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Acute Vision Loss


Christopher J. Brady

, MD, Wilmer Eye Institute, Retina Division, Johns Hopkins University School of Medicine

Last full review/revision May 2021| Content last modified May 2021

Loss of vision is usually considered acute if it develops within a few minutes to a couple of days. It may affect one or both eyes and all or part of a visual field. Patients with small visual field defects (eg, caused by a small retinal detachment) may describe their symptoms as blurred vision.

Pathophysiology of Acute Vision Loss

Acute loss of vision has 3 general causes:

  • Opacification of normally transparent structures through which light rays pass to reach the retina (eg, cornea, vitreous)
  • Retinal abnormalities
  • Abnormalities affecting the optic nerve or visual pathways

Etiology of Acute Vision Loss

The most common causes of acute loss of vision are

In addition, sudden recognition of loss of vision (pseudo-sudden loss of vision) may manifest initially as sudden onset. For example, a patient with long-standing reduced vision in one eye (possibly caused by a dense cataract) suddenly is aware of the reduced vision in the affected eye when covering the unaffected eye.

Presence or absence of pain helps categorize loss of vision (see table Some Causes of Acute Vision Loss).

Most disorders that cause total loss of vision when they affect the entire eye may affect only part of the eye and cause only a visual field defect (eg, branch occlusion of the retinal artery or retinal vein, local retinal detachment).

Less common causes of acute loss of vision include

  • Anterior uveitis (a common disorder, but one that usually causes eye pain severe enough to trigger evaluation before vision is lost)
  • Aggressive retinitis
  • Certain drugs (eg, methanol, salicylates, ergot alkaloids, quinine)

Some Causes of Acute Vision Loss


Suggestive Findings

Diagnostic Approach

Acute loss of vision without eye pain

Amaurosis fugax

Monocular blindness lasting minutes to hours (typically < 5 minutes when due to cerebrovascular disease)

Consideration of

Carotid ultrasonography


MRI or CT of the brain

Electrocardiography (ECG)

Continuous monitoring of cardiac rhythm

Arteritic ischemic optic neuropathy (usually in patients with giant cell [temporal] arteritis)

Sometimes headache, jaw or tongue claudication, temporal artery tenderness or swelling, pale and swollen optic disk with surrounding hemorrhages, occlusion of retinal artery or its branches

Sometimes proximal myalgias with stiffness (due to polymyalgia rheumatica)

Sometimes only vision loss

Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), platelet count

Temporal artery biopsy

Functional loss of vision (uncommon)

Normal pupillary light reflexes, positive optokinetic nystagmus, no objective abnormalities on eye examination

Often inability to write name or bring outstretched hands together

Sometimes indifferent affect despite severity of claimed loss of vision

Sometimes exaggerated severity of an organic eye disorder

Clinical evaluation

If diagnosis is in doubt, ophthalmologic evaluation and visual evoked responses

Macular hemorrhage due to neovascularization in age-related macular degeneration

Blood within or deep to retina in and around the macula

Clinical evaluation

Nonarteritic ischemic optic neuropathy

Optic disk edema and hemorrhages

Sometimes loss of inferior and central visual fields

Risk factors (eg, diabetes, hypertension, hypotensive episode)

ESR, CRP, and platelet count

Consideration of temporal artery biopsy to exclude giant cell arteritis

Ocular migraine

Scintillating scotomata, mosaic patterns, or complete loss of vision lasting usually 10–60 minutes and often followed by headache

Bilateral, but may be seem monocular if the scotoma is off-center (ie, a visual disturbance in the right hemifield of both eyes might be perceived as in the right eye only)

Often in young patients

Clinical evaluation

Retinal artery occlusion

Nearly instantaneous onset, pale retina, cherry-red fovea, sometimes Hollenhorst plaque (refractile object at the site of arterial occlusion)

Risk factors for vascular disease

ESR, CRP, and platelet count to exclude giant cell arteritis

Carotid ultrasonography


Consideration of MRI or CT of brain


Continuous monitoring of cardiac rhythm

Retinal detachment

Recent increase in floaters, photopsias (flashing lights), or both

Visual field defect, retinal folds

Risk factors (eg, trauma, eye surgery, severe myopia; in men, advanced age)

Clinical evaluation

Sometimes ocular ultrasonography

Retinal vein occlusion

Frequent, multiple, widely distributed retinal hemorrhages

Risk factors (eg, diabetes, hypertension, hyperviscosity syndrome, sickle cell anemia)

Clinical evaluation

Transient ischemic attack or stroke

Bilaterally symmetric (homonymous) field defects, no effect on visual acuity in the intact parts of the visual field (bilateral occipital lesions are the exception and are uncommon but can occur due to basilar artery occlusion)

Risk factors for atherosclerosis

Carotid ultrasonography


Consideration of MRI or CT of the brain


Continuous monitoring of cardiac rhythm

Vitreous hemorrhage

Previous floaters or spider web in vision

Risk factors (eg, diabetes, retinal tear, sickle cell anemia, trauma)

Possible ocular ultrasonography to assess retina

Acute loss of vision with eye pain

Acute angle-closure glaucoma

Halos around lights, nausea, headache, photophobia, conjunctival injection, corneal edema, shallow anterior chamber, intraocular pressure usually > 40 mm Hg

Immediate ophthalmologic evaluation


Corneal ulcer

Ulcer visible with fluorescein staining, slit-lamp examination, or both

Risk factors (eg, injury, contact lens use)

Ophthalmologic evaluation


Floaters, conjunctival injection, decreased red reflex, hypopyon, or a combination

Risk factors (infection after eye surgery, traumatic ruptured globe, intraocular foreign body [eg, after hammering metal on metal], fungemia, or bacteremia)

Immediate ophthalmologic evaluation with microbiologic testing (eg, gram stain and culture of aspirates for endogenous endophthalmitis, blood and urine cultures)

Optic neuritis (usually painful but not always)

Mild pain with eye movement, afferent pupillary defect (occurs early)

Visual field defects, typically central

Abnormal color vision testing results

Sometimes optic disk edema

Gadolinium-enhanced MRI to diagnose multiple sclerosis and related disorders

Evaluation of Acute Vision Loss


History of present illness should describe loss of vision in terms of onset, duration, progression, and location (whether it is monocular or binocular and whether it involves the entire visual field or a specific part and which part). Important associated visual symptoms include floaters, flashing lights, halos around lights, distorted color vision, and jagged or mosaic patterns (scintillating scotomata). The patient should be asked about eye pain and whether it is constant or occurs only with eye movement.

Review of systems should seek extraocular symptoms of possible causes, including jaw or tongue claudication, temporal headache, proximal muscle pain, and stiffness (giant cell arteritis); and headaches (ocular migraine).

Past medical history should seek known risk factors for eye disorders (eg, contact lens use, severe myopia, recent eye surgery or injury), risk factors for vascular disease (eg, diabetes, hypertension), and hematologic disorders (eg, sickle cell anemia or disorders such as Waldenström macroglobulinemia or multiple myeloma that could cause a hyperviscosity syndrome).

Family history should note any family history of migraine headaches.

Physical examination

Vital signs, including temperature, are measured.

If the diagnosis of a transient ischemic attack is under consideration, a complete neurologic examination is done. The temples are palpated for pulses, tenderness, or nodularity over the course of the temporal artery. However, most of the examination focuses on the eye.

Eye examination includes the following:

  • Visual acuity is measured.
  • Peripheral visual fields are assessed by confrontation.
  • Central visual fields are assessed by Amsler grid.
  • Direct and consensual pupillary light reflexes are examined using the swinging flashlight test.
  • Ocular motility is assessed.
  • Color vision is tested with color plates.
  • The eyelids, sclera, and conjunctiva are examined using a slit lamp if possible.
  • The cornea is examined with fluorescein staining.
  • The anterior chamber is examined for cells and flare in patients who have eye pain or conjunctival injection.
  • The lens is checked for cataracts using a direct ophthalmoscope, slit lamp, or both.
  • Intraocular pressure is measured.
  • Ophthalmoscopy is done, preferably after dilating the pupil with a drop of a sympathomimetic (eg, 2.5% phenylephrine), cycloplegic (eg, 1% cyclopentolate or 1% tropicamide), or both; dilation is nearly full after about 20 minutes. The entire fundus, including the retina, macula, fovea, vessels, and optic disk and its margins, is examined.
  • If pupillary light responses are normal and functional loss of vision is suspected (rarely), optokinetic nystagmus is checked. If an optokinetic drum is unavailable, a mirror can be held near the patient’s eye and slowly moved. If the patient can see, the eyes usually track movement of the mirror (considered to be the presence of optokinetic nystagmus).

Red flags

Acute loss of vision is itself a red flag; most causes are serious.

Interpretation of findings

Diagnosis of acute vision loss can be begun systematically. Specific patterns of visual field deficit help suggest a cause. Other clinical findings also help suggest a cause for acute vision loss:

  • Difficulty seeing the red reflex during ophthalmoscopy suggests opacification of transparent structures (eg, caused by corneal ulcer, vitreous hemorrhage, or severe endophthalmitis).
  • Retinal abnormalities that are severe enough to cause acute loss of vision are detectable during ophthalmoscopy, particularly if the pupils are dilated. Retinal detachment may show retinal folds; retinal vein occlusion may show marked retinal hemorrhages; and retinal artery occlusion may show pale retina with a cherry-red fovea.
  • An afferent pupillary defect (absence of a direct pupillary light response but a normal consensual response) with an otherwise normal examination (except sometimes an abnormal optic disk) suggests an abnormality of the optic nerve or retina (ie, anterior to the optic chiasm).

In addition, the following facts may help:

  • Monocular symptoms suggest a lesion anterior to the optic chiasm.
  • Bilateral, symmetric (homonymous) visual field defects suggest a lesion posterior to the chiasm.
  • Constant eye pain suggests a corneal lesion (ulcer or abrasion), anterior chamber inflammation, or increased intraocular pressure, whereas eye pain with movement suggests optic neuritis.
  • Temporal headaches suggest giant cell arteritis or migraine.


Erythrocyte sedimentation rate (ESR), C-reactive protein, and platelet count are done for all patients with symptoms (eg, temporal headaches, jaw claudication, proximal myalgias, stiffness) or signs (eg, temporal artery tenderness or induration, pale retina, papilledema) suggesting optic nerve or retinal ischemia to exclude giant cell arteritis.

Other testing is listed in the table Some Causes of Acute Vision Loss. The following are of particular importance:

  • Ultrasonography is done to view the retina if the retina is not clearly visible with pupillary dilation and indirect ophthalmoscopy done by an ophthalmologist.
  • Gadolinium-enhanced MRI of the brain and orbits is done for patients who have eye pain with movement or afferent pupillary defect, particularly with optic nerve swelling on ophthalmoscopy, to diagnose multiple sclerosis.

Treatment of Acute Vision Loss

Causative disorders are treated. Treatment should usually commence immediately if the cause is treatable. In many cases (eg, vascular disorders), treatment is unlikely to salvage the affected eye but can decrease the risk of the same process occurring in the contralateral eye or of a complication caused by the same process (eg, ischemic stroke).

Key Points

  • Diagnosis and treatment should occur as rapidly as possible.
  • Acute monocular loss of vision with an afferent pupillary defect indicates a lesion of the eye or of the optic nerve anterior to the optic chiasm.
  • Optic nerve lesion, particularly ischemia, is considered in patients with acute monocular loss of vision or afferent pupillary defect without eye pain and in those with or without optic nerve abnormalities on ophthalmoscopy but no other abnormalities on eye examination.
  • Corneal ulcer, acute angle-closure glaucoma, endophthalmitis, or severe anterior uveitis is considered in patients with acute monocular loss of vision, eye pain, and conjunctival injection.

Drugs Mentioned In This Article

Drug Name Select Trade
phenylephrine No US brand name

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