Polypoidal Choroidal

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Information about Polypoidal Choroidal

Published on March 21, 2014

Author: badhon821

Source: slideshare.net

Polypoidal Choroidal Vasculopathy Dr. Md Mominul Islam Fellow Vitreo - Retina

Introduction  PCV is an exudative maculopathy with features similar to neovascular AMD with hemorrhage, pigment epithelium detachment and neurosensory detachment.  Pathogenesis mostly unknown  It remains controverial as to weather PCV represents a sub type of neovascular AMD

History • In 1982 By Yannuzzi et al • At annual meeting of American academy of ophthalmology as :-  Polypoidal , subretinal, vascular lesions associated with serous and hemorrhagic detachments of the RPE in a series of patients (10/11 patients were woman).  The entitity was initially called Idiopathic polypoidal choroidal vasculopathy.

History (contd) In 1984 Kleiner et al Described as:-  A peculiar hemorrhagic disorder of the macula and sub retinal pigment epithelium bleeding in middle aged black woman ,which they term posterior uveal bleeding syndrome.  Later a study from the same group of authors showed an expanded clinical spectrum for PCV

Pathogenesis  It is a primary abnormality of the choroidal circulation, characterized by :-  An inner choroidal vascular network of vessels ending in an aneurysmal bulged or outward projection often visible as a reddish – orange, spheroid ,polyp like structure.  PCV primarily involves the inner choroidal vasculature that is well differentiated from the middle and larger choroidal vessels by histology.

Histopathological Features  Kuroiwa reported from surgically excised specimens from 5 patients with PCV had been diagnosed by ICGA :--  Results - arteriosclerosis appears to be an important pathological feature in the choroidal vessels of PCV subjects.

Histopathological Features (Contd) In another histopathologic group : • Nakashizuka et al, who also examined from surgically excised specimens from 5 patients with PCV Results :- little granulation tissue from any of the specimens. On the other hand all the specimen exhibited:- • Massive exudative change and leaking ,all the vessels exhibited hyalinization and chorio-capillaris had disappeared ,in which RPE had been preserved.

Immuno ChemistryThis group demonstrated that : • PCV is not the same as choroidal neovascularization. • CD-34 is a marker of vascular endothelial growth factor • CD-34 staining revealed  Discontinuity in the vascular endothelium.  Smooth muscle actin was negative in hyalinized vessels  There was disruption and injury of smooth cells causing dilation of vessels

Demography Prevalence of PCV in presumed neovascular AMD • US -7.8% • Belgian – 4.0% • Italian - 9.8 % • Greek – 8.2% • Japanese – 23.0-54.7% • Chinese – 22.3% • Korean – 24.6%

Demography (contd)  Varies with age  Predominantly middle aged ,one or two decade earlier than classical AMD  Commonly occur both gender ( more in Asian man than woman)  More prevalent in black, Japanese and other Asian than in white.  Incidence is high in Asian.

Course Natural course of disease is Variable:-  May be relatively stable  May repeated bleeding and leakage with vision loss and chorioretinal atrophy  With or without fibroitic scarring  Reddish- orange nodules alone or nodule and small sub- retinal hemorrhage and absence of hard exudates.  May association with other condition like thrombocytopenia and massive hemorrhage has been reported  Also association with sickle cell disease and irradiation.

Clinical feature Usually bilateral  Protruding orange –red elevated lesion often with nodular elevations of RPE.  Also described as –  Polypoidal lesion ,polyp like or grasp like  Association serous exudation and hemorrhage , that may lead to detachment of the RPE and sometimes neurosensory retina  Sometime associated features recurrent hemorrhage and vitreous hemorrhage.

Clinical feature (contd) Location of the lesion:  In the macular area -69.5%  Under the temporal retinal vascular arcade 15%  Peripapillary area (within one disc diameter of disc edge -4.5%.  Also mid peripheral area

Clinical feature (contd)Lesions may active or inactive. • Lesions considered as active on the evidence of clinical, OCT, FFA any one of the following: 1. Vision loss of 5 or more letters (ETDRS chart) 2. Subretinal fluid with or without intraretinal fluid. 3. PED 4. Subretinal hemorrhage or fluorescence leakage.

ICGA :- • Accepted as the gold standared for diagnosis of PCV. • Better visualization in ICGA than FFA  ICG absorbs and emit near infrared light, which readily penetrates the RPE and enhancing veiwing of choroidal lesions  ICG binding affinity with plasma proteins, that means – it does not leak from chorio-capillaries in the same way as fluorescence, so choroidal lesions are less obscured.

Characteristics feature of PCV in ICGA:-  A branching network of inner choroidal vessels.  Nodular polypoidal aneurysm or dilations at the edge of these abnormal vessels network, which correspond to orange sub-retinal nodules.  Presence of single or multiple focal nodular areas of hyperfluorescence arising from choroidal circulation within the first 6 minutes

Classification According to Japanese group on PCV Quiescent: Polyps in the absence of subretinal or intraretinal fluid or hemorrhage. Exudative : Exudation without hemorrhage, which may include sensory retinal thickening, Neuro-sensory retinal detachment, PED, subretinal lipid exudation. Hemorrhagic: Any hemorrhage with or without other exudative characteristics

Differential Diagnosis  AMD  CSCR

Treatment Thermal laser Photocoagulation: To be beneficial ,albeit it with short term follow up and for extra foveal lesion. In some studies  Improve and stabilize vision- in 55-100%  Vision loss – in 13-45%  Whole lesion compared with polyps only appears to be more efficacious.

Photodynamic therapy:  Regression or resolution of the polyp by in angio occlusive mechanism of action  Restrict loss of letters on ETDRS chart to less than 15 letters or improved vision 80-100% patient after 1 year.

Anti VEGF therapy:  Intravitreal Ranibizumab resolving the macular oedema, polypoidal complexes decreased in 4/12 (33%) eyes.  Intravitreal Bevacizumab 1/11 (9.09%) eyes

Combination therapy:  Both combination therapy and vertiporfin PDT monotherapy superior to ranibizumab monotherapy in achieving complete polyp regression at 6 months.  Improvement in BCVA and central retinal thickness also favored combination therapy.


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