RETINAL BURNS IN PHOTIC RETINOPATHY: THREE CASE REPORTS

SUMMARY

Photic retinopathy (PR) is due to retinal phototoxicity, especially affecting the macula, resulting from exposure to sun, welding devices and lasers. It leads to oxidative damage to the retinal pigment epithelium (RPE) and the surrounding photoreceptors. Early recognition of this visual threatening condition, follow-up lesion evolution, and prevention of prolonged ocular exposure to lights is warranted. We herein report the three principal types of retinal burns due to solar retinopathy, laser pointer-induced maculopathy and arc welding maculopathy.

Introduction

Photic retinopathy (PR) is defined as retinal damage, especially affecting the macula. Apart from the classic solar maculopathy, new forms of PR are due to exposure to artificial light, including welding devices and lasers.¹ This phototoxicity leads to reactive oxygen species generation and thus, oxidative damage to the retinal pigment epithelium (RPE) and the surrounding photoreceptors.¹ Therefore, PR is a visual-threatening pathology that may cause permanent retinal injury.²

Material and methods

We aim to offer an integrated view of the three principal types of retinal burns due to PR, involving solar retinopathy, laser pointer-induced maculopathy and arc welding maculopathy.

Results - case reports

A series of three patients, with different PR, underwent history taking and extensive ocular examination, including best corrected visual acuity (BCVA), spectral domain optical coherence tomography (SD-OCT) and 3 x 3 OCT-angiography scans (OCT-A, OptovueRTVue-XR Avanti).

Clinical case 1: solar retinopathy

The first case was a 29-year-old man, with history of sungazing, who presented with blurred vision and central scotoma in his left eye (LE) with BCVA limited to 2/10. Ophthalmological evaluation revealed a normal anterior segment, anda round, yellowish-white discoid macular lesion on fundoscopy (Fig. 1a). SD-OCT showed interdigitation zone discontinuity (Fig. 1b). OCT-A was normal (Fig. 1c). Diagnosis of solar retinopathy was established. Long-term follow-up showed no complications and visual acuity improvement to 10/10 in the LE.

Fig. 1.

Multimodal imaging in solar retinopathy: a) fundus photography of the RE, showing round and yellowish-white discoid macular lesion (yellow arrow); b) macular spectral domain-optical coherence tomography, revealing a localized interdigitation zone discontinuity (yellow arrow); c) optical coherence tomography – angiography of the RE showed no abnormalities.

Clinical case 2: laser pointer-induced maculopathy

The second case was a 26-year-old man, with a history of self-inflicted handheld laser exposure, who presented with blurred vision in his LE. Ophthalmological evaluation showed a BCVA limited to 5/10 in both eyes and a normal anterior segment. Fundus examination disclosed bilateral and asymmetric yellow macular lesions (Fig. 2a,2b). SD-OCT revealed disruption of the ellipsoid zone (EZ) and the retrofoveal RPE. These lesions were more marked in the LE (Fig. 2c,2d). On OCT-A, a localized peri-foveal anastomotic arcade rupture was noted, as well as an irregular central avascular zone with hyporeflective areas in the outer retina and the choriocapillaris layers (Fig. 2e,2f). Our patient had a laser-pointer-induced maculopathy. Long-term follow up revealed VA improvement to 10/10 bilaterally with persistent central scotoma.

Fig. 2.

Multimodal imaging in laser pointer-induced maculopathy: a,b) fundus photography showing bilateral yellow macular lesions – (a) right eye (b) left eye; c,d) spectral domain-optical coherence tomography exhibiting disruption of the ellipsoid zone (EZ) and the retrofoveal RPE more marked in the LE (blue circles); e,f) optical coherence tomography-angiography revealing a localized peri-foveal anastomotic arcade rupture and an irregular central avascular zone with hyporeflective areas in the outer retina and the choriocapillaris layers (red circles) - (e) right eye (f) left eye

Clinical case 3: arc-welding maculopathy

The third case was a 25-year-old man, who performed electric arc welding for a few minutes without wearing a protective device. He subsequently experienced eye discomfort and blurry vision in both eyes. His BCVA was 10/10 in the right eye and 3/10 in the LE. Anterior segment examination revealed the presence of conjunctival hyperemia and superficial punctate keratitis. Fundoscopy of the LE revealed a yellowish spot in the macula with loss of foveal reflection (Fig. 3a). SD-OCT showed subfoveal rectangular hyporeflectivity in the ellipsoid zone (EZ) and the photoreceptor outer segments in the LE (Fig. 3b). OCT-A was normal. Ophthalmologic evaluation after three months revealed a VA improvement to 5/10 in the LE (Fig. 3c). No complications were noted.

Fig. 3.

Multimodal imaging in arc-welding maculopathy: a) fundus photography of the LE, showing a yellowish spot in the macula with loss of foveal reflection; b) spectral domain-optical coherence tomography of the LE, exhibiting subfoveal rectangular hyporeflectivity in the ellipsoid zone and the photoreceptor outer segments; c) macular optical coherence tomography - angiography of the LE was normal.

Discussion

Photic retinopathy results from prolonged exposure to solar radiation or other bright light devices, like flash burns, laser pointers or arc welding lights.² The most frequent causative agent for PR is sunlight, through solar eclipse viewing or sungazing, responsible for “eclipse retinopathy” or “solar retinopathy”.

Solar retinopathy is known as the oldest form of PR. It can occur after sungazing in patients with mental disturbance, or psychotropic drug consumers. Symptomatology is usually bilateral and asymmetric. Patients can complain of visual blurring, scotoma, photopsia or metamorphopsia.²

It has been demonstrated that the retina receives greater radiation, about 100,000 times more compared to the cornea, due to the ocular dioptrium design.³

At first, the physiopathology of solar retinopathy was considered to be a thermal mechanism. However, exposure to the sun results in a temperature rise of 2°C approximately, while protein denaturation is produced beyond an increase of 10°C.^1,4

Therefore, Vos et al. concluded that PR would be caused by a “non-thermal” mechanism, in solar retinal burns. They suggested that the main pathophysiology is a metabolic photochemical phenomenon: indeed, after prolonged light exposure, an oxidation process is produced at a molecular level, and toxic metabolites are generated. Products resulting from metabolic poisoning cause retinal tissue damage, if not rapidly removed.⁴

Acute retinal phototoxicity after use of welding devices is very uncommon. Some cases described retinal lesions occurring after short-time exposure of 30 seconds. Retinal phototoxicity secondary to chronic exposure is more frequent and can be considered as a professional risk.¹

As for laser pointers, both children and adults who misuse this high-powered device, either for demonstration or entertainment, are at risk of self-inflicted retinal injury.⁵ A male predominance was reported. Children, especially those with learning difficulties or behaviour, seem to encounter more danger due to the lack of protective reactions to laser pointers.⁶

Lasers are classified in eight groups, lining up to the UK classification (Class 1, 1C, 1M, 2, 2M, 3R, 3B and 4). The most dangerous category is Class 4. The World Health Organisation (WHO) concluded that “laser pointers higher than class 2 are considered too powerful for general use as laser pointers and present an unacceptable risk in the hands of consumers because they may cause eye injury.”⁷ According to the Food and Drug Administration, tolerated laser pointers should not exceed 5 mW of power within the visible wavelength range, between 400 and 710 nm.⁸

In PR, characteristic anatomic changes during the acute phase are a consequence of the high metabolic rate that causes shedding in the outer retinal segment components.⁹

Several factors contribute to photic-related retinal damage such as the size of the pupil, the degree of retinal pigmentation, the proximity of incident beam to the fovea and the refraction status.¹⁰

SD-OCT imaging has been thought to be a great advance in the diagnosis of photic maculopathy. All types of PR are responsible for retinal structural changes. Chronologic evolution is represented by hyperreflectivity in inner layers at acute stage, and cystlike hyporeflectivity localized in the EZ at chronic stage, as a sign of photoreceptor layer injury. A pathognomonic feature is outer retinal disruption, in association to foveal atrophy and photoreceptors and RPE abnormalities.^2,11,12 OCT-A of choriocapillaris layer is normal in acute PR.

SD-OCT and OCT-A are promising imaging techniques, in the study of PR, bringing information in vivo to better understand its physiopathological mechanisms.

No consensus concerning management of PR is available. Some authors prescribed corticosteroids to treat this entity without scientific evidence.¹ Visual prognosis seems to be good, even in the absence of treatment. Visual acuity may improve or be maintained. Structural changes can reveal EZ recovery on long-term follow-up. However, patients may complain of residual central scotomas. In more severe forms, lesions progressed to lamellar macular holes.^1,2 Subjects exposed to arc welding ought to abandon photosensitizing drugs.

Finally, prevention in this affection remains essential. Indeed, patients with mental disorders as well as long-term psychotropic drug takers are more at risk of solar retinopathy.¹³ Moreover, parents and professionals ought to be aware of the ocular danger of laser pointer and arc welding misuse, especially in children and workers.⁵ This risk should be also considered while manufacturing these instruments, because of their visual threatening consequences.

Conclusion

Retinal burns can result from light toxicity and include different types of photic maculopathies: solar retinopathy as the most classic form and more recently, welding devices and laser pointers. Multimodal imaging techniques including SD-OCT and OCT-A are promising tools to better characterize structural changes in PR. Early recognition of this entity and follow-up lesion evolution is warranted. Prevention from prolonged exposure to sun or artificial light is essential.