1162 Keratoconus in an Adolescent with Obstructive Sleep Apnea

Abstract Introduction Obstructive sleep apnea (OSA) is common in pediatrics. Signs of OSA vary between patients commonly reflecting an obstructed upper airway with hypoventilation and hypoxemia. There is less knowledge of the ophthalmologic findings in OSA. Corneal thickness is sensitive to oxygen desaturations that occur during sleep and may contribute to the development of keratoconus. Based on the IRIS Registry, the prevalence of keratoconus in adults is 2.9% compared to 0.27% in pediatrics. We describe a pediatric patient with keratoconus, who was found to have severe OSA. Report of case(s) 14-year-old male with history of obesity, tonsillar hypertrophy and bilateral keratoconus s/p corneal crosslinking was admitted to the hospital for corneal transplant. Post-operatively, it was difficult to wean the patient off oxygen and inpatient he required 3L oxygen due to significant nocturnal hypoxemia. With concurrent morning headaches, witnessed apneas and weight gain (BMI 52.7, >99th percentile) the patient underwent an inpatient split night polysomnogram. Results revealed severe OSA (AHI 123/hr) and hypoxemia (O2 baseline 89-91%, nadir 64% O2, ODI 105.1/hr, < 90% for 40% of TST) without significant hypoventilation (PETCO2 43 - 54mmHg, >50mmHg for 1% TST). He was titrated to CPAP 15cm H2O with resolution of sleep apnea (AHI 0.7, SpO2 92 - 98%). Echocardiogram showed normal right ventricular size, ejection fraction and negative for signs of pulmonary hypertension. Chest x-ray was unremarkable. He was initiated on PAP therapy, and subsequently underwent adenotonsillectomy 5 months later. He continues to follow with ophthalmology and uses prednisolone eyedrops regularly. Conclusion Ocular presentations are a less recognized sign of OSA particularly in pediatric patients. In adults, the intermittent hypoxemia and airflow limitations could contribute to ocular pathology and severity in presentation. Keratoconus has been associated with elevated levels of matrix metalloproteinases and protease inhibitors, which may play a role in corneal thinning in individuals with OSA. Pediatric keratoconus has been described as more aggressive compared to adults leading to more rapid deterioration. The progression of ocular disease in our patient may have been a consequence of untreated OSA. Our report highlights the importance of early recognition and treatment of OSA in pediatric patients. Support (if any)