We examined children assessed for OSAS by overnight RP, to investigate for early signs of ocular changes related to airway obstruction during sleep, poorly documented and understood in the previous literature[10–11].
Retina and optic nerve have been examined in OSAS paediatric patients with adenotonsillar hypertrophy with controversial results. Cinici and Tatar found no significant alterations of RNFL thickness, while Simsek et al showed that OSAS seems to influence RNFL and IOP parameters. Both studies highlighted the potential risk of long-term optic injury due to blood intermittent hypoxia and recommend prompt treatment of OSAS in young people. None evaluated corneal alterations in OSAS paediatric patients.
The major limitation of these studies was the assessment of OSAS diagnosis by questionnaire, contrasting with AAMS recommendations . The questionnaires, indeed, are sensitive just for severe grades of apnoea so they are not suitable for children and could under-diagnose the disease.
Despite the gold standard for diagnosis of OSAS is the polysomnography, it is an expensive test, the setup can be challenging, and the placement of numerous electrodes can be difficult in children.
In our study, we investigated the OSAS using RP in a dedicate room, according with J. Corral et al. that found RP management was similarly effective to polysomnography, with a substantially lower cost .
None of the children enrolled in the study had visual impairment and all reached 0.00 logMar, with or without optical correction, without anomalies during ophthalmological examination.
However, although corneal parameters were within normal range in both OSAS and non-OSAS group, statistically significant differences were found for SAI and TCT values (p = 0.02 and p = 0.04, respectively).
SAI is the index of asymmetry of the corneal surface and is based on the specular correspondence between the two hemicorneas (superior and inferior), which normally does not exceed small physiological differences (< 0.5). Values greater than 1, result in a notable corneal asymmetry which is suggestive for ectasia[17–18].
Our results suggest that OSAS children have a higher corneal asymmetry than non-OSAS. This finding, added to the detection of a lower TCT, leads to suspect a possible evolution towards ectasias. In fact, we found one OSAS patient with suspect corneal ectasia. This would be in keeping with the previous literature on the correlation between OSAS and keratoconus in adult patients[8, 9]. The SAI values within the normal range, found in this study, could be explained by the shorter period of exposure to OSAS in children patients compared to adult ones. Indeed, the latter have generally several years of exposure to OSAS when a diagnosis of keratoconus is made. Therefore, a possible evolution towards ectasia in young patients should be suspected.
Similar behaviour has been found in RNFL parameters, whose values were found within the normal range in all patients . However, the OSAS group showed higher RNFL thickness in all quadrants, reaching statistically significant difference in the average values and in the nasal quadrant values.
The relation between OSAS and optic injury is well known in middle-aged adults and the elderly and most of the studies reported reduction in RNFL thickness [8, 9]. Recently, Lee et al confirmed this relation also in young OSAS patients (aged 19–22 years) reporting RNFL thinning in inferotemporal and superotemporal segments .
This study shows that a correlation between OSAS and optic nerve fibers is already detectable also in very young patients, but not in terms of a reduced RNFL thickness when compared with non-OSAS group. On the opposite, our data showed increased RNFL in OSAS patients. These changes could reflect a mild swelling of the optic nerve fibres secondary to capillaries dilatation, due to hypoxic condition, or to a possibly increased intracranial pressure, which are common conditions in OSAS patients [20–22].
The peripapillary and retinal capillary tone, indeed, is under local vascular control and it responds to O2 and CO2 concentration in the blood. Moreover, Jaki Mekjavic et al.  described in patients under experimental condition that hypoxia and acute hypercapnia induce dilation of retinal vessels and radial peripapillary capillary network, causing the increasing of RNFL thickness, as compensatory response.
As know, in adults with moderate-severe OSAS, RNFL thickness is significantly reduced compared to healthy subjects and is associated with macular retinal thinning due to ganglion cells loss . However, already other authors have noted that probably the optic nerve head changes through the stage of subtle edema in the mild and moderate OSAS groups and pass to a secondary phase of reduction in RNFL thickness in patients with long-standing severe OSAS .
The fact that in our study a mild increase in RNFL thickness was not associated to any visual disturbances and CMT and RV appeared within normal limits could be a sign of very early and potentially reversible change.
Most of our patients were newly diagnosed with a mild stage of OSAS, with a disease duration likely to be relatively short due to the young age of the patients. We cannot exclude that, in case of OSAS is left untreated and progress with time to more severe disease stages, optic nerve head changes could evolve over the years to chronic nerve fibres distress with reduction of RNFL thickness.
In this study, OSAS children show higher RNFL thickness in all quadrants, reaching statistically significant difference in the average and in the nasal one. Furthermore, the significant increase in RNFL only in the nasal sector could be explained by the swelling disc scheme proposed by Frisen , which showed that edema begins precisely in the nasal part of the disc.
In our study, the correlation between OSAS and increased RNFL thickness could represent an early modification of the peripapillary nerve fiber layers, due to apneas and desaturation events. A limitation of this study is the lack of measurement of retinal ganglion cell layer values.
No significant differences were found in CMT and MV, however higher values were found in the OSAS group. These findings could be due to the vascular response of retinal capillary network in OSAS group.
Further investigations with larger populations in paediatric patients with OSAS are needed to confirm our hypotheses.
This is the first study that found a correlation between OSAS and corneal alterations in childhood, contributing to the knowledge of the ocular implications related to OSAS.
Ocular damages in children are completely asymptomatic and these early signs could give insight on pathogenesis of corneal and optic disc changes that appear clinically evident in the adult population. So, based on our evidence, we suggest to plan earlier ophthalmological examination including evaluation of corneal asymmetry and RNFL thickness in paediatric patients affected by OSAS.