{"title":"Hypertension and the Eye","authors":"S. Graham, Angela M Schulz","doi":"10.15713/INS.JOHTN.0198","DOIUrl":null,"url":null,"abstract":"The retina provides a unique opportunity to assess the systemic circulation in vivo and has long been recognized as an important site for identifying systemic vascular changes in disorders such as hypertension and diabetes. The progressive changes in the vessels occurring in hypertension are readily visible and the accompanying hemorrhages, exudates and infarcts have been described as early as 1939 in a grading system for hypertensive retinopathy by Keith-Wagener-Baker (the KWB system).[1] More recently this has been simplified to a 3-step grading system by Mitchell and Wong,[2] which has been suggested to be easier to apply in practice [Table 1].[3,4] The pathophysiology of sustained hypertension involves initially a vasoconstriction of the retinal arteries, followed by progressive thickening of the elastic lamina and hyaline degeneration.[5] This may be recognized on fundoscopy as focal narrowing of vessels, arteriovenous crossing changes (referred to as “nipping or nicking”) where the hardened artery compresses the vein as it crosses with a shared adventitia, and a progressive change in the vessel wall reflectivity termed copper wiring and silver wiring. With sustained hypertension, small hemorrhages, focal areas of infarction (“cotton-wool spots” – so-called because of their white appearance), as well as lipid exudates from break-down of the blood retinal barrier occur. Lipids can form a visible “macular star” pattern. These changes occur in the inner retinal circulation which is derived from the central retinal artery. The choroid, which is the deeper vascular layer of the eye directly beneath the retina supplying the photoreceptors, derives its circulation from the long and short posterior ciliary arteries, which branch from the ophthalmic artery. In severe hypertension, choroidal changes can also occur,[6,7] including choroidal infarcts (represented as Elschnig’s spots – seen as pale, yellow lesions) and pigmentation lines along the larger choroidal vessels (termed Siegrist streaks). Severe hypertension can also lead to optic disc swelling through raised intracranial pressure and optic disc ischemia – termed hypertensive optic neuropathy, and this stage has been termed “malignant hypertension.” The risk of stroke and systemic organ damage is high at this stage, as discussed below. Abstract","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Hypertension Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15713/INS.JOHTN.0198","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
The retina provides a unique opportunity to assess the systemic circulation in vivo and has long been recognized as an important site for identifying systemic vascular changes in disorders such as hypertension and diabetes. The progressive changes in the vessels occurring in hypertension are readily visible and the accompanying hemorrhages, exudates and infarcts have been described as early as 1939 in a grading system for hypertensive retinopathy by Keith-Wagener-Baker (the KWB system).[1] More recently this has been simplified to a 3-step grading system by Mitchell and Wong,[2] which has been suggested to be easier to apply in practice [Table 1].[3,4] The pathophysiology of sustained hypertension involves initially a vasoconstriction of the retinal arteries, followed by progressive thickening of the elastic lamina and hyaline degeneration.[5] This may be recognized on fundoscopy as focal narrowing of vessels, arteriovenous crossing changes (referred to as “nipping or nicking”) where the hardened artery compresses the vein as it crosses with a shared adventitia, and a progressive change in the vessel wall reflectivity termed copper wiring and silver wiring. With sustained hypertension, small hemorrhages, focal areas of infarction (“cotton-wool spots” – so-called because of their white appearance), as well as lipid exudates from break-down of the blood retinal barrier occur. Lipids can form a visible “macular star” pattern. These changes occur in the inner retinal circulation which is derived from the central retinal artery. The choroid, which is the deeper vascular layer of the eye directly beneath the retina supplying the photoreceptors, derives its circulation from the long and short posterior ciliary arteries, which branch from the ophthalmic artery. In severe hypertension, choroidal changes can also occur,[6,7] including choroidal infarcts (represented as Elschnig’s spots – seen as pale, yellow lesions) and pigmentation lines along the larger choroidal vessels (termed Siegrist streaks). Severe hypertension can also lead to optic disc swelling through raised intracranial pressure and optic disc ischemia – termed hypertensive optic neuropathy, and this stage has been termed “malignant hypertension.” The risk of stroke and systemic organ damage is high at this stage, as discussed below. Abstract