Optical coherence tomography (OCT) has been shown to be beneficial in the diagnosis of posterior vitreous detachment (PVD) and vitreomacular traction. In 2001, ultrahigh-resolution OCT (UHR-OCT), capable of 3-μm axial resolution in the human eye, has demonstrated refined visualization of outer retinal layers.1 Dramatic advances in the imaging speed of OCT enable high pixel density, high-definition imaging with further improved image quality.2 The following is a case of bilateral photoreceptor disruption secondary to PVD, imaged using high-speed UHR-OCT.
A 66-year-old man underwent cataract extraction and placement of a posterior chamber intraocular lens (PCIOL) in the left eye. One day after surgery, his visual acuity returned to 20/20 OS. One week after surgery, he reported a decline in vision in the left eye associated with a floater. Best-corrected visual acuity was 20/25 OD and 20/40 OS. Anterior ocular examination findings revealed moderate nuclear sclerosis in the right eye and a well-placed PCIOL in the left eye. Dilated fundus examination revealed a Weiss ring in both eyes. In the asymptomatic right eye, high-speed UHR-OCT demonstrated vitreofoveal attachment (seen in some OCT images; image not shown herein), slight foveal thickening, irregular fovea, and minimal interruption of the photoreceptor outer segment layer (Figure, A). In the symptomatic left eye, there was a detached posterior hyaloid with an associated pseudooperculum, interruption of the foveal photoreceptor outer segment layer, and an irregular fovea (Figure, B).
Four months later, visual symptoms had improved in the left eye, although the floater persisted. No ocular symptoms were noted in the right eye. On examination, best-corrected visual acuity was 20/25 OU. Anterior and posterior ocular examination findings remained unchanged in both eyes. High-speed UHR-OCT imaging was again performed, which revealed progression to complete vitreomacular separation in the right eye with return of normal foveal contour, as well as greater interruption of the foveal photoreceptor outer segment layer (Figure, C). In the left eye, the photoreceptor outer segment layer abnormality had decreased, and foveal contour had returned to normal (Figure, D).
This case demonstrates bilateral lucencies within the foveal photoreceptor outer segment layer secondary to PVD as visualized using high-speed UHR-OCT. In the asymptomatic right eye, an increase in photoreceptor disruption was observed on detachment of the posterior hyaloid. In the symptomatic left eye, a larger interruption in the photoreceptor outer segment layer, associated with foveal posterior hyaloid separation, was evident at the initial examination. Four months later, foveal photoreceptors had returned to normal, and visual acuity had improved.
Zambarakji et al3 reported similar OCT findings in patients with macular microholes. Their patients had small foveal lesions evident on biomicroscopy. On standard resolution OCT 3 imaging, most of the patients had small outer retinal defects, and many had partial PVD. In contrast, our patient had no evidence of foveal abnormalities on biomicroscopy. The initial manifestation of our patient's right eye is also similar to cases reported by myself and colleagues.4 However, those patients had vitreofoveal traction without evidence of photoreceptor disruption and with the added symptom of metamorphopsia, which our patient did not have.
This case demonstrates small abnormalities in the outer retina occurring as a result of PVD. These interruptions in the outer segment layer may represent a shift in outer segment orientation causing attenuation of OCT signal or may represent actual outer segment damage. We postulate that these small photoreceptor outer segment abnormalities result from mechanical traction from the detaching posterior hyaloid causing secondary interruption of outer retinal orientation, similar to what may happen in the early stages of macular hole formation. High-speed UHR-OCT aids in visualization of small photoreceptor abnormalities undetected on biomicroscopy. Visual symptoms may occur as a result of outer retinal disruption. Foveal anatomy may return to normal over time, with resolution of visual symptoms.
Correspondence: Dr Reichel, New England Eye Center, Tufts–New England Medical Center, Tufts University, 750 Washington St, Boston, MA 02111 (EReichel@tufts-nemc.org).
Financial Disclosure: Drs Fujimoto and Schuman receive royalties from intellectual property licensed by the Massachusetts Institute of Technology to Carl Zeiss Meditec. Dr Schuman receives research support from Carl Zeiss Meditec.
Funding/Support: This study was supported in part by grants R01-EY11289 and R01-EY13178 from the National Institutes of Health, by grant ECS-01-19452 from the National Science Foundation, and by grant FA9550-040-1-0046 from the Air Force Office of Scientific Research.
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