Download ocular injuries caused by lightning strikes: review of the literature

OCULAR INJURIES CAUSED BY LIGHTNING STRIKES: REVIEW OF THE
LITERATURE AND PRESENTATION OF TWO CLINICAL CASES
JeannethToquica Osorio, MD
Hector Fernando Gómez Goyeneche, MD
Department of Ophthalmology, Hospital Militar Central, Bogota, Colombia
Corresponding author: Jeanneth Toquica-Osorio
Cll152 # 12 c 12 unit 315 Bogotá Colombia
Tel: 3138897669
Email: [email protected]
Funding: None
Proprietary/Financial interest: None
Date of submission Date of Approval
Short head running title: Toquica-Osorio J, Gomez-Goyeneche HF. Eye and lightning
strikes.
Abstract: Secondary injuries caused by lightning strikes are not frequent;
however, survivors have important sequel in organs and tissues. We describe
two cases. The first one with lightning-induced maculopathy and the other case
involving lens damage. This paper discusses factors that determine the extent of
injuries and review the management for each one. The study and data collection
complained with local legislation and with the principles of the Declaration of
Helsinki.
Key words: lightning strike; eye injury; maculopathy; cataract; electric shock.
INTRODUCTION
Electrocution by lightning or electrofulguration is the most frequent cause of
injuries by natural phenomena and it is associated with high mortality (20-30%)
and morbidity (75%) with permanent sequel among survivors.1-3 Asystolic cardiac
arrest4 or ventricular fibrillations are the most frequent mechanisms of death5,6
and these are caused by different degrees of cardiac depolarization.
The injuries caused by electricity are classified as low voltage (less than 1000
volts), high voltage (more than 1000 volts) or lightning (3 to 200 million volts).7
Several factors determine the magnitude of the injuries, these include: voltage,
current (amperage), type of current (alternate or direct), current pathway across
the body, duration of contact with the current source, and individual susceptibility,
among others.8,9
Although ocular involvement is infrequent for victims of low-voltage electrical
burns, in victims of electrocution by lightning, it can reach up to 50%. 10 The most
affected ocular tissues are generally the cornea (where epithelial erosions
predominate11 and the lens where the percentage of formation of anterior and
posterior subcapsular cataracts can reach 6-7%.12 A minor percentage of victims
can present with uveitis, iridocyclitis, intraocular hemorrhage or thrombosis,
macular cysts, thermal papillitis, and chorioretinitis. Glaucoma is more frequent in
electrocution survivors compared to the general population.
The army as a profession is ranked in first place for being at high risk of electrical
accidents caused by lightning.13 These young people have high morbidity and
mortality and suffer from important sequel.
We report on two cases of ocular injuries caused by lightning among Colombian
soldiers. Anatomical involvement is seen at different levels: the first one initially
presented with unilateral uveitis, which was then associated with a cataract and
subfoveolar cyst; the second case later developed a subcapsular bilateral
cataract. We describe the clinical presentation, tomography, management, and
include a review about the pathophysiologic mechanisms that generated the
ocular injury in each case.
CASE REPORT 1
A 20-year-old soldier came to the ophthalmology service after being struck by
lightning in the left frontal region of the head. He reported intense ocular pain and
moderate visual loss in the left eye. On examination his best-corrected visual
acuity was 20/20 RX + 0.50-0.25x 160 in the right eye and 20/400, RX +0.750.50x 40 in the left. Ocular bilateral movements were preserved. The eyelids,
adnexa, anterior segment, and tonometry of the right eye were all normal. The
left eye had a clear cornea with cellularity ++ in the anterior chamber.
He was treated with topical corticosteroids and cycloplegic agents for several
days and he experienced clinical improvement. A week later, he presented again
with iritis associated with important lens opacification (Figure 1) and macular
pigmentary changes in the left eye upon ophtalmoscopic examination. He was
treated for two more weeks with topical corticosteroids and cycloplegic agents
that controlled the iritis, but a new control demonstrated a full-thickness macular
hole with retinal traction. Optical coherence tomography confirmed the
detachment of the pigmentary epithelium, a subfoveal cyst (Figure 2), and
thickness of the internal retinal membrane (Figure 3) and the hyaloid. The patient
required a surgical approach with phacoemulsification with intraocular lens
implantation, vitrectomy, laser, and gas achieving the complete closing of the
hole and retinal attachment. One week postoperative his best-corrected visual
acuity was counting fingers at a distance of 50 cm from the left eye. After five
months, his best-corrected visual acuity was 20/50 and the retina was attached.
CASE REPORT 2
An asymptomatic 26-year-old soldier is evaluated after being struck by lightning.
The ophthalmological examination is completely normal with a visual acuity of
20/20 AO. Thirteen months later, he consults for progressive bilateral visual loss.
His best-corrected visual acuity is 20/60 and there is lens opacification (Figure 4)
in both eyes. Ocular intrinsic and extrinsic movements are preserved and there
are no changes in pupil reflexes, intraocular pressure, or retinal mapping.
Interferometry
reached
20/30.
Phacoemulsification
with
intraocular
lens
implantation was consecutively done in both eyes with improvement in his visual
acuity to 20/30 one week postoperative. Two months later, his visual acuity was
20/20 in both eyes.
DISCUSSION
The pathological effects of electrical power are seen in several active
mechanisms. The current destroys cells, damages the integrity of the cellular
membranes and alters their potential; the consequences are edema and
irreversible cellular damage. This process is called electroporation.
The current can initiate its pathway across the orbit; in this case, it produces
alterations in the annexes like the loss of eyebrows and eyelashes. Painless
deep burns form unaesthetic scars with or without lagophthalmos 12 and even
ankyloblepharon10 in the eyelids. The metallization of the skin is typical at the
point of contact with the current source.
The pathway of electrical current across the body produces changes and
reactions in tissues and organs that exponentially increase in cases of
electrofulguration. These reactions affect the organism’s structural composition
on several levels (anatomical, histological, and biochemical) and make for a
series of electric traumas.14
The changes that are observed in the conjunctiva can be hyperemia, with some
degree of ciliary injection, and/or chemosis. Eventually hyposphagma and
hematic impregnation of the cornea have been described, especially when the
electric shock is intense.
Different injuries can occur in the cornea: from dotted epitheliopathy, to punctate
erosions, localized or diffused subepithelial opacities. Sometimes widespread
transitory edema appears, but a localized edema that topographically
corresponds with lens opacity is the most typical sign.
According to Waardenburg et all15, injuries begin appearing 24 hours after the
trauma, with disturbances occurring in the deepest layers of the stroma. After a
week, the whole cornea is cloudy, slowly becoming transparent nearly six weeks
later. If an electrical burn formed, the epithelium necrotized, and was associated
with the loss of the corneous sensation and suffered permanent scarring. In the
worst cases, a purulent infiltration of the whole cornea appeared, with extensive
necrosis of the tissues, which culminated in perforation and phthisis.16
In the iris and ciliary body, inflammatory changes occurred frequently. The iritis is
moderate and transitory, generally beginning between 1 and 8 weeks after the
trauma.17 Although it is infrequent in severe traumas, an intense iridocyclitis18 can
cause the formation of hypopyon and synechiae.19 It is interesting that in all
cases, including ours, uveitis has been associated with cataracts—suggesting
that lens capsule disruption leads to the release of angiogenic substances. 20
The appearance of hyphema is exceptional. Iris atrophy, either focal or
generalized, can be associated with the pigment of the anterior lens capsule,
superficial stroma of the iris, endothelium, and trabecular meshwork, being able
to cause a secondary glaucoma.21
The early changes that can be recognized in the lens consist of multiple vacuoles
directly behind the anterior capsule.22 These vacuoles are located in half of the
periphery and for this reason; they can go unnoticed if the patient is not dilated.
These changes do not produce an immediate reduction of visual acuity. A few
days or weeks later, these vacuoles disappear and are replaced by thin, linear
irregular opacities in the anterior subcapsular region. In some cases, especially in
young patients, all of these lens opacities disappear, returning to transparency.23
Cataracts are not generally diagnosed immediately (usually, within two to six
months after the trauma);24 however, cataracts have been identified immediately
up until eleven years after the trauma. If they are bilateral, the nearest eye to the
point of contact is the most affected. In general, industrial accidents affect the
anterior cortical of the lens, whereas the injuries caused by light imply the
involvement of the anterior and posterior subcapsular areas.
The mechanisms of these lens changes are not clear. Ferreiro et al25 postulated
that the voltage does not influence the severity of the cataract as much as the
point of contact with the electrical current. An existing hypothesis states that the
current coagulates the proteins of the lens’ cells. Galezowski and Knies26 suggest
that the contraction force of the ciliary muscle mechanically displaces the fibers of
the lens, in the same way that occurs in contusions. Other proposed mechanisms
include changes in the permeability of the lens capsule, vascular involvement of
the previous eye segment, and direct injury by heat or absorption of radiant
energy.
Lightning retinal injuries are rare; the most frequent are macular edema and
dotted pigmentary degeneration, which generally persist as pigmentary atrophy.
The macula is particularly sensitive to the thermal damage because of its high
concentration of melanocytic granules that lead to major dissipation of the heat
when it is injured by the electrical current. The elevated temperature found in the
retina’s pigmented epithelium and choroidal ischemia caused by focal vascular
changes can explain macular injuries. Edema can be a temporary reaction or it
may be followed by the formation of cysts or holes.27 There are few reports in the
literature of these macular cysts and holes like those found in our patient. 28,29
Other retinal changes described are arteriolar constriction, intra and sub retinal
hemorrhages secondary to venous thromboses or arterial occlusions for edema,
and clots in the intimate layer.30 In the periphery, we can find patches of
chorioretinal atrophy that resemble traumatic chorioretinitis31, a serious injury
such as retinal detachment.32,33
Nervous injuries can be thermal papillitis, unilateral or bilateral neuropathy, optic
atrophy, and paralysis of extraocular muscles, ptosis, nystagmus, facial paralysis
and Horner's syndrome, among others.34 These injuries lead to functional
alterations such as photophobia and blepharospasm. Visual loss ranges from
transitory blindness to a permanent decrease of all or part of the field of vision.
Ring scotomas and concentric field reductions have also been described.
The injury of the nervous tissues takes place in several mechanisms. The
nervous tissues can present a decrease in the conductivity or necrosis for
coagulation similar to the one observed in the muscle. In addition, it can suffer a
consequential damage in the patient’s vascular supply or myelinic injury. The
signs of neuronal injury can appear immediately or delay several hours or even
days to appear.35
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