Excessive dynamic airway collapse leading to cardiac arrest due to airway obstruction

IF 1.5 Q2 MEDICINE, GENERAL & INTERNAL
Shinichi Kida, Reiki Kumashiro, Naoki Yonezawa
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引用次数: 0

Abstract

An 85-year-old woman (body mass index 30.7 kg/m2), a never-smoker with a two-year history of a seal-like barking cough, presented with sudden-onset dyspnea. Examination revealed a respiratory rate of 21 breaths/min, expiratory wheezing, and an oxygen saturation of 90% on room air. Chest radiography revealed superior mediastinal widening with rightward tracheal deviation (Figure 1A), later attributed to an incidental thoracic aortic aneurysm. Computed tomography revealed pronounced posterior tracheal membrane collapse (Figure 1B) in the absence of emphysema. Shortly after imaging, the patient experienced a severe coughing episode, followed by stridor, choking, and cardiac arrest. Spontaneous circulation was restored after one cardiopulmonary resuscitation cycle and emergency intubation. Fiberoptic bronchoscopy (Video S1), performed with pressure support (positive end-expiratory pressure of 5 cm H2O), showed a normal trachea during inspiration (Figure 1C) and pronounced posterior wall bulging during expiration (Figure 1D). These findings confirmed severe excessive dynamic airway collapse (EDAC), implicated in the cardiac arrest. On day 11, an uncovered self-expanding metallic stent was placed in the trachea, enabling successful extubation.

EDAC, often underdiagnosed, can mimic or coexist with inflammatory airway diseases.1 It is characterized by expiratory collapse of the posterior membranous tracheal wall, hypothesized to result from an imbalance between intraluminal and pleural pressures, exacerbated by reduced wall tone and pressure drops caused by the Bernoulli effect in tapering airways,2 particularly when elastic recoil is reduced.3, 4

The authors declare no conflicts of interest.

Approval of the research protocol: None.

Informed consent: Published with the written consent of the patient.

Registry and the registration no. of the study/trial: None.

Animal studies: None.

Abstract Image

过度动态气道塌陷,因气道阻塞导致心脏骤停
85岁女性(体重指数30.7 kg/m2),从不吸烟,有两年海豹样吠叫性咳嗽史,表现为突发性呼吸困难。检查显示呼吸频率为21次/分钟,呼气性喘息,室内空气氧饱和度为90%。胸片显示上纵隔增宽伴气管右偏(图1A),后归因于偶发的胸主动脉瘤。在没有肺气肿的情况下,计算机断层扫描显示明显的气管后膜塌陷(图1B)。成像后不久,患者出现严重咳嗽,随后是喘鸣、窒息和心脏骤停。经1个心肺复苏周期及紧急插管后,患者恢复自主循环。在压力支持下(呼气末正压5cm H2O)进行的纤维支气管镜检查(视频S1)显示吸气时气管正常(图1C),呼气时气管后壁明显膨大(图1D)。这些发现证实了严重的过度动态气道塌陷(EDAC),涉及心脏骤停。第11天,气管内放置无盖自膨胀金属支架,成功拔管。EDAC常被误诊,可与炎性气道疾病相似或共存它的特征是气管后膜壁的呼气塌陷,假设是由腔内和胸膜压力不平衡引起的,壁张力降低和逐渐变细的气道中的伯努利效应引起的压力下降加剧,特别是当弹性后坐力减少时。3,4作者声明无利益冲突。研究方案批准:无。知情同意:经患者书面同意发表。注册表及注册编号研究/试验:无。动物实验:没有。
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来源期刊
Acute Medicine & Surgery
Acute Medicine & Surgery MEDICINE, GENERAL & INTERNAL-
自引率
12.50%
发文量
87
审稿时长
53 weeks
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