The authors report spectral-domain optical coherence tomography findings of laser pointer–induced maculopathy in a 25-year-old man after accidental laser pointer exposure of less than 1 second. The Class 3R laser pointer (output wavelength 532 nm and output power 3.5 to 4.5 mW [continuous wave]) had U.S. Food and Drug Administration certification. One day after exposure, he had visual blurring and metamorphopsia of his right eye. He was treated with a systemic high-dose corticosteroid. Spectral-domain optical coherence tomography disclosed a hyperreflective band in the foveal region. After 1 week of treatment, disappearance of hyperreflectivity was observed on spectral-domain optical coherence tomography. At 6 months, residual disruption of the outer retinal layer at the fovea remained unchanged. Spectral-domain optical coherence tomography was a useful and sensitive tool for evaluating retinal damage and subsequent resolution after treatment.
SD-OCT Features of Laser Pointer Maculopathy Before and After Systemic Corticosteroid Therapy
From the Ophthalmology Department and Ophthalmic Research Center (MH, JB, MS), Labbafinejad Medical Center, Shahid Beheshti Medical University, Tehran, Iran; Shiraz University of Medical Sciences (RS), Kish, Iran; and the Department of Ophthalmology (GAP), University of Arizona Health Science Center, Tucson, Arizona.
Supported by Ophthalmic Research Center of Shahid Beheshti University of Medical Sciences, Tehran, Iran.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Gholam A. Peyman, MD, 10650 W. Tropicana Circle, Sun City, AZ 85351. E-mail: email@example.com
Received: February 18, 2011
Accepted: October 28, 2011
Posted Online: December 16, 2011
Lasers have many applications for science, industry, medicine, and the military. Lasers produce a beam of light that is coherent, monochromatic, and unidirectional, and can converge most of its radiant power over small areas, even at great distances. There is great concern about potential for eye damage by commonly used hand-held laser pointers.1–4
High-resolution spectral-domain optical coherence tomography (SD-OCT) offers extremely high image resolution of macular pathologies.5 We report a case of laser pointer–induced maculopathy in a 25-year-old man after accidental laser pointer exposure of less than 1 second. SD-OCT findings before and after treatment with systemic corticosteroid are described.
A 25-year-old man was referred the day after accidental laser pointer exposure of less than 1 second. He had visual blurring and metamorphopsia of the right eye. The laser pointer was a Class 3R device with U.S. Food and Drug Administration certification (Orion Skyline Deluxe, Santa Cruz, CA) with output wavelength of 532 nm and output power of 3.5 to 4.5 mW (continuous wave). Best-corrected visual acuity was decreased to 20/200 in his right eye and was 20/20 in his left eye. On dilated fundus examination, a yellow-white spot at the center of the foveola was evident (Fig. 1). SD-OCT showed preserved foveal contour with an enhanced rod-shaped full-thickness hyperreflective signal strength in the foveal region extending from the retinal pigment epithelium (RPE) and photoreceptor outer segment to the inner layer of the retina. A small region of hyporeflectance was evident, punching out through the hyperreflecting layer of the outer segments of the photoreceptors and partially into the RPE hyperreflecting layer (Fig. 2). Oral prednisolone (1 mg/kg) was immediately started.
Figure 1. Fundus photograph of right eye of 25-year-old man after accidental laser pointer exposure of less than 1 second shows a foveal yellow spot.
Figure 2. Spectral-domain optical coherence tomography shows full-thickness retinal hyperreflectivity at the foveal region.
Seven days later, symptoms were substantially improved. Visual acuity of his right eye improved to 20/40, but an annoying central visual scotoma and mild metamorphopsia remained. On fundus examination, the foveolar yellow spot was no longer present. Repeated SD-OCT showed resolution of the hyperreflective band, but a small region of hyporeflectance seen on first examination was still evident (Fig. 3). Fluorescein angiography was within normal limits and could not explain the patient’s residual symptoms (Fig. 4). SD-OCT at 6 months showed residual disruption of retinal layers (Fig. 5).
Figure 3. Spectral-domain optical coherence tomography 2 days after treatment with systemic high-dose corticosteroid shows resolution of the hyperreflective band and disruption of retinal layers up to the retinal pigment epithelium/photoreceptors.
Figure 4. Fluorescein angiography 2 days after treatment with systemic high-dose corticosteroid shows no pathologic finding to justify symptoms of vague central scotoma and metamorphopsia.
Figure 5. Fundus photograph (left) and spectral-domain optical coherence tomography (right) at 6 months shows residual disruption of outer retinal layers.
Although laser pointers are accessible—even to the point of being used as children’s toys—there is great concern about their safety. There is controversy surrounding potential damage of the laser pointer beam to retinal tissue.6–9 Some authors believe that macular injury from laser pointers will not cause permanent eye damage, even if used inappropriately.6–8 Robertson et al. reported on radiation safety of widely available laser pointers in a clinicopathologic study of three patients with uveal melanomas who were scheduled for enucleation.8 They documented no fluorescein angiographic or histologic evidence of damage to the eyes.
We present SD-OCT findings of laser pointer–induced maculopathy and correlation of findings with this type of OCT to the patient’s symptoms. Our patient presented with a hyperreflective band on OCT that correlated with funduscopic findings. Decreased visual acuity was consistent with OCT findings, showing abnormalities in the outer and inner segments of the photoreceptors with concurrent involvement of the inner retinal layer in the macular region at presentation. After 7 days of systemic high-dose corticosteroid therapy, OCT revealed resolution of inner retinal hyperreflectivity, which was consistent with visual acuity improvement and funduscopy findings. However, patient complaints of vague central scotoma and meta-morphopsia continued. Fluorescein angiography could not explain symptoms at this stage, but SD-OCT revealed a small region of hyporeflectance disrupting the entire foveal retinal layer with extension to the hyperreflecting layer of the outer segments of the photoreceptors and RPE layer. This finding was closely correlated with residual symptoms. Systemic high-dose corticosteroid therapy rapidly improved full-thickness retinal hyperreflectivity at the foveal region, but SD-OCT revealed full-thickness retinal layer disruption up to the photoreceptor/RPE layers.
SD-OCT facilitates microstructural imaging to an unprecedented histologic level. SD-OCT findings of retinal structural changes in laser pointer maculopathy and their resolution during follow-up closely paralleled the patient’s vague symptoms. SD-OCT findings were invaluable for evaluation of laser pointer–induced macular damage and provided a better understanding of the pathogenesis and prediction of final visual outcome in this case. SD-OCT may provide an objective monitoring tool for possible efficacy of steroid therapy in these patients. The laser pointer described in this report was labeled Class 3R with U.S. Food and Drug Administration certification, indicating potentially damaging laser radiation. We suggest that with the help of sensitive imaging techniques such as SD-OCT, ultrastructurally fine disruption of normal retinal anatomy could be elucidated in such cases. Although in some reports laser pointer macular injury has been described as negligible, SD-OCT investigation may help detect underestimated laser damage in such cases.
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