DOS_dec_2010

Contents

E5 ditorial Clinical Monthly Meeting

Focus 53 Clinical Case-1: The Big Oil Leak……A Surgeon’s Nightmare

11 Optic Neuritis S.P .Chaudhary, Manisha Agarwal

57 Clinical Case-2: The Big Bug!

Manisha Acharya MS, Umang Mathur MS

Retina F69 orthcoming Events

33 Polypoidal Choroidal Vasculopathy (PCV) Columns

Priyank Garg, Samarth Agarwal, Arindam Chakravarti, S. Natarajan 71 Membership Form

OCuloplasty Tear sheet

39 CT Imaging of the Orbit 79 Keratoconus: Diagnosis and Management

Samarjit S. Ghuman, Seema Sud Ritu Arora, Parul Jain

Miscellaneous

49 New Venture – Realising Dreams

Vipin Sahni MS

www.dosonline.org 3

Editorial

My Dear Friends and Colleagues,

A Very Happy and Joyful New Year 2011 to all of you.
DOS Marches Ahead in the new year with sparkling new initiatives to benefit Ophthalmologists.

The DOS PhacoFellowship Course.
We worked hard to bring it to you and we have finally succeeded. Probably the first time that a society is organizing
such a high value fellowship programme for its members. We all know that all of us do not have access to latest
technology and we at DOS have always looked for ways to rectify it. And now we have it for you.

The Hands On Two Wks Phaco Fellowship.
There are 8 seats everyyear at present ; 4 for Delhi Doctors and the rest for Ophthalmologists from outside Delhi.
The DCRS system that we already have in place will be the basis of selection of the candidates. We are thankful to Venu Eye Institute for
starting the fewllowship which will be supported by M/s. Zeiss Ltd.

Those of you who wish to join this fellowship programme are requested to apply to the DOS office immediately.

Observerships in Subspecialities. We are planning to start Observership
In the best Ophthalmology Institutes in Delhi, with highly trained faculty and the latest tech. First hand experience and training. learn to
use new equipments and get retrained in Ophthalmic Subspecialities of Retina, Oculoplasty, Squint, Glaucoma and Cornea etc. One to Two
weeks of Observership and intense training. Again a first by any society.

The Annual Conference.
We wish to invite you to our 62nd Annual Conference from 15th to 17th April 2011 at Hotel Ashok, Delhi. “Trends in Ophthalmology” A
Showcase of the latest and the best Ophthalmology practice in India. Please keep these dates free and please register well in time.Online
registration is open. Please visit:http://www.dosonline.org/ for further assistance. The registration date has been extended to 15th January, 2011.

Dr. Omparkash Oration:
The Annual Dr Omparkash Oration starts this year at the annual conference. We begin with the most distinguished speaker Dr. Michael
Knorz from Germany. He is a pioneer of Lasik in Germany and has the singular achievement of training many Indian Ophthalmologists in
Lasik, when it first came to India. We are Proud to Present Him to you.

Diabetic Retinopathy Screening Camps.
We are organizing DR screening in association with Delhi Medical Association on 16th January, 2011. Delhi Members are invited to volunteer
for this programme.

Dear Friends,

We have taken several new initiatives during this year and we wish to do more. We welcome your suggestions and your ideas.

Yours Truly.

Thanking you,

Dr Amit Khosla
Secretary,

Delhi Ophthalmological Society

Email: [email protected]

Himanshu R. Gupta MS

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Optic Neuritis Focus

Dr. S. Ambika Dr. J.L. Goyal Dr. Ramesh Kekunnaya Dr. Satya Karna Dr. Anshu Rohatgi
DNB MD, DNB MD, FRCS DO, DNB DM, MD, DNB

Optic Neuritis is an inflammatory disease of the optic nerve, characterized by sudden loss of vision (partial or complete),
or sudden blurred, “foggy” or defective vision, and pain on movement of the affected eye. In most of the cases the
appearance of the optic disc is normal and swelling may be seen in very few cases.It is necessary to differentiate it from
other causes of disc edema, as optic neuritis as such has a relatively benign ophthalmic course usually, while other causes
may point towards a severe CNS sequele. It is also important to identify optic neuritis, as depending upon the clinical
situation it may be associated with multiple sclerosis (MS). Timely identification and appropriate intervention may reduce
the morbidity due to MS.

Dr. S. Ambika (SA), DNB, Director, Neuro-Ophthalmology Department, Sankara Nethralaya, Medical Research Foundation,
Chennai. Dr. J.L. Goyal (JLG), MD, DNB, Director, Professor and Head of Neuroophthalmology, Guru Nanak Eye Centre,
MAMC, New Delhi. Dr. Ramesh Kekunnaya (RK), MD FRCS, Pediatric Ophthalmology & Neuro-Ophthalmology, L.V.
Prasad Eye Institute, Road No 2, Banjara Hills, Hyderabad. Dr. Satya Karna (SK), DO, DNB, Consultant Ophthalmologist,
Max Hospital and Shroff Eye Centre, New Delhi. Dr. Anshu Rohatgi (AR) DM, MD, DNB, Hony. Senior Consultant,
Department of Neurology, Sir Ganga Ram Hospital, New Delhi, India.

Dr. Ankur Sinha (AS) MD (AIIMS), Consultant Ophthalmologist, Specialist Strabismology, Glaucoma and Neurophthalmology,
Max Vision Eye Care Centre, 305, Vinayak Enclave, Opp Post Office, Between Nursery Circle and Amrapali Circle, Viashali
Nagar, Jaipur

AS: What clinical signs and Symptoms suggest Optic disc hyperemia, oedema (polar blurring in initial stages),
Neuritis? papillary and peri-papillary haemorrhages, vitreous cells
in the posterior vitreous, sometimes hard exudates in
SA: The hallmark symptom of optic neuritis is acute vision macular area, venous dilatation, loss of venous pulsations
loss with painful ocular movements. Optic neuritis and temporal pallor if patient comes late. Transient visual
signs include all features of optic nerve dysfunction like obscuration is the common symptom in papilloedema.
reduced visual acuity, color vision and contrast sensitivity,
classical field defects are central defects. Optic nerve head RK: Optic neuritis (ON) can present in four forms, Retrobulbar
appearance can range from normal disc [retrobulbar Neuritis (RBN), Papillitis, Perineuritis and Neuroretinitis.
neuritis] to swollen optic disc [papillitis / neuroretinitis] RBN is the most common form. Perineuritis and
Neuroretinitis are not associated with the risk of Multiple
JLG: Decreased / blurred vision/ dyschromatopsia/decreased sclerosis (MS).
brightness of the same torch in the affected eye, associated
with Pain on ocular movements (due to inflammation SK: Typical Optic neuritis presents as mostly unilateral sudden,
of dural sheath) which is usually abrupt with / without painful, blurring of vision with rapidly progressive loss
prior H/O fever / sinusitis (atypical optic neuritis) are the of vision over the first few days to a week. Color vision is
symptoms. Decreased visual acuity ( decreasing further affected much more than the visual acuity. Vision ranges
after exercise or hot bath called pulfrich phenomenon), from 6/6 with a field defect to NPL. Fundus exam shows
sluggish pupils, RAPD (must) in u/l cases, impaired normal disc in half of the cases (retrobulbar neuritis) and
contrast sensitivity (normal 1.65 or more on pelli - robson disc edema (papillitis) in the rest. Presence of RAPD is
charts) dyschromatopsia (relative impairment of brightness suggestive of an optic neuropathy. Bilateral simultaneous
of colour vision),central /centrocaecal scotomas in visual optic neuritis is seen most often in children and is
fields, are the signs which must be looked for. Also I have associated with papillitis.
seen patients of amblyopia being referred (without doing
refraction) for optic neuritis. On fundus examination we AR: Typically ON (optic neuritis) presents with acute unilateral
may have normal disc in retrobulbar optic neuritis, or vision loss progressing to nadir in hours to days

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The most common visual symptoms are scotoma (45%) be mistaken for functional vision loss and so performing
and visual blurring (40%). optic nerve function tests can only differentiate these two
conditions.
Pain is present is approximately 92% of patient and may be
constant and is usually worse with eye movement. JLG: Papilloedema, Benign intracranial hypertension, AION,
Pseudoneuritis, Optic nerve drusen, venous occulusions,
Positive visual phenomenon including colors and flashing pituitary adenomas, amblyopia, high hyperopia, sometimes
lights are reported in 30% of cases of ON. uveitis and malignant hypertention.

AS: What cardinal signs and Symptoms are a must for RK: Ischemic optic neuropathy (ION), Compressive optic
diagnosis of Optic Neuritis? neuropathy (CON), Infiltrative optic neuropathy (INON)
and rarely Papilloedema, Malingering.
SA: The cardinal symptoms of optic neuritis are painful sudden
drop in vision and central scotoma and the cardinal signs SK: The common differentials are atypical optic neuritis, AION,
include all features of optic nerve dysfunction like reduced compressive optic neuropathy.
vision, color vision and contrast sensivity, RAPD Relative
afferent papillary defect [in case of unilateral involvement], AR: (1). AION (2). PION (3). Toxic Neuropathy (4). LHON
swollen /normal disc and central field defects. (5). Nutritional optic neuropathy.

JLG: Blurring / Decreased visual acuity , Impaired brightness of AS: How can one differentiate other causes of Disc Edema
light/ colours, impaired contrast sensitivity, RAPD, visual from Optic Neuritis?
field defects in the central/paracentral area , disc hyperemia
with polar blurring (may be absent in retrobulbar neuritis), SA: Any disc edema has to be differentiated whether it is a
venous dilatation and loss of venous pulsations. PVEP will true or pseudo disc edema before proceeding further
always show prolonged latency and decreased amplitude as investigations. Optic neuritis always manifests all features
compared to other eye by more than 20%. Normal values of optic nerve dysfunction. Acute optic neuritis disc
in our machine are 100+/- 10 m.sec latency and >5uv edema has hyperemia with elevation and haemorrhages
amplitude. [occasionally]. In case of chronic presentation it can have
associated pallor, unlike an ischaemic optic neuropathy
RK: The classic clinical triad includes vision loss, pain on where disc edema with sectoral pallor is the hallmark. Not
motility and dyschromotopsia. RAPD also is one of the key only the clinical appearance of the disc edema is helpful
signs. The presenting vision may vary from 6/6 to PL. In to derive at the diagnosis but the history and associated
cases where vision is very good, contrast vision and visual features as mentioned earlier are useful in differentiating
filed defects aid in the diagnosis. the optic neuritis disc edema from other disc edema.

SK: Painful loss of vision is a symptom in majority except MS JLG: Examine BP to rule out hypertention, Refraction to rule
patients who might have painless recurrences. Presence of out Refractory error and amblyopia, S/L examination
RAPD is a must, except in bilateral cases where the extent to rule out uveitis, USG, OCT, CT Scan, FA to rule
of visual loss is similar in both eyes. Colour vision loss out buried drusen. I have seen few cases of pituitary
should be out of proportion of visual loss. adenomas being treated as retrobulbar neuritis by pulse
steroids. In these cases visual acuity improves by systemic
AR: • Decreased visual acuity. pulse steroids because of decreased compression due to
decrease in edema by steroids further strengthening the
• Decreased color perception, particularly red appears misdiagnosis. Visual field examination may reveal field
less intense defects respecting vertical midline, or MRI with contrast
is required to clinch the diagnosis. Papilloedema/benign
• RAPD (relative afferent pupillary defect) intracranial hypertension will have symptoms of recurrent
headaches with nausea or vomiting, normal/ near normal
• Abnormal visual fields – no specific pattern. visual acuity, transient visual obscuration, disproportionate
massive disc edema, dilatation and tortuousity of veins,
• Optic disc is normal in two-third of cases (reterobulbar haemorrhages, loss of venous pulsations which can not be
optic neuritis) induced even after pressing the globe, MRI with contrast
will be most important to prove ICSOL. Benign intracranial
• Optic disc edema is present in 1/3 of cases. Disc edema hypertension patients have typical papilloedema. They
is mild, nonfocal and only rarely associated with are usually obese females, on oral contraceptives, with
hemorrhage, retinal exudates or vitreous cells. persistent headache have normal/ small ventricles on
MRI, may have empty sella, normal CSF composition, on
• When severe edema/ hemorrhage is present, diagnosis MRV may show closed dural sinuses. AION will have H/O
of idiopathic ON is in question. diabetes, hypertension, collagen disorder, usually present
with acute loss of vision in the morning probably due to
AS: What are common differentials for Optic Neuritis? nocturnal hypotension. In Arteritic AION, ESR, ASO titre,
CRP will be raised, temporal artery may be palpable and
SA: Any optic neuropathy of infectious / ischemic /compressive/ tender, may need biopsyto confirm arthritic AION. Venous
infiltrative origin can be the differential for classical optic
neuritis. Typical optic neuritis is classical in its presentation
which cannot be missed if the aforementioned features
are evaluated. A case of retrobulbar neuritis can easily

12 DOS Times - Vol. 16, No. 6, December 2010

occlusions are usually U/L with lot of hemorrhages with sugar, lipid profile, Sarcoid workup [ serum ACE, Lysozyme
H/O diabetes, hypertension or other systemic diseases. and calcium ] Chest X ray, Mantoux, Quantiferon TB gold,
Visual acuity in venous occlusion is much better than RA, ANA,VDRL etc.
expected with that type of picture in optic neuritis.
• Optic neuritis patients with spine signals or NMO suspicion
RK: ION affects older individuals usually more than 50 years of are subjected for Aquaporin 4 Antibody evaluation.
age, typically those who have altitudinal field defects. The
presenting signs include sectoral, pallid disc edema and • VEP is ordered to document the optic pathway dysfunction
Nerve Fiber Layer (NFL) hemorrhages. which usually shows delayed P2 latency and it has an
important role in case of retrobulbar neuritis.
CON cases may experience gradual decrease in vision,
diffuse field loss, severe disc edema (rarely can present Lumbar puncture and CSF analysis are advised only for
without disc oedema). atypical optic neuritis patients and in case of recurrent
optic neuritis with high risk for CDMS.
INON will have gradual decrease in vision with severe disc
edema and hemorrhages. There may be history suggestive JLG: Examination protocol includes visual acuity, contrast
of associated ocular or systemic diseases. sensitivity, color vision with ishihara charts, pain during
eye movements, change in visual acuity after hot bath or
Papilloedema is bilateral and they will have only transient exercise, visual fields 30-2 ( altitudinal defects in AION,
obscurations of vision. central scotomas in optic neuritis, enlarged blind spot
in papilloedema), bitemporal field defects in pituitary
Malingering patients will not have RAPD. Color vision and adenoma, pupillary reaction, RAPD, Fundus examination
field of vision will be normal. They may show cloverleaf (blurring of disc margins, hyperemia, venous dilatation,
pattern on field test. hemorrhages, exudates, venous pulsations – spontaneous/
induced/ totally absent) Pattern VEP (Flash VEP if the
SK: Optic neuritis is painful as against AION which is painless. visual acuity is less than 3/60), USG, OCT, FFA for optic
Typical optic neuritis occurs in individuals between 20-40 nerve drusens, AION and venous occlusion.. These tests
years of age. Childhood optic neuritis is atypical as it is will lead you to the extent and etiology of optic neuritis.
bilateral. Optic neuritis above 40 years of age is suggestive of Always look for field defects and VEP abnormalities in the
ischemic etiology (AION) unless proven otherwise. Rarely fellow eye which is supposedly normal. Upto 70% of these
optic neuritis above 40 may be painless as in MS. Also, eyes may show some abnormality which the patient does
uveitis may be associated with unilateral optic neuritis. not complain.
Progression of vision loss beyond 10 days with or without
treatment should suggest compressive optic neuropathy. RK: Detailed ocular and relevant neurological history, Vision,
Color vision, Look for RAPD, Fundus evaluation, HVF
AR: • In disc edema usually no visual loss only visual 30-2, Visually Evoked Potential (VEP) and MRI SCAN
obscuration.
SK: My examination protocol for all patients in the OPD is
• Pupillary reaction is not affected in disc edema BCVA, RAPD check, anterior segment examination by slit
lamp, applanation tension, ocular movements and dilated
• Color vision not affected in patients with disc edema fundus examination with indirect ophthalmoscope. In a
patient who complaints of blurring of vision where the
AS: What is your examination protocol for work-up of a case cause is not apparent and in any patient I detect RAPD, I
of Optic Neuritis? perform a color vision test and confrontation fields also.
This examination protocol leads to the correct diagnosis of
SA: If the diagnosis of optic neuritis is confirmed with the optic neuritis in majority of cases. In all optic neuropathies
clinical examination. All patients are subjected to these (detected by RAPD) I order Humphrey Visualfields Test
following investigations. 30-2.

• Visual fields – [Humphrey visual field 30-2 standard AR: Clinical Examination
programme with size 3 stimulus], few patients with visual
acuity less than 6/60 may be able to perform a Humphrey • Visual acuity
fields with size 5 stimulus. Confrontation fields are very
useful in patients who are unable to perform fields tests • Pupillary reaction
due to poor vision.
• Fundus evaluation
• All Typical optic neuritis patients are advised for an MRI
Brain and Orbit. MRI Brain and orbit with post contrast • Color vision
fat suppression is the preferred imaging modality of choice
for optic neuritis patients. • Visual Fields

• As per ONTT recommendation no laboratory tests or • Ancillary Investigation
lumbar puncture is needed for Typical Optic neuritis
• VEP
• If we suspect an infectious / granulomatous optic neuritis
patients are advised for Complete Haemogram, Blood • OCT

• MRI (brain) + Orbit + Spine.

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AS: What systemic investigations do you order for patients Some examples are progressive visual loss, painless visual
with Optic Neuritis? loss, hemorrhage out of proportion to the disc edema,
associated uveitis, associated meningitis etc.
JLG: Complete Hemogram, ESR, blood sugar, Mx and Xray
chest,VDRL, BP, MRI brain and orbit with contrast with AR: One should suspect Atypical optic Neuritis
FLAIR sequence (preferably 3 Tesla. MRI for better
resolution), ACE levels, ANA, CSF (for pleocytosis, If
abnormal proteins and sugar, oligoclonal band) and
mitochondrial DNA studies in LHON. Lumbar puncture • Lack of pain.
however do not provide any additional value if MRI is done
in multiple sclerosis. Look for enhancing demyelination • Visual deficiency beyond 14 days.
plaques around lateral ventricles, brainstem, posterior
cranial fossa and optic nerves in MRI. • Ocular findings are suggestive of inflammatory
process.
RK: None for typical optic Neuritis, other than MRI.
• Evidence of systemic conditions.
SK: In all cases of optic neuritis I order MRI Brain and orbits
with contrast. In cases of atypical optic neuritis where MRI Causes
is normal and clinical signs suggest uveitis or systemic
illness, I order complete blood counts, Serum ACE, serum • Vasculitis
Calcium, phosphorus, VDRL, TPHA, RA factor, ANA,
dsDNA, Chest Xray, Mantoux test. I do not do any systemic • AIDS
investigations for patients with optic neuritis unless they
have any systemic illnesses like diabetes, hypertension etc. • Viral infections

AR: Blood glucose, Vasculitis markers, Complete blood counts, • Endophthalmitis
ESR, CRP.
• LHON
AS: What is typical and atypical Optic Neuritis? How would
one differentiate? Granulomatous inflammation – Sarcoidosis, T.B.

SA: Any optic neuropathy which occurs in middle to elderly AS: Is there any difference between optic neuritis in children
age group patient, painless, bilateral, progressive with and adults?
insidious onset, with or without disc edema are defined
as an atypical optic neuropathy. We can differentiate an SA: Optic neuritis in children is mostly of infectious origin,
atypical optic neuritis only by a detailed history, stepwise but in adults idiopathic optic neuritis is common. Children
clinical approach [as mentioned earlier in answer] and by commonly develop optic neuritis following a systemic
performing careful optic nerve function tests. illness like viral fever /post vaccination. Usually children
develop bilateral papillitis. In children VEP is useful to
JLG: Typical optic neuritis is usually unilateral, between 18-45 asses the optic pathway dysfunction due to lack of detailed
years of age, pain on ocular movements, with visual acuity history.
varying from no PL to 6/12, dyschromatopsia. Visual loss
does not progress beyond 2days. JLG: Otic neuritis in adults isunilateral while in children it
is bilateral. In adults optic neuritis is more retro-bulbar
Atypical optic neuritis means optic neuritis associated with than in children where it is usually anterior with glaring
systemic/Local illnesses like fever, bilaterality, visual loss disc oedema, disc oedema is 70% in children and 30% in
progressing beyond 1 week, more frequent recurrences at adults. In adults association with MS is high while it is
shorter intervals, neuro-retinitis, LHON, infectious ( viral, hardy seen associated with MS in children. Visual Prognosis
tubercular, syphilis, and cat scrach fever) or auto-immune is poorer in children as compared to adults. In children
neuritis, toxic optic neuropathies, paraneoplastic eg lung response to steroids is excellent and they become steroid
carcinomas, and uveitis. They mimick optic neuritis. dependent also. In adults response to steroids is variable.
It is usually post infectious in children while in adults it is
RK: The features of typical optic neuritis include sudden onset MS/ idiopathic.
central visual loss in a young adult, pain on eye movement,
unilateral involvement and enhancement of optic nerve on RK: The bilateral involvement and Papillitis type of ON is more
MRI. common in children as compared to adults.

The features of atypical ON include bilateral involvement, SK: Optic neuritis in children is often bilateral, presents as
slowly progressive vision loss, severe vision loss, lack of pain papillitis, responds very well to steroids but is steroid
on eye movement, disc edema associated with hemorrhage, dependant in some cases, i.e. vision loss recurs when
normal MRI scan. steroids are tapered. In children, optic neuritis is generally
not associated with MS.
SK: Typical optic neuritis is described in Q.1 above. Atypical
optic neuritis is any clinical presentation other than that. AR: In children papillitis is seen more commonly than
reterobulbar neuritis and bilateral involvement is seen
commonly.Optic neuritis is seen more commonly
following viral infections in children.

14 DOS Times - Vol. 16, No. 6, December 2010

AS: Role of VEP, when do you need to repeat it? AR: OCT is a means of quantifying retinal nerve fiber layer
(RNFL) thickness and may be useful prognosticating the
SA: VEP has a vital role in retrobulbar neuritis / malingering / optic neuritis.
paediatric optic neuritis. I feel a careful pupillary assessment
will be more useful than a VEP. The necessity to repeat a Patients of ‘ON’ those with progress to multiple sclerosis
VEP is to confirm whether the optic nerve functions are show a progressive loss of RNFL whereas RNFL remains
restored or worsened .Most of the time we have ample stable in patients with isolated optic neuritis.
clinical evidence to prove the optic nerve function status
so I don’t believe in repeating a VEP for same. AS: What is your standard treatment protocol? When do you
prefer to start Steroid Treatment? Does steroid treatment
JLG: VEP should be done in the beginning. VEP is done to have a bearing on final visual outcome of a patient?
confirm the optic nerve conduction defect and to quantify
the extent of damage. VEP is repeated usually after one SA: All optic neuritis patients particularly the demyelinating
month when a good amount of recovery has occured and at optic neuritis should receive Intravenous methyl
3 months when the recovery is almost complete. The patient predninsolone 1gm /day x 3 days followed by tapering
also is satisfied to see the objective improvement. Always oral steroids.
look for VEP abnormality in the supposedly normal eye
which also is abnormal in majority of the cases. Difference I prefer to treat all optic neuritis patients even if they are
of 20% in latency/ amplitude between the two eyes I take 2-3 weeks of onset of vision loss, but always early initiation
it as abnormal. of intravenous steroids are proven to be very beneficial.

RK: The VEP is very useful in arriving at a diagnosis when the According to ONTT trial Intravenous steroids prevent
clinical features are not very clear. We do it in all cases as a relapses and hastens the recovery, but it does not affect the
baseline investigation and also in recurrent cases. The key final visual outcome.
thing to look at is delayed latency.
JLG: As soon as the patient comes, we send the blood
SK: Majority of typical optic neuritis cases are of viral etiology. investigations, order Gadolinium enhaunced MRI, VEP,
VEP is indicated in most cases of optic neuritis, when MS MX test, visual fields central 30-2. We start intravenous
is suspected either clinically or on MRI, along with BAER Methyl prednisolone sodium succinate (once we are sure
and SSEP for conformation of MS. VEP shows delayed that patient is not having diabetes, tuberculosis, any fever,
latency of the waveform which persists for many months infection, usually by next day) in a dose of 500mgm I/V in
after the visual parameters have recovered. 300ml of 5% dextrose fast in 30-45 minutes twice a day for
three days followed by tab prednisolone 40 mgm per day
AR: VEP is helpful in establishing diagnosis especially in after breakfast for 11 days, then oral steroids are tapered in
patients with retro bulbar neuritis. another 2-3 weeks. Steroids definitely hasten recovery. Also
when the patient is in agony because of rapid loss of vision
It is also helpful in prognosticating visual recovery and plcebo therapy will lose patient’s faith in you. Although
follow up, however clinical recovery occurs much faster ONTT says ultimate outcome is same I have a feeling that
and earlier than change in VEP. I/V steroids definitely should have better visual outcome
at the end. In our country. We are not dealing with pure
AS: Does RNFL measurement have any role in management MS Cases, some have mixed etiology. It is always better
of optic neuritis? to control the damage to optic nerve as early as possible.
More the duration of edema more will be the axon death
SA: OCT can be done in optic neuritis patients to measure RNFL which is irreversible because optic nerve fibres do not have
thickness which can be correlated with the visual outcome. neurilemma for axon recovery.
Measurement of RNFL thickness pre and post treatment
is more helpful for follow up. Optic neuritis patients show RK: IVMP 250 mg q.i.d X 3 days followed by oral steroids
good clinical signs and history of recovery which are more 1mg/kg body wt for 11 days. We start treatment as early as
useful in evaluating them. RNFL measurement may be an possible and generally go up to a maximum of 8 days from
ancillary tool in the follow-up of optic neuritis. onset.

JLG: OCT is being used for RNFL Thickness to know the ONTT showed above protocol did not have any bearing on
demyelinated nerve fibres of RNFL. Retinal nerve fibre layer the final visual outcome. It expedites the process of vision
decreases in MS and compressive neuropathies. Decrease in improvement.
RNFLT thickness in compressive lesion means poor visual
outcome after decompression of tumor according to some SK: The standard treatment protocol I follow is Intravenous
studies. It will become a routine vestigation in future in all Methylprednisolone 1gram per day slow IV in NS/5%
cases of optic neuropathies. Dextrose for 3 days. This is followed by Oral prednisolone
1mg/kg/day tapered every 3 days by 10mg for a period
RK: We do it in all cases mainly for academic purpose. of 11-15 days. Along with this oral antacid, calcium and
multivitamins are prescribed.
SK: RNFL measurement is useful in cases of Retrobulbar
neuritis on followup, in case baseline RNFL has been I prefer to start Steroids if the presentation is within the first
measured and it shows loss of NFL it implies recurrence 2 weeks of onset. Steroid treatment hastens the recovery of
and is suggestive of MS.

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vision and reduces the number of recurrences in the next 3 diabetes, hypertension etc. If the patient has systemic
years in most cases. The final visual outcome at 3-6 months illnesses, I get blood sugar, both fasting and PP, CBC, LFT,
is similar in cases with or without treatment. Chest Xray, Urine routine and ECG done.

AR: The patients should be started on intravenous methyl When the patient is on steroids we monitor blood sugar,
prednisolone 1gm in a injection over 4-6 hours daily for both fasting and PP and Blood pressure.
3-5 days as soon as diagnosis of optic neuritis is made.
AR: The evaluation of a patient with a first event of optic neuritis
This should be followed by oral prednisolone at 1mg /kg/ is important for diagnostic and prognostic reasons.
day to be continued in tapering doses over next 2 week.
Blood Investigations - CBC, ESR, CRP
Treatment with intravenous methyl prednisolone improves
the rate of visual recovery, acuity, color vision, contrast ANA
sensivity and visual field.
VDRL
Patients on methyl prednisolone – intravenous had a lower
rate of progression to clinically definite multiple sclerosis BI2 level
vs placebo in ONTT trial.
ACE level

AS: What work-up would you like to perform before starting They are helpful to rule out BI2 deficencies and any
steroids? Any investigations would you like to monitor underlying inflammatory process.
when the patient is on Steroids?
Routine CSF examination is not required
SA: All patients who are receiving steroids are evaluated by
our physician. They get a complete haemogram, FBS, lipid MRI brain with MRI optic nerve in patients with
profile, urea, creatinine, ECG, Blood pressure recording retreobulbar neuritis.
before starting them on systemic steroids. All patients are
informed about the possible side effects of steroids and Patients on steroid treatment need to be monitored for
we receive an informed consent from the patient before blood sugar elevation at base line and frequently thereafter
intravenous steroids therapy. on treatment with oral steroids.

When the patient is on steroids we advise them to get weekly AS: What is the role of oral steroids in management of optic
blood counts, sugar and blood pressure recording ,serum neuritis in current scenario?
urea, calcium screening.
SA: In current scenario of demyelinating optic neuritis it is
JLG: Local Work up includes visual acuity, contrast sensitivity, advisable to give a short oral steroids taper ONLY following
color vision with ishihara charts, visual fields 30-2 , IV steroids and NEVER put the patient on isolated oral
Record of pupillary reaction, RAPD, Fundus examination steroids. We have sufficient literature evidence to support
(blurring of disc margins, hyperemia, venous dilatation, that ONTT treatment protocol definitely prevents
hemorrhages, exudates, venous pulsations – spontaneous/ recurrences and hastens recovery, but has no impact on
induced/ totally absent) Pattern VEP (Flash VEP if the the final visual outcome.
visual acuity is less than 3/60), if VEP is not possible
record pupil cycle time (PCT) in both eyes (time taken JLG: Oral steroids we give when the patient is having diabetes,
for excursion of one constriction and dilatation of pupil , or partially controlled hypertention. Monitoring these
measure 100 cyles on slit lamp putting slit at the edge of the conditions is better with oral steroids as compared to
pupil using stop watch and take average , Normal values I/V steroids. I still give oral steroids in our set of patients
are 850-950 msecs which is increased in optic neuritis with mixed etiology knowing fully well that ONTT has
markedly). condemned its use in multiple sclerosis cases. Recurrences
however are a bit more but the patients recover fast.
Systemic work up includes Complete Hemogram, ESR,
blood sugar, Mx and Xray chest,VDRL, BP, MRI brain SK: There is no role of oral steroids alone in the management
and orbit with contrast with FLAIR sequence ( preferably of typical optic neuritis as it may increase the risk of
3 Tesla. MRI for better resolution), ACE levels, ANA. recurrences.

Before starting steroids we must rule out diabetes, active AR: There is no role of oral steroids even in Indian scenario.
infection, see serum electrolytes because steroids will cause
hypokalemia. When the patient is on I/V steroids we have AS: Do you think dexamethasone has a role in the Indian
to monitor pulse for any arrhythmia, may order ECG in scenarios?
case of doubt and call cardiologist. By and large steroids are
safe. We did come across arrhythmic pulse in a few patients SA: I don’t advise dexamethasone to optic neuritis patients,
but they were all declared to be safe and cardiologist asked but there are few reports in the literature which have used
us to continue I/V steroids. dexamethasone in the management of opticneuritis.

SK: I do not do any systemic investigations for patients with JLG: We did a study on comparison of I/V dexamethasone
optic neuritis unless they have any systemic illnesses like (100mgm I/V in 5% dextrose OD for three days without
following up with oral steroids) verses I/Vmethyl
prednisolone sodium succinate, 500mgm BD for three days

16 DOS Times - Vol. 16, No. 6, December 2010

followed by 11days treatment with oral steroids in optic with contrast, 2. optic nerve signals which are hypointense
neuritis cases. In both the ultimate visual outcome was not on T1WI and hyperintense on T2WI enhancing with
statistically different but cases of I/V methyl prednisolone contrast. Classical deep periventricular white matter lesions
recovered faster than I/V dexamethasone. The patients which are finger like [dawson’s fingers] are pathognomic
who cannot afford methyl prednisolone can be given I/V for M.S.
dexamethasone which is cheap and equally effective. Vials
of 100mgm of dexamethasone in 5ml are available at few JLG: One should look for Periventricular plaques which
shops and should be used. Using 4mgm /ml vials will add enhance with contrast more than 3mm in size, more than
lot of preservatives in 200mgm I/V dose which may be 3 in number and are present along the lateral ventricles,
harmful. Not significant side effects are seen except for brain stem, in the optic nerve and in the posterior cranial
increased weight gain like any other steroids. fossa suggesting demyelination as the pathology. See if
any plauque is more than 5mm which is highly significant
SK: Dexamethasone can be used as an alternative to for demyelination. We should also look for any ICSOL,
Methylprednisolone as the long term results are similar. ischemic lesions and tubercular lesions for other pathology.
Abnormal plaque lesions on MRI are seen in 46.9% of optic
AR: Trials of high dose of 100mg intravenous dexamethasone neuritis patients according to ONTT. If there are no lesion
at AIIMS have been found to be useful in treatment of on MRI 22% patients will develop MS in 10 years. If there
optic neuritis, however larger RCT are required before any are one or more lesions 56% will develop MS in 10 years
recommendations can be made. (ONTT). 35% of patients suffer another attack of optic
neuritis in 10 years.
AS: Is there any role of MRI in cases of first attack of optic
neuritis? SK: We look for Hyperintense plaques on T1 Weighted
contrast slices and with FLAIR sequence, especially in
SA: It is ideal to do MRI Brain and orbit in 1st attack of Optic the periventricular areas and optic nerves. These are not
neuritis. MRI helps us to prognosticate and follow up the symmetrical across the midline as against ischemic areas
patients who pose high risk of developing of M.S .Optic in the elderly.
neuritis patients who have periventricular signals and deep
white matter lesions on MRI Brain, are prone for CDMS AR: One should look for demyelinating plaques of multiple
[Clinically definite multiple sclerosis] in later stages. These sclerosis, which are classically seen in the white matter
patients may be benefited with initiation of early interferon oriented perpendicular to the ventricles. Further MRI also
therapy. helps to rule out any SOL/Tumor / Infarct.

JLG: Gadolinium enhanced MRI with FLAIR Sequence for brain AS: Is there a role of interferons in optic neuritis in present
and orbit should be ordered in every case of optic neuritis. scenario?
MRI should always be done to confirm multiple sclerosis,
to prognosticate future attacks, and to rule out any other SA: In present scenario Interferons are a better choice for
intracranial pathology like ICSOL, brain tuberculosis, demyelinating optic neuritis with features of systemic
vascular lesions which might give rise to visual loss. These demyelination and positive MRI Brain signals. There are
days we must do MRI in every case to be on the safer side reports like CHAMPS study which have proven early
from CPA also. We can never be clinically sure every-time. I interferon therapy being beneficial for isolated optic
have seen many cases of pituitary adenomas being treated as neuritis as presenting feature of multiple sclerosis.
retro-bulbar neuritis turning out to be pituitary adenomas
in the second attack on MRI. JLG: The patients who were having two or more plaque lesions
on MRI showed less incidence of developing MS when
SK: MRI Brain and orbits with contrast is definitely indicated Interferon beta-1a (avonex) was given than those who were
in the first attack of optic neuritis to detect demyelinating not given avonex. In India however. It has not been popular
plaques suggestive of possible MS or likelihood of and I have not seen ophthalmologists using interferons.
developing MS in the next 5 years. One reason is cost, second its effectivity in prevention of
MS (only marginally better according to CHAMP STUDY,
AR: Yes, all patients with first attack of optic neuritis should 35% treatment group patients developed MS in 3 years
undergo MRI (Brain) to rule out underlying multiple as compared to 50% in placebo group). Patient has to be
sclerosis. admitted for any side effects during therapy.

In relevant cases, (MRI spine may be required if SK: Beta interferons were useful in CHAMPS study to reduce
MRI (brain) is suggestive of multiplesclerosis risk of recurrences in 5 year followup in 50% of cases of
In reterobulbar optic neuritis, a fat suppressed MRI scan typical optic neuritis. However, these are injections, are very
demonstrates post contrast enhancement of involved optic costly and need to be given for upto 2 years on a weekly
nerve. basis. Also, there are few side effects. Hence they are being
prescribed by a limited number of neurologists as patient
AS: What finding on MRI should one look for? affordability and acceptance is a major factor.

SA: MRI Brain and orbit with post contrast fat suppression AR: The CHAMPS and BENEFIT trial have show that it is
imaging is ideal for optic neuritis .We should look for reasonable to discuss starting immunomodulatory therapy
1.diffuse thickening of the optic nerve which may enhance

www.dosonline.org 17

in all patients who present with optic neuritis and MRI JLG: Long term visual prognosis of the patients is generally good.
finding suggestive of multiple sclerosis. Beta interferons Aproximately 90% of patients of optic neuritis develop
can prevent progression from clinically isolated syndrome improvement of vision upto 6/12 or better in ONTT but
such as optic neuritis to clinical definite multiple sclerosis in Indian population we see 6/12 in approximately 40-50%
in these patients. of cases only. This is due to the fact that some cases belong
to atypical variety which do not improve much. Children
AS: How do you follow-up patient of Optic Neuritis? have better visual prognosis as compared to adults. At 15
year follow up in ONTT 72% improved to 6/6 or better.
SA: All optic neuritis patients are advised to review with us 2 Only 2% were worse than or equal to 6/12. According to
weeks post steroid therapy. Subsequently they are advised ONTT at 10years follow up those who had no lesion on
for 1 month, 3 months and 6 months follow up. In each MRI, only 22% developed MS, while those who had one or
visit they undergo all optic nerve function tests – vision / more lesion, 56% developed MS. Incidence of developing
pupil / color vision / fields / contrast sensitivity. I advise MS is reduced when the patients are treated with methyl
MRI Brain and orbit only in case of any new symptoms or prednisolone as compared to those who are on placebo.
worsening of symptoms. While in Indian scenario the development of MS what we
see is much less as compared to west. Incidence of optic
JLG: The patients are admitted initially for I/V methyl neuritis is less in children is much less as compared to adults
prednisolone for 3 days. The patient is then followed after (approximately 5%). Children have better visual prognosis
1week, 2weeks , 1month, 3months and then after 6months than adults. Chances of developing MS are much less in
or earlier in case of any blurring of vision. Best corrected children in comparison to adults.
Visual acuity, contrast sensitivity, color vision are tested
on each visit. Visual fields are tested on day 1, at three SK: Majority of cases (90%) of Optic neuritis have a good
and 6months. VEP is done at day 1, 2weeks and 3months. prognosis with recovery of 6/6 vision and subsequent
After 14 days oral steroids are reduced from 40mg to 20 recovery of color vision and fields. The rest also have a good
for 1week, then 10mg for 1week, then stopped. prognosis with IV steroid treatment, with less recurrences.

SK: I followup patients at one month after starting IV steroids The long term risk on multiple sclerosis is high in patients
and I repeat visual fields test. Subsequently for most patients who have 3 or more demyelinating plaques on MRI,
it is a yearly followup or on recurrence, whichever comes have recurrences of optic neuritis or other neurological
earlier. symptoms, or a family history of MS.

AR: These patients of ON ‘are’ require regular ophthalmological AR: • Spontaneous improvement in vision occurs over weeks
evaluation – visual acuity, color vision, visual fields and & 95% patients regain vision at 12 months.
fundus examination.
• Treatment with intravenous methyl prednisolone
AS: What is the long term prognosis of optic neuritis results increase the rate but not extent of visual recovery.
& long term risk of multiple sclerosis?
• Patients with normal MRI (brain) at baseline have
SA: Optic neuritis patients in our country don’t pose high risk 15% risk of progression to clinically definite –multiple
of developing Multiple sclerosis as much as the western sclerosis at 5 years, 22% at 10 years & 25% at 15 years.
population. Most of optic neuritis patients belong to
chronic relapsing inflammatory optic neuritis group who • Patients with abnormal MRI (brain) have a 42% risk
respond to steroids and have good visual prognosis. In a of progression to CDMS at 5 years, 56% at 10years and
retrospective 5 year analysis done in our hospital, out of 60 72% at 15 years.
patients, only 3 patients developed Multiple sclerosis after
5 yrs.

DOS Correspondent
Ankur Sinha MD

18 DOS Times - Vol. 16, No. 6, December 2010

OPHTHALMOLOGICAL Venue:
26th November, 2010 - (Friday)
Teaching Live SurgeryDOSArmy Hospital (R&R), Auditorium,
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HALMOLOGICAL Mid Term Conference

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HALMOLOGICAL Mid Term Conference

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30 DOS Times - Vol. 16, No. 6, December 2010

Polypoidal Choroidal Vasculopathy (PCV) Retina

Priyank Garg MS, Samarth Agarwal DO, Arindam Chakravarti MS, S. Natarajan DO

Upon the original recognition and description of polypoidal lesions are easily diagnosed on biomicroscopy, especially
choroidal vasculopathy (PCV) it was suggested that this when the lesions are located beneath the atrophic retinal

acquired, abnormal choroidal vasculopathy was distinct from pigment epithelium, and on ICG. The polypoidal lesions

the more typical choroidal neovascularization. Most people appear smaller when the disease affects the middle choroidal

today believe that PCV is a variant of type 1 neovascularization, vasculature. In this case, the lesions are more challenging to

as we do, although some propose PCV is a distinct vascular diagnose on clinical examination, and the preferential method

abnormality of choroidal vessels. Not just an anatomical variant, of diagnosis is ICG angiography.

there are differences in patients at risk for its development, the The choroidal vascular lesions of PCV are most commonly
associated clinical manifestations, the natural course, the response • found in the peripapillary area, although recent evidence
to treatment, and the overall visual prognosis. suggests that the lesions could also be found in the central

Pathology1 macula and in the mid-periphery. Polypoidal lesions are also

The peculiar abnormality of PCV is believed to originate in the usually located at the margin of the PED, and they may create
inner choroid. The aneurysmal vessels are of venular origin and a notch in the accompanying PED visible on angiography.
probably the pathological counterpart of the lesion identified in The lesions of PCV can be localized to a single location in
ICG angiography. It is hypothesized that the hyperpermeability the fundus or can be widespread and involve more than one
and hemorrhage due to the stasis of blood in the vessel might site.

cause edema and degeneration of the tissue. When the lesion • Variably sized serous and serosanguineous detachments of

is increasing in size, it usually does so by three proposed the neurosensory retina and pigment epithelium around the

mechanisms. The lesion may enlarge by simple vessel hypertrophy, optic nerve or in the central macula are the most frequent

by conversion of the lesion into the advancing edge of a vascular presentation.

channel, and by unfolding of a cluster of aneurysmal elements • The typical presentations for a patient who is symptomatic
and subsequent transformation into enlarging, vascular, tubular for less than three months is extensive subretinal exudation
components. The latter mechanism is usually apparent on and bleeding with minimal cystic change in the retina and a
clinical examination as a large, reddish-orange subretinal mass surprisingly good visual acuity (VA). This disparity between
that corresponds to a cluster of aneurysmal elements. On ICG the severity of the serosanguineous detachments and good
imaging, this same process is noted to be composed of multiple, vision is best explained by the minimal intraretinal changes.
polypoidal elements that project anteriorly from the inner choroid

toward outer retina. With time, these mass-like vascular lesions • For patients with symptoms longer than 3 months, there

flatten out and expand tangentially in its plane. Hyalinization of are considerable lipid depositions from proteineous leakage

choroidal vessels and massive exudation of fibrin and plasma are from active aneurysmal elements in the polypoidal vascular

prominent features in all specimens of PCV lesions.

Clinical Features2-4

• Most commonly diagnosed in patients between the ages of 50
and 65 years. Caucasian patients usually present the disease
at an older age.

• Women are involved predominantly over men by a ratio
of approximately 4.7:1 (53 to 12), men could still have
manifestations of the disorder.

• Individuals of African-American and Asian descents
are at risk for developing PCV, as the disorder seems to
preferentially affect pigmented individuals by a ratio of 4.2:1
(52 to 13).

• The polypoidal lesions could be classified as small, medium, Figure 1: Large polypoidal structures are sometimes
and large. The polypoidal lesions usually appear larger in visible in color pictures
size when the outer choroidal vessels are involved. Such

Aditya Jyot Eye Hospital Pvt. Ltd.,
Plot No. - 153, 9, Major Parmeshwaran Road,

Wadala (W), Mumbai

www.dosonline.org 33

Imaging

High speed fluorescein, ICG angiography, and high resolution
OCT are the principle diagnostic adjuncts used in imaging PCV.

Fluorescein Angiography5

Fluorescein angiography (FA) is not as useful in imaging PCV.
Some patients, however, have large polypoidal choroidal vascular
components - branching inner choroidal vessels and aneurismal
or polypoidal lesions—with overlying atrophy of the pigment
epithelium. In these eyes, FA may be able to image the PCV, but
not usually in the entire vascular abnormality.

Indocyanine Green Angiography5

With ICG, the vessels of the PCV lesion are usually found to be

more numerous and far-reaching than it is evident upon clinical

Figure 2: Pigment epithelial detachment (A) and examination. The early stages of the ICG video angiogram show
subretinal hemorrhage (B) are common manifestations. filling of the larger vessels of the PCV network prior to retinal
vessels, but the area within and immediately surrounding the
(C ) Subretinal lipid is often observed. (D) In some lesion remains hypofluorescent compared to the uninvolved
patients, progressive subretinal fibrosis can be observed choroid. Shortly after the network can be identified on the ICG

angiogram, small hyperfluorescent “polyps” become easily

abnormalities following the spontaneous resolution of the identifiable within the choroid. The polyps seem to arise from
acute serosanguineous complications, there may be signs the larger choroidal vessels and do not appear on every vessel of
of subretinal fibrosis, pigment epithelial hyperplasia, and the network. The polypoidal structures seen on ICG correspond
atrophic degeneration. Multiple or independent vascular to the reddish orange lesions visible on biomicroscopy. Although
abnormalities may appear in the same eye, and there is a the network of vessels may appear more extensive on ICG than
marked tendency toward bilaterality. As a rule, the presence on the clinical examination, the polypoidal structures routinely
of PCV in one eye generally means that the fellow eye is at appear smaller in the earlier phases of ICG angiography. During
high risk of similar clinical changes. the midphase of the angiogram, however, the size of the lesions
approximates the choroidal excrescencies observed clinically.

• Drusen may also be seen in patients with PCV, generally in The late phase of angiogram is associated with a reversal of the

white patients. Highly pigmented individuals infrequently pattern of fluorescence observed previously. The area surrounding

have drusen, and their clinical manifestations are generally the lesion becomes hyperfluorescent and the center of the lesion

in the central macula area, in contrast to white patients who demonstrates hypofluorescence.

more typically have involvement in the peripapillary area.

Figure 3: Optical coherence tomography Figure 4: A and B: Color photograph and red-free
(OCT) scan shows polypoidal structure photograph, respectively, of the right eye show the presence
attaching to the back surface of detached of atrophic changes in RPE consistent with central serous
retinal pigment epithelium (RPE) (C ) at chorioretinopathy. C: Fluorescein angiogram of the right
the region corresponding to fluorescein eye reveals the presence of the vascular network of small
angiography (FA) (A) and indocyanine green caliber vessels terminating in polyp-like structures. D: ICG

angiography (ICGA) (B) angiogram of the right eye confirms the presence of the
polypoidal lesion.
34
DOS Times - Vol. 16, No. 6, December 2010

The size of the lesion seems to influence the reversal pattern. is staining in the walls of the aneurysmal lesions and exudation
The lesions that are less than 0.5-disk diameter in size appear to into the surrounding choroid and subretinal space. The clinical
have intense uniform fluorescence, whereas internal details seem location and the course of PCV are different from that of CNV.
to be visible in larger polypoidal structures. These findings, in Subfoveal CNV tends to organize into a fibrotic or disciform
turn, suggest presence of an internal architecture. In the very late scar leading to severe macular damage and loss of vision. The
stages of ICG, the dye disappears from the lesions thus defining PED seen in association with PCV does not necessarily involve
a phenomenon termed “washout”. The “washout” is only seen central macula and virtually never forms a fibrotic scar. This, in
in non-leaking lesions; the leaking polypoidal lesions remain turn, means better prognosis for PCV than for AMD associated
hyperfluorescent throughout the late phases of the angiogram. with a PED and occult CNV.
Varying degrees of hypopigmentation of the RPE overlying an
area involved in the disease process may enhance visualization Chronic CSCR: - Some patients with PCV may present with purely
of the abnormal vessels; yet, the late ICG staining results from exudative changes masquerading a chronic decompensation
the intrinsic characteristics of the lesion rather than the RPE of RPE, a variant of central serous chorioretinopathy (CSC).
alterations. The PCV lesions presenting with symptoms of central serous
chorioretinopathy are usually small in size. The polypoidal lesions
Optical Coherence Tomography6 may resemble small PEDs both clinically and on fluorescein
angiography. The diagnosis becomes especially challenging when a
OCT is especially useful in identifying PCV by detecting patient presents with chronic central serous chorioretinopathy and
abnormalities surrounding the polypoidal lesions. High-resolution lipid deposition in the central macula due to subfoveal polypoidal
OCT images demonstrate that polypoidal structures exist beneath lesion. The principle way of differentiating a small serous PED
RPE and attach at the back surface of RPE. C-scans, which can be from a polypoidal lesion is with ICG. Late staining of the PED
reconstructed from the linear B-scans on several of the spectral- is seen with fluorescein angiography and hypofluorescence
domain OCT platforms, may reveal separation of blood into with ICG. On the other hand, the polypoidal lesion is usually
its corpuscular and serous components, a phenomenon called hyperfluorescent with ICG due to its vascular nature.
the ‘‘hematocrit sign’’. Sometimes, C-scan representation may
demonstrate the vascular network in its entirety, which is termed Treatment
the ‘‘bola sign’’. The polypoidal lesions detected by ICGA often
correspond to the location of pigment epithelial detachments on Several methods of treatment for PCV have been reported.
the OCT. The principle therapies are laser photocoagulation, PDT, anti-
vasogenic drug, and combinations of these.
Natural Course7
Photocoagulation10
The natural history of PCV depends on factors including location
(peripapillary vs macular), size of the lesion, and associated Initially, laser photocoagulation was used in the treatment of
bleeding and exudation - which may resolve or progress, polypoidal lesions. Photocoagulation is recommended only if the
sometimes to extensive subretinal fibrosis. The history is probably lesion is extrafoveal & if it is feasible to treat the entire polypoidal
heavily influenced by the racial background and individual genetic lesion.
makeup and modified by systemic factors such as hypertension.
There appears to be a difference in the clinical features between Intravitreal Bevacizumab Or Ranibizumab11,12
early and late stage PCV: ‘‘the longer the disease period, the
larger the lesion.’’ Microrips of RPE at the margin of the pigment In 2008, Gomi et al evaluated the efficacy of intravitreal
epithelial detachment are not uncommon in PCV; however, they bevacizumab for PCV. The ICGA at 3 months showed resolution
often disappear spontaneously. of polyps in one eye, but residual or enlarged lesions in the other
10. Vision did not improve significantly. Although the follow up
Differential Diagnosis8,9 was relatively short, they concluded that intravitreal injection of
bevacizumab may reduce the fluid from PCV, but seems to be
Wet AMD: - Vascular proliferative changes associated with non- ineffective for diminishing its choroidal vascular changes. These
polypoidal type of CNV tend to produce small caliber vessels results suggest that polypoidal dilation of choroidal vessels in
that are associated with a “dirty gray membrane” or a grayish PCV may not depend on VEGF to the same extent as ‘‘normal’’
discoloration of the overlying retina. On the contrary, the patients age-related neovascularization. This hypothesis is consistent with
with vascular changes typical of PCV form a network of vessels the finding that the VEGF levels in aqueous humor in PCV are
ending with saccular polypoidal lesions that are red to orange in significantly lower than those in neovascular AMD. In another
color and evident with slit-lamp biomicroscopy unless they are study using intravitreal ranibizumab, polyps disappeared on ICG
camouflaged by overlying exudate or blood. Both fluorescein angiography in 9 out of 13 lesions (69.2%). Several studies reported
and ICG angiography can be used to distinguish the two types decreased retinal thickness on OCT following injection. PCV
of vascular abnormalities. In both of these studies, CNV is appears likely to be refractory to anti-VEGF therapy.
characterized by diffuse late staining plaque. PCV is demonstrated
by ICG angiography as a prominent vascular network in the Photodynamic Therapy13-15
early stages of the study and an area of clearing or so called
“washout” of the dye in the late stage. The late phase of PCV is Sixteen published reports concern the results of PDT for PCV. In
also distinguished by a characteristically appearing outline of the all of the reports with a follow-up of at least 1 year, preservation
non-leaking large choroidal vessels. If the vessels are leaking, there and improvement of VA was achieved in more than 80% of
patients.

www.dosonline.org 35

Subretinal hemorrhage can occur after PDT. This is occasionally 7. Uyama M, Wada M, Nagai Y, et al. Polypoidal choroidal vasculopathy:
massive and can lead to vitreous hemorrhage and a poor visual natural history. Am J Ophthalmol. 2002; 133(5):639—48
prognosis.
8. Ahuja RM, Downes SM, Stanga PE, et al. Polypoidal choroidal
Recurrent bullous detachment and chorioretinal anastomosis after vasculopathy and central serous chorioretinopathy. Ophthalmology.
PDT has also been reported. 2001;108(6):1009—10.

The one major concern regarding the efficacy of PDT for PCV is 9. Tamura H, Tsujikawa A, Otani A, et al. Polypoidal choroidal
the recurrence or the development of new polypoidal lesions with vasculopathy appearing as classic choroidal neovascularization on
longer follow-up. PDT can reduce the size of polypoidal lesions, fluorescein angiography. Br J Ophthalmol. 2007; 91(9):1152—9.
but may not destroy them completely. Persistent branching vessels
in the network may be origins of new active polypoidal lesions. 10. Yuzawa M, Mori R, Haruyama M. A study of laser photocoagulation
Periodical ICGA would be needed to detect abnormal choroidal for polypoidal choroidal vasculopathy. Jpn J Ophthalmol.
vascular changes during long-term follow-up after PDT. 2003;47(4):379—84.

Combination Therapy16-18 11. Gomi F, Sawa M, Sakaguchi H, et al. Efficacy of intravitreal
bevacizumab for choroidal vasculopathy. Br J Ophthalmol.
Anti-angiogenic drugs do not appear to work adequately as 2008;92(1):70—3.
monotherapy, nor does PDT.
12. Reche-Frutos J, Calvo-Gonzales C, Donate-Lopez J, et al. Short-
The current treatment regimen includes PDT followed by three term anatomic effect of ranibizumab for polypoidal choroidal
intravitreal injections of ranibizumab. The patient is reassessed vasculopathy. Eur J Ophthalmol. 2008;18(4):645—8.
monthly with OCT & 6 monthly with ICGA. If polyps are found,
even not active, reinjection of ranibizumab is recommended. 13. Akaza E, Mori R, Yuzawa M. Long-term results of photodynamic
therapy of polypoidal choroidal neovascularization. Retina.
References 2008;28(5):712—22.

1. Nakashizuka H, Mitsumata M, Okisaka S, et al. Clinicopathological 14. Kusashige Y, Otani A, Sasahara M, et al. Two-year results of
findings of polypoidal choroidal vasculopathy. Invest Ophthalmol photodynamic therapy for polypoidal choroidal vasculopathy. Am
Vis Sci. 2008;49(11):4729—37. J Ophthalmol. 2008;146(4):513—9.

2. Yannuzzi LA, Wong DWK, Sforzolini BS, et al. Polypoidal choroidal 15. Otani A, Sasahara M, Yodoi Y, et al. Indocyanine green angiography:
vasculopathy and neovascular age-related macular degeneration. guided photodynamic therapy for polypoidal choroidal vasculopathy.
Arch Ophthalmol. 1999;117(11): 1503—10. Am J Ophthalmol. 2007; 144(1):7—14.

3. Ciardella AP, Donsoff IM, Huang SJ, et al. Polypoidal choroidal 16. Lai TY, Chan WM, Liu DT, et al. Intravireal bevacizumab
vasculopathy. Surv Ophthalmol. 2004;49(1) 25—37 (Avastin). with or without photodynamic therapy for the
treatment of polypoidal choroidal vasculopathy. Br J Ophthalmol.
4. Imamura Y, Engelbert M, Iida T, Freund KB, et al. Polypoidal 2008;92(5):661—6.
choroidal vasculopathy. Surv Ophthalmol. 2010; 55: 501-515.
17. Shima C, Gomi F, Sawa M, et al. One-year results of combined
5. Yannuzzi LA, Nogueira FB, Spaide RF: Idiopathic polypoidal photodynamic therapy and intravitreal bevacizumab injection for
choroidal vasculopathy: a peripheral lesion. Arch Ophthalmol retinal pigment epithelial detachment secondary to age-related
116:382–3, 1998. macular degeneration. Graefes Arch Clin Exp Ophthalmol.
2009;247(7):899—906.
6. Saito M, Iida T, Nagayama D. Cross-sectional and en face
optical coherence tomographic features of polypoidal choroidal 18. Gomi F, Tano Y. Polypoidal choroidal vasculopathy and treatments.
vasculopathy. Retina. 2008;28(3):459—64. Curr Opin Ophthalmol. 2008;19(3):208—12.

First Author
Priyank Garg MS

Congratulation

Dr. Suneeta Dubey the Best Scientific Paper Award in the 5th International Glaucoma Surgery Congress which
was held in Delhi between 11th to 13th November.

36 DOS Times - Vol. 16, No. 6, December 2010

CT Imaging of the Orbit Oculoplasty

Samarjit S Ghuman MBBS, MD, Seema Sud DNB

CT scanners have come a long way since the time of the first the other compartments. The optic canal forms the apex of
generation scanners with present generation scanners capable the pyramidal orbit, and the optic septum the base of the orbit
of achieving slice thickness of 0.3 mm. Multi detector CT (MDCT) anteriorly, with the lids forming the anterior compartment1,2
is able to provide isotropic multiplanar reconstructions and
along with volume rendering techniques is able to display both CT In orbital pathology
bone and soft tissues with exquisite detail. CT is relatively cheap,
with a wider availability than MRI, and is much faster. It images Trauma
calcification and bone in exquisite detail and has very high spatial
and temporal resolution. The disadvantages include use of ionizing CT is the procedure of choice in evaluating patients with orbital
radiation and beam hardening artefacts from dental amalgam. trauma. It is a rapid test that can detect bony and soft tissue
injury, haemorrhage and foreign bodies. Trauma may be blunt,
Diagnostic strategy penetrating or involve implantation of foreign bodies. The classical
injury seen in blunt trauma is the blowout fracture. This commonly
Several approaches to the diagnosis of orbital pathology are in involves the floor and medial wall of the orbit.3 Features which
use. A common strategy is to localize the pathology to one of the indicate likely extraocular muscle entrapment include muscle
defined compartments of the orbit. These have been described prolapse, and a “tear drop” shape pointing toward the fracture,
as the muscle cone, formed by the four rectus muscles, dividing indicating muscle sheath tethering. A suggestive finding which
the orbit into intraconal and extraconal compartments, with
the optic nerve within the central part of the muscle cone, and
the extraocular muscles forming separate compartments. The
extraconal compartment is bordered by the bony orbit and
subperiosteal compartment. The lacrimal gland and globe form

Figure 2: Coronal and oblique sagittal
multiplanar CT images showing a

depressed floor of orbit fracture with no muscle
entrapment

Figure 1: showing normal axial anatomy of the orbit. Figure 3: Axial CT showing dislocated lens in left eye
(AC =Anterior chamber, PS=posterior segment,
ON = optic nerve, L= Lens) 39

Department of CT Scan & MRI
Sir Ganga Ram Hospital, New Delhi

www.dosonline.org

Figure 4: Axial CT showing metallic intra ocular Infection
foreign body in left eye
Orbital infections may originate from skin and eyelid disease,
or be related to sinusitis. In the former, preseptal swelling if
often seen, with intraorbital involvement later. Sinusitis may be
complicated by subperiosteal abscess formation, and intraorbital
extraconal inflammatory collections. Progression to cavernous
sinus thrombosis, meningitis or sudden visual loss may occur 4. CT
and MRI are the main imaging modalities. Chronic infection may
result in mucocoeles which may present as orbital mass lesions
with proptosis. These most commonly occur in the frontoethmoid
sinuses5.

Thyroid eye disease

Graves disease is an autoimmune disorder associated with
excess thyroid gland secretion. Thyroid eye disease is the most
common cause of unilateral and bilateral proptosis in adults. It
is four times more common in women and peaks in the 4th and
5th decades. Imaging features are typically enlargement of the
extraocular muscles with inferior and medial recti most commonly
involved (75%), followed by superior and lateral recti (50%).
Other diagnoses should be considered with isolated lateral rectus
involvement. Sagittal imaging with CT or MRI is useful to visualize
the entire length of the superior and inferior recti6.

Figure 5: Axial CT displays fracture of Rt optic canal

Figure 7: Axial contrast enhanced CT showing left
anterior ethmoid sinusitis with

subperiosteal abscess in medial left orbit

Figure 6: Axial CT demonstrates right lid swelling and Figure 8: CT in patient with bilateral frontoethmoid
preseptal inflammatory swelling mucocoeles presenting with bilateral orbital masses

should raise suspicion of a blowout fracture is the presence of DOS Times - Vol. 16, No. 6, December 2010
orbital emphysema. Evaluation for involvement of the optic canal,
and bone fragments in the vicinity of the optic nerve should be
made. Both axial and particularly coronal reformatted sections
are useful.

40

Figure 11: Orbital pseudotumour presenting as
infiltrative soft tissue mass in left orbit

on axial CT with loss of normal tissue planes (arrow)

Figure 9: Patient presenting with bilateral proptosis.
CECT demonstrates

typical enlargement of the muscle belly with sparing
of the tendons bilaterally

Figure 12: Orbital pseudotumour presenting as
right lacrimal fossa mass

Figure 10: Axial CT showing unilateral proptosis with diffuse Figure 13: Axial, contrast enhanced CT showing
enlargement of the muscle including the tendinous insertion patient with lymphomatous mass involving the

Inflammation lacrimal gland of left orbit

Orbital inflammatory mass or orbital pseudotumour is one of the 41
most common causes of an intraoribital mass. It is one of the most
common causes of unilateral exophthalmos, with bilateral disease
alson common. The typical clinical triad is a patient with proptosis,
pain and impaired ocular movement. Age of presentation ranges
from 10 to 40 years commonly. Typical radiological findings are
contrast enhancing uveal-scleral thickening. This may be isodense
to slightly hyperdense on CT with moderate enhancement usual.
Involvement of the rectus muscles, obliteration of retrobulbar soft
tissue planes, lacrimal gland, or optic nerve sheath may occur
mimicking opthic nerve sheath meningioma.7,8.

www.dosonline.org

Figure 14: Axial, oblique saggital and coronal Figure 16: Axial bone window CT a showing bony
contrast enhanced CT showing patient with preseptal expansion of the left ethmoid and sphenoid sinus
as well as left greater wing sphenoid in patient with
lymphomatour mass
fibrous dysplasia

Figure 17: Coronal CT, showing hyperostosis of left
greater wing second day to meningioma

Fibrous dysplasia

Figure 15: Axial and coronal contrast enhanced CT Fibrous dysplasia most commonly involves the frontal or sphenoid
of patient with lymphomatous bone. It characteristically produces expansion of the bone shown
Infiltrate in both lacrimal glands as prominent calcified bone density material on CT. Due to fibrous
stroma and osteoid material, it typically shows low T1 and T2
signal on MR with enhancement after gadolinium10. The bone
expansion may lead to foraminal narrowing and impingement
of the optic nerve.

Meningioma

Tumours Meningiomas may arise either primarily from the optic nerve
sheath or periosteum of the orbital wall, or secondarily from the
The diagnostic approach to tumours of the orbit focus on sphenoid ridge or tuberculum sellae and extend into the orbit.
anatomical location – in the globe, intraconal space, extraconal They comprise approximately one third of primary optic nerve
space, preseptal space, bony orbit, paranasal sinues, lacrimal gland, tumours and more commonly present in middle age females.
optic nerve and globe. Useful features on CT are density including Bilateral meningiomas are seen in neurofibromatosis. Secondary
calcification and contrast enhancement. meningiomas present with hyperostosis and expansion of the
bones adjacent to the orbit. Primary meningiomas typically
Lymphoma have a perineural location with enhancing tissue surrounding
optic nerve11. Presence of calcification helps confirm diagnosis.
Lymphoma may present with unilateral or bilateral disease, and Secondary meningiomas may present with visual impairment
manifest in the orbit as the primary site or as part of systemic secondary to compression of the optic nerve.
disease. It may present in any compartment, though lacrimal
gland involvement with clinical manifestation of lid swelling Optic nerve glioma
and a palpable mass is most common. It may mimic orbital
inflammatory mass. A more diffuse form with infiltration of the These tumours commonly present in children with 50% less than
retroconal space effacing normal tissue planes may occur. On CT 5 years of age. They may be unilateral or bilateral. They have
it appears commonly as hyperdense contrast enhancing mass. well defined margins. Calcification is rare in absence of previous

42 DOS Times - Vol. 16, No. 6, December 2010

Axial contrast enhanced CT in patient
with intraconal cavernous heamangioma

showing well defined margins and
enhancement after contrast

Figure 19: Axial CT revealing calcifred intra-ocular
mass in the (R) eyeball suggested of retinoblastoma

flow, the determination of which affects therapy12. CT or MR
angiography may be used, though catheter angiography offers
option of endovascular treatment

Rhabdomyosarcoma

Figure 18: Well defined lalulated ultra cana Rhabdomyosarcomas are the most common mesenchymal
SOI s/o heneyronia childhood tumours. Incidence peaks at approximately 8 to 9
years of age. These tumours may present with rapid proptosis. CT
radiotherapy. There is no orbital hyperostosis unlike meningioma. shows a mass similar in density to muscle with irregular margins
Heterogeneous enhancement is related to mucin deposits which with most in the extraconal space though half have intraconal
appear as mottled lucent areas. Widened optic canal occurs in up extension. These are aggressive tumours with bone erosion and
to 90% more common than with meningioma. Bilateral disease intracranial extension seen.
strongly suggests neurofibromatosis
Retinoblastoma
Capillary haemangioma
Retinoblastomas are tumours arising from the retina. They
This is the most common childhood benign orbital tumour, usually occur in children younger than 5 years of age and may be
is more common in females, appears within first 2 weeks post hereditary or nonhereditary. They may present with leukocoria
partum, is non encapsulated, and may be very large. The tumour in about half of patients. It is the most common intraocular
has irregular margins with prominent enhancement and may be tumour of childhood. Typical findings on non contrast CT are
difficult to distinguish from rhabdomyosarcoma. speckled calcification. MR is useful for evaluating extraocular
and intracranial disease
Cavernous haemangioma
External angular dermoid
These are the most common benign intraorbital lesions in adults
and most commonly present in the 2nd to 5th decades. They These are the most common congenital childhood masses. They
typically present with painless slowly progressive proptosis and typically present superolaterally adjacent to the orbital rim.
are mostly intraconal. They have smooth margins, homogeneous These tumours are slow growing and appear as well defined non
in density, show uniform enhancement and are easily separated enhancing low density lesions on CT. Bony erosion may occur
from the optic nerve and extraocular muscles related to their slow growth

Caroticocavernous fistula Conclusion

Caroticocavernous fistula may be traumatic or occur spontaneously. A systematic evaluation using an anatomical compartment
They represent a communication between the internal carotid strategy, evalution of imaging features, as well as correlation with
artery and the cavernous sinus. They may be slow flow or high clinical presentation and patient age is useful in the diagnosis of
patients with orbital disease.

www.dosonline.org 43

References 7. Yuen SJ, Rubin PA. (2002) Idiopathic orbital inflammation: ocular
mechanisms and clinicopathology. Ophthalmol Clin North Am
1. Bloching M, Beck R, Knipping S, Mir-Salim PA, Duncker GI, 15:121-6. 3.
Berghaus A (2001) Orbital space-occupying lesions. Practical aspects
of imaging. HNO 49:21-28 8. Weber AL, Romo LV, Sabates NR. (1999) Pseudotumour of the orbit.
Clinical, pathologic, and radiologic evaluation. Radiol Clin North
2. Wichmann W, Muller-Forell W (2004) Anatomy of the visual system. Am 37:151-68. .
Eur J Radiol 49:8-30
9. Valvassori GE, Sabnis SS, Mafee RF, Brown MS, Putterman A (1999).
3. Gilbard SM, Mafee MF, Lagouros PA, Langer BG (1985) Orbital Radiol Clin N Am 37(1): 135-150
blowout fractures. The prognostic significance of computed
tomography. Ophthalmology 92(11): 1523-8 10. Z i m m e r m a n R A , G i b b y WA , C a r m o d y R F ( 2 0 0 0 )
Neuroimaging:Clinical and Physical Principles. New York: Springer-
4. Eutis HS, Mafee MF, Walton C, Mondoca J. (1998) MR imaging and Verlag
CT of orbital infections and complications in late rhinosinusitis.
Radiol Clin N Am 36(6):1165-83 11 Johns TT, Citrin CM, Black J, Sherman JL.(1984) CT evaluation of
perineural orbital lesions: evaluation of the ‘tramtrack sign’. AJNR
5. Lloyd G, Lund VJ, Savy L, Howard D. (2000) Optimum imaging for Am J Neuroradiol 5:587–90.
mucocoeles. Journal of Laryngology and Otology 114: 233-236 11.
12. Debrun GM (1997) Endovascular management of carotid cavernous
6. Kahaly GJ: Imaging in thyroid-associated orbitopathy. Eur J fistulas. In: Valavanis A, editor. Interventional neuroradiology.
Endocrinol (2001) 145(2): 107-1812. Berlin: Springer; p. 23–34

First Author
Samarjit S. Ghuman MBBS, MD

44 DOS Times - Vol. 16, No. 6, December 2010

New Venture – Realising Dreams Miscellaneous

Vipin Sahni MS

If you want to build home what do you do? You search a land Facility Makeover
and buy it or take a flat. Hire an architect to make a plan. He
discusses with you your requirements. He makes a plan. Then It requires work of many different kind of work force. In big cities
according to your requirements, you suggest some changes in all the work are done by single contractor who works on turnkey
plan. Then according to the feasibility and space available he makes basis. But in medium and small city it requires a lot of effort as all
changes. You accept the plan. Then you hire a contractor who the contractors (like civil work, woodwork plumbing, electricity,
builds’ the building for you. You always visit to see the quality is POP, Painting etc.) for different works are different. Facility
being maintained or not. After the civil work is complete you hire makeover is done according to the expected clientele needs. If you
plumber carpenter to do the job. Who then work according to plan are making a charitable set up anything will do; avoid using glass
to create fixtures and fittings. Then you hire a painter who do the unless must. But for upscale practice, you should hire an interior
paint work. After this your house is complete to enter. Then you decorator and everything should be according to plan. Lighting,
organise a puja and “Grihpravesh” and make that place your home. paints, false ceilings use of glass and aluminum and laminates is
done as required.
Similarly stablishing a new practice is not an easy task it requires
a lot of planning and efforts. It has many stages. Instrumentation

Conception As you start makeover of the facility make a list of Instruments
you are going to buy. In today’s’ scenario following are the must
First you have to decide that you want to open a practice. Where- buy for a general ophthalmologists.-
This is very important, because on this your future depends. First
you should decide what type of practice you want to open. It is • Refraction unit
general ophthalmology or multi-specialty. Similarly you should
decide you want to do upscale/medium scale or charity practice. • Slit lamp
Always consider the locality where you want to open your practice
is an upscale locality like GK / Sufderjung Enclave or Geeta • Autorefractometer
colony/ Shahdara. Usually in most places both type of localities
exists but difference is in numbers. Once you decide locality and • Refraction sets
type of practice you want to open you decide about investments
you are going to do, because amount of investment depends • A scan biometer
solely on above two things. If you are opening multi-specialty
then investment is going to be more than general ophthalmology • Keratometer (if not with autoref.)
practice. And if you are opening in posh locality then investments
are going to be more than an ordinary middle class locality. When • Microscope
deciding for locality and investments please remember your skills.
Upscale patient is very demanding if you are not a fluent orator • Cautery
and your surgical skills are not among the best in the market
don’t take risk. • Phacoemulsification unit

Planning • OT table

After you have decided the place and type of practice you • Autoclave
want to open, start planning for facility design. Hire an expert
architect who is specialist in hospital designing and tell him your • Surgical Instruments
requirements. In the mean time start arranging the finance for the
practice. Get a Project report made by a charted accountant. Talk There are some optional instruments which some people buy are
to the financers/ bankers or your near and far relatives. Before even
leasing or purchasing the property, you should not only have clear • Perimeter
outline in your mind, from where you are arranging finances to
start the practice but you should talk to your financiers and take • Nd YAG LASER
confirmation. In the mean time architect will make the basic plan
discuss everything with him about how the facility will look like • Non contact tonometer
and what the expected cost of facility design and makeover is.
• Synaptophore

• Dehumidifier

• Pulse oxymeter

• Ultrasound cleaner

• ETO Steriliser

Kaushalya Devi Eye Institute • Refraction unit (If you are planning separate Refraction room)
Pilibhit / Shahjahanpur, U.P. • RF Cautery

www.dosonline.org 49

• Aplanation Tonometer condition. Now a days it is preferred to do official “Inauguration”
function after working for few days. Invitations for the function
• Lensemeter should be extended to all who matter in your practice. Don’t be
miser in distributing invitations, it should be done generously.
• Fundus Camera Also invite some of your old satisfied patients.

• OCT etc. Working

While buying equipment you should remember you have to use This is the most important activity for which a practice is
that for a long time, so never go for cheap alternatives. Otherwise stablished. Quality Eye care should be the only work for which one
after some time you have to buy new good equipment and your opens an eye practice. Patients should not wait very long, so that
earlier investment will go waste. they are annoyed. Doctors and refractionists should be cordial in
their behavior while talking and examining the patients. Doctor
Staffing should patiently hear the patients and their attendants. If in any
procedure patient has to suffer some discomfort he should be
Staffing depends you reach near to your inauguration you start informed beforehand. Prognosis should be explained to patients
hiring appropriate staff for your setup. Number and Level of staff and if you feel this patient may create problems latter either take
depends on the setup you are creating. If you are creating a very everything in writing whatever have you explained to him or avoid
big Eye institute in a metro staff requirement will be different but that patient. Flow of patients should be smooth. Don’t hesitate to
if you are opening a small eye clinic then it will be different. But take second opinion of your trusted colleagues. Try to satisfy each
usual staff is as follows: patient with diligence.

• Receptionist Cash flow

• Refractionist All the above activity involve small or large amount of expences.
Even if you spend miserly and do only must do expences you are
• Councilor spending more than rupees twenty lacs. Our estimated expences
in for each of the activity are as following.-
• OT technitian
Name of activity Expences in Rupees
• Peon or Bell boy
1. Conception 10,000
• Sweeper etc 2. Planning 20,000
3. Facility makeover 3,00,000
Hiring the staff is the only first step of staffing. You should give 4. Instrumentation 1,70,0000
appropriate training and tell each of them separately what you 5. Staffing 10,000
expect from them. If you don’t have time or you think they should
get better training then hire an outside source who is expert in
training staff. Otherwise recruit fully trained staff only. You should
remember even if you are best in the world but your team does not
perform well you cannot achieve what you expect or you should.
Making a good team is very important. If you expect good returns,
then you should hire the best staff available.

Marketing 6. Marketing 50,000

Telling people that you and your services are available is part of 7. Inauguration 20,000
marketing. Giving advertisement in news papers distributing 8. working 1,00,000
handbills etc. are other ways of marketing. But nothing beats word 2,21,0000
of mouth publicity in India. So if you have treated some patients Total
of the same locality earlier send them mailers or invite them in
your Inauguration and ask one of the most satisfied patients to tell These expences may vary a little according to place or scale of
his experience about your services or the treatment he received practice. If you want to realize your dreams of having your own
from you. But now a days I have seen eye practices are advertising private practice in ophthalmology, you should work on keeping
like other commodity products one I have seen on many metro these points in your mind. This will help you to establish your
stations in Delhi. If your marketing budget is more than you can practice in a planned manner. May all your dreams come true.
resort to these tactics also.

Inauguration

Inauguration of your practice is one of the most important Author
functions of your practice. I have seen some people do it half Vipin Sahni MS
heartedly. Some others are in hurry and they do inauguration
when all the equipments are not installed or even before the paint
has been done. Some others do it as family affair. But what I feel
it should be done after completion of all the work and when all
the instruments and equipments are installed and are in working

50 DOS Times - Vol. 16, No. 6, December 2010

The Big Oil Leak……A Surgeon’s Nightmare Clinical Meeting: Clinical Case-1

S.P .Chaudhary MS, FMRF, Manisha Agarwal MS, FMRF

A62- year-old female patient was referred to us after an After successful scleral rupture repair, shallow retinal detachment
uneventful vitreoretinal surgery (pars plana vitrectomy + was noted, but break could not be identified. Drainage retinotomy
scleral buckling + laser photocoagulation+ perfluorocarbon liquid was done followed by endolaser and silicon oil exchange. At
+silicon oil injection) for retinal detachment 2 weeks back, with conclusion, retina was attached throughout with well formed
the complaints of irritation and oily fluid coming out from the globe.
left eye. She was a known case of high myopia for last 40 years.
There was no history of trauma with no other significant ocular Patient was comfortable on first post op day. Ant Segment showed
or systemic history. well formed globe and well covered scleral patch graft. There was
no evidence of active leakage. Anterior chamber was formed with
On examination, the best corrected visual acuity was 6/36, N 12 in few DMF. Digital Tension was normal. On fundus examination,
the right eye and counting fingers in the left eye. Anterior segment media was hazy due to corneal edema, however a red glow could
examination showed pseudophakia in both eyes. Left eye showed be seen suggestive of attached retina .
corneal edema with mild conjunctival congestion and button
holing in the superotemporal quadrant with silicone oil leakage At the final follow up (3 months), the BCVA was FC 2 meter and
corresponding to the site of the supero-temporal sclerotomy anterior segment was stable with well covered scleral patch graft
(Figure 1). Fundus examination of the right eye showed a myopic (Figure 3 ab). Fundus showed attached retina with high SB effect
fundus and the left eye showed well attached retina with sclera and silicon oil in situ (Figure 3c).
buckle effect in the periphery and silicon oil in situ. The left eye
was hypotonus with an under fill of the silicon oil. Discussion

Left eye was diagnosed to have silicon oil leak status post Scleral rupture is a rare but serious complication of RD
vitreoretinal surgery with high myopia, probably due to breakage surgery,which has also been reported as surgical complication
of the sclerotomy suture. Based on this diagnosis she was planned during local ocular anaesthesia (Peribulbur/ retrobulbar), during
for re-suturing of the sclerotomy and re-silicon oil injection in Squint surgery, scleral buckle procedure and status post SB
the left eye under local anesthesia with guarded visual prognosis. (intrusion of buckle)1,2.

Intra-operatively limited conjunctival peritomy and fixing of As per literature search, all cases reported are during the surgery,
the infusion cannula was done in the infero-temporal quadrant. none has been reported after uneventful VR surgery. Tabandeh
Supero-temporal sclerotomy suture was found to be intact, while H et al has reported , 14 Cases of scleral rupture following 5000
silicon oil was noticed in the sub-conjucntival space coming out consequetive RD Surgery cases ( status post SB and PPV +/- SB)
from a posterior location. The silicon oil was mopped out with occurring over a period of 4 years (1993–1997) at Moorfields Eye
the bud but further leakage of silicon oil with fluid was noted, still Hospital3 . Caprineto et al has also reported single case report of
the source of leakage could not be identified. management of scleral rupture with scleral patch graft and scleral
buckle placement during the re-detachment surgery4.
Superior rectus muscle was tagged and the leakage was further
traced to the supero-nasal quadrant. Finally, medial rectus muscle
was also tagged and scleral buckle suture cut and removed to
explore the site of leakage. Gush of silicon oil with fluid was
noted leaking from superonasal quadrant at the posterior edge
of previously placed scleral buckle (Figure 2a). A large scleral
rupture extending from 9 to 12 O’clock, at the posterior edge of the
buckle (approx 9 mm from the site of muscle insertion) was noted
(Figure 2b). Sclera under the buckle was avascular and margins
of the scleral rupture were edematous and tethered.

Scleral suturing was attempted with 7-0 vicryl suture, but failed
to stop the leakage due to tethered, edematous scleral margins,
posterior location and constant leakage of large amount of fluid
(Figure 2c). Finally, scleral patch graft was placed covering the
scleral rupture and extending beyond superior and medial rectus
and sutured with 7-0 vicryl suture (Figure 2d). The leakage still
persisted, so patch graft was supported with scleral buckle # 280
(Figure 2e).

Vitreo-retina Services Figure 1: Conjuntival button holing with silicon oil leak
Dr Shroff’s Charity Eye Hospital, Darya Ganj, New Delhi

www.dosonline.org 53

Figure 2: Per-operative: a) Blob of silicon oil with fluid, b) Scleral rupture in the
superonasal quadrant, c) Scleral suturing with 7-0 vicryl, d) Scleral patch graft

suturing , e) Scleral buckle placement # 280

Figure 3: Final post operative (3 months): Anterior segment (a, b) and Fundus photo (c)

Pre-existing scleral pathosis (thin sclera, Scleritis with scleral pressure. Such situations are difficult to manage due to ocular
thinning, active necrotizing scleritis.), myopia and re-surgery after hypotony, distortion of the globe and posterior location. Presence
failed scleral buckle procedure have been reported as risk factors3. of haemorrhage might also interfere with visualization and
Cryotherapy, SBP, or other ocular surgery may be associated with treatment of retinal breaks.
scleral inflammation, thinning and necrosis and weakening of the
sclera which further increases the risk of scleral rupture. In all Repair of scleral rupture has been described as suturing
buckle revision surgery cases, site of rupture was found to be in (interrupted/ mattress) along with scleral patch graft and
the bed of the previously placed scleral buckle3. placement of a scleral buckle over the site. A number of graft
materials are also available, including allograft materials such
Cause of scleral rupture in our case could be scleral thinning as lyophilized donor scleral material or cadaveric dura mater,
secondary to high myopia along with surgical inflammation as an autologous grafting with fascia lata, or periostium5,6.
inciting factor. Possibility of systemic collagen vascular disorder
should also be kept in mind; however our patient did not have To summarize, a high myopic patient presented with hypotony
any systemic disease. and silicon oil leak s/p SB+VR surgery 2 weeks back for retinal
detachment. Presumed to be a case of opened sclerotomy, however
Risk of recurrent retinal detachment is high in such cases. In our it turned out to be an occult scleral rupture. Scleral rupture was
case, re-detachment occurred during the wound exploration; difficult to suture, due to large size, thinned out sclera, tethered
however no break could be identified. Probable mechanism of margins, and posterior location but was managed successfully
retinal detachment in our case was separation of ora (dialysis) with scleral patch graft, sclera buckle and re- silicon oil injection .
along the site of scleral rupture, which could be explained in
absence of an identifiable break. Conclusion

Scleral rupture can result in secondary intraoperative complications Rupture of the sclera is a less common but more serious
such as choroidal, subretinal, and vitreous hemorrhage, and retinal complication of RD surgery. Spontaneous scleral rupture should
incarceration. After restoration of the globe integrity, these be kept as differential in case of hypotony/oil leak after an
intraoperative complications may require further management. uneventful RD surgery. Pre-existing scleral pathology, myopia
and scleral buckling are important risk factors. Scleral patch graft
Immediate management goals in a case of scleral rupture are to with scleral buckle is a successful option in cases not amenable
limit the loss of intraocular contents and restoration of intraocular to scleral suturing.

54 DOS Times - Vol. 16, No. 6, December 2010

References 4. Management of scleral rupture during retinal detachment surgery:

a case report. Carpineto P et al. Eur J Ophthalmol. 2002 Nov-Dec;

1. Localized, extreme scleral thinning causing globe rupture during 12(6):553-5.

strabismus surgery. Haugen OH, Kjeka O. J AAPOS. 2005 Dec; 5. Chechelnitsky M, Mannis MJ, Chu TG. Scleromalacia after retinal

9(6):595-6. detachment surgery. Am J Ophthalmol. 1995; 119:803–804.

2. Inadvertent ocular perforation and intravitreal injection of an
anesthetic agent during retrobulbar injection. Wadood AC, Dhillon 6. Mauriello JA, Pokorny K. Use of split-thickness dermal grafts to
repair corneal and scleral defects—a study of 10 patients. Br J
B, Singh J. J Cataract Refract Surg. 2002 Mar; 28(3):562-5.
Ophthalmol. 1993; 77:327

3. Scleral rupture during retinal detachment surgery: risk factors,

management options, and outcomes. Tabandeh H et al.

Ophthalmology. 2000 May;107(5):848-52

First Author
S.P. Chaudhary MS, FMRF

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

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

Selection Procedure

Nomination should be signed by one of the following:

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

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

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

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

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

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

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

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

DOS Election 55

Applications are invited from Delhi Members of Delhi Ophthalmological Society for the posts of : Vice President (1 Post),
Secretary (1 Post), Joint Secretary (1 Post), Treasurer (1 Post), Editor (1 Post), Library Officer (1 Post), & Executive Member
(8 Posts).
The eligibility criteria for different Posts prescribed in DOS Constitution (1998) will be followed. Application should be
submitted on a plain paper duly proposed and seconded by a member of DOS (not in arrears). Application should reach
Secretary Office latest by 1st February, 2011 (2 p.m.). Last date of withdrawal is 1st March, 2011 (5 p.m.) Election will be
held during the Annual DOS Conference on 17th April, 2011.

Secretary, DOS

www.dosonline.org

A64 year old male presented to Dr Shroff ’s Charity Eye Hospital The Bugging Bug! Clinical Meeting: Clinical Case-2
with complaints of mild irritation and watering in the left eye
for 1 month. There was history of Penetrating Keratoplasty which Manisha Acharya MS, Umang Mathur MS
was done 10 months ago for pseudophakic bullous keratopathy
and a recent suture removal 1 week back elsewhere. He was Figure 2
being treated for suture infiltrate with topical antibiotics and
Prednisolone 1% eye drop 2 times /day.

On examination the Right Eye was a quiet pseudophakic with
Iris Claw lens and vision of 6/6. The best corrected Visual Acuity
of Left Eye was 6/60. On Slit Lamp examination a 3.0 mm x 2.0
mm infiltrate which was creamy white in colour and had mid
stromal branching with needle like opacities without evidence
of inflammation was present adjacent to the graft host junction
(Figure 1). The infiltrate was confined to the donor cornea and
the overlying epithelium was intact.

A clinical diagnosis of Infectious crystalline keratopathy (ICK)
post suture removal status post Penetrating Keratoplasty with
Pseudophakia was made in the left eye.

No microbiological work up was done at this stage, and he was
empirically treated with topical Moxifloxacin 0.5% eye drops 2
hourly, prednisolone 1% eye drop 2 times /day and CMC 0.5% eye
drops 4 times a day. The lesion remained localised and status quo
for the next 10 weeks. At 3 month follow up visit, the infiltrate
had increased in size and had crossed the host- graft junction
(Figure2). The rest of the graft was still clear and compact.

Figure 1 Figure 3

Cornea and Refractive Surgery Services Corneal Scraping was performed but no organism was
Dr Shroff’s Charity Eye Hospital, isolated. This was not surprising as the infiltrate was deep with
intact overlying epithelium. Prednisolone 1% eye drops was
5027 Kedarnath Road, Daryaganj, Delhi discontinued for 48 hours. Cessation of topical steroids resulted
in sudden increase in infiltration, stromal edema and epithelial
www.dosonline.org breakdown (Figure 3). A repeat corneal scraping was performed
now and the culture revealed growth of Candida albicans (an
uncommon organism to be isolated in a tropical country like
India). The patient was started on Tab Itraconazole – 2 times
a day, Natamycin eyedrops -2 hourly, Fluconazole eyedrops -2
hourly, Atropine eyedrops – 3 times.

57

Figure 4 Figure 5

In the course of the next two weeks, the infiltration became Figure 6
organised and reduced in size and intensity. The infected lesion
responded to antifungal treatment which was noted by reduction Alpha-hemolytic streptococci of the viridans group are the most
in size and density of infiltration and finally scarred over a period frequent isolates in ICK1,10,8,11,12 but other bacteria and fungi have
of 2 months. The graft stromal edema cleared without addition of also been implicated4,7,9,13,14,18.There are only a few anecdotal case
topical steroids.Three months post treatment the graft was clear reports of Candida species as causative organism of ICK7, .15,16,17
with a pupillary membrane for which Nd YAG Membranectomy
was done and post membranectomy, he attained BCVA of 6/18 In our case recurrence occurred with the same organism after
(Figure 4) and was on maintenance therapy of low dose steroids. quiescent period of 7 months. Darryl et al has reported recurrence
of ICK caused by Candida glomerulli in a post Keratoplasty
Seven months after the quiescent phase the patient presented patient15. The ability of Candida cells to build biofilms could have
with needle like infiltration at the site of previous scar on a facilitated its survival in corneal stroma16,19,20 even after specific
routine follow up visit. The patient was asymptomatic at this antifungal treatment. This possibly led to recurrence in our case.
stage. A recurrence of Infectious crystalline keratopathy (ICK)
was suspected. The steroid eye drops was stopped for 48 hours. Our case highlights that etiology of Candida Albicans should be
Cessation of topical steroids again flared up the lesion with suspected as a causative agent of ICK even in a tropical country
infiltrate crossing the host-graft junction and associated stromal like India. The organism can remain dormant in biofilms leading
edema and epithelial breakdown (Figure 5). Corneal scraping to recurrence even after long quiescence.
was done and heavy growth of Candida albicans in blood agar
and chocolate agar was observed .The patient was started on Tab
Itraconazole, Fluconazole, Amphotericin (0.15%) and Atropine
eye drops. Subsequently the lesion started responding and healed
with scarring and thinning over 6 weeks.

On final follow up visit the infiltrate scarred with vascularisation
with stromal edema persisting inferiorly and a dense retrocorneal
membrane in visual axis (Figure 6). The patient has been planned
for optical penetrating keratoplasty with due risk of recurrence
explained to the patient.

Discussion

Infectious crystalline keratopathy (ICK) was first described in
the 1980’s as a unique corneal infection characterized by slow
progression, a paucity of inflammation, and the formation of
sharply demarcated, gray-white, branching, round, stellate,
or needle like opacities in the corneal stroma. The minimal
inflammatory response in ICK is credited to the nature of the
affected cornea, the causative agent2,3,4 and the use of topical
corticosteroids.

58 DOS Times - Vol. 16, No. 6, December 2010

Reference 12 Remeijer L, van Rij G, Mooij CM, et al. Infectious crystalline
keratopathy Doc Ophthalmol 1987;67:95–103.
1. Gorovoy MS, Stern GA, Hood CI, et al. Intrastromal noninflammatory
bacterial colonization of a corneal graft. ArchOphthalmol 13 Ching-Long Chen,Ming-Cheng Tai, Jiann-Torng Chen,Chiao-
1983;101:1749–175 Hong Chen. Infectious Crystalline Keratopathy Caused by Serratia
marcescen.s Cornea 2007;26:1011–1013
2. Meisler DM, Langston RH, Naab TJ, et al. Infectious crystalline
keratopathy. Am J Ophthalmol 1984;97:337–43. 14 Lênio Alvarenga, Denise Freitas ,Ana Luísa Hofling-Lima, Rubens
Belfort Jr., Jorge Sampaio Luciene Sousa. Infectious Post-LASIK
3. McDonnell PJ, Kwitko S, McDonnell JM, et al. Characterization Crystalline Keratopathy Caused by Nontuberculous Mycobacteria.
of infectious crystalline keratitis caused by a human isolate of Cornea 21(4): 426–429, 2002
Streptococcus mitis. Arch Ophthalmol 1991;109:1147–51.
15 Darryl J.Ainbinder, Vernon C. Parmley, Thomas H. Mader, and Mark
4. Khater TT, Jones DB, Wilhelmus KR. Infectious crystalline L. Nelson, Infectious Crystalline Keratopathy caused by Candida
keratopathy caused by gram-negative bacteria. Am J Ophthalmol guilliermondii. Am J Ophthalmol1998;Vol125No5;723-724
1997;124: 19–23.
16 Elder MJ, Matheson M, Stapleton F, Dart JKG. Biofilm formation in
5. Sutphin JE, Kantor AL, Mathers WD, et al. Evaluation of infectious infectious crystalline keratopathy due to Candida albicans. Cornea
crystalline keratitis with confocal microscopy in a case series. Cornea 1996;15:301–304
1997;16:21–6.
17 Rhem MN, Wilhelmus KR, Font RL. Infectious crystalline
6. James CB, McDonnell PJ, Falcon MG. Infectious crystalline keratopathy caused by Candida parapsilosis. Cornea 1996;15:543-
keratopathy.Br J Ophthalmol 1988;72:628–30. 545

7. Wilhelmus KR, Robinson NM. Infectious crystalline keratopathy 18 Kamna Verma, Rasik B. Vajpayee, Jeewan S. Titiyal,Namrata
caused by Candida albicans. Am J Ophthalmol 1991;112:322–5. Sharma. Post-LASIK Infectious Crystalline Keratopathy Caused by
Alternaria. Cornea 2005;24:1018–1020
8. Salabert D, Robinet A, Colin J. Infectious crystalline keratopathy
occurring after penetrating keratoplasty. J Fr Ophtalmol 1994; 19 Ramage G, Vande Walle K, Wickes BL, Lo´ pez-Ribot JL.
17:355–7. Standardized method for in vitro antifungal susceptibility testing
of Candida albicans biofilms. Antimicrob Agents Chemother 2001;
9. Lubniewski AJ, Houchin KW, Holland EJ, et al. Posterior infectious 45:2475–2479
crystalline keratopathy with Staphylococcus epidermidis.
Ophthalmology 1990;97:1454–9. 20 lejandra E. odrı´guez . Polymerase chain reaction and DNA typing
for diagnosis of infectious crystalline keratopathy; J Cataract Refract
10 Meisler DM, Langston RH, Naab TJ, et al. Infectious crystalline surg - Vol 32, December 2006
keratopathy.Am J Ophthalmol 1984;97:337–43

11 Patitsas C, Rockwood EJ, Meisler DM, et al. Infectious crystalline
keratopathy occurring in an eye subsequent to glaucoma filtering
surgery with postoperative subconjunctival 5-fluorouracil.
Ophthalmic Surg 1991;22:412–3

First Author
Manisha Acharya MS

DOS Election

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

Secretary, DOS

Resolutions / Suggestions for General Body Meeting 59

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

– Secretary DOS

www.dosonline.org

Forthcoming Events: National

January 2011 March 2011
16-17 CHENNAI 20-24 SYDNEY

Chrysalis 2011 Asia Pacific Academy of Ophthalmology
International Conference on Oculofacial Reconstructive (APAO) Congress
and Aesthetics Surgery Contact Person
Organizing Secretary John Deeth, Executive Director
Dr. Shubhra Goel APAO Sydney - 2011
E-mail: [email protected] Phone: (Mobile): 0417 667 926
Ph.: 044-28254177, Mobile: 91-9382832910, Office: 61 2 9690 1001
Website: www.sankaranethralaya.org/chrysalis2011 Email: [email protected]
Website: www.apaosydney2011.com
February 2011
3-6 GUJARAT April 2011
15-17 NEW DELHI
69th AIOS Annual Conference
Gujarat University Convention Centre, Ahemadabad Annual Conference
Conference Secretary, Delhi Ophthalmological Society
Dr. Tejas D. Shah Venue: Hotel Ashok, Chanakya Puri, New Delhi
Amdavad Eye Laser Hospitals Pvt. Ltd. Contact Person & Address
Vision Complex, Polytechnic Cross Roads, Dr. Amit Khosla, Secretary DOS
Ahmedabad, 380015. India Room No. 2225, 2nd Floor, New Building,
Fixed: +91 79 26303208, Fax: +91 79 26303308 Sir Ganga Ram Hospital,
Website: www.aioc2011.com, Rajinder Nagar, New Delhi - 110 060
E-mail: [email protected] Ph.: 011-65705229, E-mail: [email protected],
Conference Help Line: 96248 96248 Website: www.dosonline.org

Dr. Shroff’s Charity Eye Hospital

Presents International conference on

“ Paediatric Cataract“

On 9th January 2011 10.00 a.m. – 4.00 p.m.

International Guest Faculty: National Guest Faculty:
Dr. Ken Nischal, Dr. Noshir Shroff, Shroff Eye Centre, Delhi
Prof. Dr. Sudarshan Khokhar,
Great Ormond Street Hospital for Children, U.K AIIMS, R.P.Center, Delhi
Prof. Dr. Jagat Ram, PGI, Chandigarh
Prof. Pawan Sinha, Dr. G.V. Rao, ORBIS International

Massachusetts Institute of Technology, U.S.A, Address for Correspondence:

Dr. Yuri Ostrovsky, Ms. Kalpana Gupta

Massachusettes Institute of Technology, U.S.A, [email protected]
Dr. Shroff’s Charity Eye Hospital
Organizing Secretary, 5027, Kedar Nath Road, Daryaganj
Delhi – 110002 (Mobile): 09899195676
Dr. Suma Ganesh

Head of Paediatric Ophthalmology
[email protected]

The registration fee is complimentary.

www.dosonline.org 69

Delhi Ophthalmological Society

(LIFE MEMBERSHIP FORM)

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

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

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

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

FOR OFFICIAL USE ONLY

Dr._______________________________________________________________has been admitted as Life Member of

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

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

drawn on __________________________________________________________________.

(Secretary DOS)

www.dosonline.org 71

INSTRUCTIONS

1. The Society reserve all rights to accepts or reject the application.
2. No reasons shall be given for any application rejected by the Society.
3. No application for membership will be accepted unless it is complete in all respects and accompanied by a Demand Draft of

Rs. 3100/- in favour of “Delhi Ophthalmological Society” payable at New Delhi.
4. Every new member is entitled to receive Society’s Bulletin (DOS Times) and Annual proceedings of the Society free.
5. Every new member will initially be admitted provisionally and shall be deemed to have become a full member only after formal ratification by

the General Body and issue of Ratification order by the Society. Only then he or she will be eligible to vote, or apply for any Fellowship/Award,
propose or contest for any election of the Society.
6. Application for the membership along with the Bank Draft for the membership fee should be addressed to Dr. Amit Khosla,
Secretary, Delhi Ophthalmological Society, Room No. 2225, 2nd Floor, New Building, Sir Ganga Ram Hospital, Rajinder Nagar,
New Delhi - 110 060
7. Licence Size Coloured Photograph is to be pasted on the form in the space provided and two Stamp/ Licence Size Coloured photographs are
required to be sent along with this form for issue of Laminated Photo Identity Card (to be issued only after the Membership ratification).
8. Applications for ‘Delhi Life Member’ should either reside or practice in Delhi. The proof of residence may be in the form Passport/Licence/
Voters Identity Card/Ration Card/Electyricity Bill/MTNL (Landline) Telephone Bill.

Notice for General Body Meeting*

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

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

72 DOS Times - Vol. 16, No. 6, December 2010

Delhi Ophthalmological Society Fellowship for Partial
Financial Assistance to Attend Conferences

Applications are invited for DOS Fellowship for partial financial assistance to attend conference(s).

Conferences Points Awarded

International: Three fellowships per year (Two fellowships can be 1) Age of the Applicant Points
awarded at a time if committee feels that papers are very good) a) < 35 years 10
b) 36 to 45 years 07
• Maximum of Rs. 35,000/- per fellowship will be sanctioned c) 45 years plus 05

National: Three fellowships per year (Only for AIOS) 2) Type of Presentation 12
a) Instructor/ Co-instructor of Course 07
• Maximum of Rs. 10,000/- per fellowship will be sanctioned b) Free Paper (Oral) / Video 05
c) Poster
Eligibility 15
3) Institutional Afſliation 20
• DOS Life Members (Delhi Members only) a) Academic Institution
b) Private Practitioner 05
• 75 or More DCRS Points 08
4) DCRS Rating in the immediate previous year
• Accepted paper for oral presentation, poster, video or instruction a) 75-150
course. b) > 150

Time since last DOS Fellowship c) < 75 not eligible for fellowship
Preference will be given to member who has not attended conference in
last three years. However if no applicant is found suitable the fellowship Documents
money will be passed on to next year. Members who has availed DOS
fellowship once will not be eligible for next fellowship for a minimum • Proof for age. Date of Birth Certificate
period of three years.
Authorship • Original / attested copy of letter of acceptance of paper for oral pre-
sentation / video / poster or instruction course.
The fellowship will be given only to presenting author. Presenting
author has to obtain certificate from all other co-authors that they are • Details of announcement of the conference
not attending the said conference or not applying for grant for the same
conference. (Preference will be given to author where other authors are • Details of both International & National Conferences attended in
not attending the same conference). If there is repeatability of same author previous three years.
group in that case preference will be given to new author or new group
of authors. Preference will also be given to presenter who is attending • Copy of letter from other national or international agency / agencies
the conference for the first time. committing to bear partial cost of conference if any.
Quality of Paper
• At least one original document should be provided, that is ticket,
The applicant has to submit abstract along with full text to the DOS boarding pass or registration certificate along with attendance cer-
Fellowship Committee. The committee will review the paper for its tificate of the conference.
scientific and academic standard. The paper should be certified by the
head of the department / institution, that the work has been carried out • Fellowship Money will be reimbursed only after submission of all
in the institution. In case of individual practitioner he or she should the required documents and verified by the committee.
mention the place of study and give undertaking that work is genuine.
The fellowship committee while scrutinizing the paper may seek further • Undertaking from the applicant stating that above given information’s
clarification from the applicant before satisfying itself about the quality are true.
and authenticity of the paper. Only Single best paper has to be submitted
by the applicant for review (6 copies). Quality of the paper will carry • If found guilty the candidate is liable to be barred for future fellow-
50% weightage while deciding the final points. ships.
Poster and Video
Application should reach Secretary’s ofſce and should be addressed
The applicant will need to submit poster and video for review. to President, DOS before 30th July, 31st October and 31st January
Credit to DOS for International Conference and before 30th September for National
Conference. The committee will meet thrice in a year in the month of
The presenter will acknowledge DOS partial financial assistance in August, November and February with in 2 weeks of last date of receipt
the abstract book / proceedings. of applications. The committee will reply within four week of last date
The author will present his or her paper in the immediate next DOS of submission in yes/no to the applicant. No fellowship will be given
conference and it will be published in DJO/DOS Times. retrospectively, that means prior sanction of executive will be necessary.

Dr. Amit Khosla
Secretary
Delhi Ophthalmological Society
Room No. 2225, 2nd Floor, New Building,
Sir Ganga Ram Hospital, Rajinder Nagar
New Delhi - 110060
Ph : 011-65705229
Email : [email protected]

www.dosonline.org 77

Tear Sheet www.dosonline.org 79

Keratoconus: Diagnosis and Management

SUBCLINICAL KCONUS ‐ Close follow up GRADE 4 KCONUS
DALK if no descemet’ s scar
EARLY KCONUS ‐ Spectacles, CL PK if descemet’s scar or unsuccessful DALK

Serial VKG

GRADE 1 ,2 KCONUS GRADE 3 KCONUS KERATOCONUS CLASSIFICATION BASED ON KRUMEICH AND
CO‐AUTHORS
CL trial CL IF POSSIBLE
Rose K/ softperm CL INTACS STAGE I – CORNEAL RADII</= 48D, VOGT’S STRIAE ,NO
SCARS
C 3R if progression C3R if CCT>370microns STAGE II – CORNEAL RADII</= 53D, NO CENTRAL SCARS,
CORNEAL THICKNESS>/=400 MICROMETRES
PTK if apical scarring PENTACAM ANALYSIS STAGE III ‐ CORNEAL RADII>53D, NO CENTRAL SCARS,
CORNEAL THICKNESS 200 TO 400 MICROMETRES
RABINOWTZ CRITERIA Indices (ISV,IVA,KI,CKI) STAGE IV – CORNEAL RADII>55D, CENTRAL SCARS,
PERFORATION, CORNEAL THICKNESS 200 MICROMETRES
VKG of patients with keratoconus‐ Distance between thinnest and apex>1mm
K’CONUS SUSPECT :No clinical finding,No Scissoring,AB/SRAX
à Central K > 47.2( averaging the K over central 3 mm) Pachy. Difference between thinnest and pattern on VKG
apex >10 u
EARLY K’CONUS:No slit lamp finding,Scissoring reflex,AB/SRAX
à I‐S asymmetry Anterior elevation map difference>+15u— pattern
> 1.4<1.9 ‐k’conus suspect ,>1.9Kconus 9mm zone BFS
>+8u‐‐‐8 mm zone BFS K’CONUS:Stromal thinning,Vogt’s striae , Scissoring of reflex on
refraction,AB/SRAX VKG pattern
ORBSCAN ANALYSIS Posterior elavation map difference>20u—9
Higher mean posterior elevation (>40µ) mm zone BFS Ritu Arora MD, Parul Jain,
3mm, 5mm irregularity
>16u‐‐‐8 mm zone BFS Guru Nanak Eye Centre, Maharaja Ranjit Singh Marg, New Delhi

Thinnest cornea < 500µ

ORBSCAN II IS MORE SENSITIVE