Nonarteritic Anterior Ischemic Optic Neuropathy Pdf Free
Emoni Rasner
Anterior ischemic optic neuropathy occurs due to decreased blood supply to the optic nerve head. It is divided into a) Arteritic anterior ischemic optic neuropathy (A-AION) and b) Non-arteritic anterior ischemic optic neuropathy (NAION). These two conditions have entirely different ethology and approach to their diagnosis and management is completely different. This activity will focus on the role of the interprofessional team in the diagnosis and management of NAION.
Objectives:
- Identify the etiology of NAION.Summarize the evaluation of NAION.Outline the management options available for NAION.Discuss interprofessional team strategies for improving care coordination and communication to advance NAION management and improve outcomes.
The pathophysiology of NAION is not completely understood, but it is accepted that relative hypoperfusion of the optic nerve head, as well as structural or other factors, lead to edema and infarction of optic nerve fibers, most often in the superior half of the ONH.[6]
NAION is the most common cause of optic neuropathy in adults over 50 years of age.[1] The prevalence of NAION in the US has been estimated to be anywhere between 2.3 to 10.2 per 100000. It is less common in blacks and is most common in Caucasians presumably because blacks tend to have a larger cup to disc ratio and are thus less likely to have small optic nerve cups, which is the biggest risk factor for developing NAION.
As mentioned above, the exact pathophysiology of NAION; however, the main theory is that the hypoperfusion of short posterior ciliary arteries supplying the optic nerve head leads to localized edema of the involved axons.[9] As the scleral canal through which optic nerve passes into its intra-orbital compartment is small, in predisposed individuals (those with small cup-to-disc ratio) localized optic nerve head edema leads to a compartment syndrome where the swelling is propagated by affecting the neighboring axons. This eventually leads to severe axonal swelling/ischemia and apoptosis with loss of function of the involved axons.
Complete neuro-ophthalmological history should be obtained emphasizing the onset of visual loss (typically sudden in NAION and semi-acute in optic neuritis) and any other associated symptoms (about 10-15% of patients with NAION experience pain in and around the eye but not with eye movements as is typical in optic neuritis).
Medications history with specific attention to the use of PD-5 inhibitors and anti-hypertensive medications, especially the use of these medications at night, as well as the use of amiodarone, which can be associated with the anterior optic neuropathy whose presentation can be similar to NAION.
The diagnosis of NAION is a clinical one: all patients must have optic nerve edema at the time of presentation and over 97% of patients would have a disc-at-risk in the fellow eye with the cup to disc ratio of 0.2 or less.
While many medications and treatment strategies have been tried over the years, none have been proven to be effective. One of the very few randomized controlled clinical trials in neuro-ophthalmology was done evaluating whether patients with NAION will benefit from optic nerve head decompression via vitrectomy and demonstrated that surgery was not beneficial and potentially harmful.[3]
Recently, a clinical trial evaluating intravitreal injection of QRK207, a caspase 2 inhibitor preventing apoptosis, in patients with recent (within 14 days from onset) onset of NAION did not demonstrate its efficacy and was stopped early.
Currently, the only clinical trial that is ongoing includes subcutaneous injections of RPh201, an isolated botanical extract of gum mastic, for patients who had an onset of NAION within 1-5 years prior to enrollment.
The natural course of the disease in NAION has been elucidated by the results of the optic nerve decompression treatment trial which demonstrated that 1/3 of patients will re-gain 3 or more lines of vision at 2 years follow up, 30% will lose 3 or more lines at 2 years, and the rest will demonstrate unchanged visual acuity.[14] In reality, most patients likely maintain the vision they have after the resolution of acute optic nerve head edema, and the improvement seen was secondary to their learned ability to fixate around their scotomas.
There are several risk factors of anterior ischemic optic neuropathy, which can be modified. Patients are advised to have a sleep study, and if diagnosed with sleep apnea to start treatment for this condition, modifications of vascular risk factors should be recommended to all patients, avoidance of nocturnal hypotension has been suggested by many clinicians to be an important strategy to prevent NAION in the fellow eye as well. The use of phosphodiesterase inhibitors should also be discussed.
The correct diagnosis and management of ischemic optic neuropathies are essential to ensure that all potential risk factors are modified in order to decrease the chance of a patient developing this condition in the fellow eye. The possible associations like diabetes, hypertension, hyperlipidemia, when present, should be managed by the interprofessional team, including endocrinologists and general physicians. The team can also include optometrists, neurologists, and ophthalmologists. The nurses participate in patient education and follow up, informing the ophthalmologist of any new issues.
Non-arteritic anterior ischemic optic neuropathy (NAION) refers to loss of blood flow to the optic nerve (which is the cable that connects the eye to the brain). This condition typically causes sudden vision loss in one eye, without any pain. In many cases, the patient notices significant loss of vision in one eye immediately upon waking up in the morning. The visual loss typically remains fairly stable, without getting markedly better or worse once it has occurred.
The exact mechanism causing reduced blood flow to the optic nerve in NAION is not proven, but it is known that this condition occurs more often when a patient has conditions such as diabetes, high blood pressure, and sleep apnea. Smoking may also elevate the risk of developing NAION. Most patients with NAION have an anatomical variation of the optic nerve, making its contents very tight and crowded. This anatomy probably contributes to the impaired circulation that causes NAION.
Although it is controversial, some researchers believe that another risk factor for NAION may be the use of blood pressure medications at nighttime, contributing to lower blood pressure during sleep. Another controversy regarding the cause of NAION concerns the use of medications for erectile dysfunction. The link to these medications is not proven, and current studies are trying to carefully address this question.
After taking a thorough history, the doctor will perform a careful examination that includes measuring the visual acuity, color vision, and peripheral visual field. In most cases of ischemic optic neuropathy, the doctor will see swelling of the optic nerve in the back of the eye. Depending on other clinical factors, some blood work may be done to exclude other diseases that affect the optic nerve. For example, it is important to exclude the possibility of Temporal Arteritis, which requires urgent treatment to prevent loss of vision in the other eye. Imaging studies (such as a CT or MRI scan) are not usually needed to diagnose NAION, but might be performed in an atypical case.
Unfortunately, there are no treatments for NAION that are proven to be effective. There have been many clinical trials studying over a dozen different therapies, but none have convincingly improved the visual outcome in patients with NAION. Some studies have investigated the use of corticosteroids (prednisone) and suggested a mild improvement, but these studies did not use rigorous scientific methods, and it remains unknown if steroids are actually helpful.
Eyeglasses do not correct the vision loss due to NAION. Eyeglasses are used to focus light in front of the eye. With NAION, the problem causing loss of vision is in the back of the eye, where the optic nerve exits to connect to the brain. If the affected eye has a separate problem of near-sightedness or far-sightedness, then glasses can be used for that reason, but they do not help the loss of vision due to an injured optic nerve.
To try to reduce the risk that NAION occurs in the other eye, the doctor might suggest regular exercise, a healthy diet, and other measures to treat the risk factors of diabetes, high blood pressure, and sleep apnea. For a patient that has had NAION, it is probably reasonable to avoid taking high blood pressure medications before bedtime. It is also often recommended to take daily aspirin, although this treatment is not supported by definite evidence.
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Based on histopathology, electron microscopic corrosion cast studies, optic nerve blood flow studies, and clinical data, the pathogenesis of idiopathic nonarteritic ischemic optic neuropathy includes the following features: (1) structurally crowded optic discs are predisposed; (2) laminar and retrolaminar regions are the most common locations for infarction; (3) there is flow impairment in the prelaminar optic disc during the acute phase; (4) lack of consistent choroidal flow impairment and the retrolaminar location of infarcts suggest vasculopathy within or distal to the paraoptic branches of the posterior choroidal arteries; (5) diabetes is the most consistently identified vasculopathic risk factor; (6) impaired autoregulation of the disc circulation by atherosclerosis, with a possible contribution from serotonin and endothelin-mediated vasospasm, may play a role; and (7) progression may be caused by secondary cell death after the initial ischemic insult or compression from cavernous degeneration and mechanical axonal distortion.
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