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Case 1: ProgressionImages from 2022:Subretinal fluid and VA controlled with Eylea q6wks

Case 1: Progression Images from 2022:  

Case 1: ProgressionImages from 2021:DLS still present OS now with large PED adjacent. antiVEGF agent changed to Eylea OS q6wk. SDD conversion to CNVM is often more recalcitrant to treatment.

Case 1: Fundus Photography Images from 2020:SDDs are now obvious OD>OS in ribbon inter-laced pattern, concentrated more superior paramacula 

Case 1: Conversion to CNVM OS Images from 2020:New Double Layer Sign (DLS) was present OS only, FA confirmed leakage from CNVM OS and antiVEGF was initiated (started with Avastin q4wks) 

Case 1: ProgressionWe have been monitoring q6mo with serial OCT and dilated fundus examinations.He continued to monitor with Amsler Grid at homeHas noted no change to VA or Amsler Grid over the next 2 years  Images from 2019: 

Case 1: Diagnosis and Plan Clinically, most would diagnose this patient with age-related drusen or perhaps early AMD. Educate and monitor q1yr. However - due to his significant functional delay (dark adaptation) and presence of SDDs and hypertransmission defects I recommended management of this patient similar to an intermediate AMD patient: Full discussion on

Case 1: baseline OCT 2017  VA 20/20 OD, 20/20 OS 20/20 OS  OCT shows presence of SDDs and significant amount of hyper-transmission defects, especially for how mild the clinical appearance is. Presence of SDDs and a generally “sick” macula is the reason why the dark adaptation is so delayed.

Case 1: baseline Dark Adaptometry 2017 While the maculae did not appear clinically severe, this patient had a significant delay in dark adaptation. He is not adapting even after a 20 minute period. But why does this not match the clinical picture? Neither drusen nor early AMD causes this type of delay.  

Case 1: baseline Fundus Photography 2017 Pinpoint and small, hard drusen noted in the macula OU.Further testing recommended…