Features

Solar retinopathy describes a focal retinal injury occurring in the setting of intense light exposure, characteristically associated with sun-gazing. It is also known as eclipse retinopathy, eclipse burn, solar retinitis, and solar chorioretinal burn. Historical anecdotes linking direct sun-gazing to ocular damage date back to the time of Plato. Case reports began in the 17th century, and the first fundus findings were described with the advent of ophthalmoscopy in the early 20th century.

The primary mechanism implicated in solar retinopathy is a photochemical retinal injury from intense light exposure. Early studies reported thermal damage from light exposure leading to heat absorption and subsequent protein denaturation. Later studies have articulated the role of photochemical damage inciting free radical formation, DNA injury, and metabolic damage.

The degree of injury in solar retinopathy is determined by the intensity and duration of light exposure. Patients with emmetropia and low hyperopia are at increased risk given the sharp focus of light on the macula. Greater pupillary size at the time of exposure increases risk of retinal damage. Aphakic and young patients are also at greater risk as age-related lens changes yield progressive protective absorption of ultraviolet (UV) light not filtered by the cornea. The dominant eye is also at greater risk given the tendency to squint in the nondominant eye when sun-gazing. Thus, although solar retinopathy is a bilateral process, the damage can be asymmetric between the two eyes.

84.1.1 Common Symptoms

Common symptoms are blurred vision (usually 20/30 to 20/100), central or paracentral scotoma, dyschromatopsia, metamorphopsia, photophobia, and headache. Events preceding the onset of solar retinopathy include eclipse viewing without protective eyewear and protracted sun-gazing. Risk factors include psychiatric predisposition (e.g., schizophrenia), hallucinogenic drug use, or select religious rituals. Occurrence among sunbathers and aviation military personnel has been reported. Patients with direct exposure to visible-light laser pointers may present with similar symptoms. Patients may not readily connect the exposure event to the subsequent symptoms.

84.1.2 Exam Findings

In the acute phase (e.g., 1–7 days after exposure), fundus examination reveals a yellowish-gray spot or spots at or near the fovea (▶ Fig. 84.1, ▶ Fig. 84.2). Approximately 2 weeks after exposure, an oval-shaped outer lamellar defect is evident in the fovea, or juxtafoveal area. There may be associated pigmentary changes if the retinal pigment epithelium (RPE) is involved. In the chronic phase, pigmentary changes may abate, but cystoid or cavitary spaces remain (▶ Fig. 84.3, ▶ Fig. 84.4).

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