March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
Pattern of Retinal Ischemia during Acute Retinal Hypoperfusion
Author Affiliations & Notes
  • Feng Liang
    CHNO des 15-20, Paris, France
  • José-Alain Sahel
    CHNO des 15-20, Paris, France
  • Jean-françois Girmens
    CHNO des 15-20, Paris, France
  • Michel Paques
    CHNO des 15-20, Paris, France
  • Footnotes
    Commercial Relationships  Feng Liang, None; José-Alain Sahel, None; Jean-françois Girmens, None; Michel Paques, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5652. doi:
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      Feng Liang, José-Alain Sahel, Jean-françois Girmens, Michel Paques; Pattern of Retinal Ischemia during Acute Retinal Hypoperfusion. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5652.

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

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Purpose: : The retina may be affected by several diseases leading to an acutely decreased blood flow and hence global ischemia. Yet, little is known about the locoregional variations of the sensitivity of the retina to ischemia. The aim is to document the topography of acute retinal ischemia in patients with panretinal hypoperfusion.

Methods: : Clinical examination and spectral domain optical coherence tomography (SD-OCT) imaging were performed in patients with acute retinal hypoperfusion, due to central artery occlusion (CRAO, n=5), central vein occlusion (CRVO, n=5), and CRVO with cilioretinal artery infarction (n=3) at presentation and at 1 year follow-up. SD-OCT from mice with branch AO were also analyzed.

Results: : Acute ischemia led to a highly reflective inner nuclear layer (INL). With increasing severity of hypoperfusion, focal retinal edema extended more or less laterally and toward the vitreoretinal interface. During follow-up, INL atrophy occurred in the previously oedematous territory, sparing the outer nuclear layer. Surprisingly, the nerve fiber layer was spared in all cases except CRAO. Final vision depended on the preservation of the papillomacular bundle of axons. In mice, BRAO led to opacification of the inner nuclear layer and outer part of the inner plexiform layer, sparing the immediate vicinity of adjacent veins. From these results a model of extension of cytotoxic edema in relation to the severity of ischemia is proposed.

Conclusions: : During acute hypoperfusion, that is, with persistence of residual flow, the observed pattern of retinal ischemia sensitivity matches the distribution of oxygen from precapillary arterioles, hence supporting the theory of Krogh cylinders. Axons that are located closely nearby the arterioles are less affected by acute ischemia, probably accounting for the elective preservation of the papillomacular bundle during a cilioretinal artery occlusion. Similarly, this may account for the elective sensitivity of the subvenular INL area, which is the area located farthest from arterioles. In BRAO, the opposite pattern is seen, i.e. there is sparing of the perivenular retina. Acute, global retinal ischemia due to generalized hypoperfusion affects differentially retinal layers. Subvenular INL is the area the most sensitive to acute ischemia. From a clinical point of view, these findings are useful for the retrospective diagnosis of an episode of acute retinal hypoperfusion.

Keywords: imaging/image analysis: clinical • retina • vascular occlusion/vascular occlusive disease 

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