Spark ImageWise 63

Multiple branch retinal artery occlusion and its aftermath

Dr. Shashank Somani, Dr. Sarang Lambat, Dr Prabhat Nangia, Dr. Vinay Nangia
Suraj Eye Institute, 559, New Colony, Sadar, Nagpur- 440001.

Case Description

A female, 59 years of age, came with a complaint of sudden diminution of vision in her left eye for the last 7 days. Her best corrected visual acuity (BCVA) was 6/6, N6 in the right eye (OD) and CF 1m, N36 in the left eye (OS). Anterior segment examination showed pseudophakia in the right eye and an early cataract in the left eye. Intraocular pressure recorded by the Goldmann applanation tonometer was 18 mm Hg in both eyes. She was a known case of diabetes mellitus and systemic hypertension for the last 16 years.

*Please enlarge the images for a better viewing experience.

Figure 1: Fundus photograph of the right eye shows the presence of a few drusen inferotemporal to the fovea (yellow arrow). Multiple cotton wool spots can be seen superiorly (blue arrows). There is a presence of RNFL defect in the inferotemporal quadrant (ITQ) (white arrows).  
Figure 2: Fundus photograph of the left eye shows the area of retinal infarct involving the superior half of the macula sparing the fovea (green arrows).
Figure 3: The optical coherence tomography line scan of the left eye passing through the fovea shows increased hyperreflectivity of inner retinal layers nasal to the fovea in the area of the lesion (green arrow). The inner retinal layers can still be distinguished as shown in the white box.
Figure 4b: Fundus photograph of LE shows a significant decrease and resolution of the area of cloudy swelling. (yellow arrow) as compared to the photograph in the initial presentation in fig 4a (green arrow). The patient underwent an intravitreal anti-VEGF bevacizumab injection on day 8 following the onset of symptoms.

Her visual acuity on day 21 after the first presentation was improved to 6/24, N18 in the Left eye.

Figure 5a and 5b: The optical coherence tomography vertical line scan of the left eye passing through the fovea on day 7 shows disorganization and increased hyperreflectivity of the inner layers of the retina in the area of the lesion (Fig 5b. green arrow). Increased thickness and hyperreflectivity can be seen in the outer plexiform layer (pink arrow). There is some increased reflectivity of the outer nuclear layer seen (Fig 5b, blue arrow). The total retinal thickness in the area of the lesion (orange arrow) is about 380um and the thickness between the internal limiting membrane and outer plexiform layer is about 277um.
Figure 5c and 5d: The optical coherence tomography vertical line scan of the left eye passing through the fovea at day 21 shows increased hyperreflectivity of inner retinal layers nasal to the fovea in the area of the lesion (Fig 5d green arrow). There is a decrease in the retinal thickness with atrophic changes in the outer retinal layers in the area of the lesion on day 21 (Fig 5d). The total retinal thickness at the same location on day 7 was 380um and on day 21 was (orange arrow)  243um and the thickness between the internal limiting membrane and outer plexiform layer on day 7 was 277um and on day 21 ( Fig 5d, orange arrow) was about 62um suggesting significant inner retinal layers atrophy.
The total retinal thickness in RE at the same relative location was 313um and the inner retinal layers thickness was 128um
Figure 6a: FFA of the right eye in late arteriovenous phase showing normal vascular architecture. A few microaneurysms can be seen in the macular area (blue arrow). We can appreciate the blocked fluorescence caused by the presence of multiple cotton wool spots in the superior area (pink arrows). 
Figure 6b: FFA of the left eye on day 7 in the late arteriovenous phase shows the area of nonperfusion suggestive of branch retinal artery occlusion in the macular area (yellow arrow). There is generalized reduced vascularity in the LE as compared to that of RE in fig 6a.
Figure 6d: FFA of the left eye on day 21 in the late arteriovenous phase shows a significant increase in the perfusion in the macular area. The vessels denoted by pink, blue, and green arrows in fig 6b are seen to be reperfused in fig 6d.
Figure 7a: OCTA of RE showing normal superficial capillary plexus.
Figure 7b: On Day 7, OCTA of LE. The superficial capillary plexus (SCP) shows significantly reduced vasculature and fragmented reflections from the vasculature in the area of the infarct (yellow arrow). 
We can also appreciate the increased size of the vessel reaching up to the macula suggestive of increased blood flow (green arrow vessel no. 3). 
Figure 7c: On day 21, OCTA of LE. The SCP shows an increase in the density of vessels in the area of the lesion (yellow arrow). The dilated vessel which was seen in the previous scan is seen to have reduced in width size (green arrow).
Figure 8a: OCTA of RE showing normal intermediate vascular plexus.
Figure 8b: OCTA of LE on Day 7. The intermediate vascular plexus (ICP) shows a large area of decreased vascular density in the area of the lesion (yellow arrow). 
Figure 8c: OCTA of LE on day 21. The ICP shows a significantly improved density of vessels in the area of the lesion (yellow arrow).
Figure 9a: OCTA of RE showing normal deep vascular plexus.
Figure 9b: OCTA of LE, day 7.  The deep vascular plexus (DCP) shows a large area of decreased vascular density in the area of the lesion (yellow arrow). 
Figure 9c: OCTA of LE, day 21. The DCP shows a mild improvement in the density of vessels in the area of the lesion (yellow arrow).


Branch retinal artery occlusion is the interruption of blood flow through a branch retinal artery by thromboembolism or vasospasm with or without retinal ischemia.

What we know as cloudy swelling is considered to be retinal cell death attributable to ischemia on the basis of pathological, imaging or other objective evidence of retinal focal ischemic injury in a defined vascular distribution or clinical evidence of retinal focal ischemic injury based on symptoms persisting > 24 hours or until death with other causes excluded. Retinal infarction/ clinical cloudy swelling does not manifest fluid spaces and may be largely intracellular. We have noticed previously that it presses on the blood vessels narrowing them further in patients with branch artery occlusion

Our patient underwent an intravitreal injection of bevacizumab. While there is no evidence that it may help in such a patient, the basis was the expectation that it may reduce the amount of swelling seen in the retinal layers in the area of infarct, thereby reducing the pressure and narrowing of the vessels, and allowing perhaps the vessels to not collapse and stay open to enable blood flow.  What follows is an image-based description of the retinal layers and the vasculature on Day 7 of symptoms, when our patient presented to us and on day 21 when she came for a follow-up.  

The Colour photo shows an area of occlusion (fig 2, yellow arrows). We could not make out any cilioretinal artery though the shape of the cloudy swelling may have suggested that that was the case. Three blood vessels marked (Fig 2, 4b)1, 2 and 3   show occlusion at different distances from their origin. On follow up there is a disappearance of cloudy swelling, but the macula takes on a darker shade compared to the unaffected eye (Fig 4b, yellow arrow). This is often an indication of superficial retinal layer loss and is also seen in the loss of RNFL and GCL in some other conditions. 

OCT shows the presence of swelling of the inner and middle retinal layers up to the outer plexiform layer (Fig 5b). The outer nuclear layer shows some loss of transparency and relative hyperreflectivity, especially in the region of the foveal pit.  The degree of swelling of the retina is mostly confined to the swelling of the inner and middle retinal layers and not so much the outer retinal layers (Fig 5b) Indicating that following branch retinal artery occlusion, the thickness of the outer retinal layers may not be affected significantly and also indicating relative preservation of the health of outer retinal layers including the photoreceptors, largely perhaps because these layers derive their nutrition from the choroid. 

The vision dropped abruptly to CF after the episode when on the 7th day she was examined for the first time. On the next visit, (day 21) the vision had recovered to 6/24. We do not have the baseline VA  prior to the occlusive episode, but from the history the vision in both eyes was good. While the foveal pit made up of largely the outer nuclear layer and the photoreceptor layers and the RPE-BM complex may have undergone some damage, it is difficult to appreciate and define the extent of the damage. The sudden deterioration of vision may be due to the sudden insult to the retinal layers and the recovery may be due to the pliability of the retinal layers to reorganise and recover from the insult and be able to transmit impulses to the optic disc and onward. On the OCT, the sub-foveal pit photoreceptor tissues do not appear to show any significant changes that would explain the recovery of vision.

The FFA in the first visit shows the closure of vessels especially in the area superior to the fovea. However, 2-3 weeks later the FFA shows the presence and partial recovery of circulation in the three vessels going towards the macula ( 1,2,3).  In the initial FFA, these vessels are dilated and in the follow-up visit all of these vessels appear to be narrow, however, the fluorescein dye goes further into the area, which was initially ischaemic, indicating recovery of  a degree of circulation in the ischaemic area and perhaps function also. 

On OCTA the superficial capillary plexus (SCP) located in the ganglion cell layer shows considerable reduction of the vasculature (Fig 7b) and in 7C there is increased visibility of the blood vessels in this area, indicating the return of blood flow. The Intermediate capillary plexus (ICP) which is located along the inner boundary of the inner nuclear layer bordering the inner plexiform layer shows a significant recovery from day 7 to day 21 (Fig 8b and 8c). The deep vascular plexus (DVP) located at the outer boundary of the inner nuclear layer bordering the outer plexiform layer shows a mild improvement in the detection of vessels (Fig 9c) on day 21. 

It is significant to see a return of circulation to some extent in all three layers, but especially in the intermediate capillary plexus and we may be liberal to think that there may be a flow of nutrients to more layers than just the junction of the inner nuclear and inner plexiform layer.  This finding is important and it does prove, that there is some return of functional circulation with a reasonably significant formation of the intermediate capillary plexus even as compared to the ICP of the RE ( Fig 8a). Theoretically one may rationalise, that it may have enabled the visual recovery to an extent. 

Our patient presented with a devastating complication resulting in significant visual loss. These situations are difficult to treat. Most suggested treatments do not result in significant improvement. In this situation, based on the rationale, that an antiVEGF would help to reduce the cloudy swelling, we gave an intravitreal injection of bevacizumab. It should not be construed from this case, that it was helpful since there is no incontrovertible evidence to say so. It may be that it helped in some way, but we may not be able to say that with certainty. The recovery that took place in the circulation as seen on the OCT is a little difficult to explain but it is known to occur. The Superficial vascular complex flows into the deep vascular complex in a linear fashion. Based on this simplistic thinking one might have assumed that with significant loss of the superficial capillary plexus,  there may not be a recovery of the intermediate or deep capillary plexus.   However, there may yet be many dynamics of the recovery of the retinal vascular plexus that we do not understand and are unable to explain. In spite of the considerable recovery of the intermediate capillary plexus, one may note the thinning and disorganisation of the inner retinal layers, including the inner nuclear and plexiform layers and the associated disorganisation. 

It is open to conjecture whether the return of the circulation has in some manner helped in the recovery of the vision. We may at least consider that it may have helped in preventing further deterioration and atrophy of the retinal layers. 

The patient underwent a cardiovascular evaluation, but there were no positive findings to explain this event. From the images, it is probable that in our patient there were multiple branch retinal artery occlusions, resulting from vasospasm causing retinal infarction. This may explain the vascular recovery.


  1. Scharf J, Freund KB, Sadda S, Sarraf D. Paracentral acute middle maculopathy and the organization of the retinal capillary plexuses. Progress in Retinal and Eye Research. 2021 Mar 1;81:100884.
  2. Mac Grory, B., Schrag, M., Biousse, V., Furie, K.L., Gerhard-Herman, M., Lavin, P.J., Sobrin, L., Tjoumakaris, S.I., Weyand, C.M., Yaghi, S. and American Heart Association Stroke Council; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Hypertension; and Council on Peripheral Vascular Disease, 2021. Management of central retinal artery occlusion: a scientific statement from the American Heart Association. Stroke52(6), pp.e282-e294. DOI: 10.1161/STR.0000000000000366

Dr Vinay Nangia
Department of Ophthalmology
Suraj eye Institute
Email –


1. Which of the following layers are affected in paracentral acute middle maculopathy?
A. Inner nuclear layer
B. Inner plexiform layer
C. Outer plexiform layer
D.  All of the above

2. Monocular vision loss in CRAO is more commonly due to – 
A. Vitreous hemorrhage
B. Retinal detachment
C. Ischemic optic neuropathy
D. Sub-retinal bleeding

3. Cherry red spot is seen in which of the following conditions? 
A. Central retinal artery occlusion
B. Tay Sachs disease
C. Niemmen Pick disease
D. All of the above

4. Vascular risk factors for CRAO are- 
A. Tobacco intake?
B. Hypertension
C. Hyperlipidemia
D. All of the above

5. The superficial capillary plexus is positioned in which of the retinal layer?
A. Ganglion cell layer
B. Inner plexiform layer
C. Outer plexiform layer
D. Outer nuclear layer

6. Conservative approaches to save vision in CRAO include – 
A. Topical intraocular pressure-lowering agents 
B. Anterior chamber paracentesis
C. Carbogen therapy (inhaling a 95% O2/5% CO2 mixture
D. Ocular massage
E. All of the above

7. Non-embolic causes of BRAO include vasospasm secondary to which of the following conditions?
A. Migraine
B. Cocaine abuse
C. Behcet’s disease
D. All of the above.  

8. Which of the following aspects of vision is affected by CRAO?
A. Central vision
B. Stereopsis
C. Visual field
D. Color vision
E. All of the above

9. Systemic risk factors for the development of BRAO are
A.  Hypertension, 
B. Carotid occlusive disease 
C. Coronary artery disease
D. Hypercholesterolemia
E. All of the above

10. Vascular secondary prevention after CRAO does not include – 
A. Lifestyle modifications
B. Antiplatelet therapy 
C. Regular check-ups with neurologist and ophthalmologist
D. Ocular massage


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