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. (See Managing sudden vision loss, page 690.)
If the patient’s vision loss occurred gradually, ask him if the vision loss affects one eye or both and all or only part of the visual field. Is the visual loss transient or persistent? Did the visual loss occur abruptly, or did it develop over hours, days, or weeks? What is the patient’s age? Ask the patient if he has experienced photosensitivity, and ask him about the location, intensity, and duration of any eye pain. You should 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.
Don’t touch the patient’s eye if he has perforating or penetrating ocular trauma. The first step in performing the eye examination is to assess visual acuity, with best available correction in each eye. (See Testing visual acuity, page 691.)
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 551) and the effect of accommodation. Evaluate extraocular muscle function by testing the six cardinal fields of gaze.
With amaurosis fugax, recurrent attacks of unilateral vision loss may last from a few seconds to a few minutes. Vision is normal at other times. Transient unilateral weakness, hypertension, and elevated intraocular pressure (IOP) in the affected eye may also occur.
With a cataract, usually, painless and gradual visual blurring precedes vision loss. As the cataract progresses, the pupil turns milky white. Night blindness and halo vision may be early signs of this disorder.
Immediately or shortly after blunt head trauma, which causes a concussion, vision may be blurred, double, or lost. Generally, vision loss is temporary. Other findings include headache, anterograde and retrograde amnesia, transient loss of consciousness, nausea, vomiting, dizziness, irritability, confusion, lethargy, and aphasia.
With diabetic retinopathy, retinal edema and hemorrhage lead to visual blurring, which may progress to blindness. The patient may also have a loss of central vision and color vision.
Typically, endophthalmitis follows penetrating trauma, I.V. drug use, or intraocular surgery, causing possibly permanent unilateral vision loss; a sympathetic inflammation may affect the other eye. The patient with endophthalmitis may also experience headache, photophobia, and ocular discharge.
Glaucoma 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. Findings are 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 open-angle glaucoma is usually bilateral, with an insidious onset and a slowly progressive course. It causes peripheral vision loss, aching eyes, halo vision, and reduced visual acuity (especially at night).
When herpes zoster affects the nasociliary nerve, bilateral vision loss is accompanied by eyelid lesions, conjunctivitis, skin lesions that usually appear on the nose, and ocular muscle palsies.
With a hyphema, blood in the anterior chamber can reduce vision to light perception only. Other effects include moderate pain, conjunctival injection, and eyelid edema. Most hyphemas are the direct result of blunt trauma to the normal eye.
Keratitis (inflammation of the cornea) may lead to complete unilateral vision loss. Other findings include an opaque cornea, increased tearing, irritation, and photophobia.
Following eye injury, sudden unilateral or bilateral vision loss may occur. Vision loss may be total or partial and permanent or temporary. The eyelids may be reddened, edematous, and lacerated; intraocular contents may be extruded.
Optic atrophy (degeneration of the optic nerve) 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.
Optic neuritis usually produces temporary but severe unilateral vision loss. Pain around the eye occurs, especially with movement of the globe. This may occur with visual field defects and a sluggish pupillary response to light. Ophthalmoscopic examination commonly reveals hyperemia of the optic disk, blurred disk margins, and filling of the physiologic cup.
With Paget’s disease, bilateral vision loss may develop as a result of bony impingements on the cranial nerves. This occurs with 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 the optic disk from increased intracranial pressure; both optic disks are affected. Acute papilledema may lead to momentary blurring or transiently obscured vision, whereas chimeric 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.
Retinal artery occlusion is a painless ocular emergency that 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 retinal detachment, painless vision loss may be gradual or sudden and total or partial. Macular involvement causes total blindness.
With partial vision loss, the patient may describe visual field defects or a shadow or curtain over the visual field as well as visual floaters.
Most common in geriatric patients, retinal vein occlusion is a painless disorder that causes a unilateral decrease in visual acuity with variable vision loss. IOP may be elevated in both eyes.
Occurring in elderly patients, senile macular degeneration 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.
Vision loss and visual blurring with a throbbing, unilateral headache characterize temporal arteritis. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
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.
With vitreous hemorrhage, sudden unilateral vision loss may result from intraocular trauma, ocular tumors, or systemic disease (especially diabetes, hypertension, sickle cell anemia, or leukemia). Visual floaters and partial vision with a reddish haze may occur. The patient’s vision loss may be permanent.
Chloroquine therapy may cause patchy retinal pigmentation that typically leads to blindness. Phenylbutazone may cause vision loss and increased susceptibility to retinal detachment. Cardiac glycoside derivatives, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause vision loss.
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.
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, and retina or by decreased function of the rods, cones, and other neural elements. Elderly patients often have difficulty turning their eyes upward. IOP also increases with age.
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. Instruct him to wash his hands often and to avoid rubbing his eyes. If necessary, prepare him for surgery.
Read excerpts from these other book chapters related to Fleeting blindness:
Copyright Details: Signs & Symptoms: A 2-in-1 Reference for Nurses, Copyright © 2008 Williams & Wilkins.
|
More About This Book:
Title: Signs & Symptoms: A 2-in-1 Reference for Nurses Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-318-1 
|
|
What do you think about the features of this website? Take our user survey and have your say:
Next articles:
Tools & Services:
Medical Articles:
Search Specialists by State and City
By using this site you agree to our Terms of Use. Information provided on this site is for informational purposes only; it is not intended as a substitute for advice from your own medical team. The information on this site is not to be used for diagnosing or treating any health concerns you may have - please contact your physician or health care professional for all your medical needs. Please see our Terms of Use.
Copyright © 2009 Health Grades Inc. All rights reserved.
