Sleep-disordered breathing, of which OSA is the most common, is estimated to affect up to 24% of men and 9% of women in the United States.14
In addition, there are a projected 18 million believed to be untreated.15
As the prevalence of obesity continues to rise, more and more patients will be at risk. OSA is associated with endothelial dysfunction, systemic vasculopathy, and is an independent risk factor for increased cardiovascular morbidity and mortality making it imperative that patients be diagnosed and treated expeditiously.
Floppy eyelid syndrome, primary open angle glaucoma, normal tension glaucoma, NAION, optic disc edema and the degree of diabetic retinopathy have been all been linked to OSA.5
The majority of ophthalmic associations in OSA have potential vascular etiologies. During apneas, transient hypotension and hypoxemia may occur with repeated oxyhemoglobin desaturations as low as 30%. This hypotension and hypoxemia has been proposed as a possible etiologic factor for glaucoma and NAION secondary to ischemic damage to the optic nerve. Optic disc edema may be secondary to the catecholamine release seen at termination of the apnea which results in blood pressure surges and increased intracranial pressure. Boland et al, examined the retina in patients with OSA looking for microvascular abnormalities including microaneurysms, hemorrhages, exudates, macular edema, intraretinal microvascular abnormalities, venous beading, neovascularization, and vitreous hemorrhage.16
Their study concluded that there was no notable relationship between sleep-disordered breathing and retinal abnormalities. In patients with both OSA and diabetes, the AHI and level of oxyhemoglobin desaturation have been shown to correlate with the degree of diabetic retinopathy.17
To our knowledge, the status of retinal vascular tortuosity has not yet been reported in OSA.
In our series, patients with OSA demonstrate increased retinal vascular tortuosity as compared to controls. The venous system in OSA was significantly more tortuous at both the 5DD and 10DD marks while the arterial system was more tortuous at the 10DD mark. As both diabetes and hypertension are associated with increased retinal vascular tortuosity we attempted to match the control group for these comorbidities.10
In our small cohort of patients, the increased tortuosity in OSA appears to be independent of the presence of hypertension or diabetes.
The mechanism of increased retinal vascular tortuosity in OSA is likely multi-factorial. Apneas result in significant intermittent arterial blood pressure surges, increased venular pressure, and increased intracranial pressure which can potentially lead to tortuosity due to increased shear wall stress.18
In addition, patients with OSA may have hypercapnia which has been shown to be associated with increased retinal arteriolar and capillary blood flow.19
The alteration of retinal blood flow may also be related to impaired cerebral autoregulation in OSA making ophthalmic vasculature more susceptible to shear stress during arterial and venous pressure swings during apneas.20
We hypothesize that hypercapnia, blood pressure surges, and disrupted cerebral autoregulation may result in increased blood flow or blood volume in the retinal vasculature causing tortuosity.
While the significance of increased tortuosity is not yet clear, this finding is interesting in light of the recent associations made between vein occlusion and OSA.9
It is possible that increased tortuosity may result in turbulence or stagnation of blood flow predisposing these patients to retinal occlusive disease. There is also evidence that OSA is associated with a hypercoagulable state which would explain both the increased risk of cerebral stroke and retinal vein occlusion.21
There are several limitations to this study. First, this study is limited by the small number of patients in both the control and study groups. Second, the influence of hypertension or diabetes on our findings cannot be totally excluded. However, due to the comparable frequency of these two comorbidities, it is unlikely that they have a major effect on the difference in observed retinal vascular tortuosity. Third, we cannot exclude the effect of positive airway pressure treatment or obesity on retinal vascular changes. Finally, the severity of sleep apnea with respect to the apnea-hypopnea index and oxyhemoglobin saturations during sleep are important factors to evaluate in future studies. Although our study size is small, the patients with OSA demonstrated a wide range in the AHI and nadir oxyhemoglobin saturations showing that patients with both mild and severe sleep apnea displayed increased tortuosity.
In conclusion, patients with OSA have increased retinal vascular tortuosity. These retinal vascular changes may be related to the underlying systemic inflammatory state and alterations in cerebral hemodynamics seen in OSA. A prospective study with a larger sample size will be necessary to further explore this relationship and its clinical significance.