Clinicopathological correlations and surgical outcomes in a case of electric cataract

Oli, Avadhesh MS; Waikar, Shrikant MS; Sebastien, Tintu K. MBBS

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doi: 10.1097/j.jcro.0000000000000036
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A 40-year-old man reported with a 3-month history of painless, progressive diminution of vision in both eyes, which was disabling in the daytime and bright light. He had difficulties in performing his duties at the workplace because of haziness of vision. He denied a history of steroid intake in any form, recurrent red eye treated with long-term topical drops, or trauma. His presenting corrected distance visual acuity was 6/9 in the right eye and 6/12 in the left eye. The anterior segment examination was within normal limits except for posterior subcapsular cataract in both eyes (with left eye affected more) involving the pupillary axis (Figure 1, A). Fundus in both eyes showed no abnormality. He also had a well-healed scar on the left side of his forehead, and on the enquiry about the scar, he gave a history of high voltage electric shock 1 year before (Figure 1, B). He sustained this high voltage shock at his workplace from an 11 kV electric transmission cable. The current resulted in an entry wound over the left side of the forehead and an exit wound on left axilla. The patient did not have any ocular symptoms until 8 to 9 months after the electric shock when he noticed haziness of vision in both eyes, with more difficulty in the left eye, worsening over the next 3 months.

Figure 1.
Figure 1.:
A: Slitlamp photograph showing posterior subcapsular opacity in retroillumination. B: Entry point on the forehead (yellow arrow) and exit point in the left axilla (white arrow).

He underwent phacoemulsification and posterior chamber intraocular lens implantation in the left eye. Postoperative period was uneventful with corrected distance visual acuity of 6/6, N6 in left eye at the end of 1 week (Figure 2, A). The anterior capsule was subjected to a histopathological examination with hematoxylin and eosin staining that showed disruption of architecture of basement membrane and calcium deposition (Figure 2, B).

Figure 2.
Figure 2.:
A: Postoperative clinical picture. B: Histology of the anterior capsule with calcification (yellow arrow).


Electrical injuries are not infrequent in the developing world and can be potentially life-threatening.1 Domestic and industrial accidents with exposure to high voltage currents might lead to visual impairment. Ocular injuries due to high voltage electric currents might manifest as conjunctival hyperemia, corneal opacification, iridocyclitis, accommodative spasm, cataract, macular edema, optic atrophy, and retinal detachment. Electric cataract can develop following electric shock immediately or after a latent period.2

Cataract formation usually occurs after a period of latency varying from a few days after the injury, until a few years. Our patient became symptomatic in the form of reduced vision 9 months after the electrical shock. The exact incidence of electric cataract is not known; however, it ranges from 0.7% to 8.0%. Degree of cataractous changes is not related to the strength of the current. Cataract results from 5% to 20% of electric injuries ranging from 220 to 50 000 V.3 The occurrence of electric cataract has been reported after administration of electric shocks used in electric chair punishments and cardioversion.2 The propensity for cataract development increases with proximity of electric injury to the eye. Although the exact pathogenesis of electric cataract formation is not clear, extensive epithelial damage could be the cause of the lenticular opacities. It is also postulated that circulatory changes associated with inflammation result in cataractous changes.4 The appearance of multiple fine vacuoles just beneath the anterior capsule is the earliest change that can be identified. These changes can be missed in undilated pupils if lenticular opacities are located in the midperiphery. Damage to the subcapsular epithelium leads to osmotic changes and direct coagulation of lens proteins.5 Opacities might form in the capsule and subcapsular layers of anterior cortex commonly, but posterior cortex might also get affected. In our case, the entry point of electric current was on the forehead, and the exit point was left axilla. Similarly, the symptoms and lenticular opacity in the left eye was more than that in the right eye.

In our case, histopathological examination of anterior capsule showed disruption of architecture of basement membrane and calcium deposition. The deposition of calcium is not reported earlier; however, the most common finding reported earlier was fibrosis.5 This finding could help us understand the pathogenesis of electric cataract.

In this case, the patient did not give a history of electric injury, but the forehead scar gave a clue regarding the possibility of complicated electric cataract. In a young patient, detailed history and physical examination is mandatory in the case of presenile cataract. Visual outcomes after phacoemulsification with posterior chamber intraocular lens implantation are excellent if the injury is not accompanied with other significant damage in the anterior and posterior segments. This case also highlights the importance of preventive measures at the individual level and engineering modifications to avoid chances of high voltage–related electrical injuries.


  • Accidental exposure to high voltage current causes electric cataract, and modern cataract surgery results in good visual outcome.


  • The pathological changes are more pronounced near point of entry and exit of electric current.
  • Deposition of calcium in the lens is an unreported new histopathological finding.


1. Raina UK, Tuli D. Bilateral electrical cataract. Br J Ophthalmol 1999;83:1088
2. Long JC. Electric Cataract: a clinical and experimental study. Am J Ophthalmol 1963;56:108–133
3. Rathi M, Bhatt N, Dhull C, Sachdeva S, Phogat J. Electric cataract: a report of two cases and a review of the literature. Egypt J Cataract Refract Surg 2016;22:54–55
4. Reddy SC. Electric cataract: a case report and review of the literature. Eur J Ophthalmol 1999;9:134–138
5. Hashemi H, Jabbarvand M, Mohammadpour M. Bilateral electric cataracts: clinicopathologic report. J Cataract Refract Surg 2008;34:1409–1412
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