Approved and Indexed by PMDC & Pak MediNet ABC Certified ... · Ophthalmology Update Vol. 11. No....

Ophthalmology Update Vol. 11. No. 1, January-March 2013 i

Published quarterly by Ophthalmic Newsnet from 267-A, St: 53, F-10/4, Islamabad - PakistanPhones:051-2222922 ext.1255, 051-4414091 Mob: 0333-5158885, Fax:051-2299113

E-mail: [email protected] at PanGraphics (Pvt) Ltd., Islamabad.

INTERNATIONAL

Approved and Indexed by PMDC & Pak MediNetABC Certified

www.ophthalmologyupdate.comwww.prime.edu.com

www.pakmedinet.com

AN OFFICIAL JOURNAL OF PESHAWAR MEDICAL COLLEGE

THE TRUSTED JOURNAL OF OPHTHALMIC SCIENCES

Established 1998 ISSN 1993-2863

Vol. 11. No. 1 January-March 2013

Update

CHIEF ADVISER CHIEF EDITOR

Prof. Najib ul Haq Prof. M.Yasin Khan Durrani

OPHTHALMIC SECTION

INTERNATIONAL BOARDProf. Arthur S.M. Lim (Singapore), Prof. Robert N. Weinrub (USA)Prof. Khalid Tabbara (S. Arabia), Dr. Syed Sikandar Hasnain (USA)Prof. Emeritus Diljeet Singh (India), Dr. Sakkaf Ahmed Aftab (UK)

Dr. Madiha Durrani (UAE)

ASSOCIATE EDITORSProf. Syed Imtiaz Ali, Prof. Hafeez ur Rehman, Prof. Akbar Hyder Soomro

Prof. Jahangir Akhtar, Prof. Shahid Wahab

ASSISTANT EDITORSProf. Nadeem Qureshi, Prof. Naqaish Sadiq, Prof. B.A. Naeem, Prof. Imran Azam Butt

Dr. Ghulam Sabir, Dr. Inam ul Haq Khan, Dr. Liaqat Ali Shaikh, Dr. Munira ShakirDr. Syeda Aisha Bukhari, Prof. Niamatullah Kundi, Dr. Mahfooz Hussain

Dr. Zeeshan Kamil, Dr. Shakir Zafar, Balbir Singh Bhura

GENERAL SECTION

ASSISTANT EDITORSProf. Zahoor Ullah, Prof. Zafar Iqbal, Dr. Faiz-ur-Rehman

Dr. Misbah Durrani

MANAGING EDITORDr. Jahanzeb Durrani

Registered vide No. 3405/2/(63) under Press and Publication Ordinance ‘98 Govt. of Pakistan

ii Ophthalmology Update Vol. 11. No. 1, January-March 2013

ContentsEDITORIAL

Significant Progress in Fuchs’s Corneal Dystrophy (FCD) (Role of E2-2 Protein)Prof. M. Y. K. Durrani ----------------------------------------------------------------------------------------------------------------01

ORIGINAL ARTICLES

Do we need to Redefine Laser Indications in Diabetic Maculopathy?Sanaullah Jan et al -------------------------------------------------------------------------------------------------------------------- 04

Ocular Trauma Associated with Bomb BlastJunaid Faisal Wazir et al ------------------------------------------------------------------------------------------------------------ 08

Photorefractive Keratectomy and Patient Satisfaction LevelM. Abdul Moqeet ----------------------------------------------------------------------------------------------------------------------12

To Know about Timely Referral System for Retinopathy of Prematurity (ROP)in three Leading Hospitals of Peshawar, (KPK)Junaid Faisal Wazir et al ------------------------------------------------------------------------------------------------------------ 16

Comparison of Preoperative Injection vs. Intraoperative application of Mitomycin Cin Recurrent PterygiumZakir Hussain et al ------------------------------------------------------------------------------------------------------------------- 21

Frequency of Different Types of Age Related Cataracts (Study of 250 cases)Naseer Ahmad et al ------------------------------------------------------------------------------------------------------------------- 25

Role of Intravitreal Bevacizumab in the Treatment of Acute Central Serous Chorio-retinopathyZakir Hussain et al ------------------------------------------------------------------------------------------------------------------- 30

Comparison of Frequency of Recurrence after Surgery for Primary Pterygiumusing free Conjunctival Autograft Transplantation & Bare Scleral TechniqueSaber Mohammad et al --------------------------------------------------------------------------------------------------------------- 34

Visual Outcome after the use of Neodymium-Yttrium- Aluminum Garnet (YAG) Applicationfor Posterior Capsular OpacificationNuzhat Rahil et al -------------------------------------------------------------------------------------------------------------------- 40

Efficacy of Excimer Laser Photorefractive Keratectomy in High MyopiaM. Abdul Moqeet and Dr. Madiha Durrani --------------------------------------------------------------------------------------- 44

The effect of Intracameral Preservative free 1% Xylocaine on the Corneal Endothelium duringPhacoemulsification ProcedureMushtaq Ahmad et al ---------------------------------------------------------------------------------------------------------------- 50

Postoperative Endophthalmitis, role of SubconjunctivalAntibiotics Intraoperatively during Cataract SurgeryMuhammad Naeem et al ------------------------------------------------------------------------------------------------------------- 54

Ophthalmology Update Vol. 11. No. 1, January-March 2013 iii

Contents

Penetrating Keratoplasty: Indications, Visual outcomes,and Complications in Tertiary Care HospitalAfzal Qadir et al ---------------------------------------------------------------------------------------------------------------------- 57

Role of Amniotic Membrane in Ocular Surface DiseasesAfzal Qadir et al ---------------------------------------------------------------------------------------------------------------------- 60

Prevalence of Glaucoma in Low Myopic VS High Myopic Patients:(A Study of 300 Cases)Mohammad Alam et al --------------------------------------------------------------------------------------------------------------- 64

CURENT RESEARCH

Arcuate Field Defects in GlaucomaSyed S. Hasnain M.D. et al ---------------------------------------------------------------------------------------------------------- 67

REVIEW ARFTICLES

Glaucoma: Beyond Intraocular PressureProf. Marianne L. Shahsuvaryan MD --------------------------------------------------------------------------------------------- 74

Change in Intraocular Pressure following Phacoemulsification Technique of Cataract SurgeryMuhammad Imran Saleem et al ----------------------------------------------------------------------------------------------------- 79

Postoperative Astigmatism following Phacoemulsification: Versus Extracapsular Cataract ExtractionFaisal Nawaz Khan------------------------------------------------------------------------------------------------------------------- 83

FEATURE

A Simple Method to Diagnose GlaucomaSyed S. Hasnain M.D. et al ---------------------------------------------------------------------------------------------------------- 88

PITFALLS OF RESEARCH (A non-conventional analysis)Abbas Hasnain ------------------------------------------------------------------------------------------------------------------------ 93

OPHTHALMOLOGY NOTEBOOK

Letters to the Editor ---------------------------------------------------------------------------------------------------------------- 94

Apple fruit (Malus domestica) nutritional factsZainab Inam--------------------------------------------------------------------------------------------------------------------------- 95

iv Ophthalmology Update Vol. 11. No. 1, January-March 2013

viewers.Abstract: Abstract of original article should be in

structured format with the following sub-headings:Objective, Design, Place and duration of Study, Patients& Methods, Result and Conclusion.

Introduction: This should include the purpose ofthe article. The rationale for the study or observationshould be summarized.

Methods: Study design and sampling methodsshould be mentioned. The selection of the observationalor experimental subjects (patients or experimentalanimals, including controls) should be describedclearly. The methods and the apparatus used shouldbe identified and procedures described in sufficientdetails to allow other workers to reproduce the resultsand references to established methods. All drugs andchemicals used should be identified precisely,including generic names, doses, routes ofadministration.

Results: These should be presented in a logicalsequence in the text, tables and illustrations. Onlyimportant observations should be emphasized orsummarized.

Discussion: The author’s comments on the result,supported with contemporary references, includingarguments and analysis of identical work done byothers. Brief acknowledgement may be made at the end.

Conclusion: Conclusion should be provided underseparate heading and highlighting new aspects arisingfrom the study. It should be in accordance with thestudy.

Copyright: Material printed in this journal is thecopyright of the publisher of Ophthalmic Newsnet/Ophthalmology Update and may not be reproducedwithout the permission of the editor/publisher. Thepublisher only accepts the original material forpublication with the understanding that except forabstracts, no part of the data has ycccccccccccc beenpublished or will be submitted for publicationelsewhere before appearing in the journal. The EditorialBoard makes every effort to ensure the accuracy andauthenticity of the material printed in the journal.However, conclusions and statements expressed are theviews of the authors and do not necessarily reflect theopinions of the Editorial Board. Publishing ofadvertising material does not imply an endorsementby the Ophthlmic Newsnet /Ophthalmology Update.

Address for Correspondence: The Chief Editor,Ophthalmology Update, 267-A, St: 53, F-10/4, Islamabad,Pakistan. E-mail: [email protected]

Instructions to the authors

All materials submitted for publication should besent to the journal ‘Ophthalmology Update’. Articles/research papers which have already been published oraccepted elsewhere for publication should not besubmitted. A paper that has been presented at ascientific meeting, if not published in full in proceedingor similar publication may be submitted. Press reportsof meetings will not be considered as breach of thisrule.

Ethical Aspects: If articles, tables, illustrations orphotographs, which have already been published, areincluded, a letter of permission for republication (orits excerpts) should be obtained from the author(s) aswell as the editor of the journal where it was previouslypublished.

Material for Publication: The material submittedfor publication may be in the form of original research,a review article, short communications, a case report,recent advances, new techniques, review on clinical/medical/ophthalmic education, a letter to the editor,medical quiz, Ophthalmic highlights/update, newsand views related to the field of medical sciences.Editorials are written by invitation. Report onOphthalmic obituaries should be concise. Authorshould keep one copy of the manuscript for reference,and send three copies (laser or inkjet) to the ManagingEditor, Ophthalmology Update through E-mail/CD orby post in MS word. Photocopies are not accepted. Anyillustrations or photographs should also be sent induplicate. Authors from outside Pakistan can also e-mail their manuscript. It should include a title page, E-mail address, fax and phone numbers of thecorresponding author. There should be no more than40 references in an original/review article. If preparedon computer, a CD should be sent with the manuscript.

Dissertation/Thesis Based Article: An articlebased on dissertation submitted as part of therequirement for a Fellowship can be sent forpublication after it has been approved by the relevantinstitution. Dissertation based article should be re-written in accordance with the instructions to authors.

References: References should be numbered in theorder in which they are called in the text. At the end ofthe article, the full list of references should give thenames and initials of all authors in Vancouver stylebased on the format used by the NLM in IndexMedicus. It verify the references against the originaldocuments before submitting the article.

Peer Review: Every paper will be read by at leasttwo staff editors of the editorial board. The paperselected will then be sent to one or more external

Instructions to the Authors

Ophthalmology Update Vol. 11. No. 1, January-March 2013 1

Significant Progress in Fuchs’s Corneal Dystrophy (FCD)(Role of E2-2 Protein)

Editorial

Corneal dystrophies are a group of genetic, oftenprogressive, eye disorders in which abnormal materialoften accumulates in the clear transparent cornea.Corneal dystrophies may not cause symptoms(asymptomatic) in some individuals; in others they maycause significant vision impairment. The age of onsetand specific symptoms vary among the different formsof corneal dystrophy. The disorders have some similarcharacteristics; most forms of corneal dystrophy affectboth eyes, do not affect other areas of the body, andtend to run in families. Most forms are inherited asautosomal dominant traits; a few autosomal recessivetraits, taking into account the chromosomal loci as wellas the responsible genes and their mutations.

Fuchs’s Corneal Dystrophy (FCD) is characterizedby dysfunction of the corneal endothelium, leading toreduced vision. The prevalence of FCD has beenestimated at about 5% among persons over the age of40-50 years affecting women 4 times more than themenand is the most common indication for cornealtransplantation. The ability to diagnose FCD beforesymptoms develop and knowledge of the biologicpathways leading to the disorder are important.

Corneal transparency is critically dependent on amono-layer of endothelial cells to maintain thedehydration and hence the clarity of its collagenousstroma, which makes up 90% of corneal thickness. Thecornea shows extracellular deposits, usually calledguttae which confer a “beaten-metal” appearance to theinnermost endothelial layer.These excrescences (guttae)are the clinical hallmark of FCD and become morenumerous with progression of the disease. As theendothelial layer develops confluent guttae in thecentral cornea, the cornea swells and becomes cloudybecause the remaining endothelial cells are not sufficientto keep the cornea dehydrated and clear.There isreduced water movement out of the cornea, causingstromal hydration. This process impairs cornealtransparency, giving rise to glare and blurred vision,most noticeably on waking in the morning. Cataractsurgery in such patients can accelerate endothelial-cellloss, resulting in further edema of all corneal layers,

loss of vision, and a blind, painful eye.Most cases of corneal dystrophy are inherited as

an autosomal dominant trait with variable expressivity.Genetic diseases are determined by the combination ofgenes for a particular trait present on the chromosomesreceived from the father and the mother. Dominantgenetic disorders occur when only a single abnormalgene is necessary for the appearance of the disease. Thisabnormal gene can be inherited from either parent, orcan be the result of a new mutation in the affectedindividual. The risk of passing the abnormal gene fromaffected parent to offspring is 50 % for each pregnancyregardless of the sex of the resulting child. Variableexpressivity means that some individuals who inheritthe same gene for a dominant disorder may not developthe same symptoms.The chance for a child to receivenormal genes from both parents and be geneticallynormal for that particular trait is 25 %. The risk is thesame for males and females.

Investigators have determined that several cornealdystrophies occur due to disruptions or changes(mutations) of the Transforming Growth Factor Beta-induced (TGFB1) gene located on the long arm (q) ofchromosome 5 (5q31). Each chromosome has a shortarm designated “p” and a long arm designated “q”.Chromosomes are further sub-divided into many bandsthat are numbered. For example, “chromosome 5q31”refers to band 31 on the long arm of chromosome 5.The numbered bands specify the location of thethousands of genes that are present on eachchromosome.

FCD is thought to be a genetically complex traitthat has been observed in 38%of the first-degreerelatives of probands. Although rare genetic variationthat contributes to both early onset of familial diseaseand late onset of age-related disease has been identified,no common variants have been reported.Early onset hasbeen linked to mutations in the COL8A2 gene, encodingthe α2sub-unit of collagen VIII, a component of theendothelial basement membrane.

Researchers identified two regions of the genomethat appear to contribute to FCD. The first region spans

2 Ophthalmology Update Vol. 11. No. 1, January-March 2013

theTCF4 (Transcription Factor4) locus and wassignificantly associated with FCD at the genomewidelevel. The second region, spanning theProtein TyrosinePhosphatase Receptor type G (PTPRG) locus, wasstrongly associated with FCD, but the association didnot reach genomewide significance. Genetic variationacross the TCF4 locus may explain the linkage signalwith FCD previously observed on chromosome 18q21.The high impact on disease risk suggests that a pathwayregulated by E2-2, the protein encoded by TCF4, is amajor contributor to FCD.E2-2 is expressed in thedeveloping corneal endothelium and is an attractivecandidate for FCD.

PTPRG belongs to the protein tyrosinephosphatase (PTP) family, members of which regulatea wide array of cellular functions, including growth,cell mobility, gene expression, cellular adhesion, ionchannel control and oncogenesis. It has yet to bedetermined whether PTPRG interacts with Zinc FingerE-Box binding homoeo box1(ZEB1) or E2-2.

The biologic pathways that are implicated by thecontribution of TCF4 and probably ZEB1 gene, whichencodes the zinc finger E-box binding homeo box1protein, and PTPRG variants to typical FCD suggestseveral mechanisms of pathogenesis as seen in patientswith FCD. Another mechanism could be increasedcellular stress through abnormal development of thebasement membrane, abnormal ion-channel regulation,

or premature senescence.In conclusion, the findings suggest that genetic

variation in the TCF4 locus substantively contributesto the risk of FCD. The genetic risk appears to localizeto multiple regions of the TCF4 locus and the presenceof these haplotypes confers a high risk of FCD.

As far as the treatment is concerned, severalfactors determine what therapy may be used, keepingin view of the severity of symptoms, the rate ofprogression and the patients’ overall health and qualityof life.It is mostly symptomatic and supportive.Individuals who have mild symptoms may not requiretreatment and may instead be regularly observed todetect progression of the disease. Specific treatmentmay include eye drops, ointments, laser and cornealtransplant. Recurrent corneal erosions, a commonfinding, may be treated with bandage contact lens. Ifrecurrent erosions persist, additional measures such ascorneal scrapings or use of Excimer laser therapy, whichcan remove abnormalities from the corneal surface(photo-therapeutic keratectomy), may be undertaken.In individual with advanced symptoms, Keratoplastyis highly successful. However, there is a risk that thelesion may eventually develop in the graft.

Though multiple factors have been accrued in thedevelopment of FCD, yet the subject is a challenge toresearchers.In our country, cases are not very frequentlyseen in our daily practice and we do have a very

Editorial

Features of Fuchs’s Corneal Dystrophy (FCD)In Panel A, a clinical photograph shows severe corneal edema caused by FCD, with an associated loss of corneal clarity. In Panel B, aconfocal photomicrograph of the corneal endothelium in a control subject shows the normal appearance of the endothelial monolayer, with aregular mosaic of small, densely packed cells. In Panel C, a confocal photomicrograph of the corneal endothelium in a patient with FCDshows larger but fewer endothelial cells. The dark areas are sub-endothelial deposits called guttae. (Courtesy: NEJM - UK)


skeptic outlook pertaining to the course and prognosisof the disease . So far no attempt has ever been made toundertake the genetic study of FCD by our scientists ofMolecular Biology except a scanty research which hasbeen reported against Retinitis Pigmentosa. Moreover,there is hardly any data available regarding theincidence of FCD in our country.

Hence, it is important and the need of the hour toembark on research for hereditary/genetic disordersin Pakistan, where consanguineous marriages are morecommon in our society and hereditary disorders areoften seen in our daily practice.No doubt, our scientistsare well versed in the study of Genetics and MolecularBiology, there is a word of advice for them to undertakemore research on the challenging topics rather wastingtime on already researched or stereotyped projects, atrend commonly observed today.However, geneticcounseling may be beneficial to the affected individualand his family.REFERENCES1. Hindorff LA, Junkins HA, Hall PN, Mehta JP, Manolio TA.

A catalog of published genome-wide association studies.Bethesda, MD: National Human Genome ResearchInstituteGoldstein DB. Common genetic variation and humantraits. N Engl J Med 2009;360:1696-1698

2. Manolio TA. Genomewide association studies andassessment of the risk of disease. N Engl J Med 2010;363:166-176

3. Vitart V, Rudan I, Hayward C, et al. SLC2A9 is a newlyidentified urate transporter influencing serum urateconcentration, urate excretion and gout. Nat Genet2008;40:437-44

4. Budarf ML, Labbe C, David G, Rioux JD. GWA studies:rewriting the story of IBD. Trends Genet 2009;25:137-146

5. Donoso LA, Vrabec T, Kuivaniemi H. The role of complementFactor H in age-related macular degeneration: a review.SurvOphthalmol 2010;55:227-246

6. Baratz KH, Tosakulwong N, Ryu E, et al. E2-2 protein andFuchs’s corneal dystrophy. N Engl J Med 2010;363:1016-1024

7. Hogan MJ, Wood I, Fine M. Fuchs’ endothelial dystrophy ofthe cornea: 29th Sanford Gifford Memorial lecture. Am JOphthalmol 1974;78:363-383

8. Adamis AP, Filatov V, Tripathi BJ, Tripathi RC. Fuchs’endothelial dystrophy of the cornea. SurvOphthalmol1993;38:149-168

9. Krachmer JH, Purcell JJ Jr, Young CW, Bucher KD. Cornealendothelial dystrophy: a study of 64 families. ArchOphthalmol 1978;96:2036-2039

10. Flora A, Garcia JJ, Thaller C, Zoghbi HY. The E-protein Tcf4interacts with Math1 to regulate differentiation of a specificsubset of neuronal progenitors. ProcNatlAcadSci U S A2007;104:15382-15387

11. Thiery JP, Acloque H, Huang RY, Nieto MA. Epithelial-mesenchymal transitions in development and disease. Cell2009;139:871-890

12. Eger A, Aigner K, Sonderegger S, et al. DeltaEF1 is atranscriptional repressor of E-cadherin and regulatesepithelial plasticity in breast cancer cells. Oncogene2005;24:2375-2385

13. McGowan SL, Edelhauser HF, Pfister RR, Whikehart DR.Stem cell markers in the human posterior limbus and cornealendothelium of unwounded and wounded corneas. Mol Vis2007;13:1984-2000

14. Takacs L, Toth E, Berta A, Vereb G. Stem cells of the adultcornea: from cytometric markers to therapeutic applications.Cytometry A 2009;75:54-66

15. Riazuddin SA, Zaghloul NA, Al-Saif A, et al. Missensemutations in TCF8 cause late-onset Fuchs corneal dystrophyand interact with FCD4 on chromosome 9p. Am J Hum Genet2010;86:45-53

16. Moshirfar M, Feiz V, Feilmeier MR, Kang PC. Laser in situkeratomileusis in patients with corneal guttata and familyhistory of Fuchs’ endothelial dystrophy. J Cataract RefractSurg 2005;31:2281-2286

17. Vision 2020: the cataract challenge. Community Eye Health2000;13:17-19

Prof. M. Yasin Khan DurraniMBBS.,DO.,FRCOphth (Lond)Editor in ChiefE.Mail>[email protected]

Editorial


————————————————————————————————*This study was presented in the Khyber Eye Symposium atNathia Gali and won 2nd best paper award.————————————————————————————————1Assistant Professor, Vitreo-retina, 2Trainee Medical Officer,3Senior Registrar, 4Medical Officer, 5Trainee Medical Officer,Department of Ophthalmology, Khyber Girls Medical College,Hayatabad Medical Complex, Peshawar.————————————————————————————————Correspondence: Dr. Sanaullah Jan, H.No:101, St. NO: 10,Sector: J-2, Phase II,, Hayatabad, Peshawar.Ph: 03138584819 (Mob), 0092 91 5815071 (Res), 0092 912562929 (Clinic).Email: [email protected]————————————————————————————————Received: July’2012 Accepted: Sep’2012————————————————————————————————

INTRODUCTION:Diabetic retinopathy (DR) is a disorder of retinal

vasculature that affects almost all individuals with longstanding diabetes mellitus1. Blindness occurs 25 timesmore commonly in diabetic individuals compared tonormal individuals2. The fastly growing global epidemicof diabetes mellitus and the resultant complications

including diabetic retinopathy is the serious concernfor the health care authorities. Diabetic maculopathy(DM) is the common cause of visual loss in diabeticindividuals3,4. It is secondary to compromise vascularpermeability and accumulation of hard exudates atmacula which can occur at any stage of retinopathy3. Indiabetic individuals of more than 20 years duration,Clinically Significant Macular Edema (CSME) is presentin 29% of patients4. Diabetic maculopathy prevalenceis reported to be 17.6% in diabetics as reported by oneof the national study2. The Early Treatment DiabeticRetinopathy Study (ETDRS) was the first study toclinically grade the severity of macular edema5. Thisstudy established the benefits of laser therapy formacular edema and concluded that laser treated eyeshad decreased risk of having moderate visual lossversus observation group and greatest benefits wereshown in eyes with CSME5,6. EDTRS data provided thebasis for global acceptance of laser therapy as the first

Do we need to Redefine Laser Indicationsin Diabetic Maculopathy?*

Sanaullah Jan1, Yousaf Jamal Mahsood2, Muhammad Naeem Khan3

Samina Karim4, Zakir Hussain5

ABSTRACT:Objective: To determine the inter ophthalmologists bias while diagnosing the diabetic maculopathy as Clinically SignificantMacular Edema (CSME) in diabetic individuals.Study Design: An observational case series.Place and Duration: Department of ophthalmology, Hayatabad Medical Complex , Peshawar, Pakistan from 1st Jan 2011to 31st May 2011 (for the duration of seven months).Methodology: This observational case series included all the diabetic patients of both gender after informed verbalconsent. Diabetic individuals with any severity of diabetic maculopathy irrespective of stage of diabetic retinopathy wereincluded. Eyes with co-morbities like cataracts or corneal opacities and complications like vitreous bleed which rendersfundus examination impossible or doubtful were excluded. Eyes with co-morbidities like Age Related Macular Degeneration(ARMD) and hypertensive retinopathy (as agreed by both consultants) were excluded as they may mimic Diabetic MacularEdema (DME). The data was collected using a predesigned proforma. All the patients were examined by two consultantophthalmologists with at least eight years of postgraduate experience with 78D lens on slit lamp biomicroscopy. Bothconsultants were blinded regarding the clinical assessment and decision of one another. Consultants decision was recordedwhether maculopathy is clinically significant or not clinical significant. Their confidence level regarding their decision wasalso assessed as >80%, 61-80% and 51-60%. The data was analyzsed by means of SPSS software version 17.Results: Total of 83 eyes of 45 patients were included in the study (both consultants excluded one eye of seven patientsdue to media opacities). However in one consultant commented only on 82 eyes excluding another eye because of mediaopacities. Consultant-II commented on 82 eyes only. Mean age of our patients was 53.64 years. Male were 25 (55.6%)and female were 20 (44.4%). Eight (17.8%) patients were of type I diabetes while 37 (87.2%) were having type II.Maculopathy was clinically significant in 38 (45.8%) eyes and in 45 (54.2%) eyes, the consultant-I classified maculopathynon-significant. While consultant II diagnosed CSME in 39 (47.6%) eyes out of 82 eyes. In 2.4% eyes, diagnosis of bothconsultants were different from each other (Age related maculopathy versus CSME respectively). Confidence levels ofboth consultants regarding their clinical decisions was also varied with 80% or more confidence level in 88% and 63%respectively.Conclusion: The clinical diagnosis of CSME show statistically insignificant difference or error among ophthalmologists ofalmost same clinical experience. However the confidence with which CSME is diagnosed vary even among ophthalmologistsof same experience.Key words: Clinically Significant Macular Edema; CSME; Diabetic macular edema; Laser for CSME.

Original Article

Dr. Sanaullah Jan


line of treatment for diabetes maculopathy which isstill in practice. However, EDTRS defined diagnosis ofCSME was subjective and based on clinical assessmentby ophthalmologist by slitlamp biomicroscopy with78D. No objective tools were used to grade the macularedema as a clinical significant in this study. As peravailable evidence, laser treatment is indicated only ineyes having CSME. There are studies which reportedthat the retinal thickness may not be detected by clinicalobservation only7,8. Now, as the clinical expertise andexperience may vary among different ophthalmologists,the subjective assessment of CSME may show errors.This condition of CSME may be under or overdiagnosed. As a result, by following the ETDRS definedindications for laser in macular edema, we may be overor under treating our patients. There may be a numberof eyes which will benefit from laser but may be missedwhile there may be eyes which does not requiretreatment but may be receiving treatment with noevidence based visual benefits. This treatment practicemay be just because of over or under diagnosis of CSMEby ophthalmologists in patients with diabetes mellitus.This mis-directed management may also havesignificant socioeconomic impact on our nationalresources and eye care services. This hypothesis thatthe diagnosis of CSME may be biased due to inter-ophthalmologists clinical assessment variation, urgedus to design and conduct this study to determine theinter-ophthalmologists bias while diagnosing thediabetic maculopathy as CSME in diabetic individuals.METHODOLOGY

This observational case series was conducted atthe Department of Ophthalmology, Hayatabad MedicalComplex , Peshawar, Pakistan from 1st Jan 2011 to 31st

May 2011(for the duration of seven months). All thediabetic patients of both gender were included into thestudy after informed verbal consent. Diabeticindividuals with any severity of diabetic maculopathyirrespective of stage of diabetic retinopathy wereincluded. Known diabetics of type I and type II diabetesmellitus or individuals with typical features of diabeticretinopathy and maculopathy who were theninvestigated to be diabetic (fasting plasma glucose >7mmol/l or random plasma glucose >11.1mmol/l asrecommended by WHO) were included in our study.Eyes with co-morbities like cataracts or corneal opacitiesand complications like vitreous bleed which rendersfundus examination impossible or doubtful (as perconsultant decision) were excluded. Eyes with co-morbidities like Age Related Macular Degeneration(ARMD) and hypertensive retinopathy (as agreed byboth consultants) were excluded as they may mimicDME. The data was collected using a predesignedproforma. All the patients were examined by two

consultant ophthalmologists with at least eight yearsof postgraduate experience in the tertiary care teachinginstitute. Both consultants examined the eyes by 78Dlens on slit lamp biomicroscopy. Both consultants werekept blinded regarding the clinical assessment anddecision of one another. Consultants decision wasrecorded whether maculopathy is clinically significantor not clinically significant. Their confidence levelregarding their decision was also assessed as >80%, 61-80% and 51-60%. The data was analyzed by means ofSPSS software version 17.RESULTS :

Total of 83 eyes of 45 patients were included inthe study. Both consultants excluded one eye of sevenpatients due to media opacities. However in one patient,one consultant commented while the other consultantdidn’t comment because of media opacities. Thecomments of consultant-II were recorded on 82 eyesonly. Mean age of our patients was 53.64 years. Malewere 25 (55.6%) and female were 20 (44.4%). There were8 (17.8%) patients from type I diabetes while 37 (87.2%)were having type II. Maculopathy was classified asclinically significant in 38 (45.8%) eyes and non-significant in 45 (54.2%) eyes by the consultant I. Whileconsultant II diagnosed CSME in 39 (47.6%) eyes andnonsignificant maculopathy in 43 (52.4%) out of 82 eyes.Clinical diagnosis of CSME in our patients is shown inTable I. The difference between accuracy of clinicaldecision to diagnose CSME between consultants wasnot statistically significant (P-value of 0.44 and 0.51respectively) in our study. Confidence levels of bothconsultants regarding their clinical decisions is shownin Table II. It was interesting to note that 2 (2.4%) eyesof one patient which were diagnosed as having CSMEby consultant II were regarded to be having drusen byconsulant I. Similarly one eye classified as having CSMEby consultant I, was labelled by consultant II as havingARMD.DISCUSSION :

Although the pathogenesis of macular edema indiabetic individuals is complex and it results secondaryto compromised blood retinal barrier and collection ofintra retinal fluid, proteins and other blood constituentsat the macula9-12. Diabetic Macular Edema (DME) isgraded as clinically significant or non-significantmacular edema for the purpose of laser treatment as apart of standard care and protocol based onrecommendation of ETDRS5,6. CSME if present in eyesand CSME which involves the foveal center has the riskof moderate visual loss in 24% and 33% eyesrespectively within 3 years if not treated by laserapplication5. As per evidence till date, the laser therapyis only indicated when the diabetic macular edema isclassified as CSME. However the grading of DME as

Do we need to Redefine Laser Indications in Diabetic Maculopathy?


clinically significant is based on clinical assessment anddecision of ophthalmologist after examining the patientfundus on slitlamp biomicroscopy with 78 Diopterlens13. Although Fundus Fluorescein Angiography(FFA) can show different patterns by classifying theCSME as having focal and diffuse patterns thusaugmenting the execution of laser application but is notessential for diagnosing of CSME. At the same time,the leakage on FFA is not diagnostic for retinal edemaas the retinal edema or thickness is the end result ofcompromised balance between fluid leakage into theretina and fluid clearance out of retina by retinalpigment epithelium pump mechanism13. As thediagnosis of CSME is based on clinical assessment byophthalmologists, are the indications for laserapplication in DME. The subjective basis for definitionof CSME may show errors in diagnosis and may resultin mis-management of diabetic eyes with diabeticmaculopathy. Our study was designed to determinewhether the statement that “there may be subjectivevariations in diagnosing DME as CSME” is valid or not.We purposely included assessment of our patients’ eyeby two consultants of almost similar clinical experienceand even then we had encountered difference ofopinion regarding status of CSME in eye with signs ofdiabetic maculopathy. Although the difference betweenaccuracy of clinical decision to diagnose CSME betweenophthalmologists of almost same experience was notstatistically significant (P-value of 0.44 and 0.51respectively) in our study. It is also worthy to mentionthat in ophthalmic community, the clinical expertise,

experience and level of stereopsis of clinicians widelyvaries. Thus we presume that difference of opinionregarding diagnosing of CSME may also widely vary ifophthalmologists of different level of experience andexpertise are included in future studies. At thesametime, it is also obvious from the our data, thatconfidence levels of both consultants widely varied andwas different regarding their own assessment anddecision to classify the maculopathy as “clinicallysignificant” or “clinically not significant”. It is alsoworthy to note that in 2.4% eyes consultants haddiagnosed totally different pathologies i.e., (CSMEversus ARMD). This difference of opinion in diagnosisof CSME raises serious concern regarding subjectivedefinition of CSME based solely on the clinical expertiseof different ophthalmologists. Besides clinical expertise,the clinical experience, quality of stereopsis and visualstatus also vary among practicing ophthalmologiststhus affecting their assessment and final decision toclassify the DME as clinically significant. Ultimatelysuch subjective errors in diagnosis will affect thedecision of laser application in our patients with diabeticmaculopathy and the significance of under or overtreatment of eyes with diabetic maculopathy can notbe overestimated. Although the search for bettertreatment options continues but standard care ofdiabetic macular edema is laser application, which isstill in practice globally. We hope that our study willbe considered as part of “icebreaking” and basis forplanning multi-centered, large sample-sized studieswhich will be able to better answer the question ofchallenging the subjective diagnosis of clinicallysignificant macular edema.

At present, there are plenty of recent availabletools such as Optical Coherence Tomograghy (OCT),retinal thickness analyzers etc which can better classifythe macular edema quantitatively and moreobjectively7,14. At the same time, OCT is a non- invasivetool and is well tolerated by patients. Such objectivetools like OCT can benefit the patients in terms ofdiagnosis in the early stages of DME which yet maynot be obvious clinically and at the sametime will behelpful by exactly measuring the macular edema whilepracticing various treatment options to decreasemacular edema and to improve visual function in theaffected eyes or vice versa. Although such objectiveclassification also need to be tested by multi-centerrandomized controlled trials of standard, similar to thatof ETDRS for the purpose of evolving better treatmentstrategies.

The living search to find better treatment optionsfor DME to have better visual outcomes, surelycontinues. This search has resulted in evolving andemerging options of intravitreal anti-VEGF, intravitreal

Table I Clinical diagnosis of CSME

CSME Consultant Consultant IIn (%) n (%)

YES 38 (45.8%) 39 (47.6%)

NO 45 ( 54.2%) 43 (52.4%)

TOTAL 83 ( 100%) 82 (100%)CSME: Clinically Significant Macular Edema, n : number,% : percentage

Table II, Confidence levels of consultants regarding clinicaldecision in diagnosing CSME

Confidence level Consultant I Consultant IIn (%) n (%)

>80% 73 (88%) 52 (63.4%)

61-80% 07 (8.4%) 26 (31.7%)

51-60% 03 (3.6%) 04 (4.9%)

TOTAL 83 (100%) 82(100%)CSME: Clinically Significant Macular Edema, n: Number,%: Percentage, >: More than



steroids (including sustained release implants), otherrecent therapeutic options, recent laser therapy withmore accuracy and less collateral damage to retinalpigment epithelium and sensory retinal tissue, andvarious combinations of different treatmentoptions3,15-24. The indications to treat DME need to bebased on objective assesment and various treamentoptions need to be tested in terms of efficacy to decreasemacular edema, improve visual functions and theirsafety. Therefore in this evolving era of moderntechnology and recently introduced promisingtreatment options, ophthalmic care community need todetermine more objective indications to treat DME withbest options after evolving evidence based globallyaccepted standerd protocols. Such management willsurely result in provision of better eye care to diabeticindividuals by avoiding the errors due to subjectiveassessment of CSME by clinical ophthalmologists.CONCLUSION:

The clinical diagnosis of CSME show statisticallyinsignificant difference or error amongophthalmologists of almost same clinical experience.However the confidence with which decision is madeto diagnose CSME varies even among ophthalmologistof same experience.REFERENCES:1. Raman R, Rani PK, Rachepalle SR, Gnanamoorthy P, Uthra

S, Kumaramanickavel G, Sharma T. Prevelence of diabeticretinopathy in india: Sankara Nethralaya DiabeticRetinopathy Epidemiology and Molecular Genetics StudyReport 2. Ophthalmology 2008; 116: 311-18.

2. Din J, Qureshi MB, Khan AJ, Khan MD, Ahmed K. Prevalenceofdiabetic retinopathy among individuals screened positivefordiabetes in five communitiy-based eye camps in northKarachi, Pakistan. J Ayub Med Coll Abbottabad 2006; 18(3):40-3.

3. O’Doherty M, Dooley I, Hickey-Dwyer M. Interventions fordiabetic maculer edema: a systemic review of literature. Br JOphthalmol 2008; 92:1581-90.

4. Klein R, Klein BE, Moss SE, Cruickshanks KJ. TheWisconsinEpidemiologic Study of diabetic Retinopathy, XVII: the 14-year incidence and progression of diabetic retinopathy andassociated risk factors in type 1 diabetes. Ophthalmology 1998;105:1801 – 15.

5. Early Treatment Diabetic Retinopathy Study research group.Photocoagulation for diabetic macular edema: Earlytreatment Diabetic Retinopathy Study report number 1. ArchOphthalmol 1985; 103:1796-806.

6. Early Treatment Diabetic Retinopathy Study Research Group.Treatment techniques and clinical guidelines forphotocoagulation of diabetic macular edema: Early treatmentDiabetic Retinopathy Study Report Number 2. Ophthalmology1987; 94:74

7. Strom C, Sander B, Larsen N, Larsen M, Andersen HL.Diabetic Macular Edema assessed with Optical CoherenceTomography and Stereo Fundus Photography. InvestOphthalmol Vis Sci 2002; 43(1):241-5.

8. Browning DJ, Mcdowen MD, Bowen RM, O’Marah TL.Comparison of the Clinical Diagnosis of Diabetic MacularEdema with Diagnosis by Optical Coherence Tomography.Ophthalmology 2004; 3(4):712-5.

9. Ehrlich R, Harris A, Ciulla TA, Kheradiya N, Winston DM,Wirostko B. Diabetic macular oedema: Physical,Physiological and molecular factors contribute to thispathological process. Acta Ophthalmol 2010; 88:279-91.

10. Singh A, Stewart JM. Pathophysiology of diabetic macularedema. Int Ophthalmol Clin 2009; 49:1-11.

11. Antcliff RJ, Marshall J. The pathogenesis ofedema in diabeticmaculopathy. Semin Ophthalmol 1999; 14(4):223-32.

12. Browing DJ, McOwen MD, Bowen RM Jr, O’Marah TL.Comparison of the clinical diagnosis of diabetic macularedema with diagnosis by optical coherence tomographyOphthalmology 2004; 111(4):712-5.

13. Bhagat N, Grigorian RA, Tutela A, Zarbin MA. Diabeticmacular edema: Pathogenesis and treatment. Surv Ophthalmol2009; 54:1-32.

14. Deak GG, Bolz M, Kriehbaum K, Prager S, Mylonas G,Scholda C, et al. Effect of retinal photocoagulation onintraretinal lipid exudates in diabetic macular edemadocumented by optical coherence tomography.Ophthalmology 2010; 117(4):773-79.

15. Wright AD, Dodson PM. Medical management of diabeticmaculopathy: fenofibrate and ACCORD Eye studies. Eye 2011;25:843-9.

16. Wenick AS, Bressler NM. Diabetic Macular Edema: Currentand Emerging Therapies. Middle East Afr J Ophthalmol 2012;19(1):4-12.

17. Diabetic Retinopathy Clinical Research Network (DRCR.net);Beck RW, Edwards AR, Aiello LP, Bressler NM, Ferris F,Glassman AR, et al. Three-year follow-up of a randomizedtrial comparing focal/grid photocoagulation and intravitrealtriamcinolone for diabetic macular edema. Arch Ophthalmol2009; 127(3):245-51.

18. Diabetic Retinopahty Clinical Research Network; Elman MJ,Aiello LP, Beck RW, Bressler NM, Bressler SB, Edwards AR,et al. Randomized trial evaluating ranibizumab plus promptor deferred laser or triamcinolone plus prompt laser fordiabetic macular edema. Ophthalmology 2010; 117(6):1064-77,e35.

19. Elman MJ, Bressler NM, Qin H, Beck RW, Ferris FL 3rd,Friedman SM, et al. Expanded 2-year follow-up ofranibizumab plus prompt or deferred laser or triamcinoloneplus prompt laser for diabetic macular edema. Ophthalmology2011; 118:609-14.

20. Kozak I, Oster SF, Cortes MA, Dowell D, Hartmann K, KimJS, et al. Clinical evaluation and treatment accuracy indiabetic macular edema using navigated laserphotocoagulator NAVILAS. Ophthalmology 2011; 118:1119-24.

21. Lavinsky D, Cardillo JA, Melo LA Jr, Dare A, Farah ME,Belfort R Jr. Randomized clinical trial evaluating mETDRSversus normal or high-density micropulse photocoagulationfor diabetic macular edema. Invest Ophthalmol Visual Sci 2011;52:4314-23.

22. Luttrull JK, Musch DC, Mainster MA. Subthreshold diodemicropulse photocoagulation for the treatment of clinicallysignificant diabetic macular oedema. Br J Ophthalmol 2005;89:74-80.

23. Haller JA, Kuppermann BD, Blumenkranz MS, Williams GA,Weinberg DV, Chou C, et al. Randomized controlled trial ofan intravitreous dexamethosone drug delivery system inpatients with diabetic macular edema. Arch Ophthalmol 2010;128:289-96.

24. Boyer DS, Faber D, Gupta S, Patel SS, Tabandeh H, Li XY, etal. Dexamethasone intravitreal implant for treatment ofdiabetic macular edema in vitrecotomized patients. Retina2011; 31:915



————————————————————————————————1Assistant Professor, Vitreo-retina, 2Trainee Medical Officer,3Senior Registrar, 4Medical Officer, 5Trainee Medical Officer,Department of Ophthalmology, Khyber Girls Medical College,Hayatabad Medical Complex, Peshawar.————————————————————————————————Correspondence: Junaid Faisal Wazir, [email protected]: 0302 5586596————————————————————————————————Received: April 2012 Accepted August 2012————————————————————————————————

Ocular Trauma Associated with Bomb Blast

Junaid Faisal Wazir1, Inayatullah Khan2, Imran Ahmad3

Sabir Mohammad4, Zaman Shah5

ABSTRACTObjective: To study the type and severity of ocular trauma associated with bomb blast.Methods: It was a descriptive case series. The study was conducted at the Department of Ophthalmology, KhyberTeaching Hospital, Peshawar from December, 2009 to February, 2011. Detailed history was taken and complete ocularexamination was done. B-scan was done to know about any posterior segment pathology (when required). Digital X-rayorbit and/or computed tomography were done to rule out intraocular foreign body. The treatment and follow up variedaccording to the type and extent of eye injury.Results: Total number of patients were 79. Out of them 78 (98.73%) males and 1 (1.26%) female. Mean age of patientswas 23.43 ± 10.67 years. Ocular injury was unilateral in 50 (63.29%) and bilateral in 29 (36.70%) patients . Forty-one(37.96%) eyes had closed globe injury and 67 (62.03%) had open globe injury. The most common type of injury wascorneal/scleral perforation (48.14%) followed by vitreous haemorrhage (38.88%) and traumatic cataract (30.55%). Themost commonly performed surgery was corneal/scleral repair (in 33 eyes). Final best corrected visual acuity (BCVA)improved in 56 (51.85%) eyes, remained unchanged in 49 (45.37%) eyes and worsened in 03 (2.77%) eyes.Conclusion: Bomb blast related ocular trauma are becoming increasingly common. In severely injured eyes the visualprognosis remains poor despite development of advanced microsurgical techniques and better methods of visualrehabilitation.Keywords: Digital X-ray, Computed Tomography (CT), Ocular trauma.

Original Article

INTRODUCTION Ocular trauma is an important and potentially

preventable cause of ocular morbidity.1 Ocular traumaform approximately 5-10% of all ophthalmic hospitaladmissions in non-industrialized areas and 39-42% inthe industrialized community.2 Every year more thanhalf a million potentially blinding ocular trauma occurglobally. There are approximately 1.6 million peoplewho go blind from eye injuries, 2.3 million with bilateralvisual impairment and 19 million with unilateral visualloss world-wide; thus ocular trauma is the commonestcause of unilateral blindness.3 In the United Statesapproximately 2.5 million new eye injuries occurannually and around 40% of monocular blindness isdue to eye trauma.4 Eye injuries can be broadly dividedinto 2 groups i.e. closed globe and open globe. Closedglobe injuries are divided into contusion and lamellarlaceration. Open globe injuries are divided into ruptureand laceration.5 Etiologically ocular trauma can beclassified into domestic, occupational, sports, road

traffic accidents, iatrogenic, fights and assaults and warinjuries.6 Almost 100 years ago more than 70% of allserious ocular trauma occurred at the workplace.7 Inthe 1960s and 1970s, road traffic accidents became themost common cause of serious ocular injury.8 In the1980s, sport and leisure activities became commoncauses of serious eye injuries.9-11 The home is now themost common location for eye injuries.12 However,bomb blast and battlefield ocular trauma are becomingincreasingly common in different parts of the world.13-

15 In blast victims ocular injury may result from primaryblast exposure. The blast effect shock wave propagatesthrough the different medium of eyeball causingcontusion and concussion injuries. Primary blast injurycomprises non-penetrating mechanical injuries such ashyphema, globe rupture, subconjunctival haemorrhage,commotio retine and orbital fracture.16,17 However,ocular trauma is most commonly the result of secondaryblast effects, in which debris displaced by the blastcauses physical trauma to the eye and/or orbit.Secondary blast injury comprises penetrating or blunt-force injury to any part of the eye or orbit; open globeinjuries, lacerations of the lacrimal system and eyelidscomprise the majority of injuries in this group.18,19

The spectrum of eye injuries in blast victims rangesfrom very mild, innocuous to extremely serious withpotentially blinding consequences. The purpose of ourstudy was to study the type and severity of oculartrauma in blast victims, so that a comprehensive plan

Dr. Junaid


could be made for proper management of these patients.PATIENTS AND METHODS:

This prospective study was conducted atOphthalmology Department of Khyber TeachingHospital, Peshawar, from December 2009 to February2011. The study was done in collaboration with anorganization which was working for people sufferingfrom war injuries. All the patients were victims of bombblast or mine blast, belonging to Afghanistan, FederallyAdministered Tribal Areas (FATA) and Swat. Thepatients were completely assessed by a team ofphysicians and surgeons and any serious systemicinjuries were properly managed. Patients were thenreferred to us for the management of ocular trauma.

It was a descriptive case series study. Patients ofall age groups and both genders, having blast-relatedinjury to the eyeball were included in the study. Patientswho had only ocular adnexal injury and those who didnot come for follow up were excluded. Consecutivesampling technique was employed i.e. all the patientswho met the inclusion criteria were studied. The studywas approved by the ethical review board of theinstitution. Informed (verbal) consent was taken fromall the patients and written informed consent was takenfrom those who needed surgery.

All patients were evaluated for types of ocularinjury and extent of damage. Detailed history was takenand complete ocular examination was done includingassessment of best corrected visual acuity (BCVA) witha Snellen’s chart, assessment of pupillary reaction withtorch and slit lamp examination (Takagi SM-70, Japan).Intraocular pressure (IOP) was checked with Perkin’stonometer MK2 (Clement Clarke, London), whenfeasible. Fundus examination was done with 90 diopterlens (Volk, USA) and/or indirect ophthalmoscope(Neitz, Japan). In those patients with poor or no viewof fundus, B-scan ultrasonography was done with AB5500+ A/B Scan (Sonomed, USA). In those with openglobe injury, B-scan was performed after restoring theglobe integrity. Digital X-ray orbit was done in allpatients. In those with high suspicion of intraocularforeign body (IOFB), a CT orbit (2mm section) wasundertaken.

Primary repair was done under generalanaesthesia (GA), in emergency, in those with cornealor scleral perforation. Evisceration was performed inpatients with shattered globe (where repair was notpossible) or if there was globe perforation withendophthalmitis. Subsequent management and followup varied according to the type and extent of eye injury.Complete ocular examination was conducted at eachfollow up. SPSS-10 was used for data analysis.RESULTS

Total number of patients was 79, including 78

males (98.73%) and 1 female (1.26%). Age ranged from5 to 60 years with a mean of 23.43 ± 10.67 years. Age ofthe patients was < 10 years in 6 (7.59%) patients, 11-20years in 28 (35.44%), 21-30 years in 31 (39.24%), 31-40years in 10 (12.65%), 41-50 years in 2 (2.53%) and 51-60years in 2 (2.53%) patients. The interval between thetime of injury and presentation to ophthalmologistranged from 1 to 10 days in 44 patients (60 eyes) andwas more than 10 days in 35 patients (48 eyes). Ocularinjury was unilateral in 50 (63.29%) patients andbilateral in 29 (36.70%) eyes. Forty-one (37.96%) eyeshad closed globe injury and 67 (62.03%) had open globeinjury. Of these 67 eyes, 25 (37.31%) had zone I injury,6 (8.95%) had zone II injury and 36 (53.73%) had zoneIII injury. The most common type of injury was corneal/scleral perforation (48.14%) followed by vitreoushaemorrhage (38.88%) and traumatic cataract (30.55%).The types of eye injury noted in our patients is given inTable-1.

The treatment varied according to the type of in-jury. Forty eyes (37.03%) were treated medically and68 (62.96%) eyes were treated surgically. These patientsunderwent from 1 to 4 surgeries. Corneal/scleral re-pair was the most commonly performed surgery (33eyes). Evisceration was done in 19 eyes; it was done inthose with shattered globe (where repair was not pos-sible) with poor visual potential or if there was globeperforation with endophthalmitis. Vitreo-retinal sur-gery was required in patients who had non-resolvingvitreous haemorrhage, retinal detachment or posteriorsegment intraocular foreign body (IOFB) and in 2 pa-tients with endophthalmitis. The type and number ofsurgeries are given in Table-2.

In addition, 360 argon laser was done in 17(15.74%) eyes, panretinal photocoagulation (PRP) wasdone in 2 (1.85%) and Nd: YAG laser capsulotomy in 2(1.85%) eyes which had undergone cataract extractionwith intraocular lens (IOL) implantation. The initial andfinal best corrected visual acuities (BCVA) are given infigure I.

Final BCVA improved in 56 (51.85%) eyes,remained unchanged in 49 (45.37%) and worsened in 3(2.77%) eyes.

In our study the initial visual acuity was noperception of light (NPL) in 25 (23.14%) eyes, perceptionof light (PL+) in 27 (25.0%), hand movement (HM) in20 (18.51%), counting fingers (CF) in 14 (12.96%), 6/60to 6/18 in 8 (7.40%) and 6/12 to 6/6 in 14 (12.96%) eyes.While the final VA was NPL in 27 (25.0%) eyes, PL+ in13 (12.03%) eyes, HM in 8 (7.40%), CF in 13 (12.03%),6/60 to 6/18 in 13 (12.03%) and 6/12 to 6/6 in 34(31.48%) eyes. In 61 (56.48%) eyes the final BCVA was< 6/60. Final BCVA improved in 52 (48.14%) eyes,remained unchanged in 52 (48.14%) and worsened in 4



Table 1:Type and number of eye injury

Type of injury No. of eyes (%) Type of injury No. of eyes (%)

Corneal/Sceral perforation* 52 (48.14%) Vitreous hamorrhage 42 (38.88%)

Cataract 33 (30.55%) IOFB+ 22 (20.37%)

Subconjunctival hemorrhage 22 (20.37%) Corneal foreign bodies 19 (17.59%)

Corneal oedema 18 (16.66%) Retinal detachment 16 (14.81)

Increased IOP++ 15 (13.88%) Sealed perforation # 15 (13.88%)

Hyphema 13 (12.03%) Retinal hemorrhage 08 (7.40)

Endophthalmitis 08 (7.40%) Macular scaring 06 (5.55%)

Corneal epithelial defect 01 (0.92%) Corneal lameller laceration 01 (0.92%)

Iridodialysis 01 (0.92%) Optic atrophy 01 (0.92%)

* – Including corneal perforation in 22 eyes, sceral perforation 07 eyes and carneo-scleral perforation in 23 eyes.+– 21 eyes had posterior segment IOFB and 1 eye had anterior segment IOFB++– Increased IOP was due to topical steroids in 8 eyes, due to free lens matter in 2 eyes, due to peripheral anterior synechiae in 2 eyes,silicone oil in 2 eyes and due to single recession in 1 eye.# – It was corneal in 03 eyes, limbal in 01 eye and scleral in 11 eyes

Table 2:Type and number of surgeries*

Type of Surgery No. of Surgeries

Corneal/Sceral repair + 33Evisceration 19Vitrectomy ++ 14Cataract Extraction 12Vitrectomy + Cataract extractgion # 10OthersRemoval of silicon oil 3Trabeculectomy 1Opening of peripheral iridectomy 1Pupiloplasty 1Corneal autograft 1Corneal autograft + Cataract extraction 1Amniotic membrane graft 1Removal of FB from limbus 1Total 98

* – In 46 eyes 1 surgery was performed in 14 eyes 2 surgries wereperformed, in 06 eyes 3 surgeries were performed and in 01 eye 4surgeries were performed.+ – Including corneal repair in 21 eyes, scleral repair in 7 eyes andcorneo-scleral repair in 5 eyes, IOFB removal was done in 1 eye.++ – With IOFB removal in 5 eyes.# –With IOFB removal in 6 eyes.

(3.70%) eyes.The time of presentation was an important

prognostic factor in our study as 91.66% of the patientswho presented > 10 days after eye injury had finalBCVA < 6/60. Patients presenting within 10 days ofinjury had better visual outcome; out of these patients

53.33% had BCVA of 6/12-6/6, 18.33% had BCVA of6/60-6/18 and 28.33% had BCVA < 6/60.DISCUSSION

Trauma is a common cause of ocular morbidity.The effect of trauma may be apparent immediately ormay develop later as a secondary complication. Oculartrauma can cause permanent visual or cosmetic defectin the affected individuals and is a major cause ofmonocular blindness and visual impairmentthroughout the world.20

Ocular trauma victims are predominantly youngmales,21 as was the case in our study, with 78 (98.73%)males and 1 (1.26%) female. The causes of ocular traumavaries at different times and at different places.7,12 Bombblast and mine blast are becoming increasingly commoncauses of ocular as well as systemic injuries. In the study



conducted by Sethi MJ et al, bomb blast injuriesaccounted for 3% of ocular trauma.6 In another studyblasts were responsible for 9% cases of ocular trauma.22

The majority of blast-related ocular trauma occur inindividuals who present with other life-threateninginjuries that require immediate intervention. Surgicalstabilization of any life-threatening injuries, as well ashaemodynamic stability is required prior to initialevaluation by the ophthalmologist. Therefore, initiationof emergent ophthalmic care often occurs hours afterinjury.18 In our study, before being referred to us thepatients were assessed by a team of physicians andsurgeons and any serious systemic injuries wereproperly managed. Therefore, in most patients theinitial eye evaluation was delayed for a few days. Visualoutcomes for patients with ocular trauma due to blastinjuries vary, and prognosis depends upon the type ofinjury sustained. The majority of poor visual outcomesarise from perforating injuries: only 21% of patients withperforating injuries with initial visual acuity of lightperception had a final BCVA better than 6/60. Patientswho have choroidal haemorrhage, perforating orpenetrating globe injury, retinal detachment, traumaticoptic neuropathy, and subretinal macular haemorrhageare more likely to have BCVA worse than 6/60. Reportsfrom Operation Iraqi Freedom indicate that 42% ofsoldiers with globe injuries had a BCVA equal to orbetter than 6/12 six months after injury.18,19,23 DuringAfghan-Russia war the bomb blast injuries in Afghanrefugees led to blindness in 27.2% cases.24

The final visual outcome also depends on the typeof eye injury.18 In our study, open globe injuries hadpoor visual outcome; 73.13% of these eyes had finalBCVA < 6/60. On the other hand, only 29.26% of closedglobe injuries had final BCVA < 6/60 while 58.65% hadBCVA > 6/18. Initial visual acuity of NPL or PL+, thepresence of relative afferent pupillary defect (RAPD),central corneal opacity, retinal detachment,endophthalmitis, macular scarring and optic atrophywere other factors associated with poor final visualoutcome.CONCLUSION

The visual prognosis in ocular trauma is variable.Bomb blast associated ocular trauma are becomingincreasingly common. Bomb blast victims usually havevery severe eye injuries. In such cases the visualprognosis still remains very poor despite developmentof advanced microsurgical techniques and bettermethods of visual rehabilitation.REFERENCES 1. Gothwal VK, Adolph S, Jalali S, Naduvilath TJ. Demography

and prognostic factors of ocular trauma in South India. AustNZ J Ophthalmol 1999; 27: 318-25.

2. Stegmann D. Treatment of Anterior Segment Ocular trauma.Montreal Medicopia 1996; 7-12.

3. Negrel AD, Thylefors B. The global impact of eye injuries.Ophthalmic Epidemiol 1998; 5: 143-69.

4. May DR, Kuhn FP, Morris RE, Witherspoon CD, Danis RP,Matthews GP, et al. The epidemiology of serious eye injuriesfrom the United States Eye Injury Registry. Graefes Arch ClinExp Ophthalmol 2000; 238: 153-7.

5. Kuhn F, Morris R, Witherspoon CD, Mester V. TheBirmingham Eye Trauma Terminology system (BETT). J FrOphtalmol 2004; 27: 206-10.

6. Sethi MJ, Sethi S, Khan T, Iqbal R. Occurrence of oculartrauma in patients admitted in Eye Department KhyberTeaching Hospital Peshawar. J Med Sci 2009; 17: 106-9.

7. Garrow A. A statistical enquiry into 1000 cases of eye injuries.Br J Ophthalmol 1923; 7: 65-80.

8. Canavan YM, O’Flaherty MJ, Archer DB, Elwood JH. A 10-year survey of eye injuries in Northern Ireland, 1967-76. Br JOphthalmol 1980; 64: 618-25.

9. MacEwen CJ. Eye injuries: a prospective survey of 5671 cases.Br J Ophthalmol 1989; 73: 888-94.

10. Jones NP. One year of severe eye injuries in sport. Eye 1988;2: 484-7.

11. MacEwen CJ. Sports associated eye injuries: a casualtydepartment survey. Br J Ophthalmol 1987; 71: 701-5.

12. Desai P, MacEwen CJ, Baines P, Minaissian DC.Epidemiology and implications of ocular trauma admittedto hospital in Scotland. J Epidemiol Community Health 1996;50: 436-41.

13. Treister G. Ocular casualties in the Six Day War. Am JOphthalmol 1969; 68: 669-75.

14. Belkin M. Ocular trauma in the Yom Kippur War. J OculTherapy Surg 1983; 2: 40-9.

15. Newmann TL, Russo PA. Ocular sequelae of BB injuries toeye and surrounding adnexa. J Am Optom Assoc 1998; 69:583-90.

16. United States Department of Defense, Joint Publication 1-02,Department of Defense Dictionary of Military and AssociatedTerms. 2008, amended 2011; 171.

17. Harlan JBX, Pieramici DJ. Evaluation of patients with oculartrauma. Ophthalmol Clin North Am 2002; 15: 153-61.

18. Weichel ED, Coyler MH. Combat ocular trauma and systemicinjury. Curr Opin Ophthalmol 2008; 19: 519-25.

19. Wolf SJ, Bebarta MV, Bonnet CJ, Pons PT, Canhill SV. Blastinjuries. Lancet 2009; 374: 405-15.

20. Jackson H. Bilateral blindness due to trauma in Cambodia.Eye 1996; 10: 517-20.

21. Tielsch JM, Parver LM. Determination of hospital chargesand length of stay for ocular trauma. Ophthalmology 1990;97: 231-7.

22. Khan MD, Mohammad S, Islam Z, Khattak MN. An 11 yearsreview of ocular trauma in North West Frontier Province ofPakistan. Pak J Ophthalmol 1991; 7: 15-8.

23. Ramasamy A, Harrisson SE, Clasper JC, Stewart MP. Injuriesfrom roadsideimprovised explosive devices. J Trauma 2008;65: 910-4.

24. Friesen H, Asmat AA, Salim AG, Khan I. Incidence ofincurable blindness in the Afghan refugees in Pakistan. PakJ Ophthalmol 1990; 6: 61-3.



————————————————————————————————*Associate Professor, Pakistan Institute of Ophthalmology,Al-Shifa Trust Eye Hospital Rawalpindi————————————————————————————————Correspondence: [email protected] Dr. M. Abdul Moqeet,Associate Professor, Pakistan Institute of Ophthalmology,Al-Shifa Trust Eye Hospital Rawalpindi————————————————————————————————Received: September’2012 Accepted Nov’2012————————————————————————————————

Photorefractive Keratectomy andPatient Satisfaction Level

M. Abdul Moqeet*

ABSTRACT:Objective: To subjectively assess the overall patient satisfaction and self-perceived response to quality of visionfollowing bilateral photorefractive keratectomy (PRK) with the help of a questionnaire.Study Design: Qualitative survey.Participants and Methods: The study was conducted at the department of Cornea and Refractive Surgery of Al-ShifaTrust Eye Hospital Rawalpindi on 34 out of 59 consecutive patients who underwent bilateral PRK for myopia ranging from-1.5 to -20 diopters with a minimum of six months follow up since the last surgery. A specially designed questionnaire wasfilled by all patients and the response of 34 patients (68 eyes) who were randomly picked up for analysis was evaluated.Their baseline myopia ranged from -1.50 to -20.00 diopters (DS) with a refractive cylinder ranging between -1.5 to -6.00D.Cyl. They were all treated with Omni Med U.V 270300 excimer laser with an ablation zone one (5.oo mm) zone two(6.oo mm) and zone three (6.50 mm) diameter.Results: Ten patients (29.41%) required glasses at times for distance vision however nobody used glasses permanentlyduring six months duration. Twenty four (70.59%) subjects were enjoying life without wearing spectacles. Twenty three(67.65%) participants had clear vision, whereas, 11 (32.35%) subjects had some complaints as to quality of their visiondue to foggy vision. Twenty six (76.47%) subjects were happy with the overall result at completion of six months, whereas,8 (23.53%) subjects were not much comfortable with the overall outcome.Conclusion: The level of satisfaction six months after PRK was generally high and quite encouraging in this survey.Subjective visual symptoms such as night vision problems and halo phenomenon did not have significant influence onoverall patient satisfaction.

Original Article

Dr. Abdul Moqeet

INTRODUCTON:Myopia may be corrected satisfactorily with

glasses and contact lenses but many people desire clearvision without dependence on any corrective opticaldevices 1. Strong desire of myopes to get rid oftraditional optical corrections by glasses and contactlenses led to introduction of a variety of surgicalprocedures to correct myopia. PRK was invented in theearly 1980s. FDA approved laser PRK for the firsttime in 1995. It modifies the anterior corneal curvatureby laser ablation of superficial corneal tissue to correctmyopia2. Due to relatively high patient satisfaction withthe results, PRK rapidly gained popularity throughoutthe world as an effective alternative to glasses andcontact lenses. PRK has arrived as a boon to the myopicpopulation who previously has had to depend on othermeans of visual correction3

. This article evaluated theoverall patient satisfaction with this modality of

treatment six months after the surgery.PATIENTS AND METHODS

The study was conducted at the department ofCornea and Refractive Surgery of Al-Shifa Trust EyeHospital Rawalpindi on 34 out of 59 consecutivepatients who underwent bilateral PRK for myopia.Inclusion Criteria:• Patients considered fit for refractive surgery after

initial assessment.• Age: 18-35 years old• Mentally and physically in a stable health

condition• Able to read and understand the language of

questionnaire• Willing to participate in the study and

communicated well with investigator• Agreed to follow-up at scheduled timesExclusion Criteria:• Unable to read simple questionnaire and

communicate conveniently·• Any corneal pathology which could interfere the

visual outcome after surgery.• Any other condition that would prevent

completion of the questionnaireThe study was a prospective evaluation of

patients’ satisfaction with PRK. Approval from thehospital ethical committee was taken for conducting thestudy. All the participants had healthy corneas before


surgery and no one had any systemic or ocular disease.All the patients were above 18 years and refractive errorbelow -6.00 Diopters having stable myopia at leastduring the last one year. The refractive status of thesubjects was as follows:1. Myopia ranging from -1.50 to -6.00 D.S (Diopter

Sphere) without astigmatism or with astigmatismup to -1.50 D.C (Diopter Cylinder)

2. Myopia from -6.25 to -20.00 D.S, withoutastigmatism or with astigmatism up to -4.00 D.C,Candidates were counseled before surgery that

the procedure was intended to correct distance visionand they may require correction for the best distancevisual acuity and eventually presbyopic glasses. Allthe multi zone procedures were performed, by onesurgeon over a period of four months, entering sphericalequivalent refraction by Omni Med U.V 270300 ( SummitTechnology Inc; Waltham MA) excimer laser, withaffluence of 180 mj/cm2 at a frequency of 10 Hz.Postoperative medications included tobramycin 0.3%and dexamethasone sodium phosphate solutions fourtimes a day for a period of two weeks followed byflouromethalone 0.1% four times a day up to threemonths. An eye pad was placed on operated eye for atleast 48 hours or till the completion of re-epithelialization of ablated area on the thirdpostoperative day. A thorough examination was doneat completion of six months after PRK, specific pointswere noted, glasses were prescribed if required ordesired by the patients and a questionnaire was filledout by the patients at random. Answers were recordedwithout any prompting, to see overall satisfaction ofthe patient with the procedure.

The patients were asked the following sixquestions1. Do you experience night vision problems?

a) Permanentlyb) Sometimesc) None

2. Do you experience halo phenomenon around lightsource?a) Permanentlyb) Sometimesc) None

3) How the night vision problem and halo pheno-menon changed with time over the past sixmonths?a) Improvedb) Unchangedc) Worsened

4) Are you using glasses for distance vision?a) Permanentlyb) Sometimesc) None

5) Do you have foggy vision?a) Yesb) No

6) Are you happy with the overall result?a) Yesb) NoThe results were analyzed using statistical

software SPSS version 13.RESULTS:

All the participants, both male 18 (52.95%) female16 (47.05%), had good socioeconomic background andeducation and almost the same intelligence level. Allwere between18 and 35 years of age group with a meanof 24.34 (±4.35) years, representing full range of myopiatreated.

Following results were found after the analysis ofquestionnaires of 34 patients (Table 1,2,3,4,5). Tenpatients (29.41%) required glasses at times for distancevision however nobody used glasses permanentlyduring six months duration. Twenty four (70.59%)subjects were enjoying life without wearing spectacles.Twenty three (67.65%) participants had clear vision,whereas, 11 (32.35%) subjects had some complaints asto quality of their vision due to foggy vision. Twentysix (76.47%) subjects were happy with the overall resultat completion of six months, whereas, 8 (23.53%)subjects were not much comfortable with the overalloutcome. In short, none of these participants was reallyunhappy or annoyed but the level of satisfaction variedgreatly as the expectation of some persons might bequite extraordinary.DISCUSSION

Many factors contribute to patient satisfactionincluding accessibility and convenience of services,institutional structure and interpersonal relationships,competence of health professionals and patient’s ownexpectations and preferences4. It has been proposed thatmultiple outcomes should be assessed, and that patientsatisfaction with surgery is an important outcomemeasure to include in the assessment of surgicaloutcomes5.

Subjective patient satisfaction is the mostimportant in the basic objective data points by whichrefractive surgery procedures can be judged6. As suchthe number of studies is relatively small and researchhas tended to focus on objective clinical outcomes suchas visual acuity and refractive errors, or symptoms suchas the degree of halo, or glare. Previous results fromstudies carried out by telephone and questionnaire haveindicated a high level of patient satisfaction from 84.6%to 92%1,2. The satisfaction is not a one-dimensionalconcept that is, patient may be satisfied, with overallresult, but may be, not be satisfied with the sub-component of the eventual outcome, such as, the

Photorefractive Keratectomy and Patient Satisfaction Level


Table 1:Night vision problems after PRK

Total= 34 patients

Duration Number Percentage

Permanent 03 08.82

Sometimes 08 23.52

Never 23 67.66

Table 2:Halo problems reported after PRK


Permanent 05 14.71

Sometimes 08 23.52

Never 21 61.78

Table 3:Progress in halo and night vision problems at 6months after PRK

Status Number Percentage

Improved 11 32.35

Unchanged 18 52.95

Worsened 05 14.70

Table 4:Need for spectacle correction 6months after PRK


Permanent 0 0

Sometimes 10 29.41

Never 24 70.59

Table 5:Foggy vision problem reported after PRK


Yes 11 32.35

No 23 67.65

necessity to wear spectacles occasionally. Keeping allthese considerations in mind, a questionnaire wasconstructed including questions related to night vision,halo problems, foggy vision and need to wear glassesafter PRK. But the lack of questionnaire standardizationmakes it difficult to compare different studies andresults. Furthermore level of satisfaction varies fromindividual to individual and it could be different indifferent situations and economic set up. Educationalbackground and intelligence can affect the level of

satisfaction of a patient with the procedure.This study can be compared well with the one

conducted by Nystrom and others in 1995, 36 patientsafter PRK, using 3.50 to 5.00 mm diameter ablation zone.They found 70% of the patients were happy with theoverall results and 30% of patients had some complaintsas to the quality of vision7. We had 76.47% happy withthe overall result and 23.53% were not very muchcomfortable with overall result. They also reported that34% of patients always, 26% sometimes and 40% neverexperienced halo problems. Night vision and haloproblems improved in approximately 50% of cases withtime. Respective percentage of this study is 14.70%,23.52%, and 61.78%. Nystrom et al, further reported thatpermanent night vision problems were experienced by40%, 30% reported them sometimes and 30% reportedno problem at all. Respective percentage of the currentstudy is 8.82%, 23.52%, and 67.66%. Situation of nightvision and halo problem also improved significantlywith time. The difference in the results is due todifference in ablation diameters used to treat myopia.With the small optical zones (4.3 to 4.5 mm) of PRK,one would expect problems with glare and worseningof vision at night8. Similarly halo phenomenon (halosaround light sources) is common in patients treated with3.5 mm zones 9, which is also evident in the comparison.Problems with glare, night halos, and blurred visionhave been found in other studies but these tend todiminish with time10. Nystrom et al further reportedthat 60% never needed to use glasses after treatment,30% sometimes did,and 10 % always wore distanceglasses 3 years after surgery. In the current study 70.59%never needed glasses after PRK, whereas 29.41%required sometimes. The difference of 10% may be dueto the difference of duration after which the study wasconducted. Majority of the patients who have achievedgood refractive and visual results at six months appearto remain stable11, but the regression of effect, especiallyin higher refractive errors and need of glasses to furtherimprove the vision for reading and driving, is quitepossible with the passage of time. It is quite evidentfrom both the studies that the level of satisfactioncorrelates well with the freedom from spectacle state.

It is reported that the most important reason forundergoing excimer laser treatment was to improveunaided vision (85.6%),or to be free from spectacles(83.35%),whereas 72.7% reported difficulties withcontact lens wear as being very important. Improvedunaided vision enabling subjects to participate (70%)in supports and improved cosmetic appearance (59.5%)were also considered important12.

Brett Holliday did similar study; the questionnaireshowed that between 15% and 30% of patients(depending on initial degree of myopia) were



disappointed with the result10 . Thus the level ofsatisfaction varies greatly from individual toindividual11. Our study showed that majority of patientswere happy and satisfied with the final outcome at sixmonths. A number of patients were not satisfied; eitherdue to initial halo and night vision problems or withfoggy vision and needed to wear glasses at times. Butnone of them was really unhappy or annoyed with theexperience.

Shan et al tried to find out patient satisfaction levelone year after PRK. Patients considered their results tobe as follows: 82.3% good or excellent, 14.9%worthwhile, and 2.8% were disappointed with theoutcome. A high percentage of patients were satisfiedwith the outcome following PRK. However, a fairnumber (14%) of patients considered the treatment tobe worthwhile but it did not meet their expectations13.

As much depend upon the patients expectationswith the procedure, a patient with 6/6 visual acuity maynot be satisfied owing to problems of glare and halosaround light source12. These problems resolve over thetime and can be reduced significantly by avoidingeccentric ablation and using larger ablation zonediameter. The satisfaction and acceptance of thepostoperative results can be much improved byimproving on the preoperative consultative process,which must include the reason for seeking the treatmentto determine the level of expectation of patient withthe procedure, generally decline from low to highmyopia.

But dissatisfied patients are seen in everyrefractive group10.It is best to describe the outcomespecific activities rather than an achieved level of visualacuity such as vision that is good enough to play sports,watch TV, and drive a car without correction. Butglasses for reading, night driving, or bad weatherdriving may be required sometimes11.CONCLUSION:

Taking in to account the rang of myopia treated,the level of satisfaction six months after PRK was

generally high and quite encouraging in this survey.Subjective visual symptoms such as night visionproblems and halo phenomenon did not havesignificant influence on overall patient satisfaction.REFERENCES:1. Waring GO, Lynn MJ, McDonnel PJ. On the PERK study

group; Results of the Prospective Evaluation of RK (PERK)Study 10 years surgery. Am J Ophthalmol 1994;112:1298-1308.

2. Kamiya K., Miyata K., Takunaga T., Kiuchi T., Hiraoka T,Oshika T. Structural analysis of the cornea Using scanning—Slit Corneal Topography in eyes undergoing Excimer LaserRefractive Surgery. Cornea .2004; 23:59-63.

3. Janakeraman P, Rajendran B, Increasing the number ofphotorefractive keratectomy procedures from a singleexcimer laser gas fill. J Refract Surg 1995;11:319-20.

4. Myles PS, Williams DL, Hendrata M, Anderson H, and WeeksAM. Patient satisfaction after anaesthesia and surgery : resultsof a prospective survey of 10811 patients. Br J Anaesthesia2000:84:6-10.

5. Conner Spady, S. Sanmugasunderam,P. Courtright, J.JMacgGraran ,T.W Noseworthy, the steering committee of thewestern Canada waiting list project. Determinants of patientsatisfaction with cataract surgery and length of time on thewaiting list. Br J ophthalmol 2004:88: 1305-9.

6. Doane JF, Nordan LT, Baker RN, Slade SJ, . Basic tenets ofLamellar Refractive Surgery. Ocular Surgery News(International ) 1996 ;7:20.

7. Nystrom HH, Tengroth B, Fagerholm P, Epstein d, K WastEM , Patient Satisfaction following Photorefractivekeratectomy for myopia. J Refract Surgery 1995;11:335-6 .

8. Epstein D, Tengroth B, Fagerholm P, Nystrom HH. ExcimerRetreatment of Regression after photorefractive keratectomy. Am J Ophthalmol 1994; 117:456—61.

9. Seiler T, Mc Donnell PJ. Excimer Laser Photorefractivekeratectomy( Major Review) Survey of ophthalmology1995;40:89-118.

10. Holliday B. Refractive and Visual Results and patientsatisfaction after excimer laser photorefractive keratectomyfor myopia Br J Ophthalmol 1995 ; 79: 881-7

11. Machat JJ. Excimer Laser Photorefractive Keratectomy:Practice and principal, Slake Inc, U.S.A 1996; 3-211.

12. Mc Ghee CNG, Orr D , Kidd B, Stark C, Bryce IG, AnastasNC. Physiological Aspects of Excimer Laser Surgery formyopia Reasons for seeking treatment and patientsatisfaction. Br J Ophthalmol 1996; 80: 874-9.

13. Shah S, Perera S, Chatterjee A. Satisfaction after Photorefractive Keratectomy. J Refract Surg 1998 Apr; 14(2 Suppl):S226-7.



To Know about Timely Referral Systemfor Retinopathy of Prematurity (ROP)

in three Leading Hospitals of Peshawar, (KPK)

Junaid Faisal Wazir1, Inayatullah Khan2, Imran Ahmad3, Sabir Mohammad4, Shafqatullah5

ABSTRACTObjective: Retinopathy of prematurity (ROP) is emerging as a significant avoidable cause of childhood blindness indeveloping countries. This study was conducted to assess the referral system for ROP in the leading health care centersinvolved in the provision of services to newborns in Peshawar, and to assess the awareness of this condition amonghealth care workers in these centers.Methods: A purposeful sampling technique was employed to select ten health care centers in Peshawar, Pakistan, whichhad the highest number of deliveries per year. Key informants interviews were held with the health care providers involvedin the decision-making at these centers. A content analysis was performed on their responses.Results: A total of 10 physicians (2 neonatologists and 8 pediatricians) were interviewed. Most of the surveyed centersdid not have any referral system for ROP. The two centers that did have a referral system were not following standardprotocol for such referrals. Most interviewees had inadequate knowledge of ROP. Only 3 out of 10 physicians were awarethat ROP can lead to blindness.Conclusion: There was no referral system for ROP screening at most of the surveyed centers. The few centers that didhave a referral system were not following international screening guidelines for such referrals. There is lack of recognitionof ROP as a sight-threatening condition as shown by the inadequate knowledge of ROP among the concerned staff.Key Words. Retinopathy of prematurity (ROP) ,low birth weights (LBW)

————————————————————————————————1Assistant Professor, Vitreo-retina, 2Trainee Medical Officer,3Senior Registrar, 4Medical Officer, 5Trainee Medical Officer,Department of Ophthalmology, Khyber Girls Medical College,Hayatabad Medical Complex, Peshawar.————————————————————————————————Correspondence: Junaid Faisal Wazir, [email protected]: 0302 5586596————————————————————————————————Received: April 2012 Accepted August 2012————————————————————————————————

Original Article

INTRODUCTION Retinopathy of prematurity (ROP) is an important

cause of childhood blindness which can lead to a lifetime of social, emotional and economical challenges.Currently, at least 50, 000 children world wide are blindfrom ROP.1 Its major risk factors include prematurity,low birth weight and exposure to high oxygenconcentration.2

The proportion of children who are affected byROP varies depending on the level of development ofthe country and the effectiveness of ROP screeningprogrammes in place.3 With improved survival rates ofpremature and low birth weight infants, especially inthe developing countries, ROP is emerging as animportant cause of blindness in children worldwide.This has been referred to as the “third epidemic” ofROP.1,3 However, if appropriate screening strategies areimplemented, it is a potentially avoidable cause ofblindness.4

A key strategy used by ROP screening

programmes is the timely referrals of high risk children.The idea of this study stems from our experience ofseeing several cases of advanced ROP as a result ofdelayed referral. All these children were high-risk forROP but their parents were not made aware by healthcare providers of the condition, its management andblinding consequences. They were all born in theleading hospitals of Peshawar, reportedly adequatelyequipped to deal with premature births. Based on thisexperience, we conducted a study in the 3 leading healthcare centers across Peshawar to assess if they had areferral system for ROP. We also assessed the level ofawareness of this condition among health care workersdirectly involved in decision-making and provision ofservices to the new borns in these centers.Methods

A purposeful sampling technique was employedto select 3 hospitals in Peshawar with the highestnumber of deliveries per year (Table 1).

The selected centers included private and publicsector hospitals and maternity homes in differentlocalities of the city, catering to large populations.Informed written consent to conduct the study wasobtained from the administrators of the respectivecenters. In each center, information about referrals forROP and related practices, and whether a standardprotocol was being followed, were obtained from twopaediatricians or neonatologists, involved in theprimary decision making regarding the care of all

Dr. Junaid


newborns. We assessed if the selected centers werefollowing a standard protocol for ROP screening. Bystandard protocol we mean, the joint statement onscreening guidelines for preterm infants, which wasissued by the American Academy of Ophthalmology,Section on Ophthalmology, American Academy ofPediatrics, & American Association for PediatricOphthalmology and Strabismus in 2006.5 Theseguidelines recommend that “infants with a birth weightof less than 1500 g or with a gestational age of 32 weeksor less (as defined by the attending neonatologist) andselected infants with a birth weight between 1500 and2000 g or gestational age of more than 32 weeks withan unstable clinical course, including those requiringcardiorespiratory support and who are believed by theirattending paediatrician or neonatologist to be at highrisk, should have retinal screening examinationsperformed after pupillary dilation using binocularindirect ophthalmoscopy to detect retinopathy ofprematurity (ROP).” Each interview lasted for aroundhalf an hour. The interview with the primary decisionmakers also asked open-ended question about theirawareness and practices (Appendix-1).

Relevant records and documents were examinedand field notes were taken through interviews anddocument reviews. Content analysis technique wasused to identify key features from the responses givenby the interviewees regarding their practices of dealingwith preterm infants. The typical responses that wereobtained have been discussed here.RESULTS

A total of 3 centers providing maternity servicesin Peshawar were invited to participate in the study.All decided to participate. The annual number of babiesborn ranged from approximately 700 to 16,000(Table-2).

A range of responses were obtained for thequestions we asked at these centers (Table-3).Ophthalmic referral system for premature babies:

Most (8 out of 10) of the surveyed centers did nothave any referral system for ROP. The two centers that

Table 1:Characteristics of the surveyed hospitals and

maternity homes in Peshawar

Centre(Hospital/ Public/Private No. of deliveries No. of pretermMaternity sector per year* births per year*

Home)

A Public 7,000 1200-1400

B Public 9,000 1200-1800

C Public 16,000 3000-3600*Average number of deliveries and preterm births as reported bythe respective centers

Appendix 1

1. What advice would you give to the parents of a baby with gesta-tional age <32 weeks or birth weight <1500 grams?

2. What are the criteria for giving oxuygen to babies in your cen-ter?

3. If oxygen is given, what is the usual saturation and duration inyour center?

4. What do you think could be the benefits and adverse effects ofgiving oxygen?

5. Have you ever heard of retinopathy of prematurity? If yes, whathave you heard?

6. Do you routinely advise an eye examination for premature ba-bies? If yes, at what age?

did have a referral system were not following standardprotocol for such referrals. Prematurity and low birthweights were not considered reasons for referral to anophthalmologist. Generally if the baby was stable,regardless of gestational age, no advice was given otherthan for follow up with a paediatrician. At a hospitalwhere approximately 7200 deliveries take place a year,the neonatologist said:

Table 2:Key findings of the study

Most of the surveyed hospitals did not have any referral systemfor ROP screening.

Prematurity and LBW are not considered as reasons for givingan ophthalmologic referral.

If a preterm and LBW baby is stable no advice is given to theparents besides follow up with the paediatrician.

Though health care providers were aware of ROP, the extent ofawareness was minimal.

The most common misperception is that only those prematurebabies who are given exygen are at risk of developing ROP

In the 2 hospitals where preterm, low birth weight (LBW) infantswere given ophthalmologic referral, the timing for the first oph-thalmologic visit was not in accordance with international guide-lines.

Although most doctors were aware that excessive exposure tooxygen could lead to eye problems, the oxygen saturation andduration of oxygen therapy were not properly standardized.

Table 3:Response by the Physicians

Responses n = 20

No advice is given other than follow up with thepaediatrician if a premature baby is stable 16

We routinely refer preterm, low birth weight infantsfor eye examination 4

Oxygen was given if the baby was in distress, appearedcyanosed and oxygen saturation was less than 85-90% 20

To Know about Timely Referral System for Retinopathy of Prematurity (ROP) in three Leading Hospitals of Peshawar, (KPK)


“We do not advise parents to have their child’seyes examined, unless the baby was given oxygenwhich would lead to retrolental fibroplasia. In that casewe advise them to visit an ophthalmologist, or weadvise an eye examination if there is any ‘obviousabnormality’. But we do perform eye examination onevery baby ourselves as well.” When asked when thefirst eye examination on a new born baby should takeplace, the interviewee replied that the timing dependson the parents. At one of the hospitals where prematurebabies were regularly seen by an ophthalmologist, thesenior registrar said that he was not sure of the age atwhich the child was seen by an ophthalmologist. Amajor misconception among the interviewees was thatonly those premature babies who received oxygen wereat risk of developing ROP. Only few were aware thatROP can lead to blindness. Another pediatrician cited“discharge from their baby’s eyes” as the reason forreferral to an ophthalmologist.

In another hospital where nearly 800 babies wereborn annually, the paediatrician said that parents wereadvised to have their baby’s first eye examination at 6-8 weeks of life. One center that did have a referralsystem were not following standard protocol for suchreferrals. In one of these hospitals, all babies in theNeonatal Intensive Care Unit with birth weight less than1500 grams were examined by a visitingophthalmologist once a week. One maternity home,which caters to a large population of a very lowsocioeconomic stratum, where nearly 9600 deliveriestake place per year, the pediatrician said. “Giving advicefor eye examination is useless as no ophthalmologistvisits our hospital from the institutes where [expertisein ROP management] exist. How can we refer ourchildren? Our patients cannot afford to and will not seekany medical care outside of this charity hospital.”Availability and use of oxygen therapy:

All surveyed hospitals had incubators. 10 out of10 physicians we interviewed mentioned that oxygenwas given if the baby was in distress, appearedcyanosed and oxygen saturation was less than 85-90%.However, in one out of ten hospitals premature babieswere not given oxygen if they did not have any signs ofrespiratory distress. According to most interviewees,duration of oxygen therapy depended on the conditionof the baby.

Regarding the appropriate use of oxygen in thepreterm infants, in 2 out of the 3 selected centers thepractice was to maintain oxygen saturation above 95%.However, some of the centers reported not monitoringoxygen saturation levels because of lack of human andcapital resources to do so. Instead, the practice was togive 1 to 2.5 liters of oxygen per minute till baby’scondition improved.

Regarding the harmful effects of supplementaloxygen, the common responses were damage to lungsdue to hyperoxia, retinopathy, metabolic alkalosis andfree radical injuries. Fourteen physicians said that theywere aware that excessive exposure to oxygen can haveharmful effects on the brain and eyes.Awareness of ROP and its risk factors:

When asked if they had ever heard of ROP andwhat its main risk factors were, majority of therespondents were aware of the fact that it was acondition of premature infants with excessive exposureto supplemental oxygen being the main risk factor.However, only few mentioned that it can result inirreversible blindness. Several interviewees confessedto having no or very little knowledge of the condition.As one senior doctor, where nearly 9000 deliveries occurper year, said: “Yes, I have heard of ROP, but I do notknow anything about it.”

A pediatrician in a maternity home where 3000-3600 babies are born per year, with 120-240 preterm,LBW infants said: “I have as much knowledge [of ROP]as a final year MBBS student. I am aware of thepathophysiology and outcome. Every child who is givenoxygen should have an eye examination.”DISCUSSION

Our study revealed that majority of the leadinghealth centers and maternity homes in KPKs’ largestcity, Peshawar, do not refer preterm and low birthweight infants at risk of developing ROP to anophthalmologist. Majority interviewees, irrespective ofwhere they worked, showed inadequate knowledge ofROP, its risk factors and screening. Timely referral ofthe high risk babies is critical as it prevents theoccurrence of threshold disease as recommended byguidelines titled, Screening examination of prematureinfants for retinopathy of prematurity.5 Ocularexamination of premature infants should be performedby an ophthalmologist trained to deal with preterminfants, with sufficient expertise and knowledge to beable to identify the location and sequence of the disease.“The International Classification of Retinopathy ofPrematurity Revisited” should be used as a guidelinefor recording these retinal findings.6 The firstexamination should normally be performed between 4and 6 weeks of post natal age and the follow upexaminations should be scheduled by the examiningophthalmologist.5 However, it was disturbing to notethat in our study prematurity and low birth weightswere not considered as reasons for advising neonatalophthalmologic examination. In addition, the majorityof interviewees were not aware of its pathology, riskfactors and consequences. We identified a number ofmisperceptions, the most common being that only thosepremature babies who were given oxygen therapy were



at risk of developing ROP. To date, there is in-sufficientevidence to suggest what the optimal oxygen saturationis or PaO2 values to aim for in preterm infants whoreceive oxygen. Research has shown that despite thecommon belief that oxygen therapy increases the riskof ROP, it can occur even with carefully controlledoxygen therapy and therefore, prematurity is the mostimportant risk factor.2

In two hospitals where ophthalmologic referralwas given for premature, low birth weight infants, thetiming for the first ophthalmic visit was not inaccordance with international guidelines; parents wereadvised to visit an ophthalmologist either at 6-8weeksafter birth, immediately after first visit to a pediatricianor no time frame was given. Lack of attention to ROPas an important cause of childhood blindness in medicalcurriculum and the limited number of trained peoplein neonatal care may explain these misconceptions. Aprior local study, which reported the incidence of ROPas 32.4% in a tertiary care center, revealed that a largenumber of infants who satisfied the screening criteriaremained unscreened in our country and could havedeveloped ROP with consequent blindness.7 Thus,implementation of proper screening guidelines inhospitals and maternity homes with special focus onthe education of staff involved is essential.

According to World Health Organization —Vision 2020 program, after corneal scarring and cataract,ROP is one of the leading causes of avoidable childhoodblindness worldwide.4 Due to improvements inneonatal care in the developing world, more prematureinfants are surviving. Thus ROP is emerging as a causeof blindness in middle and low-income countries.Prematurity and low birth weights are important issuesin our country contributing to infant morbidity andmortality. In Pakistan 35% of neonatal mortality is dueto prematurity and related complications.8 Withimprovements in neonatal care, more premature infantsare now surviving in developing countries such as ours.Therefore, there is a much greater percentage ofpopulation that is “at risk” of developing Retinopathyof Prematurity in our part of the world. Due to limitedresources the economic burden of the disease is alsohigher in such countries.

An important question which arises is that whoshould be making the decision for referral in thesecenters and where these babies should be referred to.Unless there are appropriate ROP services availablewith effective linkages to maternity homes and otherhealth care facilities, referrals cannot be meaningful. Inindustrialized countries, effective screeningprogrammes and high standard of neonatal care hasresulted in reduced rates of blindness due toROP.1 Screening programmes are also being

implemented in India, however they show a need todevelop region specific guidelines.9,10

A strength of our study was that it involved allmajor hospitals and maternity homes with the highestrates of births, in all the major parts of the city. It wouldbe important to see if the same pattern of inadequateknowledge of ROP and variable referral system existin smaller units. A qualitative methodology was chosenbecause this topic is not very well explored in our partof the world. Such a method was useful in providingan in-depth understanding of the issues explored.

One limitation of our study was that we could notconfirm the reliability of the responses we obtainedsince we did not directly observe the practices regardingROP referrals in the selected centers and our conclusionsare based on the responses we received from the healthcare providers in these places.CONCLUSION

In conclusion, there is no referral system forpremature infants at the surveyed hospitals andmaternity homes which have the highest number ofdeliveries in the city. There is lack of recognition of ROPas a sight-threatening condition as shown by theinadequate knowledge of ROP among the concernedstaff.

We recommend that all at-risk babies born inhospitals and maternity homes should be registered andbe automatically referred to ophthalmologists. Staffinvolved in the care of premature infants should betrained in ROP through workshops and seminars.Parents of all prematurely born babies should beinformed about the risk of development of ROP, andthe importance of timely ophthalmologic review andfollow-up should be stressed. The importance of acritical time window for successful treatment andblindness as a possible consequence of untreateddisease should be emphasized.REFERENCES 1. Gilbert C. Retinopathy of prematurity: a global perspective

of the epidemics, population of babies at risk and implicationsfor control. Early Hum Devel 2008; 84: 77-82.

2. Karna P, Muttineni J, Angell L, Karmaus W. Retinopathy ofprematurity and risk factors: a prospective cohort study. BMCPediatr 2005; 5: 18.

3. Gilbert C, Fielder A, Gordillo L, Quinn G, Semiglia R, VisintinP, et al. Characteristics of infants with severe retinopathy ofprematurity in countries with low, moderate, and high levelsof development: implications for screening programs.Pediatrics 2005; 115: e518-25.

4. Gilbert C, Foster A. Childhood blindness in the context ofVISION 2020—the right to sight. Bull World Health Organ2001; 79: 227-32.

5. Section on Ophthalmology American Academy ofPaediatrics; American Academy of Ophthalmology;American Association for Paediatric Opthalmology andStrabismus. Screening examination of premature infants forretinopathy of prematurity. Pediatrics 2006; 117: 572-6.

6. The International Classification of Retinopathy of



Prematurity revisited. Arch Ophthalmol 2005; 123: 991-9.7. Taqui AM, Syed R, Chaudhry TA, Ahmad K, Salat MS.

Retinopathy of prematurity: frequency and risk factors in atertiary care hospital in Peshawar, Pakistan. J Pak Med Assoc2008; 58: 186-90.

8. Mufti P, Setna F, Nazir K. Early neonatal mortality: effectsof interventions on survival of low birth babies weighing1000-2000g. J Pak Med Assoc 2006; 56: 174-6.

9. Vinekar A, Dogra MR, Sangtam T, Narang A, Gupta A.


Retinopathy of prematurity in the Indian population. It’s timeto set our own guidelines! Indian J Ophthalmol 2007; 55: 329-30.

10. Vinekar A, Dogra MR, Sangtam T, Narang A, Gupta A.Retinopathy of prematurity in Asian Indian babies weighinggreater than 1250 grams at birth: ten year data from a tertiarycare center in a developing country. Indian J Ophthalmol2007; 55: 331-6.

STAY ON TOPWITH

Approved & indexed by PMDC, PakMedinet & H.E.C

Quarterly

Update


————————————————————————————————*Department of Ophthalmology, Khyber Institute of OphthalmicMedical Sciences, Hayatabad Medical Complex, Peshawar.————————————————————————————————1.2.3. Trainee Medical Officers, HMC, Peshawar, 2. Senior RegistrarHMC Peshawar————————————————————————————————Correspondence: Dr Zakir Hussain, H.NO: 624, St. No:21, Sector:F-5, Phase 6, Hayatabad, Peshawar. Cell: 0334 9123070 Email:>[email protected]————————————————————————————————Received August ’2012 Accepted Oct’2012————————————————————————————————

Comparison of Preoperative Injection vs.Intraoperative application of Mitomycin C

in Recurrent Pterygium*

Zakir Hussain1, Hamid ur Rehman2

Muhammad Bilal3

Objectives: to study the efficacy of preoperative subconjunctival injection of mitomycin C with intraoperative mitomycinin recurrent pterygiumStudy design: Randomize control trial.Place and duration of study: The study was carried out at Eye Unit, District Headquarter Hospital, Lakki Marwat betweenMay 2011 and November 2011.Patients and methods: Patients underwent full preoperative evaluation (complete history and ophthalmologicalexamination). Patients were randomly divided into two groups. In group A, 20 eyes received 0.1 ml of 0.20 mg/ml MitomycinC injected subconjunctivally into the head of the pterygium one day before surgical excision using the bare sclera technique.In group B, 20 eyes underwent surgical removal with the bare sclera technique and intraoperative topical application of0.20 mg/ml of mitomycin C. Preoperative subconjunctival injection of mitomycin C (MMC) was done at the outpatientclinic under aseptic conditions one day before surgery.Results: The study included 40 eyes divided into two groups. Both groups had recurrent pterygium encroaching onto thecornea (3 to 5 mm in size) that had been operated within one year prior to inclusion. The mean preoperative best correctedvisual acuity (BCVA) was 0.53 th + 0.15 in the group A and 0.58th + 0.20 in the group B upon inclusion into the study. Themean postoperative BCVA was 0.8 + 0.11 in the group A and 0.83+ 0.16 in the group B. There was a highly statisticallysignificant difference between the preoperative and postoperative results (P<0.05), while the difference between the twogroups was statistically insignificant (P>0.05) One year postoperatively, the recurrence rate was one (5%) eye in thegroup A (a 5-mm pterygium that was removed after reported growth by the patient) and two (10%) eyes in the group B (a4-mm pterygium that was removed for proximity to visual axis and a 3-mm pterygium that was removed after reportedgrowth by the patient). The difference in the recurrence rate between both groups was statistically insignificant (P>0.05)Conclusions: Preoperative subconjunctival injection of mitomycin C in low dose (0.1 ml of 0.20 mg/ml) a day beforepterygium surgery is a simple and effective modality for management of recurrent pterygium.Key words: Pterygium, Mitomycin C

Original Article

INTRODUCTIONPterygium is a common external eye disease, seen

more frequently in tropical and subtropical areas whereexposure to ultraviolet sunlight is high. Pterygiumcreates many problems for the patient includingsymptoms of irritation, foreign body sensation andlacrimation, cosmetic disfigurement, and functionalproblems such as reduced visual acuity, diplopia andproblems fitting contact lenses. The mainhistopathological change in primary pterygium iselastodysplasia and elastodystrophy of subepithelialconnective tissue.1 The exact cause of pterygium is not

well understood. However, long-term exposure tosunlight, especially ultraviolet rays and chronic eyeirritation from dry, dusty conditions seem to play animportant role. 1,2 Surgical treatment of pterygium isdirected at excision, prevention of recurrence andrestoration of ocular surface integrity. Simple excisionof the pterygium alone has a very high rate ofrecurrence, about 30-70%.3 Even conjunctivalautografting to cover the bare sclera is associated withrecurrence rates of 2% - 39%.4 Various adjunctivestrategies such as irradiation treatment, anti-metabolites, conjunctival autograft, limbal autograftand amniotic membrane graft have been employed overthe years to reduce the high recurrence rate.4,5 In thelast decade, mitomycin C had been used morecommonly in pterygium surgery. The mechanism ofaction of mitomycin C seems to inhibit fibroblastproliferation at the level of the episclera. The use ofintraoperative application of mitomycin C gives a highsuccess rate, however, serious complications have beenreported.6 Subconjunctival injection of mitomycin C asadjunctive therapy before surgery allows exact titrationof mitomycin C delivery to activated fibroblasts and

Dr. Zakir Hussain


minimizes epithelial toxicity.7 We designed this studyto compare the efficacy of preoperative injection versusintraoperative application of mitomycin c in recurrentpterygium surgery.MATERIAL AND METHODS

A randomized comparative case series study wasconducted between May 2011 and November 2011 inEye Unit, District Headquarter Hospital, Lakki Marwat;where 40 eyes of 40 patients with recurrent pterygiumfollowing simple excision were included in the study.Patients with other ocular surface diseases, dry eye andprogressive ocular disease unrelated to cornealcondition were excluded from the study. Patientsunderwent full preoperative evaluation (completehistory and ophthalmological examination). Patientssigned an informed consent after complete discussionof the procedure before included in the study. Patientsnot coming for follow-up were excluded from the study.

Patients were randomly divided into two groups.In group A, 20 eyes received 0.1 ml of 0.20 mg/mlmitomycin C injected subconjunctivally into the headof the pterygium one day before surgical excision usingthe bare sclera technique. In group B, 20 eyes underwentsurgical removal with the bare sclera technique andintraoperative topical application of 0.20 mg/ml ofmitomycin C. Preoperative subconjunctival injection ofmitomycin C (MMC) was done at the outpatient clinicunder aseptic conditions one day before surgery. Withthe patient in supine position and magnifying loupe,surface anesthesia was achieved by benoxinate 0.4% eyedrops; then eye speculum was applied and MMC wasinjected into the head of the pterygium at the limbususing 30G needle followed by pressure with micro-sponge to prevent drug leakage and irrigation with50ml balanced salt solution. Ofloxacin 0.3% anddexamethasone 0.1% eye drops (four times/day) wereprescribed and the eye was patched for one day beforescheduled surgery next morning. Patients underwentpterygium excision by bare sclera technique in theoperating room under surgical microscope. Afterpreparing and draping the eye in normal sterile fashion,the lids were opened using eye speculum. Surfaceanesthesia was achieved with Alcaine eye drops.Lignocaine 0.5 ml of 2% solution was injected into thepterygium. The head of the pterygium was graspedwith toothed forceps and excision was done with No.15 Bard-Parker blade about 0.5 mm ahead of thepterygium and carried down clearly to the limbus. Theconjunctiva and subconjunctival tissue were thencleaned over the sclera towards the insertion of themedial rectus muscle and excision of the pterygium wascarried out to 4 mm posterior to the limbus. Hemostasiswas ensured. No conjunctival sutures were used.

In the group A, intraoperative eye irrigation with

200 mL of balanced salt solution was done followingpterygium excision to wash out residualsubconjunctival MMC. In the group B, intraoperativeapplication of mitomycin C was done using 5-mmsurgical sponge soaked with 0.20 mg/ml mitomycin Csolution and placed on the exposed scleral surface for2 min. After the sponge was removed, the eye surfacewas irrigated with 200 mL of balanced salt solution.Postoperative treatment included ofloxacin 0.3% anddexamethasone 0.1% eye drops (four times/day) andcombined tobramycin and dexamethasone eye ointmentat bedtime for four weeks in both groups.

Postoperative follow-up visits were scheduled oneday, one week, one month, two months, three months,six months and 12 months after surgery. In each visit,complete ophthalmological examination was done withspecial attention to pterygium recurrence andcomplications of mitomycin C such as corneal edema,glaucoma, corneal or scleral melting, keratitis andcataract. Recurrence of pterygium was defined as afibro-vascular growth beyond the limbus into the corneawith conjunctival drag. Data was coded, entered andanalyzed using SPSS Version 10.0 software for analysis.RESULTS:

The study included 40 eyes divided into twogroups. The group A consisted of 9 (45%) women and11 (55%) men with mean age 30.15±15.57 years. Whilethe group B consisted of 12 (60%) women and 8 (40%)men with mean age 33.11±114.23 years. Both groupshad recurrent pterygium encroaching onto the cornea(3 to 5 mm in size) that had been operated within oneyear prior to inclusion. The indications for pterygiumsurgery are shown in Table I. There was no statisticaldifference (P>0.05) between the two groups asregarding the age and sex. So the two groups werestatistically comparable. The mean preoperative bestcorrected visual acuity (BCVA) was 0.53 th + 0.15 in thegroup A and 0.58th + 0.20 in the group B upon inclusioninto the study. The mean postoperative BCVA was 0.8+ 0.11 in the group A and 0.83+ 0.16 in the group B.There was a highly statistically significant differencebetween the preoperative and postoperative results(P<0.05), while the difference between the two groupswas statistically insignificant (P>0.05).

One year postoperatively, the recurrence rate wasone (5%) eye in the group A (a 5-mm pterygium thatwas removed after reported growth by the patient) andtwo (10%) eyes in the group B (a 4-mm pterygium thatwas removed for proximity to visual axis and a 3-mmpterygium that was removed after reported growth bythe patient). The difference in the recurrence ratebetween both groups was statistically insignificant(P>0.05). Recurrence of pterygium was noted three tofive months postoperatively. As regards postoperative

Comparison of Preoperative Injection vs. Intraoperative application of Mitomycin C in Recurrent Pterygium


complications, delayed epithelization (more than twoweeks) occurred in two eyes (10%) in the group A andin one eye (5%) in the group B. Scleral thinning wasreported in one eye (5%) in the group B which occurredat one month and resolved within three weeks underconservative treatment with topical lubricant therapy;no other serious postoperative complications werereported.DISCUSSION:

Simple excision of pterygium is associated with ahigh recurrence rate ranging from 30 to 70%,5,8 Toreduce this high recurrence rate, different methods like,beta irradiation, mitomycin C, and amniotic membranehave been used.3,4 However, serious complications suchas secondary glaucoma, uveitis, scleromalacia andcorneal perforation are associated with these methods.Mitomycin C is commonly recommended to reducerecurrence. Mitomycin C is an antineoplastic antibioticwith radiomimetic properties, that selectively inhibitDNA, RNA and protein synthesis. Adjunctivemitomycin C (MMC) in pterygium surgery was firstdescribed in Japan by Kunitomo and Mori in1963.9 Since then several modalities of usage have beendescribed including preoperative injection andintraoperative application.7,10 MMC is an effectiveintraoperative treatment for preventing recurrence ofpterygium.10-12

The effect of the drug depends on the dose andthe time of application.13 Unfortunately, complicationsfrom intraoperative MMC application in pterygiumsurgery have been reported including vision-threatening complications such as glaucoma, cornealedema, corneal perforation, scleral melting, and cataractformation. 6 Subconjunctival application of MMC allowsexact dose delivery with minimal epithelial and scleraltoxicity. Subconjunctival MMC was investigated inanimal models, glaucoma, ocular cicatricial pemphigoidand pterygium surgery without serious complica-tions.14 -17

The concept of the study originated from aprevious study by Donnenfeld and co-workers whoreported a case series of subconjunctival MMC injectionone month before surgery in recurrent pterygium. Theirresults showed that pterygia were less vascular and less

Table I Indication of surgery

S. Indication for surgery Group A Group BNo. (No of eyes) (No of eyes)

1 Decrease Visual acuity 7 6

2 Reported growth by patient 9 11

3 Symptoms of irritation 4 3

Total 20 20

inflamed at one month and all pterygia were quiescentat the time of surgical excision. However, the recurrencerate was comparable to previous studies with MMCapplication.7The major endpoint of pterygium removalrelates to recurrence. As long as there are no evidence-based guidelines to relate recurrence to the surgicalindications or characteristics of the pterygium, judgingon the effective duration between MMC injection andsurgery on the basis of changes in pterygiumcharacteristics will be unsupported, as recurrence ratewill remain the final decision of any duration. Goodpenetration of MMC following topical application wasdocumented in animal models through either intact ornon-intact corneal epithelium, where MMC wasdetected in the aqueous humor 10 min after topicalapplication, with a statistically significant differencebetween intact or non-intact corneal epithelium. Theaqueous humor concentration of MMC increased in adose-dependent manner with increasing exposure timeand application concentration17,18 Based on these reportsof ocular penetration of MMC, the drug could bedetected in the aqueous humor 10 min after topicalapplication, and could penetrate the eye more easilythrough non-intact epithelium like that followingpterygium excision. A study of low-dose MMC throughsubconjunctival injection with shorter duration ofexposure before pterygium excision seemed logic tomaintain the efficacy of the drug and avoid longunnecessary exposure with subsequent penetration ofMMC.

In our comparative case series the recurrencerate was 5% in the group A and 10% in the group B.These results are considered as effective as othermodalities of preoperative and intraoperative adjuvantMMC in recurrent pterygium, and better than somereports like Luanratanakorn and co-workers whoreported a recurrence rate 52.6% with amnioticmembrane transplantation and 21.4% with conjunctivalautograft for recurrent pterygium after a six-monthfollow-up period.19Recurrence rates reported withintraoperative MMC application as adjuvant treatmentin recurrent pterygium surgery ranged from 12.5-42.9%depending on the MMC concentration and duration ofapplication.20,21 Combining conjunctival advancementor graft with intraoperative MMC reduced recurrencerates and improved safety. 22

In the clinical non-comparative case series ofDonnenfeld and co-workers, 36 eyes with recurrentpterygium received 0.1 ml of 0.15 mg/ml MMCsubconjunctivally one month before surgery; thereported recurrence rate was 6% over a mean follow-up of 24.4 months.7 In another trial preoperativeinjection of MMC into primary pterygium one monthprior to combined pterygium and cataract surgery



resulted in no recurrence and no serious complicationsup to 23 months of follow-up.23

As regards postoperative complications, only oneeye (5%) had mild avascular scleral thinning in thegroup B that resolved within three weeks after surgeryand no other serious complications were reported.Complications occurring after pterygium surgery withadjunctive MMC have been well reported with differentmodalities of application, concentrations and durations.Avascularized scleral thinning was reported in 13 outof 36 eyes (34.2%) following the use of topical MMC0.02% eye drops after primary pterygium excision.24

Carrasco and co-workers reported local scleral necrosisin a patient who received subconjunctival 0.15 mg/mlMMC one month before pterygium excision. However,that patient had severe dry eye with history of punctalcauterization.25 These findings should be seen inconsideration of the limitation of our work includingthe small number of patients in each group whichprobably limited the value of the statistical comparison.Further research to assess endothelial toxicity,intraocular pressure changes and long-term follow-upfollowing subconjunctival MMC injection is requiredto judge its safety and efficacy. Preoperativesubconjunctival low-dose MMC injection one daybefore bare sclera excision showed encouraging clinicalresults in the management of recurrent pterygium inappropriate patient population with comparablesuccess to topical application of mitomycin. Thesubconjunctival injection negates the ability of tear filmto dilute the medication, increasing exposure time tothe subconjunctival tissue and decreasing the ocularpenetration through the intraoperative keratectomy.CONCLUSION:

Preoperative subconjunctival injection ofmitomycin C in low dose (0.1 ml of 0.20 mg/ml) a daybefore pterygium surgery is a simple and effectivemodality for management of recurrent pterygium. Ithas the advantage of low recurrence and complicationsrate.REFERENCES:1. Austin P, Jakobiec FA, Iwamoto T. Elastodysplasia and

elastodystrophy as the pathologic bases of ocular pterygiaand pinguecula. Ophthalmology 1983;90:96-109.

2. Saw SM, Tan D. Pterygium: Prevalence, demography andrisk factors. Ophthalmic Epidemiol 1999;6:219-28

3. Hirst LW. The treatment of pterygium. Surv Ophthalmol2003; 48:145-80.

4. Murube J. Pterygium: Its treatment with beta therapy. OculSurf 2009; 7:3-9.

5. Kenyon KR, Wagoner MD, Hettinger ME. Conjunctivalautograft transplantation for advanced and recurrentpterygium. Ophthalmology 1985;92:1461-70.

6. Rubinfeld RS, Pfister RR, Stein RM, Foster CS, Martin NF,Stoleru S, et al. Serious complications of topical mitomycin

C after pterygium surgery. Ophthalmology 1992; 99:1647-54.7. Donnenfeld ED, Perry HD, Fromer S, Doshi S, Solomon R,

Biser S. Subconjunctival mitomycin C as adjunctive therapybefore pterygium excision. Ophthalmology 2003; 110:1012-6.

8. Shimazaki J, Kosaka K, Shimmura S, Tsubota K. Amnioticmembrane transplantation with conjunctival autografts forrecurrent pterygium. Ophthalmology 2003; 110:119-24.

9. Kunitomo N, Mori S. Studies on pterygium, Repot IV: Atreatment of the pterygium by mitomycin C installation. ActaSoc Ophthalmol Jpn 1963;67:601-7

10. Mastropasqua L, Carpineto P, Ciancaglini M, Enrico GallengaP. Long term results of intraoperative mitomycin C in thetreatment of recurrent pterygium. Br J Ophthalmol1996;80:288-91

11. Manning CA, Kloess PM, Diaz MD, Yee RW. Intraoperativemitomycin C in primary pterygium excision: A prospectiverandomized trial. Ophthalmology 1997;104:844-8

12. Panda A, Das GK, Tuli SW, Kumar A. Randomized trial ofintraoperative mitomycin C in surgery for pterygium. Am JOphthalmol 1998; 125:59-63.

13. Yamamoto T, Varani J, Soong HK, Lichter PR. Effects of 5-flurouracil and mitomycin C on cultured rabbitsubconjunctival fibroblast. Ophthalmology 1990; 97:1204-10.

14. Kee C, Pelzek CD, Kaufman PL. Mitomycin C suppressesaqueous humor flow in cynomolgus monkeys. ArchOphthalmol 1995;113:239-42

15. Gandolfi SA, Vecchi M, Braccio L. Decrease of intraocularpressure after subconjunctival injection of mitomycin inhuman glaucoma. Arch Ophthalmol 1995; 113:582-5.

16. Donnenfeld ED, Perry HD, Wallerstein A, Caronia RM,Kanellopoulos AJ, Sforza PD, et al. Subconjunctivalmitomycin C for the treatment of ocular cicatricialpemphigoid. Ophthalmology 1999; 106:72-9.

17. Torres RM, Merayo-Lloves J, Daya SM, Blanco-Mezquita JT,Espinosa M, Nozal MJ, et al. Presence of mitomycin C in theanterior chamber after photorefractive keratectomy. JCataract Refract Surg 2006; 32:67-71.

18. Song JS, Kim JH, Yang M, Sul D, Kim HM. Concentration ofmitomycin C in rabbit corneal tissue and aqueous humor aftertopical administration. Cornea 2006;25(10 Suppl 1):S20-3

19. Luanratanakorn P, Ratanapakorn T, Suwan-Apichon O,Chuck RS. Randomized controlled study of conjunctivalautograft versus amniotic membrane graft in pterygiumexcision. Br J Ophthalmol 2006;90:1476-80

20. Rubinfeld RS, Stein RM. Topical mitomycin-C for pterygia:Is single application appropriate? Ophthalmic Surg Lasers1997; 28:662-9.

21. Lam DS, Wong AK, Fan DS, Chew S, Kwok PS, Tso MO.Intraoperative mitomycin C to prevent recurrence ofpterygium after excision: A 30-month follow-up study.Ophthalmology 1998; 105:901-5.

22. Lam DS, Wong AK, Fan DS, Chew S, Kwok PS, Tso MO.Intraoperative mitomycin C to prevent recurrence ofpterygium after excision: A 30-month follow-up study.Ophthalmology 1998; 105:901-5.

23. Avisar R, Bar S, Weinberger D. Preoperative injection ofmitomycin C in combined pterygium and cataract surgery.Cornea 2005;24:406-9

24. Rachmiel R, Leiba H, Levartovsky S. Results of treatmentwith topical mitomycin C 0-02% following excision ofprimary pterygium. Br J Ophthalmol 1995; 79:233-6.

25. Carrasco MA, Rapuano CJ, Cohen EJ, Laibson PR. Scleralulceration after preoperative injection of mitomycin C in thepterygium head. Arch Ophthalmol 2002; 120:1585-6.



————————————————————————————————1.Resident Medical Officer LRBT Free Eye Hospital Mansehra.2.Associate Ophthalmologist LRBT Free Eye Hospital Mansehra.3.Senior Registrar Ophthalmology PGMI LRH, Peshawar. 4.MedicalOfficer, Ophthalmology, PGMI LRH, Peshawar. 5.Medical OfficerLRBT Free Eye Hospital, Mansehra.————————————————————————————————Correspondence: Dr. Naseer Ahmed, Resident Medical Officer,LRBT Eye Hospital, Mansehra. Abbotabad, KPKCell: 0345 0108558 E.Mail> [email protected]————————————————————————————————Received: July’2012 Accepted Nov’2012————————————————————————————————

INTRODUCTIONGlobally, cataract accounts for 50% of blindness

and remains the leading cause of visual impairment allover the world. Among the ocular ailments, a largebacklog of cataract blindness exists in the developingcountries and cataract is the most common cause ofreversible blindness1.This ocular morbidity is theleading cause of blindness in the world and about 18

million people are being affected by cataract2,3 despiteimprovements in surgical outcomes (WHO 2005). Theunderprivileged population of the world fails to availeye care services and the most important barriers areinsufficient financial resources, lack of awareness aboutexisting eye care facilities and inaccessibility4,5,6.Cataractsurgery has been in evolution phase from couching inthe ancient times by Susruta to reaching at the dawn ofKelman method of surgery who is the pioneer of recentadvanced technique of Phacoemulcification andlaunched in 1967.Despite what modern technology hasdone to advance the treatment of cataract, the greatestchallenge in our field continues to be the large andincreasing backlog of cataract blindness in thedeveloping countries7.This number is expected to risedue to an aging population and increase in lifeexpectancy. Cataract, an opacification of the crystallinelens in the eye, can be caused by many factors includingthe natural aging process, metabolic abnormalities,

Frequency of Different Types of Age Related Cataracts(Study of 250 cases)

Naseer Ahmad DOMS1, Faisal Nawaz Khan FCPS2, Mohammad Alam3,

Mohammad Idris4, Muddasir Hussain5

ABSTRACTObjective: To find out the frequency of different types of age related cataracts in patients admitted for cataract surgery atdepartment of Ophthalmology, Khyber Institute of Ophthalmic Medical Sciences (KIOMS), Lady Reading Hospital Peshawar.Materials and Methods: This study was conducted at department of Ophthalmology, Khyber Institute of OphthalmicMedical Sciences (KIOMS), Lady Reading Hospital Peshawar, from April 15, 2011 to November 15, 2011. Approval wastaken from ethical committee of Post Graduate Medical Institute (PGMI), Peshawar, before starting the study.250 patientssuffering from age-related cataract (with age range from 40 to 83 years) were selected, in which 128 (51.2%) were maleand 122 (48.8%) were female. An informed written consent was obtained from each patient. The patients evaluated forinclusion criteria. A proper proforma was designed for evaluation and documentation of patients. Anterior segment and ifpossible posterior segment examination was done with direct, indirect ophthalmoscope and slit lamp bimicroscopy. Afterdilation of the pupil (in individuals judged not to have occludable angles), the patient were graded as nuclear, cortical, andposterior sub capsular cataract by comparison with standard photographs based on the WHO adaptation of the LensOpacity Classification System III (LOCS III). The cases that satisfied the inclusion and exclusion criteria were included.Results: In our study the posterior sub capsular cataract (PSC) 142(56.8%) is the most common entity followed bynuclear cataract 66(26.4%) and finally is the cortical cataracts 42(16.8%). According to the Lens Opacity ClassificationSystem III (LOCS III) of cataracts, in the sub types of cortical cataracts cases 42(16.8%) mostly the patients presented inGrade 3 (> 4 mm) 17(40.48%) but the same ratio of patients 10(23.81%) presented in Grade 0 (an opacity < 1 mm invertical diameter) and Grade 2 (between 2 and 4 mm) of cortical cataracts.In the sub types of Nuclear cataract (NC),66(26.4%) cases, mostly the patients also presented in Grade 3 (is at least as extensive as standard photograph 3)26(39.39%) and Grade 2 (defined in analogous fashion with regard to standard photographs 2 and 3) 25(37.89%) nuclearcataracts. The percentage of grades show that Grade 2 and Grade 3 patients presented almost in the same ratio. Whilethe sub types of Posterior Sub capsular Cataract (PSC) 142(56.8%) cases, mostly the patients presented in Grade 3(greater than one half of lens circumference) 61(42.96%) and Grade 2(one fourth to one half of cortical circumference)42(29.57%) cortical cataracts. In our study most of the respondents observed is having Grade 3 and Grade 2 of differenttypes of age related cataract followed by Grade 2.While the Grade 1 and Grade 0 presented very rarely except in thecortical cataract.Conclusion: the posterior sub capsular cataract 142(56.8%) is the most common entity followed by nuclear cataract66(26.4%) and finally is the cortical cataract 42(16.8%).Abbreviation / Key words: Visual acuity (VA), Best corrected visual acuity (BCVA), Posterior Sub capsular (PSC),Cortical Cataract (CC), Nuclear Cataract (NC), Lens Opacity Classification System III (LOCS III)

Original Article

Dr Naseer


nutritional disorders, chronic ocular inflammation andtrauma. Many causes of cataract are classified by theirmorphology like size, shape, location or etiology. Agerelated cataract is the one related with old age8. In asurvey conducted in Pakistan, the prevalence of cataractin 16402 adults above the age of 30 years (20.9%) mainlyassociated with the increasing age. The fact that thepattern in a large proportion, different grades of cataractwere seen amongst older people as observed in manyUS-based populations. The incidence of higher agegroup rates of nuclear11 and cortical12 cataract has beenreported for women in previous population-basedstudies among both African and European populations.This finding is not completely understood. Onehypothesis is that changes in the hormonal milieu atmenopause somehow increase the risk of lens opacityamong women. Evidence in favor of this theory includesa decreased risk of nuclear sclerosis among current usersof estrogen replacement therapy and a protective effectof younger age at menarche and older age at menopauseagainst nuclear and cortical opacities, respectively 13.The most prevalent form of cataract in Africanpopulation is nuclear cataract (NSC). This differs fromthe preponderance of cortical cataract (CC), which hasbeen reported for African-derived populations inBarbados and Maryland. One reason for this observeddifference appears to be a low prevalence of CC in ourstudy (8.8%) compared with either Barbados (34%) orSalisbury (54% for African-American subjects). Severaldifferent types of explanations may be considered forthis14. Differences in the prevalence rates of the differenttypes of age-related lens opacity are of more thantheoretical interest. The degree of visual disabilityassociated with the different types of cataract has beenreported to vary, with posterior sub-capsular cataract(PSC) and NSC in particular being more likely to resultin vision loss requiring cataract surgery15. Diagnosis ismade with ocular examination using slit-lampbiomicroscopy. Although cataracts are not preventable,their surgical treatment is one of the most cost-effectiveinterventions in healthcare.MATERIALS AND METHODS:

This hospital based cross sectional study wasconducted at department of Ophthalmology, KhyberInstitute of Ophthalmic Medical Sciences (KIOMS),Lady Reading Hospital, Peshawar, from April 15, 2011to November 15, 2011. Purposive (Non probabilitySampling) technique was used in this study.Inclusion Criteria:

o All admitted patients of age related cataractsof 40 years or above age in Ophthalmology unit LRHand willing to answer the questionnaire.Exclusion Criteria:

o All patients of age related cataracts of age less

than 40 years.o All patients having systemic association with

cataracts like Diabetes Mellitus and hypertension etc.o All the patients who declined to be interviewed.Approval was taken from ethical committee of

PGMI Peshawar, before starting the study. 250 patientssuffering from age-related cataract with age range from40 to 83 years were selected, in which 128 (51.2%) weremale and 122 (48.8%) were female. They were havingrelatively old age, with an average age of 58.58+11.56SDyears. Regarding the sex of the patients 128(51.2%)patients were male and 122 (48.8%) were females(Table I). An informed written consent was obtainedfrom the patient. The patients evaluated for inclusioncriteria. A proper proforma was designed for evaluationand documentation of patients. Anterior segment andif possible posterior segment examination was donewith direct, indirect ophthalmoscope and slit lampbimicroscopy. After dilation of the pupil (in individualsjudged not to have occludable angles), the patient aregraded as nuclear, cortical, and posterior sub capsularcataract by comparison with standard photographsbased on the WHO adaptation of the Lens OpacityClassification III System (LOCS III). The cases thatsatisfied the inclusion and exclusion criteria wereincluded. Data was entered and analyzed using SPSSversion 10. Mean and standard deviation werecalculated for numerical variable i.e. age whilepercentages and frequencies were computed forcategorical variable respondent / age of the patients,sex, main type and sub types of cataract etc. The entirevariables were presented in the form of tables andcharts.RESULTS

A total of 250 cases participated in this study. Ageof the respondents ranged from 40 to 83 years. Theywere having relatively old age, with an average age of58.5 years. Regarding the sex of the patients 128(51.2%)patients were male and 122 (48.8%) were females(Table 1). In our study the presenting visual acuity ofthe 176 (73.2%) cases were between the visual acuity of6/24 and 1/60, Hand Movement (HM) of 44(17.6%) andProjection of light (PL) of remaining 23(9.2%) cases(Table II).This shows that mostly the presenting visualacuity was between 6/24 and 1/60 (Counting Fingerone meter).

In the frequency of different types of age relatedcataracts, the Posterior Sub Capsular cataracts142(56.8%) are the most common followed by nuclearcataract 66(26.4%) and finally is the Cortical cataract42(16.8%) (Table III).

According to the Lens Opacity ClassificationSystem III (LOCS III) of cataracts, in the sub types ofcortical cataracts cases 42(16.8%) mostly the patients

Frequency of Different Types of Age Related Cataracts


presented in Grade 3 (> 4 mm) 17(40.48%) but the sameratio of patients 10(23.81%) presented in Grade 0 (anopacity < 1 mm in vertical diameter) and Grade 2(between 2 and 4 mm) of cortical cataracts. (Table IV)

In the sub types of Nuclear cataract (NC),66(26.4%) cases, mostly the patients also presented inGrade 3 (is at least as extensive as standard photograph3) 26(39.39%) and Grade 2 (defined in analogous fashionwith regard to standard photographs 2 and 3)25(37.89%) nuclear cataracts. The percentage of gradesshow that Grade 2 and Grade 3 patients presentedalmost in the same ratio. (Table V) While the sub typesof Posterior Sub capsular Cataract (PSC) 142(56.8%)cases, mostly the patients presented in Grade 3 (greaterthan one half of lens circumference) 61(42.96%) andGrade 2 (one fourth to one half of cortical circumference)42(29.57%) cortical cataracts. (Table VI) In our study

most of the respondents observed is having Grade 3and Grade 2 of different types of age related cataractfollowed by Grade 2.While the Grade 1 and Grade 0presented very rarely except in the cortical cataracts.DISCUSSION:

In the present study, it was observed that olderpeople aged between 40 -83 years especially men aremost likely to develop age related cataract which maybe associated to different conditions like DiabetesMellitus and Hypertension etc.The burden of agerelated cataract was higher among the 60 years agegroup and above. Patients with cataract weresignificantly older (58.58 years). There were 52% maleand 48% female with senile cataract out of the 250 casesstudied. According to World Health Organization,cataract is the leading cause of reversible blindness andvisual impairments in more than 17million (47.8%) ofthe 37 million blind individuals worldwide, and thisnumber is projected to reach 40 million by 2020. (WHO2005) and in the Beaver Dam Eye Study (BDES), theprevalence of cataract increases with age It reportedthat 38. 8 % of men and 45.9% of women older than 75years had visually significant cataract. (Klein et al. 1998).

In Pakistan, cataract formation is more commonlyobserved among adult subjects. It is the leading causeof avoidable blindness. The elderly suffer dispro-portionately with a loss of vision from eye diseases. Theelderly are more likely to have ocular disease and suffergreater severity of the disease. Blindness has profoundhuman and socio economic consequences in all societies.

Table – V:Subtypes of Nuclear cataract (N=66)

Grade of Cataract Frequency Percent

Grade 0 3 4.54

Grade 1 12 18.18

Grade 2 25 37.89

Grade 3 26 39.39

Total 66 100.0

Table – VI:Subtypes of Posterior Sub Capsular cataract (N= 142)

Grade of Cataract Frequency Percent

Grade 0 9 6.34

Grade 1 30 21.13

Grade 2 42 29.57

Grade 3 61 42.96

Total 142 100.0

Table – I:Showing gender distribution. Total 250

Gender No of Patients % age

Male 128 51.2%

Female 122 48.8%

Table – II:Presenting Visual acuity of Pts of age related cataracts (N=250)

Presenting VA Frequency Percent

6/24 25 10.0

6/36 32 12.8

6/60 44 17.6

5/60 4 1.6

4/60 6 2.4

3/60 13 5.2

2/60 29 11.6

1/60 30 12.0

HM 44 17.6

PL 23 9.2

Total 250 100.0

Table – IIITypes of cataract (N=250)

Type of cataract Frequency Percentage

Cortical 42 16.8

Nuclear 66 26.4

Post Sub capsular 142 56.8

Total 250 100.0



The costs of lost productivity and of rehabilitation andeducation of the blind constitute a significant economicburden for the individual, the family and society. Thenumber of cataract blind is expected to increasedramatically in coming decades as the number ofelderly in the world’s population increases. In theabsence of more widespread availability of cataractsurgery in the developing world, or the identificationof interventions that retard the development orprogression of cataracts, population projections suggestthat the number of cataract blind could reach close to40 million by the year 2025.16

While cataract blindness is largely a problem inthe developing world, where access to surgicalintervention is often limited, blindness registry datacollected by several US states as recently as 1970suggested that cataracts were the third leading causeof blindness and accounted for about 9 percent of allblindness in the United States. Many changes in cataractmanagement, including an extremely large increase inthe number of cataract operations since 1970, haveapparently reduced the number of cataract blind indeveloped countries.17 How ever, a recently publishedsurvey from East Baltimore indicated that un operatedage-related cataract was the leading cause of blindnessin blacks, accounting for almost one-third of allblindness in this population.18 In the United States, age-related lenticular changes have been reported in 42%of those between the ages of 52 and 64, 19 60% of thosebetween the ages 65 and 74 20 and 91% of those betweenthe ages of 75 and 85.19.Data from the Framingham EyeStudy (FES) indicated that age-related lens changes,ranging from mild early changes (vacuoles, water clefts,spokes and lamellar separations) to later changes(cortical cuneiform opacities, nuclear sclerosis, posteriorsub capsular opacities, aphakia), were present in 42percent of persons aged 52-64.20 The prevalence of thesechanges increased to 91 percent for persons aged 75-85.In the same study, age-related cataract (corticalcuneiform opacities, nuclear sclerosis, posterior subcapsular opacities, or aphakia accompanied by areduction in visual acuity to 6/9 or worse) ranged from4 percent at age 52-64 to 50 percent at age 75-85.21 Eyeexaminations conducted during the 1971-72 NationalHealth and Nutritional Examination Survey (NHANES)showed that approximately 60 percent of persons in theage group 65-74 years had lens opacities.14 Theprevalence of lens opacities causing a decrease in visionto 6/7.5 or worse was 28 percent in persons aged 65-74.Few incidence data are available for age-relatedcataract. Podgor, Leske, and Ederer have used age-specific prevalence data from the Framingham EyeStudy to estimate 5-year incidence rates for lensopacities and cataract.22 For lens opacities, the 5-year

incidence estimates for ages 55, 60, 65, 70, and 75 were10, 16, 23, 31,and 37 percent, respectively. Thebiochemical and structural changes that take placewithin the human crystalline lens have been likened todegenerative processes that occur in other parts of thebody as a consequence of aging.CONCLUSION:

About 50% of all 60-70 years old suffer from acataract requiring surgery. More males are having agerelated cataracts than the females out of the 250 casesstudies. Age related cataracts are mostly presented inGrade 2 and Grade 3 of different types of cataract. Themost common type of cataract in our study populationis Posterior Sub Capsular cataract as shown inTable III, although the cortical cataract is more prevalentin the black African community as discussed else where.The Grade 2 and Grade 3 of the LOCS III classificationis more prevalent in our study, although Grade 0 ofPosterior Sub capsular Cataract is also in age group of60 years and above. This result was consistent with otherstudy elsewhere and support the hypothesis that withthe exception of confounders, cataractogenesis isconnected to the aging process, associated withincreased osmotic and oxidative stress, reducedefficiency of metabolic processes and a decline inantioxidant defenses.REFERENCES:1. Thylefors B.Negrel AD, Pararajasegaram R, Dadzie

KY.Global data on blindness. Bull World Health Organ 1995;73:115-21.

2. Foster A,Resnikoff S(2005).The impact of vision 2020 onglobal blindness.Eye;19:1133-35.

3. Ceklic L, Latinovic S, Aleksic P (2005). Cataract as a leadingcause of visual disability and blindness in the region ofEastern Sarajevo and Eastern Herzegovina. Med Pregl.2005;58:449-52.

4. Melese M, Alemayehu W,Friedlander E,CourtrightP(2004).Indirect costs associated with accessing eye careservices as a barrier to service use in Ethopia. Trop Med IntHealth.2004;9:426-31.

5. De Lima DM, Ventura LO, Brandt CT(2005).Barriers in theaccess to senile cataract treatment at Altino VenturaFoundation. Arq Bras Ophthalmol.2005;68:357-62.

6. Sapkota Y D,Pokarel G P,Dulal S,Byanju R N,Maharjan IM(2004).Barries to uptake cataract surgery in Gandakizone,Nepal.Katmandu Univ Med J(KUMJ).2004;2:103-12.

7. World Health Organization. Data on file. Last accessed: Dec14, 2005.Available at: http://www.who.int/pbd/blindness/vision_2020/ priorities/en/index1.

8. Kanski JJ. Extra capsular cataract extraction in: Lens. ElsevierButterworth-Heinemann. 6th ed.2006: 337-67.

9. Shah SP, Dineen B, Jadoon Z, Bourne R, Khan MA, JohnsonGJ, et al. Lens opacities in adults in Pakistan: prevalence andrisk factors. Ophthalmic epidemiology 2007; 14:381-9.

10. West SK, Munoz B, Schein OD, Duncan DD, Rubin GS. Racialdifferences in lens opacities: the Salisbury Eye Evaluation(SEE) project. Am J Epidemiology. 1998; 148:1033–1039.

11. Leske MC, Connell AM, Wu SY, Hyman L, Schachat A.Prevalence of lens opacities in the Barbados Eye Study. ArchOphthalmol. 1997; 115:105–111.

12. Mitchell P, Cumming RG, Attebo K, Panchapakesan J.



Prevalence of cataract in Australia: the Blue Mountains EyeStudy. Ophthalmology 1997; 104:581–588.

13. Klein BE, Klein R, Ritter LL. Is there evidence of an estrogeneffect on age-related lens opacities? The Beaver Dam EyeStudy. Arch Ophthalmol 1994; 112:85–91.

14. Leske MC, Connell AM, Wu SY, Hyman L, Schachat A.Prevalence of lens opacities in the Barbados Eye Study. ArchOphthalmol 1997; 115:105–111.

15. Klein BE, Klein R, Moss SE. Incident cataract surgery: theBeaver Dam eye study. Ophthalmology 1997; 104:573–580.

16. Kupfer C: Bowman Lecture. The conquest of cataract: Aglobal challenge. Trans Ophthal Soc UK 104:1, 1984.

17. Stark WJ, Sommer A, Smith RE: Changing trends inintraocular lens implantation. Arch Ophthalmol 107:1441,1989.

18. Sommer A, Tielsch JM, Katz J, et al: Racial Differences in the

cause-specific prevalence of blindness in East Baltimore. NEngl J Med 1991;325:1412-1417.

19. Sperduto RD, Seigel D., Seigel D. Sperduto RD (Jul 1980).“Senile lens and senile macular changes in a population-based sample”. Am J Ophthalmol 90 (1): 86–91.PMID 7395962.

20. Kahn HA, Leibowitz HM, Ganley JP, Kini MM, Colton T,Nickerson RS, Dawber TR (Jul 1977). “The Framingham EyeStudy. I. Outline and major prevalence findings”. Am JEpidemiol 106 (1): 17–32. PMID 879158.

21. Kahn HA, Leibowitz HM, Ganley JP, et al: The FraminghamEye Study I. Outline and major prevalence findings. Am JEpidemiology 106:17, 1977

22. Podgor MJ, Leske MC, Ederer F: Incidence estimates for lenschanges, macular changes, open-angle glaucoma and diabeticretinopathy. Am J Epidemiol 118:208-212, 1983.



————————————————————————————————*Siad Anwar Medical Center, Dabgari Garden, Peshawar.————————————————————————————————1.3.4.5. Trainee Medical Officers, HMC, Peshawar, 2. SeniorRegistrar HMC Peshawar————————————————————————————————Correspondence: Dr Zakir Hussain, H.NO: 624, St. No:21, Sector:F-5, Phase 6, Hayatabad, Peshawar. Cell: 0334 9123070 Email:>[email protected]————————————————————————————————Received August ’2012 Accepted Oct’2012————————————————————————————————

Role of Intravitreal Bevacizumabin the Treatment of

Acute Central Serous Chorio-retinopathy*

Zakir Hussain1, Muhammad Tariq Khan2

Hamid ur Rehman2, Ziauddin5

ABSTRACTObjectives: To report the beneficial effect of intravitreal bevacizumab (Avastin) injection in patients with acute centralserous chorio-retinopathy (CSCR).Place and duration of study: The study was carried out at private eye clinic in Said Anwar Medical Center, DabgariGarden, Peshawar from March 2011 to August 2011.Patients and methods: Patients with symptomatic CSCR of less than 6-months duration were prospectively recruitedbetween March 2011 and August 2011. The diagnosis of CSC was established by the presence of serous maculardetachment on fundus examination and fluorescein leak on fundus fluorescein angiography. Patients received only asingle intravitreal injection of bevacizumab (1.25 mg in 0.05 mL), 3.5 mm from the corneal limbus, using a 27-gaugeneedle. The primary outcome of the study was the time measured from baseline to complete absorption of subretinal fluidduring follow-up. Secondary outcome measures included serial changes in the logarithm of the minimum angle of resolution(logMAR) visual acuity and OCT.Results: Fifteen eyes of 15 patients (10 men, 5 women) with CSCR were treated with intravitreal bevacizumab injection.Their age at the time of treatment ranged from 32 to 55 years (mean 43.4). Pretreatment visual acuity ranged from 20/25to 20/100. All patients had complete or nearly complete clinical resolution of macular fluid and had improvement in visualacuity within 1 month after treatment. Mean pretreatment LogMAR visual acuity was 0.32 and improved to 0.04 at 6months’ follow-up, which was statistically significant. No patient lost vision or suffered from any significant complicationsrelated to the treatment.Conclusions: Intravitreal bevacizumab injection for acute central serous chorioretinopathy may result in prompt resolutionof neurosensory detachment and reduction of angiographic leakage. These short-term results suggest that intravitrealbevacizumab injection may constitute a promising therapeutic option in acute central serous chorioretinopathy.Key words: Bevacizumab; Central serous chorioretinopathy.

Original Article

INTRODUCTIONCentral serous chorioretinopathy (CSCR) is one

of the ten most common diseases of the posteriorsegment of the eye, involving serous detachment of theneurosensory retina occurs over an area of leakage fromthe choriocapillaris through the retinal pigmentepithelium (RPE).1 In most of the patients, CSCR is self-limited, and visual prognosis is good. However, in somecases of CSCR, patients develop progressive visual lossdue to persistent serous retinal detachment, cystoidmacular degeneration, or retinal pigment epitheliumdecompensation.2,3 Clinicians usually elect to observepatients with acute CSCR, because these patientsgenerally show self-remission, and standard treatments

like laser photocoagulation or photodynamic therapymay cause complications.4,5 However, patients withacute CSCR often desire more rapid resolution of theirdisease.

The mechanism for the development of CSCRremains unclear. According to one of the hypothesizedmechanisms, abnormalities in choroidal perfusion canbe causative factors in CSCR. Recent indocyanine greenangiography in patients with CSCR has demonstratedevidence of choroidal lobular ischemia and choroidalvenous congestion, and also revealed multiple areas ofchoroidal vascular hyperpermeability in intermediatestages of the study.4 The cause of the venous congestionhas not been determined, but it may be a response toischemia and delayed arterial filling or a consequenceof outflow obstruction. Choroidal hyperpermeability atfoci of subretinal fluorescein leakage is a frequentfinding, but choroidal hyperpermeability can also befound without associated fluorescein leakage,suggesting more generalized retinal pigmentepithelium (RPE) or choroidal vascular disturbance.5

Vascular endothelial growth factor (VEGF) has beenimplicated as the major factor responsible for increased

Dr. Zakir Hussain


vascular permeability.6 Recently, bevacizumab(Avastin), an antibody to VEGF, has been shown to haveanti-permeability properties. Intravitreal injection ofbevacizumab (IVB) has been reported to be associatedwith visual improvement and reduced neurosensorydetachment without adverse events in patients withCSC.7 In this study, we investigated the effect of IVB inpatients with acute CSC.MATERIAL AND METHODS

Patients with symptomatic CSC of less than 6-months duration were prospectively recruited betweenMarch 2011 and August 2011. The diagnosis of CSCRwas established by the presence of serous maculardetachment on fundus examination and fluorescein leakon fundus fluorescein angiography. Patients who hadreceived any previous treatment, includingphotodynamic therapy or focal thermal laserphotocoagulation for CSCR, or who had evidence ofchoroidal neovascularization, polypoidal chorio-vasculopathy, or other maculopathy on clinicalexamination, fluorescein angiography, were excludedfrom the study. Informed consent was obtained fromall subjects. Patients received only a single intravitrealinjection of bevacizumab (1.25 mg in 0.05 mL), 3.5 mmfrom the corneal limbus, using a 27-gauge needle, inthe inferotemporal quadrant under aseptic conditions.Eyes were injected less than one week after diagnosisin our clinic. Each patient underwent clinicalassessments, including best-corrected visual acuitymeasurement in Snellen units, applanation tonometry,fundus examination, fluorescein angiography andoptical coherence tomography (OCT) at baseline.Regarding follow-up, the patients were examined at4-week intervals with slit-lamp biomicroscopy andOCT, and fluorescein angiography was performed atthe discretion of the examiner. No other treatment forCSCR was performed during the study. The primaryoutcome of the study was the time measured frombaseline to complete absorption of subretinal fluidduring follow-up. Secondary outcome measuresincluded serial changes in the logarithm of theminimum angle of resolution (logMAR) visual acuityand OCT. Statistical analyses were performed using acommercially available statistical software package(SPSS).RESULTS:

Fifteen eyes of 15 patients (10 men, 5 women) withCSC were treated with intravitreal bevacizumabinjection. Their age at the time of treatment ranged from32 to 55 years (mean 43.4). Pretreatment visual acuityranged from 20/25 to 20/100. All patients had recentexacerbation of visual changes before receivingtreatment and none of them had received othertreatments before. All patients had one or more focal

RPE leaks responsible for the neurosensory detachment,and these serous detachments of the central maculawere confirmed by OCT. All patients had complete ornearly complete anatomic resolution of macular fluidand had improvement in visual acuity within 1 monthafter treatment. Mean pretreatment LogMAR visualacuity was 0.32 and improved to 0.04 at 6 months’follow-up, which was statistically significant. No patientlost vision or suffered from any significantcomplications related to the treatment Table 1.DISCUSSION:

Typical acute CSCR is characterized by durationof symptoms and/or retinal detachment of less than 6months and monofocal or paucifocal fluoresceinangiographic retinal pigment epithelium leakage.5,8 Thetreatment of CSCR is based largely on observation. Thehigh spontaneous remission rate favors conservativemanagement, lifestyle counseling, and discontinuationof glucocorticoid medication as first-line therapeuticoptions. But there is some evidence supporting thebenefit of early treatment for CSCR. A potential benefitfor early resolution may be mediated by a lower rate ofRPE degeneration in the treated eye,9,10 which is alsowarranted because of an uncertain relation between theonset of detachment and that of symptoms11 and specialoccupational demands for binocular visional function.Although there is no definite evidence about earlytreatment for CSC, many retinal specialists tend toconsider laser photocoagulation, PDT with verteporfinand some medical treatment as early treatment.9,12,13

Table I

S. Age Gender Eye Episode duration VA beforeNo before treatment treatment

1 47 M Right 1 month 20/40

2 52 M Left 2 weeks 20/30

3 54 F Right 2 months 20/60

4 45 M Right 3 weeks 20/30

5 35 F Right 2 months 20/25

6 42 F Left 1 month 20/100


8 42 M Left 1 month 20/40

9 46 M Left 2 months 20/100

10 43 M Left 1 month 20/25

11 40 F Right 1 month 20/50


13 51 M Right 4 months 20/30

14 48 F Left 2 months 20/40

15 32 M Right 1 week 20/40

Role of Intravitreal Bevacizumab in the Treatment of Acute Central Serous Chorio-retinopathy


Laser photocoagulation and PDT with verteporfinaccelerate the resolution of detachment, 13-20 but theyshould be used with caution because they can inducepermanent damage to the RPE or choriocapillary, severeinjury to retina, subretinal choroidal neovascularization,often many years after the primary incident .21,22

One experimental study showed that PDT withverteporfin resulted in morphologic and functionalbreakdown of the outer blood-retinal barrier andfunction of RPE or RPE cells themselves with increasingconcentration of verteporfin .23

Vascular endothelial growth factor has profoundeffects on vascular permeability. Bevacizumab is a full-length antibody that binds all isoforms of VEGF. Agrowing number of reports in the literature support itssafety and efficacy in many disorders. The mechanismby which intravitreal bevacizumab therapy amelioratesRPE leak and resorption of subretinal fluid in CSCR isunknown. But indocyanine green angiography inpatients with CSCR has demonstrated evidence ofchoroidal lobular ischemia, choroidal venouscongestion 24-26 and also multiple areas of choroidalvascular hyperpermeability, suggesting a moregeneralized RPE or choroidal vascular disturbance.27-33

Choroidal ischemia in CSC may induce an increase inthe concentration of VEGF. The reduction of VEGFconcentration may have the desired effect in patientswith CSCR, with breaking the chain of events leadingto neurosensory detachment.

In this small case series, we demonstrated thatintravitreal bevacizumab injection in patients withCSCR can bring on rapid resorption of subretinal fluid,which can be associated with rapidly improved vision.This result provided the basis for the current study andprompted further exploration of the treatment.

Although this case series demonstrated successfultreatment of acute CSCR and none of the patientsexperienced a significant adverse event with intravitrealbevacizumab injection, it is limited by small number ofpatients and short follow-up. Furthermore, individualswith CSCR may experience spontaneous resolution oftheir symptoms and leakage; our lack of a control groupalso does not allow one to determine if the resolutionof the serous detachment and RPE leaks in our caseswas actually a result of treatment or was due to thenatural resolution of the disease. But the temporalcourse suggests that the improvement is likely due tothe intravitreal bevacizumab injection. These results arepromising. We also need to make further investigationsinto the possible role of VEGF in the pathogenesis ofCSCR and treatment of CSCR with anti-VEGF agentsto understand more precisely the risk and benefit ofthe therapy for patients with CSCR.CONCLUSION:

Intravitreal bevacizumab injection for acutecentral serous chorioretinopathy may result in promptresolution of neurosensory detachment and reductionof angiographic leakage. These short-term resultssuggest that intravitreal bevacizumab injection mayconstitute a promising therapeutic option in acutecentral serous chorioretinopathy.REFERENCES:1. Gass JD. Pathogenesis of disciform detachment of

neuroepithelium: II. Idiopathic central serous choroidopathy.Am J Ophthalmol 1967;63:587–615.

2. Levine R, Brucker AJ, Robinson F. Long-term follow-up ofidiopathic central serous chorioretinopathy by fluoresceinangiography. Ophthalmology 1989;96:854–9.

3. Loo RH, Scott IU, Flynn HW Jr, et al. Factors associated withreduced visual acuity during long-term follow-up of patientswith idiopathic central serous chorioretinopathy. Retina2002;22:19–24.

4. Chan WM, Lai TY, Lai RY, et al. Half-dose verteporfinphotodynamic therapy for acute central serouschorioretinopathy: one-year results of a randomizedcontrolled trial. Ophthalmology 2008;115:1756–165.

5. Wang M, Munch IC, Hasler PW, et al. Central serouschorioretinopathy. Acta Ophthalmol 2008;86:126–45.

6. Tolentino MJ, McLeod DS, Taomoto M, et al. Pathologicfeatures of vascular endothelial growth factor-inducedretinopathy in the nonhuman primate. Am J Ophthalmol2002;133:373–85.

7. Torres-Soriano ME, Garcia-Aguirre G, Kon-Jara V, et al. Apilot study of intravitreal bevacizumab for the treatment ofcentral serous chorioretinopathy (case reports). Graefes ArchClin Exp Ophthalmol 2008;246:1235–9.

8. Eandi CM, Ober M, Iranmanesh R, et al. Acute central serouschorioretinopathy and fundus autofluorescence. Retina2005;25:989–93.

9. Wang MS, Sander B, Larsen M: Retinal atrophy in idiopathiccentral serous chorioretinopathy. Am J Ophthalmol2002;133:787–93.

10. Fuhrmeister H: A long-term study of morphological andfunctional developments after central serous chorioretinitis.Klin Monatsbl Augenheilkd 1983;182:549–51.

11. Wang M, Sander B, la Cour M, Larsen M: Clinicalcharacteristics of subretinal deposits in central serouschorioretinopathy. Acta Ophthalmol Scand 2005;83:691–96.

12. Ober MD, Yannuzzi LA, Do DV, et al: Photodynamic therapyfor focal retinal pigment epithelial leaks secondary to centralserous chorioretinopathy. Ophthalmology 2005;112:2088–94.

13. Pikkel J, Beiran I, Ophir A, Miler B: Acetazolamide for centralserous retinopathy. Ophthalmology 2002;109:1723–25.

14. Burumcek E, Mudun A, Karacorlu S, et al: Laserphotocoagulation for persistent central serous retinopathy:results of long-term follow-up. Ophthalmology 1997;104:616–22.

15. Canakis C, Conway MD, Livir-Rallatos C, et al: Ocularphotodynamic therapy in choroidal neovascularizationcomplicating idiopathic central serous chorioretinopathy.Ophthalmic Surg Lasers Imaging 2004;35:168–71.

16. Canakis C, Livir-Rallatos C, Panayiotis Z, et al: Ocularphotodynamic therapy for serous macular detachment in thediffuse retinal pigment epitheliopathy variant of idiopathiccentral serous chorioretinopathy. Am J Ophthalmol2003;136:750–2.

17. Cardillo Piccolino F, Eandi CM, Ventre L, Rigault de laLongrais RC, Grignolo FM: Photodynamic therapy forchronic central serous chorioretinopathy. Retina 2003;23:752–



63. 18. Valmaggia C, Niederberger H: Photodynamic therapy in the

treatment of chronic central serous chorioretinopathy. KlinMonatsbl Augenheilkd 2006;223:372–5.

19. Chan WM, Lam DS, Lai TY, et al: Treatment of choroidalneovascularization in central serous chorioretinopathy byphotodynamic therapy with verteporfin. Am J Ophthalmol2003;136:836–45.

20. Yannuzzi LA, Slakter JS, Gross NE, et al: Indocyanine greenangiography-guided photodynamic therapy for treatment ofchronic central serous chorioretinopathy: a pilot study. Retina2003;23:288–98.

21. Penha FM, Aggio FB, Bonomo PP: Severe retinal thermalinjury after indocyanine green-mediated photothrombosis forcentral serous chorioretinopathy. Am J Ophthalmol2007;143:887–9.

22. Kanyange ML, De Laey JJ: Long-term follow-up of centralserous chorioretinopathy (CSCR). Bull Soc Belge Ophtalmol2002;284:39–44.

23. Mennel S, Peter S, Meyer CH, et al: Effect of photodynamictherapy on the function of the outer blood-retinal barrier inan in vitro model. Graefes Arch Clin Exp Ophthalmol2006;244:1015–21.

24. Hayashi K, Hasegawa Y, Tokoro T: Indocyanine greenangiography of central serous chorioretinopathy. IntOphthalmol 1986;9:37–41.

25. Prünte C: Indocyanine green angiography findings in central

serous chorioretinopathy. Int Ophthalmol 1995;19:77–82.26. Prünte C, Flammer J: Choroidal capillary and venous

congestion in central serous chorioretinopathy. Am JOphthalmol 1996;121:26–34.

27. Stanga PE, Lim JI, Hamilton P: Indocyanine greenangiography in chorioretinal diseases: indications andinterpretation: an evidence-based update. Ophthalmology2003;110:15

28. Piccolino FC, Borgia L: Central serous chorioretinopathy andindocyanine green angiography. Retina 1994;14:231–42.

29. Piccolino FC, Borgia L, Zinicola E, Zingirian M: Indocyaninegreen angiographic findings in central serouschorioretinopathy. Eye 1995;9:324–32.

30. Slakter JS, Yannuzzi LA, Guyer DR, Sorenson JA, Orlock DA:Indocyanine-green angiography. Curr Opin Ophthalmol1995;6:25–32.

31. Spaide RF, Hall L, Haas A, Campeas L, Yannuzzi LA, FisherYL, Guyer DR, Slakter JS, Sorenson JA, Orlock DA:Indocyanine green videoangiography of older patients withcentral serous chorioretinopathy. Retina 1996;16:203–13.

32. Yuzawa M, Kawamura A, Yamaguchi C, Shouda M, ShimojiM, Matsui M: Indocyanine green videoangiographic findingsin detachment of the retinal pigment epithelium.Ophthalmology 1995;102:622–9.

33. Guyer DR, Yannuzzi LA, Slakter JS, et al: Digital indocyaninegreen videoangiography of central serous chorioretinopathy.Arch Ophthalmol 1994;112:1057–62.



————————————————————————————————1Registrar Eye A ward, Department of Ophthalmology, KhyberTeaching Hospital, Peshawar, 2Assistant Professor, Khalifa GulNawaz Hospital, Bannu(BMC), 3Medical Officer, Department ofOphthalmology Khalifa Gul Nawaz Hospital, Bannu, 4Senior RegistrarEye A Ward, Khyber Teaching Hospital,Peshawar————————————————————————————————Correspondence: Dr. Saber Muhammad, 13 New Flat, DoctorColony, Khyber Teaching Hospital, PeshawarEmail- [email protected] Tel No. 0346-9155303————————————————————————————————Received Oct’2012 Accepted: Nov’2012————————————————————————————————

Comparison of Frequency of Recurrenceafter Surgery for Primary Pterygium

using free Conjunctival Autograft Transplantation &Bare Scleral Technique

Saber Mohammad,FCPS1, Sanaullah Khan, FCPS,2 Hussain Ahmad, MBBS,3

Zaman Shah, FCPS4

ABSTRACT:Purpose: The main objective of this study was to compare the frequency of recurrence of Pterygium after surgery withfree conjunctival autograft transplantation and bare scleral technique.Materials and Methods: All patients were admitted to the Eye “A” unit of KTH Peshawar. They were all having primaryPterygium. Patients were selected on the basis of inclusion and exclusion criteria and details were recorded on predeveloped proforma. We divided patients into two groups. Group A and group B. Equal number of patients (41) wereincluded in each group randomly on the basis of lottery method. We applied bare sclera technique on group A and freeconjunctival autograft on group B. All patients were operated under sub conjunctival anesthesia. Patients were followed at1 week, 3 months & 6 months, and were examined for recurrence and any other complications. All surgeries were performedby one surgeon.Results: Total number of patients were 82 (41 for each group), Fifty five (67%) were male and 27(33%) were female. Theage of the patients ranged from 20-50 years. Occupations wise 30 (36.6%) were farmers, 20 (24.4%) fell in labors, 15(18.3%) were students, 11 (13.4%) housewives and 6 (7.3%) were teachers.The mean age and Standard Deviation (SD) in Group A and Group B are,32.78±7.62 and 34.12±6.21 respectively. In ourstudy right eye was involved in 60 cases (73.2%) and left eye in 22 patients (26.8%).In Group A, right eye involved in 26(31.7%) cases while left eye involved in 15 (18.3%) cases. In Group B, right eye involved in 34 (41.5%) cases while Lefteye in 7 (8.5%) cases. Regarding the type of pterygium 51 (62.2%) were type II, and 31 (37.8%) patient presented werein type III. 39.02% recurrence was noted in group A and 12.9% recurrence was noted in group B. P value is 0.0054 highlysignificant.Conclusion: It is concluded that free conjunctival autograft transplantation is the better technique, for prevention ofrecurrence after Pterygium surgery. It is associated with low recurrence rate, minimal complications and cosmeticallyacceptable as compared to the bare sclera technique. However, this technique is not recommended in eye with scarredconjunctiva or if the conjunctiva has to be preserved for future glaucoma filtering surgery.Key Words: Pterygium , conjunctival autograft transplantation(CAT), bare sclera technique.(BST)

Original Article

Dr Saber

INTRODUCTIONPterygium is a fibrovascular growth of

degenerative bulbar conjunctiva over the limbus ontothe cornea.1 It is mostly on nasal side and is morefrequent in areas with more ultraviolet radiation in hot,dry, windy, dusty and smoky environments.2

Ultraviolet radiations A and B are most important inits pathogenesis3 It has got a broad base on nasal (morecommon) or temporal epibulbar surface and an apexon the cornea. A gray zone precedes the apex or head

and is generally known as the “cap”. The cap is a flat,grayish white avascular zone located in thesubepithelial corneal tissue, surrounding the head ofthe pterygium like a halo4.

In some cases of pterygium, a golden yellow ironline_ “the Stocker’s line” is seen in the cornealepithelium adjacent to the head.4 The head is an elevatedstructure which is firmly attached to the globe; whereasbody of pterygium can be easily lifted from theepibulbar surface. The body is a fleshy, highlyvascularized tissue that is delineated from normalconjunctiva both superiorly and inferiorly by sharpfolds. The epithelial surface of the body and corneaimmediately in front of the head may show punctatestaining. Corneal dellen formation may occur inassociation with pterygia.5

The growth of pterygium across the cornea is aslow process and it usually takes several years to reachthe visual axis. Progressive pterygium is characterizedby a fleshy and congested appearance, whereasregression or inactivation is characterized by the


absence of episodic congestion, disappearance ofpunctate staining over the body and shrinkage of thecap.6 The lesion may remain stationary for several yearsand finally involution occurs. The head gets flattenedand thinned out leaving behind a scar that blends withadjacent cornea and the body gets changed into amembrane-like structure with few fine blood vessels.Its incidence varies across geographical locations.7

Pterygium is a common disease in tropical andsubtropical countries including Pakistan.2 Pterygiumhas three types. Type I , which extends less than 2mmonto the cornea. The lesion is often asymptomatic. TypeII , which Involves upto 4mm of cornea and may beprimary or recurrent following Surgery. It may interferewith precorneal tear film and induce astigmatism. TypeIII , Invade more than 4mm of cornea and involve visualaxis.1 The clinical features include chronic irritation,conjunctivitis, reduced vision and cosmetic concern.8

The indications for surgery include:1. Reduced vision due to direct involvement of the

visual axis or due to astigmatism,9

2. Chronic irritation,3. Recurrent inflammation,4. Restriction of ocular motility, and5. Cosmesis.

To prevent recurrence, several adjunctivetherapies, including the use of beta irradiation andMitomycin C, have been recommended due to theiranti-fibrotic and anti-angiogenic properties but theyhave serious side effects2. .There are several techniquesused for pterygium surgery. The simplest one is barescleral technique but it has high recurrence frequencyi.e. 38.09%10. Amniotic membrane and buccal mucosalgrafts are also used for the treatment of pterygium butthey are time consuming procedures and needssurgically skilled hands2 .The procedure which gainedpopularity in recent years for pterygium is freeconjunctival autograft transplantation. It is simple, safeand highly effective with low recurrence i.e. 13.3%11 .Inthis procedure ipsilateral bulbar conjunctiva fromsuperotemporal quadrant is removed and free graftedonto episcleral bed of excised pterygium.12Differencesin study methodology, patient characteristics, natureof pterygium, geographic area, definition of recurrenceand duration of follow-up are some of the factorsresponsible for difference in the recurrence frequencies.

As the pterygium is very common in our countryand the surgery is demanding, we decided to gaininformation about the frequency of recurrence ofpterygium after excision with bare sclera technique ascompared to free conjunctival autograft.MATERIAL AND METHODS

This study was conducted from December 2010to September 2011 at the Department of

Ophthalmology, Khyber Teaching Hospital Peshawar.A total of 82 patients meeting eligibility criteria withprimary Pterygium were enrolled. After enrollmentcomplete ocular examination was done. Before theirallocation into groups, the procedure was fullyexplained to the patients informing them that they couldbe allocated into either of the two groups. An informedconsent was obtained from them for the surgery.

We divided patients into two groups. Group Aand group B. Equal number of patients 41 were includedin each group randomly on the basis of lottery method.We applied bare sclera technique on group A and freeconjunctival autograft on group B. Fifty five were maleand 27 were female. Patients’ age ranged from 20-50years in each group.

All variables were noted from all patients andentered into typed proforma. All the procedures wereperformed in eye department Operation theatre underoperating microscope by the same surgeon. The ocularsurface was anesthetized with topical instillation ofproparacaine hydrochloride 0.5% in combination withan additional subconjunctival injection in the bed ofPterygium with 0.5ml of 2% lidocaine hydrochloridewith 0.001% adrenaline in all patients and 0.5ml at thedonor site in free conjunctival autograft. First head ofpterygium was excised from the cornea with BardParker No 15. blade and then cut it with scissor 2-3mmaway from the limbus. Then cornea was shaved.

In free conjunctival autograft, bare sclera wasmeasured with caliper.Haemostasis was achieved. Theglobe was rotated downward using stay sutures toexpose the superotemporal bulbar conjunctiva. Themeasured dimensions were marked on exposedconjunctiva. Saline solution was injected underconjunctiva to facilitate the sole dissection ofconjunctiva. Dissection began from fornix to limbus. Thegraft was flipped over onto the cornea and tenon’sattachment at limbus was meticulously dissected. Theflap was then excised and moved onto the bare scleraand stitched with 8/0 virgin silk to the conjunctiva.

Post operatively topical corticosteroid- antibioticointment was used and a pressure patch applied for 24hours. Antibiotic-steroid drops were administered 4times a day and tapered during the following 2-3months. After 1 week, follow up was done. Recurrenceand other complications were noted. Patients wereadvised for next visit after three months and then aftersix months from the date of surgery. Data was analyzeson SPSS version 11.RESULTS

We analyzed the data for 82 patients. Fifty five(67%) were male and 27(33%) were female. The age ofthe patients ranged from 20-50 years. Patients wereequally divided into two groups, group A and group

Comparison of Frequency of Recurrence after Surgery for Primary Pterygium


B. Shown in table II.In group A , patients underwent pterygium

excision with bare sclera technique while in group B,pterygium excision with free conjunctival autografttransplantation.

Patients’ data was analyzed for the mainparameters of the study such as age, sex, frequency ofrecurrence and occupation. The quantitative variable,age was analyzed for mean and standard deviation andwe found that mean age was 33.45 and SD is ±6.94.Themean age and SD in Group A and Group B are,32.78±7.62 and 34.12±6.21 respectively. It is shown intable I. Regarding the Type of pterygium 51 (62.2%)were type II , and 31 (37.8%) patient presented were intype III. Twenty nine (35.4%) patients in group A, whounderwent bare sclera technique and 22 (26.8%) ingroup B, who had free conjunctival autograft presentedas type-II pterygium. Ten (34.5%) patients hadrecurrence in group A while no patient had recurrencein group B. P-Value is 0.0021 which is statistically verysignificant.

In patients with type III pterygium, out of 31patients 12 (14.6%) were in group A while 19 (23.2%)were in group B. Recurrence occurred in 6 (50%) patientin group A and 5 case (26.3%) in group B. (P-Value was0.1795, which is not statistically significant). The resultsare shown in table no III. In our study right eye wasinvolved in 60 cases (73.2%) and left eye in 22 patients(26.8%).In Group A , right eye involved in 26 (31.7%)cases while left eye involved in 15 (18.3%) cases. InGroup B, right eye involved in 34 (41.5%) cases whileLeft eye in 7 (8.5%) cases. In our study age range in 55male patients was 20 to 50 years. Out of ten patients in

group A with age rang 20-30 years 3 (30%) hadrecurrence while in group B, 1 case (12.5%) out of 8 (PValue=0.3749).Age class of 31 to 40 years, out of 12patients 5 (41.66%) had recurrence in group A while ingroup B, 2 (16.66%) out of 12 had recurrence (P value=0.1779). In age range 41-50 years male patient in groupA, 2 (40%) out of 5 had recurrence, while 1(12.5%) outof 8 patients in group B suffered recurrence (Pvalue=0.2522).

There were 27 female patients. In group A, 1 (25%)patient out of 4 had recurrence while no patient sufferedrecurrence in group B in age group 20-30 years female(P-Value =0.4386). In 31-40 years, 4 (50%) out of 8 hadrecurrence in group A while 1 (10%) out of 10 patientssuffered recurrence in group B (P-value = 0.0597). In41-50 years, 1 (50%) out of 2 patients in group A hadrecurrence while no such recurrence in group Boccurred. (P-Value = 0.3865).

Occupations wise 30 (36.6%) were farmers, 20(24.4%) fell in labors, 15 (18.3%) were students, 11(13.4%) housewives and 6 (7.3%) were teachers.18 (22%)were in group A and 12 (14.6%) were in group B infarmer group. In this group recurrence frequency was8 (44.4%) out of 18 patients in group A while it was 2(16.7%) out of 12 patients in group B. The P-Value is0.1138 which is not statistically significant. In 20laborers, 12 (14.6%) were in group A and 8 (9.8%) werein group B who underwent bare sclera technique andfree conjunctival autograft technique respectively. Therecurrence frequency in laborers was 5 (41.7%) in groupA and 3 (37.5%) in group B. P-Value is 0.8522 which isstatistically insignificant. Similarly in 15 students, 4(4.9%) were in group A while 11(13.4%) were ingroup B. The recurrence frequency in group A was2(50%) while there was no recurrence in group B. P-Value is 0.0118 which is statistically significant.

Six patients were teachers, 2(2.4%) in group A and4(4.9%) in group B. Recurrence occurred only in groupA which was 1(50%) patient. P-Value is 0.1213 which is

TABLE NO. I (b)Mean and standard deviation of age

N Minimum Maximum Mean Std.Deviation

Age of patients 82 20 47 33.45 6.94

Group A 41 20 47 32.78 7.62

Group B 41 21 46 34.12 6.21

TABLE I (a)

TABLE II



not statistically significant.As compare to laborers, farmers, students and

teachers, house wives had no recurrence for any surgicaltechniques. All these results are shown in table IV. Twoseparate surgical techniques were performed for groupA & B. In group A, where bare sclera technique wasapplied recurrence was in 16 patients (39.02%). Ingroups B where free conjunctival autograft was done,recurrence was noted in 5 cases (12.2%).P valuecalculated by chi-square test (7.746), is 0.0054, which ishighly statistically significant showing high recurrencefrequency in Group A. It is shown in table V.DISCUSSION

Pterygium is one of the most common disordersin tropical and subtropical regions including Pakistan.2

The most important risk factor is exposure to sunlight.13

It affects the visual acuity either by directly affectingthe visual axis or by producing changes in the cornealcurvature.14

In our study maximum number of patients werefarmers 30 (36.6%) and laborers 20 (24.4%), who had towork outside for long periods of time and were exposedto hazardous effects of the infrared and ultravioletradiations present in the sunlight.

In this study there was significant associationbetween pterygium and UV-rays. According to Khoo –Jet al15 there was high association between the out door

TABLE NO. IIITypes of pterygium and recurrence in group A & group B

S.No Type of Group A Recurrence Group B Recurrence P ValuePterygium

1 Type-II 29 (35.4%) 10(34.5%) 22(26.8%) Nil 0.0021*

2 Type-III 12 (14.6%) 6 (50%) 19 (23.2%) 5 (26.3%) 0.1795

*Statistically significantGroup A = Bare sclera technique (BST)Group B = Free conjunctival autograft (FCA)

TABLE NO. IVOccupation wise distributions and recurrence of the patients

in group A & group B

S.No Occupation Group A Recurrence Group B Recurrence P-Value

1 Farmers 18 (22%) 8 (44.4%) 12 (14.6) 2 (16.7%) 0.1138

2 Laborers 12 (14.6%) 5 (41.7%) 8 (9.8%) 3 (37.5%) 0.8522

3 Students 4 (4.9%) 2 (50%) 11 (13.4) Nil 0.0118

4 Housewives 5 (6.1%) Nil 6 (7.3%) Nil

5 Teachers 2 (2.4%) 1 (50%) 4 (4.9%) Nil 0.1213Group A = Bare sclera techniqueGroup B = Free conjunctival autograft

work and pterygium which may be related to highexposure to sunlight and dust. The same idea wassupported by Wilder et al 16 and Threfall –TJ.13 McCartyCA also documented that pterygium was a significantpublic health problem in rural areas primarily as a resultof ocular sun exposure.17

There are multiple surgical techniques to treatpterygium but recurrence is common. Adjunctivetreatment after bare sclera excision with β-irradiationreduced recurrence frequency to as low as 0.5%-16%16,but was associated with significant complications likescleral necrosis. 18 The use of Mitomycin C was alsoassociated with complications such as secondaryglaucoma, corneal edema, iritis, corneal perforation,endophthalmitis and cataract. We performed pterygiumexcision with two different techniques and comparedthe results. 19 Bare sclera technique is easiest methodbut recurrence frequency ranging from 30-82%20 andassociated with high rate of complications. In our studyrecurrence frequency after this technique was 39.02%.Conjunctival autograft is a time consuming procedureand need surgical skill, recurrence frequency reportedfrom 0-13.3%11 and less complications. In our studyfrequency was 12.9%. This study showed that freeconjunctival autograft was superior to bare scleratechnique, P-Value=0.0054 which is highly statisticallysignificant.



TABLE NO.VRecurrence of pterygium in bare sclera technique

and free conjunctival autograft

S. Surgical Total no of No of %No. procedure patients recurrence age

1 Bare sclera 41 16 39.02%

technique

2 Free conjunctival 41 5 12.9%

autograftChi-square test = 7.746P-Value = 0.0054 (Highly statistically significant)

The result of bare sclera technique was favoredby Ashaye who gave 40% recurrence frequency.21

Another study done by Dash and Bapori who observed25% recurrence frequency.22 Stark et al reported 30-70%23 and Singh et al showed 73% recurrencefrequency.24

These variations may be due to occupation of thepatient, morphology of pterygium and number ofpatients studied. There are few complications whichcan occur with bare scleral technique like scleralnecrosis, conjunctival cyst formation, symblepharonand tenon granuloma. The cause being abnormalexposure of tenon tissues without adequate cover byconjunctival tissue or the incarceration of tenon in theconjunctival wound. Cameron also noted thesecomplications.25 Conjunctival autograft is cosmeticallyacceptable technique and related to no recurrence orlow recurrence frequency.

This is due to transplantation of normalconjunctiva that forms barrier to the proliferation andadvancement of residual abnormal tissues towards thelimbus.7 The recurrence frequency has been reportedfrom 0-13.3%.11 A study by Hille K et al noted recurrencefrequency of 12.2%26 after pterygium excision with freeconjunctival autograft. These results are similar to ourstudy (12.9%). Other study done by Kenyon et al notedrecurrence frequency 5.3% after pterygium excisionwith conjunctival autograft.27 Study conducted byFigueriredo et al observed a low recurrence afterpterygium excision with Free Conjunctival Autograft28

(They did not define low recurrence). Study by Frau29

on the treatment of pterygium with free conjunctivalautograft noted no recurrence. While Chaidaroon noted5% of recurrence of pterygium treated with freeconjunctival autograft.30 Study done by Kmiha et al 31,noted 10% recurrence frequency. Mejia noted 1.8%recurrence frequency with free conjunctival autograft.12

Tan & De Keizer noted 2% and 6.6% recurrencefrequency after free conjunctival autograft.32,33

Recently,Prabhasawat et al used amniotic membrane

graft as an alternative to conjunctival autograft but withrecurrence of 10.9% for primary pterygium and 37.5%for recurrent pterygium as compared to 2.6% and 9.1%of conjunctival autograft. 34 These variations may be dueto sample size and geographic variations.

No intraoperative complications were noted in ourstudy. Post operative complications can occur like, graftedema and hemorrhage, graft retraction, subtenongranuloma in the superotemporal region. Conjunctivalautograft have successful results and are widelyaccepted in the management of pterygium. Howeverthis technique cannot be used in eyes in whichconjunctiva is already scarred from previous surgeryor if the conjunctiva has to preserved for futureglaucoma filtering surgery. In our study the freeconjunctival autograft technique was found superior tobare sclera technique as the recurrence frequency wasstatistically low (12.9%vs 39.02% P-Value =0.0054). Inconclusion, this is safe technique, have low recurrenceand cosmetically acceptable.CONCLUSION

It is concluded that free conjunctival autografttransplantation is more effective associated with lesscomplication then bare sclera technique (P-value=0.0054). All pterygium excision should be donewith free conjunctival autograft transplantation.REFERENCES1. Kanski JJ. Conjunctiva. In: Kanski JJ(edi). Clinical

ophthalmology. A systemic approach. 6th Ed. Edinburgh:Butterworth Heinemann 2006; 215-45.

2. Narsani AK, Jatoi SM, Dabir SA. Results of conjunctivalautograft for primary and recurrent pterygium atHyderabad.Pak J Ophthalmol 2006; 22:170-3.

3. Baig MSA,Khokar AR,Ali MA,Khan MS,AhmedI.Conjunctival autograft for primary and recurrentpterygium.Pak J Surg 2008;24:173-6

4. Gupta, Tandon R, Vajpayee RB. Disorders of conjunctiva. In:Textbook of ophthalmology vol-2. Lids, adnexa and orbitexternal eye diseases cornea and refractive surgery 1st Ed.New Delhi: Japee Brothers; 2002; 838-9.

5. Alpar JJ. Treatment of pterygium in 8th Afro Asian congressof Ophthalmology Lahore. Pakistan, 1984, Wajidalis LtdLahore, 1984; 141-7.

6. Chatter Jee’s BM. Anatomy and disease of the conjunctiva.In: Handbook of Ophthalmology. 6th Ed. New Delhi: CBS;1997; 41-84.

7. Doughman DJ. In discussion: Kenyon KR, Weagoner MD,Hettinger ME. Conjunctival autograft transplantation foradvanced and recurrent pterygium. Ophthalmology 1985:1470-73.

8. Srinivasan S,Dallen M,MacAllen P,Berger Y,RootmanDS,Solmovic AR et al.Fibrin glue versus sutures for attachingthe conjunctival autograft in pterygium surgery; aprospective observer masked clinical trial.Br J Ophthalmol2009;93:215-8.

9. Ashaye AO. Refractive astigmatism and pterygium. J FrOphthalmol 2001; 24: 729-32.

10. Alpay A, Ugurbas SH, Erdogan B.Comparing techniques forpterygium surgery.Clin Ophthalmol 2009; 3:69-74.

11. Fahmi MS, Sayed J, Ali M. After removal of pterygium roleof mitomycin and conjunctival autograft.Ann Abbasi



Shaheed Hosp.Karachi Med Dent Coll 2005; 10:757-61.12. Mejia LF, Sanchez JG, Escobar H.Management of primary

pterygia using free conjunctival and limbal-conjunctivalautografts without antimetabolites. Cornea 2005; 24:972-5.

13. Threfall TJ, English DR. Sun exposure and pterygium of theeye: a dose- response curve. Am J Ophthalmol 1998; 128:280-87.

14. Holladay JT, Lewis JW, Allison ME et al. Pterygia as a causeof post cataract with the rule astigmatism. Am Intraocularimplant Soc J 1985; 11: 176.

15. Khoo J, Saw SM, Banerjee K, Chia SE, Tan D, Int Ophthalmol,1998; 22: 293-98.

16. Wilder RB, Buatti JM, Kittelson JM, et al. Pterygium treatedwith excision and postoperative beta irradiation. Int J RadiatOncol Biol Phys 1992; 23: 533-37.

17. Mc Carty CA, FU-CL, Taylor HR. Br J Ophthalmol 2000; 84:289-92.

18. Mackenzie FD, Hirst LW, Kynaston B et al. Recurrence rateand complications after beta irradiation for pterygia.Ophthalmology1991; 98: 1776-81.

19. Rubinfeld RS, Pfister RR, Stein RM, et al. Seriouscomplications of topical mitomycin C after pterygiumsurgery. Ophthalmology 1992; 99: 1647-54.

20. Lewallen S. A randomized trail of conjunctival autograftingfor pterygium in the tropics. Ophthalmology 1989; 96: 1612-14.

21. Ashye AO. Pterygium in Ibadan west afr-J. Med 1991; 10:232-43.

22. Dash RG, Bopari MS. Pterygium evaluation of management.Indian J Ophthalmol 1986; 34:7-10.

23. Stark T, Kenyon KR, Serrano F. Conjunctival autograft forprimary and recurrent pterygia: surgical technique andproblem management. Cornea 1991; 10: 196-202.

24. Singh G,Wilson MR,Foster CS.Longterm followup study ofmitomycin eye drops as adjunctive treatment of pterygia and

its comparison with conjunctival autograft transplantation.Cornea 1990; 9:331-34.

25. Cameron ME. Pterygium throughout the worlds. Spring fieldIII, Thomas, 1965; 141-71.

26. Hille K, Hon H, Gross A, Ruprecht KW. Prospective studyof surgical therapy of pterygium: bare sclera technique vs.free conjunctiva – limbus transplant. Ophthalmology 1996;93: 224 – 6.

27. Kenyon KR,Wagoner MD,Hettinger ME.Conjunctivalautograft transplantation for advanced and recurrentpterygium.Ophthalmology 1985;92:1461-70

28. Figueiredo RS, Cohen EJ, Gomes JAP, et al. Conjunctivalautograft for pterygium surgery: how well dose at preventrecurrence? Ophthalmic Surg Lasers 1997; 28:99-104.

29. Frau E, Labetoulle M, Lautier-Frau M, Hutchinson S, OffretH. Corneo-conjunctival autograft transplantation forpterygium surgery. Acta Ophthalmol 2004; 82: 59-63.

30. Chaidaroon W, Wattananikorn S. Conjunctival autografttransplantation for primary pterygium. Cornea 2003; 22: 763.

31. Kmiha N, Kamoun B, Trigui B, Fourati M, Chaabouni M.Effectiveness of conjunctival autograft transplantation andpterygium surgery. J Fr Ophthalmol 2001; 24: 729-32.

32. Tan DTH, Chee SP, Dear KBG, et al. Effect of pterygiummorphology on pterygium recurrence in a controlled trialcomparing conjunctival autografting with bare sclera. ArchOphthalmol. 1997; 115: 1235-40.

33. De Keizer RJ. Pterygium excision with free conjunctivalautograft versus postoperative strontium 90 beta irradiation.J Fr Ophthalmol 2001; 86: 111-15.

34. Prabhasawat P,Barton K,Burkett G,Tseng SC.Comparision ofconjunctival autografts,amniotic membrane grafts andprimary closure for pterygium excision.Ophthalmology.1997;104:974-85.



————————————————————————————————1.Junior Registrar , Eye Deptt, Lady Reading Hospital, Peshawar2.

Trainee Medical Officer3. Senior Registrar————————————————————————————————Correspondance: Dr Nuzhat Rahil , Junior Registrar , Eye Deptt,Lady Redaing Hospital Peshawar. Cell: 0321-9036959————————————————————————————————Received: September’12 Accepted: October’12————————————————————————————————

INTRODUCTIONVisual impairment is a global health problem.1 It

is estimated that 37 million of the world population isblind and 124 million have severe visual impairment.1

According to previous studies cataract is responsiblefor 50% of blindness worldwide.2 The treatment ofcataract available today has passed through evolution.3

Of the long term complications of cataract surgery,posterior capsule opacification (PCO) is the mostcommon4. The incidence of PCO varies from 10% - 50%when followed for 2 years postoperatively5. PCOformation is a manifestation of proliferation ofequatorial epithelial cells across the posterior capsule.6

It causes reduction in visual acuity (VA) and contrastsensitivity by obstructing the view or by scattering thelight that is perceived by patients as glare.7-8-9 It alsodecreases the field of view during therapeutic anddiagnostic procedures.10

Before the Neodymium- Yttrium- Aluminum-Garnet (Nd: YAG) laser came into use, the treatment ofPCO was surgical capsulotomy, which is not free fromdrastic complications such as endophthalmitis. TodayPCO is treated with Nd: YAG laser, which is safer, more

effective and an out-patient procedure. The decreasedrate of complications and faster recovery has made Nd:YAG laser capsulotomy a popular approach for thetreatment of PCO.11

Nd: YAG Laser is a photo disruptive laser whichproduces extreme heat of about 10,000 C° along withan acoustic shock wave at the site being focused andthus causes disruption of tissues. This property of Nd:YAG Laser is used to disrupt the posterior lens capsulein order to create an opening in it12. This causessignificant improvement in visual acuity (mean decimalvisual acuity 0.49±0.14 SD before and 0.6 ±0.19 SD afterNd: YAG laser posterior capsulotomy).13

Nd: YAG Laser posterior capsulotomy isfrequently performed in our hospital but no study hasbeen undertaken on the subject in the recent past. Thisstudy has been designed to determine improvement inVA by Nd: YAG laser capsulotomy in patients withPCO.MATERIAL AND METHODS.

This study was conducted at out-patientdepartment, Ophthalmology Unit, KIOMS, PGMI, LRHPeshawar. Prior to the start, permission from hospitalethical committee was obtained. Patients were includedin the study after fulfilling inclusion and diagnosticcriteria that included: a) Posterior capsular opacificationseen on slit lamp examination b) Visual acuity between6/24 to 6/60 seen on Snellen’s VA chart. The patientswere evaluated for inclusion and exclusion criteria. Aspecial data collection proforma was filled for each

Visual Outcome after the use ofNeodymium-Yttrium- Aluminum Garnet (YAG) Application

for Posterior Capsular Opacification

Nuzhat Rahil1, Romana Rehman2, Rahil Malik3

ABSTRACTObjectives: To determine the frequency of improvement in visual acuity after Nd: YAG Capsulotomy. Improvement isdefined here by 2 or more lines on Snellen’s visual acuity chart.Material and Methods: This cross sectional observational study was conducted at Out Patient Department, Ophthalmologyunit, Khyber Institute of Ophthalmic Medical Sciences (KIOMS), PGMI, Lady Reading Hospital, Peshawar. Study durationwas 6 months (from July 2010 to December 2010) in which a total of 251 patients were treated and assessed for the visualstatus after YAG laser capsulotomy carried out for secondary posterior capsular opacification that had developed aftercataract surgery.Results: In this study mean age was 54 years with standard deviation +13.51. 64% patients were male and 34% werefemale. Frequency of improvement was very high as 91% of patients showed improvement of minimum of two linepositive change on Snellen distant acuity scoring system while only 9% patients did not show any improvement.Conlcusion: It is concluded that visual acuity in patients who developed secondary posterior lens capsule opacificationafter cataract extraction after intraocular lens implantation is better after Neodymium: YAG Laser posterior capsulotomythan the visual acuity before the use of Neodymium: YAG Laser, (p-value < 0.05).Key Words: Cataract extraction, Posterior capsule opacification, Nd: YAG laser capsulotomy.

Original Article

Dr Nuzhat


patient and had a detailed record of the diseaseincluding name, age , gender, address etc.

After enrollment in the study, detailed history,visual acuity (VA) using standard Snellen’s visualacuity chart, slit lamp examination, IOP by Goldmannapplanation tonometer, direct and indirectophthalmoscopy, and B-scan ultrasonography in casesof dense PCO, was carried out by same senior surgeonbefore YAG laser capsulotomy to avoid any biasedstudy.

Patients were dilated and properly prepared priorto the procedure. Proper instructions were given to thepatients before the procedure. 3-4 mm of capsulotomywas done by same senior surgeon using same lasermachine, if clinically indicated.

Confounders and bias were controlled by strictlyfollowing exclusion and by proper follow up. Patientswere instructed to come for follow up after one week.On follow up visual acuity was checked using standardsnellen’s visual acuity chart. The data was recorded ina proper proforma. All the analysis was done in SPSS10.1. Frequency and percentage were calculated forcategorical variables like gender, improvement in visualacuity . Mean + standard deviation was computed fornumerical variables like age, and pre procedure V.A .All the results were presented in the form of graphsand tables.Inclusion Criteria:1) All patients whether male or female, from 10 to

60 years of age having PCO and visual acuitybetween 6/24 and 6/60 on Snellen’s VA chart.

2) Pseudophakic patients of more than 6 monthsduration of cataract surgery with posteriorchamber intraocular lens.

Exclusion Criteria:1) Infants, children less than 10 years of age and very

old patients who are unable to cooperate becauseit is not possible to perform Nd:yag lasercapsulotomy on them.

2) Patients with ocular complications likeendophthalmitis dislocated IOL, IOL in traumaticcataract because these complications will furtherreduce visual acuity.

RESULTSThis study was conducted at Khyber Institute of

Ophthalmic Medical Sciences (KIOMS), Lady ReadingHospital, Peshawar in which 251 patients were observedand the results were analyzed.

Age distribution among 251 patients wereanalyzed as n=15(6%) patients were in age ranged 10-20 years n=40(16%), 21-30 years n=53(21%), 31-40 yearsn=65(26%), 41-50 years n=78(31%) and 51-60 years.Mean age was 54 years with standard deviation+13.51.Minimum age was 31 years while maximum age was

80 years. Gender distribution among 251 patients wereanalyzed as n=161(64%) patients were males whilen=90(34%) were females. There were n=141(56%)patients had posterior lens capsule opacification in theright eye while n=110(44%) patients had posterior lenscapsule opacification in the left eye after extracapsularcataract extraction and phacoemulsification withposterior chamber intraocular lens implantation.

The pre-procedure assessment of distant visualacuity of the patients was 6/12 in n=30(12%) patients,6/18 in n=33 (13%) patients, 6/24 in n=55(22%) patients,6/36 in n=88(35%) patients and 6/60 in n=45(18%)patients. (as shown in Table No 1)

The post-treatment distant visual acuity of thepatients was 6/06 in n=30(12%) patients, 6/09 inn=38(15%) patients, 6/12 in n=85(34%) patients, 6/18in n=82(33%) patients, 6/24 in n=8(3%) patients and 6/36 in n=8(3%) patients. (as shown in Table No 2)

The mean decimal pre-treatment visual acuity was0.2307+0.1235. The mean decimal post-treatment visualacuity was 0.5121+0.2231. Difference between pre andpost treatment decimal visual acuity by applying pairedsample t-test was significant. (P-value = 0.000). Thushypothesis is proved that visual acuity improved afterNd: YAG laser capsulotomy in patients withextracapsular cataract extraction and phacoemul-sification with posterior chamber intraocular lensimplantation.

Frequency of improvement is also very higher asn=228(91%) of patients showed improvement ofminimum of two line positive change on Snellen’sdistant acuity scoring system while only n=23(9%)patients did not show any improvement. (as shown inTable No 3)

The pre and post treatment visual acuity wascompared using paired T-test which shows significantdifference in visual acuity with p-value=0.000.DISCUSSION

There were 251 patients involved in the study withmean age range of 54.78+13.51 years. The mean age ofsuch patients in one study done in Manchester EyeHospital, UK was 75.2 years.14 While in another study

TABLE NO 1:Pre-procedure assessment of distant visual acuity (n=251)

Pre-procedure Distant Visual Acuity Frequency Percent

6/12 30 12%

6/18 33 13%

6/24 55 22%

6/36 88 35%

6/60 45 18%

Total 251 100.0%

Visual Outcome after the use of Neodymium-Yttrium- Aluminum Garnet (YAG) Application for Posterior Capsular Opacification


TABLE NO 2:Frequency distribution of post-treatment distant visual acuity

(N=251)

Post-treatment Distant Visual Acuity Frequency Percent

6/6 30 12%

6/9 38 15%

6/12 85 34%

6/18 82 33%

6/24 8 3%

6/36 8 3%

Total 251 100.0%

TABLE NO 3:Frequency distribution of post Nd: Yag Laser distant visual acuity

(N=251)

Post Nd:YAG laser distant visual acuity Frequency Percent

Not Improved 23 9%

Improved 228 91%

Total 251 100.0%

the mean age range was 65.08+10.47.15 This is becauseall patients had age-related cataract which was operatedand they developed PCO.16

Out of total 251 patients, 160(63.3%) were maleand 91 (36.7%) were female in our study. There were14 (53.8%) females and 12 (46.2%) males in a study donein UK.14 There were 19 (55.9%) male and 15 (44.1%)females in study done in Greece. And 46% male and54% females in study done in Eye HospitalHyderabad.14,15

According to our study, the mean durationbetween the cataract surgery and Nd: YAG lasertreatment was found to be 3.138±1.282 years. In anotherstudy it was found to be 10 months to 15 months15. Instudy of 500 cases, the average time from cataractsurgery to Nd: YAG laser capsulotomy was 2.06 years,the minimum 3 months and the maximum more than 4years.19 The majority of patients (46%) had PCO between3 months to 12 months post-operatively.16 Apple DJ hasnoted the incidence of PCO up to 50% by two yearspostoperatively,17 while other authors have reported theincidence of PCO up to 43% in five years duration afterextra capsular cataract extraction18 and in study of 369eyes noted the frequency of PCO in 1.6%, 12.3% and26.5% after cataract surgery in the duration of 1, 2 and3 years respectively19.

There were 141(56%) patients had posterior lenscapsule opacification in the right eye while 110(44%)patients had posterior lens capsule opacification in the

left eye after extracapsular cataract extraction andphacoemulsification with posterior chamber intraocularlens implantation.

The pre-treatment distant visual acuity of thepatients was 6/12 in 30(12%) patients, 6/18 in 33(13%)patients, 6/24 in 55 (22%) patients, 6/36 in 88(35%)patients and 6/60 in 45(18%) patients. While in a studyof Greece, 2.9% patients had VA 20/32 and 20/60, 20.6%had VA 20/40, 14.7% had 20/50 and 20/60, 17.6% hadVA 20/80 and 26.6% had VA 20/100.15,23 While in studyof Hyderabad, 80.4% of patients had pre-Laser VA >20/30, among them 52.4% had VA above 6/60.23,,24

According to our study the post-treatment distantvisual acuity of the patients was 6/6 in 30 (12%) patients,6/9 in 38 (15%) patients, 6/12 in 85(34%) patients, 6/18in 82(33%) patients, 6/24 in 8 (3%) patients and 6/36 in8 (3%) patients. The study of Greece showed that out of34 patients only 1 (2.9%) patient had post treatment VA20/80 while other patients (85.3%) recover well and hadVA less than 20/60 and concluded that Nd:YAGcapsulotomy seems to be a safe and effective procedurefor eyes that have previously undergone combinedphacoemulsification and vitrectomy surgery.15 Thestudy of Hyderabad showed that there were no patientsthat had VA 6/6-6/12 pre-treatment but after treatmentthere were 372 (74.4%) had VA 6/6-6/12.21

In our study the mean decimal pre-treatmentvisual acuity was 0.2307+0.1235 and mean decimal post-treatment visual acuity was 0.5121+0.2231. Differencebetween pre and post treatment decimal visual acuityby applying paired sample t-test was significant. Thushypothesis is proved that visual acuity improved afterNd: YAG laser capsulotomy in patients withextracapsular cataract extraction andphacoemulsification with posterior chamber intraocularlens implantation.20

Frequency of improvement is also very high. 228(91%) of patients showed improvement of minimum oftwo line positive change on Snellen’s distant acuityscoring system while only 23 (9%) patients did not showany improvement in our study. Similar results wereseen in study done in Hyderabad. Researchers found93.9% had improved visual acuity (more than 2 lineimprovement in Snellen’s lines).CONCLUSION

Thus it is concluded that visual acuity in patientswho develop secondary posterior lens capsuleopacification after cataract extraction with intraocularlens implantation is better after Neodymium: YAGLaser posterior capsulotomy than the visual acuitybefore the use of Neodymium: YAG Laser, (p-value <0.05).REFERENCES1. Foster A, Resnikoff S. The impact of Vision 2020 on global



blindness. Eye 2005;19: 1133–5.2. Polack S, Kuper H, Wadud Z, Fletcher A, Foster A. Quality

of life and visual impairment from cataract in Satkhiradistrict, Bangladesh. Br J Ophthalmol 2008;92: 1026-30.

3. Apple DJ, Kincaid MC, Mamalis N, Olson RJ. Intraocularlenses; evolution, designs, complications, and pathology.Baltimore MD. Williams & Wilkins. 1989; 370-7.

4. Awasthi N, Guo S, Wagner BJ. Posterior capsularopacification: a problem reduced but not yet eradicated. ArchOphthalmol 2009;127: 555-62.

5. Dawood Z, Mirza SA, Qadeer A. Review of 560 cases of YAGlaser capsulotomy. J Liaqat Uni Med Health Sci 2007;6(1):3-7.

6. Lukaszewska-Smyk A. Posterior capsule opacification inpseudophakic eyes-etiopathogenesis, clinical picture,possibilities of prevention and therapy. Klin Oczna 2007;109:464-9.

7. Krajcova P, Chynoransky M, Strmen P. Posterior capsuleopacification following the implantation of various types ofIOL-part II. Different intraoperative findings. Cesk SlovOftalmol 2008;64:13-5.

8. Nejim R, Miyata K, Honobou M. A prospective, randomizedcomparison of single and three piece acrylic foldableintraocular lenses. Br J Ophthalmol 2004;88:746-9.

9. Kanski JJ. Clinical Ophthalmology, a systemic approach. 6th

edition. London. Butterworth Heinemann. 2007;358-60.10. Niazi MK, Hanif MK, Khan HA, Yaqub MA. Neodymium:

YAG; capsulotomy rates following implantation of PMMAand Arylic Intraocular lenses. Professional Med J2006;13(4):538-42.

11. Aslam TM, Devlin H, Dhillon B. Use of Nd: YAG lasercapsulotomy. Surv ophthalmol 2003;48:594-612.

12. Panezai MN, Shawani MA, Hameed K. Posterior capsularopacification (PCO) and Nd: YAG laser capsulotomy inHelpers Eye Hospital, Quetta. Pak J Ophthalmol 2004;20:115-8.

13. Hayashi K, Nakao F, Hayashi H. Influence of size of

neodymium: yttrium-aluminium-garnet laser posteriorcapsulotomy on visual function. Eye 2010;24:101-6.

14. Aslam TM, Patton N. Methods of assessment of patients forNd: YAG laser capsulotomy that correlate with final visualimprovement. BMC Ophthalmol 2004;4:13.

15. Georgalas I, Petrou P, Kalantzis G, Papaconstantinou D,Koutsandrea C, Ladas I. Nd: YAG capsulotomy for posteriorcapsule opacification after combined clear cornealphacoemulsifi cation and vitrectomy. Therapeutics andClinical Risk Management 2009;5:133–7.

16. Khanzada MA, Jatoi SM, Narsani AK, Dabir SA, Gul S.Experience of Nd: YAG Laser Posterior Capsulotomy in 500cases. J Liaqat Uni Med Health Sci 2007;6:109-15.

17. Apple DJ, Solomon KD, Tetz MR. Posterior capsuleopacification. Surv Ophthalmol 1992;37:73-116.

18. Sundelin K, Sjostrand J. Posterior capsule opacification 5years after extracapsular cataract extraction. J Catarct RefractSurg 1999;25:246-50.

19. Erie JC, Hardwig PW, Hodge DO. Effect of intraocular lensdesign on neodymium:YAG laser capsulotomy rates. JCataract Refract Surg 1998;24:1239-42.

20. Paz SH, Verma R, Klein R, Wu J, Azen SP. Noncompliancewith vision care guidelines in Latinos with type 2 diabetesmellitus. The Los Angeles Latino Eye study. Optholmol2006;113:1372 – 7.

21. Kohner EN, Porta M. Screening for Diabetic Retinopathy inEurope: A Field Guide-Book. Copenhagen: WHO RegionalOffice for Europe, 1992.

22. Ahmed AA. Prevention of blindness due to diabetes in theMiddle East (Editorial). Middle East J Ophthalmol 1994;2:68-9.

23. Yeo KT, Lim ASM, Ling SL. Mass screening for diabeticretinopathy in the prevention of blindness. Asia-Pacific JOphthalmol 1995;7:2-10.

24. Kayani H, Rehan N, Ullah N. Frequency of retinopathy amongdiabetics admitted in a teaching hospital of Lahore. J Ayub MedColl Abbottabad 2003;15(4):53-6.



Efficacy of Excimer Laser Photorefractive Keratectomyin High Myopia

M. Abdul Moqeet FCPS,1 Madiha Durrani, MCPS, FRCS2

Pakistan Institute of Ophthalmology, Al-Shifa Trust Eye Hospital, Rawalpindi

ABSTRACT:Objective: To assess the efficacy and safety of excimer laser photorefractive keratectomy in high myopic Pakistanipopulation.Study Design: It is a prospective interventional study conducted during August, 1995 to August 1996.Participants and Methods: Forty nine (49) operated eyes were enrolled in this study with a refractive error ranged from-6.25 to -20.00 diopters. Range of the astigmatism was from -0.50 to -4.0 diopters giving an average of 0.93. Six (12.24%)eyes did not turned up for final visit and 43 (87.76%) eyes were followed till last visit six months after photorefractivekeratectomy.Results: At 1 month, 3 months and 6 months after PRK, 14.28%, 20.40% and 20.97% eyes respectively achieved 6/6visual acuity without glasses. At six months postoperatively 10 (23.25%) eyes were hypermetropic, 10 eyes (23.25%)were myopic between 1 to 4 diopters spherical equivalent, 4 (09.30%) eyes had spherical equivalent refraction between-6.00 to-8.25 diopters, 10 (23.25%) eyes presented with astigmatism more than +1.0 DC and 11 (25.58 %) eyes with morethan -1.0 DC at the end of six months. All the 43 eyes presented with various degree of corneal haze at six months followup visit. No serious complication was reported.Conclusion: The short term follow up revealed PRK to be less effective and predictable for the correction of high myopiamainly due to corneal haze and regression of effect.

Original Article

————————————————————————————————Correspondence: Dr. M. Abdul Moqeet, Associate ProfessorPakistan Institute of Ophthalmology, Al-Shifa Trust Eye HospitalRawalpindi. E.Mail: [email protected] Mobile: 03335135233Phone: 051 -5487820-4 Fax: 051 -5487827————————————————————————————————1.Associate Professor, 2.Ophthalmic Surgeon, Dubai (UAE)————————————————————————————————Received: Sept 2012 Accepted Oct’2012————————————————————————————————

INTRODUCTION:Myopia can be corrected satisfactorily with

spectacle and contact lenses but many people want clearvision without dependence on corrective opticaldevices1. Refractive surgery came as harbinger ofhappiness for these people. As the Argon Fluorideexcimer laser found its use as cutting device it led tothe development of photo refractive keratectomy (PRK).Excimer laser photorefractive surgery modifies theanterior corneal curvature by laser ablation of cornealtissue2. Since birth of PRK several countries worldwidehave been evaluating 193nm argon fluoride excimerlaser for myopia. Numerous studies have used theexcimer laser to correct refractive error .Good resultshave been reported for low myopia and somewhat lesspredictable results for high myopia3. This study wascarried out to asses/check the efficacy, safety andpredictability of PRK for high myopia in ourpopulation.

PARTICIPANTS AND METHODS:It was a prospective interventional study done at

Al-Shifa Trust Eye Hospital Rawalpindi. Approval ofthe study was taken from the Hospitals Ethicalcommittee. Only high myopic between - 6.25 to -20 DSwith a range of astigmatism between -0.50 to – 4 DCwere evaluated in this study. Eligible candidates wereat least 18 years of age with relatively stable myopiaduring the last one year. Patients suffering from anyocular or systemic disease were excluded .All patientsgave written informed consent at the time of enrollmentin the study. Contact lens wear was stopped at leastone month before surgery. All patients had detailed slitlamp biomicroscopy. Unaided and best corrected visualacuity was recorded using snellen visual acuity chart.Meticulous refraction was done with auto refractor andretinoscope in each case without any cycloplegics.Applanation tonometery was done. Direct and indirectophthalmoscopy was performed on each case and 90Diopter lens was used, whenever required.

PRK was performed with Omni Med U.V 270300excimer laser system, using an energy density of 180mj/cm2 with a repetition rate of 10 Hz. (Summittechnology (USA), approved by Food and DrugAdministration (FDA) for therapeutic use. Localanesthesia was achieved with Alcaine (Proparacain0.50%) or Novesin (Oxy buprocain hydrochloride (0.4%)eye drops. Chloramphenicol 0.50 % eye drops were used

Dr. Abdul MoqeetAuthor

Dr. Madiha DurraniCo-Author


as prophylactic antibiotic. Few drops of 2% Pilocarpinewere instilled to constrict the pupil. The eye was keptopen during laser delivery by wire speculum. Eachpatient was supposed to maintain self fixationthroughout the procedure. 100 % manifest refraction atthe corneal plane was entered. Three zones wereentered for each eye. 100% of the manifest refractionwas entered in zone one (5.0 mm), 70% in zone two(6.00mm) and only 30 % in zone three (6.50 mm).Epithelium of about 7 mm zone was removedmechanically with a Beaver blade 64. Methyl cellulosewas used on weck sponge to smooth the corneal surfaceafter epithelial removal. Surface was dried with wecksponge and then laser ablation was performed.Medication used included one drop of each, 2%Homatropine, 0.5% Chloramphenicol, Ocufen(Flurbiprofen Sodium 0.04 %) and Chloramphenicol eyeointment in each eye before applying occlusivebandage for 48 hours. Postoperative examinations wereperformed after 2nd day and 1, 3and 6 months. Tobrex(Tobramycin 0.3%) and Maxidex (dexamethasonesodium phosphate 0.1 %) eye drops, four times a daywere advised after epithelialization, to be replaced aftertwo weeks by FML eye (Flouromethalone 0.1 %) dropsfour times a day.RESULTS :

The study group comprised 49 eyes within rangeof -6.25 to -20.00 diopters refractive error. Range ofastigmatism was -0.50 to –4.00 diopters with an averageof 0.93. Six eyes (12.24%) did not turned up for finalvisit. 43 (87.76%) eyes were examined at final visit perschedule at six months postoperatively. 26 (54%) eyescompleted epithelialization on 3rd postoperative day,22 eyes (44%) on 4th postoperative day and one eye(02%) took the 7 days to complete the healing process.Moderate to severe postoperative pain was experiencedby every one for three days, which gradually subsidedwith epithelial healing. Three patients presented withtransient rise in IOP in their both eyes (12.24%) onemonth after PRK. IOP remained between 28 mm of Hgto 32 mm of Hg. Potent steroids (Maxidex) werereplaced with mild steroids (FML eye drops). Twopatients were given 0.5% Betagan eye drops two timesa day and one was not given, IOP was controlled in allafter one week. Detailed results of the study at onemonth, three months and six months follow up visitsare as under:

At one month: One eye achieved (2.04 % ) visualacuity between counting fingers ( CF) and handmovements( HM ), 05 eyes (10.20%) achieved 6/60, 06eyes (12.24%) achieved 6/36, 09 eyes ( 18.36 % )achieved 6/24, 11 eyes (22.48%) achieved 6/18 ,05 eyes(10.20%) achieved 6/12, another 05 eyes (10.20%)achieved 6/9 and 07 eyes (14.28%) achieved 6/6 visual

acuity without any optical aid. (Table No. 1 ).It was found that 03 eyes ( 6.12 %) could be

corrected up to 6/60 , another 03 eyes (06.12 %) up to6/36 , 06 eyes (12.24 % ) up to 6/24,07 eyes(14.28%) upto 6/18, 06 eyes (12.24%) up to 6/12 ,10 eyes (20.40%)up to 6/9 and14 eyes (28.60%)up to 6/6. (Table No.2).It was also observed that 08 eyes (16.32%) wereovercorrected by +1 diopter spherical equivalent, 19eyes (38.80%) ranged between +1.25 to +2.00 diopterspherical equivalent. Seven eyes (14.28%) were foundwithin the range of +2.25 to +3.00 diopters sphericalequivalent. One eye (2.4%) was overcorrected by +4 .00diopters spherical equivalent. Four eyes (08.16 %)ranged from +4.25 to +5.00 diopters sphericalequivalent. Two eyes (4.08%) were with in range of+5.25 to +6.00 diopters spherical equivalent. Three eyes(06.12%) revealed under correction up to -1.00 diopterspherical equivalent and 02 eyes (4.08%) by -1.50 and-2.00 diopter spherical equivalent. Two eyes (4.08 %)had residual myopia of -2.50 –3.00 dipoters sphericalequivalent .Only one eye (2.4%) was emmetropic (TableNo. 3). Twenty five eyes (51.02%) had astigmatism ofmore than +1.00 diopters. Only one eye (02.04%) hadastigmatism more than -1.00 diopters. Eighteen eyes(36.75 %) scored grade 1 corneal haze, 23 eyes (46.93%)were given grade 2 corneal haze, and 03 eyes (6.12%)had grade 3 degree corneal haze at one monthpostoperatively. (Table No.4).

At three months: 6/60 visual acuity was recordedin 05 eyes (10.20%) ,6/36 in 03 eyes (06.12%) ,6/24 in 08eyes (16.32%) ,6/18 in 16 eyes (32.68%) ,6/9 in07eyes(14.28%)and only 10 eyes (20.40%) reached to 6/6without glasses at the end of three months follow upvisit.(Table No.1). Two eyes (4.08%) achieved 6/60 ,04 eyes (8.16%) 6/36 , 14 eyes (28.59%) 6/18 , 03 eyes(6.12%) 6/12 , another 03 eyes (6.12%) 6/9 and 23 eyes(46.93%) achieved 6/6 after correction with glasses.(Table No. 2).

Thirteen eyes (13) eyes (26.53%) were found withhypermetropia up to +1.00 DSE. Another group of 08eyes (16.32%) ranged +1.25 to +2.0 DSE. Seven eyes(14.28%) were between +2.25 to +3.00 DSE. Three eyes(6.12%) had hypermetropia of +3.50 to +4.00 DSE. Oneeye (2.4%) presented with hypermetropia of +5.75 DSE.Seven eyes (14.28%) were myopic up to -1.00 DSE. Threeeyes (6.12%) were myopic within -1.25to -2.0 DSE. andanother three eyes (6.12%) ranged between-2.25 to -3.0DSE, 03 eyes (6.12%) were emmetropic. Properrefraction could not be done in one eye.(TableNo3).Seventeen eyes (34.69%) were left withastigmatism of more than +1.00 diopter. Three eyes(06.12%) with more than -1.00 diopter cylinder. Threemonths after PRK, 09 eyes (18.36%) showed grade 1corneal haze, 22 eyes (44.92%) showed grade 2 corneal

Efficacy of Excimer Laser Photorefractive Keratectomy in High Myopia


haze, 10 eyes (20.40%) showed grade 3 and 03 eyes(6.12%) had grade 4 corneal haze .Rest of the corneaswere clear. (TableNo.4).

At six months: Forty three (43) eyes from thisgroup appeared for the final visit at six months. Theyshowed the following results:

Three eyes (6.97%) had C F, 12 eyes (27.90%) had6/60, 03 eyes (6.97%) had 6/36, 06 eyes (13.95%) had6/24 another 06 eyes (13.95%) had 6/18, 01 (02.32%)had 6/12, 03 eyes (06.97%) had 6/9 and 09 (20.97%)eyes had 6/6 vision without any correction. (TableNo.1).02 (04.65%) had counting fingers, 04 eyes (09.30 %) had6/60, 03 eyes (06.97%) had 6/36, 02 eyes (04.65%) had6/24, 07 eyes (16.27%) had 6/18, 04 eyes (09.30%) had6/12, 05 eyes (11.62%) had 6/9 and 16 eyes (37.24%)had gained 6/6 visual acuity with spectacles. (TableNo.2). It was found that 05 eyes (11.62%) hadhypermetropia up to +1.00 DS .05 eyes (11.62%) weregrouped in hypermetropia ranging from + 1.25 to +2.0DS Three eyes (06.97%) were grouped together withhypermetropia ranging from +2.25 to +3.00 DSE.Another group of 02 eyes (04.65%) had hyper metropiaof +3.50 DS. 04 eyes (9.30%) were found with emetropiaat six months after surgery. Five eyes (11.62%) hadmyopia within -1.00 DS, 04 eyes (9.30%) had myopiawithin -1.25 to -2.0 DS, 06 eyes (13.95%) fell between -3.00 to -4.00 DS. One eye (02.32 %) had attained myopiaof -6.50 DS; another pair of 02 eyes (04.65%) attained -7.50 DS. Still another eye (02.32%) attained -8.25 DS asevaluated, six months postoperatively. Retiniscopycould not be done in five eyes (11.62%). Ten eyes(23.25%) were still overcorrected by more than +1.00diopter spherical equivalent. Fourteen eyes (33.54 %)had regressed/under corrected by more than -1.00 DS(Table No3). 10 eyes (23.25%) presented with +1.00diopter cylinder and eleven 11 eyes (25.58%) with morethan - 1 diopter cylinder. It was noted that 08 eyes(18.61%) were seen grade 1 haze, 09 eyes (20.94%) with

grade 2 degree corneal haze .16 eyes (37.20%) withgrade 3 degree corneal haze and 10 eyes (23.25 %) with4.0 degree corneal haze. (Table No.4)DISCUSSION:

Excimer Laser PRK has been shown to be safe,predictable, stable and effective for myopia up to -6.0diopters by many studies, myopia exceeding this limit,however, has shown contradictory results4. This studywas designed to asses the outcome of excimer laser PRKin Pakistani population, for myopia of -6.00 to -20.0diopters. All the patients experienced moderate tosevere pain shortly after the excimer laser applicationand reported to peak twenty four hours after treatment.It subsided over next two days. We also concluded likeother reports that simple analgesics and tranquilizerscannot control post laser pain effectively. It is acceptedthat combination of the disposable contact lenses andtopical Diclofenac sodium (3-4 times a day) gives thebest results in suppressing the pain following PRK5.Topical NSAIDS offer several potential benefits overtraditional systemic agents for ocular pain relief6. Animportant routine is that topical steroids should be usedin combination with NSAIDS preparations to reducethe incidence of sterile infiltrates7. Despite theintroduction of topical non steroidal and bandagecontact lenses approximately 5% to 10 % of patientscontinue to experience moderate to severe painrequiring oral narcotic agent. Ice packs or cold compresscan significantly improve comfort level in thesepatients8. It is also reported that vitamin A and E;significantly decreased re-epithelialization time, hazeformation, and myopic regression occurrence9.However pain disappeared completely once thereepithelialization was completed. In generalepithelium heals over promptly after PRK10. Ifmechanical debridement is performed, re-epithelialization occur within 2-4 days8. Epithelialhealing usually requires 3 days to complete , but many

Table No. 1 Unaided postoperative visual acuity

Visual Acuity 1Month (n=49) 3Months (n=49) 6Months (n=43)No. of eyes (%) No. of eyes (%) No. of eyes (%)

CF 01(02.04%) 00(00.00%) 03(06.97%)

6/60 05(10.20%) 05(10.20%) 12(27.90%)

6/36 06(12.24%) 03(06.12%) 03(06.97%)

6/24 09(18.36%) 08(16.32%) 06(13.95%)

6/18 11(22.48%) 16(32.68%) 06(13.95%)

6/12 05(10.20%) 00(00.00%) 01(02.32%)

6/9 05(10.20%) 07(14.28%) 03(06.97%)

6/6 07(14.28%) 10(20.40%) 09(20.97%)



patients require 4 days and some as long as 1 week10.In this study group re-epithelialization occurred

in 54% (26 eyes) within 72 hours. Twenty two eyes (44%)completed healing on fourth postoperative day. Only

one eye (02%) healed in one week. It is comparable withmost of the international studies, which has reportedcompletion of re-epithelialization within 72 to 96 hours.Higher refractive errors require deeper ablations as

Table No.2 Best spectacle corrected visual acuity

Visual Acuity 1Month (n=49) 3Months (n=49) 6Months (n=43)No. of eyes (%) No. of eyes (%) No. of eyes (%)

CF 0(00.00%) 0(00.00 %) 02(04.65%)

6/60 03(06.12%) 02(04.08%) 04(09.30%)

6/36 03(06.12%) 04(08.16%) 03(06.97%)

6/24 06(12.24%) 00(00.00%) 02(04.65%)

6/18 07(14.28%) 14(28.59%) 07(16.27%)

6/12 06(12.24%) 03(06.12%) 04(09.30%)

6/9 10(20.40%) 03(06.12%) 05(11.62%)

6/6 14(28.60%) 23(46.93%) 16(37.24%)

Table No. 3 Postoperative spherical equivalent refraction

Refraction (DSE) 1Month (n=49) 3Months (n=49) 6Months (n=43)No. of eyes (%) No. of eyes (%) No. of eyes (%)

+0.25to +1.00 08(16.32%) 13(26.53%) 05(11.62%)

+2.25to+3.00 07(14.28%) 07(14.28%) 03(06.97%)

+3.25to+4.00 01(02.04%) 03(06.12%) 02(04.65%)

+4.25 to +5.00 04(08.16%) 00(00.00%) 00(00.00%)

+5.25 to+6.00 02(04.08%) 01(02.04%) 00(00.00%)

-0.25to-1.00 03(06.12%) 07(14.28%) 05(11.62%)

-1.25to-2.00 02(04.08%) 03(06.12%) 04(09.30%)

-2.25to-3.00 02(04.08%) 03(06.12%) 00(00.00%)

-3.25to-4.00 00(00.00%) 00(00.00%) 06(13.95%)

-6.50 00(00.00%) 00(00.00. %) 01(02.32%)

-7.50 00(00.00%) 00(00.00%) 02(04.65%)

-8.25 00(00.00%) 00(00.00%) 01(02.32%)

00.00 01(02.04%) 03(06.12%) 04(09.30%)

Table No. 4 Distribution of corneal haze after PRK

Grade 1Month (n=49) 3Months (n=49) 6Months (n=43)No. of eyes (%) No. of eyes (%) No. of eyes (%)

0 05(10.20%) 05(10.20%) 00.00

1 18(36.75%) 09(18.36%) 08(18.61%)

2 23(46.93%) 22(44.92%) 09(20.94%)

3 03(06.12%) 10(20.40%) 16(37.20%)

4 00.00 03(06.12%) 10(23.25%)



compare to smaller refractive errors and take relativelylonger healing time, showing some relationshipbetween rate of reepithelialization with depth ofablation.

In one series 15% of 255 patients had delayedepithelial healing and in other series 116 (9.4%) of 1236eyes required more than four days for closure of theepithelial defect. Delay in epithelial healing is oftenassociated with increased postoperative haze10. In 1995Kim and Jung performed PRK using new multi-zonesoft ware of the Summit Omni Med Excimer laser onthirteen high myopic eyes from -9.00 diopters to -14.00diopters and reported that epithelial wound wascompletely healed within five days in all cases11.Whereas, Rajendran and Janakeraman used the samesoftware and technique in 124 eyes for myopia of 8 to23 diopters and found good epithelial healing within72 hours after treatment12. We found epithelial healingon 4th day in all case except one. Three patients werefound with rise in IOP in their both eyes (12.24% of 44eyes). Rise in IOP was confined between 28 mm of Hgto 32 mm of Hg. Potent steroids were replaced withmild ones. Mild steroids continued till completion ofthree months without any problem. Betagan 0.5% eyedrops (Levobunolol hydrochloride 0.5%) were addedin the regimen for a few days.

One study reported an increase of 24 mm of Hgin 8 of 273 eyes, all responded promptly to topical beta–blockers and returned to normal levels when steroidsand beta-blocker was discontinued13. Intra ocularpressure (IOP) must be monitored while patient is ontopical steroid therapy .More frequent monitoring isrequired if IOP is elevated by 5 to 8 mm of Hg, but stillwithin normal range .It should be kept in mind thatIOP may be under estimated with flat corneas postPRK7. The higher myopes in this study showed a largevariation in uncorrected visual acuity and refractiveresults during six months follow up. 30.26 % eyes wereable to read 6/12 or better uncorrected at six monthsafter surgery. Nystrom et al, 1995 reported the sameresult (30 %) after nine months follow up for myopiafrom -10.00 to -18.00 diopters14. None of the eyes inthis study group lost best corrected visual acuity,though loss of one or two lines is not uncommon afterexcimer laser PRK15. As the data indicates thatpostoperative spherical equivalent refraction was within +/- 1.00 diopters in 10of 43 eyes (23.25 %), within +/- 1.25 to +/- 2.00 in 09 of 43 eyes (20.93%).Five of 43eyes were (11.62%) were overcorrected by +2.25 to +3.75DS and 10 of 43 eyes (23.25%) were under corrected/regressed by more than-3.00 DS at six months followup. Four (09.30%) were emmetropic. 14 of 43 eyes(32.55%) regressed by more than -1.0 DS. This studyhad shown that density and distribution of corneal haze

gradually increased and no decrease in corneal hazewas observed even after six months. All the eyespresenting at six months had corneal haze of variousdegree. Chan et al, 1995, studied high myopia (-6.00 to-18.00 diopters) and reported that 77% of the eyes hadnone or trace corneal haze, 23 % had mild to moderatecorneal haze4. As compare to other international studiesrelatively greater corneal haze was observed in ourpopulation. Corneal haze has been described variouslyin different studies. This may be due to the fact thatgrading the haze being used at present is not objectiveand grading may differ from report to report. Thishigher incidence of corneal haze, compare to otherreports may be due to the greater depth of ablationrequired to correct high myopia resulting in anaggressive wound healing tissue response in ourpopulation like elsewhere in the body.

The literature suggests that the results of excimerlaser surgery to correct myopia are more variable forhigh and extreme myopia. Predictability of refractionand uncorrected and best corrected visual acuityprogressively decreases with increasing myopia. Thelikelihood of loosing lines of best corrected visual acuityand corneal haze has tendency to increase withincreasing myopia16. Therefore patients with higherdegrees of myopia are more likely to show someregression and under correction to the extent that asecond ablation may be required17. Major disadvantageof PRK (especially for high myopia) is that theprocedure is performed over visual axis and patientwho experience exuberant healing will develop visualhaze usually temporary, rarely it can have permanentscarring of the cornea18. Though we had our share ofcomplications, but none was vision threateningpermanently.CONCLUSION:

It seems that postoperative haze in high myopiais the most significant problem in our population.Predictability and stability decreases with increase indiopteric power and ablation depth as does the cornealhaze. High myopes showed more postoperative hazeand regression on initially achieved effect,compromising the predictability and the stability of theprocedure.REFERENCES:1. Waring G.O., Lynn M.J., McDonnell P.J., On the PERK Study

Group; Results of the Prospective Evaluation of RK (PERK)Study 10 Years After Surgery. Am J Ophthalmol 1994; 112:1298-1308.

2. Kamiya K, Miyata K, Tokunaga T , Kiuchi T , Hiraoka T,Oshika T. Structural Analysis of the Cornea Using Scanning-Slit Corneal Topography in Eyes Undergoing Excimer LaserRefractive Surgery. Cornea 2004;23: s59-s63.

3. Levin S, Carson CA, Garreth SK. Prevalence of Central Islandsafter Excimer Laser Refractive Surgery. J CataractRefractSurg. 1995;21:21-25.



4. Chan W.K., Heng W.J., Tseng P. et al, PhotorefractiveKeratectomy for Myopia of 6 to 12 Diopters. J Refract Surg.1995; 11: s286-291 .

5. Belluci R, Morselli S, Pucci V. Disposable Contact Lensesand Diclofenac Sodium Yield Minimum Pain After PRK.Ocular Surgery News (International) 1996; 7: (8): 28.

6. Rizman M. , Helga P. Sandoval, Ketherine stern , AmadaVanDenberg , Janet k. Cheetam , Pharm D. , Rehet Schittman, Safety and Efficacy of Ketorolac Tormethamine 0.4%Ophthalmic Solution in Post Photorefractive Keratectomy , JCataract Refract. Surg. 2004;30:1653-1660

7. Machat.J.J. Excimer Laser Photorefractive Keratectomy:Practice and Principles, Slack incorporated, U.S.A, 1996: 3-211.

8. Stein R. NSAIDs Bandage lens Have Led to a DramaticReduction in Photorefractive PRK Pain; Ocular SurgeryNews (International ) 1996;7; 21.

9. Vetrungo M. , Maino A. ,Cardia G. , Quaranta G. M. , CardiaL. , A Randomized, Double Masked , Clinical Trial of HighDose Vitamin A and Vitamin E Supplementation AfterPhotorefractive Keratectomy, Br J Ophthalmology 2001;85:537-539

10. Seiler T. , and McDonnell P. J. , Excimer Laser PhotorefractiveKeratectomy (Major Review).Survey of Ophthalmology 1995;

40: 89-11811. Kim H.M., Jung H.R., Multizone Photorefractive Keratectomy

for Myopia of 09 to 14 Diopters; J Refract.Surg.1995;11(Supply.):s293-s297

12. Rajendran B., Janakeraman P., Multizone PhotorefractiveKeratectomy for Myopia of 08 to 23 Diopters; J Refract. Surg.1995:11(Suppl.): s298 –s301

13. Bahcecioglu H., Ozdamar A., Aktunc R., et al, Simultaneousand Sequential Photorefractive Keratectomy. Journal ofRefractive Suegery.1995; 11: s261-s262.

14. Nystrom H.H., Fangerhom P., Sjoholm C., Tengroth B.Photorefractive Keratectomy for 1.5 to 18 Diopters of Myopia;J Refract. Surg.1995; 11 (suppl.); s265-s267.

15. Amano and Shimizu, 1995, Excimer Laser PRK for Myopia:Two year Follow up, J. Cataract Refract.Surg. 1995; 11(Suppl.)s253-s260

16. Taylor H.R., Mc Carty C.A., Aldred G.F., Predictability ofExcimer Laser Treatment of Myopia .Arch Ophthalmol.1996114:248-251.

17. Snibson G.R., Carson C.A., Aldred G.F., Taylor H.R., OneYear Evaluation of Excimer Laser PRK for Myopia andMyopic Astigmatism. Arch Ophthalmol.1995; 113: 994-1000.

18. Winsly S., Refractive Surgery Overview: OphthalmologyWorld News (Review Edition) 1995:Vol.1: 6



————————————————————————————————1Senior Registrar Ophthalmology Department, Hayatabad MedicalComplex,Peshawar. 2Postgraduate Trainee, OphthalmologyDepartment, Hayatabad Medical Complex,Peshawar. 3Post graduateTrainee, Radiology Department, Hayatabad Medical Complex,Peshawar. 4Assistant Professor, Khaleefa Gul Nawaz Hospital,Bannu.————————————————————————————————Correspondence: Dr Mushtaq Ahmad, House No. 31BStreet No 2, Sector N4, Phase 4, Hayatabad, Peshawar.E.Mail> [email protected] Cell: 0333 9119605————————————————————————————————Received: Oct’2012 Accepted: Nov’2012————————————————————————————————

The effect ofIntracameral Preservative free 1% Xylocaine

on the Corneal Endothelium duringPhacoemulsification Procedure

Mushtaq Ahmad FCPS1, Muhammad Naeem2, Hina Mehwish Khan3, Sanaullah Khan FCPS4

ABSTRACTPurpose : To evaluate the effect of intracameral preservative-free 1% xylocaine on the corneal endothelium as an adjuvantto topical anaesthesia during phacoemulsification cataract surgery.Material & Methods: This is a randomized control trial containing96 patients with soft to moderately dense (Grade 1-3)senile cataract and corneal endothelial cell density of >1500/mm2 were randomized into two groups one was xylocainegroup(n=48) and control group(n=48). Central endothelial specular microscopy and ultrasound corneal pachymetry wereperformed preoperatively. On the first postoperative day the eyes were evaluated for corneal oedema and Descemet’sfolds. Ultrasound corneal pachymetry was performed at 1, 3 and 12 months. Specular microscopy was performed at 3and 12 months. Cell loss was expressed as a percentage of preoperative cell density. Six patients could not complete oneyear follow-up. Chi-square and paired t test (2 tail) statistical tests were applied for analysis.Results:Four (8.33%) patients in the xylocaine group and 5 (10.41%) in the control group had a few Descemet’s foldsassociated with mild central stromal oedema. Corneal thickness increased from 549.3µ ± 37.2µ to 555.5µ ± 36.5µ in thexylocaine group and from 553.1µ ± 36.2µ to 559.3µ ± 40.5µ in the control group at the one-month postoperative visit.Thickness returned to the preoperative level in xylocaine group 549.6µ ± 34.5µ and control group 554.7µ ± 41.1µ at threemonths. (P=0.484) The percentage of cell loss was 4.47 ± 2.53% in the xylocaine group and 4.49 ± 3.09 % in the controlgroup at one year. (P=0.97)Conclusion:Intracameral preservative-free 1% xylocaine does not appear to affect corneal endothelium adversely duringphacoemulsification.Keywords: Topical anaesthesia, phacoemulsification, intracameral xylocaine, endothelial specular microscopy, ultrasoundcorneal pachymetry

Original Article

INTRODUCTIONTopical and intracameral anaesthesia are new

options for pain management in phacoemulsification.Injection of anaesthetic agents has been associated withcomplications such as ocular perforation, retrobulbarheamorrhage, retinal vascular occlusion, optic nervetrauma and extraocular muscle malfunction1,2. Topicalanaesthesia has advantage of rapid visual recovery afterphacoemulsification.3 Topical anaesthesia for cataractsurgery, popularised by Fichman, has been in use since1992.4 Though peribulbar anaesthesia gives akinesia,phacoemulsification can be performed satisfactorilywithout inducing akinesia. Topical anesthesia has

gained wide acceptance as an effective, efficient,practical and safe form of ocular anaesthesia for clearcorneal phacoemulsification.5 The survey of membersof the American Society of Cataract and RefractiveSurgeons (ASCRS) in 2000 revealed an increase in theuse of topical anesthesia to 49% of surgeons from 5% in1995 and 45% in 1999.6 However, topical anaesthesiaalone may not work in certain cases because of painand discomfort arising from frequent pressure changesduring phacoemulsification. Gills suggestedpreservative-free 1% xylocaine for intracameralanaesthesia to control intraoperative discomfort.

Since the introduction of intracameral anaesthesiain cataract surgery, many investigational and clinicalstudies have verified its safety postoperatively.5

Nevertheless, some authors advise caution with the useof intracameral anaesthetic agents because of theirpossible toxic effects on intraocular structures, inparticular damage to the corneal endothelium.7 Changesin the ultrastructure of corneal endothelial cells and anincrease in polymorphism and cellular oedema havebeen reported.8 Such alterations also occur withpreservative-free 1% xylocaine, the concentration mostoften used for intracameral anaesthesia in cataractsurgery.9 This study evaluated the longterm effect of

Dr. Mushtaq


intracameral preservative-free 1% xylocaine onendothelial cell loss after phacoemulsification withfoldable IOL implantation in Indian patients andcompared the endothelial cell loss rate with thatfollowing topical anaesthesia alone.MATERIAL AND METHODS

This is arandomized control trail conducted atophthalmology department HMC from March, 2011to March, 2012. It comprised 96 patients scheduled forphacoemulsification under topical anaesthesia. Patientswith soft to moderately dense senile cataract (Grade 1to 3 on a scale of 1 to 5) and corneal endothelial celldensity of > 1500/mm2 were included in the study.Obese and short-necked patients were also included.Patients with hard cataract (grade 4 and 5), uveitis,glaucoma, previously operated eye, a single eye andwhite mature cataract were excluded. Patients withdiabetes, hypertension and those with whomcommunication could not be established, for reasonssuch as hearing disability or language barrier were alsoexcluded.

Patients were evaluated for visual acuity onSnellen’s chart, intraocular pressure (IOP) and anteriorsegment pathology. The endothelium was examined byslit lamp with 16 X magnification for changes likeguttatae. Fundus examination was done with direct andindirect ophthalmoscope. Specular microscopyphotographs of the corneal endothelium were takenwith a Konan SP 8000 nonconROBO specularmicroscope (Konan Medical, Inc, Japan). Theendothelial cell density (CD) was estimated countingcell numbers by a computer assisted measuring systemafter 100 cells in a cluster. Cell density is one of the mostimportant indices. Cell density of 2000 cells/mm2 ormore is considered normal. The specular microscope isprogrammed to select a central location which can beconfirmed by a highlighted mark on the monitor. Thiscentral location was standardised in all patients.However, it is possible that measurements were nottaken at exactly same location. Ultrasound cornealpachymetry (Humphrey Instruments Inc.) was done inthe center of the cornea by advising the patient to lookat the fixation light. Once again there was a possibilityof missing the same point every time.

Using the envelope method patients wererandomly assigned to receive either 0.2 ml preservative-free 1% xylocaine (xylocaine group) or BSS (controlgroup). The surgeon and observer were masked to therandomization. The technique of anaesthesia andsurgery was standardised. All surgeries wereperformed under topical anaesthesia. 4% xylocainewasinstilled twice at intervals of 5 minutes duringpreoperative preparation. Xylocaine was reinstilled justprior to the placement of the temporal corneal incision

and also before enlargement of incision for intraocularlens implantation. This technique was followed in allcases. Additional supplementation for breakthroughpain during surgery was given based on the surgeon’ssubjective impression when the patient complained ofpain. If wound integrity was suspected,supplementation with topical 4% xylocaine was avoidedjust prior to intraocular lens insertion. Surgeries weredone by a single surgeon. After making a 3.5 mm pre-planed superior corneal tunnel, either 0.2 ml.preservative-free 1% xylocaine or BSS was injected inthe anterior chamber through main tunnel. After 20seconds, 2% HPMC was injected. Anteriorcapsulorhexis was performed under methylcellulosefollowed by hydrodissection and rotation of nucleus.Our phacoemulsifi-cation technique includes initialsculpting followed by step-by-step chop-in situ andlateral separation10and stuffing of nucleus fragmentwith the stop, chop, chop and stuff technique.11 Cortexremoval was done with irrigation aspiration cannula.Acry Sof I. Qwas implanted in the bag through injector.Intraoperative details like average phaco power, totalphaco time and total infusion fluid volume werenoted.Postoperatively, eyes were evaluated forpresence or absence of corneal oedema and Descemet’sfolds. Quantification of aqueous flare and cells weremade using Hogan’s criteria.12 Intraocular pressure andvisual acuity were also recorded. Eyes were examinedon day 1, at 1 week and 1, 3, 6 and 12 monthspostoperatively. Ultrasound corneal pachymetry wasperformed at 1, 3 and 12 months. Endothelial specularmicroscopy was performed at 3 and 12 months andparameters like cell denstiy, coefficient of variation andhexagonal cells were recorded. All the readings ofspecular microscopy and corneal pachymetry wereperformed by a single observer to avoid bias, both preand postoperatively. Chi-square and paired t Test (2tail) were applied for statistical analysis.RESULTS

Six patients could not complete more than 6months of follow-up as four had to travel a considerabledistance and two died during the period. Averagefollow-up was 12 months. Demography, preoperativeintraocular pressure, infusion fluid volume used andcumulative dissipated energy are comparable in bothgroups as shown in Table - 1. 4 (7.54%) patients inxylocaine and 5 (9.43%) patients in control group had afew Descemet’s folds associated with mild centralstromal oedema on first postoperative day. All corneashad cleared at the one week visit. Uveal inflammatoryresponse as noted on first postoperative day was notstatistically significant (P=0.662). IOP on firstpostoperative day was on an average of 14.4 ± 2.8mmHg in xylocaine group and 14.4 ± 3.6 mmHg in

The effect of Intracameral Preservative free 1% Xylocaine on the Corneal Endothelium during Phacoemulsification Procedure


control group (P=0.895)Table - 2. Three patients inxylocaine group had an IOP of 32, 28, 27 mmHgrespectively. These patients on second postoperativeday had an IOP of 14, 17, 15 mmHg with Timololmaleate 0.5% eye drops twice a day. Similarly in thecontrol group, four patients had an IOP of 30, 29, 24, 23mmHg. On second postoperative day IOP recorded was17, 15, 18, 14 mmHg respectively with Timolol maleate0.5% eye drops twice a day. Best spectacle visual acuityat one year was >6/12 in 48 (90.57%) patients of thexylocaine group and 47 (88.67%) patients of the controlgroup (P=0.646). The other two patients of the xylocainegroup had 6/18 best spectacle visual acuity due to agerelated macular degeneration (ARMD). In the controlgroup two patients with ARMD had 6/18 and one withamblyopia had 6/24 best spectacle visual acuity.Percentage of cell loss is comparable in both groups atthe 3 and 12-month postoperative visit. No patientneeded conversion to injection anaesthesia. No patientdeveloped serious complications such as posteriorcapsule rupture, vitreous loss or zonular dialysis.DISCUSSION

Topical anaesthesia for phacoemulsification hasgained popularity since the introduction of clear cornealincision.13 Better understanding of phacodynamics,improved surgical skill and use of foldable IOLs alsohave helped popularise topical anaesthesia. Globemanipulation can be done easily to the surgeon’s

Table 1.Demographic data and operative detail

Xylocaine Control P value(n:48) (n:48)

Age 58± 7.78 56± 7.2 0.14

Male 35(72.91%) 33(68.75%) 0.87

Female 13(27.08%) 15(31.25%) 0.87

Fluid used 324.9± 117.2 295.7± 91.2 0.14

CDE 0.765± 0.336 0.66± 0.297 0.12

IOP9(mmHg) 13.8± 3.7 14.1± 3.9 0.78Preoperative

Table 2. Postoperative outcome: First postoperative day

Xylocaine Control P value(n:48) (n:48)

Cornea- Clear 44(91.66%) 43(89.58%)5 0.75

Descemets folds 4(8.33%) (10.41%)

Cells - Mild 38(79.16%) 37(77.07%) 0.66

Moderate 8(16.66%) 8(16.66%)

Severe 2(4.16%) 3(6.80%)

IOP(mmhg) 14.4+2.7 14.4+3.5

comfort during surgery under topical anaesthesia. It isparticularly valuable in cases of one eyed patients asall possible complications of peribulbar and retrobulbaranaesthesia are avoided. Selection criteria would varyfrom surgeon to surgeon. Preoperative counseling andintraoperative communication improve the surgicalperformance and the final outcome. Topically appliedxylocaine effectively penetrates the eye through thecornea and can be found in aqueous humour at levelsthat involve analgesic activity.14 but in patients withanxiety and complicated ocular history as in cases ofprolonged surgical time, topical anaesthesia alone maynot be sufficient. Pressure changes induced by suddendeepening of the anterior chamber duringphacoemulsification are more frequent in youngindividuals, high myopic and in post vitrectomisedeyes. In situations like these intracameral xylocaine hasbeen found beneficial.

Intracameral xylocaine appears to act by twomechanisms. (1) “Uveal anaesthesia” - decrease thesensation induced by stretching of iris root, cliliary bodyand zonules during inflation-deflation of globe. (2)Decrease sensitivity to microscope light by anaestheticeffect on the retina-ganglion cell-optic nerve complex.Studies have shown that high concentrationsintracameral xylocaine (2% or 4%) are toxic to thecorneal endothelium and cause corneal oedema. 1%xylocaine hydrochloride is safe. A survey of ASCRSmembers in 2000 revealed that 82% of the surgeonsusing topical anesthesia used it in combination withintracameral preservative-free 1% xylocaine.

This study addresses the long term safety ofintracameral xylocaine.We have included soft tomoderately dense cataracts (Gr. 1 to 3). As the effect ofhard cataract emulsification on endothelium ismultifactorial, we have excluded grade 4 and 5cataracts.15 We also feel that the effectiveness of the drugcould be different in diabetic and hypertensive patients.Flare and cells response in immediate postoperativeperiod was acceptable in both groups. There was short-term rise of the IOP in 3 (6.25%) patients of the xylocainegroup and in 4 (8.33%) patients of the control group.The glaucoma was controlled with topical timololmaleate 0.5% and no patient required longterm anti-glaucoma medications.

We could not explain the increase in IOP in thesepatients. They did not have exaggerated postoperativeinflammatory response and there was no history ofglaucoma in any patient. The changes produced inendothelium cell density, hexagonality and coefficientof variation in cell area are informative in evaluatingthe safety of new agents for intracameral use.16

Preoperative specular parameters and pachymetrywere comparable in both xylocaine and control groups.



Though preoperative cell density is less than otherreported studies, it represents the cell density in thePakistani population.17

In our study, 4 (8.33%) eyes in xylocaine groupand 5 (10.41%) eyes in control group developedDescemet’s folds and mild central stromal oedema onfirst the postoperative day. As genesis of oedema nearthe incision is multifactorial, we decided to focus oncentral corneal oedema. All corneas cleared within aweek. Percentages of cell loss in our study are withinthe range reported by other authors.18There was nosignificant difference in specular parameters both preand postoperatively in patients who developed cornealstromal oedema compared to the patients withoutstromal oedema postoperatively. Pachymetry givesuseful information of the endothelial function. Asreported in previous studies19 corneal thickness returnsto the preoperative level by 3 months postoperatively.

A few studies reported in the literature had astudy design similar to ours with xylocaine and controlgroups. All these studies did not report any significantchange on the study eyes with intracameral xylocine.Several other studies have used injection anaesthesiaas a control group. These studies also did not show anysignificant endothelial cell loss in the study or thecontrol eyes. The study by Heuermann et all withfollow-up of 20 months reported that longtermpostoperative endothelial cell course with topicalanaesthesia combined with intracameral injection ofpreservative-free 1% xylocaine is a safe alternative toperibulbar anaesthesia. Similarly, our study evaluatedlongterm endothelial cell loss and found no statisticallysignificant differences between topical anaesthesiacombined with intracameral preservative-free 1%xylocaine (xylocaine group) and topical anaesthesiawith injection of BSS (control group) one year aftersurgery.

Although we have not done fundus fluoresceinangiography, there was no evidence of macular oedemaon fundus examination. There was no evidence ofphototoxicity. In summary, intracameral preservative-free 1% xylocaine does not appear to affect the cornealendothelium adversely during phacoemulsification.CONCLUSION

Intracameral preservative-free 1% xylocaine doesnot appear to affect corneal endothelium adversely

during phacoemulsification.REFERENCES:1. Davis DB, Mandel MR. Posterior peribulbar anesthesia : an

alternative to retrobulbar anesthesia. J. Cataract Refract Surg.1986;12:182-84.

2. Bloomberg LB. Administration of periocular anesthesia. J.Cataract Refract Surg. 1986;12:677-79.

3. Hoh HB, Bourne R, Baer R. Visual recovery afterphacoemulsification using topical anesthesia. J. CataractRefract Surg . 1988;24:1385-89.

4. Fichman RA. Use of topical anesthesia alone in cataractsurgery. J. Cataract Refract Surg. 1998;22:612-14.

5. Gills JP, Cherchio M, Raanan MG. Upreserved lidocaine tocontrol discomfort during cataract sugery using topicalanesthesia. J. Cataract Refract Surg. 1997;23:545-50.

6. Leaming DV. Practice style and preferences of ASCRSmembers - 2000 survey. J Cataract Refract Surg . 2001;27:948-55.

7. Kadonosono K, Ito N, Yazama F, Nishide T, Sangita M,Sawada H. et al. Effect of intracameral anesthesia on thecorneal endothelium. J Cataract Refract Surg . 1998;24:1377-81.

8. Judge AJ, Najafi K, Lee DA, Miller KM. Corneal EndothelialToxicity of Topical Anesthesia. Ophthalmology1997;104:1373-79.

9. Kim T, Holley GP, Lee JH, Broocker G, Edelhauser HF. TheEffects of Intraocular Lidocaine on the Corneal Endothelium.Ophthalmology , 1998;105 :125-30

10. Vasavada AR, Singh R. Step-by-step, chop-in-situ andseparation of very dense cataracts. J Cataract Refract Surg .1998;24:156-59.

11. Vasavada, Desai JP. Stop, chop, chop and stuff. J CataractRefract Surg . 1996;22:526-29.

12. Hogan MJ, Kimura SJ, Thygeson P. Signs and symptoms ofuveitis. I. Anterior uveitis. Am J Ophthalmol1959;47 (5, ptII):155-170.

13. Fine IH, Fichman RA, Graben HB, editors. Clear CornealCataract Surgery and Topical Anesthesia .Thorofare, NJ. SlackInc; 1993.

14. Belluci R, Morselli S, Pucci V, Zordan R, Magnolfi G.Intraocular penetration of topical lidocaine 4%. J CataractRefract Surg . 1999;25:644-47

15. Singh R, Vasavada AR, Janaswamy G. Phacoemulsificationof brunescent and black cataracts. J Cataract Refract Surg .2001;27:1764-69.

16. By committee on Ophthalmic Procedure Assessment CornealEndothelial Photography (Three year revision).Ophthalmology;1997;8:1360-65.

17. Desai J, Vasavada AR, Singh R. The corneal endothelium:Phacoemulsification - Part-I. Emmetropia - J IntraocularImplant &Refract SocIndia , 1998;1:78-81.

18. Zetterstrom C, Laurell CG. Comparison of endothelial cellloss and phacoemulsification energy during endocapsularphacoemulsification surgery. J. Cataract Refract Surg . 1995;21:55-58.

19. Ventura ACS, Walti D, Bohnke. Corneal thickness andendothelial density before and after cataract surgery. Br JOphthalmol 2001;85:18-20.



————————————————————————————————1.Post graduate Trainee Ophthalmology Department HayatabadMedical Complex,Peshawar.2.Senior Registrar OphthalmologyDepartment Hayatabad Medical Complex,Peshawar.3.Post graduateTrainee Radiology Department Hayatabad MedicalComplex,Peshawar.4.TMO Ophthalmology Department HayatabadMedical Complex,Peshawar5.TMO Ophthalmology DepartmentHayatabad Medical Complex,Peshawar————————————————————————————————Correspondence: Dr Mushtaq Ahmad House no 31B, street no 2,sector N4, Phase 4, Hayatabad,Peshawar E.Mail>[email protected] Cell:03339119605————————————————————————————————Received: Oct’2012 Accepted: Nov’2012————————————————————————————————

Postoperative Endophthalmitis,role of Subconjunctival Antibiotics

Intraoperatively during Cataract Surgery

Muhammad Naeem1.Mushtaq Ahmed FCPS2,Hina Mehwish Khan3

Yousaf Jamal Mesud,4 Tariq Shehnam5

ABSTRACTPurpose: To determine role of subconjuctival antibiotics regarding prevention of postoperative endophthalmitis aftercataract surgery.Material and Methods: The study was conducted in the Department of Ophthalmology at Hayatabad Medical Complex,Peshawar, from 1st January 2010 to 30th June 2011. In this study evaluation of 800 eyes listed for senile cataract surgerywere randomized into two groups, one received subconjunctival gentamicin at the end of the surgical procedure and theother group did not receive any subconjunctival antibiotic. All other methods of sterilization and prophylaxis werestandardized for both the groups. All patients received antibiotic-steroid combination eye drops postoperatively and werefollowed up for six weeks. Patients with any major intraoperative complication or who were lost to follow-up were excluded.Results: A total of 760 eyes were included in the study. Females patients were 372(48.94%) and the mean age of patientswas 61.66 years. Manual small incision cataract surgery (MSICS) with IOL was performed in 470 (61.84%) patients,phacoemulsification with IOL in 290 (38.15%) patients. Subconjunctival gentamicin injection was given in 400(52.63%)patients at the end of the procedure, while 360(47.36%) eyes were not injected. Only 01 case developed postoperativeendophthalmitis, and this case was given subconjunctival antibiotic injection during manual small incision cataract surgerywith IOL.Conclusion:Cataract surgery with subconjunctival gentamicin seems to be no role in prevention of endophthalmitis.Key words: Endophthalmitis, Phacoemulsification, Manual small incision cataract surgery.

Original Article

INTRODUCTIONPostoperative endophthalmitis, though rare, is one

of the most devastating complications of intraocularsurgery. It is also the most common form ofendophthalmitis, accounting for approximately 70% ofinfective endophthalmitis.1In approximately 30-45% ofcataract operations, intraocular contamination occurswith facultative pathogenic bacteria from the ocularsurface without the development of endophthalmitis.2

The infectious agent generally enters the eye duringintraocular surgery (postoperative), following apenetrating injury of the globe (post traumatic) or fromhematogenous spread of bacteria to the eye from adistant anatomical site (endogenous). Althoughuncommon, endophthalmitis can also result from

infective keratitis if left untreated.3

The incidence of postoperative endophthalmitisvaries from 0.05 to 0.2% (1/2000 to 1/500 cataractoperations) 4-8. At present there is no clear robustevidence withregards to, which prophylactic methodsto use to prevent postoperative endophthalmitis aftercataract surgery. Most surgeons empirically use avariety of prophylactic techniques includingpreoperative topical antibiotics, povidone-iodinepreparation for periocular skin and conjunctivalinstillation, intraoperative antibiotics both intracameraland subconjunctival and postoperative antibioticstopical or systemic9,10. Our aim of this study was todetermine the role of gentamicin injection in preventionof post operative endophthalmitis.MATERIAL AND METHODS

Patients listed for senile cataract surgery wererandomized into two groups. One receivedsubconjunctival gentamicin injection 20 mg / 0.5 ml atthe end of the surgical procedure and the other groupdid not receive any subconjunctival injection. All themethods of sterilization were standardized for both thegroups. These methods included:1. Pre-operativemoxifloxacin eye drops single drop every half an hourstarting two hours before surgery. 2. Povidone–iodine10% over and around the eyelids. 3. Povidone – iodine5% eye drops for conjunctival instillation. 4. Proper

Dr. Naeem


draping, covering the eye lashes and lid margins. 5.Standard sterilization of surgical instruments. 6.Standard scrubbing of the surgeon and assistant. 7.Single drop of moxifloxacin eye drops at the end ofsurgery.All patients received antibiotic-steroidcombination eye drops postoperatively, and werefollowed up for six weeks to assess for onset ofpostoperative endophthalmitis. Patients were seen on1st day, one week and then six weeks postoperatively.Patients were asked to contact urgently if they developany redness, pain or blurring of vision.The softwareSPSS version 11 was used for data analysis.RESULTS

A total of 800 eyes of 724 patients were initiallyincluded in the study. We excluded 40 eyes due to eitheran intraoperative complication or due to loss of follow-up. The mean age of our patients was 61.60 years.Females constituted 372 (48.94%) cases.Table 1 showsthat, Manual small incision cataract surgery (MSICS)with IOL was performed in 470 (61.84%) cases.Subconjunctival gentamicin injection was given in400(52.63%) eyes at the end of the procedure, and thisgroup included different types of surgeries, Manualsmall incision cataract surgery and phacoemulsificationas shown in table 2 . Only one case developedpostoperative endophthalmitis, and this case was givensubconjunctival antibiotic injection during manualsmall incision cataract surgery with IOL. Theendophthalmitis was diagnosed clinically; culture wasnegative on vitreous tap. It was treated with intravitralceftazidime and the vision recovered to 6/18. Theincidence of postoperative endophthalmitis in our studywas 0.13%.DISCUSSION

Postoperative endophthalmitis is one of the mostfeared complications following intraocular surgery andit is the second common cause of endophthalmitis after

trauma in Pakistan with poor visual outcome11,12.However, due to the low incidence of postoperativeendophthalmitis, it has been difficult to assess theefficacy of various prophylactic measures. There aretwo approaches for prophylaxis; the first is to reduceocular surface flora by using topical antisepticpreparation or antibiotics and the second is, to eradicatebacteria that enter the eye during surgery, by the use ofantibiotics through intracameral, subconjunctival,topical or systemic route13.

The most common source of organisms inpostoperative endophthalmitis is the patient’s ownocular surface flora, so it is recommended to instillpreoperative 5% povidoneiodine in the conjunctivalsac14,15. A review by Ciulla 16 has found that povidoneiodine antisepsis of skin, lids and conjunctiva to be theonly recommended practice on the basis of the currentevidence. Ciulla TA had also reported that, all otherprophylaxis interventions (including preoperative lashtrimming, preoperative saline irrigation, preoperativetopical antibiotics, antibiotic-containing irrigatingsolutions and postoperative subconjunctival antibioticinjection) are possibly relevant but not definitely relatedto clinical outcome.The European Society of Cataractand Refractive Surgeons (ESCRS) guideline onprevention of postoperative endophthalmitisrecommend intracameral cefuroxime and does notencourage subconjunctival antibiotics17,18for threereasons; 1. Intracameral cefuroxime achieves higheraqueous concentration after surgery thansubconjunctival cefuroxime. 2. The use ofsubconjunctival antibiotics has been questionable intheir affectivity in preventing postoperativeendophthalmitis. 3. The potential complications causedby subconjunctival injections like subconjunctivalhaemorrhage and penetration of sclera and theextraocular muscles.

However subconjunctival antibiotics have been astandard method used to prevent postoperativeendophthalmitis all over the world, including Pakistanand the great majority of United Kingdom surgeonsroutinely gives subconjunctival antibiotics at the endofcataract surgery, and that is due to the concernsregarding ocular toxicity from intracameralantibiotics19,20. Lehmann OJ 21 and Ng JQ 22in their studieshad favoured the use of subconjunctival antibiotics asprophylaxis against endophthalmitis and reported thatit reduces the risk by 50%.To change our routine practicewe did this study, which showed no case ofendophthalmitis in 180 cases that were not givensubconjunctival injections.It had proved that not usingsubconjunctival antibiotics did not put patients on extrarisk of getting endophthalmitis. Incidentallyendophthalmitis occurred in one case out of 200 eyes

Table:1 Types of surgery

MSICS+IOL Phaco+IOL Total

470 (61.84%) 290 (38.15%) 760 (100%)MSICS: Manual small incision cataract surgery

Table:2 Sub conjunctival antibioticsin different types of surgeries

Surgical Injected Not Grandprocedure injected Total

MSICS + IOL 248(52.76%) 222(47.23%) 470(61.84%)

Phaco + IOL 152(52.41%) 138(47.58%) 290(38.15%)

Total 400(52.63%) 360(47.36%) 760(100%)MSICS: Manual small incision cataract surgery

Postoperative Endophthalmitis, role of Subconjunctival Antibiotics Intraoperatively during Cataract Surgery


which were given subconjunctival gentamicin injection.This patient underwent manual small incision cataractsurgery with IOL. In this study regarding the patternsof endophthalmitis prophylaxis in Canada it wasreported that only 26% of surgeons give intraoperativeantibiotics intracamerally or subconjunctivally, whilethe majority of surgeons (74%) are using similarmethods of prophylaxis as were used in our study likeperfect draping technique and instillation of povidoneiodine 5% into the conjunctival sac prior to surgery. Thelimitation of this study may be that we included onlysenile cataract. We excluded all other surgeries alongwith any eventful surgery such as posterior capsulartear or vitreous loss which carries a significant risk forthe development of postoperative endophthalmitis.This was done to avoid any extra risk to be put onpatients with high risk.CONCLUSION

Cataract surgery with subconjunctival gentamicinseems to be no role in prevention of endophthalmitis.REFERENCES1. Forster R.K, Abbott RL, Gelender H. Management of

infectious endophthalmitis.Opthalmology 1980;87:313-15.2. Sherwood DR, Jacobs RWJ, Hart JS, et al. Bacterial

contamination of intraocular and extraocular fluids duringextracapsular cataract extraction. Eye. 1989; 3: 308-12.

3. Callegan MC, Engelbert M, Parke DW, et al.Bacterialendophthalmitis: epidemiology, therapeutics, andbacteriumhostinteractions. Clin Microbiol Rev. 2002; 15: 111-24.

4. West ES, Behrens A, McDonnell PJ, et al. The incidence ofendophthalmitis after cataract surgery among the USMedicare population increased between 1994 and 2001.Ophthalmology 2005; 112: 1388-94.

5. Kamalarajah S, Silvestri G, Sharma N, et al. Surveillance ofendophthalmitis following cataract surgery in the UK. Eye2004; 18: 580-7.

6. Schmitz S, Dick HB, Krummenauer F, et al. Endophthalmitisin cataract surgery: results of a German survey.Ophthalmology. 1999; 106: 1869-77.

7. Wong TY, Chee SP. The epidemiology of acuteendophthalmitis after cataract surgery in an Asianpopulation. Ophthalmology. 2004; 111: 699-705.

8. Lalitha P, Rajagopalan J, Prakash K, et al. Postcataractendophthalmitis in South India incidence and outcome.Ophthalmology. 2005; 112: 1884-9.

9. Gupta MS, McKee HD, Stewart OG. Perioperativeprophylaxis for cataract surgery: survey of ophthalmologistsin the north of England. J Cataract Refract Surg. 2004; 30:2021-2.

10. Rosha DS, Ng JQ, Morlet N, et al. Cataract surgery practiceand endophthalmitis prevention by Australian and NewZealand ophthalmologists. Clin Experiment Ophthalmol2006; 34: 535-44.

11. Babar TF, Masud Z, Saeed N, et al. A two years audit ofadmitted patients with the diagnosis of endophthalmitis.Pak J Med Res 2003; 42: 105-11.

12. Hussain I, Kundi NK. Visual outcome in infectiveEndophthalmitis. J Med Sci 2005; 13: 151-3.

13. Ou JI, Ta CN. Endophthalmitis prophylaxis. Ophthalmol ClinN Am. 2006; 19: 449-56.

14. Speaker MG, Milch FA, Shah MK, et al. Role of externalbacterial flora in the pathogenesis of acute postoperativeendophthalmitis. Ophthalmology 1991; 98: 639-49.

15. Speaker MG, Menikoff JA. Prophylaxis of endophthalmitiswith topical povidone-iodine. Ophthalmology 1991; 98: 1769-75.

16. Ciulla TA, Starr MB, Masket S. Bacterial endophthalmitisprophylaxis for cataract surgery: an evidence – based update.Ophthalmology 2002; 109: 13-24.

17. Barry P, Seal DV, Gettinby G, et al. ESCRS EndophthalmitisStudy Group. ESCRS study of prophylaxis of postoperativeendophthalmitis after cataract surgery: Preliminary reportof principal results from a European multicenter study. JCataract Refract Surg. 2006; 32: 407-10.

18. Yu-Wai-Man P, Morgan SJ, Hildreth AJ, et al. Efficacy ofintracameral and subconjunctival cefuroxime in preventingendophthalmitis after cataract surgery. J Cataract Refract Surg2008; 34: 447-51.

19. Dinakaran S, Crome DA. Prophylactic measures prevalentin the United Kingdom. J Cataract Refract Surg. 2002; 28: 387-8.

20. Ang GS, Barras CW. Prophylaxis against infection in cataractsurgery: A survey of routine practice. Eur J Ophthalmol. 2006;16: 394-400.

21. Lehmann OJ, Roberts CJ, Ikram K, et al. Association betweennonadministration of subconjunctival cefuroxime andpostoperative endophthalmitis. J Cataract Refract Surg. 1997;23: 889-93.

22. Ng JQ, Morlet N, Bulsara MK, et al. Reducing the risk forendophthalmitis after cataract surgery: Population-basednested case-control study: Endophthalmitis Population Studyof Western Australia: sixth report. J Cataract Refract Surg.2007; 33: 269-80.

23. Hammoudi DS, Abdolell M, Wong DT. Patterns ofperioperative prophylaxis for cataract surgery in Canada.Can J Ophthalmol 2007; 42: 681-8.

Postoperative Endophthalmitis, role of Subconjunctival Antibiotics Intraoperatively during Cataract Surgery


————————————————————————————————1. Registrar Ophthalmology Department Hayatabad Medical ComplexPeshawar. 2Associate Prof. 3Registrar. 4,5Medical Officers————————————————————————————————Correspondence Dr Afzal Qadir Registrar OphthalmologyDepartment Hayatabad Medical Complex Peshawar Email address;[email protected] Cell No. 0321-9128247 Fax. 091-9217189,Mailing Address: House no 40, Street 2, N/4, Phase 4, Hayatabad,Peshawar.————————————————————————————————Received: July’2012 Accepted: Oct:2012————————————————————————————————

Penetrating Keratoplasty:Indications, Visual outcomes, and Complications

in Tertiary Care Hospital

Afzal Qadir1, Mir Zaman2, Umer Khan3, Ashfaq-u-Rehman4, Inayat ullah Khan5.

ABSTRACTPurpose: To evaluate the indications, visual outcomes, and complications of penetrating keratoplasty in tertiary carehospital Khyber Pakhtoonkhwha (KPK).Material and Methods: Retrospective case series of 441 patients of penetrating keratoplastys (PKPs) which was performedby a single experienced surgeon in a tertiary care teaching hospital in the Department of Khyber Institute of OphthalmicMedical Sciences (KIOMS), Hayatabad Medical Complex, Peshawar from May 2004 to May 2011. Preoperative evaluationfor indications, surgical technique, operative, postoperative complications, and Snellen acuity were analysed.Results: In our total 441 patients 315 (71.42%) were male and 126 (28.58%) were female. In 275 patients right eye whilein 171 patients left eye was involved. Age range (5-70 years), mean age group was 40 years. Mean follow-up was 18months (1-24 months). The most common indication for keratoplasty was keratoconus 305 (69.16%), followed by infectedcorneal ulcer 41 (9.29%) and corneal scar 24 (5.44%). Pre-operative visual acuity were counting fingers in 265 (60%) ofpatients. 6/60 – 1/60 in 176 (40 %) of patients. Post-operatively 150 (34%) patients had best corrected visual acuity of 6/6 – 6/12. In 130 (29.47%) of patients had a best corrected visual acuity of 6/18 – 6/36.Most common complication was astigmatism, posterior sub capsular cataract, toxic anterior segment syndrome, graftfailure and rejection.Conclusions: PK is currently an effective long-term treatment option for improving visual function in various cornealdiseases depending upon the underling cause. Keratoconus and infective corneal ulcer were the most common indicationfor PK in our setup.Keywords: Corneal transplantation, graft survival, visual acuity, complications.

Original Article

INTRODUCTIONThe cornea is normally avascular tissue that

refracts or bends light rays as they enter the eyesallowing them to focus on the retina.1,2 Penetratingkeratoplasty (PK) is a corneal transplant procedure inwhich full thickness diseased host corneal tissue isreplaced with healthy donor corneal tissue.3 Cornealtransplant is the most common tissue transplant worldwide.4 Modern day success of transplantation isattributed to eye bank storage techniques, ocularpharmacology and improved surgical techniques.5,6

keratoplasty may lamellar or full thickness. Lamellerkeratoplasty: which is a partial thickness cornealgrafting and penetrating keratoplasty: is a full thicknesscorneal grafting. The indications of keratoplastyinclude; optical to improve visual acuity by replacingthe opaque host tissue by a healthy donor cornea.

Tectonic in patients with stromal thinning,descemetoceles and corneal perforation to preservescorneal anatomy and integrity. Therapeutic is removalof inflamed or infected corneal tissue refractive totreatment by antibiotics or antiviral drugs. Cosmetic inpatients with corneal scar giving a whitish opaque hueto the cornea.7

The purpose of penetrating keratoplasty inmajority of cases is to improve visual acuity, followedby relief from pain and to save the globe integrity. Theindication for penetrating keratoplasty is not onlyvaried country to country but institution to institutionin the same country.4 If corneal perforation seems likely,urgent management is required, since cornealperforation has high morbidity and keratoplasty is acommon procedure.8

METHODS AND MATERIALS:Retrospective case series of 441 patients of

penetrating keratoplastys (PKPs) which performed bya single experienced surgeon in a tertiary care teachinghospital of Khyber Pakhtoonkhwa in the Departmentof Khyber Institute of Ophthalmic Medical Sciences(KIOMS), Hayatabad Medical Complex, Peshawar fromMay 2004 to May 2011. All patients were admitted.Informed consent was signed and prepared for local orgeneral anesthesia. Preoperative evaluation were donewith detail history of ocular and systemic diseases,

Dr. Afzal Qadir


family history of ocular and systemic diseases, drughistory with previous record if available, socioeconomicstatus of the patient. Recipient factors included age,indication for transplantation, prior grafts, preoperativeocular conditions (glaucoma, uveitis, infection, ocularsurface disease, and corneal vascularisation (numberof quadrants of superficial and deep vascularisation)anterior segment and posterior segment slit lampexamination with high magnification, as well as indirectophthalmosocpy to look for posterior segmentpathology and systemic examination were performed.B-scan ultrasonography was performed in suspectedcases, corneal topography in keratoconus patients, toget proper diagnosis for surgical indications. Operative,postoperative complications, and best corrected Snellenacuity were analysed. Associated surgical proceduresat the time of surgery, such as intraocular lens (IOL)implantation, exchange or removal were alsodocumented.Surgical technique:

Corneal transplantation was performed in all casesby a single experienced surgeon. Donor cornea wasobtained from Murad Eye Bank of the Hospitalinspected and then trephined. The donor cornea wassutured to the recipient using 10/0 nylon interruptedsutures as a routine, and subconjunctival antibiotic andsteroid were given. The Eye was bandaged with contactlens. If required, Cataract extraction was performedusing an extracapsular technique following a can openeror continuous curvilinear capsulorhexis. Soft lensmatter was aspirated using manual Simco aspiration.Insertion of an IOL was decided on a case-to-case basis.

Routine postoperative medication consisted oftopical dexamethason combined with topicaltobramycin antibiotic one hourly daily for one week.Following discharge, the patient was examined onweekly basis for the first month, fortnightly for threemonths and monthly for one year. Topically, antibioticwas reduced over the subsequent postoperative monthand dexamethason tapered down over 3 months witha change to fluromethalon 0.1% once daily for sixmonths. All sutures were generally removed between12 and 24 months. Following removal, steroids wereincreased to four times daily and reduced to once dailyover 1 week with covering antibiotics. In general,episodes of immunological endothelial transplantrejection were treated with hourly prednisolone 1% for1 week and reduced dependent on response. In severecases, a single pulsed dose of i.v. methylprednisolone500mg has been used. Transplant failure was definedas described by Price et al.9 The timing of transplantfailure was defined as the time of the first postoperativeexamination when the corneal graft was described asfailed. Graft failure because of endothelial

decompensation was considered secondary to rejectionif evidence of keratic precipitates and endothelialrejection lines or definite episodes of rejection had beendocumented.RESULTS:

Out of total 441 patients 315 (71.42%) were maleand 126 (28.58%) were female. In 275 patients right eyewhile in 171 patients left eye were involved. Age rangedfrom (5-70 years), mean age group was 40 years. Meanfollow-up was 18 months (1-24 months). The mostcommon indication for keratoplasty was keratoconuswhich were 305 (69.16%) of the patients, followed byinfective corneal ulcer 41 (9.29%) of patients. Cornealscar were 24 (5.44%), pseudophakic bullous keratopathy20 (4.53%), aphakic bullous keratopathy 13 (2.94%),band keratopathy were 08 (1.81%), Fuch’s endothelialdystrophy were 10 (2.26%), Corneal macular dystrophywere 09 (2.04%). Re-grafting were done in 10 (2.26%) ofpatients. In total 441 patients 25 (5.66%) had gone underopen sky procedure. In all these cases pre-operative andpost-operative snellen visual acuity assessment wasdone. Pre-operative visual acuity were counting fingersin 265 (60%) of patients while 6/60 – 1/60 in 176 (40%)of patients. Which improved post operative by 6/6 –6/12 in 150 (34.0%), followed by 130 (29.47%) had 6/18– 6/36. One (2%) had become no perception of light(NPL) shown in table II. Toxic anterior segmentsyndrome was observed in 05 (1.337%) of patients.Secondary glaucoma occurred in 23 (5.21%) of patients.Graft rejection occurred in 38 (8.61%) of patient in themean interval of 4 months. While graft failure occurredin 27 (6.12 %) of patients. Posterior sub capsular cataractwas observed in 05 (1.337%) of cases. 130 (29.47%) ofpatients had astigmatism were corrected with glassesor contact lenses. Hyphaema occurred in 07 (1.5%) ofcases. Paretic pupil (iris sphincter paralysis fixed mid-dilated pupil) occur in 03 (0.68%) of patients.

Penetrating Keratoplasty: Indications, Visual outcomes, and Complications in Tertiary Care Hospital


DISCUSSION:Penetrating keratoplasty (PK) can visually

rehabilitate many of those who suffer from blindnessor visual impairment due to corneal diseases. Theprognosis, however, is dependent on the pathologyresponsible for causing corneal blindness or visualimpairment. The purpose of this study was to documentthe indication of penetrating keratoplasty in tertiarycare hospital of the province.

Keratoconus remain the most common indication69.16% for penetrating keratoplasty in our series whichcan better be compared with national and internationalstudies.5,9 while a study by Ngamti et al in MaharajNakorn hospital showed that the leading indicationsfor PK were bullous keratopathy (28.9%), which is(7.47%) in my study because of socioeconomic factor.11

Mohammad H D et al12 had performed PK in 43% forcorneal scar, and 20% for keratoconus. The rate ofcorneal transplant rejection in most studies is between9.9 and 17.2%13 and we had a graft rejection rate of 8.61%and failure rate of 6.12% which occur in patients withcorneal ulcer, superficial and deep corneal visual acuity6/12 or better in 34% of cases and 6/18 – 6/36 in 29.47%of cases as compare with Bhatti et al 33.3% and 41.7%respectively.13 Spontaneous loosening or breakage ofsutures occurred in 40 patients (9.07%) and suturerelated abscesses were seen in 12 patients (2.72%) at anaverage of 6 months follow-up.14

CONCLUSIONPK is currently an effective long-term treatment

option for improving visual functions. Depending uponthe underline cause. Keratoconus and infective cornealulcer remain the most common indication for PK in oursetup.REFRENCES:1 Godeiro KD, Coutinho AB, Pereira PR, et al.

Histopathological diagnosis of corneal button specimens: Anepidemiological study. Ophthalmic Epidemiol 2007;14(2):70-5.

2 Kanavi MR, Javadi MA, Sanagoo M. Indications forpenetrating keratoplasty in Iran. Cornea 2007;26(5):561-3.

3 Verdier DD, Penetrating keratoplasty In: Krachmer JH,Mannis MJ, Holland EJ, editor: cornea. Vol.III. Surgery ofcornea and conjunctiva. St. Louis: Mosby, 1997: 1581-92.

4 I Rahman, F Carley, C Hillarby, A Brahma and A B Tullo.Penetrating keratoplasty: indications, outcomes, andcomplications. Eye (2009) 23, 1288–1294;

5 N-Al-Yousf, I Mavrikakis, E Mavrikakis, SM Daya.Penetrating keratoplasty: indications over a 10 years period.Br J Ophthalmol. 2004 August; 88(8): 998-1001.

6 Chen WL, Hu FU, Wang IJ. Changing indications forpenetrating keratoplasty in Taiwan from 1987 to 1999. Cornea2001; 20: 141-4.

7 Buehler PO, Schein OD, Stamler JF, Verdier DD, Katz J. (1992).The increase risk of ulcerative keratits among disposable softcontact lens users. Arch Ophthalmol; 110 : 1555-8.

8 Portnoy SL, Insler MS, Kaufman HE. Surgical managementof corneal ulceration and perforation. Surv Ophthalmol.1989;34:47–58.

9 Price FW, Whitson WE, Marks RG. Graft survival in fourcommon groups of patients undergoing penetratingkeratoplasty. Ophthalmology 1991; 98: 322–328.

10 Khan WA, Indications of penetrating keratoplasty at Al-ShifaTrust Eye Hospital Rawalpindi. Pakistan Armed ForcesMedical Journal. 2005, (01): 09.

11 Ngamti phkorns, Parasit slip. Clinical indication for PK inMaharaj Nakorn chaing Mai Hospital. J Med Assos 2003; 86(3):206-11.

12 Mohammad H D, Amini A. Clinical Indications ofPenetrating Keratoplasty: An Epidemiological Study inTeaching Hospitals of Birjand Iranian Journal ofOphthalmology 2008;20(4):30-33.

13 Bhatti NM, Zaman Y, et al. Outcome of penetratingkeratoplasty from a corneal unit in Pakistan. Pak JOphthalmol 2009; 25 (3): 152-59

14 Asfour W, Shaban R. Suture-related complications afterpenetrating keratoplasty at King Hussein Medical Center.Journal of the Royal Medical Services March 2011; 18(1): 30-33.

Table I: Indication for Keratoplasty (N-441)

Indications No of patientsKeratoconus 305 (69.16%)Infective corneal ulcer 41 (9.29)Corneal scar 24 (5.44%)Pseudophakic bullous keratopathy 20 (4.53%)Aphakic bullous keratopathy 13 (2.94%)Band keratopathy 08 (1.81%)Fuch’s endothelial dystrophy 10 (2.26%)Corneal macular dystrophy 09 (2.04)Regrafting 10 (2.26%)

Total 441

Table II: Pre-operative and post-operative visual acuity (N-441)

Visual acuity Preoperative Postoperative6/6 – 6/12 0 150 (34%)6/18 – 6/36 0 130 (29.47%)6/60 – 1/60 176 (40%) 90 (20.40%)CF 265 (60%) 70 (15.87%)NPL 0 1 (2%)

CF: counting fingerNPL: No perception of light

Table III: Post-operative complications (N-441)

Complications No of patientsAstigmatism 130 (29.47%)Graft rejection 38 (8.61%)Graft failure 27 (6.12%)Secondary glaucoma 23 (5.21%)Hyphaema 07 (1.5)TASS 05 (1.337%)Post: sub capsular cataract 05 (1.337%)

Paretic pupil 03 (0.68%)

TASS: Toxic anterior segment syndrome

Penetrating Keratoplasty: Indications, Visual outcomes, and Complications in Tertiary Care Hospital


————————————————————————————————1.Registrar Ophthalmology Department Hayatabad Medical ComplexPeshawar. 2Associate Prof. 3,4,5Medical Officers.————————————————————————————————Correspondence Dr Afzal Qadir Registrar OphthalmologyDepartment Hayat abad Medical Complex Peshawar Email address;[email protected] Cell No. 0321-9128247 Fax. 091-9217189,Mailing Address: House no 40, Street 2, N/4, Phase 4, Hayatabad,Peshawar.————————————————————————————————Received: July’2012 Accepted: Oct:2012————————————————————————————————

Role of Amniotic Membrane in Ocular Surface Diseases

Afzal Qadir1, Mir Zaman2, Irfanullah Shah3, Zakir Hussain,4 Inayat-ullah Khan5

ABSTRACT

Objectives: Efficacy of amniotic membrane in ocular surface diseases.Material and Methods: This interventional case series was conducted in the Department of Khyber Institute of OphthalmicMedical Sciences (KIOMS) Hayatabad Medical Complex, Hayatabad, Peshawar from January 2009 to January 2011. Inthis study 186 patients with various diseases of ocular surface were treated with amniotic membrane transplantation overa period of two years. Surgeries were performed as needed under local and general anesthesia, amniotic membrane wasused as a therapeutic contact lens. Significant improvement in sign and symptom, like ocular pain, irritation, photophobia,discharge, and visual acuity was noted.Results: Out of 186 patients 70% were male and 30% were female. In ocular surface disorder, 50 patients were pterygium,40 patients with infectious keratitis, 30 patients with shield ulcer, 15 patients with impending perforation, 12 patients withband keratopathy, 08 patients with bullous keratopathy, 08 patients with penetrating keratoplasty, 06 patients with chemicalinjury, 06 patients with recurrent corneal epithelium erosion, 04 patients with neurotrophic keratitis, 02 patients withmooren ulcer, 02 patients with stevens johnson syndrome, 02 patients with filtering bleb and 01 patient with conjunctivalsquamous cell carcinoma.Conclusion: Amniotic membrane is a safe, effective and useful treatment for the treatment of ocular surface disorders.Keywords: Amniotic membrane, ocular surface diseases.

Original Article

INTRODUCTION:The normal ocular surface is covered by epithelial

cells which can be damaged by certain systemicinflammatory diseases,1 primary ocular diseases, andtrauma resulting in the breakdown of ocular surface.2

If the normal epithelialization process fails, ocularsurface defect becomes chronic. Chronic inflammationleads to neovascularization, corneal scarring,opacification, corneal thinning, corneal melting andpossible corneal perforation. Traditional treatments forocular surface disorders include correcting underlyingpathology, suppressing inflammation and promotinghealing process. Currently, artificial tears, lubricants,fibronectins,3,4 growth factors,5 and substance P6 areused. However, if defect persists and stromal thinningdevelops, more invasive surgical options like tissueadhesive,7 bandage contact lens,8 conjunctival flap,9

penetrating keratoplasty, Boston keratoprosthesies andtarsorrhaphy can be performed.10 But these treatmentshave their own complications. In this background

amniotic membrane can be considered as an option fortreating the ocular surface defects.3,4

In 1910, Davis reported the use of fetal membranein skin transplantation for the first time.11 Amnioticmembrane transplantation in ophthalmology wasreported by De Roth in 1914 who achieved partialsuccess in treatment of conjunctival epithelial defects.12

There was very little information available inophthalmic literature until the study by Kim and Tsengin 1995 who used amniotic membrane transplantationfor ocular surface reconstruction of severely damagedcornea in rabbit model. Since that experimental study,amniotic membrane transplantation has been used forpersistent corneal epithelial defects, neurotrophiccorneal ulcers, conjunctival surface reconstruction,bullous keratopathy, chemical or thermal burns and inpatients of Steven-Johnson syndrome.13-15 Ocular surfacedisorders are a common problem and currentmanagement is not satisfactory. Amniotic membranetransplantation has shown better results in treatingthese disorders. In Pakistan, a very little work has beendone so far in this regard. So, I scientifically studiedthis new technique in the local setup.MATERIAL AND METHODS:

This interventional case series was conducted inthe Department of Khyber Institute of OphthalmicMedical Sciences (KIOMS), Hayatabad MedicalComplex, Hayatabad Peshawar from January 2009 toJanuary 2011. In this study evaluation of over a periodof two years of 186 patients were included. Age rangingfrom 3 years to 70 years. Patients with globe perforation

Dr. Afzal Qadir


were excluded from this study. Informed writtenconsent was taken. Detail ocular and systemic historyand examination were performed to get properdiagnosis.Preparation of Amniotic membrane:

Amniotic membrane was obtained fromprospective donors undergoing elective Caesareansection, who were negative for communicable diseasesincluding HIV, hepatitis and syphilis. Differentprotocols exist for the processing and storage. We usedprotocol described by Kim et al.16 According to whichplacenta is cleaned and stored with balanced saltsolution containing a cocktail of antibiotics (Table 1)under sterile conditions.Surgical TechniquesI. Inlay or graft technique: When Amniotic

membrane is tailored to the size of the defect, ismeant to act as a scaffold for the epithelial cellsand which then merges with the host tissue, it isreferred to as a graft.17 Amniotic membrane wassecured with its basement membrane or epithelialside up to allow migration of the surroundingepithelial cells on the membrane.

II. Overlay or patch technique: When the Amnioticmembrane is used akin to a biological contact lensin order to protect the healing surface defectbeneath; it is referred to as a patch.18 A patch alsoreduces inflammation by its barrier effect againstthe chemical mediators from the tear film. Whenused as patch the membrane is secured with itsepithelial side up which either falls off or isremoved.

III. Filling-in or layered technique: In this techniquethe entire depth of an ulcer crater is filled withsmall pieces of AM trimmed to the size of thedefect. A larger graft is sutured to the edges ofthe defect in an inlay fashion and an additionalpatch may help in preserving the deeper layersfor a longer duration.19 Preoperative evaluationwas applied to all patients with special attentiongiven to patient’s symptoms with respect to pain,photophobia and best corrected visual acuity.Follow up was observed at first post operativeday, 1st week, 2nd week and 1 month for bestcorrected visual acuity, ocular symptoms (painand photophobia) and complications. The datawas analyzed by SPSS version 10.00, the variablesof outcome measures (pain, photophobia, bestcorrected visual acuity, graft uptake) waspresented as proportions and ratios. The variablesof outcome were compared with some of variablesof demography. Since this study was a quasi-experimental, no test of significance wasnecessary.

RESULTS:Of the 186 patients of different ocular surface

disorders included in this study. 70% were males and30 % were females of ocular surface disorders of varioustypes. The most common ocular surface disorder 50(26.88%) patients were pterygium, followed by 40(21.50%) patients of infectious keratitis, 30 (16.12%)patients of shield ulcer, 15 (8.06%) patients withimpending perforation, 12 (6.45%) patients with bandkeratopathy, 08 (4.30%) patients were bullouskeratopathy, 08 (4.30%) patients with penetratingkeratoplasty, 06 (3.22%) patients with chemical injury,06 (3.22%) patients with recurrent corneal epitheliumerosion, 04 (2.15%) patients with neurotrophic keratitis,02 (1.075%) patients with mooren ulcer, 02 (1.075%)patients with stevens johnson syndrome, 02 (1.075%)patients with filtering bleb, and 01 (0.53%) patient withconjunctival squamous cell carcinoma.

The ocular surface defects were present in botheyes of (40.0%) cases. (53.3%) cases had these defectsin right eye, while (6.7%) cases left eye was involvedout of total 186 cases. Ocular pain was one of the mostimportant variable of study. It was recorded on the painscale from grade 0 – 4 as described by the patient. 30(16.12%) patients did not complain any pain (Grade 0).40 (21.50%) cases had mild pain (grade 1). 12 (6.45%)cases were having moderate pain (grade 2). 08 (4.30%)patients described severe pain. After one month ofamniotic membrane transplantation, most of thepatients 160 (86.02%) were having no pain (grade 0).Only 6 (3.22%) and 4 (2.15%) patients described mild(grade 1) and moderate (grade 2) pain. No patientdescribed grade 3 and 4 level of pain. 60 (32.25%) of thepatients were photophobic, rest of them were notcomplaining of photophobia. A remarkableimprovement was noted in this regard. At one monthafter surgery, 180 (96.77%) patients did not complainof photophobia and only 6 (3.22%) cases were stillcomplaining of photophobia. There was animprovement of best corrected visual acuity noted, afterone month of surgery 80 (43.01%) had best correctedvisual acuity of 6/12, while 30 (16.12%) case had 6/18and 26 (13.97%) patients were having visual acuity 6/24. 50 (26.88%) were still having best corrected visualacuity of 6/60 or less.

Table 1: Contents and concentrations of antibiotics solution usedfor cleaning and preservation of amniotic membrane.

Antimicrobial Agent DosePenicillin 50 mg/mlStreptomycin 50 ìg/mlNeomycin 100 mg/mlAmphotericin B 2.5 mg/ml



Table 2: Causes of ocular surface diseases (N 186)

Ocular surface diseases Number of patients

Pterygium 50 (26.88%)

Infectious keratitis 40 (21.50%)

Shield ulcer 30 (16.12%)

Impending perforation 15 (8.06%)

Band keratopathy 12 (6.45%)

Bullous keratopathy 08 (4.30%)

Penetrating keratoplasty 08 (4.30%)

Chemical injury 06 (3.22%)

Recurrent corneal epithelial erosion 06 (3.22%)

Neurotrophic keratitis, 04 (2.15%)

Mooren ulcer 02 (1.075%)

Stevens johnson syndrome 02 (1.075%)

Filtering bleb 02 (1.075%)

Conjunctival squamous cell carcinoma 01 (0.53%)

Total 186

DISCUSSIONOcular surface disorders are a common problem

that presents not only with decrease of vision but alsopain and photophobia. Unfortunately, So far its medicalor surgical treatment has not shown satisfactory results.Amniotic membrane that had been used for otherpurposes like biological dressing to cover the openwounds and skin transplantation, have also shown goodresults in ocular surface defects healing and thusrelieving the symptoms of ocular irritation. Humanamniotic membrane is derived from the fetalmembranes and is loosely attached to the chorion.20 Itis composed of three layers: a single epithelial layer,thick basement membrane, and avascular stroma.

Human amniotic membrane has been shown to containcollagen types III and V. It also contains collagen typesIV and VII similar to corneal epithelial basementmembrane as well as fibronectin and laminin.21

Additionally, it contains fibroblast and other growthfactors. Amnion prevents inflammatory cell infiltrationand reduces apoptosis in keratocytes aftertransplantation onto the corneal surface.22 Due to allthese properties amniotic membrane transplantation isfound to be an important tool for reconstruction ofocular surface disorders.

Reduction in symptoms of ocular irritation thatincludes pain and photophobia was 90 % in our studywhich is comparable to the other studies.23 Increasedcomfort level, improved the quality of life of thepatients. There was no remarkable improvement in bestcorrected visual acuity observed in our study. The finalvisual acuity less than 6/60 was recorded in 67 % ofcases in our study which was quite similar to study byPrabhasawat P, Tesavibul N who also observed thesimilar ratio in their study.23 However increased comfortlevel improved the quality of life of these patients andvisual acuity was not the issue in these patients. Failurewas noted in 3 (10%) cases in our study. This was dueto graft necrosis, active infection and intractable cornealperforation. This failure points out the limitations ofAMT in treating ocular surface disorders.

The possible causes of failure could be, continuoustissue destruction compounded with active infectionunderneath the graft, had retarded healing andsecondly there might have been inadequate limbal stemcells and intact sensory innervations which aremandatory for repairing and maintaining ocular surfaceintegrity.24 Thirdly normal keratocytes from adjacentarea might be important in restoring stromal integrityafter AMT. The results of stud y showed that amnioticmembrane transplantation is effective in ocular surfacedisorders when all other existing methods ofmanagement fail.CONCLUSION

Amniotic membrane transplantation appears tobe a useful method to alleviate symptoms of ocularsurface irritation like pain, photophobia and lacrimationcaused by the ocular surface disorders. It does not onlyheal the corneal surface defect but also helps inpreserving the globe. The future studies are requiredfor further elaboration of usefulness of this tissue.REFERENCE1. Mejia LF, Acosta C, Santamaria P. Use of nonpreserved

human amniotic membrane for the reconstruction of ocularsurface. Cornea. 2000; 19: 288-91

2. Sangwan VS, Tseng SCG. New Perspectives in ocular surfacedisorders. An integrated approach for diagnosis andmanagement. Indian J Ophthalmol. 2001; 49:153-68.



3. Spigelman AV, Deutsch TA, Sugar J. Application ofhomologous fibronectin to persistent human cornealepithelial defects. Cornea. 1987; 104: 494-501.

4. Nishida T, Nakagawa S, Manabe R. Clinical evaluation ofibronection eye drops on epithelial disorders after herpetickeratitis. Ophthalmology. 1985; 92: 213-16.

5. Feldman ST. The effect of epidermal growth factor on cornealwound healing: practical consideration of therapeutic use.Refract Corneal Surg. 1991; 7: 232-9.

6. Brown SM, Lamberts DW, Reid TW, et al. Neurotrophic andanhidrotic keratopathy treated with substance P andinsulinlike growth factor I. Arch Ophthalmol. 1997; 115: 926-7.

7. Globovic S, Paronovic A. Cyanoacrylate glue in the treatmentof corneal ulcerations. Fortschr Ophthalmol. 1990; 87: 378-81.

8. Pfiser RR. Clinical measures to promote corneal epithelialhealing. Acta Ophthalmol. 1992; 70: 78-83.

9. Lugo M, Arentsen JJ. Treatment of neurotrophic ulcers withconjunctival flaps. Am J Ophthalmol. 1987; 103: 711-2.

10. Welch C, Baum J. Tarsorrhaphy for corneal disease in patientswith rheumatoid arthritis. Ophthalmol Surg. 1988;19:31-32

11. Davis JW. Skin transplantation with a review of 550 cases atthe Johns Hopkins Hospital. Johns Hopkins Med J. 1910; 15:307-96.

12. De Rotth A. Plastic repair of conjunctival defects with fetalmembranes. Arch Ophthalmol. 1940; 23: 522-5.

13. Shimazaki J, Yang HY, Tsubota K. Amniotic membranetransplantation for ocular surface reconstruction in patientswith chemical and thermal burns. Ophthalmology. 1997; 104:2068-76.

14. Meller D, Pires RT, Mack RJS. Amniotic membranetransplantation for acute chemical and thermal burns.Ophthalmology. 2000; 107: 980-90.

15. Ucakhan OO, Koklu G, Firat E. Nonpreserved humanamniotic membrane transplantation in acute and chronicchemical eye injuries. Cornea. 2002; 21: 169-72.

16. Kim JC, Tseng SC. Transplantation of preserved humanamniotic membrane for surface reconstruction in severelydamaged rabbit corneas. Cornea. 1995; 14: 473-84.

17. Sippel KC, Ma JJ, Foster CS. Amniotic membrane surgery.Curr Opin Ophthalmol. 2001; 12: 269-81

18. Azuara-Blanco A, Pillai CT, Dua HS. Amniotic membranetransplantation for ocular surface reconstruction. Br JOphthalmol. 1999; 83: 300-402.

19. Hanada K, Shimazaki J, Shimmura S, et al. Multilayeredamniotic membrane transplantation for severe ulceration ofthe cornea and sclera. Am J Ophthalmol. 2001;131:324-31

20. Trelford JD, Trelford-Sauder M. The amnion in surgery, pastand present. Am J Obstet and Gynecol. 1979; 134: 833-45.

21. Fukada K, Chikama T, Nakamura M, et al. Differentialdistribution of subchains of the basement membranecomponents type IV collagen and laminin among theamniotic membrane, cornea, and conjunctiva. Cornea. 1999;18: 73-9.

22. Wang M, Gray T, Prabhasawat P, et al. Corneal haze isreduced by amniotic membrane matrix in excimer laserphotoablation in rabbits. Invest Ophthalmol Vis Sci. 1997;38: 405.

23. Prabhasawat P, Tesavibul N, Omolsuradej W. Single andmultilayer amniotic membrane transplantation for persistentcorneal epithelial defect with and without stromal thinningand perforation. Br J Ophthalmol. 2001; 85: 1455-63.

24. Van Herendael BJ, Oberti C, Brosens I. Microanatomy of thehuman amniotic membranes. Am J Obstet Gynecol. 1978; 131:872-8.



————————————————————————————————1Senior Registrar Department of Ophthalmology PGMI Lady ReadingHospital Peshawar2. TMO Ophthalmology PGMI LRH Peshawar.3.District Eye Specialist DHQH Kohat.————————————————————————————————Correspondence: Dr. Mohammad Alam, Senior RegistrarOphthalmology, Lady Reading Hospital, Peshawar. Address: C/OKhattak Pharmacy Opposite Gynae OPD Gate Lady ReadingHospital Peshawar Email: [email protected]————————————————————————————————Received: Sep’2012 Accepted: Nov’2012————————————————————————————————

Prevalence of Glaucoma inLow Myopic VS High Myopic Patients:

(A Study of 300 Cases)

Mohammad Alam FCPS1, Jamal Hussain2, Awalia Jan3

ABSTRACT:Objective: To compare the prevalence of glaucoma in low myopic VS high myopic patients.Materials and Methods: This comparative study of four years duration was conducted in Eye Care Centre Karak fromJanuary 2008 to December 2011. Total 300 patients with myopic refractive error were selected comprising of 171 maleand 129 female with age ranging from 15 years to 50 years. Informed consents were taken. They were divided into twogroups A & B both had 150 patients. Group A patient had spherical equivalent of myopia from 0.5D- 4.0 diopter sphericalwhile group B patients had spherical equivalent of myopia more than4.0 diopter spherical. Intraocular pressure was checked with applanantion Tonometer. Perimetry was done by confrontationmethod in advanced stage while in initial stage by Humphrey Visual Field Analyser. Fundoscopy with dilated pupils wasdone with direct and indirect ophthalmoscope and indirect slit lamp bimicroscopy. Myopic error was checked with retinoscopeand auto-refractometer.Results: In Group A 5 (3.33%) patients had high intraocular pressure with glaucomatous cup-disc and visual fieldschanges while in Group B 7(4.66%) patients had glaucomatous cup disc and visual fields changes with high Intraocularpressure.Conclusion: Glaucoma has association with myopia and the prevalence increases with increase in refractive error.Abbreviation: Intraocular pressure (IOP) visual filed (VF) Refractive error (R.E) Primary Open-Angle Glaucoma (POAG).Diopter Spherical (DS).

Original Article

Dr. Alam

INTRODUCTION:Myopia is a major refractive error. It has

association with other ocular morbidities likedegenerative changes in fundus like macular hole andeven retinal detachment. One of the importantassociations of Myopia is with POAG. Myopicassociation with POAG has been documented for manydecades in numerous studies1, 2, 3, 4. Some studies havereported high frequency of Myopia in young patientspresenting with POAG 5. Chihara, E, study has reportedthe association of POAG only in patients with highMyopia6 .In some large case control studies myopia wasfound to have strong association with ocularhypertension7.

In Barbados Eye Study and Blue Mountain EyeStudy it was concluded that Glaucomatous optic nervedamage was more in myopic patients as compared tohyperopic8, 9. These finding were in consonance with

hospital based studies in which axial Myopia had beenreported to be a risk factor for Glaucomatous opticneuropathy10

Myopic patients usually go unnoticed whilehaving association with POAG. This negligence lateron may result in advanced stage of cupped disc beingirreversible. Histopathological and clinical investigationhave shown that optic nerve head appearance variesbetween patients with high Myopia and with patientsof low to moderate Myopia11,12,13. This comparativestudy is based on the prevalence of POAG in patientwith low Myopia verses high Myopia.MATERIALS AND METHODS:

This comparative study of prevalence of POAGwith low myopia verses high myopia was conductedin eye care center Karak from January 2008 to December2011 spanning four years duration. Total three hundred(300) patients after informed consent were included inthis study comprising of 171 male and 129 female (TableI). The age range was from 15-50years. They weredivided into two groups A and B both have 150 patients.Myopic RE was taken as spherical equivalent. RE wasmeasured with retinoscope and auto refractor. GroupA patients had Myopic RE from 0.5- 4 DS while groupB patients had Myopic RE more than 4 DS (Table II).

Angle of anterior chamber of the patients wasexamined with van Herrick method with slit lamp. IOPwas checked with applanantion Tonometer. Perimetry


was done in Tertiary level hospital by visual fieldanalyser as well as by confrontation method inadvanced stage of POAG. Pupils were dilated withTropicamide Eye drop and Fundoscopy was done withdirect/indirect ophthalmoscope and indirect slit lampbimicroscopy.Inclusive criteria:1. Myopic patients2. patients with high IOP3. patients with cup disc changes4. patients with visual field changesExclusive criteria:1. Aphakic / Pseudophakic patients2. Traumatic patients3. Patients with high IOP but no cup disc and

visual field changes.RESULTS:

In group A with low Myopic RE 5(3.33%) patientshad POAG while in group B with high Myopic RE7(4.66%) patients had POAG (Table III).As far as thegender is concerned in group A 3(60%) patients weremale and 2(40%) were female who had POAGassociated with Myopia. In group B 5(71.42%) patients

Table I showing total patients with gender: N 300

Gender No of Patients Percentage

Male 171 57%

Female 129 43%

Table II showing refractive error:

Group Myopic error in No of Patients Percentagesphericalequivalent

A 0.5-4DS 150 50%

B >4DS 150 50%

Table III showing prevalence of glaucoma:

Group Myopic Patients Myopic Patients withwithout Glaucoma Glaucoma

A 145 (96.66%) 5 (3.33 %)

B 143 (95.33%) 7 (4.66 %)

Table IV showing Gender Distribution of Glaucoma:

Group Male Female

A 3 (60%) 2 (40%)

B 5 (71.42 %) 2 (28.57%)

were male while 2(28.6%) were female who had POAGassociated with Myopic RE (Table IV)DISCUSSION:

According to this study prevalence of POAG wasmore in high Myopic than low Myopic patients whichsuggests high glaucoma susceptibility in eyes withmarked myopia.

There are multiple studies which have shown thatPOAG does have association with Myopia. Study ofPaul Mitchell, Flever Houirhan et al has reportedassociation POAG with myopia. This study revealed4.2% patients had POAG with low myopia comparedto 4.4% patients with moderate to high myopia whichis nearly comparable to our study14. Many case controland clinic based studies have reported a relationshipbetween POAG and myopia. No previous populationbased studies have searched the association in detailwhile taking into account the effects of other knownGlaucoma risk factors. Confirmation that myopia is afrequent risk factor for Glaucoma should help toidentify this group whose participants need earlier andregular ophthalmic screening and follow up.

Study of Liang XU, Yaxing Wang, Shuang Wanget al has reported the association of Glaucoma with highmyopia15. This study has shown that hypermetropic andemmetropic population had no changes in the cup discwhile Glaucomatous optic neuropathy was more in highmyopic patients as well as prevalence of Glaucoma hadhigher incidence.

The Blue Mountain Eye Study has reportedprevalence of glaucoma ranged from 1.5% inemmetropic to 4.4% in myopia. The Barbados Eye Studyrevealed that myopia increases the odds of havingGlaucoma while hypermetropia has decreased the oddsfor Glaucoma.

Our study is supported by another InternationalStudy of Malmo Eye Survey based on early manifestGlaucoma Trail over a large number of population 16, 17

.This study has shown strong association of Glaucomawith myopia. Chihiro Mayama, Yasoyaki Suzuki,Makato Arai et al had reported in their study that highmyopia constitutes a threat to visual field in advancedGlaucoma18.

Aaron A, Kuzin, Rohit varma et al study hasdemonstrated that prevalence of glaucoma was 8.1%in myopic patients19. This ratio is higher than our studyresults. The reasons may be due to sample size and levelof myopia. As evident from all the international studiesprevalence of Glaucoma increases with increase inmyopic error. However the Beaver Dam Eye Study20

did not show the pattern of increasing severity ofmyopia. These differences could be explained by racialvariations, difference in definition of Glaucoma, or inanalytical approaches.

Prevalence of Glaucoma in Low Myopic VS High Myopic Patients: (A Study of 300 Cases)


Study of Nelsa I, Loyo, Berrios, Joseph et al hasreported the evidence of increase risk of POAG amongmyopic patients is stronger for moderate and highmyopia and not for mild myopia21.

The prevalence of POAG with myopia has beensupported by population based cross-sectionalepidemiologic study conducted by Yosuuki Suzuki,Aiko Iwse; Makato Arai etal22.This study has provedthat myopia is a significant risk factor for POAG.CONCLUSION:

This study has shown that primary open glaucomais associated with myopia. If myopia has been onlytreated, it means that some important ocular co-morbidities like glaucoma has been left as suchuntreated. So all the myopic patients must be screenedfor glaucoma.REFERENCES:1. Fong DS, Epstien DL, Allingham RR. Glaucoma and myopia:

Are they related? Int Ophthalmol Clin 1990; 30:215-82. Perkins ES, Phelps CD. Open angle glaucoma, ocular

hypertention, low tention glaucoma, and refraction.ArchOphthalmol 1982; 100:1464-7.

3. Mastropasqua L,Lobefalo L, Mancini A, et al. Prevalence ofmyopia in open angle glaucoma. Eur J Ophthalmol 1992; 2:33-5.

4. Phelps CD Effect of myopia on prognosis in treated primaryopen-angle glaucoma. Am J Ophthalmol 1982; 93:622-8.

5. Goldwyn R, Waltman SR, Becker B. Primary open-angleglaucoma in adolescents and young adults. Arch Ophthalmol1970; 84:579-82.

6. Chihara E, Liu X, Dong J, et al. Severe myopia as a risk factorfor progressive visual field loss in primary open-angleglaucoma, Ophthalmologica 1997; 211:66-71.

7. Seddon JM, Schwartz B, Flowerdew G. Case-control studyof ocular hypertension. Arch ophthalmol 1983; 101:891-4.

8. Leseke MC, Connell AM, Wu SY, et al. Risk factors for open-angle glaucoma: the Barbados Eye Study. Arch Ophthalmol1995; 113:918-24.

9. Mitchell P, Hourihanh F, Sandbach J, Wang JJ. The relationbetween glaucoma and myopia: the blue Mountains EyesStudy Ophthalmology 1999; 106:2010-5.

10. Jonas JB, Budde WM. Optic nerve damage in highly myopiceye with chronic open-angle glaucoma. Eur J Ophthalmol2005; 15:41-7.

11. Jonas JB, Berenshtien E, Hiolbac L. Lumina cribrosa thicknessand spatial relationships between intraocular space andcerebrospinal fluid space in highly myopic eyes. InvestOphthalmol Vis sci 2004; 45:2660-5.

12. Dichtl A Jonas JB, Naumann GO. Histomorphormetry of theoptic disc in highly myopic eyes with absolute secondaryangle closure glaucoma. Br J Ophthalmol 1998; 82:286-9.

13. Jonas JB, Gusek GC, Naumann GO. Optic disc morphometryin high myopia. Greafeas Arch Clin Exp Ophthalmol 1998;226:587-90.

14. Paul Mitchell, Fleur H, Jen S, et al. The relationship betweenGlaucoma and myopia. Ophthalmology 1999; 160:2010-15.

15. Ling Xu, Yaxing Wang, Shang Wang, et al. High Myopia andGlaucoma Susceptibility. The Beijing Eye Study.Ophthalmology 2007; 114:216-220.

16. AGIS Investigators. The advance Glaucoma InterventionStudy (AGIS): Baseline risk factors for sustained loss of visualfield and visual acuity in patient in advanced glaucoma. AmJ Ophthalmol 2002; 134:499-512.

17. Leske MC, Heijl A, Hussein M, et al. Factor for glaucomaprogression and the effect of treatment: The early ManifestGlaucoma Trail. Arch Ophthalmol 2003; 121:48-56.

18. Chihiro Mayama, Yasuyuki Suzuki, Makoto Araie, et al.Myopia and Advanced Stage Open-angle Glaucoma.Ophthalmology 2002; 109:2072-2077.

19. Aaron A. Kuzin, Rohit Verma, et al. Ocular Biometry andOpen-angle Glaucoma: The Los Angeles Latino Eye Study.Ophthalmology 2010; 117:1713-1719.

20. Wong TY, Klien BE, Klien R, et al. Refractive errors,intraocular pressure, and glaucoma in white population.Ophthalmology 2003; 110:211-7.

21. Nilsa I, Loyo-Berrios, Joseph N et al. Primary-Open angleGlaucoma and Myopia: A Narrative Review. WisconsinMedical Journal 2007.Volume 106, No.2.

22. Yasuyuki Suziki, Aiko Iwase, Makoto Araie et al. Risk Factorsfor Open- Angles Glaucoma in a Japanese Population. TheTajimi Study Ophthalmology 2006; 113:1613-1617.

Prevalence of Glaucoma in Low Myopic VS High Myopic Patients: (A Study of 300 Cases)


Current Research

Arcuate Field Defects in Glaucoma

Syed S. Hasnain M.D1, Sikandra Hasnain B.A.2

Original Article

Dr. S. Hasnain

——————————————————————————————1General Ophthalmologist, 2Medical student————————————————————————————————Correspondence: General Ophthalmology, 560 W. Putnam Ave.Suite #6, Porterville, CA 93257 Tel: 559.781.7482Fax: 559.781.8446 E. Mail: [email protected]————————————————————————————————

INTRODUCTION:The arcuate field defects, produced due to

selective destruction of the arcuate fibers, are apathognomonic feature of both high-tension (HTG) andnormal-tension glaucoma (NTG), the statisticallynormal range of intraocular pressure is 10 to 21mmHg.Although these arcuate field defects were discoveredmore than 100 years ago by Bjerrum and Ronnie, westill have not come to a consensus as to why they areproduced. The arcuate field defects are so sharplydefined, it is as though the arcuate fibers have beendeliberately excised with a pair of scissors. There areseveral theories, ranging from: the undue sensitivity ofthe arcuate fibers to raised intraocular pressure (IOP),to their increased vulnerability due to larger size holesin the region of arcuate fibers in the lamina cribrosa.1

However, none of these theories satisfactorily explainthe selective destruction of arcuate fibers in the earlystages of glaucoma. This article focuses on thiscontroversial subject as this may be the crucial key tofinding the true pathogenesis of glaucoma.

Visual field defects in glaucoma are produced ina specific sequence; indicating that the nerve fibers arebeing destroyed methodically and not haphazardly. Themost peripheral temporal fibers are destroyed first,resulting in the loss of most peripheral nasal field.However, the very early nasal field loss has littlediagnostic value because of normal variation in theextent of peripheral fields. Moreover, there are hardlyany noticeable glaucomatous changes occurring in theoptic disc at this early stage. However, when the nasalfield loss extends inward and produces a horizontalnasal step, this feature becomes diagnostic of glaucoma.This initial stage is followed by production of isolatedscotomas in the 10 to 20 degrees of the paracentral

region which coalesce to form superior and inferiorarcuate field defects. Both arcuate field defectscombined together are called ring scotoma.

Before we discuss as to why the nerve fibers inglaucoma are being destroyed in a specific sequence, itis imperative to mention the arrangement of the nervefibers in the retina and optic disc. There are about onemillion nerve fibers originating from the retinalganglion cells (RGC) which leave the eye ball throughmeshwork of the lamina cribrosa and form the opticdisc.

There are four main aspects in which the nervefibers are arranged in the retina and in the optic disc.First, the nerve fibers in the retina are arranged in layerssuperficial to deep. Second, the most central visionfibers originate closest to the disc lie most superficial(closest to vitreous) and exit from the most central partof the disc. In contrast, the most peripheral fibersoriginate from the most distant retina or farthest fromthe optic disc lie deepest (closest to sclera) and exitclosest to the edge of the scleral opening. Figure 1 Third,the nerve fibers originating from the nasal retinaproceed directly to the nasal part of the optic disc.However, the situation is different in the temporal retinabecause of the presence of the macular fibers. The fibersoriginating from the nasal aspect of macular areaproceed directly to the central temporal part of the disc.The fibers originating from the temporal macular andperipheral retina have to arch above and below themacular fibers to reach the superior and inferior polesof the optic disc respectively, and hence are known asarcuate fibers. Figure 2 Fourth, the nerve fibers of thesuperior and inferior hemifield are separated byhorizontal meridian and do not cross over to theopposite hemifield.

Based on the glaucomatous visual field defects,the nerve fibers, invariably, are being destroyed in aspecific sequence and an orderly fashion, yet neverhaphazardly in glaucoma. This important feature oforderly destruction of the nerve fibers will be the focusof our presentation in finding the pathogenesis of

Ms. SikandraCo-author


arcuate field defects in glaucoma.DISCUSSION:

By reviewing the literature, the subject ofpathogenesis of glaucomatous field loss appears quitecontroversial. There are two main theories: mechanicaland vascular, which were put forward 150 years ago,the time chronic glaucoma was given a separate entity.According to mechanical theory, the raised IOP directlycompresses the nerve fibers or causes posterior bowingof the lamina cribrosa resulting in distortion of thelaminar holes.(1) This in turn causes interruption of theaxoplasmic flow resulting in the death of RGCs.

The second school of thought, vascular theory,suggests that the raised IOP directly compresses theblood vessels resulting in ischemia and thus death ofthe RGCs/nerve fibers. Some believe that bothmechanical and ischemic events are occurring inglaucoma.

Duke-Elder,2 Henkind,3 Harrington,4 and Hayreh5

were proponents of the vascular theory. Henkindsuggested the occlusion of radial peripapillarycapillaries as the cause of selective destruction of thearcuate fibers. It has also been suggested that glaucomais due to varying degree of sensitivity of the nerve fibersto IOP: the ocular hypertension cases would be thosein whom the nerve fibers are the most resistant whereasnormal-tension glaucoma subjects will have the nervefibers least resistant to IOP. Neuro-degeneration is alsobeing implicated in glaucoma akin to Alzheimer’s orParkinson’s disease.

There was very comprehensive discussion on“Pathogenesis of Visual Field in Glaucoma” by EdwardMaumenee, published in Controversy in Ophthal-mology.(6)

Maumenee had challenged the direct role ofboth mechanical and vascular theory for the productionof the glaucomatous field defects. Maumenee arguedagainst the vascular theory because of normal electro-retinogram and fluorescein angiography in glaucoma,which he expected to be abnormal if vascular theorywas valid. Maumenee remarked that both mechanicaland vascular theory were not convincing and concluded“the exact cause of loss of visual field in glaucoma isnot known at present time”. This well-reasonedconclusion was stated almost 35 years ago, to ourdismay, it still holds true today. Now we would discussthe orderly destruction of nerve fibers in view of presenttheories of glaucoma.Can the nerve fibers be destroyed in an orderlyfashion, if cupping of the optic disc is occurring?

The term ‘cupping’, given by Heinrich Muller in1856(2), implies that the pathology starts from the centralpart of the disc and extends peripherally. However,according to the distribution of nerve fibers in retina,the fibers for the central vision originate closer to the

optic disc lie superficial (closer to the vitreous) and exitfrom the central part of the disc. (Figure 1) Therefore, ifcupping was truly occurring then the central visionfibers should have been destroyed first and peripheralfibers at the last, but in actuality, the opposite isoccurring in glaucoma. Moreover, if cupping was takingplace, there should have been immediate blindness dueloss of central vision fibers in the earliest stages ofglaucoma. Therefore, keeping in view the distributionof the nerve fibers in the retina/optic disc and theglaucomatous field defects, the cupping theory appearsto be invalid and mistakenly given 150 years ago.Can the nerve fibers be destroyed in an orderlyfashion due to direct role of raised IOP?

It has been postulated over 150 years ago thatretinal nerve fibers are destroyed either due to directeffect or via ischemia induced by direct compression ofthe blood vessels by raised IOP.

Arguments against the direct role of IOP: how isit possible that raised IOP, acting directly, will alwaysdestroy the peripheral fibers first, followed byparacentral arcuate fibers and ending with the centralfibers and IOP will never destroy the nerve fibersrandomly?

It is also hypothesized that raised IOP causesposterior bowing of the lamina cribrosa, resulting indistortion of its holes and causing the interruption ofthe axoplasmic flow leading to the death of the RGCs.1

Arguments against the posterior bowing of the lamina:the central vision fibers being located at the apex of thebowed lamina, should be destroyed first not theperipheral fibers.

Moreover, if the bowing of the lamina wasoccurring due to high IOP then how can we explain thebowing of the lamina occurring in NTG in which theIOP is within normal range. It appears unlikely that anypathology occurring within the holes of the laminacribrosa can be as precise as to result in an orderlydestruction of nerve fibers. In view of the aboverationale, it appears unlikely that bowing of the laminawould result in selective destruction of arcuate fibersin the early stages of glaucoma.Can the nerve fibers be destroyed in an orderlyfashion if glaucoma is a neurodegenerative disease?

Glaucoma is implicated as a neurodegenerativedisease akin to Parkinson’s disease, Alzheimer’s orAmyotrophic Lateral Sclerosis (ALS). Argumentsagainst glaucoma being a neurodegenerative diseasewill also be based on the orderly destruction of nervefibers occurring in glaucoma.

The random degeneration of the neurons is acharacteristic feature of a neurodegenerative disease,therefore the course of a neurodegenerative diseasevaries in each individual. Therefore, it would be



unlikely that neurodegeneration, in glaucoma, willalways start first with those RGCs, which serve theperipheral vision and not occur randomly. Glaucomais considered a neurodegenerative disease due tounexplained death of neurons in the lateral geniculatenucleus (LGN) occurring concurrently with the deathof retinal ganglion cells.7 The reason for theirsimultaneous death will be discussed later in thispresentation under section of paradigm shift.

Other theories for the production of the arcuatefield defects include occlusion of radial peripapillarycapillaries3 because of their arcuate shaped bloodvessels distribution. It would be an unlikely scenariothat occlusion of the radial peripapillary capillariescould produce ischemia so precise and well defined thatit would cause an orderly destruction of nerve fibers inglaucoma. It has also been mentioned that glaucoma isdue to varying degree of sensitivity of the nerve fibersto IOP; ocular hypertension subjects having the mostresistant nerve fibers to IOP whereas the NTG subjectsthe least resistant to IOP. If the aforementioned is true,then someone born with undue sensitivity of the nervefibers to IOP should develop NTG in early childhood,not after the age 50 or more. It would be difficult toconvince ourselves that subjects although born withvariable sensitivity of the nerve fibers yet would havean orderly destruction of nerve fibers starting with theperipheral fibers in glaucoma. If the nerve fibers arebeing destroyed in an orderly fashion, then we shouldexpect the mechanism causing their destruction to bean orderly as well. In fact, the raised IOP, ischemia,neurodegeneration, undue sensitivity or any pathologyacting directly on the RGCs or nerve fibers cannot resultin the orderly destruction of the nerve fibers inglaucoma.Then, why are the nerve fibers being destroyed in anorderly fashion in glaucoma?

In order to answer above intriguing question, wewill have to change the current ‘cupping disc’ paradigmwith ‘sinking disc’ - a paradigm shift. We hypothesizethat the optic disc may be sinking, not cupping inglaucoma. 8-9

PARADIGM SHIFTDue to sinking of the disc, the prelaminar nerve

fibers, prior to their entry in the lamina cribrosa, arebeing stretched as one end is attached to the RGC andthe other end anchored in the sinking optic disc andultimately severed against the scleral edge. In otherwords the optic disc may be herniating in the scleralcanal- a mechanical problem. If this is true then thenerve fibers are being severed, not atrophied inglaucoma. Severing of the nerve fibers appears to be aunique phenomenon occurring in the glaucomatousdisc. Glaucoma may not be an optic disc neuropathy

but an axotomy.Now we will discuss if the orderly production of

visual field defects in glaucoma can be produced incontext of severance of the nerve fibers. Since theperipheral nerve fibers lie deeper and exit closer to thescleral edge, the peripheral fibers would be the first tobe affected and severed if the sinking of the disc isoccurring and this is shown by peripheral field loss inearly stages of glaucoma. As the peripheral fibers arebeing severed, the central fibers will move towards theperiphery to occupy the vacant space. Figure 3 Thismovement of the central fibers to the periphery willbreak or enlarge the physiological cup which may bemistaken as true cup enlargement, known as cupping.Severance of the nerve fibers may explain the death ofthe neurons in LGN due to Wallerian degeneration,whereas the retrograde degeneration would result inthe death of RGCs. I believe aforementioned concurrentdeath of the neurons in the LGN and of RGCs may bethe reason the glaucoma is considered a neuro-degenerative disease.Returning to our main question: why are the arcuatefibers being selectively destroyed in glaucoma?

Due to inherent temporal tilt of the optic disc, theentire group of temporal fibers (macular, superior andinferior arcuate) are being stretched and severed.Figure 4 However, the superior and inferior arcuatefibers being fewer in number compared to the macularfibers will be depleted earlier, resulting in arcuate fielddefects/ring scotoma. Figure 5 During this process ofsporadic depletion, there would initially be isolatedscotomas in the paracentral area, but as glaucomaprogresses and all the arcuate nerve fibers are severedand depleted, these isolated scotomas will coalesce toform complete arcuate field defects. The severing of thenerve fibers may explain the selective destruction ofthe arcuate fibers in glaucoma. Therefore, the severance,not the degeneration/atrophy of the nerve fibersappears to be involved in the production of the arcuatefield defects. It would be an unlikely event that anypathology could result in atrophy only of the arcuatefibers out of one million densely packed nerve fibers ina 1.5 mm optic disc. Sinking of the disc will becomeself-propagated due to severance of nerve fibers, whichalso provide anchorage to the optic disc as roots do to atree. Sinking of the disc will continue until all the nervefibers are severed in an orderly sequence from theperipheral to central fibers. Figure 3 Therefore, thesinking of the disc and severing of the nerve fibers canexplain the orderly visual field loss starting with theperipheral and ending with the central field inglaucoma.Since we have proposed, the nerve fibers are beingsevered in glaucoma: do we have any evidence?



Figure 2. Arrangement of nerve fibers in the retina and optic disc.The arcuate fibers, arch above and below the macular fibers, areselectively destroyed in the early stages of glaucoma.

Figure 1. Normal Disc: Arrangement of nerve fibers in retina andoptic disc. The most peripheral fibers (5) originate farthest from theoptic disc, lie deep, closest to the sclera and exit closest to thescleral edge. Whereas, the most central fibers (1) originate closestto the disc, lie superficial, closest to the vitreous and exit from mostcentral part of the disc.

Figure 3. Due to sinking of the disc, the most peripheral and deepestprelaminar fibers (5) are stretched and severed against the scleraledge (red arrows) first, and ending with the most central fibers (1).Thus, the central fibers move to be periphery (black arrows) resultingin enlargement of the original cup, known as cupping.

Figure 4. Due to temporal sinking, all of the temporal fibers (macular,superior and inferior arcuate) are being stretched and severed.However, the arcuate fibers being fewer in number, compared tomacular fibers will be depleted earlier, resulting in arcuate fielddefects as shown in figure 5.

Although we may never witness the actual processof severing of the nerve fibers, we may infer this factby deductive reasoning of the changes occurring in aglaucomatous disc. The continuous severing of thenerve fibers is supported by the phenomenon ofprogressive thinning of the RNFL as observed on opticalcoherence tomography (OCT). Moreover, the end-stage

histology of glaucomatous disc resembles an emptybean-pot. Interestingly, the bean-pot appears quite hugecompared to the size of original disc. Is this large emptybean-pot really a deeply cupped disc (lamina)? Is thelamina so inflatable that it has ballooned into a largebean-pot? If not, where did the lamina and nerve fibersgo?



Figure 5. Right eye: Double arcuate/ ring scotoma produced afterseverance and depletion of the arcuate fibers. Due to macular fibersbeing abundant, the central vision is retained until the end. Thismay explain the selective destruction of the arcuate fibers in theearly stages of glaucoma.

Figure 7. Flat disc atrophy due to Multiple Sclerosis. Note the nervefibers though shrunken are still present, in contrast to totaldisappearance of nerve fibers in glaucomatous disc in figure 6. Thereis no excavation since no sinking and thus no severance of nervefibers is occurring in flat disc atrophy. Copy from Yanoff, OcularPathology: Harper& Row. 1975

Figure 8. Interaction between ciliary pressure and IOP. Normallythe ciliary pressure supplying the border tissue should be higherthan IOP for good perfusion as in column (1). In column (2) the IOPis increased to 30 whereas the ciliary pressure remains the same at25, resulting in high -tension glaucoma. In column (3) the ciliarypressure is decreased to 15 but the IOP remains the same, normalat 20, resulting in normal- tension glaucoma.

Figure 6. End-stage glaucomatous disc. Not a deeply cupped discbut a large crater left over after the severance and disappearanceof all of nerve fibers.Copy: Kolker AE, Hetherington Jr J. Becker-Shaffer’s diagnosis andtherapy of the glaucoma, Mosby, 1976, p146.

In order to answer the aforementioned questions,we will compare the histology of both glaucomatousdisc and of the non-glaucomatous atrophic disc suchas due to multiple sclerosis. The histology of end-stageglaucomatous disc reveals a large crater (bean-pot), withan entrance appearing to be the scleral opening and itsbelly formed of dura mater, not the lamina cribrosa.

Figure 6 In contrast, the histology of a flat atrophicdisc reveals shrunken and collapsed nerve fibers, notan empty bean-pot. Figure 7 Moreover, the non-glaucomatous atrophic disc is flat, there is neithersloping/kinking of the blood vessels at the disc marginnor excavation of the disc occurring as in theglaucomatous discs.



The flat atrophic discs are not sinking in the scleralcanal, therefore no severance of the nerve fibersoccurring and thus no excavation in the flat atrophicdisc. Therefore, distinctly different pathological processare taking place in the flat atrophic discs and in theglaucomatous discs. In the flat atrophic disc, the nervefibers are being atrophied whereas in glaucomatous discthe nerve fibres are being severed. The severance of thenerve fibres appears to be the unique feature ofglaucoma. End-stage glaucomatous disc is not a deeplycupped disc, but a leftover empty crater after theseverance of all of the nerve fibers and the freed laminamay be lying at the bottom. The end-stageglaucomatous disc resembling an empty crater can onlybe explained by severance, not due to atrophy of thenerve fibers.Do we have any evidence of sinking disc?

I believe we do. First, the photographs of theglaucomatous optic discs vividly reveal sloping andkinking of the blood vessels at the disc margin prior toany change in the contour of the physiological cup. Thissuggests that the optic disc may be sinking, not cuppingin glaucoma. The physiological cup may not be trulyenlarging, but instead, disintegrating and excavatingdue to severance of the nerve fibers. Second, the newenhanced imaging technique of the optic disc (EDI-SD-OCT) has enabled us to visualize the deeper structuresin the scleral canal well beyond the entire width of thelamina cribrosa which was previously not possible withstandard SD-OCT. Therefore, EDI technique hasopened a new chapter and is providing us very valuableinformation of the glaucomatous disc. EDI of theglaucomatous optic disc, in vivo, has shown theposterior migration of the lamina cribrosa as far backas pia mater or in other words total sliding outward ofthe lamina from the scleral opening, from the very earlystages of glaucoma.10-13 This is very significant discoveryas it suggests that lamina (optic disc) is detachable fromthe scleral wall and is able to slide posteriorly (sink) inthe scleral canal. EDI findings support the phenomenonof sinking, not cupping of the disc. If true, then chronicglaucoma may be a mechanical problem, in fact, aherniation of the disc.Why is the optic disc sinking in both HTG and NTG?

We hypothesize that the collagenous border tissueof Elschnig lying between the lamina cribrosa and thescleral edge may be the primary site of pathology, notthe lamina cribrosa itself. Border tissue acts like an ‘O’ring seal which keeps the optic disc firmly anchored inthe scleral opening. If the border tissue atrophies, theoptic disc will start sinking in the scleral canal. Whywould the border tissue atrophy in both HTG and NTG?It is a complex and multifactorial subject. First, theinteraction between the circulation of the border tissue

and IOP. Second, the structural integrity of the bordertissue itself, inherent or acquired. The border tissue issupplied exclusively by the short posterior ciliaryarteries, a weaker pressure compared to the centralretinal artery, which unfortunately, does not participatein the blood supply of the border tissue.14

The systemic ciliary pressure and IOP areopposing forces. Normally the ciliary pressure of theborder tissue should be higher than the IOP for its goodperfusion and healthy maintenance. However, if eitherthe IOP becomes higher than the ciliary circulatorypressure due to an ocular disease or the ciliary pressuresupplying the border tissue becomes lower than IOP,due to some systemic problems like chronichypotension then the IOP will take the upper hand andwill compress the circulation of the border tissue,resulting in chronic ischemia and its atrophy. In thelatter scenario, if the ciliary pressure becomes lowerthan any normal range IOP level then that normal rangeIOP level will act as a higher IOP for that subject, thusNTG will result. Figure 8 Therefore it is still the IOP,whether within or above the statistically normal range,appears to be the culprit in both HTG and NTG.Moreover, it is not only the IOP level important, butalso the compromised oxygen carrying capacity of theblood which may also cause chronic hypoxia andatrophy of the border tissue. This may explain thehigher incidence of NTG in cases of long- term smokersand those with sleep apnea. Therefore, the normal-tension glaucoma may be a systemic disease.

In addition to circulation we may have to considerthe structural integrity of the border tissue. If someoneis endowed with strong border tissue then thatparticular subject may tolerate the circulatory imbalancefor a longer period compared to someone who has weakborder tissue such as in high myopia or various collagentissue disorders. Keeping all these factors in view, thepathogenesis of atrophy of the border tissue becomesmultifactorial.CONCLUSION:

In fact, the sinking of the optic disc is a herniationin the scleral canal- a mechanical problem. Due tosinking of the optic disc, the nerve fibers are stretchedand ultimately severed at the scleral edge. Theseverance of the nerve fibers can explain the selectivedestruction of the arcuate fibers in the early stages ofglaucoma. The sinking of the disc and severance of thenerve fibers can explain the orderly destruction of thenerve fibers, starting with the peripheral and endingwith the central fibers. Glaucoma may not be an opticdisc neuropathy but an optic disc axotomy.REFERENCES1. Quigly HA, Addicks EM. Regional differences in the structure

of the lamina cribrosa and their reaction to the glaucomatousdamage. Arch Ophthalmol.1981; 99: 137-43.




2. Duke-Elder S, Barrie J. Diseases of the lens and vitreous,glaucoma and hypotony, System of Ophthalmology, Vol. X1.London: Henry Kimpton; 1969. p 476.

3. Henkind, P; new observations on the radial peripapillarycapillaries. In symposium on Glaucoma: Invest Ophthalmol.6: 103, 1967.

4. Harrington, D, O Pathogenesis of glaucomatous visual fielddefects: Individual variations in pressure sensitivity inglaucoma. In Transactions of Fifth Macy Conference , 1960.Princeton , N.J., Josiah Macy, Jr. Foundation, 1961, p259

5. Hayreh S.S: Pathogenesis of visual field defects: role of ciliarycirculation. Br. J. Ophthalmol, 54: 289, 1970.

6. Maumenee E: The pathogenesis of Visual Field Loss inGlaucoma: Brockhurst R et al ,editors Glaucoma inControversy in Ophthalmology. Philadelphia: W.B. SaundersCompany; 1977 p 301-11

7. Hasnain SS. Is glaucoma a Neurodegenerative Disease?Ophthalmology Update. July-September 2012; 10 (3); 299-301

8. Hasnain SS. Optic Disc may be Sinking in Chronic glaucoma.Ophthalmology Update. Oct-Dec. 2010; 8 (4); 22-28

9. Hasnain SS. Scleral edge, not optic disc or retina is theprimary site of injury in chronic glaucoma. MedicalHypothesis 2006; 67(6) ;1320-1325

10. Anderson, DR Probing the Floor of the Optic Nerve Head inGlaucoma Ophthalmology 2012;119:1-2

11. Yang H. et al. Posterior(outward) migration of the laminacribrosa and early cupping in monkey experimentalglaucoma. Invest Ophthalmol Vis Sci 2011;52:7109-21

12. Yang H. Optic Nerve Head (ONH) Lamina Cribrosa InsertionMigration and Pialization in Early Non-Human PrimateExperimental Glaucoma. Poster Presentation ARVO meetingMay 03, 2010.

13. Park SC et al. In-vivo, 3-dimentional imaging of the laminacribrosa horizontal central ridge in normals and laminacribrosa deformation in glaucoma. Invest. Ophthalmol VisSci 2011;52:3063

14. Hayreh SS. Structure and blood supply of the optic nerve.In:Heilmann K, Richardson KT, editors. Glaucoma;Conceptions of a disease. Stuttgart: Thieme;1978. p78.


————————————————————————————————*Professor of Ophthalmology 8th Hospital, Yerevan State MedicalUniversity, 7 Ap., 1 Entr.,26 Sayat-Nova Avenue, Yerevan, 0001,Republic of Armenia————————————————————————————————Received Oct’2012 Accepted: Nov’2012————————————————————————————————

INTRODUCTIONGlaucoma is second only to cataract among visual

disorders, but it is a major cause of worldwideirreversible blindness. Bilateral blindness will be presentin 5.9 million people with open-angle glaucoma and5.3 million people with angle-closure glaucoma in 20201.

By 2020, India will become second overall innumber with glaucoma, surpassing Europe. There willbe six million more Chinese people with glaucoma. In2020, the Europe region will still contain the greatestnumber of people with open-angle glaucoma, and theproportion of all those with angle-closure glaucomathat live in Asian regions will increase further to 87.6%1.It is important to improve diagnostic and therapeuticapproaches to glaucoma that can be applied worldwide.

Glaucoma is currently recognized to be amultifactorial, progressive, neurodegenerativedisorder. It is characterized by the acquired death ofretina ganglion cells (RGC) and loss of their axons aswell as optic nerve atrophy and loss of neurons in thelateral geniculate nucleus and the visual cortex 2. Thisconcept emphasizes that several pressure-independentmechanisms are responsible for the development andprogression of glaucomatous neuropathy and that highintra-ocular pressure (IOP) and vascular insufficiencyin the optic nerve head are merely risk factors for thedevelopment of glaucoma. The central role of raisedIOP is being questioned as many patients continue to

demonstrate a clinically downhill course despite controlof initially raised IOP 3. In addition, up to one-sixth ofpatients with glaucoma develop it despite normal IOP4.

Chronic heart failure is associated with lower ocularperfusion pressure, and glaucomatous optic nerve headchanges 5. Visual field loss and RGC death continue tooccur in patients with well controlled intraocularpressures and, thus, a consensus has recently emergedthat additional treatment strategies are needed 6.

In humans, the optic nerve consists ofapproximately one million axons; whose cell bodies areprimarily located in the ganglion cell layer 7. RGC death,therefore, represents the final common pathway ofvirtually all diseases of the optic nerve includingglaucomatous optic neuropathy. There is histologicaland electrophysiological evidence to suggest thatganglion cells are the sole neurons affected inglaucoma7. All animal cells are programmed forcarrying out self-destruction when they are not needed,or when damaged. Apoptosis is a process rather thanan event. It has been labeled a programmed cell death,or cell suicide. It is not unique to RGCs or glaucomaalone. Following an initial insult, the cells try tominimize or buffer the damage done through a varietyof processes. Generation of “suicide triggers” could beone of the consequences of these processes andinteractions and these molecules may start the processof apoptosis which is characterized by an orderlypattern of inter-nucleosomal DNA fragmentation,chromosome clumping, cell shrinkage and membraneblebbing8. Abnormally high Ca2+ concentration leadsto inappropriate activation of complex cascades ofnucleases, proteases and lipases. They directly attackcell constituents and lead to the generation of highly

Glaucoma: Beyond Intraocular Pressure

*Prof. Marianne L. Shahsuvaryan MD, Ph.D, D.Sc (Medicine),Professor of Ophthalmology, Yerevan State Medical University,

Republic of Armenia

ABSTRACTBack Ground: Glaucoma is currently recognized to be a multifactorial, progressive, neurodegenerative disorder. It ischaracterized by the acquired death of retina ganglion cells (RGC) and loss of their axons as well as optic nerve atrophyand loss of neurons in the lateral geniculate nucleus and the visual cortex. The central role of raised intraocular pressure( IOP) is being questioned as many patients continue to demonstrate a clinically downhill course despite control of initiallyraised IOP. The protection from retinal ganglion cell loss, one of the main characteristics of glaucoma, would be a straightforward treatment for this disorder.Objective: This review focuses on cellular events associated with neurodegeneration due to glaucoma, and discussespharmacological agents believed to have a neuroprotective role in this disease . New intervention as pharmacologicalneuroprotection remains an important strategy to limit the morbidity of glaucoma representing significant health problem.Key words: Glaucoma, optic neuropathy, apoptosis, pharmacological neuro-protection

Current Research

Prof. Marianne

Review Article


reactive free radicals and activation of the nitric oxidepathway9. The resulting interaction betweenintermediate compounds and free radicals leads toDNA nitrosylation, fragmentation and activation of theapoptotic programme.TREATMENT Neuroprotective Therapy:

The strategy of treating a disease by preventingneuronal death is termed neuroprotection. The term isused more narrowly to describe therapies to addressfinal common pathways of damage in manyneurological diseases ranging from Amyotrophic lateralsclerosis(ALS), Alzheimer’s disease and, in the contextof the eye, glaucoma. The potential role ofneuroprotective agents is to rescue of sick and dyingcells and to maintain the integrity of healthy cells byproviding resilience to a variety of hostile factors oragents 2.

The objective of neuroprotective therapy is toemploy pharmacologic or other means to attenuate thehostility of the environment or to supply the cells withthe tools to deal with these changes 10. According tothis approach, any chronic degenerative disease maybe viewed to have, at any given time, some neuronsundergoing an active process of degeneration whichcontributes to the hostility of the environmentsurrounding it. The exponential loss of cells aftersecondary degeneration stems from the damagebrought on other neurons that either escaped or wereonly marginally damaged by the primary injury 11.Neuroprotection attempts to provide protection to suchneurons that continue to remain at risk12. The idea oftreating glaucoma with neuroprotection goes back tothe 1990s, with Weinreb and Levin13 writing in Archivesof Ophthalmology that, at the very least,neuroprotection should be an adjunctive therapy, alongwith lowering IOP. The concept of neuroprotectivetherapy for glaucoma is that damage to retinal ganglioncells may be prevented by intervening in neuronal deathpathways 14-16.

Wheeler et al.17 proposed four criteria to assessthe likely therapeutic utility of neuroprotective drugswith demonstrated utility in animal studies: The drugshould have a specific receptor target in the retina/ opticnerve; activation of the target must trigger pathwaysthat enhance a neuron’s resistance to stress or mustsuppress toxic insults, the drug must reach the retina/vitreous in pharmacologically effective concentrationsand the neuroprotective activity must be demonstratedin clinical trials.

The major causes for cell death followingactivation of NMDA receptors are the influx of calciumand sodium into cells, the generation of free radicalslinked to the formation of advanced glycation end-products (AGEs) and/or advanced lipoxidation

endproducts (ALEs) as well as defects in themitochondrial respiratory chain18,19.

Calcium channel blockers have been shown toneutralize glutamate-NMDA-induced intracellularCa2+ influx. Neuroprotective effect of calcium channelblockers against retinal ganglion cell damage underhypoxia was shown by Yamada et al. 20, and also byGarcia-Campos et al. 21. The general consensus is thatintracellular concentrations of calcium ion are increasedin apoptosis 22-25.

These findings suggest that calcium channelblockers may potentially inhibit ganglion cells andphotoreceptor apoptosis in glaucoma 26. Understandingof the role of extracellular calcium transport across cellmembranes in modulating various intracellularsignaling processes, including the initiation of theapoptotic cascade, represents part of the rationale forinterest in investigating calcium-channel blockers forneuroprotection in glaucoma.

The objective of this review is to evaluate theevidence and discuss the rationale behind the recentsuggestions that calcium channel blockers may be usefulin the treatment of glaucoma.PHARMACOLOGICAL NEUROPROTECTION

Calcium channel blockers generally dilate isolatedocular vessels and increase ocular blood flow inexperimental animals, normal humans, and patientswith open-angle glaucoma and in patients who havevascular diseases in which considerable vascular toneis present 26-28. As well, contrast sensitivity in patientswith normal tension glaucoma was found amelioratedby calcium channel inhibition29-30.

In a retrospective study of normal-tension andopen-angle glaucoma patients who happened to betaking calcium channel blockers, Netland et al.31

demonstrated a decrease in glaucoma progressionrelative to controls. Kittazawa et al.32 suggested visualimprovement in a significant number of patients whotook Nifedipine in a 6-month prospective study.Flunarizine, a potent calcium channel blocker has beendemonstrated to enhance RGC survival after optic nervetransection in mice33. These findings suggest thatcalcium channel blockers may potentially inhibitganglion cells and photoreceptor apoptosis inglaucoma26 .

Otori et al.34 evaluated the effect of Diltiazem oninhibition of glutamate-induced apoptotic retinalganglion cells death and concluded that application ofDiltiazem do not appear to reduce apoptosis.

Nimodipine is an isopropyl calcium channelblocker which readily crosses the blood-brain barrierdue to its high lipid solubility. Its primary action is toreduce the number of open calcium channels in cellmembranes, thus restricting influx of calcium ions into



cells.Several clinical trials have unequivocally shown

that Nimodipine is capable of preventing neurologicaldeficits secondary to aneurysmal subarachnoidhaemorrhage. The results of the VENUS (very earlyNimodipine use in stroke) study do not support theconcept that early Nimodipine exerts a beneficial effectin stroke patients 35 . On the other hand oral Nimodipineshowed an enhanced acute reperfusion if applied within12 hours of onset of acute stroke20,35,36. Yamada et al.20

in experimental in vitro model revealed thatNimodipine have a direct neuroprotective effect againstretinal ganglion cells damage related to hypoxia.

Michelson et al., 37 have evaluated the impact ofNimodipine on retinal blood flow in double-blind, two-way, crossover study of healthy subjects and found thatorally administered at a dosage of 30 mg three times aday Nimodipine significantly increases retinalperfusion in healthy subjects. The impact of Nimodipineon ocular circulation in normal tension glaucoma havebeen evaluated in many clinical studies.

Piltz et al., 38 have described a performance-corrected improvement in visual field deviation andcontrast sensitivity in patients with normal tensionglaucoma (NTG) and in control subjects in aprospective, placebo-controlled double-masked studyafter oral administration of Nimodipine (30 mg twicea day). Other authors 39 also stated that a single dose of30mg Nimodipine normalizes the significantly reducedretinal blood flow in NTG patients with clinical signsof vasospasmic hyperactivity. Luksch et al. 27 haveexamined the impact of 60 mg Nimodipine in NTGpatients 2 hours after oral administration. Resultsdisclosed that Nimodipine increased the blood flow ofthe optic nerve head by 18% and improved color-contrast sensitivity. Thus, Nimodipine is potentiallyuseful calcium channel blocker for eye disorderstreatment due to its high lipid solubility and ability tocross the blood-brain barrier.

Recent experimental evidences suggest thatNilvadipine appear to have beneficial effects ondifferent ocular structures. Ogata et al.40 have evaluatedthe effects of Nilvadipine on retinal blood flow andconcluded that this agent may directly and selectivelyincrease retinal tissue blood flow, while having onlyminimal effect on systemic circulation including arterialblood pressure. Another experimental study conductedby Uemura and Mizota41 have also advocated the useof Nilvadipine for the treatment of glaucoma or otherretinal diseases that have some relation to apoptosis,based on claims that Nilvadipine has high permeabilityto retina and neuroprotective effect to retinal cells. Otoriet al.34 in the experimental study of different calciumchannel blockers protective effect against glutamate

neurotoxicity in purified retinal ganglion cells has foundthat Nilvadipine significantly reduce glutamate-induced apoptosis.

In addition to direct effects of calcium channelblockers on intracellular concentrations of calcium ionin ganglion cells, other indirect effect is expected suchas increased choroidal blood flow28. Several clinicaltrials have shown the effectiveness of Nilvadipine inglaucoma.

Yamamoto et al.42, Tomita et al.43, Niwa et al.44

have found that Nilvadipine reduces vascular resistancein distal retrobulbar arteries and significantly increasesvelocity in the central retinal artery in patients withnormal tension glaucoma. Tomita et al.43 also statedthat reduced orbital vascular resistance after a 4-weektreatment with 2 mg oral Nilvadipine consequentlyincreases the optic disc blood flow.

Koseki et al.28 conducted a randomized, placebo-controlled, double-masked, single-center 3-year studyof Nilvadipine on visual field and ocular circulation inglaucoma with low-normal pressure. No topical ocularhypotensive drugs were prescribed.

The authors concluded that Nilvadipine (2 mgtwice daily) slightly slowed the visual field progressionand maintained the optic disc rim, and the posteriorchoroidal circulation increased over 3 years in patientswith open-angle glaucoma with low normal intraocularpressure. The results of this study add to the growingbody of evidence that Nilvadipine may be useful forneuroprotection in glaucoma.

Thus, Nilvadipine is potentially useful calciumchannel blocker for eye disorders treatment due to itshydrophobic nature with high permeability to thecentral nervous system, including the retina and thehighest antioxidant potency among calcium channelblockers.

The latest experimental study45 evaluated aneuroprotective effect of another new calcium channelblocker – Lomerizine. The authors stated thatLomerizine alleviates secondary degeneration of retinalganglion cells induced by an optic nerve crush injuryin the rat, presumably by improving the impairedaxoplasmic flow. Tamaki et al.46 also investigated theeffects of Lomerizine on the ocular tissue circulation inrabbits and on the circulation in the optic nerve headand choroid in healthy volunteers and have found thatLomerizine increases blood velocity, and probablyblood flow, in the optic nerve head and retina in rabbits,and it also increases blood velocity in the optic nervehead in healthy humans, without significantly alteringblood pressure or heart rate.CONCLUSION

Currently, glaucoma is recognized as amultifactorial, progressive, neurodegenerative disorder



and is characterized by the acquired death of retinaganglion cells, loss of their axons as well as optic nerveatrophy, loss of neurons in the lateral geniculate nucleusand the visual cortex. This concept emphasizes thatseveral pressure-independent mechanisms areresponsible for the development and progression ofglaucomatous neuropathy and that high intra-ocularpressure and vascular insufficiency in the optic nervehead are merely risk factors for the development ofglaucoma, and at the same time has led to a quest foridentifying neuro-protective agents that can be used tosafeguard the optic nerve.

Understanding of the role of extracellular calciumtransport across cell membranes in modulating variousintracellular signaling processes, including the initiation ofthe apoptotic cascade, represents part of the rationale forinterest in investigating calcium-channel blockers forpharmacological neuroprotection in glaucoma. Taken intoaccount the abovementioned eligibility criteria forneuroprotective drug, Nilvadipine meets them entirely andit is potentially useful calcium channel blocker forglaucoma treatment due to its hydrophobic nature withhigh permeability to the central nervous system,including the retina and the highest antioxidant potencyamong calcium channel blockers.

With exciting data now emerging from manyresearch laboratories, it is obvious that pharmacologicalneuroprotection for glaucoma without doubt representsan exciting development in the search for a treatmentmodality for this debilitating disease.REFERENCES 1. Quigley HA, Broman AT. The number of people with

glaucoma worldwide in 2010 and 2020.. Br J Ophthalmol2006;90(3):262-7.

2. Kaushik S, Pandav SS, Ram J. Neuroprotection in glaucoma.J Postgrad Med 2003;49:90

3. Osborne NN, Ugarte M, Chao M, et al. Neuroprotection inrelation to retinal ischemia and relevance to glaucoma. SurvOphthalmol 1999;43(Suppl):102-28.

4. Brubaker RF. Delayed functional loss in glaucoma. LIIEdward Jackson Memorial Lecture. Am J Ophthalmol1996;121:473-83.

5. Meira-Freitas D, Melo LA Jr, Almeida-Freitas DB, ParanhosA Jr. Glaucomatous optic nerve head alterations in patientswith chronic heart failure Clin Ophthalmol. 2012;6:623-9.

6. Chidlow G, Wood JP, Casson RJ. PharmacologicalNeuroprotection for Glaucoma. Drugs 2007; 67(5):725-59.

7. Lisegang TJ. Glaucoma: changing concepts and futuredirections. Mayo Clin Proc 1996 7;689-94.

8. Farkas RH, Grosskreutz CL. Apoptosis, neuroprotection andretinal ganglion cell death: An overview. Int Ophthalmol Clin2001;41:111-30.

9. Naskar R, Dreyer EB. New horizons in neuroprotection. SurvOphthlamol 2001;45(Suppl 3):S250-6.

10. Kaufman PL, Gabelt BT, Cynader M. Introductory commentson neuroprotection Surv Ophthalmol 1999; 43(Suppl):S89-90.

11. Schwartz M, Belkin M, Yoles E,et al. Potential treatmentmodalities for glaucomatous neuropathy: neuroprotectionand neuroregeneration. J Glaucoma 1996;5:427-32.

12. Chew SJ, Ritch R. Neuroprotection: the next break throughin glaucoma? Proceedings of the third Annual Optic NerveRescue and Restoration Think Tank. J Glaucoma 1997; 6:263-66.

13. Weinreb RN, Levin LA. Is neuroprotection a viable therapyfor glaucoma? Arch Ophthalmol 1999;117:1540-4.

14. Danesh-Meyer H V. Neuroprotection in glaucoma: recent andfuture directions. Current Opinion in Ophthalmology2011;22(2):78-86.

15. Chang EE, Goldberg JL. Glaucoma 2.0: neuroprotection,neuroregeneration neuroenhancement. Ophthalmology 2012;119(5):979-86.

16. Sena DF, Ramchand K, Lindsley K. Neuroprotection fortreatment of glaucoma in adults. Cochrane Database ofSystematic Reviews 2010, Issue 2. Art. No.: CD006539. DOI:10.1002/14651858.CD006539.pub2.

17. Wheeler LA, Gil DW, WoldeMussie E. Role of alpha-2adrenergic receptors in neuroprotection and glaucoma. SurvOphthalmol 2001;45(Suppl)3:S290-6.

18. Schmidt K-G, Bergert H, Funk RHW. NeurodegenerativeDiseases of the Retina and Potential for protection andRecovery. Curr Neuropharmacol. 2008; 6(2): 164–178.

19. Hayashi H, Eguchi Y, Fukuchi-Nakaishi Y. et al. A PotentialNeuroprotective Role of Apolipoprotein E-containingLipoproteins through Low Density Lipoprotein Receptor-related Protein 1 in Normal Tension Glaucoma. J. Biol. Chem.2012 ;287: 25395-406.

20. Yamada H, Chen YN, Aihara M, et al. Neuroprotective effectof calcium channel blocker against retinal ganglion celldamage under hypoxia. Brain Res.2006; 1071(1):75-80.

21. García-Campos J, Villena A, Díaz F, et al. Morphological andfunctional changes in experimental ocular ocularhypertension and role of neuroprotective drugs. HistolHistopathol.2007; 22(12):1399-1411.

22. Nicotera P and Orrenius S . The role of calcium in apoptosis.Cell Calcium. 1998; 23(2-3):173-180.

23. Delyfer MN, Leveillard T, Mohand-Said S, et al. Inheritedretinal degenerations: therapeutic prospects. Biology of theCell. 2004;96(4):261-269.

24. Sanges D, Comitato A, Tammaro R, et al. Apoptosis in retinaldegeneration involves cross-talk between apoptosis-inducingfactor (AIF) and caspase-12 and is blocked by calpaininhibitors. Proceedings of the National Academy of Sciencesof the United States of America. 2006;103(46):17366-17371.

25. Paquet-Durand F, Johnson L, Ekstrom P . Calpain activity inretinal degeneration. Journal of Neuroscience Research.2007;85(4):693-702.

26. Araie M and Yamaya C . Use of calcium channel blockers forglaucoma. Prog Ret Eye Res.2011; 30:54-71.

27. Luksch A, Rainer G, Koyuncu D, et al. Effect of nimodipineon ocular blood flow and color contrast sensitivity in patientswith normal tension glaucoma. Br.J.Ophthalmol. 2005; 89:21-25.

28. Koseki N, Araie M, Tomidokoro A . A placebo-controlled 3-year study of a calcium blocker on visual field and ocularcirculation in glaucoma with low-normal pressure.Ophthalmology.2008; 115(11):2049-2057.

29. Yu DY, Cringle S, Valter K, et al. Photoreceptor death, trophicfactor expression, retinal oxygen status, and photoreceptorfunction in the P23H rat. Investigative Ophthalmology andVisual Science.2004; 45(6):2013-2019.

30. Boehm AG, Breidenbach KA, Pillunat LE, et al. Visualfunction and perfusion of the optic nerve head afterapplication of centrally acting calcium-channel blockers.



Graefes Arch Clin Exp Ophthalmol. 2003; 241:24-38.31. Netland PA, Chaturvedi N, Dreyer EB. Calcium channel

blockers in the management of low tension and open angleglaucoma. Am J Ophthalmol 1993;115:608-13.

32. Kittazawa Y, Shirai H, Go FJ. The effect of ca2+ antagoniston visual field in low-tension glaucoma. Graefes Arch ClinExp Ophthalmol 1989;227:408-12.

33. Eschweiler GW, Bahr M. Flunarizine enhances rat retinalganglion cell survival after axotomy. J Neurol Sci 1993;116:34-40.

34. Otori Y, Kusaka S, Kawasaki A, et al. Protective effect ofnilvadipine against glutamate neurotoxicity in purifiedretinal ganglion cells. Brain Res.2003; 31;961(2):213-219.

35. Horn J.de Haan RJ,Vermeulen M. Very Early NimodipineUse in Stroke (VENUS): a randomized, double-blind, placebo-controled trial.Stroke.2001;32:461-465.

36. Infeld B, Davis SM, Donnan GA. Nimodipine and perfusionchanges after stroke. Stroke.1999;30:1417-1423.

37. Michelson G, Wärntges S, Leidig S, et al. Nimodipine plasmaconcentration and retinal blood Invest Ophthalmol Vis Sci.2006;47(8):3479-86

38. Piltz JR, Bose S, Lanchoney D . The effect of nimodipine, acentrally active calcium antagonist, on visual function andmascular blood flow in patients with normal-tensionglaucoma and control subjects. J Glaucoma.1998; 7(5):336-342.

39. Michalk F, Michelson G, Harazny J, et al. Single-dosenimodipine normalizes impaired retinal circulation in normaltension glaucoma. J Glaucoma.2004; 13:158-162.

40. Ogata Y, Kaneko T, Kayama N, et al. Effects of nilvadipineon retinal microcirculation and systemic circulation. NipponGanka Gakkai Zasshi. 2000;104(10):699-705. Japanese.

41. Uemura A, Mizota A . Retinal concentration and protectiveeffect against retinal ischemia of nilvadipine in rats. Eur JOphthalmol.2008; 18(1):87-93.

42. Yamamoto T, Niwa Y, Kawakami H, et al. The effect ofnilvadipine, a calcium-channel blocker on the hemodynamicsof retrobulbar vessels in normal-tension glaucoma. JGlaucoma.1998; 7(5):301-305.

43. Tomita G, Niwa Y, Shinohara H, et al. Changes in optic nervehead blood flow and retrobular hemodynamics followingcalcium-channel blocker treatment of normal-tensionglaucoma. Int Ophthalmol.1999; 23(1):3-10.

44. Niwa Y, Yamamoto T, Harris A, et al. Relationship betweenthe effect of carbon dioxide inhalation or nilvadipine onorbital blood flow in normal-tension glaucoma. J Glaucoma.2000;9(3):262-267.

45. Karim Z, Sawada A, Kawakami H, et al. A new calciumchannel antagonist, lomerizine, alleviates secondary retinalganglion cell death after optic nerve injury in the rat. CurrEye Res.2006; 31(3):273-283.

46. Tamaki Y, Araie M, Fukaya Y, et al. Effects of lomerizine, acalcium channel antagonist, on retinal and optic nerve headcirculation in rabbits and humans. Invest Ophthalmol VisSci. 2003 44(11):4864-71. [13]. Wheeler LA, Gil DW,WoldeMussie E. Role of alpha-2 adrenergic receptors inneuroprotection and glaucoma. Surv Ophthalmol2001;45(Suppl)3:S290-6



————————————————————————————————1Medical Officer/Registrar, Department of Ophthalmology, EyeUnit-I, B.V. Hospital Bahawalpur. 2Medical Officer/Registrar,Department of Ophthalmology, Eye Unit-I, B.V. Hospital Bahawalpur,3Resident Medical Officer, Department of Ophthalmology, EyeUnit-I, B.V. Hospital Bahawalpur.————————————————————————————————Correspondence: Muhammad Imran Saleem, Eye unit-I,Department of Ophthalmology, B.V.Hospital , Bahawalpur.E.Mail: [email protected]————————————————————————————————Received: Sep’2012 Accepted. Oct’2012————————————————————————————————

INTRODUCTION:The advent and refinement of modern

phacoemulsication techniques have revolutionized theability to rehabilitate the patients with vision losssecondary to cataract. Cataract surgery is, far and away,the most commonly performed ophthalmic surgicalprocedure of any kind, and the use of phacoemulsifi-cation to remove cataract is increasing at a rapid paceworldwide.1 Although the postoperative visual andrefractive outcomes of cataract extraction have beenwell studied, the concomitant changes in anteriorchamber anatomy and physiology remain unclear.There is very little information on aqueous humordynamics following phacoemulsication.

It has been widely reported that modern cataractextraction results in a long-term reduction in intraocular

pressure (IOP); however, the magnitude and clinicalsignificance of this change continues to bedebated.2,3,4

This situation is especially pertinent in patients withglaucomatous comorbidities, in whom the decision toperform concomitant incisional glaucoma surgery alongwith cataract removal via phacoemulsication must beassessed taking into account the additional risksassociated with such combined surgery. The ability ofa surgeon to prospectively predict the postoperativeIOP course of patients with coexistent cataract andglaucoma undergoing phacoemulsication wouldgreatly advance ophthalmic care.MATERIAL & METHODS:Change in the IOP following cataract surgery:

Both the short and long-term effects of cataractextraction on IOP have been studied for many years.Although the technique and instrumentation forcataract extraction has advanced dramatically since theadvent of modern phacoemulsication and minimallyinvasive clear cornea incisions, the long-termpostoperative results with regard to visualimprovement have been more or less unchanged overthe past two decades. Similarly, there has been noevidence to suggest that the recent evolution ofphacoemulsication with smaller, temporally locatedincisions and more efficient removal of lens material

Change in Intraocular Pressure followingPhacoemulsification Technique of Cataract Surgery

Muhammad Imran Saleem1, Muhammad Arshad2

Muhammad Farhan Saleem3

ABSTRACTObjective:The objective of this study was to review the current ophthalmic literature regarding the effect of cataractsurgery (Phacoemulsification) on intraocular pressure (IOP).Study Design: Literature Review.Place of Study: Eye unit-I, Department of Ophthalmology, B.V. Hospital, Bahawalpur.Results: There are a number of articles in the recent literature which demonstrate that a modest but long-standingdecrease in the IOP is achieved following cataract extraction by phacoemulsification technique. This postoperative declinein IOP can be demonstrated in patients having normal preoperative IOP as well as in patients having primary open-angleglaucoma, ocular hypertension or angle closure glaucoma. The mechanism of this pressure-lowering effect of cataractsurgery is not yet completely understood. The postoperative reductions in IOP seen in patients with angle closure glaucomaare said to be more pronounced than those in patients having open angle glaucoma. Patients with higher levels ofpreoperative IOP tend to have greater reductions in IOP postoperatively.Conclusion: It is now well recognized that cataract extraction by phacoemulsification leads to a modest but sustainedreduction in IOP during the postoperative period. There are several limitations in the studies conducted so far on thistopic. The implication of this reduction in IOP on the algorithms for care in patients having open angle glaucoma andcoexistent cataract remain unclear. In contrast, there are substantial benefits of cataract surgery in patients having acuteor chronic angle-closure glaucoma. This fact has been well studied and is now widely accepted by the practicingophthalmologists throughout the world. An improved understanding of the patho-physiological mechanisms of IOP declineafter cataract extraction may help us better predict the patients most likely to benefit from cataract surgery alone. Thismay obviate the need for a combined cataract and glaucoma surgery in these patients.Keywords: Cataract, glaucoma, Intraocular pressure, Phacoemulsification.

Review Article

Dr ImranSaleem


have had anysignicant impact on the postoperative IOPcourse.

Matsumura et al2, approximately 15 years ago,prospectively analyzed 93 patients undergoing cataractsurgery alone and demonstrated a 1.5-mmHgreductionin IOP at 3 years. In contrast, Suzuki et al3,during the same era, showed no signicant change inpostoperative versus preoperative IOP at 10 years incircumstances in which preoperative IOP was less than20 mmHg.

A few years later, Jahn4 demonstrated a consistent2-mmHgreduction of IOP at greater than 5 years in 80%of patients undergoing uncomplicated phacoemulsifi-cation. Tong and Miller5 similarly found an approxi-mately 2-mmHg reduction at 6–8 months post-operatively in patients undergoing cataract extractionwith either a scleral tunnel or a clear corneal incision.A subset analysis of the study by Tong and Miller5

further demonstrated no signicant impact of woundconstruction technique or anesthesia type (topicalversus retrobulbar injection) indeterminingpostoperative IOP reduction. In contrast, Schwennet al.6,in 2001, demonstrated an IOPreduction of 1.5 mmHgwith a clear cornea incision, versus a 0.6-mm reductionwith a scleral tunnel approachat 5 months post-operatively, in 100 patients undergoing uncomplicatedcataract extraction.

The contradictory results of these early studiesmay reflect unique surgical techniques andmethodologies for study design, data collection, andinterpretation employed by each investigative group.Pohjalainen et al7 demonstrated a large, approximately3.5 mmHg, IOP reduction postoperatively in 160patients undergoing phacoemulsication alone, with afollow-up of between 1.0 and 2.7 years.

Shingleton et al8 demonstrated a more modestdecline of 1.5 mmHg in ‘cataract surgery-only patients’,and further showed larger decreases in patientsdiagnosed as or being suspicious for primary open-angle glaucoma (POAG). Recent reviews of the subjecthave reported a range of IOP reduction from 0.63 to2.5 mmHg. Given this degree of variability inpostoperative response, Issa11, in 2005, demonstrated anovel index for predicting the degree of IOP reductionbased on a ratio of the preoperative IOP and anteriorchamber depth (pressure to depth ratio). This studydemonstrated a consistently greater than 4-mmHg IOPreduction in patients with a pressure to depth ratio ofmore than 7 (IOP inmmHg/anterior chamber depth inmm). In these patients with supposedly normalanterior chamber anatomy, the anterior chamber depthwas found to decrease, on an average, by 1.10 mmpostoperatively. A recent study by Kimet al13 on thesame subject demonstrated a 1.5-mmHg postoperative

reduction in IOP at 1 month, with no change in diurnalIOP uctuation relative to thepreoperative period.RESULTS:Change in the IOP following Cataract Surgery inpatients having Glaucoma:

A series of retrospective and prospective analysesover the last decade have consistently demonstratedreductions in IOP after cataract extraction inpatientswith glaucoma. These analyses havedemonstrated large variability in the magnitude of IOPreduction apparently related, at least in part, topreoperative angle anatomy. Although it would beexpected that one would achieve large magnitudereductions in patients with partially or completelyclosed angles, the mechanisms for the IOP reductionnoted in patients with open angles remain poorlyunderstood. Regardless, it is clear that carefulpreoperative examination including gonioscopy, andcertain investigations i.e anterior chamber opticalcoherence tomography (AS-OCT) and ultrasoundbiomicroscopy (UBM) may improve the practitioner’sability to predict the postoperative IOP course inselected cases during the preoperative period.DISCUSSION:Change in the IOP following Cataract Surgery inpatients having Open-Angle Glaucoma:

Although Matsumura et al2 demonstrated a 1.5-mmHg reduction of IOP in ‘cataract surgery-only’patients, they found 2.5- and 5.5-mmHg reductions inIOP for patients with controlled versus uncontrolledPOAG, respectively, with a 3-year postoperative follow-up. In 2002, Friedman14 published a meta-analysis usingthe Cochrane methodology on approximately 40 studiesof almost 5000 patients with various types of glaucomaand cataract undergoing cataract and/or incisionalglaucoma surgery.This analysis revealed an estimated2–4-mmHg IOP reduction with extracapsular cataractextraction (ECCE) or phacoemulsication, butdetermined that strong evidence for sustained long-term IOP control was found only for patients whounderwent combined cataract extractionwithtrabeculectomy. Tezel et al15, in the late 1990s, hadpreviously reported that approximately 95% of eyesthat underwent combined phacoemulsication andtrabeculectomy maintained IOPs of less than 20 mmHgwithout medication as compared with 82% attainingthe same result with cataract surgery alone over anaverage postoperative period of 15 months. Cimetta andCimetta12, in 2008, demonstrated a 3-mmHg greater IOPreduction postoperatively in patients with pseudo-exfoliation when compared with normal individuals(3.5 mmHg versus 0.48-mmHg reduction, respectively).Shingleton et al 8 showed a modestly greater reductionin postoperative IOP for patients with cataract with

Change in Intraocular Pressure following Phacoemulsification Technique of Cataract Surgery


coexisting POAG (1.8 mmHg) versus those with cataractwithout coexistent POAG (1.8 mmHg) at 5 years. In a2008 retrospective review, this group furtherdemonstrated that the postoperative IOP decline wasstatistically correlated with the preoperative IOP;patients with higher preoperative IOP obtained largermagnitude sustained reductions in IOP postoperativelyrelative to those with lower preoperative IOP.16 Poley17

substantiated these findings in a retrospective study ofalmost 600 patients undergoing simple cataractextraction, with upto 10 years of follow-up (range of 1–10 years, with over 50% having at least 4 years offollow-up). Patients were grouped on the basis of theirpreoperative IOP, and the largest magnitude reductionsin postoperative IOP were found in patients in thehighest pre-operative IOP group: a decrease of 6.5mmHg in the 23–31-mmHg group, 4.8 mmHg in the20–22-mmHg group, 2.5 mmHg in18–19-mmHg group,1.6 mmHg in the 15–17-mmHg group, and an increaseof 0.2 mmHg in the 9–14-mmHg group. Other studieshave demonstrated postoperative IOP reductionsranging from 1.85 mmHg to almost 4.5 mmHg in POAGpatients.9,18–24

There is increasing evidence to suggest that themagnitude of IOP reduction following cataract surgeryis positively related to the level of preoperative IOP.Although this effect appears logical and is supportedby data, one must not discount the importance of thestatistical phenomenon known as regression to themean. IOP varies substantially around the mean in mostpatients, particularly in those with high-pressure levels,and numerous baseline IOP measurements should betaken (phasing) to understand the full effect of any IOP-lowering therapy. The number of baseline preoperativeIOP measurements is not always apparent in severalpublished articles on this topic.

A review of patients undergoing cataractextraction with either acute or chronic angle-closureglaucoma (ACG) further illustrates the impact of thepreoperative diagnosis on IOP-lowering effect.

Change in the IOP following Cataract surgery inpatients havingAngle-Closure Glaucoma:

Wishart et al 24 demonstrated in the late 1980s inaprospective analysis of 22 patients with primary CACGthat ECCE resulted in IOPs of less than 21 mmHg in65% of patients, whereas a retrospective analysis of 21patients with POAG did not demonstrate the samefindings. Hayashi et al25, in 2001, studied 74 patientswith CACG and 68 with a diagnosis of POAG, andshowed that although the IOP was signicantlyreducedin both groups, a larger percentage of patientswithCACG (40.0%) did not require glaucoma medicationspostoperatively relative to those with POAG(19.1%).

Gunning and Greve26 demonstrated a remarkable

15-mmHg IOP decrease with combined trabeculec-tomy/cataract extraction and a 12-mmHg decrease withcataract extraction alone in patients with CACG at amean follow-up of approximately 5 years. They furtherfound anequal proportion of patients (68%) obtainingIOP control, with either combined cataract/trabeculectomy or cataract surgery alone, but the meannumber of medications required for such control waslower in the combined surgery group. Similarly, Ge etal 27, in a retrospective analysis of patients with eitheracute or chronic angle closure, demonstrated a greaterthan 11-mmHg IOP decrease after cataract extractionat approximately 8 months postoperatively.

In the acute treatment of angle closure glaucomas,studies comparing laser peripheral iridotomy (LPI) withprimary cataract extraction have also demonstrated IOPlowering, with the later group attaining more significantreductions. Both Lam 28 and Hata29 in 2008 demonstrated2.4- and 2.8-mmHg additional decreases in IOP forcataract surgery patients as compared with thoseundergoing LPI alone, respectively. Pachimkul andIntajak30 demonstrated an almost 6-mmHg IOPreduction in 58 eyes with acute angle closure glaucomaor CACG when treated with primary phacoemulsifi-cation and lens implantation. Mierzejewski20, also in2008, demonstrated 4.4- and 6.0-mmHg IOP reductionsfollowing phacoemulsication in POAG and CACGpatients, respectively.

It can be ascertained from all of these studies thatthe presence of closed-angle anatomy predisposespatients undergoing cataract extractions to largerdecreases in IOP when compared with normal andPOAG counterparts. Euswas and Warrasak31, in 2005,further quantified these differences bydividing angle-closure patients into two groups, distinguished by thedegree of closure; group- I included those with less than180 degrees of such closure, whereas group-II showedless than 270 degrees of peripheral anterior synechiae.They demonstrated a 3-mmHg greater IOP reductionpostoperatively in patients from group-II versus thosein group-I (5 versus 2 mmHg, respectively).CONCLUSION

Although there is definitive evidence showing thatIOP is reduced, on average, following phacoemulsifi-cation, in patients with or without glaucomatousdisease, the magnitude and duration of this effect needsfurther studies. Patient-specific factors, including angleanatomy, likely predict the expected postoperativereduction; yet, elucidation of such factors has beensuboptimal to date. Further, the mechanisms that leadto IOP reduction following cataract surgery in patientswith open angles remain poorly understood. It has beentheorized that phacoemulsification surgery increasesthe postoperative aqueous outow facility, and cultured



trabecular meshwork cells have been found to releaseinterleukins and tumor necrosis factors, which may leadto increased synthesis of matrix metalloproteinases inthetrabecular meshwork.32 Further research will likelyallow a better understanding of these postoperativechanges.

In contrast, it has been shown that the magnitudeof IOP reduction following cataract surgery in patientswith angle-closure glaucoma is related to the degree ofsuch closure. There is substantial evidence in supportof the use of cataract surgery as an important treatmentmodality for both acute angle-closure glaucoma andCACG in phakic individuals. Cataract and glaucomaare the two leading causes of morbidity associated withdiseases of sense organs worldwide. Given the frequentcoexistence of these two conditions, the managementof patients requiring simultaneous cataract removal andIOP lowering warrants furtherstudies, with regard toboth basic mechanisms and clinical outcomes.REFERENCES:1. Resnikoff S, Pascolini D, Etya’ale D, et al. Global data on

visual impairment inthe year 2002. Bull World Health Organ2004; 82:844–851.

2. Matsumura M, Mizoguchi T, Kuroda S, et al. Intraocularpressure decreaseafter phacoemulsication-aspiration andintraocular lens implantation inprimary open angle glaucomaeyes [in Japanese]. Nippon GankaGakkaiZasshi 1996;100:885–889.

3. Suzuki R, Kuroki S, Fujiwara N. Ten-year follow-up ofintraocular pressure afterphacoemulsication and aspirationwith intraocular lens implantation performed by the samesurgeon. Ophthalmologica 1997; 211:79–83.

4. Jahn CE. Reduced intraocular pressure afterphacoemulsication and posterior chamber intraocular lensimplantation. J Cataract Refract Surg 1997;23:1260–1264.

5. Tong JT, Miller KM. Intraocular pressure change aftersutureless phacoemulsication and foldable posterior chamberlens implantation. J Cataract RefractSurg 1998; 24:256–262.

6. Schwenn O, Dick HB, Krummenauer F, et al. Intraocularpressure after smallincision cataract surgery: temporalsclerocorneal versus clear corneal incision. J Cataract RefractSurg 2001; 27:421–425.

7. Pohjalainen T, Vesti E, Uusitalo RJ, Laatikainen L. Intraocularpressure afterphacoemulsication and intraocular lensimplantation in nonglaucomatouseyes with and withoutexfoliation. J Cataract Refract Surg 2001; 27:426–431.

8. Shingleton BJ, Pasternack JJ, Hung JW, O’Donoghue MW.Three and veyear changes in intraocular pressures after clearcorneal phacoemulsicationin open angle glaucoma patients,glaucoma suspects, and normal patients.J Glaucoma 2006;15:494–498.

9. Mathalone N. Long-term intraocular pressure after clearcornea phacoemulsication in glaucoma patients. J CataractRefract Surg 2005; 31:479–483.

10. Damji KF. Intraocular pressure following phacoemulsicationin patients withand without exfoliation syndrome: a 2 yearprospective study. Br J Ophthalmol2006; 90:1014–1018.

11. Issa SA. A novel index for predicting intraocular pressurefollowing cataractsurgery. Br J Ophthalmol 2005; 89:543–546.

12. Cimetta DJ, Cimetta AC. Intraocular pressure changes afterclear corneal phacoemulsication in nonglaucomatouspseudoexfoliation syndrome. Eur JOphthalmol 2008; 18:77–81.

13. Kim KS, Kim JM, Park KH, et al. The effect of cataract surgeryon diurnalintraocular pressure uctuation. J Glaucoma 2009;18:399–402.

14. Friedman D. Surgical strategies for coexisting glaucoma andcataract: anevidence-based update. Ophthalmology 2002;109:1902–1913.

15. Tezel G, Kolker AE, Kass MA, Wax MB. Comparative resultsof combinedprocedures for glaucoma and cataract:extracapsular cataract extractionversus phacoemulsicationand foldable versus rigid intraocular lenses.Ophthalmic SurgLasers 1997; 28:539–540.

16. Shingleton BJ. Effect of phacoemulsication on intraocularpressure in eyeswith pseudoexfoliation: single surgeon series.J Cataract Refractive Surg2008; 34:1834–1841.

17. Poley BJ. Long term effects of phacoemulsication withintraocular lensimplantation in normotensive and ocularhypertension eyes. J Cataract Refractive Surg 2008; 34:724–742.

18. Kim DD. Intraocular pressure reduction followingphacoemulsication cataract extraction with posteriorchamber lens implantation in glaucoma patients.OphthalmicSurg Lasers 1999; 30:37–40.

19. Pohjalainen T. Phacoemulsication and intraocular lensimplantation in eyeswith open angle glaucoma.ActaOphthalmologicaScandinavica 2001;79:313–316.

20. Mierzejewski A. Cataract phacoemulsication and intraocularpressure inglaucoma patients. KlinOczna 2008; 110:11–17.

21. Damji KF. Intraocular pressure following phacoemulsicationin patients withand without exfoliation syndrome: a 2 yearprospective study. Br J Ophthalmol2006; 90:1014–1018.

22. Merkur A. Intraocular pressure decrease afterphacoemulsication in patientswith pseudoexfoliationsyndrome. J Cataract Refract Surg 2001; 27:528–532.

23. Yalvac I. Phacoemulsication with and withouttrabeculectomy in patients with glaucoma. Ophthalmic SurgLasers 1997; 28:469–475.

24. Wishart PK, Atkinson PL. Extracapsular cataract extractionand posteriorchamber lens implantation in patients withprimary chronic angle-closureglaucoma: effect on intraocularpressure control. Eye (Lond) 1989; 3 (Pt 6):706–712.

25. Hayashi K, Hayashi H, Nakao F, Hayashi F. Effect of cataractsurgery onintraocular pressure in glaucoma patients. JCataract Refract Surg 2001;27:1779–1786.

26. Gunning FP, Greve EL. Lens extraction for uncontrolledangle-closure glaucoma: long-term follow-up. J CataractRefract Surg 1998; 24:1347–1356.

27. Ge J, Guo Y, Liu Y, et al. New management of angle-closureglaucoma byphacoemulsication with foldable posteriorchamber intraocular lens implantation. Yan KeXueBao 2000;16:22–28.

28. Lam DS. Randomized trial of early phacoemulsication versusperipheraliridotomy to prevent intraocular pressure rise afteracute primary angleclosure. Ophthalmology 2008; 115:1134–1140.

29. Hata H. Preliminary outcomes of primary phacoemulsicationplus intraocularlens implantation for primary angle-closureglaucoma. J Med Invest 2008;55:287–291.

30. Pachimkul P, Intajak Y. Effect of lens extraction on primaryangle closure in aThai population. J Med Assoc Thai 2008;91:303–308.

31. Euswas A, Warrasak S. Intraocular pressure control followingphacoemulsication in patients with chronic angle closureglaucoma. J Med Assoc Thai2005; 88 (Suppl 9):S121–S125.

32. Wang N, Chintala SK, Fini ME, Schuman JS. Ultrasoundactivates the TMELAM-1/IL-1/NF-kB response: a potentialmechanism for intraocular pressure reduction afterphacoemulsication. Invest Ophthalmol Vis Sci 2003;44:1977–1981.



————————————————————————————————1Associate Ophthalmologist, LRBT free Eye Hospital Mansehra2,3,5Medical Officers, 4Medical Officer PGMI, LRH, Peshawar————————————————————————————————Correspondence: Dr Faisal Nawaz Khan. LRBT Eye Hospital ,Mansehra. KPK E.Mail. [email protected]————————————————————————————————Received: Oct’2012 Accepted. Nov’2012————————————————————————————————

Postoperative Astigmatism followingPhacoemulsification:

Versus Extracapsular Cataract Extraction

Faisal Nawaz Khan.1, Naseer Ahmed, DOMS2, Amir Naseem3,Muhammad Idrees4, Muddasar Hussain5

Objective: To compare the magnitude of postoperative induced astigmatism and visual acuity following phacoemulsificationversus extracapsular cataract extraction.Materials and Methods: This study was conducted at LRBT Free Secondary Eye Hospital, Mansehra from June 2012 toSeptember 2012 . This was a comparative study in which total of 60(100%) patients were selected from amongst patientswho presented in the OPD with cataract. These patients were divided into 2 groups designated Group-A and Group-Brespectively. In Group-A, patients were included whom Phacoemulsification with posterior chamber rigid intraocular Lenswas implanted. In Group-B, Standard Extracapsular Cataract Extraction followed by posterior chamber rigid intraocularlens implantation was carried out. These cases were followed up as two separate groups. Preoperatively their visualacuities and K-readings were taken from which any astigmatism was calculated by simple subtraction method.Postoperatively these variables were recorded on each follow-up visit, which were scheduled at 1st day postoperativelyday followed by one week, three weeks, six to eight weeks and twelve weeks. Finally the visual outcome in terms of visualacuity and surgically induced astigmatism were compared between the two groups on each follow-up visit.Results: Post-operative induced astigmatism was less in group A patients as compared to group B patients in all follow upvisits. Post operative visual acuity was significantly better in group A as compared to group B patients all through thefollow up.Conclusion:• Surgically induced astigmatism is significantly more following standard ECCE as compared to the small incisionphacoemulcification followed by posterior chamber IOL implantation.• Phacoemulsification is clinically superior to ECCE.Keywords :Phacoemulcification, Astigmatism, Extra capsular cataract extraction, Visual acuity, Intra ocular lens.

Review Article

INTRODUCTIONAccording to the World Health Organization

(WHO), cataract is the leading cause of blindness andvisual impairment throughout the world. With thegeneral aging of the population the overall prevalenceof visual loss as a result of lenticular opacities increaseseach year. In 2002, the WHO estimated that cataractscaused reversible blindness in more than 17 million(47.8%) of the 37 million blind individuals worldwide,and this number is increasing to reach 40 million by2020. The WHO proposes that between 2000 and 2020,the number of cataract surgeries performed worldwidewill need to triple in order to keep pace with the needsof the population. (1)

Cataract surgery is possibly the oldest surgicalprocedure and is now the most frequently performedsurgical procedure in the western world.(2) It isperformed with the aim of improving vision and

surgery has considerably been changed in recent years.Advancement in techniques and improvements ininstruments have enabled surgeons to achieve a bettervisual outcome. In the past the cataract surgeonsconcentrated on removal of the opaque lens so as toallow the passage of light into the globe. Withadvancement efforts were made not only to remove thecataractous lens but also to ensure that light is broughtto an optimum focus on the retina, so that the patientcould have good uncorrected visual acuity.

The evolution of cataract surgery in the recent pastsaw intracapsular cataract extraction falling in disregardand its place being taken over by extracapsular cataractextraction. The advent of intraocular lens furtherimproved the post operative visual acuity as itdispensed the need for aphakic glasses. More recentlyadvances of small incision surgery usingphacoemulsification have revolutionized cataractsurgery. It is now performed with high expectations ofsuccess by both surgeons and patients alike.

The major part of the focusing power of the eye iscontributed by the cornea and not the lens. Therefore itis obvious that a slight change in the corneal curvaturecan affect the precision with which light is focused onto the retina. The technique of surgery, the incisionsmade for the surgery and the stitches applied, all have


the potential to alter the corneal shape and refractionof the eye.

It has been known for quite sometime that cataractsurgery is associated with changes in corneal curvaturewhich can bring about alteration in the refractingsurface of the cornea i.e. the anterior surface. Thesechanges can be associated with induction of astigmatismand thus limit visual rehabilitation post operatively.Originally, all extracapsular techniques involvednuclear expression, but in 1967 Charles Kelman MD,developed phacoemulsification, which differed fromconventional ECCE with nuclear expression by the sizeof he incision and the method of nucleus removal. (3)

The main difference between extracapsularcataract extraction and phacoemulsification lies in theremoval of the lens nucleus. In the former the nucleusis removed in one piece through a 9-10mm incisionwhereas in the latter it is remove piece-meal throughan incision of 3mm, which can be increased if a non-foldable lens is used. Since the incision length is themost important factor for the surgically inducedastigmatism,(4) therefore the small incision used inphacoemulsification would induce minimal postoperative astigmatism, less post operative inflammationand early visual recovery. The better visual resultsachieved using phacoemulsification has transformedcataract surgery from an operation to restore vision toa refractive procedure in which the surgeonmanipulates the surgical parameters to provide thepatient with the best possible vision both with andwithout spectacles. Few operations give such animprovement in health (5).

Since cataract is one of the main causes ofpreventable blindness, therefore to counteract thisincreasing backlog, efforts have been made to increasethe output of cataract surgery services in the country.However the outcome of this surgery is not always asdesired and so much more attention needs to be givento this aspect of the procedures followed.

A study was carried out at LRBT Free Eye HospitalMansehra from June 2012 to September 2012, toevaluate the surgically induced astigmatism followingphacoemulcification using a 5.5mm incision andconventional extracapsular cataract extraction followedby posterior chamber non-foldable intraocular lensimplantation in both groups.

Visual acuity and astigmatism were recorded onboth groups preoperatively followed by the twodifferent procedures. Postoperatively the same wereagain recorded and compared on each follow up visit.It was hypothesized that the patients undergoingphacoemulcification will have less induced astigmatismand a better postoperative visual acuity at everycheckup of this study.

MATERIALS AND METHODS:This study was conducted at LRBT Free secondary

eye hospital Mansehra from June 2012 to September2012. Ethical committee approval was taken fromResearch Ethics Committee LRBT Karachi. This was acomparative study in which total of 60(100%) patientswere selected from amongst patients, presented in theOPD with cataract. These patients were divided into 2groups designated Group-A and Group-B respectively.In Group-A patients were included whomphacoemulcification with posterior chamber rigidintraocular Lens was implanted. In Group-B, StandardExtracapsular Cataract Extraction followed by posteriorchamber rigid intraocular lens implantation was carriedout. These cases were followed up as two separategroups. Preoperatively their visual acuities and K-readings were taken from which any astigmatism wascalculated by simple subtraction method.Postoperatively these variables were recorded on eachfollow-up visit, which were scheduled at 1st daypostoperatively day followed by one week, three weeks,six to eight weeks and twelve weeks. Finally the visualoutcome in terms of visual acuity and surgicallyinduced astigmatism were compared between the twogroups on each follow-up visit.

TABLE – 1 Total number of patients in the study

GROUPS NO. OF PATIENTS PERCENTAGE

Group – A 30 50%

Group – B 30 50%

TOTAL 60 100%

TABLE – 2 Distribution of patients according to sex( n = 60 )

GENDER GROUP – AGROUP – BNo of Pts %age No of Pts %age

Male Patients 17 56.66% 14 46.66%

Female Patients 13 43.33% 16 53.33%

TOTAL 30 100% 30 100%

TABLE – 3 Age wise distribution

AGE GROUP – AGROUP – BNo of Pts %age No of Pts %age

50 – 55 years 10 33.33% 0 0%

56 – 60 years 8 26.66% 2 6.66%

61 – 65 years 6 20% 11 36.66%

66 – 70 years 6 20% 17 56.66%

TOTAL 30 100% 30 100%

Postoperative Astigmatism following Phacoemulsification: Versus Extracapsular Cataract Extraction


DISCUSSIONThis study was conducted at LRBT Free Eye

Secondary Hospital Manshera to compare clinicaloutcome in terms of surgically induced astigmatism andpostoperative visual acuity at predetermined follow upvisits. In this study, a total of 60 patients were dividedinto two groups comprising 30 cases each. Group-Aunderwent phacoemulsification with a clear cornealincision, which was later extended to 5.5mm toaccommodate a non-foldable posterior chamber IOL.Group-B patients underwent ECCE with a 9-10mmincision followed by posterior chamber IOLimplantation.

In Group-A, the mean magnitude of inducedastigmatism on the first postoperative day was around2.02D and on the last follow up visit there was almostno difference with the preoperative values. In Group-

B, there was marked change on the first postoperativeday with the mean of 3.48D and towards the end of thestudy there still remained a significant degree ofastigmatism, although the trend was that ofneutralization towards its preoperative keratometryvalues.

Mission and Birmingham(6) has done a study onkeratometry and postoperative astigmatism. Theystated that postoperative refractive astigmatism andKeratometric corneal astigmatism were determined inpatients following cataract surgery by comparing theresults of the two methods. The value of keratometry isthat it is a simple and quick procedure for identificationof surgically induced astigmatism. It is proposed thatthis method should be used before final refraction inan attempt to increase clinical efficiency and to reducefurther follow-up appointments resulting fromsurgically induced astigmatism.

The results of our study are comparable to the onecarried out by Watson and Sunderraj (7) who carried outa comparative study of small incisionphacoemulcification with standard ECCE. Theycompared postoperative astigmatism and visualrecovery. These results are comparable to our study.They carried out a prospective study on astigmatismand visual acuity (corrected and uncorrected) followingphaco and ECCE.

47 eyes were implanted a 5x6mm optic IOL,through with 5mm scleral incision after phaco and 50eyes were implanted with 7mm diameter IOL afterECCE. Uncorrected visual acuity of 6/9 or better wasachieved in 25% of eyes on the first day following phaco,36% at one week and 57% at 12 weeks. These results(and also the best corrected visual acuity) weresignificantly better than those following ECCE. Lessastigmatism was induced by phaco than ECCE

TABLE – 6 Comparison of amount of post-operative astigmatism in both groups

Visit Group 0-1.0D 1.1D to2.0D 2.1D to 3.0D 3.1D to 4.0D >4.0 D

1st Day Group-A 2(6.66%) 18(60%) 7(23.33%) 3(10%) 0

Group-B 0 0 9(30%) 19(63.33%) 2(6.66%)

1st week Group-A 5(16.66%) 19(63.33%) 4(13.33%) 26.66%) 0

Group-B 0 0 11(36.66%) 16(53.33%) 3(10%)

3rd week Group-A 14(46.66%) 13(43.33%) 3(10%) 0 0

Group-B 0 1(3.33%) 13(43.33%) 15(50%) 1(3.33%)

6-8 weeks Group-A 19(63.33%) 11(36.66%) 0 0 0

Group-B 0 3(10%) 14(46.66%) 13(43.33%) 0

12th week Group-A 26(86.66%) 4(13.33%) 0 0 0

Group-B 0 7(23.33%) 18(60%) 5(6.66%) 0

TABLE – 4 Distribution of patients according to treatment

Eye GROUP – AGROUP – BNo of Pts %age No of Pts %age

Left eye 13 43.33% 14 46.66%

Right eye 17 56.66% 16 53.33%

TOTAL 30 100% 30 100%

TABLE – 5 Comparison of amount ofpre-operative astigmatism in both groups

ASTIGMATISM GROUP – AGROUP – BNo of Pts %age No of Pts %age

0D to 0.5D 9 30% 6 20%

0.51D to 1.0D 19 63.33% 20 66.67%

1.1D to 2.0D 2 10% 4 13.33%

TOTAL 30 100% 30 100%



measured at all postoperative time intervals.(7)

Small incision cataract surgery allows for earlyrehabilitation of patients and improved control ofpostoperative astigmatism. The astigmatism was verylow and the required astigmatism correction was in theorder of 0.75D.(8) These were conclusions of a studycarried out by Hashmani, Haider and Ali. Theconclusions of our study are to similar effect.

In a study conducted at Sheik Zayed Hospital, itwas found that almost 70% of the patients undergoingphaco with IOL implantation, a best corrected visualacuity of 6/6 to 6/12 was achieved.(9)

In our study in Group-A, 86% of patients hadinduced astigmatism of less than 1.0D at 12 weeks time.This could be favorably compared with a studyconducted by Afzal and Khawaja in which theyreviewed 120 cases of phacoemulsification. They foundthat 64% patients had less than 1.0D of astigmatism and37% had less than 2.0D of induced astigmatism.(10)

In a study carried out at Liaquat Medical Collegeit was reported that better postoperative visual acuitywith minimum induced astigmatism was achievedfollowing phaco as compared to the conventional ECCEtechnique. The results of our study are comparable withthis study.(11)

In an audit carried out at Addenbrook’s Hospital-UK, the final visual acuity of 6/12 or better was achievedin 81% of cases undergoing cataract surgery throughphaco. This is comparable with our results of group-Apatients.(12)

The difference between phaco and ECCE lies inthe incision size, therefore not only phaco but any smallincision surgery would yield better results incomparison to a large incision surgery. A study on theselines was done and was found that a procedure referredto as manual small incision cataract surgery would givebetter uncorrected visual acuity. This study reportsoutcome at 1 week and 6 weeks after and it showspersistent better visual outcome for patients undergoingmanual small incision cataract surgery. (13)

In a study published by Malik, Qazi and Gilbert itwas revealed that the visual outcome in eyes operatedon using phaco and those undergoing ECCE weresimilar. Since this outcome is different from our study,it is possible that bias could have played a role in this.The most likely bias could be that phaco is a difficultprocedure to master and therefore in the hands of a notso experienced surgeon its results would be similar toECCE. In our study the source of bias in favor of phacois the age factor. Patients were comparitively moreyounger than those undergoing ECCE. Thereforepredictably the visual outcome would be better.Another bias is that in the group undergoing ECCE thecataract is more mature as mature cataract patients wereexcluded from the phaco group.(14)

CONCLUSION:• Surgically induced astigmatism is significantly

more following standard ECCE as compared tothe small incision phacoemulsification followedby posterior chamber IOL implantation.

• Visual acuity is better at every postoperative stageand visual rehabilitation rapid following cases

TABLE – 7 Comparison of pre-operative visual acuity in bothgroups

VISUAL ACUITY GROUP – AGROUP – BNo of Pts %age No of Pts %age

UPTO 6/24 3 10% 0 0%

6/36 – 6/60 25 83.33% 17 56.67%

CF / PL 2 6.67% 13 43.33%

TOTAL 30 100% 30 100%

TABLE – 8 Comparison of post-operative uncorrected Visual acuity in group-A & group-B

Visit Group 6 / 6 TO 6/24 6/36 OR LESS TOTAL

1st Day Group-A 13(43.33%) 17(56.66%) 30

Group-B 3(10%) 27(90%) 30

1st week Group-A 22(73.33%) 8(26.66%) 30

Group-B 3(10%) 27(90%) 30

3rd week Group-A 27(90%) 3(10%) 30

Group-B 7(23.33%) 23(76.66%) 30

6-8 weeks Group-A 29(96.66%) 1(3.33%) 30

Group-B 14(46.66%) 16(53.33%) 30

12th week Group-A 30(100%) 0 30

Group-B 23(76.66%) 7(23.33%) 30



undergoing phacoemulsification in comparison toECCE.

• Phacoemulsification is clinically superior to ECCEREFERENCES:1. Ophthalmology AA. Basic and clinical science course (Sec-

II). Lens and cataract. San Francisco 2011-2012;6:71.2. Spalton D. The constant evaluation of cataract surgery. Br

Med J 2000;321:1304.3. Ophthalmology AA. Basic and clinical science course (Sec-

II). Lens and cataract. San Francisco 2011-2012;6:104.4. Van Rij G, Waring GD. Changes in corneal curvature induced

by sutures and incisions. Am J Opth 1984;98:773-83.5. Raftery J, Stevens A. Cataract Surgery. London NHS

Executive 1994.6. Mission GP, Birmingham. Keratometry and post operative

astigmatism. Eye 1992; 63-65.7. Watson A, Sunderraj P. Comparison of small incision

phacoemulsification with standard ECCE surgery:Postoperative astigmatism and visual recovery. Eye 1992; 6:626-29.

8. Hashmani S, Haider I, Khan MA. Phacoemulsification resultsand complications during the learning curve. Pak JOphthalmol 1997; 13: 132-6.

9. Hussein M, Durrani J, Ajmal N. Phacoemulsification a reviewof 210 cases. Pak J Ophthalmol 1996; 12: 38-43

10. Afzal M, Khawaja H. Comparison of pre and postoperativeastigmatism : review of 120 cases of phacoemulsification .Pak J Ophthalmol 1999; 15: 69-71.

11. Junejo SA, Khan SA. Phacoemulsification by stop and choptechnique: review of 200 cases. Pak J Ophthalmol 1999; 15:138-41.

12. Kamal Z. An audit of 100 cases of phacoemulsificationcataract surgery. Ann King Edward Med Coll 2000; 6-4: 349-50.

13. Gogate PM, Deshpande M, Wormald RP, Deshpande R,Kulkarni SR. Extracapsular cataract surgery compared withmanual small incision cataract surgery in community eye caresetting in western India: a randomized controlled trial. Br JOphthalmol 2003; 87: 667-672.

14. Malik AR, Qazi ZA, Gilbert C. Visual outcome after highvolume cataract surgery in Pakistan. Br J Ophthalmol 2003;87: 937-940.



——————————————————————————————1General Ophthalmologist, 2Medical student————————————————————————————————Correspondence: Syed S. Hasnain M.D. General Ophthalmology,560 W. Putnam Ave. Suite #6Porterville, CA 93257, USA.Tel: 559.781.7482, Fax: 559.781.8446Email: [email protected] Web: www.hasnaineye.com————————————————————————————————

INTRODUCTION:A simple method to diagnose glaucoma is being

presented which is based on the hypothesis that theoptic disc is sinking, not cupping, in chronicglaucoma.1,2, 3 In order to diagnose glaucoma based onthe sinking optic disc, we must replace currently usedschool of thought: cupping and optic disc neuropathy,with the following new paradigms.Paradigm 1.

The optic disc is sinking in the scleral canal.Paradigm 2.

Due to sinking of the disc, the nerve fibers arebeing stretched and ultimately severed against thescleral edge, an optic disc axotomy.

The term “cupping” which implies gradualenlargement of the physiological cup in glaucoma ismisnomer for two reasons. First, the physiological cupis not truly enlarging but disintegrating, in glaucoma.Second, we are already using the term cuppingdescribing various sizes of physiological cups, therefore,the use of term pathological cupping causesunnecessary confusion in glaucoma diagnosis.What is a physiological cup of the optic disc?

The physiological cup of the optic disc is of varioussizes that are produced by varying degrees of atrophyof Bergmeister papilla 4, a tuft of hyaloid vessel in fetallife. If we review the histology of the normal optic disc,the remnant of the papilla base is identified as centralconnective tissue meniscus lying superficially on thesurface of the nerve fibers layer. The meniscus formsthe base of the physiological cup, therefore the largerthe meniscus, the bigger the size of the cup.Consequently, a larger cup would be covering morearea of the nerve fibers and thus smaller exposed areaor rim of the disc.

It has been mentioned that the axons areconcentrated in the rim area only, and the cup itself isdevoid of axons. However, the histology of a normaloptic disc reveals that underneath the meniscus, theentire lamina is packed with nerve fibers and there ishardly any empty space 5. In fact, the physiological cupis not an integral part of the optic disc and has no clinicalsignificance. Many optic discs have minimal cup or noneat all. Since the physiological cups are composed offibrous tissue, it is unlikely they would become enlargeddue to raised IOP because of lack of elasticity.

This presentation will demonstrate that thechanges occurring in the glaucomatous disc are mainlydue to severing of the prelaminar nerve fibers and bloodvessels as a result of sinking disc- a mechanical problem.These pathological events are supported bymorphological and histological findings of theglaucomatous discs.What happens to the optic disc after severance ofnerve fibers?

Severing of the nerve fibers results in excavationor empty spaces in the disc, whereas severing of theblood vessels results in hemorrhages at the disc margin,peripapillary atrophy and characteristic pallor devoidof inflammation. Severance of the nerve fibers resultsin thinning of the RNFL as revealed by optical coherencetomography (OCT). Severing of the nerve fibers and ofblood vessels is a unique feature of glaucoma as no otheroptic disc disease exhibits such a phenomenon.In addition to the border tissue, the optic disc isanchored in the scleral canal by 360 degrees of the nervefibers, similarly to the roots anchoring a tree. As theoptic disc starts sinking due to atrophy and weaknessof the border tissue, the prelaminar nerve fibers becomestretched and ultimately severed at the scleral edge. Dueto depletion of the nerve fibers, the anchorage of theoptic disc is weakened and disc sinks further resultingin severing of additional nerve fibers. The cascade ofsinking and severing of the nerve fibers become self-propagated and will continue until all the nerve fibersare severed. This phenomenon may explain as to why

A Simple Method to Diagnose Glaucoma

Syed S. Hasnain M.D1, Sikandra Hasnain B.A.2

Feature

Ms. SikandraDr. S. Hasnain


glaucoma cannot be halted despite lowering of the IOPmaximally.Evaluation of the optic disc for glaucoma.

While evaluating the optic disc for glaucoma wehave to keep two things in mind: the glaucomatousdisc is sinking and as a result the nerve fibers andvasculature are being severed. If we observe themorphological features of the glaucomatous disc in thecontext of severing of the nerve fibers, then we wouldnot only determine the glaucoma in its earliest stage,but every stage of the glaucomatous disc with our nakedeye; all we may need is an ophthalmoscope orpreferably a digital fundus camera.How do we determine if the optic disc is sinking?

By observing the course of blood vessels as theycross at the junction of the retina and the optic disc: ifthe course of blood vessels from the retina on to thesurface of the disc is straight and the optic disc appearsflush with the retina then, of course, the disc is notsinking. We should observe the course of the bloodvessels at the disc margin, not to confuse with thenormal bending of the blood vessels occurring at themargin of the physiological cup. As the optic disc startssinking, the blood vessels will also start sloping inpursuit of the sinking disc. The aforementioned simpleobservation with our naked eye will clearly tell us ifthe disc is sinking or not.

This article will present the pictures ofglaucomatous discs from their earliest to the late stage

of the six glaucoma subjects and we would evaluatethem in the context of severing of the nerve fibers andits vasculature as a result of the sinking disc.Stages of the glaucomatous discs:

Since the changes occurring in the glaucomatousdiscs are gradual and continuous, it is difficult to dividethem into definitive stages. However, arbitrarilyglaucomatous changes may be divided into three stages.Early Stage:

Due to the inherent temporal tilt of the disc, thetemporal part will reveal glaucomatous changes first.Temporal area will appear pale due to severance of thesmaller blood vessels, whereas the temporal scleraledge/border area will appear prominent and visibledue to severance and thus thinning of RNFL. Fig 1-6.Splinter hemorrhages may also appear due to severingof the blood vessels at the disc margin. In the early stagethere is usually no change in the contour of thephysiological cup. There may be generalized peripheralfield constriction but usually no arcuate field defects atthis stage.Intermediate stage:

Due to severing of the nerve fibers the excavationor empty spaces are produced in the optic disc. In casesof optic discs with minimal physiological cups thesinking of the disc appears more obvious. Fig 4Notching in the superior and inferior pole of thephysiological cup will start appearing due to severanceand depletion of the arcuate fibers. Since the

Figure 1 same subject: A. Early glaucoma left eye: Temporal pallor and increased visibility of the temporal scleral edge/rim area. B.Intermediate glaucoma right eye: Inferotemporal area appears pale, sunken and sloping of .blood vessels. Increased visibility of the scleraledge due to thinning of RNFL.Arcuate field defects present.

A simple method to diagnose glaucoma


Figure 2 same subject: A. Early glaucoma right eye: Temporal pallor, increased visibility of the temporal scleral edge due to thinning of RNFL.Physiological cup still intact. B. Intermediate glaucoma left eye: Temporal area more sunken, increased visibility of rim and more sloping of theblood vessels. Physiological cup being obliterated due to excavation created by severance of the RNFL.

Figure 3 same subject: A. Early glaucoma left eye: Temporal pallor, increased visibility of the scleral edge. B. Intermediate glaucoma righteye: Inferotemporal area pale, sunken and sloping of temporal vessels. Scleral edge area more visible due to thinning of RNFL.Arcuate fielddefects present.



Figure 4 same subject: A. Early glaucoma right eye: Temporal pallor, increased visibility of the temporal scleral edge and sloping of the bloodvessels. B. Late glaucoma left eye: Temporal area more pale, sunken and marked visibility of the scleral opening due to thinning of RNFL.Nasal shifting of blood vessels due to severance of the temporal nerve fibers.

Figure 5 same subject: A. Early glaucoma right eye: Temporal pallor and increased visibility of the temporal scleral edge. Physiological cupstill intact. B. Late glaucoma left eye: Marked pallor, excavation and kinking of the vessels at the entire rim. Entire scleral opening is visibledue to extreme thinning of the RNFL.



Figure 6 same subject: A. Early glaucoma right eye: Temporal pallor, increased visibility of the temporal scleral edge and sloping of thetemporal vessels. Physiological cup still intact. B. Late glaucoma left eye: Marked pallor, excavation and kinking of the blood vessels at thescleral edge. Entire scleral opening is visible due to severance and thinning of the RNFL. Pallor, excavation and kinking of the vessels at theentire rim. Entire scleral opening is visible due to extreme thinning of the RNFL.

physiological cup is now obliterated, it may be calledan intermediate stage.

At this stage the visual field defects would startappearing in the paracentral area due to severance anddepletion of arcuate fibers. The sloping of the bloodvessels will turn into kinking due to progressivedepletion of nerve fibers. The central retinal vessels willbegin to shift nasally due to loss of anchorage resultingfrom the severance of temporal nerve fibers.

Analogy: if the roots of a tree are severed fromone side, the tree will shift to the opposite side.Late to End-stage:

In the late stages of glaucoma, the more of the discarea becomes pale and excavated. Due to extremethinning of the RNFL the entire scleral opening willbecome visible. Fig 4-6 The area around the disc marginwould appear bald due to severance and disappearanceof the smaller blood vessels whereas the larger bloodvessels would remain hanging on the scleral edge,Fig4-6.

In summary, the histology of the end-stageglaucomatous disc resembles a totally empty bean-pot

which can only be explained if severance, not atrophyof the nerve fibers is occurring. The glaucomatous discsillustrated in this presentation are of six subjects inwhich one eye has early glaucoma and the contralateraleye in an intermediate or late stage. All theseglaucomatous discs reveal the same pattern from thevery early to the late glaucoma stage, resulting fromthe severing of the nerve fibers and vasculature. Ibelieve my colleagues would find my presentationappealing and may agree: if there is no sinking of thedisc then there is no glaucoma, irrespective of cuppingReferences:1. Hasnain SS. Optic Disc may be Sinking in Chronic glaucoma.

Ophthalmology Update. Oct-Dec. 2010; 8 (4); 22-282. Hasnain SS. Scleral edge, not optic disc or retina is the

primary site of injury in chronic glaucoma. MedicalHypothesis 2006; 67(6) ;1320-1325

3. Hasnain SS, Hasnain AB. Is glaucoma a NeurodegenerativeDisease? Could it be a mechanical problem and not aneurodegenerative disease? Ophthalmology Update July-Sept, 2012 10(3); 299-301

4. Wolff E. Anatomy of the Eye and Orbit. Revised by Last R.J.6th ed London H.K. Lewis & CO;1968. p. 438

5. Wolff E. Anatomy of the Eye and Orbit. Revised by Last R.J.6th ed. London: H.K. Lewis & Co;1968. Fig. 294, p. 326



PITFALLS OF RESEARCH(A non-conventional analysis)

Abbas HasnainDoctor of Jurisprudence, California, USA

Men love to wonder, and that is the seed of science - Ralph Waldo Emerson.

——————————————————————————————Note: Mr. Hasnain is a senior medical student at University Autonomaof Guadalajara, Mexico with plans of entering Ophthalmology. Alsohaving a law degree, Mr. Hasnain plans to practice law as an attorneyto defend physicians alleged to be involved in medical malpracticecases.————————————————————————————————Correspondence: Abbas Hasnain, JD. 560 W. Putnam Ave. Suite#6, Porterville, CA 93257 Tel: 559.781.7482Fax: 559.781.8446 E. Mail: [email protected]————————————————————————————————

Feature

While attending medical school in Latin America,I was in utter perturbation to listen to my professortelling me that only peer-reviewed articles from theUnited States would be accepted for our oralpresentation. I was disheartened because I was unableto utilize any extraordinary and intriguing articleswritten by my host country’s outstanding physiciansand scientists. Left and perched in utter confusion, Iwondered the loss of great ideas and studies from thefertile and fruitful minds, which are not necessarilypeer-reviewed and published in glossy journals.Moreover, I was saddened to realize that majority ofthe peer-reviewed journals are available at exorbitantcosts for subscription. This leaves much of the scientistsin the world not being able to be involved in theexchange of ideas and sharing of experiences of evensenior colleagues.

In fact, non peer-reviewed forms of research,ideas, and studies are deprived of ever being consideredfor discussion. Journal clubs, presentations, citations,are all steadily requiring research to be from journalswith much rigid safeguarding essentially making othersobsolete and unread. Thus, we are creating anundesirable tradition for the younger generations wherethey are being subjected to ignore anything that is notaccessible via PubMed or any indexing agency.

There are myriad of articles written on importantand current scientific topics that major journals chooseto ignore because there is no ‘scientific consensus’ onsuch material. However, the question arises of howwould there ever be a consensus if the journals have noroom for such unorthodox articles? We are convincedthat these ideas would be ignored forever unless we

intrinsically review and motivate ourselves to readbeyond the typical peer-reviewed manuscripts. Let’snot forget, that in 1875 German researchers hadhypothesized that bacteria may be the culprit for gastriculcers, but these studies never received any attentionbecause of not having shown any acceptable scientificbasis. It is not until 1984 did they rediscovered thecausative relation between H. Pylori and the gastriculcers. Had the scientific community cared to take aserious notice of this scientific innovation, they wouldhave saved the humanity from immense sufferings.There are hundreds and thousands of scientificparadigms, theorems, hypothesis and inventions whichwere evaded under careless and arguably selfishmotives, resulting in great scientific backlogs.

Apparently, the policy behind the much-emphasized importance of peer-reviewed journals is toremove scientific material that is not agreed upon byparticular peers, editors, or associations. Suchpublications are inherently flawed as they leaves noroom for novel and unorthodox ideas to ever becomeintroduced to the flourishing minds. Such ideas, thoughfewer in number as compared to approved articles ofnormal scientific research. These ideas are left tojournals of small circulation and online presentations.

Our advice to the students, residents, andphysicians is to pay attention to such open-accessedjournals, which provide a platform for progressivescientific ideas of equal importance. In fact, it is anamalgamation of all these ventures whether peer-reviewed or not, that we evolve a scientific consensuswhether these ideas fit within scientific domain. And ifthese ideas do not fit the current scientific consensus,do not completely discard them; let us utilize ourinquisitive scientific inquiry to evaluate its possiblevalidity. It is only with this non-conventional analysisthat we can maximize and direct the growth of scientificstudy and its application.

Finally, in the words of Ralph Waldo Emerson:“Men love to wonder, and that is the seed of science.”

Abbas Hasnain


Ophthalmology Notebook

Letters to the EditorCONGRATULATIONS - RECOGNITION BY HEC

Dear Prof Durrani, I am pleased to learn the Ophthalmology Update beingapproved and recognized by the Higher EducationCommission. Congratulations, this will definitely solve manyproblems of the ophthalmic faculty members from medicaluniversities of the country. Well done. Best Regards

Prof. Khalid Talpur, Hyderabad.——————————

Dear Prof Durrani,AOA, Congratulations Sir, great achievement for

yourself and all the contributing ophthalmologists. Regards

Prof. Brig Majeed Malik, CMH Lahore Medical College——————————

Respected: Prof. M.Yasin Khan DurraniEditor-in-Chief, Ophthalmology Update

Sir, Let me share sincere compliments on achievingsuch a great honor and excellence. It is a marvelousachievement and great landmark in your career that you havejoined the fraternity of success by getting the journalrecognized by HEC. This is Almighty’s befitting reward foryour concerted efforts. It is only because of your most angelicnature. Sir, you have a character of sterling excellence. Younever leave your work of today for the next day. TheAlmighty Allah gives this opportunity to those who arefavorite to Him. We offer you whole hearted congratulationson this remarkable feat.Most sincerely

Professor Dr. Sameen Afzal Junejo, Dept. of OphthalmologyLiaquat Uni. of Medical and Health Science, Jamshoro.President Elect: OSP Hyderabad/Sindh.Cell: 0300-3013012

——————————Dear Prof. Yaseen Durrani

Congratulations for recognition of Ophthalmo-logyUpdate by HEC. Regards

Dr. Ghulam Rabbani Dahri, President OSP Hyderabad.——————————

Dear Prof. DurraniCongratulations! Prof. Durrani for this fertile

achievement.

Prof. Syed Imtiaz Ali Shah, Dean, SBB Medical University,Head of Ophthalmology,Chandka Medical College, Larkana

——————————Very Respected Prof. Durrani,

Sir , I am really thankful for your thoughtfulness andkindness for accepting my article for publication. I must availthis opportunity to express my heart felt andhumble appreciations for your dedication , commitment , and

endless efforts to make this journal a success, in particular,recognition by HEC and to serve the cause of ophthalmologyin general. With a lot of regards.

Dr. M. Abdul Moqeet, Assoc. Professor,PIO, Al-Shifa Trust Eye Hospital, Rawalpindi

——————————Dear Prof. Durrani,

I gratefully acknowledge the receipt of International‘OPHTHALMOLOGY Update’ Vol: 10 No:4 October-December’2012, it is excellent in both, contents andpresentation. The copy has been placed in Shifa Library toattract a wider readership. With regards,

Maj. Gen. (Retd) Professor Muhammad AslamPrincipal, Shifa College of Medicine &VC, Taamir-i-Millat University, Islamabad

——————————Dear Prof. Yasin Durrani

I hope you must be enjoying EID. May Allah bless youand your family with all the happiness of the life. Amin! Youare very blessed and spiritual person and very close to Allah.Your dedication in publication of Ophthalmology Update isa proud achievement.

When I first knew about you and your Journal I wasamazed to find your dedication in publishing a high classinternational Journal at your own. I said to myself “ Thefuture of Pakistan can’t be bleak if Pakistan is blessed with dedicatedpersons like you” It is not at all easy to publish at your ownand that is why Journals are published by the associations.It is really very commendable that you are publishing forthe past 10 years.

I was only 26 when I left Pakistan and have lived mostpart of my life outside Pakistan. I have done nothing forPakistan whereas you have dedicated your entire life servingPakistan. Yourself and other ophthalmologists serving inPakistan had the same opportunity as I had in settling in thedeveloped countries abroad, but you chose to serve Pakistan.I salute you and all the other ophthalmologists serving inPakistan despite difficult circumstances.

When I had intuition of my ‘sinking disc hypothesis’I was so excited that if I am correct then my discovery willnot only be a pride for Pakistan but for the entire Muslimworld. This is the only consolation I have for not settling inPakistan because in Pakistan I believe I would have got sobusy by the enormous workload that most probably I wouldnot had time to think outside the box. Accept heartiestfelicitations for acceptance of the journal by HEC. Manythanks and best regards

Syed S. Hasnain M.D. General Ophthalmology560 W. Putnam Ave. Suite #6Porterville, CA 93257 USATel: 559.781.7482Fax: 559.781.8446

——————————


Apples belongsto Rosaceae family, originallycultivated in the mineral-rich mountains of Kazakhstan,and now in many parts of the world.

Delicious and crunchy apple fruit is one of the mostpopular fruits, favorite of health conscious, fitness loverswho believe in the concept “health is wealth.” Thiswonderful fruit is packed with rich phyto-nutrients that inthe true senses indispensable for optimal health. Theantioxidants in apple have much health promoting anddisease prevention properties, thus truly justifying theadage, “an apple a day keeps the doctor away.”

Apples are low in calories, 100 g of fresh fruit provideonly 50 calories. They, however, contain no saturated fats

or cholesterol. Nonetheless, the fruit is rich in dietary fiber,which helps prevent absorption of dietary-LDL or badcholesterol in the gut. The fiber also saves the colon mucousmembrane from exposure to toxic substances by bindingto cancer-causing chemicals inside the colon.

Apples are rich in antioxidant phyto-nutrientsflavonoids and polyphenolics. The total measured anti-oxidant strength (ORAC value) of 100 g apple fruit is 5900TE. Some of the important flavonoids in apples arequercetin, epicatechin, and procyanidin B2. Additionally,they are also good in tartaric acid that gives flavor to them.Altogether, these compounds help the body protect fromdeleterious effects of free radicals.

Apple fruit contains good quantities of vitamin-C andbeta-carotene. Vitamin C is a powerful natural antioxidant.Consumption of foods rich in vitamin C helps the bodydevelop resistance against infectious agents and scavengeharmful pro-inflammatory free radicals from thebody.Further, apple fruit is a good source of B-complexvitamins such as riboflavin, thiamin, and pyridoxine(vitamin B-6). Together these vitamins help as co-factorsfor enzymes in metabolism as well as in various syntheticfunctions inside the body.

Apple also contains a small amount of minerals likepotassium, phosphorus, and calcium. Potassium is animportant component of cell and body fluids helpscontrolling heart rate and blood pressure; thus, countersthe bad influences of sodium. It helps in maintainingoverall good health, preventgs early ageing processspecially maintaining good vision by preventing cataractand age-related macular degeneration. Fresh apples canbe kept at room temperature for few days and stored insidethe refrigerator for two to three weeks. Wash them in cleanrunning cold water before use to remove any surface dustand pesticide/fungicide residues.Eat apple fruit along withtheir peel in order to get maximum health-benefits.Slicedapple turns brown (enzymatic brownish discoloration) onexposure to air due to conversion in iron form from ferrousoxide to ferric oxide. If you have to serve them sliced, rinseslices in water added with few drops of fresh lemon.Applefruit is also used in the preparation of fruit jam, pie, andfruit salad.Safety profile

According to the environmental-working groupreports, apple fruit is one of the heavily pesticide-contaminated product. The most common pesticides foundon apple are organo-phosphorous and organo-chloridepesticides like Permethrin and DDT. Therefore, it isrecommended to wash the fruit thoroughly before use.

Apple fruit (Malusdomestica)Fresh, Nutritive value per 100 g

(Source: USDA National Nutrient data base)Energy 50 Kcal 2.5%Carbohydrates 13.81 g 11%Protein 0.26 g 0.5%Total Fat 0.17 g 0.5%Cholesterol 0 mg 0%Dietary Fiber 2.40 g 6%VitaminsFolates 3 µg 1%Niacin 0.091 mg 1%Pantothenic acid 0.061 mg 1%Pyridoxine 0.041 mg 3%Riboflavin 0.026 mg 2%Thiamin 0.017 mg 1%Vitamin A 54 IU 2%Vitamin C 4.6 mg 8%Vitamin E 0.18 mg 1%Vitamin K 2.2 µg 2%ElectrolytesSodium 1 mg 0%Potassium 107 mg 2%MineralsCalcium 6 mg 0.6%Iron 0.12 mg 1%Magnesium 5 mg 1%Phosphorus 11 mg 2%Zinc 0.04 mg 0%Phyto-nutrientsCarotene-ß 27 µg —Crypto-xanthin-ß 11 µg —Lutein-zeaxanthin 29 µg —

Health is Wealth

Apple fruit (Malusdomestica)nutritional facts

Zainab Inam, Nowshera


Next Meeting of theSAUDI OPHTHALMOLOGICAL SOCIETY

“SAUDI OPHTHALMOLOGY”to be held from 3-6 March’2013 at

King Fahd Cultural Centre, RiyadhPlease Contact:

[email protected] & [email protected]

For assistance, Visa and Pre-registration FormsPlease Contact:

Ophthalmology Update267-A , Street 53, F-10/4, Islamabad

Phone: 0333 5158885E.Mail: [email protected]

35th Annual National Ophthalmic Conference& KAROPHTH 2013

8-10 March 2013Pearl Continental Hotel Karachi

Secretary Scientific Committee Chairman, Registration committeeDr Alyscia Cheema Dr Vasdev Harani

Secretary Organizing Committee Chairman Organizing CommitteeDr Qazi M. Wasiq Prof. Shahid Wahab

For further information please contact:Mr. Muhammad Usman Tariq

Cell: 0345-2233942OSP Office, PMA House,Agha Khan III Road Karachi.

Email: [email protected]

Date post:	12-Jul-2020
Category:	Documents
Upload:	others
View:	1 times
Download:	0 times

Approved and Indexed by PMDC & Pak MediNet ABC Certified ... · Ophthalmology Update Vol. 11. No....

Documents