Polypoidal Choroidal Vasculopathy – A Type I Polypoidal Subretinal Neovasculopathy

Gregg T Kokame*
Division of Ophthalmology, Department of Surgery, University of Hawaii John A Burns School of Medicine, Honolulu, Hawaii; Retina Consultants of Hawaii, Honolulu, Hawaii, The Retina Center at Pali Momi, An Affiliation of Hawai’i Pacific Health, USA

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© Gregg T Kokame; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Retina Center at Pali Momi, 98-1079 Moanalua Road Suite 470, Aiea, Hawaii 96701, USA; Tel: 1-808-487-3699; Fax: 1-808-487-8928; E-mail:


This 47 year old female developed the new onset of a polypoidal subretinal neovascular membrane in the left eye 13 years after having polypoidal choroidal vasculopathy (PCV) treated in the right eye. The indocyanine green (ICG) angiography of the left eye at initial presentation showed a normal choroidal vascular pattern without PCV. The new development of a PCV complex on ICG angiography demonstrates that PCV is truly a type of subretinal neovascularization, and not a choroidal vascular abnormality. The optical coherence tomography shows that the polypoidal vascular complex lies above Bruch’s membrane and beneath the retinal pigment epithelium, and not within the choroid. Treatment with high dose ranibizumab (2.0 mg) resulted in excellent polyp closure and regression of the branching vascular network. The documented new development of polypoidal subretinal vessels on ICG angiography and the response to ranibizumab supports that PCV is a polypoidal neovasculopathy (PNV).

Keywords:: Subretinal neovascularization, polypoidal choroidal vasculopathy, ranibizumab, serous retinal detachment, branching vascular network, macular edema.