Prevalence of Glaucoma in Obstructive Sleep Apnea Patients
Prevalence of Glaucoma in Obstructive Sleep Apnea Patients
The main cause of all complications associated with OSA is the decreased oxygenation of vital structures during sleep.
Hyperventilation and resultant hypoxia occur normally during sleep, and particularly during rapid eye movement (REM) sleep. During the deepest stages of sleep, autoregulation of cerebral blood flow does not function perfectly, even in normal subjects, and this regulation appears to be severely disturbed in OSA. In patients with OSA, blood flow to the ONH may be altered and may result in glaucoma.
The ophthalmic artery is a branch of the internal carotid artery and shows similar characteristics regarding autoregulation of blood flow. In patients with OSA, the cerebral blood flow in response to hypoxia returns to normal levels after treatment with CPAP for a period of 6 weeks.
A high prevalence of glaucoma was found in patients with OSA, and especially in severe cases. The prevalence of glaucoma in OSA shows a wide range of fluctuation. Bendel et al reported a higher prevalence of NTG (27%) in patients with OSA. According to another study, the prevalence of NTG in all types of OSA was 5.7%, and increased to 7.1% in moderate and severe OSA cases. Tsang et al reported that moderate to severe OSA was associated with a higher incidence of visual field defects and glaucomatous changes in the optic nerve. These findings are in accordance with our study results. Although we found a higher prevalence of glaucoma in the severe OSA group compared with the moderate OSA group, a statistically significant difference could not be attained (P=0.4). This was primarily due to the low number of study subjects. We also found that, in the category of poorly controlled severe OSA, a deterioration of the visual field and OCT ensued in four patients. Two of these were already classified as glaucoma and the other two were from the previously non-glaucoma group, and the latter was eventually included in the glaucoma category.
Sergi et al reported that the prevalence of NTG was higher in OSA patients compared with a control Caucasian population of same age, and that OSA may be an important risk factor for NTG. These studies further support our findings that OSA is an important risk factor for the development and progression of glaucoma, and especially NTG.
Mojon et al reported that sleep apnea was more prevalent among patients with POAG than a normal control group. In a 5-year retrospective study published in 2013, Lin et al found a statistically significant increase in the incidence of open angle glaucoma in OSA patients compared with non-OSA patients.
Silva et al reported that in a 24-h IOP monitoring study involving 11 patients with OSA, the mean IOP was highest at 0600 hours and while the patients were in the lying position. Although the study is not specifically mentioning whether it is supine or prone position, the increase in IOP during lying can be a critical factor in the development or progression of glaucoma in patients with OSA.
On the contrary, a study conducted by Girkin et al failed to support the relevance of sleep apnea in comparison to other risk factors in the eventual development of glaucoma. However, the significance of these findings is in doubt, because there is overwhelming evidence supporting OSA as a risk factor for the development of glaucoma.
Boland et al recently conducted a detailed evaluation of factors that can contribute to the development of glaucoma, and sleep apnea was considered to be one of the risk factors. Vascular insufficiency and elevated IOP can cause death of retinal ganglion cells and lead to development of glaucoma. Vascular insufficiency may result from reduced ocular blood flow, decreased ocular perfusion pressure, generalized vascular deregulation, or increased trans-lamina cribrosa pressure.
One significant drawback of the current study is the relatively small number of patients studied. However, the number of subjects was kept small to ensure meticulous follow-up for a period of 3 years and avoid errors in assessments of visual fields and OCT results. Patients with doubtful findings were screened repeatedly during their follow-up visits to obtain conclusive evidence for classifying them as glaucoma or non-glaucoma subjects.
Although control of IOP is the most important aspect of managing NTG, it is imperative to explore the presence of other factors that may influence perfusion of the ONH. Kremmer et al reported that two cases of NTG became stabilized after treatment of OSA with nasal CPAP, and this approach may be applicable for managing other types of glaucoma with symptoms of OSA. Considering the findings described above, and our own results, we strongly endorse the need to screen all OSA patients for glaucoma. Also, glaucoma patients with symptoms suggestive of OSA should be advised to undergo a detailed sleep study; a concept also supported by Marcus et al.
Discussion
The main cause of all complications associated with OSA is the decreased oxygenation of vital structures during sleep.
Hyperventilation and resultant hypoxia occur normally during sleep, and particularly during rapid eye movement (REM) sleep. During the deepest stages of sleep, autoregulation of cerebral blood flow does not function perfectly, even in normal subjects, and this regulation appears to be severely disturbed in OSA. In patients with OSA, blood flow to the ONH may be altered and may result in glaucoma.
The ophthalmic artery is a branch of the internal carotid artery and shows similar characteristics regarding autoregulation of blood flow. In patients with OSA, the cerebral blood flow in response to hypoxia returns to normal levels after treatment with CPAP for a period of 6 weeks.
A high prevalence of glaucoma was found in patients with OSA, and especially in severe cases. The prevalence of glaucoma in OSA shows a wide range of fluctuation. Bendel et al reported a higher prevalence of NTG (27%) in patients with OSA. According to another study, the prevalence of NTG in all types of OSA was 5.7%, and increased to 7.1% in moderate and severe OSA cases. Tsang et al reported that moderate to severe OSA was associated with a higher incidence of visual field defects and glaucomatous changes in the optic nerve. These findings are in accordance with our study results. Although we found a higher prevalence of glaucoma in the severe OSA group compared with the moderate OSA group, a statistically significant difference could not be attained (P=0.4). This was primarily due to the low number of study subjects. We also found that, in the category of poorly controlled severe OSA, a deterioration of the visual field and OCT ensued in four patients. Two of these were already classified as glaucoma and the other two were from the previously non-glaucoma group, and the latter was eventually included in the glaucoma category.
Sergi et al reported that the prevalence of NTG was higher in OSA patients compared with a control Caucasian population of same age, and that OSA may be an important risk factor for NTG. These studies further support our findings that OSA is an important risk factor for the development and progression of glaucoma, and especially NTG.
Mojon et al reported that sleep apnea was more prevalent among patients with POAG than a normal control group. In a 5-year retrospective study published in 2013, Lin et al found a statistically significant increase in the incidence of open angle glaucoma in OSA patients compared with non-OSA patients.
Silva et al reported that in a 24-h IOP monitoring study involving 11 patients with OSA, the mean IOP was highest at 0600 hours and while the patients were in the lying position. Although the study is not specifically mentioning whether it is supine or prone position, the increase in IOP during lying can be a critical factor in the development or progression of glaucoma in patients with OSA.
On the contrary, a study conducted by Girkin et al failed to support the relevance of sleep apnea in comparison to other risk factors in the eventual development of glaucoma. However, the significance of these findings is in doubt, because there is overwhelming evidence supporting OSA as a risk factor for the development of glaucoma.
Boland et al recently conducted a detailed evaluation of factors that can contribute to the development of glaucoma, and sleep apnea was considered to be one of the risk factors. Vascular insufficiency and elevated IOP can cause death of retinal ganglion cells and lead to development of glaucoma. Vascular insufficiency may result from reduced ocular blood flow, decreased ocular perfusion pressure, generalized vascular deregulation, or increased trans-lamina cribrosa pressure.
One significant drawback of the current study is the relatively small number of patients studied. However, the number of subjects was kept small to ensure meticulous follow-up for a period of 3 years and avoid errors in assessments of visual fields and OCT results. Patients with doubtful findings were screened repeatedly during their follow-up visits to obtain conclusive evidence for classifying them as glaucoma or non-glaucoma subjects.
Although control of IOP is the most important aspect of managing NTG, it is imperative to explore the presence of other factors that may influence perfusion of the ONH. Kremmer et al reported that two cases of NTG became stabilized after treatment of OSA with nasal CPAP, and this approach may be applicable for managing other types of glaucoma with symptoms of OSA. Considering the findings described above, and our own results, we strongly endorse the need to screen all OSA patients for glaucoma. Also, glaucoma patients with symptoms suggestive of OSA should be advised to undergo a detailed sleep study; a concept also supported by Marcus et al.
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