Case 1B

ABELLO, ANTHONY ACERO, RIA ACOSTA, ANDRE AGCAOILI, NIKKI AGCAOILI, ROMARICO

HISTORY
62 year old, female
Sudden loss of vision in her right eye an hour ago

HISTORY
Vision was hand movement right eye
20/20 left eye Right pupil does not respond to light directly; reacts

consensually
Left pupil responds to light directly; does not react

consensually
Pale retina with a reddish spot on macular area

DIAGNOSIS

Central Retinal Artery Occlusion

Central Retinal Artery Occlusion

Painless catastrophic visual loss occurring over a period of

few seconds
Antecedent Transient Visual Loss (amaurosis fugax)

Visual acuity ranges between counting fingers and light

perception in 90% of eyes at initial examination

Central Retinal Artery Occlusion

Afferent pupillary defect can appear within seconds,

preceding the fundus abnormalities by an hour

25% of eyes with CRAO have cilioretinal arteries that spare

macular retina
potentially preserving central vision

Pathophysiology of signs and symptoms

Pathophysiology
Obstruction of the central retinal artery

Loss of blood supply to the inner layer of the retina

Inner layer edema and pyknosis of the ganglion cell nuclei

Ischemic Necrosis

Visual Loss

Pathophysiology
Causes
Systemic hypertension seen in two thirds of patients Diabetes mellitus Cardiac valvular disease seen in one fourth of patients

Pathophysiology
Causes
Embolism
This is most commonly cholesterol but can be calcific, bacterial,

or talc from intravenous drug abuse. This is associated with poorer visual acuity and higher morbidity and mortality. Emboli from the heart are the most common cause of CRAO in patients younger than 40 years.

Pathophysiology
Causes
Atherosclerotic changes
Carotid atherosclerosis is seen in 45% of cases of CRAO, with

60% or greater stenosis in 20% of cases. Atherosclerotic disease is the leading cause of CRAO in patients aged 40-60 years.
Other

Pathophysiology
Retina becomes

opacified and yellowwhite in appearance

takes as little as 15

minutes to several hours before becoming evident resolves in 4-6 weeks

Foveal cherry red spot

Visualization of the

choroidal pigment and retinal pigment epithelium

Diagnostic Procedures

Diagnostic Procedures
Laboratory Studies

helpful in determining the etiology of central retinal artery occlusion (CRAO)

CBC count

to evaluate anemia, polycythemia, and platelet disorders

Erythrocyte Sedimentation Rate (ESR)

evaluation for giant cell arteritis

Fibrinogen, antiphospholipid antibodies, prothrombin time/activated partial thromboplastin time (PT/aPTT), and serum protein electrophoresis

to evaluate for coagulopathies

Diagnostic Procedures
Fasting blood sugar, cholesterol, triglycerides, and lipid

panel
to evaluate for atherosclerotic disease

Blood cultures to evaluate for bacterial endocarditis and septic emboli

Diagnostic Procedures
Imaging studies
helpful in determining the etiology of CRAO

Carotid ultrasound imaging to evaluate atherosclerotic disease. This appears to be more sensitive than carotid Doppler, which only determines the flow. Magnetic resonance angiogram may be more accurate in detecting obstruction.

Diagnostic Procedures

Fluorescein angiogram
Delay in arteriovenous transit time (<11 seconds is in the reference

range) Delay in retinal arterial filling Normal choroidal filling (begins 1-2 seconds before retinal filling and completely filled within 5 seconds of dye appearance in healthy eyes). A delay of 5 seconds or greater is seen in 10% of patients. Consider ophthalmic artery occlusion or carotid artery obstruction if there is a significant delay in choroidal filling. Arterial narrowing with normal fluorescein transit after recanalization

Other Diagnostic Procedures

ECG
to evaluate for possible atrial fibrillation (A 24-h Holter monitor

may be necessary if arrhythmia is suspected but not detected on ECG testing.)

Electroretinogram
shows a diminished b-wave corresponding to Muller and/or bipolar

cell ischemia.

Echocardiogram (not necessarily an emergency department test)

To evaluate valvular disease, wall motion abnormalities, and mural

thrombi To evaluate vegetations that may cause septic emboli

Management

Aim of Management
restore the blood circulation to the retina as quickly as

possible
increasing the perfusion of blood through the artery

Management
Reduction of intraocular pressure
by ocular hypotensive drugs (acetazolamide IV) intermittent digital massage over the closed eyelid

5-15 seconds repeated for up to 15 minutes.

anterior chamber paracentesis

dislodge an embolus

inhalation of a mixture of 5% carbon dioxide and 90% oxygen

Complications & Prognosis

Complications
Neovascularization and the development of neovascular

glaucoma - occurs in about 16% of patients and warrants treatment.

Partial or complete loss of vision in the affected eye Similar problem occurring again in the same or the other

eye

Prognosis
Patients with a retinal artery occlusion often maintain

good to fair vision, but vision loss is often profound with central artery occlusion, even with treatment.
Once retinal infarction has occurred, vision loss is

permanent.