Cornea and Refractive Atlas of Clinical Wisdom [1st ed.] 1556428677, 9781556428678

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Cornea and Refractive Atlas of Clinical Wisdom, edited by Dr. Samir A. Melki and Dr. Mark A. Fava, gathers unique observations that experienced eye surgeons have learned in their daily treatment of patients. Each chapter begins with a detailed description of the condition from diagnosis to symptoms to complications to eventual treatment methods. Features Include: • Practical tips, as opposed to the theoretical aspects of the disease. • Diagnostic and medical management of the disease. • Anecdotal experience that has been proven correct over the years versus the type of information that is awaited for from a large clinical trial. • Full color images reinforce the information presented in the book. Cornea and Refractive Atlas of Clinical Wisdom also includes a condensed summary of diagnostic pearls acquired through the years from personal experience with a focus on diagnosis and medical management. Some Topics Include: • Imaging and diagnostics: IOL power, corneal topography • Ocular surface disorders: Ocular chemical injury, dry eye syndrome • Infectious diseases: Fungal keratitis, epidemic keratoconjunctivitis • Inflammatory diseases: Scleritis, Stevens-Johnson syndrome • Neoplasia and epithelial downgrowth: Melanocytic lesions of the ocular surface • Dystrophies and degeneration: Keratoconus, corneal transplant rejection • Refractive surgery: LASIK flap folds, corneal ectasia aer LASIK All ophthalmologists, regardless of level of experience, will have an interest in the clinical diagnosis and medical management information gathered inside the pages of Cornea and Refractive Atlas of Clinical Wisdom.

Samir A. Melki and Mark A. Fava Dimitri T. Azar James Chodosh Reza Dana Claes H. Dohlman C. Stephen Foster Gary N. Foulks Mark S. Gorovoy Kenneth J. Hoffer

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I N C O R P O R A T E D

MEDICAL/Ophthalmology

ATLASOF CLINICALWISDOM

SLACK

slackbooks.com

Cornea and Refractive

Cornea and Refractive ATLASOFCLINICALWISDOM

ATLASOF CLINICALWISDOM

Melki • Fava

Cornea and Refractive

Kenneth R. Kenyon Peter R. Laibson Mark J. Mannis Deborah Pavan-Langston Carol L. Shields Roger F. Steinert Elmer Y. Tu

SLACK Incorporated

2/1/2012 11:42:42 AM

Edited by

Samir A. Melki, MD, PhD Director, Boston Eye Group Ophthalmology Medical Director, UK Specialist Hospitals Attending Physician, Massachusetts Eye and Ear Infirmary Harvard Medical School Boston, Massachusetts

Mark A. Fava, MD, FRCSC Boston Eye Group Attending Surgeon, Beth Israel Deaconess Hospital Boston, Massachusetts

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ISBN: 978-1-55642-867-8 Copyright © 2011 by SLACK Incorporated All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without written permission from the publisher, except for brief quotations embodied in critical articles and reviews. The procedures and practices described in this book should be implemented in a manner consistent with the professional standards set for the circumstances that apply in each specific situation. Every effort has been made to confirm the accuracy of the information presented and to correctly relate generally accepted practices. The authors, editor, and publisher cannot accept responsibility for errors or exclusions or for the outcome of the material presented herein. There is no expressed or implied warranty of this book or information imparted by it. Care has been taken to ensure that drug selection and dosages are in accordance with currently accepted/recommended practice. Off-label uses of drugs may be discussed. Due to continuing research, changes in government policy and regulations, and various effects of drug reactions and interactions, it is recommended that the reader carefully review all materials and literature provided for each drug, especially those that are new or not frequently used. Any review or mention of specific companies or products is not intended as an endorsement by the author or publisher. SLACK Incorporated uses a review process to evaluate submitted material. Prior to publication, educators or clinicians provide important feedback on the content that we publish. We welcome feedback on this work. Published by: SLACK Incorporated 6900 Grove Road Thorofare, NJ 08086 USA Telephone: 856-848-1000 Fax: 856-848-6091 www.slackbooks.com Contact SLACK Incorporated for more information about other books in this field or about the availability of our books from distributors outside the United States. Library of Congress Cataloging-in-Publication Data Cornea and refractive atlas of clinical wisdom / [edited by] Samir A. Melki, MD, PhD, Mark A. Fava, MD, FRCSC. p. ; cm. Includes bibliographical references and index. ISBN 978-1-55642-867-8 (alk. paper) 1. Cornea--Diseases--Atlases. 2. Eye--Refractive errors--Atlases. I. Melki, Samir A., 1965- editor. II. Fava, Mark A., 1972- editor. [DNLM: 1. Corneal Diseases--therapy--Atlases. 2. Clinical Medicine--methods--Atlases. 3. Refractive Errors-therapy--Atlases. WW 17] RE336.C6325 2011 617.7’19--dc22 2010054466 For permission to reprint material in another publication, contact SLACK Incorporated. Authorization to photocopy items for internal, personal, or academic use is granted by SLACK Incorporated provided that the appropriate fee is paid directly to Copyright Clearance Center. Prior to photocopying items, please contact the Copyright Clearance Center at 222 Rosewood Drive, Danvers, MA 01923 USA; phone: 978-750-8400; web site: www.copyright.com; email: [email protected]. Printed in the United States of America. Last digit is print number: 10 9 8 7 6 5 4 3 2 1

Dedication To my mother, Sima, Thank you for being a role model of dedication, perseverance, and compassion. Your selfless love and devotion will always be an example for all of us to follow. —SAM

To Erin, Thank you for your love, support, and lighting the way for this and all of our journeys. —MAF

Contents Dedication ...................................................................................................................................................................................... v Acknowledgments ..........................................................................................................................................................................xi About the Editors ........................................................................................................................................................................ xiii Contributing Authors ................................................................................................................................................................... xv Preface .........................................................................................................................................................................................xvii Foreword by Joan W. Miller, MD ..............................................................................................................................................xix

Section I

Imaging and Diagnostics ...................................................................................................1

Chapter 1

Intraocular Lens Power Calculation .................................................................................................................3 Kenneth J. Hoffer, MD, FACS

Chapter 2

Corneal Topography ......................................................................................................................................... 15 Isaac W. Porter, MD and Dimitri T. Azar, MD

Section II

Ocular Surface Disorders.................................................................................................21

Chapter 3

Dry Eye Syndrome and Lid Margin Disease ..................................................................................................23 Gary N. Foulks, MD, FACS

Chapter 4

Recurrent Erosion Syndrome .......................................................................................................................... 33 Peter R. Laibson, MD

Chapter 5

Persistent Corneal Epithelial Defects .............................................................................................................. 39 Kenneth R. Kenyon, MD

Chapter 6

Pterygium: Medical and Surgical Management............................................................................................. 55 Kenneth R. Kenyon, MD and Mark A. Fava, MD, FRCSC

Chapter 7

Ocular Chemical Injury ...................................................................................................................................63 Kenneth R. Kenyon, MD and Michael D. Wagoner, MD, PhD

Section III Infectious Diseases ...........................................................................................................77 Chapter 8

Ocular Herpes Simplex ....................................................................................................................................79 Deborah Pavan-Langston, MD, FACS

Chapter 9

Herpes Zoster Ophthalmicus ..........................................................................................................................85 Deborah Pavan-Langston, MD, FACS

Chapter 10

Epidemic Keratoconjunctivitis ........................................................................................................................ 91 James Chodosh, MD, MPH

Chapter 11

Bacterial Keratitis .............................................................................................................................................97 Mark Krakauer, MD, MPhil and Dimitri T. Azar, MD

Chapter 12

Fungal Keratitis ............................................................................................................................................... 101 Elmer Y. Tu, MD

Chapter 13

Acanthamoeba Keratitis .................................................................................................................................. 107 Elmer Y. Tu, MD

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Contents

Chapter 14

Staphylococcal Marginal Keratitis ................................................................................................................ 113 Peter R. Laibson, MD

Section IV Inflammatory Diseases .................................................................................................. 117 Chapter 15

Episcleritis ....................................................................................................................................................... 119 Reza Dana, MD, MSc, MPH

Chapter 16

Scleritis ............................................................................................................................................................125 C. Stephen Foster, MD, FACS, FACR and Sana S. Siddique, MD

Chapter 17

Peripheral Ulcerative Keratitis....................................................................................................................... 131 C. Stephen Foster, MD, FACS, FACR and Luis Alonso Gonzalez-Gonzalez, MD

Chapter 18

Stevens-Johnson Syndrome ........................................................................................................................... 141 C. Stephen Foster, MD, FACS, FACR and Laura Amorese, MD

Chapter 19

Ocular Cicatricial Pemphigoid ...................................................................................................................... 149 C. Stephen Foster, MD, FACS, FACR and Ribhi Hazin, MD

Chapter 20

Steroid Use in Corneal Disease...................................................................................................................... 153 Claes H. Dohlman, MD, PhD and Simon Wu, MD

Section V

Neoplasia and Epithelial Downgrowth.........................................................................157

Chapter 21

Ocular Surface Squamous Neoplasia ............................................................................................................ 159 James Chodosh, MD, MPH

Chapter 22

Melanocytic Lesions of the Ocular Surface .................................................................................................. 165 Carol L. Shields, MD

Chapter 23

Epithelial Downgrowth .................................................................................................................................. 171 Claes H. Dohlman, MD, PhD; Mark A. Fava, MD, FRCSC; and Daniel Cherfan, BSc(Hon), MA/MS

Section VI Dystrophies and Degenerations ....................................................................................179 Chapter 24

Keratoconus..................................................................................................................................................... 181 Mark J. Mannis, MD, FACS and Jennifer Y. Li, MD

Chapter 25

Fuchs’ Dystrophy and Bullous Keratopathy ................................................................................................. 187 Mark S. Gorovoy, MD

Chapter 26

Stromal Dystrophies ....................................................................................................................................... 191 Jessica Jer-Heng Wong, MD and Dimitri T. Azar, MD

Chapter 27

Corneal Transplant Rejection ........................................................................................................................ 197 Reza Dana, MD, MSc, MPH

Section VII Refractive Surgery ......................................................................................................... 205 Chapter 28

Diffuse Lamellar Keratitis..............................................................................................................................207 Samir A. Melki, MD, PhD and Mark A. Fava, MD, FRCSC

Chapter 29

Epithelial Ingrowth After LASIK .................................................................................................................. 211 Samir A. Melki, MD, PhD and Mark A. Fava, MD, FRCSC

Contents

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Chapter 30

Corneal Ectasia After LASIK ......................................................................................................................... 217 Roger F. Steinert, MD

Chapter 31

LASIK Flap Folds ............................................................................................................................................227 Roger F. Steinert, MD

Chapter 32

Corneal Scarring and Refractive Surgery ..................................................................................................... 233 Samir A. Melki, MD, PhD; Daniel Cherfan, BSc(Hon), MA/MS; and John Mauro, DO

Financial Disclosures .................................................................................................................................................................. 241 Index ........................................................................................................................................................................................... 243

Acknowledgments Was it difficult to convince these well-established and published authors to share personal experience while their careers have been based on more evidence-based science? We were pleasantly surprised to find that all of them shared our view concerning the value of personal observation in the practice of medicine. They have wholeheartedly taken the bold step to say loudly what they have been thinking quietly throughout the course of their careers. We would like to extend our greatest thanks to all of the contributing authors who were gracious enough to participate in this project despite their demanding schedules. We thank them for sharing our belief that personal experience in medicine is just as important as rigorous scientific method. This group of authors is among the most proficient and accomplished practitioners in the field, and we have attempted to capture the intangible of human experience in print. We also wish to thank Jennifer Briggs and John Bond from SLACK Incorporated for believing in the concept of this book while providing unwavering support in the process.

AbouttheEditors Samir A. Melki, MD, PhD, is the founder and medical director of the Boston Eye Group. He is an attending physician on the Cornea and Refractive Surgery Service at the Massachusetts Eye and Ear Infirmary. He teaches at Harvard Medical School where he holds a title of assistant clinical professor. Dr. Melki obtained his BSc from the American University of Beirut followed by an MD, PhD degree from Vanderbilt University. He completed his residency at Georgetown University and additional fellowship training at the Massachusetts Eye and Ear Infirmary. Dr. Melki’s special interest lies in refractive and corneal surgery. His daily practice encompasses clinical duties, teaching, and research. Dr. Melki is also the ophthalmology medical director for the UK Specialist Hospitals, providing high volume cataract surgery for National Health Service patients in the United Kingdom.

Mark A. Fava, MD, FRCSC, began his interest in the visual sciences conducting research under the direction of Professor Kathryn Murphy, PhD, of the Visual Neuroscience Laboratory at McMaster University where he obtained his Bachelor of Science. He then went on to complete his medical degree at the University of Western Ontario. After completing his ophthalmology training at Queen’s University in Kingston, Ontario, Dr. Fava was awarded the E. A. Baker Foundation for the Prevention of Blindness Fellowship through the Canadian National Institute for the Blind to pursue training in cornea, refractive surgery, and external disease under the supervision of Dr. Melki, founder of the Boston Eye Group. During his fellowship, Dr. Fava acted as an assistant in ophthalmology at the Massachusetts Eye and Ear Infirmary and associate staff at Beth Israel Deaconess Medical Center in Boston. Dr. Fava is currently practicing at the Boston Eye Group and as an attending surgeon at Beth Israel Deaconess Medical Center where his main focus of practice is corneal, anterior segment, and refractive surgery.

ContributingAuthors Laura Amorese, MD (Chapter 18) Research Fellow Massachusetts Eye Research and Surgery Institution Cambridge, Massachusetts Preliminary Internal Medicine North Shore Medical Center Salem, Massachusetts Dimitri T. Azar, MD (Chapters 2, 11, 26) B. A. Field Chair, Ophthalmologic Research Professor and Head Department of Ophthalmology and Visual Sciences Illinois Eye and Ear Infirmary University of Illinois at Chicago Chicago, Illinois Daniel Cherfan, BSc(Hon), MA/MS (Chapters 23, 32) Medical Student Royal College of Surgeons in Ireland Dublin, Ireland James Chodosh, MD, MPH (Chapters 10, 21) Massachusetts Eye and Ear Infirmary Harvard Medical School Boston, Massachusetts Reza Dana, MD, MSc, MPH (Chapters 15, 27) Claes H. Dohlman Professor of Ophthalmology Vice Chairman and Associate Chief of Ophthalmology (Academic Programs) Director, Cornea and Refractive Surgery Services Massachusetts Eye and Ear Infirmary Senior Scientist and W. Clement Stone Scholar Schepens Eye Research Institute Boston, Massachusetts Claes H. Dohlman, MD, PhD (Chapters 20, 23) Professor of Ophthalmology Harvard Medical School Chief Emeritus Massachusetts Eye and Ear Infirmary Boston, Massachusetts C. Stephen Foster, MD, FACS, FACR (Chapters 16, 17, 18, 19) Founder and President Massachusetts Eye Research and Surgery Institution Founder and President Ocular Immunology and Uveitis Foundation Cambridge, Massachusetts Clinical Professor of Ophthalmology Harvard Medical School Boston, Massachusetts

Gary N. Foulks, MD, FACS (Chapter 3) Arthur and Virginia Keeney Professor of Ophthalmology Department of Ophthalmology and Vision Science University of Louisville School of Medicine Louisville, Kentucky Luis Alonso Gonzalez-Gonzalez, MD (Chapter 17) Research Fellow Massachusetts Eye Research and Surgery Institution Ocular Immunology and Uveitis Foundation Cambridge, Massachusetts Mark S. Gorovoy, MD (Chapter 25) Gorovoy MD Eye Specialists Fort Myers, Florida Ribhi Hazin, MD (Chapter 19) Massachusetts Eye Research and Surgery Institution Cambridge, Massachusetts Kenneth J. Hoffer, MD, FACS (Chapter 1) Clinical Professor of Ophthalmology Jules Stein Eye Institute University of California Los Angeles, California Kenneth R. Kenyon, MD (Chapters 5, 6, 7) Cornea Consultants International Associate Clinical Professor Harvard Medical School Senior Surgeon Massachusetts Eye and Ear Infirmary Senior Clinical Scientist Schepens Eye Research Institute Boston, Massachusetts Mark Krakauer, MD, MPhil (Chapter 11) Department of Ophthalmology and Visual Sciences Illinois Eye and Ear Infirmary University of Illinois at Chicago Chicago, Illinois Peter R. Laibson, MD (Chapters 4, 14) Director Emeritus Cornea Service Wills Eye Institute Professor of Ophthalmology Thomas Jefferson University School of Medicine Philadelphia, Pennsylvania

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Contributing Authors Jennifer Y. Li, MD (Chapter 24) UC Davis Health System Eye Center Sacramento, California Mark J. Mannis, MD, FACS (Chapter 24) Professor and Chair UC Davis Health System Eye Center Sacramento, California John Mauro, DO (Chapter 32) Attending Ophthalmologist New York Eye and Ear Infirmary New York, New York Stony Brook University Medical Center Stony Brook, New York North Shore Eye Care Smithtown, New York Deborah Pavan-Langston, MD, FACS (Chapters 8, 9) Professor of Ophthalmology Harvard Medical School Massachusetts Eye and Ear Infirmary Boston, Massachusetts Isaac W. Porter, MD (Chapter 2) Illinois Eye and Ear Infirmary University of Illinois at Chicago Chicago, Illinois Carol L. Shields, MD (Chapter 22) Co-Director, Ocular Oncology Service Wills Eye Hospital Professor of Ophthalmology Thomas Jefferson University Philadelphia, Pennsylvania Sana S. Siddique, MD (Chapter 16) Massachusetts Eye Research and Surgery Institution Ocular Immunology and Uveitis Foundation Cambridge, Massachusetts

Roger F. Steinert, MD (Chapters 30, 31) Irving H. Leopold Professor and Chair of Ophthalmology Professor of Biomedical Engineering Director, Gavin Herbert Eye Institute University of California, Irvine Irvine, California Elmer Y. Tu, MD (Chapters 12, 13) Director, Cornea and External Disease Service Associate Professor of Clinical Ophthalmology Department of Ophthalmology and Visual Sciences Illinois Eye and Ear Infirmary University of Illinois at Chicago Chicago, Illinois Michael D. Wagoner, MD, PhD (Chapter 7) Professor of Ophthalmology Department of Ophthalmology and Visual Sciences University of Iowa Carver College of Medicine Iowa City, Iowa Jessica Jer-Heng Wong, MD (Chapter 26) Illinois Eye and Ear Infirmary University of Illinois at Chicago Chicago, Illinois Simon Wu, MD (Chapter 20) Assistant in Ophthalmology Massachusetts Eye and Ear Infirmary Boston, Massachusetts

Preface Where does personal experience fit into the world of evidence-based medicine, meta-analysis, and randomized clinical trials? Are personal impressions merely biased ex cathedra statements from experts who value their own opinions over the scientific method? A dictionary definition of experience states: “knowledge or practical wisdom gained from what one has observed, encountered, or undergone”…. In setting to write this book, we asked men and women of experience to share their clinical wisdom acquired through thousands of clinical encounters. We believe that empirical experience can be invaluable when handled objectively and wisely. This does not diminish the necessity of the rational scientific method but ignoring it would surely deprive us from a precious side of medicine, the clinician’s intuition. In a 1939 paper examining “The Phrase Art and Science of Medicine,”1 Otto Guttentag emphasizes the possibility and necessity of looking from 2 qualitative angles at patients…. the term scientific connotes the aim to judge by measuring while the art is used to indicate the attitude of the clinician toward nature and patient, which is quite similar to that of an artist toward nature and his creation. In this book we have strived to balance the 2 approaches allowing accomplished physicians to convey to the reader the essence of what they personally learned over many years of clinical observation.

References 1.

Guttentag O. The phrase art and science of medicine. Cal West Med. 1939;50(2):86-87.

Foreword Physicians aspire to practice evidence-based medicine whenever possible, applying findings from randomized clinical trials when available. Often, though, data are not available to support clinical decisions, particularly in uncommon disorders or when our patients do not match those enrolled in the clinical trials. The knowledge shared by experienced physicians remains a fundamental cornerstone of high-quality care, and textbooks like Cornea and Refractive Atlas of Clinical Wisdom provide a collection of wonderful insights and useful “pearls.” Drs. Samir Melki and Mark Fava have compiled in this volume not just a comprehensive array of conditions and problems faced by anterior segment practitioners and methods of treatment: make no mistake, the facts presented are comprehensive and valuable to any anterior segment ophthalmologist. What sets this volume apart is that it captures, through its “In My Experience” sections on each topic, the fine details of diagnosis and treatment that each highly experienced author has learned through years of seeing patients and carrying out research. These sections will benefit any ophthalmologist seeking greater insight into the diagnosis and management of some of the difficult conditions encountered by anterior segment physicians and will be of great use for posterior segment ophthalmologists whose updated knowledge of these conditions will allow them to provide the most comprehensive and accurate diagnoses for those diseases that they see less often and that may impact the vision of their patients. —Joan W. Miller, MD Chief of Ophthalmology Massachusetts Eye and Ear Infirmary Massachusetts General Hospital Chair, Department of Ophthalmology Harvard Medical School Boston, Massachusetts

SectionI

ImagingandDiagnostics

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chapter 1 Intraocular Lens Power Calculation Kenneth J. Hoffer, MD, FACS Since Sir Harold Ridley experienced a 21-diopter (D) “surprise” in lens power calculation on his first two cases in 1949–1950, we have been seeking ways to calculate intraocular lens (IOL) power with greater accuracy (Figure 1-1). Without a reasonable calculation of IOL power, IOLs would never have proceeded to the standard of care they are today. This entire subject is based on the formula to calculate the power of the IOL, which requires input of specific biometric data that must be collected for each individual patient. Let us first discuss the foundation of the formula and then the collection of the biometry. When the human lens is replaced with an IOL, the optical status becomes a two-lens system (cornea and IOL) projecting an image onto the fovea. The distance (X) between the two lenses affects the refraction, as does the distance (Y) between the two-lens system and the fovea. X is defined as the distance from the anterior surface (vertex) of the cornea to the effective principal plane of the IOL in the visual axis. Y is defined as the distance from the principal plane of the IOL to the photoreceptors of the fovea in the visual axis. It is easy to see that X + Y is equal to the visual axis axial length of the eye (A). Therefore, knowing X and A will allow the calculation of Y (Y = A − X). To calculate the IOL power (P), we must know the vergence of the light rays entering the cornea (refractive error, R). For emmetropia, R is zero. The relationship of these factors (X, Y [A − X], P, K, R) is such that a formula can be written to describe it. Knowing the values of any four of these variables will allow for the calculation of the fifth.

Biometry Axial Length If the crystalline lens (cataract) is to be removed, obtaining an accurate axial length (AL) is mandatory. If the lens has already been removed (aphakia/pseudophakia) or will not be removed (phakic IOL), an AL is not always necessary because the correct implant lens power can be calculated using a refraction formula (see below). Because this formula requires an accurate vertex distance, it is not dependable in cases of aphakia where errors in the vertex distance of a high-powered refraction can have a significant effect.

Axial Length Measurement Instruments Up to 1999, all AL-measuring instruments have been A-scan ultrasound units. In 1999, Carl Zeiss Meditec AG (Jena, Germany) introduced a new instrument that uses laser coherent interferometry to measure AL. The IOLMaster performs five functions: it (1) measures the AL, (2) measures the corneal power (K or r), (3) measures the anterior chamber depth (ACD), (4) measures the corneal white-towhite diameter (the latter three by optical means), and (5) performs the formula IOL power calculations using four modern third-generation theoretic formulas (the Haigis, the Hoffer Q, the Holladay I, and the SRK/T). A multitude of reports in the literature conclude that the IOLMaster (Ver 5) is extremely accurate and reproducible but cannot obtain results in about 5% of eyes because of either posterior subcapsular cataract, the density of a cataract, or the patient’s

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Melki SA, Fava MA, eds. Cornea and Refractive Atlas of Clinical Wisdom (pp 3-14). © 2011 SLACK Incorporated

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Chapter 1

inability to fixate. We have so far noticed increased success with posterior subcapsular cataracts with the latest (2008) version of the instrument software. In 2009, Haag-Streit (Koeniz, Switzerland) introduced a similar unit called the Lenstar LS-900 (Figure 1-2).

ImmersionUltrasound Technique The immersion technique of Ossoinig1 has been shown to be more accurate than the standard applanation contact technique in several studies over the past 15 years.2-6 They report a mean average shortening of the AL of 0.25 to 0.33 mm using applanation compared to immersion. Arguments against using the immersion technique are that it is time consuming, more expensive, messy, and requires the patient to be totally supine. On the contrary, the evaluation can be performed in a standard ophthalmic examination chair reclined backward at a 45-degree angle with the headrest set back so that the patient’s AL is perpendicular to the floor (Figure 1-3). To maintain a nonleaking fluid bath in the Ossoinig scleral shell (Hansen Ophthalmic Development Labs, Coralville, Iowa), we use a 50/50 dilution of 2.5% hydroxypropyl methylcellulose (Goniosol) in Dacriose solution. Once the eye is anesthetized topically, the scleral shell is gently placed between the lids and filled three-quarters full with the solution. Any air bubbles should be vacuumed with a short silicone tube attached to a syringe. The latter can also be used to remove the solution at the completion of the procedure. The ultrasound probe is placed into the solution and positioned parallel to the axis of the eye (Figure 1-4). Axiality is judged by watching for the correct spike patterns on the oscilloscope screen as the probe position is adjusted. First, the corneal and retinal spikes must be identified and equally maximized. An undilated pupil aids the examiner by the fact that eliminating the iris spikes improves the chances of being more axial; a dilated pupil eliminates this advantage.

Ultrasound Velocities The nominal average velocity for the normal range AL eye is 1555 m/s. Because of the inversely proportional change in the axial ratio of solid to liquid as the eye increases in length, the average phakic velocity of a short, 20-mm eye is 1560 m/s and that of a long, 30-mm eye is 1550 m/s (Figure 1-5). This factor amounts to only a small (0.25 D) error in the extremes of AL, but it can be corrected. The inversely proportional relationship is greater in pseudophakic eyes but is not a factor at all in aphakic eyes (1534 m/s). If an eye has been measured using the wrong velocity, it can be easily corrected without remeasuring the eye by using the following formula:

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ALCORRECTED = (ALMEASURED) × (VCORRECT) ÷ VMEASURED where V = ultrasound velocity. This is because the instrument does not measure length or distance (d) directly. Instead, it measures the time (t) it takes the sound to traverse the eye and converts it to a linear value using the velocity (V) formula where d = V × t.

Retinal Thickness Factor Some formula writers add a value to the ultrasonic AL measurement to take into account the additional distance from the surface of the retina to the level of the receptive end of the retinal cones. This value has been estimated to be 0.20 to 0.25 mm and is automatically added to the AL in some formulas (Binkhorst, Holladay) and not used at all in others (Colenbrander, Hoffer Q).

Corneal Power The first lens in the eye’s optical system is the cornea. We usually think of corneal power in terms of diopters of optical power, but really we are measuring the radius of curvature of the anterior surface and making assumptions regarding the curvature of the back surface based on the Gullstrand eye. It has been proposed by many that we should convert to using the radius of curvature (r) rather than diopters, but that may take a long time, especially in America.7

Instrumentation A manual keratometer measures only the front surface of the cornea and converts the radius of curvature (r) obtained to diopters (K reading) using an index of refraction (IR) of 1.3375 (some units use a different IR). The formula to change from D to r is (r = 337.5/D) and from r to D is (D = 337.5/r). Many postulate that this index is too high and that lower ones should be used. Corneal topography units also supply simulated corneal power values, as do the newer Scheimpflug camera instruments such as the Pentacam and Galilei units.

Astigmatism Regular astigmatism is not a factor in IOL power calculation because the goal is to predict the postoperative spherical equivalent refractive error. Therefore, the average of the two K readings is the only value used.

Keratoconus Eyes Because a cornea with keratoconus can become very steep, it is important to consider the fact that formulas that use the K reading to estimate the ultimate IOL position may overestimate this actual PO position. One should be aware

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Intraocular Lens Power Calculation that the K reading has less of this effect in the Hoffer Q formula than the other modern theoretic formulas. It is not a factor with the Haigis formula because it does not use the K reading at all in estimating the effective lens position (ELP).

Previous Corneal Refractive Surgery Previous corneal refractive surgery causes three errors in IOL power calculation: (1) error in obtaining K readings, (2) error due to the change in the cornea’s IR (not a factor in a radial keratotomy eye), and (3) modern theoretic formulas use the flat K reading to estimate the IOL position. The first error is the fact that most keratometers measure at the 3.2-mm zone of the central cornea, which often misses the central flatter zone of effective corneal power; the flatter the cornea, the larger the zone of measurement. There are now many methods proposed to more accurately estimate the corneal power in these refractive surgery eyes. There are also methods proposed that adjust the calculated IOL power using standard data.

Corneal Transplant Eyes A problem also arises when attempting to predict what the corneal power will be after corneal transplantation. Some have suggested using the corneal power of the fellow eye (if it is available) or using an average of one’s posttransplant corneal powers, but published reports show a very large range of prediction and refractive errors using these methods. Performing the IOL implantation after the corneal transplant has settled was suggested by this author in 1986, and in 1990, Geggel reported excellent refractive results using this two-stage approach, with 66% of eyes achieving 20/40 or better visual acuity without correction.7,8 A secondary piggyback toric IOL or toric phakic IOL is another alternative to correct residual ametropia in these cases.

Eyes With Corneal Scarring The problem of obtaining an accurate corneal power measurement in eyes with corneal scarring and irregular astigmatism has not received much attention. Cua et al9 studied this in two eyes needing IOL exchange due to large IOL surprises of +5.00 and −7.50 D. They compared six methods to ascertain the corneal power and found the hard contact lens over refraction method to be the most accurate, decreasing the error they would have obtained with the manual keratometer of +4.00 to 5.00 D to -0.40 to 1.60 D. This may be a useful clinical tool in such cases.

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Intraocular Lens Axial Position This factor was historically referred to as the anterior chamber depth (ACD) because the optic of all IOLs in the early era was positioned in front of the iris, in the anterior chamber. Because most IOLs today are positioned behind the iris, new terminology has been offered such as ELP. ACD is defined as the axial distance between the two lenses (cornea and lens or IOL) or, more exactly, the distance from the central front surface (anterior vertex) of the cornea to the effective principal plane of the IOL (or front surface of the crystalline lens). This value is required for all formulas and it is incorporated into the A-constant specific to each IOL style for SRK formulas or as an ACD, both supplied by the manufacturer. Some researchers have proposed that it would be useful to measure the preoperative anatomic ACD (corneal epithelium to anterior lens capsule) either with an A-scan unit or by optical pachymetry. The author performed such a comparison study on 44 eyes and showed that the optical method (Haag-Streit Optical Pachymeter II) resulted in a mean 0.20 ± 0.35 mm deeper ACD than obtained by immersion ultrasound using 1548 m/s (3.14 vs 2.93 mm). The IOL position has been considered the least important of the three variables as a cause of IOL power error, but IOL position has received the most attention from formula authors over the past 15 years. The major effort has been toward better prediction of where the IOL will ultimately rest.

Retinal Detachment Eyes: Hoffer Double-Axial Length Method This method, proposed by the author in 2000, uses two ALs. The PO retinal detachment AL of the eye is used to calculate the IOL power. Because most postencircling band retinal detachment eyes have a 1.0 mm increase in AL, and the ACD is not affected by the encircling band, we use the AL - 1 mm in the part of the formula that calculates the predicted ELP. This amounts to making the IOL a little weaker than would be predicted using all the modern formulas. Alternatively, one would just lower the power of the recommended IOL in such retinal detachment eyes.

Formulas10-28 The first IOL power formula was published by Fyodorov in 1967. Colenbrander wrote his in 1972, followed by the Hoffer formula in 1974. In 1982, the author demonstrated a direct relationship between the position of a polymethyl methacrylate (PMMA) posterior chamber IOL and the AL and presented a formula to better predict ACD. In 1988, Holladay proposed a direct relationship between the steepness of the cornea and the position of the IOL (Holladay I). In 1992, the Hoffer Q formula was developed using a

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Chapter 1

tangent function to accomplish the same effect. In 1990, Olsen proposed using the preoperative ACD and other factors to better estimate the postoperative IOL position and published algorithms for this. After several studies showed that the Holladay I formula was not as accurate as the Hoffer Q in eyes shorter than 22 mm, Holladay used the preoperative ACD measurement as well as corneal diameter, lens thickness, refractive error, and age to calculate an estimated scaling factor that multiplies the IOL-specific ACD. This Holladay II formula has been promulgated since 1996 but has yet to be published. In 1999, Wolfgang Haigis proposed using three constants to predict the position of the IOL based on the AL and preoperative ACD measurement.

tors, and computer programs that run on DOS, Windows, and Macintosh systems as well as for the handheld Palm PDA operating system (Figure 1-7). You can also program the published ones yourself on a spreadsheet program. It is important to check the errata in the Hoffer Q and SRK/ T publications.25,27 The most popular commercial programs are the Hoffer Programs System (the first computer program for IOL power in 1994) and the Holladay IOL Consultant (1997), which include several formulas and the ability to personalize them as well as routines to deal with unusual clinical situations.

Refraction Formula

The concept of personalizing a formula based on a surgeon’s past experience and data was introduced by Retzlaff and colleagues19 using the A-constant to refine the formula. Holladay incorporated this concept into backsolving for the Surgeon Factor, and Hoffer backsolved for his personalized ACD. Several studies have proven that formula personalization definitely improves formula accuracy significantly. The following parameters are required from postoperative eyes: z AL (preoperative)

Holladay published a formula in 199329 to calculate the IOL power for an aphakic eye or ametropic pseudophakic eye (piggyback IOL) or a refractive lens for a phakic eye. It does not need the AL but requires the corneal power, preoperative refractive error, and desired postoperative refractive error as well as the vertex distance of both.

Formula Usage The author’s study of 450 eyes27 (by one surgeon using one IOL style; Figure 1-6) showed that in the normal range (72%) of AL (22.0 to 24.5 mm) almost all formulas function adequately but that the SRK I formula is the leading cause of poor refractive results in eyes outside this range. It also showed that the Holladay I formula was the most accurate in medium-long eyes (24.5 to 26.0 mm; 15%) and the SRK/T was more accurate in very long eyes (>26.0 mm; 5%). In short eyes (0.0001) in an additional large study of 830 short eyes as well as in a multiple-surgeon study by Holladay. This recommendation was conclusively proven statistically by an 8108 eye study from the United Kingdom.30 A more recent study performed on 317 eyes31 showed that the Holladay II formula equaled the Hoffer Q in short eyes but was not as accurate as the Holladay I or Hoffer Q in average and medium-long eyes. It appears that in attempting to improve the accuracy of the Holladay formula, the addition of more biometric data input has improved the Holladay II formula in the extremes of AL but deteriorated its excellent performance in the normal and medium-long range of eyes (22.0 to 26.0 mm), which is 82% of the population.

Methodology There are several means by which to use these newer formulas, including A-scan instruments, handheld calcula-

9781556428678Ch01.indd 6

Personalization

z

Corneal power (preoperative)

z

IOL power

z

Postoperative refractive error (stable)

All eyes should have the same lens style by one manufacturer implanted by one surgeon. The same biometry instruments and technician should also have been used. Eyes with postoperative surprises or acuity worse than 20/40 should not be included in the analysis due to poor accuracy in obtaining refractive error. Personalization can be easily performed using the Hoffer Programs or Holladay IOL Consultant computer programs.

ClinicalVariables Special Circumstances Monocular Cataract in Bilateral High Ametropia The dilemma is to either make the surgical eye emmetropic or match the large ametropia of the fellow eye, which may never need surgery. Until now, I have convinced most patients to accept a monocular contact lens or ignore the other eye and go for the “brass ring” of emmetropia. In the future, those who cannot tolerate contact lenses could have a phakic IOL either placed in the fellow eye or placed over the IOL to eliminate aniseikonia and have it removed if the fellow eye ultimately has surgery.

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Pediatric Eyes Children have always posed a dilemma in IOL power selection in that the eye will grow in length (Figure 1-8) and become more myopic if a fixed emmetropic power is implanted. The study of pediatric eyes by Gordon and Donzis32 shows a steep AL growth rate from premature babies to age 2, increasing by 6 mm (~20 D), whereas corneal power drops from 54.00 to 44.00 D offsetting 10 D. If IOLs are used in this age group it might be best to place piggyback lenses, with the more posterior IOL having the average adult emmetropic power and the anterior IOL being the added power needed to reach emmetropia. As the child grows, he or she can be corrected with myopic spectacles until old enough to have the anterior IOL removed. Between the ages of 2 and 5 years, growth slows to approximately 0.4 mm per year and increases only another 1 mm from age 5 to 10 years, while corneal power remains stable. From age 2 to 10 years, it might be wise to aim for 1.50 to 2.00 D of hyperopia postoperatively, which allows for reasonable uncorrected vision and mild spectacle correction in amblyopia treatment. When the child matures, he or she will become emmetropic or mildly myopic, depending on age at implantation. Growth slows after age 10 to 15 years and emmetropia can be the aim. Future use of implantable phakic refractive lenses on top of IOLs may be very helpful in these children because they can easily be exchanged as the eye grows, keeping them emmetropic throughout life. Plager et al33 reported 38 eyes of 27 patients receiving an IOL in childhood. Based on their results, they recommend the following scheme for the refractive goal for children depending upon their age: Age

3

4

5

6

7

8

10

13

Goal +5.00 +4.00 +3.00 +2.25 +1.50 +1.00 +0.50 Plano

Multifocal Intraocular Lenses In 1983, the author invented the first multifocal IOL; five were manufactured by Iolab (thanks to its president, Peter LaHaye) and were optically measured and sterilized by Ioptex (thanks to its president, Ken Rainin), three of which were implanted in three patients at Santa Monica Hospital in 1985. The IOL was a split-bifocal with one-half the optic 20.00 D and the other half 24.00 D. The story of this experience was published in the 1991 book by Maxwell and Nordan on multifocal IOLs.34 In 1991, the author35 reported that to obtain −2.75 D myopia (reading at 14 to 16 inches) the IOL power in the near vision region must be approximately 3.75 to 4.00 D stronger than the emmetropic power. It was also shown that the amount of this additional power in a bifocal IOL

9781556428678Ch01.indd 7

7

is not affected at all by the AL and very little by the corneal power. It is affected, however, by the IOL position and an anterior chamber lens needs less add power than a posterior chamber lens. Obviously, to negate the need for spectacles, it is important to aim for emmetropia, but mild postoperative hyperopia is far better than even the mildest myopia. Distance vision will be reasonable in the former (the patient can easily obtain readers if necessary), whereas in the latter it will not. Bifocal IOL patients with myopia can be dissatisfied and everything should be done to avoid this situation since minus power readers are not readily available. In the future, a phakic IOL could be implanted on top of the bifocal to make the eye emmetropic.

Silicone Oil Refractive Effect The second problem that arises when the vitreous is replaced with silicone oil is that the refractive index of the oil is much less than that of the vitreous and it acts as a negative lens in the eye, which must be offset with more power in the IOL. This effect is dependent upon the shape factor of the back surface of the IOL such that a biconvex IOL creates a worst problem and a concave posterior lens (no longer commercially available) causes practically no effect. Between the two IOLs is the plano-posterior lens, which is recommended in these cases. With a plano-convex lens, 2 to 3 D must be added to the IOL power to compensate for this silicone effect. For a biconvex IOL, +5 to 6 D must be added.

Piggyback Lenses Piggyback lenses can be placed primarily or the second lens placed secondarily over a previously healed IOL. In the former, the anterior IOL forces the posterior IOL more posteriorly a distance equal to the central thickness of the anterior lens. This causes the posterior lens (whose focal point is moved more posteriorly) to require more power to maintain the same focus. This effect diminishes the thinner (lower power) the anterior lens is, and a thinner lens is easier to remove if necessary. Primary piggyback lenses need special calculations to adjust for the posterior lens shift. One can simply add one-half the central thickness of the anterior IOL to the ACD value being used by the formula. Secondary lenses can be calculated using the refraction formula or by a more simple formulation based on the fact that the healed primary IOL is more stable. Due to the different effect on vertex power changes between plus and minus lenses, the following formulation works well: Hyperopic Error: Piggyback IOL = 1.5 × Rx ERROR Myopic Error: Piggyback IOL = 1.0 × Rx ERROR where Rx = PO spherical equivalent refractive error.

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Chapter 1

InMyExperience In My Experience... by Kenneth J. Hoffer, MD, FACS General Warnings z

Measuring the AL of both eyes is prudent and customary.

z

If the AL is very difficult to obtain and the eye appears to have a length greater than 25 mm, suspect a staphyloma. Use the IOLMaster or the Shammas method36: by direct ophthalmoscopy (with patient fixating on the cross-hair target), measure the distance from the target (macula) to the edge of the optic nerve (in disc diameters). A B-scan exam is then performed to measure the AL at that distance from the edge of the optic nerve shadow (Figure 1-9).

z

Measuring an eye containing a silicone IOL with standard phakic velocity (1555 m/s) can amount to an error of 3.00 to 4.00 D.

z

If planning silicone oil injection into the vitreous space, perform an accurate AL measurement before doing so and make this information available to the patient. It is practically impossible to measure a silicone oil–filled eye (try using a velocity of 1000 m/s.) Using the Zeiss IOLMaster is the only way to obtain an accurate measurement in silicone oil–filled eyes. Alternatively, consider performing a secondary IOL implantation after the aphakic refraction is obtained.

z

Always measure AL to the nearest hundredth of a millimeter and record it carefully. Errors in AL are the most significant and amount to ~2.50 D/mm in IOL power, but it is important to be aware that this error drops to ~1.75 D/mm in very long eyes (30 mm) but jumps to ~3.75 D/mm in very short eyes (20 mm). Greater care must be taken in measuring short eyes.

z

Hard contact lenses (including gas permeable) should be removed permanently for at least 2 weeks prior to measuring corneal power for IOL power calculation. Do this one eye at a time.

z

An IOL intended for capsular bag placement should be decreased by 0.75 to 1.50 D (depending upon the IOL power) when placed in the ciliary sulcus.

Post-Refractive Biometry To make it easier for the surgeon to analyze these many methods, we created the Hoffer/Savini LASIK IOL Calculation Tool (Figures 1-10 and 1-11), which automatically calculates the results using all the methods available. This tool is available for free by downloading the MS Excel template from www.EyeLab.com.

Biphakic Eyes (Phakic Eye With a Phakic Intraocular Lens) The problem here is eliminating the effect of the sound velocity through the phakic lens when measuring the AL using ultrasound. I published a method to correct for this potential error by using the following formula: ALCORRECTED = AL1555 + (C × T) where AL1555 = the measured AL of the eye at sound velocity of 1555 m/s, T = the central thickness of the phakic IOL, and C = the material specific correction factor of

9781556428678Ch01.indd 8

+0.42 for PMMA, −0.59 for silicone, +0.11 for collamer, +0.23 for acrylic, and +0.247 for Alcon Laboratories’ (Ft Worth, Texas) acrylic anterior chamber phakic IOL. The publications contain tables showing the phakic IOL central thickness for each dioptric power for each phakic IOL on the market today.37,38

Refractive Surprises A major problem is an unacceptable postoperative refractive error. The sooner it is discovered, the sooner it can be corrected and the patient made happy. Therefore, it is wise to perform K readings and a manifest refraction on the first postoperative day. The author has long recommended immediate surgical correction (24 to 48 hours), which allows easy access to the incision and the capsular bag, only one postoperative period, and produces excellent uncorrected vision. The majority of medicolegal cases today are due to a delay in diagnosis and treatment of this iatrogenic problem. Until now, we could correct this problem only by lens exchange, which creates the dilemma of

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Intraocular Lens Power Calculation determining the factor that created the IOL power error— AL, corneal power, or mislabeled IOL or a combination of all three. Today, with the advent of low-powered IOLs, the best remedy may be a piggyback IOL. When using a piggyback IOL, it is not necessary to determine what caused the error or to remeasure the AL of the freshly operated pseudophakic eye. It is important to remember that a shallow anterior chamber can lead to as much as 3.00 D of myopia (depending on the power of the IOL), which will disappear when the anterior chamber reforms. A radial keratotomy eye has a propensity for the cornea to flatten postoperatively, causing large hyperopic surprises. It may take up to 3 or 4 months for the cornea to resteepen; therefore, surgical correction should not be attempted until then.

FinalThoughts Simple steps and attention to detail can be very useful in preventing IOL power errors, and recent advances in IOL power range availability have made this problem more easily corrected. Since the first American ultrasound IOL power calculation in 1974, the past 36 years have seen great improvement in the accuracy of postoperative refractive prediction. Future improvements may someday eliminate the problems we have left.

References 1.

Ossoinig KC. Standardized echography: basic principles, clinical applications, and results. Int Ophthalmol Clin. 1979;19(4):127-210. 2. Shammas HJ. A comparison of immersion and contact techniques for axial length measurements. J Am Intraocul Implant Soc. 1984;10(4):444-447. 3. Artaria LG. Axial length measurements with different ultrasound devices. Klin Monast Augenheilkd. 1986;188:492-494. 4. Schelenz J, Kammann J. Comparison of contact and immersion techniques for axial measurement and implant power calculation. J Cataract Refract Surg. 1989;15(4):425-428. 5. Olsen T, Nielsen PJ. Immersion versus contact technique in the measurement of axial length by ultrasound. Acta Ophthalmol (Copenh). 1989;67(1):101-102. 6. Watson A, Armstrong R. Contact or immersion technique for axial length measurement? Aust N Z J Ophthalmol. 1999;27(1):49-51. 7. Geggel H. Intraocular lens implantation after penetrating keratoplasty. Improved unaided visual acuity, astigmatism, and safety in patients with combined corneal disease and cataract. Ophthalmology. 1990;97(11):1460-1467. 8. Hoffer KJ. Triple procedure for intraocular lens exchange. Arch Ophthalmol. 1987;105(6):609-610. 9. Cua IY, Qazi MA, Lee SF, Pepose JS. Intraocular lens calculations in patients with corneal scarring and irregular astigmatism. J Cataract Refract Surg. 2003;29(7):1352-1357. 10. Fyodorov SN, Kolonko AI. Estimation of optical power of the intraocular lens. Vestnik Oftalmologic (Moscow). 1967;4:27.

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11. Colenbrander MC. Calculation of the power of an iris clip lens for distant vision. Br J Ophthalmol. 1973;57(10):735-740. 12. Hoffer KJ. Intraocular lens calculation: the problem of the short eye. Ophthalmic Surg. 1981;12(4):269-272. 13. Van der Heijde GL. A nomogram for calculating the power of the prepupillary lens in the aphakic eye. Bibl Ophthalmol. 1975;83:273-275. 14. Binkhorst RD. The optical design of intraocular lens implants. Ophthalmic Surg. 1975;6(3):17-31. 15. Gills JP. Regression formula. J Am Intraocul Implant Soc. 1978;4(4):163-164. 16. Gills JP. Minimizing postoperative refractive error. Contact Intraocular Lens Med J. 1980;6:56-59. 17. Retzlaff J. A new intraocular lens calculation formula. J Am Intraocul Implant Soc. 1980;6(2):148-152. 18. Sanders DR, Kraff MC. Improvement of intraocular lens power calculation using empirical data. J Am Intraocul Implant Soc. 1980;6(3):263-267. 19. Sanders D, Retzlaff J, Kraff M, et al. Comparison of the accuracy of the Binkhorst, Colenbrander and SRK implant power prediction formulas. J Am Intraocul Implant Soc. 1981;7(4):337-340. 20. Hoffer KJ. Biometry of the posterior capsule. In: Emery JC, Jacobson AC, eds. Current Concepts in Cataract Surgery (Eighth Congress). New York, NY: Appleton-Century Crofts; 1983:56-62. 21. Hoffer KJ. The effect of axial length on posterior chamber lenses and posterior capsule position. Curr Concepts Ophthalmic Surg. 1984;1:20-22. 22. Binkhorst RD. Biometric A scan ultrasonography and intraocular lens power calculation. In: Emery JE, ed. Current Concepts in Cataract Surgery: Selected Proceedings of the Fifth Biennial Cataract Surgical Congress. St. Louis, MO: Mosby CV; 1987:175-182. 23. Sanders DR, Retzlaff J, Kraff MC. Comparison of the SRK II formula and other second generation formulas. J Cataract Refract Surg. 1988;14(2):136-141. 24. Holladay JT, Prager TC, Chandler TY, Musgrove KH, Lewis JW, Ruiz RS. A three-part system for refining intraocular lens power calculations. J Cataract Refract Surg. 1988;14(1):17-24. 25. Retzlaff J, Sanders DR, Kraff MC. Development of the SRK/T intraocular lens implant power calculation formula. J Cataract Refract Surg. 1990;16(3):333-340. Erratum: 1990;16(4):528. 26. Olsen T, Oleson H, Thim K, Corydon L. Prediction of postoperative intraocular lens chamber depth. J Cataract Refract Surg. 1990;16(5):587-590. 27. Hoffer KJ. The Hoffer Q formula: a comparison of theoretic and regression formulas. J Cataract Refract Surg. 1993;19(6):700-712. Errata: 1994;20(6):677 and 2007;33(1):2-3. 28. Haigis W. The Haigis formula. In: Shammas HJ, ed. Intaocular Lens Power Calculations. Thorofare, NJ: SLACK Incorporated; 2003:41-57. 29. Holladay JT. Refractive power calculations for intraocular lenses in the phakic eye. Am J Ophthalmol. 1993;116(1):63-66. 30. Aristodemou P, Knox Cartwright NE, Sparrow JM, Johnston RL. Formula choice: Hoffer Q, Holladay 1, or SRK/T and refractive outcomes in 8108 eyes after cataract surgery with biometry by partial coherence interferometry. J Cataract Refract Surg. 2011;37:63-71. 31. Hoffer KJ. Clinical results using the Holladay 2 intraocular lens power formula. J Cataract Refract Surg. 2000;26(8):12331237. 32. Gordon RA, Donzis PB. Refractive development of the human eye. Arch Ophthalmol. 1985;103(6):785-789.

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33. Plager DA, Kipfer H, Sprunger DT, Sondhi N, Neely EN. Refractive change in pediatric pseudophakia: 6 year followup. J Cataract Refract Surg. 2002;28:810-815. 34. Hoffer KJ. Personal history in bifocal intraocular lenses. In: Maxwell A, Nordan LT, eds. Current Concepts of Multifocal Intraocular Lenses. Thorofare, NJ: SLACK Incorporated; 1991:127-132. 35. Holladay JT, Hoffer KJ. Intraocular lens power calculations for multifocal intraocular lenses. Am J Ophthalmol. 1992;114:405-408.

36. Berges O, Siahmed K, Puech M, Perrenoud F. B-mode guided biometry. In: Shammas HJ, ed. Intraocular Lens Power Calculations. Thorofare, NJ: SLACK Incorporated; 2004:161167. 37. Hoffer KJ. Ultrasound axial length measurement in biphakic eyes. J Cataract Refract Surg. 2003;29(5):961-965. 38. Hoffer KJ. Addendum to ultrasound axial length measurement in biphakic eyes: factors for Alcon L12500–L14000 anterior chamber phakic IOLs. J Cataract Refract Surg. 2007;33:751-752.

Figure 1-1. Photo taken by the author in 1975 of an eye implanted by Sir Harold Ridley in 1951 using his original IOL. Uncorrected visual acuity was 20/20.

Figure 1-2. (A) Carl Zeiss Meditec IOLMaster. (Reprinted with permission of Carl Zeiss Meditec.) (B) Haag-Streit Lenstar LS-900.

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Figure 1-4. Immersion ultrasound probe in cup with patient supine in examination chair with A-scan facing examiner. Figure 1-3. Examination chair reclined 45 degrees for immersion A-scan procedure.

Figure 1-5. Phakic sound velocity is lower in longer eyes and higher in shorter eyes.

B A BEST RESULTS, WITHIN +/- 0.50D SHORT

HOFFER Q

67% = 24

MEDIUM

HOFFER Q

67% = 219

Med LONG

HOLLADAY

71% = 47

Very LONG

SRK/T

57% = 13 303/450 = 67% 303

Figure 1-6. (A) Hoffer Q paper reports results of 450 eyes showing that different formulas perform better in different axial length ranges.27 (B) Ranges of prediction error show the regression formulas to be the worst.

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A

B

C

D

Figure 1-7. Palm Hoffer Programs System screens.

Figure 1-8. Pediatric eye growth showing the change in AL as a child grows. Figure 1-9. B-scan of an eye with a staphyloma showing the anatomical axis (blue) and the visual axis (red).

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Figure 1-10. Hoffer/Savini tool without any data entered.

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Figure 1-11. Hoffer/Savini tool with all data entered for one patient.

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chapter 2 Corneal Topography Isaac W. Porter, MD and Dimitri T. Azar, MD An accurate depiction of the corneal power and shape through corneal topography is a great clinical tool. The normal cornea is aspheric, steeper centrally, and flattens toward the periphery.1 There are many commercial systems available for determining corneal topography, and they predominantly employ Placido-based, scanning slit, or rotating Scheimpflug technology to model the cornea.

Placido-Based Topography The Placido disk was developed in the 1800s, and the same general principles are still used today. An early disk was composed of alternating light and dark rings with an observation hole in the center. The corneal reflection of the rings was viewed through the opening, allowing the viewer to infer variations of the anterior cornea by the shape and the position of the rings. This led to the development of the illuminated handheld keratoscope by Klein.2 Recently, as computer technology became widely available, photographs with Placido disk reflections could be scanned and assessed using mathematical algorithms.3 The relative thickness of the rings and the spacing between the rings are analyzed to determine the shape and curvature of the cornea. Later, analysis software was combined with a videokeratoscope, creating an integrated system. A significant advance came with the corneal modeling system, which included imaging and analysis systems with both Placido ring and slit-beam images.4 Variations on this platform form the basis for many modern videokeratoscopes.

Measurements from Placido-based systems have been proven to be accurate and reliable.5 However, only a limited amount of information can be obtained by using this reflection from the anterior cornea and tear film. The actual shape and true elevation of the cornea cannot be determined, and no information can be gathered from the posterior corneal surface. This has prompted the development of scanning slit and rotating Scheimpflug systems to provide additional data.

Scanning Slit Topography Scanning slit-beam topographers use cross-sectional images of the cornea to obtain information about the entire cornea in a manner similar that of a thin slit beam is used with the slit-lamp biomicroscope. This overcomes the shortfalls of Placido-based imaging and is able to measure actual elevation data as well as corneal thickness and posterior curvature (Figure 2-1). Slit beams are projected from the left and right of the cornea, and the resulting corneal cross-section is stored as two-dimensional images. The actual location of the corneal surface is spatially localized in three dimensions using triangulation calculations. The analysis of the posterior corneal surface requires more advanced triangulation that must account for the refractive variables of the cornea and curvature data acquired from Placido-based scans.3 The accuracy of the scanning slit is considered to be similar to that of other topographers.

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Rotating Scheimpflug Topography A later development in corneal topography used the principles of Scheimpflug imaging to create a model of the cornea. Scheimpflug imaging is based on the light-scattering principle and measures the density of light that is reflected back to a camera from a slit beam. A blue LED light (475 nm) is used as a slit light source to obtain 25 to 50 cross-sectional images around a 180-degree rotation centered on the corneal vertex.6 Like the scanning slit method, true elevation data, corneal thickness, and posterior corneal curvature can be measured (Figure 2-2). Rotating Scheimpflug scans penetrate deeper into the eye and can also provide detailed information on the anterior chamber, iris, and lens, including objective measurements of lens opacity. This system has also been validated and found to be accurate and reliable.5

Topographical Maps The images created from the combined analyses in all forms of topography are output in colored maps. A scale is

created with red, orange, and yellow colors for the steeper areas, green for intermediate, and blues for f latter areas. Attention must be paid to the scale because the intervals between colors can vary and give the impression of a more or less curved surface. Usually, half-diopter steps are used with a standard scale.1 For anterior surface topography, power maps are displayed as axial or tangential maps. Axial models provide a broader view of the corneal curvature, because each point is shown with its radius of curvature projected to the primary axis of the cornea. Tangential models will give a more immediate, localized view of curvature by showing the true instantaneous radius of curvature at each point. The tangential topography offers useful information for patients who had previous excimer keratectomy and can be utilized to differentiate intraoperative treatment from treatment shift (Figures 2-3 through 2-5). When the posterior corneal curvature can be accurately determined, as with scanning slit and rotating Scheimpflug systems, many other maps can be created, including pachymetry, surface elevation maps, and representations of anterior and posterior curvatures. Higher order aberrations may also be mapped to topography data, fitting the information to Zernike or other higher order representations.

In My Experience In My Experience...

by Dimitri T. Azar, MD

We use information from corneal topography to make decisions every day in our practice. This is particularly important in evaluating patients for refractive surgery, managing astigmatism after keratoplasty, diagnosing corneal disease, and for preoperative evaluation of patients with cataracts. We rely on all aspects of corneal topography (including Placido-based axial and tangential images). These maps are familiar and are performed routinely on all our new arrival and cataract patients; for example, the diagnoses of forme fruste and early keratoconus are made more easily with the help of topography when other clinical signs may be subtle. Our preferred method for the removal of sutures following penetrating keratoplasty involves the use of corneal topography. The topographic map provides more information than can be obtained with simple keratometry regarding the actual astigmatism that is present. We will usually remove a single interrupted suture in the steep meridian with guidance from the topography in a patient who has unacceptably high astigmatism (higher than can be comfortably managed with spectacles). With the advent of premium intraocular lenses, management of corneal astigmatism becomes even more important. Preoperatively, it is critical to determine whether a patient has corneal or lenticular astigmatism. Multifocal lenses perform best when there is low postoperative astigmatism, and toric lenses must be aligned with the steep corneal meridian to have the most effectiveness. In both of these instances, we rely on topography to confirm the axis of astigmatism. Elevation data maps are valuable in planning treatments with phototherapeutic keratectomy for the treatment of corneal irregularities in the absence of corneal opacities. These can highlight areas that need to be flattened to restore a more even anterior corneal surface. This approach is not reliable when phototherapeutic keratectomy is used to treat corneal opacities; ultrasound pachymetry is necessary to confirm the accuracy of optical pachymetry. (continued )

Corneal Topography

In My Experience... (continued)

17

by Dimitri T. Azar, MD

Having a measured pachymetry map of the entire cornea from the scanning slit and Scheimpflug systems is useful. Previously, we would rely on a central corneal thickness measurement by ultrasound or a series of ultrasound measurements in cardinal positions. The availability of adjunctive maps seems to reduce the variability of pachymetry readings taken by different personnel or on different days. We have used these maps in conjunction with ultrasound pachymetry to monitor corneal edema, plan lamellar surgery, and evaluate patients for excimer laser procedures. As mentioned above, we use tangential topography when evaluating patients for retreatment. In assessing keratoconus suspects before refractive surgery, we first look at axial topography, then we look at Orbscan (Bausch & Lomb, Rochester, New York) elevation topography, and then we make sure that the pachymetry is above 500 μm. We use the automatic calculation of the inferior-superior value available on most topographers. We also calculate it by the number of half-diopter steps between the superior and inferior cornea. We still use the Azar-Lu MEEI criteria.7 Extra attention should be paid to patients with corneal irregularities and against-the-rule astigmatism because of the risk of pellucid degeneration masquerading as against-the-rule astigmatism (Figure 2-6). Questions regarding when to take the posterior elevation into consideration are still unresolved. The location of the posterior elevation and the location of thinnest pachymetry may affect the diagnosis. Posterior elevation may be irregular in patients who have corneal anterior surface abnormalities, but they are extremely helpful in patients with subtle changes in the anterior corneal surface. With the “best-fit sphere” as a reference, a posterior elevation of 50 μm will alert us to examine the topography very carefully for other signs of keratoconus or forme fruste keratoconus. In the absence of corneal abnormality, posterior elevation data may help in advising patients on whether to do surface ablation versus laser in situ keratomileusis (LASIK). It may also help in predicting results after refractive surgery (predictability, efficacy, and safety measures). Very few patients have a significant posterior elevation and no other signs of keratoconus. Nevertheless, abnormal posterior elevation remains an important screening criterion in younger patients where they would be advised to switch to surface ablation versus LASIK. Differences between the Pentacam (Oculus Optigeräte GMbH, Wetzlar, Germany) and Orbscan and their usefulness and accuracy following refractive surgery are minimal. The Orbscan involves a scanning slit beam and the Pentacam involves Scheimpflug imaging. Both methods can be used after refractive surgery to map the curvature and measure corneal thickness, especially when evaluating patients for retreatment. An emerging technology is the Visante Omni (Carl Zeiss Meditec, Jena, Germany), which uses topography and Visante to calculate posterior elevation. Data regarding the added value of combining topography with optical coherence tomography are not available for the screening of patients for refractive surgery. Finally, two important aspects in all topography machines are avoiding common mistakes when performing the test and recognizing poor scans that should be repeated.

References 1.

2. 3.

4.

Koch DD, Haft EA. Introduction to corneal topography. In: Sanders DR, Koch DD, eds. An Atlas of Corneal Topography. Thorofare, NJ: SLACK Incorporated; 1993:3-15. Klein M. A new keratoscope with self-luminous placido disc. Br J Ophthalmol. 1958;42(6):380-381. Cairns G, McGhee CN. Orbscan computerized topography: attributes, applications, and limitations. J Cataract Refract Surg. 2005;31(1):205-220. Gormley DJ, Gersten M, Koplin RS, Lubkin V. Corneal modeling. Cornea. 1988;7(1):30-35.

5.

6.

7.

Read SA, Collins MJ, Iskander DR, Davis BA. Corneal topography with Scheimpflug imaging and videokeratography: comparative study of normal eyes. J Cataract Refract Surg. 2009;35(6):1072-1081. Shankar H, Taranath D, Santhirathelagan CT, Pesudovs K. Anterior segment biometry with the Pentacam: comprehensive assessment of repeatability of automated measurements. J Cataract Refract Surg. 2008;34(1):103-113. Carr J, Hersh P, Tsubota K. Patient evaluation for refractive surgery. In: Azar DT, Gatinel D, Hoang-Xuan T, eds. Refractive Surgery. 2nd ed. St. Louis, MO: Elsevier-Mosby; 2007:81-88.

18

Chapter 2

Figure 2-1. Topographical map generated by the Orbscan showing the elevation data, corneal thickness, and posterior curvature.

Figure 2-2. Topographical map of the same patient shown in Figure 2-1 generated by the Pentacam.

Corneal Topography

19

Figure 2-3. Tangential topographic analysis of a right eye 1 month after photorefractive keratectomy, showing high inferotemporal displacement of laser treatment zone (r = 0.81 mm). Visual acuity of 20/20 was achieved. The black circle and black cross on the map represent the pupillary margin and the position of the pupillary center, respectively. (Reprinted from Am J Ophthalmol, Vol 124, Azar DT, Yeh PC, Corneal topographic evaluation of decentration in photorefractive keratectomy: treatment displacement vs intraoperative drift, 312-320, © 1997, with permission from Elsevier.)

Figure 2-4. Comparison of laser drift in two patients with similar amounts of treatment decentration (displacement). The contour and the pupillary center are represented by the black circle and black cross, respectively. (Left) Tangential topography showing a laser-drift effect in the superior direction. The treatment, with an intended myopic correction of −6.20 D, was slightly shifted inferotemporally (r = 0.21 mm). Note that the area of greatest ablation (blue) was drifted upward, resulting in a nonuniform central ablation power. The change in central ablation power in the central 4 mm2 relative to the pupillary center was 3.00 D and the arc of the second flattest area was 3.07 radii. The shortest distance from the center of ablation to the flattest area was 1.00 mm. The drift index was 0.98. The best-corrected visual acuity 1 month after photorefractive keratectomy was 20/40. (Right) Tangential topography of a left eye with an intended myopic correction of −5.50 D with similar degree of displacement as in the map at left (0.31 mm). Compared with the panel at left, the central power is more homogeneous, without gross drift effect (drift index = 0.03). Visual acuity of 20/20 was achieved. (Reprinted from Am J Ophthalmol, Vol 124, Azar DT, Yeh PC, Corneal topographic evaluation of decentration in photorefractive keratectomy: treatment displacement vs intraoperative drift, 312-320, © 1997, with permission from Elsevier.)

20

Chapter 2

Figure 2-5. (Left) Tangential topographic map showing high displacement (0.67 mm) in the superotemporal direction and low drift index (0.00). Visual acuity achieved was 20/20. (Right) Tangential topographic map showing high displacement (0.95 mm) superotemporally and high drift index (3.27), resulting in 20/40 postoperative visual acuity. In each map, the contour and the pupillary center are indicated by the black circle and black cross, respectively. (Reprinted from Am J Ophthalmol, Vol 124, Azar DT, Yeh PC, Corneal topographic evaluation of decentration in photorefractive keratectomy: treatment displacement vs intraoperative drift, 312-320, © 1997, with permission from Elsevier.)

Figure 2-6. Claw-shaped patterns on Orbscan II (Bausch & Lomb, Rochester, New York; hardware version 2GOT4.0 and software version 31257SP3) mean keratometric axial power maps of representative patients with pellucid marginal degeneration (A-C) with peripheral corneal thinning in an arcuate or crescenteric pattern on slit-lamp photography (D). Claw-shaped patterns were also seen in representative patients with keratoconus (E-G) with central corneal thinning on slit-lamp photography (H) and in patients with postoperative ectasia (I-K). The slit-lamp photos shown in (D) and (H) were taken from patients whose topographic maps are shown in (C) and (G), respectively. (Reprinted from Am J Ophthalmol, Vol 144, Lee BW, Jurkunas UV, Harissi-Dagher M, Poothullil AM, Tobaigy FM, Azar DT, Ectatic disorders associated with a claw-shaped pattern on corneal topography, 154-156, © 2007, with permission from Elsevier.)

SectionII

OcularSurfaceDisorders

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chapter 3 Dry Eye Syndrome and Lid Margin Disease Gary N. Foulks, MD, FACS Dry eye and lid margin disease are the most common conditions seen in clinical practice. The problems often occur simultaneously and can exacerbate symptoms and signs of both diseases. Dry eye disease is estimated to occur in 7.8% of women and 3.9% of men over age 55 in the United States.1,2 Lid margin disease has been identified in 39% of patients evaluated for contact lens fitting.3 An appreciation of the interrelationship of both diseases provides more effective therapeutic strategies to manage these clinical conditions.

DryEyeDisease The International Dry Eye Workshop (DEWS) defines dry eye disease as “a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.”4 The DEWS classification system recognizes two major forms of dry eye phenotypes: aqueous deficient dry eye, in which tear production is below normal, and evaporative dry eye, in which secretion is normal but evaporation is excessive (Figure 3-1). Both forms produce tear film instability and elevated tear film osmolarity. Although the two phenotypes are described, it is recognized that both mechanisms may occur together in as much as 34% to 40% of cases.5 The phenotype of the condition may be determined not only by the initiating pathophysiology of the disease but also by modifications of the host compensatory response.6

Symptoms of dry eye disease include discomfort often described as burning, itching, gritty, or foreign body sensation that is aggravated by conditions of low humidity or excess air current as well as activities such as reading or computer use during which blink frequency is decreased. Conjunctival vessel engorgement and intermittent mucous accumulation are often present. Intolerance of contact lens wear is frequently a result of dry eye disease and lid margin disease. Interestingly, symptoms can occur with marked severity even in the mild or early stages of the condition possibly due to increased corneal sensitivity, although symptoms may be less severe even in advanced stages of disease probably as a result of decreased corneal sensation due to inflammation. Symptoms and signs do not correlate well over the spectrum of dry eye disease.7 Signs of dry eye disease include reduction of the tear meniscus height, instability of the tear film, and staining of the ocular surface with supravital dyes such as fluorescein, rose bengal, and lissamine green. A postulated cause of aqueous deficient dry eye disease is inflammation of the lacrimal glands (main and accessory) and the ocular surface that may be due to declining androgen levels that otherwise suppress inflammation.8,9 Evaporative dry eye is most often caused by meibomian gland dysfunction, which is a part of the spectrum of lid margin disease and which also may be due to declining hormonal support of meibomian gland function. Diagnosis of dry eye disease is made by a combination of recognition of the symptoms produced by the disease and identification of the signs of the disease that verify tear instability (rapid tear breakup time; Figure 3-2), reduced tear volume or change in volume (reduced Schirmer test;

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Chapter 3

Figure 3-3), elevated tear osmolarity (tear osmometry; Figure 3-4), and/or ocular surface staining (fluorescein, rose bengal, lissamine green; Figure 3-5). Recognition of meibomian gland dysfunction as a contributor to tear film evaporation is also an important diagnostic feature of evaporative dry eye (Figure 3-6).

LidMarginDisease Lid margin disease is often described by the term blepharitis, but it is important to differentiate between inflammation of the skin of the eyelid (cutaneous blepharitis) and the lid margin, which can be affected in the anterior portion of the lid at the base of the eyelashes (anterior blepharitis; Figure 3-7) or in the posterior portion of the lid in the meibomian glands (posterior blepharitis; Figure 3-8). A more extensive clinical summary of meibomian gland dysfunction is presented in Figure 3-9.10 Abnormalities of the secretion of the meibomian glands can occur without inflammation as meibomian gland dysfunction. Meibomian gland disease commonly occurs in patients with rosacea. Symptoms of blepharitis and meibomian gland dysfunction are often similar to those of dry eye but also include swelling and redness of the eyelid margin as well as debris on the eyelashes in the case of anterior blepharitis. Signs of meibomian gland dysfunction include conjunctival vascular engorgement but more specifically those related to the

In My Experience...

eyelid margin, including swelling, redness, plugging of the meibomian gland orifices, and abnormalities of the gland secretion (ease of expression and character of secretion).10 Diagnosis of blepharitis is made by identifying the location (anterior vs posterior) of inflammation of the eyelid margin or plugging of the meibomian gland orifices by epithelial plugs or inspissated secretions (Figure 3-10). There is usually instability of the tear film with meibomian gland dysfunction and frequently fluorescein staining of the inferior cornea occurs (Figure 3-11).

Therapy Management of dry eye disease is increasingly determined according to the severity of the disease (Tables 3-1 and 3-2).11 Mild cases can be treated with topical lubricant drops, but more advanced disease may require pulse topical steroid and/or topical cyclosporine therapy.12,13 Oral omega 3 essential fatty acid therapy has been advocated but with variable response. Punctal plugging can be performed once surface inflammation is controlled to retain tears and increase tear volume. In severe recalcitrant cases, topical autologous serum drops can be prepared at a concentration of 20% for use four times daily. Management of blepharitis begins with lid hygiene and massage following application of warm compresses to the eyelid, but use of topical azithromycin solution once daily or daily oral doxycycline often is required.

by Gary N. Foulks, MD, FACS

My orientation to cornea and external disease was conditioned by my fellowship training at the Massachusetts Eye and Ear Infirmary and the Eye Research Institute of the Retina Foundation (now known as the Schepens Eye Research Institute). My fellowship began in 1976 and for 2 years I worked closely in the laboratory with Richard Thoft, MD, and Judith Friend, who taught me the techniques of evaluating and treating the ocular surface. My interaction with Frank Holly, PhD, and Marshall Doane, PhD, was critical to my developing understanding of the importance and the role of the tear film in maintaining ocular surface health. Clinical insights came from Arthur Borchoff, MD; Claes Dohlman, MD; and Deborah Pavan-Langston, MD. Jules Baum, MD, was a mentor who stimulated interest in pursuing the “clues” to eye disease that was presented in the clinic but often had to be explained in the laboratory. Working with bright and enthusiastic co-fellows such as Dave Lamberts, MD; Henry Perry, MD; and Ken Kenyon, MD, further defined my appreciation of both clinical and laboratory investigations. After completing the 2-year fellowship, I joined the faculty of the Duke University Eye Center in Durham, North Carolina, and enjoyed the stimulation of working with impressive colleagues like Gordon Klintworth, MD, PhD, and Diane Hatchell, PhD, to explore the nuances of corneal disease. My collaborations with Fred Sanfilippo, MD, PhD, to investigate the immune basis of corneal allograft rejection and corneal inf lammation helped me to appreciate the role of the immune response in cornea and external disease of the eye. My career expanded into clinical trial research and the experiences in conducting numerous trials in treatment of dry eye shaped my orientation and prompted the offering of these personal observations. (continued )

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Dry Eye Syndrome and Lid Margin Disease

In My Experience... (continued)

25

by Gary N. Foulks, MD, FACS

The classical description of ocular surface staining with fluorescein, rose bengal, or lissamine green is that of an interpalpebral horizontal band. In my experience, the inferior and particularly the inferonasal area of the cornea is stained earliest with fluorescein and the inferonasal conjunctiva is stained earliest with rose bengal or lissamine green. Our studies confirm previously published observations14,15 that normal, non-dry eye patients can demonstrate peripheral corneal micropunctate staining, particularly in the inferonasal cornea, 39% of the time. Central corneal micropunctate staining occurs in 5% of normal patients. The superior cornea is usually spared until the more advanced stages of the disease. The condition of dry eye disease is usually recognized by the practitioner, but the contribution of lid margin disease is often not well appreciated. Therefore, initial treatment is not as effective as when therapy of the meibomian gland dysfunction is added. Lid massage following hot compresses works about 80% of the time to improve the condition, but the remaining 20% of patients will require either topical azithromycin therapy once daily for 4 weeks or oral doxycycline therapy daily for 2 to 3 months. The advanced formulation lubricants and tear enhancers can be effective in stabilizing the tear film and protecting the ocular surface. In my experience, Soothe metastable emulsion is most effective in evaporative dry eye associated with meibomian gland dysfunction, and Systane gelling solution is very effective in protecting the ocular surface and reducing friction of the blink in aqueous-deficient and evaporative dry eye. Optive compatible solute lubricant can be effective in protecting the surface against the hyperosmolarity of the tear film in dry eye. Systane and Optive work well in conjunction with topical cyclosporine. Topical cyclosporine emulsion therapy twice daily is effective in reducing symptoms and signs of dry eye disease in about 75% of patients with moderate to severe disease, but concurrent use of a topical lubricant such as Systane increases effectiveness of treatment. Use of topical steroid concurrently with the initiation of cyclosporine therapy reduces the discomfort and potential intolerance of topical cyclosporine but should be tapered rapidly to avoid side effects of elevated intraocular pressure or cataract. If relapse on long-term cyclosporine occurs, another pulse of topical steroid therapy often controls the flare-up. I have not found topical nonsteroidal anti-inflammatories to be of value in treating inflammation of dry eye, and there are potential epithelial-toxic effects that can occur with their chronic use. Advanced dry eye disease that is unresponsive to the standard therapies can be treated with use of topical autologous serum. Blood obtained by venipuncture into a sterile, unheparinized collection tube and then centrifuged allows serum to be collected in a sterile manner and delivered into artificial tear containers with a dilution of 1 cc serum to 4 cc artificial tear. Patients need to be advised of the risk of infection and not to contaminate the tear container. The containers should be refrigerated or, if multiple bottles are stored, frozen until ready to use. Lubricating gels (eg, Genteal gel) can be helpful in prolonging contact time but often are best used at bedtime because they tend to blur vision. Ointments are even more likely to blur vision, although they can further prolong lubricant effect. I recommend them for nighttime use. Lacrisert dissolvable inserts can be used to extend lubrication of the surface and they work best if instilled in the inferior conjunctival cul-de-sac behind the lower lid at night. Dissolution occurs during the night and day such that the insert can be replaced the next night. Punctal plugs are still valuable as adjunctive therapy but are best used after inflammation is controlled to avoid aggravation of symptoms by retention of inflammatory tears. In my experience, plugs are useful in patients wearing contact lenses with early dry eye who still have adequate reflex tearing. The use of contact lenses in patients with dry eye depends upon severity of disease. Intolerance of contact lenses (either soft or rigid) can be a manifestation of early dry eye disease. Placement of punctal plugs in these patients can prolong their tolerance of the lenses. Patients with moderate to severe dry eye are often able to wear soft contact lenses if they are simultaneously treated with topical cyclosporine. The use of a bandage soft contact lens can be helpful in managing filamentary keratopathy in the moderate to severe dry eye patient, but contact lens deposits are often a problem. Scleral contact lenses have been a major step forward in managing ocular surface damage and discomfort in dry eye disease and are worth the high cost and the time necessary for instruction in application and removal techniques in those patients with severe ocular surface disease. (continued )

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Chapter 3

In My Experience... (continued)

by Gary N. Foulks, MD, FACS

Another option for retention of tears or reduction of evaporation is the use of protective eyewear. Applying side shields (eg, Eagle Vision, Memphis, Tennessee) is an easy option, but in my experience, the most effective protection is the use of sealed-edge spectacles. Panoptx (Pleasanton, California) spectacles are very effective, particularly in high-velocity wind conditions, but are more expensive. The microenvironment glasses developed by Richard Yee, MD (Houston, Texas), are now available and provide ample protection with a very cosmetically acceptable option. Such spectacles are especially helpful in those patients who must spend prolonged periods reading or working with video terminal displays. Oral secretagogues such as pilocarpine (Salagen) or cevimeline (Evoxac) are sometimes helpful in patients with Sjögren’s syndrome, but the stimulatory effect is greater for salivary secretion than for tear secretion. The drug usefulness is often limited by the cholinergic side effects of gastrointestinal stimulation or sweating. The use of topical vitamin A has been controversial in the treatment of dry eye disease, and I find that topical vitamin A is helpful in those patients with epithelial keratinization demonstrable by rose bengal/lissamine green staining in a nonwetting area of the ocular surface. I have not found it helpful in patients with early disease. The future will probably bring additional approved therapies including topical secretagogues, such as diquafosol or rebamipide, but the path to regulatory approval has been difficult given the fact that signs and symptoms of dry eye disease do not correlate well with or without therapeutic effect of topically applied agents.

References 1.

2.

3.

4.

5. 6.

7.

8.

Schaumberg DA, Sullivan DA, Buring JE, Dana MR. Prevalence of dry eye syndrome among US women. Am J Ophthalmol. 2003;136(2):318-326. Schaumberg DA, Dana R, Buring JE, Sullivan DA. Prevalence of dry eye disease among US men: estimates from the Physicians’ Health Studies. Arch Ophthalmol. 2009;127(6):763768. Hom MM, Martinson JR, Knapp LL, Paugh JR. Prevalence of Meibomian gland dysfunction. Optom Vis Sci. 1990;67(19): 710-712. Lemp MA. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):75-92. Mathers WD. Ocular evaporation in meibomian gland dysfunction and dry eye. Ophthalmology. 1993;100(3):347-351. Bron AJ, Yokoi N, Gaffney E, Tiffany JM. Predicted phenotypes of dry eye: proposed consequences of its natural history. Ocul Surf. 2009;7(2):78-92. Nichols KK, Nichols JJ, Mitchell GL. The lack of association between signs and symptoms in patients with dry eye disease. Cornea. 2004;23(8):762-770. Bron AJ, Smith JA, Calonge M. Methodologies to diagnose and monitor dry eye disease: report of the Diagnostic Methodology Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):108-152.

9781556428678Ch03.indd 26

9.

10.

11.

12.

13.

14. 15.

Sullivan DA: Sex and sex steroid influences on dry eye syndrome. In: Pflugfelder SC, Beuerman RW, Stern ME, eds. Dry Eye and Ocular Surface Disease. New York, NY: Marcel Dekker Inc; 2004. Foulks GN, Bron AJ. Meibomian gland dysfunction: a clinical scheme for description, diagnosis, classification, and grading. Ocul Surf. 2003;1(3):107-126. Pflugfelder SC. Management and therapy of dry eye disease: report of the Management and Therapy Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):163-178. Sall K, Stevenson OD, Mundorf TK, Reis BL. Two multicenter, randomized studies of the efficacy and safety of cyclosporine ophthalmic emulsion in moderate to severe dry eye disease. CsA Phase 3 Study Group. Ophthalmology. 2000;107(4):631-639. Pflugfelder SC, Maskin SL, Anderson B, et al. A randomized, double-masked, placebo-controlled, multicenter comparison of loteprednol etabonate ophthalmic suspension, 0.5%, and placebo for treatment of keratoconjunctivitis sicca in patients with delayed tear clearance. Am J Ophthalmol. 2004;138(3):444-457. Norn MS. Vital staining of the cornea and conjunctiva. Acta Ophthalmol (Copenh). 1962;40:389-401. Korb D, Korb J. Corneal staining prior to contact lens wear. J Am Optom Assoc. 1970;41(3):228-232.

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Dry Eye Syndrome and Lid Margin Disease ETIOLOGICAL CLASSIFICATION OF DRY EYE

27

DRY EYE

Effect of the Environment Milieu Interieur Low blink rate Behavior VTU; microscopy, wide lid aperture, gaze position, aging Low androgen pool Systemic drugs; antihistamines, beta-blockers, antispasmodics, diuretics, and some psychotropic drugs Milieu Exterieur Low relative humidity High wind velocity Occupational environment

Aqueous-deficient Sjögren Syndrome Dry Eye Primary

Evaporative Intrinsic

Non-Sjögren Dry Eye

Meibomian Cil Deficiency

Secondary Lacrimal Deficiency Lacrimal Gland Duct Obstruction Reflex Block

Poor Lid Congruity or Dynamics Low Blink Rate

Extrinsic

Vitamin A Deficency Topical Drugs Preservatives Contact Lens Wear

Drug Action Accutane

Oc Surface Disease eg Allergy

Systemic Drugs

Figure 3-1. International Dry Eye Workshop classification of dry eye disease. (Reprinted with permission from Ethis Communications Inc. Lemp MA. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5[2]:75-92.)

Figure 3-3. Reduced Schirmer strip wetting. Figure 3-2. Rapid tear film breakup identified with fluorescein.

Figure 3-4. Osmolarity measured by the TearLab osmometer.

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Chapter 3

A

C

Figure 3-6. Meibomian gland dysfunction associated with evaporative dry eye.

B

Figure 3-5. (A) Fluorescein staining of the cornea. Note filaments. (B) Rose bengal staining of the interpalpebral ocular surface. (C) Lissamine green staining of the conjunctival surface.

Figure 3-7. Anterior blepharitis. Note the crusts and debris on the eyelashes.

Figure 3-8. Posterior blepharitis. Note the plugging of the meibomian gland orifices.

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Dry Eye Syndrome and Lid Margin Disease

29

Meibomian Gland Disease

Congenital lack

Replacement dystichiasis

Meibomian gland dysfunction (MGD)

Neoplastic lid disease

High delivery

Low delivery

Simple MGD

Hyposecretory

1˚ ?

2˚ Retinoids

Other

2˚ Seborrheic dermatitis Acne rosacea Atopy Psoriasis Icthyosis EEC Turner syndrome Fungal infection

Cicatricial MGD

1˚ Primary

Hypersecretory meibomian seborrhoea

2˚ Trachoma Pemphigoid Erythema multiforme Acne rosacea Atopy

b

Meibomian keratoconjunctivitis (MKC-meibomianitis)

1˚ Primary

2˚ Seborrheic dermatitis Acne rosacea

Evaporative dry eye

Figure 3-9. Clinical classification of meibomian gland disease. (Reprinted with permission from Ethis Communications Inc. Foulks GN, Bron AJ. Meibomian gland dysfunction: a clinical scheme for description, diagnosis, classification, and grading. Ocul Surf. 2003;1[3]:107-126.)

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30

Chapter 3

A B

C D

Figure 3-10. (A) Turbid meibomian gland secretion easily expressed. (B) Turbid with clumps in meibomian gland secretion more resistant to expression. (C) Solid pasty meibomian gland secretion that is difficult to express. (D) Obstruction of meibomian gland orifice with epithelial plug.

Figure 3-11. Inferior corneal staining seen with advanced meibomian gland dysfunction.

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Dry Eye Syndrome and Lid Margin Disease

31

Table 3-1

Treatment Recommendations by Severity Level Level • • • •

1 Education and environmental/dietary modifications Elimination of offending systemic medications Artificial tear substitutes, gels/ointments Eyelid therapy

Level 2 If Level 1 treatments are inadequate, add • Anti-inflammatories • Tetracyclines (for meibomianitis, rosacea) • Punctal plugs • Secretagogues • Moisture chamber spectacles Level 3 If Level 2 treatments are inadequate, add • Serum • Contact lenses • Permanent punctal occlusion Level 4 If Level 3 treatments are inadequate, add • Systemic anti-inflammatory agents • Surgery (lid surgery, tarsorrhaphy, mucus membrane, salivary gland, amniotic membrane transplantation) Modified from International Task Force Guidelines for Dry Eye. Reprinted with permission from Ethis Communications Inc.

Table 3-2

Disease Severity Grading for Dry Eye* DRY EYE SEVERITY LEVEL 1

2

3

4

Discomfort severity and frequency

Mild and/or episodic Occurs under environ stress

Moderate episodic or chronic Stress or no stress

Severe frequent or constant Without stress

Severe and/or disabling and constant

Visual symptoms

None or episodic Mild fatigue

Annoying and/or activity limiting Episodic

Annoying, chronic, and/ or constant Limiting activity

Constant and/or possibly disabling, requires signs and symptoms

Conjunctival injection

None to mild

None to mild

None to mild

Mild to moderate

Conjunctival staining

None or mild

Variable

Moderate to marked

Marked

Corneal staining (severity/location)

None or mild

Variable

Marked central

Severe punctate erosions

Corneal/tear signs

None to mild

Mild Decreased debris meniscus

Filamentary keratitis, mucus clumping Increased tear debris

Filamentary keratitis Epithelial defect ulceration

Lid/meibomian glands

Variable

Variable

Frequent

Trichiasis Keratinization Symblepharon

Tear break-up time (sec)

Variable