Purpose: Vascular changes have been observed among glaucoma patients, but it is not yet known whether these vascular changes occur primary or secondary to glaucomatous damage. In this study, a theoretical mathematical model of the retinal vasculature is applied to a set of oximetry data obtained from healthy individuals and glaucoma patients and is used to propose possible explanations for the clinically observed increases in venous blood oxygen saturation in advanced glaucoma patients.
Methods: Given clinical measurements of intraocular pressure (IOP), mean arterial pressure and arterial blood oxygen saturation from healthy persons and advanced (visual field mean defect (MD) ≥ 10 dB) primary open angle glaucoma (POAG, IOP > 21 mmHg) patients and advanced normal tension glaucoma (NTG, IOP ≤ 21 mmHg)patients, the model is used to predict the oxygen demand or Krogh cylinder tissue width that would yield the clinically-measured venous oxygen saturation in each population.
Results: A decrease in retinal tissue oxygen demand (M0), an impairment in blood flow autoregulation, or a decrease in Krogh cylinder tissue width (d) can independently lead to increased venous saturation. The model predicts that a decrease in M0 or a decrease in d is more likely to yield the increased venous saturation levels observed in POAG patients, while impairing blood flow autoregulation with no change in M0 or d is more likely to yield the increased venous saturation levels observed in NTG patients.
Conclusions: The combined theoretical and clinical model predictions suggest that the mechanisms leading to increased venous saturation might differ between POAG and NTG patients. The model predictions are used to hypothesize that a decrease in oxygen demand might be more relevant to the increase in venous saturation observed in advanced POAG, while impairment in autoregulation mechanisms might be more relevant to the increase in venous saturation observed in advanced NTG.