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Year : 2002  |  Volume : 50  |  Issue : 3  |  Page : 224-225

An unusual case of late ocular changes after lightning injury.

Department of Ophthalmology, Bankura Sammilani Medical College, Bankura, West Bengal, India

Correspondence Address:
H Datta
Department of Ophthalmology, Bankura Sammilani Medical College, Bankura, West Bengal
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Source of Support: None, Conflict of Interest: None

PMID: 12355702

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We describe a case of late ocular changes after lightning injury. One year after the injury, complete ankyloblepharon, severe dry eye, corneal opacity, healed iritis and mature cataracts were noted in both eyes of the patient.

Keywords: Lightning injury, ocular trauma, sequelae ankyloblepharon

How to cite this article:
Datta H, Sarkar K, Chatterjee PR, Datta S, Mukherjee U. An unusual case of late ocular changes after lightning injury. Indian J Ophthalmol 2002;50:224-5

How to cite this URL:
Datta H, Sarkar K, Chatterjee PR, Datta S, Mukherjee U. An unusual case of late ocular changes after lightning injury. Indian J Ophthalmol [serial online] 2002 [cited 2020 Jul 9];50:224-5. Available from: http://www.ijo.in/text.asp?2002/50/3/224/14778

Electric injury due to lightning is not uncommon. Although only about 25% of lightning victims die, as many as 75% of survivors have permanent sequelae.[1] Longterm sequelae of lightning injury include hearing loss, cataracts, burn scars, psychiatric illness, paresis and neuritis with painful neuralgia.[1] More than 50% of all lightning victims suffer from some form of ophthalmic injury.[1]

  Case report Top

A 32-year-old man presented with complete adhesion of eyelids in both the eyes (ankyloblepharon). He also had scarring over part of the scalp (with alopecia of the affected area), part of the face, neck, chest and abdomen on the left side of the body and contracture of both hands. He gave a history of injury by lightning a year before. Records revealed that he had been admitted elsewhere in a deep coma though his vital signs were normal. His level of consciousness improved over a week though he remained amnestic about the event. He experienced decreased vision in both eyes (up to finger counting), vertigo, and a total inability to hear with perforation of left tympanic membrane. Second degree burns were present over scalp, face, chest, abdomen and both arms. Ophthalmic injuries included corneal haze in both the eyes without any cataract or iridocyclitis and second degree burns of both eyelids which initially responded to antibiotic ointment and eye patching. Otologic reports revealed bilateral conductive and sensorineural hearing loss. The vertigo responded spontaneously. Standard wound dressing helped heal the body wounds.

Recurrent episodes of iritis, corneal ulerations and dryness of both the eyes persisted. He was discharged from the hospital after one month. He continued visiting the local ophthalmologist and the records revealed that he had been experiencing recurrent attacks of iritis, corneal ulcerations with gradual diminution of vision and the symptoms persisted throughout this period. About three months after the injury symblepharon and ulceration of the lid margins with temporary adhesion developed and the lids were repeatedly separated manually by glass rods. After six months the follow-up visits became irregular.

He presented to us one year after the injury with lid adhesions, which he described as having gradually developed during last four months. On examination, his visual acuity was perception of light only with accurate projection of rays in both eyes. Loss of eyebrows and eyelashes were noted in both eyes. There was complete adhesion of upper and lower lids in both the eyes (Figure).

General anaesthesia was used to separate the eyelids. This was done with the help of blunt tipped scissors. There was total symblepharon and complete restriction of ocular movements in both the eyes. The conjunctiva in both eyes were grossly adherent (bulbar and palpebral parts) and scarred. The fornices were reconstructed with symblepharon rings in both the eyes. Subsequent ocular examination revealed the conjunctiva to be markedly adherent to the underlying structures in both the eyes, bilateral corneal opacities, irregularities of pupils, evidence of healed iritis without any cells and flare and mature cataracts. Slitlamp examination showed that the corneal opacifications involved the anterior one-third of the stroma without any vascularization. They were bilateral and diffusely distributed. The epithelium in both eyes lacked lustre and had no epithelial defects (ulcerations/erosions). Bilaterally the endothelial surfaces showed keratic precipitates with pigment dispersions. Applanation tonometry readings were 14 in the right eye and 13 in the left. Ultrasonography (combined A and B scans) showed echogenically clear vitreous and flat retinas in both eyes. The patient had extremely dry eyes; the Schirmer test results were 3 mm in both the eyes. Later, buccal mucous membrane grafts[2] from cheeks were attempted in both the eyes after the devitalized conjunctiva was excised without any encouraging results. Due to the presence of extreme dryness, cataract surgeries were not attempted. The patient was advised to continue artificial tears.

  Discussion Top

Lightning involves a transfer of electric charge. It develops when warm, low pressure air rises through colder, higher pressure air. An electrical potential is created between the negatively charged inferior aspect of the cloud and the positively charged ground. When the voltage difference exceeds the insulator strength of the air (approximately 30,000 volts),[1] electrical energy is discharged as lightning. People may be injured by lightning in five possible ways:

  1. Direct strike (most dangerous) -when the major current flows directly through the victim and is facilitated by metal objects;

  2. Contact - when lightning strikes an object the victim is in contact with;

  3. Splash (most common) - where lightning strikes an object first and then jumps to a nearby person of low resistance;

  4. Ground current - the bolt strikes the ground, and radiates towards the victim; and

  5. Blunt injury-from shock wave.

Standard electrical injuries are different from those caused by lightning. Electrical injuries caused by alternating currents fix the victim to the current source by tetanic muscle spasm. In such instances there is longer contact, causing skin to break down even though the voltage is lower. Lightning contact, on the other hand, is instantaneous with less time (exposure time usually lasts only 1 to 100 milliseconds) to cause injury.[3] The cells are destroyed by both heat and electrolysis. The high resistance offered by non-nervous tissue accounts for the thermal effects of electrical injuries, which result in immediate coagulation of the proteins of the cells.[4] The high temperature generated can cause carbonification of the skin and the underlying tissue.[5] When the current traverses the skin, energy from the current is converted into heat, producing coagulation and necrosis of the striated muscles and blood vessels through which it passes.

More than half of all lightning victims suffer from some form of ophthalmic injury, most commonly involving the cornea.[1] Damage is the result of a combination of electrical energy and intense brightness. Epithelial lesions may disappear rapidly but deep opacities do not regain their transparency for long. The sensitivity of the cornea may deteriorate, leading to ulceration and even perforation. If serious ulceration becomes recurrent, a permanent scar may develop.[4] Such a mechanism most probably caused the stromal opacity in the cornea of our patient. Cataracts are the most common longterm sequelae (occuring in 5% of the patients).[4] Cataracts associated with lightining injury are usually bilateral. They can occur months or years after the initial injury. They are typically posterior subcapsular.[6] Surgeries are usually attempted in these cases, if no spontaneous resolution occurs over time.[7] In this case, though bilateral mature cataracts were found, surgery was not attempted due to the presence of extreme dry eyes.

Iridocyclitis and hyphaema following lightning injury are common.[8],[9] This patient also had signs of healed iritis in the form of multiple posterior synechiae and irregular pupils in both the eyes. Usually the lesions of the eyelids following lightning injury are typical. The lesions are pale, grey necrotic areas with no surrounding hyperaemia. They are painless, dry and aseptic and usually heal rapidly. This patient had total adhesion of both lids in both the eyes (total ankyloblepharon) and extreme dry eyes.

Though ulcerated necrotic eyelid lesions have been reported in literature,[9] we did not find any report of ankyloblepharon following lightning injury, as was the case in this patient. In our opinion this atypical ankyloblepharon may have resulted as a result of extensive destruction of conjunctival tissue followed by granulation and cicatrisation similar to contact thermal burns.[10] It is also known that the lower the skin resistance the more serious are the internal injuries.[8] The eyelid skin because of its anatomical peculiarity (absence of subcutaneous adipose tissue) produced least resistance, and the extensive damage to the inner structures and tissues may have occurred through the eyelids.

The dry eye is probably due to damage to the meibomian gland openings at the lid margins and destruction of the conjunctival mucin secreting glands. Thermal energy causes superficial moisture (sweat, rainwater, tears, or saliva) to turn to steam. Thus, exposed moist mucous membranes are frequent sites of injury. Other ocular findings seen in lightning injuries such as retinal oedema, retinal haemorrhage, retinal detachment, cystic macular oedema, macular hole, retinal folds, optic neuritis, mydriasis, loss of pupillary reflex, anisocoria and Horner's syndrome were not noticed in this patient at any stage.[7][8][9],[11] Available treatments for severe ocular surface disease are not very satisfactory and attempted buccal membrane graft in this case was a failure.

  References Top

Edelstein J, Peters W, Cartotto R. Lightning injury: A review and case presentations. Canadian J Plastic Sur 1994;2:164-68.  Back to cited text no. 1
Roper-Hall MJ. Stallard's Eye Surgery. 7th ed. Bombay: Verghese Publishing House, 1989. pp 393-94.  Back to cited text no. 2
Dimick AR. In: Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, et al, editors. Harrison's Principles of Internal Medicine. 14th ed. New York: McGraw-Hill Health Professions Division, 1998. Vol.2. p 2559.  Back to cited text no. 3
Duke-Elder Sir S, Macfaul PA. In: Duke-Elder Sir S, editor. System of Ophthalmology. Vol XIV, Part 2. London; Henry Kimpton, 1972. pp 813-35.  Back to cited text no. 4
Wallace JF. In: Braunwald E, Isselbacher KJ, Petersdorf RG, Wilson JD, Martin JB, Fauci AS, editors. Harrison's Principles of Internal Medicine. 11th ed. New York: Mcgraw-Hill Health Professions Division.1987. Vol.1. pp 859-60.  Back to cited text no. 5
Lagreze Wolf-Dietrich A, Bomer Thomas G, Aiello LP. Lightning-Induced Ocular Injury. Arch Ophthalmol 1995;113:1076-77.  Back to cited text no. 6
Portellos M, Orlin SE, Kozart DM. Electric Cataracts. Arch Ophthalmol 1996;114:1022.  Back to cited text no. 7
Casten JA, Kytilia J. Eye symptoms caused by lightning. Acta Ophthalmol 1964;42:39-43.  Back to cited text no. 8
Bullock John D. History of Ophthalmology (Daniel MA, section editor): Was Saint Paul Struck Blind and Converted by Lightning? Survey of Ophthalmology. 1994;39:151-60.  Back to cited text no. 9
Duke-Elder Sir S, Macfaul PA. In: Duke-Elder Sir S, editor. System of Ophthalmology. London: Henry Kimpton. 1972. Vol.XIV, Part 2. Pp 760-65.  Back to cited text no. 10
Noel LP, Clarke WN, Addison D. Ocular complications of lightning. J Pediatr Ophthalmol Strabismus 1980;17:245-46.  Back to cited text no. 11

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