Self-induced maculopathy in a 12-year-old boy – Tips & Results

A 12-year-old male patient presented to the hospital with complaints of central scotomas in both eyes, worse in the right than the left. He and a friend had been playing with a laser pointer and, over the course of a few hours, experienced multiple bursts of laser light directed at his eyes for 20 to 30 seconds. The laser pointer was 650 nm and had an output power of less than 100 mW.

The patient is not taking any medication and is in good health. Eye history positive for myopia and wears soft contact lenses; However, he did not wear his contact lenses for the examination. His family history is free of charge. His uncorrected visual acuity was 20/80 OD and 20/80 OS. Pinhole visual acuity was 20/60-2 OD and 20/50+2 OS. Amsler grid confirms key shortcomings OU.

Pupils, eye muscles, intraocular pressure, confrotational visual fields and anterior segment examination with slit lamp were normal OU. Posterior segment examination revealed loss of foveal light reflexes and central areas of hypopigmentation OD>OS (illustration 1). Optical coherence tomography (OCT) shows disruption of the outer layers of the retina and focal loss of the photoreceptor integrity line (PIL) OU (numbers 2 and 3). Peripheral examination was normal OU.

diagnosis and discussion

On examination we noticed a central yellowish lesion with irregular borders in both eyes. OCT scans show an area of ​​hyperreflection from the retinal pigment epithelium (RPE) to the outer plexiform layer OU. No obvious cysts or pigment epithelial detachments are noted. Based on the thorough medical history, examination and OCT findings, the patient was diagnosed with laser pointer maculopathy in both eyes.

Laser pointers are ubiquitous and injuries associated with this device are not uncommon. Laser stands for Light Amplification by Stimulated Emission of Radiation; This means that the light emitted by laser devices is usually monochromatic, has the same energy and phase, and can be highly focused (minimally divergent).1 Because of their high focus, lasers can transfer large amounts of energy to a very small area.2 Lasers applied to the human body can have mechanical, thermal and photochemical effects on tissues and cells and can therefore be of therapeutic value. However, if used improperly, they can damage these cells and tissues.2

The amount of energy emitted by a laser is measured in joules (J) and the rate at which that energy is emitted is measured in joules per second or watts (W).2 There is an inverse relationship between energy and wavelength, so the smaller the wavelength, the more energy.3

Related: OCT in glaucoma treatment: green is not always clean

Lasers sold in the United States fall into 4 classifications based on maximum power. Class 1 lasers are the safest and are not believed to damage human tissue. Their maximum output power is less than 0.4mW. Class 2 lasers have a maximum power of less than 1mW and are unlikely to cause damage with short exposures. Class 3a lasers have a power of 1 to 5 mW. These can cause eye injuries if viewed for long periods – most laser pointers sold in the US fall into this category. Class 3b lasers have a power of 5 to 500 mW and can cause eye damage even with very fast vision. Finally, Class 4 lasers have a maximum output power of more than 500 mW. These are military or commercial lasers and can cause significant eye damage.4

Laser pointer retinopathy has similar effects on the retina as that caused by solar retinopathy. Melanin within the retina, particularly the RPE, is highly susceptible to thermal damage.2 The heat from the laser is absorbed by the RPE faster than it can emit it, causing damage.2 Lasers can also cause photochemical damage, particularly in the photoreceptor layer. Laser pulses cause photochemical damage that breaks down the molecular bonds of proteins and nucleic acids.2 Clinically, ophthalmologists see a yellowish lesion and RPE changes shortly after exposure.5.6 OCT scans show subretinal and RPE irregularities as well as cystic spaces and hyper- and hypo-reflectivity in the photoreceptor layer.5.6 Patients commonly report decreased visual acuity, central scotomas, and metamorphopsia.5.6

management and tracking

The prognosis is fairly good in most cases, with many patients reporting a reduction—and in some cases complete resolution—of their symptoms over the course of weeks to months; however, long-term complications such as subretinal and intraretinal hemorrhage, subretinal neovascularization, epiretinal membranes, and macular holes have been reported.7

There are no agreed guidelines, and treatment is observation-only in most cases.2,7,8 There have been reports of oral steroid treatment in animal models, but results have been mixed.2.7 Another area of ​​interest is antioxidants, since photochemical damage often leads to the formation of free radicals. High-dose antioxidants may play a role in maculopathy, but require further investigation.8th

Related: OCT, OCTA show promise in screening for DR

Back to our patient

The interfering laser in this case was probably a class 3a laser, and fortunately it had a longer wavelength (650nm). We had an extensive discussion with the patient and his mother and decided to observe. He was due to return in 3 to 4 weeks, received an Amsler grid and was instructed to return to the clinic as soon as possible should he see any deterioration.

At follow-up, he reported a significant improvement in the size and density of the central scotomas, as well as an improvement in his visual acuity. It was 20/20 in each eye and we noted the return of the foveal reflexes and the resolution of the hypopigmented lesions. OCT scans showed improvement in outer segments OU and macular contour OU. We recommended that he continue Amsler grid testing and follow-up every 6 months. We reviewed the long-term effects of laser damage to the retina and emphasized continued care.

In this case, the patient was lucky in that the outer segments of his retina did not appear to be permanently damaged. In cases with more severe damage, OCT scans often show focal loss of photoreceptors and RPE and the absence of the PIL.

references

1. laser definition. Dictionary.com. Accessed August 11, 2021. http://www.dictionary.com/browse/laser

2. Barkana Y, Belkin M. Laser eye injuries. Surv Ophthalmol. 2000;44(6):459-478. doi:10.1016/s0039-6257(00)00112-0

3. Keating MP. Geometric, physical and visual optics. Butterworth-Heinemann. 2002

4. Peterson JD. Wills Eye patient case series – diagnosis and discussion. Rev Ophalmol. May 2, 2011. Accessed August 11, 2021. https://www.reviewofophthalmology.com/article/wills-eye-resident-case-series-diagnosis-and-discussion

5. Stangos AN, Petropoulos IK, Pournaras JAC, Zaninetti M, Borruat FX, Pournaras CJ. Optical coherence tomography and multifocal electroretinogram findings in chronic solar retinopathy. Am J. Ophthalmol. 2007;144(1):131-134. doi:10.1016/j.ajo.2007.03.003

6. Hossein M, Bonyadi J, Soheilian R, Soheilian M, Peyman GA. SD-OCT features of laser pointer maculopathy before and after systemic corticosteroid therapy. Ophthalmic surgical laser imaging. 2011;42 Online:e135-138. doi:10.3928/15428877-20111208-03

7. Muslubaş IS, Hocaoğlu M, Arf S, Özdemir H, Karaçorlu M. Macular burns from nonmedical lasers. Turk J Ophthalmol. 2016;46(3):138-143. doi:10.4274/tjo.29577

8th. Chen KC, Jung JJ, Aizman A. High-resolution spectral-domain optical coherence tomography results in three patients with solar retinopathy and a review of the literature. Open Ophthalmol J 2012;6:29-35. doi:10.2174/1874364101206010029

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