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Optic Coherence Tomography Angiography Findings of Bilateral Choroidal Neovascularization Associated with Optic Disc Drusen Treated with Intravitreal Aflibercept Injection.

1. Introduction

Optic disc drusen (ODD) are calcified hyaline-like deposits in the optic nerve head that are mainly located in front of the lamina cribrosa. They are often bilateral (67%-91%), and their incidence is 0.4%-20.4% in general population while there is female preponderance in their prevalence. They are usually benign and vision sparing; however, they may rarely complicate with visual field defects, haemorrhages, choroidal neovascularization (CNV), serous maculopathy, vascular occlusion, and nonarteritic ischemic optic neuropathy (NAION) [1].

Various imaging methods have been used in order to detect ODD accurately and reliably, which include ultrasonography (USG), enhanced depth imaging-OCT (EDIOCT), fluorescein fundus angiography (FFA), and fundus autofluorescence (FAF), and the newest application is optical coherence tomography angiography (OCTA, Optovue, Inc., Fremont, CA, USA) [2].

Noninvasive imaging of the retina, choroidal, and disc microvasculature is now possible with OCTA and without the use of exogenous intravenous dye injection. It can provide information for the evaluation of both structure and blood flow. It particularly allows the assessment of CNV morphology and features activity as well as the timing of and response to anti-VEGF treatment of CNV [3, 4]. It has been increasingly used for the diagnosis and imaging of paediatric retinal vascular disease and especially CNV as it is both reliable and noninvasive [5].

The OCTA studies in the literature mainly focus on microvascular changes associated with optic disc drusen. To the best of our knowledge, only Ong et al. demonstrated inactivate CNV associated with ODD in 1 case with OCTA in a series of 8 paediatric patients with CNV. However, this is the first time to report an interesting change in CNV after injection and long-term follow-up findings.

2. Case Report

A 14-year-old girl was referred to us with complaints of visual loss and metamorphopsia in both eyes that had persisted for 1 week. Her best-corrected visual acuity (BCVA) was 20/32 in the right eye and 20/25 in the left eye. Her ocular and systemic history was unremarkable. Her intraocular pressure and anterior segment examination were normal. Dilated fundus examination revealed elevated optic discs with blurred margins in both eyes. In addition, slightly elevated yellow lesion extending from optic nerve head to the macula was observed bilaterally (Figures 1(a) and 1(d)). The patient underwent imaging with colour fundus photography, FAF, FFA, spectral-domain optic coherence tomography (SD-OCT, Cirrus HD OCT 5000, Carl Zeiss Meditec Inc., Dublin, CA, USA), OCTA, orbital USG, and computed tomography (CT). FAF showed bilateral aspect of white refractile and hyperautofluorescence bodies on the surface of the optic nerve linked with the drusen and a hypoautofluorescent and hyperautofluorescent lesion in the papillomacular region (Figures 1(b) and 1(e)). FFA showed no hyperfluorescence or leakage with blurred borders of the optic disc, and early hyperfluorescence and intense leakage that might be associated with CNV were observed in both eyes with the right eye predominance (Figures 1(c) and 1(f )). The peripheral retina was normal. B-mode USG showed hyperechogenic appearance, and orbital CT revealed papilla as bright spots which might be associated with optic disc drusen (Figure 1(g)). SD-OCT showed retinal thickening, subretinal hyperreflectivity in the papillomacular region bilaterally, and subfoveal fluid in the right eye (Figures 1(h) and 1(i)). Furthermore, macular and retinal nerve fiber layer (RNFL) thickness measurements were recorded (Table 1).

OCTA revealed superficial and deep capillary density, foveal avascular zone, flow, and en face images in the macula (Table 2). A large circular CNV complex with main trunk, multiple dense thin capillaries branching from the main trunk in a tree-like manner, and frequent anastomoses was observed in the papillomacular region of the right eye in the outer retina and choriocapillaris cross-sections (Figures 2(a) and 2(b)). In the left eye, CNV with main trunk, minimal vessel loops, and capillaries was observed, which was considered as slightly activated (Figures 2(c) and 2(d)). Moreover, radial papillary capillary density was measured with OCTA (Table 2). Density was lower in the areas associated with nasal quadrant compared to the other quadrants.

All evaluations suggested CNV secondary to ODD, and intravitreal aflibercept was injected in 3 doses to the right eye and a single dose to the left eye. Three doses were injected to the right eye every other month. After the first injection, BCVA remained as 20/32 and increased to 20/25 after the second one. After the third dose of injection to the right eye and the first one to the left eye, BCVA was 20/20 in both eyes. After the injections in both eyes, SDOCT revealed RPE irregularity in the temporal region of the optic disc and complete regression of the subretinal fluid. OCTA interestingly showed that the entire CNV compete including the main trunk disappeared (Figures 3(a) to 3(d)). CNV complex was not observed with OCTA, and no significant change was observed in the peripapillary and macular vascular density measurements, and findings which might be correlated with RNFL measurements were not detected in 1-year follow-up. BCVA was preserved, and no additional injections were needed.

3. Discussion

CNV associated with ODD is a very rare complication, which has been reported in both adults and children [6]. In most of the patients, CNV membranes associated with ODD occur nasally; however, they may also occur temporally resulting in serous haemorrhagic maculopathy, cystoid macular edema, and macular scarring [7]. Its pathogenesis is unknown. Possible mechanisms involved in this complication include the compressive effect of drusen on the surrounding blood vessels, which leads to mechanical impairment of peripapillary vascular integrity, vascular congestion, or ischemia. Retinal ischemia and the release of VEGF may be the factors that trigger the development of CNV [8, 9]. Treatment must be provided if vision is jeopardized. The modern antivascular endothelial growth factor (VEGF) medications, photodynamic therapy, and surgical removal have each been demonstrated to be successful [10]. Anti-VEGF agents have been increasingly preferred as the first-line treatment because they ensure high visual acuity and disease stabilization usually with fewer intravitreal injections especially in paediatric cases, and recurrence is almost never observed. Gan and Long reported complete resolution after 3 doses of injection in cases for whom aflibercept was injected for the first time [11]. Knape et al. reported rapid and atraumatic resolution with the combination of bevacizumab and focal laser photocoagulation [12]. Alkin et al. emphasized that CNV secondary to ODD might be more sensitive than CNV secondary to age-related macular degeneration (AMD) in cases injected with a single dose of ranibizumab [13]. We achieved rapid response and did not observe recurrence in cases injected with 3 doses of aflibercept in the right eye and a single dose of aflibercept in the left eye and whom we followed for 12 months with OCTA.

4 different CNV patterns associated with exudative agerelated macular degeneration can be detected with OCTA: Medusa pattern: central feeder vessel, circular peripheral anastomosis, thin branches, and hypointense halo; seafan pattern: eccentric feeder vessel, thin branches, and hypointense halo; indistinct network pattern: thin branches and hypointense halo; and pruned vascular tree pattern: persis tence of main vascular trunks [14]. Pruned vascular tree pattern is considered as inactivate and usually followed up. The morphology of CNV and structural response to anti-VEGF treatment are strongly correlated. Anti-VEGF is ineffective for the vascular trunk while it is effective for especially the newly formed capillaries from preexisting vascular trunks while there is a correlation between better functional outcomes an increased vascularity of the CNV [15]. Spaide demonstrates reprofileration 20-50 days after the injection [16]. However, long-term inactivation can be ensured with fewer anti-VEGF injections in cases of CNV associated with high myopia, punctate inner choroidopathy (PIC), choroidal osteoma, optic nerve drusen like our patient, and idiopathic with lower activity than AMD [17-20]. The literature does not contain wide range of data which can be used to assess why stabilization can be achieved with fewer injections and make comparisons with CNV patterns of AMD with OCTA as highlighted above and assess reproliferation.

The most striking finding after injection in our case was the absence of CNV visualization in OCTA. The absence of CNV visualization in OCTA was associated with clinical and SD-OCT exudative inactivity [14]. In fact, inactive lesions are visualized as pruned vascular tree pattern, presence of large linear vessel with no or minimal anastomosis in OCTA. This may be due to other reasons such as the masking effect generated by a high PED, media opacities, or the presence of haemorrhages [21]. However, they were not observed in the follow-up of our patient. Hua and Ning demonstrated the development of atrophy in the CNV complex after 3 doses of anti-VEGF injections in PIC cases with high myopia and round dark region visualization due to no-perfusion/hypopefusion zone in the choriocapillaris [22]. This situation which was also observed in our case can be interpreted as decreased signal due to inactivity, but the absence of pruned vascular tree pattern may at least contribute to explaining why atrophy/shrinkage can develop in the main vascular trunk and why non-AMD CNV causes are more benign and can be stabilized longer with fewer injections.

In the literature, only Ong et al. demonstrated inactive CNV associated with ODD in 1 case with OCTA in a series of 8 paediatric patients with CNV. A 12-year-old female patient first underwent injection and photodynamic therapy in the left eye; however, OCTA revealed two large calibre vessels and a lack of fine capillaries, anastomoses, and vessel loops, which was considered as inactive sub-RPE CNV lesion [23]. This is the first paper to report a case with an interesting change in CNV visualization after injection and followed up for a long term for both CNV and vascular density. On the other hand, studies on OCTA for ODD mainly focus on microvascular changes. Bicer and Atilla showed that macular vascular density located in different regions decreased both at the superficial and deep capillary layer in cases with bilateral ODD, and there was a density loss in the peripapillary area especially the nasal region. They reported that ODD findings could be used to demonstrate that enlarged ODD might cause acute or chronic ischemia by compressing nerve fibers or surrounding vessel [24]. Aghdam et al. compared patients with ODD, NAION, and normal individuals and reported that optic nerve head vessel density was lower in the NAION group than in the other groups [25]. Cennamo et al. reported that flow rate measurements were correlated with ganglion cell layer thickness and OCTA examination can be an early marker to show the axonal damage in patients with ODD [26]. Similarly, Engelke et al. demonstrated the correlation between vascular density and RNFL and ganglion cell complex (GCC) and peripapillary capillary density loss compared to the normal group [27]. In our case, however, peripapillary capillary density evaluation revealed that the vascular density in the nasal quadrants was lower than those in the other quadrants, which was an interesting finding. However, changes that might be correlated in both RNFL and disc and macular vascular density measurements were not detected contrary to the abovementioned reports.

In conclusion, it is possible to evaluate vascular density, presence of associated CNV, and response to injection with OCTA in patients with optic nerve diseases such as ODD. Nonetheless, there is a need for further studies to confirm the changes in CNV visualization like in our case with OCTA that has been increasingly used.

https://doi.org/10.1155/2020/8398054

Disclosure

The authors have no proprietary or commercial interest in any materials discussed in this article.

Conflicts of Interest

The authors declare that they have no conflict of interest. Authors' Contributions

Melih Akidan, Mehmet Bulut, and Lutfiye Yaprak did the surgical and medical practice. Melih Akidan, Mehmet Bulut, Lutfiye Yaprak, and Elcin Suren developed the concept. Melih Akidan, Mehmet Bulut, Muhammet Kazim Erol, and Elcin Suren designed the study. Melih Akidan, Mehmet Bulut, Lutfiye Yaprak, and Muhammet Kazim Erol are responsible for the data collection or processing. Melih Akidan, Mehmet Bulut, Lutfiye Yaprak, and Elcin Suren analyzed and interpreted the data. Melih Akidan, Mehmet Bulut, and Muhammet Kazim Erol performed the literature search. Melih Akidan, Mehmet Bulut, Lutfiye Yaprak, Muhammet Kazim Erol, and Elcin Suren wrote the manuscript.

References

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[13] Z. Alkin, A. Ozkaya, I. Yilmaz, and A. T. Yazici, "A single injection of intravitreal ranibizumab in the treatment of choroidal neovascularisation secondary to optic nerve head drusen in a child," Case Reports, vol. 2014, 2014.

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[15] Y. Ichiyama, T. Sawada, Y. Ito, M. Kakinoki, and M. Ohji, "Optical coherence tomography angiography reveals blood flow in choroidal neovascular membrane in remission phase of neovascular age-related macular degeneration," Retina, vol. 37, no. 4, pp. 724-730, 2017.

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[19] Q. Chen, X. Yu, Z. Sun, and H. Dai, "The application of OCTA in assessment of anti-VEGF therapy for idiopathic choroidal neovascularization," Journal ofOphthalmology, vol. 2016, Article ID 5608250, 8 pages, 2016.

[20] J. T. Szelog, M. A. Bonini Filho, D. R. Lally, T. E. de Carlo, and J. S. Duker, "Optical coherence tomography angiography for detecting choroidal neovascularization secondary to choroidal osteoma," Ophthalmic Surgery, Lasers and Imaging Retina, vol. 47, no. 1, pp. 69-72, 2016.

[21] R. F. Spaide, J. G. Fujimoto, and N. K. Waheed, "Image artifacts in optical coherence tomography angiography," Retina, vol. 35, no. 11, pp. 2163-2180, 2015.

[22] R. Hua and H. Ning, "Using optical coherence tomography angiography to guide the treatment of pathological myopic patients with submacular haemorrhage," Photodiagnosis and Photodynamic Therapy, vol. 28, pp. 105-109, 2019.

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[25] K. A. Aghdam, M. A. Khorasani, M. S. Sanjari et al., "Optical coherence tomography angiography features of optic nerve head drusen and nonarteritic anterior ischemic optic neuropathy," Canadian Journal of Ophthalmology, vol. 54, no. 4, pp. 495-500, 2019.

[26] G. Cennamo, S. Tebaldi, F. Amoroso, D. Arvanitis, M. Breve, and G. Cennamo, "Optical coherence tomography angiography in optic nerve drusen," Ophthalmic Research, vol. 59, no. 2, pp. 76-80, 2018.

[27] H. Engelke, M. Shajari, J. Riedel, N. Mohr, S. G. Priglinger, and M. J. Mackert, "OCT angiography in optic disc drusen: comparison with structural and functional parameters," British Journal Ophthalmology, 2019.

Melih Akidan [ID]. (1) Mehmet Bulut [ID], (2) Lutfiye Yaprak, (2) Muhammet Kazim Erol [ID], (2) and Elcin Suren (2)

(1) Department of Ophthalmology, Antalya Kepez State Hospital, Antalya, Turkey

(2) Department of Ophtalmology, Antalya Education and Research Hospital, Antalya, Turkey

Correspondence should be addressed to Melih Akidan; melcihhh@yahoo.com

Received 10 December 2019; Accepted 20 February 2020; Published 10 March 2020

Academic Editor: Alexander A. Bialasiewicz

Caption: Figure 1: On the first day. (a and d) Fundus image of the right and left eyes; elevated optic disc with blurred margin and slightly elevated yellow lesion extending from optic nerve head to the macula. (b and e) FAF image of the right and left eyes; hyperautofluorescence bodies on the surface of the optic nerve linked with the drusen and hyperautofluorescent lesion in the papillomacular region. (c and f) FFA image of the right and left eyes; hyperfluorescence and intense leakage that might be associated with CNV. (g) Orbital CT image of the right and left eyes; bright spot on papilla associated with optic disc drusen. (h) SD-OCT image of the right eye; retinal thickening, subretinal hyperreflectivity, and subfoveal fluid in the papillomacular region. (i) SD-OCT image of the left eye; retinal thickening and subretinal hyperreflectivity in the papillomacular region.

Caption: Figure 2: On the first day. (a) Unified and coloured OCTA image of the right eye; circular CNV complex with main trunk, multiple dense thin capillaries branching from the main trunk and frequent anastomoses (yellow). (b) Outer retina cross-section and en face OCTA image of the right eye. (c) Unified and coloured OCTA image of the left eye; CNV with main trunk, minimal vessel loops, and capillaries (yellow). (d) Outer retina cross-section and en face OCTA image of the left eye.

Caption: Figure 3: At 3 months. (a and b) Outer retina, choriocapillaris cross-sections, and en face OCTA image of the right eye; CNV complex including the main trunk disappearance. (c and d) Outer retina, choriocapillaris cross-sections, and en face OCTA image of the left eye; entire CNV compete of including the main trunk disappearance.
Table 1: On the first day, 3rd month, and 12th month; OCT and RNFL
thickness measurements.

Thickness ([micro]m)        Day 1         Month 3      Month 12

Macular
Fovea                        232    250   236   248    239    251
Parafovea                    337    340   339   335    338    348
  Superior-hemi              339    342   340   338    339    350
  Inferior-hemi              335    337   337   333    336    345
  Temporal                   323    319   328   316    327    328
  Superior                   348    349   349   344    349    358
  Nasal                      335    350   335   347    332    354
  Inferior                   343    340   344   334    343    350
Perifovea                    318    322   316   316    316    325
  Superior-hemi              322    328   317   322    315    330
  Inferior-hemi              315    316   314   310    316    320
  Temporal                   293    296   299   292    297    302
  Superior                   322    330   320   323    318    333
  Nasal                      341    349   330   342    329    346
  Inferior                   317    313   314   307    318    320
Retinal nerve fiber layer
Whole                        129    126   126   125    129    134
  Superior-hemi              123    130   121   129    122    142
  Inferior-hemi              137    122   131   121    136    126
  Nasal superior             111    107   116   102    117    110
  Nasal inferior             107    97    100    91    108    98
  Inferior nasal             145    146   142   141    149    147
  Inferior temporal          195    173   202   182    211    184
  Temporal inferior          108    74    87     78     82    80
  Temporal superior          100    97    88    100     91    107
  Superior temporal          176    179   173   185    174    201
  Superior nasal             118    157   119   150    117    174

Cells are divided into two to show the results of the right and left
eyes separately.

Table 2: On the first day, 3rd month, and 12th month; OCTA macula
and disc vascular density, FAZ, and flow measurements.

                           Day 1           Month 3        Month 12

Disc-capillary density
Radial peripapillary (%)
Whole                      49.1    48.6    49.2    48.1   48.2   48.5
Inside disc                46.9    45.3    45.9    43.3   40.6   45.9
Peripapillary              51.7    51.0    51.1    49.5   50.7   50.4
  Superior-hemi            50.7    50.8    51.2    49.9   50.7   50.5
  Inferior-hemi            52.8    51.2    50.9     49    50.7   50.2
  Nasal superior           45.8    47.8     46     47.1   46.1   46.3
  Nasal inferior           49.1    46.6    48.4    46.6   49.6   46.3
  Inferior nasal           53.1    50.9    52.3    45.4   51.8   48.3
  Inferior temporal        53.8    57.2    52.3    53.1   49.7   57.2
  Temporal inferior         56     51.5    51.4    52.2   51.7   51.1
  Temporal superior        57.3    55.3    57.1     56    56.7   58.2
  Superior temporal        56.1    53.2    55.9    53.3   52.4   50.9
  Superior nasal           45.7    47.9    47.2    43.9   48.2   47.7
Macula-capillary density
Superficial (%)
Whole                      52.4    53.2    54.5    54.1   53.5   51.9
Superior-hemi              53.5     53     54.8    53.7   53.3   51.9
Inferior-hemi              54.6    50.8    54.2    54.5   53.6   51.9
Fovea                      15.2    17.1    14.6    17.7   15.7   15.3
Parafovea                  55.3    53.6    58.2    58.1   56.8    55
  Superior-hemi            57.1    53.5    57.8    56.6   55.9   54.1
  Inferior-hemi            56.8    56.8    58.6    59.6   57.7    56
  Temporal                 56.2    52.8    55.5    56.5   56.1   54.1
  Superior                 58.5    55.6    58.8    57.4   57.2   53.6
  Nasal                    56.7    59.3    57.5    57.9   55.4   55.6
  Inferior                  60     55.9     61     60.5   58.4   56.8
Perifovea                  52.8    51.8    54.3    54.5   53.3   52.9
  Superior-hemi            53.1    53.5    54.7    54.3   52.9   53.2
  Inferior-hemi            53.6    54.1    53.9    54.7   53.6   52.7
  Temporal                 50.3     52     51.8    52.2   50.8   52.5
  Superior                 54.2    54.7    54.7    53.9   52.4   53.1
  Nasal                    57.5    53.4    57.7    58.2   57.4   55.2
  Inferior                 53.4    52.4    52.6    53.8   52.2   50.9
Deep (%)
Whole                      48.1    47.6    48.3    48.4    48    46.9
Superior-hemi              49.9    47.9    50.3    47.9   49.7   47.4
Inferior-hemi              46.4    48.5    46.4     49     46    46.4
Fovea                      32.3    30.1    30.6    29.1   32.7   29.2
Parafovea                  55.8    53.9    56.4    55.1   55.5   55.7
  Superior-hemi            56.7    55.7    56.7    55.2   56.2   55.9
  Inferior-hemi            55.6    56.2     56     54.9   54.8   55.5
  Temporal                 55.8    57.5     55     57.4   55.6   57.8
  Superior                 56.5    53.4    57.8    53.7   55.5   55.3
  Nasal                    57.9    55.2    58.3    55.9   58.1   55.8
  Inferior                 52.3    51.8    54.4    53.4   52.8   53.9
Perifovea                  50.1    48.3    50.7    50.1   48.1   46.3
  Superior-hemi            50.2    48.6    52.8    49.8    49    46.7
  Inferior-hemi            48.5    47.4    48.6    50.4   47.2   45.8
  Temporal                 54.8    54.3    56.1    54.6   55.5   49.5
  Superior                 49.4    49.2    53.3    49.4   47.3   47.4
  Nasal                    43.9    43.4    46.4    46.5   44.6   42.8
  Inferior                 46.7    48.1    47.8     50    45.8   45.3
Foveal avascular zone
 ([mm.sup.2])
Retina                      352     376     347    389    358     386
Foveal flow
Outer retina               0.558   0.732   0.346   0.846  0.602  0.665
Choriocapillaris           2.101   2.068   2.087   2.091  2.195  2.058

Cells are divided into two to show the results of the right and left
eyes separately.
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Title Annotation:Case Report
Author:Akidan, Melih; Bulut, Mehmet; Yaprak, Lutfiye; Erol, Muhammet Kazim; Suren, Elcin
Publication:Case Reports in Ophthalmological Medicine
Date:Mar 31, 2020
Words:4220
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