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IM BOARD REVIEW GREGORY W.

RUTECKI, MD, Section Editor

CME LEARNING OBJECTIVE: Readers will assess the possible causes of acute monocular vision loss
CREDIT
JUSTIN R. ABBATEMARCO, MD RUSHAD PATELL, MD JANET BUCCOLA, MD MARY ALISSA WILLIS, MD
Neurology Resident, Cleveland Clinic Internal Medicine Resident, Department of Hospital Medicine, Mellen Center for Multiple Sclerosis
Cleveland Clinic Medicine Institute, Cleveland Clinic; Treatment and Research, Neurological
Clinical Assistant Professor, Cleveland Clinic Institute, Cleveland Clinic; Assistant
Lerner College of Medicine of Case Western Professor, Cleveland Clinic Lerner College of
Reserve University, Cleveland, OH Medicine of Case Western Reserve University,
Cleveland, OH

Acute monocular vision loss:


Dont lose sight of the differential
A n 83-year-old man presented to the
emergency department with acute, pain-
less loss of vision in his left eye. His vision in
disciplinary effort, early evaluation and triage
of this potential medical emergency is often
done by clinicians without specialized train-
that eye had been normal in the middle of the ing in ophthalmology.
night when he woke to use the restroom, but The physiology of vision is complex and
on awakening 6 hours later he could perceive the list of possible causes of vision loss is long,
only light or darkness. but the differential diagnosis can be narrowed
He denied headache, scalp tenderness, jaw quickly by considering the time course of vi-
claudication, fever, weight loss, myalgia, or sion loss and the anatomic localization.1
other neurologic symptoms. He had not ex- The time course (including onset and
perienced any recent change in his vision be- tempo) of vision loss can classified as:
fore this presentation, including halos around Transient (ie, vision returned to normal by
lights, floaters, eye pain, or redness. However, the time seen by clinician)
6 months ago he had undergone left cataract Acute (instantaneous onset, ie, within sec-
surgery (left phacoemulsification with intra- onds to minutes) He woke up
ocular implant) without complications. And Subacute (progression over days to weeks)
he said that when he was 3 years old, he had that morning
Chronic (insidious progression over months
sustained a serious injury to his right eye. to years). and could not
His medical history included ischemic heart Although acute vision loss is usually dra- see out of his
disease and hypertension. His medications in- matic, insidious vision loss may occasionally
cluded losartan, furosemide, amlodipine, atorv- be unnoticed for a surprisingly long time until left eye; 6 hours
astatin, and aspirin. the normal eye is inadvertently shielded. earlier it had
Anatomic localization. Lesions anterior to been normal
CAUSES OF ACUTE MONOCULAR the optic chiasm cause monocular vision loss,
VISION LOSS whereas lesions at or posterior to the chiasm
lead to bilateral visual field defects. Problems
1 Which of the following is the least likely cause
of this patients acute monocular vision loss?
leading to monocular blindness can be broadly
divided into 3 anatomic categories (Figure 1):
Ocular medial (including the cornea, an-
Optic neuritis
Retinal vein occlusion terior chamber, and lens)
Retinal artery occlusion Retinal
Pituitary apoplexy Neurologic (including the optic nerve and
Retinal detachment chiasm).
Acute vision loss is often so distressing to the Clues from the history
patient that the emergency department may A careful ophthalmic history is an essential
be the first step in evaluation. While its diag- initial step in the evaluation (Table 1). In ad-
nosis and management often require an inter- dition, nonvisual symptoms can help narrow
doi:10.3949/ccjm.84a.16096 the differential diagnosis.
CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 84 NUM BE R 10 O CT O BE R 2017 779
MONOCULAR VISION LOSS

Cornea icits (eg, bitemporal hemianopia) but is less


Trauma likely to cause monocular vision loss.1
Keratitis
Anterior chamber CASE CONTINUED: EXAMINATION
Acute angle-closure glaucoma
Hyphema On examination, the patient appeared com-
Uveitis fortable. His temperature was 97.6F (36.4C),
Lens problems pulse 59 beats per minute, respiratory rate 18
Acute trauma per minute, and blood pressure 153/56 mm Hg.
Dislocation Heart and lung examinations were nota-
ble for a grade 3 of 6 midsystolic, low-pitched
murmur in the aortic area radiating to the
neck, bilateral carotid bruits, and clear lungs.
The cardiac impulse was normal in location
Retina and character. There was no evidence of aor-
Detachment tic insufficiency (including auscultation dur-
Vascular occlusion ing exhalation phase while sitting upright).
Eye examination. Visual acuity in the
right eye was 20/200 with correction (owing
Optic nerve to his eye injury at age 3). With the left eye,
Neuropathy (ischemic, inflammatory, or infectious process) he could see only light or darkness. The con-
Papilledema
junctiva and sclera were normal.
FIGURE 1. Common causes of monocular vision loss can arise The right pupil was irregular and measured
in the media (cornea, anterior chamber, or lens), retina, or 3 mm (baseline from his previous eye injury).
optic nerve. The left pupil was 3.5 mm. The direct pupil-
lary response was preserved, but a relative
Nausea and vomiting often accompany afferent pupillary defect was present: on the
acute elevation of intraocular pressure. swinging flashlight test, the left pupil dilated
Insidious vision Focal neurologic deficits or other neuro- when the flashlight was passed from the right
logic symptoms can point to a demyelinating
loss may be to the left pupil. Extraocular movements were
disease such as multiple sclerosis. full and intact bilaterally. The rest of the neu-
unnoticed for Risk factors for vascular atherosclerotic rologic examination was normal.
a surprisingly disease such as diabetes, hypertension, and An ophthalmologist was urgently con-
coronary artery disease raise concern for reti- sulted. A dilated funduscopic examination of
long time until nal, optic nerve, or cerebral ischemia.
the left eye revealed peripapillary atrophy, tor-
the normal eye Medications with anticholinergic and ad- tuous vessels, a cherry red macular spot, and
is inadvertently renergic properties can also precipitate mon- flame hemorrhages, but no disc edema or pal-
ocular vision loss with acute angle-closure lor (Figure 2).
shielded glaucoma.
Can we rule out anything yet? FURTHER WORKUP
Our patient presented with painless monocular
vision loss. As discussed, causes of monocular
vision loss can be localized to ocular abnormal-
ities and prechiasmatic neurologic ones. Reti-
2 Which of the following investigations
would be least useful and not indicated at
this point for this patient?
nal detachment, occlusion of a retinal artery or Carotid ultrasonography
vein, and optic neuritis are all important po- Electrocardiography and echocardiography
tential causes of acute monocular vision loss. Magnetic resonance angiography
Pituitary apoplexy, on the other hand, is of the brain
characterized by an acute increase in pituitary Computed tomographic (CT)
volume, often leading to compression of the angiography of the head and neck
optic chiasm resulting in a visual-field defect. Testing for the factor V Leiden and
It is most often characterized by binocular def- prothrombin gene mutations
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TABLE 1
Acute monocular vision loss: Diagnostic clues from the history
Feature Common conditions Additional features
Eye pain Acute angle-closure glaucoma Age > 60 and family history
Deep brow, headache with nausea and vomiting
Halos around lights

Optic neuritis Pain worsens with eye movements


Loss of color vision (red desaturation)

Keratitis Sharp superficial pain (grittiness)


(inflammation of the cornea)
Discharge from the eye

Conjunctival hyperemia Acute angle-closure glaucoma See above


(red eye)
Keratitis See above

Uveitis Redness prominent at limbus (convergence between


cornea and sclera)
Photophobia
Systemic features suggesting autoimmune disease

Headache Giant cell arteritis Age > 50


Scalp tenderness (new onset, temporally based headache)
Jaw claudication
Proximal muscle pain

Migraine Younger patients


Preceded by migraine prodrome
Symptoms resolve within hour

Photopsia Retinal detachment Myopia


(flashes of bright light)
Recent history of ophthalmic procedures
Partial loss of peripheral field

Preceding trauma Keratitis or uveitis Accompanying milder trauma

Hyphema History of blunt trauma


(blood in the anterior chamber)
Recent history of ophthalmic procedures

Lens dislocation or rupture Predisposed by congenital conditions


Associated small, irregular pupil

Information from references 2 and 3.

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MONOCULAR VISION LOSS

ritis) or nonarteritic (due to atherosclerotic


vascular disease).
Thus, carotid ultrasonography, electro-
cardiography, and transthoracic and trans-
esophageal echocardiography are important
components of the further workup. In addi-
tion, urgent brain imaging including either
CT angiography or magnetic resonance an-
giography of the head and neck is indicated
in all patients with central retinal artery oc-
clusion.
Thrombophilia testing, including tests
for the factor V Leiden and prothrombin
gene mutations, is indicated in specific cas-
es when a hypercoagulable state is suggested
by components of the history, physical ex-
amination, and laboratory and radiologic
testing. Thrombophilia testing would be
FIGURE 2. The patients funduscopic examination revealed low-yield and should not be part of the first-
a cherry red spot (arrow), a characteristic finding in central line testing in elderly patients with several
retinal artery occlusion. atherosclerotic risk factors, such as our pa-
tient.
A systematic ocular physical examination can
offer important diagnostic information (Table CASE CONTINUED:
2). Ophthalmoscopy directly examines the LABORATORY AND IMAGING EVIDENCE
optic disc, macula, and retinal vasculature.
Initial laboratory work showed:
To interpret the funduscopic examination,
Central retinal we need a basic understanding of the vascular Mild microcytic anemia
Erythrocyte sedimentation rate 77 mm/
artery occlusion supply to the eye (Figure 3). hour (reference range 110)
For example, the cherry red spot within
can be either the macula in our patient is characteristic C-reactive protein 4.0 mg/dL (reference
nonarteritic of central retinal artery occlusion and high- range < 0.9).
lights the relationship between anatomy and The rest of the complete blood cell count
or arteritic pathophysiology. The retinas blood supply is and metabolic profile were unremarkable. His
compromised, leading to an ischemic, white hemoglobin A1c value was 5.3% (reference
background (secondary to edema of the inner range 4.8%6.2%).
third of the retina), but the macula continues A neurologist was urgently consulted.
to be nourished by the posterior ciliary arter- Magnetic resonance imaging of the brain
ies. This contrast in color is accentuated by without contrast revealed nonspecific white-
the underlying structures composing the fo- matter disease with no evidence of ischemic
vea, which lacks the nerve fiber layer and gan- stroke.
glion cell layer, making the vascular bed more Magnetic resonance angiography of the
visible.2,3 head and neck with contrast demonstrated
Also in our patient, the marked reduction 20% to 40% stenosis in both carotid arteries
in visual acuity and relative afferent pupil- with otherwise patent anterior and posterior
lary defect in the left eye point to unilateral circulation.
optic nerve (or retinal ganglion cell) dys- Continuous monitoring of the left carotid
function. The findings on direct funduscopy artery with transcranial Doppler ultrasonogra-
were consistent with acute central retinal phy was also ordered, and the study conclud-
artery ischemia or occlusion. Central retinal ed there were no undetected microembolic
artery occlusion can be either arteritic (due events.
to inflammation, most often giant cell arte- Transthoracic echocardiography showed
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TABLE 2
Key physical examination features in monocular vision loss
Physical examination Helpful techniques Results
Visual acuity Vision screening apps (eg, EyeChart Pinhole test corrects refractory error by permitting central
Vision Screening App by Dok LLC) rays of light into the eye; will not correct underlying neuro-
logic impairment
Use corrective lens or pinhole
occluder

Visual field Monocular assessment Scotoma: discrete area of visual impairment surrounded by
intact vision; positive scotoma (seeing something that is not
Confrontation visual field testing there) may be a sign of retinal damage; negative scotoma
uses small-amplitude finger move- may indicate optic nerve dysfunction
ments in all quadrants
Hemianopia: bilateral visual impairment suggesting a le-
Central fields tested by Amsler grid sion posterior to optic chiasm

Color testing Use red objects (sharps container Unilateral color desaturation: optic nerve dysfunction
or bottle cap)

Pupillary Examine for size, shape, symmetry Afferent pupillary defect: optic nerve dysfunction
examination
Swinging flashlight examination:
paradoxical dilation when stimu-
lating ipsilateral eye after shining
light into contralateral eye

Red reflex Performed with ophthalmoscope Loss of reflex: localizes to media and possibly retinal detachment
when standing 1 foot away from
patient

Direct Use dilating drops to enhance the Cherry red macula: ischemic retina from central retinal artery
ophthalmoscopy examination occlusion that contrasts with nourished macula supplied by
posterior ciliary arteries
Disc: neuroretinal fibers entering
the eye Hollenhorst plaque: cholesterol emboli signifies atheroscle-
rotic disease in carotid or aortic arch
Macula: located temporally to disc
and lacking blood vessels Pale and swollen optic nerve head: ischemic optic neuropathy
from posterior ciliary artery obstruction
Information from references 2 and 3.

aortic sclerosis with no other abnormalities. CENTRAL RETINAL ARTERY OCCLUSION:


Ophthalmic fluorescein angiography was NONARTERITIC VS ARTERITIC CAUSES
performed and showed patchy choroidal hy-
poperfusion, severe delayed filling, and exten-
sive pruning of the arterial circulation with no 3 Which of the following is least useful to
differentiate arteritic from nonarteritic
causes of central retinal artery occlusion?
involvement of the posterior ciliary arteries.
Given the elevated inflammatory markers, Finding emboli in the retinal vasculature
pulse-dose intravenous methylprednisolone on funduscopy
was started, and a temporal artery biopsy was Temporal artery biopsy
planned. Measuring the C-reactive protein level
CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 84 NUM BE R 10 O CT O BE R 2017 783
MONOCULAR VISION LOSS

Anterior ciliary

Long posterior ciliary

Short posterior ciliary

Central retinal

Ophthalmic

Internal carotid

FIGURE 3. Vascular supply to the eye. The internal carotid arterys first major branch is the
ophthalmic artery. Four major vessels break off from the ophthalmic artery:
Central retinal artery: large-diameter vessel that supplies the retina (vulnerable to em-
bolic disease)
Short and long posterior ciliary arteries: small vessels that supply the optic nerve and
macula (susceptible to small-vessel disease)
Anterior ciliary arteries supply the iris and ciliary body.
Information from references 4 and 5.

and the erythrocyte sedimentation rate to nonarteritic central retinal artery occlusion
Echocardiography is similar to the evaluation of patients with
Positron-emission tomography (PET) an acute cerebral stroke.4 Studies have shown
Retinal fluorescein angiography that 25% of patients diagnosed with central
In patients diagnosed with central retinal ar- retinal artery occlusion have an additional
tery occlusion, the next step is to differentiate ischemic insult in the cerebrovascular system,
between nonarteritic and arteritic causes, since and these patients are at high risk of recurrent
separating them has therapeutic relevance. ocular or cerebral infarction. Workup includes
The carotid artery is the main culprit for diffusion-weighted MRI, angiography, echo-
embolic disease affecting the central retinal ar- cardiography, and telemetry.5
tery, leading to the nonarteritic subtype. Thus, Arteritic central retinal artery occlusion is
evaluation of acute retinal ischemia secondary most often caused by giant cell arteritis. The
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American College of Rheumatology classifica- claudication, or scalp tenderness once steroids


tion criteria for giant cell arteritis include 3 of are initiated also helps support the diagnosis
the following 5: of giant cell arteritis.7
Age 50 or older Unfortunately, visual symptoms may be ir-
New onset of localized headache reversible despite treatment.
Temporal artery tenderness or decreased Our patients central retinal artery occlusion
temporal artery pulse This case highlights how difficult it is in prac-
Erythrocyte sedimentation rate 50 mm/ tice to distinguish nonarteritic from arteritic
hour or greater central retinal artery occlusion.
Positive biopsy findings.6 Our patient had numerous cardiovascular
Temporal artery biopsy is the gold stan- risk factors, including known carotid and cor-
dard for the diagnosis of giant cell arteritis onary artery disease, favoring a nonarteritic
and should be done whenever the disease is diagnosis.
suspected.7,8 However, the test is invasive and On the other hand, his elevated inflamma-
imperfect, as a negative result does not com- tory markers suggested an underlying inflam-
pletely rule out giant cell arteritis.9 matory response. He lacked the characteristic
Although a unilateral temporal artery bi- headache and other systemic signs of giant cell
opsy can be falsely negative, several studies arteritis, but this has been described in about
evaluating the efficacy of bilateral biopsies did 25% of patients.15 If emboli are seen on fun-
not show significant improvement in the diag- duscopy, further workup for arteritic central
nostic yield.10,11 retinal artery occlusion is not warranted, but
Ophthalmic fluorescein angiography is emboli are not always present. Then again,
another helpful test for distinguishing nonar- absence of posterior ciliary artery involvement
teritic from arteritic central retinal artery oc- on fluorescein angiography pointed away from
clusion.12 Involvement of the posterior ciliary giant cell arteritis.
arteries usually occurs in giant cell arteritis,
and this leads to choroidal malperfusion with CASE CONTINUED: FINAL DIAGNOSIS
or without retinal involvement. The optic If giant cell
nerve may also be infarcted by closure of the Biopsy of the left temporal artery showed in-
timal thickening with focal destruction of arteritis
paraoptic vessels fed by the posterior ciliary
vessels.12,13 Such involvement of multiple ves- the internal elastic lamina by dystrophic cal- is suspected,
sels would not be typical with nonarteritic cification with no evidence of inflammatory it is essential
central retinal artery occlusion. Thus, this infiltrates, giant cells, or granulomata in the
finding is helpful in making the final diagnosis adventitia, media, or intima. Based on the re- to start
along with supplying possible prognostic in- sults of biopsy study and fluorescein angiogra- intravenous
formation.13 phy, we concluded that this was nonarteritic
central retinal artery occlusion related to ath- pulse-dose
PET-CT is emerging as a test for early
inflammation in extracranial disease, but its erosclerotic disease. methylpred-
utility for diagnosing intracranial disease is Methylprednisolone was discontinued. nisolone early
limited by high uptake of the tracer fluoro The patient was discharged on aspirin, losar-
deoxyglucose by the brain and low resolu- tan, furosemide, amlodipine, and high-dose
tion.14 Currently, it has no established role in atorvastatin for standard stroke prevention.
the evaluation of patients with central retinal He was followed by the medical team and the
artery occlusion and would have no utility in ophthalmology department. At 6 weeks, there
differentiating arteritic vs nonarteritic causes was only marginal improvement in the visual
of central retinal artery occlusion. acuity of the left eye.
If giant cell arteritis is suspected, it is es-
sential to start intravenous pulse-dose methyl MANAGEMENT
prednisolone early to prevent further vision
loss in the contralateral eye. Treatment should
not be delayed for invasive testing or temporal
artery biopsy. Improvement in headache, jaw
4 Management of nonarteritic central reti-
nal artery occlusion could include all of
the following except which one?
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MONOCULAR VISION LOSS

Ocular massage but has no value in nonarteritic central retinal


Intravenous thrombolysis artery occlusion.
Intra-arterial thrombolysis Vision recovery in nonarteritic central ret-
Risk-factor modification inal artery occlusion is variable, but the prog-
Intraocular steroid injection nosis is generally poor. The visual acuity on
In patients with acute vision loss from nonar- presentation, the onset of the symptoms, and
teritic central retinal artery occlusion, acute collateral vessels are major factors influencing
strategies to restore retinal perfusion include long-term recovery. Most of the recovery oc-
noninvasive standard therapies and throm- curs within 7 days and involves peripheral vi-
bolysis (intravenous or intra-arterial). Unfor- sion rather than central vision. Several studies
tunately, consensus and guidelines are lacking. report some recovery in peripheral vision in ap-
Traditional therapies include sublingual proximately 30% to 35% of affected eyes.2022
isosorbide dinitrate, systemic pentoxifylline,
inhalation of a carbogen, hyperbaric oxygen, PROMPT ACTION MAY SAVE SIGHT
ocular massage, intravenous acetazolamide and Vision loss is a common presenting symptom
mannitol, anterior chamber paracentesis, and in the emergency setting. A meticulous his-
systemic steroids. However, none of these have tory and systematic physical examination can
been shown to be more effective than placebo.16 narrow the differential diagnosis of this neu-
Thrombolytic therapy, analogous to the ro-ophthalmologic emergency. Acute retinal
treatment of patients with ischemic stroke or ischemia from central retinal artery occlusion
myocardial infarction, is more controversial in is the ocular equivalent of an ischemic stroke,
acute central retinal artery occlusion.13 Data and they share risk factors, diagnostic workup,
from small case-series suggested that intra- and management approaches.
arterial or intravenous thrombolysis might Both etiologic subtypes (ie, arteritic and
improve visual acuity with reasonable safety.17 nonarteritic) require prompt intervention by
On the other hand, a randomized study from front-line physicians. If giant cell arteritis is
the United Kingdom that compared intra-ar- suspected, corticosteroid therapy must be ini-
Suspicion terial thrombolysis within a 24-hour window tiated to save the contralateral retina from
of central and conservative measures concluded that ischemia. Suspicion of central retinal artery
thrombolysis should not be used.18 occlusion warrants immediate evaluation by a
retinal artery neurologist to consider thrombolysis. Prompt
Thrombolysis is thus used only in selected
occlusion patients on a case-specific basis with involve- action and interdisciplinary care involving an
warrants ment of a multispecialty team including stroke ophthalmologist, neurologist, and emergency
neurologists, especially if patients present or internal medicine physician may save a pa-
immediate within hours of onset and have concomitant tient from permanent visual disability.
evaluation by neurologic symptoms.
Treatment beyond the acute phase fo- KEY POINTS
a neurologist
cuses on preventing complications of the eye Monocular vision loss requires urgent
ischemia and aggressively managing systemic evaluation with a multidisciplinary man-
atherosclerotic risk factors to decrease the agement approach.
incidence of further ischemic events. Other There are no consensus treatment guide-
interventions include endarterectomy for sig- lines for nonarteritic central retinal artery
nificant carotid stenosis and anticoagulation occlusion, but the workup includes a com-
to prevent cardioembolic embolization (such prehensive stroke evaluation.
as atrial fibrillation). Most experts agree on Arteritic central retinal artery occlusion is
the addition of an antiplatelet agent.13,19 most often due to giant cell arteritis, and
Intraocular steroid injection can be used when it is suspected, the patient should be
in the management of some retinal disorders empirically treated with steroids.

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