June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Topographic OCT Segmentation of Inner and Outer Retina in Progressive Hydroxychloroquine Retinopathy
Author Affiliations & Notes
  • Michael F. Marmor
    Ophthalmology, Stanford University School of Medicine, Stanford, CA
    Byers Eye Institute, Palo Alto, CA
  • Luis de Sisternes
    Radiology, Stanford University School of Medicine, Stanford, CA
  • Julia Hu
    Ophthalmology, Stanford University School of Medicine, Stanford, CA
    Byers Eye Institute, Palo Alto, CA
  • Daniel L Rubin
    Radiology, Stanford University School of Medicine, Stanford, CA
    Medicine (Biomedical Informatics), Stanford University School of Medicine, Stanford, CA
  • Footnotes
    Commercial Relationships Michael Marmor, None; Luis de Sisternes, None; Julia Hu, None; Daniel Rubin, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 1786. doi:
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      Michael F. Marmor, Luis de Sisternes, Julia Hu, Daniel L Rubin; Topographic OCT Segmentation of Inner and Outer Retina in Progressive Hydroxychloroquine Retinopathy. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1786.

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

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Abstract
 
Purpose
 

Progression of hydroxychloroquine (HCQ) retinopathy has been documented before and after cessation of the drug, in proportion to the severity of damage. Several papers have implicated involvement of inner as well as outer retina. We use a new topographic segmentation of the retina to independently assess inner and outer damage both during and after usage of HCQ.

 
Methods
 

A new automated image analysis system developed at Stanford has been applied to produce pixel-by-pixel OCT analysis of different retinal layers across the entire macula. OCT records from a prior clinical study of HCQ patients with retinopathy were re-analyzed to show inner and outer retinal integrity at different stages of retinopathy, and progression after the cessation of therapy.

 
Results
 

The topographic images confirmed a prior finding that in early and moderate retinopathy (no RPE damage), the retina gets slightly thinner only during the first year after HCQ is stopped. However, we found this change resulted entirely from damage to the outer retina, and inner retinal thickness was essentially unaffected by HCQ (even in severe retinopathy with a visible bull’s eye). Prior reports might have recorded inner retinal deformation as it fills in focal parafoveal outer retinal damage. Our topographic images revealed that outer retinal thinning after drug cessation was not limited to a parafoveal bull’s eye zone, but occurred diffusely across the macula. The development of bull’s eye thinning occurred primarily while patients were taking the drug, and before the damage reached the RPE level.

 
Conclusions
 

Topographic segmentation shows clearly that inner retina is not affected by HCQ to any major degree. It also shows that while HCQ toxicity targets the parafovea as it develops during drug exposure, damage after the HCQ is stopped is diffuse across the macula. Finally, it confirms the clinical observations that while visible bull’s eye maculopathy may progress for years after stopping HCQ, progression of HCQ retinopathy is very limited if detected before a stage of RPE damage. This provides a strong rationale for regular screening with sensitive procedures.

 
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