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TRANSSCLERAL DELIVERY OF Nd: YLF LASER AT 1,047 nm CAUSES VASCULAR OCCLUSION IN EXPERIMENTAL PIGMENTED CHOROIDAL MELANOMA

Damico, Francisco Max MD, PhD*,†; Takahashi, Beatriz S. MD; Acquesta, Felipe B.

doi: 10.1097/IAE.0b013e3182a2e723
Original Study

Purpose: The aims of this study were to determine the scleral attenuation of focused neodymium: yttrium–lanthanum–fluoride laser at 1,047 nm applied transsclerally and whether transscleral delivery can close the vascular supply at the base of experimental choroidal melanoma in rabbits.

Methods: Fifty-two New Zealand albino rabbits were included. Scleral laser attenuation was measured across fresh sclera. B16F10 melanomas were established in the subchoroidal space of 49 rabbits. Twenty-one animals were killed immediately after transscleral treatment, 14 were followed for 2 weeks to 4 weeks, and 14 were followed without treatment. Ophthalmoscopy, fundus photographs, and fluorescein angiography were performed before treatment, immediately after, and weekly during the follow-up. Eyes were examined by light microscopy.

Results: Sclera attenuated laser energy by 31% ± 7%. Immediately after treatment, angiography showed diffuse hypofluorescence in 71% (15 of 21 rabbits). Light microscopy showed vascular occlusion extending at least two thirds of the tumor thickness from the base. Seven of the 14 tumors followed for 15 days ± 8 days were eradicated. There was no correlation between tumor height and eradication.

Conclusion: Rabbit sclera attenuated 31% ± 7% of laser energy. A single transscleral treatment causes tumor vascular closure at the base and may serve as an adjuvant therapy to ensure destruction of deep and intrascleral tumor cells.

This study evaluates the effects of transscleral neodymium: yttrium–lanthanum–fluoride laser at 1,047 nm in experimental choroidal melanoma in rabbits. Rabbit sclera attenuates 31% of laser energy. A single transscleral treatment causes tumor vascular closure at the base and may serve as an adjuvant therapy to destroy deep and intrascleral tumor cells.

*Retina Service, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA; and

Department of Ophthalmology, University of Sao Paulo Medical School, Sao Paulo, Brazil.

Reprint requests: Francisco Max Damico, MD, PhD, Department of Ophthalmology, University of Sao Paulo Medical School, Av. Dr. Eneas Carvalho de Aguiar, 255–6° Andar, São Paulo SP 05403-900, Brazil; e-mail: fmdamico@usp.br

Supported in part by Massachusetts Lions Eye Research Fund.

None of the authors have any financial/conflicting interests to disclose.

© 2014 by Ophthalmic Communications Society, Inc.