A Rare Mechanism of Inhalation Injury: Direct Thermal Damage to the Lower Airway

In patients with inhalation injury associated with major burns, the primary mechanism of tissue harm depends on the location within the respiratory tract. Proximal to the trachea, the upper respiratory tract epithelium is classically injured via direct thermal injury. Such injury occurs due to the inhalation of high-temperature air. These upper airway structures and the tracheobronchial tree’s dense vasculature protect the lower airways and lung parenchyma from direct thermal damage. The lower respiratory tract epithelium and lung parenchyma typically become injured secondary to the cytotoxic effects of chemical irritants inhaled in smoke as well as delayed inflammatory host responses. This paper documents a rare case in which a patient demonstrated evidence of direct thermal injury to the lower respiratory tract epithelium. A 26-year-old Caucasian male presented to the emergency room with 66% total body surface area thermal burns and grade 4 inhalation injury after a kitchen fire. Instead of visualizing carbonaceous deposits in the bronchi, a finding common in inhalation injury, initial bronchoscopy revealed bronchial mucosa carpeted with hundreds of bullae. Despite the maximum grade of inhalation injury per the abbreviated injury score and a 100% chance of mortality predicted with the revised Baux score, as well as a clinical course complicated by pneumonia development, bacteremia, and polymicrobial external wound infection, this patient survived. This dissonance between his expected and observed clinical outcome suggests that the applicability of current inhalation injury classification systems depends on the precise mechanism of injury to the respiratory tract. The flaws of these grading scales and prognostic indicators may be rooted in their failure to account for other pathophysiologic processes involved in inhalation injury. It may be necessary to develop new grading and prognostic systems for inhalation injury that acknowledge and better account for unusual pathophysiologic mechanisms of tissue damage.