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Brief Communication

Peripapillary retinal thermal coagulation following electrical injury

Tandon, Manjari; Agarwal, Aniruddha; Gupta, Vishali; Gupta, Amod

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Indian Journal of Ophthalmology: May 2013 - Volume 61 - Issue 5 - p 240-242
doi: 10.4103/0301-4738.109532
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Abstract

Electrical injury from high-tension wires can result in a significant ocular morbidity. Tissue damage can occur through the transmission of electrical current directly through the tissues, and conversion of electrical energy to thermal energy, which gets subsequently absorbed by tissues, thus causing end-organ ischemia either by generalized vascular constriction or by cardiac arrhythmia. The extent of damage to the tissues depends on the intensity of the current, duration of tissue exposure, and the tissue's resistance to the current.[1] The optic nerve and retina have a low resistance and are thought to be primarily affected by ischemia resulting from coagulation and necrosis of the vascular tissues that feed them.[123] The sequence of events following such an injury to retinal tissues is not known. We report a case which illustrates that the initial acute response following electric shock injury is the retinal opacification with increased retinal thickness that subsequently progresses to retinal atrophy.

Case Report

A 20 year old boy presented to our department with decreased vision, redness and watering of both eyes following electrocution with overhead transmission wires six days ago. The electricity transmission wires were carrying a high voltage of approximately 20,000V. He had multiple eschars on the back, scalp and arms along with facial erythema [Fig. 1]. His best-corrected visual acuity was light perception in the right eye and counting fingers in the left eye with normal intraocular pressures. There was a lid scaling and charring of the eyelashes. Anterior segment examination showed bilateral circumcorneal congestion, sluggish pupillary reactions, superficial punctate keratitis and cataract in the left eye. Fundoscopy revealed an area of peripapillary retinal opacification and a dull foveal reflex in both eyes [Figs. 2 and 3]. Fundus fluorescein angiogram showed a normal retinal circulation with late hyperfluorescence corresponding to the area of opacification. Optical coherence tomography (OCT) showed retinal thickening with few cystoid spaces in the right eye [Fig. 4]. Similar changes were seen the left eye (not shown). Patient was started on oral corticosteroids (prednisolone 30 mg/day) and acetazolamide (750 mg/day in three divided doses). Steroids were given to control inflammation arising from the injury, if any, and oral carbonic anhydrase inhibitor were added to reduce cystic fluid collection by possible stimulation of the retinal pigment epithelium (RPE) pump.[4] Acetazolamide was withdrawn after 1 month and oral steroids were discontinued after another month by gradual tapering. One month later, his best corrected visual acuity was counting fingers 1 meter in the both eyes with posterior subcapsular cataract and peripapillary retinal atrophy in both the eyes [Fig. 5]. OCT of both the eyes showed retinal atrophy with disorganization of all retinal layers and the RPE [Fig. 6]. Patient underwent cataract surgery after 6 months from the time of injury in both the eyes with no improvement in the visual acuity.

Figure 1
Figure 1:
Photograph of the face of the patient in the study following electrical burn showing eschars, erythema and facial erythem
Figure 2
Figure 2:
Fundus photograph of the right eye of the patient in the study at presentation showing areas of peripapillary retinal opacification with a dull foveal reflex
Figure 3
Figure 3:
Fundus photograph of the left eye of the patient in the study at presentation showing areas of peripapillary retinal opacification with a dull foveal reflex
Figure 4
Figure 4:
Optical Coherence Tomography of right eye of the patient in the study at presentation showing presence of retinal thickening and few cystic spaces. The retinal thickening is predominantly nasal with disruption of the inner segment /outer segment (IS/OS) junction and retinal pigment epithelium (RPE). Localized areas of posterior vitreous detachment can be observed
Figure 5
Figure 5:
Fundus photograph of both eyesof the patient in the study taken at 1 month following injury showing almost complete resolution of retinal opacification with appearance of retinal atrophy in both eyes. The area of retinochoroidal atrophy can be seen as patches of pigmented and depigmented retina. Right eye shows pallor of the optic disc and attenuation of inferior peripapillary retinal vessels is noted
Figure 6
Figure 6:
Optical Coherence Tomography of right eye of the patient in the study at one month following injury showing retinal atrophy with disorganization of retinal layers and clumps of photoreceptor cells (left eye not shown)

Discussion

Optic nerve is very good conductor of electricity, with the nerve tissue conducting electricity as any metal rod.[1] The retina usually suffers thethermal effects of injuries in the form of immediate coagulation of proteins and cells,[5] – and thus the initial whitening/opacification of the retina can be explained. The absorption of energy by the RPE results in retinal damage which was evident in the peripapillary and macular area in our patient. A normal fluorescein angiogram indicates that the retinal opacification was not as a result of ischemia, but was due to the thermal coagulation of the retinal tissue. According to a recently published report, peripapillary meridional changes in the eye have been noted in a patient suffering from electric injury. However, OCT changes underlying the pathology have not been studied in that study.[6] Our case illustrates that initial acute response following electric shock injury is the retinal opacification with increased retinal thickness, that subsequently progresses to retinal atrophy.

1. Grover S, Goodwin J. Lightning and electrical injuries: Neuro-ophthalmological aspects Semin Neurol. 1995;15:335–41
2. Al Rabiah SM, Archer DB, Millar R, Collins AD, Shepherd WF. Electrical injury of the eye Int Ophthalmol. 1987;11:31–40
3. 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;12:458–62
4. Marmor MF, Maack T. Enhancement of retinal adhesion and subretinal fluid resorption by acetazolamide Invest Ophthalmol Vis Sci. 1982;23:121–4
5. Miller BK, Goldstein MH, Monshizadeh R, Tabandeh H, Bhatt MT. Ocular manifestations of electrical injury: A case report and review of the literature CLAO J. 2002;28:224–7
6. Jin CJ, Ye HY, Luo GW, Chen WR, Lai KB. Electrical injury induced bilateral peripapillary meridional retino-choroidal atrophy: A case report Retin Cases Brief Rep. 2011;5:237–40

Source of Support: Nil,

Conflict of Interest: None declared.

Keywords:

Cystoid edema; electrical injury; retinal opacification; retinal atrophy

© 2013 Indian Journal of Ophthalmology | Published by Wolters Kluwer – Medknow