EDAC can become unexpectedly severe such that mechanical ventilation becomes difficult and the resulting hypoxia and hypercapnia are life-threatening. Smoking, chronic inflammation, administration of steroids or beta-agonists, and ischemia (caused, for example, by introducing the endotracheal tube, tracheostomy, thyroid tumor, or vascular anomaly) can lead to degeneration of the smooth muscle fibers in the posterior membrane of the tracheobronchial tree [1, 2]. As air travels in the direction of the larynx, the intraluminal pressure decreases from alveolus toward the larynx during expiration. Because the smooth muscle of the trachea and main bronchi is affected with atrophies in EDAC patient, the posterior membrane bulges toward the anterior wall at the part where the intraluminal pressure is below the intrathoracic pressure [1]. One study found the prevalence of EDAC defined by expiratory airway collapse ≥ 75 to be 1.6% (1/62) in non-smokers without obstructive lung disease and 30.7% (62/202) in non-smokers with asthma [3]. Our patient may have been prone to EDAC because of her untreated asthma. The same study also reported the prevalence of EDAC to be 6.8% in a mild asthma group and 69.2% in a severe asthma group [3], indicating that patients with more severe asthma are at higher risk of EDAC.
However, EDAC is not widely recognized by anesthesiologists, probably because it is not clinically serious unless there is a significant narrowing of the airway. The symptoms of airway narrowing are paroxysmal cough, wheeze, and stridor [4]. Those symptoms are also common in asthma and chronic obstructive pulmonary disease. Given the slow progression of EDAC, patients may not notice airway narrowing in everyday life. Although our patient did not have symptoms suggesting airway collapse before surgery during spontaneous breathing, general anesthesia with neuromuscular blockade seemed to cause an increase in intrathoracic pressure, leading to worsening of airway collapse. Furthermore, the choice of sevoflurane and administration of a bronchodilator might have worsened the EDAC by causing relaxation of the smooth muscle.
There has been another report of expiratory central airway collapse after induction of general anesthesia with isoflurane [5]. However, in that case, collapse affected in a limited portion of the trachea, as demonstrated by immediate improvement after the endotracheal tube was advanced 3 cm further down the trachea. In contrast, our case had more severe collapse, extending from the trachea to the main bronchi, as evident from our review of the preoperative CT scans. Our patient was extubated on POD 11. We speculate that improvement in the ileus and a return to spontaneous breathing may have helped reduce the intrathoracic pressure, leading to the improvement of EDAC.
Dynamic bronchoscopy or paired inspiratory-dynamic expiratory CT is often used for the diagnosis of expiratory central airway collapse [4]. In our case, we first detected the airway collapse using bronchoscopy. This incident diagnosis of EDAC was also supported by preoperative non-dynamic CT findings. Non-dynamic CT scans are usually acquired during breath-holding in the end-inspiratory phase, so images of expiratory airway collapse would not usually be obtained. However, the patient’s chest might have been scanned during the expiratory phase due to tachypnea and cognitive decline. Harada et al. [6] also reported incidental detection of EDAC with non-dynamic CT.
PEEP can serve as a useful pneumatic stent if EDAC is suspected during general anesthesia, as in our case. Lyaker et al. [7] reported a case in which EDAC consistently worsened soon after extubation. In severe cases, noninvasive positive pressure ventilation might be necessary after extubation; this was not needed in our patient after extubation, probably because we continued mechanical ventilation until she had recovered satisfactorily. Some reports describe the use of PEEP of 6–10 cmH2O as treatment for EDAC not related to anesthesia [6, 8]. In another study, expiratory flow in children with TBM improved at noninvasive positive expiratory pressures of 5, 10, and 15 cmH2O but worsened at 20 cmH2O [9]. Although these were not cases of intraoperative EDAC, PEEP of 5–15 cmH2O may be adequate to improve EDAC that occurs during general anesthesia. In our case, we carefully added PEEP of 5 cmH2O and were able to decrease the PIP. However, it is possible that a higher PEEP could have further improved the airway obstruction. If a mechanical ventilator has a function of displaying flow-volume loops, the lowest PEEP value that can get the highest maximum expiratory flow will be a suitable setting. Considering the patient had already presented a hypoxia and a pleural effusion before the operation, we probably should have applied PEEP when mechanical ventilation was initiated.
