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This journal is the official scientificpublication of the Al SalamaInstitute of Ophthamology & itsallied hospitals with two issuesbeing published every year. Itwelcomes original articles, reviews,case reports, book reviews & othermaterials of academic interest inophthalmology & medicine

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  • AIO Journal of Ophthalmology 1

    Know Thy Instrument

    Chief EditorDr. K. Preetha

    Editorial CommitteeDr. Priya NambiarDr. Divya MenonDr. Dolly Nazia P.M.

    Editorial BoardDr. J. MuthiahDr. Rajesh P.Dr. M.A. SafarullaDr. Kunal KumarDr. Manish ShyamkulDr. Syed BasheerDr. Dheeresh KadukanvelliDr. Shaji Hussain

    Advisory BoardDr. Muhammed Swadique

    Dr. K. PreethaConsultant Ophthalmologist

    Al Salama Eye Hospital, Arayidathupalam Junction, Calicut - 673004Emai l : [email protected] : 9895878764Landline : 0495 3930123

    This journal is the official scientific

    publication of the Al Salama

    Institute of Ophthamology & its

    allied hospitals with two issues

    being published every year. It

    welcomes original articles, reviews,

    case reports, book reviews & other

    materials of academic interest in

    ophthalmology & medicine.

    AIO Journal of OphthalmologyVolume I, Issue I, September 2013

    Address for correspondence

  • AIO Journal of Ophthalmology 3

    conTenTs

    5 Editorial

    OriginalArticle7 Role of corneal wavefront guided LASIK treatment in highly aberrated corneas MuhemmedSwadique,PadmajaKrishnan

    Reviews14 Blepharoptosis

    KunalKumar

    20 Recurrent corneal erosion DivyaMenon

    25 Contracted socket

    KunalKumar

    28 Phakic Intraocular Lens

    DollyNaziaP.M

    Cuttingedgeophthalmology31 Refractive lenticule extraction (ReLEx)

    PriyaNambiar

    conTenTs

  • 4 AIO Journal of Ophthalmology

    conTenTs

    CaseKorner34 Posterior embryotoxon and its significance

    ManishShyamkul

    36 Ankyloblepharon filiforme adenatum

    ManishShyamkul

    KnowThyInstrument38 Optical coherence biometry: How coherent is the master ?

    K.Preetha

    Eureka!45 This is all about smart phone-o-graphy

    ShajiHussain

    TheOphthalmicParaphernalias48 Oculocardiac reflex an overview

    MuhammadHasifM.K.

    50 AnOphthalmicPotpourri

    K.Preetha

    51 Fun-Tastica

    K.Preetha

    53 ReadyReckoner

    MuhemmedSwadique

  • AIO Journal of Ophthalmology 5

    editorial

    Greetings from the editorial desk!

    Welcome!

    In your hands is the maiden issue of AIO JOURNAL OF OPHTHALMOLOGY. As the tag line states this journal is the official scientific journal of the Al Salama Institute of Ophthalmology (AIO) & its allied hospitals. Envisaged as a half yearly journal with a minimum of two issues a year, we plan to make this journal a forum for ophthalmic interactions of the highest quality.

    Ophthalmology is in the midst of a knowledge boom with quite a few journals coming out every year. The fate of most of these publications is that the ophthalmologist flips through most of them cursorily without actually going through the material. Our endeavor is to make this journal interesting enough so that the reader is enticed to read it thoroughly.

    Inside this issue, The Review Section features articles on Ptosis, RCES, Contracted Socket & Phakic IOL. The section Original Articles features an interventional study on the role of corneal wave front guided lasik treatment in highly aberrated corneas . The results are promising with a significant reduction in corneal higher order aberrations with coma components.

    The section Cutting Edge Ophthalmology focuses on the latest innovation in refractive surgery- ReLex. Case Korner features two interesting cases seen in our hospital. In Know Thy Instrument the focus is on the IOL Master recently acquired at our Calicut branch. Our guest column Ophthalmic paraphernalias features a writeup on oculocardiac reflex a nemesis for surgeons; Eureka features a brilliant innovation to use smart phones for slit lamp photography, Potpourri is an aviyal of ophthalmology information while funtastica is the dessert after the feast. We finally wind off with a Ready Reckoner on the present day modalities for managing Keratoconus.

    Here is hoping that this information collage is as interesting for you to peruse as it was for us to assemble. Please feel free to give your reviews, opinions & criticism about this issue & also about any novel ideas you want incorporated in the journal.

    RegardsEditorial Board

  • AIO Journal of Ophthalmology 7

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    RoleofCornealWavefrontGuidedlasikTreatmentinHighlyAberratedCorneas

    Dr. Muhemmed Swadique, FRCS, Prof. Padmaja Krishnan, MS

    Introduction

    Laser in situ keratomileusis (LASIK), is developed to correct refractive errors. It involves moulding of corneal surface with the help of excimer laser. It is a safe and effective procedure.1 Even though the un aided acuity of vision improves, the quality of vision decreases after LASIK procedure. This is due to the increase in the in-duced aberrations which reduces the contrast sensitivity2-4 and also causes photic phenomena like glare and halos. The optical aberrations may be the cause for non attain-ment of maximal acuity of retinal limit of 6/35.

    The aim of refractive surgery has shifted to maintain or even improve the quality of vision6. This target can be attained by decreasing the induced aberrations and also by decreasing the pre-existing aberrations6. This can be at-tained by the use of Corneal wavefront guided LASIK treat-ment.

    This study aims at evaluating the safety and efficacy of Corneal wavefront guided LASIK treatment in highly aber-rated corneas. Also it evaluates the changes in the higher order aberrations, glare, halos and contrast sensitivity.

    Materials and MethodsThis non randomised, interventional, prospective study comprised 76 consecutive symptomatic eyes of 38 pa-tients with a hyperopic or myopic spherical equivalent (SE). Inclusion criteria were symptomatic myopia, hyperopia, or astigmatism and a significant level of primary corneal coma aberration. The level of corneal coma was considered significant when the associated root mean square (RMS) for the corneal primary coma (measured over a pupil of 6.0 mm) was higher than 0.5 m.

    This criterion was chosen based on previously reported physiologic levels of corneal HOAs16; that is, the 0.5 m cut-off point was selected because the associated probability of it being a normal value was less than 1%.16 Exclusion cri-teria were formal contraindication to LASIK.

    Patients wearing contact lenses to correct the residual error were instructed to discontinue lens use for at least 4 weeks before the preoperative examination. Before

    surgery, patients received a complete explanation of the surgery and its risks and benefits and signed an informed consent in accordance with the Declaration of Helsinki. No treatment was performed if the refraction was not stable at 2 consecutive examinations performed at least 3 weeks apart. The target postoperative refraction was emmetropia in all cases. The postoperative follow-up was 6 months.

    Preoperative ExaminationThe preoperative examination included uncorrected deci-mal visual acuity (UCVA); best spectacle-corrected decimal visual acuity (BSCVA); manifest and cycloplegic refractions; slitlamp biomicroscopy; applanation tonometry; ultrasonic pachymetry; scotopic, low, and high mesopic pupillome-try; contrast sensitivity, corneal topography (Opticon Kera-ton Scout); and fundus evaluation.

    Corneal aberrations were derived from corneal topog-raphy following the protocol described below in Corneal Aberrations. In addition, patients were asked to evaluate the levels of halos and glare they perceived at night using the following qualitative scale: none, low, moderate, high, or severe.

    Ablation ProfileThe corneal wavefrontguided customized ablation was designed and calculated using commercially available ORK-CAM software. With this system, after the Opticon Keraton Scout corneal topography file is imported into the ORK-CAM software and clinical information (eg, patient age, subjective spherocylindrical refraction, central corneal pachymetry, flap thickness) is introduced, the software au-tomatically designs the ablation profile to best minimize all corneal aberrations.

    The calculation requires a topographic examination during which at least 7.0 mm of corneal area is analyzed in all meridians. Then, the optical zone is modified accord-ing to the pachymetry and the more significant or disturb-ing terms from the Zernike decomposition are chosen for inclusion in the calculation of the customized ablation.

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    The main goal of the designed ablation in all cases was to minimize the primary coma aberration Z(3,1). Therefore, the ablation profile was designed according to the corneal shape and refractive error and by modifying the optical zone and number of Zernike terms treated.

    The aim was to create a corneal surface with an el-evation profile that would generate a minimally distorted wavefront. In addition, all treatments were designed to leave an expected residual stromal bed thicker than 300 m in the central cornea.

    Surgical TechniqueAll LASIK procedures were performed by the same surgeon at Al Salama Eye Hospital, Perinthalmanna, Kerala, India. First, the treatment designed using ORK-CAM software was loaded into the computer of the excimer laser (Esiris, Schwind eye-tech-solutions). The surgeon then reviewed and confirmed the data. The Esiris is a flying-spot laser with a para-Gaussian spot of 0.8 mm diameter.

    The laser incorporates an eye-tracker system with a frequency of 330 Hz. The temperature and humidity condi-tions were maintained within the ranges indicated by the laser manufacturer. The optical zone of the treatment was selected according to the preoperative scotopic pupil size. Depending on the pachymetry, optical zones with a diam-eter at least as large as the scotopic pupil were targeted to prevent unwanted optical phenomena.

    Corneal AberrationsCorneal aberrations were derived from the data of the anterior surface of the cornea obtained with the Optikon Keraton Scout topography system. The systems software converts the corneal elevation profile into corneal wave-front data using Zernike polynomials with an expansion up to the 7th order.

    This topography system analyzes 6144 corneal points on a corneal area enclosed in a circular annulus defined by an inner radius of 0.33 and an outer radius of 10.0 mm re-

    spective to the corneal vertex. Aberration coefficients and RMS values for a 6.0mmpupil were obtained in all cases. The total RMS value was calculated based on all existing optical errors. In addition, the RMS was computed for the primary coma, Z(3, 1)

    Postoperative Follow-upPatients were examined on the first postoperative day and at 1, 3, and 6 months. On the first postoperative day, a de-tailed slitlamp examination was performed to evaluate the flap position and integrity of the cornea. At the other post-operative visits, UCVA, manifest refraction, BSCVA, slitlamp biomicroscopy, contrast sensitivity and corneal wavefront aberrations were recorded. In addition, patients were asked again about night-vision symptoms using the same criteria as preoperatively. An independent observer performed all the postoperative examinations.

    Statistical AnalysisStatistical analysis was performed using SPSS software for Windows (version 16 SPSS, Inc.). The Student t test for paired data was used for comparison. The significance of differences between preoperative and postoperative data was calculated. Differences were considered statistically significant when the P value was less than 0.05.The efficacy index was calculated as the ratio of postoperative UCVA to preoperative best corrected visual acuity (BCVA) and the safety index, as the ratio of postoperative BCVA to preop-erative BCVA.

    ResultsThe mean age of the 38 patients was 23.56 years 9.79 (SD) (range 18 to 35 years). The mean preoperative SE was -2.99 1.96 diopters (D) (range -6.88 to +1.63 D). Seventy five eyes (98.6%) had a myopic SE and one eye (1.32%), a hyperopic SE. The mean preoperative scotopic pupil size was 6.38 0.05 mm and the mean optical zone, 6.23 0.24 mm (range 6.00 to 7.00 mm). The mean total ablation zone

    UCVA=uncorrectedvisualacuity,BCVA=bestcorrectedvisualacuity,SE=sphericalequivalent

    Table 1. Refractive outcome over time

    Mean SD (Range)

    Parameter Pre Operative Post op 1 Month Post op 3 Months Post op 6 Months

    UCVA (decimal) 0.4440.19 (0.1 to 0.8 0.900.17 (0.4 to 1.5) 0.900.17 (0.4 to 1.5) 0.900.17 (0.4 to 1.5)

    Spherical Equivalent (D) -2.99 1.96 (-6.88 to 1.63) -0.7 0.24 (-1.25 to 0.12) -0.057 0.22 (-1.25 to 0.12) -0.04 0.13 (-1.25 to 0.12)

    BCVA (decimal) 0.9 0.17 (0.3 to 1) 0.9 0.17 (0.4 to 1.5) 0.9 0.16 (0.4 to 1.5) 0.92 0.16 (0.4 to 1.5)

    Efficacy 1.02 0.23 (range1 to 3)

    Safety 1.05 0.2.1 (range 1 to 3)

  • AIO Journal of Ophthalmology 9

    Wavefront lasik

    designed with ORK-CAM software was 7.31 0.06 mm (range 6.50 to 8.50 mm).

    Refractive OutcomesTable 1 shows the refractive results. Statistically signifi-cant reductions were observed in sphere and cylinder at 1 month (both P < .01, Student t test for paired data) (Table 3). The mean SE was -2.99 1.96 diopters (D) (range -6.88 to

    UCVA=uncorrectedvisualacuity,BCVA=bestcorrectedvisualacuity,SE=sphericalequivalent

    Table 2. Change in corneal aberrations over time

    Mean SD (Range)

    Parameter Pre Operative Post op 1 Month Post op 3 Months Post op 6 Months Total reduction

    Total RMS (m) 6.712.97(0.97 to 13.23) 3.461.60 (0.65 to 8.10) 3.441.60 (0.65 to 8.10) 3.401.56 (0.65 to 8.10) 3.313.03 (6.01 to 9.38)

    Coma (m) 0.72 0.23 (0.50 to 2.03) 0.270.30 (0.01 to 1.6) 0260.30 (0.01 to 1.6) 0.260.29 (0.01 to 1.6) 0.450.28 (0.99 to 10.7)

    mal BCVA postoperatively. Eleven eyes (14.47%) gained one to two lines of Snellen BCVA The loss of 2 to 3 lines in 2 eyes (2.63%) was due to numular keratitis.

    The contrast sensitivity is significantly improved at 6 months P > 0.01. (Table 3 )

    Corneal Aberrations:Table 2 shows the changes in corneal aberrations postop-

    Paired Differences

    Mean Std. Deviation Std. Error 95% Confidence Interval t df Sig. Mean of the Difference (2-tailed) Lower Upper

    Table 3. Paired Samples Test

    Pair 1 UCVA Preop - UCVA 6M -0.4599 0.2573 0.0295 -0.5187 -0.4011 -15.581 75 0

    Pair 2 BCVA pre op - BCVA 6M -0.0224 0.1015 0.0116 -0.0456 0.0008 -1.922 75 0.058

    Pair 3 HOA total RMS Pre Op - HOA total RMS 6M 3.31E+00 3.030499 0.347622 2.618686 4.003683 9.525 75 0

    Pair 4 Coma Pre Op - Coma 6M 0.456763 0.288005 0.033036 0.390951 0.522575 13.826 75 0

    Pair 5 SE Pre Op - SE 6 M -2.958 1.985 0.228 -3.412 -2.505 -12.994 75 0

    Pair 6 SPH pre op - SPH 3 M -2.4441 2.014 0.231 -2.9043 -1.9839 -10.58 75 0

    Pair 7 CYL pre op - CYL 3 M -1.047 0.826 0.095 -1.237 -0.857 -10.977 74 0

    Pair 8 CS Pre Op - CS 6 M 4.868 7.023 0.806 3.264 6.473 6.044 75 0

    Pair 9 Halos Preop - Halos 6M 1.737 1.204 0.138 1.462 2.012 12.575 75 0

    Pair 10 Glare Pre Op - Glare 6 M 1.513 0.931 0.107 1.3 1.726 14.171 75 0

    eratively. At 1 month, there was a statistically significant reduction in total RMS (P < .01, paired Student t test), astig-matic and coma RMS (P < .01, paired Student t test). There were no significant changes in these aberrometric param-eters between 3 months and 6 months.

    Subjective SymptomsGraph 1 & 2 summarizes patients perceptions of halos and glare at night. For both phenomena, the center of the dis-tribution of the answers moved from the high and severe levels preoperatively to the none and low levels postopera-tively. At 6 months, 93.42% of eyes did not perceive ha-

    +1.63 D), preoperatively and -0.05 1.37D (range -1.25 to +0.12 D) 1 month postoperatively; the difference between the 2 time points was not statistically significant (P = .06, paired Student t test). At 6 months, 97.36% of eyes had an SE within 0.50 D of emmetropia and 100%, within 1.50 D. At 6 months, the mean efficacy index was 1.02 0.23 (range1 to 3) and the mean safety index, 1.05 0.16 (range 1 to 3). (Table 1)

    Six months postoperatively, the UCVA was statistically significant better (P < .01, paired Student t test), although the change in BCVA was not significant. (P = .06, Student t test for paired data). (Table 3) shows the changes in deci-

  • 10 AIO Journal of Ophthalmology

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    6 M

    3 M

    1 M

    Pre Op

    7

    7

    2711

    1612

    2 38

    68

    68

    020

    4060

    80

    2

    Number of patients

    0 - No glare 1 - Minimal 2 - Mild 3 - Moderate 4 - Severe

    Number of patients 0 - No haloes 1 - Minimal 2 - Mild 3 - Moderate 4 - Severe

    Time Pe

    riod

    Time Pe

    riod

    Pre Op

    1 M 18

    0 20 40 60 80

    63

    63

    3 M

    6 M

    Graph 1. Change in subjective symptoms over time - Glare

    Graph 2. Change in subjective symptoms over time Halos

  • AIO Journal of Ophthalmology 11

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    los and 94.73% of eyes had no glare or a low level of glare.

    ComplicationsNo flap related or ablation related complications occurred during the treatment. No eye required retreatment dur-ing the postoperative follow-up. There were two eyes with reduced BCVA by two lines at 6 months due to nummular keratitis.

    DiscussionOcular or total wavefrontguided ablations are effective in correcting aberrations in eyes without previous refractive surgery.1722 This type of treatment partially reduces HOAs and minimizes the induction of new aberrations. In addi-tion, total wavefrontguided ablations have been shown to be safe and effective in the correction of low to moder-ate levels of HOAs, providing only partial reduction in cases with more extreme aberrations.810, 2326 The wavefront sen-sors available today analyze up to only 1452 points18.

    Therefore, this type of customized ablation is less effec-tive in patients with high levels of corneal aberrations (eg, previous refractive surgery with older algorithms, surgical complications during LASIK, corneal scars or wounds and patients with high levels of primary corneal aberrations). Other limitations of ocular wavefront sensing include the crowding or superimposition of the light spots or the as-sumption that the slope of the wavefront in each analyzed portion is locally flat in highly aberrated eyes. With topog-raphy systems, more than 6000 points can be studied and an exhaustive analysis performed. Although topography-guided and corneal wavefront guided ablations have been evaluated by several authors,1115 the changes in HOAs were not recorded in all cases.

    The terms topography guided and corneal wavefront guided can be confusing. Normally, systems that try to re-duce corneal irregularity by changing the corneal shape without considering corneal wavefront analysis are called topography guided. These systems are less accurate and thus were improved by the introduction of corneal wave-front data derived from corneal elevation data in the cal-culation of the ablation profile. Nevertheless, this nomen-clature can vary depending on the investigator. Several studies2731 report the results of corneal wavefrontguid-ed technology in highly aberrated corneas, such as after complicated refractive surgery, keratoplasty, or corneal penetrating injury. The results in these studies confirm the applicability of these excimer laser profiles. In addition, we found several justifications for the use of corneal wave-frontguided ablations:

    1. The first refractive interface corresponding to air

    cornea is the most important contributor to the total pow-er of the eye because the greatest difference in refractive indexes between materials in the eye is found at that point.

    2. In highly aberrated corneas, the contribution of the aberrations in the cornea generated by the surgery will be the most significant source of optical errors.

    3. The sample provided by most ocular wavefront sen-sors or aberrometers is more limited than that obtained with corneal topographers.

    4. Ocular wavefront sensors or aberrometers have limi-tation in the analysis of highly aberrated eyes; drawbacks include the crowding or superimposition of the light spots or the assumption of a flat slope for each analyzed portion of the wavefront (Hartmann-Shack devices).

    Therefore, treatment using corneal wavefront guided ablations seems to be the best option to restore quality of vision in corneas that are highly aberrated. In our study, we evaluated the usefulness of the corneal wavefrontguided ablations generated with ORK-CAM software in improving visual performance and optical quality in patients with high levels of corneal higher order aberrations and coma. The correction of higher order aberrations with the ORK-CAM ablations was successful. In terms of SE, predictability has proved to be excellent.

    The mean UCVA improved significantly, although the mean BSCVA did not change. The improvement in UCVA was mainly due to the reduction of the higher order com-ponents, which have the strongest effect on visual quality. One case with a significant loss of lines of BSCVA is related to numular keratitis. Regarding the optical properties of the cornea, the total RMS and Coma decreased significant-ly in all cases.

    Mean reduction in total HOA was 3.31. There was a significant reduction of the primary coma, with the mean postoperative RMS close to the physiologic range.16 One limitation of the customized refractive surgery technique we used is the size of the laser spot. The ideal spot for com-plete correction of HOAs is 0.5 mm or smaller.32 The Esiris laser had a spot size of 0.8 mm, which could have been re-sponsible for the partial correction of some HOAs.

    Another limitation of customized refractive surgery is the wound-healing response of the cornea. The cornea is made of complex structural composite material that un-dergoes biomechanical changes and healing responses after damage or injury.33 The ablation of tissue with the excimer laser could generate subtle unexpected modifica-tions that could limit the effect of a customized ablation34.Therefore, although the ablation profile was planned to achieve a more regular corneal surface, biomechanical changes and wound-healing responses could reduce

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    the effectiveness of the customized ablation. The improve-ment observed in corneal aberrations after the corneal wavefrontguided enhancement was related to a reduc-tion in the bothersome symptoms perceived by patients preoperatively. Specifically, the presence of night halos and glare was studied because patients with highly aberrated corneas often report these symptoms and they are easy to describe and understand.

    An increase in HOAs increases the incidence of night-vision complaints,7 especially after refractive surgery. These optical errors significantly increase image distortion, espe-cially when the pupil dilates because the most aberrated part of the ocular optical system takes part in the genera-tion of the retinal image. We did not report other symptoms associated with aberrated vision, such as double vision or ghost images. In future research of wavefront-guided re-fractive surgery, a standardized survey including all subjec-tive symptoms associated with aberrated vision must be used to allow complete analysis of the patients subjective perceptions. Corneal wavefrontguided LASIK treatment using the ORK-CAM software was useful in treating cases of high levels of primary coma. It provided excellent safety and efficacy for correction of higher order components. In addition, primary coma was significantly reduced and night-vision symptoms were decreased.

    ConclusionCorneal wave frontguided ablation using is a valuable safe and effective refractive surgical procedure to correct cases with significant corneal higher order aberrations with coma components. This treatment modality reduces higher order aberrations and coma. The quality of vision significantly improves with the procedure.

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    30. Rajan MS, OBrart DPS, Patel P, et al. Topography-guided customized laser-assisted subepithelial keratectomy for the treatment of postkeratoplasty astigmatism. J Cataract Refract Surg 2006; 32:949957

    31. Lee D-H, Seo SJ, Shin S-C. Topography-guided exci-mer laser ablation of irregular cornea resulting from penetrating injury. J Cataract Refract Surg 2002; 28:186188

    32. Latkany RA, Haq FE, Speaker MG. Advanced epithelial ingrowth 6 months after laser in situ keratomileusis. J Cataract Refract Surg 2004; 30:929931

    33. Lumba JD, Hersh PS. Topography changes associ-ated with sublamellar epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg 2000; 26:14131416

    34. Dupps WJ Jr, Wilson SE. Biomechanics and wound healing in the cornea. Exp Eye Res 2006; 83:709720

    35. Roberts C. Biomechanics of the cornea and wave-front-guided laser refractive surgery. J Refract Surg 2002; 18:S589S592 l

    Dr. Muhemmed Swadique, D.O.,D.N.B.,M.N.A.M.S,F.I.C.O.,F.R.C.S.,M.B.AiscurrentlytheMedicaldirector,AlSalamaEyeHospital.Heisacataractandrefractivesurgeonwithspecialinterestsinglaucoma&cornea

  • 14 AIO Journal of Ophthalmology

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    Ptosis refers to drooping or inferior displacement of any anatomic tissue. This short form is often used in place of the more accurate term, blepharoptosis, to describe drooping or inferior displacement of the upper eyelid.

    CLASSIfICATIOn Of PTOSIS (Table 1)

    Depending on onset1.Congenital present from birth.2. Acquired occurs anytime after birth due to an aetiology.

    Depending on aetiology 1. Myogenic 2. Aponeurotic 3. Neurogenic4. Mechanical 5. Traumatic

    Blepharoptosis

    Congenital simple ptosisCongenital myogenic ptosis is the commonest variety in this group (Fig 1). Rather than normal muscle fibers,

    fibrous and / or adipose tissue is present in the muscle belly, diminishing the ability to contract (leads to ptosis) and relax (leads to lid lag on looking down and lagophthalmos).

    Amount of levator function is an indicator of the amount of

    Blepharoptosis

    TruePtosis

    Congenitalptosis

    Congenitalsimpleptosis(CSP)CSP+Sup.Rectusweakness

    BlepharophimosisSynkinesis

    Acquiredptosis

    AponeuroticptosisMyogenicptosisNeurogenicptosisMechanicalptosisTraumaticptosis

    Pseudoptosis

    Vertical and horizontal shorten-ing of palpebral fissure height.Superior orbital rim flattening.Nasal bridge hypoplasia.

    SynkinesisIt may occur as:l Marcus Gunn jaw wink-

    ing Synkinesis. There is aberrant connection between motor division of Vth cranial nerve and levator muscle. (Fig 3a, 3b)

    Dr. Kunal Kumar, DO, FMRF

    Table 1. Classification of Blepharoptosis

    normal muscle present.It is characterised by a shallow / absent lid crease.

    Congenital simple ptosis with superior rectus weakness (Monocular elevation deficiency / Double elevator palsyThere is maldevelopment of the superior rectus muscle along with the congenital simple ptosis.

    There is an associated poor Bells phenomenon and / or vertical strabismus.

    Blepharophimosis: (Fig 2)It is an autosomal dominant condition characterised by:

    Telecanthus i.e. increased distance between the two medial and lateral canthus.Epicanthus inversus skin fold from lower to upper eyelid.

    Fig1Simplecongenitalptosis

    Fig2:Blepharophimosissyndrome

  • AIO Journal of Ophthalmology 15

    Blepharoptosis

    l Congenital IIIrd cranial nerve palsy.l Congenital Horner syndrome.l Duane retraction syndrome.

    Aponeurotic ptosisIt is the commonest type of acquired ptosis and is due to failure of aponeurosis to insert in its normal position (Fig 4).

    Because of involutional changes, chronic ocular inflam-mation, surgical trauma, repetitive trauma like frequent eye rubbing or insertion and removal of rigid contact lenses, the levator aponeurosis undergoes disinsertion, dehiscence or stretching.

    It is characterised by good levator function as levator muscle is healthy and high or absent upper eyelid crease because of loss of insertion of levator fibres into the skin. This type of ptosis may worsen on reading due to frontalis muscle relaxation.

    Myogenic ptosisIt is an uncommon variety of ptosis occurring due to local-ised or diffuse muscular disease e.g.l Myasthenia gravis.l Muscular dystrophy.l Chronic progressive external ophthalmoplegia.l Oculopharyngeal dystrophy.

    Neurogenic ptosisIt may be due to:l IIIrd cranial nerve palsy: Vasculopathic aetiology

    (diabetes, hypertension, atherosclerosis) usually spares the pupil and spontaneously resolves within 3 months. If it does not resolve by 3 6 months, than it requires further investigations. Compressive aetiol-ogy (neoplastic / aneurysms) affects the pupil and requires further investigations.

    l Horner syndrome.l Iatrogenic botulism.l Guillain Barre syndrome.

    Mechanical ptosisLarge chalazion or tumor like capillary haemangioma (Fig 5), squamous cell carcinoma, etc. may mechanically pull the eyelid down. It can even be caused by post traumatic or post surgical oedema.

    Traumatic ptosisBlunt or sharp trauma to the aponeurosis or muscle can lead to ptosis.

    Eyelid laceration exposing the pre aponeurotic fat indi-cates transection of orbital septum and possible damage to the levator aponeurosis.

    PseudoptosisApparent eyelid drooping without any pathology in the lid may be due to:l Abnormally low eyelid as in: Hypotropia Lid follows the eye downwards. Enophthalmos. Microphthalmos. Anophthalmos. Phthisis bulbi. Superior sulcus defect.l Contralateral upper eyelid retraction (Fig 6 ).l Dermatochalasia: excess upper eyelid skin over-

    hangs eyelid margin.l Brow ptosis

    Fig3A&B:MarcusGunnjawwinkingphenomenon Fig4:Aponeuroticptosis Fig5:Mechanicalptosis

    Fig6Righteyeptosiscausingthepseudolidretractionoflefteye

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    EvALuATIOn Of PTOSIS

    HistoryTo suggest the provisional diagnosis of the ptosis:l Duration: Congenital / Acquired.l Pre-disposing factors: h/o pregnancy and delivery,

    trauma, surgery, medical conditions.l Progression.l Variability: time of day, jaw winking.l Functional limitation: restricted superior field / full

    field of vision. difficulty while readingl Associated symptoms: diplopia, dysphonia, dys-

    phagia, dyspnoea (Myasthenia gravis)l Family history: Blepharophimosis, some forms of

    congenital ptosis.

    ExaminationTo confirm provisional diagnosis and decide on treatment.Full ocular and adnexal examination with emphasis on:l Facial examination: Chin up, frontalis overaction,

    brow ptosis, dermatochalasia, telecanthus, epican-thus inversus.

    Presence of ptosisl Vertical palpaebral fissure height: Patient fixates on

    a distant object in primary gaze. Measure the widest point between upper and lower eyelid (Fig 7 ). Value of < 9 mm indicates ptosis.

    l Margin reflex distance (MRD): MRD1 = With patient looking at the torch in the primary

    gaze, the distance from the upper eyelid margin to the cor-neal light reflex is measured. Normal MRD1 value is 4 to 4.5 mm.

    Light may be obstructed by the eyelid in severe cases and therefore have a zero or negative value.

    MRD1 helps to exclude cases of lower lid malposi-tions which lead to decreased palpaebral fissure height.

    Grading of ptosisIn unilateral cases, one can compare the droop with the contralateral eyelid position. However in bilateral ptosis (can be used also for unilateral ptosis), we have to measure the difference between a point 9 mm above the inferior limbus and the upper eyelid margin in primary position.

    Using MRD1, ptosis can be graded as the amount in mm, the MRD1 value is less than the normal value of 4 mm.

    2 mm is Mild ptosis3 mm is Moderate ptosis 4 mm is Severe ptosis.

    Levator functionIt is measured as the amount of upper eyelid excursion from extreme downgaze to extreme upgaze, with the frontalis muscle immobilised by the examiner manually fixing the eyebrow in its normal position (Fig 8 ).

    Levator action in mm Functional classification10 15 Excellent8 9 Good5 7 Fair0 4 Poor

    l In infants and uncooperative young children, the ILI-FF sign is elicited to determine the levator function. When the upper lid is everted in infants with fair to good levator function, the agitated infant is able to flip back the lid to its normal position. If levator function is poor to nil, the lid will not return to its normal position and will have to be manually reinverted.

    l Lid position in downgaze:Lid lag compared to the contralateral upper eyelid on downgaze in the absence of previous surgery or trauma suggests dystrophy of the levator muscle which will nei-ther relax nor contract properly (Fig 9). This is the impor-tant finding in congenital ptosis. In involutional ptosis, drooping of the lid may worsen on downgaze because of frontalis muscle relaxation.

    Cong. Myogenic ptosis Acquired Aponeurotic ptosis

    Lid crease Absent / weak Higher position

    Levator function Reduced Near normal

    On downgaze Eyelid lag Eyelid drop

    Comparison between:

    Fig7:MeasurementofPalpebralfissureheight

  • 17

    Blepharoptosis

    Fig8:Measurementoflevatorfunction Fig9:Lidlagondowngaze Fig10:Bellsphenomenon

    l Upper eyelid skin crease:Skin crease is often shallow or absent in congenital ptosis. Margin crease distance (MCD) is the distance between the upper eyelid crease and the eyelid margin. The high crease (large MCD) suggests an aponeurotic defect.

    l Aberrant eye movements:On lateral jaw movement or eye movements:Marcus Gunn jaw winking Synkinesis.Aberrant regeneration of the Vth cranial nerve.Duane retraction syndrome.

    l Refractive error and vision:To diagnose amblyopia due to occlusion of pupil, high astigmatism or strabismus.

    l Pupillary examination:Horner syndrome will present with miosis while IIIrd cra-nial nerve palsy will present with mydriasis.

    l Ocular motility:

    To diagnosePtosis with superior rectus weakness.IIIrd cranial nerve palsyChronic progressive external ophthalmoplegia

    Myasthenia gravis

    l Ancillary tests:Tests for Horner syndrome: Cocaine and amphetamine test.

    Test to rule out Pancoast tumor, carotid artery aneurysm or dissection.

    Tests for Myasthenia gravis:Edrophonium chloride (Tensilon) testIce pack testAcetylcholine receptor antibody test.

    l Test to predict post-op complication:LagophthalmosBells phenomenon (Fig 10 ) Evaluation for dry eye Corneal sensation

    TREATMEnT (Table 3) Choice of surgery depends upon:l Type of ptosis.l Amount of ptosis.l Degree of levator function.l Surgeons experience with various type.

    Ptosis

    ModerateMild Severe

    Good

    FasanellaServat

    FairGood Poor

    LargeResection

    ModerateResection SupramaximalMaximalResection/Sling

    Sling

    Fair Poor

    Table 3. Decision making in ptosis surgery

    AIO Journal of Ophthalmology

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    Surgical Procedures

    Fasanella Servat procedure:Principle: The upper border of tarsus is excised with the lower part of Mullers muscle and the conjunctiva (Fig 11).

    Indications: l Mild congenital ptosis with a levator function better

    than 10 mm

    l Horners syndromel Mild involutional ptosis if not associated with frank

    aponeurotic weakness.

    Levator resection:The extent of the resection is modified by the degree of the ptosis.

    Levator function Resection8 10 mm 14 18 mm6 7 mm 18 22 mm4 5 mm 22 26 mm

    If the superior rectus muscle is weak, the resection should be increased by about 4 mm.

    Anterior approach levator resection:PrincipleThe aponeurosis is ap-proached through a skin incision.The muscle is shortened and sutured to the tarsus. The skin crease reformed with sutures which pick up the underlying levator muscle (Fig 12).

    Fig11A,Fig11BandFig11CFasanellaServatprocedure

    IndicationsA ptosis with 4 mm or more of levator function;Lid exploration;Maximum levator resection;Preservtion of tarsus and conjunctiva;Skin crease defect.

    Aponeurosis surgery:It is indicated for patients with an aponeurotic defect and good levator function i.e. usually better than 10 mm. Intra operatively, the lid is set at the same level or a little higher than the other side.

    Anterior approach aponeurosis repair:

    PrincipleThe aponeurosis is approached through a skin incision. It is advanced and sutured to the tarsus or the defect is re-paied directly. Excess skin is excised and the skin crease reformed with sutures which pick up the underlying aponeurosis.

    IndicationsRepair or exploration of an aponeurotic defect, especially if there is an excess skin to be excised.

    Brow suspension

    PrincipleThe frontalis muscle normally lifts the eyebrow and con-tributes to eyelid elevation. This action of lifting the eyelid is enhanced by connecting the frontalis muscle and eye-brow to the eyelid with a subcutaneous sling for which various materials can be used. A unilateral sling will always produce asymmetrical result on downgaze. For a definitive cosmetic procedure it is better to do a bilateral suspension with weakening of other levator muscle if this is normal.

    Fig12:LigationofLPSduringLPSresectionsurgery

  • AIO Journal of Ophthalmology 19

    Blepharoptosis

    IndicationsPtosis with less than 4 mm of levator function; The prevention of amblyopia in an infant with severe pto-sis in whom an assessment of levtor function is not pos-sible;Following a levator excision.

    Levator division or excision:

    PrincipleThe action of the levator muscle is abolished by dividing or excising it.IndicationsThe abolition of aberrant eye movement e.g. jaw winking. To promote the use of frontalis muscle and create sym-metry in patients undergoing a bilateral brow suspension procedure for a unilateral ptosis.

    Post Operative Complications:

    Exposure keratitis.UndercorrectionOvercorrectionContour defects, notching of lid margin.Lash ptosis and entropionLash eversion and ectropionDefective skin creaseConjunctival prolapseSymblepharonExtra ocular muscle involvement (Strabismus)HaemorrhageInfection.

    Congenital ptosis with superior rectus weakness:If the eye is straight in the primary position of gaze but the superior rectus muscle is weak, more extensive ptosis sur-gery is required to lift the lid by a given amount since the superior rectus muscle normally contributes to upper lid movement via its common sheath with the levator mus-cle. When a levator resection is performed, an extra 4 mm

    of levator muscle is arbitrarily resected. If the eye is hypo-tropic in the primary position, it must be elevated before the ptosis correction is undertaken.

    Blepharophimosis:l The treatment of the ptosis depends on the levator

    function. This is usually poor and bilateral brow sus-pension procedure is required. The epicanthus and telecanthus should be corrected 6 months prior to ptosis surgery. For telecanthus trans nasal wiring or medial canthoplasty can be done.

    Marcus Gunn jaw winking Synkinesis:l If the ptosis is the main problem, it can be corrected

    with the ptosis surgery based on levator function.

    If the aberrant movement of the eyelid is the main problem, it can be corrected by leva-tor excision and brow suspension procedure. This can be done bilaterally to obtain the most sym-metrical result.

    References

    l Orbits, eyelids and lacrimal system. Section 7. Basic and clinical science course. Edition: 2000-2001. The Foundation of the American Academy of Ophthal-mology. Blepharoptosis. Pages: 189 204.

    l J.R.O. Collin. Manual of systematic eyelid surgeries. 2nd Edition. Butterworth Heinemann. Ptosis. Pages: 41 72.

    l Homblass A (Ed). Oculoplastic, Orbital, and recon-structive surgery, 1988, Williams & Wilkins, Balti-more, MD

    l Ptosis, Chapter 24, Repair and Reconstruction of or-bital region, C.Beard and J.C. Mustarde, pages 411-443. l

    Dr. Kunal Kumar,DO,FMRF-(Orbit,Oculoplasty&ReconstructiveSurgery)SankaraNetralaya.,ChennaiiscurrentlyworkingasOrbit&OculoplasticsurgeonintheAlSalamagroupofEyeHospitalsCalicut&Perinthalmanna

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    RecurrentCornealErosionSyndrome

    Etiology

    Recurrent corneal erosion is a disorder of the eyes characterized by the failure of the cornea's outer-most layer of epithelial cells to attach to the under-lying basement membrane (Bowman's layer). Defective adhesion of the epithelium to the Bowman's membrane causes recurring cycles of epithelial breakdown. Multiple recurrences are common, because the epithelial cells re-quire at least 8-12 weeks regenerating or repairing the epithelial basement membrane .The condition is excruci-atingly painful because the loss of these cells results in the exposure of sensitive corneal nerves.

    Typically, recurrent corneal erosion syndrome (RCES) develops 3-10 days after the insult but in some cases, it may not develop until several months later. There is often a history of previous corneal injury (corneal abrasion or ulcer), but also may be due to corneal dystrophy or cor-neal diseases. In other words, one may suffer from corneal erosions as a result of another disorder, such as map dot fingerprint disease. [1]

    The common causes that trigger the process off are:

    a) superficial trauma to the cornea including corneal abrasions due to contact lens wearing

    b) A clean cut abrasion (such as a paper cut) is more likely to cause the problem than a ragged abrasion.

    c) Other types of trauma may include alkali burns, for-eign bodies and exposure keratopathy,entropion,ectropion,blepharitis,lagophthalmos.

    There may be more unusual trigger factors (all involv-ing disruption of the epithelial basement membrane) such as following cataract surgery or refractive surgery. Other iatrogenic causes include vitrectomy (surgical removal of the vitreous) and photocoagulation.[2]

    Systemic diseases which may predispose to this condition includel Diabetes[1] l Junctional epidermolysis bullosa

    l Alport's syndrome l Mnchausen's syndrome l Malnutrition

    Drugs associated with the development of RCES includel Thiomersal (found in contact lens solutions). l High-dose topical neomycin. l Topical paromomycin. l Topical diamidines and propamidine. To a certain extent, all topical anaesthetic medication causes some degree of epithelial cell damage but this is most marked with cocaine, which is associated with RCES more than others. A variety of RCES associated with au-tosomal dominant inheritance has been described but is rare.

    Epidemiology [2]l There are no accurate statistics relating to the exact

    incidence and prevalence of this condition as it often goes undiagnosed or misdiagnosed.

    l It tends to occur slightly more commonly in females.l It is a problem seen in adulthood, usually from the

    fourth decade of life onwards, unless it is associated with one of the corneal dystrophies (eg Reis-Bcklers dystrophy) or Alport's syndrome, in which case it can arise in children.

    SymptomsSymptoms include recurring attacks of severe acute ocular pain, foreign-body sensation, photophobia (i.e. sensitivity to bright lights, this occurs if corneal oedema develops)), and tearing often at the time of awakening or during sleep when the eyelids are rubbed or opened, decreased visual acuity. In its early stages, the condition may be asympto-matic. Later, there may be recurrent attacks of acute pain (typically towards the end of sleep or on waking) associ-ated with lacrimation, photophobia and a foreign body sensation. There may be an associated blepharospasm (inability to open the lids). The problem may be unilateral

    Dr. Divya Menon, D.O.M.S., FICO

  • AIO Journal of Ophthalmology 21

    rces

    or bilateral. Symptoms may gradually subside over the course of the day and then start all over again the next morning. The unpredictability of these episodes may lead to an associated anxiety.

    SignsSigns of the condition include corneal abrasion or lo-calized roughening of the corneal epithelium, some-times with map-like lines, epithelial dots or micro-cysts, or fingerprint patterns. An epithelial defect may be present, usually in the inferior interpalpebral zone. Loose edges, intraepithelial cysts,stromal edema,blepharospasm. (Fig 1)

    Diagnosis Diagnosis is made on history and examination. Severe cas-es may warrant corneal topography to outline the degree of corneal damage or help in the diagnosis of a corneal dystrophy (most of which are diagnosed on examination).The erosion may be seen by a doctor using the magnifica-tion of a slit lamp biomicroscope , although usually fluo-rescein stain must be applied first and a blue-light used. (Fig 2). In vivo confocal microscopy and videokeratogaphy are other methods of diagnosis.

    Management of episodesThe type of tears being produced has little adhesive prop-erty. Water or saline eye drops tend to be ineffective. Rath-er a 'better quality' of tear is required with higher 'wetting ability' (i.e. greater amount of glycoproteins) and so artifi-cial tears are applied frequently. Individual episodes may settle within a few hours or days but additional episodes (as the name suggests) will recur at intervals.

    The easy remedy for recurrent attacks is to apply a pressure patch.

    Prevention Since episodes tend to occur on awakening and managed by use of good 'wetting agents', approaches has to be tak-en to help prevent episodes .Prophylaxis revolves around long-term lubrication in the first instance, eg night-time lubricating ointment for three months.[7] The success of this approach depends on the patient understanding the importance of continuing this treatment in the absence of symptoms. More severe cases may require a protective bandage contact lens.

    There is evidence to suggest that a 12-week course of systemic tetracyclines (eg oxytetracycline 250 mg bd) may be beneficial (they inhibit matrix metalloproteinase activ-ity and promote epithelial stability)

    Fig1 Fig2

    Prevention includesa) Environmental Ensuring that the air is humidified rather than dry, not overheated and without excessive airflow over the face. Also avoiding irritants such as cigarette smoke.[2] l Use of protective glasses especially when gardening

    or playing with children.[2]

    b) General personal measures l Maintaining general hydration levels with adequate

    fluid intake.[2] l Not sleeping-in late as the cornea tends to dry out

    the longer the eyelids are closed.[2]

    c) Pre-bed routine l Routine use of long-lasting eye ointments applied

    before going to bed.[2] l Occasional use of the anti-inflammatory eyedrops

    before going to bed if the affected eye feels inflamed, dry or gritty

    l Use of a hyperosmotic ointment before bed reduces the amount of water in the epithelium, strengthen-ing its structure

    l Use the pressure patch as mentioned above.

    d) Waking options l Learn to wake with eyes closed and still and keeping

    artificial tear drops within reach so that they may be instilled under the inner corner of the eyelids if the eyes feel uncomfortable upon waking.[2]

    l It has also been suggested that the eyelids should be rubbed gently, or pulled slowly open with your fin-gers, before trying to open them, or keeping the af-fected eye closed while "looking" left and right to help spread lubricating tears. If the patient's eyelids feel stuck to the cornea on waking and no intense pain is present, use a fingertip to press firmly on the eyelid to push the eye's natural lubricants onto the affected

  • 22 AIO Journal of Ophthalmology

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    area. This procedure frees the eyelid from the cornea and prevents tearing of the cornea.[2]

    Surgical A punctal plug may be inserted into the tear duct by an ophthalmologist, decreasing the removal of natural tears from the affected eye. [5]

    The use of thin contact lenses may help prevent the abrasion during blinking. However they need to come for frequent follow-up visits because there is an increased risk of infection.[2]

    Alternatively, under local anaesthetic, the loose cor-neal layer may be gently removed with a fine needle and cautery (heat or laser) or 'spot welding can be attempted with laser. The procedures are not guaranteed to work, and in a minority may exacerbate the problem.

    Anterior Stromal Puncture is an effective and simple treatment. This is a minor procedure carried out under topical anaesthesia in the eye clinic. Numerous tiny punc-tures are made away from the central visual axis, which induces cicatrisation and promotes more permanent epi-thelial adherence. It may be performed using Nd-YAG la-ser.[5] or 24-26G needle.

    An option for minimally invasive and long-term effec-tive therapy [6] is laser phototherapeutic keratectomy. Laser PTK involves the surgical laser treatment of the cor-nea to selectively ablate cells on the surface layer of the cornea. It is thought that the natural regrowth of cells in the following days are better able to attach to the base-ment membrane to prevent recurrence of the condition. Laser PTK has been found to be most effective after epi-thelial debridement for the partial ablation of Bowman's lamella[7], which is performed prior to PTK in the surgical procedure. This is meant to smoothen out the corneal area that the laser PTK will then treat. In some cases, small-spot PTK[8], which only treats certain areas of the cornea may also be an acceptable alternative

    .Keratectomy is the removal of corneal tissue and is reserved for severe and difficult cases (usually in patients with associated corneal dystrophies).[3] It involves either laser treatment or surgical removal (knife, diamond burr): the entire epithelium is removed and allowed to regrow from new over the following 5-7 days. It can be carried out more than once if the problem recurs. It can also be com-bined with a refractive correction.

    Presence of blepharitis,meibomitis,and filaments over the corneal surface should be treated accordingly.

    30-60 days autologous serum drops can be given. We have to educate the patient regarding the refrigeration and sterile preservation of the drops .

    Alcohol delamination is a newer procedure that has shown good efficacy and safety.[6]

    Medical Patients with recalcitrant recurrent corneal erosions often show increased levels of matrix metalloproteinase (MMP) enzymes.[9] These enzymes dissolve the basement mem-brane and fibrils of the hemidesmosomes, which can lead to the separation of the epithelial layer.

    Treatment with oral tetracycline antibiotics (such as doxycycline or oxytetracycline) together with a topical corticosteroid (such as prednisolone), reduces MMP activ-ity and may rapidly resolve and prevent further episodes in cases of unresponsive to conventional therapies.[10][11] Some have now proposed this as the first line therapy after lubricants have failed.[3]

    Assessmentl Check the patient's visual acuity (a drop of local an-

    aesthetic will temporarily relieve the pain and the as-sociated blepharospasm).

    l Examine as much of the anterior segment of both eyes (even if symptoms are unilateral). This includes fluorescein staining of the cornea. The idea is to rule out other possible differentials .

    Differential diagnosisl Corneal abrasion. l Corneal foreign body. l Contact lens-related problem. l Dry eye syndrome. l One of a variety of corneal dystrophies. l Floppy eyelid syndrome. l Herpes simplex keratitis. l Other form of keratitis.

    Recurrent corneal erosion syndrome (RCES) can also occur following prolonged eye patching.

    Staging There is no formal staging of recurrent corneal erosion syndrome (RCES) but a note is made of the depth of cor-neal involvement, as this dictates treatment options and prognosis.

    ManagementFirst if there is an abrasion, cover with an antibiotic (such as a topical fluoroquinolone given as directed in the pre-scribing information) and a bandage contact lens until healed. Once the cornea is reepithelialized, the following

  • AIO Journal of Ophthalmology 23

    rces

    regimen can be followed for the treatment of RCE.a) 5%hypertonic saline (5% NaCl) ointment at bedtime

    for 2 months. This helps reduce overnight edema and improves epithelial adherence just prior to the morn-ing (when most RCEs occur).

    b) Preservative free lubricating drops 4 times a day.

    c) (loteprednol etabonate 0.5%) or fluoromethalone four times a day for 2 weeks, then twice a day for 6 weeks (check intraocular pressure within 1 month).

    d) Oral doxycycline (either 20mg or 50 mg) twice a day for 2 months.

    long-term, management, especially in cases of epithelial basement membrane dystrophy, should include:

    a) Cyclosporine 0.05% twice a day b) Artificial tear substitutionc) Omega-3 free fatty acid supplementationd) Lubricating eye ointment for 2 months during night

    time. The negative pressure in the sac is neutralised with this.

    e) Soft BCL for 2-3 weeks.

    Note: Avoid topical steroid till the epithelium is healed .

    Complicationsl Infectious keratitis. l Corneal scarring. l Decreased visual acuity (due to either of the above).

    PrognosisWith the right treatment, generally the prognosis is good with most patients responding well to topical treatment.[2] This relies on any underlying conditions being diagnosed and treated and good patient education on the long-term management. Few patients will have their vision perma-nently affected.

    further reading & references1. Kanski J. Clinical Ophthalmology; A Systematic Ap-

    proach (5th Ed) Butterworth Heinemann (2003) 2. Recurrent corneal abrasions/erosion, Kinshuck D, Good

    Hope Eye Department, Heart of England NHS Founda-tion Trust; (excellent patient resource with good dia-grams)

    3. Ramamurthi S, Rahman MQ, Dutton GN, et al; Patho-genesis, clinical features and management of recurrent

    corneal erosions. Eye (Lond). 2006 Jun;20(6):635-44. Epub 2005 Jul 15.

    4. Verma A et al, Corneal Erosion, Recurrent, Medscape, Jun 2009

    5. Ewald M, Hammersmith KM; Review of diagnosis and management of recurrent erosion syndrome. Curr Opin Ophthalmol. 2009 Jul;20(4):287-91.

    6. Watson SL, Barker NH; Interventions for recurrent corneal erosions. Cochrane Database of System-atic Reviews 2007, Issue 4. Art. No.: CD001861. DOI: 10.1002/14651858.CD001861.pub2.

    7. Tsai TY, Tsai TH, Hu FR, et al; Recurrent corneal ero-sions treated with anterior stromal puncture by neo-dymium: Ophthalmology. 2009 Jul;116(7):1296-300. Epub 2009 May 8.

    8. Singh RP, Raj D, Pherwani A, et al; Alcohol delamina-tion of the corneal epithelium for recalcitrant recur-rent corneal Br J Ophthalmol. 2007 Jul;91(7):908-11. Epub 2007 Feb 14.

    9. Das S, Seitz B; Recurrent corneal erosion syndrome. Surv Ophthalmol. 2008 Jan-Feb;53(1):3-15

    10. Review of Ophthalmology, Friedman NJ, Kaiser PK, Trattler WB, Elsevier Saunders, 2005, p. 221

    11. Verma A, Ehrenhaus M (August 25, 2005) Corneal Ero-sion, Recurrent at eMedicine

    12. Wang L, Tsang H, Coroneo M (2008). "Treatment of recurrent corneal erosion syndrome using the combination of oral doxycycline and topical cor-ticosteroid". Clin. Experiment. Ophthalmol. 36 (1): 812. doi:10.1111/j.1442-9071.2007.01648.x. PMID 18290949.

    13. Liu C, Buckley R (January 1996). "The role of the ther-apeutic contact lens in the management of recurrent corneal erosions: a review of treatment strategies". CLAO J 22 (1): 7982. PMID 8835075.

    14. Tai MC, Cosar CB, Cohen EJ, Rapuano CJ, Laib-son PR (March 2002). "The clinical efficacy of sili-cone punctal plug therapy". Cornea 21 (2): 1359. doi:10.1097/00003226-200203000-00001. PMID 11862081.

    15. Baryla J, Pan YI, Hodge WG (2006). "Long-term effi-cacy of phototherapeutic keratectomy on recurrent corneal erosion syndrome.". Cornea 25 (10): 11501152. doi:10.1097/01.ico.0000240093.65637.90. PMID 17172888.

    16. Kampik D, Neumaier K, Mutsch A, Waller W, Geerling G (2008). "Intraepithelial phototherapeutic keratec-tomy and alcohol delamination for recurrent corneal erosions--two minimally invasive surgical alterna-tives.". Klinische Monatsbltter fr Augenheilkunde

  • 24 AIO Journal of Ophthalmology

    reVIeW - rces

    225 (4): 27680. doi:10.1055/s-2008-1027174. PMID 18401793.

    17. Van Westenbrugge JA. (2007). "Small spot photother-apeutic keratectomy for recurrent corneal erosion.". J Refract Surg 23 (7): 7214. PMID 17912944.

    18. Ramamurthi S, Rahman M, Dutton G, Ramaesh K (2006). "Pathogenesis, clinical features and manage-ment of recurrent corneal erosions.". Eye 20 (6): 63544. doi:10.1038/sj.eye.6702005. PMID 16021185.

    19. Hope-Ross M, Chell P, Kervick G, McDonnell P, Jones H (1994). "Oral tetracycline in the treatment of recur-rent corneal erosions.". Eye 8 (Pt 4): 3848. PMID 782^ Review of Ophthalmology, Friedman NJ, Kaiser PK, Trattler WB, Elsevier Saunders, 2005, p. 221

    20. Verma A, Ehrenhaus M (August 25, 2005) Corneal Ero-sion, Recurrent at eMedicine

    21. Wang L, Tsang H, Coroneo M (2008). "Treatment of recurrent corneal erosion syndrome using the combination of oral doxycycline and topical cor-ticosteroid". Clin. Experiment. Ophthalmol. 36 (1): 812. doi:10.1111/j.1442-9071.2007.01648.x. PMID 18290949.

    22. Liu C, Buckley R (January 1996). "The role of the ther-apeutic contact lens in the management of recurrent corneal erosions: a review of treatment strategies". CLAO J 22 (1): 7982. PMID 8835075.

    23. Tai MC, Cosar CB, Cohen EJ, Rapuano CJ, Laib-son PR (March 2002). "The clinical efficacy of sili-cone punctal plug therapy". Cornea 21 (2): 1359. doi:10.1097/00003226-200203000-00001. PMID 11862081.

    24. Baryla J, Pan YI, Hodge WG (2006). "Long-term effi-cacy of phototherapeutic keratectomy on recurrent corneal erosion syndrome.". Cornea 25 (10): 11501152. doi:10.1097/01.ico.0000240093.65637.90. PMID 17172888.

    25. Kampik D, Neumaier K, Mutsch A, Waller W, Geerling G (2008). "Intraepithelial phototherapeutic keratec-tomy and alcohol delamination for recurrent corneal

    erosions--two minimally invasive surgical alterna-tives.". Klinische Monatsbltter fr Augenheilkunde 225 (4): 27680. doi:10.1055/s-2008-1027174. PMID 18401793.

    26. Van Westenbrugge JA. (2007). "Small spot photother-apeutic keratectomy for recurrent corneal erosion.". J Refract Surg 23 (7): 7214. PMID 17912944.

    27. Ramamurthi S, Rahman M, Dutton G, Ramaesh K (2006). "Pathogenesis, clinical features and manage-ment of recurrent corneal erosions.". Eye 20 (6): 63544. doi:10.1038/sj.eye.6702005. PMID 16021185.

    28. Hope-Ross M, Chell P, Kervick G, McDonnell P, Jones H (1994). "Oral tetracycline in the treatment of recur-rent corneal erosions.". Eye 8 (Pt 4): 3848. PMID 782

    29. Kampik D, Neumaier K, Mutsch A, Waller W, Geerling G (2008). "Intraepithelial phototherapeutic keratec-tomy and alcohol delamination for recurrent corneal erosions--two minimally invasive surgical alterna-tives.".

    Klinische Monatsbltter fr Augenheilkunde 225 (4): 27680. doi:10.1055/s-2008-1027174. PMID 18401793.

    30. Van Westenbrugge JA. (2007). "Small spot photother-apeutic keratectomy for recurrent corneal erosion.". J Refract Surg 23 (7): 7214. PMID 17912944.

    31. Ramamurthi S, Rahman M, Dutton G, Ramaesh K (2006). "Pathogenesis, clinical features and manage-ment of recurrent corneal erosions.". Eye 20 (6): 63544. doi:10.1038/sj.eye.6702005. PMID 16021185.

    32. Hope-Ross M, Chell P, Kervick G, McDonnell P, Jones H (1994). "Oral tetracycline in the treatment of re-current corneal erosions.". Eye 8 (Pt 4): 3848. PMID 7821456.

    33. Dursun D, Kim M, Solomon A, Pflugfelder S (2001). "Treatment of recalcitrant recurrent corneal erosions with inhibitors of matrix metalloproteinase-9, doxy-cycline and corticosteroids.". Am J Ophthalmol 132 (1): 813. doi:10.1016/S0002-9394(01)00913-8. PMID 11438047. l

    Dr. Divya Menon,D.O.M.S.,FICOiscurrentlyworkingasConsultantinGeneralOphthalmologyattheAlSalamaEyeHospitalPerinthalmanna

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    Dr. Kunal Kumar, DO, FMRF

    ContractedSocket

    Congenital anophthalmia is the congenital ab-sence of any ocular tissue in the orbit resulting from failure of budding of optic vesicle. Clinical anophthalmia refers to reduced volume socket result-ing in small cul-de-sac, lid phimosis, eyelid malposition and peripalpebral fibrosis. The term microphthalmia is reserved for a structurally normal, small eye, with axial length two standard deviations below that of the popu-lation age-adjusted mean. The eye is essentially normal except for its decreased total axial length and typically correlates to an axial length below 21 mm in adult eyes. Anophthalmia and microphthalmia are thought to be caused by disturbances of the morphogenetic pathway that controls eye development. Contracted Socket is an anophthalmic socket which cannot support a prosthetic eye. A contracted socket has been classified based upon the clinical presentation (Table 1).

    Socket Contracture

    CongenitalThis involves contracted socket due to conditions such as anophthalmia and microphthalmia where there is virtually no stimulus for the bony growth.

    AcquiredAn acquired contracted socket is the result of tissue shrink-age due to various factors (as discussed below) which leads to inadequate space for the prosthesis to be retained properly. Tumors such as retinoblastoma pose a special problem when the suffering patient is treated with irradia-tion. Physical trauma such as globe rupture necessitating the removal of precious tissue like conjunctiva leads to posterior lamellar shortening. Chemical insult due to alkali burns are a big hurdle in the management of the resultant contracted socket. Mustarde called them the Malignantly Contracted Sockets as these are very difficult to manage. The anterior and posterior lamellae are lost partially or completely and the recurrent cicatricial process yields to repeated failure of any treatment modality. Staphylococ-cal infections especially in post traumatic infections, cause necrosis and destruction of tissue causing contracture. Iatrogenic factors also play an important role in causa-

    tion of a contracted socket. An enucleation done badly or with inadequate knowledge about the anatomy of the lid and socket very often leads to tissue deficiency. Failure to place a conformer immediately after enucleation or evis-ceration procedure or when placed initially, not using it in post operative period for adequate duration result in shal-lowing or obliteration of fornices

    PathophysiologyThe exact cause of a contracted socket is not been clearly understood. It has however been attributed to factors such as volume deficit and volume redistribution. Vol-ume deficit can be because of loss of the globe and tis-sue, inadequate sized implant and deficient conjunctiva. Volume redistribution refers to an alteration in the quality or placement of the tissue such as contraction of Tenons capsule, retraction of periocular muscle (eyelid retractors) and downward and forward shifting of orbital fat. There is also a role of myofibroblast which is controversial.

    Clinical featuresA patient with a contracted socket presents to the clinic with cosmetic deformity and problems in prosthesis fit which causes a nuisance, embarrassment and mental de-pression to the patient. Features of a contracted socket are sunken socket, inability to retain prosthesis in the socket, lagophthalmos, ptosis, entropion, pain and discharge. Post Enucleation Socket Syndrome (PESS) refers to a condition of contracture of socket following enucleation character-ized by enophthalmos, ptosis, entropion and superior sul-cus deformity.

    Clinical EvaluationClinical evaluation of a case of contracted socket includes a detailed history, indication and age at enucleation/ evis-ceration, previous history (trauma, tumor), presence or absence of implant at primary procedure, history of any radiation therapy and allergy to some medication. Exami-nation of eyelids includes measuring the amount of ptosis, lagophthalmos, and vertical and horizontal palpebral fis-sure height. Adequacy of the cul-de-sac, superior sulcus deformity and presence of cicatricial element (scar/band/contracture) should be noted. Keeping the possibility

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    Table 1. Classification of contracted socketClassification IMild Superficial Contraction of conjunctival fornixSevere Superficial Contraction of eyelids and conjunctival fornixMild Deep Contraction of conjunctival fornix and orbital fatSevere Deep Absence of fornix and severe contraction of orbital fatTotal All of the above with bony abnormalityClassification IIMild l Mild entropion l Fairly deep socket/ fornix l Minimal shortening of the posterior lamella.

    Moderate l Inferior fornicial shallowing l Mild increase in superior sulcus deformity l Prosthesis overrides the lower lid margin l Prosthesis starts getting displaced

    Severe Upper and lower fornicial shallowing Palpebral fissure height and length shortening No space to introduce examiners fingers Prosthesis cannot be retained

    Classification III

    Congenital Anophthalmia Microphthalmia

    Acquired Tumor Trauma l Physical l Chemical Irradiation Infection Iatrogenic

    of a membrane graft in mind, one should also examine the condition of oral mucosa, oral hygiene and the ability of the patient to open mouth.

    ManagementThe primary aim in the management of a contracted sock-et is to make the socket capable enough to maintain the prosthesis and provide better cosmesis for the patient. The management of a contracted socket can be divided into surgical and prosthetic treatment.

    Congenital contracted socketThe aim of managing a congenital contracted socket is to stimulate the growth of the orbit. Maximum growth oc-curs in the first year of life and hence intervention should be initiated as early in life as possible. Since there is an ab-sence of globe which does not provide any stimulus for the bony development, placement of conformers of in-creasing sizes act as substitutes. Mild to moderate contrac-tion is managed conservatively by insertion of conform-

    ers. A conformer of increasing size is changed every week for socket and soft tissue expansion followed by a change every month to provide bony expansion. The end point is when a suitable sized prosthesis can be worn. Severe contraction requires volume replacement using implants, expanders and dermis fat grafts and often need orbital os-teotomies. Conjunctival sac and lid reconstruction may be beneficial to the overall cosmetic effect.

    Mildly contracted socket (fig 1)This is associated with mild en-tropion resulting from shorten-ing of posterior lamella. The for-nices are fairly deep and there is no problem with the fitting of a prosthesis. A transverse blepha-rotomy (lid split) with marginal rotation (Weis procedure) is the

    preferred surgical procedure for the entropion. If hori-zontal lid laxity is also present, the marginal rotation can be combined with horizontal lid shortening procedure (Quickert procedure).

    Moderately contracted socket (fig 2)A moderately contracted socket is associated with loss of both superior and inferior fornices along with some amount of volume deficit. Contractures, bands or sym-blepharon when present can be easily treated with band release followed by Z plasty with placement of a con-former. For extensive contractures, either a split thick-ness graft or a full thickness mucus membrane graft can

    be used. However, a full thick-ness mucus membrane graft is preferred over a split thickness graft because of less contrac-ture. Volume deficiency can be managed by a secondary ball implant, dermis fat graft (DFG) or a temporary muscle flap transfer.

    Severely contracted socket (fig 3)In a severely contracted socket, there is complete oblit-

    eration of the fornices with or without bony deformity making it impossible to place or retain prosthesis. For severe bony de-formity, extensive craniofacial reconstruction with external wiring can be undertaken al-

    Fig1,Mildcontractedsocketwithmildentropion

    Fig2,Moderatecontract-edsocketwithInferiorfornicialshallowing

    Fig3,Severlycontractedsocketfollowingenucleation

  • AIO Journal of Ophthalmology 27

    contracted socket

    though the whole procedure is tedious, time consuming and may not always yield satisfactory results. Surface defi-cit can be managed by split thickness graft or a full thick-ness mucus membrane graft. Secondary ball implant, der-mis fat graft (DFG) or a temporary muscle flap transfer can address the volume replacement.

    Graft MaterialsVarious types of graft materials have been used in the past for the replacing the damaged or deficient palpebral la-mella such as conjunctiva, mucus membrane grafts (inner side of the lower lip, gums, buccal mucosa, opening of the parotid duct near the upper second molar avoiding the Stensons duct, hard palate mucosa, nose, nasal septum or nasal cartilage with mucosal lining, prepuce, vagina, labia minora, and rectum), hard palate, skin, muscle flaps, tem-poralis fascia, and dermis fat graft (DFG).

    General PrinciplesAll scar must be removed. All raw surfaces must be cov-ered with grafts that will survive. Size of mucus membrane graft should be 1.5 to 2.0 times the size of defect since some amount of tissue shrinkage is unavoidable. All grafts must be placed on a vascularized tissue and that absolute immobility of the graft is achieved. Shifting of the graft can result in loss of blood supply. Skin and mucosa should not be mixed in the same socket (Fig 4 and Fig 5).

    ComplicationsThe incidence and occurrence of complication of a con-tracted socket depends on the surgical technique, pres-ence of infection and tissue reactivity. The various com-

    plications are graft failure, oral cicatrix formation, mucus membrane granuloma formation, socket infection, recur-rence of contractures, and ankyloblepharon

    Prevention of socket contractureInadequate dissection of the tissues leads to socket con-tracture in the early post operative period. Care should be taken to carefully dissect and preserve as much Tenons capsule and conjunctiva as possible and suture them in separate layers over the implant without tension.

    Adequate and prolonged expansion of fornicial tissue is essential for socket expansion and prevention of forni-cial shortening. The prosthesis should be frequently evalu-ated for roughening of the surface and ill fitting. This can be a source of constant irritation and discomfort to the patient and can result in disuse of the prosthesis which in turn would cause socket contracture. At this stage, palpe-bral phimosis and symblepharon formation can result in severe socket contracture which is difficult to manage.

    References:1) Complex socket deformities, Stephen Bosniak, Page

    no: 97-1422) Ophthalmology monographs, AAO, Surgery or eyelid

    orbit and lacrimal system, vol 3, page no: 128-1323) Smiths Ophthalmic plastic and reconstructive sur-

    gery, page no: 1114- 11204) Color atlas and text of Ocular plastic surgery, page no:

    275- 2975) Repair and reconstruction in the orbital region, by

    J.C.Mustarde. Page no: 335-340 l

    Fig4

    Preserveconjunctivaasfaraspossible Limitedfornicialdissection CorrectEOMplacementtopreventfornicialshortening Placementofconformerpostoperativelyforlongerduration Useofimplants Properfittingofprosthesis

    Precautions to prevent Contracted Socket

    Fig5

    Dr. Kunal Kumar,FMRF-(Orbit,Oculoplasty&ReconstructiveSurgery)SankaraNetralaya.,ChennaiiscurrentlyworkingasOrbit&OculoplasticsurgeonintheAlSalamagroupofEyeHospitalsCalicut&Perinthalmanna

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    Dr Dolly Nazia P.M., MD (Ophthalmology), FICO

    PhakicIntraocularLens

    Phakic intraocular lenses are intraocular lenses im-planted in eyes with normal crystalline lens for re-fractive correction. The history of PIOL dates back to 1953 when Italian surgeon Benedetto Strampelli success-fully implanted a PIOL in the anterior chamber for correc-tion of myopia. But PIOL fell into disrepute because of in-creased incidence of post operative complications, lack of microsurgical devices and poor understanding of endothe-lial functions.

    Even though laser vision correction is simpler and easily accepted by patients, it yields less than satisfactory results in case of patients with high myopia (>10 D).These patients, albeit being 2% of myopic population, constitutes 13 15% of patients presenting for refractive surgery. LASIK in such patients may result in significant residual error, loss of best spectacle corrected visual acuity, induction of iatrogenic keratectasia, higher order aberrations and tear film abnor-malities. In recent years, phakic intraocular lens (PIOL ) has emerged as a reliable and predictable alternative to laser refractive correction, in higher grades of refractive error.

    Indications for PIOLl Myopia > - 12Dl Hyperopia >+4Dl Corneal thickness < 480 micronsl Residual bed thickness after LASIK likely to be < 280 micronsl Topography suggestive of keratoconus

    Types of phakic IOLsDepending on site of insertion they are of 3 types (fig. 1, 2, 3)

    Angle supported PIOLFirst generation PIOL.eg- Baikoff, NUVITA. Foldable eg- Vi-varte( Ciba), and Acrysof (Alcon).

    Iris supported anterior chamber PIOLAlso called iris clip lens ; fixate the IOL to mid peripheral iris by enclavation of loop tips, to produce a pillar of iris tissue over most peripheral part of haptics. The size of this type of PIOL is not dependent on the eye dimension one size fits all. Eg : Artisan (Ophtec) and Verisyse (AMO)

    Posterior chamber PIOL: (figure4a,figure4b)

    Figure1AnglesupportedPIOL1

    STAAR Implantable contact lens (ICL) available in India. It is made of highly biocom-patible silicone collagen co-polymer called collamer. It is available in powers from -2 to -20D and +3 to +17 D. Toric version available with myopic powers can correct up to 6D of astigmatism.

    CIBA Vision Phakic refractive lens (PRL) made of ultra thin hydrophobic silicone. it has no anatomical fixation site and floats on layer of aqueous humor in posterior chamber.

    IOLTECH Sticklens: made of hydrophilic acrylic material, which sticks to anterior surface of crystalline lens.

    Pre requisites for PIOLl Age >18 years, refractive status stable for at least 1yearl Endothelial count >2000/ sq mml Anterior chamber depth >3mml Angle width >30 degreel Pupil smaller than 6mm in scotopic luminancel No refractive eye pathology l No systemic pathologyl 2 Fully patent Nd : YAG laser iridotomies made 1 to2

    weeks before surgery

    ContraindicationsPreexisting intraocular disease such as a compromised cor-neal endothelium, iritis, significant iris abnormality, rube-osis iridis, cataract

    Power calculation for PIOLThree essential parameters for PIOL power calculation arel Spectacle power at vertex distance of 12mml Anterior chamber depthl Horizontal and vertical radii of curvature of corneaThe measures are sent to the manufacturer and exact IOL power is calculated using specific software and normo-

    Figure2IrissupportedPIOL

    Figure3SulcussupportedPIOL

  • AIO Journal of Ophthalmology 29

    PHaKIc Iol

    grams (figure 5).For iris clip lens the Vander Heijde formula is used, and

    for ICL and PRL, Olson Feingold and Holladay Refractive formulae respectively are used.

    Clinical Examination: l Uncorrected visual acuityl Manifest and cycloplegic refractionl Spectacle and/ contact lens corrected visual acuityl Slit lamp examination of anterior segment and adnexal Intra ocular pressurel Pupil size under scotopic conditionsl Biometry to calculate the axial length and anterior

    chamber depthl White to white corneal diameter in case of angle sup-

    ported and posterior chamber PIOLl It is measured with calipers under a microscope and

    verified with an orbscan to obtain appropriate size of lens. Sizing is important to ensure appropriate vault and separation between back of PIOL and the anterior capsule.

    l Keratometry and VKG - Fundus examination by indi-rect ophthalmoscopy

    l Field charting

    Surgical procedure for insertion of posterior chamber PIOL(figure 6)Surgery is done under topical or peribulbar anesthesia with the pupil fully dilated and preferably through a temporal clear corneal or near limbal incision. The loading of these lenses has to be precise and there are markers (different for spherical and toric versions; current PRL has 2 tiny dots on the haptics to avoid inverted implantation) to indicate and assist in proper placement of lens. Low molecular weight viscoelastics are recommended for both loading of lens and during surgical procedure.

    The ICL / PRL is injected through a less than 2.5mm in-cision. Smooth and gentle retro positioning of footplates involves maneuvering the haptics through 1 mm side ports with sandblasted visco cannula or specifically designed

    STAARPIOLinsituFig4a:onslitlamp

    tuckers. Bimanual irrigation aspiration is then done to re-move the viscoelastic agent.

    Post operative complicationsAngle supported PIOL: progressive pupillary distortion, UGH syndrome, corneal decompensation.

    Iris supported anterior chamber PIOL: anterior chamber inflammation, glaucoma, iris atrophy on fixation sites, IOL decentration, dislocation, endothelial cell loss.

    Posterior chamber PIOL: inverted implantation el-evated IOP, cataractogenesis, endothelial cell damage, de-centration, inflammation and pigment dispersal.

    Advantages of PIOL:l Additive procedure, not subtractive as in LASIKl Preservation of corneal sphericityl Preservation of accommodation (versus refractive lens

    exchange)l Rapid visual recovery and stable post operative refrac-

    tionl Excellent refractive accuracy even with significant

    astigmatisml Optical advantage of PIOL placed much closer to

    nodal point of eye; hence the effective optical zone of PIOL is 1.25 times on corneal surface

    l No initial investment on costly equipmentl Technique can be comfortably incorporated into prac-

    tice by good anterior segment surgeon

    Disadvantages of PIOLl It is an intra ocular surgery. Even though very low,

    chances of endophthalmitis and retinal detachment are present.

    l Steep learning curve is present. Surgical dexterity is essential as the intra ocular surgical maneuvering has to be performed in the 3 mm space between corneal endothelium and anterior lens capsule.

    l Cost of imported phakic intra ocular lens is high.l Long term data on performance of PIOL is sparse.

    Recent Literaturek Meta-analysis of randomized controlled trials compar-ing excimer laser and phakic intraocular lenses for myopia be-tween 6.0 and 20.0 diopters.Barsam A, Allan BD. Cornea. 2012 Apr;31(4):454-61.

    ResultsThis review included 3 RCTs with a total of 228 eyes. The range of myopia was 6.0 to 20.0 D with up to 4.0 D of astig-matism. The PIOL group was less likely to lose 2 or more

    Fig4bScheimpflugphotography

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    Figure5:softwareforpowercalculationofsulcusfixatedPIOL

    lines of best spectacle-corrected visual acuity at 12 months (odds ratio, 0.35; 95% confidence interval, 0.19-0.66, P = 0.001). PIOL surgery scored more highly on patient satisfac-tion/preference questionnaires.

    ConclusionsThe results of this systematic review show that PIOLs are safer within 1 year of follow-up compared with excimer laser surgical correction for myopia between 6 and 20 D. There is weaker evidence for superior visual quality in PIOL recipients. Further RCTs adequately powered for subgroup analysis with long-term follow-up are necessary to establish the ideal myopic range for excimer laser & PIOL treatments.

    k (Foldable iris-fixated phakic intraocular lens vs femtosec-ond laser-assisted LASIK for myopia between -6.00 and -9.00 diopters. Albarrn-Diego C, Muoz G et al. J Refract Surg. 2012 Jun;28(6):380-6.)

    MethodsForty-six myopic patients were randomized to undergo bi-lateral Artiflex (Ophtec BV) PIOL implantation or bilateral femtosecond laser-assisted conventional LASIK with the VISX S2 (Abbott Medical Optics). Refraction, uncorrected (UDVA) and corrected (CDVA) distance visual acuity, con-trast sensitivity, corneal endothelial cell count, rate of re-

    treatment, and complications were compared.

    ResultsTwelve months after surgery, no statistically significant differences were noted in spherical equivalent refrac-

    tion (P=.19) or UDVA (P=.28), whereas CDVA was better in the PIOL group (P.99). The percentage of eyes gaining lines of CDVA was significantly higher in the PIOL group (50.0% vs 8.7%; P

  • AIO Journal of Ophthalmology 31

    cuTTIng edge oPHTHalmology

    Dr. Priya Nambiar, M.S., D.O., FICO

    RefractiveLenticuleExtraction(Relex)

    From a humble beginning more than half a century ago, refractive surgery has witnessed a technology explosion with an exciting array of microkeratomes ,excimer lasers, femtosecond lasers and a wide variety of procedures to choose from. ReLEx is an exciting new procedure in the refractive surgical armamentarium that holds the potential to herald a paradigm shift for the fu-ture of refractive surgery, since it addresses most of the risks and variables related to the microkeratome blade and excimer laser.

    BackgroundLamellar refractive surgery was developed from the con-cepts and work of Dr.Jose Barraquer in the 1950s. In the 1980s, microkeratome was developed and in 1982, Trokel and coworkers suggested the use of excimer laser for cor-neal reprofiling. Pallikaris described the use of automated microkeratome to make a hinged corneal flap followed by excimer laser ablation and called it LASIK. The last decade has witnessed many advancements and refinements in microkeratomes and excimer lasers leading to significant improvement in clinical outcomes. Later on, femtosecond laser technology was developed and LASIK with femtosec-ond flaps became popular.

    ReLEx is an all femtosecond laser vision correction, utilizing it for the creation and extraction of a refractive lenticule from the corneal stroma so that the radius of cur-vature of the tear film- anterior corneal interface is altered as