Central Retinal Artery Occlusion (CRAO) for undergraduate MBBS Students. Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of CRAO. Also encompasses salient points for PGMEE

1. CENTRAL RETINAL ARTERY
OCCLUSION(CRAO)
Dr. Abhishek Onkar

3. Blood supply of O.N.

5. THE OCULAR BLOOD SUPPLY
 The eye receives its blood supply from the ophthalmic artery (a branch of the
internal carotid artery) via the retinal artery, ciliary arteries and muscular
arteries.
 The conjunctival circulation anastomoses anteriorly with branches from the
external carotid artery.
 The anterior optic nerve is supplied by branches from the ciliary arteries.
 The retina is supplied by arterioles branching from the central retinal artery.
These arterioles each supply an area of retina with little overlap. Obstruction
results in ischaemia of most of the area supplied by that arteriole.
 The fovea is so thin that it requires no supply from the retinal circulation. It is
supplied indirectly, as are the outer layers of the retina, by diffusion of oxygen
and metabolites across the retinal pigment epithelium from the choroid.

8. CRAO
 An abrupt diminution of blood flow through the central retinal artery
severe enough to cause ischemia of the inner retina •
 A branch retinal artery obstruction occurs when the site of blockage is
distal to the lamina cribrosa of the optic nerve.
 Retinal artery obstructions selectively affect the inner retina only.

9. EPIDEMIOLOGY
 Elderly population
 Arteritic: > 60-70 years of age
 Non-arteritic: > 50 years
 Can be seen in young adults
 M:F=2:1
 UNIOCULAR: 98%

11. Aetiology

12. Pathophysiology

13. SYMPTOMS
• Monocular
• Sudden loss of vision
• severe
• painless
• Occurs acutely, possibly over the span of a few seconds.
• In some cases, premonitory episodes of amaurosis fugax may be reported.
Amaurosis fugax represents transient acute retinal ischemia and typically
suggests an embolic source of occlusion

14. SIGNS
1) Visual acuity:
 at the time of initial presentation ranges from counting fingers to light perception
 • Central visual acuity may be near normal in patients who have a transient CRAO or a
cilioretinal artery providing sufficient vascular supply to the fovea.
 • The absence of light perception is rare; therefore, in such cases, concomitant
choroidal circulation deficit (e.g., due to ophthalmic artery occlusion) or optic nerve
involvement should be considered •
 Visual acuity tends only to improve within the first week of onset with minimal chance
for appreciable improvement subsequently
 • Visual recovery after treatment has been shown to correlate with presenting visual
acuity and the duration of visual impairment

15.  2) RAPD
 3) INTRAOCULAR PRESSURE is often normal at presentation but may
become elevated in the setting of rubeosis iridis

16.  4) FUNDUS CHANGES
 • Cherry-red spot (90%)
 • Posterior pole retinal opacity or whitening (58%),
 • Box-carring of retinal arteries and veins (19% and 20% respectively) •
Retinal arterial attenuation (32%)
 • Optic disc edema (22%), and optic nerve pallor (39%)
 • The retinal findings were predominantly located in the posterior pole
with a normal-appearing periphery

18. BRAO

20. Cherry Red Spot
 • GM2 gangliosidoses (Tay-Sachs & Sandhoff)
 • GM1 gangliosidoses
 • Sialidosis
 • Metachromatic leukodystrophy
 • Niemann-Pick Type A
 • Farber lipogranulomatosis
 • CRAO
 • Trauma (retinal edema)

21.  Fluorescein angiography demonstrates the slow rate of filling of the retinal
circulation and the normal filling of the cilioretinal artery and choroid

22.  Retinal emboli are visible in 20–40% of eyes with CRAO .The most common
variant is a yellow, refractile cholesterol embolus (Hollenhorst plaque)
 Retinal emboli consist of CHOLESTEROL in 74% of cases, CALCIFIED MATERIAL
in 15.5%, and PLATELET AND FIBRIN in 15.5%
 • 1 Cholesterol emboli (Hollenhorst plaques) are frequently asymptomatic.
 Calcific emboli may originate from atheromatous plaques in the ascending aorta
or carotid arteries, as well as from calcified heart valves. They may cause
permanent occlusion of the central retinal artery or one of its main branches.
 Fibrin-platelet emboli :They may cause a retinal transient ischaemic attack (TIA),
with resultant amaurosis fugax, and occasionally complete obstruction.

24. Neuro/cardio prompt referral
 forestall the development of permanent neurological sequelae as patients
with retinal embolization have an increased risk of developing a
permanent stroke over the next few months
 • It should be noted that the leading cause of death in patients with retinal
arterial obstruction is cardiovascular disease

25.  The optic nerve is acutely edematous in nearly all cases of arteritic CRAO
as a result of the associated anterior ischemic optic neuropathy that is
typically observed in these patients.
 In the acute phase of nonarteritic CRAO, the disc may be normal,
hyperemic, edematous, and, rarely, pale. •

26. EVALUATION
 R/o GCA
 • carotid Doppler imaging and echocardiography
 • Since the cardiac morbidity and mortality are significant in patients with
retinal artery occlusion, a baseline electrocardiogram is recommended
 • A hypercoagulability evaluation should be considered for patients less
than 50 years of age with a suggestive history (e.g.,prior thrombosis,
miscarriage, or family history) or unknown embolic source
 • Other tests for monoclonal gammopathy, cancer, • infection, and
disseminated intravascular coagulation may be ordered depending on the
clinical circumstance

28. TREATMENT
 • Adoption of a supine posture might improve ocular perfusion •
 Ocular massage
 • sublingual isosorbide dinitrate
 • intravenous acetazolamide,
 • intravenousmannitol or oral glycerol,
 • anterior-chamber paracentesis,
 • Intravenous methylprednisolone, streptokinase

30.  HBO
 CARBOGEN

31.  Iris neovascularization develops after acute CRAO in approximately 18% of
eyes, with a mean time interval of approximately 4- 5 weeks -typically
earlier than in CRVO 3 months.
 Full-scatter PRP is effective in eradicating the new iris vessels in about two
thirds of cases •
 Intravitreal injection of an anti-VEGF agent is first-line therapy for iris,
trabecular meshwork, or optic disc neovascularization

32.  Treatment of carotid disease In patients with a localized stenosis of the
artery, endarterectomy significantly reduces the risk of subsequent stroke.
 • If endarterectomy is contraindicated, medical treatment with drugs that
reduce platelet stickiness (aspirin, dipyridamole) or anticoagulants may be
used to reducing the frequency of transient ischaemic attacks and the risk
of a major stroke.

33.  FOLLOW-UP • The patient should be seen by an ophthalmologist in 3–4
weeks and again a month later in order to detect incipient
neovascularization, particularly of the anterior segment.
 PROGNOSIS • Patients with visualized retinal artery emboli, whether or not
obstruction is present, have a 56% mortality rate over 9 years, compared to
27% for an age-matched population without retinal artery emboli. • Life
expectancy of patients with CRAO is 5.5 years compared to 15.4 years for
an age-matched population without CRAO