Glaucoma Potpurri - DOS TIMES Bhalotra, Amit Khosla 93 F orthcoming Events C olumns 95 Membership Form Attention DOS Member DOS Times is not published in the month of May & June each

3www.dosonline.org

5 Editorial

Focus7 Glaucoma Potpurri

13 Outgoing Presidential Address

15 Incoming President Address

17 Secretary’s Report 2009-2011

19 Highlights: Annual DOS Conference

Retina59 Descemet’s Membrane Detachment Manisha Acharya, Jyoti, Umang Mathur, Kapil Arneja

65 Macular Hole Priyank Garg, Arindam Chakravarti, Sundaram Natarajan

Glaucoma

75 Post Traumatic Glaucoma Manav Sachdev, Usha Yadava

Miscellaneous

81 Myopia: An Overview Kapil Khurana, S.P. Chaudhary, Manisha Agarwal

87 Ocular TB Bobby Bhalotra, Amit Khosla

93 Forthcoming Events

Columns

95 Membership Form

Attention DOS MemberDOS Times is not published in the month

of May & June each year

Contents

DOS Times - Vol. 16, No. 10, April, 20114

SO YC TIE

D IE L H

DOExecutive Members

Delhi Ophthalmological Society SO YC TIE

D IE L H

DO

B.P. Guliani MSVice-President

[email protected]

P.V. Chadha DOMSPresident

[email protected]

Alkesh Chaudhary DO, MSJoint-Secretary

[email protected]

Amit Khosla MD, DNBSecretary

[email protected]

Ashu Agarwal Executive Member

MS

[email protected]

(Major) Arun Baweja Executive Member

MS

[email protected]

Subhash C. Dadeya Executive Member

MD

[email protected]

Rohit Saxena MDEditor

[email protected]

Harbansh Lal MSLibrary Officer

[email protected]

Pawan GoyalExecutive Member

MD

[email protected]

A.K. JainExecutive Member

DO, MS

[email protected]

Rohit NandaExecutive Member

DO, DNB

[email protected]

Deependra Vikram Singh Executive Member

[email protected]

MD

Rajesh Sinha MD, Executive Member

DNB

[email protected]

Sharad Lakhotia MSEx-Officio Member

[email protected]

Namrata Sharma MD

[email protected] Member

Sanjay Chaudhary MS

DOS Representative to AIOSEx-Officio Member &

[email protected]

Rajendra Khanna DOMS, FRSMDOS Representative to [email protected]

Ruchi Goel MSTreasurer

[email protected]

EditorialDear Colleagues and Friends,

Before I say Goodbye,

This is the last issue of DOS Times that I publish as the secretary of this august institution. The annual conference was a resounding success and my last waltz is now over.

I do however, leave the DOS secretary ship with a feeling of pride and achievement.

It is not easy to better something that is already the best and this is what i tried to do, with the help of all of you.

Some firsts and some innovations:• EPosters-introducedforthefirsttimeinDOSconference.

• LiveWebcasting-ofTheMidtermConf,andofOurSkillTransfercourses.

• JointSessionwithBJOattheannualconference.

• DOSonFacebook-hundredsofeducationalvideosuploaded-fromConferencesandDOSTprogramme.

• PublicAwarenessCompaignsOnDiabetesandGlaucomainassocwiththeDMAandGlaucomaSociety.

• DOSWebsite-totalupgradationanduserfriendlyinterfacewithlivewebcastedvideosavailableforallmembers.

• DirectoryofDOSmembersonCD-nowfullysearchableandonyourdesktop.

Friends,itisnotjusttheachievementswemadethatmakemeproud.ItistheloveandencouragementIrecievedfromeachand everyone of you. During these two years I have made hundreds of new and valuable friends. My live has been enriched, intellectually and socially and I am definitely going to miss this excitement.

Butlifegoesonandthiswholeworldwillkeeponturning.

KalAurAayengeyMehfilmeinkhiltikaliyanchuneneywaley;

Mujhseybehtarkehneywaley,tumseybehtarsuneneywaley:

I danced my last waltz, I sang my swan song and now I wish the incoming secretary all the very best and assure my commitment to this society till my last breath.

Thankingyou,

Dr Amit KhoslaSecretary, Delhi Ophthalmological Society

Editor-in-chiefAmit Khosla MD, DNB

Room No. 2225, 2nd Floor,New Building, Sir Ganga Ram Hospital,Rajender Nagar, New Delhi - 110 060Tel.: 91-11-65705229Email: [email protected]: www.dosonline.org

H.K. Tewari

J.K.S. Parihar

Sudershan Khokhar

MD, FAMS, DNB

Ashok K. Grover MS FRCS

MS, DNB

Shashi N. Jha MD

MD

Nidhi Tanwar Gagan Bhatia Vipul Nayar Daraius Shroff Ritika Sachdev

MD

DOMS

DOMS, DNB, MNAMS

MS

MS

MS

MS

MS

MD

MD

MD

MS

MS, DNB

S.K. Mishra J.S. Guha Manisha Agarwal Hardeep Singh Kapil Midha Deependra Vikram Singh Sanjiv Mohan Ajay Kumar Agarwal

Anuj Mehta Deven Tuli Prakash Agarwal V. Rajshekhar Jasmita Popli Himanshu R. Gupta Palak Shah

MS

MS

MD

MS

MS

MS

MBBS

Editorial Board

DOS OfficeDOS CorrespondentsAdvisors

Cover Design by: Amit ChauhanPublished by: Dr. Amit Khosla for

Delhi Ophthalmological Society Printers: Symmetrix

E-mail: [email protected]

Ruchi Goel MS, DNB, FICS

MD, DNB

MS

MS

MD

MS

MS

Sanjeev Gupta Sanjay Khanna Y.C. Gupta Sarita Beri Devindra Sood Umang Mathur Rajesh Sinha MD, DNB

MD

MS, DNB

MS

MD, DNB

MD

Rohit Saxena Hemlata Gupta

Neeraj Verma Vivek Gupta Amit Gupta

Rajiv Sudan Neera Agarwal Poonam Jain

MD

MS

MS

Rajpal

A.K. Singh

MD

S.P. Garg MD, MNAMS

MS

J.L. Goyal MD, DNB

7www.dosonline.org

Glaucoma Medical Management

DS: Opportunistic glaucoma screening or case detection in the clinic?

MK: First of Applanation tonometry is always done as a routine for all our patients.

Secondly, all the patients of shallow anterior chamber (< 2 mm) are screen with gonioscopy examination. Sometimes weuseAS-OCT to see the angle configuration indarksituationtodetectPAC.

It is also done for family history of glaucoma and suspicious lookingopticnerveheadeg.largecup.

SJ: I think opportunistic glaucoma screening or casedetection does not exist to a greater extent especially in a larger perspective. This is so as majority of the general ophthalmologist donotmeasure IOPof everypatient.MostmeasuretheIOPonlywhentheyfindthedisctobesuspicious on direct ophthalmoscopy.

The scenario in which opportunistic screening for glaucoma islikelytooccuris:

a) Whenanewdiagnostictoolsuchasperimeter,OCT

etc is acquired and every patient is subjected to these tests.

b) TobeapartoftheWorldGlaucomaWeekcelebrations,glaucoma diagnostic camps are organized

In both these scenarios, the interest to continue screening is short lived. This is because glaucoma diagnosis, many a times is confusing in view of many variables associated with it. Also most glaucoma patients and glaucoma suspectseatintoalotofOPDslotsandcounselingtimeandenergy. Hence it is better to avoid opportunistic glaucoma screening.TheenthusiasmtocelebrateWorldGlaucomaWeek should bemore focused at creating awarenesscampaigns rather than diagnostic camps.

RM: I feel that both have their own importance. the idea is not to miss any opportunity we come across for detecting glaucoma.

DS: How can we improve case detection?

MK: Properhistorytaking,Applanationtonometry,pachymetry,gonioscopy, stereoscopic optic disc viewing using 90D or 78D lens on slit lamp, use of imaging in special situations improves case detection.

ParagraphforrelatedGlaucomaMedicalManagement

Dr. Mayuri Khammar (MK): Head Glaucoma Service, Raghudeep Eye Clinic, AhmedabadDr. Sunil Jain (SJ): DNB, DO, FLVPEI, The Eye Super Specialities & Infiniti Eye Hospital, MumbaiDr. Rajat Maheshwari (RM): MS, Fellow LVPEI (Glaucoma), Maheshwari Eye Center, Muzaffarnagar, U.P.

Dr. Devindra Sood (DS): MS, FACS, DO, MS, Glaucoma Imaging Centre, P-13, South Extension Part-II,, Ground Floor, New Delhi - 110049

Focu

s

Dr. Sunil JainDNB, DO, FLVPEI

Dr. Rajat MaheshwariMS

Dr. Mayuri KhammarMS

8 DOS Times - Vol. 16, No. 10, April, 2011

SJ: Casedetectionofanydiseasecanbeimprovedbyfollowingaprotocol.Whatisthisprotocol?Thisprotocolisimportanthistorytakingfollowedbygoodclinicalexamination.Inmedicine this protocol is taught to us right at the beginning of our student career i.e. when the clinical postings start in undergraduate days.

However once we step into clinical practice, following this protocol is what we forget. This results in failure of early case detection.

InageneralOPD,glaucomacasedetectioncanbeimprovedby ‘sticking to thebasics’ i.e.history takingkeeping thecommonriskfactorsinmindsuchasfamilyhistory,historyof trauma, use of steroids etc. Following the history measure theIOP,examineeverytissueoftheeyefromlidstoretinaand optic nerve in every patient and perform gonioscopy if any doubt.

RM: Everypatientseenintheclinicneedstoundergoscreeningfor glaucoma. whether the patient has come for simple change of glasses or just watering & itching in eyes.

DS: Providing cost effective treatment in India : medical/laser/surgical treatment?

MK: Before one decade for India surgical treatment was considered cost effective. But for POAG, todaywithavailability of many cheaper drugs with once daily dose and lesser side effects has improved the compliance of patientsandmedicaltreatmentiscosteffectiveforPOAG.ForPACGthelaserPIisstillafirstchoiceofthetreatment.

SJ: I think the initialmodalityof treatment inglaucoma ismedical.Laseriridotomybecomestheimmediatemodalityof treatment in angle closure glaucoma.

• Medical: In providing cost effective medical treatment, one can consider starting with time tested molecules such as betablockers, pilocarpineor evengenericprostaglandins. However my choice would be based onthe initialIOP,discandfielddamageandhencethetargetIOP.Alsoonehastoevaluatetheefficacyand any contraindications of a particular molecule in a particular patient. In providing an effective treatment, Iwouldnot like a tradeoffbetweencostand compliance i.e. cheaper drop but more number of instillations.

• Laser: In treatment of angle closure glaucoma, laser iridotomy is one of the most cost effective treatments. The same cannot be said for selective laser trabeculoplasty in treatment of open angle glaucoma.

• Surgery:Amongthedifferentanti-glaucomasurgeries,trabeculectomy is probably the most cost effective surgery. However this should not be the criteria in advising trabeculectomy as the first modality of treatment in glaucoma management. This is because of the short and long termrisks andcomplicationsinvolved with trabeculectomy.

RM: Depends on what type of glaucoma & what profile of patient i am dealing with. would not generalize my opinion here. sometimes simple YAG iridotomy is all that is required to takecareofthepathology&hencemostcosteffective!butyes patient profile has to be considered before prescribing life long expensive medical therapy to them.

DS: How early case detection helps maintains QOL for our glaucoma patients?

MK: Appropriate treatment gives better control and delays progressionmaintainsgoodQoL.

Lesser drugs are needed in early disease improvescomplianceandQoL.

SJ: Early case detection helps in early awareness onpart of the patient and early treatment on part of the treatingophthalmologist.Earlierthediagnosis,lesserthemedications needed, better is the compliance. Also early treatment prevents progression of field damage and hence maintainstheQOL.

RM: Putting thepatient onmultiple IOP loweringdrugs&increasingfieldloss,bothaffecttheQOLofpatientsinabigway.earlycasedetectionhelps thepatientby takingcare of both the issues.

DS: Is Goldmann applanation tonometry (GAT) still the gold standard for measuring the IOP?

MK: Yes.

SJ: Yesverymuch.Itistheslit-lampmountedGAT,whichisthegoldstandardandnotthehandheldPerkinstonometer.

RM: Withbetterunderstandingof corneal bio-mechanics&introductionofnewertonometerslikeDynamicContourTonometer (DCT) & Ocular Response Analyzer (ORA), thereisabigquestionmarkontheaccuracyofcurrentgoldstandard GAT. For most of the patients, yes GAT is still the gold standard. Newer tonometers have to withstand the test of times & prove their worth before they can replace GAT as the gold standard.

DS: Should medical treatment come before surgery?

MK: Yes forPOAG, laser iridectomyfirst forPACS,PAC&PACG.

SJ: Yesverymuch.Becauseattimesthepost-operativecoursein glaucoma surgery can be very unpredictable in the best ofhands.Alsoifthesurgeryfailsi.e.IOPrises,onehastorestartmedicaltreatmenttocontrolIOP.Andthesuccessrate reduces with every subsequent surgery.

RM: Yes, medical therapy comes before surgical treatment for almost all of my patients.

DS: Solving compliance related issues amongst Indian patients:?

MK: - Surgery

- Selectdrugswithlesserfrequencydosing,nosideeffects

- goodcouncellingregardingthedisease.

9www.dosonline.org

SJ: Thecomplianceofanypatientimproveswhenheorsheunderstands the disease, its course, the treatment options andtheneedofaregularfollow-upvisit.Allthishastobe done on the first visit, by the treating ophthalmologist andre-emphasisedon follow-up.Theunfortunate thingabout this counseling is the amount of time required on partoftheophthalmologistespeciallyinabusyOPD.Butthis according to me the sure shot solution for improving compliance. If a doctor is not serious about a chronic disease, nor will the patient be. In addition reducing the

fear-psychosisaboutgoingblindenhancesthefaithinthetreating ophthalmologist.

RM: Good & proper counseling is most important. once the importanceoftherapy&24hourIOPcontrolisimpresseduponthepatient,mostofthepatientssticktoit.anotherveryimportantthingistoaskthepatientabouttheirroutine& discuss with them the timing of instillation of the drops. This way they realize the importance & ultimately improves their compliance with therapy.

DOS CorrespondentDevindra Sood MS, FACS

13www.dosonline.org

Outgoing Presidential Address - 2011

GoodEvening,LadiesandGentlemen.

LastyearwhenItookovertheresponsibilityofthisjob,IpausedtoreflectonmyroleastheheadoftheDOSfamily.Mytrainingperiodasthevicepresidentwasalittledifficultand thus this important question caused some distress in my mind. After deliberation from many quarters, I concluded that it was most important for DOS to function smoothly and honestly.

Frankly,Ineverthoughofmakinganydrasticordramaticchangesinthefabricofthesociety.Already,itsperformanceisratedhighinallaspects;thereforethecredibilityfactorwas the only major point in my mind. And, I am pleased to say that we have been able to enhancethesociety’scredibilityoverthelastoneyear.

Theprecedingyearsawtwomajoreventsthatwerealittledifferent.Threefull-dayskillstransferworkshopstookplaceinRPCentreandGuruNanakEyeCentre.About90-100ophthalmologistsparticipatedineachoneofthem.Theseworkshopscoveredmoreofthepracticalaspectsofvarioussubjects.

You all are aware of the rising menace of Diabetes and its implications on the eye. A Diabetic retinopathy screening programmewasconductedintheUnionTerritoryofDelhi.In30clinicsofGeneralPractitionersandPhysicians,our DOS members conducted the screening programme on a Sunday and guided the future treatments of these patients.ThesetypesofprogrammesdoproduceanawarenessofthediseaseintheGPS,Physiciansandthepatients.Such events need to be continued so as to contain the disastrous effects of Diabetes.

A Glaucoma detection programme was also conducted in the DMA house by DOS members. A large number of new patients of Glaucoma were diagnosed and their treatment instituted.

OurExecutiveconsistedofthebestoftalents;theirinputsandeffortsarecommendable.Oursecretary,DrAmitKhosla, treasurer Dr Ruchi Goel and editor Dr Rohit Saxena made a very comprehensive team. All deserve a strong patontheirbacks.

ProfessorBPGuliani,theincomingpresident,isafarsightedpersonwithwisdomandknowledge.Ipersonallyfeel that the society is bound to progress and perform better under his guidance. I wish him and his entire team lotsofluck.

LadiesandGentlemen,finallytoeachoneofyou,allIwouldliketosayisabigwhole-heartedthankyou!

Dr. Prem Vijay ChadhaPresident DOS (2010- 2011)

15www.dosonline.org

Dr.P.V.ChadhaoutdoingPresident,Dr.AmitKhoslasecretary,Dr.RuchiTreasure,RespectedseniorsanddearfriendsIamacommonophthalmologisthavingatremendouszealtoworkforgrowthanddevelopmentofthis3000strongophthalmiccommunityknownforitsintegrity,strength and academic excellence. It is popular all over the world. I am proud to get an opportunity toheadthissocietyforwhichIamthankfultoallofyou.ImustspeciallythankProf.K.P.S.Malikmymentor.Prof.V.S.Guptamyguide,myparents,mywifeandchildren,mydepartmentalcolleagues and residents.

Ijoinedthissocietyin1989aslifememberwhenmycoseniorresidentDr.ArunSangalwhowassecretaryofthissocietyaskedmetobecomememberofDOS.IhaveheldvariousexecutivepostsformorethanadecadeIgotachancetoworkundertheleadershipofLateDr.Patnaik,Dr.R.V.Azad,Dr.M.P.S.Sachdev,Dr.AKGrover,Dr.N.Shroff,Dr.S.Bharti,Dr.LalitVerma,Dr.Lakhotia,Dr.P.V.Chadha.

Incoming Presidential Address -2011

Manyofmyyoungfriendsneedtoknowthatthissocietystartedwithhumblebeginningofhalfadayofannualconferencehas grown to a three day annual conference by day and night efforts of these ophthalmic stalwarts. I salute all those hard workingandacademicallyexcellentophthalmologistswhomadethispossible.Mymaincontributiontothesocietyismyinvolvement for obtaining registration as charitable society meaning thereby that the society does not pay any income tax on itsincome.Thisexemptionwasallowedtothesocietyduringmytenureastreasureinyear1999.

Whatisgoodaboutthissociety?

• Unityindiversityofvariousstreamsofophthalmologistsi.epractitioners,teachersandresidents

• RichacademicfeastthroughouttheyearintheformofDOST,Monthlyclinicalmeetingsandtwoconferences

• Healthyindustrialsupport

• Varioussocialeventslikepicnicandculturalprogrammes

• AlloutinvolvementinstrengtheningofvariouscommunityprogramsinvolvedinalleviatingthemenaceofblindnesslikeDMandglaucoma

I assure all of you that I will put all my efforts for smooth conduct all such activities.

My vision:

• Motivatingallteachinginstitutionstoactivelyparticipateinmonthlyclinicalmeetings.Thisisrequiredforstrengtheningthe roots of society.

• DevelopmentofinfrastructureforthesocietysomethinglikeAIOShouse

• theissueofrecognitionofdaycarecenters,

• IssueoflowremunerationbyTPAs

I resolve to solve these issues.

Whatisexpectedfromyou?

I need your valuable suggestions for

• Properutilizationofcorpusamount

• Improvingutilizationoflibraryfacility

• QualityarticlesforDelhijournalofOphthalmology

• Suggestionsforconstitutionofscientificcommittee

Changeiswayoflife.Exerciseforchangeinconstitutionhasalreadybegun.Feelfreeforsendingyoursuggestionsforanychange to [email protected] or even directly to me at [email protected].

Thankyou.

Dr. B P GulianiIncoming President, DOS


ExEcutivE MEMbERS

Dr. Amit Gupta

Dr. Hardeep Singh

Dr. M. Vanathi

Dr. Prem Tanwar

Dr. R.K. Bhandari

Dr. Umesh Bareja

Dr. Vinay Kumar Garodia

Dr. Vipul Nayar

PRESiDEntDr. B.P. Guliani

vicE PRESiDEntDr. Harbansh Lal

SEcREtaRyDr. Rohit Saxena

Joint SEcREtaRyDr. Ajay Aurora

tREaSuRERDr. Ashu Agarwal

EDitoRDr. Rajesh Sinha

LibRaRy officERDr. Subhash C. Dadeya

congratulationsFollowing members have been elected as Office bearers and executive Members of the

Delhi Ophthalmological Society for the year 2011-2012 & 2013.

Respected Senior Colleagues & Dear Friends.

Iwould like to thankall theDOSmembers forhelpextended incarryingoutvibrantDOSactivitiesthroughouttheyear.I’mthankfultoSecretary,JtSecretary,Treasurer,LibraryOfficerandEditorforbeingveryhardworking&progressive.I’dalsoliketoplaceonrecordcommandableworkdonebytheentireexecutive for smooth running of the entire tenure.

Dos attained new heights and its credibility was all time high as evidenced by record participation during Annual Conference. Bye Bye & best wishes to all of you. Dr. Sharad LakhotiaPast President DOS

Outgoing President Address for 2009-2010

17www.dosonline.org

Dear Friends and Colleagues,

HonorablePresidentDr.P.V.Chadha, IncomingPresidentDr.B.P.Guliani, respectedSeniorMembers of the society and my dear friends. I on behalf of the executive welcome you all to this GeneralBodyMeetingofDelhiOphthalmologicalSociety2011.

Ibeginby expressingmyheartfelt thanks to all of you for yourkind support and constantencouragementthroughoutyear.Lookingback,wecantakesomeprideinafewachievementsand innovations.

The DOS membership continues to grow. This year we have had a record increase in our membership.541Newmemberswereadded(outofwhich28arefromDelhi)andtodaywehave6103membersfromalloverIndiaandabroad.

Outgoing Secretary Report - 2011

DOS Times is as popular as ever and we made sure to publish all the issues, sorted out the distribution issues and made it available online on our website.

TheDOSTProgrammewasgivenanewshotinthearmbyarrangingafulldayDOSTlivesurgeryworkshoponalltopicsexceptLasikandPhacoatArmyHospital(R&R)on26thNovember,2010,whichincludedVitreous,Glaucoma,Squint,CorneaandOculoplasty surgery. This was webcast live.

TheMidTermConferencewasorganizedon27thto28thNovember,2010.ThethemeoftheconferencewasTechniquesandInnovations.Alivesurgeryworkshopwasorganizedon27thNovemberfromSirGangaRamHospital,MedfortSharpSightCentre,CentreforSight&ShroffEyeCentre.ItwassponsoredbyM/s.AppasamyAssociates,M/s.IntraOcularCare(IOC)M/s.AMO,M/sZeissandM/sBausch&Lomb.TheMidtermConferencewasextremelysuccessfulwithmoreattendancethanever.Theconferencewasattendedby1136membersandtheacademiccontentwaswellappreciated.

Severalnovelintroductionsmadetheconferencemorelivelyandcontemporary;Viz:

FreePaperSession_afirsttimeforthemidtermDOSConference

E-Posters-introducedforthefirsttime.

SMSQuiz-againanovelconceptwhichwaswellappreciated.

LiveWebcastingoftheMidtermConference

Cultural programme

Nine monthly clinical meetings were held which were well attended and were of high quality academic content. They were all recordedandvidoesgrouponfacebook.-DOSonline.

DOSTeachingprogrammewasheldatArmyHospital(R&R)on8th&9thJanuary,2011.180studentsattendedthemeeting.LectureandCasePresentationandOSCEformedthesalientfeaturesofthisprogramme.Theprogrammewaswebcastlive.

TheDOSlibraryhasanonlinejournalfacilitywhichwaswell–utilizedbythemembers.WehadOVIDaccessto18journals,we have updated the website so the members can directly request for full text articles which are sent by email.

DelhiJournalOphthalmology(DJO):TheDJOhasmaintainedhighscientificqualityandhasbeenpublishedregularly.Afteralonggapofmorethan10yearsalltheissuesofDJOhavebeenpublished.

The DOS travel fellowship have been increased to 3 per year from 2 per year. The international travel fellowship amount has beenincreasedfromRs.25,000toRs.30,000/-andnationalfellowshipincreasedfromRs.5000toRs.10,000/-.

3 Skill transferprogrammeswereorganizedSquint SkillTransferProgramme, atR.P.Centre,Oculoplasty SkillTransferProgramme,atGuruNanakEyeCentre&GlaucomaSkillTransferProgrammeatR.P.Centreheldforpostgraduatesandthecomprehensive ophthalmologist which were attended by about 300 doctors.

TheWebsiteofDOShasbeenthoroughlyupgradedandmadeuserfriendly.LiveWebcasting:Skilltransferworkshoponsquint,Oculoplasty,Glaucoma.MidtermConferenceDOSTeachingprogrammeandDOSTlivesurgeryworkshopwerewebcastlive-forthefirsttimeever.Eventhosewhocould’ntattendarenowabletoparticipateandbenefit.AllthewebcastedvideosareavailabletotheDOSmemberstoseeandtolearn.TheDOSlivesurgerywasseenby242visitorsDOSMidtermconference1stdayby296and2nddayby211.


DOSonFacebook:ThiswasagreateffortonthepartoftheDOSofficeandentailedalotofhardwork.Wehaveuploadedhundreds of educational videos from the conferences, DOST and monthly meetings and we continue to do so. A wealth of info is available to anyone who joins the group.

WehaveincreasingusedthemediumofSMS,Email&Facebooktokeepthemembersinformedoftheactivitiesofthesociety.

PublicAwarenessCampaigns:AuniqueconceptandaboldinitiativeonthepartofDOStoinvolveotherassocinthePublicAwareness and Screening camps on Diabetes, Glaucoma etc. The Delhi Medical Assoc, Glaucoma Society of India and the Indian Optometric Association were involved and jointly we organized this drive for the general public.

FreeDiabeticRetinopathy screeningprogrammewereheld at 22 centres in associationwithDMA.Posters forDiabeticRetinopathy were distributed to all DMA members.

FreeGlaucomaScreeningCampfortheDoctorsofDelhiatDMAhallduringtheglaucomaweekwherealltheinvestigativefacilitiesweremadeavailablemarkedthehighpointofourinteractionwithotherorganizations.ManyDOSmembersorganizedfree glaucoma screening camps in their clinics.

PhacofellowshipTraining-Keepinginmindthatalargenumbersofmembersdonothaveaccesstomoderntechnologyandtraining,wehavestartedaphacotrainingfollowshipatVenuEyeInstituteandoutof8seatsavailableatpresent,4havebeenreservedforDelhiDOSmembersand4forNon-Delhi,DOSmembers.WethankM/s.Zeissforsupportingthisprogramme.TheallotmentisonDCRSratingandattendanceofmid-termandAnnualConference.

TheAnnualconferencewasheldfrom15thto17thApril,2011.Itwasattendedbymorethan3000delegates.Thethemeofthe conference was “Trends in Ophthalmology” giving exposure to delegates for contemporary topics and latest cutting edge technologyavailable.Livesurgerywasheldon15thAprilfromVenuEyeInstitute,ShroffEyeCentre,CentreForSightandChaudharyEyeCentre.ItwassponsoredbyM/s.Appasamy,M/s.AMO,M/s.CarlZeiss,M/s.StaarSurgicals,M/s.Bausch&Lomb&M/s.Alcon.Thescientificsessionwasspreadoutacross8hallswithatotalof63sessionswithmorethan400facultyincludingforeignfaculty.ManyInstructioncourseswereheld.Thetotalnumberofscientificpresentationswere219whichincludes18videopresentationand68posterpresentation.

LandMarksattheAnnualConference

Dr.OmParkashOrationhasbeenstartedforthefirsttime,Prof.MichaelKnorzfromGermanywhoisaninternationalPioneerinLasikgavethefirstorationonfemtosecondcataractsurgery.

Dr.S.N.MitterOrationwasgivenDr.LalitVermaandDr.P.K.JainOrationwasgivenDr.K.P.S.Malik.

JointSessionwithBJO-Anewconcepthasbeenintroducedattheannualconferenceandthesessionon“HowtoPublish”wassuccessfulwiththechiefeditoroftheBJOhimselfparticipating.

In short Highly Successful annual conference with the maximum attendance ever and a superlative cultural programme are other points worth mentioning.

ThetradeexhibitionwaswellattendedinthefrontlawnsoftheAshokHotel.

WehavedistributedaDVDwithaDOSDirectory,withagoodSearchfacility.TheDVDalsocontainssurgicalconsentformsinEnglish&Hindiandlast5yearstearsheets.

For the first time we have recorded the proceeding of the Annual Conference and these will put on the website.

TheAIOSisplanningtoholdtheAIOSannualconference(2013)inNewDelhialongwiththeAPAOconference.

Dear Friends,

Iknow Iwalk in the footstepsof giants,mypredecessorshaveworkedhardand tirelessly tomake thisorganization aninternationalforceandit isonlybefittingthatIputinmyutmosthardworkandwhichIdid.Ifeelprivilegedtobethesecretary of this greatest of all societies and today I feel highly emotional and proud. I wish all the best with full force at my command for the incoming executive.

Dr. Amit KhoslaSecretary, DOS (2009-2011)

DELHI OPHTHALMOLOGICAL SOCIETY Live Surgery

15th - 17th April 2011, Hotel Ashok, New Delhi ANNUAL CONFERENCE

Delhi Ophthalmological SocietySO YC TIE

D IE HL

D O

MOL LOA GHT ICH AP L

O

SO YC TIE

D IE HL

D O S

SO YC TIE

D IE HL

D O


O

SO YC TIE

D IE HL

D O S

15th-17th April 2011, Hotel Ashok, New Delhi

ANNUAL CONFERENCE

ANNUAL CONFERENCE


D IE HL

D O


O

SO YC TIE

D IE HL

D O S

SO YC TIE

D IE HL

D O


O

SO YC TIE

D IE HL

D O S

15th-17th April, 2011, Hotel Ashok, New Delhi

ANNUAL CONFERENCE

15th - 17th April 2011, Hotel Ashok, New Delhi


ANNUAL CONFERENCE

ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE

15th - 17th April 2011, Hotel Ashok, New Delhi 15th - 17th April 2011, Hotel Ashok, New Delhi

ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


ANNUAL CONFERENCE


DELHI OPHTHALMOLOGICAL SOCIETY Cultural Evening


ANNUAL CONFERENCE

DELHI OPHTHALMOLOGICAL SOCIETY Cultural Evening

15th - 17th April 2011, Hotel Ashok, New Delhi ANNUAL CONFERENCE

ANNUAL CONFERENCE


DELHI OPHTHALMOLOGICAL SOCIETY Oration

ANNUAL CONFERENCE


D IE HL

D O


O

SO YC TIE

D IE HL

D O S

SO YC TIE

D IE HL

D O


O

SO YC TIE

D IE HL

D O S

15th-17th April, 2011, Hotel Ashok, New Delhi

DELHI OPHTHALMOLOGICAL SOCIETY Major Sponsors


ANNUAL CONFERENCE



ANNUAL CONFERENCE



ANNUAL CONFERENCE


Various Trophies - 2011Dr. Sudhank Bharti

Dr. Krishna Sohan Singh Trophyfor Best Clinical Talk in Monthly Clinical Meeting

Dr. Neha RathiDr. H.S. Trehan Trophy

for Best Case Presentation in Monthly Meeting

Guru Nanak Eye CentreDr. Bodh Raj Sabharwal Trophy

Institution for Holding Best Monthly Clinical Meeting

Dr. Neha GoelDr. A.C. Agarwal Trophy

for Best Free Paper Presentation Session - 1

Dr. M. VanathiDr. T.P. Agarwal Trophy

for Best Free Paper Presentation Session (Cornea-2)

Dr. Anoop Kishore Gupta & Dr. Mohit Jain (RPC)Dr. V.K. Kalra Memorial Trophy

Trophy for Quiz Winners

Sir Ganga Ram HospitalDr. Minoo Shroff Trophy

for Most Popular Monthly Clinical Meeting

Certificates of Merit 1. Dr. Supita Ghosh 4. Dr. Shivcharan L. Chandravanshi for Best Free Paper Cornea Session – 3 for Best Free Paper Oculoplasty Session – 6

2. Dr. Nandini Chandak 5. Dr. Neha Mohan for Best Free Paper Glaucoma Session – 4 for Best Free Paper Cataract Session – 7

3. Dr. Neha Goel 6. Dr. Subhender Kumar Boral for Best Free Paper Retina Session – 5 (A) and (B) for Best Video Presentation

7. Dr. Parul Jain for Best E-Poster Presentation

Life Time Achievement Award1. Dr. R.B. Jain 2. Dr. L.D. Sota Life Time Achievement Award Life Time Achievement Award

49www.dosonline.org

1. Dr.DineshKalra2. Dr. Namrata Sharma 3. Dr. Sanjit Kumar Saha 4. Dr. Satish Kumar Mehta 5. Dr. Amit Raj 6. Dr.(Col.)J.K.S.Parihar7. Dr.HarbanshLal8. Dr.K.P.S.Malik9. Dr. Subhash C. Dadeya 10. Dr.UmeshBareja11. Dr.V.JayaPrakash12. Dr.MahipalS.Sachdev

13. Dr.RajendraKhanna14. Dr.S.Bharti15. Dr.AshokKumarDubey16. Dr.AshokKumarGrover17. Dr.B.Ghosh18. Dr.OmPrakash19. Dr.RajeshSinha20. Dr. Raj Anand 21. Dr.RohitSaxena22. Dr.P.V.Chadha23. Dr. Rishi Mohan Bhatnagar 24. Dr.SureshKumarVerma

25. Dr.AnitaPanda26. Dr.RajeshKumarChhoker27. Dr.ParveenKumarMongre28. Dr. (Major) Arun Baweja 29. Dr.AlkeshChaudhary30. Dr.S.C.Lakhotia31. Dr.SuchetaTripathy32. Dr.PrabinBasumatary33. Dr. Ruchi Goel 34. Dr. Deven Tuli 35. Dr.N.K.Pattnaik36. Dr.RajendraPrasad

List of Members Achieving more than 100 DCRS Credits

Dr. R.N. Sabharwal Gold Medalsfor 100% Attendance of Monthly Clinical Meetings

1. Dr. N.K. Pattnaik 2. Dr. Prabin Basumatary

3. Dr. Rajendra Prasad 4. Dr. Sucheta Tripathy

5. Dr. Vinod Kumar

Distinguished Resource Teachers of the SocietyFor achieving more than 200 DCRS Credits

1. Dr. Amit Khosla 2. Dr. Neha Goel 3. Dr. Vinod Kumar

Dr. P.K. Jain & Dr. S.N. Mitter Oration - 20111. Dr. K.P.S. Malik 2. Dr. Lalit Verma Dr. P.K. Jain Oration Dr. S.N. Mitter Oration

Dr. Om Prakash Oration 2011Prof. Dr. Michael C. Knorz

Dr. Om Prakash Oration


Application Invited from Institutions for Holding the DOS Monthly Clinical MeetingsAspertheDCRSratingstwoinstitutionswillbedroppedfromthemonthlycalenderof2011-2012.Werequestalltheinstitutions/hospitalsinterestedinholdingtheDOSmonthlymeetingtokindlyseeiftheyfulfillthecriteriagivenbelow.TheymayapplytotheSecretary’sOfficewithdetailslatestby15thJune,2011.NomeetingisheldinMayandJune.MeetingsareusuallyheldonthelastSaturdayorSundayofthemonth.

Criteria for selection of a place: (a) Seatingcapacityof100-200persons,preferablyACminiauditorium/halldefinitelywithinthepremisesoftheinstitutions.(b) AudioVisualfacilitiestobeavailable –movingmike 1set –multimediaprojector 1set –doubleslideprojectors1set(c) Instituteshouldsendthedetailsofthemeetings/CMEetc.,heldatthatinstituteinpast1yearstotheDOSoffice.(d) AsizeablestaffinOphthalmologywhowouldbeabletoconductthemeetingthemselveswithoutanymajoroutsideparticipationasspeakers/presenters. – Before the submission of application for holding the DOS clinical meeting, all the above mentioned criteria should be met. –ThesemaybeverifiedbyPresidentandSecretary.

Secretary, DOS

Proceeding Protocol for Monthly Clinical Meetings1. TheHost(usuallytheophthalmicchiefoftheHostingInstitution)willwelcometheDOSandrequestthePresidentandSecretaryofthe

DOS to come to the Dais and start the Meeting.

2. ThePresidentandtheSecretarywilltakeuptheirseatsonthesideoftheDais,whichisoppositetotheLectern.(Theywouldcontinueto be in the same position through out the Meeting, including the Mini Symposium.) The Chairman of the Symposium will be invited toaThirdseatnexttothePresidentonthesametable,afterthe‘ClinicalTalk’.TheSpeakers,whoiftheyformaPanelwouldbeseatedonthesamesideastheLectern.

3. ThePresidentwilldeclaretheMeetingopen.4. ThePresidentandtheSecretarywillthenconductthemeeting.5. Thecasepresentations(2inno.)willformthefirstpartoftheclinicalmeeting.Eachpresenterwillbeallotted10min.timeforhis/her

presentation.Thiswillbefollowedbydiscussionwiththeaudienceonboththecases(Totaltimeallottedis15min.).ThecasepresentationwillbefollowedbyaClinicalTalkof15min.duration.Thiswillbefollowedbydiscussionwiththeaudienceonthetopicfor10min.

6. Afterthefirstpartofthemeetingisover,thePresidentwillintroducethesubjectoftheMiniSymposium(whichwillbeof1hourduration)andinvitetheChairpersonoftheSymposiumtotheDaistoconducttheSymposium.AllthespeakersmaybeinvitedtoassumetheirseatsontheDaisatthistimeoronebyoneaftertheyhavepresentedtheirTalks(atthediscretionofthechairpersonofthe symposium).

7. AftertheSymposiumisover,thePresidentwillthanktheSpeakersandtheChairpersonandrequestSecretarytomakeanyAnnouncements,includingthePrizesetc.

8. Bythetime,theClinicalMeetingistobedeclaredclosedbythePresident,theHostorhisrepresentativewouldbeattheLecternto(takethefloorimmediatelyaftertheMeetingisclosed)thankpeople,firmswhohadhelpedhiminhostingtheMeetingandinvitetheMembers of the DOS for Refreshments.

9. Venue : The monthly clinical meeting will definitely be held in the premises of the allotted institution. 10. Day:ThemeetingshallbeheldonthelastSaturday/Sundayofthemonth,whichevertheinstitutiondeemsfeasible.11. Presenter : Thepresentingfaculty/resident/fellowsshouldbefromthesameinstituteforclinicalcasepresentationsandtheclinical

talk.12. Onepersonwillbeallowedonlyone-presentationfortheaward-winingsessioninthesameacademicyear.13. Exchange of dates : In case two institutions want to exchange the date of the meeting, it can be done with mutual agreement by the

headsofthedepartmentandwithinformationtothesecretary’soffice,wellinadvance.14. Mini Symposium : It shall be organized by the institution but other DOS members can be invited to participate, if required. There should

notbemorethan3speakersintheminisymposium.15. Toqualifyfortheretentioninthemonthlymeetingcalendar,aminimumattendanceof70membersisrequired(inclusiveofthemembers

of the host institute).16. For the Best Clinical Meeting award i.e. Bodhraj Sabharwal Trophy, the overall assessment of the meeting will be made purely on the

overallmarksbyoutsidedelegatesandforDr. Minoo Shroff Trophy the award will be given to the most popular meeting (based on total attendance including outside and inside delegates as per the attendance register).

17. TheattendancewillbemarkedintheregisterwhichwillbeataseparatecounterandwillbemanagedbytheDOSStaff.Atthecloseoftheclinicalmeeting,theattendanceregisterwillbesignedbytheSecretaryandthePresidentonthesameday.

18. MeetingsinthemonthofMayandJunemaybeopenedfromthenextyearifthereareapplicationsforthesame.19. Noalcoholicdrinkswillbeservedduringorafterthemeeting;onlyrefreshments/snacks/lunchwillbeserved.

51www.dosonline.org

A-4310 DR. ANJALI A.R-4343 DR. ARYA A.R.T-4463 DR. MANOJ A.T.A-4195 DR. TANUJA ABHILASHA-4296 DR. JAGMOHAN PRASAD AGARWALA-4367 DR. MANOJ AGARWALA-4455 DR. VISHNU KUMAR AGARWALA-4495 DR. SHRI KANT AGARWALA-4568 DR. SAMARTH AGARWALA-4570 DR. ARTI ELHENCE AGARWALA-4579 DR. PRERANA AGARWALA-4257 DR. MUKESH AGGARWALA-4350 DR. PARUL AGGARWALAD-1477 DR. SHIKHA AGGARWALA-4484 DR. NAMITA AGGARWALA-4131 DR. PRASHANT SOMES AGNIHOTRIA-4221 DR. ANUGYA AGRAWALA-4432 DR. RAJ KUMAR AGRAWALA-4554 DR. SURABH JWALAPRASAD AGRAWALA-4569 DR. SANTOSH AGRAWALA-4193 DR. FAREED AHMADA-4368 DR. SOFIA AHMADA-4402 DR. VAZEEM AHMADA-4509 DR. FURQUAN AHMADAD-1470 DR. ISHITA ANANDA-4433 DR. ATUL ANANDA-4468 DR. ABHISHEK ANANDA-4405 DR. AMRITA ANEJAT-4425 DR. TIWARI ANJANAA-4483 DR. ANKITAA-4502 DR. BENAZIR ANSARIA-4412 DR. ANSHUMANA-4408 DR. KAMSON ANTHONYA-4242 DR. ATIF ANWARA-4120 DR. S.D. ARAIYERA-4218 DR. AMAN SUMEET ARORAA-4369 DR. MEGHANA R. ARORAA-4385 DR. PRIYANKA ARORAA-4403 DR. PRIYANKA ARORAA-4416 DR. DIVYA JYOTI ARORAA-4443 DR. VISHAL ARORAA-4590 DR. GAGANDEEP ARORAA-4558 DR. NOWSHEEN ABDULIAH ATTARB-4238 DR. NAVEEN B.B-4283 DR. JAYA SHREE B.B-4255 DR. PANMAND PRATIBHA BABANB-4400 DR. AADITYA BAJAJB-4480 DR. PRACHI N. BAKAREBD-1478 DR. UANDANA BALACHANDRANB-4513 DR. POOJA BANDIVADEKARB-4138 DR. KARISHMA P. BANDIVDEKARB-4181 DR. CHITRABHANU BANDYOPADHYAYB-4212 DR. ADITYA BANSALB-4334 DR. REENA BANSALBD-1475 DR. SMRITI BANSALB-4422 DR. PREETI BANSALBD-1479 DR. MAYANK BANSALB-4504 DR. NISHAT BANSAL

B-4594 DR. ASHISH BANSALB-4505 DR. MANU BANSALB-4264 DR. SONAWANE ASHWINI BARKUB-4429 DR. NABANITA BARUAB-4538 DR. SUNIL BATRAB-4119 DR. ABHISHEK C. BAWDEKARB-4137 DR. MADHUSMITA BEHERAB-4144 DR. FATHIMA BENAZIRB-4516 DR. VIMLA BENIWALB-4519 DR. SUMANTA KUMAR BERAB-4277 DR. RENU BERIB-4229 DR. SHARADA BHAGAWATB-4587 DR. SHYAM BHARGAVAB-4466 DR. GAURAV BHATIBD-1482 DR. HARSIMRAN KAUR BHATIAB-4254 DR. GATI MARKANDBHAI BHATTB-4361 DR. DEBANSHU BHATTACHARYAB-4122 DR. ANUBHA BHATTIB-4299 DR. DHARMESH PRAVIN CHANDRA BHUPTANIB-4225 DR. KARMA LODAY BHUTIAB-4280 DR. TWINKEY BHUTIAB-4435 DR. ANKITA BISANIB-4549 DR. GOVIND BALLABH BISHTB-4184 DR. SHEKHAR PRASAD BISWASB-4488 DR. MRINAL MODHUR BORGOHAINB-4426 DR. SANJIB BURAGOHAINBD-1469 DR. SHALINI BUTOLAA-4398 DR. ANTONY C.L.P-4139 DR. SHARMILA C.P.L-4607 DR. MADHAVI CATHAC-4199 DR. AMAR KANTI CHAKMAC-4353 DR. PRAGYAN CHAKRABORTYC-4652 DR. RISHAB CHANDC-4274 DR. VINIT CHANDAKC-4493 DR. NANDINI CHANDAKC-4149 DR. B.S. ANIL CHANDRAM-4591 DR. BISEN PRIYANKA CHANDRAMOHANC-4344 DR. NEHA CHATURVEDIC-4160 DR. MANISHA PRANAV CHAUDHARYC-4323 DR. KANAN NANUBHAI CHAUDHARYC-4391 DR. KULBHUSHAN PRAKASH CHAUDHARYC-4565 DR. BRAJESH CHANDRA CHAUDHARYC-4182 DR. JAYASHREE CHAUDHURIC-4295 DR. DEBARPITA CHAUDHURYCD-1465 DR. NEHA CHAWLAC-4518 DR. RUPALI CHOPRAC-4414 DR. VINEET CHOUDHARYC-4602 DR. HIMADRI CHOUDHURYC-4152 DR. RACHNA CHOURASIAC-4520 DR. RAVINDRA KUMAR CHOWDHURYD-4116 DR. RUCHI DABASD-4186 DR. SONAL DANGDAD-4557 DR. MOHAMMAD AHSAN DARD-4561 DR. MOHAMAD AYOUB DARD-4394 DR. TAPAS DASS-4104 DR. KAILASH DAVEDD-1467 DR. ABHISHEK DAVED-4512 DR. MANISH DAVE

D-4301 DR. BANSRI HARSHAD DAWDAD-4571 DR. ARINDAM DEBD-4200 DR. NEHA K. DESAID-4268 DR. MAMTA SHANTHNU DESHPANDED-4406 DR. SMITA BHARAT DESHRAJD-4140 DR. SABITA DEVID-4282 DR. KUNWAR VIKRAM SINGH DHALIWALD-4448 DR. VRUSHALI DILIP DHAMALED-4300 DR. MRS. SUPRIYA DHARD-4430 DR. JASDEEP SINGH DHESID-4117 DR. VIVEK DHILLOND-4112 DR. BHAG SINGH DHIMAND-4302 DR. PARIKSHIT DHIRV-4265 DR. MAYUR KUMAR DILIPSINGH VAGHELAD-4313 DR. BRAHMBHATT DIVYANGD-4428 DR. WANGCHUK DOMAD-4165 DR. UDBHAV DORWALD-4497 DR. ASHISH KUMAR DUTTAD-4314 DR. DAISY DWIVEDIE-4451 DR. DUKALE SAGAR EKNATHE-4472 DR. EKTAF-4556 DR. SHEIKH MOHO FAROOQFD-1488 DR. JAVED HUSSAIN FAROOQUIG-4173 DR. VAIJAYANTI PRASANNA GADREG-4187 DR. VIVEK GAGNEJAG-4234 DR. UDAY RANCHHODDAS GAJIWALAG-4427 DR. HEGDE DEEPA GANAPATIG-4322 DR. DEEPTI GANAPULEG-4237 DR. MOIZA TABIR GANIG-4445 DR. GURPREET SINGH GARCHAG-4373 DR. RAJNEESH GARGG-4377 DR. RAHUL GARGG-4521 DR. PAYAL GARGG-4419 DR. HARSHAVARDHAN G. GHORPADEG-4365 DR. KAJAL PRASAD GHOSHG-4189 DR. VIPUL GOELD-4473 DR. VAISHALI GOKHALE NEE DESHMUKHR-4550 DR. GANISETTI GOPALA RAOG-4258 DR. PREETI GOYALGD-1463 DR. ISHA GULATIG-4330 DR. PARMOD GULERIAG-4147 DR. DIVYA GUPTAG-4203 DR. NAMRATA RAJIVKUMAR GUPTAG-4232 DR. ARUNIMA GUPTAG-4249 DR. PINAKI SEN GUPTAG-4279 DR. SHWETA GUPTAG-4292 DR. SANDEEP GUPTAG-4307 DR. PRABHA GUPTAGD-1474 DR. SHUCHI GUPTAG-4363 DR. DEEPSHIKHA GUPTAG-4371 DR. NAVDEEP GUPTAG-4389 DR. VINAY GUPTAG-4475 DR. REENA GUPTAG-4485 DR. PAYAL GUPTAGD-1483 DR. SHYAM KUMAR GUPTAG-4506 DR. AMISHA GUPTAGD-1485 DR. POOJA GUPTAG-4517 DR. RAJEEV GUPTA

DOS New Members List


G-4567 DR. VIBHOR KUMAR GUPTAG-4585 DR. HIMANSHU RAVI GUPTAG-4275 DR. MAUSAM GUTPAH-4128 DR. SUHAS HALDIPURKARP-4529 DR. PAREKH MUKUL HARKISHORH-4464 DR. SMITA WASUDEORAO HARNEHD-1473 DR. RAZI HASSANH-4583 DR. SHEERAZ HASSANH-4333 DR. AARTI SUBHASH HEDAK-4297 DR. POURNAMI I.K.I-4577 DR. JASIYA ISHTIAQI-4490 DR. RAFI UL ISLAMJ-4153 DR. SWETHA JADAPALLIJ-4233 DR. VIJAYKUMAR NARAYAN JADHAVJ-4312 DR. RANA JAGDISHJ-4108 DR. NEHA JAINJ-4174 DR. RUPA JAINJ-4251 DR. PARUL JAINJ-4486 DR. SANDEEP JAINJ-4487 DR. ASTHA JAINJ-4496 DR. ALOK JAINJ-4514 DR. AMIT BHURMAL JAINJ-4541 DR. PRACHI JAINJ-4601 DR. POONAM JAINJ-4340 DR. VISHAL JAISWALK-4458 DR. DIPAK KUMAR JALANIJ-4410 DR. RANADE KAUSTUEH JAYANTM-4449 DR. MEHTA RACHARA JAYESHKUMARJ-4404 DR. AMIT KUMAR JAYSWALJ-4357 DR. MONIKA J. JETHANIJ-4164 DR. MAHENDRA KUMAR JHARWALV-4236 DR. AANAL JIGISH VYASJ-4311 DR. MADHAV RANCHHODBHAI JODHANIJ-4332 DR. LIBY JOSEPHJ-4145 DR. JYOTIK-4262 DR. MANJULA K.P-4491 DR. PRASAD K.S-4413 DR. PRIYA K.S.B-4191 DR. BALAN RESHMA K.T.K-4528 DR. CHANDAN KALLAK-4123 DR. RAVI PREET KALSIK-4457 DR. SURESH PRASAD KALWANIYAK-4574 DR. HARSHLI KAMATK-4135 DR. SAURABH KAPOORK-4269 DR. STOTI KAPURK-4584 DR. MANISHA KARKIK-4540 DR. ANJU KATIYARK-4284 DR. RAVLEEN KAURK-4321 DR. MANDEEP KAURK-4605 DR. LOBO ANEESHA KENNETHK-4178 DR. NABAB ALI KHANK-4347 DR. ASIF KHANK-4555 DR. SHABANA KHANK-4614 DR. TEJASWINI PRASHANT KHANDGAVEKD-1487 DR. TANVI KHANNAK-4603 DR. GAURISH KHANNAK-4240 DR. ANITA ARORA KHANOOJAK-4409 DR. VARUN KHARBANDA

W-4560 DR. EJAZ AKBAR KIANIK-4179 DR. ZAINULIDDIN AHMAD KIDWAIK-4563 DR. RAJITHA KONDAMK-4267 DR. LEENA SANTHOSH KONDEK-4510 DR. JACOB KOSHYK-4379 DR. ANITA ARORA KOULK-4124 DR. KUMAR KRISHNAK-4610 DR. VARHA NITIN KULKARNIK-4121 DR. RAJIV KUMARK-4127 DR. ANIL KUMARK-4151 DR. ARVIND KUMARKD-1462 DR. VISHAL KUMARK-4176 DR. AMARENDRA KUMARK-4180 DR. SANJEEV KUMARK-4208 DR. PRADEEP KUMARK-4241 DR. ASHOK KUMARK-4260 DR. P. ARUN KUMARK-4270 DR. ARVIND KUMARK-4294 DR. SATISH KUMARK-4308 DR. SUSHIL KUMARK-4337 DR. BIRENDRA KUMARK-4360 DR. ASHISH KUMARK-4395 DR. BIPUL KUMARK-4396 DR. PANKAT KUMARK-4397 DR. ANAND KUMARK-4503 DR. ASHOK KUMARKD-1486 DR. (MRS.) DIMPY KUMARK-4588 DR. PRADEEP KUMARK-4592 DR. SAROJ KUMARS-4597 DR. SANJAY KUMARKD-1468 DR. REENA KUMARIK-4303 DR. ANUPAMA KUMARIK-4327 DR. SUNITA KUMARIK-4372 DR. ARCHANA KUMARIL-4465 DR. NIKHIL A. LABHSETWARL-4420 DR. ROSHAN LALL-4386 DR. NINGTHOUJAM LINTHOINGAMBIL-4209 DR. MILIND LOTKEL-4331 DR. SAURABH KUMAR LUTHRAM-4142 DR. DEEPA M.M-4202 DR. SAJITHA M.M-4326 DR. BHANUPRAKASH M.M-4593 DR. KAVITHA M.J-4133 DR. VENKATESAN M.J.K-4206 DR. KANWALJEET H. MADANM-4479 DR. MADHUM-4566 DR. SABNIS MILIND MADHUKARM-4576 DR. RITU MAHANAM-4383 DR. PRAFULLA KUMAR MAHARANAM-4143 DR. MAHESHMD-1471 DR. CHARU MALIKM-4316 DR. ANU MALIKM-4335 DR. MAMTAM-4217 DR. SEEMA KRISHNA MANEA-4444 DR. TARANNUM MANSOORIM-4559 DR. AAKIFA MAQBOOLM-4589 DR. SANGITA MARLECHAM-4185 DR. SURENDRA MATHUR

M-4439 DR. KAMLESH KUMAR MAYWADM-4370 DR. RAVINDRA KUMAR MEENAM-4543 DR. MEENAKSHIM-4359 DR. NAMRATA MEHRAM-4537 DR. JUNI MENONM-4609 DR. SONALI AJAY MHETREM-4105 DR. REWTI SHARAN MISHRAM-4141 DR. SUCHI SMITA MISHRAMD-1480 DR. SHAILY MISHRAM-4454 DR. ANURAG MISHRAM-4462 DR. SANTOSH KUMAR MISHRAM-4226 DR. CHANDANA MISRAM-4305 DR. SOMEN MISRAM-4388 DR. SHAILI MISRAM-4205 DR. APOORVA MITTALM-4207 DR. SAURABH MITTALM-4276 DR. RUCHI MITTALM-4407 DR. DEEPAK MITTALM-4526 DR. NITIN MITTALM-4582 DR. (MRS.) BELA MOHANN-4163 DR. NAIR DIVYA MONANCHANDRANM-4342 DR. LAKSHMI P. MOORTHYM-4211 DR. MEETA MUNGALEM-4552 DR. SURAJ MUNJALM-4612 DR. DEEPA MUZUMDART-4474 DR. SRINIVAS NAYAKA N.T.N-4230 DR. VIPUL KUMAR NAGARN-4508 DR. SONALI G. NAGPUREN-4362 DR. KARTIK KUMAR NAMDEVN-4418 DR. ASHOK KUMAR NANDAN-4522 DR. RUPALI NANDWANIN-4527 DR. DEEPTI NANWANIND-1481 DR. ARJUN NARANGN-4476 DR. ANURAG NARULAN-4564 DR. D. DWARAK NATHN-4243 DR. MANJIRI SANJAY NATUJ-4492 DR. JADEJA JAGRUTI NAVALSINHJIN-4381 DR. SHAH NAWAZN-4341 DR. DEEPAK N. NAWKHAREN-4188 DR. PRAFULLA KUMAR NAYAKN-4224 DR. ASHA NEGIN-4380 DR. RAHUL NEHATEN-4256 DR. SIRISH NELIVIGID-4132 DR. (MISS) MANECK D. NICHOLSONN-4457 DR. VISHAL NIGAMN-4159 DR. KUNAL HARICHANDRA NIKALEN-4470 DR. SABINA NISART-4194 DR. RAJESH O.T.O-4287 DR. (SQN. LDR) AVADHESH OLIS-4436 DR. SUVITHA P.K.ST-4239 DR. JYOTHI P.T.P-4125 DR. MEENAKSHI PANDEP-4235 DR. UMA PANDEYP-4288 DR. PRADEEP KUMAR PANDEYP-4390 DR. M.L. PANDEYP-4338 DR. RANJANA PANDEYAP-4114 DR. ARUN KUMAR PANIGRAHID-4450 DR.DESAI SAUDHAN PANKAJBHAI


53www.dosonline.org

P-4223 DR. PRAVEEN KUMAR PANWARP-4525 DR. SAMIR RAMESH PARABP-4102 DR. (CAPT.) CHANDRA PRAKASH PATELP-4107 DR. RAMESHBHAI NARAYANBHAI PATELP-4201 DR. BHARATI DASHARATHLAL PATELP-4213 DR. AMIT KUMAR PATELP-4507 DR. ASHWINI S. PATILP-4595 DR. BIJAY KUMAR PATTANIKP-4219 DR. REMYA MAREEN PAULOSEP-4355 DR. GRANTHALI ATMARAM PAWARP-4545 DR. SUNEEL KUMAR PENTYALAP-4150 DR. PIYUSH PRABHAKAR PATILPD-1476 DR. ABHINAV PRAKASHP-4431 DR. PRAGYAN PRAKASHP-4246 DR. K. SRINIVAS PRASADP-4304 DR. MUKTA PRASADP-4596 DR. CHANDRA SHEKHAR PRASADP-4228 DR. PANIKKAR KARTIK PRASANNAKUMARP-4546 DR. PRASHANTHIP-4245 DR. RAJSHREE PRAVEENN-4500 DR. NARANG PRIYAP-4573 DR. PRASHANT PRIYADARSHIP-4411 DR. DAVID PUDUKADANP-4253 DR. SURESH PRASAD PUTHALATHR-4248 DR. SANDHYA R..R-4548 DR. TASNA RABIA RAHMANR-4146 DR. JAINENDRA SHIVADAS RAHUDR-4329 DR. NIRAV DILIP RAICHURAR-4196 DR. (MAJOR) BIRESH RAJR-4129 DR. BASA DIVYA RAJESHWARRAOR-4478 DR. K.C. RAJINIR-4320 DR. BAL RAMR-4110 DR. MINU RAMAKRISHNANR-4606 DR. MEET MAVJIBHAI RAMANIR-4113 DR. MODI ROHIT RAMESHT-4215 DR.THORAT MANISHA RAMESHR-4447 DR. RAJASREE P. RAMKRISHANB-4154 DR. CHAUDHARY MRUGESH RAMSANGBHAIR-4155 DR. PUSHPANJALI RAMTEKER-4168 DR. RANVIR SINGH RANAR-4118 DR. VEERABHADHRA RAOR-4467 DR. M. SAMBASIVA RAOR-4214 DR. ABDUL RASHIDR-4134 DR. RAMIT ASHOK KUMAR RASTOGIRD-1464 DR. VANDANA RATHIR-4210 DR. PRATIBHA M. RATHIR-4161 DR. PRADEEP SINGH RATHORER-4136 DR. VANRAJ RATHWAR-4306 DR. ASHISH RAWALR-4273 DR. ACHIN RAWATR-4539 DR. MOTI LAL RAWATR-4375 DR. MARAM VENKATA RAMANA REDDYR-4126 DR. SANGEETHA KOLLAPURI RENUKAYT-4423 DR. SANTOSH TIB REWALAR-4252 DR. RASHMI RHAINAJ-4446 DR. RIMALJEETR-4278 DR. JONAKI ROYR-4553 DR. SANGEETA ROY

S-4349 DR. SHWETA VASVDEO SABNISS-4536 DR. ABU OBAID BANI SADATS-4613 DR. RAKHEE SANJAY SAGARS-4271 DR. R.N. SAHAS-4535 DR. RINKI SAHAS-4599 DR. SAIRENGLIANA SAILOS-4376 DR. MURALI SAJJAK-4216 DR. KUMAR SAMBHAVN-4499 DR. NARANG SAMIRS-4261 DR. JASDEEP SINGH SANDHUS-4319 DR. SMRITA SANDHUS-4227 DR. AGASHE VAIBHAVI SANJEEVS-4434 DR. RASHMI SANKHES-4608 DR. ARTI SAREENS-4231 DR. SAPNA DEB SARKARS-4399 DR. SAMIR SARKARS-4501 DR. HEMA SAROCHS-4171 DR. MADHU SWAROOP SAXENAS-4197 DR. MANISH SAXENAS-4318 DR. T. SELVARANIS-4534 DR. KETAN SELWARIAS-4417 DR. SAURABH SEVERIAS-4106 DR. ALKA BHUPENDRABHAI SHAHS-4192 DR. SMITESH KIRAN SHAHS-4198 DR. SONALI S. SHAHS-4244 DR. MIKEEN KAMLESH SHAHS-4324 DR. MAYUR RAMESHCHANDRA SHAHS-4364 DR. ANKIT ARVINDBHAI SHAHS-4356 DR. PURVA PRAKASH SHAHAPURKARS-4170 DR. RAJA ABU SHAHMAC-4115 DR. AVINASH SHANDRAS-4166 DR. PAWAN SHARMAS-4169 DR. VIVEK SHARMAS-4204 DR. DHARMIK R. SHARMAS-4222 DR. ARPANA SHARMAS-4263 DR. NEHA SHARMAS-4285 DR. VIKAS SHARMAS-4382 DR. SOURABH SHARMAS-4387 DR. BHUMIKA SHARMAS-4392 DR. VINOD SHARMAS-4415 DR. RAM PRAKASH SHARMAS-4438 DR. SNEHA SHARMAS-4515 DR. ASHOK KUMAR SHARMAS-4533 DR. ANUJ SHARMAS-4247 DR. HARSHA SAHEBRAO SHEJAOSD-1466 DR. HIMANSHU SHEKHARS-4530 DR. SHIKHAS-4611 DR. KHUSHBOO SHIKHANGIS-4183 DR. VIJAY BHAGWAN SHINDES-4220 DR. PRADEEP SHINGALS-4130 DR. LOKHANDE SWATI SHIVLINGS-4336 DR. ZAMBRE PRACHI SHRIKANTS-4532 DR. HIMANSHU SHUKLAS-4250 DR. MANISH V. SHYAMKULS-4156 DR. AYUSH SINGALS-4103 DR. AMANDEEP SINGHS-4148 DR. KARAMJIT SINGHS-4167 DR. IRWINDER PAL SINGH

S-4272 DR. TEJPAL SINGHS-4289 DR. KRISHNA PRATAP SINGHS-4339 DR. VISHWA PAL SINGHS-4384 DR. HARSH INDER SINGHS-4440 DR. GANPATI BAHADUR SINGHS-4441 DR. RAJMISH BAHADUR SINGHS-4481 DR. SONALI SINGHS-4489 DR. GYANENDRA SINGHS-4498 DR. KULVINDER SINGHS-4531 DR. SUBODH KUMAR SINGHS-4598 DR. PUNIT KUMAR SINGHS-4600 DR. KUNWAR KANT SINGHS-4604 DR. TANPREET PAL SINGHS-4175 DR. REKHA SINGHALSD-1484 DR. AMIT SINGHALS-4351 DR. VINOD SINGLAS-4378 DR. VIJAY RAJ SINGH SINGRAURS-4523 DR. NEHA SINHAS-4309 DR. BARKHA SOLANKIS-4459 DR. SHREYANS SONIS-4524 DR. SURABH KUMAR SONIS-4581 DR. ANKIT SONIS-4259 DR. SHISHIR SOODS-4575 DR. SUSHANK SOODSD-1489 DR. SHAGUN SOODP-4346 DR. DUDU SREEDEVIPRIYAS-4190 DR. RAMYASHRI SRIKANTAIAHS-4266 DR. ASHITA SUDS-4421 DR. CHANDAN SUDS-4477 DR. POONAM SUNDERK-4580 DR. KARANDE SUNITA SUNILS-4162 DR. CHITRA SUNOVS-4328 DR. SAMEER SUBHASHBHAI SURATWALAC-4424 DR. CHHAJED SHAILESH SURESHP-4325 DR. PATEL CHETNA SURESHBHAIS-4547 DR. PEREIRA SAVIO SYLVANT-4453 DR. BIMISHA T.T-4109 DR. OMKAR JAGDISH TELANGD-4511 DR. NEEPA THACKER DAVET-4317 DR. RAJARATHNA THANGAVELT-4293 DR. ANKUJ TINNAT-4469 DR. SANA TINWALAT-4172 DR. EVA RANI TIRKEYT-4290 DR. SATYA PRAKASH TIWARYT-4452 DR. ROSE MARY TOMYT-4298 DR. PARAG TUPEU-4482 DR. VALVEKAR PURVA UMAKANTV-4315 DR. JARIWALA MANAN UMESHCHANDRAU-4157 DR. ANAND UPADHYAYU-4544 DR. ASHOK KUMAR UPADHYAYU-4494 DR. ATUL TRIVIKRAM URSEKARV-4471 DR. M.S. USHAV-4354 DR. BIJU V.V-4393 DR. JYOTHI V.V-4461 DR. ARJUN V.V-4542 DR. RAVI KUMAR VADAPALLIV-4366 DR. ALKA VARGHESEV-4401 DR. PRASHANT VASHISHT


Contd.. page 73

59www.dosonline.org

Descemet’smembranedetachment (DMD) is an importantcause of surgery related corneal edema that may lead to

corneal decompensation. As clear corneal incision cataract surgery has advanced, increased surgical manipulation at the edgeofdescemet’smembrane(DM)hasincreasedtheprevalenceofDMdetachment.Promptrecognitionandmanagementofthiscomplication gives dramatic improvement in corneal edema and thus enhances visual outcome.

The first systemic description of DMD was made by Bernard SamuelsintheAmericanliteraturein1928.1 Descemet's membrane detachment is neither rare, nor always a benign problem. The most common cause is a localized detachment occurring during instrumentationincataractsurgery.Whenandhowtointervenefor DMD has been an area of controversy because the prognosis andnaturalhistoryofDMDarestillunclear.Inaddition,non-surgical detachments have been reported in birth injury, blunt or sharp trauma, congenital glaucomaandkeratoconus. Somepatients may be anatomically predisposed to DMD possibly because of an abnormality in the fibrillary stromal attachment to descemet’smembrane.2

Themostcommoncauseofdescemet’smembranedetachmentis mechanical separation near the incision site by an instrument, fluidorviscoelasticsubstance.3,4,5

Predisposing Factors

• Shallowanteriorchamber

• Complicatedorrepeatedsurgeries

• Inadvertent insertionof instrumentsbetween the cornealstroma and descemet's membrane

• Anteriorandshelvedincisions

• Bluntblades

• Engagingthedescemet'smembraneduringintraocularlensimplantationorwiththeirrigation/aspirationdevice(whenmistakenasananteriorcapsularremnant).

Classification

• Mackool and Holtz’ Classification based on clinical presentation - ClassificationbyMackoolandHoltzhelpsindeterminingtheprognosisofDMD.Planardetachmentsarelikelytoresolvespontaneouslyandnon-planarshouldberepaired early.3,4

• Planar(<1mmseparationfromthestroma)

• Peripheraldetachmentonly

• Combinedperipheral&centraldetachment

• Non-Planar(>1mmseparationfromthestroma)

• Peripheraldetachmentonly

• Combinedperipheral&centraldetachment

Dr Jacob’s Classification based on etio-pathogenesis6

• Strippeddescemet’smembranedetachment

• Tautdescemet’smembranedetachment

Descemet’s Membrane DetachmentManisha Acharya MS, DNB, Jyoti MS, Umang Mathur MS, Kapil Arneja MS

Dr. Shroff ’s Charity Eye HospitalDaryaganj, New Delhi-110002

Causes of Descemet’s Membrane Detachment

Surgical

Complicated/uncomplicatedCataractsurgery

• Phacoemulsificaton

• SICS

• ECCE

Glaucoma surgery –

• Viscocanalostomy

• Deepsclerectomy

• Trabeculectomy

• Iridectomy

• holmiumlasersclerostomy

Inadvertent intracorneal injections

• Viscoelstics

• Balancedsaltsolution

• Adrenaline

• Antibiotics

Penetratingkeratoplasty

Parsplanavitrectomy

Non- surgical

Birth injury

Trauma-blunt/sharp

Congenital glaucoma

Cornealectasia-keratoconus

Anatomical predispositionRe

tina


Strippeddescemet’smembranedetachment-Strippeddescemet’smembrane detachment is generally induced during viscoelastic injection or during insertion of blunt instruments or intraocular lens.

Tautdescemet’smembranedetachment-Along-standingstrippeddescemet’smembranedetachment could sometimes adhere tointraocular contents with secondary fibrosis, thus turning into a taut descemet’smembrane detachment. It could be due toinflammation involving thedescemet’smembrane, secondaryincarcerationof thedescemet’smembrane inan inflammatoryprocess,eg,inperipheralanteriorsynechiaeorwithinthegraft-hostjunction;orsecondaryincarcerationinawound/suturewithsubsequent contraction.

Morphological classification7

• DMDwithnon-scrollededges

• DMDwithscrollededges

Role of Imaging Technology

Diffusecornealedemacanobscure theslit-lampview into theanteriorchamber,makingthediagnosisandsubsequentsurgicalplanning difficult. Ultrasonographic biomicroscopy (UBM) has been advocated as a means of imaging DMD through an opaquecornea,butthisprocedurerequiresaskilledtechnician,a cooperative patient, and substantial time investment.8Anterior segment OCT may be superior alternative to UBM because of the speed and ease of image acquisition, the ability to acquire images without direct corneal contact, and the ability to image patients in the upright position.9 It determines the extent of detachment (planar or non-planar) and degree of tautness. A strippeddescemet’smembranedetachmentisseenasanundulatinglinearhyper-reflective echo in the anterior chamberwhereas a tautdescemet’smembranedetachmentisseenasastraight,tautlinebetween two points of attachment.6

Management

Conservative Approach:PlanarDMDsarevisually insignificantandresolvespontaneously(reattachment)withinfewweekstofewmonths. Conservative approach including medical treatment in the form of topical steroids and hyperosmotic agents is indicated withaclosefollow-up.

Reattachment:Spontaneousresolutionofdescemet’smembranedetachment has been reported within days to 3 months. The actual

nature of this reattachment is unclear. It has been hypothesized that the persistent pumping action of the healthy endothelium might exert an appositional force to appose detached corneal descemet’smembrane.Fortunately,theviabilityoftheendothelialcells is maintained, and they function well even after months of descemet’smembraneseparation.Thedescemet’sridgespresentfollowing reattachment are usually visually insignificant.10

Interventional Approach:Non-planarDMDsmaycausevisionlossbecause of subsequent corneal decompensation. Swift action in nonplanar DMD is essential

Internal temponade : One should be vigilant enough to notice even asmallDMDintra-operatively,immediatelyonitsoccurrence.If

Conservative approach Interventional approach

Topical steroids

Hyperosmotic agents Internal temponade – Air

Descemetopexy -14% C3F8, 20%SF6)

Transcorneal suturing

Descemetotomy

Penetratingkeratoplasty

Figure 1: anterior segment OCT of a stripped planar DMD

Figure 2: anterior segment OCT of a strippednon-planar DMD

61www.dosonline.org

stripping of descemet's mem¬brane is recognised at the time of surgery attempt may be made to reposit the same using an iris re¬positor. Sterile air should be injected at the end of surgery. Due to its short life, air is reserved for small incision detachments.11 If anterior chamber gas injection cannot be carried out at the end of the surgery, it must be done on the first day after the surgery.

Descemetopexy:Intracameralinjectionwitheitheriso-expansilesulfur hexafluoride (SF6) or iso-expansile perfluoropropane(C3F8)gashasgainedincreasingacceptanceasanefficientandeffectivetreatmentoptionfordescemet’smembranedetachments.SF6(20%)istheleasttoxicfortheendothelium.12 However, C3F8 (14%)hadlowestnumberofcomplicationsinthestudiesfoundin literature13. In addition, this procedure can be performed at the slit-lampandmaybe repeated ifnecessary. Itmayalsobecombined with transcorneal suturing if DMD is very large or having scrolled edges.

Technique of descemetopexy: After appropriate sterile draping, a few drops of topical anaesthetic are applied to the eye, and the eyelid speculum is inserted. A 26 G cannula on a 5 ml

Figure 3: Descemet’s membrane detachment

Figure 4: optical section illustrating DMD

Figure 5: 14% C3F8 Bubble in anterior chamber

Figure 6: Optical section (descemetopexy)

disposable syringe is inserted through a stab incision near the areaofattacheddescemet’smembrane(opposite to theareaofdetacheddescemet’smembrane).Cannulamaybebeplacedinareasofprevious corneal/scleralorparacentesis incision sites.Theplungeronthesyringeisslowlydepressedtoinject14%C3F8or20%SF6tofillapproximately60%oftheanteriorchamber.Whenadequategasinjectionhasoccurred,cannulaisremovedfrom the eye. The eyelid speculum is then removed following theinstillationoftopicalantibioticdrops.Postoperativeregimenincludes topicalantibiotic4 timesdaily for1weekandtopicalsteroidadministration in taperingdoses.Regular follow-up ismandatory to monitor the position and size of intraocular gas bubbleandreattachmentofthedescemet’smembrane.Figures3to8illustratecompletereattachmentofDMD2weeksfollowingdescemetopexywithiso-expansileC3F8(14%).

Complications of descemetopexy

• Raisedintraocularpressureduetopupillaryblockduetolargegas bubble or because of movement of the gas bubble behind theiris.Asimpleparacentesiswillrelievethepupillaryblock.


• Endothelialfalloutmayoccurduetoincreasedinstrumentationassociated with descemetopexy

• Despite successful reattachment, a horizontal opacity, ordescemet's membrane haze may remain at the location of the original detachment.

• Irregularastigmatismmayresultowingtotheformationofwrinklesindescemet'smembrane.

Transcorneal Suturing: It is reserved for refractory largenon-planar DMD. It is not recommended as the initial treatment duetotheriskofseverecomplicationsandinfections,wrinklesin the membrane and residual leucoma.14 Manipulations with surgicalinstrumentsshouldbelimitedduetotheriskofcausingendothelial damage.11

Combined Descemetotomy and Descemetopexy: A detached descemet membrane that is scrolled, shredded, or severely damaged isunlikely tobe repairedusingdescemetopexy andmay require more delicate surgical manipulation.7 Relaxing descemetotomy incisionsactbybreaking the stress forces thatare actingon thedescemet’smembraneandholding it taut. Itmakesthedescemet’smembranelaxandthusallowsanairorgasbubbletoapposeitagainstthecornealstroma.Long-actinggasispreferred,asitmaysometimestakelongertimetoadherewell,thus requiring a longer period of tamponade.6

Penetrating keratoplasty: It is the last resort for visual rehabilitation of scarred cornea due to DMD.

Prevention

Descemet’smembranedetachmentisaremediablebutpotentiallyblinding cause of postoperative corneal oedema. Several factors shouldbeborneinmindtohelpminimisetheriskofDMD:

• Instrumentationshouldbegentleandminimal,

• UseofBluntkeratomesandbladesshouldbeavoided,

• Early intraoperativedetection is imperative toavoidrapidprogression,

• The incision's inner corneal aspect shouldbe equal to,orslightly greater than, the incision's outer scleral aspect to prevent undue trauma during insertion and removal of phaco probesorirrigation/aspirationdeviceswithirrigatingsleeves.

Conclusion

Acarefulslit-lampexaminationaugmentedbyananteriorsegmentOCTifneeded,candiagnosedescemet’smembranedetachmentincases of corneal oedema following cataract surgery, especially if the procedurehasbeenuneventful.Variousmanagementapproacheshave been described in literature but an early descemetopexy with 14%iso-expansileC3F8or20%SF6offersbettersurgicaloutcomeboth in terms of visual acuity and resolution of corneal edema. DescemetopexyshouldbeundertakenevenifdetectionofDMDis as late as 2 months postoperatively.

References

1. Samuels B.Detachment ofDescemet’smembrane. TransAmOphtahlmolSoc1928;26:427-37.

2. Kansal, SukeshM.D.; Sugar, JoelM.D.ConsecutiveDescemetMembraneDetachmentAfterSuccessivePhacoemulsification.Cornea:August2001-Volume20-Issue6-pp670-671

3. MackoolRJ,Holtz SJ.Descemetmembranedetachment.ArchOphthal1977;95:459-63

4. IradierMT,MoreonoEetal.LatespontaneousresolutionofamassivedetachmentofDescemet’smembrane afterphacoemulsification.JCRS2002;28:1071-3

5. Hoover DL, Giangiacomo J, Benson RL. Descemet’smembrane detachment by sodium hyaluronate. Arch Ophthalmol.1985;103:805-808

6. Soosan Jacob,AmarAgarwal.Relaxingdescemetotomy relievesstress forces in tautDescemet’smembranedetachment.Ocularsurgerynews.U.S.EDITIONOctober10,2010

7. Marcon AS, Rapuano CJ, JonesMR, Laibson PR, Cohen,EJ.Descemet'smembrane detachment after cataract surgerymanagementandoutcome.Ophthalmology2002;109:2325-30

Figure 8: 2 weeks after descemetopexy (complete rereattachment)

Figure 7: 1 week after descemetopexy (partial re-attachment)

63www.dosonline.org

8. MorinelliEN,NajacRD,SpeakerMG,TelloC,LiebermannJM,RitchR. Repair of Descemet's membrane detachment with the assistance of intraoperativeultrasoundbiomicroscopy.Am JOphthalmol.1996;121(6):718-720

9. RadhakrishnanS,Goldsmith J,HuangD; et al.Comparisonofoptical coherence tomography and ultrasound biomicroscopy for detection of narrow anterior chamber angles. Arch Ophthalmol. 2005;123(8):1053-1059.

10. VMenezo,YFChoong,NRHawksworth.ReattachmentofextensiveDescemet’smembranedetachment followinguneventfulphaco-emulsificationsurgeryEye(2002)16,786–788.

11. SevillanoC,VisoE,Millán-RodríguezAC.Descemet'smembranedetachmentasacomplicationofcataractsurgery].ArchSocEspOftalmol.2008Sep;83(9):549-51

12. LeeDA,WilsonMR,YoshizumiMO,HallM.Theoculareffectsofgases when injected into the anterior chamber of rabbit eyes. Arch Ophthalmol1991;109:571-575.

13. ShahM,BathiaJ,KothariK.RepairoflateDescemet'smembranedetachment with perfluoropropane gas. J Cataract RefractSurg.2003;29(6):1242-1244.

14. JengBH,MeislerDM.Acombined technique for surgicalrepairofDescemet´smembranedetachments.OphthalmicsurgeLasersImaging2006;37:291-297.

First AuthorManisha Acharya MS, DNB

Shabu James

Rectangle

65www.dosonline.org

The term Macular Hole implies that a part of macula is missing.These are an important cause of vision loss in elderly.

Thesecanbe:-

• Partial-Thickness.

• Full-Thickness.

Partial-Thickness Macular Hole

Two types of partial-thickness holes occur: -

• Outerlamellarhole(OLH).

• Innerlamellarhole(ILH).

Outer Lamellar Hole(OLH): -

Causes: -

• Collapseofouterwalloflargecyst.

• Trauma-thereisabreakdownouterblood-retinalbarrierattheRPE.

• Opticpitsassociatedwithmacularschisis.

• Solarretinopathy.

Clinical Features: -

• Visionvariesfrom20/20(6/6)to20/400(3/60),dependingon the size & degree of photoreceptor destruction of the & on the cause (e.g., traumatic, solar).

• Onbiomicroscopic examination, a slightly irregulardeep,round, or oval excavation is seen with intact inner retinal tissue.

• F/A-demonstrates a variable degree of “windowdefect”resultingfromtheRPEatrophy&mayfortuitouslyshowdyeinaretinalcapillarydirectoverlyingpartofOLH.

• OLHsmay increase in size over time,with subsequentdecrease in vision.

• TheymayalsotransformintoFTMHiftheintactinnerretinaatrophies or is avulsed by vitreal traction.

• Thereisnoknowntreatment.

Inner Lamellar Hole(ILH): -

• AnILHismuchmorecommonthananOLH&maybeanintermediate stage in the development of some FTMHs.

Macular Hole2Priyank Garg MS, FNB, 1Arindam Chakravarti, 1,3Sundaram Natarajan

1. Aditya Jyot Eye Hospital Pvt. Ltd., Mumbai, Maharashtra, India.

2. Dept. of Ophthalmology, LLRM Medical College, Meerut, UP.

3. TNMGR University, Chennai, Tamilnadu, India.

• It represents an excavation of the inner layers of retinacharacterized by recognizable retinal tissue at its base.

Causes: -

• ChronicCME.

• Radiationretinopathy.

• Idiopathicperifovealtelangiectasia.

Clinical Features: -

• Visualacuityrangesfrom20/20(6/6)to20/80(6/24).

• DistortionmaybenotedwithoutscotomaonAmslergridtesting.

• BordersmaynotappearassharpasinFTMHsbecauseofsloping margins & thin, irregular edges.

• Thereisusuallynocuffofsurroundingsubretinalfluid&noRPEalteration.

• CanbedifferentiatedfromFTMHby“slit-beamtest”.

• F/A–EithernotransmittedfluorescenceorminimalwindowdefectiftheILHisnearlyaFTMH.

• Progression to aFTMHwith subsequent fall in vision ispossible, but rare, if the ILHhas beenpresent formanymonths.

• Thereisnoknowntreatment.

Full-Thickness Macular Hole

AnFTMHisaroundbreakthatinvolvesallthelayersoftheretina,from the internal limiting membrane through the outer segments of photoreceptor layer.

Etiology

• MostMacularHolesoccurintheabsenceofantecedentinjury& are referred to as idiopathic.

• Trauma(4-5%).

• PathologicalMyopia.

• Laser.

• ElectricCurrent.

• Misc.causes

Idiopathic Macular Hole

Introduction: (ICD-9 #362.54)

• The termMacularHole implies that a part ofmacula ismissing.

Retin

a


• Thisisanimportantcauseofvisionlossinelderly.

Epidemiology

• PrevalencerateofmacularholeinIndiaisareported0.17%,withameanageof67years.1

• Idiopathicmacularholesdeveloppredominantly inolderpatientsatanincidencerangingfrom0.03%to0.05%.2

• Theprevalence is three timesgreater amongwomen thanmen.2

• MacularHolesarebilateralinupto29%ofpatients.3

• Peakincidenceisseeninseventhdecadeoflife.

• Inacase-controlstudy,72%oftheidiopathicmacularholesoccurredinwomenandmorethan50%ofthemacularholesoccurredinpatients65to74yearsold.Only3%werefoundto occur in patients under age 55 years.4

Risk Factors

• Largelyunknown.

• A fewepidemiologic risk factorsofuncertain importancehave been reported:

• Hypertension.

• Diabetesmellitus.

• Coronaryarterydisease.

• Previouscerebrovascularaccident.

• Elevatedplasmafibrinogenlevels.

Pathogenesis

Vitreoustraction,anteroposterioraswellastangential,playsanimportant role in thepathogenesisofmacularholes.Posteriorvitreousdetachmentdecreasestheriskforfuturemacularholeformation. Fellow eyes with vitreomacular separation have less thana5%riskformacularhole18,19,20versusashighasa29%riskfor macular hole in eyes with no posterior vitreous detachment20. As described above, tangential traction caused by the condensed perifoveal cortical vitreous was supposed to be the main factor inthe initiationandprogressionofmacularhole formation17.Evaluationof the early stagesofhole formationwithOCTbyGaudric et al21 led to the postulation of a new mechanism for macularhole formation,which is basedonanterior-posteriortractional forces. These investigators have documented that posterior hyaloid detachment begins in the posterior pole around the macula and gradually spreads with focal attachment to the

Historical Timeline of Macular Hole Theories

Year Author Description

1869 Knapp Firstcasedescriptionofmacularhole(traumatic)5

1871 Noyes Firstdetailedclinicaldescriptionofmacularhole(traumatic)6

1900 Ogilvie Publishedcaseseries&proposedterminologyincludingmacularhole7

1900 Kuhnt Atraumatictheoriesofcysticretinaldegenerationleadingtomacularhole8

1901 Fuchs Earlyhistopathologicdescriptionsofmacularholeincludingcysticretinalchanges9,10

1907 Coats

1912 Zeeman Histopathologicrecognitionofpremacularvitreouscondensation219

1924 Lister Vitreousforcesand“vitreoustractionbands”(anteroposterior)maycausemacular holes11

1967 Reeseetal Vitreousseparationcriticaltomacularholeformation12

1982 McDonnelletal Possiblefemalehormonalinfluenceonvitreousseparationandmacularholeformation2

1983 Avilaetal Vitreousseparationnotnecessaryinformationofamacularhole13

1986 Morgan&Schatz Involutionalmacularthinningisapremacularholecondition14

1988 Gass&Johnson TangentialvitreoustractionandGassbiomicroscopicclassificationofJohnsonpremacular hole and macular hole lesions15,16

1995 Gass Centrifugaldisplacementofretinalreceptorswithumbodehiscence

Reappraisal of biomicroscopic classification of premacular hole and macular hole lesions17

67www.dosonline.org

foveal center. This focal attachment creates retinal convexity consistentwithanterior-posteriorvitreoretinaltraction.

More recently, Gass has emphasised the importance of the foveal Muller cell “cone”,22 originally described by Yamada23 and Hogan et al24 in histological studies of the normal human foveola. These studies showed the foveola to be composed of an inverted cone of Muller glia with a truncated apex up to the external limiting membrane(ELM).BetweentheapexandtheELMwereradiallyoriented inner cone segments radiating towards the beginning of the outer nuclear layer of cone nuclei. The base of the cone formed the umbo and extended into the clivus in the perifoveolar region.The internal limitingmembrane (ILM) lining thebaseoftheconewasextremelythin(10–20nm)comparedwiththeperipheral fovea. The sides of the cone were apposed to radiating inner segments centrally and cone nuclei in the outer nuclear layer more peripherally towards the perifoveolar region.

Staging&Clinicalfeatures:-

Basedonclinicalobservations,Gassin1988proposedafour-stageclassification for macular holes15,16&modifieditin199517.

Stage 1:

Further sub-divided into 2 stages: -

• Stage1a(ImpendingMacularHole):

• Rarelyseenclinically.

• Usuallydetectedinapatientwithafullthicknessmacularhole in other eye.

• Lossofthefovealdepressionandayellowishfovealspot(100to200micronsindiameter)

• Localizedshallowdetachmentoftheperifovealvitreouscortex with persistent adherence to the foveola initially

• Vitreofoveolartractionmaycauseasplitoftheretinaatthe fovea (“pseudocyst”) that corresponds to the yellow spot

• Epiretinalmembranesareuncommon

• Visualacuity20/25to20/80

• Stage1b(OccultMacularHole):

• Yellowring200to350micronsindiameter

• Posteriorextensionofthe“pseudocyst”withdisruptionof the outer retinal layer

• Roof remains intactwithpersistent adherenceof theposterior hyaloid to the retina



• Results fromcentrifugaldisplacementof the foveolarretina & xanthophyll.

• Characterizedbyayellowringwithbridginginterfaceof vitreous cortex.

• Maybeassociatedwithrecentmilddecreaseinvisualacuity or metamorphosia.

• F/A:-Fainthyperfluorescenceornoabnormalities.

• Visualacuitymaybeonlymildlyreduced&Amslergridabnormalitiesaredetectedonly50%ormoreofthetime.

• About50%ofholesresolvefollowingspontaneousvitero-foveolar separation.

Stage 2 (Early FTMH): -

• Smallfullthickness(lessthan300micronsindiameter)retinaldefectinaneyewithastage1macularhole


• Visual symptoms includemetamorphopsia anddecreasedvision


• Atthisstage,theposteriorcorticalvitreousisstillattachedatthe fovea and, in many cases, radial tractional striae may be visible around the edges of the hole at the level of the inner retina and internal limiting membrane.

• Inaddition, intraretinal cystoid spaces appear around theedges of the hole.

• Twoconfigurationsmayoccuratstage2:

• Centric:Thefullthicknesstearbeginsatthecentreofthefovea (umbo dehiscence) and expands in a symmetric fashion.

• Pericentric:Afullthicknessteararisesataneccentricposition in the fovea and extends in a “can opener” fashion to form a crescentic hole progressing to a “horseshoe” shaped hole and eventually, when the can opener is complete, to a round hole with a fully detached operculum of tissue suspended on the posterior vitreous cortexintheprefovealplane.Thisconfigurationistypicalinthemajorityofstage2FTMH(80–90%).

Stage 3 (Established FTMH): -

• Fullthicknesshole300to400micronsindiameter

• Posteriorhyaloidiscompletelyseparatedoverthemaculabutmay be attached to the optic disc and more peripherally

• Operculumoraflapontheposteriorhyaloidovertheholeusually evident on optical coherence tomography (Figure 4) and may be apparent clinically

• Cuffofsubretinalfluid,intraretinaledema,andcysts

• Drusen-likedeposits(mayrepresentmacrophagesatthelevelof the retinal pigment epithelium and may indicate chronicity of disease) often in the base of the hole.

• Rimofretinalpigmentepitheliumhyper/hypopigmentationoften present at the junction between edematous or detached retina and normal-appearing, attached retina in long-standing cases.


• Epiretinalmembranesmaybepresent

• Visualacuity20/100to20/400.

• Characterizedbyaroundretinaldefectgreaterthan400µwith an attached posterior vitreous face with or without an overlyingpseudo-operculum.

• NoWeiss’ringpresent.

• Rimofelevatedretinawithorwithoutprefoveolaropacity.

Stage 4: -

• Characterizedbyenlargementoftherounddefectwhichisnowsurroundedbycuffofsub-retinalfluid&exhibitstinyyellowishdepositsatthebaseofthecrater(Figure1,2&3).

• Theposteriorvitreousiscompletelydetached,asevidencedbyaWeissring.

• Visualacuitytendstodeteriorateprogressively,stabilizingat6/60orworseastheholereachesitsmaximumdiameter.

• Somepatients achieve better visual acuity by employingeccentric fixation.

Diagnostic Tests

Watzke-Allen Test: -

• Performedbyprojectinganarrowslitbeamoverthecentreof the hole both vertically & horizontally with a 90D or 78D lens.

• Pt.Withmacularholewillreportthatthebeamisbrokenorthinned.

Laser aiming beam test: -

• Performedbyprojectinga50µspotofalaseraimingbeam(e.g.He-Ne)atthecentreofthehole.

• Apatientwithmacularholewill report that the spothasdisappeared.

Figure 1: Colour Photo of Full Thickness Macular Hole

Figure 2: Red Free Photo of Full Thickness Macular Hole

Figure 3: SD-OCT of Full Thickness Macular Hole

Figure 4: SD-OCT of Full Thickness Macular Hole with operculum

69www.dosonline.org

Fluorescein Angiography:-

• Showsacorrespondingareaofhyperfluorescence.

• This result from unmasking of background choroidalfluorescencecausedbyawindowdefectinxanthophylld/tcentrifugal displacement.

Optical coherence tomography:-

• Provideshigh resolutionoptical sectionsof the retina&affordsmeasurementofretinalthickness.

• It’susefulindiagnosis&stagingofmacularholes.

• Italsomeasuresthevolumeoffull-thicknessmacularhole.

Scanning Laser ophthalmoscopy:-

• Itisusedtoevaluatethecharacteristicsofmacularholes&outcomes of surgery.

Retinal Thickness Analyzer: -

• Thishasshownpromiseindetecting&accuratelymeasuringmacular holes.

Fundus Autofluorescence:-

• Hasbeenusedasindicationoftheleveloflipofuscinintheretinal pigment epithelium.

• Normally,autofluorescenceoftheretinalpigmentepitheliumunderlying the fovea is decreased because the overlying macular yellow pigments absorb the exciting light.

• Withouttheoverlyingabsorptivepigments,amacularholecreatesawindowdefectsothatautofluorescenceisincreased.

• Thus,thischangeinvisibleautofluorescencecanbeusedasanindicationofafull-thicknessmacularholeoroffailureofsurgical repair.

Natural History: -

• Thenaturaloutcomesofstages1,2,3&4FTMHsisdifferent.

• Stage1macularholeswithoutaPVDwerefoundtoprogresstoanFTMHin33%ofpatientsbutnostage1lesionswithaPVDprogressedtoanFTMH.

• Most stage 2FTMHsprogress to stage 3or 4 (especiallycentricstage2holeswith“pericentralhyperfluorescence”&eccentric stage 2 holes).

• Stage2FTMHsthatare400micronsorsmallerwithoutaPVDmayhaveagreaterriskofenlargingwithalargerrimofsub-retinalfluid&decreasedvisualacuity.

Figure 8: SD-OCT showing Type 2 Closure of Macular Hole

Figure 5: Full Thickness Macular Hole with Retinal Detachment

Figure 6: SD-OCT of Full Thickness Macular Hole with Retinal Detachment

Figure 7: SD-OCT showing Type 1 closure of Macular Hole


• ThevitrectomyforPreventionofMacularHoleStudyGroupfoundthat:-

• theriskofprogressiontoanFTMHwasmuchhigherineyeswithstage1macularholewhohadbest-correctedvisualacuity20/50orworse.

• Stage2holesprogressed84%ofthetime,stage3holesprogressed55%ofthetime&stage4holesenlarged16%.

• Visualacuitydecreasedtwoormorelinesinthemajorityofstage2holes(68%)&lesssignificantlyfortheotherstages(stage1-30%;stage3-29%;stage4–13%).

• Inanotherstudy–

• 96%ofstage2holesprogressedtostage3or4,with71%having a two or more line reduction in visual acuity.

• Theauthorsconcludedthateventhoughvitreomacularseparation may improve the prognosis of a macular hole, stage 2 lesions usually will develop an enlarged hole and decreased visual acuity.

• TheincidenceofdisappearanceofidiopathicFTMHsislow.

Differential Diagnosis: -

Pseudoholes: -

• Mostpseudoholes areoftenundiagnosed&are the resultof a dehiscence of a portion of gliotic preretinal membrane overlying the macula, producing a lesion with surprisingly sharp but often irregular borders.

• Seenmostofteninassociationwith:-

• Idiopathicepiretinalmembraneformation

• Vitreomaculartractionsyndromes

• Proliferativediabeticretinopathy

• Rhegmatogenousretinaldetachment

• Intraocularinflammation

• Venousocclusivedisease

• Trauma.

• Whitedotfovea

Visual acuity: -

• Maybenormalorslightlyreduced.

• Contractionofassociatedfibrousproliferationmayproducemacularpucker,whichmayeffectvisionbyvirtueofdistortionmore than acuity decline, since the retina underneath is intact.

Stage Management Follow up

1A Observation • Promptreturnifnewsymptoms.

1B • Every4 to6months in the absenceofsymptoms.

2 PPV+BBGassistedILMpeeling+C3F8+ • 1to2dayspostop,then1to2weeks

Pronepositionfor2weeks • Ifnosurgery,every4to8months

3 • 1to2dayspostop,then1to2weeks

4

Hole form factor (HFF) = c + d/aa = base diameter

b = minimum diameterc = left arm length

d = right arm length

Macular Hole Index (MHI) = b/a

71www.dosonline.org

• Acirculardehiscenceinaprefovealmembranemayallowforsurprisingly good visual acuity.

• Extensive preretinalmembranesmaybe associatedwithperifoveal axoplasmic debris accumulation, which may influencethevisualstatus.

Fluorescein angiography: -

• Noabnormalfluorescenceexceptfortraction-inducedretinalvascularleakage.

• However,faintcentralfluorescencecoincidentwithchoroidalfilling that later fades occurs in pseudoholes with epiretinal membranes.

• Red-freephotographyishelpfulinoutliningtheextentofthepreretinal membrane bordering the defect.

Prognosis: -

• Usuallygoodbutdependson theunderlyingcauseof thepreretinal membrane.

• Progressivecontractionmayincreaseperifovealintraretinalvascularleakage(macularedema).

Treatment: -

• Thereisnoevidencethatlasertreatment,evenineyeswithassociatedangiographicleakage,isofvalue.

• Indeed,photocoagulationmayworsen contractionof themembrane on the surface of retina because of thermal energy absorption.

• Surgeryissuccessfulinvastmajorityofcases.

• Ifthevisionis20/80orless&thepatient’svisionisdisturbedby distortion then vitrectomy surgery to peel the epiretinal membrane is justified, this relieves surface traction.

• Thismanagementhasyet tobeevaluatedsince thereturnofvisionisusuallyincomplete&therisksofvitrectomy&progression of nuclear sclerosis always exist.

Macular Cysts: -

• Ithasanintactinner&outerretinallayerwithfluidpresentintraretinally.

• Cysticmaculardegenerationinvolvesextensiveinnerretinalischemic atrophy with loss of nerve fiber layer, ganglion cells, inner plexiform & inner aspects of inner nuclear layers.

• Cystoidspacesinthemaculadevelopfromdegenerationofmuller cells & eventually progress to irreversible liquefaction necrosis of these cells & neuronal degeneration.

• Collapseofsmallercysticcavities,creatingalargeconfluentcyst, in chronicor severeCMEcreates a lesion thatmayappear similar to macular hole on direct ophthalmoscopy.

• CMEmaybeassociatedwith:-

• Useofintraoculargas.

• Choroidaltumors.

• Retinalvascularocclusivedisease.

• Trauma.

• Ocularinflammation.

• Exudativemaculardegeneration.

• Diabetesmellitus.

• Macularpucker.

• Retinitispigmentosa.

• Maculartelangiectasias.

Visual acuity : -

• Usuallyrangesfrom20/20to20/100.

Fluorescein Angiography:-

• Revealspoolingofthedyeinthecystoidspacesinthelatevenous phase.

• AnRPEdetachmentcanbedistinguishedbyslow&completesubpigmentepithelialleakage&neurosensorydetachmentwillbeassociatedwithafocalRPEleak.

• Tractionneurosensory retinal detachmentwill shownoabnormalfluorescence.

Diagnosis: -

• Watzke-Allentestdifferentiatesaholefromacyst.

• Ifacompleteinterruptionoraninterruptiongreaterthanonehalf the width of the slit then FTMH.

• Nointerruptionorslightnarrowingordistortionintheslitcorrelates – pseudohole, cyst or lamellar hole.

• TheAmslergridalthoughsensitiveisnotspecific.

Prognosis:-

• Dependsontheunderlyingcause.

• Thesize&chronicityofthecystoidedema,associatedvitrealtraction & disruption in the anatomic architecture of the perifoveal tissue may lead to inner lameller or FTMH.

Treatment : -

• NotreatmentisindicatedexceptinpatientswithpartialPVDwith ongoing traction to a cystic macula, esp. in a patient with poor vision in the fellow eye.

• Parsplanavitrectomyisusedtoseparatepartiallydetachedposterior hyaloid face from underlying cystic retina.

Treatment of FTMH: -

Indications of Surgery: -

• Stage2MHwithVA<6/12

• Stage3or4MH

Case Selection: -

• Carefulpatientselectioniscriticaltoasuccessfuloutcome.


• Ideal candidatewouldbe apatientwithbilateralholesofrecent onset, with vision in his better eye inferior or equal to 6/36.

• Patientswith symptomatic unilateral holeswith recentlyreducedvisionto6/24orworsearealsogoodcandidates.

• Sincestage1macularholeshaveahighrateofspontaneousresolution & reported studies have failed to demonstrate any benefit from vitrectomy, surgery is not usually recommended for this early stage.

Prognostic Factors

i) Stage of hole – earlier the better

ii) Pre-opVA–thegoodthebetter

iii) Pre-opLensStatus–theclearerthebetter

iv) Duration of hole – longer the duration, grim surgical results.

v) Hole Form Factor (HFF) – indirect indicator of the size of hole.ThehigherthevalueofHFF(>0.9)thebetteraretheresults.Calculatedasfollows:-

vi) Macular hole Index (MHI)– is basically the ratio of hole height with base diameter. Higher MHI (≥0.5) correlates with better visual outcomes.

vii)No.ofsurgeries-Patientswhohavehadtwofailedsurgeriesfor a macular hole generally derive little or no visual benefit even if a third surgery closes the hole.

viii)Scanning LaserMicroperimetry –maximumpara holesensitivity showedapositivecorrelationwithpost-opVA.Stimuli are positioned on the retina around the macular hole. Thefirst stimuli arepresented at 15–20dB. If thepatientidentified all stimuli around the hole or if none of the stimuli are seen, the intensity was adjusted until some stimuli are seen. The intensity is then decreased gradually until the patient did not see any stimuli around the hole, which is defined as the “maximum para hole sensitivity”.

ix) Shorter axial length

Results: -

Twotypesofholeclosurehasbeendefined:-

• Type 1 closure indicates that themacular hole is closedwithout foveal defect of the neurosensory retina (Figure 7).

• Type 2 closure indicates that a foveal defect of theneurosensory retina persists postoperatively although the whole rim of the macular hole is attached to the underlying RPEwithflatteningofthecuff(Figure8).

• Visualimprovementisachievedin55%to85%ofeyeswithafinalvisualacuityof6/12orbetterinupto65%.

• Stage2holesrandomizedtosurgeryhadasignificantlylowerincidence of hole enlargement.

• Bilateral visual function improves after successfulFTMHsurgery,especiallyinpatientswithsubnormal(<20/40)visualacuity in fellow eye.

Chemical vitrectomy/ Enzymatic Vitrectomy: -

• Aninofficeprocedure

• Enzymaticmanipulationofposteriorhyaloids&vitreouscortex is carried out using 0.4 IU autologous plasmin & the solutionislavagedfollowedby14%C3F8.

Adjunctive Agents: -

Thrombin:-

• AknownstimulatorofRPE&glialcells.

• Failedtoshowmarkedincreaseinthesuccessrateofmacularhole closure.

• Increasedpost-opinflammation.

Gelatin plugs: -

• Preliminaryresultsofvitrectomyfollowedbyplacementofanabsorbablecross-linkedgelatinpluginstages3&4havebeen encouraging.

• Recommendeduseinhighmyopeswithposteriorstaphylomaor recurrent macular hole.

TGF ß-2: -

• Itappearstopromotewoundhealingbystimulatingcollagenfibril growth, glycoproteins & proteoglycans.

• Studies have suggested a potential benefit usinghumanrecombinantTGFß-2forpersistentFTMHsfollowingfailedprimary surgery & for traumatic holes.

Autologous platelet concentrate: -

• It induces a localizedfibrocellular response that seals theretinectomyedge,involvingamixedpopulationofglial,RPE& fibroblastic cells.

• Ithasabeneficialeffect inprimaryFTMHsurgery&alsoincreased the surgical success rate in reoperations combined with rigorous epiretinal membranectomy.

References

1. SenP,BhargavaA,VijayaL,GeorgeR.Prevalenceof idiopathicmacular hole in adult rural and urban south Indian population. ClinExperimentOphthalmol2008;36:257–60.

2. McDonnellPJ,FineSL,HillisAI:Clinical featuresof idiopathicmacularcystsandholes.AmJOphthalmol93:777–786,1982

3. EzraE,Wells JA,GrayRH, et al. Incidence of idiopathic full-thicknessmacularholesinfelloweyes:a5-yearprospectivenaturalhistorystudy.Ophthalmology1998;105:353–359.

4. The EyeDiseaseCase-Control StudyGroup. Risk factors foridiopathicmacularholes.AmJOphthalmol1994;118:754-61.

5. Knapp H: Ueber isolerte zerreissungen der aderhaut in folge von traumenaufdemaugapfel.ArchAugenklinik1:6–29,1869

6. Noyes HD: Detachment of the retina, with laceration at the macula lutea.TransAmOphthalmolSoc1:128–129,1871

7. Ogilvie FM: On one of the results of concussion injuries of the eye (“holes”atthemacula).TransOphthalmolSocUK20:202–229,1900

73www.dosonline.org

8. Kuhnt H: Uber eine eigenthumliche veranderung der netzhaut ad maculam (retinitis atrophicans sive rareficans centralis).ZtschrAugenheilk3:105–112,1900

9. CoatsG:Thepathologyofmacularholes.RoyLondonHospRep17:69–96,1907

10. FuchsE:Zurveranderungdermaculaluteanachcontusion.ZtschrAugenheilk6:181–186,1901

11. ListerW:Holes in the retinaand their clinical significance.Br JOphthalmol8:1–20,1924

12. ReeseAB, Jones IS,CooperWC:Macular changes secondary tovitreoustraction.AmJOphthalmol64:544–549,1967

13. AvilaMP, JalkhAE,MurakamiK:Biomicroscopic studyof thevitreousinmacularbreaks.Ophthalmology90:1277–1283,1983

14. MorganCM,SchatzH:Involutionalmacularthinning:Apremacularholecondition.Ophthalmology93:153–161,1986

15. Gass JD: Idiopathic senilemacular hole: Its early stages andpathogenesis.ArchOphthalmol106:629–639,1988

16. JohnsonRN,Gass JD: Idiopathicmacularholes:Observations,stages of formation, and implications for surgical intervention. Ophthalmology95:917–924,1988

17. GassJD:Reappraisalofbiomicroscopicclassificationofstagesofdevelopmentofamacularhole.AmJOphthalmol119:752–759,1995

18. FisherYL, Slakter JS,YannuzziLA, et al.Aprospectivenaturalhistory study and kineticUltrasound evaluation of idiopathicmacularholes.Ophthalmology1994;101:5–11.

19. LewisML,CohenSM,SmiddyWE.Bilateralityofidiopathicmacularholes.GraefesArchClinExpOphthalmol1996;234:241–5.

20. TrempeCL,WeiterJJ,FurukawaH.Felloweyesincasesofmacularhole:biomicroscopicstudyofthevitreous.ArchOphthalmol1986;104:93–5.

21. GaudricA,HaouchineB,MassinPetal.Macularholeformation:new data provide by optic coherence tomography. Arch Ophthalmol 1999;117:744–51.

22. GassJDM.Mullercellcone,anoverlookedpartoftheanatomyofthefovea centralis. Hypotheses concerning its role in the pathogenesis of macular hole and foveomacular retinoschisis. Arch Ophthalmol 1999;117:821–3.

23. YamadaE. Some structural featuresof the fovea centralis in thehumanretina.ArchOphthalmol1969;82:152–9.

24. HoganMJ,AlvaradoJA,WeddellJE.Histologyofthehumaneye.Anatlasandtextbook.Philadelphia:WBSaunders,1971:492–7.

First AuthorPriyank Garg MS, FNB

V-4460 DR. V. PANIMALAR A. VEERAMANIV-4158 DR. BRAJESH SINGH VERMAV-4177 DR. SANJEEV VERMAV-4345 DR. GAJENDRA KUMAR VERMAV-4442 DR. RAJEN VERMAV-4572 DR. HEMENDRA KUMAR VERMAV-4286 DR. V.R. VIJAYARAGHAVAN

V-4281 DR. GHARAT MIHIR VINAYK-4586 DR. KULKARNI SHRINIVAS VINAYAKRAOV-4374 DR. PRIYANKA VIRMANIV-4111 DR. NASTA NIKHIL VISHNUV-4348 DR. MEGHANA R. VYASW-4456 DR. MITHUN PRAFULKUMAR WADEKAR

WD-1472 DR. BATRITI SHYMPLIANG WALLANGW-4437 DR. ASHWINI JAGANNATH WAVAREY-4291 DR. VINOO KUMAR YADAVY-4358 DR. BINDU YADAVY-4352 DR. VINOD BHAUSAHEB YENAGEZ-4578 DR. MD. MASIH UZ ZAMAN

New Members List (Contd....) from page 53

75www.dosonline.org

Glaucomaisawellknowncomplicationinvariousformsofeye trauma. It is the major cause of unilateral blindness world

wide.PropermanagementofglaucomarequirescarefulhistorytakingandexaminationineverycaseofeyetraumasoastodetectGlaucoma early and to manage it effectively.

Classification Glaucoma after trauma can be categorized by

• Typeofinjury

• Onsetofglaucoma

According to Onset of Glaucoma causes can be Immediate and Delayed Onset.

Immediate

• Contusion

• Trabeculardisruption

• Hyphema

• Massivechoroidalhaemorrhage

• Chemicalinjury

Delayed

• Anglerecession

• Peripheralanteriorsynechiae

• Lensinduced

• Subluxation

• phacomorphic

• phacolytic

• lensparticle

• GhostcellGlaucoma

• Closureof cyclodialysis cleftAccording toTypeof injuryresponsible for causing glaucoma

• FibrousepithelialdowngrowthBlunttrauma

• RetainedIntraocularforeignPenetratingtrauma

• BodyChemicalinjury

• RhegmatogenousRDRadiationinjury

• Surgery

Blunt trauma is the most common cause of glaucoma throughout theworld.Highriskgroupsinclude.

Post Traumatic GlaucomaManav Sachdev MBBS, Usha Yadava

• Men

• Agelessthan30

• Professional athletes particularlyBoxingAndBall gamesSuchAsvolleyball,toygunpellet,badmintonshuttle,cricket,tennis

• assault

• Childabuse

• African-americanrace

• Sicklecelldisease

Contusion Injury

In this there active inflammationof the trabecularmeshworksoonafter the injury, leading to transientdecrease inoutflowfacility from the TM. There is no evidence of angle recession, angle disruption or Hyphema, angles are typically open.. It is a self limiting condition. Sometimes topical and hyperosmolar agents mayberequiredtocontroltheIOP.

Trabecular Disruption

If gonioscopy is done within 48 hours of the injury damage to the angle structures can be identified. There might be haemorrhage in totheschlemm’scanalordamagetotrabecularmeshworkwhichmightberestrictedtooutersheetsortheremightbefullthicknessinjurytotheTM.AflapofinjuredTMiscreatedjustbelowthesight of rupture which hinges at the scleral spur.

Hyphema

BloodinACcanbeeitherduetoBluntorPenetratinginjury,inblunttraumathereisantero-posteriorcompressionandequatorialexpansion leading to damage to ciliary body and TM. There are shearing forces acting on the angle structures and the ciliary body leading to damage to the anterior face of ciliary body and damage to major arterial circle acusin the hyphema,

Penetrating injury leads tohyphemabydamaging the bloodvessels and due to hypotony. Certain conditions lead to HYPHEMAeveninMINORTRAUMA–Rubeosisiridis,juvenilexanthogranuloma, iris melanoma, iris leiomyosarcoma, myotonic dystrophy , vascular iris tufts blood dyscrasias.

Hyphema resorption occurs by anterior surface of the iris and TM. Uncomplicatedhyphemasareclearedwithin1week.

Grading

• grade1:<1/3thofAC

• grade2:1/3oth-1/2ofAC

• grade3>½ofAC

• grade4:totaloreightballhyphema.Guru Nanak Eye CentreMaharaja Ranjit Singh Marg, New Delhi

Glau

com

a


Complications of Hyphema

• IncreasedIOP:variouscausesofhighiopinhyphemaare:

• occlusionoftrabecularmeshworkbyclot,inflammatorycells, erythrocytic debris.

• papillaryblockduecollarbuttonshapedclot.

• Peripharalanteriorsynechiae:PASareformedifhyphemapesistsformorethanaweek.

• Opticatrophy:opticatrophyinhyphemacanoccurbecauseofhigh IOP , contusion to theopticnerve, secondary todamage to short posterior ciliary arteries. Risk of opticatrophyincreaseswhenthIOPis>50mmHgfor5daysor35mmHgormorefor7days.PatientswithsicklecelldiseasehaveopticatrophyevenatnormalorslightlyraisedIOP.

• Corneal blood staining:. Factorswhich influence cornealblood staining include: rebleeding, prolongd clot duration, sustainedincreaseinIOPandcornealendothelialdysfunction.

Twomain risk factors of corneal blood staining includeIOP>25mmHgand>6daysduration.

Earliest sign of corneal blood staining is a straw coloureddiscoloration of deep stroma, presence of tiny yellow granules in posterior1/3rdofthecornea.

In sunlight the haemoglobin gets converted in to porphyrins, which toxic to the corneal endothelium therefore patching might have a role in management of hyphema.

Corneal blood staining can cause decreased visual acquity and depriviation amblyopia in children.

• Secondary haemorrhage: rebleed occurs because of clotretraction on and after day 4. signs of rebleed incude increase in size of hyphema, layer of freas RBCs over previous clot, changeofcolourfromdarkredtobrightred.

Chancesofrebleedaremorewithblackraceandchildren

• Accomodativeimpairment

Massive Choroidal Haemorrhage

It is rare cause of pressure elevation in trauma signs include shallowAC,poorredreflex,choroidalelevationinIO.IndicationsofsurgicalinterventionincludepersistentelevationofIOP,lenscorneaapposition,kissingchoroidals

Chemical Injury

Alkaliburnsare themaincauseofglaucomaamonstchemicalinjuries.Mechanismisbyshrinkageoftheoutercoatsoftheeye,releaseofprostaglandins,andblockageofTMbyinflammatorycellsformationoPAS

Late Onset Glaucoma after Trauma

Angle Recession

COLLINSwasthefirstpersontodescribeanglerecessionduetoblunttraumain1892.WolfandZimmermanin1962linkedanglerecession to development of Glaucoma.

Anglerecessionoccurs in20-94%casesofeyetrauma.Studiesindicate that incidence of glaucoma in angle recession ranges from7-9%.

Pathologicallyanglerecessionisaseparationbetweenthecircularand the longitudinal fibers of the ciliary body, longitudinal muscles remain attached to the scleral spur. There might be associated cyclodialysis, iridodialysis, damage to the lens manifested as cataract,subluxation,dislocation,hyphema.Latertheinnerlaterof ciliary body atrophies leading to broadand fusiform ciliary band appearance on gonioscopy.

GradingisdoneaccordingtoHoward’sClassificationasGradeI(shallow), grade II (moderate), grade III (deep)

Gonioscopic findings:

• deepeningofangle

• wideningofexposedfaceofciliarybody

• posteriordisplacementofirisroot

• disruptionofuvealprocesses

• abnormalwhiteningofscleralspur

• greywhitemembraneovertheTM

Bilateral simultaneous gonioscopy is a very effective way detecting even the subtle changes in the angle.

MechanismofelevatedIOPisdamagetotheTMinsteadoftheactual angle recession. Angle recession indicates the extrent and severity of the injury. It is advised to do gonioscopy within 48 hours of trauma to detect trauma to the TM.

Peripheral Anterior Synechiae

PAScanformduetovariousreasonsasthereis inflammation,apposition of iris to the cornea, there might be hyphema leading toorganizationofblood.Penetrating traumacan lead toPASformation by chronic shallowing of AC, endothelialization of angle.EpithelialorfibrousdowngrowthintotheAC.

Ghost Cell Glaucoma

Campbell described a condition in cases of blunt trauma with vitreous haemorrhage and hyphema. Hyphema cleared with in 2 weeksbutRBCsinvitreouslosttheirHBanddegeneratedittogostcellin2weeks.Duetotheassociatedbreakintheanteriorhyloid phase these cell come in to the AC and being less pliable theyblock theTM leading to elevationof IOPwhichusuallyoccurs2weeks–3monthsaaftertheinjury.theasecellshaveacharacteristic ochre color can form a layer of cells in AC leading toapsuedohypopyonandmaygiverisetoCandy-StripeSign

Lens Induced Glaucoma

This group has lens as a common pathogenic cause, the angle mightbeopenorclosed.Variouscausesare

• Lens swelling: trauma can lead to swelling of the lens and cataract. Swollen lens pushes the iris len diaphragm forwards andcausespapillaryblockleadingtoHIGHIOP

• Lens dislocation/subluxation: lens may be dislocated in to theACleadingtopapillaryblockmechnicallyoritmaybe

77www.dosonline.org

dislocated posteriorly leading to vitreous coming in to the ACandcausingpapillaryblock

• Phacolytic glaucoma. An open angle glaucoma occurs due to release of lens proteins through an intact lens capsule.

• Lens particle glaucoma:duetofranklydisruptedlenscapsulefrgamentsoflensandproteinblocktheTM.

Delated Closure of Cyclodialysis Cleft

Formation of a cyclodialysis cleft leads to hypotony due to decreasedproductionofaqueous,whichleadstodecreasedflowacrosstheTMresultinginreducedpermeabilityoftheTM.Whenclosureofthecleftoccurs,IOPincreasesacutelyleadingtopain,cornealedema,DOV,openangles.

Retained Intraocular Foreign Body

iron foreign body might lead to siderotic glaucoma which is associatedwithheterochromia,mydriasis,rustlikediscolorationanterior subcapsular ares of lens and the posterior surface of cornea.

Retinal Detachment

Glaucomacanbeattributedtotrabecularinflammationleadingtodecreasedoutflow,blockageofTMbypigmentorphotoreceptors.RepairingtheRDcasespermanentdecreaseinIOPprovidedthereis no other abnormality in TM.

Management of Post Traumatic Glaucoma

InacutelyelevatedIOPismanagedbygivingtopicalantiglaucomaagents as well as systemic carbonic anhydrase inhibitors, hyperosmolaragentsuntilthetrabecularinflammationsubsides.However certain cases needs specific interventions which are mentioned here

Hyphema: Medical Management:

• Anti fibrinolytic agents:epsilonaminacaproicacid(EACA)and Tranexamic acid are used to prevent rebleed in cases of hyphema

EACA(amicar )binds to lysinemolecules in the clot vialysine binding site and inhibits fibrin clot digestion. Its dose is100mg/kgevery4hourstoamaximumdoseof30g/dayby mouth for 5 days.

Side effects include nausea, vomiting, diarrhea, postural hypotention,pruritis,musclecramps,rash,nasalstuffiness,arrhythmia, confusional state. Rhabdomyolysis and myoglobinuria are rare.. Contraindications include drug allergy, active intravascular clotting, history of thrombosis hematuria, renal failure and hemophilia.

Tranexamic acid also has similar mechanism. Side effects are lesser as compared to amicar

The results of various studies indicate that both amicar and tranexamic acid have beneficial effect on rate of secondary haemorrhage but none of them had improved the final visual outcome.

• Corticosteroids:bystabilizingtheblood-ocularbarrierandby directly inhibiting fibrinolysis corticosteroids decrease th

incidence of secondary haemorrhage.predinislone in dase of 40mg/dayor0.6mg/kginchildreniseffectiveinreducingthe incidence of rebleed statistical analysis indicates that coticosteroids decreased the incidence of rebleeding without having any effect on the longterm visual outcome.

• StudiesadvocateuseofmydriaticsastheyrelieveciliaryspasmandprenentsformationpfPAS.Aspirinshouldnotbegivenin cases of hyphema

• Outpatientmanagement : canbe considered in followingCases(Waltonetal):

• noassociatedinjury

• hyphema<½ofACvolume

• satisfactoryIOP

• noblooddyscrasia

• safehomeenvironment

• goodpatientcompliance

• goodfollowup(notimedelayatpresentation)

• Indicationsforsurgicalmanagement(irrigation,vitrectomy,trabeculectomy)-waltonetal:

• microscopiccornealbloodstaining

• Riscofoptic atrophy/CRAO(sickle cell disease/tait,IOPavg>25mmHg>24hoursorspikesrepeatedly>30mmHg,IOP>60mmHgfor2daysOR50mmHgfor>4days,presenceofpre-existingglaucomatousopticatrophyand“unacceptable”IOP.

• Riscofcornealbloodstaining(e.g4daysftertheonsetofglaucoma,>½-totalhyphemawithIOP>25mmHg>6days

• Riscofsynechiaeformation(e.g>50%hyphemafor>8 days.

Alkali Injury

Topical antiglaucoma agents which reduce the formation of aqueousproductioncanbeusedtolowertheIOP.IfIOPisveryhigh systemic drugs can be used. Corticosteroids can used in thefirstweek after injurywhichdecreases inflammation andpreventsfibrosis.Steroidsshouldnotbeusedafterfirstweekdueto risc of corneal melting. Since prostaglandins are responsible forinflammationandhighIOP,indomethacinandotheragentswhich decrease their production can be used.

Angle Recession

Management consists of medical therapy followed by ndYAG laser trabeculoplasty. Filteration surgery can be done if conjuntiva is not injured by primary injury

PAS

Iridogonioplasty with Argon laser can be used to pull the iris away from the angle, failing which surgical goniosynechiolysis may be effective in reopening the angle.


Ghost Cell Glaucoma

Treatment involves conventional medical therapy followed by surgical treatment if it doe not respond. According to Campbell only less than half of thesecases respond on medical therapy alone. Surgical intervention in form of AC irrigation along with pars plana vitrectomy to clear blood components trapped in vitreous if required.

Lens Induced Glaucoma

Dislocation: treatmentofpapillaryblockbyLASERorsurgicalIridectomy.Lensectomymaybedoneifpupillaryblockrecursorvisualrehabilitationisnotpossible.Lensectomycanbedon

by intrcapslar approach with anterior vitrectomy or pars plana lensectomy with vitrectomy can be done.

Lens swelling: cataract extraction along with iridectomy or trabeculectomyisthetreatmentofchoice.TreatmentofPASasmentioned above can be required.

Phacolyticandlensparticleglaucomaaremanagedbyconventionalmedical and surgical methods.

Retained Intraocular Foreign Body

Foreign body removal has to be done as soon as possible along with vitrectomy to prevent further damage and irreversible vision loss.

First AuthorManav Sachdev MBBS

81www.dosonline.org

Refractive error, predominantly myopia (short sightedness), is the most common eye disease and thus the major cause of

reduced vision worldwide.1 Myopia is a condition in which parallel rays of light are brought to a focus in front of the retina, which leads to blurred distance vision. This leads to loss of productivity andco-morbidityduetovisionimpairment,aswellasthedirectcosts of correction through glasses, contact lenses, and surgical treatment.2 The major structural correlate of myopia is an increase in the axial length of an eye.

Epidemiology

Mildormoderatemyopia currently affects at least 25%of thepopulationsinEuropeandNorthAmerica,approximately5%inAfrica,andupto80%inEastAsia.4-9 In contrast, “pathological myopia” (very severe) affects less than 3% ofmost of thepopulations. Myopia in several Indian age groups increases from 16.1%inthelateteensto20-50%inthe70s.3Womenareaffectedtwice as commonly as men.

Pathogenesis

The pathogenesis of myopia in general, and progressive myopia in particular, is unclear, but both heredity and environment play a role. The mode of inheritance may be autosomal recessive or dominant, but it also can appear sporadically. The most widely accepted environmental influence is excessive near work.Sustainedaccommodationandintraocularpressure(IOP),bothbasalandphasic,aresuspectedtoinfluenceaxialelongationineyes that have decreased scleral resistance.4

Genetic Factors: The most widely accepted theory of the cause of myopia is that it is mainly hereditary. Measures of the heritability ofmyopiahaveyieldedfiguresashighas89%,andrecentresearchhas identified genes that may be responsible: defective versions ofthePAX6geneseemtobeassociatedwithmyopia.Accordingtothistheorytheeyeisslightlyelongatedfronttobackduringdevelopment, causing images to be focused in front of the retina rather than directly on it.

Environmental Factors: Another theory is that myopia is caused byweakeningoftheciliarymusclewhichcontroltheeye'slens.Theweakmuscleisunabletoadjustthelensenoughtoseefardistances,causingfar-offthingstobeblurred.Thistheorystatesthatthemuscle'sweaknessisusuallycausedbydoinglotsof"nearwork",likereadingbooksorusingacomputerscreen.Sincetheeye rarely has to focus on far distances, the muscle is rarely used and,asaresult,becomesweak.

Other factors: Myopia is seen commonly in individuals of hyperinsulinemia and also commonly in prematurity with or withoutROP(MyopiaofPrematurity-MOP).5 Many theories have

Myopia: An OverviewKapil Khurana DOMS, S.P. Chaudhary MS,FMRF, Manisha Agarwal MS, DNB, FMRF

Dr. Shroff ’s Charity Eye Hospital, Darya Ganj, New Delhi

been put forward to explain how myopia develops in premature babies. These include bone deficiency, temperature, light, visual deprivation and retinal dysfunction.

Threetypesofmyopiaareassociatedwithprematurebirth:(1)physiological and temporarymyopia (2)myopiawithoutROP(MOP)and(3)myopiainducedbysevereROPdisease.

Physiological and temporary myopia

Myopia is probably the normal refractive state in infants before full term with the eye becoming more hypermetropic in early infancy. Compared with the eye of the full term baby the features ofthismyopiaareshorteraxiallength,flatteranteriorchamber,and more spherical lens.

Figure 1: Color fundus photograph of both eyes showing Optic Disc crescent

Mis

cella

neou

s


Myopia without ROP (myopia of prematurity-MOP)

Thistypeofmyopiahasanearlyonsetandcomparedwithfull-termandjuvenileonsetmyopestheMOPeyeexhibitsarelativelyhighlycurvedcornea,shallowanteriorchamberandthicklens.Axial lengths are shorter than expected for the dioptric value. ThehallmarkofMOPisarresteddevelopmentofocularanteriorsegment.

Myopia induced by severe ROP disease

The prevalence of myopia increases with the presence and severity ofROP.There isadramatic jumpin theprevalenceofmyopiawhenstage3ROPisreached.6ROPinducedmyopiacannotbefully explained by increased axial length as it is also associated with evidence of arrested development of the anterior segment: microcornea, steepcorneal curvatureand thickened lens.Thiscould be due to a mechanical restriction of ocular growth.

Classification of myopia

• Donder’s classification (1864)- based on the rate ofprogression

• Stationary

• Temporarilyprogressivemyopia

• Permanentlyprogressivemyopia

• DukeElder’sclassification(1949)

• Simplemyopia(generallylessthan-6D)-occurringasa result of normal biological variation.

• Degenerativemyopia(morethan-6D)

• Grosvenor’s(1987)classification-basedontheageofonset

• Congenitalmyopia (present at birth and persistingthrough infancy)

• Youth-onsetmyopia(<20yearsofage)

• Earlyadult-onsetmyopia(20-40yearsofage)

•Lateadult-onsetmyopia(>40yearsofage)

• Accordingtodegreeofmyopia

• Low(≤-3D)

• Medium(-3Dto-6D)

• High(≥-6D)

Ocular associations of Myopia

Thevariousocularassociationsare:-

• Prematurenuclearsclerosis

• Posteriorsubcapsularopacities(lesscommon)

• Glaucomawheretheprevalenceofglaucomaisrelatedtothedegree of myopia. All myopic discs should be evaluated with high suspicion of glaucoma

• Strabismusespeciallyexophoriaandexotropia

Systemic associations of Myopia

• Albinism

• CongenitalrubellaGyrateatrophy—hyperornithinemia

• Laurence–Moon–Bardet–Biedlsyndrome

• Marfan’ssyndrome

• PierreRobin’ssyndrome

• Stickler’ssyndrome

• deLange’ssyndrome

• Down’ssyndrome

• Ehlers–Dahlossyndrome

Among all theseMarfan’s syndrome, Stickler syndrome andalbinism are commonly associated with myopia.

Fundus changes in high myopia

Excessiveaxialelongationoftheglobeinhighmyopiacancausemechanical stretching and thinning of the choroid and retinal pigment epithelium (RPE) layers, resulting in various retinaldegenerative changes.Highmyopicshavean increased riskofretinal complications such as peripheral retinal degenerations, retinal tears, retinal detachment, posterior staphyloma, chorioretinal atrophy, retinal pigment epithelial atrophy, lacquer cracks, choroidal neovascularization (CNV) andmacularhaemorrhage.

Optic disc crescent

This is an early change in the myopic fundus and is due to a pullingawayofthechoroidandRPEusuallyfromthetemporaledge of the nerve to expose the sclera .The incidence of crescent formation is significantly associated with increasing axial length in high myopics.

Figure 2: Color fundus photograph of the left eye showing Foster Fuchs’ Spot

83www.dosonline.org

Posterior staphyloma

Aposterior staphyloma is a backward ectasia of the fundus,thehallmarkbeing tessellationandpallorof thearea involved(Figure3).Posteriorstaphylomacanbeoffivetypes7:-

Type1-Theareaoftessellationandpallorincludestheregionofthe optic disc and macula. It is the most common type

Type2-includestheregionofthemacula

Type3-involvestheperi-papillaryregion

Type4-extendsnasallyfromthedisc

Type5-mostrareandinvolvesthefundusinferiortotheopticdisc

Steidl andPruett et al8. suggested that eyes with the shallow staphylomas showed larger drop in visual acuity and a greater occurrenceofCNVandmacularhemorrhage.Thepossiblereasonfor this could be the better preserved choriocapillaris underneath the shallow staphylomas.

Peripheral retinal degenerations and rhegmatogenous retinal detachment

Latticedegeneration is themost importantperipheral retinaldegeneration which can predispose to rhegmatogenous retinal detachment (RRD). This is because retinal tears can develop secondary to posterior vitreous detachment (PVD), at theposterior and lateral margins of the lattice degeneration where strongvitreoretinaladhesionsexist.SymptomsofPVDandretinalbreakformationincludesuddenorgradualincreaseinthenumberoffloatersand/orflashesoflight.

Dilated fundus examination should be carried out in patients with these symptoms as soon as possible to detect early development ofretinalbreakorretinaldetachment.

Laserphotocoagulationisusedforthetreatmentofeyeswhichhavedevelopedretinalholeorbreak.

In eyes with retinal detachment either pneumatic retinopexy, scleral buckling (SB)with cryopexyorparsplana vitrectomy

(PPV)surgerywithgasorsiliconeoiltamponadeisperformedunder local or general anesthesia.

Myopic foveoschisis and macular hole

Recent advancement in retinal imaging technology using optical coherence tomography (OCT) has demonstrated that high myopic patients with posterior staphylomas are predisposed to develop macular pathologies such as myopic foveoschisis and macular hole.

Myopic foveoschisis is the splitting of the retinal layers in the macula and can result in metamorphopsia and blurring of vision. In more advanced stage, myopic macular hole can develop which may be associated with retinal detachment and patients will suffer from severe visual losswith reduced visual acuity.PPVwithpeeling of the internal limiting membrane and gas or silicone oil tamponade followed by post operative prone positioning is performed for treating macular holes.

Lacquer cracks

LacquercracksareformedbyspontaneousrupturesintheBruch'smembrane and small hemorrhages may develop within the lacquercracks.Lacquercracksmaycausesuddenlossofvisionsecondary to thedevelopmentofaCNVincloseproximity tothelacquercracks.

Foster Fuchs’ Spot

FosterFuchs’spotsappearasroundorellipticallesionsthatarepredominantlydarkbut canhaveagray, yellow, red,orgreencoloration.Theyarisedue toproliferarationofRPEassociatedwith choroidal hemorrhage.9

Choroidal neovascularisation in high Myopia

MyopicCNVisoneofthemostvisionthreateningcomplicationsofhighmyopia(Figure2).MyopicCNVMdevelopsinaround5to10%oftheeyeswithhighmyopiaandisthecommonestcauseofCNVinyoungindividuals.

Figure 3: Fundus fluorescein angiography of the left eye showing early hyperfluorescence with late leakage in the macula suggestive of classic myopic CNV


TheincidenceofmyopicCNVinthesecondeyeinpatientswithpre-existingmyopicCNVinthefelloweyeisashighas30%withineight years after the first eye.10

Therefore Amsler grid monitoring of the second eye is very importantforearlydetectionoftheCNVinthesecondeye.PoorprognosticfactorsforpatientswithmyopicCNVincludeageofgreaterthan40years,largerCNV,andworseinitialvisualacuity.11

CurrentlymyopicCNVaretreatedwithanti-vascularendothelialgrowthfactor(anti-VEGF)agentssuchasRanibizumab(Lucentis),Bevacizumab (Avastin) and pegaptanib sodium (Macugen) given as an intravitreal injection under topical anesthesia and aseptic precautions.

Conclusions

Individuals with high myopia are subject to various retinal pathologies including peripheral retinal degenerations, retinal detachment,andposteriorpolepathologiessuchasCNV,lacquercracksandmacularhaemorrhages.Theseretinalpathologiesmaycauseserioussight-threateningcomplications.Thereforepatientswith high myopia should be educated about the symptoms of posteriorvitreousdetachmentsuchasflashesandfloaters,fallingofablackcurtainin-frontoftheeyeordevelopmentofacentralscotomasecondarytoamyopicCNV.Patientsshouldbeadvisedtoseekpromptmedicalcareshouldsuchsymptomsarise.Promptdiagnosis and treatment may greatly help in preventing severe visual loss secondary to retinal complications arising in high myopic patients.

References

1. ThyleforsB.Aglobal initiative for the eliminationof avoidableblindness.AmJOphthalmol1998;125:90–3.

2. JavittJ,ChiangYP.Thesocioeconomicaspectsof laserrefractivesurgery.ArchOphthalmol1994;112:1526–30

3. LopesMC,AndrewT,CarbonaroF,etal.Estimatingheritabilityandshared environment effects for refractive error in twin and family studies.InvestOphthalmolVisSci2009;50:126–31

4. VitaleS,EllweinLB,CotchMF,etal.PrevalenceofrefractiveerrorintheUnitedStates,1999-2004.ArchOphthalmol2008;126:1111–9.

5. LingCS,FleckBW,WrightE,AndersonC,Laing I.Diode lasertreatment for retinopathy of prematurity: structural and functional outcome.BrJOphthalmol1995;79:637–41.

6. ScharfI,ZonisS,ZeltzerM.Refractioninprematurebabies.MetabOphthalmol1978;2:395–6.

7. HoffmanDJ,HeathDA.(1987)Staphylomaandotherriskfactorsinaxialmyopia.J.Am.Optom.Assoc.58:907-913

8. SteidlSM,PruetRC.(1997)Macularcomplicationsassociatedwithposteriorstaphyloma.Am.J.Ophthalmol.123:181-187

9. KleinRM,CurtinBJ. (1975)Lacquercrack lesions inpathologicmyopia.Am.J.Ophthalmol.79:386-392

10. CurtinBJ,KarlinDB.(1971)Axiallengthmeasurementsandfunduschangesofthemyopiceye.Am.J.Ophthalmol.71:42-53

11. MorsePH.(1989)Vitreoretinaldisease2nded,YearBookMedicalPublishers,Chicago.

First AuthorKapil Khurana DOMS

87www.dosonline.org

Ocular TBBobby Bhalotra MD, Amit Khosla MD

Department of Chest Medicine Sir Ganga Ram Hospital,

Rajinder Nagar, New Delhi

Tuberculosis [TB] is a serious global public health problem. In areportfromasanatoriumintheUSA,1.4percentof10524

patientsweretreatedforocularTBbetween1940and1966.Theincidence of TB uveitis in India has varied from two to thirty per cent. The large variation in the incidence rates in different reports possibly stems from differences in the diagnostic criteria used in thestudiesreportinghigherincidencerates;thediagnosisofTBuveitiswasoftenbasedonapositivetuberculinskintest[TST].

OcularmanifestationsofTBareprotean.WhileTBcanaffectall areas of the visual system, the choroid is probably the most commonly affected intraocular structure. Choroidal tubercles constitute the most common intraocular manifestation of TB. Woods estimated that-the choroid is involved in about oneper cent of patientswith pulmonaryTB. PrimaryTBof theeyelid, conjunctival sac and optic nerve is rare. Rarely, serious manifestations, such as panophthalmitis or endophthahnitis can also occur. Certain ocular mani festations, such as vasculitis due toTB[e.g.,Eale’sdisease]arepresumablyduetohypersensitivityto a sequestered antigen rather than TB disease per se.

Primary and Secondary Ocular Tuberculosis

The term “primary ocular TB” has been used when the TB lesions are confined to the eyes and no systemic lesions are clinically evident. “Secondary” ocular TB has been defined as ocular infection resulting from congruous spread from adjacent structures or haematogeneous spread from the lungs.

Definitive diagnosis of ocular TB can be made only by demonstrating Mycobacterium tuberculosis in the ocular tissues. However, obtaining ocular tissue for diagnostic purposes is notonlydifficult,but isalsoassociatedwithsignificantocularmorbidity. Hence, the diagnosis of TB can rarely be definitely confirmed before enucleation. Only 25 per cent of patients with ocular TB give past history of TB and 50 per cent have normal chest radio graphs. Orbital radiographs may reveal bony erosions.

Ahighdegreeofclinicalsuspicionis,therefore,thekeytoearlydiagnosis. Easily accessible sites, such as eyelid, conjunctiva, lacrimal gland and sclera , should preferably be biopsied to demonstrate the charac teristic findings of caseating granulomas withLanghans’giantcellsandMycobacterium tuberculosis. Despite all investigations patients with clinically suspicious lesions should receive empirical standard antituberculosis treatment and should becarefullyfollowed-upfortherapeuticresponse.

A positive TST in a patient with granulomatous uveitis was considered to be a positive evidence of ocular TB. A positive TST is, however, only indicative of infection with Mycobacterium. tuberculosis anddoesnotnecessarilyreflectthediseaseactivity.‘Wernik calculated that a patientwith uveitis and a positive

TST test has only one per cent probability of having active TB. However,recentconversionofapreviousnon-reactorfavorsthediagnosis of TB.

Useofsystemiccorticosteroidsforsevereocularinflammationcaninterfere with the TST results. Therefore, though a routine TST has been advocated in patients with uveitis, it is rarely diagnostic. In countries where TB is highly endemic, a caution is advocated before interpreting a positive TST result in isolation. A positive TST can be considered to be supporting evidence in a patient with a clinical picture highly suggestive of TB such as choroidal tubercles or tuberculoma or when other investigations such as a chest radiograph also have findings compatible with TB. On the other hand, a negative TST is considered by some as being more relevant as it rules out TB if the patient is immunocom petent. This, however, is also not always true as there are several causes of anergy.

In patients with ocular TB, it is seldom possible to procure adequate tissue for diagnosis and the number of organisms present may be too small to be detected by conventional methods. The utility of serological tests in the diagnosis of ocular TB needs furtherevaluationinwell-designedstudieswithalargesamplesize.Polymerasechainreactionappearstobeapromisingtoolto establish the definitive diagnosis of ocular TB, if the sample is takenfromtherepresentativetissue

Despite rapid advances in medicine, ocular TB still remains an important diagnostic challenge. The criteria for the diagnosis of ocular TB differ greatly and very often the diagnosis is based on a compatible clinical picture and good therapeutic response to antituberculosis treatment rather than mycobacterial isolation.

Earlier,ithasbeensuggestedthatclinicaldiagnosisofocularTBbebased on the presence of at least three of the following five features [i] suggestive clinicalpicture; [ii] exclusionofother aetiology;[iii]positiveTST; [iv] therapeutic response toantituberculosistreatment;and[v]presentorpasthistoryofTB.

In patients with a clinical picture suggestive of intra ocular TB. The criteria shown below can be helpful.

Major criteria

Evidenceofpulmonaryorothersystemicpathologyconsistentwith TB occurring concurrently with the ocular disease. Response of ocular and systemic disease to antituberculosis treatment [with or without steroids]

Exclusionofother etiological causes, like sarcoidosis, tumors,secondary metastases

Minor criteria

PositiveQuatiferongoldessayorTST

PositivePCRforMycobacterium tuberculosis inocularfluidsorbiopsy

Mis

cella

neou

s


Allmajorcriteria fulfilled=highlyprobable intraocularTB;2majorand1minorcriterionfulfilled=probableintraocularTB

WhenpatientswithTBelsewhere in thebodydevelopclinicalfeatures of ocular involvement, thorough ophthalmologic evaluation is warranted. Similarly when patients are detected to have ocular involvement, a complete systemic evaluation must be done. Treatment of ocular TB is on the same lines as treatment of TB elsewhere in the body. The disease is said to respond well to standard antituberculosis treatment and there is no role for topical treatment

However, as significant damage can occur to ocular tissues from infectionaswellasinflammation,itisprudenttoaddsystemiccorticosteroids as an adjuvant to the standard antituberculosis treatment. This must be done in consultation with a physician

Anteriorsegmentinflammationshouldbemanagedwithtopicalsteroids and cycloplegics. Treatment of TB phlyctenulosis also involves topical corticosteroids and cycloplegic agents in addition to standard antituber culosis treatment. Conjunctival lesions causing only mild symptoms may respond to local astringents. Muco-purulentdischargesuggestssecondarybacterialinfectionand should be treated accordingly. Conjuctival lesions heal without scarring, but corneal phlyctenules leave superficial scars of variable severity.

Antituberculosis Treatment Induced Ocular Toxicity

Several antituberculosis drugs can cause ocular adverse effects, which if not recognized early can result in an irreversible loss of vision. Often patients are referred to ophthalmologists for evaluation of ocular toxicity following prescription of drugs for

Suspected case of Tuberculosis

Pulmonary Disease is Suspected

Send

1. Threeinducedorspontaneous(respiratoryisolation)1cm.spectures samples for AFB staining and microscopy:

• 5to10ml.each,acceptinwisteryspecimens

2. OnesputumsampleforMTbcomplexPCR:

3. Samethreesputumsamplesforculture;

4. It effusion is present, consider sending diagnostic thoracentedssampleforsmear,culture,PCR,andadenminedeaminase(ADA)testing-pleuralbiopsyhashigherculturesensitivity.

5. Consider early morning gastric aspiration of 50 ml in childrenorfailedsputuminductions;and,

6. ConsideranIFNbasedawayonsacrumorTuberculinSkinTest – negative text does not exclude disease.

Other than pulmonary disease is suspected

Send:

1. Samplesanyouwouldforsuspectedpulmonarydisease;and,

2. Sample from suspected site. For these collection, collect both with and without formalies.

a. Lymphmode

• Exclusionalbiopsypreferred

• Fine needle aspiration if unable to obtainexclusional biopsy, e.g. CT guided biopsy in setting of mesenteric adenitis.

• AFBsmearandculture

• Histopathologicanalysis

b. CSF

• Cellcountanddifferential

• Chemistriestoincludeglucoseandprotein

• AFBsmear(typicallyergative)andculture(10ml.offers required)

• ConsiderPCR

c. Pleuralpericardial,orasdiskfluid

• Cellcountanddifferential

• Chemistriestoincludeglucoseandprotein

• AFB smear and culture (lining biopsies havehigher yield)

• ConsiderADAanalysis

• PCR

d. Other theses (bonemarrow, skin, liver, spices…kidney)

• AFBsmearandculture

• Histopathologicanalysis,mayconsider,specializedAFBstaining,andsubsequenttargetedPCR

• PCR

e. Blood

• Culture

• PCR

f. Stool, consider, intestinal biopsy

• Culture

• PCR

g. Urine(firstmorningmid-voidstreamcollections,threedaily samples

• Urinalysisandconventionalculture

• Culture

• PCR

89www.dosonline.org

TB elsewhere in the body. Sometimes patients themselves notice a diminution in vision while on antituberculosis treatment and get evaluated by an ophthalmologist. Ocular toxicity due to ethambutol, isoniazid and streptomycin has been well documented. Of these, ethambutol has the greatest potential to cause ocular toxicity. In general, adverse drug reactions occur less frequently in patients receiving intermittent regimens as compared to daily regimens.

Three types of optic neuritis have been described with ethambutol These include the axial, the periaxial and the mixed type. Both eyes are usually involved and the visual loss may vary from mild to severe. Colour vision is also variably affected. In the axial form ofopticneuritis,onvisualfield recordingpericentralorperi-pheral scotoma may be evident. Quadrantic field defects have also been commonly found. Although mild disc hyperaemia and disc oedema have been reported, fundus examination may be normal intheacutephaseofethambutoltoxicity.Peripapillarysplinterhaemorrhages, macular oedema and focal pigmentary changes havealsobeendescribed.Ethambutolrelatedoculartoxicity isstrongly dose related .

As the incidence of ethambutol toxicity is low with the currently favoureddose of 15 to 20mg/kg/ day, and also because it isreversible in most cases, sophisticated electrophysiological tests like electroretinographyandVERarenot required in allcases. However, in all patients receiving ethambutol, a baseline best corrected visual acuity and colour vision record should be routinely obtained. Thereafter, patients should be questioned monthly about any changes in vision. Any significant alteration in vision needs to be promptly investigated.

The most common adverse effect of rifampicin in the eye is conjunctivitis. It can result in the production of tears that are orange coloured and this can stain contact lenses. Rifabutin has beenassociatedwiththedevelopmentofanendophthalmitis-likeresponse. Clofazimine has been associated with several ocular side effects;theseinclude:abrownishdiscolourationoftheconjunctiva,brownswirlsinthecornealandbull’seyemaculopathyresultingin visual loss due to macular degeneration.

Laboratory Diagnosis of Tuberculosis in Primary Care

Laboratorydiagnosis of tuberculosis requires a multimodality approach, as well as recognition that empiric therapy often is appropriate.

Diagnosisoftuberculosisistricky,upto20%ofU.S.tuberculosis cases are clinically diagnosed. CDC surveillance data from 2004 reveals42%smear-negativeand17%culture-negativerates forpulmonary tuberculosis.Smear-negativeindexcasescontributetoasmuchas17%ofnewlytransmittedcases.

Laboratoryfeaturesofatuberculosis are the following:

Algorithm for the laboratory diagnosis of tuberculosis.

Bacteriology and Microscopy

Tuberculosis is caused by a bacillus of the Mycobacterium tuberculosis complex.Evaluationof sputumsmearsand tissuesamples is accomplishedwith twomain stains:Ziehl–Neelsenandauramineorangefluorescence.

Auramineorangefluorescencestainingofthreesputumsamplesperpatientdetected7ofevery10cases.Thefalse-positiverate

was2in10.Inotherstudieswithculture-provendisease,asinglesputumsampledetecteddiseaseinone-halftotwo-thirdsofcases,whilethreeorfourspecimensdetectedasmanyas9ofevery10cases.

In most cases bronchoscopy or lavage is required when sputum smears are negative in the setting of a known radiographiclesion allowing focused lavage. Induced sputum collection and bronchoalveolar lavagecanbeusedtogether,detecting8of10patients.

Auramine staining of sputum is superior. It has greater sensitivity with a requirement for fewer screened microscopic fields as a lower magnification can be used. Stain superiority in tissue samples is not clear.Typically,104to106organisms/mlarerequiredfordetection,although concentration techniques can lower this number.

Histopathology: Thehallmarkfindingonhistopathologyisthenecrotizingorcaseatinggranuloma.Whenfound,tuberculosis should be presumed until disproven.

Culture

Culture remains the gold standard for diagnosis.Egg-basedplatemediasuchasLöwenstein–Jensenareused,butagarmediasuchas Selective7H11and liquid-basedmedia (Becton–DickinsonandCo.,BACTEC™andBACTEC™MGIT™)nowarethestandard.Growthoftencanbedetectedwithin2weeks.Typicalholdperiodsarefor4to6weeks.Useofthesesystemsalsoallowsexpeditiousdrug susceptibility assessment when agents are added into the liquid media.Culture yields in extrapulmonary tuberculosis are significantly lower than from sputum samples.

ImprovementsinsampleprocessingforuseinPCRhaveincreasedcultureyields,resultingindetectionoflessthan102organisms/mL.Pleuralcultureyieldsrangefrom23to67%fromfluid,and90to97%frombiopsy.Despitehighyields,findingproviderstoperform pleural biopsy is problematic.

Molecular Methods: NAA/PCR

NAA assays allow rapid turnaround time (24 to 48 hours) when samplesaresmearpositiveandcanbedoneonsmear-negativespecimens, but with less sensitivity and specificity. They are performed directly on specially processed specimens to provide simultaneous detection and identification. Culture of the organism is still necessary to confirm the identification and to perform drug-sensitivitytests.Moleculartargetsusuallyincludebothaninsertionsequenceanda16SrRNAsequence.

Two FDA-approvedmolecular tests are available for rapiddiagnosis: a revised Amplified Mycobacterium Tuberculosis Direct Test (MTD) byGen-Probe, and theMycobacteriumTuberculosis Test (MTT) by Amplicor.

Molecular Methods: Inflammatory Marker Measurements

Inflammatorymarkermeasurements exploit differences inthe predominating immune response to different pathogens. Adenosinedeaminase (ADA) and interferongamma (IFN-ã)sometimes are used to diagnose tuberculous effusions. Combined PCR,ADA,andculturetechniqueshavebeenused.

Fluid Cell Counts and Chemistries, Nonspecific Changes

Fluid analysis may provide helpful clues in the diagnosis of tuberculosis.Involvedpleural,pericardial,andCSFfluidmay


manifest neutrophilia, although a lymphocytosis eventually predominates.Proteiniselevatedandglucoselevelsmaybeloworlownormal.Lactatedehydrogenaseusuallyiselevatedaseffusionsmostoftenareexudative.Persistentsterilepyuriainanillpatientshould raise suspicion for tuberculosis

New technologies such as proteomics and microarrays may soon find their place in the evaluation of patients. However, sputum and tissue analysis remain the cornerstone of laboratory diagnosis.

Diagnosing Latent Tuberculosis Infection in the 20th Century

The biology of latent tuberculosis infection (LTBI) is poorlyunderstood, and the condition has hitherto been defined by a positive tuberculin skin test (TST) result in an asymptomatic person exposed to tuberculosis with no clinical or radiographic signs of active tuberculosis. The clinical relevance of this definition isthatitcarriesasmallbutsignificantforwardriskofprogressionto active tuberculosis, which is significantly increased in persons with suppressed or immature (ie, young children) cellular immune systems. Unfortunately, the TST has poor specificity in bacille

Calmette-Guérin (BCG)-vaccinatedpersons, low sensitivity inpeoplewithweakened cellular immunity, and several logisticdrawbacks.

Recent advances in mycobacterial genomics and human cellular immunology have resulted in two new blood tests that detect tuberculosis infection bymeasuring in vitro T-cellinterferon (IFN)-b release in response to two unique antigens that are highly specific for Mycobacterium tuberculosis but absent frombacilleCalmette-Guérin (BCG)vaccineandmostnontuberculousmycobacteria.One assay, the enzyme-linkedimmunospot (ELISpot) [T-SPOT.TB;Oxford Immunotec;Oxford,UK] enumerates IFN-b–secreting T cells, while the other assaymeasures IFN-ãconcentration in supernatant byenzyme-linkedimmunosorbentassay(ELISA) [QuantiFERON-TBGold;Cellestis;Carnegie,Australia].A large andgrowingclinical evidence base indicates that both tests are more specific thantheskin test becausetheyarenotconfoundedbypriorBCGvaccination.Inactive tuberculosis,ELISAhassimilarsensitivitytotheskin test,whileELISpotissignificantlymoresensitive.

AuthorBobby Bhalhotra MD

(Surgeon with Experience in Phaco / Vitreo Retinal Surgery)

Freshers can also ApplyFor Modern, Equipped Eye Hospital with Dedicated

• EyeBankwithSpecularMicroscopeandDSAEK&DALK• CorneaCentrewithConfocalMicroscope&CrossLinking• GlaucomaclinicwithCO2Laser,YagLaser,HFA&HRT• CataractwithColdPhaco,IOLMasterandMultifocal&ToricIOL’s• VitreoRetinalsetupwithAcurus,FFA,GreenLaser&HDOCT• CarlZeissLumeraTOperatingMicroscope• RefractiveSurgerywithLasikLaser• Charitable&FreeCaseswithMobileEyeUnit

Salary will commensurate with experienceAccommodation will be provided.

Apply with detailed bio-data to

Dr. Sunil Sah, ChairmanSahHospital,J.12/9D,Ramkatora,Varanasi

Tel.:0542-2202263,64Email:[email protected]

RequiRedOphthalmOlOgist

Sah hoSpital(AN ISO 9001:2008 CERTIFIED HOSPITAL)

(MostAdvanceCentreofEasternU.P.)(Recognised Centre for Fellowship by ARC (AIOS)

Shabu James

Rectangle

93www.dosonline.org

Forthcoming Events: National

October 20117-9th RISHIkESH, UTTARAkHAND The VIII annual conference of UKSOS, UTTARA EYECON -11 Himalayan Institute of Medical Sciences SwamiRamNagar,Rishikesh Contact Person Dr. Renu Dhasmana, Uttaraeyecon11 Department of Ophthalmology Himalayan Institute of Medical Sciences Swami Ram Nagar, Dehradun Mobile: 08954785343, Phone:0135-2471355,0135-2471440 Email: [email protected]

October 20119th SITAPUR, U.P. 1st Meeting of “Association of Children Eye Specialists of India” Regional Institute of Ophthalmology Contact Person Dr. V.B. Pratap SitapurEyeHospital,Sitaput,U.P. Mobile: 09336838343 E-mail: [email protected]

April 201115-17 NEw DELHI Annual Conference Delhi Ophthalmological Society Venue: HotelAshok,ChanakyaPuri,NewDelhi Contact Person & Address Dr. Amit Khosla, Secretary DOS Room No. 2225, 2nd Floor, New Building, Sir Ganga Ram Hospital, RajinderNagar,NewDelhi-110060 Ph.:011-65705229,E-mail: [email protected], Website: www.dosonline.org

May 201129th PILIBHIT, UTTAR PRADESH Mid-term Converence of UPSOS UP State Ophthalmic Society Conference Secretariat Dr. Vipin Sahni KaushalyaDeviEyeInstitute NearChhatariChauraha,Pilibhit,U.P. E-mail: [email protected] Website: www.practicesolutions.in (M):91-9897504744

SITUATION VACANTFor

OPTHALMOLOGISTFor60beddedModrenEye

Hospital[ Estd 1992]Contact/SendCVto:

GANGA MATA EYE HOSPITALSapatRishiLinkRoadHARIDWAR-249410Fax:01334260175M:09412931046

[email protected]

Shabu James

Rectangle

95www.dosonline.org

Name (In Block Letters) _______________________________________________________________________________________________

S/D/W/o ____________________________________________________________________________ Date of Birth ___________________

Qualifications ________________________________________________________________________ Registration No. ________________

Sub Speciality (if any) ________________________________________________________________________________________________

ADDRESS

Clinic/Hospital/Practice __________________________________________________________________________________________

_____________________________________________________________________________ Phone _______________________

Residence ____________________________________________________________________________________________________

_____________________________________________________________________________ Phone _______________________

Correspondence _______________________________________________________________________________________________

_____________________________________________________________________________ Phone _______________________

Email ____________________________________________________________ Mobile No. _____________________________

Proposed by

Dr. _______________________________________________ Membership No. __________ Signature _________________________

Seconded by

Dr. _______________________________________________ Membership No. __________ Signature _________________________

[Must submit a photocopy of the MBBS/MD/DO & State Medical Council / MCI Certificate for our records.]

i agree to become a life member of the Delhi ophthalmological Society and shall abide by the Rules and Regula-tions of the Society.(Please Note : Life membership fee Rs. 3100/- payable by DD for outstation members. Local Cheques acceptable, payable to Delhi Ophthalmo-logical Society)

Please find enclosed Rs.___________in words ____________________________________________________ by Cash

Cheque/DD No.____________________ Dated_____________ Drawn on______________________________________

Three specimen signatures for I.D. Card.

Delhi Ophthalmological Society

(LifE MEMbERShiP foRM)

foR officiaL uSE onLy

Dr._______________________________________________________________has been admit ted as Li fe Member of

the Delhi Ophthalmological Society by the General Body in their meeting held on________________________________

His/her membership No. is _______________. Fee received by Cash/Cheque/DD No._______________ dated_________

drawn on __________________________________________________________________.(Secretary DOS)

Signature of Applicant with Date

SubmiSSiOn online www:dosonline.org


INSTRUCTIONS

1. TheSocietyreserveallrightstoacceptsorrejecttheapplication.

2. No reasons shall be given for any application rejected by the Society.

3. No application for membership will be accepted unless it is complete in all respects and accompanied by a Demand Draft of Rs.3100/-infavourof“Delhi Ophthalmological Society” payable at New Delhi.

4. EverynewmemberisentitledtoreceiveSociety’sBulletin(DOSTimes)andAnnualproceedingsoftheSocietyfree.

5. Everynewmemberwillinitiallybeadmittedprovisionallyandshallbedeemedtohavebecomeafullmemberonlyafterformalratification by the General Body and issue of Ratification order by the Society. Only then he or she will be eligible to vote, or apply foranyFellowship/Award,proposeorcontestforanyelectionoftheSociety.

6. ApplicationforthemembershipalongwiththeBankDraftforthemembershipfeeshouldbeaddressedtoDr.AmitKhosla,Secretary, Delhi Ophthalmological Society, Room No. 2225, 2nd Floor, New Building, Sir Ganga Ram Hospital, Rajinder Nagar, NewDelhi-110060

7. LicenceSizeColouredPhotographistobepastedontheforminthespaceprovidedandtwoStamp/LicenceSizeColouredphotographsarerequiredtobesentalongwiththisformforissueofLaminatedPhotoIdentityCard(tobeissuedonlyaftertheMembership ratification).

8. Applicationsfor‘DelhiLifeMember’shouldeitherresideorpracticeinDelhi.TheproofofresidencemaybeintheformPassport/Licence/VotersIdentityCard/RationCard/ElectyricityBill/MTNL(Landline)TelephoneBill.

Documents

Glaucoma Potpurri - DOS TIMES Bhalotra, Amit Khosla 93 F orthcoming Events C olumns 95 Membership Form Attention DOS Member DOS Times is not published in the month of May & June each