An Objective Analysis of the Effect of Obstructive Sleep Apnea on Anterior Segment Parameters

Objectives: To evaluate the effect of obstructive sleep apnea syndrome (OSAS) on corneal anterior segment parameters compared with body mass index (BMI)-matched and polysomnography (PSG)-negative healthy controls. Methods: This cross-sectional case-control study included 42 patients with OSAS and 25 age-sex BMI-matched and PSG-negative healthy volunteers. Obstructive sleep apnea syndrome was diagnosed by the polysomnographic sleep test, and the control subjects were determined from a negative overnight PSG. Maximum keratometry (Kmax), central corneal thickness, corneal symmetry index (SI), keratoconus vertex (KV), Baiocchi–Calossi–Versaci (BCV), anterior chamber volume (ACV), anterior chamber angle (ACA), and anterior chamber depth (ACD) values from topographic measurements and endothelial cell density (ECD), coefficient of variation, and hexagonality percentage (Hex) values from specular microscopic measurements were recorded. Results: In our study, 48 eyes of 24 patients with mild-moderate OSAS (Group 1) and 36 eyes of 18 patients with severe OSAS (Group 2) and 50 eyes of 25 BMI-matched and PSG-negative volunteers (Group 3) were evaluated. Among the keratoconus index values, front and back KV values were significantly higher in the OSAS group compared with the control group ( P =0.001, P :0.003, respectively), while there was no significant difference in SI and BCV values ( P >0.05). Central corneal thickness was statistically lower in the severe OSAS group compared with the control group. There was no statistically significant difference between patients with OSAS and controls in Kmax, ACD, ACA, and ACV values. Among the specular microscopic measurements, the ECD value was significantly lower in the severe OSAS group ( P <0.05). Conclusion: In the study comparing age-sex and BMI-matched groups, some abnormal changes in corneal endothelial morphology and topographic keratoconus screening indices were observed in patients with OSAS. We assume that these corneal changes are due to intermittent hypoxia and hypoxia-induced inflammatory response during apnea–hypopnea episodes in OSAS.