Ophthalmic Surgery, Lasers and Imaging Retina

Clinical Science 

Optical Coherence Tomography Angiography in Monitoring Proliferative Macular Telangiectasia Type 2 Treatment Response

Rania G. Estawro, FRCS; Sherif N. Embabi, MD

Abstract

BACKGROUND AND OBJECTIVE:

Difficulty exists in the follow-up of proliferative macular telangiectasia type 2 (MacTel 2) cases after anti-vascular endothelial growth factor (VEGF) treatment due to staining in fluorescein angiography (FA) and alteration in retinal layers by optical coherence tomography (OCT). Herein, the authors report three cases in which OCT angiography (OCTA) could resolve this issue.

PATIENTS AND METHODS:

In this retrospective, observational case series, diagnosis of MacTel 2 was made based on clinical examination, FA, OCT, and OCTA at presentation. Regression of neovessels was monitored by OCT and OCTA.

RESULTS:

OCTA could delineate neovessels before treatment in all cases and facilitate differentiation between active and regressed lesions after treatment. Simultaneous OCT images were less easily appreciated due to altered retinal structure secondary to degenerative nature of the disease.

CONCLUSION:

OCTA could be the tool of choice to monitor neovascular response to anti-VEGF treatment in proliferative MacTel 2.

[Ophthalmic Surg Lasers Imaging Retina. 2019;50:485–491.]

Abstract

BACKGROUND AND OBJECTIVE:

Difficulty exists in the follow-up of proliferative macular telangiectasia type 2 (MacTel 2) cases after anti-vascular endothelial growth factor (VEGF) treatment due to staining in fluorescein angiography (FA) and alteration in retinal layers by optical coherence tomography (OCT). Herein, the authors report three cases in which OCT angiography (OCTA) could resolve this issue.

PATIENTS AND METHODS:

In this retrospective, observational case series, diagnosis of MacTel 2 was made based on clinical examination, FA, OCT, and OCTA at presentation. Regression of neovessels was monitored by OCT and OCTA.

RESULTS:

OCTA could delineate neovessels before treatment in all cases and facilitate differentiation between active and regressed lesions after treatment. Simultaneous OCT images were less easily appreciated due to altered retinal structure secondary to degenerative nature of the disease.

CONCLUSION:

OCTA could be the tool of choice to monitor neovascular response to anti-VEGF treatment in proliferative MacTel 2.

[Ophthalmic Surg Lasers Imaging Retina. 2019;50:485–491.]

Introduction

Macular telangiectasia type 2 (MacTel 2) is a neurodegenerative disease1,2 in which there is loss of Müller cells within the temporal juxta foveal area, resulting in ellipsoid zone loss, retinal pigment epithelium (RPE) changes, structural collapse, and alteration of juxtafoveal retinal layers in association with various forms of vascular changes.1–5 These changes may start in subclinical form and can be complicated by neovascularization in advanced stages (proliferative MacTel 2).2,6–9

Intravitreal injection of anti-vascular endothelial growth factor (VEGF) is recommended in proliferative MacTel 2.10 Response to treatment was observed by decreased leakage in fluorescein angiography (FA) and/or decreased retinal thickness in optical coherence tomography (OCT).11,12

FA could be confusing due to persistent staining after neovascular regression.13 OCT could be challenging too due to structural alterations in line scans, minimal reduction of central subfield thickness (CST),11,14 or even no reduction in the central macular thickness after regression of neovascularization, as reported by Sandhu and Hamilton.15

OCT angiography (OCTA) has shown promising results in diagnosis and classification of MacTel 2.3,16–18 More detailed visualization of possible complicating neovascularization was observed, even in dense staining by FA or in decreased CST by OCT.5,8,19

This study describes the OCTA morphologic features of three cases of proliferative MacTel 2 after treatment with intravitreal anti-VEGF injection.

Patients and Methods

Our study adhered to the tenets of the Declaration of Helsinki and to the local ethics committee of Watany Research Development Center standards, which has come to the conclusion to waiver the need for review by an institutional review board.

Three patients with proliferative MacTel 2 were enrolled in this study, and data from clinical visits and imaging modalities were reviewed. All three patients underwent FA (HRA; Heidelberg Engineering, Heidelberg, Germany). Two patients were imaged by spectral-domain OCT (Spectralis; Heidelberg Engineering, Heidelberg, Germany) and OCTA (Cirrus 5000; Zeiss, Jena, Germany). The third patient was imaged using OCT and OCTA (RTVue XR; Optovue, Fremont, CA).

At baseline, patients underwent Snellen best-corrected visual acuity (BCVA) testing and complete ocular examination. Diagnosis was confirmed by FA, OCT, and OCTA. Patients received intravitreal ranibizumab (Lucentis; Genentech, South San Francisco, CA) injection, and then OCT and OCTA were repeated 4 weeks after injection to assess treatment response and the need for further injection treatment. Visual acuity (VA) was recorded after regression of neovascularization based on OCT and OCTA features.

In addition to the commercially available automated segmentation strategy in each OCTA machine, a custom segmentation by author was performed between the outer retinal boundary and the inner aspect of the choriocapillaris as recommended by Zhang et al.19 to observe the detailed microvascular structure of neovascularization. No subsequent image modification or processing was performed.

Results

Case 1

A 64-year-old female with history of well-controlled type 2 diabetes mellitus and essential hypertension presented to our clinic due to decrease of vision in the right eye (OD). Prior ophthalmic history was noncontributory. BCVA was 20/400 and anterior segment examination was unremarkable. Fundus examination was remarkable for foveal pigment mottling, juxtafoveal spot hemorrhage, and angulated venule with no diabetic or hypertensive retinopathy changes.

FA showed temporal juxtafoveal hyperfluorescent lesion with progressive leakage and fuzzy edges. OCT showed CST 268 μm (Figure 1D) and temporal juxtafoveal deep heterogeneous hyperreflective lesion associated with overly intraretinal edema and adjacent rim of subretinal fluid (Figure 1G). Simultaneous OCTA showed temporal juxtafoveal angulated venule with interruption of temporal foveal avascular zone (FAZ) at the level of superficial capillary plexus (SCP), downward displacement of the angulated vessel with temporal interruption of FAZ at the level of deep capillary plexus (DCP), custom segmentation slab revealed branching vascular network with circular peripheral anastomosis, and surrounding dark area (Figure 1A). The decision to treat with intravitreal anti-VEGF (ranibizumab [Lucentis; Genentech, South San Francisco, CA]) treatment was made.

Case 1 with proliferative macular telangiectasia type 2. (A) Optical coherence tomography angiography (OCTA) is shown before treatment with branching vascular network and tiny peripheral anastomosis. (B) OCTA is shown after first anti-vascular endothelial growth factor injection with partial disappearance of neovascularization. (C) OCTA is shown after second injection, with complete disappearance of neovascularization. (D) Retinal thickness map before treatment with a central subfield thickness (CST) of 268 μm. (E) Retinal thickness map after first injection with a CST of 302 μm. (F) Retinal thickness map after second injection with a CST of 264 μm. (G) OCT line scan is shown before treatment with temporal juxtafoveal deep heterogeneous hyperreflective lesion with overly intraretinal edema and adjacent rim of subretinal fluid. (H) OCT line scan is shown after first injection with more homogeneity of the deep hyperreflective lesion, flattened foveal contour, and thickened vitreoretinal interface. (I) OCT line scan is shown after second injection with minimal change of the lesion, flattened foveal contour, and thickened vitreoretinal interface.

Figure 1.

Case 1 with proliferative macular telangiectasia type 2. (A) Optical coherence tomography angiography (OCTA) is shown before treatment with branching vascular network and tiny peripheral anastomosis. (B) OCTA is shown after first anti-vascular endothelial growth factor injection with partial disappearance of neovascularization. (C) OCTA is shown after second injection, with complete disappearance of neovascularization. (D) Retinal thickness map before treatment with a central subfield thickness (CST) of 268 μm. (E) Retinal thickness map after first injection with a CST of 302 μm. (F) Retinal thickness map after second injection with a CST of 264 μm. (G) OCT line scan is shown before treatment with temporal juxtafoveal deep heterogeneous hyperreflective lesion with overly intraretinal edema and adjacent rim of subretinal fluid. (H) OCT line scan is shown after first injection with more homogeneity of the deep hyperreflective lesion, flattened foveal contour, and thickened vitreoretinal interface. (I) OCT line scan is shown after second injection with minimal change of the lesion, flattened foveal contour, and thickened vitreoretinal interface.

After the first anti-VEGF injection, OCT showed increased CST of 302 μm (Figure 1E), and line scan showed more homogeneity of the deep hyperreflective lesion, flattened foveal contour, and thickened vitreoretinal interface (Figure 1H). Simultaneous OCTA custom slab showed partial disappearance of vascular network with residual abnormal flow nasally (Figure 1B). The decision was made for another injection.

After the second injection, OCT showed a reduction of CST to 264 μm (Figure 1F), and line scan showed minimal change in comparison to the previous scan (Figure 1I). Simultaneous OCTA custom slab showed complete disappearance of the vascular network, leaving behind a dark area and blunted large vessel (Figure 1C). BCVA improved to 20/100, and the decision was made for no further injections.

The patient maintained stable VA at the 3-month follow-up visit after the second injection.

Case 2

A 67-year-old female with history of well-controlled essential hypertension presented to our clinic due to a decrease of VA in the OD. The patient was diagnosed with MacTel 2 10 years ago, with a previous ocular history of three anti-VEGF injection in the left eye (OS). BCVA was 20/32 and anterior segment examination was unremarkable. Fundus examination was remarkable for foveal pigment mottling and angulated venule, with no signs of hypertensive retinopathy OD.

FA showed a temporal juxtafoveal hyperfluorescent lesion with progressive leakage and fuzzy edges OD. OCT showed a CST of 317 μm (Figure 2D) and a tiny temporal juxtafoveal deep hyperreflective lesion with overly minimal intraretinal edema associated with preserved foveal contour and a tiny RPE interruption (Figure 2G). Simultaneous OCTA showed a temporal juxtafoveal angulated venule with telangiectatic vessels temporal to the FAZ at the level of the SCP, telangiectatic vessels at the level of the DCP, custom segmentation slab revealed small branching vascular network with tiny peripheral anastomosis, and a surrounding dark area (Figure 2A). The decision to treat with intravitreal anti-VEGF (ranibizumab) injection was taken.

Case 2 with proliferative macular telangiectasia type 2. (A) Optical coherence tomography angiography (OCTA) is shown before treatment with branching vascular network and tiny peripheral anastomosis. (B) OCTA is shown after first anti-vascular endothelial growth factor injection with complete disappearance of neovascularization. (C) OCTA is shown after 3 months with the same angiographic features. (D) Retinal thickness map before treatment with a central subfield thickness (CST) of 317 μm. (E) Retinal thickness map after first injection with a CST of 293 μm (middle right). Retinal thickness map after 3 months with a CST of 275 μm. (F) OCT line scan is shown before treatment with tiny temporal juxtafoveal deep hyperreflective lesion with overly minimal intraretinal edema and preserved foveal contour in association with tiny retinal pigment epithelium interruption. (H) OCT line scan is shown after first injection, with more homogenous appearance of the deep temporal juxtafoveal lesion and dry retinal layers. (I) OCT line scan is shown after 3 months, with preservation of the foveal contour and formation of focal choroidal excavation.

Figure 2.

Case 2 with proliferative macular telangiectasia type 2. (A) Optical coherence tomography angiography (OCTA) is shown before treatment with branching vascular network and tiny peripheral anastomosis. (B) OCTA is shown after first anti-vascular endothelial growth factor injection with complete disappearance of neovascularization. (C) OCTA is shown after 3 months with the same angiographic features. (D) Retinal thickness map before treatment with a central subfield thickness (CST) of 317 μm. (E) Retinal thickness map after first injection with a CST of 293 μm (middle right). Retinal thickness map after 3 months with a CST of 275 μm. (F) OCT line scan is shown before treatment with tiny temporal juxtafoveal deep hyperreflective lesion with overly minimal intraretinal edema and preserved foveal contour in association with tiny retinal pigment epithelium interruption. (H) OCT line scan is shown after first injection, with more homogenous appearance of the deep temporal juxtafoveal lesion and dry retinal layers. (I) OCT line scan is shown after 3 months, with preservation of the foveal contour and formation of focal choroidal excavation.

After the first anti-VEGF injection, OCT showed mild reduction of CST to 293 μm (Figure 2E), a more homogenous appearance of the deep temporal juxtafoveal lesion, and dry retinal layers in the line scan (Figure 2H). Simultaneous OCTA custom slab showed a complete disappearance of the vascular network, with a residual dark area and blunted large vessel (Figure 2B). BCVA improved to 20/25, and the decision was made for no further injections.

The 3-month follow-up visit showed maintained BCVA, and OCT showed further reduction of CST to 275 μm (Figure 2F), preservation of foveal contour, and formation of focal choroidal excavation at lesion site on the line scan (Figure 2I). Simulations OCTA custom slab showed stable angiographic featured (Figure 2C).

Case 3

A 61-year-old male with a history of well-controlled type 2 diabetes mellitus and essential hypertension presented to our clinic due to decrease of VA OD. Prior ophthalmic history was noncontributory. BCVA was 20/80 and anterior segment examination was unremarkable. Fundus examination was remarkable for foveal pigment mottling and angulated venule with no diabetic or hypertensive retinopathy.

FA showed a temporal juxtafoveal hyperfluorescent lesion with progressive leakage and fuzzy edges. OCT showed CST of 417 μm (Figure 3D) and a subretinal hyperreflective lesion with overly intraretinal edema, cystic cavities, and loss of foveal contour on line scan (Figure 3G). Simultaneous OCTA showed temporal juxtafoveal angulated venule with telangiectatic vessels temporal to the FAZ at the level of the SCP, telangiectatic vessels at the level of the DCP; custom segmentation slab revealed a branching vascular network with tiny peripheral anastomosis and a surrounding dark area (Figure 3A). Decision to treat with an intravitreal anti-VEGF ranibizumab treatment was taken.

Case 3 with proliferative macular telangiectasia type 2. (A) Optical coherence tomography angiography (OCTA) is shown before treatment with branching vascular network and tiny peripheral anastomosis. (B) OCTA is shown after first anti-vascular endothelial growth factor injection, with complete disappearance of neovascularization. (C) OCTA is shown after 1 month with same angiographic features. (D) Retinal thickness map before treatment with a central subfield thickness (CST) 381 μm. (E) Retinal thickness map after first injection with a CST of 295 μm. (F) Retinal thickness map after 1 month with a CST of 287 μm. (G) OCT line scan is shown before treatment with subretinal hyperreflective lesion with overly intraretinal edema, cystic changes, and loss of foveal contour. (H) OCT line scan is shown after first injection, with more homogeneity of the deep hyperreflective lesion, residual intraretinal edema, cystic cavitation, flattened foveal contour, and thickened vitreoretinal interface. (I) OCT line scan is shown after 1 month with preservation of the foveal contour and formation of focal choroidal excavation.

Figure 3.

Case 3 with proliferative macular telangiectasia type 2. (A) Optical coherence tomography angiography (OCTA) is shown before treatment with branching vascular network and tiny peripheral anastomosis. (B) OCTA is shown after first anti-vascular endothelial growth factor injection, with complete disappearance of neovascularization. (C) OCTA is shown after 1 month with same angiographic features. (D) Retinal thickness map before treatment with a central subfield thickness (CST) 381 μm. (E) Retinal thickness map after first injection with a CST of 295 μm. (F) Retinal thickness map after 1 month with a CST of 287 μm. (G) OCT line scan is shown before treatment with subretinal hyperreflective lesion with overly intraretinal edema, cystic changes, and loss of foveal contour. (H) OCT line scan is shown after first injection, with more homogeneity of the deep hyperreflective lesion, residual intraretinal edema, cystic cavitation, flattened foveal contour, and thickened vitreoretinal interface. (I) OCT line scan is shown after 1 month with preservation of the foveal contour and formation of focal choroidal excavation.

After the first anti-VEGF injection, OCT showed reduction of CST to 285 μm (Figure 3E), more homogeneity of the deep hyperreflective lesion, flattened foveal contour, thickened vitreoretinal interface on line scan associated with residual retinal thickening, and residual cavitation (Figure 3H). Simultaneous OCTA custom slab showed a complete disappearance of the vascular network with a residual dark area (Figure 3B). BCVA improved to 20/50, and the decision was made for no further injections.

The 3-month follow-up visit showed maintained BCVA. OCT showed minimal reduction of CST to 287 μm (Figure 3F) and the same structural changes on B-scan (Figure 3I). Simultaneous OCTA custom slab showed stable angiographic features (Figure 3C).

Discussion

OCTA has recently become an important tool for the appraisal of retinal vasculature. MacTel 2 was described as the ideal disease to study using OCTA because it is a vascular pathology contained within the central macula.20 In this study, OCTA imaging could not only delineate neovascularization in MacTel 2 at presentation but also monitor response to anti-VEGF treatment.

Automated segmentation is quite tricky in those patients because Müller cell depletion results in posterior displacement of temporal juxtafoveal vascular layers, as mentioned by Spaide et al.5 In our study, custom segmentation by author between the outer retinal boundary and the inner-most aspect of the choriocapillaris revealed detailed microvascular structure of the neovascularization, which supports the finding reported by Zhang et al.19

In the current study, baseline OCTA custom segmentation slab revealed active neovessels taking the appearance of a branching network with tiny peripheral anastomosis, deep to the angulated vessel. An adjacent area of hyporeflectivity at the level of the choriocapillaris (dark halo) was noted, which may indicate element of choroidal hypoperfusion, as suggested in wet AMD.20 Complete regression of neovessels was noted by OCTA as complete disappearance of the abnormal vascular network, leaving behind a dark flow void area at the level of the outer retinal layers and choriocapillaris.

Neovascularization disappearance after treatment by OCTA can be explained by obliteration of abnormal vessels, or by reduced flow velocity below a detectable threshold, as postulated previously.19

BCVA and OCTA features were maintained at follow-up visits for up to 3 months after the last injection in all patients. This confirms the stability of the condition after complete regression of neovessels.

It is worth mentioning that regression of neo-vessels was observed on OCTA as the disappearance in custom slab in all patients, despite using two different machines with two different accusation algorithms, which supports that these features are disease-related not machine-related.

Notably, OCTA images permitted more accurate judgment of neovascular regression, in relation to OCT images done on the same follow-up visits. For example, Case 1 showed partial disappearance of the neovascularization after the first injection on OCTA, whereas OCT performed on the same visit showed increased CST (+34 μm). Complete disappearance of neovessels on OCTA was achieved in Case 1 after the second injection, whereas subtle changes were observed on OCT line scan. Case 2 showed complete disappearance of neovascularization after single injection on OCTA and a minor change of CST (−24 μm) by OCT. Case 3 showed complete disappearance of the neovascular network by OCTA after a single injection, whereas residual retinal thickening and cystic cavitation were noted on OCT line scan. These results support our assumption that OCTA images can be an effective tool in monitoring proliferative MacTel 2 treatment response in comparison to OCT.

The patient with the largest neovascular membrane size (Case 1) required two injections and had the worst final VA. On the other hand, the patient with the smallest membrane size (Case 2) required a single injection and had the best final visual outcome. This supports previous results that better response can be achieved with smaller-sized membranes.1,6 Hence, we recommend using OCTA in follow-up of MacTel 2 patients to ensure early detection of complicating neovascularization and to have the chance of a better visual outcome.

To the best of our knowledge, this is the first study describing utility of OCTA in monitoring proliferative MacTel 2 in response to intravitreal anti-VEGF treatment. The limitation of this study is the small number of included cases, which can be explained by rarity of the disease,7,21 and raises the need for further validation through a larger number of patients.

In conclusion, OCTA enables objective monitoring of neovascular response to anti-VEGF treatment in proliferative MacTel 2 and can facilitate differentiation between active and regressed lesions. This novel imaging method could become an essential tool in clinical management of this rare disease.

References

  1. Powner MB, Gillies MC, Zhu M, Vevis K, Hunyor AP, Fruttiger M. Loss of Müller's cells and photoreceptors in macular telangiectasia type 2. Ophthalmology. 2013;120(11):2344–2352. doi:10.1016/j.ophtha.2013.04.013 [CrossRef]
  2. Wu L, Evans T, Arevalo JF. Idiopathic macular telangiectasia type 2 (idiopathic juxtafoveolar retinal telangiectasis type 2A, Mac Tel 2). Surv Ophthalmol. 2013;58(6):536–559. doi:10.1016/j.survophthal.2012.11.007 [CrossRef]
  3. Gaudric A, Krivosic V, Tadayoni R. Outer retina capillary invasion and ellipsoid zone loss in macular telangiectasia type 2 imaged by optical coherence tomography angiography. Retina. 2015;35(11):2300–2306. doi:10.1097/IAE.0000000000000799 [CrossRef]
  4. Shen W, Fruttiger M, Zhu L, et al. Conditional Müller cell ablation causes independent neuronal and vascular pathologies in a novel transgenic model. J Neurosci. 2012;32(45):15715–15727. doi:10.1523/JNEUROSCI.2841-12.2012 [CrossRef]
  5. Spaide RF, Klancnik JM Jr., Cooney MJ, et al. Volume-rendering optical coherence tomography angiography of macular telangiectasia type 2. Ophthalmology. 2015;122(11):2261–2269. doi:10.1016/j.ophtha.2015.07.025 [CrossRef]
  6. Charbel Issa P, Gillies MC, Chew EY, et al. Macular telangiectasia type 2. Prog Retin Eye Res. 2013; 34:49–77. doi:10.1016/j.preteyeres.2012.11.002 [CrossRef]
  7. Shukla D, Gupta SR, Neelakantan N, et al. Type 2 idiopathic macular telangiectasia. Retina. 2012;32(2):265–274. doi:10.1097/IAE.0b013e31822091b0 [CrossRef]
  8. Balaratnasingam C, Yannuzzi LA, Spaide RF. Possible choroidal neovascularization in macular telangiectasia type 2. Retina. 2015;35(11):2317–2322. doi:10.1097/IAE.0000000000000887 [CrossRef]
  9. Yannuzzi LA, Bardal AM, Freund KB, Chen KJ, Eandi CM, Blodi B. Idiopathic macular telangiectasia. 2006. Retina. 2012;32Suppl 1:450–460. doi:10.1097/IAE.0b013e31823f9a59 [CrossRef]
  10. Narayanan R, Chhablani J, Sinha M, et al. Efficacy of anti-vascular endothelial growth factor therapy in subretinal neovascularization secondary to macular telangiectasia type 2. Retina. 2012;32(10):2001–2005. doi:10.1097/IAE.0b013e3182625c1d [CrossRef]
  11. Toygar O, Guess MG, Youssef DS, Miller DM. Long-term outcomes of intravitreal bevacizumab therapy for subretinal neovascularization secondary to idiopathic macular telangiectasia type 2. Retina. 2016;36(11):2150–2157. doi:10.1097/IAE.0000000000001035 [CrossRef]
  12. Mandal S, Venkatesh P, Abbas Z, Vohra R, Garg S. Intravitreal bevacizumab (Avastin) for subretinal neovascularization secondary to type 2A idiopathic juxtafoveal telangiectasia. Graefes Arch Clin Exp Ophthalmol. 2007;245(12):1825–1829. doi:10.1007/s00417-007-0567-8 [CrossRef]
  13. Villegas VM, Kovach JL. Optical coherence tomography angiography of macular telangiectasia type 2 with associated subretinal neovascular membrane. Case Rep Ophthalmol Med. 2017; 2017:8186134.
  14. Kovach JL, Rosenfeld PJ. Bevacizumab (avastin) therapy for idiopathic macular telangiectasia type II. Retina. 2009;29(1):27–32. doi:10.1097/IAE.0b013e31818ba9de [CrossRef]
  15. Sandhu R, Hamilton R. Treatment of proliferative idiopathic macular telangiectasia type 2 with intravitreal bevacizumab. IOVS2013;54: ARVO E-Abstract 4655. http://iovs.arvojournals.org/article.aspx?articleid=2149537. Accessed April 18, 2018.
  16. Runkle AP, Kaiser PK, Srivastava SK, et al. OCT angiography and ellipsoid zone mapping of macular telangiectasia type 2 from the AVATAR Study. Invest Ophthalmol Vis Sci. 2017;58(9):3683–3689. doi:10.1167/iovs.16-20976 [CrossRef]
  17. Spaide RF, Klancnik JM Jr., Cooney MJ. Retinal vascular layers in macular telangiectasia type 2 imaged by optical coherence tomographic angiography. JAMA Ophthalmol. 2015;133(1):66–73. doi:10.1001/jamaophthalmol.2014.3950 [CrossRef]
  18. Chidambara L, Gadde SG, Yadav NK, et al. Characteristics and quantification of vascular changes in macular telangiectasia type 2 on optical coherence tomography angiography. Br J Ophthalmol. 2016;100(11):1482–1488. doi:10.1136/bjophthalmol-2015-307941 [CrossRef]
  19. Zhang Q, Wang RK, Chen CL, et al. Swept source optical coherence tomography angiography of neovascular macular telangiectasia type 2. Retina. 2015;35(11):2285–2299. doi:10.1097/IAE.0000000000000840 [CrossRef]
  20. Coscas GJ, Lupidi M, Coscas F, Cagini C, Souied EH. Optical coherence tomography angiography versus traditional multimodal imaging in assessing the activity of exudative age-related macular macular degeneration: A new diagnostic challenge. Retina. 2015;35(11):2219–2228. doi:10.1097/IAE.0000000000000766 [CrossRef]
  21. Gass JD, Blodi BA. Idiopathic juxtafoveolar retinal telangiectasis. Update of classification and follow-up study. Ophthalmology. 1993;100(10):1536–1546. doi:10.1016/S0161-6420(93)31447-8 [CrossRef]
Authors

From Al-Watany Eye Hospital, Cairo, Egypt.

The authors report no relevant financial disclosures.

Address correspondence to Rania G. Estawro, FRCS, Al-Watany Eye Hospital, Thawra Street, Egyptian Army Bridge, Qism El Nozha, Cairo, Egypt 11775; email: restawro@hotmail.com.

Received: August 06, 2018
Accepted: January 17, 2019

10.3928/23258160-20190806-02

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