History of present illness
A 13-year-old boy was referred by an outside ophthalmologist for bilateral reduced central vision for 3 months. The vision loss was painless, constant, and symmetrical. The patient denied any recent trauma. Medical history was significant for multiple psychiatric conditions including attention deficit hyperactivity disorder, depression, generalized anxiety disorder, and posttraumatic stress disorder.
Ocular exam findings
On examination, best-corrected visual acuity was 20/50 in the right eye and 20/60 in the left eye. Intraocular pressures, pupils, confrontational visual fields, and extraocular motility were within normal limits. The anterior segment examination was unremarkable. Dilated fundus examination revealed yellow-gray mottled lesions of the fovea in both eyes ( Fig. 61.1 ).
Imaging
Optical coherence tomography (OCT) and fluorescein angiogram (FA) were obtained. OCT of both eyes showed outer retinal loss with hyperreflective bands extending from the retinal pigment epithelium (RPE), consistent with pigment migration ( Fig. 61.2 ). FA showed hypofluorescence with surrounding hyperfluorescence of the central lesions, consistent with pigment staining ( Fig. 61.3 ).
Questions to ask
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Did the patient have any family history of known eye conditions?
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The patient was adopted with his biological sister, who had no known medical or ocular problems. Other family history was unknown.
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Did the patient have any other systemic conditions?
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Besides the known psychiatric history, the patient denied any other medical problems in the review of systems.
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Did the patient have access to a laser pointer?
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The patient’s parents reported that he did have access to a laser pointer purchased online and often self-isolated in his room playing with the laser.
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Had the patient ever stared into the laser pointer?
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The patient adamantly denied self-harm, though his parents stated that it was highly possible.
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Assessment
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A 13-year-old man without known family history of ocular problems reported subacute onset of bilateral, symmetrical, painless vision loss and was found to have central macular pigment mottling in the setting of prior exposure to a laser pointer.
Differential diagnosis
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Hereditary macular dystrophy, including Stargardt disease
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Solar retinopathy
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Drug-induced toxicity
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Trauma
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Multifocal choroiditis
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Ocular histoplasmosis syndrome
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Placoid retinopathy
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Laser-induced maculopathy
Working diagnosis
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The sudden onset, lack of family history, and exposure to a laser pointer in a young patient with an extensive psychiatric history strongly suggest laser pointer–induced maculopathy.
Multimodal testing and results
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Color fundus photographs reveal foveal pigmentary changes. The fovea is often affected in these patients due to fixation on the laser light source.
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FA demonstrates blockage and staining associated with the foveal pigment mottling. Fluorescein can be helpful in clearly delineating the outline of the pigment clumps. A key diagnostic clue in this and other cases of laser-induced maculopathy is often the presence of vertical linear lesions, which are thought to occur because of a reflexive Bell phenomenon. In the left eye ( Fig. 61.3 ), there is a vertical linear lesion superior to the fovea that is better visualized compared with the fundus photograph.
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OCT through these lesions shows RPE irregularities with intraretinal migration. This can be a useful imaging modality to monitor the patient and observe for any evidence of subsequent choroidal neovascularization.
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Electroretinogram (ERG) can be performed in cases of diagnostic uncertainty when a macular dystrophy is also suspected. In these situations, the full field ERG is normal because the pathology is limited to a small area of the macula only.
Management
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There currently exists no standard of care in treating retinal damage associated with laser-induced maculopathy.
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The severity of damage varies with duration of exposure, device output power, and laser wavelength. Blue laser light is thought to be the most damaging wavelength because of its ready absorption by foveal xanthophyll pigment and melanin.
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In most cases, providers have observed these lesions with spontaneous mild visual recovery noted by some.
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There are a few case reports of improvement with systemic administration of corticosteroids (e.g., 1 mg/kg of oral prednisone), but it is unclear whether these patients would have spontaneously improved without intervention.
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Sequelae such as full-thickness macular hole, epiretinal membrane, and premacular hemorrhage can develop and are usually managed with the standard of care for these conditions (e.g., surgical intervention such as pars plana vitrectomy).
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It is critical to ensure the laser pointer is removed from the patient’s possession and appropriate psychiatric care is established to prevent further self-harm in cases of intentional injury.
Follow-up care
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After initial injury, patients should be followed closely (e.g., monthly) to monitor for worsening and/or continued insults.
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Once stability has been established, follow-up can be slowly extended.
Algorithm 61.1 : Algorithm representing the differential diagnosis of central macular pigmentary changes
