Sir,

Ocular complications of electrical trauma are widely reported. This presentation of a severe macular subretinal haemorrhage following an electrical shock has not been described previously.

Case report

A 58-year-old man presented with a 24 h visual deterioration in his left eye following an accidental electrical shock (230 V AC) to his left forearm, lasting a few seconds. There was no relevant past ocular or medical history. His left visual acuity was reduced to counting fingers. Fundus examination showed a large, elevated subretinal haemorrhage at the macula (Figure 1), with no other abnormalities. The right eye was normal, with no risk factors for choroidal neovascularisation such as drusen or retinal pigment epithelial changes. Fluorescein and indocyanine green angiography were not performed. The haemorrhage took several months to resolve (Figure 2). At 2 years, a dense macular scar remains (Figure 3) with visual acuity of counting fingers. There are no lens opacities or other abnormalities noted.

Figure 1
figure 1

Large, elevated subretinal haemorrhage at the macula, 24 h following trauma.

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Figure 2
figure 2

Resolving subretinal haemorrhage.

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Figure 3
figure 3

Macular scar remains 2 years following injury.

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Comment

The first documented case of electrical trauma to the eye was reported by St Yves in 1722 when a field worker developed cataracts following a lightning strike.1 Since then, ocular complications of electrical trauma have been widely reported.

Tissue damage from electricity may occur from its direct transmission, conversion to thermal energy, or ischaemia caused by vascular constriction. The extent of damage is influenced by numerous factors including voltage, duration of contact, tissue sensitivity, and area of contact.2 Cases have been described following contact varying from 220 to 80 000 V.3

The presence of ocular sequelae, which can affect any structure, depends on the proximity of the route travelled by the electrical current.2 The latency of complications following trauma secondary to lightning is shorter when compared to those following contact with lower voltages.4

Anterior subcapsular cataracts are most common, developing from 1 month to 2 years after the injury.3 These range from fine vacuoles to linear or mossy opacities and may regress.5 The contact area is usually the head or neck.2

The retina and choroid are thought to be affected by ischaemia resulting from coagulation and necrosis of the vasculature. Macular oedema, retinal pigment epithelium changes, macular holes, retinal haemorrhages, and detachments have been described, occurring months to years after the original insult.2, 5 This necessitates serial ophthalmologic examinations.

Subretinal haemorrhages have been associated with conditions such as systemic hypertension and blood dyscrasias, including idiopathic thrombocytopaenic purpura and von Willebrand's disease.6, 7 The use of aspirin or warfarin increases the risk of subretinal haemorrhage, especially in patients with age-related macular degeneration.8, 9 These conditions were not present in this case, although polypoidal choroidal vasculopathy could not be excluded as the cause of this haemorrhage, due to the lack of angiography.10

Our patient was managed conservatively. Other approaches include vitrectomy and pneumatic displacement using intravitreal sulphur hexafluoride or perfluoropropane gas. These aim to minimise damage by removing the blood from the macula. Both techniques can be used with tissue plasminogen activator, which liquefies and facilitates reabsorption of the thrombus.11

To the best of our knowledge, this is the first reported case of subretinal macular haemorrhage following electrical trauma. The acute history and low voltage involved is also unusual, when compared to previous reports.