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Editors Selection IGR 9-3

Clinical glaucoma: RNFL and OSAS

Comment by David Greenfield on:

12506 Retinal nerve fibre layer measurements are reduced in patients with obstructive sleep apnoea syndrome, Kargi SH; Altin R; Koksal M et al., Eye, 2005; 19: 575-579

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Prior reports have suggested an association between obstructive sleep apnea syndrome (OSAS) and glaucoma. The mechanism has been thought to involve intermittent upper airway obstruction during sleep producing relative hypoxia, vascular dysregulation, and secondary ischemic optic nerve damage. The study by Kargi et al. (514) investigates the RNFL thickness in 34 subjects with OSAS and 20 age-matched controls using a scanning laser polarimeter with fixed corneal compensation. The authors found reduced RNFL thickness in patients with OSAS compared to controls; a more modest reduction was observed in patients classified as having severe OSAS. A weak correlation (p = 0.01) was identified between OSAS severity and RNFL thickness.

This study adds further evidence that patients with OSAS may be at risk for the development of glaucomatous optic neuropathy. The authors correctly point out that ischemia injury may represent a possible mechanism for RNFL loss. A syndrome characterized by progressive optic nerve cupping and axonal loss has been described in primate models of chronic ischemia.¹

I would propose an alternative hypothesis that may co-exist in such patients. Intermittent upper airway obstruction may produce increased intra-thoracic pressure resulting in increased episcleral venous pressure and increased nocturnal IOP. The authors report that enrolled subjects had a recorded intraocular pressure below 21 mmHg (presumably a diurnal IOP measured in the habitual position). Twenty-four hour patterns of intraocular pressure fluctuation have been recently described in normal subjects and persons with glaucoma² and investigators with access to sleep laboratories may have an opportunity to further explore the characteristics of the supine nocturnal IOP in this patient population.

Kargi and colleagues are to be congratulated for this welcome addition to the literature. It is worth noting that the findings observed in this study should be substantiated using the latest commercial scanning laser polarimeter with variable corneal compensator which determines and neutralizes eye-specific corneal polarization axis and magnitude.

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