Facciolongo Nicola, Menzella Francesco, Lusuardi Mirco, Piro Roberto, Galeone Carla, Castagnetti Claudia, Cavazza Alberto, Carbonelli Cristiano, Zucchi Luigi, Salsi Pier Paolo
Pulmonology Unit, Department of Cardiology, Thoracic and Vascular Surgery and Critical Care Medicine, Azienda Ospedaliera ASMN, Istituto di Ricovero e Cura a Carattere Scientifico, Reggio Emilia, Italy.
Respiratory Rehabilitation, AUSL Reggio Emilia, S. Sebastiano Hospital, Reggio Emilia, Correggio Italy.
Multidiscip Respir Med. 2015 Mar 8;10(1):9. doi: 10.1186/s40248-015-0002-7. eCollection 2015.
Bronchial thermoplasty (BT) is a new therapeutic option for severe refractory asthma not controlled despite high dose inhaled corticosteroids plus long-acting bronchodilators and omalizumab in selected cases. Risk of pulmonary atelectasis after BT in severe asthma has been described in literature, but no details have been reported on the possible mechanisms of the complication.
A 49-year-old male with severe uncontrolled asthma was referred to BT. One hour after the first procedure, acute respiratory failure occurred with PaO2/FiO2 < 300. A CT scan showed atelectasis of the right lower and middle lobes. A new bronchoscopy was performed under non-invasive ventilation; the right lower and middle lobe bronchus were occluded by bronchus-shaped plugs, that were very difficult to remove despite repeated saline washings and fragmentation with forceps. The patient had a rapid resolution of respiratory failure. Four weeks later, 6 hours after the second session of BT, severe bronchospasm occurred with respiratory failure. Chest X-Ray showed atelectasis of the left lower lobe, prompting to perform a new flexible bronchoscopy on non-invasive ventilation. The exam showed again a plug occluding the left lower lobar bronchus, removed with forceps and washings. The histological analysis of the plugs demonstrated the massive presence of fibrin with mucus debris, rare Charcot-Leyden crystals, scattered macrophages, neutrophils, eosinophils and bronchial epithelial cells.
The originality of our case report is related to the recurrence of bronchial plugging with lobar atelectasis within one and five hours respectively, after two sequential BT procedures. At the histological evaluation the bronchial plugs appeared very different from the typical mucoid asthma plugs, being composed prevalently by fibrin. It can be hypothesized that intense thermal stimulation of the bronchial mucosa may represent a strong boost for inflammation in susceptible patients, with microvascular alteration induced directly by heat or through the release of mediators. Although in severe asthma a risk of atelectasis from the classical asthma mucoid plugs may be expected, the peculiarity of our case resides in the formation of fibrin plugs whose direct correlation with BT should be considered.
支气管热成形术（BT）是一种针对重度难治性哮喘的新治疗选择，在某些病例中，尽管使用了高剂量吸入性糖皮质激素加长效支气管扩张剂以及奥马珠单抗，但哮喘仍未得到控制。文献中已描述了重度哮喘患者接受BT治疗后发生肺不张的风险，但尚未详细报道该并发症的可能机制。
一名49岁重度未控制哮喘男性患者接受了BT治疗。首次治疗后1小时，患者出现急性呼吸衰竭，动脉血氧分压/吸入氧分数值（PaO2/FiO2）<300。CT扫描显示右下叶和中叶肺不张。在无创通气下进行了一次新的支气管镜检查；右下叶和中叶支气管被支气管样栓子阻塞，尽管反复用生理盐水冲洗并用钳子破碎，栓子仍很难清除。患者呼吸衰竭迅速缓解。四周后，在第二次BT治疗6小时后，患者发生严重支气管痉挛并伴有呼吸衰竭。胸部X线显示左下叶肺不张，促使在无创通气下再次进行柔性支气管镜检查。检查再次显示一个栓子阻塞左下叶支气管，用钳子和冲洗将其清除。栓子的组织学分析显示大量纤维蛋白与黏液碎片、罕见的夏科-莱登结晶、散在的巨噬细胞、中性粒细胞、嗜酸性粒细胞和支气管上皮细胞。
我们病例报告的独特之处在于，在连续两次BT治疗后，分别在1小时和5小时内出现了伴有肺叶肺不张的支气管阻塞复发。在组织学评估中，支气管栓子与典型的黏液性哮喘栓子非常不同，主要由纤维蛋白组成。可以推测，对支气管黏膜的强烈热刺激可能是易感患者炎症的强大促进因素，热直接或通过介质释放诱导微血管改变。尽管在重度哮喘中可能预期会因经典的哮喘黏液栓子而发生肺不张，但我们病例的独特之处在于形成了纤维蛋白栓子，应考虑其与BT的直接相关性。
