A Review of Central Retinal Artery Occlusion
A Review of Central Retinal Artery Occlusion
The central retinal artery (CRA) is a branch of the ophthalmic artery (OA), which is the first branch of the internal carotid artery. The CRA supplies blood to the surface layer of the optic disc. From here it divides into two main branches (superior and inferior); these then further divide into temporal and nasal branches, which supply blood to the four quadrants of the retina. The outer retina is supplied by the choriocapillaris of the choroid that branches off the ciliary artery. Both of these must be functioning to maintain retinal function, as both CRA and ciliary artery originate from the OA.
One important variation to this is the presence of a cilioretinal artery. A study on 1000 consecutive patients, using fundus fluorescein angiography (FFA), found a cilioretinal artery to be present in 49.5% of patients. When present, it supplies the papillomacular bundle, which contains the maximum amount of photoreceptors essential for central vision. In these patients, the macula may still be perfused in acute CRAO. This means it is possible for good vision to be maintained. However, this does not always occur. A detailed study of 260 eyes with CRAO showed the presence of cilioretinal artery in 35 eyes. Of these, 60% had an initial VA of 6/30 or worse. Such poor results are due to the variability in size of the cilioretinal artery and the area it supplies. Therefore, CRAO infarcts will deprive retinal blood supply, reducing the thickness of the inner retinal layers. However, a cilioretinal artery, if present, will maintain the thickness of the retina to variable extents, depending on how much of the retina it supplies.
The exact location where CRAO occurs is debated. Anatomical studies show that the narrowest part of the CRA lumen is where it pierces the dural sheath of the optic nerve and not the lamina cribrosa, and that this was the most common location where CRAO occured (Figure 1). Embolism is the most common cause of CRAO, the major source of this being carotid artery disease, usually due to atherosclerotic plaques. Carotid stenosis and the heart are other important sources of emboli. In all, 74% of these emboli are shown to be made of cholesterol, 10.5% were calcific material, and 15.5% were fibrin. It is equally probable that an occlusive thrombus at the level immediately posterior to the lamina cribrosa also causes CRAO.
(Enlarge Image)
Figure 1.
Figure showing the narrowest part of the central retinal artery (common site for embolus), where it pierces the dural sheath of the optic nerve (arrowhead) and showing the site of an thrombus in the central retinal artery behind the lamina cribrosa (star). Abbreviations: PCA, posterior ciliary artery; CRA, central retinal artery; ON, optic nerve; dura, duramater; Pia, piamater (reproduced from [65]).
Once the CRA is occluded, the ability of the retina to recover depends on whether the offending embolus or thrombus is dislodged, and more importantly by the retinal ischaemic tolerance time. Conclusions from electrophysiological, histopathological, and morphometric studies showed that in old atherosclerotic hypertensive rhesus monkeys, no detectable damage was done with CRAO of 97 min. However, between 105 and 240 min there was a variable degree of partial retinal recovery seen on visual-evoked potential. A large degree of interindividual variability in regard to the relationship between the length of CRAO and the extent of retinal damage was found. At 240 min, complete or almost total optic nerve atrophy and nerve fibre damage resulting in massive irreversible retinal damage was found in all eyes. This suggests that the time window for intervention is finite and inversely proportional to the degree of recovery. The exact retinal tolerance time when irreversible damage occurs is not yet known, but would appear to be no longer than 4 h.
Anatomy and Pathophysiology
The central retinal artery (CRA) is a branch of the ophthalmic artery (OA), which is the first branch of the internal carotid artery. The CRA supplies blood to the surface layer of the optic disc. From here it divides into two main branches (superior and inferior); these then further divide into temporal and nasal branches, which supply blood to the four quadrants of the retina. The outer retina is supplied by the choriocapillaris of the choroid that branches off the ciliary artery. Both of these must be functioning to maintain retinal function, as both CRA and ciliary artery originate from the OA.
One important variation to this is the presence of a cilioretinal artery. A study on 1000 consecutive patients, using fundus fluorescein angiography (FFA), found a cilioretinal artery to be present in 49.5% of patients. When present, it supplies the papillomacular bundle, which contains the maximum amount of photoreceptors essential for central vision. In these patients, the macula may still be perfused in acute CRAO. This means it is possible for good vision to be maintained. However, this does not always occur. A detailed study of 260 eyes with CRAO showed the presence of cilioretinal artery in 35 eyes. Of these, 60% had an initial VA of 6/30 or worse. Such poor results are due to the variability in size of the cilioretinal artery and the area it supplies. Therefore, CRAO infarcts will deprive retinal blood supply, reducing the thickness of the inner retinal layers. However, a cilioretinal artery, if present, will maintain the thickness of the retina to variable extents, depending on how much of the retina it supplies.
The exact location where CRAO occurs is debated. Anatomical studies show that the narrowest part of the CRA lumen is where it pierces the dural sheath of the optic nerve and not the lamina cribrosa, and that this was the most common location where CRAO occured (Figure 1). Embolism is the most common cause of CRAO, the major source of this being carotid artery disease, usually due to atherosclerotic plaques. Carotid stenosis and the heart are other important sources of emboli. In all, 74% of these emboli are shown to be made of cholesterol, 10.5% were calcific material, and 15.5% were fibrin. It is equally probable that an occlusive thrombus at the level immediately posterior to the lamina cribrosa also causes CRAO.
(Enlarge Image)
Figure 1.
Figure showing the narrowest part of the central retinal artery (common site for embolus), where it pierces the dural sheath of the optic nerve (arrowhead) and showing the site of an thrombus in the central retinal artery behind the lamina cribrosa (star). Abbreviations: PCA, posterior ciliary artery; CRA, central retinal artery; ON, optic nerve; dura, duramater; Pia, piamater (reproduced from [65]).
Once the CRA is occluded, the ability of the retina to recover depends on whether the offending embolus or thrombus is dislodged, and more importantly by the retinal ischaemic tolerance time. Conclusions from electrophysiological, histopathological, and morphometric studies showed that in old atherosclerotic hypertensive rhesus monkeys, no detectable damage was done with CRAO of 97 min. However, between 105 and 240 min there was a variable degree of partial retinal recovery seen on visual-evoked potential. A large degree of interindividual variability in regard to the relationship between the length of CRAO and the extent of retinal damage was found. At 240 min, complete or almost total optic nerve atrophy and nerve fibre damage resulting in massive irreversible retinal damage was found in all eyes. This suggests that the time window for intervention is finite and inversely proportional to the degree of recovery. The exact retinal tolerance time when irreversible damage occurs is not yet known, but would appear to be no longer than 4 h.
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