DOS MONTHLY CLINICAL MEETING FOR NOVEMBER, 2004 · November, 2004 5 DOS Times - Vol.10, No. 5 Roop...

3November, 2004 DOS Times - Vol.10, No. 5

Dear Colleagues,

As the festive season comes to an end the seasonof conferences begin with our very own DOSMidterm meeting. You all must have receivedthe Midterm brochure by now & I am sure each& every one is eagerly looking forward for themeet just as I am. This issue of DOS Times comeswith a mix of old & new topics which all of uswould like to go through once in a while. DOSTimes is quite popular among students of Oph-

EDITORIAL

thalmology because of the fact that importanttopics of academic and those of clinical impor-tance in day to day practice are dealt in a simpleand concise manner.I would also like to invite non-institutional DOSmembers to actively participate in clinical talk& case presentation in our monthly meetings.See you all on 21st November, 2004 at IndiaHabitat Centre.

Dr. Jeewan S. Titiyal

Venue : Conference Hall, Dr. Shroff’s Charity Eye Hospital,Daryaganj, New Delhi

Date & Time : 27-11-04 (Saturday) at 2:30 PM

Case Presentation

1. Unusual complication of a dislocated pseudophakos ................: Dr. Umang Mathur (10 Min)

2. Sterile endophthalmitis due to endotoxins ..................................: Dr. Suneeta Dubey (10 Min)

Clinical Talk

• Update on ARMD ...................................................................................: Dr. Manisha Aggarwal (20Min)

Mini Symposium : Recent Advances

Chairman : Dr. B. PatnaikCo-Chairman : Dr. Noshir M. Shroff, Prof. J.C. Das

1. Adjustable suture techniques in strabismus surgery...................: Dr. Suma Ganesh (15 Min)

2. Tube implants in glaucoma ..........................................................: Dr. Suneeta Dubey (15 Min)

3. Newer phaco technologies ...........................................................: Dr. Umang Mathur (15 Min)

Discussion - 15 Min

DOS MONTHLY CLINICAL MEETING FOR NOVEMBER, 2004


This is to pay my gratitude for the deepfeelings and sympathy at this hour of grief ofmine and my family which includes my onlydaughter and son-in-law. Dr. Agarwal's endcame suddenly in the evening of 24thSeptember, 2004. He was working till end. Itwas a sudden end. This is a saintly death. Notime was left for medical aid.

Dr. Agarwal is well known for his vastcontribution in Ophthalmology in developingit and in sending the message far and wide.He founded a world known center, Dr. R. P.Centre at the All India Institute of MedicalSciences, New Delhi where many sub-specialties were developed adding to ScientificResearch and teaching advances and newdimensions were added to Ophthalmology.The students were made to work very hard, asa result they showed brilliance in all aspectsincluding other sub-specialties like Pathology,Pharmacology and Bio-Chemistry etc.wherever they went, here or abroad. They arespread throughout the world.

He was a visionary and could see manythings ahead of his times. He was associatedwith many Institutions and Organisations ofSpain, U.K., U.S.A., Africa, Pakistan, Sri Lanka,Japan either as a member, editor, or visitor. Heremained a Member of International Councilof Ophthalmology, Life Fellow ofInternational Academy of Ophthalmology.

He served as chairman of SteeringCommittee of WHO for development ofGlobal Programme of Prevention of Blindnessas well as Regional Committees of WHO forPrevention of Blindness.

His contribution in developing aProgramme for Prevention of Blindness andalleviation of blindness as advisor in theMinistry of Health which has been named as"National Programme for Prevention of VisualImpairment and Control of Blindness", wasadopted throughout the country and abroad.

quoted in books, journals and seminars. Hewas associated with various journals, Nationaland International, as editor or member like"Ophthalmogica" and "Vision".

Dr. Lalit P. Agarwal was Ophthalmologyand Ophthalmology was his.

He founded a Federation of Ophthal-mology roping in many Ophthalmologiststhroughout the country and enthused in themthe zeal for public work and training of thedoctors and paramedical staff.

Since some time past he was devotinghimself to producing paramedical staffthroughout the country through theFederation of Ophthalmic Research andEducation Centres. The course includes notonly Optometry and refraction but manyadvances in Modern Ophthalmology besidesbasic Pharmacology, Anatomy, Physiology andMicrobiology. He developed in the students anallround personality in dealing with public,theatre work, enterpreneurship, accounts andcomputer education. This is an example ofvision far ahead of the time. He is termed the"father of Modern Ophthalmology" in Asiaand other countries. He will be rememberedas such. He was a man of action throughouthis life and a great visionary.

It will be an appropriate tribute to him andfor the peace of his soul if his mission is carriedforward.Thanking you,Dr. (Mrs.) Savitri AgarwalW/o Dr. (Prof.). L.P. AgarwalAnd familyDr. Kavita A. Sharma (Daughter)Mr. J.C. Sharma (Son-in-law)

He penned about 22books in variousdisciplines of Ophthalmol-ogy and more than 350research papers inNational and Interna-tional Journals. They are

Tribute to Prof. (Dr.) L.P. AgarwalTRIBUTE


Roop NetralayaRun by : Meerut Laser and Eye Care Centre Pvt. Ltd.Opp. N.A.S. College, E.K. Road, Meerut-250 001

Phaconit-without SurgeRoop MD, Sangeeta MS

Whenever there is break of occlusion duringphacoemulsification sudden outflow of fluid occurs fromanterior chamber (AC). If not compensated by adequateinflow in the AC, it leads to momentary collapse of AC.This is what we call surge. Importance of surge is everincreasing because of use of higher vacuum and less phacopower to consume nuclear pieces in conventional phaco.Now with availability of phaco systems in which notmuch heat is generated at phaco tip (AMO SovereignWhitestar, STAAR Sonic, Alcon Neosonix and Aqualaseand Dodick Nd-YAG laser photolysis)1 and IOLs whichcan be inserted through sub 2mm incisions (Acri.Smart,Thin optX (Ultrachoice), Medennium Smart IOL, Microl)2,sleeveless phaco or phaconit or bimanual phaco or microincision cataract surgery is being practiced morefrequently now. However, it is the presence of surge, whichis preventing most of the ophthalmic surgeons to convertto phaconit. In the present article we attempt to analyzecauses of surge in phaconit and find innovative ways toprevent it on the basis of our experience of phaconit.

Compliance of Tubing

This simple innovation not only helps us in reducingsurge, it also makes the whole system more efficient. Asthe effect of changes occurring in the AC needs to betransmitted to the sensor located in the console throughthe tubing and the corresponding changes in pumpʹsspeed takes some time for its effect to come in AC. Thelonger the tubing the more the time lag. Smaller tubingreduces this time lag and the sensor and pump locatedin the console become more responsive to surgeonʹscommands by the foot-switch. All the positive featuresof a particular system controlling fluidics become moreeffective. By reducing the length of aspiration tubing eventhe fluidics of lower end machines becomes more effective.

The Kick of the PumpAnother important cause, which has not been

adequately emphasized, is the kick of the pump. By kickwe mean the initial thrust that pump makes to overcomethe inertia of static state. Just to understand theimportance of this phenomenon as far as surge isconcerned, put the test chamber over the handpiece. Nowfill the test chamber with fluid and go to foot pedalposition 2. Now pinch the aspiration tubing near its endat the peristalsis pump. Allow the vacuum to build to the

CURRENT PRACTICE

The compliance of tubing is one of the most wellrecognized cause of surge. By compliance of tubing wemean that when occlusion occurs at the phaco tip thevacuum rises in the aspiration tubing. Due to thecompliance, tubing, walls collapse partially and asocclusion breaks these come to their normal shapecausing sudden outflow of fluid from AC, which is for ashort period of time much more than the maximum flow-rate we have set in the machine. To make tubings lesscompliant thicker walled tubings are now being usedwhich allow us to use higher vacuums. To further reducesurge due to tubing ʹs compliance we employ aninnovative way. We have changed the way we place ourphaco system in relation to the instrument trolley andthe patientʹs head in such a way that we can work withhalf of the original length of the tubing supplied by themanufacturer. Using the half the length of the aspirationtubing we can reduce the compliance of the tubing to lessthan half. It allows us to increase the maximum vacuumsettings by at least 50 mm / Hg without anycorresponding increase in the surge. It has proven to bethe most simple and least cumbersome way to reducesurge without increasing any cost. The most importantthing is that this innovation would work with allmachines, all types of pumps, all sets of parameters, alltypes of cataracts and all kinds of techniques used forphaco.

maximum set limit. When the maximum vacuum isreached and pump stops release the tubing. One has toremain in foot pedal position 2 throughout. As the tubingis released the test chamber collapses. This part of surgeis caused by the kick of the pump as we have avoided thepart of the surge caused by tubing by pinching the tubingat the end of its aspirating part. Now one can vary theflow rate and repeat the experiment and realize that

Reducing the surge bydecreasing the length

of the tubing

Compliance of tubing


higher the flow rate greater the kick is. This means thatthe kick of the pump is proportionate to the flow rate setand is responsible for much of the post occlusion surgewe see in our phaco surgery.

To avoid the surge caused by the kick of the pumpduring phaconit we make use of the occlusion mode of ourphaco system (The Sovereign Whitestar). The occlusionmode allows the surgeon to have two sets of parameters,which automatically change, at a preset level of vacuumcalled the threshold. During our conventional phacosurgery we keep the flow rate at 24cc /min which changesto 30cc/min at the threshold vacuum of 100mm of Hg. Thehighest vacuum is set at 350mm of Hg. At these parametersroutine phaco is done speedily without any surge andsame parameters are used for chopping and also forconsuming the chopped nuclear pieces. But sameparameters cannot be used safely in phaconit even withhalf the size of aspiration tubing. For phaconit we usedifferent parameters for chopping nucleus into 6 piecesand different parameters to consume chopped nuclearpieces. For chopping, the flow rate is kept at 12cc/minwhich changes to 24cc/min at threshold vacuum of100mm of Hg.The maximum vacuum is kept at 300mmof Hg.This gives good hold for chopping while notincreasing the rise time significantly. As during choppingthe occlusion breaks gradually there is no surge even at300mm of Hg vaccume. For consuming the nuclear piecesthe flow rate is kept at 24cc/min to give goodfollowability. The threshold vacuum is set at 250mm Hgat which level the flow rate changes to only 8cc/min. Thehighest vacuum is 300mm Hg.Till 250mm Hg the rise timeis fast then nuclear pieces start being sucked and as theflow rate drops most of the nuclear pieces get suckedbefore highest vacuum is reached or pump stops. In thisway surge due to kick of the pump is all together avoided.Even if the pump stops due to reaching highest vacuumthe kick is mild due to low flow rate of just 8cc/min.

Phaco Power and SurgeAnother observation we have made and which is not

yet discussed in literature is the relationship of phacopower with surge. To appreciate it, while consumingrelatively softer nuclear pieces, keep all other parameterssame and consume one piece with 40% phaco power andanother similar piece with 10% phaco power and one canfind that post occlusion surge is more when higher poweris used. The explanation for this observation is that withlow phaco power larger pieces of nucleus get sucked intothe tubing and hence offer greater resistance to flow tillthey are cleared from the other end of the tubing thuscausing less surge. While when we use higher phacopower the nuclear pieces are emulsified into smaller piecesquickly and they offer less resistance to fluid flow in thetubing causing more surge. To take advantage of thisphenomenon during phaconit we set the phaco power at30% continuous, which is used just to impale the nuclearfragment and which at threshold vacuum of 100mm Hg

changes to 3 long pulses per second with whitestar onwith 33% on duty cycle. Thus even pulses are composedof micro pulses with the time interval between micropulses being double of each micropulse.As phaco poweris also linearly controlled, the foot pedal is depressed tothe minimal level in position 3 to further minimize theuse of phaco power.

Discussion To reduce surge in phaconit other modalities used areuse of air pump3, use of Star cruise control device4 anduse of posterior segment system5 to work as air injector.

The use of air pump allows more fluid to flow in ACto avoid surge. It is an effective way to control surge butit involves use of one extra gadget. The AC at timesbecomes very deep due to high positive pressure and itmay be deleterious in patients with compromised opticnerve perfusion and patients with weak zonules. With theuse of air pump the tunnel needs to be slightly longreducing the maneuverability of instruments in AC andalso distorts the cornea reducing the visibility. Anotherdisadvantage that we have experienced is that whenpump is put off due to positive pressure in the bottle thefluid comes back in the tubing of the pump causingfrequent breakdown of the pump. Due to these problemsthe air pump has not become very popular.

Another alternative is the use of Star Cruise Controldevise. Its cost and disposable nature are obviousdisadvantages. Apart from this as it works on theprinciple of reducing the smallest aspirating internallumen to 0.3mm it reduces the actual outflow from ACcausing the reduction in followability to a significantextent. One can do a simple experiment to understandthis. By collecting the fluid aspirated at the outflow endof the tubing, we measured the fluid using 20 gauze phacotip and using 0.3mm I/A tip. When we set the flow rateas 40cc/min the actual fluid collected with I/A tip is lessby about 66% as compared with the phaco tip. As theactual outflow from AC is responsible for the followabilityduring surgery the smaller internal aspirating lumendecreases the followability during surgery for the samesettings of flow rate set in the machine.

Now even the use of posterior segment machine -Accurus Surgical System has been described for injectingair into the bottle in place of separate air pump but theavailability of this machine with cataract surgeons is alimitation.

Thus reducing the length of the aspirating tubing tothe minimum required, judicious use of occlusion modein our existing machines and minimum use of phacopower are the most cost-effective and least cumbersomeway to reduce surge in phaconit.

Till today we were trying to reduce surge by reducingthe compliance of tubings by making the changes in thewall of the tubing, but nobody thought of reducing thelength of the tubing to reduce the total compliance of the


tubing. The simplicity, the cost effectiveness and theunquestionable effectiveness of this innovative conceptcan be used to improve our existing machines. This alsogives an idea to phaco machine manufacturers to designconsoles in such a way that the length of aspirationtubing can be minimized. It is helpful even in conventionalphaco and surgeons with lower end machines can alsoincrease their maximum vaccume settings by reducing thelength of aspiration tubing.

Our observations also emphasize the importance ofkick of the pump in causing post occlusion surge. We havealso suggested the use of occlusion mode of our machinesto avoid surge caused by the kick of the pump. May bettersoftware be developed in future to take care of this kickof the pump.

References1. Bovet J,Chiou A,Mehta CK.Phaconit Bimanual

Phacoemulsification.Journal of Intraocular Implant andRefractive Society,India2004;1(3):7-11

2. PandeySK,WernerL,MamalisN,OlsonRJ.UltrasmallIncision Intraocular Lenses.Journal of Intraocular Implantand Refractive Society,India 2004;1(3):29-33

3. Agarwal A, Agarwal S, Agarwal A,et al. Antichambercollapser. J Cataract Refract Surg 2002;28: 1085-1086

4. Chang F C. 400 mm Hg High-Vacuum Bimanual PhacoAttainable with the Staar Cruise Control Device. JCataract Refract Surg 2004;30:932-933

5. Arteaga A P. Anterior Vented Gas Forced Infusion Systemin Phaconit. J Cataract Refract Surg 2004;30:933-935

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CASE REPORT

Department of Ophthalmology,Ministry of Health Hosptial, Ramia,Taif, Kingdom of Saudi Arabia

Central Retinal Vein Occlusion (CRVO)In a Young PatientD.N. Saksena, M.S.

Introduction

Central Retinal Vein Occlusion (CRVO) is a conditionin which central retinal central retinal vein is compressedby arteriosclerotic central retinal artery where the twoshares common sheath (adventia) i.e. just behind laminacribirosa and at arteriovenous crossings. Here a case ofCRVO in young patient is reported.

A 25 year old male patient presented in eye clinicwith complaints of disturbance of vision in right eye ofapproximately one week duration. There was no historyof pain in right eye and previous episodes of suchcomplaints. Ocular examination revealed a best correctedvisual acuity of 6/12 in right eye and 6/6 in left eye, normalpapillary reactions and intraocular pressure 17.3 mm Hgin both eyes. Fundus examination showed generalizedtortusity of retinal veins and occasional flame shapedfresh hemorrhages along retinal veins. No retinal ormacular oedema except foveal reflex was indistinct. Inview of these symptoms and findings of transient visualobscurations, provisional diagnosis of impending retinalvenous occlusion was thought off and patient was put oftablet Aspirin (100 mg.) one tablet daily. The relevantlaboratory investigations were requested like bleedingtime, clotting time, Hb, TLC, DLC. ESR, Platelet count,Mauntex test, X-ray chest. Patient was asked to come forfollow up after one week. In the mean time results ofrequested investigations were received and all werewithin normal limits. On follow up visit, patient reportedfurther detoriation in vision in right eye. On examinationvisual acuity in right eye was 6/36 and left eye 6/6. Fundusexam showed extensive flame shaped dot and blothemorrhages in all quadrant of retina with occasional softexudates. There was moderate degree of macular oedemaand mild disc swelling. This was typical picture of centralretina vein occlusion (CRVO) clinically. In view ofextensive hemorrhages Flourescein Angiography wasdelayed to a later date.

In view of possible causes of CRVO in young patient,presenting symptoms, fundus findings and associatedgross diminution of visual acuity in right eye, patient wasprescribed tablet Prednisolone (10 mg.) one tablet q.i.d.

for one week and tablet aspirin (100 mg.) one tablet dailyfor three weeks. On subsequent follow up, patient waslooking happy and on examination his vision in right eyeimproved to 6/9 and left eye 6/6. Fundus examinationshowed almost 90% resolution of retinal hemorrhages andmacular and disc oedema. Flourescein angiographyrevealed prolongation of retinal circulation time withcompromised retinal capillary permeability and minimalnon perfusion areas in retina. This also suggests thatCRVO is of non ischaemic type. In the next follow up visitafter one month, it was found that patientʹs vision wasmaintained and stabilized at 6/9 in right eye with norecurrence and fundus picture further improved. Therewas no neovascularization of iris and therefore laserphotocoagulation was not required as patient respondedwell to medical treatment.

Discussion

Central retinal vein occlusion (CRVO) is caused bycompression of central retinal vein by atheroscleroticcentral retinal artery where the two share the commonadventia i.e. just behind lamina cribirosa and at arteriovenous crossings. This leads to turbulence, thrombusformation and endothelial damage. Typical picture ofCRVO consist of dilated tortuous retinal veins, intraretinal hemorrhages, dot and blot and flame shaped fierylooking fundus picture along with retinal and discoedema. Predisposing factors in elderly are age (6th and7th decade), associated systemic diseases likehypertension, diabetes mellitus and also associatedprimary open angle glaucoma. In young patients like thisone, causes are blood dyscrasia by causing eitherhypercellularity ( Leukaemias, polycythaemia) or changein plasma proteins (macroglobunaemias), sickle celldisease, periphlibitis (Bechets, diseases, sarcoidosis). Thispatient was young and all investigations were normal,therefore no specific cause could be identified.

CRVO is of two types.

a. Non ischaemic

b. Ischaemic

Non ischaemic type of CRVO can convert to ischaemictype so visual prognosis should be guarded as vision inlatter type is much compromised.

Effects of Venous Occlusion on Retinal


Circulation

Management

Regarding management of CRVO in non ischaemictype, no treatment is effective but in this case medicaltreatment did help and laser photocoagulation is helpfulonly if iris revascularization is present according to CRVOstudy group. In this particular case improvement invisual acuity is either due to spontaneous resolution dueto development of collateral circulation or as effectivenessof medical treatment.

Conclusion

I thought of reporting this case as patient was young andCRVO is uncommon in young patients and secondly allinvestigations were normal still patient responded verywell to medical treatment and finally this patientpresented as case of impending CRVO and went on todevelop as full blown case of CRVO in spite of startingtreatment well in time.

Reference :

1. Zagarra H., Gutman, F.A. Zakov, N.et al (1983) PartialCentral retinal Vein Occlusion. American Journal ofOphth. 96, 330-337.

2. The Central Retinal Vein Occlusion Study Group.Natural history and clinical management of CRVOArch. Ophthalmol. 1997; 115:486-491.

3. Kohner, E.M. Laatikainen, L., Oughton, J (1983) Themanagement of central retinal occlusionOphthalmology 90, 484-487.

Sl.No. Non ischaemic Ischaemic

1. Also known as Hemorrhagic orVenous Stasis complete CRVORetinopathy orIncomplete CVRO

2. More common 75% Less Common 3. Visual acuity moderately Final visual acuity

reduced and final visual not good usuallyout come good. less than 6/60

4. RAPD- Minimal Maximum due toretinal ischaemia

5. Rubiosis Iridis- PresentNot present

6. Fundus minimal soft Maximal softexudates exudates &

extensivehemorrhages.

Differences between non-ischaemic and ischaemic typeof CRVO

Corrigendum

In the last issue of DOS Times (Oct, 2004 Vol. 10 No. 4) the article titled “Chemical Injuries of the eye” byDr. Tishu Saxena et. al. had a table of Ropper- Hall (Ballen) Classification, which was not complete. We areprinting the complete table for the benefit of our readers. The error is regretted.

Editor DOS Times

Grade Prognosis Cornea Conjunctival limbus

I Good Corneal epithelial haze No limbal ischaemia

II Good Corneal haze, iris details visible No limbal ischaemia

III Guarded Total epithelial loss, stromal haze,iris details obscured 1/3-1/2 limbal ischaemia

IV Poor Cornea opaque ,iris and pupil obscured >1/2 limbal ischaemia

Roper- Hall MJ. Thermal and chemical burns. Tras Ophthalmol Soc UK 1965; 85: 631-61.

(Table 1) Ropper -Hall (Ballen) Classification


Dark AdaptometryParul Sony, MD, Vandana Kori, BSc, Pradeep Vankatesh, MD.

Exposure of an eye to a bright light reduces the visualsensitivity of retina. In dark the retinal sensitivity to lightshows a marked increase. Out of rods and cones, rods(containing rhodopsin pigment) are extremely sensitiveto low levels of illumination and are responsible for dark-adapted vision or the scotopic vision and the cones areresponsible for the photopic vision or the light-adaptedvision.The scotopic vision is characterized by• A high retinal sensitivity to light (1000 times higher

than sensitivity in light adapted state),• Low resolution visual acuity.• Absence of color perception.The photopic vision is characterized by presence of• Low sensitivity to light• A high resolution visual acuity• Presence of color perception.

Light exposure results in depletion of photopigmentby bleaching. Rhodopsin is decomposed in bright light,making the rods nonfunctional. Dark adaptation requiresbiochemical regeneration of rhodopsin pigment requiringexpenditure of metabolic energy. It has been shown thatthe recovery of visual sensitivity in dark corresponds wellwith curves of rhodopsin regeneration. As rods are absentin the foveal region scotopic vision shows a relative fovealdepression of visual sensitivity. The visual sensitivity ismaximum 7o away from fixation where the density of rodsis maximum.

Light minimum or absolute threshold is theminimum intensity of light that an eye can see andperceive under a dark-adapted state. To measurethreshold perception in a dark adapted eye initially arelatively bright light is projected and then the durationof its exposure is adjusted on the basis of repeated trialso that an observer can detect only 50% of its presentation.It can be calculated by obtaining mean of threshold ofappearance and threshold of disappearance in an eye, darkadapted for at least 40 minutes. The duration of the flashis altered in proportion to the change in luminance.Generally an intense light need not remain for a longduration as a weaker light requires.

Dark adaptation refers to the ability of the visualsystem, (both rods and cones mechanisms) to recoversensitivity following exposure to light. Whenever asubject is taken from a bright light to a dark room the

REVIEW

retinal sensitivity changes and this change/ or recoveryfollows a characteristic pattern known as course of darkadaptation. The recovery is faster in the cones as comparedto rods. However, the absolute level of sensitivity isgreatest in the rods.

Instruments called photometers or adaptometers,which can control and vary the amount of light to adefinite and known extent are used to record the courseof dark adaptation. Most primitive model that wasinitially used was photometer of Richard Forster.Hemispherical adaptometers are used nowadays(Goldman-Weeker by Haag Streit). Goldmann-Weekeradaptometer has various advantages such as it can beused both for binocular/ uniocular testing, it can testentire retina/ only macula/ or any specific peripheral partof retina. It allows determination of absolute threshold ofsensitivity; and has good objectivity.The absolute threshold values of dark adaptation dependon following variables:-• State of adaptation (preadaptation)• Stimulus variables (wavelength)• Methodological variables• Variability of the sensitivity of the retina depending

on retinal locationPupillary size affects the amount of illumination

entering into the eye and therefore has important impacton the measurement of dark adaptation. It is best to fixthe pupil with pilocarpine (3 drops of 1% pilocarpine at3 minutes interval) and measure it both prior to and afterthe completion of the test. Depending on the pupillary sizethe correction factor (by Reeve et al) is used to know theexact intensity of light used.

Temperature of illumination should also be keptconstant. Therefore the changes in light intensity aremade by filters or diaphragm and not by a rheostat thatcan alter the temperature of the light.Dark adaptation takes about 15-30 minutes. It has twomechanisms1. Neural adaptation which is fast and represents

reversal of neural light adaptation of photoreceptorsand other retinal cells.

2. Photochemical adaptation is a slow phenomenoninvolving pigment regeneration.

Technique• Pupil is fixed with pilocarpine• Preadaptation / light adaptation of eye is performed

by 10 minutes of pre-exposure of the eye to a diffuselyDr. R.P. Centre for Ophthalmic SciencesAIIMS, New Delhi -110 029


illuminated hemisphere of the adaptometer with astandard and constant illumination of 1500miliambert. This bleachs the photoreceptor pigments.

• The light is turned of and threshold sensitivity isdetermined immediately by presenting a series offlashes of light 7o - 10 o below fixation. The intensityof the flashes is controlled by neutral density filter.The readings are repeated every few minutes till apoint is reached when no further rise in sensitivityis recognized. The results are plotted as log units ofbrightness against time. A biphasic sensitivity curveis obtained. The initial rapid segment represents acone function and the second slower segmentrepresents the rod function. The kink on the curvewhere the rod segment begins is called rod-cone break(alpha point).Normally the whole process of dark adaptation

requires 15-30 minutes. The alpha-point occurs after 7-10 minutes of dark adaptation. The threshold measuredon the cone and rod plateaus are the absolute thresholdsof the cone and rod mechanism.

Dark Adaptation curve varies with the location of theretina where the test is performed. When performed at50 a typical biphasic curve is obtained (Figure 1). At thestart the threshold is very high, then it falls rapidly inthe initial phase and gradually in the next phase andreaches its lowest value over 30 minutes.00 curve: If the flash of light is focused on foveola onlycone plate is obtained as rods are absent at foveola.Clinical applications1. Disorders of pigment degeneration

a. Vitamin A deficiency: Threshold for darkadaptation is increased for both rods and coneswith a decrease in serum Vitamin A levels. Timerequired for dark adaptation is also increased.

b. Fundus albipunctatus: This is autosomalrecessive hereditary disorder where theregeneration time for visual pigment is prolonged.It requires several hours for dark adaptationinstead of the usual 30 minutes. The fundus hasscattered white dots and the serum Vitaminlevels are normal.

2. Disorders of neural adaptationa. Oguchi ʹs disease requires hours for dark

adaptation. Though the rate of rodhopsinregeneration is normal, the rod arm is prolonged.

b. Congenital stationary night blindness (CSNB) ischaracterized by absence of any rod adaptation.

Chloroquine toxicity: Rod limb of the dark adaptationcurve is unaffected however the cones are selectivelydestroyed thus cone limb is absent. Retinitispigmentosa Type II (due to damaged photoreceptornot the visual pigment cycle) shows a prolonged cone-rod break time, normal final rod threshold.

Abnormal dark adaptation curves in tapetoretinaldegeneration (Figure2)• Type I normal• Type II biphasic curve with cone arm normal and

rods segment is delayed.• Type III rod adaptation never develops• Type IV monophasic curve and represents the

adaptation of foveal cones• Type V the adaptation of foveal cone is defective

Apart from these other conditions like high myopia,glaucoma and extreme miosis may also result inabnormal dark adaptation function.

Visual field in dark-adapted eye gives an overallsurvey of functioning of rods. It shows a central scotomaat the fovea. The sensitivity is greatest between 10-200eccentric to fovea and it again declines in the peripheryespecially superiorly.

Time in dark (minutes)

Thre

shol

d In

tens

ity

Figure 1: The normal dark adaptation curve

Figure 2: Typical adaptation curves in tapetoretinal degeneration

Time in dark (minutes)

Thre

shol

d In

tens

ity

Suggested Readings1. Steffins L, Blair H, Sheard C. Dark Adaptation and

dietary deficiency in vitamin A. Am J Ophthalmol1940;23-1325-1329.

2. Hecht S, Haig C, Wald G, Dark adaptation of retinalfields of different size and location. J Gen Physiol1935;19:321-330.

3. Dowling JE. Night blindness, dark adaptation and theelectroretinogram. Am J Ophthalmol 1960;50:875-878.


Diplopia WorkupHarinder Singh Sethi, MD, DNB,FRCS, Rohit Saxena, MD

REVIEW

Double vision, also called diplopia, causes a personto see two images of a single object. It is often the firstmanifestation of many systemic disorders, especiallymuscular or neurologic processes. The cause of diplopiamust be resolved to diagnose and manage itappropriately.

The diplopia can be uniocular or binocular.Binoculardiplopia can be differentiated from uniocular diplopia bycovering either eye; monocular diplopia persists in oneeye despite covering the other eye while binoculardiplopia disappears. Causes of uniocular diplopia are asevere corneal deformity or marked astigmatism(keratoconus), a mass or swelling in the eyelid, Dryeye,more than one pupil or opening in the iris, refractiveanomalies within the eye (early cataracts or partiallydisplaced lenses as in Marfan syndrome), and retinalabnormalities (macular scarring and distortion). It can bedifferentiated from the binocular diplopia by followingmethods a)Monocular occlusion :Uniocular diplopia maybe present in each eye (eg cortical diplopia) or in one eyeonly. Uniocular diplopia persists on covering the other eyeand disappears on covering the affected eye.b) Visualacuity with and without pin-hole : Refractive monoculardiplopia will normally disappear through a pinhole. c)Amsler chart : Metamorphopsia if present, indicates anassociation with macula & pathology.

Binocular diplopia is encountered almost exclusivelyin adults or in those with mature visual systems becausechildren may not be able to express this symptom andthe immature visual system deals with diplopia bysuppressing the poorer image, possibly resulting inirreversible amblyopia. Children with obvious andmarked ocular malalignment from strabismus arecomfortable and content because the visual image fromthe deviating eye is suppressed and not noticed. Incontrast, adults who have mature visual processingpathways cannot easily ignore the second image, thismanifests as diplopia.

Causes of binocular diplopia are :

Damage to III, IV,VI cranial nerves controlling theextraocular muscles - Nerves can be involved by infection,multiple sclerosis, stroke, head trauma or a brain tumor,Diabetes and hyertension

Myasthenia gravis.

Gravesʹ disease

Trauma to the eye muscles

Evaluation of a Patient with Diplopia.

A. History

The patient typically presents with a history ofdouble vision, where 1 object appears as 2 objects.

The most important symptom to be elicited iswhether the diplopia is horizontal (2 images are side byside) or vertical (2 images are above each other). Obliquediplopia (2 images are separated both horizontally andvertically) should be considered as a manifestation ofvertical diplopia.

The patient should be enquired about onset (abruptor slow), severity, duration, location, associatedsymptoms, and aggravating and relieving factors. Thisevaluation is as important as performing appropriateexaminations and ordering special tests. Determine ifdiplopia worsens when the muscles are fatigued ( eg, atthe end of the day, after strenuous use as in Myastheniagravis). On presentation of any acute onset diplopia, oneof the most difficult but important decisions to make iswhether it is of recent onset or due to the decompensationof a long standing deviation. This is especially importantin cases of congenital superior oblique palsies. A detailedhistory of systemic diseases (eg diabetes, vascular disease,or hypertension; headache and other neurologiccomplaints), as well as a past surgical and medical historyshould be taken.

History of recent trauma to the face and the headshould be ruled out. Blunt injury to the cheek can resultin a blow-out fracture of the orbit with hematoma orentrapment of the soft tissues and extraocular muscles,restricting upward and downward eye movement. Blunthead injury is associated with nonspecific sixth cranialnerve (abducens) weakness. Evaluate old photographs todetermine if the head posture is long-standing or of recentonset.

B. Examination of a patient with diplopia

Abnormal head posture ( AHP )

It often gives clues towards the underlying etiology.It is developed to compensate for an incomitancy bymoving the eyes into a position of comfortable binocularvision. The presence of an AHP normally indicates that

Dr. R.P. Centre for Ophthalmic SciencesAIIMS, New Delhi -110 029


the patient has the capacity for good binocular functions.Head posture has three components:

a) Chin elevation or depression (vertical),

b) Face turn to right or left side (horizontal)

c) Head tilt to right or left shoulder (torsional).

The patient prefers a head posture at which the oculardeviation is the least, and image can be fused. Forexample, the head posture in a case of left superior oblique(LSO) palsy will have chin depression, face turn to theright, and head tilt to the right shoulder. It can beexplained as follows :- LSO being a depressor, chindepression occurs, it being an intorter, a head tilt towardsthe opposite shoulder occurs. And a face turn to the rightbrings the eyes in abduction so that the verticalmovements can be executed by the vertical recti. Thus thehead posture ensures that the eye is out of the field ofaction of the paralytic muscle. Rarely a head posturewhich causes the maximal deviation is chosen so that theperipheral image can be easily suppressed or ignored.

Lid position

Ptosis of the upper eyelid indicates possible third-nerve lesions, while eyelid retraction suggests thyroidophthalmopathy.

Pupils

Pupil asymmetry is a sinister sign when associatedwith diplopia because it indicates involvement of the thirdcranial nerve (oculomotor nerve).

Cover test

The cover test should be performed, at least initially,using an accommodative target for fixation. Where thereis an incomitancy, the angle of deviation normally differsdepending on the fixating eye, with the secondarydeviation being larger than the primary. The primarydeviation is the angle when fixating with the unaffectedeye and the secondary deviation is the angle whenfixating with the affected eye. The cover test should berepeated with and without any AHP. Normally, the angleof deviation will reduce with the head posture and apreviously manifest deviation will become latent. It isnecessary to determine whether the diplopia andmanifest deviation are constant or intermittent, andwhether the angle of deviation varies with fixationdistance.

Ocular motility

Complete ocular motility examination should bedone. The alternate cover test should be performed in thedifferent directions of gaze to reveal the full angle of thedeviation. Subjective responses can be improved by the

wearing of red and green goggles. Suppression is less likelyand the patient can report on the direction and separationof the images. The use of a vertical bar-light as a fixationtarget allows for the assessment of torsion, and can beplotted as a ʹdiplopia chartʹ.

Mechanical or myogenic versus neurogenic:

Observation of the smoothness of eye movements canhelp differentiate between a mechanical and neurogenicdefect. In a neurogenic lesion, as the eyes move into thedirection of the defect, the under-acting eye will movesmoothly but more slowly than the normal eye. In amechanical deviation, the eye movements will be smoothand symmetrical until meeting the obstruction, at whichpoint there will be an abrupt slowing of the defective eye.

Another clue to differentiating a neurogenic from amechanical lesion is by observing the diplopia. If the distalimage changes in opposite directions of gaze (e.g. theimage seen by the right eye is inferior on down gaze andsuperior on up gaze), then this indicates a mechanicaldeviation, and is described as a crossing of diplopia.

A neurogenic lesion generally results in an under-action of the eye movement. In a mechanical restriction,the eye is often tethered, such that it cannot move intothe stipulated direction. This mechanical tethering can putpressure on the globe, causing an increase in intra-ocularpressure (IOP) on an attempted movement in the directionof the restriction.

Further the neurogenic lesion can be differentiated fromthe myogenic one by the forced duction test (FDT) andelectromyography. In a mechanical defect, theelectromyographic activity will be normal or increasedon attempting to look in the direction of the restriction,whereas the activity will be reduced with a neurogeniclesion.

Investigations of a case of diplopia

Ocular investigations

Near point of convergence Measuring the near pointof convergence is of clear value in patients complainingof asthenopic symptoms. Assessment of convergence canalso provide useful information in differentiating asupranuclear from an infranuclear defect.

Measurement of the angle of deviation

Measurement of the deviation in different directionsof gaze helps to confirm the direction of maximummisalignment of the visual axes. In true incomitancies,the angle of deviation differs depending on which eye isfixating. It can be measured with prism cover test. Itshould be measured in 9 gazes with each eye fixing. Inorder to use the prism cover test to measure the angle


when fixating with the right eye, for example, the strengthof prism should be adjusted until the movement of theleft eye is nulled. When fixating with the right eye, theangle of the left eye is being measured, and when fixatingwith the left eye, the angle of the right eye is beingmeasured. As the secondary angle of a deviation is thegreater, measurement of the angle of deviation fixatingeach eye in turn can help determine the eye with thedefect.

Maddox double rod testMaddox rods at the same orientation in front of each

eye (normally vertically orientated to produce ahorizontal streak) can be used to assess the angle oftorsion. If the streaks seen by each eye are not parallel,then the rods can be rotated until the streaks becomeparallel and horizontal, thus giving a measure of therotation required and hence the torsion. This test ismaximally dissociating and can produce erroneousresults (possibly as a result of small angles of head tilt).

Bielschowskyʹs head tilt testDue to the development of the muscle sequelae, the

eye movement pattern in a longstanding SO palsy in oneeye can be difficult to differentiate from a SR palsy of theother eye. A positive Bielschowsky head tilt test canconfirm the culprit as the SO, but a negative result isinconclusive. Normally, as the head is tilted towards theright shoulder, for example, the right SR and right SOwork in partnership to intort the eye, the opposingvertical actions of the two muscles cancelling out. If apatient has a SO palsy, as the head is tilted towards theaffected side, the SR acts unopposed, so it not only intortsthe eye but also elevates it. To perform the test, seat thepatient upright, maintaining steady fixation straightahead at a distance of 3m, so that fixation doesnʹt favoureither the SO or SR. Tilt the head towards the eye withthe suspected SO palsy (the hypertropic eye) and if thevertical angle of the deviation increases, the defectivemuscle is confirmed as the SO ).

Parks used this information to devise a three step testfor differentiating the four vertically acting extra-ocularmuscles. Parks 3-step test helps to elucidate which of the4 extraocular muscles responsible for vertical eyemovements may be weak, thereby causing verticaldiplopia. Although first appearing impossibly complex,this test follows a logical progression to progressivelyeliminate groups of muscles from the 4 pairs.

First, determine which eye appears higher with thehead in a normal position, with the head turned to theleft and to the right, and with the head tilted left and tiltedright. Then, answer the questions in the following steps:

Step 1: Which eye is higher in primary gaze? Thisreduces the possibilities of muscles from 4 pairs to 2 pairs.

For example, if the right eye is higher, the weaknessresides either in the muscles depressing the right eye(right superior oblique muscle and right inferior rectusmuscle) or in the elevators of the left eye (left superiorrectus muscle and left inferior oblique muscle).

Step 2: Is the deviation greater with left head turnor with right head turn? Now, only one pair remains. Ifthe right eye deviates most when the head is turned tothe right (both eyes are turning to the left), then only theright superior oblique muscle or the left superior rectusmuscle remains.

Step 3: Is the deviation greatest with tilting the headto the left or to the right? Called the Bielschowsky headtilt, it relies on the torsional balancing reflexes provokedby head tilt. The higher eye extorts (because of the inferioroblique muscle), while the lower eye intorts (because ofthe superior oblique muscle).

By combining steps 1-3, only one muscle remains.However, the astute clinician can reduce this process byrecognizing that the superior oblique muscle is by far theone muscle most likely to be responsible. A head tilt tothe same side as the involved muscle exacerbates theproblem. Alternately, the eye that is highest in adductionʺpoints atʺ the muscle that is affected.

Fusional ReservesMeasurement of fusional reserves can be of

diagnostic value when differentiating a long standingvertical muscle palsy from one of recent onset. CongenitalSO palsies, for example, can have vertical fusionalreserves in excess of 10D, whereas a recent onsetdeviation will usually have a normal vertical fusionrange (4D - 6D). Vertical fusion ranges can also increaseover a long period of gradual change in the direction ofthe visual axes, such as in dysthyroid eye disease.

Past PointingPast pointing can be used to differentiate a recent

onset cause from a long-standing condition. On occlusionof the unaffected eye, the patient is asked to rapidly lookat, and point towards, an object in the field of action ofthe palsied muscle. In recent onset incomitancies, theinput required to look at the object will be greater thannormal, so the object will be perceived as more peripheralthan its actual position, and the patient will tend to pointtowards a more eccentric location.

Diplopia ChartA vertical bar of light is viewed through red and

green goggles at a fixed distance from the eye. The barlight is moved into each direction of gaze, and the patientdescribes the image separation and appearance. Theimage separation can be measured. By convention, thered filter is always placed before the right eye. The


symbol `$ ʹ is used to describe the two lines assuperimposed. When interpreting a diplopia chart, itshould always be remembered that the most distal imagebelongs to the under-acting eye. The position of the imageis the reverse of the position of the eye. Ideally, the distanceof fixation and image separation should also be recorded.

Field of binocular single vision (BSV)The field of BSV is a test used to describe the areas

of BSV, and hence diplopia. It is of particular value in themanagement of symptomatic incomitancy. It is verysimple to do using a kinetic perimeter, or to approximatefrom ocular motility. The patient is seated at theperimeter, with the chin central to fixation. The target ismoved outwards until the patient recognizes diplopia,and the point is marked. The target is then moved furtheruntil one image disappears, normally due to occlusion byfacial contours, and this point is marked. The inner ringdescribes the area of BSV, the outer ring describes thelimits of the binocular field of fixation.

Hess chart/ Lees screenThe patient should be seated squarely facing the

screen being plotted, with the head centred on the centralfixation spot. Ideally, plot the centre position first, thenthe 15° fixation points, and finally as many of the 30°points as can be seen without moving the head. There area number of basic rules for interpreting a Hess plot:1. The smaller field belongs to the eye with the defect.2. Neurogenic pareses will show the muscle sequelae to

a greater or lesser extent (dependent on the durationof the condition and the eye used for fixation). Thelargest underaction is normally in the direction ofaction of the paretic muscle and the largest over-action is normally the contralateral synergist.

3. Mechanical defects show a compressed field. There isnot normally an obvious over-action of the directantagonist, nor under-action of the contralateralantagonist, so the effects of the defect are limited tothe direction of action of the mechanical restriction.The most obvious feature of a mechanical defect isnormally the marked overaction of the contralateralsynergist.

Systemic investigationsThey are indicated to detect or confirm the underlying

suspected cause of pathological binocular diplopia asindicated by the history and detailed work up of thepatient.

Magnetic resonance imaging (MRI) or computedtomography (CT) scan of head and orbit may be requiredto find the cause of oculomotor nerve palsies, to check forsigns of trauma, tumor or blood vessel malformations etc.

Tensilon test should be done in cases suspected to bedue to Mysthenia gravis

Thyroid profile in cases of diplopia due to thyroidophthalmopathy

To summarize, many patients complaining of diplopiawill have conditions that can be appropriately managedin practice while other cases will need referral . Those forwhom the condition is more sinister and require neuro-ophthalmologic investigation are, fortunately, uncommon.In an adult or a child, recent, acute onset diplopia due toa concomitant or incomitant deviation with an uncertainaetiology should be referred urgently for a neuro-ophthalmologic investigation.The consequences ofinappropriate action, however, can be life threatening. Thelong-standing deviations which are cosmeticallyunacceptable may be assisted by surgery or prisms.

References1. Bielschowski A: Disturbance of vertical motor muscles of

the eyes. Arch Ophthalmol 1938; 20: 175-200.

1. Sharma Pradeep, Strabismus Simplified. ModernPublishers, New Delhi 1999.

2. Walsh and Hoytʹs Clinical Neuro-Ophthalmology. 4th ed.Baltimore, Md: Lippincott Williams & Wilkins; 1985:707-715.

3. Richardson LD, Joyce DM: Diplopia in the emergencydepartment. Emerg Med Clin North Am 1997 Aug; 15(3):649-64.

4. Glaser, JS Neuro-ophthalmology, 3rd edition. 1999.Philadelphia, Lippincott Williams andWilkins.

5. von Noorden, GK. Binocular Vision and Ocular Motility.Theory and management of strabismus 5th Edition. 1990.St Louis, Mosby.30. von Noorden GK, Hansell R (1991)

Where is my copy of DOS Times ?Dear DOS members, anyone who could not receive DOS Times from the monthof October, 2004 onwards. Please Contact:

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Vitreous HemorrhageCyrus M. Shroff, MD

Vitreous hemorrhage is defined as the presence ofextravasated blood within the space outlined by theinternal limiting membrane of the retina posteriorly andlaterally, the non-pigmented epithelium of the ciliary bodyantero-laterally and the lens zonular fibers and posteriorlens capsule anteriorly

Symptoms:

Patients present with sudden painless diminution ofvision, floaters, photopsia, and the perception of shadowand cobwebs.

Signs:

1. Slit lamp examination: - Red blood cells can beappreciated when the light beam is focused posteriorto the lens. Mild afferent pupillary defect may bepresent.

2. Ophthalmoscopy:- In severe vitreous hemorrhage, thered fundus reflex may be absent, and there may beno fundus view. In mild vitreous hemorrhage, bloodobscures part of the retina and retinal vessels.

Chronic vitreous hemorrhage has a yellow ochreappearance secondary to the break down ofhemoglobin.

Depending on the etiology there may be otherabnormalities.

Pathologic Mechanisms.

There are three main pathologic mechanisms forvitreous hemorrhages.

REVIEW

1. Bleeding from diseased retinal vessels or abnormalnew vessels, as in proliferative diabetic retinopathy,proliferative retinopathy secondary to retinal veinocclusion, Ealesʹ disease, sickle cell retinopathy andretinopathy of prematurity. The common pathologicmechanism in this group of diseases is retinalischaemia, which results in formation of new vesselscaused by the production of angiogenic factors.Occasionally vitreous hemorrhage can occur frominflamed obstructed retinal vessels as in severevasculitis or acute central retinal vein occlusion.

2. Tearing of retinal vessels caused either by formationof retinal break or posterior vitreous detachment dueto adherence of cortical vitreous to retinal vessels.

3. Less frequently it is caused by extension ofhemorrhage through the retina from other sourceslike from subretinal hemorrhage as in age relatedmacular degeneration and choroidal melanoma.

Infrequently vitreous hemorrhage occurs incoagulation disorders and in patients on anticoagulanttherapy.

Etiology

Children:1. Trauma

a. Birth Traumab. Shaken Baby Syndromec. Traumatic Child abuse

2. Retinopathy of Prematurity3. Retinal Break4. Retinal Detachment5. Retinoblastoma

Shroff Eye Centre (SEC) andDr. Shroff's Charity Eye Hospital (SCEH)New Delhi


6. Congenital Retinoschisis7. Pars Planitis8. PHPV9. TERSONʹSAdult :A. Bleeding from diseased retinal vessels or

abnormal new vesselsDiabetic RetinopathyEalesʹ Disease

a. Neovascular Diseaseb. Acute Severe Vasculitis

Retinal Vein OcclusionCentrala. Neovascularizationb. Acute Central Vein Occlusion

BranchSickle Cell RetinopathyRetinal Capillary AngiomaHypertensive RetinopathyRadiation RetinopathyMacroaneurysm

B. Rupture of Normal Retinal vessels.Retinal breaksRetinal DetachmentPosterior Vitreous DetachmentTrauma

C. Extension of hemorrhage from other sourcesAge related macular degeneration with CNVMIntraocular Tumour - Choroidal Melanoma

D. MiscellaneousTersonʹs SyndromeBleeding …..

Workup1. History: History of ocular or systemic disease

especially diabetes, hypertension, trauma, retinalbreak or detachment in the other eye, family historyof detachment.

2. Complete ocular examination including slit lampexamination to check for neovascularization of iris,intraocular pressure measurement and a dilatedfundus examination of both eyes using indirectophthalmoscope. This may be supplemented by slitlamp biomicroscopy using 78D or 90D lens or funduscontact lens. Contralateral eye examination is often

diagnostic e.g. diabetes, age related maculardegeneration, Ealesʹ retinopathy of prematurity.Presence of peripheral retinal lesions in the other eyeshould alert one to possibility of retinal break. Incases of spontaneous vitreous hemorrhage withoutobvious vascular disease it is important to do anindirect ophthalmoscopic examination with scleraldepression. Retinal breaks are commonly locatedsuperiorly in cases of dense vitreous hemorrhage. Intraumatic vitreous hemorrhage (especially open globeinjuries) scleral depression is avoided for the first 3-4 weeks.

3. Ultrasonography : When there is no fundal glow aBscan Ultrasound helps in a diagnosis of vitreoushemorrhage as well as in detection of any associatedposterior vitreous detachment, retinal detachment(traction or rhegmatogenous), intraocular tumor,retinal break ( if large), scleral rupture . In fresh, mildhemorrhage, dots and short lines are displayed on B-Scan, and a chain of low amplitude spikes is foundon A-Scan. The more dense the hemorrhage, the moreopacities are seen on B-Scan and the higher is thereflectivity on A-scan. If the blood organizes, largerinterfaces are found which have higher reflectivity onA-Scan and may be confused with retinal detachment.Kinetic echography shows undulating aftermovements on B-Scan which are to be differentiatedfrom the less mobile retinal and choroidaldetachment.

4. Fluorescein angiography may aid in defining theetiology although the quality of the angiogram maydepend on the density of the hemorrhage.Angiography is especially useful in diagnosis ofproliferative retinopathies, wherein abnormal newvessels show leakage of the dye into the vitreouscavity, and in age related macular degeneration,where there is subretinal leak. Fluoresceinangiography of the contra lateral eye is also animportant diagnostic aid.

Differential Diagnosis1. Vitritis : The onset is rarely as sudden as in vitreous

hemorrhage. History is very important. Pain orredness at onset can alert one to vitritis. History ofany surgical intervention is important. Thepossibility of trivial undiagnosed trauma should bespecifically asked for and explored. Detailed historyof systemic illnesses must be taken if vitritis issuspected. There may also be antecedent signs ofanterior or posterior uveitis. Pars planitis should belooked for. On slit lamp examination there may bepresence of vitreous cells in the anterior vitreous. If


unexplained ʹvitritisʹ is seen, masquerade syndromeslike intra-ocular lymphoma should be ruled out.

2. Retinal Detachment: may occur without a vitreoushemorrhage, yet the symptoms may be identical. Thefundus view may be difficult in a fresh retinaldetachment with dense vitreous hemorrhage.However, the retina can usually be viewed withindirect ophthalmoscopy by an experienced observor.Ultrasonography is indicated in case of doubt.

3. Very advanced ʹbrown ʹ or ʹblack ʹ cataract cansometimes give an impression of vitreous hemorrhageon indirect ophthalmoscopy. The ability to see someretinal detail despite the advanced cataract can oftenhelp to differentiate the two conditions. If a doubtpersists a combined A & B Scan is helpful.

Natural History and PrognosisThe natural history and prognosis of vitreous

hemorrhage depends on the underlying disease. Ingeneral, patients with diseases that have no tendency forrecurrent bleeding, such as avulsion of a vessel associatedwith a retinal tear or posterior vitreous detachment havegood prognosis for resolution of the vitreous hemorrhageand restoration of vision. Clearance of blood from thevitreous is a slow process, with a time constant in theorder of 1% per day. Hemorrhage in the vitreous gelremains suspended in a lamellar fashion until the vitreousliquifies and the blood sinks to the bottom of the vitreouscavity where it is absorbed.

Patients with diabetic retinopathy as the underlyingdisease process have a relatively poorer prognosis forspontaneous clearing of vitreous hemorrhages andrestoration of vision especially after recurrent bleeds.Among patients with vitreous hemorrhage secondary toretinal vein obstruction, branch vein occlusion patientshave the best visual prognosis, hemi-central veinocclusion patient inter-mediate and central retinal veinocclusion worst. Natural history of vitreous hemorrhagesecondary to Eales Disease and retinal arterial macroaneurysms is generally good while that following agerelated macular degeneration and sickle cells retinopathyis poor.

Visual recovery following trauma is unpredictableand depends on the nature and extent of injury.

ManagementOnce the diagnosis of vitreous hemorrhage has been

made, the patient must be referred to an ophthalmologistwith special interest in vitreo-retinal disease and well-versed with indirect ophthalmoscopy. Unlike retinaldetachment, vitreous hemorrhage is usually not a surgicalemergency. However, prompt examination especially fora first time bleed is important as surgical interventionmay be required if there is retinal detachment. IF other

causes like AMD with CNVM, intra-ocular tumour aresuspected these must be specifically investigated for andtreated promptly. In most other cases one can safely waitfor a few weeks for the hemorrhage to clear upspontaneously. The patient must be reassured and theplan of management explained. The treatment modalitiesare:A. Conservative Management: Bed rest with head end

of the bed elevated. Eye movements maintain RBCin the vitreous cavity in diffuse suspension. If the eyemovements are diminished, the blood gravitates tothe bottom of the space. Sometimes bilateral patchingis advised as this accelerates the settling of the bloodcells. Settling of blood enables visualization of thesuperior retina for examination and treatment. Ifdense vitreous hemorrhage persists, and the etiologyremains unknown, the patient is followed with a B-scan ultrasound every 1-3 weeks to rule out a retinaldetachment.Eliminate asprin, nonsteroidal anti-inflammatorydrugs and other anticlotting agents unless they aremedically necessary.

B. Photocoagulation or cryotherapy: Laserphotocoagulation or cryotherapy is used to sealretinal breaks. Photocoagulation is done as soon asmedia is clear enough to permit it. Indirectophthalmoscopic laser delivery especially with 810-nm diode laser is very useful when it may not bepossible to achieve adequate laser burns with thegreen laser. As these retinal breaks are associatedwith vitreous traction they should be surroundedcompletely by 3-4 rows of confluent laser burns.Patents must be informed that if retinal detachmentoccurs before firm chorio-retinal adhesion is formed,surgery in the form of scleral buckling or vitrectomymay be required.If there are large retinal tears and the media is notclear enough for adequate prophylactic treatment theoption of early surgery has to be seriously considered.In the case of vascular retinopathies it is usually saferto wait for longer periods for the hemorrhage to clearbefore starting laser photocoagulation. The other eyemust have a fundus fluorescein angiography to detectproliferative vascular disease and receive immediatelaser photocoagulation if new vessels are present.Some surgeons advocate peripheral retinalcryotherapy for non-resolving vitreous hemorrhage.Peripheral retinal cryotherapy accelerates theresorption rate of vitreous hemorrhage by causing abreakdown of the blood retinal barriers and anincrease in tissue plasminogen activator and has been


used as a treatment modality for non-resolvingvitreous hemorrhage. However this should be usedwith caution in cases where organisation andcontraction of the vitreous gel can precipitate atraction retinal detachment. This is especially truein cases where there is no PVD or very limited PVD.

C. Posterior Hyaloidotomy: Hemorrhage locatedbetween the internal limiting membrane and theretina may cause permanent macular changes beforespontaneous resolution occurs. In few cases posteriorhyaloidotomy may be performed using a Nd-YAGlaser which disrupts the internal limiting membraneand releases blood cells into the vitreous cavity.

D. Pars Plana Vitrectomy: Pars plana vitreous surgeryhas revolutionised the management of vitreoushemorrhage, dramatically improving the prognosisin a number of cases and enabling quicker visualrehabilitation in may others. Vitrectomy or surgicalremoval of blood is usually performed for:-

Urgent:1. Vitreous hemorrhage accompanied by RD2. Neovascular AMD with vitreous hemorrhage and

subretinal hemorrhage.3. Certain cases of trauma.Early: Vitreous hemorrhage secondary to vascular

retinopathies:1. Bilateral hemorrhage.2. Associated with early iris neovascularization3. Associated with hemolytic ʺghost cellʺ glaucoma4. With severe progressive fibrovascular proliferation5. Dense premacular hemorrhage.

Late/Elective :Chronic vitreous hemorrhage with no traction on

retina or other associated problems, with good vision inthe other eye may be observed almost indefinitely if thepatient is not handicapped, or for medical reasons, is nota good candidate for surgery.

Summary :-Vitreous hemorrhage is a common presenting sign in

patients with a vitreo-retinal disorder. It is alarming tothe patient as it produces dramatic visual symptoms andoften marked visual loss. Though, most of the time,vitreous hemorrhage is not a surgical emergency thepatient should be examined and investigated verycarefully to detect those who do require earlyintervention. Appropriate management ensures goodprognosis in most cases of vitreous hemorrhage.

Monthly Meetings CalendarFor The Year 2004-2005

1st August, 2004 (Sunday)Army Hospital (R&R)

29th Auguest, 2004 (Sunday)Sir Ganga Ram Hospital

6th November, 2004 (Saturday)Rescheduled : Hindu Rao Hospital

30th October, 2004 (Saturday)R.P. Centre for Ophthalmic Sciences

21st November, 2004 (Sunday)DOS Midterm Conference

27th November, 2004 (Saturday)Dr. Shroff’s Charity Eye Hospital

18th December, 2004 (Saturday)Venu Eye Hospital & Research Centre

29th January, 2005 (Saturday)Safdarjung Hospital

26th February, 2005 (Saturday)M.A.M.C. (GNEC)

27th March, 2005 (Sunday)Mohan Eye Institute

2nd & 3rd April, 2005 (Saturday & Sunday)Annual DOS Conference

Attention DOS MembersThe Hi-tech DOS Library is functioning on

Ground Floor, Dr. R.P. Centre, Delhi Oph-thalmic Sciences, AIIMS, New Delhi-110029from 12.00 Noon to 9.00 P.M. on week days and10.00 A.M. - 1.00 P.M. on Saturday, Sunday. TheLibrary will remain closed on Gazetted Holidays.Members are Requested to utilise the FacilitiesAvailable i.e. Computer, Video Journals View-ing, Latest Books and Journals. We are planningto subscribe two journals member can give sug-gestion in this regard.

Dr. Lalit Verma, Library Officer, D.O.S.


CURRENT PRACTICE

Issues in Diagnosis and Treatment of Macular HolesAtul Kumar MD, Gunjan Prakash MD

holes? Interestingly, the first surgery attempted was forimpending macular holes. De Bustros and colleagues hy-pothesized that we may be more successful treating orpreventing holes before rather than after they form. There-fore, the first clinical trial focused on Stage 1 macular holes.As that trial evolved, however, the technique for matchingStage 2 and Stage 3 macular holes was developed. We foundthat operating on Stage 1 holes was as likely to cause themto progress to Stage 2 or 3 as to cause improvement. Wehad a high success rate in closure when operating on Stage2 or 3 macular holes. Consequently, we now observe Stage1 holes. With Stage 2 holes, we tend to operate in order toprovide early intervention and success. The days of wait-ing unit a patient’s vision deteriorates to 20/100 or 20/200to repair their macular holes are behind us.

Of course, chronic Stage 3 and Stage 4 holes have a lowerrate of anatomic closure, and visual outcomes tend to bepoorer. A patient who has had a macular hole for 5 or 6years is unlikely to benefit from surgery. The patients witha good surgical prognosis tend to be those with Stage 2holes or Stage 3 holes with relatively recent changes invisual acuity.

Peeling the Internal Limiting Membrane

Other important issues include the advisability of peel-ing the internal limiting membrane (ILM), the type of in-traocular tamponade, and managing complications. Thesuccess rate has gradually increased in macular hole sur-gery. Looking at anatomic closure, we can now see successrates that exceed 90%. Peeling the internal limiting mem-brane may play a critical role in the improvement of suc-cess rate.

Macular hole surgery was first described in 1991. Untilthat time, there was no known treatment for the condi-tion, and we would customarily tell patients that nothingcould be done to save their vision. In the early 1990’s, Kellyand Mandel demonstrated that by separating the poste-rior hyaloid, performing an air-fluid exchange and posi-tioning the intravitreal gas bubble on the macular holewith the patient in a facedown position, they could suc-cessfully close the macular hole. Our knowledge of macu-lar holes has evolved since that time, but several issuesstill remain open to question.

DiagnosisDiagnosis of macular holes is easiest using slit-lamp

biomicroscopy of the fovea. A specific diagnostic test, theWatzke-Allen, involves passing a slit beam over the cen-tral fovea and identifying a break in the line. This test,however, is not very reliable, so we must depend uponmany ancillary tests to help us diagnose macular holes.The best ancillary test now available is Optical CoherenceTomography (OCT).

Surgery

When should we operate on patients with macular

Vitreoretina ServicesDr. R. P. Centre for Ophthalmic SciencesAIIMS, New Delhi - 110 029

Colour photograph showing full thicknessMacular Hole

Intraoperative photographdepicting ICG enhanced ILM

being peeled

Intraoperative photograph depict-ing completely peeled ILM from

Posterior Pole

OCT showing full thickness Macular Hole


Several studies have yielded varied results. Our studyat RP Centre found benefit in ILM peeling, but other re-search has suggested it is less critical. Working with agroup of 18 eyes, we were able to have anatomic closure in83.33% in the year 2000-2001. Preoperative visual acuitywas also a factor in the outcomes.

There are a variety of techniques of ILM peeling. Aftervitrectomy has already been done, and the posterior hya-loid has been removed from the retinal surface, we injectICG dye into the vitreous cavity over the macular hole,taking care not to put any in the macular hole itself. Thesolution is diluted to 0.5 %, which is weaker than the solu-tion used in the anterior segment. We then aspirate theICG dye out of the vitreous cavity. An optimal startingpoint for ILM-peel is chosen within the arcade vessels butremote from the fovea. The site is chosen to lie outside themaculopapular bundle. Tano’s Diamond Dusted MembraneScraper (Synergetics, Inc., USA) is used to raise a small ILMflap. In this way, engaging the neurosensory retina isavoided. The ILM flap is then grasped with end-openingforceps (Grieshaber, Alcon Laboratories, Inc. 6201 SouthFreeway, Fort Worth, TX 76134, USA) and a “rhexis”(smooth-edged continuous tear) is created by slowly tear-ing the ILM in a circular motion, concentric with the fovea,keeping the direction of force always following the naturalcourse of the nerve fibres (Figure No. 1). Most of the timesthe ILM can be removed as single piece, but if the tear isincomplete, the ILM can simply be-grasped at the new edge,and the rhexis resumed. This is how the process works.

Some researchers noticed that some of the patients weredeveloping poor visual acuity after ILM peeling. Some pa-tients experienced toxicity in the discrete area of RPE drop-out in the macular hole. Tissue culture studies were car-ried where RPE cells were grown and then treated withICG. No histological damage occurred. However, when vi-ability of the cells was measured using a mitochondrialdehydrogenase assay, it was found a definite decrease inthe viability of the RPE cells when they were exposed toICG. And the combination of the light exposure to the ICGenhanced the effect. So it is hypothesized that ICG mightactually be a photosensitizer like Visudyne. Now use oflower doses of ICG and lower light levels is advised, be-lieving this will be safer way to take advantage of ICGwithout causing harm to the macula.

Internal Tamponade

Whether gas or air should be used for internal tampon-ade is still open to question. Most ophthalmologists useeither SF6 or C3F8; both are adequate provided the patientmaintains a face-down position. Some, in particularMcCuen and colleagues, report very good results using a

silicone oil tamponade. The advantage of a silicone oil tam-ponade is that patients do not have to be as compulsiveabout maintaining their face-down positioning in the post-operative period, and visual rehabilitation occurs moreimmediately, the disadvantages are that patients need asecond operation to have the oil removed.

On the other hand, a gas internal tamponade leads tocataracts, which will result in a second operation any-way. In a study on a series of patients comparing oil to gas,the closure rate was basically the same with the twogroups. The overall closure rate was 89% with oil and 91%with gas. Perhaps the rate was somewhat higher with gasbecause of the somewhat higher surface tension. But thegroups differed in visual acuity. Close to 40% of patientshas 20/100 or better visual acuity with gas, whereas only25% has 20/100 or better vision with oil. Because of thedifference in visual acuity, it is currently recommend touse a gas tamponade.

Reducing ComplicationsAnother question to resolve is the recommended length

of the postoperative face-down positioning. We generallyadvise patients to be extremely compulsive about main-taining this position for 1 week. Finally, we must considerthe issue of cataract management in these eyes. These pa-tients develop acceleration of cataract/nucleus sclerosis.In order to maximize their visual recovery, patients willneed cataract surgery within 1 or 2 years of the macularhole surgery. Cataract surgery on a vitrectomized eye in-troduces more difficulty than the usual procedure. Highlyexperienced cataract surgeons say they prefer to operateon these eyes earlier rather than later. Waiting too longallows the nucleus to get very hard, and it is technicallydifficult to phacoemulsify harder nuclei in the absence ofvitreous.

Overall, we have found macular hole surgery to be oneof the most exciting innovations in our specialty. This con-dition that was considered totally inoperable previouslynow is treated with a success rate of over 90%. This is avery dramatic turnaround. Patients have high expecta-tions from the results, and we owe it to them to try tooptimize their visual outcome.Suggested Readings:1. ICG enhanced maculorhexis in macular hole surgery. Ind J

Ophthalmol 20022. Visual outcome of macular hole surgery with ILM peeling.

Jpn J Ophthalmol 20023. Clinicopathologic correlation of a macular hole treated by

cortical vitreous peeling and gas tamponade. Ophthalmol-ogy 1994

4. A Multicentered Clinical Study of Serum as AdjuvantTherapy for Surgical Treatment of Macular Holes. ArchOphthalmol. 1999


JOURNAL ABSTRACTS

Corneal Reinnervation after LASIK:Prospective 3-Year Longitudinal Study.Calvillo MP, McLaren JW, Hodge DO, BourneWM.

Invest Ophthalmol Vis Sci. 2004 Nov;45(11):3991-6.

The Study measured the return of innervation to thecornea during 3 years after LASIK. Seventeen corneas of11 patients who had undergone LASIK to correct myopiafrom -2.0 D to -11.0 D were examined by confocalmicroscopy before surgery, and at 1, 3, 6, 12, 24, and 36months after surgery. In all available scans, the numberof nerve fiber bundles and their density (visible lengthof nerve per frame area), orientation (mean angle), anddepth in the cornea were measured. The number anddensity of subbasal nerves decreased >90% in the firstmonth after LASIK. By 6 months these nerves began torecover, and by 2 years they reached densities notsignificantly different from those before LASIK. Between2 and 3 years they decreased again, so that at 3 yearsthe numbers remained <60% of the pre-LASIK numbers(P < 0.001). In the stromal flap most nerve fiber bundleswere also lost after LASIK, and these began recoveringby the third month, but by the third year they did notreach their original numbers (P < 0.001). In the stromalbed (posterior to the LASIK flap interface), there were nosignificant changes in nerve number or density. As thesubbasal nerves returned, their mean orientation did notchange from the predominantly vertical orientationbefore LASIK. Nerve orientation in the stromal flap andthe stromal bed also did not change. The study concludedthat both subbasal and stromal corneal nerves in LASIKflaps recovered slowly and did not return to preoperativedensities by 3 years after LASIK. The numbers ofsubbasal nerves appeared to decrease between 2 and 3years after LASIK.

Concurrent use of 5% natamycin and2% econazole for the management offungal keratitis.Cornea. 2004 Nov;23(8):793-6.

Prajna NV, Nirmalan PK, Mahalakshmi R, LalithaP, Srinivasan M.

PURPOSE:: To determine if concurrent use of 5%natamycin and 2% econazole offers greater benefits thanmonotherapy with 5% natamycin for the management

of fungal keratitis. METHODS:: Subjects presenting to thecornea service were treated with 5% natamycin and 2%econazole used concurrently. We compared the resultswith a historical control of patients treated with 5%natamycin in the same calendar year. The same clinicaland examination protocol including inclusion andexclusion criteria was used for both groups. RESULTS::We compared results of 47 subjects on concurrent use of5% natamycin and 2% econazole with all 53 subjects whohad received 5% natamycin in a previous study(historical controls). Baseline characteristics were similarbetween the 2 groups. There were no significantdifferences (P = 0.9) between the 2 arms for success(defined as a healed or healing ulcer). CONCLUSIONS::Concurrent use of 5% natamycin and 2% econazole doesnot appear to offer additional benefits over monotherapywith 5% natamycin for the management of fungalkeratitis.es remains predominantly vertical.

Intraocular pressure, safety and qualityof life in glaucoma patients switchingto latanoprost from adjunctive andmonotherapy treatments.Eur J Ophthalmol. 2004 Sep-Oct;14(5):407-15.

Haverkamp F, Wuensch S, Fuchs M, Stewart WC.

The authors evaluated efficacy, safety and quality of lifein ocular hypertensive or open-angle glaucoma patientschanged to latanoprost from previous therapy. The studywas a prospective, multicenter, active-controlled designin which qualified patients had their previous therapysubstituted for latanoprost and were followed for at leastthree months. In 1068 patients, latanoprost wascontinued 92% throughout the 36-month observationperiod. Latanoprost treatment reduced the intraocularpressure (1OP)(p < 0.001) when compared to previousmonotherapies including: beta-blockers (-4.0 +/- 3.7mmHg, 42%), alpha-antagonists (-3.9 +/- 3.0 mmHg, 14%),miotics (-3.8 +/- 3.5 mmHg, 2%), or carbonic anhydraseinhibitors (CAI) (-3.8 +/- 3.6 mmHg, n = 16%), andadjunctive therapy including: beta-blocker and CAI (-3.7+/- 3.1 mmHg, n = 12%), alpha-agonist (-3.7 +/- 3.4 mmHg,n = 5%), or pilocarpine (-3.4 +/- 3.7 mmHg, n = 6%), orCAI and alpha-agonist (-4.6 +/- 6.4 mm Hg, n = 2%)(p <0.0017). The most common adverse event withlatanoprost was ocular allergy (1.5% incidence). Patientsshowed a preference for latanoprost for many systemicand ocular quality of life measures on a non-validated


questionnaire (p < 0.05). The authors concluded that ina clinical setting, patients who have their mono- andadjunctive therapy treatment substituted for latanoprostmay on average experience reduced IOP, decreased sideeffects and increased quality of life measures.

Cost effectiveness of photodynamictherapy with verteporfin for agerelated macular degeneration: the UKcase.Br J Ophthalmol. 2004 Sep;88(9):1107-12.

Smith DH, Fenn P, Drummond M.

AIM : To estimate the potential cost effectiveness ofphotodynamic therapy (PDT) with verteporfin in the UKsetting. METHODS: Using data from a variety of sourcesa Markov model was built to produce estimates of thecost effectiveness (incremental cost per quality adjustedlife year (QALY) and incremental cost per vision yeargained) of PDT for two cohorts of patients (one withstarting visual acuity (VA) of 20/40 and one at 20/100)with predominantly classic choroidal neovasculardisease over a 2 year and 5 year time horizon. Agovernment perspective and a treatment cost onlyperspective were considered. Probabilistic and one waysensitivity analyses were undertaken. RESULTS: From thegovernment perspective, over the 2 year period, theexpected incremental cost effectiveness ratios range from286 000 (starting VA 20/100) to 76 000 UK pounds(starting VA 20/40) per QALY gained and from 14 000 (20/100) to 34 000 UK pounds (20/40) per vision year gained.A 5 year perspective yields incremental ratios less than5000 UK pounds for vision years gained and from 9000(20/40) to 30 000 UK pounds (20/100) for QALYs gained.Without societal or NHS cost offsets included, the 2 yearincremental cost per vision year gained ranges from 20000 (20/100) to 40 000 UK pounds (20/40), and the 2 yearincremental cost per QALY gained ranges from 412 000(20/100) to 90 000 UK pounds (20/40). The 5 year timeframe shows expected costs of 7000 (20/40) to 10 000 UKpounds (20/100) per vision year gained and from 38 000(20/40) to 69 000 UK pounds (20/100) per QALY gained.CONCLUSION: This evaluation suggests that earlytreatment (that is, treating eyes at less severe stages ofdisease) with PDT leads to increased efficiency. Whenconsidering only the cost of therapy, treating people atlower levels of visual acuity would probably not beconsidered cost effective. However, a broad perspective

that incorporates other NHS treatment costs and socialcare costs suggests that over a long period of time, PDTmay yield reasonable value for money.

Cost utility of photodynamic therapyfor predominantly classic neovascularage related macular degeneration.Br J Ophthalmol. 2004 Aug;88(8):982-7.

Hopley C, Salkeld G, Mitchell P.

Centre for Vision Research, University of Sydney, Departmentof Ophthalmology, Westmead Millennium Institute, Australia.

Age related macular degeneration (AMD) is the leadingcause of severe vision impairment and blindness in olderpeople throughout the developed world and currentlyaffects around 420 000 UK citizens. Choroidalneovascularisation (CNV) is treatable withphotodynamic therapy (PDT) but is expensive at overpound 1200 per treatment. The aim of this study was toassess the cost utility of PDT for better eye,predominantly classic, subfoveal choroidal neovascularlesions secondary to AMD. Cost utility analysis (CUA)was conducted to estimate the cost effectiveness of PDTfor scenarios involving reasonable (6/12) and poor (6/60)visual acuity. The models incorporated data from theTreatment of Age-related Macular Degeneration with PDT(TAP) Study and patient based utilities. The incrementalCUA was based on decision analytical models,comparing treatment to a placebo comparator. Extensiveone way sensitivity analysis of parameters wasconducted to determine the robustness of the model. Adiscount rate of 6% was used for costs and qualityadjusted life years (QALY). RESULTS: Model 1: in peoplewith reasonable initial visual acuity, the cost utility oftreating applicable neovascular AMD lesions was pound31 607 per QALY saved, with a sensitivity analysis rangefrom pound 25 285 to pound 37 928. Model 2: in peoplewith poor initial visual acuity, the cost utility was pound63 214 per QALY saved, with a sensitivity analysis rangefrom pound 54 183 to pound 75 856. CONCLUSIONS: PDTtreatment is the only available treatment for some formsof neovascular (“wet”) AMD. Under these assumptions,PDT can be considered moderately cost effective for thosewith reasonable visual acuity but less cost effective forthose with initial poor visual acuity. These findings haveimplications for ophthalmic practice and healthcareplanning.


TEAR SHEET

Approach to Leukocoria

Harish Pathak, MD, Vijay B. Wagh, MD, M.S. Bajaj, MDDr. R. P. Centre for Ophthalmic SciencesAIIMS, New Delhi - 110 029


DOS Midterm Conference21st November, 2004Contact : Dr. Jeewan S. Titiyal, Secretary DOSR.No. 476, 4th Floor,Dr. R.P. Centre for Ophthalmic SciencesAIIMS, Ansari Nagar, New Delhi – 110029Ph : 91-011-26589549, 265888852-65 Ext. 3146Fax : 91-011-26588919Email : [email protected] : www.dosonline.org

63rd All India Ophthalmological Society Conference13-16th January, 2005Contact : Dr. B. K. Tripathy, Organising Secretary,Bimal Tripathy Lane, Mahatab Road,Cuttack – 753001, OrissaPh : 0671-2310111, 2332483 Fax : 0671-2330111E-mail : [email protected]

Annual DOS Conference2nd & 3rd April, 2005Contact : Dr. Jeewan S. Titiyal, Secretary DOSR.No. 476, 4th Floor,Dr. R.P. Centre for Ophthalmic SciencesAIIMS, Ansari Nagar, New Delhi – 110029Ph : 91-011-26589549, 265888852-65 Ext. 3146Fax : 91-011-26588919Email : [email protected]

FORTHCOMING EVENTS

NATIONALINTERNATIONAL

20th Asia Pacific Academy of Ophthalmology Congress27-31st March, 2005Kuala Lumpur, MalaysiaThe 20th Asia Pacific Academy of OphthalmologyCongressTel : +603-7956-3113 Fax : +603-7960-8297Email : [email protected] : www.apao2005.com.my

5th International Glaucoma Symposium20th March, 2005 – 2nd April, 2005Cape Town, South AfricaContact : Kenes InternationalTel : +41-22-908-04-88 Fax : +41-22-7322850Email : [email protected] : www.kenes.com/glaucoma

ASCRS/ASOA Meeting Congress16-20th April, 2005Washington, DCContact : ASCRSTel : +1-703-591-2220 Fax : +1-703-591-0614Web : www.ascrs.org

!! Congratulations !!1. Prof. R.B. Vajpayee, Dr. Namrata Sharma & Dr. Tushar Agarwal for being awarded

Best Scientific Video Presentation in American Academy of Ophthalmology, NewOrleans, USA, 2004.

2. Dr. Mohita Sharma & Dr. Angshuman Goswami, Tirupati Eye Centre, Noida forrecieving Awadh Dubey Award for paper presentation in 39th Annual U.P. StateOphthalmological Society in October, 2004 at Agra.

3. Dr. Neeraj Sanduja for recieving Dr. Prem Chandra award for Best Free PaperPresentation in Annual Conference of North Zone Ophthalmological Society, 2004& Rashtriya Gaurav Award for Year 2004.


DOS has always been in the forefront of efforts toensure that its members remain abreast with the latestdevelopments in Ophthalmology. Among the importantobjectives formulated by the founders of ourconstitution was the cultivation and promotion of theScience of Ophthalmology in Delhi.

The rapid strides in skills and knowledge havecreated a need for an extremely intensive ContinuingMedical Education programme.

DOS Credit Rating System (DCRS)

If any of the presentations is given an Award – Addi-tional 20 bonus Credits.

Member who have earned 100 Credits, are entitled to:

a) Certificate of Academic Excellence in OphthalmicPractice.

b) Eligible for DOS Travel fellowship for attendingconference.

If any member earns 200 Credits, he/she shall, inaddition to above, be awarded Certificate of Distin-guished Resource-Teacher of the Society.

Institutional assessment for best performance will bebased on the total score of members who attend dividedby number of members who attended. Institutional as-sessment regarding decision to retain the institute forthe next year will be based on total score by all delegateswho attend the meeting divided by average attendenceof all 8 meetings.

In a bid to strengthen our efforts in this directionDOS had DOS Credit Rating System (DCRS), the detailsof which are given below. Our Primary objective is topromote value-based knowledge and skills inOphthalmology for our members and give recognitionand credit for efforts made by individual members toachieve standards of academic excellence in OphthalmicPractice.

DOS CREDIT RATING SYSTEM (DCRS)DCRS Max.

1) Attending Monthly Clinical Meeting* † (For full attendence) 10 902) Making Case Presentation at Monthly Meeting** 15 —3) Delivering a Clinical Talk at Monthly Meeting** 15 —4) Free Paper Presentation at Annual Conference (To Presenter)** 15 305) Speaker/Instructor** in : Monthly Symposium 15 30

: Mid Term Symposium 15 30: Annual Conference 15 30

6) Registered Delegate at Mid Term DOS Conference 20 —7) Registered Delegate at Annual DOS Conference 30 —8) Full Article publication in Delhi Journal of Ophthalmology/DOS Times 30 609) Letter to editor in DOS Times 10 2010) Letter to editor in DJO 15 30——————————————————————————————————————————————

Please note that the Institutions’ grading increases ifthe attendance at its meeting is higher (i.e. more thanthe average attendence of the eight monthly meetings).——————————————————————* Based on Signature in DCAC** Subject to Submission of Full Text to Secretary, DOS† Credits will be reduced in case attendence is only forpart of the meeting.

DCRS !! Attention !!* Members are requted to sign on monthly meeting at-tendance register and put their membership number.* The DCRS paper will be issued only after the validsignature of the member in the attendance register.* Please submit your DCRS papers to the designatedDOS Staff only.* The collected DCRS papers will be countersigned byPresident and Secretary and sealed immediately ofterthe meeting is over.


1. Vertical saccade is controlled by the ____________

2. ____________variety of Adenoid cystic carcinoma of the lacrimal gland is associated with the worstprognosis.

3. Blood staining of the cornea is caused by the presence of ____________within the cornea

4. Bitots spots is caused by goblet cell hyperplasia - True/False

5. Wedl cells occur in____________type of cataract.

6. Rosenthal fibres are seen in____________

7. Sympathetic ophthalmitis is prevented by removal of the exciting eye within___________weeks of injury

8. Term retinoblastoma was coined by____________

9. Ocular bobbing is associated with haemorrhages in ____________________ area of the brain

10. KF ring starts at____________clock hour.

Rules:• Please send your entries to the DOS office latest by 10th December, 2004.• Prize Rs. 500/- Courtesy: Syntho Pharmaceuticals

1. What is the frequency of acoustic waves used in ophthalmology?

2. What is the normal thickness of optic nerve in imaging.......?

3. Who described first external dacryo cystorhinostomy..........?

4. Who is the Editor of Journal Survey of Ophthalmology.......?

5. Most Common location of juvenile retinoschisis is...............?

6. Most common organism causing post operative endophthalmitis?

7. Classical visual field finding in hysteria is................... ?

8. Toutan giant cell is seen in ................?

9. Abraham lens has a focusing button of .............?

10. Angle between optical and visual axis is known as ................?

ANSWERS OF DOS QUIZ NO. 13

10 MHz

2.4 to 3.4 mm

Toti

B. Schwartz

Inferotemporal

Staph. Epidermidis

Symmetrical field constriction

Juvenile xanthogranuloma

66D

Alpha Angle

DOS QUIZ NO. 15


DOS Credit Rating System Report CardDCRS July 2004 – Army Hospital (R&R)

Total No. of Delegates ................................................................................................................................................................. 83Delegates from Out side (N) ........................................................................................................................................................ 75Delegates from Army Hospital (n) ................................................................................................................................................ 8Overall assessment by outside delegates (M) ..................................................................................................................... 610.5Assessment of case presentation-I (Dr. Lt. Col. R. Maggon) by outside delegates ............................................................... 549Assessment of case presentation-II (Dr. Lt. Col. (Mrs.) Madhu Bhaduria) by outside delegates ...................................... 541.5Assessment of clinical talk (Dr. Col. Ajay Banajee) by outside delegates .......................................................................... 572.5Rejected Form Army Hospital (n) .................................................................................................................................................. 2

Rejected Form Out side (N) ........................................................................................................................................................... 2

DCRS August, 2004 – Sir Ganga Ram HospitalTotal no. of Delegates (Valid DCRS forms) .................................................................................................................................. 86Delegates from Out side (N) ........................................................................................................................................................ 76Delegates from Sir Ganga Ram Hospital (n) ............................................................................................................................... 10Overall assessment by outside delegates (M) ........................................................................................................................ 552Assessment of case presentation-I (Deepti Manocha) by outside delegates ...................................................................... 475Assessment of case presentation-II (Dr. Piyush Kapoor) by outside delegates .................................................................... 498Assessment of clinical talk (Prof. H.K. Tewari) by outside delegates ...................................................................................... 571Total no. of invalid DCRS forms .................................................................................................................................................. NIL

DCRS September, 2004 – Hindu Rao HospitalTotal No. of Delegates ................................................................................................................................................................. 45

Delegates from Out side (N) ........................................................................................................................................................ 32

Delegates from Hindu Rao Hospital (n) ...................................................................................................................................... 13

Overall assessment by outside delegates (M) ..................................................................................................................... 225.5

Assessment of case presentation-I (Dr. Vikas Anand / Dr. Ruchi Goel) by outside delegates .......................................... 214.5

Assessment of case presentation-II (Dr. Bithi Chowdhury) by outside delegates ................................................................ 216

Assessment of clinical talk (Dr. Ruchi Goel) by outside delegates ......................................................................................... 229

Rejected Form Hindu Rao Hospital (n) ...................................................................................................................................... NIL

Rejected Form Out side (N) ............................................................................................................................................................ 1

DCRS October, 2004 – Dr. R.P. Centre for Ophthalmic SciencesTotal No. of Delegates ................................................................................................................................................................. 57

Delegates from Out side (N) ........................................................................................................................................................ 38

Delegates from Dr. R.P. Centre (n) ................................................................................................................................................ 19

Overall assessment by outside delegates (M) ..................................................................................................................... 272.5

Assessment of case presentation-I (Dr. Balasubramanya R.) by outside delegates ............................................................ 261

Assessment of case presentation-II (Dr. Arun Singhvi) by outside delegates ....................................................................... 264

Assessment of clinical talk (Dr. Rajesh Sinha) by outside delegates ..................................................................................... 300

Rejected Form Dr. R.P. Centre (n) ................................................................................................................................................... 2

Rejected Form Out side (N) ........................................................................................................................................................ NIL


Emergencies in Ophthalmology1. CRAO2. Post Operative Endophthalmitis3. Traumatic Optic Neuropathy4. Acute Angle Closure Glaucoma5. Orbital Cellulitis6. Cornea Scleral Perforation with Lens Rupture7. Impending or Perforated Corneal Ulcer8. Acute Lime Injury

Forenoon Session: 11:30 AM - 1:30 PM

Difficult Intra Operative surgical situations: How to manage them?1. Accidental Needle Perforation in RD Surgery

a) With Subretinal Hemorrhageb) With incarceration of retina

2. Accidental Slippage of Muscle in Squint Surgery3. Phaco in Torn Capsulorhexis4. Intra- op Zonular Dialysis5. Posterior Capsular Rent6. Damaged / Wrong IOL7. Nucleus / IOL Drop8. LASIK Incomplete Flaps and Buttonholes

Afternoon Session : 2:30 PM - 4:30 PM

Diagnostic & Management DilemmasCorneal & Refractive cases:

1. Post Mito-C Scleral Necrosis2. Cystoid Cicatrix following P.K.3. Unusual presentation of Scleral abscess

Neuro-Ophthalmology Cases:1. Disc Oedema diagnostic deliema

Three CasesOculoplasty Cases

1. Unusual Presentation of lacrimal gland tumour2. Three Cases

Vitreo Retina / Uvea Cases1. Three Cases

SCIENTIFIC PROGRAMME

SCIENTIFIC PROGRAMMEMid Term Conference of DOS : Crisis Management

Forenoon Session : 9:00 AM - 11:00 AM


Name (In Block Letters) __________________________________________________________________________

S/D/W/o _____________________________________________________________ Date of Birth _____________

Qualifications _________________________________________________________ Registration No. __________

Sub Speciality (if any) ___________________________________________________________________________

ADDRESS

Clinic/Hospital/Practice ______________________________________________________________________

_______________________________________________________________ Phone __________________

Residence ________________________________________________________________________________

_______________________________________________________________ Phone __________________

Correspondence ___________________________________________________________________________

_______________________________________________________________ Phone __________________

Email___________________________________________________________ Fax No. ________________

Proposed by

Dr. ____________________________________ Membership No._________ Signature __________________

Seconded by

Dr. ____________________________________ Membership No._________ Signature __________________

[Must submit a photocopy of the MBBS/MD/DO Certificate for our records.]

I agree to become a life member of the Delhi Ophthalmological Society and shall abide by the Rules andRegulations of the Society.(Please Note : Life membership fee Rs. 3100/- payable by DD for outstation members. Local Cheques acceptable, payableto Delhi Ophthalmological Society)

Please find enclosed Rs.____________in words _______________________________________________________ by Cash/

Cheque/DD No._______________________ Dated_____________ Drawn on_______________________________________

Three specimen signatures for I.D. Card.

DELHI OPHTHALMOLOGICAL SOCIETY

(LIFE MEMBERSHIP FORM)

Signature of Applicantwith Date

FOR OFFICIAL USE ONLY

Dr.___________________________________________________________________has been admitted as Life Member of

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

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

drawn on __________________________________________________________________.(Secretary DOS)


INSTRUCTIONS

1. The Society reserve all rights to accepts or reject the application.

2. No reasons shall be given for any application rejected by the Society.

3. No application for membership will be accepted unless it is complete in all respects and accompanied by aDemand Draft of Rs. 3100/- in favour of “Delhi Ophthalmological Society” payable at New Delhi.

4. Every new member is entitled to received Society’s Bulletin (DOS Times) and Annual proceedings of theSociety free.

5. Every new member will initially be admitted provisionally and shall be deemed to have become a full memberonly after formal ratification by the General Body and issue of Ratification order by the Society. Only then heor she will be eligible to vote, or apply for any Fellowship/Award, propose or contest for any election of theSociety.

6. Application for the membership along with the Bank Draft for the membership fee should be addressed to Dr.Jeewan S. Titiyal, Secretary, Delhi Ophthalmological Society, R.No. 476, 4th Floor, Dr. R.P. Centre for Oph-thalmic Sciences, AIIMS, Ansari Nagar, New Delhi – 110029.

7. Licence Size Coloured Photograph is to be pasted on the form in the space provided and two Stamp/ LicencesSize Coloured photographs are required to be sent along with this form for issue of Laminated Photo IdentityCard (to be issued only after the Membership ratification).

!!Attention!!Case Presentation in the Monthly Meetings

by Non Institutional MembersThere will be one non Institutional case presentation/Clinical talk by one ofthe DOS member during the monthly meeting. The presentation will be doneby a non Institutional member where monthly meetings are not being held.The presenter will be allowed to present a case or a clinical talk for sameamount of time as it is given for other presentations in the monthly meeting.Interested members should contact secretary DOS at least two weeks before themonthly meeting with details of their presentation. If there are more than onerequest then they will be given opportunity in the next monthly meeting. ThePresident and Secretary will review the presentation for its clinical and scien-tific contents. These non Institutional presentation will be graded for the bestcase presentation/Clincal talk as it is done for Institutional presentations andthey will be eligible for best presentation award.

DOS MONTHLY CLINICAL MEETING FOR NOVEMBER, 2004 · November, 2004 5 DOS Times - Vol.10, No. 5 Roop...

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