THE RISK OF NON ARTERITIC OPTIC NEUROPATHY IN HYPERTENSION PEOPLEEiffel (112014090), Selley Kenanga (112014102), Gio Vano Beril Karel Naihonam (112014127), Steaffie Eunike Cassandra (112014169), Elcha (112014172)ABSTRACTIntroduction: Non Arteritic Optic Neuropathy Anterior is the most common acute optic neuropathy in people older than 50 years. It is characterized by sudden vision loss in one eye, usually painless, which can increase the risk of vision loss in the contralateral eye. Although definite cause has not been determined, NAION is thought to occur following an idiopathic ischemic event involving the short posterior cilliary arteries that supply blood to the most anterior part of the optic nerve. Other factors that have been hypothesized to associate with NAION include high cholesterol, arteriosclerosis, stroke, cardiac and intraocular surgery, tobacco use, nocturnal hypotension, blood loss, glaucoma, hiperhomocsyteine and sleep apneu. The most common cause of NAION is hypertension. The condition of high blood pressure can damage to the retina, which can changes light and images that enter the eye into nerve signals that are sent to the brain. It also can damage to the nerves in the eye (ischemic optic neuropathy) due to poor blood flow.Method: The literature review is conducted by several major steps such as searching journals and books associated to NAION pathogenesis according to hypertension, the progression of NAION, and reviewing the risk factor of the hypertension individuals to NAION.Results: The sympathetic nervous control and autoregulatory mechanisms of the retinal and choroidal vasculatures are briefly reviewed. In hypertensive choroidopathy focal occlusion of choriocapillaris leads to necrosis of retinal pigment epithelium (Elschnig spots). Hypertensive retinopathy is described in vasoconstrictive, exudative, and sclerotic phases, followed by complications of the sclerotic phase. Hypertensive optic disc edema is influenced by the blood supply and extracellular tissue fluid pressure of the optic nerve head. In baboons with hypertensive disc edema, accumulation of axoplasmic components is observed in the optic nerve head.Conclusions: Systemic hypertension, arteriosclerosis, vasospasm or medications may reduce the autoregulatory capacity of the optic disc. Vasoactive substances might be released in response to ischemia that influence the autonomic control of blood vessels; prove the hypothesis the correlation between hypertension with NAAION.Keyword: NAION, hypertension, optic neuropathy.INTRODUCTIONHypertension is one of the most common worldwide diseases afflicting humans. Hypertension has been described as the most important modifiable risk factor for coronary heart disease, stroke, congestive heart failure, and end stage renal disease. The prevalence of hypertension in 2003-2004 was 25,8 % at the 18-39 age group. Hypertension is usually asymptomatic until the damaging effects of hypertension. Because of assymptomatic, high blood pressure is undertreated and underdiagnosed among all races and genders. Beside of macrovascular effect, the condition of high blood pressure can damage to retina, which can damage to the nerves in the eye (ischemic optic neuropathy). The acute elevation of blood pressure typically causes reversible vasoconstriction in retinal blood pressure, and hypertensive crisis may cause optic disk edema. More prolonged or severe hypertension leads to exudative vascular changes, a consequences of endothelial damage and necrosis.METHODSThe objective of this study is to provide knowledge regarding NA-AION and to introduce fellow medical students and people about the risk of NA-AION as a complication of hypertension.The method used for this paper is literature review. This study is conducted by several major steps such as searching the worldwide websites, journals and articles associated to NA-AION pathogenesis, identifying the possible etiological factors of NA-AION, looking for the correlation between NA-AION and hypertension, and reviewing the risk of NA-AION in people with hypertension.RESULTSIschemic optic neuropathies are the most frequent acute optic neuropathies in patients > 50 years of age. Depending on the segment of optic nerve affected, they are subdivided into anterior and posterior ischemic optic neuropathies. Optic disc edema from ischemia to the anterior nerve is present in anterior ischemic optic neuropathy (AION) and absent in posterior ischemic optic neuropathy (PION). AION is much more common than PION, accounting for 90% of cases of optic nerve ischemia.1,2AIONs are subdivided into non-arteritic and arteritic etiologies. Arteritic anterior ischemic optic neuropathy (AAION), classically due to Hortons giant cell arteritis (inflammation of mid-sized arteries), is an ophthalmologic emergency, requiring prompt recognition and treatment to prevent devastating blindness. About 9095% cases of AION are non-arteritic anterior ischemic optic neuropathy (NAAION). 1-3Non-arteritic anterior ischemic optic neuropathy (NAION) is the most common acute optic neuropathy in patients over the age of 50 and is the second most common cause of permanent optic nerve-related visual loss in adults after glaucoma.3The Risk Factors of NA-AIONNA-AION may be mainly recognized as a multi-factorial disease, with many risk factors collectively contributing to its pathophysiology. The most commonly proposed pathogenic theory involves an insufficiency of the optic disc circulation, exacerbated by structural crowding of nerve fibers and supporting structures at the nerve head, resulting in inadequate oxygenation, ischemia and swelling of the disc. 4,5NA-AION could be caused by several combined factors which is the increasing blood flow resistance, arterial hypotension, and reduction of perfusion pressure. Increasing blow flow due to systemic and local causes including aging processes, arterial hypertension, diabetes mellitus, atherosclerosis, hypercholesterolemia or increased blood viscosity due to haematologic disorder. Arterial hypotension mainly caused by nocturnal arterial hypotension during sleep or by intensive antihypertensive medication. Reduction of perfusion pressure intended as the difference between the mean systemic blood pressure and the intraocular pressure (IOP) which may be due to arterial hypotension but also to a relevant rise of the IOP. Thus, according to the available evidence, ischemic optic neuropathy, and particularly the NA-AION, is a multifactorial disease: this means that each patient may have a special combination of systemic and local factors that all together may have caused it.4,5NAION typically presents with rapid onset, stable course, unilateral loss of visual acuity and/or field and generally poor recovery. The visual loss in NAION is commonly first noted upon awakening, and may progress over several hours to days, and rarely even weeks. Visual acuity may range from 20/15 to no light perception, though severe visual loss may prompt investigation for alternative types of optic neuropathy such as AAION or optic neuritis. Patients also tend to have mild to moderate dyschromatopsia consistent with the degree of acuity loss.6With respect to the visual field defect in NAION, though any pattern of loss may develop, the most common are an inferior altitudinal or arcuate defect. Visual field patterns in NAION resemble the nerve fiber bundle defects of glaucoma and typically obey the horizontal midline. An altitudinal field defect, usually involving the inferior field, is most common, but generalized depression, broad arcuate scotomas, and cecocentral defects also are seen.6

Figure 1. Typical inferior altitudinal/arcuate visual field defect in NAION.5Fundus examination of the optic nerve may reveal disc edema with possible peripapillary hemorrhaging. The end stage finding is pallor of the nerve head which can be diffuse or sectoral depending on the amount of initial edema. Examination of the fellow eye may show a disc at risk.. This term is used to describe the appearance of the fellow nerve, which is small and crowded with blood vessels, with minimal to no cup-to-disc ratio. This anatomical presentation is thought to compromise the blood supply to the optic nerve, leaving it at risk for possible future involvement. NAION is a diagnosis of exclusion and A-AION should be ruled out. Test results show a normal ESR and CRP as the condition is not inflammatory but vascular in nature. Also, patients will rarely have episodes of amaurosis fugax, or systemic symptoms suggesting GCA. If a temporal artery biopsy is performed, it will also be negative.6

Figure 2. Appearance of affected and unaffected optic discs in a patient with NAION. a, optic disc in eye with NAION is swollen and hyperaemic. Note several peripapillary flame-shaped haemorrhages. b, optic disc in unaffected eye is small and has no cup.5NA-AION Current ManagementThere are no accepted treatment guidelines although numerous surgical and medical therapies have been proposed including: optic nerve decompression, aspirin, anti-coagulants, thrombolytics, vasodilating agents, systemic steroids, intravitreal triamcinolone, anti- vegf agents, levodopa, diphenylhydantoin and hyperbaric oxygen. Literature on these treatments, however, is mostly of retrospective or prospective case series with the largest study on NA-AION treatment, the Ischemic Optic Neuropathy Decompression Trial, showed that treatment actually exacerbated the condition. The general consensus among clinicians is that the systemic vascular diseases that precipitate the condition should be well managed in hopes of averting or delaying bilateral ocular involvement and further systemic involvement.6,7HypertensionHypertension is a chronic elevation of blood pressure that, in the long term ,causes end-organ damage and results in increase morbidity and mortality. Blood pressure is the product of cardiac output and systemic vascular resistance. It follows that patients with arterial hypertension may have an increase in cardiac output, an increase in systemic vascular resistance, or both. In the younger age group, the cardiac output is often elevated, while in older patients increased systemic vascular resistance and increased stiffness of the vasculature play a dominant role. Vascular tone may be elevated because of increased -adrenoceptor stimulation or increased release of peptides such as angiotensin or endothelins. The final pathway is an increase in cytosolic calcium in vascular smooth muscle causing vasoconstriction. Table 1. JNC 7: Hypertension Classification.8Hypertension can effect the retina, choroid, and optic nerve of the eye, particularly with stage 2 hypertension. These changes can be appreciated with inspection of the retinal vessels by direct ophthalmoscopy, photography, or angiography. In acute or advanced hypertension, the retinal vasculature may be injured sufficiently to cause occlusion or leakage. These changes may be manifested as nerve fiber layer infarcts (soft exudates or cotton-wool patches), extravascular edema (hard exudates), intra retinal hemorrhages, and retinal arterial macroaneurysms.8,9DISSCUSIONThe pathogenesis of NAAION is clearly multifactorial; acute blood loss, migraine, periarteritis nodosa, and other vascular disorders predispose patients to ischemic optic neuropathy on less frequent occasions. Several observers have found focal areas of infarction, post mortem, in the retrolaminar region of the optic nerve in patients with ischemic optic neuropathy. The almost invariably anterior location of the infarction produces disk edema, not only through ischemia, but also by compromise of venous and perhaps axoplasmic flow through the inexpansile scleral canal with its rigid supporting network, the lamina cribrosa. Certain vascular anatomic factors, some still unknown, may render this region especially vulnerable to infarction. Functional properties of the disk vasculature may also play a role in this vulnerability.8,9 Loss of blood supply within the posterior cilliary arteries deprives the optic nerve tissue of oxygen and results in damage to part or all of the optic nerve. This is a small "stroke" in the optic nerve but unlike other strokes is unassociated with weakness, numbness, or loss of speech, nor is there an increased risk of a classic stroke later. It is also not associated with pain. Patients may become aware of decreased vision or difficulty seeing above or below the center of gaze. Loss of the blood supply results in swelling of the optic disc, often associated with hemorrhages. The hemorrhages and swelling will go away within several weeks leading to the development of a pale disc (optic atrophy). As the swelling resolves, some of the affected portion of the nerve fiber layer disappears from the surface of the retina and the axons will be permanently lost.8,9CONCLUSION1. Non-Arteritic Anterior Ischemic Optic Neuropathy (NAAION) is the leading cause optic neuropathy in persons over age 50 and associated with hypertension.2. Main proccess in NAAION pathogenesis is insufficiency of the optic disc circulation, exacerbated by structural crowding of nerve fibers and supporting structures at the nerve head, resulting in inadequate oxygenation, ischemia and swelling of the disc.3. Hypertension can effect the retina, choroid, and optic nerve of the eye, particularly with stage 2 hypertension. The retinal vasculature may be injured sufficiently to cause occlusion or leakage. Loss of blood supply within the posterior cilliary arteries deprives the optic nerve tissue of oxygen and results in damage to part or all of the optic nerve; prove the hypothesis that people with hypertension have a higher risk of NAAION.REFERENCES1. Giusti C. (2010). Bilateral non-arteritic anterior ischemic optic neuropathy (NA-AION): case report and review of the literature. European Review for Medical and Pharmalogical Sciences 14: 141-42. Banik R. (2013). Nonarteritic anterior ischemic optic neuropathy: an update on demographics, clinical presentation, pathophysiology, animal models, prognosis, and treatment. J Clin Exp Ophthalmol S3: 004.3. Lin MC, Hsu FM, Sheu SJ. (2007). Nonarteritic ischemic optic neuropathy. J Chin Med Assoc 70:2.4. Brouzas D, Charakidas A, Ladas I, Apostolopolous M. (2009). Nonarteritic anterior ischemic optic neuropathy associated with chronic anemia: a case series of myelodysplastic syndrome patients. Clinical Ophthalmology 3:133137.5. Miller NR, Arnold AC. (2015). Current concepts in the diagnosis, pathogenesis and management of non artheritic anterior ischaemic optic neuropathy. Eye 29: 65-79.6. Bahkhri R. (2014). Ischemic optic neuropathy. California Optometry Jan/Feb:44-507. Hayreh SS. (2008). Non-arteritic anterior ischemic optic neuropathy: role of systemic corticosteroid therapy. Graefes Arch Clin Exp Ophthalmol Jul; 246(7):10291046.8. Chobanian AV, et all. (2003). Hypertension: seventh report of the national committee on prevention, detection, evaluation, and treatment of high blood pressure. AHA Journals: 42: 1206-529. Fox P, Sear JW. (2004). Hypertension: pathophysiology and treatment. In: Continuing education in anaesthesia, critical care & pain. 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