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ST Schuschereba, J Brown Jr, DR Clarkson, LM Valo, BE Stuck; Bridging Choroidal Neovascular Complexes Between Two Nd:YAG Laser-induced Retinal Lesions are Facilitated by Coalescence of Large and Confined Subretinal Hemorrhages . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1259.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To determine funduscopic criteria that will help predict when bridging choroidal neovascular (CNV) complexes will develop after laser trauma and to define early preventive treatment targets. Methods: Ten rhesus monkeys were used and all animal handling was according to NIH guidelines. Retinal lesions were produced by Nd:YAG exposures (20ns, 1-2mJ, 1064nm, min. spot size) simulating human accidental laser trauma to the central fundus. Funduscopy and fluorescein/ICG angiography were conducted at day 1, 4, and 14, and at 2 and 4 months, and animals terminated for histologic evaluation. Seventeen isolated lesions with confined subretinal hemorrhages were compared to 5 sets of two lesions showing coalescing and confined subretinal hemorrhages and 8 sets of two lesions with coalescing edges where one contained a vitreous hemorrhage and the other a confined subretinal hemorrhage. Results: Evidence of elevated fibrovascular complexes (CNV) of either type I or II were present in all of the 17 lesions with confined subretinal hemorrhages. All 5 lesion sets that showed initial coalescing subretinal hemorrhages formed bridging CNV scars between the two involved lesions. Extensive secondary photoreceptor losses occurred in confined hemorrhage zones and directly above and along the length of the scar bridges. Fibrovascular growth in directions external to the involved two-lesion zone was limited. In all 8 lesion sets involving a vitreous hemorrhage adjacent to a confined subretinal hemorrhage, no bridging CNVs occurred. Other lesions not involving hemorrhages, but with equidistant locations to the hemorrhagic two-lesion sets, did not show bridging CNVs. In hemorrhagic lesions, pathology also included retinal holes, inner lamellar holes, retinal thinning, retinal gliosis, chorioretinal adhesions, cystoid changes, vitreous adhesion/traction, epiretinal membranes, RPE hypopigmentation, choriocapillaris obliteration, and choroidal vascular bed atrophy. Conclusion: Trauma presenting with evidence of coalescing and confined subretinal hemorrhages between two adjacent lesions has a high chance of forming choroidal neovascular bridge complexes between the involved lesions. Confined subretinal hemorrhages may promote CNV formation, which may be related to the long residence time, break down products, and clearance processes of extravasated blood. Therefore, in these injuries, removal of trapped blood and possible use of anti-angiogenic and anti-proliferative agents may help curtail CNV formation and photoreceptor losses.
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