Vascular Occlusions

Presenters: Dr Adithi K Murthy

Dr Neha
Dr Hage Angku
Dr Mousumi Banerjee
Preceptor: Prof. Pradeep Venkatesh
 Retinal arteries vs veins-
A 1. Veins are darker in colour than arteries.
V
V
A 2. Arteries are thinner than adjacent
veins.
3. Central reflex is wider in arteries
than in comparably sized veins.
The diameter of retinal arterioles and venules
are measured 1-2 DD from the optic disc
edge.1

1.Hemminki V, Kähönen M, Tuomisto MT, Turjanmaa V, Uusitalo H. Determination of retinal blood vessel
diameters and arteriovenous ratios in systemic hypertension: comparison of different calculation formulae. Graefes
Arch Clin Exp Ophthalmol. 2007 Jan;245(1):8-17.
 Central Retinal Artery: Anatomy

• Arises from ophthalmic artery

• Runs below optic nerve, pierces dura and

arachnoid 1.25 cm behind the eyeball

• Runs with CRV in optic nerve and enters

eyeball through lamina cribrosa

• Circle of Zinn - small anastomosis between

pial vessels and vessels of sclera
• Cilioretinal artery : in 15-20% patients
supplies papillo-macular bundle
Central Retinal Artery: Anatomy

• Divides into superior and inferior papillary arteries

 nasal and temporal branch.

• The four arteries supply four quadrants of retina-

no overlap/ anastomosis.

• Veins- Larger and more central.

• Normal A:V ratio = 2:3.

Central Retinal Vein: Anatomy

• Union of tributaries of central retinal artery.

• Occasionally – two trunks present.

• CRV lies lateral to the artery in the optic

nerve.

• The vein pierces the dural sheath farther

from the eyeball than the artery.

• Drains into cavernous sinus or

superior ophthalmic vein.

 Retinal Artery Occlusion

Central Retinal Branch Retinal Cilio-retinal

Artery Occlusion Artery Occlusion Artery Occlusion

• CRAO more common than BRAO.

CRAO: Pathogenesis

EMBOLI
 Retinal Vein Occlusion

Central Retinal Vein occlusion Branch retinal vein occlusion

Hemi-Central Retinal Vein Tributary Vein
Occlusion Occlusion

• BRVO is the second most common cause of retinal vascular disease after diabetic retinopathy
• BRVO two to three times more common than CRVO.
 CRVO: Pathogenesis

1. Occlusion of the vein by external compression by

sclerotic adjacent structures

2. Occlusion by primary venous wall disease

(degenerative/ inflammatory)

3. Hemodynamic disturbances produced by a variety of

factors.
 NON- ISCHEMIC CRVO ISCHEMIC CRVO
• 80% • 20%
• Occlusion further back from retrolaminar region • Occlusion at Lamina cribrosa/ retrolaminar area
• Nocturnal hypotension converts partial thrombus to • Marked increase in venous pressure ( fewer
a complete thrombus collaterals)  Precipitous fall in perfusion pressure
• Gradual increase in size of thrombus leading to leading to retinal ischemia
complete occlusion • Return of arterial pressure to normal / hypertensive
• Further back the occlusion- milder retinopathy  rupture of weakened capillaries
(collaterals) extensive hemorrhages
 HCRVO- Hemi central retinal vein occlusion

• Embryologically two trunks exist,

one usually disappears before birth.

• 20% - two trunks persist.

• Similar mechanism as CRVO.

• Occurs in superior or inferior trunk of central

retinal vein.
BRVO: Pathogenesis
• Site of occlusion- AV crossing

• Most common site: Supero-temporal (larger number of AV crossings).

• Risk factors:

• Age: most important - >50% occur in > 65 years

• Hypertension

• Hyperlipidemia

• Diabetes mellitus

• Oral contraceptives
 RISK FACTORS

WITHIN THE VESSEL

OUTSIDE THE VESSEL IN THE VESSEL WALL
WALL

• AGE
• BEHCET’S • MYELOPROLIFERATIVE
• ARTERIOSCLEROSIS DISORDERS
• SARCOIDOSIS
• HYPERTENSION • INHERITED AND
• WEGENERS ACQUIRED
• GLAUCOMA GRANULOMATOSIS HYPERCOAGULABLE
• GOOD PASTURE STATES
SYNDROME