Transverse Maxillary Deficiency Predicts Increased Upper Airway Collapsibility during Drug‐Induced Sleep Endoscopy

Abstract

AbstractObjectiveTo examine the relationship between craniofacial skeletal anatomy and objective measures of pharyngeal collapse obtained during drug‐induced sleep endoscopy. We hypothesized that transverse maxillary deficiency and an increased pharyngeal length will be associated with higher levels of pharyngeal collapsibility.Study DesignCross‐sectional analysis in a prospective cohort.SettingUniversity Hospital.MethodsA cross‐sectional analysis was conducted in a cohort of consecutive patients from the positive airway pressure (PAP) alternatives clinic who underwent computed tomography (CT) analysis and drug‐induced sleep endoscopy for characterization of upper airway collapsibility. PAP titration was used to determine pharyngeal critical pressure (PCRIT) and pharyngeal opening pressure (PhOP). CT metrics included: Transverse maxillary dimensions (interpremolar and intermolar distances) and pharyngeal length (posterior nasal spine to hyoid distance).ResultsThe cohort (n = 103) of severe obstructive sleep apnea (Apnea and Hipopnea Index 32.1 ± 21.3 events/h) was predominantly male (71.8%), Caucasian (81.6%), middle‐aged (54.4 ± 14.3 years), and obese (body mass index [BMI] = 30.0 ± 4.9 kg/m2). Reduced transverse maxillary dimensions were associated with higher PCRIT (intermolar distance: β [95% confidence interval, CI] = −.25 [−0.14, −0.36] cmH2O/mm; p = .03) and PhOP (Interpremolar distance: β = −.25 [−0.14, −0.36] cmH2O/mm; p = .02). Longer pharyngeal length was also associated with higher PCRIT (β = .11 [0.08, 0.14] cmH2O/mm, p = .04) and PhOP (β [95% CI] = .06 [0.03, 0.09] cmH2O/mm, p = .04). These associations persisted after adjustments for sex, age, height, and BMI.ConclusionOur results further the concept that skeletal restriction in the transverse dimension and hyoid descent are associated with elevations in pharyngeal collapsibility during sleep, suggesting a role of transverse deficiency in the pathogenesis of airway obstruction.