1 Department of Internal Medicine, 2 Lung Research Institute, Hallym University College of Medicine, Chuncheon, Korea.
J Thorac Dis. 2014 Jun;6(6):617-24. doi: 10.3978/j.issn.2072-1439.2014.04.11.
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.
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.
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.
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.
火灾产生的烟雾中含有不完全燃烧产生的有毒气体和大量化学物质,可能会对气道造成损伤。吸入烟雾损伤后的后遗症包括气道反应性增加和肺功能下降。本研究旨在评估火灾吸入性损伤患者早期的肺功能。
共纳入 15 名火灾吸入性烟雾(火灾烟雾组)患者和 15 名患有慢性咳嗽但无肺部疾病既往史的患者(慢性咳嗽组)。为诊断吸入性损伤,我们在入院时进行了支气管镜检查、高分辨率计算机断层扫描(HRCT)以及动脉血碳氧血红蛋白(COHb)检测。分析比较两组的临床特征、肺功能检查(PFTs)和甘露醇支气管激发试验(BPTs)。
在火灾烟雾组中,初始 COHb 水平和 PaO2/FiO2 比值分别为(14.8±18.49)%和 425.7±123.68。7 名进行 HRCT 的患者中,有 4 名(57.1%)显示符合吸入性损伤肺部受累的 CT 表现。支气管扩张剂后用力肺活量(FVC)的百分比和 1 秒用力呼气量(FEV1)分别为(76.0±24.27)%和(79.8±27.82)%。支气管扩张剂前后 25%至 75%用力肺活量之间的呼气流量(FEF25-75)和预测值 FEF25-75 分别为 2.41±1.47 与 2.65±1.45 L(P=0.045)和(68.7±37.29)%与(76.4±36.70)%(P=0.031)。2 名患者(13.3%)出现阳性支气管扩张剂反应(BDR)。在火灾烟雾组和慢性咳嗽组中,所有患者的甘露醇 BPTs 均在正常范围内。
火灾吸入烟雾导致火灾烟雾损伤患者早期出现轻度阻塞性小气道功能障碍。然而,需要进一步研究来确定气道对吸入甘露醇的狭窄与烟雾吸入损伤之间的关系。