The document discusses retinal arterial occlusion, including the central retinal artery and its branches. It describes the anatomy and blood supply of the retina. There are several potential mechanisms of retinal arterial occlusion, most commonly atherosclerosis-related thrombosis. Clinical presentations vary depending on the site of occlusion, such as central retinal artery occlusion presenting with a cherry red spot and cilioretinal artery occlusion causing pericentral scotomas. Management includes treating the acute event to restore vision as well as workup and management of any underlying systemic conditions. However, visual recovery is often poor due to retinal infarction.

1. RETINAL ARTERIAL
OCCLUSION

2. Ophthalmic artery
• Ophthalmic artery constitutes the main source of blood supply to
orbital structures
• Ophthalmic artery arises from medial side of the convexity of the
fifth bend of the internal carotid artery, just after it has left the roof
of cavernous sinus after piercing the dura
• At its origin ophthalmic artery is medial to ant clinoid process & inf to
the optic nerve

3. Central retinal artery
• Central retinal artery branch of ophthalmic artery
• Originates from ophthalmic artery close to optic foramen, & runs a
wavy course forward below the optic nerve.
• Here it lies outside the dura but it is adherent to it
• At about 10-15mm behind the eyeball it bends upwards & pieerces
the dura & arachnoid to enter subarachnoid space.

4. Central retinal artery
• In the subarachnoid space it bends forwards & after a short course it
again bends upwards at right angle & invaginate pia to reach the
centre of nerve
• So here it is surrounded by pia matter along with pial vessels & also
by sympathetic nerve plexus (nerve of tiedemann)
• In the centre of optic nerve it bends forwards & then accompanying
with vein (on temp side) it passes anteriorly & pierces lamina
cribrosa to appear inside the eye

5. Central retinal artery
• In the optic nerve head it lies superficially in the nasal part of
physiological cup
• Here it divides into two branches superior & inferior
• Each of which subdivides into a temporal & nasal branch at or near
the margin of the optic disc
• In the retina the 4 terminal branches of central retinal artery divide
dichotomously as they proceed towards the ora serrata where they
end without anastomosis

6. • The retinal arteries and arterioles remain in the inner retina
• Only capillaries are found as deep as the inner nuclear layer
• When two vessels cross, the artery usually lies anterior to the vein
• And the two vessels share a common adventitial coat
• Many more arteriovenous crossings occur temporally than nasally
because the nasal vessels assume a much straighter course
• The crossings are important because they represent the most common
site of branch retinal vein obstructions.

7. Blood supply of the retina
• Outer 4 layers of the retina RPE, photoreceptors, ELM, ONL get their
nutrition from choriocapillaries
• Inner 6 layers OPL, INL, IPL, GCL, NFL, ILM get their blood supply from
central retinal artery
• OPL gets its blood supply from both central retinal artery &
choriocapillaries
• Fovea is relatively avascular, get its blood supply from
choriocapillaries

8. Blood supply of the retina
• Macular region get its blood supply from temporal branches of
central retinal artery
• Sometimes cillioretinal artery is seen originating in a hook shaped
manner within the temp margin of the disc
• It runs towards the macula & supplies it
• Applied :- when present it helps to retain central vision in CRAO

9. Venous drainage
• The venous drainage of the retina generally follows the arterial
supply
• Veins corresponding to arteries join to form central retinal vein which
drains into superior ophthalmic vein
• Near the superior orbital fissure it is joined by inferior ophthalmic
vein
• Leave the fissure & ultimately drains into cavernous sinus

10. Arterial occlusions

11. Demography
•Retinal arterial occlusions may occur at any age,
but the average age of patients with CRAO found in
two large series is 62 & 67 yrs
•Most series demonstrate a slight male
predominance
•No racial predilection
•The right and left eyes appear to be involved
equally
•Common systemic risks factors for retinal arterial
occlusive disease include
Hypertension,
Diabetes,
Lipid disorders,
Cardiac and systemic atherosclerotic disease

12. Mechanism of occlusion
• The principal mechanisms operative in occlusion of the retinal
arterial system are
• Embolic,
• Thrombotic,
• Vaso spastic,
• Extravascular compression,
• Vasculitic
• Other mechanisms such as radiation and elevated intraocular
pressure occur much less commonly

13. • More than one mechanism may occur
• An embolism to the retinal arterial circulation can originate as a
venous thrombosis reaching the arterial circulation via a right to left
cardiac shunt
• CRAO secondary to giant cell arteritis is primarily a vasculitic
phenomenon, with thrombosis being the ultimate occlusive event.

14. Atherosclerosis-related thrombosis
• Atherosclerosis-related thrombosis at the level of the lamina
cribrosa is by far the most common underlying cause of CRAO
• About 80%
• The incidence of atherosclerosis increases with age & is accelerated
by
• Hypertension,
• Hyperlipidaemia,
• Diabetes,
• Oral contraceptives and
• Hyperhomocysteinaemia
• Other risk factors include obesity, tobacco smoking and a sedentary
lifestyle

15. Carotid embolism
• Origin of emboli is most often from an atheromatous plaque at
carotid bifurcation and sometimes from aotic arch.

16. Types of emboli
• Emboli may be of following types:
• 1.Cholesterol emboli-hollenhorst plaques
•Intermittent showers of minute ,bright, refractile ,
golden to yellow-orange crystals,
•Often located at arteriolar bifurcation
•Rarely cause significant obstruction

18. Types of emboli
• 2.calcific emboli
• Single,non-scintillating often on or close to the disc
•They may be overlooked when present on the disc
•They are more dangerous because they may cause
permanent occlusion

20. Types of emboli
• 3.fibrin –platelet emboli:
•Dull grey, elongated particles, usually multiple
,occasionally fill the entire lumen
•They may cause a retinal transient ischaemic attack
and resultant amaurosis fugax
•Occasionally they may cause permanent
obstruction

22. Uncommon causes
• Giant cell arteritis
• Cardiac emboli
• Periarteritis: Dermatomyositis, SLE, PAN, Wegener granulomatosis,
Bechet syndrome
• Thrombophilic disorders: defects of natural anticoagulants,
antiphospholipid antibody syndrome, hyperhomocystenaemia
• Sickle cell disease
• Migrane (reflex vasospasm)
• Susac syndrome: triad of retinal artery occlusion, sensorineural
deafness and encephalopathy

23. Local conditions in the eye and orbit
•Peripapillary arterial loop
•Optic nerve head drusen
•Intraocular foreign body
•Elevated intraocular pressure secondary to angle-
closure glaucoma
•External compression of the ophthalmic artery or
central retinal artery caused by orbital cellulitis,
orbital hemorrhage, abscess formation, cavernous
sinus thrombosis, and neoplastic disease

24. BRAO in right eye secondary to prepapillary arterial loop

25. Inferior BRAO secondary to intraocular foreign body imbedded in
the retina with distal occlusion of the inferior temporal artery.
There is hemorrhage overlying the intraocular foreign body.

26. Histopathology
RAO
Reduced/no perfusion
Reduced glucose & O2 delivery
Ischaemia
Opacification of ganglion cell layer

27. •The opacification is most prominent in the macular
region where the multiple layers of ganglion cells
reside
•Retinal opacification generally decreases toward the
periphery as the ganglion cell population
diminishes, and is also absent from the avascular
zone of the foveola where ganglion cells are absent.
•The classic ‘cherry red spot’ is a result of the visible
red reflex of the perfused choroid at this location

28. CRAO
• Sudden ,profound, painless loss of vision
• VA : severely reduced except if a portion of papillomacular bundle is
supplied by cilioretinal artery ,where central vision is preserved
• Afferent pupillary defect
• Visual fields are depressed in the area of the ischemic retina
• The retina shows ischemic whitening
• the retinal arterials and veins manifest boxcarring
• Cherry red spot
• FFA: delay in arterial filling and masking of background choroidal
fluorescence by retinal swelling

30. Characteristics Findings on OCT
•Increase in inner layer reflectivity and
• Muted outer layer reflectivity around the
foveola
•With normal reflectivity of the retinal pigment
epithelium beneath the foveola

31. • OCT of CRAO demonstrating increased thickness in the inner retinal layers and
muted outer layer/retinal pigment epithelium reflectivity surrounding the
foveola.
• Note that there is normal reflectivity of the retinal pigment epithelium at the
foveola

32. Prognosis
• Poor due to retinal infarction
• After few days oedema disappears ,arteries remain attenuated .
• Inner layers of retina become atrophic.
• Optic atrophy,permanent loss of vision
• Rubeosis iridis may require PRP,NVD
• NVG

33. OPHTHALMIC ARTERY OCCLUSIONS
• Profound painless unilateral loss of vision
• Visual acuity ranges from CF to no PL
• An afferent pupillary defect
• Fundus picture is that of an acutely infarcted retina with extensive
retinal whitening
• Pallid swelling of the optic disk
• No cherry red spot
• Boxcarring or segmentation of the blood column of the retinal vessels
• FFA :- no or markedly delayed background choroidal flush and minimal
or delayed filling of the retinal vasculature

34. Chronic ophthalmic artery occlusion in right eye.
Pale disk and ischemic retinal arteries and veins.

35. • Visual recovery is rare in cases of ophthalmic artery occlusion.
• Electroretinographic testing can help differentiate ophthalmic artery
occlusions from CRAO
• In ophthalmic artery occlusions, both the B wave and A wave are
absent
• In CRAO with intact choroidal perfusion, the A wave is present.

36. BRANCH RETINAL ARTERY OCCLUSIONS
• Presentation : painless loss of visual field in the distribution of the
occluded artery
• Fundus: narrowing of arteries and veins with sludging and segmentation
of blood column.
• Cloudy white retina may not occur in nasal branch artery occlusions due
to the single layer of ganglion cells present there
• FFA:- delayed transit of the dye through the affected vessel, and often
retrograde filling of the vessel can be observed later in the angiogram

37. Inferior BRAO with calcific emboli at
inferior margin of the optic disk beneath
overlying vein.
Fluorescein angiogram of inferior BRAO
showing delayed perfusion of inferior retina
with retrograde filling of inferior retinal veins

38. RE fundus photo revealing whitening of the superior retina with a calcified plaque at the disc
within the supero temporal artery (arrow); (B) SDOCT revealed hyper-reflectivity and increased
thickness of the inner retinal layers in the superior compared to inferior retina, decreased
reflectivity of the outer retinal layers (including retinal pigment epithelial layer) in the superior
retina as compared to inferior retina probably due to optical shadowing

39. CILIORETINAL ARTERY OCCLUSIONS
• 35% of eyes and 50% of people have cilioretinal arteries
• Typical symptom pericentral scotomas, often subtle, in the
distribution of the artery
• APD are often not present
• Although any of the described mechanisms of occlusion may be
operational
• May occur in conjunction with central retinal venous occlusive
disease and anterior ischemic optic neuropathy

40. Cilioretinal artery occlusion. (A) Isolated; (B) combined with central retinal vein occlusion; (C)
combined with anterior ischaemic optic neuropathy; (D) FA shows hypofluorescence at the
macula due to lack of filling and masking by retinal swelling

41. Management
1. Management of the acute occlusive event in an attempt to restore
visual function
2. Workup of the patient looking for potential systemic conditions
requiring treatment
3. Management of the remote complications and sequelae of the
arterial occlusive event

42. Management of the acute occlusive event
• Digital ocular massage
• Simple treatment with low morbidity
• No statistical benefit has been noted
• Reduction of intraocular pressure through ocular antihypertensives
and paracentesis
• Which theoretically may also dislodge an embolus
• Have been attempted to improve retinal arterial circulation.
• Studies have shown no significant difference in final versus initial
visual outcomes in use of topical beta blockers, oral acetazolamide,
or paracentesis

43. • Medical vasodilatation utilizing sublingual nitroglycerin, calcium
channel blockers and pentoxifylline
• Used to improve the retinal arterial circulation.
• While results of one study found that the pentoxifylline group had
less neovascularization compared to standard treatment, there was
no definitive improvement in visual outcomes
• To date there are only anecdotes of effectively treating CRAO with
nitroglycerin

44. • Carbogen 95% oxygen and 5% carbon dioxide
• inhalation treatment that may cause dilation of retinal arterioles
• not shown benefit to final visual outcome and is generally no longer
used
• thrombolytic therapy
• There are case reports of thrombolytic therapy improving visual
recovery even when initiated more than 2 h after occlusion.
• However, less than 16% of CRAO cases are due to platelet fibrin
obstruction

45. • lack of clinical evidence of improved visual outcome
• potential for systemic complications, and inherent difficulty
establishing nonembolic etiology
• The decision to attempt fibrinolytic therapy using drugs like TPA
should be made carefully.
• in patients with CRAO, if giant cell arteritis is suspected by clinical and
laboratory parameters, high-dose steroid therapy should be initiated
while awaiting temporal artery biopsy

46. Surgical treatments
• Laser photo disruption of an embolus
• Vitrectomy with cannulation of the central retinal artery
• No randomized trial data have confirmed the efficacy of any of these
treatments.

47. Systemic workup
In up to 30% of patients, no systemic associated condition
leading to arterial occlusion is documented

48. Thank-you