To describe the sequential evolution of outer retinal tubulations (ORTs) in patients diagnosed with choroidal neovascularization and/or retinal pigment epithelium atrophy.
Retrospective evaluation of spectral domain optical coherence tomography of a consecutive cohort of patients with various retinal conditions.
We reviewed the clinical findings of 238 eyes of 119 consecutive patients (54 men and 65 women) with a mean age of 76.2 ± 14.2 years (range: 57–90) and a mean follow-up of 3 ± 1.6 years (range 1–7). Over the follow-up period, ORTs were diagnosed in 67 of 238 eyes (28.1%), 9 of which were imaged with sequential, eye-tracked spectral domain optical coherence tomography dating from the beginning of ORT formation. The presence of geographic atrophy and subretinal hyperreflective material at baseline were found to be risk factors for ORT development (P < 0.001 and P < 0.001, respectively). Outer retinal tubulations were divided into forming versus formed morphologies. The latter was comprised open and closed ORTs of which the open subtype was the most common. The formation of ORTs was significantly associated with microcystic macular lesions in the inner nuclear layer and the downward displacement of the outer plexiform layer, referred to as the outer plexiform layer subsidence sign (P < 0.001).
Outer retinal tubulation is a frequent optical coherence tomography finding in eyes with choroidal neovascularization and geographic atrophy. Open ORTs with progressive scrolled edges and shortened diameter were significantly associated with microcystic macular lesions in the inner nuclear layer and the outer plexiform layer subsidence sign.
Outer retinal tubulations were divided into forming versus open and closed outer retinal tubulations. Open outer retinal tubulations with progressive scrolled edges were significantly associated with microcystic macular abnormalities in the inner nuclear layer and the outer plexiform layer subsidence sign. The pathophysiology of inner nuclear layer microcystic macular abnormalities may involve Müller cell degeneration.
*Division of Ophthalmology, University of São Paulo Medical School, São Paulo, Brazil;
†Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, California; and
‡Greater Los Angeles Veterans Affairs Healthcare Center, Los Angeles, California.
Reprint requests: Rony C. Preti, MD, PhD, Av. Ramalho Ortigão, 269 ap. 54, Vila Gumercindo, CEP 04130-010, São Paulo, Brazil; e-mail: firstname.lastname@example.org
None of the authors has any financial/conflicting interests to disclose.