Sudden Visual Loss 

Updated: May 18, 2016
Author: Gino A Farina, MD, FACEP, FAAEM; Chief Editor: Edsel Ing, MD, MPH, FRCSC 



Sudden visual loss is a common complaint with variable presentations among patients of different ages.

The differential diagnoses of sudden vision loss are vast. In general, monocular vision loss usually indicates an ocular problem. Binocular vision loss is usually cerebral in origin. Monocular vision loss may respect the horizontal midline. Binocular vision loss may respect the vertical midline.

Some patients describe their symptoms as a gradually descending gray-black curtain or as blurring, fogging, or dimming of vision. Symptoms usually last a few minutes but can persist for hours. Variation in frequency ranges from a single episode to many episodes per day; recurrences may continue for years but more frequently occur over seconds to hours.

Many different causes of sudden visual loss are recognized; however, the most common reason for painless sudden visual loss is ischemia. Vision loss with positive scotoma may be seen with migraine. Vision loss with a negative scotoma may be seen with amaurosis fugax.  Ischemia, often via mechanical obstruction, can affect any aspect of the visual system. Those who develop ischemia of the eye often have other evidence of atherosclerotic disease, such as coronary artery disease and peripheral vascular disease, which increases their susceptibility to ischemic events in other parts of the body. Risk factors include smoking, hypercholesterolemia, and hypertension.

Other etiologies of sudden visual loss include infection/inflammation, vasculitis, trauma, mechanical dysfunction, and idiopathic causes.


Ischemia compromises cell metabolism by reducing delivery of oxygen and other important nutrients to tissues. The resulting functional deficit may be temporary or permanent, depending on the degree of damage. Nomenclature of eye ischemia as given by Hedges and others includes the following[1] :

  • Transient visual obscuration (TVO) - Episodes lasting seconds that are associated with papilledema and increased intracranial pressure

  • Amaurosis fugax - Brief, fleeting attack of monocular partial or total blindness that lasts seconds to minutes

  • Transient monocular visual loss (TMVL) or transient monocular blindness (TMB) - A more persistent vision loss that lasts minutes or longer

  • Transient bilateral visual loss (TBVL) - Episodes affecting one or both eyes or both cerebral hemispheres and causing visual loss

  • Ocular infarction - Persistent ischemic damage to the eye, resulting in permanent vision loss



Sudden visual loss is uncommon.


Transient monocular visual loss (TMVL) in a person younger than 45 years may be benign; many attacks are probably vasospastic or due to migraine.

Transient bilateral visual loss (TBVL) is almost always associated with severe occlusive disease of the internal carotid artery (ICA), aortic arch, or bilateral occipital lobe ischemia.

Patients with ICA disease often have other systemic evidence of atherosclerosis, such as coronary and peripheral vascular disease. Other risk factors include smoking, hypercholesterolemia, and hypertension.


Whites, especially men, have a high incidence of ICA-origin atherosclerosis.

Blacks and Chinese and Japanese persons have a higher incidence of intracranial occlusive disease.


A strong male predominance (2:1) exists among patients with severe ICA disease.




For any patient with sudden visual loss, the following information should be obtained:

  • Age

  • Duration of visual loss or changes

  • Whether one eye or both eyes affected

  • History of trauma

  • Prior episodes/ophthalmologic history

  • Symptoms - Photophobia, headache, pain

It is important to ask about comorbid conditions such as arrhythmia, hypertension, hypercholesterolemia, collagen vascular disease, hematological disorders, cancer, or drug use.


The inspection of vision loss can be approached anatomically, from anterior (refraction and tear film) to posterior (occiput). Inspect the extraocular area and assess the refraction, visual acuity, color vision, visual fields, pupil reactivity (including the presence or absence of a relative afferent pupillary defect), and extraocular motility.

Sudden changes in refractive error may be seen with diabetes mellitus or shallowing of the anterior chamber with topiramate. Corneal edema due to endothelial decompensation or hydrops may cause abrupt vision loss. Cataract opacity that encroaches the visual axis may be interpreted by patients as sudden vision loss.

Initial examination of the external appearance of the eye is part of a good systematic approach. The appearance of the eye is key. A non-injected eye may be painful owing to optic neuritis, cluster headaches, sinusitis, or dental pain. Normal findings on this examination eliminate extraocular causes of visual loss.

Red and painful eyes should be examined with a slit lamp, both with and without fluorescein staining. Corneal and conjunctival findings such as inflammation, edema, or defect are associated with etiologies such as abrasions, keratopathy, ulcers, and infection, which should become apparent with this examination.

Intraocular pressure should be measured in patients who have red, painful eyes with normal findings on corneal staining. Elevated pressure points to a diagnosis of acute glaucoma.

The anterior chamber should be evaluated for hyphema, cells, and floaters. See the image below.

Hyphema - Blood in anterior chamber resulting from Hyphema - Blood in anterior chamber resulting from trauma.

In injected, painful eyes with normal fluorescein examination and pressure, the presence of inflammatory cells in the anterior chamber suggests iritis or endophthalmitis, especially with any recent history of ocular surgery.

Visual field testing with hand movement is used to assess if central or peripheral field vision deficiency is present. In general, field defects that respect the horizontal midline suggest an ocular lesion. Field loss that respects the vertical midline suggests cerebral pathology.

Careful fundus examination is part of a complete ophthalmic assessment. On funduscopy, a detached retina appears gray and detached.

An optokinetic drum may be helpful in functional vision loss. If optokinetic nystagmus occurs, the patient usually has at least 20/400 vision. Moving a mirror (placed close to the patient's face) will cause the eyes to move if vision is present. To differentiate physiologic from functional ("hysterical") visual field loss, the examiner can double the distance between the patient and the tangent screen (ie, visual screen test). In physiologic visual loss, this results in doubling of the size of the central visual field, whereas in hysterical visual loss, the visual field remains the same.

Funduscopy and visual field testing can be challenging and, when negative, cannot completely rule out retinal detachment, as the retina is only partially visualized with these methods. If available, ultrasound is a useful adjunct to the physical examination of the eye. When the fundus cannot be visualized, ocular ultrasonography may reveal retinal detachment, vitreous detachment, vitreous hemorrhage, ocular tumors, intraocular foreign bodies, retrobulbar hematoma, and increased intracranial pressure.[2] Retinal detachment is evident by a taut, linear opacity seen in the vitreous chamber that moves in conjunction with eye movement. Vitreous detachment appears as an opaque line separated from the retina that floats in the vitreous humor. Vitreous hemorrhage appears as curved strands connecting with the retina as the eye moves. Severe vitreous hemorrhage causes complete opacification of the vitreous chamber.

The examination should also include complete cardiac and neurologic evaluation, including murmurs and carotid bruits.


Multiple conditions are associated with transient visual loss. They can be classified according to origin or pathogenesis, but for the purpose of this article, they are outlined by source. Wray has classified TMVL into 3 different groups based mostly on pathogenesis; they include the following:[3]

  • Type 1 is characterized by loss of all or a portion of vision in one eye, lasting seconds to minutes, with full recovery. It is usually secondary to an embolic phenomenon. The attacks have been related to an ICA origin associated with ulceration but not critical narrowing.

  • Type 2 includes visual loss due to hemodynamically significant, occlusive, low-flow lesions in the ICAs or ophthalmic arteries. Symptoms are more frequent, less rapid in onset, and longer in duration than type 1 attacks, with gradual vision recovery.

  • Type 3 is thought to be due to vasoconstriction or vasospasm.


The pathophysiology of some types of visual loss can be explained by atherosclerotic cerebrovascular disease. The visual disturbances are usually described as dark or gray, or obscuration by a "descending shade." Visual loss lasts for minutes (10-15 min) and painlessly returns to normal afterwards.


Retinal arteriolar emboli are the most important and common ophthalmoscopic abnormality arising from the carotid artery, aorta, cardiac valves, or the heart itself. Particles consist mostly of platelets or fibrin, calcified emboli, or cholesterol crystals.

Cholesterol crystals are observed most frequently. These are called Hollenhorst plaques and are found at the bifurcation of the retinal arterioles. They arise from atherosclerotic plaques in the ICA in the carotid siphon or the aorta, and are usually bright, refractile, and small (10-20 µm in diameter). They infrequently impede flow or occlude vessels, and they tend to disappear rapidly and rarely damage the vessel wall. They are difficult to see, but placing pressure on the eye may cause the crystals to move and become visible through the ophthalmoscope.

Platelet-fibrin emboli are gray-white in color and commonly extend to the small retinal arteries. In contrast to the Hollenhorst plaques, they tend to occlude vessels and obstruct blood flow.

Finally, calcified emboli arise most commonly from calcified heart valves. They are white and usually remain in one position, blocking blood flow. Calcific emboli typically reside directly on the optic disc and remain in that location serving as a reminder of calcific aortic valve disease in that patient.

Stenotic vascular disease

This includes carotid or vertebral artery atherosclerotic disease, fibromuscular dysplasia, arteritis, and dissection.

Cardiac disease

Cardiac causes include atrial myxomas, endocarditis, or a dyskinetic wall segment. They predispose patients to the formation of platelet-containing emboli.

Dissection usually involves the pharyngeal ICA and can be precipitated by trauma or can begin spontaneously. Pain in the neck, jaw, face, or head, ipsilateral Horner syndrome, ipsilateral spells of TMVL, and transient hemispheric attacks are frequent features.

Ocular Ischemic Syndromes

Persistent eye ischemia can be classified into central retinal artery occlusion (CRAO), branch retinal artery occlusion (BRAO), or ischemia of the optic nerve, which is caused by involvement of the posterior choroidal blood supply of the nerve (anterior ischemic optic neuropathy [AION]).

Origin of CRA from the ophthalmic artery is variable. The vessel has several segments on its way to the retina. To reach the fundus, the CRA penetrates the lamina cribrosa. At this point, it narrows; the tissue around the vessel acts as a mechanical barrier to dilatation. This area is not visible by ophthalmoscope and is most often the site of embolic or inflammatory diseases (eg, giant cell arteritis). The narrowest area of the CRA is where the artery enters through the dural sheath of the optic nerve,[4] also making this region susceptible to emboli.

The major symptom of CRAO is sudden, painless blindness with persistent visual loss. Perception of hand movement or light can be preserved in parts of the visual field. Diagnosis is confirmed by ophthalmoscopy, which reveals partial or complete arrest of retinal circulation. Cardinal signs include attenuated retinal arteries and veins (very early only), and a cloudy whitening of the retina (ie, edema) with the consequent cherry-red spot in the macula in a patient who has lost vision in one eye. Shortly after occlusion, segmentation of the blood column with slow streaming of veins is seen without recovery of vision. If the occlusion lasts more than 1 hour, the retina becomes irreversibly infarcted.

In BRAO, visual defect and retinal ischemia are more focal and have an altitudinal, lateral, or scotomatous quality. The incidence of carotid artery and valvular disease is not very different than in CRAO, but temporal arteritis is less often the cause.

In AION, the patient usually develops painless visual loss in the eye, which is noted on awakening in the morning without worsening thereafter. The degree of loss is variable but most often incomplete. Ophthalmoscopy shows edema of the optic disc and splinter hemorrhages at the disc margins. When the ischemia is posterior to the disc, the disc may look normal, but this is quite uncommon and may point toward arteritis as the cause. Subsequent involvement of the other eye is common.

Other ocular ischemic syndromes involve the retinal vein. Retinal vein occlusions are retinal vascular disorders that are classified clinically as branch retinal vein occlusion (BRVO), hemispheric vein occlusion, and central retinal vein occlusion (CRVO). See the image below.

Central retinal vein occlusion - Diffuse retinal h Central retinal vein occlusion - Diffuse retinal hemorrhages extending to periphery of fundus, "blood and thunder" appearance.

BRVO involves one of the branch retinal veins. Most involve the superior or inferior temporal arcades and occur at an arteriovenous crossing where the vein is compressed by a sclerotic artery. The superior or inferior temporal arcades cause macular vein occlusion with profound visual deficit. Hemispheric vein occlusion involves the venous drainage of either the superior or inferior retina.

BRVO affects males and females equally, occurring most frequently in adults aged 60-70 years. Regardless of the primary pathogenic processes, it is clear that disease of the arterial wall and the presence of common adventitia between the artery and the vein at arteriovenous crossings play a role in the pathogenesis. The common symptoms of BRVO are blurring and distortion of vision. During the acute stage, multiple superficial and deep retinal hemorrhages are seen in a pie configuration in the distribution of the affected vein. The veins in the occluded segment usually are dilated and tortuous.

Fluorescein angiography is helpful to delineate the hemodynamic changes that occur in the retinal vasculature. Angiography usually shows slow venous return without complete occlusion of the vein. Approximately 50% of patients recover good visual acuity, although 2 complications may lead to reduced visual acuity—macular edema, which develops in more than 50% of patients, and retinal neovascularization. Management of both involves photocoagulation to ablate the ischemic peripheral retina.

CRVO involves occlusion of the main central vein, which usually occurs at the level of the lamina cribrosa. This occlusion interferes with the drainage of the whole retina. Consequent macular edema may develop, with reduction in visual acuity.[5] The mechanism is unknown, but the most important local factor is chronic open-angle glaucoma, which is present in over 20% of patients. CRVO is primarily a disease of the elderly persons, but well-documented cases in younger persons have been reported. Risk factors for CRVO include hypertension, chronic open angle glaucoma, and diabetes mellitus.[6]

CRVO has 2 types: nonischemic and ischemic. These types are characterized by the severity of the retinal vein ischemia, although both have very similar ophthalmological findings.[7] Nonischemic is the more common form and occurs when blood flow and oxygen delivery are restored following vein blockage.[5] Visual complaints vary from mild to moderate blurring of vision, which may be transient. Visual fields are usually normal except for occasional central scotomas.

Ophthalmoscopic features of nonischemic CRVO include moderate dilatation and tortuosity of all retinal veins with multiple punctate hemorrhages in the peripheral retina and few scattered retinal hemorrhages in the posterior pole. Most hemorrhagic activity resolves over several months. Some patients may be left with some permanent visual loss from the nonresolving cystoid macular edema, macular cystic degeneration, macular retinal pigment epithelial changes, and preretinal fibrosis.

Ischemic CRVO occurs in older individuals who have a higher incidence of systemic vascular disease, preexisting glaucoma, and ocular hypertension. These patients have sudden, painless vision loss. Vision usually is decreased markedly, but the majority of patients will be able to count fingers or see hand movement. Peripheral visual fields are almost always normal with a dense central or centrocecal scotoma. One definition includes the presence of an afferent pupillary defect in the affected eye, which has been found to be both sensitive and specific.[5]

In nonarteritic ischemic optic neuropathy (NAION), the patient develops painless visual loss in the eye, decreased central visual acuity, peripheral visual field loss, or both. The etiology of NAION is unknown, but pallid swelling of the optic disc is observed. Patients are at risk during the next 5 years to develop involvement of the other eye; risks for fellow eye involvement include poor baseline acuity and diabetes mellitus, but interestingly not age, sex, smoking, or aspirin use. Spontaneous improvement of vision may occur.[8]

The ophthalmoscopic features of ischemic CRVO include marked tortuosity and dilatation of all the retinal branch veins, diffuse retinal hemorrhages extending from the optic disc to the periphery of the fundus, and multiple cotton-wool patches. The prognosis is poor; central vision seldom recovers, owing to ischemic maculopathy or cystic macular degeneration, macular holes and cysts, macular epithelial fibrosis, ocular neovascularization, or secondary glaucoma.[5] Although none of the following methods has proven efficacious, laser photocoagulation (panretinal), thrombolysis with t-PA, and surgical interventions have been used to attempt to restore or improve visual acuity.[6] In the last few years, treatment with antivascular endothelial growth factor (VEGF) has shown promise.[9]


Hematological causes of visual loss, such as hypercoagulable states, antiphospholipid syndrome, and anemia, may affect vision through the formation of clots or platelet-containing emboli.

Local orbital or ocular disease

Angle-closure glaucoma: Often, onset of this disease results in painful vision loss and red eye. In open-angle glaucoma, the aqueous humor has access to the trabecular meshwork, whereas in angle-closure glaucoma, this access is blocked by the peripheral iris.

The iris may close the angle in one of 3 ways: (1) pupillary block, in which the iris is bowed forward by aqueous humor, which is unable to get through the pupil because it is adherent to the lens (posterior synechiae); (2) obstruction of the trabecular meshwork directly without pupillary block as a result of posterior pressure from the ciliary body, vitreous, or lens or because of anterior rotation and swelling of the ciliary body; and (3) peripheral anterior synechiae, which are adhesions formed between the peripheral iris and the angle structures.

The diagnosis is not difficult when the presentation is typical; a painful, red eye with increased intraocular pressure that is accompanied by diaphoresis, nausea, and vomiting. Atypical presentations include chronic angle closure or an acute closure without pain. The presence of a midposition, fixed pupil in an eye with reduced vision can suggest unrecognized angle-closure glaucoma. All presentations can be confirmed by tonometry or gonioscopy. Treatment consists of topical miotics and beta-blockers, systemic carbonic anhydrase inhibitors, hyperosmotic agents, and perhaps analgesics and antiemetics. Ophthalmologic consult is warranted; when pupillary block is suspected, iridectomy or iridotomy remains the primary surgical management.[10]

Papilledema/neoplasm: Intracranial hypertension causes persisting visual loss by mechanically compressing or physiologically destroying the optic nerve. The visual consequences of postpapilledema optic atrophy start with peripheral visual field constriction, typically most prominent in the inferior nasal or upper nasal quadrant, followed by loss of central visual field with decline in central acuity and dyschromatopsia. A relative afferent pupillary defect can be found in most instances in which visual field or acuity loss is asymmetric between eyes. Visual field defects can include central/paracentral and arcuate scotomas, or nasal steps. Ophthalmoscopy will show a swollen, pale, or normal retina. Patients with papilledema may have unilateral or bilateral transient vision loss and this may be aggravated by standing up or bending over.

Intraocular foreign bodies: These are small particles that have penetrated the cornea or sclera. This commonly occurs in the workplace; the signs can be subtle, causing only mild erythema and local discomfort. Visual acuity often is decreased markedly, but normal visual acuity is possible and does not rule out an intraocular foreign body. Smaller objects may produce few, if any, signs or symptoms and may be difficult to discover without a high index of suspicion. With large objects, disruption of the anterior segment, a visible penetration site, hyphema, or cataract may be obvious.

Ruptured globe: This results from full-thickness traumatic disruption of the sclera or cornea as a result of blunt or penetrating trauma to the eye.

Open globe should be suspected in any patient who has a history of trauma to the eye, especially with a laceration or puncture wound that extends through the eyelid, followed by pain and decreased visual acuity.

On examination, visual acuity often is decreased. Flattening of the anterior chamber or hyphema may be present. Note alteration of the pupil size, shape, or location and conjunctival edema or hemorrhage. Extrusion of ocular contents may be seen, and the eye may have a deflated appearance. Leakage of aqueous humor from the anterior chamber may become apparent during examination with fluorescein staining (i.e., Seidel test). Intraocular pressure frequently is decreased, although it should not be measured if an open globe is suspected.

Other eye disorders that can cause sudden painless vision loss include a detached retina. A patient with a detached retina presents with the sensation of painless vision loss in one eye, described in the classic presentation as a wall slowly developing over the visual field. The patient may also complain of flashing lights (like an ambulance car light gleaming) or "spider webs" in the peripheral field.


Optic neuritis is usually seen in patients younger than 45 years and often causes pain upon eye movement. Vision loss may be worse with heat or exertion.

Pituitary apoplexy can cause sudden peripheral field loss, usually associated with ocular motility deficit.

Occipital stroke may cause homonymous visual field loss with no appendicular or speech deficits.



The patient with hysterical blindness or loss of vision will, despite alleged loss of vision, still be capable of maneuvering in a room. The pupillary reactions are normal. The loss of vision is a subconscious conversion symptom. A purely functional loss of vision can be assumed when the visual field is markedly constricted, orientation when walking is intact, and pupillary reactions to light are normal.

The transition between a hysterical or malingering patient and one with an aggravated loss of vision is fluid. If the patient indicates a unilateral loss of vision, the examination should be conducted in such way that the patient does not know which eye is being tested or the actual size of the optotypes, and a relative afferent pupillary defect should be present.

Drugs, such as quinidine, sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis)

Sudden monocular visual loss due to nonarteric anterior ischemic optic neuropathy (NAION) has been reported in a small number of patients taking the above medications for erectile dysfunction. The US Food and Drug Administration (FDA) has advised health care professionals of the potential risk of sudden visual loss that may be attributed to the use of phosphodiesterase-5 (PDE-5) inhibitors. The visual loss is typically altitudinal and the visual acuity loss is typically mild; severe vision loss with PDE-5 inhibitors should suggest a different etiology.

As of May 2005, the FDA has received a total of 43 postmarketing reports of ischemic optic neuropathy in patients using these drugs. Vascular risk factors for NAION overlap with those of erectile dysfunction such as age older than 50 years and a history of heart disease, high blood pressure, high cholesterol, or smoking; hence, the causal role of PDE-5 inhibitors remains unclear.

Patients should be advised to discontinue the use of these medications and seek immediate medical attention if they experience a sudden decrease or loss of vision in one or both eyes. For more information, please visit US Food and Drug Administration Center for Drug Evaluation and Research.


Migraine or scintillating scotoma: This may occur on a persistent basis or may recur after an absence of decades. The physiologic and anatomic bases have not been explained fully but are thought to involve vasospasm. Shimmering scotomas with or without perception of color or movement are reported commonly, usually as a binocular symptom but occasionally monocular. Most commonly, these last less than 30 minutes.





Laboratory Studies

Individualize the evaluation of patients with transient monocular visual loss (TMVL).

Because common causes of TMVL are ischemic, cardiac and cerebrovascular related laboratory studies should be evaluated.

Laboratory studies should include blood counts and coagulation studies.

Obtain erythrocyte sedimentation rate, C-reactive protein level, and platelet count in patients older than 55 years with suspected giant cell arteritis.

Imaging Studies

Treating transient monocular blindness (TMB) and atherosclerosis is important because they increase the risk of stroke.

Noninvasive evaluation of the carotid artery and heart (eg, echocardiography, carotid Doppler) is useful in patients older than 40 years; this evaluation provides information on the degree of stenosis. Noninvasive study of the heart can detect abnormal valves, dyskinetic wall segments, and arrhythmias, all of which predispose to the formation of emboli.

Ulceration is more difficult to detect noninvasively than invasively, so angiography remains the diagnostic standard for detecting carotid atherosclerotic disease.

Fluorescein angiography is helpful for detecting embolic retinal vascular occlusion. The most common embolic particles are cholesterol crystals, which are often small; they disappear rapidly but not without damaging the vessel wall.

Fluorescein angiography may show hyperfluorescent crystals or areas of fluorescein leakage that are caused by crystal-related endothelial damage.

Other Tests

Holter monitoring is the preferred method to screen for intermittent cardiac arrhythmias.

Temporal artery biopsy is performed often to rule out giant cell arteritis. A clinician should perform biopsies frequently. The risk of missing the diagnosis of giant cell arteritis far outweighs the minor inconvenience of this very benign procedure.



Medical Care

Medical care for patients with sudden visual loss includes the following:

Aspirin is believed to be beneficial in patients with no hemodynamically significant disease of the carotid artery (ie, greater than 1 mm residual lumen) or in those who are poor surgical candidates.

In general, aspirin together with modification of risk factors (eg, decreasing serum cholesterol level, controlling systemic hypertension) reduces the likelihood of myocardial infarction. It is also very effective in reducing the risk of stroke.

Aspirin was once believed to be most effective in high doses, but recent evidence has shown that similar benefits can be achieved with low-dose aspirin at 81 mg a day.

Advise patients with frequent or severe headaches to stop smoking. Women who smoke and take birth control pills are at increased risk for stroke.

Clopidogrel (Plavix) has been shown to be effective in reducing the risk of stroke and in a study comparing its efficacy to aspirin, was shown to be only minimally better. It can be used easily in patients who are aspirin intolerant. Whether the combination of clopidogrel plus aspirin is better than either medication alone is currently unknown.

Aggrenox (aspirin plus dipyridamole) has been shown to be effective in reducing stroke risk. In a comparison with either agent alone, it was found to be significantly more effective.

The recent results of the PROFESS trial showed that aspirin plus dipyridamole and clopidogrel were equivalent in efficacy. Either medication is an acceptable starting medication for the patient at risk for future stroke.

Inferior retinal detachment is treated with the patient sitting up. Superior detachment is treated with the patient lying prone, so to avoid worsening of the detachment by gravity.

Current guidelines for optic neuritis are based on one randomized control trial (Optic Neuritis Treatment Trial) and suggest either high-dose intravenous methylprednisolone or no treatment. In a review article reporting on 750 participants across 6 randomized trials looking at low-dose, high-dose, oral, and intravenous steroids for optic neuritis, there was no evidence of benefit in terms of recovery of visual acuity, visual field, or contrast sensitivity with either oral or intravenous corticosteroids compared with placebo at 6 months.[11] There was, however, indication that treating with steroids hastened the rate of return of vision to normal compared with placebo. When choosing this treatment, oral steroids must be preceded by intravenous steroids, as oral steroids alone resulted in fewer patients achieving normal visual acuity compared with controls and may in fact be associated with increased recurrence rates.

In cases of acute CRAO, conservative therapy may include the following:[12]

  • Ocular massage

  • Topical glaucoma medications

  • Acetazolamide

  • Mannitol

  • Glycerol

  • Calcium channel blockers

  • Prostaglandin E1

  • Lidocaine hydrochloride

  • Acetylcholine

  • Pentoxifylline

  • Hemodilution

  • Methylprednisolone

  • Hyperbaric oxygen

  • Heparin IV

  • Paracentesis

  • Carbogen inhalation

None of these strategies has been proven more effective than any other. A randomized study by Schumacher et al (EAGLE study) compared these conservative treatments with a more invasive method called local intra-arterial fibrinolysis.[13]

For patients with nonischemic CRVO, there has been much investigation in the last several years into effective treatments to both correct vision and prevent progression to ischemic CRVO. Some treatments to help with the aftermath of the disease include panretinal laser photocoagulation, lowering intraocular pressure, treating underlying medical conditions,[7] laser-induced chorioretinal venous anastomosis (L-CRA),[14] intravitreal anti-VEGF, and intravitreal triamcinolone treatments. The latter 2 methods are proposed to decrease subsequent macular edema from CRVO, whereas L-CRA is intended to directly treat the venous occlusion.

Limited studies have evaluated the efficacy of triamcinolone injections, and it has been found to have only a temporary effect with risk of significant adverse effects.[14]

While anti-VEGF injections have come to the forefront in CRVO and BRVO therapy, further studies are required to target treatment groups that would benefit most from these therapies, as well as to determine specific dosing regimens and window for treatment initiation.

A small, retrospective, single-center study by Ferrara et al demonstrated improved visual acuity and decreased macular edema in patients with CRVO of less than 3 months who were given bevacizumab. In this study, 5 patients (6 eyes) who received intravitreal bevacizumab were tested for visual acuity and retinal appearance before and after treatment.[15] However, small sample size and the nonrandomized nature of the study and other studies evaluating this method limits its use as standard therapy at this time.

In a phase II, double-masked, multicenter, randomized sham-controlled trial of pegaptanib sodium for nonischemic CRVO of less than 6 months duration, by Wroblewski et al, 98 patients were randomized to receive either 0.3 mg, 1 g, or sham injections of an anti-VEGF drug, pegaptanib.[16] Subjects who received the 1-mg injection were most benefited in terms of visual acuity compared with the sham group, whose visual acuity declined. Both treatment groups had a significantly lower risk for loss of visual acuity (6-9% of subjects) compared with 31% of controls. Further, there was greater reduction in central retinal thickness compared with controls.

Later analysis reported possible risk of bias due to incomplete outcome data and found that it was not possible to exclude selective reporting.[5] The small sample size resulted in insufficient power to investigate outcome differences between the treatment doses, and the lack of protracted observation allows only for speculation of short term treatment with pegaptanib.

Intravitreal anti-VEGF injection with ranibizumab (approved by the FDA for treatment neovascular age-related macular degeneration in 2006) has shown promise in the short-term treatment of nonischemic CRVO–related macular edema, with recently published follow-up study data and FDA approval of ranibizumab for retinal vein occlusion. In the CRUISE trial, a phase III randomized, double-masked, multicenter, injection-controlled trial by Campochiaro et al, 392 patients with macular edema after CRVO were randomized to receive monthly 0.3-mg, 0.5-mg, or sham intravitreal injections of ranibizumab over 6 months. Those patients who received ranibizumab injections were shown to have significantly improved visual acuity (46.3-47.7%) compared with study controls (16.9%), as well as decreased central foveal thickening.[17]

In a similar prospective, randomized, sham injection–controlled, double-masked, multicenter clinical trial, BRAVO, by Campochiaro et al, intravitreal ranibizumab was also found to improve visual acuity (55.2-61.1%) in patients with BRVO compared with controls (28.8%), in addition to decreased central foveal thickness.[18] Follow up data from both trials, BRAVO and CRUISE, for the subsequent 6 months showed that patients with both conditions continued to improve with repeated injections with no increase in adverse events.[19, 20]

The HORIZON trial, by Heier et al, which included a cohort of patients who completed the BRAVO and CRUISE trials, found no new adverse safety events after an additional year of treatment with ranibizumab.[21] It did, however, find that during the second year of treatment, the clinical improvement of patients with BRVO was persistent, whereas CRVO patients tended to have a decline in vision, perhaps related to a decreased frequency of injections or the differing degrees in retinal damage.[9]

Although the HORIZON study was terminated early secondary to FDA approval of ranibizumab for RVO, several limitations of the aforementioned studies exist and questions remain regarding the utility of ranibizumab for RVO. Follow-up data at the 6-month time point eliminated the control group of sham-injection patients and provided rescue laser treatment for all patients,[22] neither the BRAVO nor CRUISE trials had enough power to investigate differences between the 2 treatment doses,[5] ischemic CRVO was excluded in these trials, and optimal timing of initial treatment has not yet been determined, which is also limited by the small amount of data regarding the disease progression and prognosis of untreated CRVO-related macular edema.

Surgical Care

Carotid artery stenosis increases the risk of hemispheric stroke. This risk is greater after hemispheric ischemic symptoms than after retinal ischemic symptoms. Amaurosis fugax with a carotid stenosis of 70% or greater definitely increases a person's risk of stroke, but with less risk than if the ischemic symptoms were cerebral.

Carotid endarterectomy subsequent to episodes of transient cerebral or retinal ischemia is known to reduce the risk of cerebral infarction. This effect is seen after cerebral ischemia with stenosis greater than 50%. It is seen after retinal ischemia only if stenosis is 70% or greater. Therefore, endarterectomy is advocated in the retinal patient only if the stenosis is 70% or greater while advocated for hemispheric events with stenosis of 50% or greater. Recommendations for this procedure must be individualized. It should be considered for patients with TMB or amaurosis fugax only if the surgical complication rate is less than 2%. For patients with cerebral transient ischemic attacks (TIAs), a complication rate of 3% or less is acceptable.

Local arterial fibrinolysis for the treatment of central retinal artery occlusion (CRAO)

A nonrandomized, single center, interventional study by Aldrich et al. demonstrated improved visual acuity in patients who received local intra-arterial aliquots of tissue plasminogen activator (tPA). In this small study, 21 patients received 3 mg aliquots of intra-arterial tPA and 76% of these patients had improved visual acuity compared with 33% of the patients in the standard therapy group. The authors cautioned that because of the nonrandomized nature of this and previous studies, local arterial fibrinolysis cannot be recommended as standard therapy in daily clinical practice pending the publication of randomized clinical trials.[23]

In a more recent study, results from the first interim analysis of the first randomized clinical trial comparing efficacy of conservative treatment to local arterial fibrinolysis (the European Assessment Group for Lysis in the Eye [EAGLE] study) found no difference in efficacy between the treatment groups.[13] In addition, despite having similar visual improvements in both groups, local intra-arterial fibrinolysis (57%) and conservative treatment (60%), results showed higher occurrences of adverse events in the local intra-arterial fibrinolysis group; thus, the study was discontinued.[13]

Nonarteritic-Ischemic Optic Neuropathy

No good surgical option or therapeutic treatment for nonarteritic ischemic optic neuropathy has yet been elucidated.[24] In a study by Dickersin et al, an optic nerve decompression surgery involving cutting 2 or more slits within the tissue around the optic nerve with the intention to allow CSF to escape and reduce pressure around the nerve was stopped early for futility.[25] Surgical patients experienced both intraoperative and postoperative adverse events, including CRAO during surgery and light perception vision at 6 months. There was also immediate loss of light perception following surgery and loss of vision that persisted to the 12-month visit.

Central Retinal Vein Occlusion

Surgical options for CRVO include radial optic neurotomy, chorioretinal venous anastomosis, vitrectomy, and retinal vein injection with tPA. None of these surgical treatments has been proven to be more effective than nonsurgical methods for improving vision loss and are still experimental at this time.[6]


Ophthalmic consultation is prudent in any case of sudden visual loss that cannot be easily and confidently explained and managed by emergency department physicians.

Cardiac and neurologic consultation is recommended. A complete cardiac and neurologic examination, including murmurs and carotid bruits, should be performed.



Medication Summary

The goals of pharmacotherapy in sudden visual loss are to reduce morbidity and prevent complications.

Antiplatelet agents

Class Summary

Inhibit platelet function perhaps by blocking cyclooxygenase and subsequent aggregation. Antiplatelet therapy has been shown to reduce mortality by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients at risk.

Aspirin (Ascriptin, Aspirtab, Aspercin, Bayer Aspirin, Buffinol)

Irreversibly inhibits the formation of cyclooxygenase, thus preventing the formation of thromboxane A2, a platelet aggregator and vasoconstrictor. Platelet inhibition lasts for the life of the cell (approximately 10 d).

Clopidogrel (Plavix)

Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Aspirin and dipyridamole (Aggrenox)

Aspirin irreversibly inhibits formation of cyclooxygenase, thus preventing formation of thromboxane A2, a platelet aggregator and vasoconstrictor. Platelet-inhibition lasts for life of cell (approximately 10 d).

Dipyridamole is a platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity leading to increased cyclic-3', 5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.

Each tablet contains 25 mg aspirin and 200 mg dipyridamole for total of 50 mg aspirin and 400 mg dipyridamole per day.



Further Outpatient Care

Patients should receive follow-up care as needed.


Transfer of patients with sudden visual loss is necessary when emergent ophthalmologic consultation (if warranted) is unavailable at the initial treatment location.


Potential complications depend on the etiology.


Prognosis depends on the etiology.

Patient Education

Patients should seek professional care.

For excellent patient education resources, visit eMedicineHealth's Eye and Vision Center and Cholesterol Center. Also, see eMedicineHealth's patient education articles Anatomy of the Eye, High Cholesterol, and Cholesterol FAQs.