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Ophthalmologic Manifestations of Hypertension 

  • Author: Kean Theng Oh, MD; Chief Editor: Hampton Roy, Sr, MD  more...
Updated: Apr 21, 2016

Acute and Chronic Changes to the Eyes

Acute and chronic hypertensive changes may manifest in the eyes, respectively, from acute changes from malignant hypertension and chronic changes from long-term, systemic hypertension.

Ocular involvement in the setting of malignant hypertension was first described by Liebreich, in 1859. Hayreh, over the course of the 1970s and 1980s, elucidated pathophysiologic mechanisms for ocular involvement and described clinical findings through direct patient management observations and animal models. Fundamentally, the ocular effects of hypertension arise from hypertension's impact on the ocular vasculature.

Ocular changes can be the initial finding in an asymptomatic patient with hypertension, necessitating a primary care referral. In other instances, a symptomatic patient may be referred to an ophthalmologist for visual problems caused by hypertensive changes.

Prompt and accurate diagnosis of hypertensive retinopathy, especially when associated with malignant hypertension, is necessary to avoid visual and systemic morbidity. In addition, appropriate patient education regarding proper diet, exercise, and medication compliance is crucial. For excellent patient education resources, visit eMedicineHealth's Eye and Vision Center and Diabetes Center. Also, see eMedicineHealth's patient education articles Ocular Hypertension, High Blood Pressure, and Diabetic Eye Disease.


Retinal arteries are histologic arterioles with 100 µm calibers and no internal elastic lamina or continuous muscular coat. Changes in the luminal diameter of the arterioles are the most important component in regulating systemic arterial blood pressure. The resistance of flow is equivalent to the fourth power of the diameter. Therefore, a 50% decrease in the lumen results in a 16-fold increase in the pressure.

Retinal arterioles and capillaries are similar in anatomy to cerebral vessels in that they exhibit autoregulatory mechanisms and tight junctions to maintain the blood-ocular barrier. Choroidal arterioles and capillaries have fenestrations (ie, no blood-ocular barrier) and do not exhibit autoregulation. Optic nerve–head vessels exhibit intermediary characteristics with autoregulation but an incompetent blood-ocular barrier as a result of the peripapillary choroidal vessels.

Because of the vascular differences between the retina, the choroid, and the optic nerve, each of these anatomic regions responds differently to hypertension. Together, however, they represent the clinical picture of the ocular response to systemic hypertension.

For more information, see Hypertension.

Hypertensive vascular changes

Arteriosclerotic changes are chronic changes resulting from systemic hypertension. In the retina, atherosclerosis and arteriolosclerosis predominate.

According to Spencer, the normal light reflex of the retinal vasculature is formed by the reflection from the interface between the blood column and vessel wall.[1] Initially, the increased thickness of the vessel walls causes the reflex to be more diffuse and less bright. Progression of sclerosis and hyalinization causes the reflex to be more diffuse and the retinal arterioles to become red-brown. This is known as copper wiring.

Advanced sclerosis of the retinal vasculature leads to increased optical density of the retinal blood vessel walls; this is visible on ophthalmoscopy as a phenomenon known as sheathing of the vessels. When the anterior surface becomes involved, the entire vessel appears opaque (pipe-stem sheathing). The patency of such vessels has been demonstrated by fluorescein angiography. When sheathing encircles the wall, it produces a silver-wire vessel.

Generalized attenuation of the arterioles results from diffuse vasospasm, which occurs when a significant elevation of blood pressure has persisted for an appreciable period. A relationship has been noted between the narrowing of the caliber of the arteriole and the height of the diastolic pressure. Increased intraluminal pressure either in the retinal arterioles or in the central artery of the retina causes narrowing of the arterioles.

Wang et al reviewed the incidence of microvascular changes associated with systemic arterial hypertension in 2058 subjects. They identified that focal arteriole narrowing was closely related to control of hypertension. They postulated that the presence of focal arteriole narrowing was the precursor to more recognized microvascular abnormalities associated with hypertension.[2]

Focal narrowing occurs from spasm of local areas of the vascular musculature. Spencer speculated that either edema in and around the vessel wall or vascular spasm leads to focal narrowing, which can become permanent with fibrosis.

In arteriovenous nicking (the Gunn sign), impeded circulation results in a dilated or swollen vein peripheral to the crossing, causing hourglass constrictions on both sides of the crossing and aneurysmal-like swellings. Ikui noted that arteriole and venous basement membranes are adherent with shared collagen fibers at the crossing points. Thickening of the basement membrane and the media of the arteriole in hypertension impinge on the vein and cause the crossing phenomenon.[1] Mimatsu asserted that the crossing changes were due to sclerotic thickening of the wall of the venule and not by compression by the arteriole, whereas Seitz attributed the crossing phenomenon to vascular sclerosis and perivascular glial cell proliferation and not to venous compression.[1]

Sclerosis may shorten or elongate retinal arterioles, with the branches coming off at right angles. This change in length deflects the veins at the common sheath and changes the course of the vein (Salus sign). According to Albert et al, the original crossing angle, the degree of vascular thickening, and the pressure differential influence this phenomenon.[3]

Acute hypertensive retinal changes (hypertensive retinopathy)

Changes in the retinal circulation in the acute phase of hypertension primarily involve the terminal arterioles rather than the main retinal arterioles. Main retinal arteriole changes are seen and recognized as a response to chronic systemic hypertension.

First described by Hayreh, focal intraretinal periarteriolar transudates (FIPTs) are observed in malignant arterial hypertension. Consisting of small, white, focal, oval lesions deep in the retina, they are associated with major arteriole vessels and are among the earliest retinal lesions caused by malignant hypertension.

FIPTs may be related to dilation of terminal arterioles and the breakdown of autoregulatory mechanisms due to an acute, malignant increase in blood pressure. This results in the breakdown of the blood-retinal barrier, allowing transudation and accumulation of macromolecules. FIPTs are not associated with capillary obliteration and are not cotton-wool spots. They are hyperfluorescent and leak on fluorescein angiography.

Fluffy, white lesions found at the level of the nerve fiber layer, inner retinal ischemic spots, also called cotton-wool spots, are located more commonly at the posterior pole and are related to the distribution of the radial peripapillary capillaries. These cotton-wool spots last approximately 3-6 weeks before fading away. Their fluorescein angiographic appearance is hypofluorescent due to nonperfusion and capillary dropout.

Capillary obliteration results in the development of microaneurysms, shunt vessels, and collaterals. Hayreh noted that the development of blot retinal hemorrhages is neither an early nor a conspicuous finding associated with malignant hypertension.

Acute hypertensive choroidopathy

The effects of hypertension on the choroid are related to the anatomic and functional differences found in the choroidal vasculature, as compared with the retinal vasculature. Sympathetic innervation makes terminal arterioles more susceptible to vasoconstriction. Fenestrations in the capillaries and the consequent lack of a blood-ocular barrier allow free passage of macromolecules. No autoregulation increases susceptibility to elevated perfusion pressures.

Acute ischemic changes in the choriocapillaris and overlying retinal pigment epithelium result in acute, focal retinal pigment epithelium lesions. These focal, white spots at the level of the retinal pigment epithelium are similar to FIPTs.

Serous retinal detachments, which preferentially affect the macular region, cause neurosensory retinal detachments (NSRD) and cystoid macular edema. Ischemic damage to the retinal pigment epithelium leads to breakdown of the blood-retinal barrier. Hayreh observed that the presence of NSRDs was correlated to the degree of choroidal circulation disruption.

Acute hypertensive optic neuropathy

Optic disc edema is a primary manifestation of hypertensive optic neuropathy. The blood supply to the optic nerve arrives via posterior ciliary arteries and peripapillary choroidal vessels. Vasoconstriction and choroidal ischemia in the setting of malignant hypertension result in optic disc edema and axoplasmic flow stasis.[4]

Chronic hypertensive retinal changes

Chronic hypertensive changes to the retina include the following (see Hypertensive Vascular Changes):

  • Arteriolosclerosis - Localized or generalized narrowing of vessels
  • Copper wiring and silver wiring of arterioles as a result of arteriolosclerosis (See Assessment.)
  • Arteriovenous (AV) nicking as a result of arteriolosclerosis
  • Retinal hemorrhages
  • Nerve fiber layer losses
  • Increased vascular tortuosity
  • Remodeling changes due to capillary nonperfusion, such as shunt vessels and microaneurysms

Chronic hypertensive choroidal changes

Retinal pigment epithelium changes include the development of diffuse pigmentary granularity and a moth-eaten appearance. Areas of retinal pigment epithelium clump and atrophy (Elschnig spots), forming from the focal acute white retinal pigment epithelium lesions. Triangular patches of atrophy result from the occlusion of a larger-caliber choroidal vessel

Chronic hypertensive optic nerve changes

Optic disc pallor develops in chronic hypertension.



Extravascular retinal lesions

Most patients are asymptomatic. However, symptomatic patients most commonly present with headaches and blurred vision.

Extravascular lesions of the retina include the following:

  • Microaneurysms
  • Retinal hemorrhages
  • Retinal and macular edema
  • Retinal lipid deposits
  • Cotton-wool spots
  • FIPT

Postulated to occur at localized areas of capillary wall weakness, microaneurysms are most visible by angiography. Stasis engorgement of the capillaries may lead to anoxia and poor nutrition, which contributes to microaneurysm formation.

In addition to microaneurysms, loss of endothelial integrity leads to extravasation of plasma, which leads to retinal hemorrhages. Streak hemorrhages located in the nerve fiber layer predominate over the blot hemorrhages located deeper in the outer plexiform layer.

Absorption of the plasma component of retinal edema leads to protein accumulation. Histologically, there is accumulation of edema residue and lipid-containing macrophages (the above-mentioned retinal lipid deposits). Although the deposits assume many shapes and appear in many parts of the retina, the macular star is the most predominant appearance, and this appearance is due to the radially oriented nerve fiber layer of Henle.

Wong and McIntosh assessed these changes in light of cardiovascular morbidity and mortality. The presence of these extravascular retinal lesions, specifically microaneurysms, hemorrhages, and cotton wool spots, were strongly associated with cardiovascular disease, independent of blood pressure and other risk factors. Milder hypertensive signs such as AV nicking were only weakly associated with these diseases.[5]


The original classification system for hypertensive retinopathy was conceived in 1939 by Keith and colleagues. Since that time, there have been several criticisms of the original system concerning the reproducibility and the relevance of the system to clinical practice. Some, including Hayreh, believe that the retinopathy grades may not correlate with the severity of systemic hypertension. However, others have suggested that classifications may be correlated with cardiovascular disease. Specifically, recent work links the modified Keith-Wagener-Barker system described by Mitchell and Wong to end-organ target damage.[6]

Keith-Wagener-Barker classification (1939)

Patients were grouped according to their ophthalmoscopic findings. As such, this was the first system to correlate retinal findings with the hypertensive disease state. Classifications are as follows:

  • Group 1 - Slight narrowing, sclerosis, and tortuosity of the retinal arterioles; mild, asymptomatic hypertension
  • Group 2 - Definite narrowing, focal constriction, sclerosis, and AV nicking; blood pressure is higher and sustained; few, if any, symptoms referable to blood pressure
  • Group 3 - Retinopathy (cotton-wool patches, arteriolosclerosis, hemorrhages); blood pressure is higher and more sustained; headaches, vertigo, and nervousness; mild impairment of cardiac, cerebral, and renal function
  • Group 4 - Neuroretinal edema, including papilledema; Siegrist streaks, Elschnig spots; blood pressure persistently elevated; headaches, asthenia, loss of weight, dyspnea, and visual disturbances; impairment of cardiac, cerebral, and renal function

Mitchell-Wong simplification of the Keith-Wagener-Barret system​

Grading is as follows:

  • Grade 1 (mild retinopathy) - Arteriolar narrowing (generalized and focal), AV nicking, and/or arteriolar wall opacity
  • Grade 2 (moderate retinopathy) - Hemorrhage, microaneurysm, cotton wool spot, and/or hard exudate
  • Grade 3 (malignant retinopathy) - Moderate retinopathy plus optic disc swelling

Scheie classification (1953)

Staging under this system is as follows[7] :

  • Stage 0 - Diagnosis of hypertension but no visible retinal abnormalities
  • Stage 1 - Diffuse arteriolar narrowing; no focal constriction
  • Stage 2 - More pronounced arteriolar narrowing with focal constriction
  • Stage 3 - Focal and diffuse narrowing, with retinal hemorrhage
  • Stage 4 - Retinal edema, hard exudates, optic disc edema

The Scheie classification also grades the light reflex changes from arteriolosclerotic changes, as follows[7] :

  • Grade 0 - Normal
  • Grade 1 - Broadening of light reflex with minimal arteriolovenous compression
  • Grade 2 - Light reflex changes and crossing changes more prominent
  • Grade 3 - Copper-wire appearance; more prominent arteriolovenous compression
  • Grade 4 - Silver-wire appearance; severe arteriolovenous crossing changes

Modified Scheie classification

Staging is as follows:

  • Grade 0 - No changes
  • Grade 1 - Barely detectable arterial narrowing
  • Grade 2 - Obvious arterial narrowing with focal irregularities
  • Grade 3 - Grade 2 plus retinal hemorrhages and/or exudates
  • Grade 4 - Grade 3 plus disc swelling

Differential diagnosis

The differential diagnosis includes the following:

In general, the degree and the duration of hypertension are the primary determinants of hypertensive retinopathy. However, the changes described in the above sections are not unique for hypertension. These changes may be seen in other diseases with vascular risk factors, such as diabetes.[8] The retinopathy may also be more severe and more progressive when diabetes and hypertension are associated. Other factors, such as hyperlipidemia, may make the retinopathy worse as well.


Treatment & Management

Medical care for hypertensive optic complications involves evaluation of secondary causes and appropriate medical management involving lifestyle changes and pharmacotherapy.

In the presence of hypertensive optic neuropathy, a rapid reduction of blood pressure may pose a risk of worsening ischemic damage to the optic nerve. The optic nerve demonstrates autoregulation, so there is an adjustment in perfusion based on the elevated blood pressure. A precipitous reduction in blood pressure will reduce perfusion to the optic nerve and central nervous system as a result of their autoregulatory changes, resulting in infarction of the optic nerve head and, potentially, acute ischemic neurologic lesions of the central nervous system.

Surgical management is indicated to address certain secondary causes of systemic hypertension.

Contributor Information and Disclosures

Kean Theng Oh, MD Consulting Staff, Associated Retinal Consultants, PC

Kean Theng Oh, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Michigan Society of Eye Physicians & Surgeons

Disclosure: Nothing to disclose.


Nader Moinfar, MD Consulting Staff, Vitreoretinal Department, Magruder Eye Institute

Nader Moinfar, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.


Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting

Bradley M Hughes, MD, Assistant Professor, Department of Ophthalmology, Retina and Vitreous Service, University of Arkansas for Medical Sciences

Bradley M Hughes, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

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