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I was interested to read the article by Garcia-Arumi and colleagues
on "Surgical embolus removal in retinal artery occlusion". The authors
claim that "Surgical removal of retinal arterial emboli seems to be an
effective and safe treatment for RAO (retinal artery occlusion)".
Briefly, the study was based on 6 eyes with temporal branch retinal
artery occlusion (BRAO) and one with central re...
Briefly, the study was based on 6 eyes with temporal branch retinal
artery occlusion (BRAO) and one with central retinal artery occlusion
(CRAO). The surgery was performed in BRAO eyes 4, 12, 19, 22, 28, and 33
hours after onset and in CRAO eye 29 hours after visual loss. The first
post-operative evaluation, 48 hours after surgery, showed reperfusion of
the occluded branch retinal artery in 4 and none in one; in the
no evaluation was possible for 2 weeks because of vitreous hemorrhage.
the 6 eyes with BRAO, pre-operative visual acuity was: hand motion,
counting fingers, 20/400, 20/200, 20/200 and 20/25, at 48 hours it was
20/200, 20/100, 20/100, 20/200, 20/100 and 20/30 respectively, and final
visual acuity was 20/50, 20/30, 20/80, 20/200, 20/25 and 20/25
respectively; in the CRAO eye, visual acuity remained hand motion all
It is worth noting, initially, that a conclusion based on 6 eyes is
limited. However, the matter of
apparent improvement in visual acuity claimed by the authors deserves
1. All 6 of the eyes had temporal BRAO. In the vast majority of
temporal BRAO eyes the border between the ischemic and non-ischemic
passes through the fovea, as their figures 2 and 3 show. Also the
fluorescein angiogram in Figure 2 shows a patent cilioretinal artery.
These are extremely important facts in determining whether the visual
improvement noted was result of removal of the embolus or simply the
natural history of the disease. Having studied the natural history of
200 BRAO eyes, I recently stated: "In cilioretinal artery occlusion,
branch retinal artery occlusion and CRAO with cilioretinal artery
the junction between the infarcted and normal retina may often pass
through the fovea. In many of these eyes, I have seen marked spontaneous
visual acuity improvement occurring within several days or weeks, from
almost 20/200 or worse to even normal. This spontaneous improvement is
often erroneously attributed to an advocated treatment."
When the junction between the normal and infarcted retina passes
through the fovea, in such eyes, the retinal edema associated with
infarction most probably also involves to some extent the adjacent
foveal retina shortly after the occlusion; over the following weeks the
normal foveal retina recovers spontaneously, resulting in natural visual
improvement. In the series of Garcia-Arumi and colleagues a significant
visual improvement at final visit seen in 4 of 6 eyes is not uncommon in
such eyes, as a part of the natural history in my experience. Moreover,
the eye in figure 2, not only had the junction between the normal and
infracted retinal passing through the fovea but also had patent
cilioretinal artery, which is an important factor in natural visual
improvement not only in BRAO but also in CRAO.
2. Having studied more than 450 patients with BRAO and CRAO, I have
found another common confounding factor involving visual acuity testing.
At the initial visit, because of sudden visual loss, the patient is
emotionally upset, and tends to test poorly; for instance a patient with
only temporal BRAO with the border between the ischemic and normal
passing through fovea should not have hand motion or even 20/400 visual
acuity, if tested properly because the other half of the macula and
is still functioning normally. Moreover, later on it is not unusual to
find patients with central scotoma learning to fixate eccentrically and
show better visual acuity, which may erroneously be interpreted as
improvement. In my studies on various ocular vascular occlusive diseases
have found that unless improvement in visual acuity corresponds with
improvement in central scotoma, it is not a genuine improvement but due
3. Since visual acuity testing assesses only the function of the
fovea and not of the entire involved retina, visual fields, particularly
with a Goldmann perimeter, give us much better information about the
extent of visual loss and change. In my study, every eye with BRAO had
visual fields plotted with a Goldmann perimeter; that showed that the
visual fields of BRAO eyes often did show reduction in size of the
field defect as a part of the natural history. Garcia-Arumi and
state that they recorded the visual fields with Humphrey perimeter but
give no information on the visual fields of their cases. Moreover,
the Goldmann perimeter, Humphrey perimeter provides information about
the central 240 - 300 and not the entire involved retina.
4. In the series of Garcia-Arumi and colleagues, 6 of 7 eyes had
acute retinal ischemia for 12 to 33 hours and in one for 4 hours. We
evaluated the retinal tolerance time to acute ischemia experimentally in
rhesus monkeys and found that in CRAO, ischemic retina can recover
function from acute ischemia of 97 minutes, but after that the longer
ischemia, the more extensive the irreversible damage so that acute
ischemia lasting for 240 minutes results in massive irreversible retinal
damage. Therefore, it does not seem logical that restoration of
circulation in BRAO 4 to 33 hours after the occlusion would restore
function in an already irreversibly damaged retina. Moreover, they found
restoration of circulation in 4 of the 6 eyes on fluorescein angiography
first done 48 hours after the surgery. They argue that "in branch RAO
because some degree of perfusion at the macular area may be supplied by
the contralateral temporal artery."  This may be true, but it may also
another factor in the spontaneous marked visual recovery in such eyes as
part of natural history.
In conclusion, based on my studies on the natural history in BRAO
eyes, I feel the visual acuity improvement attributed by Garcia-Arumi
colleagues to embolectomy simply represents natural history.
1. Garcia-Arumi J, Martinez-Castillo V, Boixadera A, et al.
embolus removal in retinal artery occlusion. Br J Ophthalmol
2. Hayreh SS. Prevalent misconceptions about acute retinal vascular
occlusive disorders. Prog Retin Eye Res 2005;24:493-519.
3. Hayreh SS, Zimmerman B. Central Retinal Artery Occlusion: Visual
Outcome. Am J Ophthalmol 2005;140:376-91.
4. Hayreh SS, Zimmerman B, Kardon RH. Visual improvement with
corticosteroid therapy in giant cell arteritis. Acta Ophthalmol Scand
5. Hayreh SS, Zimmerman MB, Kimura A, et al. Central retinal
occlusion. Retinal survival time. Exp Eye Res 2004;78:723-36.
Sohan Singh Hayreh, MD, PhD, DSc, FRCS, FRCOphth
Professor Emeritus of Ophthalmology & Director Ocular Vascular