The Whimsical Nature of Airway Obstruction during Drug-Induced Sleep Endoscopy

INTRODUCTION

Drug-induced sleep endoscopy (DISE) is used in the evaluation of obstructive sleep apnea (OSA) to characterize the anatomic location and pattern of upper airway collapse. DISE exams are utilized to guide patient selection for positive-airway-pressure-alternative treatment, however outcomes are variable. More recently, our group has applied objective measures of airflow and respiratory effort to the DISE exam¹ which can alter surgical decision-making.² Herein, we present a DISE exam in which the addition of quantitative airflow and pressure measurements demonstrated multiple, dynamically moving sites of pharyngeal collapse which were associated with changes in respiratory effort.

CASE REPORT

A 47-year-old man with a BMI of 28 kg/m² presented with severe OSA (apnea-hypopnea index [AHI] 46 events/hour) by in-lab polysomnography. He could not tolerate continuous positive airway pressure (CPAP) therapy and sought an evaluation for hypoglossal nerve stimulation (HGNS). To determine candidacy for upper airway surgical intervention, including HGNS, the patient underwent an enhanced DISE protocol (University of Pennsylvania IRB: 849542).¹ In brief, the patient was anesthetized with propofol, then two Mikro-Cath pressure catheters (Millar Inc, Houston, TX) were positioned 1) just inferior to the distal rim of the soft palate and 2) posterior to the epiglottic petiole. Finally, a nasal CPAP mask was connected to pneumotachometer that monitored airflow (Figure 1).

Figure 1:

The enhanced recording platform integrates nasolaryngoscopy video with synchronized upper airway physiology tracings including nasal airflow and pharyngeal manometry via catheters just distal to the soft palate (P_US) and posterior to the epiglottic petiole (P_DS).

Once the patient had reached the targeted plane of anesthesia, a baseline examination was performed to determine the sites and severity of upper-airway collapse. A three-minute snapshot of nasal airflow, catheter pressures, endoscopic images, and blood oxygen saturation during the baseline exam is shown in Figure 2. This patient demonstrated three distinct patterns of upper airway collapse during two successive apneas. The first apnea, shown in Figure 2A, endoscopic footage displayed partial collapse of the tongue-base and complete collapse of the epiglottis. Nasal airflow and pharyngeal manometry measurements confirmed that the flow limiting site was located between the upstream catheter (shown in blue) and the downstream catheter (shown in green). The negative pressure generated by a contracting diaphragm was registered only by the downstream catheter while the upstream catheter and airflow remained flat (zero).

Figure 2:

A three-minute snapshot of this patient’s DISE. Three illustrative flow and pressure patterns were observed. (A) Oropharyngeal collapse. (B) Multilevel collapse of the velum and oropharyngeal airway. (C) Velum collapse.

For subsequent inspirations in the first apnea, shown in Figure 2B, the endoscope was repositioned superiorly, and complete collapse of the velum was observed. Additionally, nasal airflow and pharyngeal manometry revealed that the flow limiting site migrated proximal to the upstream catheter. Nasal airflow remained zero (flow had ceased) while both the upstream and downstream catheter pressures deflected downward together at the start of inspiration. As inspiration proceeded, the upstream and downstream pressures dissociated, demonstrating that a secondary site of collapse developed distal to the upstream catheter as inspiratory effort increased. At the start of the second apnea, highlighted in Figure 2C, the endoscopic image again showed complete collapse of the velum and physiologic tracings showing that both the upstream and downstream catheters deflected downward without inspiratory airflow, thus confirming that the flow-limiting site remained proximal to the upstream catheter.

DISCUSSION

This case highlights the complementary information provided by the addition of a nasal flow sensor and two pressure sensors to the standard DISE exam, which typically relies solely on video-endoscopy. Our enhanced evaluation allowed for the sites of anatomic collapse to be identified on endoscopy and simultaneously evaluated for their impact on respiratory dynamics. Results of this case revealed two important findings: 1) the flow limiting site (or site of airflow obstruction) can migrate within an apnea, and 2) increased inspiratory effort causes a secondary site of pharyngeal collapse to develop downstream from the initial flow limiting site. These findings have significant therapeutic implications as described below.

The flow-limiting site is defined as the anatomic region where pressure and flow first dissociate.³ In this case, the flow-limiting site was either proximal or distal to the upstream catheter. In the patient’s first apnea the initial site of flow limitation was located distal to the upstream catheter (Figure 2A). The endoscopic image acquired at this time identified a posteriorly placed tongue and collapsed epiglottis as the culprit responsible for flow limitation. As the apnea progressed, however, the flow-limiting site migrated proximal to the upstream catheter. This may be due to phasic increases in genioglossal tone, which can stiffen the retroglossal airway or increase pharyngeal collapsibility such that the velum became the most collapsible segment.

In both apneas, endoscopic evaluation showed complete collapse of the velum. While the endoscope was not inserted distal to the velum in either apnea after complete collapse was observed, catheter pressure tracings indicated that a secondary collapse site developed distal to the soft palate. As highlighted in Figure 2B, the upstream and downstream pressures dissociated as inspiration progressed. A previous study which utilized pharyngeal manometry in natural sleep found that 15/30 patients had multilevel pharyngeal obstruction and that sites of airway collapse could evolve within a single apnea.⁴ These findings may suggest that downstream secondary sites of collapse were a consequence of increased respiratory effort caused by a primary upstream site of flow-limitation in the velopharynx.

Delineating between primary and secondary sites of obstruction is clinically meaningful. Multilevel collapse is a common finding on DISE exams. Nevertheless, it is not known whether all collapsing sites observed on DISE should be treated surgically. In a retrospective study of 24 patients who underwent either single-level or multi-level surgery for OSA, 8/14 patients in the responder group (post-op AHI < 10 and >50% reduction) had a collapse site on DISE that was not surgically addressed.⁵ Treating the primary collapse site may therefore relieve flow limitation, abolish supraphysiologic respiratory effort and prevent secondary sites from collapsing. Understanding the impact of collapse on inspiratory flow is therefore crucial to tailor individualized treatment strategies.

CONCLUSION

While endoscopic evaluation during DISE remains a valuable tool for modeling factors contributing to pharyngeal obstruction during sleep, this case report highlights insights gained by coupling anatomic and visual assessment with objective measurements of airway pressures that characterize primary and secondary sites of airway obstruction. This case emphasizes the need for a comprehensive assessment of upper airway dynamics in OSA to aid in surgical decision making.