Solar retinopathy (also known as, photic retinopathy, foveomacular retinitis, solar retinitis, and eclipse retinopathy) refers to a photochemical toxicity and resultant injury to retinal tissues, usually occurring at the fovea. This entity is commonly associated with sun-gazing or eclipse viewing, and often results in mild-to-moderate visual acuity deficit and/or central or paracentral scotomata. Recovery is spontaneous in nature and occurs over the course of 3-6 months after the inciting event, though visual recovery may be incomplete and patient may suffer from permanent visual acuity deficits and central or paracentral scotomata.
- 1 Disease Entity
- 2 Diagnosis
- 3 Management
- 4 Additional Resources
- 5 References
Disease Entity[edit | edit source]
ICD9: 363.31 Solar Retinopathy ICD10: H31.029 Solar Retinopathy, unspecified eye
Disease[edit | edit source]
Solar (or photic) retinopathy refers to a pathophysiologic entity causing visual disturbance sustained during or after prolonged or high intensity exposure of the foveomacular retinal tissue to light energy.
Etiology[edit | edit source]
The disease entity has been recognized, to some degree since the times of Classical Greece1. While this disease process is classically associated with sun-gazing and eclipse viewing, a number of reports have found phototoxic foveomaculopathy to occur secondary to a myriad of other mechanisms, including from ophthalmic operating microscopes2,5, endoillumination techniques utilized during vitreoretinal surgeries3, occupational hazards such as welding arcs4 and laser pointers8, and even photographical illumination mechanisms6.
Risk Factors[edit | edit source]
Aside from sustained or high-intensity light exposure, common factors predisposing patients to phototoxic injury to the retina include7: 1. Young age 2. Clear intraocular lens 3. Photosensitizing drugs: tetracycline, psoralens 4. Mental impairment 5. Prolonged staring to Sunrise or Sunset under certain drug effects
Protective factors include the following7: 1. High refractive error 2. Cataract 3. Darkly pigmented Fundi
General Pathology[edit | edit source]
Histopathalogic analysis of rhesus monkey retinae after prolonged light exposure helped characterize the histopathologic changes observed in solar other photoxic retinopathies. As early as day 2 post-exposure, major changes were observed mainly in and about the retinal pigmented epithelium (RPE). RPE disruption was evident throughout the exposed area, sometimes associated with choroidal damage. Pigmentary changes of the RPE were noted as macrophages were observed engulfing melanosomes in the subretinal space. Resolution of these findings can be seen by 10 days after injury.10
In 1993, ultrastructural pathologic changes of solar retinopathy were explored by Hope-Ross, et al., who had the cooperation of a 65 year-old man scheduled for enucleation for choroidal melanoma. The patient agreed to stare into the sun 6 days prior to enucleation. Findings included photoreceptor changes including vesiculation and fragmentation of photoreceptor lamellae, the presence of whirls within disc membranes, mitochondrial swelling and nuclear pyknosis. Retinal Pigment epithelial cells in the affected area showed plasma membrane changes, smooth endoplasmic reticulum swelling, and changes in lipofuscin granule structure.11
Pathophysiology[edit | edit source]
The mechanism by which retinal tissue damage occurs in solar retinopathy is photomechanical in nature. Photochemical retinal injury is believed to be a product of free radical formation. Two mechanisms of free radical formation have been proposed. First, absorption of light energy by a molecule causes an electron to enter an “excitation state”, with free radical formation being a means by which such an electron can return to the “ground state” energy level. In returning to the “ground state” energy level, an excited state electron splits a bond within another molecule, forming a free radical.9 Second, light energy absorption can cause excitation of and direct transfer of energy from an intraretinal chromophore – flavoproteins, heme proteins, melanosomes, lipofuscin, and photoreceptors themselves – to oxygen, creating a reactive oxygen species.9 Furthermore, the photochemical injury to the retinal tissues may be thermally enhanced8.
Primary prevention[edit | edit source]
Prevention of solar retinopathy is in fact the mainstay of therapy. Primary prevention of solar retinopathy includes refraining from direct sun-gazing or eclipse-viewing.
Diagnosis[edit | edit source]
Diagnosis is made based on history and examination findings including physical/biomicroscopic examination of the fundus, as well as diagnostic imaging, such as FA and OCT.
History[edit | edit source]
Obtaining a good history is important for making a clinical diagnosis of solar or photic retinopathy. Sun-gazing, eclipse-viewing, occupational hazards such as welding without a welding helmet or welding goggles, repeated flash-photography, recent cataract extraction or other ophthalmologic operative procedures may be endorsed by the patient or may require pointed interrogation. Furthermore, cognizance on the part of the ophthalmologist of solar and other astronomical phenomena, such as solar eclipse, may aid in teasing out pertinent history from patients that raise suspicion for solar retinopathy.
Symptoms[edit | edit source]
Symptoms commonly present within hours of exposure and include blurry vision and central or paracentral blind spot in one, or more commonly, both eyes. Additional complaints may include dyschromatopsia, metamorphopsia, micropsia, frontotemporal headache
Signs[edit | edit source]
Decreased Visual Acuity, usually to a level of 20/25 - 20/100, but possibly worse depending on the extent of exposure.7
Physical Examination[edit | edit source]
A full 8 point examination should be performed on all patients presenting with visual complaints.
Fundus biomicroscopic changes tend to be bilateral, however mild cases may show no fundus abnormalities whatsoever. More moderate to severe cases show dynamic fundus changes. In the first few days after injury, the fundus may display a yellow-white spot at the fovea. Subsequently, this spot may be seen to take on a more red appearing color. This red spot is often surrounded by a halo of pigment. Approximately 2-3 weeks after the injury, a small 100-200 µm lamellar hole or foveal depression can be seen. 7
Diagnostic Imaging[edit | edit source]
Optical Coherence Tomorgraphy[edit | edit source]
OCT of a patient diagnosed with Solar Retinopathy illustrated changes and focal disruption at the level of the sub-foveal RPE and outer retinal bands with an otherwise normal retinal architecture and contour.
Differential diagnosis[edit | edit source]
Add text here
Management[edit | edit source]
Medical therapy[edit | edit source]
No known beneficial treatment exists for solar retinopathy. Prevention is through education is paramount.
Medical Follow-up[edit | edit source]
Regular follow-up through the acute phase of disease is at the discretion of the physician.
Prognosis[edit | edit source]
The bulk of visual acuity improvement has been noted to take place in the first 1 and 6 months after the photoxic event.7,13,14 Despite more moderate vision loss at presentation, most patients ultimately return to a visual acuity level of 20/20-20/40.7 Improvement has been shown to be achieved earlier and more robustly in patients with visual acuity of 0.2 logMAR (20/30 Snellen visual acuity) at presentation.12 Furthermore, a correlation was found between initial visual acuity and fundoscopic appearance 2 weeks after the phototoxic event.12 Unfortunately, metamorphopsia and central or paracentral scotomata, including those that show some improvement initially, may become permanent.7, 14
Additional Resources[edit | edit source]
Add text here
References[edit | edit source]
1. Yannuzi LA, Fisher YL, KruegerA, et al. Solar Retinopathy: A photobiological and geophysical analysis. Tr. Am. Ophth Soc. 1987; 85:120-158.
2. Michels M, Sternberg P, Operating microscope-induced retinal phototocicity: pathophysiology, clinical manifestations and prevention. Surv Ophthalmol. 1990; 34:237-252.
3. Yang C, Shao D, Ding X, et al. Chronic phototoxic maculopathy caused by welding arc in occupational welders. Can J Ophthalmol. 2012; 47(1):45-50.
4. Michels M, Lewis H, Abrams GW, et al. Macular phototoxicity caused by fiberoptic endoillumination during pars plana vitrectomy. Am J Ophthalmol. 1992; 114(3):287-96.
5. Long VW, Woodruff GH. Bilateral retinal phototoxic injury during cataract surgery in a child. J AAPOS. 2004; 8(3):278-9.
6. Tarigopula S, Chod R. Unpublished Case. St. Louis University Eye Institute. St. Louis University, St. Louis, MO.
7. American Academy of Ophthalmology. "Solar Retinopathy." Section 12: Retina and Vitreous. Singapore, 2013-2014. 332-334.
8. Robertson DM, Lim TH, Salomao DR, et al. Laser pointers and the human eye: a clincopathologic study. Arch Ophthalmol. 2000; 118(12):1687-1691.
9. Youseff PN, Sheibani N, Albert DM. Retinal light toxicity. Eye (Lond). 2011; 25(1):1-14.
10. Ham, WT, Ruffolo JJ, Mueller HA, et al. Histologic analysis of photochemical lesions produced in rhesus retina by short-wave-length light. Invest Ophthalmol Vis Sci. 1978; 17(10):1029-35.
11. Hope-Ross MW, Mahon GJ, Gardiner TA, et al. Ultrastructural findings in solar retinopathy. Eye (London). 1993; 7:29-33.
12. Atmaca LS1, Idil A, Can D. Early and late visual prognosis in solar retinopathy. Graefes Arch Clin Exp Ophthalmol. 1995; 233(12):801-4.
13. MacFaul PA. Visual prognosis after solar retinopathy. Brit. J. Ophthal. 1969; 53: 534-41
14. Rothkoff L, Kushelevsky A, Blumenthal M. Solar retinopathy: visual prognosis in 20 cases. Isr J Med Sci. 1978; 14(2):238-43.