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E.R. Crouch, J.E. Thompson, R. Vorona, C. Ware, F. Lattanzio, Jr, P. Sammuel; Retinal Vascular Changes in Obstructive Sleep Apnea Syndrome . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3278.
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Purpose: The obstructive sleep apnea syndrome (OSAS) manifests with repetitive upper airway obstruction with consequent fragmentation of sleep and arterial oxygen desaturation. Ophthalmic manifestations of OSAS include glaucoma, optic neuropathy, papilledema, floppy eyelid syndrome and keratoconus. However, studies have found no relation between sleep disorders and retinal vascular abnormalities. Recently, we noted retinal vascular tortuosity in patients with a reported history of OSAS. This study was initiated to investigate the prevalence of such changes in OSAS as compared to controls and postulate as to the etiology. Methods: Patients were diagnosed with OSAS based on initial history, physical examination and nocturnal polysomnography. Patients then underwent full ophthalmic examination including visual acuity, slit–lamp exam, applanation tonometry, dilated fundus exam and fundus photography. A series of non–OSAS historical controls with and without diabetes was used. For both groups exclusion criteria included sickle cell disease, history of central retinal vein occlusion, history of chronic obstructive pulmonary disease, and retinopathy of prematurity. Ophthalmologists, masked to the sleep study results, rated fundus photographs by the degree of vascular tortuosity on a 0–4+ scale.The criteria for tortuosity was four out of five ophthalmologists giving a 3+ or 4+ rating. Results: Incidence of tortuosity was 22.2% (n=8/36) in OSAS, 0% (0/46) in non–diabetic controls and 10% (n=4/40) in diabetic controls. Incidence was greater in diabetic controls vs. non–diabetic controls (p=<0.001), and also in OSAS patients vs. non–diabetic controls (p=<0.006). No difference exists between OSAS patients and diabetic controls (p=<0.992). 33% (n=12/36) of all OSAS patients and 10% (n=2/8) of OSAS patients with tortuosity had diabetes or a family history of diabetes. Conclusions: OSAS is associated with increased sympathetic activation. We hypothesize that sympathetic over activity leads to vasoconstriction and kinking of the retinal vessels manifesting as tortuosity. Loss of pericytes in diabetic vascular disease reduces support of the vessel wall. The diabetic control group had an increased prevalence of tortuosity supporting this as a mechanism. The highest observed incidence of tortuosity occured in OSAS patients, 33% of whom were diabetic, suggesting a combination of loss of pericytes and recurrent vasoconstriction contributed to the tortuosity.
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