Breathing on the Brink: Emergent Tracheostomy for Undiagnosed Subglottic Stenosis

INTRODUCTION

Sub-glottis is the part of the upper airway extending from below the vocal cords to the lower border of the cricoid cartilage. It is the only part of the upper airway encircled by a complete cartilaginous ring- the cricoid cartilage. The sub-glottic mucosa comprises pseudostratified ciliated columnar epithelium, basement membrane and lamina propria, which is rich in fibroblasts and leukocytes.¹ These factors render the sub-glottis more susceptible to inflammation, fibrosis, scarring and stenosis, resulting in narrowing of the airway at this level.²

Sub-glottic stenosis can be congenital, acquired, or idiopathic, of which acquired sub-glottic stenosis is the most common type. The aetiology of acquired sub-glottic stenosis is multifactorial and includes prolonged intubation or tracheostomy, trauma, gastroesophageal reflux disorder (GERD), inhalational injuries, autoimmune diseases like granulomatosis with polyangitis, sarcoidosis, and systemic lupus erythematosus.^3,4 Iatrogenic Sub-glottic stenosis was first theorised in 1969 to be the result of tissue ischemia due to excessive endotracheal tube cuff pressures compromising mucosal blood flow, leading to sub-glottic inflammation, scarring, fibrosis and eventual stenosis.⁵ Though rare, the incidence of post-intubation sub-glottic stenosis is estimated to be 4.9 cases per million per year.⁶ The primary diagnosis often gets delayed and misdiagnosed as asthma or chronic bronchitis until intubation is attempted.⁷ We report one such case of failed intubation in the emergency department secondary to undiagnosed sub-glottic stenosis.

CASE REPORT

A 24-year-old male presented to the emergency department with shortness of breath for two days, which was gradually progressive in nature. The patient was tachypneic with an oxygen saturation of 85% at room air and 98 % with 8 litres of oxygen through a face mask. There was no chest rise with the patient using neck and abdominal muscles for respiration, and the chest was silent on auscultation. Arterial blood gas (ABG) showed type 2 respiratory acidosis. He was initially diagnosed with possible exacerbation of obstructive airway disease based on the above findings and started on nebulization with beta agonists and inhaled corticosteroids. As the patient did not improve, noninvasive ventilation (NIV) with bi-level positive airway pressure (BiPAP) was initiated. Past history was significant for a two-month period prior to endotracheal intubation for a duration of 12 days in view of traumatic head injury.

The patient was becoming restless and could not tolerate NIV (non invasive ventilation). Endotracheal intubation was planned, and on direct laryngoscopy, a Cormack Lehane grade 1 view of the glottis was visualised.⁸ Bougie assisted intubation was attempted with an 8.0 endotracheal tube, which failed. This was followed by serial unsuccessful attempts with 7.0, then 6.0 and lastly 5.5 sizes of endotracheal tube by a senior emergency physician. The patient had a hypoxic cardiac arrest, and cardiopulmonary resuscitation (CPR) was initiated. Return of spontaneous circulation could be achieved after one cycle of CPR. The failed airway algorithm was followed, and a laryngeal mask airway was placed and connected to the mechanical ventilator at this point, and the patient started maintaining saturations. Simultaneously, an airway ultrasound was done, which showed a narrowed sub-glottic diameter. Following this, with a probable differential of sub-glottic stenosis in mind, where emergency cricothyrotomy would not be helpful, an emergency tracheostomy was done under local anaesthesia at the bedside. A tracheostomy tube of size 7.0 was secured in place, and the patient was placed back on mechanical ventilation. The patient was transferred to the intensive care unit, where he remained stable, with improvement in Glasgow Coma Scale (GCS) to 15. Once stabilised, a contrast-enhanced CT neck was done, which was suggestive of near-complete sub-glottic stenosis for a length of 15 mm, with a residual lumen measuring 2 mm. [Figures 1 and 2] He was discharged on day 5 with a tracheostomy tube in situ in a neurologically intact state post-CPR and advised to see an otolaryngologist. The timeline of events is described in Table 1.

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Figure 1:

Antero-posterior view of contrast-enhanced CT neck with the red arrow showing the site of maximum stenosis. CT: Computed tomography

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Figure 2:

Sagittal view of contrast-enhanced CT neck with yellow arrow showing the site of maximum stenosis. CT: Computed tomography

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DISCUSSION

Acquired sub-glottic stenosis occurs as a result of trauma to the mucosal layers of the trachea that leads to scarring and formation of granulation tissue over time. Prolonged endotracheal intubation is a common cause of acquired subglottic stenosis with a documented incidence of 1-8 %.^9,10

The severity of sub-glottic stenosis is given by the Cotton-Myer grading system.¹¹ [Table 2]

Table 2: Cotton-Myer grading system for sub-glottic stenosis

These patients with sub-glottic stenosis usually present to the emergency room with symptoms of upper airway obstruction like dyspnea, wheeze, stridor and cough, which might rapidly progress to cardiopulmonary arrest unless the airway is secured emergently.¹²

This patient had a grade 3 sub-glottic stenosis, likely secondary to previous intubation, which remained undiagnosed until he presented to the emergency room with acute respiratory distress. The diagnosis of sub-glottic stenosis causing upper airway obstruction had not been in the differential diagnosis initially due to the absence of the usual signs of upper airway obstruction. The trial of non-invasive ventilation had failed due to lack of patient cooperation, and this was followed by several attempts at endotracheal intubation, which resulted in failed intubation and possibly exacerbated his airway oedema. At this point, an airway ultrasound was done, and the possibility of sub-glottic stenosis was added to the differential diagnosis. Emergency surgical tracheostomy was decided as the method of choice for securing the airway.

An undiagnosed subglottic stenosis presents significant challenges in an emergent setting, including misdiagnosis as obstructive airway disease, delayed definitive airway management, difficult endotracheal intubation, and the need for emergent surgical airway instead of a planned elective surgical management.¹³ There are several options available in our armamentarium for securing the airway in these patients, including fibreoptic intubation, cricothyrotomy and tracheostomy. Though a good modality in elective settings, allowing for visualisation and assessment of the stenosis, fibreoptic bronchoscopy is time-consuming and impractical in the emergent setting. Between cricothyrotomy and tracheostomy, despite cricothyrotomy being the first line of management in a “cannot intubate, cannot oxygenate” situation, the stenosis often involves the cricothyroid membrane, rendering this procedure difficult. Hence, in higher grades of subglottic stenosis, tracheostomy is the preferred choice in an emergent situation.¹⁴ An earlier recognition of sub-glottic stenosis and an earlier airway ultrasound might have led to securing the airway earlier through front-of-neck-airway and would have helped avoid prolonged resuscitation and hypoxic cardiopulmonary arrest.

CONCLUSION

Few reports exist where emergency tracheostomy was done by the emergency physician in the emergency department for previously undiagnosed sub-glottic stenosis. This case shows why it is crucial for emergency physicians to consider sub-glottic stenosis in the differential diagnosis of airway obstruction with acute respiratory distress and perform early airway ultrasound, especially in patients with a previous history of endotracheal intubation.