Electric Shock Retinopathy: Case Report of a Late Retinal Manifestation

Abstract

Purpose:

This is a case report of a male patient who suffered a high-voltage electrical burn and presented with bilateral pigmentary retinopathy.

Methods:

A 40-year-old man presented with bilateral vision loss following a high-voltage electrical injury sustained 10 years earlier. Family history, ocular history, and anterior segment evaluation were unremarkable.

Results:

Fundus examination revealed bilateral optic disc pallor, widespread areas of chorioretinal atrophy, and pigmentary changes surrounding the optic disc that partially involved the macula with some spared areas located on the superior retina.

Conclusions:

Retinal manifestations following a high-voltage electrical injury can resemble other hereditary and inflammatory diseases with similar clinical patterns, therefore, a meticulous family, medical, and clinical evaluation is essential.

Introduction

High-voltage electrical currents may produce damage in ocular tissues at several levels, and many factors including cell membrane disruption, heat generation, vasoconstriction, and ischemia may result. The most common reported injuries are cataracts ^{1 -3}  and macular and retinal alterations. ^4,5

Several mechanisms, including direct transmission from the electrical current through tissues, thermal burn, tissue ischemia, or even direct mechanical injury from the electrical shock wave, warrant consideration. ^{6 -8} Electrical currents travel through the retinal pigment epithelium (RPE) cells, then create heat and produce tissue damage; the absorption of energy by the RPE cells contributes to the damage of the overlying retina. ⁵  Because higher concentrations of melanin pigments are found in the macula (thicker and tightly packed RPE cells), it causes more production of heat and thermal damage; additionally, although the macula is the most affected site, the entire retina can be affected. ⁹  Macular manifestations include full-thickness macular hole, macular edema, and cysts. ^8,10,11

The extent of tissue damage depends on the current intensity, tissue exposure time, and tissue resistance to the current. ^6,12,13  Damage to the optic nerve is mainly caused by its low resistance to electrical currents and by ischemia. ^4,6  Retinal abnormalities from high-voltage electrical currents can be nonspecific and highly variable (eg, retinal edema, pigmentary alterations, macular hole, chorioretinal rupture, vitreous hemorrhage, central vein occlusion, and retinal detachment). ^4,5  We report a case of a patient who suffered a high-voltage electrical burn and presented with a bilateral pigmentary retinopathy as a late manifestation several years after the accident.

Methods

Case Report

A 40-year-old man presented with bilateral visual loss from an electrical injury suffered 10 years earlier. Electrocution resulted from a work-related incident when his head accidentally touched an exposed electrical wire; he also reported a brief period of unconsciousness. At that time, he reportedly sustained multiple burns (head, scalp, back, and arms) and he required minor facial surgeries. Several months after the accident, his vision began to worsen and he was diagnosed with bilateral cataracts; phacoemulsification with intraocular lens implantation was performed at that time with no improvement of visual acuity (VA). No significant family or ocular history was documented, and at that time, the patient was clinically diagnosed as having a bilateral pigmentary retinopathy.

Results

Ten years after this injury, at the time of presentation, the patient’s best-corrected VA was counting fingers and 1.3 (Snellen 20/400; logarithm of the minimum angle of resolution) in the right and left eye, respectively. An in-the-bag intraocular lens was found in the anterior segment evaluation of each eye; the rest of the exam was unremarkable. Both fundi showed pale optic discs and an extensive area of chorioretinal atrophy surrounding the optic nerve (which extended up to the midperipheral fundus) that partially involved the macula, associated with widespread RPE hyperplasia, with some spared areas seen on the superior retina (Figures 1 and 2). Optical coherence tomography (OCT) images showed diffuse severe choroidal and retinal atrophy in the affected areas with retinal thinning of the outer retinal layers of the less-affected superior retina (Figures 1 and 2). Fluorescein angiography (FA) showed extensive areas of hypofluorescence and hyperfluorescence due to a blockage and transmission window defects, respectively (Figure 3). The patient also had burn scars on his head, scalp, left hand, and leg.

Figure 1.

On the left side, color fundus photography of the left eye shows extensive peripapillary chorioretinal atrophy with widespread retinal pigment epithelium hyperplasia, pale optic disc, and normal spared superior retina with mild generalized vascular attenuation. On the right side, optical coherence tomography images of the areas corresponding to the white dotted lines in the fundus photograph reveal severe choroidal and retinal atrophy in affected areas and diffuse retinal thinning on the less-affected superior retina.

Figure 2.

On the right side, color fundus photography of the right eye shows extensive peripapillary chorioretinal atrophy with widespread retinal pigment epithelium hyperplasia, pale optic disc, and normal spared superior retina with mild generalized vascular attenuation. On the left side, optical coherence tomography images reveal corresponding areas (white dotted lines) of severe choroidal and retinal atrophy in affected areas and diffuse retinal thinning on the superior less-affected retina.

Figure 3.

Fluorescein angiography of both eyes shows extensive areas of hypofluorescence and hyperfluorescence due to blockage and transmission window defects, respectively. Optical coherence tomography images reveal choroidal and retinal atrophy in affected areas and diffuse retinal thinning on the less-affected superior retina (white dotted lines, respectively).

Injuries resulting from high-voltage electrical injuries can be very severe, and the resulting damage can be related to several mechanisms. ⁶  For example, the direct transmission of high-voltage electrical currents through tissues generates cell membrane disruption and direct cell injury. ^12,13  The acute cell membrane depolarization also leads to cellular dysfunction and death. ¹³  Electrical injuries induce tissue damage by converting electricity into heat-producing thermal burns; additionally, the thermal energy generates dissipated heat and causes severe burns at the entry and exit points, and all along the path of the current. ¹²  The thermal energy is absorbed by tissues, causing tissue ischemia, which is also caused by generalized vascular constriction leading finally to necrosis. ¹³  The thermal effects of electrical injuries are caused by the RPE's absorption of energy in the form of immediate coagulation of proteins and cells. ⁵

Direct mechanical injury resulting from high-voltage electrical shock wave also has been noted in the literature. ^4,5 The optic nerve is reportedly a good conductor of electricity, ⁷  thus, these manifestations are mainly seen surrounding the optic nerve and peripheral retina. However, several factors make the macula particularly sensitive to high-voltage electrical injuries. ⁸  Foveal avascularity increases the risk of ischemic damage to the macula. ¹⁴  The higher concentration of pigments at the macula causes more heat production and subsequently more thermal damage. ^10,11  The macula is also one of the sites of strongest vitreoretinal adhesion and may be more at risk from mechanical injuries from concussive forces of the high-voltage current, resulting in vitreomacular traction due to thermal shrinkage of the vitreous. ⁸

Retinal findings may be nonspecific (Table 1), ⁵  ranging from retinal whitening, edema, ¹⁵ hemorrhages, Purtscher-like retinopathy, ¹⁶ choroidal rupture, and retinal detachment ^{17 -19} in the acute phase to widespread chorioretinal atrophy in late stages. ^{4,10,15,17,18,20 -22} Retinal vascular damage and optic atrophy may also occur. ^15,23 Unilateral or bilateral optic neuropathy, ^23,24 as well as ischemic anterior optic neuropathy, have been noted in the literature. ^7,23 Macular cysts are also frequently reported findings, and can progress to full-thickness macular holes and even retinal detachment. ^5,10,17,21

Table 1.

Retinal Manifestations From Electric Injury.

Manifestation	References
Bilateral retinal detachment	Faustino et al, 17 Koytak et al, 18 Mitra et al 19
Retinal edema	Tandon et al, 15 Sharma et al 16
Chorioretinal atrophy	Verma et al, 20 Choe and Park 22
Pigmentary retinopathy	Verma et al 20
Purtscher-like retinopathy	Sharma et al 16
Optic neuropathy	Biro and Pamer 24
Ischemic optic neuropathy	Izzy et al, 23 Grover and Goodwin 7
Macular cysts	Sony et al 10 , Faustino et al 17 , Miller et al 5 , Lakosha et al 21 , Mitra et al, 19 Ranjan et al 9
Macular hole	Choe and Park, 22 Ouyang et al, 11 Rajagopal et al 8
Spontaneous recovery	Ranjan et al 9

Conclusions

Our case illustrates a patient with retinal findings noted several years after an electrical injury. Other entities may share similar clinical patterns (hereditary and inflammatory diseases) ²²  and must be differentiated with a detailed personal and family history regarding symptoms of night and/or color blindness in addition to the presence of consanguinity. Extensive areas of chorioretinal atrophy may be present in hereditary and inflammatory conditions, and differentiating them from other entities based only on electroretinography is difficult.

Inflammatory diseases usually present with anterior chamber or vitreous inflammatory reaction, a greater extent of retinal involvement, vascular changes (sheathing), and recurrent episodes associated with poorer vision. OCT findings may range from normal to some chronic cystoid changes or central thinning depending on the stage of inflammatory disease. FA and OCT showed nonspecific defects (widespread chorioretinal atrophy with RPE hyperplasia) in the present case.

Retinal manifestations following an electrical injury are nonspecific, and late manifestations such as the ones reported in the present case are very difficult to distinguish from other entities without a meticulous medical, family, and clinical history.

Retinal pigmentary changes with chorioretinal atrophy after a high-voltage electrical injury can clinically resemble hereditary and inflammatory diseases, rendering medical history and clinical evaluation of great importance.