Airway leak syndrome occurs when air escapes from the lung into extra-alveolar spaces causing respiratory symptoms. A variety of clinical presentations may be seen depending on the location of the air, which can include pneumothorax, pneumomediastinum, pulmonary interstitial emphysema, and pneumopericardium. Known predisposing factors for airway leak syndrome are prematurity, RDS, and bronchitis [
7]. Our case was a 27-week-old premature infant with RDS but had no signs of bronchitis like fever or leukocytosis.
Pulmonary barotrauma can be another cause of airway leak syndrome; though, large airways are less likely to be damaged by barotrauma, with injury more commonly affecting the distal airways. The pathophysiology of barotraumatic air leak typically begins with overdistended alveoli, leading to alveoli rupture, not bronchial rupture [
11]. Among iatrogenic causes, the most common etiology of tracheobronchial injury is acquired damage during intubation [
12]. In our case, this preterm infant was intubated immediately after birth, re-intubated on his 3rd day, and subsequently deteriorated on day 5. It is not suspected that injury occurred from intubation, as the deterioration started 2 days after re-intubation and, endotracheal tube was in the proper position on all imaging studies. There are previously reported pediatric cases of premature neonates who were intubated and experienced air leaks with endotracheal tube suctioning [
8,
9]. The mechanism of injury in these reports were mainly from tissue trauma causing perforations in the trachea or the right bronchial tree. The respiratory system’s cartilage tissue development begins anywhere from the 51-54th day of gestational life. According to Carnegie staging, tracheal cartilage tissue development starts as a ventromedial mesenchymal condensation and continues throughout pregnancy until it reaches its mature characteristic horseshoe shape, which wraps around the trachea 320 degrees [
13]. However, in preterm neonates, the immaturity of this cartilagenous tissue makes the trachea more susceptible to rupture. Eckenhoff et al. describes that, unlike adults, the cricoid ring is the narrowest part to encounter during any airway intervention until the age of 8 [
14]. Additionally, the cricoid ring mucosa lacks submucosa, making this location particularly vulnerable to iatrogenic damage from an instrument. The anatomical position of the cricothyroid membrane is also forced into a cephalic shape, in contrast to a cylinder shape in adults. Due to this difference in position, if the cricothyroid membrane is iatrogenically penetrated, perforation is expected to lead into the glottic area, not the trachea [
14].In our case, the location of the rupture was between the carina and the left bronchus, which is the cartilaginous anteroinferior part of the bronchus, drawing us away from the possibility of barotraumatic etiology. Although the exact cause of the large bronchial rupture remains unknown, we suspect the suction catheter used for endotracheal aspiration perforated the carina, given the fragility of the cartilaginous tissue, as described above.