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

Abstract

Background

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.

Case presentation

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.

Discussion

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.

Conclusion

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.

Introduction

Anterior ischemic optic neuropathy (AION) is classified into arteritic and nonarteritic types. NAION is diagnosed by excluding arteritis. It is a common optic neuropathy that severely threatens visual function [1]. NAION is associated with hypoperfusion of the short posterior ciliary arteries, which may contribute to acute ischemia and subsequent structural and functional impairment of the optic nerve. Ultimately, this condition can lead to blurred vision and even blindness. The etiology and pathogenesis of NAION are complex, involving local anatomical factors and systemic vascular risk factors. Currently, there is no clear, unified, or universally recognized treatment plan; therefore, early detection, diagnosis, and treatment have a significant impact on the prognosis of NAION. This disease predominantly affects middle-aged and elderly individuals, presenting primarily as sudden, painless vision loss and visual field defects. It is typically unilateral; however, the fellow eye may become involved after a few months or years. A relative afferent pupillary defect (RAPD) is often present. This article reports a case of NAION primarily associated with OSAHS, highlighting the importance of recognizing this risk factor [2].

Method

We present the following case in accordance with the CARE guideline.

Case presentation

The patient was a 59-year-old Chinese Han male who presented with a 6-day history of blurred vision in the left eye accompanied by a visual field defect. He denied a history of hypertension or diabetes and had no significant comorbid conditions or chronic illnesses. There was no known family history of hematological or thrombotic disorders. Physical examination revealed: right eye visual acuity (VA) 0.3, intraocular pressure (IOP) 14 mmHg; left eye VA 0.15, IOP 16 mmHg. Anterior segment examination was unremarkable. Left fundus examination revealed a blurred optic disc border, hyperemia, flat retina, vascular deformity, and an indistinct macular foveal reflex. Right fundus examination was unremarkable, with no evidence of a small or crowded optic disc. Admitted with “ischemic optic neuropathy of the left eye.” After admission, laboratory investigations were performed to assess for tuberculosis, autoantibodies, HLA-B27, anti-streptolysin O (ASO), rheumatoid factor, hepatitis B/C, syphilis, HIV, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and other relevant markers. Cranial and orbital MRI, cardiac ultrasound, cervical vascular ultrasound, and chest CT revealed no abnormalities. Following 1 week of treatment, fundus photography, optic nerve OCT, and visual field examination of the left eye were performed. Representative images included: (i) fundus photographs at early, arteriovenous, and late phases of the left eye (Fig. 1A–D) and (ii) optic disc OCT, visual field map, and fundus angiography of the left eye (Fig. 2A–D). Collectively, these findings led to a definitive diagnosis of NAION. Ambulatory blood pressure monitoring revealed no abnormalities, and other relevant risk factors were excluded, suggesting nocturnal hypoxemia as the primary risk factor for OSAHS, with an AHI of 24.09 (Fig. 2E). The patient received treatment with 80 mg oral methylprednisolone tablets to improve microcirculation, neurotrophic support, and nutritional status, with a gradual dose reduction regimen initiated. Following consultation with the Department of Respiratory and Sleep Medicine, noninvasive positive pressure ventilation (NPPV) was administered to address systemic hypoxia, promote bronchodilation, and enhance circulatory perfusion. Although the multimodal intervention was associated with partial alleviation of OSAHS symptoms and a modest improvement in the visual acuity of the affected left eye (0.2), it remains uncertain whether this visual recovery is treatment-related or simply reflects the natural history of NAION. At the 1-month follow-up, the patient’s symptoms remained stable. Symptoms first presented 6 days prior to diagnosis (T=0), at which time the diagnosis was confirmed. Symptomatic treatment was initiated and continued for 1 week, with symptom improvement observed by T=1 (1 week post-treatment initiation).

Fig. 1.

A Diffuse optic disc edema with blurred margins and papillary hyperemia. B Left eye demonstrates increased optic nerve head thickness with a decreased cup-to-disc ratio, while the right eye appears normal. C Binasal inferior altitudinal visual field defect sparing the central fixation point and extending from the physiological blind spot. D (after 1 week of treatment) Diffuse optic disc edema with resolving hyperemia and improved margin definition

Fig. 2.

A (At admission, FA at 21.00 s) early phase: blurred optic disc margins, tortuous retinal veins, and delayed choroidal filling. B, C (at admission, FA at 26.25 and 38.92 s) arteriovenous phase: progressive dilation and leakage of optic disc capillaries with heterogeneous fluorescein leakage; marked subtemporal leakage and radial hemorrhages obscuring fluorescence. D (at admission, FA at 128.78 s) late phase: intense focal leakage and fluorescein smudging at the optic disc, with preservation of the vascular arcade. E Moderate obstructive sleep apnea–hypopnea syndrome (OSAHS) with moderate nocturnal hypoxemia and disrupted sleep architecture; Apnea–Hypopnea Index (AHI) of 24.09 events/hour

Discussion

NAION is frequently associated with various systemic risk factors, particularly cardiovascular and cerebrovascular diseases, including hypertension, diabetes mellitus, dyslipidemia, and ischemic heart disease [3]. These risk factors contribute to optic disc hypoperfusion, leading to ischemia, necrosis, and subsequent optic nerve atrophy. Currently, the association between OSAHS and NAION is garnering increasing research attention [4]. Although the underlying pathogenic mechanisms of these two conditions differ, they share several common risk factors, particularly those related to hemodynamics, hypoxia, and ocular health. OSAHS is characterized by a clinical syndrome involving repetitive apnea and/or hypopnea during sleep, leading to intermittent hypoxia, hypercapnia, and sleep fragmentation. The majority of NAION episodes occur during sleep. Even after controlling for other risk factors, this nocturnal onset suggests that sleep-related systemic factors may play a significant role in the pathogenesis of NAION. Elucidating the association between OSAHS and NAION may provide a theoretical basis for the clinical prevention and management of NAION [5]. OSAHS significantly correlated with NAION in a severity-dependent manner, making it a critical target for clinical intervention. Therefore, integrating the management of OSAHS into future treatment protocols is essential, as preventing the onset and progression of OSAHS may facilitate the prevention and treatment of NAION [6]. In this case, the patient presented with optic disc edema and was subsequently managed with an appropriate regimen of corticosteroids. Currently, there is no consistently effective pharmacotherapy for NAION, and the use of corticosteroids remains a subject of ongoing controversy. Our treatment choice was based on a specific clinical rationale within this context of uncertainty [7]. Noninvasive ventilation (NIV) was initiated to manage the underlying OSA, aiming to reduce hypoxemic episodes and potentially attenuate long-term optic nerve damage. NAION may still develop despite noninvasive ventilation therapy, indicating that such intervention offers incomplete protection against the disease.

The modest gain in visual acuity (from 0.15 to 0.2) is consistent with the natural course of NAION, in which spontaneous improvement occurs in approximately 43% of cases.

The association between OSAHS and NAION is closely linked to hemodynamic disturbances; Specifically, OSAHS is significantly associated with fluctuations in optic disc perfusion pressure, which represents a key pathophysiological feature [8]. While the “non-dipper” or “reverse-dipper” blood pressure pattern in OSAHS is a known risk factor, it does not fully elucidate the mechanism of nocturnal NAION onset, as some patients experience ischemia even when mean arterial pressure is preserved. A more comprehensive explanation involves severe nocturnal hypoxemia combined with sympathetic overactivity. Recurrent apneic events trigger surges in sympathetic tone, causing systemic vasoconstriction and elevating intracranial pressure (ICP).

Simultaneously, intermittent hypoxia impairs the autoregulatory capacity of the short posterior ciliary arteries, which supply the optic nerve head (ONH) “watershed” zone, rendering them unable to compensate for these pressure changes. Consequently, the ocular perfusion pressure (OPP)—defined as the difference between mean arterial pressure and the elevated ICP or intraocular pressure—may drop below the critical threshold required to sustain metabolic demand, even if systemic blood pressure does not plummet.

This hemodynamic and hypoxic insult is particularly devastating in eyes with anatomically “small” or “crowded” discs (disc-at-risk). In these eyes, the high density of nerve fibers within the confined lamina cribrosa, coupled with hypoxia-induced endothelial dysfunction and a pro-thrombotic state, creates a “perfect storm” for ischemic injury, ultimately leading to axoplasmic stasis, edema, and infarction.

OSAHS is associated with a hemodynamically unstable environment and alterations in the blood supply of the optic nerve head, which are observed in cases of NAION. We acknowledge that in resource-limited settings, diagnostic challenges—such as the scarcity of advanced imaging and rapid diagnostic testing—may delay the detection of such complications.

Conclusion

For patients with ischemic optic neuropathy, presenting to an ophthalmologist, it is important to assess whether they have a history of obstructive sleep-disordered breathing or related symptoms [9], so as to facilitate the identification of the cause of ischemic optic neuropathy and carry out targeted treatment [10].We should enhance our clinical awareness and emphasize the necessity of screening for OSAHS.

Abbreviations

NAION

Nonarteritic anterior ischemic optic neuropathy

OSAHS

Obstructive sleep apnea–hypopnea syndrome

Author contributions

Chenjia Zhang administered the case, curated the data, reviewed the literature, and revised the manuscript. Qihang Lei prepared the initial draft. Xinzhi Song developed the conceptual framework for the case. Yuxia Fan curated the data. Xiangli Wang confirmed the diagnosis and analyzed the entire clinical course.

Funding

This work was supported by Gansu Natural Science Foundation (No. 22JR5RA675) and the Internal Research Fund project of Gansu Provincial Hospital (No. 21GSSYC-9).

Data availability

All data generated or analyzed during this study are included in this published article.

Declarations

Ethics approval and consent to participate

The identity of the patient reported herein remained fully anonymous. Ethical approval was not required for this single case report, in accordance with the institutional policy.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no competing interests.