{"title":"Hypertensive retinopathy","authors":"Kumudini Sharma , Vikas Kanaujia , Priyadarshini Mishra , Rachna Agarwal , Alka Tripathi","doi":"10.1016/j.cqn.2013.08.001","DOIUrl":null,"url":null,"abstract":"<div><p><span>The term hypertensive retinopathy is used for all the fundus changes caused by increased systemic </span>arterial blood pressure<span><span><span><span>. Retinal vasculature can be seen non-invasively through </span>fundoscopy<span><span><span> and their similarity to other microvasculature in the body make early diagnosis of hypertensive </span>retinopathy very important in hypertensive </span>risk stratification<span><span>. The usual features of chronic hypertensive retinopathy are arteriolar attenuation, nerve fiber layer infarct, superficial flame shaped hemorrhage, lipid exudates, </span>macular edema<span><span>. In malignant hypertension<span> choroidopathy and optic neuropathy can be seen in addition to retinopathy. Many of these changes resolve with time when control of blood pressure is good. For grading of hypertensive retinopathy Scheie classification and Keith-Wagener-Barker classification are most commonly used. Diagnosis of hypertensive retinopathy is clinical by ophthalmoscopy. Others like fundus photography, </span></span>fluorescein angiography, </span></span></span></span>optical coherence tomography can be used for added information. Decrease vision if occur is due to macular edema, secondary </span>retinal pigment<span> epithelial changes and due to optic neuropathy. Blood pressure lowering is the mainstay of treatment which should be in a slow and controlled manner in case of malignant hypertensive retinopathy to avoid ischemic damage.</span></span></p></div>","PeriodicalId":100275,"journal":{"name":"Clinical Queries: Nephrology","volume":"2 3","pages":"Pages 136-139"},"PeriodicalIF":0.0000,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cqn.2013.08.001","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Queries: Nephrology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2211947713000277","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The term hypertensive retinopathy is used for all the fundus changes caused by increased systemic arterial blood pressure. Retinal vasculature can be seen non-invasively through fundoscopy and their similarity to other microvasculature in the body make early diagnosis of hypertensive retinopathy very important in hypertensive risk stratification. The usual features of chronic hypertensive retinopathy are arteriolar attenuation, nerve fiber layer infarct, superficial flame shaped hemorrhage, lipid exudates, macular edema. In malignant hypertension choroidopathy and optic neuropathy can be seen in addition to retinopathy. Many of these changes resolve with time when control of blood pressure is good. For grading of hypertensive retinopathy Scheie classification and Keith-Wagener-Barker classification are most commonly used. Diagnosis of hypertensive retinopathy is clinical by ophthalmoscopy. Others like fundus photography, fluorescein angiography, optical coherence tomography can be used for added information. Decrease vision if occur is due to macular edema, secondary retinal pigment epithelial changes and due to optic neuropathy. Blood pressure lowering is the mainstay of treatment which should be in a slow and controlled manner in case of malignant hypertensive retinopathy to avoid ischemic damage.