Sudden Visual Loss

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Background

Sudden visual loss has an extensive differential diagnoses. Determining the etiology is guided by variables such as patient age, lateralization of symptoms, time course of vision loss, and associated symptoms, including the presence or absence of pain. In general, monocular vision loss indicates an ocular problem or a problem anterior to the optic chiasm, and the vision loss may respect the horizontal midline. Binocular vision loss is usually cerebral in origin and often respects the vertical midline. Sudden-onset painless vision loss is often ischemic in origin. However, if accompanied by headache, sudden vision loss can result from giant cell arteritis (GCA) and pituitary apoplexy. Vision loss with pain upon eye movement in young women should prompt consideration of optic neuritis.

Symptoms of vision loss have been described as a gradually descending gray-black curtain or as blurring, fogging, or dimming of vision and can last a few minutes to hours. The presentation of vision loss ranges from a single episode to multiple episodes per day; recurrences may continue for years and frequently occur over seconds to hours.

Numerous causes of sudden visual loss are recognized. Vision loss with positive scotoma may be seen with migraine. Vision loss with negative scotoma may be seen with amaurosis fugax. Ischemia, often via mechanical obstruction, can affect any aspect of the visual system and commonly occurs among individuals with atherosclerotic disease, such as coronary artery disease and peripheral vascular disease. Sudden changes in refractive error may be associated with diabetes mellitus or shallowing of the anterior chamber due to certain medications, including topiramate. Corneal edema due to endothelial decompensation or hydrops may cause abrupt vision loss. Cataracts encroaching on the visual axis may be interpreted by patients as sudden vision loss.

Other etiologies of sudden visual loss include infection/inflammation, vitreous hemorrhage, retinal detachment, GCA and other vasculitis, trauma, and idiopathic causes.

The management of sudden vision loss is directed at the underlying etiology.

Pathophysiology

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 includes the following[1] :

Transient vision loss can result from emboli originating from the heart, carotid artery, aorta, or peripheral vasculature.[2] TMVL can also result from arteritis, which causes inflammation of arteries and causes end organ ischemia.[3]

Epidemiology

Frequency

The estimated incidence of TMVL is 14 per 100,000 people per year.[4, 5]

Mortality/Morbidity

TMVL in a person younger than 45 years may be benign; many attacks are probably vasospastic or due to migraine.

TBVL is almost always associated with severe occlusive disease of the internal carotid artery (ICA), aortic arch, or vertebral circulation with 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.

Race

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.

Sex

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

Prognosis

The prognosis of sudden visual loss depends on the etiology.

Patient Education

Patients with sudden visual loss 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.

History

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

It is important to ask about comorbid conditions such as atrial fibrillation, thromboembolic disease, hypertension, hypercholesterolemia, nicotine use, diabetes mellitus, collagen vascular disease, hematological disorders, cancer, or drug use.[2]

Physical

The examination of vision loss can be approached anatomically, from the anterior orbit (refraction and tear film) to posterior skull (occipital lobe of the brain). Examination of patients with vision loss consists of a complete neuro-ophthalmic assessment, consisting of the following:

The physical examination is used to help narrow the differential diagnoses. Slit-lamp examination can be used to rule out an ocular cause for vision loss, including corneal abrasions, keratopathy, and ulcers, which may present as a red painful eye. A non-injected eye may be painful owing to nonocular causes, including optic neuritis, cluster headaches, sinusitis, or dental pain. Elevated intraocular pressure can be attributed to acute angle-closure glaucoma.

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



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Hyphema - Blood in anterior chamber resulting from trauma.

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

Confrontational visual field testing is used to assess for a peripheral field visual field cut. 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.

When the fundus cannot be visualized, ocular ultrasonography should be performed to exclude retinal detachment, posterior vitreous detachment, vitreous hemorrhage, ocular tumors, intraocular foreign bodies, retrobulbar hematoma, and increased intracranial pressure.[6]

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

In patients with severe monocular vision loss not involving the temporal crescent, the absence of a relative afferent pupillary defect suggests functional vision loss. Optokinetic testing can also 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. Tunneling of the visual field may differentiate physiologic from functional (psychological) visual field loss. The examiner can retest the field after doubling the distance between the patient and the target screen. In physiologic visual loss, this should double the size of the central visual field, whereas in hysterical visual loss, the visual field remains constricted.

Causes

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, as follows:[7]

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 minutes), is painless, and returns to normal afterward.

Embolic Causes

Emboli from distant sources are the most frequent cause of ischemia of the retinal artery. These distant emboli can originate from the ipsilateral carotid artery, the aortic arch, or the heart.[4] 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.

Cardiac disease

Cardiac emboli can originate from atrial fibrillation, valvular disease, mobile masses such as atrial myxomas, endocarditis, or a dyskinetic wall segment.[2] They predispose patients to the formation of platelet-containing emboli.

Carotid disease

This includes emboli originating from the carotid artery, as well as carotid artery dissection. 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.[4]

Other

Other causes that must be considered include fibromuscular dysplasia, hypercoagulable states, and vasculitides such as GCA.[4]

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 central retinal artery (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 on ophthalmoscopy and is most often the site of embolic or inflammatory diseases (eg, GCA). The narrowest area of the CRA is where the artery enters through the dural sheath of the optic nerve,[8] also making this region susceptible to emboli.

The major symptom of CRAO is sudden, painless blindness with permanent 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 the affected eye, as well as slow segmental blood flow in arterioles (ie, "box-carring").[4] If the occlusion lasts more than 1 hour, the retina becomes irreversibly infarcted.

In BRAO, visual defects 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 commonly 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 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), hemiretinal vein occlusion, and central retinal vein occlusion (CRVO). See the image below.



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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 can involve photocoagulation to ablate the ischemic peripheral retina, administration of intravitreal antivascular endothelial growth factor (VEGF) injections, or corticosteroid therapy.[9]

CRVO involves occlusion of the main central vein, which usually occurs at the level of the lamina cribrosa. Consequent macular edema may develop, with reduction in visual acuity.[10] The mechanism is unknown, but the most important local factor is chronic open-angle glaucoma, which is present in over 20% of patients. CRVO primarily affects adults aged 45 years and older,[11] but well-documented cases in younger persons have been reported. Risk factors for CRVO include hypertension, open angle glaucoma, dyslipidemia, peripheral arterial disease, and diabetes mellitus.[12, 13]

CRVO has 2 types: ischemic and nonischemic. These types are characterized by the severity of the retinal vein ischemia, although both have very similar ophthalmological findings.[14] Nonischemic is the more common form and occurs when blood flow and oxygen delivery are restored following vein blockage.[10] 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 due to nonresolving cystoid macular edema, macular cystic degeneration, macular retinal pigment epithelial changes, and preretinal fibrosis.

Ischemic CRVO presents as sudden, painless vision loss. Vision is usually markedly decreased, but most 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.[10]

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 spots. The prognosis is poor; central vision seldom recovers, owing to ischemic maculopathy or cystic macular degeneration, macular holes and cysts, macular epithelial fibrosis, macular edema, anterior segment and retinal neovascularization,[9] or secondary glaucoma.[10]

Patients with nonarteritic ischemic optic neuropathy (NAION) usually have painless vision loss and decreased central visual acuity, peripheral visual field loss, or both. The etiology of NAION is unknown, but a small cup disc and "ischemic spiral" is often associated with mild pallid swelling of the optic disc, often sectoral. Individuals with NAION are at risk during the subsequent 5 years of developing 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.[15]

Hematological

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. Whether hypercoagulability causes acute vision loss is unknown; however, given the elevated risk of stroke associated with antiphospholipid antibodies and the reversibility of hyperhomocysteinemia, testing for these in the context of transient vision loss may be beneficial.[2, 16]

Ophthalmic disease

Angle-closure glaucoma (ACG)

ACG results from obstruction of the angle from forces either pushing or pulling the iris forward against the trabecular meshwork.[17]

The angle may be obstructed via two major mechanisms: (1) pupillary block, in which the iris bows forward owing to a pressure gradient between the posterior and anterior chamber due to increased resistance to aqueous outflow from proximity between the lens and posterior iris[18, 17] or (2) nonpupillary block, which involves variable anatomical factors, including a thick peripheral iris, anteriorly positioned peripheral iris or ciliary body, and plateau iris.[17]

The typical presentation is that of a painful red eye with reduced vision due to corneal edema, a mid-dilated pupil with increased intraocular pressure accompanied by nausea, and vomiting. Treatment consists of topical miotics and beta-blockers, systemic carbonic anhydrase inhibitors, hyperosmotic agents, and perhaps analgesics and antiemetics. If pupillary block is suspected, iridectomy or iridotomy remains the primary surgical management.[19]

Papilledema/neoplasm

Intracranial hypertension is postulated to cause papilledema via mechanical axoplasmic flow stasis in the prelaminar and nerve fiber layers of the optic nerve head, resulting in vision loss.[20, 21] Affected patients may present with episodic visual obscurations lasting seconds, precipitated by postural changes. Visual field defects range from an enlargement of the blind spot and arcuate scotomas to progressive constriction of the visual field resulting in blindness. Papilledema can also cause submacular fluid and hemorrhages, which can affect central vision.[22] Fundus findings include blurring or elevation of the disc margin and retinal or choroidal folds.[23] Treatment is directed at the underlying cause of the papilledema.

Leber hereditary optic neuropathy

Leber hereditary optic neuropathy is a rare mitochondrial disease that predominantly affects men. It typically presents as painless vision loss in one eye with subsequent involvement of the other eye weeks to months later. Affected individuals commonly have dyschromatopsia, and relative afferent pupillary defect may be noted. Fundus findings include disc hyperemia, peripapillary telangiectasias, tortuosity of blood vessels, and swelling of the retinal nerve fiber layer (RNFL). The fundus may also appear normal, resulting in diagnostic delays. On optical coherence tomography (OCT), the RNFL thickens early in the disease course; however, the RNFL thins during the chronic phase. The visual field demonstrates a centrocecal scotoma that enlarges to affect central vision. The prognosis is poor, although some visual recovery occurs in a minority of cases. Most patients suffer permanent bilateral visual loss.[24]

Intraocular foreign bodies

Foreign bodies can penetrate the globe via the cornea, sclera, or limbus.[25] Visual prognosis following these types of injuries varies by patient age, length of wound, interval between injury and repair, volume of the intraocular foreign body, and subsequent complications, including retinal detachment, endophthalmitis, and relative afferent pupillary defect.[26, 27] Treatment involves removal of the foreign body.

Ruptured globe

A rupture globe is defined as a full-thickness traumatic wound through sclera, cornea, or both due to blunt or penetrating eye trauma.[28]

Open globe injuries should be suspected in patients with a history of trauma, especially with a laceration or puncture wound that extends through the eyelid, followed by pain and decreased visual acuity. Examination may reveal a shallow anterior chamber, irregular contour of the pupil (tear-drop shape), presence of subconjunctival hemorrhage, chemosis, and a positive Seidel test result or leakage of aqueous humor from the wound on fluorescein staining. The intraocular pressure may be low, although it should not be measured in cases of suspected rupture owing to the risk of extrusion of intraocular contents with applied pressure to the globe.[25]

Treatment consists of urgent surgical globe repair.

Retinal detachment

Other eye disorders that can cause sudden painless vision loss include detached retina. A patient with a detached retina presents with a "dark curtain" in their vision, flashes, and "spider webs" or floaters in their vision[29] and should be referred urgently to a retina specialist.

Neurologic

Optic neuritis is usually seen in patients younger than 45 years and often presents with pain upon eye movement. Patients describe seeing things as dark or unclear, and colors may appear pale. Vision loss may be worse with heat or exertion, known as the Uhthoff phenomenon. Vision deteriorates over a few days and subsequently nadirs within 1-2 weeks and then ultimately improves.[30]

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

Sphenoid sinusitis may cause vision loss. Phycomycosis occasionally manifests as a nasal or palatal eschar in immunocompromised patients.

Occipital stroke may cause homonymous visual field loss with no appendicular or speech deficits. Visual acuity may be normal if there is macular sparing. Patients may report homonymous paracentral scotoma.

Miscellaneous

Hysteria/malingering

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 topiramate and the PDE-5 inhibitors (sildenafil [Viagra], vardenafil [Levitra], tadalafil [Cialis])

Topiramate most commonly causes abrupt vision loss due to ciliochoroidal effusion with shallowing of the anterior chamber and myopic shift. Cessation of topiramate is required.

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 suggests a different etiology. 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.

Idiopathic

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 retinal vasospasm.[31, 2] 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.

Complications

Potential complications depend on the etiology.

Approach Considerations

The workup of sudden vision loss includes a thorough ophthalmic examination. Additional tests should be performed to narrow the differential diagnoses if not clinically evident and to facilitate secondary prevention in patients with a suspected ischemic, cardiac, or cerebrovascular etiology. Patients with acute retinal ischemia are at higher risk of stroke and MI,[4] so further workup and risk stratification in patients with transient monocular blindness is important for secondary prevention.

Laboratory Studies

Laboratory studies should include a complete blood cell count, coagulation studies, renal function testing, fasting blood glucose study, and lipid testing.

The erythrocyte sedimentation rate, C-reactive protein level, and platelet count in patients older than 50 years with suspected GCA should be obtained.

In patients with suspected optic neuritis, exclude mimicking infections (eg, Lyme disease, cat scratch disease, syphilis, herpes zoster) and noninfectious causes (eg, sarcoidosis, systemic lupus erythematosus [SLE], and other vasculitides).

Imaging Studies

Noninvasive evaluation of the carotid artery and heart (eg, electrocardiography, echocardiography, carotid Doppler) is useful, particularly in older patients. 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.

However, angiography remains the diagnostic standard for detecting carotid atherosclerotic disease.

Fluorescein angiography is helpful in retinal vascular occlusive disease. 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.

Neuroimaging is often useful unless the vision loss has an obvious ocular explanation. CT imaging can be useful to rule out vascular abnormalities and tumors and to assess for possible globe rupture in the context of ocular trauma.

Other Tests

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

GCA should be considered in elderly patients presenting with vision loss. Many authors advocate the liberal performance of temporal artery biopsy since the risk of permanent vision loss due to a missed GCA diagnosis outweighs the risks associated with biopsy. Diagnostic prediction models can help guide the decision for temporal artery biopsy but should be used in conjunction with clinical judgment.[32] In centers with radiologic expertise and high-quality imaging, tests such as Doppler ultrasonography of the temporal artery may be considered.

Medical Care

Treatment is directed at the underlying cause of vision loss.

If GCA is suspected, prednisone 1 mg/kg should be initiated before the temporal artery biopsy is performed in order to prevent involvement of the fellow eye. Similarly, if optic neuritis is suspected, acute steroid management may hasten recovery but has not been found to affect visual acuity outcomes.[30]

Treatment of papilledema is directed at the underlying cause and consists of medical and surgical management.

For cases of suspected CRAO or BRAO, treatment is directed at prevention of future ischemic events. Patients with CRAO and BRAO should be referred for urgent stroke workup and a carotid and cardiac examination. Although acute treatments have been described in the literature, none has proven beneficial in improving visual outcome beyond the expected vision based on the natural history of ischemia.[4] Thrombolytics have been used in an attempt to dissolve clots in suspected arterial occlusions, although there are no guidelines on their use owing to mixed results from conducted studies, as well as the risks associated with administration of thrombolytics.[4]

In patients with CRVO, systemic risk factors such as hypertension, diabetes, and hyperlipidemia should be treated. Patients should be monitored for macular edema and iris neovascularization. The ophthalmic complications can be treated with anti-VEGF injections, steroids, or retinal photocoagulation.[9, 33]

For ophthalmic causes of vision loss, treatment should be aimed at the underlying etiology.

Angle-closure glaucoma should be treated with topical intraocular pressure–lowering agents, and the underlying cause of the angle closure should be addressed.

Retinal detachment is treated in conjunction with retinal specialists. Treatment can include pneumatic retinopexy or surgical treatment with scleral buckle or vitrectomy.

Globe ruptures should be repaired surgically.

Surgical Care

Carotid artery stenosis increases the risk of hemispheric stroke. However, this risk is lower in patients with transient vision loss than in patients with other types of TIA. Thus, surgical management of carotid stenosis with carotid endarterectomy is indicated in patients with transient vision loss who have greater than 70% stenosis in addition to three other risk factors, which include male sex, age older than 75 years, absence of collaterals on angiography, TIA, peripheral vascular disease, and stenosis of 80%-94%.[2]

Nonarteritic-Ischemic Optic Neuropathy

No good surgical option or therapeutic treatment for nonarteritic ischemic optic neuropathy has been established.[34] The IONDT trial showed that optic nerve sheath fenestration was not beneficial.[35]

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.[12]

Consultations

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

Patients with unexplained vision loss should undergo neuroimaging.

When appropriate, cardiac and neurologic consultation is recommended. Complete cardiac and neurologic examinations should be performed.

Further Outpatient Care

Patients with sudden visual loss should receive follow-up care as needed.

Transfer

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

Medication Summary

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

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

Clinical Context:  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)

Clinical Context:  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)

Clinical Context:  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.

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.

Author

Jean Deschênes, MD, FRCSC, Professor, Research Associate, Director, Uveitis Program, Department of Ophthalmology, McGill University Faculty of Medicine; Senior Ophthalmologist, Clinical Director, Department of Ophthalmology, Royal Victoria Hospital, Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Zoya Chaudhry, MD, CM, Resident Physician, Department of Ophthalmology, McGill University Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

J James Rowsey, MD, Former Director of Corneal Services, St Luke's Cataract and Laser Institute

Disclosure: Nothing to disclose.

Chief Editor

Edsel Ing, MD, MPH, FRCSC, Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Active Staff, Michael Garron Hospital (Toronto East Health Network); Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital, Canada

Disclosure: Nothing to disclose.

Additional Contributors

Ellen M Menocal, MD, Resident Physician, Department of Emergency Medicine, Long Island Jewish Medical Center

Disclosure: Nothing to disclose.

Gino A Farina, MD, FACEP, FAAEM, Professor of Emergency Medicine, Hofstra North Shore-LIJ School of Medicine at Hofstra University; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Disclosure: Nothing to disclose.

Kilbourn Gordon, III, MD, FACEP, Urgent Care Physician

Disclosure: Nothing to disclose.

Lien Hong Lam, MD, Resident Physician, Department of Emergency Medicine, North Shore Long Island Jewish Hospital

Disclosure: Nothing to disclose.

Nicholas Lorenzo, MD, MHA, CPE, Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc; Chief Strategy Officer, Discourse LLC

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Angel Feliciano, MD, to the development and writing of this article.

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Hyphema - Blood in anterior chamber resulting from trauma.

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

Hyphema - Blood in anterior chamber resulting from trauma.

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