Validation of Retinal Oximetry in Glaucoma Patients: a Structural and Functional Correlation

Retinal ischemia is thought to play an important role in the pathogenesis of glaucoma. Up until today, very little is known about the metabolic alterations in the retina of glaucoma patients, since only techniques for surrogate measurements of metabolism (like blood flow velocities and vessel diameter) were available. Oximetry has provided us with an important tool to study metabolism in glaucoma, and to correlate these findings with the available blood flow evaluation techniques. Preliminary results by the group of Prof Stefánsson (2011) with the dual wavelength oximeter pointed out that deeper glaucomatous visual field defects are associated with decreased arteriovenous differences in retinal oxygen saturation. These data suggest that a change in oxygen metabolism occurs in glaucomatous retina. This reduced oxygen metabolism may be related to tissue atrophy. However, this explanation is still hypothetical, since the relation between these oximetry results and structural changes in the optic nerve have not been studied yet.

1. What are the oximetry values in a normal population of within the same age group as the glaucoma population? To answer this question, a normative database of the investigators retinal oximetry device needs to be constructed for healthy controls. 2. Do glaucoma patients have different retinal oximetry values than these normal patients? Are there any differences in retinal oxygenation between these glaucoma groups? To answer these questions, oximetry measurements will be performed in patients with normal tension glaucoma (NTG) and primary open angle glaucoma (POAG). 3. Is there an association between structural optic disc and retinal nerve fibre layer changes, using Heidelberg Retinal Tomography (HRT), with alterations in retinal vascular oxygen saturation in NTG and POAG patients? 4. Are blood flow measurements, using colour Doppler imaging (CDI), correlated with alteration in retinal vascular oxygen in NTG and POAG patients?