EDITORIAL
5 Back to the Future
FOCUS
11 Amlyopia & Strabismus
GRAND ROUNDS
19 Retina: Central Serous Chorioretinopathy
B.P. Guliani
HISTORY OF OPHTHALMOLOGY
23 Down the Memory Lane: Delhi Ophthalmological Society
G. Mukherjee
OCULOPLASTY
33 Management of Orbital Cellulitis
Pankaj Gupta, Nishant Nawani
41 Ocular Myiasis
Ramesh K.C. Gupta, Abhishek Anand, Sonam A. Bodh, R. Arora, J.L. Goyal
SQUINT
47 Synoptophore
P.C. Dwivedi, Charudatt Chalisgaonkar, Syed Imran
55 Accommodative Esotropia
Varshini Shanker, Srijana , Suma Ganesh , Manish Sharma
RETINA
63 Low Fluence PDT + Anti-VEGF Therapyin Subfoveal CNVM
Lalit Verma, Shaifali Gupta
69 Choroidal Hemangioma
Neha Goel, Supriya Batta, Meenakshi Thakar, Usha Kaul Raina, Basudeb Ghosh
PRACTICE ADVICE
77 Consumer Protection Act-A Nightmare
Namrata Kabra
COMMUNITY OPHTHALMOLOGY
81 Childhood Blindness due to Vitamin A DeÀciency Disorders
Noopur Gupta, Vasundhra Misra, Praveen Vashist
TEAR SHEET
95 Gonioscopy Grading Systems
Digvijay Singh
Attention DOS Member
DOS Times is not published in
the month of May & June each year
www. dosonline.org l 3
Back to the Future
Respected Seniors & friends,
They say that those who forget the past are condemned to repeat it.
Therefore as the new executive takes charge with a new look DOS Times,
DOS Website and new energy and enthusiasm; we take a peep in the past
to learn who we are. We remember the greats of yesterday so that we can
create the greats of tomorrow.
The vibrant and colorful new look of the DOS Times comes with a fresh new format and is aimed to be more
interactive. The DOS Times Quiz has been started to push you to rack your brains and test your knowledge. The
Practice Advise section is like your friend giving you valuable professional information.
The DOS website has a changed look and some new features, I request you to please see them and give your
feedback. We have hours of videos, talks and presentations, features like “Find a Doctor” and information and
education for the public. The Find a Doctor section will be giving information to patients about how to access
the nearest ophthalmologist or specialist. All our members are requested to give us their clinic address and other
information they want us to display on the website.
We have launched the DOS Community Programme in an attempt to shoulder some of our social responsibility.
Diabetic retinopathy screening camp was our Àrst effort under this programme and I hope we can work together
to make this programme a success.
The Academic Calendar is ready and we all are looking forward for the Àrst monthly meeting at Ram Manohar
Lohia hospital. The dates and venue all monthly meetings, Midterm Conference at India Habitat Centre
(12th - 13th November 2011), DOS Teaching at AIIMS (7th – 8th Jan 2012) and the Annual Conference at Hotel
Ashok (6 – 8 April 2012) have been Àxed and will help you to plan your year ahead.
The DOS ofÀce is for you and all your criticism, advice and requests are welcome.
With best wishes,
Rohit Saxena
Secretary,
Delhi Ophthalmological Society
www. dosonline.org l 5
www. dosonline.org l 7
Sunday, 2nd October, 2011
at India Habitat Centre, Lodhi Road, New Delhi
Saturday & Sunday 12th & 13th November, 2011
at India Habitat Centre, Lodhi Road, New Delhi
Saturday & Sunday 7th & 8th January, 2012
at Jawaharlal Nehru Auditorium, AIIMS, Ansari Nagar, New Delhi
Friday, Saturday & Sunday 6th, 7th & 8th April, 2012
at Hotel Ashok, Chanakaya Puri, New Delhi
Focus
Prof. Pradeep Sharma MD, FAMS, Professor, Pediatric and Strabismus Services, Dr. Rajendra Prof. Pradeep Sharma
Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi MD, FAMS
Dr. Kanwar Mohan, MS, Consultant, Pediatric Ophthalmology and Strabismus, Squint Centre, Dr. Kanwar Mohan
SCO: 833-834(2nd Floor), Sector 22-A, Chandigarh MS
Dr. T.S. Surendran, MBBS, DO, Vice Chairman and Director of Pediatric Ophthalmology Department, Dr. T.S. Surendran
Sankara Nethralaya, 18/40 College Road, Chennai MBBS, DO
Dr. P. Vijayalakshmi, DNB, MS, FRCS Chief, Paediatric Ophthalmology & Adult Strabismus Dr. P. Vijayalakshmi
Department, Aravind Eye Hospital, 1, Anna Nagar, Madurai DNB, MS,FRCS
Prof. P.K. Pandey, MD, Professor, Pediatric Ophthalmology and Strabismus Services, Guru Nanak Dr. P.K. Pandey
Eye Centre, Maharaja Ranjit Singh Marg, New Delhi MD
Dr. Ramesh Kekunnaya MD, FRCS, Consultant, Pediatric Ophthalmology & Neuro-Ophthalmology Dr. Ramesh Kekunnaya
L.V. Prasad Eye Institute, Road No 2, Banjara Hills, Hyderabad MS, FRCS
Dr. Swati Phuljhele, MD, Assistant Professor, Pediatric Ophthalmology, Strabismus and Nuero- www. dosonline.org l 11
Ophthalmology Services, Advanced Eye Centre, PGIMER, Chandigarh and Associate Editor, DOS
Times interviewed the above panelists.
Strabismology is an important aspect of paediatric ophthalmology. It may
not be a sight threating problem, but signiÀcantly affects the overall physco-
social development of a growing child. With the ever changing concepts of
neurophysiology and development of binocular vision, the management
of strabismus and amblyopia has also evolved. This questionare is focused
on the conditions which are confusing/in the gray zone. The list of panelist
includes leading Indian strabismologists of International repute who have
tried to clear the scenario.
A. AMBLYOPIA
Swati: What is the most common type of amblyopia you encounter in your practice?
P. Sharma: The most common type encountered is anisometropic followed by strabismic.
K. Mohan: I encounter strabismic amblyopia most commonly in my practice.
T.S. Surendran: Strabismic amblyopia followed by amblyopia due to refractive error is the
most frequent type of patients in my practice. Our’s is a tertiary care centre and this could be the
reason we are seeing more strabismic amblyopia cases.
P. Vijayalakshmi: Strabismic Amblyopia.
P.K. Pandey: Mixed, strabismic and anisometropic.
R. Kekunnaya: I mostly encounter anisometropic type of amblyopia in our tertiary level of
eye care.
Both aniosmetropic and strabismic amblyopia appear to be equally important causes of
amblyopia.
Swati: What is your preferred modality for managing unilateral amblyopia? Is there a
role of spectacles correction alone in the management of anisometropic amblyopia?
P. Sharma: Occlusion is the mainstay of amblyopia therapy. Refractive correction is the
foremost part of amblyopia therapy as it is also the most common culprit. Glasses alone also
work but occlusion makes it work faster. Uncorrected refractive error not leading to amblyopia
may be +1.5D sphere or +1.0D cylinder and -3.0D sphere. But also keep in mind an uncorrected
The classiÀcation of amblyopia used is based on the etiology.
(A) Refractive Error
_ Iso-Ametropic (Bilateral uncorrected or undercorrected ref. error)
_ Anisometropic (unilateral or asymmetric uncorrected or undercorrected ref. error)
This would include hypermetropia (over 1.5Dsph),astigmatism (over 1Dcyl) or myopia (usually more than–
3 or -4 Dsph)
(B) Strabismus: usually esotropia, even of smaller angles (microtropia), vertical deviations and very rarely
exotropia.
In case of the latter one should exclude associated refractive errors, vertical deviation or subclinical organic
pathology
(C) Stimulus deprivation or media opacities
(D) Organic: Subclinical foveal malfunction or malorientation of cones: this is usually considered if the vision does
not improve despite proper occlusion. In addition one should keep in mind the possibility of mixed etiology,
as also the overlay of true amblyopia over the organic pathology compromising vision.
-or under corrected hyperope may exercise his / her R. Kekunnaya: Yes, to begin with I give refractive
accommodation to develop an accommodative esotropia to correction. It improves vision signiÀcantly in many
suffer from strabismic amblyopia also. patients. After 6 weeks of refractive error correction, I add
part time patching. Duration of patching depends upon the
K. Mohan: I prefer full-time occlusion alongwith near severity of amblyopia.
vision exercises for managing unilateral amblyopia. Yes,
there is a role of spectacle correction alone (Refractive All experts agree that correction of refractive error plays
adaptation) in the management of anisometropic amblyopia. a major role in management of amblyopia in general and
I advise refractive adaptation for 6-8 weeks before I start anisometropic and ametropic amblyopia in particular. However
occlusion treatment in anisometropic amblyopes and have the patient would require additional therapy to hasten and ensure
seen visual acuity improvement by 1-2 lines in a number complete recovery and occlusion/patching appears to be the best
of patients. option.
T.S. Surendran: I feel that Occlusion – Patching is Swati: Till what age would you like to treat amblyopia?
the best modality of treatment for patient with unilateral Is it different for different types of amblyopia?
amblyopia. For patients with poor compliance, I recommend
drug and optical penalization. P. Sharma: Though amblyopia is best treated in early
childhood it can be treated at a any age, but becomes
For children with amblyopia due to refractive error, I progressively difÀcult at later age. Vision is just like
advocate glasses Àrst - the spectacles when needed, can be learning a new language, we can easily pickup our mother
a powerful treatment for amblyopia. I advice patch only if tongue (even Chinese!) in early childhood, but to do it later
poor follow up is expected or if parents are very anxious to is a tough task. Practically speaking the age is dependent
start more aggressive treatment. I feel, that the advantage on type of amblyopia, the severity, the presentation visual
of this approach is that for some children, patching or acuity, the compliance and the motivation of the case.
penalization is not needed and glass alone will result in Usually Anisometropic amblyopia is less severe and is
resolution of amblyopia. Secondarily, glasses followed treatable till late teens, whereas the strabismic (esotropic)
by patching will have better tolerance from the children is better treated by the 8-9 years of age and stimulus
as the glass improves the vision in amblyopic eye before deprivation if from early childhood may require to be
patching. I think it is right to introduce one new treatment treated infancy.
at a time, instead of initiating spectacles and patching at the
same time. K. Mohan: I would like to treat amblyopia upto age 20
years. I have already published a series of 45 patients aged
Even the Amblyopia treatment study (ATS 5) 11-15 years treated successfully with occlusion treatment
had shown that patients with previously untreated (JPOS 2004, 41:89-95). I have few ambloyopes aged 16-19
anisometropic amblyopia and treated with spectacle alone years who showed improvement with occlusion treatment.
had shown improvement. In the same study, they had There is no difference in age for treatment for different
observed that patients with strabismic amblyopia also types of amblyopia.
showed improvement with glasses.
T.S. Surendran: Of late, I am advising amblyopia
P. Vijayalakshmi: Occlusion Therapy is my prefered management till 14-16 yrs. of age, for patients with
modality. Yes, spectacle correction alone has some role. refractive and strabismic amblyopia. In the early days of
my practice I thought, as many pediatric ophthalmologists
P.K. Pandey: Occlusion and atropine penalization do that amblyopia is not effective beyond 10-12 yrs of
work well in mild to moderate amblyopia, only occlusion age. However recent evidence shows that (Amblyopia
works in severe amblyopia. Glasses alone can improve treatment study 3) some older children and teenagers will
vision in about ¼ of cases, however further treatment is respond to amblyopia treatment - optical correction with
invariably required. patching and penalization - particularly if they have had
12 l DOS Times - Vol. 17, No. 1 July, 2011
no prior amblyopia treatment. Still, we cannot discount the P. Vijayalakshmi: Recurrences are seen rarely. After
fact, that younger children show greater response to early the expected improvement, keep on maintenance dosage
amblyopia management. and taper completely in 6 months period. I will stop
treatment if there is no improvement in spite of the right
P. Vijayalakshmi: Individualised treatment. Will give type of treatment with good compliance for more than 6
a chance of therapy to any age if it was not diagnosed months.
and treated earlier, again depending upon the amount of
vision impairment, cause of amblyopia (older children P.K. Pandey: At 6 months or if there is no improvement
do well in cases of anisometropic amblyopia) demand on in VA on 2 consecutive visits, 6 weeks apart. Recurrences
academic activities etc. Younger the child- more insistence are uncommon upto 1 year of follow up.
on patching therapy.
R. Kekunnaya: Depends upon the compliance with the
P.K. Pandey: Till about 17 years. Anisometropic patching and improvement in vision. If vision is improving
amblyopia may respond slightly better. I would continue till a point its improving. Once it is stable
for 4 to 6 months, I would stop patching.
R. Kekunnaya: Most important aspect is the parent or
patient’s willingness to try the patch therapy. In hyperopes, If compliance is poor, I may consider more time for
my cut off is 10 -12 years, myopes 16 years and I try the parents to correct the patching behavior etc and advice
patching even in strabismic patients even if they, present further on reward system to enhance compliance and will
at 15-16 years. I have seen dramatic improvement in quite a continue for extra 6 months. In some cases may switch to
few patients. If there is no improvement in vision after 3 - 4 Atropine penalization.
months, I ask them to discontinue patching.
Experts recommend that occlusion should be tapered once
All our experts feel that amblyopia can be treated as late as visual acuity is stable on multiple visits over 3- 6 months and
late teens depending upon the presenting visual acuity, history of maintenance occlusion therapy is given till 8-9 years of age.
prior treatment and most importantly motivation of the patient. Weaning of occlusion should be from 6 hours to 2 hours for 6-8
However one cannot discount the fact that younger the age better weeks before stopping it completely as the risk of recurrence is
is the response to amblyopia therapy. greater when the treatment is stopped abruptly.
Swati: When and how do you consider stopping B. INFANTILE ESOTROPIA
amblyopia treatment? How often do you see recurrence?
Swati: How early would you advocate surgery in
P. Sharma: We continue occlusion (full time) till full cases of Infantile esotropia?
visual improvement has occurred as evidenced by Snellen’s
vision or no further improvement in two consecutive P. Sharma: As per the evidence till now good binocular
monthly visits. So occlusion can be stopped, when vision is only possible if the alignment is done early
acuity becomes equal in both eyes or when there is true preferably within the Àrst year of misalignment. So when
alternation of Àxation or there is no visual improvement the child presents early, ie by 4-6 months of age and the
after 3-6 months of occlusion despite good compliance deviation is larger than 30pd and stable and not corrected
One may switch to part time patching and Ànally weekly by glasses, surgery should be done to achieve alignment as
patching as age advances, and continue till 9th birth day to soon as possible after 6 months of age.
check regression which is seen in about 14% cases in a year.
Monitoring from time to time is worth its while. K. Mohan: I advocate surgery for infantile esotropia
around age one year of age.
K. Mohan: I stop full-time occlusion treatment when
there is no improvement or no further improvement in T.S. Surendran: To establish the binocularity, a
vision despite 3 months of occlusion treatment provided satisfactory alignment should be obtained before 2 years
the treatment has been carried out sincerely. I stop of age. Waiting for the child to reach sufÀcient maturity, in
maintenance occlusion treatment between 8-9 years of most cases may lead to no binocularity at all.
age. If maintenance occlusion treatment is being done
sincerely, I see recurrence of amblyopia occasionally, but if P. Vijayalakshmi: Varies. Not in less than 11 months
maintenance treatment is not being done honestly, I do see unless otherwise indicated.
recurrence of amblyopia quite often.
P.K. Pandey: It may be 4 months if angle is stable
T.S. Surendran: I like to wean prior to stopping the measuring about 30-40 PD or more, earlier the better for
treatment. Once the maximum visual acuity has been binocularity.
established, treatment may be weaned - while monitoring
to ensure that visual acuity does not worsen. For example 6 R. Kekunnaya: Around 10 to 12 months of age. I get to
hrs patching might be weaned to 2 hr daily patching for 6-8 see the child at least 2 times before, I take a decision on the
weeks prior to stopping the treatment. amount of surgery.
Also, for those patients who have not shown any Experts differ in their opinion regarding the best time for
improvement with good compliance patching for 3- 4 surgical intervention in cases of infantile esotropia. While P
months, I consider stopping the treatment. In these Sharma and P K Pandey feel that surgery can be done as early as
children, I will double check and reconÀrm that there is no 4-6 months of age, others are of the opinion that one year of age is
other organic cause for sub normal vision. the optimal time for surgery.
Less than 15% children get recurrence of amblyopia Swati: How often do you see post operative over-
after treatment is stopped. For those patients, the treatment correction in these cases?
is restarted and very slowly weaned there-after.
P. Sharma: May be about 5-10%, if it is small exotropia,
or manageable by reducing the spherical hyperopic
correction that is present, so that fusion is possible at least
www. dosonline.org l 13
for some distance, I do not bother as long as binocularity is reassessed and occlusion schedule modiÀed, if need be.
not affected. Any associated refractive error needs to be treated and if
anisometropic, occlusion monitored.
K. Mohan: I do see postoperative overcorrection once
in a while, more often in patients who have associated K. Mohan: I do not consider occlusion during the
DVD. waiting period because I feel it serves no purpose.
T.S. Surendran: I personally prefer a slight immediate T.S. Surendran: The treatment for infantile esotropia is
over-correction in these cases as the convergence will make basically surgical but before surgery, treating any existing
the eyes straight. In older patients and adults with long- amblyopia is essential. The idea is to operate on cases with
standing congenital esotropia, I prefer under correction – good visual acuity in both eyes, preferably with alternating
since they have poor fusion potential and tend to drift to Àxations. To treat amblyopia before surgery, I advise
exotropia over time. patching the dominant eye 4-6 hours per day until the
patient holds Àxation well with the other eye. I follow-up
P. Vijayalakshmi: Very rare in the immediate every 1 to 2 weeks, to test for change in Àxation preference.
postoperative period, however we do come across
consecutive deviations on long term followup. Not sure P. Vijayalakshmi: Yes.
about the percentage.
P.K. Pandey: Yes, alternate occlusion also has a role it
P.K. Pandey: Not very often, in less than 10%. DHD may even improve smooth pursuit asymmetry.
is often associated and should not be confused with
overcorrection. R. Kekunnaya: Yes. Part time patching of the dominant
eye or alternate patching if the vision is equal.
R. Kekunnaya: May be around 10 % of cases in a
follow up 5 to 6 years. This number may change with more Most of the experts feel that occlusion should be given
and more years of follow up. during the waiting period to ensure equal vision in both the eyes.
It appears that 5-10% of patients may show consecutive Swati: Do you use Botulinum toxin in cases of
exodeviation over time but can be overlooked if it is a small angle. Infantile esotropia? If so when?
Swati: How many of these patients gain binocular P. Sharma: No, I have never used botulinum toxin in
status/ stereoacuity after surgery? cases of Infantile esotropia.
P. Sharma: I do not have deÀnite statistics, but K. Mohan: I do not use botulinum toxin in treatment
binocularity is achievable in atleast about 40% cases, of infantile esotropia.
which could be better if the follow up is more meticulously
maintained by the patient. T.S. Surendran: I had worked with Dr. Scott who was
the Àrst person to use Botulinum toxin A in the ocular
K. Mohan: Though I have not complied data on muscle as an alternative to surgical procedure in the
postoperative stereoacuity gain after infantile esotropia treatment of ocular deviations. Based on that experience, I
surgery, I do not remember any patient who has gained started using Botox for infantile esotropia in my early days
binocular vision or stereoacuity. of practice. But since I encountered some complications like
transient blepharoptosis, unexpected ocular misalignment,
T.S. Surendran: Very early intervention, as young as 6 I have now stopped using Botox for ocular misalignment.
to 8 months of age, may increase the chances of achieving Also both, Botox injection and surgery requires general
binocular fusion. If the eyes are aligned after 2 years of anesthesia – So, I prefer surgical option as it has better
age, there is only a small chance of obtaining binocular predictability.
fusion. They may obtain some degree of peripheral fusion
and gross stereopsis. Motor alignment can be achieved in P. Vijayalakshmi: No.
approximately 2/3 surgical cases.
P.K. Pandey: No.
P. Vijayalakshmi: Many of them get binocular status,
only a few gain stereopsis. Not sure about the stereopsis. R. Kekunnaya: No.
P.K. Pandey: If surgery performed before 2 years, All experts feel that Botulinum toxin probably has no role in
binocularity outcomes are far better. the management of infantile esotropia since results can be non-
predictive.
R. Kekunnaya: Not many. They may have a very gross
stereopsis, in spite of early surgery. C. INTERMITTENT DIVERGENT STRABISMUS
(IDS)
Although no clear statistics are available, experts believe that
if operated early, some patients may gain binocularity although Swati: When would you consider surgery in a case of
results are not encouraging as far as stereopsis is concerned. IDS? What are the factors that inÁuence decision making?
Swati: In a case of Infantile esotropia if surgery is P. Sharma: The indications depend on age of
delayed due to systemic problems or waiting list, would presentation, presenting complaints, fusion range and
you consider occlusion during the waiting period? baseline stereopsis. In children upto 4 years of age, I would
defer surgery till the manifestation is at least 50% of time.
P. Sharma: After having obtained alternation/ equal If stereopsis is assessable I would do that too. I would
vision naturally or by age dependent occlusion, the follow such children 3-6 monthly depending on these
regression of amblyopia is prevented by maintenance parameters to decide for surgery. However in adults an IDS
occlusion which is 1:1 occlusion for a few months, in manifesting for distance and/or having affected distance/
the waiting period. In case of long waiting the child is near stereopsis would be an indication for surgery.
14 l DOS Times - Vol. 17, No. 1 July, 2011
K. Mohan: I consider surgery for IDS if deviation more P.K. Pandey: Distance stereoacuity is known to vary
than 20 PD, frequency of squint more than 50% of waking between 2 examinations hence is not very reliable in
period, suppression on FDT and a stereoacuity less than 60 isolation, I do not have the facility, I use deterioration in
sec of arc on the TNO test. binocular VA as surrogate to Distance stereoacuity.
T.S. Surendran: Surgery helps to preserve or restore R. Kekunnaya: Not really unless the above mentioned
binocular function. I prefer surgery if non-surgical factors are present.
measures (alternate patching, over correcting minus power
lens, base out prism) are not successful and control over Three of our experts believe that the surgery should be
an intermittent exotropia is deteriorating (occurrence of considered if distance stereoacuity is poor or deteriorating. The
deviation is more than 50% per day – Amount of deviation other experts feel that the previously discussed factors are more
does not make a difference). important in decision making.
Age and pre-operative stero are the main factors I Swati: What is your desired postoperative correction
consider – I wait till 4-5 years of age for the surgery. in cases of IDS?
P. Vijayalakshmi: IDS with the following characteristics P. Sharma: In children upto about 5 years age I would
– easily dissociated, either the patient or parents are aware generally aim for under correction. In adults I aim for about
of the deviation, signiÀcant angle of deviation, pattern 10 pd overcorrection.
deviation, even if it is less, confusion or double vision. The
child also should be cooperative for assessment of sensory K. Mohan: My desired postoperative correction in
function in situations when that is going to be the deciding cases of IDS is upto 10 PD esotropia.
factor. Parents should have the capacity to understand
about the surgical outcome including post op double T.S. Surendran: My objective is to achieve 10PD over
vision, consecutive and residual deviations. correct on the day after surgery. I believe that this will
prevent suppression from occurring in the immediate post
P.K. Pandey: Deteriorating control and type of IDS. operative period and also compensate for the exotropic
Those with high AC/A ratio can be managed by minus lens drift. I usually counsel the parents before the surgery, on
therapy and those with fusional convergence insufÀciency the chances of diplopia during the early post operative
can be managed by orthoptic exercises initially. period. If over correction persist more than 2-3 weeks, it
can be managed by occlusion, prisms and miotics.
R. Kekunnaya: Generally around 4 to 5 years of age.
The factors inÁuencing this decision are: P. Vijayalakshmi: Optimum correction or few prism
(less than6 to 8 ) overcorrection, collapse of patterns if any.
• Increasing amount of deviation over a period of time.
P.K. Pandey: It is a mixed bag. A small angle ET for
• Loss or signiÀcant reduction in the fusional control distance with X or ortho for near is usually stable over
(ofÀce based decision with inputs from parents) of long term, amblyopia is a real concern in small children. In
deviation. older children and adults orthotropia should be the aim as
diplopia can be troublesome.
• Psychosocial impact on child.
R. Kekunnaya: On the Àrst postoperative day, I would
Experts feel that surgery should be done if deterioration in target 10 to 15 prism diopters of overcorrection (esotropia).
sensory or motor status is seen. However it is better to try and
defer surgery till 4-5 years of age. All experts agree that up to 10 PD of over-correction is
desired in immediate post operative period.
Swati: Would you consider surgery in a case of IDS
having good fusional control but poor or deteriorating Swati: What are the factors that determine the
distance stereoacuity? restoration of normal stereoacuity in the cases of IDS?
Does good post operative motor alignment ensures
P. Sharma: In studies done by us we have found good superior stereoacuity?
correlation between good fusion control and stereopsis
and vice versa, both for distance and near. In case of poor P. Sharma: The factors that determine the restoration
fusional control especially for near only, we usually give of normal stereoacuity in the cases of IDS are: fair to
convergence exercises and operate if that does not work . good preoperative stereopsis, fusional control and postop
After operating for deteriorating stereopsis we see recovery alignment. Good post operative motor alignment deÀnitely
unless the surgery is too late is more severly affected. ensures superior stereoacuity.
K. Mohan: Yes, if there is poor or deteriorating distance K. Mohan: Patients with a younger age (below 10
stereoacuity, I would consider surgery of IDS. years) and a shorter duration (less than 5 years) of IDS have
more chances of restoration of normal stereoacuity. A good
T.S. Surendran; Distance stereoacuity can be postoperative motor alignment does not ensure a superior
measurted with global Random Dot, contour Circle test of stereoacuity.
the Mentor BVAT II-SG and Frisby-Davis Distance (FD2)
stereotest. Personally I don’t have any experience. Yes if T.S. Surendran: Post operative motor alignment is
distance steroacuity is deteriorating, it needs surgical one of the factors for restoration of the stereoacuity. I
management. personally feel, that the pre operative central fusion is the
most signiÀcant factor in determining the achievement of
P. Vijayalakshmi: We don’t measure the distance normal stereoacuity postoperatively.
stereoacuity per se, but go with the other Àndings and is
individualized. P. Vijayalakshmi: Yes, when there is good sensory
functions detected preoperative.
www. dosonline.org l 15
P.K. Pandey: Stereoacuity is a cortical function based them has been successful on long term follow up. Correction of
on horizontal disparity in Panum’s fusional area, it can be refractive error and amblyopia is of prime importance in these
aided by motor alignment but age has to be favorable. cases to improve the quality of vision.
R. Kekunnaya: A. Appropriate age for intervention. In Swati: Do you think drugs have a role in the
children less than 3-4 years overcorrection may lead on to management of infantile nystagmus syndrome (INS)?
microtropia, which may result in reduction of stereopsis.
Otherwise good postoperative alignment ensures or P. Sharma: Baclofen has been tried succesfully in
maintains good stereo acuity. acquired periodic nystagmus but not in infantile PAN.
Botox,as retrobulbar injection has also been used by some,
Experts feel that the restoration of stereoacuity after surgery but I would not be keen for that.
depends on multiple factors including the age of the patient,
duration of deviation, absence of suppression before surgery and K. Mohan: I think drugs do not have a role in the
postoperative motor alignment. management of infantile nystagmus syndrome. Drugs do
have a role in periodic alternating nystagmus.
D. NYSTAGMUS
T.S. Surendran: People have tried Gabpentin,
Swati: How would like to manage a case of nystagmus Baclofen, oral & topical carbonic anhydrase inhibitor (CAI)
without any null point? and this has showed some beneÀcial effects on measures
of nystagmus foveation quality. I don’t have any personal
P. Sharma: Unfortunately no deÀnite therapy works experience.
for a case of nystagmus without any null point. We have
tried acupuncture, auditory biofeedback, Supramaximal P. Vijayalakshmi: Some drugs like Baclofen and
recession on all four horizontal recti, as well as Hertle Gabapentin work well for acquired nystagmus. The
Dell’Osso procedure. All have short term success. Cases beneÀcial effect lasts only as long as the drug is continued.
with a periodic shifting null do well after Supramaximal Its use in congenital nystagmus is limited by the fact that
recession on all four horizontal recti. Manifest latent long term treatment is needed which automatically puts
nystagmus associated with a deviation also do well after the patient at risk of adverse drug reactions. I rarely use
strabismus surgery. them. I had tried Gabapentin in a couple of patients with
Congenital see saw nystagmus, but there was no beneÀt
K. Mohan: I would consider retroequatorial recession and we eventually stopped the drug. One of my associate
of all four horizontal rectus muscles in a case of nystagmus has tried in 5 patients and only one showed improvement,
without any null point. but still taking it for the past 5 months.
T.S. Surendran: Correction of signiÀcant refractive P.K. Pandey: No.
errors with spectacles or contact lenses in children with
nystagmus is the single most powerful therapeutic R. Kekunnaya: Not really. I haven’t used any drugs in
intervention for improving vision. Base-out prisms to this group.
induce convergence, helps to dampen the nystagmus and
plays an important role in nystagmus management. Drugs do not appear to have a role in the management of
INS.
P. Vijayalakshmi: First we should direct our attention
to optical correction and amblyopia management. Low Swati: How would you manage a case of nystagmus
vision aids may help patients with poor vision. Tinted having a null point in left gaze with left convergent
lenses can be tried in patients with cone-rod dystrophy. squint and left amblyopia?
The results of surgery are not very gratifying. P. Sharma: One should ensure the Àxating eye. In the
Retroequatorial recession (Kestenbaum Anderson situation given the right eye is preferred in adduction as
Procedure) of all the four horizontal recti can be tried. left eye is esotropic and amblyopic, one would have to
Recently Richard Hertle and Dell Osso have proposed recess the Right eye Medial rectus by augmented Anderson
that Tenotomy may work just as well. We have found that recession procedure: 9mm. No recession of Left LR is
these procedures only occasionally improve the Snellen required here! This will also take care of the left esotropia.
Acuity. But there is a marginal reduction in the amplitude If the esotropia is more marked then recession on left MR
of nystagmus and patients report that the quality of vision would also be required.
is better after surgery. Such procedures should be done
only after a careful discussion with the patient. We have K. Mohan: I think, I would consider moving the right
found that the artiÀcial divergence procedure carries a risk eye laterally in this patient.
of inducing a non-fusible exotropia and no longer practice
the same. T.S. Surendran: Amblyopia has to be tackled Àrst
by refractive correction or patching. To tackle the head
P.K. Pandey: Depends upon patient’s symptoms. turn and squint, I used to straighten the head with prism
correction over the preferred eye - like in this case right
R. Kekunnaya: I would Ànd the cause for nystagmus eye is neutralized and then the strabismic deviation is
in all these cases. measured with prism over the Left eye. With that prism
measurement, we can plan for the Recess- resect procedure
I would offer them them low vision aids. And other on each eye.
recommendations to enhance their existing vision.
P. Vijayalakshmi: A few questions Àrst.
Surgically, I offer them tenotomy and re attachment
(rectus muscle) surgery after explaining the beneÀts and • I assume that we are dealing with infantile nystagmus
risks of the surgery (Hertle Dell’ Osso proceduce). syndrome. What is the age of the patient? – we would
consider surgery only when the child is older than six
Various surgical and non-surgical options have been tried years of age.
to treat a case of nystagmus without any null point, none of
16 l DOS Times - Vol. 17, No. 1 July, 2011
• What is the vision? Is there a sensory cause? If the left RMR resection for a leash effect. If further exotropia is still
eye is deeply amblyopic, I would be conservative in present, left LR recession may not only correct the residual
treating the esotropia. exotropia but also improve the ptosis due to Àxation duress
effect.
• Has the optical correction been given?
K. Mohan: I prefer supramaximal recession of the
• Has amblyopia treatment been tried? – If not we would lateral rectus and supramaximal resection of the medial
patch the right eye Àrst. Surgery can be considered if rectus in post-traumatic third nerve palsy without aberrant
amblyopia treatment is not successful after six months regeneration. In addition, I prefer performing transposition
of full time patching. of the superior oblique to the medial rectus insertion to
prevent recurrence of exotropia. I feel periosteal anchoring
• We usually do a VNG prior to surgery. of the medial rectus is a cumbersome procedure.
• What is the angle of esotropia? What is the face turn? T.S. Surendran: The photo appears to show III nerve
Is there a pattern? Any oblique dysfunction? Have the palsy without ptosis. My decision is based upon the
tests for binocularity and stereopsis been done? patients’ desire regarding his disÀgurement, as well as the
level of disability created by diplopia. In our case, since
• The patient has a null zone in left gaze i.e a right face angle of deviation is large, chance of diplopia is relatively
turn with right eye dominance. The right eye can be less. But if patient is bothered about the disÀgurement, then
operated for esotropia and this would take care of the my goal is to improve his appearance and provide a usable
face turn as well. Say the patient has a 30 degree right Àeld of single binocular vision. First goal is achievable and
face turn with 40 degrees of left esotropia - I would do the second goal partially achievable.
recess the right medial rectus by 5mm and resects the
right lateral rectus by 8mm. If the left eye were deeply Counseling is most important in such cases and we
amblyopic, I would be more conservative. need to set realistic expectation to the patient. Surgical
option for III nerve palsy is limited. To improve the
P.K. Pandey: I would like to know whether an abnormal centration of the right eye, I would consider a maximal
head posture is adopted by the patient and whether VA recession of the lateral rectus and resection of the medial
improves by adopting it, whether it is INS or LN/MLN. rectus. As a rule I do not operate on de-enervated muscle
Strabismus surgery can be planned simultaneously or done because the contractile muscle elements are atrophic and
subsequently if required in INS. LN/MLN (fusional mal- therefore typical strabismic surgery is of little or no beneÀt.
development nystagmus syndrome) may improve with However, maximum amount of surgery can produce,
only strabismus surgery Amblyopia will need to be treated increased muscle tension by virtue of stretching the non-
keeping in mind special circumstances of nystagmus. contractile elastic elements. So, the right eye medial
rectus surgery eventually reduces the elasticity of the
R. Kekunnaya: In this situation the right eye is the muscle, tethering the right eye close to primary gaze. Post
driving eye. I would put the prisms in the ofÀce and look operatively if the diplopia is problematic, prism or fogging
for the amount of change in the head posture. Probably I one spectacle lens can be advise.
would do four-muscle (rectus) recession (asymmetrical),
taking care the amount of esotropia. P. Vijayalakshmi: Lateral rectus deactivation with
medial rectus large resection.
Correction of amblyopia should be done before proceeding for
surgery. Correction of both strabismus and face turn can be done P.K. Pandey: It does not seem to be complete 3rd
simultaneously. nerve palsy as IR seems to have recovered partially along
with LPS. We need to know whether pupil is involved,
E. INCOMITANT STRABISMUS is there pseudoptosis is 4th nerve intact and fundus
torsion. There is no single best treatment and moderate
Swati: What is your preferred surgical modality for alignment could bring diplopic images closer and be more
managing a case of post traumatic complete third nerve disturbing with loss of motor fusion due to limitation of
palsy without any aberrant regeneration? (Picture below) motility resulting from unconventionally large surgery and
induced incomitance. Pupillary involvement is invariably
present and aberrant innervation is often found if recovery
has occurred in traumatic 3rd nerve palsies. Surgical
approaches may include surgery on the normal eye and
no consensus seems to be there, as there is no single best
treatment.
R. Kekunnaya: LR weakening and Àxation to the
lateral orbital wall and MR Àxation to MPL.
There appears to be no consensus and no single best treatment
for the management of a case of complete III nerve paralysis. The
surgical decision needs to be individualized according to the
requirement of the patient.
P. Sharma: There appears to be some improvement of Associate Editor
Right ptosis on levoversion so some aberrant regeneration Swati Phuljhele MD
seems possible in this case. But Àrstly one has to evaluate
the FDT in right eye and relieve that. I would do an www. dosonline.org l 17
anchoring of the Right LR to the lateral periosteum and
Grand Rounds
B.P. Guliani
Prof. B.P. Guliani, MS
Department of Ophthalmology, Safdarjung Hospital, New Delhi
Q.1. What is the new terminology for CSR? Q.7. Give the conditions predisposing to subretinal
Àbrin exduation.
Ans. CSCR (Central Serous Chorioretinopathy)
Ans. a) Large and multiple PED’s
Q.2. Who gave the term CSR? b) Chronic and recurrent disease
c) Pregnancy
Ans. Binnel in 1955. d) Systemic use of steroids
e) Organ transplant
Q.3. What are the types of CSR? f) DM
g) Male Gender
Ans. a) Typical / Classic CSCR – mild to mod loss, one
or more focal leaks Q.8. What is the natural course of CSCR?
Ans. - 95% of cases spontaneously resolve to base line
b) Diffuse retinal pigment epithelopathy/
decompesnsated RPE/ Chronic CSC. vision within 3 to 6 months.
- 5% of cases have persistent and progressive
Chronic shallow SRF, RPE pigmentation
altered, chronic cortiocosteroid use. detachment and visual loss.
- 1/3 rd to ½ of patients have recurrences after
c) Bullous retinal detachment (INF>SUP).
1st episode.
Q.4. How do you deÀne CSCR? Q.9. Which patients are at a greater risk of visual loss?
Ans. a) Large PED’s
Ans. Active CSCR is characterized by detachment of
neurosensory retina caused by accumulation of b) Multiple recurrences
serous Áuid between the photoreceptor outer c) Multiple leaks
segments and RPE in combination with monofocal d) Dependent neurosensory detachment.
or multifocal changes in RPE. e) Subretinal Àbrin deposits.
Q.10. What are the Complications of CSCR?
Q.5. What is its Pathogenesis? Ans. a) CNVM
b) Paifoveal RPE perifoveal RPE atrophy
Ans. 1. RPE dysfunction theory c) Cystoid macular deposition/oedema.
Q.11. What are the Sequelae of CSCR?
2. Choiroid dysfunction theory Ans. a) Subretinal Àbrosis
b) Fibrotic scar especially with treatment with
Q6. What are the Clinical signs of CSCR?
steroids
Ans. a) Halo of light reÁex delineating the area of c) Peripheral dependent bullous neurosensory
neurosensory detachment.
detachment.
b) Multiple yellow while dot like deposits which d) Retinal pigment atrophic tracts.
cover the posterior surface of detached retina. e) Pigment migration atrophy
c) 1. PED’s/single & multiple.
2. Pink halo surrounding the PED is shallow
detachment of retina.
3. Presence of Àbrin in sub RPE/subretinal
space.
This may dissolve or may polymerize
causing oval yellow/grey membrane and
opaciÀcation of SRF.
d) Subretinal Àbrosis/Àbrotic scar leading to
permanent visual loss.
www. dosonline.org l 19
f) RPE tear - Late phase hyperÁourescence centrifugal in
g) Cystoid retinal changes detached area late phase.
h) CME
i) Subretinal lipid deposition - Hyperpermeability is quite diffuse even if
j) CNVM patient is asymptomatic.
k) Choriocapillary atrophy
Q.12. What is the cause of peripheral bullous Q.16. How will you differentiate between ill deÀned
neurosensory detachment CNV from diffuse CSCR.
Ans. Increase in exudation.
Q.13. What are the Systemic conditions associated in Ans. By ICG.
CSCR?
Ans. a) Pregnancy Q.17. What is the role of photocoagulation in CSCR?
b) End stage renal disease patient on
Ans. - Typically shortens the course of disease by
corticosteroids accelerating desorption of Áuid.
c) Organ transplantation
d) SLE - No effect on Ànal visual acuity.
e) Increased endogenous cortisol production
f) Endogenous mineralocortecoids - Some experts say that it reduces recurrence
g) Use of inhaled nasal corticosteroids rate.
h) Systemic corticosteroids use/treatment
i) Epidural corticoid injection Q.18. What are the Indications for LASER
j) Type a personality photocoagulation?
k) Migraine/Histeria/Neurosis
Q.14. What are the Differential diagnosis of CSCR? Ans. - Persistence of serous detachment for more than
Ans. a) POHS 3 months
b) CNVM
c) Harada’s disease - Recurrence in eyes with visual deÀcit from
d) Sympathetic ophthalmits previous episodes.
e) Choroidal hemangioma
f) Choroidal metastasis - Presence of permanent visual deÀcit from
g) Leukeamic inÀltrates. previous episodes in fellow eye.
Q.15. What are the Picture/Àndings on ICG in a case of
- Development of chronic sings i.e. cystic
CSCR? changes in neurosensory retina & widespread
Ans. - Choroidalvascular hyperpermeability espe- RPE abndmalities.
cially in mid phase - Occupational or other patient needs that
require prompt visual restoration.
Q.19. What parameters will you use for LASER
photocoagulation?
Ans. Spot size 50 to 200 Pm
Time = 0.1 to 0.2 sec.
End point – blanching without whitening of outer
retina.
Q.20. What is the Role of PDT in CSCR?
Ans. Juxtrafoveal lesion.
- Subfoveal lesion.
- Lack of clearly deÀned leakage spot.
- Concern about potential of CNV.
20 l DOS Times - Vol. 17, No. 1 July, 2011
Question From Figures
Figure 1 Figure 1a & 1b
Figure 1
Qns. What is A & B
Ans. A = PED
B = Neurosensory detachment
Figure 1A, 1B
Qns. What is 1 and 2 (in 1A) and 3 and 4 (in 1B).
Ans. 1. Hyper Áuorescence due to PED
2. Smoke stack sign of characteristic of CSR
3. Increasing Áuorescence in sub retinal space in
umbrella fashion
4. Staining of sub retinal Áuid and back of
neurosensory detachment.
Figure 2A & 2B
Qns. What is 3,4 in sequence Figure 2A, 2B?
Ans. Shows increasing intensity of mottled hyper
Áuorescence. This is due to staining of choroidal lesion
in chronic and recurrent CSR.
Figure 2a & 2b
www. dosonline.org l 21
Figure 3
Qns. What is 1 and what is your diagnosis in the given
macular OCT?
Ans. 1. Is Subretinal Áuid
The diagnosis is neurosensory detachment due to CSR.
Figure 4
Qns. This is a case of CSR? Comment upon the OCT and
discuss various treatment modalities of CSR.
Figure 3 Ans. This is serial OCT of a patient. After observing for three
months there is progression. Intervention by Laser has
resolved the CSR. For other modalities see question-
answer.
Figure 4
Figure 5
Figure 5 Figure 6
Qns. What is 1 in Figure 5 and what is your diagnosis?
Ans. Fibrin deposit and the diagnosis is chronic CSR. 2. Is PED / a defect in RPE
Figure 6 Qns. What is your conclusion?
Qns. What are 1 and 2 and what is your conclusion? Ans. Progressing CSR .
Ans. 1. Is Àbrin deposit on the back of neurosensory
detachment Neurosensory
22 l DOS Times - Vol. 17, No. 1 July, 2011
History of Ophthalmology
G. Mukherjee
G. Mukherjee, MBBS, MD, DOMS, ZO, FICS
Mukherjee Eye Clinic C.R. Park Extension, New Delhi
Past President (1998-2999), Past Secretary (1976-1978), Editor
DOS (1988-1990), DOS Representative to AIOS (1999-2002)
Delhi Ophthalmological Society (DOS) was formed with the initial years the AIOS conference was not held regularly
the primary objective of promoting dissemination of every year and only after the 1948 meeting in Delhi did the
knowledge in the Àeld of ophthalmology and promote a society organize the meetings annually.
feeling of brotherhood amongst fellow members. Though
the society had very humble beginnings and faced great The birth of Delhi Ophthalmological Society (DOS) is
challenges in its initial years, today DOS is the second largest intimately connected with the 9th AIOS conference held at
ophthalmic society in the country and is second only to the Delhi in 1948. The All India ophthalmological society had
All India Ophthalmological Society (AIOS). only 213 members on record. A small group of Delhi based
ophthalmologists had to work hard to make the conference
The history of DOS is closely related to the AIOS history a success. A few of them had migrated from the then
so it will not be out of place to put few words about the West Pakistan. The organizing Committee faced immense
origins of AIOS. The idea of forming AIOS was conceived by problems due to the assassination of Mahatma Gandhi on
Dr. George Zachariah (Madras), Dr. R.P. Ratnakar (Bombay) 30th January as the conference was scheduled to be held on
Dr. B.G.S. Acharya (Lucknow) Dr. Kugelberg (Tirupattar) 11th February, less than a fortnight of this national calamity.
and Dr. S.K. Mukherjee (Calcutta) and the society was The AIOS conference had to be postponed by a month and
formed on 16th February 1929. Delhi was lucky to host the it was even suggested to cancel the conference in view of
1st post Independence AIOS conference in the year 1948. In the prevailing circumstances in the country. It required
DOS Group Photograph 1976 - 1977
Sitting from (R - L) Dr. R.N. Sabhrawal, Dr. A.R. Sethi, Dr…, Dr…, Dr. L.P. Agarwal, Dr. Pratap Narain (President),
Dr. R.N Mathur (Guest Speaker) Dr. Tejpal Saini, Dr. N.S. Singhal, Dr.(Brig) R.C. Sharma, Dr. R.C. Agarwal
Dr. Madan Mohan, Dr. Mrs. M. Krishna Mathew
Standing in 1st Row (R - L) Dr. G. Mukherjee (Sectary), Dr. Jatinder Nath, Dr. M.S. Ravindra
Dr. N.K. Patnaik, Dr. ……, Dr. ……… Dr. N.L. Vaish, Dr. O.N. Krishna
Dr. B. Patnaik, Dr. P.K. Khosla, Dr. P.R. Karwal, Dr. Madhu Kwatra, Dr. Indrani Dasgupta, Dr. Satish Sabharwal
Standing 2nd Row (R - L) Dr. Vijay Sabharwal, Dr. Amitava Majumdar, Dr. ……, Dr. J.C. Das, Dr. Satinder Sabharwal,
Dr. …….., Dr. Dipak Sachdeva, Dr. H.K. Tiwari, Dr. Rajinder Kalsi, Dr. Subhash Goswami, Dr. R.P Sachdeva,
Dr. I.K. Bhatia, Dr. D.K. Mehta, Dr. Col. P.C. Padhi, Dr. …....
www. dosonline.org l 23
great courage on the part of late Dr. S.P. Shroff (Father of Membership was also extended to the neighboring states and
Dr. Minoo Shroff) and Late Dr. S.N. Mitter, doyens of Delhi Dr. Mohan Lal from Aligarh, Dr. Victor C. Rambo from CMC
Ophthalmology and a band of very dedicated active workers, Ludhiana and few others joined the society.
who decided to hold the conference in spite of adverse
circumstances. At that point of time there was no ophthalmic Monthly Clinical Meetings
society in Delhi. A reception committee was formed with Dr.
S.N. Mitter as organizing secretary and Dr. Tejpal Saini as In Late Fifties Monthly clinical meetings were started at
assistant secretary. All the Ophthalmologists of Delhi became hospitals by rotation on invitation. The meetings were held
members of the organizing committee. Dr. Mohan Lal from on the last Saturday of the month in the afternoon. Cases of
Aligarh founder of Mohan Eye Hospital Presently known clinical interest were presented (like live bed side evaluation)
as Gandhi Eye Hospital, contributed a lot for the success of and discussed. Occasionally other types of academic materials
conference. like clinical talks were presented by local ophthalmologists.
Once in a while distinguished ophthalmologists visiting
The All India Conference was a great success. The winding Delhi from other states were invited to deliver clinical talks.
up Ànal meeting of the Reception Committee was held on Post clinical meeting refreshments were managed through
4th, May 1948 and there was net saving of Rs. 36.75. Some voluntary contribution from consultants working in that
suggested having a party as it was a handsome sum in hospital. Minutes of the meeting including brief description
those days (Annual dinner subscription used to be Rs. 5 of academic material presented were noted by the secretary
to 6 only). Another view was to send the money to the All and were read in the next monthly meeting.
India Ophthalmological Society. The organizing Secretary,
Dr. S.N. Mitter suggested that as the local Ophthalmologists The turning point in the history of DOS came with addition
has shown great enthusiasm and keen interest in joining of few more teaching hospitals in Delhi like AIIMS, MAMC,
hands together and it would be in the Àtness of things that UCMS and their faculty and post graduate students started
this tempo is maintained and the members present decided taking active interest in DOS academic activities. The
to form the Delhi Ophthalmological Society with Rs. 36.75 as membership started to increase and by the year 1990 it was
the funds of the society. This suggestion was received with 265.
great enthusiasm and unanimously approved. History was
created on 4th May, 1948. DOS was thus born. Later a special Bodhraj Sabharwal memorial running trophy was instituted
meeting was held under the chairmanship of Late Maj. (Rtd.) for the Àrst time in 1976 for Best monthly clinical meeting
K.N. Tandon at his residence of Barakhamba Road. Reception held in a year. Many more such awards were added later.
Committee members were enrolled as founder members. Dr.
Tej Pal Saini was elected as convener of the society. Dr. D.D. Mid-term
Kapoor, Dr. D.C. Loomba and Dr. Bodh Raj Sabharwal were
requested to draft the constitution. The DOS Mid-term conference started in 1987 as a half day
Mid-term Symposium on infective keratitis. Subsequently
The Àrst dinner cum meeting was hosted by Dr. Harsukh Rai this changed to a whole day programme and now has
at his residence on Boulevard Road near Tis Hazari Court. increased to a two day conference. The Mid-term dinner
The meeting was attended by 13 members namely Dr. Bodh was added from year 1998 Golden Jubilee to increase social
Raj Sabharwal, Dr. Raja Ram, Dr. Ram Lubhaya, Dr. Harsukh interaction amongst members and their family.
Rai, Dr. S. Devichand, Dr. Umrao Singh Mudgal, Dr. S.B.
Mathur, Dr. S.P. Srivastava, Dr. B.R. Gupta, Dr. D.C. Loomba, Annual Conference
Dr. (Major) H.L. Anand, Dr. S.N. Mitter and Dr. Tej Pal Saini.
Dr. S.N. Kaul could not attend but authorized Dr. Mitter to The Annual Conference of DOS was started in the late Àfties,
put forward his views. with half a day meeting on Sundays in the lecture theater of
a hospital. With increase in the membership and addition
The Constitution of the Society was adopted at the meeting. of more number of academic institutions, DOS started to
DOS Constitution that we have today was formed in the year have a full day long conference with an annual dinner in
i.e. 1948 though many changes have being made from time the evening. Thus DOS annual meeting changed to annual
to time as and when required. The Àrst Executive Committee conference. DOS started inviting Guest speaks from other
was elected as under: states from 1977 after the society got afÀliated to AIOS and
travel assistance was given by the AIOS.
President : Dr. Harsukh Rai
DOS Library
Vice President : Dr. K.N. Tandon
DOS Library started way back in early nineteen sixties, with
Secretary cum Treasurer : Tej Pal Saini very few books and journals, mostly donated by members.
There was no library room and the books were kept in the
Members : Dr. B.R. Sabharwal secretary’s ofÀce. Books were taken by secretary to the venue
of monthly clinical meeting every time. This system went on
Dr. B.R. Gupta for almost three decades. In 1971-72 when Dr. S.R.K. Malik
was president of DOS he collected donations from members
Unfortunately due to prolong illness of Dr. S.P. Shroff and and purchased few more text books and subscribed to BJO,
active member like Dr. S.N. Mitter leaving Delhi to take up AJO and Archives of Ophthalmology. The post of library
assignment as HOD ophthalmology at K.G. Medical College ofÀcer was created in late eighties.
Lucknow, the society had to face teething problems and
few setbacks in its initial years. In the Àfties DOS was like DOS Times
a very small family. The society started organizing monthly
clinical meeting at Shroff’s Eye Hospital (Daryaganj), Irwin DOS Times started as DOS bulletin some time in 1986.
Hospital (Now L.N.J.P.) and in the residences of some of the The aim of this bulletin was to update members about
members. Membership drive was actively carried out by Dr. what is happening in ophthalmology academically and
Tej Pal Saini, Dr. Bodhraj Sabharwal and few other members. other ophthalmology related news. In the initial phase the
24 l DOS Times - Vol. 17, No. 1 July, 2011
publication was irregular but in a short time all problems 10. Delhi Journal of Ophthalmology (DJO) – 1997.
were solved and it became a regular publication.
11. DOS entered cyberspace in – 1998.
Delhi Journal of Ophthalmology (DJO)
12. DOS Golden Jubilee Cellebration – 1998.
The Delhi Journal of Ophthalmology (DJO) started as a DOS
news letter in 1993 and was named as VISICAN. Earlier 13. DJO Indexing process begins– 2010
issues of VISICAN used to have necessary information along
with few scientiÀc articles. With the increasing popularity of International Conferences held under aegis of DOS at Delhi.
VISICAN more and more of scientiÀc articles started coming
from members, so the DOS bulletin was changed to Journal 1. 19th International Congress of Ophthalmology – 1962
of DOS in the year 1995, name remained as VISICAN. In the
year 1997 a full Áedged DOS Journal was published as DJO. 2. 10th Congress of Asia PaciÀc Academy of Ophthalmology
With opening of DOS cyberspace DOS Times and DJO were – 1985
put on the web.
AIOS Conference held by DOS
Membership
1. 9th AIOS Conference 1948
Membership started with 13 founder members of DOS in
the year 1948. Membership increased at a slow pace initially 2. 31st AIOS Conference 1971
and there were 118 members in 1976, which increased to 450
members in 1993. Subsequently there was an increase in the 3. 50th Golden Jublee Conference 1992 (Dr. Harimohan,
membership with addition of more members not only from Chairman & R.B.Jain Secretery)
neighboring states but also from far off places. The present
membership is 6103, and is second only to the AIOS. 4. 55th AIOS Conference 1997
Proud Moments 5. 61st AIOS Conference 2003
Golden Jubilee of DOS was celebrated in the year 1998 Awards Trophies, Orations and prizes of DOS
with Dr. G. Mukherjee as President and Dr. Lalit Verma as
Secretary. Series of Lectures were organized as to mark the In order to improve the standard of academic meetings and
event and were delivered by distinguished DOS members. improve the quality of scientiÀc material a large number of
All lectures were memorial lectures in the name of notable trophies, awards, orations etc. were instituted from time to
DOS members eg : Dr. R.K. Seth memorial lecture, Dr. S.N. time. It started with Dr. Bodh Raj Sabharwal running Trophy
Mitter memorial lecture, Dr. S.R.K. Malik memorial lecture –in 1976 – 1977.
and Dr. Tej Pal Saini memorial lecture. Dr. S.N. Mitter oration
was instituted. DOS entered cyberspace in the golden jubilee A. Trophies
year.
1. Dr. Bodh Raj Sabharwal Running trophy for Best
DOS credit rating system (DCRS) was started for the beneÀt Monthly Clinical Meeting – 1976 – 1977
of members. A full day mid-term conference was organized
followed by a conference dinner for the Àrst time. DOS Dr. Bodh Raj Sabharwal was one of the 13 founder
fellowship to attend conference (national and international) members of DOS.
was initiated during this time to encourage younger DOS
members to present their research work in national and 2. Dr. Krishna Sohan Singh Trophy – for best Clinical
international forums. Talk in Monthly Clinical Meeting – 1977 - 1978
DOS Member time and again made their presence felt not 3. Dr. H.S. Trehan Trophy – for best Case Presentation
only at national but also at international forum in various in monthly clinical meeting.
capacities. Numerous of our members have been awarded
the National “Padma Award” the Dr. B.C Roy National Dr. H.S. Trehan was president of DOS in the year
award, American academy achievement award and many 1960-61. He was a versatile ENT and eye surgeon
more awards. in central Delhi
Land marks in DOS History 4. Dr. A.C. Agarwal Trophy – for best Free Paper
Presentation in Annual Conference.
1. Foundation Day 4th May - 1948.
5. Dr. T.P. Agarwal Trophy – for best free paper on
2. 1st DOS Constitution - 1948. Cornea in Annual Conference.
3. DOS AfÀliation to AIOS - 1976 Dr. T.P. Agarwal was a faculty in the Dept. of
Ophthalmology Pondicherry and Goa. He started
4. DOS Insignia designed - 1977 his private practice in Meerut and was the founder
Director of Agarwal eye Institute, Meerut.
5. Bodh Raj Memorial running Trophy as 1st Academic
award - 1976. 6. Dr. V.K. Kalra memorial Trophy for Quiz winners
in Annual Conference.
6. DOS Bulletin – Now DOS Times - 1986.
Dr. V.K. Kalra was a faculty at the Dr R P Centre
7. DOS Registration with Registrar Society – 1987 for Ophthalmic Sciences and was a very active
academician with a great clinical knowledge.
8. 1st Mid-term Conference – 1987.
7. Dr. Minoo Shroff Trophy for Most Pupular
9. VISICAN as quarterly Journal of DOS – 1993. Monthly meeting.
Dr. Minoo Shroff was a one of the trustee of Shroff
charity eye hospital, Daryaganj and foundry
Director of Shroff eye centre, Delhi.
www. dosonline.org l 25
(The names in red are some of the Past Presidents of DOS)
Dr. S.N.Mitter Dr. Tejpal Saini Dr. S.P. Shroff
Founder Member 1st Sectary of DOS Founder Member
Golden Jubilee Lecture
Dr. Hari Mohan
B. Orations awarded in Annual Conference of DOS Hony Surgeon to Mahatma Gandhi and President
of India.
a) Dr. P.K. Jain Oration. He was President in the year
1990 – 1991 and a well known private practioner. c) Dr. Omprakash Oration.
b) S.N. Mitter Oration He was one of the founder C. Life time achievement award started in the year 2008:
member of DOS. He was president in the year Awarded to two distinguished DOS member every year
1959 – 1960 and was Organizing Secretary of the at the Annual Conference.
9th AIOS Conference in Delhi. It was his idea D. Dr. R.N. Sabharwal Gold Medal for 100% attendance in
to form the Delhi Ophthalmological Society in monthly clinical meeting.
the year 1948. He was the Head of Department
of Ophthalmology at the King George Medical E. CertiÀcate of merits are awarded in various categories
College, Lucknow, Irwin Hospital, Delhi and and super specialties.
26 l DOS Times - Vol. 17, No. 1 July, 2011
AIOS President from DOS Acknowledgement
Facts Collected From:
DOS has given 12 AIOS presidents so far with many more to
come in the future:- 1. Personal Communication with other member.
Dr. S.N. Kaul (1938) 2. Souvenir of golden jubilee conference AIOS 1992.
Dr. V.C. Rambo (1958)
Dr. L.P. Agarwal (1977) (i) Article by Late Dr. B. Patnaik.
Dr. Madan Mohan (1988)
Dr. S.K. Malik (1989) (ii) Article by Late Dr. Tejpal Saini, Founder DOS
Dr. P.K. Khosla (1955) Sectary.
Dr. D.K. Sen (2003)
Dr. H.K. Tewari (2004) 3. Souvenir of golden jubilee conference of DOS article by
Dr. R.B. Jain (2006) Dr. Satish Sabharwal.
Dr. K.P.S. Malik (2008)
Dr. R.V. Azad (2010) 4. Annual reports of DOS presented by ofÀcial bearer from
Dr. A.K. Grover (2011) time to time since 1976.
Venue: Auditorium, PGIMER, Dr. R M L Hospital, New Delhi
Entry from Old R.K. Ashram Marg
Date & Time: 31st July 2011 (Sunday) 11:00 a.m.
BREAKFAST & Registration 10:00 a.m. - 11:00 a.m.
Clinical Session: 11:00 a.m. to 1 p.m.
Clinical Cases: : Dr. O.P. Gupta
1. Bilateral Endogenous Endophthalmitis
2. Schwannoma of Trigeminal Nerve : Dr. Shikha Jain
Clinical Talk: : Dr. Rachna Meel
Management of Retinoblastoma
Mini Symposium: Time for a paradigm shift in MICS
Chairperson: Professor Shashi Vashisht
1. Zero Phaco MICS, The HACC Technique : Dr. V. Krishna
2. OCTOPUS: Our CMICS Technique of One Percent Ultrasound : Dr. Taru Dewan
3. CALIBCHOP Technique for a safe and effective vertical chop using
: Prof. Praveen Malik
a calibrated Phacotip
20 Early Bird Prizes
www. dosonline.org l 27
Oculoplasty
Pankaj Gupta
Pankaj Gupta MS, Nishant Nawani MS
Department of Ophthalmology PGIMER, Chandigarh
Ocular adnexal and orbital infections are divided into
preseptal and orbital cellulitis. This classiÀcation
has prognostic as well as therapeutic importance. Orbital
abscesses including subperiosteal abscesses are less common
than cellulitis. Preseptal cellulitis and orbital cellulitis
are potentially sight and life threatening conditions that
need prompt management. Better understanding of the
pathophysiology and diagnostic modalities has contributed
signiÀcantly to better management of such conditions.
Surgical anatomy of orbit
The orbital septum is a strong fascial structure that is attached Figure 2: Diagram showing the surgical spaces of orbit
to the superior orbital rim in the upper eyelid and inferior
orbital rim in the lower eyelid. The orbital septum divides thinnest portion of the medial orbital wall, also called lamina
the orbit and the preseptum (Figure 1). The line of fusion papyracea. Multiple other defects are found in the lamina are
of the septum with periosteum at the orbital rim is known known as Zuckerkandl’s Dehiscences. This combination of
as the arcus marginalis and serves as barrier to spread of thin bone, numerous neurovascular foramina, and multiple
infection. In the upper eyelid, the orbital septum fuses with naturally occurring bony defects allows easy passage of
the levator aponeurosis and in the lower eyelid it inserts into infectious material between the ethmoidal air cells and the
capsulopalpebral fascia and inferior tarsal border. The orbital subperiosteal space medially.1 The most common location of
septum serves similar function in the lower eyelid as well. The a subperiosteal abscess secondary to acute sinusitis is along
orbit has four surgical spaces (Figure 2), namely the intraconal the medial orbital wall. The relatively loose adherence of
space, extraconal space, subperiosteal space and subtenon the periosteum to the bony orbit anteriorly allows abscess
space. The orbit is closely related to paranasal sinuses; material to move easily superiorly, inferiorly, and laterally
superiorly with the frontal sinus, medially with the ethmoid within the subperiosteal space. The venous drainage of the
sinus and inferiorly with the maxillary sinus (Figure 3). The middle third of the face and the paranasal sinuses is primarily
orbit is lined with periosteum which is loosely adherent to through the orbital veins (Figure 4) that are valveless and then
bones anteriorly and much more Àrmly adherent posteriorly. inferiorly through the pterygoid plexus or posteriorly to the
The periosteum also serves as protective barrier to spread of cavernous sinus that may get involved in orbital infections.
orbital infections. Numerous nerves and vessels perforate the
Etiology
Figure 1: Diagram showing the relationship of orbital septum with Table I outlines the etiology of orbital cellulitis in various
eyelids and orbital structures age groups. The commonest etiology of orbital cellulitis is
extension from adjacent periorbital structures. Upto 90%
of all cases of orbital cellulitis are caused by spread from
paranasal sinusitis2–6 with spread from ethmoid sinusitis
being the commonest followed by maxillary sinus, frontal
sinus and sphenoid sinus. Childhood infections such as
facial erysipelas and impetigo can lead to orbital infections
owing to retrograde outÁow through orbital veins and septic
thrombophlebitis. Untreated infections from hordeolum and
dacryocystitis have also been reported to be responsible for
orbital cellulitis. Odontogenic infections can lead to paranasal
sinusitis and subsequent orbital infections.
www. dosonline.org l 33
Table I
Etiology of orbital cellulitis in different age groups
Age group Etiology
Neonates (up to 1 month)
Ruptured dacryocele
Infants and toddlers Untreated blepharo-
(1 month to 5 yrs) conjunctivitis
Sinusitis
Respiratory tract
infections
Children (5yrs-15yrs) Sinusitis
Dental abscess
Adults Sinusitis
Orbital trauma
Dental abscess Figure 4: Diagram showing venous drainage of orbit
Endogenous secondary
to debilitation of orbital inÁammations (Figure 5) and does not indicate
the temporal progression of the disease process from one
type to another. A simpliÀed classiÀcation was given by
Jain and Rubin1 that classiÀed orbital inÁammations into 3
types: preseptal cellulitis, orbital cellulitis and orbital abscess
(Table III).
Preseptal cellulitis is inÁammation of tissues anterior to the
orbital septum. Some authors have used the term periorbital
inÁammation for this entity; however, the term preseptal
cellulitis is preferred over periorbital inÁammation. Orbital
abscesses can arise denovo from preexisting orbital cellulitis
or a subperiosteal abscess can rupture into the orbit and lead
to formation of orbital abscess. Cranial complications can
accompany any of these entities though it is most commonly
associated with orbital cellulitis secondary to frontal sinusitis.1
Figure 3: Diagram showing the relationship of orbit with Epidemiology
paranasal sinuses a) maxillary sinus b) ethmoidal bulla
Infections of the adnexa and orbit are commoner in children
c) ethmoid sinus d) frontal sinus e) uncinate process than adults. Preseptal cellulitis is more common than any
f) middle turbinate g) inferior turbinate h) nasal septum form of orbital cellulitis or abscess. Uzcategui found an
incidence of 84% for preseptal cellulitis versus 16% for orbital
Exogenous causes of orbital cellulitis include penetrating cellulitis in their study of 101 patients of orbital and adnexal
trauma to the orbit or blunt trauma resulting in orbital inÁammations.12 Spires and Smith reported prevalence of
fractures that can result in direct communication with an preseptal cellulitis to be 93.8% among pediatric patients
adjoining sinus with bacterial inoculation. Displaced bony having orbital and adnexal inÁammation.13 The median age of
fragment from an orbital Áoor fracture can block the ostium of children admitted due to orbital cellulitis secondary to sinusitis
the maxillary sinus, leading to concurrent sinusitis and orbital has been reported to be 4 to 14 years.1, 14, 15 There is no deÀnite
cellulitis. Orbital foreign bodies, especially contaminated sex predilection although slight female preponderance was
metallic and wood fragments, must be ruled out in cases of reported by Uy and Tuano.14 The condition is commoner in
penetrating trauma. Any orbital or periorbital surgery can winters when frequency of sinusitis increases.
lead to orbital cellulitis. Orbital cellulitis is rare complication
of strabismus surgery and scleral buckling procedures. Other Microbiology
less common causes are endogenous spread of infection from
bacterial endocarditis or other infections elsewhere in the As the commonest cause for orbital cellulitis is sinusitis, the
body7 and spread from panophthalmitis.8 microbiological Áora associated with orbital cellulitis and
orbital abscesses depends on the bacteriological etiology of
Classification sinusitis. Harris discussed the variation in bacteriology and
response to treatment of subperiosteal abscess of the orbit
Hubert categorized the orbital complications of sinusitis9 depending upon the age of the patient.16 In his series, Harris
in 1937. This categorization was modiÀed by Smith and noted that no anaerobes were isolated from the drainage
Spencer10 and later revised by Chandler11 in 1970. The cultures of children younger than 9 years.16 The pathogenic
resultant classiÀcation, given in Table II, describes the types constituencies in younger children were simpler in general,
with single aerobes recovered from 4 of the 6 culture-positive
patients aged 9 years or younger. In contrast, all patients older
34 l DOS Times - Vol. 17, No. 1 July, 2011
Table III Figure 5: Diagram showing Chandler’s classiÀcation
Jain and Rubin’s classification of orbital inflammations of orbital inÁammations
1. Preseptal cellulitis
2. Orbital cellulitis (with or without intracranial
complications)
3. Orbital abscess (with or without intracranial
complications)
• Intraorbital abscess
• Subperiosteal abscess
than 15 years had polymicrobial, mixed aerobic and anaerobic reported to be as high as 80% in children with preseptal
infections. Although the reasons for these age-associated cellulitis.19 The incidence of orbital and preseptal cellulitis
differences are not entirely clear, anatomical factors probably due to Hemophilus influenzae has decreased dramatically
play an important role. With increasing age, the sinus cavities over the last few decades, probably owing to widespread
enlarge markedly, but the ostia remain approximately the immunization.20 Hemophilus influenzae type b is no longer
same size.17,18 Relative to the cavities they must drain, the a significant pathogen in periorbital or orbital cellulitis,
ostia of young children are wide, and those of older children and management should be modified ac cordingly.
and adults are narrow. The relative width of ostia in young
children partially explains the greater incidence of acute Shuttleworth mentioned that when a preseptal cellulitis
sinusitis in this age group, as frequent upper respiratory presents after a local trauma, the most common organisms
infections tend to involve the nose and sinuses as a single are Staphylococci or beta-haemolytic Streptococci, whereas
structure. The same relative proportions between sinus Haemophilus influenzae usually is associated with an upper
ostia and cavities may prevent severe derangement of the respiratory tract infection.21
physiology and promote rapid resolution. Chronic sinusitis,
for example, is relatively rare in patients younger than 16 Clinical Features
years.
Preseptal cellulitis
The frequency of anaerobic isolates increases with the mean
age of patients. Harris16 speculated that younger children The condition is diagnosed on clinical grounds. The patients
rarely achieve strict anaerobic conditions in their sinuses, usually present with swelling and congestion of eyelids with
whereas older children and adults are prone to more complete difÀculty in opening the eye (Figure 6). The adjacent part of
sequestration and more complex infections, even with a brief cheek and eyebrow region may also be involved. Since there
duration of symptoms. The most commonly isolated bacterial are no discreet barriers in the soft tissues over the nasal bridge,
agents causing sinusitis are Streptococcus pneumoniae, other inÁammatory Áuid seeps across the nasal bridge and causes
streptococci, Staphylococcus aureus, Haemophilus inÁuenzae, and edema of eyelids of the uninvolved side. There is however,
non-spore-forming anaerobes. Anaerobic organisms include no proptosis or any other signs of orbital involvement.
Peptostreptococcus, Veillonella, Bacteroides, Fusobacterium, and Symptoms include pain and swelling of the affected eyelids,
Eubacterium. conjunctival congestion, watering and occasionally fever
that may be mild to moderate. Visual acuity is normal and
Other gram-negative organisms such as Pseudomonas, so are the extraocular movements. The condition needs to be
Klebsiella, atypical mycobacteria, Mycobacterium tuber- distinguished from viral blepharoconjunctivitis and severe
culosis, and Eikenella corrodens have also been isolated allergic dermatitis.
from orbital infections. Polymicrobial infections are
common. No clinical feature distinguishes the sinusitis Orbital cellulitis
caused by one organism from another. In young children,
Streptococcus pneumoniae is the most common sinusitis The most distinctive features of orbital cellulitis are proptosis
pathogen. Some decades ago, Hib bacteremia was and limitation of ocular motility (Figure 7). Variable signs
include conjunctival chemosis, orbital pain, reduced visual
acuity, and afferent pupillary defect. The onset of infection
www. dosonline.org l 35
Figure 6: Clinical photograph of patient with Figure 7: Clinical photograph of patient
preseptal cellulitis with orbital cellulitis
is usually acute and is characterized by headache, fever, nasopharyngeal cultures. However, predominant or resistant
eyelid edema, rhinorrhea, and increasing malaise. A organisms obtained from the latter sites may offer a clue to
minority of patients present with profound visual loss or the infectious etiology.
even blindness when Àrst seen. Intraorbital and subperiosteal
abscesses cannot possibly be detected on the basis of clinical In the past, plain radiographs were performed looking for
examination alone. The patients with orbital cellulitis mucosal thickening or sinus opaciÀcation but their value is
usually present with axial proptosis while the patients with of doubtful signiÀcance as reports have failed to demonstrate
subperiosteal or orbital abscess may present with non-axial the correlation between opaque sinuses and infection.6, 23
proptosis. The differential diagnosis includes neoplasms like Ultrasound is another imaging modality used to assess the
orbital leukemia, Burkitt’s lymphoma, rhabdomyosarcoma presence of infection posterior to the septum. It has the beneÀt
and other orbital malignancies; thyroid associated of not exposing these young patients to ionizing radiation.
orbitopathy; post-traumatic hematoma; orbital cysticercosis There are few studies to support the use of daily orbital
and idiopathic non-speciÀc orbital inÁammation. sonography to aid early diagnosis in paediatric patients.24
Mair et al., reported that the examination was tolerated well
Masquerade syndrome in the paediatric age group without the need for sedation,
however they did point out that this modality is insufÀcient
There are certain conditions that mimic orbital cellulitis to evaluate the orbital apex, paranasal sinuses or intracranial
closely and at times may be clinically indistinguishable from involvement. CT is the most widely used modality for
orbital cellulitis. Such conditions include retinoblastoma, evaluating orbital infections. It allows differentiation of
non-speciÀc idiopathic orbital inÁammation, and orbital preseptal from orbital cellulitis. The diagnosis of the latter
lymphoma among others. condition is conÀrmed if concurrent sinus disease is present
and the extent of sinus involvement can be easily deÀned. A
Aside from a thorough history and physical examination, subperiosteal abscess has a characteristic convex-appearing,
laboratory and imaging studies are crucial in narrowing the elongated shape between the rectus muscle and ethmoid
differential diagnosis of orbital cellulitis and in determining sinus, separated by a thin rim of orbital fat (Figure 8). True
its proper management. The role of ancillary tests in preseptal orbital abscesses may be extraconal or intraconal and are seen
cellulitis is less clearly deÀned. However, additional with proptosis. “Patchy enhancement” of the intraconal fat in
diagnostic tests sometimes are performed to distinguish orbital cellulitis has also been described. The presence of gas
preseptal from orbital cellulitis. or an air-Áuid level may be due to gas-forming organisms
or communication with the sinuses. True intraorbital abscess
Management may present as an enhancing ring-like peripheral mass that
can be either heterogeneous or homogeneous. One of the
All patients with orbital cellulitis require inpatient main advantages of CT as compared to ultrasonography is
management while patients with preseptal cellulitis can be that intracranial involvement such as epidural or cerebral
managed on outpatient basis. The patients with preseptal abscess can be assessed. Coronal sections are important:
cellulitis usually do not require elaborate investigations. The One-third of all abscesses were seen only in coronal sections
condition once recognised clinically can be treated with oral in one study.25 Magnetic resonance imaging (MRI) is less
antibiotics and analgesics for a week. On the other hand, reliable than CT at diagnosing the subtle signs of muscle
patients with orbital cellulitis require admission and prompt enlargement and periscleritis.26 On MRI with gadolinium
management. enhancement, orbital cellulitis may show a smearing or linear
streaking of the normal fat shadows on T2-weighted images.
Laboratory Investigations MRI is excellent for demonstrating localized Áuid collections
such as abscesses. It is also the preferred imaging modality
The patients with orbital cellulitis or abscess should for diagnosis of cavernous sinus thrombosis. In children
undergo hematological and radiological investigations for however, MRI scans are preferred over CT scans because of
conÀrmation and knowing the extent of the disease. The absence of radiations.
blood investigations needed include complete blood count,
ESR, blood urea, serum electrolytes and blood cultures. Management
The patients with orbital infections have leukocytosis and
often raised ESR. Blood cultures yield higher positive The management of patients with orbital cellulitis is
results in children than in adults. There is 5% incidence of summarized in table IV. These broad guidelines are modiÀed
bacteremia reported in adults compared to 33% in children from the work of Howe and Jones.27
younger than 4 years with orbital cellulitis.22 Blood cultures
are less sensitive but more speciÀc than are conjunctival or
36 l DOS Times - Vol. 17, No. 1 July, 2011
Table IV
Management plan for orbital cellulitis
• The patient to be admitted
• Secure IV access
• blood for cbc, blood urea, serum electrolytes, blood
culture
• Radiological imaging (CT scan / MRI scan)
• Intravenous antibiotics – amoxycillin-clavlunate,
amikacin and metronidazole
• Analgesics as necessary
Figure 8: CT scan Àlm showing ethmoid sinus haze • Nasal ephedrine 0.5% drops 8 hourly in head back
with subperiosteal abscess position
• ENT and paediatric opinions as necessary
The patients are admitted and an intravenous line is secured. • Twice daily assessment of visual acuity, eye
Blood sample is taken for investigations and broad spectrum movement and pupil reÁexes
antibiotics are given. The authors prefer iv amoxycillin-
clavlunate (50 mg/kg/day of amoxycillin in divided doses) • Surgical drainage if radiological imaging reveals
along with iv amikacin (15 mg/kg/day in divided doses) abscess
and iv metronidazole (7.5 mg/kg 8 hourly). Additional
cultures may be obtained from conjunctival discharge and Inadequate treatment can lead to the formation of a localized
nasal discharge if present. Analgesics are used as necessary. orbital abscess from orbital cellulitis. Cerebral complications
Nasal decongestants like ephedrine nose drops are given if include cavernous sinus thrombosis (1%), meningitis (2%),
the patient has rhinosinusitis. Atleast 12 hourly ophthalmic carotid occlusion, epidural abscess, subdural abscess, and
evaluation of the patient is carried out to document visual brain abscess (1%). The incidence of intracranial complications
acuity, proptosis, colour vision and extraocular movements are is surprisingly nearly equal for both preseptal and orbital
recorded. Radiological imaging is carried out and subsequent cellulitides, even though orbital cellulitis is usually a much
Otorhinolaryngological or Pediatric consultations are sought more severe infection. The incidence of cavernous sinus
if needed. When CT scan or MRI scan reveals presence of thrombosis might be higher in orbital cellulitis.
subperiosteal or orbital abscess, orbital drainage is required.
There is no evidence that undertaking more extensive sinus References
surgery is justiÀed in the absence of any other paranasal
sinus abnormalities such as polyposis. Sinus surgery in 1 Jain A, Rubin PAD. Orbital cellulitis in children. International
acutely infected patients is difÀcult because the associated Ophthalmology Clinics 2001;41(4):71-86.
hyperaemia causes marked bleeding making visibility poor
and the risk of producing adhesions and stenosis of the 2 Swift AC, Charlton G. Sinusitis and the acute orbit in children. J
frontal recess are increased. The main surgical objective is to Laryngol Otol 1990;104: 213–6.
drain the pus adequately, release the pressure on the orbit and
obtain a culture.27 Once adequate drainage has been done, iv 3 Moloney JR, Badham NJ, Mcrae A. The acute orbit: preseptal
antibiotics are continued along with supportive management (periorbital) cellulitis, subperiosteal abscess and orbital cellulitis due to
till proptosis recedes. sinusitis. J Laryngol Otol Suppl 1987;12,1–18.
Complications 4 Wagenmann M, Nacleiro RM. Complications of sinusitis. J. Allergy
Clin Immunol 1992;90:552–4.
Orbital cellulitis can lead to permanent visual loss and central
nervous system complications that may be life threatening. 5 Davis JP, Stearns MP. Orbital complications of sinusitis: avoid delays
The pathophysiology of vision loss in orbital cellulitis can in diagnosis. Postgrad Med J 1994;70: 108–10.
be because of corneal opaciÀcation secondary to exposure
keratopathy or neurotrophic keratopathy; optic neuropathy 6 Wald E.R., Pang D, Milmore GJ et al. Sinusitis and its complications
secondary to infection or inÁammation and compressive in paediatric patients. Paediatr Clin North Am 1981;28:777-96.
effects; thrombophlebitis of ocular veins; central retinal artery
occlusion secondary to compression; mechanical distortion 7 Nangia V, Hutchinson C. Metastatic endophthalmitis caused by
of globe and optic nerve (tenting); thromboembolic lesions clostridium perfringens. Br J Ophthalmol 1992;76:252-3.
to optic nerve, retina, choroid and permanent extraocular
motility deÀcits.28 Less commonly, endophthalmitis and 8 Leavelle RB. Gas gangrene panophthalmitis. Arch Ophthalmol
infective uveitis have been documented as complications of 1955;53:634-42.
orbital cellulitis.
9 Hubert L. Orbital infections due to nasal sinusitis. NY State J Med
1937;37:1559-64.
10 Smith AT, Spencer JT. Orbital complications resulting from lesions of
the sinuses. Ann Otol Rhinol Laryngol 1948;57:5-27.
11 Chandler JR, Langenbrunner DJ, Stevens ER. The pathogenesis of
orbital complications in acute sinusitis. Laryngoscope 1970;80:1414-
28.
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12 Uzcátegui N, Warman R, Smith A, Howard CW. Clinical practice 21 Shuttleworth G, Harrad R: Management of acute eyelid conditions.
guidelines for the management of orbital cellulitis. J Pediatr Ophthalmol The Practitioner 2000, 244:138–143.
Strabismus. 1998 Mar-Apr;35(2):73-9.
22 Steinkuller PG, Jones DB. Microbial preseptal and orbital cellulitis. In:
13 Spires JR, Smith RJH. Bacterial infections of the orbital and periorbital Tasman W, ed. Foundations of clinical ophthalmology. Philadelphia:
soft-tissues in children. The Laryngoscope 1986;96(7):763-7. Lippincott, 1990.
14 Uy HS, Tuano PMC. Preseptal and orbital cellulitis in a developing 23 Schramm V.L., Curtin H.D. & Kennerdell J.S. (1982) Evaluation of
country. Orbit 2007;26:33-7. orbital cellulitis and results of treatment. Laryngoscope 1982;92:732–
738.
15 Shapiro ED, Wald ER, Brozanski BA. Periorbital cellulitis and
paranasal sinusitis: a reappraisal. Pediatr Infect Dis 1982;1(2):91-4. 24 Mair M.H., Geley T., Judmaiei W. et al. (2002) Using orbital
sonography to diagnose and monitor treatment of acute swelling of the
16 Harris G. Age as a factor in the bacteriology and response to treatment eyelids in paediatric patrients. Am. J. Roentgenol. 179, 1529–1534.
of subperiosteal abscess of the orbit. Trans Am Ophthalmol Soc
1993;91:441–516. 25 Langham-Brown JJ, Rhys-Williams S. Computed tomography of
acute orbital infection: the importance of coronal sections. Clin Radiol
17 English GM. Sinusitis. In: English GM, ed. Otolaryngology, vol 2. 1989;40:471-4.
Hagerstown, MD: Harper & Row, 1980: chap 21.
26 Casteel I, DeBleecker C, Demaerel P, et al. Orbital myositis following
18 Arey LB. Developmental anatomy, ed 7. Philadelphia: Saunders, an upper respiratory tract infection: contribution of high resolution CT
1974;528. and MRI. J Belg Radiol 1991;74:45-7.
19 Smith TF, O’Day D, Wright PF: Clinical implications of preseptal 27 Howe L, Jones NS. Guidelines for the management of periorbital
(periorbital )cellulitis in childhood. Pediatrics 1978, 62:1006–9. cellulitis/abscess. Clin Otolaryngol 2004;29:725-9.
20 Barone SR, Aiuto LT. Periorbital and orbital cellulitis in the 28 Patt BS, Manning SC. Blindness resulting from orbital complications
Haemophilus inÁuenza vaccine era. J Pediatr Ophthalmol Strabismus of sinusitis. Otolaryngol Head Neck Surg. 1991 Jun;104(6):789-95.
1997;34:293–296.
38 l DOS Times - Vol. 17, No. 1 July, 2011
Oculoplasty
Ramesh K.C. Gupta
Ramesh K.C. Gupta, Abhishek Anand, Sonam A. Bodh, R. Arora, J.L. Goyal
Guru Nanak Eye Centre, Maharaja Ranjit Singh Marg, New Delhi
Myiasis - A term coined by Frederick William Hope for Figure 1: Larvae in anterior chamber
the disease caused by infestation of insect larvae, word
myiasis is derived from Greek word muia means Áy. Fritz Clinical presentation
Zumpt deÀne myiasis as “the infestation of live human and
vertebrate animals with dipterous larvae, which at least for a External ophthalmomyiasis- larvae invades external ocular
period, feed on the host's dead or living tissue, liquid body tissue like lids,periocular skin, and conjunctiva.Mainly
substances, or ingested food". producing nonspeciÀc symptoms depending on the tissue
affected. Lid and periocular myiasis resembles furuncular
Most of the time it infest animals and a major problem in myiasis of skin, appears as painful boil with central opening
livestock industry, accidently it may affect humans that leads from which sersanguineous discharge oozes along with lid
to severe tissue destruction. edema. Some larvae produces creeping eruptions that appear
tortuous thread like red line below the skin with vesicles at
ICD-10 classification of myiasis the end, vesicle contains larvae. Some larvae like hypoderma
spp. Penetrate deep inside the skin and form painful nodule
• Cutaneous – dermal and sub dermal containing dead larvae.
• Nasopharyngeal Conjunctival involvement classically described as acute
catarahal conjunctivitis with sand of grains. It presents as
• Ocular lid edema, lacrimation, foreign body sensation, conjunctival
congestion with larvae crawling over the conjunctiva in
• Intestinal accordion fashion i.e. moving away from the light. Sometimes
larvae invades conjunctiva where it may form subconjunctival
• Urogenital nodule or cyst, may reach orbit where it causes severe tissue
damage and reaction simulating orbital cellulitis.
Ophthalmomyiasis
Corneal involvement is rare and manifest as superÀcial
Infestation of ocular tissue by Dipteran Áies larvae (maggot). punctate keratitis and marginal corneal ulcer.
First human case of ophthalmomyiasis is reported by Keyt
in 1900 and in India Elliot reported the Àrst case.There are Diagnosis is made by seeing the live crawling larvae in the
three families of Áies that affect the humans; most common of fornix or sometimes hidden in sulcus tarsalis needed double
them is sheep botÁy oestrus ovis. Fly lays eggs or larvae over eversion of lid.
the skin or on mucus membrane in different body cavities
that fed on host tissue and produces symptoms. Most of the Internal ophthalmomyiasis- when larvae invades the eyeball
time it affects old debilitated people from rural background, and inhabited inside the eyeball after penetrating the sclera
a number of predisposing factor identiÀed for myiasis related and rarely via cornea,where it may remain sub-retinal or may
to both host and environment. go to vitreous cavity, lens, angle, or anterior chamber.
Host factors
• Livestock industry
• Poor self-hygiene
• Imunocompromised state
• Debilitated and Poor nutritional state
Environmental factors
• Rural background
• Improper sanitation
• Tropical climate
Ophthalmomyiasis is further classified as
• External ophthalmomyiasis
• Internal ophthalmomyiasis
• Orbital ophthalmomyiasis
www. dosonline.org l 41
Figure 2: Larvae in vitreous Figure 3: Subretinal larvae
When larvae inhabited the anterior chamber it presents with • Stratiomyidae
painful purulent iridocyclitis. Sometimes lens suluxation • Syrphidae
is also noticed. Larvae are seen as a grey white mass in the Entomologist classiÀes myiasis according to the relation
anterior chamber that moves with movement of the head. between Áies and host in three types as
Specific myiasis (Obligatory myiasis)
When the larvae resides in the sub-retinal space, it produces
creeping depigmented linear tract, RPE changes along When the larval stage needed a live vertebrate host for their
with sub retinal and vitreous hemorrhage. There is intense development at least for certain period of time
uveal reaction because of larvae movement, and may cause • Dermatobia hominis (human botÁy)
exudative retinal detachment. • Cordylobia anthropophaga (tumbu Áy)
• Oestrus ovis (sheep botÁy)
Inside vitreous cavity it usually remains silent, or produces • Hypoderma spp. (cattle botÁies or ox warbles)
mild inÁammatory reaction having self-limiting course. • Gasterophilus spp. (horse botÁy)
• Cochliomyia hominivorax (new world screwworm Áy)
Diagnosis made by seeing motile larvae (larvae show Semispecific myiasis (Facultative myiasis)
movement on stimulation by light) on slit lamp examination
or by indirect ophthalmoscopy for sub retinal and vitreous When larvae doesn’t show absolute need for their
infestation. development, but may cause myiasis if Áy layed eggs over
the open wound or on sored skin.
Orbital ophthalmomyiasis- Mostly seen in old debilitated • Lucilia spp. (green-bottle Áy)
patients suffering from nasopharyngeal and ethmoidal • Cochliomyia spp. (blue-bottle Áy)
sinus tumor. Here the larvae inhabited the orbital cavity • Phormia spp. (black-bottle Áy)
and fed on orbital tissue causing severe tissue destruction • Calliphora spp. (blowÁy)
and inÁammatory reaction. Larvae reaches the orbital cavity Accidental myiasis
either via the nasal route through ethmoidal sinus, skin and
conjunctiva. Larvae in orbital cavity mainly fed on the muscles (pseudomyiasis) Transmission occurs through accidental
and forms large cavernous spaces that are Àlled with blood deposit of eggs on oral or genitourinary openings, or by
and exudates and rotting Áesh producing a foul smelling swallowing eggs or larvae that are on food.
cavity. Patient mainly presents with pain, redness, proptosis, • Musca domestica (houseÁy)
impaired ocular motility, and foul smelling discharging • Fannia spp. (latrine Áies)
sinus. Cystic swelling may evident on examination. Lacrimal • Eristalis tenax (rat-tailed maggots)
sac involvement is presented as chronic dacryocystitis with • Muscinaspp.
or without Àstula formation.
Differential diagnosis
Diagnosis made on direct visualization of pouting larvae and
by orbital imaging. • Orbital abscess
• Pseudotumour
Entomology– Most of case of ophthalmomyiasis is caused by • Dermoid cyst
the dipteran Áy larvae belongs to the three classes named as
• Bot Áy (oestroidea)
• Blow Áy (calliphoriadae)
• Flesh Áy (sarcophagidae)
Most common of them is Oestrus ovis (sheep botÁy)
Other flies that may cause myiasis is
• Anisopodidae
• Piophilidae
42 l DOS Times - Vol. 17, No. 1 July, 2011
Figure 4: Larvae extracted from orbital myiasis ophthalmomyiasis where it can conÀrm the diagnosis and
also tell about the viability of larvae by its motility and
Figure 5: CT scan showing destruction of size of larvae where it shows hypoechoecity, especially in
ethmoidal sinuses and globe cases where it induces intense inÁammation making direct
visualization almost impossible. It also give information
• Cystecercosis about the associated other posterior segment complications
• keratoconjunctivitis (retinal detachment) that may affect management.
• Acute anterior uveitis
CT scan like x-rays aids in planning of management of
Diagnosis and treatment orbital myiasis cases by clearly deÀning the extent of bone
destruction and soft tissue involvement especially muscular
Ophthalmomyasis is mostly diagnosed by direct visualization involvement.
of larvae.
Some laboratory investigation may aid in diagnosis as MRI scan this is a very useful imaging modality in cases of
follows, Blood count shows leukocytosis and eosinophilia in orbital as well as in other ophthalmomyiasis. Not only does
cases of orbital Invasive Myasis. it give an idea of the extent of the soft tissue destruction but
Role of serology is seen in few cases but need more studies. can also tell about its cranial extension.
Imaging studies Doppler ultrasonography (DUSG)-Performed by using a high-
resolution (10-MHz) soft-tissue transducer. Its demonstrates
X-ray- aids in diagnosis as well as in planning the management circulation of Áuid within the parasite as well as the number
in cases of orbital myiasis, it can shows bone destruction and of parasites, their size, and their situation within the lesion.
soft tissue swelling and calciÀcation in cases where larvae die This is especially useful when the lesions are still small and
and induces calciÀcation around it. look like insect bites.
USG B scan- Role of B scan is mostly in cases of internal
Biopsy and histology- shows inÁammatory inÀltrate of
neutrophils, lymphocytes, giant cells, mast cells, plasma cells,
and eosinophil’s that occur in stages. The larvae can be seen
in cross-section.
Treatment- Myiasis is a self-limiting infestation with minimal
morbidity and mortality. The major reasons for treatment are
reduction of pain, cosmesis, and psychologic relief. Once the
larva has emerged or has been removed, the lesions rapidly
resolve. However, larvae such as C hominivorax (cause of
wound myiasis) can infest around oriÀces of the head and
may burrow into brain tissue.
First-line treatment - Surgical removal
Surgical removal with local anaesthesia is usually the
preferred approach in cases of external ophthalmomyiasis.
The skin lesion is locally anesthetized with lidocaine and
excised surgically followed by primary wound closure.
Alternatively, lidocaine can be injected forcibly into the base
of the lesion in an attempt to create enough Áuid pressure to
extrude the larvae out of the punctum.
Another surgical approach would be to perform a 4-5 mm
punch excision of the overlying punctum and surrounding
skin to gain better access to and visibility of the larva. The
larva can then be removed carefully using toothed forceps.
In cases of larvae crawling over the conjunctiva can be
picked by using toothed forcep under topical anaesthesia.
Sometimes double eversion of lids in needed if larvae are
hidden in subtarsalis sulcus.
In cases of severe orbital myiasis, orbitotomy with removal
of all dead tissue along with larvae is mandatory to avoid
further tissue destruction and other complications.
Furthermore, care should be taken to avoid lacerating the
larva because retained larval parts may precipitate foreign
body reaction. After the removal of the larvae, antiseptic
dressings are indicated, as well as antibiotics if secondary
infection is present.
Second-line treatment - Occlusion/suffocation approaches
These treatments include petroleum jelly, liquid parafÀn,
beeswax or heavy oil, or lard or bacon strips placed over the
central punctum, larva emerges spontaneously head-Àrst
www. dosonline.org l 43
Evidence shows Ivermectin decreased inÁammation and
destructive process if used prior to debridement. It can be
used an adjuvant therapy prior to surgical debridement and
helpful in preventing enucleation in patients with massive
orbital involvement and also avoids the difÀculties associated
with surgical removal of the larvae.
Figure 5: DUSG References
over the course of several hours, at which time, tweezers (or 1 Ofordeme KG, Papa L, Brennan DF. BotÁy myiasis: a case report. CJEM.
forceps) aid in the capture. These approaches take advantage Sep 2007;9(5):380-2
of the larva's oxygen requirements, encouraging it to exit on
its own. 2 Cestari TF, Pessato S, Ramos-e-Silva M. Tungiasis and myiasis.
Third-line treatment - Systemic/topical ivermectin4,5,6 ClinDermatol. Mar-Apr 2007;25(2):158-64
An alternative treatment for all types of myiasis is oral
ivermectin (200 mcg/kg) or topical ivermectin (1% solution), 3 Quintanilla-Cedillo MR, Leon-Urena H, Contreras-Ruiz J, Arenas R.
proven especially helpful with oral and orbital myiasis The value of Doppler ultrasound in diagnosis in 25 cases of furunculoid
myiasis. Int J Dermatol. Jan 2005;44(1):34-7
4 Osorio J, Moncada L, Molano A, et al. Role of ivermectin in the treatment
of severe orbital myiasis due to Cochliomyiahominivorax. Clin Infect
Dis. Sep 15 2006;43(6):e57-9
5 Costa DC, Pierre-FilhoPde T, Medina FM, Mota RG, Carrera CR. Use
of oral ivermectin in a patient with destructive rhino-orbital myiasis.
Eye. Sep 2005;19(9):1018-20
6 Clyti E, Nacher M, Merrien L, et al. Myiasis owing to Dermatobiahominis
in a HIV-infected subject: Treatment by topical ivermectin. Int J
Dermatol. Jan 2007;46(1):52-4
7 Agarwal DC, Singh B. Orbital myiasisFa case report. IndianJ
Ophthalmol 1990; 38: 187–188
8 Sachdev MS, Kumar H, Roop, Jain AK, Arora R, Dada VK. Destructive
ocular myiasis in a noncompromisedhost.Indian J Ophthalmol 1990; 38:
184–186.
9 DC Costa, P de Tarso Ponte Pierre-Filhoetal.Eye (2005) 19, 1018–1020
44 l DOS Times - Vol. 17, No. 1 July, 2011
Instructions:
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2. The answers should reach not later than 29th August 2011.
The quiz can also be viewed and directly answered on our website www.dosonline.org
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prize of Rs. 2100 along with a certiÀcate. If there are more than one correct entry, the winner of the cash prize
will be decided by draw of lots. At the end of the year the person who has got the maximum number of correct
entries will be awarded.
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Squint
Syed Imran
P.C. Dwivedi MS, FSVH, Charudatt Chalisgaonkar MS, Syed Imran MBBS
S.S. Medical College, Rewa, Madhya Pradesh
Synoptophore is an orthoptic instrument used for both white line on the top of tube by closing your right eye. Repeat
motor and sensory evaluation of strabismus. It is also similarly for the left eye of the subject, note down the IPD and
used for nonsurgical treatment of strabismus in the form lock it for further measurements.
of orthoptic exercises. The functioning of the synoptophore
is based on haploscopic principle. Each eye is separately Angle of Deviation
stimulated by a separate target and then binocular visual Objective Angle of Deviation
response is measured. Clement Clarke major synoptophore
is now the most commonly used version and has replaced It can be measured based on the principles of either the
the older versions like MoorÀelds Synaptophore, Lyle Major Hirschberg's test or the alternate cover test. Make sure that the
amblyoscope and Curpax Major amblyoscope.
Figure 1: Basic optics of Synoptophore. L= Lamp House,
Basic Structure P = Slide Holder, S = Scale, O = Center of rotation of arms,
The instrument has a base that contains the electrical M = Mirror, D = Convex Lens
components and controls. Attached to the base are scales (+ 6.5D) Focal length DX=DO + OP
for measuring vergence movements. Supported at the
base are two optical tubes that contain a light source; high Figure 2: Synoptophore, 1= Forehead Rest,
intensity light for after image test and Haidenger’s brushes 2= Eyepiece with Lens holder, 3 = Slide carier
and a low intensity light; a slide carrier; various scales and 4 = Lamp house, 5= Chin rest, 6= Handle for adjustment of
control knobs for measuring horizontal, vertical and tortional horizontal angle, 7 = Interpupilary Distance control,
deviations; a reÁecting mirror and an eyepiece with a +6.5D 8= Chinrest control, 9= Hand Áashing switches,
lens. Plus lenses in the eyepiece ensure relaxation of patient's
accommodation and the image appears to come from the 10 = Horizontal vergence scale.
distance. Accommodation can be induced by placing minus
lenses in the lens holder placed in front of the eyepiece.
Uses
Diagnostic Uses
• To measure interpupilary distance (IPD).
• To measure angle of deviation.
• To assess Anomalous retinal correspondence (ARC).
• To measure angle kappa (K).
• To assess various grades and anomalies of Binocular
vision.
• To measure fusional reserve.
• To measure AC/A ratio.
• To measure primary and secondary deviations.
Therapeutic Uses
• For various orthoptic exercises
• To treat convergence insufÀciency.
• To improve fusional reserve.
• To combat suppression & ARC.
Interpupilary Distance Measurment
This is the Àrst step before starting any measurement of
strabismus. Set all the scales to zero, put the slides of foveal
Àxation and ask the patient to look with his right eye into
right picture and then align the corneal reÁection with the
www. dosonline.org l 47
Figure 5: Slides of simultaneous macular perception
Figure 3: Synoptophore – Scales and controls horizontal scale and vertical scale in front of the non Àxing
1= Vertical deviation scale and control, 2= Slide holder, arm represents the objective angle of deviation.
3= Tortional deviation scale, 4= Elevation and depression scale, 5=
Subjective angle of deviation
Elevation and depression control,
6= Tortional deviation control. First measure the objective angle of deviation, if the patient
claims superimposition (the lion is the cage) at his objective
angle, this angle is also his subjective one. If this is not the
case the patient is asked to superimpose the two slides by
adjusting the angle between two slides by the handle. Reading
on the scale will give you the subjective angle of deviation.
Angle of Anomaly
Figure 4: Synoptophore – Scales and controls If subjective and objective angles of deviation are same it is
1=Horizontal deviation scale, 2=Interpupilary distance scale, called normal retinal correspondence and if it is different,
3= Horizontal vergence scale, 4= Horizontal vergence control, it is called anomalous retinal correspondence (ARC). Angle
of anomaly is the difference between the subjective and
5=Tube locking control objective angle of deviation. For instance, if a patient has an
objective angle of deviation of 25ǻBO and a subjective angle
patient is comfortably seated and correctly positioned in front of 10ǻBO, his angle of anomaly is 15ǻ. If objective angle is
of the instrument and then adjust the interpupilary distance equal to angle of anomaly i.e. subjective angle is zero, it is
and insert the Àrst grade targets. In the Hirschberg's test the called harmonious ARC. If objective angle exceeds angle of
patient is asked to look at the center of the target slides and anomaly - unharmonious ARC.
the angle of slide carrier is adjusted to make corneal reÁection
symmetrical (in the center of the pupilary area in both eyes) Measurement of Cyclodeviation
and the deviation is measured. For measuring the angle of
deviation by the alternate cover test the lion or car is placed in It can only be measured subjectively. Simultaneous
front of the Àxing eye and the cage or gate in front of the non perception slides are used, the patient is asked to look at each
Àxing eye. The arms are set to zero and the patient is Àxing at slide in turn and is asked whether the cage appears level or
the center of the slide with the Àxing eye light in front of the tilted. If the image appears to be tilted a cyclo-deviation is
Àxing eye is turned off, immediately the non Àxing eye will present. If with the left eye focusing, the cage's left-hand side
take Àxation. The non Àxing eye will move either inwards (in is lower than the right-hand side, incyclophoria or tropia is
exotropia), outwards (in esotropia), upwards or downwards present. It should be remembered that the tilt of the image is
to take Àxation. If the non Àxing eye moves out to pick up in the opposite direction to the tilt of the eye. The deviation is
Àxation, the arm is moved into a more convergent or less corrected by means of the torsional deviation screw and the
divergent position. If the eye moves in, the arm is moved amount of deviation is measured from the scale.
into a more divergent or less convergent position. If the
eye moves downward the tube has to be raised; if it moves Grades of Binocular Single Vision
upward the tube has to be lowered. The alternate Áashing is
continued and the tube adjusted until there is no movement There are three grades of binocular single vision:
in either eye when it picks up Àxation. The reading on the
• Simultaneous perception
• Binocular fusion
• Stereopsis
Simultaneous perception: It is the ability to simultaneously
perceive two images, one formed on each retina. The slides
(Figure 5) are designed so that the patient puts something
into something e.g. a lion in a cage. Either parafoveal, foveal,
or macular slides may be used. The patient who sees the lion
in the cage is seeing with each eye simultaneously and has
grade 1 binocular vision.
48 l DOS Times - Vol. 17, No. 1 July, 2011
Figure 6: Slide for fusion deviated eye switches to the pseudo-fovea. With esotropia,
the fovea is temporal to the pseudo-fovea and temporal retina
projects to the opposite hemiÀeld, so the right afterimage is
seen on the left and the after images will be crossed (Figure 9)
in esotropia. Exotropia is just the opposite, right afterimage
is seen on the right and the after images will be uncrossed.
Angle Kappa
To measure angle kappa we use a special slide (Figure 10)
that has zero at its centre and a row of numbers and letters
at 1ǻ intervals on either side. The patient is asked to look at
the zero and we observe the light reÁex on the cornea. If the
reÁex is on the nasal side of the pupil the angle is positive; if
it is on the temporal side it is negative. The patient is asked
to look in turn at either one letter or one number until the
reÁex is centered. The degree of deviation corresponding to
the letter or number is then recorded as angle kappa.
AC/A Ratio
Accommodative Convergence to Accommodation (AC/A)
Ratio is the amount of change in convergence for a speciÀc
amount of change in accommodation. Measure deviation
Figure 7: Slide for Steriopsis
Binocular fusion: Sensory fusion is the ability to fuse two Figure 8: Special slide for after image test
slightly dissimilar images and perceive them as one. These
consist of targets which are mainly the same but each has Figure 9: After image test, First image RE esotropia with
a different control on it e.g. (Figure 6) a grade 2 target may ARC-Crossed after image. Second image Re exotropia with ARC-
present to one eye a picture of a rabbit with no tail, clutching
Áowers, the other eye would be presented with a picture of Uncrossed after image
the same rabbit, but it would have a tail, and held in its hand www. dosonline.org l 49
would be a stem without Áowers. Grade 2 binocular vision is
present if the patient fuses these images and reports seeing a
tailed rabbit clutching a bunch of Áowers by a stem.
Stereopsis: It is the perception of depth based on binocular
image disparity. These slides (Figure 7) have slightly disparate
targets; the fusion of these slightly disparate images by the
brain creates the sensation of depth, or stereopis. If fused
correctly, one of the parachutes will appear distinctly in front
of the others i.e. they will perceive a three dimensional image.
After Image Test
It is a fovea-to-fovea sensory test used to measure ARC.
Special slides (Figure 8) that present the retina with a linear
strobe of light (one vertical and one horizontal) are used.
The center of the linear strobe light is masked to spare the
fovea; thus, the afterimage line has a break in the middle.
Stronger 12v lamps are used to stimulate the fovea of both
eyes separately for 15 seconds each. Patient is then asked
to close his eyes and explain about the after image that he
sees. Because the stimulus is presented under monocular
conditions, the stimulus always marks the true fovea of each
eye unless there is eccentric Àxation from dense amblyopia.
Patients with NRC will, therefore, always see a cross whether
they are orthophoric, esotropic, exotropic, or hypertropic.
Patients with ARC however, use their true fovea during
monocular viewing but, during binocular viewing, the
heterotopias. Previously orthoptics was used in the
treatment of ARC, but as per current view orthoptics is not
recommended for treating ARC. Presently, the most effective
treatment for terminating ARC is surgical alignment of eye.
For the treatment of convergence/divergence insufÀciency
Àrst measure convergence/divergence fusional reserve and
all grades of binocular single vision. Stereoscopic slides are
used as they are strongest stimulation for fusion. Patient Àrst
fuses the slides; tubes are then converged till patient is able to
maintain the fusion; when diplopia occurs patient is asked to
try to fuse the images. This exercise is continued for 5 minutes
at each weekly visit and the patient is given a home exercise
in the form of pencil convergence exercise and physiological
diplopia exercise (stereogram card) before he comes for next
visit.
Figure 10: Special slide for Angle Kapa References
without and with a -3.0 D lens in the lens holder placed in 1. Keith Lyle, Kenneth C. Wybar. Orthoptic instruments and their uses. In,
front of the eyepiece. A -3.0 D lens will induce accommodation Lyle and Jackson’s, Practical orthoptics in the treatment of squint, 5th
and measure deviation for near. Measure AC/A ratio by the edition. New Delhi, Jaypee brothers, 1979; 96-170.
given formula
AC/A =Deviation with lens - Deviation without lens 2. Gunter K. von Noorden, Emilio c. Campos. Binocular vision and ocular
motility, 6th edition. United States of America, Mosby, 2002.
3D (Accommodation induced by a -3D lens)
Determination of Fusional Amplitudes 3. Kenneth W. Wright, Peter H. Spiegel, Lisa S. Thompson. Handbook of
Pediatric
4. Strabismus and Amblyopia, 2nd edition. United States of America,
Springer Science + Business Media, 2006.
5. John A. Pratt-Johnson, Geraldine Tillson. Management of strabismus
and amblyopia: a practical guide, 2nd edition. New York, Thieme, 2001.
After determining the objective angle and the presence of Àrst
and second grades of binocular vision, the examiner blocks
the arms at the objective angle (divided equally between both
arms). By means of the horizontal vergence controls, both
arms are Àrst diverged/converged (depending on whether
divergence or convergence fusional amplitude is being
measured) and the point where fusion breaks is recorded.
The arms are then moved back to a less divergent/converged
position and the point where fusion is recovered is recorded.
The recovery point is usually 2 to 4 ΔD below break point.
Fusional amplitude should be tested slowly as vergence
movements are slow and tonic. This is recorded as follows.
Synoptophore test, with correction:
• Distance: 30ΔET, 4ΔRHT objectively and subjectively
• Fist-and second-grade fusion at angle
• Convergence to 35Δ/recovery at 30Δ
• Divergence to 8Δ/recovery at 5 Δ.
Near (with 3.0 D spheres)
• 46ΔET, 20ΔRHT objectively and subjectively
• Fist - and second-grade fusion at angle
• Convergence to 48Δ/ recovery at 40Δ
• No divergence past angle, suppression OD.
Orthoptic Exercises
Orthoptics is a training process of an individual to obtain
the best possible binocular interaction in the form of BSV.
Presently it is mainly used to improve fusional amplitudes
for the management of heterophorias and intermittent
50 l DOS Times - Vol. 17, No. 1 July, 2011
Squint
Varshini Shanker
Varshini Shanker DNB, Srijana MS, Suma Ganesh MS, Manish Sharma
Department of Paediatric Ophthalmology and Strabismus, Shroff Charity Eye Hospital, , Daryaganj, New Delhi
Accommodative esotropia is one of the most common
types of childhood strabismus. The incidence in the
population is estimated at 2%. Accomodative esotropia is
caused by overconvergence due to accommodation and is
associated with signiÀcant hypermetropia in most cases.1
Etiology
The relationship between accommodation and convergence
and uncorrected hypermetropic refractive error causes a
comitant esodeviation. Most patients with uncorrected
hypermetropia will attempt to clear the image blur by
increasing accommodative effort, which in turn causes
excessive accommodative convergence. An emmetrope needs
to accommodate 3 diopters to see clearly at 33 cm. A child
with 3 diopters of uncorrected hypermetropia will need to
accommodate 3 diopters at 6m, and 6 diopters at 33cm to see
clearly. If fusional divergence is insufÀcient to compensate
for this impulse to converge the eyes, in the presence of a
normal or high AC/A ratio, esotropia will develop.
Classification Consequences of uncorrected high hypermetropia (Adapted from
Noorden GK von, Heleveston EM: Strabismus: A Decision Making
Von Noorden1 classiÀed Accommodative Esotropia on the Approach. St Louis, Mosby 1994, p 95)
basis of underlying etiology as
1. Refractive Accommodative Esotropia times and crossing whenever the child is tired or focusing
on near objects. Although it is initially intermittent, it can
2. Non-refractive Accommodative Esotropia quickly become constant. This condition may present anytime
from infancy to late childhood, but most often between two
3. Hypo Accommodative Esotropia and four years of age with no gender or race predilection.
Decompensation of initially fully controlled deviation can
4. Partially Accommodative Esotropia occur in some cases precipitated by illness or trauma. Most
accommodative esotropes are moderate hyperopes. High
The ClassiÀcation of Eye Movement Abnormalities and hyperopes often remain orthotropic, preferring blurred
Strabismus2 (CEMAS) group classiÀed and deÀned this vision rather than the constant accommodative effort.
entity as-
Refractive Accommodative Esotropia
Accommodative Esotropia
Refractive esotropia is deÀned as an esotropia that is restored
• Pure Refractive: esotropia eliminated by hyperopic to orthophoria at all Àxation distances and in all gaze
spectacles positions by optical correction of underlying hypermetropic
refractive error.1
• Non-Refractive: esotropia at near only and eliminated
with plus lenses at near, e.g. bifocal Clinical presentation
• Mixed: esotropia at distance and greater at near associated Most commonly, refractive accommodative esotropia
with hyperopia and responds to hyperopic correction at develops around the age of 3 years, but it may develop as late
distance with bifocal for near as 6 or 7 years of age.3 Onset as early as 4 months of age has
been reported4,5 Frequently, accommodative esotropia begins
Mixed (Partially Accommodative) Esotropia as an intermittent strabismus that occurs following an illness
and may worsen or become more noticeable with fatigue.
Hyperopia with incomplete response to spectacles and Over the next several weeks to months, the esotropia will
bifocals. usually become constant.
History and Demographics
This usually presents as an acquired, intermittent esotropia.
Parents often describe the childs eyes as being straight at
www. dosonline.org l 55
Figure 1: Refractive Accommodative Esotropia fully corrected with hyperopic glasses.
The size of the deviation is variable and is typically smaller Figure 2: A 4 year old child who presented with right esotropia and
than congenital esotropia, usually measuring 20-40 PD. amblyopia. She was prescribed full cycloplegic refraction
Accommodative esotropia is associated with varying
degree of hypermetropia. Cycloplegic refraction reveals of +6.50 DS in the right eye and +3.50 DS in the left eye and
hypermetropia between +1.50 to +6.50 Dioptres.6 These started on amblyopia therapy
patients have normal AC/A ratio and normal near point of
accommodation. Figure 3: Her esotropia reduced by
20 prism diopters with the glasses
A progressive increase in the angle and frequency of deviation
is common in these patients, and dysfunction of the oblique Miotics like ecothiophate iodide (Phospholine) have been used
muscles may occur in up to 30% of cases. in the treatment of hypermetropic accommodative esotropia
and high AC/A ratio esotropia..Miotics act by facilitating
Management accomodation. As the effort for accomodation is decreased,
the resulting accomodative convergence is consequently
The goals of treatment for accommodative esotropia include reduced. Phospholine iodide (0.03%, 0.06% and 0.125%) is
maintenance of normal visual acuity in each eye, restoration of administered once or twice daily. The side effects include iris
ocular alignment and maintenance of excellent binocularity.3 cysts at the pupillary margin, induced myopia, conjunctival
hyperemia, and a prolonged response to depolarizing muscle
The Àrst step in the treatment of refractive accommodative relaxants (e.g., succinycholine chloride).
esotropia is to perform a refraction under adequate The indications for this drug are now rare and is mainly used
cycloplegia. Cyclopentolate (1%) is applied topically in three to maintain binocular alignment at all times in children non
doses, 5 minutes apart and the refraction is performed 30 compliant with bifocal glasses.
minutes after the last dose. In India, due to darkly pigmented
iris, Atropine eye ointment (1%) is the preferred cycloplegic
agent, at least at the Àrst visit. Atropine is applied twice a day
for three days and refraction is performed on the third day.
The full hypermetropic correction obtained under cycloplegia
is then prescribed. By prescribing the full spectacle correction,
the patient does not have to accommodate and therefore
converge, to see clearly.
In children with fully accommodative esotropia, the deviation
is eliminated by the appropriate spectacle correction. If
the residual esotropia with glasses is less than 8 PD and
the patient obtains fusion, nothing more needs to be done.
Wearing spectacles has been shown to be an effective means
of restoring ocular alignment, preventing amblyopia, and
maintaining stereopsis in children with accommodative
esotropia.
Patients with accommodative esotropia who are prescribed
the full hypermetropic correction demonstrate signiÀcantly
smaller angles of deviation than those who are undercorrected
by as little as one spherical dioptre. This supports the current
practice of prescribing the full hypermetropic correction in
children with esotropia.7
Contact lenses have certain optical advantages over
spectacles for children with both refractive and nonrefractive
accommodative esotropia. In children with high hyperopia,
they eliminate the ring scotoma, magniÀcation and prismatic
effect associated with spectacle use. In children with high
AC/A ratios, they reduce the accommodative effort required
for near tasks.
56 l DOS Times - Vol. 17, No. 1 July, 2011
hyperopic children without strabismus.12 The average
amount of hyperopia in individuals with accommodative
esotropia and high AC/A ratios is approximately +2.00 D,
and in those with normal AC/A ratios it is approximately
+4.50 D.13 The average age of onset is younger than the usual
age of onset of accommodative esotropia, at 2.7 years.
Determining the AC/A ratio
Figure 4: Bimedial recession was performed to correct the The method used most commonly to estimate the AC/A
residual angle resulting in fusion with low grade stereopsis ratio is to simply compare the distance to the near deviation
during clinical evaluation. A difference of greater than 10
Followup and monitoring prism diopters is considered high.
Conventional teaching states that patients with The Heterophoria Method
accommodative esotropia require follow-up examinations
at intervals of 3 to 6 months, especially before the age of 6 The deviation at distance and near and the interpupillary
years. In addition to monitoring for spectacle compliance distance are (IPD ) are used to calculate the AC/A ratio
and the development of amblyopia, this ensures detection of
decompensation to a nonaccommodative deviation, a sequela • AC/A = IPD (cm) + (Dn – Dd)/D
which affects 11% to 48%8 of these patients.The patients also
require regular monitoring to ensure the need for increased • D = Àxation distance at near in diopters
treatment measures to continue adequate control9 or to
incrementally reduce treatment to encourage the expansion • Dn = Deviation at near
of fusional divergence.10
• Dd = deviation at distance
Weaning from spectacles
The Gradient Method
Most children with refractive accommodative esotropia
continue to require spectacle correction into adulthood to This is the most accurate method. The deviation is measured
control their esotropia. However, a subset of these patients at a constant distance while plus power lenses are used to
are able to discontinue spectacle wear as they become less reduce the amount of accommodation produced. As this
hyperopic during the adolescent years.11 The spectacle power method uses a constant testing distance, it is not inÁuenced
may be gradually reduced by 0.50-1.00 dioptre on each by proximal convergence. A normal AC/A measured by the
visit after ascertaining that ocular alignment is maintained gradient method is 3:1 to 5:1.
for distance and near with the reduced prescription. This
process is continued at six-month intervals, until the child • AC/A = (D1 – D0)/D
is orthotropic without spectacles, the hyperopic correction
cannot be reduced further without inducing a manifest • D1= Deviation measured with lenses
esotropia, or the child develops symptoms of asthenopia.3
• D0= Original deviation measured without lenses
Non refractive Accommodative Esotropia
• D = power of the lens
Non refractive accomdative esotropia is deÀned as an
esotropia greater at near than at distance Àxation, unrelated Management
to an uncorrected refractive error, and caused by abnormally
high AC/A ratio in the presence normal near point of A bifocal add is indicated for the patients who are fusing in
accommodation.1 the distance but have esotropia at near that is large enough
to interfere with near fusion (>10pd). The add will relax
Clinical characteristics the near accommodation, thus reducing convergence.6 The
purpose of a bifocal is to reduce the near deviation to an extent
The diagnosis of nonrefractive accommodative esotropia is that binocular vision and fusion develop at all distances.
based on the presence of signiÀcant esodeviation at the near The power of the bifocals are calculated by measurement of
Àxation on an accommodative target, with the refractive the deviation with increasing powers of plus lenses at near.
error fully corrected, and presence of high AC/A ratio as Usually a +2.50 to +3.00 D add is required to to control the
established with the gradient method. High AC/A ratio overconvergence at near and produce fusion.
esotropia usually occurs in patients with hypermetropia but
may occur in patients with myopia or no refractive error. For children 5 years of age and younger, the bifocal add
should be prescribed as an executive or a Áat-top type, with
Children with hyperopia who develop esotropia have the top of the bifocal bisecting the pupil in primary gaze in
higher AC/A ratios when compared with similarly matched younger children and a few millimeters lower (between the
lower eyelid and lower pupillary border) in older children.
Eliminating bifocals is feasible in approximately 60% of
cases after an average of 5 years of use, by 9 to 10 years of
age. However, excellent initial response is associated with
a lower likelihood that the bifocals can be withdrawn later
without recurrence of the esotropia.14
Hypoaccomodative Esotropia
Hypoaccommmodative esotropia is deÀned as an esotropia
greater at the near than at the distance Àxation,unrelated to
an uncorrected hypermetropic refractive error and caused
by excessive convergence from increased accommodative
effort to overcome a primary or secondary weakness of
accommodation.1
www. dosonline.org l 57
Clinical Characteristics Standard surgery
It is characterized by small refractive error, remote near Standard surgical approach is based on the deviation
point of accommodation, small deviation at distance Àxation, measured with full hypermetropic correction. The target
but large esotropia at near Àxation.1 Cycloplegic agents angle is an average of the near and distance deviation
may be required to temporarily suspend the excessive with correction. However, the standard surgery has a high
accommodation, exercises may be helpful in increasing the undercorrection rate of approximately 25%.6
accommodative amplitudes and rarely plus lenses may be
prescribed for clear vision at near. Augmented Surgery
Partially Accommodative Esotropia In augmented surgery the target angle is determined by
averaging the near deviation with correction and near
An esotropia is partially accommodative when deviation without correction. Results comparing the
accommodative factors contribute to but not account for entire standard surgery to this augmented surgery formula showed
deviation.1 This entity is also described as decompensated 26% undercorrection for standard surgery, while augmented
accommodative esotropia. It is believed to be an evolution of surgery resulted in 93% success rate with 7% overcorrection.16
a purely accommodative deviation into one that has both an
accommodative component and a portion that is not corrected Differential diagnosis
by suspending the accommodative effort. Various risk factors
have been implicated in precipitating the decompensation • Decompensated esophoria/intermittent esotropia
of a fully controlled acomodative esotropia including an
age of onset less than 2 years, untreated hyperopia, poor • Infantile esotropia
compliance with glasses, prolonged ill health, aggressive
patching therapy for amblyopia and a high AC/A ratio. • Pseudoesotropia
Clinical characteristics • Acquired non-accommodative esotropia
A residual esotropia(>10PD) for distance and near exists • VI cranial nerve palsy
despite full correction of the hypermetropic refractive error or
prescription of the bifocal lenses6. It is important to repeat the • Duane Syndrome
cycloplegic refraction to ensure that no residual, uncorrected
hypermetropia is present. Prognosis
Management There should be four goals when treating a child with
accommodative esotropia: to maintain normal visual acuity
Prescribing the full cycloplegic refraction initially will provide in both eyes, to restore normal ocular alignment, to maintain
the best opportunity for restoring ocular alignment and high-grade binocularity, and to foster emmetropization2.
maintaining good visual acuity and stereopsis. Amblyopia Restoring normal visual acuity in both eyes is the easiest
may be treated with patching and/or atropine penalization, goal to achieve, with success rates as high as 80% in some
and amblyopia treatment in accommodative esotropia is series .2,16 Restoring normal ocular alignment with spectacle
usually successful. therapy alone is the next easiest goal to achieve, with success
rates around 50%. Maintaining stereopsis is a much more
Surgical Management difÀcult goal to achieve, since even several weeks of ocular
misalignment in a young child may permanently impair
Surgery is indicated in partially accommodative and binocularity. In most series only about 25% of patients
deteriorated accommodative esotropia. Strabismus surgery achieve this goal. The most difÀcult of these outcomes to
is generally performed with the goal of only correcting the achieve is to successfully discontinue spectacle wear, while
non-accommodative component of the esotropia, with the simultaneously maintaining normal visual acuity, restoring
understanding that the child will still need to wear spectacles ocular alignment, and maintaining high-grade binocularity.
postoperatively to correct the accommodative component In most series <15% of accommodative esotropes are able to
of the esotropia.Bilateral medial rectus recession is the successfully discontinue spectacle wear even after long-term
procedure of choice for partially accommodative esotropia. follow-up.
Unilateral recession/resection may also be performed on an
amblyopic eye. There is however controversy regarding how Role of refractive surgery in accommodative esotro-
to determine the target angle. pia
Prism Adaptation In older children and adults, refractive surgery has been
reported to be an effective means of correcting hyperopic
Preoperative prism adaptation15 is used to predict the refractive errors and achieving ocular alignment in
patient’s fusional capability and determine the augmented accommodative esotropes without spectacles17. However,
target angle for surgery. Fresnel prisms, split equally over the it is limited by its inability to consistently correct refractive
two eyes, are prescribed over the full hypermetropic spectacle errors exceeding 6D of hyperopia with the currently available
correction. Patients are followed at 1 to 2 week intervals technology. Several short case series show good results in
and the prism is adjusted until the deviation stabilizes at an children as well but randomized clinical trials are needed to
esotropia of 8 prism diopters or less. Surgery is done for this fully establish its safety and efÀcacy.
amount of esotropia that has been determined by prolonged
prism adaptation. Operating on the larger adapted angle References
reduces the rate of undercorrection, with the predictability
of a successful surgical outcome at 90%. The disadvantage of 1. Von Noorden G K, Campos E C. Binocular Vision and ocular
prism adaptation is the time and cost involved in prescribing motility; theory and management of strabismus. 6; Mosby: 312-
and adjusting the prisms until the deviation stabilizes. 320.
2. A ClassiÀcation Of Eye Movement Abnormalities And Strabismus
(CEMAS) Report of a National Eye Institute Sponsored Workshop,
2001
58 l DOS Times - Vol. 17, No. 1 July, 2011
3. Lambert SR: Accommodative esotropia. Ophthalmol Clin North 11. Mulvihill A, MacCann A, Flitcroft I, O’Keefe M. Outcome in
Am 14: 425-32, 2001 refractive accommodative esotropia. Br J Ophthalmol 2000;
84:746-9.
4. Pollard ZF. Accommodative esotropia during the Àrst year of life.
Arch Ophthalmol 1976;94:1912-3. 12. Von Noorden GK, Avilla CW. Accommodative convergence in
hypermetropia. Am J Ophthalmol 1990;110:287-92.
5. Coats DK, Avilla CW, Paysse EA, et al. Early-onset refractive
accommodative esotropia. J AAPOS 1998;2:275-8. 13. Pediatric Eye Disease Investigator Group. Spontaneous resolution
of early-onset esotropia: experience of the Congenital Esotropia
6. Kenneth Weston Wright, Peter.H.Speigel .Pediatric ophthalmology Observational Study. Am J Ophthalmol 2002;133:109
and Strabismus. 2 nd Ed. Springer.
14. Ludwig IH, Parks MM, Getson PR. Long-term results of bifocal
7. C J MacEwen, E G Lymburn and W O Ho. Is the maximum therapy for accommodative esotropia. J Pediatr Ophthalmol
hypermetropic correction necessary in children with fully Strabismus 1989;26:264-70.
accommodative esotropia? Br J Ophthalmol. 2008 Oct;92(10):1329-
32. 15. Prism Adaptation Research Group. EfÀcacy of prism adaptation in
the surgical management of acquired esotropia. Arch Ophthalmol
8. Ludwig IH, Parks MM, Getson PR, Kammerman LA. Rate of 1990; 180:1248-1256.
deterioration in accommodative esotropia correlated to the AC/A
relationship. J Pediatr Ophthalmol Strabismus 1988;25:8-12. 16. Wright KW,Bruce Lyle L. Augmented Surgery for esotropia
associated with hypermetropia. J pediatr Ophthalmol strabismus
9. McNeer KW. Childhood and adult strabismus surgery. In: 1993;30:167-170
Symposium on strabismus. Transactions of the New Orleans
Academy of Ophthalmology. St. Louis: CV Mosby; 1978. p.207. 17. Pehere NK, Ramappa RM. Refractive surgery in children: treatment
options, outcomes, and controversies. Am J Ophthalmol. 2010 May;
10. Dyer JA. Nonsurgical treatment of esotropia. In: Symposium 149(5):870-1
on strabismus. Transactions of the New Orleans Academy of
Ophthalmology. St. Louis: CV Mosby; 1971. p. 157.
www. dosonline.org l 59
Retina
Lalit Verma
Lalit Verma MD, Shaifali Gupta MS
Centre for Sight, Safdarjung Enclave, New Delhi
Monotherapy with vascular endothelial growth factor are endophthalmitis and retinal detachment. After one
(VEGF) inhibitors, mainly Ranidizumab is the gold intravitreal injection the incidence of these is very less,
standard of treatment of subfoveal choroidal neovascular i.e around 0.13% which is not of much signiÀcance. But
membrane. However the major drawback of these vascular the cumulative incidence of side effects after giving many
endothelial growth factor inhibitors is the need for number of injections can be of signiÀcance.
injections and side effects of frequent intravitreal injections.
The potential side effects after intravitreal VEGF inhibitors PDT has been shown to be effective in controlling both
01 May 2007
12 July 2007
09 January 2008
78 year old male had a best corrected visual acuity of 6/15 in his right eye complaining of metamorphopsia. Fundus ƀuorescein
angiography showed subfoveal choroidal neovascular membrane whish shows leakage in late phase. After low ƀuence PDT and
intravitreal injection of vascular endothelial growth factor inhibitor he improved to 6/12. His angiogram 4 weeks following treatment
showed regression of the membrane with no leakage in the late phase. After this he was on continuous follow up and 10 months
following treatment his angiogram showed a healed lesion with no leakage.
www. dosonline.org l 63
experimental choroidal neovascularization in animal models biomicroscopy and best corrected visual acuity was measured
as well as subfoveal choroidal neovascularization (CNV) in using snellen chart. Baseline fundus Áuorescein angiography
humans by causing closure of mature vessels. The therapy was done and greatest lesion diameter and least spot size
results in temporary closure of choroidal new vessels for a were measured for the low Áuence photodynamic therapy.
period of approximately 1 to 4 weeks. By 12 weeks, most Optical coherence tomography was done to conÀrm the
patients have reperfusion or reproliferation of choroidal diagnosis and to see the amount of macular edema caused by
new vessels resulting in the need for retreatment to achieve subfoveal choroidal neovascular membrane.
sustained effect and visual stabilization. On the other hand,
PDT by itself also causes upregulation of VEGF. Single Low Áuence photodynamic therapy was done using light
treatment with PDT can cause increased Àbrosis associated intensity of 50mJ/m2 at 300mW of power for 83 seconds as
with CNV in 8.6% of patients and branch retinal arteriolar or compared to standard Áuence where 100 mJ/m2 at 600mW
venular nonperfusion in 2.3%. The Àbrosis and nonperfusion of power for 83 seconds. After 5 days of photodynamic
is seen more signiÀcantly at high Áuence PDT. therapy intravitreal injection of vascular endothelial growth
factor inhibitor (lucentis / avastin) was given. Patients were
Thus in this study our aim was to reduce the number of followed up one day, one week, two weeks and four weeks
intravitreal injections of VEGF inhibitors and the side effects after intravitreal injection. At every visit best corrected visual
of monotherapy with PDT by combining Ranidizumab acuity was noted along with fundus examination. After 4
injections with low Áuence PDT. Combo therapy has the weeks repeat Áuorescein angiography and optical coherence
advantage of reducing the number of injections to three or angiography was done to see any leakage or residual
four. Hence in the series we combined low Áuence PDT with choroidal neovasular membrane respectively. If leakage or
VEGF inhibitor with the aim of having advantage of both edema is not fully resolved repeat intravitreal injection was
(i.e. countering existing vessels and preventing maturation given otherwise further follow up was done every 2 to 3
of new vessels). weeks. At next visits if needed Áourescine angiography or
optical coherence angiography was done to revaluate and
We conducted a prospective study of 12 eyes of 10 patients intravitreal injection given when needed.
who had been diagnosed as having subfoveal choroidal
neovascular membrane. Inclusion criteria were newly Out of 12 eyes of 10 patients, 6 were females and 4 were
diagnosed subfoveal choroidal neovascular membrane, males. Mean age was 58.67 years (range from 40 to 81 years).
pseudophakos or having mild cataract not responsible for The mean visual acuity pretreatment was 6/24 (range from
visual loss, no history of any other ocular disease. Exclusion Ànger counting at 2 meters to 6/9). Two patients have shown
criteria were one eyed, vision loss in other eye due to age complete regression of choroidal neovascular membrane
related macular degeneration. Each patient had undergone following single intravitreal injection of vascular endothelial
complete ophthalmoscopic examination including slit lamp growth factor inhibitors after low Áuence PDT. Five patients
Pretreatment OCT of the same patient as in previous pictures, showing subfoveal choroidal neovascular membrane along
with intraretinal edema. 6to 8 weeks following treatment there is regression of the membrane and absorption of the ƀuid,
with maintenance of normal foveal contour. 9 months following treatment with low ƀuence PDT and one intravitreal
injection patient is maintaining vision of 6/12.
64 l DOS Times - Vol. 17, No. 1 July, 2011
58 year old male at presentation he had a vision of 6/36 in his right eye and fundus ƀuorescein angiography
shows leakage in the late phase. He has received three intravitreal injections of vascular endothelial growth
factor inhibitor following low ƀuence PDT. He improved by one line and his latest angiography showed
partial regression of the neovascular membrane. He is maintaining vision of 6/24 in his right eye for the last
6 months and is on continuous follow up
www. dosonline.org l 65
S.No Age Sex Eye Pre VA Pre OCT Follow Up FFA (months) Post OCT Post VA
(thickness
1 57 F Left 6/60 0.718 micrometre) Partial Regresion 0.563 6/20
2 78 M Right 6/15 0.583 Complete Regresion 0.395 6/12
3 78 M Left 6/36 0.851 3 Partial Regresion 0.623 6/12
4 58 M Right 6/36 0.491 11 Partial Regresion 0.312 6/30
5 40 F Right 6/60 11 Complete Regresion 6/18
6 81 M Left 6/9 0.351 6 Complete Regresion 0.309 6/9
7 58 M Left 6/18 6 Complete Regresion 6/18
8 45 F Left 6/12 0.474 10 Complete Regresion 6/7.5
9 40 F Right 6/12 0.509 6 Complete Regresion 6/6
10 46 F Right FC2m 7 Complete Regresion 6/24
11 63 M Right 6/24 0.377 5 Complete Regresion 6/15
12 60 F Right 6/30 4 Complete Regresion 6/18
2
6
60 year old female complained of meta-morphopsia and was having 6/30 vision. Fundus ƀuorescein angiography showed
subfoveally leaking lesion suggestive of choroidal neovascular membrane. Low ƀuence PDT was done followed 5 days later by
intravitreal injection of lucentis. 4-6 weeks later her vision improved to 6/12 with less of meta-morphopsia and her angiogram
showed less leakage. OCT was done which showed minimal edema with small choroidal neovascular membrane and
distorted foveal contour. Second intravitreal injection was then given.4-6 weeks later she showed regression in leakage with
improvement in vision to6/9. OCT shows almost normal foveal contour. After third intravitreal injection angiogram showed
very mild leakage with normal foveal contour. She is maintaining a vision of 6/6 for last 2 months.
66 l DOS Times - Vol. 17, No. 1 July, 2011
received two intravitreal injections of vascular endothelial patients has shown partial regression and in 9 patients has
growth factor inhibitors and 5 patients received three shown complete regression of the leakage. Optical coherence
intravitreal injections of vascular endothelial growth factor angiography of the three patients showed residual choroidal
inhibitors following low Áuence PDT. Second and third neovascular membrane though it was less than the baseline
injections were generally needed at 4-6 weeks following and rest of the patients had normal foveal contour. The mean
previous injections. Fundus Áourescein angiography in 3 visual acuity postreatment was 6/9 (range from 6/60 to 6/6).
www. dosonline.org l 67
Retina
Neha Goel
Neha Goel MS DNB, Supriya Batta MBBS, Meenakshi Thakar MD FRCS(Ed),
Usha Kaul Raina MD FRCOphth, Basudeb Ghosh MD MNAMS
Vitreo retina Services, Guru Nanak Eye Centre, Maulana Azad Medical College, New Delhi
Choroidal hemangiomas are rare vascular hamartomatous (RD), cystoid macular edema (CME), subretinal Àbrosis
tumours that are the most common benign vascular and/or direct invasion of the macular region by the
tumours of the uveal tract.1 Though the incidence has not tumour.
been well documented, it has been estimated that one
choroidal hemangioma may be diagnosed for every 15-40 • Induced hyperopia (of upto 9D) may develop as the
choroidal melanomas seen in clinical practice.2 Virtually all tumour pushes forward in the macular area.
cases reported have occurred in Caucasians and there is no
sex predilection.3 Choroidal hemangiomas have no malignant • Metamorphopsia, photopsia, visual Àeld defects or, in
potential and they display a very slow rate of growth.4 very rare cases, pain secondary to neovascular glaucoma.
Classification • However, most solitary hemangiomas are discovered in
asymptomatic patients.
These tumours exist in two forms:
Clinical Characteristics (Figure 1-4)
1. Circumscribed
• Location - temporal to and near the optic disc.6
2. Diffuse - commonly associated with encephalofacial
angiomatosis (Sturge-Weber syndrome) • Size - If tumours are divided into small (upto 5mm basal
diameter and upto 2 mm thickness), medium (5 to 10 mm
In most clinical series of choroidal hemangioma, approximately basal diameter and 2 to 3 mm thickness), and large (over
50% of tumours are diagnosed as circumscribed and 50% as 10 mm basal diameter or over 3mm thickness), almost
diffuse associated with Sturge Weber syndrome.5 half the tumours are of medium size.7
Circumscribed Choroidal Hemangioma (CCH) • Solitary tumours are the rule; an eye containing more
than one CCH is extremely rare.
Clinical presentation
• Appearance - Amelanotic red-orange domelike masses
These tumours are usually diagnosed between third to sixth that blend in with the surrounding choroid.8 The tumour
decade of life.1 has less sharply demarcated margins than a malignant
melanoma.1
Symptoms and Signs1
• The nature and contour maybe difÀcult to appreciate,
• Decreased vision is the most common complaint. It especially when associated with RD. Overlying retinal
develops as a result of exudative retinal detachment pigment epithelial (RPE) changes and mild yellow-white
(a) (b) (c)
Figure 1(a): Fundus photograph of a 35 year old male showing orangish mass with indistinct margins,
superotemporal to the disc and minimal retinal exudation temporally
(b&c): Fluorescein angiogram showing mottled hyperƀuorescence which becomes more conƀuent in the late phase
www. dosonline.org l 69
(a) (b)
Figure 2(a): Right fundus photograph of a 22 year old male showing a juxtapapillary choroidal
hemangioma with surrounding RPE alterations Figure (b): Fluorescein angiogram showing
hyperƀuorescence surrounded by blocked ƀuorescence and window defects
(a) (b) (c)
(d) (e)
Figures 3(a): Right fundus photograph of a 27 year old male showing a juxtapapillary choroidal hemangioma with exudation
at the macula (b) ICG angiogram showing early hyperƀuorescence, which increases rapidly (c), (d), followed by a loss of
ƀuorescence or “dye washout” (e) in the late phase
foci on the tumour surface that correspond to areas of • angiogram, the Áuorescence increases and the initially
Àbrous metaplasia of the RPE are often observed. Pigment mottled pattern of Áuorescence becomes more conÁuent.
clumping and a surrounding rim of pigmentation around In the later stages, multiloculated accumulation of dye in
the tumour are also common features (Figure 2a).1 the outer retina develops (Figure 1,2,).3
• Although these tumours are highly vascular, dilated Indocyanine green (ICG) angiography is the most useful
and tortuous feeder vessels are typically not observed. study for demonstrating the intrinsic vascular pattern of
Retinal hard exudates are minimal or absent. CCH. It shows a well deÀned area of an early, intense,
and relatively uniform hyperÁuorescence within 30
Imaging studies6 seconds of injection of dye (Figure 3b). This is followed by
a rapid increase in the hyperÁuoresence which peaks at
• On Áuorescein angiography, irregular hyperÁuorescence
of the choroidal vessels within the tumour begins during 3-4 minutes (Figure 3c,3d,4b). Late in the ICG angiogram
the choroidal phase of angiogram before the Àlling of
the retinal arterioles. In the arteriovenous phase of the a characteristic “dye washout” is noted, with the tumour
rapidly losing its Áuorescence (Figure 3e).
70 l DOS Times - Vol. 17, No. 1 July, 2011
(a) (b)
(d)
(c)
Figure 4(a): Left fundus photograph of a 43 year old male showing
a choroidal hemangioma at the macula Figure 4(b): ICG angiogram
demonstrating corresponding hyperƀuorescence
Figure 4(c): Ultrasound B scan showing a dome shaped choroidal
mass with high internal reƀectivity Figure 4(d): Spectral domain OCT
reveals shallow SRF overlying the choroidal mass
• Optical coherence tomography (OCT) can be used to visual impairment occurs from hyperopic amblyopia or from
evaluate secondary retinal morphologic changes, such as secondary retinal detachment.6
shallow subretinal Áuid (SRF, Figure 4d) or CME.9
Patients with this tumour usually have a brighter pupillary
• On B-scan ultrasonography, a hemangioma appears as a reÁex compared to the contralateral eye. This phenomenon,
smooth contoured, dome shaped, choroidal mass which which is due to light reÁex from the highly vascularised
demonstrates high internal reÁectivity on A-scan studies tumour in the posterior pole, has been called the “tomato
(Figure 4c). catsup” fundus.6 Diffuse orange choroidal thickening is seen
clinically (Figure 5a,b). Though choroidal hemangiomas are
• The tumour enhances moderately with contrast material typically located posterior to the equator, the diffuse tumours
on CT scan. may extend as far anteriorly as the ora serrata.1
• MRI scan shows the tumour to be hyperintense to the B-scan ultrasonography demonstrates a diffuse, highly
vitreous on T1-weighted images and isointense to the echogenic thickening of the choroid.
vitreous on T2-weighted images.
Associated features – The classic skin lesion of Sturge Weber
Diffuse Choroidal Hemangioma syndrome is the facial hemangioma, referred to as nevus
Áammeus or port wine stain (Figure 6a). The typical CNS
Choroidal hemangiomas associated with Sturge-Weber feature is a diffuse leptomeningeal hemangioma ipsilateral
syndrome are congenital. There is involvement of both to the facial hemangioma (Figure 6b). This lesion can show
the choroidal vessels and the episcleral and conjunctival secondary calciÀcation and appears radiographically as a
vasculature.1 radiopaque double line called the “rail road track” sign.
Convulsions frequently occur as a result of these alterations.
Diffuse tumours are most commonly unilateral with the
tumour involving the same side as the nevus Áammeus in Differential Diagnosis
Sturge-Weber patients. If there is a bilateral nevus Áammeus,
it is not unusual to have choroidal hemangioma in both eyes. Whenever a choroidal mass is encountered on examination,
the following differentials must always be kept in mind.
Diffuse tumour is usually diagnosed when the affected patient
is young (median age 8 years), either because the associated • Amelanotic choroidal melanoma
facial hemangioma prompts a fundus examination or because
• Metastatic choroidal tumour
www. dosonline.org l 71
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