0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Research Letters |

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

Dhananjay Shukla, MS, MAMS; Abhishek Sharan, MS; Ramesh Venkatesh, MS
[+] 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.
Text Size: A A A
Published online

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.

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).

Place holder to copy figure label and caption
Graphic Jump Location

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.

Place holder to copy figure label and caption
Graphic Jump Location

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.

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.

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.

Norman ME, Albertson D, Younge BR. Ophthalmic manifestations of lightning strike.  Surv Ophthalmol. 2001;46(1):19-24
PubMed   |  Link to Article
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-S73
PubMed   |  Link to Article
Rivas-Aguiño PJ, Garcia RA, Arevalo JF. Bilateral macular cyst after lightning visualized with optical coherence tomography.  Clin Experiment Ophthalmol. 2006;34(9):893-894
PubMed   |  Link to Article
Gardner TW, Ai E, Chrobak M, Shoch DE. Photic maculopathy secondary to short-circuiting of a high-tension electric current.  Ophthalmology. 1982;89(7):865-868
PubMed
Vicuna-Kojchen J, Amer R, Chowers I. Reversible structural disruption of the outer retina in acute welding maculopathy.  Eye (Lond). 2007;21(1):127-129
PubMed   |  Link to Article
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):1483-1487
PubMed   |  Link to Article

Figures

Place holder to copy figure label and caption
Graphic Jump Location

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.

Place holder to copy figure label and caption
Graphic Jump Location

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.

Tables

References

Norman ME, Albertson D, Younge BR. Ophthalmic manifestations of lightning strike.  Surv Ophthalmol. 2001;46(1):19-24
PubMed   |  Link to Article
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-S73
PubMed   |  Link to Article
Rivas-Aguiño PJ, Garcia RA, Arevalo JF. Bilateral macular cyst after lightning visualized with optical coherence tomography.  Clin Experiment Ophthalmol. 2006;34(9):893-894
PubMed   |  Link to Article
Gardner TW, Ai E, Chrobak M, Shoch DE. Photic maculopathy secondary to short-circuiting of a high-tension electric current.  Ophthalmology. 1982;89(7):865-868
PubMed
Vicuna-Kojchen J, Amer R, Chowers I. Reversible structural disruption of the outer retina in acute welding maculopathy.  Eye (Lond). 2007;21(1):127-129
PubMed   |  Link to Article
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):1483-1487
PubMed   |  Link to Article

Correspondence

CME
Also Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
Please click the checkbox indicating that you have read the full article in order to submit your answers.
Your answers have been saved for later.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.

Multimedia

Some tools below are only available to our subscribers or users with an online account.

1,088 Views
0 Citations
×

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections
Jobs