Spark ImageWise 23 – Retina

Inflammatory Choroidal Neovascular Membrane

Dr. Shashank Somani, Dr. Sarang Lambat, Dr. Prabhat Nangia, Dr. Vinay Nangia 
Suraj Eye Institute, 559 New Colony, Nagpur 

Case Description
A male, 63 years of age, presented to us with the complaint of seeing a black spot in front of the right eye since few days. He was a known case of diabetes mellitus under treatment since 6 years. On examination his best corrected visual acuity was 6/12(p), N8 in right eye and 6/9, N6 in left eye. Anterior segment examination was normal. Intraocular pressure recorded by Goldmann applanation tonometer was 14 mmHg in both eyes. 

Figure 1: Fundus photograph of the right eye shows multiple chorioretinal atrophic patches with hyperpigmentation suggestive of healed choroiditis lesions (green arrow). A yellowish grey membrane above the fovea is seen (Yellow arrow) with surrounding macular edema and sub retinal bleed suggestive of choroidal neovascular membrane (CNVM).
Figure 2: Fundus photograph of the left eye shows multiple healed choroiditis lesions in the left eye. (green arrows)
Figure 3: The optical coherence tomography line scan of right eye passing through the fovea shows presence of hyper-reflectivity in the sub RPE space suggestive of CNVM (yellow arrow) along with hyperreflectivity in the sub retinal space suggestive of CNV growing in the subretinal space. (Blue arrow) Hypo-reflectivity in the sub retinal space adjoining the CNVM represents presence of minimal SRF (Red arrow). There is presence of minimal edema of the  outer retinal layers. These findings are suggestive of a CNV. 
The area nasal to the CNV shows loss of photoreceptors and RPE with intermittent RPE clumping along with hyperreflectivity of the choroid with evident shrinking of the choroidal vasculature suggestive of a chorio-retinal scar (Green arrow).
Figure 4: The optical coherence tomography line scan of right eye passing along one of the pre existing scar showing outer retinal tubulation (yellow arrow). RPE undulations are also seen (blue arrows) with presence of intraretinal fluid (green arrow) and subretinal fluid (red arrow). 
Figure 5: The optical coherence tomography line scan of left eye passing through the fovea with   loss of photoreceptors and RPE (blue arrow) temporal to fovea with intermittent RPE clumping (red arrow) along with hyper-reflectivity of the choroid with evident shrinking of the choroidal vasculature  (yellow arrow) suggestive of a chorio-retinal scar. 
Figure 6: OCT Angiography scan passing through the avascular complex shows increased vascular signal intensities in the area of scarring (Blue arrow). No abnormal vessels were seen in the area of the CNV. 
Figure 7: Fluorescein angiography of the right eye shows hyperfluorescent lesion in the foveal region (yellow arrow). The late phase angiogram shows progressive increase in the area and intensity of the hyperfluorescence of the foveal lesion suggestive of choroidal neovascularization (blue arrow). Window defects with staining are seen suggestive of the healed choroiditis lesions (green arrow).


Our patient presented with recent visual loss in the right eye and on the basis of characteristic findings on multimodal imaging (MMI) we were able to conclude that he had an inflammatory CNV (iCNV). The patient was advised  to undergo injection anti VEGF. Ocular inflammation though not common cause for CNVM formation, but it is just next to AMD and Myopia. This patient did not have any evidence of age related macular degeneration and he was not myopic. Diagnosis of an Inflammatory CNV is difficult especially when it is associated with areas of active or healed choroiditis. It is important to investigate such patients in detail to determine whether we are dealing with an active inflammation or an iCNV. MMI guides us to accurately distinguish between the two. 

The development of iCNV is associated with infective and non infective causes of posterior uveitis. The infective causes include histoplasmosis, toxoplasmosis, toxocariasis, tuberculosis, congenital rubella, and West Nile virus. The non infective causes include punctate inner choroidopathy, multifocal choroiditis, serpiginous choroiditis and Vogt-Koyanagi-Harada (VKH) disease. It has been thought that i-CNV can occur either directly from an angiogenic stimulus mediated by local inflammation or it can result from a degenerative disruption in the Bruch’s membrane–RPE complex, or both. Majority of i-CNVs are type 2 lesions with abnormal growth of vasculature into the outer retinal space. CNV lesion may be missed initially due to the presence of associated features such as inflammatory lesions, scars, and pigmentation, as well as intra- or subretinal fluid accumulation. It is imperative to evaluate such patients in detail and do MMI to ensure that typical findings in each imaging modality are available for accurate diagnosis. On SDOCT the retinal features of choroiditis lesions may be similar to the iCNV. Finger like projections from the iCNV in the outer retina labelled as the ‘pitchfork sign’ helps us to differentiate iCNV from ocular inflammation. Findings on each imaging modality needs to be interpreted with caution.

Anti VEGF agents are very effective in iCNV. Intravitreal dexamethasone implant, methotrexate, or triamcinolone acetonide can also be considered, which help to reduce the size of the CNV lesion.


  1. Agarwal A, Invernizzi A, Singh RB, Foulsham W, Aggarwal K, Handa S, Agrawal R, Pavesio C, Gupta V. An update on inflammatory choroidal neovascularization: epidemiology, multimodal imaging, and management. J Ophthalmic Inflamm Infect. 2018 Sep 12;8(1):13. doi: 10.1186/s12348-018-0155-6.
  2. Neri P, Lettieri M, Fortuna C, Manoni M, Giovannini A. Inflammatory choroidal neovascularization. Middle East Afr J Ophthalmol. 2009 Oct;16(4):245-51. doi: 10.4103/0974-9233.58422.

Dr. Sarang Lambat
Vitreoretinal services
Suraj Eye Institute
Email –

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