KEVIN C. CHEN, MD · JESSE J. JUNG, MD · ALEXANDER AIZMAN, MD

Solar retinopathy is retinal damage that results from exposure to solar radiation.¹ Patients with solar retinopathy classically have a history of sun exposure through religious ritual participation,² solar eclipse viewing without proper precautions,^3,4 or sunbathing,⁵ or from mental disturbances via drug intoxication or schizophrenia.^6-8

Prolonged exposure to light from the operating microscope during ophthalmic surgery⁹ can reproduce solar retinopathy, as can arc welding,¹⁰ although several cases have reported minimal to no sun exposure.^11,12

In this review, we describe the pathogenesis, clinical presentation, imaging, prognosis, and treatment of solar retinopathy.

PATHOGENESIS

Solar retinopathy occurs primarily through a photo-oxidative pathway rather than by direct thermal injury.¹³ The incident thermal damage resulting from looking at the sun through an adaptive pupil is far less than the threshold for detectable damage through ophthalmoscopy.¹⁴

Normal anatomical structures, such as the cornea, absorb and filter the shortest wavelengths of ultraviolet light (UV-C, <280 nm), while the adult lens predominantly absorbs light in the UV-B spectrum (280-320 nm) and part of the UV-A spectrum (315-440 nm) less than 365 nm.^15-17 At the other end of the light spectrum, the aqueous anterior chamber absorbs the longer wavelength infrared (IR) B and C light (1,400-10,000 nm).¹³

Figure. Ophthalmoscopy of the right and left eye of a patient with solar retinopathy, showing a normal macula with a slight reduction of the foveal reflex (top row). SD-OCT showed a maintained foveal contour, juxtafoveal microcystic cavities in the outer retina, increased foveal rod-shaped full-thickness hyper-reflectivity that extended from the outer segments of the photoreceptors and RPE to the inner layer of the retina, and a slight interruption of the external limiting membrane and the inner and outer segment junctions, with disorganized material in the “vitelliform space” (bottom row). CREDIT: HINDAWI PUBLISHING CORP.

Although these structures absorb most of the light spectrum, the longer-wavelength end of UV-A (365-440 nm), visible (400-700 nm), and near IR (IRA, 700-1,400 nm) light can still pass through the ocular media and converge on and under absorption by the photoreceptor and lipofuscin-containing retinal pigment epithelial.¹³

Histopathological studies have confirmed that both the RPE layer and the outer segments of the photoreceptor layer are the most susceptible to damage.

Phototoxicity and Anatomic Damage

This phototoxicity, mainly from the higher-energy UV-A and the shorter wavelengths of visible light, leads to generation of reactive oxygen species and subsequent oxidative damage to these epithelial cells and the surrounding photoreceptors.^18-20

Histopathological studies have confirmed that both the RPE layer and the outer segments of the photoreceptor layer are the most susceptible to damage.^21,22 Specifically, the primary lesion seems to occur in the melanosome-containing RPE layer, followed by subsequent photoreceptor damage, likely secondary to disruption of the supportive RPE.²³

CLINICAL PRESENTATION

Solar retinopathy more commonly occurs in younger patients.⁴ Hypotheses suggest this demographic is most at risk because the clearer crystalline lens at younger ages transmits more light to the retina, including some of the higher-energy UV-B light.²⁴ Men have an increased incidence of solar retinopathy than women.^4,8

Presentation and Symptoms

Patients with solar retinopathy typically present with symptoms of blurred vision, a central or paracentral scotoma, chromotopsia, metamorphopsia, photophobia, and headache.²⁵

The symptoms are often bilateral, but can only affect one eye.²⁵ Even a short duration of exposure can produce significant retinal damage, as authors have reported as little as one minute of fixation on the sun causing solar retinopathy.²⁶ Snellen visual acuity following exposure can range from 20/20 to counting fingers, but it is typically 20/40 to 20/60.

The fundus examination in solar retinopathy may initially appear normal or have macular edema that resolves.^27,28 However, after a few days it can develop a small yellowish-white spot with surrounding gray, granular pigmentation in the central fovea.¹⁹ This foveal spot may evolve over weeks into a well-circumscribed red spot, which some authors have described as pathognomonic.¹

IMAGING FINDINGS

Doctors have used multiple imaging modalities to evaluate solar retinopathy, including fundus autofluorescence (FAF), fluorescein angiography (FA), multifocal electroretinography (mfERG), and OCT

Fundus Autofluorescence And Fluorescein Angiography

FAF in solar retinopathy appears as a well-circumscribed, hypoautofluorescent fovea surrounded by an irregular ring of hyperautofluorescence.²⁹

The decreased fluorescence seems to correspond to a deficiency of lipofuscin, presumably from loss of RPE cells or photoreceptors, with consequent reduced accumulation of lipofuscin in the underlying RPE.²⁹

One report described FAF findings from five eyes of patients with clinical and time-domain OCT (TD-OCT) findings similar to solar maculopathy, but one limitation of this case series was that no patient reported a history of solar exposure.²⁹

FA may show punctate, central RPE transmission or window defects correlating with damage to the RPE and photoreceptors, as seen on histopathology as well as OCT. However, these findings may be subtle and not reliably present in all cases of solar retinopathy.¹⁹

Multifocal Electroretinography

Initially, mfERG may show reduced function in the para-fovea and perifovea that generally improves over time.³⁰ Although reduced function of the photoreceptors may occur acutely, examinations of latencies with mfERG typically show normal response times.³⁰

Functional deficits on mfERG mainly persist in chronic cases,³¹ making it a helpful adjunctive test in the diagnosis of chronic solar retinopathy.

OCT

The most sensitive diagnostic imaging technique to detect changes in solar retinopathy is OCT. Using TD-OCT, Bechmann and colleagues first described solar retinopathy as a hyper-reflective area at the fovea with all retinal layers affected.³²

Since this initial series, other OCT observations have appeared, including transient increase in foveal reflectivity,³² reduced reflectivity from the RPE,^{20,25,31,33-35} and disruption of the inner and outer segments of the photoreceptor layers.^31,33-44

In our prior case series of six eyes using high-definition spectral-domain OCT, we also observed that the inner and outer photoreceptor segments were damaged without underlying RPE defects.⁴⁵

ACUTE VS CHRONIC RETINOPATHY

Reviewing the literature based on reported OCT findings, acute changes seen on OCT predominantly include the RPE and outer photoreceptor segments, while chronic changes, defined as more than one year from exposure, primarily affect the inner and outer photoreceptor segments.^18,25,45

This pathology agrees with the proposed mechanism of injury; the RPE layer initially absorbs solar radiation, leading to acute damage followed by secondary dysfunction of the photoreceptor segments.¹⁸ In addition, the RPE can regenerate itself in a matter of weeks following damage, so RPE damage is less common in chronic vs acute solar retinopathy.^45,46

In contrast, photoreceptors cannot self-propagate because they are postmitotic,¹⁸ so they are more likely to remain damaged in patients with chronic retinopathy.⁴⁵

Long-term Changes

Worse long-term vision is significantly related to the presence of photoreceptor layer damage on OCT. In our literature review, inner photoreceptor segment lesions were correlated with worse BCVA.⁴⁵ Lesions elsewhere in the retina, including the RPE, inner high reflective layer, and outer photoreceptor segment layer, did not show a statistically significant relationship with decreased visual acuity.⁴⁵

These findings suggest that patients with extensive phototoxic damage involving the inner photoreceptor layer are most at risk for chronically decreased VA from baseline.

PROGNOSIS

The decreased VA in solar retinopathy can be transient and self-resolving, lasting less than one year.²⁰ Studies have noted that the VA in solar retinopathy is correlated with initial VA,⁴⁷ initial rate of recovery,⁴ and degree of visual impairment.⁴⁸

In a study following 86 eyes after solar eclipse exposure, eyes with pre-exposure acuity of 20/50 or better had an earlier and more favorable visual recovery.⁴⁷ In his case series, MacFaul noted that early improvement helped to predict full recovery within one to two months.⁴

Long-term VA

The degree of initial visual impairment is also important in final VA, with eyes with visual acuity no worse than 20/70 after exposure showing the best recovery in one case series.⁴⁸

While visual acuity has the potential to recover to baseline, some patients continue to experience small central or paracentral scotomas.^4,25,33 The extent of pathology may vary with the intensity, duration and light spectrum of solar exposure, ocular pigmentation, the clarity of the ocular media, and environmental conditions, such as highly reflective surroundings and reduced atmospheric ozone.³¹

TREATMENT

No guidelines exist for the treatment of solar retinopathy. Several case reports of solar retinopathy have reported the use of steroids in the treatment of macular edema with equivocal results.^4,8,21,27

In one case report, a patient with solar retinopathy was treated with systemic corticoidsteroids, which are a known risk factor for central serous chorioretinopathy. That patient developed signs of CSC after one month.⁴⁹

Physicians should be cautious if they decide to treat with steroids because of their well-known side effects, the self-resolving nature of the macular edema in solar retinopathy, and a potentially increased risk of developing CSC after solar-induced impairment of the RPE barrier function.

Worse long-term vision is significantly related to the presence of photoreceptor layer damage on OCT.

Free Radicals and Antioxidants

Because free radicals are believed to be the mechanism through which light energy damages the retina, some researchers have studied antioxidants in animal models of solar retinopathy. These results have shown that steroids may confer a retinal protective benefit from light exposure.^50,51

The Age-Related Eye Disease Study showed an advantage of several antioxidants in AMD,⁵² a separate clinical entity from solar retinopathy but one that shares similarities in its proposed pathogenesis with dysfunction of the RPE⁵³ and elevated risk from UV light exposure.⁵⁴ A study specifically looking at antioxidant use in human eyes with solar retinopathy would help to describe their potential role in future management.

Because the only way to avoid solar retinopathy and its potential chronic complications is to prevent exposure, physicians should counsel patients to protect their eyes from excessive light. This includes avoiding direct laser exposure and sun gazing, use of a pinhole camera to view solar eclipses, and wearing industrial-grade protective eyewear during arc welding.

CONCLUSION

Solar retinopathy occurs with high-energy light exposure to the retina. Patients present with an acute worsening of VA that may last several weeks to months, but this deterioration generally resolves without treatment.

Although VA may return to baseline, scotomas may persist, reflecting permanent damage to the photoreceptors. Avoidance of sun exposure is critical in decreasing the incidence of this disease. RP

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