Unilateral nonarteritic anterior ischemic optic neuropathy associated with obstructive sleep apnea–hypopnea syndrome: a case report

This report describes a case of obstructive sleep apnea–hypopnea syndrome (OSAHS) associated with nonarteritic anterior ischemic optic neuropathy (NAION). NAION is an optic neuropathy characterized by painless vision loss, visual field defects, and optic disc edema. It results from hypoperfusion of the short posterior ciliary arteries, leading to acute ischemia and structural and functional impairment of the optic nerve, which ultimately manifests as blurred vision or blindness. We report the case of a 59-year-old Han Chinese male who presented with a 6-day history of blurred vision and visual field defects in the left eye . The diagnosis was confirmed after excluding other potential etiologies. The patient was treated with 80 mg of oral methylprednisolone, which was gradually tapered, alongside neuroprotective and circulation-improving therapies. Following consultation with the Department of Respiratory and Sleep Medicine, he was initiated on noninvasive ventilation (NIV) to correct systemic hypoxia and received bronchodilators. Subsequently, the patient’s symptoms showed moderate improvement. NAION is frequently associated with a variety of systemic vascular risk factors, particularly hypertension, diabetes mellitus, dyslipidemia, ischemic heart disease, and cerebrovascular disease. These conditions compromise the microvascular supply to the optic nerve head, leading to ischemia, necrosis, and subsequent optic atrophy. Among these, OSAHS is recognized as a significant and independent risk factor. OSAHS is a clinical syndrome characterized by recurrent episodes of apnea and hypopnea during sleep, resulting in intermittent hypoxia, hypercapnia, and sleep fragmentation. OSAHS is a well-established risk factor for systemic vascular comorbidities, including cardiovascular disease and diabetes mellitus. In the present case, an association between OSAHS and NAION was observed after excluding other potential confounding etiologies. These findings highlight the clinical importance of screening for and managing OSAHS in patients with NAION, providing a rationale for optimized therapeutic strategies.