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Published by DOS DOS, 2020-05-20 06:19:47

DOS_jan_2011

DOS_jan_2011

Contents

E5 ditorial Miscellaneous

Focus 47 How to Maintain Practice Growth

13 Primary Angle Closure Glaucoma Vipin Sahni MS

49 Scheme for Participation of Voluntary Organisations

Uveitis Clinical Monthly Meeting

19 Juvenile Idiopathic Arthritis 53 Clinical Talk: Changing Trends in the Management of ARMD

Amit Khosla Manisha Agarwal MS, DNB

Cataract 61 Clinical Case-2: Tissue Plasminogen Activator Assisted Treatment

19 Management of Small Pupil in Manual Small Incision of Choroidal Neovascular Membrane
Narula Rohini Grover, H.K. Tewari, S.N. Jha, Amit Khosla,
Cataract Surgery Neeraj Manchanda, Nidhi Tanwar
Ruchi Goel, KPS Malik, Sushil Kuma
F69 orthcoming Events
Retina
Columns
31 Epiretinal Membrane
75 Membership Form
Bhuvan Chanana, Vinod Kumar, Ved Prakash Gupta
Tear sheet
Glaucoma
83 Management of Neo-vascular Glaucoma
37 Role of Ocular Response Analyzer in Measurement of IOP
Deven Tuli, Amit Khosla
Rakhi Kusumesh, Tanuj Dada, Sasikala, Anita Panda

Neurophthalmology

41 Adie’s Pupil

Shilpa Goel, Savleen Kaur, Prem Vardhan, Yuvika Bansal, Gaurav Goel

www.dosonline.org 3

4 DOS Times - Vol. 16, No. 7, January 2011

Editorial

Dear Colleagues and Friends,

A very happy new year to all of you.

We take great pride in sending you this National Issue of the DOS Times and hope you will find it useful.

Please give us your feedback and suggestions to make these issues more relevant to your practice.

Annual Conference

The Annual Conference of the Delhi Ophthalmological Society is just 3 months away.Our 62nd annual conf from
15th to 17th April 2011 at Hotel Ashok, Delhi.

We Promise you a never before conference experience. Let me share a few highlights with you:

Dr Om Parkash Oration- Starts this Year and we present to you the most distinguished Dr Michael Knorz from Germany. He is a Pioneer
of Lasik surgery and has the singular achievement of training many Indian Ophthalmologists In Lasik Surgery.

Joint Session With BJO- another first! The editor in chief of BJO Dr A D Singh is coming specially to kick off this joint session of DOS
and British Journal Of Ophthalmology.{Last Year-Dr Dua the other editor in chief of BJO gave a lecture on Stem Cell Research in a special
meeting of the DOS!}

Show CASE-Alumni Sessions. Inviting the alumni of all the medical colleges of Delhi to show case their work and research in special sessions
during the conference. All who wish to participate, my contact me immediately.

DOS is for all Indian Ophthalmologists

For Ophthalmologists from outside delhi, we now have special facilities for continuing Ophthalmic Training;

DOS on Facebook-Lectures and Presentations in the form of videos uploaded on Facebook in all Ophthalmic Subspecialities.

Skill Transfer Workshops webcast and available on the DOS website.

Phaco fellowship Training- about to begin, hands on Phaco Training in reputed delhi eye hospitals and out of 8 seats available at present , 4
have been reserved for DOS members from outside delhi.

Looking Back

Dear Friends, my tenure will end with the annual conference. I have enjoyed tremendously my two years as the secretary of this awesome
organisation and i have tried to give my best. From uploading educational videos on facebook, to live webcasting of skill transfers and now
the Phaco fellowhips and the innovations in the conference-I have tried to look beyond the horizon. I invite you to the annual conference,
and request to register as soon as possible. Online registration is open.
Yours Truly.
Thanking you,

Dr Amit Khosla
Secretary,
Delhi Ophthalmological Society

Editor-in-chief

Amit Khosla MD, DNB

Advisor DOS Correspondents DOS Office

H.K. Tewari MD, FAMS, DNB Rajpal MD Nidhi Tanwar MD Room No. 2225, 2nd Floor,
Ashok K. Grover MS FRCS S.P. Garg MD, MNAMS Gagan Bhatia DOMS New Building, Sir Ganga Ram Hospital,
J.K.S. Parihar MS, DNB A.K. Singh MS Vipul Nayar DOMS, DNB, MNAMS Rajender Nagar, New Delhi - 110 060
Shashi N. Jha MD J.L. Goyal MD, DNB Daraius Shroff MS Tel.: 91-11-65705229
Sudershan Khokhar MD Ritika Sachdev MS

Email: [email protected]

Editorial Board Rajiv Sudan MD Deependra Vikram Singh MD Website: www.dosonline.org
Neera Agarwal MS Sanjiv Mohan MS
Ruchi Goel MS, DNB, FICS Poonam Jain MS Ajay Kumar Agarwal MS, DNB Cover Design by: Amit Chauhan
Sanjeev Gupta MD, DNB Neeraj Verma MS Anuj Mehta MS Published by: Dr. Amit Khosla for Delhi Ophthalmological Society
Sanjay Khanna MS Vivek Gupta MD, DNB Naginder Vashisht MD
Y.C. Gupta MS Amit Gupta MD Deven Tuli MS Printers: Symmetrix
Sarita Beri MD S.K. Mishra MS Prakash Agarwal MD E-mail: [email protected]
Devindra Sood MS J.S. Guha MS V. Rajshekhar MS
Umang Mathur MS Manisha Agarwal MS Jasmita Popli MS
Rajesh Sinha MD, DNB Hardeep Singh MD Himanshu R. Gupta MS
Rohit Saxena MD Kapil Midha MD
Hemlata Gupta MS, DNB

www.dosonline.org 5

Emergency Retina Care

A Centre for Retina & Vitreous Surgery

8, Siri Fort Road, New Delhi - 110 049
Ph.: 65293455, E-mail: [email protected]

Helpline for

Endophthalmitis ROP (Retinopathy of Prematurity)
Nucleus Drop Ocular Trauma

Contact: Dr. Amit Khosla
(9811060501)
Dr. Sanjeev Gupta

(9810075900)

Sama Nursing Home, 8, Siri Fort Road, New Delhi

DOS Election

Applications are invited from Delhi Members of Delhi Ophthalmological Society for the posts of : Vice President (1 Post),
Secretary (1 Post), Joint Secretary (1 Post), Treasurer (1 Post), Editor (1 Post), Library Officer (1 Post), & Executive Member
(8 Posts).

The eligibility criteria for different Posts prescribed in DOS Constitution (1998) will be followed. Application should be
submitted on a plain paper duly proposed and seconded by a member of DOS (not in arrears). Application should reach
Secretary Office latest by 1st February, 2011 (2 p.m.). Last date of withdrawal is 1st March, 2011 (5 p.m.) Election will be
held during the Annual DOS Conference on 17th April, 2011.

Secretary, DOS

DOS Election

If you want to VOTE in the forthcoming DOS Election, Please ensure that your correct address (office and residential) is
available at the DOS secretariat by 15th February, 2011. Outstation members are not permited to vote in DOS Election.

Secretary, DOS

Resolutions / Suggestions for General Body Meeting

DOS members are requested to send us their suggestions or resolutions to be discussed in the general body meeting to
be held on 17th April, 2011. These will be discussed first in the executive meeting and then forwarded to General Body
Meeting. Last date of receipt 15th February 2011.

– Secretary DOS

6 DOS Times - Vol. 16, No. 7, January 2011

Primary Angle Closure Glaucoma Focus

Dr. S.S. Pandav Dr. Chandrima Paul Dr. Sirisha Senthil Dr. P. Sathyan
MS MS MS, FRCS MS

Dr. B.K. Nayak Dr. Kirti Singh
MD MD, DNB, FRCS

Blindness from angle closure glaucoma is preventable. Even though epidemiological studies show that open angle glaucoma
is more common than angle closure worldwide, the morbidity from angle closure is more. We asked a panel of Indian
glaucomatologists their opinion and views on various aspects of angle closure.

Dr. S.S. Pandav, MS, (SSP): Prof. & Head, Glaucoma Service, Post Graduate Institute of Ophthalmology, Chandigarh.
Dr. Chandrima Paul, MS, (CP): Director, Glaucoma Service, B.B. Eye Foundation, Kolkata,
Dr. Sirisha Senthil, MS, FRCS, (SS):Consultant, VST Centre for Glaucoma, L.V. Prasad Eye Institute, Hyderabad.
Dr. P. Sathyan, MS, (PS): Head Glaucoma Service, Aravind Eye Hospital, Coimbatore.
Dr. B.K. Nayak, MD, (BKN): Head Dept. of Ophthalmology, P.D..Hinduja National Hospital & MRC, Mumbai.
Dr. Kirti Singh, MD, DNB, FRCS, (KS): Professor, Glaucoma Division, Guru Nanak Eye Centre, Maulana Azad Medical
College, New Delhi.

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

DS: What is the commonest type of glaucoma you see in your DS: Angle closure is a loose term. What does it mean to you?
practice?
SSP: I means patient either has angle closure or angle closure
SSP: Secondary glaucoma both SOAG and SACG. Over half of glaucoma. PACS is usually referred to as ‘narrow angles’
our clinic patient are secondary glaucomas. But angle closure could mean any of these.

CP: Two thirds PAOG and one third ACG. CP: Those patients in whom I cannot see the trabecular
meshwork for more than 180 degrees on gonioscopy or
SS: PACG, POAG, Secondary glaucomas. those who have a shaffers grading of 2 or less in more
than 180 degrees would be labeled as probables for angle
PS: POAG and PACG in equal proportions closure.

BKN: The commonest type of glaucoma seen by me during my SS: Posterior trabeculum closed more than 180 degrees.
practice so far is Primary Open Angle Glaucoma.
PS: It means Primary Angle Closure Disease.
KS: I practice in a tertiary care teaching and referral hospital
of North India. The commonest type of glaucoma I see are: BKN: Angle closure is when the anterior chamber is shallow and
Chronic ACG > OAG> Secondary > Congenital. angles are narrow on gonioscopy with high probability of

www.dosonline.org 13

getting occluded later. It includes appositional closure as CP: Yes, family history of ACG and hypermetropia.
well as synechial closure.
SS: History has a role to find out approximately the duration
KS: An occludable angle is when the posterior pigmented of disease or if thee had been any acute episodes
trabecular meshwork is not visible for at least 3 clock hours
during gonioscopy. Narrow angle term is used when the PS: Yes history taking does have its role especially in subacute
posterior pigmented trabecular meshwork was not visible angle closure.
for at least 180°. A steep iris insertion anterior to scleral
spur also makes the case an angle closure suspect. BKN: Yes, history taking definitely has a role. It helps in diagnosis
and management in order to know the lifestyle, family
DS: What would be the number of primary angle closures history, prodromal symptoms, systemic medication and
versus the secondary angle closure seen by you in the previous episodes.
clinic setting?
KS: Not a very significant role. Headache is a pretty ubiquitous
SSP: About 50:50 complaint given by most of my patients. Coloured halos
and acute pain are very rarely reported by my patients. Poor
CP: Almost a fifty fifty. dark adaptation is a very common symptom in established
glaucoma cases.
SS: 3:1
DS: Can we depend on symtoms to diagnose angle closure?
PS: Primary angle closures versus 100 secondary angle closures
per month SSP: No. Symptoms are not reliable for the diagnosis of ACG.
If present the are useful pointers but majority have no
BKN: The ratio of primary angle closure versus secondary angle symptoms.
closure seen by me is approximately 40:1.
CP: No, but unexplained headaches could do with a gonioscopy.
KS: I see almost 50-60% angle closure glaucoma cases in my
clinic. SS: We cannot diagnose angle closure based on symptoms only
as >90% are asymptomatic.
DS: What are the common secondary angle closures seen by
you? PS: We cannot completely depend on symptoms alone for the
diagnosis.
SSP: Post surgery (cataract, corneal grafts, vitreo-retinal surery),
uveitis, trauma, phacomorphic. BKN: Yes, symptoms can be important criteria for angle closure.

CP: The commonest secondary angle closure is that following KS: Not really.
uveitis. Others are following Vitreo retinal procedures and
complicated cataract surgeries. DS: How do you diagnose angle closure in the clinic?

SS: Post PK glaucomas, post traumatic and post VR surgery. SSP: Clinical examination including Gonioscopy.

PS: Lens induced Glaucoma CP: On routine examination ( Van Herricks at the slit lamp) ,
followed by gonioscopy.
Post Retinal surgerry
SS: By gonioscopy
Post-Keratoplasty glaucoma
PS: Screening by VanHerick’s method on Slit lamp and
Uveitic glaucoma confirmation with Indentation Gonioscopy, Intraocular
pressure by Applanation Tonometry, Stereoscopi Fundus
Traumatic glaucoma evaluation and corresponding repeatable visual field
defects.
BKN: Common secondary angle closures seen by me are
phacomorphic glaucoma, neovascular glaucoma, post BKN: Diagnosis in the clinic depends on complete history taking
traumatic glaucoma, post-operative glaucoma, glaucoma including family history, signs and symptoms, gonioscopy,
secondary to certain systemic medications and post uveitic slit lamp examination, applanation tonometry, 90 diopter
glaucoma. slit lamp biomicroscopic evaluation of the optic disc.
Anterior segment OCT and UBM can also aid in making
KS: In the secondary glaucoma post pseudophakia, post uveitic the diagnosis.
and steroid induced top the list.
KS: Gonioscopy, gonioscopy and gonioscopy. In uncooperative
DS: Glaucoma is often described as a disease of signs. Does patients Anterior segment OCT, but I personally prefer
history taking have a role in angle closure? gonioscopy done in a dim lit environment.

SSP: Yes. History taking has an important role. When the DS: As a general practitioner do you suggest that we shift
problem started, how it started, course of disease, effect from gonioscopy to anterior segment OCT to diagnose
of previous medicines their side effects, family members angle closure, in view of the ongoing “ Current concepts”?
involved, associated conditions, secondary causes...... all
information comes from history. SSP: Gonioscopy is much easier, quicker and dynamic. OCT
can miss synechiae, pigmentation, NVA and is static.

14 DOS Times - Vol. 16, No. 7, January 2011

CP: No, gonioscopy is still the gold standard. For primary angle closure glaucoma laser iridotomy may
be tried if the damage is not extensive and synechial closure
SS: At this point there are no other diagnostic tests to replace is less than 180 degrees. However more often than not
Gonioscopy surgical option is required for such cases keeping in mind
that even after respite after a patent PI many will progress
PS: Not really, but in case of Ophthalmologist does not know to to further glaucomatous damage Fellow eye needs to be
do proper gonioscopy and in case of legal documentation lasered depending on the stage of disease.
or other requirements which warrant ASOCT it can be
done. DS: Is laser iridotomy a must in angle closure. Are there
situations where medical treatment would have a role?
BKN: No, sophisticated tests so far available cannot replace
gonioscopy. I think that to a large extent the “current SSP: Medical treatment has a role in reducing IOP if cornea is
concepts” is basically company driven for financial reasons. not clear or while waiting for LI and after LI if the IOP is
still high. LI is must for angle closure of primary variety.
KS: Not at all. Gonioscopy is easier, gives more information and
is softer on the pocket. For exact quantification and research CP: Laser iridotomy is a must in angle closure. Pilocarpine and
OCT is helpful but only as an adjunct not a replacement Aqueous suppressants have a role, after iridotomy
for gonioscopy.
SS: YAG pi is a must. No medications can replace it. However
DS: What treatment protocols do you follow for a primary pilocarpine will facilitate PI by stretching the iris and is
angle closure and primary angle closure glaucoma. If useful for treating plateau iris post PI.
you do not follow the mentioned classification please
mention what you do in such cases? PS: Laser iridotomy is must but in case where it cannot be
performed due to medical reasons medical treatment may
SSP: POAG: good baseline documentation including fields and have a role.
disc pictures, start with a monotherapy unless IOP is too
high or target IOP considerations demand combination BKN: In Primary angle closure Laser iridotomy is not a must but
therapy. PGA or Beta blockers are usual choice of drugs considering the nature of Indian Population I prefer to do
to start with. a peripheral laser iridotomy. In angle closure glaucoma
medical treatment has a role till peripheral iridotomy or if
PAC/PACG: Start with pilocarpine, do LI, monitor IOP, after peripheral iridotomy glaucoma is not under control.
switch to a betablocker or PGA if needed. Monitor IOP
and angles following LI. KS: Laser iridotomy is the sheet anchor. Medical therapy is an
adjunct. However laser iridotomy will only take care of
CP: Laser iridotomy along with aqueous suppressants. Followed pupil block component of ACG. For dealing with other
by filtration surgery where required. components like extensive peripheral anterior synechiae,
plateau iris or crowding of angle by lens requisite medical
SS: Yag PI first, followed by dilated disc exam and visual fields or surgical therapy has to be resorted to.
to look at the disease severity and treat them accordingly.
DS: There is now an ever increasing scientific temper about
PS: Primary Angle Closure - Yag peripheral iridotomy, if IOP is cataract extraction in angle closure. Your views with
higher to treat with appropriate antiglaucoma medications, respect to pros or cons and situation where you may or
close IOP,Visual field monitoring with periodic follow up. may not opt for the same?

Primary Angle Closure Glaucoma – Yag peripheral SSP: If it is secondary angle closure due to lens (phacomorophic)
iridotomy, antiglaucoma medications/ trabeculectomy +/- the lens has to go. In PACG if there is significant cataract
cataract extraction and close IOP, Visual field monitoring and angles do not show any improvement after LE. I would
with periodic follow-up. look at the lens thickness, chamber depth and consider
cataract extraction.
BKN: Ideally for primary angle closure only regular follow ups are
required whereas for primary angle closure glaucoma laser CP: If a patient has borderline angle closure (say schaffers
peripheral iridotomy and medical treatment for control of grade 2 in more than 180 degrees) and intumescent lens –
IOP is required. Due to high attrition rate I prefer to do definitely a cataract extraction would take care, but if the
laser peripheral iridotomy even in primary angle closure. angle is schaffers 1 or 0 and no cataract, the treatment of
However, both the above groups of patients should have choice could be laser iridotomy followed by medication or
regular follow ups. trabeculectomy.

KS: For primary angle closure laser iridotomy by Nd: YAG laser SS: In cases with PAC or early PACG associated with significant
is tried after medically controlling the IOP. Post operative cataract cataract extraction may help. In cases of PACG
steroids and anti glaucoma drugs are used for 5- 7 days. The requiring surgical treatment in the presence of even an
IOP is rechecked and gonioscopy repeated. If IOP is raised early cataract a combined surgery may be more beneficial.
then depending on disc damage and field status medical
therapy or surgical therapy is instituted. Fellow eye also PS: May opt - Convex iris configuration with thicker lens and
needs to be lasered. However follow up is must as almost early cataract. May not opt – Normal chamber depth with
30-40% will progress to glaucomatous damage in 5 years normal lens size.
despite patent PI.

www.dosonline.org 15

BKN: I am aware that there are certain people recommending BKN: I firmly believe that for glaucoma detection clinic based
clear lens extraction for angle closure which according to approach is the best approach. So far as the issue of public
me is driven by economic forces to some extent. I personally screening is concerned I am of the opinion that public
don’t do clear lens extraction in angle closure however, education and awareness is more important than public
if there is associated cataract, in such patients I do offer screening.
cataract surgery a little earlier.
KS: Most studies have concluded that public screening for
KS: In greater than 180 degree (an arbitrary figure) of synechial glaucoma is neither cost effective nor beneficial unless
closure cataract extraction logically should not and does you perform visual fields and gonioscopy too. The
not work. In cases of Nanophthalmos, microspherophakia, logistics of that are pretty daunting, so currently a clinic
subluxated lens, small globes with early changes of glaucoma based approach or glaucoma detection is the only option.
damage a clear corneal temporal phacoemulsification with Screening presbyopes coming for refractive correction and
a surgical peripheral iridectomy can be tried. at risk individuals with a family history of glaucoma can be
propagated, however the sheer numbers are tremendous.
However whenever significant glaucomatous damage is
present, when follow up is doubtful, or the other eye has DS: Any advise you would want mentioned with respect to
lost significant vision due to glaucoma I prefer to perform angle closure detection, treatment etc.?
a trabeculectomy in the hope it will control the IOP and
prevent blindness SSP: Our clinic data suggests that only 1/3rd of PAC/PACG were
diagnosed correctly by general ophthmologists. Still worse,
The types of angle closure I often see have glaucomatous only about 5% of diagnosed angle closures were offered
damage, IOP of greater than 30 mm Hg. This scenario PI or LI this could be due to lack of understanding of the
coupled with the silent nature of the disease, the probability disease of lack of availability of Yag Laser. Role or LI needs
of patient not coming for follow up or adhering to treatment to be emphasised.
makes me wary of sending the patient home with a cataract
surgery combined with peripheral iridectomy alone CP: Hypermetropes must undergo gonioscopy. Those with
without the cover of a trabeculectomy. Recently concluded reduced Anterior Chamber depth on Biometry and
reviews eg Cochrane data base of 2006 states that there Pachymetry need gonioscopy and followup.
is no published evidence supporting the efficacy of lens
extraction in chronic primary angle closure glaucoma. Before staring any anti glaucoma medication, gonioscopy
Recent reviews by Tarongoy P et al in Survey 2009, is a must.
and Walland in July issue of Clinical & Experimental
Ophthalmology 2010 emphasize that the jury is still out SS: Presence of deep AC does not rule out angle closure.
on this issue. Gonioscopy is a most, it can be replaced.

DS: The blindness from glaucoma is irreversible. Its also about PI is mandatory for treatment of angle closure glaucoma.
the economic burden on society. Do you recommend a
clinic based approach or glaucoma detection or should PS: Family screening for Angle closure glaucoma is equally
public screning be made mandatory? important as for POAG ormal appearing anterior chamber
does not mean open angles. Gonioscopy is mandatory
SSP: I would say public awareness is important. Public awareness for all (Women>35yrs and Men>40yrs) to rule out angle
along with opportunistic screening may be more cost closure disease
effective. Public screening has its pitfalls.
BKN: Ophthalmic examination for detection of angle closure
CP: The alarming rate at which the disease is increasing, should include gonioscopy. Anterior segment OCT
mandatory public screening would be recommended. or UBM is not a substitute. Medical treatment except
pilocarpine has its role only after iridotomy has been
SS: Clinic based approach is better. Above the age of 40 when performed.
a presbyopic individual visits the ophthalmologist that
may be the best opportunity to screen for the disease. KS: Please be comfortable and strict about doing a gonioscopy
Community screening has not much role as the disease in your practice. Laser iridotomy is quite easily available,
prevalence i slow and there is no sensitive and specific pretty safe and in case of doubt perform one, it may prevent
test to diagnose glaucoma; it requires a complete eye blindness in the patient prone to develop ACG. Remember
examination along with visual fields. ACG in our country is often the creeping angle type so a
silent damage goes on, a PI in time may save the eye.

PS: Though the disease has increasing prevalence still as of now
Oppurtunistic screening for glaucoma holds good

DOS Correspondent
Devindra Sood MS, FACS

16 DOS Times - Vol. 16, No. 7, January 2011

Juvenile Idiopathic Arthritis: An Overview Uveitis

*Amit Khosla MD, DNB, **Sanjeev Gupta MD, DNB, ***Sujata Sawhney MD, MBBS

JIA is the most common cause of the anterior uveitis comprising The uveitis runs a chronic course with relapses and recurrences
up to 30% of children. JIA remains one of the major causes of and is bilateral in the majority of cases.
visual impairment in children with uvietis.
The incidence of uveitis is maximum in oligo arthritis and varies
JIA is group of idiopathic arthritis with an onset before 16 years from 13-45% and is seen more in girls.
of age that persists for alteast 6 weeks.
Uveitis is rare in systemic arthritis and RF positive polyarthiritis.
It is classified into 7 sub-sets. It is important in determining
the risk of development ocular inflammation and optimizing The PSA assoc uveitis is more resistant to therapy.
screening for uveitis.
In the Enthesitis related arthritis, uveitis occur in 10-15%. It is
• Systemic Arthritis typically symptomatic with an acute onset. These patients are
HLA B-27 positive and eventually develop lumbo-sacral disease
• Oligo arthritis and sacroilitis.

• Polyarthritis (RF positive) Risk factors for developing JIA uveitis include ANA positivity,
early age of occurrence of arthritis < 6 and female sex.
• Polyarthritis (RF negative)
Paediatric Uveitis generally accounts for 5-10% of patients with
• Psoriatic arthritis uveitis1. The varied nature of clinical presentation and the nuances
of their management makes this group of patients distinctly
• Enthesitis related arthritis challenging. In addition, paediatric uveitis, can lead to significant
ocular morbidity, which increases with duration of disease and
• Undifferentiated arthritis delay in diagnosis.

The incidence of JIA associated uveitis is 1.4-25% in various series. Clinical Presentation of uveitis

The course of arthritis does not parallel the course of uveitis, The characteristic features of JIA are associated uveitis are:
therefore patients in remission for arthritis may still suffer from
active ocular inflammation. • Bilateral non granulomatous,asymptomatic anterior uveitis
(initial presentation / chronic). Most cases have simultaneous
involvement of both eyes or within few month.

• Sometimes patients may present with classical trial of cataract,
band shaped keratopathy and glaucoma due to asymptomatic
course.

• In contrast to the chronic asymptomatic form of uveitis
seen in Oligoarticular JIA, children with HLA B-27 positive
enthesitis present with acute symptomatic anterior uveitis

• Some clues which give suggestion of active/inactive uveitis
are iris atrophy, one eye with low IOP, and pigment on the

lens.

Figure 2: Colour photograph showing complicated The visual impairment in JIA uveitis is secondary to complications
cataract with band shaped keratopathy which includes cataract, BSK, glaucoma, cystoid macular edema,
hypotony and amblyopia. Factors which predict poor visual
outcome include:

• Severity of uveitis at initial examination

• Uveitis onset before or at the time of arthritis

*Department of Ophthalmology • Short duration between onset of arthritis and eye involvement.
Sir Ganga Ram Hospita, Rajinder Nagar, New Delhi
Evaluation of child with arthritis / Diagnosis of JIA
**Siri Fort Laser Eye Centre
Siri Fort Road, New Delhi JIA is a diagnosis of exclusion. Evaluation of children for presence
of JIA includes:
***Department of Paediatrics
Sir Ganga Ram Hospital, New Delhi, India

www.dosonline.org 19

Table 1: Screening Recommendation

JIA subtype at onset Risk of Developing Uveitis based on age of onset

< 7 years Frequency of Screening > 7 years Frequency of screening

Oligoarticular High Every 3-4 month Medium Every 6 months
+ ANA Medium Every 6 months Medium Every 6 months

- ANA High Every 3-4 months Medium Every 6 months
Medium Every 6 months Medium Every 6 months
Polyarticular Low Every 12 months Low Every 12 months
+ ANA

- ANA

Systemic

• Thorough clinical history ophthalmologist, the paediatric rheumatologist should be fully
aware of the start of ocular inflammation and should inform the
• General examination ophthalmologist about any changes in medication. The goal of
treatment is to achieve complete quiescence of inflammation in
• Musculor skeletal examination (joints, muscles, enthesis, soft order to prevent sight threatening complications.
tissues)
The purpose of anti-inflammatory therapy is to cause the uveitis to
• Systems review become quiescent and to prevent complications and loss of vision.
Normally a step ladder approach to treating uveitis is advocated
Laboratory tests have limited role in arriving at the diagnosis of – to begin with local steroids till complete resolution of cells in
JIA. However some patients of JIA have elevated levels of markers the anterior chamber and then to keep a low dose maintenance
of inflammation (erythrocyte sedimentation rate; C-reactive therapy. If inflammation persists steroids are administered
protein; leucocyte and platelet counts). systemically. Systemic immunosuppressive drugs are used when
steroids are ineffective in achieving remission/control in 6
In addition, ANA is present in 40-60% of children with weeks – 3 months, the dose of steroid is too high or side effects
oligoarthritis and often in those with polyarthritis and psoriatic become evident. Some uveitis in JIA may extend upto 20 years
arthritis. Test for RF is not useful for diagnosis, but for and cause morbidity. We prefer to start immunosuppressives at
appropriately classifying the child with polyarthritis. JIA uveitis the time of diagnosis. The agent of first choice is weekly low dose
can mimic uveitis secondary to other conditions. These include: methotrexate. It is given orally or sub-cutaneous which has better
bio-availability. The disease is controlled in approximately 60% of
• Connective tissue disorders eg. systemic lupus erythematosus, cases with single drug but 40% will require additional medication
dermatomyositis or replacement by other drugs to obtain uveitis resolution.

• Infectious / post infectious arthritis The other drugs which have been tried are cyclosporine,
Azathioprime and Mycophenolate mofetil. When the disease is
• Sarcoidosis resistant to these drugs then tumour necrosis factor inhibitors
can be used. The results are better for the JIA associated arthritis
• Parsplanitis than for JIA associated uveitis. The TNF inhibitors available
are Etanercept, Ifliximab and Adalimumab. Infliximab is the
• Tubuo interstitial nephritis and uveitis (T.I.N.U). commonest drug used for uveitis and is administered in the dose of
3-10 mg /kg body weight. The infusion usually are given at interval
• Vasculitis eg. Kawasaki’s disease. of 2-4 weeks. Then at 6-8 week interval. An increasing incidence
of infections are observed with TNF inhibitors eg. Tuberculosis.
Screening for uveitis in patients with JIA We prefer to add mycophenolate mofetil (MMF) in unresponsive
patients and use TNF inhibitors for resistant cases. Still a segment
The newly diagnosed patients of JIA must under go screening of patients may be resistant to treatment.
for eye diseases and therefore should be referred to an
ophthalmologist. Current guidelines for screening are summarized Among the various immunosuppressive Methotrexate has the
in Table 1 (American Academy of Paediatrics Recommendation). most evidence as an effective treatment. The efficacy of CSA is
All children with JIA should be screened by slit lamp at diagnosis relatively low, Azathioprine has a moderate effect while MMF has
of arthritis. limited case series but is being tried in trials recently.

Treatment TFN inhibitors help reduce the inflammation and allow the dosage
of other immunosuppressives to be reduced. In our series TNF
Medical inhibitors had limited response.

Medical treatment of JIA and associated uveitis requires a multi-
disciplinary approach. Collaboration between the ophthalmologist
and rheumatologist is critical for optimal management. Although,
the management of uveitis is primarily the purview of the

20 DOS Times - Vol. 16, No. 7, January 2011

Table 2: Surgical Indications in JIA Comments
Indication
1. Cataract • Strict control of uveitis prior to surgery at least for 3 months.
• Peri-operative use of systemic Immunomodulatory therapy
2. Glaucoma • Relative contraindications for intraocular lens (IOL) implantation age <4
3. Band shaped keratopathy
4. Recalcitrant chronic uveitis years, hypotony, shallow anterior chamber, fellow eye with IOL complication
• Surgical approach Parsplana lensectomy + anterior vitrectomy with aphakic
& persistent hypotony
correction Lens aspiration + IOL + Parsplana vitrectomy.
• Strict control of uveitis prior to surgery at least for 3 months.

Trabeculectomy with anti-metabolites / glaucoma drainage devices
• Chelation using ethylene diamine tetracetic acid
• Pars plana vitrectomy (PPV)
• Persistent hypotony - PPV + removal of cyclitic membranes + silicone oil

Local treatment consists of topical steroids and cycloplegics. It is is an almost unavoidable consequence of long-term alkylating
important to use short acting cycloplegics like tropicamide to keep agent use.
the pupil mobile and prevent posterior synechiae. It is important
to prevent ambylopia thus avoid longer acting cycloplegics. The medical management of glaucoma associated with JRA uveitis
is difficult. Topical beta-blockers, topical sympathomimetic
End points of treatment agents, and carbonic anhydrase inhibitors may have to be used.
Although some case reports show an association between the use
The minimal duration of Methotrexate therapy and the of latanoprost and the development of anterior uveitis. The use
tapering regimen has not been studied thoroughly. It is general of pilocarpine is probably not recommended in these patients
recommended to taper Methotrexate after 12-24 months of because of its effect on the blood aqueous barrier as well as the
remission. We keep a monthly checkup of patients on remission risk of posterior synechiae formation. Laser iridotomy is indicated
and start to taper Methotrexate after 1 year of remission. in acute angle-closure glaucoma associated with pupillary block
and iris bombe.
It is important to note that low dose (2 times per day) topical
steroids be given for 3-6 months after remission. Surgical

Chronic systemic corticosteroid therapy is associated with the The surgical intervention in JIA uveitis is usually done in the
complications of growth retardation in children, osteoporosis, setting of the following.
and the development of a cushingoid habitus, all of which are
unavoidable. Other potential complications include secondary • Chronic uveitis
diabetes, peptic ulcer, hypertension, psychosis, myopathy, and
hip necrosis. Immunosuppressive therapy is associated with • Complications like cataract, band shaped keratopathy,
potential complications; these, however, can be avoided by regular glaucoma and hypotony.
monitoring of the patient by a pediatric rheumatologist. These
complications include bone marrow depression; hepatic, renal, These are discussed briefly in table no. 2.
and pulmonary toxicity; infection; and alopecia. Concerns have
also been raised about the development of malignancies in patients The surgical management of cataract in JRA has been the
treated with single-agent immunosuppressive chemotherapy; may subject of many recent studies. It is recommended that cataract
decrease immune surveillance and, hence, enhance malignancies surgery be performed in only those eyes that have been free
associated with the Epstain Barr Virus. of all inflammation for at least 3 months, and aggressive anti-
inflammatory therapy should be provided both before and after
Alkylating agents have been used fairly extensively in uveitis the surgery.
associated with certain other disorders. Concerns with these
drugs include those of sterility and the development of secondary Traditional glaucoma surgery with trabeculotomy has shown poor
malignancies. Sterility is generally not considered a major issue results because of low scleral rigidity and fibrous proliferation
in prepubertal children at the doses and for the duration we at the surgical site. The use of aqueous drainage devices such
recommend for use in these children. Studies show that some as Ahmed valves and Molteno implants may improve surgical
prepubertal children treated with alkylating agents later go on to success. Band keratopathy is treated with debridement followed
bear normal offspring. In postpubertal children, however, sterility by chemical chelation and topical application of ethylene
diaminetetracetic solution.

www.dosonline.org 21

Prognosis shorter duration of uveitis and short delay before presentation to
a specialist have been shown to be significantly associated with a
JRA – associated uveitis is a difficult disease that often extracts a visual outcome of 20/40 or better.
“silent” toll from its victims if smoldering, low-grade, inflammation
is allowed to go uncontrolled. Seventy-five percent of children with It is important to note that children who present with uveitis
moderate to severe uveitis experience visual loss due to ocular without arthritis should be evaluated for JIA. They must have an
complications. Functional blindness occurs in between 22% and ANA test. It suspicion points towards JIA, then patient should be
38% of patients if inflammation is not controlled. In children with started on immunosuppressives.
JRA-associated uveitis, approximately 25% have inflammation
unresponsive to local therapy. Factors associated with a poor visual It is important to have a joint management with a rheumatologist
prognosis include young age at onset, oligoarticular arthritis, a to monitor the side effects and monitor issues like growth
chronic course, the presence of uveitis prior to arthritis, female retardation, recurrent infection and issues related to vaccination.
gender, ANA positivity, and rheumatoid factor negativity.
The parents need to be counselled that the disease is chronic and
Earlier detection and aggressive treatment to prevent ocular will require monitoring till adulthood and despite treatment some
complications can improve the visual outcome further, in fact, a of the children will develop ocular morbidity.

Author
Amit Khosla MD, DNB

OPHT HALMOLOGICAL

SOCIETY DOS Phaco Training Fellowship

DE LHI

Supported by 4 Slots for Delhi Members
4 Slots for Non Delhi Members
M/s. Zeiss Pvt. Ltd. (Based on DCRS Rating)

15 days Duration
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at Venu Eye Institute, New Delhi

Starting, January 2011

Apply at: [email protected]

22 DOS Times - Vol. 16, No. 7, January 2011

Management of Small Pupil in Manual Cataract
Small Incision Cataract Surgery

*Ruchi Goel MS,DNB, FICS, **KPS Malik MS, DOMS, MNAMS, FICS, *Sushil Kumar MD

Apupil that fails to dilate beyond 4 mm, with the routine • Switching from miotics to alternative intraocular pressure
dilating protocol during the preoperative work up should put lowering agents a week prior to surgery
the surgeon on his guard. Besides causing impaired visualization
due to its size a small pupil may be a harbinger of other co • Starting topical nonsteroidal anti-inflammatory group of
morbidities and predispose to increased tissue damage, retained drugs thrice a day a week prior to surgery
lens material, vitreous loss and cystoid macular edema due to
prostaglandin release because of excessive handling of iris tissue. Intra operative measures

The causes of a non dilating pupil are pseudoexfoliation syndrome The ultimate aim is to create a capsular opening of at least 6mm
which may be associated with zonular weakness, diabetes mellitus, to enable the nuclear prolapse out of the bag into the anterior
chronic use of miotics, uveitis, senile miosis, iridoschisis, atonic chamber.
pupil due to systemic drugs like tamsulosin, anterior segment
dysgenesis, and previous ocular surgery/laser or iris sphincter High molecular weight viscoelastics such as sodium hyaluronate
fibrosis, e.t.c. 2.3% is used both for the purpose of viscodilation as well as
minimizing the iris prolapse. The actual capsulorrhexis can often
The preoperative planning should comprise of the following: extend beyond the actual pupil margin, and a second instrument
may be used to temporarily retract the iris.
• Accessibility of devices for pupil expansion and capsular bag
stability The nucleus can be brought out of a small pupil using two handed
technique. The anterior chamber is filled with viscoelastic, two
• Shifting from topical to peribulbar anaesthesia as iris handling Sinskey’s hooks are used. One is inserted through the side port
would cause pain if topical anaesthesia is used and one through the main port and the nucleus is brought out
using hand over hand manoeuvre. (Figure 1)
• Performing the surgery under steroid cover in patients of
uveitis Nonpreserved epinephrine 0.5 mL in 500 mL of Balanced Salt
Solution is used for infusion during surgery.1

Intracameral irrigation with 1% lidocaine followed by a wash with
basic salt solution can also be tried.

If these measures fail, sector iridectomy which is sutured after
intraocular lens implantation (rarely used nowadays), mechanical

Figure 1: Nucleus prolapse out of the bag using Figure 2: Mechanical stretching using dialers
hand on hand maneuvre
23
*Guru Nanak Eye Centre
MAMC, Maharaja Ranjit Singh Marg, New Delhi
**Subharti Medical College, Meerut & Visitech Eye Care Center

South Extension Part II, New Delhi
*Guru Nanak Eye Centre,

MAMC, Maharaja Ranjit Singh Marg, New Delhi

www.dosonline.org

Figure 3: Mechanical stretching using Kuglen hooks Figure 4: Mechanical stretching by
Beehler pupil dilator

stretching, mini-sphincterotomy, iris hooks, ring expanders and
iris sutures are other available options.

Posterior synechiae, if present, are swiped with the cannula of
the viscoelastic syringe or a vitreous sweep. A synechial ring can
be present, which is best stripped with a pair of capsulorrhexis
forceps akin to carrying out a rhexis.

Mechanical stretching is a simple manoeuvre which is accomplished
by using a pair of hooks such as Kuglen or Sinskey’s which either
push or pull the iris respectively in opposite directions. (Figure
2&3)

Stretching can also be done using a Beehler’s pupil dilator. (Figure Figure 5: Mini sphincterotomy: crescentric
4) It has two to three microfingers and one hook attached to the cuts using Vanna’s scissors
tube of the instrument to stretch the pupil in an asymmetric four
quadrant pattern.

Disadvantages of mechanical stretching:

• Does not prevent progressive miosis Now days, metal retractors have been replaced by nylon with
silastic sleeve.
• May increase iris prolapse related to atonicity
The anterior chamber is deepened with viscoelastic. Symmetrically
• The iris sphincter may sustain more stretching in one placed side ports are created using MVR knife. The sleeve on the
particular meridian than is necessary iris hook is pulled back. It is held with a suture tying forceps and
introduced keeping the hook parallel to the iris plane. Once it
• Accidental anterior capsular tear reaches the pupillary edge it is rotated to engage the pupillary
margin and pulled centrifugally. The silastic sleeve is then pulled
Mini-sphincterotomies can be performed with either a pair of centripetally. (Figure 7,8)
Vanna’s scissors or a retinal scissor. (Figure 5,6) The retinal scissors
have the advantage that it can be passed through the paracentesis Disadvantages of iris hook:
and it can cut subincisionally as well.2,3 Crescentic cuts make a
more normal pupil appearance postoperatively.

Iris hooks were initially described by Mackool4 using titanium • Peripheral shallowing of anterior chamber with little working

hooks attached to a square titanium base and an iris repositor. space in patients with shallow anterior chamber. Once the

24 DOS Times - Vol. 16, No. 7, January 2011

the Malyugin ring system. Injector systems are available for all
these devices.

Perfect Pupil is a grooved polyurethane ring with an internal
diameter of 7.0 mm. (Figure 9) It has an integral arm at one end
of the ring which is kept at one end of the incision and helps in
removal of the device. The ring is open for 450 to allow passage
of instruments.7

Morcher pupil dilator ring is a fixed, rigged 7.5mm polymethyl
methacrylate (PMMA) ring without an integral arm. (Figure 10)

Graether 2000 pupil expander system is an incomplete soft silicone
ring with an internal diameter of 7.0mm and a grooved outer
circumference to engage the iris sphincter.8 (Figure 11) A 3.75mm
gap in the ring is bridged by a slender strap which facilitates
access to the pupillary plane. The insertion tool is critical in this

Figure 6: Mini sphincterotomy: radial cuts using Figure 7: Iris hooks dilating the pupil
Vanna’s scissors Figure 8: Iris hooks dilating the pupil

capsulotomy is done, it is better to remove the hooks and 25
then prolapse the nucleus in the anterior chamber to avoid
endothelial damage

• Too many ports have a tendency to leak and hinder the
built of anterior chamber pressure which is vital for nuclear
progress outwards. This can be managed by increasing the
bottle height or injecting 2% methylcellulose through the
anterior chamber maintainer in the Modified Blumenthal
technique.5 Viscoelastic can also be injected through the side
port at 6 o’clock position to push the nucleus outwards

• Improper placement of hook can cause raised iris platform
between the hooks.

• Improperly constructed side ports can result in iris prolapse

• Injury to anterior capsule occurs if the hooks are introduced
in an incorrect direction or if the anterior chamber becomes
shallow

• Injury to descemet’s membrane can also occur due to the
reasons cited above

• Irregular postoperative pupil function6

Ring expanders cause circumferential expansion in the physiologic
plane along with stabilization and protection of pupil margin.
The available ring expanders are the Perfect Pupil, the Morcher
pupil dilator ring, the Graether 2000 pupil-expander system and

www.dosonline.org

Figure 9: The Perfect pupil

Figure 11: Graether 2000 pupil expander

Figure 10: Morcher pupil dilator ring Figure 12: Malyugin ring system

device since it lacks adequate annular rigidity to allow forward Conclusion
advancement along the pupil margin.7
Small pupil management is no longer fraught with complications
The Malyugin ring system consists of a holder and inserter with availability of so many devices in the armoury. In
packaged together with each ring. The inserter is used to withdraw small incision cataract surgery, unlike phacoemulsification a
the ring from the holder. It also introduces the ring into the capsulorhexis though desirable is not a must. Also the size of
anterior chamber and removes the ring from the eye. the capsular opening should be 6.0mm or larger. Majority of the
patients can be comfortably managed by intracameral adrenaline,
It is friendlier to the eye due to its well distributed stretching, gentle viscodilation and stretch pupilloplasty. Ring expanders are less
holding of delicate iris tissue, and the easier and less traumatic traumatic and do not require additional ports unlike iris hooks
implantation. (Figure 12) It has no sharp or pointed ends that can but are expensive and are rarely required for manual small incision
damage the eye. 9 cataract surgery.

The 10-0 nylon iris sutures can be used when iris hooks and other References
devices are unavailable. Four 1-1.5mm stab incisions are made
at the limbus, followed by capture of the peripheral iris in these 1. CF Kranemann. Small pupil management in cataract surgery.
incisions with the aid of a fine forceps. The captured iris is then Techniques in Ophthalmology 2003:1; 81-84.
sutured to clear cornea with a 10-0 nylon suture.10

26 DOS Times - Vol. 16, No. 7, January 2011

2. Fine IH. Pupilloplasty for small pupil phacoemulsification. J Cataract 8. Graether JM. Graether pupil expander for managing the small pupil

Refract Surg. 1994; 20:192-196. during surgery. J Cataract Refract Surg 1996; 22:530-535.

3. Pham DT, Volkmer C, Leder K, et al. Partial sphincterectomy 9. Malyugin B Malyugin ring for small pupil phaco cases. Cataract &

in cataract surgery. Clinical and patho-histologic results. Refractive Surgery today Europe 2008; March:59-62.

Ophthalmologe. 1998; 95:635-638. 10. Freitas LL,CasanovaFH,Bonomo PP.Small pupil phacoemulsification

4. Mackool RJ. Small pupil enlargement during cataract extraction: a using iris sutures: a new method ? Ophthalmic Surg Lasers Imaging

new method. J Cataract Refract Surg 1992; 18:523-526. 2004; 35: 434-437.

5. Malik KPS, Goel R. Nuclear Management with Blumenthal (An excerpt from 2nd Edition of Manual
technique: Anterior chamber maintainer. IJO:2009;57:23-5. of Small Incision Cataract Surgery, CBS

6. Goldman JM, Karp CL. Adjunct devices for managing challenging Publishers, 2011, under print)
cases in cataract surgery: pupil expansion and stabilization of the
capsular bag. Curr Opin Ophthalmol 2007; 18: 44-51.

7. Kershner RM. Management of the small pupil for clear corneal
cataract surgery. J Cataract Refract Surg 2002; 28:1826-1831.

First Author
Ruchi Goel MS, DNB, FICS

ARPANA HOSPITAL VACANCY

A Multi Specialty Hospital with well FOR
equipped Eye Wing. VITREO RETINA CONSULTANT

Requires AT
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(Surgeon with Experience in Phaco /
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27
www.dosonline.org

Epiretinal Membrane Retina

Bhuvan Chanana MD, DNB, MNAMS, FICO; Vinod Kumar MD, DNB, MNAMS, FRCS; Ved Prakash Gupta MD, DNB

Epiretinal membrane (ERM), first described in 1865, is an or even pigmented membrane. Retinal changes are observable as
avascular, fibrocellular membrane that proliferates on the surface wrinkling, vasculature distortion, cystoid macular edema
inner surface of retina. Macular ERMs are visually disturbing. or pseudohole.
The prevalence of macular ERMs is 2% under the age of 60 years
and 12% in those over 70 years.1 These membranes have been classified into three grades by Gass
based on the appearance of the membrane and the underlying
Etiology retinal tissue and vessels: 5

Epiretinal membranes may be idiopathic and found in otherwise Grade 0: Cellophane maculopathy – Fine membrane over macula
healthy eyes, or secondary. Idiopathic ERMs are associated with causing a glistening light reflex , no retinal distortion, visual acuity
posterior vitreous detachment (PVD). PVD can create minor normal with no or minimal symptoms
damage to the retina, stimulating exudate, inflammation, and
leucocyte response.2 These cells can form a transparent layer Grade 1: Crinkled cellophane maculopathy/ surface wrinkling
gradually and, like all scar tissue, tighten to create tension on the maculopathy - Inner retinal folds are visible with retinal
retina which may bulge and pucker, and also cause macular edema. vasculature distortion, less than half of ERM is opaque causing
obscuration of underlying retina and vasculature, vision is slightly
Secondary ERMs may result from ocular inflammation, trauma, affected but symptoms like metamorphopsia are present
intra-ocular surgery like post-retinal detachment repair, retinal
laser, and cryotherapy.3 Grade 2: Macular pucker - Thick opaque membrane over
inner retina, causing marked distortion and obscuration of
Epiretinal membranes comprise glial cells, retinal pigment underlying retina and vasculature, gross puckering of the macula
epithelial (RPE) cells, macrophages, fibrocytes, and collagen fibres. may be present; visual acuity is less than 20/200 with marked
Different proportions of these components are associated with metamorphopsia
a different etiology. Those from retinal breaks, previous retinal
detachments, or cryopexy are composed mainly of dispersed Role of OCT in ERM
RPE cells, while cells of glial origin predominate in idiopathic
pathology. Laminocytes are the fundamental cell type in idiopathic • To view fine ERM (Grade 0)
ERMs. These cells are frequently found in small and dispersed
numbers in eyes containing a PVD.3,4 • Presence of Vitreo-macular traction

Clinical Presentation • Assess retinal thickness and CME

Epiretinal membrane is symptomatic only if the macular or peri- • Differentiate pseudohole from true macular hole
macular area is involved. Most other cases are asymptomatic. • Monitor macular changes following surgery
Bilateral eye involvement has been reported in 31% of cases.3

The common presenting symptoms are: Foos classified ERM into simple, intermediate and complex based
on clinical appearance and etiology:6
• Decreased visual acuity
Simple – No contraction feature or associated ocular disease
• Metamorphopsia
Intermediate – Thicker than simple ERM and contain contraction
• Other symptoms include micropsia, macropsia, and features and pigment
monocular diplopia.
Complex – Such ERMs are secondary to retinal detachment
The severity of symptoms is related to the area of involvement surgery or trauma. Tractional retinal detachment may develop
and the thickness of ERM. Occasionally, the membrane may as a result of contraction of such membranes.
spontaneously detach from the retina and thereby improve
symptoms. Fluorescein angiography (FA) can aid diagnosis. FA shows retinal
distortion such as straightened retinal vessels, retinal vascular
Diagnosis tortuosity, foveal ectopia and macular dragging (Figure 1).

Slit lamp biomicroscopic examination is the best method to view Optical coherence tomography (OCT) is an important tool in
the membrane over the macula. An ERM is seen as a glistening evaluating patients with ERM. OCT helps to view the vitreo-
light reflex if it is thin, or as an obvious transparent, translucent, macular junction and fine ERMs can be visualized on the retinal
surface (Figure 2). OCT may be considered the “Gold standard” for
Vitreo-retina Services, Department of Ophthalmology monitoring changes in macula following surgery.7,8 Examination
University College of Medical Sciences & with high-resolution spectral-domain OCT (SD-OCT) allows
Guru Teg Bahadur Hospital, Delhi

www.dosonline.org 31

Figure 1: Fundus photo and fluorescein angiography showing retinal vascular
distortion due to ma cular epiretinal membrane

Figure 2: Spectral optical coherence tomography showing ERM causing traction over macula and resulting in
macular edema. 3D picture of macula (right) showing grayish-white membrane with macular thickening (red color)

three-dimensional visualization of the dynamics of epiretinal The SD-OCT with 3-D image reconstruction provides
tractions that had not previously been obtainable. Epiretinal unprecedented visualization of VMT and idiopathic ERM (Figure
membranes can be clearly distinguished and their tractional 2). ERM attachment to the macula viewed on OCT can be classified
effects can be traced through all retinal layers up to the pigment into two groups, focal and broad. ERM with broad attachment
epithelium.9 As a result of the postoperative elimination of the may further be subclassified into ERM adhered uniformly to
tractions, the morphological alterations of the individual retinal underlying macula and ERM with multifocal attachments.
layers can be observed with spectral OCT (Figure 3 & 4). The posterior hyaloid phase of vitreous can also be visualized

32 DOS Times - Vol. 16, No. 7, January 2011

Figure 3: (Patient 1) Pre-operative fundus photo (Figure 5). Koizumi H et al 8 examined 36 eyes with idiopathic
and OCT (above) showing ERM over macula ERM; 30 had complete posterior vitreous detachment (PVD),
five had partial PVD associated with attached posterior hyaloid
causing macular edema. 1 month post-operatively at some peripheral portion of the ERM, and one had no PVD.
OCT (bottom right) shows complete absence of
ERM and absence of macular edema. Normal Management
foveal contour is observed
Surgical removal of the membrane will improve visual acuity and
reduce metamorphopsia in most cases. It has not been customary
to treat patients with mild and non-progressive symptoms since
results are generally unsatisfactory. Nonetheless, advances in
surgery and instrumentation now allow patients with relatively
good visual acuity but significant metamorphopsia to be
offered a choice of surgery. Grade 1 ERM may cause significant
metamorphopsia with relative sparing of visual acuity. Early
surgical removal can relieve the disturbing symptom and stabilize
the vision that may worsen later. Surgery involves pars plana
vitrectomy, removal of ERM, with or without peeling of the
internal limiting membrane (ILM). Different methods of staining,
and peeling of ERM, have been described.10

Vitrectomy

A subtotal vitrectomy is performed; this decreases the risks of
intra-operative lens damage and peripheral retinal tear. In many
cases, PVD has occurred. If the posterior hyaloid is adherent
to the retina, PVD should be induced. Accelerated cataract is a

Figure 4: (Patient 2) Pre-operative fundus photo and OCT (above) showing ERM over macula causing traction 33
on all retinal layers. 1 week post-operatively OCT (bottom right) shows complete absence of ERM. The traction

has also disappeared and a decrease in macular edema is observed.

www.dosonline.org

Complications

Epiretinal membrane peeling is generally a safe operation and
complications are few. Intra-operative complications include
retinal petechiae, vitreous hemorrhage, and peripheral iatrogenic
retinal breaks. Most can be successfully managed if promptly
identified intra-operatively. Careful inspection of the peripheral
retina with indentation must be performed intra-operatively to
search for iatrogenic retinal breaks.

Figure 5: SD-OCT showing ERM uniformly adhered to the Postoperative complications include the recurrence of ERM (3-
underlying retina with macular thickening 12%), accelerated nuclear sclerosis of crystalline lens, and retinal
detachment.12

Outcome

common complication after vitrectomy: hence a combination After surgery, vision is improved in most eyes but complete
of cataract surgery and ERM has been suggested. Nonetheless, normalization of visual acuity is rare. Similarly, the appearance
phacoemulsification, which is performed first, can produce of the retina tends to return to normal but not completely: 60%
corneal epithelial edema especially in eyes with significant to 87% of eyes improve by 2 Snellen lines. The improvement
cataract. This may obscure the surgeon’s view during subsequent continues for more than 6 months and the mean time to achieve
ERM surgery. With modern cataract surgery, corneal edema is best final vision is about 1 year.13
seldom severe enough to warrant separate surgery for posterior
vitrectomy and the corneal epithelium can be scrapped to get a Prognostic factors associated with the visual outcome include:14,15
clearer view if needed.
• Preoperative visual acuity

• Duration of symptoms prior to surgery

• Intra-operative complications

Membrane removal • Etiology

After vitrectomy, the edge of the membrane is searched. A bent- • Patient’s age
tip needle or an intravitreal microforceps such as ILM or pick
forceps is used to lift it up. Subsequent peeling is completed with Eyes with worse preoperative vision demonstrate greater
forceps. If there is no obvious edge, a cut is made at the centre of improvement following surgery. Ultimately though, the final
the membrane using a microvitreoretinal (MVR) blade. An edge vision is better in eyes with better preoperative visual acuity. Eyes
is created and forceps are used to lift off the membrane. with a longer history of blurred vision have poorer visual acuity
postoperatively and less improvement in vision. This may be due
Indocyanine green to the longer traction damage on the retina by the ERM. Young
patients and those with secondary ERM have more recurrences,
Indocyanine green is hydrophilic and the acellular collagen of thus final outcome is usually less satisfactory.
the ILM is stained positively. In contrast, cellular ERM is stained
negatively. It provides a ‘negative staining’of ERM. Internal limiting References
membrane peeling is commonly adopted in macular hole surgery,
but its effect on ERM surgery is uncertain. The presence of long 1. Mitchell P, Smith W, Chey T, Wang JJ, Chang A. Prevalence and
segments of ILM within the histopathological specimen appears associations of epiretinal membranes. The Blue Mountains Eye
to indicate a less favourable visual outcome. Recurrence of ERM Study, Australia. Ophthalmology 1997; 104:1033-1040.
is also possible at the margins of ILM removal. This makes the
removal of ILM unfavourable for the outcome of ERM surgery. 11 2. Miller B. Epiretinal macular membranes: pathogenesis and
treatment. Dev Ophthalmol 1997; 29:61-63.
Trypan blue
3. Fraser-Bell S, Guzowski M, Rochtchina E, Wang JJ, Mitchell P. Five-
Trypan blue at a concentration of 0.2%, gives a bluish discolouration year cumulative incidence and progression of epiretinal membranes:
of ERMs that facilitates surgery. The stain not only makes the ERM the Blue Mountains Eye Study. Ophthalmology 2003; 110:34-40.
more easily identified, but enables a more complete removal of
the membrane. 4. Appiah AP, Hirose T, Kado M. A review of 324 cases of idiopathic
premacular gliosis. Am J Ophthalmol 1988; 106:533-535.
The area of ERM is usually larger than that estimated
ophthalmoscopically. With the stain, a larger area of the membrane 5. Gass JDM. Macular dysfunction caused by epiretinal membrane
can be identified and removed. contraction. In: Stereoscopic Atlas of Macular Diseases: Diagnosis
and Treatment. Vol 2. 4th ed. St. Louis, Mo: Mosby; 1997:938-950.
Triamcinolone acetonide
6. Foos RY. Vitreoretinal juncture—simple epiretinal membranes.
Triamcinolone acetonide (TA) is also used to stain ERM and it Graefes Arch Clin Exp Ophthalmol 1974; 189:231–250.
also has a beneficial effect of reducing macular edema.
7. Sayegh RG, Georgopoulos M, Geitzenauer W, Simader C, Kiss C,
Schmidt-Erfurth U. High-resolution optical coherence tomography
after surgery for vitreomacular traction: a 2-year follow-up.
Ophthalmology. 2010; 117(10):2010-2017, 2017.e1-2.

34 DOS Times - Vol. 16, No. 7, January 2011

8. Koizumi H, Spaide RF, Fisher YL, Freund KB, Klancnik JM Jr, 12. Margherio RR, Cox MS Jr, Trese MT, Murphy PL, Johnson J, Minor
Yannuzzi LA. Three-dimensional evaluation of vitreomacular LA. Removal of epimacular membranes. Ophthalmology 1985;
traction and epiretinal membrane using spectral-domain optical 92:1075-1083.
coherence tomography. Am J Ophthalmol. 2008; 145(3):509-517.
13. Pesin SR, Olk RJ, Grand MG, et al. Vitrectomy for premacular
9. Georgopoulos M, Geitzenauer W, Ahlers C, Simader C, Scholda C, fibroplasia. Prognostic factors, long-term follow-up, and time course
Schmidt-Erfurth U. High-resolution optical coherence tomography of visual improvement. Ophthalmology 1991; 98:1109-1114.
to evaluate vitreomacular traction before and after membrane
peeling. Ophthalmologe. 2008; 105(8):753-760. 14. Rice TA, De Bustros S, Michels RG, Thompson JT, Debanne
SM, Rowland DY. Prognostic factors in vitrectomy for epiretinal
10. Lee JW, Kim IT. Outcomes of idiopathic macular epiretinal membranes of the macula. Ophthalmology 1986; 93:602-610.
membrane removal with and without internal limiting membrane
peeling: a comparative study. Jpn J Ophthalmol. 2010; 54(2):129-134. 15. Ting FSM, Kwok AKH. Treatment of epiretinal membrane: an
update. Hong Kong Med J 2005;11:496-502
11. Kadonosono K, Itoh N, Uchio E, Nakamura S, Ohno S. Staining
of internal limiting membrane in macular hole surgery. Arch
Ophthalmol 2000; 118:1116-1118.

First Author
Bhuvan Chanana MD, DNB, MNAMS, FICO

Delhi Ophthalmological Society
Monthly Clinical Meeting, January 2011

Venue: Auditorium, Guru Nanak Eye Centre
Date & Time: 30.1.2011, (Sunday) 11:00 a.m.

BREAKFAST 10:30 am - 11:00 am

Clinical Session: 11:00 am onwards

Clinical Cases: : Dr. Neha Rathi 10 mins.
1 Bilateral Medial Rectus Aplasia
10 mins.
Moderator: Dr. P.K. Pandey 10 mins.

2. A case of B/L infromedial Space occupying lesion : Dr. Saurabh Kamal
Moderator: Dr. Sushil Kumar
Discussion

Clinical Talk: : Dr. J.L. Goyal 15 mins.
Neuro-ophthalmic manifestation of Trauma 10 mins.

Discussion

Video Assisted Symposium: Management of Sequalae of Ocuar Trauma
Chairman: Dr. B. Ghosh Co-Chairman: Dr. Kamlesh & Dr. Usha Yadava

1. Chemical Burns : Dr. Ritu Arora 10 mins.
2. Canalicular injury
3. Traumatic dislocation of crystalline Lens & IOLs : Dr. Ruchi Goel 10 mins.
4 Management traumatic Superior Oblique palsy
5. Trauma in operated Trabeculectomy & Glaucoma : Dr. Meenakshi Thakker 10 mins.

drainage devices : Dr. Subhash Dadeya 10 mins.

: Dr. Kirti Singh 10 mins.

20 Early Bird Prizes Followed by Lunch

www.dosonline.org 35

Role of Ocular Response Analyzer in Glaucoma
Measurement of IOP

Rakhi Kusumesh, Tanuj Dada MD, Sasikala, Anita Panda MD,MRCO, FICS

Understanding the role of ocular biomechanical properties The ocular response analyzer (ORA) was developed with a similar
may be key in the future of glaucoma management. The purpose in mind. This instrument evaluates several biomechanical
biomechanical properties of the anterior segment, such as properties of the cornea and then corrects the IOP according to
hydration, elasticity, hysteresis and rigidity, have substantial and these properties.
widely variable influence on IOP measurement. So, achieving
accurate estimates of intraocular pressure remains difficult. Thus, It provides four variables:
an understanding of the differences in corneal biomechanics
between individuals may explain why some optic nerve heads are 1. Goldmann-correlated IOP (IOPG)
more susceptible to damage by variations in IOP.
2. Corneal-compensated IOP (IOPcc)
Over the past few years, several new instruments have been tried
in an effort to resolve the limitations of conventional tonometry. 3. Corneal resistance factor (CRF)
The current gold standard for IOP measurement in the laboratory
setting is manometry, however, the use of such manometric 4. Corneal hysteresis (CH)
devices is not feasible in routine clinical care. IOP measurement in
the routine is generally obtained using one or more of the following Reichert has produced an instrument, the Ocular Response
instruments: Indentation tonometry, Goldmann applanation Analyzer (ORA; Reichert Corporation; Depew, USA), that
tonometery, tono-Pen, and the pneumotonometer and Dynamic measures the corneal response to indentation by a rapid air pulse,
Contour Tonometry. based on the principles of non-contact tonometry, in which the
IOP is determined by the air pressure required to applanate
Indentation tonometry, these were early efforts to monitor IOP, the central cornea. It is a new type of air-puff tonometer that
which essentially measured how easily the globe was compressed, ejects 20 msec of air impulse and monitors the time course
this techniques was highly dependent on rigidity of the ocular causes the cornea to move inward, past applanation, and into
tissue. Thus, they typically overestimated true IOP in eyes with a slight concavity (inward shift - applanation - slight concavity
more rigid corneas and underestimated true IOP in eyes with -second applanation - and a return to normal convex curvature).
softer corneas.1 Then Goldmann applanation tonometer (GAT) Milliseconds after applanation, the air pump shuts off, and the
quickly became the preferred method to measure intraocular cornea gradually recovers its normal configuration, passing
pressure, primarily because it is far less affected by ocular rigidity through a second applanation state. An electro-optical system
than schiotz tonometry.2 Others were the Tono-Pen, and the monitors the deformation of corneal curvature in the central 3.0-
pneumotonometer. mm diameter throughout the entire process, and two independent
values are obtained for the inward and outward applanation events
Two particularly interesting techniques have emerged during the because of energy absorption or damping in the cornea, resulting
last few years: Pascal Dynamic Contour Tonometry (DCT) and in two different pressures. The difference between ‘‘inward’’ and
Ocular Response Analyzer (ORA) tonometry. ‘‘outward’’ applanation pressure depends on the viscoelastic
properties of the corneoscleral shell, because of energy absorption,
Recent studies performed using the new dynamic contour the inward and outward applanation events are delayed, resulting
tonometer (DCT) seem to indicate less dependence on central
corneal thickness of its pressure measurements, compared with
those of conventional tonometry. DCT uses a concave “contour
matching” surface that allows transcorneal measurement of
IOP without significant applanation of the cornea. This helps to
overcome the influence of corneal biomechanical characteristics
(including central corneal thickness).3,4 To date, several studies
have found that DCT measurements are relatively independent of
central corneal thickness, while GAT measurements consistently
demonstrate significant relationships with corneal thickness.5
Additionally, intracameral manometric studies using harvested
human eyes have demonstrated a strong correlation between true
IOP (per manometry) and DCT measurements of IOP.6

Cornea Services Applanation plot for Reichert Ocular Response
Dr Rajendra Prasad Centre for Ophthalmic Sciences, Analyzer (ORA)

All India Institute of Medical Sciences, New Delhi,

www.dosonline.org 37

in two different pressures. The average of these two pressures between CH and glaucoma damage. The effect of topical treatment
provides a reproducible Goldmann-correlated IOP, and the on corneal biomechanics is currently unknown. There is some
difference between the two pressures is called corneal hysteresis. suggestion that the use of topical prostagland in analogues may
alter the extracellular matrix of the cornea making it a less stiff
Corneal hysteresis: Corneal hysteresis is an indication of viscous structure,although to date there have been no in vivo studies that
damping in the cornea, due to the viscoelastic resistance of the support this hypothesis.14
cornea to a deformation pulse by an air jet of the tonometer,
reflecting the capacity of corneal tissue to absorb and dissipate Diurnal variation in CH & IOP: Although both CCT and IOP
energy. Previous studies have revealed that this measure ascribed are higher during the nocturnal period than during the diurnal
to corneal tissue is independent of the radius of curvature of the period, the nocturnal IOP elevation cannot be explained by the
cornea, corneal astigmatism, visual acuity, or axial length.11 In nocturnal increase in CCT when examining both the timing
eyes with keratoconus or Fuchs’ dystrophy or those undergoing and magnitude of the change. Teruyo K et al studied 24- hour
corneal refractive surgery, the corneal hysteresis is significantly changes of corneal biomechanical properties and their influences
reduced with respect to eyes with normal corneas. on measurement of IOP and found no evidence of association
between change in IOP in healthy young adults with a 24-hour
Goldmann-correlated IOP: The average of the inward (P1) and change in known corneal biomechanical parameters.15
outward (P2) applanation pressures. This parameter is closely
correlated with GAT-IOP. In summary, the understanding of ocular biomechanics has
greatly improved in recent years, and it seems likely that additional
Corneal-compensated IOP: It is a pressure measurement that research in this area will have a substantial impact on future
utilizes the new information provided by the corneal hysteresis glaucoma treatments. While measurement of central corneal
measurement to provide an IOP that is less affected by corneal thickness has now become a routine part of practice, it seems
properties. Similar to DCT-IOP findings, several published clinical highly likely that future diagnostic procedures in glaucoma will be
studies have reported that corneal compensated IOP is unrelated directed toward the measurement of anterior segment properties
to central corneal thickness.7 beyond simple geometric thickness. Additionally, the impending
capability to clinically measure biomechanical properties of the
Corneal Resistance Factor: It is derived from corneal hysteresis, optic nerve and adjacent tissues will greatly enhance our ability
is an indicator of the overall resistance of the cornea, which, to determine an individual’s susceptibility to glaucoma. It will
according to previous data, seems to be related to central also allow us to better target and specifically tailor our treatment
corneal thickness and GAT-determined IOP but not to corneal- options.
compensated IOP. The thicker the cornea and/or the higher
the IOP GAT, the greater the corneal resistance factor. Corneal References
compensated IOP is unaffected by the corneal resistance factor, the
latter being significantly correlated with central corneal thickness 1. Friedenwald JS. Clinical significance of ocular rigidity in relation
and IOP GAT. to the tonometric measurement. Trans Am Acad Ophthalmol
Otolaryngol 1949 Jan-Feb;53:262-4.
Ocular Biomechanics and the Risk for Glaucoma
2. Singh RP, Goldberg I, Graham SL, et al. Central corneal thickness,
Biomechanical properties may be more predictive of glaucoma tonometry, and ocular dimensions in glaucoma and ocular
development and progression than IOP level. The best evidence hypertension. J Glaucoma 2001 Jun;10(3): 206-10.
for this hypothesis is the Ocular hypertension treatment study
(OHTS) finding that suggested CCT is the strongest predictor 3. Siganos DS, Papastergiou GI, Moedas C. Assessment of the Pascal
for conversion from ocular hypertension to primary open-angle dynamic contour tonometer in monitoring intraocular pressure in
glaucoma.8 Besides CCT, CH and CRF suggest that these factors unoperated eyes and eyes after LASIK. J Cataract Refract Surg 2004
may also provide unique value in risk analysis.9 In multivariate Apr;30(4):746-51.
analysis that included CCT, axial length, refractive error and ORA
variables, CH was the only variable that was associated with any 4. Francis BA, Hsieh A, Lai MY, et al. Los Angeles Latino Eye Study
degree of posterior laminar deformation. This relationship was Group. Effects of corneal thickness, corneal curvature, and
significant for subjects with glaucoma, but not normal subjects.10 intraocular pressure level on Goldmann applanation tonometry and
These results suggest that CH, an anterior segment biomechanical dynamic contour tonometry. Ophthalmology 2007 Jan;114(1):20-6.
metric, may be related to distensibility of the posterior segment/
optic nerve complex. 5. Ku JY, Danesh-Meyer HV, Craig JP, et al. Comparison of intraocular
pressure measured by Pascal dynamic contour tonometry and
Recent studies have suggested that a thinner CCT is a risk factor for Goldmann applanation tonometry. Eye 2006 Feb;20(2):191-8.
the development of glaucoma, although this risk may be explained
by the effect of CCT on IOP measurement such that eyes with 6. Kniestedt C, Nee M, Stamper RL. Dynamic contour tonometry: a
thin corneas present at later stages of the disease progress.11,12 In comparative study on human cadaver eyes. Arch Ophthalmol 2004
a recent hospital-based, crosssectional study by Congdon and Sep;122(9):1287-93.
co-workers, CH was measured in a cohort of glaucoma patients
and a retrospective chart review used to determine the degree 7. Medeiros FA, Weinreb RN. Evaluation of the influence of corneal
and progression of glaucoma in each patient. The study found biomechanical properties on intraocular pressure measurements
that low CH was predictive of visual field progression.13 This is using the Ocular Response Analyzer. J Glaucoma 2006 Oct;15(5):364-
one of the first studies to determine an independent association 70.

8. Congdon NG, Broman AT, Bandeen-Roche K, et al. Central corneal
thickness and corneal hysteresis associated with glaucoma damage.
Am J Ophthalmol 2006 May;141 (5):868-75.

38 DOS Times - Vol. 16, No. 7, January 2011

9. Kirwan C, O’Keefe M, Lanigan B. Corneal hysteresis and intraocular demographic patient data: prospective analysis of biophysical
pressure measurement in children using the Reichert Ocular parameters in tertiary glaucoma practice populations. J Glaucoma
Response Analyzer. Am J Ophthalmol 2006 Dec;142(6):990-2. 2006 Apr;15(2):91-7.

10. Wells AP, Poostchi A, Wong T, et al. Corneal biomechanics and optic 13. Congdon NG, Broman AT, Bandeen-Roche K, et al: Central corneal
nerve head compliance: corneal hysteresis but not corneal thickness thickness and corneal hysteresis associated with glaucoma damage.
correlates with optic nerve surface deformation in glaucoma patients. Am J Ophthalmol 2006 may;141(5):868—75.
Invest Ophthalmol Vis Sci 2008 Mar 3. [Epub ahead of print].
14. Wu KY, Wang HZ, Hong SJ: Effect of latanoprost on cultured porcine
11. Gordon MO, Beiser JA, Brandt JD, et al: The Ocular Hypertension corneal stromal cells. Curr Eye Res 2005 Oct;30(10):871-9.
Treatment Study: baseline factors that predict the onset of primary
open-angle glaucoma. Arch Ophthalmol 2002 jun;120(6):714—20. 15. Teruyo K, John H. K. L, Robert N. W. Effect of 24- hour corneal
biomechanical changes on intraocular pressure measurement. Invest
12. Kniestedt C, Lin S, Choe J, et al: Correlation between intraocular Ophthal Vis Sci. 2006 Oct;47(10):4422-6.
pressure, central corneal thickness, stage of glaucoma, and

Author
Anita Panda MD, MRCO, FICO

Notice for General Body Meeting*

To be held on 17th April, 2011 at 4.30 p.m. at
Hotel Ashok, Chanakya Puri, New Delhi

*As per the decision of the last Annual General Body Meeting, 2001 the Annual GBM will be held along with the
ęrst monthly clinical meeting in July, 2002.

www.dosonline.org 39

Adie’s Pupil

1Shilpa Goel, Savleen Kaur, 2Prem Vardhan, 1Yuvika Bansal, 1Gaurav Goel

Adie's tonic pupil1 refers to a dilated, poorly reactive pupil, the spinal ganglion. Some people think this is due to an attack by
resulting from damage to postganglionic parasympathetic a virus; other think it is "auto-immune". Lesions in the Edinger-
fibers of ciliary ganglion that innervates sphincter pupillae. The Westphal nucleus or anywhere along the course of the third nerve
tonic pupil is a common cause of anisocoria, or unequal pupils. may damage the parasympathetic outflow and lead to pupillary
dilation. Usually the postciliary ganglionic lesions cause pupillary
Adie’s syndrome is a neurological disorder that affects the pupil parasympathetic supersensitivity to a lower concentration of
of the eye and the autonomic nervous system. It is known by a pilocarpine, but preciliary ganglionic lesions can also induce this
number of names as shown by the table below2. condition

• Adie’s pupil Tonic pupils have been attributed to various diseases, including

• Adie-Holmes syndrome • Syphilis

• Holmes-Adie syndrome • herpes zoster

• Kehrer-Adie syndrome • orbital trauma

• Markus' syndrome • temporal arteritis

• Markus-Adie syndrome • endometriosis

• Weill’s syndrome • paraneoplastic syndromes

• Weill-Reys syndrome • There is typically no association with underlying disease of the
eye, nerves or brain, with the exception of Adie's syndrome
• Weill-Reys-Adie syndrome (70% of patients) In Adie's syndrome, the deep tendon reflexes
may be decreased.
pupillotonic pseudostrabismus
Clinical Features
• Saenger’s syndrome
It presents with mydriasis, loss of deep tendon reflexes (DTRs), and
Historical Background diaphoresis. Ten percent of cases are bilateral and the prognosis is
benign. Adie syndrome presents with three hallmark symptoms,
The London ophthalmologist James Ware (1756-1815) described namely abnormal pupil size (mydriasis), loss of deep tendon
some of the features of this syndrome in 1813. John Hughlings reflexes and diaphoresis. Other signs may include hyperopia due
Jackson (1835-1911) described the syndrome fully in 1881, and to accommodative paresis, photophobia and difficulty in reading.
in 1902 Max Nonne (1861-1959), Julius Strasberger, and Alfred
Saenger. Oloff in 1914 appears to have been the first to show that • Most people have no symptoms from Adie's tonic pupil.
the disorder is not syphilitic in origin. Joint publication in 1926 by
G. Weill and L. Reys, and described by Adie in 1931 as a disease sui • At first, it may only cause the loss of deep tendon reflexes
generis of the autonomous nervous system. At the time of Adie’s on one side of the body, but then progress to the other side.
publication more than 60 similar cases had been described. Adie The eye and reflex symptoms may not appear at the same
recognised the work of his colleague, Foster Moore, who, from time. Sensitivity to bright lights (because the pupil isn't
1924 onwards published altogether 15 cases – and later expressed constricting) is the most common symptom.
his dissatisfaction with not having been ascribed the eponym.
The eponymic term Adie’s syndrome was coined by the French • Vision symptoms are not common but may include glare or
neurologist Jean-Alexandre Barré in 1934,”syndrome d’Adie”. diminished ability to focus at near.

The prevalence of the Adie's pupil is about two cases per 1000 • Over years, the resting pupil size can become smaller and
population. Although patients of all ages are affected, the mean more normal appearing, although a normal response to light
age is 32 years, and there is a female predominance (2.6:1) for the doesn't usually recover. The tonic pupil may become smaller
idiopathic variety. (miotic) over time which is referred to as "little old Adie's
pupil”.
Etiology
• Sometimes over time the second eye becomes affected. A
In many cases the cause of Adie's tonic pupil is unknown. It is related condition called Adie's syndrome occurs when there
thought to be the result of a viral or bacterial infection that causes is loss of deep tendon reflexes as well.
inflammation and damage to neurons in the ciliary ganglion, and
• Patients with tonic pupil may also sweat excessively,
1. Guru Nanak Eye Center, sometimes only on one side of the body. The combination of
Maharaja Ranjit Singh Marg, New Delhi , these 3 symptoms – abnormal pupil size, loss of deep tendon
2. Eye Q Hospital, Gurgaon, Haryana

www.dosonline.org 41

(a) (b)

(c) (d)

Figure 1: Anisocoria in dim light and Figure 2: Right eye pupil constricted with
bright light (a-d) 0.125% pilocarpine

reflexes, and excessive sweating – is usually called Ross’s in adrenergic mydriasis the pupil is unusually large,the palpabral
syndrome fissure is widened and conjunctiva is blanched. Accommodation
is not impaired and very bright light can overcome the mydriasis.
On examination one should look for the following features:
Treatment
• Anisocoria that increases in bright light. (Figure1 a-d)
The loss of deep tendon reflexes is permanent. Some symptoms
• Light near dissociation: direct light reflex is absent while of the disorder may progress.
near reflex is present or tonic due to abberant reinervation
of sphincter by accommodative neurons. • Prescribe reading glasses to compensate for impaired vision
in the affected eye,
• Slit lamp examination shows sectoral vermiform movements
of the iris due to segmental denervation.90% of Adie’s pupil • Pilocarpine drops to be applied 3 times daily to constrict the
have some residual light reaction that is segmental. dilated pupil.

• Testing with low dose (0.125%) pilocarpine constricts the • For most individuals, pilocarpine drops and glasses will

tonic pupil3 due to cholinergic denervation supersensitivity. improve vision. Thoracic sympathectomy, which severs the

A normal pupil will not constrict with the dilute dose of involved sympathetic nerve, is the definitive treatment for

pilocarpine. (Figure 2) excessive sweating in Ross syndrome.

Differential Diagnosis References

Traumatic mydriasis: Traumatic pupil is usually not round and 1. Adie, WJ. Pseudo-Argyll Robertson pupils with absent tendon

slit lamp examination will not show any consistent iris movements, reflexes: a benign disorder simulating tabes dorsalis. Br Med J 1931;

while other signs of ocular trauma like sphincter tear, iris border 1:928.

transillumination will be seen. 2. National Institute of Neurological Disorders and Stroke. Page”.

Third nerve palsy: Third nerve palsy seldom present with an Retrieved 2008-01-21

isolated weakness of the iris sphincter. Partial third nerve palsies 3. Leavitt, JA, Wayman, LL, Hodge, DO, Brubaker, RF. Pupillary

with aberrant reinnervation may show a segmental palsy of response to four concentrations of pilocarpine in normal subjects:

iris sphincter( e.g. due to diabetic neuropathy).Such pupil may application to testing for Adie tonic pupil. Am J Ophthalmol 2002;

constrict with miotic dose of pilocarpine(1%). 133:333.

Pharmacological mydriasis: In atropinic mydriasis the entire
sphincter is palsied(360%) and pilocarpine miosis is blocked, while

First Author
Shilpa Goel

42 DOS Times - Vol. 16, No. 7, January 2011

How to Maintain Practice Growth Miscellaneous

Vipin Sahni MS

“Only the fools and dead never change” – Anonymous where as vertical line shows earnings in lacs. In initial phase it
grows rapidly this can last for a few years.In the next phase it
If you are an ophthalmologists in your mid 40s or 50s you must grows slowly again for few years, then a phase comes when the
have seen changes coming in India. If you consider the changes practice reaches a plateu and growth comes to a standstill, this
in society then it is changing so fast that it is difficult to enumerate may remain for many more years . You keep the earnings nearly
them. Remember your days in college hostel. If you wanted to the same year after the year. Then the phase of decline starts and
phone home then one would go to a post office to make a call back the practice starts declining. Slowly it cascades down.
home. There were no Malls, no Metro, and no Mobiles. Only elite
class used to travel by air. Movies were the only entertainment But the practice graph (Figure 2) of a visinary eye surgeons does
as there was only Doordarshan that too broadcasting a very few not follow the usual path. This graph shows they develop their
programs. TVs were not found every household. Roads used to practice from scratch then there is phase of medium to rapid
be empty when the serials Ramayana or Mahabharata used to growth. In the next phase there is some stagnation which makes
come on TV. them change their mind , and they work smartly to take their
practice to a newer height. In the next phase again they notice
Similarly remember your residency days. ICCE was the standard their practice has stopped growing and then they again start
surgery. People use to retire when they had cataract because working harder to take their practice to a new high. Here you
outcome of cataract surgery was very uncertain. There were only must remember working smartly and working harder are different
one or two odd microscopes in the departments that too were strategies for growth of your practice.
exclusively for the use of our professors. As our professors and
lecturers were learning ECCE and IOLs sometime we use to I have shown in figure 2 graphs has a time zone of five years, but
consider ICCE was a better surgery. (As even today some people for the surgeons who are very vigilant about their practice may
think Phacoemulsification and in bag IOL is no better than not have any slag period or very small slag period say for one to
simple PCIOL or SICS). No NCTs, OCTs, IOL masers, Nd YAG two years.
Lasers, Excimers or other lasers only big Argon Laser Machine
used to come. We used to do field testing on a chart hung on How to achieve this continuous practice growth? There are some
wall. Ophthalmology was considered the poorest branch, largely rules to follow –
because charges were very low and the old ophthalmologists used
to visit to patients at their home for cataract surgery. Change with the changing time. If you have a mindset that you are
the best it is good but to keep yourself as best you have to change
But today everything has changed in the society as well as in with changing times. I have seen some best practices which did
our branch Ophthalmology. There are Famto Lasers, Multifocal not change with changing technology and failed miserably in the
lenses, MIOLs, Multi point retinal lasers, 25G vitrectomy etc.
The Scenario is completely changed. Those who are changing
with time are riding the horse and galloping ahead. But there are
many practices which are not growing; there are many reasons for
it. Some are not growing because of the increasing competition,
others because of lack of initiative by the owner. Others are starved
due to lack of investments; some others are old timers who have
not changed with the changing times. Let us see what the growth
strategies are in today’s rapidly changing scenario.

Is no growth an option? Since travelling and meeting new people
is my hobby, I meet so many peoples and it is not surprising
to note many of them think they do not want any growth. As
they want to avoid the complications of growth. Growth brings
with it – crowds of patients, more surgeries, to see them and to
manage them they have to spend more time in practice which
they do not want, so they avoid growth. There is another set of
ophthalmologists who do not have a son/heir who they can take
care of their practice after them, so they do not want to invest and
grow more. Managing the growth is not an easy task. It involves
a lot of efforts and time which people do not want to spend. So
no growth is a very viable option.

The usual graph of a practice of an average eye specialist is like
Figure 1. Horijontal line shows time lapsed in practice in years,

Kaushalya Devi Eye Institute
Pilibhit / Shahjahanpur, U.P.

www.dosonline.org 47

latter part of life. Some failed to change from ICCE to ECCE with Diversification in the practice is very important. First let us talk
PCIOL; some other could not do Phaco-emulsification (or failed about services. I have seen those Retina Surgeons who are also
in providing Phaco surgery at their centers). Some failed to unite doing phaco-emulsification are now becoming more successful
for LASICS and hence are losers today. They missed the bus. I than pure Retina Surgeons, or it is difficult to survive as pure
am not saying that they are doing badly but they missed the spot LASIK surgeon then cataract and refractive surgeon. In the same
where they could have reached if they had changed themselves way if you have an optical and medical dispensary at your centre
with the changing time. then you can have more per patient revenue, which you may not
be earning otherwise. Another way to think about diversity is to
Upgrade, upgrade and upgrade. If you fail to upgrade your facility examine the source of your patients. In the typical setting, 70% of
someone else will provide those facilities some day and you will new patients come from alumni, patient-to-patient referrals, and
lose your hard earned practice. So don’t starve your practice of rest of the patients come from marketing, optometric, medical
investments. Regular feeding of your practice is must. Suppose and minor other referral sources. Such a practice has literally
you are practicing for years and your A- Scan gives good results thousands and thousands of referral sources, and is extremely
but with the advancement in technology now a day’s immersion resistant to the loss of any one source.
A-Scan is preferred. So you should also get an immersion A- Scan Service area diversity is also important. If you are working in a
for your practice. This will cut down your post Op. refractive place where most of your patients come from one particular area,
surprises. In the same way if you are doing toric IOLs and locality or town then it is dangerous. If due to some reason one
multifocal lenses, then IOL master is the best choice. You have to area is cut then you may be in trouble soon. Initially most of my
upgrade your facilities to get premium patients. patients were coming from the tarai regions of Kumaun but when
Uttarakhand was formed then bus services to the region were cut
Marketing Guru Phillip Kotler has rightly said that “With any off and I lost my clientele.
amount of publicity or marketing you can never force anybody Examine your current procedure and service mix. Are you
to buy poor quality products twice”. So quality of eye care is very providing all the possible surgeries and procedures in your
important. Some of my colleagues ask me what quality you always practice? It doesn’t take much time to examine this. Open your OT
talk about. By the quality I mean it’s like Mc Donald. When ever register/ procedure report for the last year. How many different
you go there and order a Mc Chicken Burger, you know what it procedures/ surgeries did you perform last year. Look for any gaps,
will be like – it will have two sesame seed coated buns with two especially in special investigations and plastics. I have seen many
chicken cutlets with cheese cream sauce and lettuce in it. All the surgeons not focusing on other surgical cases except the cataracts
tables will be always clean and toilets will be clean and dry. Staff but in all the other surgical cases usually make 20% of practice.
will be young and courteous to you. Service will be quick and All of this diversity will almost certainly command a substantial
within few minutes your order will be served. This you will get in increase in the scale of your practice.
every Mc Donald, whether it is in Las Vegas in US or Phuket in If you see the demography of India, It has some unique features-
Thailand or on NH -24 in India. Similarly in your practice when • Population is increasing rapidly.
ever anyone comes staff should be polite and courteous, facility • Around 40% population is between 15 – 40 years of age.
should be clean, he should be attended promptly and good quality • Life expectancy is rising. It has reached around 68 years.
eye care should be provided to him. • Cataract is occurring at a younger age.
• As the surgical out comes have improved, more immature
If you feel you are not providing quality eye care, before doing
anything else, you should try to improve it in all aspects. If you cataracts are going in for surgery as compared to the early
fear some other groups coming to your town and capturing more days when only mature cataracts were willing for surgery.
practice and patients then it is must for you to improve your • You are willing to operate on patients even with 6/9 vision,
level of eye care. The quality must be visible and perceived by whereas earlier we used to advise surgery when vision was
everybody coming to your centre, whether he/she is coming for less than 6/24.
OPD or Surgery or attendant of the patient or even some body If you consider these points, then future of ophthalmologists is
making professional call to you. There is a patient in every home very bright in India. Even if you do nothing special your practice
and every family, if a person is satisfied he will surely refer you a will grow in future.
patient or bring in the patient some day. If you apply even few of these tips to your practice, then the graph
of your practice will change permanently. And you will be able to
Quality of treatment or eye care is what patient comes for, and do much better in your practice. It is must to change yourself with
gets when he visits in your clinic. Whether it is OPD treatment the changing time to acquire results you dream.
or some procedure or a surgery, if people know that you provide “Progress is impossible without change; and those who do not
good treatment, they come to you only. In earlier times a doctor change with times cannot change anything.”
could behave anyway to his patients and their attendants, but now
the patient has to be treated with respect and kindness, to let him Author
come back to you later also. Vipin Sahni MS

Facility modification and upgraded facility looks are very
important. If you had a good setup twenty years ago then you
must have used mosaic floors, ten years ago marble was in and
now vitrified tiles are the norm. So one has to uplift the facility
looks and design according to the time. Visible quality is one
which everyone can see. Your patients waiting lounge must be
clean, walls should be properly painted, and there should be no
stains on floor or walls.

48 DOS Times - Vol. 16, No. 7, January 2011

Scheme for Participation of Voluntary Organisations Miscellaneous

Non-recurring Grant-in-aid for Development of iv) The applicant NGO should have preferably hand on
Mobile Ophthalmic Units with Tele-Ophthalmic experience/in handing teleophthalmology project.
Network and few fixed Tele-Models
v) The NGO should have matching contribution of the amount
sanctioned under the scheme upto maximum of 60 lakhs.

Non-recurring Grant-in-aid for Development of Mobile vi) Recent investments made by the NGO on above-mentioned
Ophthalmic Units with Tele-Ophthalmic Network and few items during preceding three years (03) can be taken as
fixed Tele-Models (up to maximum of Rs. 60 lakhs) contribution from NGO as matching grant. For long-term
sustainability and resource participation, following recurring
One of the objectives of the NRHM is to provide the rural costs shall be borne by the NGO:
population access to healthcare services. In this context,
Telemedicine, an information and communication technology i) Salaries of staff
based tool, has the potential to assist in electronic delivery of
diagnostic and healthcare services to remote rural population even ii) Cost of consumables
in the absence of physical infrastructure in place thus creating
a platform to network India. Telemedicine helps to provide iii) Costs on maintenance of equipment and vehicles, POL,
healthcare where there is none and improve healthcare where etc.
there is some. The fact is that while 70% of our population lives
in rural India; 90% of secondary & tertiary care facilities are in iv) Administrative overheads
the cities and towns far away from the rural India. At the same
time, it is also a fact that a significant proportion of patients in Population to be served
remote locations in tribal/ underserved area could be successfully
managed with some advice and guidance from specialists and The Tele-Ophthalmology project is primarily for the underserved
super-specialists in the cities and towns. population of the rural, tribal and hilly areas with specific focus
to the north eastern States. The NGO shall serve an area of 150
Financial Assistance kms from the district headquarter.

Non-recurring Assistance: Upto Rs. 60 lakh towards development Infrastructure Requirement: This shall consist of two
of Mobile Ophthalmic units with Tele-Ophthalmic Network and component:
few fixed Tele-Models* (with equal contribution from NGO in
the form of building, equipment and vehicle(s) or cash from 1. Base hospital
management / donations). The assistance for Mobile Van with
essential ophthalmic equipments is upto Rs.20 lakh. The assistance 2. Peripheral Unit (Fixed/ Mobile Unit)
for Tele-Ophthalmic Network/Tele-Model is upto Rs. 40 lakh for
any of the following purposes: Base Hospital

• Construction, renovation & furnishing* a) Manpower requirement:

• Ophthalmic equipment, instruments and other machines Category of personnel Minimum Minimum
(List attached) No. No. in difficult

(*Not more than 33% of GIA can be utilized on capital works / terrain
construction activities in case of fixed models).
Ophthalmic Surgeons 4 2
Eligibility Criteria: The organization should have: (Skilled enough to handle 8 4
Subspecialties)
i) Should satisfy general eligibility conditions mentioned at page 4 2
no. 2 of the document (except eligibility clauses) Para Medical Ophthalmic
Assistant (Ophthalmic
ii) Organizations having experience in providing eye care Assistant / Technician /
services for 5 years will be considered. Optometrists / Ophthalmic
Nurse.)

Support Staff (Counselor/
Social worker/Accountant /
Administrator)

iii) Operated on at-least 2000 cases per year of cataract or b) At-least 20 bed IPD facility
combination of cataract and other ophthalmic diseases
(as approved in the scheme) in the preceding 2 Years of c) In addition, the applicant NGO should have adequate
application. In case of difficult terrain (e.g. North eastern infrastructure and equipment for OPD services, Operation
states), relaxed criteria of 200/600 operations in the preceding and Management of the tele-Ophthalmic Services admitted
1 year / 2 Year shall be applicable respectively. patients.

www.dosonline.org 49

d) At least one of the eye surgeon in the base hospital should 10. Optical dispensing equipment: Edger zeta, lensometer, frame
have experience in handling posterior segment disorder like warmer
Diabetic Retinopathy, Glaucoma and others.
11. Autorefractor
Peripheral Unit (Fixed/ Mobile Unit) 12. Computer/Laptop with UPS
13. Printer cum scanner
The fixed model tele-ophthalmic and the mobile units 14. Mobile phone
shall consist of the basic infrastructure and manpower
requirement as follows:

Minimum Requirements: 15. Still digital camera

i) Manpower: There should be at least one Paramedical 16. Tele-ophthalmology software
Ophthalmic Assistant (PMOA) in both fixed or mobile units 17. 2GB Pen/thumb drive
18. Inverter with battery
ii) In case of fixed facility the OPD Room shall be at least one 19. 5 kva Genset
room with minimum length of 6 meters/3 meters will be
required.

iii) In case of the mobile unit, the OPD shall be conducted in the 20. Video conference camera and projector
Mobile Van with the provision of examining the patients 21. 8 port switch-1 no.
22. Picture grabber card
iv) IT Connectivity 23. CAT cable straight-1 no.; Cross-1 no (with RJ 45)-100 meters
24. All in one memory card reader
Services to be Rendered 25. Pc to video converter

i) Identification of conditions requiring services like cataract,
glaucoma and Red eye etc. and refer patients to affiliated at
Service Centre;

ii) Vision testing & prescription / dispensing of glasses; Optical 26. Audio visual aid
shop can be set up or outsourced.
27. Furniture and fixture: table (4x2 feet)-2 no.; bench (8x1)-4
iii) Conducting school eye screening program & IEC. no.; plastic chair-5 no.; examination stool-2 no.; dismountable
black room; sponsor displaying unit
iv) Organizing screening camps at the vision centre or other
places. 28. Others: umbrella, travelling bag and battery charger-1 no.

v) Participation in training of link workers, volunteers and Expected Output: NGOs receiving non-recurring grants Shall
teachers; and
Cataract and other Eye Diseases:
vi) Imparting eye health education to the community.
i) Commit to take the responsibility of active screening of
vii) Maintain village wise blind registry. population of villages allocated by the District Health Society
and in addition, cater to the patients from adjoining area.
viii) Furnish data in prescribed format on number of patients,
refractions and school eye screening. ii) Prepare and maintain village wise Blind Registers in
prescribed format (Annexure II)
Equipment: The approved list of equipment instruments,
mobile van, furniture, fixture is as under: iii) Complete the construction & procurement of equipments &
vehicle, if any within one year after following due procedures.
Approved list of items under Grant-in-aid to Tele-ophthalmology
project iv) Provide & maintain Cataract Surgical Cards for the patients
operated in the base hospital and other OPD / Indoor wards
1. Mobile unit including fabrication records (Annexure – III)

2. Slit lamp v) The NGO should be committed to perform free of cost
operations of 1) Cataract and/or other ophthalmic diseases
3. Schiotz Tonometer like Diabetic retinopathy, Glaucoma, Keratoplasty, Childhood
Blindness- Squint correction, ROP, Retinoblastoma upto a
4. Fundus camera value of 50 % of the sanctioned amount. For the purpose of
this scheme, the deemed value of one cataract operation is
5. Retinoscopy Rs. 750/-only and for other diseases it is Rs. 1000/- per case.

6. Direct ophthalmoscope

7. Trial set and frame vi) Maintain proper record & submit monthly report on cases
8. Vision charts screened, treated and operated in the prescribed Performa
9. Torch light (Annexure – VII) in addition to reports as may be sought
from the institution from time to time.

50 DOS Times - Vol. 16, No. 7, January 2011

vii) Prepare and maintain Diabetic Retinopathy Register Disposal of Assets
(Annexure – XII), Glaucoma Register (Annexure – XIII),
Squint Register (Annexure – XIV), Keratoplasty Register NGO shall maintain a register of Assets acquired wholly or
(Annexure XV). substantially out of Government grants as per the prescribed
proforma at (Annexure–VI). Assets acquired wholly or
viii) Commit to perform at least 2000 cases (Cataract Surgeries substantially out of the Government grants will not be disposed
and others interventions) per year for succeeding 5 years. of, encumbered or utilized for any purpose other than those for
which the grants are sanctioned. If such assets are disposed of after
Procedure for Approval of Grants due sanction, the money thus received will be credited to State
Health Society. Goods declared as obsolete and unserviceable or
Two copies of application in with details of the proposed tele condemned as per the prescribed procedure may be disposed by
project would be submitted by applicant NGO along with NGO after prior approval of State Health Society.
necessary documents in support of qualifying criteria to the
State Programme Officer (SPO), NPCB. The SPO would examine Monitoring and Evaluation
the proposal in terms of eligibility criteria, and depute a team
of expert(s) (2-3) from the State/district to visit the NGO for The State Programme Officer/district Health Society shall inspect
assessing present facilities and requirements. This entire work the work done as and when required and shall also obtain monthly
should be completed within maximum of three months from the report from the NGO of the work done. The grantee NGO shall
date of receipt of applications complete in all respects. The SPO be duty bound to submit such reports on a timely basis.
may thereafter, forward his recommendation to the competent
authority for final disposal. Audited Statement of Accounts & Utilization Certificate

Competent authority NGO shall get its accounts audited by a Chartered Accountant and
submit these accounts within three months of the closure of every
Secretary (Health)/Mission Director NRHM of the State would be financial year till the completion of conditions in the prescribed
the competent authority to approve/reject applications in writing Bond to the State Health Society under intimation to the District
giving reasons for rejection, in case of disapproval. Health Society. NGO will also have to furnish a certificate of actual
utilization of the non-recurring Grant-in-aid for the purpose for
Release of Grant which it was received within a period of 3 months of the closure
of the financial year. Utilization Certificate shall be submitted in
The NPCB shall release funds for this scheme to State Health the prescribed Performa at Annexure – VIII. The account of NGO
Society on the basis of proposal in the State PIP. The State Health shall be open to inspection by the sanctioning authority whenever
Society shall release Grant-in-aid to approved grantees in two the institution is called upon to do so.
installments on completion of following necessary documents.
Nomination by Government
Execution of bond on a hundred rupee Non-Judicial Stamp paper
by the grantee institution /NGO in the prescribed Pro forma The Central Government and State Health Society will nominate
(Annexure–IV). one officer as its representative to the governing body of the NGO
receiving Grant-in-aid.
Penalties

The Government of India/State Government reserves the right Reprint from Scheme for Participation of
to inspect the premises / accounts of the NGO. Any violation of Voluntary Organisation, National Programme
conditions will lead to suspension of any Government grant to for Control of Blindness July, 2009 Edition.
the organization in future.

ICARE Eye Hospital & PG Institute SITUATION VACANT

Consultants/Associate Consultants for OPTHALMOLOGIST

(Pediatric/Glaucoma/ [MD/MS/DNB]
Cornea- Refractive/Vitreo-Retina)
Experienced-preffered for 60 Bedded
Min 1-3 yrs of exp. post fellowship Hi-Tech Exclusive Eye Hospital [Estd 1992]
e-mail or post your resume:
Gangamata Eye Hospital
ICARE Eye Hospital
Sapat Rishi Link Road, HARIDWAR - 249410
E-3A Sector 26, Noida-201301 FAX-01334-260175 Š M: 09412931046
Ph: 9811357232, [email protected] Emai :[email protected]

www.dosonline.org 51

Changing Trends in the Management of ARMD

Manisha Agarwal MS, DNB

Age related macular degeneration is the leading cause of Management of Wet AMD
irreversible visual loss among the elderly across the globe.
This is due to the increase in the life expectancy at birth. The Wet age related macular degeneration was believed to be largely
prevalence of AMD increases from 1.6% (52-64 yrs) to 11% (65- untreatable, but developments in the last two years have challenged
74 yrs). this view.

Diagnosis of AMD Past management of wet AMD

• Complete ocular examination including a dilated fundus The main aim of management was to limit the spread of the
evaluation with slit lamp biomicroscopy (+90/+78 dioptre) uncontrollable disease irrespective of the vision.

• Fundus fluorescein angiography (FFA)- it is an invasive Thermal laser photocoagulation (PHC)
procedure
The choroidal neovascular membrane was burnt using a thermal
• Optical coherence tomography (OCT)- it is a non invasive laser which was equivalent to amputation in general surgery.
procedure Macular photocoagulation study (MPS)3-7 in 1982 showed the
role of thermal laser photocoagulation for angiographically well
• Indocyanine green angiography (ICG)- an invasive defined – extrafoveal or juxtafoveal CNVM. (Figure 3) However
procedure, especially useful for the diagnosis of retinitis the subfoveal CNVM treated with thermal laser showed an
angiomatous proliferans (RAP), idiopathic polypoidal immediate and permanent loss of central vision due to damage
choroidal vasculopathy (IPCV) and an occult CNVM

Newer diagnostic modalities are as follows:-

• Ultra high resolution FD OCT

• Combination of OCT-SLO

• Combination of OCT-ICG

• Fundus autofluorescence -novel imaging method that allows
mapping of lipofuscin and other fluorophores in RPE cell
monolayer, outer retina and sub-sensory retinal space. It is
promising for diagnosing dry ARMD. (Figure 1)

Management of Dry AMD

A patient of Dry AMD is managed by providing the following:-

• Best spectacle correction

• Amsler Grid monitoring to pick up early conversion to wet
AMD (Figure 2)

• Diet supplements

• Low vision aids

• Vitamin supplements

Several clinical trials have been conducted to recommend the
best dosage of the various macronutrients and micronutrients for
a patient of AMD eg. AREDS-1, AREDS-2, LUNA study,1 LAST
study, POLA study2 etc.

Miniature implantable telescopes (IMT) have got FDA approval Figure 1: Fundus autofluorescence
in July- 2010 and appear promising for patients having a central
scotoma secondary to AMD.

Shroff Charity Eye Hospital
Darya Ganj, New Delhi

www.dosonline.org 53

Figure 2: Amsler grid chart Then came the era when the aim of treatment was to selectively
eliminate the CNVM but preserve the vision with least damage
to the overlying normal retinal tissue. This lead to the following
modalities of treatment

Feeder vessel photocoagulation

The aim of this treatment is to eliminate the source of the CNVM.
This requires a high speed or dynamic ICG angiography using a
scanning laser ophthalmoscope to identify the feeder vessel to the
sub-foveal CNVM. A thermal laser PHC was done to the feeder
vessel supplying the CNVM.8 However it is possible in selected
patients only where the feeder vessel can be identified. (Figure 4)

Transpupillary thermotherapy (TTT)

A thermal laser (Diode 810nm) is used .The laser is used having
a long pulse, low energy and large spot size.9 This leads to low
hyperthermia with downward heat-sink effect by choroidal
circulation. (Figure 5) The disadvantages of this treatment were
that the laser parameters and the results were very variable in
every treated patient. Sparingly used now days.

Figure 4: Feeder vessel supplying the CNVM

Figure 3: Thermal laser photocoagulation of CNVM Figure 5: Transpupillary thermotherapy (TTT)
DOS Times - Vol. 16, No. 7, January 2011
to the retinal pigment epithelium (RPE) and the photoreceptors.
The recurrence rate of the CNVM was as high as 50%.
The current status of this modality of treatment is that it is
recommended for extrafoveal classic CNVM.

54

Figure 6: Submacular removal of CNVM Figure 7

Photodynamic therapy (PDT)

Introduced in 2000. Verteporfin (photosensitive dye) is injected
through the intravenous route for five minutes which is said to
selectively get concentrated in the CNVM. After ten minutes the
CNVM is then exposed to a laser of 689 nm for 83 sec, energy-
600mW/cm.sq. and total light dose-50J/cm.sq. Laser spot diameter
is kept 1mm larger than the greatest linear diameter of the entire
lesion complex. This causes non-thermal photothrombosis of
the CNVM.

The following clinical trials were conducted to study the role of Figure 8
PDT in different types of CNVM:-

• TAP trial- benefit in predominantly classic sub-foveal Anti-VEGF drugs
CNVM10-11
Vascular endothelial growth factor-A (VEGF-A) was found to
• VIP trial-benefit in smaller occult sub-foveal CNVM with be the key mediator for increasing vascular permeability and
recent progression angiogenesis. (Figure 7) This lead to the discovery of the various
anti-VEGF drugs:-
• VIO trial- Visudyne in occult CNVM
• Pegaptanib sodium (Macugen)-It is the first anti-VEGF drug
• VIM trial-benefit in smaller minimally classic lesions to be discovered for ophthalmic use. It was approved by the
FDA for ophthalmic use in 2004. Macugen comprises of
• VALIO study- Verteporfin with Altered (delayed) light in aptamers which are chemically synthesized strands of RNA
occult CNVM selectively blocking VEGF 165.13

• VER study- Visudyne early Re-treatment for subfoveal • V.I.S.I.O.N trial - was conducted in which intravitreal
choroidal neovascularization macugen was given every six weeks for 54 weeks and it
showed macugen to be effective in all subtypes of CNVM
Surgical management secondary to AMD. At the end of 2 years there was a
relative benefit of 45 % and 7% patients lost > 15 letters
Submacular surgery involving the direct removal of the large and despite the macugen injection given every 6 weeks.14
poorly demarcated CNVM (Figure 6) and macular translocation
surgery12 involving moving the fovea over a healthier choroid was These results lead to the search for agents which would block all
done. However these surgeries had higher rates of complications the isoforms of VEGF -A thereby blocking all it’s actions – Pan
in comparison to the benefit to the patient. These are rarely VEGF Blockers such as
performed in the current time.
• Ranibizumab (Lucentis)- It is a recombinant humanized
Present management of Wet AMD antibody fragment which inhibits biologically active plasmin
cleavage product of all isoforms of VEGF-A
The aim of management is to selectively eliminate the CNVM
and to improve the visual acuity of the patient. To achieve this
search for a more targeted treatment was done which lead to the
following:-

www.dosonline.org 55

injections and PDT for 24 months. Two year results
showed 94% (0.3mg) and 96% (0.5mg) lost <15 letters
in comparison to 64% in the PDT group and 36% (0.3mg)
and 40% (0.5mg) gained >15 letters Vs 6% in the PDT
group.16

This required giving an intravitreal injection every month which
was not practical and had the risk of associated complications such
as endophthalmitis, retinal detachment etc. Therefore alternate
dosing regimens were tried which lead to the following clinical
trial:-

PIER Trial: To evaluate the efficacy and safety of ranibizumab
administered monthly for three months and then quarterly in
patients with sub-foveal CNVM secondary to AMD.

Results: In first 3 months the results were comparable to Anchor
and Marina but then the average visual acuity decreased as the
quarterly injections were unable to maintain the improvement
seen with monthly injections initially. The conclusion drawn from
these results were that probably some patients required more
frequent injections to maintain their vision.17

Figure 9: Bevacizumab (Avastin) injection It was thought that a set dosing regimen may not work for all the
patients therefore the concept of individualizing the treatment for
each patient was considered and this lead to the following trial:-

PrONTO Trial: Prospective Optical coherence tomography
imaging of patients with Neovascular AMD Treated with intra-
ocular ranibizumab (Lucentis)

All subtypes of CNVM secondary to AMD were treated with
intravitreal Ranibizumab for the first two months (3 injections)
followed by the PRN (pro re nata) dosing. The retreatment was
done if there was a new hemorrhage, persistent sub-retinal
fluid,new area of classic CNVM, VA loss > 5 letters, macular
thickness >100m,enlargement of PED. The results got with this
trial were comparable to Marina trial and Anchor trial however
the average number of injections had reduced to 9.9 in comparison
to 24 injections in Marina and Anchor trials. (Figure 8)

• Bevacizumab (Avastin)- Anti-VEGF humanized antibody
fragment developed in 2005. It is FDA approved for colorectal
cancer and breast cancer treatment. An off label use of
bevacizumab is done in the eye. Several small patient series
have shown results comparable to Ranibizumab (Lucentis).

Figure 10 CATT Trial: Comparison of age related macular degeneration

treatments trial- To determine the safety and efficacy of Avastin

compared with Lucentis .It is a head to head, prospective

randomized masked clinical trial.
• MARINA Trial- was conducted to know the role

ranibizumab in treating minimally classic or occult Other ongoing trials: VIBERA,IVAN and GEFAL

CNVM secondary to AMD by monthly intravitreal Low fluence PDT
injections of Lucentis (dose-0.3mg/0.5mg) Vs sham

injections for 24 months. Results of two years study In comparison to the full fluence PDT, here the energy used is
showed that 90% patients lost <15 letters in comparison 300mW/cm. square for 83 sec and total light dose is 25J/cm.sq.
to 53% in the sham group and 26-33% gained >15 letters The rationale is that the delivery of the light photon becomes
Vs 4% in the sham group.15 the rate limiting step in photochemical reaction leading to

• ANCHOR Trial-was conducted to know the role of selective treatment of the CNVM with lesser side effects on the
ranibizumab in treating predominantly classic CNVM choriocapillaris and RPE cells.

secondary to AMD with monthly intravitreal injections • VIM trial- the effect of low fluence PDT – Phase IV clinical
of Lucentis (dose-0.3mg/0.5mg) Vs sham PDT Vs sham
trial

56 DOS Times - Vol. 16, No. 7, January 2011

Figure 11: Neovista Figure 12: Depot of
Anecortaveacetate

Combination treatment

A combination treatment was though of because of the following
reasons:

• A multi-factorial etiology maybe responsible for the
formation of a CNVM secondary to AMD. (Figure 10)

• The anti-VEGF agents used in combination with others may
target the non-VEGF components of the disease and together
they may provide a synergistic effect.

• This may offer the potential for a reduced course of treatments.

• May improve the outcomes got with monotherapy

• May reduce the no. of injections and the risk of associated Figure 13: Retinal prosthesis
ocular and systemic side effects

The above reasons lead to the trial of various combination
therapies such as:-

• PDT + anti VEGF

• PDT + intravitreal triamcinolone (IVTA) EVIZON (Squalamine lactate)
• Triple therapy - PDT+ anti-VEGF+ dexamethasone
• Strontium 90 beta radiation + anti-VEGF Squalamine is an amino sterol purified from the dogfish shark. It
• Anti- VEGF + steroids inhibits growth factors signaling VEGF, integrin and cytoskeletal
formation.

Future management of AMD NEOVISTA

VEGF Trap It is an epiretinal brachytherapy in which ß radiation is applied to
the macula using strontium 90 isotope.(Figure 11)
A recombinant protein which binds and inactivates circulating
VEGF. Phase II studies have shown mean improvement of 5.7 Retaane
letters and reduction in macular thickness in all groups at 12
weeks. Phase III study (VIEW II): recruiting 1200 subjects It is a depot of anecortave acetate.It is an angiostatic agent
worldwide including some centers in India is comparing efficacy administered as a periocular posterior juxtascleral depot.
of VEGF Trap to Ranibizumab (Lucentis). (Figure 12)

Sirna-027 and C and 5 OT-551 ophthalmic solution

Chemically modified short interfering RNA which down regulates This is in the form of eye drops. It is said to safely and effectively
VEGF production. treat geographic atrophy in AMD.

www.dosonline.org 57

Oxygen ozone therapy 8. Photodynamic therapy increases the eligibility for feeder vessel
treatment of choroidal neovascularization caused by age related
Copaxone macular degeneration. Piemarocchi S, Giudice GL,Sartore M et al.
AJO 2002 Apr;133(4): 572-5.
It is an immunomodulatory substance to arrest the progression
as well as the conversion of dry AMD to wet AMD. 9. Transpupillary thermotherapy for choroidal neovascular membrane
in age related macular degeneration. M Agarwal, Mahesh P
• RPE transplantation Shanmugam, L Gopal, N Shetty et al. Indian J Ophthalmol 2004;
52(1):45-49.
• Retinal prosthesis (Figure 13)
10. Photodynamic therapy of subfoveal choroidal neovascularization in
• Photo-microchip and artificial vision age-related macular degeneration with verteporfin: one-year results
of 2 randomized clinical trials--TAP report. Treatment of age-related
• Nanotechnology to regenerate retinal synapses macular degeneration with photodynamic therapy (TAP) Study
Group. Arch Ophthalmol 1999 Oct;117(10):1329-45.
• Gene therapy
11. Bressler NM. Treatment of Age-Related Macular Degeneration with
An ideal treatment for age related macular degeneration would Photodynamic Therapy (TAP) Study Group. Photodynamic therapy
require attacking multiple patho-physiological pathways to of subfoveal choroidal neovascularization in age-related macular
address the complex disease mechanisms that lead to visual loss. degeneration with verteporfin: two year results of 2 randomized
clinical trials- TAP report 2. Arch Ophthalmol 2001;119: 198-207.
References
12. Machemer R,Steinhorst U. Retinal separation ,retinotomy, and
1. Trieschmann M,Beatty S,Nolan JM et al.Changes in macular macular relocation. A surgical approach for age related macular
pigment optical density and serum concentrations of its constituent degeneration. Graefes Arch Clin Exp Ophthalmol.1993;231:635-41.
carotenoids following supplemental lutein and zeaxanthin:LUNA
study.Experimental Eye research.2007;84(4):718-728. 13. Gragoudas ES,Adamis AP,Cunhingham ET et al.for the VEGF
inhibition study in ocular neovascularization clinical trial group.
2. Delcourt C,Cristol JP,Tessler F et al.Age related macular degeneration Pegaptanib for neovascular age related macular degeneration. N
and anti oxidant status in the POLA Study. Arch Ophthalmol Engl J Med 2004;351:2805-2816.
1999;117: 1384-1390.
14. Moshfegi A and Puliafito C. Pegaptanib sodium for the treatment
3. Macular Photocoagulation Study. Argon laser photocoagulation for of neovascular age-related macular degeneration. Expert Opin.
senile macular degeneration. Results of a randomized clinical trial. Investig. Drugs (2005)14(5):671-682.
Arch Ophthalmol 1982; 100: 912-918.
15. Rosenfeld PJ,Brown DM,Heier JS et al, for the MARINA Study
4. Macular Photo coagulation Study Group. Argon laser Group. Ranibizumab for neovascular age related macular
photocoagulation for neovascular maculopathy. Five-year results degeneration. N Engl J Med.2006;355: 1419-1431.
from randomized clinical trials. Arch Ophthalmol1986;104: 694-701.
16. Ranibizumab for predominantly classic neovascular age related
5. Macular Photo coagulation Study Group. Argon laser macular degeneration:Subgroup analysis of first year ANCHOR
photocoagulation for neovascular maculopathy. Five-year results Results. Am J Ophthalmol 144;6:850-857.
from randomized clinical trials. Arch Ophthalmol1991;109: 1109-
1114. 17. Randomized double masked,sham controlled trial of Ranibizumab
for neovascular age related macular degeneration: PIER Study Year
6. Macular Photocoagulation Study Group. Kr ypton laser 1.Am J Ophthalmol 2008;145:239-248.
photocoagulation for neovascular lesions of age related macular
degeneration.Results of a randomized clinical trial. Arch 18. An optical coherence tomography guided variable dosing regimen
Ophthalmol1990;108: 816-824. intravitreak ranibizumab(Lucentis) for neovascular age related
macular degeneration.Fung AF,Lalwani GA,Rosenfeld PJ et al. Am
7. Macular Photocoagulation Study Group. Laser photocoagulation J Ophthalmol 2007;143:566–583.
for juxtafoveal choroidal neovascularisation. Five-year results from
randomized clinical trials. Arch Ophthalmol1994; 112: 500-509.

Author
Manisha Agarwal MS, DNB

58 DOS Times - Vol. 16, No. 7, January 2011

Tissue Plasminogen Activator Assisted Treatment of
Choroidal Neovascular Membrane

Rohini Grover DNB, H.K. Tewari MD, S.N. Jha MD, Amit Khosla MD, DNB, Neeraj Manchanda DO, DNB, Nidhi Panwar MD

Submacular hemorrhage is an important cause of sudden Case Report
visual loss in patients suffering with Age Related Macular
Degeneration. The visual outcome for patients with submacular A 60 year old male presented to us with chief complaints of sudden,
hemorrhage is typically poor1, especially if the hemorrhage is painless diminution of vision in right eye for last one week. There
thick, involves the fovea, and covers a large area of the macula. The was no associated history of trauma or any recent surgery. He was
visual prognosis is even worse if there is an underlying choroidal a known case of diabetes mellitus for past 5 years. Patient was
neovascular membrane.2,3 non hypertensive.

Therefore prompt displacement of blood from the fovea is the key On examination patient was fully conscious and well oriented
to success for early and good final visual acuity. Management of with normal systemic examination. On ophthalmic examination
submacular hemorrhage includes variety of options; one of them his best corrected visual acuity in right eye was 20/400 (+0.25 sph/
is recombinant tissue plasminogen activator (rtPA) which assists +1.25 cyl at 60 deg) and in left eye was 20/60 (+0.75 sph /+0.75
in liquefying subretinal blood. cyl at 12 deg). Pupillary reactions were normal in both the eyes.
Anterior chamber in both eyes had normal depth and content.
Subretinal bleed There was no significant change in lens. The IOP in both eyes
was 16 mmHg. Fundus examination showed an elevated reddish
Right Eye coloured lesion of around 5-6 disc diameter with retinal vessels

(a) Right Eye

Left Eye

(b) Left Eye

Figure 1: R/E showing subretinal bleed Occult CNVM
Figure 2(a): Blocked fluorescence (suretinal bleed)
Department of Ophthalmology Figure 2(a): Stippled fluorescence (Occult CNVM)
Sir Ganga Ram Hospital,
61
Rajinder Nagar, New Delhi

www.dosonline.org

CNVM Neurosensery detachment

Right Eye (a) Left Eye (b)

Figure 3(a): R/E OCT showing sub RPE hemorrhage PED
Figure 3(b): L/E OCT showing neurosensery detachment, CNVM and PED

Gas (SF6) bubble Submacular bleed displaced
from fovea

Figure 4: Fundus photos of first post-operative day

seen over the lesion with obscured choroidal vessels suggestive of Clinical and ophthalmic investigations were suggestive of right
submacular bleed. Clinically left eye did not reveal any significant eye submacular hemorrhage due to wet ARMD and left eye
change on fundus examination. neurosensory detachment with choroidal neovascular membrane.

On investigating the patient, biochemical and haematological On the same day of presentation, the patient was administered
investigations were normal. Patient showed his fluorescein right eye intravitreal injection of tissue plasminogen activator (50
angiography and optical coherence tomography reports ug in 0.1cc) with SF6 (0.3 cc) and advised strict prone position.
(conducted elsewhere). Fluorescein angiography of right eye Topical antibiotic and antiglaucoma medication were given
showed blocked fluorescence with visible retinal vessels over the postoperatively. On day one postoperatively, right eye showed
lesion with obscured choroidal vessels, suggestive of submacular displacement of submacular bleed from fovea. A fluorescein
bleed. In left eye, the late phase angiogram revealed stippled angiogram now revealed an underlying CNVM in right eye
hyperfluoresecence with poorly defined margins indicating occult which was otherwise masked under subretinal bleed and an
choroidal neovascularization. occult CNVM in left eye. Three days later, the left eye was treated
with intravitreal injection of Ranibizumab (0.3mg in 0.05cc). A
On OCT horizontal line scan passing through the foveal centre week later, after administration of rtPA with SF6, we again treated
in right eye showed dome shaped lesion with hyperechoic spots right eye with intravitreal injection of Ranibizumab. On follow
indicating haemorrhage just below Retinal Pigment Epithelium. up, patient was advised to use Amsler grid, a monthly fundus
Signal attenuation was noted due to overlying subfoveal bleed. In examination, OCT and 2 more injections of Ranibizumab in
left eye a small hyperreflective area indicating CNVM with PED each eye one month apart then extend the treatment as and when
and a hyporeflective area suggestive of neurosensory detachment. required according to (prn) criteria.

62 DOS Times - Vol. 16, No. 7, January 2011

(a) (b)

Figure 5(a): R/E FFA revealing underlying CNVM Figure 5(b): L/E FFA showing CNVM
(a)

(b)

Figure 6: Fundus photo following rtPA with SF6
and IV ranibizumab

There was two line improvement in right eye following rtPA with Figure 7(a): Final OCT showing loss of dome
SF6 and after intravitreal injection of ranibizumab the final visual shaped contour in R/E
outcome was 20/200. In left eye visual acuity improved to 20/40
from 20/60. Figure 7(b): L/E decrease in size of
neurosensory detachment

Discussion

The visual outcome in ARMD with submacular hemorrhage is Heriot6, in 1996, presented a new procedure to lyse and displace
poor because of thick blood covering a large macular area and also submacular blood by injecting intravitreal tissue plasminogen
ferrous ion is toxic to photoreceptors4,5. Animal studies have shown activator and a bubble of long acting expansile gas into the
that the most immediate damage from subretinal blood may be vitreous cavity. Heriot’s technique used 100ug of intravitreal tPA,
due to the shearing of photoreceptors during clot retraction. The intravitreal gas and face down positioning directly compressing
thick blood forms a mechanical barrier preventing metabolic the macula and displacing the sumacular blood inferiorly.
exchange between the retina and retinal pigment epithelium.
The earlier the removal of subretinal blood the lasser will be the
retinal damage.

www.dosonline.org 63

Mechanism of action of tPA Drug cost is a prime consideration for treatment of chronic and
progressive disease like AMD.
Binding of tPA and plasminogen to the fibrin
To avoid monthly expensive injections of Ranibizumab/
Conformational change Bevacizumab, variable treatment strategies have arisen. This
comprise of pro re nata (PRN) basis of treatment in which a
Plasminogen to plasmin loading phase, monthly injections of anti-VEGF for first three
moths is needed to maximize the initial response. Followed by a
dissolving the clot. maintaince phase which is flexible treatment regimen based on
OCT findings. This reduces injection related risks as well as lost
The recombinant tissue plasminogen activator has been used factor.
systemically in the management of acute myocardial infarction
since 19847. Its ophthalmic use began in 1988 to lyse fibrin from References
anterior chamber in postvitrectomised eyes8.
1. Bennett AR, Folk JC, Blodi CF, Klugman M. Factors prognostic
Mechanism of action of tPA of visual outcome in patients with subretinal hemorrhag. Am J
Ophthalmol. 1990;109-33.
tPA is a serine protease that converts plasminogen to plasmin.
Plasmin in turn lyses fibrin into soluble degradation products. 2. Avery RL, Fekrat S. Howkins BS, Bressler NM. Natural history of
subfovea subretinal hemorrhage in age-related degeneration. Retina.
Molecular weight of tPA is the same as albumin so its diffusion 1996;16 183-189.
into subretinal space is proven in animal study9. tPA begins its
action of liquefying subretinal hemorrhage as early as 12-36 hrs 3. Berrocal MC, Lewis ML, Flynnn HW. Variations in the clinical course
following intravitreal injection, in cases of acute hemorrhage of submacular hemorrhage. Am J. Ophthalmol. 1996;122:486-493.
which are 2-4 days old10.
4. Glatt H, Machemer R. Experimental subretinal hemorrhage in
Drug dose rabbits. Am J. Ophthalmol. 1982;94:762-773.

Heriot6 used 100ug of tPA in his technique. In animal studies eyes 5. Toth CA, Morse LS, Heijlmeland LM, Landers MB III. Fibrin directs
treated with 100ug of tPA has shown toxic retinal damage like early retina damage after experimental subretinal hemorrhage. Am
retinal holes, bullous retinal damage , attenuation of retinal blood J. Ophthalmol. 1991;109-73-79.
vessels and marked early reduction in b –wave amplitude on ERG.
Studies have shown no toxic retinal change with the dose of 25 to 6. Heriot WJ. Intravitreal gas and tPA: an outpatient procedure for
50 ug on indirect ophthalmoscopy, ERG or light microscopy11,12. submacular hemorrhage. Paper presented at: American Academy
of Ophthalmology Annual Vitreo-retinal Update; October 1996;
Safety and efficacy Chicago, III.

Handwerger et a l12, using low doses of tPA, described complete 7. Collen D, Topol EJ et al Ceronary thrombolysis with recombinant
displacement of submacular hemorrhage from the fovea in 10 of leuman tissue type plasinogen activate a prospective, randenized,
14 patients. Hassan et al13 reported that 10 (71%) of 14 patients placebo-controlled trial. Circulation 1984;70:1012-13.
with AMD had visual acuity of 20/400 or better. Studies12 have
shown that symptomatic submacular hemorrhage of less than 8. Williams GA, Jaffe GA et al treatment of post vitrectomy fibrin
3 weeks, thick blood under the fovea with retinal elevation and formation with intraocular tPA. Arch ophthalmol 1988; 106:1055-8.
hemorrhage of at least 3DD have shown displacement of blood
and uncovered underlying macular pathology in 93% patients 9. Takeuchi A, Kricorian G, Yao XY, et al. The rate and source of
after prone posturing for 1 to 5 a minimum of 24 hrs. Ojhi14 and albumin entry intrasaline-filled experimental retinal detachment.
colleagues speculated that solid blood clots that are present for Invest Ophthalmol Vis Sci. 1995 36:1875-1884.
more than 1 week may not be displaced by gas compression alone.
10. Kimura AE, Reddy CV, Folk JC, Farmer SG. Removal of subretinal
New era of treatment for wet ARMD hemorrhage facilitated by preoperative intravitreal tissue
plasminogen activator. Retina. 1994 14:83-84.
Anti VEGF (Ranibizumab/Bevacizumab) delivered directly into
the eye by injection and attack anormal VEGF in the retina of the 11. Irvine WD, Johnson MW, Hernandez E, Olsen KR. Retinal toxicity
eyes with wet ARMD. of human tissue plasminogen activator in vitrectomized rabbit eyes.
Arch Ophthalmol. 1991;109:718-722.
ANCHOR and FOCUS trial showed superior results of
combination therapy (ie. PDT +Ranibizumab) over PDT alone. 12. Handwerger Beth A, Barbara A.B. etl al treatment of submacular
hemorrhage with low-dose intravitreal tPA injection and preumatic
MARINA and ANCHOR trials proposed regular monthly Displacement Arch Ophthalmol. 2001;119:28-32.
intravitreal injections of Ranibizumab for 2yrs and found good
results. 13. Hassan AS, Johnson MW, Schneiderman TE, et al. Management
of submacular hemorrhage with intravitreal tPA injection and
pneumatic displacement. Ophthalmology. 1999;106:1900-1907.

14. Ohji M, Saito Y, Hayashi A, Lewis J, Tano Y. Pneumatic displacement
of sub-retinal hemorrhage without tissue plasminogen activator.
Arch Ophthalmol. 1998 116:1326-1332.

First Author
Rohini Grover DNB

64 DOS Times - Vol. 16, No. 7, January 2011

Life Time Achievement Award

Details of the awards, eligibility criteria and procedure to apply are given below:

General Conditions

1. Any Member of the Society who is eligible for the Award shall be entitled to be considered for the same.

2. Nomination should be signed by one of the following:

a. Any of the Past Awardees b. Any of the Past Presidents

c. At least 5 members of the Executive Committee d. At least 15 members of the Delhi Members of DOS.

3. Recommendations should be sent to the Secretariat, DOS with 5 copies of BIO-DATA and Photograph.

4. The person shoud have significant Life time achievements in the field of Ophthalmology.

5. Recipient of the Award shall be selected and recommended by the Selection Committee, which has to be approved by the
executive.

Eligibility

1. The Member should be 65 years of age or more
2. Active participation in Society for 20 years
3. Contribution in improvement of standard of Ophthalmology in India
4. Award will carry a citation.
Periodicity
1. Maximum 2 Awards in a year.
2. The nominations must be received in DOS Secretariat no later than 5.00 p.m. on February 15th, 2011.

Secretary, DOS

Dr. P.K. Jain Oration & Dr. S.N. Mitter Oration

Nominations are invited for the above orations. The nominee should be a voting member of the Delhi Ophthalmological
Society.

Selection Procedure

Nomination should be signed by one of the following:

1. Any of the Past Awardees 2. Any of the Past Presidents

3. At least 5 members of the Executive Committee 4. At least 15 members of the Delhi Members of DOS.

The nomination must include an introductory paragraph justifying the nomination, a biodata of the nominee, a statement to the

effect that the nominee would accept the award if awarded and would deliver an oration of his choice at the annual conference

of the DOS. The topic should be intimated to the society at least 4 weeks before the conference and a typed script of the same

should be sumitted at least 15 days before. The awardee will have to transfer the copyright of the text of his talk to the society.

Selection Process
The selection will be made by a Selection Committee consisting of the President, Secretary and 3 senior, distinguished members
from 3 different sub-specialties of Ophthalmology. The Executive Committee would take the final decision on the basis of the
recommendations of the Selection Committee. The nominations must be received in DOS Secretariat no later than 5.00 p.m.
on February 15th, 2011.

Advance copy of the nominations may be sent by email. The hard copy must however be received in the DOS Secretariat by the
last date for receiving the nominations.

www.dosonline.org 67

Forthcoming Events: National

January 2011 Ahmedabad, 380015. India
16-17 CHENNAI Fixed: +91 79 26303208, Fax: +91 79 26303308
Website: www.aioc2011.com,
Chrysalis 2011 E-mail: [email protected]
International Conference on Oculofacial Reconstructive Conference Help Line: 96248 96248
and Aesthetics Surgery
Organizing Secretary April 2010
Dr. Shubhra Goel 15-17 NEW DELHI
E-mail: [email protected]
Ph.: 044-28254177, Mobile: 91-9382832910, Annual Conference
Website: www.sankaranethralaya.org/chrysalis2011 Delhi Ophthalmological Society
Venue: Hotel Ashok, Chanakya Puri, New Delhi
February 2011 Contact Person & Address
3-6 GUJARAT Dr. Amit Khosla, Secretary DOS
Room No. 2225, 2nd Floor, New Building,
69th AIOS Annual Conference Sir Ganga Ram Hospital,
Gujarat University Convention Centre, Ahemadabad Rajinder Nagar, New Delhi - 110 060
Conference Secretary, Ph.: 011-65705229, E-mail: [email protected],
Dr. Tejas D. Shah Website: www.dosonline.org
Amdavad Eye Laser Hospitals Pvt. Ltd.
Vision Complex, Polytechnic Cross Roads,

Ophthalmologist R.K. Netralaya Eye
Required Hospital Pvt. Ltd.

Application are invited for consultants (An Advance & Growing Eye Centre of Eastern UP)
Ophthalmologist
Requires Full Time
M.S./D.N.B./DO Having experience in
1. Phaco/SICS Ophthalmologist

2. Paediatric Ophthalmology (Surgeon with Experience in Phaco/ Vitreo
Apply immediately with full details to: Retinal Surgery)

Director Freshers can also apply
Salary will Commensurate with Experience
Khairabad Eye Hospital
Apply with detailed bio-data to:
Swaroop Nagar, Kanpur (U.P.)
Mobile: +91 0336118273, 9415174742, Dr. R.K. Ojha-Director

Fax: 91-5120549430 R.K. Netralaya Eye Hospital Pvt. Ltd.
Email: [email protected]
Address: D-63/10, B-1A DAYAL ENCLAVE, MAHMOORGANJ,
www.dosonline.org VARANASI (UP)-221010

Tel: 0542- 2223580, 2223581 Fax: 2223579
Email: [email protected]

69

Delhi Ophthalmological Society

SUBMISSION online www:dosonline.org

(LIFE MEMBERSHIP FORM)

Name (In Block Letters)_______________________________________________________________________________________________
S/D/W/o ____________________________________________________________________________ Date of Birth___________________
Qualifications________________________________________________________________________ Registration No. ________________
Sub Speciality (if any) ________________________________________________________________________________________________
ADDRESS

Clinic/Hospital/Practice __________________________________________________________________________________________
_____________________________________________________________________________ Phone _______________________
Residence ____________________________________________________________________________________________________
_____________________________________________________________________________ Phone _______________________
Correspondence _______________________________________________________________________________________________
_____________________________________________________________________________ Phone _______________________
Email ____________________________________________________________ Mobile No. _____________________________
Proposed by
Dr. _______________________________________________ Membership No. __________ Signature _________________________
Seconded by
Dr. _______________________________________________ Membership No. __________ Signature _________________________
[Must submit a photocopy of the MBBS/MD/DO & State Medical Council / MCI Certificate for our records.]

I agree to become a life member of the Delhi Ophthalmological Society and shall abide by the Rules and Regula-
tions of the Society.
(Please Note : Life membership fee Rs. 3100/- payable by DD for outstation members. Local Cheques acceptable, payable to Delhi Ophthalmo-
logical Society)
Please find enclosed Rs.___________in words ____________________________________________________ by Cash
Cheque/DD No.____________________ Dated_____________ Drawn on______________________________________

Signature of Applicant Three specimen signatures for I.D. Card.
with Date

FOR OFFICIAL USE ONLY

Dr._______________________________________________________________has been admitted as Life Member of

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

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

drawn on __________________________________________________________________.

(Secretary DOS)

www.dosonline.org 75

INSTRUCTIONS

1. The Society reserve all rights to accepts or reject the application.

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

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

4. Every new member is entitled to receive Society’s Bulletin (DOS Times) and Annual proceedings of the Society free.

5. Every new member will initially be admitted provisionally and shall be deemed to have become a full member only after formal
ratification by the General Body and issue of Ratification order by the Society. Only then he or she will be eligible to vote, or apply
for any Fellowship/Award, propose or contest for any election of the Society.

6. Application for the membership along with the Bank Draft for the membership fee should be addressed to Dr. Amit Khosla,
Secretary, Delhi Ophthalmological Society, Room No. 2225, 2nd Floor, New Building, Sir Ganga Ram Hospital, Rajinder Nagar,
New Delhi - 110 060

7. Licence Size Coloured Photograph is to be pasted on the form in the space provided and two Stamp/ Licence Size Coloured
photographs are required to be sent along with this form for issue of Laminated Photo Identity Card (to be issued only after the
Membership ratification).

8. Applications for ‘Delhi Life Member’ should either reside or practice in Delhi. The proof of residence may be in the form Passport/
Licence/Voters Identity Card/Ration Card/Electyricity Bill/MTNL (Landline) Telephone Bill.

We wish all DOS Members success in the forthcoming AIOS Election.

Dr. P.V. Chadha Dr. Amit Khosla
President, DOS Secretary, DOS

The online voting for AIOS office bearers will be starting at 5.30 AM on 20th January 2011 and will
be open upto midnight of 26th January 2011. Following are the modes of voting:

1. Online Voting:
(A Any one who has an Email ID which is registered with the AIOS office will get a link through their

email which can be accessed on 20/01/11 (05.30 AM onwards) and they will have to follow the
instructions to cast their votes.
(B Those who have not registered their Email IDs with the AIOS office will get a letter informing
them about their login ID and password which have been created for voting purpose. Please
preserve the letter and use the given ID and password to execute your vote between the 20th
and 26th of January 2011 through AIOS website.

2. EVM Voting:
All those who have not voted by midnight of 26th January 2011 through the online voting system
will be able to vote through electronic voting machine at Ahmedabad during the AIOC Conference
on 4th February, 2011 between 9:00 AM and 3:00 PM.

76 DOS Times - Vol. 16, No. 7, January 2011

Management of Neo-vascular Glaucoma

NVG

Medical Management

Seeing eye Non Seeing eye

Clear Media Hazy Media Cyclodestruction
Anti VEGF Cyclocryo or
PRP
(Aggressive) as Ant. Cornea Vit. Hge Cyclophotocoagulation (CPC)
as possible + Anti-VEGF + lens Anti VEGF +
hazy
Ant. Retinal
Controlled un-Controlled Vitrectomy Cryopexy
+ endolaser
+
Ant-Retinal Medical Management
Cryopexy
+
Anti-VEGF

Anti-VEGF

NVI Regression No Repeat Laser /
Anti-VEGF
Yes IOP not
No
IOP IOP not controlled
controlled
controlled

NVI free areas

present

Periodic followup Trab with MMC with Shunt
releasable sutures

IOP on target No

Yes No Shunt CPC*
Sectorial
(May repeat)

Shunt

* CPC - Cyclophotocoagulation / Cyclocryopexy
* Vit. Hg. - Vitreous Haemarrhage

*Deven Tuli MS, **Amit Khosla MD, DNB

*Bharti Eye Hospital, Greater Kailash-1, New Delhi
**Department of Ophthalmology, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi

& Siri Fort Laser Eye Centre, Siri Fort Road, New Delhi

www.dosonline.org 83


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