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Iris-claw lens explantation due to acute anterior neovascularization postvitrectomy surgery

Poster Details

First Author: S.Iglesias Cerrato SPAIN

Co Author(s):    G. Garrido Ceca   J. Gonzalez Guijarro           

Abstract Details


Reporting a case of acute anterior neovasculararization post vitrectomy surgery that required an iris-claw lens explantation.


Department of Ophthalmology, La Princesa Hospital, Madrid, Spain


Case Report


A 51-year-old man with a history of retinal detachment (RD) 15 years ago that was treated with panphotocoagulation. Residual peripheral RD anterior was reported. Phacoemulsificacion and intraocular lens (IOL) implantation with insertion of a capsular tension ring (CTR) due to zonular instability was performed. The BCVA improved from 0.2 previously to 0.5. Postoperatively, an early subluxation within the capsular bag was observed, so the patient underwent an IOL explantation surgery and implantation of an iris-claw lens in anterior chamber. The postoperative BCVA achieved 0,4. Spectral Domain - Optical Coherence Tomography (SD-OCT) reported cystoid macular edema (CME) and epiretinal membrane (EM) with bad response to topic ketorolac and subtenon triamcinolone. One year after iris-claw lens implantation, vitrectomy surgery including inner limiting membrane and EM peeling was done. In the early postoperative period, widespread anterior neovascularization including the angle and IOL deposits was reported, with complete regression after two intravitreal bevacizumab injections. Two weeks later, insidious iris neovascularization was reported so after a spontaneous anterior chamber bleeding, it was decided to remove the iris-claw lens. Two months after surgery, the patient was aphakic and there was no evidence of anterior neovascularization.


Secondary implantation of aphakic IOLs is effective, predictable, and safe for the correction of aphakia in eyes without capsule support. Nevertheless, complications such as corneal endothelial loss, pigment precipitates on the optic surface or haptics of the IOL (most of them transient), positive vitreous pressure, elevated intraocular pressure, IOL dislocation, pupillary block glaucoma, retinal detachment, pupil ovalization, hyphema, and CME have been reported. No cases of anterior neovascularization have been reported yet. Possible mechanisms of acute anterior neovascularization after the vitrectomy in this case includes ocular pathology present before: retinal ischemia due to chronic periferical RD, deep panretinal photocoagulation and subacute inflammation maintained by the iris-claw lens. Intravitreal bevacizumab injection had good result in the neovascularization regression, but only temporarily. We think that a subacute inflammation related with the iris-claw IOL (expressed as IOL deposits and greater neovascularization on the iris-claw areas) could keep the angiogenic stimulation triggered by vitrectomy surgery; so that, only removing IOL we can get a permanent regression until current date. Probably the chronic peripheral RD also had a main role in initiating the anterior neovascularization. FINANCIAL INTEREST: NONE

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