The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne
Review Article
Primary Care
B LURRED V ISION
BRADFORD J. SHINGLETON, M.D.,
AND MARK W. O’DONOGHUE, O.D.
B
LURRED vision is the most common symp-
tom related to the eye. It is manifested in many
ways and has a wide variety of causes. Here we
review for nonophthalmologists the examination tech-
niques and diagnostic algorithms that are useful in the
evaluation of blurred vision. We also describe how
to determine when patients need urgent ophthalmo-
logic consultation and treatment.
THE EYE EXAMINATION
History
In evaluating a patient with blurred vision, it is
important to note the time of onset and how the pa-
tient first noticed the symptoms. Was the blurring of
vision sudden in onset, or was it gradual? Did it occur
with or without pain? Was the blurred vision unilat-
eral or bilateral? The differentiation of cases of blurred
vision on the basis of these characteristics will facil-
itate making the proper diagnosis.1 It is also important
to note any other associated conditions or events.
For example, the patient should be asked about ac-
companying auras preceding migraines and about fo-
cal neurologic signs. Is there a history of blunt trau-
ma, penetrating injury, or exposure to a foreign body
that might lead to blurred vision? Medications such
as steroids (systemic, injectable, topical, or inhaled)
may be associated with cataracts, glaucoma, and ker-
atitis due to the herpes simplex virus. Effects on
vision from antibiotics, antimalarial drugs, psycho-
tropic agents, and other medications are rare, but tox-
ic effects on the retina and optic nerve are possible.
Other clues that can be useful for diagnosing blurred
vision are a family history of glaucoma or macular
degeneration and a personal history of symptoms sim-
ilar to the current ones.2
Examination Techniques
The eye examination, as performed by a practi-
tioner who is not an ophthalmologist, is divided into
six parts: visual acuity, visual field, pupils, movement
of extraocular muscle, anterior segment, and posteri-
or segment. Because some serious eye conditions are
From Ophthalmic Consultants of Boston, Boston. Address reprint re-
quests to Dr. Shingleton at 50 Staniford St., Suite 600, Boston, MA 02114,
or at bjshingleton@eyeboston.com.
©2000, Massachusetts Medical Society.
556 · Aug u s t 2 4 , 2 0 0 0
The New England Journal of Medicine as published by New England Journal of Medicine.
Downloaded from www.nejm.org on August 19, 2010. For personal use only. No other uses without permission.
Copyright © 2000 Massachusetts Medical Society. All rights reserved.
not readily apparent, systematic progression through
all six parts of the eye examination is essential for ev-
ery patient with blurred vision.
Visual Acuity
Blurred vision is most often associated clinically
with a reduction in visual acuity. Visual acuity should
be tested one eye at a time, with glasses or contact
lenses in place if they are normally worn by the pa-
tient. First, the patient is asked to read a standard eye
chart. If the acuity at a distance is less than 20/40,
the acuity is rechecked by placing a pinhole occluder
over the patient’s glasses, a maneuver that will give
an approximation of the best corrected vision. If the
patient is unable to read any of the figures on the
chart, the patient is asked to count the fingers on
the examiner’s hand. If the patient is unable to count
the fingers, the distance at which the patient can de-
tect hand movements is determined. If the patient is
unable to detect hand movements, the practitioner
should determine whether the patient can perceive
light. The precise level of visual acuity and the dis-
tance at which it was achieved are recorded. The doc-
umentation of visual acuity is important for making
comparisons with the results of future examinations
and for legal reasons.
Visual Field
Blurred vision that is due to neurologic disease or
retinal detachment is occasionally manifested as a de-
fect in peripheral vision. The confrontation method
of testing peripheral vision is a quick and simple way
to identify defects in the visual field. With each eye
tested separately, the normal visual field of the exam-
iner is used as a base line for comparison with that
of the patient in the superior, inferior, nasal, and tem-
poral quadrants. If the test is performed properly,
homonymous field defects that are associated with
cerebral vascular accidents can be identified, as can
quadrantic or hemispheric defects associated with ret-
inal detachments. Another quick way to test the cen-
tral visual field is with an Amsler’s grid (Fig. 1). The
patient looks at the central dot with one eye and
identifies any zones of distortion or loss of the visual
field. The grid is particularly helpful in diagnosing
blurred vision in patients with retinal disease.
Pupils
The pupils should be black, round, of the same size,
and reactive to light. A nonblack pupil suggests the
opacification of refracting media, which is often due
to the formation of cataracts. Misshapen or eccentric
pupils occur after blunt or penetrating trauma and
may be associated with serious ocular injuries, such
as ruptured globes. In up to 20 percent of cases, pu-
 PRIMA RY CA R E
Figure 1. An Amsler’s Grid, Used to Test the Central Visual Field.
From a distance of 40 cm (16 in.) and with eyeglasses or con-
tact lenses used for reading in place, the patient looks at the
central dot with one eye at a time and identifies any zones of
distortion or loss of the central visual field.
pillary asymmetry may be the only obvious sign of
serious eye injury on examination with a penlight.
Abnormal pupillary size or reactivity to light may be
important clues to the presence of intracranial dis-
ease. An afferent pupillary defect (with paradoxical
pupillary dilatation in response to light) is an impor-
tant sign of optic-nerve disease or injury. If present,
it confirms that damage to the optic nerve or retina
has occurred. Every practitioner should be comfort-
able performing this part of the examination.
Movement of Extraocular Muscles
Occasionally, the patient may interpret diplopia due
to disorders in ocular motility as blurred vision. Oc-
ular motility is tested by asking the patient to follow a
penlight up and down and to the left and right with
the eyes. The extraocular muscles should work in
concert, and the movements in each eye should be
smooth, unrestricted, and symmetrical. Limitation of
movement in any of the four cardinal positions of gaze
should be noted.
Anterior Segment
The anterior segment includes the sclera, conjunc-
tiva, cornea, anterior chamber, iris, and lens. The en-
tire anterior segment can be examined adequately
with simple illumination by penlight and careful ob-
servation. The sclera and conjunctiva are examined
The New England Journal of Medicine as published by New England Journal of Medicine.
Downloaded from www.nejm.org on August 19, 2010. For personal use only. No other uses without permission.
Copyright © 2000 Massachusetts Medical Society. All rights reserved.
for discharge, swelling, and vascular injection. The
corneal reflection of light may be the most impor-
tant sign to evaluate. The reflection of light should be
clear, free of irregularities, and sharp. The applica-
tion of topical fluorescein, in conjunction with illu-
mination with cobalt-blue light, is useful for further
evaluating acute irregularities in the corneal surface.
Irregularities imply corneal disease or trauma. When
present in an eye with nontraumatic redness, they may
herald a vision-threatening corneal ulcer or herpes
simplex infection.
The anterior chamber is the space between the
cornea and the iris that is filled with aqueous humor.
When trauma has occurred, it is inspected for blood
(hyphema); it is inspected for pus (hypopyon) in any
patient who has had eye surgery. The iris is evaluated
for alterations in shape or contour. Trauma may lead
to pupillary dilatation, and in iritis, the pupil on the
involved side may be miotic. The lens is situated in
the pupillary axis, behind the diaphragm of the iris.
Opacification of the lens, which is normally clear, in-
dicates the formation of a cataract. A cataract may
appear white when illuminated by a penlight or as a
focal dark area against the normally uniform red re-
flex produced by direct ophthalmoscopy.
Posterior Segment
The posterior segment consists of the vitreous, the
retina, and the optic nerve. Direct ophthalmoscopy
is used to assess the clarity of the refracting media
and the posterior segment. Dilation of the pupil great-
ly facilitates examination of the posterior segment; it
should be carried out by the medical practitioner if
important diagnostic information can be obtained
and if there are no neurologic contraindications. We
favor the use of 1 percent tropicamide and 2.5 per-
cent phenylephrine for routine dilation.
The red reflex as seen through the direct ophthal-
moscope should look the same in all angles of view.
Alteration in the reflex may occur with cataracts, hem-
orrhage in the vitreous gel, retinal detachment, and
choroidal detachment. The image of the retina should
be clear. The margins of the optic nerve normally ap-
pear flat and well demarcated. Pathologic elevation
occurs with papilledema, papillitis, and ischemic optic
neuropathy; an afferent pupillary defect is associated
with papillitis and ischemic optic neuropathy. Optic-
disk drusen (Fig. 2) are probably the most common
form of pseudopapilledema. The arteries and veins
should be of normal caliber, and the retinas should
be free of hemorrhages, exudates, and ischemic cot-
ton-wool spots.
NONPATHOLOGIC CAUSES
OF BLURRED VISION
Refractive Errors
Refractive errors are the most common cause of
blurred vision and account for the vast majority of
Vol ume 343 Numb e r 8 · 557
 The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne
Figure 2. Optic-Disk Drusen.
Elevation of the optic disk is commonly caused by optic-disk
drusen, but this condition can be misdiagnosed as pathologic
edema of the optic disk. The drusen typically appear as irregu-
lar, white, hyaline concretions in the substance and at the bor-
der of the head of the optic nerve.
visits to eye specialists. Blurred vision that is caused by
refractive errors is generally bilateral, of gradual on-
set, painless, dependent on distance, and responsive
to correction with a pinhole. Specific refractive errors
include myopia (nearsightedness), hyperopia (farsight-
edness), astigmatism, and presbyopia (age-related ac-
commodative loss and impaired vision for reading).
Amblyopia occurs as a monocular condition in chil-
dren, usually before five years of age. It results from
a failure of the neurosensory connections of the visual
system to develop fully, because of a loss of a clear
monocular image or because of binocular misalign-
ment. Precipitating conditions include strabismus, un-
equal refractive error, and monocular occlusions of
the ocular media (congenital cataract). Amblyopia
may be responsive to treatment if therapy is initiated
while the child is in the critical developmental period
(up to seven years of age). It is important not to con-
fuse reduced vision due to amblyopia with blurred
vision of recent onset.
Functional Loss of Vision
Blurred visual acuity that results from a perceptual
or psychological malfunction is termed functional
loss of vision. It represents real but usually transient
loss of visual acuity that is often due to severe psy-
chological trauma. The most common diagnostic clin-
ical finding is tubular visual fields.2
PATHOLOGIC CAUSES
OF BLURRED VISION
The pathologic causes of blurred vision are much
less common but far more urgent than the nonpatho-
logic causes. For patients who cannot see well, a di-
agnostic algorithm based on the chronology of onset,
whether the symptom is unilateral or bilateral, and the
558 · Aug u s t 2 4 , 2 0 0 0
The New England Journal of Medicine as published by New England Journal of Medicine.
Downloaded from www.nejm.org on August 19, 2010. For personal use only. No other uses without permission.
Copyright © 2000 Massachusetts Medical Society. All rights reserved.
Figure 3. Nonproliferative Diabetic Retinopathy Showing Hem-
orrhages and Exudates in the Posterior Pole, with No Evidence
of Neovascularization.
presence or absence of pain helps in the categoriza-
tion of the many and varied causes of blurred vision.
The ophthalmic branch of the fifth cranial nerve
provides ocular sensation. The areas of the eye that are
sensitive to pain are the ocular surface, the iris, and
the ciliary body. The periorbital areas are also sensi-
tive to pain; therefore, inflammation around the op-
tic nerve can cause pain as well as blurred vision. The
retina, the vitreous, and the optic nerve within the
globe are relatively insensitive to pain.
Sudden, Unilateral, Painless Loss of Vision
Sudden, unilateral, painless loss of vision often re-
sults from an abnormality in the posterior segment
of the eye. Facility with the ophthalmoscope is crit-
ical for diagnosing these problems. Each of the fol-
lowing problems deserves urgent ophthalmologic con-
sultation.
Vitreous hemorrhage associated with diabetes or
trauma is a common cause of sudden, unilateral, pain-
less loss of vision.3 The red reflex and details of the
retina will be obscured when viewed through the di-
rect ophthalmoscope. Patients with diabetes may also
present with hemorrhages, exudates, microaneurysms,
edema, and neovascularization in the posterior seg-
ment, which result in sudden changes in vision (Fig.
3).4 Most vitreous hemorrhages are allowed to clear
spontaneously, but in patients with diabetes who have
neovascularization, emergency retinal photocoagula-
tion may be indicated.
Serous elevations of the macula5 and hemorrhagic
macular changes due to choroidal neovascular mem-
branes and age-related macular degeneration will oc-
casionally present as sudden, unilateral, painless loss
of vision (Fig. 4).6,7 Age-related macular changes can
be identified with the direct ophthalmoscope.8 Pa-
 PRIMA RY CA R E

Figure 6. A Central Retinal-Vein Occlusion, with Widespread In-

Figure 4. A Subretinal Hemorrhage Due to a Choroidal Neovas-
traretinal Hemorrhages.
cular Membrane in a Patient with Age-Related Macular Degen-
eration.

Figure 5. A White, Billowing, and Elevated Retina, Characteris- Figure 7. Occlusion of the Central Retinal Artery.
tic of Retinal Detachment. The retina appears white because of widespread edema, and
the preserved choroidal circulation underneath shines through
as a cherry-red spot at the fovea.

tients with these problems should undergo urgent
angiography with fluorescein to determine whether
the macular lesion is amenable to laser treatment.
Retinal detachments are diagnosed most easily by
an ophthalmologist using indirect ophthalmoscopy
through a dilated pupil, but occasionally the medical
practitioner can see the white, billowing retinal sep-
aration (Fig. 5).9 Retinal detachments require urgent
surgical repair.
Retinal-vein occlusions are characterized by intra-
retinal hemorrhages.10,11 These hemorrhages can be
widespread and diffuse throughout the fundus in an
occlusion of the central retinal vein (Fig. 6) or may
be localized to one quadrant with occlusions of the
branches of the retinal vein. Retinal photocoagula-
tion may be indicated in cases of serious edema or
of neovascularization of the iris.
Episodes of amaurosis fugax (temporary loss of vi-
sion) may precede frank occlusion of the retinal ar-
tery.12 Occlusion of the central retinal artery is associ-
ated with profound loss of vision, an afferent pupillary
defect, and a cherry-red spot in the macula (Fig. 7).
An embolus, or Hollenhorst, plaque may be visible.
Patients with this condition benefit from an urgent
neurovascular workup to search for the source of the
embolus. Nonarteritic anterior ischemic optic neurop-
athy tends to occur in older patients and is associated
with an afferent pupillary defect and congestion and
elevation of the optic disk (Fig. 8).13,14
One type of presentation of sudden, unilateral,
painless loss of vision could be termed suddenly per-
ceived unilateral, painless loss of vision. A slowly pro-
gressive condition, usually in the nondominant eye,
is suddenly noticed when the unaffected eye is inad-

Vol ume 343 Numb e r 8 · 559

The New England Journal of Medicine as published by New England Journal of Medicine.
Downloaded from www.nejm.org on August 19, 2010. For personal use only. No other uses without permission.
Copyright © 2000 Massachusetts Medical Society. All rights reserved.
 The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne

Figure 8. Anterior Ischemic Optic Neuropathy, Characterized by Figure 9. A Corneal Ulcer, Appearing as a White Infiltrate in the
Swelling and Hemorrhages of the Optic Disk. Cornea.
In this fungal infection, the ulcer is associated with a ring of in-
flammatory cells and hypopyon.

vertently covered, making apparent the reduced vi-

sion in the other eye. To help in determining wheth-
er the condition has presented in such a fashion, the
patient should be asked how he or she first noticed
the blurred vision. Conditions that commonly have
this presentation include refractive errors, cataracts,
and age-related macular degeneration without hem-
orrhage or exudation.
Sudden, Unilateral, Painful Loss of Vision
The conditions that most commonly cause sud-
den, unilateral, painful loss of vision are centered in
the cornea and anterior chamber and are associated
with a red eye.15 The corneal causes include abrasion,
infection, and edema.16,17 Infection (corneal ulcer) is Figure 10. An Epithelial Ulcer (Arrow) Due to Herpes Simplex In-
the most critical condition to recognize. Patients with fection, Which Has a Typical Dendritic Pattern When Stained
infectious ulcers typically have a white infiltrate in the with Topical Fluorescein and Illuminated with Cobalt-Blue Light.
cornea (Fig. 9) and require emergency ophthalmo-
logic referral, cultures, and intensive treatment with
topical antibiotics. Herpes simplex ulcers often present
with a dendritic pattern, which is most easily identi-
fied with topical fluorescein (Fig. 10).
Inflammation of the iris, of the ciliary body, and of condition medically to minimize problems with in-
the anterior uveal tract causes mildly decreased vision creased intraocular pressure and to reduce the threat
that is commonly associated with photophobia.18 Most of recurrent bleeding.
cases of inflammation (uveitis) are idiopathic, but A rapid increase in intraocular pressure (acute glau-
some may be associated with sarcoid, collagen vascular coma) causes pain and corneal edema, which results
diseases, syphilis, and tuberculosis. All are clinically di- in a moderate-to-severe reduction in visual acuity. Pa-
agnosed with use of the slit lamp and are treated with tients with acute angle-closure glaucoma require emer-
topical corticosteroids. Because topical corticosteroids gency laser iridectomy to relieve the pupillary block-
may be associated with the development of cataracts, age that leads to angle closure.
with glaucoma, and with reactivation of herpes sim- Temporal arteritis tends to present in older patients,
plex virus infection, nonophthalmologic medical prac- with pain and tenderness over the scalp and temple
titioners should not prescribe these medications. and symptoms of polymyalgia rheumatica. Loss of vi-
Traumatic hyphema is most often associated with sion results from ischemic optic neuropathy, and an
pain and reduces visual acuity in proportion to the afferent pupillary defect is present. The erythrocyte
amount of blood in the anterior chamber.19 After re- sedimentation rate is elevated, and prompt treatment
ferral, the ophthalmologist will treat patients with this with systemic corticosteroids is indicated to minimize

560 · Augus t 2 4 , 2 0 0 0
The New England Journal of Medicine as published by New England Journal of Medicine.
Downloaded from www.nejm.org on August 19, 2010. For personal use only. No other uses without permission.
Copyright © 2000 Massachusetts Medical Society. All rights reserved.
 PR IMA RY CA R E

the risk of bilateral ocular involvement.20 A biopsy of

the temporal artery is indicated; the results of the
biopsy are not altered by short-term use of cortico-
steroids.
Optic neuritis generally occurs in younger patients
and may be associated with multiple sclerosis.21,22 The
reduction in visual acuity can be profound and is of-
ten accompanied by pain on movement of the eyes.
An afferent pupillary defect is generally present, and
the optic nerve may appear swollen in patients with
anterior papillitis (Fig. 11) and normal in patients
with retrobulbar neuritis. Prompt diagnosis is impor-
tant, because some patients may benefit from inten-
sive systemic treatment with corticosteroids.23
Orbital cellulitis is a vision-threatening and, in rare Figure 11. Optic Neuritis (Papillitis) with a Swollen Optic Nerve.
instances, life-threatening infection of the retro-orbit-
al space. Deep orbital involvement is heralded by pain,
decreased vision, limited extraocular motility, propto-
sis, an afferent pupillary defect, and optic-nerve con-
gestion.24,25 Referral to an ophthalmologist and an
otorhinolaryngologist is indicated, with a workup
that includes cultures, computed tomographic scan-
ning, and treatment that incorporates intravenous an-
tibiotics. Treatment is particularly critical in immu-
nosuppressed patients.
Sudden, Bilateral, Painless Loss of Vision
Loss of vision that is sudden, bilateral, and pain-
less is extremely rare. It may be caused by sudden re-
fractive changes due to the swelling of the lens in pa-
tients with poorly controlled diabetes or in response
to medications.26,27 Medications that contain anticho-
linergic agents, cholinergic agents, and corticoster-
oids can exacerbate refractive errors or induce sud- Figure 12. A Posterior Subcapsular Cataract as It Would Appear
den refractive changes. through the Direct Ophthalmoscope When Highlighted against
the Pupillary Red Reflex.
Sudden, Bilateral, Painful Loss of Vision
Trauma to the anterior segment in the form of for-
eign bodies, chemical spills, and welder’s exposure to
ultraviolet radiation may present as sudden, bilateral,
painful loss of vision. Corneal infections, iritis, and is another common cause of gradual, unilateral, pain-
acute glaucoma, which are all associated with a red less loss of vision in older patients. It may appear as
eye, very rarely present bilaterally.28 Temporal arteri- focal yellow spots (drusen) or as variable areas of hy-
tis may also rarely be associated with permanent bi- perpigmentation or hypopigmentation in the macula
lateral, painful loss of vision. (Fig. 13). Patients with this condition need routine
ophthalmologic consultation so that possible foci of
Gradual, Unilateral, Painless Loss of Vision hemorrhage or exudation, which may not be readily
Blurred vision is commonly manifested as loss of apparent but are potentially treatable with a laser,
vision that is gradual, unilateral, and painless. Cata- can be located.
racts are the primary cause in the elderly population. In rare instances, slowly compressive lesions in the
Cataracts may appear as a hazy opacification of the orbit and intracranial space may cause this type of vi-
pupillary space when the eye is examined with a pen- sion loss. When loss of vision occurs as a result of a tu-
light, and they impair visualization of the posterior mor compressing the optic nerve, optic atrophy and
segment when the direct ophthalmoscope is used defects in the visual field are invariably present.29,30
(Fig. 12). For cataracts, routine, nonurgent ophthal-
mologic follow-up should be planned. Gradual, Unilateral, Painful Loss of Vision
Age-related macular degeneration without hem- Gradual, unilateral, painful loss of vision is rare.
orrhage or exudation (“dry” macular degeneration) Slowly progressive inflammatory or neoplastic proc-

Vol ume 343 Numb e r 8 · 561

The New England Journal of Medicine as published by New England Journal of Medicine.
Downloaded from www.nejm.org on August 19, 2010. For personal use only. No other uses without permission.
Copyright © 2000 Massachusetts Medical Society. All rights reserved.
 The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne
Figure 13. Macular Drusen in Age-Related Macular Degenera-
tion without Hemorrhage or Exudates.
esses of the cornea or retrobulbar space are possible
causes. Orbital granulomas and optic neuromas have
been reported.31,32 Computed tomography or mag-
netic resonance imaging is ordered by the ophthal-
mologist in these cases.
Gradual, Bilateral, Painless Loss of Vision
Cataracts and age-related macular degeneration are
the most common causes of gradual, bilateral, pain-
less loss of vision. Rare, but deserving of ophthal-
mologic monitoring, are conditions caused by ocular
toxicity, such as that associated with hydroxychloro-
quine or ethambutol.33-35 Treatment involves discon-
tinuing the offending medication, although visual loss
in these cases is usually irreversible. In rare instances,
compressive lesions at the level of the chiasm may
present as painless bilateral loss of vision.29,30 Testing
of the visual field is critical in this condition.
Gradual, Bilateral, Painful Loss of Vision
Gradual, bilateral, painful loss of vision is exceed-
ingly rare and is most likely to be due to a chronic
inflammatory process, as might occur in collagen vas-
cular disease or sarcoidosis.
CONCLUSIONS
Blurred vision is a complex symptom with myriad
causes, ranging from simple refractive errors correct-
able with eyeglasses to life-threatening illnesses. The
ability of the clinician to distinguish pathologic causes
from nonpathologic causes is of paramount impor-
tance. Fortunately, simple tools common to all med-
ical offices and a systematic diagnostic approach can
help the medical practitioner make an important start
in this critical delineation.
562 · Augus t 2 4 , 2 0 0 0
The New England Journal of Medicine as published by New England Journal of Medicine.
Downloaded from www.nejm.org on August 19, 2010. For personal use only. No other uses without permission.
Copyright © 2000 Massachusetts Medical Society. All rights reserved.
REFERENCES
1. Barresi BJ, Higgins JD. Vision loss. In: Barresi BJ, ed. Ocular assessment:
the manual of diagnosis for office practice. Boston: Butterworths, 1984:35-41.
2. Albert DM, Jakobiec FA. Principles and practice of ophthalmology.
Philadelphia: W.B. Saunders, 1994.
3. Spraul CW, Grossniklaus HE. Vitreous hemorrhage. Surv Ophthalmol
1997;42:3-39.
4. Fong DS, Ferris FL III, Davis MD, Chew EY. Causes of severe visual
loss in the Early Treatment Diabetic Retinopathy Study: ETDRS report no.
24. Am J Ophthalmol 1999;127:137-41.
5. Mathews DE. Idiopathic central serous chorioretinopathy. Optom Clin
1996;5:175-84.
6. Bressler NM, Bressler SB, Fine SL. Age-related macular degeneration.
Surv Ophthalmol 1988;32:375-413.
7. Bressler SB, Maguire MB, Bressler NM, Fine SL. Relationship of drusen
and abnormalities of the retinal pigment epithelium to the prognosis of
neovascular macular degeneration. Arch Ophthalmol 1990;108:1442-7.
8. Frederick AR Jr, Morley MG, Topping TM, Peterson TJ, Wilson DJ.
The appearance of stippled retinal pigment epithelial detachments: a sign
of occult choroidal neovascularization in age-related macular degeneration.
Retina 1993;13:3-7.
9. Elfervig LS, Elfervig JL. Retinal detachment. Insight 1998;23:66-70.
10. Krakau CE. Disk hemorrhages and retinal vein occlusions in glauco-
ma. Surv Ophthalmol 1994;38:Suppl:S18-S22.
11. Wong VK. Retinal venous occlusive disease. Hawaii Med J 1997;56:
289-91.
12. Kosmorsky GS. Sudden painless visual loss: optic nerve and circulatory
disturbances. Clin Geriatr Med 1999;15:v, 1-13.
13. Hayreh SS, Podhajsky PA, Zimmerman B. Nonarteritic anterior ische-
mic optic neuropathy: time of onset of visual loss. Am J Ophthalmol 1997;
124:641-7.
14. Warner JE, Lessell S, Rizzo JF III, Newman NJ. Does optic disc ap-
pearance distinguish ischemic optic neuropathy from optic neuritis? Arch
Ophthalmol 1997;115:1408-10.
15. Gaston H. Managing the red eye. Practitioner 1989;233:1566-72.
16. Shingleton BJ. Eye injuries. N Engl J Med 1991;325:408-13.
17. Whitcher JP. Corneal ulceration. Int Ophthalmol Clin 1990;30:30-2.
18. Rosenbaum JT. Systemic associations of anterior uveitis. Int Ophthal-
mol Clin 1991;31:131-42.
19. Gottsch JD. Hyphema: diagnosis and management. Retina 1990;10:
Suppl 1:S65-S71.
20. Gordon LK, Levin LA. Visual loss in giant cell arteritis. JAMA 1998;
280:385-6.
21. Cleary PA, Beck RW, Bourque LB, Backlund JC, Miskala PH. Visual
symptoms after optic neuritis: results from the Optic Neuritis Treatment
Trial. J Neuroophthalmol 1997;17:18-28.
22. Landau K. Visual symptoms after optic neuritis: results from the Optic
Neuritis Treatment Trial. Surv Ophthalmol 1998;42:491.
23. Kapoor R, Miller DH, Jones SJ, et al. Effects of intravenous methyl-
prednisolone on outcome in MRI-based prognostic subgroups in acute op-
tic neuritis. Neurology 1998;50:230-7.
24. Donahue SP, Schwartz G. Preseptal and orbital cellulitis in childhood:
a changing microbiologic spectrum. Ophthalmology 1998;105:1902-6.
25. Uzcategui N, Warman R, Smith A, Howard CW. Clinical practice
guidelines for the management of orbital cellulitis. J Pediatr Ophthalmol
Strabismus 1998;35:73-9, 110-1.
26. Eva PR, Pascoe PT, Vaughan DG. Refractive change in hyperglycae-
mia: hyperopia, not myopia. Br J Ophthalmol 1982;66:500-5.
27. Fledelius HC. Myopia and diabetes mellitus with special reference to
adult-onset myopia. Acta Ophthalmol (Copenh) 1986;64:33-8.
28. Silverman H, Nunez L, Feller DB. Treatment of common eye emer-
gencies. Am Fam Physician 1992;45:2279-87.
29. Trevino R. Chiasmal syndrome. J Am Optom Assoc 1995;66:559-75.
30. van Dalen JT, Verbeeten BJ, Peeters FL. Chiasmal syndrome: ophthal-
mological and neuro-radiological aspects. Doc Ophthalmol 1982;52:259-78.
31. Freeman NR, Shraberg D. Alternating painful ophthalmoplegia. South
Med J 1980;73:1398-400.
32. Martin CJ. Orbital pseudotumor: case report and overview. J Am Op-
tom Assoc 1997;68:775-81.
33. Mazzuca SA, Yung R, Brandt KD, Yee RD, Katz BP. Current practices
for monitoring ocular toxicity related to hydroxychloroquine (Plaquenil)
therapy. J Rheumatol 1994;21:59-63.
34. Sammartino JP, Soll DB. Ocular toxicity of systemic drugs. Am Fam
Physician 1985;31:226-9.
35. Fraunfelder FT, Meyer SM. Ocular toxicity of antineoplastic agents.
Ophthalmology 1983;90:1-3.