ISSN 0972-0200 Delhi Journal of OphthalmologyDelhi Journal of Ophthalmology Vol. 22, No. 2, October - December, 2011 [email protected] 79 ISSN 0972-0200 Vol.22, No.2, October - December,

Delhi Journal of Ophthalmology

Vol. 22, No. 2, October - December, 2011 [email protected] 79

ISSN 0972-0200 Vol.22, No.2, October - December, 2011

Editor-in- Chief

Associate EditorManaging Editor

Advisory Board

Editorial Board

Rajesh Sinha

Harinder S. Sethi Sumit Khanduja

M.Vanathi

Rajvardhan AzadAshok K. GroverLalit K.VermaYograj SharmaHarbans LalMahipal S. SachdevK.P.S. MalikAtul Kumar Namrata Sharma Rishi Mohan Tanuj Dada Rajinder Khanna Rohit Saxena Sanjiv Mohan Tushar Agarwal

Rasik B. VajpayeeHem K.TiwariB.P.GulianiS.P.GargJeewan S. TitiyalB.GhoshAnita PandaRadhika TandonSudarshan Khokhar Zia ChaudhuriRitu Arora Amit Khosla Neelam Pushkar Ruchi Goel

Saptorishi MajumdarShorya V. AzadRaghav GuptaSangeeta RoyTarun AroraRavi BBhaskar JhaAnasua GangulySubodh SinghKoushik Tripathy

Digvijay SinghVarun Gogia ReetikaSri Vatsa SehraKumar VivekRebika DhimanMayank BansalRajshri Hirawat Manik MittalVishal Arora

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General InformationDelhi Journal of Ophthalmology (DJO), once called Visiscan,

is a quarterly journal brought out by the Delhi Ophthalmological Society. The journal aims at providing a platform to its readers for free exchange of ideas and information in accordance with the rules laid out for such publication. The DJO aims to become an easily readable referenced journal which will provide the specialists with up to date data and the residents with articles providing expert opinions supported with references.

Contribution Methodology

in carrying out the work and it should be original. It should be accompanied by a letter of transmittal.The article can be sent by email to the Editor or a hard copy posted. Articles received will be sent to reviewers whose comment will be emailed to the author(s) within 4-6 weeks. The identity of the authors and the reviewers will not be revealed to each other by the editorial team. Detailed instructions to the contributors and for advertisement are included at the end of the journal.

Editorial ProcessThe DJO has Dr Rajesh Sinha as its Editor who is assisted by

a team of renowned ophthalmologists and an illustrous editorial

form the back bone of the journal by setting standards for the published work.

DisclaimerThe journal does not take any responsibility for the articles

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Published by Dr Rajesh Sinha,Editor DJO,Delhi Ophthalmological Society


Cover Page Designed By Amit Chauhan



Major Review

83. Editorial ........Dr. Rajesh Sinha

Contents

85. Current Trends – Intermittent Exotropia Management Pradeep Agarwal

93. Endoscopic Dacryocystorhinostomy Ruchi Goel , Saurabh Kamal , Sonam Angmo Bodh , Smriti Nagpal , Smriti Bansal , Kshitij Aditya

99. Edge Light Pupil Cycle Time as A Measure of Optic Nerve FunctionJ L Goyal , Sarmi Malik , Parul Jain , Ritu Arora

105. Effect Of Intracameral Heparin In Post Operative Inflammatory Reaction And Posterior Capsular Opacification After Cataract Surgery In High Risk Cases Eva R Tirkey , Shivcharan L. Chandravanshi , Mahesh K. Rathore , Kriti Sharma

Original Article

115. Endoillumination assisted Scleral Buckling: The future approach to Retinal Detachment SurgeryPradeep Venkatesh , Tarun Arora , Satpal Garg

Techniques

Case Report 119. Orbital Soft Tissue Mass as a Masquerading Presentation Preceding Acute Myeloblastic

Leukemia and Chloroma in a Child with Down SyndromePasumala Lakshminarayana , Basudev Ghosh , Meenakshi Thakkar , Shyama Jain , Seema Kapoor , Amit Bhatia

125. Large Post Traumatic Ocular Foreign Body With Good Visual OutcomeAnoop Kishore Gupta , Sourabh Sharma , Neelam Pushker , Mahesh Chandra

123. A Typical Lens Coloboma – A Rare Cause of Childhood Blindness Punita Garg , Parul Aggarwal , H.K Sidhu

131. Corticosteroid Implant for Vascular OcclusionsSavleen Kaur , Nishant Sachdev

Recent Advances

Contents (Contd.........)

Vol. 22, No. 2, October - December, 201182


149. Retinal Haemorrhage as an Unusual Presenting Feature of Metastatic Pancreatic Carcinoma

Parul Jain , Vasu Kumar , P K Pandey , B Ghosh , Chittaranjan Mishra

Photo Essay

153. Brinzolomide A new Star in Anti Glaucoma Armamentarium Brinolar

155. HOYA Launches the NEW MICS ≤2.0 mm Single-piece Hydrophobic Acrylic IOL in India Hoya

Industry News

Information to Author

135. Ophthalmic Drug Delivery Systems : An Update Nihar Ranjan Biswas

Allied Ophthalmic Sciences : Ocular Pharmacology

Copy Right Form

141. Cosmetic Contact Lens Induced Corneal UlcersKhushnood Sheikh

143. Letter to editorSupriya Arora, Tarun Arora, Vinod Kumar Tewari

Brief Communication



What makes a journal good ?

Dear Colleagues,To consider a journal as good requires it to be readable and be able to provide information, at least part of which should be new to the readers. It should be having different formats of articles so as to avoid monotony and also to keep it interesting for not only the readers but also to the authors. There should be a good reviewing system of the manuscript so that the quality of the articles is maintained high.

“It is reasonable to have perfection in our eye that we may always advance toward it, though we know it can never be reached”.

Samuel Johnson

We at Delhi journal of ophthalmology also strive towards perfection, trying to bring out the best articles in every new edition. With increasing participation of various ophthalmologists from the country, generation of new thoughts is at

new issue to a standard that it is now expected of us is a challenge that I am beginning to love. However, if we are to take the journal further ahead, we need quality submissions from everyone, and only then we can hope to achieve our goal of a peer-reviewed indexed journal.

I made a promise during the previous issue that we will strive to make every issue of DJO bigger and better than

online article submission platform. This makes it easier and safer for all of you there to submit your valuable article and also for keeping a proper record of the articles. The website http://submission.djo.org.in has been activated for online submission of articles to the Delhi Journal of Ophthalmology. We need your valuable inputs in order to make this submission process appropriate and successful. There may be initial hiccups but with the involvement of all the members of the society, we can cross the hurdles and march ahead.

Rajesh SinhaMD, DNB, FIACLE, FRCS



Abstract

Del J Ophthalmol 2011;22(2):85-92.Key Words:

Major Review

Current Trends – Intermittent Exotropia Management

Pradeep Agarwal MS

Intermittent exotropia is a divergent squint intermittently controlled by fusional mechanisms. Unlike a true phoria, intermittent exotropia spontaneously breaks down into a manifest exotropia. Of all the exotropia, intermittent exotropia comprises about 50 to 90% of the cases and is usually preceded by a stage of exophoria.1,2 It usually affects 1% of general population. Exodeviation occurs more commonly in middle east, subequatorial Africa and the Orient than in the United states. Not all the intermittent exotropia are progressive. In some cases, the deviation may remain stable for many years, and in few cases it may even improve.3 Thus the patient should be carefully followed over time to determine whether the deviation is stable or deteriorating. Many studies have revealed variable results like Von Noorden found that 75% of 51 untreated patients showed progression over an average follow up period of 3.5 years while 9% did not change and 16% improved while on the other hand Romanchuk found that 23% of 109 untreated patients showed progression more than 10 prism dioptre over an average follow up period of 9 years while 58% did not change and 19% improved by more than 10 prism dioptre.4

Stages of Intermittent ExotropiaAccording to Calhounz et al intermittent exotropia can

be divided into following 4 Stages.

1. Exophoria at distance, orthophoria at near: Asymptomatic.

2. Intermittent exotropia at distance, orthophoria/ exophoria at near: Symptomatic for distance.

3. Exotropia for distance, exophoria or intermittent exotropia at near: Binocular vision for near, suppression scotoma for distance.

4. Exotropia for distance as well as near: Lack of binocularity.

EtiologyAccording to Duane exodeviations are caused

by innervational imbalance that upsets the reciprocal relationship between active convergence and active divergence mechanisms.4 Bielschowsky claims Duane’s theory that the majority of exodeviations are based on hyperactive tonic divergence. According to him, Duane’s theory did not take into account the abnormal position of rest associated with exodeviation. This abnormal position is determined by anatomic and mechanical factors like size and shape of eyeball, orientation, size and shape of orbit, volume and viscosity of retrobulbar tissue, functioning of eye muscles as determined by their insertion, length, elasticity, anatomical and structural arrangement as well



as on condition of ligament and fascias of orbit. But now most of the theory combines the concepts of innervational and mechanical factors.5,6 According to Cooper and Medow the AC/A ratio is either normal or slightly higher than the normal in patients who have intermittent exotropia.7

Kushner in 1988 found that approximately 60% patients with true divergence had a high AC/A ratio, and 40% had a normal AC/A ratio.8 According to Knapp and Jampolsky the ability to suppress temporal vision allows the eye to diverge.9,10 According to Ignacio Serrano-Pedroza and others patients with intermittent exotropia develop sophisticated mechanisms to maintain single vision during periods of

ability to adapt to disruption early in development.11 As the accommodative effort is less than normal in myopic patient especially in uncorrected myopic patient, these patients have the tendency for exodeviation according to Donder.12 Similarly in patients with high degree of uncorrected hypermetropia no effort is made to overcome the refractive error by accommodation and clear vision is not possible,13 this may lead to exodeviation on the basis of under stimulated and thus under active convergence mechanism that causes the AC/A ratio to remain low. Thus refractive errors through their effect on accommodation are prime causes of misalignment.

ClassificationBurian’s well known intermittent exotropia

and divergence.14

1. Basic intermittent exotropia - Exodeviation in the distance is within 10 to 15 prism dioptres of the near deviation. These patients have normal fusional convergence, normal accommodative convergence and normal proximal convergence.

2. True Divergence excess – Distance deviation is 10 to 15 prism dioptres more than the near deviation, even after doing patch test.15 To diagnose this, while still dissociated fusion by patch test, re-measure the near deviation after putting +3.00D lens in trial frame, if near deviation increases by 20 prism dioptres or more then

Kushner found that approximately 60% patients with true divergence had a high AC/A ratio and remaining about 40% patients had normal AC/A ratio. The group with high AC/A ratio is prone to have post-operative over-correction if the distance measure was used as a target angle

3. Pseudo/ Simulated Divergence excess - is present when distance deviation is 10 to 15 prism dioptres more than near deviation, but near deviation also increases with in 10 prism dioptres of distance deviation after doing patch test for 30 to 60 minutes. This occurs because monocular occlusion of 30 to 60 minutes dissipates

fusional convergence thereby disclosing the full latent deviation.

4. - when near deviation is 10 to 15 prism dioptres more than the distance deviation.

Characteristics Intermittent exotropia is most common type of exodeviation

16,17,18

Younger children are usually asymptomatic because of hemiretinal temporal suppression.10 Older children and adults without suppression may develop asthenopic symptom, blurred vision, transient diplopia and diplophotophobia. Diplophotophobia is closure of one eye in bright sun light, because bright light dazzles the retina so that fusion is somehow disrupted causing the deviation to become manifest,19 thus one eye is closed in order to avoid diplopia. In general these patients have good binocular vision and stereoacuity for near is good but suppress for distance. It is important to obtain a baseline evaluation as well as to monitor deterioration and progression of intermittent exotropia. Intermittent exotropia can be a sign of reduced visual acuity.20

Two new method of assessment of control are -

1- New Castle control score - Reliable method for grading the severity of intermittent exotropia.21 It incorporates both subjective (Home control) and objective (clinical control) criteria in to a scale to grade severity.22

Subjective / Home control – parents are asked to look for outside deviation of eye or monocular closure of eye and grading of severity is done as following :-

Never – 0

< 50% of time for distance – 1

> 50% of time for distance - 2

> 50% of time for distance, and also for near - 3

Objective / clinical control - Cover test is done for distance and near and scored separately as following –

Immediate realignment after cover test – 0

No realignment or spontaneously manifest – 2

In both subjective and objective method the score can vary from 0 to7. Score of 3 or more are unlikely to attain cure without surgery.23 Recently there is a revised version of the NCS in a UK study (Improving outcomes in intermittent exotropia study). In this revised scale all components of NCS are same except the most severe categories with in the clinic control components have been divided into two categories “remains manifest after

Hence, the total NCS now ranges from 0 to9. It is envisaged

grading the severity of childhood intermittent exotropia.24



2 – Mayo clinic exotropia score 25 - Again the cover test is done to dissociate the images for distance and near both and scoring is done as following-

Never exotropia unless dissociated,

recovery in < 1 second – 0


recovery in 1-5 second – 1


recovery in > 5 second – 2

Exotropia < 50% of time before dissociation – 3

Exotropia > 50% of time before dissociation – 4

Constant exotropia – 5

Mayo clinic exotropia score can vary from 0 to 10. Score 0 signifying a phoria with no tropic components at either distance or near, even after dissociation, and 10 denoting

26

Because Newcastle scale consider parental report score to

observation could profoundly alter the overall score and subsequent management. While Mayo clinic score provides a quantitative measure of the severity and duration of the manifest component of the exodeviation, so Mayo exotropic scaling system suits best for the management of cases and decision making. Distance stereoacuity provides an objective assessment of both control of the deviation and the deterioration of fusion that occurs early in intermittent exotropia. Distance stereoacuity can also be checked by Frisby-Davis Distance (FD2) Test27 and Distance Randot (DR) Test.28 Frisby- Davis Distance Stereo (FD2) Test is based on real world contour based targets. These targets stimulate fusion in intermittent exotropia even when distance control is poor so even in early stages of intermittent exotropia distance stereoacuity is comparatively good. In contrast Distnce Randot (DR) Test is based on new polaroid vectograph and is very sensitive to disturbance of stereoacuity so even in early stage of intermittency test performances deteriorates.29,30 Halt SR and others advocated that nearly half of children with intermittent exotropia show marked changes in stereoacuity and control over the course of a single day. When based on isolated measures, an apparent change in distance stereoacuity between visits should be interpreted with caution.31,32

Measuring the Angle of DeviationDue to variable angle of deviation, measurement in

routine alternate cover prism test. Prolonged alternate cover testing should be used in patients with intermittent exotropia to suspend tonic fusional convergence. If after

a patch test is indicated. The patients who show consistent measurements and no distance/near discrepancy do not need patch test. Patch test should be done before +3.0 D Test to measure near deviation, to avoid misdiagnosing high AC/A Ratio. Monocular occlusion in patch test suspend/relaxes fusional convergence while + 3.0 D lens suspend/ relaxes accommodative convergence.

Patch Test This test is used to control the tonic fusional

convergence to differentiate the pseudo-divergence excess from true divergence excess and to reduce angle variability.

convergence to reveal the actual amount of deviation.33

Earlier full day patching of 24 hours is now no more in practice.

+ 3.0 D Near Add Test (Lens Gradient Method) This test has been devised to diagnose the patients of

divergence excess type who have true divergence excess due to high AC/A Ratio. This test uses the lens gradient method to measure the AC/A Ratio. This test should be done in patients who have a distance deviation more than the near deviation of 10 to 15 prism dioptres or more after patch test. After the patch test while still dissociated, re-measure the deviation at near with +3.0 D lens add. If the near deviation increases by 20 prism dioptres or more the diagnosis of high AC/A Ratio true divergence excess type intermittent exotropia is made. These patients are one who will continue to have distance/ near disparity post-operatively, and may require bifocal glasses after surgery for consecutive esotropia at near.

Far Distance Measurement

the measurement variability and helps in uncovering the full deviation by reducing the near convergence. Combining the patch test and far distance measurement can reduce the under-correction and has improved the overall results. In a prospective randomised trial, 86% of patients who underwent surgery for the largest angle at far distance had a satisfactory result, compared with 62% who were operated on for the standard 6 meter distance deviation.34

ManagmentNon-surgical treatment

Although not much effective but has the advantage that some time intermittent exotropia may get resolved spontaneously and we can always change our mind later. But still conservative therapy can be done in patients with small (<20 prism dioptres) exodeviation35, very young patients



in whom surgical over-correction can lead to amblyopia

general anaesthesia and those who want to delay surgery.36

Conservative options include

1-Glasses

Corrective lenses based on cycloplegic refraction should be given especially in cases of myopia, anisometropia, high hypermetropia.37 Role of spectacles in low hypermetropia is controversial but should be given in small exodeviation initially. Overcorrecting minus lens therapy is based on stimulating accommodative convergence that can reduce exodeviation,38,39 especially helpful in high AC/A ratio type of exodeviation. Watts and others suggest that Newcastle Control Score is a useful method to indicate the success in the control of intermittent exotropia with conservative treatment with minus lens therapy.21

2- Orthoptic Exercise

This should not be used as substitute of surgery but rather than as supplement. The aim is to make the patient aware of manifest deviation and to improve the patient’s control over it.40 Active anti-suppression exercise and diplopia awareness techniques can be used in cases with suppression. Convergence exercise can be helpful in cases of patients with remote point of near convergence.

Some times prism are useful in improving fusional control and some time as a temporary measure either pre-operatively41 or post-operatively.

4- Part Time Occlusion

This technique can be useful in very young children. This is a passive anti-suppression technique as opposed to the active technique involving awareness of diplopia. Part-time occlusion of non-deviating eye for 3 to 6 hours daily may convert intermittent exotropia in to phoria.42 Alternate

preferences.

Surgical Treatment

As a general rule the most important indication of squint surgery is preservation or restoration of binocular function and cosmetic. In intermittent exotropia one of the important indication is an increasing tropia phase. If the frequency or duration of tropia phase increases, this indicates diminished fusional control and the potential for losing binocular function. Infact some school going age group children may experience the progression of their disease and have fear

of teasing and harassment from playmates and looking different from other children, thus have a negative impact on self-esteem and personality development. These negative psychological impact are one of the indication if the children is complaining about this. Childhood intermittent exotropia also seems to affect parent health-related quality-of-life.43,44

Progression should be monitored by documenting the size of deviation, duration of manifest exodeviation and ease of regaining fusion after dissociation from cover-uncover test. Deteriorating fusional control is an indication for surgery.

Signs of progression of intermittent exotropia

1- Increase in size of basic deviation

2- Gradual loss of fusional control as evidenced by increasing frequency of manifest phase of squint.

4- Development of suppression as indicated by absence of diplopia during manifest phase.

5- Decrease of stereoacuity.

Timing of SurgeryA lot of controversy is there about the surgery of

children less than 4-5 years of age because in contrast to congenital esotropia these children have intermittent fusion and excellent stereopsis.45,46 Knapp and others advocated early surgical intervention to prevent the development of sensory changes.47,48,49 Saunders and Trivedi achieved high-grade stereopsis in some cases by early surgical intervention.50 Jampolsky advocated delayed surgery, citing

amount of deviation. Although few study reported better outcomes in children who were under the age of 4 years, while at the same time other studies failed to show that age at the time of surgery makes any difference in outcomes51,52

Based on all these studies now most of the surgeons reserve the surgery in this age group in whom rapid loss of control is documented. Recently Kushner explained the presence

present preoperatively. Many of these patients manifest a constant microtropia preoperatively and hence should not

exotropia is more appropriately descriptive.53

Choice of ProcedureAs a general rule in divergence excess type of

intermittent exotropia most of the surgeons prefer bilateral lateral rectus recession, in basic type of intermittent exotropia unilateral lateral rectus recession and medial

intermittent exotropia bilateral medial rectus resection. However recently it has been shown that in all type of exotropia bilateral lateral rectus recession works well except



no doubt bilateral medial rectus resection works well. Symmetrical bilateral surgery is preferred over unilateral recession/resection because recession/resection may

diplopia to the side of the operated eye. As a general rule surgeons should operate for the largest distance deviation that can be repeatedly documented. Adjustable suture techniques are helpful in cooperative patients.54,55 Koklanis

the surgical treatment of intermittent exotropia.56

Surgical Dosage

In cases of exotropia of 60 prism dioptres or more, there is need of 3 muscle surgery i.e. bilateral lateral rectus recession and right/left medial rectus resection. Surgical dosages are shown in Table 2.

intermittent exotropia we should plan bilateral medial rectus resection in dosage as shown in Table 3.

In cases where the exotropia is minimal, we can plan single eye recession of lateral rectus muscle in following dosage as shown in Table 4.

Lateral Gaze Incomitance

gaze in comparison to primary position. Parks and Moore recommended that patients with preoperative lateral incomitance are much more likely to be overcorrected with surgery. This is true regardless of the type of intermittent exotropia. A 20% or greater decrease in lateral gaze

surgical dosage is advisable.57

Goals of Surgery Many Ophthalmologist have proposed that for

intermittent exotropoia a small (5-15 prism dioptres) surgical over-correction is desirable because eyes tend to drift out over time.58,59 Small over-correction i.e. esotropia in initial post-operative phase stimulate the development of fusional vergences and stabilize post-operative alignment. One must keep the age of the patient in mind when planning for surgery, since consecutive esotropias in visually immature children can have the consequences of amblyopia and loss of binocularity. In oldren children and adults who develop intermittent exotropia after the age of 10 years, diplopia is usually present with little or no suppression. In these patients the surgical goal should be orthotropia on

60

Beside adults with longstanding intermittent exotropia will often tolerate under-correction, but will have symptomatic diplopia when overcorrected. So in intermittent exotropia surgical amount of over-correction, under-correction or full correction depends on the age of patient. Recently Pineles SL and colleagues found that long-term surgical results in intermittent exotropia are less encouraging when

Deviation (prism dioptres)

Both eye lateral rectus recession (mm)

Right or Left eye Medical rectus resection (mm)

60 8 665 8.5 670 8.5 6.575 9 6.580 9.5 6.585 9.5 790 10 7

Deviation (prism dioptres) Both eye Medical rectus recession (mm)

20 425 530 5.535 640 6.5

Deviation (prism dioptres) Unilateral lateral rectus recession (mm)

15 720 825 9

Deviation (prism dioptres)

Bilateral lateral rectus recession (mm)

Unilateral lateral rectus recession & medial rectus resection (mm)

20 5 5 425 6 6 4.530 7 6.5 535 7.5 7 5.540 8 7.5 645 8.5 8 650 9 8.5 6.555 9.5 9 6.560 10 10 7

The amount of surgical dosage in terms of recession and resection is shown in Table 1.



sensory status is added to evaluation (38% in comparison to 64% when considering only motor criteria). Patients with anisometropia, lateral incomitance and immediate postoperative under-correction are risk for poor outcome.61

A and V PatternIntermittent exotropia may be associated with true or

pseudo over-action of superior or inferior oblique muscle. If

V pattern (3+, 4+ action) then simultaneous surgery should be done on oblique muscle. Supra-placement or infra-placement of horizontal muscle can be done depending of A or V pattern, if surgeon is not interested in doing surgery on oblique muscle. Mild A or V pattern (1+, 2+ action) are mostly pseudo A or V pattern62 due to tight lateral rectus muscle due to long standing exotropia which causes slippage of the globe under the tight lateral rectus muscle in extreme lateral gaze. This up-shoot and down-shoot of the eyeball will mostly be corrected by recessing the tight lateral rectus muscle and does not require any surgery on oblique muscle. Also small vertical deviation less than 8 prism dioptres associated with intermittent exotropia should be ignored since these vertical phorias usually disappear after surgery.

Post-Operative TreatmentDepends on the position of eye post-operatively.

The eyes may be in orthoposition, may show residual exodeviation (under-correction) or may show consecutive esotropia (over-correction). E kdawi and others showed excellent alignment in 50% children from a population based cohort.63

OrthopositionAs mentioned above older children and adults who

develop intermittent exotropia after the age of 10 years usually present with diplopia and in these patients orthoposition in immediate post-operative phase is desirable. In contrast in children less than 10 years of age group a small consecutive esotropia of 8 to 10 prism dioptres is desirable because there is always a tendency of the eyes to diverge postoperatively. If these children less than 10 years of age are ortho in immediate post-operative phase then it is very important to strengthen the positive fusional convergence with orthoptic exercises in order to improve

Residual Exodeviation/Undercorrection 1) Small residual exotropia (<15 prism dioptres) - Should

be managed by non-surgical measures. Any refractive error like myopia should be fully corrected. In emmetropic and hypermetropic patient full cycloplegic correction should be

given and orthoptic exercises in the form of anti-suppression exercises and fusional convergence exercises should be done till the proper alignment is achieved. Base in prism can be tried to provoke convergence if patient is not improving with above measures.64,65,66,67

2) Large residual exotropia (>15 prism dioptres)- Post-operatively >15 prism dioptres with in 1st week of operation will probably not improve and will require additional surgery. It is better to wait 2-3 months before re-operating on residual exotropia. If the primary surgery was bilateral lateral rectus recession of 6.0 mm or less, re-recession of the lateral rectus can be done. If the primary recession was greater than 6.0 mm, then perform unilateral or bilateral resection of medial rectus muscle carefully as over-corrections are common after resecting against a large recession.

Consecutive Esotropia (over-correction)As mentioned above small (5-15 prism dioptres)

esotropia in early post-operative period is desirable in children as eye has the tendency to drift out. But if the consecutive esotropia is little more (15-25 prism dioptres) then at the same time there is danger of developing amblyopia thus these patients require special attention. Any refractive error especially hypermetropia should be fully corrected and bifocals should be given if near deviation is more than distance. In children under the age of 8 years alternate patching should be done to prevent amblyopia and to facilitate straightening of eyes. If these measures are not able to correct consecutive esotropia with in 4-6 weeks then base-out prism should be given to allow fusion.68,69 If still after 20 weeks esotropia persist then a re-operation should be considered.70 Unilateral or Bilateral recession of medial rectus is procedure of choice, especially if esotropia is greater at near. In case of lateral incomitance advancement of lateral rectus can be considered. Overall non-surgical management of over-correction should be tried at least 4-6 weeks because of high likelihood of spontaneous resolution.71 An unusually large over-correction with gross limitation of abduction on

rectus muscle. Such cases should be taken up for surgery as soon as possible.

ConclusionWe should not wait unnecessary for the natural

miracles if there is straight forward indication for surgery or deterioration of fusional control over time. Most of the tests in practice measure only near stereoacuity and already there is a lot more compromise in distance stereoacuity at this stage. Frisby-Davis Distance test and Distance-Randot test for distance stereoacuity are not accessible in routine pediatric ophthalmology practice. So even in the absence of these tests we should plan the surgery at appropriate time aiming for stereopsis and not only for cosmetic purpose.



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24 Buck D, Clarke MP, Haggerty H, Hrisos S, Powell C, Sloper J et al. Grading the severity of intermittent distance exotropia: the revised Newcastle Control Score. Br J Ophthalmol 2008;92:577.

25 S. Hatt, B. Mohney, D. Leske, J. Holmes. Variability of stereoacuity in intermittent exotropia. Am J Ophthalmol 2008;145:556-61.

assessing control in intermittent exotropia. Strabismus2006;14:147-50.

27 J. Holmes, S. Fawcett. Testing distance stereoacuity with the Frisy-Davis 2 (FD2) test. Am J Ophthalmol2005;139:193-5.

28 Leske DA, Birch EE, Holmes JM. Real depth vs randot stereotests. Am J Ophthalmol 2006;142:699-701.

29 Birch EE, Holmes JM. Assessment of a new distance Randot stereoacuity test. J AAPOS 2006;10:419-23.

30 Adams WE, Hatt SR, Haggerty H, Buck D. Improvement in distance stereoacuity following surgery for intermittent exotropia. J AAPOS 2008;12:141-4.

31 Hatt SR, Mohney BG, Leske DA, Holmes JM. Variability of control in intermittent exotropia. Ophthalmology2008;115:371-6.

32 Hatt SR, Mohney BG, Leske DA, Holmes JM. Variability of stereoacuity in intermittent exotropia. AmJ Ophthalmol 2008;145:556-61.

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34 Kushner BJ. The distance angle to target in surgery for intermittent exotropia. Arch Ophthalmol 1998;116:189-94.

35 Richardson S, Gnanaraj L. Interventions for intermittent distance exotropia. Cochrane Database Syst Rev.2006;3:CD003737.

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37 Iacobucci IL, Archer SM, Giles CL. Children with exotropia responsive to spectacles correction of hyperopia. Am J Ophthalmol 1993;116:79-83.

38 Caltreider M, Jampolsky A. Overcorrecting minus lens therapy for treatment of intermittent exotropia. Am J Ophthalmol 1983;90:1160-5.

39 Rowe FJ, Noonan CP, Freeman G, DeBell J. Intervention for intermittent distance exotropia with overcorrecting minus lenses. Eye (Lond) 2009;23:320-5.

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1 Govindan M, Mohney BG, Diehl NN, Burke JP. Incidence and type of childhood exotropia: a population based study. Ophthalmology 2005;112:104-8.

2 Von Noorden GK. Binocular Vision and Motility. Theory and Management of Strabismus 5th ed Mosby: St Louis 1996;343.

3 Romanchuk KG, Dotchin SA, Zurevinsky J. The natural history of surgically untreated intermittent exotropia – Looking into the distant future. J AAPOS 2006;10:225-31.

the eyes based on physiological principles together their symptoms, diagnosis and treatment. Ann. Ophthalmol Otolaryngol 1896;5:969.

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6 Costenbader FD. The physiology and management of divergent strabismus. St. Louis, Ed Allen JH. Strabismic Ophthalmic Symposium I 1950 Mosby- Year Book, Inc.

7 Muscle Cooper J, Medow N. Intermittent Exotropia, basic and divergence excess type. Binoc Vis Eye Surg1993;8:185-6.

8 Kushner BJ. Exotropic Deviations AND A Functional Am Orthopt

J 1988;38:81-3.9 Knapp P. Intermittent Exotropia AND Evaluation and

Therapy. Am Orthopt J 1953;3:27-3.10 Jampolsky A. Differential Diagnostic Chracterstics of

Intermittent Exotropia and true Exophoria. Am Orthopt J 1954;4:48-5.

11 Ignacio Serrano-Pedraza, Michael P Clarke, Jenny CA Read. Single vision during ocular deviation in intermittent exotropia. Ophthalmic Physiol Opt2011;31:45-55.

12 Donders FC. An essay on the nature and consequences of anomalies of Refraction. Ed. Oliver CA. Philadelphia 1899. P. Blakiston’s son and co,59.

13 Von Noorden GK, Avilla CW. Accomodative convergence in hyermetropia. Am J Ophthalmol1990;110:287-92.

14 Burian HM, Spivey BE. The Surgical Management of Exodeviations. Am J Ophthalmol 1965;59:603-20.

15 Von Noorden GK. The patch test and plus lenses in the diagnosis of exodeviation. The Prism 1982.

16 Mohney BG, Huffaker R.K. Common forms of childhood exotropia. Ophthalmology 2003;110:2093-6.

17 Govindam M, Mohney BG, Diehl NN, Burke JP. Incidence and types of childhood exotropia : A population-based study. Ophthalmology 2005;112:104-8.

18 Mohney BG. Common forms of childhood Strabismus in an incidence cohort. Am J Ophthalmol 2007;144:465-7.

Manley D ed.: Symposium on horizontal ocular deviations. St. Louis. 1971. Mosby-Year book Inc.128.

20 Buck D, Powell C, Cumberland P, Davis H, Dowson E, Rahi J et al. Presenting features and early management of childhood intermittent exotropia in the UK: inception cohort study. Br J Ophthalmol 2009;93:1620-4.



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41 Veronneau-Troutman S: Frensel prism membrane in the treatment of strabismus. Can J Ophthalmol 1971;6:249.

42 Freeman RS, Isenberg SJ: The use of part time occlusion for early onset unilateral exotropia. J AAPOS 1989;26:94-6.

43 Hatt SR, Leske DA, Yamada T, Bradley EA, Cole SR, Holmes JM. Development and initial validation of quality-of-life questionnaires for intermittent exotropia. Ophthalmology 2010;117:163-8.

44 Hatt SR, Leske DA, Holmes JM. Comparison of quality-of-life instruments in childhood intermittent exotropia. J AAPOS 2010;14:221-6.

45 Abroms AD, Mohney BG, Rush DP, Parks MM, Tong PY. Timely Surgery in intermittent and constant exotropia for superior sensory outcome. Am J Ophthalmol 2001; 131:111-6.

46 Asjes-Tydeman WL, Groenwoud H. Timing of surgery for primary exotropia in children. Strabismus 2007;15:95-101.

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49 Richard JM, Parks MM: Intermittent exotropia: Surgical results in different age groups.Ophthalmology1983;90:1172-7.

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52 Stoller SH, Simon JW, Liniger LL. Bilateral lateral rectus muscle recession for exotropia. A Survival Analysis. J AAPOS 1994;31:89-92.

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Major Review

Endoscopic DacryocystorhinostomyRuchi Goel MS, DNB, FICS , Saurabh Kamal MS , DNB , Sonam Angmo Bodh MS, DNB , Smriti Nagpal MBBS ,

Smriti Bansal MBBS , Kshitij Aditya MBBS

Symptomatic epiphora due to nasolacrimal duct obstruction (NLDO) is a common disorder and external dacryocystorhinostomy (DCR) is still considered the gold standard for its treatment.1,2 But with minimally invasive scar less surgery becoming the demand of the modern day ophthalmic surgery, there has been a renewed interest in the development of endoscopic technology3. Using an endoscope, the DCR can be performed by endonasal route using either laser 4,5 or surgical instruments 6,7 or both.8

Laser transcanalicular endonasal DCR is also becoming popular due to its inherent advantages over endonasal laser delivery systems such as the laser direction being away from the globe and the approach being more familiar to the ophthalmic surgeon.

The transnasal approach to DCR was initially described a century ago.9 A rekindling of interest in this route led to the use of lasers in DCR. Initially the argon laser was employed10,11 followed by the carbon dioxide and potassium titanyl phosphate (KTP) lasers12,13. The other laser systems used are Holmium:yttrium aluminium garnet (Hol:YAG),8

Erbium:yttrium aluminium garnet (Erb:YAG), Neodymium: yttrium aluminium garnet (Nd:YAG) and diode.14 In this article we made an attempt to highlight the contemporary techniques of endoscope assisted DCR.

Indications for endonasal DCR1. NLDO causing epiphora or infection as for external

DCR 15-17

3. NLDO with previous paranasal sinus surgery or trauma in selected patients 17-19

4. Atypical forms of dacryostenosis including NLD cyst formation 20,21

5. Revision surgery following external or endonasal DCR22,23

Contraindications to endonasal DCR (Relative)1. Suspicion of lacrimal system neoplasia 24-26

2. Severe mid facial trauma with secondary hyperostosis or altered anatomy involving the bones surrounding the lacrimal sac and NLD 24-26

3. Dacryolithiasis 27

4. Diverticula arising from lacrimal sac and extending to the lid28

5. Wegners granulomatosis and sarcoidosis due to poor success rates29

Advantages of endonasal DCR compared to external DCR1. Avoidance of cutaneous scar 10,30

2. Less disruption of medial canthal anatomy and lacrimal pump function 6,8,10,30

3. Decreased operative time 6,10,17,20

4. Decreased intraoperative hemorrhage 10,11,26,31

5. Decreased postoperative morbidity and enhanced recovery 11,32,33

6. Correction of nasal/paranasal sinus abnormalities through the same surgical approach 19,26,30

Abstract

Del J Ophthalmol 2011;22(2):93-97.Key Words: endoscopic DCR, epiphora, nasolacrimal duct obstruction.



7. Management of acute dacryocystitis with abscess formation 34,35

8. Performance of the procedure on out patient basis under local anaesthesia 36

9. Simultaneous surgery on both the sides 37

Disadvantages of endonasal DCR1. High capital equipment costs and ongoing material and

technical support expenses related to lasers 23,38

2. Laser ablation of lacrimal sac mucosa precludes submission of mucosal specimen for biopsy purposes 38

3. Radiologic studies may be required more frequently to rule out lacrimal system mass or sinonasal disease 19,26

39,40

5. Decreased nasal mucociliary clearance due to damage to nasal mucosa 41

Tissue response to LaserLasers in endonasal surgery involve instant

vaporization/ablation of tissue and delayed tissue loss by coagulative effect.3

limited. Diode and Nd:YAG lasers induce large coagulation zones, whereas the CO2 laser induces the most precise ablation with the smallest coagulation zones.42 There is

in laser treated tissues. Based on the current data, it is unclear as to which laser is the best. The development of the

14

Techniques of Endonasal DCRAnaesthesia: The vast majority is performed under

local anaesthesia unless the patient expresses a personal preference for general anaesthesia. An additional extra injection of lignocaine with adrenaline is given into the nasal mucosa overlying the proposed rhinostomy site under direct view of nasal endoscope for reducing sensations and blood splatter during the procedure. 29A 10% lignocaine spray can also be applied through the affected nostril.43

Endoscopic endonasal surgical DCR: 43 (Figure1)The lacrimal puncta on the affected side is dilated

and irrigated with saline solution. Then either a 20 gauge

lacrimal probe is inserted through either punctum into the lacrimal sac to tent the mucosa of lateral nasal wall. A circular incision of nasal mucosa around the underlying probe tip is performed using a sickle knife. The mucosal

elevated from the region anterior to the middle turbinate

constituted by the anterior lacrimal crest of the maxilla anteriorly and lacrimal bone posteriorly. The bone may be removed by means of a microdrill and the bony window may be enlarged using a gouge and a rongeur. The medial wall of the lacrimal sac adjacent to the bony window is tented by a lacrimal probe, incised with a sickle knife and removed by an angled forceps.

Endoscopic endonasal laser DCR: (Figure 2)

light pipe is inserted into the lacrimal sac via lower or upper canaliculus and visualised endonasally with 0 or 300 Hopkins rigid endoscope. The light pipe is directed

Figure 1 : Intraoperative endoscopic surgical dacryocystorhinostomy. Figure 2 : Intraoperative endonasal laser dacryocyst-orhinostomy. Figure 3 : Intraoperative transcanalicular laser dacryocystorhinostomy.

figure 1 figure 2 figure 3



to the lower part of the lacrimal sac. Moore et al37 usedHolmium:YAG (2100nm) laser with 0.6 J at 10 Hz(6 W) setting to ablate the nasal mucopeiosteum, increased the laser power to 1.0 J at 10 Hz(10 W) to ablate and vaporize the bone mainly lacrimal bone and create a rhinostomy measuring 6X6mm. If the lacrimal sac was not opened by the above, the laser setting was reduced again to ablate the medial wall of the lacrimal sac. Panwar et al used KTP laser at a setting of 5 watts for mucosa and 10 watts for bone.44

Laser transcanalicular/endocanalicular endona-sal DCR : 45 (Figure 3)

canaliculus so that it comes in contact with the medial wall of the lacrimal sac. At this point the aiming beam is switched on. The beam is visualized through the endoscope in the

beam is at its brightest and not scattered. Switching off the light source of the endoscope helps in better visualization of

is still in the sac and not touching the lacrimal bone. The light

the anterior attachment of the middle turbinate. The mucosa overlying the sac is vaporized. The bone over the lacrimal

repositioning the cannula. Diode laser (980nm) at a setting of 8 W in continuous mode is used for this purpose. Rosen et al 46used Nd:YAG laser(1064nm) with Helium-neon as aiming beam. The laser delivered 200 W of peak power at a pulse width of 20 to 40 msec with a repetition rate of 10 pulses per sec. The total energy used to create the ostium was 18 to 34 J. In recent years, microdrills, microronger, and radiosurgery have been used in conjunction with laser for widening the bony window.11,39 Higher success rates have been reported in groups where additional surgical instruments were used due to creation of larger ostium. Silbert has reported a 92% success rate with 9mm balloon assisted endoscopic DCR.47 Several authors have emphasized the use of saline, methycellulose, or a viscoelastic material such as sodium hyaluronate to dissipate heat and protect the canaliculi and common canaliculus during treatment.48,49

Ostium size and locationSome authors recommend creating a small ostium 10,25

involving primarily the inferior portion of the lacrimal bone while others 19,26 suggest that a larger ostium should be created by removing the frontal process of maxilla that comprises the anterior lacrimal crest. A 6-8mm ostium is mostly acceptable with laser DCR. Linberg et al 50 showed that a mean intranasal ostium size of 1.8 mm was enough to be successful in external DCR. The lower success rates with endoscopic laser DCR were probably due to inability to directly suture the nasal mucosa and the mucosa of the lacrimal sac.43 Available data do not support the clear superiority of a particular option in terms of ostium size and location.

Stent placement and removalIn a retrospective analysis of endoscopic surgical DCR,

Saeed reported that stents were not always necessary provided the obstruction was postsaccal and a good exposure with maximum sac exposure and marsupialisation was performed.51

Many surgeons elect to insert bicanalicular silicone stents at the time of surgery6,8,23,26 while others prefer not to use them because of concerns related to silicone

compromise long term ostium patency.52 The success rates without using the stents ranged from 81% 53to 90%.54

Analysis of Boush et al series showed that majority of the surgical failures occurred within 4 months after endoscopic surgery. 11 Zilelioglu et al 43 preferred to leave the siliastic tubes for 4-6months after endoscopic surgery. The stent interval proposed by different authors range from 4 weeks to 24 weeks. 55 The longer duration of tube retention is associated with higher chances of infection. The reported success rates with intubation range from 70 to 100%.

Mitomycin CThe decrease in size of the healed intranasal ostium after

surgery is the result of a normal wound healing reponse. Intraoperative application of mitomycin C favourably affects the wound healing process. It has been used in different concentrations and time by various authors such as 0.5mg/ml concentration for 2.5 minutes 43, 5 minutes and 10 minutes. Also 0.4 mg/ml has been used for 3minutes 24 and 5 minutes 22. Dolmetsch reported a success rate of 95 % with adjunctive use of MMC (0.5mg/ml for 10 minutes) in a follow up of 18.2 months in non laser endoscopic endonasal DCR. She also reported that intubation for more than 3 months was associated with higher rates of obstruction.56

Postoperative carePostoperative drug application includes antibiotic

or combination of antibiotic steroid drops, intranasal saline irrigation, intranasal steroid sprays and endonasal debridement of the DCR ostium.

Complications1. The most common complication of endonasal DCR is

failure11,24,40 of the procedure which usually occurs 1-3 months after surgery due to

8

the middle turbinate

the nasal septum



not drained by the surgical procedure.

2. Intraoperative and postoperative haemorrhage26 (non laser surgical manipulation)

3. False passage creation by light pipe

4. Punctal erosion related to silicone intubation 29

5. Silicone tubing prolapse

6. Canalicular obstruction

7. Thermal injury to the canaliculus 57

8. Orbital fat herniation30

9. Orbital and subcutaneous emphysema 30

58

11. Retrobulbar haemorrhage

12. Transient medial rectus paresis 32

ConclusionsAn ophthalmologist embarking on the journey of

nasal cavity and use of the endoscope. Both the advantages and limitations of the procedure relative to external DCR should be carefully discussed with the patient. The endoscopic DCR may be taken up on a primary basis or as a revisional surgery. In paediatric age group, one investigator had poor8 results whereas others have noted success.21 The technique of endoscopic DCR whether surgical or laser depends on the surgeons preference. The surgical outcomes of both endocanalicular and endonasal laser techniques are similar59. The success rates can be improved by careful selection of the patients with a detailed preoperative nasal examination, use of stents and Mitomycin C. Barring the expense incurred in the purchase and maintenance of equipment, endoscopic DCR, especially the laser assisted technique is a promising procedure for patients demanding a scarless surgery with quick recovery.

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Original Article

Edge Light Pupil Cycle Time as A Measure of Optic Nerve Function

J L Goyal MD , Sarmi Malik MD , Parul Jain MBBS , Ritu Arora MD

AbstractPurpose:Methods:

Results:

Conclusion:

Del J Ophthalmol 2011;22(2):99-101.Key Words :

The normal human pupil varies in size from 2.5 to 4mm in diameter. It is 7.5 – 8mm in full mydriasis and 1.5 to 2mm when fully miosed. The amount of light reaching the retina is regulated by the iris, which constantly adjusts the pupil size. The pupil remains in a constant state of unrest called hippus.

of the sympathetic and parasympathetic innervations of the iris muscles which are in an unsteady equilibrium. The time taken for one oscillation of constriction and dilatation is called pupil cycle time (PCT).

PCT is determined by measuring the duration of pupil oscillations while directing a thin beam of light at the pupil margin .As the retina receives rays of light from the edge of the pupil , the pupil constricts causing the edge light to go out of the papillary marginandthe stimulus for constriction is lost leading to the pupillary dilataion.. Following dilation of the pupil, the retina receives edge light rays again and the pupil constricts once more. Thus a repetitive constriction and dilatation of pupil is set up. PCT is determined by calculating the time taken for one such cycle of constriction and dilatation.

PCT was studied by Campbell and Whiteside1 in 1950 and was later shown to be useful in the diagnosis and investigation of optic nerve compression2, demyelinating disease3 and optic neuritis.2-4 While there is adequate literature regarding PCT in Caucasian eyes, no study has been done on Indian eyes. In this paper, we compare PCT between Indian eyes and the available literature.

MethodsThe sampling frame consisted of subjects suffering from

refractive error who were recruited from the outpatient department of a tertiary eye care centre (Guru Nanak eye centre, New Delhi). A detailed history and ocular examination was undertaken to exclude patients with any other detectable ocular disorders which may confound the results. Patients aged below 16 years and those who were

also excluded. The pupil cycle time was recorded using a slit lamp and stopwatch by the method described by Miller and Thompson5. In this method, a 1 mm wide horizontal beam of light of the lowest intensity is directed at the lower border of the pupil while the patient maintains a steady gaze at a distant object. The time taken for 100 pupil cycles (constriction and dilation) is measured (to the nearest 0.1 sec) using the hand held stopwatch. The PCT is calculated as number of cycles per second and reported as milliseconds per cycle.



Figure : 1(a) shows pupil with no light falling on it. Figure 1(b) shows light falling on the edge of the pupil. Figure 1(c) shows constriction of pupil in response to light. Figure 1(d) dilatation of pupil since the stimulus for constriction is gone.

Age Sex PCT(ms) Right Left

Differencebetween eye

18 F 1049 1043 76

18 F 951 978 2719 F 1003 1061 5820 F 1000 1062 6221 F 949 963 1423 F 1046 1055 925 F 1021 1078 5725 F 1092 1126 34

25 F 964 986 2229 F 1070 1054 1630 F 1076 1126 5043 F 1011 986 2945 F 955 1054 2345 F 1014 1126 048 F 1125 982 3551 F 1040 978 6555 F 1128 1111 1755 F 1078 1014 6455 F 1075 1134 5958 F 1041 1079 3860 F 1075 1041 3416 M 1030 1043 1317 M 1053 986 6718 M 1013 1038 25

51 M 1068 1046 22

Age Sex PCT(ms) Right Left

Differencebetween eye

19 M 1060 1079 19

20 M 1000 974 2621 M 1013 1064 5122 M 961 954 7

23 M 1112 1117 524 M 1075 1110 3525 M 1038 961 7725 M 982 1091 109

30 M 1092 1078 1431 M 1035 1076 4132 M 1004 961 1635 M 1050 1027 2335 M 1104 1046 5835 M 1137 109 4440 M 1081 1112 3141 M 1016 1026 1042 M 1030 1126 9642 M 1080 1086 642 M 1075 993 8244 M 1076 1095 1945 M 878 954 7645 M 1086 1075 1145 M 1049 964 8545 M 993 1011 1850 M 1111 1129 18

34.56 Years 1041 1047 37Average

A B C D



ResultsHundred eyes of 50 patients (29 males, 21 females)aged

between 16 to 60 years(mean 34.6 years) were studied. The PCT ranged from 878ms to 1160ms with a mean value of 1044±56.16 ms. The mean difference in the PCT between the two eyes was 37±52.66ms. The mean PCT in males was 1045.12 ± ms 54.70 while in females it was 1042.45 ± 56.42 ms. Table 1 depicts the pupil cycle time for each eye of the subjects with regard to the age.

DiscussionThe pupil cycle of a particular individual depends on

certain inherent factors. These include the latent period and duration of contraction of iris and the latent period and duration of dilataion of iris.1 These in turn depend upon speed, frequency and intensity of afferent nerve impulses, synaptic delays, delays in efferent nerve impulses and on the integrity of the iris motor apparatus (sphincter and dilator pupillae). These factors in turn depend on synaptic delays, delays in efferent nerve impulses and structural integrity of iris itself.

Our mean value of PCT (1044ms) was higher as compared to previously reported values of 870 ± 148 ms (Campbell and Whiteside)1, 980 ± 97 ms (Wybar)3 and 822 ± 69 ms (Miller and Thompson)5. The reason for the higher values is not clear. We hypothesize that it may have relation to the fact that the Indian eyes are more pigmented as compared to the Caucasian counterparts and also possibly the contractility of iris sphincters may be less. The latter can only be proved or disproved by in vitro testing but by virtue of Indian iris’ being thick and pigment laden, there may be logic in this possibility. Measurement of PCT has

neuritis, demyelinating disease,optic nerve compression ,familial dysautonomia and barbiturate and benzodiazepine intake.2-4,6,7 Although PCT is less sensitive than visual evoked potential, it has been shown to detect and quantitate subclinical defects in optic nerve conduction time.2,4,8,9

Measurement of the PCT is an easy and rapid procedure with the advantages of not requiring any

eye separately. Despite this certain drawbacks exist such as requirement of high patient cooperation, presence of an intact afferent and efferent pathway and unreliability in severe optic nerve diseases. Pupil cycle time is often compared to visual evoked potential and rightly so as both measure the function of the visual pathway. While PCT

the delay in the appearance time of the impulse at the occipital cortex. Although PCT is less sensitive than VEP, it can objectively aid diagnosis of optic nerve conditions

5 Campbell and Whiteside1 found a tendency for PCT to become prolonged as the retina remained adapted to light. They also reported an increase in PCT with a 94% decrease in stimulus intensity. Miller and Thompson5 found that PCT was not affected by variables such as sex, iris color, visual acuity, refractive error and side of eye, pupil size and amplitude of oscillations.So far, there was no normative data in Indian eyes to quatify any PCT delays, this test was deemed to have little objective

keeping in view, the ease and rapidity of this measurement without the requirement for sophisticated instruments, we recommend that this test be a prelimanry screening and

References

1. Campbell FW, Whiteside TCD. Induced papillary oscillations. Br J Ophthalmol.1950;34:180-89.

2. Weinstein JM, Gilder JCV, Thompson HS. Pupil cycle time in optic nerve compressions. Am J Ophthalmol.1980;89:263-67.

3. Wybar KC. Ocular manifestations of disseminated sclerosis. Proceedings of royal society on medicine 1952;45:315-20.

4. Miller SD, Thompson HS. Pupil cycle time in optic neuritis. Am J Ophthalmol.1978;85:635-42.

5. Miller SD, Thompson HS. Edge light pupil cycle time. Br J Ophthalmol.1978;62:495-500.

6. Gadoth N, Schalen N, Maschkowski D, Bechar M. The pupil cycle time in familial dysautonomia. Metab Pediatr System Ophthalmol.1983;7:131-34.

of central depressant drugs on pupil function:an evaluation with the pupils cycle induction test.Ophthalmologica.1981;183:214-19.

8. Hamilton W, Drewry RD. Edge light pupil cycle time and optic nerve disease. Ann Ophthalmol.1983;15:714-21.

9. Mc Kissock W, Taylor JC, Bloom WH, Till K. Extradural haematoma. Lancet 1960;2:167-72.



Original Article

Effect Of Intracameral Heparin In Post Operative Inflammatory Reaction And Posterior

Capsular Opacification After Cataract Surgery In High Risk Cases

Eva R Tirkey MS , Shivcharan L. Chandravanshi MS , Mahesh K. Rathore MS , Kriti Sharma MS

AbstractPurpose:

Design:Methods:

Results:

Conclusion:


Cataract surgery has a higher incidence and more

groups such as congenital, traumatic, complicated cataract, diabetic patients and lens induced glaucoma. They have a

when compared to normal eyes, leading to augmented protein leakage and cellular reactions in aqueous humor.1 This reaction

adjacent structures such as the iris, remnants of retained cortical material and immunological reactions to the implanted foreign body; that is, the intraocular lens.2,3

precipitates over the IOL surface, formation of synechiae and

capsular opacity (PCO).

antiproliferative and anticoagulant properties.4,5 Heparin in irrigating solution during cataract surgery results in less disturbance of blood aqueous barrier (BAB) and helps in

6-9 The use of

popularity because of their higher cost.8 This prospective study was conducted to evaluate the effect of intracameral heparin



Age in years Congenital cataract

Traumatic cataract

Complicated cataract Diabetic patients Lens induced

glaucomaTotal no of

patients

70-79 - - - 6 4 10

60-69 - 3 - 8 2 13

50-59 - 2 - 4 6 12

40-49 - 3 1 3 - 7

30-39 - 11 4 - - 15

20-29 - 4 - - - 4

10-19 4 8 - - - 12

5-9 3 - - - - 3

1-4 4 - - - - 4

Total 11 31 5 21 12 80

TABLE 1. Distribution of Type of Cataract in Study (Group-A) and Control Group (Group-B)

Materials & MethodsWe conducted a prospective and randomized study in 80

eyes of high risk cases, ranging in age from 2 years to 80 years, who underwent manual small incision cataract extraction with posterior chamber intraocular lens implantation at tertiary eye care centre, India from April 2007 to March 2008. Informed consent comprising a frank discussion between surgeon and the patients or their family on the possible merits and demerits of the procedure was obtained from all patients. Demographic and surgical data were recorded. All patients had complete preoperative medical check up including documenting evidence of prior bleeding tendencies and were routinely instructed to avoid preoperative and postoperative use of anticoagulant drugs. Patients were randomly assigned to one of two groups; during surgery 40 mg of low molecular weight heparin sodium was added to the 500 ml irrigating solution of

salt solution as the intraocular irrigating infusion in 40 eyes.

Preoperative systemic steroid were used when ever necessary in both the groups. Ocular aseptic preparation was done including using aqueous povidone-iodine 5% on the lids and conjunctival sac and using plastic drapes. The edges of the plastic drape were isolating lashes and lid margins from the eye. One experienced surgeon (ERT) performed all the cases and using same techniques. In too young patients, surgery was done under general anesthesia, while adult patients were operated under peribulbar anesthesia. After making a 6 to 6.5 mm scleral tunnel incision which was 1.5 to 2 mm away from the limbus, side port was made at 9 o’ clock position just 1 mm inside the limbus. The anterior chamber was entered with the help of 3.2 mm keratome and a 5 to 5.5 mm capsulorhexis or if the capsulorrhexis was unsuccessful, a can opener capsulotomy was created. Hydrodissection was performed with hydrodissection cannula. Cataractous lens was prolapsed

Figure 1 : Slit lamp photograph of a uveitis patient in Group A. (a) Pre-operative. (b) Day 1 post-operative photograph showing quite anterior chamber with primary PCO.

Figure 2 : (a)Preoperative slit lamp photograph of a traumatic cataract showing ruptured anterior lens capsule and synechiae. (b) Same patient on 1st postoperative day, slit lamp photograph showing anterior chamber reaction, air in anterior chamber and fibrinoidal response, in which heparin was not used.

(a) (b) (a) (b)



Type of Cataract Group A (with Heparin)(40 eyes)

Group B (without Heparin)(40 eyes)

Congenital Cataract 6 5

Traumatic Cataract 15 16

Complicated Cataract 2 3

Diabetic Patients 10 11

Lens Induced Glaucoma 7 5

Total 40 40

TABLE 2. Distribution of Type of Cataract in Study and Control Group

into anterior chamber and removed by sandwich technique. The cortical clean-up was done by bimanual irrigation aspiration cannula. All eyes having intraocular lens (IOL) implantation

Viscoelastic was used and washed out at completion of surgery. Stromal hydration was performed to prevent leaking from side-port. At the completion of surgery, the eye was patched after subconjunctival injection of steroid and antibiotic. Next day the patch was removed and the patients received corticosteroid eye drops (Prednisolone acetate 1%) and antibiotic eye drops

had a complete eye examination including slit lamp, retinal examinations and measurement of the intraocular pressure preoperatively and at 1st, 7th, 28th day, 8th week, 3rd month and

assessed at all visits with slit lamp biomicroscopy and the

to the number of cells present in the anterior chamber and

examination. Early and late postoperative intraocular reaction

10

The results were reported as the average grading.

ResultsTwo groups were comparable with age distribution and

types of high risk group cataract (Table-1). The median age of the patients was 40 years. 80 eyes of 76 patients were included in this study. 40 eyes had intraocular infusion of enoxaparin (group-A) and 40 eyes were operated without intraocular enoxaparin (group-B). Both of the groups were high risk cases like congenital, traumatic, complicated cataract, lens induced glaucoma and diabetic patients (Table-2 ). Follow up of patients was 100% at 1st postoperative day and 75% at 1 year. On days 1

found, while in control group (group B) there is statistically

were raised on 1st and 7th postoperative days in control group (P<0.003). None of the eyes of group A was having +4 cells and

groups peaked at 1st postoperative day with a subsequent decrease thereafter. Similar reestablishment of the blood-aqueous-barrier (BAB) between groups was found (Table-3)

7 (17.5%) eyes on 1st postoperative day while 19 (19.75%) eyes

related complications such as precipitates over IOL surface, posterior synechiae and optic capture. Seven (17.5%) of 40 eyes that underwent surgery without heparin had precipitates over IOL surface, pupillary membrane, posterior synechiae and optic capture related to postoperative complication. None of the patients of either group developed cyclitic membrane. We did not observe intraoperative or postoperative complications attributed to heparin supplementation. All corneas in study

Figure 3 :Late post-operative photos of group A patients showing complication. (A) Optic Capture, iris pigment dispersion over anterior lens surface and early PCO formation. (B) Posterior capsular opacity with iris pigment dispersion over anterior lens surface.

(a) (b)



CELLS D-1 D-7 D-28 8th Week 3rd month 1 year

± 22 20 17 21 20 15

+ 1 14 12 8 0 0 0

+ 2 4 4 0 0 0 0

+ 3 0 0 0 0 0 0

+ 4 0 0 0 0 0 0

N 40 36 25 21 20 15

FLARE D-1 D-7 D-28 8th Week 3rd month 1 year

0 24 18 18 21 18 15

+ 1 13 13 7 0 0 0

+ 2 3 5 0 0 0 0

+ 3 0 0 0 0 0 0

+ 4 0 0 0 0 0 0

N 40 36 25 21 18 15

CELLS D-1 D-7 D-28 8th Week 3rd month 1 year

± 0 0 2 8 4 2

+ 1 2 4 10 8 8 6

+ 2 12 10 11 4 2 1

+ 3 24 19 5 0 0 0

+ 4 2 1 0 0 0 0

N 40 34 28 20 16 12

FLARE D-1 D-7 D-28 8th Week 3rd month 1 year

0 0 0 3 9 5 2

+ 1 3 6 9 8 7 5

+ 2 12 11 13 3 2 1

+ 3 23 16 3 0 0 0

+ 4 2 1 0 0 0 0

N 40 34 28 20 16 12

TABLE 3. Grading of anterior chamber reaction after cataract surgery

Group Examination

Group A (With Heparin)

Group B (With out Heparin)



and control group remained clear for the entire follow up period. We also did not observe adverse effects that may be attributed to heparin such as hyphema (Table 4).The posterior capsule was examined with direct ophthalmoscope and graded

slit lamp grading of PCO. Only grade 4 PCO was taken for consideration because it only involves visual axis and termed

in group A were having grade 0 PCO and no one was having grade 4 while in group B 12 (30%) patients were having grade 4 PCO. Similarly at 1 year not even a single patient was having grade 4 PCO in group A while in group B, 15 (30%) patients were having the same (Table 5).

Discussion The major challenge in case of high risk cataract surgery

formation that is responsible for postoperative complications

new therapeutic approaches are being invented to prevent postoperative complications of high risk cases. Two factors

trauma and foreign body reaction to the intraocular lens.2,3,11

Surgical trauma causes breakdown of blood aqueous barrier

leading to augmented protein leakage and cellular reaction in the aqueous humor.1 We minimized surgical trauma by avoiding excessive handling of the iris. Early use of systemic and frequent instillation of topical corticosteroid also decreased

groups in a similar manner. One senior experience surgeon (ERT) performed all the surgeries using the same surgical technique and same type of PMMA intraocular lens. Thus the effect of two factors that could have resulted in trauma and

12,13 Iverson et al demonstrated that an infusion of low molecular weight heparin

and retinotomy in rabbits.14 Heparin has been shown to induce apoptosis in human peripheral neutrophils which may help

15 Heparin also inhibits reactive oxygen species generation by mononuclear and polymorphonuclear leucocytes.16 In addition, heparin

inhibit activation of the complement system.17,18 Enoxaparin was added to the infusion solution which has a potential

after cataract surgery in the eyes prone to postoperative

enoxaparin was infused into the anterior chamber during

agree with those of Khonen et al, who observed reduced 7 Heparin inhibits

leucocyte migration and pigment deposition.18

cells originate from the uveal tissue, enter the anterior chamber and are frequently found over IOL surface. We found that at 1st postoperative day group-A had no IOL precipitates over the anterior surface (p < .001) (Table-3). This may also explain decrease in late postoperative complications such as

and optic capture. Indeed in our study, these complications were absent in group-A treated with intraoperative heparin infusion while common in group-B without heparin infusion. We also did not observe the side effects that may attribute to enoxaparin such as development of postoperative corneal opacity or hyphema.2 The anticoagulant effect of enoxaparin has long been known. Enoxaparin is composed of heparin

TABLE 4. Early and Late Postoperative Complications

Some patients had more than one complication.

Grade 0 36 6 28 2 20 1

Grade 1 4 8 5 5 6 1

Grade 2 - 6 3 5 4 3

Grade 3 - 8 - 9 - 10

Grade 4 - 12 - 15 - 15

Total 40 40 36 36 30 30

TABLE 5. Grades of PCO in study group and control group at 1 month, 6 month and 1 year

Grade of PCO 1 month 6 month 1 year

Group – A Group – B Group - A Group - B Group - A Group – B

ComplicationsGroup A

(With Heparin)(40 eyes)

Group B (With-out Heparin)

(40 eyes)

EarlyFibrin in anterior chamber

Mild 4 8 Moderate 1 7

Severe 2 4Intraocular lens precipitates 0 2

LatePupillary Membrane 0 4Posterior Synechiae 0 3

Optic capture 0 3



fragments in different lengths.19,20 Heparin acts indirectly at multiple sites in both the intrinsic and extrinsic blood clotting systems. Heparin binds to antithrombin III to form heparin-AT complex. This inactivates a number of coagulation enzymes including thrombin factor IIa and IXa, Xa.21 Of this thrombin IIa and factor Xa are most responsible for the result. As such

response by coagulation pathway and inhibit formation of a

heparin is known to have antiproliferative effects. It stabilizes the dividing lens epithelial cells at equators and prevents them to move onto the posterior capsule. None of our patients had grade 3 and 4 PCO in heparin infusion group. Our study agree with Knorr et al who demonstrated anti-proliferative effect in cultured bovine lens epithelial cells.5 Zaturinsky et al described reduced secondary cataract formation following extracapsular cataract extraction (ECCE) with heparin infusion solution.6

Our study showed that the addition of 40 mg enoxaparin in 500 ml infusion solution during manual small incision cataract

in high risk groups is associated with intense postoperative

complications.22

compromise with visual acuity even after successful cataract surgery. In recent studies, it has been found that because of its

PCO. Although the safety of cataract surgery has dramatically improved in past years, high risk cases are predisposed to

heparin sodium to the irrigating solution might help in

surgery. In addition it is safe, economical, non-toxic, easily available and easy to use.

References

1. Miyake K. Fluorophotometric evaluation of the blood- ocular barrier function following cataract surgery and intraocular lens implantation. J Cataract Refract surg 1988;14(5):560-8.

2. Obstbaum SA. Biologic relationship between poly(methyl methacrylate) intraocular lenses and uveal tissue. JCataract Refract Surg 1992;18(3):219-31.

3. Kruger A, Schauersberger J, Findl O, Petternel V, Svolba

corneal and sclerocorneal incisions. J Cataract Refract Surg1998;24(4):524-8.

4. Matzner Y, Marx G, Drexler R, Eldor A. The inhibitory effect of heparin and related glycosaminoglycans on neutrophil chemotaxis. Thromb Haemost 1984;52(2):134-7.

5. Knorr M, Wunderlich K, Steuhl KP, Thiel HJ, Dartsch PC. [Effect of heparin on proliferation of cultivated bovine lens epithelial cells]. Ophthalmologe 1992;89(4):319-24.

6. Zaturinsky B, Naveh N, Saks D, Solomon AS. Prevention

of heparinized irrigating solution during extracapsular lens extraction in rabbits. Ophthalmic Surg 1990;21(6):431-4.

7. Kohnen T, Dick B, Hessemer V, Koch DD, Jacobi KW.

following small incision cataract surgery. J Cataract Refract Surg 1998;24(2):237-43.

8. Dada T, Dada VK, Sharma N, Vajpayee RB. Primary posterior capsulorhexis with optic capture and intracameral heparin in paediatric cataract surgery. ClinExperiment Ophthalmol 2000;28(5):361-3.

9. Kruger A, Amon M, Abela-Formanek C, Schild G, Kolodjaschna J, Schauersberger J. Effect of heparin in the

cellular reaction on the intraocular lens surface. J Cataract Refract Surg 2002;28(1):87-92.

10. Sellman TR, Lindstrom RL. Effect of a plano-convex

from Elschnig pearl formation. J Cataract Refract Surg1988;14(1):68-72.

11. Sinskey RM, Amin PA, Lingua R. Cataract extraction and intraocular lens implantation in an infant with a monocular congenital cataract. J Cataract Refract Surg1994;20(6):647-51.

12. Johnson RN, Balyeat E, Stern WH. Heparin prophylaxis Ophthalmology 1987;94(6):597-601.

13. Johnson RN, Blankenship G. A prospective, randomized, clinical trial of heparin therapy for postoperative

Ophthalmology 1988;95(3):312-7.14. Iverson DA, Katsura H, Hartzer MK, Blumenkranz

infusion of low-molecular-weight heparin during vitrectomy. Arch Ophthalmol 1991;109(3):405-9.

15. Manaster J, Chezar J, Shurtz-Swirski R, Shapiro G, Tendler Y, Kristal B, et al. Heparin induces apoptosis in human peripheral blood neutrophils. Br J Haematol 1996;94(1):48-52.

16. Dandona P, Qutob T, Hamouda W, Bakri F, Aljada A, Kumbkarni Y. Heparin inhibits reactive oxygen species generation by polymorphonuclear and mononuclear leucocytes. Thromb Res 1999;96(6):437-43.

17. Schwartz CF, Kilgore KS, Homeister JW, Levy BA, Lucchesi BR, Bolling SF. Increased rat cardiac allograft survival by the glycosaminoglycan pentosan polysulfate.J Surg Res 1999;86(1):24-8.

18. Ekre HP, Naparstek Y, Lider O, Hyden P, Hagermark

and its derivatives: inhibition of complement and of lymphocyte migration. Adv Exp Med Biol 1992;313:329-40.

19. Hirsh J, Levine MN. Low molecular weight heparin. Blood1992;79(1):1-17.

20. Hammer RH. Anticoagulants, coagulants and plasma extenders. In: Foye WO, Lemke TL, Williams DA, editors. Principles of medicinal chemistry, 4th edition. Baltimore: Williams and Wilkins, 1995:393.

21. Fareed J. Heparin, its fractions, fragments and derivatives.Some newer perspectives. Semin Thromb Hemost1985;11(1):1-9.

In: Naumann GOH, Apple DJ, eds, Pathology of the eye. Berlin, Springer-Verlag, 1986;99-184.



Techniques

Endoillumination Assisted Scleral Buckling:The future Approach to Retinal Detachment Surgery

Pradeep Venkatesh MD , Tarun Arora MBBS , Satpal Garg MD

Abstract


Rhegmatogenous retinal detachment is presently managed by conventional scleral buckling, pneumatic retinopexy or vitreoretinal surgery.1-3 Vitreoretinal surgery was initially advocated for patients with complex retinal detachments such as giant retinal tear or higher grades of proliferative vitreoretinopathy (PVR). With increasing experience with vitreous surgery and advances in surgical instrumentation, vitreoretinal surgery is now being more frequently used in the primary management of even simple retinal detachments. This is despite the known sequelae of primary vitreoretinal surgery. One of the reasons for this shift is that scleral buckling surgery, as advocated today, is a procedure that depends on indirect ophthalmoscopy and hence cannot be carried out completely under the surgical microscope. Here in we describe a new approach that enables all steps of conventional buckling surgery to be performed under the surgical microscope.

Surgical Technique In this new technique localization of the break is

achieved using

1. Self retaining endoilluminators

2. Wide angle viewing lenses

Figure 1 : Placement of 23 G Awh Self retaining endoilluminator



Technological advances have enabled commercial availability of small gauge (23G/ 25G/ 27G) powerful light sources for endoillumination.4 These endoilluminators are self retaining and can be placed at a desired location through the pars plana (Figure 1).

Steps involved are1) Preoperatively the pupil is dilated with tropicamide 1%

eye drops.

2) The surgery is performed under peribulbar block using a 10ml syringe containing 5 ml bupivacaine 0.75% plain plus 5ml lignocaine 2% with hyaluronidase 75 units added to it.

3) A 5 to 10% povidone-iodine solution (Betadine) is instilled for 5 min before the start of the surgery to minimize risk of post-operative infection.

4) Peritomy is done 360 degrees at the limbus with two relaxing incisions 180 degrees apart.

5) Additional blunt dissection between tenon`s capsule and the sclera is performed posteriorly to bridle and hook the rectus muscles.

6) Encircling band is passed underneath the recti muscles with a temporary knot tied.

7) 23 G PPV port made at 4mm (in phakic patients) from the limbus using trocar cannula.

8) Volk's Reinverting Operating Lens System (ROLS) wide angle viewing system is used to examine the fundus (Figure 2).

9) Scleral indentation to visualize the breaks is done under

10) Retinal cryopexy is done under direct visualization (Figure 3).

11) Buckle is placed and sutured at the localized break.

12) ROLS viewing system is used for draining subretinal

buckle.

13) Endoilluminator and cannula removed (Figure 4).

14) Conjunctival peritomy closed with 8’0 vicryl.

15) Subconjunctival gentamicin (20mg) and dexamethasone (2 mg) injected.

DiscussionThis new approach combines the advantages of

visualization provided by vitreoretinal instruments (endoillumination and wide angle viewing) and safety and simplicity of conventional scleral buckling surgery. This is likely to improve surgical results even in eyes with rigid

Figure 2 : ROLS wide angle viewing system in place (as in VR surgery)

Figure 3 : Internal localization and cryotherapy of retinal break

Figure 4 : Site of entry for placement of endoilluminator seen after its removal (after completion of cryotherapy)



Once there is endoillumination, wide angle viewing lenses enable visualization of the retina right up to the ora serrata.5,6 Scleral indentation can be performed by the surgeon sitting at the microscope without having to wear an indirect ophthalmoscope and move around the operating table. Visualization is excellent even in the presence of

cataract. With this approach it is not only possible to locate the number and location of breaks more accurately while seated at the microscope, but also undertake cryopexy of

height of detachment is maximum and also titrate the buckle height to achieve an ideal buckle-break relationship. The self retaining endoilluminator can be removed at the end of the procedure after looking for induced retinal arterial pulsation. The site at which the endoilluminator was placed may need to be closed with a single stitch in some patients.

Success of conventional scleral buckling surgery is dependent on accurate localization of retinal break(s) and its subsequent closure using silicone buckle sutured to the scleral surface.7 Accurate localization of retinal breaks during this surgery is dependent on skill of the surgeon with indirect ophthalmoscopy. Indirect ophthalmoscopic localization of the retinal break(s) during buckling surgery is however considered tedious. This is because surgeons have to move around the operation table with the indirect ophthalmoscope mounted on the head. Moving from the operating microscope time and again tends to make the surgery more cumbersome. To do away with the need for indirect ophthalmoscopy surgeons are now more inclined towards primary vitreoretinal surgery even in simple retinal detachment. Other factors towards this trend include lesser emphasis on teaching the ‘art of buckling’; medical insurance issues and market forces.8

Localization of retinal break(s) is also dependent on adequacy of visualization through the pupillary aperture of the patient. Factors that limit visualization are non-

vitreous hemorrhage and opacities in the crystalline lens.

presence of a bullous retinal detachment. In such situations, the current approach to mange the retinal detachment is vitreoretinal surgery.

Vitreoretinal surgery has the advantage that it decreases the risk of missing any retinal breaks. This is because of the endoillumination and wide angle viewing systems used during the surgery. However, standard three post vitreous surgery also carries with it disadvantages like progression of cataract, creation of iatrogenic tears, placement of long acting vitreous substitutes like intraocular gas or silicone oil, silicone oil glaucoma, and silicone oil keratopathy.9 Even in the case of a successful surgery, the visual rehabilitation time following VR surgery is more prolonged than following scleral buckling surgery. To overcome the above

patients with simple retinal detachments, we hypothesize

the possibility of achieving good results with an alternate surgical approach to carry out conventional buckling surgery. The new technique hence allows every step of conventional buckling surgery to be performed entirely under the microscope. It removes the disadvantages of the current approach that of using an indirect ophthalmoscope to view the retina, localize and cryo the break and for

microscopic retinal detachment surgery is likely to gain wider acceptance and may become the future approach to undertaking conventional scleral buckling surgery.

References

1. Lincoff H, Kreissig I. The treatment of retinal detachment

of the Custodis procedure, Part VI). Trans Am Acad Ophthalmol Otolaryngol 1972; 76: 1221-32.

2. Hilton GF, Grizzard WS. Pneumatic retinopexy. A two step outpatient operation without conjunctival incision. Ophthalmology 1986; 93: 626-41.

3. Machmer R, Beuttner H, Norton EWD et al. Vitrectomy: A pars plana approach. Trans Am Acad Ophthalmol Otolaryngol 1971; 75: 813-20

4. Chow DR. Shedding some light on current endoillumination. Retinal physician. 2005; 2: 37-39.

5. Bovey EH, Gonvers M. A new device for noncontact wide angle viewing of the fundus during vitrectomy. Arch Ophthalmol 1995; 113: 1572-73.

6. Nakata K, Ohji M, Ikuno Y et al. Wide angle viewing lens for vitrectomy. Am J Ophthalmol 2004; 137: 760-62.

7. Lincoff H, Gieser R. Finding the retinal hole. ArchOphthalmol 1971; 85: 565-69.

8. Lincoff H, Kressig I. Changing patterns in the surgery for retinal detachment: 1929 to 2000. Lin Monatsbl Augenheilkd 2000; 216: 352-59.

9. Heimann H, Schmidt KUB, Bornfeld N et al. Scleral buckling versus primary vitrectomy in rhegmatogenous retinal detachment. A prospective randomized multicenter clinical study. Ophthalmology 2007; 114: 2142-54.



Case Report

Orbital Soft Tissue Mass as a Masquerading Presentation Preceding Acute Myeloblastic

Leukemia and Chloroma in a Child with Down Syndrome

Pasumala Lakshminarayana1 MD , Basudev Ghosh2 MD, MNAMS , Meenakshi Thakkar2 MD, FRCS ,Shyama Jain3 MS , Seema Kapoor4 MD , Amit Bhatia5 MS

Abstract

Del J Ophthalmol 2011;22(2):119-121.Key Words:Ectopic

Pre leukemic syndrome is seen in 25% of patients with acute myeloblastic leukemia (AML).1 It presents as anemia and other cytopenias months to years preceding the development of overt leukemia. In Down syndrome AML is 400 times more common and has long pre leukemic phase. Chloromas (granulocytic sarcomas) are sites of extra medullary granulopoesis which can presents at multiple sites like orbits, sinuses, skull, spine,

years.3,4 Orbital chloromas present as proptosis, orbital tumour, dacrocystitis or orbital cellulitis, with leukemic or atypical cells seen on histopathology.5 The present work reports an unusual case of a two and half years old girl with Down syndrome with simultaneous presentation of cheek chloroma and Acute Myeloblastic Leukemia 3 months after a suspicious episode of orbital soft tissue mass in the pre leukemic phase of AML.

Case ReportA two and half years old karyotypically proven case of Down

syndrome (Fig1a) presented to us with acute onset soft tissue mass of both eyes (OD>OS) and restricted ocular movements in elevation and abduction in right eye (Fig 1b). She had received two blood transfusions in past two months for anemia. On examination the child was comfortable, afebrile and non toxic. In both the eyes cornea, pupils and fundus were within normal limits. Orodental and examination of the paranasal sinuses ware non contributory. General physical examination and systemic examination did not reveal any abnormality. Hemogram showed low hemoglobin (10 gm%), low total leukocyte count (3600/

Fig 1c. The patient responded partially to systemic intravenous antibiotics (Fig 1d) and CT scan showed a persisting orbital soft tissue density (Fig 1e). Fine needle aspiration cytology (FNAC) from the orbital mass showed no atypical cells. Two weeks later, the patient developed hepatosplenomegaly and repeat haemogram showed pancytopenia (Hb:5 gm%, TLC: 3000/mm3, platelets: 20,000/mm3). Bone marrow biopsy revealed a picture of megaloblastic aneamia which partially responded to Vitamin B 12 injections and packed blood cell transfusions. The child was discharged after the improvement. Three months later child



Figure 1 (a) Karyotypying of the patient showing trisomy 21 ; (b) A two and a half year old female at presentation showed soft tissue mass of both eyes (OD>OS) and restricted ocular movements in elevation and abduction in right eye ; (c) CT scan showing homogenously enhancing soft tissue density in the preseptal region (right more than left) extending into the extraconal space in the right eye ; (d) Persisting soft tissue swelling in both eyes after intravenous antibiotic therapy ; (e) CT scan showing persisting soft tissue density (right more than left) ; (f) The patient presenting three months later with a rapidly growing firm, non-mobile and nontender mass over the right cheek with increased soft tissue swelling of both eyes.

1(a) 1(b) 1(c)

1(d) 1(e) 1(f)

Figure 2 (a) FNAC from the cheek mass low power showing immature atypical granulocytic cells (blasts) ; (b) ) FNAC from the cheek mass high power showing immature atypical granulocytic cells (blasts) with moderate cytoplasm, cytoplasmic granules, 2-3 prominent nucleoli, nuclear lobulation and positive for myeloperoxidase ; (c) Peripheral blood smear low power: showing blasts cells ; (d) Peripheral blood smear high power showing a typical “smudge cell” ; (e) The patient showing complete disappearance of cheek and orbital mass two weeks after chemotherapy ; (f) CT scan showing disappearance of orbital soft tissue density two weeks after chemotherapy both eyes.

2(a) 2(b) 2(c)

2(d) 2(e) 2(f)



non-tender mass over the right cheek with increased soft tissue swelling in both eyes (Fig 1f). FNAC obtained from the cheek mass was diagnostic of chloroma (Fig 2 a & b). Peripheral smear showed 12% blast cells (Fig 2 c & d) and bone marrow aspirate showed 32% blast cells diagnostic of AML. The child was started on induction chemotherapy with Cytosine arabinoside, Daunorubicin and Etoposide. Two weeks later the cheek (Fig 2e) and orbital mass (Fig 2f) disappeared completely and blood picture improved.

DiscussionThere is astonishingly high incidence of AML in Down

syndrome, which is nearly 400 times greater than in normal children6 and is said to be unique clinically in terms of a long pre leukemic phase, increased incidence of trisomy 8 and a high cure rate7. Chloromas derive there name from the greenish hue of the granulocytic cells on myeloperoxidase staining. Chloromas develop preferentially in bones or periosteum and from there they spread via haversian canals to penetrate periosteum and form a soft tissue mass. They tend to mold to contiguous structures demonstrating little bony destruction8. Chloromas

5 to 16 months) and at the time of presentation it may have no constitutional signs or symptoms3. The shortest interval between the development of chloroma and AML has been reported to be 3 months4, but in our case cheek chloroma and AML

appeared simultaneously. The orbital soft tissue mass which appeared 3 months before cheek chloroma and AML could be orbital chloroma because it increased with appearance of cheek chloroma and AML and it responded to chemotherapy, but initial FNAC from orbital mass did not show any atypical cells.

Chloroma of the orbit can present in various forms. In a retrospective analysis of 33 patients, the ophthalmic manifestations of chloroma were reviewed5 and in two patients

until peripheral smear became positive and in one child, the

diagnosed as chloroma on repeat biopsy. In case of our child who was a known case of Down syndrome the presentation of features of acute orbital soft tissue mass without fever and systemic toxicity but with evidence of pancytopenia later prompted us to think in terms of pre leukemic phase of AML and a close follow up yielded the results. It was further substantiated by the development of a full blown systemic AML and chloroma on the cheek 3 months after the initial presentation of orbital soft tissue mass. Chloroma and AML responded well to Chemo

necessitates close follow up for later development of systemic AML but it also needs to be emphasized that close follow up of children with Down syndrome with suspicious presentations of orbital soft tissue masses helps in early diagnosis of AML which has a good prognosis in these children if treated early.

References

1. Bagby GC. The pre leukemic syndrome (hematopoietic dysplasia). Blood Rev 1988;2(3):194-205.

2. Bulas RB, Laine FJ, Das Narla L. Bilateral Orbital granulocytic sarcoma (chloroma) preceding the blast

Peadiatr Radiology1995;25:488-89.3. Rebecca Stein-Wexler, Sandra L.Woolton-Gorges,

Daniel C West. Orbital granulocytic sarcoma: an unusual presentation of AML. Paediatric Radiology2003;33:136-39.

4. Atul Kapur, Sanjay Khetarpal. Multifocal chloromas preceding AML. Indian Peadiatrics 1995;32(March):370-73.

5. Lorenz E, Zimmerman, Ramon L. Font. Ophthalmic manifestations of granulocytic sarcoma (myeloid sarcoma or chloroma) Am J Ophthalmol 1975;80(6):975-90.

6. Lange BJ, Kobrinsky N, Barnard DR, et al. Distinctive demography, biology, and outcome of AML and myelodysplastic syndrome in children with down syndrome. Blood 1998;91:608-15.

7. Zipursky A, Thorner P, De Harven E, Christensen H, Doyle J. Myelodysplasia and AML in Down syndrome. Leuk Res 1994;18:163-71.

8. Jacobiec FA. Granulocytic Sarcoma. Am J Neuroradiol1991;12:263-64.



Case Report

A Typical Lens Coloboma – A Rare Cause of Childhood Blindness

Punita Garg MS , Parul Aggarwal MS , H.K Sidhu MS,

Abstract


A lens coloboma is characterized by its notching at

the zonules at that site.1 Colobomas of the lens are divided into typical colobomas (those that occur at the site of the

2 Superior lens coloboma is rare. We present a case identifying a superior lens coloboma with iris coloboma causing amblyopia.

Case A 16 years old female reported to OPD with

diminished vision in right eye. On ocular examination, BCVA was Finger Counting at 3m. On retinoscopy, eye was hypermetropic with refractive error of 3.25DS/2.50DC at axis of 100.There was coloboma of iris in superotemporal quadrant. Post dilated Slit lamp biomicroscopy revealed notching at equator of the lens in superotemporal quadrant. Persistant pupillary membrane was present partially. On Gonioscopy angle was open. Fundus was normal.K1 was 37.25 and K2 was 41.75.Axial length was 21.74.

Discussion Congenital anomalies, though rare, are important

cause of childhood blindness. Congenital anomalies of lens

include ectopia lentis, microphakia, microspherophakia, lentiglobus, lens coloboma. Coloboma of lens is a condition with autosomal dominant inheritance and occurs at about 4 month of gestation.1,2 It represents an incomplete

completely. It can occur in isolation or with other ocular

indentation of the lens. It is usually unilateral but may be bilateral. Size of coloboma may vary. It is usually inferior-nasal but may occur anywhere along the circumference of the lens.2 Colobomas of the lens are divided into typical colobomas (those that occur at the site of the embryonic

Figure 1 : Iris Coloboma



A lens coloboma is characterized by its notching at

the zonules at that site.1 Colobomas of the lens are divided into typical colobomas (those that occur at the site of the

2 Superior lens coloboma is rare. We present a case identifying a superior lens coloboma with iris coloboma causing amblyopia.

Case A 16 years old female reported to OPD with

diminished vision in right eye. On ocular examination, BCVA was Finger Counting at 3m. On retinoscopy, eye was hypermetropic with refractive error of 3.25DS/2.50DC at axis of 100.There was coloboma of iris in superotemporal quadrant. Post dilated Slit lamp biomicroscopy revealed notching at equator of the lens in superotemporal quadrant. Persistant pupillary membrane was present partially. On Gonioscopy angle was open. Fundus was normal.K1 was 37.25 and K2 was 41.75.Axial length was 21.74.

Discussion Congenital anomalies, though rare, are important

cause of childhood blindness. Congenital anomalies of lens include ectopia lentis, microphakia, microspherophakia, lentiglobus, lens coloboma. Coloboma of lens is a condition with autosomal dominant inheritance and occurs at about 4 month of gestation.1,2 It represents an incomplete

completely. It can occur in isolation or with other ocular

indentation of the lens. It is usually unilateral but may be bilateral. Size of coloboma may vary. It is usually inferior-nasal but may occur anywhere along the circumference of the lens.2 Colobomas of the lens are divided into typical colobomas (those that occur at the site of the embryonic

Figure 2 : Lens Coloboma

References

1. Bavbek T, Ogut MS, Kazokoglu H. Congenital lens coloboma and associated pathologies. Doc Ophthalmol1993; 83:313-22.

2. Onwochei BC, Simon JW, Bateman JB, Couture KC, Mir E. Ocular Colobomata. Surv Ophthalmol 2000; 43:175-94.

3. Duke-Elder S. System of Ophthalmology vol 3, part 2. St. Louis:Mosby; 1963.

4. Khan AO, Al-Assiri A. Lens coloboma associated with a ciliary bodycyst. Ophthalmic Genet 2007; 28:208-9.

5. Barber A.N. Embryology of the lens. En: Barber A.N., editors.Embryology of the human eye. St Louis: CV Mosby;1955:50-63.

6. Ozanics V, Jacobiec F.A. Ocular anatomy, embryology and teratology.En:Jacobiec F.A., editors. Prenatal development of the eye and its adnexa. Philadelphia: Harper & Row; 1982. 11-9.

absence of the zonules at that site.1,2 So it is often a misnomer and might better be called coloboma of the zonules or of the ciliary body, as the process actually involves the segmental notching and contraction of the lens due to an absence of the zonules in that location.3 The zonules fail to form in the anterior secondary vitreous or the marginal bundle of Druault during the 3rd - 4th month of gestation, due either to the failure of condensation and differentiation of the vitreous substance or to the failure of the lens to induce such change.

of zonules that usually occur without an apparent cause.4

eye is established. The embryological basis of atypical coloboma is uncertain; various theories propose that it

5,6 It may also result from persistence of mesodermal tissue of embryonic vascular origin blocking the forward growth of the neuroectoderm, thus causing a defect in the ciliary body and iris.2 Lens coloboma has been documented to cause an astigmatic refractive error.1,2

refractive error is left uncorrected, refractive, meridional or anisometropic amblyopia may develop as a result as seen in our patient.

Localised lens opacities may be found in the region of coloboma and capsular tension ring implantation may

coloboma may be associated with complicated retinal detachment. The prognosis of visual recovery in cases where visual disability has occurred will depend upon the time of detection (better prognosis inside the sensitive period ) and the willingness of the patient to attempt rehabilitation.



Figure 1(a) clinical photograph showing foreign body in right eye, (b) clinical photograph of explanted foreign body

Large Post Traumatic Ocular Foreign Body With Good Visual Outcome

Anoop Kishore Gupta MD , Sourabh Sharma MBBS , Neelam Pushker MD , Mahesh Chandra MD

AbstractPurpose:Method: Results:

Conclusion:


Ocular bullet injuries are vision threatening injury because of high speed of bullet they penetrate the globe and ultimately result in blind eye. However patients without open globe injuries have better visual prognosis. This case report enumerates ocular pellet injury in a 30-year-old female presenting as intrascleral foreign body without globe penetration.

Case ReportA thirty year old female, presented with complaints of

pain and redness in right eye with mild blurring of vision since 4 hours. There was history of trauma to right eye with aluminum bullet from a toy gun which was followed by sudden redness and later pain and mild blurring. (Figure 1a).

There was no history of any systemic illness. Her general physical examination was within normal limits. Her best corrected visual acuity was 20/40 in right eye and 20/20 in left eye. Right eye examination showed normal size and shape of globe with normal ocular movements. Eyelids and lacrimal system was normal. There was congestion of conjunctiva medially with a foreign body seen in the medial lower fornix.

Case Report

(a) (b)



It looked like a barrel shaped foreign body, black in

normal with intact sensation. Both direct and consensual pupillary reactions were present. Intraocular pressure was normal. Anterior chamber depth was normal with clear lens. On indirect ophthalmoscopy, retinal hemorrhage was seen in the right inferomedial compartment just anterior to equator. Rest of fundus was normal. Left eye examination was within normal limits. X- ray orbit was done both anteroposterior and lateral view which showed intraorbital

was given injection tetanus toxoid 0.5 ml IM and injection diclofenac 0.5 IM to alleviate pain. Patient was then planned for right eye exploration for any occult scleral perforation and intraorbital foreign body removal under general anesthesia.Under general anesthesia, peritomy was done around the foreign body which was found to be adherent to sclera. It was then carefully removed and underlying sclera was examined. Lamellar perforation was noted which

was repaired with 6-0’ vicryl. The globe was examined in detail for any other occult perforation. Peritomy was closed with 8-0’ vicryl. Subconjunctival injection of antibiotics

vision was 20/40 in right eye. There was mild congestion

hydrochloride (0.5%) q.i.d, prednisolone acetate ( 1%) q.i.d and topical lubricants q.i.d. At 1st week follow up vision

DiscussionOcular bullet injuries are usually vision threatening

and result in open globe injuries which have poor visual prognosis than closed globe injuries.1 In cases in which an ocular foreign body is suspected, prompt diagnosis and treatment is crucial. Retained foreign bodies can lead

2 In our case no intraocular foreign body was seen on indirect ophthalmoscopy but retinal hemorrhage were seen which

that point. Surgical manipulation revealed only lamellar perforation of the sclera. The inner coat of eyeball was intact.

1 ( visual acuity > or = 20/40 ), Zone 1 ( limited to bulbar conjunctiva, sclera, cornea ) according to Proposed Ocular

3 This case presents one of the modes of closed globe injuries with good prognosis. Few cases of intrascleral foreign bodies and situations simulating intrascleral foreign bodies have been reported previously. Nazimul et al reported a case of ocular bullet injury presenting as intrascleral foreign body3. Park et al reported a case of intrascleral foreign body simulating as extrascleral extension of uveal melanoma.4 Our case was fortunate that the foreign body just stopped before penetrating all the coats of the eye. Our case report is one of the unique occurrences

visual prognosis.

Figure 2 (a) x ray orbit lateral view showing foreign body in right orbit (b) x ray orbit antero posteior view showing foreign body in right orbit

Figure 3 : clinical photograph at 1st week post operative showing healthy wound

(a) (b)



References

1. Schein O D, Enger C, Tielsh J M. The context and consequences of ocular injuries from airguns. Am J Ophthalmol1994;117;501-506.

2. Vincent A. Deramo, Gaurav K. Shah, Caroline R. Baumal, Mitchell S. Fineman, Zélia M. Corrêa, William E. Benson Ultrasound biomicroscopy as a tool for detecting and localizing occult foreign bodies after ocular trauma. Ophthalmology1999;106;301-305

3. Kuhn F, Morris R, Witherspoon C D; A Standardized

Exp Ophthalmol 1996; 234; 399-403. 4. Nazimul Hussain, Narendra Laddha, Anjili Hussain, S

Natrajan; Ocular Bullet Injury Presenting As Intraocular Foreign Body: BOA journal Jan – march 2002;20-21.

5. Park S S, Theodossiadis P G, Gragoudas ; Intrascleral foreign body simulating extrascleral extension of uveal melanoma. Arch Ophthalmol 1994; 112 ; 1620.

Announcement Delhi Journal of Ophthalmology

The Best “Original article” published in the Delhi journal of ophthalmology in a calender year will be awarded in the DOS Annual Conference.

Dr.Rajesh SinhaEditor, DJO & Associate Proff.of Ophthalmology

Room. No. 479, Dr.R.P. Centre for Ophthalmic Sciences,AIIMS, Ansari Nagar, New Delhi - 110029







Recent Advances

Corticosteroid Implant for Vascular OcclusionsSavleen Kaur MS , Nishant Sachdev MS

The pathophysiology of macular edema (ME) involves a breakdown of the blood-retinal barrier, with contributory

(e.g. prostaglandins and interleukins), and increased amounts of vascular permeability factors (e.g. vascular endothelial growth factor). Corticosteroids are thought to

therapeutic concentrations of steroids to the retina while limiting systemic exposure is the greatest challenge in the use of steroids today. Intravitreal injections of the corticosteroid triamcinolone have shown promise in the treatment of ME. Dexamethasone, a more potent corticosteroid than triamcinolone, has been shown to produce high intravitreal levels of the drug, however, a short intraocular half-life after intravitreal injection (approximately 3 hours) has led to the investigation of other delivery methods.

Retinal Vein Occlusion Retinal vein occlusion is a blockage of the venous

circulation draining the retina. It is second only to diabetic retinopathy as the most common retinal vascular cause of visual loss1. When vein occlusion occurs, pressure builds up

and blood. This can lead to ME and ischemia of the macula. Macular edema is the most important cause of visual loss in patients with vein occlusions which are of 2 basic types:

1. Central retinal vein occlusion (CRVO): ischemic and non ischemic

Abstract


2. Branch retinal vein occlusion (BRVO)

The various treatment options for CRVO include photocoagulation (PRP) for the treatment of neovascular complications and intravitreal injection of triamcinolone and bevacizumab for macular edema. Other treatments tried

corticosteroids, local anti-coagulation with intravitreal injection of alteplase.

The ProtocolDuring the past 2 decades, the management of macular

edema associated with RVO has been based on 2 pivotal trials conducted by the National Institutes of Health (NIH): the Branch Vein Occlusion Study (BVOS) 2 and the Central Vein Occlusion Study (CVOS).3 In BVOS, patients with BRVO and macular edema after 3 years of follow-up gained an average of 1.33 lines with focal laser photocoagulation compared with 0.23 lines in the nontreatment group. Also, the investigators recommended waiting 3 months before considering laser treatment as one third of the patients improved spontaneously. The CRVO study group summarized that prophylactic PRP did not prevent angle and iris neovascularization in ischemic CRVO, but resulted in regression of angle and iris neovascularization and reduced progression to neovascular glaucoma. The CVOS investigators did not recommend laser treatment for macular edema due to CRVO. Over the years various authors have concluded that there is a limited strategy for any intervention to improve visual acuity in patients with CRVO. Although laser photocoagulation has been the gold standard for the treatment of macular edema, the limited functional outcomes achievable by means of laser treatment have prompted researchers to try alternative options.



Corticosteroids as Treatment

stabilize endothelial cell tight junctions, and inhibit the synthesis of VEGF, prostaglandins, and other cytokines.4

The Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) Study compared 1-mg and 4-mg intravitreal triamcinolone with standard care in patients with non resolving macular edema due to vein occlusions (i.e. grid photocoagulation in eyes without dense hemorrhage and deferral of photocoagulation until hemorrhage clears in eyes with dense macular hemorrhage for BRVO and observation for CRVO).

At the 12-month visit, there was no statistically

with BRVO. However, the adverse rate event, particularly elevated intraocular pressure and cataract, were highest in the 4-mg group. The SCORE investigators advised that grid photocoagulation remain the benchmark against which other treatments are compared in clinical trials evaluating BRVO.5,6

In contrast, intravitreal triamcinolone was determined to be superior to observation for macular edema in patients with CRVO with more side effects like cataract in the 4mg group. Corticosteroid could reduce vision loss due to CRVO-ME and that treated patients were also 5 times more likely to regain vision after 1 year than patients who were under observation. The SCORE investigators recommended 1-mg intravitreal triamcinolone for up to1 year and possibly 2 years in patients of CRVO.5,6

Dexamethasone ImplantDexamethasone is a potent corticosteroid that has anti

acetonide resevoir implant, which contains half the drug as the Retisert implant to decrease the side-effects seen with Retisert. OZURDEX (dexamethasone intravitreal implant) 0.7 mg is a biodegradable implant injected into the vitreous to treat adults with macular edema (Figure 1). Allergan’s Ozurdex (called Posurdex everywhere except in the US) has been approved by the US Food and Drug Administration (FDA) to treat patients of macular edema due to vein occlusions and non infectious posterior uveitis. Ozurdex

AdvantageThe DEX implant has two many potential advantages

over other therapies currently employed for macular edema secondary to vein occlusion.4

Figure 1 a & b : OZURDEX (dexamethasone) intravitreal implant

Figure 2 : Applied under aseptic precautions as an outpatient procedure

(a) (b)



1. The continuous release of medication maintains a consistent level of the drug within the eye for about an year, eliminating the need for monthly or bimonthly injections, as might be necessary with intravitreal anti-VEGF agents. Additionally, the sustained release formulation provides the potency of DEX while compensating for the short intraocular half-life of the medication.

2. It may be most appropriate for motivated patients with branch vein occlusions associated with macular

for repeated anti-VEGFtherapy, or for patients who have demonstrated intolerance or recalcitrant edema following anti-VEGF therapy.

3. It may also be a suitable choice for patients with CRVO, particularly those who are already pseudophakic and not steroid responders, and who are not good candidates for anti-VEGF agents for other reasons such as intolerance or pre-existing thromboembolic disease.

implant, additional implants are not recommended. Some authors give consideration to combination therapy with both an anti-VEGF agent and DEX.

Proven Trials1. An early trial of the DEX implant compared 0.35 mg and

0.7 mg doses to a noninjection observation group for the treatment of macular edema of various etiologies.

7

2. Chang-Lin et al recently published their results on the pharmacokinetics and pharmacodynamics of Ozurdex in monkeys and reported a steady state concentrations of dexamethasone in monkey eyes with peak concentration on day 60.8

3. Two randomized, prospective, masked, sham-controlled studies were conducted at 167 clinical sites

Ozurdex over an initial 6-month period followed by a 6-month open-label extension. Proportion of eyes achieving at least a 15-letter improvement from baseline BCVA was greater in the treatment groups at month 1 and month 3 but not at month 6. 9,10

Adverse Events

include:

The most common ocular adverse reactions reported

included increased intraocular pressure (25%), conjunctival hemorrhage (20%), eye pain (7%), conjunctival hyperaemia (7%), ocular hypertension (4%), cataract (4%), vitreous detachment (3%), and headache (3%).

Very few cases report some of the products that may lead to drug interactions with Ozurdex including nonsteroidal

Bromfenac eye drops, Diclofenac eye drops, Flurbiprofen eye drops, Ketorolac eye drops, Nepafenac ophthalmic suspension.

Contraindications

The dexamethasone implant is contraindicated in pa-tients with:

1. Active or suspected ocular or periocular infections including most viral diseases of the cornea and conjunctiva, including active epithelial herpes simplex keratitis,vaccinia, varicella.

2. Mycobacterium infections.

3. Fungal diseases.

4. Infections of sclera and episclera.

5. Steroid responders and advanced glaucoma.

The FutureAlthough the rates of elevated IOP (up to 41%) and

higher in the SCORE study than in patients receiving the DEX implant, these results, as well as those showing

comparative controlled trials.

There are ongoing clinical trials examining Ozurdex for the treatment of diabetic ME, however, the trials are not expected to be completed until 2014.

An ongoing trial on Ozurdex for Combined Pseudophakic Cystoid Macular Edema and Diabetic Macular Edema After Cataract Surgery: Completion Date: January 2012

Ranibizumab has also been used with success in the treatment of macular edema associated with both BRVO and CRVO. The recently published BRAVO and CRUISE studies

a 15-letter improvement with an average of almost one



injection per month but currently, there is no randomized controlled trial comparing anti-VEGF agents and Ozurdex directly.

Our personal experience says that dexamethasone implant is a promising therapy for patients having macular edema recalcitrant or minimally responsive to anti VEGF

and also improving visual acuity. But randomized trials comparing the DEX implant to grid laser in BRVO, intravitreal anti-VEGF agents, and triamcinolone, are anticipated to help decide the best choice in patients of macular edema.

References

1. Rogers S, McIntosh RL, Journ GD, et al. The prevalence of retinal vein occlusion: pooled data from population studies from the United States, Europe, Asia, and Australia. Ophthalmology 2010;117:313–19.

2. The Branch Vein Occlusion Study Group. Argon laser photocoagulation for macular edema in branch vein occlusion. Am J Ophthalmol 1984;98:271–82.

3. The Central Vein Occlusion Study Group. Evaluation of grid pattern photocoagulation for macular edema in central vein occlusion: the Central Vein Occlusion Study Group M report. Ophthalmology 1995;102:1425–33.

4. Chan A, Leung L, Blumenkranz M S. Critical appraisal of the clinical utility of the dexamethasone intravitreal implant (Ozurdex®) for the treatment of macular edema related to branch retinal vein occlusion or central retinal vein occlusion. Clinical Ophthalmology 2011;5:1043–49

5. Ip MS, Scott IU, VanVeldhuisen PC, et al. A

of intravitreal triamcinolone with observation to treat vision loss associated with macular edema secondary to central retinal vein occlusion: the Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) study report 5. Arch Ophthalmol 2009;127:1101–14.

6. Scott IU, Ip MS, VanVeldhuisen PC, et al. A

intravitreal triamcinolone with standard care to treat vision loss associated with macular Edema secondary to branch retinal vein occlusion: the Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) study report 6. Arch Ophthalmol 2009;127:1115–28.

7. Kuppermann BD, Blumenkranz MS, Haller JA, et al. Randomized controlled study of an intravitreous dexamethasone drug delivery system in patients with persistent macular edema. Arch Ophthalmol2007;125:309–17.

8. Chang-Lin JE, Attar M, Acheampong AA. Pharmacokinetics and pharmacodynamics of a sustained-release dexamethasone intravitreal implant. Invest Ophthalmol Vis Sci 2011;52:80–86.

9. Haller JA, Dugel P, Weinberg DV, et al. Evaluation of the safety and performance of an applicator for a novel intravitreal dexamethasone drug delivery system for the treatment of macular edema. Retina. 2009;29:46–51

10. Haller JA, Bandello F, Belfort R, et al. Randomized, Sham-Controlled Trial of Dexamethasone Intravitreal Implant in Patients with Macular Edema Due to Retinal Vein Occlusion. Ophthalmol 2010;117: 1134–46.



Allied Ophthalmic Sciences : Ocular Pharmacology

Ophthalmic Drug Delivery Systems : An UpdateNihar Ranjan Biswas MD , DNB, DM

Abstract


Topical drug treatment of ocular disease has the

desired site of action. For ocular drugs, to be effective ideal drug delivery systems (DDS) should provide the drug at the receptor site of the ocular tissue in relatively higher concentrations to elicit the desired pharmacological response.1 The tight junctions of iris capillaries and retina acts as a barrier to the diffusion of drugs from the blood into the aqueous and vitreous and the cornea acts as a barrier to drugs applied topically.2 Most important factor, which

thereby increasing the contact time of the drug to the ocular tissues. The duration of the drug action in the eye can be extended by

(i) improving corneal drug penetration.

(ii) reducing drainage through the use of viscosity enhancing agents. Factors that affect the bioavailability of ocular drugs include pH, salt form of the drug, vehicle composition, osmolarity, toxicity and viscosity.3

The most frequently used ocular therapeutics are eye drops, ointments and inserts. In dependence on the physico-chemical properties of the therapeutical substance and the kind of disease, one has to formulate the form of the drug in the manner to obtain its maximal bioavailability. By increasing their viscosity one can keep the watery solutions in the conjunctival sac for around 60 minutes. Mainly

the viscosity of the solution and size of the molecules suspended in it limit the time of contact of the drug, given in the form of suspension. The ointments stay on the surface of the eye up to 2 hours. The ocular inserts secure

The compounds penetrate into the anterior chamber of eye mainly through the cornea. Therefore the physiological

by the therapeutical substance. Carbomer based hydrogel with timolol maleate (T-Gel) used for the study as a vehicle

T-Gel 0.05% (0.05% timolol), T-Gel 0.025% (0.025% timolol) and commercial timolol ophthalmic solution (TOS 0.1% timolol) determined and compared. Timolol detected in the washings up to 1 hr after instillation of test products; the highest levels observed after T-Gel 0.05 %. This study concluded that the new vehicle obviously improves the bioavailability of topically applied timolol.

Medication forms used in Ophthalmology Solutions, Ointments, Sprays, Gels, Lid scrubs

Solutions

Most of the topical ocular preparations are commonly available as solutions which are applied directly to the eye. Eye drops is one of the most common forms of drug delivery systems. A "pouch method of eye drop instillation" has been used whereby the patient looks up and the lower eyelid is held everted. The eye drop is placed into the exposed lower cul-de-sac and allowed to pool there. The eyelids are then gently closed and kept closed for 25 minutes so that blinking does not activate the lacrimal pump system.3,4



Ointments

results from the prolonged contact time with eye. Ointments are especially useful for treating children who may not cooperate for topically applied solutions. Ointments are especially useful for medicating ocular injuries such as corneal abrasions where the eye needs to be patched. A

of delivering a small volume of medication. The ribbon of ointment cannot be easily separated from the tubing without contacting the eye, which contaminates the tube. The commonly used ophthalmic ointment bases and liquid oily vehicles are made up of lanolin, petrolatum and peanut oil, which are toxic to the interior of the eye, causing endothelial damage, corneal oedema, vascularisation, and scarring. For this reason, ophthalmic medications in ointment or oily liquid vehicles should not be instilled into the interior of the eye. Experimental studies showed that introduction of 0.1 ml of any of these substances into rabbit eyes caused severe reactions with secondary glaucoma.5

This form is specially used for paediatric patients and solution is administered using a sterile perfume atomizer or plastic spray bottle. Mydriatic-cycloplegics can be admministered as spray to the closed eye to dilate the pupil.3

Gels

Corticosteroids dispensed in gel vehicles may contain therapeutic levels 5 times or more than in ordinary liquid vehicles. Ophthalmic gels are similar in viscosity and clinical usage to ophthalmic ointments. Experimental trials indicate that delivery of pilocarpine in viscous gel vehicles instilled twice daily may control intraocular pressure as well as solutions of equal drug strength instilled 4 times daily.

Lid scrubs

Eyelid cleansers, antibiotic solutions or ointments can be applied directly to the eyelid margin for the treatment of blepharitis. This is ideally achieved by applying the medication tipped applicator and then scrubbing the eyelid margins several times daily.

Ocular Drug Delivery Devices in Ophthalmology

Soluble ocular drug inserts (SODI) are made of polymers of ethylacrylate, vinyl pyrolidone and acrylamide. SODI dissolve in cul-de-sac and is capable to provide detectable drug levels in the cornea upto 48 hours. Wafers are inserts made of succinylated collagen.6 Wafers are 6 mm x 12 mm in size and are inserted into the inferior cul-de-sac. In the treatment of kerato-conjunctivitis sicca, a 12 mg cellulosic polymer rod is itself the active ingredient. The rod is supplied sterile, without preservative. When inserted in the lower cul-de-sac in the morning, the substance slowly

7 A particular advantage of this method is that no preservative is necessary. Thiomersol and chlorbutanol may be toxic to the dry eye. Benzalkonium chloride, a detergent, de-

Higher water content with large intermolecular pore size contact lens has the capability to absorb water-soluble drugs and release gradually.8-10 Dexamethasone, antibiotics and pilocarpine can be delivered through hydrogel contact lens. Maximum drug delivery is obtained by pre-soaking the lens. The permeability of drug is related to thickness of the lens. A thinner lens allows a greater amount of topically applied drug to pass into the lens-cornea interface.11-14 It is used in the treatment of dry eye syndromes and in bullous keratopathy. In comparison with soft contact lens delivery vs subconjunctival delivery of chloramphenicol, gentamicin

higher aqueous drug levels than subconjunctival injection.15

Collagen shields have been studied extensively for their potential usefulness as drug delivery devices because the drug is released as the shield dissolves.16-20 Collagen shields are made of thin membranes of porcine or bovine scleral collagen.21-25 Collagen shields are packaged in a dehydrated state and require rehydration before application, when a shield is rehydrated in a solution containing a water-soluble drug, the drug becomes trapped in the collagen matrix, and



shields dissolve as a result of proteolytic degradation by the

healing time of herpes simplex keratitis compared with traditional antiviral eye drop therapy.26-28 Clinical experience indicates that the collagen shield is relatively safe when used as a drug delivery device. Drug delivery using impregnated collagen shields is potentially more comfortable and reliable than frequent applications of eye drops or subconjunctival injections.29-30 Collagen shields are superior to topical eye drops or soft contact lenses in delivering water-soluble drugs to the human cornea. Following are the limitations to use collagen shields.

It consists of a rod shaped pellet of hydroxy propyl cellulose without preservative. Each lacrisert is 1mm in diameter and 4 mm in length at dehydrated state and it contains 5 mg of the synthetic polymer. Lacrisert is inserted into the inferior conjunctival fornix. After placement into the conjunctival sac, its hypertonicity causes it to absorb

conjunctiva, and swells, becoming a gelatinous mass. After several hours, the insert dissolves and releases the polymer

to relieve symptoms. This device is useful for the patients with moderate to severe dry eye syndrome. Blurring of

or release polymer to the eye and treatment may be failure with this device.

A new ocular drug delivery of high molecular weight (400 KDa) linear polyethylene oxide (PEO) in gel-forming erodible

tested in vitro and in vivo.31-33 Inserts of 6 mm diameter, 20

by powder compression. In vitro drug release from inserts is mainly controlled by insert erosion. The rate of insert erosion dependent on the strength of inter-polymer interactions in the compounds, and on the hydrophilic balance of compounds.

into the aqueous humor is both retarded and prolonged by the PEO-EUDNa 17% inserts. C(max), AUC(0-2) are strikingly increased by plain PEU inserts with respect to commercial eye drops.34-35

strips. Fluorescein impregnated paper strips eliminates the risk of solution contamination with Pseudomonas aeugenosa. For administration, the drug-impregnated paper strip moistened with a drop of normal saline, and the applicator is gently touched to the superior or inferior bulbar conjunctiva or to the inferior conjunctival sac.

A pledget is constructed by simply teasing the cotton tip of an applicator to form a small (5 mm) elongated body of cotton. These devices allow prolonged ocular time with solutions that are normally topically instilled into the eye. After placing one or two drops of the ophthalmic solution on the pledget, the device is placed into the inferior conjunctival fornix. This device of drug delivery allows maximum mydriasis in attempts to break posterior synechiae or dilate sluggish pupils.

The ocusert is a device with a two-membrane sandwich with a pilocarpine reservoir in the centre. The co-polymeric membrane is ethylene vinylacetate with a pilocarpine reservoir in the centre. A white titanium dioxide ring incorporated between the membrane that helps in visualizing and handling the inserts. Ocusert are

the upper or lower lid. Ocusert provide a zero-order rate of delivery by steady-state diffusion whereby drug is

membrane controlled drug delivery has advantages and is effective in some patients, the inserts have not gained widespread use, likely due to their cost and the fact that

solid insert in the cul-de-sac. Drugs that can be delivered through ocusert are pilocarpine, antibiotics, steroids and carbachol.3

The mechanism of micro-emulsions is based on the absorption of the nanodroplets representing the internal phase of the micro-emulsion, which constitutes a reservoir for the drug on the cornea. The micro-emulsions are a promising dosage form for the natural defence of the eye because they are prepared by inexpensive processes

They are stable and have a high capacity of dissolving the ocular drug. In vivo results and preliminary studies on healthy volunteers have shown a delayed effect and an increase in the bioavailability of ophthalmic drug.36



Extra-ocular irrigation is used to dislodge foreign material in the initial treatment of acute chemical burns and ocular foreign bodies. It consists of the container of irrigating solution and a tissue paper or towel with which to collect

position with head tilted toward the side to be irrigated with the upper and lower lids retracted; the clinician gently bathes the extra ocular surfaces with the solution.

Most methods that have been devised for continuous ocular irrigation are suitable for short periods in non-ambulatory patients. Polyethylene tubing is sometimes simply passed with a minor surgical procedure through the

be perfused is supplied from an overhead infusion bottle. The tubing is anchored to the skin with sutures and may also be secured by tape. In cases in which it is undesirable

of tubing, loops, rings and haptic contact lens shells have been successfully used. The Morgan lens is the convenient commercially available system. This system is capable of

eyelid, avoiding contact with damaged ocular tissues.

are involved in the disease. These drugs are then able to act directly on their relevant targets. For other diseases,

location, the disease could be treated more effectively with reduced side effects.37 To overcome this problem, drugs are incorporated into small particles, which could release their drug at the site of interest. It has been found that the particles need to be very small, around 50-150 nm in diameter to reach suitable targets. Also that the particles need to be coated to make them invisible to the body's immune system to avoid them being prematurely removed by organs likes the cornea and liver. The best coatings to use are very hydrophilic molecules such as polyethylene glycol (PEG), which do not interact with these defence receptors. The nanoparticles are produced by an instantaneous self-assembly process and are micellar in nature with the poly lactide (PLA) segments forming the core of the particle and the PEG segments forming a mobile corona. The PLA core is solid, and the density of the PEG corona varied as the block sizes of the PLA and the PEG are changed. Investigations are done with both biodegradable particles with adsorbed surface layers and micellar type particles made by phase

separation techniques from block copolymers of poly lactide-polyethyleneglycol (PLA-PEG). The resulting polymers are used to make nanoparticles which were characterised by a variety of physico-chemical techniques including: transmission electron microscopy (morphology), Infrared (IR) spectroscopy (hydrodynamic diameter), NMR (structure of particles in D20), hydrophobic interaction chromatography, colloidal stability in salt solutions. The biological performance of nanoparticles is believed to

PEG layer. Following three drugs are under development for nanoparticles delivery applications - Conventional low molecular weight drugs, protein and polypeptide drugs, and DNA for oligonucleotide or gene therapy.37 Solid lipid nanoparticles (SLN) as carriers for topical ocular delivery of tobramycin have been reported.38 It was found that when compared with an equal dose of aqueous tobramycin eye

higher bioavailability in the aqueous humor. Furthermore, polycyanoacrylate nanoparticles were loaded with amikacin sulphate and evaluated for their ability to improve the corneal penetration of this hydrophilic drug. This study

the cornea and aqueous humor in nanoparticle formulation as compared to the control solution.39

It was reported that topical application of liposome formulation is capable of increasing the intraocular

42 Water soluble penicillin G and water insoluble indoxole-loaded liposome instillation

the rat cornea as compared to the drug applied using polysorbate-80.40 Moreover, positively charged liposomes showed better penetration as compared to negatively charged liposomes. The proof of the concept of positively charged liposomes interacting with the cornea came from a study conducted to visualize the interaction on rat cornea. This study reported the interaction of liposome entrapped propidium iodide and horseradish peroxidase (which is impermeable to epithelium) on the outer epithelium

41 A single topical application of tobramycin (3.5 mg/0.1 ml) multi-

overlaying bandage contact lens was studied in the model of Pseudomonas keratitis in rabbits and showed that this method comparatively decreased the bacterial count in the cornea.43

Iontophoretic system is the technique which uses electric potential to drive charged drug molecules towards the opposite polarity. Transcorneal and trans-scleral iontophoresis were compared to subconjunctival injection in the delivery of gentamicin into rabbit eyes.



This study assessed the potential corneal toxicity of trans-corneal iontophoresis by measuring corneal thickness and endothelial cell counts before and 3 days after trans-corneal iontophoresis of gentamicin; balanced saline solution served as control. It is of interest that this study showed no

44 In another study, the effects of iontophoretic application of tobramycin on the corneal concentration was compared by Hobden and co-workers in the resistant P. aeruginosa-infected and normal rabbit corneas.45 Corneas infected with P. aeruginosa were treated 22 hrs after infection with tobramycin delivered by either iontophoresis, mock iontophoresis, or application of

at 10 mg/ml showed a one log reduction in the number of

of bacteria compared to other treatments.46 Corneal iontophoresis using soft stable hydroxyethyl methacrylate hydrogel discs (80% water content) loaded with gentamicin sulphate which were mounted on an iontophoresis probe was reported by Frucht-Pery et al. in rabbits.47 This study reported that a current of 0.6 mA used for 60 sec

having an established key role in ophthalmic therapeutics, using iontophoresis with more cumbersome efforts to achieve drug concentration in the aqueous humor becomes unattractive.

References

1. Barza M, Kane A, Baum J. Oxacillin for bacterial endophthalmitis: subconjunctival, intravenous, both, or neither? Invest Ophthalmol Vis Sci 1980;19:1348-54.

2. Rizzolo LJ. Development and role of tight junctions in the retinal pigment epithelium. Int Rev Cytol2007;258:195-234.

3. Velpandian T. Intraocular penetration of antimicrobial agents in ophthalmic infections and drug delivery strategies. Expert Opin. Drug Deliv 2009;6(3):255-70.

4. Kitagawa K, Fukuda M, Sasaki K. Intraocular penetration of topically administered acyclovir. LensEye Toxic Res 1989;6:365-73.

5. Robin JS, Ellis PP. Ophthalmic ointments. SurvOphthalmol 1978;22:335-40.

6. Mundada AS, Shrikhande BK. Design and evaluation of soluble ocular drug insert for controlled release

Drug Dev Ind Pharm2006;32:443-8.

7. Felt O, Baeyens V, Buri P, et al. Delivery of antibiotics to the eye using a positively charged polysaccharide as vehicle. AAPS PharmSci 2001;3:E34.

8. Praus R, Brettschneider I, KrejcaL, Kalvodova¡ D. Hydrophilic contact lenses as a new therapeutic approach for the topical use of chloramphenicol and tetracycline. Ophthalmologica 1972;165:62-70.

9. Matoba AY, McCulley JP. The effect of therapeutic soft contact lenses on antibiotic delivery to the cornea. Ophthalmology 1985;92:97-9.

10. Rootman DS, Willoughby RP, Bindlish R, et al.

to rabbit cornea and aqueous humor. J Ocul Pharmacol1992;8:317-23.

11. Busin M, Spitznas M. Sustained gentamicin release by presoaked medicated bandage contact lenses. Ophthalmology 1988;95:796-8.

12. Tian X, Iwatsu M, Kanai A. Disposable 1-day Acuvue

rabbits’ eyes. CLAO J 2001;27:212-5.13. Tian X, Iwatsu M, Sado K, et al. Studies on the uptake

lenses. CLAO J 2001;27:216-20.14. Hehl EM, Beck R, Luthard K, et al. Improved penetration

aqueous humour of patients by means of Acuvue contact lenses. Eur J Clin Pharmacol 1999;55:317-23.

15. Jain MR. Drug delivery through soft contact lenses. Br J Ophthalmol 1988;72:150-4.

16. Dorigo MT, De Natale R, Miglioli PA. Collagen shields delivery of netilmicin: a study of ocular pharmacokinetics. Chemotherapy 1995;41:1-4.

17. Phinney RB, Schwartz SD, Lee DA, et al. Collagen-shield delivery of gentamicin and vancomycin. ArchOphthalmol 1988;106:1599-604.

tobramycin-soaked collagen shields vs tobramycin eyedrop loading dose for sustained treatment of experimental Pseudomonas aeruginosa-induced keratitis in rabbits. Am J Ophthalmol 1992;113:418-23.

19. Pleyer U, Legmann A, Mondino BJ, et al. Use of collagen shields containing amphotericin B in the treatment of experimental Candida albicans-induced keratomycosis in rabbits. Am J Ophthalmol 1992;113:303-8.

20. Robin JB, Keys CL, Kaminski LA, et al. The effect of collagen shields on rabbit corneal reepithelialization after chemical debridement. Invest Ophthalmol Vis Sci1990;31:1294-300.

21. Liang FQ, Viola RS, del Cerro M, et al. Non-cross-linked collagen discs and cross-linked collagen shields in the delivery of gentamicin to rabbits eyes. Invest Ophthalmol Vis Sci 1992;33:2194-8.

22. Kuwano M, Horibe Y, Kawashima Y. Effect of collagen cross-linking in collagen corneal shields on ocular drug delivery. J Ocul Pharmacol Ther 1997;13:31-40.

23. Hosaka S, Ozawa H, Tanzawa H, et al. In vivo evaluation of ocular inserts of hydrogel impregnated with antibiotics for trachoma therapy. Biomaterials1983;4:243-8.

24. Silbiger J, Stern GA. Evaluation of corneal collagen shields as a drug delivery device for the treatment of experimental Pseudomonas keratitis. Ophthalmology1992;99:889-92.

shields as a surgical adjunct. J Cataract Refract Surg1988;14:492-5.

26. Hobden JA, Reidy JJ, O’Callaghan RJ, et al. Quinolones in collagen shields to treat aminoglycoside-resistant pseudomonal keratitis. Invest Ophthalmol Vis Sci1990;31:2241-3.



27. Baziuk N, Gremillion CM Jr, Peyman GA, et al. Collagen shields and intraocular drug delivery: concentration of gentamicin in the aqueous and vitreous of a rabbit eye after lensectomy and vitrectomy. Int Ophthalmol1992;16:101-7.

28. Wang JM, Chu RY, Li YT. Cephradine delivery into the eye with domestic collagen shield. Zhonghua Yan Ke Za Zhi 1994;30:131-3.

29. Taravella M, Stepp P, Young D. Collagen shield delivery of tobramycin to the human eye. CLAO J 1998;24:166-8.

30. Taravella MJ, Balentine J, Young DA, et al. Collagen J Cataract

Refract Surg 1999;25:562-5.31. Di Colo G, Zambito Y, Burgalassi S, et al. Effect of

chitosan on in vitro release and ocular delivery of

oxide). Int J Pharm 2002;248:115-22.32. Kaiser RR, Rãckert PR. Hydrogel, a new galenic form in

ophthalmology. Klin Monatsbl Augenheilkd 1990;196:405-6.

weight sodium hyaluronate in the treatment of bacterial corneal ulcers. Graefes Arch Clin Exp Ophthalmol1992;230:20-3.

34. Srividya B, Cardoza RM, Amin PD. Sustained

in situ gelling system. J Control Release 2001;73:205-11.35. Sultana Y, Aqil M, Ali A. Ion-activated, Gelrite-based in

with conventional eye drops. Drug Deliv 2006;13:215-9.36. Ghelardi E, Tavanti A, Celandroni F, et al. Effect

of a novel mucoadhesive polysaccharide obtained from tamarind seeds on the intraocular penetration

J Antimicrob Chemother 2000;46:831-4.

37. Douglas SJ, Davis SS, Illum L. Nanoparticles in drug delivery. Crit Rev Ther Drug Carrier Syst 1987;3(3):233-61.

38. Cavalli R, Gasco MR, Chetoni P, et al. Solid lipid nanoparticles (SLN) as ocular delivery system for tobramycin. Int J Pharm 2002;238:241-5.

39. Losa C, Calvo P, Castro E, et al. Improvement of ocular penetration of amikacin sulphate by association to poly(butylcyanoacrylate) nanoparticles. J Pharm Pharmacol 1991;43:548-52.

40. Schaeffer HE, Krohn DL. Liposomes in topical drug delivery. Invest Ophthalmol Vis Sci 1982;22:220-7.

41. Velpandian T, Gupta SK, Gupta YK, et al. Ocular drug targeting by liposomes and their corneal interactions. J Microencapsul 1999;16:243-50.

42. Velpandian T, Gupta SK, Gupta YK, et al. Enhanced

on rabbit cornea. Proceedings of XII International conference of Eye Research held at Yokohama, Japan, 1996.

43. Frucht-Perry J, Assil KK, Ziegler E, et al. Fibrin-enmeshed tobramycin liposomes: single application topical therapy of Pseudomonas keratitis. Cornea1992;11:393-7.

44. Grossman RE, Chu DF, Lee DA. Regional ocular gentamicin levels after transcorneal and transscleral iontophoresis. Invest Ophthalmol Vis Sci 1990;31:909-16.

45. Hobden JA, Rootman DS, O’Callaghan RJ, et al. Iontophoretic application of tobramycin to uninfected and Pseudomonas aeruginosa-infected rabbit corneas. Antimicrob Agents Chemother 1988;32:978-81.

46. Hobden JA, O’Callaghan RJ, Hill JM, et al. Tobramycin iontophoresis into corneas infected with drug-resistant Pseudomonas aeruginosa. Curr Eye Res 1989;8:1163-9.

47. Frucht-Pery J, Mechoulam H, Siganos CS, et al. Iontophoresis-gentamicin delivery into the rabbit cornea, using a hydrogel delivery probe. Exp Eye Res2004;78:745-9.

Medical and surgical Retina Specialist exp 2 to 3 yrs.

Pediatric ophthalmologist – exp 2 to 3 yrs.

General Ophthalmologist (community) exp 2 to 3 yrs.

Excellent work environment. Salary Negotiable for deserving candidate.

Chairman & Managing Director

Sushil Eye Hospital & Brahma Laser Center

25 Krushinagar, College Road Near Janlakshmi Bank, Nasik, Maharastra

Ph.: 09909909082 Email: [email protected]

Sushil Eye Care Multispecialty Hospital @ Nasik(Maharashtra) requires



Brief Communication

Cosmetic Contact lens Induced Corneal Ulcers Khushnood Sheikh MS

A corneal ulcer is a break, erosion or open sore in the cornea. If not treated in time it may result in blindness due to scar formation. The most common cause of corneal ulcer is an abrasion or scratch caused by an injury or as a result of long wearing of contact lens. Other causes may include viral

malnutrition, chemical injury, exposure to ultraviolet light, prolong use of corticosteroid eye drops and autoimmune diseases. In this era of modernization the uses of cosmetic soft contact lenses are increasing. People especially the younger generation want to show themselves as a different personality specially in festival season and for this they purchase cosmetic and coloured contact lenses from

any proper guidance. When they use this for longer period, due to low quality of material and poor personal hygiene, they develop complications related to this.

We observed 10 cases of corneal ulceration by the use of extended wear cosmetic contact lenses between August 2010 and December 2010. They developed corneal ulcers after wearing cosmetic contact lens purchased directly from shop without proper consultation and without proper cleaning for more than three days. Out of these 60 % were males and 40% were females. Eight patients presented with pain, watering, red eye, dimness of vision and foreign body sensations while two patients had only foreign body sensations. On examination there was presence of a corneal

and in two patients there was a central ulcer with double

than 3 mm in both eyes. The visual acuity was 6/60 in two cases, 6/36 in six cases and 6/24 in remaining two cases at the time of presentation. Corneal scrapping was taken and slides were prepared for KOH, Gram’s staining, and Ziehl-Nielson staining and for culture and sensitivity.

The microbiological reports showed presence of Gram negative bacilli and culture reports revealed pseudomonas

0.5% one hourly initially for 12 hours followed by two hourly

one hourly and cyclopentolate drops three times a day. Oral analgesic was given 8 hourly to all patients. On third day of follow up 8 cases showed improvement. On subsequent

follow up eight patients responded well to treatment and recovered completely. The patient with paracentral corneal

nebulomacular opacity and resolved within 15 days having

visual acuity of greater than 6/60. Use of cosmetic contact lenses in younger generation is increasing day by day in view of increasing cosmetic awareness more so due to the

easily available in the shops and can be worn even without proper guidance and care of trained ophthalmologists and optometrists. Due to this, there are risks of corneal complications. As observed in studies done by Cohen et al2 and Weissman et al3 the causative organism was pseudomonas. Early diagnosis with suitable treatment resulted in complete healing of the ulcer with reasonable visual recovery in my study. The complication of corneal ulceration can be prevented by good hygienic care and proper guidance along with use of good quality contact lenses.

References

1. Kanski J. Clinical ophthalmology; microbial keratitis, 5th edition, 2003 P-102.

2. Cohen EJ, Laibson PR, Arentsen JJ, Clemons CS. Corneal ulcer associated with cosmetic extended wear soft contact lenses. Ophthalmology 1987; 94 (2): 109 -14.

3. Weissman BA, Pearson TR.Clinical management of cosmetic extended-wear contact lens failure. J Am Optom Assoc 1986;57(6):448-50.



Brief Communication ; Letter to editor

Dear editor,I found the review on small gauge vitrectomy published in the last edition to be very good. The physics and dynamics

of the different gauge system have been very clearly explained. Even the complications associated with the system have been nicely mentioned. However there is no mention of the comparison in the learning curve and the duration of the surgery in between 23 G and 25 G. Studies comparing the pain score between the two systems could also have been mentioned. There is little doubt now about the success of 23 G and 25 G instrumentation despite the initial criticism it received.What we have to look is the direction these advances will take us!

Dr. Supriya Arora

Guru Nanak Eye CentreMaulana Azad Medical College

Dear editor,

time and it gives a nice feel of pictorial story telling. Very concisely written it gave a good idea of the disease with all the appropriate photos to imprint in your mind. But a postoperative photograph to show the resolution of the disease would

management protocol could also have been included.

Dr.Tarun Arora

Rajendra Prasad Centre for Ophthalmic Sciences All India Institute of Medical Sciences

Dear editor,The section on Industry news last time, The EX-Press Glaucoma Filtration Device was very informative. For private

practitioner like me, this section helps me to know the latest advances in the industry as and when it is available. If the companies can also mention the price range of the product it would be more appropriate. Also a video link demonstrating the application of the device along with associated research about the advantages and complications associated with the device should be available.

Dr.Vinod Kumar Tewari

Tewari Eye CentreGhaziabad



Photo Essay

Parul Jain MBBS , Vasu Kumar MS, DNB , P K Pandey MD , B Ghosh MD, MNAMS , Chittaranjan Mishra MBBS

Periampullary neoplasms include carcinomas of the duodenum , ampulla of Vater, distal common bile duct and pancreas. They are considered collectively because of their

them without the examination of the resected specimen.1,2

More than half of the cases have distant metastases at

diagnosis.3-7 To the best of our knowledge this is a rare report of presumed isolated retinal metastases from periampullary cancer. A 52 year old male, diagnosed with periampullary carcinoma was referred by the treating surgeon for sudden visual loss in his left eye. He had no history of hypertension,diabetes mellitus, heart disease or cerebral infarction. On examination the visual acuity was 20/20 OD and light perception OS. Intraocular pressure was 14mm Hg OD and 12 mmHg OS. A relative afferent pupillary defect was observed in his left eye. The extraocular movements were full and free and the slit lamp examination of the anterior segment of both eyes was normal.

1(a) 1(b) 2 3

4 5 6

7 8 9

Figure 1 a & b: Anterior segment photographs; Figure 2: Fundus photo (montage) of the left eye at presentation showing a large preretinal bleed overlying the macular area with multiple intraretinal and subretinal haemorrhages with patchy yellow lesions confined to retinal vasculature; Figure 3: Fundus photo of the right eye showed normal macula and retinal vasculature; Figure 4: Fundus photo immediate post yag hyaloidotomy; Figure 5: Fundus photo at 8 weeks follow up showing resolved haemorrhages; Figure 6: USG B scan (left eye) showing pvd with preretinal bleed.no evidence of rd/choroidal lesion; Figure 7: x 20 hematoxylline stain; tumor cells with prominent hyperchromatic nuclei ; Figure 8: Chromogranin staining for tumor cells positive highly suggestive for tumor cells; Figure 9: FFA left eye showing areas of blocked fluorescence due to residual haemorrhages.

Retinal haemorrhage as an unusual presenting feature of metastatic pancreatic carcinoma



Dilated fundus examination of the right eye showed a cup-disc ratio of 0.3:1 with normal disc, macula, retinal vasculature and peripheral retina. Examination of the left eye showed a normal disc with a large preretinal haemorrhage overlying the macular area with multiple preretinal and subretinal hemorrhages scattered at the posterior pole with

retinal periphery was unremarkable (Figure 2-5).

An ultrasound B scan was performed the same day which revealed the presence of total posterior vitreous detachment with organized preretinal bleed. There was no evidence of any choroidal lesion or retinal detachment. (Figure 6) The differential diagnosis at presentation was combined preretinal and subretinal hemorrhages due to bacterial endocaditis, Purtscher’s retinopathy and in this setting metastatic tumor cell embolism. In view of the large premacular bleed, Yag hyaloidotomy was done and the patient was advised a battery of investigations.

The patient underwent echocardiography which did not reveal any evidence of endocarditis. His serum amylase levels were also found to be normal. He was thus presumed to have tumor cell embolism and was advised a comprehensive metastatic work up. He underwent PET scan and there was evidence of nodal metastases.

He was asked to follow up after three weeks. During this period the patient underwent Whipple’s pancreaticoduodenectomy for his primary malignancy and subsequently advised chemotherapy. The specimen’s

pancreatic endocrine neoplasm with nodal meatstasis (PT3N1) (Figure 7). The retropancreatic resection margin showed the presence of a tumor thrombus in a vessel wall (Figure 8).

The patient came for follow up after a gap of four

with accurate projection of rays 0S and on examination the haemorrhages had partially resolved .There were no fresh retinal /choroidal lesions. At 8 weeks follow up ,a

(Figure 9). The patients visual acuity at the last follow up visit was 7/200 and he was on palliative chemotherapy.

DiscussionMetastatic tumors are the most common malignant

neoplasms of the eye8 with the choroid being the most common site for growth.

Intraocular metastases isolated to the retina are rare.9

was secondary to a gastroesophageal adenocarcinoma. In a historical review of retinal metastases, Pelzek and Schachat9

summarized the literature which at that time consisted of 20 additional cases of intraocular metastases localized to the retina and 4 cases of retinal metastases that were associated with additional intraocular metastases. There have been isolated reports of intraocular metastasis from pancreatic cancer11.12.All these patients had choroidal metastases.

The initial manifestation of the metastases in our case is of interest because of the presence of multiple intraretinal and subretinal hemorrhages with a larger preretinal bleed that while highly suspect in this patient with known disease, would have presented a greater diagnostic dilemma in a 52 -year-old man. In this case, it is reasonable to assume that a collection of cells with metastatic potential entered the retinal vasculature and that the hemorrhages resulted from their early disruption of the retinal microvasculature.

As there was no evidence of any choroidal metastases the patient was presumed to have isolated retinal metastasis due to tumor cell emboli which is a very rare entity. Morbidity and mortality from pancreatic cancer is conspicuously associated with metastasis; the most frequent sites of metastasis are local lymph nodes, lung, liver, adrenal glands, kidney and bones. Patients with pancreatic cancer have only very rarely been reported to develop metastatic lesions to the eye, brain, skin, and larynx .

To the best of our knowledge, this is a rare case of isolated retinal metastases of metastatic periampullary pancreatic endocrine carcinoma presenting as a large preretinal bleed presumed to be due to tumor cell embolism. This case highlights the importance of maintaining a high index of suspicion for metastasis in a patient with diagnosed carcinoma. Investigations must be tailored

able to institute appropriate palliative therapy as early as possible.

References

1. Berberat PO, Künzli BM, Gulbinas A, Ramanauskas T, Kleeff J, Müller MW, Wagner M, Friess H, Büchler MW: An audit of outcomes of a series of periampullary carcinomas. Eur J Surg Oncol 2009,35:187-91.

2. Diener MK, Knaebel HP, Heukaufer C, Antes G, Büchler MW, Seiler CM: A systematic review and meta-analysis of pylorus-preserving versus classical pancreaticoduodenectomy for surgical treatment of periampullary and pancreatic carcinoma.Ann Surg2007, 245:187-200.

3. Edwards BK, Howe HL, Ries LA, Thun MJ, Rosenberg HM, Yancik R,Wingo PA, Jemal A, Feigal EG: Annual report to the nation on the status of cancer, 1973-1999, featuring implications of age and aging on U.S. Cancer 2002, 94:2766-92.

4. Yendluri V, Centeno B, Springett GM: Pancreatic cancer presenting as a Sister Mary Joseph’s nodule: case report and updateof the literature. Pancreas 2007, 34:161-4.



5. Caricato M, Borzomati D, Ausania F, Garberini A, Rabitti C, Tonini G,Coppola R: Cerebellar metastasis from pancreatic adenocarcinoma. A case report. Pancreatology 2006, 6:306-8.

6. Hafez H: Cutaneous pancreatic metastasis: A case report and review of literature. Indian J Cancer 2007, 44:111-4.

7. Oku T, Hasegawa M, Watanabe I, Nasu M, Aoki N: Pancreatic cancer with metastasis to the larynx.JLaryngol Otol 1980,94:1205-9.

8. Castro PA, Albert DM, Wang WJ, et al. Tumors metastatic to the eye and adnexa. Int Ophthalmol Clin1982; 22: 189-223

9. Pelzek CD, Schachat AP. Retinal metastases. In: Ryan SJ, ed. Retina. St Louis, Mo: Mosby; 2001:608-616.

10. Smoleroff JW, Agatston SA. Metastatic adenocarcinoma of the retina: report of a case, with pathologic observations. Arch Ophthalmol. 1934;12:359-65.

11. Lin CJ, Yang CM, Chen MS. Intraocular metastasis of pancreatic cancer: report of two cases. Retina 2001; 21: 666-9.

12. Nagpal M, Nagpal K, Nagpal PN. Choroidal metastasis secondary to pancreatic carcinoma: a case report. AsiaPac J Ophthalmol 1998; 10: 30-2.

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Original article Case report Technique Photoessay Brief Communication Allied Ophthalmic Sciences Recent Advences


The corresponding author is required to sign the authorship responsibility, disclosures and copyright transfer form on behalf of all authors and send in the signed form ( by fax or email) to the Editor, Delhi Journal of Ophthalmology, Room No 479 4th Floor, Dr R P Centre, AIIMS, Ansari Nagar, New Delhi [email protected] SinhaEditorDelhi Journal of Ophthalmology



Delhi Journal of Ophthalmology accepts articles which are original and not being considered for publication in any other journal. All submitted manuscripts are subject

submit your manuscripts with a covering letter to the Editor of the journal.

Manuscript SubmissionAt Delhi Journal of Ophthalmology, we are soon

starting the online submission of manuscript, the information regarding which will be soon provided in DOS times, DJO and the website of DJO and DOS. Till date we have managed our relationship with authors on a personal level and authors have been sending their

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Authors are responsible for the content of material and views expressed in the manuscripts. Authors must

of interest (including sources of funding) should be summarized in a separate section of the published article.

of) must be declared in the ‘Disclosure’ section of the manuscript. The corresponding author of articles accepted for publication, will be required to send us a signed copyright transfer form on behalf of all the authors.

Policies on ethical conduct of research where articles include publication of original data related to human or animal experimental investigations, appropriate institutional review board approval is required and should be described within the article. For those investigators who do not have formal ethics review committees, the principles outlined in the Declaration of Helsinki should be followed. In attempting to maintain patient anonymity, identifying details should be omitted where they are not essential. However, patient data should never be amended

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Preparation of Manuscript

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Article

email

Original Article to be prepared under following headings Introduction Methods Results Discussion References and acknowledgements Legends for display items (Figures and Tables)

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appearance in the text, with a descriptive heading/ legend provided for each. Abbreviations and footnotes are to be placed immediately below the

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are NOT ACCEPTABLE.

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