Solar retinopathy: A literature review

Abstract

Solar retinopathy (SR) refers to retinal injury that results from unprotected excessive exposure to light. It has been associated with direct sungazing, sunbathing, laser pointers, and welding arc exposure. Symptoms are typically bilateral and are characterized by asymmetric decreased vision, central or paracentral scotoma, photophobia, metamorphopsia, and headache. In most cases, recovery occurs spontaneously with no specific treatment within weeks to 6 months after exposure. However, few cases have been reported in the literature using steroids in acute SR because of their anti-inflammatory effects. The aim of this review is to present an update about this entity, describing the pathogenesis, risk factors, and diagnostic methods, with focus on management and outcomes of SR.

Introduction

Solar retinopathy (SR), which is also known as solar retinitis,[1] photic retinopathy,[2] or eclipse retinopathy,[3] has been recognized for centuries. Most cases that have been documented in the literature were the result of direct sungazing[4] or solar eclipse viewing without proper precautions.[5] It was also reported in welding arc exposure,[6] in sunbathers without a clear history of sungazing,[7] under the influence of some drugs,[8] in individuals following religious rituals,[9] and in patients with mental disorders.[10] With the development of technology, photic maculopathy was described after laser-induced plasma flash exposure,[11] during cataract,[12] and vitreoretinal surgeries.[13] Furthermore, solar retinal injury was documented lately during drone flying without protective eyewear.[14] However, some cases have been reported after indirect sunlight exposure, reflected from water,[1] desert sand,[15] snow,[16] or even screens.[17] Laser pointer maculopathy is a related entity that has increased in incidence in recent years due to the easy access to cheap laser pointers and was described after blue laser pointer exposure.[18] Excessive exposure to light leads to a concentration of photic energy at the macula, ultimately causing photochemical and thermal damage to the photoreceptor cells and retinal pigment epithelium (RPE) that may lead to permanent vision impairment and significant restriction in patient’s ability to perform daily activities.[19] This review aims to provide a comprehensive overview of the course of the disease and discusses prognosis and management of SR.

Methods of Literature Search

A comprehensive search of PubMed and Google Scholar databases was conducted for “SR” and each of the following keywords: solar retinitis, photic retinopathy, eclipse retinopathy, and laser pointer maculopathy. Inclusion criteria were studies documenting SR course with a minimum 1-month follow-up or until complete visual acuity (VA) recovery. Studies not reporting initial or final VA, papers not describing management method, and patients with multiple ocular pathologies were excluded from the review. The search was conducted in May 2023 and was limited to articles that were written in English or the abstracts were in English. All abstracts were screened and relevant articles were included in this review.

This study followed the[20] Preferred Reporting Items for Systematic Reviews and Meta-Analyses of Individual Participant Data guidelines [Figure 1].

Figure 1.

The Preferred Reporting Items for Systematic Reviews and Meta-Analyses of individual participant data flow diagram of the inclusion process

Mechanisms of Retinal Damage

A multifactorial pathogenesis has been proposed in the development of SR. Light can damage the retina through photothermal, photochemical, and photomechanical mechanisms.[21,22] Thermal damage occurs from light absorption by melanosomes of the RPE and melanocytes of the choroid, leading to temperature rise in the retinal tissues. The damage can generate from excess near-infrared radiation[19] and occurs when the temperature in the retina is raised by at least 10°C.[21]

Many investigators observed different mechanisms of retinal light damage in animal studies. The retinal damage was reported in low-energy light sources, suggesting that these low-energy light injuries could not be thermal.[23,24] White et al.[25] showed that chorioretinal temperature elevation in sungazing is far too low for retinal photocoagulation. This was a strong evidence to suggest the combination of photothermal and photochemical injury in SR, or the photochemical injury to the retina may be thermally enhanced.[26,27,28]

Photochemical injury has been observed after long-term exposure to bright light, causing damage in the melanosome of the RPE, followed by subsequent damage in the outer segment layer (perhaps secondary to loss of RPE function).[29] Basically, the damage occurs from excessive illumination with blue light as lipid and protein peroxidation can be seen in RPE cells.[7] The third mechanism of retinal damage is photomechanical, which can occur from acoustic transients and shock waves in the retina created by mode-locked or Q-switched lasers.[21,30]

Risk Factors

Pathology is strongly dependent on intensity, duration of exposure, wavelength light, clarity of the ocular media, ocular pigmentation, individual characteristics, and environmental conditions.[31,32]

SR is more common in people with emmetropia and low hypermetropia because of the refraction state of the eye that focuses the light sharply on the retina.[30] It is also common among young men with clear ocular media.[33] In contrast, cataract development reduces the transmission of radiant energy to the retina and considered a protective factor in the development of SR.[34,35]

Since the lens protects the retina from photochemical damage by ultraviolet (UV) absorption, aphakic and pseudophakic eyes are at greater risk of development SR; however, UV protection is routinely included in intraocular lenses since the 1980s.[30,36]

The amount of radiant energy incident on the retina depends on the pupillary diameter; hence, dilated pupils are associated with an increased risk of retinal damage; therefore, any activity that causes mydriasis such as anxiety, exercise, or some drugs[8] may also predispose individuals to SR.[37]

Environmental conditions also play a big role in SR. Highly reflective surroundings (water, snow, sand, and glass) and reduced atmospheric ozone are considered risk factors in SR.[30] It is more reported among high altitude residents, where UV-B (260–315 nm) radiation increases.[7,38]

Assessment and Diagnosis

Since most patients present with a history of direct sungazing or solar eclipse viewing, thorough history taking is essential in SR. Fundus photography may reveal central foveal changes in the form of a yellow-white spot with reduction of foveal reflex in the acute phase which may fade with time.[32,39]

Spectral-domain optical coherence tomography (OCT) is the most common and reliable tool in the diagnosis of SR. The findings on OCT correlate with time from exposure to examination. If patients present early in the 1^st days after solar exposure, spectral-domain OCT may show focal area of hyperreflectivity in the fovea involving the outer segments of the photoreceptors and RPE that can involve all layers of the retina and disappear later on in the follow-up period.[19,40,41] In late SR, OCT shows characteristic findings of focal disruption of the myoid zone, ellipsoid zone, outer segment layer of photoreceptors, and RPE in the fovea (outer retinal hole) [Figure 2], which considered a common trait in SR.[29,39,42,43]

Figure 2.

Optical coherence tomography of a patient with solar retinopathy showing disruption of outer retinal layers. The arrow points to the foveal outer retinal hole

Fundus autofluorescence (FAF) represents an effective and noninvasive tool that utilizes the fluorescent properties of lipofuscin within the RPE to detect subtle changes in it. Accordingly, FAF may show a well-circumscribed hypoautofluorescent central area that corresponds to the RPE defect surrounded by an irregular halo of hyperautofluorescence.[32,44] It is thought that the hypoautofluorescent area is due to photoreceptor cells loss, secondary to RPE cells injury, whereas the hyperautofluorescent halo is caused by the accumulation of outer segments in the outer retina after photoreceptor cells damage.[44]

Retinal functional changes can be detected using microperimetry that shows areas of decreased sensitivity, presenting central or paracentral scotomas.[19,45] These changes resolve in time and scotomas decrease in size or disappear few months after exposure.[46,47] Retinal function can also be evaluated by multifocal electroretinography which considered an essential sensitive tool in detecting subtle changes in the macula. It can demonstrate macular dysfunction even when other tests cannot detect any changes in the retina.[48,49] Central retinal dysfunction can be revealed as reduced amplitudes in the fovea and the parafovea that improve over time.[48,50] Moreover, residual retinal dysfunction can be verified in patients with complete visual recovery; therefore, it can be very helpful in the diagnosis and follow-up of SR.[47,48]

Management and Prognosis

No specific therapy

The visual prognosis of SR is usually favorable and most patients report a complete recovery of vision with no specific treatment within weeks to 6 months after exposure [studies are summarized in Table 1].

Table 1.

Clinical studies of solar retinopathy with no specific treatment

Study		Number of subjects		Length of follow-up		Outcomes
Michaelides et al.[51]		70 patients		6 months		Complete VA recovery
Choi et al.[2]		1 patient		1 month		Complete VA recovery
Marticorena et al.[17]		2 patients		2–5 months		Complete VA recovery
Dhir et al.[3]		10 eyes		3 weeks–3 months		Complete VA recovery in eight eyes, no change in VA in 1 eye and visual deterioration in 1 eye
Yannuzzi et al.[30]		4 patients		6 months		Complete VA recovery with persisted relative scotoma in all eyes
Hope-Ross et al.[9]		4 patients		6 weeks–6 months		Partial to complete VA recovery with persisted scotoma in all eyes
Rai et al.[52]		319 patients		20 months		Good VA recovery to 20/40 or more in 80% of the patients
Awan et al.[53]		36 patients		7 years		Complete VA recovery in 26 patients, partial recovery in 7 patients and no improvement in 3 patients
Khatib et al.[54]		4 patients		3 weeks–1 year		Complete VA recovery in 3 patients and no improvement in the fourth patient
Moran and O’Donoghue[55]		1 patient		1 year		Complete VA recovery with persisted scotoma in 1 eye
Gregory-Roberts et al.[56]		3 patients		5 months		Good VA recovery
Abdellah et al.[40]		10 eyes		1 year		Good to complete recovery in 9 eyes and partial recovery in 1 eye
Yeh et al.[57]		1 patient		6 months		Poor VA
Eke and Wong[58]		20 patients		21 months		Complete VA recovery and resolution of all symptoms
Alsulaiman et al.[59]		14 patients		Few months		Poor outcome and severe retinal injuries in most patients that required surgical intervention
Zamir et al.[60]		1 patient		2 months		Complete VA recovery with persisted symptoms
Sell and Bryan[61]		1 patient		11 months		Good VA recovery and resolution of all symptoms
Chen et al.[62]		1 patient		4 years		Good VA recovery with persisted pigment epithelium changes

VA: Visual acuity

Michaelides et al.[51] reported the changes in 70 cases of SR from a solar eclipse on August 11, 1999. All patients showed a complete visual recovery and resolution of all symptoms within 6 months postexposure. Good prognosis was also described by Choi et al. presenting a case of retinal injury induced by plasma arc welding exposure. At presentation, the patient suffered from acute loss of vision and central scotoma in both eyes. After 1 month, the patient reported complete visual recovery with the resolution of all symptoms.[2] Marticorena et al. also demonstrated two cases of SR after sunlight exposure reflected from the screen of mobile devices and reported complete visual recovery within 2–5 months after exposure.[17]

However, in some cases, VA did not recover completely and/or patients were still aware of having central scotoma in their visual field over a long period of time. Dhir et al. described ocular changes in patients who suffered from varying degrees of SR during a solar eclipse on February 16, 1980. Eight of the ten eyes who were available for follow-up reported complete visual recovery to 20/20 or better within 3–12 weeks after exposure. Only one patient suffered from visual deterioration in one eye (20/60) after developing a true lamellar macular hole, while the second eye did not show any change in VA.[3]

Yannuzzi et al. reported a series of four young sunbathers who developed SR after sun exposure; however, all of them denied any history of direct sungazing. Three patients were bilateral emmetrope, while the fourth patient was low myopic who wore corneal contact lens at the time of sun exposure. Their VA improved gradually (to 20/30 or better) with no specific treatment within weeks to 6 months after exposure. To note, the presence of a relative central scotoma was documented in all patients at the last follow-up.[30]

Hope-Ross et al. presented four cases of SR following sungazing during religious rituals. All patients complained of visual deterioration and black spots in front of their eyes. Three weeks postexposure, one patient reported improvement of VA to 20/20 in both eyes, whereas she was still complaining of bilateral central scotoma. Two patients were followed up for more than 6 months. One of them reported partial visual recovery (from 20/60 to 20/40), while the other presented with complete visual recovery in his affected eye.[9]

Rai et al. described a large study of 319 patients with SR, 126 of whom had a history of sungazing during a solar eclipse. They found a good prognosis of VA over 20 months of follow-up, as more than 80% of patients reported visual improvement and final VA of 20/40 or more with no specific treatment.[52] Similarly, Awan et al. reported various outcomes of 36 patients with SR who suffered from poor VA after solar eclipse observation. Visual improvement was observed between 2 weeks and 6 months after exposure with complete visual recovery in 26 patients.[53]

In 2014, Khatib et al. published a case series of four patients with acute SR after solar eclipse observation. Three patients reported complete visual recovery to 20/20 with no symptoms within 3 weeks to 6 months after exposure. Unfortunately, the fourth patient had poor VA (20/80) and did not show any improvement over 1-year follow-up.[54]

Moran and O’Donoghue reported a case of bilateral SR that was managed conservatively and observed over 1 year. There was full resolution of symptoms in one eye; however, a central scotoma persisted in the other eye at the end of the follow-up.[55] Gregory-Roberts et al. described VA changes in five eyes of three children who experienced various degrees of visual deterioration from SR. Although ellipsoid and interdigitation zone abnormalities persisted in some eyes at 5 months postexposure, all children reported good VA recovery.[56]

Another study by Abdellah et al. described VA changes in ten eyes over 1-year follow-up. The improvement in VA started 1–2 weeks after solar exposure and reached the maximum at 6 months. After 1-year, nine eyes (90%) showed visual recovery to 20/25 or more, while one eye (10%) showed the modest improvement to be 20/50 from 20/60.[40] Whereas, Yeh et al. presented poor visual recovery in a patient who suffered from SR after sungazing for about 3 h. The patient complained of blurred vision, erythropsia, and central scotoma in one eye. Over 6 months of observation, the patient developed a lamellar hole in the fovea that was detected by OCT with no change in VA (20/200).[57]

Rarely, it may take more than 6 months for complete visual recovery. Eke and Wong described 20 cases of symptomatic SR, after watching the solar eclipse of August 11, 1999. Sixteen patients reported resolution of all symptoms within weeks to months, while four patients still complained of a central scotoma for up to 7 months after exposure. Three patients who were available for follow-up were still aware of a central scotoma in dim lighting conditions at 14 months, and it took them up to 21 months for resolution of all symptoms.[58]

Regarding laser pointer maculopathy, Alsulaiman et al. described a case series of 14 patients who presented with retinal injury after high-power handheld blue laser exposure. Patients suffered from various types of maculopathies including full-thickness macular hole, foveal outer retinal disruption, premacular hemorrhage, and epimacular membrane formation. To note, only four eyes (29%) improved spontaneously with increase in vision, whereas ten eyes (71%) required surgical intervention. The mean VA improved from 20/290 at presentation to 20/35 at last follow-up.[59]

Zamir et al. published a case of photic maculopathy postlaser pointer exposure. The patient presented with decreased vision (20/40) and complains of two small pericentral scotomata in one eye. After 8 weeks, VA improved to 20/20, but a subjective relative decrease in brightness of objects viewed was apparent.[60] Similarly, Sell and Bryan reported a 11-year-old girl who developed unilateral photic maculopathy after diode laser pointer exposure. The patient was examined for the first time 3 weeks postexposure. Her VA was 20/60 in the injured eye, while Amsler grid test revealed a relative central scotoma involving the center 2°. The patient managed conservatively and reported complete resolution of all symptoms with increased VA (20/25) 11 months after injury.[61]

Recently, Chen et al. reported the poor outcome in a case of laser pointer-induced maculopathy. The patient complained of severe bilateral reduced vision to count fingers in both eyes. With no specific treatment and over the following 4 years, VA did not recover completely and slowly improved to 20/30 in both eyes, while the lesions were still present on OCT.[62]

Steroid therapy

Although no specific therapy exists for SR, some studies suggested steroids as treatment in acute SR because of their anti-inflammatory effects.[63,64] Studies are summarized in Table 2.

Table 2.

Clinical studies of solar retinopathy with steroid therapy

Study		Number of subjects		Route of delivery		Length of follow-up		Outcomes
MacFaul[65]		7 eyes		Systemic steroid		1–6 months		Three eyes reported complete VA recovery with persisted scotoma in two of them, 2 eyes showed partial recovery, while 1 eye showed no improvement
Schatz and Mendelblatt[8]		2 eyes		Systemic steroid		4 months		Complete VA recovery with persisted scotoma in both eyes
Weber et al.[66]		2 eyes		Topical steroid		2 months		Complete VA recovery
Bruè et al.[32]		4 eyes		Systemic steroid		4–6 months		Complete VA recovery
Nakamura et al.[67]		2 eyes		Systemic steroid plus sub-Tenon triamcinolone in one eye		21 weeks		Complete VA recovery
Marashi et al.[68]		1 eye		Suprachoroidal triamcinolone acetonide		4 months		Complete VA recovery
Raevis and Shrier[18]		2 eyes		Systemic steroid and topical nonsteroidal anti-inflammatory drug		22 weeks		Complete VA recovery
Mtanes et al.[69]		8 eyes		Systemic steroid		2–12 months		Good VA recovery in all 7 eyes, while one showed no improvement
Cankurtaran and Şekeryapan Gediz[70]		1 eye		Sub-Tenon triamcinolone acetonide		3 months		Complete VA recovery
Farassat et al.[71]		5 eyes		Systemic steroid		2 weeks–96 months		Partial VA recovery in 4 eyes

VA: Visual acuity

In 1969, MacFaul demonstrated visual prognosis of 19 patients with SR, four (seven eyes) of whom received systemic steroid therapy and showed various visual outcomes. Only three (two patients) of the seven treated eyes showed complete visual recovery in 1 month after treatment; however, two (one patient) of them were still able to detect small scotoma in their visual field. Partial recovery was reported in two eyes of two patients; the first eye showed improvement to 20/30 in 1 month, whereas the other was still only 20/60 after 6 months. Unfortunately, one patient showed no improvement in his both eyes (20/80) for over a month; therefore, he was placed on the partially sighted register.[65]

Schatz and Mendelblatt presented the treatment of SR in a patient who gazed at the sun, while he was under the effect of lysergic acid diethylamide. The patient complained of decreased vision and central scotoma in his both eyes; hence, systemic steroid therapy was recommended. At last examination, 4 months after injury, VA completely recovered to 20/20 in both eyes, but the patient was still aware of small scotoma in front of his eyes.[8]

Weber et al. reported a case of bilateral SR in a young girl who suffered from severe visual deterioration and central scotoma in her both eyes. At presentation, her VA was 20/400 and 20/200 and macular pigmentary changes were noted in fundus examination; therefore, topical prednisolone (0.5 mg 5 times daily) was prescribed. Good visual recovery was seen in both eyes and VA returned to normal after 8 weeks.[66] Similarly, in 2013, Bruè et al. described two cases of SR who presented with decreased vision and metamorphopsia in both eyes. After systemic steroid therapy, VA improved gradually and showed complete recovery 4–6 months postexposure.[32]

Later on, Nakamura et al. presented the outcomes of steroid therapy in a bilateral subacute SR. The patient complained of bilateral central scotoma and decreased vision after sungazing several times 7 weeks before his first visit to the clinic. His best-corrected VA (BCVA) was 0.8 in his right eye and 0.7 in his left eye. The patient received oral prednisolone (30 mg per day) with a decrease over a 3-month tapering period and a posterior sub-Tenon triamcinolone injection in his right eye. Visual improvement was noted 9 weeks after initiation of the therapy with an increase to 1.2 in his right eye and 1.0 in his left eye. However, loss of the interdigitation zone was observed on OCT after 12 weeks in the right eye and 21 weeks in the left eye.[67]

Using a suprachoroidal injection of triamcinolone acetonide, Marashi et al. described treating a 17-year-old girl who developed SR after sun exposure. The patient reported decreased vision to 0.4 in one eye, while her VA was 1.0 in the other. Visual improvement was observed 1-week posttreatment and gradually reported complete recovery to 1.0 at week 16.[68]

In 2017, Raevis and Shrier reported a case of bilateral laser pointer maculopathy of a 12-year-old boy who was treated with oral steroids. The patient presented 5 days after exposure with complains about decreased vision (20/40 in both eyes) and central scotoma. Twenty-two weeks after steroid therapy, complete VA recovery was observed in both eyes with no residual scotoma on Amsler grid testing.[18] Later, Mtanes et al. described the clinical finding in seven patients (eight eyes) with laser pointer maculopathy. At presentation, VA ranged from counting fingers to 20/20, while all patients complained of a central/paracentral scotoma in front of their eyes. A round, well-defined deep yellowish-orange discoloration was seen on fundus examination in the fovea. All patients received oral steroids and were followed up for 2–12 months. At the last follow-up, VA was improved to 20/25–20/20 in all eyes except in one which remained poor at counting fingers from two meters with no further improvement.[69]

Cankurtaran and Şekeryapan Gediz described using sub-Tenon triamcinolone acetonide injection in a patient with laser pointer maculopathy. The patient complained about decreased vision (20/32) and paracentral scotoma in one eye; hence, the patient was treated with a sub-Tenon injection of triamcinolone acetonide. Three months posttreatment, complete VA with no treatment-related adverse events was observed.[70]

Recently, Farassat et al. evaluated the long-term outcome of laser pointer-induced maculopathy in seven children (ten eyes). Four children (five eyes) received oral prednisolone, while in the other three children (five eyes), no treatment was prescribed. VA improved slightly in four out of the five treated eyes (median BCVA at the first presentation 20/32, range 20/50–20/20; median BCVA at the last follow-up 20/25, range 20/40–20/20), whereas only one eye in the untreated group reported visual improvement median (BCVA at first presentation 20/20, range 20/40–20/16; median BCVA at the last follow-up 20/20, range 20/40–20/16). However, visual improvement between first and last presentation was not significantly different between both the groups.[71]

Discussion

SR is a self-limited entity with a complete visual recovery within weeks to months in most cases. Rarely, retinal injury may lead to permanent visual impairments and significant restriction in patient’s ability to perform daily activities.[3,65]

MacFaul found that the rate of VA recovery in early stages postexposure is a better guide to prognosis than the degree of initial visual impairment, and if the patient reports early improvement then full recovery can occur within month to six weeks.[65] Atmaca et al. reported that improvement in vision was more prominent and earlier in the eyes that had VA of 20/100 or more after exposure.[72]

Although steroid therapy demonstrated a rapid visual recovery after treatment, no superiority over conservative management was seen regarding final VA as full visual recovery and resolution of all symptoms was not seen in all treated patients.[65] Furthermore, ocular side effects of steroids should be considered when treating patients with SR, such as cataract progression, intraocular pressure elevation, or central serous chorioretinopathy (CSCR).[73] Bouzas et al. reported the development of CSCR in one case of SR posttreatment with steroids, suggesting that localized RPE damage from solar exposure might be the permissive factor in developing CSCR.[73]

Despite isolated cases of success in treating SR with steroids, obviously, the best available treatment in the moment is prevention. Future randomized clinical trials with sensitive imaging tools and long-term follow-up period are needed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.