From the University Eye Clinic of Ioannina (MS, AK, EV, NA), Ioannina, Greece. Dr. Kaloudis is in private practice in Corfu, Greece.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Andreas Katsanos, MD, PhD, University of Ioannina, Ophthalmology Department, Leof. Stavros Niarchos, 45500 Ioannina, Greece. E-mail: firstname.lastname@example.org
Lightning accidents represent the second most common cause of death from natural elements after floods in many parts of the world.1 The interactions of lightning with the human body are diverse and unpredictable: direct strike, ground current (from a strike at the victim’s vicinity), contact injury (from a strike on an object that the victim is touching), side flash (from current splashing on the victim from a nearby object), and blast injury (from the lightning-induced shock wave).2 Due to the different mechanisms of tissue damage, a variety of ocular injuries have been described in victims of lightning strikes. For example, eyelid burns, corneal injuries, ocular motility disorders, cataract, optic neuropathy, macular edema and macular hole formation, retinal detachment, choroidal rupture, retinal vascular occlusions, and uveitis have all been reported.3–7
We present the case of a man with lightning-induced chorioretinal burn who was followed up with spectral-domain optical coherence tomography (SD-OCT).
A 60-year-old man without previous ophthalmic and general medical history was referred to the University Eye Clinic of Ioannina, Greece. According to the patient’s report, lightning struck a few meters away the previous day, leaving him with blurred vision in the right eye.
Best-corrected visual acuity was 3/10 and 10/10 in the right and left eyes, respectively. Other findings in the right eye were eyelid swelling, conjunctival hyperemia, superficial punctate keratopathy, mid-dilated pupil with small iris sphincter lacerations, mild anterior chamber flare with +1 cells, and a clear crystalline lens. The intraocular pressure was 23 and 16 mm Hg in the right and left eyes, respectively. Funduscopy revealed normal disc and retinal vessels in both eyes. However, chorioretinal edema with a whitish, fluffy appearance of the posterior pole affecting the macula was noted in the right eye (Figs. 1 and 2). SD-OCT detected significant morphological changes, particularly at the temporal and inferior aspect of the parafoveal region. Figure 3 shows photoreceptor layer thinning, retinal pigment epithelium (RPE) damage resulting in RPE layer unevenness, and abnormal choroidal reflectivity presumably due to loss of the overlying RPE and possibly choroidal damage. Findings in the left eye were unremarkable and no other organ injuries were found.
Figure 1. Funduscopic view of the right eye at presentation. Chorioretinal edema of the posterior pole.
Figure 2. Spectral-domain optical coherence tomography topographic view of the macular area at presentation.
Figure 3. Spectral-domain optical coherence tomography section of the right macula at presentation.
Diclofenac and dexamethasone eye drops three times daily were prescribed in the right eye. Over the next few days, the anterior chamber cleared and the intraocular pressure returned to the mid teens. In the course of several weeks, a gradual extension of the area with clinically evident chorioretinal injury was noted. Nonetheless, the visual acuity improved. At 5 months’ follow-up, the area of chorioretinal damage was larger than at presentation (Fig. 4), the lens remained clear, and best-corrected visual acuity improved to 6/10 and 10/10 in the right and left eyes, respectively. SD-OCT revealed posterior vitreous detachment, several small parafoveal intraretinal cysts, partial recovery of the photoreceptor cell layer thickness, RPE layer unevenness, and reversal of choroidal changes (Fig. 5).
Figure 4. Spectral-domain optical coherence tomography topographic view of the macular area at 5 months of follow-up.
Figure 5. Spectral-domain optical coherence tomography section of the right macula at 5 months of follow-up.
Lightning-induced tissue injuries are caused by the photochemical, thermal, and shock wave (photo-mechanical) effects of the high-voltage discharge.2–4 In this case, the patient had a brief exposure to the electric arc without current actually passing through his body. We assume that lesions such as eyelid edema and iris sphincter ruptures were caused by the shock wave effect of lightning. The mild anterior chamber reaction and the resulting increase in intraocular pressure could be related to vascular damage with blood–aqueous barrier breakdown and mild iritis. The macular lesions may have resulted from a combination of direct photo-chemical, thermal, and shock wave effects. Thus, chorioretinal damage may have occurred primarily due to heat and blunt trauma; this may have caused secondary damage due to vasospasm, edema, ischemia, and reperfusion.3,4 All of these tissue responses have been previously described and may account for the diverse clinical picture often encountered in victims of lightning strikes.4–9 In cases of lightning, the pigment granules contained in the iris, choroid, and RPE may act as resistors to electrical conduction.3 As a consequence, this resistance to electrical current may generate heat that can cause further injury to neighboring tissues. The macular area in particular may be more vulnerable to the thermal effects of high-voltage discharge because the retinal pigment epithelium at this location has a high content of melanin.3 Therefore, the overlying retina and the adjacent choroid may be particularly at risk.
Armstrong et al. also described changes documented with SD-OCT in lightning maculopathy.10 The authors found subfoveal cystic spaces that had already started forming 3 days after the injury but had nearly disappeared approximately 2 months later. In their report, the patient’s visual acuity declined to 1/10 over 4 months due to foveal atrophy. On the contrary, our patient developed small intraretinal cystic spaces adjacent to the foveola. These were clearly evident even 5 months after the incident (Fig. 5). Luckily, our patient’s visual function improved to 6/10 during the follow-up period. Earlier, lower resolution versions of the OCT platform were used by Moon et al.6 and Rivas-Aguino et al.9 to document lightning-induced maculopathy. Unfortunately, potential changes in macular topography were not documented because neither of the reports provided macular OCT images taken shortly after the injury. Similar to our case, however, these reports have shown that functional improvement can occur in the course of months or years. Such differences in clinical severity and prognosis may be attributed to differences in physical properties of the electric discharge, mode of injury due to the variable contribution of photochemical, thermal, and shock wave effects, and dissimilar tissue responses.
This report offers SD-OCT documentation of outer retina and RPE lesions in lightning-induced ocular injury. As evidenced by this case, although sequelae of macular lightning injuries can be sight-threatening, at least some functional improvement may be anticipated. However, long-term follow-up for complications such as cataract or macular hole formation is necessary.
- Curran BE, Holle RL, Lopez RE. Lightning fatalities, injuries and damage reports in the United States from 1959–1994. National Oceanic & Atmospheric Administration (NOAA) Technical Memorandum NWS SR-193. Available at: http://www.nssl.noaa.gov/papers/techmemos/NWS-SR-193/techmemo-sr193.html. Accessed September 2011.
- Ritenour AE, Morton MJ, McManus JG, Barillo DJ, Cancio LC. Lightning injury: a review. Burns. 2008;34:585–594. doi:10.1016/j.burns.2007.11.006 [CrossRef]
- Wu J, Seregard S, Algvere PV. Photochemical damage of the retina. Surv Ophthalmol. 2006;51:461–481. doi:10.1016/j.survophthal.2006.06.009 [CrossRef]
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- Lee MS, Gunton KB, Fischer DH, Brucker AJ. Ocular manifestations of remote lightning strike. Retina. 2002;22:808–810. doi:10.1097/00006982-200212000-00023 [CrossRef]
- Boozalis GT, Purdue GF, Hunt JL, McCulley JP. Ocular changes from electrical burn injuries: a literature review and report of cases. J Burn Care Rehabil. 1991;12:458–462. doi:10.1097/00004630-199109000-00012 [CrossRef]
- Rivas-Aguino PJ, Garcia RA, Arevalo JF. Bilateral macular cyst after lightning visualized with optical coherence tomography. Clin Experiment Ophthalmol. 2006;34:893–894. doi:10.1111/j.1442-9071.2006.01377.x [CrossRef]
- 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:S70–S73. doi:10.3928/15428877-20101031-02 [CrossRef]