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Dr.Pranita Chaudhary, P19932, Dr.Rakesh Juneja, Dr.Navneet Mehrotra, Dr.Manish Nagpal

Introduction:

Choroidal neovascular membrane (CNVM) is a rare but well-known sight-threatening complication of posterior segment intraocular inflammation affecting eyes with active or inactive inflammatory pathologies.1 Because of the association with various inflammatory conditions of posterior segment, these CNVMs are termed as “inflammatory CNVM.” The development of inflammatory CNVM results either directly from an inflammation-mediated angiogenic drive and/or secondary to a degenerative disruption in the Bruch membrane–retinal pigment epithelium complex.

Inflammatory CNVM is usually Type 2 or classic CNVM which grows beneath the neurosensory retina and anterior to retinal pigment epithelium.2 The different uveitic entities associated with CNVM include toxoplasmosis, punctuate inner choroidopathy

(PIC) (17–40%), idiopathic multifocal choroiditis (MC) (33%), and serpiginous choroiditis 3. It is also reported in ten eyes (9%) of seven patients in a follow-up of 58 patients (116 eyes) with Vogt-Koyanagi-Harada syndrome 4.

FA is currently the gold standard for identifying inflammatory CNV 5. In various uveitic choroidal disorders such as multifocal choroiditis (MFC) or punctate inner choroidopathy (PIC), the major cause of vision loss may be related to direct inflammatory damage of the retina and RPE 6, and secondary invasion of inflammatory CNV 7. Making the distinction between inflammatory versus neovascular lesions is mandatory to optimize therapy.

The typical presentation of inflammatory CNV on FA is early hyperfluorescence with late leakage 5, while inflammation displays early hypofluorescence or isofluorescence with late hyperfluoresence 5. However, CNV may not always illustrate obvious early hyperfluorescencedue to blockage from the inflammatory component, fluid, or hemorrhage. Furthermore, inflammatory lesions may display early hyperfluorescence because of RPE damage causing a window defect. It is therefore challenging to distinguish inflammatory CNV from purely inflammatory lesions by FA. OCTA, however, has improved the sensitivity and specificity of CNV detection in inflammatory choroidal disorders. The microvascular morphological detail may be more precisely detected with OCTA, and the area and the density of the inflammatory CNV can be quantitatively measured.

In this study, we report our OCTA findings in a case series of patients with posterior uveitis complicated with CNV.

Methods and materials:

Consecutive patients of posterior segment intraocular inflammation who presented with inflammatory CNVM, treated with intravitreal anti-VEGF agents, and followed for 6 months at least were included in this retrospective case series. An institutional review board approval was taken for this retrospective review. We searched the electronic database of medical record department to find out cases of inflammatory CNVM diagnosed during the last 5 years. Medical record of these patients with inflammatory CNVM fulfilling the inclusion criteria was further reviewed manually for relevant data abstraction. The diagnosis of active CNVM was made based on fundus biomicroscopy (presence of serous retinal detachment with or without subretinalhemorrhage), fluorescein angiography (presence of early phase hyperfluorescence with late-phase leakage), optical coherence tomography and optical coherence tomography angiography (OCTA). All patients diagnosed with active CNVM were advised either intravitreal injection of ranibizumab (0.5 mg in 0.05 mL) or bevacizumab (1.25 mg in 0.05 mL). All the details related to both anti-VEGF agents were explained to the patients, and injection was given according to the patient’s choice of selection after taking informed consent. Same anti- VEGF injection was repeated at monthly intervals till complete anatomical resolution of CNVM defined as complete resolution of subretinal or intraretinalfluid.OCTA images of 3 mm × 3 mm were acquired and centered at the fovea, using Nidek 3000 Advance RS.

Results:

Eighteen eyes of 10 patients (8 women and 2 men) with posterior uveitis (7 serpiginous like choroiditis, 3 APMPPE) met the inclusion criteria. The mean age was 42.9 ± 13.4 years (range, 23.5–60.1). The mean spherical equivalent was 26.2 ± 5.3 diopters (range, 0 to 213). The median Early Treatment Diabetic Retinopathy Study chart visual acuity at baseline was 63.1 ± 25.7 letters (range, 5–85). No patient reported a preexisting autoimmune disease or systemic complaints.

All 18 included eyes had a macular CNV. The mean follow-up of 9patients was 19.1 ± 12.8 months (range, 1.1–51.3). One patient was evaluated only once. On OCTA, 6 patients (9 eyes) had a mean follow-up of 7.2 ± 3.2 months (range, 2–10.6), whereas for 4 patients (9 eyes), only one OCTA was available.

Choroidal Neovascularization on Multimodal Imaging

Ten eyes had a history of CNV. During the follow-up period of OCTA data acquisition, nine eyes showed signs of activity on multilodal imaging andone did not. All nine active CNVs had a hyperautofluorescent- surrounding halo and a slight hyperautofluorescencein the center. One inactive CNVs had a slightly hyperautofluorescent surrounding ring. A subretinalhyperreflectivity and disruption of the outer retinal hyperreflective lines was visible in active CNV and not in inactive CNV. Exudative signs on SD-OCT (subretinalfluid and intraretinal cysts) were present in 6/9 eyes (66.7%), of which 2 eyes presented were treatmentnaive CNV. We did not find the homogenous choroidal increased light transmission beneath the CNV. Nevertheless, CNV presented a heterogenous choroidal hyperreflectivity, probably corresponding to areas of previous RPE damage (Figures 2, 4).

On OCTA images, all nine eyes with active CNV presented a highly organized dense high flow neovascular network in the outer retinal segmentation, equally visible in the choriocapillaris as a projection artifact. 2 eyes with active CNV were followed up by OCTA for a mean time of 8.8 ± 1.56 months (range, 6.8–10.6) and treated in average with 4.8 ± 2.6 intravitreal injections of anti-VEGF. After treatment, the CNV decreased in size and the collaterals decreased.

Discussion:

FA is currently the gold standard for identifying inflammatory CNV 5. In various uveitic choroidal disorders, the major cause of vision loss may be related to direct inflammatory damage of the retina and RPE 6, and secondary invasion of inflammatory CNV 7. Making the distinction between inflammatory versus neovascular lesions is mandatory to optimize therapy. Both illustrate elevation of the RPE by homogeneous hyper-reflective material with SD-OCT analysis [8, 9]. When avascular, these inflammatory lesions may appear small and conical [8]. It is unclear exactly what comprises the sub-RPE material. Inflammation and CNV are not mutually exclusive and may both be present in certain lesions. Even with multimodal imaging, the differentiation between active inflammatory lesions and inflammatory CNV may not be possible because both have the potential to cause infiltration and exudation with breakdown in the blood–retina barrier.

FA is currently the gold standard for identifying CNV 10. The typical presentation of inflammatory CNV on FA is early hyperfluorescence with late leakage 5, while inflammation displays early hypofluorescence or isofluorescence with late hyperfluoresence 5. However, CNV may not always illustrate obvious early hyperfluorescence due to blockage from the inflammatory component, fluid, or hemorrhage. Furthermore, inflammatory lesions may display early hyperfluorescence because of RPE damage causing a window defect. It is therefore challenging to distinguish inflammatory CNV from purely inflammatory lesions by FA.

OCTA, however, has improved the sensitivity and specificity of CNV detection in inflammatory choroidal disorders. The microvascular morphological detail may be more precisely detected with OCTA, and the area and the density of the inflammatory CNV can be quantitatively measured. OCTA has shown remarkable accuracy in distinguishing inflammatory CNV from avascular inflammatory lesions that were poorly identified using other imaging modalities 8, 11. However, OCTA cannot reliably determine which lesions are clinically active 7.

References

  1. Perentes Y, Van Tran T, Sickenberg M, Herbort CP. Subretinalneovascular membranes complicating uveitis: frequency, treatments, and visual outcome. OculImmunolInflamm 2005;13:219–224.
  2. Dhingra N, Kelly S, Majid MA, et al. Inflammatory choroidal neovascular membrane in posterior uveitis-pathogenesis and treatment. Indian J Ophthalmol 2010;58:3–10.
  3. Kuo IC, Cunningham ET Jr. Ocular neovascularization in patients with uveitis. IntOphthalmolClin. 2000 Spring;40(2):111-26.
  4. Moorthy RS, Chong LP, Smith RE, Rao NA. Subretinalneovascularmembranes in Vogt-Koyanagi-Harada syndrome. Am J Ophthalmol. 1993 Aug 15;116(2):164-70. DOI: 10.1016/S0002- 9394(14)71280-2.
  5. Kotsolis AI, Killian FA, Ladas ID, Yannuzzi LA (2010). Fluorescein angiography andoptical coherence tomography concordance for choroidal neovascularisation in multifocal choroidtis. Br J Ophthalmol Nov;94(11):1506-1508.
  6. Thorne JE, Wittenberg S, Jabs DA (2006) Multifocal choroiditis with panuveitis incidence of ocular complications and of loss of visual acuity. Ophthalmology 113:2310–2316.
  7. Levison AL, Baynes KM, Lowder CY, Kaiser PK, Srivastava SK (2017). Choroidal neovascularisation on optical coherence tomography angiography in punctate inner choroidopathy and multifocal choroiditis. Br J Ophthalmol 101(5):616–622.
  8. Pichi F, Sarraf D, Arepalli S, Lowder CY, Cunningham ET Jr, Neri P, Albini TA, Gupta V, Baynes K, Srivastava SK (2017) The application of optical coherence tomography angiography in uveitis and inflammatory eye diseases. ProgRetin Eye Res. Jul;59:178-201.
  9. Agrawal RV, Biswas J, Gunasekaran D (2013). Indocyanine green angiography in posterior uveitis. Indian J Ophthalmol. Apr;61(4):148-159
  10. Pichi F, Carrai P, Srivastava SK, Lowder CY, Nucci P, Neri P (2016). Genetic of uveitis. IntOphthalmol 36(3):419–33.
  11. Zahid S, Chen KC, Jung JJ, Balaratnasingam C, Ghadiali Q, Soreson J, Rofagha S, Freund KB, Yannuzzi LA (2016). Optical coherence tomography angiography of chorioretinal lesions due to idiopathic multifocal choroiditis. Retina [Epub ahead of print]

 

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