Purchase this article with an account.
G. Leroux les Jardins, A. Glacet-Bernard, G. Coscas, E. Souied, G. Soubrane; Obstructive Sleep Apnea Syndrome and Retinal Vein Occlusion: What’s the Link. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5214.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Obstructive sleep apnea syndrome (OSAS) is a very common disease and has been recently increasingly implicated in the initiation and progression of numerous cardiovascular, neurologic and ophthalmologic diseases. The already known risks of undiagnosed obstructive sleep apnea include heart attack, stroke, impotence, irregular heartbeat, high blood pressure and heart disease.In ophthalmologic practice, it would be linked with glaucoma, nonarteritic anterior ischemic optic neuropathy, visual field defects, papilledema, and floppy eyelid syndrome. Because of personal observations, we investigated its link with retinal vein occlusion (RVO).
We report the observations of 3 patients who presented with retinal vein occlusion. These patients had a complete medical investigation to find predisposing factors. Surprisingly we founded an OSAS (clinically suspected and then diagnosed with polysomnography) as one of the only abnormality of the complete check-up. In the last patient, a rapid conversion into an ischemic form was observed, resulting in neovascular glaucoma at the end of the first month. The OSAS, which was the only predisposing factor, was suspected to be responsible for the particularly rapid aggravation.
The local and systemic effects of OSAS could explain, in some patients, the occurrence and the aggravation of RVO. First stage effects of OSAS are nocturnal hypoxemia, reoxygenation, hypercapnia, intra-thoracic pressure changes, arousals and sleep fragmentation. RVO could be to consequence of a slow-down of blood flow circulation secondary to hypoxemia and elevated nocturnal intracranial pressure. The arousals cause an acute increase of blood pressure. Ancillary effects are increased platelet aggregability, an increased sympathic activation, oxydative stress, vascular endothelial dysfunction, inflammation and metabolic dysregulation. These mechanisms could account for the aggravation of the symptoms in some patients.
This short series of RVO patients presenting with OSAS suggests that there is maybe an independent relationship between both disorders. It could be interesting to systematically screen for OSAS (at least by questioning the patients) in each RVO, as there are effective treatments available for OSAS.
This PDF is available to Subscribers Only