Vision loss—the inability to perceive visual stimuli—can be sudden or gradual and temporary or permanent. The deficit can range from a slight impairment of vision to total blindness. It can result from an ocular, a neurologic, or a systemic disorder or from trauma or the use of certain drugs. The ultimate visual outcome may depend on early, accurate diagnosis and treatment.
Sudden vision loss can signal an ocular emergency. Don’t touch the eye if the patient has a perforating or penetrating ocular trauma. (See Managing sudden vision loss, page 802.)
If the patient’s vision loss occurred gradually, ask him if it affects one eye or both and all or only part of the visual field. Is the vision loss transient or persistent? Did it occur abruptly or develop over hours, days, or weeks? What is the patient’s age? Ask the patient if he has experienced photosensitivity, and ask about the location, intensity, and duration of any eye pain. Also, obtain an ocular history and a family history of eye problems or systemic diseases that may lead to eye problems, such as hypertension; diabetes mellitus; thyroid, rheumatic, or vascular disease; infections; and cancer.
The first step in performing the eye examination is to assess visual acuity with the best available correction in each eye. (See Testing visual acuity, page 803.)
Carefully inspect both eyes, noting edema, foreign bodies, drainage, or conjunctival or scleral redness. Observe whether lid closure is complete or incomplete, and check for ptosis. Using a flashlight, examine the cornea and iris for scars, irregularities, and foreign bodies. Observe the size, shape, and color of the pupils, and test the direct and consensual light reflex (see “Pupils, nonreactive,” page 654) and the effect of accommodation. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 246.)
In this disorder, recurrent attacks of unilateral vision loss may last from a few seconds to a few minutes. Vision is normal at other times. Other findings may include transient unilateral weakness, hypertension, and elevated intraocular pressure (IOP) in the affected eye.
Typically, painless and gradual visual blurring precedes vision loss. As the cataract progresses, the pupil turns milky white.
Immediately or shortly after blunt head trauma, the patient may develop blurred, double, or lost vision. Vision loss is usually temporary. Other findings include headache, anterograde and retrograde amnesia, transient loss of consciousness, nausea, vomiting, dizziness, irritability, confusion, lethargy, and aphasia.
Some corneal dystrophies cause vision loss with associated pain, photophobia, tearing, and corneal opacities.
Retinal edema and hemorrhage lead to visual blurring, which may progress to blindness.
Typically, this intraocular inflammation follows penetrating trauma, I.V. drug use, or intraocular surgery, causing unilateral vision loss that may be permanent; a sympathetic inflammation may affect the other eye.
This disorder produces gradual visual blurring that may progress to total blindness. Acute angle-closure glaucoma is an ocular emergency that may produce blindness within 3 to 5 days. It’s characterized by rapid onset of unilateral inflammation and pain, pressure over the eye, moderate pupil dilation, nonreactive pupillary response, a cloudy cornea, reduced visual acuity, photophobia, and perception of blue or red halos around lights. Nausea and vomiting may also occur.
Chronic angle-closure glaucoma has a gradual onset and usually produces no symptoms, although blurred or halo vision may occur. If untreated, it progresses to blindness and extreme pain.
Chronic open-angle glaucoma usually has an insidious onset, progresses slowly, and affects both eyes. It causes peripheral vision loss, aching eyes, halo vision, and reduced visual acuity (especially at night).
When this disorder affects the nasociliary nerve, bilateral vision loss is accompanied by eyelid lesions, conjunctivitis, skin lesions (usually on the nose), and ocular muscle palsies.
Blood in the anterior chamber can reduce vision to light perception only. Most hyphemas are the direct result of blunt trauma to the normal eye.
This inflammation of the cornea may lead to complete unilateral vision loss. Other findings include an opaque cornea, increased tearing, irritation, and photophobia.
Sudden unilateral or bilateral vision loss may occur after an eye injury. Vision loss may be total or partial and permanent or temporary. The eyelids may be reddened, edematous, and lacerated; intraocular contents may be extruded.
Degeneration of the optic nerve, optic atrophy can develop spontaneously or follow inflammation or edema of the nerve head, causing irreversible loss of the visual field with changes in color vision. Pupillary reactions are sluggish, and optic disk pallor is evident.
An umbrella term for inflammation, degeneration, or demyelinization of the optic nerve, optic neuritis usually produces temporary but severe unilateral vision loss, pain around the eye (especially with movement of the globe), a sluggish pupillary response to light and, possibly, visual field defects. Ophthalmoscopic examination commonly reveals hyperemia of the optic disk, blurred disk margins, and filling of the physiologic cup.
In this disorder, bony impingements on the cranial nerves may cause bilateral vision loss, which may be accompanied by hearing loss, tinnitus, vertigo, and severe, persistent bone pain. Cranial enlargement may be noticeable frontally and occipitally, and headaches may occur. Sites of bone involvement are warm and tender, and impaired mobility and pathologic fractures are common.
Papilledema is characterized by swelling of both optic disks from increased intracranial pressure. Acute papilledema may lead to momentary blurring or transiently obscured vision, whereas chronic papilledema may lead to vision loss.
As a pituitary adenoma grows, blurred vision progresses to hemianopia and, possibly, unilateral blindness. Double vision, nystagmus, ptosis, limited eye movement, and headaches may also occur.
This painless ocular emergency causes sudden unilateral vision loss, which may be partial or complete. Pupil examination reveals a sluggish direct pupillary response and a normal consensual response. Permanent blindness may occur within hours.
Depending on the degree and location of detachment, painless vision loss may be gradual or sudden and total or partial. Macular involvement causes total blindness. Other effects include visual floaters, light flashes, and a sensation of a shadow or curtain over the visual field.
Most common in geriatric patients, this painless disorder causes a unilateral decrease in visual acuity with variable vision loss. IOP may be elevated in both eyes.
Inflammation of the retina is a complication of this viral disease that may result in some degree of permanent vision loss. Typical signs and symptoms include fever, myalgia, weakness, dizziness, and back pain. A small percentage of patients may develop encephalitis or hemorrhagic fever that can lead to shock and hemorrhage.
Occurring in elderly patients, this disorder causes painless blurring or loss of central vision. Vision loss may proceed slowly or rapidly, eventually affecting both eyes. Visual acuity may be worse at night.
Corneal scarring from associated conjunctival lesions produces marked vision loss, which may be accompanied by purulent conjunctivitis, eye pain, and difficulty opening the eyes. Additional findings include widespread bullae, fever, malaise, cough, drooling, inability to eat, sore throat, chest pain, vomiting, diarrhea, myalgia, arthralgia, hematuria, and signs of renal failure.
Vision loss and visual blurring with a throbbing, unilateral headache characterize this disorder. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
This rare disorder may initially produce varying degrees of vision loss and a mild infection resembling bacterial conjunctivitis. Conjunctival follicles, red and edematous eyelids, pain, photophobia, tearing, and exudation also occur. After about 1 month, conjunctival follicles enlarge into inflamed yellow or gray papillae.
Inflammation of the uveal tract may result in unilateral vision loss. Anterior uveitis produces moderate to severe eye pain, severe conjunctival injection, photophobia, and a small, nonreactive pupil. Posterior uveitis may produce insidious onset of blurred vision, conjunctival injection, visual floaters, pain, and photophobia. Associated posterior scar formation distorts the shape of the pupil.
This condition, which may result from intraocular trauma, ocular tumors, or systemic disease (especially diabetes, hypertension, sickle cell anemia, or leukemia), can cause sudden unilateral vision loss, visual floaters, and a reddish haze. The vision loss may be permanent.
Chloroquine therapy may cause patchy retinal pigmentation that typically leads to blindness. Digoxin derivatives, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause vision loss.
Any degree of vision loss can be extremely frightening to your patient. To ease his fears, orient him to his environment and make sure it’s safe, and announce your presence each time you approach him. If the patient reports photophobia, darken the room and suggest that he wear sunglasses during the day. Obtain cultures of any drainage, and instruct him not to touch the unaffected eye with anything that has come in contact with the affected eye. Instruct him to wash his hands often and to avoid rubbing his eyes. If necessary, prepare him for surgery.
Children who complain of slowly progressive vision loss may have an optic nerve glioma (a slow-growing, usually benign tumor) or retinoblastoma (a malignant tumor of the retina). Congenital rubella and syphilis may cause vision loss in infants. Retrolental fibroplasia may cause vision loss in premature infants. Other congenital causes of vision loss include Marfan syndrome, retinitis pigmentosa, and amblyopia.
In elderly patients, reduced visual acuity may be caused by morphologic changes in the choroid, pigment epithelium, or retina or by decreased function of the rods, cones, or other neural elements.
Read excerpts from these other book chapters related to Fleeting blindness:
Copyright Details: Professional Guide to Signs & Symptoms (Fifth Edition), Copyright © 2008 Williams & Wilkins.
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Title: Professional Guide to Signs & Symptoms (Fifth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2006 ISBN: 1-58255-510-9 
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