medical & vision research foundations

18 Pages·2014·1.46 MB·English

June 2014 Volume XXXII No 2
insight
Scientifi c Journal of
MEDICAL & VISION RESEARCH FOUNDATIONS
www.sankaranethralaya.org
insight
Scientifi c Journal of Medical & Vision Research Foundations
Sankara Nethralaya – The Temple of the Eye.
It was in 1976 when addressing a group of doctors, His
Year: 2014
Holiness Sri Jayendra Saraswathi, the Sankaracharya of
the Kanchi Kamakoti Peetam spoke of the need to create
a hospital with a missionary spirit. His words marked the
Issue: Vol. XXXII | No. 2 | June 2014 | Pages 19–32
beginning of a long journey to do God’s own work. On the
command of His Holiness, Dr. Sengamedu Srinivasa
Badrinath, along with a group of philanthropists founded a
Editor: Parthopratim Dutta Majumder
charitable not-for-profi t eye hospital.
Sankara Nethralaya today has grown into a super specialty
institution for ophthalmic care and receives patients from
all over the country and abroad. It has gained international
excellence and is acclaimed for its quality care and
compassion. The Sankara Nethralaya family today has
Typeset at: Techset Composition India (P) Ltd., Chennai, India over 1400 individuals with one vision – to propagate the
Nethralaya philosophy; the place of our work is an Alaya and
Printed at: Gnanodaya Press, Chennai, India
Work will be our worship, which we shall do with sincerity,
©Medical and Vision Research Foundations dedication and utmost love with a missionary spirit.
Contents
Guest Editorial: The Tale of Refractive Surgery 19
Prema Padmanabhan
Major Review: MicroRNA: Potential Therapeutics of Eye Cancer 20
Swathi Lingam
Tips and Tricks: Tips and Pearls in Corneal Examination 23
A. Shweta, B. Sumanta and A. Bharti
Case Report: Spontaneous Resolution of Congenital Glaucoma 25
L. Vijaya and M. Baskaran
Case Report: Unilateral Full Thickness Macular Hole in Association with Serpiginous Choroiditis 27
P. Ranganathan and J. Biswas
Residents’ Corner: Intravitreal Medications in Uveitis 29
A. Maheshwari
Optics & Refraction: Cycloplegic Refraction in Children 30
L. Jayalakshmi, N. Kalpa and R. Srikanth
Inquiries or comments may be mailed to the editor at [email protected]
Cover photo: Mr. M.S. Krishna, Senior photographer,
Department of Ophthalmic Photography, Sankara Nethralaya
Guest editorial
The Tale of Refractive Surgery
Prema Padmanabhan
Director,DepartmentofCornea “It was the best of times, it was the worst of times, it was the age of
andRefractiveSurgery, wisdom,itwastheageoffoolishness,itwastheepochofbelief,itwasthe
SankaraNethralaya
epoch of incredulity, it was the season of Light, it was the season of
Darkness, it was the spring of Hope, it was the winter of Despair….” This
couldwellbeaDickensoniansummaryof“TheTaleofRefractiveSurgery”.
Correspondenceto:
PremaPadmanabhan,
It would be no are more types of diagnostic gadgets that the
MedicalDirector
exaggeration to say surgeon can now use for patient screening and
SankaraNethralaya,
Chennai600006, thatno otherfieldin selection. The proper interpretation of the
India. Ophthalmology has ‘displays’ on some of them can be more confusing
E-mail:[email protected] seensomanychanges than is apparent and calls foran understanding of
in so short a time as its working principle and equally, of its
Refractive Surgery limitations.
has in the last 25 years. Once considered an Whentheright patientandthe mostsuitedpro-
experimental hobby, it has gradually gained a cedurearechosen,everypatientdeservesadetailed
level of acceptance even among its most vocal counseling.Justasitisimportantforthesurgeonto
critics. It has, in this short span of time, become understand the needs and expectations of the
the most commonly performed elective procedure patient, it is no less important for the patient to
done on the human body. A meta-analysis of the understand the possibilities and limitations of the
USFDA approved Lasik device studies across the procedure. Disclosing the unvarnished truth about
globe 8 years ago, found that 96% of patients possible side-effects is a moral responsibility, we
reported satisfaction. With improved technology owe our patients and sets the patients expectations
that is used today, that figure would be even tomorerealisticlevels.
higher. This can only mean that refractive surgery The introduction of the Femtosecond laser has
has met the physical, emotional and financial raisedthebarintermsofprecisionandhasopened
expectationsofitsclientale. newwindowsofpossibilities.Thefemtosecondlaser
Ametropia is now correctable by a myriad sur- allows the surgeon to choose the diameter, shape,
gical techniques—each more clever in design and thickness,depth,angleandlocationofcornealflaps
imaginative in name than the other. Although and hinges and makes customized laser refractive
today the term “Refractive Surgery” is almost syn- surgerymoreachievablethanitearlierwas.
onymous with Laser Refractive Surgery, there are Extending the versatility of the Femtosecond
severalnon-lasertechniquesaswellthatasurgeon laser to perform flapless refractive surgery by
can choose from. The multiple procedures and extracting a lenticule fashioned entirely by the
their acronyms make for a colorful landscape, but femtosecond laser, maybean importantmilestone
they could all fall into one of four broad categor- in the journey of Refractive surgery. By avoiding
ies—incisional (RK being the most notorious and flap-related complications, it would enhance the
AK the most handy), thermal (like CK that was safetyoftheprocedure,butwedoneedtowaitfor
born only to be buried), lamellar (which theresultsofcurrentclinicaltrials.
began with ALK but soon gave way to Laser The possibilities are mind-boggling. But unless
Refractive Surgery in all its forms) and intraocular each new procedure passes the test of scientific
surgery (IOLs that may or may not replace scrutinyandcriticalanalysis,unlesswell-designed
the crystalline lens). With so many choices, the studieswithcleardocumentationarehealthilydis-
challenge, in Refractive Surgery, lies in choosing cussed, unless there is an honest self-reporting of
theappropriate procedureforeacheye. Sometimes, failures and complications, we would be guilty of
however, the bigger challenge lies in determining creatinganophthalmicFrankenstein.
the appropriateness of refractive surgery itself for The complexity of the optical design of the
the eye. Failure to do so has resulted in catastro- humaneyeisevenmoremind-boggling.Novelideas,
phies. But the more genuine difficulty in “smelling brillianttechnology,deftsurgeryhavenotbeenable
the rat” has often resulted in the landmine to improve the quality of the biological optical
blowing into the surgeons’s face. Iatrogenic systemofthehumaneye,atleastuntilnow.Evenas
keratectasia is probably the most feared—and we applaud human achievement and serendipidity,
embarrassing—exampleofacomplicationresulting, letuspauseforamovementinsilentreverenceforall
most often, from improper patient selection. There thatthecorneahasgivenandforgiven.
Howtocitethisarticle PremaP.TheTaleofRefractiveSurgery,SciJMed&VisResFoun2014;XXXII:19.
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SciJMed&VisResFounJune2014|volumeXXXII|number2|
Major review
MicroRNA: Potential Therapeutics of Eye Cancer
Swathi Lingam
SwathiLingam, MicroRNAs (miRNAs) are small single stranded retinoblastoma development. It was found that
ProjectAssistant, nucleotides that are ∼22 base pairs long. They PAX6 expression was inhibited by this miRNA,
DepartmentofOcularPathology were first identified in Caenorhabditis elegans.1 andthatitfunctionedasatumorsuppressor.9
Functionally, they are involved in post transcrip- Cancer associated miRNAs are of two types;
tional regulation of gene expression by binding to those associated with oncogenes (called onco-
Correspondenceto:
SwathiL,ProjectAssistant, the 30 untranslated regions of transcribed mRNA. miRNA’s or oncomirs), and those linked to tumor
DepartmentofOcularPathology. Mature miRNA also interact with Argonaute pro- suppressor genes, as described in the previous
E-mail:swathi.lingam89@gmail. teins, and are inducted into the RNA induced section.
com silencingcomplexwhichisinvolvedingenesilen- The miR-17-92 cluster is a cluster of oncogene
cing.2 Gene silencing occurs when a mutation associated miRNA, which has been shown to be
causes the gene to lose its function. Recently, involved in retinoblastoma. The first study that
miRNAs have been found to be associated with indicated this association was carried out by
diseasessuchascardiovasculardisease,3metabolic Conkrite et al. in theyear 2011. They were able to
diseases4andcancer.5 provethat Rbgene deletion leadstoan increasein
the levels of the polycystrionic miR-17-92 cluster.
Retinoblastoma The expression of these miRNA appeared to be
Studying the role of miRNA in retinoblastoma directlyproportionaltotherateofdiseaseprogres-
could be very important since it has a potential sioninvitro,andinanRb-mousemodel.10
for development into a treatment strategy. The Epithelial cell adhesion molecule (EpCAM) is a
earliest report of an association between miRNA glycoprotein that is expressed only in epithelial
and retinoblastoma was made in the year 2009 by cells and epithelial neoplasms. In retinoblastoma,
Dalgard et al. They investigated the role of it was identified as a possible cell surface marker,
miR-34a and were able to identify its differential and its regulation of the miR-17-92 cluster was
expression in retinoblastoma cell lines, and com- studied. It was found that the miR-17-92 cluster
prehensively proved that it acts as a tumor sup- can be positively correlated to EpCAM expression,
pressor miRNA. miR-34a is associated with p53, a and is involved in retinoblastoma progression
known tumor suppressor gene, whose pathway is in vitro.11 This is a promising result since this
inactivated in a subset of retinoblastoma tumors. correlation can be used as a potential target for
As a result of their study, it was possible to retinoblastoma therapy. If EpCAM is knocked
hypothesize that increasing miR-34a expression down, it will lead to the reduction of miR-17-92,
can possibly activate the p53 tumor suppression which in turn can cause tumor regression. This
pathway, and ultimately lead to cancer cell apop- effect was observed in vitro, but has to be studied
tosis7 thus paving way for a possible future in animal models before it can be taken to the
miRNA-based therapy of retinoblastoma. Just like clinical trial level. These tumor suppressor and
miR-34a, miR-449a and miR-449b are also tumor onco-miRNAappeartobeusefultargetsforfuture
suppressor miRNA. Their over expression in ret- retinoblastomatherapy. miRNA-based therapy can
inoblastoma cell lines has been associated with be used independently or in conjunction with
decreased cell proliferation and increased apop- current forms of therapy to improve the qualityof
tosis.8 Since miRNAs are regulators of gene lifeforaretinoblastomapatient.
expression, their interactions with genes involved Identification of miRNA that are differentially
in retinoblastoma have been studied. One such expressed in retinoblastoma is possible using
study identified miR-365b-3p, an miRNA that is microarray technology. This helps in the identifi-
down regulated in retinoblastoma, and interacts cation of novel miRNA, consequently increasing
with PAX6, a gene that is involved in the number of miRNA that can be targeted for
miRNAsassociated miRNAsassociatedwith
withoncogenes tumorsuppressorgenes
Examples miR-17-92cluster miR-34a,miR-449a,miR-449b,miR-365b-3p,miR-9,
miR-182,miR-124a
Roleineyecancer Progressionofretinoblastomaby Suppressionofretinoblastomaand/oruveal
(experimental) overexpressionduetoRbgene melanomaprogressionthroughinteractionswith
deletion tumorsuppressorgenepathways
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SciJMed&VisResFounJune2014|volumeXXXII|number2|
Major review
therapy. On comparing 12 retinoblastoma tumors miR-124a is yet another tumor suppressor that
to 3 normal retinae, Martin et al.12 were able to is involved in uveal melanomatumor suppression.
identify 41 differentially expressed miRNA in ret- In an in vitro study, transfecting uveal melanoma
inoblastomatissue. cell lines with miR-124a showed a significant
miRNA released into the serum are also emer- decrease in tumor cell growth, invasion and
ging as possible biomarkers of disease. In an migration. In an in vivo study, tumor suppression
efforttoidentifyserumbiomarkersforretinoblast- was observed. It was found to be epigenetically
oma, microarray technology was utilized, and regulated during melanoma progression, leading
yielded 45 differentially expressed miRNA in ret- toitsdownregulation.17
inoblastoma serum compared with normal age
matched serum. Of these, 21 were upregulated, Conclusion
and 24 were down regulated. It was also possible Since the discovery of miRNA little over a decade
to identify the gene targets of these miRNA.13 ago, the fact that they are associated with disease
This information is invaluable as it opens many conditions has opened up an entire area of
doors for research into serum biomarkers for research. There are exciting possibilities for disease
retinoblastoma. treatment and early diagnosis by using miRNA as
biomarkers. This approach is especially important
Uveal melanoma in cancer, where associated miRNA are of two
Melanoma is a cancer of pigment cells (melano- types, oncomiRNA and tumor suppressor miRNA.
cytes). In the eye, this cancer originates from the By regulating their target genes, oncomiRNA
melanocytes in the uvea (iris, ciliary body and promote tumor progression, whereas tumor sup-
choroid). The treatments of choice for uveal mel- pressormiRNAhavetheoppositefunction.
anoma are local radiation using Iodine 125 In the section above, several tumor suppressor
plaques, and in extreme cases, eyeball removal. and oncomiRNA involved in retinoblastoma and
miRNAs are also being investigated as possible uvealmelanomahavebeendescribed.Theirrolein
therapeutic targets for uveal melanoma. miR-34a tumor progression, their possible tumor biology,
was previously correlated with tumor suppression and what this means for treatment have been
in retinoblastoma. Two members of the same hypothesized. Theoretically, if an oncomiRNA is
family, namely miR-34b/c have been associated down regulated, and atumor suppressor miRNA is
with suppression of uveal melanoma migration upregulated, tumor progression should be arrested.
andcellproliferation.Itwasfoundthattheyactas However,theprocess isneverthatstraightforward.
tumor suppressors through the down regulation of The pathways involved in tumor progression are
several genes involved in the cell cycle.14 Just as complex,andthereareseveralregulatorymechan-
inretinoblastoma,overexpressionofthesemiRNA isms. Also, this cancer related miRNA have many
canhelpindiseaseregression. gene targets, and just turning them on and off
Nuclear factor kappa B (NF-κB) is a transcrip- may not necessarily have the expected effect on
tion factor family that is involved in cell prolifer- tumor progression. What is required is a cumula-
ation, angiogenesis and tumor metastasis. tive approach involving manipulation of onco-
NF-κB1, a member of this family is a target of genes and tumor suppressor genes and controlling
miR-9,whichisassociatedwithtumorsuppression expression of tumor suppressor miRNA,
in uveal melanoma. Liu et al. showed that expres- oncomiRNA and their target genes. Once a suc-
sion of miR-9 can be associated with tumor sup- cessful combination leading to tumor progression
pression through its interaction with NF-κB1. This arrest/cancer cell apoptosis has been identified, it
same group was also able to show that miR-9 has to show a significant effect in cell lines, in
inhibits genes in the NF-κB pathway, such as vas- animal models and lastly, human clinical trials
cular endothelial growth factor A, MMP-2 and beforeitcanbeusedasaformoftherapy.
MMP-9 (matrix metalloproteinase). Such an asso- The use of circulating miRNA in blood plasma
ciation makes miR-9 a suitable target for treat- and serum as biomarkers of early stage disease,
mentofuvealmelanoma.15 however, is a more achievable target. Since cancer
Another tumor suppressor miRNA found to miRNAs are indicators of the disease, accurately
inhibit uveal melanoma progression in vitro is quantifying their expression levels can throw
miR-182. Yan et al. were able to prove that on light on the presence of the disease, and the stage
transfecting miR-182 into uveal melanoma cell of the cancer. This is a very important discovery
lines, there was increased cell cycle arrest and as it can eliminate the need for invasive methods
apoptosis. Furthermore, they were able to identify of diagnosis. This is important in tumors such as
that miR-182 works by targeting the 30 UTR retinoblastoma where tumor sampling is not
regions of MITF, BCL2 and Cyclin D2, which are possible.
involved in tumor progression. The expression of In conclusion, miRNA-based therapy and diag-
miR-182 is dependent on p53 expression, which is nosis could be the future in the fight against
aknowntumorsuppressorgene.16 cancer. miRNA and gene manipulation will have
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SciJMed&VisResFounJune2014|volumeXXXII|number2|
Major review
to be used in conjunction with existing treatment retinoblastomacellsbytargetingPAX6.FEBSLett2013;587
strategies,andthiswillbeapotentcombination. (12):1779–1786.
10. ConkriteK,etal.miR-17∼92cooperateswithRBpathway
mutationstopromoteretinoblastoma.GenesDev2011;25(16):
1734–1745.
References 11. KandalamMM,etal.OncogenicmicroRNA17-92clusteris
1. LeeRC,FeinbaumRL,AmbrosV.TheC.elegansheterochronic regulatedbyepithelialcelladhesionmoleculeandcouldbea
genelin-4encodessmallRNAswithantisensecomplementarity potentialtherapeutictargetinretinoblastoma.MolVis2012;
tolin-14.Cell1993;75(5):843–854. 18:2279–2287.
2. KimVN,HanJ,SiomiMC.BiogenesisofsmallRNAsin 12. MartinJ,etal.DifferentiallyexpressedmiRNAsin
animals.NatRevMolCellBiol2009;10(2):126–139. retinoblastoma.Gene2013;512(2):294–299.
3. QuiatD,OlsonEN.MicroRNAsincardiovasculardisease:from 13. BetaM,etal.Identificationandinsilicoanalysisof
pathogenesistopreventionandtreatment.JClinInvest2013; retinoblastomaserummicroRNAprofileandgenetargets
123(1):11–18. towardspredictionofnovelserumbiomarkers.BioinformBiol
4. Fernandez-HernandoC,etal.MicroRNAsinmetabolicdisease. Insights2013;7:21–34.
ArteriosclerThrombVascBiol2013;33(2):178–185. 14. DongF,LouD.MicroRNA-34b/csuppressesuvealmelanoma
5. ChenPS,SuJL,HungMC.DysregulationofmicroRNAsin cellproliferationandmigrationthroughmultipletargets.Mol
cancer.JBiomedSci2012;19:90. Vis2012;18:537–546.
6. LohmannDR,GallieBL.Retinoblastoma1993. 15. LiuN,etal.MicroRNA-9suppressesuvealmelanomacell
7. DalgardCL,etal.DifferentialmicroRNA-34aexpressionand migrationandinvasionthroughtheNF-kappaB1pathway.
tumorsuppressorfunctioninretinoblastomacells.Invest OncolRep2012;28(3):961–968.
OphthalmolVisSci2009;50(10):4542–4551. 16. YanD,etal.RoleofmicroRNA-182inposterioruveal
8. MartinA,etal.MicroRNAs-449aand-449bexhibittumor melanoma:regulationoftumordevelopmentthroughMITF,
suppressiveeffectsinretinoblastoma.BiochemBiophysRes BCL2andcyclinD2.PLoSOne2012;7(7):e40967.
Commun2013;440(4):599–603. 17. ChenX,etal.MicroRNA-124aisepigeneticallyregulatedandacts
9. WangJ,etal.miR-365b-3p,down-regulatedinretinoblastoma, asatumorsuppressorbycontrollingmultipletargetsinuveal
regulatescellcycleprogressionandapoptosisofhuman melanoma.InvestOphthalmolVisSci2013;54(3):2248–2256.
Howtocitethisarticle SwathiL.MicroRNA:PotentialTherapeuticsofEyeCancer,SciJMed&VisResFoun2014;
XXXII:20–22.
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SciJMed&VisResFounJune2014|volumeXXXII|number2|
Tips & Tricks
Tips and Pearls in Corneal Examination
A Shweta, B Sumanta and A Bharti
AssociateConsultant, Examination of an eye is like a jigsaw puzzle. Etiology Disease Distributionof
DepartmentofCornea&Ocular Everysymptom and sign givesyou aclue to com- filaments
SurfaceDisorder,
plete your puzzle. A complete examination would
SankaraNethralaya Viral Herpessimplex Usuallysingle
include a detailed history, visual acuity, slit lamp
filament
examination, intraocular pressure measurements,
Trauma Cornealabrasion Usuallysingle
Correspondenceto: fundus evaluation and ancillary tests like staining
layer
ShwetaAgarwal, andschirmers.
AssociateConsultant, Let us go through some common corneal signs Surgery Multiplesurgeries Diffuse
DepartmentofCornea&Ocular and see what each one tells us, however, it is Others Dryeye Interpalpebral
SurfaceDisorder,
beyond the scope of this article to cover all Superiorlimbic Upperonethird
SankaraNethralaya.
diseases. keratoconjunctivitis ofcornea
E-mail:[email protected]
1.Superficialpunctuatekeratitis: Neurotrophickeratopathy Interpalpebral
Toxicmedicamentosa Loweronethird
ofcornea
3. Epithelial defect: a breach in the continuity
oftheepitheliumiscalledasanepithelialdefect.
Dendritic:herpessimplex,herpeszoster,healing
epithelialdefect
Sign Symptoms Differentialdiagnosis
Minimallyraised Irritation Lids:concretions,
superficial FBsensation granuloma,papillae,
punctuate Watering foreignbody,blepharitis,
stainingpattern Photophobia meibomiangland
disease
Conjunctiva:
conjunctivochalasis
Ocularsurface
conditions:dryeye,
allergicorinfective 4. Ulcer: an epithelial defect associated with
keratoconjunctivitis,viral inflammation. An ulcer has varied presentations.
keratitiscontactlens
But based on its location, edges, shape, depth of
induced,toxic
involvement associated hypopyon a fair idea of
medicamentosa
etiologycanbemade.
2. Filamentary keratitis: filaments appear as
Ringulcer:fungal,acanthamoeba,pseudomonas,
mucoiddepositsadherenttothecornealsurface. severecornealburn,cornealforeignbody
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SciJMed&VisResFounJune2014|volumeXXXII|number2|
Tips & Tricks
5. Scar: final outcome of any inflammatory 7.Vascularization:
lesion. Depending on the layerof corneal involve-
ment it is three types nebular, macular and
leucomatous.
Typesof Etiology
vascularization
Superficial LSCD,Clwear,blepharitis,
Sign Symptom
chronicinflammation
Whiteopaque,no Minimalphotophobiano Deep Interstitialkeratitis,viral
epithelialdefect, painorwatering keratitis
well-definedmargins,
quieteye
Furtherreading
1. KrachmerJayH,MannisMarkJ,HollandEdwardJ.Cornea,vol
6. Edema: due to accumulation of fluid in
1;Examiningandimagingthecorneaandexternaleye.
cornealstromaand/orepithelium. 2. BasicandClinicalsciencecourse.AAO.Externaldiseaseand
cornea(section8)2013–2014.
Etiology Presentation
Primaryendothelialfailure Primarilystromal,
(Fuchs,CHED) diffuseprogressive
Secondaryendothelial Primarilystromal,
failure(viralkeratitis, focalordiffuse
trauma)
ElevatedIOPwithnormal Primarilyepithelial,
endothelium microcyticedema
Howtocitethisarticle ShwetaA,SumantaB,BhartiA.TipsandPearlsinCornealExamination,SciJMed&VisRes
Foun2014;XXXII:23–24.
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SciJMed&VisResFounJune2014|volumeXXXII|number2|
Case report
Spontaneous Resolution of Congenital Glaucoma
L Vijaya and M Baskaran
Correspondenceto:VijayaL, Abstract Gonioscopy revealed anterior insertion of iris with
Director,SriJadhavbaiNathmal, To report clinical features in five eyes of three irisprocess.Opticdiscswerehealthy.
SinghviGlaucomaServices,
cases with spontaneously resolved congenital Case 3: A 3-year old presented with a history
SankaraNethralaya,Chennai
glaucoma. All eyes showed megalocornea, deep of blunt trauma to the left eye 2 months back.
600006,India.
anterior chambers and refractive status of either Examination showed that the child was able to
E-mail:[email protected]
high myopia or astigmatism. Gonioscopy revealed fixate and follow the objects well with right eye
high anterior insertion of iris with iris processes. while there was no perception of light in the left
Three eyes showed Haab’s striae, two eyes showed eye.Therefractiveerrorintherighteyewas−2.00
features of Reiger’s anomaly. Repeated intraocular diopters spherewith −2.00 dioptercylinderataxis
pressure measurements were in normal range. of 200. Slit lamp biomicroscopy showed megalo-
Congenital glaucoma can resolve on its own cornea, Haab’s Striae (Fig. 1) and a deep anterior
leaving behind features suggestive of previous chamber in both eyes. In addition, the left eye
raisedintraocularpressure. showed complicated cataract. Gonioscopy revealed
anterior insertion ofiris with iris processes (Fig. 2)
the right eye optic nerve head showed glaucomat-
Introduction ous cupping and ultrasonography of the left eye
Congenital glaucoma occurs in one out of 10,000 revealedtotalretinaldetachment.
births and prevalence is 0.01–0.04% of general Megalocornea, Haab’s striae with axial myopia
ophthalmic patients.1 Spontaneous resolution of or astigmatism are suggestive of previously raised
such congenital glaucoma has rarely been intraocular pressure. Breaks in Descemet’s mem-
reportedintheliterature.1,2Mostofthetimessuch brane (Haab’s Striae) from increased intraocular
cases have been diagnosed on a presumptive pressure rarelyoccurafterage 3.4This suggests all
basis, that is, from subsequent findings rather five eyes possibly had raised intraocular pressure
than actual documentation of resolution of glau- before 3 years of age. Lockie and Elder2 reported
coma.3 We report five eyes of three patients where three cases of documented spontaneous resolution
in typical clinical sings of congenital glaucoma of glaucoma, out of the three cases one case was
were seen with consistent normal intraocular seen before and after disappearance of glaucoma.
pressure indicating the spontaneously resolved Their series did not mention about gonioscopic
condition. None of them had surgery or medical features. Primary infantile glaucoma has very
treatment for raised intraocular pressure prior to characteristic angel features.1 The presence or
presentation. absence of congenital glaucoma can be judged
Case 1: A 15-year old male with history of
defective vision in left eye and enucleation of
righteyeattheageof7years.Examinationofleft
eye revealed visual acuity of 6/9 with a refractive
correction of +1.00 diopter sphere and −5.00
dioptercylinderataxisof900.Slitlampbiomicro-
scopy showed megalocornea, Haab’s striae and a
deep anterior chamber. Gonioscopy revealed
anterior insertion of iris with prominent iris pro-
cesses. Intraocular pressure was 17mmHg with
applanation tonometer. Optic nerve head evalu-
ation with 90 diopter lens using slit lamp bio-
microscopy showed cup disc ratio of 0.6:1 with
healthyneuralrim.
Case 2: A 9-year old female presented with a
history of defective vision in both eyes.
Examination revealed visual acuity of 3/36 with
−7.00 diopter sphere in right eye 6/36 with
−14.00 diopter sphere in the left eye. Slit lamp
biomicroscopy showed megalocornea, deep
anterior chamber and corectopia. Applanation
tonometry showed intraocular pressure of 17 and Figure1. Case3:externalphotographyofthe
18mmHg in the right and left eyes, respectively. righteyeshowingHaab’sStriae.
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SciJMed&VisResFounJune2014|volumeXXXII|number2|
Case report
Figure2. Case3:gonioscopicphotographyoftherighteyeshowinganteriorinsertionofiris.
from non-gonioscopic signs and symptoms, but References
gonioscopy confirms the diagnosis of congenital 1. DeLuiseVP,AndersonDr.Primaryinfantileglaucoma
glaucoma. In our series, all eyes showed anterior (congenitalglaucoma).SurvOpthalmol1983;28:1–19.
2. LockieP,ElderJ.Spontaneousresolutionofprimarycongenital
insertion of iris, which eliminates possibility of
glaucoma.AustNZJOphthalmol1989;17(1):75–77.
secondary glaucoma during childhood and con-
3. MalbranE,DoddR.Megalocorneaanditsrelationtocongenital
firms the diagnosis of congenital glaucoma. The glaucoma.AmJOphthalmol1960;49:908–921.
mechanism of spontaneous resolution is unclear; 4. WaringGD,LaibsonPR,RodriguezM.Clinicalandpathological
it isthought to be due to continuous development alterationofDescemet’smembrane.SurvOpthalmol1974;18:
of angel even after birth with disappearance of 325–368.
theembryologicaltissuethatcausesprecanalicular 5. AndersonDR.Thedevelopmentofthetrabecularmeshworkand
obstuction.5 Spontaneous resolution of congenital itsabnormalityinprimaryinfantileglaucoma.TransAm
OpthalmolSoc1981;79:458–485.
glaucomaisdefiniteentity,thoughrare.
Howtocitethisarticle VijayaL,BaskaranM.SpontaneousResolutionofCongenitalGlaucoma,SciJMed&VisRes
Foun2014;XXXII:25–26.
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