Choroidal neovascularization following laser pointer-induced macular injury: case report and overview

Neovascularização de coroide após lesão macular induzida por laser-pointer: Relato de caso e revisão de literatura

Abstract

The purpose is to report a case of laser pointer-induced maculopathy and to describe its characteristics using spectral-domain optical coherence tomography (SD-OCT), further the outcome of treatment with intravitreal injections. A 35-year-old man presented with a 6-day history of central vision loss in his right eye (RE) after an accidental laser pointer discharge (wavelength of 532 nm). He underwent a full ophthalmologic examination, including SD-OCT, which suggested the presence of subfoveal choroidal neovascularization (CNV). This was not confirmed due to the unavailability of tools such as fluorescein angiography, indocyanine green angiography and OCT angiography. Best-corrected visual acuity (BCVA) was inicially 20/400 in the RE. Thus, considering a presumed CNV, three intravitreal injections of bevacizumab (the first one combined with triamcinolone acetonide) were performed in the RE. BCVA acuity in his RE improved to 20/25 at 3 months after the first intravitreal injection, with complete resolution of exudation. Over the following 12 months, BCVA remained stable, and no evidence of progression or development of neovascularization was observed. Laser pointer may cause subfoveal CNV when accidently directed toward the eye. In this case, the presumed CNV induced by laser had an excellent response to bevacizumab and triamcinolone acetonide injections.

Keywords:
Lasers; Eye injuries; Choroidal neovascularization; Intravitreal injections; Bevacizumab; Triamcinolone acetonide

Resumo

O objetivo é relatar um caso de lesão macular induzida por laser pointer e descrever suas características utilizando a tomografia de coerência óptica de domínio espectral (SD-OCT), assim como o resultado do tratamento com injeções intravítreas. Um homem de 35 anos apresentou uma história de perda da visão central no olho direito (OD) de 6 dias de evolução após um disparo acidental de laser (comprimento de onda de 532 nm). O paciente foi submetido a exame oftalmológico completo, incluindo SD-OCT, que sugeriu a presença de neovascularização coroidal (CNV) subfoveal. Isso não foi confirmado devido à indisponibilidade de ferramentas como angiografia fluoresceínica, angiografia com indocianina verde e angiografia por OCT. A acuidade visual (AV) com melhor correção foi inicialmente de 20/400 no OD. Assim, considerando uma CNV presumida, três injeções intravítreas de bevacizumabe (a primeira combinada com triancinolona acetonida) foram realizadas no OD. A AV melhorou para 20/25 aos 3 meses após a primeira injeção intravítrea, com resolução completa da exsudação. Nos 12 meses seguintes, a AV permaneceu estável e nenhuma evidência de progressão ou desenvolvimento de neovascularização foi observada. O laser pointer pode causar CNV quando acidentalmente direcionado para o olho. Nesse caso, a suposta CNV induzida por laser teve uma excelente resposta às injeções de bevacizumabe e triancinolona acetonida.

Descritores:
Lasers; Traumatismos oculares; Neovascularização da coroide; Injeções intravítreas; Bevacizumabe; Triancinolona acetonida

Introduction

Light is a portion of the electromagnetic spectrum that is visible to the human eye and is responsible for the sense of sight,⁽¹⁾ while LASER (acronym for Light Amplification by Stimulated Emission of Radiation) is originated by a process of optical amplification based on the stimulated emission of electromagnetic radiation. ⁽²⁾ First produced in 1960, ⁽³⁾ laser has been effectively used in several applications in modern medicine and industry, further for private purposes. High-powered laser pointers have become commercially available and it has been observed an increased incidence of laser pointer induced retinal injuries in several countries, especially in the paediatric population. ^(4-12)

The first case of macular injury induced by laser pointer was reported in 1999, by Luttrull and Hallisey.⁽¹³⁾ Since then, several cases were described. The spectrum of damage ranges from focal photoreceptor defects to macular holes and retinal hemorrhages associated with loss of visual acuity and central scotoma. ⁽¹⁴⁾ Besides, there are a few cases of choroidal neovascularization following laser pointer injury.^(10,15-17)

The purpose of this article is to report a laser-induced maculopathy in a healthy 35-year man and to describe its characteristics using spectral-domain optical coherence tomography, as well as the outcome of treatment with intravitreal bevacizumab and triamcinolone acetonide injections.

Case presentation

A 35-year-old white healthy man presented with a 6-day history of central vision loss in his right eye (RE) after using a laser pointer. He reported an accidental discharge toward his RE while he was testing the device. It was a high-powered laser (200mW), with 532nm wavelength and the pointer was classified as a Class IIIB laser product (Figure 1A).

Figure 1
Laser pointer-induced maculopathy. 1A: Photograph of the device used in the injury with a magnified view (inset) of its label. 1B: Spectral domain optical coherence tomography image taken six days after laser injury shows a subfoveal hyperreflective material above the retinal pigment epithelium (white asterisk), associated with intrarretinal cysts (white arrow), subretinal fluid (red arrowhead) and disruption of the ellipsoid zone (white arrowhead). 1C: Spectral domain optical coherence tomography image taken thirty days after third bevacizumab intravitreal injection shows a remaining pigment epithelial detachment (black arrow), besides disruption of the ellipsoid zone

On examination, his best corrected visual acuity (BCVA) was 20/400 in the RE and 20/20 in the left eye (LE). Biomicroscopy was unremarkable in both eyes and pupillary reflexes were normal. In the RE, fundus examination disclosed an elevated foveal lesion, surrounded by a subrretinal haemorrhage in the parafoveal region. On Spectral-domain optical coherence tomography (SD-OCT) (Cirrus, Carl Zeiss Meditec, Dublin, CA), macular thickness map revealed increased central subfield thickness (429µm). On cross-sectional assessment, a subfoveal hyperreflective material was shown above the retinal pigment epithelium (RPE), associated with intrarretinal cysts, subretinal fluid and disruption of the ellipsoid zone (Figure 1B). Both fundus examination and SD-OCT were normal in the LE. Tools such as fluorescein angiography, indocyanine green angiography and OCT angiography were unavailable.

Presuming a laser-induced CNV, intravitreal injection of bevacizumab combined with triamcinolone acetonide was performed in the RE. One month later, mean central macular thickness decreased from 429 μm to 220 μm and BCVA improved from 20/400 to 20/100. Complete resolution of subretinal fluid and intrarretinal cysts were seen. The patient underwent two additional intravitreal bevacizumab injections in a monthly interval. BCVA and macular thickness evolution during intravitreal injections are shown in Table 1. Final central subfield thickness was 217µm and BCVA was 20/25. Macular scanning presented a residual pigment epithelial detachment, with no signs of activity (Figure 1C). Over the following 12 months, BCVA remained stable, and no evidence of progression or development of neovascularization was observed.

Table 1
Evolution of best corrected visual acuity (BCVA) and central macular thickness

Time	BCVA (Snellen)	Central macular thickness
Before treatment (six days following laser injury)	20/400	429 µm
30 days after first intravitreal injection (Bevacizumab + Triamcinolone Acetonide)	20/200	220 µm
30 days after second intravitreal injection (Bevacizumab)	20/60	219 µm
30 days after third intravitreal injection (Bevacizumab)	20/25	217 µm

Discussion

It is well-known that retina is the most vulnerable structure to laser irradiation, because laser is focused by the refractive media of the eye on a very small retinal point, less than 50 micron in diameter. This focusing results in a very considerable increase in energy concentration, about 10,000 fold higher. Therefore, very little laser energy entering the eye can damage the retina.⁽¹⁸⁾

When laser light reaches a tissue surface, it can be reflected, refracted, scattered, absorbed, or transmitted. The fractional intensity of these different processes depends on the optical properties of the tissue, as well as the laser parameters.⁽¹⁹⁾ The mechanisms of the light interaction may vary according to wavelength, intensity and duration of the exposure. There are three general mechanisms of light induced ocular damage: thermal, mechanical and chemical. In this context, thermal is the most important one in laser injury, since it leads to protein denaturation, loss of cell integrity and secondary inflammatory reactions.⁽²⁰⁾ It is more pronounced in short-wavelength light, like in the reported case (green laser pointer; wavelength 490–575 nm), compared with long-wavelength light (red laser pointer; wavelength 635–750 nm). ⁽²¹⁾

The morphology of retinal injuries caused by laser is highly variable. There are some documented cases of disruption of the outer retinal layers,^(22-24) macular-holes,^(4,5,25-33) retinal haemorrhage,^{(5,25-27,34-36)} and streak-like lesions.^(24,37,38) Laser pointer injury rarely leads to secondary complications, but laser-induced perforation of Bruch’s membrane can cause secondary CNV, like it was seen in a few reported cases^(10,15-17) and in animals models.⁽³⁹⁾

The treatment of retinal injury associated with laser pointer is limited and controversial. Systemic corticosteroids have been used in differing regimes and with differing results.^(20,23) Observation is also an option, as many of these patients will have stabilization of visual acuity over time.⁽¹⁴⁾ However, if a CNV forms as a result of direct trauma from the laser to Bruch’s membrane, a vascular endothelial growth factor inhibitor is recommended to arrest neovascular growth.10 In our case, SD-OCT suggested the presence of subfoveal CNV, but it was not confirmed due to the unavailability of tools such as fluorescein angiography, indocyanine green angiography and OCT angiography. Assuming a CNV, we chose to associate an antiangiogenic drug with an intravitreal corticosteroid, due to the inflammatory nature of the process. After that, we got an excellent result, with central macular thickness decrease and sustained improvement of BCVA.

In conclusion, laser pointers can be harmful to the eye, with several manifestations. Although CNV is very uncommon, it can be found in some cases. Treatment options after laser pointer-induced ocular injury are limited. In our case, association of bevacizumab and triamcinolone played an important role to disease control, besides morphological and functional improvement.

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Publication Dates

• Publication in this collection
  07 Aug 2020
• Date of issue
  May-Jun 2020

History

• Received
  27 May 2019
• Accepted
  3 Sept 2019