Introduction
Pathophysiology:
- Primarily due to 2 key processes
- The first is atherosclerosis
- Process by which plaques form inside arteries, causing a focal narrowing of the vascular lumen
- Arthritic plaques generally contain lipid-containing foam cells and smooth muscle cells, covered by a cap of connective tissue
- This begins to prolliferate and multiply, creating a focal limitation of lumen size, limiting BF
- Occlusion forms when embolisms become stuck
- Subtype of arteriosclerosis
- Typically, CRAO has a sudden and profound painless loss of vision
The second is embolism:
- This is a term used to describe a detached mass that travels throughout the vasculature, and is carried by the normal systemic circulation. Isn't a thrombus, since it moves
Occlusion Sites:
- 58% occur just at the point where the central retinal artery pierces the ON sheath. This point is most narrow and thus most vulnerable
- Surprisingly more common than branch artery occlusion.
Dead Giveaways
Acute
Branch RAO
The result of atherosclerosis and or emboli that travels through the circulatory system and becoming stuck at a part where the arterial lumen narrows.
This usually occurs at the point in which the CRA pierces the dura mater.
An arterial occlusion blocks oxygenated blood to affected area of the retina, causing ischaemia and lack of perfusion
May be preceded by amaurosis fugax. Becomes sudden and severe if not relieved within a few hours. Can impact VF as well
Appears white and opaque due to retinal ischaemia. Note the relative attenutation of retinal arteries in the affected superior region Another feature is the box-car/cattle-truck vessel:
The segmenting of the arteries is referred to as box-carring or cattle-trucking In OCT:
Ischaemia is shown at the parts where the retinal layers are less discernible Retinal changes occur due to the loss of blood supply
Central RAO
If a blockage occurs at the point in which the CRA crosses the dura mater and it is not cleared within 90 minutes, unilateral CRAO will occur
Causes oedema of the inner retinal layers as well as death of GCL. In the chronic phase, loss of retina and retinal transparency occurs, along with thinning of the inner retinal layers
There is widespread whitening as well as a cherry red fovea, which is a classical feature of CRAO RNFL is typically swollen in this stage
50% of Px will have a cilioretinal artery. This allows for a better prognosis due to partial sparing
Cilioretinal artery supplies the papillomacular bundles, leading to a relative hypo-reflectivity
Chronic
Ischaemia triggers VEGF and neovascularisation, but is very rare as the dead retina cannot produce VEGF.
Typically no neovascularisations.
They also cannot generate collateral vessels
The RNFL will drastically thin
Shown on the left, there is RNFL thinning
diagnostic features
Embolus:
Three major embolus exists:
Hollenhorst Plaques
Yellow orange in colour, and usually found at the bifurcation of the arteries.
Consists of cholesterol and are often asymptomatic
Calcium Emboli
Second type and less common
Much whiter in appearance and often found near or at the optic disc
This makes them more dangerous, as they are likely to occlude larger retinal vessels
Fibrin Platelet
Dull green colour, often elongated. Can lead to amaurosis fugax
CRAO
In acute CRAO, the blockage will lead to RAPD being present
As a rule of thumb, unless treated within 90 minutes, prognosis is poor
After 240 minutes, total ON atrophy and nerve fibre damage occurs. This is irreversible