Hypertension and the Eye

Q4 Medicine
S. Graham, Angela M Schulz
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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
高血压与眼睛
视网膜提供了一个独特的机会来评估体内的体循环,长期以来被认为是识别高血压和糖尿病等疾病的全身血管变化的重要部位。高血压患者血管的进行性改变很容易看到,并且伴随的出血、渗出液和梗死早在1939年keith - wagner - baker (KWB系统)的高血压视网膜病变分级系统中就有描述。[1]最近,Mitchell和Wong将其简化为三步评分系统[2],并建议在实践中更容易应用[表1]。[3,4]持续高血压的病理生理包括视网膜动脉最初的血管收缩,随后是弹性层的进行性增厚和透明变性[5]。在眼底镜检查中可识别为血管局灶性狭窄,动静脉交叉改变(称为“夹击或划痕”),硬化的动脉在与共享外膜交叉时压迫静脉,血管壁反射率进行性改变,称为铜线和银线。如果高血压持续存在,就会出现小出血、梗死灶(“棉絮斑”——因为它们的外观呈白色而被称为“棉絮斑”)以及因血液视网膜屏障破裂而渗出的脂质。脂质可形成可见的“黄斑星型”。这些变化发生在视网膜内循环,起源于视网膜中央动脉。脉络膜是眼内较深的血管层,位于视网膜下方,供应光感受器,它的循环来源于长、短后睫动脉,后者是眼动脉的分支。在严重高血压患者中,脉络膜也会发生改变,[6,7]包括脉络膜梗死(表现为Elschnig斑点——呈淡黄色病变)和沿较大脉络膜血管的色素沉着线(称为Siegrist条纹)。严重的高血压也可通过颅内压升高和视盘缺血导致视盘肿胀——称为高血压性视神经病变,这一阶段被称为“恶性高血压”。中风和全身器官损伤的风险在这个阶段是很高的,如下所述。摘要
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来源期刊
Open Hypertension Journal
Open Hypertension Journal Medicine-Cardiology and Cardiovascular Medicine
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