与阻塞性睡眠呼吸暂停低通气综合征相关的单侧非动脉炎性前部缺血性视神经病变：一例病例报告

文献信息

中文摘要

背景： 本报告描述了一例与阻塞性睡眠呼吸暂停低通气综合征（OSAHS）相关的非动脉炎性前部缺血性视神经病变（NAION）。NAION是一种视神经病变，以无痛性视力丧失、视野缺损和视盘水肿为特征。它由睫状后短动脉灌注不足引起，导致急性缺血及视神经的结构和功能损害，最终表现为视物模糊或失明。
病例介绍： 我们报告一例59岁汉族男性，表现为左眼视物模糊和视野缺损6天。在排除其他潜在病因后确诊。患者接受口服甲泼尼龙80 mg治疗并逐渐减量，同时辅以神经保护和改善循环治疗。经呼吸与睡眠医学科会诊后，开始无创通气（NIV）以纠正全身性缺氧，并接受支气管扩张剂治疗。随后，患者症状出现中度改善。
讨论： NAION常与多种全身血管危险因素相关，尤其是高血压、糖尿病、血脂异常、缺血性心脏病和脑血管疾病。这些疾病损害视神经乳头的微血管供血，导致缺血、坏死及随后的视神经萎缩。其中，OSAHS被认为是重要的独立危险因素。OSAHS是一种临床综合征，以睡眠期间反复发生呼吸暂停和低通气为特征，导致间歇性缺氧、高碳酸血症和睡眠片段化。
结论： OSAHS是全身血管合并症（包括心血管疾病和糖尿病）的公认危险因素。在本病例中，排除其他潜在混杂病因后，观察到OSAHS与NAION之间的关联。这些发现强调了在NAION患者中筛查和管理OSAHS的临床重要性，为优化治疗策略提供了依据。

英文摘要

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.