CASE REPORT

Corneal manifestations in chemical injury with stannouschloride

Prachi Jain • Sumeet Khanduja •

Joginder Pal Chugh

Received: 12 December 2012 / Accepted: 8 January 2013 / Published online: 3 February 2013

� Springer Science+Business Media Dordrecht 2013

Abstract Chemical injuries are potentially devas-

tating ocular accidents that can lead to permanent

damage to the ocular surface and visual loss. The

majority of serious chemical injuries occur in factory

workers who are exposed to hazardous chemicals in

their day-to-day life. The ocular effects of commonly

encountered acids and alkalis are well documented in

the literature. Here we report briefly on the corneal and

other ocular effects of stannous chloride, which is

sparsely reported in the currently available literature.

Keywords Acid injuries � Stannous chloride �Corneal manifestations

Case description

A 24-year-old male presented to us with a history of

accidental instillation of stannous chloride (SnCl2)

solution in both eyes after an explosion in a pipeline

containing the chemical. There was charring of the

forehead skin, eyelids and right upper limb skin. He

complained of pain, difficulty in opening eyes and

blurred vision in both eyes. On examination, Snellen’s

acuity was 6/60 and 4/60 in the right and left eye,

respectively. Bilateral temporal limbal ischemia up to

2 h was observed along with central corneal edema

mainly confined to the posterior stroma and endothe-

lium, particularly in the left eye (Fig. 1a, b). A small

crescent-shaped epithelial defect was present inferiorly

in both eyes. After examination, the patient was

prescribed oral analgesics and vitamin C, topical

prednisolone acetate 1 %, homatropine 2 %, moxiflox-

acin 0.5 %, timolol 0.5 % and preservative-free

lubricating eye drops. Successive follow-ups were

performed daily. Initially the epithelial defects pro-

gressed to involve almost the entire cornea in both eyes

followed by complete epithelial regeneration within

2 weeks. Corneal edema subsided gradually over

4 weeks with residual subepithelial and anterior stromal

haze. After 6 weeks, superficial, fine corneal vascular-

ization involving 2–3 h was noted inferiorly in both eyes

(Fig. 2a, b). Best-corrected visual acuity improved to

6/12 in both eyes. Endothelial cell morphology was

poorly defined on specular microscopy. Intraocular

pressure was within normal limits during the follow-up

visits. The skin lesions healed completely in 2 weeks.

Discussion

The severity of chemical injury depends upon the area

of contact and degree of penetration. Most chemical

P. Jain (&) � S. Khanduja � J. P. Chugh

Regional Institute of Ophthalmology, Pt. B.D Sharma Post

Graduate Institute of Medical Sciences, c/o Dr. J.P Chugh,

172-R, Model Town, Rohtak 124001, Haryana, India

e-mail: drprachi04@gmail.com

S. Khanduja

e-mail: drkhanduja@gmail.com

J. P. Chugh

e-mail: chughjoginder@yahoo.co.in

123

Int Ophthalmol (2013) 33:725–727

DOI 10.1007/s10792-013-9720-z

injuries are mild in extent, occurring in males of

working age. Industrial accidents and assaults often

cause bilateral involvement. Alkalies tend to penetrate

more readily than acids as they cause saponification of

the cell membranes, leading to an acute rise in aqueous

pH and depletion of ascorbate levels [1]. Acid injuries

produce coagulation of cell membrane proteins and

remain confined to the ocular surface. Acute injury

may result in damage to limbal stem cells, conjunc-

tival and corneal epithelium, corneal nerves, corneal

stroma and endothelium, keratocytes, trabecular mesh-

work, iris, lens and ciliary body epithelium. According

to the new classification of ocular surface burns by Dua

et al. [2], ocular surface burns involving 0–6 h of

corneal limbus and up to 50 % of conjunctiva (grade

I–III) have a good prognosis, involvement of 6–9 h of

limbus and 50–75 % of conjunctiva (grade IV) have

intermediate prognosis, while limbal involvement

[9 h and conjunctival involvement [75 % (grade

V–VI) signifies poor outcome.

Any chemical injury to the eye requires prompt

intervention. Decontamination of the conjunctival sac

should be performed by copious irrigation for at least

30 min followed by early referral to an ophthalmol-

ogist. Management should be directed towards halting

the ongoing tissue damage, promoting ocular surface

healing and re-epithelization and controlling inflam-

mation. Medical measures in the early phase include

broad-spectrum topical antibiotics, and cycloplegic

and antiglaucoma therapy. Topical corticosteroids

should be given 6 h to minimize cellular infilteration

and inflammation; however, they should be rapidly

tapered off in cases of persistent epithelial defects after

10 days as they may lead to corneal melting especially

in alkali burns where the reparative process is severely

compromised due to depletion in ascorbate levels.

Other measures to promote corneal epithelization are

topical lubricants, bandage contact lens, autologous

serum drops, topical fibronectin and topical retinoic

acid. Topical and systemic ascorbate therapy promotes

stromal healing and halts ulceration if instituted during

the early course.

In 1997, Davis et al. [3] reported on a series of 30

patients with alkali burns in which all cases were treated

with a prolonged intensive regimen of topical cortico-

steroids in conjunction with topical and systemic

Fig. 1 a, b Central corneal

edema in right and left eye,

respectively

Fig. 2 a, b Fine superficial

corneal vascularization in

inferior quadrant after

6 weeks in right and left eye,

respectively (arrow)

726 Int Ophthalmol (2013) 33:725–727

123

vitamin C. They concluded that topical corticosteroids

in conjunction with topical and systemic ascorbate

therapy markedly reduces the incidence of corneoscleral

melting by repleting aqueous ascorbate levels which are

critical for collagen synthesis .

Although most of the chemical injuries encountered

in day-to-day life are mild and can be managed

medically, severe injuries often require surgical man-

agement for corneal complications. Impending cor-

neal perforations may be dealt with by Tenon’s

advancement or amniotic membrane grafting. Small

perforations can be managed with tissue adhesives

while larger ones ([2 mm) require patch grafting or

therapeutic penetrating keratoplasty. Once the active

process is quiescent long-term rehabilitative measures

like penetrating keratoplasy, keratoprosthesis or

limbal stem cell grafting can be used. Complications

like secondary glaucoma and cataract should be dealt

with accordingly.

Kuckelkorn et al. [4] reported on a series of 66

patients with 90 severely burnt eyes. Cataract occurred

in 23 (25.6 %) eyes shortly after the burn and early

secondary glaucoma in 14 (15.6 %) eyes. In the

further clinical course, 41 (45.6 %) eyes developed a

secondary cataract and 20 (22.2 %) eyes developed a

late secondary glaucoma. Penetrating keratoplasty

was performed in 55 eyes—35 of them were unsuc-

cessful as a consequence of graft rejection or increas-

ing vascularization. One-third of the patients achieved

a long-term visual acuity of C0.1.

Sharma et al. [5], in a series of 31 eyes with severe

alkali burns, concluded that despite appropriate treat-

ment these eyes responded poorly and carried a

guarded visual prognosis. They also concluded that

visual recovery in cases of chemical injury depends

upon the severity of the initial injury.

Hong et al. [6] reported on a case series of 239 eyes

of 190 patients with severe ocular chemical injury, in

which only five eyes (2.1 %) achieved visual acuity of

6/60 or better.

Stannous chloride (SnCl2) is a highly acidic com-

pound (pH range 1–2) widely used as a reducing agent

and catalyst in the dye industry, pharmaceuticals and

as a tanning agent. It is stable in anhydrous form and

undergoes hydrolysis in hot water [7].

SnCl2 þ H2O$ Sn OHð ÞClþ HCl

It causes burns by all exposure routes. It is harmful

to eyes and skin. Ingestion and inhalation is poisonous.

Chronic exposure can damage liver, kidneys and red

blood cells. Natural history of ocular manifestations

following chemical insult with stannous chloride is not

available and not yet reported to the best of our

knowledge. Chemical injury with stannous chloride in

our case led to involvement of all corneal layers with

consequent damage to endothelial cell layer morphol-

ogy. Although the epithelial layer completely healed

along with resolution of corneal edema with medical

management, residual sub-epithelial haze and fine

corneal neovascularization was the tell-tale sign. No

evidence of anterior chamber and posterior segment

involvement was seen. Through this brief communi-

cation an effort has been made to update the limited

available data on ocular toxicity of stannous chloride

exposure.

References

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Ophthalmol 41:275–313

2. Dua HS, King AJ, Joseph A (2001) A new classification of

ocular surface burns. Br J Ophthalmol 85:1379–1383

3. Davis AR, Ali QH, Aclimandos WA, Hunter PA (1997)

Topical steroid use in the treatment of ocular alkali burns. Br

J Ophthalmol 81:732–734

4. Kuckelkorn R, Kottek A, Reim M (1994) Intraocular com-

plications after severe chemical burns—incidence and sur-

gical treatment. Klin Monbl Augenheilkd 205(2):86–92

5. Sharma N, Singh D, Sobti A et al (2012) Course and outcome

of accidental sodium hydroxide ocular injury. Am J Oph-

thalmol 154(4):740–749

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