COVID-19肺炎拔管后喘鸣:刚性气管镜优于支气管镜以避免气道损害1例

G. Palmer, D. Buus, P. Kasznica, F. Jamous
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引用次数: 0

摘要

简介:拔管后喘鸣,或拔管后吸气噪声,在拔管后患者中经常观察到,由于气道操作继发的喉部水肿。在2019冠状病毒病大流行期间,拔管后喘鸣日益引起人们的关注,因为再次插管和由此导致的不良后果的风险很高。我们报告一例在COVID-19肺炎背景下因气管粘液堵塞而引起的拔管后喘鸣。病例介绍:一名61岁女性,诊断为COVID-19肺炎,右下叶肺栓塞,左肺气胸伴胸管,因呼吸衰竭接受非创伤性插管和13天的通气支持。拔管后4天患者出现喘鸣,需氧量增加。患者给予外消旋肾上腺素0.5mL x 2次剂量,静脉注射固美醇40mg BID x 4次剂量,BiPAP维持血氧饱和度91%。软性喉镜下直接观察可见后连合处小肉芽组织,气管内有结块和干燥粘液。第二天,患者表现出更严重的喘鸣、声音嘶哑和呼吸困难。考虑支气管镜检查与气管镜检查。胸部CT显示近端气管内有中度碎片。由于担心支气管镜检查对气道的损害,患者行喉镜检查和气管镜检查,并用气道钳取出气管塞。手术后患者的喘鸣和声音嘶哑得到改善,在出院前的2 - 3天内氧气需求下降。讨论:拔管后喘鸣可发生在近10%的重症监护病房患者,通常是由于喉水肿。在本病例中,我们的患者接受了类固醇和外消旋肾上腺素治疗来解决这个可能的原因,但没有临床改善。胸部CT进一步表征,发现近端气管内有中度碎片。我们假设气管碎片堆积是由于COVID-19疾病、长时间插管和无力咳嗽无法清除气道分泌物所致。既往研究表明,COVID-19肺炎可引起双侧弥漫性肺泡损伤,纤维黏液样渗出导致气道粘液过多。这种多余的粘液导致气道阻力增加和肺泡气体交换减少。危重疾病后的虚弱和长时间插管可能导致患者无法清除这些分泌物,导致气管积聚,氧气需求增加和喘鸣。气管碎片患者的支气管镜检查和/或插管可能是有害的,因为气管内管阻塞或粘液塞移动到远端支气管和随后的呼吸衰竭。因此,在评估拔管后的喘鸣时保持广泛的鉴别诊断非常重要,特别是在COVID-19肺炎患者中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Post-Extubation Stridor in COVID-19 Pneumonia: A Case for Rigid Tracheoscopy Over Bronchoscopy to Avert Airway Compromise
Introduction: Post-extubation stridor, or inspiratory noise following extubation, is frequently observed in patients post-extubation, due to laryngeal edema secondary to airway manipulation. Post-extubation stridor is of increasing concern during the COVID-19 pandemic, as risk for re-intubation and consequent poor outcome is high. We present a case of post-extubation stridor due to tracheal mucus plugging in the setting of COVID-19 pneumonia. Case Presentation: A 61-year-old female diagnosed with COVID-19 pneumonia, right lower lobe pulmonary embolus, and left lung pneumothorax with chest tube experienced a nontraumatic intubation and 13 days of ventilatory support due to respiratory failure. Four days following extubation patient developed stridor and increased oxygen requirement. Patient was given racemic epinephrine 0.5mL x two doses and IV solumedrol 40mg BID x four doses, maintaining oxygen saturation >91% on BiPAP. Direct visualization under flexible laryngoscopy showed small granulation tissue in posterior commissure and concretions and dried mucus in the trachea. The following day, patient displayed worsening stridor, hoarseness, and respiratory difficulty. Bronchoscopy versus tracheoscopy was considered. CT chest displayed moderate debris within the proximal trachea. Due to concern for airway compromise with bronchoscopy, patient underwent laryngoscopy and tracheoscopy with tracheal plug removal by airway forceps. Stridor and hoarseness improved following procedure;oxygen requirements declined in following two-three days leading to discharge. Discussion: Post-extubation stridor can occur in nearly 10% of intensive care unit patients, frequently due to laryngeal edema. In the present case, our patient underwent steroid and racemic epinephrine therapy to address this possible cause with no clinical improvement. Chest CT was performed for further characterization, which discovered moderate debris within the proximal trachea. We hypothesize the tracheal debris accumulation was due to illness with COVID-19, prolonged intubation, and a weak cough unable to clear airway secretions. Previous studies have shown that COVID-19 pneumonia causes bilateral diffuse alveolar damage with fibromyxoid exudates leading to excessive airway mucus. This excess mucus leads to increased airway resistance and decreased alveolar gas exchange. Weakness after critical illness and prolonged intubation likely contributed to our patient's inability to clear these secretions, leading to tracheal accumulation, increased oxygen requirement, and stridor. Bronchoscopy and/or intubation in patients with tracheal debris may be detrimental due to endotracheal tube obstruction or mucus plug mobilization into distal bronchi and subsequent respiratory failure. Therefore, it is important to maintain a broad differential diagnosis while assessing stridor after extubation, particularly in patients with COVID-19 pneumonia.
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