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Published by DOS Secretariat, 2020-05-15 02:58:39

DOS_dec_2009

DOS_dec_2009

Contents

E5 ditorial Neurophthalmology

Focus 45 Traumatic Optic Neuropathy

11 Amblyopia J.L. Goyal, Deepa Gupta, Ritu Arora

Refractive Surgery Oculoplasty

17 All Femtosecond Refractive Surgery 49 Vascular Lesions of the Orbit

Sharad Lakhotia Gaurav Bharti, Taru Dewan, Akhila Prasad, Shashi Vashisht

Cataract Clinical Monthly Meeting

21 Current Status of IOL Power Calculations 55 Clinical Case -1: Congenital Glaucoma in a 5 Day Old Infant

S. Venkatesh Shivani Kochar, K.P.S. Malik, V.S. Gupta

Glaucoma 59 Clinical Case -2: An Unusual case of Discharing Sinus

29 Diagnostic Ability of GDx VCC for Glaucoma Diagnosis Aniket Shastri, Anuj Mehta, KPS Malik, Sangeeta Abrol, Malvika Gupta

Tutul Chakravarti Miscellaneous

Cornea 63 DNB Paper Cracked

37 Collagen Cross: Linking with Riboflavin (C3R for Treatment A69 bstracts

of Keratoconus) F73 orthcoming Events
Neera Agarwal
Columns

75 Membership Form

DOS Election 3

The posts of Vice President Last date of withdrawal is 15th March, 2010 (5 p.m.) Election will be held
during the Annual DOS Conference on 18th April, 2010.
Secretary, DOS

www.dosonline.org

Editorial

Dear Friends and fellow Ophthalmologists,

Foggy mornings, delayed flights and everyone has a story to tell. Who sat longer in the plane before
take off ? And the winner is…………! Actually this contest stands nowhere in front of “Who were
forced to deboard the plane” contest. And it was not funny. As a matter of fact, it was extremely painful.

But sunny days are with us again. Merry sunshine and balmy weather. Delhi-at its best.

At DOS we are continuously striving to innovate and do something more useful for the members.
Training of residents and the young Ophthalmologist is an area ; where we are totally focused. The
DOST programme is a testimony to that, and it keeps on evolving.

Solved Question Paper of The DNB exam: A team of experts has specially solved the previous year’s DNB question paper and
we are publishing it in this issue. I hope all the residents find it a useful adjunct, in their preparations.

Mock OSCE:The highlight of this years DOST teaching weekend at R&R Hosp {13th and 14th Feb}. Another first on our part and
our passionate hope that you will find it useful.

Quest For Uniformity in training of Residents: Training programmes lack uniformity and vary in quality-and if a resident is not
well trained, he suffers due to none of his fault. We should rectify this and produce excellent young ophthalmologists; well
armed and fully equipped to sail in the choppy waters of Ophthalmic Practice. “The boat rocks, but we row on.”

The Next Level: It is now our endeavour to make fellowship and observership available to all residents who are DOS Members,
in the various excellent Private Eye Hospitals and Institutes in Delhi. The DOS Mach 3 skill sharpener. We will definitely make this
happen. For all of you. For all of us.

The Annual Conference:

I hope the Pleasant Weather continuous till The Conference and all of us have a great conference. The theme is “Ophthalmology
Now”.

The focus: “Consensus building on Ophthalmic Controversies.”

And above all: To give you a fantastic and memorable conference.

Yours Truly.
Thanking you,

Dr Amit Khosla
Secretary,
Delhi Ophthalmological Society

www.dosonline.org 5

From the President Desk 7

Dear Friends & respected Senior Colleagues,

Warm Greetings. I’m indebted to you all, for the confidence & support reposed
in me to carryout DOS activities. I congratulate Dr. R.V. Azad our past
President, who besides a great Ophthalmologist, a great motivator, protagonist
for equality for all, to be installed as President ‘All India Ophthalmological
Society’. I also Congratulate Dr. Noshir Shroff for being awarded Padma
Bhushan. I also congratulate other friends for attaining different milestones
in their professional and personal front.

Now only 2 months are left in my tenure and I wish every moment, I’d contribute something to DOS.
I’ve kept 4hrs daily for DOS and would love to hear suggestions, ideas and execute work assigned to me.
I’m fortunate to have a wonderful executive and a dynamic Secretary with us to present combined
performance. I attribute all our success to the entire executive for their cooperation, help, support and
judicious thinking.

In my endeavor for ‘CHANGE’ I might have caused displeasure to some for which I apologise. My
intentions had been to take the team along for the journey called success. My performance can’t be
compared to towering personalities of previous Presidents but nevertheless my enthusiasm & desire
to excel has received appropriate appreciation.

DOS guest house/office is our immediate requirement as land values are escalating in Delhi and fixed
deposit values are depreciating. We should immediately put our fixed deposit to real estate, which can
give us additional rental up to 1 lakh rupees/ month besides appreciation of land value. If need be, the
place can be utilized for DOS purposes.

DOS Annual Conference is our best show. All of us are equally responsible for the respect and stature,
it has achieved in academic circles. Let us pledge this year also, we make it a spectacular, grandeur show
of academic excellence coupled with great trade & personal get together. Please do not hesitate to write
or speak to me if you find things, not up to the mark of DOS. I’m personally supervising all activities
with great support from our Secretary and the entire executive.

Thanks,

Dr. Sharad Lakhotia
President, DOS
[email protected]
09312255311

www.dosonline.org

Amblyopia Focus

Prof. Pradeep Sharma MD Dr. Subhash C. Dadeya MD

Amblyopia, also termed as lazy eye, is defined by poor vision in the absence of any organic cause. The prevalence of this
entity in the normal population is 1-5%. It hypothesized that it may be caused by poor visual transmission of visual image
to the brain in the early childhood. Since there is significant prevelence of this disease in the general population, it becomes
all the more necessary to understand and diagnose and to start its treatment at the earliest. Here, we question some of the
pioneers from the field of strabismology to highlight upon various issues of amblyopia.

(PS): Dr. Pradeep Sharma MD, MNAMS, Professor of Ophthalmology, Dr. R.P. Centre For Opthalmic Sciences, All India
Institute of Medical Sciences, Ansari Nagar, New Delhi

(SCD): Dr. Subhash C. Dadeya MD, Associate Professor Department of Ophthalmology, Guru Nanak Eye Centre,
Maulana Azad Medical College, Maharaja Ranjit Singh Marg, New Delhi

(AA): Dr Ashish Amar, MS, FRCS, DNB, Senior Resident at Guru Nanak Eye Centre, Maulana Azad Medical College, New Delhi.

AA: How do you define Amblyopia? Pit falls in its definition? SCD: We see 4-5 cases in each OPD of around 100 patients and
20-30% patients in squint clinic are amblyopic.
PS: The definition of Amblyopia includes unilateral or bilateral
diminution (not loss) of vision despite best refractive AA: How do you diagnose Amblyopia and what are difficulties
correction and excluding any media opacity or any organic and pit falls encountered during diagnosis?
pathology on the visual pathway. The difference of two
lines on Snellen may be used for clinical purpose but for PS: The diagnosis of amblyopia differs in the different age
the end point one has to ensure not only equal vision but groups. In the literate children the letter charts are used, in
also equal (alternating) preference of fixation. The younger children the E or C charts are used and in still
underlined words underline the common pitfalls. smaller (preverbal children) we depend on indirectly looking
for the amblyogenic causes. So if there is an esotropia or
SCD: Clinically amblyopia has been defined as unilateral or vertical squint one should suspect it. Also the use of
bilateral reduction in best corrected visual acuity caused by Bruckner’s red reflex should be made to look for the media
form vision deprivation and or abnormal binocular opacity, refractive error or squint. It is then further
interaction, without a visible organic cause commensurating confirmed with the help of noticing the preference of
with this visual loss. This significant reduction in corrected fixation behavior. An observation of central/ eccentric,
central visual acuity is labeled to vision less than 6/12 in steady/unsteady and maintained/not maintained fixation,
bilateral amblyopia and a difference of two or more lines semi-quantifies the fixation.
between normal and amblyopic eye in unilateral amblyopia,
this is correctable, if appropriate measures are applied at One has to always look at the fundus and rule out any
appropriate time. However, amblyopia remains a diagnosis organic fundus pathology. Any purported diminution of
of exclusion. vision due to amblyopia should be supported by an
amblyogenic cause and the diagnosis of amblyopia should
AA: What is prevalence of amblyopia in your setting? be the last diagnosis.

PS: The prevalence of amblyopia in our clinical practice is higher SCD: It is not uncommon to see clinicians getting puzzled over the

because of the referral nature. In the general population it diagnosis of a case of diminution of vision. In Indian

should be about 5% or more. circumstances, the inadequate history and hurried decision

www.dosonline.org 9

1. on part of clinician due to increased patient load leads to 3. Crowding phenomenon
2. more confusion, the cause may be pathogenic rather than
3. functional. It is important to remember that diagnosis of Although not specific to amblyopia, it may be more
amblyopia is incomplete until following conditions are fulfilled pronounced in amblyopic eye compared to better eye.
10 Presence or absence of crowding phenomenon has
Evidence of reduced visual acuity usually unilateral but may prognostic implication. This difference between linear
be bilateral and isolated acuities should be noted at each visit. This
difference is a way of quantifying the depth of amblyopia
Presence of amblyopiogenic factor e.g. strabismus, unequal from visit to visit. Furthermore near visual acuity is
and uncorrected refractive error of a significant degree, more reliable indicator during amblyopia therapy as
any evidence of obstacle to vision (e.g. visual deprivation) near acuity often improves faster than distant visual
by way of congenital cataract, ptosis, corneal opacity, and acuity.
uncorrected aphakia in a child in amblyopiogenic age group.
4. Effects of neutral filter
No alternate explanation for visual loss
If we apply neutral density filter before normal eye, it
Amblyopia is diagnosed, when the criteria are met and leads to decrease in visual acuity however, if we apply
cause is identified. It is our duty to ensure that it is detected neutral density filter before amblyopic eye, the vision
at the earliest so that therapy can be started immediately does not decreases on the other hand it might improve.
for the maximum benefit to the patient. The diagnostic That means amblyopic eye act under mesopic conditions.
features of amblyopia are.
5. Colour vision
1. Confirm the diminution of vision
Color vision is usually normal in amblyopic eye. It is
1a) The hallmark of amblyopia is decreased foveal acuity. abnormal only in dense amblyopia and that to
Most clinical studies have defined unilateral secondary to reduced vision or eccentric fixation.
amblyopia as a minimum of two-line difference
between eyes on snellens chart/2-octave difference by 6. Contrast sensitivity
preferential looking method
Strabismus or anisometropic amblyopia show contrast
For bilateral amblyopia the visual acuity should be sensitivity loss affecting cither all spatial frequencies or
less than 6/12 in each eye. The amblyopia treatment limited to high spatial frequencies. There is loss of high
study (ATS) defined amblyopia as visual acuity of frequencies in stimulus deprivation amblyopia. Contrast
20/40 or worse with at least 3 Log MAR line difference sensitivity improves during amblyopia therapy and can
between the eyes be used to monitor progress.

In children it is difficult to determine visual acuity 7. Accommodation
and there is debate which method should be used to
measure visual acuity at which ages. However, it is Accommodation has been found to be normal or
easier in cases of unequal vision as child resist closure reduced in some amblyopic eye. However, visual acuity
of better eye. to near fixation has been found to be better than at
distance
1b)Stereo acuity- Any defective stereopsis indicates
further investigations for strabismus and amblyopia. 8. Fixation pattern

2. Fixation reflex Eccentric fixation is characteristic of amblyopic eye and
is usually seen in 23-89%of patients
One of the most commonly used clinical method for
diagnosing amblyopia in preverbal children is subject ii) Search for amblyopiogenic factors
assessment of fixation response as described by Zipt.
The presence of alternate fixation rules our amblyopia. Search for amblyopiogenic factors is a useful strategy for
However, preference of fixation for one eye suggests poor early detection of amblyopia, even when vision recording
vision in other eye in presence of squint. Furthermore, and detailed examination is not possible. Presence of
behavioral response to unilateral occlusion is another unilateral congenital cataract, ptosis or other media
commonly employed method for amblyopia opacities may have high amblyopiogenic tendency,
assessment. The child resists occlusion of sound eye, but bilateral cataract and opacities and opacities should no
will not care, if amblyopic eye is covered. A central, steady be ignored. Presence of high refractive error especially
and maintained fixation in each eye implies good visual hypermetropia of more than 3.5 diopter and astigmatism
acuity in each eye of >1.5 diopter should to taken as suspicious of amblyopia.
Presence of microtropia and small angle esodeviations
Fixation preference testing remains one of the most are also associated with amblyopia in significant number
valuable clinical methods for diagnosis and follows up of cases. Corneal reflex test & Buckner’s reflex tests are
of amblyopic patients and should be practiced by all the methods, which can be applied to assess amblyopia
ophthalmologist to assess vision in infants and preschool indirectly & unilateral amblyopia is usually associated
children. with strabismus (esotropia more commonly compared to

DOS Times - Vol. 15, No. 6, December 2009

Exotropia), visual deprivation (ptosis, corneal opacity/scar Anisometropic amblyopia is most commonly
cataract and vitreous hemorrhage), or refractive error encountered in our clinical practice; however strabismic
(Hypermetropia >3.5 Diopter & Astigmatism >1.5 amblyopia is detected at the earliest.
Diopter). Similarly bilateral amblyopia is also associated
with refractive errors and visual deprivation. If no AA: What is Your 1st line of Therapy in amblyopia?
plausible evidence for amblyopia factor is seen reconsider,
your diagnosis of amblyopia. PS: The first line is removal of the amblyogenic cause with
occlusion as per age. So along with proper glasses as the
Ruling out alternate causes of visual loss cycloplegic assessment, occlusion is started: patching the
good eye more than the amblyopic eye, alternating as per
Complete ocular examination by means of proper history age in ratio 2:1, 3:1, 4:1, 5:1, or 6:1 respectively for age under
and examination is mandatory to rule out any organic 2 year, 3 year, 4 year, 5 year, 6 year and above 6 years.
lesions like macular pathology, optic nerve or retinal diseases
before making diagnosis of amblyopia .However, two SCD: Full time occlusion is my preferred treatment modality in
conditions may coexist. Fundus examination is must .if treatment of amblyopia
uncertainty persists, a trial of occlusion for 3-4 weeks is worth.
AA: Does refractive correction has any role in treatment of
AA: How do you Classify amblyopia and which sort of amblyopia and what amount of refractive error if not
amblyopia do you see most commonly? corrected is amblyogenic?

PS: The classification of Amblyopia used is based on the PS: Refractive correction is the foremost part of amblyopia
etiology. therapy as it is also the most common culprit. Glasses
alone also work but occlusion makes it work faster.
(A) Refractive Error Uncorrected refractive error not leading to amblyopia may
be +1.5D sphere or +1.0D cylinder and -3.0D sphere. But
Iso-Ametropic (Bilateral uncorrected or also keep in mind an un-or under corrected hyperope may
undercorrected ref. error) exercise his / her accommodation to develop an
accommodative esotropia to suffer from strabismic
Anisometropic (unilateral or asymmetric uncorrected amblyopia also.
or undercorrected ref. error)
SCD: Refractive correction alone improves visual acuity in at least
This would include hypermetropia (over 1.5Dsph), 25-33 % patients in cases of anisometropic amblyopia. It is
astigmatism (over 1Dcyl) or myopia (usually more than–3 mandatory to carry out cycloplegic refraction in every case of
or -4 Dsph) amblyopia and proper optical correction should be
prescribed in every case of amblyopia .1% atropine in
B) Strabismus: usually esotropia, even of smaller angles children less than 7 years of age and 1% cyclopentolate in
(microtropia), vertical deviations and very rarely exotropia. older children are used by authors to carrying out the
In case of the latter one should exclude associated refractive refraction in their routine practice .ATS-5 Eye glass phase
errors, vertical deviation or subclinical organic pathology has concluded that amblyopia improved with optical
correction by more than 2 lines in 77% patients and
C) Stimulus deprivation or media opacities amblyopia resolved with optical correction in 27 % patients.

D) Organic: Subclinical foveal malfunction or malorientation Hypermetropia >3.5 Diopter & Astigmatism >1.5 Diopter
of cones: this is usually considered if the vision does not and myopia of more than 5 diopter are amblyogenic.
improve despite proper occlusion.
AA(a): What is the role of occlusion in treatment of amblyopia?
In addition one should keep in mind the possibility of mixed
etiology, as also the overlay of true amblyopia over the PS: Occlusion is the main part of amblyopia therapy.
organic pathology compromising vision.
SCD: There is neither a substitute nor a shortcut for full time
The most common type encountered is anisometropic occlusion in the treatment of amblyopia despite recent
followed by strabismic. recommendation of amblyopia study group. Occlusion
therapy prevents the fixating eye from taking part in the act
SCD: Strabismic of vision so that the patient is forced to use the amblyopic
eye.In addition, it removes the inhibitory stimuli to
Anisometropic amblyopic eye that arise from stimulation of the fixating
eye
Deprivation
AA (b): Which schedule of occlusion does you advice?
Isometropic
PS: The schedule used is described in Answer to Q.5
Idiopathic Undoubtedly the full time patch with good compliance is
the most effective and rapid, Recourse to part-time patch
Organic can be made in moderate amblyopia or partially recovered
amblyopia to maintain the visual gains, or in situations
Hysterical

Meridional

www.dosonline.org 11

where compliance to full-time patch is not possible. In the and it was concluded through intermediate reports that
latter situation the fact that a compromise is better than no minimal patching (2 hours / day) is as effective as moderate
treatment is to be understood. patching (6 hours/day) in treatment of moderate amblyopia
and prescribing greater number of hours of patching does not
SCD: We prescribe occlusion according to the thumb age rule. In seems to have significant effect during first four months of
children of 0-1 year of age, we occlude the better eye for treatment.
three days and amblyopic eye for one day. In children of 2-
3 years of age, we occlude the better eye for 4 days and AA: What is the role of penalization in amblyopia therapy? Is
amblyopic eye for one day. In children of 4-6 years of age penalization as effective as occlusion?
we occlude the better eye for 5 days and amblyopic eye for
one day . In children of more than 6 years of age we PS: Penalization is an effective alternative in select cases and
occlude the better eye for 6 days and amblyopic eye for one needs to be individualized depending on the refractive
day. Once occlusion therapy has been initiated, the child errors of the two eyes and associated esodeviation if any. A
must be reexamined at frequent intervals for several reasons fixation switch “needs to be established for its effect. It may
be done with atropine ointment used hs in cases of
AA (c): When do you stop occlusion? hyperopes or with over plus glasses in low hyperopes or
myopes. The former penalizes for near and latter for
PS: We continue occlusion (full time) till full visual improvement distance. Both may be combined in select cases. Usually
has occurred as evidenced by Snellen’s vision no further penalization in the form of atropine or partial blurring by
improvement in two consecutive monthly visits. One may scotch tapes or transparent nail-varnish is used for
switch to part time patching and finally weekly patching as maintenance therapy.
age advances, and continue till 9th birth day to check
regression. Monitoring from time to time is worth its while. SCD: We are of the opinion that occlusion remains gold standard
in the treatment of amblyopia and penalization can be tried
SCD: 1. The occlusion can be stopped ,when acuity becomes as an alternative line of therapy in patients of occlusion
equal in both eyes failure, or as maintaince therapy.

2. When there is true alternation of fixation In view of the difficulties encountered with occlusion therapy
in some patients and the occasional complication of
3. There is no visual improvement after 3-6 months of occlusion amblyopia, alternative therapies have been tried.
occlusion despite good compliance (depending on the Penalization is therapeutic technique performed by optically
age of patient). defocusing the eye with better vision by using cycloplegics
or by altering the eyeglass lens to cause decreased vision in
AA (d): What are adverse effects of occlusion seen in your setting? non amblyopic eye; it may be either pharmacological or
optical. Penalization has the advantage being cosmetically
PS: The risk of occlusion amblyopia is rare with the age related acceptable, but it does not inhibit the abnormal binocular
alternating regime also because we follow-up with timely interaction, which is the essential cause for amblyopia. It rarely
monitoring. If it occurs and is detected timely it can be decreases the vision of the good eye, below that of
easily reversed. amblyopic eye: therefore, its indication is limited:

SCD: Occlusion amblyopia 1. Moderate amblyopia in uncooperative patients

Constant manifest déviation 2. Anisometropic amblyopic eye

Psychological problems 3. Maintenance therapy

Diplopia 4. Occlusion failures

Increase in angle of deviation 5. Nystagmus

Skin rash Amblyopia treatment study was initiated to address whether
occlusion or atropine penalization is best initial, treatment
AA (e): Is minimum intensity patch as effective as full time patch? for moderate amblyopia (20/40-20/100) and it was concluded
that both the treatment were well tolerated and the effect of
SCD: No atleast not in our experience. However, amblyopia each treatment seemed consistent. Patching has a potential
treatment study 2 was initiated to address following advantage of a more rapid improvement in visual acuity and
question possibly a slightly better acuity outcome, whereas atropine
has the potential advantage of easier administration and lower
1. Is minimal intensity patching (two hours/day) as effective cost. Atropine or patching for 6 months period produced a
as moderate intensity patching (6 hours day) in treatment similar improvement in amblyopia 2 years after the treatment.
of moderate amblyopia (20/40 to 20/80)?
However, there are certain drawbacks of ATS, so before
2. Is full time patching (all waking hours) more effective than applying these conclusions in Indian circumstances, we have
part time patching (6 hours /day) in treating severe to keep in mind the following limitation of ATS.
amblyopia (20/100to 20/400) ?

3. What is recurrence rate and what are the factors influencing
recurrence after cessation of therapy in successfully treated
amblyopia?

12 DOS Times - Vol. 15, No. 6, December 2009

1. The strict inclusion criteria hampered the study by a research project titled Role of television exercises as a
including a limited number of patients. form of near vision activities and initial results are
encouraging.
2. Methodology was not strict, thereby making the results
subject to many questions. AA: Is there any role of LASIK surgery in amblyopia and do
you have any personal experience?
3. Ethnic variation to treatment always remains a factor,
so the results cannot be generalized to other countries. PS: The role of LASIK surgery in cases of high unilateral myopia
or high anisometropia is worth while, but this should be
4. Is atropine safe in tropical countries. done preferably after the amblyopia is treated with glasses
and occlusion and also after establishing the stability of the
5. Compliance was not monitored objectively in PEDIG refractive error over two-three years. This would help in
and therefore makes it harder to interpret the result. rehabilitation if high unilateral refractive errors and prevent
the regression of amblyopia therapy.
6. ATS-I did not answer the effect of atropine on fusion
and stereopsis as the patients were under the effect of SCD: Refractive surgery in children to reduce the amblyiopiogenic
the drug at the time of final examination. The difference level of refractive error is proving to be relatively stable.
in the visual input from the two eyes has been shown to Recently Astle et al. have described that LASIK is an effective
reduce fusion and stereopsis this may be a potential surgical alternative to improve visual acuity in
disadvantage with atropine. anisometropic amblyopia treatment or in whom other
therapy fails. However, we are of the opinion that Lasik
7. In ATS there was selection bias as limited centers were should be used as a last resort to treat only desperate cases
included. of amblyopia. Idonot have any personal experience of using
Lasik for amblyopia.
8. There was a lack of an untreated control group
AA: Is it mandatory to treat amblyopia prior to surgery?
9. Improvement in visual acuity may have been due to
learning and adaptation PS: Amblyopia therapy should always be treated prior to
surgery as it is easy to monitor, convince the patient and
These are the valid objections and should be taken into parent and maintain their compliance prior to surgery.
account before applying recommendations of ATS Moreover there is a risk of recurrence of squint due to
occlusion therapy in some cases if is done after surgery.
Despite all the benefits of penalization its major Further the success of squint surgery is better in treated
disadvantages include: causes of amblyopia, as harmony is better established
amongst the equals!
1. Active inhibition is not eliminated
It has been traditionally taught that treatment of amblyopia
2. The risk of occlusion amblyopia persists should be done prior to surgical intervention. Surgery may
have to be postponed till completion of amblyopia therapy
3. Cost of drugs resulting in its delay for months or year in intractable
amblyopia, thus depriving the benefits of early surgery to
4. Injury with drug vial these patients. Lam et al. have suggested that performing
surgery before the completion of amblyopia therapy does
5. Allergic reaction to drugs not affect the motor or sensory outcome adversely
provided amblyopia therapy is continued postoperatively.
AA: What is the role of near activities in treatment of Hence, the question that arises is why wait till completion
amblyopia? of amblyopia therapy and deny the benefits of early surgery
to these patients?
PS: The role of near activities in treatment of amblyopia is as
important as occlusion therapy. It may be said that Home We conducted a study to resolve this issue and concluded
Active Vision Exercises (HAVE to be done!), be it for near that it is not mandatory to treat amblyopia prior to surgery
like reading, writing, drawing or playing video games or if amblyopia therapy is continued postoperatively, unless it
even distance – watching good (approved by mothers!) is a case of infantile esotropia with moderate amblyopia.
programs on television.
AA: How do you record vision in a case of amblyopia with
Along with proper glasses and occlusion HAVE is the most nystagmus and how do you treat it?
effective way of treating amblyopia. Whether one uses the
computer games at home or office / clinic, obviously the PS: For recording of vision in cases of nystagmus one has to
former is better as it can be done for more time and daily, keep in mind two things (a) null position if any as vision is
provided somebody ensures regularity. best in this position, but also check the vision in primary
position to know the deterioration (b) Latency of
SCD: It has been suggested that near activities like threading beads, Nystagmus: in manifest latent nystagmus (MLN) when the
tracing pictures and reading fine print plays a significant binocular vision is better that monocular vision in either
role in the improvement of vision in amblyopia and children eye. If that be so, reassess the monocular vision with +
should be encouraged to do near activities. Park et al studied 6.0Ds lens to fog the other eye.
the outcome of part time occlusion combined with near
activities and found that combining the near activities with
occlusion causes improvement in vision. We are conducting

www.dosonline.org 13

Conventional occlusion (patching the dominant eye) can 7. Type of occluder: If the proper occluder is not prescribed, it
still be used in amblyopia associated with MLN. The vision might compromise the prognosis. An adhesive skin patch
deteriorates initially but gradually even the nystagmus is always preferable
becomes better as vision recovers.
8. Near exercises: Occlusion treatment augmented with near
SCD: Visual acuity testing in nystagmus requires blurring of other visual exercises such as threading, beads tracing and reading
eye with high plus lens (plus 6 diopter lens.) visual acuity fine prints is considered to hasten visual improvement and
should be measured separately in each eye. Testing of should be advised. Although this aspect is under study by
binocular vision and near vision is mandatory inpatient ATS, initial results are promising, long-term results are not
with nystagmus.Visual acuity should be tested using same known.
parameters at each visit
9. Patient compliance: Compliance is the most important factor
If nystagmus is idiopathic infantile, then the patient has to for occlusion treatment to be successful, better the
treated in a conventional way. However, in manifest latent compliance, better the result
nystagmus, partial patching doesn’t work and full time
patching is required, but, we have to keep in mind that 10. Presence of astigmatism: The patients with presence of
occluding one eye makes the nystagmus worse. Hence, significant astigmatism (>1.5D) are less likely to achieve
atropine has been suggested as an alternative to a skin successful outcome
occluder, but it is usually less effective.
11. Method of treatment termination: The method of
AA: What are the prognostic considerations in treatment of terminating occlusion treatment affects prognosis in
amblyopia? amblyopia, ATS found that when occlusion is applied for 6
or more hours, there is less likely regression of visual acuity
PS: For prognosticating the amblyopia therapy the factors are compared to 2 hours of patching, and when it is stopped
(a) presenting vision (b) age at treatment and (c) compliance abruptly.
and motivation of the patient to do amblyopia therapy.
Counseling the patient and parent and proper monitoring 12. Previous treatment: Although, some studies report that
helps in improving the prognosis. Assessment of near vision presence or absence of previous treatment has no effect on
as also single letter acuity vs line acuity helps in amount of visual acuity improvement achieved. Other
prognosticating the recovery of vision as also reinforcing studies reports that a new treatment‘s outcome may simply
the success to the patient. The speed of reading is a very constitute reestablishment of the previous regimen’s
useful tool of assessment in monitoring progress. outcome, thus compromising maintaince.

SCD: Success of occlusion therapy depends upon several factors, 13. Refractive correction: The effect of refractive correction
which should be kept in mind while treating amblyopia needs to be controlled for evaluating any other amblyopia
treatment, because, if refractive correction is improper, the
1. Age of patient, younger the child better the prognosis, efficacy of treatment is reduced
however it depends on duration of amblyopiogenic
experience AA: What are differential diagnoses for amblyopia?

2. Types of amblyopia: Occlusion is most effective in strabismic PS: The differential diagnosis of amblyopia in the form of
amblyopia, because it is detected early. Stimulus deprivation organic pathologies should be recognized in the initial visit
amblyopia has the poorest prognosis. Anisometropic itself to prevent forcing an unnecessary occlusion on a child.
amblyopia had prognosis somewhere in between. But the fact that a concurrent functional amblyopia may be
Hypermetropic anisometropia has a poorer prognosis in over-riding an organic pathology, mandates an occlusion
comparison to myopic anisometropic amblyopia. trial for a few weeks. In cases of failed occlusion therapy
despite good compliance on two successive visits, one
3. Treatment duration: ATS, found no relationship, between should rule out sub-clinical macular degeneration by
hours of treatment prescribed and final visual acuity electrophysiological tests.
outcome.
SCD: Functional causes
4. Pretreatment visual acuity: If the pretreatment visual acuity
is comparatively good, visual prognosis is better, due to Strabismic
better patient compliance to occlusion treatment .However;
initial poor vision does not necessarily mean a poorer Strabismus
prognosis.
Refractive
5. Type of occlusion: Conventional full time occlusion of the
better eye is preferred and gives better result as compared Uncorrected anisometropia
to part time and partial occlusion.
Combined aniso-strabismus
6. Types of fixation: Amblyopia with foveal fixation responds
more quickly to therapy and the success rate is better than Uncorrected astigmatism
that with eccentric fixation.
Irregular astigmatism

Visual –deprivation cause

14 DOS Times - Vol. 15, No. 6, December 2009

Occlusion amblyopia Hypoplasia of optic nerve
Early complete bleopharoptosis
Congenital cataract Keratoconus
Corneal opacity
Psychogenic cause Macular pathology
Hysteria
Malingering Optic atrophy
Structural / Pathological causes
Vitreous Hemorrhage Retrobulbar neuritis
Fundus coloboma
Medullated nerve fibres AA: Have your treatment plan changed after report of
amblyopia treatment study groups recommendations?

PS: The recent ATS by PEDIG and our own studies on the role
of atropine penalization and part time occlusion has
prompted us to use these two modalities in moderate
amblyopia and recovered amblyopia for maintaining and
preventing recurrences as well as in poor compliant cases.

SCD: No

DOS CORESSPONDENT
Ashish Amar MS, FRCS, DNB

Kindly send New E-mail address for DOS Correspondence
Email: [email protected]

Online Journal Available

Many New Journals at DOS Library

Dear DOS Members,

We are pleased to announce that DOS has subscribed to online access of the following 18 journals. We are also in the process of adding a few
more journals. These journals can be accessed at the DOS library situated at Room No. 2225, 2nd Floor, New Building, Sir Ganga Ram Hospital,
Rajinder Nagar, New Delhi-60. The timings are from 10.00 A.M. to 5.00 P.M. on week days and 10.00 A.M. - 2.00 P.M. on Saturday. The
Library will remain closed on Gazetted Holidays. Members are requested to utilise the available facilities i.e. Computer with Video Editing
& Conversion facility VHS to VCD, Journals Viewing, Books and Journals etc. The DOS members can get the full text articles of the current
issues as well as many back issues of these subscribed journals. You need to send the request for the article needed. We will email you full text.

E-mail ID is: [email protected]

• Acta Ophthalmologica • Acta Ophthalmologica Scandinavica
• Acta Ophthalmologica Scandinavica Supplement • Archives of Ophthalmology
• British Journal of Ophthalmology • Clinical & Experimental Ophthalmology
• Contemporary Ophthalmology • Cornea
• Current Opinion in Ophthalmology • Evidence-Based Eye Care
• Evidence-Based Ophthalmology • International Ophthalmology Clinics
• Journal of Glaucoma • Journal of Neuro-Ophthalmology
• Journal of Pediatric Ophthalmology & Strabismus • Journal of Refractive Surgery
• Ophthalmic Surgery & Lasers • Ophthalmic Surgery, Lasers & Imaging
• Ophthalmology Management • Retina
• RETINAL Cases & Brief Reports • Techniques in Ophthalmology

www.dosonline.org 15

All Femtosecond Refractive Surgery Refractive Surgery

Sharad Lakhotia MS, CAMS

Femtosecond is an ultrafast laser generating pulses as short as with this procedure are more stable than Lasik including high
one quadrillionth of a second (10-15). The world Femto came myopia patients. If the lenticule is dissected above, then it is very
from Danish word for number 15. easy to identify inferior surface by having enough resistance and
empty spaces. Once dissected, it is very easy to lift flap by simple
It uses infrared beam to separate tissues by photo disruption. pull with forceps or spatula.

All Femtosecond Refractive Correction Journey from Flex to smile is easy and has advantage of small
incision thus providing all Femtosecond laser solution to refractive
Femtosecond lenticule extraction or FLEx using Visumax (Carl problems.
Zeiss meditec, Jena Germany) have reported excellent results for
total refractive correction. INTRACOR procedure also uses Initial results with hyperopia suggest FLEx can be a good option.
Femtosecond laser to interact with stroma to give vision correction. There was some regression as with Eximer laser but data at 1
month interval was great. In hyperopia, the flap is just 0.5mm
Lenticular Extraction with Visu Max Femtosecond laser larger in diameter then the lenticule. The main point for
consideration is that lenticule should not have sharp edge other
Dr. Walter Sekundo & Dr. Marcus Blum were first surgeons to wise it will result in regression. So the main challenge is to find an
perform this procedure in August 2008. Over 1000 eyes have been optimal form for lenticule edge.
operated till now at all centres including one at Baroda run by Dr.
Rupal Shah besides 3 other international sites. In FLEx treatment, Complication
Femtosecond laser creates two cuts, a refractive and a non-
refractive as a single step. The first cut is made at the bottom of They were minimal. Mild transient haze like reaction and
the refractive lenticle while the second one at its roof. Once the microstria were reported which cleared. There were some problems
cuts are made, flap is lifted and refractive lenticule is removed. in separating the refractive lenticule in 2 cases of which one resolved
The flap is reposited in usual manner. It is important to make after 6 months. However no patient showed signs of diffuse
manipulation at correct plane between flap & lenticule and separate lamellar keratitis or transient light sensitivity syndrome.
lenticule edge.
Benefits of Visumax System
The lenticule can be of different diameters from 6mm to 7.3 mm
equivalent to optical zone of Excimer laser. The remaining stromal While designing Femtosecond laser a balance has to be kept
zone is usually 300 micron or more. between increasing pulse rate and focusing power & decreasing
spot size & energy. The optics of Visu Max produce tightly focused
Walter Sekundo reported good results in 6 months follow up. 9% beam with following effects.
gained 2 lines of visual acuity, 43% gained one line, 39% remain
unchanged and 7% lost one line visual acuity. 74% patients were 6/
6 or better.

Dr. Rupal Shah reported slow visual recovery at 1 week but
changing scanning pattern produced good results. While scanning
in spirals, they used to cleave posterior surface of the lenticule
from centre to periphery. The flap was then cleaved from periphery
to centre. They changed direction i.e. posterior surface of lenticule
was separated by scanning from periphery to centre and anterior
surface from centre to periphery. This led to dramatic
improvement in visual recovery. 89% reached to pre operative
BCVA after 1 week. With upgraded 500 Hz Visumax, 95% reached
or improved to pre- operation BCVA level at 1 week.

Some of the investigators are doing a modified version called
small incision lenticular extraction or Smile. This technique makes
the procedure less invasive where by the entire lenticule can be
extracted through a small incision without lifting up the flap.

Osama Ibrahim reported 90% of patients having better than 20/25 Visumax Femtosecond Laser
visual acuity after one month. He is of the opinion that results (Carl Zeiss Meditec AG, Jena)

Lakhotia Eye Centre & Laser Institute
E-544, Greater Kailash Part-II, New Delhi

www.dosonline.org 17

(i) The accuracy of pulse placement is optimized.

(ii) Tissue dissection is carried out with low energy.

(iii) Energy drop off from point of impact is steep thus causing
less collateral tissue damage & hence faster recovery.

Some Femtosecond lasers require scleral suction & flat FLEx procedure in stages
applanation. High suction in such cases can cause discomfort &
subconjunctival hemorrhages. In Visumax the rise is intraocular
pressure is low enough for patients to see & does not discomfort
the patient. A curved contact glass and corneal suction allows IOP
below 90 or 100mg. In one study rise in IOP during flap creation
was 84.9 ± 7.3mmHg for Visumax, 180.6 ± 21.6 mmHg for intralase
and 150.9 ± 17.2 mmHg for LDV. Thus anxiety level of patient is
less, patient can visualize fixation light and so better fixation is
achieved during treatment.

Flap centration on corneal vertex is well achieved as it was intended been tried. However the results are not very accurate. Also its
for FLEx procedure. The vertex of cornea fit well in to vertex of role in presbyopia has been emphasized as it causes a biomechanical
contact glass of Visu Max Femtosecond laser. The problem of change in cornea that shifts centre slightly forward creating a
opaque bubble layer is very thin as it dissipates very rapidly. Walter pattern of hypersphericity thus allowing some near vision while
Sekundo considers this to be standard procedure with potential retaining distance vision.
to revolutionize the course of refractive surgery.

INTRACOR procedure:- is an intrastromal procedure done on The surgeon can expand circle diameter or add radial intrastromal
TECHNOLAS Femtosecond work station. It applies energy inside incision similar to those created in radial Keratotomy and is
the cornea without bringing it to the surface. There is no incision effective in biomechanically correcting small degree of myopia.
of epithelium, endothelium or Bowman’s or Descemet’s
membrane and thus ensure better healing with minimal risk of INTRACOR brings hope for correcting presbyopia with low
infection. The pulses are placed on concentric intrastromal circles refractive errors by biomechanical methods.
centered about visual axis and extended at least up to 100 microns
from the surface. The concentric patterns of cut fibers shift the Thus Visumax Femtosecond has shown a great stride as an
centre of cornea slightly anteriorly and create a hyperprolate alternative as all Femtosecond laser option for all refractive errors
shape. At present myopia up -3D and astigmatism up to 2D have with small incision lenticular extraction.

Author
Sharad Lakhotia MS, CAMS

18 DOS Times - Vol. 15, No. 6, December 2009

Current Status of IOL Power Calculations Cataract

S. Venkatesh MS, FICO, FRCS

In modern day ophthalmic practice the buzz word seems to be In a similar fashion a “Standard Emmetropia” lens power can be
precision. Precision with a view to achieving perfection and one calculated by adding +1.25D to the calculated power of an
the greatest challenges to this quest is the restoration of normal or EMMETROPIA lens to restore emmetropia.
near normal vision after cataract surgery. This could only be possible
if we had the ability to predict the power of the IOL with an Educated guesses – not good enough!
unprecedented degree of accuracy.
With these crude types of calculations, ophthalmologists were
The Past- Educated Guesses happy if they achieved post operative results within 1.0D of targeted
outcomes. However in the present scenario when we are dappling
But thirty years ago, before 1980s, IOL power calculations could with multifocals and offering accomodative IOLs that cost about
be at best described as educated guesses based primarily and a lakh of rupees we need to be able not only to achieve much
solely on the patient’s previous refractive status before the onset greater levels of precision but also be able to achieve this precision
of cataractous changes. If the patient was an emmetrope before consistently.
the onset of cataractous changes then he received an ‘Idem lens’.
The IOL power prediction formulae:
The IDEM Lens
To achieve greater levels of accuracy in predicting IOL power that
The IDEM lens or the “ideal emmetropia lens”, was that IOL power would result in desired post operative spherical outcomes, 4
which when implanted within the eye restored emmetropic status generations of IOL formulae were enumerated.
after cataract surgery. The power of this lens was mathematically
deduced to be +17.0 D for an AC lens, +19.0D for an iris fixated • First Generation - were the SRK- 1 and the Binkhorst formula.
lens and +21.0D for a posterior chamber lens.
• Second Generation – SRK-2

The Standard lens • Third Generation – SRK T, Hollday. Hoffer-Q

Since the preferred practice pattern at that time was to make the • Fourth Generation – Hollday 2, HAIGIS.
patient myopic by about 1.0D, in order to strike a balance between
distance and near vision, a “Standard Lens” was implanted. This Broadly speaking these formulae could either be ‘Theoretical
lens had +1.25D added to the IDEM lens power, this add being the formulae’ which are based on mathematical principles revolving
adjustment for moving the 1.0 D of myopia from the spectacle to around the ‘schematic eye’, or they could be ‘regression formulae’
the IOL plane. which were arrived at by looking at post operative outcomes and
working backwards in what is known as the regression analysis to
The Emmetropia lens order to arrive at the IOL power. The Third and fourth generation
formulae incorporate a bit of both which was called the “Fudge
If the patient had previous ammetropia, he received an factor” by duke elder.
“Emmetropia Lens” which would effectively take care of the pre
existing error and restore the patient to an emmetropic status
after cataract surgery. The power of such a lens was calculated by
multiplying the pre existing refractive error with a conversion
factor of 1.25 and algebraically adding it on to the IDEM lens
power.

For example: if a patient had an axial myopia of 3.0D before the
onset of cataract. The power of the emmetropia lens may be
calculated thus:

• 3.0 x 1.25 = 3.75.

• Idem lens power for a PC IOL = 21.0D

• Emmetropia lens power = 21.0 + (-3.75)

• = +17.25D.

Figure 1: Dual Lens System

Old No. 21, New No. 3, ‘TUSHARA’ 21
Navarathna Gardens, Ekkaduthangal,

Chennai, Tamilnadu

www.dosonline.org

coined by Dr. Jack Holladay will also play a pivotal role in
determining its power. In fact the strength and predictability of
the various IOL formulae depends upon their ability to accurately
predict the ELPo

“One of the most important and challenging tasks in IOL power
calculation is to predict the ELPo for a given eye,” - Dr. Haigis

THE ELPo

There are several factors that will influence the ELPo.

Figure 2: Effective IOL position Anatomical factors: like the axial length, the steepness of the cornea
(average K), the limbal white to white measurements, the pre-
Understanding how these Formulae Work- Basic Facts operative anterior chamber depth and the lens thickness. In fact
one large group study conducted by Dr. Haigis showed that the
Before we unravel the complexities enshrouding the various IOL position of the capsular bag equator from the corneal vertex can
formulas we need to take a look at some basic facts. The normal be arrived at by adding the pre op ACD and 40% of the crystalline
human eye has two refracting surfaces – the cornea and the lens thickness. Dr Holladay showed in his study that the depth of
crystalline lens. The aqueous and the vitreous serve as a uniform the anterior chamber had a positive and partial relationship to the
conducting medium having a RI of 1.337 limbal white to white measurement (avg.11.7mm). The 1st and
2nd generation IOL formulae tried to predict the ELPo based on
Therefore the human eye functions as a dual lens system. In any anatomical factors alone.
dual lens system if the primary or the objective lens as well as the
distance of the focusing screen are fixed – then the effective power IOL and surgery related factors: The shape, the length, the flexibility,
of this system of lenses will depend on the power and the position the anterior angulation if any and the material of the haptic of the
of the second lens. Let us say that for a given power of the second IOL will affect the ELPo. The shape and design and the material of
lens the light get focused on the screen. If this secondary lens the optic will also have a profound effect. Certain lenses like the
moves towards the primary lens its effective power is increased ‘Acrysof ’ hydrophobic lenses and the ‘Technis-One’ lenses have a
and the light will focus in front of the screen and if it is moved negative shape factor because of their asphericity. In these lenses
away from the primary lens its effective power is decreased and about 80% of the principle plane of the IOL power is situated close
now the light will come to a focus behind the screen. In the normal to its posterior surface which is why these lenses have a higher A
Phakic eye the position of the cornea and the retina is fixed and constant of 118.8 in contrast with the biconvex, non aspheric design
the effective power of the eye is increased, as say, during of hydrophilic acrylic and silicon lenses where the principle plane
accommodation not by changing the position of the crystalline of the IOL power is closer to its midpoint and anterior surface
lens but by increasing its curvature. But this is not the case in a which explains why their A constants are close to 118.0 for the
Pseudophakic eye. In a Pseudophakic eye the effective IOL power same in the bag implantation.
will not only depend on the IOL power printed in the label of the
IOL box but also upon where it is positioned within the eye. Individual Surgeon’s Technique: in addition the surgeon’s individual
surgical technique can also influence the ELPo;
Assimilating this fact we understand that the effective power of an
IOL will depend on its position within the eye. In fact the very The most important surgical factor is the manner in which you
concept of an IOL power is rather a relative phenomenon. For fashion the CCC with respect to its size and centration; this is
example if the calculated power for an “in the bag” IOL is 21.0D because the ELPo is directly related to the post operative position
and during the surgery you end up placing it in the sulcus with an of the capsular bag equator. Too large a CCC will allow the optic
anterior displacement of 0.5mm, its effective power will increase to prolapse out of the bag increasing its effective power. The ideal
and it will function as a 22.0 lens leading to a myopic shift in the CCC should overlap the optic and keep it in place. Capsular fibrosis
post operative period. Similarly if you change the model of your will cause the forward movement of the bag.
IOL and implant a lens with a 10 degree angulation into the bag
which may produce a 0.5mm shift posteriorly then the effective In addition, inadequate removal of visco-elastic from behind the
power of the lens will decrease and it will now behave like a 20.0D IOL can cause a capsular block syndrome and induce progressive
lens leading to a hyperopic shift. The message in this explanation myopia. Certain plate haptic lenses especially of the thin lens design
is that although the power of the IOL is function of the corneal can vault anteriorly with the onset of capsular fibrosis producing a
power and the axial length, its effective position within the eye myopic shift that cannot be explained solely on the basis of an
which is known as the ELPo or the effective lens position -a term anterior displacement. The 4th generation IOL formulas can
optimize these surgeon factors.

Bag to Sulcus shift

It could sometimes happen that certain factors like a posterior
capsular rent or a loss of the integrity of the anterior capsule may
require that the IOL is placed in the sulcus. In such a situation
most surgeons would empirically deduced 0.50D – 0.75D from
the calculated IOL power in order to compensate for the increase

22 DOS Times - Vol. 15, No. 6, December 2009

Power at Power at Bag / Sulcus Subtract from The manufacturer’s lens constant

Capsular Bag Ciliary Sulcus Difference Bag Power Since the post operative effective lens position is dependant upon
a myriad of factors, the various IOL formulae incorporate a variable
+30.00 D +28.55 D -1.45 D -1.50 D into the computation. This variable known as the “A constant” of
+29.50 D +28.09 D -1.42 D -1.50 D the SRK formula, the ‘Surgeon Factor’ or the ‘SF’ of the Holladay
+29.00 D +27.61 D -1.39 D -1.50 D formula or the ‘pACD’ or the ‘personalized ACD constant’ of the
+28.50 D +27.14 D -1.36 D -1.50 D Hoffer-Q formula all contribute towards accurately predicting
+28.00 D +26.67 D -1.33 D -1.00 D the ELPo and each of them can be ‘optimized’ to enhance the
+27.50 D +26.20 D -1.30 D -1.00 D predictability of the IOL formula. For a specific surgeon with a
+27.00 D +25.73 D -1.27 D -1.00 D reproducible surgical technique, the A-Constant will depend upon
+26.50 D +25.26 D -1.25 D -1.00 D the material of the IOL and its deemed position within the eye.
+26.00 D +24.79 D -1.22 D -1.00 D This ‘A constant’ is worked out by the manufacturer of the IOL
+25.50 D +24.31 D -1.19 D -1.00 D and this information is printed on the box of the IOL.
+25.00 D +23.84 D -1.16 D -1.00 D
+24.50 D +23.36 D -1.13 D -1.00 D This value represents where we anticipate the IOL to sit in
+24.00 D +22.89 D -1.11 D -1.00 D relationship to the cornea. Specifically, how near or far from the
+23.50 D +22.42 D -1.08 D -1.00 D cornea. The “constant” will decrease with an AC IOL as compared
+23.00 D +21.94 D -1.05 D -1.00 D to a PC IOL.
+22.50 D +21.47 D -1.03 D -1.00 D
+22.00 D +21.00 D -1.00 D -1.00 D Fallacies of the manufacturer’s lens constant
+21.50 D +20.53 D -0.97 D -1.00 D
+21.00 D +20.05 D -0.95 D -1.00 D But there are certain pitfalls with the computation and calculation
+20.50 D +19.58 D -0.92 D -1.00 D of these lens constants. Firstly, the ‘A constants’ have been calculated
+20.00 D +19.11 D -0.89 D -1.00 D for an eye with an axial length of 23.5mm, a central corneal power
+19.50 D +18.63 D -0.87 D -1.00 D or 43.86D and limbal white to white diameter of 11.7mm. Which
+19.00 D +18.16 D -0.84 D -1.00 D is the reason why most IOL formulae work well within values that
+18.50 D +17.69 D -0.82 D -1.00 D approximate the normal schematic eye with a range of axial lengths
+18.00 D +17.21 D -0.79 D -1.00 D between 22.0mm – 26.0mm and a central corneal power of 41.0D
+17.50 D +16.73 D -0.77 D -1.00 D – 46.0D, while outside this range their predictability seem to be
+17.00 D +16.26 D -0.74 D -0.50 D erratic.
+16.50 D +15.78 D -0.72 D -0.50 D
+16.00 D +15.31 D -0.69 D -0.50 D Secondly, for many IOL models the ‘A constant’ is not individually
+15.50 D +14.83 D -0.67 D -0.50 D computed based on trials but merely approximated from similar
+15.00 D +14.35 D -0.64 D -0.50 D lens design models.
+14.50 D +13.88 D -0.62 D -0.50 D
+14.00 D +13.40 D -0.60 D -0.50 D And finally these calculations have been based on data obtained
+13.50 D +12.93 D -0.57 D -0.50 D by applanation A scans and manual keratometry.
+13.00 D +12.45 D -0.55 D -0.50 D
+12.50 D +11.97 D -0.53 D -0.50 D Although the A constant is representative of the effective lens
+12.00 D +11.49 D -0.50 D -0.50 D position within the eye it only needs to be used as guide and needs
+11.50 D +11.02 D -0.48 D -0.50 D to be optimized to enhance your surgical results.
+11.00 D +10.54 D -0.46 D -0.50 D
+10.50 D +10.07 D -0.43 D -0.50 D The IOL formulas – A closer look
+10.00 D +9.58 D -0.41 D -0.50 D
+9.50 D +9.11 D -0.39 D -0.50 D The SRK formula
+9.00 D +8.63 D -0.37 D No Change
+8.50 D +8.16 D -0.35 D No Change Was described by Donald Sanders, John Retzlaff and Kraff in the
+8.00 D +7.68 D -0.32 D No Change mid 1980’s. The formula attempted to predict the IOL power based
+7.50 D +7.20 D -0.30 D No Change on the axial length and the average central corneal power.
+7.00 D +6.72 D -0.28 D No Change
+6.50 D +6.24 D -0.26 D No Change • IOL power = A – 2.5 L – 0.9 K.
+6.00 D +5.76 D -0.24 D No Change
+5.50 D +5.28 D -0.22 D No Change • L = axial length in mms

• K = average central corneal power in Diopters.

The first generation SRK formula worked well for axial length
ranges between 22.0m – 24.5mm but was erratic outside this range.

in effective IOL power. However this compensation will depend In order to increase its predictability the SRK 2 formula was
upon the ‘base power’ of the IOL. The following table needs to be introduced in which additions were made to the A constant in
displayed in all operating rooms and gives us a guideline as to how axial lengths less than 22mms and 0.5 was subtracted from the A
much we need to subtract from the calculated IOL power in a bag constant for axial lengths over 24.5mms. This was an attempt to
to sulcus shift provide a ready made ‘optimization’ of the A constant.

www.dosonline.org 23

SRK 2 patient. The pACD – the personalized A constant was the
equivalent of the A-Constant in the SRK formula. The construction
• Axial length 21-22mm, add 1 to A of the Hoffer –Q formula was such that it was extremely reliable
in short eye balls with an axial length of less than 22.0mms.
• 20-21 add 2
The Fourth Generation Formulae
• < 20 add 3
Haigis
Long eyes:
Holladay 2
Over 24.5mm subtract 0.5mm from the A.
HAIGIS Formula:
With this modification the SRK 2 formula was reliable in predicting
IOL powers between the axial length range of 20.0mm- 26.0mm (1) DL = L - d n/z - d
but was still unreliable in shorter and longer eye balls.
—— - ———
SRK T Formula
ref nC - 1
The SRK T formula is a third generation formula, described in
1990 by John Retzlaff and Donald Sanders. It combines the benefits with z = DC + ————— and DC = ———
of both the theoretical and regression formulae. The SRK T
formula uses theoretical elements like predicted post operative 1 - ref dBC RC
anterior chamber depth, retinal thickness adjusted axial length
and refractive indices of the cornea .The regression element is • D : refractive power of IOL
primarily used to optimize the ‘A constant’. This formula works in
eyes of normal length and moderately long and very long eyes. • DC: refractive corneal power
The SRK T formula has made the SRK 2 formula obsolete since it
combines all the advantages of the SRK 2 formula and also enables • RC : corneal radius
you to optimize the A-Constant
• nC : (fictitious) refractive index of cornea
Optimization is the process of making a formula more predictable
by refining and defining the manufacturer’s lens constant. In simple • ref : desired refraction
terms optimization is achieved by analyzing post operative
outcomes with respect to the targeted refraction for a given surgical • dBC : vertex distance between cornea and glasses
technique and a specified model or design of IOL as well as for a
given range of axial lengths. This optimization is then added on to • d : optical ACD
the ‘A constant’ to make the formula more predictable.
• L : axial length
Why Optimize
• n : refractive index of aequeous and vitreous (1.336)
As we have already seen almost all the IOL power prediction
formulae seem to work for axial lengths between 22.0mm – The calculation according to HAIGIS is given by:
26.0mm. However in shorter or longer eye balls they tend to
become inaccurate for two important reasons • nC = 1.3315

The A- constant is computed based on an average axial length of • dBC = 12 mm
23.50mm.
• L : axial length as measured by ultrasound
The reason for the failure of the 1st and 2nd generation IOL
formulae in accurately predicting the IOL power in very long or With the optical ACD d obtained by regression from preoperatively
very short eyes is because their calculations are based on certain measured acoustical data:
assumptions. These formulae assume a directly proportional
relationship between the axial lengths and the anterior chamber (2) d = a0 + a1 VKpr + a2 ALpr
depth and a similar association between corneal steepness or
curvature and the AC depth. It has been subsequently proved by (3) with a0 = ACD-Konst - a1 MW(VKpr) - a2 MW(ALpr)
Dr Holladay that this assumption is incorrect.
• VKpr : preop. anterior chamber depth measured ultrasonically
The Hoffer-Q formula: Third generation formula
• ALpr : (=L) preop. axial length from ultrasound
• Was described by Dr. Kenneth Hoffer in 1993.
• MW(..) : means of VKpr (=3.37) mm and ALpr (=23.39) mm
• P = f (A, K, Rx, pACD)
• ACD-Konst: ACD constant of manufacturer
• A: axial length
The Haigis formula is a 4th generation formula which was an
• K: average corneal refractive power (K-reading) adaptation of the formula first suggested by Gernet, Ostholt and
Werner as early as 1970, which is the reason why this formula is
• Rx: refraction also called the GOW 70 formula. The versatility of the formula lies
in the three individualized A constants namely a0, a1 and a2. The
• pACD personalized ACD (ACD-constant) a0 is linked to the manufacturers lens constant. The a1 is linked to
the pre operative ultrasonically measured ant chamber depth (this
This formula predicted IOL power as a function of the axial length, has a default value of 0.4) and a2 which is linked to the axial length
average central corneal power and the previous refraction of the measurements and which has a default value of 0.1.

The three ‘A constants’ enable us to customize each component
of the IOL formula. When fully optimized this formula will work
across the entire range of axial length values and you may not
need to use different formulae for different axial lengths.

24 DOS Times - Vol. 15, No. 6, December 2009

The Nine Types of Eyes Model Practical Tips: Chosing the Right
Formula in your Day to Day Practice

Figure 3: Nine types of eyes model – Dr.Holladay Figure 4: prediction accuracy of the various IOL
formulas to within 0.5D of target refraction

Holladay 2: 4th Generation Formula axial lengths between 22.0 and 26.0mm but also in 80% of short
eyes and 90% of patients with long eyes. It is this breakthrough
The Holladay 2 (1998) - 4th generation formula is currently the finding that has contributed to the enhanced predictability of the
most sophisticated formula that you could possible lay your hands Holladay 2 formula.
upon. It is an improvement on the Holladay 1 formula.
This formula now is available as part of a package called the
The unprecedented success of the formula lies in the fact that Dr ‘Holladay IOL consultant which also provides the necessary
Jack T Holladay has attempted to increase its accuracy and information to optimize every component of the ‘SF’ or the
predictability by incorporating seven different parameters into surgeon factor. This package costs 995$ and can be ordered from
the framework of the formula. These parameters all contribute the following web site- (713) 668-7337; docholladay @
towards the accurate estimation of the ELPo. docholladay.com

• Axial length. When fully optimized the Holladay 2 formula works across the
entire range of axial lengths.
• Central corneal power (K)
The most pertinent question now, is what formula do we need to
• Anterior chamber depth use in our day to day practice. In any surgical practice the majority
of the patient population (about 90%) would fit into the normal
• Lens thickness measurement range of axial length. For these patients any 3rd generation IOL
formula would work. But I recommend the SRKT or the Holladay
• Limbal white to white measurement 1 formula. Both these formulae are available with most biometers.
Remember there is no place for the SRK2 formula in today’s practice
• Age of the patient because the SRKT formula possesses all the advantages of SRK 2
formula and more. For these normal axial length population you
• Previous refraction of the patient. can further enhance your post operative outcomes by optimizing
the ‘A constant’ in the SRK T or the SF in the Holladay 1 formula.
The second reason for the success of this formula is the
development of the ‘nine types’ of eyes model by Dr. Holladay. For eyes shorter than 22.0mm the construction of the Hoffer-Q
This model overcame the discrepancies in all the other IOL formula makes it a better choice.
formulae, which revolved around the assumption that there was a
constant relationship between the central corneal power (K), the For long (axial length more than 26.0mm) and extremely long
pre operative anterior chamber depth and the axial length eyes (axial length more than 27.5mm) the SRK T formula works
measurement. For instance in eye ball with long axial lengths the better than any other formula.
formulae automatically assumed that the anterior chamber depth
would also be longer and vice versa and similarly in a steeper If you can purchase the fully optimized version of the Haigis and
cornea the formula presume a greater anterior chamber depth the Holladay 2 formula they would work across the entire range
and vice-versa. This is the principal reason why the various of axial lengths.
standard IOL power prediction formulae do not work in post
refractive surgery patients. How do we optimize

The surprising finding in this model that exposes the inadequacies Optimization helps to fine tune our post operative results. Since
of the 1st 2nd and even the 3rd generation formulae is that there most of us have access to the SRK T formula lets see how we go
is no direct correlation between the axial length measurements about this task:
and the anterior chamber size. Dr. Holladay found that the anterior
chamber depth was found to be normal in 96% of eyes with normal

www.dosonline.org 25

Table: Electronic spreadsheet to optimize A constant for different IOL formulae
Initial IOL Constant Calculation Sheet
Warren E. Hill, MD, FACS

Pt. name Axial length ACD pre-op K1 pre-opK2 IOL power Target SE post op ref calculated SE final va

• A minimum of 25 cases must be studied. Conclusion

• All cases must be operated upon using more or less the same Success in IOL power calculation should not be a product of chance

surgical technique. but instead needs to be the end result of sound scientific knowledge,

• All cases must receive the same IOL model. meticulous attention to detail and an ability to consistently achieve
targeted outcomes case after case. Several surgeons like Dr.Warren

• The A scan and keratometry must be performed by the same E Hill who have fully optimized their IOL formula have achieved a

technician. In case you are using applanation A scans it is a post operative prediction accuracy of 0.25D. This is what he has to

good time to move to immersion scans. In case you are using say regarding the future of successful IOL power prediction:

manual keratometry – calibrate the instrument at least once “If we can consistently lie within 0.25D of the target refraction we
in 3 months. can now set our sights on far more sophisticated endeavors like

• Analyze your post operative results at the end of 6 weeks or correcting third and fourth order aberrations during cataract

at the time of prescription of glasses. Look at the discrepancies surgery…..”

between your target refraction and your actual post operative References
result.

1. Ophthalmic Surg. 1990 Apr;21(4):266-71. A simple modified SRK

• Cumulatively enter all these details into an electronic spread formula for severely myopic eyes. Kora Y, Suzuki Y, Inatomi M,

sheet that can be downloaded from the internet at Ozawa T, Fukado Y. Department of Ophthalmology, Showa

hill@doctor_hill.com. University, Tokyo, Japan.

• As data is fed into the spreadsheet you can develop your own 2. Klin Oczna. 2005;107(10-12):615-9. [Accuracy of the SRK II, SRK/
optimization of the A constant, which will help you to achieve T, Holladay and Hoffer Q IOL power calculation formulas in
hyperopic patients after phacoemulsification]
more predictable post operative results.
3. Szaflik J, Kamiñska A, Gajda S, Jedruch A. Z Katedry i Kliniki

• In third generation IOL formulae like the SRK T, the Hoffer- Okulistyki II Wydzia u Lekarskiego Akademii Medycznej w

Q, or the Hollady1 formula there is only a single A constant Warszawie.

that affects the entire formula. Hence you need to optimize 4. doctor_hill.com Calculating Bag vs. Sulcus IOL Power.
the formula for a given range of axial lengths – like short eye
5. IOL Power Calculation, Personalizing the A-constant is key. BY
balls (20.0mm – 22.0mm) , normal axial lengths (22.0mm – AMY ORAVEC, MANAGING EDITOR (cataract and refractive
24.5mm) or long eye balls (24.5mm – 26.0mm). If for example surgery today)

the SRK T formula has been optimized for short axial lengths,
this optimization factor will not work if applied to longer axial 6. J. Cataract Refract Surg. 1990 May;16(3):341-6. Comparison of the
SRK/T formula and other theoretical and regression formulae Sanders
lengths. DR, Retzlaff JA, Kraff MC, Gimbel HV, Raanan MG. Department

• Optimization for the 4th generation IOL power prediction of Ophthalmology, University of Illinois, Chicago.

formulae can be done across the entire range of axial lengths 7. GERNET H, OSTHOLT H, WERNER H: Die praeoperative

as the Haigis formula has three different a constants linked Berechnung intraocularer Binkhorst-Linsen. 122. Vers. d. Ver. Rhein.-

not only to the manufacturer’s lens constant but also to the Westfäl. Augenärzte. Balve, Verlag Zimmermann. S. 54-55, 1970

post operative anterior chamber depth and the axial length. 8. SANDERS DR, RETZLAFF J, KRAFF MC: Comparison of the SRK
However to optimize the 4th generation formula you need
II formula and other second generation formulas. J Cataract Refract

upward of 200 cases and not merely 25 cases. Surg 14: 136-141, 1988

• For surgeons who are just getting initiated into the world of 9. Highly Accurate IOL Calculations, Pearls for achieving consistent
outcomes. By Warren E. Hill, MD, FACS (Cataract and refractive
refractive cataract surgery – optimization of the formula can
surgery today).
be greatly facilitated by visiting the following web site:

www.augenklinik.uni-wuerzburg.de/ulib. The ULIB site

developed by Dr. Haigis gives us optimized A- constant values

for different IOL designs and models and various axial lengths.

These guideline ‘A constants’ could be used as a starting point

instead of the manufacturer’s lens constant for your Author
optimization. S. Venkatesh MS, FICO, FRCS

26 DOS Times - Vol. 15, No. 6, December 2009

Diagnostic Ability of GDx VCC for Glaucoma
Glaucoma Diagnosis

Tutul Chakravarti MBBS, DO, DNB

Glaucoma is an optic neuropathy resulting in the loss of ganglion GDx NFA, GDx VCC
cells and their axons in the retina. The functional defect is
usually manifested by the loss of the visual field (VF) owing to Two new diagnostic instruments, the GDx/ Nerve Fiber Analyzer
diffuse or wedge defects of the ganglion cells and retinal nerve (GDx/NFA) (Laser Diagnostics Technology, San Diego, CA) and
fiber layer (RNFL). the Optical Coherence Tomograph (OCT) provides real-time
quantitive and objective assessments of the RNFL. Each of them is
RNFL defects based on different optical principles and different properties of
light to measure RNFL thickness.
Clinical examination for glaucoma has traditionally included
measurements of intraocular pressure, funduscopic examination Evolution of the Nerve Fiber Analyzer
of the optic disc and retinal nerve fiber layer (RNFL), and visual
function testing. However, it has long been recognized that axon The first commercially available version of the NFA in 1993 is now
loss in the RNFL can precede changes in the optic nerve head known as the NFA I. It has been upgraded several times since
(such as increased cup-to-disc ratio) and visual field loss. Studies then, changing names in the process. The second type was called
showed that in 60% of eyes with reproducible visual field defects, NFA II, and the next generations are NFA GDx, GDx VCC and
abnormalities of the RNFL were present six years before functional GDx ECC.
change and loss of visual field occurred. Therefore, delineating of
early glaucomatous RNFL damage might improve diagnosis and Nerve Fiber Analyzer GDx
monitoring of progressive glaucomatous damage.
The RNFL exhibits substantial linear birefringence with its slow
However, it is not yet proven that structural changes always precede axis parallel to the direction of nerve fibre bundles. This
functional damage. birefringence probably results from birefringence of closely spaced
cylindrical structures in the RNFL. This unique property of the
Preperimetric Glaucoma RNFL provides a basis for SLP (Scanning Laser Polarimetry) to
assess the RNFL thickness by measuring total retardation in the
The stage before functional loss detection is known as light reflected from the retina. Retardation is proportional to the
preperimetric glaucoma. Diverse techniques have been used to RNFL birefringence and the RNFL thickness.
distinguish normal eyes from glaucomatous eyes in preperimetric
stages. The current SLP system, GDX VCC (Carl Zeiss Meditec Inc.,
Dublin, CA,USA), is a confocal scanning laser ophthalmoscope
RNFL Photography integrated with a polarimeter. Images of the ocular fundus are
formed by scanning the beam of a near- infrared laser (780nm) in
RNFL defects are often difficult to identify using standard clinical a raster pattern. The field of view is 40 degree horizontally x 20
examination techniques. degree vertically at a density of 256x128 pixels, respectively. The
scanned area includes the peripapillary region around the ONH
RNFL photography is widely used as a qualitative detection method and macular region around the fovea.
owing to difficulties in measuring the thickness of the RNFL. Both
analog and digital photographs are usually done in black and white The GDX VCC produced a reflection image that was generated
by using a fundoscopic camera and a red –free filter. This method from light reflected back from the fundus of the eye. In addition,
has been validated and is widely used for detecting early changes it produced a retardation image that had been constructed from
in the RNFL loss. the 32,768 pixels (256x128) individual retardation value.

RNFL photography has been documented as having sensitivity Influence of the Cornea
and specificity averaging 80-94% for differentiation of
glaucomatous and non glaucomatous eyes. However, high –quality The GDx VCC is equipped with a variable corneal compensator.
photographs are often difficult to obtain and RNFL photography As the corneal stroma is composed of parallel collagen fibres, it
is only performed regularly at a few academic centers. In addition, has significant polarizing properties, which must be effectively
photographic methods are limited by the need for pupil dilation, compensated for valid SLP measurement of RNFL thickness.
clear media and qualitative review of the photograph at the patient’s Therefore, a fixed corneal compensation FCC with a fixed angle
next clinic visit. and magnitude as featured in older generations of the GDx (Carl
Zeiss Meditec inc., Dublin, CA, USA) has been shown not to be
Glaucoma Research Fellow completely successful. Anterior segment birefringence,
Rotterdam Eye Hospital Rotterdam, predominately the corneal birefringence, is a confounding factor
in SLP assessments of the RNFL.
Netherlands
In the GDx VCC, a variable corneal compensator (VCC) thus

www.dosonline.org 29

neutralizes the anterior segment birefringence. Anterior segment
birefringence is measured from the macular “bow tie” pattern
resulting from the linear anterior segment birefringence and the
radial birefringence of Henle’s fibre layer. With compensation by
VCC, the retardation image reveals both Henle’s fibre layer and
the RNFL.

The polarizing properties of the lens, which are considerably
smaller than those of cornea, are also compensated by VCC.

Although compensation of anterior segment birefringence in the
individual eye seems to be adequate with SLP-VCC in general, a
small amount of residual anterior segment birefringence can be
observed in some eyes which may lead to erroneous
measurements of the RNFL. As an alternative the existing VCC
method, a new software method, named enhanced corneal
compensation (ECC), was developed that requires no hardware
modification to the GDx VCC system and provides individualized
corneal compensation with enhanced SLP measurement sensitivity.
In myopic eyes, it is believed that the assessment of RNFL thickness
by SLP should be conducted with caution because of the incidence
of abnormal retardation pattern (ARP). In contrast to VCC, the
use of ECC dramatically reduced the presence of ARP.

Interpretation of GDx printout

The printout’s key areas are: 1) The Fundus image, 2) The RNFL Figure 1: Printout of a healthy subject. The TSNIT plots
thickness map, 3) The RNFL deviation map 4) The TSNIT graph and are within normal range. In addition, these plots are
5) The parameter table.
symmetrical for the two eyes. All parameters are within
Normal example normal limits. The NFI is below 35

The printout (Figure 1) shows a normal example. When
interpreting a scan, it is helpful to go through the five key areas of
interest sequentially.

Fundus image age and ancestry matched database. Each superpixel represents
the average of 16 individual pixels (4X4). Only superpixels whose
The first thing to consider in the interpretation of a scan is whether value is below the 5th percentile will be colour coded dark blue for
it is of high quality. Every image has a Q score representing the those below the 5th percentile, light blue below the 2nd percentile,
overall quality of the scan. The Q score ( displayed above the yellow below the 1st and red below the 0.5th. The deviation map
fundus image) ranges from 1-10, with values 8-10 representing makes it easy to see RNFL bundle defects and areas of abnormality.
acceptable quality.
TSNIT Plots
Thickness map
The TSNIT (temporal-superior-nasal-inferior-temporal) plots
The retardation /thickness map (panels below the fundus image) (bottom panel) reflect the peripapillary RNFL thickness along the
reflect the phase shift of the polarized laser light passing through measurement circle, which is approximately 3.2 mm in diameter
the RNFL, which is proportional to the thickness. Measurements in an emmetropic eye. The normal 95% range of the TSNIT plot is
are taken in a 20 degree X 20 degree field of view. The amount of shown as a shaded area. For comparison of the two eyes, their
phase shift has been converted to a thickness measure, and colour- TSNIT plots have been superimposed on the central bottom panel.
coded according to the scale shown on the printout. Bright, warm
colors (yellow, orange, red) represent thicker areas; dark, cool The parameter table
colours (black, blue) represent thinner areas. A healthy eye may
show a typical “hour-glass” distribution of warmer colours Parameters
superiorly and inferiorly and cooler colours nasally and temporally.
Loss of warmer colours corresponds to thinning of the RNFL. In Six parameters are printed in the central top panel. They are
healthy eyes, retardation is present adjacent to the thicker blood constructed from data along the measurement circle:
vessels superior and inferior to the ONH. There is a large
variability in the appearance of the RNFL in healthy eyes. 1. TSNIT Average: The average RNFL thickness around the entire
calculation circle.

Deviation map 2. Superior Average: The average RNFL thickness in the superior

The deviation maps (below the retardation maps) compare the 120 degree region of the calculation circle.

retardation value of “superpixels” with corresponding areas the 3. Inferior Average: The average RNFL thickness in the inferior

30 DOS Times - Vol. 15, No. 6, December 2009

• Abnormality in the retardation image can present itself as
generalized loss ( the double hump pattern shows a flat line),
or a defect of one bundle only. Poor modulation is also very
specific finding.

• In some cases, wedge defects can be seen.

• It is expected that an assessment of the entire printout will
improve the accuracy of GDx VCC for diagnosing glaucoma.

Figure 2: GDX Parameters Different studies show that the parameters analysed by the GDx
120 degree region of the calculation circle. VCC are useful for discriminating between normal and
glaucomatous subjects with slight to moderate Automated
Perimetry (AP) defects. Most of the parameters showed significant
differences between normal subjects or those with ocular
hypertension and glaucomatous subjects. NFI stands out among
all the parameters as that having the best diagnostic ability. In
different studies, RNFL parameters of the GDx VCC were
compared among four groups namely healthy controls, ocular
hypertensive eyes, Glaucoma suspects, and glaucomatous eyes.
Most parameters of GDx VCC exhibited differences between
glaucoma group and the rest of the groups. Some parameters

4. TSNIT Std. Dev.: This measure captures the modulation (peak
to trough difference) of the double-hump patern. A normal
eye will have high modulation in the double-hump RNFL
pattern, while a glaucomatous eye will typically have low
modulation in the double-hump pattern.

5. Inter-Eye Symmetry: Measures the degree of symmetry
between the right and left eyes by correlating the TSNIT
functions from the two eyes. Values range from -1 to 1, where
values near one represent good symmetry. Normal eyes have
good symmetry with values around 0.9.

6. NFI: (The Nerve Fiber Indicator) The NFI is a global measure
based on the entire RNFL thickness map. The output of the
NFI is a single value that ranges from 1-100 and indicates the
overall integrity of the RNFL. The NFI is not colour coded
based on probability like the other parameters, but rather it
is based on an absolute scale.

Diagnostic Ability of GDx VCC For glaucoma Diagnosis

The best parameter

The NFI is the best parameter for discriminating between
glaucoma and healthy eyes. Data suggest that glaucoma eyes rarely
have an NFI < 35, and healthy ones almost never have an NFI > 44.
For NFI values between 35 and 44, which are probably borderline.

Other data in the GDx VCC printout may be indicative of the Figure 3: Printout of a glaucoma patient whose right
diagnosis of glaucoma eye has lost retardation in the superior temporal and
inferior region. These regions have also been flagged in
• Prior to any interpretation, the image quality should be the deviation map. In addition, the TSNIT plot shows
assessed that the thickness of the RNFL is below the normal

• It is preferable to examine the print-outs systematically: first range in the same regions. Most parameters are
one should look for typical signs of normality and then for flagged at P< 0.5%. The NFI is 79. The left eye shows
typical signs of abnormality, before drawing a conclusion. a loss of retardation superiortemporal to the ONH. In
the inferotemporal region, a localized, wedge-shaped,
• One should know to recognize split bundle as being a common defect of the RNFL is visible as a flagged area in the
anatomical variation, with prevalence of approximately 8.0%. deviation map. There is asymmetry in the TSNIT plot

between the two eyes.

www.dosonline.org 31

Figure 4: Printout of a glaucoma patient were also different between healthy patients and glaucoma
RE:GHT Outside normal limits. MD -7.86 dB (P< suspects.

0.5%). PSD 14.24dB (P< 0.5%). NFI is a global indicator of the state of the RNFL and is based on
LE: GHT Outside normal limits. MD -0.69dB. PSD an advanced system of neural network analysis measuring the
complete RNFL profile and reached a number that represents its
1.94 dB (P< 10%). integrity.

It is plausible that by combining the parameters in discriminant
equations one may reach a higher diagnostic ability, as has been
shown (different studies) by evaluating different RNFL objective
evaluation systems. In the GDx NFA, by using the discriminant
equation (proposed by Weinreb), a greater diagnostic ability was
observed than with the <<number>> that the analyzer provides.
This << number>> is equivalent to the NFI of the GDx VCC laser
polarimeter. GDX VCC laser polarimeter has shown a good ability
to discriminate between healthy eyes and eyes with early or
moderate glaucomatous loss through different studies. It can be
concluded that the use of parameter combinations or other RNFL
analysis methods can support diagnosing glaucoma early on and
should therefore be studied.

References

1. Optic nerve Head and Retinal Nerve fibre analysis.. Editors: Michele
Lester. David Garway-Heath. Hans Lemij.

2. Nerve Fiber Analysis With Variable Corneal Compensation...
Professor Dr. H. G. Lemij, The Rotterdam Eye Hospital.

3. A Guide to the Clinical Interpretation of GDx VCC Measurements,
Cases: Nic J. Reus, MD and Hans G. Lemij, MD, PhD. The Rotterdam
Eye Hospital, Glaucoma Service.

Author
Tutul Chakravarti MBBS, DO, DNB

Guidelines for Presentation in
Annual DOS Conference

All presentations should be made in MS-Office 2007.
Any Fonts and Animations if used which are not a part of the standard MS Office XP pack should be included with
the Presentation CD and this should be specified to the Audio Visual in charge at the Preview Room well in
advance.
Videos when included should be ideally in avi or mpeg and if any other format is used its codec should be also be
included.
If any different format is used deviating from the above mentioned format the same should be informed well
before the conference so alternative arrangements can be made where ever possible.
The medium of storage used by the presenters can be CD, DVD, Flash Drive, USB HDD, PCI MCI card. Also any
deviation from this should be informed so that alternative arrangements can be made if possible.
All speakers should submit their presentations 3 hrs before their presentation in the Preview Room.
No personal Laptops are allowed for the presentation.
Speakers are requested to timely adhere to these guidelines.

32 DOS Times - Vol. 15, No. 6, December 2009

Collagen Cross: Linking with Riboflavin Cornea
(C3R for Treatment of Keratoconus)

Neera Agarwal MBBS, MS

Keratoconus is a bilateral non-inflammatory corneal ectasia Quality of Beam
(Figure 1) with an incidence of approximately 1 per 2,000 in
the general population. It normally presents in early teens or All safety considerations regarding the Cross-Linking procedure
twenties and is known to be progressive. Despite intensive clinical assume an optically homogenous irradiation of the cornea. Optical
and laboratory investigation, the aetiology of keratoconus remains in-homogeneities can lead to damage to corneal endothelium,
unclear. Thinning of the corneal stroma, breaks in Bowman’s layer, which represents most endangered structure. Thus, having
and deposition of iron in the basal layers of the corneal epithelium homogenizing optics and as well as pre-compensation for corneal
comprise a triad of the classical histopathologic features found in curvature in the system is important (Figure 5).
keratoconus.

Till date, accepted methods of treatment have been contact lenses,
intra-stromal corneal rings (INTACS), Photo-refractive
keratectomy and cornea transplant. Cornea transplant is reserved
for advanced cases in which vision can not be improved with contact
lenses. Unfortunately none of these modalities prevent the
progression of the disease. Now with the advent of Collagen Cross-
Linking with Riboflavin and UVA, there is scope to arrest the
progression of disease in these patients. Moreover, it is technically
simple and less invasive than all other surgical therapies proposed
for Keratoconus.

Mechanism of action

Similar to photo polymerization of polymers, Collagen Cross-
Linking of Cornea using ultraviolet light and the Photo-sensitizer
Riboflavin was developed to treat corneal thinning and ectasia by
increasing the biomechanical strength of the tissue. This procedure
is also addressed by various eponyms such as C3R, CXL and CCL.

First studies in Photobiology began in 1990’s, with attempts to
identify biological glues that could be activated by heat or light to
increase resistance of stromal collagen2. It was discovered that the
gluing effect was mediated by oxidative mechanism associated
with hydroxyl radical release. A similar mechanism of natural
hardening and thickening of collagen fibres has been demonstrated
in corneal aging3. Similarly, young diabetics never develop
progressive keratoconus due to natural cross linking effect of
glucose, which increases corneal resistance.

Collagen cross linking results in an increase in inter-fibrillar covalent
bonds by photosensitized oxidation (Figure 2), and causes bio-
mechanical stabilization of cornea. A significant increase of 328.9%
in the biomechanical rigidity of human corneas has been
documented after collagen cross linking4.

Riboflavin plays a dual role in the procedure; it not only acts as a
photo sensitizer for the photo-oxidative cross linking process but
also has a barrier effect. It acts like a shield and prevents UV
induced collateral damage to sensitive ocular structures like
Corneal Endothelium, Lens and Retina.

Figure 1: Natural Progression of Keratoconus
in a patient over 1.5 years

Neera Eye Centre & Laser Vision
Daryaganj, New Delhi

www.dosonline.org 37

Figure 2: Mechanism of action: C3R

Figure 3: Effect of Collagen Cross
Linking on Corneal Collagen

Indications Figure 4: Effect of Cross linking on Cornea

Most common indications are – equivalent power, Decentration component and Irregular
astimatism component and calculation their yearly rate of
1. Mild to moderate Keratoconus – In a case of Keratoconus, the progression. It is generally accepted that 1 dioptre increase in
selection criteria for C3R are as follows - the power of cone per year is an indicator of progression of
Keratoconus. It can also be seen as steepening of Keratometry
• There should not be corneal scarring. readings17

• There should be reasonably good acuity with glasses or contact DOS Times - Vol. 15, No. 6, December 2009
lenses.

• Corneal thickness should be more than 450 microns (400
microns after epithelium removal) at thinnest point. This is
based on the fact that UV light can penetrate cornea up to a
thickness of 350 microns and will damage endothelium if
enough corneal thickness is not there. That is why some people
advocate doing specular microscopy before and after the
procedure.

• Age should more than 16 yrs.

• Maximum K readings should be < 60Diopters.

• Keratoconus must be documented to be progressive.
Progression of Keratoconus is ideally determined by Kaplan
Meier or Fourier analysis which are based on Spherical

38

Figure 5: Quality of beam for C3R

Figure 7: Effect of Cross-linking on cornea

Figure 6: C3R being done in a patient Hydrochloride (0.5%) eye drops & Xylocaine 4% drops. Central 7-
8 mm of corneal epithelium is removed by mechanical debridement
2. Post Lasik Ectasia – Good results have been reported in (gentle scraping with hockey stick knife) or Alcohol. My personal
treatment of post Lasik ectasia 13. preference is mechanical debridement.
3. Progressive Hyperopia post RK – good results have been
reported12. This is followed by instillation of 0.1% Riboflavin (3 mg Riboflavin
4. Pellucid Marginal Degeneration - 5 Phosphate in 3 ml of Dextran-T-500 20% solution) eye drops at
5. Bullous Keratopathy – reduces Corneal oedema by increasing every 2 minute interval for 30 minutes (15 times).
stromal compaction after Cross-linking. It may be combined with
Intra-stromal administration of 0.1% Riboflavin with the help of To confirm adequate penetration of Riboflavin into the cornea,
Femtosecond laser (Can also be staged i.e. anterior and posterior the patient may be examined on slit lamp. A greenish flare, similar
separately)16. to that seen with fluorescein dye instillation, may be seen in anterior
6. Infective Keratitis – to prevent Corneal Perforation by chamber, signifying penetration through the thickness of cornea.
increasing resistance to the effect of collagen digesting enzymes.16
7. Scleral CXL for Glaucoma and Pathological Myopia16 There are studies available which say that epithelial debridement
Technique is not necessary. However, it’s mandatory to demonstrate the
The procedure is conducted in an operating room under sterile penetration of the riboflavin in the corneal stroma when
conditions. Topical anaesthesia is given by Proparacaine performing the treatment without removing the epithelium.

Following this, the cornea is subjected to Ultraviolet A radiation
(365nm) from a distance of 5 cm (Peschke Meditrade UVX system
was used) for the next 30 minutes (Figure 6). During this period,
topical Riboflavin drops are again instilled at 5 minute intervals, to
complete photo-sensitization and provide photo-protection by

www.dosonline.org 39

Results

• C3-R appears to stabilize corneas up to six months after
treatment.

• In a 5 year study, it was noted that in all treated eyes, the
progression of keratoconus was at least stopped. About 70%
eyes show regression with a reduction of the maximal
keratometry readings by 2 dioptres and of the refractive error
by 1 D was found14. Best-corrected visual acuity improved by
1.4 lines. I have personally experienced similar results in my 8
month experience with the procedure.

• The addition of C3-R to the INTACS procedure results in
greater keratoconus improvements compared to INTACS
alone10.

Figure 8: Absorption of UVA by Cornea • There are reports available that surface ablation procedures
could be used to correct refractive errors following C3R in
Keratoconus patients but conclusive evidence is lacking.

the ‘barrier’ effect. Thereby, a dose of 3 mW/ Sq cm (+ 0.3 Mw) Safety
(5.4 J/Sq cm) UV-A is delivered. The UV-A radiation lamp is
checked for calibration with a UV- meter before and after the During corneal Cross-Linking, 95% of UVA energy is absorbed by
treatment. On completion of the treatment, eye is patched with only 350 microns of Riboflavin soaked Cornea (Figure 8). As long
antibiotic eye ointment or sterile bandage lens is applied. as the treated cornea has a minimum thickness of 400 microns
(after removal of epithelium), the corneal endothelium will not
Post-operative Care experience damage, nor will deeper structures such as lens and
retina.
Topical antibiotics along with lubricants and viscous tear substitute,
mild steroids are prescribed 4-5 times a day for 3-4 weeks. Complete The light source should provide a homogenous irradiance,
re-epithelization usually occurs in 3-4 days. Patients may experience avoiding hot spots.
mild pain and discomfort for first 2 days, for which oral analgesics
are also required to keep them comfortable. It has been seen that corneal and lens transparency, endothelial
cell density, and intraocular pressure remained unchanged after
A mild epithelial haze with transient, mild stromal oedema may the procedure9.
be seen in some cases after C3R, which usually disappears
completely in a few weeks. There is no damage to the corneal Conclusion
endothelium.
Cornea Collagen Cross-linking with Riboflavin is a simple, safe
Histopathological changes in cornea post C3R and effective procedure in the management of early progressive
ecstatic disorders of the cornea.

C3R treatment leads to a dose-dependent keratocyte apoptosis1 References
that can be expected in human corneas to a depth of 300 microns
from the anterior surface utilising a surface UV-A dose of 5.4 J/ sq 1. Apoptosis After Corneal Collagen Cross-linking using Riboflavin/
cm. In the first few weeks after the procedure, a ‘vertical transition UVA treatment. Wollensak G. et al. Cornea 2004; 23: 43-49
line’ may be visible on the slit lamp, delineating the anterior cross-
linked zone with the posterior unaffected stroma (Figure 7). 2. Photodynamic biologic tissue glue. J. Khaderm, T. Truong, J.T. Ernest.
Cornea 1994;13: 406-410
Repopulation of corneal stroma may take up to 6 months. It is well
documented that the corneal epithelium attains a regular 3. Collagen fibrils in the Human corneal stroma . structure and aging.
morphology and density within 5 days after C3R. Initially, A. Dover, K. Misof et al. Invest. Ophthalmol. Vis. Sc. 1998; 39: 644-
disappearance of the sub-epithelial stromal nerve fibres was 648
observed in the treated area and initial re-innervation was seen
one month after the procedure. Complete recolonization of the 4. Stress-strain measurements of human and porcine corneas after
anterior sub-epithelial stroma by the keratocytes was observed in Riboflavin- ultraviolet-A induced cross-linking. Wollensak G.,Spoerl
6 months after C3R, with restoration of corneal sensitivity. E., Seiler T. J Cataract Refract Surg. 2003;29:1780-1785

Histopathologically, it has been demonstrated that there is a 5. Increased resistance of cross-linked cornea against enzymatic
significant increase in collagen fibre diameter after collagen cross digestion. Seiler T., Wollensak G., Spoerl E. Curr. Eye Res. 2004
linking. After Collagen Cross-Linking, the cornea shows an July; 29(1): 35-40.
increase in thermo-mechanical stability as well as a markedly
increased resistance to collagen digesting enzymes5. 6. Thermo-mechanical behaviour of collagen cross linked porcine
cornea. Spoerl E., Wollensak G., Dittert D.D., Seiler T.,
Ophthalmologica.2004, Mar-Apr; 218(2):136-140

7. C3-R Treatment Opens New Frontiers for Keratoconus and Corneal
Ectasia. Roberto Pinelli, MD. Eyeworld 2007, 34-36

40 DOS Times - Vol. 15, No. 6, December 2009

8. Safety of C3-R UVA at the Retinal Level and Compared to Outdoor 13. Visual rehabilitation and outcomes of ectasia after corneal refractive

UVA Exposure Leonard Yuen, MD and Brian S. Boxer Wachler, surgery. Woodward MA, Randleman JB, Russel B, Lynn MJ, Ward

MD MA, Stulting RD - J. cataract Ref. surg. 2008 mar; 34(3): 383-8

9. Safety of UVA-Riboflavin Cross-Linking of the Cornea Eberhard 14. Riboflavin/UVA induced collagen cross-linking for treatment of

Spoerl, PhD, Michael Mrochen, PhD, David Sliney PhD, Stephen Keratoconus. G. Wollensak, MD et al, Am. J. Ophthal. 2003 May;

Trokel, MD, Theo Seiler, MD, PhD, Cornea 2007; 26:385-389 135(2) : 620-627

10. The Effect of Inferior Segment Intacs with and without Corneal 15. Staged Intra-stromal Delivery of Riboflavin with UV-A Cross-
Collagen Crosslinking with Riboflavin (C3-R) on Keratoconus. Colin linking in Advanced Bullous Keratopathy. Krueger RR, Ramos-
C.K. Chan, MD, FRANZCO, Munish Sharma, MD, Brian S. Boxer Esteban JC, Kannelopoulos J – J. Refract. Surg. 2008; 730-736
Wachler MD, J Cataract Refract Surg 2007;33:75-80
16. Corneal Cross-linking for Different Corneal Diseases. Aylin Kilic
11. No Progression of Keratoconus 5 Years after C3-R. Wollensak G. Ertan – Cataract & Refractive Surgery Today Europe. April 2009;
Crosslinking treatment of progressive keratoconus: new hope. Curr 25-28
Opin Ophthalmol. 2006 Aug; 17:356-60.
17. Progression of Keratoconus Assessed by Fourier Analysis of
12. C3-R for Stabilization of Progressive Hyperopia (Farsightedness) Videokeratography Data. Tetsuro Oshika, Tatsuro Tanabe, Atsuo
after Radial Keratotomy and Laser Ablation. Presented at the Tomidokoro, Shiro Amano – Ophthalmology 2002; 109:339-342
American Academy of Ophthalmology Annual Meeting, 2006

Author
Neera Agarwal MBBS, MS

Attention DOS Members

DOS Executive nominated Dr. G. Mukherjee as Chairman of the
Election Commission for the next DOS election for

the post of the Vice President to be held on 18th April, 2010.
The members of the Commission are

Dr. Noshir M. Shroff and Dr. Sudhank Bharti

www.dosonline.org 41

Traumatic Optic Neuropathy Neuropathalmology

J.L.Goyal MD,DNB, Deepa Gupta MBBS, Ritu Arora MD,DNB

Traumatic optic neuropathy refers to an acute injury of the space. At the posterior foramen of the optic canal, the optic nerve
optic nerve secondary to trauma. Injury may be direct or sheath fuses with an overlying falciform fold of dura that lines the
indirect and visual loss may be partial or complete. Direct TON calvaria .Any blunt force applied in the frontotemporal area leading
result from an anatomical disruption of nerve fibers by penetrating to elastic deformation of sphenoid can transmit forces directly to
orbital trauma, bony fragments within the canal and nerve sheath the optic nerve resulting in localized contusion or even laceration,
hematoma .In contrast, indirect injury results from transmission in severe cases, of optic nerve. Contusion of axons and pial
of forces to the nerve. vasculature produces localized nerve ischemia and edema leading
to further neural compression with in fixed bony canal setting a
Incidence positive feedback loop resulting in further damage. Also,
reperfusion injury has been cited as a mechanism in which
In setting of closed traumatic head injury, its incidence varies reperfusion of axons leads to production of free radicals
between 0.5-5%1,2. vast majority seen in males (85%) mean age contributing to the damage by causing neuronal cell loss.
being 34yrs. Motor vehicles and bicycle accidents account for the
majority of causes followed by falls and assaults. TON has also Intracranial
been associated with penetrating trauma (stab wounds, gunshot
wounds, foreign bodies) and recreational sports (e.g. paintball This is the next most common site usually lead to characteristic
injury). VF changes especially in chiasmal region. Vision loss may vary.

Etiopathogenesis- Nerve course is anatomically divided into 4 parts Presentation
– intraocular (about 1mm), intraorbital (20-30mm), intracanalicular
(5-11mm) and intracranial (3-16mm). Hence, trauma can lead to Comprehensive care of head injury patients requires trauma
various clinicopathological consequences according to the site. physician, head and neck surgeon, ophthalmologists and
neurosurgeons. Association of such trauma with loss of
Intraocular consciousness warrants ophthalmic assessment at earliest
opportunity.
Violent rotations of globe produces avulsion of optic nerve leading
to a picture of partial ring of hemorrhage at optic nerve head. This Visual Acuity – Varies mainly between 20/200 to no light
may b self inflicted known as oedipism OR autoeneucleation. perception. More recent reports suggests even milder vision loss
in TON. Role of refraction can’t be underestimated in this scenario.
Intraorbital
Pupils- In case of unilateral involvement, RAPD can be quantitated
Trauma in this region is mainly coz of inraorbital hemorrhage or using photographic neutral density filters. These are calibrated in
emphysema causing either ischemia or elevated intraorbital log units that measure the reduction in transmitted light. APD
pressure compromising the circulation of optic nerve known as >2.1 log units indicates poor prognosis4.
orbital compartmental syndrome. Hemorrhage may occur directly,
surgically induced, post thrombolytic therapy, injection of local Fundus- Disc pallor may not be present initially n takes about 3-4
anesthetics or even following retrobulbar block (0.4-3%)3. Optic weeks to develop. Fundus may vary according to the site of insult
nerve in intraorbital compartment runs a sinuous course which in relation to the origin of central retinal vessels. Posterior injuries
can withstand stretching of upto 9mm. hence , indirect injuries are may lead to disc edema due to hhgs in nerve sheath whereas
commoner whilst direct injuries are rare here. anterior injuries lead to venous obstruction and traumatic AION.
Findings like commotion retinae and choroidal rupture may also
Intrcanalicular be present.

It is the most common site of trauma characteristically associated Other than these, palpation of orbital rim may reveal fracture,
with high momentum decelerating injuries especially in periorbital swellings; other anterior segment evidences of
frontotemporal region. Mid facial trauma have also been observed penetrating injuries must be sought.
to result in similar picture. Studies using laser interferometry
suggests that forces applied to frontal bone are transferred and Investigations
concentrated in optic canal. Throughout its intraorbital course,
the optic nerve remains surrounded by pia, arachnoid, and dura Neuroimaging studies (CT scanning or MRI) are an important
mater, which move along with the optic nerve during normal eye part of the assessment when TON is suspected. In the post-trauma
movements. Within the optic canal, the sheath of the optic nerve setting, CT scanning is the preferred modality for demonstrating
is fused to the sphenoid periosteum, and, as a result, the nerve the presence of an optic canal fracture, a displaced bony fragment
and its sheath are tightly fixed to the bony canal within this confined impinging upon the optic nerve, a metallic foreign body in the
orbit, orbital emphysema, or an optic nerve sheath hematoma. A
Guru Nanak Eye Centre brain and orbit MRI may be useful in certain settings to delineate
Maulana Azad Medical College, New Delhi the extent of hemorrhage involving the neurovascular structures
at the orbital apex or to rule out inflammatory or infiltrative causes
for an optic neuropathy.

www.dosonline.org 45

Others - The findings of the NASCIS trials significantly influenced clinical
practice and led to an increased use of steroids in treating
Visual field perimetry TON. However, the clinical improvement was modest in these
studies, and concern existed that the clinical benefit demonstrated
Automated perimetry can be obtained only in patients who retain for those patients treated in the first eight hours with mega dose
adequate vision/acuity. Patients with poor visual acuity (worse steroids was the result of a statistical bias.
than 20/200) may be assessed with Goldmann perimetry or with
confrontational visual field testing. In 2005, the results of the Corticosteroid Randomization After
Significant Head Injury (CRASH)8trial raised concerns regarding
No visual field loss pattern is pathognomonic for traumatic optic the use of mega dose steroids (same dose as given in the NASCIS
neuropathy (TON), although a dense central scotoma is 2 study) in traumatic brain injury. This study was the largest
characteristic. Recovery of optic nerve function may be documented randomized study that evaluated steroids in patients with traumatic
via serial visual field testing. brain injury and was stopped early due to the significantly increased
risk of death in patients that received mega dose steroids at their
Visual evoked potential (VEP) 6-month follow-up when compared with the placebo group.

VEP can be helpful to document the presence of TON in Furthermore, concerns have been raised regarding the
unresponsive patients or in cases with concomitant ocular injuries. extrapolation of data from spinal cord injury studies to TON.
Patients can also be followed with serial VEP examinations to There are important histologic distinctions between the spinal
document recovery of function when clinical parameters are cord and optic nerve; for example, the optic nerve is a pure white
equivocal. However, in settings of polytrauma it may not be matter tract and the spinal cord is a mixed gray and white matter
possible at all to shift the patient to electrophysiological lab. tract. As a result, significant biologic differences may exist between
the repair mechanisms of the optic nerve axons and insults to the
In unilateral cases of TON, a flash VEP amplitude ratio (affected spinal cord.
side/normal side) greater than 0.5 appears predictive of a favorable,
long-term visual outcome. Visual recovery is considered unlikely The International Optic Nerve Trauma Study (IONTS)9 was a
when VEP amplitudes are nonrecordable.5 Retinal nerve fiber nonrandomized intervention trial that compared visual outcomes
layer (NFL) imaging: Scanning laser polarimetry and optical for patients with TON treated with observation, systemic steroids,
coherence tomography can be used to assess and monitor retinal or optic canal decompression. Published in 1999, the study included
NFL axonal loss during the period of follow-up. 133 patients who were evaluated and treated within 7 days of the
traumatic event, with most of the patients being treated with either
Newer modalities like multifocal VEP can also be used as a corticosteroids (n=85) or surgical decompression of the optic canal
prognostic indicator. (n=33). Follow-up results showed that visual acuity increased by
more than 3 lines in 32% of the surgery group, 52% of the
Management corticosteroid group, and 57% of the observation group. However,
the study was nonrandomized and uncontrolled, and the small
Medical Therapy numbers of patients in the observation group (n=9) limited the
strength of the study’s statistical power.
The main treatment options for traumatic optic neuropathy (TON)
include systemic corticosteroids and surgical optic nerve Recent animal studies have also NOT demonstrated any beneficial
decompression, either alone or in combination. Review and analysis effect for steroid therapy in animals with TON, and one study; in
of the literature are complicated by the variety of therapeutic particular, found that steroids exacerbated axonal loss as evidenced
approaches and a lack of randomized, controlled studies on the by a dose-dependent decline in axonal counts with increasing doses
use of these modalities for TON. Steroid therapy for TON can be of steroids. Such findings may suggest that steroids can exert a
categorized as follows: moderate dose (60-100mg of oral negative effect on ganglion cell survival, especially at higher, mega
prednisolone), high dose (1 gram of intravenous dose levels, due to their suppression of endogenous
methylprednisolone/day), or mega dose (30 mg/kg loading dose neuroprotective pathways.10
of intravenous methylprednisone, followed by 5.4 mg/kg/h for 24
hours).6 Steroids have been used in TON since the early 1980s Surgical therapy
because of their perceived benefits in various animal models of
central nervous system injury. Steroids were thought to provide The rationale for surgical therapy in indirect TON is to decompress
neuroprotection in traumatic central nervous system injury the optic nerve at the site of injury, which is often the intracanalicular
through their antioxidant properties and inhibition of free radical- segment. Surgical decompression is thought to help reduce optic
induced lipid peroxidation. nerve compression and subsequent vascular compromise that
may occur as a result of the indirect injury. Additionally, surgery
In 1990, Bracken and colleagues published their findings on the has been postulated to remove bone fragments that may be
use of mega dose corticosteroid therapy in the National Acute impinging on the optic nerve within the optic canal.
Spinal Cord Injury Study 2 (NASCIS 2)7. The NASCIS 2 was a
multicenter clinical trial that evaluated patients with acute spinal However, no randomized, controlled studies have been performed
cord injury treated with placebo, methylprednisolone, or naloxone. to evaluate the role of surgery in TON. As mentioned previously,
The study showed that methylprednisolone (30 mg/kg loading one of the largest series is from the IONTS, which did not provide
dose, followed by 5.4 mg/kg/h for 24 hours) started within 8 hours any convincing evidence that surgical decompression of the optic
of injury was associated with a significant improvement in both canal in TON is superior to observation or corticosteroid therapy.
motor and sensory function compared with patients treated with
a placebo.

46 DOS Times - Vol. 15, No. 6, December 2009

Additionally, in cases in which bony fragments are impinging on 3. Ruben S. The incidence of complications with retrobulbar injection of
the optic nerve within the canal, the prognosis of visual recovery is anaesthetic for ophthalmic surgery. Acta Ophthalmologica
extremely poor because the bony fragments are more likely to 1992;70:836—838.
have anatomically disrupted the optic nerve axons, leading to
irreversible visual loss. 4. Alford MA, Nerad JA, Carter KD. Predictive value of the initial quantified
relative afferent pupillary defect in 19 consecutive patients with traumat
The variety of surgical approaches used in optic nerve optic neuropathy. Ophthal Plast Reconstr Surg 2001;17:323—327.
decompression include intracranial, extra cranial, orbital,
transethmoidal, endonasal, and sublabial approaches, and the 5. Holmes MD, Sires BS. Flash visual evoked potentials predict visual
selection of the technique tends to be based on the surgeon’s outcome in traumatic optic neuropathy. Ophthal Plast Reconstr
training, background, and experience.17,20 Patients with profound Surg. Sep 2004;20(5):342-6.
vision loss and a visualized bone fragment impinging on a segment
of the intracanalicular optic nerve on neuroimaging have been 6. Yu-Wai-Man P, Griffiths PG. Steroids for traumatic optic
considered to be the best candidates for surgical intervention. neuropathy. Cochrane Database Syst Rev. Oct 17 2007;CD006032
Although anecdotal reports of impressive visual recovery exist for
such patients, most cases with direct injuries to the optic nerve do 7. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled
not improve as the injury to nerve axons becomes irreversible trial of methylprednisolone or naloxone in the treatment of acute spinal-
and the risk of possible surgical complications such as cerebrospinal cord injury. Results of the Second National Acute Spinal Cord Injury
fluid leak or postoperative bleeding cannot be ignored. Cadaveric Study. N Engl J Med. May 17 1990;322(20):1405-11
studies have shown that transphenoidal medial wall decompression
of optic nerve canal with dural sheath opening may induce physical 8. Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a
damage to nerve. randomised placebo-controlled trial of intravenous corticosteroid in
adults with head injury-outcomes at 6 months. Lancet. Jun 4-
Conclusion 10 2005;365(9475):1957-9.

Based on the current evidence, a therapeutic role for corticosteroids 9. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic
in the management of TON is unsubstantiated. If steroids are neuropathy: the International Optic Nerve Trauma
considered for TON, they should not be used in cases with Study. Ophthalmology. Jul 1999;106(7):1268-77.
concomitant traumatic brain injury or in patients that present 8
hours or more after initial injury. Whether clinicians should use 10. Steinsapir KD. Treatment of traumatic optic neuropathy with high-dose
mega dose rather than lower doses of steroids for selected cases corticosteroid. J Neuroophthalmol. Mar 2006;26(1):65-7.
of TON is also not clearly defined by the literature.
11. Steinsapir KD, Goldberg RA, Sinha S, et al. Methylprednisolone
Also, at this time, conclusive evidence that surgical decompression exacerbates axonal loss following optic nerve trauma in rats. Restor Neurol
has a beneficial role for most patients with TON does not exist. Neurosci. 2000;17(4):157-163. .
Because a significant rate of spontaneous recovery is found in
cases of TON, a randomized controlled trial comparing observation 12. Steinsapir KD, Seiff SR, Goldberg RA. Traumatic optic neuropathy: where
with optic canal decompression is the only reliable way to evaluate do we stand?. Ophthal Plast Reconstr Surg. May 2002; 18(3):232-4.
the therapeutic benefit for surgical intervention. The decision to
perform surgical decompression of the optic canal should be made 13. Cook MW, Levin LA, Joseph MP, et al. Traumatic optic neuropathy. A
on a case-by-case basis, with the patient being informed that, to meta-analysis. Arch Otolaryngol Head Neck Surg. Apr 1996; 122(4):389-
date, surgery has not been shown to improve the prognosis over 92.
observation alone.
14. Wang BH, Robertson BC, Girotto JA, et al. Traumatic optic neuropathy:
Hence, to conclude, the treatment of traumatic optic neuropathy a review of 61 patients. Plast Reconstr Surg. Jun 2001; 107(7):1655-64.
is more of a trail based and more data is required for any modality
to have proven benefit over observation alone. 15. Bracken MB, Shepard MJ, Holford TR, et al. Administration of
methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours
References in the treatment of acute spinal cord injury. Results of the Third National
Acute Spinal Cord Injury Randomized Controlled Trial. National Acute
1. Turner JWA. Indirect injury of the optic nerves. Brain 1943;66:140—151. Spinal Cord Injury Study. JAMA. May 28 1997; 277(20):1597-604.

2. Russell WR. Injury to cranial nerves including the optic nerves and 16. Carta A, Ferrigno L, Salvo M, et al. Visual prognosis after indirect traumatic
chiasma. In Brock S, ed. Injuries of the Skull, Brain and Spinal Cord. optic neuropathy. J Neurol Neurosurg Psychiatry. Feb 2003;74(2):246-8
London, Bailliere, 1940:113—122
17. Girard BC, Bouzas EA, Lamas G, et al. Visual improvement after
transethmoid-sphenoid decompression in optic nerve injuries. J Clin
Neuroophthalmol. Sep 1992;12(3):142-8Goldberg RA, Steinsapir KD.

18. Extracranial optic canal decompression: indications and
technique. Ophthal Plast Reconstr Surg. Sep 1996;12(3):163-70.

19. Goldenberg-Cohen N, Miller NR, Repka MX. Traumatic optic neuropathy
in children and adolescents. J AAPOS. Feb 2004; 8(1):20-7.

20. Kountakis SE, Maillard AA, El-Harazi SM, et al. Endoscopic optic nerve
decompression for traumatic blindness. Otolaryngol Head Neck
Surg. Jul 2000;123 (1 Pt 1): 34-7.

21. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic
neuropathy: the International Optic Nerve Trauma Study. Ophthalmology’.

First Author
J.L. Goyal MD, DNB

www.dosonline.org 47

Vascular Lesions of the Orbit Oculoplasty

Gaurav Bharti DOMS, Taru Dewan MS, FRCSEd, Akhila Prasad MD, Shashi Vashisht MS

Vascular lesions of the orbit are relatively uncommon, usually different lesions. Doppler, CT scan and MRI are thus the important
benign lesions in the orbit producing proptosis and more diagnostic tools for diagnosis and categorization of these lesions.
rarely visual disturbances in all age groups. As knowledge increased Although ultrasound echography, CT, MRI and angiography have
their pathogenesis and morphology has become clearer and so greatly changed the diagnostic work up of orbital lesions, diagnosis
the classifications. Traditionally vascular lesions are classified on is still made with errors in certain cases. And most cases demand
the basis of their growth pattern, clinical features and histologic a thorough knowledge of the clinical behavior, radiological
composition. Because of their uncommon presentations and appearance and histological features to come to the confirmatory
rareity such lesions still present a diagnostic dilemma. Mulliken diagnosis.
and Glowacki classified these lesions on basis of their natural
history, including their growth pattern and histologic composition Capillary Hemangioma
in the following groups
Capillary hemangiomas are the most common benign lesion of
• Capillary hemangiomas the orbit. These are usually unilateral, nonencapsulated, poorly
circumscribed, often lobulated, and largely extraconal lesions these
• Venous vascular malformations (cavernous malformations are present during birth or present at two-three months of infancy.
and orbital varices) They are more common in females and premature infants and
tend to involute gradually after a short growth phase. The tumor
• Venous lymphatic malformations (capillary, cavernous, and is marked by two phases, a proliferative phase which lasts for 8-18
cystic lymphatic malformations) months and is marked by rapid tumor growth and an involutional
phase which comes at an age of 5 years marked by tumour
• Arterial and arteriovenous lesions (arteriovenous regression. Due to their rapid growth during childhood these lesions
malformations, arteriovenous fistulas and ophthalmic artery can be differentiated from lymphangiomas and AV malformations
aneurysms) which may present at the same time but grow slowly.

• Neoplasms (hemangioblastomas, hemangiopericytomas, The benign tumor presents as proptosis which increases on crying,
choroidal hemangiomas, choroidal melanomas and vascular and with periocular cutaneous involvement or telltale sign of same.
metastases) Proptosis in general is mild, but can be severe enough to cause
corneal exposure. The tumor is mostly extraconal but intraconal
• Miscellaneous (Coats disease). extensions are also found in some cases especially through the
optic canal and the superior orbital fissures. The tumor may spread
Hemodynamics is an important factor which affects the across various tissue planes and can involve the lacrimal gland and
presentation and the treatment modality of a vascular growth. the extraocular muscles. Although benign in nature, hemangiomas
The clinical properties of orbital vascular malformations are in certain locations can impede vital functions, causing problems
determined by their relations with a major vessel type (arterial, such as airway obstruction (laryngeal hemangiomas), high-output
venous or lymphatic). The same is true of shunts and new growths. cardiac failure (large hepatic hemangiomas), and visual impairment
For Example, An AV malformation getting a supply from the (periocular hemangiomas). The Kasabach-Merritt syndrome
artery drains directly into SOV or IOV which further drain into presents with a consumption coagulopathy and thrombocytopenia
cavernous sinus. This lesion, lacking intervening capillaries act as a secondary to platelet sequestration in large visceral hemangiomas
high-flow shunt and present as rapid proptosis with pulsations,
turbulence, progressive arterializations and potential thrombosis. Hemangiomas are classified using the Ceisler classification system
as follows:
Vascular lesions of orbit typically present as gradual onset proptosis
at birth or at early adulthood. A history of trauma may be a • Type 1: small, flat periocular hemangioma with no ptosis.
precipitating factor in AV-shunts and orbital varices. These lesions
usually increase on valsalva or lifting heavy weights. Forced • Type 2: small, localized, raised, superficial periocular
expiration against resistance (valsalva) raises venous pressure in hemangioma
the neck, face and head, such that orbital masses with significant
draining veins will increase in volume, evidenced by transient • Type 3: diffuse, bulky periocular hemangioma
increase in proptosis. This phenomenon is typically demonstrable
in the presence of congenital venous varices or AV malformations, • Type 4: diffuse, nonbulky periorbital hemangioma
but may also be seen with acquired carotid-cavernous fistula or
with primary or secondary bony defects which transmit intracranial • Type 5: deep bluish lesion with no superficial component
pressure to the orbital contents. Such effect may be seen in infants
during crying or on head hanging. Histology forms the hallmark Along with the clinical features various forms of diagnostic tests
for the final diagnosis of a vascular lesion but certain characteristics are of most value for diagnosis of hemangiomas. On CT they are
seen on radiological studies and Doppler are also typical for non encapsulated, usually lobulated, heterogenous but shows
immense enhancement on contrast injection. They may also
Department of Ophthalmology demonstrate phlebolith formation and can have both intraconal
Dr. Ram Manohar Lohia Hospital, New Delhi and extraconal extensions (Figure 1). On MRI they are usually
hypointense on T1-weighted images and iso- to hyperintense on
T2-weighted images (Figure 2). They enhance intensely on contrast

www.dosonline.org 49

Figure 1: CT scan of a Figure 2: MRI (T2 image) of a Capillary
capillary hemangioma hemangioma showing a hyperintense image
showing phleboliths and intracranial
extension of the lesion

injection and show both intralesional and perilesional flow voids. Figure 3: Doppler exhibiting both venous
Doppler shows both venous and arterial component with a high and capillary flow in a case of orbital
velocity flow (Figure 3). Pathological findings include capillary haemangioma

The morbidities associated with capillary hemangiomas is the effect on the surrounding structures can lead to symptoms like
threat of compressive optic neuropathy, extraocular muscle decreased vision, diplopia, extraocular muscles or pupillary
dysfunction, amblopia and cosmetic disfigurement. The first-line disturbances. Zauberman and Feinsod described a pregnancy-
treatment of capillary hemangiomas is simple observation. Since induced increase in symptomatology of these lesions. Most
most of these lesions regress on their own, there is no need to cavernous angiomas are found between the optic nerve and
intervene unless one of the above criteria is met. Corticosteroids, extraocular muscles within the intraconal space. Biopsy of these
in various formulations, also have been used in the treatment of lesions may lead to uncontrollable haemorrhage and is not
capillary hemangiomas. Radiotherapy and corticosteroids are both recommended. Clinical presentation and radiological evidences
effective in individual cases, but many lesions are resistant to all are the hallmark for the diagnosis of cavernous hemangioma,
forms of present treatment. Interferon alfa-2a has emerged as a confirmed by histology of the excised specimen.
new modality to combat the life-threatening and vision-
threatening hemangiomas of infancy that are resistant to steroid CT scan detects an oval or round shaped, sharply marginated,
treatment. Laser therapy has been attempted but is still homogenous lesion. They occasionally contain microcalcifications
controversial. Incisional surgical techniques also have had variable
success. Surgical ligation of the hemangiomas produces equivocal
results. Vascular embolization of the lesions should be used for
large extraorbital hemangiomas only. Primary excision also has
been advocated for infantile hemangiomas. Early surgical
intervention can be considered as a primary treatment option in
selected, isolated capillary hemangiomas without a significant
cutaneous component.

Cavernous Haemangioma

Cavernous hemangiomas are most common benign orbital tumors
found in adults, most commonly in females aged 18-72. They are
well-encapsulated tumors found in the intraconal space and
composed of very large vascular channels. The vessel walls contain
smooth muscles and there is fibrous tissue in the trabeculae that
separates the vessels. Cavernous hemangiomas produce a slow
painless progressive proptosis which is usually axial .The mass

50 DOS Times - Vol. 15, No. 6, December 2009

Figure 4: Axial T1-weighted MR image shows a Figure 5: Cavernous haemangioma ,
well-circumscribed, hypointense intraconal T1-weighted fat-suppressed MR image, post
cavernous hemangioma lesion contrast shows inhomogenous enhancement

(phleboliths) and may produce expansion of the orbital walls to a change in hemodynamics of the orbit induced by extraorbital
Ultrasound study can find a uniform high-echogenicity on A-scan. lesions, such as carotid-cavernous fistula, dural fistula, brain
These reflections are secondary to the septae found within the arteriovenous malformation, or intracranial dural sinus occlusion.
lesion. Doppler flow study may reveal subdued blood flow within A true varix is in direct communication with the vein and shows a
the angioma. T1-weighted MR image demonstrates an intraconal, pulsating proptosis on valsalva or on crying, and the patient may
lobulated, regularly marginated lesion with hypointense signal experience extreme pain during such episodes. The patient may
and small serpentine flow voids (Figure 4). T2-weighted fat- be enophthalmic at rest because of the enlarged orbits and fat
suppressed image shows the same lesion with slight signal atrophy. An anteriorly located lesion may lead to lid edema and
hyperintensity, characteristic fine internal septa, and flow voids. marked restriction of ocular motility.
Contrast-enhanced T1-weighted fat-suppressed image
demonstrates homogeneous intense enhancement of the lesion Proptosis with resulting enlargement of mass can be demonstrated
and provides improved delineation of the flow voids (Figure 5). during imaging procedures. On ultrasound the finding of an
Fine needle aspiration of these lesions reveales only the blood intermittently anechoic retrobulbar lesion that exhibits intrinsic
harbored in the large cavernous spaces. Histology shows engorged flow during the Valsalva maneuver is indicative of a varix, and
vascular channels, which are tightly knit and separated by fibrous color Doppler imaging may demonstrate a reversal of flow toward
septae and a dense fibrous pseudocapsule. Axial proptosis, the transducer during the Valsalva maneuver. Plain orbital x-ray
extraocular muscle dysfunction, and compressive optic neuropathy and CT shows enlarged orbital walls and small, round areas of
are the sequelae that can occur due to enlarging cavernous calcifications as result of recurrent thrombosis. A mass of veins or
hemangiomas. a massively enlarged vein may be seen on venography. MR imaging,
varices have hypo- to hyperintense signal on T1-weighted images,
The lesions are usually managed conservatively, and surgical have hyperintense signal on T2-weighted MR images, and usually
excision is reserved for those compressing on the optic nerve, enhance intensely after the administration of contrast material.
cosmesis or those causing ocular symptoms like diplopia.
There are only two indications for intervention in an orbital varix.
Orbital Varix Extreme orbital pressure with functional deficit or intractable pain,
and cosmetic disfigurement. A varix rarely leads to visual loss or
Varices are the most common cause of spontaneous orbital extreme pain unless there is spontaneous intraorbital hemorrhage
hemorrhage. Orbital varix is an intraorbital mass composed of or unexpected thrombosis. Methods of treatment of orbital varix
abnormally large veins. A varix like anywhere else can either be a include surgical excision, electrothrombosis, injection of sclerosing
single vessel with saccular dilatations or can be multiple vessels agents, and venous embolization with microcoils. Most primary
tangled together. Varices have been differentiated by Lloyd into orbital varices do not require aggressive treatment. In cases of
primary and secondary. A primary varix is usually present since acute thrombosis or hemorrhage, surgery may be required to
birth or may manifest by the early part of the second decade. remove a hematoma or clotted vessel. For patients with severe
Secondary or acquired varices are secondary to a trauma or related intermittent exophthalmos and cosmetic disfigurement, treatment

www.dosonline.org 51

by embolization after surgical exposure is a safe and relatively Figure 6: AV Malformation MRI ( T1)
easy procedure, particularly if the orbital varix is consistent with
saccular or segmental venous dilatations. treatment. A through evaluation by use of contrast angiography is
though required before planning any procedure. Other treatment
Arteriovenous Communications modalities include embolization, electrothrombosis of the fistula,
and direct surgery.
In arteriovenous (AV) communications, blood flows from arterial
circulation directly into the venous circulation without passage Dural shunts represent arteriovenous shunts from a dural artery
through intervening capillaries. AV malformations can occur as a to either one of the major sinuses or into variceal cortical veins.
congenital disorder or occur spontaneously after trauma. They Patients usually present between the ages of 20 and 79 years. Post
may present as orbital swelling and chemosis, increased episcleral menopausal women are most commonly affected. Spontaneous
and intraocular pressure, and pulsatile exophthalmos (High-flow dural shunts can occur in the elderly patients and have been
states). A low-flow state displays similar signs and symptoms but reported in patients with Ehlers-Danlos syndrome, osteogenesis
to a lesser degree. AV communications are classified into either imperfecta, and pseudoxanthoma elasticum. Etiologic factors
AV malformations, Carotid-cavernous sinus fistulas (CCF) or dural include trauma, surgery, infection, and sinus thrombosis. The
shunts. clinical presentations of dural shunts depend on the location of
the shunt and include tinnitus, cranial nerve palsies, and/or signs
Congenital arteriovenous malformations (AVM) are developmental related to venous congestion in the orbit. CT scan alone is usually
anomalies that occur when the embryonic vascular network fails not useful in demonstrating the dural shunt. Superselective
to differentiate. AV malformation gets a direct inflow from a angiography of both the internal and external carotid can help to
dedicated vessel of an arterial system and out flow through a determine the exact location and haemodynamic features. USG
normal vein downstream. In case of orbit the down flow channel and CT reveals enlargement of SOV and extra ocular muscles in
is either the SOV or IOV which drain into the cavernous sinus. the involved orbit. Surgical intervention is indicated in patients
The elevated pressure in the venous pathways draining the orbit with progressive proptosis, intractable glaucoma and debilitating
produces orbital venous congestion. The congestion is reflected diplopia in primary gaze. External carotid artery feeder vessels are
by dilation of the veins on the surface of the sclera, producing embolized with detachable balloons, isobutylcyanoacrylate, or
chemosis. Congestion and pulsatile proptosis is also apparent on polyvinyl alcohol particles. Embolization of ICA is not
increased pressure states produced during valsalva, lifting heavy recommended because of high success rate embolization of EC
weights and bending forward. A bruit is produced by the feeders and the borderline patency of circle of willis in elderly.
arterialized turbulent flow entering the veins. Over time the thin Other techniques include electrothrombosis of fistula and direct
wall of the AVMs veins rupture causing spontaneous bleeding surgery. Hemodynamically active vascular lesions of the orbit are
within the brain. The pulsation and bruit can usually be diminished often clinically challenging to treat, both because of the complexity
by compression of the ipsilateral common carotid artery. US, CT of the vascular anatomy and the delicacy of the cardinal structures
with standard and angiographic protocols, and MR imaging that are involved and vulnerable to damage.
(Figure 6) with standard and angiographic protocols can help
diagnose arteriovenous fistulas; however, conventional catheter- Hemangipericytoma
based angiography typically is required for precise definition and
treatment planning. On histology mature arteries and veins are Hemangiopericytoma is a highly vascular tumor that is relatively
seen in the tumour. Intraorbital AVMs are exceptions to common in the musculoskeletal system (lower extremities), pelvis,
endovascular treatment because embolization of the central retinal
artery, a distal branch of the ophthalmic artery, can complicate the
procedure and devastate a patient’s vision. The small caliber and
tortuous course of the ophthalmic artery make selective
catheterization difficult. Embolization is possible only in a few
extraorbital AVMs. Surgery plays an important role in such lesions.

Carotid-cavernous fistulas are direct communications between
internal carotid and cavernous sinus. It may occur spontaneously
or follows ocular or head trauma. Majority occurring after basal
skull fractures or penetrating orbital injuries affecting the medial
or inferomedial orbital wall as well as superior orbital fissure, or
occur after carotid artery surgery or aneurysmal rupture.
Spontaneous carotid cavernous fistulas have been reported in
patients with Ehlers-Danlos syndrome, osteogenesis imperfecta,
and pseudoxanthoma elasticum. The fistulas often manifest with
the classic triad of pulsatile exophthalmos, conjunctival chemosis,
and an auscultatory bruit. The fistulas occur in middle to late
adulthood and are more common in women. The patient presents
with chemosis, orbital swelling, episcleral venous congestion,
elevated intraocular pressure and retinal hemorrhages and
ischemia. Third and sixth nerve palsy may be associated. Surgery
is indicated in cases where vision is threatened. Balloon
catheterization through an endoarterial route forms the optimal

52 DOS Times - Vol. 15, No. 6, December 2009

and retroperitoneum. Approximately 15% of these tumors arise hemangioblastomas, and the term retinal angioma is therefore a
in the extracranial part of the head and neck. Origin within the misnomer. Hemangioblastomas represent 1%–2% of all primary
orbit is rare. The tumors may occur at any time, from infancy tumors of the central nervous system. Seventy percent of patients
through late adult life. Overall, hemangiopericytomas demonstrate who present with a hemangioblastoma do not have a family
no predilection for either sex. Hemangiopericytomas most often history of von Hippel-Lindau disease. However, patients with a
manifest with slowly progressive, sometimes painful proptosis sporadic nonhereditary hemangioblastoma should undergo
and decreased visual acuity, extraocular motility abnormalities, further evaluation for evidence of von Hippel- Lindau disease.
visual field deficits, and congestion of the retinal and choroidal Ocular abnormalities due to a retinal hemangioblastoma are the
vessels. They can be both benign and malignant or have features earliest manifestations of von Hippel-Lindau disease in about 50%
of both and are capable of metastasizing to distant organs like of cases. The hemangioblastoma typically appears as a dilated
lungs, bone and liver. The typical location is extraconal; lesions artery leading from the optic disc to a peripheral (most often
commonly arise in the adjacent paranasal sinuses. On Ultra temporal) tumor with an engorged draining vein that leads back
sonography, hemangiopericytomas are moderately hyperechoic, to the optic disc. Less commonly, the lesion is near or on the optic
with high vascularity on color Doppler images, a feature that disc. Patients with a retinal hemangioblastoma are usually
permits their differentiation from cavernous hemangiomas. At asymptomatic until the 3rd decade of life, although the
CT, they are typically homogeneous and lobulated. The lesions enlargement of a centrally located lesion may produce an earlier
may be well circumscribed and confined to the orbit, or they may vision loss. A retinal hemangioblastoma may be a predisposing
have indistinct, irregular margins. When large, they may cause factor for retinal detachment, macular edema, and glaucoma. Early
osseous erosion and remodeling and may involve the central detection, followed by laser coagulation or cryotherapy, may
nervous system. Rarely, intralesional calcification is present. On prevent vision loss.
dynamic contrast-enhanced CT, hemangiopericytomas exhibit
marked early arterial phase and early venous phase enhancement References
followed by rapid washout. On MR imaging, the signal intensity of
hemangiopericytomas is similar to that of gray matter on T1- and 1. Rodgers R, Arthur S, Grove Jr. Vascular lesions of the orbit. Principle and
T2-weighted images, a feature that helps differentiate these lesions Practice of Ophthalmology (Jakobiec). 2nd Edition, Vol 4, section 8:3144-
from cavernous malformations. Digital subtraction angiography 3155.
demonstrates a prominent arterial supply with an early florid
blush and persistent tumor staining, features that help differentiate 2. Haik BG, Jakobiec FA, Ellsworth RM, Jones IS. Capillary hemangioma of
hemangiopericytomas from meningiomas (which typically contain the lids and orbit: an analysis of the clinical features and therapeutic results
multiple vessels and show a late tumor blush) and schwannomas in 101 cases. Ophthalmology. 1979:86;760-792.
(which typically show no tumor blush).
3. Dubois J, Garel L. Imaging and therapeutic approach of hemangiomas
Hemangiopericytomas are usually lobulated, encapsulated, and and vascular malformations in the pediatric age group. Pediatr Radiol.
well circumscribed, but they may have infiltrative margins. 1999;29:879-893.
Histologic findings range from benign to malignant characteristics,
with many tumors demonstrating both. Diagnostic criteria include 4. Plesner-Rasmussen HJ, Marushak D, Andersen M. Sequelae of capillary
the number of mitotic figures per high-power field, the degree of hemangioma of lids and orbita. Scand J Plast Reconstr Surg.
cellularity and the degree of nuclear atypia. These mesenchymal 1983;17(3):241-5.
tumors arise from the pericytes of Zimmerman, contractile cells
that surround the outer aspect of small vessels and that are thought 5. Millischer-Bellaiche AE, Enjolras O, Andre C, et al. Eyelid hemangiomas
to regulate lumen size and produce collagen. Histologic analysis in infants: contribution of MRI. J Radiol. 2004;85:2019-2028.
demonstrates staghorn-like capillary spaces lined by plump,
proliferating pericytes, with intervening fibrous septa. The 6. Brackup AH, Haller ML, Danber MM. Hemangioma of the bony orbit.
standard treatment is wide surgical excision. On surgery they are Am J Ophthalmol 1980;90:258–261.
solid and dark blue to violaceous and may bleed extensively and
maybe exceedingly friable. Postoperative irradiation is 7. Relf SJ, Bartley GB, Unni KK. Primary orbital intraosseous hemangioma.
recommended for incompletely excised lesions. Local recurrence Ophthalmology 1991;98:541–547.
in approximately 30% of cases has been reported, and lesions may
recur up to 30 years after initial treatment. 8. Rootman, Kao SC, Graeb DA. Multidisciplinary approaches to
complicated vascular lesions of the orbit. Ophthalmology. 1992
Hemangioblastomas sep;99(9):1440-6.

Hemangioblastoma is a benign vascular tumor that is commonly 9. Ranchod TM, Frieden IJ, Fredrick DR. Corticosteroid treatment of
associated with von Hippel- Lindau disease. Most periorbital haemangioma of infancy: a review of the evidence. Br J
hemangioblastomas that occur within the orbit are located in the Ophthalmol. 2005 Sep;89(9):1134-8.
retina, although locations within the optic nerve have been
reported. Von Hippel-Lindau disease is an autosomal dominant 10. Huna-Baron R, Setton A, Kupersmith MJ, Berenstein A. Orbital
genetic disorder with variable expressivity that is localized to arteriovenous malformations mimicking cavernous sinus dural
chromosome 3. It is characterized by both benign and malignant arteriovenous malformation. Br J Ophthalmology. 2000 jul;84(7):771-4.
tumors. Without a family history, at least two cerebellar
hemangioblastomas or one hemangioblastoma plus one associated 11. Meyer E, et al. Fine-needle aspiration of orbital lesions. Ann Ophthalmol.
visceral tumor (renal cell carcinoma, pheochromocytoma) are 1983 Jul;15(7):635-8.
necessary for a diagnosis of von Hippel-Lindau disease.
Histologically, the retinal tumors first described by von Hippel are 12. Char DH. Management of orbital tumours. Mayo Clin Proc. 1993
Nov;68(11):1081-96.

13. Wendy R. K. Smoker, MD, Lindell R. Gentry, MD, Norbert K. Yee, MBBS,
Deborah L. Reede, MD, and Jeffrey A. Nerad, MD. Vascular Lesions of
the Orbit: More than Meets the Eye.Radiographics. 2008 jan;28:185-204.

14. Bilaniuk, Larissa T. Vascular lesions of the orbit in children. Neuroimaging
clinics of North America. 2005-Feb;15(1):107-20.

15. Sachin Mehta MS, Zia Chaudhuri MS, MNAMS, FRCS. Orbital
Lymphangioma. DOS Times.2007;13(5):55-57.

16. Jayanta Kumar Das. Color Doppler Imaging of the Orbital Disorders.
www.Natboard.edu.in. Online training program for DNB students.

First Author
Gaurav Bharti DOMS

www.dosonline.org 53

Congenital Glaucoma in a 5 Day Old Infant Clinical Meeting: Clinical Case 1

Shivani Kochhar MBBS, K.P.S. Malik MS, MNAMS, V.S. Gupta MS

A5 day old female child, born out of a consanguineous marriage Table 1: Findings on examination under anaesthesia done pre
in a Muslim family, presented to the out-patient services of operatively (day 2)
Safdarjung hospital with the chief complaints of both side big
sized eyes and whitish opacity in the black part of eye since birth R/E L/E
and not opening eyes to bright light. Mother gave No h/o excessive
watering / discharge /redness. Cornea Hazy Hazy
Stromal edema + Stromal edema +
Birth history: full term normal vaginal delivery with no H/O birth Habb’s striae + Habb’s striae +
trauma/ systemic illness/ topical medication use. The Obstetric
history was uneventful. Corneal diameter

Family history: child is the 4th child from a consanguineous marriage Horizontal 13 mm 13 mm
with no H/O of similar complaints in the family/ siblings.
Vertical 13 mm 13 mm
On Examination: General physical examination, head to toe was
within normal limits with no systemic abnormality. IOP (schiotz) 65 mmHG 70 mmHG

Local examination: photophobia present/ blepharospasm present, Fundus Glow + Glow +
with bilateral symmetrical enlargement of eyeball, the corneal Optic disc: Optic disc:
vertical and horizontal diameters appeared enlarged, corneal haze appears normal appears normal
was present (L/E>R/E), sclera appeared thin and blue, digital
tension was raised bilaterally, regurgitation on pressing over the CDR : 0.2 CDR: 0.2
lacrimal sac area was negative. Posterior segment could not be
evaluated due to hazy media (edematous cornea). Rest details not Rest details not
seen cur to seen cur to
Provisional Diagnosis of B/L congenital glaucoma hazy media hazy media

Management Following this, the child was seen once weekly and features like
photophobia, blepharospasm and epiphora were assessed which
Examination under anaesthesia was done on day 2 (Table 1, showed marked improvement The examination under anaesthesia
Figure1), followed by R/E trabeculotomy with trabeculectomy using was repeated at post operative week 6 (Table2, figure 2 {right eye},
Mitomycin-C, 0.04%, applied for 2 minutes. The L/E was started Figure 3{left eye}) which showed increased clarity of cornea and
on topical medication (E/D dorzolamide 2% TDS and E/D timolol considerable decrease in the corneal haze with tension reducing to
0.25% BD) which was then taken up for similar procedure 1 week 11 mmHG in both eyes.
later.
Discussion

The incidence of congenital glaucoma is 1 in 10,000 live births (in
Europe/US)1 and 1 in 3300 in AP, India1.

Glaucoma as a cause of childhood blindness is 7%2,3(North/South
India) and 4.9% (Delhi)4 . It is Bilateral in 65-80%1, with male
predominance (65%)1, onset in 1st yr of life is seen in >80% of
children1 but diagnosed at birth in less than 25% cases1.

Figure 1: Microscopic picture of right eye and Figure 2: Microscopic picture of right eye preoperatively
left eye preoperatively showing corneal haze, (right) and post operartive at week 6 (left)

stromal edema and haab’s striae 55

Department of Ophthalmology
Safdarjung Hospital, New Delhi

www.dosonline.org

Table 2: Findings on examination under anaesthesia done post
operatively (week 6)

R/E L/E

Cornea Decreased edema
(R>L) Clarity
better Pupil seen

Corneal diameter

Horizontal 13 mm 13 mm

Vertical 13 mm 13 mm

IOP (schiotz) 11 mmHG 11 mmHG Figure 3: Microscopis picture of left eye
bleb preoperatively (right) and post operative at
Well formaed / Well formaed /
diffuse/ diffuse/ week 6 (left)
avascular avascular

Fundus Glow + Glow +
Optic disc: Optic disc:
appears normal appears normal In deciding upon simultaneous B/L surgery, the possible risk of B/
L endophthalmitis has to be balanced against the advantages of
CDR : 0.2 CDR: 0.2 one anaesthesia versus two cost effectiveness and early visual
rehabilitation. Wheeler performed a survey of 500 pediatric
Background Background ophthalmologists and glaucoma specialist who did not recommend
appears normal appears normal B/L pediatric intraocular surgery .18

Congenital glaucoma is essentially a surgical disease with medical Visual rehabilitation is as important in the management of the
management being a temporary option. Various studies advocate disease as is intraocular pressure control and involves correction
that the surgical procedure of Choice for congenital glaucoma is of refractive error, anisometropia, amblyopia, media
“Primary combined trabeculotomy–trabeculectomy” 5,6,7,8 opacities(corneal scarring) and timely keratoplasty if required.

Intra Ocular Pressure rise in young children can result in severe Post operative protocol for follow up as given by Mandal et al
visual morbidity due to corneal opacification induced myopia, 19says that the child should be seen weekly in the OPD and the
amblyopia and glaucomatous optic atrophy. Hence, timely reduction degree of relief from photophobia/ tearing/ blepharospasm
of IOP and stabilisation of refractive error are essential to avoid should be assessed. The examination under anaesthesia should
these sequalae. Therefore various studies advocate “surgery as be repeated post surgery 3-4 weeks, if IOP is stable then every 3
early as in the first week of life, may improve the chances of cure” months, followed by quarterly interval for the first 1 year, then
biannually until the child is cooperative for OPD examination.
9,10,11 Such children have to be kept in follow up indefinitely.

Surgery in infants can be very challenging since they have to be put Salient features
under general anaesthesia at a very early age in life and also because
an infant’s eye behaves differently from that of an adult by virtue • It is very important to diagnose and surgically treat a child of
of congenital glaucoma at the earliest to prevent severe visual
morbidity.
• Definition of surgical limbus is more difficult
• Combined surgery with MMC has shown a high net success
• Abnormally stretched limbus makes it difficult to fashion the rate in children < 6 months of age.
scleral flap and cannulate it
• The available literature does not allow a formal comparison
• More rapid healing and exuberant scarring processes leading between the risks involved in multiple anaesthesia and the
to a high failure rate. possible risks of B/L endophthalmitis.

The use of mitomycin C (MMC) as an adjunct intraoperative drug • And since the rate of complication goes up with the use on
was first described by Chen et al in 1983 following which number mitomycin C, we recommend one eye at a time.
of studies have reported a success rate varying between 60-95%12,
13, 14, 15, 16..Ali A hazmi et al reported that the success rate of the • It is imperative to inform and educate the parents about the
glaucoma filtering surgery utilizing MMC goes up with increasing need to follow up which is life long.
age but so does the complication rate” and concluded that the net
success rate was highest in the age group <6 months .17 A very low References
rate varying from 0-8% of endophthalmitis post combined surgery
with MMC has been reported12, 13, 16 1. Anil K Mandal, Peter A Netland; The pediatric glaucomas; 2006.

2. Dorairaj et al ophthalmic epidemiology 2008.

56 DOS Times - Vol. 15, No. 6, December 2009

3. Harsha Bhattacharjee, Kalyan Das, Rishi Raj Borah et al Causes of 11. Rajeev Jain et al Trabeculectomy with Mitomycin-C (MMC) As
childhood blindness in the northeastern states of India IJO Primary Surgery In Congenital Glaucoma, AIOC 2006.
2008,56,6;495-499
12. Susanna R, Oltrogge et al. Mitomycin as adjunct chemotherapy in
4. Titiyal et al, Causes and temporal trends of blindness and severe congenital and developmental glaucoma. J Glau 1995.
visual impairment in children in schools for the blind in North
India, BJO aug 2003 13. Mandal Ak, Walton DS et al MMC augmented trabeculectomy in
refractory congenital glaucoma ophthalmol 1997.
5. Anil K mandal at el Outcome of surgery on infants younger than 1
month with congenital glaucoma, presented as a paper at the annual 14. R Ehrlich, M Snir, et al Augmented trabeculectomy in paediatric
meeting of the AAO,oct 2003,110,10,1909-1915 glaucoma BJO 2005.

6. Anil K. Mandal, Prashant G. Bhatia et al, Ophthalmology Long- 15. A Al-Hazmi, A Awad et al, Correlation between surgical success
term Surgical and Visual Outcomes in Indian Children with rate and severity of congenital glaucoma. BJO 2005.
Developmental Glaucoma Operated On within 6 Months of Birth
2004. 16. Jair Giampani Junior et al, Efficacy and safety of trabeculectomy
with MMC in childhood glaucoma: a study of results with long-
7. Laudo Silva Costa, Reoberta Martins da silva costa, Combined term follow-up, clinics 2008.
Trabeculotomy–Trabeculectomy as a First Surgical Procedure for
Primary Congenital Glaucoma, Annals of Ophthalmology 2006. 17. Ali Al hazmi, johan zwaan et al, Effectiveness and complications of
mitomycin C use during pediatric glaucoma surgery, ophthalmol
8. São Paulo, Long-term surgical outcomes of primary congenital 1997.
glaucoma in China ,Clinics vol.64 no.6 June 2009.
18. Wheeler DT, Stager DR et al endophthalmitis following pediatric
9. Shaffer RN, Prognosis of goniotomy in primary infantile glaucoma intraocular surgery for congenital cataract and congenital glaucoma
(trabeculodysgenesis). Trans Am Ophthalmol Soc. 1982. J pediatr ophthalmol strabismus 1992.

10. Shaffer RN, Hoskins HD. Montgomery lecture. Goniotomy in the 19. Anil K Mandal, Current concepts in the diagnosis and management
treatment of isolated trabeculodysgenesis. Trans Ophthalmol Soc of developmental glaucomas, IJO 1993.
UK. 1983.

First Author
Shivani Kochhar MBBS

Congratulations

Dr. Noshir M. Shroff, Senior Eye Surgeon, Shroff Eye Centre, Kailash Colony, New Delhi has been awarded
Padma Bhushsan by President of India on 26th January 2010.

Lt. Gen. D.P. Vats SM, VSM, a renowned expert in the field of Ophthalmology has assumed the appointment of
Director and Commandant of the prestigious Armed Forces Medical College, Pune

Dr. (Lt. Col. ) Sanjay Kumar Mishra has been awarded Vishist Seva Medal by President Of India on 26 January
2010. He is posted at Army Hospital (Research & Referral) Delhi Cantt and is at present pursuing long term training
in Vitreo-retinal surgery at the prestigious R.P. Centre AIIMS. He hails from Uttar Pradesh.

Dr. Gopal Lal Verma & Dr. Tarun Sharma have been nominated by American Academy of Ophthalmology
for International Ophthalmic education award -2009 at san francisco.

Dr. Noopur Gupta, Dr. Radhika Tandon and Dr. J.S. Titiyal for being awarded the ORBIS International Medal
for the best paper contributing to prevention and blindness in the developing world at XXVII Congress of
European Society of Cataract & Refractive Surgery, Barcelona 2009.

www.dosonline.org 57

An Unusual case of Discharging Sinus Clinical Meeting: Clinical Case 2

Aniket Shastri MBBS, Anuj Mehta MS, KPS Malik MS, MNAMS, Sangeeta Abrol MS, Malvika Gupta DO

We present a case of a 25 year old healthy adult male; who Provisional Diagnosis
presented to us with discharge from inner aspect of the
right upper lid since 15 days. With this we made a diagnosis of fracture of the right medial wall
of the orbit with (?) impaction of soft tissue with (?) orbital cellulitis
History revealed a fall from his bicycle about a month back when with a discharging sinus
he sustained injury to the right side of the face. He developed
swelling in his right upper and lower lids along with wound/abrasion Investigations
in upper lid on the inner aspect. He visited a nearby doctor and
was given first aid treatment. A CT scan was done then. After Routine investigations were within normal limits. Chest X ray was
about 15 days later he noticed that there was a purulent discharge normal. He produced a CT scan report which read as a Normal
from inner aspect of the right upper lid, which was present study of eyeball with fluid collection in extra ocular space with a
throughout the day. This was associated with restriction of eye medial wall fracture.
movements and diplopia on looking towards the left side. He
complained of pain, more so on extra ocular movements. Redness An Ultrasound B-scan was done on the same day that showed
of the eye was present. No past history of tuberculosis or contact linear hyper-echoic lesion with a surrounding hypoechoic area
with Tuberculosis.

On Examination

He had a Vision of 6/9 in both the eyes with a normal near and
color vision. The orbital margins were normal with no discontinuity
or tenderness. On examination of extra-ocular movements the
right eye showed limited adduction, elevation and levo-versions.
The eyeball showed a right exotropia and hypotropia.

There was right upper and lower lid edema, upper lid erythema
with an Ulcer about 2 *1 cm- about 2 cm from lid margin and 1cm
from the medial canthus. This was associated with purulent
discharge from medial aspect of the ulcer (Figure 1). Rest of the
examination was within normal limits except for a mild congestion
of conjunctiva.

Figure 2: Ultrasound B Scan Image showing linear
hyper-echoic lesion with a surrounding hypoechoic

area. No post acoustic shadowing

Figure 1: Ulcer with discharging sinus Figure 3: Coronal scans of CT showing well
defined, round hypodense lesion in the medial
Department of Ophthalmology
Safdarjung Hospital, New Delhi wall of the right orbit

www.dosonline.org 59

Figure 4: Axial CT scans showing hypodense lesion with Figure 5: Trans-caruncular
size of the hollowness same throughout- extending from approach showing removal of the
the equator of globe to the posterior ethmoidal sinuses.
40 mm wooden piece

(suggestive of probably an intra orbital foreign body) in the medial
side of the orbit (Figure 2). There was no post acoustic shadowing
(probably non-metallic) with a mass effect on the eyeball. Pus was
sent for culture and sensitivity. Review of the CT scan films was
done.

Sequential coronal non contrast CT of nasal sinuses in bone window
showed a well defined, round hypodense lesion with attenuation
similar to air in the medial wall of the right orbit (Figure 3). This
lesion was seen pushing the optic nerve supero-laterally with
preservation of the fat plane in between indicating no involvement
of the optic nerve. It was seen extending into right middle and
posterior ethmoidal sinuses. The axial view (Figure 4) is showing
the hypodense lesion with size of the hollowness same throughout-
extending from the equator of globe to the posterior ethmoidal
sinuses.

Summarizing the radiological findings- Figure 6: The foreign body; multiple
• Hypodense lesion-attenuation similar to air wooden pieces

• Well Defined, Circumscribed and also as the suspected lesion was not felt anteriorly. NCCT also
showed the suspected lesion to be relatively posterior.
• Size of hollowness was same throughout- suggestive of foreign
body On exploration of the sinus, we were able to pick out approximately
9-10 pieces of wood with a forceps from the medial part of the
• No post acoustic shadowing on U/S B scan- suggestive of orbit- with the largest measuring 35 MM. On further probing a
non-metallic hard mass was felt inside. On pulling it out using an artery forceps,
a thick hollow piece of wood of size 40 MM was seen (Figure 5&6).
• Hyperechoic on ultrasound
Post Op: On the first post-op day patient had mild upper lid edema
Final Diagnosis and conjunctival congestion with limitation of adduction
(Figure 7). Shows the clinical picture at post-op day 7- with complete
Foreign body in the medial part of the right orbit-non-metallic, healing of the ulcer and the sinus.
probably, wood or glass.

Treatment

Meanwhile the patient was started on Intra-venous antibiotics An ultrasound B scan was performed and it showed no evidence
and anti-inflammatory. of foreign body.

Exploration for a suspected Foreign Body under General Discussion
Anesthesia was planned. On the decision about how to approach,
a trans-caruncular approach was chosen over the eyelid skin crease Amongst the various causes of a periorbital discharging sinus, two
approach. This was done to avoid damage to the lid structures important ones are

60 DOS Times - Vol. 15, No. 6, December 2009

metallic foreign bodies. Wooden foreign bodies may be missed
on CT scanning or may be misdiagnosed as intraorbital air.

MRI scans are better at demonstrating wooden foreign bodies
and should be performed after a negative CT scan if there is a
possibility of a wooden Intra orbital Foreign Body. An MRI scan
may be performed before a CT scan if there is a definite history of
a wooden Intra Orbital Foreign Body.

Orbital Ultrasonography is a complementary modality.
Ultrasonography may be useful when CT and MRI do not
demonstrate a wooden Intra Orbital Foreign Body.

Figure 7: Post operative picture day 7. Wooden foreign bodies are notorious for remaining quiescent for a
Note the ulcer has healed and sinus closed long time, before presenting with a variety of complications. The
wound of entry may often be small and self-sealing. Wooden foreign
• retained periorbital foreign body bodies also show a propensity to break during attempted removal.
Intraorbital wood is often not detected by standard diagnostic tests
• periorbital tuberculosis like the computed tomography scan, adding to the diagnostic
dilemma
The diagnosis of periorbital tuberculosis is made on the basis of
clinical features supported by radiological investigations. Wood, plastic and Air have radiologically similar characteristics-
Polymerase chain reaction and Acid Fast Bacilli cultures provide very difficult to distinguish. Air, when trapped inside a foreign
the investigative evidence body, will take shape conforming to primary object. This is an
important clue to presence of foreign body.
Intra orbital foreign bodies (IOrbFbs) usually occur after a high-
velocity injury such as a gunshot or industrial accident but, may The presence of an intraorbital mass with a discharging sinus
occur after relatively trivial trauma to the extent that the history should evoke suspicion of a retained foreign body, regardless of
may be unclear the time interval between the trauma and current presentation. It
is imperative to maintain a high index of suspicion in such cases to
A high index of suspicion is required in the setting of projectile avoid misdiagnosis
injuries or in the setting of persistent orbital inflammation after a
history of periocular trauma, no matter how trivial it seems This case again emphasizes the necessity for careful assessment of
penetrating wounds of the orbit, however trivial they may appear
Clinical features may be varied- superficially.

• Orbital mass References

• Pain on eye movements 1. Roberts CF, Leehey PJ 3rd. Intraorbital wood foreign body mimicking
air at CT. Radiology 1992;185:507–8

• Orbital abscess 2. Green BF, Kraft SP, Carter KD, et al. Intraorbital wood. Detection

• Orbital cellulitis by magnetic resonance imaging. Ophthalmology 1990;97:608–11.
3. Glatt HJ, Custer PL, Barrett L, Sartor K. Magnetic resonance imaging

• Diplopia and lagophthalmos and computed tomography in a model of wooden foreign bodies in

• Finding on computed tomography scan the orbit. Ophthalmic Plast Reconstr Surg 1990;6:108–14.

4. John SS, Rehman TA, John D, Raju RS. Missed diagnosis of a wooden

A CT scan is the standard diagnostic test, because it demonstrates intra-orbital foreign body. Indian J Ophthalmol. 2008 Jul-

most Intra Orbital Foreign Bodies, and it is safe in the presence of Aug;56(4):322-4.

First Author
Aniket Shastri MBBS

www.dosonline.org 61

DNB Paper Cracked Miscellaneous

Important Links to Common Questions

DNB Paper 1 Scleritis: Conjunctival and Scleral Disorders: Merck Manual
www.merck.com/mmpe/sec09/ch101/ch101f.
Q1) Clinical picture and management of epidemic Local Treatment of Necrotizing Scleritis with Cyclosporin A
keratoconjunctivitis? Hoffmann, F.; Wiederholt, M.Cornea. 4(1):3-7, March 1985.
Q4 Traumatic hyphaema?
Ans. Links Ans. Links
Hyphema: eMedicine Ophthalmology
Keratoconjunctivitis, Epidemic: eMedicine Ophthalmology. emedicine.medscape.com › ... › Anterior Chamber
emedicine.medscape.com › ... › Ophthalmology › Conjunctiva Management of traumatic hyphema
www.ncbi.nlm.nih.gov/pubmed/12161209
Epidemic Keratoconjunctivitis Factsheet - NSW Department of Clinical management of hyphaema
Health www.safpj.co.za/index.php/safpj/article/viewFile/715/621
The medical management of traumatic hyphaema: a survey
www.health.nsw.gov.au/factsheets/.../keratoconjunctivitis. of opinion ...
html www.ncbi.nlm.nih.gov/pmc/articles/PMC1294050/
Treatment of traumatic hyphaema
ISPUB - New Management Of Epidemic Viral www.ncbi.nlm.nih.gov/pmc/articles/PMC506390/
Keratoconjunctivitis Q5. MARINA and FOCUS Trials?
Ans. Links
www.ispub.com/ostia/index.php?xmlFilePath=journals/ http://www.mrcophth.com/MARINATRIAL.htm
http://www.dostimes.org/FullText.aspx?id=201
EPIDEMIC KERATOCONJUNCTIVITIS New data from two leading clinical studies show Lucentis® is
first hugin.info/134323/R/1002762/153861.pdf
www.ncbi.nlm.nih.gov/pmc/articles/PMC2135294/ http://www.ncbi.nlm.nih.gov/pubmed/16935211
Q7. Ischaemic CRVO?
Treatment of Epidemic Keratoconjunctivitis With Idoxuridine Ans. Links
(IUDR) archopht.highwire.org/cgi/reprint/73/1/49.pdf http://www.dostimes.org/FullText.aspx?id=112
http://www.dostimes.org/FullText.aspx?id=287
Q2. Fungal Corneal Ulcer? Central Retinal Vein Occlusion: eMedicine Ophthalmology
emedicine.medscape.com/article/1223746-overview
Ans. Links Management of central retinal vein occlusion.
www.ncbi.nlm.nih.gov/pubmed/12660480
http://www.dostimes.org/FullText.aspx?id=503 Q8. Sarcoid Uveitis?
Ans. Links
Corneal Ulcer: Diagnosis and Management - Prashant Garg ... Sarcoidosis of the Eye
www.cehjournal.org/0953-6833/12/jceh_12_30_021.html www.sarcoidosisnetwork.org/documents/sarcoideye.html
Sarcoid Uveitis
Corneal Ulceration and Ulcerative Keratitis: eMedicine jnm.snmjournals.org/cgi/reprint/33/10/1851.pdf
Emergency emedicine.medscape.com › ... › Ophthalmology Uveitis associated with sarcoidosis and angiotensin converting
enzyme.
Practice Patterns in the Management of Fungal Corneal Ulcers www.ncbi.nlm.nih.gov/pmc/articles/PMC1311705/
Cornea. 28(8):856-859, September 2009.

Concurrent Use of 5% Natamycin and 2% Econazole for the
Management of Fungal Keratitis Cornea. 23(8):793-796,
November 2004.

The Epidemiological Features and Laboratory Results of
Fungal Keratitis: A 10-Year Review at a Referral Eye Care
Center in South India

Gopinathan, Usha; Garg, Prashant; Fernandes, Merle; Sharma,
Savitri; Athmanathan, Sreedharan; Rao, Gullapalli N. Cornea.
21(6):555-559, August 2002.

Q3. Necrotising Scleritis?

Ans. Links

Scleritis: eMedicine Ophthalmology emedicine. medscape.com
› ... › Ophthalmology › Sclera

Scleritis lmk23.tripod.com/scleritis.html

Scleritis and Streptococcus pneumoniae Altman, Adam J.;
Cohen, Elisabeth J J.Cornea. 10(4):341-345, July 1991.

www.dosonline.org 63

Q9. Retinopathy of Prematurity Screening? http://www.ojoonline.org/article.asp?issn=0974-620X;
year=2009;volume=2;issue=1;spage=23;epage=26;
Ans. Links aulast=Mahdy;type=0

http://www.dostimes.org/FullText.aspx?id=113 Q3. Factors influencing sclerotomy sites for vitrectomy?

http://www.dostimes.org/FullText.aspx?id=125 Retina 4th Edition, by Stephen Ryan, Volume 3, Page 2150-51.

Screening Examination of Premature Infants for Retinopathy Atlas of Vitreo Retinal Surgery, by H. Mackenzie Freeman
of ... and Felipe I. Tolentino, Jaypee Brothers Publications, Chapter
aappolicy.aappublications.org/cgi/content/full/pediatrics;108/ 6, Page 47.
3/809
Q4. Indications, procedures and complications of
Retinopathy of Prematurity Lateral Orbitotomy?
www.mrcophth.com/.../Retinopathy % 20 of % 20 Prematurity.
htm Ans. Links

Q10. Vision Assessment in Preschool Child? http://www.medscape.com/viewarticle/405714_3

Ans. Links http://www.dostimes.org/FullText.aspx?id=213

Measuring Vision in Children http://www.dostimes.org/FullText.aspx?id=553
www.ncbi.nlm.nih.gov/pmc/articles/PMC1705714/
http://www.ncbi.nlm.nih.gov/pubmed/8919143?itool=
Vision testing of infants in a child health clinic and at home. EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.
www.ncbi.nlm.nih.gov/pmc/articles/PMC1228044/ Pubmed_RVDocSum&ordinalpos=4

Infant Vision Screening-Teller Acuity Test for Pediatric Visual. http://www.ncbi.nlm.nih.gov/pubmed/3940134?ordinalpos=
www.stereooptical.com/html/teller-acuity-cards.html - Cached 1&itool=EntrezSystem 2.PEntrez. Pubmed.Pubmed_
- Similar ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_
RA&linkpos=5&log$=relatedreviews& logdbfrom=pubmed.

DNB Paper 2 Q5. Clinical Picture and Management of Congenital
Glaucoma?
Q1. Methods to reduce PCO?
Ans. Links
Ans. Links
http://www.emedicinehealth.com/primary_congenital_
http://www.dostimes.org/FullText.aspx?id=285 glaucoma/article_em.htm

http://www.ijo.in/article.asp?issn=0301 4738;year=2004; http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi? book=
volume=52;issue=2;spage=99;epage=112; aulast=Pandey gene&part=glc

http://www.ncbi.nlm.nih.gov/pubmed/10627830 http://www.ijo.in/article.asp?issn=0301-4738;year=1993;
volume=41;issue=2;spage=51;epage=70; aulast=Mandal
http://bjo.bmj.com/content/89/11/1389.1.full
http://www.iovs.org/cgi/reprint/7/2/127.pdf
http://www.ncbi.nlm.nih.gov/pubmed/19365040?itool=
EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel. http://www.dostimes.org/FullText.aspx?id=265
Pubmed_RVDocSum&ordinalpos=2
Q6. Fuch’s Heterochromic Cyclitis?
Q2. Indications and methods of pterygium surgery. How
to prevent recurrences? Ans. Links

Ans. Links http://emedicine.medscape.com/article/1208706-overview

http://www.ncbi.nlm.nih.gov/pubmed/19668546?itool= www.uveitissociety.org/pages/diseases/fhu.pdf
EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC504237
Pubmed_RVDocSum&ordinalpos=7 Q7. Prevention and Management of PBK?
Ans. Links
http://www.dostimes.org/FullText.aspx?id=77 http://www.dostimes.org/FullText.aspx?id=588
http://emedicine.medscape.com/article/1194994-overview
http://www.dostimes.org/FullText.aspx?id=437 http://www.dostimes.org/FullText.aspx?id=320

h t t p : / / w w w. i j o . i n / a r t i c l e . a s p ? i s s n = 0 3 0 1 4 7 3 8 ; y e a r =
1998;volume=46;issue=4;spage=203;epage=209;
aulast=Rao;type=0

64 DOS Times - Vol. 15, No. 6, December 2009

Q8. Recent Methods for Treatment of Keratoconus? Q3 Differential Diagnosis Malignant Lid Tumors?

Ans. Links Ans. Links

http://www.dostimes.org/FullText.aspx?id=127 www.springerlink.com/index/M035P8H24K343M13.pdf

http://www.dostimes.org/FullText.aspx?id=130 http://www.aafp.org/afp/980600ap/carter.html
http://www.dostimes.org/FullText.aspx?id=239 linkinghub.elsevier.com/retrieve/pii/S0161642099001359
http://www.ncbi.nlm.nih.gov/pubmed/12750109 Clinicopathological Features of Eyelid Skin Tumors. A
Q9. Acute Management of Alkali Burns? Retrospective Study of 5504 Cases and Review of Literature
Ans. Links
http://www.emedicinehealth.com/chemical_eye_burns/ Q4. Non Arteritic AION?
page2_em.htm
http://www.dostimes.org/FullText.aspx?id=483 Ans. Links
http://www.dostimes.org/FullText.aspx?id=551
http://emedicine.medscape.com/article/798696-overview http://www.dostimes.org/FullText.aspx?id=168
Q10. Indications, Contraindications and Complications http://emedicine.medscape.com/article/1216891-overview
of Phakic IOLs for High Myopia? www.eyeassociates.com/understanding_a_stroke_of_the_
Ans. Links op.htm
www.iovs.org/cgi/reprint/34/7/2260.pdf
www.ncbi.nlm.nih.gov/pubmed/3229901
http://webeye.ophth.uiowa.edu/dept/aion/12-AION-
incipient.htm

http://www.dostimes.org/FullText.aspx?id=536 www.ajnr.org/cgi/content/full/27/2/255
http://www.dostimes.org/FullText.aspx?id=143
http://www.dostimes.org/FullText.aspx?id=234 http://jnnp.bmj.com/content/53/10/830.abstract
http://emedicine.medscape.com/article/1221908-overview
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684439. Q5. Role of HBA1c, Blood Pressure and Blood Cholesterol
in Prevention and Management of Diabetic
Retinopathy?

Ans. Links

DNB Paper 3 http://www.nei.nih.gov/health/diabetic/retinopathy.asp
http://www.sma.org.sg/smj/4106/articles/4106ra1.pdf
Q1. Clinical Picture & Management of Congenital http://www.ncbi.nlm.nih.gov/pubmed/7622004
Epiphora. Indications for Surgical Intervention? http://linkinghub.elsevier.com/retrieve/pii/S0002939407005351
http://www.dostimes.org/FullText.aspx?id=95
Ans. Links Q6. Modern methods for the diagnosis and
http://www.dostimes.org/FullText.aspx?id=218 management of POAG?
http://www.dostimes.org/FullText.aspx?id=513 Ans. Links
http://bjo.bmj.com/content/85/3/314.abstract http://www.dostimes.org/FullText.aspx?id=76
www.ncbi.nlm.nih.gov/pmc/articles/PMC1772826/ http://www.dostimes.org/FullText.aspx?id=115
Congenital epiphora as a potential cause of amblyopia http://www.dostimes.org/FullText.aspx?id=175
www.opt.indiana.edu/ce/peddz/epiphora.htm http://emedicine.medscape.com/article/1206147-overview
http://linkinghub.elsevier.com/retrieve/pii/S016164209990
Q2. Clinical Picture of Heredomacular Degeneration and 458X
its mode of Inheretence?

Ans. Links

http://www.ijo.in/article.asp?issn=0301-4738;year=1983; ftp://fastlink.nih.gov/pub/staff/schaffer/webpapers/
volume=31;issue=3;spage=115;epage=118;aulast=Khosla POAGhg.pdf

http://bjo.bmj.com/content/56/11/817.full.pdf http://www.replaylearning.com/mediaLibrary/images/
english/5780.pdf

www.dosonline.org 65

http://www.college-optometrists.org/filemanager/root/ Q9. Indications and complications of intravitreal
site_assets/cmg/glaucoma_primary_open_angle_poag_ steroids?
v12_final.pdf
Ans. Links
Q7. Classification and management of primary
divergent squint? http://www.dostimes.org/FullText.aspx?id=389
http://www.boamumbai.com/journalpdfs/jan-mar2004/
Trans Am Ophthalmol Soc. 1891; 6: 165–168 dudaniivitsteroids.pdf
http://www.ncbi.nlm.nih.gov/pubmed/18348879
J Pediatr Ophthalmol Strabismus. 2010 Feb 8:1-5. doi: 10.3928/ h t t p : / / w w w. n a t u r e . c o m / e y e / j o u r n a l / v 2 1 / n 1 1 / f u l l /
01913913-20100118-03. [Epub ahead of print] 6702551a.html
http://linkinghub.elsevier.com/retrieve/pii/S0161642000003948
Common forms of childhood exotropia http://linkinghub.elsevier.com/retrieve/pii/S1529183905000321
Ophthalmology, Volume 110, Issue 11, November 2003, Pages http://cme.medscape.com/viewarticle/564818?src=rss
2093-2096 ht t p : / / w w w. l i b r a r y. n hs . u k / E Y E S / Vi e w R e s ou rc e . a s px ?
resID=304981
Understanding squints: Diagnosis and management
Current Paediatrics, Volume 7, Issue 1, March 1997, Pages 23-27 Q10. Pharmacological properties, mechanism of action
and side effects of antiviral drugs ophthalmology
Strabismus simplified by Dr Pradeep Sharma , Chapter 8,
Page 98-104 Ans. Links

Q8. Anatomical & functional prognostic factors in the http://www.dostimes.org/FullText.aspx?id=340
management of rhegmatogenous RD? http://www.ncbi.nlm.nih.gov/pubmed/1324532
http://linkinghub.elsevier.com/retrieve/pii/003962579290003C
Ans. Links http://www.eyeupdate.com/pages/antiviral_drug.html
http://www.iovs.org/cgi/content/abstract/14/8/628
http://www.dostimes.org/FullText.aspx?id=528

http://www.ncbi.nlm.nih.gov/pubmed/19123157

http://linkinghub.elsevier.com/retrieve/pii/S0886335004007011

http://cat.inist.fr/?aModele=afficheN&cpsidt=14571488

http://archopht.highwire.org/cgi/reprint/105/4/503.pdf

http://www.springerlink.com/content/18446118r4777523/

Reviewd by
Ramendra Bakshi MS

66 DOS Times - Vol. 15, No. 6, December 2009

Anti-VEGF Therapy for Glaucoma Abstracts

Michael B. Horsley, Malik Y. Kahook, MD
Current Opinion in Ophthalmology 2010, 21:112–117

Department of Ophthalmology, Rocky Mountain Lions Eye Institute, University of
Colorado School of Medicine, 1675, Aurora Ct Mail Stop F731, Aurora, CO 80045, USA

INTRODUCTION

A lot of research is going on to understand the mechanism of action of anti VEGF drugs and their role in various diseases is being
investigated. Recently, their usage in glaucoma is also being talked about. The current article reviews various studies exploring the
utility of these agents in wound modulation after trabeculectomy.

A major factor in the success of a trabeculectomy is body’s innate healing response which might at times can lead to a failure of the
filtering surgery. With the coming up of MMC and 5 FU there has been a tremendoud improvement in the success rate of glaucoma
filtering surgeries.

The recent proposal of anti VEGFin trabeculectomy is based on the thought that it would take care of the angiogenic stimulus while the
anti mitotic agents would take care of the fibroblastic part. Thus, one may get a healthier bleb with less scarring and better long term
IOP control. Various case reports support the above, where subconjunctival bevacizumab during or after trabeculectomy has been
used in the dose of 1.25 mg/0.05 ml. This drug could also control the intractable cases of neovascular glaucoma who were treated with
preop PRP with intravitreal avastin and trabeculectomy later on.

Although, the above mentioned clearly point towards the benefits of anti VEGF in glaucoma, further studies are still needed to better
understand their functioning, the best route of administration, the dosage and the side effects if any in such a scenario.

Conjunctivitis and other Eye Manifestations in Swine Flu

Viroj Wiwanitkit, MD

Iranian Journal of Ophthalmology 2009;21(3):3-4 © 2009

CWiwanitkit House, Bangkhae, Bangkok Thailand

INTRODUCTION

The leatest pandemic of swine flu is due to the genetic assortment of the influenza virus and is considered a major threat on health
worldwide. A human to human transmission has already been confirmed, since the clinical manifestations of this disease overlap with
those of classical influenza, it becomes all the more important to look for its other specific manifestations.

The routes of entry of most respiratory viruses are via mouth and nose. Swine flu virus may also affect by passing through the
conjunctiva because the molecular size of this virus is smaller than the conjunctival barrier pore (as is true with human immunodeficiency
virus). This clearly reflects the role of dirty hands in helping the virus enter the human body via mouth, nose or conjunctiva.

Importance of eye manifestations in swine flu-

Even the classical influenza can have conjunctivitis as its manifestation, possibly due to inflammation caused by infection. In may also
be due to scratching and sneezing. In swine flu patients, there is no specific data on this topic but due to the above mentioned facts and
no clear cut figures, it may be assumed that conjunctivitis may be a presenting feature of swine flu but should not be considered as
marker of viral load or a hallmark of the disease.

Correspondence Author
Nidhi Tanwar MD

www.dosonline.org 69

Forthcoming Events: National

January 2010 April 2010
21-24 KOLKATA 16-18 NEW DELHI

AIOC 2010: Joint Meeting of the 68th AIOS Annual Annaul Conference
Conference & 15th Afro-Asian Congress of Delhi Ophthalmological Society
Ophthalmology Venue: Hotel Ashok, Chankaya Puri, New Delhi
Contact Person & Address Contact Person & Address
Dr. Ashis Kumar Bhattacharya Organising Secretary Dr. Amit Khosla, Secretary DOS
IMA House, Room No. 8, 53 Room No. 2225, 2nd Floor, New Building,
Creek Row, Kolkata - 700014 Sir Ganga Ram Hospital,
Tel: 033-22371679, 033-22366350, Rajinder Nagar, New Delhi - 110 060
Mobile : +09831019779 Email : [email protected] Ph.: 011-65705229, E-mail: [email protected],
Website: www.dosonline.org

Forthcoming Events: International

February, 2010 September, 2010
18-21 PALM BEACH, FLORIDA 16-20 BEIJING, CHINA

5th International Conference on Ocular Infections APAO-AAO Joint Congress
The Breakers Hotel, Palm Beach, Florida China National Convention Centre, Beijing
Conference Secretariat APAO Central Secretariat
Paragon Conventions Secretariat, Asia Pacific Academy of Ophthalmology
18, Avenue Louis-Casai, 5th Floor C/o. The Chinese University of Hong Kong,
1209 Geneva, Switzerland Dept. of Ophthalmology & Visual Sciences, Hong Kong
Tel: +41 (0)22 747 7930, Fax: +41 (0)22 747 7999 Eye Hospital, 3/F, 147K Argyle Street, Kowloon,
Email: [email protected] Hong Kong
Website: www.ocularinfections.com Email: [email protected]
Tel: (852) 2762-3042, Fax: (852) 2715-9490,
Website: www.apao2010beijing.org

Monthly Clinical Meetings Calendar 2009-2010

Dr. R.P. Centre for Ophthalmic Sciences Venu Eye Institute & Research Centre
26th July, 2009 (Sunday) 29th November, 2009 (Sunday)
Safdarjung Hospital
Shroff Charity Eye Hospital 27th December, 2009 (Sunday)
23rd August, 2009 (Sunday) Bharti Eye Foundation
31th January, 2010 (Sunday)
Base Hospital
4th October, 2009 (Sunday) Centre for Sight
28th February, 2010 (Sunday)
Sir Ganga Ram Hospital Guru Nanak Eye Centre
1st November, 2009 (Sunday) 28th March, 2010 (Sunday)

Midterm Conference of DOS
14th & 15th November, 2009 (Saturday - Sunday)

Annual Conference of DOS 16th-18th April, 2010 (Friday, Saturday & Sunday)

www.dosonline.org 73


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