April 2014
Volume 55, Issue 13
ARVO Annual Meeting Abstract  |   April 2014
Intravitreal triamcinolone acetonide with anti-VEGF therapy for the management of polypoidal choroidal vasculopathy
Author Affiliations & Notes
  • Gisela Velez
    Central Massachusetts Retina and Uveitis Center, Worcester, MA
    Ophthalmology, Univ of Massachusetts Med School, Worcester, MA
  • Footnotes
    Commercial Relationships Gisela Velez, Allergan (C), Regeneron (C)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 3905. doi:
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      Gisela Velez; Intravitreal triamcinolone acetonide with anti-VEGF therapy for the management of polypoidal choroidal vasculopathy. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3905.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: Polypoidal choroidal vasculopathy (PCV), considered by some a variant of exudative age-related macular degeneration (wet ARMD), is particularly resistant to management with anti-VEGF therapy alone. Although responsive to anti-VEGF agents, complete resolution of subretinal fluid can be a challenge. We explore the use of intravitreal triamcinolone acetonide in a subset of patients resistant to therapy with anti-VEGF agents.

Methods: We performed a retrospective review of all patients with wet ARMD in our practice. Patients with PCV were confirmed by indocyanine green (ICG) angiography (Spectralis, Heidelberg). Nine patients were identified, with a total of 12 eyes treated. Failure to treatment was defined as (1) persistent subretinal fluid (SRF) on SD-OCT (Cirrus 4000, Zeiss); or (2) loss of more than 1 line of Snellen visual acuity (VA).

Results: Seven patients (10 eyes) were treated with a variety of anti-VEGF agents alone, including bevacizumab (1.25mg), ranibizumab (0.5mg) and aflibercept (2 mg). Two patients (2 eyes) were treated with low dose intravitreal triamcinolone acetonide (2mg) in addition to anti-VEGF therapy. Median VA pre and post-treatment was 20/50, with a range from 20/25 to CF. Five eyes (5 patients) responded to anti-VEGF therapy alone. Two eyes (2 patients) were maintained on bevacizumab q 4 weeks. Three eyes (3 patients) were stabilized with intravitreal aflibercept q 4 weeks. Of the 7 eyes (5 patients) that failed treatment, 6 failed as a result of persistent SRF while maintaining stable VA, while 1 eye failed due to loss of vision secondary to hemorrhage. Of these eyes, 3 (2 patients) were treated with aflibercept, while 4 eyes (3 patients) were treated with bevacizumab. Two eyes (2 patients) were treated with supplemental intravitreal triamcinolone acetonide while continuing monthly anti-VEGF treatments. Both patients received 2 injections an average of 14 weeks apart. Both patients achieved complete but temporary resolution of SRF, with a sustained effect of up to 11 weeks. Injections of intravitreal triamcinolone acetonide were tolerated well with no evidence of increased intraocular pressure.

Conclusions: Low dose intravitreal triamcinolone acetonide can be successfully and safely used as a supplement to anti-VEGF therapy in the treatment and management of PCV. Further studies are warranted.

Keywords: 412 age-related macular degeneration • 453 choroid: neovascularization • 487 corticosteroids  

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