Original Article
Pulmonary function assessment in the early phase of patients with smoke inhalation injury from fire
Abstract
Objectives: Fire smoke contains toxic gases and numerous chemical compounds produced by incomplete combustion, and may cause injury to the airways. Increased airway reactivity, as well as a decrease in lung function, has been reported as a sequela of smoke inhalation injury. This study was undertaken to assess lung functions in the early phase of patients with smoke inhalation damage from fires.
Methods: A total of 15 patients with fire smoke inhalation (fire smoke group) and 15 subjects with chronic cough but no previous history of lung disease (chronic cough group) were enrolled. For diagnosis of inhalation injury, we performed bronchoscopy, high-resolution computed tomography (HRCT), as well as arterial carboxyhemoglobin (COHb) at admission. Clinical characteristics, pulmonary function tests (PFTs) and mannitol bronchial provocation tests (BPTs) were analyzed and compared between the two groups.
Results: In fire smoke group, initial COHb levels and the PaO2/FiO2 ratio were (14.8±18.49)% and 425.7±123.68, respectively. Of seven patients performing HRCT, 4 (57.1%) showed the CT findings compatible with lung involvement of inhalation injury. Post bronchodilator value of the percent of forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) were (76.0±24.27)% and (79.8±27.82)%, respectively. Pre-and post- bronchodilator forced expiratory flow between 25% and 75% of the FVC (FEF25-75) and the percent predicted FEF25-75 were 2.41±1.47 vs. 2.65±1.45 L (P=0.045), and (68.7±37.29)% vs. (76.4±36.70)% (P=0.031), respectively. Two patients (13.3%) had positive bronchodilator response (BDR). In fire smoke and chronic cough group, all the subjects showed mannitol BPTs within normal limits.
Conclusions: Fire smoke inhalation leads to mild obstructive small airway disease pattern of pulmonary function in the early phase of patients with fire smoke damage. Further studies, however, need to be followed to identify the relationship between airway narrowing to inhaled mannitol and smoke inhalation injury.
Methods: A total of 15 patients with fire smoke inhalation (fire smoke group) and 15 subjects with chronic cough but no previous history of lung disease (chronic cough group) were enrolled. For diagnosis of inhalation injury, we performed bronchoscopy, high-resolution computed tomography (HRCT), as well as arterial carboxyhemoglobin (COHb) at admission. Clinical characteristics, pulmonary function tests (PFTs) and mannitol bronchial provocation tests (BPTs) were analyzed and compared between the two groups.
Results: In fire smoke group, initial COHb levels and the PaO2/FiO2 ratio were (14.8±18.49)% and 425.7±123.68, respectively. Of seven patients performing HRCT, 4 (57.1%) showed the CT findings compatible with lung involvement of inhalation injury. Post bronchodilator value of the percent of forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) were (76.0±24.27)% and (79.8±27.82)%, respectively. Pre-and post- bronchodilator forced expiratory flow between 25% and 75% of the FVC (FEF25-75) and the percent predicted FEF25-75 were 2.41±1.47 vs. 2.65±1.45 L (P=0.045), and (68.7±37.29)% vs. (76.4±36.70)% (P=0.031), respectively. Two patients (13.3%) had positive bronchodilator response (BDR). In fire smoke and chronic cough group, all the subjects showed mannitol BPTs within normal limits.
Conclusions: Fire smoke inhalation leads to mild obstructive small airway disease pattern of pulmonary function in the early phase of patients with fire smoke damage. Further studies, however, need to be followed to identify the relationship between airway narrowing to inhaled mannitol and smoke inhalation injury.
