Abstract
Purpose::
A known risk factor for the development of sleep apnea syndrome (SAS) is a neck circumference greater than 17 inches for men and 16 inches for women. Patients with SAS belong to a population at high risk for developing glaucoma. Also, a large number of patients with normotensive glaucoma and primary open angle glaucoma carry a diagnosis of SAS. The purpose of this study is to determine if there is a significant difference in the change of sitting to supine intraocular pressures (IOP) between two groups of patients: those with a risk factor for the development of SAS (i.e. a neck circumference greater than 17 inches (men), greater than 16 inches (women)) and those without such a risk factor. A significant difference may indicate that additional mechanical stresses such as increased head and neck venous congestion while supine are impeding aqueous outflow.
Design::
Observational study.
Participants::
64 consented adults without previous diagnoses glaucoma in an internal medicine, ambulatory clinic. 48 patients had neck circumferences less than or equal to 16 or 17 inches. 16 patients had neck circumferences of greater than 16 or 17 inches.
Methods::
Neck circumference was measured using a soft measuring tape marked in inches. Topical anesthetic was instilled in the right eye. Sitting IOP was measured in the right eye using a calibrated Tonopen. IOP was then reassessed in the right eye using the Tonopen after the patient had been in the supine position for greater than two minutes.
Results::
For the group of patients with smaller neck circumferences, the mean IOP change from sitting to supine was 1.708mmHg. For the group of patients with larger neck circumferences (greater than 17 inches for men and 16 inches for women), the mean IOP change from sitting to supine was 2.000mmHg (t(15)=0.964, p > 0.05, 95%CI [1.469-2.531]).
Conclusions::
Although the mean change from sitting to supine intraocular pressures was higher in the group with larger neck circumferences, the increase was not statistically significant. This data suggest the underlying mechanism of optic nerve head damage in patients with SAS is not related to an elevation in IOP due to additional mechanical stresses impeding aqueous outflow (e.g. neck venous congestion and rise in venous pressure). However the sample size in this study was small and IOP measurements were not repeated at different times of day to account for diurnal variation. Future research can correct for these limitations. In addition, future research may include examining the effect of medications known to increase aqueous outflow on IOP changes in these two populations.
Keywords: intraocular pressure