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contact with the milky latex. There is burning sensation,
pain,photophobia and lacrimation which may worsen over hourseven
a!er copious irrigation. At rst, there is mild diminutionof vision,
but may diminish further to 20/200 or countingngersto hand
movements within 24 h as Case 2 in this report. Oninitial
examination, the corneal epithelium may be intact or withmild
punctate epitheliopathy, but eventually it may show frankepithelial
defect on the next day.[10]It takes around four to seven
days for the epithelium to heal completely. There is stromal
edemawith Descemets fold which decreases with time. The degree
ofanterior uveitis is variable and is particularly marked with
certainspecies as in Case 1 and Case 3 in this report.[3]The degree
ofocular inammation may also vary with the amount of sap thatenters
the eye. Neglected cases can progress to blindness due tocorneal
scarring, complicated uveitis, and anterior staphyloma.[3,4]
The species of Euphorbia causing ocular toxicity reportedearlier
were mostly with E. royaleana, E. lathyris an dE.
tirucalli.[4,5,11,12]Only one case of ocular toxicity with E.
trigonawas reported earlier by Sco$et al.[5]and they reported only
cornealepithelial defect without edema and anterior chamber
reaction.But in our Case 1, there was gross corneal edema with
moderateanterior uveitis and secondary elevated IOP. This was
possiblydue to a greater amount of sap entering into the RE in our
case.There was only one case report on E. miliiby Eke et al.[6]and
thepatient presented with corneal epithelial defect and edema
withmild anterior uveitis which was similar to our third case. To
the
best of our knowledge which includes MEDLINE search, wecould not
nd any case report of ocular toxicity by the sap of E.neriifolia
(Indian Spurge tree). If the patient presents early within24 h, the
treatment is antibiotic eye drops, topical
corticosteroids,cycloplegics, tears substitute and IOP-lowering
medications ifnecessary. No patching is required. With appropriate
supportivetherapy and close daily observation, the condition
generallyresolves completely within 10-15 days. In case of
suspected
bacterial infection and in the presence of a hypopyon,
topicalcorticosteroids may be started later once the epithelial
defect
gets healed.[10]
In conclusion, the clinical course may be a"ected by
particularspecies of Euphorbia, the amount of sap exposure, the
time betweenexposure and irrigation, and host factors.
Ophthalmologistsmanaging Euphorbia keratouveitis should warn the
patient that
vision may get worse on the next day before it improves. It
isalways advisable to ask the patient to bring a sample of the
plantfor identication. People who work with Euphorbiaspecies
shouldwear protective goggles while handling the plant.
Acknowledgement
We acknowledge the contribution of Mr. Volker Buddensiek,
Editor, Euphorbia World, and Mr. Tim Marshall, Seed
BankSecretary, International Euphorbia Society, 17 High
Street,Wighton, Norfolk, NR23 1AL, UK, for identication of
Euphorbianeriifoliaplant.
References
1. Webster GL. Irritant plant in Spurge family (Euphorbiaceae).
ClinDermatol 1966;4:36-45.
2. Elder S Duke. System of Ophthalmology. Vol XIV. London:
Kimpton;1972, p. 1185.
3. Grant WM, Schuman JS. Toxicology of the eye. In: Charles C
Thomaseditor 4thed. Springeld, IL: Thomas Publishers; 1993, p.
680-2.
4. Sofat BK, Sood GC, Chandel RD, Mehrotra SK. Euphorbia
royaleana
latex keratitis. Am J Ophthalmol 1972:74;634-7.5. Sco$IU, Karp
CL. Euphorbia sap keratitis: Four cases and possible
pathologic mechanism. Br J Ophthalmol 1996:80;823-6.
6. Eke T, Al-Husainy S, Raynor MK. The spectrum of ocular
inammationcaused by Euphorbia plant sap. Arch Ophthalmol
2000;118:13-6.
7. Available from: http://www.desert- tropical s.com/Plan
ts/Euphorbiaceae/Euphorbia.html. [last accessed on 2008 Jun
22].
8. Available from:
h$p://en.wikipedia.org/wiki/List_of_Euphorbia_species. [last
accessed on 2008 Jun 22].
9. Available from: http://www.euphorbia-international.org/.
[lastaccessed on 2008 Jun 22].
10. Merani R, Sa-Ngiampornpanit T, Kerdraon Y, Billson F, Mc
Clellan KA.Euphorbia lactea sap keratouveitis: Case report and
review of the
literature. Cornea 2007;26:749-52.11. Crowder JI, Sexton RR.
Keratoconjunctivitis resulting from the sap of
candelabra cactus and the pencil tree. Arch Ophthalmol
1964:72:476-84.
12. Sood GC, Sofat BK, Chandel RD. Injury to the eye by the sap
ofEuphorbia royaleana. Br J Ophthalmol 1971;55:856-7.
Aniridia associated with congenitalaphakia and secondary
glaucoma
Mayur Moreker1, Rajul Parikh2, Shefali R Parikh1,
Ravi Thomas1,3
We report a case of aniridia associated with congenital
aphakiaand secondary glaucoma. A 35-year-old male presented
withaniridia, congenital aphakia and secondary glaucoma in
botheyes. A!er an unsuccessful medical management, he
underwenttrabeculectomy with mitomycin C and anterior vitrectomy
underlocal anesthesia in his le!eye. Postoperatively, at the end of
six
months, intraocular pressure (IOP) in his le!eye was
controlledwithout medications. This case highlights the rare
association ofaniridia with congenital aphakia and secondary
glaucoma.
Key words:Aniridia, congenital aphakia, secondary glaucoma
Indian J Ophthalmol: 2009;57:313-314
DOI:10.4103/0301-4738.53061
Aniridia is a phenotypically heterogeneous condition thatcan be
inherited as an autosomal dominant disorder or as
1VST Center for Glaucoma Care, L.V. Prasad Eye Institute,
Hyderabad,2Bombay City Eye Institute and Research Center, Mumbai,
India.3Queensland Eye Institute, Brisbane, Australia, 4University
ofQueensland, Brisbane, Australia
Correspondence to Dr. Rajul Parikh, Bombay City Eye Institute
andResearch Center, 5, Babulnath Road, Mumbai - 400 007,
Maharashtra,India. E-mail: [email protected]
Manuscript received: 03.02.08; Revision accepted: 28.08.08
Brief Communications
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314 IndianJournal of Ophthalmology Vol. 57 No. 4
part of several systemic syndromes. It has been linked
toChromosomes 1 and 2 and associated with the deletion of thep-13
band of Chromosome 11.[1] Aniridia involves not onlythe iris, but
also the retina, optic nerve, lens and cornea. [2]Visual acuity
deteriorates as a result of nystagmus, glaucoma,cataract, corneal
opacities and retinal hypoplasia. There arenumerous reports of
association of aniridia with congenitalcataract but there is no
report in literature showing association
of aniridia and congenital aphakia. We report a patient
withaniridia, congenital aphakia and secondary glaucoma.
Case Report
A 35-year-old male presented with complaints of decreasedvision
in both eyes for 15 years. There was no history ofintraocular
surgery in either eye. His best-corrected visualacuity was no
perception of light in the right eye and 20/400in the le! eye with
+ 9.0 diopter sphere (Dsph). Horizontalpendular nystagmus was noted
in both eyes. Examination ofthe right eye revealed corneal stromal
edema and an intercalarystaphyloma. The cornea in the le!eye had
mild corneal haze.Both eyes had aniridia and were aphakic. The view
in the
le!
eye was clearer and showed aphakia with total absenceof zonules
[Fig. 1]. Intraocular pressure (IOP) measured byGoldmann
applanation tonometry was 28mm Hg and 36mmHg in the right and left
eye respectively. Corneal edemaobscured visualization of the angle
in the right eye. Gonioscopyin the le! eye with a four-mirror lens
showed open anglesup to the cilliary body inferiorly; the stump of
the iris hadformed peripheral anterior synechia (PAS) superiorly.
Fundusdetails were not clear in the right eye but a total
glaucomatousoptic atrophy was noted. Fundus examination of the
le!eyeshowed a near total glaucomatous optic atrophy (vertical
discdiameter of 2.1 mm, 0.9 : 1 cup disc ratio with bipolar
notch)as well as foveal hypoplasia. As the IOP was uncontrolled
withtopical 0.5% timolol maleate eye drops and 0.15%
brimonidinetartarate eye drops, the patient underwent
trabeculectomywith Mitomycin C under local anesthesia in his
le!eye. Partialanterior vitrectomy was performed at the same
time.
At ve weeks postoperatively the patient maintained
abest-corrected visual acuity of 20/400 (using + 9 Dsph and
1diopter cylinder (D cyl) at 180 degree) in the le!eye [Fig. 2].At
the three-month follow-up the vision remained the same;there was a
di"use bleb and the IOP was 7mm Hg withoutany anti-glaucoma
medications. When last seen (six monthspostoperatively), the
best-corrected visual acuity of 20/400 wasmaintained; the IOP was 6
mm Hg without any anti-glaucomamedications.
Discussion
The visual function in aniridia varies from near normal
toblindness. The more serious cases where blindness occurs arenot
due to the aniridia but due to associated conditions likecataract,
glaucoma, foveal hypoplasia, corneal dystrophy, andnystagmus.
Deletion or mutations involving the PAX6 genehave been implicated
in the pathogenesis of various anteriorsegment anomalies including
congenital aphakia.[3]However,
to our knowledge there is no reported case in literature of
aniridia associated with congenital aphakia. Such an
association
could be expected to occur by a chance alone in
approximately
one in 490,000,000 live births. (Chance associations
calculated
based on approximate prevalence of aniridia in one in 70,000
live births and approximate prevalence of congenital aphakia
in one in 70,000 live births.)
This case highlights the rare association of aniridia with
aphakia and secondary glaucoma.
References
1. Nelson LB, Spaeth GL, Nowinski TS, Margo CE, Jackson
L.Aniridia: A review. Surv Ophthalmol 1984;28:621-42.
2. Ivanov I, Shuper A, Shohat M, Snir M, Weitz R. Aniridia:
Recent
achievements in paediatric practice. Eur J Pediatr
1995;154:795-800.
3. Johnson BL, Cheng KP. Congenital aphakia: A
clinicopathologic
report of three cases. J Pediatr Ophthalmol Strabismus
1997;34:35-9.
Figure 1:Left eye of the patient with aphakia and aniridia. The
patients
left cornea has mild haze. Aniridia and aphakia can be noted
Figure 2:Left eye of the patient with diffuse bleb
(postoperatively)
