A 1 day old, 560 g female, 23 weeks and 6 days gestation developed labored breathing immediately after birth. Intubation was deemed necessary and the NICU team proceeded with direct laryngoscopy. Despite a grade I Cormack Lehane view with visualization of the endotracheal tube (ETT) traversing the glottic inlet, three attempts yielded no end-tidal carbon dioxide (EtCO₂) on capnography. After confirming functional capnography equipment, video laryngoscopy was tried. No supraglottic and glottic abnormalities were identified, and correct ETT placement was directly visualized, however EtCO₂ remained undetectable. The NICU team did not comment on chest rise with positive pressure or bilateral breath sounds on auscultation after intubation. The patient was extubated and temporized on nasal BiPAP (Pinsp of 16 cmH₂O, positive end expiratory pressure of 6 cmH₂O and FiO₂ of 0.4) and transferred to our pediatric hospital for urgent rigid bronchoscopy to evaluate for tracheoesophageal fistula (TEF).

To facilitate bronchoscope insertion, we provided deep sedation while maintaining spontaneous ventilation. This was challenging given the size of the patient. We accomplished this by administering dexmedetomidine (diluted to 1 mcg/ml) boluses incrementally, totaling 4 mcg/kg IV, in addition to a propofol (diluted to 2.5 mg/ml) infusion at 300 mcg/kg/min. Bronchoscopy demonstrated an edematous epiglottis (Fig. 1A), 2 lacerations on the posterior pharyngeal wall (Fig. 1B), and mild tracheomalacia (Fig. 1C, D), however, no TEF was identified. Additionally, successful orogastric tube placement made esophageal atresia unlikely. The trachea was then intubated using a Wisconsin 00 laryngoscope with an uncuffed 2.5 mm ETT over a 2 mm telescope with care taken to maintain tube depth at 7 cm. However, no chest-rise, bilateral breath sounds on auscultation or EtCO₂ was observed with subsequent manual ventilation. When the inspiratory pressure applied during manual ventilation was increased to 40 cmH₂0, lack of EtCO₂ remained. The patient was briefly turned into a lateral decubitus position with continued ventilation to rule out mass effect given the lack of preoperative echocardiography, but this was to no avail. A suction catheter could not be passed down the 2.5 mm ETT given its small size. After a min of high peak inspiratory pressure with shorter inspiratory times, a subtle increase in chest-rise was observed and EtCO₂ was detected. The procedure was complicated by a brief episode of severe hypoxemia (SpO₂ 37%) and bradycardia (HR 20) during bronchoscopy (Fig. 2), for which epinephrine 1 mcg/kg was given. After stabilization, the patient was transferred to the NICU for further monitoring. During the patient’s hospital course, a hemodynamically significant patent ductus arteriosus (PDA) was identified by echocardiogram and confirmed by cardiac catheterization. The patient returned to the operating room for thoracotomy and patent ductus arteriosus closure, which was uncomplicated.

To our knowledge, this is the first report of an extremely premature un-intubated micropremie requiring rigid bronchoscopy with goals of maintaining spontaneous ventilation. Aspects of this case that make it uniquely challenging include the combination of: (i) a micropremie with failed detection of EtCO₂ on repeated successful intubations with suspicion of TEF; (ii) need for an TIVA technique to maintain spontaneous ventilation for airway surgery (iii) need for positive pressure ventilation post intubation with no prior surfactant administration in an extremely premature neonate with suspected NRDS; (iv) no preoperative echocardiogram done given the urgency of the case. When confirmation of successful endotracheal intubation using standard clinical measures such as capnography was delayed, a broad differential diagnosis was considered, including technical, anatomical, and pathophysiological causes. Ultimately, when higher peak inspiratory pressure was applied during manual ventilation to overcome the intrinsic resistance of poorly compliant, surfactant-deficient alveoli, EtCO₂ was detected, confirming successful intubation, and implying effective ventilation. The presence of a hemodynamically significant PDA could have contributed to the lack of EtCO₂ post-intubation with high positive pressure ventilation, but the lack of chest rise, or presence of bilateral breath sounds on auscultation, make this sole cause less likely.

Quantitative capnography is a valuable and feasible monitoring modality, notwithstanding its limitations when applied to the premature neonatal population [1]. The absence of EtCO₂ following intubation prompts consideration of a broad differential, including dysfunctional capnography equipment as well as various patient factors and conditions. Intubation in extremely premature neonates is technically challenging owing to small maneuverability. However, ETT placement over a telescope ruled out esophageal intubation in our case. It is essential to consider TEF or associated airway anomalies in the differential diagnosis of lack of EtCO₂ following intubation of a neonate. In our case, this was ruled out by performing urgent diagnostic bronchoscopy with successful orogastric tube placement [2]. Finally, conditions which may present as an inability to detect EtCO₂, including severe bronchospasm, laryngospasm, obstructive shock, and cardiovascular collapse, were inconsistent with our clinical scenario. In our case, failure to detect EtCO₂ implied ineffective ventilation secondary to reduced lung compliance and marked adhesive atelectasis in the setting of surfactant deficiency.

A common cause of respiratory failure in neonates is NRDS. Anesthesiologists should consider this condition and its implications on airway management and respiratory function when caring for premature neonates. The mainstay of treatment in NRDS is endotracheal surfactant replacement [3]. Endotracheal surfactant replacement (200 mg/kg) is indicated when NRDS is suspected and has been shown to reduce morbidity and mortality [4]. This intervention may have optimized conditions for ventilation. Furthermore, we postulate that mechanistically, surfactant therapy given upfront may have prevented the delay in detecting EtCO₂ by mitigating the development of adhesive atelectasis. Previous studies have shown that the difference between measured EtCO₂ and PaCO₂ decreases following endotracheal surfactant administration, which supports our hypothesis [5]. Surfactant administration may have also mitigated the need for high inspiratory pressures, and the resulting risk of barotrauma. From an institutional case, it was atypical that intubation did not occur in the NICU prior to transfer, resulting in no pre-operative surfactant administration.

Our case overviews considerations for airway management in micropremies with suspected NRDS and illustrates the importance of multidisciplinary collaboration to promote favorable outcomes for micropremies.