Quantitative evaluation of the upper airway during nasopharyngoscopy with the Müller maneuver.

OBJECTIVE: To quantitatively examine changes in the upper airway caliber of normal subjects at graded negative inspiratory pressures generated during nasopharyngoscopy with a Müller maneuver. STUDY DESIGN: Eighteen normal subjects prospectively underwent nasopharyngoscopy with Müller maneuvers. Subjects performed graded and maximal effort Müller maneuvers while sitting upright, and maximal-effort Müller maneuvers in the supine position. Two regions of the upper airway--the retropalatal and retroglossal--were examined. METHODS: Images from the endoscopic examination were objectively analyzed by adjusting manually traced airway contours using full-width, half-maximum edge detection algorithm software. The adjusted tracings' area and dimensions through the airway centroid were measured. RESULTS: Müller maneuvers performed at -40 cm H2O resulted in a 64%+/-17% (P = .0001) reduction in upper airway area that consisted of a 51%+/-20% (P = .0001) reduction in the lateral dimension and a 21%+/-24% (P = .0026) reduction in antero-posterior dimension. Müller maneuvers in the retroglossal region did not significantly reduce airway area (P = .575), but demonstrated an altered airway conformation that consisted of lateral narrowing and an increase in antero-posterior dimension. Changes in body position did not result in significant differences in either airway caliber or airway dimension. CONCLUSIONS: Airway caliber during forced inspiration is mediated primarily through changes in the lateral pharyngeal walls. This study has also shown that antero-posterior and lateral airway structures are largely independent in their response to Müller maneuvers. Similarly, the retropalatal and retroglossal regions of the upper airway respond differently to forced negative intraluminal pressure.

State-related changes in upper airway caliber and surrounding soft-tissue structures in normal subjects.

State-dependent changes in upper airway caliber were studied with magnetic resonance imaging (MRI) techniques. We hypothesized that changes in airway caliber during sleep in normal subjects would result from positional and dimensional changes in upper airway soft-tissue structures, including the lateral pharyngeal walls, tongue, and soft palate. We used MRI to study 15 normal subjects during wakefulness and sleep. Sleep was facilitated by one night of sleep deprivation prior to MRI. During sleep, the volume of the retropalatal (RP) airway was reduced by 19% (p = 0.03). The volume of the retroglossal (RG) airway was not significantly reduced during sleep, suggesting that the RP region may be more likely to collapse. The mean minimal cross-sectional airway area was reduced by 228% (p = 0.004) in the RP and by 22% (p = 0.02) in the RG region during sleep as compared with values in anatomically matched axial images during wakefulness. Airway anteroposterior (AP) and lateral dimensions were also significantly reduced in the RP region. Airway narrowing in the RP region was associated with a 7% increase in thickness of the lateral pharyngeal walls (p = 0.04). In nine subjects, sagittal data showed significant posterior displacement of the soft palate during sleep as compared with wakefulness. Multiple linear regression analyses indicated that reduction in the RP airway area during sleep resulted from posterior movement of the soft palate, thickening of the lateral pharyngeal walls, and an increase in tongue oblique distance. We conclude that the lateral pharyngeal walls play an important role in upper airway narrowing during sleep in normal subjects.

Pleural effusion due to herpes simplex type II infection in an immunocompromised host.

Pleural effusions caused by herpes simplex viruses are rare. We report a case of a young woman with acute lymphocytic leukemia (ALL) and prolonged neutropenia who developed pleural space infection with herpes simplex type II virus (HSV II), as confirmed by cytologic and microbiologic studies. We believe that this is the first report of a pleural effusion caused by HSV II, and suggest that this virus now be considered in the differential diagnosis of an unexplained exudative pleural effusion, especially in an immunocompromised host.