The inability to perceive visual stimuli, vision loss 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, neurologic, or systemic disorder or from trauma or the use of certain drugs. The ultimate visual outcome may depend on early, accurate diagnosis and treatment.
Act Now: Sudden vision loss can signal central retinal artery occlusion or acute angle-closure glaucoma — ocular emergencies that require immediate intervention. If the patient reports sudden vision loss, immediately notify an ophthalmologist for an emergency examination, and perform the following interventions.
For a patient with suspected central retinal artery occlusion, perform light massage over his closed eyelid. Increase his carbon dioxide level by administering a set flow of oxygen through a Venturi mask, or have the patient rebreathe in a paper bag to retain exhaled carbon dioxide. These steps will dilate the artery and, possibly, restore blood flow to the retina.
For a patient with suspected acute angle-closure glaucoma, measure intraocular pressure (IOP) with a tonometer. IOP can also be estimated without a tonometer by placing a finger over the patient’s closed eyelid. A rock-hard eyeball usually indicates increased IOP. Instill timolol drops and administer I.V. acetazolamide to assist in decreasing IOP.
Sudden vision loss can signal an ocular emergency. Don’t touch the eye if the patient has perforating or penetrating ocular trauma.
If the patient’s vision loss occurred gradually, ask him if it developed over hours, days, or weeks. Does it affect one eye or both? Does it affect all or part of the visual field? Is the vision loss transient or persistent? What’s the patient’s age? Ask whether he has experienced photosensitivity, and ask him about the location, intensity, and duration of eye pain. Obtain an ocular history, including history of eye problems or systemic diseases that may lead to eye problems, such as infections, cancer, hypertension, diabetes mellitus, and thyroid, rheumatic, or vascular disease.
Assess visual acuity and determine the best available vision correction in each eye. (See Testing visual acuity.)
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. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 306.) Observe the size, shape, and color of the pupils, and test the direct and consensual light reflex and the effect of accommodation. (See Vision loss: Causes and associated findings, pages 308 and 309.)
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 commonly have difficulty turning their eyes upward. IOP also increases with age.
With this 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 IOP in the affected eye may also occur.
ALERT: Acute angle-closure glaucoma is an ocular emergency that may produce blindness within 3 to 5 days.
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 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).
Some dystrophies cause vision loss with associated pain, photophobia, tearing, and corneal opacities.
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.
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.
An inflammation of the cornea, keratitis 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.
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 occurs, especially with movement of the globe. This may occur with visual field deficits 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.
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.
A painless ocular emergency, retinal artery occlusion 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.
With partial vision loss, the patient may describe visual field deficits or a shadow or curtain over the visual field as well as visual floaters.
Most common in elderly 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.
A viral disease, Rift Valley fever causes inflammation of the retina and may result in some permanent vision loss. Typical signs and symptoms include fever, myalgia, weakness, dizziness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever that can lead to shock and hemorrhage.
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.
Corneal scarring from associated conjunctival lesions produces marked vision loss. Purulent conjunctivitis, eye pain, and difficulty opening the eyes occur. Additional findings include widespread bullae, fever, malaise, cough, drooling, an 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 temporal arteritis. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
A rare disorder, trachoma may initially produce varying 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 an 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 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. Digoxin, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause visual disturbances and possibly vision loss.
Any degree of vision loss can be extremely frightening. To ease the patient’s fears, orient him to his environment and make sure that it’s safe. 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. If necessary, prepare him for surgery.
Discuss safety measures to prevent injury. Emphasize the importance of frequent hand washing and to avoid rubbing the eyes. If the loss is progressive or permanent, refer the patient to the appropriate social service agencies, community support services, and related associations for assistance with adaptation and equipment.
Read excerpts from these other book chapters related to Blind spot:
Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2008 Williams & Wilkins.
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Title: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-624-5 
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