Hyperopia and Presbyopia

Hyperopia and Presbyopia edited by

Kazuo Tsubota Tokyo Dental College Ichikawa City, Chiba, Japan

Bn'an S. Boxer Wachler Boxer Wachler Vision Institute Beverly Hills, California, U.S.A.

Dimitri T. Azar Massachusetts Eye and Ear Infirmary Schepens Eye Research Institute and Harvard Medical School Boston, Massachusetts, U.S.A.

Douglas D. Koch Cullen Eye Institute Baylor College of Medicine Houston, Texas, U.S.A.

» DEKKER

MARCEL DEKKER, INC.

NEW YORK • BASEL

Although great care has been taken to provide accurate and current information, neither the author(s) nor the publisher, nor anyone else associated with this publication, shall be liable for any loss, damage, or liability directly or indirectly caused or alleged to be caused by this book. The material contained herein is not intended to provide specific advice or recommendations for any specific situation. Trademark notice: Product or corporate names may be trademarks or registered trademarks and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data A catalog record for this book is available from the Library of Congress. ISBN: 0–8247–4107–2 This book is printed on acid-free paper. Headquarters Marcel Dekker, Inc. 270 Madison Avenue, New York, NY 10016, U.S.A. tel: 212–696–9000; fax: 212–685–4540 Distribution and Customer Service Marcel Dekker, Inc. Cimarron Road, Monticello, New York 12701, U.S.A. tel: 800–228–1160; fax: 845–796–1772 Eastern Hemisphere Distribution Marcel Dekker AG Hutgasse 4, Postfach 812, CH–4001 Basel, Switzerland tel: 41–61–260–6300; fax: 41–61–260–6333 World Wide Web http://www.dekker.com The publisher offers discounts on this book when ordered in bulk quantities. For more information, write to Special Sales/Professional Marketing at the headquarters address above. Copyright  2003 by Marcel Dekker, Inc. All Rights Reserved. Neither this book nor any part may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, microfilming, and recording, or by any information storage and retrieval system, without permission in writing from the publisher. Current printing (last digit): 10 9 8 7 6 5 4 3 2 1 PRINTED IN THE UNITED STATES OF AMERICA

REFRACTIVE SURGERY

Series Editors

Dimitri T. Azar, M.D. Massachusetts Eye and Ear Infirmary Schepens Eye Research Institute and Harvard Medical School Boston, Massachusetts

Douglas D. Koch, M.D. Cullen Eye Institute Baylor College of Medicine Houston, Texas

1. LASIK: Fundamentals, Surgical Techniques, and Complications, edited by Dimitri T. Azar and Douglas D. Koch 2. Hyperopia and Presbyopia, edited by Kazuo Tsubota, Brian S. Boxer Wachler, Dimitri T. Azar, and Douglas D. Koch

ADDITIONAL VOLUMES IN PREPARATION

Preface

Heil dir, Sonne! Heil dir, Licht! With the explosion of refractive surgical technologies and techniques we have witnessed increased success in the treatment of hyperopia, but we still stand restrained in our ability to free our patients from presbyopic spectacles. We eagerly await the moment of overcoming the seemingly insurmountable obstacles of presbyopic correction to echo Bru¨nhilde’s greetings of the sun and of the light in the third act of Wagner’s opera Siegfried, at the time of her resurrection after decades of slumber: Long was my sleep. Who is the hero who awakened me? Siegfried forged “Nothung,” the famous sword that could be forged only by a man who did not know fear, and used it to slay the dragon Fafner (and recover the magical Ring and Tarnhelm). He defied the gods and entered Loge’s impenetrable circle of flames to rescue the sleeping Bru¨nhilde. We are on the verge of facing a similar success story in refractive surgery. Many unsung heroes are paving the way for the next discovery that will change the way we treat hyperopia and revolutionize the surgical correction of presbyopia. The wide range of investigations covered in this book indicates that it will not be long before we will be able to fulfill our quest to conquer these two frontiers in refractive surgery. This book is the second of a series of books dedicated to refractive surgery published by Marcel Dekker, Inc. The focus of the first volume in this series was LASIK fundamentals, surgical techniques, and complications, a topic that has received a lot of coverage in both the peer- and non-peer-reviewed literature. For this book, we asked Drs. Tsubota iii

iv

Preface

and Boxer Wachler to edit the manuscripts, and they have worked diligently with the contributors to ensure maximal coverage and minimal redundancy. It may come as no surprise to the reader that the methods of treatment of hyperopia and presbyopia are grouped in a single refractive surgical textbook. The classical teachings of physiological optics separate these two areas, but many of the surgical techniques employed for the correction of hyperopia may have applications for presbyopia. The introductory section is written by experts in the fields of basic optics, mechanisms of accommodation, aging of the lens, and contact lens basics. Among topics discussed in the section on hyperopia are LASIK and PRK for hyperopia and hyperopic astigmatism, laser thermokeratoplasty, conductive keratoplasty, hyperopic intracorneal segments, phakic IOLs. The section on presbyopia includes discussions of monovision refractive surgery, multifocal corneal approach, scleral relaxation, scleral expansion bands, multifocal IOLs, refractive lens exchange with a multifocal intraocular lens, Phaco-Erstaz, and accommodating and adjustable IOLs. The topographical changes, corneal surface profiles, wavefront contrast sensitivity changes, and wound healing after hyperopic surgery are discussed in a separate section with special emphasis on clinical applications. The contributors draw on first-hand experiences with the aim of providing an engaging book covering these important topics. We are indebted to the coeditors, students, residents, and colleagues who have made valuable contributions to this book. We are grateful for their effort in integrating the sometimes limited information in peer-reviewed literature with the knowledge derived from their clinical experiences and interactions with colleagues. We hope that this provides a text that is both clinically relevant and as evidence-based as possible. We thank Dr. Geoffrey Greenwood and Elizabeth Curione of Marcel Dekker, Inc., for their commitment to this project. Special thanks go to Leona Greenhill, for her editorial assistance, and to Rhonda Harris, who managed this project with care and precision. Her attention to detail and her dedication have enabled us to work coherently in the face of adversity. We take the opportunity to acknowledge the pioneering surgeons and researchers in the field of refractive surgery. Their work and vision have provided the basis not only for current advances in hyperopia and presbyopia that we can offer to our patients, but also for future advances to be made by the next generation of thoughtful contributors to this important field. Dimitri T. Azar Douglas D. Koch

Contents

Preface Contributors

1. Introduction Kazuo Tsubota

iii ix

1

2. Basic Optics of Hyperopia and Presbyopia Michael K. Smolek and Stephen D. Klyce

17

3. The Helmholtz Mechanism of Accommodation Adrian Glasser

27

4. Schachar’s Theory of the Mechanisms of Accommodation Jay S. Pepose and Moonyoung S. Chung

47

5. Aging and the Crystalline Lens: Review of Recent Literature (1998–2001) Leo T. Chylack, Jr.

55

6. Hyperopia Ivo John Dualan and Penny A. Asbell

63 v

vi

Contents

7. Surgical Treatment Options for Hyperopia and Hyperopic Astigmatism Paolo Vinciguerra and Fabrizio I. Camesasca

69

8. Laser Thermokeratoplasty and Wavefront-Guided LTK Shahzad I. Mian and Dimitri T. Azar

83

9. Conductive Keratoplasty for the Correction of Low to Moderate Hyperopia Marguerite B. McDonald, Jonathan Davidorf, Robert K. Maloney, Edward E. Manche, Peter Hersh, and George M. Salib

95

10. Intracorneal Segments for Hyperopia Laura Gomez and Arturo S. Chayet

107

11. Anterior Chamber Phakic Intraocular Lenses in Hyperopia Georges Baı¨koff

115

12. Hyperopic Phakic Intraocular Lenses Thanh Hoang-Xuan and Franc¸ois Malecaze

119

13. Hyperopia and Presbyopia: Topographical Changes Stephen D. Klyce, Michael K. Smolek, Michael J. Endl, Vasavi Malineni, Michael S. Insler, and Marguerite B. McDonald

129

14. Corneal Surface Profile After Hyperopia Surgery Damien Gatinel

141

15. Wavefront Changes After Hyperopia Surgery Maria Regina Chalita and Ronald R. Krueger

151

16. Contrast Sensitivity Changers After Hyperopia Surgery Lavinia C. Coban-Steflea, Tommy S. Korn, and Brian S. Boxer Wachler

163

17. Wound Healing After Hyperopic Corneal Surgery: Why There Is Greater Regression in the Treatment of Hyperopia Renato Ambro´sio, Jr., and Steven E. Wilson

173

18. Monovision Refractive Surgery for Presbyopia Dimitri T. Azar, Margaret Chang, Carolyn E. Kloek, Samiah Zafar, Kimberly Sippel, and Sandeep Jain

189

19. Multifocal Corneal Approach to Treat Presbyopia Janie Ho and Dimitri T. Azar

201

20. Scleral Relaxation to Treat Presbyopia Hideharu Fukasaku

209

21. The Scleral Expansion Procedure Chris B. Phillips and Richard W. Yee

219

Contents

vii

22. Multifocal IOLs for Presbyopia Hiroko Bissen-Miyajima

237

23. Refractive Lens Exchange with a Multifocal Intraocular Lens I. Howard Fine, Richard S. Hoffman, and Mark Packer

249

24. The Limits of Simultaneous Ametropia Correction in Phaco-Ersatz Arthur Ho, Fabrice Manns, Viviana Fernandez, Paul Erikson, and Jean-Marie Parel

259

25. Accommodating and Adjustable IOLs Sandeep Jain, Dimitri T. Azar, and Rasik B. Vajpayee

279

26. Accommodative Amplitude Measurements After Surgery for Presbyopia David L. Guyton

287

27. Complications of Hyperopia and Presbyopia Surgery Liane Clamen Glazer and Dimitri T. Azar

291

28. Future Developments Brian S. Boxer Wachler

315

Index

319

Contributors

Renato Ambro´sio, Jr., M.D. Department of Ophthalmology, University of Washington, Seattle, Washington, U.S.A., University of Sa˜o Paolo, Sa˜o Paolo, and Department of Cornea and Refractive Surgery, Clinica e Microcirurgia Oftalmolo´gica Renato Ambro´sio, Rio de Janeiro, Brazil Penny A. Asbell, M.D. Mount Sinai Medical Center, New York, New York, U.S.A. Dimitri T. Azar, M.D. Corneal and Refractive Surgery Services, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A. Georges Baı¨koff, M.D. Clinique Montecelli, Marseille, France Hiroko Bissen-Miyajima, M.D., Ph.D. Department of Ophthalmology, Tokyo Dental College, Suidobash Hospital, Tokyo, Japan Brian S. Boxer Wachler, M.D. nia, U.S.A. Fabrizio I. Camesasca, M.D. tas, Milan, Italy

Boxer Wachler Vision Institute, Beverly Hills, Califor-

Department of Ophthalmology, Istituto Clinico Humani-

Maria Regina Chalita, M.D. Department of Refractive Surgery, Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A. ix

x

Contributors

Margaret Chang, M.S. Corneal and Refractive Surgery Services, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A. Arturo S. Chayet, M.D. Codet Aris Vision Institute, Tijuana, B.C., Mexico Moonyoung S. Chung, M.D.

Pepose Vision Institute, Chesterfield, Missouri, U.S.A.

Leo T. Chylack, Jr., M.D. Department of Ophthalmology, Harvard Medical School and Center for Ophthalmic Research, Brigham and Women’s Hospital, Boston, Massachusetts, U.S.A. Lavinia C. Coban-Steflea, M.D. Department of Ophthalmology, Bucharest University Hospital, and Carol Davila University of Medicine and Pharmacy, Bucharest, Romania Jonathan Davidorf, M.D. Davidorf Eye Group, West Hills, and Maloney Vision Institute, Los Angeles, California, U.S.A. Ivo John Dualan, M.D. Mount Sinai Medical Center, New York, New York, U.S.A. Michael J. Endl, M.D. Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A. Paul Erickson, O.D., Ph.D. Cooperative Research Centre for Eye Research and Technology, The University of New South Wales, Sydney, New South Wales, Australia Viviana Fernandez, M.D. Ophthalmic Biophysics Center, Bascom Palmer Eye Institute, University of Miami Medical School, Miami, Florida, U.S.A. I. Howard Fine, M.D. Department of Ophthalmology, Casey Eye Institute, Oregon Health and Science University, Portland, Oregon, U.S.A. Hideharu Fukasaku, M.D.

Fukasaku Eye Centre, Yokohama, Japan

Damien Gatinel, M.D. Fondation Ophthalomogique Adolphe de Rothschild and Bichat Claude Bernard Hospital, Paris, France Adrian Glasser, Ph.D. College of Optometry, University of Houston, Houston, Texas, U.S.A. Liane Clamen Glazer, M.D. Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A. Laura Gomez, M.D. Codet Aris Vision Institute, Tijuana, B.C., Mexico David L. Guyton, M.D. Department of Ophthalmology, The Wilmer Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A.

Contributors

xi

Peter Hersh, M.D. Cornea and Laser Vision Center, Teaneck, New Jersey, U.S.A. Arthur Ho, M.Optom., Ph.D. Cooperative Research Centre for Eye Research and Technology, The University of New South Wales, Sydney, New South Wales, Australia Janie Ho, M.D. Department of Ophthalmology, University of California at San Francisco, San Francisco, California, U.S.A. Thanh Hoang-Xuan, M.D. Fondation Ophthalomogique Adolphe de Rothschild and Paris University, Paris, France Richard S. Hoffman, M.D. Department of Ophthalmology, Casey Eye Institute, Oregon Health and Science University, Portland, Oregon, U.S.A. Michael S. Insler, M.D. Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A. Sandeep Jain, M.D. Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical Schoool, Boston, Massachusetts, U.S.A. Carolyn E. Kloek, B.A. Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A. Stephen D. Klyce, Ph.D. Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A. Tommy S. Korn, M.D. University of California–San Diego, and Sharp Rees-Stealy Medical Group, San Diego, California, U.S.A. Ronald R. Krueger, M.D. Department of Refractive Surgery, Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A. Franc¸ois Malecaze, M.D. Hoˆpital Purpan, Toulouse, France Vasavi Malineni, M.D. Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A. Robert K. Maloney, M.D. Maloney Vision Institute, Los Angeles, California, U.S.A. Edward E. Manche, M.D. Stanford University School of Medicine, Palo Alto, California, U.S.A. Fabrice Manns, Ph.D. Ophthalmic Biophysics Center, Bascom Palmer Eye Institute, University of Miami Medical School, Miami, and Department of Biomedical Engineering, University of Miami College of Engineering, Coral Gables, Florida, U.S.A.

xii

Contributors

Marguerite B. McDonald, M.D. Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A. Shahzad I. Mian, M.D. Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A. Mark Packer, M.D. Department of Ophthalmology, Casey Eye Institute, Oregon Health and Science University, Portland, Oregon, U.S.A. Jean-Marie Parel, Ph.D. Ophthalmic Biophysics Center, Bascom Palmer Eye Institute, University of Miami Medical School, Miami, Department of Biomedical Engineering, University of Miami College of Engineering, Coral Gables, Florida, U.S.A., and University of Liege, CHU Sart-Tilman, Liege, Belgium Jay S. Pepose, M.D., Ph.D. Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, and Pepose Vision Institute, Chesterfield, Missouri, U.S.A. Chris B. Phillips, M.D. Department of Ophthalmology, Hermann Eye Center and University of Texas Health Science Center at Houston Medical School, Houston, Texas, U.S.A. George M. Salib, M.S., M.D. Department of Ophthalmology, Tulane University School of Medicine, New Orleans, Louisiana, U.S.A. Kimberly Sippel, M.D. Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A. Michael K. Smolek, Ph.D. Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A. Kazuo Tsubota, M.D. Department of Ophthalmology, Tokyo Dental College, Ichikawa City, Chiba, Japan Rasik B. Vajpayee, M.D. Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A. Paolo Vinciguerra, M.D. Milan, Italy

Department of Ophthalmology, Istituto Clinico Humanitas,

Steven E. Wilson, M.D. Department of Ophthalmology, University of Washington, Seattle, Washington, U.S.A.

Contributors

xiii

Richard W. Yee, M.D. Department of Ophthalmology, Hermann Eye Center and University of Texas Health Science Center at Houston Medical School, Houston, Texas, U.S.A. Samiah Zafar, M.B.B.S. Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A.

1 Introduction KAZUO TSUBOTA Tokyo Dental College, Ichikawa City, Chiba, Japan

SUMMARY A new era of refractive surgery is on the horizon in the field of hyperopia and presbyopia correction. Corneal intervention, corneal implants, corneal rings, intraocular lenses, and scleral intervention are the major treatment strategies. Although this field is new and some of the novel surgeries may not endure into the future, this book covers all of the clinical and basic research activities available as of the year 2003.

A. OVERVIEW Refractive surgery is currently evolving toward a new stage. Although high myopia and irregular astigmatism cannot be corrected fully, laser-assisted in situ keratomileusis (LASIK) for myopia and myopic astigmatism has already become an established technology, with millions of patients benefiting from LASIK every year all over the world. The next challenge will be the correction of hyperopia and presbyopia. In most advanced countries, life spans have been increasing annually and have now passed the 80-year mark. Baby boomers in the United States, Japan, Europe, and other countries are getting older, with an expected mean age of 50 to 60 years by the year 2005. Although the ratio of hyperopia cases is lower at younger ages, hyperopia becomes increasingly significant in the later stages of life. It has been estimated that around 20% of the U.S. population are hyperopic at the age of 40, and the rate is above 60% at age 65. Even in Japan, where myopia is the dominant refractive error, the ratio increases from 15% at age 40 to 30% at age 65. People may develop cataracts, possibly indicating phacoemulsification and intraocular lens implantation, but the majority of the elderly still do not have cataract 1

2

Tsubota

Table 1 Medical and Surgical Correction of Hyperopia Medical correction Glasses Contact lenses

Surgical correction Photorefractive keratectomy (PRK) or laserassisted in situ keratomileusis (LASIK) Phakic intraocular lenses (IOLs) Clear lens extraction with IOLs Laser thermal keratoplasty (LTK) Conductive keratoplasty (CK) Diode laser keratoplasty Corneal implant Intracorneal ring (ICR) modification

surgery. It is well known that nearly everyone develops presbyopia with age. Thus, in an aging society, correction of hyperopia and presbyopia is anticipated to become more important than it currently is. This book covers the current medical and surgical treatments for the correction of hyperopia and presbyopia. An effort is also made to cover new technologies, although these are still preliminary and controversial. In this sense, this is no ordinary textbook based only on authority and established principles. Rather, it is a new comprehensive information book introducing current technology and developmental trials. The emerging innovation of thermal or conductive keratoplasty as well as corneal implants for hyperopic correction now provide exciting potential. Furthermore, the new Schachar theory of presbyopia is now attracting attention as a strategy for the treatment of presbyopia. Scleral relaxation, using a diamond knife or laser, and scleral expansion rings are also potential technologies. All of the established as well as the new medical and surgical treatments are described in this book, with the relevant theoretical backgrounds, clinical results, and possible complications indicated (Tables 1 and 2, Figs. 1 and 2).

Table 2 Medical and Surgical Correction of Presbyopia Medical correction Bifocal and multifocal glasses Bifocal and multifocal HCL Bifocal and multifocal SCL Bifocal disposable SCL

Surgical correction Monovision by LASIK Multifocal LASIK IOL with multifocal Hinged IOL Scleral expansion ring Scleral incision Scleral relaxation by laser Small-diameter corneal lens

Key: HCL, hard contact lens; SCL, soft contact lens; LASIK, laser-assisted in situ keratomileusis; IOL, intraocular lens.

Introduction

Figure 1 Surgical correction of hyperopia.

Figure 2 Surgical correction of presbyopia.

3

4

Tsubota

B. HISTORY OF MEDICAL AND SURGICAL CORRECTION OF HYPEROPIA The most commonly used corrective devices for hyperopia are glasses and contact lenses. Since surgical correction is still in its preliminary stages, most patients around the world still use glasses or contact lenses. Before discussing the current technology, let us broadly review some older ideas. In the history of surgical correction, there have been several methods that are no longer popular. One technology was keratomileusis as originally proposed by Jose Barraquer in Colombia (1–3). He developed a technique in which a central lamellar keratectomy is performed and a resected disk is shaped using a Barraquer cryolathe (4). The shaped disk is then sutured in place. For hyperopic correction, more tissue is removed from the periphery of the disk, producing a steepening of the central portion of the cornea (5,6). In order to minimize the complexity of the procedure, a donor disk is also used. This is called keratophakia. The corneal lenticule is obtained from a donor cornea, frozen, and shaped with a cryolathe into a refractive disk with central thickness (2). A lamellar flap is made on the host cornea, the disk is inserted intrastromally, and the lamellar cut is replaced. Kaufman and Werblin further developed this technique of epikeratoplasty (7,8). Donor corneal tissue is prelathed into the proper shape and sutured onto a recipient, de-epithelialized cornea in which Bowman’s layer and the stroma are intact. This technique is described by the term living contact lens. The change in curvature of the anterior surface produced by the lenticule provides the refractive correction. First, the corneal epithelium of the host cornea is removed and an annular keratectomy is performed. A partial lamellar dissection peripheral to the trephine is used as a groove for lenticule suturing. Interrupted and running 10–0 nylon sutures are used to secure the tissue and are removed 10 weeks later (Figs. 3 and 4). This technique was originally developed for aphakia and keratoconus (7,9). The results were slightly disappointing relative to predictions, and the technique was abandoned. (10) Hexagonal keratotomy is another refractive procedure formerly employed for hyperopia. The procedure consists of making a series of paracentral incisions in a hexagonal pattern with subsequent steepening of the central cornea (11). This curvature change is due to weakening of the central cornea, which has been incised and separated from the peripheral cornea, resulting in bulging of the center due to intraocular pressure. The initial results seemed promising, but this procedure was later found to frequently be associated with glare, photophobia, fluctuating vision, and irregular astigmatism (12). Thus, this

Figure 3 Diagram of epikeratophakia. Donor corneal lens is placed on the Bowman’s layer with stromal pockets sutured with 10–0 nylon.

Introduction

5

Figure 4 Photograph of epikeratophakia. Note the corneal lens on the top of the cornea.

technique was abandoned. Predictability was not adequate, such that the procedure did not gain popularity. In the specific situation of postoperative hyperopia after radial keratotomy, suturing of the corneal incision is useful for the correction of hyperopia up to 2 diopters. It is believed to stabilize refractive status, thus minimizing corneal shape fluctuation (13,14). Automated lamellar keratoplasty is another method for the correction of hyperopia. Historically, the idea for this also came from keratomileusis. Steepening of the central cornea was observed to occur with lamellar keratotomy alone. Recently, ectasia of the cornea after myopic LASIK has become a major long-term safety concern. Progressive ectasia in a significant percentage of eyes, another major concern, also renders this technique unattractive. When the cut is deep, more ectasia unavoidably occurs with this procedure. The amount of ectasia depends on the optical zone. When the optical zone is small, the curvature is relatively high. When the optical zone is large, the curvature is low. The nomogram was developed on the basis of this observation (15,16). When the optical zone is 6.6 mm, the correction is 1.0 D; whereas the correction is 6.5 D with an optical zone of 5.0 mm. The cut should be deep—e.g., 65%. The initial results were promising, but the nomogram is not always predictable. With the development of hyperopic LASIK, use of this procedure is now limited (17). The mechanical corneal contouring device invented by Eiferman and Nordquist is another means of correcting hyperopia (18). The principle is based on the observation that when the peripheral cornea is flattened, the central optical power is increased. The instrument consists of a vacuum chamber and steel blades positioned at orthogonal angles. When a Teflon stopper is added to the blade and the stopper pressed down on the eye, the peripheral cornea bulges, such that the blades can remove more tissue in the periphery than at the central cornea. The clinical results remain unknown. C. CURRENT SURGICAL CORRECTION OF HYPEROPIA Photorefractive keratectomy (PRK) for hyperopia is useful for the correction of hyperopia up to Ⳮ3.0 to 4.0 D; however, healing of the corneal epithelium has effects on the final

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result, such as regression and/or haze (19–23). Predictability is still poor for moderate to high myopia. LASIK, which was originally developed for the correction of myopia (24–26), is considered theoretically to be more advantageous for the correction of hyperopia because it is possible to ablate the corneal midperiphery by stromal photorefractive ablation and to prevent strong epithelial regression with an overlying flap (27–29). With the expansion of optical zone treatment, LASIK has now become an acceptable treatment for hyperopia of up to 5 D (30–36). This method is fully discussed in Chapters 7, 13–15. The Phakic IOL has also been used for the correction of hyperopia as well as for aphakia and high myopia (37–40). The use of posterior chamber phakic IOL, such as the Staar Collamer implantable contact lens (Staar Surgical, AG, Nidau, Switzerland) appears to be promising, although there is a risk of cataract formation. The recent development of very light floating lenses, such as the Medennium (Ciba Vision, Duluth, GA), may be another innovation. The lens is very light, almost floating, and does not touch the patient’s own lens. Iris-claw lenses in phakic eyes, to correct hyperopia, are also promising (Fig. 5), despite the risks of glaucoma and corneal degeneration. Very thin anterior chamber phakic IOLs, angle support lenses such as Nuvita (Bausch & Lomb Surgical, Rochester, NY), and new foldable lenses designed by Baı¨koff (fully discussed in Chapter 11) are other promising technologies. These are discussed in detail in Chapters 11 and 12. Clear lens extraction can produce cystoid macular edema and retinal detachment and is less accurate and predictable for hyperopia below Ⳮ 3.0 D (41,42). Reshaping the corneal curvature by heating of the peripheral cornea is another major approach for hyperopic correction. Currently, there are three ways to do this. One is laser thermal keratoplasty (LTK) (43–46). This employs a holmium laser technique, called the Sunrise LTK Procedure (Sunrise Technologies International, Inc. Fremont, CA), to heat the corneal collagen in several spots in the periphery. The resulting thermal contraction steepens the central corneal curvature, thus correcting hyperopia. This procedure has received approval from the U.S. Food and Drug Administration (FDA). The treatment range will be up to 2.5 D. The second method is conductive keratoplasty (CK) (Refractec, Inc,

Figure 5 Artisan hyperopia 5 mm, phakic intraocular lens (IOL) for the correction of hyperopia. (Figure provided courtesy of OPHTEC BV, Groningen, The Netherlands.)

Introduction

7

Figure 6 Conductive keratoplasty for the correction of hyperopia. (Figure provided courtesy of Refractec, Inc., Irvine, CA, USA.)

Irvine, CA) (Fig. 6). This method uses a radiofrequency generator as the energy source instead of a holmium:YAG laser. The energy is delivered through a microtip inserted deep into the stroma. The procedure is considered to minimize regression relative to LTK because the energy is applied deep in the cornea, thereby creating an affected spot that is uniform in depth. The CK was approved by the FDA in April 2002. Diode laser treatment is a third approach (47–49). This procedure uses a 1.8-U diode laser as an energy source (Rodenstock, Munich, Germany). The application is similar to CK in that the probe is in contact with the peripheral cornea. The diode laser has not yet obtained FDA approval. All three technologies are described in detail in Chapters 8 and 9. The ICS娃 (Intrastromal Corneal Segments) or “Hyperopia Segments” is a variation of the INTACS威 Prescription Inserts (Addition Technology, Inc., Fremont, CA) under investigation in the United States, Europe, Brazil, Mexico, Singapore, and the U.K. While INTACS威 inserts correct for myopia by flattening the central portion of the cornea, the ICS is designed to correct hyperopia by steepening the anterior corneal curvature by the insertion of the ring materials at the limbal area, instead of inserting at the 7-mm central zone as for myopic correction. The ICS may also be used for hyperopia concurrent with astigmatism or hyperopic astigmatism. Clinical investigations have been initiated in both Mexico and Europe for the treatment of hyperopia using the ICS clinical product. The results are most encouraging, with stability achieved around the Month 3 exam and hyperopic corrections of up to 4.63 D (based MRSE) at Month 6 (n⳱43) and slightly less than 3.0 diopters of hyperopic correction (2.75 D) at the Month 12 exam. Manifest Refraction stability is demonstrated through the Month 12 time point. Clinical trials in Europe are ongoing. Corneal implants have long been an attractive idea, but lack of suitable materials has inhibited the development of this technology. New materials have again made it attractive. Historically, Barraquer, who inserted glass materials into the corneal stroma in animals, developed the intracorneal technique. There was always a loss of transparency, with vascularization and extrusion of lenses. It was not known at that time that nutrients such as

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amino acids and glucose come from the aqueous humor and that oxygen is supplied from the ambient air. The glass lens interfered with the exchange of these components through the corneal stroma. Then, fenestrated intracorneal polysulfone lenses were developed to enhance the exchange of metabolic components. However, opacification was associated with these fenestration techniques. This was a major obstacle to the implementation of this technology. The recent development of a small-diameter lens made of a hydrogel copolymer (Chiron Corporation, Emeryville, CA), with a water content of 45%, for correction of presbyopia, has paved a new pathway for this technology (53). Since the lens is small in diameter (1.8–2.2 mm), nutrient diffusion is not impaired (54). Lindstrom suggested the usefulness of this technology for a select group of patients (53). Anamed, Inc., recently developed novel biocompatible, clear, and permeable hydrogel materials with substantially higher permeability than typical hydrogels with similar water content. The refractive index of the material is essentially identical to that of corneal tissue (1.376 D), and has a water content exceeding 70%. The lens diameter ranges from 4.5 to 6.0 mm, depending on the diopter correction needed. The meniscus design includes a central thickness of 50 ␮m and an edge thickness of 20 ␮m. A preliminary animal study showing the safety and efficacy of this lens and a limited clinical trial were both performed by Dr. Stephen G. Slade, M.D., Director of the Laser Center of Houston, Texas. He reported that there was no haze formation except in one patient with minimal haze (Ⳮ1), which later resolved. No lines of best-corrected visual acuity were lost and the refractive correction was accurate. A flap is made with a microkeratome and the lens is placed in the center of the pupil. Since making a flap with a microkeratome is now a standard technique in refractive surgery, this technique is relatively simple for most surgeons currently performing LASIK. In LASIK, it is necessary for the correction of hyperopia to remove twice as much tissue as the same myopic diopter correction with certain regression, such that the intracorneal approach is reasonable. The FDA approved Phase I of the clinical trial for the PermaVision威 intracorneal lens, involving 10 eyes, which began in November 2001 (Fig. 7). An interim clinical analysis has been completed and submitted to the FDA, along with a

Figure 7 PermaVision intracorneal lens for the correction of hyperopia. (Figure provided courtesy of Anamed Inc., Lake Forest, CA, USA.)

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request to move into Phase II of the clinical protocol. As of November 2002, Anamed is awaiting FDA approval to begin Phase II. This is considered to be a promising technology. However, the long-term complications—such as corneal stromal and epithelial thinning as well as endothelial change—must be evaluated in terms of safety. D. CURRENT MEDICAL AND SURGICAL CORRECTION OF PRESBYOPIA The major means of correction are simple glasses or simple contact lenses (55). The development of bifocal glasses provided the first convenience, allowing the use of only one pair of glasses throughout the day. Bifocal contact lenses are another popular method for the correction of presbyopia (56). According to the 1999 contact lens spectrum reader profile survey, 21.5% were fit with monovision, 9% with soft multifocals, 3% with rigid gas permeable (RGP) multifocals, and 5% with single-vision contact lenses and reading glasses. The remainder had spectacles only. A major disadvantage of this method is compromised visual quality (57). Success depends on the patient having a realistic expectation. Monovision contact lenses are also used (58,59). The increasing prevalence of dry eye in the elderly might be an obstacle to the application of this technique for many patients. Since the introduction of disposable bifocal contact lenses (Vistakon’s Acuvue Contact Lenses, Jacksonville, FL) in 1999 (60), use of bifocal contact lenses for the correction of presbyopia has been increasing. With further development of materials and designs from companies such as Ciba Vision and Bausch & Lomb, Inc., bifocal contact lenses have apparently become the major corrective method for presbyopia. The intraocular lens with multifocal optics is another method for correcting presbyopia. This method is based on a theory termed “the simultaneous vision principle,” whereby separate images of near and distant objects are formed and, if the power difference between the two optical systems is more than 3.0 D, the images are dissimilar enough for the brain to interpret them as separate. The brain therefore selects the highly focused image and suppresses the other. This IOL can be achieved with two distinct optical elements (bifocal IOL) (61) or by means of diffractive optics (62), in which concentric diffractive zones are applied to the posterior surface of the implant in order to focus light from near objects. Both types of IOLs require central fixation and are relatively successful in younger patients. Monovision intraocular lenses are also the choice for presbyopic correction (61). The IOL with real accommodative power has long been studied by Japanese and other researchers. The gel technology reached a certain level, using monkey eyes, in which the lens capsule was filled with soft gel. However, clinical application has not yet begun. Recently, a hinged haptic accommodative lens was developed and has attracted considerable attention. The proper functioning of the lens is dependent on movement of the remaining lens capsule, contracted by the ciliary muscle. When the lens capsule expands, the lens changes position and focuses. There are now several companies working on this technology (Fig. 8). Like the multifocal intraocular lens, LASIK can also offer the multifocal effect by means of changing the corneal shape. It was first observed that regional variation in corneal curvature in the eyes of patients 45 years of age or older sometimes provides good near vision without correction (63). The regional variation in corneal power apparently explained how the multifocal lens effect could be achieved. Thus, intentional multifocal LASIK is a potential technology, which is still under investigation (64). Another practical method is monovision LASIK. Monovision is defined as providing optical correction of

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Figure 8 Finite-element computer simulation of accommodative intraocular lens (IOL), a flexible micro-optic with accommodative features. (Figure provided courtesy of Human Optics AG, Erlangen, Germany.)

one eye for distance vision and of the other eye for near vision. This is usually achieved with contact lenses or intraocular lenses after cataract extraction, but can be achieved by LASIK as well (65). The ideal diopter difference necessary for both distant and near vision has not yet been determined. Since most patients with presbyopia undergoing LASIK still have some accommodative ability, there are several components that should be evaluated and determined for mass application of LASIK monovision. This is fully discussed by Azar in Chapter 18. The concept of anterior ciliary sclerotomy (ACS) is a new challenge in the treatment of presbyopia (66). This surgery is based on the theory that the lens is ectodermal in origin and constantly grows throughout life, gradually filling the eye and leaving no space for accommodation (67,68). Loss of lens elasticity might contribute to the mechanism of presbyopia, and this theory raises the possibility that reduced space is the cause of the reduced accommodative power of the lens. Thus, somehow expanding the globe by ciliary sclerotomy can provide space for the ciliary body and lens for accommodation. Along this line, the original anterior sclerotomy as well as Fukasaku incisional surgeries have been developed (69). Since there is regression of the results due to wound healing, Fukasaku recently developed a method of inserting silicon plugs for the maintenance of the incision (69). Furthermore, the erbium:YAG laser has also been applied to making a wide scleral incision that may not heal quickly, thus maintaining the effect (Figs. 9 and 10). I have personal experience of two patients who had previously undergone LASIK. Both were Japanese males, aged 58 and 48 years. Both had 1.0 far vision without correction and near vision of 0.3 without correction, and both were having difficulty with reading. I applied the laser to a limbal-scleral area 4.0 mm in length. A total of 8 lasers were applied in a radial configuration. One day after surgery, both patients had 0.6 to 0.7 near

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A

B

C Figure 9 (A) Scleral relaxation by laser. The eight incisions at the sclera. The incision is 4 mm in length and 0.5 mm from the limbus. The parallel incisions are 2 mm apart. (B) Possible mechanism of scleral relaxation for the treatment of presbyopia. (C) Scleral incision by Erbium:YAG laser. Optics are applied directly to the sclera where the conjunctiva is opened.

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Figure 10 Slit-lamp view of the sclera incision by Erbium:YAG. The arrow indicates the incision fully covered by the conjunctiva.

vision without correction, reporting that they could read the newspaper without glasses. The technique must be evaluated in regard to long-term safety and efficacy, but the results appear to be promising. Recently, Schachar et al. proposed a new surgical treatment using a scleral expansion ring based on the same theory (Fig. 11) (67). Since several negative reports have been published on this theory and surgery (70,71), this area is discussed in Chapters 3, 20, and 21.

Figure 11 Slit-lamp view of the Schachar scleral band. Note that the scleral band is visible and slightly elevated.

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REFERENCES 1. 2. 3. 4. 5. 6. 7.

8.

9. 10.

11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

21. 22. 23. 24. 25.

Barraquer JI. Queratoplastia. Arch Soc Am Oftal Optom 1961; 3:147. Barraquer, JI. Keratophakia. Trans Ophthalmol Soc U K 1972; 92:499–516. Barraquer, JI. Keratomileusis for myopia and aphakia. Ophthalmology 1981; 88:701–708. Barraquer, JI. Results of hypermetropic keratomileusis, 1980–1981. Int Ophthalmol Clin 1983; 23:25–44. Troutman, RC, Swinger, C. Refractive keratoplasty: keratophakia and keratomileusis. Trans Am Ophthalmol Soc 1978; 76:329–339. Troutman, RC, Swinger C. Refractive keratoplasty. Keratophakia and keratomileusis. Metab Pediatr Syst Ophthalmol 1982; 6:299–304. Werblin, TP, Kaufman HE, Friedlander MH, Sehon KI, McDonald MB, Granet NS. A prospective study of the use of hyperopic epikeratophakia grafts for the correction of aphakia in adults. Ophthalmology 1981; 88:1137–1140. Werblin TP, Kaufman HE, Friedlander MH, Granet N. Epikeratophakia: the surgical correction of aphakia. III. Preliminary results of a prospective clinical trial. Arch Ophthalmol 1981; 99: 1957–1960. Kaufman HE, Werblin TP. Epikeratophakia for the treatment of keratoconus. Am J Ophthalmol 1982; 93:342–347. Goosey JD, Prager TC, Goosey CB, Bird EF, Sanderson JC. A comparison of penetrating keratoplasty to epikeratoplasty in the surgical management of keratoconus. Am J Ophthalmol 1991; 111:145–151. Grady FJ. Hexagonal keratotomy for corneal steepening. Ophthalm Surg 1988; 19:622–623. Basuk WL, Zisman M, Waring GO III, Wilson LA, Binder PS, Thompson KP, Grossniklaus HE, Stulting RD. Complications of hexagonal keratotomy. Am J Ophthalmol 1994; 117:37–49. Damiano RE, Forstot SL, Dukes DK. Surgical correction of hyperopia following radial keratotomy. Refract Corneal Surg 1992; 8:75–79. Damiano RE, Forstot SL, Frank CJ, Kasen WB. Purse-string sutures for hyperopia following radial keratotomy. J Refract Surg 1998; 14:408–413. Kezirian GM, Gremillion CM. Automated lamellar keratoplasty for the correction of hyperopia. J Cataract Refract Surg 1995; 21:386–392. Manche EE, Judge A, Maloney RK. Lamellar keratoplasty for hyperopia. J Refract Surg 1996; 12:42–49. Kliger CH. Hyperopic automated lamellar keratoplasty. Arch Ophthalmol 1999; 117:416, discussion 417. Eiferman R, Nordquist R. The corneal contouring device for hyperopia. In: Sher N, ed. Surgery for Hyperopia and Presbyopia, Baltimore: Williams & Wilkins, 1997:201–210. Jackson WB, Mintsioulis G, Agapitos PJ, Casson EJ. Excimer laser photorefractive keratectomy for low hyperopia: safety and efficacy. J Cataract Refract Surg 1997; 23:480–487. Jackson WB, Casson E, Hodge WG, Mintsioulis G, Agapitos PJ. Laser vision correction for low hyperopia. An 18-month assessment of safety and efficacy. Ophthalmology 1998; 105: 1727–1737; discussion 1737–1738. Dausch D, Klein R, Schroder E. Excimer laser photorefractive keratectomy for hyperopia. Refract Corneal Surg 1993; 9:20–28. Dausch DG, Klein RJ, Schroder E, Niemczyk S. Photorefractive keratectomy for hyperopic and mixed astigmatism. J Refract Surg 1996; 12:684–692. Dausch D, Smecka Z, Klein R, Schroder E, Kirchner S. Excimer laser photorefractive keratectomy for hyperopia. J Cataract Refract Surg 1997; 23:169–176. Buratto L, Ferrari M, Genisi C. Myopic keratomileusis with the excimer laser: one-year followup. Refract Corneal Surg 1993; 9:12–19. Brint SF, Ostrick DM, Risher C, Slade SG, Maloney RK, Epstein R, Stulting RD, Thompson KP. Six-month results of the multicenter phase I study of excimer laser myopic keratomileusis. J Cataract Refract Surg 1994; 20:610–615.

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26. Pallikaris IG, Papatzanaki ME, Stathi EZ, Frenschock O, Georgiadis A. Laser in situ keratomileusis. Lasers Surg Med 1990; 10:463–468. 27. Ditzen K, Huschka H, Pieger S. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg 1998; 24:42–47. 28. Argento CJ, Cosentino MJ. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg 1998; 24:1050–1058. 29. Knorz MC, Lierman A, Jendritza B, Hugger P. LASIK for hyperopia and hyperopic astigmatism—results of a pilot study. Semin Ophthalmol 1998; 13:83–87. 30. Zadok D, Maskaleris G, Montes M, Shah S, Garcia V, Chayet A. Hyperopic laser in situ keratomileusis with the Nidek EC–5000 excimer laser. Ophthalmology 2000; 107:1132–1137. 31. Argento CJ, Cosentino MJ. Comparison of optical zones in hyperopic laser in situ keratomileusis: 5.9 mm versus smaller optical zones. J Cataract Refract Surg 2000; 26:1137–1146. 32. Buzard KA, Fundingsland BR. Excimer laser assisted in situ keratomileusis for hyperopia. J Cataract Refract Surg 1999; 25:197–204. 33. Williams DK. One-year results of laser vision correction for low to moderate hyperopia. Ophthalmology 2000; 107:72–75. 34. Esquenazi S, Mendoza A. Two-year follow-up of laser in situ keratomileusis for hyperopia. J Refract Surg 1999; 15:648–652. 35. O’Brart DP, Stephenson CG, Baldwin H, Ilari L, Marshall J. Hyperopic photorefractive keratectomy with the erodible mask and axicon system: two year follow-up. J Cataract Refract Surg 2000; 26:524–535. 36. Lindstrom RL, Linebarger EJ, Hardten DR, Houtman DM, Samuelson TW. Early results of hyperopic and astigmatic laser in situ keratomileusis in eyes with secondary hyperopia. Ophthalmology 2000; 107:1858–1863; discussion 1863. 37. Davidorf JM, Zaldivar R, Oscherow S. Posterior chamber phakic intraocular lens for hyperopia of Ⳮ4 to Ⳮ11 diopters. J Refract Surg 1998; 14:306–311. 38. Rosen E, Gore C. Staar Collamer posterior chamber phakic intraocular lens to correct myopia and hyperopia. J Cataract Refract Surg 1998; 24:596–606. 39. Sabbagh LB. Phakic IOLs revisited; the current FDA trials. J Refract Surg 2000; 6:664–667. 40. Vetrugno M, Cardascia N, Cardia L. Anterior chamber depth measured by two methods in myopic and hyperopic phakic IOL implant. Br J Ophthalmol 2000; 84:1113–1116. 41. De Smedt SK, Vrijghem JC. Clear lens extraction to correct hyperopia in presbyopic eyes with or without arcuate keratotomy for pre-existing astigmatism. Bull Soc Belge Ophtalmol 2000; 277:43–51. 42. Lyle WA, Jin GJ. Clear lens extraction to correct hyperopia. J Cataract Refract Surg 1997; 23:1051–1056. 43. Koch DD, Kohnen T, Anderson JA, Binder PS, Moore MN, Menefee RF, Valderamma GL, Berry MJ. Histologic changes and wound healing response following 10-pulse noncontact holmium:YAG laser thermal keratoplasty. J Refract Surg 1996; 12:623–634. 44. Koch DD, Kohnen T, McDonnell PJ, Menefee RF, Berry MJ. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty. United States phase IIA clinical study with a 1-year follow-up. Ophthalmology 1996; 103:1525–1535; discussion 1536. 45. Alio JL, Ismail MM, Sanchez Pego JL. Correction of hyperopia with non-contact Ho:YAG laser thermal keratoplasty. J Refract Surg 1997; 13:17–22. 46. Eggink CA, Meurs P, Bardak Y, Deutman AF. Holmium laser thermal keratoplasty for hyperopia and astigmatism after photorefractive keratectomy. J Refract Surg 2000; 16:317–322. 47. Brinkmann R, Koop N, Geerling G, Kampmeier J, Borcherding S, Kamm K, Birngruber R. Diode laser thermokeratoplasty: application strategy and dosimetry. J Cataract Refract Surg 1998; 24:1195–1207. 48. Geerling G, Koop N, Tungler A, Brinkmann R, Wirbelauer C, Birngruber R, Laqua H. Diode laser thermokeratoplasty. Initial clinical experiences. Ophthalmologe 1999; 96:306–311.

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49. Geerling G, Koop N, Brinkmann R, Tunglar A, Wirbelauer C, Birngruber R, Laqua H. Continuous-wave diode laser thermokeratoplasty: first clinical experience in blind human eyes. J Cataract Refract Surg 1999; 25:32–40. 50. Schanzlin DJ. Studies of intrastromal corneal ring segments for the correction of low to moderate myopic refractive errors. Trans Am Ophthalmol Soc 1999; 97:815–890. 51. Cochener B, Savary-LeFloch G, Colin J. Effect of intrastromal corneal ring segment shift on clinical outcome: one year results for low myopia. J Cataract Refract Surg 2000; 26:978–986. 52. Asbell PA, Ucakhan OO, Durrie DS, Lindstrom RL. Adjustability of refractive effect for corneal ring segments. J Refract Surg 1999; 5:627–631. 53. Lindstrom R. Small diameter intracorneal inlay lens for the correction of presbyopia. In: Sher N, ed. Surgery for Hyperopia and Presbyopia. Baltimore: Williams & Wilkins. 1997:195–199. 54. Keates RH, Martines E, Tennen DG, Teich C. Small-diameter corneal inlay in presbyopic or pseudophakic patients. J Cataract Refract Surg 1995; 21:519–521. 55. Fonda G. Presbyopia corrected with single vision spectacles or corneal lenses in preference to bifocal corneal lenses. Trans Ophthalmol Soc Aust 1966; 25:78–80. 56. Back A, Grant T, Hine N. Comparative visual performance of three presbyopic contact lens corrections. Optom Vis Sci 1992; 69:474–480. 57. Atwood JD. Presbyopic contact lenses. Curr Opin Ophthalmol 2000; 11:296–298. 58. Westin E, Wick B, Harrist RB. Factors influencing success of monovision contact lens fitting: survey of contact lens diplomates. Optometry 2000; 71:757–763. 59. Josephson JE, Caffery BE. Monovision vs aspheric bifocal contact lenses: a crossover study. J Am Optom Assoc 1987; 58:652–654. 60. Key JE, Yee JL. Prospective clinical evaluation of the Acuvue Bifocal contact lens. Clao J 1999; 25:218–221. 61. Chateau N, Baude D. Simulated in situ optical performance of bifocal contact lenses. Optom Vis Sci 1997; 74:532–539. 62. Gray PJ, Lyall MG. Diffractive multifocal intraocular lens implants for unilateral cataracts in prepresbyopic patients. Br J Ophthalmol 1992; 76:336–337. 63. Moreira H, Garbus JJ, Fasano A, Lee M, Clapham TN, McDonnell PJ. Multifocal corneal topographic changes with excimer laser photorefractive keratectomy. Arch Ophthalmol 1992; 110:994–999. 64. Anschutz T. Presbyopic PRK. In: Sher N, ed. Surgery for Hyperopia and Presbyopia. Baltimore: Williams & Wilkins, 1997:63–77. 65. Hom MM. Monovision and LASIK. J Am Optom Assoc 1999; 70:117–122. 66. Thornton S. Anterior ciliary sclerotomy (ACS), a procedure to reverse presbyopia. In: Sher N, ed. Surgery for Hyperopia and Presbyopia. Baltimore: Williams & Wilkins, 1997:33–36. 67. Schachar RA. Cause and treatment of presbyopia with a method for increasing the amplitude of accommodation. Ann Ophthalmol 1992; 24:445–447, 452. 68. Schachar RA. Pathophysiology of accommodation and presbyopia. Understanding the clinical implications. J Fla Med Assoc 1994; 81:268–271. 69. Fukasaku H, Marron JA. Anterior ciliary sclerotomy with silicone expansion plug implantation: effect on presbyopia and intraocular pressure. Int Ophthalmol Clin 2001; 41:133–141. 70. Glasser A, Kaufman P. The mechanism of accommodation in primates. Ophthalmology 1999; 106:863–872. 71. Mathews S. Scleral expansion surgery does not restore accommodation in human presbyopia. Ophthalmology 1999; 106:873–877.

2 Basic Optics of Hyperopia and Presbyopia MICHAEL K. SMOLEK and STEPHEN D. KLYCE Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A.

A. INTRODUCTION It normally comes as a surprise that there are more hyperopes than myopes in the general population. The reason for this is that hyperopes can hide behind their accommodative capacity until at least age 40, when the aging process takes away the ability to alter the power of the natural lens. In this chapter, we examine the optical basis and interrelationships between hyperopia and presbyopia.

B. FAR POINT The simplest and preferred clinical method of determining the refraction of the eye is still the far point method, in which the patient subjectively determines the furthest distance at which he or she can clearly see a target without using any accommodation. The far point location of the eye can also be determined objectively by an examiner using a retinoscope, an automated refractor, or similar method. By definition, the far point is the focal point in object space that is conjugate to the focus at the retina and is, therefore, seen clearly by the subject. Again, because of the spherical aberration (multifocality) of the eye’s optics and the physical size of the pupil, there may actually be a distance range that appears to be in focus simultaneously (i.e., a depth-of-field effect), but a single far point is specified. The far point of the eye is distinct from the near point of the eye, which is the location at which one can maximally accommodate in order to clearly see the closest possible target to the eye. 17

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For the emmetrope, the far point is located at optical infinity, and no power correction is needed to image a distant target onto the retina (Fig. 1). In myopia, the far point lies close to and a finite distance in front of the eye, so that light from the far point target enters the eye with a certain amount of negative vergence. The amount of negative vergence cancels the excess power inherent within the myopic eye, and the light comes to a focus at the retina. The specific location of the far point for the “nearsighted” myope depends on the level of myopic error; the higher the error, the nearer the far point will be to the eye. In order for the myope to clearly see a target located at optical infinity, negative power must be added to reduce the vergence of the distant light to a negative amount before it enters the eye; otherwise the excessive power of the eye’s optics must be reduced, as through flattening of the cornea by laser surgery. Myopic error is always expressed with a negative sign indicative of the negative power that must be added to achieve correction for viewing distant targets. In hyperopia, the far point is commonly said to exist “beyond infinity,” because only converging rays can be brought to a focus onto the retina in the uncorrected hyperope (Fig. 1). Actually, it is more accurate to say that the far point of the hyperope is a virtual object that is located a finite distance behind the retina. The far point of the hyperope can be found by noting the location where the converging rays entering the eye would come to a focus if the eye were not present to intercept the light. Because hyperopic eyes have insufficient plus power to see targets clearly at infinity, positive vergence must be added to the light entering the eye and the refraction is signified by a plus sign. Plus power can be added to the light entering the eye or the eye itself can be made to have relatively more power by making the cornea steeper through laser surgery. However, many young to middle-aged hyperopes can fully correct their distance vision error by adding enough plus power through accommodation to shift the far point to infinity. This ability to self-correct their refractive error gives these hyperopes a distinct advantage over myopes, who cannot “disaccommodate” to move the far point away from the eye. It also explains why these hyperopes can be considered to be farsighted, because they in fact become self-corrected for far vision. Unfortunately, as hyperopes age, the ability to

Figure 1 Far point location specified for three refractive states. R is the location of the far point, defined as the most remote distance at which the unaccommodated eye can see clearly. R’ is the conjugate focus of the far point, which is always located at the retina. D refers to the vergence power entering the eye to bring light to a focus on the retina: zero for emmetropia, negative for myopia, and positive for hyperopia.

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Figure 2 Graphic representation of the decline in accommodative amplitude with age (2).

accommodate diminishes (Fig. 2); thus they lose their ability to see clearly at any distance, while older myopes still retain at least a portion of their ability to see clearly at some distance. C. ACCOMMODATION FOR NEAR VISION The closer an object is to the cornea, the greater the divergence of light entering the eye and the greater the need for more plus power to make the near object conjugate with the retina. In youth, accommodation allows viewing at a variety of distances from infinity to very near targets. As a person ages, however, the accommodative ability decreases, and the near point moves away from the eye. Because uncorrected hyperopes often use a portion of their accommodative ability to correct their refractive error for distance, the near point is located farther from the eye; therefore hyperopes often experience near vision problems at an earlier age than myopes or emmetropes. It should be noted that some myopes may not experience any near vision problems in the uncorrected state if their refractive error maintains a clear image within a comfortable working distance that is neither too close nor too far from their eyes. It is important to appreciate that there is a limited and diminishing amount of accommodation available at any given age and that the amount available depends in part on whether accommodation is being used to correct for a hyperopic error. This amount of accommodation in play is specified by the amplitude of accommodation, which is defined as the vergence difference between the far point and the near point. The relationship between age and accommodative amplitude was established by Donders (1) and later refined by Duane (2), who presented what has since become the classic representation of accommodative amplitude as a function of age (Fig. 2). Duane’s data show that accommodation begins to decrease in early adulthood, well before the decline is noticed during the performance of near vision tasks, such as reading. For adolescents, accommodative amplitude is approximately 14 D, which corresponds to a near point of approximately 7

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cm for an emmetrope. By age 45, this accommodative amplitude drops, due to changes in the accommodative apparatus controlling the crystalline lens power, to about 4 D and results in at best a 25-cm near point distance for that same emmetrope. Normal reading distance is considered to be around 15 in. or 37 cm, which is still within the range of a person in his or her mid- to late forties. However, it must be remembered that a continuous and excessive need to accommodate can be tiring and uncomfortable, so the decline in accommodative amplitude will be noticed by many subjects who are only in their midforties and who still have a fair amount of accommodative amplitude in reserve. If the eye has insufficient accommodative amplitude, which normally occurs with advancing age and requires a plus lens addition for comfortable near vision, the condition is called presbyopia. There are no specific values that define the absolute onset of presbyopia, because its effects are dependent on a number of factors including the refractive error, age, amplitude of accommodation, and the near vision tasks and lifestyle of a particular patient. Because using accommodation to correct for distance vision is often tiring in itself, the hyperope will be more likely to complain of tired eyes, eyestrain, and diplopia, and may do so at an earlier age. Children do not normally experience vision problems from mild amounts of hyperopia because their accommodative reserve is large. However, those with moderate to high levels of hyperopia may experience visual problems ranging from mild eyestrain and headaches after near work to more severe problems such as strabismus and amblyopia (3). Some of these complaints are associated specifically with the ability of the two eyes to fuse images binocularly, because the accommodative process is neurologically tied to the convergence of the eyes. There is a clinical distinction made between accommodative amplitude, which is the optical difference between the near and far point measured in diopters, and the range of accommodation, which is the linear difference between the far point and the near point in terms of physical distance. In the uncorrected myope, the far point may be located very close to the eye. The myope’s range of accommodation is thus very limited, whereas prepresbyopic low hyperopes may have a range that allows vision to infinity, just as in emmetropia (Fig. 3). D. MANIFEST VERSUS LATENT HYPEROPIA The refractive state of the eye is measured at rest with respect to the far point, but achieving a totally unaccommodated state can be problematic, especially in the uncorrected hyperope who uses accommodation to self-correct for distance vision. Consequently, refractions are separated into two basic types—manifest and latent refractions—which can give different refraction values for the same eye. A manifest refraction is the obvious, nonhidden part of the refraction that is based on the elimination of any natural stimulus to accommodate. Generally this is best accomplished by providing additional positive vergence of a known amount to the incoming light to the extent that the eye is made artificially myopic. The process is referred to as fogging. The far point thus moves to a finite distance in front of the eye, which in itself is beneficial with respect to interacting with and measuring the location of the far point. Of course, once the myopia-shifted far point is measured, the added vergence power is subtracted to provide the true far point location. While fogging a patient removes the manifest portion of the total accommodation that may be in play, it does not necessarily remove the latent or hidden portion of accommodation that may still exist. Latent accommodation is that part which cannot be relaxed due to excessive, spastic tonicity of the ciliary apparatus controlling accommodation. Self-

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A

B

C Figure 3 Example of the possible range of accommodation for three refractive states at three different ages. R is the far point and P is the near point. The dark line refers to the theoretical region in which unaided clear vision is possible. (A) In emmetropia, objects at optical infinity can be seen at any age. (B) In myopia, objects seen clearly are always located a finite distance in front of the eye, but objects at optical infinity cannot be seen clearly. (C) In hyperopia, objects at optical infinity can usually be seen clearly in youth and middle age; by the time late presbyopia occurs, however, no objects can be seen clearly at any distance unless the hyperopic error is corrected.

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correcting hyperopes tend to be prone to accommodative excess because they are constantly demanding additional plus power from the lens for both near and far tasks, and this effort builds up a constant level of spastic tonicity in the ciliary muscle. Therefore a cycloplegic drug is used to completely relax the spastic tonicity of the ciliary muscle, after which a refraction is performed to determine the full latent refractive error. Typically, the latent accommodation may account for approximately 1 D of total accommodation, so the difference between manifest and latent refractions may be clinically significant. E. MAGNIFICATION AND VISUAL ACUITY A refractive error can be fully corrected and image blur eliminated, but the retinal image may be smaller or larger than it would be in the uncorrected state; therefore the ability to resolve details in the image may be harder or easier to accomplish. Suppose we have a hyperope with a Ⳮ5 D correction in a spectacle plane 1.2 cm from the cornea. The apparent image size will be reduced by 6% if the correction is moved to the corneal plane, as in the case of laser refractive surgery or contact lens wear (Table 1). If the spectacle correction is increased to Ⳮ10 D, the amount of minification for a corneal plane correction likewise doubles to 12%. The general rule of thumb is that spectacle magnification in percent equals the power of the spectacle lens in diopters multiplied by the distance between the spectacle plane and the cornea in centimeters. Because we are considering an image projected from the eye in order to assess the apparent visual angle change experienced by the subject, distances are considered positive when measured from the cornea to the spectacle plane and negative when moving from the spectacle plane back to the cornea. Thus, moving a correction from the cornea to a spectacle plane in the hyperope causes magnification of the retinal image, and the further the spectacle plane is from the eye, the greater the change in the magnification. However, when the correction is moved from the spectacle plane back to the cornea, the retinal image becomes physically smaller in the hyperope. Therefore, Snellen letters subtend a relatively smaller angle in the visual field and appear smaller to the patient and harder to distinguish. The opposite relationship holds true for the myope; moving the correction from the spectacle plane to the cornea causes Snellen letters to appear slightly larger to the myope corrected by refractive surgery or a contact lens. Applegate and Howland calculated the effects of magnification on Snellen visual acuity and, as expected, showed that the effective change in acuity was nonlinear and greater for myopes than for hyperopes (4). Whereas myopes had a positive effect of gaining more letters of visual acuity, hyperopes lost letters of acuity. For example, a Ⳮ5

Table 1 Magnification Effect of Moving a Correction from the Spectacle Plane to the Cornea Spectacle power (D) ⫹2 ⫹2 ⫹5 ⫹5 ⫹10

Spectacle plane distance (cm) ⫺1.2 ⫺1.5 ⫺1.2 ⫺1.5 ⫺1.2

Spectacle magnification (%) ⫺2.4 ⫺3.0 ⫺6.0 ⫺7.5 ⫺12.0

Loss of letters for Snellen distance visual acuity ⬃1 ⬃1 ⬃2 ⬃2 ⬃3

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D hyperope wearing glasses who has successful refractive surgery is expected to lose two to four letters of acuity as a result of moving the correction to the cornea, depending on the exact distance of the spectacle plane from the cornea (Table 1). F. HYPEROPIA AND BIOMETRIC CHANGES DURING LIFE Based on spherical equivalent data obtained during cycloplegic refractions, the average eye is hyperopic through most of life (Fig. 4). The average refraction is approximately Ⳮ2.25 D at birth and reaches a hyperopic peak around 8 years of age, after which the refraction becomes increasingly less hyperopic during adolescence and comes close to being emmetropic during early adulthood (5). In the Beaver Dam Eye Study of adults, hyperopia was more prevalent than myopia in age-matched subjects (49 vs 26.2%, respectively, p ⳱ 0.0001) (6). Hyperopia increases in later adulthood from 22.1% between ages 43 and 54 to 68.5% at age 75 and above; however, Slataper noted that the refraction tends to drift back toward myopia with very advanced age (5). The hyperopic shift for older adults between the ages of 45 and 65 has been attributed to reductions in the axial length of the eye and changes in the focal power of the lens (7). The cause of the myopic drift in advanced age may be attributed to a shrinking radius of curvature of the cornea, which leads to a higher corneal power (8). This effect occurs predominantly in females (9). Passive growth of the eye during childhood tends to be a correlated, uniform expansion of ocular dimensions (7,10). By “correlated” we mean that as eye growth causes the retina to recede from the optical elements of the eye, we also see changes in the lens and cornea that ideally allow emmetropia to be achieved if the eye is hyperopic or retained if the eye is already emmetropic. Furthermore, it must be remembered that as axial length increases, there is a reduction in the vergence power required to focus an image on the

Figure 4 Graph based on Slataper’s data (5) of average refractive error during life. Note that the error tends to be hyperopic throughout life and relatively stable from young adulthood to middle age. N ⳱ 34,570 eyes assessed by cycloplegic refractions.

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retina. During childhood, corneal power decreases by about 2 D because the radius of curvature of the cornea increases as part of the expansive growth of the corneoscleral shell (11). In addition, the anterior chamber depth decreases, which reduces the effective power of the lens, and the lens itself decreases in power as the radius of curvature of the front and back surfaces increases by up to 1 mm (11). Sorsby noted lens power to be on average 23 D at age 3 and only 20 D at age 14 (12). The lens also thins from an average of 3.6 mm at age 6 to about 3.4 mm at age 10, after which thinning essentially halts (11). The overall lens thinning can be attributed to a compression of the nucleus, even though the cortex grows and thickens at this time. There appears to be an active growth mechanism that uses feedback from the blur of the retinal image to make corrective growth changes to the ocular component dimensions (7,10). A defect in an active growth feedback pathway might be responsible for a runaway increase in axial length, which is often seen with myopia; but the active growth mechanism does not adequately explain hyperopic error. Hyperopia seems more likely to be a failure of the passive growth mechanism, such that the eye retains slightly immature globe dimensions into adulthood. Hyperopic eyes tend to be smaller in all dimensions (not just in axial length) compared to corresponding age-matched emmetropic eyes. Using high-resolution magnetic resonance imaging to measure dimensions in the major axes of the eye, Cheng and coworkers found that, on average, the hyperopic eye is consistently smaller overall than the mean emmetropic eye and significantly smaller than the mean myopic eye (Fig. 5) (13). Strang et al. used biometric data from 53 human subjects with refractive errors of up to Ⳮ10 D and found that there was a strong correlation between the mean hyperopic

Figure 5 Data based on the findings of Cheng et al. (13) of eye size relative to refractive error. Error bars indicate standard deviations. The general trend is that myopic eyes are larger and hyperopic eyes smaller than eyes with no refractive error. The differences in globe dimension between hyperopic and myopic eyes are significant.

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error and the axial length of the globe (r2 ⳱ 0.611, p ⳱ 0.0001) (14). There was also a weak but significant correlation between mean corneal radius and mean refractive error (r2 ⳱ 0.128, p ⳱ 0.009). Grosvenor also found that hyperopic eyes were smaller and tended to have flatter corneas than emmetropic eyes (15). G. OPTICS OF THE CRYSTALLINE LENS The lens has an average index of refraction that higher than the index of corneal stroma (1.427 vs. 1.376) (16). However, the contribution of the lens to the total power of the eye is about half that of the anterior corneal surface, because the lens is surrounded by fluid with an index near 1.336, whereas the cornea is exposed to air with an index of 1.0, which greatly increases its refractivity. While a single index of refraction of the lens is useful for simple calculations, in reality, the lens cannot be defined by a single value. Mapping the gradient index of the lens has proved difficult. Simple models using concentric shells of varying index gradients do not yield accurate ray-tracing results, and the models do not agree with refractive index measurements made by tissue probes (17). It is interesting to find that significant levels of transient hyperopia have been attributed entirely to changes in the refractive index of the lens. Saito and coworkers noted hyperopia peaking between 1 to 2 weeks after abrupt decreases in plasma glucose and attributed this effect to water influx into the lens (18). Okamoto et al. also noted hyperopia after treatment for hyperglycemia and found no changes in lens thickness or anterior chamber depth, thus implicating a change entirely due to the refractive index of the lens (19). Although the lens is the primary component associated with accommodation for near vision, the contribution of depth of focus of the eye should not be discounted, particularly in presbyopic eyes. Brighter viewing conditions or the use of miotics that constrict the pupil increase the depth of focus and help to extend the effective range of accommodation. H. OPTICAL ABERRATIONS The shape of the gradient index profile across the lens as well as shape changes due to accommodation alter not only effective power but also the spherical aberration of the eye (20). By accommodating to approximately 3 D (a 33-cm viewing distance), the negative spherical aberration of the lens corrects for much of the positive spherical aberration induced by the cornea (21). Further accommodation tends to give the eye an overall negative spherical aberration, but the exact amount varies among individuals (22). In general, near accommodation tends to increase the monochromatic wavefront aberrations of the eye (23). Fourth-order aberrations can either increase or decrease with increasing accommodation, but higher-order aberrations tend to increase (22). It has been suggested that there is no correlation between the change in aberration during accommodation and the total amount of aberration for the relaxed eye (22). It can be concluded that any clarity of vision provided by refractive surgery must diminish by a measurable extent with accommodation, but certainly more work needs to be done to ascertain the significance of aberration change on visual performance. REFERENCES 1. Donders FC. On the Anomalies of Accommodation and Refraction of the Eye. London, 1864. 2. Duane A. Normal values of accommodation at all ages. JAMA 1912; 59:1010–1013.

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3. Moore B, Lyons SA, Walline J. A clinical review of hyperopia in young children. The Hyperopic Infants’ Study Group, THIS Group. J Am Optom Assoc 1999; 70:215–224. 4. Applegate RA, Howland HC. Magnification and visual acuity in refractive surgery. Arch Ophthalmol 1993; 111:1335–1342. 5. Slataper FJ. Age norms of refraction and vision. Arch Ophthalmol 1950; 43:466–481. 6. Wang Q, Klein BEK, Klein R, Moss SE. Refractive status in the Beaver Dam Eye Study. Invest Ophthalmol Vis Sci 1994; 35:4344–4347. 7. Brown NP, Koretz JF, Bron AJ. The development and maintenance of emmetropia. Eye 1999; 13:83–92. 8. Hayashi K, Hayashi H, Hayashi F. Topographic analysis of the changes in corneal shape due to aging. Cornea 1995; 14:527–532. 9. Goto T, Klyce SD, Zheng X, Maeda N, Kuroda T, Ide C. Gender and age related differences in corneal topography. Cornea 2001; 20:270–276. 10. van Alphen GWHM. On emmetropia and ametropia. Ophthalmologica Suppl 1961; 142:1–92. 11. Zadnik K, Mutti DO, Fusaro RE, Adams AJ. Longitudinal evidence of crystalline lens thinning in children. Invest Ophthalmol Vis Sci 1995; 36:182–187. 12. Sorsby A, Benjamin B, Sheridan M. Refraction and Its Components During the Growth of the Eye from the Age of Three. MRC special report series no. 301. London: Her Majesty’s Stationery Office, 1961. 13. Cheng H-M, Singh OS, Kwong KK, Xiong J, Woods BT, Brady TJ. Shape of the myopic eye as seen with high-resolution magnetic resonance imaging. Optom Vis Sci 1992; 69:698–701. 14. Strang NC, Schmid KL, Carney LG. Hyperopia is predominantly axial in nature. Curr Eye Res 1998; 17:380–383. 15. Grosvenor T. High axial length/corneal radius ratio as a risk factor in the development of myopia. Am J Opt Physiol Opt 1988; 65:689–696. 16. Mutti DO, Zadnik K, Adams AJ. The equivalent refractive index of the crystalline lens in childhood. Vis Res 1995; 35:1565–1573. 17. Pierscionek BK. Refractive index contours in the human lens. Exp Eye Res 1997; 64:887–893. 18. Saito Y, Ohmi G, Kinoshita S, Nakamura Y, Ogawa K, Harino S, Okada M. Transient hyperopia with lens swelling at initial therapy in diabetes. Br J Ophthalmol 1993; 77:145–148. 19. Okamoto F, Sone H, Nonoyama T, Hommura S. Refractive changes in diabetic patients during intensive glycaemic control. Br J Ophthalmol 2000; 84:1097–1102. 20. Smith G, Pierscionek BK, Atchison DA. The optical modelling of the human lens. Ophthalmic Physiol Opt 1991; 11:359–369. 21. Koomen MJ, Tousey R, Scolnik R. The spherical aberration of the eye. J Opt Soc Am 1949; 39:370–376. 22. He JC, Burns SA, Marcos S. Monochromatic aberrations in the accommodated human eye. Vis Res 2000; 40:41–48. 23. He JC, Marcos S, Webb RH, Burns SA. Measurement of the wave-front aberration of the eye by a fast psychophysical procedure. J Opt Soc Am A Opt Image Sci Vis 1998; 15:2449–2456.

3 The Helmholtz Mechanism of Accommodation ADRIAN GLASSER College of Optometry, University of Houston, Houston, Texas, U.S.A.

“There is no other portion of physiological optics where one finds so many differing and contradictory ideas as concerns the accommodation of the eye, where only . . . in the most recent time have we actually made observations where previously everything was left to the play of hypotheses.” H. Von Helmholtz (1909)

A. INTRODUCTION In 1853 Hermann von Helmholtz described the mechanism of accommodation of the human eye. This was not the first description of how the human eye accommodates. Many descriptions of and much research on accommodation preceded the work of Helmholtz (1), yet the accommodative mechanism of the human eye is still generally referred to as the “classic Helmholtz accommodative mechanism.” Helmholtz succeeded where others had failed at providing a comprehensive and consistent explanation of how accommodation occurs. It was comprehensive in that he described the functions of all of the major elements of the accommodative apparatus, and it was consistent in that it required no significant modifications of what was known with certainty at the time regarding how accommodation occurs. B. THE ANATOMY OF THE ACCOMMODATIVE APPARATUS In order to understand how accommodation occurs, it is necessary to have a clear understanding of the accommodative apparatus and the relationships of the accommodative structures to each other. While in recent years there has been some limited debate over 27

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Figure 1 Hermann Ludwig Ferdinand von Helmholtz (b, 1821; d, 1894) was not the first to describe the accommodative mechanism of the human eye, but he provided the first comprehensive and most accurate description based on the experiments he had performed and on the work done by many preceding him. Helmholtz succeeded where others had failed at providing a consistent and harmonious description of how accommodation occurs. Although the description that Helmholtz provided was largely accurate, subsequent experimental studies have shown that some aspects of the accommodative mechanism are not as Helmholtz described. For example, Helmholtz believed that the posterior surface of the lens did not move with accommodation and that the iris played an important role in mediating the accommodative changes in the lens.

the gross anatomy of the accommodative apparatus, in general there is a consensus, and has been for some time (2). The primary accommodative structures of the eye consist of the ciliary body, the ciliary muscle, the posterior and anterior zonular fibers, the lens capsule, and the lens substance. C. THE CILIARY MUSCLE The ciliary muscle consists of three subgroups of muscle fiber cells differentiated by their positions and orientations within the ciliary body (3). The muscle fibers group are (1) the longitudinal fibers, sometimes referred to as meridional fibers or Bru¨cke’s muscle (4); (2) the radial or reticular fibers; and (3) the equatorial or circular fibers. The longitudinal fibers are located most peripherally in the eye, just inside the sclera at the ciliary region. Inward of the longitudinal fibers and closer to the vitreous are the radial fibers, and inside these are the circular fibers, located most anteriorly in the ciliary body and closest to the lens (5). The ciliary muscle is located within the ciliary body, bounded externally by the

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sclera of the eye and the collagen fibers, fibroblasts, and melanocytes of the outer surface of the ciliary body (3). The inner surface of the ciliary muscle is bounded anteriorly by the pars plicata and posteriorly by the pars plana of the ciliary body. Anteriorly, the ciliary muscle inserts into the scleral spur and the trabecular meshwork, which serve as a relatively fixed anterior anchor point against which the ciliary muscle contracts (3). Posteriorly, the ciliary muscle attaches via the elastic tendons to the stroma of the choroid. D. THE ZONULAR FIBERS The zonular fibers of the eye can broadly be broken down into two subgroups. The posterior zonular fibers or the pars plana zonule and the anterior zonular fibers. The pars plana zonule extends from the posterior insertion of the zonule at the posterior attachment of the ciliary muscle near the ora serrata of the retina to the ciliary processes.(6) The anterior zonular fibers span the circumlental space between the ciliary processes and the equatorial region of the lens (Fig. 2). From their posterior origin, the posterior zonular fibers extend longitudinally toward the pars plicata of the ciliary body as a mat or meshwork of interlacing fibers, following a straight path toward the tips of the ciliary processes (7). The majority of the posterior zonular fibers course forward to the pars plicata region of the ciliary body and enter the valleys between the ciliary processes, inserting into the walls of the valleys of the ciliary processes (8). The pars plicata region of the ciliary body separates the

Figure 2 Early anatomists had an excellent knowledge of the anatomy of the crystalline lens (A) and the ciliary region of the eye. The lens is composed of lens fiber cells arranged in concentric layers. New lens fibers develop from the germinative zone at the anterior equatorial region of the lens. The lens capsule surrounds the lens. The anterior surface of the lens is to the left. (From Ref. 2.) (B) Similarly, investigators whose work preceded that of Helmholtz (1) had already provided excellent anatomical information on the structure and relationships of various elements of the accommodative apparatus to each other. In particular, the arrangement of the zonular fibers passing from the ciliary body to the lens equator shows a picture remarkably consistent with subsequent descriptions of this tissue, but quite unlike that postulated in recent controversial and anatomically inaccurate theories (i.e., Refs. 9 and 43). (From Ref. 2.)

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posterior zonule from the anterior zonule (8). Some zonular fibers pass from the pars plana through the valleys between the ciliary processes and on toward the lens (6,8). A spanning or tension fiber system of many finer strands forms the zonular plexus, which attach the zonule to the ciliary epithelium in the valleys of the ciliary processes (6). This serves to anchor the anterior and pars plana zonule to the ciliary epithelium of the ciliary body. As the anterior zonular fibers near the lens equator, they fan out to insert into the lens capsule around the equatorial region of the lens. The individual zonular fibers terminate within zonular lamellae of the lens capsule (6). No discrete zonular fiber bundles can be seen to selectively insert specifically to the lens anterior, equatorial, and posterior surfaces, as suggested by Schachar (9); instead, the zonular fibers form a uniform distribution or meshwork of fibers inserting all around the equatorial region of the lens (10,11). E. THE LENS AND CAPSULE The lens capsule is a thin, acellular, elastic membrane surrounding the lens. It is principally composed of type IV collagen with some glycosaminoglycans (12). The capsule is not of uniform thickness. Fincham, in 1937, found it to be thickest at the peripheral anterior surface and thinner toward the lens equatorial region. On the lens posterior surface, the capsule is thinnest at the region of the posterior pole of the lens but thicker toward the periphery (13). The lens consists of a monolayer of epithelial cells on the anterior surface beneath the capsule, with elongated lens epithelial cells at various stages of maturation. The lens fiber cells are arranged in layers to form the younger peripheral cortex and the more mature central lens cortex (Fig. 2). The human lens does not shed any of its cells and grows throughout life by adding lens fibers at its outer equatorial zone. Isolated lenses show a linear increase in mass with age (14–16). The axial thickness of the lens increases with increasing age. Its axial thickness can readily be measured in vivo in the living eye with A-scan ultrasound or Schiempflug (17–19). Since the lens thickness increases with accommodation, it is important to measure this dimension in unaccommodated eyes to draw conclusions about changes due to aging. As the lens grows, there is an increase in the anterior and posterior surface curvatures of the unaccommodated lens as measured with Schiempflug slit-lamp photography (20,21). While the axial thickness and surface curvatures of the lens can readily be measured in the living eye, lens diameter, until recently, could not. Based on the observation that the diameter of lenses removed from postmortem human eyes increases with increasing age (22), it has been suggested that there is a growth-related increase in the lens equatorial diameter throughout life (23–25). However, Smith (22) recognized that his measurements of isolated lenses did not reflect a growth-related increase in diameter. When lenses are removed from the eye, the outwarddirected zonular tension on the lens equator is removed. Isolated lenses are therefore in an accommodated form, rather more so for the younger than the older lenses (3). Advances in magnetic resonance imaging (MRI) have recently allowed lens diameter to be measured in the living eye. The MRI measurements do not show an increase in lens diameter with age (26). F. OPTICAL CHANGES WITH ACCOMMODATION 1. Increased Optical Power of the Eye Accommodation is defined as a dioptric change in power of the eye (27). The increase in refractive power or the change in refractive state of the eye is the predominant optical

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change of accommodation and is readily measured. The cornea, the anterior and posterior lens surfaces, and the lens gradient refractive index provide optical refractive power to the eye. In the unaccommodated, emmetropic eye, the optical refracting power allows the image of a distant object to be focused on the retina. In this case, parallel rays of light from the distant object enter the eye and become convergent to focus the image on the retina. A near object, closer to the eye than optical infinity, however, has diverging light rays entering the cornea. In order for the divergent rays to be drawn to a focus on the retina, the optical power of the eye must increase. During accommodation, this is accomplished primarily by an increase in curvature of the anterior and posterior lens surfaces. In addition, lens thickness increases and anterior chamber depth and, to a lesser degree, vitreous chamber depth decreases during accommodation. All these changes contribute to an increase in optical refracting power. If the optical power or the refraction of a young eye is measured with an objective refractometer during accommodation, it is clear that the optical power increases, resulting in a myopic shift in the refraction. 2. Depth of Field The accommodative triad describes the neuronally coupled accommodation, convergence, and pupil constriction that occur with an accommodative effort. Both accommodation and pupil constriction contribute to near visual acuity. Depth of field is the distance an object can be moved in object space without appreciably altering image focus or, in the case of the eye, without appreciably altering the eye’s visual acuity. This plays an important role in the perception of a sharply focused image on the retina. An eye with a large pupil diameter has a small depth of field. This means that the eye can detect a change in focus of the retinal image with small movements of the object toward or away from the eye. An eye with a small pupil diameter has a large depth of field. In this case, the object can be moved a greater distance toward or away from the eye without appreciably altering the retinal image focus. The pupillary constriction that occurs with accommodation results in an increased depth of field, which also contributes to maintaining a clear image of a near object on the retina. Pupillary constriction can also occur without accommodation, as with increased illumination. This too improves depth of field and hence near reading ability, but without accommodation. Pupillary constriction and increased depth of field are important for improving near reading ability but are very different from the refractive change that accompanies accommodation. 3. Aberrations of the Eye The imperfect optics of the eye mean that the eye suffers from optical aberrations. The low-order aberrations, such as defocus and astigmatism, can be corrected with optical prescriptions, but higher-order aberrations cannot. These higher-order aberrations include spherical aberration and coma, for example. While the presence of aberrations in the eye reduces retinal image quality, they also have important implications for accommodation. Ocular aberrations result in decreased retinal image quality and contribute to a larger depth of field of the eye due to its inability to detect small changes in image focus as an object is moved closer or further from the optimal point of focus. Before the accommodative mechanism was fully understood, Sturm (2) proposed that astigmatism could explain how the eye could see at different distances. An optical system with astigmatism has two line foci at orthogonal meridians separated by a distance called the interval of Sturm. No perfect image focus is attained anywhere between the two line foci, so if an object is

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moved such that the interval of Sturm remains on the retina, only a modest change in image quality occurs, but without a distinct perception of a change in focus. Thus subjective accommodation testing may suggest the presence of accommodation in an individual with ocular aberrations even when no functional accommodation occurs. This illustrates the importance of considering of the optical aberrations of the eye—how they can contribute to near vision but yet are clearly distinct from active accommodation. G. THE HELMHOLTZ DESCRIPTION OF ACCOMMODATION Helmholtz (2) provided the first accurate description of the eye’s accommodative anatomy and mechanism. He described that in the unaccommodated state, resting tension on the

Figure 3 Sections of the (A) unaccommodated and (B) accommodated ciliary muscle. Eyes were placed in a fixative after maximal contraction of the ciliary muscle with eserine or maximum relaxation of the ciliary muscle with atropine. These histological diagrams illustrate that the inner apex of the ciliary body moves forward and toward the axis of the eye with accommodation. Notice that in the unaccommodated state, the inner apex of the ciliary muscle resides behind the scleral spur; but in the maximally accommodated state, this portion of the ciliary muscle has moved forward of the scleral spur. (From Ref. 2.) (C) The Helmholtz accommodative mechanism. In the left half of the diagram, the eye is shown in the unaccommodated state, focused for far (F), and the right half, in the accommodated state, focused for near (N). A contraction of the ciliary muscle moves the ciliary body closer to the lens equator. Resting zonular tension is released. The anterior lens surface is shown to move forward with accommodation and the posterior lens position to remain unchanged. (From Ref. 2.)

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zonular fibers at the lens equator pull and hold the lens in a flattened and unaccommodated state. The zonular fibers extend from the ciliary processes to their insertion on the lens capsule at the lens equatorial region. When the ciliary muscle contracts with an accommodative effort, it undergoes a forward redistribution of its center of mass (Fig. 3). This moves the anterior-inward apex of the ciliary body toward the lens equator to release the resting zonular tension. When the zonular tension is released, the elastic lens capsule molds the lens to decrease equatorial diameter, increase thickness, and allow the lens anterior and posterior surfaces to undergo an increase in curvature (Fig. 3). H. TSCHERNING’S THEORY OF ACCOMMODATION Tscherning (28) challenged the Helmholtz theory of accommodation, believing that with accommodation there is an increase in traction of the zonular fibers at the lens equator and that the curvatures of the central lens increase while those at the periphery flatten on account of the greater resistance and steeper curvatures of the lens nucleus (Fig. 4). In other words, with a traction of the zonular fibers, the softer cortex is molded around the harder nucleus, so that the central lens surface curvatures more closely resemble the steeper central curvatures of the lens nuclear surface. Tscherning also believed that the vitreous provided a force on the lens posterior surface to aid in the accommodative mechanism. Tschering’s accommodative mechanism required no significant modification of the anatomy of the accommodative apparatus as Helmholtz had described it.

Figure 4 Tscherning (Ref. 28.) proposed an alternative mechanism of lenticular accommodation. (A) The unaccommodated lens is shown as a solid line with the accommodated lens superimposed as a dashed line. Tscherning believed that the accommodative change in the form of the lens occurred as a consequence of an increase in traction of the zonular fibers at the lens equator. Thus, as depicted by Tscherning, the unaccommodated lens has a larger diameter, but the lens undergoes no change in axial thickness. The anterior surface of the lens is to the left. (B) Tscherning believed this change in form of the lens occurred as a consequence of the relatively softer cortex being molded around the relatively hardened nucleus. He believed the surfaces of the nucleus to be more steeply curved than the surfaces of the lens. With an increase in traction of the zonular fibers at the lens equator the peripheral lens surfaces are flattened while at the middle of the lens the curvatures increase. The cornea and anterior lens surface are on the left of the diagram. (From Ref. 28.)

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I. SCHACHAR’S THEORY OF ACCOMMODATION Schachar too has proposed that accommodation occurs through an increase in zonular tension, essentially restating Tscherning’s theory. Unlike Tscherning’s theory, however, Schachar’s theory requires significant modification of the accommodative anatomy. Schachar requires that the zonular fibers insert into the anterior face of the ciliary muscle, which Schachar believes moves backward in the eye with an accommodative effort. Schachar’s theory also requires that separate and discrete zonular fiber bundles insert to that lens anterior, equatorial, and posterior surfaces and that the tension on these discrete subgroups be differentially adjusted with accommodation. Like Tscherning, Schachar proposes that when the ciliary muscle contracts with accommodation, there is an increase in zonular tension at the lens equator, but that the tension of the zonular fibers on the lens anterior and posterior surfaces relax during accommodation. Schachar believes that the increased zonular tension at the lens equator results in an increase in lens equatorial diameter, but that the release of zonular tension on the lens anterior and posterior surfaces results in a flattening of lens peripheral surfaces and an increase in curvature at the center of the lens.

J. DEBATE OVER THE ACCOMMODATIVE MECHANISM Central to the debate over the Helmholtz and Schachar theories of accommodation is the mechanism by which the ciliary muscle/zonular complex acts on the lens. Cramer (29), by observing minification of Purkinje images reflected off the anterior lens surface with accommodation, first unequivocally demonstrated that the crystalline lens anterior surface undergoes an increase in curvature with accommodation (see appendix in Ref. 29). Cramer’s belief that this was mediated by a contraction of the iris sphincter was later disproved by von Graefe (31), who observed that an aniridic patient had normal accommodation. Helmholtz, apparently unaware of Cramer’s work, subsequently and independently also observed minification of Purkinje images of the anterior lens surface with accommodation. It is beyond debate that for accommodation to occur, the lens power must increase, and that this is accomplished in part through an increase in the lens anterior surface curvature. However, the Helmholtz accommodative mechanism on the one hand and the Tscherning/ Schachar theories on the other are at odds as to how this occurs.

K. TSCHERNING’S STUDIES Young (32) stated that the amplitude of accommodation diminishes toward the periphery of the pupil. Tscherning observed in his own eye that, with accommodation, the refraction at the center of his pupil increased more than the refraction at the periphery. Tscherning arrived at this conclusion from observations of the change in the appearance of the pointspread of his eye and by positioning Young’s double-slit optometer in the center and toward the periphery of his pupil during accommodation. Tscherning believed the Helmholtz accommodative mechanism to be incorrect because it provided no obvious explanation for this observation. Tscherning believed that this could be explained only by a steepening of the central lens and a flattening of the peripheral lens.

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In an attempt to prove his accommodative mechanism, Tscherning studied the behavior of bovine lenses (Fig. 5). He observed that when inward pressure was applied at the lens equator, the anterior and posterior surface curvatures flattened; but when outward zonular tension was applied at the lens equator, the anterior surface curvature increased. Schachar also performed similar experiments on bovine lenses to provide experimental support for his accommodative mechanism and recorded an increase in optical power of the lens with outward-directed zonular tension at the lens equator (33). The bovine eye and lens bear little resemblance to that of the primate. The bovine eye is unlikely to accommodate, since it has a diminutive ciliary muscle (34) and a lens that is considerably thicker, more spherical, and harder than the primate lens. The paradoxical optical results that Tscherning and Schachar et al. (28,35) observed from tests on bovine lenses may be due to the fact that the bovine lens is structurally and functionally quite different from the primate lens. It is inappropriate to draw conclusions on the accommodative performance of the primate lens or on the primate accommodative mechanism from observations of the

Figure 5 Tscherning (Ref. 28.), like Schachar et al. (33), performed experiments on bovine lenses. (A) When Tscherning applied a squeezing force to the equator of the bovine lens, a peripheral flattening and central steepening resulted (solid line) relative to unstressed lens (dashed line). (B) Tscherning believed that the nucleus was harder and had steeper curvatures than the surfaces of the lens and so provided a resistive force around which the cortex is molded. (C) When Tscherning applied a stretching tension to the lens equator (solid line), the softer lens cortex was molded around the hardened nucleus such that there is an increase in curvature at the center of the lens relative to the unstretched lens (dashed line). Note that there is no change in thickness of the lens with either squeezing or stretching. While this may be an accurate depiction of the behavior of the bovine lens, this lens is harder and more spherical than that of the primate lens and is from an animal that probably has no accommodation. Results from studies on bovine lenses cannot be extrapolated to prove anything about the accommodative performance of the human lens or the accommodative mechanism of the human eye. It is well established, for example, that there is an increase in axial thickness of the human lens during accommodation. (From Ref. 28.).

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performance of bovine lenses. Tscherning found no change in axial thickness of the bovine lens with stretching, and Schachar (33) does not mention lens thickness. It is well established that the lens thickness increase by 10% with accommodation in the human eye (35,36). Our recent results show a 23% increase in lens thickness with 12D of accommodation in young rhesus monkey eyes (unpublished observations). When accommodation tests are performed on primate lenses known to be capable of accommodation, very different results from those of Tscherning and Schachar are found. Outward-directed zonular tension applied to young primate lenses causes a decrease in power due to flattening of the lens surface curvatures, in accordance with the Helmholtz accommodative mechanism (11). The extent of change in lens power at any age matches the expected accommodative amplitude (11). It is possible to demonstrate paradoxical optical effects of mechanical stretching on bovine lenses (33), artificial fluid-filled lenses (37–39), or air-filled Mylar balloon lenses (40). However, these lenses bear little resemblance to the primate lens, so there is little that can be concluded about accommodation in primates from tests on such lenses. Both Tscherning’s and Schachar’s theories require some part of the anterior-internal aspect of the ciliary muscle to recede to increase zonular tension at the lens equator during accommodation. Subsequent to Helmholtz’s description of accommodation, even Tscherning (28) himself was aware of reports that described how, in aniridic patients, the ciliary processes could be observed to move (“swell”) toward the lens equator and that the lens diameter was observed to decrease with accommodation. Lens diameter is observed to decrease with accommodation in human eyes (41). Ultrasound biomicroscopy and goniovideography shows similar accommodative movements in monkey eyes (Fig. 6) (42). These observations contradict the mechanistic descriptions of Tscherning and Schachar. Schachar has postulated how the ciliary muscle contracts to increase zonular tension based on an analysis of a histological section (43). However no direct evidence exists to support the proposed movements of the ciliary muscle, and ultrasound biomicroscopy of the accommodative movements of the ciliary body (42) does not support the mechanism of action required by Schachar. L. MEASUREMENT OF ACCOMMODATION Tscherning begins his chapter on the accommodative mechanism with a section on the measurement of the amplitude of accommodation, in which he writes “to determine [the near point] exactly is generally of little practical importance.” The significance of this misconception is no more certain than today. Despite claims that accommodation is restored in presbyopes, there are no published objective measurements to demonstrate this. Subjective near reading tests used to determine if scleral expansion restores accommodation (44) are inaccurate and unreliable and do not unequivocally measure accommodation. The only documented attempt to measure accommodation postoperatively in scleral expansion patients using objective methods found none (45). Accurate, objective measurement of accommodation is imperative to establish the efficacy of surgical procedures claimed to restore accommodation. Tscherning did not have access to infrared optometers and other objective instruments that are available today to measure accommodation. Unlike the push-up test that is used clinically, these instruments are capable of unequivocally measuring accommodation dynamically and objectively. While the push-up test provides an indication of near reading ability, in some cases this may have no relationship to accommodative ability. For example if the push-up test were used to measure accommoda-

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Figure 6 Recent experiments on iridectomized rhesus monkeys using Edinger-Westphal stimulated accommodation are in agreement with the Helmholtz accommodative mechanism (42). (A) A gonioscopy lens placed on the temporal cornea allows visualization of the ciliary processes and lens equator. (B) The movements of these structures can be observed during accommodation. (C) The subtracted image pair shows that the eye remains relatively stable during accommodation, but there is a pronounced movement of the ciliary processes and lens equator away from the sclera with accommodation. (D) The ciliary muscle and lens equator can be observed with ultrasound biomicroscopy (UBM). (E) The apex of the ciliary muscle and the lens equator move away from the sclera during accommodation. (F) The subtracted image pair shows that while the eye is relatively stable, the ciliary muscle and lens equator move away from the sclera during accommodation. (G) The entire equatorial diameter of the lens can be seen when a Goldman lens is placed on the cornea. (H) With accommodation, there is a concentric decrease in equatorial diameter of the crystalline lens and an inward movement of the ciliary processes. (I) The subtracted image pair shows that the eye remains relatively stable relative to the pronounced accommodative movements that are observed. Each of the movements observed are in accordance with the Helmholtz accommodative mechanism and opposite to those proposed by Schachar. The accommodative movements observed, such as a concentric decrease in lens diameter (G–I), cannot be explained by eye movements. (From Ref. 42.)

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tion in a presbyope wearing multifocal contact lenses, one might erroneously conclude that active accommodation is present. The multifocal contact lenses may provide functional distance and near reading ability but obviously without restoring accommodation. Clearly the push-up test does not unequivocally measure accommodation and cannot differentiate multifocality from functional accommodation. An objective optometer that dynamically measures the refraction of the eye is the appropriate method to unequivocally demonstrate the presence of accommodation. While Tscherning may not have appreciated the importance of accurate measurement of accommodation, he was aware of good methods to stimulate accommodation. Tscherning described the use of topical instillation of a muscarinic agonist to stimulate accommodation. Muscarinic agonists such as pilocarpine and carbachol act directly on the acetylcholine receptors of the ciliary muscle and cause it to contract. If the optical refractive power of the eye is measured with an objective optometer before and after the instillation of topical pilocarpine, for example, the optometer will record a change in refraction as accommodation occurs. Depending on the drug’s concentration, its penetration into the eye, and the amount absorbed by the ciliary muscle, the accommodative response may vary. While pharmacological stimulation may not stimulate maximal accommodation and would therefore not provide an accurate measure of the full accommodative amplitude, it will provide an objective demonstration of whether accommodation is present. M. HELMHOLTZ’S CONTRIBUTION From his observations of the eye during accommodation, Helmholtz noted that the anterior surface of the crystalline moves forward and that the anterior lens surface curvature increases (a decrease in the radius of curvature). This latter observation was demonstrated by observing the minification of the third Purkinje image reflected from the anterior lens surface. Helmholtz also observed an apparent minification of the posterior lens surface’s Purkinje images and concluded from calculations that the curvature of the posterior lens surface increases slightly with accommodation but without appreciable movement of the posterior lens surface. Helmholtz suggested that these observations meant that the lens axial thickness increased by about 0.5 mm with accommodation and, that since the lens volume is constant, the equatorial diameter of the lens must be reduced with accommodation. As to the mechanism by which the observed accommodative changes occur, Helmholtz was less certain due to the difficulties in observing the accommodative movements of the ciliary body directly. Prior to Helmholtz, Cramer and Donders believed that the iris and the ciliary muscle induced accommodation of the lens. They supposed that the iris pushed backward on the peripheral anterior surface of the lens and that the ciliary muscle increased the vitreous pressure behind the lens. Helmholtz recognized that this was inconsistent with the increase in lens thickness that he had observed. Helmholtz believed that the mechanism proposed by Cramer and Donders would tend to decrease lens thickness and flatten the posterior lens surface. Helmholtz believed that when the eye is focused at distance, the lens is stretched by the zonule attached to the lens equator. Based on an understanding of the anatomical attachment of these zonular fibers to the ciliary body, Helmholtz hypothesized that with a contraction of the ciliary muscle, the zonular insertion in the ciliary body is moved toward the lens to release the tension at the lens equator, allowing a decrease in lens diameter, an increase in lens thickness, and an increase in both lens surface curvatures.

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Observations of accommodation in a patient with a paralyzed iris and in another with a completely detached iris convinced Helmholtz that the iris did not cause the accommodative change in the lens. Helmholtz also observed that the form of the lens is changed and that it becomes thicker on cutting the zonule. He did not believe that the lens was composed of a lens muscle (musculus crystallinus), as others had suggested, but, in describing the accommodative mechanism, he also failed to provide an explanation why this change in the form of the lens occurs. From his observations, Helmholtz ultimately concluded that the ciliary muscle was responsible for inducing accommodation. Helmholtz was aware of Mu¨ller’s (5) description of circular fibers of the ciliary muscle and appreciated that it acted as a sphincter muscle in conjunction with the meridional and radial fibers. In particular, a contraction of the circular and meridional fibers moves the tip of the ciliary processes toward the lens equator to release zonular tension. Helmholtz was unsure if the ciliary processes push directly on the lens equator, as occurs in birds eyes with accommodation, since he could not directly observe the edge of the lens. Although this is unlikely to occur in human eyes, it is observed to occur at maximum accommodation in iridectomized monkey eyes (42). Thus, Helmholtz recognized that, at rest, zonular tension pulls outward on the lens equator and that a contraction of the ciliary muscle moved the ciliary processes toward the lens equator and released tension on the zonule, allowing an increase in lens anterior and posterior surface curvatures, an increase in lens thickness, a decrease in lens diameter, a forward movement of the lens anterior surface, and little or no movement in the posterior lens surface. Although Helmholtz provided a comprehensive and accurate description of how accommodation occurs, he gave no indication of how or why the lens becomes accommodated, simply assuming that it did this through its supposed elasticity. He made no mention of a role for the lens capsule, the posterior zonular fibers, or the elasticity of the posterior attachment of the ciliary muscle to the choroid, all anatomical structures now known to play important roles in accommodation. Helmholtz also believed that the posterior lens surface does not move with accommodation, but this is now well documented to occur (46,47). N. GULLSTRAND’S CONTRIBUTION Gullstrand also contributed to our current understanding of accommodation in the appendix to Helmholtz’s posthumous third edition of the Treatise on Physiological Optics. Gullstrand’s descriptions built on the groundwork that Helmholtz had laid. On summarizing the knowledge concerning the lens posterior surface, Gullstrand wrote: “The only definitive conclusions that can be drawn from these investigations is that as yet there is no proof of a change in position of the posterior surface of the lens in accommodation, and that the curvature of the posterior surface of the lens increases in accommodation, though to a very slight extent.” Gullstrand’s investigations suggested that with accommodation, the anterior lens surface radius of curvature decreased from 10.0 to 5.33 mm and that the anterior lens surface moved forward by 0.4 mm. More recent measurements suggest forward movement of the anterior lens surface of between 0.2 to 0.3 mm with accommodation (46). Gullstrand inferred a role for the lens capsule in describing the intracapsular accommodative mechanism. He described that the lens undergoes accommodative changes as a consequence of the extracapsular accommodative changes.

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Helmholtz had correctly postulated that zonular tension at the lens equator is released during accommodation. Gullstrand showed that evidence for this had been presented by Hess (48), who demonstrated that, with a strong accommodative effort, the lens sags downward in the direction of gravity, that there is an increase in amplitude of accommodation when the head is bent forward and a decrease when the head is bent backward, and that the lens sags sagittally downward in the frontal plane after administration of eserine to induce accommodative spasm. O. FINCHAM’S CONTRIBUTION Fincham (13) made significant contributions to what we understand about accommodation today. He showed that the zonule is an elastic tissue and repeated observations made by Tscherning, Helmholtz, and others on the accommodative changes in curvature, lens thickness, anterior chamber depth, and vitreous chamber depth. Fincham identified that the lens thickness increases to a greater degree than the anterior chamber decreases with accommodation and therefore that the lens posterior surface moves backward with accommodation. From his measurements of accommodation in an eye with traumatic aniridia, Fincham observed centripetal movement of the ciliary processes and a smaller decrease in lens diameter. He also observed that with accommodation, both the lens nucleus and lens surface undergo similar change in curvature, demonstrating that the whole of the lens substance rather than just the lens cortex is involved in accommodation. Together with Graves (49), Fincham observed that in the empty capsular bag of a patient with traumatic aphakia, the anterior and posterior capsular surfaces were flattened and parallel to each other in the unaccommodated state but became flaccid, widely separated, and wrinkled during an accommodative effort. Fincham concluded that the capsule is held under tension in the unaccommodated state and that the tension is released with accommodation. Fincham also measured greater changes in the anterior chamber depth with accommodation when a subject is looking down than when looking forward, supporting an accommodative release of zonular tension. He observed, in a young enucleated eye, that the lens takes on a more accommodated form, with increased anterior surface curvature, when the zonule is cut and the lens freed from the zonular suspension and that when the capsule is removed, the lens substance tends to take on the unaccommodated form. All these observations led Fincham to the inevitable conclusion that accommodation is caused by capsular molding of the plastic lens substance into an accommodated form. Fincham studied the capsules of various animal species in histological section and found them to be of relatively uniform thickness in nonaccommodating mammals, but in humans it was thinnest at the posterior pole and of maximum thickness on the anterior surface about 2 mm from the equator and on the posterior surface about 1 mm from the equator. Fincham described how these variations in capsular thickness allow the lens polar surfaces to undergo steeper changes in curvature with accommodation than the peripheral lens surfaces, thus allowing the accommodated lens to take on a conoidal form. Finally, Fincham restates the Helmholtz accommodative mechanism, but now with the recognition that resting zonular tension pulls the lens into a flattened and unaccommodated form and that the capsular forces mold the lens into an accommodated form when zonular tension is released. Fincham recognized that presbyopia and the loss of accommodative amplitude can be explained simply by the lens substance losing its elasticity and the capsule failing to be able to mold the hardened lens. In accordance with Smith’s (22) observation that the equatorial diameter of isolated lenses does not reflect the diameter of the lens in the living eye, Fincham stated that when

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Figure 7 (A) Fincham (13) showed that the primate lens capsule is not of uniform thickness. A diagram of the capsule, in which thickness is exaggerated relative to size, shows the posterior surface to be thinner than the anterior surface and regions of increased thickness on the anterior and posterior peripheral surfaces. The elasticity of the capsule provides the force to mold the lens substance into an accommodated form. In the absence of the capsule, the lens substance is in a flattened and maximally unaccommodated form. When outward-directed zonular tension is released with accommodation, the capsule molds the lens to increase the lens anterior and posterior surface curvatures. (B) In support of this capsular theory of accommodation, Fincham cites the evidence from Graves (49) of the behavior of the empty capsular bag in a patient with traumatic aphakia. In the unaccommodated state, the anterior and posterior capsular surfaces were flat against each other. With a voluntary accommodative effort, the two surfaces became more flaccid and separated slightly. After the iris was dilated and accommodation was stimulated with eserine, the two surfaces of the capsule separated widely and the posterior surface (P) moved backward in the eye, becoming flaccid and wrinkled, while the anterior surface (A) showed a forward curve. (From Ref. 13.)

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removed from the eye and isolated from external zonular forces, younger lenses tend to become accommodated while older presbyopic lenses do not undergo a change in shape. P. EVIDENCE AGAINST SCHACHAR’S THEORY OF ACCOMMODATION While Schachar’s theory of accommodation has been widely discussed, when scrutinized with results from the nearly 150 years of research on accommodation since Helmholtz, numerous inconsistencies appear. Schachar’s theory requires that accommodation occur through an increase in the lens surface curvatures consequent to an increase in zonular tension at the lens equator, but without any significant change in the lens thickness. If anything, increased tension on the zonule at the lens equator would be expected to decrease its thickness. However, the lens is well documented to undergo an increase in axial thickness with accommodation. This is readily documented by A-scan ultrasonography (50) but has most convincingly been documented by studies in which an ultrasound transducer was vacuum suctioned to the sclera of the eye to ensure that the transducer did not move with respect to the axis of the eye when accommodation occurred (36). In addition, increases in lens thickness have also been measured during accommodation to an aligned optical target with partial coherence interferometry, a noncontact, high-precision measurement technique (46). These studies show a 0.5-mm increase in the lens axial thickness with accommodation. An increase in thickness of this magnitude could not occur under Schachar’s theory, with an increase in zonular tension. These studies of accommodative changes in the lens also show that the lens posterior surface moves backward in the eye to decrease vitreous chamber depth and that the lens anterior surface moves forward to decrease anterior chamber depth. It is impossible, under Schachar’s theory, to explain how lens thickness can increase and anterior chamber depth and vitreous chamber depth decrease during accommodation with an increase in zonular tension at the lens equator. Schachar’s theory requires that that the zonule at the lens equator be composed of three separate and distinct subgroups—anterior, posterior, and equatorial bundles (43,51). Scanning electron micrographic studies (6) and direct examination of the zonule in enucleated human eyes (11) do not support this view. Further, Schachar’s theory requires that the equatorial zonular fibers be attached to the anterior face of the ciliary muscle just beneath the root of the iris—the region of the ciliary muscle that Schachar believes to move outward to selectively increase the tension on the equatorial zonular bundle (43). Direct examination of the ciliary body shows that the zonular fibers attach all along the pars plicata and not to the anterior face of the ciliary muscle, as required by Schachar’s theory. Ultrasound biomicroscopy shows this anterior face of the ciliary muscle to move forward with accommodation (42) rather than backward, as required by Schachar’s theory. Schachar’s theory requires that the lens equator move toward the sclera by 50 ␮m with accommodation (52). Independent experiments have imaged movements of the lens equator in several different ways during centrally or pharmacologically stimulated accommodation in iridectomized monkey eyes (42). Swan-Jacob gonioscopy and ultrasound biomicroscopy showed a 0.25-mm movement of the lens equator away from the sclera during accommodation. Imaging with a Goldman lens showed a concentric decrease in the crystalline lens diameter with accommodation. Pharmacologically stimulated accommodation, not subject to the systematic convergent eye movements that occur with centrally stimulated accommodation, also showed movement of the lens equator away from the

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sclera and a concentric decrease in lens diameter. The lens was also observed to sag downward under the influence of gravity during accommodation irrespective of the orientation of the head, thus demonstrating that zonular tension is reduced rather than increased as required by Schachar’s theory. Sutures were placed beneath the medial and lateral rectus muscles to reduce eye movements that occur with centrally stimulated accommodation.

Q. EVIDENCE AGAINST SCHACHAR’S THEORY OF PRESBYOPIA Schachar’s theory of presbyopia also fails on scrutiny at many levels. Fundamental to Schachar’s theory of presbyopia is his claim that the lens grows throughout life, increasing in equatorial diameter by 20 ␮m per year. It is this increased lens diameter that Schachar suggests results in crowding of the posterior chamber with a consequent loss of resting zonular tension. Schachar’s claims for an increase in lens diameter come from a single study in which lens diameter was measured in isolated human lenses (22). Rafferty (23) cites this study when stating that the lens undergoes an increase in diameter of 0.02 mm/ year. Rafferty (23) is the single source cited by Schachar to support the notion that the lens grows in equatorial diameter (24,25,40,51–53). Smith (22) recognized that his measurements of the diameter of the isolated lens do not reflect the diameter of the lens in the living eye. Smith (22) states that when the lens is removed from the eye, it undergoes a change in shape becoming more accommodated, relatively more so for the younger than the older lenses. These data do not reflect equatorial growth of the lens. Only recently has technology become available to measure lens diameter in vivo in living human eyes. Lens diameter measured with MRI in living eyes shows no increase with increasing age (26). The MRI study does show an age-dependent decrease in circumlental space or distance between ciliary processes and lens equator. However; this is clearly not due to increased lens diameter but may be due to an age-related change in configuration of the ciliary body (54). Based on his theory of accommodation and presbyopia, Schachar has suggested that accommodation can be restored by scleral expansion (24). Setting the numerous problems with Schachar’s theory of accommodation aside, under the classic notion that presbyopia occurs due to an increased hardness or “sclerosis” of the lens, it is hard to understand how accommodation could be restored by scleral expansion. Mechanical stretching experiments of human eye bank eyes suggests that the presbyopic lens is incapable of being made to undergo accommodative changes (11). These experiments show that young lenses can be made to undergo accommodative changes in focal length matching accommodative amplitudes in youth, but that when lenses over the age of 60 years are subjected to the same mechanical tests, they fail to undergo any change in focal length. This result is supported by the MRI studies showing that in presbyopes, accommodative movements of the ciliary body occur, but without changes in the lens (26). The human lens undergoes a fourfold increase in hardness over the human life span (16). Scleral expansion cannot restore the accommodative capacity to the crystalline lens. While scleral expansion possibly may increase resting zonular tension or even enhance the efficacy of ciliary muscle contraction, this is unlikely to provide sufficient force to enable presbyopic lenses to accommodate. In any event, whatever serendipitous beneficial consequences scleral expansion surgery may have would be undermined by the inevitability of cataract and the required removal of the crystalline lens in cataract surgery.

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R. DOES SCLERAL EXPANSION SURGERY RESTORE ACCOMMODATION? Regardless of the accommodative mechanism or the causes of presbyopia, it is theoretically possible that scleral expansion surgery may restore accommodation through some unknown mechanism. However, the only published objective measurements of accommodation in patients with postoperative scleral expansion show that no accommodation is restored (45). Subjective tests suggest that near reading distance may be temporarily improved following scleral expansion (44). It is not clear why this would occur. The pushup or near reading test that is typically used to assess accommodation postoperatively is inappropriate to determine if accommodation occurs. The push-up test does not unequivocally measure accommodation and is subject to errors due to depth of focus of the eye and ocular aberrations. By definition, accommodation is a dioptric change in optical power of the eye. If accommodation occurs, this can be measured with objective instrumentation designed to measure the optical power of the eye. Unilateral scleral expansion surgery reportedly improves near vision bilaterally. A physiological explanation for this is unlikely, but it may reflect the inadequacy of subjective accommodation testing. It is possible, for example, that scleral expansion surgery may inadvertently introduce corneal or lenticular aberrations or some degree of multifocality to the eye. While this may prove beneficial to provide some degree of functional near vision, it is clearly not accommodation. Schachar has suggested that this is not the cause of the improved near vision, since keratometry is unaltered by scleral expansion (24). However, this does not address the possibility of aberrations in the lens. In addition to instrumentation available to measure accommodation objectively, excellent wavefront technology exists to objectively measure the aberrations of the eye. These measurements should be made pre- and postoperatively, in conjunction with objective and appropriate measurements of accommodation to demonstrate if there are any benefits to scleral expansion. REFERENCES 1. von Helmholz H. Ueber die Accommodation des Auges. Arch Ophthalmol 1853; 1:1–74. 2. von Helmholz HH. Handbuch der Physiologishen Optik. In: Southall JPC, trans. Helmholtz’s Treatise on Physiological Optics. New York: Dover, 1962:143–172. 3. Tamm ER, Lu¨tjen-Drecoll E. Ciliary body. Micro Res Tech 1996; 33:390–439. 4. Bru¨cke E. Ueber den Musculus Cramptonianus und den Spannmuskel der Choroidea. Arch Anat, Physiol Wissenschaft Med 1846; 1:370. ¨ ber einen ringfo¨rmigen Muskel am Ciliarmuskel des Menschen und u¨ber den 5. Mu¨ller H. U Mechanismus der Akkommodation. Graefes Arch Ophthalmol 1858; 3:1. 6. Rohen JW. Scanning electron microscopic studies of the zonular apparatus in human and monkey eyes, Invest Ophthalmol Vis Sci 1979; 18:133–144. 7. Glasser A, Croft MA, Brumback L, Kaufman PL. Ultrasound biomicroscopy of the aging rhesus monkey ciliary region. Optom Vis Sci 2001; 78(6):417–424. 8. Farnsworth PN, Burke P. Three-dimensional architecture of the suspensory apparatus of the aging lens of the rhesus monkey. Exp Eye Res 1977; 25:563–576. 9. Schachar RA. Zonular function: a new hypothesis with clinical implications. Arch Ophthalmol 1994; 26:36–38. 10. McCulloch C. The zonule of Zinn: its origin, course, and insertion, and its relation to neighboring structures. Trans Am Ophthalmol Soc 1954; 52:525–585. 11. Glasser A, Campbell MCW. Presbyopia and the optical changes in the human crystalline lens with age. Vision Res 1998; 38:209–229.

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12. Paterson CA, Delamere NA. The Lens. In: WM Hart, ed. Adler’s Physiology of the Eye, 9th ed. St. Louis: Mosby 1992:348–390. 13. Fincham EF. The mechanism of accommodation. Br J Ophthalmol Monogr VIII. 1937:7–80. 14. Scammon R, Hesdorffer M. Growth in mass and volume of the human lens in postnatal life. Arch Ophthalmol 1937; 17:104–112. 15. Weale RA. The Lens. In: The Aging Eye. New York: Harper & Row, 1963:69–102. 16. Glasser A, Campbell MCW. Biometric, optical and physical changes in the isolated human crystalline lens with age in relation to presbyopia. Vision Res 1999; 39:1991–2015. 17. Weekers R, Delmarcelle Y, Luyckx-Bacus J. Biometrics of the crystalline lens. In: J Bellows J, ed. Cataract and Abnormalties of the Lens. Grune & Stratton, 1975:134–147. 18. Koretz JF, Cook CA, Kaufman PL. Accommodation and presbyopia in the human eye. Changes in the anterior segment and crystalline lens with focus. Invest Ophthalmol Vis Sci 1997; 38: 569–578. 19. Dubbelman M, Van der Heijde GL, Weeber HA. The thickness of the aging human lens obtained from corrected Scheimpflug images. Optom Vis Sci 2001; 78:411–416. 20. Dubbelman M, Van Der Heijde GL. The shape of the aging human lens: curvature, equivalent refractive index and the lens paradox. Vision Res 2001; 41:1867–1877. 21. Brown N. The change in lens curvature with age. Exp Eye Res 1974; 19:175–183. 22. Smith P. Diseases of the crystalline lens and capsule: on the growth of the crystalline lens. Trans Ophthalmol Soc U K 1883; 3:79–102. 23. Rafferty NS. Lens morphology. In: Maisel H, ed. The Ocular Lens Structure, Function, and Pathology. New York: Marcel Dekker, 1985:1–60. 24. Schachar RA. Cause and treatment of presbyopia with a method for increasing the amplitude of accommodation. Ann Ophthalmol 1992; 24:445–452. 25. Schachar RA. Pathophysiology of accommodation and presbyopia: understanding the clinical implications. J Fla Med Assoc 1994; 81:268–271. 26. Strenk SA, Semmlow JL, Strenk LM, Munoz P, Gronlund-Jacob J, DeMarco KJ. Age-related changes in human ciliary muscle and lens: a magnetic resonance imaging study. Invest Ophthalmol Vis Sci 1999; 40:1162–1169. 27. Keeney AH, Hagman RE, Fratello CJ. Dictionary of Ophthalmic Optics. Boston: ButterworthHeinemann, 1995:4. 28. Tscherning M. Physiologic Optics, 4th ed. Philadelphia: The Keystone Press, 1924:192–228. 29. Cramer A. Het accommodatievermogen der oogen, physiologisch toegelicht. Natuurkundige Verhandelingen vande Hollandsche Maatschappij der Wetenschappen te Haarlem 1853; 1: 139-Haarlem: De Erven Loosjes. 30. Guthoff R, Ludwig K. The Accommodative ability of the eyes. In: Current Aspects of Human Accommodation. Heidelberg: Kaden Verlag, 2001:171–200. 31. Graefe A. Fall von acquirirter Aniridie als Beitrag zur Accommodattionslehre. Arch Ophthalmol 1861; 7:150–161. 32. Young T. On the mechanism of the eye. Phil Trans R Soc Lond 1801; 91:23–88. 33. Schachar RA, Cudmore DP, Black TD. Experimental support for Schachar’s hypothesis of accommodation. Arch Ophthalmol 1993; 25:404–409. 34. Samuelson D. A reevaluation of the comparative anatomy of the eutherian iridocorneal angle and associated ciliary body musculature. Vet Comp Ophthalmol 1996; 6:153–172. 35. Koretz JF, Kaufman PL, Neider MW, Goeckner PA. Accommodation and presbyopia in the human eye—aging of the anterior segment. Vision Res 1989; 29:1685–1692. 36. Beers APA, Van Der Heijde GL. In vivo determination of the biomechanical properties of the component elements of the accommodative mechanism. Vision Res 1994; 34:2897–2905. 37. Schachar RA, Cudmore DP, Black TD, Wyant JC, Shuang VW, Huang T, Mckinney RT, Rolland JP. Paradoxical optical power increases of a deformable lens by equatorial stretching. Ann Ophthalmol 1998; 30:10–18.

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38. Schachar RA, Cudmore DP, Torti R, Black TD, Huang T. A physical model demonstrating Schachar’s hypothesis of accommodation. Ann Ophthalmol 1994; 26:4–9. 39. Schachar RA, Cudmore DP, Black TD. A revolutionary variable focus lens. Ann Ophthalmol 1996; 28:11–18. 40. Schachar RA. Theoretical basis for the scleral expansion band procedure for surgical reversal of presbyopia (SRP). Ann Ophthalmol 2000; 32:271–278. 41. Wilson RS. Does the lens diameter increase or decrease during accommodation? Human accommodation studies: a new technique using infrared retro-illumination video photography and pixel unit measurements. Trans Am Ophthalmol Soc 1997; 95:261–267. 42. Glasser A, Kaufman PL. The mechanism of accommodation in primates. Ophthalmology 1999; 106:863–872. 43. Schachar RA, Anderson D. The mechanism of ciliary muscle function. Ann Ophthalmol 1995; 27:126–132. 44. Malecaze FJ, Gazagne CS, Tarroux MD, Gorrand J. Scleral expansion bands for presbyopia. Ophthalmology 2001; 108:2165–2171. 45. Mathews S. Scleral expansion surgery does not restore accommodation in human presbyopia. Ophthalmology 1999; 106:873–877. 46. Drexler W, Baumgartner A, Findl O, Hitzenberger CK, Fercher AF. Biometric investigation of changes in the anterior eye segment during accommodation. Vision Res 1997; 37:2789–2800. 47. Findl O. IOL movements induced by ciliary muscle contraction. In: Guthoff R, Ludwig K, eds. Current Aspects of Human Accommodation. Heidelberg: Kaden Verlag. 2001:119–135. ¨ ber einige bisher nicht gekannte Ortsvera¨nderungen der menschlichen Linse wa¨hrend48. Hess C. U der Akkommodation. Ber. u¨ber die XXV. Vers. d. Ophth. Ges. Heidelberg. 1896. 49. Graves B. The Response of the lens capsules in the act of accommodation. Trans Am Ophthalmol Soc 1925; 23:184–196. 50. Abramson DH, Coleman DJ, Forbes M, Franzen LA. Pilocarpine. Effect on the anterior chamber and lens thickness. Arch Ophthalmol 1972; 87:615–620. 51. Schachar RA. Is Helmholtz’s theory of accommodation correct? Ann Ophthalmol 1999; 31: 10–17. 52. Schachar RA, Tello C, Cudmore DP, Liebmann JM, Black TD, Ritch R. In vivo increase of the human lens equatorial diameter during accommodation. Am J Physiol 1996; 271:670–676. 53. Schachar RA, Black TD, Kash RL, Cudmore DP, Schanzlin DJ. The mechanism of accommodation and presbyopia in the primate. Ann Ophthalmol 1995; 27:58–67. 54. Tamm S, Tamm E, Rohen JW. Age-related changes of the human ciliary muscle. A quantitative morphometric study. Mech Aging Dev 1992; 62:209–221.

4 Schachar’s Theory of the Mechanisms of Accommodation JAY S. PEPOSE Washington University School of Medicine, St. Louis, and Pepose Vision Institute, Chesterfield, Missouri, U.S.A. MOONYOUNG S. CHUNG Pepose Vision Institute, Chesterfield, Missouri, U.S.A.

A. KEY FEATURES THAT DIFFERENTIATE HELMHOLTZ’S VERSUS SCHACHER’S THEORIES The term accommodation refers to the change in the refractive power of the eye that allows images of near objects to be focused on the retina. The most widely accepted theory to account for the mechanism of accommodation was proposed by Hermann von Helmholtz in 1855 in his Treatise on Physiological Optics. He observed that accommodation involves pupillary constriction and anterior movement of the iris. Helmholtz carefully observed the Purkinje images of the crystalline lens during accommodation using crossed glass plates placed between the subject’s eye and the observer viewing the eye with a telescope. He observed an increase in curvature of the anterior and posterior surfaces of the lens, although the anterior surface became more convex than the posterior surface. He noted that the sagittal thickness of the lens increased and hypothesized that the equatorial diameter of the lens decreased during accommodation. He proposed that these events occurred through contraction of the ciliary muscle. This anterior and axial movement of the muscle results in relaxation of zonular tension, which allows the lens (which is surrounded by its elastic capsule) to round up and increase in optical power, with the lens equator moving away from the sclera (1,2). Helmholtz’s universally accepted theory has recently been challenged by Ronald Schachar’s new theory of the mechanisms underlying accommodation. Schachar (2) pro47

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Figure 1 Effect of equatorial stretch on a deformable lens.

poses that in the unaccommodative state (i.e., when there is minimal optical power), the equatorial zonules are under minimal tension. He suggests that during accommodation, the anterior radial muscle fibers of the ciliary muscle move toward the sclera, with increased tension exerted on the lens exclusively via the equatorial zonules. There is relaxation of the anterior and posterior zonules as the posterior longitudinal and posterior radial fibers are displaced anteriorly. The increase in equatorial zonular tension causes the lens equator to move toward rather than away from the sclera. Schachar proposes that this transduction in the force of the ciliary muscle to the lens via the equatorial zonules results in steepening of the central lens and flattening at its periphery. This causes an increase in optical power along with a reduction in spherical aberration. To illustrate this type of lens deformation, Schachar utilizes a Mylar balloon to demonstrate his theory (Figs. 1 and 2). If the equator of a biconvex air-filled Mylar balloon is stretched, the reflections from the center of the balloon minify while the reflections from its periphery enlarge, demonstrating that the center of the balloon is steepened with equatorial stretching while the periphery is flattened. Schachar also states that since the effective working distance between the ciliary muscle and the equator of the lens decreases throughout life secondary to normal lens growth, the force that the ciliary muscle can

Figure 2 Effect of equatorial stretch on periphery of a deformable lens.

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apply to the lens equator decreases linearly with age, resulting in a linear decrease in the amplitude of accommodation (i.e., presbyopia). 1. Schachar’s Supporting Data Schachar first showed experimental support of his theory by progressively stretching the sclerae and ciliary bodies of bovine eyes and then measuring the change in focal length and equatorial diameter of the lens. All eyes showed a decrease in focal length and therefore an increase in the optical power as well as an increase in equatorial diameter (3). Schachar (4) has also constructed a physical model of the variable-focus lens using a gelatin-filled balloon that can change optical power to 10 D, simulating an aspect of his theory of accommodation. Profile photographs were taken of a gelatin-filled balloon relaxed and stretched at the equator. He was able to prove, both with the photographs and mathematically, that with equatorial stretching, the central anterior lens becomes steeper, the peripheral anterior lens becomes flatter, and there is no change in the posterior radius of curvature. Schachar (5) used a vertical scanning interference microscope to measure the mean radius of curvature of both anterior and posterior surfaces of constant-volume, deformable, waterfilled lenses prior to and during stepwise equatorial stretching. Central steepening and peripheral flattening of the lens was again demonstrated. In another study, high-frequency, high-resolution anterior segment ultrasound biomicroscopy was used to measure in vivo changes occurring at the lens equator in 12 young human subjects during pharmacologically controlled accommodation (6). The patients ranged in age from 20 to 34 years with a mean age of 26 years and a standard deviation of 5 years. The patients had a correctable visual acuity of 20/20 and accommodative mean amplitude of 9.5 D. One drop of 1% tropicamide was placed in the right eye. The pupil and the near point without correction were measured 25 min later using four-point print. Ultrasound biomicroscopy (UBM) was performed using the Humphrey Instruments biomicroscope to image the lens equator in the unaccommodated state. A video recording was made of the UBM images. Later, one drop of 2% pilocarpine was administered in the right eye, and 1 h later the pupil and the near point without correction were measured. Ultrasound biomicroscopy was then performed, after which a video recording was made of the UBM images. The induced accommodation was the difference between the near point measurements after pilocarpine and tropicamide. A frame-by-frame comparison was made between the two videos for each patient, using a video mixer and computer subtraction techniques. Over 20,000 images of each of the 12 subjects were compared. Separate and different images of the same patient in the unaccommodated and the accommodated states were superimposed. The cornea and sclera were used as positional references, which provided a reliable method to avoid errors that accompany misalignment and rotation, since the cornea and sclera do not change position during accommodation. In this study it was demonstrated that, during accommodation, the lens equator moves toward the sclera. The mean displacement of the lens equator toward the sclera was 6.8Ⳳ1 ␮m for each diopter of increase in accommodation (6). This confirmed predictions of previous mathematical and physical models (4,7,8) and was consistent with the increase in the optical power of the bovine lens with equatorially stretching that occurred in Schachar’s previous study (3). Schachar and his colleagues mathematically modeled the human crystalline lens to approximate both the Schachar and the Helmholtz theories of accommodation (9). They used nonlinear finite-element analysis that included the material properties and proper

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boundary conditions approximating the human crystalline lens. They used ANSYS 5.6, a general-purpose, nonlinear, finite-element computer program to perform their analysis. They calculated the amount of force necessary to produce a given amount of equatorial displacement. The thick-lens formula was used to establish the optical power of the crystalline lens. Then the longitudinal spherical aberration of various levels of crystalline lens accommodation was investigated using Zemax EE, an optical computer program. The results of nonlinear finite-element analysis by Schachar et al. demonstrated that only the tension produced solely by the equatorial zonules was able to produce the known properties of the accommodative process, which include an increase in central optical power, and also accounts for the physiological force limitations of the ciliary muscle. They also demonstrated that the increase in equatorial diameter associated with the tension produced by the equatorial zonules was consistent with the ultrasound biomicroscopy measurements showing that the lens equator moves toward the sclera during pharmacologically controlled accommodation. The analysis demonstrated that when the anterior and posterior zonules or all three sets of zonules totally relax, the central optical power of the crystalline lens would decrease, not increase. These results contradict Helmholtz’s theory of accommodation. 2. Clinical and Experimental Data Supporting Helmholtz’s Theory Schachar’s hypothesis of accommodation has recently been challenged. Glasser and Campbell (11,12) isolated human lenses from 27 human eyes aged 10 to 87 years. An in vitro scanning laser technique was used to measure the focal length and spherical aberration of the lenses as the lenses were exposed to increasing and decreasing radial stretching forces through the ciliary body–zonular complex. They demonstrated that for the three youngest lenses (11,31, and 39 year old), the focal length did change with stretch. On the other hand, the older lenses, 54 and the 87 years old, demonstrated no change in focal length over the extent of stretch applied. These results contradict Schachar’s hypothesis of accommodation, which maintains that the lens remain malleable even with increasing age. In a different investigation by Glasser and Campbell (12,13), another group of 19 lenses 5 to 96 years of age were studied. In this group, which included older lenses with signs of early cataract, the focal length increased up to approximately age 65, but then their focal length decreased. Both studies demonstrated that over the years when accommodation is gradually lost due to presbyopia, the focal length of the unstretched lenses gradually increased linearly, supporting a lens/capsule compliance and elasticity-based theory of presbyopia. Glasser and Kaufman (14) studied the accommodative mechanism in six cynomolgus monkeys (10 to 13 year old) and eight rhesus monkeys (6 to 17 years old) with stimulated accommodative amplitudes ranging from 7 and 18 D. The monkeys had complete bilateral iridectomies. Stimulating electrodes surgically implanted in the Edinger-Westphal nucleus were used to induce varying amplitudes of accommodation. Accommodation was also induced and reversed in several other cynomolgus and rhesus monkeys. Carbachol chloride iontophoresis, topical pilocarpine hydrochloride, and systemic pilocarpine hydrochloride were the agents used to stimulate accommodation, and topical and systemic atropine sulfate was used to reverse the accommodation. Goniovideography of the iridectomized eyes was performed, demonstrating the tips of the ciliary processes, the anterior zonular fibers, and the lens equator. Ultrasound biomicroscopy was also performed using the Humphrey Instruments biomicroscope. Gonioscopy

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was imaged and recorded at the slit lamp. Measurements of the movement of the lens equator and ciliary processes were taken from image analysis of the goniovideography sequences. The refractive state of the eye during accommodation was recorded using the Hartinger coincidence refractometer (Jenoptik, Jena, Germany). Refractions at baseline and with accommodation were recorded at each stimulus amplitude. The accommodative amplitude at each stimulus was the difference between the two refractions. The results of these studies of dynamic accommodation showed that the ciliary body and the lens equator moved away from the sclera during both centrally and pharmacologically stimulated accommodation, contrary to Schachar’s theory of accommodation, which states that the lens equator moves toward the ciliary processes. Schachar has claimed that the experiments by Glasser and Kaufman were flawed (15). He states that because the sutures placed in the cornea as a reference point and the corneal Purkinje images did not subtract out, there was eye movement between the imaging device and the eye. He then states that Glasser and Kaufman did not have any controls to prove that the small amount of eye movement seen in their experiments did not account for the changes in the crystalline lens size. In Glasser and Kaufman’s experiments, when they fixated the lateral rectus to reduce eye movement, the crystalline lens equator moved toward the sclera with anterior and posterior zonular relaxation. The authors state that this movement of the lens was secondary to lateral translation of the crystalline lens, but Schachar has argued that this mechanism is mechanically impossible. He states that with anterior and posterior zonular relaxation, because the crystalline lens is denser than water and vitreous, the crystalline lens equator can only move toward the temporal sclera by an active force generated by the equatorial zonules. Wilson and Merin (16–18) also demonstrated, using infrared videophotography in a young human subject with ocular albinism, that the lens equator moved away from the sclera and that its diameter decreased during accommodation. However, Schachar (15) has challenged their study. He states that since the measurements were taken only when the circular light was concentric with the pupil and that, in order to keep the light concentric with the pupil, the alignment between the eye and the camera must have changed between the measurements made of the unaccommodated and accommodated states, since the pupil moves nasally during pupillary constriction. He also notes the presence of rotation of the eye relative to the axis of the camera, which is demonstrated by measuring the horizontal diameter of the cornea in the unaccommodated and accommodated states. Strenk et al. used high-resolution magnetic resonance imaging (MRI) to examine changes in the human ciliary muscle and crystalline lens during minimal and maximal accommodation (18). Magnetic resonance images from 25 subjects, ranging from 22 to 83 years of age, were taken. Measurements of the ciliary muscle ring’s diameter, lens thickness, and equatorial diameter of the lens under minimum and maximal accommodation were obtained from the magnetic resonance images. A nonmagnetic accommodative stimulus device was used to provide a minimal (0.1 D) or a strong (8.0 D) binocular accommodative stimulus during magnetic resonance imaging. They found that ciliary muscle contractile activity remained active in all the subjects and was reduced only slightly with advancing age. They did find a decrease in the diameter of the unaccommodated ciliary muscle ring and retrolenticular space that correlated highly with advancing age. There was an age-related increase in the unaccommodated lens thickness, but the lens thickness under accommodative effort was only modestly age-dependent. Of note, the lens equatorial diameter did not show any significant change with advancing age in either accommodative state. This latter finding appears to directly challenge one of Schachar’s

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basic tenets—i.e., that a primary mechanism underlying presbyopia is crowding of the ciliary muscle because of a linear increase in lens diameter with age. [Others (12) have argued that the early studies of the diameter of isolated lenses of enucleated eyes did not reflect the diameter of the unaccommodated lens in the living eye, because the younger lenses rounded up when the zonules were cut.] This stresses the importance of being able to make reliable in vivo measurements using techniques such as MRI. As to the subject of reliable measurements, Schachar contends that the results of the MRI study by Strenk et al. were caused by artifact (15). He states that an MRI image of their patient’s eye during accommodation showed that the eye was turned nasally and that there was a change in configuration of the orbital bones, demonstrating that the head and the eye moved during accommodation. He further attests that the measurements of the transverse diameter of the globe, the corneal diameter, and the equatorial diameter of the lens all decrease during accommodation, demonstrating that the image plane of the eye in the unaccommodated and accommodated states was not the same. 3. Studies of Scleral Expansion Surgery to Improve Near Vision Based upon his theory of accommodation and presbyopia, Schachar has developed a number of surgical techniques to expand the sclera, using bands or segments (22), in an effort to increase the effective working distance between the ciliary muscle and the equator of the crystalline lens. Others have attempted to expand the sclera by incisions or laser treatment (15), and these cumulative studies have shown some significant albeit nonuniform improvement in near vision using standard subjective testing. Whether such surgical methods truly restore accommodation has recently been challenged by Matthews (10), who examined three presbyopic patients shortly after scleral expansion surgery and three young control subjects. The presbyopic patients ranged between 50 and 58 years of age. The control subjects were 22, 27, and 29 years of age. All of the patients were asked to focus on an approaching target while accommodation was monitored with a high-speed infrared optometer. The accommodative targets used were either the Maltese cross or a reduced Snellen chart presented monocularly in a Badal optical system. The target luminance was 100 cd/m. The accommodative stimulus changed in increments of 1 D every 10 s, ranging from 0 to 4 D. The investigator concluded that scleral expansion surgery did not restore accommodation in the presbyopic patients tested with this optometer device, which monitors the central 2.2 mm of the pupil. There was no difference in accommodative responses between the two preoperative presbyopic patients and the three postoperative presbyopic patients tested at each incremental accommodative stimulus level. There was also no accommodative response in either presbyopic group. This is in contrast to the three young control subjects, in whom the accommodative response increased by about 450 A/D values per diopter of accommodative stimulus change. Schachar’s response to Matthews’ study can be summarized as follows. First, this group of patients was independently examined by Yang and coworkers (20), who documented a significant improvement in near vision without a change in distance refraction, axial length, or corneal power. Matthews’ study with the optometer did not include any near vision measurements using standard testing methods. The patients had an early prototype of the scleral expansion band (rather than segments) not currently in use, and they were all tested in the very early postoperative period, when tear film abnormalities and superficial punctate keratitis were present. In addition, the infrared optometer, which is generally

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operated in a darkened room, does not offer the usual accommodative stimulus but relies purely on defocus. The instrument, which requires the subject to use a bite plate for stability and alignment, generally takes practice to obtain reliable data, and it was unclear if this level of training and reproducibility was achieved. Glasser and colleagues (12) have speculated that the possible restoration of near vision via scleral expansion could function via nonaccommodative mechanisms, such as inducing multifocality of the crystalline lens. A number of patients in the phase I clinical trial of scleral expansion in the United States are now undergoing wavefront analysis to provide an objective measurement and assess mechanisms that may underlie improvement in near vision after this procedure.

B. CONCLUSION There are few subjects in ophthalmology capable of generating as much lively debate as that of accommodation and presbyopia. The processes of accommodation and disaccommodation are complex, to say the least, and involve changes in muscular, lenticular, and extralenticular components. At some time, almost every one of these components has been proposed as a factor in the development of presbyopia. We have tried in this chapter to present a balanced view of Schachar’s versus Helmholtz’s theory of accommodation, along with experimental evidence and arguments that have been espoused by proponents of both sides. In a number of key respects, the proposed mechanisms are antithetical. The universal nature of presbyopia and the intense interest in its reversal justifies further research in this area to elucidate its pathophysiology.

ACKNOWLEDGMENT Supported by the Midwest Corneal Research Foundation, Inc.

REFERENCES 1. Koretz JF. Accommodation and Presbyopia. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology: Basic Sciences. Philadelphia: Saunders, 1994:270–282. 2. Schachar RA. Is Helmholtz’s theory of accommodation correct? Ann Ophthalmol 1999; 31(1): 10–17. 3. Schachar RA, Cudmore DP, Black TD. Experimental support for Schachar’s hypothesis of accommodation. Ann Ophthalmol 1993; 25:404–409. 4. Schachar RA, Cudmore DP, Black TD. A revolutionary variable focus lens. Ann Ophthalmol 1996; 28:11–18. 5. Schachar RA, Cudmore DP, Black TD, Wyant JC, Shung VW, Huang T, Mckinney RT, Rolland JP. Paradoxical optical power increase of a deformable lens by equatorial stretching. Ann Ophthalmol 1998; 30(1):10–18. 6. Schachar RA, Tello C, Cudmore DP, Liebmann JM, Black TD, Ritch R. In vivo increase of the human lens equatorial diameter during accommodation. Am J Physiol (United States) 1996; 271(3 pt 2): R670–R676. 7. Schachar RA, Cudmore DP, Torti R, Black TD, Huang T. A physical model demonstrating Schachar’s hypothesis of accommodation. Ann Ophthalmol 1994; 26:4–9. 8. Schachar RA, Huang T, Huang X. Mathematical proof of Schachar’s hypothesis of accommodation. Ann Ophthalmol 1993; 25:59. 9. Schachar RA, Bax AJ. Mechanism of accommodation. Int Ophthalmol Clin 2001; 41(2):17–32.

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10. Mathews S. Scleral expansion surgery does not restore accommodation in human presbyopia. Ophthalmology 1999; 106:873–877. 11. Glasser A, Campbell MCW. Presbyopia and the optical changes in the human crystalline lens with age. Vis Res 1998; 38:209–229. 12. Glasser A, Croft MA, Kaufman PL. Aging of the human crystalline lens and presbyopia. Int Ophthalmol Clin 2001; 41(2):1–15. 13. Glasser A, Campbell MCW. Biometric, optical and physical changes in the isolated human crystalline lens with age in relation to presbyopia. Vis Res 1999; 39:1991. 14. Glasser A, Kaufman PL. The mechanism of accommodation in primates. Opthalmology 1999; 106(5):863–872. 15. Schachar RA. Presbyopia: Cause and Treatment. In: Schachar RA, Roy FH eds. Presbyopia: Cause and Treatment. The Hague, The Netherlands: Kugler, 2001:1–20. 16. Wilson RS. Does the lens diameter increase or decrease during accommodation? Human accommodation studies: a new technique using infrared retro-illumination video photography and pixel unit measurements. Trans Am Ophthalmol Soc 1997; 95:261–270. 17. Wilson RS, Merlin LM. Infrared video photographic analysis of human accommodation. Invest Ophthalmol Vis Sci 1997; 38(suppl):S986. 18. Wilson RS, Merlin LM. Infrared video photographic analysis of the lens-zonular-ciliary space in human accommodation. Invest Ophthalmol Vis Sci 1998; 39(suppl):S312. 19. Strenk SA, Semmlow JL, Strenk LM, Munoz P, Gronlund-Jacob J, DeMarco JK. Age-related changes in human ciliary muscle and lens: a magnetic resonance imaging study. Invest Ophthalmol Vis Sci 1999; 40(6):1162–1169. 20. Yang GS, Yee RW, Cross WD, Chuang AZ, Ruis RS. Scleral expansion: a new surgical technique to correct presbyopia. Invest Ophthalmol Vis Sci 1997; 38(suppl):S497. 21. Smith P. Disease of the crystalline lens and capsule: on the growth of the crystalline lens. Trans Ophthalmol Soc UK 1883; 3:79. 22. Schachar RA. Cause and treatment of presbyopia with a method for increasing the amplitude of accommodation. Ann Ophthalmol 1992; 24:445–452.

5 Aging and the Crystalline Lens Review of Recent Literature (1998–2001)

LEO T. CHYLACK, JR. Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, U.S.A.

This chapter on aging and the crystalline lens is based on a review of the literature between 1998 and 2001. Due to the limits on the length of this chapter and the numerous recent publications in this field, I have not been able to cite many important earlier works. I extend my apologies to the authors of these works. Bron et al. (1) published an excellent general summary of the aging lens in 2000. The avascular lens grows throughout life. Being enclosed by a capsule and lacking a means of shedding cells, the lens is an excellent organ in which to study aging. There are changes in lens size, shape, and mass throughout life that occur at different rates. The sagittal diameter of the lens is approximately constant at 9.0 mm., but the anteroposterior distance varies from 2.5 to 3.5 mm. These dimensions may increase in the mature/hypermature cataract. In spite of decreases with age in the radius of the anterior surface of the lens and changes in the points of zonular insertion, the clear lens retains its ability to focus an image clearly on the retina. Although the central epithelial cells divide rarely, they survive throughout life. The germinative epithelial cells are actively dividing cells, and the equatorial epithelial cells undergo terminal differentiation. As lens fibers form, they lose their nuclei and other intracellular organelles; in the deeper cortex, fiber cells are essentially organelle-free. The slightly tortuous course of the long fiber cells as they arch over the equator and meet near the opposite pole to form sutures has been illustrated in elegant studies by Kuszak et al. (2–4). The complexity of these sutures increases with age and may account for the increased light scattering in the zones of disjunction seen biomicroscopically. Lens protein synthesis in the epithelium and superficial cortex continues throughout life, but these proteins undergo several posttranslational changes, among 55

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which are chemical and photochemical oxidation, glycation, and racemization. Antioxidant defense mechanisms may ameliorate some of these posttranslational changes. Also, with increasing age monomeric proteins associate in covalently bound aggregates to form highmolecular-weight aggregates whose hydrodynamic radii approach in size the wavelengths of visible light. As size increases, light scattering also increases to the point of lens opacification and frank cataract. Changes with age in protein conformation and phospholipid composition of fiber membranes increase nuclear rigidity and contribute to presbyopia. This chapter considers many of these changes in more detail. In the past 15 years, epidemiological research on age-related cataracts (ARCs) has revealed risk factors that pertain to behavior (e.g., diet, smoking, lifestyle, drug use) and suggested that ARC may be a preventable disease (5,6). This is most encouraging, for each year increasing percentages of public and private health care budgets are used to provide surgical care for ARC. A. AGING AND CHANGES IN LENS SIZE AND SHAPE Several authors (7–12) have documented the growth of the lens throughout life. Koretz et al. analyzed (24) Scheimpflug photographs of the unaccommodated lens in 100 subjects from 18 to 70 years of age to determine the regions that changed with time. With Scheimpflug optics the lens image is in focus from the anterior to posterior pole. The geometric distortion of Scheimpflug images can be corrected (14), so that accuratemeasures of the lens can be obtained. Koretz et al. measured the lens with Hough transforms and other image analysis methods. The radii of the anterior and posterior surfaces of the whole lens decrease, but the volume increases with increasing age. In contrast, neither the shape nor the volume of the nucleus changes with age. The central clear zone and center of mass of the nucleus move anteriorly with age. The correlation between lens shape and location (relative to the cornea) is very high, confirming earlier results. Also, the anterior movement of the lens with age increases the likelihood of phakic IOL–lenticular touch and complications. Another study (15) explored the relationship of accommodative convergence per unit of accommodative response (AC/A ratio), refractive error, and age to determine if the AC/A ratio was a risk factor for myopia. A high AC/A ratio was associated with—and a risk factor for—rapid onset of myopia. A higher AC/A ratio, associated with a flatter crystalline lens, increased the effort to accommodate, or “pseudocycloplegia.” Accommodative deficits in myopia may be the functional consequence of myopic enlargement of the eye. This enlargement was documented in a study (16) of changes in biometric measurements and refractive errors over a 3-year period in eyes of university students. After 3 years, the mean change in refractive error (in OD) was ⳮ0.52 Ⳮ/ⳮ 0.45D (p ⬍ 0.05). The mean lens thickness increased by 0.07 Ⳮ/ⳮ 0.10 mm (p ⬍ 0.05), and the mean elongation of the vitreous chamber was 0.27 Ⳮ/ⳮ 0.30 mm (p ⬍ 0.05). Regardless of the original refractive error, the change in refractive error over the 3-year period was toward myopia. There were no statistically significant changes in the curvature of the cornea or depth of the anterior chamber. The authors concluded that the myopic shift was due to an elongation of the vitreous chamber. In a study of 1-year-old chickens (17), form deprivation vision such as is obtained through translucent glass or eyelids that have been sutured closed, even in fully grown birds, was associated with a myopic shift that was similar but not as large as that in neonatal chicks. The decreases in retinal dopamine seen in neonatal chicks were also seen

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to a lesser degree in 1-year-old chickens. These studies suggest that form deprivation is one of the mechanisms controlling eye growth and causing myopia. B. AGING AND CHANGES IN REFRACTIVE ERROR The modulation transfer function (MTF) has been used (18) to estimate the overall optical performance of the eye with increasing age. In qualitative terms, the MTF is used to assess optical quality of lens combinations by measuring the degree to which a point source of light is dispersed to a spot, in this case on the retina. The average MTF was determined as a function of age and pupillary size. Not surprisingly, the MTF declined in an approximately linear fashion with age, but it did not vary with gender. The decline in MTF may account for the decline in contrast sensitivity function (CSF) with age. C. PRESBYOPIA In an important paper appearing in 1988 (19), Fisher recounted the classic argument that presbyopia was related to the force of contraction of the ciliary muscle and the resistance to deformation of the crystalline lens. He recounted the view of Donders (20), that presbyopia was caused by a decrease in the force of contraction of the ciliary muscle with age, and the opposing view of Helmholtz (21), that the lens became more difficult to deform with age due to lenticular sclerosis. Fisher found that, in fact, the ciliary muscle undergoes a compensatory hypertrophy as accommodative amplitude decreases with age. The force of contraction is about 50% greater at the onset of presbyopia than in youth. However, because of increased lenticular resistance, its effect on the amplitude of accommodation is small. Fisher claimed that the lens becomes more difficult to deform not because of lenticular sclerosis, since the lens substance does not lose water, but because the capsule loses its elastic force with age and the lens fibers, particularly in the nucleus, become more compacted with age. In fact, the nuclear fiber mass becomes more rigid with age, as was shown in subsequent studies. Since Fisher’s work, considerable progress has been made in our understanding of the mechanisms of presbyopia. In 1991 (22), Pau and Kranz used a fine conical probe and a dynamometer to measure the resistance to penetration of various layers of the lens. The resistance to penetration increased with age, due primarily to a hardening of the nucleus. The cortex did not show this hardening. In an interesting study of the dynamic aspects of accommodation (23), Heron et al. showed that accommodation gain decreased and the phase lag increased with age. Reaction time, response time, and accommodative velocity did not change with age for a target oscillating sinusoidally in a predictable manner at modest amplitude. The main aging effect was a longer than predicted phase lag. In spite of decreasing amplitude of accommodation, other aspects of accommodative function were quite robust in the middle-aged eye. In a very elegant study of accommodation in vivo using magnetic resonance imaging (MRI) in humans, Strenk et al. (24) showed that the muscle’s contraction decreased only slightly with increasing age. A decrease in the diameter of the unaccommodated ciliary muscle ring was highly correlated with advancing age. Unaccommodated lens thickness increased with age, but the thickness of the lens under accommodative effort was only slightly age-dependent. Their data shed light on what has been a lens paradox—namely, the decrease in the ciliary muscle’s diameter and an increase in lens thickness in the unaccommodated eye. These changes showed the greatest correlation with increasing age.

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They concluded that presbyopia was actually due to the loss in ability to disaccommodate due to increases in lens thickness, the inward movement of the ciliary ring, or both. The issue of whether the changes in the human lens are due to changes in the lens fiber mass or changes in the lens capsule were addressed directly in a recent study (25) of the biometric, optical, and physical properties of capsulated and decapsulated lenses. Lens focal lengths, thicknesses, surface curvatures, and spherical aberrations were measured for paired eye-bank lenses. Decapsulating the lens caused changes in focal length similar to those occurring in lenses stretched into an unaccommodated state. These phenomena were attributed to nonsystematic changes in lens curvatures. These data support the concepts that lens hardening is an important factor in presbyopia and that aging changes in the lens are not limited to the loss of accommodation and cataract. In addition there are substantial changes in the optical and physical properties of the lens with aging. It is known that myopes have shallower accommodative stimulus/response functions (26), due possibly to reduced sensitivity to defocus. Jiang and White showed that a near task caused a small increase in the static accommodative response. In both emmetropes and late-onset myopes, near tasks also increased the interval for relaxing accommodation. These data suggest the existence of two subsystems that adapt differently to prolonged accommodative effort. Heron et al. studied dynamic accommodation responses to small, abrupt changes in an accommodation stimulus (27). They concluded that for small stimuli within the amplitude of accommodation, the response dynamics (reaction and response times) over the adult age range (16 to 48 years) remained remarkably constant even though the amplitude of accommodation decreased progressively with age. D. AGING, OXIDATIVE STRESS, LENS OPACIFICATION AND CATARACT Considerable evidence has accumulated implicating oxidative stress as a major risk factor in age-related cataract (ARC) formation. Both chemical oxidation (H2O2) and photo-oxidation (secondary to UV irradiation) have been implicated. In addition to a cumulative increase with age in the oxidative damage to lens proteins and lipids, there is also a gradual reduction in the potency of the lens antioxidant defenses. In a recent study (28), the thiol and carbonyl contents of 62 cataractous (age-related idiopathic, diabetic, and myopic) lenses and age- and sex-matched clear lenses from patients undergoing vitrectomy or giant retinal tear surgery were compared. There was a statistically significant (p ⬍ 0.01), ageassociated inverse relationship between the contents of P-SH and protein carbonyls. The changes were greater in cataractous than clear lenses and greater in diabetic and myopic cataracts than in age-related cataracts. The decrease in P-SH occurred earlier in diabetic and myopic cataracts than in ARCs. An increase in protein carbonyls ⬎2 nmol/mg protein and a decrease in P-SH of ⬍10 to 12 nmol/mg protein were always associated with lens opacification. The tripeptide glutathione (GSH) is present at high concentrations (4 to 6 mM) (29) in the young lens and in the cortex of older lenses. It has been identified as one of the major antioxidant defenses in the lens. The GSH-redox cycle is very active in lens epithelium and cortex. Via this cycle, the lens detoxifies hydrogen peroxide, other active oxygen species, and dehydroascorbic acid. There appear to be separate mechanisms in LECs for the detoxification of hydrogen peroxide and hydroxyl radical. Recently, Truscott (30) and Moffat et al. (31) demonstrated a barrier to free diffusion of GSH within the lens that increases

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with age. The low ratio of GSH/P-SH and the relatively inactive GSH-redox cycle in the nucleus make the nucleus more susceptible to oxidative stress than the cortex. That, indeed, this is the case has been demonstrated in animal models with hyperbaric oxygen (32), UVA irradiation (33,34), and the glutathione peroxidase knockout mouse (35–37). With increased oxidative stress in nuclei of lenses in these animal models, there is an increase in protein disulfides and light scattering. Also with reduced activity of the GSH-redox cycle, there is damage to NaⳭ, KⳭ-ATPase (an enzyme involved with many of the active transport mechanisms in LECs), to cytoskeletal proteins, and to membrane proteins involved in regulating membrane permeability. An excellent review of these topics has recently been published (38). As oxidative stress increases and the size of the GSH pool decreases, some proteins thiols (P-SH) are converted to protein-thiol mixed disulfides (29), either protein-S-Sglutathione (PSSG) or protein-S-S-cysteine (PSSC). The formation of PSSG precedes the formation of PSSP (29) and increases insolubilization of lens proteins. Lou et al. (29) discovered that the early oxidative damage could be reversed if the oxidant was removed in time. This reversal is mediated by the enzyme thiol transferase (TTase), recently found in the lens. Lou et al. showed that recombinant TTase, although requiring GSH for activity, was much more efficient in dethiolating lens proteins than GSH alone. TTase favored PSSG over PSSC and gamma-crystallin-S-S-G over alpha-crystallin-S-S-G. TTase was also remarkably resistant to oxidation. The TTase dethiolase activity reactivates enzymes deactivated by S-thiolation. It is this ability to regulate and repair SH-dependent enzymes that suggests that TTase plays an important role in ARC formation. In a study (39) of ascorbate oxidation and advanced glycation in the lens, the major advanced glycation end product (AGE), N(epsilon)-carboxymethyl-L-lysine (CML), was found to have an EDTA-like (chelator) structure that might bind copper. Ascorbylation led to increased CML formation, copper binding, and free radical formation in the lens. These results suggested that there is a vicious cycle in the lens between AGE formation, lipoxidation, metal binding, and oxidative damage. It is possible that chelators may play a role in the therapy of ARC. In another interesting study of the possible value of antioxidants in the treatment of ARC (40), it was shown that chronic administration of vitamin E, but not of sodium ascorbate, restored the age-associated decrease in GSH content in rat lenses to levels comparable to those in younger rats. The age-associated decrease in lenticular glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase was not reversed by chronic administration of either vitamin E or sodium ascorbate (40). In addition to the age-associated change in lens proteins, there are age-associated changes in lens lipids. The percentage of sphingolipid nearly doubles with age, and there is also an increase in hydrocarbon chain saturation with age. These increases were much greater in the deeper layers of the lens (41). These data support the idea that the degree of lipid hydrocarbon order is determined by the amount of lipid saturation, and this, in turn, is regulated by the content of saturated sphingolipid. Hyperbaric oxygen treatment increases the lipid disorder in the nucleus and the levels of lipid hydroxyl, hydroperoxyl, and aldehydes. The transparency of the nucleus is also reduced as these lipid oxidation products accumulate in the lens. The Roche European-American Cataract Trial (REACT) (42,43), the first prospective, randomized, placebo-controlled clinical trial of oral vitamins E and C, and betacarotene suggested that antioxidant treatment might slow the progression of ARC. A small but statistically significant deceleration of ARC was found after 3 years of treatment in

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a cohort of American and British patients. In this study, the beneficial effect was seen in the entire cohort and in the subgroup of American patients but not in the subgroup of British patients. The basis for the different responses of American and British patients to the antioxidant treatment was not clear but may have been due to the fact that the British patients had slightly more advanced cataracts at entry. E. AGING AND THE ZONULE There has been very little research on the effects of aging on the zonule. Recently, however, a light and electron microscopic study of the human ciliary zonule has been published (44). The organization of the zonule as it inserts into the ciliary body was studied. Fibrillin is the major constituent of the zonule and also of microfibrils. Mutations in the fibrillin gene are thought to underlie the zonular abnormalities of Marfan’s syndrome. With aging, the zonular fiber becomes more fragile, increasing the risk of ocular pathology. REFERENCES 1. Bron AJ, Vrensen GF, Koretz J, Maraini G, Harding JJ. The ageing lens. Ophthalmologica 2000; 214:86–104. 2. Kuszak JR, Sivak JG, Herbert KL, Scheib S, Garner W, Graff G. The relationship between rabbit lens optical quality and sutural anatomy after vitrectomy. Exp Eye Res 2000; 71: 267–281. 3. Kuszak JR, Sivak JG, Weerheim JA. Lens optical quality is a direct function of lens sutural architecture. Invest Ophthalmol Vis Sci 1991; 32:2119–2129. 4. Kuszak JR, Bertram BA, Macsai MS, Rae JL. Sutures of the crystalline lens: a review. Scan Electron Microsc 1984; 3:1369–1378. 5. Rowe NG, Mitchell PG, Cumming RG, Wans JJ. Diabetes, fasting blood glucose, and agerelated cataract: the Blue Mountains Eye Study. Ophthalm Epidemiol 2000; 7:103–114. 6. Klein BE, Klein R, Lee KE. Diabetes, cardiovascular disease, selected cardiovascular disease risk factors, and the 5-year incidence of age-related cataract and progression of lens opacities: the Beaver Dam Eye Study. Am J Ophthalmol 1998; 126:782–790. 7. Kwok LS, Coroneo MT. Temporal and spatial growth patterns in the normal and cataractous human lens. Exp Eye Res 2000; 71:317–322. 8. Bron AJ, Vrensen GF, Koretz J, Maraini G, Harding JJ. The ageing lens. Ophthalmologica 2000; 214:86–104. 9. Treton J and Courtois Y. Evidence for a relationship between longevity of mammalian species and a lens growth parameter. Gerontology 1989; 35:88–94. 10. Brown N. The change in lens curvature with age. Exp Eye Res 1974; 19:175–183. 11. Nordmann J, Fink H, Hockwin O. Growth curve of the human lens. Graefes Arch Klin Exp Ophthalmol 1974; 191:165–175. 12. Spencer RP. Change in weight of the humanlens with age. Ann Ophthalmol 1976; 8:440–441. 13. Koretz JF, Cook CA, Kaufman PL. Aging of the human lens: changes in lens shape at zerodiopter accommodation. J Opt Soc Am A Opt Image Sci Vis 18:2665–2672. 14. Richards DW, Russell SR, Anderson DR. A method for improved biometry of the anterior chamber with a Scheimpflug technique. Invest Ophthalmol Vis Sci 1988; 29:1826–1835. 15. Mutti DO, Jones LA, Moeschberger ML, Zadnik K. AC/A ratio, age, and refractive error in children. Invest Ophthalmol Vis Sci 2000; 41:2469–2478. 16. Kinge B, Midelfart A, Jacobsen G, Rystad J. Biometric changes in the eyes of Norwegian university students—a three-year longitudinal study. Acta Ophthalmol Scand 1999; 77: 648–652.

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17. Papastergiou GI, Schmid GF, Laties AM, Pendrak K, Lin T, Stone RA. Induction of axial eye elongation and myopic refractive shift in one-year-old chickens. Vis Res 1998; 38:1883–1888. 18. Guirao A, Gonzalez C, Redondo M, Geraghty E, Norrby S, Artal P. Average optical performance of the human eye as a function of age in a normal population. Invest Ophthalmol Vis Sci 1999; 40:203–213. 19. Fisher RF. The mechanics of accommodation in relation to presbyopia. Eye 1988; 2:646–649. 20. Donders FC. On the anomalies of accomodation and refraction of the eye: with a preliminary essay on physiological dioptrics. London: The New Sydenham Society, 1864. 21. von Helmholtz H. Treatise on Physiological Optics, translated from the 3d German ed. Vol 1. JPC Southall, ed. Handbuch der physiologischen Optik. (English) Rochester, NY: The Optical Soc America, 1924. 22. Pau H, Kranz J. The increasing sclerosis of the human lens with age and its relevance to accommodation and presbyopia. Graefes Arch Clin Exp Ophthalmol 1991; 229:294–296. 23. Heron G, Charman WN, Gray LS. Accommodation responses and ageing. Invest Ophthalmol Vis Sci 1999; 40:2872–2883. 24. Strenk SA, Semmlow JL, Strenk LM, Munoz P, Gronlund-Jacob J, DeMarco JK. Age-related changes in human ciliary muscle and lens: a magnetic resonance imaging study. Invest Ophthalmol Vis Sci 1999; 40:1162–1169. 25. Glasser A, Campbell MC. Biometric, optical and physical changes in the isolated human crystalline lens with age in relation to presbyopia. Vision Res 1999; 39:1991–2015. 26. Jiang BC, White JM. Effect of accommodative adaptation on static and dynamic accommodation in emmetropia and late-onset myopia. Optom Vis Sci 1999; 76:295–302. 27. Heron G, Charman WN, Schor C. Dynamics of the accommodation response to abrupt changes in target vergence as a function of age. Vis Res 2001; 41:507–519. 28. Boscia F, Grattagliano I, Vendemiale G, Micelli-Ferrari T, Altomare E. Protein oxidation and lens opacity in humans. Invest Ophthalmol Vis Sci 2000; 41:2461–2465. 29. Lou MF. Thiol regulation in the lens. J Ocul Pharmacol Ther 2000; 16:137–148. 30. Truscott RJ. Age-related nuclear cataract: a lens transport problem. Ophthalmic Res 2000; 32: 185–194. 31. Moffat BA, Landman KA, Truscott RJ, Sweeney MH, Pope JM. Age-related changes in the kinetics of water transport in normal human lenses. Exp Eye Res 1999; 69:663–669. 32. Borchman D, Giblin FJ, Leverenz VR, Reddy VN, Lin LR, Yappert MC, Tang D, L Li. Impact of aging and hyperbaric oxygen in vivo on guinea pig lens lipid and nuclear light scatter. Invest Ophthalmol Vis Sci 2000; 41:3061–3073. 33. Balasubramanian D. Ultraviolet radiation and cataract. J Ocul Pharmacol Ther 2000; 16: 285–297. 34. Weinreb O, vanRijk FA, Steely HT, Dovrat A, Bloemendal H. Analysis of UVA-related alterations upon aging of eye lens proteins by mini two-dimentional polyacrylamide gel electrphoresis. Ophthalm Res 2000; 32:195–204. 35. Spector A, Kuszak JR, Ma W, Wang RR, Ho YS, Yang Y. The effect of photochemical stress upon thelenses of normal and glutathione peroxidase–1 knockout mice. Exp Eye Res 1998; 67:457–471. 36. Spector A, Ma W, Wang RR, Yang Y, Ho YS. The contribution of GSH peroxidase-1, catalase, and GSH to the degradation of H2O2 by the mouse lens. Exp Eye Res 1997; 64:477–485. 37. Reddy VN, Lin LR, Ho YS, Magnenat JL, Ibaraki N, Giblin FJ, Dang L. Peroxide-induced damage in lenses of transgenic mice with deficient and elevated levels of glutathione peroxidase. Ophthalmologica 1997; 211:192–200. 38. Giblin FJ. Glutathione: a vital lens antioxidant. J Ocul Pharmacol Ther 2000; 16:121–135. 39. Saxena P, Saxena AK, Cui XL, Obrenovich M, Gudipaty K, Monnier VM. Transition metalcatalyzed oxidation of ascorbate in human cataract extracts: possible role of advanced glycation end products. Invest Ophthalmol Vis Sci 2000; 41:1473–1481.

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40. Campisi A, Di Giacomo C, Russo A, Sorrenti V, Vanella G, Acquaviva R, Li Volti G, Vanella A. Antioxidant systems in rat lens as a function of age: effect of chronic administration of vitamin E and ascorbate. Aging (Milano) 1999; 11:39–43. 41. Borchman D, Giblin FJ, Leverenz VR, Reddy VN, Lin LR, Yappert MC, Tang D, Li L. Impact of aging and hyperbaric oxygen in vivo on guinea pig lens lipids and nuclear light scatter. Invest Ophthalmol Vis Sci 2000; 41:3061–3073. 42. Chylack Jr LT, Wolfe JK, Friend J, Tung W, Singer DM, Brown NP, Hurst MA, Kopcke W, Schalch W. Validation of methods for the assessment of cataract progression in the Roche European-American Anticataract Trial (REACT). Ophthalm Epidemiol 1995; 2:59–75. 43. Chylack Jr LT, Phelps-Brown N, Bron A, Hurst M, Kopcke W, Thien U, Schalch W, the REACT Group. The Roche European American Cataract Trial (REACT): a randomized clinical trial to investigate the efficacy of an oral antioxidant micronutrient mixture to slow progression of age-related cataract. Ophthalm Epidemiol 2002; 9:49–80. 44. Hanssen E, Franc S, Garrone R. Fibrillin-rich microfibrils: structural modifications during ageing in normal human zonule. J Submicrosc Cytol Pathol 1998; 30:365–369.

6 Hyperopia IVO JOHN DUALAN and PENNY A. ASBELL Mount Sinai Medical Center, New York, New York, U.S.A.

A. CONTACT LENS VS REFRACTIVE SURGERY 1. History of Contact Lens Why would anyone choose contact lenses over refractive surgery? Contact lenses have been around for decades and are therefore true, tried, and tested. Surgical procedures, on the other hand, are still considered innovative, and no long-term follow-up data are yet available. Contact lenses were first described and used well over a century ago but came into popular use after World War II, where the first hard contact lenses, made of polymethylmethacrylate (PMMA), were introduced. In the 1960s the advent of soft lens materials made of hydroxy-ethyl methacrylate (HEMA) led to the widespread use of contact lenses in the United States. In the 1970s rigid gas-permeable lenses were introduced, and in the 1980s astigmatic and presbyopic connecting lenses became available. Flexibility of lens use increased with the introduction of extended-wear contact lenses in the 1980s and disposable lenses that can be replaced weekly, monthly, and even daily. The last decade has seen advances in contact lenses for correcting presbyopia, including bifocal and multifocal contact lenses. 2. Market Information Currently, it is estimated in the United States that over 30 million people use contact lenses. Some 80% are using soft lenses and approximately 20% are using rigid gas-permeable lenses. Contact lenses offer individuals a readily available method of correcting refractive errors that can be personalized to their individual needs. Excellent visual acuity is routinely attained with contact lenses; 100% likely see 20/40 or better and well over 95% achieve 20/20 or better, though visual “results” with contact lenses are rarely reported. Contact 63

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lenses are relatively inexpensive, and though there are ongoing costs in terms of replacing the lenses, the lens care solutions, and having follow-up care, the expenditures are modest compared to the significant initial outlay for refractive surgery. Contact lenses can easily be exchanged as patient’s refractive error changes and so allows children and young adults to be fitted even before the refractive error has completely stabilized. In addition, older individuals have an option to change to presbyopic contact lenses as the need for additional correction for good near vision increases. Perhaps the key to the success of contact lenses is their flexibility: the ability to change lenses to meet patients’ changing visual needs and even give them the ability to return to spectacles or other vision correction method at any time. Most refractive surgery procedures are permanent and irreversible. If for any reason a patient is unhappy or dissatisfied with the surgical results, he or she “cannot go back again.”

B. REFRACTIVE SURGERY VERSUS CONTACT LENSES FOR THE CORRECTION OF REFRACTIVE ERRORS 1. The Contact Lens Candidate As with any patient seeking correction of a refractive error, a complete eye exam is indicated. This would include obtaining a good history. It is important to determine how the patient will be using the refractive correction and whether it is to be used for a specific activity such as skiing, swimming, computer use, etc. Medical problems that might increase the risk of wearing contact lenses could include diabetes mellitus, immunosuppression, severe allergies, and possibly occupational hazards such as exposure to volatile gases. The eye examiner needs must be particularly attentive to lid function, since spreading of a tear film by blinking is central for the good fit of a contact lens. Evaluation for possible dry eyes is essential, since a poor tear film can interfere with the patient’s ocular health and/ or comfort with lenses. Relative contraindications to contact lens wear are not different from those being considered when a patient is being evaluated a patient for refractive surgery: the inability to understand the risks and benefits of the correction modality, immunosuppressed patients, patients with only one functional eye, history of previous ocular problems including herpetic keratitis, previous ocular surgery such as glaucoma filtering procedures, chronic use of topical medications such as steroids, severe dry eyes, neovasclarization of the cornea, corneal dystrophies, and pregnancy. The key issues regarding more of contraindications that are specific to the fitting of contact lenses include patients who are unable or not willing to participate in appropriate lens care and follow-up care, patients who are unable to learn to insert and remove contact lenses or do not have a family member who can assist with this process, and patients who may have poor hygiene, which may put them at increased risk for infections associated with contact lens use.

C. SOFT CONTACT LENSES Soft contact lenses are made of a plastic called hydrogel that can be shaped into lenses but maintains its flexibility and provides immediate quality vision and comfort for most patients.

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1. Advantages of Soft Contact Lenses Immediate comfort is clearly the advantage of these lenses. Soft contact lenses are generally large in diameter and extend beyond the cornea and limbus and fit under the upper lid margin. Though there is slight movement with each blink because of the size of the lens and the flexibility of the material, little sensation is associated with soft contact lens use. Adaptation to soft contact lenses is rapid and patients can begin enjoying quality vision almost from the moment the lenses are placed. Key advantages of soft contact lens use are Adaptation Comfort High-quality visual acuity Ability to use on an intermittent basis Ease of fitting Ease of contact lens care Correction of a wide range of refractive errors Soft contact lenses can usually be fitted in one visit, with a brief follow-up to ensure that they continue to provide excellent comfort and vision. Few unscheduled visits are required, and patients typically return every 6 to 12 months for a follow-up that includes evaluation for other ocular diseases, such as glaucoma and to ensure the general ocular health as well continued proper use of the contact lenses. 2. Disadvantages of Soft Contact Lenses Unlike myopes, hyperopes may have difficulties with visualization of contact lenses during handling, since these patients do not have any near point in focus. Deposits can develop on the lenses, which can interfere with comfort and vision. Patients who may be exposed to environmental hazards such as volatile chemicals and those who have poor or inadequate tear film are presently not good candidates for the use of soft contact lenses. 3. Lens Selection There are a variety of things to be considered in picking a soft contact lens for a particular patient. Most soft lenses come in predetermined parameters from the manufacturer, though some can be custom-ordered for a particular prescription, such as lenses for patients with high astigmatism. Soft contact lenses vary in water content: low range (30 to 45% water), medium content (40 to 58% water), and high content (60 to 80% water). The amount of water is a factor in the oxygen permeability of the lens and also influences comfort and ease of handling. Contact lens parameters include the base curve of the central optic zone and the diameter of the lens. Typically, a trial lens will be placed to evaluate the fit and determine the refractive correction needed to account for the reduced vertex distance and residual astigmatism. Many manufacturers supply practitioners with trial lenses that can then be dispensed on the initial visit. Replacement lenses can then be sent directly to the patient’s home or work for added convenience. Another key consideration in fitting a soft lens is the wear schedule. For patients who might need intermittent correction, as for social events or sports, one-day disposable lenses may very well be suitable. Other patients do well with daily-wear disposable lenses that are replaced weekly or biweekly. Soft lenses can also be used on a flexible replacement

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schedule: weekly, monthly, or quarterly. They can also be dispensed as extended-wear lenses, typically being left in place for 6 to 7 days and then removed and disposed of and replaced by new contact lenses. Past studies suggest that the use of extended-wear contact lenses significantly increases the risk of corneal infections. However, new lens materials have become available that have significantly increased oxygen permeability and disposability of lenses and possibly may have reduced the risks of extended-wear usage. Conventional lenses that are used day in and day out are still available but are less commonly prescribed, since they offer none of the advantages of disposable lenses, including the regular use of a Fuch sterile lens offering assured quality vision and comfort with each new lens. D. RIGID GAS PERMEABLE CONTACT LENS The original cosmetic lenses made of a hard material (PMMA) and are still available today but are rarely used in new fittings in the United States. Newer materials afford increased oxygen to the cornea and greater comfort while providing better rigidity than soft contact lenses. Several rigid gas-permeable (RGP) materials are available, including silicone acrylate and fluorine copolymers as well as others. 1. Key Advantages of RGP The key advantages of RGP contact lenses are that they are manufactured “to order,” allowing for adjustments for an individual’s visual needs to achieve the best fit. RGPs allow for sharp, excellent visual quality and lens durability. The advantages of rigid gas permeable lenses are Quality of vision Durability of lens material Ability to correct astigmatism In-office modification possible Resistance to formation of lens deposit Increased suitability in patients with poor tear film Ease of lens handling 2. Disadvantages of Gas-Permeable Contact Lenses A period of adaptation is needed for the patient to become comfortable with the lenses. This varies from patient to patient but usually is about 2 weeks long. Comfort is not “instantaneous,” and these lenses are less likely to provide the “wow factor,” which may be routine with soft contact lenses. Fitting RGP lenses can be more challenging, but modifications can allow for the best fit for an individual patient. Possible corneal thinning with long-term contact lens wear is another disadvantage. 3. Lens Selection (RGP) Lens selection criteria for RGP materials will include choosing the material based on its oxygen permeability and its ability to resist deposit formation. Other parameters that need to be considered are the base curve and the peripheral (secondary and tertiary) curves to provide a good fit. Aspheric lenses are also available; these can provide less optical distortion and better-quality visual acuity. As with other lens modalities, wear schedules will

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depend the material chosen and patient’s visual needs, whether these involve daily wear or extended-wear use. More recently, frequent lens replacement has been introduced even for rigid gas permeable lenses. Intermittent use is inadvisable, since an adaptation period is needed to achieve maximum comfort with RGP lenses. E. ASTIGMATISM Soft contact lenses can be used in patients needing astigmatic corrections. If the patient’s refractive error demonstrates only a small amount of astigmatism (under 1.00 D) and the astigmatism is a small amount of the spherical correction (less than one-third), a soft spherical contact lens will adequately correct vision. However, greater degrees of astigmatism can easily be corrected with toric soft contact lenses. RGP lenses can be used to correct astigmatism whether it is corneal or lenticular in origin. Various methods have been developed to stabilize the soft lens to match the orientation of the astigmatic correction. These include prism ballast (weighting the lens more heavily on the bottom), truncation (removing a section of the upper and/or lower part of the lens), or a combination of the two methods, and “slab off” (a change in the lens periphery using pressure from the eyelids to maintain the position). The fitting of soft toric lenses usually involves using a trial set and then ordering the appropriate lenses for an individual patient. These lenses have a surface orientation mark to demonstrate whether there is lens rotation, indicating that the astigmatism might not be corrected. One must observe the orientation mark on the soft contact lens when it is fitted on the eye. Typically, the mark is located at the 6 o’clock position, and one must observe whether the rotation is clockwise or counterclockwise. A mnemonic that can help the fitter to remember how to order the appropriate lens is LARS: left add, right subtract. This means that if the lens rotates to the left, one adds to the amount of trial lens rotation to the axis from the spectacle refraction. However, if the rotation, is to the right, then one subtracts the amount of lens rotation from the axis obtained in the spectacle refraction. Soft lenses come in a variety of astigmatic corrections, which are available in disposable or frequent lens replacement styles, for correcting 2 to 3 D. These lenses are not indicated for greater amounts of astigmatism and irregular astigmats. RGP contact lenses, on the other hand, easily correct corneal astigmatism. Typically a spherical RGP contact lens may correct up to 3 D of astigmatism. For greater amounts of astigmatism, a toric RGP lens can be made. Most manufacturers provide customer service information over the telephone or by e-mail through the Internet. This procedure can help in fitting patients who have significant astigmatism that may not be adequately corrected with standard lens materials. F. PRESBYOPIA 1. Monovison Currently refractive surgery also offers presbyopic correction primarily with the use of monovison, where one eye is corrected for distance and the other eye for near use. This procedure has been used successfully for many years with contact lens patients. In fact, before refractive surgeries, often a trial monovison using contact lenses is indicated to help a patient decide if this is appropriate for the planned permanent refractive procedure to be done. Monovision offers simplicity both for the patient and the contact lens fitter.

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However, some patients do not get used to the 2 D of anisometropia induced with monovision fitting and note reduced stereopsis; they sometimes need an overrefraction in spectacles for driving and other demanding visual tasks. Another option in such patients is to reduce the anisometropia to approximately 1.25 D, which usually resolves symptoms, but by doing so the patient should understand there will be an increased need for glasses for closer vision compared to midrange vision. 2. Bifocal Contact Lenses There are basically two designs in bifocal contact lenses. Alternating-vision bifocal contact lenses provide for a slight range movement of the patient’s gaze from distance to near. A slight twist of the lens provides an altered path for the light rays into the eye and how it is refracted. The lenses can be made in a segmented bifocal-style, similar to bifocal spectacles, or they can be made in a concentric bifocal style. The distance vision is in the central part of the lens and the peripheral portion of the lens is for near vision. In both styles, the lens must move slightly for patients to have good vision as they change their focus from distance to near. An alternative bifocal contact lens design provides simultaneous vision, whereby light rays from both distant and near object pass through the lens and pupil. The patient’s brain then selects the object to regard and bring into focus. This type of lens is available in several different types, including the concentric bifocal which has an annular design, with distance vision in the center and the near vision in the peripheral part of the contact lens; an aspheric “multifocal” design, where there is an increase in plus power as one moves from the center to the periphery of the lens as a result of the changing curvature of the lens as oppose to a single based curve; and the diffractive bifocal type, which has small concentric circular facets of varying refractive ability that are alternated to provide the appropriate additional power needed for near vision near the center of the lens. Lenses differ in their ability to be fitted, requiring careful attention to centering of the lens and the relationship of the lens size to the patient’s pupil size. Typically, a practitioner becomes expert in one or two bifocal lens types and acquires the experience and knowledge to pick patients appropriately and fit them quickly. The availability of soft bifocal contact lenses, which may also disposable, allows for an easier fit with the use of trial lenses. As with refractive surgery, however, monovision probably continues to be the mainstay, considering the presbyopic patient today. G. CONCLUSION In conclusion, we will probably always have patients who prefer to use contact lenses and spectacles for their refractive correction. These modalities offer quality visual acuity as well as stability and affordability. In addition, the development of new materials for contact lenses, particularly those offering extended wear, may very likely present a competitive alternative to refractive surgery. This is especially true if the material for extended wear demonstrates increased safety and comfort compared to older lens materials. It remains to be seen whether this goal of extended wear and comfort can in fact be associated normal corneal physiology and the maintenance of a risk-free use of contact lenses. With further research and an increasing number of people seeking “hassle free” vision correction, we may yet see the emergence of “permanent” contact lenses.

7 Surgical Treatment Options for Hyperopia and Hyperopic Astigmatism PAOLO VINCIGUERRA and FABRIZIO I. CAMESASCA Istituto Clinico Humanitas, Milan, Italy

A. TREATMENT OF HYPEROPIA With initial experience, the refractive surgeon may more or less consciously consider the treatment of hyperopia as a situation opposite to but similar to myopia. Disappointingly, laser refractive surgery for hyperopia has often led to more unsatisfactory results and complications than for myopia (1–3). If we examine carefully a corneal surface after hyperopic ablation, we may notice several important peculiarities. The main concern is the transition zone: in treating myopia we create just one transition zone; while in the treatment of hyperopia, central corneal curvature is increased and two transition zones are needed, featuring double change in curvature and a median flexus point (Fig. 1). This double transition zone is the most critical point of hyperopia treatment (4). The most central of these two transition zones cannot be considered as part of the optical zone (Fig. 2). This portion of the induced curvature is used to generate a refractive effect but features a flexus with variation in curvature and is connected to the peripheral corneal curvature through the second curvature zone. Therefore, in comparing myopic and hyperopic treatments with the same ablation diameter, the hyperopic optical zone will be smaller than the myopic one. With the hyperopic ablation, the corneal curvature is changed, but the corneal physiology is maintained up to the middle periphery. The ablation diameter must be planned to fit the zone of curvature inversion right where the normal peripheral cornea flattens. Using the elevation map, the surgeon must calculate the maximal corneal diameter and place the flexus on the flat peripheral cornea, thus preserving the normal corneal physiology (Fig. 3). If the flexus area is positioned centrally, far from this peripheral area of physiological corneal flattening, multifocality and high-order optical aberrations will be induced. 69

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Figure 1 Hyperopic ablation. Central corneal curvature is increased and two transition zones are induced, leading to a double change in curvature.

Figure 2 Hyperopic ablation. The central part of the transition zone (A to B) cannot be considered part of the optical zone.

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Figure 3 Importance of corneal diameter in hyperopic refractive surgery.

Also, hyperopic ablation generates a negative longitudinal spherical aberration with worse vision quality, due to the fact that para-axial light rays will pass through the first curvature flexus, which imparts a hyperopic shift (Figs 4 and 5). However, it is important to remember that these problems are sometimes reduced by the anatomical characteristics of hyperopic eyes. Generally speaking, the size of the optical zone is less important for a hyperopic patient than for a myopic one. The hyperopic eye features smaller axial length, anterior chamber, and corneal diameter. Given the same ablation diameter, an eye with a shallow anterior chamber will enjoy a larger optical zone than one with a deep chamber (Fig. 6), and will have a larger percentage of corneal surface involved by the treatment. Moreover, the two transition zones mentioned above will lie peripherally, positioned in a corneal area with lesser curvature and lesser influence on refraction. In a hyperopic eye with a shallow anterior chamber, the treatment results will be less influenced by pupil diameter: even an optical zone of small size may cover the pupillary area sufficiently, since the treated corneal arc will be closer to the pupillary area and thus able to cover the pupil halos during mydriasis (Fig. 6). What is really important is that the optical zone be truly homogeneous.

Figure 4 Myopic ablation. With a wide ablation area, the optical zone is wide and uniform, without aberrations induced on para-axial rays.

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Figure 5 Hyperopic ablation. When the optical zone is small, para-axial light rays will pass through the first curvature flexus, with consequent hyperopic shift, negative longitudinal spherical aberration, and worse vision quality.

These and the following observations can be assumed to be valid both for photorefractive keratectomy (PRK) and laser-assisted in situ keratomileusis (LASIK) treatment. Therefore, with some important exceptions, we henceforth refer to refractive treatment as including both PRK and LASIK. 1. Keratorefractive Indexes Several parameters may be taken into account in evaluating the quality of an ablation. 1. Corneal eccentricity. A concept of foremost importance is that of corneal eccentricity. Eccentricity is the measure of corneal asphericity; therefore it expresses

Figure 6 Given a 6.5-mm optical zone ablation, an eye with a low chamber will enjoy a larger optical zone than one with a deep chamber, and even a small optical zone may sufficiently cover the pupillary area.

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the way the cornea changes from a flatter periphery to a more curved central portion. Eccentricity values (e values) are positive when the cornea is prolate, negative when it is oblate. Normal eccentricity values range between Ⳮ0.5 and Ⳮ0.6 (normally prolate cornea, curved in the center, flat in the periphery). A hyperopic treatment increases the e value; Figures 7 through 11 show cases with progressively higher e values, approaching a keratoconus-like situation. Central keratoconus, featuring a high eccentricity, with e values of Ⳮ1.5 or more, amplifies the physiological situation of transition from a curved central cornea to a flat periphery. On the contrary, a myopic treatment induces negative eccentricity, inverting the normal morphology. 2. Longitudinal spherical aberration (LSA). LSA expresses the aberration induced by corneal multifocality. It is a measure of spherical aberration; its increase indicates a decrease in contrast sensitivity. 3. Root mean square (RMS). RMS is a measure of the irregularity of curvature, expressing the amount of deviation from a regular corneal curvature. 4. Surface asymmetry index (SAI). SAI is a measure of corneal symmetry in the pupillary area. Its increase leads to an increase in coma. In the past, it was generally thought that excessively high corneal curvature values would lead to a keratoconus-like situation. From our studies, it appears that an important factor for this complication is the corneal curvature gradient (eccentricity). Interestingly,

Figure 7 through 11 Eyes with progressively higher e values, approaching a keratoconus-like situation.

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Figure 8.

Figure 9.

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Figure 10.

Figure 11.

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we may observe patients with corneal curvature values of 46 D who show good visual acuity, while others with, for example, 45 D do not enjoy such good vision. In a patient with 46 D and normal eccentricity, there is no marked peripheral flattening and visual acuity will be good. Another patient, with a keratoconus and a corneal curvature within normal values, such as 45 D, will inevitably show a high eccentricity and therefore a marked (e.g., spherical) optical aberrations, a very small homogeneous optical zone, and reduced vision quality. Highly positive eccentricity values (above 1.0 to 1.2) are typical of keratoconus and some cases of hyperopic ablations. A whitish scar may occur in the stroma following PRK or LASIK. This scar correspond topographically to the point of maximal corneal curvature (Figs. 12 and 13). In these cases there is always a high eccentricity value. At present, the etiology of this scar remains uncertain; there is an inhomogeneous tear film as well as lid trauma to the centrally steepened area. For photorefractive treatments, the scar was believed to be the result of denervation of the central corneal area due to the depth of the peripheral ablation. This hypothesis is no longer held, however, because the scar is observed at the point of greatest corneal curvature and not at that of maximal corneal ablation. Furthermore, the scar is not observed with a greater frequency in LASIK eyes, where central corneal denervation is more complete. However, a similar scar is present in posttraumatic corneal leukomas, always at the point of greatest corneal curvature. In these cases of corneal leukoma, topographic analysis may very often be misleading due to problems with the elaboration of the map. Keratoscopy must always be obtained and examined. Correction of hyperopia with LASIK is more successful, even in the presence of high e values. As a matter of fact, the flap does not follow the new shape of the stromal bed, perfectly thus reducing the eccentricity created by the ablation. In PRK, corneal epithelium follows the newly imparted morphology faithfully. However, above certain values of eccentricity, even LASIK fails. Retreatment with PTK of these fibrotic areas in hyperopia leads to limited or no result at all, if corneal eccentricity remains positive (e ⳱ 1.0 ⳮ 1.5), with recurrence of

Figure 12 Keratoscopy of an eye with a subepithelial (PRK) whitish scar, corresponding topographically to the point of maximal corneal curvature.

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Figure 13 Topography of same eye as in Figure 12.

the scar at the point of greatest corneal curvature. On the other hand, when eccentricity is decreased, as with corneal excimer laser smoothing, recurrence is prevented. A key point of hyperopic ablation is thus to maintain a corneal eccentricity as much as possible close to physiological values. Corneal topography offers the advantage of an accurate evaluation of the quality of hyperopic ablation. A wide, homogeneous central area is necessary for improved visual quality, and the surgeon must strive to achieve it as well as to monitor the result topographically. The aberrometric map allows evaluation of central corneal dioptrical homogeneity as well as detection of irregularities that may generate aberrations. The wider the central treatment, the less important is the second, peripheral part of the transition zone (Figs. 1 and 2). Our experience with the Nidek OPD aberrometer shows that, with good topographical indexes, we have a satisfactory aberrometric map: more than 80% of optical aberrations are caused by the first corneal surface. The future is represented by a larger optical zone (in relation to corneal diameter), of 6.5 mm or greater, with a first, more smooth and homogeneous transition zone up to 9 mm, and a second, limbal transition zone, of more than 9 mm. Let us remember that the corneal periphery offers also the advantage of a greater thickness (Fig. 14).

8 Laser Thermokeratoplasty and Wavefront-Guided LTK SHAHZAD I. MIAN and DIMITRI T. AZAR Cornea and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A.

The use of thermokeratoplasty in order to change corneal curvature has been evaluated extensively but has shown limited success due to significant regression of refractive effect. With an improved understanding of corneal response to thermal injury and technological advances that have allowed for better control of thermal injury to the cornea, real-time wavefront-guided thermokeratoplasty may become a safe and effective surgical technique for the management of hyperopia. A. HISTORY Lans first demonstrated the use of thermal energy to change corneal curvature (1). He applied electrocautery to the peripheral corneas of rabbits to induce central corneal steepening. Corneal cautery was later used to treat patients with high astigmatism, but with limited stability of results (2,3). Thermokeratoplasty has also been used to treat patients with keratoconus, but with poor predictability and a high incidence of regression (4–6). There have also been reports of complications, including delayed epithelial healing, corneal scarring, recurrent erosions, corneal neovascularization, and iritis (7–9). However, thermokeratoplasty may have a role in the management of patients with keratoconus in countries with limited availability of corneal tissue (10). Radiofrequency energy has also been used to induce corneal steepening with collagen shrinkage, but with poor predictability and scarring (11). Fyodorov first used thermokeratoplasty to treat hyperopia by developing radial thermokeratoplasty (12). He used a retractable nichrome thermal probe to coagulate the midperipheral cornea at a depth of 85 to 90% with temperatures up to 600⬚C for 0.3 s. The 83

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corneal burns were made in a radial pattern with eight rows and comprised of three or four applications, each up to a premarked optical zone. Trials with radial thermokeratoplasty showed limited clinical benefit because of regression of refractive effect and poor predictability (13–15). Like previous methods of thermokeratoplasty, there were also reports of endothelial damage, corneal decompensation, and corneal necrosis. Improvement in laser technology has led to advancement in thermokeratoplasty techniques. Prior to the use of infrared laser sources, the complications with thermokeratoplasty techniques were partly related to nonuniform heating of corneal stroma at high temperatures. Laser thermokeratoplasty (LTK) allows for controlled delivery of heat to the corneal stroma while preventing excessive injury to the epithelium and endothelium. Several lasers have been investigated to induce stromal injury. The carbon dioxide laser (CO2, wavelength: 10.6 ␮m) leads only to superficial retraction of collagen, with early regression of effect (16,17). The yttrium-erbium-glass laser (Yt-Er-glass, wavelength: 1.54 ␮m) allows for deep penetration of corneal stroma with good refractive results, but its use may lead to corneal tissue necrosis and iris damage (18). The cobalt:magnesium fluoride laser (wavelength: 1.85 ⬎ to 2.25 ␮m) and the continuous-wave hydrogen fluoride chemical laser (wavelength: 2.61 ␮m) have also been evaluated in animal studies, with stable results (19,20). Initial trials with a pulsed holmium:yttrium-aluminum-garnet laser (Ho:YAG, wavelength: 2.06 ␮m) in human eyes resulted in a hyperopic shift of up to 5 D, which remained stable for 4 months (21). The advantages of the Ho:YAG laser include a corneal stromal penetration depth of about 400 to 450 ␮m and a cone-shaped profile. Unlike the cylindrical profile of thermal probes, the Ho:YAG laser produces a cone-shaped coagulation, allowing for greater shrinkage of anterior stromal collagen compared to the posterior stroma (22). Controlling the magnitude and depth of stromal coagulation allows for greater refractive effect and increased stability of results. In addition, the Ho:YAG laser uses solid-state technology, which is relatively inexpensive to manufacture and maintain. B. MECHANISM The basic mechanism of thermokeratoplasty involves change in corneal curvature through heat-induced injury of stromal collagen. Stringer and Parr first reported that the temperature required to shrink corneal collagen is 55 to 58⬚C (23). Heating above 65 to 70⬚C causes collagen relaxation, while even higher temperatures lead to stromal collagen necrosis (24). Refractive outcome with LTK is based on optimal corneal stromal shrinkage, determined by the following parameters (25): 1. Temperature. Collagen shrinkage without destruction of collagen fibrils occurs in a narrow temperature range between 55 and 58⬚C. When the corneal stroma is heated to 55 to 60⬚C, the tropocollagen helical structure collapses due to dissociation of interpeptide hydrogen bonds, unwinding of the triple helix, crosslinkage between tropocollagen molecules, and dehydration of the stroma. This causes the corneal collagen to shrink maximally, to one-third of its original size. The temperature threshold increases with age due to a greater number of thermally stable cross-linked hydrogen bonds (26). Increasing the temperature to 78⬚C or more leads to relaxation of contracted collagen and loss of tissue elasticity (24). 2. Tissue elasticity. The refractive effect is dependent on tissue resistance to collagen shrinkage (24). In younger patients, rigid corneal tissue will lead to limited initial response; greater elasticity of corneal tissue will increase regression of effect (25).

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3. Keratocyte response. Keratocyte injury occurs when stromal collagen is heated to 79⬚C, which induces wound healing, including extracellular matrix remodeling and keratocyte activation (27). These changes contribute to postoperative regression of induced refractive effect. 4. Stability of corneal collagen. Normal replacement of treated collagen by newly synthesized collagen may also contribute to regression of refractive effect. Collagen turnover in the cornea is very slow, with a half-life of 10 years; the stability of corneal collagen after LTK is unknown (28,29). C. CONTACT AND NONCONTACT LTK The Ho:YAG laser delivery system can be used with a contact probe (Summit Technology, Waltham, MA, and Technomed, Baesweiler, Germany) or a noncontact device (Sunrise Technologies, Fremont, CA) (22,30). The contact probe allows for sequential delivery of laser pulses into premarked spots using a fiberoptic handpiece brought into direct contact with the cornea. The spot size is variable and dependent on the diameter of the fiber optic handpiece (Summit Technology, Waltham, MA, 0.7 mm; Technomed, Baesweiler, Germany, 0.55 mm). Depending on the degree of hyperopia, rings of eight spots are applied with a treatment zone of 6.5 and 9.0 mm, 7.0 and 9.0 mm, and 7.5 mm with the Summit Ho:YAG LTK and 6, 7, or 8 mm with the Technomed Ho:YAG LTK. The noncontact Ho:YAG laser device allows for simultaneous delivery of eight laser pulses using a slit-lamp, with a fixed spot size of 0.60 mm. One, two or three radial or staggered concentric octagonal rings are placed at 6-to 8-mm ring diameters. This technology can be coupled with real-time wavefront measurements to minimize the unpredictability of the surgery. D. PATIENT SELECTION The noncontact Ho:YAG laser (Hyperion, Sunrise Technologies, Freemont, CA) was approved by the U.S. Food and Drug Administration (FDA) in June 2000 for the temporary reduction of hyperopia in patients with the following indications: 1. 2. 3. 4.

Age ⱖ 40 years Manifest refraction spherical equivalent of Ⳮ0.75 to Ⳮ2.5 diopters Cylindrical correction ⱕ Ⳳ 0.75 diopters Stable refraction 6 months prior to the procedure

LTK is contraindicated in patients: 1. During pregnancy or while nursing 2. With keratoconus 3. With clinically significant corneal dystrophy or scarring in the 6-or 7-mm central zone 4. With a history of herpetic keratitis 5. With an autoimmune disease, collagen vascular disease, clinically significant atopic syndrome, insulin-dependent diabetes or an immunocompromised state Patient evaluation includes visual assessment with both uncorrected and best-corrected visual acuity with cycloplegic refraction. Intraocular pressure should be measured to exclude narrow-angle glaucoma in hyperopic patients. A poor LTK effect is observed in patients with high intraocular pressure (31). Corneal topography is performed to determine

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presence of irregular astigmatism. Pachymetry is helpful, because thinner corneas have greater effect with LTK. Systemic anti-inflammatory medications should be avoided 2 months preoperatively and 3 months postoperatively due to their contribution to regression of refractive effect. Wavefront-guided LTK studies are underway, but have not been approved as of yet by the FDA. E. SURGICAL PROCEDURE 1. Contact LTK With the contact Ho:YAG laser (Summit Technology, Waltham, MA, and Technomed, Baesweiler, Germany), energy is delivered through a quartz fiberoptic probe handpiece and focused by a disposable tip at the corneal surface with a cone angle of 120⬚ (32). Preoperatively, patients are given topical tetracaine anesthesia and the pupil is constricted with 1% pilocarpine. The optical zone center is located using coaxial fixation and marked over the center of the pupil. Probe placement is guided by using a specially designed marker with radial and arcuate marks. The probe tip is applied perpendicular to the corneal surface at the intersection of the radial and arcuate marks. The laser energy is set at 19 mJ per pulse for 25 pulses, pulse duration of 300 ms, with a repetition rate of 15 Hz. The patients receive either 8 or 16 spots at variable optical zones. Loose epithelium is debrided with a weck-cell sponge from the treatment areas after and the eye is patched after administering antibiotic/steroid ointment. Postoperatively, patients receive tobramycin 0.3%/dexamethazone 0.1% ointment five times daily until re-epithelialization. 2. Noncontact LTK The noncontact Ho:YAG laser (Hyperion, Sunrise Technologies, Fremont, CA) is a solidstate, pulsed laser connected to a slit-lamp delivery system (Nikon) capable of projecting eight uniform beams in an octagonal ring (33). Each beam has an individual shutter with adjustable optical zone diameters, allowing for different treatment patterns. The laser energy is set from 21 to 25 mJ per pulse for 5 to 10 pulses with a repetition rate of 5 Hz applied over several seconds. Two HeNe laser beams are used for alignment, centration, and coaxial focusing. Preoperatively, topical anesthetic drops (0.5% proparacaine solution) are administered, starting 20 min before treatment, for a total of four drops. A lid speculum is inserted to allow the eyelids to be held open for 3 min before laser application to dry the tear film. This helps standardize the effects of epithelial swelling and corneal hydration on delivery of laser energy to the corneal stroma. The patient is instructed to fixate on a flickering red light during laser application. The ring diameter and number of rings applied depends on the desired correction. Postoperatively, patients are given 0.3% tobramycin and diclofenac sodium drops four times daily until the epithelium is healed. Patients may also take acetaminophen or acetaminophen with codeine for pain management. In realtime wavefront-guided LTK, the energy per pulse can be adjusted to improve the surgical outcomes. F. VISUAL OUTCOMES 1. Contact LTK The safety of contact Ho:YAG LTK was initially established in 33 human cadaver and 4 blind human eyes (21). Sixteen coagulations on two concentric rings, with diameters of 6 and 9 mm, were applied. This resulted in central corneal steepening with a refractive

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change that increased with the applied pulse energy above a threshold of 10 mJ per pulse, remaining constant between 15 and 35 mJ per pulse. Hyperopic shifts of up to 5.00 D were obtained, decreasing linearly with increasing diameter of treatment zone, which remained stable for 4 months. Durrie et al. conducted FDA phase I and II trials for contact Ho:YAG LTK for low to moderate hyperopia (32). Patients in phase I had a mean spherical equivalent of Ⳮ4.17 D (Ⳮ2.25 to Ⳮ6.62 D). However, because of limited efficacy with higher refractive corrections, phase II included patients with a mean spherical equivalent of Ⳮ1.50 D (0.00 to Ⳮ4.25 D). One or two ring treatments with eight spots were applied at 7.0, 7.5, 7.0, and 9.0 and 6.5 and 9.0 mm. No patients saw J2 or better preoperatively, and 75% saw J2 or better 6 months postoperatively. In phase II, 79% of patients were within 1 D of emmetropia, and 89% of patients had uncorrected visual acuity of 20/40 or better at 1 year follow-up. After initial regression, the refractive results were stable at the 6-month follow-up for patients in both phase I and phase II. The phase I patients were followed for 1 year with further regression of effect. Tutton et al. treated 22 eyes by placing two rings with eight laser spots at 6.5 and 9.0 mm to produce a 4-D correction (34). Only 25% of patients were within Ⳳ1.00 D of intended correction. In addition, Ⳮ1.25 to Ⳮ2.50 D astigmatism was induced with 50% regression of refractive effect at 2 years postoperatively. Eggink et al. treated 55 hyperopic eyes with one ring of eight spots with a treatment diameter of 6, 7, or 8 mm (35). The 6- and 7-mm-diameter treatments were more effective than the 8-mm-diameter treatment zone. Twelve-month follow up did not show stability, and there was limited additive effect of retreatment. Contact Ho:YAG LTK has also been used for correction of astigmatism (36–38). Corneal coagulation produces flattening in the peripheral cornea, accompanied by central steepening. This can be an effective treatment for steepening the flat axis in astigmatism. There is also a myopic shift in the spherical equivalent equal to one-half the steepening of the flat axis. Thompson et al. treated 30 eyes with four coagulation treatments with two spots placed on either side of an 8.5-mm ablation zone in the flat axis of the cylinder (38). The preoperative cylinder ranged from Ⳮ1.50 to Ⳮ4.00 D, with the average astigmatic correction obtained being 1.69 D (Ⳮ0.4 to Ⳮ3.98 D). Uncorrected distance visual acuity improved by two or more lines in 18 eyes and remained unchanged in the other 8 eyes. There was a trend toward more astigmatic correction with increasing age as well as a trend toward a myopic shift in spherical equivalent. With limited efficacy of results and a high rate of regression of refractive effect, the FDA trials for contact LTK were discontinued. 2. Noncontact LTK The safety of noncontact Ho:YAG LTK was initially established in humans with poorly sighted eyes. Ariyasu et al reported no evidence of endothelial cell loss, corneal thinning or neovascularization, persistent epithelial defects or change in intraocular pressure. (39) Table 1 summarizes the clinical trials conducted for noncontact Ho:YAG LTK. In the United States, the FDA phase II trial for low hyperopic correction by noncontact Ho:YAG LTK was conducted with 1-year follow-up (40). Twenty-eight patients with a preoperative spherical equivalent of Ⳮ2.21 Ⳳ 0.89 D (0.5 to 3.88 D) were treated with either one or two symmetrical staggered rings of eight spots per ring, with a diameter of 6 mm (one ring) or 6 and 7 mm (two rings). Ten pulses of laser light were applied at 5-Hz pulse frequency, with pulse energy ranging from 208 to 242 mJ. At 1 year postoperatively,

24 18

12

12

15 12

42 43

44

46

47 49

17 8 15 15 7 8 8 6 6 18 57 182

Patients n 6 6/7 6 6 6/7 6/7/8 6/7/81 5/6 6/7 6.5/7.5 6/7 or 8 5 to 7.5

D (mm) 8 8/8 8 8 8/8 8/8/8 8/8/8 8/8 8/8 8/8 8/8 8/8⫾8

N 10 10/10 10 10 10/10 7/7/7 7/7/7 5/5 5/5 5/5 10/10 5/5⫾5

M

240 240 240 215–255 240

208–242 224–240 160–199 208–242 224–240 NA

Ep (mJ)

LTK Treatment parameters

20/63→20/32 20/125→20/50 20/125→20/50 20/63→20/40 20/125→20/63 20/105→20/36 20/118→20/47 20/160→20/80 20/200→20/40 20/200→20/50 20/30→20/40 20/80→20/40

⌬UDVA

⌬Cyl (D) 0.25⫾0.29 0.47⫾0.53 0.16⫾0.49 0.30⫾0.37 0.25⫾0.29 0.15 0.15 0.92⫾1.46 0.17⫾0.38 0.15⫾0.58 NA NA

⌬SE (D) ⫺0.55⫾0.33 ⫺1.64⫾0.61 ⫺0.79⫾0.65 ⫺0.52⫾0.35 ⫺1.41⫾0.53 ⫺2.15 ⫺1.50 ⫺2.08⫾1.13 ⫺1.83⫾0.88 ⫺1.22⫾0.88 ⫺2.07⫾0.11 ⫺1.25

0.54 0.43 0.59 0.49 0.38 0.41 0.29 0.62 0.62 0.46 0.58 0.60

Stability

One-Year Postoperative results

Key: n, number of patient eyes; D, centerline ring diameter(s); N, number of spots; M, number of pulses; Ep, pulse energy; ⌬UDVA, change in uncorrected distance visual acuity (pre→post); ⌬SE, change in spherical equivalent; ⌬Cyl, change in cylinder; Stability, ratio of mean change in spherical equivalent values for 1 day to 1 month postoperatively divided by 1 year postoperatively; NA, not available.

12

40

Reference Follow-up, no. months

Table 1 Noncontact Ho: YAG LTK Clinical Studies

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uncorrected distance visual acuity improved in all patients. The mean change in spherical equivalent was ⳮ0.55 Ⳳ 0.33 D (one-ring treatment) and ⳮ1.64 Ⳳ 0.61 D (two-ring treatment). After initial regression, there was good stability of refractive effect after 6 months. The mean induced refractive astigmatism was 0.25 Ⳳ 0.29 D (1 ring) and 0.47 Ⳳ 0.53 D (two rings). The extent of refractive change in each group was correlated with the amount of laser pulse energy using the following algorithms: for one-ring treatment, change in spherical equivalent (diopters) ⳱ 3.20 ⳮ 0.0171 ⳯ pulse energy; for two-ring treatment, change in spherical equivalent (diopters) ⳱ 14.47 ⳮ 0.0685 ⳯ pulse energy. Corneal topographic changes confirm peripheral corneal flattening and central corneal steepening, with a greater change in curvature being produced with two-ring treatment.(41) Two-year follow-up of low hyperopic treatment with eight spots at a 6 mm diameter revealed stable refractive effect, similar to the 1-year data (42). Eighteen-month follow up of low hyperopia treatment with two octagonal staggered rings at 6- and 7-mm diameter also confirmed stability of refractive results (43). Two-ring treatments may be performed with radial or staggered rings of eight spots. Vinciguerra et al. compared the effects of the two treatment patterns in the correction of hyperopia with Ho:YAG LTK (44). The treatment consisted of 24 spots in three concentric rings of eight spots each, with ring diameters of 6, 7, and 8 mm. Each spot received seven pulses of laser energy. One eye of each patient received the radial ring pattern, while the fellow eye was treated with the staggered ring pattern. The radial and staggered patterns effectively corrected low hyperopia, and both were subject to regression. However, the radial pattern produced faster postoperative recovery of spectacle-corrected visual acuity and demonstrated greater refractive stability. Histopathological studies of rabbit and human corneas have shown a direct correlation between the amount of pulse radiant energy and resulting acute tissue injury (25,45). These studies have shown that Ho:YAG laser irradiation produces acute epithelial and stromal tissue changes, which stimulate a brisk wound-healing response. The wound healing response has been correlated to rapid early regression of refractive effect. In order to determine whether regression correlates to initial pulse energy, a clinical trial was conducted using five pulses of laser light (1.2 J of total energy compared to 2.35 J with 10 pulses) for treatment of low to moderate hyperopia (46). Thirty-nine eyes with preoperative spherical equivalent of Ⳮ2.95 Ⳳ 0.97 D (1.50 to 4.75 D) were treated with two radial rings of eight spots with diameters of 5 and 6 mm (Group A), 6 and 7 mm (Group B), or 6.5 and 7.5 mm (Group C). Uncorrected distance visual acuity improved in all three groups at 1-year follow-up. The mean change in spherical equivalent was ⳮ2.08 Ⳳ 1.13 D for Group A, ⳮ1.83 Ⳳ 0.88 D for Group B and ⳮ1.22 Ⳳ 0.88 D for Group C. In comparing the 10-pulse with the 5-pulse Ho:YAG treatment, there was less initial refractive effect with the 5-pulse treatment. However, there was also less regression, with increased stability of refractive effect. In addition, the duration of treatment for five pulses is reduced to 1 s, which is more comfortable for patients and less likely to produce irregular effects due to motion. Group C also showed reduced refractive effect when compared to groups A and B because of reduction in areal energy density with peripheral treatment. The induced refractive cylinder was greatest with group A, corresponding to the proximity of treatment spots to the central visual axis. Regression of initial refractive effect can be large with Ho:YAG LTK. Alio et al. demonstrated a direct relationship between refractive regression, age, and measurements of central corneal thickness (47). In this study, 57 eyes, with a mean preoperative spherical equivalent of Ⳮ3.80 Ⳳ 0.22 D (1.50 to 5.00 D), were treated with Ho:YAG LTK, applying

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two or three rings of eight spots, with 6-, 7-, and 8-mm-zone diameters. The mean spherical equivalent at 15 months was reduced to Ⳮ1.73 Ⳳ 0.16 D. In all, 57.8% of the eyes were Ⳳ1.00 D of intended correction, while 21% were Ⳳ0.50 D of intended correction. Patients with 75 to 100% regression were compared to those with 25% or less regression. Full regression was more common in patients between 18 and 30 years of age, with an inverse correlation with increasing age. Gezer et al. reported 18% regression in patients older than 20 years and 48% in patients less than 20 years of age (48). Corneal thickness correlated directly with regression. Patients with central corneal thickness of 525 ␮m or less experienced the least amount of regression. Average keratometry did not influence regression. Alio et al. hypothesize that the regression of effect might be due to the elasticity of Bowman’s membrane and stromal collagen in younger patients, or due to thicker corneas, allowing the cornea to return to its original shape. In addition, the thermal effectiveness of Ho:YAG LTK may depend on the water content of the corneal stroma, which may be age-dependent. Alio et al. have developed a formula for preoperative evaluation of the potential amount of postoperative regression: % of regression ⳱ average keratometry x pachymetry/15 x age. Since regression is common after Ho:YAG LTK, retreatment may be necessary. Nano and Muzzin conducted a study with 182 eyes with low hyperopia with mean preoperative spherical equivalent of Ⳮ2.50 Ⳳ 0.87 D (0.75 to 4.75 D) (49). At 12 months, the mean spherical equivalent was Ⳮ1.25 Ⳳ 0.96 D, with 45% regression in manifest refraction. Seventeen percent of the operated eyes were retreated (31 eyes). Eighteen (56%) eyes were retreated with Ho:YAG LTK, which has been reported to have a success rate between 50 and 70%. In the Sunrise LTK clinical trials, 85% of eyes were within Ⳳ1.0 D of emmetropia after retreatment (50). Excimer laser retreatment with laser-assisted in situ keratomileusis (LASIK) or photorefractive keratectomy (PRK) may also be performed after LTK. Nano and Muzzin treated 14 (45%) eyes with PRK (49). Portellinha et al. treated 12 eyes with hyperopic LASIK for residual hyperopia after LTK (51). The mean preoperative cycloplegic spherical equivalent refraction was Ⳮ3.31 D (1.00 to 6.50 D). Postoperatively, all eyes achieved reduction in hyperopia to a mean postoperative refraction of Ⳮ0.88 D. No morphological changes were observed in the radial thermal scars. Attia et al treated 50 eyes with hyperopic LASIK for regression after LTK (52). The mean spherical equivalent refraction improved from Ⳮ2.92 Ⳳ 1.60 D to Ⳮ0.36 Ⳳ 1.48 D; the predictability and efficacy were less than with primary LASIK for hyperopia. This study reported confluent haze between previous LTK spots in most eyes, as LASIK ablation took place at the sites of the LTK spots. The haze was greater when the LASIK flap cut coincided with the LTK spots. However, the corneal scarring did not seem to influence the visual results. Both studies conclude that LASIK after LTK is a good alternative for management of hyperopic regression. 3. LTK for PRK-Induced Hyperopia Myopic treatment with PRK may result in a significant overcorrection in 2 to 5% of patients. Ho:YAG LTK has been evaluated for the correction of hyperopia induced by PRK (53–56). Alio et al. evaluated the use of noncontact Ho:YAG LTK in 14 eyes with hyperopia induced by PRK with a mean spherical equivalent of Ⳮ4.20 Ⳳ 1.80 D (Ⳮ1.75 to Ⳮ6.25 D) (54). The Ho:YAG laser spots were applied outside the previous ablation zone to avoid confluence of haze. After 12-month follow-up, there was no difference between the mean preoperative spectacle-corrected visual acuity and the mean postopera-

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tive uncorrected visual acuity. There was a mean increase of Ⳮ4.60 Ⳳ 1.20 D in central keratometric power. Contact Ho:YAG LTK was also evaluated for correction of hyperopia and astigmatism after PRK. Eggink et al. reported limited efficacy and predictability in 16 eyes treated with contact Ho:YAG LTK (55). However, there were no sight-threatening complications. Goggin and Lavery reported treatment of 11 eyes with mean preoperative spherical equivalent of Ⳮ2.06 Ⳳ 1.02 D and postoperatively to Ⳮ0.511 Ⳳ 0.55 D after 1-year follow-up. (56) a total of 91% were 20/40 or better and 82% were within Ⳳ1.00 D of the target spherical equivalent. 4. LTK for LASIK-Induced Hyperopia LASIK is a safe and effective technique for correction of moderate to high myopia. However, 2 to 8% of patients may have significant overcorrection (57). The efficacy and safety of noncontact Ho:YAG LTK for correction of hyperopia after LASIK was evaluated in 13 eyes (58). After 18 months of follow-up, the mean cycloplegic refraction changed from Ⳮ4.6 Ⳳ 1.4 D (Ⳮ2.50 to Ⳮ7.25 D) to Ⳮ0.76 Ⳳ 0.11 D. All of the patients were within Ⳳ1.50 D of emmetropia, and no patient lost lines of best-corrected visual acuity. G. COMPLICATIONS Mild pain, tearing, photophobia, and foreign-body sensation have been reported 1 to 3 days after surgery.(21,39,42,46,50) These complications were related to laser-induced epithelial injury, which resolved within 3 days in most patients. Opacities in each treatment spot decreased over time, becoming undetectable in most patients in room light; however, the opacities were observed with slit-lamp biomicroscopy even after 2 years (42). Astigmatism has been shown to be induced by Ho:YAG LTK, especially with the smaller treatment diameters (32,42,50). No significant changes in endothelial cell density occurred up to 12 months postoperatively (33,44). There was no significant loss of contrast sensitivity and no change in glare test measurements (33,46,50). H. CONTINUOUS-WAVE DIODE LTK Compared to pulsed Ho:YAG lasers, diode lasers provide continuous heat to the target tissue with more uniform stromal heating. This potentially allows for higher and more stable refractive correction. Wavelength settings of 1.854, 1.870, 1.885, and 2.1 ␮m have been studied (59–63). The shorter wavelengths achieve greater corneal depth, with a wavelength of 1.854 ␮m causing extensive local endothelial damage (0.8 to 1.2 mm in diameter) (61,62). A wavelength of 1.885 ␮m has a penetration depth of 380 ␮m, comparable to the absorption of the Ho:YAG laser emitting at 2.07-␮m wavelength. Continuouswave diode LTK has been tested in eight blind human eyes (63). A wavelength of 1.854 or 1.870 ␮m with 100 to 150 mW power was applied for 10 s. The radiation was focused into the corneal stroma between 400 and 600 ␮m or 1000 ␮m with one or two eight-spot rings. The refractive change increased with higher laser power and smaller ring diameters. Two rings provided higher and more stable refractive effect of up to Ⳮ5.66 D. The refractive effect stabilized between 3 and 6 months. Greater endothelial damage was noted with a wavelength of 1.854 ␮m. Ho:YAG LTK offers an alternative treatment for the correction of hyperopia up to Ⳮ2.50 D. There is an initial overcorrection followed by regression, dependent on age and

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corneal thickness. Clinical studies have established the safety and efficacy of Ho:YAG LTK up to 2 years after treatment. LTK may also be used to treat PRK and LASIKinduced hyperopia. Diode lasers may help further improve stability of refractive effect with LTK. Wavefront-guided LTK may further improve the predictability of this procedure and allow for predictable outcomes even for retreatments of initial undercorrections. REFERENCES 1. Lans LJ. Experimentelle Untersuchungen u¨ber Entstehung von Astigmatismus durch nichtperforirende Corneawunden. Graefes Arch Ophthalmol 1898; 45:117–152. 2. Terrien F. Dystrophie marginale symme´trique des deux cornee´s avec astigmatisme regulier consecutif et guerison par la cauterisation ignee. Arch Ophthalmol (Paris) 1900; 20:12–21. 3. Wray C. Case of 6 D of hypermetropic astigmatism cured by the cautery. Trans Ophthalmol Soc UK 1914; 34:109–110. 4. Gassett AR, Shaw EL, Kaufman HE, Itoi M, Sakimoto T, Ishii Y. Thermokeratoplasty. Trans Am Acad Ophthalmol Otolaryngol 1973; 77:OP–441–OP–454. 5. Shaw EL, Gassett AR. Thermokeratoplasty (TKP) temperature profile. Invest Ophthalmol Vis Sci 1974; 13:181–186. 6. Keates RH, Dingle J. Thermokeratoplasty for keratoconus. Ophthalm Surg 1975; 6:89–92. 7. Fogle JA, Kenyon KR, Stark WJ. Damage to epithelial basement membrane by thermokeratoplasty. Am J Ophthalmol 1977; 83:392–401. 8. Aquavella JV, Smith RS, Shaw EL. Alterations in corneal morphology following thermokeratoplasty. Arch Ophthalmol 1976; 94:2082–2085. 9. Arensten JJ, Rodrigues MM, Laibson PR. Histopathologic changes after thermokeratoplasty for keratoconus. Invest Ophthalmol Vis Sci 1977; 16:32–38. 10. Itoi M. Computer phtokeratometry changes following thermokeratoplasty. In: Schachar RA, Levy NS, Schachar L, eds. Refractive Modulation of the Cornea. Denison, TX: LAL Publishers, 1981:61–69. 11. Rowsey JJ, Doss JD. Preliminary report of Los Alamos Keratoplasty techniques. Ophthalmology 1981; 88:755–760. 12. Neumann AC, Fyodorov S, Sanders DR. Radial thermokeratoplasty for the correction of hyperopia. J Refract Corneal Surg 1990; 6:404–412. 13. Neumann AC, Sanders D, Raanan M, DeLuca M. Hyperopic thermokeratoplasty: clinical evaluation. J Cataract Refract Surg 1991; 17:830–838. 14. Neumann AC. Thermokeratoplasty for hyperopia. Ophthalmol Clin North Am 1992; 5: 753–772. 15. Feldman ST, Ellis W, Frucht-Perry J, Chayet A, Brown SI. Regression of effect following radial thermokeratoplasty in humans. J Refract Corneal Surg 1989; 5:288–291. 16. Beckman H, Fuller TA, Boyman R, Mandell G, Nathan LE Jr. Carbon dioxide laser surgery of the eye and adnexa. Ophthalmology 1980; 87:990–1000. 17. Peyman GA, Larson B, Raichand M, Andrews AH. Modification of rabbit corneal curvature with use of carbon dioxide laser burns. Ophthalm Surg 1980; 11:325–329. 18. Kanoda AN, Sorokin AS. Laser correction of hypermetropic refraction. In: Fyodorov SN, ed. Microsurgery of the Eye: Main Aspects. Moscow: MIR Publishers, 1987:147–154. 19. Horn G, Spears KG, Lopez O, Lewicky A, Yang XY, Riaz M, Wang R, Silva D, Serafin J. New refractive method for laser thermal keratoplasty with the Co:MgF2 laser. J Cataract Refract Surg 1990; 16:611–616. 20. Koch DD, Padrick TD, Menefee RL. Laser phtothermal keratoplasty: nonhuman primate results. Invest Ophthalmol Vis Sci 1992; 33(suppl):768. 21. Seiler T, Matallana M, Bende T. Laser themokeratoplasty by means of a pulsed holmium:YAG laser for hyperopic correction. J Refract Corneal Surg 1990; 6:335–339.

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22. Durrie DS, Seiler T, King MC. Application of the holmium:YAG laser for refractive surgery. SPIE Proc 1992; 1644:56–60. 23. Stringer H, Parr J. Shrinkage temperature of eye collagen. Nature 1964; 204:1307. 24. Allain JC, Le Lous M, Cohen-Solal S, Bazin S, Maroteaux P. Isometric tensions developed during hydrothermal swelling of rat skin. Connect Tissue Res 1980; 7:127–133. 25. Koch DD. Histological changes and wound healing response following noncontact holmium: YAG laser thermal keratoplasty. Tr AM Ophth Soc 1996; 94:745–802. 26. Bakerman S. Distribution of the alpha- and beta-components in human skin collagen with age. Biochim Biophys Acta (Amst) 1964; 90:621. 27. McCally RL, Bargeron CB, Green WR, Farrell RA. Stromal damage in rabbit corneas exposed to CO2 laser radiation. Exp Eye Res 1983; 37:543–550. 28. Smelser GK, Polack FM, Ozanics V. Persistence of donor collagen in corneal transplants. Exp Eye Res 1965; 4:349–354. 29. Lass JH, Ellison RR, Wong KM, Klein L. Collagen degradation and synthesis in experimental corneal grafts. Exp Eye Res 1986; 42:201–210. 30. Koch DD, Berry MJ, Vassiliadis A. Non-contact holmium:YAG laser thermal keratoplasty. In: Salz JJ, ed. Corneal Laser Surgery. Philadelphia: Mosby-Year Book, 1994:247–254. 31. Alio´ JL, Pe´rez-Santonja JJ. Correction of hyperopia by laser thermokeratoplasty (LTK). In: Agarwal S, Agarwal A, Pallikaris IG, Neuhann TH, Knorz MC, Agarwal A, eds. Refractive Surgery. New Delhi: Jaypee, 2000:583–591. 32. Cavanaugh TB, Durrie DS. Holmium YAG laser thermokeratoplasty: synopsis of clinical experience. Semin Ophthalmol 1994; 9(2):110–116. 33. Koch DD, Kohnen T, McDonnell PJ, Menefee RF, AAS, Berry MJ. Hyperopia correction by noncontact holmium: YAG laser thermal keratoplasty. United States phase IIA clinical study with a 1-year follow-up. Ophthalmology 1996; 103(10):1525–1535. 34. Tutton MK, Cherry PM. Holmium:YAG laser thermokeratoplasty to correct hyperopia: two years follow-up. Ophthalm Surg Lasers 1996; 27(5 suppl):S521–S524. 35. Eggink CA, Bardak Y, Cuypers MHM, Deutman AF. Treatment of hyperopia with contact Ho:YAG laser thermal keratoplasty. J Refract Surg 1999; 15(1):16–22. 36. Lim KH, Kim WJ, Wee WR, Shin DE, Lee JH, Chang BL. Holmium: YAG laser thermokeratoplasty for astigmatism in rabbits. J Refract Surg 1996; 12(1):190–193. 37. Hennekes R. Holmium:YAG laser thermokeratoplasty for correction of astigmatism. J Refract Surg 1995; 11(3 suppl):S358-S360. 38. Thompson V. Holmium: YAG laser thermokeratoplasty for correction of astigmatism. J Refract Corneal Surg 1994; 10:S293. 39. Ariyasu RG, Sand B, Menefee R, AAS, Hennings D, Rose C, Berry M, Garbus JJ, McDonnell PJ. Holmium laser themokeratoplasty of 10 poorly sighted eyes. J Refract Surg 1995; 11: 358–365. 40. Koch DD, Kohnen T, McDonnell PJ, Menefee RF, Berry MJ. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty. United States phase IIA clinical study with a 1-year follow-up. Ophthalmology 1996; 103(10):1525–1535. 41. Kohnen T, Husain SE, Koch DD. Corneal topographic changes after noncontact holmium:YAG laser thermal keratoplasty to correct hyperopia. J Cataract Refract Surg 1996; 22:427–435. 42. Koch DD, Abarca A, Villarreal R, Menefee R, AAS, Kohnen T, Vassiliadis A, Berry M. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty. Clinical study with two-year follow-up. Ophthalmology 1997; 104(11):1938–1947. 43. Kohnen T, Koch DD, McDonnell PJ, Menefee RF, Berry MJ. Noncontact holmium:YAG laser thermal keratoplasty to correct hyperopia: 18-month follow-up. Ophthalmologica 1997; 211: 274–282. 44. Vinciguerra P, Kohnen T, Azzolini M, Radice P, Epstein D, Koch DD. Radial and staggered treatment patterns to correct hyperopia using noncontact holmium:YAG laser thermal keratoplasty. J Cataract Refract Surg 1998; 24:21–30.

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45. Koch DD, Kohnen T, Anderson JA, Binder PS, Moore MN, Menefee RF, AAS, Valderamma GL, Berry MJ. Histologic changes and wound healing response following 10-pulse noncontact holmium:YAG laser thermal keratoplasty. J Refract Surg 1996; 12:623–634. 46. Kohnen T, Villarreal V, R, Menefee R, Berry M, Koch DD. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty: five-pulse treatments with 1 year follow-up. Graefes Arch Clin Exp Ophthalmol 1997; 235:702–708. 47. Alio´ JL, Ismail MM, Sanchez Pego JL. Correction of hyperopia with non-contact Ho:YAG laser thermal keratoplasty. J Refract Surg 1997; 13(1):17–22. 48. Gezer A. The role of patient’s age in regression of holmium:YAG thermokeratoplasty-induced correction of hyperopia. Eur J Ophthalmol 1997; 7(2):139–143. 49. Nano HD, Muzzin S. Noncontact holmium:YAG laser thermal keratoplasty for hyperopia. J Cataract Refract Surg 1998; 24:751–757. 50. Aker AB, Brown DC. Hyperion laser thermokeratoplasty for hyperopia. Int Ophthalmol Clin 2000; 40(3):165–181. 51. Portellinha W, Nakano K, Oliveira M, Simoceli R. Laser in situ keratomileusis for hyperopia after thermal keratoplasty. J Refract Surg 1999; 15(2 suppl):S218–S220. 52. Attia W, Pe´rez-Santonja JJ, Alio´ JL. Laser in situ keratomileusis for recurrent hyperopia following laser thermal keratoplasty. J Refract Surg 2000; 16:163–169. 53. Pop M. Laser thermal keratoplasty for the treatment of photorefractive keratectomy overcorrections: a 1-year follow-up. Ophthalmology 1998; 105(5):926–931. 54. Alio´ JL, Ismail MM, Artola A, Pe´rez-Santonja JJ. Correction of hyperopia induced by photorefractive keratectomy using non-contact Ho:YAG laser thermal keratoplasty. J Refract Surg 1997; 13:13–16. 55. Eggink CA, Meurs P, Bardak Y, Deutman AF. Holmium laser thermal keratoplasty for hyperopia and astigmatism after photorefractive keratectomy. J Refract Surg 2000; 16:317–322. 56. Goggin M, Lavery F. Holmium laser thermokeratoplasty for the reversal of hyperopia after myopic photorefractive keratectomy. Br J Ophthalmol 1997; 81:541–543. 57. Pe´rez-Santonja JJ, Bellot J, Claramonte P, Ismail MM, Alio´ JL. Laser-in-situ keratomileusis to correct high myopia. J Cataract Refract Surg 1997; 23:372–385. 58. Ismail MM, Alio´ JL, Pe´rez-Santonja JJ. Noncontact thermokeratoplasty to correct hyperopia induced by laser-in-situ keratomileusis. J Cataract Refract Surg 1998; 24:1191–1194. 59. Bende T, Jean B, Oltrup T. Laser thermal keratoplasty using a continuous wave diode laser. J Refract Surg 1999; 15:154–158. 60. Brinkmann R, Koop N, Geerling G, Kampmeier J, Borcherding S, Kamm K, Birngruber R. Diode laser thermokeratoplasty: application strategy and dosimetry. J Cataract Refract Surg 1998; 24(9):1195–1207. 61. Koop N, Wirbelauer C, Tu¨ngler A, Geerling G, Bastian GO, Brinkmann R. Thermal damage to the corneal endothelium in diode laser thermokeratoplasty. Ophthalmologe 1999; 96(6): 392–397. 62. Wirbelauer C, Koop N, Tu¨ngler A, Geerling G, Birngruber R, Laqua H, Brinkmann R. Corneal endothelial cell damage after experimental diode laser thermal keratoplasty. J Refract Surg 2000; 16:323–329. 63. Geerling G, Koop N, Brinkmann R, Tu¨ngler A, Cand med.m, Wirbelauer C, Birngruber R, Laqua H. Continuous-wave diode laser thermokeratoplasty: first clinical experience in blind human eyes. J Cataract Refract Surg 1999; 25:32–40.

9 Conductive Keratoplasty for the Correction of Low to Moderate Hyperopia MARGUERITE B. McDONALD Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A. JONATHAN DAVIDORF Davidorf Eye Group, West Hills, and Maloney Vision Institute, Los Angeles, California, U.S.A. ROBERT K. MALONEY Maloney Vision Institute, Los Angeles, California, U.S.A. EDWARD E. MANCHE Stanford University School of Medicine, Palo Alto, California, U.S.A. PETER HERSH Cornea and Laser Vision Center, Teaneck, New Jersey, U.S.A. GEORGE M. SALIB Tulane University School of Medicine, New Orleans, Louisiana, U.S.A.

A. HYPEROPIA CORRECTION BY CONDUCTIVE KERATOPLASTY 1. Thermokeratoplasty Procedures Surgical correction of hyperopia has been a greater challenge to ophthalmology than the correction of myopia. Attempts to steepen the central cornea by non-ablative methods, such as thermal keratoplasty, date back to the rabbit studies by Lans in the nineteenth century. During the 1980s, hot-wire thermokeratoplasty, a technique developed in the 95

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Soviet Union, was used to produce thermal burns (up to 600⬚C) that penetrated to 95% of corneal depth (1). Studies showed substantial overcorrection followed by marked regression (2–4). Evaluation of the procedure through well-designed clinical trials before adoption and dissemination was recommended (5). The failure of high-temperature probes to produce a stable, predictable, and safe hyperopic correction led to the investigation of other modalities of thermal keratoplasty, including contact holmium: YAG laser thermal keratoplasty (Holmium 25, Technomed, Baesweiler, Germany) (6–8), pulsed, noncontact holmium:YAG laser keratoplasty (noncontact LTK, Hyperion System, Sunrise Technologies, Fremont, CA) (9–18), continuouswave diode laser thermokeratoplasty (DTK, Rodenstock, ProLaser Medical Systems, Inc., Dusseldorf, Germany) (19–20), and radiofrequency-based conductive keratoplasty (CK) (Refractec, Inc., Irvine, CA) (21). These techniques have been more successful than the original hot-needle technique, although regression and induction of astigmatism have continued to be concerns with some techniques. In addition to thermokeratoplasty procedures, ablative methods, such as photorefractive keratectomy (PRK) (22–27) and laser in situ keratomileusis (LASIK) (28–34), have been used to correct hyperopia. Generally, attempted hyperopia corrections with these methods have been higher (⬎3.00 D) than the range recommended for CK. 2. Conductive Keratoplasty: The Mechanism The conductive keratoplasty procedure performed with the ViewPoint CK System (Fig. 1) is designed to treat spherical, previously untreated hyperopia of 0.75 to 3.00 D. Treatment of astigmatism, presbyopia, and over- or undercorrections following LASIK or other refractive procedures are other potential applications. Conductive keratoplasty delivers low-energy, high-frequency (radiofrequency, 350 kHz) current directly into the corneal stroma by means of a Keratoplast tip inserted into the peripheral cornea at eight or more treatment points (Fig. 2). Collagen within the targeted treatment zone is heated in a gentle, controlled fashion as a result of the natural resistance of stromal tissue to the flow of the current (35). Because resistance to the flow of the

Figure 1 The ViewPoint Conductive Keratoplasty (CK) System: console, probe, and specula.

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Figure 2 The CK Keratoplast tip shown next to a 7–0 suture. (Courtesy of Refractec, Inc., Irvine, CA.)

current increases with increasing dehydration of collagen, the process tends to be selflimiting. A thermal model predicts a cylindrical footprint approximately 150 to 200 ␮m wide by 500 ␮m deep that extends to approximately 80% of the depth of the mid-peripheral cornea at each treated spot (36). Striae form between the treated spots, creating a band of tightening that increases the curvature of the central cornea, thereby decreasing hyperopia. The Hyperion noncontact LTK technique, on the other hand, applies heat directly to the surface of the cornea, heating tissue in a gradient, and generates a conical footprint (10). B. THE CONDUCTIVE KERATOPLASTY PROCEDURE 1. The Conductive Keratoplasty Device The Viewpoint CK system consists of a radiofrequency energy-generating console, a handheld, reusable, pen-shaped handpiece attached by a removable cable and connector, a speculum (choice of two, Lancaster or Barraquer) that provides a large surface for an electrical return path, and a pedal that controls release of radiofrequency energy. Attached to the handpiece is the Keratoplast tip, a single-use, disposable, stainless steel penetrating tip, 90 ␮m in diameter and 450 ␮m long, that delivers the current directly to the corneal stroma. At the very distal portion of the tip is a Teflon-coated stainless-steel stop that assures correct depth of penetration. 2. Patient Selection a. Suitable Patients Patients suitable for treatment with the Viewpoint CK System should have 0.75 to 3.00 D of spherical hyperopia and ⱕ0.75 D of refractive astigmatism. Visual acuity should be correctable to at least 20/40 in both eyes. Hard or rigid gas-permeable lenses should be

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discontinued for at least 3 weeks and soft lenses for at least 2 weeks prior to the preoperative evaluation. Wearers of hard contact lenses should have two central keratometry readings and two manifest refractions taken at least 1 week apart. The manifest refraction measurements must not differ from the earlier measurements by more than 0.50 D in either meridian. Keratometry mires must be regular. b. Unsuitable Patients Patients with a peripheral pachymetry reading at the 6-mm optical zone of less than 560 ␮m are not suitable for treatment with the Viewpoint CK System. Also unsuitable are those who have had strabismus surgery; have anterior segment pathology; have residual, recurrent, active ocular or uncontrolled eyelid disease or any corneal abnormality; or have signs of progressive or unstable hyperopia. Other relative contraindications are a history of herpes zoster keratitis, herpes simplex keratitis, glaucoma, a history of steroid-responsive rise in intraocular pressure (IOP), a preoperative IOP ⬎21 mmHg, or narrow angles. Patients with diabetes, diagnosed autoimmune disease, connective tissue disease, an immunocompromised state, current treatment with chronic systemic corticosteroid or other immunosuppressive therapy that may affect wound healing; a history of keloid formation; intractable keratoconjunctivitis sicca; or pregnancy are also contraindicated to receive the CK treatment. 3. Examinations Preoperative examinations should include a manifest and cycloplegic refraction, an uncorrected and best spectacle-corrected visual acuity (distance and near), a slit-lamp and fundoscopic examination, applanation tonometry, central keratometry, ultrasonic pachymetry, and computed corneal topography. 4. Performing the CK Procedure Correct the patient’s full cycloplegic spectacle refraction. Administer one drop of topical anesthetic three times at 5-min intervals and monitor the patient for degree of anesthesia. Do not use pilocarpine. Insert the CK lid speculum to provide corneal exposure and act as an electrical return path. Do not use a lid drape, for it may prevent direct contact of the lid speculum and eyelid, which would disrupt the electrical current return path. Tape the fellow eye closed. Position the operating microscope or slit-lamp biomicroscope over or in front of the eye to be treated. Mark the cornea with the CK marker, and remind the patient to fixate on the light from the microscope. Dampen the CK marker with gentian violet or rose bengal stain. Center the marker’s cross hairs over the center of the pupil and apply light pressure on the marker to make a circular mark with eight intersections on the cornea. If using gentian violet, irrigate with balanced salt solution to remove excess ink. Dry the surface of the cornea thoroughly with a fiber-free sponge to avoid dissipation of applied energy by a wet surface. Set the appropriate treatment parameters on the console according to the nomogram (Table 1). The default setting for treatment is 350 kHz, 60% power (0.6 W) for 0.6 s. Inspect the Keratoplast tip under the microscope to ensure it is not damaged or bent prior to application. When treating 0.75 to 0.875 D of hyperopia (eight spots), treat only at the 7-mm optical zone, beginning treatment at the 12 o’clock position and continuing in the sequence shown in Figure 3. When treating higher levels of hyperopia, follow the nomo-

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Table 1 Conductive Keratoplasty Nomogram Diopters to be corrected ⫹0.75 D to ⫹0.875 D ⫹1.00 D to ⫹1.625 D ⫹1.75 D to ⫹2.25 D ⫹2.375 D to ⫹3.00 D

Number of CK treatment spots 8 16 24 32

CK—Conductive Keratoplasty

gram and application sequence. For example, for treating 1.00 to 1.625 D of hyperopia, apply a total of 16 spots: 8 spots at the 6-mm optical zone and 8 at the 7-mm optical zone. Begin application at each of these optical zones at the 12 o’clock position and continue in sequence until the full circle of spots has been completed. For treating 1.75 to 2.25 D, apply treatment at the 6-, 7-, and 8-mm optical zones for a total of 24 spots. For treating 2.375 D to 3.00 D, apply treatment to the 6-, 7-, and 8-mm optical zones and then to each of the eight sectors between the previously treated spots at the 7-mm optical zone for a total of 32 spots. To treat each spot, place the tip of the delivery probe at the treatment mark on the cornea, perpendicular to the corneal surface. Apply light pressure until the tip penetrates the cornea down to the insulator stop. Depress the foot pedal to apply the radio frequency energy. A tone will sound as the energy is applied. At each treatment spot, keep the tip in place until the preprogrammed treatment time has been completed (the tone stops). Clean the tip with a fiber-free sponge after each treatment spot to remove any tissue debris,

Figure 3 Number, location, and sequence of treatment spots. (Courtesy of Refractec, Inc., Irvine, CA.)

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taking care not to damage the tip. Perform intraoperative keratometry after completing the full circle of treatments to check for any induced cylinder. 5. Postoperative Care The surgeon may follow his or her usual refractive surgery postoperative care regimen. Administration of one drop of a topical ophthalmic antibiotic solution and one drop of an ophthalmic nonsteroidal anti-inflammatory drug, continued for up to 3 days, according to product labeling, is recommended. Administration of topical corticosteroids is not recommended. A bandage contact lens may be used for comfort for 24 to 48 h postoperatively but is usually not necessary.

C. UNITED STATES MULTICENTER CLINICAL TRIAL 1. Patients and Methods A 2-year, multicenter, prospective clinical trial is being conducted in the United States to evaluate the safety, efficacy, and stability of conductive keratoplasty when performed on eyes with 0.75 to 3.00 D of hyperopia and less than 0.75 D of cylinder. Each procedure was performed by one of 14 surgeons at 20 centers according to methods described above. All eyes were treated at the default setting of 350 kHz, 60% power for 0.6 s. No retreatments were performed. A total of 231 patients were treated; 361 eyes were treated with the current nomogram for CK and an additional 29 were treated with an earlier nomogram that had a tendency to undercorrect (Table 2). These 29 eyes were excluded from analysis of efficacy variables. Thus, data from 361 eyes were evaluated for efficacy, stability, and safety, while data from 390 eyes were evaluated for stability and safety only. At 12 months, a total of 96 eyes were available for stability and safety analyses and 127 were available for stability, safety, and efficacy analyses. Uncorrected distance visual acuity (UCVA) preoperatively was 20/40 or worse in 81% of the eyes, and uncorrected near visual acuity was J5 or worse in 95%. Postoperative care and examinations followed the methods described above.

Table 2 Clinical Study Eyes Eyes

Attribute

Evaluated for safety and stability variables only Evaluated for all variables (Efficacy, safety, stability) Available at 12 months for stability and safety analyses Available at 12 months for safety, efficacy, and stability analyses Age Mean Preoperative MRSE Mean Preoperative CRSE

N ⫽ 390 N ⫽ 361 N ⫽ 96 N ⫽ 127

MRSE—Manifest refractive spherical equivalent CRSE—Cycloplegic refractive spherical equivalent

55 ⫾ 5.4 years (40 to 74) ⫹1.82 ⫾ 0.60 D (0.75 to 3.00 D) ⫹1.76 ⫾ 0.60 D (0.75 to 3.25 D)

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Figure 4 Postoperative UCVA over time.

2. Results a. Efficacy Twelve months postoperatively, UCVA was 20/20 or better in 53/96 (55%), 20/25 or better in 73/96 (76%), and 20/40 or better in 87/96 (91%) of the eyes (Fig. 4). Near UCVA increased an average of six Jaeger lines. Mean MRSE values showed 53/96 (55%) within Ⳳ0.50 D of intended correction, 87/96 (91%) within Ⳳ1.00 D, and 94/96 (98%) within Ⳳ2.00 D (Fig. 5). A summary of the efficacy results with conductive keratoplasty is shown in Table 3.

Table 3 Summary of Efficacy Results with Conductive Keratoplasty Compared with FDA Guidelines for Refractive Procedures

UCVA ⱖ 20/20 UCVA ⱖ 20/25 UCVA ⱖ 20/40 MRSE ⫾ 0.50 D MRSE ⫾ 1.00 D MRSE ⫾ 2.00 D

FDA guideline

6 Months (N⫽348)

9 Months (N⫽276)

12 Months (N⫽96)

50% Not stipulated 85% 50% 75% Not stipulated

46% 65% 90% 60% 88% 99%

48% 72% 92% 66% 88% 99%

55% 76% 91% 55% 91% 98%

FDA ⫽ Food and Drug Administration UCVA ⫽ Uncorrected Visual Acuity MRSE ⫽ Manifest Refractive Spherical Equivalent

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Figure 5 Accuracy of achieved MRSE.

b. Corneal Topography Corneal topography of a typical eye with an MRSE of Ⳮ3.25 D and UCVA of 20/125 preoperatively shows central steepening postoperatively surrounded by a midperipheral flattening (Fig. 6). Twelve months postoperatively, this eye had an MRSE of Ⳮ0.25 D and UCVA of 20/20.

Figure 6 Conductive keratoplasty case study. Corneal topography of a typical eye with an MRSE of Ⳮ3.25 preoperatively D and UCVA of 20/125 preoperatively shows post-CK central steepening surrounded by a midperipheral flattening. Twelve months postoperatively, this eye had an MRSE of Ⳮ0.25 D and UCVA of 20/20.

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Table 4 Stability of Manifest Refraction through 12 Months (Cohort of Patients with All Postoperative Visits, N ⫽ 115) Change in MRSE

3–6 Months

6–9 Months

9–12 Months

ⱕ0.50 D ⱕ0.75 D ⱕ1.00 D Mean Change (SD) (paired differences) 95% Confidence Interval

73% 90% 96% 0.27 D (0.43)

85% 94% 97% 0.09 D (0.40)

83% 97% 97% 0.15 D (0.39)

0.19,0.35

0.01,0.17 D

0.07,0.23

MRSE—Manifest Refractive Spherical Equivalent

c. Stability Refractive stability after the procedure was demonstrated by the mean change in residual SE refraction for all treated eyes at three intervals during the study (Table 4). During the last two intervals (6 to 9 months, 9 to 12 months), the mean MRSE changed 0.09 D (confidence interval 0.01, 0.17) and 0.16 D (confidence intervals 0.07 and 0.22), respectively. The mean change in MRSE between postoperative visits from 0.50 D or less in 73% of the eyes between the 3- and 6-month visits, in 85% of the eyes between the 6and 9-month visits, and in 83% of the eyes between the 9- and 12-month visits and in 83% of the eyes between the 9- and 12- month visits (Fig. 7). The refraction appeared to stabilize at approximately 6 months.

Figure 7 Change in MRSE between postoperative visits. N ⳱ 115 (patients present for all followup visits).

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Figure 8 Slit-lamp view of treatment spot 1 h after CK showing bands of striae between spots. The surface leukomas are small because all of the energy is delivered within the stroma. (Courtesy of Refractec, Inc., Irvine, CA.)

d. Slit Lamp One hour after treatment, the opacities at each treatment spot were visible by slit lamp as small surface leukomas, with a band of striae connecting the treatment spots (Fig. 8). These leukomas are small because CK delivers energy deep into the stroma rather than on the surface. The striae between treatment zones remain visible at 3, 6, and 12 months, as reported by the United States CK clinical trial investigators, and suggest that the effect of treatment on the stroma is long-lasting. e. Safety No eye had lost two or more lines of BSCVA and no eye had BSCVA worse than 20/40 at 12 months (Table 5). A total of 1/127 (1%) of eyes had an increase of ⬎2.00 D of

Table 5 Summary of Safety Results with Conductive Keratoplasty Postoperative visit

2 Lines loss of BSCVA ⬎2 Lines loss of BSCVA BSCVA Worse than 20/40 Increase 2.00 D Cylinder Increase ⬎ 2.00 D Cylinder BSCVA ⬍20/25 if better than 20/20 Pre-op

1 Month (N⫽390)

3 Months (N⫽390)

6 Months (N⫽384)

9 Months (N⫽218)

12 Months (N⫽79)

6% 2% 0% 3% 3% 4%

5% 1% 0% 2% 2% 2%

4% 1% 0% 1% 1% 1%

2% ⬍1% 0% 0% ⬍1% 1%

0% 0% 0% 0% 1% 0%

BSCVA—Best Spectacle-Corrected Visual Acuity

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cylinder at 12 months and 0/127 had an increase of 2.00 D. Seventy five percent had no change (within Ⳳ 0.50 D) in cylinder. No eye with BSCVA of 20/20 or better preoperatively was worse than 20/25 postoperatively. No intraoperative complications or adverse events occurred during the surgeries, and there were no treatment-related adverse events. D. CONCLUSION The 12-month results in the ongoing 2-year prospective clinical study of the CK technique for correcting low to moderate spherical hyperopia are encouraging. Postoperative visual acuity and predictability of refraction were excellent and are comparable to or better than results obtained with PRK or LASIK for low hyperopia (17–34). The CK refractive effect appears to stabilize by 6 months, surpassing the early studies of refractive stability results seen following the noncontact LTK method (11–16). However, recent LTK postmarketing approval data from phase 3 FDA clinical trials shows that LTK is stable after 3 months. Availability of the 2-year results will confirm the efficacy, predictability, and safety of results seen with CK at 1 year and provide validation of this nonlaser option for the treatment of low to moderate hyperopia. REFERENCES 1. Fogle JA, Kenyon KR, Stark WJ. Damage to the epithelial basement membrane by thermokeratoplasty. Am J Ophthalmol 1977; 83:392–401. 2. Neumann A, Sanders D, Raanan M, DeLuca M. Hyperopic thermokeratoplasty: clinical evaluation. J Cataract Refract Surg 1991; 17:830–838. 3. Feldman S, Ellis W, Frucht-Pery J, Chayet A, Brown S. Regression of effect following radial thermokeratoplasty in humans. J Refract Surg 1995; 18:288–291. 4. Charpentier D, Nguyen-Khoa J, Duplessix M, Colin J, Denis P. Intrastromal thermokeratoplasty for correction of spherical hyperopia: a 1-year prospective study. J Fr Ophthalmol 1995; 18: 200–206. 5. McDonnell PJ. Radial thermokeratoplasty for hyperopia: I. The need for prompt investigation. Refract Corneal Surg 1989; 5:50–52. 6. Durrie DS, Schumer JD, Cavanaugh TB. Holmium:YAG laser thermokeratoplasty for hyperopia. J Refract Corneal Surg 1994; 10:S277–S280. 7. Eggink CA, Bardak Y, Cuypers MHM, Deutman AF. Treatment of hyperopia with contact Ho:YAG laser thermal keratoplasty. J Refract Surg 1999; 15:16–22. 8. Eggink CA, Meurs P, Bardak Y, Deutman AF. Holmium laser thermal keratoplasty for hyperopia and astigmatism after photorefractive keratectomy. J Refract Surg 2000; 16:317–322. 9. Koch DD, Kohnen T, McDonnell PJ, Menefee RF, Berry MJ. Hyperopia correction by noncontact holmium:YAG laser thermokeratoplasty; United States phase IIA clinical study with a 1-year follow-up. Ophthalmology 1996; 103:1525–1536. 10. Koch DD, Kohnen T, Anderson JA, Binder PS, Moore MN, Menefee RF, Valderamma GL, Berry MJ. Histologic changes and wound healing response following 10-pulse noncontact holium: YAG laser thermal keratoplasty. J Refract Surg 1996; 12:623–634. 11. Koch DD, Abarca A, Villarreal R, Menefee R, Kohnen T, Vassiliadis A, Berry M. Hyperopia correction by non-contact holmium: YAG laser thermokeratoplasty: clinical study with twoyear follow-up. Ophthalmology 1996; 103:731–740. 12. Koch D, Kohnen T, McDonnell P, Menefee R, Berry M. Hyperopia correction by noncontact holmium: YAG laser thermal keratoplasty. Ophthalmology 1997; 104:1938–1947. 13. Nano HD, Muzzin S. Noncontact holmium:YAG laser thermal keratoplasty for hyperopia. J Cataract Refract Surg 1998; 24:751–757.

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14. Koch DD, Kohnen T, McDonnell PJ, Menefee R, Berry M. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty: United States phase IIA clinical study with a 2year follow-up. Ophthalmology 1997; 104:1938–1947. 15. Alio JL, Ismail MM, Sanchez Pego JL. Correction of hyperopia with non-contact Ho:YAG laser thermal keratoplasty. J Refract Surg 1997; 13:17–22. 16. Alio JL, Ismail MM, Artola A, Perez-Santonja JJ. Correction of hyperopia induced by photorefractive keratectomy using non-contact Ho:YAG laser thermal keratoplasty. J Refract Surg 1997; 13:13–16. 17. Pop M. Laser thermal keratoplasty for the treatment of photorefractive keratectomy overcorrections: A 1-year follow-up. Ophthalmology 1998; 105:926–931. 18. Ismail MM, Alio JL, Perez-Santonja JJ. Noncontact thermokeratoplasty to correct hyperopia induced by laser in situ keratomileusis. J Cataract Refract Surg 1998; 24:1191–1194. 19. Bende T, Jean B, Oltrup T. Laser thermal keratoplasty using a continuous wave diode laser. J Refract Surg 1999; 15:154–158. 20. Geerling G, Koop N, Brinkmann R, Tungler A, Wirbelauer C, Birngruber R, Laqua H. Continuous-wave diode laser thermokeratoplasty in blind human eyes. J Refract Surg 1999; 25:32–40. 21. Mendez A, Mendez Noble A. Conductive keratoplasty for the correction of hyperopia. In: Sher NA, ed. Surgery for Hyperopia and Presbyopia. Williams & Wilkins; 1997:163–171. 22. Jackson WB, Mintsioulis G, Agapitos PJ, Casson EJ. Excimer laser photorefractive keratectomy for low hyperopia: safety and efficacy. J Cataract Refract Surg 1997; 23:480–487. 23. Daya SM, Tappouni FR, Habib NE. Photorefractive keratectomy for hyperopia. Six month results in 45 eyes. Ophthalmology 1997; 104:1952–1958. 24. Vinciguerra P, Epstein D, Radice P, Azzolini M. Long-term results of photorefractive keratectomy for hyperopia and hyperopic astigmatism. J Refract Surg 1998; 14:S183-S185. 25. Pietila J, Makinen P, Pajari S, Uusitalo H. Excimer laser photorefractive keratectomy for hyperopia. J Refract Surg 1997; 13:504–510. 26. O’Brart DP, Stephenson CG, Oliver K, Marshall J. Excimer laser photorefractive keratectomy for the correction of hyperopia using an erodible mask and axicon system. Ophthalmology 1997; 104:1959–1970. 27. Dausch D, Klein R, Schroder E. Excimer laser photorefractive keratectomy for hyperopia. J Refract Surg 1993; 9:20–28. 28. Davidorf DM, Eghbali F, Onclinx T, Maloney RF. Effect of varying the optical zone diameter on the results of hyperopic laser in situ keratomileusis. Ophthalmology 2001; 108:1266–1268. 29. Argento CJ, Cosentino MJ. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg 1998; 24:1050–1058. 30. Ditzen K, Huschka H, Pieger S. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg 1998; 24:42–47. 31. Esquenazi S, Mendoza A. Two-year follow-up of laser in situ keratomileusis for hyperopia. J Refract Surg 1999; 15:648–652. 32. Goker S, Er H, Kahvecioglu C. Laser in situ keratomileusis to correct hyperopia from Ⳮ4.25 to 8.0 D. J Refract Surg 1998; 14:26–30. 33. Rashad KM. Laser in situ keratomileusis for the correction of hyperopia from Ⳮ1.25 to 5.00 diopters with the Keracor 117C laser. J Refract Surg 2001; 17:123–128. 34. Tabbara KF, El-Sheikh HF, Islam SM. Laser in situ keratomileusis for the correction of hyperopia from Ⳮ0.50 to 11.50 diopters with the Technolas Keracor 117C laser. J Refract Surg 2001; 17:113–122. 35. Goth P, Stern R. Conductive Keratoplasty, Principles and Technology, presented at the American Society for Cataract and Refractive Surgery, Boston, April, 2000. 36. Data on File, Refractec, Inc.

10 Intracorneal Segments for Hyperopia LAURA GOMEZ and ARTURO S. CHAYET Codet Aris Vision Institute, Tijuana, B.C., Mexico

A. BACKGROUND The intracorneal segments (ICS) for hyperopia reshape the anterior surface of the cornea without permanently changing the structure or function of the natural eye and are intended to be an alternative to eyeglasses, contact lenses, or irreversible refractive surgery procedures for hyperopic patients. The radially placed segments create a flattening of the peripheral cornea by shortening the chord length tangential to the limbus. This peripheral flattening causes the central cornea to steepen and the corneal radius to decrease, thus correcting for hyperopia (Fig. 1). Implantation of the segments does not involve the central cornea and no tissue is removed. In addition, the cornea maintains its asphericity and normal prolate shape when the segments are implanted—an advantage also reported for the intrastromal corneal ring segments for myopia (Intacs) (1,2). The ICS for hyperopia are designed to be permanent; however, they can be removed if desired. The ICS were conceptualized and developed by Steven M.Verity and David Schanzlin. They initiated these studies in cadaver eyes using wires as the implantable intracorneal devices. The ICS for hyperopia were manufactured by Kera Vision, a vision correction company, founded in 1986 with the purpose of giving people clear vision without using corrective lenses or undergoing surgeries that cut or remove tissue from the central optical zone of the cornea. The company filed for bankruptcy in 2001, and these segments are currently not produced. However, the segments have been licensed to another entity, which may produce them in the future. The ICS are inserted radially between the layers of the corneal stroma through six or eight small incisions made in the periphery of the cornea. When surgically placed at approximately two-thirds depth into the corneal stroma, these segments reshape the anterior corneal curvature, steepening the central cornea and thereby correcting for hyperopia (Fig. 107

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Figure 1 Diagram showing how the intrecorneal segments (ICS) work. The six radially placed segments create a flattening of the peripheral cornea by shortening the chord length between each segment in the direction of the arrows. This peripheral flattening causes the central cornea to steepen, correcting for hyperopia

2). The degree of corneal steepening achieved using the ICS is directly related to the thickness of the ICS product implanted. The segments are made of polymethylmethacrylate (PMMA) and vary in length from 1.5 to 2.0 mm. Each segment has a hexagonal cross section and is tapered along the internal side to facilitate implantation. The ICS thicknesses that we tested were 0.35, 0.40, and 0.45 mm. The width of the segments was 0.5 or 0.8 mm. The 1.8 mm length with 0.8 mm width has been the most used.

Figure 2 A 42-year-old woman with six ICS in place 18 months postoperatively.

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Most of the initial ICS surgeries worldwide in human eyes were performed by the authors (AC and LG) in Tijuana, Mexico. A small European trial was started. In the United States, there is no experience with this technique in human eyes. B. INDICATIONS/CONTRAINDICATIONS The intracorneal segments for hyperopia are intended for the correction of low hyperopia with a cylinder less than or equal to Ⳳ0.75 D. Our experience included patients with a cycloplegic spherical equivalent refraction between Ⳮ1.00 to Ⳮ5.00 D; however, we found that this technique did not correct hyperopias greater than Ⳮ2.0 D. Patients should have a documented stability of their refraction as demonstrated by a change of less than or equal to 0.50 D in spherical and cylindrical components of the manifest refraction for the prior 6 months. The ICS are contraindicated in Pregnant or nursing women Patients with signs of keratoconus Patients with clinically significant corneal dystrophy or scarring in the 6- or 7-mm central zone Patients with a history of herpetic keratitis Patients with an autoimmune disease, collagen vascular disease, clinically significant atopic syndrome, insulin-dependent diabetes or an immunocompromised state C. PREOPERATIVE PREPARATION A complete ocular exam of both eyes should be performed. This includes visual acuity testing with and without correction using standardized ETDRS (Early Treatment Diabetic Retinopathy Study) visual acuity charts, slit-lamp examination, corneal topography, keratometry, manifest and cycloplegic refractions, tonometry, and ultrasound pachymetry of the central and peripheral cornea and funduscopy. D. SURGICAL TECHNIQUE The operative eye was prepared with povidone-iodine 10% solution and the eyelid margins and cilia were draped to fully isolate the surgical field. Topical anesthesia was achieved using two drops of 0.5% tetracaine hydrochloride. A Barraquer wire speculum was placed to hold the lids apart. One eye was treated at a time. The surgical procedure started with the identification of the geometric center of the cornea using a blunt Sinskey hook. A preinked marker was centered on the cornea to provide a visual guide for the placement of the six circumferential incisions and the placement of each segment at a 6.0-mm optical zone. Corneal pachymetry (DHG Technology, Exton, PA) was performed over the site of each incision. A 15-degree diamond knife (KMI, Philadelphia, PA) was used to make a 1.0-mm incision at a depth of 67% of the pachymetry reading along the peripheral corneal marks. A modified Suarez spreader was used to begin a lamellar corneal dissection at the base of each incision. Specially designed instruments (KeraVision, Fremont, CA) were used to create an intrastromal pocket toward the previously marked 6-mm optical zone. It is very important to make sure that the tunnels

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are made at approximately two-thirds of the corneal depth, otherwise the segments are placed too superficially; this may lead to extrusion of the segments or undercorrection. Each segment is then manually inserted into each tunnel with the use of specially designed forceps (Kera Vision, Fremont, CA). All ICS were supplied sterile. The ICS were sterilized with ethylene oxide (EtO) and subjected to aeration to remove residual EtO. The segments should be introduced far enough that they are left at the 6.0-mm optical zone. Leaving them too close to the limbus increases the possibility of neovascularization. The 1.8-mm segments are easier to insert, as they are shorter. There is generally no need to suture the incisions. In our hands the surgical procedure takes 15 to 17 min in all. E. POSTOPERATIVE CARE After the procedure is completed, topical gentamicin 0.3% eyedrops and topical diclofenac 0.1% are instilled into the eye before removal of the speculum. The patient is then discharged wearing a protective eye shield. No patch is necessary. The postoperative management for ICS placement is similar to that for Intacs (3). Patients are instructed to apply 0.3% tobramycin and 0.1% dexamethasone four times daily for 1 week. Artificial tears are used as needed. Patients should be examined the day after the procedure for wound revision. The incision sites will show a linear fluorescein staining for 3 to 5 days. By the first postoperative week most of the staining, is resolved. Each subsequent postoperative visit should include a manifest and a cycloplegic refraction with and without correction visual acuity testing, slit-lamp examination, tonometry, keratometry, and topography examination. After 3 months of follow-up on the operative eye and if refractive stability is achieved, the patient’s contralateral eye can be surgically corrected. F. VISUAL OUTCOMES We have performed over 50 ICS implantations in men and women under 58 years of age. We have implanted all the types of segments manufactured to date: the 2.0-, 1.8- and 1.5mm segments and a variety of thinner segments. The hyperopias we have treated have not exceeded the manifest refraction spherical equivalent (SE) of Ⳮ2.75 and cycloplegic refraction SE of Ⳮ4.5 D. Visual recovery after the ICS procedure was not as rapid as after Intacs (4). Patients experienced blurry vision for distance but were able to read without glasses after a week. Near (uncorrected visual acuity) (UCVA) was better than distance UCVA because there was an initial overcorrection. Improvement in UCVA occurred earlier with the 1.8-mm segments than with the others. Some 71% of the patients achieved 20/20 or better UCVA 2 weeks after the surgery compared with 27% in the 2.0-mm segment group. Ghost images and halos were a frequent complaint in this first postoperative period. Visual acuities continued to improve over the following weeks; by the first month, 76% of the patients were 20/20 or better in the 1.8mm segments and 64% in the 2.0-mm group. The visual acuity and visual recovery were similar to those reported for other keratorefractive procedures, and the results remained constant at 18 months (5,6). The procedure has not been associated with loss of best spectacle-corrected visual acuity (BSCVA), demonstrating the safety of the procedure. Moreover, no patient had a BSCVA less than 20/20. This can be attributed to the fact that the central cornea is not

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Figure 3 Corneal topographies of the right and left corneas showing the central steepening of the cornea produced by the ICS.

touched during the procedure. Some 25% of the patients in the 2.0-mm group and 35% of the patients in the 1.8-mm group experienced a gain of one line of BSCVA at 18 months. This advantage is due to the preservation of the corneal positive asphericity with this procedure. Refractive stability was achieved later than in the Intacs for myopia (4). After the initial overcorrection, stability is obtained by the third month postoperatively. Corneal topographies showed the central steepening of the cornea with an optical zone between 5 and 6 mm in diameter (Fig. 3). Continuing follow-up however, has demonstrated that there is no long-term stability of the correction and visual outcome achieved. We followed these patients for over 3 years and found that there is progressive hyperopic drift with time, which is observed after the second year. This finding is similar to that observed with laser thermokeratoplasty, where one sees a good initial correction but loss of effect with time (7). With the ICS, only 60% of the initial manifest refraction correction and 46% of the cycloplegic refraction is maintained after 3 years. Eyes with higher corrections (hyperopias greater than Ⳮ2.0 D) show a greater tendency to lose correction with time. The average amount of hyperopic drift is 0.9 D, ranging from 0.5 to 1.75 D. Although the amount of loss of correction has been small, considering that the attempted correction was 2.0 D, this change is significant for these patients. Similarly, by 3 years, only 9% of the patients have an UCVA of 20/15 or better. G. COMPLICATIONS Most of the complications we encountered were related to the fact that the surgical technique is mostly manual. Among the single segment complications we encountered, the presence of neovascularization was the most common. Segments placed too peripherally and close to the limbus will predispose for growth of neovessels surrounding the segments. These neovessels can grow deeply in the stromal tunnel and will eventually surround the segment. We encountered this complication in 19% of the patients. In our experience,

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topical steroids did not stop the growth of the vessel at any time during the active growth stage. We recommend removal of the affected segment, especially if the patient is symptomatic. Coagulation of the vessel with argon laser might stop the vessel growth. However, typically such vessels recanalize; therefore we do not recommend intervention with laser. A shallow placement of the segments will produce superficialization of the segments with time, superficial punctate keratitis, and thinning of the overlaying cornea. Spontaneous extrusion of a single segment is a rare complication that is related to shallow implantation of the segment. Epithelial ingrowth can occur around the segment and is surgically induced. We have found that by avoiding corneal de-epithelization during the procedure and by dissecting each tunnel as tightly as possible, this complication is almost completely eliminated. When these complications occur, the segments can be removed and subsequently reinserted. In our experience, most single segments can be successfully reinserted without complications or loss of preoperative BCVA. In the case of the shallow segments, a deeper tunnel can be dissected and the segments reinserted more deeply at the same surgical sitting as the explantation. In the presence of neovascularization, it is recommended to wait until the vessels have regressed and then to proceed with reinsertion of the segment. With experience, we have found that these types of complications are significantly reduced, which tells us that there is a learning curve with this technique. Some complications are related to the presence of the segments per se. These were white, chalky crystalline lamellar deposits that developed only in the inner most third of the segments (Fig. 4). The lamellar deposits present around the segments are similar to those reported adjacent to hydrogel corneal inlays (8,9) and in some patients after Intacs (10). These deposits are presumably caused by separation of the corneal lamellae. Lamellar deposits were seen in 80% of the eyes. Half of them were fully confluent, and no iris detail could be seen. They started to appear between 2 to 3 months after the procedure and peaked at 9 months. Only rarely were they noticeable to the patient. However, in one case, they were so severe and esthetically visible, that all the segments had to be explanted. After explantation, the deposits tend to disappear. In our experience, if the segment is not removed, the deposits do not recede, as it appears to be the case with Intacs (3). They generally do not produce visual symptoms. Other causes for removal of all segments in

Figure 4 White, chalky lamellar deposits typically seen in the inner portion of the segments.

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one eye are varied. Undercorrection and patient dissatisfaction with the refractive result, usually due to induced irregular astigmatism, are among the most common causes. Removal of the intracorneal segments is performed under topical anesthesia (tetracaine 0.5%) after sterilization of the eye with topical povidone-iodine solution. The patient is prepared and draped in the same fashion as in the original surgery. A speculum is inserted to hold the eyelids apart. The incision is reopened with a diamond blade, as this allows minimally traumatic reopening of the incision. In our experience, attempts at blunt dissection with instruments like a Sinskey hook are more traumatic than reopening with a sharp blade. After the incision is opened, the tunnel is approached with a corneal spreader spatula designed for this purpose. The spatula is used to reopen the tunnel and loosen each segment within the tunnel. Subsequently, two small hooks are used to slide the segments into the corneal tunnel and bring them through the incision. There is no positioning hole at the tip of the segments to engage each segment and facilitate its removal. Care is taken to do this in a minimally traumatic manner. The explantation of the ICS for hyperopia is not an easy procedure, unlike the explantation of the Intacs for myopia (4,11). The exceptions are when single segments are explanted in the presence of neovascularization. These segments are usually loose, close to the limbus, and easy to remove. When the segments are inserted close to the 6.0mm optical zone, they are harder to loosen, and no instruments are available to grasp the segment and pull it out through the tunnel and out of the incision. Potential problems can also be encountered when there have been difficulties with wound healing. Postoperative care after total explantation of the ICS for hyperopia is moderately painful; patients usually require systemic analgesia and topical anti-inflammatory drops. Reversibility of the refractive effect, as demonstrated with the return of BSCVA and manifest refraction to preoperative levels, is on average achieved at 3 months after the explantation, rarely before. Removal of these segments can be followed, if desired, by a safe and effective Lasik or PRK for low to moderate myopia. This procedure is not intended to produce astigmatism; however, we induced 1D or more of astigmatism in 23% of our cases. All segments should be placed symmetrically and at the same depth in order to avoid this complication. Rarely, patients have reported occasional pain without apparent cause or an unexplained photophobia. We have not seen cases of glare or halos 6 months after the surgery and beyond. H. SUMMARY The ICS procedure reduces low hyperopic errors without astigmatism while sparing the visual axis. They work better for patients with hyperopias of less than 2.0 D. As opposed to laser thermokeratoplasty and conductive keratoplasty, the ICS procedure offers the benefit of reversibility and preservation of the positive corneal asphericity. The procedure is safe and there has been no loss of BSCVA in any treated patient so far. The effect of ICS implantation appears to stabilize after the first 3 months and is maintained for 18 to 24 months after the procedure. However, after the second year there is a progressive loss of correction, which leads us to question the benefit of performing this procedure. Complications with ICS implantation are mostly related to the surgical technique, which is manual. In general, removal of these segments can be followed by a safe and effective segment reinsertion or, if preferred, LASIK or PRK for low to moderate myopia.

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REFERENCES 1. Nose W, Neves RA, Burris TE. The intrastromal corneal ring: 12-month sighted myopic eyes. J Refract Surg 1996; 12:20–28. 2. Holmes-Higgin DK, Baker PC, Burris TE, Silvestrini TA. Characterization of the aspheric corneal surface with the intrastromal corneal ring segments. J Refract Surg 1999; 15:520–528. 3. Asbell PA. Intrastromal corneal ring. In: Kaufman HE, Barron BA, McDonald M, eds. Cornea, 2nd ed. Boston: Butterworth-Heinemann, 1997: 1037–1044. 4. Gomez L, Chayet A. Laser in situ Keratomileusis results after intrastromal corneal ring segments (intacs). 2001; 108:1738–1743. 5. Anschutz T. Laser correction of hyperopia and presbyopia. Int Ophthalmol Clin 1994; 34: 107–137. 6. Jackson WB, Casson E, Hodge WG, Mintsioulis G, Agapitos PJ. Laser vision correction for low hyperopia. Ophthalmology 1998; 105:1727–1737. 7. Koch DD, Berry MJ, Vassiliadis A. Noncontact holmium: YAG laser thermal keratoplasty. In: Salz JJ, ed. Corneal Laser Surgery. St Louis: Mosby, 1995:247–254. 8. McCarey B, Andrews D. Refractive keratoplasty with intrastromal hydrogel lenticular implants. Invest Ophthalmol Vis Sci 1981; 21:107–115. 9. Gomez ML, Barraquer JI. Permalens hydrogel intracorneal lenses for spherical ametropia. J Refract Surg 1997; 13:342–348. 10. Reinstein DZ, Srivannaboon S, Holland SP. Epithelial and stromal changes induced by Intacs examined by three-dimensional very high-frequency digital ultrasound. J Refract Surg 2001; 17(3):310–318. 11. Asbell PA, Ucakgan O, Odrich M. Photorefractive keratectomy after intrastromal corneal ring segment explantation. Am J Ophthalmol 1999; 128(suppl 6):755–756. 12. Koch DD, Kohnen T, McDonnell PJ, Menefee R, Berry M. Hyperopia correction by noncontact holmium: YAG laser thermal keratoplasty: US phase IIA clinical study with 2-year followup. Ophthalmology 1997; 104(suppl 11):1938–1947. 13. Brinkmann R, Radt B, Flamm C, Kampmeier J, Koop N, Birngruber R. Influence of temperature and time on thermally induced forces in corneal collagen and the effect on laser thermokeratoplasty. J Cataract Refract Surg 1995; 26:744–754. 14. Asbell PA, Maloney RK, Davidorf J, Hersh P., McDonald M, Manche E. Conductive Keratoplasty Study Group. Conductive keratoplasty for the correction of hyperopia. Trans Am Ophthalmol Soc 2001; 99:79–84, discussion 84–87.

11 Anterior Chamber Phakic Intraocular Lenses in Hyperopia GEORGES BAI¨KOFF Clinique Montecelli, Marseille, France

INTRODUCTION: BACKGROUND Nowadays, several methods of surgery may be applied to treat myopia. These methods may be combined to achieve the surgical goal. While photorefractive keratectomy (PRK), laser assisted in situ keratomileusis (LASIK) and intracorneal rings (ICR), may be used to treat low myopia, LASIK is the method of choice for up to 10 diopters. Higher levels of myopia may require phakic intraocular lenses (IOLs) or even clear lens extraction. However, treatment of the most common cause of ammetropia, presbyopia, is still under investigation. Several techniques have been assessed including presbyopic LASIK, intracorneal inlays, clear lens extraction followed by multifocal IOL implantation, scleral rings and recently phakic presbyopic IOLs. Among these techniques, additive surgeries benefit adjustibility, adaptibility, and reversibility. This is why we have been investigating the design of phakic multifocal IOLs for the past 18 months. A. ANTERIOR CHAMBER PHAKIC IOLS Phakic intraocular lenses may be divided in 3 main categories: Posterior chamber IOLs Anterior chamber IOLs with iris fixation Anterior chamber IOLs with angle fixation Since 1986 we have been designing anterior chamber lenses with angle fixation (ZB, ZB5M, NUVITA, GBR, VIVARTE), we now aim to apply the multifocal concept to the most recent generation lenses. 115

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We decided on foldable anterior chamber lens that may be inserted using a 3.2 mm incision. A 2 piece implant has been designed: the haptics with PMMA properties have a “2” shape that ends with three footplates fixated in the angle. A very soft optic, in hydrophilic acrylic, binds tangentially to the haptics. This design allows maintaining a stable anterior chamber as well as a gentle fixation in the angle (with the hydrophilic acrylic footplates). The len’s profile is equivalent to that of the NUVITA. Indeed, prospective and retrospective studies demonstrated the short and long term safety of the ZB5M and the NUVITA on the endothelium. The only problem detected with these lenses was cosmetic: moderate pupil deformations (that may give a cat’s eye aspect) have been rarely reported (less than 5% of the cases). In order to reduce the risk of pupil ovalization, a special interest has been held on a precise measurement of the anterior chamber. The measurement from sclera to sclera using a caliper is indeed inaccurate. It is the reason we developed an objective technique based on the retro-illumination of the anterior segment. This method allows precise and accurate assessment of the angle-to-angle inner diameter of the anterior chamber and therefore to exactly adjust the size of the implant. Additionally, a plastic stick has been designed to confirm this measurement preoperatively. B. FOLDING OF THE OPTIC The optic was initially folded in two; the aperture was then either anterior (with a risk of endothelial touch) or posterior (with a risk of iris contact). It was therefore necessary to expand significantly the anterior chamber with healon. A special folding device is now available to overcome this problem. Indeed, an “N shaped” folding system has been designed to allow an aperture of the implant parallel to the iris plan. The first model of presbyopic implant favors far vision in the center of the optic, while the middle and the peripheral parts allow near and far vision respectively. Many other possibilities may be evaluated throughout the future clinical trials. C. INDICATIONS AND CONTRAINDICATIONS The current indication includes presbyopic patients with emmetropia and without astigmatism. It is known that pseudophakic emmetropic patients without astigmatism implanted with multifocal lenses have a success rate of 70%; which means that they do not wear glasses for either near or far vision. If either an ametropia or an astigmatism exists, this success rate falls down to 30%. Accordingly, in the first set of investigation, the implantation of presbyopic intraocular lenses is only proposed to emmetropic and stigmatic patients in order to obtain optimal results. However, it may be possible in the near future to develop implants with spherical power to treat low myopia or hyperopia. The only method currently available to treat an associated astigmatism is to perform LASIK. CONTRAINDICATIONS Contraindications are those of anterior chamber implant surgery, including the need to respect a 3 mm anterior chamber depth, an endothelial cell count over 2500 cells per mm2, and the absence of other disorders of the anterior chamber (cataract, uveitis, corneal dystrophy, glaucoma, etc.).

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D. PREOPERATIVE MANAGEMENT Preoperative management is generally easy. The eye to be treated, obviously lacking any signs of conjunctival or corneal infection, must be in therapeutic myosis. E. SURGICAL TECHNIQUE The first patients have been operated under general or loco-regional anesthesia. In the future topical anesthesia may be used. A 3.2 mm surgical incision, using a pre-calibrated phako knife is first performed. The incision, performed in an auto-sealed fashion, may be placed at 12 o’clock while one or two lateral paracenthesis may be performed to help the manipulations. The anterior chamber is then deepened using viscous material to: 1. Protect the endothelium 2. Enhance the volume of the anterior chamber to facilitate the lens aperture without any danger for either endothelium or iris. The implant removed from its container is then placed on the folder. Once folded in N, the implant is held with a special forceps that will allow the anterior chamber followed by the rest of the inferior handle. The haptic may be easily folded to pass through the 3.2 mm incision. Subsequently, the optic is introduced in the anterior chamber and the inferior footplates are directed towards the opposite angle. Once the optic is entirely introduced, the superior blocks the implant and the inserting forceps is removed. The optic gently opens in the anterior chamber parallel to the iris. The last manipulation of the insertion is to place the trailing haptic in the anterior segment using either a forceps or a Leister hook. Gonioscopy is performed to check the correct location of the handles, then viscous is removed. F. VISUAL OUTCOMES/COMPARISON OF RESULTS As of today, 6 eyes of 5 patients benefited the implantation with more than 1 year follow up (thanks to professor Eva VOLKOVA in BRNO, Czech Republic). As the first implanted lenses were prototypes, the correct sizes were not available for all the treated eyes. Two have been removed due to an oversizing, the 4 remnants are still in place. No anatomical complications have been detected on these eyes and visual outcome is excellent. Three eyes recovered 20/20 and the other 20/25 without additional correction in the 1st day postoperatively. No complications could be observed on this first series. G. SUMMARY Presbyopic phakic IOLs implantation is an emergent technique that will become more and more important in the future due to its simplicity. The benefit of a foldable implant is to be inserted with a small auto sealed incision without induced astigmatism. The technique has been simplified since the beginning and it will soon be feasible under topical anesthesia. The major interest of this technique is to adjust the power of the addition to the patient’s presbyopia and to be reversible in case of unfavorable outcome. Multicentric studies must be performed to better assess the quality of the optic.

12 Hyperopic Phakic Intraocular Lenses THANH HOANG-XUAN Fondation Ophthalomogique Adolphe de Rothschild and Paris University, Paris, France FRANC ¸ OIS MALECAZE Hoˆpital Purpan, Toulouse, France

A. BACKGROUND The use of phakic intraocular lenses (IOLs) in refractive surgery started in the 1950s and was initially aimed only at correcting high myopia (1). It is now also indicated in moderate myopia, particularly when photorefractive keratectomy (PRK) and laser-assisted in situ keratomileusis (LASIK) are contraindicated. Surgical correction of hyperopia is more recent. Hexagonal keratotomy (2), epikeratoplasty (3) and automated lamellar keratoplasty (4) are no longer used, and holmium: YAG laser thermokeratoplasty (5), conductive keratoplasty (16), PRK, and LASIK are only effective in low hyperopia (Ⳮ4 D or less) (6,7). The only surgical procedures to correct high hyperopia are phakic IOL implantation and clear lens extraction associated with one- or two-(piggyback) posterior chamber (PC) IOL implantation. Disadvantages of clear lens extraction associated with PC IOL implantation include loss of accomodation, difficulties with IOL power calculation, and irreversibility (8,9). Only the iris-fixed and PC phakic IOLs can be used to correct hyperopia. Anglesupported phakic IOLs are contraindicated in hyperopic patients because they often have or will have narrow angles. The literature on correction of hyperopia using phakic IOLs is scant, since this surgical procedure is is relatively new for this indication. Only five reports have been published: one on the Artisan iris-claw lens (10) and four on PC phakic IOL (11–14). B. PHAKIC IOL TYPES 1. Iris-Fixed Phakic IOL (Artisan) The Artisan hyperopia lens is a biconvex lens manufactured by Ophtec. It is fixed to the iris at its midperiphery, which is immobile, by enclavation of a fold of anterior iridal 119

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Figure 1 Hyperopic Artisan phakic intraocular lens. (Courtesy of Ophtec, Groningen, the Netherlands.)

tissue into the two diametrically opposed “claws” of the lens. It is a one-piece, UVabsorbing, polymethylmethacrylate lens with an overall length 8.5 mm (IOLs 7.5 mm long may also be available) and a diameter of the optical part of 5.0 mm. Its power range is Ⳮ1.0 to Ⳮ12.0 D with a 0.5–increment increase (Figs. 1 and 2). 2. Posterior Chamber Phakic IOL The only marketed hyperopia PC phakic IOL is the STAAR Collamer intraocular lens, also called an implantable contact lens (ICL) and manufactured by STAAR Surgical. It is made of a flexible hydrophilic collagen copolymer, a compound combining HEMA and porcine collagen (less than 0.1%). Its refractive index is 1.45 at 35⬚C. It is available with lengths of 11.0 to 13 mm. The diameter of the optical zone is 5.5 mm, and the dioptric power ranges from Ⳮ3 to Ⳮ17 D (Fig. 3). C. INDICATIONS/CONTRAINDICATIONS The best indications are hyperopes of 4 D or more who do not tolerate contact lens, cannot wear spectacle correction for occupational or psychological reasons, and cannot or do not want to undergo alternative refractive procedures. Candidates are often middle-aged or older patients whose visual discomfort is increased by presbyopia. Hyperopes also experience more difficulties in inserting their contact lenses. Contraindications include One-eyed patients Unstable refraction History of ocular disease, including glaucoma, cataract, uveitis, and progressive and/ or severe retinal/choroidal disease

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Figure 2 Hyperopic Artisan phakic intraocular lens. (Courtesy of Ophtec, Groningen, the Netherlands.)

Figure 3 Hyperopic Artisan phakic intraocular lens.

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History of connective tissue disease Corneal endothelial disease and/or endothelial cellular density less than 2000 mm2 Central anterior chamber depth less than 3.0 mm for the Artisan iris-claw lens, and 2.8 mm for the ICL STAAR lens Pupil larger than 6.0 mm in scotopic luminance Patients who will obviously not be compliant for lifelong ophthalmological followup D. PREOPERATIVE PREPARATION 1. IOL Power Calculation The Artisan iris-claw lens dioptric power is calculated on the basis of the curvature of the cornea (K), the anterior chamber depth, and the spectacle correction by applying the van der Heijde formula (15). It is approximatively the same as the power of the spectacles at a vertex distance of 12 mm. The STAAR Collamer’s IOL dioptric power is determined using Feingold’s formula (proprietary) that utilizes the refraction, keratometric power, corneal thickness, and anterior chamber depth. The IOL length is the horizontal limbal white-to-white measurement Ⳳ0.5 mm (not well defined). 2. Anesthesia Most patients are operated on on an outpatient basis. The anesthesia methods are based on patient and surgeon preferences: general anesthesia or peribulbar injection. Topical anesthesia can be applied for STAAR Collamer lens implantation but not for Artisan irisclaw lens surgery, for which full akinesia and analgesia are required. 3. Pupil Size Artisan iris-claw lens implantation requires preoperative miosis to protect the natural lens during the insertion and fixation of the IOL. A constricted pupil also facilitates proper centration of the lens. For this purpose, two argon laser marks can be made on the iris at diametrically opposite sites to facilitate proper centration of the IOL during the surgery, contrary to STAAR Collamer phakic lens implantation, which requires full pupillary dilation. 4. Prevention of Pupil Block A perioperative peripheral surgical iridotomy is performed during the Artisan iris-claw lens implantation procedure, rather than preoperative laser iridotomies. Two generous peripheral laser iridotomies separated by 80 degrees are required before implantation of the STAAR Collamer phakic lens. E. SURGICAL TECHNIQUE 1. Artisan Iris-Claw Lens Two side port incisions and a 5.2-mm (superior or temporal) clear corneal or (superior) scleral tunnel incision are made. High-viscosity sodium hyaluronate is injected, and the

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Figure 4 ICL hyperopic phakic intraocular lens.

phakic IOL is introduced with a specially designed fixation forceps into the anterior chamber through its smaller diameter. It is then rotated 90 degrees, its long axis becoming parallel to the incision. Most surgeons use specially designed iris entrapment needles introduced through the side port incisions to enclavate the iris folds into the lens claws (Figs. 4 and 5). Intraocular acetylcholine chloride can be added if miosis is not sufficient. Accurate centra-

Figure 5 ICL phakic intraocular lens.

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Figure 6 Trapping of an iris fold between the claws of a hyperopic Artisan phakic intraocular lens using an enclavation needle.

tion and fixation of the IOL is crucial to prevent postoperative glare or halos. A 1-mm fold of midperipheral iris tissue is created under the claw using the iris entrapment needle; a gentle pressure of the claw over the fold entraps it. The peripheral iridotomy is then performed, the viscoelastic substance removed, and the wound tightly closed with 10–0 nylon sutures. Postoperative care consists of steroidal and antibiotic eyedrops for 2 weeks and a regular follow-up, particularly long-term evaluation of the corneal endothelium’s density using specular microscopy. Patients also must be instructed not to rub their eyes after surgery.

Figure 7 Introduction of an ICL hyperopic phakic intraocular lens into the eye using an injector.

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Figure 8 Positioning of the haptic of the ICL phakic intraocular lens into the sulcus using a tucker.

2. STAAR Collamer Phakic IOL A side port incision is performed and viscoelastic material is injected. The foldable implant is inserted through a 3.2-mm clear corneal beveled incision on the steepest axis, either with an injector (Fig. 6) or MacPherson forceps. Care must be taken to orient the lens properly while it unfolds and to avoid any central touch of IOL with the natural lens. The optic disk is centered, and gentle downward pressure using a specially designed instrument makes it possible to place each footplate one after the other behind the iris (Figs. 7 and 8). Then, the viscoelastic material is removed and acetylcholine chloride is injected into the anterior chamber. Postoperative care consists of steroidal and antibiotic eyedrops for 1 to 2 weeks. F. VISUAL OUTCOMES/COMPARISON OF RESULTS (Tables 1 and 2) 1. Artisan Iris-Claw Lens Fechner et al. (10) published in 1998 the only study on hyperopic correction using the iris-claw phakic lens. A total of 67 hyperopes were divided into three groups: Ⳮ6.0 to Ⳮ8.9 D (group 1), Ⳮ9.0 to Ⳮ11.9 D (group 2), and more than Ⳮ12.0 D (group 3). In all groups, the standard deviation between intended and final postoperative uncorrected visual acuities was less than 2.80 D. The refractive results were stable at a follow-up of 4 months, and there was no loss of the mean best corrected postoperative best-corrected visual acuity (BCVA). We implanted nine hyperopic patients, Ⳮ4.4 to Ⳮ8.1 D, with a mean follow-up of 12 months (personal communication). Postoperative spherical equivalent (SE) ranged from ⳮ0.75 to Ⳮ0.75 D; 100% and 66.7% of eyes were within 1.00 and 0.50 D of emmetropia, respectively. Because of the loss of magnification, 78% of patients demonstrated a loss in postoperative spectacle BCVA compared to the preoperative spectacle BCVA.

STAAR

STAAR

STAAR

STAAR

Artisan

Artisan

Authors

Fechner (10) (1998) Hoang-Xuan and Malecaze (2001) (unpublished data) Rosen (11) (1998) Davidorf (12) (1999) Pesando (13) (1999) Sanders (14) (1999)

Phakic IOL type

10

15

24

9

9

67

No. of eyes

8.4 (1 to 18) 12 (6 to 18) 6

3

78.1 (12 to 120) 12

Follow-up (months)

Table 1 Visual and Refractive Outcomes

ES (D) postop ⫺5 to ⫹ 3.5 (⫹0.07 ⫾ 2.03) ⫺0.75 to ⫹ 0.75 ⫺0.08 ⫾ 0.71 ⫺0.12 to ⫹ 0.50 ⫺3.88 to ⫹ 1.25 (⫺0.39 ⫾ 1.29) ⫺1.00 to ⫹ 1.50 (⫹ 0.02 ⫾ 0.64) ⫺0.50 to ⫹ 1.50 (⫹ 0.20 ⫾ 0.61)

ES (D) preop ⫹6 to ⫹ 18 (⫹9.98 ⫾ 2.6) ⫹4.40 to ⫹ l8.12 ⫹6.61 ⫾ 0.35 ⫹2.25 to ⫹ 5.62 ⫹3.75 to ⫹ 10.50 (⫹6.51 ⫾ 2.08) ⫹4.75 to ⫹ 11.75 (⫹7.77 ⫾ 2.08) ⫹ 2.50 to ⫹ 10.88 (⫹ 6.23)

80

69.25

58

88.8

66.7

Refractive outcome (D) ⫾ 0.50 (% eyes)

90

92.3

79

100

Refractive outcome (D) ⫾ 1.00 (% eyes)

100

46.15

63

89

67

70

0

8

44

11

Uncorrected Uncorrected VA postop VA postop 20/40 orbetter 20/20 or better (% eyes) (% eyes)

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Table 2 Safety of Hyperopic Phakic Intraocular Lenses Phakic IOL type

Loss of BSCVA (% eyes)

Authors

Artisan

Fechner (10) (1998)

Artisan

22.2 (1 line) 55.5 (⬎2 lines)

STAAR

Hoang-Xuan and Malecaze (2001) (unpublished data) Rosen (11) (1998)

STAAR

Davidorf (12) (1999)

25 (1 line)

Unchanged BSCVA (% eyes)

0

22.2 (1 line)

44.4 33

22.2 (1 line) 22.2 (2 lines) 29 (1 line)

76.92

4 (2 lines) 4 (⬎2 lines) 15.38

4 (⬎2 lines) STAAR

Pesando (13) (1999)

7.69

STAAR

Sanders (14) (1999)

0

Gain of BSCVA (% eyes)

2 (3 lines)

Complications One glaucoma and corneal edema (in two eyes of same patient) None

Three pupillary block glaucomas

Two pupillary block glaucomas One lens opacity None

2. STAAR Collamer Phakic IOL Four studies on hyperopic correction using the STAAR Collamer phakic lens have been published (11–14). These studies included 9, 24, 15, and 10 hyperopes respectively, the latter study (14) being a phase I clinical trial sponsored by the U.S. Food and Drug Administration. In total, 58 patients underwent STAAR Collamer phakic IOL implantation. Cumulative data show that preoperative SE ranged from Ⳮ2.25 to Ⳮ11.75 D. Mean follow-up ranged from 3 to 12 months. Postoperative SE ranged from ⳮ3.88 to Ⳮ1.50 D; 58 to 80% of eyes were within 0.50 D of emmetropia and 79 to 92.3% of eyes were within 1.00 D of emmetropia. In Rosen’s study (11), the efficacy index was 0.98, which was superior to the index for myopic patients implanted with the same type of phakic IOL in series published by the same authors. Davidorf et al. (12) also compared their results favorably to the predictability in their series of high myopic eyes. Seven of 24 eyes (29%) (12) and one of 15 eyes (7.69%) (13) lost one or more lines of postoperative BCVA. Conversely, only 8% of hyperopic eyes operated on by Davidorf et al (12) demonstrated a gain in postoperative spectacle BCVA compared to the preoperative spectacle BCVA. This is explained by the loss of magnification induced by the surgery. G. COMPLICATIONS In Fechner’s series of the artisan lens, one patient had glaucoma and corneal edema in both eyes (10). In our study, no complications occurred and no change in endothelial cell density was noted after a follow-up of 1 year (personal communication).

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For the ICL, postoperative pupillary block glaucoma occurred in 3 of 24 eyes and in 2 of the 15 eyes in the series of Davidorf et al. (12) and Pesando et al. (13), respectively. This complication was due to iridotomies that were too small. H. SUMMARY Two types of phakic IOLs are available to correct hyperopia: the Artisan iris-claw lens and the STAAR Collamer PC IOL. These represent the only surgical refractive procedures capable of correcting hyperopia of Ⳮ4 D or more. There have been very few publications, but the results are encouraging. The predictibility, efficacy, stability, and safety of these procedures are excellent, as well as the quality of the resultant vision. The time of recovery is short and the surgeries are reversible. Long-term follow-up is, however, mandatory with respect to delayed complication such as iris atrophy at the fixation sites and progressive endothelial cell loss (iris-claw lens), and cataract and pigmentary dispersion (PC phakic lens). REFERENCES 1. Strampelli B. Sopportabilita di lenti acriliche in camera anteriore nella afachia o nei vizi di refrazione. Ann Ottamol Clin Oculist Parma 1954; 80:75–82. 2. Basuk WL, Zisman M, Waring III GO, Wilson LA, Binder PS, Thompson KP, Grossniklaus HE, Stulting RD. Complications of hexagonal keratotomy. Am J Ophthalmol 1994; 117:37–49. 3. Ehrlich MI, Nordan LT. Epikeratophakia for the treatment of hyperopia. J Cataract Refract Surg 1989; 15:661–666. 4. Lyle WA, Jin GJC. Hyperopic automated lamellar keratoplasty: complications and visual results. Arch Ophthalmol 1998; 116:425–428. 5. Koch DD, Kohnen T, McDonnell PJ, Menefee RF, Berry MJ. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty; United States phase IIA clinical study with a 1-year follow-up. Ophthalmology 1996; 103:1525–1536. 6. Jackson WB, Casson E, Hodge WG, Mintsioulis G, Agapitos PJ. Laser vision correction for low hyperopia. An 18-month assessment of safety and efficacy. Ophthalmology 1998; 105: 1727–1738. 7. Arbelaez MC, Knorz MC. Laser in situ keratomileusis for hyperopia and hyperopic astigmatism. J Refract Surg 1999; 15:406–414. 8. Kolahdouz-Isfahani AH, Rostamian K, Wallace D, Salz JJ. Clear lens extraction with intraocular lens implantation for hyperopia. J Refract Surg 1999; 15:316–323. 9. Holladay JT, Gills JP, Leidlein J, Cherchio M. Achieving emmetropia in extremely short eyes with two piggyback posterior chamber intraocular lenses. Ophthalmology 1996; 103: 1118–1123. 10. Fechner PU, Singh D, Wulff K. Iris-claw lens in phakic eyes to correct hyperopia: preliminary study. J Cataract Refract Surg 1998; 24:48–56. 11. Rosen E, Gore C. Staar Collamer posterior chamber intraocular lens to correct myopia and hyperopia. J Cataract Refract Surg 1998; 24:596–606. 12. Davidorf JM, Zaldivar R, Oscherow S. Posterior chamber phakic intraocular lens for hyperopia of Ⳮ4 to Ⳮ11 diopters. J Refract Surg 1998; 14:306–311. 13. Pesando PM, Ghiringhello MP, Tagliavacche P. Posterior chamber Collamer phakic intraocular lens for myopia and hyperopia. J Refract Surg 1999; 15:415–423. 14. Sanders DR, Martin RG, Brown DC, Shepherd J, Deitz MR, deLuca MC. Posterior chamber phakic intraocular lens for hyperopia. J Refract Surg 1999; 15:309–315. 15. van der Heijde GL, Fechner PU, Worst JGF. Optische Konsequenzen der Implantation einer negativen Intraokularlinse bei myopen Patienten. Klin Mbl Augenheilk 1988; 193:99–102. 16. McDonald MB, et al. Ophthalmology 2002; 109:1978–1989.

13 Hyperopia and Presbyopia Topographical Changes

STEPHEN D. KLYCE, MICHAEL K. SMOLEK, MICHAEL J. ENDL, VASAVI MALINENI, MICHAEL S. INSLER, and MARGUERITE B. McDONALD Louisiana State University Health Sciences Center, New Orleans, Louisiana, U.S.A.

A. INTRODUCTION Techniques for refractive surgery have made tremendous strides since the pioneering work of Jose Barraquer and the introduction of radial keratotomy in the late 1970s (1). Traditional outcome measures for the efficacy of specific refractive surgeries are primarily uncorrected and best-corrected visual acuities and cycloplegic and manifest refractions. Corneal topography analysis has not been considered a primary outcome measure for clinical trials in the United States—this despite the fact that corneal topography is now the standard of care for preoperative screening of refractive surgical candidates and analysis of postoperative results and is a mainstay of anterior segment practice. Direct analysis by corneal topography has clearly shown the causes of visual loss after eventful refractive surgery. The best examples include the formation of central islands and peninsulas after surface ablation with the excimer laser (2) and induced generalized irregular astigmatism after automated lamellar keratectomy (3). In this chapter, the topographic characteristics of the presbyope and the current modalities for the correction of hyperopia are reviewed.

B. KERATOFRACTIVE PROCEDURES FOR HYPEROPIA—TOPOGRAPHICAL CORRELATES Kohnen et al. (4) used computed videokeratography to demonstrate peripheral corneal flattening and central corneal steepening following noncontact Ho:YAG laser thermal keratoplasty (LTK) for the correction of hyperopia. Greater changes in corneal curva129

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ture and smaller amounts of topographical regression were noted when a two-ring laser treatment pattern was applied. When the topography was analyzed, several forms of induced astigmatism were observed: bowtie (both symmetrical and asymmetrical), irregularly irregular, and semicircular patterns. Only one eye in the entire study group was observed to have a homogeneous pattern. At present, noncontact LTK appears to be most promising for low hyperopia up to approximately 2 D. Regression of the effect appears to limit the procedure’s usefulness for refractive errors higher than 2 D. Furthermore, factors such as younger age (less than age 30) and increased preoperative corneal thickness may also contribute to faster rates of regression (5). Early hyperopic photorefractive keratoplasty (H-PRK) ablations consisted of small optical zones (approximately 4.0 mm) with small transition zones, creating an overall treatment zone diameter of 7 to 8 mm. Small optical zones increase the patient’s sensitivity to small decentrations. Likewise, small transition zones produce abrupt topographical and refractive changes between treated and untreated tissue. This “lack of smoothness” promotes more aggressive stromal and epithelial regeneration and thus refractive regression (6). It should also be noted that in myopic PRK, significant decrements in the character and magnitude of corneal optical aberrations have been found with larger optical and transition zones. Larger optical and transition zones result in a more natural physiological pattern of measured aberrations in myopic PRK (6), and a similar result would be expected in approaches to correct hyperopia. These considerations have led to larger optical zones of 6.0 mm, with overall hyperopic ablations now reaching 9.0 mm. With these considerations, induced aberrations after H-PRK have been carefully evaluated (7). Corneal topography after H-PRK showed a change from positive to negative spherical aberration on the order of 3 D. It is known that the positive spherical aberration of the cornea and the spherical aberration of the crystalline lens act in concert to decrease the overall aberrations of the eye. However, if hyperopic procedures over correct for corneal spherical aberration, a negative impact on visual function is expected. This effect can be seen in Figure 1. Even with larger ablation sizes, difficulties remain. By the nature of the procedure, the functional optical zone becomes smaller as the attempted correction increases in size. This is undoubtedly one of the most significant factors contributing to the poor success rate of both H-PRK and hyperopic laser assisted in situ keratomileusis (H-LASIK) for the correction of Ⳮ5.00 D or greater. Moreover, Choi et al. (8a) report an increased risk of irregular astigmatism based on topographic analyses when corrections above this level are attempted. The comfort level in this respect seems to be surgeon-related; therefore some surgeons limit attempted corrections to Ⳮ4.0 D or less. In reference to H-LASIK, a 9.0-mm ablation size requires the creation of a 9.5-mm flap. Although modern microkeratomes may provide for this flap size, some patients with small eyes or thin corneas are unsuitable candidates for this treatment. Larger flap diameters and larger amounts of correction increase the chances of striae formation, which can translate to irregular astigmatism on corneal topography. H-LASIK is gaining widespread use as a procedure to correct primary hyperopia as well as to modify consecutive hyperopia after overcorrection from LASIK for myopia; it is said to be safe and effective (8). Two typical case reports are given below to illustrate the topography obtained. Each patient underwent hyperopic LASIK with the VISX, Inc., Star Excimer Laser System. The diameter of the optical zone was 5.00 mm, with a total treatment zone of 9.00 mm OU.

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Figure 1 H-LASIK effect on corneal topography and total eye aberration measured with NIDEK OPD-Scan. (1) (top left panel) standard corneal topography showing off-center treatment; (2) skiascopic (pointwise refraction) map: in the postoperative period, corneal aberrations for this eye account for the bulk of the total ocular aberrations; (3) placido image; (4) wavefront map showing induction of excess negative spherical aberration and coma.

Case 1. A 66-year-old woman with no prior history of ocular surgery underwent H-LASIK for a refraction of Ⳮ0.75 Ⳮ 1.00 ⳯ 170 OD and Ⳮ0.25 Ⳮ1.25 ⳯ 180 OS. Her best spectaclecorrected visual acvity (BSCVA) was 20/20 (ⳮ2) OU. The patient requested refractive surgery for monovision. Her preoperative K-readings were 44.3/44.5 at 118 OD and 44.4/44.8 at 163 OS. The laser was programmed to correct OD for Ⳮ1.00 Ⳮ 1.25 ⳯ 170 and OS for Ⳮ2.50 Ⳮ 1.50 ⳯ 180. The total ablation depth was 20 ␮m OD and 38 ␮m OS. Optical zone diameter was 5.00 mm. Her visual acuity without correction on postoperative day 1 was 20/200 OD and 20/80 OS. Two weeks postoperatively, her visual acuity without correction was 20/70 (ⳮ1) OD and 20/200 OS and her BSCVA was 20/25 OD and 20/40 OS. The manifest refraction was ⳮ0.75 Ⳮ 1.00 ⳯ 050 OD and ⳮ2.50 Ⳮ 0.75 ⳯ 055 OS. At 4 weeks postoperatively, her visual acuity without correction was 20/30 (ⳮ2) OD and 20/25 (ⳮ2) OS. Her refraction at this time was ⳮ0.75 Ⳮ 0.75 ⳯ 055 OD and ⳮ1.50 Ⳮ 0.75 ⳯ 165 OS, with BSCVA being 20/25 OD and 20/25 (ⳮ2) OS. Postoperative corneal topography

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A

B Figure 2 H-LASIK 1-month postoperative topography for 66-year-old requesting monovision. (A) OD; attempted correction: Ⳮ1.00 Ⳮ1.25 ⳯ 170. (B) OS; attempted correction: Ⳮ2.50 Ⳮ1.50 ⳯ 180.

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showed the extent of induced cylinder, revealed a steepening of the central 5 mm of the cornea, and produced simulated keratometry readings (SimKs) of 46.13/44.17 at 96 with a potential visual acuity (PVA) of 20/25 to 20/30 OD and 47.41/46.68 at 94 with a PVA of 20/20 to 20/30 OS (Figure 2). Case 2. A 26-year-old woman presented for refractive surgery evaluation. She had a refractive error of Ⳮ4.75 Ⳮ 0.50 ⳯ 083 OD and Ⳮ5.25 Ⳮ 0.75 ⳯ 095 OS. Her BSCVA was 20/25 OU. Her keratometry readings were 44.1/45.6 at 091 OD and 44.1/46.0 at 099 OS. The desired correction for the right eye was Ⳮ6.00 Ⳮ 0.50 ⳯ 083 and for the left eye was Ⳮ6.00 Ⳮ 0.50 ⳯ 105. Total ablation depth was 65 ␮m OU. Optical zone diameter was 5.00 mm. On postoperative day 1 her uncorrected visual acuity was 20/30 OD and 20/40 OS. Six months postoperatively, BSCVA was 20/25 (Ⳮ1) OD with no improvement with manifest refraction. BSCVA OS was 20/25 (Ⳮ1) with a manifest refraction of Ⳮ1.00 Ⳮ0.75 ⳯ 165. There was some evidence of regression OS. Postoperative keratometry readings were 48.70/49.18 at 058 OD and 47.24/48.07 at 051 OS (Figure 3).

Hence, H-LASIK seems a good choice of procedures at least for the temporary correction of hyperopia. Long-term stability will need to be demonstrated for this approach, as for others discussed in this chapter. Conductive keratoplasty (CK) is being developed as an alternative procedure for treating hyperopia. It is argued that if the collagen is heated to a carefully controlled critical temperature, the shrinkage and changes in corneal shape might be more permanent.

Figure 3 Six-month postoperative corneal topography of H-LASIK patient showing good centration OU. (Central green irregularities OS are temporary, from tear film breakup.)

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Figure 4 Preoperative and postoperative topographies after CK. Note large uniform area of increased power.

Conductive keratoplasty uses radiofrequency energy to generate heat in the corneal periphery. As with LTK, the shrinkage of the collagen occurs from the production of a ring pattern of treatment spots around the corneal periphery. This shrinkage creates a pursestring effect to steepen the central cornea. One of the immediately appreciated benefits of CK over H-LASIK is the larger functional optical zone (Figure 4). C. MULTIFOCAL EFFECTS As the number of patients undergoing refractive surgery expands, the curious phenomenon of presbyopic patients presenting with functional near and far vision after refractive surgery is being more frequently reported for both myopic and hyperopic corrections. Described as a “multifocal” effect, this side effect of the surgery deserves scrutiny. It was Benjamin Franklin who conceived the first bifocal spectacle in 1874, initiating what is perceived to be a sequence of developments (Figure 5). Deliberate multifocality was introduced to the contact lens field prior to 1967 (9) and to the intraocular lens (IOL) arena before 1987 (10). While early models of IOLs and contact lenses exhibited pronounced aberrations that reduced contrast sensitivity, current renditions have enjoyed a measure of patient acceptance, at least with contact lenses. Unintentional iatrogenic multifocality was first identified with corneal topography in 11 eyes after radial kerato-

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Figure 5 Historical use of multifocality in vision correction: Ben Franklin’s bifocal spectacles, bifocal contact lenses, bifocal IOLs, multifocality in radial keratotomy (11) and in photorefractive keratectomy for myopia (13).

tomy, and although the possibility of complications from degradation of contrast sensitivity as well as monocular diplopia was anticipated, no patient complaints of this type were in fact reported (11). However, shortly after this report, additional analysis showed that certain patients with the multifocal effect after radial keratotomy could experience visually debilitating irregular astigmatism. This should be considered a complication of surgery (12). Multifocal effects have also been found following PRK (13) for myopia and contribute to a form of artificial accommodation in pseudophakic eyes (14). It is well known that patients with an extreme amount of irregular corneal astigmatism often refract over a large range of powers. This is the basis for the so-called multifocal effect; in spectacles, distinctly separate areas of the lens are prepared with different specific powers, whereas the power distributions of the multifocal cornea are more continuously graded and are analogous to gradations of refractive powers of the Varilux contact lens system. It might therefore be more accurate to describe the multifocal property as one of varifocality. A topographical multifocal effect can be assessed by direct examination of the distribution of corneal powers over the entrance pupil. The standard statistical metric for measuring the width of such distributions is the coefficient of variation; hence, an appropriate topographic definition of corneal multifocality is the coefficient of variation of corneal power (CVP) (15). The increase in the range or width of the distribution of central corneal

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Figure 6 Corneal power distribution in the central 3 mm before and after conductive keratoplasty. Note the broader distribution of corneal powers after surgery, which will enhance the multifocal effect. This is an analysis of the topography shown in Figure 3.

powers is illustrated in Figure 6. It can be noted that the power distribution is broad and without distinct peaks; hence the appellation varifocal. Conversely, Benjamin Franklin’s bifocals would produce a bimodal distribution: two peaks whose widths directly relate to the precision of manufacture. Despite the promising aspects of artificially inducing accommodation with controlled corneal multifocality, significant levels of uncontrolled multifocality can lead to a reduction

Figure 7 The effect of irregular astigmatism on vision can be simulated by placing the measured surface into a model eye and doing ray tracing. CTView V3.12 (Sarver and Associates, Merritt Island, FL) was used for this calculation.

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Figure 8 After correction for distance vision with conductive keratoplasty for hyperopia, uncorrected near vision (UNVA N) also improves (p ⬍ 0.001). (Data courtesy of Refractec, Inc., lrvine, CA).

in contrast sensitivity and symptomatic vision. The effect of varifocality in corneal surgery can be evaluated mathematically by fitting the surface with Zernike polynomials and calculating from this the modulation transfer function. This will give the global optical characteristics of the corneal surface and allow the simulation of multifocal effects on vision, as shown in Figure 7. With hyperopic keratorefractive surgery, there is another effect that comes into play under the guise of multifocality. In one cohort of patients undergoing the conductive keratoplasty procedure for the correction of low hyperopia, postoperative near vision either remained constant or was enhanced at 1 month for every eye in the study (Figure 8). The average improvement was statistically significant (p ⬍ 0.001). This is a striking effect that generally contrasts with myopic keratorefractive surgeries, where functional near vision typically worsens in the presbyopic patient population (16). This effect can be explained. Presbyopes who are mildly myopic often have excellent near vision without correction. With keratorefractive surgery, near vision is sacrificed for improved distance vision. On the other hand, presbyopic hyperopes have very poor uncorrected near vision, and when keratorefractive surgery is used to correct their distance vision, this brings their near focal point closer to the eye and improves vision at the near reading distances. Multifocality and better than expected near vision after keratorefractive surgery for the correction of hyperopia are due to a combination of factors. Focus over a range of distances is made possible by the varifocal nature of some postoperative corneal topographies. Residual accommodation in younger patients can enable uncorrected near vision. Use of the pinhole effect and bright illumination make a contribution as well. Finally, improvements in uncorrected near vision can be expected after hyperopic corrections because the near focal plane is brought closer to the eye, whereas with myopic corrections, it is moved further away. D. DIAGNOSTIC IMPLICATIONS Several approaches have been developed to provide for the automatic interpretation of corneal topography (17). Among these, neural networks appear to have the greatest poten-

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tial for success (18–20). A principal consideration in developing a strategy for the training of such a network is data collection. Generally, 20 to 30 examples of each class of corneal topography are collected to provide a broad range of “experience” for the neural network. In this way the network can “learn” the hallmarks of each corneal condition and then be able to classify new corneal maps accordingly. With the widespread success of refractive surgery, there is concern that donor corneas for transplantation might be compromised by previous surgery. As a result, a class of corneas was developed that are referred to as having “myopic refractive correction.” There appear to be no consistent features among the various myopic refractive corrections that persist to allow differentiation between the various types. This even includes radial keratotomy, because the lower power over the incision sites tends to be erased with time. Fortunately, no other corneal condition or disorder is known that has the principal feature of uniform central corneal flattening. With hyperopia, central corneal steepening is the principal characterizing feature, and again, differentiation among the several corneal surgical approaches may not be possible. However, the central corneal steepening after hyperopic correction, unlike correction for myopia, outwardly mimics the characteristics of keratoconus, with a centralized cone (Figure 9). This may confound the clinician, as well as the automated classification algorithms that detect keratoconus. Patient history and corneal pachymetry may be required for differentiation between hyperopia-corrected corneas and keratoconus unless some distinguishing topographical metric is found.

Figure 9 Postoperative topography of H-LASIK. Note the fairly typical appearance of keratoconus as a consequence of the surgery. Corneal topography classification programs will need to be retrained to determine whether it is possible to automatically differentiate H-LASIK from keratoconus.

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E. SUMMARY Corneal topographic analysis is helpful in elucidating the strengths and weaknesses of refractive surgical procedures, and surgery for hyperopia is no exception. Centration is critical, and a large treatment zone size is technically difficult to achieve. A hyperopic procedure’s stability can be objectively and precisely measured with corneal topography. However, the results of stability measurements may be confounded by the fact that people in this age group (50–65 years) are undergoing progressive hyperopia naturally; this must be taken into account. Several factors, including varifocality of corneal topography, contribute to better than expected near visual function after the surgery. With advancing age, qualities of the tear film diminish, and this leads to fine surface irregularities, while the induction of coma results from global asymmetrical changes in shape. REFERENCES 1. Waring GO. Refractive Keratotomy for Myopia and Astigmatism, St Louis: Mosby, 1992. 2. Lin DT, Sutton HF, Berman M. Corneal topography following excimer photorefractive keratectomy for myopia. J Cataract Refract Surg 1993; 19(suppl):149. 3. Klyce SD, Martinez CE. Corneal topography. In: Albert DM, Jakobiec F, eds. Principles and Practice of Ophthalmology. Philadelphia: Saunders, 2000: 668–694. 4. Kohnen T, Husain SE, Koch DD. Corneal topographical changes after noncontact holmium: YAG laser thermal keratoplasty to correct hyperopia. J Cataract Refract Surg 1995; 22: 427–435. 5. Alio JL, Ismail MM, Pego JLS. Correction of hyperopia with noncontact Ho:YAG laser thermal keratoplasty. J Refract Surg 1997; 13:17–22. 6. Endl MJ, Martı´nez CE, Klyce SD, McDonald MB, Coorpender SJ, Applegate RA, Howland HC. Effect of larger ablation zone and transition zone on corneal optical aberrations after PRK. Arch Ophthalmol 2001; 119:1159–1164. 7. Oliver EM, O’Brart DPS, Stephenson CG, Applegate RA, Tomlinson A, Marshall J. Anterior corneal optical aberrations induced by photorefractive keratectomy for hyperopia. J Refract Surg 2001; 17:406–413. 8. Ziff SL. Multifocal contact lenses. Am J Optom Arch Am Acad Optom 1967; 44:222–225. 8a. Choi RY, Wilson SE. Hyperopic laser in situ keratomileusis: primary and secondary treatments are safe and effective. Cornea 2001; 20:388–393. 9. Keates RH, Pearce JL, Schneider RT. Clinical results of the multifocal lens. J Cataract Refract Surg 1987; 13:557–560. 10. Werblin TP, Klyce SD. Epikeratophakia: the surgical correction of aphakia: I. Lathing of corneal tissue, Curr Eye Res 1981; 1:123–129. 11. McDonnell PJ, Garbus J, Lopez PF. Topographic analysis and visual acuity after radial keratotomy. Am J Ophthalmol 1988; 106:692–695. 12. Maguire LJ, Bourne WM. A multifocal lens effect as a complication of radial keratotomy. Refract Corneal Surg 1989; 5:394–399. 13. Scher K, Hersh PS. Disparity between refractive error and visual acuity after photorefractive keratectomy: multifocal corneal effects. J Cataract Refract Surg 1997; 23:1029–1033. 14. Fukuyama M, Oshika T, Amano S, Yoshitomi F. Relationship between apparent accommodation and corneal multifocality in pseudophakic eyes. Ophthalmology 1999; 106:1178–1181. 15. Martinez CE, Klyce SD, Waring III GO, El Maghraby A. The topography of LASIK. In: Pallikaris IG, Siganos DS, eds. LASIK. Thorofare, NJ: Slack, 1997:339–357. 16. Wright KW, Guemes A, Kapadia MS, Wilson SE. Binocular function and patient satisfaction after monovision induced by myopic photorefractive keratectomy. J Cataract Refract Surg 1999; 25:177–182.

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17. Maeda N, Klyce SD, Smolek MK, Thompson HW. Automated keratoconus screening with corneal topography analysis. Invest Ophthalmol Vis Sci 1994; 35:2749–2757. 18. Maeda N, Klyce SD, Smolek MK. Application of neural networks to the classification of corneal topography: preliminary demonstration. Invest Ophthalmol Vis Sci 1995; 36: 1327–1335. 19. Maeda N, Klyce SD, Smolek MK. Comparison of methods for detecting keratoconus using videokeratography. Arch Ophthalmol 1995; 113:870–874. 20. Smolek MK, Klyce SD. Current keratoconus detection methods compared with a neural network approach. Invest Ophthalmol Vis Sci 1997; 38:2290–2299.

14 Corneal Surface Profile After Hyperopia Surgery DAMIEN GATINEL Fondation Ophthalomogique Adolphe de Rothschild and Bichat Claude Bernard Hospital, Paris, France

The desired change in corneal curvature to correct for hyperopia with current excimer laser systems is based on principles of geometric optics and the precise interaction of the excimer radiation with the corneal tissue. In comparison to myopic correction in which the goal is to flatten the central cornea, in hyperopia the central corneal area must be steepened to increase its optical power. This central steepening makes the planned correction of the hyperopic eye more difficult because the steepened central corneal portion has to join the peripheral unablated area of lower curvature via a transition area. These represent the important special features of the correction of hyperopic errors, which are emphasized in this chapter. A. CORRECTION OF PURE SPHERICAL HYPEROPIC ERRORS The profile of ablation to correct for spherical hyperopia is radially symmetrical and predominates in the periphery in an annular fashion. A subtraction shape model based on geometric optics allowed Munnerlyn et al., in 1988, to announce the principles of laserguided photoablation in the central corneal area (effective optical zone) (1). The modifications of the corneal profile are analyzed separately below for the optical zone and for the transition zone. 1. Optical Zone Design Conforming to the pioneering work of Munnerlyn et al., the change in paraxial corneal power can be predicted by considering the initial unablated and the final ablated corneal 141

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Figure 1 Schematic representation of the lenticule ablated for the correction of spherical hyperopia. The profile of ablation is outlined along two perpendicular meridians (green). The thickness of the lenticule is maximal at its edges and null at its center.

surface as two spherical surfaces with a single but different radius of curvature. The removal of tissue is equivalent to adding a thin lens of equal but opposite power. This permits the calculation of the ablation profile over the optical zone for a spherical hyperopic error (see Appendix 1). To generate a three-dimensional graphic representation of the theoretical shapes of the lenticules ablated during laser-assisted in situ keratomileusis (LASIK) of similar amounts of spherical and cylindrical ablation, we used a digital modeling software that allow to visualize the results of Boolean operation on orientated three-dimensional surfaces (see Appendix 2). The difference between each of the radii of curvature was exaggerated as compared to the surgical range so as to facilitate the spatial visualization of the contour features of the generated lenticules. Spherical hyperopic ablation results in the ablation of a concave lenticule within the optical zone, which is represented on Figure 1. Its thickness is null in the center and increases progressively toward the periphery, where it reaches its maximum at the edge of the optical zone. In first-order approximation, the maximum thickness of the edge of the ablated lenticule over the optical zone is proportional to the magnitude of the hyperopic treatment and to the square of the chosen optical zone diameter. The volume of tissue ablation needed to steepen the cornea is thus delimited by the initial anterior surface and the final postoperative steeper spherical surface over a circular optical zone. 2. Transition Zone Design For necessary geometric feature, Any cornea that has had tissue removed centrally to steepen its curvature (optical zone) while leaving the periphery untouched must undergo an additional ablation to sculpt a smooth blending zone (transition zone). This flatter area, commonly referred to as the transition zone, thus represents a constant feature that ideally would have no undesirable optical effects and would ensure the stability of the induced refractive changes in the optical zone by limiting unwanted biological and biomechanical changes.

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When we address theoretical considerations on the different approaches to blend a steepened optical zone to the untouched peripheral cornea, some constraints had be taken into consideration (2). Should this be done by a noncontinuous constant curvature profile, avoiding the induction of a continuous negative curvature, or by minimizing the slope of the transition zone with a continuous change in its curvature but inducing negative curvature (Fig. 2)? Because the patterns of ablation for the hyperopic transition zone are proprietary, it is difficult to find confirmations of the use and interest of any of the transition zone profile design characteristics. It seems, however, reasonable to postulate that any profile of ablation should be “smooth” in a mathematical sense—i.e., avoiding local discontinuities to prevent epithelial hyperplasia. A continuous profile of ablation with a very gradual change in its curvature seems a better option to correct for hyperopia while limiting regression. This pattern implies the need of two points of inflexion (inversion of the sign of the local curvature) to prevent the occurrence of discontinuities (Fig. 2). Some publications have emphasized on the need for a large transition zone outer diameter in order to improve biological tolerance and minimize regression (3–5). Conversely, enlarging the optical zone diameter, although desirable to preserve the quality of vision and reduce the risk of decentration, represents a limiting factor, since the depth per diopter at the edge of the optical zone will increase with the square of the optical zone diameter. This could account for the low success rate observed for corrections over 5 or 6 D of hyperopia. The determination of the diameter of the ablation zone should logically

Figure 2 Profile of ablation for the spherical hyperopic error. O, ablation center; OZ, optical zone; TZ, transition zone; dotted black line, preoperative corneal profile; full black line, postoperative corneal profile; blue line, postoperative profile over the transition zone with no local curvature discontinuities but negative slope between the points of inflexion T and N; red line, postoperative transitional profile having a constant positive slope, but with a noncontinuous junction with the edge of the optical zone.

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depend on the diameter of the optical zone. For example, a planned optical zone of 6.0 mm would require an ablation zone of 8.5 to 9.0 mm. Otherwise, effective optical zone diameters might be diminished by epithelial filling of the peripheral ring of ablation in case of high-magnitude of treatment. In LASIK, the corneal flap covering of the ablation zone minimizes the epithelial healing response (6). This might account for the better reported results of this technique over photorefractive keratectomy (PRK). Because the total ablation zone diameter is equal to the outer diameter of the transition zone, it is mandatory to obtain large flap sizes for hyperopic LASIK procedures (7). B. CORRECTION OF PURE CYLINDRICAL HYPEROPIC ERRORS 1. Optical Zone Design The principles of the Munnerlyn pattern can be extended to the correction of astigmatism by taking into consideration the meridional variations in corneal apical power. In the case of pure hyperopic astigmatism, a “cylindrical profile of ablation” can be generated, which aims to selectively steepen the initial flatter principal meridian. This pattern has no center but there is axis symmetry along each of the principal meridians. A three-dimensional representation of the etched corneal lenticule for such correction over a circular optical zone is depicted in Figure 3. The depth of ablation is maximal at the edge of the optical zone along the flat meridian, while the steep meridian is untreated by the laser. 2. Transition Zone Design The shape of the transition zone is dictated by the features of the optical zone. As for the optical zone, the central symmetry is broken. The step in tissue height is maximal at the boundary of the optical zone along the flat meridian. This discontinuity then tapers slowly and becomes null along the untreated steep meridian. To alleviate this variation, the diameter of the transition zone should be longer along the flat meridian and minimal (equal to

Figure 3 Schematic representation of the lenticule corresponding to the correction of a pure hyperopic astigmatism. Its thickness is null along the steep meridian (S) and maximal in the periphery along the flat meridian (F). The profile of ablation along the flat meridian is underlined in green.

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A

B Figure 4 (A) Schematic representation of the lenticule corresponding to the correction of a pure hyperopic astigmatism with the transition zone. The ablation along the flat meridian is highlighted in green. (B) Representation of the volume of the transition zone alone. Its outer perimeter is elliptical, since the groove to blend reaches its maximum depth over the flat axis.

that of the optical zone) and minimal along the steep meridian while having a constant slope over the optical zone. The shape of the outer limit of the transition zone is thus elliptical (Fig. 4A and B). This might be clinically relevant in optimizing the position of the hinge in LASIK procedures by placing it perpendicular to the flat meridian. C. CORRECTION OF COMPOUND CYLINDRICAL HYPEROPIC ERRORS The refraction as commonly done clinically is an arc-based mathematical expression limited to the principal major and minor axes, and any compound hyperopic astigmatic refractive error can be expressed by different equivalent expressions. Thus, different sequential treatment strategies for the correction of compound hyperopic astigmatism have been proposed: they all consist in the combination of spherical and cylindrical treatments of equal or opposite signs.

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1. The positive-cylinder approach (ablating the cylinder along the flattest meridian and then treating the residual spherical component) 2. The negative-cylinder approach (ablating the cylinder along the steepest meridian and then treating the residual spherical component) 3. The cross-cylinder approach (ablating half of the power of the cylinder along the steepest meridian and the remaining half along the flattest meridian before the residual spherical equivalent is treated) Even if the optical result may be the same, these strategies may result in different amount and depths of tissue ablation. The increasing number of reports of corneal ectasia following LASIK suggests that the strategies that remove less of the corneal tissue should be preferred for the treatment of any compound astigmatism. Recently Azar et al. compared the theoretical ablation profiles and depths of tissue removal in the treatment of compound hyperopic astigmatism and of mixed astigmatism (8). They found that strategies combining the use of hyperopic spherical and myopic cylindrical corrections incur the greatest amount of corneal tissue ablation. Three-dimensional drawings were generated to depict the theoretical shapes of the volumes of corneal tissue ablated to treat similar amounts of compound astigmatic hyperopic errors (Fig. 5A–C). These images can be interpreted more easily and quickly than abstract mathematical functions. The shapes and volumes of the corresponding lenticules can be analyzed for different strategies of ablation, and this makes if possible to estimate the theoretical differences in the amount of ablated corneal volume. In compound hyperopic astigmatism, all the corneal meridians have excessive flattening. The negative cylinder and the cross cylinder approaches both imply an additional flattening that will cause redundant ablation by necessary additional positive spherical treatment.

Figure 5 Schematic representation of the lenticules ablated for the correction of compound hyperopic astigmatism for three different strategies to treat the same refraction: Ⳮ3 (Ⳮ2 ⳯ 0 degrees). The optical zone diameter is identical for each of the depicted strategies. (A) Positive-cylinder approach. The positive cylinder (2 ⳯ 0 degrees) ablated lenticule is represented above, with its section along the flat axis outlined in light green. The spherical ablated lenticule (Ⳮ3) is represented below, with two meridian outlined in dark green.

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Figure 5 Continued. (B) Cross-cylinder approach. The astigmatic component is split in two parts: (Ⳮ1 ⳯ 0 degrees) and (ⳮ1 ⳯ 90 degrees). The corresponding lenticules are represented (the profile of ablation along the principal meridians are outlined in red and light green for the negative and positive cylinders, respectively). The remaining spherical equivalent (Ⳮ4) is then treated by the ablation of a positive spherical lenticule (two perpendicular meridian outlined in dark green). (C) Negative-cylinder approach. The refraction is treated as: (ⳮ2 ⳯ 90 degrees)Ⳮ5. The lenticules corresponding to the negative-cylindrical and the positive-spherical treatments are shown with their meridian outlined in red and dark green, respectively. The positive-cylinder approach minimizes the volume of ablation and induces no ablation at the center of the optical zone. The cross-cylinder approach induces an additional volume of ablation compared to the positive-cylinder approach. The negative-cylinder approach induces the maximum volume of ablated tissue.

D. CUSTOMIZED ABLATION In the preceding text, we have studied the changes in corneal profile induced by the correction of simple spherocylindrical errors. Customized ablations aim to correct both the spherocylindrical error and the higher-order aberrations based on the collection of wavefront or corneal topography data. This induces variations of the amount of tissue removed at specific locations, and the ablation profile thus specified will have specific features. For example, taking into account the corneal apical radius asphericity will induce variations in the ablation depth. This might, however, not alter the “global pattern” of the

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ablation profile for patients with hyperopic errors but rather induce radially asymmetrical variations in the peripheral “step” at the edge of the optical zone. The transition zone pattern will have to take this variability in account and its optimized slope will have to be determined to ensure the stability of the induced changes over the optical zone. E. CONCLUSION For several reasons, the correction of hyperopia with PRK or LASIK is more difficult than for myopia. The patterns of the profiles of ablation to steepen the cornea might account for the limited success in excimer laser surgery for hyperopia. Refinements based on simple geometrical considerations and the incorporation of customized data might improve the results of such surgery. APPENDIX 1 To correct for a spherical hyperopic error, Munnerlyn et al., by considering the initial unablated and the final ablated corneal surface as two spherical surfaces with a single but different radius of curvature (Fig. 6), proposed the following formula for the ablation profile over the optical zone: t(y) ⳱ R2 ⳮ R1 Ⳮ

兹R 21 ⳮ y2 ⳮ 兹R 22 ⳮ y2

where t(y) expresses the depth of tissue removal as a function of the distance y from the center of an optical zone diameter of S when R1 and R2 are the initial and final corneal anterior radii of curvature, respectively. The power of the removed lenticule (D) corresponds to the intended refractive change and is related to R1, R2, and the index of refraction (n) as follows:

Figure 6 Schematic representation of the profile of ablation for spherical hyperopia along a corneal meridian. Both initial and final surfaces are assumed to be spherical of radius R1 and R2 respectively. The gray portion corresponds to the material to be removed to steepen the anterior part of the cornea over an optical zone diameter of S mm.

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D ⳱ (n ⳮ 1)

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冢R1 ⳮ R1 冣 2

1

where R2 ⬍ R1 for hyperopic ablations The maximal depth occurs at the edge of the optical zone of diameter S and is equal to: t(S/2) ⳱ R2 ⳮ R1 Ⳮ

兹R 21 ⳮ (S/2)2 ⳮ 兹R 222 ⳮ (S/2)2

APPENDIX 2 To generate a conceptual graphic representation of theoretical shapes of the lenticules ablated during LASIK treatments of similar amounts of spherical and cylindrical treatment, we used a digital modeling software that makes it possible to visualize the results of Boolean operation on orientated three-dimensional surfaces (Bryce 3D, Metacreation Corp. Dublin, Ireland). Using these Boolean operations (subtraction of one object from another) on geometrical primitives such as spheres, cylinders, or toroidal ellipsoids, three-dimensional representations of the theoretical ablated volumes were generated (Fig. 7). The optical zone was circular and the final corneal surface was spherical in all cases. For spherical corrections, the initial and final corneal surfaces were modeled as two spherical surfaces of different radii of curvature (the latter being flatter for myopic spherical corrections and steeper for hyperopic correction). For pure cylindrical corrections, the initial corneal surface was modeled as a spherocylinder with two major apical radii of curvature along the principal meridians, the final surface being spherical. In cases of myopic cylindrical correction, one of the principal radii of curvature of the initial surface was shorter, the other being equal to that of the final corneal surface. In the case of hyperopic cylindrical corrections, one of the principal radii of curvature of the initial surface was longer, the other being equal to that of the final corneal surface. The three-

Figure 7 Model of the ablated lenticule for the correction of pure hyperopic astigmatism. This volume is generated by boolean operation on primitive figures such as sphere, ellipsoid, cylinder, in accordance with assumptions regarding subtraction shape models.

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dimensional representation of a lenticule was obtained by first subtracting the volume of the primitive modeling of the final theoretical corneal surface from the primitive volume modeling of the initial corneal surface. These primitives were aligned and centered on the Z axis. The ablated lenticule for the correction of pure cylindrical myopic astigmatism was generated by adjusting the distance between the apex of each surface so that they would intersect along the steep meridian within a predetermined circular optical zone. The difference between each of the radii of curvature was exaggerated as compared to the clinical and surgical range to facilitate the spatial visualization of the contour features of the generated lenticules. However, in comparing different strategies, the initial and final surfaces were identical and were rescaled to the same ratio for purposes of comparison. This made it possible to estimate the theoretical differences in the amount of ablated corneal volume by the different available strategies that combine the ablation of these elementary lenticules to correct for a given compound hyperopic astigmatic refractive error. The transition zone was modeled as a spherical (constant positive curvature) surface encompassing the circular inferior edge of the ablated lenticule and joining the peripheral unablated cornea. To facilitate the visualization and the distinction of the shapes of the ablated lenticules, cross-sectional color outlines were added along the principal meridians. REFERENCES 1. Munnerlyn C, Koons S, Marshall J. Photorefractive keratectomy: a technique for laser refractive surgery. J Cataract Refract Surg 1988; 14:46–52. 2. Dierick HG, Missoten L. Corneal ablation profiles for correction of hyperopia with the excimer laser. J Refract Surg, 1996; 12:767–773. 3. Chayet AS, Assil KK, Montes M, Castellanos A. Laser in situ keratomileusis for hyperopia: new software. J Refract Surg 1997; 13(suppl):S434–S435. 4. Arbelaez MC, Knorz MC. Laser in situ keratomileusis for hyperopia and hyperopic astigmatism. J Refract Surg 1999; 15:406–414. 5. Ditzen K, Huschka H, Pieger S. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg 1998; 24:42–47. 6. Pallikaris IG, Siganos DS. Excimer laser in situ keratomileusis and photorefractive keratectomy for correction of high myopia. J Refract Corneal Surg 1994; 10:498–510. 7. Rashad KM. Laser in situ keratomileusis for the correction of hyperopia from Ⳮ1.25 to 5.00 diopters with the Technolas Keracor 117C laser. J Refract Surg 2001; 17:113–122. 8. Azar DT, Primack JD. Theoretical analysis of ablation depths and profiles in laser in situ keratomileusis for compound hyperopic and mixed astigmatism. J Cataract Refract Surg 2000; 26(8):1123–1136.

15 Wavefront Changes After Hyperopia Surgery MARIA REGINA CHALITA and RONALD R. KRUEGER Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

A. BASIS OF WAVEFRONT ANALYSIS 1. Definition of Wavefront and Aberrations In physical optics, light is considered as a wave, and the light wave spreads in all directions as a spherical wave. The wavefront is the shape of light waves that are all in phase (1). The ideal eye, defined as an emmetropic eye without any aberrations, has a perfect wavefront, described as a plane perpendicular to the line of sight (Fig. 1) (2). For real eyes, wavefronts that converge toward the retina are not spherical, so perfect imaging never occurs. Wavefront aberration is defined as the difference between the actual wavefront and the ideal wavefront in the plane of the eye’s exit pupil (Fig. 2) (3). Ocular aberrations are not constant during life (4); they increase with age (5) and may change during accommodation (6,7). In optics, aberrations are classified in two different types: monochromatic and chromatic (8). 2. Monochromatic Aberrations Monochromatic aberrations involve specific wavelengths of visible light and can be subdivided into defocus (spherical refractive error), astigmatism (cylindrical refractive error), coma, spherical aberration, and other terms of higher-order aberrations. Defocus and astigmatism are considered low-order aberrations and can be corrected with glasses, contact lenses, or refractive surgery (9). They correspond to approximately 85% of the average wavefront error. Coma, spherical aberrations, and others are high-order aberrations (refractive distortions, that limit the vision of healthy eyes to less than the retinal limits) and cannot be corrected with spherocylinder lens or with standard refractive surgery (10). 151

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Figure 1 The Shack-Hartmann wavefront sensor forms a regular lattice of image points for a perfect plane wave front of light.

They are responsible for approximately 15% of the average wavefront error. For coma, the wavefront is asymmetrical about the perfectly spherical wavefront, producing a cometshaped pattern on the emmetropic plane. For spherical aberration, the converging wavefront looks spherical near the center of the pupil but changes its curvature toward the edge of the pupil. This aberration gives a continuum of foci and results in point images with halos. Other terms of higher order aberrations are a group of all other deviations of the converging wavefront from perfect sphericity. 3. Chromatic Aberrations Chromatic aberrations are errors that result of dispersion in optical elements of the eye. Refractive surgery techniques cannot correct chromatic aberration, since this error is inherent to the properties of the ocular materials and not to the shape of the ocular components (11).

Figure 2 The Shack-Hartmann wavefront sensor forms an irregular lattice of image points for an aberrated wavefront of light.

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Figure 3 Three-dimensional pictorial directory of Zernike modes 0 to 20.

Aberrations are also classified in terms of orders using Zernike polynomials (12). The wavefront error (difference in shape between the aberrated wavefront and the ideal wavefront) for myopia, hyperopia, and astigmatism is well represented by a polynomial of second order. These aberrations are therefore called second-order aberrations. Following the same principle, coma is a third-order aberration and spherical aberration a fourth-order aberration (Fig. 3). Laser surgery [photorefractive keratectomy (PRK) and laser-assisted in situ keratomileusis (LASIK)] increases high-order optical aberrations in human eyes, especially spherical aberration and coma (13,14). This increase in high-order optical aberrations after corneal laser surgery is correlated with a significant decrease in quality of vision, especially under scotopic conditions (15). 4. Detection of Wave Aberration: History of Shack-Hartmann Most of the methods of wave aberration detection and reconstruction have been based on ray tracing. These methods were first described in1900 by Hartmann. About 5 years earlier, Tscherning constructed an aberroscope: a grid superimposed on a 5-D spherical lens where a subject could see a shadow image of the grid on the retina. From the distortions of the grid, one could infer the aberrations of the eye. Over 70 years later, Howland invented the crossed cylinder aberroscope. Instead of using a spherical lens, he used a crossed cylinder lens of 5 D with the negative axis at 45 degrees (16,17). In 1961, Smirnov developed another method where a grid is viewed by the entire aperture of the eye minus a single central intersection, which is viewed through a small

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aperture made to scan the entire pupil sequentially. In 1998, Webb and coauthors made a modern implementation of Smirnov’s method that computes the wave aberration and reduces it to Zernike polynomials. Last, the Shack-Hartmann sensor was developed in 1970 by Shack in order to improve the images of satellites taken from earth. The first practical application was in 1984 by Wilson to test large telescopes. In 1989, Bille was the first to publish using the ShackHartmann in ophthalmology to measure the profile of the cornea and in 1997 he became the first to project a source onto the retina and use the Shack-Hartmann sensor to measure aberrations of the eye. In the same year, Williams became the first to use the ShackHartmann sensor with adaptative optics to measure and correct aberrations of the eye (18). 5. Principles of Shack-Hartmann The Shack-Hartmann aberrometer has an objective lens that is actually an array of tiny lenses. With this kind of lens the reflected light is broken into many individual beams, thereby producing multiple images of the same retinal spot of light. For a perfect eye, the reflected plane wave will be focused into a perfect lattice of point images, each image falling on the optical axis of the corresponding lenslet. By contrast, the aberrated eye reflects a distorted wavefront. By measuring the displacement of each spot from its corresponding lenslet axis, we can deduce the slope of the aberrated wavefront when it entered the corresponding lenslet. The wavefront should be analyzed as soon as it passes through the eye’s pupil (19,20). B. WAVEFRONT OF HYPEROPIC TREATMENT 1. Profile of Hyperopic Correction In 1988 Munnerlyn and coworkers described the equations that served as a starting point for developing current ablation algorithms. For a hyperopic ablation, the preoperative cornea is modeled as a sphere of lesser curvature than the desired postoperative cornea, which is also modeled as a sphere. Tissue is removed from the peripheral area, flattening this region and producing increased postoperative corneal curvature as a final result. This concept is referred to as the shape-subtraction model of refractive surgery; it permeates current thinking in refractive surgery and forms the basis for both topography and wavefront-guided procedures (21). 2. Wavefront Measurements and Aberration Changes Before and After Conventional Hyperopic LASIK In our service, we use the Alcon LADARWave Device (Orlando, FL) to study visual aberrations. The LADARWave Device makes detailed measurements of the aberrations present using the Shack-Hartmann principles. We can measure defocus, astigmatism, and higher-order aberration that can be decomposed into coma, spherical aberrations, and other terms of higher order aberrations (Fig. 4). If we imagine a normal cornea with its normal prolate shape without any kind of surgery done, we will find higher-order aberrations but in low amounts. The pattern of each higher-order aberration is well defined: coma has a comet-shaped pattern with an elevated area (semicircle of hyperopia) just next to a depressed area (semicircle of myopia) in the same meridian (Fig. 5). Spherical aberration has a central elevated area (focus of

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Figure 4 LADARWave image showing the total wavefront pattern of a patient with hyperopic LASIK to achieve monovision.

Figure 5 Coma pattern in a normal eye (LADARWave).

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Figure 6 Spherical aberration pattern in a normal eye (LADARWave).

hyperopia) surrounded by a depressed circle (annulus of myopia) and with normalization in the far periphery (resembling a flat sombrero) (Fig. 6). Other terms such as trefoil, quadrafoil, and secondary astigmatism generally have lower values (Fig. 7A and B). Patients that underwent hyperopic treatments have an accentuated prolate corneal pattern (Fig. 8) (22,23). When we analyze the spherical aberration pattern of these eyes, we can notice a decrease in the magnitude of spherical aberration and an inversion in the shape pattern. This is because the waves that come from the peripheral ablated zone converge less, so this area looks like a peripheral elevated red ring (annulus of relative hyperopia) and the central rays converge more, giving a central depressed area (focus of relative myopia). We call this pattern a flipped over sombrero hat, which is the opposite pattern of myopic treated eyes (Fig. 9). C. COMPARISON OF HYPEROPIC VERSUS MYOPIC TREATMENT WAVEFRONT 1. Profile of Myopic Correction As described by Munnerlyn in 1988, for a myopic ablation, the preoperative cornea is modeled as a sphere of greater curvature than the desired postoperative cornea, which is also modeled as a sphere within the treated zone. The apex of the desired postoperative cornea is displaced from the preoperative cornea by the maximal ablation depth, which is determined by the ablation zone size. The intervening tissue is simply removed or “subtracted” to produce the final result.

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A

B Figure 7 (A) Trefoil pattern. (B) Quadrafoil pattern.

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Figure 8 LADARWave image showing defocus, astigmatism, and higher-order aberrations of a hyperopic patient.

Figure 9 Spherical aberration after hyperopic treatment showing negative asphericity, as represented by a flipped over sombrero.

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Figure 10 LADARWave device showing defocus, astigmatism, and higher-order aberrations in a myopic patient.

Patients who have undergone myopic treatments have an oblate corneal pattern (Fig. 10) (24). The wavefront pattern shows a flattening or concavity to the otherwise bowlshaped wavefront of myopia. Analyzing the wavefront of these myopic treatments, we notice that the spherical aberration increases in number and size, with the depressed and elevated areas being accentuated. We describe this kind of pattern as a sombrero hat (Fig. 11). 2. Comparison of Aberration Changes in Hyperopia Versus Myopia In a study of 113 candidates for LASIK surgery, analyzing all aberrations, defocus and astigmatism were dominant. When analyzing only higher-order terms, coma and spherical aberrations were the most significant. Another study described the pre-and postwavefront measurements of patients submitted to LASIK for myopia or hyperopia and myopic PRK. It was found that, for LASIK, postoperative total error was significantly smaller for myopes than hyperopes (p ⬍ 0.05). Both myopic and hyperopic LASIK patients exhibit modest regression in defocus. In analyzing higher-order aberrations, it was noticed that spherical aberration decreased in hyperopic treatments and increased in myopic corrections. All other higher-order terms increased after either type of correction. In the postoperative interval, coma was the most dynamic higher-order aberration, with an overall decrease over time until 6-months postoperatively.

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Figure 11 Spherical aberration after myopic treatment showing increased positive asphericity, as represented by a sombrero hat.

REFERENCES 1. Applegate RA, Thibos LN, Hilmantel G. Optics of aberroscopy and super vision. J Cataract Refract Surg 2001; 27:1093–1107. 2. Maeda N. Wavefront technology in ophthalmology. Curr Opin Ophthalmol 2001; 12:294–299. 3. Huang D. Physics of customized corneal ablation. In: MacRae SM, Krueger RR, Applegate RA, eds. Customized Corneal Ablation: The Quest for Supervision. Thorofare NJ: Slack, 2001: 51–62. 4. Mrochen M, Kaemmerer M, Seiler T. Wavefront-guided laser in situ keratomileusis: early results in three eyes. J Refract Surg 2000; 16:116–121. 5. Kaemmerer M, Mrochen M, Mierdel P, Krinke HE, Seiler T. Clinical experience with the Tscherning aberrometer. J Refract Surg 2000; 16:S584–S587. 6. Krueger RR, Mrochen M, Kaemmerer M, Seiler T. Understanding refraction and accommodation through “retinal imaging” aberrometry. Ophthalmology 2001; 108:674–678. 7. Artal P. Understanding aberrations by using double-pass techniques. J Refract Surg 2000; 16: S560–S562. 8. Schwiegerling J. Theoretical limits to visual performance. Surv Ophthalmol 2000; 45(2): 139–146. 9. Applegate RA. Limits to vision: Can we do better than nature? J Refract Surg 2000; 16: S547–S551. 10. Williams D, Yoon GY, Porter J, Guirao A, Hofer H, Cox I. Visual benefit of correcting higher order aberrations of the eye. J Refract Surg 2000; 16:S554–S559. 11. Thibos LN. The prospects for perfect vision. J Refract Surg 2000; 16:S540–S546. 12. Thibos L. Wavefront data reporting and terminology. J Refract Surg 2001; 17:S578–S583.

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13. Oshika T, Klyce SD, Applegate RA, Howland HC, Danasoury MAE. Comparison of corneal wavefront aberrations after photorefractive keratectomy and laser in situ keratomileusis. Am J Ophthalmol 1999; 127:1–7. 14. Mrochen M, Kaemmerer M, Mierdel P, Seiler T. Increased higher-order optical aberrations after laser refractive surgery. A problem of subclinical decentration. J Cataract Refract Surg 2001; 27:362–369. 15. Mrochen M, Kaemmerer M, Seiler T. Clinical results of wavefront-guided laser in situ keratomileusis 3 months after surgery. J Cataract Refract Surg 2001; 27:201–207. 16. Howland HC. The history and methods of ophthalmic wavefront sensing. J Refract Surg 2000; 16:S552–S553. 17. Mrochen M, Kaemmerer M, Mierdel P, Krinke HE, Seiler T. Principles of Tscherning aberrometry. J Refract Surg 2000; 16:S570–S571. 18. Platt BC, Shack R. History and principles of Shack-Hartmann wavefront sensing. J Refract Surg 2001; 17:S573–S577. 19. Krueger RR. Technology requirements for Summit-Autonomus CustomCornea. J Refract Surg 2000; 16:S592–S601. 20. Thibos L. Principles of Shack-Hartmann aberrometry. J Refract Surg 2000; 16:S563–S565. 21. Roberts C, Dupps Jr WJ. Corneal biomechanics and their role in corneal ablative procedures. In: MacRae SM, Krueger RR, Applegate RA eds. Customized Corneal Ablation: The Quest for Supervision. Thorofare, NJ: Slack, 2001:109–131. 22. Argento CJ, Consentino MJ. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg 1998; 24:1050–1058. 23. McDonald M. Summit—Autonomus CustomCornea Laser in situ keratomileusis outcomes. J J Refract Surg 2000; 16:S617–S618. 24. Pettit GH, Campin J, Liedel K, Housand B. Clinical experience with the CustomCornea measurement device. J Refract Surg 2000; 16:S581–S583.

16 Contrast Sensitivity Changes After Hyperopia Surgery LAVINIA C. COBAN-STEFLEA Bucharest University Hospital and Carol Davila University of Medicine and Pharmacy, Bucharest, Romania TOMMY S. KORN University of California–San Diego and Rees-Stealy Medical Group, San Diego, California, U.S.A. BRIAN S. BOXER WACHLER Boxer Wachler Vision Institute, Beverly Hills, California, U.S.A.

A. INTRODUCTION Understanding the importance of contrast sensitivity can be easier if we emphasize its relationship to spatial vision, which is the core of the visual perception (1). Spatial frequency theory of image processing is based on spatially extended patterns called sinusoidal gratings, which are characterized by four parameters: spatial frequency, orientation, amplitude, and phase. The contrast sensitivity function is a measure of the observer’s sensitivity to gratings at different frequencies and is determined by the lowest contrast at which the sinusoidal gratings can still be detected (2). Over 200 years ago, contrast sensitivity began to be acknowledged as a clinical tool for doctors in studying visual disorders (3). In 1760 Bouguer defined and gave a value to the term light-difference threshold, the first denomination of contrast threshold. Since then other researchers have made a great number of contributions to this field: Bjerrum (1884) with letter charts, the first low-contrast letter acuity tests, and Young (1918) with the ink spot test, an easy method to measure the lightdifference threshold. More recently Schade (1956) applied his knowledge of television technology to contrast sensitivity testing. The work of Campbell and Green contributed to a better understanding of the optical and neural mechanism of contrast sensitivity testing and inspired further studies regarding alterations of contrast sensitivity in ocular diseases. 163

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Correction of hyperopia has been a constant concern of ophthalmologists over the past decades. Some of the surgical procedures that have been developed—hexagonal keratotomy (4,5), keratophakia, keratomileusis, and epikeratophakia (6–9)—have been abandoned because of limited applicability or side effects. Among current corrective procedures undoubtedly laser-assisted in situ Keratomileusis (LASIK) and Ho:YAG laser thermal keratoplasty (LTK) are the most widespread. Recently published clinical results emphasize the fact that LASIK is a procedure with good predictability, stability, efficacy, and safety for the correction of low to moderate spherical hyperopia (10). Long-term predictability with occurrence of undercorrection is influenced by the preoperative keratometric values and ablation zone diameter (11). Other studies point out the importance of corneal thickness and width of the flap for LASIK feasibility (12). The effectiveness of LASIK for severe hyperopia and hyperopic astigmatism is reduced (13,14). For treatments over Ⳮ5.00 D, the incidence of loss of best-corrected visual acuity was increased. Current nomograms require the cut of a larger flap in order to enlarge the ablation zone and to decrease the risk of halos, glare, and night vision difficulties for patients with high hyperopia and astigmatism (15). A lower predictability for astigmatic corrections was also reported after LASIK for myopia (16) in spite of in situ axis alignment (17,18). Encouraging results have been reported with respect to the safety, predictability, and stability of LASIK correction, for small degrees of hyperopia that were secondary to previous radial keratotomy (RK), and for automated lamellar keratoplasty (ALK) (19). The degree of regression after H-LASIK was reported to be higher relative to myopic corrections but lower, even in high hyperopia, than with the PRK procedure (20). Flap irregularities, epithelium, infection, or nonspecific inflammation at the flap interface have been reported complications of the LASIK procedure (21). Loss of vision can occur in cases of buttonholes, free cap, or amputation of the flap (22). Correction of hyperopia and astigmatism by thermal keratoplasty was reported more than 100 years ago (23–25). The actual mechanism by which this procedure alters the anterior corneal curvature has been clarified with the discovery of shrinkage temperature of corneal collagen by Stringer and Parr (26). In 1970s and 1980s, keratoconus was the focus of theromokeratoplasty technology. A number of clinical studies done have evaluated thermal keratoplasty potential to replace penetrating keratoplasty in keratoconus treatment (27–30). In spite of the fact that initial flattening of the cone followed the procedure, regression occurred within a few weeks postoperatively. It was not uncommon for these keratoconus treatments to be accompanied by complications such as corneal scarring, vascularization, and bullous keratopathy. Additionally, poor predictability and stability contributed to the withdrawing of the procedure from clinical use for keratoconus. A more recent approach to thermal keratoplasty is credited to Fyodorov, who developed a technique, using controlled thermal burns of corneal stroma with a retractable probe tip heated to 600⬚C and applied in a radial pattern. The procedure was eventually abandoned because of the high incidence of postoperative regression (31). In spite of repeated challenges to achieve predictable and stable refractive outcomes, researchers did not give up on probe technology but took another avenue, which was the use of lasers to deliver controllable amounts of energy to the stroma. Lasers such as continuous CO2 and cobalt magnesium fluoride have been used in experimental studies on rabbit corneas, with transient results (32,33). Reports of clinical studies that used the erbium:glass laser (34) have shown good results for hyperopia higher than Ⳮ3.00 D. Over the past decade, ophthalmologists in the United States have directed their work at evaluating two Ho:YAG laser systems: the noncontact system (Sunrise Tech-

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nologies, Fremont, CA) and the contact system (Summit Technologies, Waltham, MA). The Sunrise Ho:YAG is a pulsed laser that emits laser light at a wavelength of 2.13 ␮m. Other technical characteristics include pulse repetition frequency of 5 Hz and pulse energy in the range of 226 to 258 in correlation with the amount of refractive correction required. The energy is applied to the cornea in a noncontact mode through a fiberoptic slit-lamp system; the treatment pattern is represented by rings of spots concentric to the pupil (35). Sand, who was granted a patent for performing infrared LTK, was an important contributor to the development of this technology. Initial in vitro investigations have been made on swine and human cadaver eyes (36,37) in an attempt to establish a treatment protocol. Further studies done on human poorly sighted eyes showed a mean change in corneal curvature of 1.10 D followed by some amounts of regression (38). Results of clinical trials done outside the United States, which used the eight-spot treatment pattern applied at different diameters (6, 7, or 8 mm), had shown that the procedure works best up to Ⳮ3.00 D. They also proposed a treatment algorithm adjusted to variables such as age and central corneal thickness (39). Other studies have demonstrated that the amount of refractive change is increased when a two-ring treatment is applied at the 6- and 7-mm center line in a radial instead of a staggered pattern (40,41). The U.S. phase III study protocol has defined the efficacy criteria for the LTK procedure as improvement in distance UCVA and reduction in hyperopia manifest refraction spherical equvalent (MRSE) ⬎ 0.5 D. Evaluation at 2 years showed that 69.4% of patients had more than two lines of improvement in distance uncontrolled visual acuity (UCVA) and no eyes had lost more than two lines of best spectacle corrected visual acuity (BSCDVA) (35). B. CONTRAST SENSITIVITY IN LASIK AND LTK In understanding the outcomes of contrast sensitivity, we conducted a study to evaluate the quality of vision through its changes in LASIK and noncontact Ho:YAG LTK for the correction of low to moderate spherical hyperopia. We analyzed the results of two groups of patients who had LASIK and LTK, respectively, as primary procedures. There was no history of ocular diseases or surgery. We compared best-corrected contrast sensitivity values preoperatively and at 3 months postoperatively. Contrast sensitivity was measured with the self-calibrated, internally luminated CSV-1000E Vector Vision (Dayton, OH) at 12 cycles per degree (cpd) spatial frequency. The patient was instructed to identify whether the bars were in the top circle, bottom circle, or neither. The last correct identification has been taken as the contrast sensitivity. On the contrast sensitivity chart the numbers represent normalized ratios where values greater than 1.0 correspond to percent contrasts sensitivity above the population average and values below 1.0 represent percent of the average contrast sensitivity below the population average (42). Visual acuity was measured with the Vector Vision acuity chart using a scoring method of the U.S. Food and Drug Administration for refractive surgery clinical trials (43). All visual function tests were done with best spectacle-corrected visual acuity. Data were analyzed with the StatView (SAS Institute Inc., Cary, NC) statistical package. Visual acuity data were analyzed in logMAR values. Normalized contrast sensitivity values were converted to log values and used for statistical analysis. The LASIK study group comprised 94 eyes of 49 patients, 21 men and 28 women. Mean patient age was 59.67 years Ⳳ7.95 SD, range 44 to 78 years. Preoperatively, mean deviation from target manifest refraction was Ⳮ2.4 D Ⳳ1.2 D, SD, (range Ⳮ0.37 to Ⳮ5.60 D). LASIK procedures were performed by the same surgeon (B.B.W.) using the

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Table 1 H-LASIK Group—Preoperative and Postoperative Log Contrast Sensitivity Values and Best Spectacle-Corrected LogMAR Visual Acuity Values

Preop log CS Postop log CS Preop logMAR VA Postop logMAR VA

Mean

Standard deviation

Minimum

Maximum

1.30 1.23 ⫺0.01 0.02

0.22 0.27 0.08 0.10

0.61 0.61 ⫺0.20 ⫺0.20

1.69 1.54 0.20 0.50

Moria LSK (Doylestown, PA) microkeratome and the Summit Apex Plus Laser (Summit Technology Inc., Waltham, MA); the treatment zone was centered on the pupil. Results have shown a mean postoperative deviation from target manifest refraction of ⳮ0.09 D Ⳳ0.88 D, SD, (range ⳮ2.25 to Ⳮ2.00 D) at 3 months. Table 1 shows the mean preoperative and postoperative log contrast sensitivity values, standard deviations, and maximum and minimum values. At 3 months postoperatively the mean log contrast sensitivity value was not statistically significantly different compared to preoperative levels (p ⳱ 0.18). The mean best spectacle-corrected logMAR visual acuity value at 3 months was statistically significantly worse relative to preoperative value (p ⳱ 0.008). However, the change was not clinically significant, as the logMAR conversion was a loss of 1.5 letters on the acuity chart. There was a statistically significant correlation between achieved refraction and changes in log contrast sensitivity values (p ⳱ 0.006) (Fig. 1) (r ⳱ 0.29, p ⳱ 0.006). This indicated that higher amounts of hyperopic correction were associated with greater loss of best-corrected contrast sensitivity. No statistically significant correlation was ob-

Figure 1 Correlation between changes in log contrast sensitivity values and achieved refraction in the H-LASIK group.

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Figure 2 Correlation between changes in best spectacle-corrected logMAR visual acuity values and achieved refraction in the H-LASIK group.

served between achieved refraction and changes in best spectacle-corrected logMAR visual acuity (r ⳱ 0.05, p ⳱ 0.58)(Fig. 2). The LTK study group comprised 55 eyes of 35 patients, 16 males and 19 females. Mean patient age was 57.61 years Ⳳ7.35, SD, with a range of 39 to 71 years; mean deviation from target manifest refraction of treated eyes was Ⳮ1.5 D Ⳳ0.59 D, SD, range 0 to Ⳮ3.00 D. Noncontact Ho:YAG LTK treatments were performed by the same surgeon (B.B.W.) using the Sunrise Hyperion Holmium Laser Corneal Shaping System (Sunrise Technologies Inc., Fremont, CA). The treatment was centered on the corneal purkinje image of the patient fixation light. The light reflex closely approximates the visual axis. Therefore, in cases of positive angle kappa, the treatment was not centered on the pupil. Laser parameters included wavelength, 2.13 ␮m; pulse duration, 250 ␮s; pulse repetition frequency, 5 Hz; pulse energy, adjustable from 226 to 258 mJ/pulse. In the current study we used a two concentric radial 8-spot ring treatment pattern centered around the fixation light reflex on the cornea. Postoperatively, results showed a mean deviation from target manifest refraction of ⳮ0.36 D Ⳳ0.84 D, SD, range ⳮ3.50 to Ⳮ1.25 D. Mean log contrast sensitivity value was not statistically significantly decreased (p ⳱ 0.07) (Table 2) and mean best spectacle-corrected logMAR visual acuity value was statistically signifi-

Table 2 LTK Group—Preoperative and Postoperative Log Contrast Sensitivity Values and Best Spectacle-Corrected LogMAR Visual Acuity Values

Preop log CS Postop log CS Preop logMAR VA Postop logMAR VA

Mean

Standard deviation

Minimum

Maximum

1.28 1.19 ⫺0.01 0.04

0.24 0.29 0.08 0.11

0.61 0 ⫺0.2 ⫺0.1

1.69 1.84 0.2 0.6

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Figure 3 Correlation between changes in log contrast sensitivity values and achieved refraction in the LTK group.

cantly worse (p ⳱ 0.0067) relative to preoperative values. The change in acuity was not clinically significant as the change represented approximately four letters on the acuity chart. No statistically significant correlation (R ⳱ 0.16, p ⳱ 0.25) was found between achieved refraction and changes in log contrast sensitivity values (Fig. 3). Figure 4 shows the lack of correlation between achieved refraction and best-spectacle corrected logMAR visual acuity values (r ⳱ 0.15, p ⳱ 0.26).

Figure 4 Correlation between changes in best spectacle-corrected logMAR visual acuity values and achieved refraction in the LTK group.

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C. DISCUSSION As new surgical procedures are added to the refractive surgery armamentarium, assessing visual outcome becomes more difficult. Information regarding postoperative visual acuity and refractive changes is no longer satisfactory to evaluate the quality of the image projected on the retina (44). Contrast sensitivity, as a functional method, has been shown to be directly affected by the distorted image following excimer laser surgery (45). Using digitized retroillumination, Vinciguerra has shown that corneal distortion arising from prominent flap striae may be overlooked by the customary slit-lamp examination (46). Our results have shown a slight decrease in contrast sensitivity at 12 cpd spatial frequency postoperatively after LASIK procedure. However the difference was not statistically significantly different (p ⳱ 0.18). Previous literature data that have demonstrated that spatial frequency of 12 cpd is mostly affected by degradation in optics, such as aberration or blur (47). Other studies reported a loss of contrast sensitivity at 12 months after LASIK of up to one line for low hyperopia and of more than two lines for high hyperopia with no statistical significance (13). An interesting finding in the LASIK group was the significant correlation between achieved refraction and change in contrast sensitivity, demonstrating that larger amounts of correction are accompanied by larger loss of contrast sensitivity. This indicates that with the Summit Apex Plus laser used for LASIK and centered on the pupil, higher degrees of hyperopic treatment as associated with a higher risk of loss of best-corrected contrast sensitivity. Contrast sensitivity showed little change after the LTK procedure. The minimal decrease observed was not statistically significant (p ⳱ 0.07). Furthermore, contrast sensitivity changes showed no correlation with the amount of spherical correction attempted. Clinical trials at 1 and 2 years after LTK reported that mean contrast sensitivity increased at all follow-up visits for the two-ring treatment group at Regan charts (40,48). Postoperatively visual acuity did not vary significantly (p ⳱ 0.0067) and was not influenced by the amount of correction, although the amount of hyperopia corrected in the LTK group was less than that corrected in the LASIK group. We conclude that measuring contrast sensitivity after refractive surgical procedures should be encouraged and further developed in order to assess the limits of safety for given procedures and devices used for such procedures. Studies should be directed at identifying laser characteristics and treatment patterns that are able to optimize the optical system of the eye, thus increasing safety. REFERENCES 1. Palmer SE. Vision Science—Photons to Phenomenology. Cambridge, MA: MIT Press, 1999: 146–198. 2. Blakemore C, Campbell FW. On the existence of neurons in the human visual system selectively responsive to the orientation and size of retinal images. J Physiol 1969; 203:237–260. 3. Shapley R, Man-Kit Lam D. Contrast Sensitivity: Proceedings of the Retina Research Foundation Symposia. Vol. 5. Cambridge, MA: MIT Press, 1993: 253–266. 4. Werblin TP. Hexagonal keratotomy. Should we still be trying? J Refract Surg 1996; 12: 613–620. 5. Grandon SC, Sanders DR, Anello RD, Jacobs D, Biscaro M. Clinical evaluation of hexagonal keratotomy for the treatment of primary hyperopia. J Cataract Refract Surg 1995; 21:140–149. 6. Swinger CA, Barraquer JI. Keratophakia and keratomileusis—clinical results. Ophthalmology 1981; 88:709–715.

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7. Barraquer JI. Keratomileusis. Int Surg 1967; 48:103–117. 8. Morgan KS, Stephenson GS, McDonald MB, Kaufman HE. Epikeratophakia in children. Ophthalmology 1984; 91:780–784. 9. Anshutz T. Laser correction of hyperopia and presbyopia. In: ed. International Ophthalmology Clinics. Refractive Surgery. Boston: Little, Brown, 1994:107–137. 10. Boxer Wachler BS, O’Brien TP, Tauber S. Vision Correction—Seeing the Future. Current Laser Refractive and Surgical Alternatives for the Correction of Hyperopia. Oxford Institute for Continuing Education, 2000:3–5. 11. Esquenazi S, Mendoza A. Two-year follow-up of laser in situ keratomileusis. J Refract Surg 1999; 15:648–652. 12. Rosa JL, Febbraro DS. Laser in situ keratomileusis for hyperopia. J Refract Surg 1999; 5(2 suppl):S212–S215. 13. Arbelaez MC, Knorz MC. Laser in situ keratomileusis for hyperopia and hyperopic astigmatism. J Refract Surg 1999; 15:406–414. 14. Barraquer C, Gutierrez AM. Results of laser in situ keratomileusis in hyperopic compound astigmatism. J Cataract Refract Surg 1999; 25:1198–1204. 15. Lipner M. Distant visions: how practitioners outside the United States are treating hyperopia. Eye World 1999; 4:17–18. 16. Knorz MC, Wiesinger B, Liebermann A, Seiberth V, Liesenhoff H. Laser in situ keratomileusis for moderate and high myopia and myopic astigmatism. Ophthalmology 1998; 105:932–940. 17. Stevens JD. Astigmatic excimer laser treatment: theoretical effects of axis misalignment. Eur J Implant Ref Surg 1994; 6:310–318. 18. Vajpayee RB, McCarthy CA, Taylor HR. Evaluation of axis alignment system for correction of myopic astigmatism with the excimer laser. J Cataract Refract Surg 1998; 24:911–916. 19. Buzard KA, Fundingsland BR. Excimer laser assisted in situ keratomileusis for hyperopia. J Cataract Refract Surg 1999; 25:197–204. 20. Reviglio VE, Luna JD, Rodriguez ML, Garcia FE, Juarez CP. Laser in situ keratomileusis using the LaserSight 200 laser: results of 950 consecutive cases. J Cataract Refract Surg 1999; 25:1062–1068. 21. Wilson SE. LASIK: management of common complications (review). Cornea 1998; 17: 459–467. 22. Farah SG, Azar DT, Gurdal C, Wong J. Laser in situ keratomileusis: literature review of a developing technique (review). J Cataract Refract Surg 1998; 24:989–1006. 23. Lans LJ. Experimentelle Untersuchungen uber die Entstehung von Astigmatismus durch nichtperforierende Corneawunden. Graefes Arch Clin Exp Ophthalmol 1898; 45:117–152. 24. Wray C. Case of 6 D of hypermetropic astigmatism cured by the cautery. Trans Ophthalmol Soc UK 1914; 34:109–110. 25. O’Connor R. Corneal cautery for high myopic astigmatism. Am J Ophthalmol 1933; 16:337. 26. Striger H, Parr J. Shrinkage temperature of eye collagen. Nature 1964; 204:1307. 27. Gasset AR. Thermokeratoplasty in the treatment of keratoconus. Am J Ophthalmol 1975; 79: 226–232. 28. Aquavella JV, Buxton JN, Shaw EL. Thermokeratoplasty in the treatment of persistent corneal hydrops. Arch Ophthalmol 1977; 95:81–84. 29. Itoi M. Computer photokeratometry changes following thermokeratoplasty. In: Schachar RA, Levy NS, Schachar L, eds. Refractive Modulation of the Cornea. Denison, TX LAL Publishers, 1981. 30. Rowsey JJ, Doss JD. Preliminary report of Los Alamos keratoplasty techniques. Ophthalmology 1981; 88:755–760. 31. Caster AI. The Fyodorov technique of hyperopia correction by thermal coagulation: a preliminary report. J Refract Surg 1988; 4:105–108. 32. Peyman GA, Larson B, Raichand M, Andrews AH. Modification of rabbit corneal curvature with use of carbon dioxide laser burns. Ophthalmic Surg 1980; 11:325–329.

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33. Horn G, Spears KG, Lopez O, Lewicky A, Yang X, Riaz M, Wang R, Silva D, Serafin J. New refractive method for laser thermal keratoplasty with the Co: MgF2 laser. J Cataract Refract Surg 1990; 16:611–616. 34. Kanoda AN, Sorokin AS. Laser correction of hypermetropic refraction. In: Fyodorov SN, ed. Microsurgery of the Eye: Main Aspects. Moscow: MIR Publishers, 1987:147–154. 35. Aker AB, Boxer Wachler BS, Brown DC. Vision Correction—Seeing the Future. Noncontact Holmium:YAG Laser Thermal Keratoplasty for the Treatment of Hyperopia. Oxford Institute for Continuing Education, 2000:3–5. 36. Koch DD, Berry MJ, Vassiliadis AJ, Abarca AA, Villarreal R, Haft EA. Noncontact holmium: YAG laser thermal keratoplasy. In: Salz JJ, ed. Corneal Laser Surgery. Philadelphia: Mosby, 1995:247–254. 37. Moreira H, Campos M, Sawusch MR, McDonnell JM, Sand B, McDonnell PJ. Holmium laser thermokeratoplasty. Ophthalmology 1993; 100:752–761. 38. Ariayasu RG, Sand B, Menefee R, Hennings D, Rose C, Berry M, Garbus JJ, McDonnell PJ. Holmium laser thermal keratoplasty of 10 poorly sighted eyes. Refract Surg 1995; 11:358–365. 39. Alio JL, Ismail MM, Sanchez Pego JL. Correction of hyperopia with noncontact Ho:YAG laser thermal keratoplasty. J Refract Surg 1997; 13:17–22. 40. Koch DD, Kohnen T, McDonnell PJ, Menefee RF, Berry MJ. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty. US phase IIA clinical study with a 1-year follow-up. Ophthalmology 1996; 103:1525–1536. 41. Vinciguerra P, Kohnen T, Azzolini M, Radice P, Epstein D, Koch DD. Radial and staggered patterns to correct hyperopia using noncontact holmium:YAG laser thermal keratoplasty. J Cataract Refract Surg 1998; 24:21–30. 42. Boxer Wachler BS, Kruger RR. Normalized contrast sensitivity: a new notation for mainstream contrast sensitivity testing in refractive surgery. Invest Ophthalmol Vis Sci 1997; 38:530. 43. Boxer Wachler BS, Durrie DS, Assil KK, Kruger RR. Role of clearance and treatment zones in contrast sensitivity: significance in refractive surgery. J Cataract Refract Surg 1999; 25: 16–23. 44. Pallikaris IG. Quality of vision in refractive surgery. J Refract Surg 1998; 14:551–557. 45. Boxer Wachler BS, Frankel RA, Kruger RR, Durrie DS, Assil KK. Contrast sensitivity and patient satisfaction following photorefractive keratectomy and radial keratotomy. Invest Ophthalmol Vis Sci 1996; 37(suppl):S19. 46. Vinciguerra P, Azzollini M, Radice P. A new corneal analysis after excimer laser ablation: digitized retroillumination. In: Pallikaris IG, Siganos DS, eds. LASIK. Thorofare, NJ: Slack, 1997:331–337. 47. Campbell FW, Green DS. Optical and retinal factors affecting visual resolution. J Physiol 1965; 181:576–593. 48. Koch D, Abarca A, Villarreal R, Menefee R, Kohnen T, Vassiliadis A, Berry M. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty. Clinical study with twoyear follow-up. Ophthalmology 1996; 103:731–740.

17 Wound Healing After Hyperopic Corneal Surgery Why There Is Greater Regression in the Treatment of Hyperopia

´ SIO, JR. RENATO AMBRO University of Washington, Seattle, Washington, U.S.A., University of Sa˜o Paolo, Sa˜o Paolo, and Clı´nica e Microcirurgia Oftalmolo´gica Renato Ambro´sio, Rio de Janeiro, Brazil STEVEN E. WILSON University of Washington, Seattle, Washington, U.S.A.

A. INTRODUCTION Biological diversity in the corneal wound-healing response is a major factor in the outcomes of all keratorefractive surgical procedures (1,2). It is one of the most important determinants for overcorrection, undercorrection, and other complications, such as haze (3) and irregular astigmatism, which occur with laser-assisted in situ keratotomileusis (LASIK) and photorefractive keratectomy (PRK) in the treatment of myopia (4,5), hyperopia (6,7), or astigmatism (8,9). This response is very similar in different species, facilitating the creation of animal models for better characterization of the wound-healing response. There are quantitative and qualitative variations in specific processes that comprise the cascade. There is also variability depending on the inciting injury within a species. For example, thermal, incisional, lamellar, and surface scrape injuries are followed by wound-healing responses that are similar in some respects but different in others. Corneal wound healing following correction of hyperopia may be more complex than that associated with corrections of myopia (10). Steepening of the central cornea is required for hyperopic treatments. This leads to the creation of a corneal contour with a steeper central area and a flatter paracentral area. 173

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Refractive regression is defined as a gradual, partial, or total loss of the initial correction. It limits the predictability of all refractive surgery procedures performed on the cornea. It has been hypothesized that changes occurring as a result of corneal wound healing lead to addition of new tissue. Epithelial hyperplasia and stromal remodeling are the two mechanisms that are thought to underlie this phenomenon (3,11,12). 1. Keratocytes Disappear in Response to Epithelial Injury—Keratocyte Apoptosis One of the earliest observations that debunked the prior dogma regarding the quiescence of keratocytes was detection of disappearance of superficial keratocytes following corneal epithelial scrape injury. This observation was made first by Dohlman and coworkers in 1968 (16). Studies by later investigators confirmed that keratocytes in the anterior stroma disappear following corneal epithelial scrape injury (17–20) as well as thermokeratoplasty (21). The mechanism of disappearance of the keratocytes was not elucidated in these studies. The authors of these studies suggested that the disappearance of the keratocytes was attributable to several factors, such as osmotic changes from the loss of epithelium, exposure to the atmosphere, or even artifact. In 1996, Wilson and coworkers (20) first demonstrated that the early disappearance of keratocytes that follows epithelial injury is mediated by apoptosis (13–15,22–29). Cell shrinkage, blebbing with formation of membrane bound bodies, condensation, fragmentation of the chromatin, and DNA fragmentation consistent with apoptosis were detected in anterior stromal keratocytes after epithelial scrape wounds by transmission electron microscopy. Nuclear DNA fragmentation was confirmed by the TUNEL assay for 3′hydroxyl DNA ends. Apoptosis is a programmed form of cell death that occurs without the release of lysosomal enzymes or other intracellular components that could damage the surrounding tissue or cells. Uncontrolled release of cellular contents is characteristic of necrotic cell death (26). Studies have suggested that apoptosis is mediated by cytokines released from the injured epithelium, such as interleukin 1 (IL-1) (22), the Fas/Fas ligand system (27), bone morphogenic proteins (BMP) 2 and 4 (28), or tumor necrosis factor (TNF) alpha (29). Virtually any type of epithelial injury induces keratocyte apoptosis. These include mechanical scrapes (22–25), corneal surgical procedures like PRK and LASIK (24), herpes simplex keratitis (14), incisions (25), and even a plastic ring pressed firmly against the epithelial surface (24). Keratocytes undergo apoptosis after epithelial injury to a depth of one-third to onehalf the stromal thickness, depending on the species and the type of injury. Cellular processes, known as gap junctions, connect keratocytes in the unwounded cornea to form a syncytium (31,32). It is possible that signals transmitted by cytokines to the most superficial keratocytes are relayed to deeper keratocytes via these intercellular communication channels. Alternatively, the proapoptotic cytokines may penetrate into the stroma after injury. The keratocyte apoptosis response in the stroma varies with the type of corneal epithelial injury (25). Thus, injuries such as scraping of the epithelium (25) or viral infection of the epithelium (14) triggers keratocyte apoptosis in the superficial stroma. A lamellar cut across the cornea produced by a microkeratome also induces keratocyte apoptosis. This can be detected at the site of epithelial injury and along the lamellar interface (Figure

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Figure 1 (A) Apoptosis detected along the lamellar interface by TUNEL assay in rabbit eye that had LASIK and (B) on the surface in rabbit eye that had PRK.

1). Localization of keratocyte apoptosis in LASIK is thought to be attributable to tracking of epithelial material, including proapoptotic cytokines, into the interface by the microkeratome blade (22–25). Alternatively, cytokines from the injured peripheral epithelium could diffuse along the lamellar interface and into the central stroma (22–25). Apoptosis has also been correlated with severe complications. Meitz et al. (33) reported a severe case of acute corneal necrosis following PRK for hyperopia that required penetrating keratoplasty. Histopathological studies of the excised tissue were negative for micro-organisms. Utilizing light microscopy, an anterior zone of corneal necrosis was found to be present, with a moderate amount of acute inflammation at the interface between necrotic and viable corneal stroma; in addition, keratocytes with typical features of apoptosis were detected by TUNEL assay and electron microscopy (Figure 2). 2. Keratocyte Proliferation and Migration: Myofibroblasts After the loss of keratocytes caused by apoptosis within the first few hours of corneal epithelial injury, there will be an area of stroma devoid of keratocytes. Zieske and coworkers (34) demonstrated that remaining keratocytes in the posterior and peripheral cornea begin to undergo mitosis about 12 to 24 hours after the injury (34). Keratocyte mitosis can be detected using bromodeoxyuridine incorporation or immunocytochemical staining for a mitosis-specific antigen called Ki-67 (34).

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Figure 2 Transmission electron microscopy (TEM) of rabbit cornea, 24 hours after Hi PRK (ⳮ9.0D): Keratocyte apoptosis and a PMN.

The cell types derived from the keratocytes that undergo mitosis following corneal epithelial injury remain to be completely characterized. Studies have suggested that myofibroblasts are an important cell type generated following injury (38–41). These studies, however, are primarily in vitro tissue culture-based investigations. Little information is available regarding the fate of the cells that undergo mitosis following PRK (41). Nothing has been reported about the status of these cells following LASIK. 3. Resolution of The Wound-Healing Response—Return to “Normalcy” In the months following injury to the cornea, the wound-healing response is completed and there is a return to normal morphology and function. This process is associated with elimination of some of the cells associated with wound healing and remodeling of disordered collagen that was produced by myofibroblasts or keratocytes during the woundhealing process (54–55). This process begins within a few weeks after injury and can continue for years following severe injury. The corneal epithelium may undergo hyperplasia following corneal injury (1,56) as well as refractive surgery (11,12,21,57–59) as a part of the wound-healing response. Hyperplasia may vary between individuals, the eyes of a single individual, and with different types and levels of refractive correction. This is thought to be an important mechanism for regression of many keratorefractive procedures (1,12,56–59). There may be a return to a normal epithelial thickness over a period of months to years, and this may result in instability of the refractive effect of PRK or LASIK. The regulatory mechanisms that modulate this return to normal corneal epithelial morphology have not been characterized. B. CONSIDERATIONS ON HYPEROPIC CORRECTIONS: WHY ARE THEY DIFFERENT FROM MYOPIC CORRECTIONS? The surgical correction of hyperopia remains challenging, especially for corrections greater than 4 to 5 D. While corneal surgery for myopia requires flattening the cornea with an

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Table 1 Classification of Hyperopic Refractive Surgery 1. 2. 3. 4. 5.

Excimer laser procedures Collagen shrinkage procedures Corneal implants and inlays Phakic intraocular lens (IOL) Clear lens extraction with IOL (also piggyback; multifocal IOL)

appropriate effective optical zone, hyperopic treatments require steepening of the central cornea. This leads to the creation of more complex compound curves, which are steeper in the center and flatter in the paracentral area. Currently, options for refractive surgery to treat hyperopic patients can be separated into five categories (Table 1). The present chapter discusses only the first two options. The excimer laser allows reshaping of the corneal surface to a desired contour with submicron precision and reproducibility (65). Several issues must be considered in differentiating hyperopic and myopic corrections using the excimer laser. In myopic corrections, the laser is applied in the center of the cornea. Hyperopic treatment with the excimer laser consists of an annular zone of ablation to cause a relative flattening of the corneal periphery and a concomitant relative steepening of the center (optical zone) to achieve the desired refractive effect. Hyperopic corrections require more complex laser delivery systems (66). Since the treatment is typically longer and performed in the periphery, careful alignment of the laser beam is critical in order to prevent decentration. Thus, a greater chance of decentration may be noted. Optical zone and ablation zone sizes are fundamental to the efficacy of these procedures. A blend transitional zone must be created to avoid abrupt steps on the corneal surface, which would be likely to lead to regression via epithelial hyperplasia (67). The maximum ablation depth will be in an annulus between the optical zone and the outer diameter of the ablation zone. Larger outer zones may provide for less regression of the refractive effect (68,69) (Figure 3). However, AronRosa and Febbraro noted that when using an ablation zone of 5.5 ⳯ 8.25 mm with LASIK,

Figure 3 Diagram showing epithelial hyperplasia after hyperopic cornea surgery.

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there was better predictability and stability than with an ablation zone of 5.5 ⳯ 9.0 mm (70). One possible explanation for this observation is that the corneal flap size may have been smaller than the periphery of the hyperopic treatment. In such settings, a smaller ablation zone may be preferable. Excimer laser surgery for hyperopia may induce more astigmatism than for myopia. Significant change in the astigmatism power and axis was noted 3 months following hyperopic spherical LASIK in a two-step approach for treating hyperopic or mixed astigmatism (71). This could be related to centration issues in the treatment of hyperopia relative to myopia. Attempts to shrink the peripheral corneal collagen with thermal energy (thermokeratoplasty) were first reported by Lans over a century ago (72). Central steepening of the cornea is achieved by thermal shrinkage of the midperipheral corneal tissue. The use of different types of lasers and radiofrequency energy in the corneal stroma to shrink the collagen lamellae is an active topic of study and is discussed elsewhere in this book. Recent reports have shown that these procedures may be effective in correcting low hyperopia, although corrections were subject to regression (73). Age-dependent corneal factors were shown to influence the effectiveness of thermal energy on stromal collagen and regression (74). Stability following thermokeratoplasty may be related to the type of lesion produced. A perfect thermal lesion, delivered at the perfect depth, with a perfect geometry, and for the perfect length of time would cause a permanent change in the collagen fibers in the cornea, so that regression would be less likely to occur. It remains to be seen whether such a “perfect thermal lesion” that is permanent can be created or whether ever-vigilant keratocytes will eventually detect these anomalies in the collagen fibers and repair them. Corneal iron pigmentation lines or rings can be observed after hyperopic corneal surgery (75–78). Corneal iron deposition has been seen in the normal cornea with aging (Hudson-Stahli line) and in pathological corneal conditions such as keratoconus (Fleischer ring), pterygia (Stocker-Busacca line), and filtering blebs (Ferry’s line). Stellate iron lines were also described after radial keratotomy (79) and in cases of central island (80). The most likely explanation for the formation of such lines is that the iron is derived from the tear film and deposited in the corneal epithelium in those areas where there is tear pooling. Since keratorefractive procedure for hyperopia sculpts the cornea to resemble a convex lens, a furrow-like ring zone in the corneal periphery is produced. This can be observed when looking at the corneal elevation map after H-LASIK. (Figure 4). Tear pooling occurs and subsequently triggers iron deposition. It may also prolong the exposure time to tear film cytokines (81,82) causing epithelial hyperplasia in this midtransition zone (junction of the optical and ablated zones) (11). C. MECHANISMS OS REGRESSION A complete understanding of the mechanisms underlying regression after keratorefractive surgery in vivo require the study of the wound-healing response and factors related to biomechanics. A thorough understanding of corneal microstructure can now be obtained using new methods. High-frequency (50-MHz) ultrasound biomicroscopy (UBM and VHF) (83–86) (Figure 5) and optical coherence tomography (OCT) (87–89) are two promising technologies that have the capacity to measure the thickness of each layer within the cornea. These measurements could help us to distinguish between epithelial hyperplasia and stromal remodeling as the cause of the refractive regression in individual eyes. Confocal microscopy allows for optical sectioning through intact living cornea, obtaining images

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Figure 4 Elevation map before and after hyperopic LASIK.

of the cornea at its cellular level in four dimensions (x, y, z, and t-time) (3,10,90,91). It has been difficult, however, to obtain reliable measurements of epithelial thickness using this technology. Slit-based videokeratography instruments like the Orbscan (Bausch & Lomb, Orbtek, Inc., Salt Lake City, UT) may be useful for assessing pachymetric values through the entire cornea as well as for measuring posterior curvature (92,93). However, uncertainty regarding the meaning of values derived from the posterior surface of the cornea is a limiting factor. Studies have shown that corneal thickness measurements are inaccurate with this instrument (94,95). At the present time, therefore, it appears that high-frequency ultrasound or OCT provides the best opportunity for monitoring epithelial thickness following refractive surgery procedures. Studies are in progress using these methods. Animal model studies have been performed to characterize corneal wound healing following surgery for hyperopia (11,21,96–99). It is important to recognize the possible limitations of the rabbit model in assessing the nature of the wound-healing response in humans. Wound healing is thought to be more vigorous in rabbits, and qualitative as well as quantitative differences may exist. It is feasible to perform studies in patients who

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Figure 5 Corneal image using ultrasound biomicroscopy.

undergo surgery for enucleation or exenteration, as well as before penetrating keratoplasty, to clarify these potential differences between humans and animal models (21). Our working hypothesis at the present time is that regression after LASIK or PRK surgery for hyperopia is due to a combination of epithelial hyperplasia and stromal regrowth in the ablation zone. Using confocal microscopy and histological examination in a rabbit model, Hosoda at al. detected subepithelial proliferative changes in the ablated zone that progressed for 1 month after surgery, then decreased by the third month (96). In a similar study by Dierick et al. (11), mean stromal regrowth after 10-D hyperopic PRK was 50% of ablated tissue. Deposition showed a lenticular pattern and could account for up to 5.00 D of regression (11). In addition, the epithelium thickened 20% at the midtransition zone (junction of the optical and ablated zones), contributing to more refractive regression (11). A key question is whether the epithelial hyperplasia is attributable to an increased wound healing response due to the size of the ablation zone, the altered surface topography associated with steepening the central contour, or a combination of both these factors. With smaller ablation zone diameters that have been tested in the past, rapid regression may have been largely due to abrupt changes in corneal curvature in the midperiphery of the ablation. With wider ablations that allow a more gradual transition than with smaller ablation zones, there is less tendency for regression, suggesting that the influence of this factor has been reduced. Differences in tear pooling and distribution on the corneal surface between smaller and larger ablation zone diameters could play a role. Well-controlled studies of varying ablations with careful measurements of epithelial hyperplasia and stro-

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mal regrowth should help to increase our understanding of regression associated with the laser correction of hyperopia. Other sources of regression may be a greater than average wound-healing response in individual patients or variations in surgery that promote increased healing. For example, a thin flap may be associated with regression, since the stromal wound-healing response and epithelium-modulating modulating growth factor production are more likely to be in proximity to the epithelium (13). This is probably a major factor promoting epithelial hyperplasia. Other factors such as epithelial defects produced by the microkeratome and diffuse interface keratitis may also be associated with a stronger wound-healing response and therefore regression. The rate of enhancement in a recent series was significantly higher (53 versus 16%; p⳱0.02) following DLK than for eyes that did not have DLK (Wilson and Ambro´sio, unpublished data, 2001). Since the treatment for hyperopia is typically performed in the periphery of the cornea, closer to the limbus, it is likely that a stronger inflammatory reaction will follow those surgeries. A study involving an animal model comparing hyperopic and myopic PRK, using specific antibodies for inflammatory cells as well as cytokines, might be helpful for elucidating this hypothesis. The higher the level of correction attempted for hyperopia, the more likely regression due to wound healing will occur. In our experience with hyperopic LASIK and PRK, regression is most common in eyes where the attempted correction is over 4 to 5 D. Intraocular pressure could be a factor in the regression of hyperopic LASIK in some cases with high-pressure increases. A case of acute angle-closure glaucoma was reported by Paciuc et al. 1 year after hyperopic LASIK (100). The glaucoma attack was treated with laser peripheral iridotomy and a prophylactic iridotomy was performed in the fellow eye. Corneal topography was performed 2, 5, and 18 weeks after the acute episode and a myopic shift occurred in the eye that had angle closure. This resolved over 3 months. It is important to consider that the eye blinks over 10,000 times per day (101) at lid velocities up to 30 cm/s (102). Each blink has enough force to raise intraocular pressure 10 to 70 mmHg (103). Koch and coworkers (21) studied Ho:YAG LTK on three human corneas 1 day before their removal at penetrating keratoplasty in patients with corneal edema secondary to Fuchs endothelial dystrophy (without bullous epithelial changes) and on six New Zealand white rabbit corneas followed for up to 3 months. The pulse radiant energy level was noted to be proportional to the acute tissue injury. In human corneas, changes in the irradiated zones included epithelial cell injury and death, loss of fine filamentous structure in Bowman’s layer, disruption of stromal lamellae, and keratocyte injury and death. A cone-shaped zone of increased stromal hematoxylin uptake extending posteriorly for 90% of stromal thickness was noted in the treatment areas. Special immunohistochemical stains to detect apoptosis were not used, although transmission electron microscopy findings suggested that they might play a role. In the rabbit corneas, similar acute changes were noted. By 3 weeks, epithelial hyperplasia and stromal contraction were present. Wound healing in the rabbits included repair of the epithelial attachment complex, keratocyte activation, synthesis of type I collagen, and partial restoration of stromal keratin sulfate and type VI collagen. There was also a marked endothelial proliferative response in the rabbit corneas. Attempted corrections with LTK of greater than 2 D are associated with significant regression. This is likely related to stromal remodeling, with the keratocytes functioning to repair the altered collagen over time.

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D. FUTURE DIRECTIONS AND CONCLUSIONS The ability to modulate corneal wound healing to achieve better clinical outcomes would be beneficial to extend the efficacy and safety of keratorefractive corrections of hyperopia. Apoptosis is the first detected event in the complex cascade of the corneal wound healing. Differences in this initiator and subsequent events in healing between eyes likely is a major determinant of variation between eyes following laser correction for hyperopia. Development of methods to control this first event may be useful for normalizing the response between patients. A better understanding of the mechanisms associated with regression, especially differentiating between the key determinants epithelial hyperplasia and stromal remodeling, would provide specific strategies to improve stability. Corneal implants and inlays may become an option for hyperopic treatment in the future. New alloplastic materials with acceptable permeability for corneal tissue, with refractive indices and clarity equal to those of the cornea, may provide a reversible refractive procedure for hyperopia. Intracorneal lenses with higher refractive indexes than the cornea and therefore intrinsic refractive power would not rely on changing the cornea’s shape. They could attenuate epithelial hyperplasia as a factor in regression. Corneal surgery for hyperopia has lagged behind that of myopia primarily due to issues related to efficacy, stability, and safety. Several procedures were abandoned during the past decade. Understanding and respecting the limits of the available procedures is key for achieving success with hyperopic patients. Intraocular procedures for hyperopia, such as phakic intraocular lenses and clear lens extraction, may have an important role in treating this group of patients if safety can be improved. ACKNOWLEDGMENTS Supported in part by an unrestricted grant from Research to Prevent Blindness, New York, N.Y., and U.S. Public Health Service grant EY 10056 and EYO1730 from the National Eye Institute, National Institutes of Health, Bethesda, Maryland. PROPRIETARY INTEREST STATEMENT The authors have no proprietary or financial interest in relation to this manuscript. REFERENCES 1. Wilson SE, Mohan RR, Hong JW, Lee JS, Choi R, Mohan RR. The wound healing response after laser in situ keratomileusis and photorefractive keratectomy: elusive control of biological variability and effect on custom laser vision correction. Arch Ophthalmol 2001; 119:889–896. 2. Wilson SE, Mohan RR, Mohan RR, Ambrosio R Jr, Hong J, Lee J. The corneal wound healing response: cytokine-mediated interaction of the epithelium, stroma, and inflammatory cells. Prog Ret Eye Res. 2001 9; 20(5):625–637. 3. Moller-Pedersen T, Cavanagh HD, Petroll WM, Jester JV. Stromal wound healing explains refractive instability and haze development after photorefractive keratectomy: a 1-year confocal microscopic study. Ophthalmology 2000; 107:1235–1245. 4. Kim JH, Kim MS, Hahn TW, Lee YC, Sah WJ, Park CK. Five year results of photorefractive keratectomy for myopia. J Cataract Refract Surg 1997; 23:731–735.

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5. Shah SS, Kapadia MS, Meisler DM, Wilson SE. Photorefractive keratectomy using the summit SVS Apex laser with or without astigmatic keratotomy. Cornea 1998; 17:508–516. 6. Esquenazi S, Mendoza A. Two-year follow-up of laser in situ keratomileusis for hyperopia. J Refract Surg 1999; 15:648–652. 7. Zadok D, Maskaleris G, Montes M, Shah S, Garcia V, Chayet A. Hyperopic laser in situ keratomileusis with the Nidek EC–5000 excimer laser. Ophthalmology 2000; 107: 1132–1137. 8. Hersh PS, Abbassi R. Surgically induced astigmatism after photorefractive keratectomy and laser in situ keratomileusis. Summit PRK-LASIK Study Group. J Cataract Refract Surg 1999; 25:389–398. 9. Kapadia MS, Krishna R, Shah S, Wilson SE. Surgically induced astigmatism after photorefractive keratectomy with the excimer laser. Cornea 2000; 19:174–179. 10. Vesaluoma MH, Petroll WM, Perez-Santonja JJ, Valle TU, Alio JL, Tervo TM. Laser in situ keratomileusis flap margin: wound healing and complications imaged by in vivo confocal microscopy. Am J Ophthalmol 2000; 130:564–573. 11. Dierick HG, Van Mellaert CE, Missotten L. Histology of rabbit corneas after 10-diopter photorefractive keratectomy for hyperopia. J Refract Surg 1999; 15:459–468. 12. Lohmann CP, Guell JL. Regression after LASIK for the treatment of myopia: the role of the corneal epithelium. Semin Ophthalmol 1998; 13:79–82. 13. Wilson SE, Mohan RR, Mohan RR, Ambrosio Jr R, Hong J-W, Lee J-S. The corneal wound healing response: Cytokine-mediated interaction of the epithelium, stroma, and inflammatory cells. Prog Ret Eye Res 2001; 20:625–637. 14. Wilson SE, Pedroza L, Beuerman R, Hill JM. Herpes simplex virus type–1 infection of corneal epithelial cells induces apoptosis of the underlying keratocytes. Exp Eye Res 1997; 64:775–779. 15. Wilson SE. Role of apoptosis in wound healing in the cornea. Cornea 2000; 19(suppl): S7–S12. 16. Dohlman CH, Gasset AR, Rose J. The effect of the absence of corneal epithelium or endothelium on stromal keratocytes. Invest Ophthalmol Vis Sci 1968; 7:520–534. 17. Nakayasu K. Stromal changes following removal of epithelium in rat cornea. Jpn J Ophthalmol 1988; 32:113–125. 18. Campos M, Szerenyi K, Lee M, McDonnell JM, McDonnell PJ. Keratocyte loss after corneal deepithelialization in primates and rabbits. Arch Ophthalmol. 1994; 112:254–260. 19. Szerenyi KD, Wang X, Gabrielian K, McDonnell PJ. Keratocyte loss and repopulation of anterior corneal stroma after de-epithelialization. Arch Ophthalmol 1994; 112:973–976. 20. Polack FM. Keratocyte loss after corneal deepithelialization in primates and rabbits. Arch Ophthalmol 1994; 112:1509. 21. Koch DD, Kohnen T, Anderson JA, Binder PS, Moore MN, Menefee RF, Valderamma GL, Berry MJ. Histologic changes and wound healing response following 10-pulse noncontact holmium: YAG laser thermal keratoplasty. J Refract Surg 1996; 12:623–634. 22. Wilson SE, He Y-G, Weng J, Li Q, Vital M, Chwang EL. Epithelial injury induces keratocyte apoptosis: hypothesized role for the interleukin–1 system in the modulation of corneal tissue organization. Exp Eye Res 1996; 62:325–338. 23. Wilson SE. Molecular cell biology for the refractive corneal surgeon: programmed cell death and wound healing. J Refract Surg 1997; 13:171–175. 24. Wilson SE. Keratocyte apoptosis in refractive surgery: Everett Kinsey Lecture. CLAO J 1998; 24:181–185. 25. Helena MC, Baerveldt F, Kim W-J, Wilson SE. Keratocyte apoptosis after corneal surgery. Invest Ophthalmol Vis Sci 1998; 39:276–283. 26. Kim WJ, Mohan RR, Mohan RR, Wilson SE. Caspase inhibitor z-VAD-FMK inhibits keratocyte apoptosis, but promotes keratocyte necrosis, after corneal epithelial scrape. Exp Eye Res 2000; 71:225–232.

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27. Mohan RR, Liang Q, Kim W-J, Helena MC, Baerveldt F, Wilson SE. Apoptosis in the cornea: Further characterization of Fas/Fas ligand system. Exp Eye Res 1997; 65:575–589. 28. Mohan RR, Kim W-J, Mohan RR, Chen L, Wilson SE. Bone morphogenic proteins 2 and 4 and their receptors in the adult human cornea. Invest Ophthalmol Vis Sci 1998; 39
26–2636. 29. Mohan RR, Mohan RR, Kim WJ, Wilson SE. Modulation of TNF-alpha–induced apoptosis in corneal fibroblasts by transcription factor NF-kb. Invest Ophthalmol Vis Sci 2000; 41: 1327–1336. 30. Gao J, Gelber-Schwalb TA, Addeo JV, Stern ME. Apoptosis in the rabbit cornea after photorefractive keratectomy. Cornea 1997; 16:200–208. 31. Watsky MA. Keratocyte gap junctional communication in normal and wounded rabbit corneas and human corneas. Invest Ophthalmol Vis Sci 1995; 36:2568–2576. 32. Spanakis SG, Petridou S, Masur SK. Functional gap junctions in corneal fibroblasts and myofibroblasts. Invest Ophthalmol Vis Sci 1998; 39:1320–1328. 33. Mietz H, Severin M, Seifert P, Esser P, Krieglstein GK. Acute corneal necrosis after excimer laser keratectomy for hyperopia. Ophthalmology 1999; 106:490–496. 34. Zieske JD, Guimaraes SR, Hutcheon AEK. Kinetics of keratocyte proliferation in response to epithelial debridement. Exp. Eye Res 2001; 72:33–39. 35. Kamiyama K, Iguchi I, Wang X, Imanishi J. Effects of PDGF on the migration of rabbit corneal fibroblasts and epithelial cells. Cornea 1998; 17:315–325. 36. Andresen JL, Ehlers N. Chemotaxis of human keratocytes is increased by platelet-derived growth factor-BB, epidermal growth factor, transforming growth factor-alpha, acidic fibroblast growth factor, insulin-like growth factor-I, and transforming growth factor-beta. Curr Eye Res 1009; 17:79–87. 37. Kim W-J, Mohan RR, Mohan RR, Wilson SE. Effect of PDGF, IL–1 alpha, and BMP2/4 on corneal fibroblast chemotaxis: expression of the platelet-derived growth factor system in the cornea. Invest Ophthalmol Vis Sci 1999; 40:1364–1372. 38. Masur S, Dewal HS, Dinh TT, Erenburg I, Petridou S. Myofibroblasts differentiate from fibroblasts when plated at low density. Proc Natl Acad Sci USA 1996; 93:4219–4223. 39. Jester JV, Huang J, Barry-Lane PA, Kao WW, Petroll WM, Cavanagh HD. Transforming growth factor (beta)-mediated corneal myofibroblast differentiation requires actin and fibronectin assembly. Invest Ophthalmol Vis Sci 1990; 40:1959–1967. 40. Jester JV, Petroll WM, Cavanagh HD. Corneal stromal wound healing in refractive surgery: the role of myofibroblasts. Prog Retin Eye Res 1999; 18:311–356. 41. Moller-Pedersen T, Cavanagh HD, Petroll WM, Jester JV. Neutralizing antibody to TGF beta modulates stromal fibrosis but not regression of photoablative effect following PRK. Curr Eye Res 1998; 17:736–747. 42. Jester JV, Moller-Pedersen T, Huang J, Sax CM, Kays WT, Cavanagh HD, Petroll WM, Piatigorsky J. The cellular basis of corneal transparency: evidence for “corneal crystallins.” J Cell Sci 1999; 112:613–622. 43. Weng J, Mohan RR, Li Q, Wilson SE. IL-1 upregulates keratinocyte growth factor and hepatocyte growth factor mRNA and protein production by cultured stromal fibroblast cells: interleukin-1 beta expression in the cornea. Cornea 1996; 16:465–471. 44. Kaji Y, Obata H, Usui T, Soya K, Machinami R, Tsuru T, Yamashita H. Three-dimensional organization of collagen fibrils during corneal stromal wound healing after excimer laser keratectomy. J Cataract Refract Surg 1998; 24:1441–1446. 45. El-Shabrawi Y, Kublin CL, Cintron C. mRNA levels of alpha1(VI) collagen, alpha1(XII) collagen, and beta ig in rabbit cornea during normal development and healing. Invest Ophthalmol Vis Sci 1998; 39:36–44. 46. Girard MT, Matsubara M, Fini ME. Transforming growth factor-beta and interleukin-1 modulate metalloproteinase expression by corneal stromal cells. Invest Ophthalmol Vis Sci 1991; 32:2441–2454.

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47. Strissel KJ, Rinehart WB, Fini ME. Regulation of paracrine cytokine balance controlling collagenase synthesis by corneal cells. Invest Ophthalmol Vis Sci 1997; 38:546–552. 48. West-Mays JA, Strissel KJ, Sadow PM, Fini ME. Competence for collagenase gene expression by tissue fibroblasts requires activation of an interleukin 1 alpha autocrine loop. Proc Natl Acad Sci USA 1995; 92:6768–6772. 49. Ye HQ, Azar DT. Expression of gelatinases A and B, and TIMPs 1 and 2 during corneal wound healing. Invest Ophthalmol Vis Sci 1998; 39:913–921. 50. Ye HQ, Maeda M, Yu FS, Azar DT. Differential expression of MT1-MMP (MMP–14) and collagenase III (MMP–13) genes in normal and wounded rat corneas. Invest Ophthalmol Vis Sci 2000; 41:2894–2899. 51. O’Brien T, Li Q, Ashraf MF, Matteson DM, Stark WJ, Chan CC. Inflammatory response in the early stages of wound healing after excimer laser keratectomy. Arch Ophthalmol 1998; 116:1470–1474. 52. Tran MT, Tellaetxe-Isusi M, Elner V, Strieter RM, Lausch RN, Oakes JE. Proinflammatory cytokines induce RANTES and MCP–1 synthesis in human corneal keratocytes but not in corneal epithelial cells. Beta-chemokine synthesis in corneal cells. Invest Ophthalmol Vis Sci 1996; 37:987–996. 53. Hong JW, Liu JJ, Lee JS, Mohan RR, Mohan RR, Woods DJ, He YG, Wilson SE. Proinflammatory chemokine induction in keratocytes and inflammatory cell infiltration into the cornea. Invest Ophthalmol Vis Sci 2001; 42(12):2795–2803. 54. Lee RE, Davison PF, Cintron C. The healing of linear nonperforating wounds in rabbit corneas of different ages. Invest Ophthalmol Vis Sci 1982; 23:660–665. 55. Cintron C, Covington HI, Kublin CL. Morphologic analyses of proteoglycans in rabbit corneal scars. Invest Ophthalmol Vis Sci 1990; 31:1789–1798. 56. Kim W-J, Helena MC, Mohan RR, Wilson SE. Changes in corneal morphology associated with chronic epithelial injury. Invest Ophthalmol Vis Sci 1999; 40:35–42. 57. Gauthier CA, Holden BA, Epstein D, Tengroth B, Fagerholm P, Hamberg-Nystrom H. Role of epithelial hyperplasia in regression following photorefractive keratectomy. Br J Ophthalmol 1996; 80:545–548. 58. Gauthier CA, Holden BA, Epstein D, Tengroth B, Fagerholm P, Hamberg-Nystrom H. Factors affecting epithelial hyperplasia after photorefractive keratectomy. J. Cataract Refract Surg 1997; 23:1042–1050. 59. Spadea L, Fasciani R, Necozione S, Balestrazzi E. Role of the corneal epithelium in refractive changes following laser in situ keratomileusis for high myopia. J Refract Surg 2000; 16: 133–139. 60. Warbling TP. Hexagonal keratotomy—should we still be trying? (See comments). J Refract Surg 1996; 12:613–617; discussion 617–620. Comment in: J Refract Surg 1997; 13:128. 61. Lyle WA, Jin GJC. Hyperopic automated lamellar keratoplasty: Complications and visual results. Arch Ophthalmol 1998; 116:425–428. 62. Holladay JT, Waring GO. Optics and topography of radial keratotomy. In: Waring GO, ed. Refractive Keratotomy for Myopia and Astigmatism. St Louis: Mosby–Year Book, 1992. 63. Kezirian GM, Gremillion CM. Automated lamellar keratoplasty for the correction of hyperopia. J Cataract Refract Surg 1995; 21:386–392. 64. Manche EE, Judge A, Maloney RK. Lamellar keratoplasty for hyperopia. J Refract Surg 1996; 12:42–49. 65. Trokel SL, Srinivasan R, Braren B. Excimer laser surgery of the cornea. Am J Ophthalmol 1983; 96:710–715. 66. O’Brart DP. The status of hyperopic laser-assisted in situ keratomileusis. Curr Opin Ophthalmol 1999; 10:247–252. 67. Maloney RK, Friedman M, Harmon T, Hayward M, Hagen K, Gailitis RP, Waring GO, III. A prototype erodible mask delivery system for the excimer laser. Ophthalmology 1993; 100: 542–549.

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68. Argento CJ, Cosentino MJ. Comparison of optical zones in hyperopic laser in situ keratomileusis: 5.9 mm versus smaller optical zones. J Cataract Refract Surg 2000; 26:1137–1146. 69. Davidorf JM, Eghbali F, Onclinx T, Maloney RK. Effect of varying the optical zone diameter on the results of hyperopic laser in situ keratomileusis. Ophthalmology 2001; 108:1261–1265. 70. Aron-Rosa DS, Febbraro JL. Laser in situ keratomileusis for hyperopia. J Refract Surg 1999; 15(suppl):S212–S215. 71. Ambro´sio R Jr, Wilson SE. Two step LASIK for hyperopic or mixed astigmatism with the VisX S2 laser. Invest Ophthalmol Vis Sci (Suppl) 2001; 42:S7224. 72. Lans U. Experimentelle Utersuchungen uber die Entstehung von Astigmatismus durch nichtperforierende Corneawunden. Graefes Arch Clin Exp Ophthalmol 1898; 45:117. 73. Vinciguerra P, Kohnen T, Azzolini M, Radice P, Epstein D, Koch DD. Radial and staggered treatment patterns to correct hyperopia using noncontact holmium:YAG laser thermal keratoplasty. J Cataract Refract Surg 1998; 24:21–30. 74. Gezer A. The role of patient’s age in regression of holmium: YAG thermokeratoplasty–induced correction of hyperopia. Eur J Ophthalmol 1997; 7(2):139–143. 75. Bilgihan K, Akata F, Gurelik G, Adiguzel U, Akpinar M, Hasanreisoglu B. Corneal iron ring after hyperopic photorefractive keratectomy. J Cataract Refract Surg 1999; 25:685–687. 76. Ozdamar A, Aras C, Sener B, Karacorlu M. Corneal iron ring after hyperopic laser-assisted in situ keratomileusis. Cornea 1999; 18:243–245. 77. Molina CA, Agudelo LM. Corneal iron pigmentation after LASIK for hyperopia (letter). J Refract Surg 2000; 16:755–756. 78. Probst LE, Almasswary MA, Bell J. Pseudo-Fleischer ring after hyperopic laser in situ keratomileusis. J Cataract Refract Surg 1999; 25:868–870. 79. Steinberg EB, Wilson LA, Waring III GO, Lynn MJ, Coles WH. Stellate iron lines in the corneal epithelium after radial keratotomy. Am J Ophthalmol 1984; 98:416–421. 80. Krueger RR, Tersi I, Seiler T. Corneal iron line associated with steep central islands after photorefractive keratectomy. J Refract Surg 1997; 13(4):401–403. 81. Tervo T, Vesaluoma M, Bennett GL, Schwall R, Helena M, Liang Q, Wilson SE. Tear hepatocyte growth factor (HGF) availability increases markedly after excimer laser surface ablation. Exp Eye Res 1997; 64:501–504. 82. Wilson SE, Li Q, Mohan RR, Tervo T, Vesaluoma M, Bennett GL, Schwall R, Tabor K, Kim J, Hargrave S, Cuevas KH. Lacrimal gland growth factors and receptors: lacrimal fibroblastic cells are a source of tear HGF. Adv Exp Med Biol 1998; 438:625–628. 83. McWhae J, Willerscheidt A, Gimbel H, Freese M. Ultrasound biomicroscopy in refractive surgery. J Cataract Refract Surg 1994; 20:493–497. 84. Reinstein DZ, Silverman RH, Sutton HF, Coleman DJ. Very high-frequency ultrasound corneal analysis identifies anatomic correlates of optical complications of lamellar refractive surgery: anatomic diagnosis in lamellar surgery. Ophthalmology 1999; 106:474–482. 85. Holland SP, Srivannaboon S, Reinstein DZ. Avoiding serious corneal complications of laser assisted in situ keratomileusis and photorefractive keratectomy. Ophthalmology 2000; 107: 640–652. 86. Reinstein DZ, Silverman RH, Raevsky T, Simoni GJ, Lloyd HO, Najafi DJ, Rondeau, MJ Coleman DJ. Arc-scanning very high-frequency digital ultrasound for 3D pachymetric mapping of the corneal epithelium and stroma in laser in situ keratomileusis. J Refract Surg 2000; 16:414–430. 87. Maldonado MJ, Ruiz-Oblitas L, Munuera JM, Aliseda D, Garcia-Layana A, Moreno-Montanes J. Optical coherence tomography evaluation of the corneal cap and stromal bed features after laser in situ keratomileusis for high myopia and astigmatism. Ophthalmology 2000; 107:81–87; discussion 88. 88. Ustundag C, Bahcecioglu H, Ozdamar A, Aras C, Yildirim R, Ozkan S. Optical coherence tomography for evaluation of anatomical changes in the cornea after laser in situ keratomileusis. J Cataract Refract Surg 2000; 26:1458–1462.

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18 Monovision Refractive Surgery for Presbyopia DIMITRI T. AZAR, MARGARET CHANG, CAROLYN E. KLOEK, SAMIAH ZAFAR, KIMBERLY SIPPEL, and SANDEEP JAIN Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A

A. INTRODUCTION Many refractive surgery patients are in the presbyopic or prepresbyopic age group and often experience difficulties with near vision after their myopia is corrected. Preoperatively, many of these patients are able to read by taking off their glasses; postoperatively, they may find they are no longer able to do so. Most patients choose to undergo refractive surgery in order to decrease their dependence on spectacles and are therefore not happy with the prospect of needing reading glasses (1–3). One means of addressing the problem of presbyopia is monovision refractive surgery, in which one eye is surgically corrected for distance vision and the other eye for near vision (1–7). The near vision eye may be placed in focus at a reading distance (33 cm) or at an intermediate distance (for example, at 50 cm for computer use). The monovision approach has been successfully applied to laser-assisted in situ Keretomileusis (LASIK) and to presbyopic contact lens wearers. Monovision can be used to circumvent the presbyopia problem in refractive surgery patients. The procedure entails using photorefractive keratotomy (PRK) or LASIK to correct one eye for distance and undercorrecting the other eye by 1 to 2 D. For those refractive surgery patients able to adapt, monovision represents a means of markedly decreasing dependence on spectacles for both near and distance work. However, not every patient is a good candidate for monovision. The monovision option may be associated with compromises of binocular visual function, and some people are not able or willing to accept these compromises (3). 189

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B. THE IDEAL MONOVISION RESULT Ideally, the monovision patient should be able to see clearly at all distances. The depth of focus under binocular viewing conditions should be continuous and equal to the sum of the monocular depths of focus (4). Inherent in the monovision concept is the fact that at any given distance, the image in one eye will be blurred and the image in the other eye in focus. Ideally, at any given distance, a patient should be able to suppress the blurred image from one eye so that it does not interfere with the image from the other eye (known as interocular blur suppression) (5). Any compromises in binocular visual function (such as in visual acuity, contrast sensitivity, or stereopsis) as a result of monovision should not interfere with the patient’s ability to function comfortably at home, while driving, or at work. Monovision patients may require spectacle correction in order to obtain optimal visual functioning for certain tasks such as night driving or fine near vision tasks. Monovision is considered successful in a given individual if it is satisfactory 85% of the time and spectacles over monovision are needed only 15% of the time (3).

C. MONOVISION SUCCESS RATES AFTER CONTACT LENSES Many published reports address monovision success rates in contact lens wearers. The reported monovision success rates vary considerably and in large part because differing definitions of monovision success are applied and study designs vary. Jain and associates reviewed 19 articles that met their definition of monovision success, which was the adequate adaptation to 1.00 to 2.00 D of monocular blur after 3 or more weeks of acclimatization (2). In an attempt to predict success rates after refractive surgery, these authors included only reports that studied contact lens patients above 40 years of age with astigmatism of less than 1.00 D, no previous monovision experience, and no previous contact lens intolerance. The mean monovision success rate was found to be 76%. When failures related to contact lens intolerance were excluded, the success rate increased to 81%. The latter figure is important because of its applicability to monovision success rates after refractive surgery (3).

D. MONOVISION REFRACTIVE SURGICAL OUTCOMES We have evaluated a group of 97 patients over 45 years of age who satisfied the criteria for strict monovision (n ⳱ 60) and minimonovision (n ⳱ 37) after LASIK surgery (Table 1). Best-corrected visual acuity (BCVA) before LASIK ranged from 20/15 to 20/30. The average SE before LASIK was ⳮ3.71 Ⳳ 2.73 D OD and ⳮ3.77 Ⳳ 2.93 D OS. The lasers used were both the VISX and the Summit (7). After LASIK, the average SE for eyes corrected for distance was ⳮ0.12 Ⳳ 0.29 D and ⳮ1.32 Ⳳ 0.54 D for near vision. The mean anisometropia was ⳮ1.20 Ⳳ 0.06 D. BCVA after LASIK ranged from 20/15 to 20/30. The mean Snellen uncorrected visual acuity (UCVA) after LASIK in the distance eye was 20/23 (range: 20/15 to 20/60); and in the near eye, it was 20/53 (range: 20/20 to 20/400). Satisfied and dissatisfied patients had similar distance and near UCVA. The average follow-up time was 6.1 Ⳳ 4.7 months (7).

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Table 1 Monovision Subdivision Criteria A. Based on near spherical equivalent (SE) Strict monovision Distance SE: ⫺0.5 to ⫹0.5 D Near SE: ⬍ ⫺1.0 D to ⫺3.75 D Anisometropia ⱖ0.75 D Minimonovision Distance SE: ⫺0.5 D to ⫹0.5 D Near SE: ⫺0.5 D to ⫺1.0 D B. Based on ocular dominance Uncrossed monovision Dominant eye corrected for distance Nondominant eye corrected for near Crossed monovision Nondominant eye corrected for distance Dominant eye corrected for near C. Based on near Spherical Equivalent and ocular dominance Conventional monovision Strict monovision Uncrossed monovision Crossed minimonovision Minimonovision Crossed monovision

E. SATISFACTION WITH MONOVISION AFTER REFRACTIVE SURGERY Of our 97 LASIK patients, 78 (80.4%) reported satisfaction with visual outcome after LASIK; 19 (19.6%) were not satisfied; 37 (47.4%) of the satisfied patients were happy with visual outcome, and 41 (52.6%) expressed no complaints. Of those who were not satisfied with their outcome, 4 (21.1%) were unhappy with the quality of distance vision, 3 (15.8%) were unhappy with near vision, 2 (10.5%) were unhappy with both distance and near vision, and 6 (31.6%) complained of imbalance. Four patients (21.1%) were unhappy for reasons unrelated to monovision; three complained of dry-eye symptoms and one of floaters. Satisfaction was unrelated to age, gender, dominance, myopia, type of laser, and type of microkeratome (␹2 ⳱ NS). Of the 78 satisfied patients, 29 (37.2%) fulfilled criteria for minimonovision; of these, 10 (34.5%) had crossed monovision. Of the 78 satisfied patients, 49 (62.8%) fulfilled criteria for strict monovision; 12 of the 49 (24.5%) had crossed monovision. There was no statistically significant difference in satisfaction between strict and minimonovision groups or between uncrossed and crossed monovision groups. The average anisometropia of the unsatisfied patients was 1.05 D and of the satisfied patients 1.23 D; the difference was not significant. There was also no statistically significant relationship between lines of BCVA lost after LASIK and satisfaction with visual outcome. Patients who were treated with strict monovision versus minimonovision were similar with regard to distribution of age, gender, dominance, myopia, type of laser used, and type of microkeratome used. Minimonovision patients had an average anisometropia of

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0.68 D; strict monovision patients, 1.52 D (P ⬍ .001). Twenty-nine (78.4%) minimonovision patients and 49 (81.7%) strict monovision patients were satisfied with visual outcome after LASIK. The difference in satisfaction between the two groups was not statistically significant. Only three patients in our entire study were monovision failures requiring retreatment; all had strict monovision before retreatment. One was dissatisfied with distance vision, and two complained of imbalance. Other studies have examined monovision success rates after refractive surgery. In 42 presbyopic myopic patients with monovision induced by refractive surgery, Jain and associates found a monovision success rate of 88% (1). One case report examined an aircraft pilot who underwent PRK with intentional undercorrection of the dominant eye. Postoperatively, the patient noted no deleterious visual effects and was still able to pilot an aircraft (8). Wright and colleagues studied binocular function and patient satisfaction in 21 presbyopic myopic patients between the ages of 37 and 53 in whom monovision induced by refractive surgery (9). Sixteen emmetropic patients served as a control group. In the monovision group, 20 patients (95.2%) had binocular visual acuity of 20/25 or better. No patient in the monovision group used reading glasses postoperatively, whereas 4 of 16 patients (25%) in the control group used such glasses. Stereoacuity was slightly lower in the monovision group but not statistically significantly so. Patient satisfaction was very high in the monovision group. Anecdotal evidence indicates that refractive surgery patients are often able to read better than their refractive error would suggest; for example, a 50-year-old myope corrected to plano in one eye and ⳮ0.75 D in the other may still able read fine print. This phenomenon has been attributed to the creation of a multifocal corneal topography after refractive surgery (10,11). Therefore, a smaller degree of anisometropia may be required to obtain adequate visual function for near and distance for refractive surgery monovision patients. This would serve to preserve binocular visual function and increase monovision success rates compared to monovision contact lens users. F. PREOPERATIVE COUNSELING All patients who opt for monovision should be informed of the adverse effect monovision may have on some visual function parameters (2,3). Specifically, they need to be informed of the risks of reduced binocular visual acuity, stereoacuity, and contrast sensitivity. In addition, they need to be made aware of the risk of distance and near ghosting as a result of incomplete blur suppression. Blur suppression appears to be particularly problematic under night driving conditions because, as mentioned earlier, interocular blur suppression becomes less effective under dim illumination conditions (2,3). Therefore, patients must be advised of the need for distance glasses when driving. Liability is an important consideration when selecting a refractive patient for monovision (3,12). Therefore, discussions of the risks and benefits associated with monovision need to be carefully documented in a patient’s chart. It is important to ascertain the personal preference of the patient. Some patients (particularly those who are active in sports) wish to have the most optimal distance vision possible and are willing to tolerate difficulties with near vision and associated need for reading glasses in order to achieve this. These patients should be fully corrected for distance vision in both eyes. Other patients (particularly those who do a lot of reading or other fine near work) may be willing to tolerate mildly decreased binocular distance vision in

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order to be able to perform near tasks comfortably without glasses. These patients may wish to be undercorrected in both eyes (3). G. MONOVISION TRIAL Although the best way to demonstrate the effects of monovision preoperatively is with a monovision trial with contact lenses (13,14), this is often impractical. A monovision trial can also be performed with spectacles. However, spectacles may induce magnification and minimization effects and, therefore, a monovision trial is more accurately conducted with contact lenses. If a patient has a refractive error of approximately ⳮ1.00 to ⳮ2.00 D, a monovision surgical trial can be performed (12). Instead of a bilateral procedure, surgery is initially performed on only one eye, which is targeted for distance. If the patient is unable to adapt to the monovision situation, the other eye is treated and targeted for plano. It is important to allow for at least a 3-week acclimatization period before concluding whether or not monovision is appropriate for a given individual. If a patient experiences difficulties with a monovision contact lens trial, two problems must be ruled out before one declares that monovision has failed in that patient. First, accurate contact lens fitting must be ascertained. Second, the clinician must ensure that all residual astigmatism has been corrected by performing a spherocylindrical overrefraction. As mentioned previously, even small amounts of uncorrected astigmatism can have a substantial negative effect on binocular distance visual acuity (3). A major benefit of a contact lens trial is that adjustments to the monovision arrangement can be made before refractive surgery is performed. For example, switching the distance and near eyes can serve to relieve undesirable visual symptoms (16). One common complaint with monovision is blur at an intermediate distance. Slightly reducing the add in the near eye can relieve this symptom, although this change may compromise near vision. Plus power may also be added to the distance eye, although this change may reduce distance vision. Even small (0.25-D) changes can make a large difference in creating an acceptable monovision situation for a patient (3,17). An unsuccessful contact lens trial does not necessarily mean that surgically induced monovision will be unsucessful (17). A patient may respond to refractive surgery with a gradual transition into monovision as a result of regression of the refractive result, in contrast to a contact lens trial. For example, a patient may initially be Ⳮ0.75 D in the distance eye and ⳮ0.25 D in the near eye but, after several weeks, may have regressed to plano in the distance eye and ⳮ1.00 D in the near eye. This gradual transition may allow for an easier adaptation to monovision. H. DETERMINING THE EYE FOR DISTANCE Different approaches have been used for selecting the distance-vision eye. Among these are (1) correcting the left eye for distance for increased driving safety (18); (2) using handedness to determine which eye is corrected for distance, (i.e., matching the selected eye to the patient’s handedness) (19); (3) designating as the near-vision eye the eye with the closer near point of convergence; and (4) using the “swinging-plus test” to select the near eye. In the latter test, the patient walks around the examination room with a Ⳮ1.50 lens first over one eye, then over the other eye, and the eye that is most comfortable with the plus lens then is designated as the near-vision eye (3,4).

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The most commonly used approach, however, is determining which eye is the dominant eye and correcting that eye for the most commonly used viewing distance (11), which is generally considered to be the far distance. The dominant eye has been shown to be superior for spatial-locomotor tasks such as walking, running, or driving a car (2,20). Blur suppression appears to be greater when the dominant eye is corrected for the most commonly used distance (i.e., far) (3). Correcting the dominant eye for distance also produces less esophoric shifts (21). The dominant eye is generally identified by use of sighting dominance tests (22). One of the more common tests is the hole test (8), for which the patient is asked to frame an object that lies at an intermediate distance from him or her with a triangle created by his or her outstretched arms while keeping both eyes open. The eye that is in alignment with the object and the hole is considered the dominant eye. I. CROSSED MONOVISION Crossed monovision occurs when the nondominant eye is corrected for distance and the dominant eye for near. This can happen either accidentally or intentionally (1). Crossed monovision may be the intended goal when, for example, a contact lens monovision trial demonstrates better visual function if the nondominant eye is corrected for distance. A patient may also change his or her mind regarding monovision versus full distance correction for both eyes after the nondominant eye has already been treated for distance and the dominant eye has not yet been treated. Patients who wish to have only one eye treated and who are markedly more myopic in the nondominant eye may elect to have the nondominant eye corrected for distance (1,3). Unintentional crossed monovision can occur when correction in the dominant eye is less than expected in patients requesting full distance correction for both eyes. Conversely, in patients desire equivalent undercorrection in both eyes, an overcorrection in the nondominant eye can produce crossed monovision. Unintentional crossed monovision is a result of the fact that refractive surgery is not a completely predictable procedure (1). J. UNCROSSED MONOVISION VERSUS CROSSED MONOVISION Of our 97 LASIK patients, 69 (71.1%) had uncrossed monovision, and 28 (28.9%) had crossed monovision. The average age was 51.7 Ⳳ 0.5 years for patients with uncrossed monovision and 49.7 Ⳳ 0.7 years for patients with crossed monovision (p⳱0.04). The two groups were similar with regard to distribution of gender, dominance, myopia, type of laser used, and type of microkeratome used (␹2⳱NS). The average anisometropia of uncrossed monovision patients was 1.28 D, and of crossed monovision patients 0.98 D (p⳱0.03). Of the 69 uncrossed monovision patients 56 (81.2%) were satisfied after LASIK, as were 22 (78.6%) of the 28 crossed monovision patients. Two (33.3%) of the 6 patients dissatisfied with crossed monovision and 2 (15.4%) of the 13 patients dissatisfied with uncrossed monovision were unhappy for reasons unrelated to monovision, such as dryeye symptoms and floaters. One patient each (16.7%) complained of poor distance vision, poor near vision, imbalance, and poor overall quality of vision in the crossed monovision group. Of the 13 dissatisfied uncrossed monovision patients, 3 (23.1%) complained of poor distance vision, 2 (15.4%) were unhappy with near vision, 5 (38.5%) felt imbalanced, and 1 (7.7%) was unhappy with overall quality of vision.

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Among minimonovision patients, 19 of the 24 (79.2%) patients with uncrossed monovision were satisfied, as were 10 of the 13 (76.9%) with crossed monovision. Of the monovision patients, 37 of the 45 (82.2%) patients with uncrossed monovision were satisfied, as were 12 of the 15 (80.0%) crossed monovision patients. Of the 3 patients who were monovision failures, 2 had crossed monovision. One patient with crossed monovision was retreated to uncrossed monovision, while the other two patients did not have a change in crossed monovision status. The patient with uncrossed monovision before and after retreatment remained dissatisfied. K. VISUAL PERFORMANCE IN MONOVISION 1. Monovision Failures All 13 patients dissatisfied with monovision outcome were offered retreatment, but only 3 (23.1%) elected to undergo a second procedure. Most patients chose to defer retreatment for one of three reasons (1) the patient was unwilling to sacrifice near and intermediate vision for sharper distance vision, (2) symptoms were not bothersome enough to merit risks of additional surgery, and (3) the patient was willing to give additional time to adjust to monovision. Patients were then prescribed glasses for distance vision or reading, depending on the complaint, or were to be re-evaluated for retreatment following some period of adjustment. Many patients were then lost to follow-up. This suggests that the degree of dissatisfaction was relatively mild and that many patients eventually adjust to monovision or wear glasses on occasion for specific activities. Overall patient satisfaction with monovision after LASIK was 80.4%, compared to 80.6% in contact lens wearers after exclusion of contact lens intolerance. Furthermore, the satisfaction among strict monovision, minimonovision, uncrossed monovision, and crossed monovision groups did not differ significantly from satisfaction in contact lens wearers. Due to the retrospective nature of most monovision refractive surgical studies, there was no standardized instrument to measure patient satisfaction. Rather, patient dissatisfaction was noted if the patient had any complaints or negative comments about vision at the last follow-up visit. In addition, near vision was not documented in many charts and could not be analyzed as an outcome. It was also difficult to determine from charts whether monovision was intended or whether regression of one or both eyes led to a monovision result. These factors may be better analyzed through a prospective study. 2. Interocular Blur Suppression Two tests used to measure the ability to suppress interocular blur are the anisometropic blur-suppression test and the American Optical vectographic test. The anisometropic blursuppression test indicates that the interocular suppression of blur is greater for smaller degrees of anisometropia (2). Both testing modalities indicate that blur suppression is greater when the dominant eye is corrected for distance. Monovision success is dependent on interocular blur suppression. In successful wearers of monovision lenses, the interocular suppression of blur was found to be approximately two orders of magnitude greater than in unsuccessful wearers of monovision lenses (2). Of note, interocular blur suppression becomes less effective under dim illumination conditions (2), which accounts for the well-known poorer visual performance of monovision patients under night driving circumstances.

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3. Binocular Visual Acuity Jain and colleagues (1,2) reviewed six articles addressing the effect of monovision on binocular visual acuity and found the effect to be mild. High-contrast and low-contrast visual acuities at standard room illumination were found to be reduced by 0.04 to 0.08 logMAR unit and 0.04 to 0.09 logMAR unit, respectively. This reduction was slightly higher (0.10 logMAR unit) under low illumination conditions. The effect on visual acuity was particularly pronounced when the dominant, distance-corrected eye had a residual astigmatic error at an oblique axis (23). 4. Stereoacuity Reduced stereoacuity is considered to be the major disadvantage associated with monovision (24). Jain and coworkers reviewed twelve articles that examined the effect of monovision on stereoacuity (1,2). When near stereoacuity under monovision conditions was compared to stereoacuity under binocular viewing conditions, a mean decrease of 37 arc seconds (from 87 to 124 arc seconds) was found. The average normal value for stereopsis is 20 arc seconds and, for persons over 40 years of age, 58 arc seconds (13,25). A more recent paper by Kirschen and coworkers found that near stereoacuity decreased from a median of 50 arc seconds with bifocal contact lenses to 200 arc seconds with monovision (26). Patients in whom monovision is successful exhibit a lower reduction in stereoacuity than do unsuccessful monovision patients. Patients in whom monovision was unsuccessful were found to have a 50 to 62 arc seconds greater reduction in stereoacuity as compared to successful monovision patients (1). 5. Contrast Sensitivity When two eyes are used instead of one, visual performance, and especially contrast sensitivity, greatly improves (binocular summation). Contrast sensitivity increases by a factor of 兹2 when the stimulus is viewed binocularly; therefore, binocular contrast sensitivity is 42% greater than monocular contrast sensitivity. With increasing monocular defocus, the binocular contrast sensitivity decreases steadily until it is actually worse than monocular contrast sensitivity (binocular inhibition) (27). If the defocus is increased beyond Ⳮ2.50 D the binocular contrast sensitivity reverts back to the monocular level, indicating suppression of the defocused eye. Because monovision results in loss of binocular summation, or may even result in binocular inhibition, monovision results in a significant reduction in contrast sensitivity, especially at higher spatial frequencies (greater than 4 cycles per degree). L. PERIPHERAL VISION AND VISUAL FIELDS Monovision appears to have no significant effect on peripheral visual acuity and only a minimal effect on binocular visual field width (14). 1. Binocular Depth of Focus The binocular depth of focus is the range in which an image may move without noticeable blur under binocular viewing conditions (without changing accommodation). In patients in whom neither eye is clearly dominant (i.e., in whom there is no sighting preference),

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the binocular depth of focus is approximately equal to the sum of the monocular depths of focus. However, in patients with a strong sighting preference, the image becomes blurred as the object moves from the monocular clear range of the dominant eye to the monocular clear range of the nondominant eye. Therefore, in patients with a strong sighting preference, the depth of focus under monovision conditions is considerably less than the sum of the monocular depths of focus (3). 2. Phorias Patients using monovision tend to exhibit a small-angle esophoric shift. At distance, this manifests as an esophoria. At near, the effect is offset by the fact that presbyopes generally exhibit a moderate to large exophoria at near. The magnitude of the esophoric shift is believed to correlate with the degree of binocular stress created by monovision. The esophoric shift at distance in successful monovision contact lens (0 to 0.6 prism diopters) was found to be less than the shift in unsuccessful monovision wearers (2.1 to 2.2 prism diopters) (7,28). Interestingly, the magnitude of esophoric shift is less when the dominant eye is corrected for distance, thus lending support to the generally accepted custom of correcting the dominant eye for distance (21). 3. Task Performance Monovision appears to be associated with adverse effects on, in particular, stereoacuity and contrast sensitivity in particular. The question is whether these effects have clinical significance. The effect of monovision on the performance of various visually oriented near tasks can be assessed by comparing an individual’s performance of these tasks under monovision conditions, under monocular viewing conditions (i.e., with one eye covered), and under binocular viewing conditions (i.e., with full near correction for both eyes). Use of this method revealed that monovision reduced performance of the tasks by 2 to 6% when compared to performance of the tasks under binocular viewing conditions. However, this reduction was quite minimal when compared with the 30% reduction seen under monocular viewing conditions with near tasks requiring high stereopsis (29). M. FACTORS INFLUENCING MONOVISION SUCCESS On the basis of the above-mentioned findings, poor candidates for monovision are patients who exhibit minimal interocular suppression of blur, patients with large esophoric shifts with monovision, and patients with a significant reduction in stereoacuity with monovision. Certain psychological and personality factors also appear to play a role in determining the success of monovision (30). An additional consideration is sighting preference. The inputs from the two eyes are not identical in their relative influence on cortical cells: the dominant eye produces a greater response to a given stimulus than does the input from the other eye. Those individuals who do not have a strong sighting preference (i.e., who have alternating dominance) appear to have constant interocular blur suppression and therefore tend to be more successful with monovision. Furthermore, the choice of eye that is corrected for distance, whether the dominant or the nondominant eye, appears to have an effect on monovision success. In 16 articles reviewed by Jain and coworkers, the average age of successful monovision users ranged from 48 to 55 years (1,2). No articles were found that compared the success rate in younger versus older presbyopes. Two articles examined the difference

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between the average age of successful versus unsuccessful monovision patients but failed to find any statistically significant difference in age between the two groups (5,31). N. CONCLUSIONS Monovision has been evaluated extensively in contact lens users, but few studies comment on its success in refractive surgery. Furthermore, the impact of the magnitude of anisometropia created in monovision patients has not been fully characterized. We have introduced a new term, minimonovision, to characterize monovision patients with a lesser degree of near vision correction than full monovision (7). The inclusion criteria for strict monovision and minimonovision are mutually exclusive. We found that strict monovision and minimonovision groups had comparable satisfaction rates. We also found that crossed monovision patients overall were as satisfied as uncrossed monovision patients, and that within the minimonovision and monovision subgroups, crossed monovision did not affect satisfaction. The rate of satisfaction for monovision after LASIK was similar to the rate in contact lens wearers. Monovision is associated with some compromises of visual function, the extent of which depend on the particular individual and the requirements imposed by different viewing conditions. However, for those refractive surgery patients willing and able to adapt, these compromises constitute reasonable a trade-off for reducing dependence on near-vision correction. Refractive surgery may be used to take advantage of the monovision option in presbyopic refractive surgery patients. However, this option should be pursued only after careful preoperative screening and counseling of the patient. Creating a monovision situation with refractive surgery constitutes a practical alternative to other surgical treatment modalities for presbyopia, such as scleral expansion/relaxation and multifocal corneal treatment. REFERENCES 1. Jain S, Ou R, Azar DT. Monovision outcomes in presbyopic individuals after refractive surgery. Ophthalmology 2001; 108:1430–1433. 2. Jain S, Arora I, Azar DT. Success of monovision in presbyopes: review of the literature and potential applications to refractive surgery. Surv Ophthalmol 1996; 40:491–499. 3. Sippel KC, Jain S, Azar DT. Monovision achieved with excimer laser refractive surgery. Int Ophthalmol Clin 2001; 41:91–101. 4. Schor C, Erickson P. Patterns of binocular suppression and accommodation in monovision. Am J Optom Physiol Opt 1988; 65:853–861. 5. Schor C, Landsman L, Erickson P. Ocular dominance and the interocular suppression of blur in monovision. Am J Optom Physiol Opt 1987; 64:723–730. 6. Fonda G. Presbyopia corrected with single vision spectacles or corneal lenses in preference to bifocal corneal lenses. Trans Ophthalmol Soc Aust 1966; 25:78–80. 7. Chang MA, Kloek CE, Zafar S, Jain S, Azar DT. Analysis of strict monovision and minimonovision LASIK surgery in presbyopes. Arch Ophthalmol 2002. Submitted. 8. Maguen E, Nesburn AB, Salz JJ. Bilateral photorefractive keratectomy with intentional unilateral undercorrection in an aircraft pilot. J Cataract Refract Surg 1997; 23:294–296. 9. Wright KW, Guemes A, Kapadia MS, Wilson SE. Binocular function and patient satisfaction after monovision induced by myopic photorefractive keratectomy. J Cataract Refract Surg 1999; 25:177–182.

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10. Wilson SE, Klyce SD, McDonald MB, Liu JC, Kaufman HE. Changes in corneal topography after excimer laser photorefractive keratectomy for myopia. Ophthalmology 1991; 98: 1338–1347. 11. Moreira H, Garbus JJ, Fasano A, Lee M, Clapham TN, McDonnell PJ. Multifocal corneal topographic changes with excimer laser photorefractive keratectomy. Arch Ophthalmol 1992; 110:994–999. 12. Harris MG, Classe JG. Clinicolegal considerations of monovision. J Am Optom Assoc 1988; 5:491–495. 13. Emmes AB. A statistical study of clinical scores obtained in the Wirt steropsis test. Arch Am Acad Optom 1961; 38:398. 14. Collins MJ, Brown B, Verney SJ, Makras M, Bowman KJ. Peripheral visual acuity with monovision and other contact lens corrections for presbyopia. Optom Vis Sci 1989; 66: 370–374. 15. Hom MM. Monovision and LASIK. J Am Optom Assoc 1999; 70:117–122. 16. Bennett ES, Henry VA. Bifocal contact lenses. In: ES Bennett, VA Henry, eds. Clinical Manual of Contact Lenses. Philadelphia: Lippincott, 1994; 362–398. 17. McLendon JH, Burcham JL, Pheiffer CH. Presbyopic patterns and single vision contact lenses II. South J Optom 1968; 10:33–36. 18. Sanchez FJ. Monovision: which eye for near? Contact Lens Forum 1988; 13:57. 19. Lebow K, Goldberg J. Characteristics of binocular vision found for presbyopic patients wearing single vision contact lenses. J Am Optom Assoc 1975; 48:1116–1123. 20. Trevarthan CB. Two mechanisms of vision in primates. Psychol Forsch 1968; 31:299–348. 21. Rigel L. Which modality works best? When monovision makes sense. Rev Optometry 1998; 13:90. 22. Coren S, Kaplan CP. Patterns of ocular dominance. Am j Optom Arch Acad Optom 1973; 50:283–292. 23. Collins M, Goode A, Brown B. Distance visual acuity and monovision. Optom Vis Sci 1993; 70:723–728. 24. Erickson P, Schor C. Visual function with presbyopic contact lens correction. Optom Vis Sci 1990; 67:22–28. 25. Wirt SE. A new near-point stereopsis test. Optom Weekly 1947; 38:647–649. 26. Kirschen DG, Hung CC, Nakano TR. Comparison of suppression, stereoacuity, and interocular differences in visual acuity in monovision and Acuvue bifocal contact lenses. Optom Vis Sci 1999:832–837. 27. Pardhan S, Gilchrist J. The effect of monocular defocus on binocular contrast sensitivity. Ophthal Physiol Opt 1990; 10:33–36. 28. McGill EC, Erickson P. Sighting dominance and monovision distance binocular fusional ranges. J Am Optom Assoc 1991; 62:738–742. 29. Sheedy JE, Harris MG, Busby L, Chan E, Koga I. Monovision contact lens wear and occupational task performance. Am J Optom Physiol Opt 1988; 65:14–18. 30. Du Toit R, Ferreira JT, Nel ZJ. Visual and nonvisual variables implicated in monovision wear. Optom Vis Sci 1998; 75:119–125. 31. Koetting RA. Stereopsis in presbyopes fitted with single vision contact lenses. Am J Optom Arch Am Acad Optom 1970; 47:557–561.

19 Multifocal Corneal Approach to Treat Presbyopia JANIE HO University of California at San Francisco, San Francisco, California, U.S.A. DIMITRI T. AZAR Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A.

A. INTRODUCTION Refractive surgery to correct presbyopia continues to be at an experimental stage despite a decade of investigation. The dilemma in presbyopia is the need for differing refractive powers of the optical media for near versus distance vision. In this chapter, we review several studies using a multifocal corneal approach to treating presbyopia. The techniques and results of the studies are presented, as well as a discussion of comparative conclusions and areas in need of further investigation.

B. HISTORICAL/EXPERIMENTAL For several decades, refractive surgery has been successfully employed in treating patients with myopia and, later, hyperopia. Nevertheless, the presbyope continues to pose a challenge to refractive surgeons, owing to the need for differing optical powers for near and distance vision. In the late 1980s, investigators observed a phenomenon wherein radial keratotomy patients achieved excellent uncorrected visual acuity at near and distance; however, this was inconsistent with the measured change in spherical equivalent (1,2). Further topographical analysis demonstrated an unintended multifocal lens effect of the 201

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cornea, enabling optimization of both near and distance vision through a range of optical zones. These studies offered the theoretical basis for refractive surgery to treat presbyopia using a multifocal corneal approach. The multifocal approach espouses the concept of pseudoaccomodation, or the ability to process multiple simultaneous images at the retina (3). Anschutz performed studies with photorefractive keratectomy (PRK) on polymethyl methacrylate (PMMA) lenses and porcine eyes to intentionally create multifocal corneal surfaces. A sectoral near zone as part of a concentric zone for distance was favored. He subsequently applied the models in clinical trials testing the effectiveness of PRK in treating myopia-presbyopia and hyperopia-presbyopia, described below (4). In addition, Moreira et al. investigated several modalities for achieving a multifocal surface (5). Four configurations of ablation were compared: monofocal ablation, two concentric ablations, two ablations with the smaller diameter ablation decentered inferiorly, and a single progressive ablation. The group concluded that a corneal surface with multiple refractive powers could be achieved in PMMA hemispheres and blocks, as well as, in rabbit corneas. They believed that the single progressive ablation would be the most effective, created with an iris diaphragm initially fully open to 6 mm and progressively closing until 3 mm, leaving a central zone with the preoperative refractive power (5). This technique would theoretically function in concert with pupillary miosis during near accommodation to decrease the percentage of light rays traversing the flattened zone of the cornea. Thus, degradation of the retinal image as a result of the multifocal lens effect may be reduced.

C. TECHNIQUES In March 1999, Anschutz began human clinical trials of multifocal PRK to treat myopiapresbyopia. A 193-nm Aesculap-Meditec laser was used with an iris diaphragm to bifocally sculpt the cornea (4). The investigation involved two techniques for creating zones for near and distance vision: (1) an inferior pie-shaped sectoral near zone within a concentric distance zone and (2) a central near zone within a concentric distance zone. Both techniques involved an initial circular ablation of 2 or 3 D less than the myopic baseline refraction. For technique 1, this was followed by a second ablation to the full myopic correction using a sectoral template. Technique 2 used a central nonrotating template in a similar fashion. Figure 1 demonstrates the two techniques. In treating hyperopia-myopia, Anschutz investigated the technique of an inferior sectoral steepening of the cornea, to create active myopization for near vision (4). For the initial hyperopic PRK ablation, a spiral eye mask (or double-heart mask) was used along with a rotating spiral template to correct for the complete hyperopic refraction. Next, a nonrotating presbyopic template with an oval aperture was inserted for the second ablation, to create an inferior sectoral zone of an additional 2.0 to 3.0 D presbyopic correction (Fig. 2). The hyperopia-myopia study also included a subgroup of emmetropic presbyopes. Their ablations were performed with the hyperopic spiral mask and an oval template, to create an inferior zone of steepening (3.0 D) within a transition zone of 0.5 D (4). The configuration is similar to the inferior sectoral ablation for near vision shown in Figure 1.

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Figure 1 Multifocal myopia-presbyopia PRK. Left, central near zone; right, sectoral near zone. (Adapted from Ref. 4.)

In 1998, Vinciguerra et al. published their study involving zonal PRK for treating presbyopia. The group used a 193-nm Aesculap-Meditec Mel 60 excimer laser with a mask consisting of a mobile diaphragm formed by a blunt concave blade and a blunt convex blade (6). An inferior semilunar region was ablated for a presbyopic correction of 3.00 D. Within this region, the depth of cut was progressively reduced from the corneal center to periphery as the blades of the diaphragm progressively closed upon each other.

Figure 2 Multifocal hyperopic-presbyopic PRK. (Adapted from Ref. 4.)

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Figure 3 PRK for presbyopia; inferior semilunar zone of ablation. (Adapted from Ref. 6.)

Thus, the superior pole of the ablated area served as the optical zone for near vision. Figure 3 shows the ablation zone. Multifocal laser-assisted in situ keratomileusis (LASIK) has also been employed to treat hyperopia-presbyopia. Bauerberg used a 193-nm Coherent/Schwind Keratom 2 excimer laser with an 8.2-mm-diameter, 160-␮m-thickness corneal flap (7). Ablation depth was calculated by adding 10% to the preoperative spherical equivalent. A centrally located ablation was tested as well as an inferiorly decentered ablation (by 1 mm). D. RESULTS The myopia-presbyopia PRK study by Anschutz involved 46 eyes of 23 patients with follow-up of 2 1⁄2 to 3 years (4). The preoperative refractions ranged from ⳮ2.0 to ⳮ12.0 D; patients were divided into three groups: group 1 (ⳮ2.0 to ⳮ6.0 D), group 2 (ⳮ6.25 to ⳮ10.0 D), and group 3 (ⳮ10.25 to ⳮ15.0 D). The goal was a presbyopic correction of 2.0 to 4.0 D. At 30 months, group 1 had a mean regression of ⳮ0.75 D, with an uncorrected near visual acuity (VA) of 20/22, which was three lines better than for the monofocally treated eyes. Group 2 had a mean regression of ⳮ1.5 D and an uncorrected near VA of 20/25. Group 3 had a mean regression of ⳮ4.0 D, with uncorrected near VA only 1 1⁄2 lines better than with monofocal ablation. Overall, greater regression occurred with greater preoperative myopic refraction, and multifocal PRK results were identical to those of monofocal PRK in patients with preoperative refraction greater than ⳮ6.0 D. In terms of postoperative complications, the investigators found 2 cases of loss of best corrected VA due to decentration; 1 case of wound-healing difficulties; and 2 cases of diminished near VA due to pupil sizes less than 2 mm. Glare and halo effects were also present in patients for only the first 6 months postoperatively. In addition, 20% of patients experienced “ghost pictures” and double contours for the initial 3 to 4 months postoperatively. Frequent complaints of monocular diplopia occurred in patients who received a central near zone ablation. A total of 18 eyes with follow-up of 16 to 20 months were studied by Anschutz for PRK treatment of hyperopia-presbyopia. At 18 months, patients with preoperative refractions of Ⳮ1.0 to Ⳮ4.75 D showed a mean regression of Ⳮ1.5 D and a mean near

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VA of 20/30 (4). Mean regression was Ⳮ3.5 D for patients with preoperative refractions of Ⳮ5.0 to Ⳮ8.0 D, with a postoperative mean near VA of 20/50. The investigators found a small loss of contrast sensitivity over 7 months. In addition, haze was greater in patients with higher degrees of hyperopia. Some 30% of patients complained of ghost images and 10% complained of double contours; with all complaints resolved by 6 months postoperatively. Two cases of decentration occurred during the study. Last, the improvement in VA occurred very slowly in the higher-diopter group secondary to a small optical zone (4 mm). Four emmetropic eyes were also treated for presbyopia during the same study. Uncorrected near VA at 18 months follow-up was 20/30, with postoperative spherical equivalent change of ⳮ0.25 to ⳮ0.75 D (4). The Vinciguerra et al. study of PRK for presbyopia treated three patients with a follow-up period of 24 months. A regression of 1.00 D occurred, followed by stabilization of the presbyopic correction (6). The patients read Jaeger 3 at 35 cm without near correction and were also able to read with their preoperative presbyopic correction using the 85% of the pupillary area that was not treated by PRK. A mild haze was reported in the first two postoperative months. Loss of contrast sensitivity only occurred with the 11% Regan chart. Videokeratography of a treated eye is shown in Figure 4.

Figure 4 Videokeratography of eye treated with multifocal PRK for presbyopia. Upper left, preoperative; upper right, 3 days postoperative; lower left, 1 month postoperative; lower right, 1 year postoperative. Immediate postoperative corneal steepening was almost 6.00 D. By 1 month, the presbyopic correction was within 0.25 D of the planned 3.0-D correction, remaining stable at 1 year. At 1 year, there is also a slight nasal decentration of 0.63 mm. (From Ref. 6).

PRK: concentric distance zone with inferior semilunar near zone PRK: inferior sectoral near zone PRK: inferior semilunar near zone

1. ⫹1.0 to 4.75 D 2. ⫹5.0 to 8.0 D

0 to ⫹0.5 D ⫺0.5 to ⫹1.5 D

⫹2.0 to 6.0 D

9 (18)

2 (4)

3 (3)

8 (16)

Anschutz (4)

Anschutz (4)

Vinciguerra (6)

Bauerberg (7)

LASIK: 1. central near zone or 2. inferior off-center near zone

PRK: concentric distance zone with central or inferior sectoral near zone

1. ⫺2.0 to ⫺6.0 D 2. ⫺6.25 to ⫺10.0 D 3. ⫺10.25 to ⫺15.0 D

26 (46)

Anschutz (4)

Technique

Refractive error (pre-op)

Author

Number of patients (eyes)

Table 1 Summary of Study Results

22 months

24 months

19 months

20 months

3 years

Follow-up time

⫺0.25 to ⫺0.75 D 1.0 D

1. ⫹1.5 D 2. ⫹3.5 D

1. ⫺0.75 D 2. ⫺1.5 D 3. ⫺4.0 D

Post-op regression

Significant complications

1. 20/40 or better, Jaeger 0–2 2. 20/30 or better, Jaeger 1–2

Jaeger 3 at 35 cm

Loss of contrast sensitivity with 11% Regan, transient haze Induced astigmatism

1. 20/22 Decentration, wound 2. 20/25 healing, loss of near 3. 11/2 lines better VA, transient glare, halo, ghosting, than monofocal monocular diplopia tmt Loss of contrast 1. 20/30 sensitivity, haze, 2. 20/50 decentration, transient ghosting, decentration 20/30

Post-op near VA

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The Bauerberg LASIK study for hyperopia-presbyopia involved 16 eyes of 8 patients (8 eyes with centered ablation and 8 eyes with off-center ablation) with maximum followup of 22 months (7). Preoperative refractions ranged from Ⳮ2.0 to Ⳮ6.0 D. At 12 months, the off-centered ablation eyes achieved uncorrected near VA of 20/30 or better with no loss of Snellen lines. The centered ablation eyes had uncorrected near VA of 20/40 or better with two eyes experiencing loss of 1 Snellen line. No glare was reported; however, 2 eyes had induced astigmatism. Subjectively, 6 patients preferred the eccentric inferior ablation for near vision, while 2 noticed no difference. A summary of results is presented in Table 1. E. CONCLUSIONS The multifocal corneal approach to treating presbyopia remains experimental, although the technology and techniques of multifocal corneal sculpting have been well investigated. The four studies reviewed had the drawback of low patient numbers; however, follow-up time was considerably meaningful. A most important reason for studies of greater magnitude is the need to delineate the incidence of postoperative side effects such as glare, halos, ghost images, and monocular diplopia. The reviewed studies reported that symptoms such as halos, glare, and ghost images were present for a short period of time in the limited patient groups. The presence of these symptoms was perhaps due to a temporary transition period during which wound healing and adjustment to multifocal images occurred. Stability of the presbyopic corrections and their relationship with the natural progression of presbyopia should also be followed long-term. Each of the studies revealed certain limitations for presbyopic multifocal refractive surgery as well as benefits for particular techniques. For myopia-presbyopia, Anschutz concluded that their inferior sectoral near zone is appropriate for patients with pupils greater than 2 mm diameter (4). Additionally, for patients with pupils larger than 3 mm, the central near zone may be advantageous in the case of dominant near vision, particularly in the presence of high myopia (⬎ⳮ10.0 D). The investigators also concluded that current multifocal hyperopia-presbyopia PRK is effective only for patients with a baseline refraction of less than Ⳮ5.0 D due to the high degree of regression and the small optical zone for those with refractions greater than Ⳮ5.0 D (4). Anschutz cites a need for improvement of the transition zone and aspherical reprofiling of the cornea in addition to simplifying the technique to require only one template. Vinciguerra et al. found that the zonal presbyopic correction was effective for pupils up to 6 mm (6). Advantages of their technique include a pupillary center with intact epithelium acting as a protective shield against decentration during photoablation and the need for a very superficial (10 to 15 ␮m) and small ablation zone. Because only 15% of the light entering a 3 mm pupil traverses the treated zone, contrast sensitivity was not significantly reduced. Nevertheless, Vinciguerra notes that the technique requires extreme precision to avoid erroneously aligned ablation and suboptimal presbyopic correction. In addition, for pupils greater than 6 mm, the technique may lead to an inadequate presbyopic correction. LASIK for presbyopia was shown to have stable postoperative results with minimal recovery time and complications in a small study by Bauerberg (7). However, he notes that longer follow-up is needed. He concluded that the preferred orientation of the presbyopic ablation should be inferior off-center. It may be worth considering the implications that an asymmetrical corneal contour has for flap orientation and healing. To our knowl-

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edge, no studies have been undertaken to compare multifocal PRK and LASIK in the treatment of presbyopia. Last, pupillary size appears to play a significant role in the effectiveness of multifocal refractive surgery, as shown by the aforementioned studies. Another aspect that may require investigation is the positioning of a individual’s upper and lower lid margins with respect to the treated zone during distance and near vision. Could a raised lower lid position cover up a zone of inferior corneal steepening such that the presbyopic correction has no benefit? Conversely, could the same positioning protect the patient’s vision from visual distortion by covering up a rough transition zone? REFERENCES 1. McDonnell PJ, Garbus J, Lopez PF. Topographical analysis and visual acuity after radial keratotomy. Am J Ophthalmol 1988; 106:692–695. 2. Maguire LJ, Bourne WM. A multifocal lens effect as a complication of radial keratotomy. Refract Corneal Surg 1989; 6:394–399. 3. Talamo J, Krueger R eds. The Excimer Manual. Boston: Little, Brown, 1997:106. 4. Anschutz T. Laser correction of hyperopia and presbyopia. Int Ophthalmol Clin 1994; 34(4): 107–137. 5. Moreira H, Garbus JJ, Fasano A, Lee M, Clapham TN, McDonnell PJ. Multifocal corneal topographic changes with excimer laser photorefractive keratectomy. Arch Ophthalmol 1992; 110(7):994–999. 6. Vinciguerra P, Nizzola GM, Bailo G, Nizzola F, Ascari A, Epstein D. Excimer laser photorefractive keratectomy for presbyopia: 24-month follow-up in three eyes. J Refract Surg 1998; 14(1): 31–37. 7. Bauerberg JM. Centered vs. inferior off-center ablation to correct hyperopia and presbyopia. J Refract Surg 1999; 15(1):66–69.

20 Scleral Relaxation to Treat Presbyopia HIDEHARU FUKASAKU Fukasaku Eye Centre, Yokohama, Japan

A. INTRODUCTION Accommodation has until recently been explained by the Helmholtz hypothesis. This hypothesis holds that passive anteroposterior thickening of the lens and relative curvature changes in the anterior and posterior lens surfaces result from zonular relaxation with ciliary muscle contraction (Fig. 1). Presbyopia is likewise described as the loss of accommodation due to decreasing elasticity of the lens fibers and capsule (1,2). Recent work (3,4) suggests a very different model of accommodation. Morphological changes in the lens with accommodative effort are seen as the result of active rather than passive interactions. The three components of the ciliary body—the longitudinal, radial and circular fibers—act in concert to increase tension in the equatorial zonules while decreasing tension in the anterior and posterior zonules. The result is an active elongation of the lens diameter with peripheral thinning and central thickening due to dynamic internal volume changes (Fig. 2). The net result is increased plus refracting power of the eye. The important difference between the Helmholtz model and the Schachar model is that the latter suggests a more active interaction between the ciliary muscle and the lens/ zonule complex, positing an interaction in which active effort by the ciliary muscle leads not only to passive relaxation of the lens/zonule complex but also a more complicated active differential response of different zonular types resulting in morphological changes in the lens. If this recent model of accommodation is correct, then presbyopia may not be explained by simple sclerosis of the lens fibers and capsule as previously understood. Rather, the decline in accommodative power of the eye may be due to the inability of the lens equator to expand into the posterior chamber. Thornton (5) has described this as “a crowding” of the lens in the posterior chamber as the lens grows. 209

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Figure 1 Helmholtz’s model of accommodation.

The lens is ectodermal in origin and grows throughout life, increasing in size in all dimensions. The sclera, on the other hand, is mesodermal in origin and ceases growth in and around puberty. There is a discontinuity in growth between the ectodermal lens and mesodermal scleral shell that begins around puberty. The result is an increase in the diameter of the lens and a gradual, progressive narrowing of the space between the lens

Figure 2 A new model of accommodation.

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Figure 3 Lens crowding.

equator and the ciliary body/sclera or crowding of the lens in the posterior chamber (Fig. 3). The strength of any muscle is dependent on the effective length of pull of that muscle. Decreasing the distance between the equator of the lens and the ciliary body with lens growth decreases the effective length of pull of the ciliary muscle. We visualize this as a loss of ciliary muscle/zonular apparatus “tone” (Fig. 4). With the loss of ciliary muscle/zonular apparatus tone, any given accommodative effort results in less pulling on the equatorial zonules and less relaxation of the anterior/posterior zonules, which results in less change in lens morphology and less accommodative response or presbyopia. Thus, it is not truly mechanical crowding of the lens in the posterior chamber but a progressive loss of ciliary muscle/zonular apparatus tone that causes presbyopia. This very appealing model of accommodation/presbyopia suggests a possible surgical correction for presbyopia. If the space between the lens equator and the ciliary body can be expanded, then the length of pull of the ciliary muscle/zonule apparatus should increase and accommodative tone will be restored. Thornton (5) has suggested anterior ciliary sclerotomy (ACS) as a method to safely and effectively expand the globe over the ciliary body and uncrowd the lens (Fig. 5).

Figure 4 Accommodative tone.

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Figure 5 Anterior ciliary sclerotomy (ACS).

B. ANTERIOR CILIARY SCLEROTOMY: EVOLUTION OF A PROCEDURE As first described (6), ACS involved eight equally spaced radial incisions of the conjunctiva and sclera overlying the ciliary body in each of the oblique quadrants. Our initial technique (7) modified this to include limbal peritomies overlying the oblique quadrants. This avoided excessive conjunctival bleeding and, more importantly, allowed accurate measurement of the length and depth of the incision. Incisions through the conjunctiva are always difficult to measure due to its elasticity and compressibility. In addition, we placed two parallel or tandem incisions in each quadrant for a total of eight incisions. We also introduced the use of ultrasonic biomicroscopy (UBM) to accurately measure the depth of the incision. As with radial keratotomy, an incision of insufficient depth will probably be ineffective, and since one is incising sclera overlying the highly vascular ciliary body and choroid, incisions of excessive depth might prove disastrous. UBM gives us the first accurate method of measuring scleral thickness and is absolutely essential in determining the setting for blade depth prior to incision of the sclera. Scleral/uveal border with UBM. This allows easy measurement of scleral thickness. We have found scleral thickness to be a consistent 670 ␮m, with very little variation. However, due to the possibility of scleral ectasias or staphylomas overlying the ciliary body/choroid, we continue to perform UBM scleral thickness measurements on all ACS cases. Our objective was initially to obtain 95% scleral thickness incisions. Experience with donor sclera indicated that using the Thornton Triple Edge diamond knife (MastelKOI, T–2241), the blade needed to be set at 600 ␮m. We further determined that the incision length would be 3.0 mm carried posteriorly, starting 1 mm posterior to the surgical limbus to adequately include the sclera overlying the ciliary body and posterior chamber without unnecessarily incising sclera overlying uvea and retina. UBM was used to determine the anteroposterior dimension of the ciliary body. Initial results were encouraging but limited. After initial postoperative increases of several diopters of accommodation, there was regression: within several months, only an average of 0.8 D increase in accommodation was achieved (simple ACS) (Fig. 6). Distance refraction remained stable and there were no postoperative complications such as infection or uveitis. Although the results were limited, all the patients remained enthusiastic about the improvement in their everyday near vision.

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Figure 6 Accommodative amplitude.

To enhance the surgical effect and decrease regression, we increased the sclerotomy depth to full thickness by a spreading dissection technique (Fig. 7). Following incision, we carefully spread scleral tissue using specially designed Fukasaku ACS forceps (Katena) down to the uveal plane. We termed this enhanced ACS. At first, we were quite concerned about our ability to identify this surgical plane, since entry into the uvea would surely cause hemorrhage. We found that in approaching the uveal plane, there is a distinct bluish blush from the vascular uvea, which is easily recognizable. In addition, the subscleral space, usually a potential space, opens easily to become an actual space. We have experienced no hemorrhages in this spreading dissection. The use of spreading dissection did enhance our results (Fig. 6). We now noted an initial increase in accommodative amplitude of 2.2 D. However, Within several months

Figure 7 Enhanced ACS, technique.

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of surgery, the effect rapidly regressed to near preoperative levels. Obviously, as the sclerotomy healed, any increase in globe diameter was lost. C. ANTERIOR CILIARY SCLEROTOMY WITH IMPLANTATION OF SCLERAL EXPANSION PLUGS (ACS-SEP) The marked regression in effect due to wound contraction and loss of globe expansion found with both simple and enhanced ACS suggested the addition of a material to keep the incision open. The choice of silicone for the scleral expansion plug was dictated by the need to use a stable, inert material that could be fashioned in the dimensions needed and manipulated surgically. The silicone chosen came from scleral buckle material and was shaped by hand in the operating room. The dimensions chosen, 2.5 mm length and 0.6 mm height, were determined by the estimated incision length of 3 mm and depth of 670 ␮m. The width of 0.6 mm was calculated based on the desired circumferential expansion of sclera. Given that the lens diameter change from age 20 to 90 years is 2.5 mm (6.5 to 9.0 mm lens diameter measured on post mortem specimens), there is an average increase of 0.036 mm per year in lens diameter. Hence, a 60-year-old will need to increase his or her globe diameter by 0.72 mm over that of a 40-year-old. This equates to a circumferential expansion of 2.45 mm. Pi ⳯ diameter or 2 ⳯ 3.41 ⳯ 0.36 ⳱ 2.45 mm With four silicone plugs to be implanted, the width of each plug will have to be approximately 0.6 mm. The silicone expansion plugs fashioned to the above dimensions were implanted in the depth of the sclerotomy. They were then sutured in place through both sclera and plug in a criss-cross fashion using 10–0 nylon (Fig. 8). Unlike the original simple ACS technique or our enhanced technique using spreading dissection, we used only single incisions in each oblique quadrant, not tandem incisions. The fact that there was rapid marked regression in the gained accommodative amplitude following simple ACS and enhanced ACS only with spreading dissection is not

Figure 8 ACS with SEP, technique.

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surprising. The effect depends on expansion of the scleral circumference overlying the ciliary body. As the incisions heal, there is wound closure and a reduction in scleral circumference back to near preoperative levels. The addition of silicone plugs in ACS-SEP effectively blocked this wound closure and maintained the gained scleral circumferential expansion and hence the gain in accommodative amplitude. The fact that the initial gain in accommodative amplitude with ACS-SEP was actually slightly less than either our initial ACS technique or our enhanced ACS technique using spreading dissection is probably due the effect of the sutures holding the SEP in place tending to close the wound initially. We are now careful not to place any unnecessary tension on these sutures. In addition, we are now using 11–0 Merceline, which should induce less tension and last longer than nylon. D. ANTERIOR CILIARY SCLEROTOMY AND INTRAOCULAR PRESSURE We noted also that in addition to increasing the amplitude of accommodation, ACS-SEP was also associated with a dramatic drop in intraocular pressure (IOP) (Fig. 9). Simple ACS and ACS enhanced by spreading dissection, in contrast, caused only a minimal drop in IOP that was lost fairly rapidly. The explanation probably lies in the depth and permanence of the radial incisions. Simple ACS is a shallower incision. No attempt is made to complete a full-thickness sclerotomy. ACS enhanced by spreading dissection, on the other hand, ensures a full-thickness sclerotomy by use of the Fukasaku forceps to dissect down

Figure 9 Intraocular pressure.

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to the uveal plane. This exposes the subscleral space, which is normally an anatomical potential space due to the differential embryological development of the scleral and uveal coats. With dissection, it is possible to create a limited, localized ciliochoroidal detachment that increases the uveoscleral outflow of aqueous. Traumatic cyclodialysis and surgical ciliochoroidal detachments are known to dramatically increase uveoscleral outflow and can cause hypotony (7,8). There is no evidence of wound leakage per se, as there is no filtering bleb or Seidel’s sign when fluorescein is applied to the conjunctiva overlying the wound. The loss of IOP-lowering effect with ACS enhanced by scleral spreading over a matter of several months probably reflects closure of the incision and hence closure of the ciliochoroidal detachment with a decrease in uveoscleral outflow. ACS-SEP, on the other hand, shows negligible loss in IOP-lowering effect over many months. This probably represents continued maintenance of the incision separation with the silicone plug and continued ciliochoroidal detachment with ongoing increased uveoscleral outflow. We have been very satisfied with ACS-SEP and its ability to provide a stable increase in accommodative amplitude. Patients likewise have been extremely pleased with the results. They report that they are now able to attend to the activities of daily living much better, such as reading newspapers and product labels. This despite the modest measured increase in accommodative amplitude of only 1.5 D. We expect that patient satisfaction will increase further with correction of the fellow eye. E. FUTURE DIRECTIONS Future planned improvements include replacing the criss-cross 10–0 nylon suture with a 11–0 Merceline horizontal mattress suture. We expect that we will be better able to lover the profile of the suture knot to avoid potential conjunctival irritation or erosion and achieve longer suture life. We have also redesigned the expansion plug to be broader at the base (more trapezoidal on end view) to limit forces that might extrude the plug. We are also creating preformed holes in the plug to avoid the time-consuming and difficult task of driving the small cutting needle of 10–0 or 11–0 suture. The dramatic and sustained drop in IOP with ACS-SEP suggests a possible role for this procedure in the treatment of glaucoma. The advantage of ACS-SEP in this role is that it seems to affect uveoscleral outflow. Uveoscleral outflow can account for up to 40% of total aqueous outflow (9,10). Thus, unlike beta blockers, which have little effect on IOP during sleep, stimulation of uveoscleral outflow should help to protect the patient both day and night. Thus far, IOP reduction has been a serendipitous finding in ACS-SEP in which we implant expansion plugs in each of the four oblique quadrants. The next logical step will be to attempt to titrate IOP reduction by varying the number of plugs or perhaps the size of the plugs. Again, this study is under way at our facility. We believe that ACS-SEP is a valuable procedure in the treatment of presbyopia—a procedure that is safe, effective, and well accepted by patients. Likewise, ACS-SEP promises to become another treatment modality for glaucoma, and we are working on improving its predictability. REFERENCES 1. von Helmholtz HL. Physiological Optics. New York: Dover Press, 1962: 143–172,375–415. 2. Fincham EF. The mechanism of accommodation. Br J Ophthalmol 1937; 8(suppl):5–80.

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3. Schachar RA. Histology of the ciliary muscle-zonular connection. Ann Ophthalmol 1996; 28(2):70–79. 4. Neider MW, Crawford K, Kaufman PL. In vivo videography of the rhesus monkey accommodative apparatus. Arch Ophthalmol 1990; 69:108. 5. Thornton SP, Shear NA. Surgery for Hyperopia and Presbyopia. Baltimore: Williams & Wilkins, 1997:33–36. 6. Fukasaku H. Surgical Reversal of Presbyopia. Highlights of the ’98 ASCRS meeting. CD ROM, Ophthalmology Interactive, 1998. 7. Pederson JE, Gaasterland DE, MacLellan HM. Experimental ciliochoroidal detachment. Effect on intraocular pressure and aqueous humour flow. Arch Ophthalmol 1979; 97:536–541. 8. Toris CB, Pederson JE. Effect of intraocular pressure on uveoscleral outflow following cyclodialysis in the monkey eye. Invest Ophthalmol Vis Sci 1985; 26:1745–1749. 9. Brubaker RF. Flow of aqueous humor in humans. Invest Ophthmol Vis Sci 1991; 32: 3145–3166. 10. Reiss GR, Lee DA, Topper J, Brubaker RF. Aqueous humor flow during sleep. Invest Ophthalmol Vis Sci 1984; 25:776–778.

21 The Scleral Expansion Procedure CHRIS B. PHILLIPS and RICHARD W. YEE Hermann Eye Center and University of Texas Health Science Center at Houston Medical School, Houston, Texas, U.S.A.

A. INTRODUCTION Presbyopia, or age-related loss of accommodation, becomes noticeable between 40 and 45 years (1). It is one of the first signs of aging and results from the age-related decline in the amplitude of accommodation. Some feel that presbyopia becomes apparent when the near point is greater than 22 cm (2). Since the middle 1800s, Helmholtz’s theory of accommodation (3) and its modifications (4–8) have attributed accommodation to a decrease in zonular tension and presbyopia to lens sclerosis and/or ciliary muscle atrophy. A recent theory proposed by Ronald Schachar (9–16), however, states that during accommodation the lens equatorial zonules are under increased rather than decreased tension, as postulated by Helmholtz (Fig. 1). Furthermore, Schachar attributes presbyopia to a continuous age-related increase in the equatorial diameter of the lens, with a subsequent decrease in the effective working distance of the ciliary muscle. As a direct deduction from his theory, Schachar proposed scleral expansion for the treatment of presbyopia (16). The goal of this paper is to describe the technique of scleral expansion. The descriptions of the theories of accommodation and presbyopia are presented in Chapter 4, on Schachar’s theory of the mechanisms of accommodation. 2. Early Procedures for Scleral Expansion The earliest attempts to expand the sclera in humans were made in the mid-1980s (16); they consisted of simple radial incisions in the sclera, similar to radial keratotomy (RK) The authors were supported in part by NEI core grant EY10608 and an unrestricted grant from Research to Prevent Blindness.

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C Figure 1 (A) The human lens when not accommodating. (B) Accommodation according to Helmholtz’s theory. (C) Accommodation according to Schachar’s theory.

of the cornea. This technique, however, was primarily applicable to young presbyopes, as the average increase in the amplitude of accommodation was only about 1.50 D (16). Additionally, as the incisions healed, the effect regressed. The first scleral expansion procedures using an encircling band were performed in 1992 (16). In these procedures, a plastic polymethylmethacrylate (PMMA) band (Fig. 2) was sutured to the sclera and covered with conjunctiva. The results were dramatic; however, the procedure was plagued with variable results, conjunctival erosion, and increased intraocular pressure. Various modifications were attempted to circumvent these problems. One such method involved passing portions of the bands through the sclera, forming scleral belt loops (17). This method did not include the use of scleral sutures in an effort to

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Figure 2 A complete encircling band.

simplify the surgical technique, reduce the complications, and decrease the variability of the results. In 1997 we reported six consecutive nonmyopic patients who underwent scleral expansion using a complete encircling band (17). The band was passed through four separate scleral belt loops located at the 12, 3, 6, and 9 o’clock cardinal positions (Fig. 3) (17). The bands were then ultrasonically fused together at the 1:30, 4:30, 7:30, and 10:30 o’clock positions (Fig. 4). All six patients demonstrated a marked improvement in near vision (Table 1). Surprisingly, in our study, there was a lesser but definite increase in the amplitude and near point of accommodation in the unoperated eyes of all patients. The mechanism of this finding is not clear but was postulated to be related to an increased central neurostimulation of the ciliary muscle of the unoperated eye as a result of the increased function of the ciliary muscle of the operated eye.

Figure 3 Passage of a scleral expansion band into a scleral belt loop.

69⫾1.67 1.2⫾1.33 0.42⫾0.52 ⫺0.33⫾0.5 20/43 ⫺0.85⫾0.16 20/142 ⫺0.63⫾0.14 17.2⫾2.7

NPA (cm) SEb (diopters) Cylinder Distance VAc

20.83⫾5.19 0.81⫾1.13 0.63⫾0.44 ⫺0.11⫾0.16 20/26 ⫺0.03⫾0.07a 20/21 ⫺1.95⫾1.05 16.2⫾0.84

1 month (n⫽6) 20.83⫾6.31 1.13⫾1.2 0.58⫾0.5 ⫺0.14⫾0.19 20/28 ⫺0.06⫾0.07a 20/23 ⫺2.67⫾2.63 13.6⫾1.14

a

3 months (n⫽6) 24.67⫾5.69 0.75⫾0.5 0⫾0 ⫺0.06⫾0.1 20/23 ⫺0.03⫾0.06a 20/21 ⫺0.67⫾1.66 14⫾1.73

a

6 months (n⫽3) 69⫾1.26 1.08⫾1.15 0.5⫾0.52 ⫺0.33⫾0.5 20/43 ⫺0.85⫾0.16 20/142 ⫺0.54⫾0.25 17.3⫾2.0

40.17⫾28.58 1.17⫾1.18 0.58⫾0.56 ⫺0.11⫾0.22 20/26 ⫺0.47⫾0.45 20/59 ⫺1.65⫾0.49a 16.4⫾1.5

Preop (n⫽6) 1 month (n⫽6)

27.5⫾6.12 1.06⫾1.10 0.63⫾0.52 ⫺0.12⫾0.24 20/26 ⫺0.12⫾0.21a 20/26 ⫺1.54⫾0.37a 17.1⫾1.8

b

a

3 months (n⫽6)

Nonoperated eye

Significant difference between the preop and the follow-up measurements using paired t-test (pⱕ 0.05). SE⫽spherical equivalent. c Both distance and near vision are computed based on log10 scale. The numbers below these numbers indicate the equivalent snellen refraction.

a

Blur point IOP

Near VA

Preop (n⫽6)

Variable

Operated eye

Table 1 Summary of Primary Outcome Variables at Each Follow-up Period (Mean ⫾SD)

32⫾2.65a 0.5⫾0.22 0.5⫾0.25 ⫺0.03⫾0.06 20/21 ⫺0.06⫾0.10a 20/23 ⫺0.33⫾1.61 15.8⫾0.76

6 months (n⫽3)

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Figure 4 Ultrasonic fusion of portions of a scleral expansion band.

Unfortunately, five of the six patients required removal of their scleral expansion bands 3 to 6 months later due to conjunctival erosion from the roughened areas where the PMMA bands were ultrasonically welded together. After removal of the scleral expansion bands, the accommodative amplitude of these five patients returned to preoperative values. An additional three consecutive patients subsequently underwent the same procedure. In an effort to provide a better cosmetic result with more accommodation, the scleral belt loops were made much deeper. These three patients subsequently developed anterior

Table 2 Scleral Expansion Patient Selection Ideal surgical candidate 40 to 70 years old No refractive error at distance Binocular vision Less than ⫹1.00 of hyperopia

a

Relative contraindications

Contraindications

Severe keratoconjunctivitis sicca Insulin-dependent diabetes or poorly controlled diabetes Monocular patienta Patients beyond 70 years of ageb Patients with hyperopia greater than ⫹1.00c

Previous cataract extraction Scleromalacia Previous trabeculectomy Coagulopathies Collagen vascular diseases

Important because of the investigational status of scleral expansion. These patients should be informed of the possibility of ciliary muscle atrophy and thus the possibility of a smaller range of accommodation. c These patients should have surgical correction prior to scleral expansion, as they will use a significant amount of their accommodative amplitude for distance vision, leaving less for near vision. Additionally, without prior surgical correction of hyperopia, these patients are more likely to require bilateral procedures. Source: Ref. 20. b

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Figure 5 The scleral expansion procedure. The conjunctiva is opened at the limbus from 2:30 to 10:30 o’clock and from 4:30 to 7:30 o’clock with vertical relaxing incisions at 12:00 and 6:00 o’clock. Scleral belt loops, 3.5 mm posterior to the posterior limbus, 4 mm long, 1.5 mm wide, and 300 to 400 ␮m deep are made in each of the four oblique quadrants.

ischemic syndrome (AIS) and had their bands removed 24 to 96 h after surgery. Given previous reports of treatment of AIS with hyperbaric oxygen (18,19), we opted to treat these patients with hyperbaric oxygen. All patients responded well to hyperbaric oxygen therapy and none lost vision as a result of the procedure. This was the first known occurrence of AIS as a result of scleral expansion. Despite the posterior insertions of the rectus muscles, these deeper tunnels likely resulted in a significant reduction of blood flow through the anterior ciliary arteries that perforate the sclera at the insertions of the rectus muscles. In order to avoid compression of the anterior ciliary arteries and AIS, surgeons began placing the scleral belt loops along the 45-degree meridians at 1:30, 4:30, 7:30, and 10:30 o’clock. Further modifications to the scleral expansion band followed. Unfortunately, conjunctival erosion continued to be a problem. In 1998, however, a new prototype was developed consisting of four individual PMMA segments that were not connected to each other, resulting in decreased rates of conjunctival erosion, a simplified procedure, and a significant decrease in instrumentation cost (120). To decrease the risk of AIS, these segments were also placed in scleral belt loops along the 45-degree meridians, away from the ciliary artery insertions (Fig. 5). Not everyone, however, is a candidate for scleral expansion. See Table 2 for patient selection. C. CURRENT METHOD OF SCLERAL EXPANSION 1. Preop Medications If the patient has no contraindications, it has been recommended that oral nonsteroidal anti-inflammatory drugs (NSAIDs) be started 1 to 2 days preop. Nonsteroidals decrease surgical pain and swelling and produce a smoother postoperative course. Additionally, there is some thought that NSAIDs may help to preserve anterior segment circulation (70).

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Figure 6 Marking the limbus with the quadrant marker.

Mark the 12 o’clock position at the slit lamp. This is an important reference mark to be used later for proper segment placement away from the area of ciliary arteries. If this reference mark is not made, cyclotorsion of the eye can occur when the patient lies down for the procedure. This will increase the risk of anterior ischemic syndrome from malpositioned segments. After the patient is taken to the operating room, the 12 o’clock meridian is used to align the quadrant marker in order to mark the location of the scleral expansion segments (Fig. 6.).

D. ANESTHESIA A small amount of subconjunctival anesthesia is injected at the 12:00 and 6:00 o’clock meridians to elevate the conjunctiva and produce a surgical plane for dissection. Retrobulbar and peribulbar anesthesia is generally avoided because the pupil dilates and the eye may become soft, making it more difficult to construct the scleral belt loops. Additionally, a dilated pupil precludes evaluation of iris sphincter function, which is necessary to assess anterior segment circulation. E. CONJUNCTIVAL DISSECTION A 4 to 5-mm vertical incision is placed perpendicular to the limbus at the 12 and 6 o’clock meridians. These incisions are extended circumferentially at the limbus approximately 1 mm past the oblique quadrant marks. The conjunctiva from 7:30 to 10:30 o’clock and from 2:30 to 4:30 o’clock is left intact to avoid postoperative redness in the palpebral opening. The flap is dissected approximately 5 mm posterior to the limbus, leaving no Tenon’s capsule in the area where the scleral expansion segments will be placed. As little cautery as possible should be used so as to preserve the structural integrity of the sclera.

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Figure 7 Limbus marker.

It is particularly important to avoid cauterizing the sclera between the area of the implant bed and the limbus. F. MARK THE SCLERAL BELT LOOPS The limbus and the previous oblique quadrant marks are identified. Using a specially designed marker (Fig. 7), the parallel entrance and exit ends of the scleral belt loop incisions are marked so that the anterior aspect of the exit and entrance incisions of the scleral belt loop will be 3.5 mm from the limbus (Fig. 8).

Figure 8 Marks (see arrows) are 3.5 mm posterior to the limbus.

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B

Figure 9 (A and B) The 300-␮m guarded diamond blade has a width of 1500 ␮m and makes an incision 300 ␮m deep.

G. DISSECT THE SCLERAL BELT LOOPS A specially designed scleral fixator is used to grasp the sclera. The scleral fixator should be firmly inserted approximately 1.5 to 2 mm distal to the exit side of the future scleral tunnel. Avoid setting the scleral fixator either too far forward or back to avoid significant torque and tension when making the loop and inserting the segment. A 300-␮m guarded square diamond blade (Fig. 9A and B) is used to make parallel incisions at the previously marked locations (Fig. 10A and B). The incisions should be

Figure 10 (A and B) A calibrated marker is used to check the measurements and the diamond blade is used to make the parallel incisions while stabilizing the eye with the scleral fixator.

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Figure 11 The 5-mm lamella diamond blade.

parallel to each other, not radial to the limbus. If the incisions are not parallel, the segment may rotate within the incision losing most of its lift. Care should be taken to remove all of Tenon’s capsule near the incision so as to avoid a shallow incision. Without losing scleral fixation, a 5-mm-long 1.5-mm-wide lamella diamond blade (Fig. 11) is placed in the incision located furthest from the scleral fixator. The diamond blade is slowly advanced through the sclera toward the other incision near the scleral fixator (Fig. 12). By observing the relative visibility of the lamella diamond blade through the sclera, one controls the depth of the blade. The very tip of the diamond lamella blade should not be visible as the blade is passed through the sclera. Only a slight elevation or bulge of the sclera at the lateral edges of the blade should be seen. If the blade is easily

Figure 12 The lamella diamond blade being used to make a scleral belt loop.

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Figure 13 The thickness of the scleral belt loops and the exit wound are checked with the 1.4mm-wide spatula.

seen through the sclera, then the loop is too shallow and the effect of the surgery will be greatly reduced. In making the scleral belt loop, care should be taken not to retract and advance the blade unnecessarily to avoid making blind pockets that will increase the difficulty of passing the scleral expansion segment. On nearing the exit incision with the diamond blade, the sclera is depressed with the scleral fixator to help open the exit incision. It is usually necessary to aim the lamella blade upward just before exiting to prevent a blind pocket under the exit incision. The entire lamella diamond blade is 5 mm long. The front curve of the blade is 1 mm long. Therefore, by seeing the complete front curve of the blade, the surgeon is assured that the scleral belt loop is no longer than 4 mm. In removing the lamella diamond blade, the surgeon must maintain fixation with the scleral fixator and remove the lamella blade slowly and in a controlled manner. In doing so, the surgeon avoids cutting the edges of the entrance incision, avoids perforating the belt loop, and ensures that the blade is not passed into the suprachoroidal space. If there is any doubt that the lamella blade is completely passed through the exit incision, test the incision using a 1.4-mm-wide spatula (Fig. 13). It should be possible to readily pass the spatula through the incision in the same direction that the scleral expansion segment will be passed. H. PLACE THE SCLERAL EXPANSION SEGMENTS The four scleral expansion segments (Fig. 14A and B) come packaged in much the same way as an intraocular lens (IOL). Prior to grasping the segments, place one or two drops of sterile saline into the well holding the segments. This prevents loss of the segments due to static electricity. Either a specifically designed scleral expansion segment holder or the injector can be used to pass the segment through the scleral belt loop (Fig. 15). Load the segment into the injector or segment holder curved side up. Without moving the scleral fixator, the segment is passed into the scleral belt loop. In difficult cases it is

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Figure 14 (A and B) The dimensions of the segment.

sometimes necessary to pass the segment upside down and then rotate the segment into place using the injector and heavy needle holder. Rotation of the segment will stretch the belt loop, but a slightly stretched belt loop will produce a greater effect than a thin belt loop. If it is still not possible to pass the segment, the segment may be getting caught in a blind pocket. Reapply the scleral fixator at the opposite end of the tunnel and try passing the segment in reverse by beginning at the exit side of the scleral belt loop. If the patient suddenly moves or complains of eye pain, immediately stop advancing the segment. This may indicate that the vitreous, subchoroidal space, or ciliary body has been entered. This can be confirmed by the presence of vitreous or fluid containing black pigment exiting one or both ends of the scleral belt loop. At this point, the segment should be removed and the eye examined. If the surgeon feels it is safe, it may still be possible to pass the segment upside down from the other direction. If the scleral belt loop is torn or severed, remove the segment and close the sclera. The operation may be completed after the sclera is healed in 2 or 3 months.

Figure 15 Placement of the segment.

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I. CONJUNCTIVAL CLOSURE Sutures are placed at the 12:00 and 6:00 o’clock meridians by passing the suture through the conjunctiva and back out through the sclera and burying the knot. The corners of the conjunctival incision should be overlapped. Finally, administer 20% mannitol (1 g/kg) intravenously over 30 min to avoid malignant glaucoma. J. CHECK THE PUPILS THE NEXT POSTOPERATIVE DAY The pupils should be checked for reactivity and pupil size. An irregular or dilated pupil may suggest AIS or sector AIS. If a pupillary abnormality is noted, place one drop of 0.5% pilocarpine in each eye. Pupillary constriction provides evidence that adequate anterior segment blood flow is present. The sine qua non for AIS is a dilated nonreactive pupil or a nonreactive pupillary sector. Other signs of AIS are nausea, an intraocular pressure (IOP) less than 10 mmHg, corneal edema and folds, and anterior chamber cell and flair (Fig. 16). At this point some recommend that the segment or segments causing AIS be immediately removed. Others recommend giving the patient an additional dose of intravenous manitol and 2 to 4% pilocarpine every 5 min for a total of six times in addition to oral or intravenous steroids and aspirin if not contraindicated (21). If the pupil does not respond in 2 h, repeat the manitol and six doses of pilocarpine (21). If there is still no response after another 2 h, the segments should be removed. Artificial tears, topical antibiotics, and topical anti-inflammatory or nonsteroidal agents should be administered postoperatively. It is recommended that topical antibiotics and anti-inflammatory eye drops be used for 2 weeks. Any remaining sutures should be removed after 10 to 14 days. Artificial tears should be used frequently and a bland ointment administered at night for at least 3 months. Some patients complain of a mild to severe brow ache beginning about 30 min after surgery and lasting 2 to 6 h. It may be necessary to treat these patients with analgesics. K. EYE EXERCISES Following the procedure, it is important that patients perform accommodation eye exercises for rehabilitation of the ciliary muscle (22). Patients are asked to exercise from near to

Figure 16 Characteristic photograph of a dilated pupil and corneal folds consistent with anterior ischemic syndrome.

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far rather than far to near. Patients should hold an eye chart 4 in. (10 cm) from their eye and look at the smallest line they can see. Patients are then asked to concentrate until they can see any letter on the next smaller line. Next they should hold fixation on the letter on the smaller line and slowly move it away from the eye until it is at full arm’s length. The eye chart can then be brought slowly back toward the eye while continuously holding fixation on the smaller line until the eye chart is back at 10 cm from the eye. Once they can read all the letters on that smaller line, have them move to the next smaller line and again move the eye chart to arm’s length while maintaining fixation on the smaller line, and so on. Patients should repeat this exercise as frequently as possible, but for at least 10 repetitions, four times a day, each time trying to fixate on a smaller line beginning at the close distance of 10 cm from the eye. It is much better to do frequent exercise sessions throughout the day than one long session. Following the exercises, patients will notice that they can read better. Patients will usually experience ciliary pain during the exercises for the first 2 weeks after surgery. The patients can be told that this pain is a good sign and that the exercise is strengthening their ciliary muscles. Patients should avoid the use of a near vision optical aid during their daily reading tasks. Additionally, patients should squint as little as possible during the eye exercise; if they initially have difficulty performing their daily reading tasks, encourage them to use a bright light or, only if absolutely necessary, to squint in order to avoid the use of a near optical aid. As they continue the eye exercise, the requirement to squint or use a bright light during their daily reading tasks will decrease.

L. COMPLICATIONS Only one case of AIS has been reported using the latest 5.5-mm scleral expansion segments (23). This complication may have resulted from improper positioning of the segments (23). One case of endophthalmitis has also been reported (23). This case was thought to result from a break in sterile technique (23). Additionally, one case of scleral thinning similar to that observed with scleral buckles has been reported and may have been a result of scleral expansion (24). To date, no cases of malignant glaucoma have been reported using the new scleral expansion segments. Theoretically, this is a possibility, as the segments may increase posterior pressure, blocking outflow and resulting in aqueous misdirection. Intravenous manitol is given to dehydrate the vitreous decreasing the likelihood of this complication. Other minor complications include conjunctival hyperemia, subconjunctival hemorrhage, transient ptosis, rotation or subluxation, of the scleral expansion segments, photophobia due to tear film instability, conjunctival erosion, accommodative fatigue, temporary keratoconjunctivitis, swollen or irregular conjunctiva, and astigmatism, which may last for 2 to 3 months and but subsides with intense treatment with artificial tears.

M. CLINICAL RESULTS Increases in accommodation after this technique have ranged from 1.00 to 10.00 D (13). Two different studies (20) of 29 and 7 patients have reported an increased range of accommodation in all patients, with an average of 3.02 and 3.13 D respectively. Similar to our findings, an increased range of near vision was also noted in the unoperated eye. This increase approached 20 to 50% of the increase measured in the operated eye.

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N. SCLERAL EXPANSION AND OTHER REFRACTIVE PROCEDURES Scleral expansion has been successfully performed after LASIK, PRK, and RK. With regard to LASIK, however, it is easier to perform LASIK before scleral expansion due to difficulties that may be encountered while applying the suction ring. Scleral expansion has been performed as early as 6 weeks post-LASIK. Obviously, PRK and laser epithelial keratomileusis (LASEK) are good alternatives for patients who have had previous scleral expansion procedures. O. OTHER SCLERAL EXPANSION PROCEDURES Several other methods have been used to expand the sclera. Some surgeons have made simple scleral incisions with a diamond knife to expand the sclera. The scleral incisions are limited to an accommodative range of only about Ⳮ1.50 D, and, as the incisions heal, the effect declines (R. Schachar, personal communication, 2001). In order to prevent the incisions from healing, Fukasaku has inserted silicone plugs into the scleral incisions (24a). The infrared laser has also been used to make deep scleral incisions (25). The average correction is also limited to an accommodative range of about Ⳮ1.50 D and will likely regress with time (R. Schachar, personal communication, 2001). In contrast to the above, Lin has described no regression after scleral expansion using infrared laser (J. Lin, personal communication, 2001). A major concern with the infrared laser is that it can coagulate blood vessels and lead to anterior segment ischemia. There have been two phthisical eyes as a result of making scleral incisions with the infrared laser for the treatment of presbyopia (R. Schachar, personal communication, 2001). Last, as a result of the deeper tissue ablation, the potential for rupture after blunt trauma is also a concern. P. SCLERAL EXPANSION AND GLAUCOMA While chronic open-angle glaucoma is a genetic disease, predisposed patients may benefit from scleral expansion due to anatomical modifications produced by the procedures in the ciliary muscle and trabecular meshwork (26,27). International clinical trials evaluating scleral expansion for the treatment of ocular hypertension and primary open-angle glaucoma in Canada and Mexico have demonstrated excellent preliminary results (27,28). The median decrease in IOP after scleral expansion was 7 mmHg, and the postoperative decrease in IOP appears to be equivalent to the IOP-lowering effect of the preop, physicianprescribed topical glaucoma medications (27). Q. SUMMARY Scleral expansion is a new procedure designed to treat presbyopia surgically. While the theory on which it is based continues to be a subject of intense debate, it must be noted that patients report an improved ability to read at near after scleral expansion. Given the immense impact of presbyopia, surgical reversal of presbyopia will likely continue to be an area of significant interest. In addition, scleral expansion may offer a new modality for the treatment and prevention of ocular hypertension and primary open-angle glaucoma. If scleral expansion is found to effectively decrease IOP, the adverse reactions and systemic side effects commonly observed with glaucoma medications could be avoided and potential surgical filtering and shunt procedures could be delayed or eliminated.

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ACKNOWLEDGMENT The authors would like to thank Presby Corp for their assistance in writing this chapter and the illustrations they provided. Additionally, we would like to thank Dr. Adrian Glasser and Dr. Ronald Schachar for their comments. REFERENCES 1. Donders FC. On the Anomalies of Accommodation and Refraction of the Eye. London: The New Sydenham Society, 1864:204–214. 2. May CH, Perera CA. Manual of the Diseases of the Eye for Students and General Practitioners, 17th ed. Baltimore: William Wood and Company, 1941:365–366. ¨ ber die Akkommodation des Auges. Graefes Arch Klin Exp Ophthalmol 3. von Helmholtz H. U 1855; 1:1–89. 4. Rohen JW. Scanning electron microscopic studies of the zonular apparatus in human and monkey eyes. Invest Ophthalmol Vis Sci 1979; 18:133–144. 5. Fisher RF. Presbyopia and the changes with age in the human crystalline lens. J Physiol (Br) 1973; 228:765–779. 6. Coleman DJ. Unified model for accommodative mechanism. Am J Ophthalmol 1970; 69: 1063–1079. 7. Fincham EF. The mechanism of accommodation. Br J Ophthalmol 1937; 8(suppl):5–80. 8. Stuhlman O. An Introduction to Biophysics. New York: Wiley, 1948:106–107. 9. Schachar RA. The mechanism of accommodation. Int Ophthalmol Clin 2001; 41:17–32. 10. Schachar RA. Histology of the ciliary muscle-zonular connections. Ann Ophthalmol 1996; 28:70–79. 11. Schachar RA, Tello C, Cudmore DP, Liebmann JM, Black TD, Ritch R. In vivo increase of the human lens equator diameter during accommodation. Am J Physiol (Regul Integr Comp Physiol 40) 1996; 271:R670–R676. 12. Schachar RA, Anderson DA. The mechanism of ciliary muscle function. Ann Ophthalmol 1995; 27:126–132. 13. Schachar RA, Black TD, Kash RL, Cudmore DP, Schanzlin DJ. The mechanism of accommodation and presbyopia in the primate. Ann Ophthalmol 1995; 27:58–67. 14. Schachar RA. Zonular function: a new hypothesis with clinical implications. Ann Ophthalmol 1994; 26:36–38. 15. Schachar RA, Cudmore DP, Black TD. Experimental support for Schachar’s hypothesis of accommodation. Ann Ophthalmol 1993; 25:404–409. 16. Schachar RA. Cause and treatment of presbyopia with a method for increasing the amplitude of accommodation. Ann Ophthalmol 1992; 24:445–452. 17. Yang GS, Yee RW, Cross WD, Chuang AZ, Ruiz RS. Scleral expansion: a new surgical technique to correct presbyopia. Invest Ophthalmol Vis Sci 1997; 38(suppl):S497. 18. De Smet MD, Carruthers J, Lepawsky M. Anterior segment ischemia treated with hyperbaric oxygen. Can J Ophthalmol 1987; 22:381–383. 19. Jampol LM. Oxygen therapy and intraocular oxygenation. Trans Am Ophthalmol Soc 1987; 85:407–437. 20. Cross WD, Zdenek GW. Surgical reversal of presbyopia. In: Agarwal S et al, eds. Refractive Surgery. New Delhi: Jaypee Brothers Medical Publishers, 2000:592–608. 21. Cross WD. Scleral expansion band technique treats presbyopia. Ocul Surg News 2001; 19: 28–34. 22. Ruelas V. Optometric postoperative care. In: Schachar RA, Roy FH, eds. Presbyopia: Cause and Treatment. The Hague, The Netherlands: Kugler, 2000: 105–107. 23. Zdenek G. Complications in surgical reversal of presbyopia can be avoided, managed. Ocul Surg News 2001; 19:39–44.

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24. Singh G, Chalfin S. A complication of scleral expansion surgery for treatment of presbyopia. Am J Ophthalmol 2000; 130:521–523. 24a. Fukasaku H, Marron JA. Anterior ciliary sclerotomy with silicone expansion plug implantation: effect on presbyopia and intraocular pressure. Int Ophthalmol Clin 2001; 41:133–141. 25. Johannes L. Is the end of reading glasses in sight? The Wall Street Journal. March 28, 2001, P B1. 26. Schachar RA. The scleral expansion band procedure: Therapy for ocular hypertension and primary open angle glaucoma. Ann Ophthalmol 2000; 32:87–89. 27. Rifkind AW, Yablonski ME, Shuster JJ. Effect of scleral expansion band (SEB) on ocular hypertension Canada phase 1 study. Compr Ther 2001; 27:333–340. 28. Cross WD, Marmer RH, Shuster JJ. A pilot study to determine the effect of the scleral expansion band (SEB) procedure on ocular hypertension. Submitted.

22 Multifocal IOLs for Presbyopia HIROKO BISSEN-MIYAJIMA Tokyo Dental College, Suidobash Hospital, Tokyo, Japan

A. BACKGROUND With recent advancements in refractive surgery, we can achieve sufficient results in the treatment of myopia, hyperopia, and astigmatism. Patients are able to appreciate good uncorrected visual acuity (VA), and their quality of life can also be improved. The next interest goes to how we can treat presbyopia. Several methods have been introduced. Implantation of multifocal intraocular lenses (IOLs) instead of original crystalline lenses is familiar to the ophthalmic surgeon, since we are performing this technique for cataract patients for many years. We could learn most results of multifocal IOLs from our cataract patients. 1. Cataract Surgery as Refractive Surgery When the IOL was introduced, both patients and the surgeons were impressed by the resulting relatively good vision without spectacles or contact lenses. Recently, cataract surgery has been accepted as refractive surgery, since we can correct preoperative myopia or hyperopia at the time of surgery. Even clear lens extraction following IOL implantation is accepted for the treatment of extreme myopia or hyperopia. An ideal IOL would be one that would replace the original crystalline lens at younger age. We can correct not only preoperative refractive error but also age-related presbyopia. 2. Impression of the Multifocal IOL When the multifocal IOL was first introduced, we expected it to act like bifocal spectacles, so that the patient would have clear vision at far and near. The results with first-generation multifocal IOLs were somewhat disappointing, however, since the distance visual acuity 237

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was dependent on pupil size and sometimes inferior to that with monofocal IOLs. Another concern is the loss of contrast sensitivity. Because of these unpleasant drawbacks, many surgeons went back to implanting conventional monofocal IOLs. The results of recent multifocal IOLs are more promising and the interest in this type of IOL has increased again. B. THEORETICAL BENEFITS AND CAVEATS Before describing theoretical benefits and caveats, one should understand the different designs of IOL. 1. Different Types of Multifocal IOLs a. Refractive Type The initial refractive type was two zones with a central 2-mm button for near, and this IOL was called “bull’s eye” (Fig. 1A). The center part had additional 4 D, which would be equivalent to 2.5 D in spectacles. If the pupil size was too small, the patient had insufficient visual acuity and this lens was abandoned. Then other types of refractive IOLs were introduced (Fig. 1B and C). Some are far-dominant and others are near-dominant. Recently, the zonal progressive type of AMO ARRAY (Fig. 1D) became a standard multifocal IOL in several countries. The center part is for far vision and patients usually get good distance visual acuity (VA). b. Diffractive Type Another type is the diffractive type, which is not affected by pupil size. This IOL has a 0.6-mm central zone and some 30 annular diffracting zones on its posterior surface (Fig. 1E). The light can be diffracted toward two foci; 41% for near and 41% for distance. Thus, 18% of the light would be lost, and the loss of contrast sensitivity became the biggest concern. 2. Theoretical Benefit a. Less Dependence on Spectacles Theoretical benefits of multifocal IOLs are based on their depth of focus. Figure 2 shows the results of distance visual acuity with defocus of the patient from emmetropia following AMO ARRAY. There are two spikes, which means that the patient can focus both far and near. Another interesting thing about this particular IOL is that the valley between two spikes is not deep and patients have a chance to see things at middle distance. Thus, the potential of not depending on spectacles is high. 3. Theoretical Caveat a. Decreased Contrast Sensitivity The caveat of multifocal IOLs in general is the loss of contrast sensitivity due to their design. By in a randomized study of multifocal IOLs, a significant decrease of visual acuity was reported at 11% contrast with multifocal IOLs compared to the monofocal IOLs (1). Although this problem can be detected by examination of contrast visual acuity, most patients do not have the problem in daily life.

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Figure 1 (A) IOLAB two-zone refractive type with a central 2-mm button for near. (B) IOPTEX. (C) Pharmacia. (D) AMO ARRAY. (E) Diffractive IOL (3M). This IOL has a 0.6-mm central zone and some 30 annular diffracting zones on its back surface.

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Figure 2 Defocus curve. Two spikes for far and near can be observed.

b. Glare and Halo Another caveat would be glare and halo, especially at night. When the pupil is dilated in dim light, some patients recognize halo due to its annular design. c. Incorrect Power The correct biometry is very important for this particular IOL. Especially when clear lens extraction is planned, this is critical. Patients expect better uncorrected vision at far and near. Even with perfect surgery, the results can be miserable if the IOL power calculation fails. C. INDICATIONS/CONTRAINDICATIONS Some indications and contraindications depend on the type of multifocal IOL. Recent refractive-type IOLs are indicated for most patients if they are not included in exclusion criteria (Table 1). 1. Cataract In case of cataract surgery for a younger patient, this IOL can avoid the loss of accommodation, an undesirable complication. The results in this age group may represent the possibility of treating presbyopia.

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Table 1 Exclusion Criteria Patient with multifocal IOL in the fellow eye Uncontrolled glaucoma Progressive diabetic retinopathy Corneal lesions that may affect visual acuity Other complications that may affect visual acuity Preoperative astigmatism greater than 1.5 D Frequent driving or operation of dangerous machinery at night

2. Expectation of the Patient The patient who is highly motivated is often a good candidate. The increased number of refractive surgeries has proved that many patients long for life without spectacles and contact lenses. Younger patients underage 45 are also candidates, since the most undesirable complication following cataract surgery at this age is the loss of accommodation. Despite their perfect vision at far, they may suffer from the new experience of not being able to read without spectacles. 3. Occupation Individuals with occupations that require good far and near vision in which the use of spectacles or contact lenses might be dangerous represent another good candidate group. D. PREFERRED SURGICAL TECHNIQUES The preferred surgical techniques should provide predictability of postoperative refraction and stability of IOL position. For this purpose, small incision and continuous curvilinear capsulorhexis (CCC) are recommended. 1. Incision It is well known that surgically induced astigmatism has recently been diminished by the use of small-incision cataract surgery. For this purpose, a foldable multifocal IOL is preferable. Also, a self-sealing incision should be made so as to avoid suture-induced astigmatisms. 2. IOL Position Capsular bag implantation of IOLs provides a stable position. IOL tilt or decentration causes severe complications with multifocal IOLs due to their design. Thus, CCC should be completed. If the IOL haptics position is unclear, which may cause unpleasant phenomena such as glare and halo, one should try to implant the IOL symmetrically, either both haptics in the capsular bag or in the sulcus. 3. Posterior CCC Near vision can easily be decreased by the posterior capsular opacity with multifocal IOLs. In other words, the rate of neodymium:YAG capsulotomy is higher than that of monofocal

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Table 2 Visual Acuities with Different Multifocal IOLs Lindstrom (1993)

Usui and associates (1992)

Negishi and associates (1997)

IOL Type of IOL Uncorrected distance VA Corrected distance VA

3M Diffractive 20/40 or better 53.1%

Ioptex Refractive Not described

AMO Array Refractive 20/40 or better 90.3%

20/25 or better 84.9%

20/25 or better 100%

Uncorrected near VA J1-J3 Distance-corrected near VA J1-J3 Best-corrected near VA J1-J3

82%

20/40 or better 94.9% 45.6%

92%

60.4%

62.1%

97%

94.1%

97%

62.1%

IOLs. If the opacity or the fibrosis of the posterior capsule is obvious and cannot be polished during surgery, one may perform posterior CCC. Especially when we implant multifocal IOLs in younger patients, we should consider performing posterior CCC, since a neodymium:YAG capsulotomy may be necessary earlier. a. Clinical Results There have been many reports on the results of multifocal IOLs following cataract extraction. The reports on multifocal IOL with clear lensectomy are limited. The desirable results with cataract patients persuade clear lensectomy for the patient who would like to have refractive surgery, including the correction of presbyopia. b. Visual Acuity (VA) Table 2 shows the reported results of several multifocal IOLs (2). The time-lapse changes of the mean postoperative VA in a Japanese clinical study are shown in Table 3. The average distance uncorrected VA was 20/25, best corrected VA was better than 20/20. For near, uncorrected VA was 0.39, with distance correction, it was 0.43; and best corrected

Table 3 Time Lapse Changes of the Average VA Observation

Uncorrected distance VA Corrected distance VA Uncorrected near VA Distance-corrected near VA Best corrected near VA

Pre-op

1 day

1 week

1 month

3 months

6 months

1 year

0.13 0.23 0.13 0.13 0.20

0.63 0.90 0.29 0.30 0.56

0.73 1.06 0.34 0.36 0.74

0.74 1.08 0.36 0.38 0.73

0.69 1.07 0.40 0.39 0.72

0.73 1.05 0.41 0.40 0.72

0.78 1.12 0.39 0.43 0.77

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VA was 0.77. The VA at the 1 week postoperative visit was as good as the one at 1 year. We can expect early visual recovery with this type of IOL. c. Contrast Sensitivity The loss of contrast sensitivity with multifocal IOLs is accepted as a drawback of this design. Despite previous reports, our results are encouraging. The mean contrast sensitivity at 1 year after the operation was above the lowest of normal range (Fig. 3). Contrast VA with variable-contrast charts (VCVAC) showed that the contrast VA of the eye with a multifocal IOL in 15 and 2.5% contrast was comparable to that with a monofocal IOL (Fig. 4). d. Halo and Glare Halo and glare are also of concern following multifocal IOL surgery. One year after the operation, patients were asked about halo and confirmed its intensity. At each final followup observation, 22.4% complained mild or moderate halo, which was only a transient symptom in every case against sun in daytime and/or light sources at night. This was not experienced to the extent of causing problems in daily life. Glare values were measured by Miller-Nadler Glaretester and percent glare was 5.6. No percent glare decrease was observed, potentially generating clinical problems. e. Spectacle Usage It is not easy to analyze spectacle usage, since some patients use spectacles most of the time and the others use them only when necessary. Approximately 60% were able to function comfortably without spectacles. Figure 5 shows the changes of using spectacles by the follow-up time. Until 1 month after operation, most patients were not using specta-

Figure 3 Contrast sensitivity. The mean contrast sensitivity after the operation was above the lowest of normal range.

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Figure 4 Contrast visual acuity. Contrast VA of the eye with multifocal IOL (array) in 15 and 2.5% contrast was comparable to that with monofocal IOL.

Figure 5 Changes of using spectacles.

Figure 6 Patient’s satisfaction.

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Figure 7 Vision simulation system.

cles. Once they get used to read with reading glasses, some prefer the clear letters using the zone for far with additional correction with spectacles. That is why the rate for spectacle usage increases after 3 months or 1 year. e. Patient’s Satisfaction (Questionnaire) It is important that patients be satisfied with the results (Fig. 6). Especially if clear lens extraction has been performed, patients expect better reading ability. f. Patient’s View with Model Eye a. Vision Simulation System The concern of implanting multifocal IOL is that the surgeon or patient cannot estimate the view after the surgery. Because of this, it takes a long time to explain to the patient about the results of multifocal IOL. The image through multifocal implantation was recorded using the vision simulation system developed by Ohnuma (Fig. 7) (3). b. Patient’s View Using photos taken by the vision simulation system, the view of the patient was examined. First, the view was seen by each eye while the fellow eye was covered. Then the view was compared with each eye. The photo which was most similar to the view with multifocal IOL was chosen. The results are shown in Figure 8. During the day, the vision is clearer than that with a multifocal IOL and closer to the view with a monofocal IOL. However, for near vision, the photo taken by the model eye was similar to the real view with a multifocal IOL. E. COMPLICATIONS AND MANAGEMENT 1. IOL Power Miscalculation When the biometry was not perfect and the patient ends up with myopia or hyperopia, he or she may not receive the advantage of multifocal IOL. It is known that this type of multifocal IOL should be emmetropic to slightly hyperopic (Fig. 9A). If the postoperative refraction is more than 0.5 D, the blur circles become larger at distance and near compared to emmetropia (Fig. 9B)). This will cause potential halos at night. If the postoperative

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Figure 8 Patient’s view. (A) Clinic at day. (B) Clinic at night. (C) Clock.

refraction is hyperopic, halo at night should be minimal (Fig. 9C). Thus, postoperative refraction is an important factor. IOL exchange or piggyback implantation should be considered if the patient suffers halo at night or strongly wishes better distance and near vision. 2. IOL Decentration With the introduction of CCC, clinically obvious decentration of IOL became rare. However, when it occurs, it may cause visual disturbance. Mostly, these are caused by asymmet-

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Figure 9 Refractive error and blur circles. (A) Emmetropic to slightly hyperopic (plano to Ⳮ0.5 D). (B) Myopic refraction (⬎ ⳮ0.5). (C) Hyperopic refraction (⬎ Ⳮ0.5 D).

rical fixation of the IOL. Surgical replacement of the IOL should be considered. If the replacement is not possible due to the defect of posterior capsule, one may consider exchanging the IOL to monofocal IOL. 3. Halo and Glare Vision Complications are mainly related to IOL design. Most common complaints are halo and glare at night. These are usually relieved by time. From our questionnaire, some patients

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have reported being bothered with halo and glare while they were driving at night. However, the readability of traffic signs is about the same as with monofocal IOLs. 4. Insufficient Near Vision This is caused by incorrect IOL power calculation, small pupil diameter, or opacity in the path from cornea to retina. The former two reasons are most common. If the incorrect IOL power is the main reason, one may consider IOL exchange or piggyback implantation. If the pupil diameter is smaller than the near zone, the patient will not get the advantage of near addition. F. CONCLUSIONS Treating presbyopia is still a challenge. However, we already have clinical data of implanting multifocal IOLs for cataract patients. At this time, if the patient will need cataract surgery sooner or later, multifocal IOL is a rather safe way to treat presbyopia. On the other hand, for the patient with a clear lens, this may be a decision to be made by the surgeon. The surgeon must be confident in his or her biometry and surgical technique. If the patient understands the risk of removing the lens and implanting an IOL, a multifocal IOL should always be considered as the best choice for the treatment of presbyopia. REFERENCES 1. Steinert RF, Post CT Jr, Brint SF, Fritch CD, Hall DL, Wilder LW, Fine IH, Lichtenstein SB, Masket S, Casebeer C. A prospective, randomized, double-masked comparison of a zonalprogressive multifocal intraocular lens and a monofocal intraocular lens. Ophthalmology 1992; 99:853–860. 2. Negishi K, Bissen-Miyajima H, Kato K, Kurosaka D, Nagamoto T. Evaluation of a zonalprogressive multifocal intraocular lens. Am J Ophthalmol 1997; 124:321–330. 3. Ohnuma K. Image focused by a multi-focal intraocular lens and its estimation. J Eye 2001; 18: 395–400.

23 Refractive Lens Exchange with a Multifocal Intraocular Lens I. HOWARD FINE, RICHARD S. HOFFMAN, and MARK PACKER Casey Eye Institute, Oregon Health and Science University, Portland, Oregon, U.S.A.

A. INTRODUCTION The options for treating the refractive surgery patient are greater now than at any time in ophthalmic history. Excimer laser refractive surgery is growing in popularity throughout the world, but it has its limitations. Patients with extreme degrees of myopia and hyperopia are poor candidates for corneal refractive surgery, and presbyopic patients must rely on reading glasses or monovision in order to obtain the full range of visual function. These limitations in laser refractive surgery have led to a resurgence of intraocular modalities for the correction of refractive errors. B. MULTIFOCAL LENSES Perhaps the greatest catalyst for the resurgence of refractive lens exchange has been the development of multifocal lens technology. High hyperopes, presbyopes, and patients with borderline cataracts who have presented for refractive surgery have been ideal candidates for this new technology. Multifocal intraocular lens (IOL) technology offers patients substantial benefits. The elimination of a presbyopic condition and restoration of normal vision by simulating accommodation greatly enhances the quality of life for most patients. The only multifocal IOL available for general use in the U.S. is the Array (Advanced Medical Optics; Irvine, CA). The advantages of astigmatically neutral clear corneal incisions have allowed for increased utilization of multifocal technology in both cataract and refractive lens exchange surgery. 249

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Figure 1 The AMO Array foldable silicone multifocal intraocular lens.

C. LENS DESIGN The principle of any multifocal design is to create multiple image points behind the lens. The goal of these lenses is to enable less reduction in visual acuity for a given amount of defocus by improving the depth of field. The Array is a zonal progressive intraocular lens with five concentric zones on the anterior surface (Fig. 1). Zones 1, 3, and 5 are distance dominant zones while zones 2 and 4 are near dominant. The lens has an aspherical component and thus each zone repeats the entire refractive sequence corresponding to distance, intermediate, and near foci. This results in vision over a range of distances. The lens uses 100% of the incoming available light and is weighted for optimum light distribution. With typical pupil sizes, approximately half of the light is distributed for distance, one-third for near vision, and the remainder for intermediate vision. The lens utilizes continuous surface construction and consequently there is no loss of light through defraction and no degradation of image quality as a result of surface discontinuities. The lens has a foldable silicone optic that is 6.0 mm in diameter, with haptics made of polymethylmethacrylate and a haptic diameter of 13 mm. The lens can be inserted through a clear corneal or scleral tunnel incision that is 2.8 mm wide, utilizing the Unfolder injector system (Advanced Medical Optics; Irvine, CA).

D. CLINICAL RESULTS The efficacy of multifocal technology has been documented in many clinical studies. Early studies of the one-piece Array documented a larger percentage of patients who were able to read J2 print after undergoing multifocal lens implantation compared to patients with monofocal implants (13–15). Similar results have been documented for the foldable Array (16). Clinical trials comparing multifocal to monofocal lens implantation in the same patient also revealed improved intermediate and near vision in the multifocal eye versus the monofocal eye (17,18).

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Many studies have evaluated both the objective and subjective qualities of contrast sensitivity, stereoacuity, glare disability, and photic phenomena following implantation of multifocal IOLs. Refractive multifocal IOLs, such as the Array, were found to be superior to diffractive multifocal IOLs by demonstrating better contrast sensitivity and less glare disability (19). The Array does produce a small amount of contrast sensitivity loss equivalent to the loss of one line of visual acuity at the 11% contrast level using Regan contrast sensitivity charts (14). This loss of contrast sensitivity at low levels is only present when the Array is placed monocularly; it has not been demonstrated with bilateral placement and binocular testing (20). In addition to relatively normal contrast sensitivity, good random-dot stereopsis and less distance and near aniseikonia were present in bilateral versus unilateral implants (21). One of the potential drawbacks of the Array lens has been the potential for an appreciation of halos around point sources of light at night in the early weeks and months following surgery (22). Most patients will learn to disregard these halos with time, and bilateral implantation appears to improve these subjective symptoms. Concerns about the visual function of patients at night have been allayed by a driving simulation study in which bilateral Array multifocal patients performed only slightly worse than patients with bilateral monofocal IOLs. The results indicated no consistent difference in driving performance and safety between the two groups (23). In a study by Javitt et al., 41% percent of bilateral Array subjects were found never to require spectacles, compared to 11.7% of monofocal controls. Overall, subjects with bilateral Array IOLs reported better overall vision, less limitation in visual function, and less use of spectacles than monofocal controls (24). A small recent study reviewed the clinical results of bilaterally implanted Array multifocal lens implants in refractive lens exchange patients (25). A total of 68 eyes were evaluated, comprising 32 bilateral and 4 unilateral Array implantations. Of patients undergoing bilateral refractive lens exchange, 100% achieved binocular visual acuity of 20/40 and J5 or better measured 1 to 3 months postoperatively. Over 90% achieved uncorrected binocular visual acuity of 20/30 and J4 or better, and nearly 60% achieved uncorrected binocular visual acuity of 20/25 and J3 or better (Fig. 2). This study included patients

Figure 2 Clinical results of bilateral Array implantation following refractive lens exchange.

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Figure 3 Scattergram demonstrating reduction of spherical equivalent in refractive lens exchange eyes.

with preoperative spherical equivalents between 7 D of myopia and 7 D of hyperopia, with the majority of patients having preoperative spherical equivalents between plano and Ⳮ2.50. Excellent lens power determinations and refractive results were achieved (Fig. 3). E. PATIENT SELECTION Specific guidelines with respect to the selection of candidates and surgical strategies that enhance outcomes with this IOL have been developed. AMO recommends using the Array multifocal IOL for bilateral cataract patients whose surgery is uncomplicated and whose personality is such that they are not likely to fixate on the presence of minor visual aberrations such as halos around lights. There is obviously a broad range of patients who would be acceptable candidates. Relative or absolute contraindications include the presence of ocular pathologies other than cataracts that may degrade image formation or may be associated with less than adequate visual function postoperatively despite visual improvement following surgery. Pre-existing ocular pathologies that are frequently looked upon as contraindications include age-related macular degeneration, uncontrolled diabetes or diabetic retinopathy, uncontrolled glaucoma, recurrent inflammatory eye disease, retinal detachment risk, and corneal disease or previous refractive surgery in the form of radial keratotomy, photorefractive keratectomy, or laser-assisted in situ keratomileusis (LASIK). However, a recent study has revealed comparable distance acuity outcomes in Array and

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monofocal patients with concurrent eye disease such as macular degeneration, glaucoma, and diabetic retinopathy (26). Utilization of these lenses in patients who complain excessively, are highly introspective and fussy, or obsess over body image and symptoms should be avoided. In addition, conservative use of this lens is recommended in evaluating patients whose occupations involve frequent night driving or that place high demands on vision and near work, such as engineering and architecture. Such patients must demonstrate a strong desire for relative spectacle independence in order to be considered for a refractive lens exchange with Array implantation. In our practice, patient selection has been reduced to a very rapid process. Once someone has been determined to be a candidate for refractive lens exchange, he or she is asked two questions: the first is “If an implant could be placed in your eye that would allow you to see both distance and near without glasses under most circumstances, would that be an advantage?” Patients are then asked: “If the lens is associated with halos around lights at night, would it still be an advantage?” If they do not think they would be bothered by these symptoms, they receive a multifocal IOL. If concern over halos or night driving is strong, these patients may receive monofocal lenses with appropriate informed consent regarding loss of accommodation and the need for reading glasses or consideration of a different refractive surgical procedure. Prior to receiving an Array, all candidates should be informed of the lens statistics to ensure that they understand that spectacle independence is not guaranteed. Approximately 41% of the patients who are implanted with bilateral Array IOLs will never need to wear glasses, 50% wear glasses on a limited basis as for driving at night or during prolonged reading, 12% will always need to wear glasses for near work, and approximately 8% will need to wear spectacles on a full-time basis for distance and near correction (23). In addition, 15% of patients were found to have difficulty with halos at night and 11% had difficulty with glare, compared to 6% and 1% respectively of monofocal patients.

F. PREOPERATIVE MEASUREMENTS The most important assessment of successful multifocal lens use other then patient selection involves precise preoperative measurements of axial length in addition to accurate lens power calculations. There are some practitioners who feel that immersion biometry is necessary for accurate axial length determination. However, applanation techniques in combination with the Holladay 2 formula yield accurate and consistent results with greater patient convenience and less technician time. A newer device now available, the Zeiss IOLMaster, is a combined biometry instrument for noncontact optical measurements of axial length, corneal curvature, and anterior chamber depth that yields extremely accurate and efficient measurements with minimal patient inconvenience. The axial length measurement is based on an interference-optical method termed partial coherence interferometry and measurements are claimed to be compatible with acoustic immersion measurements and accurate to within 30 ␮m. The Quantel Axis II immersion biometry unit is also a convenient and accurate device for axial length measurements. The device yields quick and precise axial length measurements using immersion biometry without requiring the patient to be placed in the supine position. Regardless of the technique being used to measure axial length, it is important that the surgeon use biometry that he or she feels yields the most consistent and accurate results.

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When determining lens power calculations, the Holladay 2 formula takes into account disparities in anterior segment and axial lengths by adding the white-to-white corneal diameter and lens thickness into the formula. Addition of these variables helps predict the exact position of the IOL in the eye and has improved refractive predictability. The SRK T and the SRK II formulas can be used as a final check in the lens power assessment; for eyes with less than 22 mm in axial length, the Hoffer Q formula should be utilized for comparative purposes. G. SURGICAL TECHNIQUE The multifocal Array works best when the final postop refraction has less than 1 D of astigmatism. It is thus very important that incision construction be appropriate with respect to size and location. A clear corneal incision at the temporal periphery that is 3 mm or less in width and 2 mm long is highly recommended (29). Each surgeon should be aware of his or her usual amount of surgically induced astigmatism by vector analysis. In preparation for phacoemulsification, the capsulorhexis must be round in shape and sized so that there is a small margin of anterior capsule overlapping the optic circumferentially (Fig. 4). This is important in order to guarantee in-the-bag placement of the IOL and prevent anterior/posterior alterations in location that would affect the final refractive status. Minimally invasive surgery is very important. Techniques that produce effective phacoemulsification times of less than 20 s and average phacoemulsification powers of 10% or less are highly advantageous and can best be achieved with power modulations (burst mode or two pulses per second) rather than continuous phacoemulsification modes (33,34). The Array is inserted most easily by means of the Unfolder injector system. Complete removal of all viscoelastic from the anterior chamber and behind the lens will reduce the incidence of postoperative pressure spikes and myopic shift from capsular block syndrome.

Figure 4 The Array multifocal intraocular lens in situ. Note the capsulorhexis overlapping the edge of the lens optic.

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H. COMPLICATIONS MANAGEMENT When intraoperative complications develop, they must be handled precisely and appropriately. In situations in which the first eye has already had an Array implanted, management of complications must be directed toward finding any possible way of implanting an Array in the second eye. Under most circumstances, capsular rupture will still allow for implantation of an Array as long as there is an intact capsulorhexis. Under these circumstances, the lens haptics are implanted in the sulcus and the optic is prolapsed posteriorly through the anterior capsulorhexis. It is important to avoid trauma to the iris since pupillary size and shape may affect the visual function of a multifocal IOL postoperatively. If the pupil is less than 2.5 mm, there may be an impairment of near visual acuity due to the location of the rings serving near visual acuity. For patients with small postoperative pupil diameters affecting near vision, a mydriatic pupilloplasty can be performed successfully with the Argon laser (35). Enlargement of the pupil will expose the near dominant rings of the multifocal IOL and restore near vision in most patients. I. TARGETING EMMETROPIA The most important skill to master in the refractive lens exchange patient is the ultimate achievement of emmetropia. Emmetropia can be achieved successfully with accurate intraocular lens power calculations and adjunctive modalities for eliminating astigmatism. With the trend toward smaller astigmatically neutral clear corneal incisions, it is now possible to address pre-existing astigmatism more accurately at the time of lens surgery. The popularization of limbal relaxing incisions by Gills and Nichamin has added a useful means of reducing up to 3.50 diopters of pre-existing astigmatism by placing paired 600-␮mdeep incisions at the limbus in the steep meridian. When against-the-rule astigmatism is present, the temporal groove of the paired limbal relaxing incisions can be utilized as the site of entry for the clear corneal incision. This is a simple and practical approach for reducing pre-existing astigmatism at the time of surgery, and since the coupling of these incisions is one to one, no alteration in the calculated lens power is needed. J. REFRACTIVE SURPRISE On occasion, surgeons may be presented with an unexpected refractive surprise following surgery. These miscalculations in lens power can be disappointing to both the surgeon and patient, but happily the means for correcting these refractive errors are increasing. When there is a gross error in the lens inserted, the best approach is to perform a lens exchange as soon as possible. When smaller errors are encountered or lens exchange is felt to be unsafe, various adjunctive procedures are available to address these refractive surprises. One of the simplest techniques to address residual myopia following surgery is a two-, three-, or four-cut radial keratotomy (RK) with a large optical zone. RK is still a relatively safe procedure with little likelihood for significant hyperopic shift with conservative incision and optical zone placement. When residual hyperopia is present following cataract surgery, conductive keratoplasty (Refractec) is an option for reducing hyperopia and appears to work best in older patients and in patients with 1 to 2 D of refractive error. Another option for reducing 0.5 to 1.0 D of hyperopia involves rotating the IOL out of

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the capsular bag and placing it in the ciliary sulcus to increase the functional power of the lens. LASIK can also be performed to eliminate myopia, hyperopia, or astigmatism following surgery complicated by unexpected refractive results. An interesting and simple intraocular approach to the postoperative refractive surprise involves the use of intraocular lenses placed in the sulcus over the primary IOL in a piggyback fashion. Staar Surgical now produces the AQ5010V foldable silicone IOL that is useful for sulcus placement as a secondary piggyback lens. The Staar AQ5010V has an overall length of 14.0 mm and is available in powers between ⳮ4.0 to Ⳮ4.0 D in whole-diopter powers. Useful for smaller eyes with larger hyperopic postoperative errors is the Staar AQ2010V, which is 13.5 mm in overall length and is available in powers between Ⳮ5.0 to Ⳮ9.0 diopters in whole-diopter steps. This approach is especially useful when expensive refractive lasers are not available or when corneal surgery is not feasible.

K. POSTOPERATIVE COURSE If glasses are required after surgery in a patient implanted with a multifocal IOL, the spherical correction should be determined by overplusing the patient to a slight blur and gradually reducing the power until the best acuity is reached. Patients are able to focus through the near portions of their IOL; thus it is possible to overminus a patient if care is not taken to push the plus power. When using this defocusing technique, it is critical to stop as soon as distance acuity is maximized to avoid overminusing the patient. The cylinder power should be the smallest amount that provides the best acuity. If add power is necessary, the full add power for the required working distance should be prescribed. If patients are unduly bothered by photic phenomena such as halos and glare, these symptoms can be alleviated by various techniques. Weak pilocarpine at a concentration of 1/8% or weaker will constrict the pupil to a diameter that will usually lessen the severity of halos without significantly affecting near visual acuity. Similarly, brimonidine tartrate ophthalmic solution 0.2% (Alphagan) has been shown to reduce pupil size under scotopic conditions (36) and can also be administered in an attempt to reduce halo and glare symptoms. Another approach involves the use of overminused spectacles in order to push the secondary focal point behind the retina and thus lessen the effect of image blur from multiple images in front of the retina. Polarized lenses have also been found to be helpful in reducing photic phenomena. Perhaps the most important technique is the implantation of bilateral Array lenses as close in time as possible in order to give patients the ability to use the lenses together, which appears to allow for improved binocular distance and near vision compared to monocular acuity. Finally, most patients report that halos improve or disappear with the passage of several weeks to months.

L. FINAL COMMENTS As this procedure becomes more popular, it will create a win-win situation for all involved. First, patients can enjoy a predictable refractive procedure with rapid recovery that can address all types and severities of refractive errors in addition to addressing presbyopia with multifocal or accommodative lens technology. Second, surgeons can offer these procedures without the intrusion of private or government insurance and establish a less disruptive relationship with their patients. Finally, government can enjoy the decreased financial burden from the expenses of cataract surgery for the ever-increasing ranks of aging baby

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boomers as more and more of these patients opt for lens exchanges to address their refractive surgery goals, ultimately reaching Medicare coverage as pseudophakes. Successful integration of refractive lens exchanges into the general ophthalmologist’s practice is fairly straightforward, since most surgeons are currently performing smallincision cataract surgery for their cataract patients. Essentially, the same procedure is performed for a refractive lens exchange, differing only in removal of a relatively clear crystalline lens and simple adjunctive techniques for reducing corneal astigmatism. Although any style of foldable IOL can be used for lens exchanges, multifocal IOLs currently offer the best option for addressing both the elimination of refractive errors and presbyopia. Refractive lens exchange with multifocal lens technology is not for every patient considering refractive surgery but does offer substantial benefits, especially in high hyperopes, presbyopes, and patients with borderline or soon to be clinically significant cataracts who are requesting refractive surgery. Appropriate patient screening, accurate biometry and lens power calculations, and meticulous surgical technique will allow surgeons to maximize their success with this procedure.

REFERENCES 1. Colin J, Robinet A. Clear lensectomy and implantation of low-power posterior chamber intraocular lens for the correction of high myopia. Ophthalmology 1994; 101:107–112. 2. Siganos DS, Pallikaris IG. Clear lensectomy and intraocular lens implantation for hyperopia from Ⳮ7 to Ⳮ14 diopters. J Refract Surg 1998; 14:105–113. 3. Pucci V, Morselli S, Romanelli F, Pignatto S, Scandellari F, Bellucci R. Clear lens phacoemulsification for correction of high myopia. J Cataract Refract Surg 2001; 27:896–900. 4. Ge J, Arellano A, Salz J. Surgical correction of hyperopia: clear lens extraction and laser correction. Ophthalmol Clin North Am 2001; 14:301–313. 5. Fine IH, Hoffman RS, Packer P. Clear-lens extraction with multifocal lens implantation. Int Ophthalmol Clin 2001; 41:113–121. 6. Pop M, Payette Y, Amyot M. Clear lens extraction with intraocular lens followed by photorefractive keratectomy or laser in situ keratomileusis. Ophthalmology 2000; 107:1776–1781. 7. Kolahdouz-Isfahani AH, Rostamian K, Wallace D, Salz JJ. Clear lens extraction with intraocular lens implantation for hyperopia. J Refract Surg 1999; 15:316–323. 8. Jimenez-Alfaro I, Miguelez S, Bueno JL, Puy P. Clear lens extraction and implantation of negative-power posterior chamber intraocular lenses to correct extreme myopia. J Cataract Refract Surg 1998; 24:1310–1316. 9. Lyle WA, Jin GJ. Clear lens extraction to correct hyperopia. J Cataract Refract Surg 1997; 23:1051–1056. 10. Lee KH, Lee JH. Long-term results of clear lens extraction for severe myopia. J Cataract Refract Surg 1996; 22:1411–1415. 11. Gris O, Guell JL, Manero F, Muller A. Clear lens extraction to correct high myopia. J Cataract Refract Surg 1996; 22:686–689. 12. Lyle WA, Jin GJ. Clear lens extraction for the correction of high refractive error. J Cataract Refract Surg 1994; 20:273–276. 13. Percival SPB, Setty SS. Prospectively randomized trial comparing the pseudoaccommodation of the AMO Array multifocal lens and a monofocal lens. J Cataract Refract Surg 1993; 19: 26–31. 14. Steinert RF, Post CT, Brint SF, Fritch CD, Hall DL, Wilder LW, Fine IH, Lichtenstein SB, Masket S, Casebeer C. A progressive, randomized, double-masked comparison of a zonalprogressive multifocal intraocular lens and a monofocal intraocular lens. Ophthalmology 1992; 99:853–861.

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15. Negishi K, Nagamoto T, Hara E, Kurosaka D, Bissen-Miyajima H. Clinical evaluation of a five-zone refractive multifocal intraocular lens. J Cataract Refract Surg 1996; 22:110–115. 16. Brydon KW, Tokarewicz AC, Nichols BD. AMO Array multifocal lens versus monofocal correction in cataract surgery. J Cataract Refract Surg 2000; 26:96–100. 17. Vaquero-Ruano M, Encinas JL, Millan I, Hijos M, Cajigal C. AMO Array multifocal versus monofocal intraocular lenses: Long-term follow-up. J Cataract Refract Surg 1998; 24:118–123. 18. Steinert RF, Aker BL, Trentacost DJ, Smith PJ, Tarantino N. A prospective study of the AMO Array zonal-progressive multifocal silicone intraocular lens and a monofocal intraocular lens. Ophthalmology 1999; 106:1243–1255. 19. Pieh S, Weghaupt H, Skorpik C. Contrast sensitivity and glare disability with diffractive and refractive multifocal intraocular lenses. J Cataract Refract Surg 1998; 24:659–662. 20. Arens B, Freudenthaler N, Quentin CD. Binocular function after bilateral implantation of monofocal and refractive multifocal intraocular lenses. J Cataract Refract Surg 1999; 25: 399–404. 21. Haring G, Gronemeyer A, Hedderich J, de Decker W. Stereoacuity and aniseikonia after unilateral and bilateral implantation of the Array refractive multifocal intraocular lens. J Cataract Refract Surg 1999; 25:1151–1156. 22. Dick HB, Krummenauer F, Schwenn O, Krist R, Pfeiffer N. Objective and subjective evaluation of photic phenomena after monofocal and multifocal intraocular lens implantation. Ophthalmology 1999; 106:1878–1886. 23. Featherstone KA, Bloomfield JR, Lang AJ, Miller-Meeks MJ, Woodworth G, Steinert RF. Driving simulation study: bilateral Array multifocal versus bilateral AMO monofocal intraocular lenses. J Cataract Refract Surg 1999; 25:1254–1262. 24. Javitt JC, Wang F, Trentacost DJ, Rowe M, Tarantino N. Outcomes of cataract extraction with multifocal intraocular lens implantation—Functional status and quality of life. Ophthalmology 1997; 104:589–599. 25. Packer M, Fine IH, Hoffman RS. Refractive lens exchange with the Array multifocal lens. J Cataract Refract Surg. 2002; 28:421–424. 26. Kamath GG, Prasas S, Danson A, Phillips RP. Visual outcome with the Array multifocal intraocular lens in patients with concurrent eye disease. J Cataract Refract Surg 2000; 26: 576–581. 27. Rodriguez A, Gutierrez E, Alvira G. Complications of clear lens extraction in axial myopia. Arch Ophthalmol 1987; 105:1522–1523. 28. Ripandelli G, Billi B, Fedeli R, Stirpe M. Retinal detachment after clear lens extraction in 41 eyes with axial myopia. Retina 1996; 16:3–6. 29. Fine IH. Corneal tunnel incision with a temporal approach. In: Fine IH, Fichman RA, Grabow HB, eds. Clear-Corneal Cataract Surgery & Topical Anesthesia. Thorofare, NJ: Slack, 1993: 5–26. 30. Gills JP, Gayton JL. Reducing pre-existing astigmatism. In: JP Gills, Cataract Surgery: The State of the Art. Thorofare, NJ: Slack, 1998:53–66. 31. Nichamin L. Refining astigmatic keratotomy during cataract surgery. Ocular Surgery News, April 15, 1993. 32. Fine IH. Cortical cleaving hydrodissection. J Cataract Refract Surg 1992; 18:508–512. 33. Fine IH. The choo-choo chop and flip phacoemulsification technique. Oper Tech Cataract Refract Surg 1998; 1,2:61–65. 34. Fine IH, Packer M, Hoffman RS. “The use of power modulations in phacoemulsification: Choo choo chop and flip phacoemulsification.” J Cataract Refract Surg 2001; 27:188–197. 35. Thomas JV. Pupilloplasty and photomydriasis. In: Belcher CD, Thomas JV, Simmons RJ, eds. Photocoagulation in Glaucoma and Anterior Segment Disease. Baltimore: Williams & Wilkins 1984; 150–157. 36. McDonald JE, El-Moatassem Kotb AM, Decker BB. Effect of brimonidine tartrate ophthalmic solution 0.2% on pupil size in normal eyes under different luminance conditions. J Cataract Refract Surg 2001; 27:560–564.

24 The Limits of Simultaneous Ametropia Correction in Phaco-Ersatz ARTHUR HO and PAUL ERICKSON The Cooperative Research Centre for Eye Research and Technology, The University of New South Wales, Sydney New South Wales, Australia FABRICE MANNS Bascom Palmer Eye Institute, University of Miami Medical School, Miami, and University of Miami College of Engineering, Coral Gables, Florida, U.S.A. VIVIANA FERNANDEZ Bascom Palmer Eye Institute, University of Miami Medical School, Miami, Florida, U.S.A. JEAN-MARIE PAREL Bascom Palmer Eye Institute, University of Miami Medical School, Miami, University of Miami College of Engineering, Coral Gables, Florida, U.S.A., and University of Liege, CHU Sart-Tilman Liege, Belgium

A. INTRODUCTION To the eye-care practitioner, the importance of presbyopia as a major concern need not be emphasized. Currently, in the United States alone, 35% of the population of 278 million (1) is presbyopic and therefore requires some form of optical aid for near vision. Further, the number of presbyopes is increasing. Statistics from the U.S. Census Bureau predict that over the next decade, the number of people over 45 years of age will increase by approximately 21 million, but the population under 45 years will remain relatively unchanged.* This trend for an increasing representation of the over-45 age group in the popula* U.S. Census Bureau, International Database, May, 2000. The projected population of the United States in the year 2010 is 300 million, on increase of 22 million from the figure for year 2001. Of this increase, the (presbyopic) age group above 45 years age will account for approximately 21 million (1).

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tion is occurring throughout the developed countries. Therefore, increasing emphasis will be placed on the provision of near vision aids to this sector of the world’s population. 1. Background to Presbyopia Restoration Unfortunately, currently available devices for near vision assistance—which we may call the “conventional” presbyopia options—suffer from a number of optical and practical disadvantages. Devices such as bifocal spectacles, diffractive intraocular lenses (IOLs), and monovision compromise the position of gaze, field of view, image contrast, or stereopsis because of the method by which they provide near focusing power. More critically, these conventional options do not recreate the continuous focusing ability of the natural young eye. Of the conventional options available, the progressive aspheric spectacle lens (PAL) most closely approaches the ideal of providing continuous near focal distance. However, the continuous focus facility of PALs compromises the position of gaze and field of view within which the required power may be used and introduces often significant optical distortions due to the need to employ sophisticated aspheric surfaces in the design (2,3). Clearly, none of the conventional options can provide a continuous near focus, full aperture, and field optical system for the presbyope. Given the deficiencies of the conventional options, many workers have been engaged in the development of strategies seeking to truly restore accommodative function to the presbyopic eye (4–8). 2. Phaco-Ersatz The strategy of Phaco-Ersatz (4,7,9–11) is to restore accommodation to the presbyopic eye. In this method (Fig. 1), the contents of the presbyopic crystalline lens is extracted

Figure 1 The procedure of Phaco-Ersatz for restoring accommodation. (A) A corneal incision is made followed by a very small diameter (⬃1 mm) capsulorhexis. The lens nucleus, cortex, and epithelial cells are extracted through the minicapsulorhexis, leaving an intact lens capsule (B). Using a fine cannula, a polymer gel with the appropriate properties is injected into the lens capsule (C), reproducing a soft, flexible de novo lens (D). The two controllable variables in this approach, which forms the basis of the strategies discussed in this chapter, are the refractive index of the polymer gel and the refilled volume of the de novo lens.

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through a small (around 1 mm in diameter) capsulorhexis and is replaced with a soft polymer gel that is injected into the intact lens capsule. Accommodation is restored by replacing the hardened lens with a polymer gel that recreates the flexibility of the young lens. Phaco-Ersatz can restore up to 4 D of accommodation in the senile nonhuman primate when a silicone gel is used as the lens refillant (9,10). The most recent developments have refined Phaco-Ersatz by using more sophisticated polymer gels that do not leak out of the capsule and by improving the delivery of the surgery (11–14). Modern Phaco-Ersatz has reached a sufficiently advanced stage that our attention may now be extended to address other patient-related issues. Certainly with the PhacoErsatz method, it is possible for the patient to employ any of the conventional options for correcting static refractive error such as spectacles and contact lenses. However, patients strongly prefer to avoid any form of ophthalmic appliance. This is evident by the increasing development in and popularity of refractive surgery. Hence, an ability to simultaneously correct refractive error while restoring accommodation would significantly enhance the attractiveness and acceptability of any such procedure for presbyopia correction. 3. Simultaneous Correction of Ametropia Surgical vision correction options such as radial keratotomy (RK), photo-refractive keratectomy (PRK), laser-assisted in situ keratomileusis (LASIK), keratoprostheses (e.g., corneal inlays) and phakic IOLs may also be used with Phaco-Ersatz. Together, these would restore accommodation as well as correct the ametropic patient. However, there are advantages in providing a Phaco-Ersatz procedure that can, by itself, simultaneously correct ametropia. For example, there would be reduced risk because only one instead of two surgical procedures is required. Further, the disadvantages [e.g., postsurgical corneal haze and discomfort in PRK and LASIK (15,16)] of some of the aforementioned vision correction options may be obviated. The purpose of this chapter is to investigate the feasibility of strategies intrinsic to the Phaco-Ersatz procedure that could simultaneously correct ametropia while restoring accommodation. 4. Two Intrinsic Approaches As the Phaco-Ersatz procedure can principally modify the crystalline lens physical parameters, we are limited to two intrinsic strategies by which ametropia may be corrected simultaneously: 1. controlling the refractive index of the refillant 2. controlling the refilled volume of the de novo lens The first strategy relies on controlling the power of the de novo lens by increasing or decreasing the refractive index of the polymer gel used for refilling. Assuming that the other properties such as curvature and thickness are not altered, this strategy is conceptually relatively straightforward. Using a polymer gel with a lower refractive index would reduce the power of the crystalline lens, thereby reducing the power of the total eye. This could be used to correct myopia. Conversely, polymer gel with a higher refractive index would increase the power of the eye and be useful for correcting hypermetropia. The implementation of this first strategy requires polymer gels with a range of refractive indices to be synthesised and made available for Phaco-Ersatz. During the opera-

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tion, the surgeon would choose a polymer gel with an appropriate refractive index for the correction of the patient’s particular amount of ametropia. The second strategy involves altering the volume of the de novo lens with a view to altering the anterior and posterior curvatures and thickness. By doing so, the power of the crystalline lens and hence the total power of the eye can also be altered. This second strategy can be implemented in two ways. Firstly the refractive error of the patient could be measured prior to operation and the appropriate volume for refilling calculated and used. Alternatively, an in-line refractometer could be used to monitor the refractive state of the eye during refilling to provide an endpoint indication to the surgeon when the correct volume has been reached. Given the simplicity of these strategies, their applicability and feasibility is worthy of evaluation. While the concepts relating to these two strategies are relatively simple, there are numerous difficulties that render the evaluation of the feasibility of these strategies impractical by physical in-surgery means. For instance, in order to evaluate the feasibility of controlling refractive index of the refillant, a range of polymers would need to be synthesized first. Even then, extraneous factors, such as the mechanical properties of the range of polymer gels, would need to be controlled in order to return valid results. With these constraints, analyses by theoretical modeling provide a good, workable, first approximation as an alternative to evaluation of the feasibility of these strategies. In the remainder of this chapter, we endeavor to evaluate, by computer-assisted modeling, the feasibility of controlling refractive index and controlling refilled volume as strategies for the simultaneous correction of ametropia with Phaco-Ersatz. 5. Controlling Refractive Index As mentioned, this strategy involves the management of the refractive status (or “error”) of the eye through controlling the power of the de novo lens by controlling its refractive index. A hint as to the feasibility of this strategy came from early studies in lens refilling that coincidentally made use of materials of a low refractive index. In those studies, the eye with de novo lenses with low refractive index were found to be hypermetropic (17). However, altering the refractive index of the lens has an accompanying effect on the amplitude of accommodation. Hence, while ametropia may be correctable by controlling the refractive index of the refillant, it is equally important to ensure that the resultant amplitude of accommodation is sufficient for near work. Therefore, any analysis of the feasibility of this strategy must take into account the range of ametropia that is correctable as well as the impact on the amplitude of accommodation. We reported on such a study (18) in which the feasibility of simultaneous correction of ametropia with Phaco-Ersatz through controlling the refractive index of the polymer gel was analyzed by theoretical modeling (Fig. 3). We analyzed a paraxial [Gullstrand no 1 Schematic Eye (19)] and a finite aspheric eye [Navarro aspheric model eye (20)] using paraxial optical equations and computerassisted optical ray tracing (Zemax version 9, Focus Software Incorporated, AZ) respectively. Both refractive and axial refractive ametropia were analyzed. In each case, the refractive index of the gel varied between 1.34 and 1.49. A backward ray trace (from retina to air) was conducted to find the corresponding far point of the eye. The accommodation state of the model eye was then set to a nominal value of 10 D and the backward ray

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trace repeated to find the near point. The amount of correctable ametropia was obtained from the first ray trace. The difference in results between the second and first ray trace yields the associated amplitude of accommodation.

B. RESULTS 1. Refractive Error Correction Using the Gullstrand model eye and a refractive index range of 1.34 to 1.49 for the refillant, the range of correctable refractive ametropia is between ⳮ11.0 D and Ⳮ14.6 D, and ⳮ12.6 D and Ⳮ12.4 D for refractive and axial ametropia, respectively (Fig. 2). For the Navarro eye, this range is between ⳮ12.4 D and Ⳮ12.2 D, and ⳮ14.6 D and Ⳮ10.9 D for refractive and axial ametropia, respectively. 2. Amplitude of Accommodation When the refractive index of the refillant ranges from 1.34 to 1.49, the amplitude of accommodation ranges from near zero to 14.6 D and 13.4 D for refractive and axial

Figure 2 Refractive and axial ametropia correctable by varying the refractive index of the polymer gel in Phaco-Ersatz for two model eyes. Interpolation of the Gullstrand results indicates that the lens cortex and nucleus may be replaced by an equivalent single uniform refractive index of 1.409 to achieve emmetropia. (From Ref. 18.)

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hypermetropia, respectively, with the Gullstrand eye model, and to 9.7 D and 8.9 D for refractive and axial hypermetropia, respectively, with the Navarro model. The nominal state of accommodation was equivalent to 10 D in all cases. 3. Discussion It should be noted that the reported theoretical analysis (18) is based on a key assumption that the shape of the refilled lens does not differ significantly from the original natural lens. This assumption is probably reasonable given that the shape of the young lens is determined largely by the properties of the capsule (21,22). Thus, provided the mechanical properties of the polymer gel refillant closely mimic those of the young natural lens, large departures from the natural shape are presumed to be unlikely (Fig. 3). The implications of controlling the refractive index of the refillant on correction of ametropia and amplitude of accommodation is shown by combining the data from Figs. 2 and 3 (Fig. 4). The amplitude of accommodation progressively decreases as we attempt to correct higher amounts of myopia. In the limiting case, the correction of a ⳮ12 D myope would result in virtually no accommodation being available. At this point, the refractive index of the refillant is almost identical to that of the surrounding ocular media and hence, the de novo lens has near zero power and consequently is also incapable of providing accommodative power.

Figure 3 Amplitude of accommodation resulting from varying the refractive index of the polymer gel in Phaco-Ersatz for two model eyes and ametropia types. (From Ref. 18.)

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Figure 4 Relationship between the amplitude of accommodation and the amount of ametropia that was correctable for two model eyes and ametropia types. (From Ref. 40.)

A practical limit to the range of ametropia that is correctable may be derived by assuming a required minimum amplitude for accommodation. For example, if a standard near work distance of 40 cm is adopted and assuming that an additional 50% of accommodative amplitude is required in reserve at all times for comfortable, prolonged reading (23), we set the acceptable minimum amplitude of accommodation at around 5 D. With this value, Figure 4 indicates that, for the Gullstrand model eye, myopia greater than ⳮ2.5 D should not be corrected by reducing the refractive index of the refillant. According to the Navarro model, no corrections for myopia are acceptable with the assumed requirements. In addition to the limitation on myopic corrections, the following practical issues may also impact the feasibility of this strategy. These issues are as follows: The need for a series of polymer gels with a large range of refractive indexes to be available for Phaco-Ersatz. The synthesis of such a range of polymers with similar mechanical properties and biocompatibility factors poses a daunting technical challenge to polymer developers. The accuracy required for correction of ametropia to an accuracy of Ⳳ0.125 D would require the refractive index to be controlled to an accuracy of Ⳳ0.0008. This accuracy needs to be maintained over its working life despite potential changes in hydration and fouling. Correction of ametropia with this strategy is limited to spherical refractive errors. Astigmatic correction is not feasible.

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Figure 5 Geometrical definitions of the two models for under- and overfilling of the crystalline lens. (A) Model 1 describes the “spherization” model. The “normal” lens is defined by an ellipsoid of revolution with major and minor axes a and b (see Table 1). When the lens is under- or overfilled, its major and minor axes are defined by a′ and b′. A scaling factor is used to determine a′ and b′ from a and b [Eq. (2a) and (2b)]. With this set of equations for defining a′ and b′, the effect is that as the lens volume changes, there is a more rapid accompanying change in the curvature of the anterior than the posterior lens surface. (B) Model 2 describes the “proportional expansion” model. In this model, a′ and b′ are set by a scaling factor according to Eqs. (3a) to (3c). This model provides for a more rapid accompanying change in the posterior curvature of the lens surface as lens volume changes. Note that the scaling factor [s in Eqs. (2a), (2b), (3b), and (3c)] is used only as a parameter for computation. The relationship between this scaling factor and lens volume is different for the two models.

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Figure 6 The relationship between the equivalent power of the crystalline lens and its thickness, with lens volume according to Models 1 and 2.

Correction of anisometropia is also not feasible, as such an attempt would result in anisoaccommodation. Further, the result at near is an induced anisometropia of the opposite sign to the original state of anisometropia. A further issue relates to ocular aberrations. There is evidence (24–26) that the spherical aberration of the eye changes over the range of accommodation (Figure 5). It has been postulated that this change in spherical aberration with accommodation is an effect of the refractive index gradient of the crystalline lens (27) (Fig. 6). When this gradient is replaced by a uniform refractive index, ocular aberration during near work with the de novo lens would differ from the natural lens and may affect near visual performance (Fig. 7). Conversely, the greater positive aberration might increase depth of focus and reduce the accommodative demand and, more significantly, permit greater tolerance in the accuracy of ametropia correction. While a number of limitations have been presented above with respect to the strategy under discussion, it should be noted that a few of these (e.g., requirement of accuracy of refractive index) apply not just to controlling refractive index within Phaco-Ersatz but also to any nonaccommodating polymer-based intracapsular ametropia correction devices (e.g., injectable IOLs) as well (Fig. 8). 4. Summary While conceptually attractive, it is clear from the foregoing findings and the number of potential implementation difficulties that significant challenges will face any attempt to introduce this strategy as a method for correcting ametropia within Phaco-Ersatz.

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Figure 7 Refractive and axial ametropia correctable by controlling the refilled volumed of the crystalline lens in Phaco-Ersatz according to models 1 and 2 using the modified Navarro eye.

Figure 8 Axial positions of the anterior cornea, anterior and posterior crystalline lens surfaces and the lens equator and retina as a function of lens volume for refractive and axial ametropia within models 1 and 2. The anterior cornea is located at the x⳱0 axial position. Note the extreme shallowness of the anterior chamber and great lens thickness associated with the correction of high amounts of hypermetropia.

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3. Controlling Refilled Volume In this section, we evaluate the feasibility of the second strategy for simultaneous correction of ametropia within Phaco-Ersatz. With this strategy, the interaction of the mechanical and geometrical properties of the lens and capsule, as well as the influence of the vitreous on lens position and potentially the shape of the lens, creates a more complex system. A number of these parameters are unknown, as they have not been measured to any acceptable level of accuracy in the living eye. For example, it is not known how the vitreous influences lens position and shape. Even more basic parameters, such as the shape of the crystalline lens at various levels of accommodation, have not been measured in a systematic manner.* Due to the lack of detailed, quantitative knowledge about many of the influencing parameters, any theoretical model of this strategy must necessarily require imposition of a number of assumptions. To facilitate our modeling analysis, we adopted the following assumptions: 1. The position and shape of the lens is not affected by the iris or vitreous regardless of the volume of refilling. 2. The position of the lens is set by its equatorial plane at all volumes of refilling and the position of the equatorial plane is fixed with respect to the eye. 4. Eye Models a. Requirements A suitable model eye for analyzing the optical effect of altering lens volume must possess the following features: 1. Accurate rendering of lens volume 2. Reasonable anatomical approximation 3. Faithful rendering of the optics of the eye The first requirement is absolute for the purpose of this study. The consequence of the second requirement is that the model lens must not only possess similar radii of curvature and thickness as the crystalline lens but that it must also have a continuous surface at the equator. Unfortunately, we have found no eye model in the literature that satisfies all of the above requirements. We therefore set out to develop an eye model for the purpose of this study by combining suitable elements from established eye and lens models. b. Modified Navarro Eye The current model is based on a modification of the Navarro aspheric eye model (20), which represents a de facto standard in finite eye models in terms of its employment and citation. The crystalline lens component of the Navarro model was replaced by a model lens, which accurately portrayed the lens volume as well as providing a reasonable approxima* Good data exist on the thickness, curvatures and optical power of a crystalline lens in the relaxed state (28,29). However, no quantitative data exist relating changes in all of these parameters with accommodation. We note that efforts are being made currently to develop measurement systems for quantifying the topography of the anterior and posterior crystalline lens surfaces at various levels of accommodation (30,31). We look forward to the availability of these data for improving the precision of our model.

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Table 1 The Prescription of the Modified Navarro Eye for Modeling the Relationship Between Refilled Lens Volume and Ametropia Correction Surface

Radius

Thickness

Index

Diameter

Q

Cornea anterior Cornea posterior Lens anterior Lens equator Lens posterior

7.72 6.50 10.20 – ⫺6.00

0.55 3.05 1.898 3.227 15.672

1.376 1.3374 1.42 1.42 1.336

– – – 8.8 –

⫺0.26 0.00 4.3740 – 0.8595

tion to the anatomical and geometrical parameters of the crystalline lens. This lens model was based on combining two half-ellipsoids of revolution, as employed by past workers (27,32). The anterior and posterior radii of curvature of the lens were the same as those of the Navarro eye. By setting the length of the major axes (perpendicular to the optical axis) of the half-ellipsoids to be identical, the continuity of the lens surface at the equator was ensured. We chose 200 ␮L as a reasonable nominal initial volume of the model lens to simulate the natural human lens (33). Given the assumed curvatures, equatorial diameter, and lens volume, the asphericity and half-thickness of each half-ellipsoid were calculated employing equations relating to the apical radius of curvature and shape factors of conic sections (34). Finally, the model eye was “emmetropized” by adjusting the vitreous chamber depth (distance between posterior lens surface and retina). The resultant prescription of the modified Navarro model eye for analysis of controlling refilled lens volume is given in Table 1. The volume of this lens model is 208 ␮L. The equatorial diameter of 8.8 mm is slightly less while the thickness of 5.12 mm is slightly greater than the respective parameters for the typical adult lens (28). However, this was necessitated by a compromise in providing reasonable optical and geometrical properties to the model. c. Refilling Model No information is available in the literature about the quantitative relationship between lens curvatures and lens volume. Hence, a validated model of the change in lens curvature with refilling is not possible at this stage. In view of this paucity of information, we developed two simple but plausible mathematical models for lens refilling. These were: 1. Model 1: “spherization” 2. Model 2: proportional expansion These two models (Fig. 5) provide contrasting relationships between lens thickness and curvature with increasing lens volume during refill. In general, Model 1 predicts that the anterior curvature and half-thickness of the lens will change more quickly than the posterior curvature and half-thickness as the lens refills during Phaco-Ersatz, while Model 2 predicts the converse. The intention of testing two such disparate models is to provide a “bracketing” of the results, such that the actual life situation might lie somewhere in between.

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Model 1: “Spherization.” This model assumes that as the lens is filled and then overfilled; it converges toward a sphere (i.e., the length of the major and minor axes at the endpoint of filling is the same). Hence, the posterior and anterior curvatures would converge with overfilling. Given that the anterior radius of curvature is greater at the “normal” volume, this model predicts that with overfilling, the anterior curvature would change more rapidly than the posterior curvature. We assumed that the lens equator expands slightly with overfilling. Model 1 is represented mathematically as follows (Fig. 5). The anterior and posterior half-lenses are represented by half-ellipsoids of revolution such that their two-dimensional cross sections may be described by x2 y2 2 Ⳮ 2 ⳱ 1 a b

(1)

where x is the distance along the optical axis y is the distance across the optical axis a is the half-length of the minor axis representing the half-thickness of the lens-half at normal volume b is the half-length of the major axis representing the half-diameter of the lens at its equator at normal volume Lens refilling according to Model 1 follows the relationship of a′ ⳱ s ⳯ (be ⳮ a) Ⳮ a b′ ⳱ s ⳯ (be ⳮ b) Ⳮ b

(2a) (2b)

where a′ is the half-thickness of the over-or underfilled half-lens. b is the half-diameter of the over-or underfilled lens. be is the radius of the endpoint sphere towards which the shape of an overfilled lens will converge. s is a scaling factor defining the amount of over-or underfilling (s ⳱ 0 is normal volume of filling, s ⬎ 0 is overfilling, and s ⬍ 0 is underfilling). Model 2: “Proportional Expansion.” Model 2 assumes that as the lens is filled and then overfilled, the posterior and anterior half-ellipsoids increase in axial dimensions (i.e., the length of the minor axis) in the same ratio. In contrast to Model 1, the posterior curvature in Model 2 would increase more rapidly than the anterior curvature as the lens overfills. As in Model 1, we assumed that the lens equator expands slightly with overfilling. Model 2 is represented mathematically as follows (Fig. 5): The anterior and posterior half-lenses are again represented by half-ellipsoids of revolution according to Eq (1). During lens refilling, Model 2 defines the following changes in lens shape: a′a ⳱ (a′p ⳯ aa)/ap a′p ⳱ s ⳯ (be ⳮ ap) Ⳮ ap b′ ⳱ s ⳯ (be ⳮ b) Ⳮ b

(3a) (3b) (3c)

where nomenclatures are as for the previous equations and subscript a ⳱ values pertaining

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to the anterior half-lens; subscript p ⳱ values for the posterior half-lens. For both models, we assumed be to be 4.9 mm. 5. COMPUTATION AND ANALYSES a. Calculation of Volume of Over-Underfilling For a lens constructed of two half-ellipsoids of revolution, the volume V can be calculated as V⳱

2 ⳯ ␲ ⳯ b2 ⳯ (aa Ⳮ ap) 3

(4)

From Eqs. (1) through (4) and assigning various values for scaling factor s, we can calculate the volume of the de novo lens at various amounts of filling. b. Calculation of Lens Power The central radius of curvature r of an ellipse is given by (34) r⳱

a b2

(5a)

and its thickness (34) d by: d ⳱ a a Ⳮ ap

(5b)

From Eqs. (1) through (3) and (5a) and (5b), the assigned refractive indices, and assigning various values for the scaling factor s, the power of the de novo lens can be calculated at various amounts of filling. c. Modeling Correctable Ametropia Armed with the calculated lens curvatures and thicknesses at different levels of lens refilling, it is now possible to calculate the associated amount of ametropia that is correctable within the two models using the modified Navarro eye model. One final variable had to be fixed—that of the position of the lens at different levels of filling. Because of the enormous complexity of the interactions between capsular tension, lens volume, vitreous influence, zonular tension and iris influence as well as the lack of precise, quantitative information in many of these factors, we assumed a simplified model in which the equatorial plane of the lens remains fixed in the axial (x) direction at all levels of filling. Under this assumption, the anterior and posterior lens surfaces would bulge forward and backward, respectively, by an amount equal to the change in the length of the minor axes of the respective half-ellipsoids. The amount of ametropia correctable was computed in two ways—assuming refractive ametropia and assuming axial ametropia. Paraxial optical equations were used in all calculations. Dioptric values of ametropia were referred to the plane of the cornea on the model eye. 6. Results Figure 6 shows the relationship between the volume of lens refilled (expressed as a percentage of a lens with normal volume) and equivalent refractive power and thickness of the resultant lens. The resultant lens thicknesses are not greatly different for Models 1 and 2.

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The refractive power of the refilled lens varied slightly more with change in refilled volume for Model 1 than for Model 2. This suggests that should lens refilling follow the shape and thickness changes predicted by Model 1, a greater amount of ametropia may be correctable. From the results shown in Fig. 6, the overall power of the eye with a refilled lens, and hence the amount of ametropia correctable, was computed. This is shown in Fig. 7, which plots the amount of ametropia that is correctable under Models 1 and 2 for both axial and refractive ametropia. The maximum ametropia that is correctable occurs using Model 1 with axial ametropia (approximately Ⳳ4 D). The minimum ametropia that is correctable occurs using Model 2 with axial ametropia. 7. Discussion a. Eye Model As noted, the geometrical dimensions of the lens model deviated from typical adult human lenses in that the equatorial diameter was slightly less and the thickness slightly higher. This compromise was necessary to enable simple ellipsoids of revolutions to be used to construct a model lens while maintaining reasonable values for the optics and geometrical parameters. A more mathematically sophisticated approach (35) has been developed to provide an anatomically precise representation of the adult human lens. However, that model employed a pair of parametric functions within a system of polar coordinates to describe the lens. Given the parametric nature of the model description, there is no direct method by which changes in volume and curvature may be modeled without a high level of mathematical complexity. Hence for convenience, we adopted the half-ellipsoids of revolution (27,32). The assumed endpoint diameter of the lens was 8.9 mm, which represents a 0.1mm increase in the diameter of a lens when overfilled to 200% (double the volume). Should this prove to be an overestimation, there would be an increase in the amount of ametropia that is correctable with controlled lens refilling due to the expected increase in curvatures. This model is able to estimate only the amount of ametropia that is correctable by controlling the refilled volume of a lens with Phaco-Ersatz. Due to a number of limitations relating to quantitative understanding of the influence of lens volume on lens shape during accommodation, it is not yet possible to study the effect of over- or underfilling on the amplitude of accommodation, as has been done for the refractive index strategy. Hence, there may be detrimental effects on the amplitude of accommodation in the application of this strategy, which are yet to be determined. The critical assumption in our lens model is that the lens capsule has a negligible effect on the change in curvature and thickness during refilling. Intuitively, this would not be the case, given that there is a difference in thickness between the anterior and posterior capsules (21,36,37), which would influence lens shape and thickness during refilling. However, we have introduced two contrasting models for refilling with the intention that the actual lens response would lie somewhere within this “bracketing.” We believe, therefore, that the robustness of the predictions within our model should be reasonable, especially considering that the two contrasting refilling models returned similar predictions. Finally, there are effects on aberrations that have not been considered. First, the gradient index of the natural lens has been eliminated by Phaco-Ersatz. This would alter

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the aberration state of the eye at both distance and, as discussed, more critically at near. Further, as the lens shape changes, it is highly likely that its surface asphericity would also change, thereby altering the aberrations at different refill volumes. These considerations are beyond the scope of the current model but merit further investigation. b. Correction of Ametropia If we accept the above assumptions and exceptions discussed, then our theoretical analysis with the eye model predicts the following: Even at the highest estimate predicted, the amount of ametropia that is correctable is too low to be practical (Model 1 and axial ametropia). Therefore controlling the refilled volume alone during Phaco-Ersatz for correcting ametropia is insufficient to correct any other than low degrees of ametropia. The reciprocal of the average slope of the four curves in Fig. 7 indicates that in order to correct ametropia with an accuracy of Ⳳ0.125 D, percentage refilling would have to be controlled to an accuracy of Ⳳ2.3%. This equates to an approximate accuracy in volume of Ⳳ5 ␮L. This may pose a technical and surgical challenge. c. Issues of Implementation There are also issues of implementation relating to this strategy. Figure 8 shows the predicted positions of the lens surfaces and retina with changes in refilled lens volume assuming a fixed position for the equatorial plane. Over the range of under-to overfilling analyzed (50 to 150%), the lens thickness changes from approximately 3.5 mm to approximately 8 mm. Even ignoring the effect of the iris and vitreous, it is certain that such a range would impose impractical values to the resultant anterior chamber depth. In particular, correction of medium to high hypermetropia would result in dangerously shallow anterior chambers. In addition to considerations of anterior chamber depth, there are other practical limits to the amount of over-and underfilling that can be achieved. The minimum amount of underfilling is set by the lowest volume that can still produce an undistorted, optically useful de novo lens. Below this limit, prism due to sagging, and distortions due to rippling, warping, or waviness as a result of a lack of sufficient capsule tension may degrade vision below acceptable limits. There is also an upper limit on the amount of overfilling. Beyond this limit, given the finite breaking strain of the capsule (38,39), rupture of the capsule would occur. While reliable data on the limits of optical imperfection with excessive underfilling and capsule rupture with excessive overfilling do not exist, a reasonable estimation may be assumed on these lower and upper limits. Experience in our laboratories, which has been conducting surgical trials of Phaco-Ersatz, suggests that a “safe” limit for over- and underfilling may be Ⳳ20% of the normal volume. Referring back to Fig. 7, introduction of this limit to the volume of refilling predicts that the range of ametropia that is correctable is significantly reduced to approximately Ⳳ2 D. This is probably not a viable range for useful correction of ametropia. In addition to the above, other implementation issues relevant to the first strategy as listed in the previous section also apply. These include a limitation in the range of correction to spherical (nonastigmatic) refractive errors.

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8. Summary Due to the complexity of the interplay between physiology, mechanics, and optics, we have been able to test only a simplified model of controlled refilling. However, even this first approximation suggests that the range of corrections achievable within this strategy would be small because of the limitations of lens thickness as well as implementation difficulties. 9. Conclusions In this chapter, we have analyzed, using theoretical modeling, the feasibility of two strategies that are intrinsic to Phaco-Ersatz for simultaneous correction of ametropia. It appears from the results and consideration of implementation issues that neither strategy on its own is sufficient or feasible for simultaneous correction of ametropia within Phaco-Ersatz. We have not investigated the feasibility of a combination of the two strategies. However, in view of the above discussions, it may be expected that those combinations would also lack sufficient range and accuracy for applicability. We therefore conclude, even in the absence of physical experimental results, that simultaneous correction using these two intrinsic strategies would be unattractive and probably not feasible. However, predictions from models are only as reliable as the assumptions made and the values for parameters assumed. We recognize that there are potential shortcomings in our theoretical analyses, which warrant further research. In particular, the lack of reliable, quantitative knowledge of relationships such as lens shape and thickness with different level of refilling—as well as the effect of the capsule thickness, vitreous, and iris on lens shape and position—merits study as well in order to refine our models. A number of studies are under way in our laboratories seeking to address such issues (13,30,31). We believe that researchers in this area should persist in their efforts to understand those relationships.

REFERENCES 1. US Census Bureau International Program Center. International Database (IDB). update May 2000. 2. Simonet P, Papineau Y, LaPointe R. Peripheral power variations in progressive addition lenses. Am J Optom Physiol Opt 1986; 63(11):873–880. 3. Sullivan C, Fowler C. Progressive addition and variable focus lenses: a review. Ophthalm Physiol Opt 1988; 8:402–414. 4. Parel J-M, Gelender H, Trefers W, Norton E. Phaco-Ersatz: cataract surgery designed to preserve accommodation. Graefes Arch Clin Exp Ophthalmol 1986; 224(2):165–173. 5. Nishi O, Hara T, Hara T, Hayashi F, Sakka Y, Iwata S. Further development of experimental techniques for refilling the lens of animal eyes with a balloon. J Cataract Refract Surg 1989; 15:584–588. 6. Hara T, Hara T, Yasuda A, Yamada Y. Accommodative intraocular lens with spring action: Part 1. Design and placement in an excised animal eye. Ophthalm Surg 1990; 21:128–133. 7. Parel JM. Phaco-Ersatz 2001: cataract surgery designed to preserve and restore accommodation. An Inst Barraquer 1991; 22:1–20. 8. Hettlich HJ, Asiyo-Vogel M. Experiments with balloon implantation into the capsular bag as an accommodative IOL. Ophthalmologe 1996; 93:73–75.

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9. Haefliger E, Parel J-M, Fantes F, Norton E, Anderson D, Forster R, Hernandez E, Feuer WJ. Accommodation of an endocapsular silicone lens (Phaco-Ersatz) in the nonhuman primate. Ophthalmology 1987; 94(4):471–477. 10. Haefliger E, Parel J-M. Accommodation of an endocapsular silicone lens (Phaco-Ersatz) in the aging rhesus monkey. J Refract Corneal Surg 1994; 10(5):550–555. 11. Parel J-M, Holden B. Accommodating intraocular lenses and lens refilling to restore accommodation (restoring accommodation). In: Azar D, ed. Intraocular Lenses in Cataract and Refractive Surgery. Philadelphia: Saunders, 2001. 12. Parel JM, Simon G. Phaco-Ersatz 2001: update. Ann Inst Barraquer 1995; 25:143–151. 13. Tahi H, Fantes F, Hamaoui M, Parel J-M. Small peripheral anterior continuous curvilinear capsulorhexis. J Cataract Refract Surg 1999; 25:744–747. 14. Tahi H, Chapon P, Parel JM, inventors; CRCERT, assignee. Mini capsulorhexis valve (MCV) for crystalline lens refilling and posterior capsule opacification (PCO) prevention procedures. United States patent US60/121,179 (US Patent Appl, 2000). PCT/US00/04339 (International Appl 2000). 15. Wilson S. LASIK: management of common complications. Laser in situ keratomileusis. Cornea 1999; 17(5):459–467. 16. Price F, Jr, Belin M, Nordan L, McDonnell P, Pop M. Epithelial haze, punctate keratopathy and induced hyperopia after photorefractive keratectomy for myopia. J Refract Surg 1999; 15(3):384–387. 17. Kessler J. Refilling the rabbit lens. Further experiments. Arch Ophthalmol 1966; 76(4): 596–598. 18. Ho A, Erickson P, Manns F, Pham T, Parel J-M. Theoretical analysis of accommodation amplitude and ametropia correction by varying refractive index in Phaco-Ersatz. Optom Vis Sci 2001; 78(6):1. 19. Gullstrand A. Appendix II: Procedure of rays in the eye. Imagery—laws of the first order. In: Southall J, ed. Helmholtz’s Treatise on Physiological Optics. 3rd ed. Optical Society of America, 1909. 20. Navarro R, Santamaria J, Bescos J. Accommodation-dependent model of the human eye with aspherics. J Opt Soc Am A 1985; 2(8):1273–1281. 21. Fincham E. The mechanism of accommodation. Br J Ophthalmol 1937; Monograph Suppl VIII:5–80. 22. Nishi O, Nishi K, Mano C, Ichihara M, Honda T. Controlling the capsular shape in lens refilling. Arch Ophthalmol 1997; 115:507–510. 23. Borish IM. Clinical Refraction, 3rd ed. Chicago: Professional Press, 1970. 24. Atchison D, Smith G. Continuous gradient index and shell models of human lens. Vis Res 1995; 35(18):2529–2538. 25. He J, Burns S, Marcos S. Monochromatic aberrations in the accommodated human eye. Vis Res 2000; 40:41–48. 26. Gray G, Campin J, Liedel K, Pettit G. Use of wavefront technology for measuring accommodation and corresponding changes in higher order aberrations. Invest Ophthalmol Vis Sci 2001; 42(4):S26. 27. Smith G, Pierscionek B, Atchison D. The optical modelling of the human lens. Ophthalm Physiol Opt 1991; 11:359–369. 28. Howcroft M, Parker J. Aspheric curvatures for the human lens. Vis Res 1977; 17:1217–1223. 29. Glasser A, Campbell M. Biometric, optical and physical changes in the isolated human crystalline lens with age in relation to presbyopia. Vis Res 1999; 39:1991–2015. 30. Hamaoui M, Manns F, Ho A, Parel J-M. Topographical analysis of ex-vivo human crystalline lens. Invest Ophthalmol Vis Sci 2000; 41(4):S428. 31. Fernandez V, Manns F, Zipper S, Sandadi S, Minhaj A, Ho A, et al. Topography of anterior and posterior crystalline lens surfaces of human eye-bank eyes. Invest Ophthalmol Vis Sci 2001; 42(4):S880.

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32. Popiolek-Masajada A. Numerical study of the influence of the shell structure of the crystalline lens on the refractive properties of the human eye. Ophthalm Physiol Opt 1999; 19(1):41–49. 33. Koretz J, Cook C, Kaufman P. Aging of the human lens: changes in lens shape at zero-diopter accommodation. J Opt Soc Am A 2001; 18(2):265–272. 34. Burek H, Douthwaite W. Axial-radial interconversion. J Br Contact Lens Assoc 1993; 16(1): 5–13. 35. Kasprzak H. New approximation for the whole profile of the human crystalline lens. Ophthalm Physiol Opt 2000; 20(1):31–43. 36. Salzmann M. Anatomy and Histology of the Human Eyeball in the Normal State: Its Development and Senescence. Chicago: University of Chicago Press; 1912. 37. Tahi H, Hamaoui M, Parel J-M. Human lens-capsule thickness: correlation with lens shape during accommodation and practical consequence for cataract surgery designed to restore accommodation. Invest Ophthalmol Vis Sci 1999; 40:S887. 38. Krag S, Andreassen T, Olsen T. Elastic Properties of the lens capsule in relation to accommodation and presbyopia. Invest Ophthalmol Vis Sci 1996; 37(3):S163. 39. Krag S. Biomechanical measurements of the lens capsule. Acta Ophthalmol Scand 1999; 77(3): 364.

25 Accommodating and Adjustable IOLs SANDEEP JAIN, DIMITRI T. AZAR, and RASIK B. VAJPAYEE Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A.

A. INTRODUCTION This chapter focuses on recent developments of accommodating and adjustable intraocular lenses (IOLs). The former group of lenses is aimed at compensating for the loss of lens accommodation after cataract surgery, whereas the latter group aims to minimize and compensate for the unpredictability of refractive outcomes after cataract surgery (1). B. ACCOMMODATING IOLs Following cataract surgery, some accommodative functions of the ciliary muscle are retained. Several ophthalmic research groups have developed aphakic IOLs that can to provide some accommodation based on the maintenance of the accommodative function of the ciliary muscle. The AT45 (C&C Vision, Aliso Viejo, CA) IOL was designed by Stuart Cumming, M.D., of Aliso Viejo (1). Khalil Hanna designed the Human Optics accommodating IOL; these lenses are placed in the capsular bag and are designed to change position once the accommodative stimulus induces ciliary muscle contraction. The success of these lenses depends on their ability to achieve high fidelity in transmitting the accommodative stimulus to the lens capsule after cataract surgery. Clinical studies with these lenses are under way, and preliminary studies are encouraging (2). 1. Description of Accommodating IOLs The accommodating AT45 lens is a conventional posterior chamber silicone lens. Its optic measures 4.5 mm in diameter. It does not have conventional plate or loop haptics but has 279

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Figure 1 New intraocular lenses from C&C are designed to move forward into the anterior chamber to accommodate much like the natural lens. (Courtesy of C&C Vision).

two flexible arms located 180 degrees apart (Fig. 1). These flexible arms allow the lens to move forward and backward in the posterior chamber on constriction and relaxation of the ciliary muscle. At the end of each arm is a T-shaped polyamide haptic that follows the curve of the capsular bag after implantation and maintains centration and stability by resting in the capsular bag. The HumanOptics designs had a modified steering wheel appearance which has been modified to allow greater accomodation. C. MULTICOMPONENT IOLs Since the advent of refractive surgery, we have been able to correct ametropia to what is achievable with spectacle and contact lens corrections. This has been especially applicable to the calculation of intraocular lens power if cataracts occur after refractive surgery. Several formulas have been used to improve the predictability of IOL calculations after

Figure 2 Intraocular lens from HumanOptics designed to move forward into the anterior chamber to accommodate, much like the natural lens. (Courtesy of HumanOptics).

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refractive surgery, but surprises are occasionally encountered. Patients who have had refractive surgery and subsequent cataract surgery demonstrate surprising hyperopic errors in IOL power determination. The ability to correct hyperopic surprises after cataract surgery in patients who have undergone previous refractive surgery would be desirable in the group of patients who are accustomed to spectacle-free vision (4). The use of adjustable or multicomponent intraocular lenses is a new concept that allows fine tuning of an already fairly accurate refractive procedure (Fig. 2). 1. Description of Multicomponent IOLs The multicomponent intraocular lens is a three-component lens consisting of a base lens and two additional refractive attachments. The base lens has a planoconvex optical, and the overall mechanical design of the lens is similar to that of currently used posterior chamber lenses. The lens is made of polymethylmethacrylate (PMMA) and consists of one piece, with a diameter of 6.0 mm and an optical aperture of 5.5 mm. The basic lens looks much like a conventional posterior chamber IOL (PCIOL). The base lens has two machined slots whose thickness is approximately 1.2 mm. These slots accept the cap lens and hold the assembly together. The base lens is placed into the posterior capsular bag permanently heals there (Fig. 3). After its implantation, it acts as a platform for the other two detachable refractive elements (3). Attached to the base lens are two additional refractive elements. The middle lens, or sandwich lens, carries the astigmatic (4.00-D sphere and 0.00 to 4.00-D diopter cylinder

Figure 3 Multicomponent IOL. (From Werblin TP. Multicomponent intraocular lens. J Refract Surg. 1996S:187–189, with permission).

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in 0.25-D increments) correction. This PMMA or silicone lens has an optical aperture of 5.5 mm. The other refractive attachment is a cap lens that has additional refractive power. This lens may be either monofocal or multifocal. This PMMA planoconvex lens has an optical clear aperture of 5.5 mm. It has a tab and two small haptics that, during the assembly, are set into slots in the base lens using a specially modified forceps. The total central thickness of a multicomponent intraocular lens is 1.88 mm for a 28.00-D lens. This is only slightly thicker than a standard silicone IOL of 20.00 D. D. LIGHT-ADJUSTED IOL This lens is also designed to help patients with cataracts who have previously undergone corneal refractive procedures, in which it is difficult to measure corneal curvature accurately for appropriate IOL calculations. Calhoun Vision has developed this lens, which may allow for noninvasive adjustment and correction of residual postimplantation refractive errors following cataract surgery by applying near-ultraviolet light to the IOL (4). The refractive power of an IOL—composed of a cross-linked silicone polymer matrix, a guest macromer, and a photoinitiator—can be adjusted. The application of the appropriate wavelength of light onto the central optical portion of the light-adjusted lens (LAL) polymerizes the macromer in the exposed region, thereby producing a difference in the chemical potential between the irradiated and nonirradiated regions. To re-establish thermodynamic equilibrium, unreacted macromer and photoinitiator diffuse into the irradiated region. As a consequence of the diffusion process and material properties of the host silicone matrix, the LAL will swell, producing a concomitant decrease in the radius of curvature of the lens and a corresponding hyperopic shift in the refractive power of the lens (Fig. 4). The process may be repeated if the surgeon wants further refractive change in the lens. The surgeon may then irradiate the entire lens, consuming the remaining, unreacted

Figure 4 Cartoon schematic illustrating the proposed mechanism of swelling. (a) Selective irradiation of the central zone of IOL polymerizes macromer, creating a chemical potential between the irradiated and nonirradiated regions; (b) to reestablish equilibrium, excess macromer diffuses into the irradiated region causing swelling; and (c) irradiation of the entire IOL “locks” the macromer and the shape change.

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macromer and photoinitiator. This action effectively locks in the refractive power of the lens (4). The surgeon may induce a myopic change by irradiating the edges of the LAL to effectively drive macromer and photoinitiator out of the lens central region, thereby increasing the radius of curvature and decreasing the power. One concern with the LAL is that after irradiation, the lens may not necessarily maintain a resolution efficiency acceptable to the patient. However, preliminary data show that this light-adjustable silicone IOL materials may provide a means to precisely and noninvasively adjust IOL power postop, after the refractive status of the eye has stabilized. E. RESULTS OF ACCOMMODATING AND MULTIFOCAL IOL IMPLANTATION Calhoun’s adjustable silicone formulations may become a platform technology useful in both pseudophakic and phakic IOLs. As additional IOLs are developed, such as the accommodating IOLs of C&C Vision and Human Optics (Erlangen, Germany), the ability to overcome imprecision in IOL power calculation by postoperative light adjustment has the potential to add value to these and other novel IOL designs (1–4). The accommodating IOL is implanted after conventional phacoemulsification surgery through a 3- or 5-mm incision. The AT45 lens is maximally positioned against the vitreous face and sealed in place with 3 weeks of atropine treatment posoperatively. At the base of the arms of lens are hinges that allow the lens to move forward, based on ciliary contraction and pressure from vitreous. Any forward movement of the lens allows for near vision, simulating natural accommodation (1,2). The early results of a phase 1 clinical trial show the lens to be safe, complicationfree, and well tolerated. The lens appeared to provide some accommodation. The lens is still in the evaluation stage and further clinical trials are in progress (2). The multicomponent lens is still in the process of development, and results of clinical trials are awaited. The multicomponent lens has been used in a cat model; at 6-month follow-up, it was well tolerated. Werblin has developed a hypothetical human surgical procedure that is analogous to routine phacoemulsification surgery with implantation of a PCIOL through a 7.00mm incision (Fig. 3) (3). Once the base lens is implanted, the cap-and-lens assembly is intraoperatively affixed by the surgeon to the base lens. The sandwich lens is oriented at the appropriate astigmatic axis, based on the preoperative assessment of anticipated postoperative astigmatism. Once refractive stability is achieved, the patient’s refractive status is evaluated and the refractive attachments can be removed or changed, depending on the amplitude and type of residual refractive error or, in case of a multifocal attachment, if the patient is not satisfied with the quality of vision. Such change or removal involves a second operative procedure consisting of opening the original wound, detaching the cap-and-sandwich lens component, and replacing it with new attachments (1,3). In contrast to accommodating and adjustable IOLs, several clinical studies have evaluated the feasibility and efficacy of multifocal IOLs (1,5–15). In a prospective study, Vaquero et al. compared the results of implanting the AMO array multifocal lenses with implanting a monofocal lens (5). Although distance acuity and contrast sensitivity were similar in both groups, patients with the multifocal lens had significantly better near acuity. In a prospective, double-masked, comparative clinical trial,

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Steinert et al. reported that significantly less correction was required in the multifocal group than the monofocal group. However, patients in the multifocal group sustained a small loss of contrast sensitivity (6). Holladay et al. have evaluated the optical performances of several multifocal lenses using laboratory and photographic studies (7). They found a two- to threefold increase in depth of field for all multifocals but also showed a 50% reduction in contrast in retinal image and a one-line drop in best corrected acuity. Percival and Setty conducted several clinical trials of multifocal lenses and found them to provide better simultaneous distance and near acuities in a significantly higher number of patients (8). Bleckman and coauthors found multifocal progressive IOLs to provide adequate visual performance at various distances but only in optimal light conditions (9). In a small-sample retrospective study, Negishi et al. demonstrated that eyes implanted with the five-zone refractive multifocal lenses showed better near visual acuity than control eyes and that the results compared favorably in other aspects of visual function (10). In a clinical trial, Wille reported a better performance of monofocal lenses for distance vision when compared to multifocal lenses (11). The mean postoperative acuity was 0.5 line higher in the monofocal than in the multifocal group. After testing contrast sensitivity and glare in patients implanted with diffractive multifocal IOLs, Winther-Nielsen and coworkers concluded that the most significant loss of contrast sensitivity is found with central glare under twilight conditions (12). In a comparative study of monofocal versus multifocal lenses, Vaqero-Ruano, et al. reported a wider depth of focus and significantly better near vision without addition in patients with multifocal lenses (13). The contrast sensitivity results at 96 and 50% were similar. Walkow et al. prospectively evaluated a diffractive versus a refractive multifocal IOL and found similar and satisfactory functional results with both except that near uncorrected vision was significantly better with the diffractive lens (14). In a case control study, Javitt et al. measured functional status and quality of life after bilateral implantation of multifocal versus a monofocal IOLs (15). The subjects with bilateral multifocal IOLs reported better overall vision, less limitation in visual function, and less spectacle usage than the control subjects with monofocal lenses. The difference was most significant in ratings of near vision without spectacles.

H. CONCLUSIONS Based on the relatively high success rate of multifocal IOLs, it is likely that several design adjustments may need to be incorporated into accommodating and adjustable IOLs before their use becomes commonplace. It is also likely that several of these technological advances may have to be combined in order to provide increased predictability for distance acuity without correction after cataract surgery as well as excellent near visual acuity. The multifocal IOLs’ ability to provide good distance and near visual acuity is not without visually disturbing loss of contrast sensitivity. Similarly, the success of monovision refractive surgery does not exceed the 80% mark in most studies (16–19). Accordingly there will be ample room for innovation in technology and surgical technique to provide excellent uncorrected distance and near acuities without optical aberrations. The successful preliminary results of accommodating and adjustable IOLs will provide the incentive for continued efforts and developments in this exciting field of research.

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REFERENCES 1. Vajpayee RB, Jain S, Azar DT. Astigmatic intraocular lenses, multifocal intraocular lenses, and other specialized intraocular lenses. In: Azar DT, ed. Intraocular Lenses in Cataract and Refractive Surgery. Philadelphia: Saunders, 2001: 299–306. 2. New IOL restored some accommodation in trial. Ocul Surg News. 1999. 3. Werblin TP. Multicomponent intraocualar lens. J Refract Surg 1996; 12:187–189. 4. Schwiegerling JT, Schwartz DM, Sandstedt CA, Jethmalani J. Light-adjustable intraocular lenses: finessing the outcome. Rev Refract Surg 2002: 23–25. 5. Vaquero M, Encinas JL, Jimenez F. Visual function with monofocal versus multifocal IOLs. J Cataract Refract Surg 1996; 22:1222–1225. 6. Steinert RF, Post CT Jr, Brint SF, Fritch CD, Hall DL, Wilder LW, Fine IH, Lichtenstein SB, Masket S, Casebeer C. A prospective, randomized, double-masked comparison of a zonal—progressive multifocal intraocular lens and a monofocal intraocular lens. Ophthalmology 1992; 99:853–861. 7. Holladay JT, van Dijk H, Lang A, Portney V, Willis TR, Sun R, Oksman HC. Optical performance of multifocal intraocular lenses. J Cataract Refract Surg 1990; 16:413–422. 8. Percival SPB, Setty SS. Prospectively randomized trial comparing the pseudoaccommodation of the AMO ARRAY multifocal lens and a monofocal lens. J Cataract Refract Surg 1993; 19: 26–31. 9. Bleckmann H, Schmidt O, Sunde T, Kaluzny J. Visual results of progressive multifocal posterior chamber intraocular lens implantation. J Cataract Refract Surg 1996; 22:1102–1107. 10. Negishi K, Nagamoto T, Hara E, Kurosaka D, Bissen-Miyajima H. Clinical evaluation of a five-zone refractive multifocal intraocular lens. J Cataract Refract Surg 1996; 22:110–115. 11. Wille H. Distance visual acuity with diffractive multifocal and monofocal intraocular lenses. J Cataract Refract Surg 1993; 19:251–253. 12. Winther-Nielsen A, Corydon L, Olsen T. Contrast sensitivity and glare in patients with a diffractive multifocal intraocular lens. J Cataract Refract Surg 1993; 19:254–257. 13. Vaquero-Ruano M, Encinas JL, Millan I, Hijos M, Cajigal C. AMO Array multifocal versus monofocal intraocular lenses: long-term follow-up. J Cataract Refract Surg 1998; 24:118–123. 14. Walkow T, Liekfeld A, Anders N, Pham DT, Hartmann C, Wollensak J. A Prospective evaluation of a diffractive versus a refractive designed multifocal intraocular lens. Ophthalmology 1997; 104:1380–1386. 15. Javitt JC, Wang F, Trentacost DJ, Rowe M, Tarantino N. Outcomes of cataract extraction with multifocal intraocular lens implantation. Functional status and quality of life. Ophthalmology 1997; 104:589–599. 16. Jain S, Azar DT. Eye infections after refractive keratotomy. J Refract Surg 1996; 12(1): 148–155. 17. Jain S, Arora I, Azar DT. Success of monovision presbyopes: review of the literature and potential applications to refractive surgery. Surv Ophthalmol 1996; 40(6):491–499. 18. Sippel KC, Jain S, Azar DT. Monovision achieved with excimer laser refractive surgery. Int Ophthalmol Clin 2001; 41(2):91–101. 19. Chang MA, Kloek CE, Zafar S, Jain S, Azar DT. Analysis of strict monovision and minimonovision LASIK surgery in presbyopes. Arch Ophthalmol. Submitted.

26 Accommodative Amplitude Measurements After Surgery for Presbyopia DAVID L. GUYTON The Wilmer Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A.

A. INTRODUCTION Several years ago in Houston, Texas, through the courtesy of Dr. Richard Yee, I had the opportunity to examine and refract two patients after surgery for presbyopia. My observations were not only surprising but also instructive. The surgery had been successful, but by a different mechanism from that proposed. The answer was in the retinoscopic reflex. Both patients had undergone Schachar’s scleral band procedures for presbyopia 2 to 3 months before. Both had experienced a beneficial optical effect, and both showed similar retinoscopic reflexes. The one with the more “complete” effect had the more striking reflexes. This patient was 56 years old. She had previously been essentially emmetropic bilaterally and had depended on reading glasses for near vision. She now went without glasses entirely, with 20/20 uncorrected visual acuity at both distance and near. She was ecstatic with the result. She had been invited to the clinic for me to examine just prior to having the scleral bands removed because of erosion through the conjunctiva. After confirming the distance and near 20/20 uncorrected visual acuity in each eye, I proceeded with the distance refraction. The retinoscopic reflex was confusing, but subjective refraction showed only small astigmatic corrections. With these minor corrections in place, I placed a small visual acuity chart beneath the peephole of my retinoscope and asked her to look from distance to near as I observed the retinoscopic reflexes. B. DYNAMIC RETINOSCOPY The technique I was using is a form of dynamic retinoscopy first described by Edward Jackson in 1895 (1). It is a marvelous method to assess the speed and completeness of 287

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Figure 1 Dynamic retinoscopy without lenses. The patient (A), wearing refractive correction if any, looks alternately between a distant target and a near accommodative target that the examiner holds just beneath the retinoscope peephole (B). Accommodation is observed objectively by neutralization of the “with” retinoscopic reflex when the patient accommodates to the plane of the near target.

accommodation, a method well described in the literature (2–4) (see Fig. 1) but not familiar to most ophthalmologists. The typical appearance is strong “with” movement with the patient looking past the edge of the retinoscope at the distance fixation target. As attention is shifted to the accommodative target just beneath the peephole of the retinoscope and as the eyes accommodate to this distance, the retinoscopic reflex broadens to neutralization over about 1/2 s. In other words, the pupil fills with light, and neither “with” nor “against” movement is visible. This striking change in the retinoscopic reflex can be observed repeatedly as the patient is instructed to look back and forth between distance and near. The speed, completeness, and stability of accommodation can thus be observed objectively. Residual astigmatism is easily detected, and when the procedure is performed under binocular conditions, anisometropia is evident by unequal neutralization of the two reflexes. To my surprise, my “rejuvenated” presbyope showed absolutely no perceptible change in the retinoscopic reflexes when looking from distance to near, and yet she could easily read the smallest letters on the near acuity chart. The clue to this total lack of objective accommodation, even though subjective accommodation appeared restored, was the shape of the retinoscopic reflexes.

C. RETINOSCOPIC REFLEXES The streak retinoscope gives a linear reflex in eyes with regular spherical or astigmatic refractive error. In other words, the streak is the same width everywhere along its length.

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Figure 2 The retinoscopic reflex seen with (A) the eye focused well beyond the retinoscope; (B) the eye focused just beyond the retinoscope; (C) a multifocal crystalline lens focused for distance in the center of the pupil and for near in the periphery of the pupil.

Typical reflexes are illustrated in Figure 2A, which shows the eye focused well beyond the retinoscope. Figure 2B shows the eye focused just beyond the retinoscope. If the eye were focused exactly in the plane of the retinoscope peephole, the red retinoscopic reflex would totally fill the pupil. D. MULTIFOCAL CRYSTALLINE LENS My patient’s reflexes correlated with neither Figure 2A nor Figure 2B but rather with Figure 2C. The streak was narrow in the center and broad at the top and bottom, in an hourglass shape. This shape persisted as the streak was rotated from one meridian to the next. Clearly the eye was focused for distance in the center of the pupil and for near in its periphery. A multifocal crystalline lens appeared to have been created by the procedure. (This appearance changed little as the retinoscope was moved off axis, indicating that the multifocal effect was in the crystalline lens, not in the cornea.) E. INCREASED DEPTH OF FOCUS It now became clear how this presbyopic patient was able to see clearly at both distances. She had been given multifocal crystalline lenses by the surgery. Because the retinoscopic reflex had not changed from distance fixation to near fixation, no true accommodation was occurring. The new multifocal effect simply created a huge depth of focus that enabled both distance and near vision without any active accommodation. By adding plus lenses to neutralize the center of the retinoscopic reflex, I observed the peripheral portion of the reflex to move strongly “against,” confirming that the periphery of the pupil was myopic with respect to the center. This type of refractive aberration is called “positive” spherical aberration, most commonly occurring naturally in young children. When it occurs naturally, however, the zones in the center and periphery are more clearly defined, with linear streak reflexes in each zone. In my “rejuvenated” presbyope, the transition from the emmetropic central zone to the myopic peripheral zone appeared more continuous, resulting in the hourglass-shaped reflex. F. TRADITIONAL TECHNIQUES FOR MEASURING ACCOMMODATION I have not yet had the opportunity to confirm this retinoscopic appearance in other patients after surgery for presbyopia. If indeed this finding is routinely present, then traditional methods for measuring accommodation are not applicable to these patients.

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Donders’s push-up method of measuring accommodative amplitude becomes instead a method of measuring the effective depth of focus of the eye, with any contribution due to true accommodation being impossible to distinguish. Similarly, adding minus lenses until blur occurs is simply a measure of depth of focus, not of accommodation. Infrared objective optometers have been used in attempts to measure accommodation after surgery for presbyopia, but without success (5). Caution must be observed in using these instruments, however, because some of them use only small portions of the pupil for the refractive measurement, and small changes in alignment can yield variable results in the presence of irregular or multifocal optics. G. WAVEFRONT ANALYSIS Wavefront analysis methods of measuring the refractive state across the pupil will be able to determine the refractive state of the multifocal zones in the altered crystalline lenses observed by retinoscopy. These new methods will also be able to detect whether or not any true optical changes occur with attempted accommodation (6). To my knowledge, these instruments have not yet been used to measure accommodation after surgery for presbyopia. I look forward to the results. H. CONCLUSION Whatever the mechanism of refractive change produced by surgical procedures for presbyopia, there is no question that a close focus can be created under certain conditions. Whether these beneficial effects will prove to be reproducible and stable and whether they will provide acceptable visual acuity and contrast remains to be seen. REFERENCES 1. Jackson E. Skiascopy and Its Practical Application to the Study of Refraction. Philadelphia: Edwards and Docker Co., 1895:86–88. 2. Guyton DL, O’Connor GM. Dynamic retinoscopy. Curr Opin Ophthalmol 1991; 2:78–80. 3. Rutstein RP, Fuhr PD, Swiatocha J. Comparing the amplitude of accommodation determined objectively and subjectively. Optom Vis Sci 1993; 70:496–500. 4. Rosenfield M, Portello JK, Blustein GH, Jang C. Comparison of clinical techniques to assess the near accommodative response. Optom Vis Sci 1996; 73:382–388. 5. Mathews S. Scleral expansion surgery does not restore accommodation in human presbyopia. Ophthalmology 1999; 106:873–877. 6. Gray GP, Campin JA, Pettit GH, Liedel KK. Use of wavefront technology for measuring accommodation and corresponding changes in higher order aberrations (abstr). Invest Ophthalmol Vis Sci 2001; 42:S26.

27 Complications of Hyperopia and Presbyopia Surgery LIANE CLAMEN GLAZER and DIMITRI T. AZAR Corneal and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Schepens Eye Research Institute, and Harvard Medical School, Boston, Massachusetts, U.S.A.

A. BACKGROUND Planning refractive surgery for a myope is like being an experienced golfer with many clubs to choose from and a good understanding of the potentials and the limitations of each club. Choosing a procedure for hyperopic refractive surgery, on the other hand, is more like being a novice golfer, still not quite sure which clubs are useful and which are optimal under different circumstances. Indeed, there is still no consensus as to the best methods for the surgical treatment of hyperopia. As one compares the treatment options that are currently available, a solid understanding of the potential complications of each refractive procedure will help one choose the most appropriate procedure for each patient. There are a number of reasons why refractive surgery for hyperopia has not been as popular as surgery to correct myopia. First, while hyperopia affects approximately 40% of the adult population, it is less visually significant than myopia (1). For example, approximately 80% of adult hyperopes require corrections of only 3.0 D or less (2). Accommodation may produce enough additional plus power to focus parallel rays of light on the retina. Thus, young hyperopes can often compensate and see well until their accommodative power weakens and they start experiencing manifest hyperopia in their mid-to late 30s. It follows that the average age of people seeking hyperopic correction is approximately 48 years, much higher than those seeking myopic correction (3–5). These older patients are more likely to suffer from presbyopia, dry eyes, glaucoma, and cataracts. Finally, hyperopic refractive surgery is more challenging than myopic surgery because it is more difficult to permanently steepen the central cornea than to flatten it. 291

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Complications plagued early attempts at hyperopic refractive surgery. The first attempts at hyperopic correction using hexagonal keratotomy, automated lamellar keratoplasty, contact laser thermal keratoplasty (LTK), epikeratophakia, and keratophakia often created more problems than they solved: irregular astigmatism, corneal ectasia, unpredictable results, or regression frequently occurred. Therefore, these methods of correcting hyperopia have been abandoned. In the evolution of hyperopic refractive surgery, the fittest procedures have proven to be PRK, LASIK, noncontact LTK, phakic intraocular lens (IOL) implantation, and clear lens extraction with IOL implantation. Of course, even these procedures can occasionally cause complications. B. COMPLICATIONS OF PRK AND LASIK Excimer lasers are used for both photorefractive keratectomy (PRK) and laser-assisted in situ keratomileusis (LASIK). When using a laser to achieve correction of hyperopia, the surgeon creates peripheral annular ablation around the central optical zone to produce central steepening. This requires excimer lasers with larger ablation diameters than those used to correct for myopia. In addition, more tissue must be removed per diopter of correction for hyperopic versus myopic LASIK or PRK. 1. Hyperopic-Photorefractive Keratectomy (H-PRK) PRK was introduced as a method for correcting refractive errors in 1983 (6–7). However, PRK for hyperopia (H-PRK) is still fairly uncommon and certainly much less common than PRK for myopia. A hyperopic ablation takes approximately three times longer to perform than a myopic ablation of similar magnitude. It simply takes longer to create a peripheral ablation zone that will steepen the central cornea than it does to create a central ablation area that flattens the central cornea (Fig. 1). The time involved increases the likelihood of dehydration and decentration (8). Decentration may cause irregular astigmatism and loss of best corrected visual acuity (BCVA). In addition, regression of effect is more likely to occur after H-PRK than after a PRK procedure for myopia. Finally, while the U.S. Food and Drug Administration (FDA) has approved PRK for the correction of hyperopia of up to Ⳮ6.00 D with less than 1.00 D of astigmatism, steepening a cornea above Ⳮ4.00 D becomes increasingly difficult: smaller optical zones and greater sensitivity

Figure 1. Hyperopic ablation profile of the VISX STAR Laser. This example of a hyperopic ablation profile demonstrates the large peripheral ablation zone necessary for H-PRK. (From Ref. 4.)

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to decentration are evident in higher hyperopic corrections. There are other potential complications of H-PRK (Table 1). For example, PRK produces large (9.5-mm) epithelial defects, leading to prolonged healing time, and an increased risk of infection while the cornea is healing. Recurrent corneal erosions are a bothersome potential complication of PRK. Haze and scar formation may also occur. Postoperative glare may be a nuisance, particularly for patients with larger pupils.

Table 1 Complications of PRK for Correction of Spherical Primary Hyperopia Mean follow-up (months)

Study

Year

No. of eyes

Technique and microkeratome used

O’Brart (12)

1997

43

6

Daya (3)

1997

25

6

Jackson (4)

1998

65

14

VISX Star Excimer Laser 9.0-mm peripheral zone/ 5.0-mm optical zone

Williams (5)

2000

41

12

VISX Star Excimer Laser 9.0-mm peripheral zone/ 5.0-mm optical zone

El-Agha (9)

2000

22

12

Haw (10)

2000

18

24

VISX Star S2 Excimer Laser 8.8- to 9.0-mm ablation diameter/5.0-mm optical zone Summit Apex Plus Excimer Laser, Combining an Erodible mask and an Axicon system 9.4-mm peripheral zone/6.5-mm optical zone

Summit Apex Plus Laser, combining an erodible mask and an Axicon system 9.5-mm peripheral zone/6.5-mm optical zone Chiron Keracor 116 Excimer Laser 8.5-mm peripheral zone/5.0-mm optical zone

Complications

Loss of best corrected visual acuity (BCVA)

• 21% subepithelial haze • 2.3% recurrent corneal erosions • 5% irregular epithelial healing • 2.3% astigmatic change • ⱕ4.4% halos • ⱕ6.7% glare (Note: Complication rates combine PRK patients with PARK patients.) • 15.4% filaments in the eyes • 21.5% epithelial erosions • 23% epithelial ridge at the site of epithelial closure • ⱕ21% haze (Note: Complication rates combine primary PRK and secondary PRK patients.) • 4.5% transient peripheral haze in the ablation zone

• 23% lost 1 line • 5% lost 2 lines

• 78% midperipheral stromal haze, sparing the optical zone

• 5.5% lost 2 or more lines under glare conditions

• 6.7% lost 2 lines

• 31% lost 1 line at 6 months • 2% lost 2 lines at 6 months • 29% lost 1 line at 18 months • No long-term loss of BCVA

• 13.6% lost 1 line • 9.0% lost 2 lines

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a. Ablation Zone Decentration A hyperopic correction, which produces a steepening of the central cornea, is less forgiving of decentration. And yet centration is more difficult during hyperopic corrective surgery because hyperopic eyes tend to be smaller, with smaller corneas, and because the ablation zone must be large. In addition, H-PRK takes up to three times longer than a comparable myopic PRK procedure; thus the risk of decentration is higher. Decentration is the HPRK complication that is most likely to cause loss of BCVA or irregular astigmatism. Decentration, with either H-PRK or H-LASIK, may occur either due to a decentered treatment throughout the ablation (shift) or due to intraoperative drift. Shift can be secondary to poor patient fixation or to the surgeon’s error. Drift occurs secondary to involuntary intraoperative eye movement or to a surgeon’s attempt to correct apparent decentration during treatment. Decentration is difficult to treat. Theoretically, one can lift the flap and retreat the patient with decentration of the treatment in the opposite direction to the previous ablation. An alternative solution is to use miotics to constrict the pupillary axis and to minimize optical aberrations. Finally, a hard contact lens may neutralize optical aberrations resulting from irregular astigmatism (13). Techniques to avoid decentration include (1) the creation of larger optical (5-mm) and ablation (9.0–9.5 mm) zones, (2) the use of faster laser pulses to decrease the ablation time, and (3) more sophisticated eye-tracking devices. Finally, performing the ablation under the lowest illumination possible can improve patient fixation. b. Regression Regression of effect after H-PRK remains one of the limitations of this procedure. It has been observed that “aggressive healers,” patients with severe corneal haze and marked scarring in the region of ablation, had significant regression of their refractive correction. This observation supports the theory that the mechanisms associated with regression are the subepithelial deposition of collagen and glycosaminoglycans which occurs during wound healing and produces a filling in of the ablation and loss of effect (12,14–15). Some ophthalmologists have given topical corticosteroids after PRK in an attempt to inhibit regression. Studies consistently show that while topical corticosteroids (fluorometholone or dexamethasone) inhibit some regression when used during the first 3 to 6 postoperative months, this effect is negated approximately 3 months after cessation of steroids (4,14–17). The development of new strategies to reduce aggressive wound healing and haze after PRK may prevent post-PRK regression. c. Haze One potential post-PRK complication is the development of haze. Fortunately, haze is less of an issue with H-PRK than it is for myopic PRK. This is because the stromal haze is most dense at the border of the ablated zone, which is in the peripheral (rather than central) cornea of eyes treated for hyperopia (Fig. 2). Nevertheless, haze can contribute to regression of effect, as mentioned above. Therefore, it is best to try to prevent haze formation. Risk factors for haze include small ablation diameters with steep transition zones, UV exposure, acute systemic viral illness, and ocular surface disorders such as dry eyes (18–20). Haze may be prevented by maintaining a good tear film layer with nonpreserved tears or punctal plugs if necessary. One can encourage patients to decrease exposure to

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Figure 2 Midperipheral ring of corneal haze, characteristic of the haze seen after PRK for hyperopia. (From Ref. 10.)

UV radiation by using sunglasses and a hat for 1 year after PRK is performed. Some authors suggest preventing formation of the corneal haze with a single intraoperative treatment of mitomycin C to suppress proliferation of keratocytes. Studies in rabbits have proven this to be very effective (21). A less aggressive approach is to wait and see if haze occurs and then to apply mitomycin C to treat corneal haze and reduce the regression that often accompanies the haze (22). One can treat stromal haze that persists beyond 6 months with excimer laser retreatment or a transepithelial PRK followed by PRK retreatment. 2. Hyperopic-Laser in situ Keratomileusis (H-LASIK) Although early trials of hyperopic LASIK (H-LASIK) reported unsatisfactory results with a high rate of BCVA loss and significant regression, H-LASIK is now supplanting HPRK as the refractive procedure of choice for hyperopia (23,24). H-LASIK is associated with a faster recovery time with less postoperative pain than H-PRK. Initially, H-LASIK was limited by small outer-zone ablations: microkeratomes that could create only small flaps as well as unrefined excimer laser algorithms contributed to the poor results of early H-LASIK. With the development of keratomes that are able to create 9.5-mm rather than the older 8.5-mm flaps, H-LASIK has become safer. In addition, better algorithms and nomograms are being developed as we accrue more experience with H-LASIK. Limitations of LASIK for the treatment of hyperopia include problems with predictability, regression, and difficulty treating hyperopia greater than Ⳮ4 D. Complications of H-LASIK can be divided into three groups. First are the complications specific to the surgical correction of hyperopia itself. As discussed above, these include the older age of the patients and the length of time of the procedure. Second, there may be intraoperative complications, including flap complications and ablation-related complications. Finally, postoperative complications include infection, flap complications, striae, diffuse lamellar keratitis, epithelial ingrowth, decentration, corneal ectasia, and, rarely, retinal complications (Table 2).

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Table 2 Complications of LASIK for Correction of Spherical Primary Hyperopia Mean follow-up (months)

Study

Year

No. of eyes

Technique and microkeratome used

Suarez (25)

1996

154

3

Ditzen (26)

1998

43

12

Goker (27)

1998

54

19

Keracor 116 Excimer Laser Automated Corneal Shaper 8.5-mm flap diameter

Knorz (28)

1998

23

12

Keracor 117 Excimer Laser Automated Corneal Shaper 8.5-mm flap diameter

Esqucnazi (29)

1999

100

12

Keracor 117CT Excimer Laser Automated Corneal Shaper 8.5-mm flap diameter

Lindstrom (30)

1999

46

6

VISX STAR S2 Excimer Laser Hansatome 9.5-mm flap diameter

Coherent/Schwind Keratom II Excimer Laser Automated Corneal Shaper 8.5-mm flap diameter MEL 60 Excimer Laser Automated Corneal Shaper 8.5-mm flap diameter

Complications • 1.3% corneal ectasia • Epithelial invasion of the interface • Traumatic flap displacement • Bilateral haze • 15% epithelial ingrowth • 2.3% haze • 7.5% scars • 4.7% vertical decentration • 2.3% central island • 4.7% free cap • 11.6% flap dislocation • 11.6% flap folds • 31.4% epithelial ingrowth • 13% regressed/undercorrected • 9.3% glare at 9 months • 3.7% transient diplopia that resolved entirely • 1.8% irregular flap cut • 1.8% decentration • 3.7% irregular astigmatism • No significant complications noted

• 6% epithelial ingrowth into the interface • 4% scars on nasal side • 2% ablation decentration • 2% transient diplopia • 5% flap folds • 6.5% transient epithelial defect • 4.3% diffuse lamellar keratitis

Loss of best corrected visual acuity (BCVA) • 2% lost 1 line • 1.3% lost 2 lines

• 9% lost 1 line • 4.7% lost 3 lines

• 5.6% lost 2 lines

• 63% of low hyperopes lost 1 line • 50% of high hyperopes lost 1 line • 6% lost 1 line at 1 year follow-up • 6% lost 2 lines at 1 year follow-up • 5% lost 2 lines at 2 year follow-up • 11% lost 1 line • 2.2% lost 2 lines (continued)

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Table 2 Continued

Study

Arbelaez (31)

Zadok (32)

Reviglio (33)

Argento (34)

El-Agha (9)

Choi (35)

Year

1999

2000

2000

2000

2000

2001

No. of eyes

192

72

50

147

26

32

Mean follow-up (months)

12

6

6

12

12

6

Technique and microkeratome used

Keracor 177C Excimer Laser Automated Corneal Shaper 9.0-mm flap diameter

Nidek EC-5000 Excimer Laser Automated Corneal Shaper 8.5-mm flap diameter Lasersight 200 Excimer Laser with 9.0 software Automated Corneal Shaper 9.0- to 9.5-mm flap diameter Keracor 117C Excimer Laser Hansatome 5.9-mm optical zone diameter, flap diameter not reported VISX STAR S2 Excimer Laser Hansatome 9.5-mm flap diameter VISX S2 Smoothscan Excimer Laser Hansatome 9.5-mm flap diameter

Complications • 4.3% epithelial cells in the interface • 2.2% haze • 2.2% mild irreg astig • 0.6% had a free cap • 0.6% sterile keratitis, (Note: Complication rates combine the 192 spherical hyperopes with the 164 toric hyperopes.) • No significant complications noted

• 2% epithelial ingrowth in the would edges associated with free caps, not requiring surgical removal • 8.2% transient epithelial ulcer • 4.5% stromal infiltrates

• No significant complications noted

• No significant complications noted

Loss of best corrected visual acuity (BCVA)

• 13% of high hyperopes lost 2 lines or more

• 1.4% lost 2 lines or more

• No eyes lost BCVA

• Less than 5.8% lost 1 line

• 19% lost 1 line • 7.7% lost 2 lines • 25% lost 1 line • 9% lost 2 lines

a. Flap Complications Intraoperative complications include free flaps, incomplete flaps, buttonholes, small flaps, and thin flaps. Free flaps, thin flaps, or incomplete flaps are more likely to occur in patients with flat (⬍41.00-D) and large (⬎11.5-mm) corneas. Unusually steep (⬎48.00-D) and small (⬍11.5-mm) corneas are more conducive to buttonholes or large flaps. The larger ablation areas necessary for H-LASIK require larger flaps. Extra care must be taken with the larger flaps because a large flap may be more prone to wrinkles

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or misalignment, which may lead to irregular astigmatism. When pannus exists, a large flap may cause bleeding, which must be cleared from the bed prior to ablation. Appropriate preoperative examinations can help one identify and discourage patients at greater risk for flap complications. Preplaced surgical landmarks that straddle the flap edge will help with accurate repositioning of the flap in the operative and postoperative period. In addition, the newer microkeratomes and suction rings create fewer flap complications. b. Epithelial Ingrowth To achieve successful H-LASIK results, the diameter of the corneal flap must be large enough. Epithelial ingrowth can result from laser energy to the periphery of the flap, or it may occur secondary to wound edge instability with migration of epithelial cells under the flap (Fig. 3). Epithelial ingrowth can progress to involve the visual axis, creating irregular astigmatism and even melting of the overlying flap (13,36). If epithelial cells under the flap progress toward the visual axis or induce stromal melting, the flap should be lifted, the stromal bed and flap undersurface should be thoroughly irrigated and scraped, and the flap should then be repositioned (37). With larger flaps of 9 to 10 mm, the risk of epithelial ingrowth is greatly reduced, most likely because this avoids ablation of epithelium beyond the edge of the flap (38). Other measures one may take to prevent epithelial ingrowth include using dedicated instruments exclusively for interface manipulation, so that these instruments do not come in contact with the surrounding epithelium. Also, one should be careful to avoid flap folds, as these may provide a conduit for cell infiltration (13). c. Decentration Decentration or small optical zones may lead to irregular astigmatism, causing loss of BCVA, glare, monocular diplopia or halos, and halo effects. The same principles of decentration described above for PRK apply here. For example, whether with PRK or LASIK, a larger optical zone is more forgiving of a slight decentration. More sophisticated LASIK ablation profiles may also diminish the risk of decentration: a more gradual transition zone between ablated and unablated tissue helps minimize epithelial and stromal regeneration, with its subsequent regression.

Figure 3 Epithelial ingrowth after LASIK. (A) Stable epithelial ingrowth at the LASIK interface. (B) Retroillumination used to view the same area of epithelial ingrowth. (From Ref. 13.)

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Figure 4 Diffuse lamellar keratitis following LASIK. (A) Diffuse lamellar keratitis 2 days after LASIK. (B) Diffuse lamellar keratitis, 5 days after LASIK, with central coalescence, scarring, and stromal melt. (From Ref. 13.)

d. Diffuse Lamellar Keratitis Although diffuse lamellar keratitis (DLK) is a recently described syndrome, not yet documented after H-LASIK, it has been reported in approximately 0.2 to 3.2% of cases of myopic LASIK (13,39–42). DLK is characterized by a proliferation of inflammatory cells at the LASIK interface (Fig. 4). It can lead to loss of BCVA due to irregular astigmatism and may also cause stromal corneal melting with induced hyperopia or hyperopic astigmatism. The cause of DLK is still unclear; thus, prevention remains a challenge. When present, however, DLK must be treated immediately with hourly topical prednisolone actate 1% and broad-spectrum topical antibiotic coverage. It has been observed that if the DLK is not resolved by the fifth postoperative day, there is typically central coalescence of the inflammatory cells, which may lead to central stromal melting and scarring. Thus, if inflammation progresses despite the steroid/antibiotic treatment, the flap should be lifted, scraped, and irrigated by the fourth postoperative day at the latest (13). The use of topical intrastromal steroid during LASIK has been proposed as a way of reducing the incidence and severity of DLK (43). e. Late Flap Dislocation One rare, potential H-LASIK complication is traumatic flap dislocation, occasionally seen months or years after LASIK (44,45). One might expect a slightly greater risk of flap dislocation in H-LASIK because the flap tends to be wider than that created for myopic LASIK. For this reason, it would be wise to avoid performing H-LASIK on high-risk patients, such as boxers. One should also encourage patients to wear safety glasses when engaging in high-risk sports activities after H-LASIK. f. Corneal Ectasia Corneal ectasia is a rare complication. For example, in one of the largest studies of HLASIK, Suarez et al. performed LASIK on 154 eyes of patients with simple hyperopia of between Ⳮ1.00 and Ⳮ8.50 D with astigmatism of less than 0.75 D. Suarez et al. had only two cases of postoperative corneal ectasia, both occurring in patients with high levels of hyperopia. Keratectasia is most likely due to the mechanical uncoupling of the posterior

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from the anterior stroma, with subsequent weakness of the cornea. Denervation of the flap or subclinical epithelial ingrowth may exacerbate this mechanical uncoupling. Other factors that may predispose to corneal ectasia include excessive ablation with less than 250 ␮m of residual stromal bed, a thicker than normal flap with consequent ablation at a deeper than planned level, and irregular corneal thickness (46). One can attempt to prevent corneal ectasia with preoperative pachymetry maps to detect borderline cases. One must also identify patients with keratoconus and prevent them from undergoing H-LASIK because they, of course, would be at great risk for postoperative corneal ectasia. g. Loss of Best Corrected Visual Acuity Loss of BCVA is more likely to occur after H-LASIK performed on high hyperopes. Choi notes that 50% of eyes with attempted corrections greater than 5 D lost two lines of BCVA. These high rates of loss of BCVA in eyes with high hyperopia may be due to induced irregular astigmatism (27–28,30–31,35). Irregular astigmatism can result from poor centration of the ablation. Even small levels of decentration can cause irregular astigmatism, leading to degraded vision quality or monocular diplopia. Knorz performed a pilot study on eyes with hyperopia and hyperopic astigmatism. In eyes with Ⳮ5.1 D to Ⳮ10 D of hyperopia (15 eyes), 53% had lost one line at 1 month, and 20% had lost two or more lines of BCVA at 1 month. For 12-month follow-up, 6 eyes were available, and 50% of these had lost one line while none had lost two or more lines of BCVA. No significant intraoperative or postoperative complications were noted. However, it was felt that the loss of acuity was due to image degradation by significant optical aberrations caused by the new corneal surface. Knorz concluded his study by suggesting that LASIK should not be used for hyperopia ⬎Ⳮ5 D.(28) Studies of myopic LASIK procedures have identified other causes of loss of BCVA to include flap folds, epithelial defects, lamellar keratitis, and epithelial ingrowth (30). 3. Conclusion As we gather more experience with hyperopic PRK and LASIK, we can achieve higher rates of predictability and accuracy by creating nomograms adjusted for preoperative refraction, keratometry, and age. Also, more sophisticated equipment can decrease complication rates for both PRK and LASIK: more sophisticated ablation profiles and better eyetracking systems can reduce decentrations. For LASIK, newer, larger microkeratomes that produce flap diameters of at least 9.0 mm should be used. C. COMPLICATIONS OF NONCONTACT LASER THERMAL KERATOPLASTY 1. Background Thermal keratoplasty (TK) was first performed in 1898 by the Dutch ophthalmologist Lendert Jan Lans in an attempt to treat astigmatism (47). Lans demonstrated that thermal energy, applied with a cautery, altered the structure of the corneal stromal collagen and changed the anterior corneal curvature. Unfortunately, using simple cauteries and probes, it was difficult to control the amount of energy applied, and TK resulted in unpredictable results and regression (48,49). Interest in TK was rekindled with the development of lasers that could heat the cornea in a more controlled manner.

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Figure 5 Slit-lamp photograph of a cornea immediately after treatment with noncontact holmium: YAG laser thermal keratoplasty. (From Ref. 55.)

In 1990, Seiler first described laser thermal keratoplasty (LTK), which utilizes the holmium:yttrium aluminum garnet (Ho:YAG) laser to correct hyperopia (50). Ho:YAG LTK avoids damage to the corneal epithelium by delivering infrared radiation to the midstroma. LTK changes the anterior corneal curvature because corneal collagen shrinks by 30 to 45% of its original length at temperatures of 55 to 60⬚C (51). Local, peripheral flattening causes central steepening, which corrects for hyperopia. Initially, both contact and noncontact LTK were performed. However, contact LTK, performed by directly applanating the cornea with a probe, tended to cause irregular astigmatism, regression and undercorrection; this form of LTK was withdrawn from U.S. Food and Drug Administration (FDA) trials (52–54). Noncontact LTK, on the other hand, has been approved by the FDA. It is traditionally performed by projecting one to three concentric rings of eight laser spots each onto the cornea through a slit lamp–mounted, fiberoptic delivery system (Fig. 5). FDA phase IIA clinical trials with 2 years of follow-up showed the uncorrected visual acuity (UCVA) was improved by one or more lines in 19 (73%) of 26 treated eyes (55). 2. Complications While a variety of complications may occur following LTK, the most common is regression of effect (Table 3). Short-term complications include discomfort immediately after LTK treatment or for 1 to 3 days post-LTK; some patients complain of mild pain (18–20%), tearing (41–43%), mild photophobia (33–41%), mild foreign-body sensation (41–54%), and other mild discomfort (29%). These side effects of laser-induced epithelial injury typically resolve within 3 days of treatment (56,58). Corneal opacities and epithelial haze and staining are common in the first week post-LTK treatment. However, by 2 years after treatment, corneal opacities at the treated sites and golden-brown intraepithelial deposits (presumably iron deposits) in or adjacent to inferior treatment spots are typically the only evidence of change to the cornea (56). Long-term damage to the central cornea has not been reported as a complication. Clearly, the principal limitation of noncontact LTK is regression. Reported rates of regression vary from 27 to 45% (55–58). In one study, 70.1% had an UCVA of 20/20 at

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Table 3 Complications of Noncontact LTK for Correction of Spherical, Primary Hyperopia No. of eyes

Mean follow-up (months)

Study

Year

Koch (56)

1996

17

24

Koch (55)

1997

28

24

Alio (57)

1997

57

15

Nano (58)

1998

182

12

Vinciguerra (59)

1998

16

12

Technique used Sunrise Technologies delivery system 1 ring of 8 spots per ring Sunrise Technologies delivery system 1–2 rings of 8 spots per ring Sunrise Technologies delivery system 2–3 rings of 8 spots per ring Sunrise Technologies delivery system 1–3 rings of 8 spots per ring Sunrise Technologies delivery system 3 rings of 8 spots per ring

Complications

Loss of best corrected visual acuity (BCVA)

• 27% had 0.5 to 1.0 D of induced astigmatism • 27% regression

• 6% lost 2 lines of BCVA

• 29% regression in the 1-ring group

• 7% lost 1 line of spectaclecorrected near visual acuity

• 31.5% had total regression

• No loss of BCVA

• 45% regression • 0.55% decentered treatment ring • 0.55% with 1 D of induced astigmatism • 25% complained of halos or ghost images at 12-month follow-up

• No loss of BCVA

• No loss of BCVA

3 months, but only 50.8% maintained this level at 15 months. In fact, by 15 months, only 57.8% were within Ⳳ1.00 D of the intended refraction (57). In addition to regression of effect, astigmatism may occur as a result of noncontact LTK. 3. Etiology of Regression Some researchers feel that regression is inherent to the current technique for LTK. The Ho:YAG LTK technique delivers pulses of energy to the cornea. The pulses themselves may trigger a mixed shrinkage/relaxation pattern. For example, if the energy pulses are too low, an insufficient amount of collagen shrinkage is achieved, and the initial refractive change may gradually be lost. On the other hand, if the laser heats the collagen fibrils to 65 to 70⬚C, collagen relaxation occurs. Regression after noncontact LTK is more common in younger patients and patients with thicker central corneas (57). Regression may be due to the elasticity of Bowman’s membrane and stromal collagen in younger patients, which causes the cornea to return to its previous shape. Similarly, thicker corneas may be more likely to resume their previous configuration. At least in rabbit models, noncontact LTK provokes procollagen synthesis by fibroblastic keratocytes, causing stromal remodeling which can produce irregularities in the anterior corneal surface leading to epithelial hyperplasia. This in turn, results in an

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altered corneal curvature (60). While the precise wound healing response to noncontact LTK in humans is not known, it is possible that both regression and astigmatism may result from a similar response. 4. Prevention Investigators are speaking optimistically about a new continuous-wave diode laser that can change the shape of the cornea without the peaks and troughs of the pulsed Ho:YAG laser (61,62). The continuous-wave diode laser is expected to avoid tissue overheating, thereby improving long-term refractive stability. In addition, FDA trials are under way on a device that uses radiofrequency energy to the peripheral cornea; this may produce more controlled shrinkage of collagen lamellae (63). 5. Conclusion One point to remember is that while regression and, less frequently, astigmatism may result from noncontact LTK, it is rare for patients to lose even one line of BCVA. No eyes have been reported to have lost two or more lines of BCVA from noncontact LTK (55–58). For risk-averse low hyperopes (Ⳮ0.75 to Ⳮ2.50 D), noncontact LTK is a procedure to consider because it causes very few BCVA-threatening complications.

D. COMPLICATIONS OF PHAKIC INTRAOCULAR LENSES AND CLEAR LENS EXTRACTIONS WITH INTRAOCULAR LENS IMPLANTS 1. Background While most types of refractive surgeries alter the cornea, the refractive power of the eye can also be changed by implanting an intraocular lens (IOL) with or without extraction of the crystalline lens. Barraquer implanted the first phakic intraocular lens in the 1950s (64). Unfortunately, many of these anterior chamber lenses were poorly finished and had sharp edges. After Barraquer had implanted almost 500 lenses, significant complications such as corneal edema occurred, and over 300 of the lenses had to be removed (65). After this experience, interest in phakic IOLs waned until labs were better able to guarantee the quality of IOLs. Intraocular lenses being made today are of much better quality than those used in the 1950s. A recent study used a scanning electron microscope to analyze the surface quality of new-generation phakic IOLs; the study showed that these lenses did not have any defects that would contraindicate their use as phakic IOLs (66). This study examined the three major types of lenses currently used as phakic IOLs: anterior chamber lenses (currently used only in myopic eyes), iris-fixated anterior chamber lenses, and posterior chamber lenses. 2. Complications Even when perfectly constructed IOLs with smooth surfaces are placed, there is still a risk of progressive corneal endothelial cell loss secondary to phakic IOLs (67–71). Other

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Table 4 Complications of Phakic Intraocular Lens Implantation for Correction of Hyperopia Mean follow-up (months)

Study

Year

No. of eyes

IOL Implanted

Davidorf (76)

1998

24

18

Staar ICL

Rosen (77)

1998

9

6

Staar ICL

Fechner (78)

1998

69

120

Pesando (79)

1999

15

18

Staar ICL

Sanders (80)

1999

10

6

Staar ICL

Pershin (81)

2000

33

12

Iris-Claw IOL

Storz Phacoprofile IOL

Complications • 12.5% pupillary block glaucoma • 8% IOL decentration of more than 1 mm • 12.5% underwent removal of their IOL • 11% pupillary block glaucoma, requiring surgical iridectomy and removal of IOL • 1.4% lens dislocation secondary to postoperative trauma • 3% uveitis, corneal edema, and glaucoma • 13% pupillary block glaucoma • 6.7% anterior • No complications • 6% anterior subcapsular cataract • 3% lens replacement was required due to calculation error • 9% pigment dispersion without IOP elevation

Loss of best corrected visual acuity (BCVA) • 4% lost 3 lines

• 22% lost 1 line

• No loss of BCVA

• 6.7% lost 2 lines • No loss of BCVA • No loss of BCVA

potential complications of IOL implantation include cataract formation, pupillary-block glaucoma, endophthalmitis, and retinal detachments (Table 4) (72–75). Currently the most popular phakic IOL for the treatment of hyperopia is the Collamer Staar Posterior Chamber IOL, also called the implantable contact lens (ICL) (Fig. 6). A recent phase I trial of silicone plate posterior chamber lenses, implanted in hyperopes, reported that 100% of patients had 20/40 or better UCVA, and 70% had 20/20 or better UCVA (80). In one study of hyperopes with phakic IOLs 1 year after implantation, opacities in the area of lens contact with the capsule developed in two eyes (6%). Pigment dispersion occurred in three eyes (9%), but without intraocular pressure elevation. One eye (3%) required a lens replacement because of a calculation error (81). Another study reported

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Figure 6 The STAAR Collamer posterior chamber phakic intraocular lens implant. (From Ref. 79.)

an anterior subcapsular cataract developing immediately after surgery in one eye (6.7%), causing a loss of two lines of BCVA (79). Because hyperopic eyes tend to be shorter, they are more prone to pupillary block after implantation of posterior chamber lenses. One study using the Staar Collamer Implantable Contact Lens (ICL) reported 2 of 15 eyes (13%) developing a severe pupillary block despite two iridotomies that had been performed 2 weeks prior to surgery. The increased intraocular pressures due to the pupillary block necessitated removal of the implants (79). Another study of the Staar ICL reported a 12.5% incidence of postoperative pupillary block. In addition, IOL decentration of more than 1 mm occurred in 2 of the 24 eyes (76). Sight-threatening complications such as endophthalmitis have been reported to occur in phakic IOL procedures for myopia and could theoretically occur for hyperopic phakic IOL implantation procedures as well (75). Occasionally, silicone plate phakic intraocular lenses need to be removed due to incorrect sizing of the lens and poor fixation within the sulcus (82). Retinal detachments after phakic IOL implantation have been reported in 4.8% of myopic eyes (74). This complication has not yet been reported in hyperopic eyes. Iris-fixated phakic IOLs for the correction of high hyperopia can be associated with serious complications such as corneal decompensation and glaucoma (Fig. 7) (78). Other risks include cataract formation and glaucoma (pupillary block glaucoma, pigmentary glaucoma, narrow-angle glaucoma, and malignant glaucoma) (76). Peripheral iridotomies can treat or prevent pupillary-block glaucoma. Shallow anterior chambers should be a contraindication to performing an ICL because of the risk of narrow-angle glaucoma. Lens decentration may also occur. 3. Clear Lens Extraction with IOL Implantation Clear lens extraction (CLE) with IOL placement has been studied as a surgical correction of hyperopia. Some of the disadvantages associated with this procedure as a treatment for myopia are not as a relevant when it is considered as a hyperopic treatment. For example,

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Figure 7 The Fechner iris-claw intraocular lens implant. (From Ref. 78.)

myopes are more prone to retinal detachments (RDs). But the increased risk of an RD after clear lens extraction surgery is less relevant in hyperopes. In addition, the loss of accomodation that accompanies removal of the crystalline lens is a moot point in the high hyperope, who can see neither at distance nor at near without correction. One problem of CLE with IOL placement encountered with hyperopes, which is not relevant in myopes, is the potential need to implant more than one IOL (piggyback IOLs) to correct for hyperopia. Several recent studies on clear lens extraction for hyperopia demonstrate that this is a safe and effective procedure. Kolahdouz-Isfahani performed clear lens extraction on 18 eyes. Two eyes lost two lines of BCVA, but no reason for the loss of BCVA was found after a complete ocular examination was performed. Complications included one case of postcapsular opacification requiring one YAG capsulotomy, one case of a lens dislocation requiring an IOL exchange, and one case of malignant glaucoma (83). Another study of 35 eyes reported that no eyes lost BCVA postoperatively. Additional procedures consisted of one IOL exchange and one PRK for overcorrection, both due to IOL miscalculations. Posterior capsular opacification developed in 19 eyes (54.2%), requiring 19 YAG capsulotomies (84). One study of 20 eyes that underwent clear lens extraction and IOL implantation reported no complications; there was no loss of BCVA and no need for further procedures. The authors did find, however, that the procedure was less accurate and less predictable for less than Ⳮ3.00 D of hyperopia (85). Pop et al. performed CLE with IOLs followed by PRK or LASIK. The only postCLE complication in this study was interlenticular opacification (ILO), which occurred in 14 eyes that had piggyback polyacrylic lenses. Of the initial 65 eyes in the study, 40 eyes received two IOLs (piggyback IOLs) because the lens power needed was higher than 30 D. Thus, 35% of all the piggybacks developed interlenticular opacification. There were no other reported complications from the CLE surgery (86).

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Other potential risks of clear lens extraction surgery with IOL implants include the risks associated with any cataract surgery, such as hemorrhage, retinal detachment, cystoid macular edema, and endophthalmitis. Approximately 10% of high hyperopes have axial lengths of less than 21 mm, predisposing them to choroidal effusions. 4. Prevention As with any type of surgery, many surgical complications of phakic IOL surgery or CLE/ IOL surgery decrease with surgeon experience. Visual complications such as halo and glare are significantly reduced with increased optic size from 5.0 to 6.0 mm. When iris-claw lenses are used, the risk of corneal decompensation can be decreased by using adequate viscoelastic during surgery, so that the IOL does not touch the cornea; ensuring sufficient anterior chamber depth; and providing long-term monitoring of the corneal endothelium (78). Glaucoma is always a potential problem associated with IOL implantation in small, hyperopic eyes. During clear lens extraction with IOL implantation, peripheral iridectomies should be performed in eyes with corneal diameters of 11.0 mm or less or axial lengths of 20 mm or less. Peripheral iridotomies should be performed prior to the implantation of phakic IOLs. 5. Conclusion While many daunting complications may occur secondary to phakic IOL implantation or CLE/IOL implantation, there are certainly many advantages to treatment of hyperopia with either of these techniques. First, IOL implantation is the only refractive procedure that can correct higher degrees of hyperopia. Second, it uses skills that physicians who perform cataract surgery have honed and polished. Finally, it does not require expensive equipment, such as lasers. Hopefully, more long-term data will be available in the future to help decrease the rate of potential complications associated with phakic IOL surgery. E. COMPLICATIONS OF INTRACORNEAL SEGMENTS AND LENSES 1. Background Intacs, the intrastromal corneal ring segment (ICRS), consists of two 160-degree polymethyl methacrylate (PMMA) segments placed in two pockets of the peripheral stroma (Fig. 8). The procedure is unique in that it retains the potential to be adjusted or reversed.

Figure 8 The Intrastromal corneal ring. (From Ref. 91.)

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In April 1999, the FDA approved Intacs for myopic correction of ⳮ1.00 to ⳮ3.00 D with Ⳮ1.00 D or less of astigmatism. Intacs can also be used to create central corneal steepening to correct for hyperopia. Studies are currently investigating the use of small linear segments placed in the peripheral cornea to create shortening of the peripheral length of the corneal arc, with subsequent central corneal steepening. By altering the thickness of the insert, one can titrate the refractive effect. Although there have been no published studies on Intacs for hyperopia, clinical trials are currently under way in Germany and Spain. These trials have produced promising preliminary results: study 噛1 enrolled 19 patients, and at 1 year 95% (18 of 19) achieved an UCVA of 20/40 or better. Of note, an induced astigmatism of 1.00 D or greater was seen in 32% (6 of 19) of the cases. Eleven patients were enrolled in study 噛2, with 6 months of follow-up. Ten of the 11 eyes (91%) were 20/40 or better, and 4 eyes (36%) experienced an induced astigmatism of 1.00 D or more. Finally, study 噛3 enrolled 9 patients with 6 months follow up. All patients had an UCVA of 20/40 or better; only 1 patient had an induced astigmatism equal to or greater than 1.00 D (87). 2. Complications Published studies of Intacs today are for the correction of myopia. However, the complications of Intacs would be similar whether the segments were placed for the correction of myopia or for hyperopia. In the FDA phase II and III studies, the incidence of adverse events was 2% of the 452 eyes enrolled. Complications of the ICRS procedure include accidental perforation into the anterior chamber (2 eyes), surface perforation of the epithelium anteriorly (3 eyes), significant decentration of the rings requiring removal or repositioning (5 eyes), and infectious keratitis (1 eye). All eyes in the group of patients with complications returned to preoperative BCVA by their 6-month follow-up appointment (88). Schanzlin reported no serious complications in the 125 eyes that received ICRS in his study. Minor postoperative problems included one case of transient conjunctivitis, three cases of filamentary keratitis, and one case of transient iritis. One patient, whose incision had gone into a region of superior pannus, developed deep stromal blood vessels. At 12 months follow-up, four patients had a two-line loss of BCVA, from 20/12.5 to 20/ 20. All four of these patients had a substantial improvement in their UCVA (89). Postoperative astigmatism is clearly a significant potential problem, with 20 of 102 patients in one group experiencing post-ICR astigmatism of 1.0 D or more at 3 months follow-up. Various theories exist as to the cause of the astigmatism; it may be related to suture tightness (90). Induced astigmatism may also result from postoperative movement of the intracorneal ring segments. Finally, Intacs-induced astigmatism can result from irregular stromal and epithelial thickening between the Intacs rings (91). Reports describe one patient with persistent focal edema due to a small Descemet’s tear from a lamellar dissection that was too deep. Although the edema necessitated ICR removal, the patient’s BCVA was 20/20 at exit from the study. One of 102 patients incurred an intraoperative perforation of Descemet’s membrane, requiring an ICRS explantation (90). Channel deposits associated with Intacs are occasionally seen but are not associated with impaired visual acuity (88,89). 3. Prevention One can attempt to prevent postimplant complications through meticulous attention to positioning, proper incision depth and pocketing, and sterile technique. In addition, proper

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attention to wound architecture along with adequate closure and tissue approximation with suturing can minimize the frequency of wound-related complications such as wound gape and epithelial cysts. One can prevent corneal neovascularization status post-ICRS by avoiding incisions that make contact with pannus or a limbal blood vessel and by warning against eye rubbing so as to prevent wound dehiscence. 4. Conclusion Intacs may prove to be a valuable tool for the correction of hyperopia. Advantages over procedures such as LASIK and PRK include the fact that the Intacs insert is placed in the peripheral cornea and the central cornea is never violated during the surgical procedure. In addition, the Intacs devices can easily be removed if necessary. Finally, the refractive effect can be adjusted by replacement of any of the implanted radial segments. The complication of induced astigmatism may become less of an issue as more Intacs devices are implanted: the cause of induced astigmatism may become better understood and thus better prevented. In addition, surgical technique will be improved as more of these surgeries are performed.

F. CONCLUSION Clearly, since hyperopic refractive surgery is entirely elective, the surgeon must have a thorough understanding of any potential complications of each type of procedure. The risk/benefit balance is tipping in favor of H-PRK, H-LASIK, or noncontact LTK for low to moderate hyperopes and toward intraocular lens implantation with or without clear lens extraction for moderate to high hyperopes. The use of ICRS for hyperopia may be useful for low to moderate hyperopes; however, long-term results of current studies have yet to be reported. Thorough preoperative evaluations and preventive techniques such as those described above can help to avoid complications. However, even with the most prepared surgeon and in the best of hands, complications may occur. Thus, it is essential to provide patients with a clear understanding of the potential risks of a procedure before proceeding.

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28. Knorz MC, Liermann A, Jendritza B, Hugger P. LASIK for hyperopia and hyperopic astigmatism—results of a pilot study. Semin Ophthalmol 1998; 13(2):83–87. 29. Esquenazi S, Mendoza A. Two year follow-up of last in situ keratomileusis for hyperopia. J Refract Surg 1999; 15:648–652. 30. Lindstrom RL, Hardten DR, Houtman DM, Witte B, Preschel N, Chu YR, Samuelson TW, Linebarger EJ. Six-month results of hyperopic and astigmatic LASIK in eyes with primary and secondary hyperopia. Trans Am Ophthalmol Soc 1999; 97:241–260. 31. Arbelaez MC, Knorz MC. Laser in situ keratomileusis for hyperopia and hyperopic astigmatism. J Refract Surg 1999; 15:406–414. 32. Zadok D, Maskaleris G, Montes M, Shah S, Garcia V, Chayet A. Hyperopic laser in situ keratomileusis with the Nidek EC–5000 excimer laser. Ophthalmology 2000; 107(6): 1132–1137. 33. Reviglio VE, Bossana EL, Luna JD, Muino JC, Juarez CP. Laser in situ keratomileusis for myopia and hyperopia using the Lasersight 200 laser in 300 consecutive eyes. J Refract Surg 2000; 16(6):716–723. 34. Argento CJ, Cosentino MJ. Comparison of optical zones in hyperopic laser in situ keratomileusis: 5.9 mm versus smaller optical zones. J Cataract Refract Surg 2000; 26(8):1137–1146. 35. Choi RY, Wilson SE. Hyperopic laser in situ keratomileusis: primary and secondary treatments are safe and effective. Cornea 2001; 20(4):388–393. 36. Castillo A, Diaz-Valle D, Gutierrez AR, Toledano N, Romero F. Peripheral melt of flap after laser in situ keratomileusis. J Refract Surg 1998; 14:61–63. 37. Walker MB, Wilson SE. Incidence and prevention of epithelial growth within the interface after laser in situ keratomileusis. Cornea 2000; 19:170–173. 38. O’Brart DP. The status of hyperopic laser in situ keratomileusis. Curr Opin Ophthalmol 1999; 10:247–252. 39. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999; 127:129–136. 40. Linebarger EJ, Hardten DR, Lindstrom RL. Diffuse lamellar keratitis: diagnosis and management. J Cataract Refract Surg 2000; 26:1072–1077. 41. Smith RJ, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998; 105:1721–1726. 42. Stulting RD, Carr JD, Thompson KP, Waring III GO, Wiley WM, Walker JG. Complications of laser in situ keratomileusis for the correction of myopia. Ophthalmology 1999; 106:13–20. 43. Peters NT, Lingua RW, Kim CH. Topical intrastromal steroid during laser in situ keratomileusis to retard interface keratitis. J Cataract Refract Surg 1999; 25:1437–1440. 44. Lemley HL, Chodosh J, Wold TC, Bogie CP, Hawkins TC. Partial dislocation of laser in situ keratomileusis flap by air bag injury. J Refract Surg 2000; 16:373–374. 45. Geggel HS, Coday MP. Late-onset traumatic laser in situ keratomileusis flap dehiscence. Am J Ophthalmol 2001; 131(4):505–506. 46. Vinciguerra P, Camesasca FI. Prevention of corneal ectasia in laser in situ keratomileusis. J Refract Surg 2001; 17(suppl):S187–S189. 47. Lans LJ. Experimentelle Untersuchungen uber Entstehung von Astigmatismus durch nichtperfoririende Corneawunden. Arch Ophthalmol 1898; 45:117–152. 48. Stringer H, Parr J. Shrinkage temperature of eye collagen. Nature 1964; 204:1307. 49. Neumann AC, Sanders D, Raanan M, DeLuca M. Hyperopic thermokeratoplasty: clinical evaluation. J Cataract Refract Surg 1991; 17:830–838. 50. Seiler T, Matallana M, Bende T. Laser thermokeratoplasty by means of a pulsed holmium: YAG laser for hyperopic correction. Refract Corneal Surg 1990; 6:335–339. 51. Allain JC, Lous LE, Cohen-Solal: Isometric tensions developed during the hydrothermal swelling of rat skin. Connect Tissue Res 1980; 7:127–133. 52. Durrie DS, Schumer DJ, Cavanough TB. Holmium:YAG laser thermokeratoplasty for hyperopia. J Refract Corneal Surg 1994; 10:S277–S280.

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75. Perez-Santonja JJ, Ruiz-Moreno JM, de la Hoz F, Giner-Gorriti C, Alio JL. Endophthalmitis after phakic intraocular lens implantation to correct high myopia. J Cataract Refract Surg 1999; 25:1295–1298. 76. Davidorf JM, Zaldivar R, Oscherow S. Posterior chamber phakic intraocular lens for hyperopia of Ⳮ4 to Ⳮ11 diopters. J Refract Surg 1998; 14:3. 77. Rosen E, Gore C. Staar Collamer posterior chamber phakic intraocular lens to correct myopia and hyperopia. J Cataract Refract Surg 1998; 24:596–606. 78. Fechner PU, Singh D, Wulff K. Iris-Claw lens in phakic eyes to correct hyperopia: preliminary study. J Cataract Refract Surg 1998; 24:48. 79. Pesando PM, Ghiringhello MP, Tagliavacche P. Posterior chamber collamer phakic intraocular lens for myopia and hyperopia. J Refract Surg 1999; 15:415–423. 80. Sanders DR, Martin RG, Brown DC, Shepherd J, Deitz MR, De Luca M. Posterior chamber phakic intraocular lens for hyperopia. J Refract Surg 1999; 15:309–315. 81. Pershin KB, Pashinova NF. Refractive Surgery of Hyperopia. J Refract Surg 2000; 16(suppl): S242-S246. 82. Zaldivar R, Oscherow S, Giselle R. The STAAR Posterior Chamber Phakic Intraocular Lens. Int Ophthalmol Clin 2000; 40:237–244. 83. Visessook N, Peng Q, Apple DJ, Gerl R, Schmickler S, Schoderbek RJ Jr, Guindi A. Pathological examination of an explanted phakic posterior chamber intraocular lens. J Cataract Refract Surg 1999; 25:216–222. 84. Kolahdouz-Isfahani AH, Rostamian K, Wallace D, Salz JJ. Clear lens extraction with intraocular lens implantation for hyperopia. J Cataract Refract Surg 1999; 15(3):316–323. 85. Siganos DS, Pallikaris IG. Clear lensectomy and intraocular lens implantation for hyperopia from Ⳮ7 to Ⳮ14 diopters. J Cataract Refract Surg 1998; 14:105–113. 86. Lyle WA, Jin GJ. Clear lens extraction to correct hyperopia. J Cataract Refract Surg 1997; 23(7):1051–1056. 87. Pop M, Payette Y, Amyot M. Clear lens extraction with intraocular lens followed by photorefractive keratectomy or laser in situ keratomileusis. Ophthalmology 2001; 108(1):104–111. 88. Verity SM. Intacs for myopia and hyperopia. Refractive Surgery 2001, American Academy of Ophthalmology Annual Meeting, New Orleans, 2001, pp 83–87. 89. Linebarger EJ, Song D, Ruckhofer J, Schanzlin DJ. Intacs: the Intrastromal Corneal Ring. Int Ophthalmol Clin 2000; 40:199–208. 90. Schanzlin DJ. Studies of Intrastromal Corneal Ring Segments for the correction of low to moderate myopic refractive errors. Trans Am Ophthalmol Soc 1999; 97:815–890. 91. Burris TE. Intrastromal corneal ring technology: results and indications. Curr Opin Ophthalmol 1998; 9:9–14. 92. Reinstein DZ, Srivannaboon S, Holland SP. Epithelial and stromal changes induced by Intacs examined by three-dimensional very high frequency digital ultrasound. J Refract Surg 2001; 17:310–318.

28 Future Developments BRIAN S. BOXER WACHLER Boxer Wachler Vision Institute, Beverly Hills, California, U.S.A.

Presently, there are several viable treatments for the correction of hyperopia and presbyopia. In order to broaden the scope of patient acceptance, current and investigative techniques will continue to develop in the future as the clinicians and researchers strive for greater efficacy, safety, and visual quality. Each area within refractive surgery will bring improvements specific unto itself. A. HYPEROPIA 1. LASIK and PRK Hyperopic laser-assisted in situ keratomileusis (LASIK) and photorefractive keratectomy (PRK) have the advantage of directly reshaping the cornea with high safety in low to moderate degrees of correction. There is growing interest in where hyperopic ablations should be centered on the eye. Conventional teaching is to center treatments on the pupillary center. This paradigm has developed from a 1987 article by Uozoto and Guyton(1) that demonstrated, through mathematical analysis, the rationale for pupil centration of refractive procedures. An opposing article by Pande and Hillman(2) used another set of analyses to show that the corneal sighted light reflex (which best approximates the visual axis of the eye) is the best location for centering refractive procedures. Positive angle kappa (corneal sighted light reflex located nasal to pupilary center) is not nearly as common in myopes as it is in hyperopes(3). Therefore, since the excimer was used initially for myopia, the potential for decentered ablations due to pupilary centration was low. I believe that the combination of delayed hyperopic excimer capability and the lower number of such patients undergoing treatments has obscured the issue that hyperopic ablations and perhaps myopic ablations as well may be better centered on the corneal sighted light reflex. Over 2 years ago, I began to question the recommendation of the Uozoto and Guyton 315

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Figure 1 Decentration of the treatment zone is seen in the right eye compared to the left eye in the hyperopic patient will bilateral angle kappa. The laser ablation was centered on the pupil in the right eye and on the coaxially sighted corneal light reflex in the left eye.

article after noting the decentrations of hyperopic LASIK was not uncommon in my practice. In one hyperopic patient with angle kappa, I centered the hyperopic treatment on the pupil on the first eye; on the second eye, the treatment was centered on the corneal sighted light reflex(4). The postoperative topographies demonstrate decentration of the treatment in the eye where the laser was centered on the pupil, while the fellow eye showed a centered ablation (Fig. 1). This area will undergo further study, evaluating not only topography but also visual acuity, contrast sensitivity, and higher-order aberrations. The dioptric limits of hyperopic excimer correction are not entirely clear. Therefore, there will be better definitions of the limitations of hyperopic ablations, which may be defined by acceptable degrees of induced higher-order aberrations. The pupil is the guardian of the aberrations of the eye. Based on individual pupil-dependent aberrations, future studies will likely determine the limits of hyperopic treatments. In myopic LASIK, the flap itself has been shown to be a source of higher-order aberrations, specifically spherical aberrations(5). In hyperopic LASIK, it is unknown what role flap-induced aberrations play. We can expect to see such evaluations in the future for hyperopic LASIK compared to hyperopic PRK. 2. Thermokeratoplasty Laser thermokeratoplasty (LTK)has the advantage of being very safe due to its noncontact modality, which also avoids surgery in the central cornea. As an indirectly acting procedure, one of its limitation is that the variable corneal steepening may occur with the same

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degree of treatment, also that some eyes have more instability of the effect than others. The future of LTK lies in the ability to perform intraoperative, real-time refractive monitoring using wavefront analysis during the treatment. This may allow the surgeon to stop the treatment when the desired refractive effect is achieved, making the treatment independent of corneal physiology, dehydration, stiffness, and surgeon technique. Preliminary results of lower-energy treatments hold promise for more stable postoperative effects. Like LTK, conductive keratoplasty (CK) offer the advantage of avoiding the central cornea. CK will be evaluated for additional uses, as for astigmatism, by steepening the flat axis (opposite to astigmatic keratotomy, whereby the steep axis is flattened). The ability of the probe to be used selectively may make this device useful for treating irregular astigmatism, as in keratoconus. Focal heat treatments of keratoconus have been evaluated in the past, but the controlled temperature gradient of CK may lead to more stability than previous probe technologies. 3. Intraocular Lenses Phakic intraocular lenses offer the advantage of high-quality of vision in higher corrections as well as being removable. Phakic lenses will continue to undergo safety evaluation with longer-term follow-up. Such lenses have the ability to treat higher degrees of hyperopia than excimer lasers. Wavefront analysis will help determine the optical advantages of phakic implants compared to excimer laser treatments. Adjustability of lens power may be achieved in the future through exchangeable optic with a haptic carrier or thoroughly laser adjustments of the optic postimplantation.

B. PRESBYOPIA 1. Scleral Expanding Bands Scleral expansion surgery, although not without controversy, has been slowly gaining credibility. The data from international and preliminary U.S. Food and Drug Administration clinical trial results demonstrate improved reading ability postoperatively. As a result, there will be greater attention paid to refining this technique and improving accommodative predictability. Ultrasound will be used to elucidate the relationship to segment positioning relative to zonules and lens capsule and how this affects postoperative accommodative amplitudes. Surgical intrumentation will improve, thus decreasing the duration of what is now an approximately 45-min procedure. The new device, called the “Focal One,” is an automated blade that creates the belt loops and has already improved efficiency in performing the procedure. 2. Multifocal LASIK and Intraocular Lenses Presbyopic LASIK has the advantage of improving near vision in carefully selected patients. Wavefront analysis will be an important adjunct to help elucidate the acceptable induced aberrations that maximize near vision without compromising quality of vision. Some monofocal intraocular lenses made with wavefront optic profiles have been reported to improve near vision with distance as well. Accomodating endocapsular intraocular lenses will continue to be evaluated for longer-term safety and efficacy.

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C. Conclusions We are beginning a new era as refractive surgery now embraces the challenge of correcting presbyopia. Through the creativity and determination of many ophthalmic care providers and investigators, greater numbers of patients are experiencing the increased freedom that comes with treating hyperopia and presbyopia. The future is very bright for the surgical correction of hyperopia and presbyopia. References 1. Uuzoto H, Guyton DL. Centering corneal surgical procedures. Am J Ophthalmol 1987; 103: 264–275. 2. Pande M, Hillman JS. Optical zone centration in keratorefractive surgery. Entrance pupil center, visual axis, coaxially sighted corneal reflex, or geometric corneal center? Ophthalmology 1993; 100:1230–1237. 3. Burian HM. The sensorial retinal relationships in comitant strabismus. Arch Ophthalmol 1947; 37:336–340. 4. Korn T, Chandra N, Boxer Wachler BS. Visual outcomes of hyperopic LASIK: centration based on pupil center versus visual axis. American Society of Cataract and Refractive Surgery Annual Meeting, April 2001. 5. Roberts C. Flap-induced spherical aberrations. Videorefractiva Italy Ophthalmology Congress. February 2001.

Index

Aberrations defined, 151 hyperopia vs. myopia, 159 Ablation zone decentration, 294 Accommodating and adjustable intraocular lens (IOL), 279–285 results, 283–284 Accommodation defined, 30–31 Fincham, 40–42 Gullstrand, 39–40 Helmholtz description, 32–33 measurement, 36–38 near vision, 19–20 optical changes, 30–32 scleral expansion surgery, 44 Accommodative amplitude, 20, 213 after surgery for presbyopia, 287–290 dynamic retinoscopy, 287–288 increased depth of focus, 289 measuring accommodation, 289–290 multifocal crystalline lens, 289 retinoscopic reflexes, 288–289 wavefront analysis, 290 Accommodative apparatus, anatomy, 27–28 Accommodative intraocular lens (IOL) finite-element computer simulation, 10

Accommodative mechanism, debate, 34 Accommodative tone, 211 Accommodative triad, 31 ACS (See Anterior ciliary sclerotomy (ACS)) ACS-SEP, 214 Age-related cataract (ARC), 58 Aging crystalline lens, 55–63 size and shape, 56–57 oxidative stress, 58–59 presbyopia, 57–58 refractive error, 57 zonule, 60 AIS, 223–224, 232 ALK, 5, 164 Alternating-vision bifocal contact lenses, 68 American Optical vectographic test, 195 Ametropia correctable modeling, 272 correction, 261 simultaneous within Phaco-Ersatz, 269 AMO ARRAY, 238, 239 foldable silicone multifocal intraocular lens, 250 Amplitude of accommodation, 19 simultaneous ametropia correction Phaco-Ersatz, 263–264 319

320 Anesthesia, hyperopic phakic intraocular lenses, 122 Anisometropic blur-suppression test, 195 Anterior chamber phakic intraocular lens hyperopia, 115–117 contraindications, 116 indications, 116 optic folding, 116 preoperative management, 117 visual outcomes, 117 Anterior ciliary sclerotomy (ACS), 9–10, 211, 212–214 enhanced, 213 future directions, 216 interocular pressure, 215–216 Anterior ciliary sclerotomy with implantation of scleral expansion plugs (ACSSEP), 214 Anterior ischemic syndrome (AIS), 223–224, 232 Antibiotics, hyperopic phakic intraocular lenses, 124 Aphakic epikaratophakia, 130 Apoptosis, keratocytes, 174–176 ARC, 58 Array implantation, 251 Array lens, 251 Array multifocal intraocular lens in situ, 254 Artisan hyperopia, 6 Artisan hyperopia lens, 119–120, 121 Artisan iris-claw lens, 125 hyperopic phakic intraocular lenses, 122–125 Artisan phakic intraocular lens (IOL) hyperopia, 124 Astigmatism, 67, 159, 178 hyperopic, 80–82 cross-cylinder technique, 80–82 treatment, 82 irregular, 136 rigid gas permeable lens, 67 thermal keratoplasty, 164 Automated lamellar keratoplasty (ALK), 5, 164 Axis variation, 82 Badal optical system, 52 Baikoff foldable contact lenses, 6 Barraquer cryolathe, 4 Beaver Dam Eye Study, 23 Best spectacle-corrected visual acuity (BSCVA), 110 Bifocal contact lens, presbyopia, 9, 68

Index Bifocal spectacle, first, 134 Binocular depth of focus, 196–197 Binocular inhibition, 196 Binocular summation, 196 Binocular visual acuity, 196 Blur circles, 247 BMP, 174 Bone morphogenic proteins (BMP), 174 Brucke’s muscle, 28 BSCVA, 110 Calibrated marker, 227 Capsulorhexis, 254 Carbon dioxide laser, 84 Cataracts age-related, 58 oxidative stress, 58–59 presbyopia multifocal IOLs, 240–241 refractive surgery, 237 Central corneal power, 136–137 Chromatic aberrations, 152–153 Ciliary muscle, 28–29, 35 magnetic resonance imaging, 51 CK (See Conductive keratoplasty (CK)) CK Keratoplast tip, 96 Clear lens extraction (CLE), with IOL placement, 305–307 Cobalt magnesium fluoride laser, 164 Coma pattern, 155 Compound cylindrical hyperopic errors, correction, 145–146 Computed videokeratography (CVK), 129 Conductive keratoplasty (CK), 133–134 device, 97 examinations, 98 hyperopia, 7, 95–105 thermokeratoplasty procedures, 95–96 mechanism, 96–97 patient selection, 97–98 performing, 98–100 postoperative care, 100 procedure, 97–98 radiofrequency-based, 96 for reducing hyperopia, 255 United States multicenter clinical trial, 100–105 corneal topography, 102 efficacy, 101 patients and methods, 100 results, 101–105 safety, 104–105 slit lamp, 104 stability, 103

Index Conjunctival closure, scleral expansion procedures, 231 Contact holmium:yttrium-aluminum-garnet laser (Ho:YAG) laser thermal keratoplasty (LTK), safety, 86–87 Contact laser thermal keratoplasty (LTK), 85, 86 visual outcome, 86–87 Contact lens Baikoff foldable, 6 bifocal, presbyopia, 9, 68 history, 63 living, 4 market information, 63–64 multifocal, 38, 68 vs. refractive surgery, 63–64 rigid gas permeable, 66–67 advantages, 66 disadvantages, 66 selection, 66–67 soft, 64–65 advantages, 65 astigmatism, 67 disadvantages, 65 selection, 65–66 Staar Collamer implantable, 6 Varilux, 135 Continuous carbon dioxide laser, 164 Continuous-wave diode LTK, 91–92 Contrast sensitivity, 196 LTK, 165–168 Contrast sensitivity changes after hyperopia surgery, 163–169 Conventional hyperopic LASIK wavefront measurements and aberration changes, 154–156 Cornea cautery, 83 collagen stability, laser thermal keratoplasty, 85 curvature, decentration, 78 curvature gradient, 73, 79–80 eccentricity, 72–73 ectasia, 299–300 folds, 231 haze, 295 image, ultrasound biomicroscopy, 180 implants, 7 pachymetry, 109 pigmentation lines, 178 surface profile, after hyperopia surgery, 141–150

321 [Cornea] thermal keratoplasty, slit-lamp photograph, 301 topography, 77, 137 conductive keratoplasty, 102 H-LASIK, 131 wound healing animal studies, 179–180 future directions, 182 Corneal collagen, peripheral thermokeratoplasty, 178 Corneal surgery, hyperopia wound healing, 173–183 Correction profile, hyperopia, 154 Criss-cross nylon suture, 216 Cross-cylinder technique, hyperopic astigmatism, 80–82 Crossed monovision, 194 Crystalline lens aging, 55–63 anatomy, 29 magnetic resonance imaging, 51 optics, 25 size and shape, aging, 56–57 CSV–1000E Vector Vision, 165 Customized ablation, 147–148 CVK, 129 Decentration, 82, 298, 316 ablation zone, 294 corneal curvature, 78 Defocus, 159 Defocus curve, 240 Deformable lens, equatorial stretch, 48 Diamond blade, 227 Diffractive multifocal intraocular lens (IOL), 238 Diffuse lamellar keratitis, 299 Dilated pupil, 231 Diode laser treatment, hyperopia, 7 Early hyperopic-photorefractive keratectomy (H-PRK) ablation, 130 Eccentricity, 73 Edinger-Westphal stimulated accommodation, 37 Elevation map, hyperopic LASIK, 179 Emmetrope, 18 Encircling band, 220, 221 Enhanced anterior ciliary sclerotomy (ACS), 213

322 Epikeratophakia, 4, 5 Epithelium hyperplasia, 177, 180 ingrowth, 298 measurement, 178–179 Equatorial stretch, deformable lens, 48 Erbium:glass laser, 164 Erbium:yttrium-aluminum-garnet (YAG) laser, 10 sclera incision, slit-lamp, 12 Excimer laser surgery, hyperopia, 178 Expansion band, 221, 223 Eye aberrations, 31–32 exercises, scleral expansion procedures, 231–232 increase optical power, 30–31 models, 269–275 implementation issues, 274 predictions using, 274 pros and cons, 273–274 requirements, 269 Far point, 17–18 Fechner iris-claw intraocular lens implant, 306 Fenestrated intracorneal polysulfone lenses, 7 Ferry’s line, 178 Field depth, 31 Fincham, accommodation, 40–42 Finite aspheric eye, 262 Finite-element computer simulation accommodative intraocular lens, 10 Flap complications, 297–298 Fleischer ring, 178 Fogging, 20 Glass lens, 7 Glaucoma, scleral expansion, 233 Glutathione (GSH), 58 Goldman lens, 42 Goniovideography iridectomized eyes, 50 GSH, 58 Gullstrand, accommodation, 39–40 Haze, 294–295 Helmholtz mechanism of accommodation, 27–44, 220 Helmholtz model, 209, 210 Hexagonal keratotomy, 4

Index H-LASIK, 295–300 case study, 131–135 corneal topography, 131 elevation map, 179 log contrast sensitivity values, 166 postoperative topography, 132, 133, 138 refraction, 166, 167 regression, 181 Holmium:yttrium-aluminum-garnet laser (Ho: YAG) laser, 85 pulsed, 84 Holmium:yttrium-aluminum-garnet laser (Ho: YAG) laser thermal keratoplasty (LTK), 96, 129, 164 H-PRK, 292–294 regression, 181 Hudson-Stahli line, 178 HumanOptics, 280 Humphrey Instruments biomicroscope, 49, 50 Hyperbaric oxygen, 59 Hyperion noncontact laser thermal keratoplasty, 97 Hyperopia, 2, 63–68 ablation, 69–80 keratorefractive indexes, 72–77 anterior chamber phakic intraocular lens, 115–117 Artisan phakic IOL, 124 astigmatism, 80–82 cross-cylinder technique, 80–82 treatment complications, 82 conductive keratoplasty, 7, 95–105 thermokeratoplasty procedures, 95–96 corneal surgery wound healing, 173–183 correction history, 4–5 vs. myopic corrections, 176–179 profile, 154 excimer laser surgery, 178 future developments, 315–317 intracorneal lens, 8 intracorneal segments, 107–113 keratofractive procedures, topographical correlates, 129–135 manifest vs. latent, 20 vs. myopia, aberration, 159 optics, 17–26 phakic intraocular lenses, 119–128 refractive surgery, 71 classification, 177 spherical aberration, 158

Index [Hyperopia] surgery, 3, 69–70 complications, 291–309 contrast sensitivity changes after, 163–169 corneal surface profile, 141–150 wavefront changes, 151–159 thermal keratoplasty, 164 treatment complications, 78–80 treatment wavefront, 154–156 vs. myopic, 156–159 Hyperopic-laser in situ keratomileusis. see H-LASIK Hyperopic LASIK. (See H-LASIK) Hyperopic-photorefractive keratectomy (HPRK), 292–294 regression, 181 ICL (See Iris-claw lens (ICL)) ICR myopia, 7 ICS (See Intracorneal segments (ICS)) Ideal monovision result, 190 IL–1, 174 Infrared videophotography, 51 Injector, 124 Interleukin 1 (IL–1), 174 Interocular blur suppression, 195 Interocular pressure, ciliary sclerotomy, 215–216 Interval of Strum, 31–32 Intracorneal lens, hyperopia, 8 Intracorneal ring (ICR), myopia, 7 Intracorneal segments (ICS) central steepening, 111 complications, 307–309 hyperopia, 107–113 complications, 111–113 contraindications, 109 indications, 109 postoperative care, 110 preoperative preparation, 109 surgical technique, 109 visual outcomes, 110–111 postoperative, 108 Intraocular lens (IOL) accommodating and adjustable results, 283–284 accommodative finite-element computer simulation, 10 diffractive multifocal, 238 future developments, 317

323 [Intraocular lens] hyperopia anterior chamber phakic, 115–117 contraindications, 116 indications, 116 optic folding, 116 preoperative management, 117 visual outcomes, 117 hyperopic Artisan phakic, 124 iris-fixed phakic, 119–120 light-adjusted, 282–283 multicomponent, 280–282 multifocal decreased contrast sensitivity, 238 glare and halo, 240 impression, 237–238 incorrect power, 240 types, 238 phakic (See Phakic intraocular lens) posterior chamber phakic, 6 power calculation, hyperopic phakic intraocular lenses, 122 refractive multifocal, 238 STAAR Collamer phakic, hyperopic phakic intraocular lenses, 125, 127 Intraocular pressure, 215 Intrastromal corneal ring, 307 IOL (See Intraocular lens (IOL)) Iridectomized eyes, goniovideography, 50 Iridotomy, laser peripheral, 181 Iris-claw lens (ICL) Artisan, 122–125, 125 Fechner implant, 306 hyperopic phakic intraocular lens, 122–125 Iris-fixed phakic intraocular lens, 119–120 Irregular astigmatism, 136–137 Keratoconus, 178 Keratocytes apoptosis, 174–176 laser thermal keratoplasty, 85 proliferation and migration, 175–176 Keratophakia, 4 Keratoplasty automated lamellar, 5, 164 thermal (See Thermal keratoplasty) Keratorefractive indexes, hyperopic ablation, 72–77 Keratoscopy, 76 Kera Vision, 107 Ki–67, 175

324 LADARWave device, 159 image, 155, 156, 158 Lamella diamond blade, 228 Lamellar deposits, 112 Lamellar flap, 4 Lamellar keratitis, diffuse, 299 Laser-assisted in situ keratomileusis (LASIK), 1, 6, 90, 96, 261 complications, 292–298 contrast sensitivity, 165–168 future developments, 315–316 induced hyperopia, LTK, 91 multifocal, future developments, 317 Laser peripheral iridotomy, 181 Laser scleral relaxation, 11 Laser thermal keratoplasty (LTK), 6, 83–92 complications, 91 contact, 85–88, 86 visual outcome, 86–87 contact and noncontact, 85 contact Ho:YAG, safety, 86–87 continuous-wave diode, 91–92 contraindications, 85–86 contrast sensitivity, 165–168 corneal collagen stability, 85 history, 83–84 holmium:YAG, 129, 164 Ho:YAG, 129 Hyperion noncontact, 97 keratocyte response, 85 LASIK-induced hyperopia, 91 log contrast sensitivity values, 167 mechanism, 84–85 noncontact, 85, 86 complications, 300–303 visual outcome, 87–88 noncontact Ho:YAG, safety, 87 patient selection, 85–86 PRK-induced hyperopia, 90–91 refraction, 168 Sunrise Procedure, 6 surgical procedure, 86 technique, Hyperion noncontact, 97 temperature, 84 tissue elasticity, 84–85 visual outcomes, 86–87 YAG, 96 LASIK. (See Laser-assisted in situ keratomileusis (LASIK)) Late flap dislocation, 299

Index Lens capsule, 30 crowding, 211 opacification, oxidative stress, 58–59 origin, 210 proteins, 59 Lenticule, schematic representation, 144–147 Lenticule ablation, 142 model, 149 Light-adjusted intraocular lens (IOL), 282–283 Light-difference threshold, 163 Limbus, marking, 225, 226 Living contact lens, 4 Longitudinal spherical aberration (LSA), 73 LTK (See Laser thermal keratoplasty (LTK)) Magnetic resonance imaging (MRI) ciliary muscle, 51 crystalline lens, 51 Magnification, visual acuity, 22–23 Medennium, 6 Merceline horizontal mattress suture, 216 Miller-Nadler Glaretester, 243 Minimally invasive surgery, 254 Monochromatic aberrations defined, 151–152 Monovision after refractive surgery satisfaction, 191–192 defined, 9 factors influencing, 197–198 failures, 195 presbyopia, 67–68 success rates after contact lenses, 190 task performance, 197 visual performance, 195–196 Monovision refractive surgery outcomes, 190 presbyopia, 189–198 preoperative counseling, 192–193 Monovision trial, 193 Moria LSK microkeratome, 166 MRI ciliary muscle, 51 crystalline lens, 51 Multicomponent intraocular lens, 280–282 Multifocal contact lenses, 38, 68 Multifocal effects, 134–136 historical, 134–136 Multifocal hyperopic-presbyopic photorefractive keratectomy (PRK), 203

Index Multifocal intraocular lens refractive lens exchange, 249–258 Multifocal intraocular lens (IOL), 249 decreased contrast sensitivity, 238 design, 250 glare and halo, 240 impression, 237–238 incorrect power, 240 presbyopia, 237–248 clinical results, 242 complications, 245–248 contraindications, 240–241 contrast sensitivity, 243 contrast visual acuity, 244 exclusion criteria, 241 halo and glare, 243, 247–248 incision, 241 indications, 240–241 insufficient near vision, 248 IOL decentration, 246–247 IOL position, 241 IOL power miscalculation, 245–246 occupation, 241 patient expectations, 241 patient satisfaction, 244, 245 patient view with model eye, 245 posterior CCC, 241–242 preferred surgical techniques, 241–245 spectacle usage, 243–244 theoretical benefits, 238–240 theoretical caveat, 238–240 vision simulation system, 245 visual acuity, 242–243 types, 238 Multifocal laser-assisted in situ keratomileusis, future developments, 317 Multifocal myopia-presbyopia photorefractive keratectomy, 203 Multifocal presbyopic photorefractive keratectomy videokeratography, 205 Musculus crystallinus, 39 Mylar balloon, 48 Myofibroblasts, 175–176 Myopia ablation, 71 correction vs. hyperopic corrections, 176–179 profile, 156–159 error, 18 vs. hyperopia aberration, 159 intracorneal ring, 7 refractive correction, 138 spherical aberration, 160

325 Navarro aspheric eye, 269–270 Near point, 17–18 Near reading test, 44 Near vision accommodation, 19–20 Neural networks, 137–138 Noncontact holmium:yttrium-aluminumgarnet laser thermal keratoplasty safety, 87 Noncontact laser thermal keratoplasty, 85, 86 complications, 300–303 visual outcome, 87–88 Nonsteroidal anti-inflammatory drugs (NSAID), 224 Non-wave diode laser thermal keratoplasty (LTK), 96 Ocular aberrations, 31–32 Optical zone design, 141–142, 144 Ora serrata, 29 Oxidative stress cataracts, 58–59 lens opacification, 58–59 Papillary constriction, 31 Paraxial eye, 262 Pars plana, 29 Pars plicata, 29 Perfect thermal lesion, 178 Peripheral corneal collagen thermokeratoplasty, 178 Peripheral vision, 196 Phacoemulsification, 254 Phaco-Ersatz, 260–261 simultaneous ametropia correction, 259–274 Phakic intraocular lens, 6 in and CLE with IOL implants, complications, 303–307 hyperopia, 119–128 complications, 127–128 contraindications, 120–122 indications, 120–122 posterior chamber phakic IOL, 120 preoperative preparation, 122 STAAR Collamer phakic IOL, 125, 127 surgical technique, 122–125 visual outcomes, 125–128 types, 119–120 Phorias, 197 Photic phenomena, 256 Photorefractive keratectomy (PRK), 5, 90, 202, 261 complications, 292–298 future developments, 315–316 induced hyperopia, LTK, 90–91

326 Pilocarpine, 38, 256 Plastic polymethylmethacrylate band, 220 Polymethylmethacrylate (PMMA) lenses, 202 Posterior chamber phakic intraocular lens, 6 Postoperative pupil check, scleral expansion procedures, 231 Presbyopia, 2, 67–68, 219 accommodative amplitude measurements after, 287–290 aging, 57–58 amplitude of accommodation, 20 bifocal contact lens, 9, 68 correction, 8–9 future developments, 317–318 keratofractive procedures, topographical correlates, 129–135 monovision, 67–68 monovision refractive surgery, 189–198 eye determination for distance, 193–194 preoperative counseling, 192–193 multifocal corneal approach, 201–208 historical and experimental, 201–202 results, 204–207 techniques, 202–204 multifocal intraocular lens, 237–248 optics, 17–26 restoration, background, 260 scleral relaxation, 209–214 surgery, 3 complications, 291–309 Presbyopic photorefractive keratectomy, 204 PRK (See Photorefractive keratectomy (PRK)) Progressive aspheric spectacle lens (PAL), 260 Proportional expansion, refilling model, 271–272 Pseudocycloplegia, 56 Pterygia, 178 Pulsed holmium:yttrium-aluminum-garnet laser, 84 Pupil block hyperopic phakic intraocular lenses, 122 Pupil check, postoperative scleral expansion procedures, 231 Pupillary constriction, 31 Pupil size, hyperopic phakic intraocular lenses, 122 Pure cylindrical hyperopic errors, correction, 144–145 Pure spherical hyperopic errors, correction, 141–144 Push-up test, 38, 44

Index Quadrafoil pattern, 157 Quantel Axis II immersion biometry unit, 253 Radial keratotomy (RK), 219–220, 255, 261 Radial thermokeratoplasty, 84 Radiofrequency-based conductive keratoplasty, 96 Radiofrequency energy, 83 Range of accommodation, 20–21 REACT, 59 Refilling model, 270–272 proportional expansion, 271–272 spherization, 271 Refractec, for reducing hyperopia, 255 Refractive error, 247 aging, 57 contact lens vs. refractive surgery, 64 simultaneous ametropia correction, PhacoErsatz, 263 Refractive index, 262–263 Refractive lens exchange scattergram, 252 with multifocal intraocular lens, 249–258 clinical results, 250–252 complications, 255 patient selection, 252–253 postoperative course, 256 preoperative measurements, 253–254 refractive surprise, 255–256 surgical technique, 254 targeting emmetropia, 255 Refractive procedures, 233 Refractive surgery cataract surgery, 237 vs. contact lens, 63–64 monovision, satisfaction, 191–192 Regression, 294, 302–303 H-LASIK, 181 H-PRK, 181 mechanisms, 178–182 Retinoscopic reflex, 287, 289 Retreatments, 80 Rigid gas permeable (RGP) lens, 66–67 advantages, 66 astigmatism, 67 disadvantages, 66 selection, 66–67 RK, 219–220, 255, 261 RMS, 73 Roche European-American Cataract Trial (REACT), 59 Root mean square (RMS), 73

Index SAI, 73 Scarring, middle periphery, 79 Schachar model, 209 Schachar’s scleral band procedures, 287 Schachar’s theory of accommodation, 34, 47–53, 220 challenged, 50 evidence against, 42–43 Schachar theory of presbyopia, 2 evidenced against, 43 Scheimpflug optics, 56 Sclera origin, 210 slit-lamp erbium:YAG, 12 Scleral belt loops, 228, 229 dissect, 227–229 scleral expansion procedures, 226 Scleral expanding bands future developments, 317 Scleral expansion, 219–233 anesthesia, 225 clinical results, 232 complications, 232 conjunctival closure, 231 conjunctival dissection, 225–226 current method, 224–225 early procedures, 219–220 eye exercises, 231–232 glaucoma, 233 patient selection, 223 postoperative pupil check, 231 scleral belt loops, 226 scleral expansion segments, 229–230 Scleral expansion segments, 229–230 dimensions, 230 placement, 230 Scleral expansion surgery accommodation, 44 Scleral relaxation, 2 presbyopia, 209–214 Shack-Hartmann wavefront sensor, 152 history, 153–154 principles, 154 Sighting preference, 197 Silicone expansion plugs, 214 Simultaneous ametropia correction Phaco-Ersatz, 259–270 results, 263–267 Simultaneous vision principle, 9 Sinskey hook, 109 Slab off, 67 Slit-lamp, sclera incision, erbium:YAG, 12

327 Snellen letters, 22 Snellen visual acuity, 22 Soft contact lens, 64–65 advantages, 65 astigmatism, 67 disadvantages, 65 selection, 65–66 Soft toric lenses, 67 Spectacle, bifocal, first, 134 Spherical hyperopia, ablation, 148 Spherical hyperopic error ablation, 143 Spherization, refilling model, 271 Sphingolipid, 59 Spreading dissection, 213 Square diamond blade, 227 Staar Collamer implantable contact lens, 6 Staar Collamer phakic intraocular lens hyperopic phakic intraocular lenses, 125, 127 Staar Collamer posterior chamber phakic intraocular lens implant, 305 Star Excimer Laser system, 130 StatView, 165 Stellate iron lines, 178 Stereoacuity, 196 Steroids, hyperopic phakic intraocular lenses, 124 Stocker-Busacca line, 178 Suarez spreader, 109 Summit Apex Plus Laser, 166 Sunrise Ho:YAG laser, 164 Sunrise LTK Procedure, 6 Surface asymmetry index (SAI), 73 Swan-Jacob gonioscopy, 42 Temperature, laser thermal keratoplasty, 84 Thermal keratoplasty, 83 astigmatism, 164 cornea, slit-lamp photograph, 301 future developments, 316–317 hyperopia, 164 peripheral corneal collagen, 178 radial, 84 Thermal lesion, perfect, 178 Thornton Triple Edge diamond knife, 212 Tissue elasticity, laser thermal keratoplasty, 84–85 TNF alpha, 174 Transition zone design, 142–145 lack, 79 Trefoil pattern, 157

328 Tschering’s studies, 34–36 Tschering’s theory of accommodation, 33 Tucker, 125 Tumor necrosis factor (TNF) alpha, 174 UBM, 49, 212 corneal image, 180 UCVA, 110 Ultrasound biomicroscopy (UBM), 49, 212 corneal image, 180 Uncorrected visual acuity (UCVA), 110 Uncrossed monovision vs. crossed monovision, 194–195 Unfolder injector, 250 Variable-contrast charts (VCVAC), 243 Varifocality, 135 Varilux contact lens, 135 VCVAC, 243 Vector Vision CSV–1000E, 165 ViewPoint Conductive Keratoplasty CK system, 97 Vision, peripheral, 196 Visual acuity, 300 best spectacle-corrected, 110

Index [Visual acuity] binocular, 196 magnification, 22–23 Snellen, 22 uncorrected, 110 Visual fields, 196 Volume calculations, 272 Von Helmholtz, Hermann Ludwig Ferdinand, 28 Wave aberration, detection, 153–154 Wavefront, defined, 151 Wavefront changes, hyperopia surgery, 151–159 Wavefront measurements and aberration changes conventional hyperopic LASIK, 154–156 Wound healing, hyperopic corneal surgery, 173–183 Zeiss IOLMaster, 253 Zemax EE, 50 Zernike modes, 153 Zonular fibers, 29–30 Zonule, aging, 60