Complete expiratory central airway collapse at general anesthesia recovery: a case report

Abstract

Expiratory central airway collapse is a degenerative tracheobronchial disease that is often overlooked because of its nonspecific clinical features. A man was admitted for evaluation of tracheal nodules. Following bronchoscopic biopsy, a significant increase in airway pressure occurred during anesthesia recovery. Laryngospasm was suspected, and tracheal intubation was performed. Bronchoscopy revealed an almost completely collapsed tracheal lumen. A Y-shaped silicone stent was placed using a rigid bronchoscope to support the airway, allowing spontaneous ventilation to resume. A retrospective review of the images suggested a diagnosis of excessive dynamic airway collapse. The silicone stent was removed after 2 weeks because of discomfort, and no subsequent dyspnea was observed. This case highlights that excessive dynamic airway collapse is easily missed. Anesthesiologists must be educated on this condition, maintain a thorough understanding of the patient’s state and illness, and have emergency airway equipment readily available to restore ventilation promptly in cases of severe airway collapse.

Introduction

Expiratory central airway collapse (ECAC) is a degenerative tracheobronchial disease that encompasses excessive dynamic airway collapse (EDAC) and tracheobronchomalacia (TBM).^1,2 EDAC involves excessive expansion of the tracheal membrane into the airway lumen during expiration without cartilage collapse, whereas TBM is characterized by collapse of the tracheobronchial cartilage.^1,3 EDAC can cause unpredictable tracheal collapse in patients under general anesthesia, potentially leading to fatal respiratory distress. ¹ The nonspecific clinical features of EDAC—such as cough, sputum retention, wheezing, and dyspnea—make it easy to overlook. This report describes a patient who experienced unexpected EDAC postoperatively despite having no respiratory discomfort before surgery and no airway collapse evident on computed tomography (CT).

Case report

The patient provided verbal informed consent for the publication of his case. The reporting of this study conforms to the CARE guidelines. ⁴ The patient’s data have been de-identified. Patient consent to biopsy was also obtained.

A male teacher in his mid-50s (body mass index, 30.5 kg/m²) was admitted to the authors’ hospital for evaluation, 3 years after a CT scan at a local hospital revealed nodules in the posterior wall of the trachea. His medical history included hypertension and fatty liver. He was a nonsmoker and reported no cough or dyspnea at admission. The admission CT scan showed no airway abnormalities (Figure 1(a), (d)), and he was scheduled for a bronchoscopic biopsy under general anesthesia.

Figure 1.

Preoperative computed tomography and intraoperative dynamic bronchoscopic images of the central airway. Preoperative transverse sectional computed tomography images of the (a) middle and (d) lower trachea during inspiration. Intraoperative bronchoscopic images of the (b) middle and (e) and lower trachea during inspiration under mechanical ventilation. Intraoperative bronchoscopy showing diffuse granular protrusions on the posterior wall of the (c) middle and (f) lower trachea during expiration under mechanical ventilation.

After premedication with phencyclidine hydrochloride 0.5 mg, anesthesia was induced with intravenous propofol 120 mg, sufentanil 30 µg, and rocuronium 30 mg. A size 4.5 laryngeal mask airway was placed. Anesthesia was maintained with propofol 350 mg/hour and dexmedetomidine 10 µg/hour to keep the entropy index between 40 and 60. Bronchoscopic evaluation revealed that the posterior wall of the middle and lower trachea and both mainstem bronchi was raised, showing diffuse granular protrusions during both the inspiratory (Figure 1(b), (e)) and expiratory (Figure 1(c), (f)) phases of mechanical ventilation. A biopsy was performed on the bulging posterior wall of the middle and lower trachea, which took 45 minutes. During anesthesia recovery, the monitor suddenly displayed a significant increase in airway pressure, loss of the end-tidal carbon dioxide waveform, and a drop in oxygen saturation (SpO₂). After checking the circuit and ruling out laryngeal mask airway displacement, the anesthesiologist initiated manual ventilation, but ventilation was unsuccessful, and the SpO₂ dropped to 90%. Suspecting laryngospasm, the anesthesiologist deepened the anesthesia and performed tracheal intubation.

The patient’s SpO₂ dropped to 20% before increasing to 92% after mechanical ventilation was restored. Repeated bronchoscopy was performed due to an airway pressure of 38 cmH₂O. Bronchoscopy revealed anterior bulging of the posterior membrane, with the tracheal lumen almost entirely collapsed (Figure 2). The right main bronchus was narrowed by more than 80%, and the left main bronchus appeared line-like and narrowed. A Y-shaped silicone stent was placed via a rigid bronchoscope to support the airway. Following the procedure, the patient’s SpO₂ improved to 98%. He was transferred to the postanesthesia care unit for recovery, during which both the SpO₂ and airway pressure returned to normal. The patient remained asymptomatic and was discharged on the second day. Pathological analysis of the biopsy revealed squamous cell metaplasia of the tracheal mucosa, and the patient was diagnosed with EDAC based on the review of intraoperative dynamic bronchoscopy images.

Figure 2.

Complete tracheal collapse observed via bronchoscopy after endotracheal intubation. (a, b) Collapse near the front of the tracheal tube tip and (c, d) Collapse in the middle trachea.

Two weeks later, the silicone stent was removed because of a persistent cough. Anesthesia for the procedure was induced and maintained with remifentanil and dexmedetomidine, supplemented with low-dose propofol and succinylcholine during induction. The operation proceeded without complications. Afterward, the patient quickly resumed spontaneous ventilation and experienced no dyspnea.

Discussion

This paper reports a case of complete ECAC during general anesthesia recovery following a bronchoscopic biopsy. Initially, the anesthesiologist suspected laryngospasm and deepened the anesthesia as a first-aid measure. When this approach failed, a Y-shaped silicone stent was placed using a rigid bronchoscope to support the airway. The patient recovered without complications and was discharged symptom-free on the second day. The diagnosis of EDAC was confirmed through a review of intraoperative dynamic bronchoscopy images.

A 50% reduction in the sagittal diameter or cross-sectional area of the airway lumen during expiration, as observed via bronchoscopy or dynamic CT, is widely recognized as a diagnostic criterion for EDAC. ⁵ However, up to 78% of healthy, asymptomatic individuals exceed the 50% threshold, leading some institutions to raise the cross-sectional area reduction threshold for ECAC diagnosis to 70%.^2,3 Diagnosing EDAC is further complicated by its nonspecific clinical presentation, which can mimic conditions such as asthma or chronic obstructive pulmonary disease. Moreover, related tests, including pulmonary function tests, lack both sensitivity and specificity.^3,6 In this case, intraoperative dynamic bronchoscopy could have facilitated an earlier diagnosis of EDAC, even before the biopsy was completed or anesthesia recovery began. However, the respiratory physician did not consider the observed airway stenosis to be clinically significant in the context of the ongoing bronchoscopy, and the anesthesiologist lacked prior experience with EDAC. As a result, the diagnosis was made retrospectively, following emergent management of the EDAC event and a review of the bronchoscopic images.

The most critical aspect of managing acute airway collapse is promptly restoring ventilation. Recommendations include using anesthesia that preserves spontaneous breathing, avoiding neuromuscular blockers, and minimizing the use of long-acting anesthetics. ¹ In cases of severe collapse with symptoms, airway stenting or tracheobronchoplasty should be considered, or extracorporeal membrane oxygenation may be necessary before anesthesia induction. For unanticipated severe ECAC, positive end-expiratory pressure–assisted positive-pressure ventilation can act as a pneumatic stent, while sugammadex can rapidly reverse muscle relaxation to restore spontaneous ventilation, with stenting or tracheotomy as additional options if required. ¹ In this case, timely deepening of anesthesia, positive-pressure ventilation after endotracheal intubation, and placement of a Y-shaped silicone stent effectively managed the crisis. While ECAC is generally a benign condition and stenting is not preferred for long-term management, a silicone stent can provide temporary relief because it is removable and minimally damaging. Persistent coughing necessitated the stent’s removal in this patient, who recovered without dyspnea; however, the degree of airway collapse post-removal was not assessed. Similar cases have been managed by using endotracheal tubes as temporary stents during inhaled general anesthesia for dental procedures. ⁷ Although silicone stents are effective in relieving ECAC-induced dyspnea, complications such as mucus obstruction, granulation tissue formation, and migration limit their long-term use.^3,8 Before placing a silicone stent, it is crucial to assess the patient’s ability to effectively clear sputum because silicone stents can lead to sputum accumulation. If the patient has difficulty expectorating, careful consideration must be given to the use of a silicone stent, and postoperative nebulized inhalation may be necessary to assist with sputum clearance. Additionally, the presence of oropharyngeal stenosis or limited neck extension must be evaluated because silicone stent placement requires the use of a rigid bronchoscope. Training anesthesiologists about the recognition and management of EDAC is essential to facilitate faster diagnosis and appropriate interventions. Early recognition of EDAC would allow timely actions, such as restoring ventilation through intubation and using a stent to maintain airway patency by repositioning the tracheal wall. Posturing may also be beneficial in managing the condition. Furthermore, innovative approaches such as laser tracheobronchoplasty and custom-designed stents are currently under investigation, but more evidence is needed to establish their effectiveness. ⁹

A previous study suggested that EDAC is common among smokers ¹⁰ ; however, the patient in this case had never smoked. It is hypothesized that long-term occupational exposure to chalk dust and second-hand smoke could also contribute to the development of EDAC, although further confirmation is required. Several factors may have played a role in the onset of severe EDAC in this patient. Rocuronium, acting on muscarinic receptors, may have caused airway smooth muscle relaxation, exacerbating airway collapse. The prolonged biopsy procedure, lasting approximately 45 minutes, could have contributed to complete tracheal collapse. Additionally, the patient’s obesity, extended supine positioning, and vigorous breathing and coughing during recovery likely increased intrathoracic pressure, further aggravating the airway collapse.^2,8

Conclusions

The key takeaway is that EDAC is often overlooked by anesthesiologists because of limited awareness and experience with the condition, underscoring the importance of targeted education. The primary management goal in such cases is to promptly restore ventilation to prevent hypoxemia or asphyxia. Assessing the degree of airway collapse preoperatively can be challenging for anesthesiologists. Therefore, they should thoroughly review the patient’s preoperative respiratory symptoms and medical history, examine imaging reports in detail, and ensure that emergency airway equipment is readily available. This preparation is vital to quickly restoring ventilation in cases of severe airway collapse, thereby preventing life-threatening complications such as hypoxemia, hypercapnia, and death.