dos_may_2016

Editor-in-chief Editorial Capsule
5 Rising Supreme with Decoration
M. Vanathi and Splendour

Section Editors DOS Exclusives
Cataract & Refractive Retina & Uvea 7 Secretary Report 2015-2016

Umang Mathur Pradeep Venketesh 11 Outgoing Presidential Address
Saurabh Sawhney Parijat Chandra 13 Address of Incoming President

Sanjiv Mohan Manisha Aggarwal Featuring Sections
S. Khokhar Shahana Majumdhar
Cornea
Cornea & Oular Surface Rohan Chawla 17 Descemet’s Membrane
Uma Sridhar Ravi Bypareddy Detachment
Deepa Gupta Ophthalmoplasty & 21 Herpetic Eye Disease in Pediatric
Population
Umang Mathur Ocular Oncology
Ramendra Bakshi Neelam Pushker Neuro-Ophthalmology
Manisha Acharya Maya Hada 27 Atypical Optic Neuritis an
Overview
Noopur Gupta Sangeeta Abrol 33 Ischemic Optic Neuropathy
Glaucoma Rachna Meel
Ocular Biochemistry
Dewang Angmo Squint & 39 Modulatory Effects of
Reena Sharma Neuro-ophthalmology 1,25 - Dihydroxyvitamin
Sunita Dubey Digvijay Singh D3 on Ocular Diseases
Viney Gupta Zia Chaudhuri
Kanak Tyagi Suma Ganesh Snapshot
Delhi Advisory Board 43 Ocular Manifestations in
Y.R. Sharma Mahipal Sachdev Takayasu’s Arteritis
Atul Kumar Radhika Tandon 47 Nevus of OTA
P.V. Chadha Jolly Rohtagi
Monthly Meeting Korner
Noshir M. Shroff J.C. Das 49 Neuro-ophthalmology
Rajendra Khanna B.P. Gulliani Grand Rounds Presentation

Vimla Menon Ritu Arora Diagnostics Discussion
H.K. Yaduvanshi Kamlesh 53 Diagnosis of Atypical Viral
Retinitis by Aqueous PCR
Anita Panda G.K. Das
Pradeep Sharma Lalit Verma DOS Crossword
Ramanjit Sihota Tanuj Dada 57 DOS CROSSWORD-
Episode 6
Harish Gandhi Abhishek Dagar
Anup Goswami Sarita Beri Quick Picks
59 Bechet Disease
Rajpal P.K. Sahu
Mandeep Bajaj Kamlesh News Watch
61 DOSCON 2016 Photograph
B. Ghosh Taru Dewan 79 Awards & Oration DOSCON 2016
Rajiv Garg H.S. Sethi 82 DOS Clinical Monthly Meet
83 Info for DOS Voting Members
R.B. Jain H.K. Tewari 85 Monthly Meeting Proceedings
National Advisory Board Protocol
R.D. Ravindran Barun Nayak 86 Obituary
Debashish Bhattacharya Venketesh Prajna 87 DOS Membership Form

R. Revathi S. Natarajan www. dos-times.org 1
Yogesh Shah Amod Gupta
Arup Charaborti Jagat Ram
Anita Raghavan Amar Agarwal
Chandna Chakraborti Mangat Ram Dogra
Sushmita Shah D. Ramamurthy
Sushmita Kaushik T.P. Lahane
Pravin Vadavalli Samar Basak
Somshiela Murthy Cyrus Mehta

Sri Ganesh Mahesh Shanmugam
M.S. Ravindra J. Biswas

Rohit Shetty Srinivas Rao
Mallika Goyal Nikhil Gokale
Partha Biswas Santosh Honavar
Nirmal Frederick Arulmozhi Varman
Abhay Vasavada Mohan Rajan
Mukesh Taneja Rakhi Kusumesh
Shalini Mohan Gopal S. Pillai
Ragini Parekh Subendu Boral

Tejas Shah Gunjan Prakash
Sujith Vengayil Pravin More

M. Kumaran Sajjad Ahmed Shiekh
Punith Kumar Santhan Gopal
Elankumaran

DOS Correspondents
Anita Ganger Dewang Angmo
Rebika Dhiman Shikha Yadav
Manish Mahabir Archita Singh
Raghav Ravani Meenakshi Wadwani

Divya Singh Mayank Bansal
Mukesh Patil Saranya

DOS TIMES
Editorial Assistance & Layout: SUNIL KUMAR

Printer: New Pusphak Printers
Cover Design: Aman Dua

DOS Times will hitherto be published once every two months by Dr. M.
Vanathi, on behalf of Delhi Ophthalmological Society, DOS Secretariat,
Dr. R.P. Centre, AIIMS, New Delhi. All solicited & unsolicited manuscripts
submitted to DOS TIMES are subject to editorial review before acceptance.
DOS TIMES is not responsible for the statements made by the contributors.
All advertising material is expected to conform to ethical standards and
acceptance does not imply endorsement by DOS TIMES. ISSN 0972-0723

DOS EXECUTIVE MEMBERS

Executive Committee:

ˆϐ‹…‡ ‡ƒ”‡”•

Dr. Cyrus M. Shroff Dr. Rishi Mohan Dr. M. Vanathi
Outgoing President Incoming President General Secretary

Dr. Arun Baweja Dr. Vipul Nayar Dr. Ruchi Goel Dr. Deven Tuli
Joint Secretary Treasurer Editor ‹„”ƒ”› ˆϐ‹…‡”
DOS Representative to AIOS
Executive Members

Dr. Jatinder Singh Bhalla Dr. Bhuvan Chanana Dr. Anshul Goyal Dr. Avnindra Gupta Dr. Ajay Aurora

Dr. Rajat Jain Dr. Deepankur Mahajan Dr. J. K.S. Parihar Dr. Manavdeep Singh Dr. Namrata Sharma

šǦ ˆϐ‹…‹‘ ‡„‡”•

Dr. Rajendra Khanna Dr. Rajesh Sinha Dr. Sanjeev Gupta
Ex-President Ex-Secretary Ex-Treasurer

DOS HALL OF FAME Tejpal Saini B. Pattnaik DOS General Secretaries
DOS PRESIDENTS Satish Sabharwal Satinder Sabharwal
A.K. Grover Hari Mohan Arun Sangal
S.N. Mitter A.C. Chadha N.C. Singhal J.C. Das R.S. Garkal R.V. Azad
H.S. Trehan M.S. Boparai Madan Mohan Gurbax Singh S.R.K. Malik B. Ghosh
Tej Pal Saini N.N. Sood Pratap Narain Noshir M. Shroff Madan Mohan Mahipal Sachdev
L.P. Agarwal P.K. Jain (Brig.) R.C. Sharma Mahipal S. Sachdev J.C. Bhutani Atul Kumar
D.C. Bhutani L.D. Sota Lalit Verma S.C. Sabharwal Lalit Verma
R.C. Aggarwal L.D. Sota B.N. Khanna S. Bharti A.C. Chadha Dinesh Talwar
S.K. Angra R.N. Sabharwal Sharad Lakhotia Pratap Narain Harsh Kumar
S.N. Kaul D.K. Mehta P.V. Chadha S.K. Angra J S. Titiyal
S.N. Kaul Y. Dayal N.L. Bajaj B.P. Guliani G. Mukherjee Harbansh Lal
H.S. Trehan K.P.S. Malik Mathew M. Krishna Harbansh Lal H.K. Tewari Namrata Sharma
Hari Mohan R.B. Jain J S. Titiyal Amit Khosla
R.S. Garkal G. Mukherjee Prem Prakash Rajendra Khanna R. Kalsi Rohit Saxena
J.C. Bhutani R.V. Azad D.K. Sen Cyrus Shroff D.K. Mehta Rajesh Sinha
S.R.K. Malik P.C. Bhatia M. Vanathi
P.K. Khosla K.P.S. Malik
K. Lall

A.K. Gupta

Sincere thanks to all DOS OFFICE STAFF : ˆϐ‹…‡ ‡…”‡–ƒ”›ǣ Parveen Kumar Š DOS Accountant: Sandeep Kumar Š DOS TIMES Assistant: Sunil Kumar
DJO Assistant: Varun Kumar Š Library Attendant: Niyaj Ahmad Š ˆϐ‹…‡ ––‡†ƒ–ǣ Harshpal

3 DOS TIMES - MAY-JUNE 2016

EDITORIAL CAPSULE

ISING UPREME WITH ECORATION AND PLENDOUR

“The best preparation for tomorrow is doing your best today.”

Ȇ Ǥ
ƒ…•‘ ”‘™ǡ
”

Dear Members

Greetings from Delhi Ophthalmological Society!

Another year passes, as DOS reigns supreme in all its academic
endeavors. I humbly acknowledge all the DOS members for the
opportunity to steer forward our society and wish to express my sincere
gratitude for their continued support as we move further into the second
year of this executive’s tenure.

Galloping forward successfully into another new year, there are

more avenues to be looked into in order to provide a heightened outlook

and image to DOS. Our society has now been able to set standards in Dr. M.Vanathi

ƒŽŽ •…‹‡–‹ϐ‹… ‡˜‡–• Š‘•–‡† —†‡” ‹–• „ƒ‡” ™‹–Š ’Š‡‘‡ƒŽ •Š‘™ ‘ˆ

delegates, faculty and ophthalmic trade presence. As we look forward to

hosting more national and international events in future, we seek active participation and contributions from

all our members, particularly all our Delhi members. Being the home ground for most of the leading teaching

colleges of the country, we can stay forward with ease in academic endeavors of the country. We have also

been able to successfully adopt new organizational approaches in our academic events and hope to be better

able to tailor it to the needs of our society in the coming future as well.

We need to work towards further increasing the strength of presence and contributions from our Delhi
members in academic publications and meetings. Our spirit of togetherness and sense of belonging to
–Š‡ •‘…‹‡–› ™‹ŽŽ †‡ϐ‹‹–‡Ž› •–”‡‰–Š‡ —• ‹ ƒŽŽ ‘—” —†‡”–ƒ‹‰• ƒ† ™‡ ‡‡† –‘ ƒ†‘’– ƒ Š‡ƒŽ–Š› –”‡† ƒ†
ƒ’’”‘ƒ…Š ‹ ƒŽŽ …‘’‡–‹–‹˜‡ …ƒ’ƒ‹‰•Ǥ ƒ …‘ϐ‹†‡– –Šƒ– ™‹ŽŽ –”‡ƒ† ˆ‘”™ƒ”† ‹–‘ –Š‡ ‡š– ƒ…ƒ†‡‹… ›‡ƒ”
with humble pride and triumphant splendor setting its bars higher in all events.

With more DOS monthly clinical meetings, teaching program, the midterm winter conference, international
DOS conference and annual conference awaiting to feature more of the academic fest, we will look forward to
another wonderful term of splendid grandeur.

With best regards.

”Ǥ Ǥ ƒƒ–Š‹ MD
Additional Prof. of Ophthalmology
Cornea, Cataract & Refractive Services
Dr R P Centre for Ophthalmic Sciences
All India Institute of Medical Sciences
New Delhi 110029, India
[email protected]

www. dos-times.org 5

DOS EXCLUSIVES

ECRETARY EPORT

(Excerpts of the secretary report presented in the GBM, April 17, 2016)
‘‘—”ƒ„Ž‡ ”‡•‹†‡– ” ›”—• Ǥ Š”‘ˆˆǡ ‹…‘‹‰ ”‡•‹†‡– ” ‹•Š‹ ‘Šƒǡ
and esteemed members of the GBM
On behalf of the executive committee, it is my pleasure and privilege to extend a warm
welcome to you all to this General Body Meeting of 67th Annual Conference of Delhi
Ophthalmological Society 2016.
I wish to express my sincere gratitude and appreciation to all the members of the entire
executive committee and all the members of DOS for extending overwhelming support
and encouragement throughout this current academic year. The DOS Executive has
been constantly striving hard to raise DOS to greater heights and set higher standards
in all its activities.
DOS Membership: DOS is the world’s largest state ophthalmological society with a
current membership of 8449 members. We are happy to announce an addition of 421 new members to our society and extend a
warm welcome to them. Of these 60 members are from Delhi. We exalt in the appreciation and commendations received as one
of the best state ophthalmic societies in India and hold this coveted position close to our heart with a pledge to take it up further.
DOS Executive and Subcommittee Meetings:
This year’s tenure of the DOS Executive had 9 executive meetings and I am indebted to the executive for contributing
constructively towards raising the standards of performance of DOS in all aspects. The following histogram depicts the high
participation of the executives in all our meetings.

Various subcommittees constituted this year include the DOS monthly meeting review subcommittee, DOS house subcommittee,
the Day care centre subcommittee, the constitution subcommittee, the appellate, disciplinary and ethics committee
subcommittee, the awards subcommittee, the TPA subcommittee, the conference advisory subcommittee and the electoral
review subcommittee. Several meetings of the various DOS subcommittees have put into place revised recommendations for
effective functioning of DOS in various aspects including the DOS election, DOS monthly meetings, DOS house, disciplinary

www. dos-times.org 7

DOS EXCLUSIVES

& appellate and awards. We wish to express our sincere thanks and appreciation to all the chairpersons (especially Dr B P
Gulliani, Dr M C Aggarwal, Dr H K Tewari, Dr P V Chadha, Dr Noshir Shroff, Dr Cyrus Shroff, Dr G Mukerjee) and members of
the various subcommittees of DOS for taking out valuable time from their busy schedules to assist the executive with their
recommendations in the concerned aspects.

DOS Monthly Clinical Meetings
Nine DOS monthly clinical meetings (DCM I – IX in the months of July 2015 – March 2016) have been held each month. All
meetings were of high clinical standard with total attendance ranging from 90 to 180 continuing in the format of two clinical
case presentations, one guest case presentation, one clinical talk & mini symposium. The current revised format of DCRS system
™Š‹…Š Šƒ• „‡‡ ƒ†‘’–‡† ‰‹˜‡• •‹‰‹ϐ‹…ƒ– ™‡‹‰Š–ƒ‰‡ –‘ ƒŽŽ –Š‡ …‘…‡”‡† ‡Ž‡‡–• ‘ˆ ‘–ŠŽ› ‡‡–‹‰•Ǥ Š‡ –‹‹‰ •…Š‡†—Ž‡
format has been introduced for all monthly meetings to ensure that all presentations conform to the time slots allotted. This has
ensured that all meetings started on time and ended on time.

DOS Subspecialty Meetings & other events
™ DESK I & II meetings (Aug 22, 2015 & March 6, 2016)
™ World Sight Day participation (October 8, 2015)
™ Eye Donation Fortnight participation (Aug 26, 2015)
™ World Glaucoma Week participation (March 6, 2016)

DOS subspecialty meetings (DESK – DOS Enhanced Subspecialty Korner) was commenced this year under which two subspecialty
meetings (DESK – I: Oculoplasty & DESK II – Glaucoma) were held.
In DESK – I, Dr Naresh Joshi from UK delivered a very enlightening talk on aesthetics in oculoplasty surgery on August 22, 2015
in IHC, along with presentation from Delhi and outside Delhi Faculty.
In DESK – II, Prevention of blindness in glaucoma: current best practices, was a full day interactive programme conducted
on March 6, 2016 in IHC by Prof Ramanjit Sihota. This, which was held in the World Glaucoma Week, along with the DOS
participation in the Glaucoma walk of GSI was a much appreciated by all.
DOS also organised the Walk for Eye Donation Awareness in conjunction with National Eye Bank on August 26, 2015, which saw
wide participation and support from DOS members.

DOS members also offered free consultation services as part of World Sight day celebrations in various centres (Shroff eye
centre, Madan Mohan Eye Tech, Chadha Eye Centre & Dr R P Centre – satellite centre in East Delhi).

DOS Times 2015 - 2016
DOS Times, the bulletin magazine of Delhi Ophthalmological Society which is the most widely-read ophthalmological bulletin
‹ †‹ƒǡ •ƒ™ ƒ ˆ—”–Š‡” Š‹‡ ‹ ‹–• ’‘’—Žƒ”‹–› “—‘–‹‡– ™‹–Š ‹–• ‡™ ‹–‡”ƒ–‹‘ƒŽ ‘—–Ž‘‘ ƒ† ‹–‡”ƒ–‹‘ƒŽ •–ƒ†ƒ”† •…‹‡–‹ϐ‹…
content which was saw wide acclaim form prominent ophthalmic fraternity across the country. Each of the six issues per year
ȋ
—Ž›Ǧ —‰—•–ǡ ‡’Ǧ …–ǡ …–Ǧ ‡…ǡ
ƒǦ ‡„ǡ ƒ”Ǧ ’”‹Žǡ ƒ›Ǧ
—Ȍ ϐ‹‰—”‡• •‡…–‹‘• ‘ˆ ƒŽŽ •—„•’‡…‹ƒŽ–› ƒ‹‰ ‹– ƒ’’‡ƒŽ‹‰ –‘ ƒŽŽ
readers of the society, innovations section, practice requisites, clinical spotlight, diagnostic discussion, DOS crossword besides
the other regular sections that were already featuring in the bulletin.

The tentative expenditure: income ratio for this year is 0.53
I wish to place a special mention of appreciation for Mr Ashish Agarwal of New Puspak printers for his printing services and he
and his team are providing us excellent quality & timely printing services for DOS TIMES and other printing requirements for
DOS.
DOS TIMES can be accessed online for current and archived articles as well (www.dos-times.org). The postal delivery of Jan –
Feb 2016 issue of DOS TIMES was clubbed with the Jan – March 2016 of DJO as an effort to curtail expenditure.

™‡„•‹–‡ ȋ™™™Ǥ†‘•‘Ž‹‡Ǥ‘”‰Ȍ
DOS website now dons a new sophisticated outlook with all its upgraded and user friendly navigation options streaming several
Š—†”‡†• ‘ˆ Š‘—”• ‘ˆ ‡†—…ƒ–‹‘ƒŽ ˜‹†‡‘•ǡ –‡ƒ…Š‹‰ ’”‘‰”ƒ‡ ƒ† ‘–ŠŽ› ‡‡–‹‰• ƒ† ƒ Š—‰‡ •…‹‡–‹ϐ‹… ”‡•‘—”…‡ ƒ–‡”‹ƒŽǡ
•‡”˜‹…‡• ƒŽŽ ‘ˆ ™Š‹…Š ’Žƒ› ƒ •‹‰‹ϐ‹…ƒ– ”‘Ž‡ ‹ ƒ‹–ƒ‹‹‰ –Š‡ •‘…‹‡–›ǯ• ’‘’—Žƒ”‹–› ™‹–Š ‘’Š–ŠƒŽ‘Ž‘‰‹•–•
across the country. The website now showcases in an organised manner the various tabs of special sections for the members
including access to the online directory, members sections, news and updates, access to the DOS times and DJO and information
about all DOS activities. DOS website navigation has been made faster with the use of latest software to make it faster and
Ž‹‰Š–‡”Ǥ ƒ…‹Ž‹–› ˆ‘” ”‘ϐ‹Ž‡ —’†ƒ–‡ ‹• ˜‡”› —•‡” ˆ”‹‡†Ž›Ǥ –Š‡” ”‡‰—Žƒ” ˆ‡ƒ–—”‡• ‘ˆ ‹ˆ‘”ƒ–‹‘ ‘ ™‡„•‹–‡ ƒ……‡•• ‹…”‘†‡–ƒ‹Ž• ƒ”‡
also available. I also wish to thank our past secretary Dr Rajesh Sinha & past President Dr Rajendra Khanna who engaged this
new platform into service which has enabled us to effectively reorganise and showcase our website services in a more effective
manner. I also wish to commend our website service provider Mr Aman Dua for the exemplary services of this team.

8 DOS TIMES - MAY-JUNE 2016

DOS EXCLUSIVES

DOS Winter Conference
The DOS winter conference or WinterDOS 2015 on the theme of “Ophthalmic Rendezvous: Current Concepts” was held on the
5th & 6th of December, 2015 at Manekshaw Centre, Delhi Cantt. was hugely successful and widely acclaimed for its new outlook,
•…‹‡–‹ϐ‹… ’”‘‰”ƒ ƒ••‡„Ž› ƒ† …‘–‡–ǡ ‡™ ˆ‡ƒ–—”‡• „› ˆƒ…—Ž–‹‡• ƒ† ‡„‡”• „‘–Š ˆ”‘ ™‹–Š‹ ƒ† ‘—–•‹†‡ ‡ŽŠ‹Ǥ Š‹•
winterDOS witnessed the highest ever trade participation and conference pre-registration. Smooth seamless transmission and
organisation of live surgery workshop on 5th of December from R & R Army Hospital and CFS was immensely appreciated by
a full house. New interactive sessions in cataract & refractive scenarios, DOL 2015 – Delhi Ophthalmic Premier League, clinical
case presentations were a huge hit. The inauguration honoured all the eminent DOS members who were Padmashree awardees
ƒ† Šƒ˜‡ …‘–”‹„—–‡† •‹‰‹ϐ‹…ƒ–Ž› ‹ –Š‡ ϐ‹‡Ž† ‘ˆ ‘’Š–ŠƒŽ‘Ž‘‰›Ǥ Š‡ ‹ƒ—‰—”ƒ–‹‘ ƒŽ•‘ ™‹–‡••‡† –Š‡ ™‡ŽŽ ƒ’’”‡…‹ƒ–‡† ˜‹†‡‘
on DOS HISTORY and a musical programme followed by dinner. WinterDOS 2015 also saw phenomenonal response for the
new introduction of physical POSTERS and there was an enthusiastic participation in this. OPHTHALMIC PHOTOGRAPHY
…‘’‡–‹–‹˜‡ †‹•’Žƒ› •‡••‹‘ ™ƒ• ‹–”‘†—…‡† –Š‹• ›‡ƒ” ‹ ™‹–‡” ǡ ϐ‹”•– –‹‡ ‹ –Š‡ …‘—–”›ǡ –‘ ‡…‘—”ƒ‰‡ ’ƒ”–‹…‹’ƒ–‹‘ ˆ”‘
private practioners with an academic inclination and for residents as well to showcase their clinical imaging skills. This also
witnessed wide participation with enthusiasm.

‡ƒ…Š‹‰ ”‘‰”ƒ‡ ȋ ʹͲͳ͸Ȍ
The 8th DOS Teaching Programme was held on 23rd and 24th January 2016, at JLN Auditorium, AIIMS which was attended
by 200 delegates from all over the country. In addition to the lectures, the delegates were also exposed to newer ophthalmic
instruments via Hands on skill transfer programme in which hands-on- clinical training was imparted to the registered delegates
in various labs at R.P. Centre, AIIMS.

67th DOS Annual conference – DOSCON 2016: Ophthalmic Panorama
The 67th DOS Annual conference was organized April 15 - 17, 2016. The conference was named `DOSCON 2016 with the theme
of “Ophthalmic Panorama’. DOSCON 2016 has witnessed the highest ever overall registrations both for delegates and exhibition
’ƒ”–‹…‹’ƒ–‹‘Ǥ ʹͲͳ͸ •…‹‡–‹ϐ‹… ’”‘‰”ƒ‡ ˆ‡ƒ–—”‡† •‡˜‡”ƒŽ ‡™ ƒ––”ƒ…–‹‘• ‹ –‡”• ‘ˆ ‹–”‘†—…–‹‘ ‘ˆ •‡Ž‡…– ‹•–”—…–‹‘
…‘—”•‡•ǡ ‡–Žƒ„• –”ƒ‹‹‰ •‡••‹‘• ‹ Ƭ ǡ ‘–ƒ…– Ž‡• Ƭ ’Šƒ…‘‡—Ž•‹ϐ‹…ƒ–‹‘ǡ •’‡…‹ƒŽ •‡••‹‘• ™‹–Š •‡˜‡”ƒŽ ƒ–‹‘ƒŽ
•‘…‹‡–‹‡•ǡ •›’‘•‹—•ǡ ϐ‹”•– –‹‡ ˆ‡ƒ–—”‹‰ ‘ˆ ƒ† Ž—‹ ‰ƒ–Š‡”‹‰• ‹ ƒ—ƒŽ …‘ˆ‡”‡…‡ ƒ’ƒ”– ˆ”‘ ƒŽŽ ‘–Š‡” ”‡‰—Žƒ”
features. The DOSCON 2016 fellowship dinner was held in Hotel Ashok, the conference venue itself which was well attended
with a Bollywood musical night and dinner.

DOS Library
The DOS library is a popular service providing excellent academic resource materials to ophthalmologists across the country.
™‘—Ž† Ž‹‡ –Šƒ –Š‡ Ž‹„”ƒ”› ‘ˆϐ‹…‡” ” ‡˜‡ —Ž‹ ˆ‘” Š‹• ‡ˆˆ‘”–• ˆ‘” ‹…”‡ƒ•‹‰ ƒ™ƒ”‡‡•• ƒ„‘—– –Š‡ —•ƒ‰‡ ‘ˆ Ž‹„”ƒ”›
services. The current contract renewal with OVID which provides the services for DOS gives us access to 7 online international
indexed journals, 45 e-books at a cost of 12500 USD.

‡ŽŠ‹
‘—”ƒŽ ’Š–ŠƒŽ‘Ž‘‰›
Delhi Journal of Ophthalmology has now become a widely read journal by all ophthalmologists, both in Delhi and around the
country. It has been published regularly and distributed to all the members. I would like to thank the editor, Dr Ruchi Goel for
the hard work that she has put in for the journal and obtaining E-ISSN number, indexing in Index Copernicus, journal seeker
research bible, open academic journal index, J gate, Cite factor, Indian Science abstract and google scholar.

DOS House
The application to DDA for a plot for DOS House has been done and is under process.

DOS Membership Drive:
‡˜‡”ƒŽ „‡‡ϐ‹–• ™‡”‡ ‡š–‡†‡† –‘ ”‡•‹†‡–• –‘ ‡…‘—”ƒ‰‡ „‡…‘‹‰ ‡„‡”•Ǥ Š‡ ‡„‡”•Š‹’ †”‹˜‡ ‹• ‘ –‘ ‹…”‡ƒ•‡
the membership further in order to extend the academic resource facilities reach to more ophthalmologists across the country.

™ƒ”†• Ƭ ”ƒ–‹‘• Dr N N Sood Dr. S.N. Mitter Oration Dr J.C. Das
The following orations were awarded Dr S C Gupta Dr. Hari Mohan Oration Dr J.L. Goyal
Life Time Achievement Award Dr Boris Malyugin Dr. B.N. Khanna Oration Dr Bhavna Chawla
Life Time Achievement Award Dr J.S. Titiyal
Dr. Om Prakash Oration
Dr. P.K. Jain Oration

Forthcoming Activites of DOS
i-DOS 2016: The next i-DOS 2016 meeting is proposed to be held in conjunction with the College of Ophthalmology of SriLanka
in December 2016 alongside the lovely shores of Colombo. The meeting is proposed to be held under the tagline ‘Christmas
in Colombo” and work is on to make this meeting a true mixture of international academics and fun & frolic. I extend a warm
™‡Ž…‘‡ –‘ ƒŽŽ ‡„‡”• ƒ† ‘–Š‡”• ƒ• ™‡ŽŽ –‘ ’ƒ”–‹…‹’ƒ–‡ ‹ –Š‹• ‡‡–‹‰ ƒ† ‡Œ‘› ‹–• „‡‡ϐ‹–•Ǥ

www. dos-times.org 9

DOS EXCLUSIVES


‘‹– Ȃ ʹͲͳ͹ǣ The 4th International meeting of WSPOS is being proposed to be held in New Delhi in conjunction with
winter DOS 2017 meeting in December 2017 in Hotel Ashok. The constant efforts of Dr Rishi Mohan, the host president for the joint
WSPOS – DOS 2017 meeting is commendable. He has been working hard to bring an international meeting into the DOS portals
ƒ† ˆ‘” –Š‡ ϐ‹”•– –‹‡ ™‹ŽŽ ™‹–‡•• ƒ ‹–‡”ƒ–‹‘ƒŽ ‡‡–‹‰ „”‹‰‹‰ ‹ –Š‡ ϐŽƒ˜‘—” ‘ˆ ‹–‡”ƒ–‹‘ƒŽ ‘’Š–ŠƒŽ‘Ž‘‰› ƒŽ‘‰ ™‹–Š ‹–
paraphernalia into the state platform. This promises to be an excellent portal to showcase our ophthalmic fraternity and standards
to the international community of paediatric ophthalmology on a scale as never before. This meeting will also witness high trade
’ƒ”–‹…‹’ƒ–‹‘ –‘ ƒ ‹–‡”ƒ–‹‘ƒŽ …ƒŽ‹„”‡ ™Š‹…Š ™‹ŽŽ ’”‘ϐ‹– ϐ‹ƒ…‹ƒŽŽ› ƒ• ™‡ŽŽǤ Š‡ …‘‘”†‹ƒ–‹‘ ƒ† ™‘”‹‰ …‘‹––‡‡ Šƒ•
„‡‡ …‘•–‹–—–‡† ƒ† ‹• ™‘”‹‰ Šƒ”† ‘ †”ƒˆ–‹‰ ƒ –Šƒ– ™‹ŽŽ „‡ „‡‡ϐ‹…‹ƒŽ –‘ Ǥ

…‘™Ž‡†‰‡‡–•
Before I conclude I wish to acknowledge every DOS member who entrusted me with this privilege of being DOS General Secretary.
I am indeed truly privileged to be surrounded, blessed, guided with the advice and affection of doyens in ophthalmology such Dr
Cyrus M Shroff, Dr Rishi Mohan, Prof Atul Kumar, Prof Radhika Tandon and several others.

I am at loss for words to express my gratitude to you all and will forever cherish this opportunity to serve you and I will strive even
‘”‡ Šƒ”† –‘ ˆ—Žϐ‹Ž ›‘—” ‡š’‡…–ƒ–‹‘•Ǥ

Our President Dr Cyrus M. Shroff has been a constant source of support and guidance at all times. Under his umbrella I was
emboldened to venture without fear to adopt new introductions and explore new options for DOS. I have learnt many new things
from him the essence of which leaves me a better human being both in the academic and personal front. He has guided me with an
‡š‡’Žƒ”› Ž‡˜‡Ž ‘ˆ ‹˜‘Ž˜‡‡– ‡š—†‹‰ ’‘•‹–‹˜‡ ‡‡”‰› ƒ– ƒŽŽ –‡•–‡† –‹‡• ‘ˆ †‹ˆϐ‹…—Ž–›Ǥ ‘ ›‘— •‹”ǡ ‰‹˜‡ › •ƒŽ—–ƒ–‹‘• ƒ† ™‹ŽŽ ’”ƒ›
for your guidance and support for the coming years too.
As I welcome our incoming president Dr Rishi Mohan who is a pillar of strength and a source of motivation for the entire executive
and to me in particular. I am awed at his attitude and approach to all situations. His steering skills are one of a kind and I fondly look
forward to working DOS to greater heights under his able guidance in the next year.

Our Treasurer Dr Vipul Nayar with his cheerful voice and smile at all times keeps the accounts in order. He is always there at all
†‹ˆϐ‹…—Ž– –—”• ™‹–Š …Š‡‡”ˆ—Ž ‰”‡‡– ƒ† ™‘†‡”ˆ—Ž ‹†‡ƒ• –‘ –Š”—•– ‡ ˆ‘”™ƒ”† ‹–‘ ‡˜‡”›–Š‹‰ ™‡ Šƒ† –‘ †‘Ǥ ‡ Šƒ• „‡‡ ƒ† ™‹ŽŽ „‡
a support as that of a brother to whom I can turn to at all times.

I wish to acknowledge the tremendous amount of support extended to DOS by Dr R P Centre for Ophthalmic Sciences, especially by
Chief Prof Atul Kumar and all the faculty and residents who have obliged every request to participate in and support all academic
activities of DOS. My sincere gratitude to the chief of Dr R P Centre, AIIMS – Prof Atul Kumar for providing all infrastructure support
–‘ Š‘—•‡ –Š‡ ‘ˆϐ‹…‡ ƒ† Š‹• ‹‡•‡ ™‹•†‘ ƒ† …‘•–ƒ– ‰—‹†ƒ…‡ Šƒ• Š‡Ž’‡† ‡ ƒ– ƒŽŽ –‹‡•Ǥ

I also wish to express my sincere gratitude to past presidents Dr Rajendra Khanna and Dr. P.V. Chadha for their support and guidance.

There can be no DOS ensemble if we do not have the backbone support of the DOS Staff. The diligence and hard work of the DOS
‘ˆϐ‹…‡ •–ƒˆˆ ’ƒ”–‹…—Žƒ”Ž› ” ƒ”˜‡‡ —ƒ” ™Š‘ ‹• ƒŽ™ƒ›• „‡ ”‡ƒ†› ˆ‘” ƒ› ƒ††‹–‹‘ƒŽ ™‘” ƒ••‹‰‡† –‘ Š‹Ǥ – ‹• ƒƒœ‹‰ –‘ •‡‡ Š‘™
well placed and organised his work table is and his skills of secretarial assistance are par excellence. Special thanks to Mr Sunil who
coordinates the typesetting of DOS times and works overboard to meet my demands for every issue. Mr Sandeep our accountant
‹• ˜‡”› Šƒ”† ™‘”‹‰ ƒ† Šƒ†Ž‡• –Š‡ ‹‡•‡ Ž‘ƒ† ‘ˆ ϐ‹ƒ…‡• –Šƒ– ‰‘‡• –Š”‘—‰Š Ǥ ” ƒ„— ‘—” Ž‹„”ƒ”› •–ƒˆˆǡ ƒŽ™ƒ›• …‘’Ž‹‡•
with any work assigned to him. Mr Varun showed exemplary skills in assisting to bring out changes in the outlook of DJO in the
previous tenure and is continuing the good job. Mr Harshpal is one fo the most reliable of all and one can count on him at all times.
My special thanks to you all who work with me like family not minding the odd hours to give the best output to DOS.

The support, guidance and patience that my husband and daughter give me almost makes them a DOS member.

I thank the Almighty for this tremendous opportunity to be at the helm of affairs for DOS this year.

I wish, to once again, thank all the members of the executive who have stood by me and supported me in all the activities and all the
members of DOS who have provided invaluable inputs to improve the working of the society and participated in large numbers in
all academic initiative of this executive.

In this past one year, I have toiled with my heart, mind and soul to inculcate and adopt new ventures, and high standards in all the
ƒ…ƒ†‡‹… ‹‹–‹ƒ–‹˜‡• ‘ˆ ‘—” •‘…‹‡–›Ǥ Šƒ˜‡ „‡‡ ƒ„Ž‡ –‘ •—……‡••ˆ—ŽŽ› –ƒ‡ ˆ‘”™ƒ”† –Š‡ •‘…‹‡–› „‘–Š ƒ…ƒ†‡‹…ƒŽŽ› ƒ† ϐ‹ƒ…‹ƒŽŽ› ‹ –Š‡
same lines as that which had been set by my predecessors. I sincerely hope I have done justice to my position and have lived up to
your expectations and promise to strive hard for more.

Closing with best regards.

”Ǥ Ǥ ƒƒ–Š‹
Secretary, DOS

10 DOS TIMES - MAY-JUNE 2016

DOS EXCLUSIVES

UTGOING RESIDENTIAL DDRESS

Dear friends,

The year under review has been an eventful and successful one for DOS.
With the untiring efforts of the executive, spearheaded by our dynamic secretary
Dr. Vanathi and contributions from numerous members, DOS continues to be the
premier state ophthalmic society of our country.

This has been a year of consolidation of our systems and processes and of
progress on many fronts. The electoral process was reviewed, improvements
suggested and loopholes plugged. As promised in the GBM last year, the Voter List
was put online. However, despite many reminders, there were very few responses
ˆ‘” ‘†‹ϐ‹…ƒ–‹‘ ‹ –Š‡ Ž‹•–Ǥ Š‡ ‹•…‹’Ž‹ƒ”› Ƭ –Š‹…• …‘‹––‡‡ ˆ”ƒ‡† ‰—‹†‡Ž‹‡•
for graded punitive action in case of misconduct by a member. The monthly meeting
ˆ‘”ƒ– ™ƒ• ƒŽ•‘ ”‡˜‹‡™‡†ǡ ‰”ƒ†‹‰ •›•–‡ ”‡ϐ‹‡† ƒ† ƒ†Š‡”‡…‡ –‘ –‹‡ ‹•‹•–‡†
upon. Thanks to the efforts of the Editor the DJO is now indexed with Index Copernicus International. The online utilization
of Library Services especially journals has been excellent and we will continue to offer this service free of charge to our
members despite a slightly higher cost to the society.

The Avastin Storm has blown over with the alert notice by DCGI being now withdrawn. Profound thanks to senior
members from AIOS, VRSI and premier institutions for their untiring efforts to achieve this, many of whom are DOS
members. Another positive development was the judgement that brought non pelvic ultrasonologists out of the PC PNDT
act with some riders and this has been a great relief to ophthalmologists of Delhi and some other states.

In the year under review, DOS successfully held Winter DOS, DOST 16 & subspecialty meetings in Glaucoma and
Ophthalmoplasty and contributed to Glaucoma week and Eye Bank fortnight and Walks.

Š‡ ‘—•‡ ƒ––‡” Šƒ• ‘– ’”‘‰”‡••‡† •‹‰‹ϐ‹…ƒ–Ž›Ǥ ˆ‡‡Ž –Š‡ ’”ƒ…–‹…ƒŽ ™ƒ› ˆ‘”™ƒ”† ‹• –‘ •‡”‹‘—•Ž› Ž‘‘ ƒ– ƒ •ƒŽŽ
‘ˆϐ‹…‡ •’ƒ…‡ ‹ ƒ …‡–”ƒŽ Ž‘…ƒ–‹‘ǡ ƒ• –Š‡ Žƒ† ƒŽŽ‘…ƒ–‹‘ǡ ˆ”‘ †‘‡• ‘– ƒ’’‡ƒ” –‘ „‡ ƒ–‡”‹ƒŽ‹œ‹‰Ǥ —” •‘…‹‡–› ƒŽ•‘
needs to step up community oriented programs for glaucoma, corneal blindness, diabetic retinopathy and school oriented
ophthalmic screening and education.

The Annual Meeting DOSCON-16 has just concluded and we hope it came upto your expectations and set even higher
standards. An I-DOS is being planned in Sri Lanka in Dec’16 and there is a proposal to hold the 4th World Congress of
‡†‹ƒ–”‹… ’Š–ŠƒŽ‘Ž‘‰› ƒ† –”ƒ„‹•—• ‹ …‘Œ—…–‹‘ ™‹–Š ‹ ‡…ǯͳ͹Ǥ Š‡ ‹• „‡‹‰ ™‘”‡† ‘—– ƒ† ‹ˆ ”ƒ–‹ϐ‹‡†ǡ ‹–
™‹ŽŽ „‡ ƒ‘–Š‡” ˆ‡ƒ–Š‡” ‹ –Š‡ …ƒ’ ‘ˆ ƒ† –Š‡ ϐ‹”•– ˆ‘” ƒ –ƒ–‡ ’Š–ŠƒŽ‹… ‘…‹‡–›Ǥ

As I come to the end of my tenure I would like to thank all of you for the privilege of being at the helm of our dynamic
society this year. It has been a great learning experience for me. A big thanks to all members of the Executive for their
•—’’‘”–Ǥ •’‡…‹ƒŽ –Šƒ• –‘ ƒŽŽ –Š‡ ‘ˆϐ‹…‡ •–ƒˆˆ ˆ‘” ™‘”‹‰ ‡š–”‡‡Ž› Šƒ”† –‘ ‡‡’ –Š‡ ƒ…–‹˜‹–‹‡• ”—‹‰ ‡ˆϐ‹…‹‡–Ž›Ǥ
also ask forgiveness for any mistake and short comings during my tenure.

I will very shortly be handing over the reins of the society to the Incoming President, Dr. Rishi Mohan. Rishi has been
closely associated with the working of our society in many capacities and I am certain, under his able guidance. DOS will
scale even greater heights.

”Ǥ ›”—• Ǥ Š”‘ˆˆ
President, DOS

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DOS EXCLUSIVES

ADDRESS OF INCOMING PRESIDENT

Respected outgoing President, Dr Cyrus Shroff, Dr Vanathi, our able Gen Secretary,
our Treasurer Dr Vipul Nayar, my dear members of the Executive, honoured Past-
Presidents, my teachers and dear colleagues, friends, ladies and gentlemen,

It’s an inordinate honour and blessing for me to be installed as President of this
outstanding Society, and a notable privilege to be able to deliver the Presidential
Address to this august House.

At the outset, I would like to thank our outgoing President, Dr Cyrus Shroff, who
has been an exemplary Leader. His clarity of thought and expression is remarkable as
‹• Š‹• ƒ„‹Ž‹–› –‘ …‘ƒ† –Š‡ ”‡•’‡…– †‡•‡”˜‡† „› ƒ ”‡•‹†‡– ‘ˆ –Š‹• †‹‰‹ϐ‹‡† ‘†›Ǥ ‹•
“—‹‡– †‡‡ƒ‘—” …ƒ‘—ϐŽƒ‰‡• ƒ ™‹ŽŽ ‘ˆ •–‡‡Ž ƒ† Š‡ Šƒ• ƒ„Ž› ‰—‹†‡† –Š‡ š‡…—–‹˜‡ ƒ†
–Š‡ ‘…‹‡–› –Š”‘—‰Š ƒ ˆƒ‹”Ž› †‹ˆϐ‹…—Ž– ›‡ƒ”Ǥ ‡ Šƒ• Ž‡ˆ– ƒ …Ž‡ƒ” ‹’”‹– ƒ† ˜‹•‹‘ ˆ‘” –Š‡
Society which I hope to be able to carry forward. We are deeply indebted to him and
ƒ”‡ …‘ϐ‹†‡– Š‡ •ŠƒŽŽ …‘–‹—‡ –‘ ‰—‹†‡ —• ‹ ‘—” ˆ—–—”‡ ‡†‡ƒ˜‘—”•Ǥ Šƒ ›‘— ˜‡”›
much, Cyrus.

The DOSCON 2016, just being concluded has beyond doubt been one of the best Conferences we’ve had and is testimony
to the faith reposed in our ability to constantly raise the bar, not only by our own members but also by our partners in the
ophthalmic industry. It’s a process which I only see as getting better each year. Its heartening to note that this is due to the
enthusiasm and undefatigable energy of our Secretary, Treasurer and Executive Committee members and which rubs off on all
who work with them.

We also owe a great debt of gratitude to our past Leaders and legends in Ophthalmology, who have brought laurels to the
DOS and lifted the status of the specialty and the Society, to international levels.

As I take over the reins of the Society in much humility, I realize that, though much has been done, there is so much more
that can be done and so little time to do it. I intend to place before you my vision and outline a plan of action as a roadmap for
the year and beyond, if necessary.
1. I realize, as has been discussed in various forums, that the opportunities for upgradation of ones clinical skills are limited

in a post-doctoral scenario.
I intend to initiate a process wherein a Committee, in consultation with the Heads of the Teaching Institutions and large
Hospitals, can examine the prospects and look into the creation of 1-4 week short-term DOS Clinical Observerships.
2. I have recognised that the DOS has tremendous potential in conducting certain research projects which may involve a
multicentric approach to collate data from the participating scientists and institutions. I propose to create a subcommittee
•’‡…‹ϐ‹…ƒŽŽ› –ƒ•‡† ™‹–Š ‹†‡–‹ˆ›‹‰ •—…Š ’”‘Œ‡…–•ǡ •‡–—’ –Š‡ ’”‘–‘…‘Ž• ƒ† ”ƒ‹•‡ ˆ—†• ˆ‘” –Š‹• ’—”’‘•‡Ǥ —„Ž‹…ƒ–‹‘ ‘ˆ –Š‡
outcomes in the DJO and the IJO would be on priority.
3. During my election campaign last year, I had made an electoral promise the Members, that I would take some small steps
to increase the exposure of the DOS internationally.
ƒ Šƒ’’› –‘ ƒ‘—…‡ ʹ •’‡…‹ƒŽ ‡‡–‹‰• ™‹–Š •‹‰‹ϐ‹…ƒ– –‡”ƒ–‹‘ƒŽ ’ƒ”–‹…‹’ƒ–‹‘ ƒ† …‘–‡– Ȃ
First, the I-DOS in Colombo, in association with the College of Ophthalmologists of Sri Lanka from Dec 22-23, 2016, very
aptly taglined “Christmas in Colombo” by our hardworking Secretary, Dr Vanathi. The details will be available very shortly
‘ ‘—” ™‡„•‹–‡ ƒ† ™‹–Š –Š‡ ˆϐ‹…‡Ǥ
Second, on behalf of the DOS, I successfully invited the World Society for Paediatric Ophthalmology and Strabismus to
…‘†—…– –Š‡‹” Ͷ–Š ‘”Ž† ‘‰”‡•• ‘ˆ ƒ‡†‹ƒ–”‹… ’Š–ŠƒŽ‘Ž‘‰› ƒ† –”ƒ„‹•—• ȋ–Š‡ ϐ‹”•– –‹‡ ‹ †‹ƒȌǡ ƒ† –Š‡ –‡”ƒ–‹‘ƒŽ
Retinoblastoma Study Group Symposium, in conjunction with our WinterDOS Meeting and which shall be held in New
Delhi from December 1-3, 2017.
[Believe me, there were other Suitors, and I must thank the previous Presidents, Secretaries and Executives, for
creating and conducting the most wonderful Conferences in the past, which allowed me to project our capabilities
and command their respect].
‘” –Š‡ „‡‡ϐ‹– ‘ˆ –Š‡ ‘—•‡ǡ ƒ –ƒ„Ž‹‰ –Š‡ ‡‘”ƒ†— ‘ˆ †‡”•–ƒ†‹‰ǡ developed after much deliberation,
between us and the World Society of Paediatric Ophthalmology and Strabismus (WSPOS), which carries the approval of our
Executive Committee. I would request your support and approval, to make this Conference a grand success.
I am also tabling the constituents of the Coordination and Working Committee of DOS Members set up for the initial
discussions and negotiations with the WSPOS. This CWC shall form the core of the Local Organising Committee which shall
take shape over the next few months.
Š‘’‡ –Šƒ– ƒŽŽ ‡„‡”• ™‘—Ž† ™Š‘Ž‡Š‡ƒ”–‡†Ž› •—’’‘”– –Š‡•‡ ‡‡–‹‰• and participate in large numbers, ensuring
their success and enhancing the Society’s academic and societal image around the world. It should be the earnest endeavor
of each Member to showcase our ophthalmic expertise, Delhi and India and our heritage of exemplary hospitality to our
foreign guests, so that there is a queue of International Societies wanting to tie up for Joint Meetings with the DOS!
4. Earlier this year, I was deeply disappointed to see 2 exceptional Leaders of our august Society, lose an election at the
National level, owing largely to a lack of communication and appreciation of each other’s strengths. I feel we did not put

www. dos-times.org 13

DOS EXCLUSIVES

our best foot forward as a cohesive Society, to mitigate these differences and thereby, the DOS lost a wonderful opportunity
to again be at the forefront of representation at the highest level on the national stage.
‹–‡† ™‡ •–ƒ† ƒ† ‹˜‹†‡† ™‡ ˆƒŽŽǤ
‹–‡† –‘ ‹•–‹–—–‡ ƒ ‡…Šƒ‹• ™Š‡”‡„› ϐ‹”•–Ž›ǡ ƒ –‡ƒ …ƒ ‡†‹ƒ–‡ „‡–™‡‡ ’”‘•’‡…–‹˜‡ …ƒ†‹†ƒ–‡• …‘–‡•–‹‰
the same post at the AIOS, and secondly, conduct a wider on-line opinion poll/survey through a referendum, the results
of which shall be made known to the contestants, whereupon I would hope that a saner and more cooperative consensus
would emerge.
ϐ‹”Ž› „‡Ž‹‡˜‡ –Šƒ– ™‡ —•– „‡ ƒ„Ž‡ –‘ …ƒ””› ‘—” –ƒ–‡ ™‹–Š —• ‹ˆ ™‡ Šƒ˜‡ ƒ› …Šƒ…‡ ƒ– –Š‡ ƒ–‹‘ƒŽ Ž‡˜‡ŽǤ
5. In the area of advocacy and improving our image in the lay public, ‹–‡† –‘ •‡– —’ ƒ †›ƒ‹… Ƭ ‹ϐŽ—‡–‹ƒŽ
”‘—’ǡ
…ƒŽŽ‡† ƒ†ƒ ™ƒ”†‡‡• Ƭ ƒ•–Ǧ ”‡•‹†‡–• †˜‹•‘”›
”‘—’ or the Promotion of Advocacy and Public Acceptance

”‘—’ ȋ‘” ǡ ˆ‘” •Š‘”–ȌǤ ŽŽ ƒ•– ”‡•‹†‡–• ‘ˆ –Š‡ ƒ†
ƒ†ƒ ƒ™ƒ”†‡‡• •ŠƒŽŽ „‡ ‡„‡”• ‘ˆ –Š‹• Š‹‰ŠǦ’”‘ϐ‹Ž‡
Group and offer to the Society our best resource to generate ideas and help improve our image and participation in various
areas.
The Group shall, in advisory capacity, be our think-tank and our sounding board. It shall have sub-Committees, along with
‡„‡”• ‘ˆ ‘—” š‡…—–‹˜‡ ‘‹––‡‡ǡ ƒ† –Š‡•‡ •—„…‘‹––‡‡• •ŠƒŽŽ „‡ •’‡…‹ϐ‹…ƒŽŽ› –ƒ•‡† ™‹–Š ƒ ƒ‰‡†ƒǤ
For assignments such as negotiation of charges with the TPA’s and Insurers, intermediation in statutes related to Clinical
establishment Laws, Registration of Nursing Homes and Daycare centres, development of the DOS House, mediation with
the Tradespeople and redressal of common grievances, communication and interactions with both Print and Electronic
Media, we earnestly require contributions from this respected Group.
Š‡ ‹ϐŽ—‡…‡ –Šƒ– –Š‹• ‡šƒŽ–‡† ‰”‘—’ ™‹‡Ž†• ‹• ‹‡•‡ ƒ† Š‘’‡ –‘ „‡ ƒ„Ž‡ –‘ …Šƒ‡Ž‹œ‡ –Š‹• ˆ‘” –Š‡ …‘‘ ‰‘‘† ƒ†
hope that I can provide a platform for discussion of contentious issues such as the ban on corneal transplants for foreigners
and in rationalizing the rates that the CGHS approves, for example.
I have personally requested and invited them to be here for this GBM and am honored by their esteemed presence.
I request the General Body to approve PAPA and also approve support for their Meetings. I hope that this Committee will
be a permanent element, though non-statutory, and not change with the change in the Executive.
6. We have for long, dedicated a lot of time, energy and resource on producing quality CME’s and Teaching Programmes for
‘—” ‡„‡”• ƒ† ”‡•‹†‡–•Ǥ Š‹• ™ƒ• –Š‡ ‡‡† ‘ˆ –Š‡ –‹‡• ƒ† Šƒ• Ž‡† –‘ •‹‰‹ϐ‹…ƒ– ‹’”‘˜‡‡– ‹ –Š‡ “—ƒŽ‹–› ‘ˆ ‘—”
training as well as the overall quality of patient care that we are able to deliver to our people. Its an area that can only get
better and better with the inputs and contributions from our Members and the high-quality teaching institutions and care-
providers that Delhi and the NCR can boast of.
However, we have failed, quite miserably, in improving the individual lot of our members. The value of a Society is in the
well-being of its individual constituents.
I intend to have a 5-pronged approach in this regard
i) ’”‘’‘•‡ –‘ ’”‘˜‹†‡ –Š‡ ‡„‡”•ǡ all 8500 of them, the opportunity to hold a DOS co-branded Credit Card with

RuPay facility. The Card shall carry the photo-ID, DOS logo and membership no. and shall be issued free of cost. This
…ƒ”† ™‹ŽŽ ˆ—Žϐ‹ŽŽ ‘—” ‡‡† ˆ‘” ‹••—‹‰ ’Š‘–‘Ǧ ƒ”†• –‘ ‘—” ‡„‡”• ƒ† •ƒ˜‡ —• …‘•–•ǡ •‹—Ž–ƒ‡‘—•Ž› ’”‘˜‹†‹‰
ϐ‹ƒ…‹ƒŽ ‹…Ž—•‹‘ –‘ ‘—” ‡„‡”•Ǥ – ™‘”• ‘—–•‹†‡ ‘ˆ ‹•ƒȀ ƒ•–‡” ƒ”†ǡ •—’’‘”–• –Š‡ ƒ–‹‘ǯ• Dz ƒ‡ ‹ †‹ƒdz …ƒ•ŠǦ
free, India mission very well, and carries the lowest transaction costs amongst all cards. Since the Card is likely to be
launched in Sept-Oct 2016, we shall have to wait till then.
††‹–‹‘ƒŽŽ›ǡ the KYC norms of the Card-issuing bank shall require continuous monitoring of the residential/work
ƒ††”‡•• ‘ˆ –Š‡ …ƒ”†ǦŠ‘Ž†‡”ǡ ™Š‹…Š ƒ› „‡ —–‹Ž‹œ‡† ˆ‘” ƒ ”‡Ǧ…‘ϐ‹”ƒ–‹‘ ‘ˆ –Š‡ ‡„‡”•ǯ ˜‘–‹‰ •–ƒ–—•Ǥ
‹‹Ȍ  –Š‡ ‹…”‡ƒ•‹‰Ž› Ž‹–‹‰‹‘—• ‡˜‹”‘‡– –Šƒ– ™‡ ϐ‹† ‘—”•‡Ž˜‡• ‹ǡ I intend to provide a framework to negotiate
with the Insurance Companies to obtain a mass Indemnity Insurance Policy for all our members to pick-up and insure
themselves at the most reasonable cost.
iii) Legal protection – I intend to create a Legal cell and a Standing Counsel for the Members of the DOS to be able to
procure advice in the event of any unfortunate mishap.
iv) ‹ˆ‡ ‹•—”ƒ…‡ –Š”‘—‰Š –Š‡ ƒ‹Ž› ‡‡ϐ‹– …Š‡‡ – As an early member of the FBS-AIOS, I was able to analyse
and understand the nuances of one of the cheapest and most-cost-effective insurance systems. I intend to publicize
the Scheme at every forum so that our Members can join up and provide security to their near and dear ones and be
„‡‡ϐ‹––‡† „› –Š‡ Ž‘™Ǧ…‘•– Ž‹ˆ‡ ‹•—”ƒ…‡ •…Š‡‡Ǥ
v) “Helping Hands of DOS”– a Charitable arm of the DOS may be commenced which shall solicit voluntary donations
ƒ”‡† ™‹–Š ͺͲ
…‡”–‹ϐ‹…ƒ–‹‘ǡ –‘ Š‡Ž’ –Š‡ ‡‡†› ƒ† –Š‡ ‹ϐ‹” ƒ‘‰•– —•ǡ ˆ‘” –”‡ƒ–‡–• ‘ˆ ‹ŽŽ‡•• ‘” —–‘™ƒ”†
instances.
7. Of late, there have been instances of complaints being circulated on various social platforms of purported unfair trade
practices by some dealers and vendors of ophthalmic equipment. I intend to introduce a mechanism to receive grievances
of this nature from our esteemed members, examine and mediate to help reconcile the issue. I hope I have your support in
this venture.
Recently, the Niti Aayog has taken up my suggestion of “Treat in India” mission to tap the tremendous potential that our
medical fraternity offers for medical tourism. I believe, activities have started to develop the theme by exploring processes to
improve and foster international patients seeking quality care in India. From the provisioning of on-line medical visas to the
logistics of delivering standardized care, all aspects are being examined.

14 DOS TIMES - MAY-JUNE 2016

DOS EXCLUSIVES

I am extremely thankful to the Dz ƒ”‰ ƒ”•Šƒ•dzǡ my mentor, teacher and father Dr Madan Mohan, Dr Rajvardhan Azad, Dr
Ashok Grover, Dr G Mukherjee, Dr RB Jain, Dr Atul Kumar, Dr Mahipal Sachdeva and Dr Lalit Verma for their guidance, advice
and support at all times. They are remarkable minds, innovators and full of ideas for the advancement of Ophthalmology and
our Society. I am deeply grateful that they have all responded to my personal invitation to be present this evening.

I must also thank my Mom, my wife Indu and daughter Avantika to whom I’m deeply indebted for putting up with my
non-availability, unreasonable behavior at times and for their understanding of the requirements of Presidential responsibility.

At the end, I hope the roadmap for the Society activities, as laid out in my address will have a positive impact and success. I
hope that I would be able to live up to your expectations and my own. My theme and vision is to review what has been achieved
by the DOS and what needs to be achieved in the decade ahead.

In conclusion, my Executive and I would like to assure the House of an eventful and action-packed Year with our promise
of active participation and collective support for all undertakings. I invite suggestions, plans, comments or feedback, both
positive and negative, from all members, researchers and thinkers to identify areas we can dwell upon. My team and I are always
available and the Secretary or any Executive member may be contacted by email.

™‘—Ž† Ž‹‡ –‘ –ƒ‡ –Š‹• ‘’’‘”–—‹–› –‘ –Šƒ ƒ”˜‡‡ ƒ† –Š‡ ‘–Š‡” ‘ˆϐ‹…‡ •–ƒˆˆ ˆ‘” –Š‡‹” •‡ŽϐŽ‡•• ™‘”ǡ –Š‡ ‡…”‡–ƒ”›ǡ
the Treasurer and the entire Executive and our Members for their encouragement and backing. I trust the 51 weeks ahead shall
be full of action and hard work.

‘‰ ‹˜‡ –Š‡ Ǩ
ƒ‹ ‹†ǨǨ
”Ǥ ‹•Š‹ ‘Šƒ
Incoming President, DOS
At this juncture, I would like to announce the introduction of the singing of our National Anthem at the conclusion of this
GBM. I hope that in the future, it will take a permanent place in our Proceedings for all time to come.

www. dos-times.org 15

CORNEA

DESCEMET’S MEMBRANE DETACHMENT

„Š‹•Š‡ ƒ˜‡ǡ ‹•Š–Šƒ ‹‰Šǡ ƒ‰ ƒ–Š—”

Descemet’s membrane (DM) is a 10 μm thick DMD can present late after an uneventful cataract surgery
specialized basement membrane present also. Clinically DMD appears as a transluscent membrane in
between the endothelium and the posterior the anterior chamber separated from the posterior stroma.
stroma. Descemet’s Membrane Detachment The overlying corneal edema may obscure the visualization of
(DMD) is an uncommon but well known DMD at times, which warrants a high index of suspicion in such

complication of cataract and other intraocular cases5. A ‘double anterior chamber’ appearance may be seen

surgeries. The detachment of the descemet’s-endothelial with large DMDs.

complex from the stroma results in failure of the endothelial

pump and hence leading to severe corneal edema1. Small, CLASSIFICATION AND GRADING OF DMD

subclinical detachments may remain undetected as they resolve ƒ…‘‘Ž ƒ† ‘Ž–œ ’”‘’‘•‡† ƒ …Žƒ••‹ϐ‹…ƒ–‹‘ •…Š‡‡ –‘
spontaneously. However, larger untreated detachments of DM help determine the prognosis for DMDs. They separated DMDs
can lead to irreversible bullous keratopathy and loss of vision. into planar and nonplanar, depending on whether Descemet’s

INCIDENCE AND CAUSES membrane was separated from the posterior corneal stroma

„› ζͳ  ‘” εͳ ǡ ”‡•’‡…–‹˜‡Ž›6. They believed that

‘……—”• ™Š‡ ϐŽ—‹† ‡–‡”• –Š‡ …‘”‡ƒŽ •–”‘ƒ planar detachments had the best prognosis for spontaneous

through a tear in Descemet’s membrane (DM) or an area of reattachment, whereas nonplanar detachments were unlikely

separation between the DM and the corneal stroma caused to spontaneously reattach and should be repaired early. Assia

during various intraocular surgeries. Cataract extraction is ‡– ƒŽ …Žƒ••‹ϐ‹‡† • ‹–‘ –Š‘•‡ ™‹–Š ƒ† ™‹–Š‘—– ƒ ”‘ŽŽ‡† •…”‘ŽŽǡ

the most common surgery associated with DMD. Other rarer and believed that those without a rolled scroll (even if there is

causes of surgical DMD include peripheral iridotomy (laser a separation for more than 1 mm) can reattach spontaneously

and surgical), trabeculectomy, non penetrating glaucoma and may be treated conservatively7.

surgeries, intracorneal ring The grading of the severity

segment implantation, deep Cataract extraction is the most of DMD has been described by
anterior lamellar keratoplasty, common surgery associated with Jain et al. It was considered to
endothelial keratoplasty and be mild if it involved < 25% of

pars plana vitrectomy2. The DMD. Other rarer causes of surgical the cornea and was peripheral,
incidence of DMD was found moderate if it involved 25% to
include peripheral iridotomy 50% cornea and was peripheral,
DMDto be 2.6% for extracapsular
(laser and surgical), trabeculectomy,
cataract extraction (ECCE) and non penetrating glaucoma surgeries, ƒ† •‡˜‡”‡ ‹ˆ ‹– ‹˜‘Ž˜‡† ε ͷͲΨ
ͲǤͷΨ ˆ‘” ’Šƒ…‘‡—Ž•‹ϐ‹…ƒ–‹‘3. intracorneal ring segment implantation, of the cornea or involved the
However, the incidence of central cornea8.
small DM scrolls along the

sclera-corneal incisions if seen deep anterior lamellar keratoplasty, DIAGNOSIS OF DMD
carefully with gonioscopy can be endothelial keratoplasty and pars plana
as high as 11-42%4. DMD during The mainstay of diagnosis
of DMD is a good slit lamp
cataract surgery can be caused vitrectomy2. The incidence of DMD biomicroscopy examination.
by blunt keratomes, anteriorly However, severe corneal
placed incisions, shallow was found to be 2.6% for extracapsular edema frequently hampers
anterior chamber, inadvertent cataract extraction (ECCE) and 0.5% for the visualization of detached

injection of saline or viscoelastic ’Šƒ…‘‡—Ž•‹ϐ‹…ƒ–‹‘ Decemet’s membrane. Anterior
in the predescemet’s space or segment optical coherence

during cortical wash, stromal tomography (ASOCT) is a

hydration to seal the incisions, intraocular lens insertion and reliable and quick modality of non-contact diagnoses of DMDs9.

intracameral antibiotic injection. An important risk factor for …ƒ ˆ—”–Š‡” †‡–‡”‹‡ –Š‡ •‹–‡ǡ …‘ϐ‹‰—”ƒ–‹‘ ƒ† ‡š–‡–

DMD is pre existing endothelial abnormality. Non surgical of the DMD, thus guiding the treatment method and monitoring

causes of DMD include trauma, chemical injuries or ectatic –”‡ƒ–‡– ‘—–…‘‡ ƒ• ™‡ŽŽǤ …Š‡‹’ϐŽ—‰ ‹ƒ‰‹‰ ‹• ƒ‘–Š‡”

corneal disorders. non-contact method of diagnosing DMD. However, it does not

CLINICAL FEATURES offer any advantage over ASOCT or slit lamp biomicroscopy

because of scattering of light in edematous corneas10.

The patient usually presents with localized or generalized Other methods which have been used in the diagnosis

…‘”‡ƒŽ ‡†‡ƒ ‘ –Š‡ ϐ‹”•– ’‘•–Ǧ‘’‡”ƒ–‹˜‡ †ƒ›Ǥ Š‡ ‡†‡ƒ …ƒ of DMD include ultrasound biomicroscopy and confocal

be as severe to cause a “cobblestone” appearance also. Rarely microscopy. But these being contact methods are not preferred

www. dos-times.org 17

CORNEA

in eyes that have undergone recent series, but, recent reports have favoured intracameral air alone. Thus there is a
surgeries. early surgical intervention to reattach tendency these days to use air injection
a DMD. Visual rehabilitation is much for all types of DMD’s. Gases with longer
MANAGEMENT OF DMD delayed if managing conservatively. Also resorption time like C3F8 are reserved
Descemet membrane detachment can for failed reattachments or long standing
There is relative scarcity in the ”‡•—Ž– ‹ …‘”‡ƒŽ ‘’ƒ…‹ϐ‹…ƒ–‹‘ǡ ϐ‹„”‘•‹•ǡ detachments. The risk for IOP elevation
literature regarding the guidelines and wrinkling of Descemet membrane, may be lower with the use of air than with
for management of DMD. To date, no thereby affecting visual recovery. Thus longstanding gases as air is absorbed
prospective studies on the management in patients with involvement of the faster.
options for DMDs have been published. visual axis, surgical intervention to
The choice to intervene surgically or promote attachment may be the favoured Pneumodescemetopexy is usually
manage conservatively is largely guided approach. Pneumodescemetopexy or performed under topical anesthesia.
by results from retrospective case series injection of gas in the anterior chamber The technique involves injecting gas
or surgeon’s preference. Whether an is the primary management strategy. with a 27G or 30 G needle with the bevel
intervention is needed in all cases of It can hasten the absorption of corneal down to reach beneath the plane of the
DMD, at what time and what agent to be edema and, thus, fasten visual recovery. detached Descemet membrane, and slow
used are still some of the unanswered Other management strategies which injection of air. The needle is then gently
questions. The management of Descemet have been described will be elaborated withdrawn and the site of entry is sealed
detachment depends on various factors, subsequently. with a surgical sponge for 1 minute. Some
such as the location and area of the •—”‰‡‘• ’‡”ˆ‘” ƒ …‘’Ž‡–‡ ϐ‹ŽŽ ˆ‘”
detachment, the degree of anteroposterior Pneumodescemetopexy 15–20 min maintaining supine position,
separation from the posterior stroma, and and then release one-third of the gas
the duration of watchful observation11. Pneumodescemetopexy is the to avoid postoperative pupillary block.
‘ †‡ϐ‹‹–‡ …Šƒ”ƒ…–‡”‹•–‹…• ƒ”‡ ‘™ –‘ injection of air or gas in the anterior Other ways of preventing postoperative
predict whether the DM will function or chamber. It causes the opposition of high intraocular pressure are by less than
not after reattachment. However Vinekar the detached DM back to the posterior …‘’Ž‡–‡ ϐ‹ŽŽǡ …›…Ž‘’Ž‡‰‹…•ǡ ’”‘’Š›Žƒ…–‹…
et al reported that attempts should be stroma. It is the preferred treatment for laser iridotomy or antiglaucoma drugs.
taken to repair DMDs that have been DMD these days because of the early The site of injection is through a limbal
detached even for a long time12. resorption of corneal edema thus fast area where the cornea is relatively
visual recovery as well as the ease of compact and DM appears apposed.
Conservative Management the procedure. Various agents have been (Figure 1 & 2) demonstrate two cases of
advocated for intracameral tamponade post cataract surgery DMD which were
Conservative management including 100% air, 14% isoexpansile managed by intracameral injection of air.
’‡”ϐŽ—‘”‘’”‘’ƒ‡ ȋ ͵ ͺȌ ƒ† ʹͲΨ Complete resolution of edema was seen
includes observation which is usually •—Žˆ—”ǦŠ‡šƒϐŽ—‘”‹†‡ ȋ ͸ȌǤ in both the cases. Other less commonly
used strategies for managing DMD have
supplemented with medical management No randomized control trial also been described.
…‘’ƒ”‹‰ –Š‡ ‡ˆϐ‹…ƒ…› ƒ† •ƒˆ‡–› ‘ˆ –Š‡•‡
with topical cortico-steroids and three agents is available till date because Suture Fixation
of the relative paucity of occurrence of
hyperosmotics (5% sodium chloride DMD. Earlier 100% air was believed to Fixation of the detached DM to
be least effective agent for tamponade, the rest of the cornea using 10-0 nylon
solution). Numerous case reports on and longstanding intracameral gases suture along with air injection has been
such as SF6 or C3F8 were shown to described16. The need for this procedure
spontaneous resolution of corneal be more successful15. However, in the in present day scenario is only limited to
recent largest retrospective case series recalcitrant detachments.
oedema have been published with by Jain et al the anatomic and functional
outcomes of descemetopexy with air Viscoelastic Tamponade
excellent visual outcome13. This occurs were found to be statistically better than
C3F8 with reduced incidence of adverse Injecting viscoelastic substance
either by spontaneous reattachment of events (pupillary block). Chaurasia for tamponading the DM has been
et al also reported 13 out of 14 eyes described17. The use of same is limited
the Descemet’s membrane or migration of which successfully reattached with due to its propensity to cause raised
intraocular pressure.
nearby endothelial cells. Observation is an

option for smaller peripheral or inferior

DMDs. Spontaneous reattachment of

DMDs usually takes several weeks to

several months.

Surgical Management

Although conservative management
in hope of spontaneous reattachment has
been reported in many case reports and

1. Cornea Services Dr. Shroff Charity Eye Hospital, Darya Ganj, New Delhi
2. Glaucoma Services Dr. Shroff Charity Eye Hospital, Darya Ganj, New Delhi

Dr.Abhishek Dave MD, FMRF, FICO1 Dr. Nishtha Singh MS2 Dr. Umang Mathur MS, FLVPEI1
18 DOS TIMES - MAY-JUNE 2016

CORNEA

Figure 1A: 2QUV 2JCEQGOWNUKſECVKQP &/&
TGF CTTQY B: ASOCT Figure 2A: 2QUV 2JCEQGOWNUKſECVKQP &/& B: #51%6 UJQYKPI EQTPGCN
EQPſTOKPI &/& C: &C[ RQUV CKT KPLGEVKQP YKVJ ENGCT EQTPGC GFGOC CPF &/& C: &C[ RQUV CKT KPLGEVKQP YKVJ ENGCT EQTPGC
D: #51%6 UJQYKPI CVVCEJGF &/ D: #51%6 UJQYKPI CVVCEJGF &/

Other Techniques management of Descemet’s membrane biomicroscopy in the early detection
of graft detachment after Descemet
Other technique like manual detachment. 2013;24:356-61. membrane endothelial keratoplasty.
repositioning of DM with cyclodialysis ‘”‡ƒ ʹͲͳͳʌ ͵Ͳǣͳ͵͸ͻȂ͹ͷǤ
saptula has been decribed. With the 3. Ti SE, Chee SP, Tan DT, et al. Descemet 11. Chaurasia S, Ramappa M, Garg P.
popularity of pneumodescemetopexy Outcomes of air descemetopexy for
this has mostly become redundant. A membrane detachment after Descemet membrane detachment after
combination of various techniques can cataract surgery. J Cataract Refract
also be used for complex DMDs. ’Šƒ…‘‡—Ž•‹ϐ‹…ƒ–‹‘ •—”‰‡”›ǣ ”‹• Surg. 2012;38:1134-9.
12. Vinekar A, Sukhija J, Brar GS, et al.
CONCLUSION factors and success of air bubble Late’ functionally successful repair of
Descemet’s membrane detachment
DMD following cataract surgery is an –ƒ’‘ƒ†‡Ǥ ‘”‡ƒ ʹͲͳ͵ʌ ͵ʹǣͶͷͶȂͷͻǤ ˆ‘ŽŽ‘™‹‰ ’Šƒ…‘‡—Ž•‹ϐ‹…ƒ–‹‘Ǥ ›‡
uncommon but well known complication. ʹͲͲ͹ʌ ʹͳǣͷͷͷȂͷ͸Ǥ
Pneumodescemetopexy with air or gas 4. Anderson CJ. Gonioscopy in no-stitch 13. Couch SM, Baratz KH. Delayed, bilateral
is an effective and simple method of Descemet’s membrane detachments
managing DMD. Though there are reports cataract incision. J cataract refract surg with spontaneous resolution:
of spontaneous reattachment of DM, but implications for on surgical treatment.
it would be wise to surgically intervene 1993;19;620-1 Cornea 2009; 28:1160-63.
timely, especially if the visual axis is 14. Mahmood MA, Teichmann KD, Tomey
involved to prevent permanent vision 5. Makley TA Jr, Keates RH. Detachment KF, AL-Rashed D. Detachment of
loss. Descemet’s membrane. J Cataract
of Descemet’s membrane (an early Refract Surg 1998; 24:827–33.
REFERENCES 15. Potter J, Zalatimo N. Descemet’s
complication of cataract surgery). membrane detachment after cataract
1. Marcon AS, Rapuano CJ, Jones MR, et extraction. Optometry 2005;76:720–4.
al. Descemet’s membrane detachment Ophthalmic Surg 1980;11:189 –91. 16. Al-Mezaine HS. Descemet’s membrane
after cataract surgery: management detachment after cataract extraction
ƒ† ‘—–…‘‡Ǥ ’Š–ŠƒŽ‘Ž‘‰› ʹͲͲʹʌ 6. Mackool RJ, Holtz SJ. Descemet •—”‰‡”›Ǥ – ’Š–ŠƒŽ‘Ž ʹͲͳͲʌ ͵Ͳǣ͵ͻͳȂ
109:2325–30. 96.
membrane detachment. Arch 17. Donzis PB, Karcioglu ZA, Insler MS.
2. Chow VW, Agarwal T, Vajpayee RB, Sodium hyalonuronate (Healon) in
Jhanji V. Update on diagnosis and ’Š–ŠƒŽ‘Ž ͳͻ͹͹ʌ ͻͷǣͶͷͻȂ͸͵Ǥ the surgical repair of Descemet’s
membrane detachment. Ophthalmic
7. Assia El, Levkovich-Verbin H, —”‰ ͳͻͺ͸ʌ ͳ͹ǣ͹͵ͷȂ͵͹Ǥ

Blumenthal M. Management of

Descemet’s membrane detachment. J

ƒ–ƒ”ƒ…– ‡ˆ”ƒ…– —”‰ ͳͻͻͷʌ ʹͳǣ͹ͳͶȂͳ͹Ǥ

8. Jain R, Murthy SI, Basu S, Ali MH,

Sangwan VS. Anatomic and Visual

Outcomes of Descemetopexy in

Post-Cataract Surgery Descemet’s

membrane detachment.

Ophthalmology. 2013;120:1366-72.

9. Wylegala E, Nowinska A. Usefulness

of anterior segment optical coherence

topography in Descemet membrane

†‡–ƒ…Š‡–Ǥ —”
’Š–ŠƒŽ‘Ž ʹͲͲͻʌ

19:723–28.

10. Moutsouris K, Dapena I, Ham L, et

al. Optical coherence tomography,

…Š‡‹’ϐŽ—‰ ‹ƒ‰‹‰ǡ ƒ† •Ž‹– Žƒ’

Financial Interest: Š‡ ƒ—–Š‘”• †‘ ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

www. dos-times.org 19

CORNEA

HERPETIC EYE DISEASE IN PEDIATRIC POPULATION

HSV EPIDEMIOLOGY

”‹ƒ”› Ǧͳ ‹ˆ‡…–‹‘• ƒ”‡ Žƒ”‰‡Ž› …‘ϐ‹‡† –‘ ‡ƒ”Ž›

Dr. Deepender Chauhan MS, DNB, FRCOphth, FLVPEI childhood and adolescence. Primary infections with HSV
Consultant manifest clinically only up 5% of the time, the rest are
Shroff Eye Centre, New Delhi asymptomatic. Therefore, clinical surveys greatly underestimate

Herpes Simplex Virus belongs to a family of the incidence and prevalence of HSV infection.
Human Herpes Viruses which also include HSV- Transmission: HSV-1 is transmitted principally by
2 and cytomegalo-virus among others. Primary
infections of HSV-1 are very common; in fact contact with infected secretions or lesions. HSV may be shed
up to 90% of our populations have positive asymptomatically at the time of primary, initial, or recurrent
infection. In Indian populations, 70 to 80% are infected
by adolescence, whereas in the developed countries this
prevalence is low.

serology markers suggesting a past HSV OCULAR HSV DISEASE EPIDEMIOLOGY
infection. These infections are mostly asymptomatic and go un-
noticed. However, whenever manifest, the clinical presentation Most of the epidemiological studies have been done in
is usually in the form of infections of mucous membranes developed countries. However, ocular HSV was evaluated in
and skin (e.g., gingivostomatitis, herpes labialis, and genital South India between 1995 and 1997. HSV eye disease accounted
infections) and rarely as disseminated or systemic forms for ~8% of all cases attending the cornea clinic. The mean age
like in case of neonatal and congenital HSV infection, eczema of the patients with ocular HSV was 29 years (range, 9 months
herpeticum, visceral HSV infections in immunocompromised –‘ ͸ͷ ›‡ƒ”•Ȍ ™‹–Š ‘ •‡ƒ•‘ƒŽ ˜ƒ”‹ƒ„‹Ž‹–› ‹†‡–‹ϐ‹‡†Ǥ

hosts, HSV encephalitis etc.

The diagnosis of a pediatric HSV infection can be OCULAR HSV DISEASE IN PEDIATRIC POPULATION

challenging. It is partly because the children cannot articulate There are studies showing differences in the clinical

well their symptoms and history, therefore, there is delayed presentation of HSV keratitis in children compared with adults.

’”‡•‡–ƒ–‹‘Ǥ  –Š‹• •‡––‹‰ ‘ˆ ‹•—ˆϐ‹…‹‡– Š‹•–‘”› ƒ† Management in the pediatric population must be tailored

description of symptoms, to address these differences
so proper treatment can be
–Š‡”‡ ƒ”‡ †‹ˆϐ‹…—Ž–‹‡• ‹ –Š‡ Herpetic eye disease is commonly seen
biomicroscopy examination of provided. Children tend to
the anterior segment as well. It in ophthalmic clinics. There are subtle have poorer visual outcomes
is not uncommon to see these variations in clinical presentation in as compared with adults

children coming to eye OPD children. This article highlights these „‡…ƒ—•‡ –Š‡› …ƒ „‡ †‹ˆϐ‹…—Ž–
only when there are repeated differences in terms of primary ocular to examine (therefore more
episodes of red eye. In fact, HSV and recurrent HSV disease in likely to get misdiagnosed),
many of these children present children not very compliant to topical
with sequels such as opacities medications, and are susceptible
and vascularization in the to amblyopia due to corneal

cornea (and not the primary scarring and astigmatism. This

disease like epithelial keratitis / blepharo-conjunctivitis). review aims to address the recent updates in management of

Š‡”‡ˆ‘”‡ǡ ‹– ‹• ‘– —…‘‘ –‘ ϐ‹† †‡Žƒ›‡† …Ž‹‹…ƒŽ HSV keratitis in children.

presentation and misdiagnosis of HSV eye disease in children.

Š‡•‡ ˆƒ…–‘”• ’‘–‡–‹ƒŽŽ› …‘’”‘‹•‡ –Š‡ ϐ‹ƒŽ ‘—–…‘‡Ǥ NEONATAL HSV (HSV IN THE NEWBORN)
•‹‰‹ϐ‹…ƒ– ’”‘’‘”–‹‘ ‘ˆ ’ƒ–‹‡–• ƒ”‡ ‹•†‹ƒ‰‘•‡† ȋͳͷǤͷΨȌ
as Staphyloccocal blepahro-kerato-conjunctival disease and Herpes simplex virus (HSV) infection of the neonate is
phlyctenular conjunctivitis. uncommon, with an estimated rate of 1 in 3,200 deliveries.
Infants present between 2nd and 3rd weeks with variable
While a red eye is the most common reason for presentations. Treatment and management of neonatal
…‘•—Ž–ƒ–‹‘ǡ ƒ •‹‰‹ϐ‹…ƒ– ’‡”…‡–ƒ‰‡ ‘ˆ ’ƒ–‹‡–• ’”‡•‡– ™‹–Š herpes falls in the domain of pediatricians, however, it is not
a corneal opacity, reported by most of the parents as a white uncommon to get referrals from neonatal-ICU regarding such
•’‘– ‘ –Š‡ ‡›‡Ǥ Š‡•‡ …Š‹Ž†”‡ ƒ”‡ Ž‹‡Ž› –‘ Šƒ˜‡ •‹‰‹ϐ‹…ƒ– patients, especially while working in a multi-specialty hospital.
astigmatism and end up with amblyopia. Also, once established

as stromal keratitis, HSV eye disease has higher recurrences RISK FACTORS
leading to further fall in vision. Primary HSV infections are more
common in childhood. There are mostly orofacial lesions and Š‡ ”‹• ‘ˆ ‡‘ƒ–ƒŽ ƒ…“—‹•‹–‹‘ ‘ˆ Ǧʹ ‹• •‹‰‹ϐ‹…ƒ–Ž›
occasionally primary ocular infections. Ocular complications Š‹‰Š‡” ™‹–Š ϐ‹”•– ‡’‹•‘†‡ ’”‹ƒ”› ȋͷ͹ΨȌ ƒ† ϐ‹”•– ‡’‹•‘†‡
include lid, conjunctival, corneal, intraocular infections and non-primary (25%) maternal infections when compared with
retinitis. This will be discussed in detail later. recurrent genital infections (2%). However, transmission of HSV-

www. dos-times.org 21

CORNEA

1 to the neonate has been documented Ocular surface has an innate resistance (Figure 2). It may be associated with
to be high irrespective of primary or to infection, provided by lysozyme, SPKs and corneal vesicles in 10% of cases
recurrent infection when compared with Interferons etc. It is followed by the (earliest sign of corneal HSV infection).
HSV-2 transmission patterns. entrance of virus into sensory nerve
terminals in the corneal epithelium. Blepharo-conjunctivitis is more
PREVENTION OF NEONATAL HSV This step requires live but not actively commonly a primary HSV infection. It is
replicating HSV. The virus then travels seen more common in children and have
Neonatal HSV is acquired during one by retrograde axonal transport to the to be differentiated from squamous and or
of three time periods as In-utero (5%), neuronal cell bodies in the trigeminal Staph blepharitis. Unilateral involvement,
Peripartum (85%) and Postnatal (10%). ganglia. Here, the virus either replicates, inter-marginal vesicles and associated
Preventive strategies include: usually killing cells, or enters into an conjunctival vesicles and follicles in
Ȉ Cesarean Delivery: Cesarean alternative replication mode called fornices usually help in diagnosis.
latency (which may involve 100 more
delivery prior to rupture of copies of the viral genome), which may It must, however, be noted that
membranes (and prevention of ’‡”•‹•– ‹ …‡ŽŽ• ‹†‡ϐ‹‹–‡Ž›Ǥ compared to adults, children tend to
disruption of mucocutaenous have bilateral blepharo-conjunctivitis
barrier by avoiding the use of Once re-activated, virus reenters into with higher recurrences. Steroids must
fetal scalp electrodes and other the productive cycle, and progeny virus be avoided and topical and oral acyclovir
instrumentation) has been proven passes anterograde along nerve exons (esp. in recurrent infection or age < 5yrs)
to be effective in preventing the to produce a recurrent bout of virus help to resolve the condition.
transmission of HSV to the neonate. replication at the initial site of infection.
Ȉ ƒ–‡”ƒŽ ƒ–‹˜‹”ƒŽ •—’’”‡••‹˜‡ EPITHELIAL HSV DISEASE
therapy BLEPHARO-KERATO-
‹•‡ƒ•‡ …Žƒ••‹ϐ‹…ƒ–‹‘ ƒ† …Ž‹‹…ƒŽ Corneal vesicles in the epithelium
presentations of Neonatal HSV CONJUNCTIVITIS: are one of the early clinical manifestations
Disseminated disease (25%) involves of acute HSV infection. These vesicles
multiple organs, including the central The condition as the name suggests, then coalesce into dendritic lesions over
nervous system, lungs, liver, adrenal, involves the entire ocular surface. It is 24 hours. If left untreated or in cases of
skin, eyes, and/or mouth. It is often usually unilateral (90%). Blepharitis topical steroid use, it may progress to
associated with viral sepsis, encephalitis, (Figure 1) is characterized by eyelid geographic corneal ulceration. Active
ARDS, respiratory failure, hepatic failure, skin vesicles, some of which coalesce to viral shedding occurs at this time as the
disseminated intravascular coagulation form giant blisters. The vesicles near the infected epithelial defect margins contain
(DIC). In fact, 40% do not develop a ‡›‡Ž‹† ƒ”‰‹• ƒ”‡ ϐŽƒ––‡” ™Š‹Ž‡ •‘‡ ‘ˆ live virus. This may rarely progress
vesicular rash during the entire illness. inter-marginal vesicles may form shallow to active stromal ulceration, melt and
CNS Disease (25%) presents with ulcers at the lid margin (unlike the waxy necrosis (necrotizing stromal keratitis).
focal/generalized seizures, lethargy, scab lesions of common blepharitis). After active infection, HSV lies dormant
irritability, poor feeding, temperature There may be associated minor bleeding within the trigeminal ganglion or in
instability, and bulging fontanelle due to from the vesicles. The vesicles actively corneal latency and may reactivate again
raised ICT. 60-70% of infants with CNS shed live virus which has a direct access to to produce any of the many varieties of
disease have skin lesions at some point conjunctival cul-de-sac. The conjunctiva ocular herpetic disease.
during the course of the illness. shows vesicular lesions (which stain with
‹•‡ƒ•‡ ȋͶͷΨȌ ‹• …‘ϐ‹‡† –‘ Fluorescein dye) and follicular response It has been noted that epithelial
the skin, eye, and/or mouth of newborns; keratitis is the most common initial
„› †‡ϐ‹‹–‹‘ǡ †‘‡• ‘– ‹˜‘Ž˜‡ ˜‹•…‡”ƒŽ
organs or the CNS. Infants present around
day 10 to 12 of life with a vesicular rash
(80%).

TREATMENT OF HSV IN THE Figure 1: *58 $NGRCJTQEQPLWPEVKXKVKU
PQVG VJG UMKP DNKUVGTU YKVJ ƀCV NGUKQPU PGCT NKF OCTIKP

NEWBORN

Treatment and management of
neonatal HSV falls under the purview
of pediatrician. Treat with parenteral
acyclovir given at 60mg/kg/day divided
every 8 hours. Treat newborns with SEM
disease for 14 days, and neonates with
CNS and disseminated disease for 21 days
or till CSF PCR becomes negative.

OCULAR HSV Figure 2: (QNNKEWNCT EQPLWPEVKXKVKU CUUQEKCVGF YKVJ DNGRJCTKVKU

Following primary infection, herpes
viruses reach the ocular surface and are
‹‹–‹ƒŽŽ› •—•’‡†‡† ‹ –Š‡ ‘…—Žƒ” –‡ƒ” ϐ‹ŽǤ

22 DOS TIMES - MAY-JUNE 2016

CORNEA

presentation (65%) of ocular HSV. In Figure 3: 0GETQVK\KPI UVTQOCN MGTCVKVKU
the Indian study on HSV epidemiology,
among the patients who presented with Figure 4: 5VTQOCN MGTCVKVKU YKVJ RTG GZKUVKPI EQTPGCN UECT
0QVG VJG JGCNGF MGTCVQWXGKVKU YKVJ
epithelial disease, 68% had dendritic UGEVQTCN KTKU CVTQRJ[ CPF ECVCTCEV KP HGNNQY G[G
keratitis, 11.1% had geographic keratitis,
and 9.8% had punctate epithelial keratitis. Figure 5: 4GUQNWVKQP QH UVTQOCN MGTCVKVKU CHVGT VQRKECN UVGTQKFU CPF VQRKECN CPVKXKTCN VJGTCR[
PQVG
Although up to 35% of all HSV cases VJG TGUKFWCN VJKPPKPI CHVGT JGCNKPI
presented with stromal disease, most
of them had recurrent ocular episodes. over 10-16 week period as relapses to time to treatment failure, proportion of
Recurrences were more frequent in men, are frequent. It must be kept in mind patients who failed treatment, proportion
consistent with other studies. Among the that topical steroids must be avoided of patients whose keratitis resolved, time
patients with stromal keratitis, disciform in any stromal keratitis associated with to resolution, or 6-month best-corrected
keratitis was present in 28.2% and epithelial defect / infection (necrotizing visual acuity. However, HEDS did not
necrotizing keratitis in 6.4%. In only 34% HSV stromal keratitis). This condition include patients with necrotizing stromal
…ƒ•‡•ǡ –Š‡ Žƒ„‘”ƒ–‘”› –‡•–• …‘ϐ‹”‡† –Š‡ —•– ϐ‹”•– „‡ –”‡ƒ–‡† ™‹–Š –‘’‹…ƒŽ keratitis. Many clinicians prefer to use
diagnosis; using multiple diagnostic tests antivirals and steroids can only be added oral Acyclovir (in therapeutic dosage) for
(viral culture, IFA for IgG, IgM and IgA). after resolution of active viral epithelial necrotizing stromal keratitis.
Up to 9-10% of epithelial keratitis cases infection (Figure 6). Neurotrophic
may develop a stromal disease or iritis. epithelial defect can develop over the ROLE OF ORAL ACYCLOVIR IN
healing stromal keratitis (Figure 7).
– –‹‡•ǡ ƒ…–‹˜‡ ˜‹”ƒŽ ‹ϐ‹Ž–”ƒ–‹‘ Š‡•‡ ’ƒ–‹‡–• „‡‡ϐ‹– ˆ”‘ –ƒ”•‘””Šƒ’Š› PROPHYLAXIS
of stroma can lead to necrotizing viral and copious lubrication.
keratitis (Figure 3). It is associated with A 1 year course of oral acyclovir
varying degrees of melt. ROLE OF ORAL ACYCLOVIR IN prevents any type of recurrence (19%
in the acyclovir group and 32% in the
Treatment of dendritic ulcer TREATMENT IN STROMAL HSV placebo group). It not only reduces the
includes gentle scraping of ulcer margins probability of recurrent stromal keratitis
(however, some experts discourage According to Herpetic Eye Disease (14% in the acyclovir group and 28%in
this because scraping may breach the Study (HEDS) there is no clinically the placebo group) but also oro-facial
Bowman’s membrane and seed the •‹‰‹ϐ‹…ƒ– „‡‡ϐ‹– ‘ˆ ‘”ƒŽ ƒ…›…Ž‘˜‹” ‹ recurrences (19% in the acyclovir group
stroma with live viral particles), topical treating HSV immune-stromal keratitis an d 36% in the placebo group). There
acyclovir ointment (5 times a day) or in patients receiving concomitant topical is no rebound in the rate of HSV disease
topical ganciclovir ointment (3 times a …‘”–‹…‘•–‡”‘‹†• ƒ† –”‹ϐŽ—”‹†‹‡ ‹ ”‡‰ƒ”† after acyclovir treatment is stopped.
day). Frequent lubricants and a weak
antibiotic like Chloremphenicol are usual
adjuvants to antiviral medication.

As per the HEDS recommendations
for patients with HSV epithelial keratitis
–”‡ƒ–‡† ™‹–Š –‘’‹…ƒŽ –”‹ϐŽ—”‹†‹‡ –Š‡”‡ ‹•
‘ ƒ’’ƒ”‡– „‡‡ϐ‹– ‘ˆ ƒ ͵Ǧ™‡‡ …‘—”•‡ ‘ˆ
oral acyclovir in preventing HSV stromal
keratitis or iritis.

STROMAL HSV DISEASE

The corneal stroma may be affected
by HSV either due to direct stromal
invasion (leading to necrotizing stromal
keratitis), or via immune reactions to
antigens in the stroma (Figure 4) leading
to immune stromal keratitis. Without
proper treatment, stromal keratitis
can lead to vision loss due to scarring
and thinning of the stroma, as well as
neovascularization, which may lead to
lipid deposition and edema.

Immune stromal keratitis responds
well to topical steroids and topical
antiviral medication (Figure 5). HEDS also
concluded that topical steroid treatment
™ƒ• •‹‰‹ϐ‹…ƒ–Ž› „‡––‡” –Šƒ ’Žƒ…‡„‘ ‹
reducing persistence or progression of
•–”‘ƒŽ ‹ϐŽƒƒ–‹‘ ƒ† ‹ •Š‘”–‡‹‰
the duration of HSV stromal keratitis.
The treatment has to be tapered slowly

www. dos-times.org 23

CORNEA

Figure 6: 4GEWTTGPEG QH GRKVJGNKCN NGUKQPU QXGTN[KPI UVTQOCN MGTCVKVKU Figure 8: %NCUUKECN UGEVQTCN KTKU CVTQRJ[ KP C JGCNGF JGTRGVKE WXGKVKU

VQRKECN UVGTQKFU CTG EQPVTCKPFKECVGF JGTG

Figure 7: 0GWTQVTQRJKE GRKVJGNKCN FGHGEV QXGTN[KPI JGCNKPI UVTQOCN MGTCVKVKU iris atrophy (Figure 8). Herpetic anterior
—˜‡‹–‹• ‹• ”ƒ”‡Ž› ‰”ƒ—Ž‘ƒ–‘—•ǡ ƒ• †‡ϐ‹‡†
ENDOTHELIITIS photophobia than the more limited forms „› ϐ‹‡ ‡”ƒ–‹… ’”‡…‹’‹–ƒ–‡• ”ƒ–Š‡” –Šƒ
‘ˆ ‡†‘–Š‡Ž‹ƒŽ ‹ϐŽƒƒ–‹‘Ǥ large ‘‘mutton fat’’ keratic precipitates.
Direct infection and subsequent Recurrences are common. There may
destruction of endothelial cells is not The condition usually responds be a role of oral acyclovir in these cases,
well documented and more common quickly to topical corticosteroids. There is along with topical corticosteroids.
hypothesis is that endotheliitis is no therapeutic role of oral acyclovir while Topical antiviral may be added to prevent
–”‹‰‰‡”‡† „› ‹ϐŽƒƒ–‘”› ”‡•’‘•‡ topical antivirals may be added to prevent epithelial recurrence. During HEDS, the
when endothelial cells express viral epithelial recurrences. ’‘••‹„Ž‡ „‡‡ϐ‹– ‘ˆ ƒ…›…Ž‘˜‹” „‡…ƒ‡
antigens. In a disciform keratitis apparent after 3 weeks of follow-up.
(Disciform endotheliitis is a better TRABECULITIS While the number of patients studied
terminology for this condition) a diffuse was too small to achieve statistically
or well-demarcated area of stromal •‘Žƒ–‡† ‹ϐŽƒƒ–‹‘ ‘ˆ –Š‡ conclusive results, the results suggested a
edema is seen. The involved endothelium trabecular meshwork is uncommon but „‡‡ϐ‹– ‘ˆ ‘”ƒŽ ƒ…›…Ž‘˜‹” ‹ –Š‡ –”‡ƒ–‡–
is characterized by keratic precipitates not rare and usually associated with of HSV iridocyclitis.
(KPs) with iritis and overlying stromal endotheliitis or iritis. Trabeculitis is often
edema. KPs if present are only present misdiagnosed as Posner Schlossmann DIAGNOSIS
under areas of stromal edema. Unless Syndrome but gonioscopy helps in
associated with iritis, there is a relative differentiating the condition. The Of the eight recognized human
’ƒ—…‹–› ‘ˆ ƒ“—‡‘—• …‡ŽŽ•Ǥ Š‡ •‹‰‹ϐ‹…ƒ– condition usually responds quickly to herpesviruses, herpes simplex virus type
ƒ“—‡‘—• ‹ϐŽƒƒ–‹‘ ‹• ’”‡•‡–ǡ –Š‡ topical corticosteroids. However, scarring 1 (HSV-1) is most frequently associated
condition is better termed as HSV of the trabecular meshwork can result with eye diseases. Herpes Simplex Viruses
kerato-uveitis. The condition responds ˆ”‘ …Š”‘‹… ‹ϐŽƒƒ–‹‘ǡ …”‡ƒ–‹‰ ƒ are large, enveloped viruses with a double
well to topical steroids but untreated, persistent increase in IOP. stranded DNA core. Whereas most cases
chronic endotheliitis can decompensate of HSV keratitis are diagnosed based on
‡†‘–Š‡Ž‹ƒŽ ˆ—…–‹‘ •—ˆϐ‹…‹‡–Ž› –‘ …ƒ—•‡ IRIDOCYCLITIS clinical exam, atypical presentations may
permanent corneal edema. „‡‡ϐ‹– ˆ”‘ Žƒ„‘”ƒ–‘”› …‘ϐ‹”ƒ–‹‘ ‘ˆ
Up to 9% of all cases of nontraumatic diagnosis. Live viral culture is the gold
Diffuse endotheliitis involves anterior uveitis and iridocyclitis may have standard for detection of HSV-1 but it is
the entire endothelium (and perhaps herpetic etiology. The main differentiating costly, time consuming and often negative
trabecular meshwork) and presents features include unilateral uveitis in the due to small sample size of corneal
with diffuse edema and KPs and high setting of pre-existing corneal scar (with/ epithelial scrapings.
IOP. Patients with diffuse endotheliitis without neovascularization), elevated
have more severe pain, redness, and IOP, occasional hyphema or blood stained Other available modalities
hypopyon and transilluminating areas of for detection of HSV include
‹—‘ϐŽ—‘”‡•‡…‡ ƒ••ƒ› ȋ Ȍǡ ƒ†
immunochromatographic assay (ICGA)
kit. Although PCR is very sensitive, it
often detects physiologic HSV shedding
also thus gives false positive results.
Therefore, a combination of PCR and IFA
is a preferredfor diagnosis of HSV.

Common differences in HSV eye
disease between children and adults:
Ȉ ‡…—””‡…‡ ‘ˆ ‡”ƒ–‹–‹• ‹• ‘”‡

24 DOS TIMES - MAY-JUNE 2016

CORNEA

likely to occur in children, with a rate oral therapy may be a considered as a higher incidence of bilateral epithelial
above 50%. In actuality, however, preferred treatment option in this group. disease.
recurrences in the pediatric Oral treatment can also avoid likely
population may be much higher as epitheliotoxic effect of topical acyclovir. Also, higher risk of bilateral and
many children present to tertiary recurrent stromal disease increases
care centers with evidence of prior Acyclovir is well tolerated in dosage the ocular morbidity in children due to
episodes of corneal disease. of 10mg/Kg body weight, 3 times a day. astigmatism, corneal scar and subsequent
Ȉ Š‡”‡ƒ• —‹Žƒ–‡”ƒŽ ’”‡•‡–ƒ–‹‘• amblyopia.
are most common, children are more Oral acyclovir dosage
ˆ”‡“—‡–Ž› ƒˆϐŽ‹…–‡† ™‹–Š „‹Žƒ–‡”ƒŽ REFERENCES
HSV blepharoconjunctivitis and Therapeutic:
keratitis as compared with adults. < 2 years: 8 mg / kg body weight (5 1. Pramod NP, Rajendran P, Kannan KA,
Ȉ  –Š‘•‡ ™Š‘ ƒ‹ˆ‡•– „‹Žƒ–‡”ƒŽ ǡ et al. Herpes simplex keratitis in South
there appears to be an increased times per day) India: clinico-virological correlation.
rate of asthma, atopy, and systemic Prophylaxis: (preferably under Jpn J Ophthalmol. 1999; 43:303–7.
disease. The sensitivity of atopic
patients to HSV infection may in part pediatrician guidance esp. when planned 2. Ching-Hsi Hsiao et al. Pediatric Herpes
result from depression of Th1-cell for more than 3 months) Simplex Virus Keratitis. Cornea Volume
activity, which is the primary effective 28:3, 2009.
immune response against ocular < 2 years: 8 mg / kg body weight (2
HSV. This puts children with atopy times per day) 3. Liesegang TJ. Epidemiology of ocular
and vernal kerato-conjunctivitis at a Adverse drug reaction: herpes simplex. Natural history in
high risk of HSV infection, especially Roschester, Minn, 1950 through 1982.
bilateral involvement. Total - 4.8% Arch Ophthalmol. 1989;107: 1160–65.
Ȉ ‡–”‘•’‡…–‹˜‡ •–—†‹‡• Šƒ˜‡ •Š‘™ Mild elevation in KFT, diarrhoea.
that 26% of children with HSV Studies on acyclovir resistant HSV- 4. Poirer RH. Herpetic ocular infections
†‹•‡ƒ•‡ Šƒ˜‡ ƒ ϐ‹ƒŽ ˜‹•‹‘ ‘ˆ ʹͲȀͶͲ 1 isolates have demonstrated cross- of childhood. Arch Ophthalmol.
or worse. Corneal scars may develop resistance between ACV, ganciclovir, 1980;98:704–706.
in up to 80% of these patients, with ƒ† ‹†‘š—”‹†‹‡ǡ „—– ‘– –”‹ϐŽ—”‹†‹‡Ǥ
as many as half of which are centrally Therefore, in suspected cases of Acyclovir 5. Beneish RG, Williams FR, Polomeno
located. In addition, patients are at ”‡•‹•–ƒ…‡ǡ ”‹ϐŽ—”‹†‹‡ –‘’‹…ƒŽ †”‘’• ƒ”‡ RC, et al. Herpes simplex keratitis
risk for refractive amblyopia caused initiated. and amblyopia. J Pediatr Ophthalmol
by keratitis-induced astigmatism. Strabismus. 1987;24:94–96.
CONCLUSION
MEDICAL MANAGEMENT 6. Beigi B, Algawi K, Foley-Nolan A, et al.
Ocular HSV is the most common Herpes simplex keratitis in children. Br
While Herpetic Eye Disease Study cause of blindness worldwide. In children, J Opthalmol. 1994;78:458–60.
(HEDS) gave important recommendation delays in treatment are related to late
for treatment of HSV keratitis, it included presentation, inadequate clinical history 7. Schwartz GS, Holland EJ. Oral acyclovir
patients above 12 years of age. Therefore, and poor compliance of a young child to for the management of herpes
the HEDS results should not be directly clinical examination. Lack of awareness simplex virus keratitis in children.
extrapolated for pediatric population. of clinical spectrum of disease and lack Ophthalmology. 2000;107:278–82.
Oral acyclovir is usually well-tolerated in of good, reliable laboratory tests also
the pediatric population. Sometimes, very delay the diagnosis, at times also lead to 8. Chong EM, Wilhelmus KR, Matoba AY,
›‘—‰ …Š‹Ž†”‡ –‡† –‘ Šƒ˜‡ †‹ˆϐ‹…—Ž–› misdiagnosis especially in children. Also, et al. Herpes simplex virus keratitis
with drops / ointment regimen, therefore, clinical response to treatment may vary in children. Am J Ophthalmol.
in children due to doubtful compliance 2004;138:474–75.
–‘ ‡†‹…ƒ–‹‘ ƒ† Žƒ… ‘ˆ †‡ϐ‹‹–‹˜‡
therapeutic guidelines. Higher and ͻǤ ‘ŽŽƒ†
ǡ …Š™ƒ”–œ
Ǥ Žƒ••‹ϐ‹…ƒ–‹‘
increasing incidence of atopy amongst of herpes simplex virus keratitis.
children also alters immune response to Cornea. 1999;18:144–54.
HSV disease. Children with atopy have a
ͳͲǤ ‹‡•‡‰ƒ‰
Ǥ Žƒ••‹ϐ‹…ƒ–‹‘ ‘ˆ Š‡”’‡•
simplex virus keratitis and anterior
uveitis. Cornea. 1999;18:127–43.

11. The Herpetic Eye Disease Study
Group. Acyclovir for the prevention
of recurrent herpes simplex virus eye
disease. N Engl J Med. 1998;339: 300–
306.

Financial Interest: Š‡ ƒ—–Š‘” †‘‡• ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

www. dos-times.org 25

NEURO-OPHTHALMOLOGY

ATYPICAL OPTIC NEURITIS AN OVERVIEW

ƒ–”‹–‹ ƒŽŽƒ‰ǡ ƒƒ ‡Š–ƒ

O’–‹… ‡—”‹–‹• ȋ Ȍ ‹• ƒ ‹ϐŽƒƒ–‘”› ‘’–‹… of the limbs and trunk, and frequently bowel and bladder
neuropathy characterised by clinical signs of dysfunction19-20. There may be a lag time that varies from a few
optic nerve dysfunction. While the term has months to decades (average 2 years), between optic neuritis
become almost synonymous with idiopathic and an attack of myelitis. Considering the risk for recurrent
or multiple sclerosis (MS) associated cause, a attack with severe residual vision loss, and differing treatment

differential diagnosis of optic neuropathy must strategies for NMO, it can be a worthwhile effort to screen all

always be kept in mind before labelling it as typical ON (Table patients of optic neuritis for NMO antibodies. The low incidence

1). and prevalence of NMO in the population, costs of testing, and

The ONTT found that 50% of patients presenting with absence of evidence based preventive or treatment protocols

‘’–‹… ‡—”‹–‹• …‘˜‡”–‡† –‘ …Ž‹‹…ƒŽŽ› †‡ϐ‹‹–‡ ‘’–‹… ‡—”‹–‹• however, go against a routine testing for antibody positivity21,22.

(CDMS) at 15 years of follow-up1. Accordingly, the clinical ”‘—† ʹͷΨ ‘ˆ ’ƒ–‹‡– ™‹–Š …Ž‹‹…ƒŽŽ› †‡ϐ‹‹–‡ ƒ”‡

’”‘ϐ‹Ž‡ ‘ˆ ‘’–‹… ‡—”‹–‹• †‡•…”‹„‡† „› –Š‡ ȋ ƒ„Ž‡ ʹȌǡ ‹• –Šƒ– seronegative and re-testing for apparently recurrent severe

of a typical case that we would assume to be either idiopathic, optic neuritis may yield a positive result in suspects23. A higher

or MS associated in aetiology2. degree of suspicion may be advisable in our set up considering

However, it should be noted that although large population the higher proportion of NMO in Asian population.

based studies are limited in India, data regarding optic neuritis The entity, relapsing optic neuropathy has been described

from the region has shown a lower proportion of MS in optic to comprise of two types: recurrent idiopathic optic neuropathy

neuritis, varying from 22-50%, as compared to data from the (RION), which is a non-progressive relapsing ON without

West3-8. This implies that up to 70% of cases would be either •–‡”‘‹† †‡’‡†‡…‡ǡ ƒ† ƒ …Š”‘‹… ”‡Žƒ’•‹‰ ‹ϐŽƒƒ–‘”›

idiopathic or due to other causes of optic neuropathy. optic neuritis (CRION) which is progressive, relapsing and

The following signs and symptoms mentioned in (Table 3) steroid dependent24. They may present as separate entities or

should raise a suspicion of an atypical optic neuritis9. part of the clinical spectrum of demyelinating disorders like

NMO, Relapsing idiopathic optic neuritis, Chronic relapsing MS or NMO as a conversion to MS or NMO has been noted25.

optic neuritis and Optic neuritis The similarity of symptoms

with collagen vascular diseases ’–‹… ‡—”‹–‹• ȋ Ȍ ‹• ƒ ‹ϐŽƒƒ–‘”› between CRION and NMO with
are the most commonly found by recurrent and severe attacks
atypical optic neuritis entities optic neuropathy characterised of optic neuritis with severe

Neuromyelitis optica clinical signs of optic nerve dysfunction. visual loss, make them clinically

is a condition similar to MS While the term has become almost indistinguishable from each
characterised by optic neuritis other although they are likely
and transverse myelitis10. It synonymous with idiopathic or multiple to be separate disease entities
is a multifocal demyelinating (Table 6)26,27.
illness, but associated with sclerosis (MS) associated cause, a Another common cause of
frequently bilateral and more differential diagnosis of optic neuropathy
atypical optic neuritis are the

severe, recurrent attacks must always be kept in mind before collagen vascular diseases.and
of ON with severe residual other autoimmune conditions
impairment, as compared to MS. labelling it as typical ON (Table 7). Distinction for optic

Š‡ …Ž‹‹…ƒŽ ’”‘ϐ‹Ž‡ ‘ˆ ’ƒ–‹‡–• neuritis associated with them

parallel that of MS, with a mean age of onset of 30 years and is a relapsing or progressive visual loss which is frequently

a female predisposition of 3:1. The prevalence is 0.3-4.4 per painful and severe28,29. They may present with systemic

100000 people11-13Ǥ Š‡ ’”‘’‘”–‹‘ ‘ˆ ‹ ‹ϐŽƒƒ–‘”› features of the underlying disease at presentation, making the

demyelinating ON varies from 1-22%, with the highest diagnosis apparent, but many case reports have described

proportions reported in non-Caucasians, including Asians14-16. optic neuritis as the initial presentation of autoimmune disease

Š‡ †‹•…‘˜‡”› ‘ˆ •’‡…‹ϐ‹… ‰
ƒ–‹„‘†‹‡• ȋƒ–‹Ǧƒ“—ƒ’‘”‹ in an otherwise asymptomatic patient30-36. An earlier diagnosis

Ͷ ƒ–‹„‘†‹‡•Ȍ „› ‡‘ ‹ ʹͲͲͶǡ …‘ϐ‹”‡† ‹– –‘ „‡ ƒ †‹•–‹…– of underlying systemic disease by an awareness and high level

clinical entity from MS17. The diagnostic criteria for NMO is of suspicion can limit the visual disability. It is also important to

given in (Table 4)18. note that up to 81% of patients of MS are ANA positive without

Š‡”‡ ƒ”‡ ‘ †‡ϐ‹‹–‡ …Ž‹‹…ƒŽ ˆ‡ƒ–—”‡• –‘ †‹•–‹‰—‹•Š SLE. However, these titres are lower as compared to patients

from NMO to that of MS (Table 5). of SLE37Ǥ ‘‡ ‹ϐŽƒƒ–‘”› †‹•‡ƒ•‡• Šƒ˜‡ „‡‡ ”‡’‘”–‡† –‘

Approximately half of patients present as isolated optic present with white matter brain lesions mimicking MS which

neuritis, of which 11-20% are bilateral in onset. 10% present are seen to resolve with corticosteroid treatment38.

with concurrent optic neuritis and myelitis, and the rest as Infectious aeitiology in relation to optic neuritis may be

isolated myelitis characterised by weakness and paraesthesias due to a direct invasion of the pathogenic organism or due to

www. dosonline.org 27

NEURO-OPHTHALMOLOGY

Table 1: Differential diagnosis of optic neuropathy Table 2: ONTT Summary

ϐŽƒƒ–‘”› ‘’–‹… ‡—”‘’ƒ–Š‹‡• Patient Female: Male: 2:1
Ȉ —–‘‹—‡ ‘’–‹… ‡—”‘’ƒ–Š› demographics Age: 20-40 years
Ȉ ‹‰Ž‡ ‹†‹‘’ƒ–Š‹… ‘’–‹… ‡—”‹–‹• ȋ Ȍ Caucasian population
Ȉ ‡…—””‡– ‘’–‹… ‡—”‹–‹•ǣ ‡Žƒ’•‹‰ ‹†‹‘’ƒ–Š‹… ‘’–‹…
Clinical presentation

neuritis (RION) Visual acuity Loss of vision 90%

Ȉ Š”‘‹… ”‡Žƒ’•‹‰ ‹ϐŽƒƒ–‘”› ‘’–‹… ‡—”‹–‹• Minimal – No light perception

(CRION) Progression over 7-10 days

Ȉ ‡—”‘›‡Ž‹–‹• ‘’–‹…ƒ ȋ Ȍ Improvement within 1st month: 90%

Ȉ …—–‡ †‹••‡‹ƒ–‡† ‡…‡’ŠƒŽ‘›‡Ž‹–‹• ȋ Ȍ ε ʹͲȀͶͲ

Ȉ ‘ŽŽƒ‰‡ ˜ƒ•…—Žƒ” †‹•‘”†‡”• ƒ† ˜ƒ•…—Ž‹–‹• Colour vision Abnormal in 80% affected eyes

Ȉ ƒ”…‘‹†‘•‹•ǡ ›•–‡‹… Ž—’—• ‡”›–Š”‡ƒ–‘•‹• Abnormal in 51% eyes with 20/20

(SLE), Behcet’s disease, Sjogrens syndrome, vision

Antiphospholipid antibody syndrome, Wegner’s Contrast sensitivity Abnormal in 99% <20/20
granulomatosis, Giant cell arteritis Pupils Abnormal in 87.2% 20/20 vision
Ȉ –Š‡” •›•–‡‹… ƒ—–‘‹—‡ †‹•‡ƒ•‡•
Ȉ ”‘Šǯ• †‹•‡ƒ•‡ǡ ›Ž‘•‹‰ •’‘†›Ž‹–‹• ƒ† RAPD

Rheumatoid arthritis, Hypereosinophilic syndrome Pain Approximately 90% (pain on eye

(HES), Tolossa Hunt syndrome movement)

Ȉ –Š‡” ‹ϐŽƒƒ–‘”› …‘†‹–‹‘• Fundus 2/3rds normal optic discs
Ȉ ‘•–Ǧ‹ˆ‡…–‹‘—•ǡ ’‘•–Ǧ˜ƒ……‹ƒ–‹‘ǡ ‡—”‘”‡–‹‹–‹• (retrobulbar neuritis)
Compressive optic neuropathies ‹•—ƒŽ ϐ‹‡Ž† 1/3rd swollen optic disc (papillitis)
Ȉ ”‹ƒ”› –—‘—”•ǡ ȋ‡‹‰‹‘ƒ•ǡ ’‹–—‹–ƒ”› –—‘—”•ǡ abnormalities Parapapillary haemorrahges, retinal
exudates uncommon
gliomas), metastasis, thyroid ophthalmopathy, arterial Treatment Macular star distinctly uncommon
aneurysms, sinus mucocoeles
Infective optic neuropathies Diffuse (48.2%), Localised
Ȉ —„‡”…—Ž‘•‹•ǡ ›’Š‹Ž‹•ǡ ›‡ǯ• †‹•‡ƒ•‡ǡ ‹”ƒŽ ‘’–‹…
neuritis, Toxocariasis, Toxoplasmosis and other (altitudinal/other nerve bundle
helminthic infections, Periorbital infection (cellulitis,
suppurative sinusitis) defects) (20.1%), Central/
Toxic and nutritional optic neuropathies
Ȉ ‹–ƒ‹ ͳʹ †‡ϐ‹…‹‡…›ǡ –‘„ƒ……‘Ȁ ‡–Šƒ‘Ž ƒ„Ž›‘’‹ƒǡ Caecocentral (8.3%), Other (23.2%)
methanol intoxication, ethambutol toxicity, other drug
Abnormalities in fellow eye in 68.8%

55.9% recovered at 1 year follow-up

related neurotoxicity IV methylprednisolone

Inherited conditions Oral corticosteroids are contraindicated

Ȉ ‡„‡”ǯ• Š‡”‡†‹–ƒ”› ‘’–‹… ‡—”‘’ƒ–Š›

Ocular causes Other differential severe vision loss is unlikely to be caused
Ȉ ‘•–‡”‹‘” •…Ž‡”‹–•ǡ ƒ…—Ž‘’ƒ–Š›ǡ ‹‰ „Ž‹† •’‘– •›†”‘‡ diagnoses of atypical by nutritional causes. Less common are
Factitious visual loss optic neuritis include the inherited optic neuropathies as well
Ȉ ƒŽ‹‰‡”‹‰ǡ ›•–‡”‹…ƒŽ compressive, toxic as retinal dystrophies associated with

and ischaemic optic optic atrophy. A family history of ocular

autoimmune reaction to antigen following neuropathies (Table 7)48. Associated disease or poor vision and associated
an infection. Various aetiologies have ‘…—Žƒ” ϐ‹†‹‰• •Š‘—Ž† ƒŽ•‘ „‡ …‘•‹†‡”‡†Ǥ ‘…—Žƒ” ϐ‹†‹‰• ƒ› Š‡Ž’ –‘ ‰—‹†‡ –Š‡
been described in both cases39-44. While In the acute phase of an ischaemic optic clinician towards the right direction
a direct invasion describes infectious ‡—”‘’ƒ–Š›ǡ ‹’‘”–ƒ– ϐ‹†‹‰• –‘ ‘–‡
ON, post infectious and post vaccination are the status of the other eye optic Š‹Ž‡ ‹˜‡•–‹‰ƒ–‹‘• Ž‹‡ ˜‹•—ƒŽ ϐ‹‡Ž†•
ON occur by the latter mechanism. Both nerve for a disc at risk, sectoral oedema, may give a clue as to the aetiology, the
infectious and parainfectious ON have and other retinal features of ischaemic ‘˜‡”ƒŽŽ …Ž‹‹…ƒŽ ’”‘ϐ‹Ž‡ ƒ† ’”‡•‡–ƒ–‹‘
been described more frequently in disease. Nutritional optic neuropathies should be looked at while interpreting
children as compared to adults45-47. usually present with mild to moderate –Š‡ ˜‹•—ƒŽ ϐ‹‡Ž†• –‡•–Ǥ ’–‹… ‡—”‹–‹• …ƒ
vision loss with bilateral optic atrophy. A ’”‡•‡– ™‹–Š ƒ› ‹† ‘ˆ ˜‹•—ƒŽ ϐ‹‡Ž†
defect, including apparently ischaemic

Department of Ppediatric Ophthalmology and Strabismus, Dr. Shroffs Charity, Eye Hospital, Daryaganj, Delhi

Dr. Batriti Wallang MS Dr. Raman Mehta MS
28 DOS TIMES - MAY-JUNE 2016

NEURO-OPHTHALMOLOGY

Table 3: atypical signs of an optic neuritis Table 6: Chronic relapsing optic
‰‡ δͳͷ ›‡ƒ”• ‘” εͷͲ ›‡ƒ”• ‡—”‹–‹• ȋ Ȍ
Bilateral or chiasm involvement
Optic atrophy at presentation (without previous ON or MS) ʹͷΨ ‘ˆ …‘˜‡”–‡† –‘ ƒ– ϐ‹˜‡
Severe optic disc oedema with vitreous reaction years
Optic disc haemorrhage Ȉ ͷͲΨ ‹ „ ’‘•‹–‹˜‡
Previous history of neoplasia Ȉ ͳͲΨ ‹ „ ‡‰ƒ–‹˜‡
Loss of vision to no perception of light with no early recovery
Painless loss of vision to <6/60 with no early recovery Bilateral involvement
‡˜‡”‡ ‘” ’‡”•‹•–‡– ’ƒ‹ εʹ ™‡‡• •‹…‡ ‘•‡– Ȉ ”‡“—‡–Ž› …‘•‡…—–‹˜‡ ™‹–Š •‡…‘†
”‘‰”‡••‹˜‡ ˜‹•‹‘ Ž‘•• εʹ ™‡‡• •‹…‡ ‘•‡– ‘ˆ ˜‹•—ƒŽ •›’–‘•
Presence of macular star (neuroretinitis) eye involvement within 1 month
ƒ… ‘ˆ ”‡…‘˜‡”› ε͵ ™‡‡• ƒˆ–‡” ‘•‡– ‘ˆ ˜‹•—ƒŽ •›’–‘• (frequently simultaneous in NMO)
Steroid dependence –deterioration of vision after withdrawal of corticosteroids
African or Afro-Caribbean patients with vision <6/12 and no early recovery Highly steroid sensitive
Ȉ ƒ’‹† ”‡•’‘•‡ ƒ† ˜‹•—ƒŽ ”‡…‘˜‡”›
Table 4. Diagnostic criteria for Neuromyelitis optica (NMO) Ȉ ‡Žƒ’•‡ ™‹–Š‹ ™‡‡• ‘ˆ –ƒ’‡”‹‰
Required
At least 1 attack of each of the following: steroids
Ȉ ’–‹… ‡—”‹–‹•
Ȉ ”ƒ•˜‡”•‡ ›‡Ž‹–‹• as well as provide a prognosis for the
Supportive patient. A knowledge of the warning
At least 2 of the following: signs and differential diagnoses is crucial
Ȉ ”ƒ‹ ǣ ‘”ƒŽ ‘” Ž‡•‹‘• ‘– ‡‡–‹‰ …”‹–‡”‹ƒ ˆ‘” in raising the suspicion of an atypical case
Ȉ ’‹ƒŽ …‘”† ǣ ‡•‹‘• ‡š–‡†‹‰ …‘–‹—‘—•Ž› ‘˜‡” ͵ ‘” ‘”‡ ˜‡”–‡„”ƒŽ •‡‰‡–• for its appropriate investigation.
Ȉ ‰
•‡”‘’‘•‹–‹˜‹–›
REFERENCES
ƒ„Ž‡ ͷǣ †‹ˆˆ‡”‡–‹ƒ–‹‰ ˆ‡ƒ–—”‡• „‡–™‡‡ ƒ†
1. ONTT group. Multiple sclerosis risk
MS NMO ƒˆ–‡” ‘’–‹… ‡—”‹–‹•ǣ ϐ‹ƒŽ ‘’–‹… ‡—”‹–‹•
treatment trial followup. Arch Neurol
MRI lesions: Periventricular, May be present: usually 2008; 65: 727-32.
Brain subcortical hypothalamic, brainstem
Spinal 1-2 segments long ε͵ •‡‰‡–• Ž‘‰ 2. The Optic Neuritis Study Group.
Š‡ …Ž‹‹…ƒŽ ’”‘ϐ‹Ž‡ ‘ˆ ‘’–‹… ‡—”‹–‹•Ǥ
CSF WBCs <50/mm3 WBC; εͷͲ͵ Ǣ Experience of the Optic Neuritis
Oligoclonal bands mononuclear 85% polymorphonuclear Treatment Trial. Arch Ophthalmol
15-30% 1991; 109: 1673-78.

Systemic autoimmune May be associated Commonly associated 3. Optic neuritis: Experience from a south
diseases occasionally Indian demyelinating disease registry.
‡Šƒ ƒ†‹–ǡ ƒŒ‡•Š Š‡––›ǡ —Ž‹ϐŽ‹
Severity of relapses Mild to moderate Moderate to severe Misri, et al.

Recovery from relapses Fair to good Fair to poor 4. Bansil S, Singhal BS, Ahuja GK, Ladiwala
U, Behari M, Friede R, et al. Comparison
Initial clinical course 85% relapsing-remitting 80-90% relapsing-remitting between multiple sclerosis in India and
the United States: A case-control study.
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Recovery from optic 5. Jain S, Maheshwari MC. Multiple
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Treatment years was 20/20 (ONTT) of follow up last thirty years. Neuroepidemiology
1985;2:96-107.
Good response to Immunosuppression
interferons Interferons can worsen the 6. Syal P, Prabhakar S, Thussu A, Sehgal
disease ǡ Šƒ†‡Ž™ƒŽ Ǥ Ž‹‹…ƒŽ ’”‘ϐ‹Ž‡ ‘ˆ
multiple sclerosis in North-West India.
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Most clinicians are well versed of associated systemic disease. A timely
diagnosis can help in the management 7. Sarma GR, Nagaraj DK. Multiple
with the ONTT and its description of of a number of otherwise potentially life sclerosis in South India. Ann Ind Acad
ON features and management. However, threatening associations, limit disability Neurol 2005;8:71-4.
a seemingly straight forward case of
8. Gangopadhyay G, Das SK, Sarda P, Aha
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Bengal. Neurol India 1999;47:18-21.

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NEURO-OPHTHALMOLOGY

ƒ„Ž‡ ͹ǣ Ž‹‹…ƒŽ ˆ‡ƒ–—”‡• ƒ† ™‘” —’ ‘ˆ ’‘••‹„Ž‡ ƒ‡–‹‘Ž‘‰› ‘ˆ ƒ–›’‹…ƒŽ ‘’–‹… ‡—”‹–‹•

Diagnosis Distinguishing clinical features Diagnostic tests

INFLAMMATORY OPTIC NEUROPATHY Steroid responsive MRI orbits and brain with
contrast.
Autoimmune optic neuritis: Typical ON without signs of demyelinating CNS MRI spine.
‹•—ƒŽ ϐ‹‡Ž†•Ǥ
Single and Relapsing optic neuritis disease. Non-progressive CBC, CRP.
Serum ANA, ACE, RF,
Š”‘‹… ‹ϐŽƒƒ–‘”› ‘’–‹… ‡—”‹–‹• Severe, recurrent, painful visual loss; bilateral, usually Antiphospholipid antibody, p
ANCA, c ANCA, AQP-4 antibody
Neuromyelitis optica (NMO) sequential. Steroid dependent. Chest radiograph.
Biopsy of accessible tissue
Acute disseminated encephalomyelitis Severe, recurrent painful vision loss; Transverse (sarcoidosis).
Lumbar puncture.
(ADEM) myelitis; severe visual disability.

‘‡…–‹˜‡ –‹••—‡ †‹•‘”†‡”•ǡ ˜ƒ•…—Ž‹–‹• Associatedvaccinationorinfection;encephalomyelitis.

and other systemic autoimmune May be bilateral.

disorders: Severe, relapsing and painful vision loss; relapse

Sarcoidosis on withdrawal of steroids; associated systemic

Systemic lupus erythematosus (SLE) manifestations of disease; often bilateral

Antiphospholipid antibody syndrome (simultaneous or sequential); other ocular

Behcet’s disease manifestations like uveitis, chorioretinitis, retinal

Wegener’s granulomatosis vasculitis, episcleritis and scleritis.

Giant cell arteritis (GCA) Bilateral (simultaneous); more common in childhood;

Crohn’s disease good visual prognosis.

Ankylosing spondylitis Optic disc edema with macular star; spontaneous

Rheumatoid arthritis recovery.

Hypereosinophilic syndrome

–Š‡” ‹ϐŽƒƒ–‘”› …‘†‹–‹‘•

Post infection and post vaccination

Neuroretinitis

Gradual and progressive vision loss; optic atrophy ‹•—ƒŽ ϐ‹‡Ž†•
Primary tumours (Meningiomas, Gliomas, Associated ocular and systemic symptoms from CNS CT or MRI orbits and brain
Pituitary tumours) space occupying lesion ( proptosis, pituitary lesion) with contrast
Metastasis Evidence of primary tumour Biopsy where appropriate
Thyroid ophthalmopathy Ocular and systemic signs of thyroid dysfunction MRA
Arterial aneurysms Painful progressive vision loss; headache
Sinus mucocoeles History of sinusitis; may have pain

INFECTIOUS OPTIC NEUROPATHIES Progressive vision loss following exposure to Appropriate serology, virology
Syphilis
Tuberculosis infectious agent; severe optic disc edema* with Blood culture
Lyme disease
Viral optic neuropathy associated anterior or posterior uveitis (retinitis, Lumbar puncture
Helminthic
vasculitis, choroiditis) Chest radiograph

Systemic features of infectious disease

(*Papillitis a more common presentation of idiopathic

optic neuritis in India)

ISCHAEMIC OPTIC NEUROPATHIES Bilateral and symmetrical; painless; poor prognosis ‹•—ƒŽ ϐ‹‡Ž†•
Anterior ischaemic optic neuropathy for visual recovery Serum Vitamin B12, Serum
(AION) Folic acid, Serum vitamin D
Posterior ischaemic optic neuropathy
(PION)
Diabetic papillopathy

HEREDITARY OPTIC NEUROPATHIES Positive family history; bilateral (simultaneous or Genetic testing
Leber’s hereditary optic neuropathy sequential); severe vision loss; poor prognosis

OCULAR CAUSES Severe pain B mode ultrasound
Posterior scleritis Painless vision loss; metamorphopsia, normal colour Electroretinogram, Fundus
Maculopathies and retinopathies vision ϐŽ—‘”‡•…‡‹ ƒ‰‹‘‰”ƒ
Big blind spot syndrome; Acute zonal ‹•—ƒŽ ϐ‹‡Ž† Ž‘••Ǣ ’Š‘–‘’•‹ƒǢ ‘”ƒŽ ˆ—†—• ‹•—ƒŽ ϐ‹‡Ž†• –‡•–‹‰
occult outer retinopathy

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35. McClelland C, Zaveri M, Walsh R,

Fleisher J, Galetta S. Optic Perineuritis

as the the presenting feature of Crohn

Disease. J Neuro-Ophthalmol 2012; 32:

345-47.

36. Lin YC, Wang AG, Yen MY. Systemic

Lupus Erythematosus-associated

Financial Interest: Š‡ ƒ—–Š‘”• †‘ ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

www. dosonline.org 31

NEURO-OPHTHALMOLOGY

ISCHEMIC OPTIC NEUROPATHY

Dr. Bithi Chowdhury MS, FRCS and retrolaminar region having blood supply as shown below.
Senior Specialist, Ȉ –‡”‹‘” ǣ –Š‡ •Š‘”– ’‘•–‡”‹‘” …‹Ž‹ƒ”› ƒ”–‡”‹‡• ƒ† …‹”…Ž‡
NDMC Medical College and Hindu Rao Hospital, Delhi
of Zinn-Haller, (formed by short posterior ciliary arteries,
Ischemic Optic Neuropathy (ION) is the most common branches of the pial arterial network, and choroidal feeder
acute optic neuropathy in patients above 50 years1. vessels).
ION is sometimes called the “stroke of the optic nerve” Ȉ ”‡Žƒ‹ƒ” ƒ† –Š‡ Žƒ‹ƒ” ’‘”–‹‘ǣ †‹”‡…– „”ƒ…Š‡• ‘ˆ –Š‡
ƒ• ‹– ‹• ƒŽ•‘ †—‡ –‘ –Š‡ ˜ƒ•…—Žƒ” ‹•—ˆϐ‹…‹‡…› ƒ† Š‡…‡ short posterior ciliary arteries and circle of Zinn-Haller
is equivalent to a brain stroke. However the etiology Ȉ ‡–”‘Žƒ‹ƒ” ”‡‰‹‘ǣ ’‹ƒŽ ƒ”–‡”‹‡• ƒ† –Š‡ •Š‘”– ’‘•–‡”‹‘”
of the two conditions is different. ION is primarily an ciliary artery system.
ischemia due to hypotension while cerebral stroke is mostly Interference with the PCA circulation results in the clinical
due to thromboembolic phenomena. picture of anterior ischemic optic neuropathy.
The disease is associated with sudden and marked visual The intraorbital optic nerve is subdivided into anterior
loss in majority of cases and recovery is variable. Limitation and posterior segments determined by the point of entry of
of space precludes a detailed discussion of this topic. This the central retinal artery. The anterior segment has 2 vascular
article provides an update on the current understanding and systems: peripheral (centripetal) and axial (centrifugal). The
management of this disease. peripheral vascular system is formed by the pial vascular
plexus which is derived from branches of the ophthalmic artery,
CLASSIFICATION whereas the axial system is supplied by branches of the central
retinal artery. The posterior segment of the intraorbital optic
ION is divided into anterior and posterior depending nerve is supplied by the pial plexus.
on the segment of optic nerve involvement. The anterior
ION presents with disc edema, visual loss and RAPD while in PATHOGENESIS
posterior ION the disc appears normal. Diagnosis of posterior
ION is by exclusion of other causes of painless sudden visual Pathogenesis of NAION
loss. However combinations of the following features are
suggestive of the diagnosis. Sudden onset visual deterioration The exact cause of NAION is unknown .It is believed that
with no other ocular, orbital or neurological abnormality to hypotension in the PCA due to any cause in the presence of a
‡š’Žƒ‹ –Š‡ ˜‹•—ƒŽ Ž‘••ǡǡ ‘’–‹… ‡”˜‡ ”‡Žƒ–‡† ˜‹•—ƒŽ ϐ‹‡Ž† †‡ˆ‡…–• ‹ susceptible disc causes sudden ischemia of the optic nerve head.
the involved eye; presence of a relative afferent pupillary defect It has been proposed that long-term elevated arterial blood
,optic disc and fundus initially normal on ophthalmoscopy and pressure interferes with the normal autoregulation system of
ϐŽ—‘”‡•…‡‹ ˆ—†—• ƒ‰‹‘‰”ƒ’Š› ƒ† †‡˜‡Ž‘’‡– ‘ˆ ‘’–‹… †‹•… „Ž‘‘† ϐŽ‘™ –‘ –Š‡ Ǥ  ‘‡ •–—†› ”‡–”‘Žƒ‹ƒ” ‹ˆƒ”…–‹‘
pallor within 6–8 weeks. ™ƒ• –Š‡ ’”‡†‘‹ƒ– ϐ‹†‹‰ ‹†‹…ƒ–‹‰ –Šƒ– …Š‘”‘‹†ƒŽ „Ž‘‘†
supply which supplies the pre and laminar portion of the optic
Anterior ION is the most common form, while posterior nerve is not involved in the disease process2.
ION is rare. Both can be divided into three subtypes:
Ȉ ”–‡”‹–‹… ȋ—•—ƒŽŽ› †—‡ –‘ ‰‹ƒ– …‡ŽŽ ƒ”–‡”‹–‹•ǡ ‹ϐŽƒƒ–‘”›ȌǢ 75% of the patents have reported visual loss on
Ȉ ‘ƒ”–‡”‹–‹… ȋ†—‡ –‘ ‘Ǧ‹ϐŽƒƒ–‘”› …ƒ—•‡•ȌǢ awakening in the morning. This has been attributed to the
Ȉ ‡”‹‘’‡”ƒ–‹˜‡Ȁ•—”‰‹…ƒŽǤ ‘…–—”ƒŽ Š›’‘–‡•‹‘ …ƒ—•‹‰ †‡…”‡ƒ•‡† „Ž‘‘† ϐŽ‘™ ‹ –Š‡
PCAs. However in another study, nocturnal hypotension was
The arteritic anterior and posterior ION are less common not found in a higher number in NAION patients compared with
than nonarteritic anterior and posterior ION, but arteritic a control group matched for age and vascular risk factors. In the
ION is a medical emergency that requires early diagnosis and presence of the other risk factors it probably plays an important
immediate treatment. role in the development and progression of visual loss. The
various risk factors are enumerated in (Table 1). The discs at
BLOOD SUPPLY OF THE OPTIC NERVE risk are small crowded disc with small cup which is present
‹ ͻͲΨ ‘ˆ ’ƒ–‹‡–•Ǥ ™‡ŽŽ‹‰ ™‹–Š‹ –Š‡ …‘ϐ‹‡• ‘ˆ ƒ –‹‰Š– †‹•…
Optic nerve has a unique blood supply (Figure 1) due to may produce a “compartment syndrome”, a vicious cycle of disc
which it is susceptible to this vascular phenomena. On the basis edema and peripapillary hemorrhages3. Ischemia of the disc
of blood supply, the optic nerve can be divided into two distinct results in edema which leads to further compression of the
regions: (1) the anterior part of optic nerve head (ONH), which vessels with worsening of the ischemia. The disc hyperaemia
is supplied primarily by the posterior ciliary artery (PCA) and peripapillary haemorrhages seen commonly in of NAION4
circulation and (2) the rest of the optic nerve, which gets its is believed to be due to occlusion of retrolaminar venules.
supply from multiple sources except the PCAs. The anterior
portion can be divided into anterior ONH, prelaminar, laminar Pathogenesis of AION

The commonest cause of AION is giant cell arteritis
which is a systemic vasculitis affecting the medium and large
sized arteries. In the eye the disease affects the PCA resulting

www. dosonline.org 33

NEURO-OPHTHALMOLOGY

Figure 1: $NQQF UWRRN[ QH QRVKE PGTXG A small or absent optic nerve cup in the
fellow unaffected eye is an important
Table 1: Risk factors for NAION …‘ϐ‹”ƒ–‘”› …Ž‹‹…ƒŽ ϐ‹†‹‰Ǥ Š‡
•–—†› ”‡’‘”–‡† ϐŽƒ‡ Šƒ‡‘””Šƒ‰‡•
Systemic risk factors Raised intraocular pressure (Figure 2) in 72% of patients and
Hypertension Small crowded disc arteriolar narrowing adjacent to the ONH
Diabetes Location of Watershed zone of the PCAs in 19% of cases.
Hypercholesterolemia on disc
Ischemic heart disease Disc drusen The arteritic variety although less
Stroke Cataract extraction common is a medical emergency and
Systemic atherosclerosis requires prompt treatment. This is
Obstructive sleep disorder because A-AION presents with a rapid
Medications- Amiodarone, vasopressors, onset of severe visual loss with a swollen
phosphodiesterease type 5 inhibitors, pale disc (Figure 3). Visual acuity is worse
vasoconstrictors than 20/200 in 75% of patients, with
nearly half of the patients presenting
in thrombotic occlusion. Depending on CLINICAL FEATURES with vision reduced to between counting
the area supplied by the occluded PCA a ϐ‹‰‡”• ƒ† ‘ Ž‹‰Š– ’‡”…‡’–‹‘Ǣ –Š‡
segmental or complete involvement of the NAION commonly presents with second eye is involved in majority of
optic nerve occurs. Other less common unilateral vision loss over hours to days cases and recovery is minimal. One must
causes of PCA vasculits are polyarteritis which is not preceded by the transient •’‡…‹ϐ‹…ƒŽŽ› Ž‘‘ ˆ‘” ‘–Š‡” •‹‰• ‘ˆ

nodosa, systemic lupus erythematosis visual loss (as is seen with arteritic-AION). like headache, scalp tenderness, jaw
and herpes zoster. ”‡•‡…‡ ‘ˆ ǡ ˜‹•—ƒŽ ϐ‹‡Ž† †‡ˆ‡…– ƒ† claudication, myalgia, anorexia, weight
colour vision defect are typically present. Ž‘••ǡ ƒ† ƒ„‘”ƒŽ •—’‡”ϐ‹…‹ƒŽ –‡’‘”ƒŽ
artery( tender, thickened with reduced or
absent pulsation). Headache is present in
50% of cases. Transient diplopia ( present
in 5% to 10% of cases), jaw claudication
and temporal artery abnormalities are
predictive features of of ischemic neuro-
ophthalmic complications. About 20%
have occult temporal arterirtis where
the patient do not have any other feature
of GCA except ischemic optic neuropathy.

The distinguishing features of
arteritic and non arteritic ION are shown
in (Table 2).

DIAGNOSIS

NAION

Diagnosis is mainly by history and
clinical examination. Visual acuity, colour

Figure 2: 0QP CTVGTKVKE ION Figure 3: #TVGTKVKE ION
34 DOS TIMES - MAY-JUNE 2016

NEURO-OPHTHALMOLOGY

Table 2: Differentiating features of arteritic and non arteritic ischemic optic neuropathy •’‡…‹ϐ‹… –‘ –Š‡ ’ƒ––‡”• ‘ˆ ˜‹•—ƒŽ ϐ‹‡Ž†
loss in NAION and has been used to
Arteritic Nonarteritic monitor RNFL edema in acute NAION
episodes and subsequent development of
Age/sex ‡†‹ƒ ƒ‰‡ ͹ͲǢ ε 50-60; M=f optic atrophy5. OCT has also shown that
•—„”‡–‹ƒŽ ϐŽ—‹† ‹ –Š‡ ƒ…—Žƒ” ”‡‰‹‘
laterality ε ͻͲΨ „‹Žƒ–‡”ƒŽ <30% have bilateral may be a contributor to the visual loss in
involvement some patients with NAION6.

Systemic features Headache, TIA, Diplopia, jaw Diabetes (25%), AION
claudication, fever, myalgia. hypertension (50%),
atherosclerosis. The hematologic indicators of
‹ϐŽƒƒ–‹‘ ‹…Ž—†‹‰ ǡ ǡ
VA at presentation Severe visual loss and 75% Normal to 6/60 ϐ‹„”‹‘‰‡ǡ ƒ† ƒ ’Žƒ–‡Ž‡– …‘—– ™Š‹…Š
have VA<6/60 should be done in all cases. A combination
of CRP and ESR has a diagnostic
Fundus : early Late Pale oedematous disc Chalky Segmental (25%) or sensitivity of over 99%. ESR is raised
(6wks-8wks) white disc with cupping Diffuse (75%) disc typically however normal or low ESR has
oedema. peripapillary hge been reported to occur in as many as 30%
Diffuse atrophy of STA biopsy proven cases of A-AION.

–Š‡” ˆ—†—• ϐ‹†‹‰• Cilioretinal artery occlusion Diabetic and hypertensive Ultrasound is a noninvasive
(20%), CRAO, BRAO Retinopathy. Small disc technique to visualize affected arteries,
and cup in the other eye. ‡˜ƒŽ—ƒ–‡ …Šƒ‰‡• ‹ „Ž‘‘† ϐŽ‘™ǡ ƒ†
†‡ϐ‹‡ ƒ”–‡”‹ƒŽ …‘—”•‡ „‡ˆ‘”‡ –‡’‘”ƒŽ
Investigations ƒ‹•‡† ǡ ϐ‹„”‹‘‰‡ ƒ† Raised blood sugar, HBAc, artery biopsy. It has 69% sensitivity and
platelet count, C reactive lipids and cholesterol, ͺʹΨ •’‡…‹ϐ‹…‹–› –‘ †‡–‡…– ƒ”–‡”‹ƒŽ ‡†‡ƒ7.
proteins Temporal artery homosystein levels
biopsy (diagnostic) Fluorescein angiography (Figure 4)
demonstrates, prolonged choroidal and
‹•—ƒŽ ϐ‹‡Ž† Altitudinal defect Infero nasal defect and …‡–”ƒŽ ”‡–‹ƒŽ ƒ”–‡”‹ƒŽ ϐ‹ŽŽ‹‰ –‹‡•ǡ ƒ†
inferior altitudinal defect …Š‘”‘‹†ƒŽ ‘’‡”ˆ—•‹‘ ‘” ϐ‹ŽŽ‹‰ †‡ˆ‡…–•8;
–Š‡•‡ ϐ‹†‹‰• Šƒ˜‡ •’‡…‹ϐ‹…‹–› ƒ• –Š‡› ƒ”‡
FFA Filling defect in choroid Moderate Leakage on not present in NAION.

supplied by the occluded PAC disc. In the very early Contrast-enhanced, high-resolution
MRI is a noninvasive method to assess
‹• •‡‡ ‹ ϐ‹”•– ˆ‡™ †ƒ›• ™Š‹…Š choroidal arterial phase —”ƒŽ ‹ϐŽƒƒ–‹‘ ƒ† –Š‹…‡‹‰Ǥ
Gadolinium contrast-enhanced imaging
is lost later due to collateral –Š‡”‡ ‹• ϐ‹ŽŽ‹‰ †‡ˆ‡…–Ȁ is used to diagnose large-vessel vasculitis
and aortitis and can also be used to
circulation. Severe leakage on delay in the prelaminar detect and grade the severity of GCA. T1-
contrast spin echo MRI with high sub-
disc region and in the millimeter spatial resolution can reliably
ƒ••‡•• ˜ƒ•…—Žƒ” ‹ϐŽƒƒ–‘”› …Šƒ‰‡• ‘ˆ
peripapillary choroid and/ •ƒŽŽ •—’‡”ϐ‹…‹ƒŽ …”ƒ‹ƒŽ ƒ”–‡”‹‡•Ǥ

or choroidal watershed Š‡ …‘ϐ‹”ƒ–‘”› –‡•– ‹• „‹‘’•› ‘ˆ
–Š‡ •—’‡”ϐ‹…‹ƒŽ –‡’‘”ƒŽ ƒ”–‡”› ȋ ȌǤ ‘
zones minimize the possibility of missing due to
skip lesions the STA biopsy should be at
OCT - Helps to locate the site of least
the ischemia by studying
the thickness of the RNFL. 2 cm in length and multiple sections
‡–‡…–• •—„ ”‡–‹ƒŽ ϐŽ—‹† ‹ from the entire length of the biopsy
macula. should be examined.

Prognosis Poor Fair Differential diagnosis

Recovery Nil 50% show no change in ION has to be differentiated from
VA. optic neuritis which is a more common
40% - improve by 3 condition occurring in the younger
Snellen line age group and also compressive optic
12% deteriorate (ONDT neuropathy which has similar clinical
study) ϐ‹†‹‰•Ǥ Š‡ •ƒŽ‹‡– †‹ˆˆ‡”‡–‹ƒ–‹‰
features of the above conditions are
Recurrence 7% risk of recurrent visual Same eye –rare (<5%) enumerated in (Table 3).
loss in the affected or fellow Contralateral eye- approx
eye during the time period of 15% over 5 years in older
steroid tapering. pts.In young pts risk is
35% in 7 months

˜‹•‹‘ǡ ˜‹•—ƒŽ ϐ‹‡Ž† ƒ† †‡‘•–”ƒ–‹‘ ‘ˆ pressure needs to be checked in all
RAPD are the most important parameters patients. The combination of a relatively
on which the diagnosis is made. inferior altitudinal defect and an absolute
Investigations are done to corroborate the inferior nasal defect is the most common
…Ž‹‹…ƒŽ ϐ‹†‹‰• ƒ† ”—Ž‡ ‘—– ‘–Š‡” …ƒ—•‡• ˜‹•—ƒŽ ϐ‹‡Ž† †‡ˆ‡…– ’ƒ––‡” †‡–‡…–‡† ‹
of neuropathy. In NAION haematological one study. Recently, optical coherence
examinations include blood sugar, lipid tomography has been used to identify
’”‘ϐ‹Ž‡ ƒ† Š‘‘…›•–‡‹ Ž‡˜‡Ž•Ǥ Ž‘‘† different patterns of RNFL involvement

www. dosonline.org 35

NEURO-OPHTHALMOLOGY

untreated group9Ǥ Š‡”‡ ™ƒ• •‹‰‹ϐ‹…ƒ–
faster resolution of disc edema in the
treated group10. This however has to be
weighed against the various side effects
of the therapy in an already predisposed
individual as most of these patients are
either diabetic or hypertensive.

Figure 4:
# %JCNM[ YJKVG QRVKE FKUE GFGOC YKVJ EKNKQTGVKPCN CTVGT[ QEENWUKQP
$ (NWQTGUEGKP AION
HWPFWU CPIKQITCO UJQYKPI GXKFGPEG QH QEENWUKQP QH VJG OGFKCN RQUVGTKQT EKNKCT[ CTVGT[ CPF PQ
ſNNKPI QH VJG EKNKQTGVKPCN CTVGT[
4GRTQFWEGF HTQO *C[TGJ High dose of systemic steroid is the
treatment of choice in GCA. Intravenous
methylprednisolone (1 to 2 g/d) for 3
to 5 days followed by 1 mg/kg/d of oral
prednisone is usually administered.
Maintenance therapy with oral

ƒ„Ž‡ ͵ǣ ‹•–‹‰—‹•Š‹‰ ˆ‡ƒ–—”‡• ‘ˆ ‹•…Š‡‹… ‘’–‹… ‡—”‘’ƒ–Š›ǡ ‘’–‹… ‡—”‹–‹• ƒ† …‘’”‡••‹˜‡ ‡—”‘’ƒ–Š›

ION Optic neuritis Compressive neuropathy

Age <40 εͷͲ Any age

Onset Sudden Over days Over months

Pain Nil Yes No

Other features Diabetes, hypertension, Uhthof’s phenomena. Headache, nausea vomiting
Features of GCA

Visual acuity Usually severe loss Mild to moderate Normal to mild loss

Bilateral involvement Depends on type of ION unilateral Unilateral

Pupil RAPD RAPD RAPD

Fundus (Disc) Sectoral edema Edema with hge Diffuse edema; opticociliary shunt
may be present. Choroidal folds

Color vision Affected affected Affected

‹•—ƒŽ ϐ‹‡Ž† Altitudnal defect Diffuse decrease in sensitivity Enlarged blind spot/hemionopia/
Central scotoma or junctional scotoma
cecocentral scotoma

FFA Š‘”‘‹†ƒŽ ϐ‹ŽŽ‹‰ †‡Žƒ› ƒ† †‹•… Mild leakage at disc Severe leakage

leakge

Other tests Raised ESR and C-reactive MRI – periventricular white USG, MRI
protein and temporal artery matter demyeleination
biopsy in GCA. Blood sugar,
lipid etc.

VEP Amplitude decreased. Latency increase. Amplitude decreased

Prognosis Poor Good Fair

TREATMENT Among these the most promising corticosteroids at a dose of 1mg/kg/d
has been oral steroid therapy. A large, is continued for 3 to 6 weeks until there
NAION prospective study, based on 696 eyes, is resolution of the systemic symptoms
comparing the visual outcome in treated and normalization of the laboratory
Š‡”‡ ‹• ‘ †‡ϐ‹‹–‹˜‡ –”‡ƒ–‡– ˆ‘” (364 eyes) versus untreated control (332 ϐ‹†‹‰•ǡ ˆ‘ŽŽ‘™‡† „› ƒ •Ž‘™ –ƒ’‡” ȋƒ„‘—–
NAION. The various treatment modalities eyes) groups, found that in eyes with 10 to 20mg every 2wks) to the lowest
tried are: initial visual acuity of 20/70 or worse, dose possible to suppress the clinical
Ȉ ’–‹… ‡”˜‡ •Š‡ƒ–Š †‡…‘’”‡••‹‘ seen within 2 weeks of onset, there was signs and symptoms and laboratory
Ȉ •’‹”‹ visual acuity improvement in 70% in the values11. For most patients, 1 to 2 years of
Ȉ ›•–‡‹… …‘”–‹…‘•–‡”‘‹† –Š‡”ƒ’› treated group compared to 41% in the chronic corticosteroid therapy is needed.
Ȉ –”ƒ˜‹–”‡ƒŽ –”‹ƒ…‹‘Ž‘‡ ƒ…‡–‘‹†‡ untreated group Similarly, among those Methotrexate has been used as an
Ȉ –”ƒ˜‹–”‡ƒŽ „‡˜ƒ…‹œ—ƒ„ seen within 2 weeks of NA-AION onset adjunct or alternative to steroid therapy
Ȉ –Š‡” ”—‰•ǣ ƒ„‹‰ƒ–”ƒǡ ‡ƒ–‹‡ǡ with moderate to severe initial visual and aspirin to reduce cardiovascular
ϐ‹‡Ž† †‡ˆ‡…–ǡ –Š‡”‡ ™ƒ• ‹’”‘˜‡‡– ‹ complications.
Pentoxyfylline, Topical Brimonidine, 40% of the treated group and 25% of the
Dalfampridine, Sunitnib
Ȉ ‡†—…–‹‘ ‘ˆ ”‹• ˆƒ…–‘”•

36 DOS TIMES - MAY-JUNE 2016

NEURO-OPHTHALMOLOGY

of ION is important as the management
is different. As of now there are no
recommended treatment for naion . A lot
of grey area exists in the understanding of
the disease and hence there is immense
•…‘’‡ ‘ˆ ”‡•‡ƒ”…Š ‹ –Š‹• ϐ‹‡Ž†Ǥ

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1. Hattenhauer MG, Leavitt JA, Hodge

DO, et al: Incidence of nonarteritic

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2. Hayreh SS. Anterior ischaemic optic

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Figure 5: 2CVJQIGPGUKU QH RQUV UWTIKECN +10
4GRTQFWEGF HTQO 0 'PI , /GF 3. Arnold AC. Pathogenesis of nonarteritic

anterior ischemic optic neuropathy. J

hip surgery, nasal surgery, thoracotomy, Neuro-Ophthalmol.2003;23:157–63
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ION entity is important not only because of Decompression Trial Research Group:
the devastating visual outcome but also
In the recent years perioperative ION because it has important medico legal Characteristics of patients with
has become an important entity because implications.
of the devastating visual outcome. In a nonarteritic anterior ischemic optic
study of 126,666 surgical procedures, TREATMENT FOR POST SURGICAL
17 patients experienced perioperative ION neuropathy eligible for the Ischemic Optic
ION, an incidence rate of 0.013 percent.
Cardiac and spinal fusion surgery had the The visual loss that occurs due to Neuropathy Decompression Trial. Arch
highest rates of perioperative vision loss. ischemia in the post surgical period is
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PATHOGENESIS Although no treatment has been found to
be effective in recovering or improving 5. Bellusci C, Savini G, Carbonelli M, et al.
The cause for post surgical ion the visual loss from perioperative PION,
(PION) is multifactorial with hypotension, anaemia, and hypotension should be ‡–‹ƒŽ ‡”˜‡ ϐ‹„‡” Žƒ›‡” –Š‹…‡•• ‹
hypovolumia and anaemia playing an ‹†‡–‹ϐ‹‡† ƒ† –”‡ƒ–‡†Ǥ ”‘’Š›Žƒ…–‹…
important role. The interplay of these measures to prevent its development nonarteritic anterior ischemic optic
various factors is shown in (Figure 5). are important. These include avoiding
Also orbital oedema and compression ƒ”–‡”‹ƒŽ Š›’‘–‡•‹‘ǡ ‡š…‡••‹˜‡ ϐŽ—‹† neuropathy: OCT characterization of the
resulting from prone position in replacement and hemodilution, pressure
spinal surgeries contributes to the on the eyeball and orbit, and dependent acute and resolving phases. Graefes Arch
development PION. The two surgeries position of the head, as well as shortening
commonly associated with ischemic the duration of surgery to the minimum. Clin Exp Ophthalmol. 2008;246:641–47.
optic neuropathy are coronary bypass
surgery and spinal surgeries probably CONCLUSION 6. Hedges TR, 3rd, Vuong LN, Gonzalez-Garcia
due to the long duration of the surgeries
and positioning of the patient in the ION is an important cause of visual ǡ ‡– ƒŽǤ —„”‡–‹ƒŽ ϐŽ—‹† ˆ”‘ ƒ–‡”‹‘”
latter. Broadly it has been observed that loss in the older age group. The diagnosis
cardiac surgery have resulted in anterior is based on high suspicion and clinical ischemic optic neuropathy demonstrated
ischemic optic neuropathy while spinal examination. It needs to be differentiated
surgery has commonly been associated from other common optic neuropathies. by optical coherence tomography. Arch
with posterior ischemic optic neuropathy Differentiating the two common varieties
. A variety of other surgical procedures Ophthalmol. 2008;126:812–5.
like radical neck dissection, orthopaedic
surgeries, venous graft in extremities, 7. Carroll SC, Gaskin BJ, Danesh-Meyer

Franzco HV. Giant cell arteritis. Clin Exp

Ophthalmol. 2006; 34:159–73.

8. Chew SSL, Kerr NM, Danesh-Meyer HV.

Giant cell arteritis. J Clin Neurosci. 2009;

16:1263–68

9. Hayreh SS, ZimmermanMB. Non-arteritic

anterior ischemic optic neuropathy:

role of systemic corticosteroid therapy.

Graefes Arch Clin Exp Ophthalmol.

2008;246:1029–46.

10. Hayreh SS, Zimmerman MB. Optic disc

edema in non-arteritic anterior ischemic

optic neuropathy.Graefes Arch Clin Exp

Ophthalmol. 2007;245: 1107–21

11. DelMonte DW, Bhatti MT . Ischemic Optic

Neuropathy.International Ophthalmology

Clinics2009; 49:35-62.

12. Holy SE, Tsai JH, McAllister RK, Smith KH.

Perioperative ischemic optic neuropathy:

A case control analysis of 126,666

surgical procedures at a single institution.

Anesthesiology 2009;110:246-53.

13. Biousse V, Newman NJ. Ischemic Optic

Neuropathy. N Engl J Med 2015;372:2428-

36.

Financial Interest: Š‡ ƒ—–Š‘” †‘‡• ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

www. dosonline.org 37

OCULAR BIOCHEMISTRY

MODULATORY EFFECTS OF 1,25 -
DIHYDROXYVITAMIN D3 ON OCULAR DISEASES

•Šƒ ‹‰Šǡ ƒ†‡‡’
‘•™ƒ‹ǡ ‘‘”ƒŒ Ǥǡ
ƒ•„‹” ƒ—”

Vitamin D plays an important role in the review will focus on the association of vitamin D with ocular
maintenance of calcium and phosphorus diseases and the potential role for vitamin D supplementation
homeostasis. Vitamin D receptors are usually in the therapy of eye diseases.
present in those organs which actively involved
in regulation of calcium level such as the CORRELATION OF VITAMIN D WITH OCULAR DISEASES
intestine, skin and kidney1. It has been revealed
by various studies that vitamin D receptors are also present Retinoblastoma
in several organs that are not involved in calcium metabolism,
such as the retina, pancreas, pituitary, muscle, brain, bone Retinoblastoma is the most common primary malignant
marrow, and thymus2,3. Vitamin D2 (ergocalciferol) and vitamin intraocular neoplasm of childhood. A study on human Y79
D3 (cholecalciferol) are the two common forms of vitamin D retinoblastoma cells revealed that these cells contain a high
found in nature. Although both forms are found in our diet, only ƒˆϐ‹‹–› ”‡…‡’–‘” •’‡…‹ϐ‹… ˆ‘” …ƒŽ…‹–”‹‘ŽǤ Š‡› ƒŽ•‘ •Š‘™‡† –Šƒ–
vitamin D3 can be synthesized by a photochemical reaction in calcitriol inhibits the growth of Y79 retinoblastomas in vitro
our skin4,5. and in vivo and the use of vitamin D or analogues of vitamin
D can be an effective drug against retinoblastoma. The human
The involvement of vitamin D in ocular diseases has been retinoblastoma cell line was not inhibited by ergocalciferol,
suggested by various studies. In particular Saulenas et al. which is an inactive, nonhydroxylated analogue of calcitriol.
revealed that human Y79 retinoblastoma cells contain a high ‡”Š‘‡ˆˆ ‡– ƒŽǤ ϐ‹”•– –‹‡ †‡‘•–”ƒ–‡† –Šƒ– ˜‹–ƒ‹ ʹ ‘”
ƒˆϐ‹‹–› ”‡…‡’–‘” •’‡…‹ϐ‹… ˆ‘” …ƒŽ…‹–”‹‘Ž ‘” ͳǡʹͷǦ†‹Š›†”‘š›˜‹–ƒ‹ ergocalciferol or one of its derivatives may be work as an effective
D3 or 1,25-(OH)2D3 and treatment of retinoblastoma cells chemotherapeutic agent against human retinoblastoma.
with calcitriol inhibits the growth of Y79 retinoblastomas in This study showed that vitamin D2 inhibits the growth of
vitro and in vivo6Ǥ ƒ–‡” Ž„‡”– ‡– ƒŽǤ •Š‘™‡† –Š‡ ‹ ˜‹˜‘ ‡ˆϐ‹…ƒ…› the human retinoblastoma cell line (Y79) grown in athymic
of 1,25-(OH)2D3 in transgenic mice with retinoblastoma. mice. In mice treated with ergocalciferol, the subcutaneous
‹–ƒ‹ ͵ –”‡ƒ–‡† ƒ‹ƒŽ• †‡‘•–”ƒ–‡† –—‘”• …‘ϐ‹‡† retinoblastomas were smaller and showed increased tumor
to the retina, whereas control animals demonstrated larger ‡…”‘•‹• ƒ† …ƒŽ…‹ϐ‹…ƒ–‹‘12. Cohen et al. present evidence that
tumors7Ǥ —”–Š‡”‘”‡ ‹ ˜‹˜‘ ‡ˆϐ‹…ƒ…› ƒ† …Ž‹‹…ƒŽ –‘š‹… calcitriol may be a useful chemotherapeutic agent against
effects of the 1,25-dihydroxy-16-ene-23-yne-vitamin D3 retinoblastoma. They have shown the decreases tumor growth
(1,25 (OH) 2-16-ene-23-yne-D3) analogue was evaluated in of subcutaneous retinoblastomas in athymic mice treated with
beta-luteinizing hormone-Tag (LH beta-Tag) transgenic mice calcitriol. Histopathologic studies showed that the calcitriol
with heritable retinoblastoma. Treated mice showed a 21% induced necrosis of the retinoblastomas but did not induce
smaller cross-sectional area compared with that in the control –—‘” …ƒŽ…‹ϐ‹…ƒ–‹‘13.
mice8. Regarding other ocular diseases, Parekh et al. studied
the associations between levels of 25-hydroxyvitamin D (25- Š‡ ‹ ˜‹˜‘ ‡ˆϐ‹…ƒ…› ‘ˆ ͳǡʹͷǦȋ Ȍʹ ͵ Šƒ• ƒŽ•‘ „‡‡
OHD) in serum and its correlation with age related macular shown by administering this agent to transgenic mice with
degeneration (AMD). They concluded the inverse associations retinoblastoma. Vitamin D treated animals demonstrated
between AMD and higher serum vitamin D levels and also –—‘”• …‘ϐ‹‡† –‘ –Š‡ ”‡–‹ƒǡ ™Š‡”‡ƒ• …‘–”‘Ž ƒ‹ƒŽ•
observed reduced prevalence of AMD among consistent demonstrated larger tumors, more often invading the vitreous,
vitamin D supplement users9. Goncalves et al. determined that anterior chamber, and choroid.
decreased serum 25-OHD concentration was associated with
primary open angle glaucoma (POAG)10. Inukai et al. reavealed Š‡ ‹ ˜‹˜‘ ‡ˆϐ‹…ƒ…› ƒ† …Ž‹‹…ƒŽ –‘š‹… ‡ˆˆ‡…–• ‘ˆ –Š‡
the inverse relationship between the severity of the retinopathy, 1,25(OH)2-16-ene-23-yne-D3 analogue was evaluated in
neovascularization, and serum 1,25-(OH)2D3 concentrations. LH beta-Tag transgenic mice with heritable retinoblastoma.
This study concluded that vitamin D, with antiproliferative, Treated mice with 1,25(OH)2-16-ene-23-yne-D3 showed a 21%
antiangiogenic, antioxidant and immunosuppressive effects, smaller cross-sectional area compared with that in the control
could play a preventive role in the pathogenesis of severe mice, without producing clinically apparent toxic effects. This
diabetic retinopathy11. Low vitamin D concentrations, certain compound may be useful as adjunctive therapy in the treatment
vitamin D receptor (VDR) gene polymorphisms and pathologies of retinoblastoma. A study proposed the antiangiogenic action
of vitamin D-binding proteins and of their gene may favor the of vitamin D compounds. Transgenic retinoblastoma mice
development of different type of ocular diseases. The present –”‡ƒ–‡† ™‹–Š ˜‹–ƒ‹ ͵ •Š‘™‡† •‹‰‹ϐ‹…ƒ–Ž› ˆ‡™‡” ˜‡••‡Ž•
than untreated controls. This result supports the hypothesis
that inhibition of angiogenesis is a mechanism of action for
vitamin D in the transgenic retinoblastoma mouse model14.

www. dos-times.org 39

OCULAR BIOCHEMISTRY

The effectiveness and toxicity of pregnacalciferol (2MbisP) in inhibiting ‹ϐŽƒƒ–‹‘ǡ ”‡–‹ƒŽ ƒ…”‘’Šƒ‰‡
vitamin D2, calcitriol, and synthetic the growth of retinoblastoma and —„‡”• ƒ† Ž‡˜‡Ž• ‘ˆ ƒ›Ž‘‹† „‡–ƒ ȋ ȾȌ
analogs were studied in the athymic/Y79 revealed that in athymic mice, 2MbisP accumulation which delayed this aging
xenograft and transgenic mouse models was effective in inhibiting RB growth process and thus improved the visual
of retinoblastoma. Calcitriol inhibited the compared with controls and should be function31.
cell growth in vitro. Calcitriol and vitamin considered for use in clinical trials of
D2 inhibited in vivo growth in xenograft RB19Ǥ  –Š‡ …—””‡– •–—†›ǡ –Š‡ ‡ˆϐ‹…ƒ…› One important AMD associated
and transgenic models, but therapeutic of combination therapy with calcitriol region in humans is located on 10q26
levels were toxic due to hypercalcemia. and cisplatin in athymic mice with and includes the two candidate genes,
Two analogs 1,25(OH)2-16-ene-23- subcutaneous Y79 human retinoblastoma age-related maculopathy susceptibility
yne-D3 and 1-alpha-hydroxyvitamin tumors was assessed. This study shows 2 (ARMS2) and HtrA Serine Peptidase 1
D2 (1-alpha-OH-D2), inhibited tumors that cisplatin given in combination with ȋ ͳȌǤ ‹•ƒ ‡– ƒŽǤ ‡š’Žƒ‹‡† –Š‡ ‹ϐŽ—‡…‡
in animal models of retinoblastoma calcitriol may be a viable multidrug of vitamin D on age-related macular
with reduced toxicity. The mechanism therapy option in the treatment of high- degeneration. First they characterized
of action appears related to increased risk retinoblastoma20. the rhesus monkey 10q26-orthologue
p53-related gene expression resulting region on chromosome 9 in detail
in increased apoptosis. 1,25(OH)2-16- AGE-RELATED MACULAR ƒ† ‹†‡–‹ϐ‹‡† –Š‡ †”—•‡Ǧƒ••‘…‹ƒ–‡†
ene-23-yne-D3 and 1-alpha-OH-D2 HTRA1 promoter SNP rs196357513 as
are effective in tumor reduction in two DEGENERATION a putative risk factor. They predicted 9
mouse models of RB with low toxicity. binding sites for the vitamin D dependent
These results warrant initiating phase 1 AMD is a progressive degenerative transcription factor vitamin D receptor
and phase 2 clinical studies in children15. condition of the retina and also a leading in the rhesus HTRA1 promoter, one of
Wagner et al. elucidated the mechanism …ƒ—•‡ ‘ˆ „Ž‹†‡••Ǥ ‡…‡–Ž›ǡ ‹ϐŽƒƒ–‹‘ which is destroyed by the rs196357513-
of anti proliferative activity of vitamin has gain importance as a potential risk risk allele. This study also revealed that
D in retinoblastoma cells. They showed factor for AMD pathogenesis21-25. Various vitamin D lowers HTRA1 promoter
that 1,25-(OH)2D3 induced programmed studies have been done which suggest an activity only for the wild type construct
death of Y79 cells by increasing the ƒ–‹Ǧ‹ϐŽƒƒ–‘”› ”‘Ž‡ ˆ‘” ˜‹–ƒ‹ ‹ and the risk allele decreases HTRA1
concentration of Bax protein and a vitro and in vivo. There is also evidence promoter activity compared to the wild
”‡†—…–‹‘ ‹ …ŽǦʹ …‘–‡–Ǥ Š‡•‡ ϐ‹†‹‰• which reveals that vitamin D reduces the type allele. Thus not only a higher HTRA1
suggest that 1,25-(OH)2D3 inhibits the proliferation of cells of the immune system expression, but an imbalance of HTRA1
growth of retinoblastoma cells by causing and may protect against AMD by virtue might cause AMD disease32.
cell cycle arrest and apoptosis16. A study ‘ˆ ‹–• ƒ–‹Ǧ‹ϐŽƒƒ–‘”› ’”‘’‡”–‹‡•26-29.
was done to determine antineoplastic Parekh et al. studied the associations Itty et al. compared the 25-OHD
effect of vitamin D analogues in a xenograft between levels of 25-OHD in serum and levels in patients with neovascular age-
model of human retinoblastoma. Vitamin its correlation with AMD. They concluded related macular degeneration (NVAMD)
D analogues appear to attenuate the inverse associations between AMD with patients with nonneovascular
retinoblastoma tumor growth in athymic and higher serum vitamin D levels and age-related macular degeneration and
mice by increasing apoptosis. Cell death is also observed reduced prevalence of AMD control patients. The levels of 25-OHD
associated with the upregulation of both among consistent vitamin D supplement ™‡”‡ •‹‰‹ϐ‹…ƒ–Ž› Ž‘™‡” ‹
p53 and p2117. —•‡”•Ǥ ‹–ƒ‹ †‡ϐ‹…‹‡…› Šƒ• „‡‡ patients versus nonneovascular age-
ƒ••‘…‹ƒ–‡† ™‹–Š ƒ …›–‘‹‡ ’”‘ϐ‹Ž‡ –Šƒ– related macular degeneration and control
Albert et al. investigated the ˆƒ˜‘”• ‰”‡ƒ–‡” ‹ϐŽƒƒ–‹‘ •—…Š ƒ• patients which emphasized the vitamin D
effectiveness of the vitamin D analogues higher C-reactive protein and interleukin †‡ϐ‹…‹‡…› ™ƒ• ‘”‡ ’”‡˜ƒŽ‡– ‹
1,25 (OH) 2-16 - ene - 23 - yne - D3 6 levels, and lower interleukin 10 levels, patients33.
and 1alpha-OH-D(2) in inhibiting which could make susceptible to AMD30.
retinoblastoma growth in large tumors ‰‡Ǧ”‡Žƒ–‡† …Šƒ‰‡• ƒ‹Ž› ‹ϐŽ—‡…‡ Graffe et al. concluded that vitamin D
in a xenograft model and with prolonged the outer retina of the eye where high ‹•—ˆϐ‹…‹‡…› ™ƒ• ƒ••‘…‹ƒ–‡† ™‹–Š ”‡†—…‡†
use in a transgenic model. They metabolic activities takes place resulting macular thickness among older patients
concluded that in athymic mice in the increase in extracellular deposition, with no patent macular dysfunction. This
large-tumor study, both 1alpha-OH-D(2) ‹ϐŽƒƒ–‹‘ǡ ƒ† …‡ŽŽ Ž‘•• ‰‹˜‹‰ ”‹•‡ ‹’Ž‹‡• –Šƒ– ˜‹–ƒ‹ ‹•—ˆϐ‹…‹‡…› ƒ›
and 1,25(OH)2-16-ene-23-yne-D3 were to visual decline. Lee et al. showed that be involved in macular thinning, and
effective in inhibiting tumor growth vitamin D3 protect against the aging ’”‘˜‹†‡• ƒ •…‹‡–‹ϐ‹… „ƒ•‡ ˆ‘” ˜‹–ƒ‹
compared with controls18. A group process. They administered vitamin D3 replacement trials in age-related macular
investigated effectiveness of 2-methylene- for only 6 weeks in aged mice which degeneration34.
19-nor-(20S)-1alpha hydroxybishomo- •Š‘™‡† •‹‰‹ϐ‹…ƒ– ”‡†—…–‹‘• ‹ ”‡–‹ƒŽ
Uro et al. examined that whether
˜‹–ƒ‹ †‡ϐ‹…‹‡…› ‹ ‘Ž†‡” ƒ†—Ž–• ‹•
associated with reduced thickness of

Ocular Biochemistry Services, Dr. Rajendra Prasad Centre for Ophthalmic Sciences,All India Institute of Medical Sciences, New Delhi

Usha Singh Dr. Sandeep Goswami Sooraj K. Prof. Jasbir Kaur

40 DOS TIMES - MAY-JUNE 2016

OCULAR BIOCHEMISTRY

the ganglion cell complex (GCC) and A group examined the association are needed before evidence-based
‘ˆ –Š‡ ”‡–‹ƒŽ ‡”˜‡ ϐ‹„”‡ Žƒ›‡” ȋ Ȍ of Taq I polymorphism of the vitamin D
or not. They concluded that vitamin D receptor with the development of severe recommendations can be made.
†‡ϐ‹…‹‡…› ‹ ‘Ž†‡” ’ƒ–‹‡–• ‹• ƒ••‘…‹ƒ–‡† DR. Frequency of wild-type genotype
with reduced mean GCC thickness, which TT was lower in patients with severe DR ACKNOWLEDGEMENT
initiate early stage of optic nerve damage, when compared with control subjects.
prior to RNFL loss35. Thus established an association between Usha Singh and Sooraj K. are
TT form (VDR) and low risk for severe
GLAUCOMA DR, and between Tt form and high risk recipients of fellowship from the Council
for severe DR40. To assess the relationship
The glaucomas are a heterogeneous Again a study was done to determine the ‘ˆ …‹‡–‹ϐ‹… ƒ† †—•–”‹ƒŽ ‡•‡ƒ”…Š
group of optic neuropathies characterized relationship between vitamin D status
by degeneration of the optic nerve and ƒ† ǡ ™Š‹…Š …‘ϐ‹”‡† –Šƒ– ’ƒ–‹‡–• and the Indian Council of Medical
’”‘‰”‡••‹˜‡ ˜‹•—ƒŽ ϐ‹‡Ž† Ž‘•• ƒ• –Š‡ ”‡–‹ƒŽ with diabetes have lower 25-OHD levels
ganglion cells die. Ocular hypertension is than those without diabetes41. Patrick Research, India respectively. We sincerely
the strongest known risk factor for POAG, et al. also found an association between
the most common form of glaucoma. severity of DR and prevalence of vitamin acknowledge the support of Department
Lowering the intraocular pressure (IOP) †‡ϐ‹…‹‡…›42.
remains the mainstay of therapy in the of Biotechnology, Govt. of India.
management of glaucoma. Galina et al. Ren et al. investigated whether
revealed by microarray analysis that 1,25-(OH)2D3 can protect DR and also REFERENCES
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”‡–‹‘„Žƒ•–‘ƒǣ Š‡ ϐ‹”•– ŽŽ•™‘”–Š ‡…–—”‡Ǥ
Ophthalmic Genet 2002;23:137-56.

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19. Albert DM, Plum LA, Yang W, Marcet M, by treatment of healthy adults with 1 39. Aksoy H, Akçay F, Kurtul N, Baykal O,
Lindstrom MJ, Clagett-Dame M, DeLuca HF. alpha, 25 dihydroxyvitamin D3. Int J Avci B. Serum 1,25 dihydroxy vitamin D
Responsiveness of human retinoblastoma Immunopharmacol 1991;13:525-30. (1,25-(OH)2D3), 25 hydroxyvitamin D (25-
and neuroblastoma models to a non-calcemic 30. Mascitelli L, Pezzetta F, Goldstein MR. OHD) and parathormone levels in diabetic
19-nor Vitamin D analog. J Steroid Biochem Macular degeneration, heart disease, and retinopathy. Clin Biochem 2000;33:47-51.
Mol Biol 2005;97:165-72. vitamin D. Ophthalmology 2010;117:194.
31. Lee V, Rekhi E, Hoh Kam J, Jeffery G. Vitamin 40. Taverna MJ, Sola A, Guyot-Argenton C, Pacher
20. Kulkarni AD, van Ginkel PR, Darjatmoko SR, D rejuvenates aging eyes by reducing N, Bruzzo F, Slama G, Reach G, Selam JL. Taq
Lindstrom MJ, Albert DM. Use of combination ‹ϐŽƒƒ–‹‘ǡ …Ž‡ƒ”‹‰ ƒ›Ž‘‹† „‡–ƒ ƒ† I polymorphism of the vitamin D receptor
therapy with cisplatin and calcitriol in the improving visual function. Neurobiol Aging and risk of severe diabetic retinopathy.
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1,25-Dihydroxyvitamin D decreases HTRA1 Rimler E, Cleveland J, Lynn MJ, Tangpricha
21. Johnson LV, Ozaki S, Staples MK, Erickson PA, promoter activity in the rhesus monkey-a ǡ ”‹˜ƒ•–ƒ˜ƒ Ǥ ‹–ƒ‹ ‹•—ˆϐ‹…‹‡…›
Anderson DH. A potential role for immune ’Žƒ—•‹„Ž‡ ‡š’Žƒƒ–‹‘ ˆ‘” –Š‡ ‹ϐŽ—‡…‡ in diabetic retinopathy. Endocr Pract
complex pathogenesis in drusen formation. of vitamin D on age-related macular 2012;18:185-93.
Exp Eye Res 2000;70:441-9. degeneration? Exp Eye Res 2013;116:234-9.
33. Itty S, Day S, Lyles KW, Stinnett SS, Vajzovic 42. Patrick PA, Visintainer PF, Shi Q, Weiss
22. Smith W, Mitchell P, Leeder SR, Wang ǡ ”—–Š›—Œƒ›ƒ Ǥ ‹–ƒ‹ †‡ϐ‹…‹‡…› IA, Brand DA. Vitamin D and retinopathy


Ǥ Žƒ•ƒ ϐ‹„”‹‘‰‡ Ž‡˜‡Ž•ǡ ‘–Š‡” in neovascular versus nonneovascular in adults with diabetes mellitus. Arch
cardiovascular risk factors, and age-related age-related macular degeneration. Retina Ophthalmol 2012;130:756-60.
maculopathy: the Blue Mountains Eye Study. 2014;34:1779-86.
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D, Annweiler C. Vitamin D and macular of 1,25-dihydroxy vitamin D3 on the
23. Johnson LV, Leitner WP, Staples MK, thickness in the elderly: an optical coherence expressions of vascular endothelial growth
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‹ϐŽƒƒ–‘”› ’”‘…‡••‡• ‹ ”—•‡ ˆ‘”ƒ–‹‘ 2014;55:5298-303. the retinas of rats with diabetes. Diabetes
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Eye Res 2001;73:887-96. A, Milea D, Annweiler C. Age-Related
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24. Wirostko E, Wirostko WJ, Wirostko BM. Reduced Macular Ganglion Cell Complex: Esquerda A, Traveset A, Granado-Casas M,
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—”Œ‘ ǡ ƒ—”‹…‹‘ Ǥ ‹–ƒ‹ ‡ϐ‹…‹‡…› •
‹ϐŽƒƒ–‘”› †‹•‡ƒ•‡ ’‘••‹„Ž› –”‡ƒ–ƒ„Ž‡ Coherence Tomography Study. PLoS One Associated with the Presence and Severity
with minocycline. Acta Ophthalmol Scand 2015;10:e0130879. of Diabetic Retinopathy in Type 2 Diabetes
2004;82:243-4. Mellitus. J Diabetes Res 2015;2015:374178.

25. Klein R, Klein BE, Tomany SC, Cruickshanks ͶͷǤ ”‘™
ǡ ƒ‹…Š‹ Ǥ ‹–ƒ‹ †‡ϐ‹…‹‡…›
KJ. Association of emphysema, gout, and and posterior subcapsular cataract. Clin
‹ϐŽƒƒ–‘”› ƒ”‡”• ™‹–Š Ž‘‰Ǧ–‡” Ophthalmol 2015; 9:1093-8.
incidence of age-related maculopathy. Arch
Ophthalmol 2003;121:674-8. 46. Jee D, Kim EC. Association between serum
25-hydroxyvitamin D levels and age-
26. Manolagas SC, Provvedini DM, Murray EJ, related cataracts. J Cataract Refract Surg
Tsoukas CD, Deftos LJ. The antiproliferative 2015;41:1705-15.

Financial Interest: Š‡ ƒ—–Š‘”• †‘ ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

RESULTS OF DOS ELECTION 2016

Vice president: ”‘ˆǤ ƒŽ‡•Š
DOS representatives to AIOS (to join executive from February-2017)

ͳǤ ”Ǥ •Š— ‰ƒ”™ƒŽ ʹǤ ”Ǥ ‘Š‹– ƒš‡ƒ

42 DOS TIMES - MAY-JUNE 2016

SNAPSHOT

OCULAR MANIFESTATIONS IN TAKAYASU’S ARTERITIS

ŠƒŽ—
—’–ƒǡ †‹–‹ ”ƒ•Šƒ”ǡ ƒŒ‡‡˜ —Ž‹ǡ Ǥ Ǥ Šƒ”ƒ

Takayasu’s arteritis (TA), also known as Figure 1: UJQYKPI NGWEQOCVQWU EQTPGCN QRCEKV[ KP . ' CPF PGDWNCT
aortoarteritis and pulseless disease, is a rare, QRCEKV[ KP 4 '
idiopathic condition. It is a form of granulomatous
arteritis, which affects large- and medium
sized arteries, primarily the aorta and its large
branches. Takayasu arteritis results in ischemic
ocular manifestations in the form of Takayasu retinopathy.
The ischemic retinal changes depend on which portions of
the carotid arteries occluded, the rate of development and
†—”ƒ–‹‘ ‘ˆ ‘…—Žƒ” ˜ƒ•…—Žƒ” ‹•—ˆϐ‹…‹‡…›ǡ ƒ† –Š‡ ‡ˆˆ‡…–‹˜‡‡••
of collateral blood supply to the eye.

CASE REPORT A detailed systemic examination was done as our patient

rb apbahvwbsnlmnllcocac1GaIoitsbaru͵eoannoeeueeloorncnnfpƒoaelleͳ)heeoofmewotintsdovnh.rgm–csagdbddttHaǤocnrrcirʹtt‡Tnehountkgetgdaraecpueatkiiigr”inhdemoosenhog,AOTehitnsrpnyaotlea ti,aaseieoahspsiede‘tchfarvoycnyclltnqeneotrslcmtnhenohthou2neloeeiactaguxoorfve egeoerocils4avǡdroniot.a5e atiraapse™iuarol.rrgmanbn–ewledmgiryisdsoTnr.weyeoŠdrrsrlnsyindry‹oh.eecrsdeahDcyhano–rrc‡aitherapeaftusuŠntdilonspueid”iefceiavsaoegewrincntllmlk ev‡aihrehavlvafraeageihfhdrhcatcyeluo itsntoaeleeyyrftseoat™s8etirreiomtnaesoaversoosso—tlwierwe’tiaecdrd.ƒsaloudrilnepaenhvnaŽyaedatou6naeohe•Ts–aieyrun,haisveeetwdmt‹f tuaclr/sudewisyehoe’scdxoue†raiscfmuutB1nesoaotiedeeuiaŽrrtllman‡nwtwhnjla‡v1.2osdonprmmasaays˜Smqidowtl euwipe4cnreamaewcr‡rcnuu6nOraiykictarns(miveauasnaŽanhwngeisaseleoFo‘nnomaustonlet‹tnaaciddmacawr7ir†’taeodcslrmnelwgttoewhvennmrbiatswrumi wiipwxaaunagtodis7ooeiegroa”uiiPanaorsnanantlhrtlamhar‡‡einnapl’.fdiseeamhLoygfteelsgyonttstϐdalT,..ohHsnirpŽczte–‡vingeshihtoonag nabnes…siineo‘eibawiTifaafsksratyo–isoidtrrˆssiooibeib‹entftert oors˜emafrierol‘noiacmgfhdongr‹envltvauwru’k–talednrheo›ehmeyaf(niarlƒfaafwsneraia. Frbtlcand…ioedrro,ogfeFso•noieie‹eoycuhemgyetfŠlFiϐnmrppcyvoorth‹rsuwenehAƒ3ar…ehoreetasmserte†ƒ(iflregiassasasrgecaeiowFdtr5o–‘atelenrhc‹,aTcaeuindo-r™sfr2r‘nviaghdata6sdtpioeiffaee-adeeu.igh’s•lso3esusrxasdr auc rhommro,ksptp‘o)ainalep‹tcacoTtae,i.ivtˆrlpoducneaiplifr ld4diOmtaa,i aezp…nclayietul)icyrsr˜t1tne‘ymrelstpdat.iektia‹rohe5dep”icingaialta–dBtuntotfrihs”tahlaggeiliyeosrl‡oas.nui‡bopaeattSwteryi‘ptsrhƒlaiirHsnuoacnedpieaprr—gilh noaaaideycetosro‹iylnei•gynndnhrayeeessrartnfmst.ǡ,,, eteitnuushh-atdliienonaac(imwfeatwwƒwaimŽsmennv5adohpranoT‡nohfhxxebpfa5eaotaaaaˆlumeoaduatropdsdcpr†A–lcbessssoaeiotrmt marerwsl rreoraŽtfloƒoaaewmyn7rI)iot‘eh4bnbmscitletsntnaw)mtmnofa™h,tinoei/aardasaue‰atln/ttahair6amdolaHhhe‡mu‹tupndthtetill‘rat0ineecei”ahigarysgdosopeei,ocdn‰oso a.reie.oodrknvsillu.ŽuS”pnnrafitssfa‹aoefasenƒseofnhpnau,niiiletrorsfsntud’lHntoedlooldpuoeurcptif„heebibŠisbdgneahvpnutwmnoxa•ensr‹omaidnPisa.oeegl… gctaerirltaanlutCnta™iLm rk.uucqCϐeoisrsitrelwtT‹phlbtosui-dl‹nilnereenaslnrza–gririeisfiemrltm.teŠt†arAaItetbgohereeasaaonihissl T‹athingototiotarrlb,ristzo’nec.rtahtwyrgntntscm‰luuiƒtscceaGtcehfoetign,.hteii•oiiŽoolrndhotvhiewvuoD’nsyǡwennedoleem bdesrreln–eraƒoaamai,,reoorbŠillan–roipnamysotearcwao‘ai‡lihendrrcotanyntsca ”ot•bb5wpcaϐlboualedot-etd†.dateicŽ›kidenuseŠanrndreiailm)etn‘Sbcb‹lofiy nllsetdardp.iƒe‘sagtytaa™phjl2gelaptsfoaabihnsao‰ifc™ekisttusnrairtns0tyoertr vwereaogptnBtv‡oeynnic‡daeadgirrridwdl‘is–r,pselimorshdco†ensmadaaorŠiil’oys•yeiracfaameucaevwgullr tdit‘usmx‹ƒuevesbniatbmlistmerr•astccib†ad–rheedae.er”rleaad nomll1–lbe‘uer‡nelsǤaeaaorenoirm‡I loooa4anryaw†ˆnxdcliafnxtastnwa fi”aw ecrofartklae0shaiura —ltictoƒesmHoatcdcecdoetr1ntrm(imauƒbe…•„hrravsiheraooydampFlcag.ios‡ armico6otl‘eortptiicfooitrtitii†nllnƒnarinymlncgpiy”waecwantrcmomaonmo›rl ,ƒoƒiaeuauelepevu,olrn(irecƒgo–trrtnmsgaarniiihctg…llaoti‘p(id.•iemnnimaeeaseh†thrnoud‘o/a4ratf—”wunoynuxtfrcraer caOtnimŽdnello›a0te eclhfn.‘Hoirn6roƒdersell cnnrepcc(ee(irr”fu..mg)”neCe”ϐginsgdPeEooopee yra‹.(Rr–‡glcksOtcahoaroe‡evvSmrFpgeSetolaatai†heesϐreRldtnf†nsee”VprgRihcr‹wtr,o—nsoowwmngm‹Žsueaaai‹tpuuo)1aaŽa)–uotn…utseuuetett‹nllbn‹llltiiisrnn2ioeheh‡hlin•yc‰traaetrtdrroiiltlaakii)ndnd0hdddd†hͳy‰eeeeeeeeecc•ssrrr-fll,,

www. dos-times.org 43

SNAPSHOT

Figure 2: (WPFWU RJQVQ UJQYKPI FQV DNQV JGOQTTJCIGU CV OCEWNC YKVJ Figure 3: (WPFWU RJQVQU UJQYKPI OGFKC JC\G YKVJ QRVKE CVTQRJ[ KP . '
PQTOCN QRVKE FKUE KP 4 '

Figure 4: ((# QH 4 ' UJQYKPI OWNVKRNG OKETQCPGWT[UOU KPXQNXKPI VJG Figure 5: %6 #PIKQ CQTVKE CTEJ UJQYKPI QEENWUKQP QH TKIJV EQOOQP
GPVKTG HWPFWU ECTQVKF CTVGT[ DKNCVGTCN UWDENCXKCP CTVGT[ QTKIKP DTCEJKQEGRJCNKE VTWPM
NGHV RTQZKOCN EQOOQP ECTQVKF CTVGT[ CPF CQTVKE CTEJ

that there was increase in number of cardiologist opinion was sought for with applanation tonometer). Anterior
dot blot hemorrhages at macula and further management, for which patient segment examination of right eye revealed
peripheral retina. There was a zone of was referred to a higher institute. Patient neovascularization of iris extending
retinal whitening at macula area with was non-compliant to her treatment. On from 3-5 o’clock and there were no
macular oedema and dilatation of veins her subsequent follow up visit after 5 •‹‰• ‘ˆ ƒ–‡”‹‘” •‡‰‡– ‹ϐŽƒƒ–‹‘
and small vessels. In view of this the months, her best corrected visual acuity (Figure 7). Gonioscopy revealed open
patient was referred to vitreoretinal in right eye was 2/60 and PL negative angle with no neovascularization.
•—”‰‡‘ ™Š‡”‡ ȋˆ—†—• ϐŽ—‘”‡•…‡‹ in left eye and intraocular pressure Dilated fundus examination revealed
angiography) was done. Keeping in view was normal in both eyes (17mm of Hg retinal ischemia with micro aneurysms,
the ischemic maculopathy, an urgent in right eye and 18 mm of Hg in left eye dot-blot hemorrhages, dilated retinal

Department of Ophthalmology, Dr. R.P.G.M.C., Kangra at Tanda, Himachal Pradesh (India)

Dr. Shalu Gupta MS Dr.Aditi Prashar MS Dr. Rajeev Tuli MS Dr. R.K. Sharma MS

44 DOS TIMES - MAY-JUNE 2016

SNAPSHOT

Figure 6: &QRRNGT KOCIKPI QH CTVGTKCN ƀQY UJQYKPI TGFWEGF EQNQT Figure 7: 5NKV NCOR GZCOKPCVKQP QH TKIJV G[G UJQYKPI PGQXCUEWNCTKUVKQP
ſNNKPI YKVJ CDPQTOCN OQPQRJCUKE ƀQY RCVVGTPU QH KTKU GZVGPFKPI HTQO QŏENQEM

vessels, arterio-venous anastomosis and infections, rheumatoid arthritis and other To delineate the type of Takayasu
neovascularization at disc (Figure 8A, collagen vascular diseases etc. Recently arteritis a peripheral angiogram is
8B). Patient was re-counselled for urgent immunopathological cause is considered required. On the basis of angiographic
cardiologist and vitreoretinal surgeon with association of interleukin-6 and ϐ‹†‹‰•Ǥ Š‡”‡ ƒ”‡ ͷ –›’‡•ǣ  ›’‡
opinion. RANTES (regulated on activation, normal ƒƒ›ƒ•— ƒ”–‡”‹–‹•ǡ –Š‡ ‹ϐŽƒƒ–‘”›
T cell expressed and secreted) in the process is localized to the arch of the
DISCUSSION pathogenesis of the disease process4. aorta and its branches. In Type II disease
the lesions involve both the ascending
ƒƒ›ƒ•—ǯ• ƒ”–‡”‹–‹• ϐ‹”•– ”‡’‘”–‡† „› According to American aorta, aortic arch and its branches
M. Takayasu, a Japanese ophthalmologist Rheumatological Society three of the (Type II a) or in addition the thoracic
in the year 1908, is a idiopathic, chronic following six criteria are necessary for a descending aorta (Type II b). In Type III
granulomatous necrotizing vasculitis †‡ϐ‹‹–‡ †‹ƒ‰‘•‹• ‘ˆ ƒƒ›ƒ•—ǯ• †‹•‡ƒ•‡ 5: disease, the thoracic descending aorta is
predominantly affecting the aorta with 1. Onset before 40 years involved along with the abdominal aorta
its branches, pulmonary and coronary 2. Claudication of the extremities and/or renal arteries. In Type IV disease
arteries1,2. The estimated incidence of 3. Absence/ decrease in the brachial involves abdominal aorta involvement or
Takayasu arteritis is 2.6 cases per million renal artery involvement, while Type V
persons per year, more common in pulse in one or both arms entails the entire aorta and its branches6.
females (F: M ratio of 1.3:1) and mostly 4. Difference of 10 mm Hg or more in It is an occlusive arteritis of the aortic
begins in second or third decade of life3. As arch branches which results in ischemic
exact pathogenesis of the arteritis is still blood pressure measured in both ocular manifestations in the form of
unknown but previously it was associated arms Takayasu retinopathy.
with tuberculosis, streptococcal 5. Audible bruit on auscultation of the
aorta or subclavian artery
6. On arteriogram, narrowing of the
aorta or its primary branches.

(A) (B)

Figure 8A and 8B: (WPFWU RJQVQ UJQYKPI TGVKPCN KUEJGOKC YKVJ OKETQ CPGWT[UOU FQV CPF DNQV JGOQTTJCIGU FKNCVGF TGVKPCN XGUUGNU CTVGTKQ XGPQWU
CPCUVQOQUKU CPF PGQXCUEWNCTKUCVKQP CV FKUE

www. dos-times.org 45

SNAPSHOT

According to Uyama and Asayma7, such as claudication, diminished or presenting with early retinopathy should
ƒƒ›ƒ•— ”‡–‹‘’ƒ–Š› …ƒ „‡ …Žƒ••‹ϐ‹‡† absent pulse, bruit, asymmetrical blood
into four stages: pressure in either the upper or lower be kept under close follow ups to detect
limbs (or both) and typical angiographic
Stage 1: characterized by distension features. The various complications of progression and ischemic changes,
of veins TA are in the form of stroke, intracranial
hemorrhages, seizures, ischemic organ as in this case there was worsening
Stage 2: micro-aneurysm formation failure, hypertensive complications,
Stage 3: the formation of arterio- heart failure , renovascular hypertension, of retinopathy from stage 2 to stage
venous anastomoses, and valvular heart disease, fetal injury and
Stage 4: the presence of ocular graft stenosis. Ͷ ™‹–Š‹ –Š‡ ‹–‡”˜ƒŽ ‘ˆ ϐ‹˜‡ ‘–Š•Ǥ
complications like cataract, rubeosis
iridis, retinal ischemia, neovascularisation For diagnosis and evaluation of Patients need to understand the nature
and vitreous hemorrhage. Less frequently Takayasu arteritis, the intraarterial
ischemic manifestations like anterior angiography is the standard diagnostic of disease and need to take medicines
ischemic optic neuropathy8, central modality but now it has been replaced
retinal artery occlusion9 and ocular by computed tomography angiography to prevent complications. When in
ischemic syndrome can occur. or magnetic resonance angiography
Approximately 10% of patients with (MRA). The goals of therapy in Takayasu remission or when experiencing mild
Takayasu arteritis are asymptomatic, with ƒ”–‡”‹–‹• ƒ”‡ –‘ ”‡†—…‡ ‹ϐŽƒƒ–‹‘ ƒ†
the disease detected based on abnormal suppress autoimmune disease. To treat form of TA, patients are tempted to stop
˜ƒ•…—Žƒ” ϐ‹†‹‰• ‘ ‡šƒ‹ƒ–‹‘Ǥ Š‡ the active disease, corticosteroids are
clinical course of the disease is divided used and gradually tapered. Cytotoxic drugs, thus increasing the risk of serious
‹–‘ ƒ ‡ƒ”Ž› ƒ…–‹˜‡ ‹ϐŽƒƒ–‘”› ’Šƒ•‡ agents such methotrexate, azathioprine,
and late chronic phase. The active phase and cyclophosphamide are the main complications. So the patient should also
lasts for weeks to months and may have therapeutic agents when the response
a remitting and relapsing course. It is to steroids is unsatisfactory. Anti-TNF be advised to monitor visual acuity at
characterized by systemic disease with agents can be used in case of relapsing
symptoms of fever, general malaise, Takayasu arteritis. The treatment of TA home and any worsening if noted, should
night sweats, loss of appetite, weight in the form of immunosuppressants can
loss, headaches, dizziness, arthralgia, lead to a dramatic improvement with seek urgent treatment for same.
skin rashes, etc. are often seen in 5-year survival rate of 94% in adults13.
children with TA. The late chronic phase REFERENCES
is the result of arterial stenosis and/ In our patient there was visual loss,
or occlusion and ischemia of organs. ‰‡‡”ƒŽ‹œ‡† ™‡ƒ‡•• ƒ† †‹ˆϐ‹…—Ž–› ‹ 1. Chun YS, Park SJ, Chung H, Lee J. The clinical
Its clinical manifestations are varied swallowing with absent pulses of both and ocular manifestations of Takayasu’s
and related to the location of arterial upper extremities, which might be arteritis. Retina.2001;21:132–40.
lesion. Initially, there are mononuclear attributed to occlusion and stenosis of
…‡ŽŽ ‹ϐ‹Ž–”ƒ–‹‘• ‹ –Š‡ ƒ†˜‡–‹–‹ƒ ƒ† branches of aorta. In 13.5% to 33% TA 2. Kothari SS. Takayasu’s arteritis in children- a
granulomas with Langerhans cells in patient may present with visual loss14. review. Paediatr Cardiol. 2002;9:4–23.
the media, followed by disruption of the The clinical features of absent arterial
elastin layer and subsequent massive pulsation in the upper limbs, head and 3. Schmidt MH, Fox AJ, Nicolle DA. Bilateral
‡†‹ƒŽ ƒ† ‹–‹ƒŽ ϐ‹„”‘•‹•Ǥ Š‡•‡ Ž‡•‹‘• neck, angiographic evidence of bilateral anterior ischemic optic neuropathy as
result in segmental stenosis, occlusion, common carotid and subclavian arterial a presentation of Takayasu’s disease. J
dilatation, and aneurysmal formation in occlusion in our case are typical of aortic Neuroophthalmol. 1997;17:156–61.
the affected vessels. arch syndrome of Takayasu’s arteritis.
Diminished or absent pulses 4. Noris M, Diana E, Gamba S, Bonazzola S,
are present in 84-96% of patients, CONCLUSION Remuzzi G. Interleukin-6 and RANTES
associated with limb claudication and in Takayasu Arteritis. Circulation.
blood pressure discrepancies between In conclusion, Takayasu arteritis 1999;100:55–60.
the two arms10. Kerr et al11 (NIH) should be considered in differential
in a study to assess disease activity diagnosis in a young patient with 5. Worrall M, Atebara N, Meredith T, Mann
in patients with Takayasu arteritis complaints of diminution of vision, ES. Bilateral ocular ischemic syndrome in
revealed some criteria of new onset or medical history positive for generalized Takayasu disease. Retina. 2001;21:75-76.
worsening of 2 or more of the following body aches and jaw claudication. The
features indicative of active disease12: detailed medical examination followed 6. Nastri MV, Baptista LP, Baroni RH,
Systemic features, such as fever and by proper investigations is necessary. Blasbalg R, de Avila LF, Leite CC, et
ƒ”–Š”ƒŽ‰‹ƒ• ȋ‘ ‹†‡–‹ϐ‹‡† …ƒ—•‡Ȍǡ ‡Ž‡˜ƒ–‡† All the patients of Takayasu arteritis al.Gadolinium-enhanced three-dimensional
erythrocyte sedimentation rate, features should be referred to ophthalmologist for MR angiography of Takayasu arteritis.
‘ˆ ˜ƒ•…—Žƒ” ‹•…Š‡‹ƒ ‘” ‹ϐŽƒƒ–‹‘ǡ evaluation of retinopathy. The patients Radiographics 2004;24:773–86

7. Uyama M, Asayma K. Retinal vascular
changes in Takayasu’s disease (Pulseless
disease). Occurrence and evolution of the
lesion. Doc Ophthalmol Proc Series. 9:549–
554.

8. Malik KP, Kapoor K, Mehta A, Dadeya S,
Guliani BP, Aggarwal S, et al. Bilateral anterior
ischemic optic neuropathy in Takayasu
arteritis. Indian J Ophthalmol. 2002;50:52–4.

9. Kaushik S, Gupta A, Gupta V, Jain S, Lal V.
Retinal arterial occlusion in Takayasu’s
arteritis. Indian J Ophthalmol. 2005;53:194–
6.

10. Johnston SL, Lock RJ, Gompels MM. Takayasu
arteritis: a review. J Clin Pathol 2002;55:481-
6.

11. Kerr GS, Hallahan CW, Giordano J, Leavitt RY,
Fauci AS, Rottem M, et al. Takayasu arteritis.
Ann Intern Med. 1994 Jun 1. 120:919-29.

12. Maksimowicz-McKinnon K, Hoffman GS.
Takayasu arteritis: what is the long-term
prognosis?. Rheum Dis Clin North Am. 2007;
33:777-86.

13. Koide K. Takayasu arteritis in Japan. Heart
Vessels Suppl. 1992;7:48-54.

14. Sagar S, Kar S, Gupta A, Sharma SK. Ocular
changes in Takayasu’s arteritis in India. Jpn
J Ophthalmol. 1994;58:97-102.

Financial Interest: Š‡ ƒ—–Š‘”• †‘ ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

46 DOS TIMES - MAY-JUNE 2016

SNAPSHOT

NEVUS OF OTA

—„Šƒ˜ Šƒ—Šƒǡ ‡‡”ƒŒ Šƒ”ƒǡ Šƒ•Š‹ ƒ–– Šƒ”ƒǡ

A40 year-old male presented to the department Figure 1: 5ENGTCN OGNCPQUKU
NGHV G[G YKVJ FGTOCN DNWKUJ RKIOGPVCVKQP
of ophthalmology of a secondary care institute KP NGHV OCNCT CTGC %JCTCEVGTKUVKE FGTOCVQNQIKECN FKUVTKDWVKQP QH VJG
of the hilly state with a history of pigmentary NGUKQP
VTKIGOKPCN PGTXG VGTTKVQT[
changes in his left eye and left upper part of
cheek since birth. The lesions did not cause Figure 2: 5MKP NGUKQP
NCVGTCN XKGY
any discomfort/trouble and he wanted to know hyperpigmentation. Mongolian spot are blue-grey patches that
whether the lesions would interfere with his vision in old age. spontaneously resolve by 3–6 years of age and typically occur
He was a labourer by occupation and had never consulted in lumbosacral area. Melasma is typically associated with
any ophthalmologist for these lesions. His medical history, pregnancy and appears as irregularly outlined gray brown
developmental history, prenatal, perinatal, postnatal and family patches, are bilateral and there is no palatal involvement. Drug
histories were all unremarkable. On examination, his speech, induced hyperpigmentation is usually acquired after ingestion
hearing, intelligence, general physical and systemic examination of drugs like minocycline, amiodarone and gold. There is no
were normal. Torch light and slit lamp examination revealed †‡ϐ‹‹–‹˜‡ †‹ƒ‰‘•‹• ˆ‘” ‡˜—• ‘ˆ –ƒǤ ‹ƒ‰‘•‹• ‹• ƒ‹Ž› „›
scleral melanosis (mulitple bluish patches) in the left eye,
superior and supero-lateral to the limbus. Rest of the slit lamp
examination was normal. His left malar area revealed patchy
dermal bluish pigmentation. His visual acquity was 6/6 in both
the eyes; pupillary reactions, ocular movements, colour vision,
fundus examination and intraocular pressure were normal.
The characteristic lesions and its site/dermatomal distribution
suggested the diagnosis of nevus of ota (Figure 1). A secondary
consultation with department of dermatology was made and
–Š‡ †‹ƒ‰‘•‹• •–ƒ›‡† …‘ϐ‹”‡†Ǥ ‡ ‡š’Žƒ‹‡† –Š‡ ’ƒ–‹‡– ƒ„‘—–
the nature of the disease and advised him a regular ophthalmic
followup while he was advised Yag laser for his malar lesion
from the department of dermatology.

Nevus of Ota (naevus fuscocaeruleus ophthalmomaxillaris)
is a rare disorder of periocular hyperpigmentation associated
with scleral melanosis. It is said to be most prevalent in Japan,
rare in Indians and is considered a congenital disorder. Ota
in 1939 described the lesion as unilateral, patchy, bluish gray
†‹•…‘Ž‘—”ƒ–‹‘ ‘ˆ –Š‡ •‹ ‘ˆ –Š‡ ˆƒ…‡ •—’’Ž‹‡† „› –Š‡ ϐ‹”•– ƒ†
second divisions of the trigeminal nerve with involvement of
the periorbital region, temple, forehead, malar area, and nose. It
is predominantly seen in females and spontaneous regression
has not been observed1.

The etiology is thought to be melanocytes that have
persisted and not migrated completely from the neural crest to
the epidermis during the embryonic stage2. It is predominantly
an asymptomatic condition though in a few case reports
sensory loss has also been reported. Aggravating factors include
infection, trauma, ultraviolet exposure, fatigue, menstruation,
insomnia and climatic changes. Ocular melanosis can affect the
sclera, cornea, iris, choroid, optic nerve, retrobulbar fat, orbit,
periosteum, and extraocular muscles3. Ocular pigmentation
is mostly ipsilateral. The pigment is deep in the conjunctiva
and does not move with it, in contrast to benign epithelial
melanosis. Besides ocular pigmentation, other features like
glaucoma, uveitis, cataracts, retinitis pigmentosa and palatal
mucosa involvement is also known.

Differential diagnosis for skin lesions of nevus of Ota
includes mongolian spot, melasma, blue nevus, and drug-induced

www. dos-times.org 47

SNAPSHOT

Figure 3: 5MKP NGUKQP
HTQPVCN XKGY papular lesions, and variegations in 2. Sharma G, Nagpal A. Nevus of Ota
color) within the involved skin, ocular with Rare Palatal Involvement: A Case
clinical examination and history. Skin tissues, or mucosal tissues. Report with Emphasis on Differential
biopsies are required only if clinical Diagnosis. Case Reports in Dentistry.
changes are suspected of malignant The treatment options for nevus of 2011;28:2011.
transformation (e.g., ulceration, new Ota includes cryotherapy, dermabrasion,
•—”‰‹…ƒŽ ‡š…‹•‹‘ ƒ† …‘•‡–‹… …ƒ‘—ϐŽƒ‰‡ 3. Kumar MA, Venkatesh E, Srikanth
but now Nd:YAG laser remains the D, Prashanth P. The case of a rare
mainstay of treatment4. In light of the nevus with palatal, facial, and scleral
above discussion, regular follow-up is pigmentation. Univ Res J Dent 2013;
mandatory for persons with nevus of ota. 3:131-3.

REFERENCES 4. Shrestha SB, Khatiwada L. Q-switched
Nd: YAG Laser Treatment of Nevus of
1. Kumari R, Thappa DM. Familial nevus Ota: A Study of 25 Nepalese Patients.
of ota. Indian J Dermatol 2006;51:198- Nepal Journal of Dermatology,
9. Venerology & Leprology 2013;11: 45-
48.

1. Deptt. of Ophthalmology, Regional Hospital Hamirpur, District Hamirpur 177001, Himachal Pradesh, India.
2. Deptt. of Dermatology, Regional Hospital Hamirpur, District Hamirpur 177001, Himachal Pradesh, India.

Dr.Anubhav Chauhan MS1 Dr. Neeraj Sharma MD2 Dr. Shashi Datt Sharma MS1

Financial Interest: Š‡ ƒ—–Š‘”• †‘ ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

48 DOS TIMES - MAY-JUNE 2016

MONTHLY MEETING KORNER

NEURO-OPHTHALMOLOGY
GRAND ROUNDS PRESENTATION

Dr. Sumit Monga MS, DNB, FRCS (Glasg),
FLVPEI (Hyderabad),
Consultant, Pediatric, Strabismus and Neuro-ophthalmology
Service, Centre for Sight, Delhi NCR

CASE NO.1 Figure 1: %NKPKECN 2TGUGPVCVKQP %CUG C 'UQFGXKCVKQP YKVJ
OKPKOCN 4KIJV CDFWEVKQP FGſEKV $ )TQUUN[ CU[OOGVTKE FKUE GFGOC
A 25 year lady (obese built) came with inward deviation of
.GHV 4KIJV
her right eye since past one month. She also experienced faint
horizontal doubling of images. She had a refractive surgery of unilateral papilledema. Optic nerve sheath anomaly was
done, elsewhere, 6 years back (no previous documents/ detailed postulated as protecting the optic nerve from high intracranial
‹ˆ‘”ƒ–‹‘ ™ƒ• ƒ˜ƒ‹Žƒ„Ž‡ȌǤ Š‡”‡ ™ƒ• ‘ Š‹•–‘”› ‘ˆ ƒ› •’‡…‹ϐ‹… pressure. Another hypothesis is a possible difference in
antecedent medical illness or medication use. On examination, the lamina cribrosa between the two optic disks. Tso et al
she had a BCVA of 6/60 in right eye (-8 D/-1 D cyl/10 degree) found that experimental elevated intracranial pressure can
and 6/6p in left eye (plano). The pupils were normal sized, cause axoplasmc blockage at the level of the lamina cribrosa.
round shaped and reacting briskly to light and near stimulus ϐŽ‘™ •–—†‹‡• ™‹–Š …‘’—–‡† –‘‘‰”ƒ’Š›Ȃƒ••‹•–‡†
in both eyes. The colour vision was normal (16/16) in left cisternography in IIH patients, who did not improve with
eye, while in right eye, the response was unreliable. Both eyes medical ICP reduction, showed impaired contrast-loaded CSF
anterior segment exam (including IOP) were within normal ϐŽ‘™ ‹–‘ –Š‡ —„ƒ”ƒ…Š‘‹† •’ƒ…‡ ‘ˆ ‘’–‹… ‡”˜‡ǡ ‹†‹…ƒ–‹‰
limits. Orthoptic review revealed an esodviation (25 PD for …‘’ƒ”–‡–ƒ–‹‘Ǥ  ‘—” …ƒ•‡ǡ ϐ‹‡ •‡…–‹‘• ‘ˆ ‘”„‹–ƒŽ ‹ƒ‰‹‰
†‹•–ƒ…‡ ƒ† ‡ƒ”Ȍ ™‹–Š ”‹‰Š– ‡›‡ ‹‹ƒŽ ƒ„†—…–‹‘ †‡ϐ‹…‹– revealed that a kink in the right eye optic nerve was present
(-1 grade, (Figure 1, top panel). On fundus exam, the media (presumably secondary to enlarged right globe of high myopia,
were clear in both eyes. The right eye optic disc was hyperemic Figure 4). This kink in the right eye optic nerve was presumably
with trace disc edema (Frisen grading grade 0), while the left ‡…Šƒ‹…ƒŽŽ› ‘„•–”—…–‹‰ –Š‡ ϐŽ‘™ –‘ –Š‡ ‘’–‹… ‡”˜‡ Š‡ƒ†
‡›‡ ‘’–‹… †‹•… •Š‘™‡† ϐŽ‘”‹† †‹•… ‡†‡ƒ ȋ ”‹•‡ ‰”ƒ†‡ ͶȌǡ ™‹–Š (leading to only a trace ONH swelling, inspite a raised CSF
peripapillary edema just stopping short of fovea (Figure 1, pressure). To the best of our knowledge, this unique anatomic
„‘––‘ ’ƒ‡ŽȌǤ Š‡ ˜‹•—ƒŽ ϐ‹‡Ž† ƒ••‡••‡– ”‡˜‡ƒŽ‡† ‘ ‰”‘•• variation in the optic nerve, leading to marked asymmetric
˜‹•—ƒŽ ϐ‹‡Ž† †‡ˆ‡…– ‹ ”‹‰Š– ‡›‡ ȋ…‘ˆ”‘–ƒ–‹‘ ϐ‹‡Ž†Ȍǡ ™Š‹Ž‡ ƒ optic disc edema in IIH, has not been reported yet in literature.
‡Žƒ”‰‡† ϐ‹‡Ž† †‡ˆ‡…– ™ƒ• †‘…—‡–‡† ‹ –Š‡ Ž‡ˆ– ‡›‡Ǥ
The learning pearl is that clinicians should not rule out
In a case of disc edema, the management approach varies, the possibility of papilledema in cases of unilateral or highly
depending on whether the edema is unilateral or bilateral asymmetric swollen disks
(Figure 2). The marked asymmetry in disc edema in our case was
perplexing and we were looking for guiding clues. On careful CASE NO.2
exam, we noted the difference in glow between the two eyes.
Axial length testing revealed marked asymmetry (32.01 mm OD An elderly gentleman (81 yr.) presented with redness and
vs. 25.18 mm OS). We proceeded ahead on lines of papilledema pain of left eye, since 3 weeks (Figure 5). Systemic medical
management (grossly asymmetric). MRI Brain imaging and history was unremarkable. He was being treated with topical
subsequent Magnetic resonance venogram (MRV) were found ƒ–‹„‹‘–‹…•ǡ ™‹–Š‘—– ƒ› „‡‡ϐ‹–Ǥ ™ƒ• ͸Ȁ͸’ ‹ „‘–Š ‡›‡•
to be unremarkable. Patient was referred to the neurologist (Left eye hazy vision). The patient was pseudophakic in the
for a cerebrospinal tap, which revealed an increased CSF ”‹‰Š– ‡›‡Ǥ ‘•‹–‹˜‡ ‘…—Žƒ” ϐ‹†‹‰• ‹ –Š‡ Ž‡ˆ– ‡›‡ ‹…Ž—†‡† ‹Ž†
opening pressure (280 mm of H2O) and normal CSF analysis. proptosis, conjunctival and episcleral congestion (with dilated,
A diagnosis of Idiopathic intracranial hypertension (IIH) was tortuous vessels) with quiet AC and cataract (grade 2) (Figure
…‘ϐ‹”‡†Ǥ Š‡ ’ƒ–‹‡– ”‡•’‘†‡† ™‡ŽŽ –‘ †‹—”‡–‹… –Š‡”ƒ’› ƒ† 5). The ocular motility was limited in the left eye (Figure 5).
optic disc edema and esodeviation of the right eye resolved in
about a month time (Figure 3).

The possibility (uncommon) of having unilateral or
asymmetric optic disc edema (difference of 2 or more grade
between the two eyes) in IIH, is reported in literature. Infact,
in IIH treatment trial (JAMA Neurology 2014), almost 7% of
patients (N=135) were having asymmetric optic disc edema.
Few hypotheses have tried to explain the atypical presentation

www. dos-times.org 49

MONTHLY MEETING KORNER

Figure 2 Figure 3: 4GUQWNVKQP QH GUQFGXKCVKQP
VQR RCPGN CPF FKUE GFGOC CHVGT
OQPVJ QH QTCN CEGVC\QNCOKFG VTGCVOGPV
DQVVQO RCPGN

Figure 4: -KPMKPI QH 4KIJV G[G 1RVKE PGTXG
FWG VQ 'NQPICVGF INQDG QH Figure 5: %NKPKECN RTGUGPVCVKQP %CUG %QPIGUVGF NGHV G[G YKVJ OKNF
JKIJ /[QRKC ECWUKPI OGEJCPKECN QDUVTWEVKQP QH %5( ƀQY RTQRVQUKU YKVJ NKOKVCVKQP QH QEWNCT OQXGOGPVU FKNCVGF VQTVWQWU
GRKUENGTCN XGUUGNU QH NGHV G[G CTG XKUKDNG KP DQVVQO RCPGNU

Figure 7

Figure 6: 4CFKQNQIKE ſPFKPIU C &KNCVGF NGHV UWRGTKQT QRJVJCNOKE XGKP $ 'PNCTIGF NGHV Figure 8: 4GUQNWVKQP QH NGHV G[G EQPIGUVKQP CPF TGUVQTCVKQP
TGEVK OWUENGU % /4+ CPIKQITCRJ[ TGXGCNGF NQY ƀQY %%(
QH QEWNCT OQVKNKV[ CHVGT ENQUWTG QH %%(

50 DOS TIMES - MAY-JUNE 2016

MONTHLY MEETING KORNER

Fundus was unremarkable in both eyes. radiologist for ruling out a carotid carotid compression maneuver
IOP was asymmetric (9 mm OD, 17 mm …ƒ˜‡”‘—• ϐ‹•–—ŽƒǤ ˜ƒŽ—ƒ–‹‘ ™‹–Š (supervised massage over neck
OS). Auscultation over the orbit revealed ƒ‰‹‘‰”ƒ’Š› ”‡˜‡ƒŽ‡† ƒ Ž‘™ ϐŽ‘™ …ƒ”‘–‹†
a faint bruit. Careful past history revealed …ƒ˜‡”‘—• ϐ‹•–—Žƒ ȋ Ȍ ȋ †‹”‡…– –›’‡ǡ area). Within 6 weeks, the patient showed
that the patient had suffered an episode †—”ƒŽ ϐ‹•–—ŽƒǢ ƒ””‘™ǯ• Žƒ•• ϐ‹•–—ŽƒȌ remarkable improvement with resolution
of drooping of the right eye with double ȋ ‹‰—”‡ ͸Ȍ Ǥ ƒ”‘–‹† …ƒ˜‡”‘—• ϐ‹•–—Žƒ• ƒ”‡ of the congestive signs of the left eye and
vision (suggestive of a third nerve of two main variety : Direct type (shunt complete restoration of ocular motility
paresis), about 1 year back. A differential between Internal carotid artery and (Figure 8). The IOP also declined in the
diagnosis of arterio-venous malformation …ƒ˜‡”‘—• •‹—•Ǣ Š‹‰Š ϐŽ‘™ ϐ‹•–—ŽƒǢȌ ƒ† left eye (OD 9 mm Hg; OS 11 mmHg). The
(cranial/ orbital), thyroid eye disease, indirect type (shunt between cavernous learning pearl: CCF should be suspected
‘Ǧ•’‡…‹ϐ‹… ‘”„‹–ƒŽ ϐŽƒƒ–‘”› †‹•‡ƒ•‡ sinus and dural branches of internal in a patient, who suddenly develops an
(NSOID), orbital space occupying lesion, carotid artery, external carotid artery acute red eye with proptosis with ocular
chronic conjunctivitis and glaucoma ‘” „‘–ŠȌ ȋ ‹‰—”‡ ͹ȌǤ Š‡ †‹”‡…– ϐ‹•–—Žƒ• ‘–‹Ž‹–› †‡ϐ‹…‹–Ǥ
were kept. Serological investigations are mostly due to head injury, while the
helped rule out vascular risk factors ‹†‹”‡…– ϐ‹•–—Žƒ• …ƒ ‘……—” •’‘–ƒ‡‘—•Ž›ǡ REFERENCES
and thyroid dysfunction. MRI imaging due to either congenital malformations
revealed dilated superior ophthalmic like preexisting aneurysms, or diseases 1. Bidot S etal. Asymmetric Papilledema in
vein and thickened extra- ocular recti causing artherosclerosis (HT, DM).
muscles (Figure 6). The patient was The patient was advised conservative Idiopathic Intracranial Hypertension. J
•’‡…‹ϐ‹…ƒŽŽ› ”‡ˆ‡””‡† –‘ ƒ ‹–‡”˜‡–‹‘ƒŽ management with an external manual
Neuro-Ophthalmol 2015; 35: 31-36.

2. Keltner etal.Dural and Carotid

Cavernous Sinus Fistulas.

Ophthalmology 94:1585-1600, 1987.

Financial Interest: Š‡ ƒ—–Š‘” †‘‡• ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

www. dos-times.org 51

DIAGNOSTICS DISCUSSION

DIAGNOSIS OF ATYPICAL VIRAL RETINITIS BY
AQUEOUS PCR

†‹–›ƒ ›ƒ‰‹ǡ ŠƒŠƒƒ ƒœ—†ƒ”ǡ •Š‹•Š ƒƒ”

A70 years old healthy lady presented with blurred
vision in the left eye since a few weeks. There
was mild pain and redness. She had suffered
herpes zoster dermatomal involvement on her
back 5 months ago.
Her BCVA was 6/6, N6 and 6/24P. The left
eye showed multiple medium sized keratic precipitates, AC cells
1-2+, early cataract (Figure 1) and vitreous cells 2+. The view of
the retina was hazy, but an area of retinitis could be seen in the
superotemporal periphery and clumps of exudates around the
optic nerve head which appeared edematous (Figure 2). Her
IOP was 20 and 34 mmhg and gonioscopy showed open angles
with pigmentation++ BE. In view of the peripheral retinitis in

Figure 1: #PVGTKQT UGIOGPV RJQVQITCRJ UJQYKPI OWNVKRNG OGFKWO Figure 2A: (WPFWU RJQVQITCRJ QH NGHV G[G UJQYKPI JC\[ OGFKC GZWFCVGU
UK\GF MGTCVKE RTGEKRKVCVGU QP FKUE UWTHCEG CPF OKNFN[ GFGOCVQWU FKUE Figure 2B: 5WRGTQVGORQTCN
SWCFTCPV UJQYKPI CP CTGC QH TGVKPKVKU

Figure 3: (WPFWU RJQVQITCRJ UJQYKPI RTQITGUUKQP QH TGVKPKVKU VQYCTFU VJG RQUVGTKQT RQNG 9KFG CPINGF ((# RJQVQ UJQYKPI C JQV FKUE CPF UVCKPKPI
KP VJG UWRGTQVGORQTCN SWCFTCPV KP VJG CTGC QH TGVKPKVKU
EQWTVGU[ &T 5JKUJKT 0CTCKP

www. dos-times.org 53

DIAGNOSTICS DISCUSSION an immunocompetent individual and a
recent history of herpes zoster infection,
Figure 4: 2%4 TGRQTV YCU RQUKVKXG HQT %/8 IGPQOG CPF PGICVKXG HQT *58 CPF CPF 8<8 a diagnosis of left hypertensive panuveitis
Figure 5: (WPFWU RJQVQITCRJ CHVGT VTGCVOGPV UJQYKPI TGUQNWVKQP QH TGVKPKVKU with acute retinal necrosis probably
due to Varicella Zoster was made and
the patient was started on intravenous
acyclovir, topical steroids, cycloplegics
and IOP lowering agents.

Though she was asked to return
earlier the patient came back a week
later and was found to have worsened
dramatically though she had strictly
adhered to the treatment advised. Her
BCVA had dropped to 3/60 and the
retinitis had progresses towards the
posterior pole. This was better visualized
‘ ™‹†‡ϐ‹‡Ž† ™Š‹…Š ”‡˜‡ƒŽ‡† ƒ Š‘–
disc and staining of the area of retinitis in
the superotemporal quadrant extending
towards the macula (Figure 3).

Investigations revealed normal
CBC+ESR, Serum ACE, VDRL, KFT, LFT,
Blood sugars and mantoux was anergic,
Elisa for both IgG and IgM for toxoplasma
was negative almost excluding it as a
causative agent. The IgG was positive for
Rubella, CMV and HSV1 and 2 but IgM was
negative for all. CECT chest was normal
except a few small sub cm lymph nodes.

As the patient was not responding to
acyclovir and the disease was progressing
”ƒ’‹†Ž›ǡ ™‡ ‡‡†‡† –‘ —”‰‡–Ž› ϐ‹† –Š‡
cause of retinitis and decided to do an
AC tap for aqueous PCR for viruses. The
report was positive for CMV genome and
negative for HSV 1 and 2, VZV (Figure
4). She was given a dose of intravitreal
gancyclovir and started on Tab
Valgancyclovir. Eventually she responded
and regained 6/24 (Figure 5).

This case is presented to exhibit the
role of PCR in establishing the diagnosis
‹ ƒ †‹ˆϐ‹…—Ž– ˜‹•‹‘ –Š”‡ƒ–‡‹‰ •‹–—ƒ–‹‘Ǥ

Cornea Services ICARE Eye Hospital, NOIDA, India.

Dr.Aditya Tyagi MBBS, DO Dr. Shahana Mazumdar MS Dr.Ashish Kakkar MS

Financial Interest: Š‡ ƒ—–Š‘”• †‘ ‘– Šƒ˜‡ ƒ› ϔ‹ƒ…‹ƒŽ ‹–‡”‡•– ‹ ƒ› ’”‘…‡†—”‡Ȁ’”‘†—…– ‡–‹‘‡† ‹ –Š‹• ƒ—•…”‹’–Ǥ

54 DOS TIMES - MAY-JUNE 2016

DOS CROSSWORD

ROSSWORD

Episode-6

Dr. Manish Mahabir MD
Senior Resident,
Dr. R.P. Centre,All India Institute of Medical Sciences,
New Delhi, India

1

2

4 6 3
5 9 7
8
10 11
12

13 14

15

ACROSS DOWN

2. Declaration of ____ gave a revision of the Hippocratic Oath(6) 1. Vertical lines on the temporal side of the disc early in the
process of papilledema(6)
ͷǤ ‘ ˜ƒŽ˜‡† ‰Žƒ—…‘ƒ ϐ‹Ž–”ƒ–‹‘ †‡˜‹…‡ ƒ†‡ ‘ˆ •–ƒ‹Ž‡••
steel(7) 3. Ring of pigment accumulation at the zonular attachments to
the lens(9)
9. Clinical triad of asymmetric and pendular nystagmus, head
nodding, and torticollis(13) 4. Preferred Reporting Items for Systematic Reviews and Meta-
Analyses(6)
10. Muscle of the lid that receives sympathetic innervation(6)
6. never to be done in Duane retraction syndrome(9)
13. Toxicity of this systemic medication causes one to see yellow 7. Yellow patches overlying area of choroidal infarction in
(Xanthopsia)(7)
hypertension(8)
14. Syndrome with absence of septum pellucidum, optic nerve 8. Principle of stereotest used in Lang’s test(11)
hypoplasia and pituitary abnormalities(9) 11. Thermal pulsation for meibomian gland dysfunction(8)
12. Paradox in probability and statistics, in which a trend that
15. Drug under trial for the treatment of aniridia(8)
appears in different groups of data disappears or reverses
when these groups are combined(8)

www. dos-times.org 57

QUICK PICKS

BECHET DISEASE

Dr. Meenakshi Wadhwani MS DIAGNOSTIC EVALUATION
Community Ophthalmology
Dr. Rajendra Prasad Centre for Ophthalmic Fluorescein angiography demonstrates early blockage
Sciences,AIIMS, New Delhi in areas of retinitis with late staining, staining and leakage of
retinal vessels in the mid to late phases, and areas of capillary
Bechet’s Disease, is a chronic, relapsing multisystem drop-out.
‹ϐŽƒƒ–‘”› †‹•‘”†‡” ‘ˆ —‘™ ‡–‹‘Ž‘‰› …Šƒ”ƒ…–‡”‹œ‡† „›
‹–”ƒ‘…—Žƒ” ‹ϐŽƒƒ–‹‘ǡ ‘”ƒŽ ƒ† —…‘•ƒŽ —Ž…‡”ƒ–‹‘ ƒ† •‹ Indocyanine green (ICG) angiography demonstrates areas
lesions. ‘ˆ Š›’‡”Ǧ ƒ† Š›’‘ϐŽ—‘”‡•…‡…‡Ǥ

EPIDEMIOLOGY TREATMENT

It is more commonly seen in patients from Mediterranean Prompt and aggressive systemic therapy with
Basin and Japan. …‘”–‹…‘•–‡”‘‹†• ƒ• –Š‡ ϐ‹”•–ǦŽ‹‡ ƒ‰‡– ‹• …”‹–‹…ƒŽǤ Š‡ ƒ‹ ‰‘ƒŽ
of treatment is to decrease the frequency and severity of the
In the United States, the prevalence is 8.6 in 1,00,000 ‹ϐŽƒƒ–‘”› ‡’‹•‘†‡•Ǥ ‹–‹ƒŽŽ›ǡ •‘‡ ’ƒ–‹‡–• ƒ› ‡‡†
persons, and is as high as 25 to 400 in 1,00,000 in Mediterranean ’—Ž•‡ •–‡”‘‹†• –‘ …‘–”‘Ž ƒ…—–‡ ‹ϐŽƒƒ–‹‘Ǥ ‡…‘† Ž‹‡
countries. agent include Immunosuppressive agents, which typically
include cyclosporine, azathioprine, mycophenolate mofetil,
OCULAR MANIFESTATIONS ƒŽ›Žƒ–‹‰ ƒ‰‡–• ȋ‹Ǥ‡Ǥǡ ›–‘šƒȌǡ ‹ϐŽ‹š‹ƒ„ǡ ‹–‡”ˆ‡”‘ǦƒŽ’Šƒǡ ‘”
a combination of these agents.
Ocular involvement occurs in approximately 70% of
’ƒ–‹‡–• ™‹–Š ‡Š…‡–ǯ• †‹•‡ƒ•‡ ƒ† ‹• –›’‹…ƒŽŽ› „‹Žƒ–‡”ƒŽ ȋε͹ͲΨȌǤ PROGNOSIS
Posterior/panuveitis is the most common form of uveitis in
these patients. Men are slightly more affected than women. It The visual prognosis depends upon the extent of the
affects young adults with the mean age of onset between 25- posterior segment involvement. Timeliness of therapy and
35 years of age. (may also occur in children). Affected patients •—•–ƒ‹‡† …‘–”‘Ž ‘ˆ ‹ϐŽƒƒ–‹‘Ǥ
are thought to have a genetic predisposition, and it has been
associated with HLA-B51. Younger age at onset, poor vision at presentation, posterior
•‡‰‡– †‹•‡ƒ•‡ǡ ’‡”•‹•–‡– ‹ϐŽƒƒ–‘”› ƒ…–‹˜‹–›ǡ ’‘•–‡”‹‘”
Signs Systemic manifestations: oral ulcers are the most synechiae, elevated intraocular pressure and hypotony are
common manifestation occurring in 98% of patients, followed poor prognostic indicators. With prompt and aggressive
by skin lesions (90%), and genital ulcers (77% to 85%). Ocular therapy, structural complications and visual impairment can be
signs usually manifest as an explosive anterior uveitis typically minimized.
™‹–Š ƒ •–‡”‹Ž‡ǡ ϐ‹š‡† Š›’‘’›‘Ǥ ‹–”‹–‹•ǡ ‡…”‘–‹œ‹‰ ”‡–‹‹–‹•ǡ
retinal vasculitis, retinal hemorrhages and retinal edema, Complications are frequent and occur in 60% to 90%
vitreous hemorrhage, retinal neovasularization, and vitreous of patients. In addition to the development of cataracts and
hemorrhage also occur. glaucoma, posterior synechiae, macular edema, epiretinal
membrane, retinal neovascularization, vitreous hemretinal
ƒ”‡ ‘…—Žƒ” ƒ‹ˆ‡•–ƒ–‹‘• ‹…Ž—†‡ ‡’‹•…Ž‡”‹–‹•ǡ ϐ‹Žƒ‡–ƒ”› vein occlusion, branch retinal artery occlusion and retinal
keratitis, conjunctivitis and extraocular muscle paralysis †‡–ƒ…Š‡– …ƒ ‘……—”Ǥ ‹‰‹ϐ‹…ƒ– ˜‹•‹‘ Ž‘•• ȋδʹͲȀʹͲͲȌ ‘……—”•
secondary to neuro-Behcet’s disease. in 20% to 30% of patients within 5 years of disease onset.

International Study Group ‘†‹ϐ‹‡†
ƒ’ƒ‡•‡ ‡…Š‡–ǯ• ‹•‡ƒ•‡ ‡•‡ƒ”…Š ‘‹––‡‡ ”‹–‡”‹ƒ
Criteria for Bechet’s Disease
Recurrent Oral ulcers ƒŒ‘” ”‹–‡”‹ƒ
ȋη ͵ –‹‡•Ȁ›‡ƒ”Ȍ Š Recurrent oral aphthous ulcers
Š Genital ulceration
† ʹ ‘ˆ –Š‡ „‡Ž‘™ …”‹–‡”‹ƒǣ Š Ocular disease
Š Recurrent genital ulcers Š Skin Disease (Erythema nodosum, cutaneous hypersensitivity,
Š Ocular disease (Uveitis)
Š Skin Lesions (Erythema nodosum, pseudofolliculitis, thrombophlebitis)

papulopustular lesions, acneiform lesions) Minor Criteria
Š Positive Pathergy test (skin prick test)
Š Arthritis
Diagnosis Criteria Š Gastro intestinal disease (Intestinal ulcers)
Š Complete type Š Vascular disease (Occlusive vasculitis,aneurysm)
Š Incomplete type Š CNS disease (Neuropsychiatric symptoms, parenchymal lesions,

Š Suspect type vascular thrombosis, vasculitis,meningitis/encephalitis)
Š Possible type:
All 4 major criteria
3 major / 2 major+2 minor criteria
it is typical ocular disease + 1 major (or 2 minor) criteria
2 major criteria (Other than ocular)
1 major criteria

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