Sir,

A unique case of neovascularization of the lens capsule (NVC) in a phakic eye without neovascularization of the iris (NVI) or angle is described.

Case report

A 30 year old male presented with pain OD since 1 month. He gave a history of post-traumatic glaucoma 13 years back for which trabeculectomy was performed. Ten years later, he presented again with chronically raised intraocular pressure (IOP), vision of light perception only, and advanced glaucomatous cupping. 360° cyclo-crotherapy was administered at this time. At present, he had lost light perception, and had low IOP (6 mm Hg) OD. Slit-lamp biomicroscopy showed a mydriatic pupil with multiple sphincter tears, absence of NVI, a mature cataract with sparse capsular pseudoexfoliation, and a fine circumferential radiating spoke like net of anterior capsular vessels (Figures 1a and b). Gonioscopy showed obscuration of the anterior chamber. Anterior segment optical coherence tomograpy (Visante, Carl Zeiss Meditec Inc., Dublin, CA, USA) and ultrasound biomicroscopy (Sonomed Escalon, Wayne, PA, USA) confirmed peripheral anterior synechiae (Figures 2a and b) and ruled out the presence of any retro-iridial proliferative membrane (Figure 2b). Fluorescein angiography demonstrated a diffuse fluorescein leakage persisting till late phase with absence of NVI (Figures 3a–c). Ultrasonography showed a closed funnel retinal detachment, and therefore no intervention was planned.

Figure 1
figure 1

(a) Figure shows complicated cataract with overlying pseudoexfoliation material; pupil is mydriatic with multiple large sphincter tears. (b) Higher magnification shows a fine net of vessels growing onto the lens capsule centripetally.

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Figure 2
figure 2

(a) Anterior segment optical coherence tomograpy showing extensive peripheral anterior synechiae. (b) Ultrasound biomicroscopy showing peripheral anterior synechiae in a mydriatic pupil. Note the absence of any proliferative membrane over the lens capsule.

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Figure 3
figure 3

(a–c) Anterior segment fluorescein angiography shows early fluorescein leakage onto the anterior lens capsule, increasing in the late phase.

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Comment

Anterior ocular neovascularization may develop in eyes with chronic anterior segment ischemia, due to peripheral retinal detachment or proliferative vitreo-retinopathy.1, 2 Deprivation of choroidal blood supply stimulates retinal pericytes, endothelial cells, and retinal pigment epithelium to produce VEGF, which follows its concentration gradient from vitreous to anterior segment causing NVI.3

NVC in our case differs from neovascular membranes, sometimes appreciated in chronic anterior uveitis, which harbor larger caliber vessels growing across the pupillary border in a random manner. In contrast, our case had a regular circumferential arrangement of vessels. In the absence of a fibro-proliferative scaffold for vessel growth behind the iris on UBM, NVC appears to be a primary event. Another possibility could be the abnormal proliferation of vessels on the ciliary body with subsequent extension through ciliary zonules onto the lens capsule. The lens capsule secretes anti-endothelial cell inhibitory factors inhibiting NVC even in the presence of concurrent iris neovascularization.4 Any injury allows the lens capsule to respond to lens specific growth factors to permit proliferation of new vessels.5 A traumatic microcapsular breach could also have precipitated NVC in our case.