The choroidal vasculature and choroidal neovascular membrane
Dr. Shashank Somani, Dr. Sarang Lambat, Dr Prabhat Nangia, Dr. Vinay Nangia
Suraj Eye Institute, 559, New Colony, Sadar, Nagpur- 440001.
A male, 59 years of age, came with a complaint of distortion of vision in right eye, along with a black spot since 6 months. He had a history of oral carcinoma for which he was on treatment. His best corrected visual acuity (BCVA) was 6/9 P, N10 in right eye (OD) and 6/9, N8 in left eye (OS). Anterior segment examination showed early cataract in both eyes. Intraocular pressure recorded by Goldmann applanation tonometer was 10 mm Hg in both eyes.
The patient was advised to undergo an intravitreal Anti-VEGF injection in the right eye. The patient underwent an intravitreal Brolucizumab injection for the right eye and was followed up after 2 weeks. The OCT findings in the right eye 2 weeks after injection are as below.
This case demonstrates the effect of anti-VEGF treatment on the choroidal structure in a patient with CNVM.
There is a high concentration of VEGF in the choriocapillaris layer. VEGF is known to play a physiologic role in the survival and maintenance of vascular endothelial cells and the choriocapillaris layer. It is also considered important for the maintenance of the choriocapillaris fenestrations. Studies in the literature  have attributed changes in the choroidal thickness with treatment to either reduced vascular hyper-permeability of the choroid or to the vasoconstrictive effect of anti-VEGF agents. The significant reduction in the CC/Sattler layer may be a result of reduced capillary permeability related to the shrinkage of choroidal neovascularization, which would indicate a positive treatment response.
Vascular hyperpermeability will only increase the thickness of the choriocapillaris but may or may not influence the outer choroidal layers. Another study also found a significant decrease in the sub-foveal choroidal thickness following anti-VEGF treatment in patients with PCV. 
In our patient of choroidal neovascularization, we assessed the response of the choroidal vasculature especially the larger choroidal vessels to Brolucizimab intravitreal injection. We found as has been mentioned previously in the literature that an anti-VEGF injection not only affects the CNVM but also influences the choroidal thickness. The choroid consists of the choriocapillaris, the Sattler’s layer, and the Haller’s layer. These vessels come from a continuation of the short and long posterior ciliary vessels through the sclera to form a part of the vascular network of the choroid. We found that following Brolucizimab injection, there was a reduction in the sub-foveal choroidal thickness from 255 to 232 microns (Fig. 3b and Fig. 5b yellow lines). When we followed up with the patient after 4 months, the sub-foveal choroidal thickness measurement was 320 microns, indicating a rebound effect (Fig. 6b, Fig. 7a). When we assessed the changes by especially measuring only the large choroidal vessels we found a similar decrease in the width (Fig. 3b and 5b) followed with a rebound effect after 4 months (Fig. 6b Green lines, and Fig. 7b)( Table 1 and Fig 8 and 9).
On OCT angiography (Fig. 7a), enface imaging shows the large Haller’s vessels measuring from 182 to 194 microns. While these measurements reflect a different dimension of the choroidal vessels, it is perhaps significant that we are now able to measure them.
It is obvious that the choroid responds not only to waning and waxing associated with the anti-VEGF therapy but also to the development of CNVM and to the regrowth of the CNVM after the effect of the anti-VEGF has decreased. The abnormal vasculature of the CNVM incites a response in the larger vessels, in this case, the posterior ciliary vessels which in some way via the choriocapillaris are linked to the CNVM. The exact implications of this finding in the etiopathogenesis of CNVM are difficult to understand. Does this have implications for the development of the feeder’s vessels? Does this influence the response of the CNVM to treatment? It is a possibility that assessing the enface images, maybe a way to identify changes in the vascular diameter, and perhaps it may serve as a biomarker for both a CNVM that occurs, recurs, and responds to treatment. It may be important to understand this phenomenon better. One may also need to study the impact on the remaining choroid away from the area of CNVM and how it may affect the health of the retina.
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- Kim HY, Lee B, Kang E, Oh J. Choroidal thickness profile and clinical outcomes in eyes with polypoidal choroidal vasculopathy. Graefe’s Archive for Clinical and Experimental Ophthalmology. https://doi.org/10.1007/s00417-020-05051-6
- Altunel O and Ozsaygili C. Assessent of Choriocapillaris/Sattler and Haller layer changes after intravitreal injection in eyes with neovascular age‐related macular degeneration: aflibercept vs ranibizumab. https://doi.org/10.1007/s10384-021-00894
- Borrelli E, Sarraf D, Freund B, and Sadda S. OCT angiography and evaluation of the choroid and choroidal vascular disorders. https://doi.org/10.1016/j.preteyeres.2018.07.002
Dr. Sarang Lambat
Suraj Eye Institute
Email – firstname.lastname@example.org
- Which of the following are considered to be layers of the choroid?
- Haller’s Layer
- Sattler’s Layer
- Ellipsoid Zone
- Interdigitation zone
2. About the Bruch’s membrane one or more of the following are true
- Bruch’s membrane is rich in collagen.
- Its thickness may vary from 2-4 microns
- Bruch’s membrane loss is associated with the development of CNVM
- It is never thrown into folds.
- It is always located 360 degrees at the margins of the clinical optic nerve.