Contents Amit Khosla Secretary, Delhi Ophthalmological Society 7 From the President Desk Dear...

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5 Editorial

Focus11 Amblyopia

Refractive Surgery

17 All Femtosecond Refractive Surgery

Sharad Lakhotia

Cataract

21 Current Status of IOL Power Calculations

S. Venkatesh

Glaucoma

29 Diagnostic Ability of GDx VCC for Glaucoma Diagnosis

Tutul Chakravarti

Cornea

37 Collagen Cross: Linking with Riboflavin (C3R for Treatmentof Keratoconus)Neera Agarwal

Neurophthalmology

45 Traumatic Optic Neuropathy

J.L. Goyal, Deepa Gupta, Ritu Arora

Oculoplasty

49 Vascular Lesions of the Orbit

Gaurav Bharti, Taru Dewan, Akhila Prasad, Shashi Vashisht

Clinical Monthly Meeting

55 Clinical Case -1: Congenital Glaucoma in a 5 Day Old InfantShivani Kochar, K.P.S. Malik, V.S. Gupta

59 Clinical Case -2: An Unusual case of Discharing SinusAniket Shastri, Anuj Mehta, KPS Malik, Sangeeta Abrol, Malvika Gupta

Miscellaneous

63 DNB Paper Cracked

69 Abstracts

73 Forthcoming Events

Columns

75 Membership Form

Contents

DOS Election

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

Secretary, DOS

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EditorialDear Friends and fellow Ophthalmologists,

Foggy mornings, delayed flights and everyone has a story to tell. Who sat longer in the plane beforetake off ? And the winner is…………! Actually this contest stands nowhere in front of “Who wereforced to deboard the plane” contest. And it was not funny. As a matter of fact, it was extremely painful.But sunny days are with us again. Merry sunshine and balmy weather. Delhi-at its best.At DOS we are continuously striving to innovate and do something more useful for the members.Training of residents and the young Ophthalmologist is an area ; where we are totally focused. TheDOST programme is a testimony to that, and it keeps on evolving.Solved Question Paper of The DNB exam: A team of experts has specially solved the previous year’s DNB question paper andwe are publishing it in this issue. I hope all the residents find it a useful adjunct, in their preparations.Mock OSCE:The highlight of this years DOST teaching weekend at R&R Hosp {13th and 14th Feb}. Another first on our part andour passionate hope that you will find it useful.Quest For Uniformity in training of Residents: Training programmes lack uniformity and vary in quality-and if a resident is notwell trained, he suffers due to none of his fault. We should rectify this and produce excellent young ophthalmologists; wellarmed and fully equipped to sail in the choppy waters of Ophthalmic Practice. “The boat rocks, but we row on.”The Next Level: It is now our endeavour to make fellowship and observership available to all residents who are DOS Members,in the various excellent Private Eye Hospitals and Institutes in Delhi. The DOS Mach 3 skill sharpener. We will definitely make thishappen. For all of you. For all of us.The Annual Conference:I hope the Pleasant Weather continuous till The Conference and all of us have a great conference. The theme is “OphthalmologyNow”.The focus: “Consensus building on Ophthalmic Controversies.”And above all: To give you a fantastic and memorable conference.Yours Truly.Thanking you,

Dr Amit KhoslaSecretary,Delhi Ophthalmological Society

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From the President DeskDear Friends & respected Senior Colleagues,

Warm Greetings. I’m indebted to you all, for the confidence & support reposedin me to carryout DOS activities. I congratulate Dr. R.V. Azad our pastPresident, who besides a great Ophthalmologist, a great motivator, protagonistfor equality for all, to be installed as President ‘All India OphthalmologicalSociety’. I also Congratulate Dr. Noshir Shroff for being awarded PadmaBhushan. I also congratulate other friends for attaining different milestonesin their professional and personal front.

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

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

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

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

Thanks,

Dr. Sharad LakhotiaPresident, DOS

[email protected]

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Amblyopia

Focu

s

AA: How do you define Amblyopia? Pit falls in its definition?

PS: The definition of Amblyopia includes unilateral or bilateraldiminution (not loss) of vision despite best refractivecorrection and excluding any media opacity or any organicpathology on the visual pathway. The difference of twolines on Snellen may be used for clinical purpose but forthe end point one has to ensure not only equal vision butalso equal (alternating) preference of fixation. Theunderlined words underline the common pitfalls.

SCD: Clinically amblyopia has been defined as unilateral orbilateral reduction in best corrected visual acuity caused byform vision deprivation and or abnormal binocularinteraction, without a visible organic cause commensuratingwith this visual loss. This significant reduction in correctedcentral visual acuity is labeled to vision less than 6/12 inbilateral amblyopia and a difference of two or more linesbetween normal and amblyopic eye in unilateral amblyopia,this is correctable, if appropriate measures are applied atappropriate time. However, amblyopia remains a diagnosisof exclusion.

AA: What is prevalence of amblyopia in your setting?

PS: The prevalence of amblyopia in our clinical practice is higherbecause of the referral nature. In the general population itshould be about 5% or more.

SCD: We see 4-5 cases in each OPD of around 100 patients and20-30% patients in squint clinic are amblyopic.

AA: How do you diagnose Amblyopia and what are difficultiesand pit falls encountered during diagnosis?

PS: The diagnosis of amblyopia differs in the different agegroups. In the literate children the letter charts are used, inyounger children the E or C charts are used and in stillsmaller (preverbal children) we depend on indirectly lookingfor the amblyogenic causes. So if there is an esotropia orvertical squint one should suspect it. Also the use ofBruckner’s red reflex should be made to look for the mediaopacity, refractive error or squint. It is then furtherconfirmed with the help of noticing the preference offixation behavior. An observation of central/ eccentric,steady/unsteady and maintained/not maintained fixation,semi-quantifies the fixation.

One has to always look at the fundus and rule out anyorganic fundus pathology. Any purported diminution ofvision due to amblyopia should be supported by anamblyogenic cause and the diagnosis of amblyopia shouldbe the last diagnosis.

SCD: It is not uncommon to see clinicians getting puzzled over thediagnosis of a case of diminution of vision. In Indiancircumstances, the inadequate history and hurried decision

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

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

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

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

Dr. Subhash C. Dadeya MDProf. Pradeep Sharma MD

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on part of clinician due to increased patient load leads tomore confusion, the cause may be pathogenic rather thanfunctional. It is important to remember that diagnosis ofamblyopia is incomplete until following conditions are fulfilled

1. Evidence of reduced visual acuity usually unilateral but maybe bilateral

2. Presence of amblyopiogenic factor e.g. strabismus, unequaland uncorrected refractive error of a significant degree,any evidence of obstacle to vision (e.g. visual deprivation)by way of congenital cataract, ptosis, corneal opacity, anduncorrected aphakia in a child in amblyopiogenic age group.

3. No alternate explanation for visual loss

Amblyopia is diagnosed, when the criteria are met andcause is identified. It is our duty to ensure that it is detectedat the earliest so that therapy can be started immediatelyfor the maximum benefit to the patient. The diagnosticfeatures of amblyopia are.

1. Confirm the diminution of vision

1a) The hallmark of amblyopia is decreased foveal acuity.Most clinical studies have defined unilateralamblyopia as a minimum of two-line differencebetween eyes on snellens chart/2-octave difference bypreferential looking method

For bilateral amblyopia the visual acuity should beless than 6/12 in each eye. The amblyopia treatmentstudy (ATS) defined amblyopia as visual acuity of20/40 or worse with at least 3 Log MAR line differencebetween the eyes

In children it is difficult to determine visual acuityand there is debate which method should be used tomeasure visual acuity at which ages. However, it iseasier in cases of unequal vision as child resist closureof better eye.

1b)Stereo acuity- Any defective stereopsis indicatesfurther investigations for strabismus and amblyopia.

2. Fixation reflex

One of the most commonly used clinical method fordiagnosing amblyopia in preverbal children is subjectassessment of fixation response as described by Zipt.The presence of alternate fixation rules our amblyopia.However, preference of fixation for one eye suggests poorvision in other eye in presence of squint. Furthermore,behavioral response to unilateral occlusion is anothercommonly employed method for amblyopiaassessment. The child resists occlusion of sound eye, butwill not care, if amblyopic eye is covered. A central, steadyand maintained fixation in each eye implies good visualacuity in each eye

Fixation preference testing remains one of the mostvaluable clinical methods for diagnosis and follows upof amblyopic patients and should be practiced by allophthalmologist to assess vision in infants and preschoolchildren.

3. Crowding phenomenon

Although not specific to amblyopia, it may be morepronounced in amblyopic eye compared to better eye.Presence or absence of crowding phenomenon hasprognostic implication. This difference between linearand isolated acuities should be noted at each visit. Thisdifference is a way of quantifying the depth of amblyopiafrom visit to visit. Furthermore near visual acuity ismore reliable indicator during amblyopia therapy asnear acuity often improves faster than distant visualacuity.

4. Effects of neutral filter

If we apply neutral density filter before normal eye, itleads to decrease in visual acuity however, if we applyneutral density filter before amblyopic eye, the visiondoes not decreases on the other hand it might improve.That means amblyopic eye act under mesopic conditions.

5. Colour vision

Color vision is usually normal in amblyopic eye. It isabnormal only in dense amblyopia and that tosecondary to reduced vision or eccentric fixation.

6. Contrast sensitivity

Strabismus or anisometropic amblyopia show contrastsensitivity loss affecting cither all spatial frequencies orlimited to high spatial frequencies. There is loss of highfrequencies in stimulus deprivation amblyopia. Contrastsensitivity improves during amblyopia therapy and canbe used to monitor progress.

7. Accommodation

Accommodation has been found to be normal orreduced in some amblyopic eye. However, visual acuityto near fixation has been found to be better than atdistance

8. Fixation pattern

Eccentric fixation is characteristic of amblyopic eye andis usually seen in 23-89%of patients

ii) Search for amblyopiogenic factors

Search for amblyopiogenic factors is a useful strategy forearly detection of amblyopia, even when vision recordingand detailed examination is not possible. Presence ofunilateral congenital cataract, ptosis or other mediaopacities may have high amblyopiogenic tendency,bilateral cataract and opacities and opacities should nobe ignored. Presence of high refractive error especiallyhypermetropia of more than 3.5 diopter and astigmatismof >1.5 diopter should to taken as suspicious of amblyopia.Presence of microtropia and small angle esodeviationsare also associated with amblyopia in significant numberof cases. Corneal reflex test & Buckner’s reflex tests arethe methods, which can be applied to assess amblyopiaindirectly & unilateral amblyopia is usually associatedwith strabismus (esotropia more commonly compared to

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Exotropia), visual deprivation (ptosis, corneal opacity/scarcataract and vitreous hemorrhage), or refractive error(Hypermetropia >3.5 Diopter & Astigmatism >1.5Diopter). Similarly bilateral amblyopia is also associatedwith refractive errors and visual deprivation. If noplausible evidence for amblyopia factor is seen reconsider,your diagnosis of amblyopia.

Ruling out alternate causes of visual loss

Complete ocular examination by means of proper historyand examination is mandatory to rule out any organiclesions like macular pathology, optic nerve or retinal diseasesbefore making diagnosis of amblyopia .However, twoconditions may coexist. Fundus examination is must .ifuncertainty persists, a trial of occlusion for 3-4 weeks is worth.

AA: How do you Classify amblyopia and which sort ofamblyopia do you see most commonly?

PS: The classification of Amblyopia used is based on theetiology.

(A) Refractive Error

� Iso-Ametropic (Bilateral uncorrected orundercorrected ref. error)

� Anisometropic (unilateral or asymmetric uncorrectedor undercorrected ref. error)

This would include hypermetropia (over 1.5Dsph),astigmatism (over 1Dcyl) or myopia (usually more than–3or -4 Dsph)

B) Strabismus: usually esotropia, even of smaller angles(microtropia), vertical deviations and very rarely exotropia.In case of the latter one should exclude associated refractiveerrors, vertical deviation or subclinical organic pathology

C) Stimulus deprivation or media opacities

D) Organic: Subclinical foveal malfunction or malorientationof cones: this is usually considered if the vision does notimprove despite proper occlusion.

In addition one should keep in mind the possibility of mixedetiology, as also the overlay of true amblyopia over theorganic pathology compromising vision.

The most common type encountered is anisometropicfollowed by strabismic.

SCD: � Strabismic

� Anisometropic

� Deprivation

� Isometropic

� Idiopathic

� Organic

� Hysterical

� Meridional

Anisometropic amblyopia is most commonlyencountered in our clinical practice; however strabismicamblyopia is detected at the earliest.

AA: What is Your 1st line of Therapy in amblyopia?

PS: The first line is removal of the amblyogenic cause withocclusion as per age. So along with proper glasses as thecycloplegic assessment, occlusion is started: patching thegood eye more than the amblyopic eye, alternating as perage in ratio 2:1, 3:1, 4:1, 5:1, or 6:1 respectively for age under2 year, 3 year, 4 year, 5 year, 6 year and above 6 years.

SCD: Full time occlusion is my preferred treatment modality intreatment of amblyopia

AA: Does refractive correction has any role in treatment ofamblyopia and what amount of refractive error if notcorrected is amblyogenic?

PS: Refractive correction is the foremost part of amblyopiatherapy as it is also the most common culprit. Glassesalone also work but occlusion makes it work faster.Uncorrected refractive error not leading to amblyopia maybe +1.5D sphere or +1.0D cylinder and -3.0D sphere. Butalso keep in mind an un-or under corrected hyperope mayexercise his / her accommodation to develop anaccommodative esotropia to suffer from strabismicamblyopia also.

SCD: Refractive correction alone improves visual acuity in at least25-33 % patients in cases of anisometropic amblyopia. It ismandatory to carry out cycloplegic refraction in every case ofamblyopia and proper optical correction should beprescribed in every case of amblyopia .1% atropine inchildren less than 7 years of age and 1% cyclopentolate inolder children are used by authors to carrying out therefraction in their routine practice .ATS-5 Eye glass phasehas concluded that amblyopia improved with opticalcorrection by more than 2 lines in 77% patients andamblyopia resolved with optical correction in 27 % patients.

Hypermetropia >3.5 Diopter & Astigmatism >1.5 Diopterand myopia of more than 5 diopter are amblyogenic.

AA(a): What is the role of occlusion in treatment of amblyopia?

PS: Occlusion is the main part of amblyopia therapy.

SCD: There is neither a substitute nor a shortcut for full timeocclusion in the treatment of amblyopia despite recentrecommendation of amblyopia study group. Occlusiontherapy prevents the fixating eye from taking part in the actof vision so that the patient is forced to use the amblyopiceye.In addition, it removes the inhibitory stimuli toamblyopic eye that arise from stimulation of the fixatingeye

AA (b): Which schedule of occlusion does you advice?

PS: The schedule used is described in Answer to Q.5Undoubtedly the full time patch with good compliance isthe most effective and rapid, Recourse to part-time patchcan be made in moderate amblyopia or partially recoveredamblyopia to maintain the visual gains, or in situations


where compliance to full-time patch is not possible. In thelatter situation the fact that a compromise is better than notreatment is to be understood.

SCD: We prescribe occlusion according to the thumb age rule. Inchildren of 0-1 year of age, we occlude the better eye forthree days and amblyopic eye for one day. In children of 2-3 years of age, we occlude the better eye for 4 days andamblyopic eye for one day. In children of 4-6 years of agewe occlude the better eye for 5 days and amblyopic eye forone day . In children of more than 6 years of age weocclude the better eye for 6 days and amblyopic eye for oneday. Once occlusion therapy has been initiated, the childmust be reexamined at frequent intervals for several reasons

AA (c): When do you stop occlusion?

PS: We continue occlusion (full time) till full visual improvementhas occurred as evidenced by Snellen’s vision no furtherimprovement in two consecutive monthly visits. One mayswitch to part time patching and finally weekly patching asage advances, and continue till 9th birth day to checkregression. Monitoring from time to time is worth its while.

SCD: 1. The occlusion can be stopped ,when acuity becomesequal in both eyes

2. When there is true alternation of fixation

3. There is no visual improvement after 3-6 months ofocclusion despite good compliance (depending on theage of patient).

AA (d): What are adverse effects of occlusion seen in your setting?

PS: The risk of occlusion amblyopia is rare with the age relatedalternating regime also because we follow-up with timelymonitoring. If it occurs and is detected timely it can beeasily reversed.

SCD: � Occlusion amblyopia

� Constant manifest déviation

� Psychological problems

� Diplopia

� Increase in angle of deviation

� Skin rash

AA (e): Is minimum intensity patch as effective as full time patch?

SCD: No atleast not in our experience. However, amblyopiatreatment study 2 was initiated to address followingquestion

1. Is minimal intensity patching (two hours/day) as effectiveas moderate intensity patching (6 hours day) in treatmentof moderate amblyopia (20/40 to 20/80)?

2. Is full time patching (all waking hours) more effective thanpart time patching (6 hours /day) in treating severeamblyopia (20/100to 20/400) ?

3. What is recurrence rate and what are the factors influencingrecurrence after cessation of therapy in successfully treatedamblyopia?

and it was concluded through intermediate reports thatminimal patching (2 hours / day) is as effective as moderatepatching (6 hours/day) in treatment of moderate amblyopiaand prescribing greater number of hours of patching does notseems to have significant effect during first four months oftreatment.

AA: What is the role of penalization in amblyopia therapy? Ispenalization as effective as occlusion?

PS: Penalization is an effective alternative in select cases andneeds to be individualized depending on the refractiveerrors of the two eyes and associated esodeviation if any. Afixation switch “needs to be established for its effect. It maybe done with atropine ointment used hs in cases ofhyperopes or with over plus glasses in low hyperopes ormyopes. The former penalizes for near and latter fordistance. Both may be combined in select cases. Usuallypenalization in the form of atropine or partial blurring byscotch tapes or transparent nail-varnish is used formaintenance therapy.

SCD: We are of the opinion that occlusion remains gold standardin the treatment of amblyopia and penalization can be triedas an alternative line of therapy in patients of occlusionfailure, or as maintaince therapy.

In view of the difficulties encountered with occlusion therapyin some patients and the occasional complication ofocclusion amblyopia, alternative therapies have been tried.Penalization is therapeutic technique performed by opticallydefocusing the eye with better vision by using cycloplegicsor by altering the eyeglass lens to cause decreased vision innon amblyopic eye; it may be either pharmacological oroptical. Penalization has the advantage being cosmeticallyacceptable, but it does not inhibit the abnormal binocularinteraction, which is the essential cause for amblyopia. It rarelydecreases the vision of the good eye, below that ofamblyopic eye: therefore, its indication is limited:

1. Moderate amblyopia in uncooperative patients

2. Anisometropic amblyopic eye

3. Maintenance therapy

4. Occlusion failures

5. Nystagmus

Amblyopia treatment study was initiated to address whetherocclusion or atropine penalization is best initial, treatmentfor moderate amblyopia (20/40-20/100) and it was concludedthat both the treatment were well tolerated and the effect ofeach treatment seemed consistent. Patching has a potentialadvantage of a more rapid improvement in visual acuity andpossibly a slightly better acuity outcome, whereas atropinehas the potential advantage of easier administration and lowercost. Atropine or patching for 6 months period produced asimilar improvement in amblyopia 2 years after the treatment.

However, there are certain drawbacks of ATS, so beforeapplying these conclusions in Indian circumstances, we haveto keep in mind the following limitation of ATS.

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1. The strict inclusion criteria hampered the study byincluding a limited number of patients.

2. Methodology was not strict, thereby making the resultssubject to many questions.

3. Ethnic variation to treatment always remains a factor,so the results cannot be generalized to other countries.

4. Is atropine safe in tropical countries.

5. Compliance was not monitored objectively in PEDIGand therefore makes it harder to interpret the result.

6. ATS-I did not answer the effect of atropine on fusionand stereopsis as the patients were under the effect ofthe drug at the time of final examination. The differencein the visual input from the two eyes has been shown toreduce fusion and stereopsis this may be a potentialdisadvantage with atropine.

7. In ATS there was selection bias as limited centers wereincluded.

8. There was a lack of an untreated control group

9. Improvement in visual acuity may have been due tolearning and adaptation

These are the valid objections and should be taken intoaccount before applying recommendations of ATS

Despite all the benefits of penalization its majordisadvantages include:

1. Active inhibition is not eliminated

2. The risk of occlusion amblyopia persists

3. Cost of drugs

4. Injury with drug vial

5. Allergic reaction to drugs

AA: What is the role of near activities in treatment ofamblyopia?

PS: The role of near activities in treatment of amblyopia is asimportant as occlusion therapy. It may be said that HomeActive Vision Exercises (HAVE to be done!), be it for nearlike reading, writing, drawing or playing video games oreven distance – watching good (approved by mothers!)programs on television.

Along with proper glasses and occlusion HAVE is the mosteffective way of treating amblyopia. Whether one uses thecomputer games at home or office / clinic, obviously theformer is better as it can be done for more time and daily,provided somebody ensures regularity.

SCD: It has been suggested that near activities like threading beads,tracing pictures and reading fine print plays a significantrole in the improvement of vision in amblyopia and childrenshould be encouraged to do near activities. Park et al studiedthe outcome of part time occlusion combined with nearactivities and found that combining the near activities withocclusion causes improvement in vision. We are conducting

a research project titled Role of television exercises as aform of near vision activities and initial results areencouraging.

AA: Is there any role of LASIK surgery in amblyopia and doyou have any personal experience?

PS: The role of LASIK surgery in cases of high unilateral myopiaor high anisometropia is worth while, but this should bedone preferably after the amblyopia is treated with glassesand occlusion and also after establishing the stability of therefractive error over two-three years. This would help inrehabilitation if high unilateral refractive errors and preventthe regression of amblyopia therapy.

SCD: Refractive surgery in children to reduce the amblyiopiogeniclevel of refractive error is proving to be relatively stable.Recently Astle et al. have described that LASIK is an effectivesurgical alternative to improve visual acuity inanisometropic amblyopia treatment or in whom othertherapy fails. However, we are of the opinion that Lasikshould be used as a last resort to treat only desperate casesof amblyopia. Idonot have any personal experience of usingLasik for amblyopia.

AA: Is it mandatory to treat amblyopia prior to surgery?

PS: Amblyopia therapy should always be treated prior tosurgery as it is easy to monitor, convince the patient andparent and maintain their compliance prior to surgery.Moreover there is a risk of recurrence of squint due toocclusion therapy in some cases if is done after surgery.Further the success of squint surgery is better in treatedcauses of amblyopia, as harmony is better establishedamongst the equals!

It has been traditionally taught that treatment of amblyopiashould be done prior to surgical intervention. Surgery mayhave to be postponed till completion of amblyopia therapyresulting in its delay for months or year in intractableamblyopia, thus depriving the benefits of early surgery tothese patients. Lam et al. have suggested that performingsurgery before the completion of amblyopia therapy doesnot affect the motor or sensory outcome adverselyprovided amblyopia therapy is continued postoperatively.Hence, the question that arises is why wait till completionof amblyopia therapy and deny the benefits of early surgeryto these patients?

We conducted a study to resolve this issue and concludedthat it is not mandatory to treat amblyopia prior to surgeryif amblyopia therapy is continued postoperatively, unless itis a case of infantile esotropia with moderate amblyopia.

AA: How do you record vision in a case of amblyopia withnystagmus and how do you treat it?

PS: For recording of vision in cases of nystagmus one has tokeep in mind two things (a) null position if any as vision isbest in this position, but also check the vision in primaryposition to know the deterioration (b) Latency ofNystagmus: in manifest latent nystagmus (MLN) when thebinocular vision is better that monocular vision in eithereye. If that be so, reassess the monocular vision with +6.0Ds lens to fog the other eye.


Conventional occlusion (patching the dominant eye) canstill be used in amblyopia associated with MLN. The visiondeteriorates initially but gradually even the nystagmusbecomes better as vision recovers.

SCD: Visual acuity testing in nystagmus requires blurring of othereye with high plus lens (plus 6 diopter lens.) visual acuityshould be measured separately in each eye. Testing ofbinocular vision and near vision is mandatory inpatientwith nystagmus.Visual acuity should be tested using sameparameters at each visit

If nystagmus is idiopathic infantile, then the patient has totreated in a conventional way. However, in manifest latentnystagmus, partial patching doesn’t work and full timepatching is required, but, we have to keep in mind thatoccluding one eye makes the nystagmus worse. Hence,atropine has been suggested as an alternative to a skinoccluder, but it is usually less effective.

AA: What are the prognostic considerations in treatment ofamblyopia?

PS: For prognosticating the amblyopia therapy the factors are(a) presenting vision (b) age at treatment and (c) complianceand motivation of the patient to do amblyopia therapy.Counseling the patient and parent and proper monitoringhelps in improving the prognosis. Assessment of near visionas also single letter acuity vs line acuity helps inprognosticating the recovery of vision as also reinforcingthe success to the patient. The speed of reading is a veryuseful tool of assessment in monitoring progress.

SCD: Success of occlusion therapy depends upon several factors,which should be kept in mind while treating amblyopia

1. Age of patient, younger the child better the prognosis,however it depends on duration of amblyopiogenicexperience

2. Types of amblyopia: Occlusion is most effective in strabismicamblyopia, because it is detected early. Stimulus deprivationamblyopia has the poorest prognosis. Anisometropicamblyopia had prognosis somewhere in between.Hypermetropic anisometropia has a poorer prognosis incomparison to myopic anisometropic amblyopia.

3. Treatment duration: ATS, found no relationship, betweenhours of treatment prescribed and final visual acuityoutcome.

4. Pretreatment visual acuity: If the pretreatment visual acuityis comparatively good, visual prognosis is better, due tobetter patient compliance to occlusion treatment .However;initial poor vision does not necessarily mean a poorerprognosis.

5. Type of occlusion: Conventional full time occlusion of thebetter eye is preferred and gives better result as comparedto part time and partial occlusion.

6. Types of fixation: Amblyopia with foveal fixation respondsmore quickly to therapy and the success rate is better thanthat with eccentric fixation.

7. Type of occluder: If the proper occluder is not prescribed, itmight compromise the prognosis. An adhesive skin patchis always preferable

8. Near exercises: Occlusion treatment augmented with nearvisual exercises such as threading, beads tracing and readingfine prints is considered to hasten visual improvement andshould be advised. Although this aspect is under study byATS, initial results are promising, long-term results are notknown.

9. Patient compliance: Compliance is the most important factorfor occlusion treatment to be successful, better thecompliance, better the result

10. Presence of astigmatism: The patients with presence ofsignificant astigmatism (>1.5D) are less likely to achievesuccessful outcome

11. Method of treatment termination: The method ofterminating occlusion treatment affects prognosis inamblyopia, ATS found that when occlusion is applied for 6or more hours, there is less likely regression of visual acuitycompared to 2 hours of patching, and when it is stoppedabruptly.

12. Previous treatment: Although, some studies report thatpresence or absence of previous treatment has no effect onamount of visual acuity improvement achieved. Otherstudies reports that a new treatment‘s outcome may simplyconstitute reestablishment of the previous regimen’soutcome, thus compromising maintaince.

13. Refractive correction: The effect of refractive correctionneeds to be controlled for evaluating any other amblyopiatreatment, because, if refractive correction is improper, theefficacy of treatment is reduced

AA: What are differential diagnoses for amblyopia?

PS: The differential diagnosis of amblyopia in the form oforganic pathologies should be recognized in the initial visititself to prevent forcing an unnecessary occlusion on a child.But the fact that a concurrent functional amblyopia may beover-riding an organic pathology, mandates an occlusiontrial for a few weeks. In cases of failed occlusion therapydespite good compliance on two successive visits, oneshould rule out sub-clinical macular degeneration byelectrophysiological tests.

SCD: � Functional causes

� Strabismic

� Strabismus

� Refractive

� Uncorrected anisometropia

� Combined aniso-strabismus

� Uncorrected astigmatism

� Irregular astigmatism

� Visual –deprivation cause

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� Occlusion amblyopia

� Early complete bleopharoptosis

� Congenital cataract

� Corneal opacity

� Psychogenic cause

� Hysteria

� Malingering

� Structural / Pathological causes

� Vitreous Hemorrhage

� Fundus coloboma

� Medullated nerve fibres

� Hypoplasia of optic nerve

� Keratoconus

� Macular pathology

� Optic atrophy

� Retrobulbar neuritis

AA: Have your treatment plan changed after report ofamblyopia treatment study groups recommendations?

PS: The recent ATS by PEDIG and our own studies on the roleof atropine penalization and part time occlusion hasprompted us to use these two modalities in moderateamblyopia and recovered amblyopia for maintaining andpreventing recurrences as well as in poor compliant cases.

SCD: No

Kindly send New E-mail address for DOS Correspondence

Email: [email protected]

DOS CORESSPONDENTAshish Amar MS, FRCS, DNB

Online Journal AvailableOnline Journal AvailableOnline Journal AvailableOnline Journal AvailableOnline Journal Available

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

E-mail ID is: [email protected]

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

17www.dosonline.org

Femtosecond is an ultrafast laser generating pulses as short asone quadrillionth of a second (10-15). The world Femto came

from Danish word for number 15.

It uses infrared beam to separate tissues by photo disruption.

All Femtosecond Refractive Correction

Femtosecond lenticule extraction or FLEx using Visumax (CarlZeiss meditec, Jena Germany) have reported excellent results fortotal refractive correction. INTRACOR procedure also usesFemtosecond laser to interact with stroma to give vision correction.

Lenticular Extraction with Visu Max Femtosecond laser

Dr. Walter Sekundo & Dr. Marcus Blum were first surgeons toperform this procedure in August 2008. Over 1000 eyes have beenoperated till now at all centres including one at Baroda run by Dr.Rupal Shah besides 3 other international sites. In FLEx treatment,Femtosecond laser creates two cuts, a refractive and a non-refractive as a single step. The first cut is made at the bottom ofthe refractive lenticle while the second one at its roof. Once thecuts are made, flap is lifted and refractive lenticule is removed.The flap is reposited in usual manner. It is important to makemanipulation at correct plane between flap & lenticule and separatelenticule edge.

The lenticule can be of different diameters from 6mm to 7.3 mmequivalent to optical zone of Excimer laser. The remaining stromalzone is usually 300 micron or more.

Walter Sekundo reported good results in 6 months follow up. 9%gained 2 lines of visual acuity, 43% gained one line, 39% remainunchanged and 7% lost one line visual acuity. 74% patients were 6/6 or better.

Dr. Rupal Shah reported slow visual recovery at 1 week butchanging scanning pattern produced good results. While scanningin spirals, they used to cleave posterior surface of the lenticulefrom centre to periphery. The flap was then cleaved from peripheryto centre. They changed direction i.e. posterior surface of lenticulewas separated by scanning from periphery to centre and anteriorsurface from centre to periphery. This led to dramaticimprovement in visual recovery. 89% reached to pre operativeBCVA after 1 week. With upgraded 500 Hz Visumax, 95% reachedor improved to pre- operation BCVA level at 1 week.

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

Osama Ibrahim reported 90% of patients having better than 20/25visual acuity after one month. He is of the opinion that results

All Femtosecond Refractive SurgerySharad Lakhotia MS, CAMS

Lakhotia Eye Centre & Laser Institute

E-544, Greater Kailash Part-II, New Delhi

with this procedure are more stable than Lasik including highmyopia patients. If the lenticule is dissected above, then it is veryeasy to identify inferior surface by having enough resistance andempty spaces. Once dissected, it is very easy to lift flap by simplepull with forceps or spatula.

Journey from Flex to smile is easy and has advantage of smallincision thus providing all Femtosecond laser solution to refractiveproblems.

Initial results with hyperopia suggest FLEx can be a good option.There was some regression as with Eximer laser but data at 1month interval was great. In hyperopia, the flap is just 0.5mmlarger in diameter then the lenticule. The main point forconsideration is that lenticule should not have sharp edge otherwise it will result in regression. So the main challenge is to find anoptimal form for lenticule edge.

Complication

They were minimal. Mild transient haze like reaction andmicrostria were reported which cleared. There were some problemsin separating the refractive lenticule in 2 cases of which one resolvedafter 6 months. However no patient showed signs of diffuselamellar keratitis or transient light sensitivity syndrome.

Benefits of Visumax System

While designing Femtosecond laser a balance has to be keptbetween increasing pulse rate and focusing power & decreasingspot size & energy. The optics of Visu Max produce tightly focusedbeam with following effects.

Visumax Femtosecond Laser(Carl Zeiss Meditec AG, Jena)

Refr

activ

e Su

rger

y


(i) The accuracy of pulse placement is optimized.

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

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

Some Femtosecond lasers require scleral suction & flatapplanation. High suction in such cases can cause discomfort &subconjunctival hemorrhages. In Visumax the rise is intraocularpressure is low enough for patients to see & does not discomfortthe patient. A curved contact glass and corneal suction allows IOPbelow 90 or 100mg. In one study rise in IOP during flap creationwas 84.9 ± 7.3mmHg for Visumax, 180.6 ± 21.6 mmHg for intralaseand 150.9 ± 17.2 mmHg for LDV. Thus anxiety level of patient isless, patient can visualize fixation light and so better fixation isachieved during treatment.

Flap centration on corneal vertex is well achieved as it was intendedfor FLEx procedure. The vertex of cornea fit well in to vertex ofcontact glass of Visu Max Femtosecond laser. The problem ofopaque bubble layer is very thin as it dissipates very rapidly. WalterSekundo considers this to be standard procedure with potentialto revolutionize the course of refractive surgery.

INTRACOR procedure:- is an intrastromal procedure done onTECHNOLAS Femtosecond work station. It applies energy insidethe cornea without bringing it to the surface. There is no incisionof epithelium, endothelium or Bowman’s or Descemet’smembrane and thus ensure better healing with minimal risk ofinfection. The pulses are placed on concentric intrastromal circlescentered about visual axis and extended at least up to 100 micronsfrom the surface. The concentric patterns of cut fibers shift thecentre of cornea slightly anteriorly and create a hyperprolateshape. At present myopia up -3D and astigmatism up to 2D have

FLEx procedure in stages

been tried. However the results are not very accurate. Also itsrole in presbyopia has been emphasized as it causes a biomechanicalchange in cornea that shifts centre slightly forward creating apattern of hypersphericity thus allowing some near vision whileretaining distance vision.

The surgeon can expand circle diameter or add radial intrastromalincision similar to those created in radial Keratotomy and iseffective in biomechanically correcting small degree of myopia.

INTRACOR brings hope for correcting presbyopia with lowrefractive errors by biomechanical methods.

Thus Visumax Femtosecond has shown a great stride as analternative as all Femtosecond laser option for all refractive errorswith small incision lenticular extraction.

AuthorSharad Lakhotia MS, CAMS

21www.dosonline.org

In modern day ophthalmic practice the buzz word seems to beprecision. Precision with a view to achieving perfection and one

the greatest challenges to this quest is the restoration of normal ornear normal vision after cataract surgery. This could only be possibleif we had the ability to predict the power of the IOL with anunprecedented degree of accuracy.

The Past- Educated Guesses

But thirty years ago, before 1980s, IOL power calculations couldbe at best described as educated guesses based primarily andsolely on the patient’s previous refractive status before the onsetof cataractous changes. If the patient was an emmetrope beforethe onset of cataractous changes then he received an ‘Idem lens’.

The IDEM Lens

The IDEM lens or the “ideal emmetropia lens”, was that IOL powerwhich when implanted within the eye restored emmetropic statusafter cataract surgery. The power of this lens was mathematicallydeduced to be +17.0 D for an AC lens, +19.0D for an iris fixatedlens and +21.0D for a posterior chamber lens.

The Standard lens

Since the preferred practice pattern at that time was to make thepatient myopic by about 1.0D, in order to strike a balance betweendistance and near vision, a “Standard Lens” was implanted. Thislens had +1.25D added to the IDEM lens power, this add being theadjustment for moving the 1.0 D of myopia from the spectacle tothe IOL plane.

The Emmetropia lens

If the patient had previous ammetropia, he received an“Emmetropia Lens” which would effectively take care of the preexisting error and restore the patient to an emmetropic statusafter cataract surgery. The power of such a lens was calculated bymultiplying the pre existing refractive error with a conversionfactor of 1.25 and algebraically adding it on to the IDEM lenspower.

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

• 3.0 x 1.25 = 3.75.

• Idem lens power for a PC IOL = 21.0D

• Emmetropia lens power = 21.0 + (-3.75)

• = +17.25D.

Current Status of IOL Power CalculationsS. Venkatesh MS, FICO, FRCS

In a similar fashion a “Standard Emmetropia” lens power can becalculated by adding +1.25D to the calculated power of anEMMETROPIA lens to restore emmetropia.

Educated guesses – not good enough!

With these crude types of calculations, ophthalmologists werehappy if they achieved post operative results within 1.0D of targetedoutcomes. However in the present scenario when we are dapplingwith multifocals and offering accomodative IOLs that cost abouta lakh of rupees we need to be able not only to achieve muchgreater levels of precision but also be able to achieve this precisionconsistently.

The IOL power prediction formulae:

To achieve greater levels of accuracy in predicting IOL power thatwould result in desired post operative spherical outcomes, 4generations of IOL formulae were enumerated.

• First Generation - were the SRK- 1 and the Binkhorst formula.

• Second Generation – SRK-2

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

• Fourth Generation – Hollday 2, HAIGIS.

Broadly speaking these formulae could either be ‘Theoreticalformulae’ which are based on mathematical principles revolvingaround the ‘schematic eye’, or they could be ‘regression formulae’which were arrived at by looking at post operative outcomes andworking backwards in what is known as the regression analysis toorder to arrive at the IOL power. The Third and fourth generationformulae incorporate a bit of both which was called the “Fudgefactor” by duke elder.

Old No. 21, New No. 3, ‘TUSHARA’

Navarathna Gardens, Ekkaduthangal,

Chennai, Tamilnadu

Figure 1: Dual Lens System

Cata

ract


Understanding how these Formulae Work- Basic Facts

Before we unravel the complexities enshrouding the various IOLformulas we need to take a look at some basic facts. The normalhuman eye has two refracting surfaces – the cornea and thecrystalline lens. The aqueous and the vitreous serve as a uniformconducting medium having a RI of 1.337

Therefore the human eye functions as a dual lens system. In anydual lens system if the primary or the objective lens as well as thedistance of the focusing screen are fixed – then the effective powerof this system of lenses will depend on the power and the positionof the second lens. Let us say that for a given power of the secondlens the light get focused on the screen. If this secondary lensmoves towards the primary lens its effective power is increasedand the light will focus in front of the screen and if it is movedaway from the primary lens its effective power is decreased andnow the light will come to a focus behind the screen. In the normalPhakic eye the position of the cornea and the retina is fixed andthe effective power of the eye is increased, as say, duringaccommodation not by changing the position of the crystallinelens but by increasing its curvature. But this is not the case in aPseudophakic eye. In a Pseudophakic eye the effective IOL powerwill not only depend on the IOL power printed in the label of theIOL box but also upon where it is positioned within the eye.

Assimilating this fact we understand that the effective power of anIOL will depend on its position within the eye. In fact the veryconcept of an IOL power is rather a relative phenomenon. Forexample if the calculated power for an “in the bag” IOL is 21.0Dand during the surgery you end up placing it in the sulcus with ananterior displacement of 0.5mm, its effective power will increaseand it will function as a 22.0 lens leading to a myopic shift in thepost operative period. Similarly if you change the model of yourIOL and implant a lens with a 10 degree angulation into the bagwhich may produce a 0.5mm shift posteriorly then the effectivepower of the lens will decrease and it will now behave like a 20.0Dlens leading to a hyperopic shift. The message in this explanationis that although the power of the IOL is function of the cornealpower and the axial length, its effective position within the eyewhich is known as the ELPo or the effective lens position -a term

coined by Dr. Jack Holladay will also play a pivotal role indetermining its power. In fact the strength and predictability ofthe various IOL formulae depends upon their ability to accuratelypredict the ELPo

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

THE ELPo

There are several factors that will influence the ELPo.

Anatomical factors: like the axial length, the steepness of the cornea(average K), the limbal white to white measurements, the pre-operative anterior chamber depth and the lens thickness. In factone large group study conducted by Dr. Haigis showed that theposition of the capsular bag equator from the corneal vertex canbe arrived at by adding the pre op ACD and 40% of the crystallinelens thickness. Dr Holladay showed in his study that the depth ofthe anterior chamber had a positive and partial relationship to thelimbal white to white measurement (avg.11.7mm). The 1st and2nd generation IOL formulae tried to predict the ELPo based onanatomical factors alone.

IOL and surgery related factors: The shape, the length, the flexibility,the anterior angulation if any and the material of the haptic of theIOL will affect the ELPo. The shape and design and the material ofthe optic will also have a profound effect. Certain lenses like the‘Acrysof ’ hydrophobic lenses and the ‘Technis-One’ lenses have anegative shape factor because of their asphericity. In these lensesabout 80% of the principle plane of the IOL power is situated closeto its posterior surface which is why these lenses have a higher Aconstant of 118.8 in contrast with the biconvex, non aspheric designof hydrophilic acrylic and silicon lenses where the principle planeof the IOL power is closer to its midpoint and anterior surfacewhich explains why their A constants are close to 118.0 for thesame in the bag implantation.

Individual Surgeon’s Technique: in addition the surgeon’s individualsurgical technique can also influence the ELPo;

The most important surgical factor is the manner in which youfashion the CCC with respect to its size and centration; this isbecause the ELPo is directly related to the post operative positionof the capsular bag equator. Too large a CCC will allow the opticto prolapse out of the bag increasing its effective power. The idealCCC should overlap the optic and keep it in place. Capsular fibrosiswill cause the forward movement of the bag.

In addition, inadequate removal of visco-elastic from behind theIOL can cause a capsular block syndrome and induce progressivemyopia. Certain plate haptic lenses especially of the thin lens designcan vault anteriorly with the onset of capsular fibrosis producing amyopic shift that cannot be explained solely on the basis of ananterior displacement. The 4th generation IOL formulas canoptimize these surgeon factors.

Bag to Sulcus shift

It could sometimes happen that certain factors like a posteriorcapsular rent or a loss of the integrity of the anterior capsule mayrequire that the IOL is placed in the sulcus. In such a situationmost surgeons would empirically deduced 0.50D – 0.75D fromthe calculated IOL power in order to compensate for the increase

Figure 2: Effective IOL position

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in effective IOL power. However this compensation will dependupon the ‘base power’ of the IOL. The following table needs to bedisplayed in all operating rooms and gives us a guideline as to howmuch we need to subtract from the calculated IOL power in a bagto sulcus shift

The manufacturer’s lens constant

Since the post operative effective lens position is dependant upona myriad of factors, the various IOL formulae incorporate a variableinto the computation. This variable known as the “A constant” ofthe SRK formula, the ‘Surgeon Factor’ or the ‘SF’ of the Holladayformula or the ‘pACD’ or the ‘personalized ACD constant’ of theHoffer-Q formula all contribute towards accurately predictingthe ELPo and each of them can be ‘optimized’ to enhance thepredictability of the IOL formula. For a specific surgeon with areproducible surgical technique, the A-Constant will depend uponthe material of the IOL and its deemed position within the eye.This ‘A constant’ is worked out by the manufacturer of the IOLand this information is printed on the box of the IOL.

This value represents where we anticipate the IOL to sit inrelationship to the cornea. Specifically, how near or far from thecornea. The “constant” will decrease with an AC IOL as comparedto a PC IOL.

Fallacies of the manufacturer’s lens constant

But there are certain pitfalls with the computation and calculationof these lens constants. Firstly, the ‘A constants’ have been calculatedfor an eye with an axial length of 23.5mm, a central corneal poweror 43.86D and limbal white to white diameter of 11.7mm. Whichis the reason why most IOL formulae work well within values thatapproximate the normal schematic eye with a range of axial lengthsbetween 22.0mm – 26.0mm and a central corneal power of 41.0D– 46.0D, while outside this range their predictability seem to beerratic.

Secondly, for many IOL models the ‘A constant’ is not individuallycomputed based on trials but merely approximated from similarlens design models.

And finally these calculations have been based on data obtainedby applanation A scans and manual keratometry.

Although the A constant is representative of the effective lensposition within the eye it only needs to be used as guide and needsto be optimized to enhance your surgical results.

The IOL formulas – A closer look

The SRK formula

Was described by Donald Sanders, John Retzlaff and Kraff in themid 1980’s. The formula attempted to predict the IOL power basedon the axial length and the average central corneal power.

• IOL power = A – 2.5 L – 0.9 K.

• L = axial length in mms

• K = average central corneal power in Diopters.

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

In order to increase its predictability the SRK 2 formula wasintroduced in which additions were made to the A constant inaxial lengths less than 22mms and 0.5 was subtracted from the Aconstant for axial lengths over 24.5mms. This was an attempt toprovide a ready made ‘optimization’ of the A constant.

Power at Power at Bag / Sulcus Subtract fromCapsular Bag Ciliary Sulcus Difference Bag Power

+30.00 D +28.55 D -1.45 D -1.50 D+29.50 D +28.09 D -1.42 D -1.50 D+29.00 D +27.61 D -1.39 D -1.50 D+28.50 D +27.14 D -1.36 D -1.50 D+28.00 D +26.67 D -1.33 D -1.00 D+27.50 D +26.20 D -1.30 D -1.00 D+27.00 D +25.73 D -1.27 D -1.00 D+26.50 D +25.26 D -1.25 D -1.00 D+26.00 D +24.79 D -1.22 D -1.00 D+25.50 D +24.31 D -1.19 D -1.00 D+25.00 D +23.84 D -1.16 D -1.00 D+24.50 D +23.36 D -1.13 D -1.00 D+24.00 D +22.89 D -1.11 D -1.00 D+23.50 D +22.42 D -1.08 D -1.00 D+23.00 D +21.94 D -1.05 D -1.00 D+22.50 D +21.47 D -1.03 D -1.00 D+22.00 D +21.00 D -1.00 D -1.00 D+21.50 D +20.53 D -0.97 D -1.00 D+21.00 D +20.05 D -0.95 D -1.00 D+20.50 D +19.58 D -0.92 D -1.00 D+20.00 D +19.11 D -0.89 D -1.00 D+19.50 D +18.63 D -0.87 D -1.00 D+19.00 D +18.16 D -0.84 D -1.00 D+18.50 D +17.69 D -0.82 D -1.00 D+18.00 D +17.21 D -0.79 D -1.00 D+17.50 D +16.73 D -0.77 D -1.00 D+17.00 D +16.26 D -0.74 D -0.50 D+16.50 D +15.78 D -0.72 D -0.50 D+16.00 D +15.31 D -0.69 D -0.50 D+15.50 D +14.83 D -0.67 D -0.50 D+15.00 D +14.35 D -0.64 D -0.50 D+14.50 D +13.88 D -0.62 D -0.50 D+14.00 D +13.40 D -0.60 D -0.50 D+13.50 D +12.93 D -0.57 D -0.50 D+13.00 D +12.45 D -0.55 D -0.50 D+12.50 D +11.97 D -0.53 D -0.50 D+12.00 D +11.49 D -0.50 D -0.50 D+11.50 D +11.02 D -0.48 D -0.50 D+11.00 D +10.54 D -0.46 D -0.50 D+10.50 D +10.07 D -0.43 D -0.50 D+10.00 D +9.58 D -0.41 D -0.50 D+9.50 D +9.11 D -0.39 D -0.50 D+9.00 D +8.63 D -0.37 D No Change+8.50 D +8.16 D -0.35 D No Change+8.00 D +7.68 D -0.32 D No Change+7.50 D +7.20 D -0.30 D No Change+7.00 D +6.72 D -0.28 D No Change+6.50 D +6.24 D -0.26 D No Change+6.00 D +5.76 D -0.24 D No Change+5.50 D +5.28 D -0.22 D No Change


SRK 2

• Axial length 21-22mm, add 1 to A• 20-21 add 2• < 20 add 3Long eyes:Over 24.5mm subtract 0.5mm from the A.With this modification the SRK 2 formula was reliable in predictingIOL powers between the axial length range of 20.0mm- 26.0mmbut was still unreliable in shorter and longer eye balls.

SRK T Formula

The SRK T formula is a third generation formula, described in1990 by John Retzlaff and Donald Sanders. It combines the benefitsof both the theoretical and regression formulae. The SRK Tformula uses theoretical elements like predicted post operativeanterior chamber depth, retinal thickness adjusted axial lengthand refractive indices of the cornea .The regression element isprimarily used to optimize the ‘A constant’. This formula works ineyes of normal length and moderately long and very long eyes.The SRK T formula has made the SRK 2 formula obsolete since itcombines all the advantages of the SRK 2 formula and also enablesyou to optimize the A-ConstantOptimization is the process of making a formula more predictableby refining and defining the manufacturer’s lens constant. In simpleterms optimization is achieved by analyzing post operativeoutcomes with respect to the targeted refraction for a given surgicaltechnique and a specified model or design of IOL as well as for agiven range of axial lengths. This optimization is then added on tothe ‘A constant’ to make the formula more predictable.

Why Optimize

As we have already seen almost all the IOL power predictionformulae seem to work for axial lengths between 22.0mm –26.0mm. However in shorter or longer eye balls they tend tobecome inaccurate for two important reasonsThe A- constant is computed based on an average axial length of23.50mm.The reason for the failure of the 1st and 2nd generation IOLformulae in accurately predicting the IOL power in very long orvery short eyes is because their calculations are based on certainassumptions. These formulae assume a directly proportionalrelationship between the axial lengths and the anterior chamberdepth and a similar association between corneal steepness orcurvature and the AC depth. It has been subsequently proved byDr Holladay that this assumption is incorrect.The Hoffer-Q formula: Third generation formula• Was described by Dr. Kenneth Hoffer in 1993.• P = f (A, K, Rx, pACD)• A: axial length• K: average corneal refractive power (K-reading)• Rx: refraction• pACD personalized ACD (ACD-constant)This formula predicted IOL power as a function of the axial length,average central corneal power and the previous refraction of the

patient. The pACD – the personalized A constant was theequivalent of the A-Constant in the SRK formula. The constructionof the Hoffer –Q formula was such that it was extremely reliablein short eye balls with an axial length of less than 22.0mms.

The Fourth Generation Formulae

Haigis

Holladay 2

HAIGIS Formula:

(1) DL = L - d n/z - d

—— - ———

ref nC - 1

with z = DC + ————— and DC = ———

1 - ref dBC RC

• D : refractive power of IOL

• DC: refractive corneal power

• RC : corneal radius

• nC : (fictitious) refractive index of cornea

• ref : desired refraction

• dBC : vertex distance between cornea and glasses

• d : optical ACD

• L : axial length

• n : refractive index of aequeous and vitreous (1.336)

The calculation according to HAIGIS is given by:

• nC = 1.3315

• dBC = 12 mm

• L : axial length as measured by ultrasound

With the optical ACD d obtained by regression from preoperativelymeasured acoustical data:

(2) d = a0 + a1 VKpr + a2 ALpr

(3) with a0 = ACD-Konst - a1 MW(VKpr) - a2 MW(ALpr)

• VKpr : preop. anterior chamber depth measured ultrasonically

• ALpr : (=L) preop. axial length from ultrasound

• MW(..) : means of VKpr (=3.37) mm and ALpr (=23.39) mm

• ACD-Konst: ACD constant of manufacturer

The Haigis formula is a 4th generation formula which was anadaptation of the formula first suggested by Gernet, Ostholt andWerner as early as 1970, which is the reason why this formula isalso called the GOW 70 formula. The versatility of the formula liesin the three individualized A constants namely a0, a1 and a2. Thea0 is linked to the manufacturers lens constant. The a1 is linked tothe pre operative ultrasonically measured ant chamber depth (thishas a default value of 0.4) and a2 which is linked to the axial lengthmeasurements and which has a default value of 0.1.

The three ‘A constants’ enable us to customize each componentof the IOL formula. When fully optimized this formula will workacross the entire range of axial length values and you may notneed to use different formulae for different axial lengths.

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Holladay 2: 4th Generation FormulaThe Holladay 2 (1998) - 4th generation formula is currently themost sophisticated formula that you could possible lay your handsupon. It is an improvement on the Holladay 1 formula.

The unprecedented success of the formula lies in the fact that DrJack T Holladay has attempted to increase its accuracy andpredictability by incorporating seven different parameters intothe framework of the formula. These parameters all contributetowards the accurate estimation of the ELPo.

• Axial length.

• Central corneal power (K)

• Anterior chamber depth

• Lens thickness measurement

• Limbal white to white measurement

• Age of the patient

• Previous refraction of the patient.

The second reason for the success of this formula is thedevelopment of the ‘nine types’ of eyes model by Dr. Holladay.This model overcame the discrepancies in all the other IOLformulae, which revolved around the assumption that there was aconstant relationship between the central corneal power (K), thepre operative anterior chamber depth and the axial lengthmeasurement. For instance in eye ball with long axial lengths theformulae automatically assumed that the anterior chamber depthwould also be longer and vice versa and similarly in a steepercornea the formula presume a greater anterior chamber depthand vice-versa. This is the principal reason why the variousstandard IOL power prediction formulae do not work in postrefractive surgery patients.

The surprising finding in this model that exposes the inadequaciesof the 1st 2nd and even the 3rd generation formulae is that thereis no direct correlation between the axial length measurementsand the anterior chamber size. Dr. Holladay found that the anteriorchamber depth was found to be normal in 96% of eyes with normal

The Nine Types of Eyes Model

Figure 3: Nine types of eyes model – Dr.Holladay

Figure 4: prediction accuracy of the various IOLformulas to within 0.5D of target refraction

Practical Tips: Chosing the RightFormula in your Day to Day Practice

axial lengths between 22.0 and 26.0mm but also in 80% of shorteyes and 90% of patients with long eyes. It is this breakthroughfinding that has contributed to the enhanced predictability of theHolladay 2 formula.

This formula now is available as part of a package called the‘Holladay IOL consultant which also provides the necessaryinformation to optimize every component of the ‘SF’ or thesurgeon factor. This package costs 995$ and can be ordered fromthe following web site- (713) 668-7337; docholladay @docholladay.com

When fully optimized the Holladay 2 formula works across theentire range of axial lengths.

The most pertinent question now, is what formula do we need touse in our day to day practice. In any surgical practice the majorityof the patient population (about 90%) would fit into the normalrange of axial length. For these patients any 3rd generation IOLformula would work. But I recommend the SRKT or the Holladay1 formula. Both these formulae are available with most biometers.Remember there is no place for the SRK2 formula in today’s practicebecause the SRKT formula possesses all the advantages of SRK 2formula and more. For these normal axial length population youcan further enhance your post operative outcomes by optimizingthe ‘A constant’ in the SRK T or the SF in the Holladay 1 formula.

For eyes shorter than 22.0mm the construction of the Hoffer-Qformula makes it a better choice.

For long (axial length more than 26.0mm) and extremely longeyes (axial length more than 27.5mm) the SRK T formula worksbetter than any other formula.

If you can purchase the fully optimized version of the Haigis andthe Holladay 2 formula they would work across the entire rangeof axial lengths.

How do we optimizeOptimization helps to fine tune our post operative results. Sincemost of us have access to the SRK T formula lets see how we goabout this task:


• A minimum of 25 cases must be studied.

• All cases must be operated upon using more or less the samesurgical technique.

• All cases must receive the same IOL model.

• The A scan and keratometry must be performed by the sametechnician. In case you are using applanation A scans it is agood time to move to immersion scans. In case you are usingmanual keratometry – calibrate the instrument at least oncein 3 months.

• Analyze your post operative results at the end of 6 weeks orat the time of prescription of glasses. Look at the discrepanciesbetween your target refraction and your actual post operativeresult.

• Cumulatively enter all these details into an electronic spreadsheet that can be downloaded from the internet athill@doctor_hill.com.

• As data is fed into the spreadsheet you can develop your ownoptimization of the A constant, which will help you to achievemore predictable post operative results.

• In third generation IOL formulae like the SRK T, the Hoffer-Q, or the Hollady1 formula there is only a single A constantthat affects the entire formula. Hence you need to optimizethe formula for a given range of axial lengths – like short eyeballs (20.0mm – 22.0mm) , normal axial lengths (22.0mm –24.5mm) or long eye balls (24.5mm – 26.0mm). If for examplethe SRK T formula has been optimized for short axial lengths,this optimization factor will not work if applied to longer axiallengths.

• Optimization for the 4th generation IOL power predictionformulae can be done across the entire range of axial lengthsas the Haigis formula has three different a constants linkednot only to the manufacturer’s lens constant but also to thepost operative anterior chamber depth and the axial length.However to optimize the 4th generation formula you needupward of 200 cases and not merely 25 cases.

• For surgeons who are just getting initiated into the world ofrefractive cataract surgery – optimization of the formula canbe greatly facilitated by visiting the following web site:www.augenklinik.uni-wuerzburg.de/ulib. The ULIB sitedeveloped by Dr. Haigis gives us optimized A- constant valuesfor different IOL designs and models and various axial lengths.These guideline ‘A constants’ could be used as a starting pointinstead of the manufacturer’s lens constant for youroptimization.

Conclusion

Success in IOL power calculation should not be a product of chancebut instead needs to be the end result of sound scientific knowledge,meticulous attention to detail and an ability to consistently achievetargeted outcomes case after case. Several surgeons like Dr.WarrenE Hill who have fully optimized their IOL formula have achieved apost operative prediction accuracy of 0.25D. This is what he has tosay regarding the future of successful IOL power prediction:

“If we can consistently lie within 0.25D of the target refraction wecan now set our sights on far more sophisticated endeavors likecorrecting third and fourth order aberrations during cataractsurgery…..”

References

1. Ophthalmic Surg. 1990 Apr;21(4):266-71. A simple modified SRKformula for severely myopic eyes. Kora Y, Suzuki Y, Inatomi M,Ozawa T, Fukado Y. Department of Ophthalmology, ShowaUniversity, Tokyo, Japan.

2. Klin Oczna. 2005;107(10-12):615-9. [Accuracy of the SRK II, SRK/T, Holladay and Hoffer Q IOL power calculation formulas inhyperopic patients after phacoemulsification]

3. Szaflik J, Kamiñska A, Gajda S, Jedruch A. Z Katedry i KlinikiOkulistyki II Wydzia u Lekarskiego Akademii Medycznej wWarszawie.

4. doctor_hill.com Calculating Bag vs. Sulcus IOL Power.

5. IOL Power Calculation, Personalizing the A-constant is key. BYAMY ORAVEC, MANAGING EDITOR (cataract and refractivesurgery today)

6. J. Cataract Refract Surg. 1990 May;16(3):341-6. Comparison of theSRK/T formula and other theoretical and regression formulae SandersDR, Retzlaff JA, Kraff MC, Gimbel HV, Raanan MG. Departmentof Ophthalmology, University of Illinois, Chicago.

7. GERNET H, OSTHOLT H, WERNER H: Die praeoperativeBerechnung intraocularer Binkhorst-Linsen. 122. Vers. d. Ver. Rhein.-Westfäl. Augenärzte. Balve, Verlag Zimmermann. S. 54-55, 1970

8. SANDERS DR, RETZLAFF J, KRAFF MC: Comparison of the SRKII formula and other second generation formulas. J Cataract RefractSurg 14: 136-141, 1988

9. Highly Accurate IOL Calculations, Pearls for achieving consistentoutcomes. By Warren E. Hill, MD, FACS (Cataract and refractivesurgery today).

Table: Electronic spreadsheet to optimize A constant for different IOL formulae

Initial IOL Constant Calculation Sheet

Warren E. Hill, MD, FACS

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

AuthorS. Venkatesh MS, FICO, FRCS

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Glaucoma is an optic neuropathy resulting in the loss of ganglioncells and their axons in the retina. The functional defect is

usually manifested by the loss of the visual field (VF) owing todiffuse or wedge defects of the ganglion cells and retinal nervefiber layer (RNFL).

RNFL defects

Clinical examination for glaucoma has traditionally includedmeasurements of intraocular pressure, funduscopic examinationof the optic disc and retinal nerve fiber layer (RNFL), and visualfunction testing. However, it has long been recognized that axonloss in the RNFL can precede changes in the optic nerve head(such as increased cup-to-disc ratio) and visual field loss. Studiesshowed that in 60% of eyes with reproducible visual field defects,abnormalities of the RNFL were present six years before functionalchange and loss of visual field occurred. Therefore, delineating ofearly glaucomatous RNFL damage might improve diagnosis andmonitoring of progressive glaucomatous damage.

However, it is not yet proven that structural changes always precedefunctional damage.

Preperimetric Glaucoma

The stage before functional loss detection is known aspreperimetric glaucoma. Diverse techniques have been used todistinguish normal eyes from glaucomatous eyes in preperimetricstages.

RNFL Photography

RNFL defects are often difficult to identify using standard clinicalexamination techniques.

RNFL photography is widely used as a qualitative detection methodowing to difficulties in measuring the thickness of the RNFL. Bothanalog and digital photographs are usually done in black and whiteby using a fundoscopic camera and a red –free filter. This methodhas been validated and is widely used for detecting early changesin the RNFL loss.

RNFL photography has been documented as having sensitivityand specificity averaging 80-94% for differentiation ofglaucomatous and non glaucomatous eyes. However, high –qualityphotographs are often difficult to obtain and RNFL photographyis only performed regularly at a few academic centers. In addition,photographic methods are limited by the need for pupil dilation,clear media and qualitative review of the photograph at the patient’snext clinic visit.

Glaucoma Research Fellow

Rotterdam Eye Hospital Rotterdam,

Netherlands

GDx NFA, GDx VCC

Two new diagnostic instruments, the GDx/ Nerve Fiber Analyzer(GDx/NFA) (Laser Diagnostics Technology, San Diego, CA) andthe Optical Coherence Tomograph (OCT) provides real-timequantitive and objective assessments of the RNFL. Each of them isbased on different optical principles and different properties oflight to measure RNFL thickness.

Evolution of the Nerve Fiber Analyzer

The first commercially available version of the NFA in 1993 is nowknown as the NFA I. It has been upgraded several times sincethen, changing names in the process. The second type was calledNFA II, and the next generations are NFA GDx, GDx VCC andGDx ECC.

Nerve Fiber Analyzer GDx

The RNFL exhibits substantial linear birefringence with its slowaxis parallel to the direction of nerve fibre bundles. Thisbirefringence probably results from birefringence of closely spacedcylindrical structures in the RNFL. This unique property of theRNFL provides a basis for SLP (Scanning Laser Polarimetry) toassess the RNFL thickness by measuring total retardation in thelight reflected from the retina. Retardation is proportional to theRNFL birefringence and the RNFL thickness.

The current SLP system, GDX VCC (Carl Zeiss Meditec Inc.,Dublin, CA,USA), is a confocal scanning laser ophthalmoscopeintegrated with a polarimeter. Images of the ocular fundus areformed by scanning the beam of a near- infrared laser (780nm) ina raster pattern. The field of view is 40 degree horizontally x 20degree vertically at a density of 256x128 pixels, respectively. Thescanned area includes the peripapillary region around the ONHand macular region around the fovea.

The GDX VCC produced a reflection image that was generatedfrom light reflected back from the fundus of the eye. In addition,it produced a retardation image that had been constructed fromthe 32,768 pixels (256x128) individual retardation value.

Influence of the Cornea

The GDx VCC is equipped with a variable corneal compensator.As the corneal stroma is composed of parallel collagen fibres, ithas significant polarizing properties, which must be effectivelycompensated for valid SLP measurement of RNFL thickness.Therefore, a fixed corneal compensation FCC with a fixed angleand magnitude as featured in older generations of the GDx (CarlZeiss Meditec inc., Dublin, CA, USA) has been shown not to becompletely successful. Anterior segment birefringence,predominately the corneal birefringence, is a confounding factorin SLP assessments of the RNFL.

In the GDx VCC, a variable corneal compensator (VCC) thus

Diagnostic Ability of GDx VCC forGlaucoma Diagnosis

Tutul Chakravarti MBBS, DO, DNB

Glau

com

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neutralizes the anterior segment birefringence. Anterior segmentbirefringence is measured from the macular “bow tie” patternresulting from the linear anterior segment birefringence and theradial birefringence of Henle’s fibre layer. With compensation byVCC, the retardation image reveals both Henle’s fibre layer andthe RNFL.

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

Although compensation of anterior segment birefringence in theindividual eye seems to be adequate with SLP-VCC in general, asmall amount of residual anterior segment birefringence can beobserved in some eyes which may lead to erroneousmeasurements of the RNFL. As an alternative the existing VCCmethod, a new software method, named enhanced cornealcompensation (ECC), was developed that requires no hardwaremodification to the GDx VCC system and provides individualizedcorneal compensation with enhanced SLP measurement sensitivity.In myopic eyes, it is believed that the assessment of RNFL thicknessby SLP should be conducted with caution because of the incidenceof abnormal retardation pattern (ARP). In contrast to VCC, theuse of ECC dramatically reduced the presence of ARP.

Interpretation of GDx printout

The printout’s key areas are: 1) The Fundus image, 2) The RNFLthickness map, 3) The RNFL deviation map 4) The TSNIT graph and5) The parameter table.

Normal example

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

Fundus image

The first thing to consider in the interpretation of a scan is whetherit is of high quality. Every image has a Q score representing theoverall quality of the scan. The Q score ( displayed above thefundus image) ranges from 1-10, with values 8-10 representingacceptable quality.

Thickness map

The retardation /thickness map (panels below the fundus image)reflect the phase shift of the polarized laser light passing throughthe RNFL, which is proportional to the thickness. Measurementsare taken in a 20 degree X 20 degree field of view. The amount ofphase shift has been converted to a thickness measure, and colour-coded according to the scale shown on the printout. Bright, warmcolors (yellow, orange, red) represent thicker areas; dark, coolcolours (black, blue) represent thinner areas. A healthy eye mayshow a typical “hour-glass” distribution of warmer colourssuperiorly and inferiorly and cooler colours nasally and temporally.Loss of warmer colours corresponds to thinning of the RNFL. Inhealthy eyes, retardation is present adjacent to the thicker bloodvessels superior and inferior to the ONH. There is a largevariability in the appearance of the RNFL in healthy eyes.

Deviation map

The deviation maps (below the retardation maps) compare theretardation value of “superpixels” with corresponding areas the

age and ancestry matched database. Each superpixel representsthe average of 16 individual pixels (4X4). Only superpixels whosevalue is below the 5th percentile will be colour coded dark blue forthose below the 5th percentile, light blue below the 2nd percentile,yellow below the 1st and red below the 0.5th. The deviation mapmakes it easy to see RNFL bundle defects and areas of abnormality.

TSNIT Plots

The TSNIT (temporal-superior-nasal-inferior-temporal) plots(bottom panel) reflect the peripapillary RNFL thickness along themeasurement circle, which is approximately 3.2 mm in diameterin an emmetropic eye. The normal 95% range of the TSNIT plot isshown as a shaded area. For comparison of the two eyes, theirTSNIT plots have been superimposed on the central bottom panel.

The parameter table

Parameters

Six parameters are printed in the central top panel. They areconstructed from data along the measurement circle:

1. TSNIT Average: The average RNFL thickness around the entirecalculation circle.

2. Superior Average: The average RNFL thickness in the superior120 degree region of the calculation circle.

3. Inferior Average: The average RNFL thickness in the inferior

Figure 1: Printout of a healthy subject. The TSNIT plotsare within normal range. In addition, these plots are

symmetrical for the two eyes. All parameters are withinnormal limits. The NFI is below 35

31www.dosonline.org

Figure 2: GDX Parameters

Figure 3: Printout of a glaucoma patient whose righteye has lost retardation in the superior temporal and

inferior region. These regions have also been flagged inthe deviation map. In addition, the TSNIT plot shows

that the thickness of the RNFL is below the normalrange in the same regions. Most parameters are

flagged at P< 0.5%. The NFI is 79. The left eye showsa loss of retardation superiortemporal to the ONH. Inthe inferotemporal region, a localized, wedge-shaped,

defect of the RNFL is visible as a flagged area in thedeviation map. There is asymmetry in the TSNIT plot

between the two eyes.

120 degree region of the calculation circle.

4. TSNIT Std. Dev.: This measure captures the modulation (peakto trough difference) of the double-hump patern. A normaleye will have high modulation in the double-hump RNFLpattern, while a glaucomatous eye will typically have lowmodulation in the double-hump pattern.

5. Inter-Eye Symmetry: Measures the degree of symmetrybetween the right and left eyes by correlating the TSNITfunctions from the two eyes. Values range from -1 to 1, wherevalues near one represent good symmetry. Normal eyes havegood symmetry with values around 0.9.

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

Diagnostic Ability of GDx VCC For glaucoma Diagnosis

The best parameter

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

Other data in the GDx VCC printout may be indicative of the

diagnosis of glaucoma

• Prior to any interpretation, the image quality should beassessed

• It is preferable to examine the print-outs systematically: firstone should look for typical signs of normality and then fortypical signs of abnormality, before drawing a conclusion.

• One should know to recognize split bundle as being a commonanatomical variation, with prevalence of approximately 8.0%.

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

• In some cases, wedge defects can be seen.

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

Different studies show that the parameters analysed by the GDxVCC are useful for discriminating between normal andglaucomatous subjects with slight to moderate AutomatedPerimetry (AP) defects. Most of the parameters showed significantdifferences between normal subjects or those with ocularhypertension and glaucomatous subjects. NFI stands out amongall the parameters as that having the best diagnostic ability. Indifferent studies, RNFL parameters of the GDx VCC werecompared among four groups namely healthy controls, ocularhypertensive eyes, Glaucoma suspects, and glaucomatous eyes.Most parameters of GDx VCC exhibited differences betweenglaucoma group and the rest of the groups. Some parameters


Figure 4: Printout of a glaucoma patientRE:GHT Outside normal limits. MD -7.86 dB (P<

0.5%). PSD 14.24dB (P< 0.5%).LE: GHT Outside normal limits. MD -0.69dB. PSD

1.94 dB (P< 10%).

were also different between healthy patients and glaucomasuspects.

NFI is a global indicator of the state of the RNFL and is based onan advanced system of neural network analysis measuring thecomplete RNFL profile and reached a number that represents itsintegrity.

It is plausible that by combining the parameters in discriminantequations one may reach a higher diagnostic ability, as has beenshown (different studies) by evaluating different RNFL objectiveevaluation systems. In the GDx NFA, by using the discriminantequation (proposed by Weinreb), a greater diagnostic ability wasobserved than with the <<number>> that the analyzer provides.This << number>> is equivalent to the NFI of the GDx VCC laserpolarimeter. GDX VCC laser polarimeter has shown a good abilityto discriminate between healthy eyes and eyes with early ormoderate glaucomatous loss through different studies. It can beconcluded that the use of parameter combinations or other RNFLanalysis methods can support diagnosing glaucoma early on andshould therefore be studied.

References

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

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

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

AuthorTutul Chakravarti MBBS, DO, DNB

� All presentations should be made in MS-Office 2007.� Any Fonts and Animations if used which are not a part of the standard MS Office XP pack should be included with

the Presentation CD and this should be specified to the Audio Visual in charge at the Preview Room well inadvance.

� Videos when included should be ideally in avi or mpeg and if any other format is used its codec should be also beincluded.

� If any different format is used deviating from the above mentioned format the same should be informed wellbefore the conference so alternative arrangements can be made where ever possible.

� The medium of storage used by the presenters can be CD, DVD, Flash Drive, USB HDD, PCI MCI card. Also anydeviation from this should be informed so that alternative arrangements can be made if possible.

� All speakers should submit their presentations 3 hrs before their presentation in the Preview Room.� No personal Laptops are allowed for the presentation.� Speakers are requested to timely adhere to these guidelines.

Guidelines for Presentation in

Annual DOS Conference

37www.dosonline.org

Keratoconus is a bilateral non-inflammatory corneal ectasia(Figure 1) with an incidence of approximately 1 per 2,000 in

the general population. It normally presents in early teens ortwenties and is known to be progressive. Despite intensive clinicaland laboratory investigation, the aetiology of keratoconus remainsunclear. Thinning of the corneal stroma, breaks in Bowman’s layer,and deposition of iron in the basal layers of the corneal epitheliumcomprise a triad of the classical histopathologic features found inkeratoconus.

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

Mechanism of action

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

First studies in Photobiology began in 1990’s, with attempts toidentify biological glues that could be activated by heat or light toincrease resistance of stromal collagen2. It was discovered that thegluing effect was mediated by oxidative mechanism associatedwith hydroxyl radical release. A similar mechanism of naturalhardening and thickening of collagen fibres has been demonstratedin corneal aging3. Similarly, young diabetics never developprogressive keratoconus due to natural cross linking effect ofglucose, which increases corneal resistance.

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

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

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

Neera Agarwal MBBS, MS

Neera Eye Centre & Laser Vision

Daryaganj, New Delhi

Quality of Beam

All safety considerations regarding the Cross-Linking procedureassume an optically homogenous irradiation of the cornea. Opticalin-homogeneities can lead to damage to corneal endothelium,which represents most endangered structure. Thus, havinghomogenizing optics and as well as pre-compensation for cornealcurvature in the system is important (Figure 5).

Figure 1: Natural Progression of Keratoconusin a patient over 1.5 years

Corn

ea

DOS Times - Vol. 15, No. 6, December 200938

Figure 2: Mechanism of action: C3R

Figure 3: Effect of Collagen CrossLinking on Corneal Collagen

Figure 4: Effect of Cross linking on Cornea

Indications

Most common indications are –

1. Mild to moderate Keratoconus – In a case of Keratoconus, theselection criteria for C3R are as follows -

• There should not be corneal scarring.

• There should be reasonably good acuity with glasses or contactlenses.

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

• Age should more than 16 yrs.

• Maximum K readings should be < 60Diopters.

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

equivalent power, Decentration component and Irregularastimatism component and calculation their yearly rate ofprogression. It is generally accepted that 1 dioptre increase inthe power of cone per year is an indicator of progression ofKeratoconus. It can also be seen as steepening of Keratometryreadings17

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2. Post Lasik Ectasia – Good results have been reported intreatment of post Lasik ectasia 13.3. Progressive Hyperopia post RK – good results have beenreported12.4. Pellucid Marginal Degeneration5. Bullous Keratopathy – reduces Corneal oedema by increasingstromal compaction after Cross-linking. It may be combined withIntra-stromal administration of 0.1% Riboflavin with the help ofFemtosecond laser (Can also be staged i.e. anterior and posteriorseparately)16.6. Infective Keratitis – to prevent Corneal Perforation byincreasing resistance to the effect of collagen digesting enzymes.16

7. Scleral CXL for Glaucoma and Pathological Myopia16

Technique

The procedure is conducted in an operating room under sterileconditions. Topical anaesthesia is given by Proparacaine

Hydrochloride (0.5%) eye drops & Xylocaine 4% drops. Central 7-8 mm of corneal epithelium is removed by mechanical debridement(gentle scraping with hockey stick knife) or Alcohol. My personalpreference is mechanical debridement.This is followed by instillation of 0.1% Riboflavin (3 mg Riboflavin- 5 Phosphate in 3 ml of Dextran-T-500 20% solution) eye drops atevery 2 minute interval for 30 minutes (15 times).

To confirm adequate penetration of Riboflavin into the cornea,the patient may be examined on slit lamp. A greenish flare, similarto that seen with fluorescein dye instillation, may be seen in anteriorchamber, signifying penetration through the thickness of cornea.

There are studies available which say that epithelial debridementis not necessary. However, it’s mandatory to demonstrate thepenetration of the riboflavin in the corneal stroma whenperforming the treatment without removing the epithelium.

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

Figure 5: Quality of beam for C3R

Figure 6: C3R being done in a patient

Figure 7: Effect of Cross-linking on cornea

DOS Times - Vol. 15, No. 6, December 200940

Figure 8: Absorption of UVA by Cornea

the ‘barrier’ effect. Thereby, a dose of 3 mW/ Sq cm (+ 0.3 Mw)(5.4 J/Sq cm) UV-A is delivered. The UV-A radiation lamp ischecked for calibration with a UV- meter before and after thetreatment. On completion of the treatment, eye is patched withantibiotic eye ointment or sterile bandage lens is applied.

Post-operative Care

Topical antibiotics along with lubricants and viscous tear substitute,mild steroids are prescribed 4-5 times a day for 3-4 weeks. Completere-epithelization usually occurs in 3-4 days. Patients may experiencemild pain and discomfort for first 2 days, for which oral analgesicsare also required to keep them comfortable.

A mild epithelial haze with transient, mild stromal oedema maybe seen in some cases after C3R, which usually disappearscompletely in a few weeks. There is no damage to the cornealendothelium.

Histopathological changes in cornea post C3R

C3R treatment leads to a dose-dependent keratocyte apoptosis1

that can be expected in human corneas to a depth of 300 micronsfrom the anterior surface utilising a surface UV-A dose of 5.4 J/ sqcm. In the first few weeks after the procedure, a ‘vertical transitionline’ may be visible on the slit lamp, delineating the anterior cross-linked zone with the posterior unaffected stroma (Figure 7).

Repopulation of corneal stroma may take up to 6 months. It is welldocumented that the corneal epithelium attains a regularmorphology and density within 5 days after C3R. Initially,disappearance of the sub-epithelial stromal nerve fibres wasobserved in the treated area and initial re-innervation was seenone month after the procedure. Complete recolonization of theanterior sub-epithelial stroma by the keratocytes was observed in6 months after C3R, with restoration of corneal sensitivity.

Histopathologically, it has been demonstrated that there is asignificant increase in collagen fibre diameter after collagen crosslinking. After Collagen Cross-Linking, the cornea shows anincrease in thermo-mechanical stability as well as a markedlyincreased resistance to collagen digesting enzymes5.

Results

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

• In a 5 year study, it was noted that in all treated eyes, theprogression of keratoconus was at least stopped. About 70%eyes show regression with a reduction of the maximalkeratometry readings by 2 dioptres and of the refractive errorby 1 D was found14. Best-corrected visual acuity improved by1.4 lines. I have personally experienced similar results in my 8month experience with the procedure.

• The addition of C3-R to the INTACS procedure results ingreater keratoconus improvements compared to INTACSalone10.

• There are reports available that surface ablation procedurescould be used to correct refractive errors following C3R inKeratoconus patients but conclusive evidence is lacking.

Safety

During corneal Cross-Linking, 95% of UVA energy is absorbed byonly 350 microns of Riboflavin soaked Cornea (Figure 8). As longas the treated cornea has a minimum thickness of 400 microns(after removal of epithelium), the corneal endothelium will notexperience damage, nor will deeper structures such as lens andretina.

The light source should provide a homogenous irradiance,avoiding hot spots.

It has been seen that corneal and lens transparency, endothelialcell density, and intraocular pressure remained unchanged afterthe procedure9.

Conclusion

Cornea Collagen Cross-linking with Riboflavin is a simple, safeand effective procedure in the management of early progressiveecstatic disorders of the cornea.

References

1. Apoptosis After Corneal Collagen Cross-linking using Riboflavin/UVA treatment. Wollensak G. et al. Cornea 2004; 23: 43-49

2. Photodynamic biologic tissue glue. J. Khaderm, T. Truong, J.T. Ernest.Cornea 1994;13: 406-410

3. Collagen fibrils in the Human corneal stroma . structure and aging.A. Dover, K. Misof et al. Invest. Ophthalmol. Vis. Sc. 1998; 39: 644-648

4. Stress-strain measurements of human and porcine corneas afterRiboflavin- ultraviolet-A induced cross-linking. Wollensak G.,SpoerlE., Seiler T. J Cataract Refract Surg. 2003;29:1780-1785

5. Increased resistance of cross-linked cornea against enzymaticdigestion. Seiler T., Wollensak G., Spoerl E. Curr. Eye Res. 2004July; 29(1): 35-40.

6. Thermo-mechanical behaviour of collagen cross linked porcinecornea. Spoerl E., Wollensak G., Dittert D.D., Seiler T.,Ophthalmologica.2004, Mar-Apr; 218(2):136-140

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

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AuthorNeera Agarwal MBBS, MS

8. Safety of C3-R UVA at the Retinal Level and Compared to OutdoorUVA Exposure Leonard Yuen, MD and Brian S. Boxer Wachler,MD

9. Safety of UVA-Riboflavin Cross-Linking of the Cornea EberhardSpoerl, PhD, Michael Mrochen, PhD, David Sliney PhD, StephenTrokel, MD, Theo Seiler, MD, PhD, Cornea 2007; 26:385-389

10. The Effect of Inferior Segment Intacs with and without CornealCollagen Crosslinking with Riboflavin (C3-R) on Keratoconus. ColinC.K. Chan, MD, FRANZCO, Munish Sharma, MD, Brian S. BoxerWachler MD, J Cataract Refract Surg 2007;33:75-80

11. No Progression of Keratoconus 5 Years after C3-R. Wollensak G.Crosslinking treatment of progressive keratoconus: new hope. CurrOpin Ophthalmol. 2006 Aug; 17:356-60.

12. C3-R for Stabilization of Progressive Hyperopia (Farsightedness)after Radial Keratotomy and Laser Ablation. Presented at theAmerican Academy of Ophthalmology Annual Meeting, 2006

13. Visual rehabilitation and outcomes of ectasia after corneal refractivesurgery. Woodward MA, Randleman JB, Russel B, Lynn MJ, WardMA, Stulting RD - J. cataract Ref. surg. 2008 mar; 34(3): 383-8

14. Riboflavin/UVA induced collagen cross-linking for treatment ofKeratoconus. G. Wollensak, MD et al, Am. J. Ophthal. 2003 May;135(2) : 620-627

15. Staged Intra-stromal Delivery of Riboflavin with UV-A Cross-linking in Advanced Bullous Keratopathy. Krueger RR, Ramos-Esteban JC, Kannelopoulos J – J. Refract. Surg. 2008; 730-736

16. Corneal Cross-linking for Different Corneal Diseases. Aylin KilicErtan – Cataract & Refractive Surgery Today Europe. April 2009;25-28

17. Progression of Keratoconus Assessed by Fourier Analysis ofVideokeratography Data. Tetsuro Oshika, Tatsuro Tanabe, AtsuoTomidokoro, Shiro Amano – Ophthalmology 2002; 109:339-342

Attention DOS Members

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

the post of the Vice President to be held on 18th April, 2010.

The members of the Commission areDr. Noshir M. Shroff and Dr. Sudhank Bharti

45www.dosonline.org

Traumatic optic neuropathy refers to an acute injury of theoptic nerve secondary to trauma. Injury may be direct or

indirect and visual loss may be partial or complete. Direct TONresult from an anatomical disruption of nerve fibers by penetratingorbital trauma, bony fragments within the canal and nerve sheathhematoma .In contrast, indirect injury results from transmissionof forces to the nerve.

Incidence

In setting of closed traumatic head injury, its incidence variesbetween 0.5-5%1,2. vast majority seen in males (85%) mean agebeing 34yrs. Motor vehicles and bicycle accidents account for themajority of causes followed by falls and assaults. TON has alsobeen associated with penetrating trauma (stab wounds, gunshotwounds, foreign bodies) and recreational sports (e.g. paintballinjury).

Etiopathogenesis- Nerve course is anatomically divided into 4 parts– intraocular (about 1mm), intraorbital (20-30mm), intracanalicular(5-11mm) and intracranial (3-16mm). Hence, trauma can lead tovarious clinicopathological consequences according to the site.

Intraocular

Violent rotations of globe produces avulsion of optic nerve leadingto a picture of partial ring of hemorrhage at optic nerve head. Thismay b self inflicted known as oedipism OR autoeneucleation.

Intraorbital

Trauma in this region is mainly coz of inraorbital hemorrhage oremphysema causing either ischemia or elevated intraorbitalpressure compromising the circulation of optic nerve known asorbital compartmental syndrome. Hemorrhage may occur directly,surgically induced, post thrombolytic therapy, injection of localanesthetics or even following retrobulbar block (0.4-3%)3. Opticnerve in intraorbital compartment runs a sinuous course whichcan withstand stretching of upto 9mm. hence , indirect injuries arecommoner whilst direct injuries are rare here.

Intrcanalicular

It is the most common site of trauma characteristically associatedwith high momentum decelerating injuries especially infrontotemporal region. Mid facial trauma have also been observedto result in similar picture. Studies using laser interferometrysuggests that forces applied to frontal bone are transferred andconcentrated in optic canal. Throughout its intraorbital course,the optic nerve remains surrounded by pia, arachnoid, and duramater, which move along with the optic nerve during normal eyemovements. Within the optic canal, the sheath of the optic nerveis fused to the sphenoid periosteum, and, as a result, the nerveand its sheath are tightly fixed to the bony canal within this confined

Traumatic Optic NeuropathyJ.L.Goyal MD,DNB, Deepa Gupta MBBS, Ritu Arora MD,DNB

Guru Nanak Eye Centre

Maulana Azad Medical College, New Delhi

space. At the posterior foramen of the optic canal, the optic nervesheath fuses with an overlying falciform fold of dura that lines thecalvaria .Any blunt force applied in the frontotemporal area leadingto elastic deformation of sphenoid can transmit forces directly tothe optic nerve resulting in localized contusion or even laceration,in severe cases, of optic nerve. Contusion of axons and pialvasculature produces localized nerve ischemia and edema leadingto further neural compression with in fixed bony canal setting apositive feedback loop resulting in further damage. Also,reperfusion injury has been cited as a mechanism in whichreperfusion of axons leads to production of free radicalscontributing to the damage by causing neuronal cell loss.

Intracranial

This is the next most common site usually lead to characteristicVF changes especially in chiasmal region. Vision loss may vary.

Presentation

Comprehensive care of head injury patients requires traumaphysician, head and neck surgeon, ophthalmologists andneurosurgeons. Association of such trauma with loss ofconsciousness warrants ophthalmic assessment at earliestopportunity.

Visual Acuity – Varies mainly between 20/200 to no lightperception. More recent reports suggests even milder vision lossin TON. Role of refraction can’t be underestimated in this scenario.

Pupils- In case of unilateral involvement, RAPD can be quantitatedusing photographic neutral density filters. These are calibrated inlog units that measure the reduction in transmitted light. APD>2.1 log units indicates poor prognosis4.

Fundus- Disc pallor may not be present initially n takes about 3-4weeks to develop. Fundus may vary according to the site of insultin relation to the origin of central retinal vessels. Posterior injuriesmay lead to disc edema due to hhgs in nerve sheath whereasanterior injuries lead to venous obstruction and traumatic AION.Findings like commotion retinae and choroidal rupture may alsobe present.

Other than these, palpation of orbital rim may reveal fracture,periorbital swellings; other anterior segment evidences ofpenetrating injuries must be sought.

Investigations

Neuroimaging studies (CT scanning or MRI) are an importantpart of the assessment when TON is suspected. In the post-traumasetting, CT scanning is the preferred modality for demonstratingthe presence of an optic canal fracture, a displaced bony fragmentimpinging upon the optic nerve, a metallic foreign body in theorbit, orbital emphysema, or an optic nerve sheath hematoma. Abrain and orbit MRI may be useful in certain settings to delineatethe extent of hemorrhage involving the neurovascular structuresat the orbital apex or to rule out inflammatory or infiltrative causesfor an optic neuropathy.

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Others -

Visual field perimetry

Automated perimetry can be obtained only in patients who retainadequate vision/acuity. Patients with poor visual acuity (worsethan 20/200) may be assessed with Goldmann perimetry or withconfrontational visual field testing.

No visual field loss pattern is pathognomonic for traumatic opticneuropathy (TON), although a dense central scotoma ischaracteristic. Recovery of optic nerve function may be documentedvia serial visual field testing.

Visual evoked potential (VEP)

VEP can be helpful to document the presence of TON inunresponsive patients or in cases with concomitant ocular injuries.Patients can also be followed with serial VEP examinations todocument recovery of function when clinical parameters areequivocal. However, in settings of polytrauma it may not bepossible at all to shift the patient to electrophysiological lab.

In unilateral cases of TON, a flash VEP amplitude ratio (affectedside/normal side) greater than 0.5 appears predictive of a favorable,long-term visual outcome. Visual recovery is considered unlikelywhen VEP amplitudes are nonrecordable.5 Retinal nerve fiberlayer (NFL) imaging: Scanning laser polarimetry and opticalcoherence tomography can be used to assess and monitor retinalNFL axonal loss during the period of follow-up.

Newer modalities like multifocal VEP can also be used as aprognostic indicator.

Management

Medical Therapy

The main treatment options for traumatic optic neuropathy (TON)include systemic corticosteroids and surgical optic nervedecompression, either alone or in combination. Review and analysisof the literature are complicated by the variety of therapeuticapproaches and a lack of randomized, controlled studies on theuse of these modalities for TON. Steroid therapy for TON can becategorized as follows: moderate dose (60-100mg of oralprednisolone), high dose (1 gram of intravenousmethylprednisolone/day), or mega dose (30 mg/kg loading doseof intravenous methylprednisone, followed by 5.4 mg/kg/h for 24hours).6 Steroids have been used in TON since the early 1980sbecause of their perceived benefits in various animal models ofcentral nervous system injury. Steroids were thought to provideneuroprotection in traumatic central nervous system injurythrough their antioxidant properties and inhibition of free radical-induced lipid peroxidation.

In 1990, Bracken and colleagues published their findings on theuse of mega dose corticosteroid therapy in the National AcuteSpinal Cord Injury Study 2 (NASCIS 2)7. The NASCIS 2 was amulticenter clinical trial that evaluated patients with acute spinalcord injury treated with placebo, methylprednisolone, or naloxone.The study showed that methylprednisolone (30 mg/kg loadingdose, followed by 5.4 mg/kg/h for 24 hours) started within 8 hoursof injury was associated with a significant improvement in bothmotor and sensory function compared with patients treated witha placebo.

The findings of the NASCIS trials significantly influenced clinicalpractice and led to an increased use of steroids in treatingTON. However, the clinical improvement was modest in thesestudies, and concern existed that the clinical benefit demonstratedfor those patients treated in the first eight hours with mega dosesteroids was the result of a statistical bias.

In 2005, the results of the Corticosteroid Randomization AfterSignificant Head Injury (CRASH)8 trial raised concerns regardingthe use of mega dose steroids (same dose as given in the NASCIS2 study) in traumatic brain injury. This study was the largestrandomized study that evaluated steroids in patients with traumaticbrain injury and was stopped early due to the significantly increasedrisk of death in patients that received mega dose steroids at their6-month follow-up when compared with the placebo group.

Furthermore, concerns have been raised regarding theextrapolation of data from spinal cord injury studies to TON.There are important histologic distinctions between the spinalcord and optic nerve; for example, the optic nerve is a pure whitematter tract and the spinal cord is a mixed gray and white mattertract. As a result, significant biologic differences may exist betweenthe repair mechanisms of the optic nerve axons and insults to thespinal cord.

The International Optic Nerve Trauma Study (IONTS)9 was anonrandomized intervention trial that compared visual outcomesfor patients with TON treated with observation, systemic steroids,or optic canal decompression. Published in 1999, the study included133 patients who were evaluated and treated within 7 days of thetraumatic event, with most of the patients being treated with eithercorticosteroids (n=85) or surgical decompression of the optic canal(n=33). Follow-up results showed that visual acuity increased bymore than 3 lines in 32% of the surgery group, 52% of thecorticosteroid group, and 57% of the observation group. However,the study was nonrandomized and uncontrolled, and the smallnumbers of patients in the observation group (n=9) limited thestrength of the study’s statistical power.

Recent animal studies have also NOT demonstrated any beneficialeffect for steroid therapy in animals with TON, and one study; inparticular, found that steroids exacerbated axonal loss as evidencedby a dose-dependent decline in axonal counts with increasing dosesof steroids. Such findings may suggest that steroids can exert anegative effect on ganglion cell survival, especially at higher, megadose levels, due to their suppression of endogenousneuroprotective pathways.10

Surgical therapy

The rationale for surgical therapy in indirect TON is to decompressthe optic nerve at the site of injury, which is often the intracanalicularsegment. Surgical decompression is thought to help reduce opticnerve compression and subsequent vascular compromise thatmay occur as a result of the indirect injury. Additionally, surgeryhas been postulated to remove bone fragments that may beimpinging on the optic nerve within the optic canal.

However, no randomized, controlled studies have been performedto evaluate the role of surgery in TON. As mentioned previously,one of the largest series is from the IONTS, which did not provideany convincing evidence that surgical decompression of the opticcanal in TON is superior to observation or corticosteroid therapy.

47www.dosonline.org

Additionally, in cases in which bony fragments are impinging onthe optic nerve within the canal, the prognosis of visual recovery isextremely poor because the bony fragments are more likely tohave anatomically disrupted the optic nerve axons, leading toirreversible visual loss.

The variety of surgical approaches used in optic nervedecompression include intracranial, extra cranial, orbital,transethmoidal, endonasal, and sublabial approaches, and theselection of the technique tends to be based on the surgeon’straining, background, and experience.17,20 Patients with profoundvision loss and a visualized bone fragment impinging on a segmentof the intracanalicular optic nerve on neuroimaging have beenconsidered to be the best candidates for surgical intervention.Although anecdotal reports of impressive visual recovery exist forsuch patients, most cases with direct injuries to the optic nerve donot improve as the injury to nerve axons becomes irreversibleand the risk of possible surgical complications such as cerebrospinalfluid leak or postoperative bleeding cannot be ignored. Cadavericstudies have shown that transphenoidal medial wall decompressionof optic nerve canal with dural sheath opening may induce physicaldamage to nerve.

Conclusion

Based on the current evidence, a therapeutic role for corticosteroidsin the management of TON is unsubstantiated. If steroids areconsidered for TON, they should not be used in cases withconcomitant traumatic brain injury or in patients that present 8hours or more after initial injury. Whether clinicians should usemega dose rather than lower doses of steroids for selected casesof TON is also not clearly defined by the literature.

Also, at this time, conclusive evidence that surgical decompressionhas a beneficial role for most patients with TON does not exist.Because a significant rate of spontaneous recovery is found incases of TON, a randomized controlled trial comparing observationwith optic canal decompression is the only reliable way to evaluatethe therapeutic benefit for surgical intervention. The decision toperform surgical decompression of the optic canal should be madeon a case-by-case basis, with the patient being informed that, todate, surgery has not been shown to improve the prognosis overobservation alone.

Hence, to conclude, the treatment of traumatic optic neuropathyis more of a trail based and more data is required for any modalityto have proven benefit over observation alone.

References1. Turner JWA. Indirect injury of the optic nerves. Brain 1943;66:140â€”151.

2. Russell WR. Injury to cranial nerves including the optic nerves andchiasma. In Brock S, ed. Injuries of the Skull, Brain and Spinal Cord.London, Bailliere, 1940:113â€”122

3. Ruben S. The incidence of complications with retrobulbar injection ofanaesthetic for ophthalmic surgery. Acta Ophthalmologica1992;70:836â€”838.

4. Alford MA, Nerad JA, Carter KD. Predictive value of the initial quantifiedrelative afferent pupillary defect in 19 consecutive patients with traumatoptic neuropathy. Ophthal Plast Reconstr Surg 2001;17:323â€”327.

5. Holmes MD, Sires BS. Flash visual evoked potentials predict visualoutcome in traumatic optic neuropathy. Ophthal Plast ReconstrSurg. Sep 2004;20(5):342-6.

6. Yu-Wai-Man P, Griffiths PG. Steroids for traumatic opticneuropathy. Cochrane Database Syst Rev. Oct 17 2007;CD006032

7. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlledtrial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord InjuryStudy. N Engl J Med. May 17 1990;322(20):1405-11

8. Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, arandomised placebo-controlled trial of intravenous corticosteroid inadults with head injury-outcomes at 6 months. Lancet. Jun 4-10 2005;365(9475):1957-9.

9. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic opticneuropathy: the International Optic Nerve TraumaStudy. Ophthalmology. Jul 1999;106(7):1268-77.

10. Steinsapir KD. Treatment of traumatic optic neuropathy with high-dosecorticosteroid. J Neuroophthalmol. Mar 2006;26(1):65-7.

11. Steinsapir KD, Goldberg RA, Sinha S, et al. Methylprednisoloneexacerbates axonal loss following optic nerve trauma in rats. Restor NeurolNeurosci. 2000;17(4):157-163. .

12. Steinsapir KD, Seiff SR, Goldberg RA. Traumatic optic neuropathy: wheredo we stand?. Ophthal Plast Reconstr Surg. May 2002; 18(3):232-4.

13. Cook MW, Levin LA, Joseph MP, et al. Traumatic optic neuropathy. Ameta-analysis. Arch Otolaryngol Head Neck Surg. Apr 1996; 122(4):389-92.

14. Wang BH, Robertson BC, Girotto JA, et al. Traumatic optic neuropathy:a review of 61 patients. Plast Reconstr Surg. Jun 2001; 107(7):1655-64.

15. Bracken MB, Shepard MJ, Holford TR, et al. Administration ofmethylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hoursin the treatment of acute spinal cord injury. Results of the Third NationalAcute Spinal Cord Injury Randomized Controlled Trial. National AcuteSpinal Cord Injury Study. JAMA. May 28 1997; 277(20):1597-604.

16. Carta A, Ferrigno L, Salvo M, et al. Visual prognosis after indirect traumaticoptic neuropathy. J Neurol Neurosurg Psychiatry. Feb 2003;74(2):246-8

17. Girard BC, Bouzas EA, Lamas G, et al. Visual improvement aftertransethmoid-sphenoid decompression in optic nerve injuries. J ClinNeuroophthalmol. Sep 1992;12(3):142-8Goldberg RA, Steinsapir KD.

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

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

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

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

First AuthorJ.L. Goyal MD, DNB

49www.dosonline.org

Vascular lesions of the orbit are relatively uncommon, usuallybenign lesions in the orbit producing proptosis and more

rarely visual disturbances in all age groups. As knowledge increasedtheir pathogenesis and morphology has become clearer and sothe classifications. Traditionally vascular lesions are classified onthe basis of their growth pattern, clinical features and histologiccomposition. Because of their uncommon presentations andrareity such lesions still present a diagnostic dilemma. Mullikenand Glowacki classified these lesions on basis of their naturalhistory, including their growth pattern and histologic compositionin the following groups• Capillary hemangiomas• Venous vascular malformations (cavernous malformations

and orbital varices)• Venous lymphatic malformations (capillary, cavernous, and

cystic lymphatic malformations)• Arterial and arteriovenous lesions (arteriovenous

malformations, arteriovenous fistulas and ophthalmic arteryaneurysms)

• Neoplasms (hemangioblastomas, hemangiopericytomas,choroidal hemangiomas, choroidal melanomas and vascularmetastases)

• Miscellaneous (Coats disease).Hemodynamics is an important factor which affects thepresentation and the treatment modality of a vascular growth.The clinical properties of orbital vascular malformations aredetermined by their relations with a major vessel type (arterial,venous or lymphatic). The same is true of shunts and new growths.For Example, An AV malformation getting a supply from theartery drains directly into SOV or IOV which further drain intocavernous sinus. This lesion, lacking intervening capillaries act as ahigh-flow shunt and present as rapid proptosis with pulsations,turbulence, progressive arterializations and potential thrombosis.Vascular lesions of orbit typically present as gradual onset proptosisat birth or at early adulthood. A history of trauma may be aprecipitating factor in AV-shunts and orbital varices. These lesionsusually increase on valsalva or lifting heavy weights. Forcedexpiration against resistance (valsalva) raises venous pressure inthe neck, face and head, such that orbital masses with significantdraining veins will increase in volume, evidenced by transientincrease in proptosis. This phenomenon is typically demonstrablein the presence of congenital venous varices or AV malformations,but may also be seen with acquired carotid-cavernous fistula orwith primary or secondary bony defects which transmit intracranialpressure to the orbital contents. Such effect may be seen in infantsduring crying or on head hanging. Histology forms the hallmarkfor the final diagnosis of a vascular lesion but certain characteristicsseen on radiological studies and Doppler are also typical for

Vascular Lesions of the OrbitGaurav Bharti DOMS, Taru Dewan MS, FRCSEd, Akhila Prasad MD, Shashi Vashisht MS

Department of Ophthalmology

Dr. Ram Manohar Lohia Hospital, New Delhi

different lesions. Doppler, CT scan and MRI are thus the importantdiagnostic tools for diagnosis and categorization of these lesions.Although ultrasound echography, CT, MRI and angiography havegreatly changed the diagnostic work up of orbital lesions, diagnosisis still made with errors in certain cases. And most cases demanda thorough knowledge of the clinical behavior, radiologicalappearance and histological features to come to the confirmatorydiagnosis.

Capillary Hemangioma

Capillary hemangiomas are the most common benign lesion ofthe orbit. These are usually unilateral, nonencapsulated, poorlycircumscribed, often lobulated, and largely extraconal lesions theseare present during birth or present at two-three months of infancy.They are more common in females and premature infants andtend to involute gradually after a short growth phase. The tumoris marked by two phases, a proliferative phase which lasts for 8-18months and is marked by rapid tumor growth and an involutionalphase which comes at an age of 5 years marked by tumourregression. Due to their rapid growth during childhood these lesionscan be differentiated from lymphangiomas and AV malformationswhich may present at the same time but grow slowly.The benign tumor presents as proptosis which increases on crying,and with periocular cutaneous involvement or telltale sign of same.Proptosis in general is mild, but can be severe enough to causecorneal exposure. The tumor is mostly extraconal but intraconalextensions are also found in some cases especially through theoptic canal and the superior orbital fissures. The tumor may spreadacross various tissue planes and can involve the lacrimal gland andthe extraocular muscles. Although benign in nature, hemangiomasin certain locations can impede vital functions, causing problemssuch as airway obstruction (laryngeal hemangiomas), high-outputcardiac failure (large hepatic hemangiomas), and visual impairment(periocular hemangiomas). The Kasabach-Merritt syndromepresents with a consumption coagulopathy and thrombocytopeniasecondary to platelet sequestration in large visceral hemangiomasHemangiomas are classified using the Ceisler classification systemas follows:• Type 1: small, flat periocular hemangioma with no ptosis.• Type 2: small, localized, raised, superficial periocular

hemangioma• Type 3: diffuse, bulky periocular hemangioma• Type 4: diffuse, nonbulky periorbital hemangioma• Type 5: deep bluish lesion with no superficial componentAlong with the clinical features various forms of diagnostic testsare of most value for diagnosis of hemangiomas. On CT they arenon encapsulated, usually lobulated, heterogenous but showsimmense enhancement on contrast injection. They may alsodemonstrate phlebolith formation and can have both intraconaland extraconal extensions (Figure 1). On MRI they are usuallyhypointense on T1-weighted images and iso- to hyperintense onT2-weighted images (Figure 2). They enhance intensely on contrast

Ocul

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sty


Figure 1: CT scan of acapillary hemangioma

showing phleboliths and intracranialextension of the lesion

Figure 2: MRI (T2 image) of a Capillaryhemangioma showing a hyperintense image

Figure 3: Doppler exhibiting both venousand capillary flow in a case of orbital

capillary haemangioma

injection and show both intralesional and perilesional flow voids.Doppler shows both venous and arterial component with a highvelocity flow (Figure 3). Pathological findings includeThe morbidities associated with capillary hemangiomas is thethreat of compressive optic neuropathy, extraocular muscledysfunction, amblopia and cosmetic disfigurement. The first-linetreatment of capillary hemangiomas is simple observation. Sincemost of these lesions regress on their own, there is no need tointervene unless one of the above criteria is met. Corticosteroids,in various formulations, also have been used in the treatment ofcapillary hemangiomas. Radiotherapy and corticosteroids are botheffective in individual cases, but many lesions are resistant to allforms of present treatment. Interferon alfa-2a has emerged as anew modality to combat the life-threatening and vision-threatening hemangiomas of infancy that are resistant to steroidtreatment. Laser therapy has been attempted but is stillcontroversial. Incisional surgical techniques also have had variablesuccess. Surgical ligation of the hemangiomas produces equivocalresults. Vascular embolization of the lesions should be used forlarge extraorbital hemangiomas only. Primary excision also hasbeen advocated for infantile hemangiomas. Early surgicalintervention can be considered as a primary treatment option inselected, isolated capillary hemangiomas without a significantcutaneous component.

Cavernous Haemangioma

Cavernous hemangiomas are most common benign orbital tumorsfound in adults, most commonly in females aged 18-72. They arewell-encapsulated tumors found in the intraconal space andcomposed of very large vascular channels. The vessel walls containsmooth muscles and there is fibrous tissue in the trabeculae thatseparates the vessels. Cavernous hemangiomas produce a slowpainless progressive proptosis which is usually axial .The mass

effect on the surrounding structures can lead to symptoms likedecreased vision, diplopia, extraocular muscles or pupillarydisturbances. Zauberman and Feinsod described a pregnancy-induced increase in symptomatology of these lesions. Mostcavernous angiomas are found between the optic nerve andextraocular muscles within the intraconal space. Biopsy of theselesions may lead to uncontrollable haemorrhage and is notrecommended. Clinical presentation and radiological evidencesare the hallmark for the diagnosis of cavernous hemangioma,confirmed by histology of the excised specimen.CT scan detects an oval or round shaped, sharply marginated,homogenous lesion. They occasionally contain microcalcifications

51www.dosonline.org

Figure 4: Axial T1-weighted MR image shows awell-circumscribed, hypointense intraconal

cavernous hemangioma lesion

Figure 5: Cavernous haemangioma ,T1-weighted fat-suppressed MR image, postcontrast shows inhomogenous enhancement

(phleboliths) and may produce expansion of the orbital wallsUltrasound study can find a uniform high-echogenicity on A-scan.These reflections are secondary to the septae found within thelesion. Doppler flow study may reveal subdued blood flow withinthe angioma. T1-weighted MR image demonstrates an intraconal,lobulated, regularly marginated lesion with hypointense signaland small serpentine flow voids (Figure 4). T2-weighted fat-suppressed image shows the same lesion with slight signalhyperintensity, characteristic fine internal septa, and flow voids.Contrast-enhanced T1-weighted fat-suppressed imagedemonstrates homogeneous intense enhancement of the lesionand provides improved delineation of the flow voids (Figure 5).Fine needle aspiration of these lesions reveales only the bloodharbored in the large cavernous spaces. Histology shows engorgedvascular channels, which are tightly knit and separated by fibrousseptae and a dense fibrous pseudocapsule. Axial proptosis,extraocular muscle dysfunction, and compressive optic neuropathyare the sequelae that can occur due to enlarging cavernoushemangiomas.The lesions are usually managed conservatively, and surgicalexcision is reserved for those compressing on the optic nerve,cosmesis or those causing ocular symptoms like diplopia.

Orbital Varix

Varices are the most common cause of spontaneous orbitalhemorrhage. Orbital varix is an intraorbital mass composed ofabnormally large veins. A varix like anywhere else can either be asingle vessel with saccular dilatations or can be multiple vesselstangled together. Varices have been differentiated by Lloyd intoprimary and secondary. A primary varix is usually present sincebirth or may manifest by the early part of the second decade.Secondary or acquired varices are secondary to a trauma or related

to a change in hemodynamics of the orbit induced by extraorbitallesions, such as carotid-cavernous fistula, dural fistula, brainarteriovenous malformation, or intracranial dural sinus occlusion.A true varix is in direct communication with the vein and shows apulsating proptosis on valsalva or on crying, and the patient mayexperience extreme pain during such episodes. The patient maybe enophthalmic at rest because of the enlarged orbits and fatatrophy. An anteriorly located lesion may lead to lid edema andmarked restriction of ocular motility.Proptosis with resulting enlargement of mass can be demonstratedduring imaging procedures. On ultrasound the finding of anintermittently anechoic retrobulbar lesion that exhibits intrinsicflow during the Valsalva maneuver is indicative of a varix, andcolor Doppler imaging may demonstrate a reversal of flow towardthe transducer during the Valsalva maneuver. Plain orbital x-rayand CT shows enlarged orbital walls and small, round areas ofcalcifications as result of recurrent thrombosis. A mass of veins ora massively enlarged vein may be seen on venography. MR imaging,varices have hypo- to hyperintense signal on T1-weighted images,have hyperintense signal on T2-weighted MR images, and usuallyenhance intensely after the administration of contrast material.There are only two indications for intervention in an orbital varix.Extreme orbital pressure with functional deficit or intractable pain,and cosmetic disfigurement. A varix rarely leads to visual loss orextreme pain unless there is spontaneous intraorbital hemorrhageor unexpected thrombosis. Methods of treatment of orbital varixinclude surgical excision, electrothrombosis, injection of sclerosingagents, and venous embolization with microcoils. Most primaryorbital varices do not require aggressive treatment. In cases ofacute thrombosis or hemorrhage, surgery may be required toremove a hematoma or clotted vessel. For patients with severeintermittent exophthalmos and cosmetic disfigurement, treatment


Figure 6: AV Malformation MRI ( T1)

by embolization after surgical exposure is a safe and relativelyeasy procedure, particularly if the orbital varix is consistent withsaccular or segmental venous dilatations.Arteriovenous Communications

In arteriovenous (AV) communications, blood flows from arterialcirculation directly into the venous circulation without passagethrough intervening capillaries. AV malformations can occur as acongenital disorder or occur spontaneously after trauma. Theymay present as orbital swelling and chemosis, increased episcleraland intraocular pressure, and pulsatile exophthalmos (High-flowstates). A low-flow state displays similar signs and symptoms butto a lesser degree. AV communications are classified into eitherAV malformations, Carotid-cavernous sinus fistulas (CCF) or duralshunts.Congenital arteriovenous malformations (AVM) are developmentalanomalies that occur when the embryonic vascular network failsto differentiate. AV malformation gets a direct inflow from adedicated vessel of an arterial system and out flow through anormal vein downstream. In case of orbit the down flow channelis either the SOV or IOV which drain into the cavernous sinus.The elevated pressure in the venous pathways draining the orbitproduces orbital venous congestion. The congestion is reflectedby dilation of the veins on the surface of the sclera, producingchemosis. Congestion and pulsatile proptosis is also apparent onincreased pressure states produced during valsalva, lifting heavyweights and bending forward. A bruit is produced by thearterialized turbulent flow entering the veins. Over time the thinwall of the AVMs veins rupture causing spontaneous bleedingwithin the brain. The pulsation and bruit can usually be diminishedby compression of the ipsilateral common carotid artery. US, CTwith standard and angiographic protocols, and MR imaging(Figure 6) with standard and angiographic protocols can helpdiagnose arteriovenous fistulas; however, conventional catheter-based angiography typically is required for precise definition andtreatment planning. On histology mature arteries and veins areseen in the tumour. Intraorbital AVMs are exceptions toendovascular treatment because embolization of the central retinalartery, a distal branch of the ophthalmic artery, can complicate theprocedure and devastate a patient’s vision. The small caliber andtortuous course of the ophthalmic artery make selectivecatheterization difficult. Embolization is possible only in a fewextraorbital AVMs. Surgery plays an important role in such lesions.Carotid-cavernous fistulas are direct communications betweeninternal carotid and cavernous sinus. It may occur spontaneouslyor follows ocular or head trauma. Majority occurring after basalskull fractures or penetrating orbital injuries affecting the medialor inferomedial orbital wall as well as superior orbital fissure, oroccur after carotid artery surgery or aneurysmal rupture.Spontaneous carotid cavernous fistulas have been reported inpatients with Ehlers-Danlos syndrome, osteogenesis imperfecta,and pseudoxanthoma elasticum. The fistulas often manifest withthe classic triad of pulsatile exophthalmos, conjunctival chemosis,and an auscultatory bruit. The fistulas occur in middle to lateadulthood and are more common in women. The patient presentswith chemosis, orbital swelling, episcleral venous congestion,elevated intraocular pressure and retinal hemorrhages andischemia. Third and sixth nerve palsy may be associated. Surgeryis indicated in cases where vision is threatened. Ballooncatheterization through an endoarterial route forms the optimal

treatment. A through evaluation by use of contrast angiography isthough required before planning any procedure. Other treatmentmodalities include embolization, electrothrombosis of the fistula,and direct surgery.Dural shunts represent arteriovenous shunts from a dural arteryto either one of the major sinuses or into variceal cortical veins.Patients usually present between the ages of 20 and 79 years. Postmenopausal women are most commonly affected. Spontaneousdural shunts can occur in the elderly patients and have beenreported in patients with Ehlers-Danlos syndrome, osteogenesisimperfecta, and pseudoxanthoma elasticum. Etiologic factorsinclude trauma, surgery, infection, and sinus thrombosis. Theclinical presentations of dural shunts depend on the location ofthe shunt and include tinnitus, cranial nerve palsies, and/or signsrelated to venous congestion in the orbit. CT scan alone is usuallynot useful in demonstrating the dural shunt. Superselectiveangiography of both the internal and external carotid can help todetermine the exact location and haemodynamic features. USGand CT reveals enlargement of SOV and extra ocular muscles inthe involved orbit. Surgical intervention is indicated in patientswith progressive proptosis, intractable glaucoma and debilitatingdiplopia in primary gaze. External carotid artery feeder vessels areembolized with detachable balloons, isobutylcyanoacrylate, orpolyvinyl alcohol particles. Embolization of ICA is notrecommended because of high success rate embolization of ECfeeders and the borderline patency of circle of willis in elderly.Other techniques include electrothrombosis of fistula and directsurgery. Hemodynamically active vascular lesions of the orbit areoften clinically challenging to treat, both because of the complexityof the vascular anatomy and the delicacy of the cardinal structuresthat are involved and vulnerable to damage.Hemangipericytoma

Hemangiopericytoma is a highly vascular tumor that is relativelycommon in the musculoskeletal system (lower extremities), pelvis,

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and retroperitoneum. Approximately 15% of these tumors arisein the extracranial part of the head and neck. Origin within theorbit is rare. The tumors may occur at any time, from infancythrough late adult life. Overall, hemangiopericytomas demonstrateno predilection for either sex. Hemangiopericytomas most oftenmanifest with slowly progressive, sometimes painful proptosisand decreased visual acuity, extraocular motility abnormalities,visual field deficits, and congestion of the retinal and choroidalvessels. They can be both benign and malignant or have featuresof both and are capable of metastasizing to distant organs likelungs, bone and liver. The typical location is extraconal; lesionscommonly arise in the adjacent paranasal sinuses. On Ultrasonography, hemangiopericytomas are moderately hyperechoic,with high vascularity on color Doppler images, a feature thatpermits their differentiation from cavernous hemangiomas. AtCT, they are typically homogeneous and lobulated. The lesionsmay be well circumscribed and confined to the orbit, or they mayhave indistinct, irregular margins. When large, they may causeosseous erosion and remodeling and may involve the centralnervous system. Rarely, intralesional calcification is present. Ondynamic contrast-enhanced CT, hemangiopericytomas exhibitmarked early arterial phase and early venous phase enhancementfollowed by rapid washout. On MR imaging, the signal intensity ofhemangiopericytomas is similar to that of gray matter on T1- andT2-weighted images, a feature that helps differentiate these lesionsfrom cavernous malformations. Digital subtraction angiographydemonstrates a prominent arterial supply with an early floridblush and persistent tumor staining, features that help differentiatehemangiopericytomas from meningiomas (which typically containmultiple vessels and show a late tumor blush) and schwannomas(which typically show no tumor blush).Hemangiopericytomas are usually lobulated, encapsulated, andwell circumscribed, but they may have infiltrative margins.Histologic findings range from benign to malignant characteristics,with many tumors demonstrating both. Diagnostic criteria includethe number of mitotic figures per high-power field, the degree ofcellularity and the degree of nuclear atypia. These mesenchymaltumors arise from the pericytes of Zimmerman, contractile cellsthat surround the outer aspect of small vessels and that are thoughtto regulate lumen size and produce collagen. Histologic analysisdemonstrates staghorn-like capillary spaces lined by plump,proliferating pericytes, with intervening fibrous septa. Thestandard treatment is wide surgical excision. On surgery they aresolid and dark blue to violaceous and may bleed extensively andmaybe exceedingly friable. Postoperative irradiation isrecommended for incompletely excised lesions. Local recurrencein approximately 30% of cases has been reported, and lesions mayrecur up to 30 years after initial treatment.Hemangioblastomas

Hemangioblastoma is a benign vascular tumor that is commonlyassociated with von Hippel- Lindau disease. Mosthemangioblastomas that occur within the orbit are located in theretina, although locations within the optic nerve have beenreported. Von Hippel-Lindau disease is an autosomal dominantgenetic disorder with variable expressivity that is localized tochromosome 3. It is characterized by both benign and malignanttumors. Without a family history, at least two cerebellarhemangioblastomas or one hemangioblastoma plus one associatedvisceral tumor (renal cell carcinoma, pheochromocytoma) arenecessary for a diagnosis of von Hippel-Lindau disease.Histologically, the retinal tumors first described by von Hippel are

hemangioblastomas, and the term retinal angioma is therefore amisnomer. Hemangioblastomas represent 1%–2% of all primarytumors of the central nervous system. Seventy percent of patientswho present with a hemangioblastoma do not have a familyhistory of von Hippel-Lindau disease. However, patients with asporadic nonhereditary hemangioblastoma should undergofurther evaluation for evidence of von Hippel- Lindau disease.Ocular abnormalities due to a retinal hemangioblastoma are theearliest manifestations of von Hippel-Lindau disease in about 50%of cases. The hemangioblastoma typically appears as a dilatedartery leading from the optic disc to a peripheral (most oftentemporal) tumor with an engorged draining vein that leads backto the optic disc. Less commonly, the lesion is near or on the opticdisc. Patients with a retinal hemangioblastoma are usuallyasymptomatic until the 3rd decade of life, although theenlargement of a centrally located lesion may produce an earliervision loss. A retinal hemangioblastoma may be a predisposingfactor for retinal detachment, macular edema, and glaucoma. Earlydetection, followed by laser coagulation or cryotherapy, mayprevent vision loss.

References

1. Rodgers R, Arthur S, Grove Jr. Vascular lesions of the orbit. Principle andPractice of Ophthalmology (Jakobiec). 2nd Edition, Vol 4, section 8:3144-3155.

2. Haik BG, Jakobiec FA, Ellsworth RM, Jones IS. Capillary hemangioma ofthe lids and orbit: an analysis of the clinical features and therapeutic resultsin 101 cases. Ophthalmology. 1979:86;760-792.

3. Dubois J, Garel L. Imaging and therapeutic approach of hemangiomasand vascular malformations in the pediatric age group. Pediatr Radiol.1999;29:879-893.

4. Plesner-Rasmussen HJ, Marushak D, Andersen M. Sequelae of capillaryhemangioma of lids and orbita. Scand J Plast Reconstr Surg.1983;17(3):241-5.

5. Millischer-Bellaiche AE, Enjolras O, Andre C, et al. Eyelid hemangiomasin infants: contribution of MRI. J Radiol. 2004;85:2019-2028.

6. Brackup AH, Haller ML, Danber MM. Hemangioma of the bony orbit.Am J Ophthalmol 1980;90:258–261.

7. Relf SJ, Bartley GB, Unni KK. Primary orbital intraosseous hemangioma.Ophthalmology 1991;98:541–547.

8. Rootman, Kao SC, Graeb DA. Multidisciplinary approaches tocomplicated vascular lesions of the orbit. Ophthalmology. 1992sep;99(9):1440-6.

9. Ranchod TM, Frieden IJ, Fredrick DR. Corticosteroid treatment ofperiorbital haemangioma of infancy: a review of the evidence. Br JOphthalmol. 2005 Sep;89(9):1134-8.

10. Huna-Baron R, Setton A, Kupersmith MJ, Berenstein A. Orbitalarteriovenous malformations mimicking cavernous sinus duralarteriovenous malformation. Br J Ophthalmology. 2000 jul;84(7):771-4.

11. Meyer E, et al. Fine-needle aspiration of orbital lesions. Ann Ophthalmol.1983 Jul;15(7):635-8.

12. Char DH. Management of orbital tumours. Mayo Clin Proc. 1993Nov;68(11):1081-96.

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

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

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

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

First AuthorGaurav Bharti DOMS

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A 5 day old female child, born out of a consanguineous marriagein a Muslim family, presented to the out-patient services of

Safdarjung hospital with the chief complaints of both side bigsized eyes and whitish opacity in the black part of eye since birthand not opening eyes to bright light. Mother gave No h/o excessivewatering / discharge /redness.

Birth history: full term normal vaginal delivery with no H/O birthtrauma/ systemic illness/ topical medication use. The Obstetrichistory was uneventful.

Family history: child is the 4th child from a consanguineous marriagewith no H/O of similar complaints in the family/ siblings.

On Examination: General physical examination, head to toe waswithin normal limits with no systemic abnormality.

Local examination: photophobia present/ blepharospasm present,with bilateral symmetrical enlargement of eyeball, the cornealvertical and horizontal diameters appeared enlarged, corneal hazewas present (L/E>R/E), sclera appeared thin and blue, digitaltension was raised bilaterally, regurgitation on pressing over thelacrimal sac area was negative. Posterior segment could not beevaluated due to hazy media (edematous cornea).

Provisional Diagnosis of B/L congenital glaucoma

Management

Examination under anaesthesia was done on day 2 (Table 1,Figure1), followed by R/E trabeculotomy with trabeculectomy usingMitomycin-C, 0.04%, applied for 2 minutes. The L/E was startedon topical medication (E/D dorzolamide 2% TDS and E/D timolol0.25% BD) which was then taken up for similar procedure 1 weeklater.

Congenital Glaucoma in a 5 Day Old InfantShivani Kochhar MBBS, K.P.S. Malik MS, MNAMS, V.S. Gupta MS


Safdarjung Hospital, New Delhi

Following this, the child was seen once weekly and features likephotophobia, blepharospasm and epiphora were assessed whichshowed marked improvement The examination under anaesthesiawas repeated at post operative week 6 (Table2, figure 2 {right eye},Figure 3{left eye}) which showed increased clarity of cornea andconsiderable decrease in the corneal haze with tension reducing to11 mmHG in both eyes.

Discussion

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

Glaucoma as a cause of childhood blindness is 7%2,3(North/SouthIndia) and 4.9% (Delhi)4 . It is Bilateral in 65-80%1, with malepredominance (65%)1, onset in 1st yr of life is seen in >80% ofchildren1 but diagnosed at birth in less than 25% cases1.

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Figure 1: Microscopic picture of right eye andleft eye preoperatively showing corneal haze,

stromal edema and haab’s striae

Table 1: Findings on examination under anaesthesia done preoperatively (day 2)

R/E L/E

Cornea Hazy HazyStromal edema + Stromal edema +Habb’s striae + Habb’s striae +

Corneal diameter

Horizontal 13 mm 13 mm

Vertical 13 mm 13 mm

IOP (schiotz) 65 mmHG 70 mmHG

Fundus Glow + Glow +Optic disc: Optic disc:appears normal appears normalCDR : 0.2 CDR: 0.2Rest details not Rest details notseen cur to seen cur tohazy media hazy media

Figure 2: Microscopic picture of right eye preoperatively(right) and post operartive at week 6 (left)


Congenital glaucoma is essentially a surgical disease with medicalmanagement being a temporary option. Various studies advocatethat the surgical procedure of Choice for congenital glaucoma is“Primary combined trabeculotomy–trabeculectomy” 5,6,7,8

Intra Ocular Pressure rise in young children can result in severevisual morbidity due to corneal opacification induced myopia,amblyopia and glaucomatous optic atrophy. Hence, timely reductionof IOP and stabilisation of refractive error are essential to avoidthese sequalae. Therefore various studies advocate “surgery asearly as in the first week of life, may improve the chances of cure”9,10,11

Surgery in infants can be very challenging since they have to be putunder general anaesthesia at a very early age in life and also becausean infant’s eye behaves differently from that of an adult by virtueof

• Definition of surgical limbus is more difficult

• Abnormally stretched limbus makes it difficult to fashion thescleral flap and cannulate it

• More rapid healing and exuberant scarring processes leadingto a high failure rate.

The use of mitomycin C (MMC) as an adjunct intraoperative drugwas first described by Chen et al in 1983 following which numberof studies have reported a success rate varying between 60-95%12,

13, 14, 15, 16..Ali A hazmi et al reported that the success rate of theglaucoma filtering surgery utilizing MMC goes up with increasingage but so does the complication rate” and concluded that the netsuccess rate was highest in the age group <6 months .17 A very lowrate varying from 0-8% of endophthalmitis post combined surgerywith MMC has been reported12, 13, 16

In deciding upon simultaneous B/L surgery, the possible risk of B/L endophthalmitis has to be balanced against the advantages ofone anaesthesia versus two cost effectiveness and early visualrehabilitation. Wheeler performed a survey of 500 pediatricophthalmologists and glaucoma specialist who did not recommendB/L pediatric intraocular surgery .18

Visual rehabilitation is as important in the management of thedisease as is intraocular pressure control and involves correctionof refractive error, anisometropia, amblyopia, mediaopacities(corneal scarring) and timely keratoplasty if required.

Post operative protocol for follow up as given by Mandal et al19says that the child should be seen weekly in the OPD and thedegree of relief from photophobia/ tearing/ blepharospasmshould be assessed. The examination under anaesthesia shouldbe repeated post surgery 3-4 weeks, if IOP is stable then every 3months, followed by quarterly interval for the first 1 year, thenbiannually until the child is cooperative for OPD examination.Such children have to be kept in follow up indefinitely.

Salient features

• It is very important to diagnose and surgically treat a child ofcongenital glaucoma at the earliest to prevent severe visualmorbidity.

• Combined surgery with MMC has shown a high net successrate in children < 6 months of age.

• The available literature does not allow a formal comparisonbetween the risks involved in multiple anaesthesia and thepossible risks of B/L endophthalmitis.

• And since the rate of complication goes up with the use onmitomycin C, we recommend one eye at a time.

• It is imperative to inform and educate the parents about theneed to follow up which is life long.

References

1. Anil K Mandal, Peter A Netland; The pediatric glaucomas; 2006.

2. Dorairaj et al ophthalmic epidemiology 2008.

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

R/E L/E

Cornea Decreased edema(R>L) Claritybetter Pupil seen

Corneal diameter

Horizontal 13 mm 13 mm

Vertical 13 mm 13 mm

IOP (schiotz) 11 mmHG 11 mmHG

bleb Well formaed / Well formaed /diffuse/ diffuse/avascular avascular

Fundus Glow + Glow +Optic disc: Optic disc:appears normal appears normalCDR : 0.2 CDR: 0.2Background Backgroundappears normal appears normal

Figure 3: Microscopis picture of left eyepreoperatively (right) and post operative at

week 6 (left)

57www.dosonline.org

First AuthorShivani Kochhar MBBS

3. Harsha Bhattacharjee, Kalyan Das, Rishi Raj Borah et al Causes ofchildhood blindness in the northeastern states of India IJO2008,56,6;495-499

4. Titiyal et al, Causes and temporal trends of blindness and severevisual impairment in children in schools for the blind in NorthIndia, BJO aug 2003

5. Anil K mandal at el Outcome of surgery on infants younger than 1month with congenital glaucoma, presented as a paper at the annualmeeting of the AAO,oct 2003,110,10,1909-1915

6. Anil K. Mandal, Prashant G. Bhatia et al, Ophthalmology Long-term Surgical and Visual Outcomes in Indian Children withDevelopmental Glaucoma Operated On within 6 Months of Birth2004.

7. Laudo Silva Costa, Reoberta Martins da silva costa, CombinedTrabeculotomy–Trabeculectomy as a First Surgical Procedure forPrimary Congenital Glaucoma, Annals of Ophthalmology 2006.

8. São Paulo, Long-term surgical outcomes of primary congenitalglaucoma in China ,Clinics vol.64 no.6 June 2009.

9. Shaffer RN, Prognosis of goniotomy in primary infantile glaucoma(trabeculodysgenesis). Trans Am Ophthalmol Soc. 1982.

10. Shaffer RN, Hoskins HD. Montgomery lecture. Goniotomy in thetreatment of isolated trabeculodysgenesis. Trans Ophthalmol SocUK. 1983.

11. Rajeev Jain et al Trabeculectomy with Mitomycin-C (MMC) AsPrimary Surgery In Congenital Glaucoma, AIOC 2006.

12. Susanna R, Oltrogge et al. Mitomycin as adjunct chemotherapy incongenital and developmental glaucoma. J Glau 1995.

13. Mandal Ak, Walton DS et al MMC augmented trabeculectomy inrefractory congenital glaucoma ophthalmol 1997.

14. R Ehrlich, M Snir, et al Augmented trabeculectomy in paediatricglaucoma BJO 2005.

15. A Al-Hazmi, A Awad et al, Correlation between surgical successrate and severity of congenital glaucoma. BJO 2005.

16. Jair Giampani Junior et al, Efficacy and safety of trabeculectomywith MMC in childhood glaucoma: a study of results with long-term follow-up, clinics 2008.

17. Ali Al hazmi, johan zwaan et al, Effectiveness and complications ofmitomycin C use during pediatric glaucoma surgery, ophthalmol1997.

18. Wheeler DT, Stager DR et al endophthalmitis following pediatricintraocular surgery for congenital cataract and congenital glaucomaJ pediatr ophthalmol strabismus 1992.

19. Anil K Mandal, Current concepts in the diagnosis and managementof developmental glaucomas, IJO 1993.

Congratulations

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

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

� Dr. (Lt. Col. ) Sanjay Kumar Mishra has been awarded Vishist Seva Medal by President Of India on 26 January2010. He is posted at Army Hospital (Research & Referral) Delhi Cantt and is at present pursuing long term trainingin Vitreo-retinal surgery at the prestigious R.P. Centre AIIMS. He hails from Uttar Pradesh.

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

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

59www.dosonline.org

We present a case of a 25 year old healthy adult male; whopresented to us with discharge from inner aspect of the

right upper lid since 15 days.

History revealed a fall from his bicycle about a month back whenhe sustained injury to the right side of the face. He developedswelling in his right upper and lower lids along with wound/abrasionin upper lid on the inner aspect. He visited a nearby doctor andwas given first aid treatment. A CT scan was done then. Afterabout 15 days later he noticed that there was a purulent dischargefrom inner aspect of the right upper lid, which was presentthroughout the day. This was associated with restriction of eyemovements and diplopia on looking towards the left side. Hecomplained of pain, more so on extra ocular movements. Rednessof the eye was present. No past history of tuberculosis or contactwith Tuberculosis.

On Examination

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

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

An Unusual case of Discharging SinusAniket Shastri MBBS, Anuj Mehta MS, KPS Malik MS, MNAMS, Sangeeta Abrol MS, Malvika Gupta DO


Safdarjung Hospital, New Delhi

Provisional Diagnosis

With this we made a diagnosis of fracture of the right medial wallof the orbit with (?) impaction of soft tissue with (?) orbital cellulitiswith a discharging sinus

Investigations

Routine investigations were within normal limits. Chest X ray wasnormal. He produced a CT scan report which read as a Normalstudy of eyeball with fluid collection in extra ocular space with amedial wall fracture.

An Ultrasound B-scan was done on the same day that showedlinear hyper-echoic lesion with a surrounding hypoechoic area

Figure 1: Ulcer with discharging sinus

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

area. No post acoustic shadowing

Figure 3: Coronal scans of CT showing welldefined, round hypodense lesion in the medial

wall of the right orbit

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

Sequential coronal non contrast CT of nasal sinuses in bone windowshowed a well defined, round hypodense lesion with attenuationsimilar to air in the medial wall of the right orbit (Figure 3). Thislesion was seen pushing the optic nerve supero-laterally withpreservation of the fat plane in between indicating no involvementof the optic nerve. It was seen extending into right middle andposterior ethmoidal sinuses. The axial view (Figure 4) is showingthe hypodense lesion with size of the hollowness same throughout-extending from the equator of globe to the posterior ethmoidalsinuses.

Summarizing the radiological findings-

• Hypodense lesion-attenuation similar to air

• Well Defined, Circumscribed

• Size of hollowness was same throughout- suggestive of foreignbody

• No post acoustic shadowing on U/S B scan- suggestive ofnon-metallic

• Hyperechoic on ultrasound

Final Diagnosis

Foreign body in the medial part of the right orbit-non-metallic,probably, wood or glass.

Treatment

Meanwhile the patient was started on Intra-venous antibioticsand anti-inflammatory.

Exploration for a suspected Foreign Body under GeneralAnesthesia was planned. On the decision about how to approach,a trans-caruncular approach was chosen over the eyelid skin creaseapproach. This was done to avoid damage to the lid structures

Figure 4: Axial CT scans showing hypodense lesion withsize of the hollowness same throughout- extending fromthe equator of globe to the posterior ethmoidal sinuses.

Figure 5: Trans-caruncularapproach showing removal of the

40 mm wooden piece

Figure 6: The foreign body; multiplewooden pieces

and also as the suspected lesion was not felt anteriorly. NCCT alsoshowed the suspected lesion to be relatively posterior.

On exploration of the sinus, we were able to pick out approximately9-10 pieces of wood with a forceps from the medial part of theorbit- with the largest measuring 35 MM. On further probing ahard mass was felt inside. On pulling it out using an artery forceps,a thick hollow piece of wood of size 40 MM was seen (Figure 5&6).

Post Op: On the first post-op day patient had mild upper lid edemaand conjunctival congestion with limitation of adduction(Figure 7). Shows the clinical picture at post-op day 7- with completehealing of the ulcer and the sinus.

An ultrasound B scan was performed and it showed no evidenceof foreign body.

Discussion

Amongst the various causes of a periorbital discharging sinus, twoimportant ones are

61www.dosonline.org

• retained periorbital foreign body

• periorbital tuberculosis

The diagnosis of periorbital tuberculosis is made on the basis ofclinical features supported by radiological investigations.Polymerase chain reaction and Acid Fast Bacilli cultures providethe investigative evidence

Intra orbital foreign bodies (IOrbFbs) usually occur after a high-velocity injury such as a gunshot or industrial accident but, mayoccur after relatively trivial trauma to the extent that the historymay be unclear

A high index of suspicion is required in the setting of projectileinjuries or in the setting of persistent orbital inflammation after ahistory of periocular trauma, no matter how trivial it seems

Clinical features may be varied-

• Orbital mass

• Pain on eye movements

• Orbital abscess

• Orbital cellulitis

• Diplopia and lagophthalmos

• Finding on computed tomography scan

A CT scan is the standard diagnostic test, because it demonstratesmost Intra Orbital Foreign Bodies, and it is safe in the presence of

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

MRI scans are better at demonstrating wooden foreign bodiesand should be performed after a negative CT scan if there is apossibility of a wooden Intra orbital Foreign Body. An MRI scanmay be performed before a CT scan if there is a definite history ofa wooden Intra Orbital Foreign Body.

Orbital Ultrasonography is a complementary modality.Ultrasonography may be useful when CT and MRI do notdemonstrate a wooden Intra Orbital Foreign Body.

Wooden foreign bodies are notorious for remaining quiescent for along time, before presenting with a variety of complications. Thewound of entry may often be small and self-sealing. Wooden foreignbodies also show a propensity to break during attempted removal.Intraorbital wood is often not detected by standard diagnostic testslike the computed tomography scan, adding to the diagnosticdilemma

Wood, plastic and Air have radiologically similar characteristics-very difficult to distinguish. Air, when trapped inside a foreignbody, will take shape conforming to primary object. This is animportant clue to presence of foreign body.

The presence of an intraorbital mass with a discharging sinusshould evoke suspicion of a retained foreign body, regardless ofthe time interval between the trauma and current presentation. Itis imperative to maintain a high index of suspicion in such cases toavoid misdiagnosis

This case again emphasizes the necessity for careful assessment ofpenetrating wounds of the orbit, however trivial they may appearsuperficially.

References

1. Roberts CF, Leehey PJ 3rd. Intraorbital wood foreign body mimickingair at CT. Radiology 1992;185:507–8

2. Green BF, Kraft SP, Carter KD, et al. Intraorbital wood. Detectionby magnetic resonance imaging. Ophthalmology 1990;97:608–11.

3. Glatt HJ, Custer PL, Barrett L, Sartor K. Magnetic resonance imagingand computed tomography in a model of wooden foreign bodies inthe orbit. Ophthalmic Plast Reconstr Surg 1990;6:108–14.

4. John SS, Rehman TA, John D, Raju RS. Missed diagnosis of a woodenintra-orbital foreign body. Indian J Ophthalmol. 2008 Jul-Aug;56(4):322-4.

Figure 7: Post operative picture day 7.Note the ulcer has healed and sinus closed

First AuthorAniket Shastri MBBS

63www.dosonline.org

Mis

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DNB Paper 1Q1) Clinical picture and management of epidemic

keratoconjunctivitis?

Ans. Links

� Keratoconjunctivitis, Epidemic: eMedicine Ophthalmology.emedicine.medscape.com › ... › Ophthalmology › Conjunctiva

� Epidemic Keratoconjunctivitis Factsheet - NSW Department ofHealth

www.health.nsw.gov.au/factsheets/.../keratoconjunctivitis.html

� ISPUB - New Management Of Epidemic ViralKeratoconjunctivitis

www.ispub.com/ostia/index.php?xmlFilePath=journals/

� EPIDEMIC KERATOCONJUNCTIVITIS

www.ncbi.nlm.nih.gov/pmc/articles/PMC2135294/

� Treatment of Epidemic Keratoconjunctivitis With Idoxuridine(IUDR) archopht.highwire.org/cgi/reprint/73/1/49.pdf

Q2. Fungal Corneal Ulcer?

Ans. Links

� http://www.dostimes.org/FullText.aspx?id=503

� Corneal Ulcer: Diagnosis and Management - Prashant Garg ...www.cehjournal.org/0953-6833/12/jceh_12_30_021.html

� Corneal Ulceration and Ulcerative Keratitis: eMedicineEmergency emedicine.medscape.com › ... › Ophthalmology

� Practice Patterns in the Management of Fungal Corneal UlcersCornea. 28(8):856-859, September 2009.

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

� The Epidemiological Features and Laboratory Results ofFungal Keratitis: A 10-Year Review at a Referral Eye CareCenter in South India

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

Q3. Necrotising Scleritis?

Ans. Links

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

� Scleritis lmk23.tripod.com/scleritis.html

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

� Scleritis: Conjunctival and Scleral Disorders: Merck Manualwww.merck.com/mmpe/sec09/ch101/ch101f.

� Local Treatment of Necrotizing Scleritis with Cyclosporin AHoffmann, F.; Wiederholt, M.Cornea. 4(1):3-7, March 1985.

Q4 Traumatic hyphaema?

Ans. Links

� Hyphema: eMedicine Ophthalmologyemedicine.medscape.com › ... › Anterior Chamber

� Management of traumatic hyphemawww.ncbi.nlm.nih.gov/pubmed/12161209

� Clinical management of hyphaemawww.safpj.co.za/index.php/safpj/article/viewFile/715/621

� The medical management of traumatic hyphaema: a surveyof opinion ...www.ncbi.nlm.nih.gov/pmc/articles/PMC1294050/

� Treatment of traumatic hyphaemawww.ncbi.nlm.nih.gov/pmc/articles/PMC506390/

Q5. MARINA and FOCUS Trials?

Ans. Links

� http://www.mrcophth.com/MARINATRIAL.htm� http://www.dostimes.org/FullText.aspx?id=201� New data from two leading clinical studies show Lucentis® is

first hugin.info/134323/R/1002762/153861.pdfhttp://www.ncbi.nlm.nih.gov/pubmed/16935211

Q7. Ischaemic CRVO?

Ans. Links

� http://www.dostimes.org/FullText.aspx?id=112� http://www.dostimes.org/FullText.aspx?id=287� Central Retinal Vein Occlusion: eMedicine Ophthalmology

emedicine.medscape.com/article/1223746-overview� Management of central retinal vein occlusion.

www.ncbi.nlm.nih.gov/pubmed/12660480

Q8. Sarcoid Uveitis?

Ans. Links

� Sarcoidosis of the Eyewww.sarcoidosisnetwork.org/documents/sarcoideye.html

� Sarcoid Uveitisjnm.snmjournals.org/cgi/reprint/33/10/1851.pdf

� Uveitis associated with sarcoidosis and angiotensin convertingenzyme.www.ncbi.nlm.nih.gov/pmc/articles/PMC1311705/

DNB Paper CrackedImportant Links to Common Questions


Q9. Retinopathy of Prematurity Screening?

Ans. Links



� Screening Examination of Premature Infants for Retinopathyof ...aappolicy.aappublications.org/cgi/content/full/pediatrics;108/3/809

� Retinopathy of Prematuritywww.mrcophth.com/.../Retinopathy % 20 of % 20 Prematurity.htm

Q10. Vision Assessment in Preschool Child?

Ans. Links

� Measuring Vision in Childrenwww.ncbi.nlm.nih.gov/pmc/articles/PMC1705714/

� Vision testing of infants in a child health clinic and at home.www.ncbi.nlm.nih.gov/pmc/articles/PMC1228044/

� Infant Vision Screening-Teller Acuity Test for Pediatric Visual.www.stereooptical.com/html/teller-acuity-cards.html - Cached- Similar

DNB Paper 2Q1. Methods to reduce PCO?

Ans. Links


� http://www.ijo.in/article.asp?issn=0301 4738;year=2004;volume=52;issue=2;spage=99;epage=112; aulast=Pandey

� http://www.ncbi.nlm.nih.gov/pubmed/10627830

� http://bjo.bmj.com/content/89/11/1389.1.full

� http://www.ncbi.nlm.nih.gov/pubmed/19365040?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=2

Q2. Indications and methods of pterygium surgery. Howto prevent recurrences?

Ans. Links




� http://www.ijo.in/article.asp?issn=03014738;year=1998 ;vo lume=46; i s sue=4;spage=203 ;epage=209 ;aulast=Rao;type=0

� http://www.ojoonline.org/article.asp?issn=0974-620X;year=2009;volume=2;issue=1;spage=23;epage=26;aulast=Mahdy;type=0

Q3. Factors influencing sclerotomy sites for vitrectomy?

� Retina 4th Edition, by Stephen Ryan, Volume 3, Page 2150-51.

� Atlas of Vitreo Retinal Surgery, by H. Mackenzie Freemanand Felipe I. Tolentino, Jaypee Brothers Publications, Chapter6, Page 47.

Q4. Indications, procedures and complications ofLateral Orbitotomy?

Ans. Links

� http://www.medscape.com/viewarticle/405714_3




� http://www.ncbi.nlm.nih.gov/pubmed/3940134?ordinalpos=1&itool=EntrezSystem 2.PEntrez. Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews& logdbfrom=pubmed.

Q5. Clinical Picture and Management of CongenitalGlaucoma?

Ans. Links

� http://www.emedicinehealth.com/primary_congenital_glaucoma/article_em.htm

� http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi? book=gene&part=glc

� http://www.ijo.in/article.asp?issn=0301-4738;year=1993;volume=41;issue=2;spage=51;epage=70; aulast=Mandal

� http://www.iovs.org/cgi/reprint/7/2/127.pdf


Q6. Fuch’s Heterochromic Cyclitis?

Ans. Links

� http://emedicine.medscape.com/article/1208706-overview

� www.uveitissociety.org/pages/diseases/fhu.pdf

� http://www.ncbi.nlm.nih.gov/pmc/articles/PMC504237

Q7. Prevention and Management of PBK?

Ans. Links




65www.dosonline.org

Q8. Recent Methods for Treatment of Keratoconus?

Ans. Links





Q9. Acute Management of Alkali Burns?

Ans. Links

� http://www.emedicinehealth.com/chemical_eye_burns/page2_em.htm




Q10. Indications, Contraindications and Complicationsof Phakic IOLs for High Myopia?

Ans. Links





� http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684439.

DNB Paper 3Q1. Clinical Picture & Management of Congenital

Epiphora. Indications for Surgical Intervention?

Ans. Links



� http://bjo.bmj.com/content/85/3/314.abstract

� www.ncbi.nlm.nih.gov/pmc/articles/PMC1772826/

� Congenital epiphora as a potential cause of amblyopia

� www.opt.indiana.edu/ce/peddz/epiphora.htm

Q2. Clinical Picture of Heredomacular Degeneration andits mode of Inheretence?

Ans. Links

� http://www.ijo.in/article.asp?issn=0301-4738;year=1983;volume=31;issue=3;spage=115;epage=118;aulast=Khosla

� http://bjo.bmj.com/content/56/11/817.full.pdf

Q3 Differential Diagnosis Malignant Lid Tumors?

Ans. Links

� www.springerlink.com/index/M035P8H24K343M13.pdf

� http://www.aafp.org/afp/980600ap/carter.html

� linkinghub.elsevier.com/retrieve/pii/S0161642099001359

� Clinicopathological Features of Eyelid Skin Tumors. ARetrospective Study of 5504 Cases and Review of Literature

Q4. Non Arteritic AION?

Ans. Links



� www.eyeassociates.com/understanding_a_stroke_of_the_op.htm

� www.iovs.org/cgi/reprint/34/7/2260.pdf

� www.ncbi.nlm.nih.gov/pubmed/3229901

� http://webeye.ophth.uiowa.edu/dept/aion/12-AION-incipient.htm

� www.ajnr.org/cgi/content/full/27/2/255

� http://jnnp.bmj.com/content/53/10/830.abstract

Q5. Role of HBA1c, Blood Pressure and Blood Cholesterolin Prevention and Management of DiabeticRetinopathy?

Ans. Links

� http://www.nei.nih.gov/health/diabetic/retinopathy.asp

� http://www.sma.org.sg/smj/4106/articles/4106ra1.pdf


� http://linkinghub.elsevier.com/retrieve/pii/S0002939407005351


Q6. Modern methods for the diagnosis andmanagement of POAG?

Ans. Links





� http://linkinghub.elsevier.com/retrieve/pii/S016164209990458X

� ftp://fastlink.nih.gov/pub/staff/schaffer/webpapers/POAGhg.pdf

� http://www.replaylearning.com/mediaLibrary/images/english/5780.pdf


� http://www.college-optometrists.org/filemanager/root/site_assets/cmg/glaucoma_primary_open_angle_poag_v12_final.pdf

Q7. Classification and management of primarydivergent squint?

� Trans Am Ophthalmol Soc. 1891; 6: 165–168

J Pediatr Ophthalmol Strabismus. 2010 Feb 8:1-5. doi: 10.3928/01913913-20100118-03. [Epub ahead of print]

� Common forms of childhood exotropiaOphthalmology, Volume 110, Issue 11, November 2003, Pages2093-2096

� Understanding squints: Diagnosis and managementCurrent Paediatrics, Volume 7, Issue 1, March 1997, Pages 23-27

� Strabismus simplified by Dr Pradeep Sharma , Chapter 8,Page 98-104

Q8. Anatomical & functional prognostic factors in themanagement of rhegmatogenous RD?

Ans. Links




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

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

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

Reviewd byRamendra Bakshi MS

Q9. Indications and complications of intravitrealsteroids?

Ans. Links


� http://www.boamumbai.com/journalpdfs/jan-mar2004/dudaniivitsteroids.pdf


� http://www.nature.com/eye/journal/v21/n11/ful l/6702551a.html



� http://cme.medscape.com/viewarticle/564818?src=rss

� http://www.library.nhs.uk/EYES/ViewResource.aspx?resID=304981

Q10. Pharmacological properties, mechanism of actionand side effects of antiviral drugs ophthalmology

Ans. Links



� http://linkinghub.elsevier.com/retrieve/pii/003962579290003C

� http://www.eyeupdate.com/pages/antiviral_drug.html

� http://www.iovs.org/cgi/content/abstract/14/8/628

69www.dosonline.org

Conjunctivitis and other Eye Manifestations in Swine FluViroj Wiwanitkit, MD

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

CWiwanitkit House, Bangkhae, Bangkok Thailand

INTRODUCTION

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

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

Importance of eye manifestations in swine flu-

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

Abst

ract

sAnti-VEGF Therapy for GlaucomaMichael B. Horsley, Malik Y. Kahook, MD

Current Opinion in Ophthalmology 2010, 21:112–117

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

INTRODUCTION

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

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

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

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

Correspondence AuthorNidhi Tanwar MD

73www.dosonline.org

Monthly Clinical Meetings Calendar 2009-2010

Venu Eye Institute & Research Centre

29th

November, 2009 (Sunday)

Safdarjung Hospital

27th

December, 2009 (Sunday)

Bharti Eye Foundation

31th

January, 2010 (Sunday)

Centre for Sight

28th

February, 2010 (Sunday)

Guru Nanak Eye Centre

28th

March, 2010 (Sunday)

Dr. R.P. Centre for Ophthalmic Sciences

26th

July, 2009 (Sunday)

Shroff Charity Eye Hospital

23rd

August, 2009 (Sunday)

Base Hospital

4th

October, 2009 (Sunday)

Sir Ganga Ram Hospital

1st

November, 2009 (Sunday)

Midterm Conference of DOS

14th

& 15th

November, 2009 (Saturday - Sunday)

Annual Conference of DOS 16th

-18th

April, 2010 (Friday, Saturday & Sunday)

January 2010

21-24 KOLKATAAIOC 2010: Joint Meeting of the 68th AIOS AnnualConference & 15th Afro-Asian Congress ofOphthalmologyContact Person & AddressDr. Ashis Kumar Bhattacharya Organising SecretaryIMA House, Room No. 8, 53Creek Row, Kolkata - 700014Tel: 033-22371679, 033-22366350,Mobile : +09831019779 Email : [email protected]

Forthcoming Events: National

February, 2010

18-21 PALM BEACH, FLORIDA5th International Conference on Ocular InfectionsThe Breakers Hotel, Palm Beach, FloridaConference SecretariatParagon Conventions18, Avenue Louis-Casai, 5th Floor1209 Geneva, SwitzerlandTel: +41 (0)22 747 7930, Fax: +41 (0)22 747 7999Email: [email protected]: www.ocularinfections.com

Forthcoming Events: International

September, 2010

16-20 BEIJING, CHINAAPAO-AAO Joint CongressChina National Convention Centre, BeijingAPAO Central SecretariatSecretariat, Asia Pacific Academy of OphthalmologyC/o. The Chinese University of Hong Kong,Dept. of Ophthalmology & Visual Sciences, Hong KongEye Hospital, 3/F, 147K Argyle Street, Kowloon,Hong KongEmail: [email protected]: (852) 2762-3042, Fax: (852) 2715-9490,Website: www.apao2010beijing.org

April 2010

16-18 NEW DELHIAnnaul ConferenceDelhi Ophthalmological SocietyVenue: Hotel Ashok, Chankaya Puri, New DelhiContact Person & AddressDr. Amit Khosla, Secretary DOSRoom No. 2225, 2nd Floor, New Building,Sir Ganga Ram Hospital,Rajinder Nagar, New Delhi - 110 060Ph.: 011-65705229, E-mail: [email protected],Website: www.dosonline.org

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