1. A 56-year-old male painter presented with sudden painless loss of vision in the right eye for 1 day. Examination found right eye visual acuity of counting fingers close to face and a cherry red spot on fundus examination, consistent with a diagnosis of central retinal artery occlusion. 2. Central retinal artery occlusion is caused by an embolism or thrombosis blocking the central retinal artery, cutting off blood supply to the retina. It typically causes sudden monocular vision loss and is more common in older males with risk factors like hypertension and smoking. 3. On examination, central retinal artery occlusion presents with right eye relative afferent pupillary defect, cherry red spot on the retina, and box

1. Case

2. Name: XXX Age/G: 56 yr/M
Occupation: Painter location: Chennai
Purpose of visit: Sudden loss of vision
Chief complaint:
RE: C/O sudden painless loss of vision for distance and near X
1day
LE: No such complaints
Previous ocular history:
H/o using Rx x 15 yrs
No h/o trauma, Sx

3. General health: Normal (H/o smoking x 30 yrs)
Family history: Not significant
Recent investigation: Nil
Current medication: Nil
Allergy: Not aware of any
Previous glass prescription:
RE: -3.00 DS/ -1.00DC x 80
LE: -2.25 DS/ -1.00DCx 90
Add: BE: +2.50 DS
Using progressive lens, good quality

4. Visual acuity (aided):
RE: CFCF, <N36
LE: 6/6, N6
Objective refraction:
RE: -3.25DS/ -1.00DC x 90
LE: -2.25DS/-1.50 DC x 100
Subjective refraction:
RE: NAG ( CFCF, <N36)
LE: -2.25DS/-1.50DC x 100 (6/6, N6)

5. Pupil examination:
RE: RAPD
LE: PERRLA, No RAPD
SLE: RE LE
upper lid normal
conjunctiva normal
cornea clear
AC depth normal
lower lid normal
Lens clear lens

6. IOP:
RE: 17mm Hg
LE: 16mm Hg
Fundus examination:
RE LE
10.05 AM
WNL
CDR- normal
Pale retina
Cherry red spot

7. Diagnosis:
?
RE: Central retinal artery occlusion

8. Central Retinal
Artery Occlusion
By,
DHINESH M

9. Introduction
Central retinal artery occlusion (CRAO) is the sudden
blockage of the central retinal artery
 retinal hypoperfusion
 rapidly progressive cellular damage
 vision loss

10. Etiology
Embolism : blockage of artery caused by any foreign body
Thrombosis . Thrombi may be due to atherosclerotic disease,
collagen-vascular disease, inflammatory states, and/or
hypercoagulable states

11. Epidemology
Incidence - 1: 100,000 ( less than 2% with bilateral presentation)
Early 60s
Male>female
RISK FACTORS:
hypertension,
smoking,
hyperlipidemia,
diabetes,
hypercoagulable states

12. Clinical features
Symptoms
Monocular vision loss
Sudden loss of vision (occurs acutely, possibly over a span of few
seconds)
Painless
In some cases, premonitory episodes of amaurosis fugax may be
reported

13. 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 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 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

14. 2. RAPD
3. Intra ocular pressure is often normal at presentation but may become
elevated in the setting of rubeosis iridis
4. Fundus changes
 Cherry red spot (90%)
 Posterior pole retinal opacity or whitening (58%)
 Box-caring/ Cattle trucking of retinal arteries and veins (19 and 20%)
 At later stages, funduscopic findings showed optic atrophy (91%),
retinal arterial attenuation (58%), cilioretinal collaterals (18%), and
macular retinal pigment epithelial changes (11%).

15. Cherry red spot

16. Box-caring

17. A patent cilioretinal artery supplying some or all of the papillomacular
bundles.

18. Retinal emboli
Retinal emboli are visible in 20 to 40 % of eyes with CRAO
1. Cholesterol emboli- golden to yellow orange crystal often located at
arteriolar bifurcation. They rarely cause significant obstruction to retinal
arteries and are frequently asymptomatic
2. Calcific emboli- single, white often close to disc, they may be easily
overlooked as they tend to merge with disc. They cause permanent
occlusion.
3. Fibrin-platelet emboli- dull grey, elongated particles. They may cause
retinal transient ischemic attack.

19. (A) Platelet-fibrin emboli (white arrow) appeared as whitish lesions within a
section of the arteriole, (B) cholesterol emboli (black arrowhead) appeared as
multiple bright yellow-white plaques on the vascular periphery, and (C) calcific
emboli (white arrowhead) appeared as whitish plaques on the bifurcation of the
arteriolar branch.

20. Diagnosis
1. OCT:
 In acute stage, OCT shows irregular macular contour with increased
reflectivity of the inner retina. This corresponds to intracellular edema
and explains the lack of intraretinal, hyporeflective fluid spaces in case of
CRAO or BRAO. The reflectivity of the outer retinal layers and RPE is
blocked by the highly reflective inner retinal layer.
 OCT can be helpful in cases of chronic CRAO where the fundus may
appear featureless but the OCT shows inner retinal atrophy with
preservation of the outer retina

21. SD-OCT shows the highly reflective thickened inner retina. The outer
retina is relatively hyporeflective because of blocking from the
thickened inner retina

22. 2. FFA:
 Initially shows some variable residual retinal circulation with
delayed and sluggish filling of the retinal vasculature. Complete
absence of retinal filling is rare

23. There is a considerable delay in filling the central retinal artery
circulation following the dye injection

24. 3. ERG:
 Typically demonstrate more severe attenuation of the b-wave than a-
wave since the inner retinal layers are more affected
 Diminution of a and b wave may suggest outer retinal damage
secondary to choroidal vascular hypoperfusion in setting of an
ophthalmic artery occlusion

26. Treatment
Adoption to supine posture might improve ocular perfusion pressure
Ocular massage
Hyperbaric oxygen
Vasodilating medications- pentoxifyline, nitroglycerin and isosorbide
dinitrate
Nd- YAG laser

27. References
Varma DD, Cugati S, Lee AW, Chen CS (June 2013). "A review of central
retinal artery occlusion: clinical presentation and management". Eye. 27 (6):
688-97. doi:10.1038/eye.2013.25. PMC 3682348. PMID 23470793
Central and branch retinal artery occlusion. Uptodate.com. Mar 14, 2012.
Kunimoto, Dr., Lecture, Vascular diseases of the retina, AT Still University
SOMA, October 2012
Hayreh SS (December 2018). "Central retinal artery occlusion". Indian
Journal of Ophthalmology. 66 (12): 1684–1694
Kanski’s clinical ophthalmology

28. Thank you