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Figure 1. Lightning-induced photic maculopathy at the initial visit. A red-free photograph of the right eye (A) and a color photograph of the left eye (B) demonstrate a pale yellow spot with a dark halo at the foveola. Spectral-domain optical coherence tomography (horizontal 6-mm scan) shows a wedge-shaped pattern of hyperreflectivity in the photoreceptor layer with interruption of the external limiting membrane and inner segment–outer segment junction, more prominent in the right eye (C) than in the left eye (D). The central macular thickness is 130 μm OD (C) and 124 μm OS (D). Fundus camera–based autofluorescence shows central dark spots corresponding to the outer lamellar defects in the right (E) and left (F) eyes, with increased autofluorescence signal in the perifoveolar macula.

Figure 1. Lightning-induced photic maculopathy at the initial visit. A red-free photograph of the right eye (A) and a color photograph of the left eye (B) demonstrate a pale yellow spot with a dark halo at the foveola. Spectral-domain optical coherence tomography (horizontal 6-mm scan) shows a wedge-shaped pattern of hyperreflectivity in the photoreceptor layer with interruption of the external limiting membrane and inner segment–outer segment junction, more prominent in the right eye (C) than in the left eye (D). The central macular thickness is 130 μm OD (C) and 124 μm OS (D). Fundus camera–based autofluorescence shows central dark spots corresponding to the outer lamellar defects in the right (E) and left (F) eyes, with increased autofluorescence signal in the perifoveolar macula.

Figure 2. Lightning-induced photic maculopathy at the final follow-up. One year after the initial visit, the central yellow spot has attenuated into a mottled, broken ring in the right (A) and left (B) eyes. Spectral-domain optical coherence tomography shows resolution of central hyperreflectivity and restoration of the external limiting membrane, and the inner segment–outer segment junction shows a minimal residual central defect in the right (C) and left (D) eyes. Autofluorescence images of the right (E) and left (F) eyes reveal normalization of the signal attenuation patterns at the central macula.

Figure 2. Lightning-induced photic maculopathy at the final follow-up. One year after the initial visit, the central yellow spot has attenuated into a mottled, broken ring in the right (A) and left (B) eyes. Spectral-domain optical coherence tomography shows resolution of central hyperreflectivity and restoration of the external limiting membrane, and the inner segment–outer segment junction shows a minimal residual central defect in the right (C) and left (D) eyes. Autofluorescence images of the right (E) and left (F) eyes reveal normalization of the signal attenuation patterns at the central macula.

1.
Norman ME, Albertson D, Younge BR. Ophthalmic manifestations of lightning strike.  Surv Ophthalmol. 2001;46(1):19-24PubMedArticle
2.
Armstrong B, Fecarotta C, Ho AC, Baskin DE. Evolution of severe lightning maculopathy visualized with spectral domain optical coherence tomography.  Ophthalmic Surg Lasers Imaging. 2010;41:(suppl)  S70-S73PubMedArticle
3.
Rivas-Aguiño PJ, Garcia RA, Arevalo JF. Bilateral macular cyst after lightning visualized with optical coherence tomography.  Clin Experiment Ophthalmol. 2006;34(9):893-894PubMedArticle
4.
Gardner TW, Ai E, Chrobak M, Shoch DE. Photic maculopathy secondary to short-circuiting of a high-tension electric current.  Ophthalmology. 1982;89(7):865-868PubMed
5.
Vicuna-Kojchen J, Amer R, Chowers I. Reversible structural disruption of the outer retina in acute welding maculopathy.  Eye (Lond). 2007;21(1):127-129PubMedArticle
6.
dell’Omo R, Konstantopoulou K, Wong R, Pavesio C. Presumed idiopathic outer lamellar defects of the fovea and chronic solar retinopathy: an OCT and fundus autofluorescence study.  Br J Ophthalmol. 2009;93(11):1483-1487PubMedArticle
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Research Letters
May 2012

Optical Coherence Tomography and Autofluorescence Findings in Photic Maculopathy Secondary to Distant Lightning Strike

Author Affiliations

Author Affiliations: Retina-Vitreous Service, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Madurai, Tamil Nadu, India.

Arch Ophthalmol. 2012;130(5):656-658. doi:10.1001/archophthalmol.2011.1807

Ophthalmic injuries due to lightning occur mainly from direct or indirect transmission of electric charge, resistance-induced heat, or heat-induced shock wave.1 Most reports of lightning-induced maculopathy quote direct or indirect electric transmission as the cause and associate maculopathy with oculofacial injuries and sometimes loss of consciousness.13 However, a high-voltage electric current can also induce photic retinopathy without contribution from the electric charge.4 We report a case of photic retinopathy caused solely by viewing a lightning strike.

Report of a Case

A 40-year-old healthy man visited our outpatient clinic with bilateral blurring of vision for 10 days, after watching a lightning strike about 2 m away through an open window. He was not using a computer or telephone at that moment and was not holding or leaning out of the window. He immediately noted a yellow after-image, but he experienced vision decline only after a day. There was no history of smoking, sun gazing, or exposure to a solar eclipse or welding arc. On examination, best-corrected visual acuity was 20/70 N10 OU. Eyelids, adnexa, and anterior segments—including the pupillary reactions—were unremarkable bilaterally. Both fundi showed a faint yellow spot at the central fovea (Figure 1A and B). Color vision, contrast sensitivity, and visual fields (Humphrey 10-2, macular program) were unaffected. The Amsler grid test revealed bilateral metamorphopsia. Spectral-domain optical coherence tomography (OCT; Topcon 1000) showed central hyperreflective echoes and disruption of the inner segment–outer segment junction in each eye (Figure 1C and D). Fundus camera–based autofluorescence (FAF; Zeiss Visupac 450 Plus IR), with excitation and barrier filters set at bandwidths of 510 to 580 nm and 650 to 735 nm, respectively, revealed bilateral increased central hypoautofluorescence and decreased parafoveolar hypoautofluorescence (Figure 1E and F). After 1 month, best-corrected visual acuity improved to 20/50 OD and 20/40 OS; the inner segment–outer segment disruption persisted in each eye. By 12 months, best-corrected visual acuity had improved to 20/25 N6 OD and 20/20 N6 OS. Fundi showed resolution of the yellow spot into a faint ring in each eye (Figure 2A and B). Optical coherence tomography revealed minimal inner segment–outer segment defects (Figure 2C and D); the macular thickness was essentially unchanged. The Amsler grid test showed minimal distortion in each eye. Imaging by FAF revealed normalization of the macular autofluorescence pattern in each eye (Figure 2E and F).

Comment

Photic maculopathy, essentially a photochemical reaction, differs from thermal foveolar burns typically attributed to lightning. Although both primarily affect macular retinal pigment epithelium, thermal energy affects the entire retinal thickness.4 Lightning maculopathy has been reported to consist of bilateral foveal cystic changes that degenerate into foveal atrophy and pigmentary disturbances over time.13 Our patient had more subtle outer retinal involvement, documented by spectral-domain OCT and FAF imaging. The hyperreflectivity and interruption of outer retinal layers, as seen on OCT in our patient, parallel the acute and chronic changes observed in welding arc and solar retinopathy.5,6 dell’Omo et al6 have demonstrated similar OCT and FAF findings in presumed chronic solar retinopathy. They attributed the decreased foveolar signal in solar retinopathy to photoreceptor death, an event unlikely in our patient, who experienced resolution of both OCT and FAF abnormalities along with visual recovery. A plausible mechanism in our case could be increased absorption of FAF signal at the foveola due to accumulation of photoreceptor debris. The increased perifoveal FAF signal was reported to result from increased lipofuscin accumulation or decreased luteal pigment.6 The former mechanism was likely in our case as well, with lightning-induced acute metabolic stress being the cause for transient accumulation of the fluorophore. This article alerts physicians to the potential for phototoxic effects from viewing lightning at close range and adds another dimension to the spectrum of lightning maculopathy.

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Article Information

Correspondence: Mr Shukla, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, 1 Anna Nagar, Madurai 625 020, Tamil Nadu, India (daksh66@gmail.com).

Author Contributions: Mr Shukla had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Financial Disclosure: None reported.

References
1.
Norman ME, Albertson D, Younge BR. Ophthalmic manifestations of lightning strike.  Surv Ophthalmol. 2001;46(1):19-24PubMedArticle
2.
Armstrong B, Fecarotta C, Ho AC, Baskin DE. Evolution of severe lightning maculopathy visualized with spectral domain optical coherence tomography.  Ophthalmic Surg Lasers Imaging. 2010;41:(suppl)  S70-S73PubMedArticle
3.
Rivas-Aguiño PJ, Garcia RA, Arevalo JF. Bilateral macular cyst after lightning visualized with optical coherence tomography.  Clin Experiment Ophthalmol. 2006;34(9):893-894PubMedArticle
4.
Gardner TW, Ai E, Chrobak M, Shoch DE. Photic maculopathy secondary to short-circuiting of a high-tension electric current.  Ophthalmology. 1982;89(7):865-868PubMed
5.
Vicuna-Kojchen J, Amer R, Chowers I. Reversible structural disruption of the outer retina in acute welding maculopathy.  Eye (Lond). 2007;21(1):127-129PubMedArticle
6.
dell’Omo R, Konstantopoulou K, Wong R, Pavesio C. Presumed idiopathic outer lamellar defects of the fovea and chronic solar retinopathy: an OCT and fundus autofluorescence study.  Br J Ophthalmol. 2009;93(11):1483-1487PubMedArticle
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