Ischemic optic neuropathy is the most common non-glaucomatous optic neuropathy in patients over 50 years of age. The disease is classified according to the presence or absence of optic disc edema at the time of vision loss, and can be divided into anterior ischemic optic neuropathy (optic disc edema) and posterior ischemic optic neuropathy (optic disc without edema). The former is more common, while the latter is relatively rare and only used as a diagnosis of exclusion. The most common is giant cell arteritis, called arteritis AION, the incidence of which is rare in China. The occurrence of anterior ischemic optic neuropathy that is not associated with systemic arteritis is called non-arteritic anterior ischemic optic neuropathy (NAION), which is a common type in China. More than 60% of non-arteritic ischemic optic neuropathies have one or more risk factors related to atherosclerosis, such as hypertension and diabetes mellitus. Therefore, patients with the “three highs” of hypertension, hyperlipidemia and hyperglycemia should be alert to diseases caused by “ischemia”, such as myocardial infarction and cerebral infarction. At the same time, optic nerve and retina can also be caused by “ischemia”, such as ischemic optic neuropathy and central retinal artery blockage, which are ophthalmic emergencies and should be treated in hospital as soon as they occur. Clinical features of ischemic optic neuropathy Anterior ischemic optic neuropathy is characterized by sudden visual loss, including visual acuity, visual field or both. The typical loss of vision is painless. In the absence of bilateral symmetric optic nerve abnormalities, relative afferent pupillary dysfunction may be present. Fundoscopic manifestations are fan-shaped or total optic disc swelling, which may be congested or pale with hemorrhage in the nerve fiber layer. Third, ischemic optic neuropathy screening and diagnosis in five steps Non-arteritic anterior ischemic optic neuropathy is the most common optic nerve disease in the Chinese elderly population, with its own characteristics of age of onset, underlying disease, anatomical structure and other aspects, which can be used as a basis for screening and diagnosis. So, how to diagnose non-arteritic anterior ischemic optic neuropathy? 1. Look at the age of onset. Non-arteritic anterior ischemic optic neuropathy usually occurs in the elderly, more than forty years of age, while optic neuritis usually occurs in young people, more than forty years of age. 2. Look at the underlying disease. Non-arteritic anterior ischemic optic neuropathy is usually combined with systemic underlying diseases, especially the three highs (hypertension, diabetes, hyperlipidemia), hypotension, anemia are also combined. 3. Look at the anatomical basis. Patients with non-arteritic anterior ischemic optic neuropathy have a typical optic papilla in the contralateral healthy eye: small cup-to-disc ratio or no cup-to-disc ratio, mostly less than 0.1. High-risk fundus of ischemic optic neuropathy. 4. Look at the optic papilla edema. Optic papillary edema in non-arteritic anterior ischemic optic neuropathy has characteristic manifestations: there is often combined hemorrhage around the optic disc, veins are more tortuous, and optic papillary edema is mostly pale edema. Optic papilledema in ischemic optic neuropathy 5. Look for visual impairment. The visual impairment of non-arteritic anterior ischemic optic neuropathy is painless vision loss, severe visual impairment, and visual field defects are mostly quadrantal. The visual field defect of ischemic optic neuropathy IV. The treatment trilogy of ischemic optic neuropathy: hormone, nutrition, and anticoagulation 1. High-dose hormone therapy for acute ischemic optic neuropathy can accelerate the recovery of visual function There has been international controversy about hormone therapy for non-arteritic ischemic optic neuropathy, according to which Hayreh and Zimmerman conducted a large sample of prospective cohort A large prospective cohort study (evidence-based clinical evidence level 2) was conducted by Hayreh and Zimmerman. A total of 613 non-arteritic ischemic optic neuropathies (696 eyes) were included, 312 (363 eyes) were given oral hormone therapy and 301 (332 eyes) were not given hormone therapy. Hormone administration: prednisone 80 mg once daily for 2 weeks; 70 mg once daily for 5 days; 60 mg once daily for 5 days; then reduced by 5 mg every 5 days. mean follow-up was 3.8 years. At month 6 of treatment, for patients with visual acuity below 20/70 treated within 2 weeks of the episode, the improvement in visual acuity was 69.8% in the hormone-treated group and 40.5% in the control group, with a statistically significant difference between the two (p = 0.001). Also at month 6 of treatment, for patients with visual acuity below 20/70 treated within 2 weeks of the episode, the rate of visual field improvement was 40.1% in the hormone-treated group and 24.5% in the control group, with a statistically significant difference between the two (P = 0.005). Therefore, high-dose hormone therapy for acute phase ischemic optic neuropathy can accelerate the recovery of visual function and effectively improve visual function. At present, a superior hormone treatment regimen can be given: methylprednisolone shock treatment regimen. 2. Neurotrophic treatment can effectively improve visual function in ischemic optic neuropathy In recent years, more and more ophthalmologists have tried to improve visual function in ischemic optic neuropathy through neurotrophic treatment. In a randomized, placebo-controlled clinical trial that included 26 patients with recovered (disease duration >6 months) non-arteritic anterior ischemic optic neuropathy randomized to cytarabine (1600 mg/d) or placebo, cytarabine was effective in improving visual function in ischemic optic neuropathy, whereas placebo did not show any improvement in visual function. Another randomized, double-blind, placebo-controlled clinical trial included 20 patients with recovered (disease duration >6 months) non-arteritic anterior ischemic optic neuropathy who were randomized to levodopa/carbidopa (levodopa 100 mg/carbidopa 10 mg, 1/d, 3 w at 9 w intervals and levodopa 100 mg/carbidopa 25 mg, 1/d, 3 w) or placebo. At 12 weeks of treatment, levodopa/carbidopa was effective in improving visual acuity by 5.9 visual standards in patients with ischemic optic neuropathy compared with placebo; levodopa/carbidopa improved visual acuity by 50% compared with 11% for placebo. Also at 24 weeks of treatment, levodopa/carbidopa was effective in improving visual acuity by 7.5 visual standards in patients with ischemic optic neuropathy; levodopa/carbidopa improved visual acuity by 70% compared to 22% with placebo. Thus, neurotrophic treatment is effective in improving visual function in ischemic optic neuropathy. The proven effective treatment regimens include (1) cytarabine 1600 mg/d orally, (2) levodopa 100 mg/carbidopa 10 mg, 1/d, 3 w at 9 w intervals, and levodopa 100 mg/carbidopa 25 mg, 1/d, 3 w. 3. Anticoagulants can prevent ischemic optic neuropathy in healthy eyes Because ischemic optic neuropathy mostly occurs in Since ischemic optic neuropathy occurs in people with “three highs”, some foreign scholars have tried to use anticoagulant drugs to prevent the re-occurrence of ischemic optic neuropathy. We pooled the results of three previously published retrospective clinical studies and found that oral aspirin was effective in reducing the risk of non-arteritic anterior ischemic optic neuropathy in healthy eyes (nearly doubled). A meta-analysis of aspirin for the prevention of ischemic optic neuropathy episodes Therefore, people at high risk for nonarteritic anterior ischemic optic neuropathy should routinely take oral aspirin to prevent reoccurrence in the contralateral eye once nonarteritic anterior ischemic optic neuropathy in one eye has occurred.