Anti-VEGF in myopic CNVM.
Dr. Ravi Daberao, Dr. Sarang Lambat , Dr. Prabhat Nangia, Dr. Vinay Nangia.
Suraj Eye Institute, 559, New Colony, Sadar, Nagpur- 440001.
A female, 33 years of age came to our hospital for the blurring of vision in the left eye since one month which was insidious in onset, gradual and progressive not associated with pain. There was no history of any systemic disease. On examination, her best-corrected visual acuity (BCVA) was 6/60 in both eyes with -14.00 DS. The anterior segment of both eyes was normal. The intraocular pressure of both eyes was 14 mmHg.
She was diagnosed to have high myopia in both eyes and left eye myopic CNVM. Intra-vitreal anti VEGF was given in her left eye. At one month follow up, her BCVA of left eye improved to 6/12p.
Our patient presented with classical features of a myopic CNVM. Figure 6 b shows a possible area of Bruch’s membrane break connecting the CNVM with the choroid (black arrow). It also shows the presence of possible communication of the short posterior ciliary arteries with the choroid and CNVM (yellow arrow). She was advised injections of anti-VEGF on PRN basis. The patient had a good response to a single injection of anti-VEGF (Fig. 5b). She was advised one more injection for further control of CNVM but the patient did not take the 2nd dose. One of the possible reasons for such a response may be that the choroid is significantly thinned out in myopic patients, due to which it may have difficulty in sustaining the CNVM for a longer duration. This may also explain the many Fuchs spots that are seen in myopic patients that represent a scarred CNVM that may have been active at some stage and has now auto regressed without any treatment and is associated with Bruchs membrane defects and surrounded by a classical area of atrophy. It is also important to consider that once there is a development of a CNVM in the macula there is a likelihood that in subjects with high myopia there may be a high possibility of this becoming a Fuchs spot, with the attendant risk of a surrounding area of myopic retinal atrophy which does not augur well for the central vision of such a patient. She was seen 10 months later and OCT showed a good foveal architecture with minimal subfoveal scarring (Fig. 6b). It may be concluded that it may not always be necessary to continue to give injections like in other non-myopic patients but a long-term follow-up is essential to detect recurrence of a CNVM.
Choroidal neovascularization (CNV) secondary to pathological myopia is one of the main causes of vision-threatening conditions in young and middle-aged patients. 5%-10% of patients with pathological myopia develop CNV. Myopic CNV is classified as type 2 CNV (located between the neurosensory retina and RPE). It is typically seen as a small greyish membrane lesion with hyperpigmented borders. Symptoms of CNV are decreased vision, central scotoma, and metamorphopsia. Diagnosis is done through fundus fluorescein angiography (FFA) and optical coherence tomography (OCT). FFA shows well-defined hyper fluorescence in an early phase and leaking in the late phase. Various treatment modalities were in existence for the treatment of myopic CNV including argon laser photocoagulation, transpupillary thermotherapy, photodynamic therapy with verteporfin, and sub-macular surgery. Currently, intravitreal injection of anti-VEGF is the safest option and it has shown promising results in the management of myopic CNV.
The prevalence of pathological myopia and associated CNV are increasing in recent times. FFA and SD-OCT should be performed to aid differential diagnosis and avoid unnecessary treatment. Especially the presence of coin-shaped hemorrhage which is a common finding in the myopic eye and does not require treatment. Classic CNV located above RPE cell layer (type 2) is better visualized by OCT. OCT has a sensitivity of 97% in detecting myopic CNV as compared with FFA. In all patients with category 3 and 4 myopic maculopathy it is essential to do a cube scan to rule out clinical and subclinical CNVM. In this case, we have shown that the use of VEGF inhibitors demonstrated significant improvement in vision. We are still unable to stop the progression of chorioretinal and RPE deterioration and the appearance of lacquer cracks which are involved in CNV and vision loss. It is more responsive and less recurrent than age-related macular degeneration. Since we are treating one modality of neovascularization, we are still facing problems like nonresponsiveness and complications resulting from injection procedure including retinal detachment and endophthalmitis.
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Dr. Sarang Lambat
Suraj Eye Institute
Email – firstname.lastname@example.org