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Ординатура / Офтальмология / Учебные материалы / Atlas of Glaucoma Second Edition Choplin Lundy 2007

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x List of Contributors

Gustavo E Gamero, MD

St. Luke’s Cataract & Laser Institute

Tarpon Springs, FL

USA

JoAnn A Giaconi, MD

Clinical Assistant

Professor of Ophthalmology

Jules Stein Eye Institute

Veterans Administration of Greater Los Angeles,

Los Angeles, CA

USA

David S Greenfield, MD

Associate Professor Clinical Ophthalmology

Bascom Palmer Eye Institute

University of Miami School of Medicine

Miami, FL

USA

Alon Harris, PhD

Department of Ophthalmology

Indiana University School of Medicine

Indianapolis, IN

USA

Jeffrey D Henderer, MD

Assistant Professor of Ophthalmology

Thomas Jefferson University School of Medicine

Assistant Surgeon

Wills Eye Hospital Glaucoma Service

Philadelphia, PA

USA

Richard A Hill, MD

Orange County Glaucoma

Santa Ana, CA

USA

Christian P Jorescu-Cuypers, MD, PhD

University of Saarland/Homburg

Homburg/Saar

Germany

L Jay Katz, MD

Professor of Ophthalmology

Thomas Jefferson Medical College

Attending Surgeon

Wills Eye Hospital Glucoma Service

Philadelphia, PA

USA

Baseer U Khan, MD FRCS

Department of Ophthalmology

University of Toronto

Toronto, ON

Canada

Paul P Lee, MD, JD

Professor of Ophthalmology

Duke University Medical Center

Durham, NC

USA

Paul S Lee, MD

James J. Peters Veteran Affairs Medical Center

Bronx, NY

USA

Jeffrey M Liebmann, MD

Professor, Clinical Ophthalmology

Director, Glaucoma Service

Manhattan Eye, Ear and Throat Hospital

New York University School of Medicine

New York, NY

USA

Diane C Lundy, MD

Captain, Medical Corps

United States Navy, Retired

Former Director of Glaucoma Services and

Residency Directory

Naval Medical Center

San Diego, CA

USA

Jonathan Myers

Associate Professor

Thomas Jefferson Medical College

Associate Attending Surgeon

Wills Eye Hospital Glaucoma Service

Philadelphia, PA

USA

Arvind Neelakantan, MD, FRCOphth

Bascom Palmer Eye Institute

Miami, FL

USA

Robert Ritch, MD

Professor, Clinical Ophthalmology

Director, Glaucoma Service

New York Eye and Ear Infirmary

New York Medical College

New York, NY

USA

Janet B Serle, MD

Professor

Department of Ophthalmology

Mount Sinai School of Medicine

New York, NY

USA

List of Contributors xi

Mark B Sherwood, MD

Department of Ophthalmology

University of Florida College of Medicine

Gainesville, FL

USA

Mary Fran Smith, MD

Department of Ophthalmology

University of Florida College of Medicine

Gainesville, FL

USA

Richard Tamesis, MD

Department of Ophthalmology

University of Nebraska Medical Center

Omaha, NE

USA

Celso Tello, MD

Associate Professor Clinical Ophthalmology

Associate Director of Glaucoma Service

The New York Eye and Ear Infirmary

New York, NY

USA

Carol B Toris, PhD

Department of Ophthalmology

University of Nebraska Medical Center

Omaha, NE

USA

Carlo E Traverso, MD

Director of Centro di Ricerca Clinica e Laboratorio per il Glaucoma e lacornea

Clinica Oculistica

Di N.O.G University di Genova

Azienda Ospedaliera Universitaria San Martino Genova

Italy

Robert N Weinreb, MD

Hamilton Glaucoma Center

Department of Ophthalmology

University of California San Diego

La Jolla, CA

USA

Jennifer S Weizer, MD

Assistant Professor

Ophthalmology and Visual Sciences

Kellogg Eye Center

University of Michigan

Ann Arbor, MI

USA

Richard Wilson, MD

Professor

Wills Eye Hospital

Philadelphia, PA

USA

Darrell WuDunn, MD, PhD

Associate Professor

Department of Ophthalmology

Indiana University School of Medicine

Indianapolis, IN

USA

Michael E Yablonski, MD

Department of Ophthalmology

University of Nebraska Medical Center

Omaha, NE

USA

Linda M Zangwill, PhD

Hamilton Glaucoma Center

Department of Ophthalmology

University of California San Diego

La Jolla, CA

USA

Foreword

Since ‘glaucoma’ encompasses a wide variety of clinical findings, diagnostic techniques, and treatment options, we thought it best to assemble a book like this one from many parts, each manufactured by someone who is an expert in that particular subject matter. Although at times it felt like we were trying to herd mercury, this project has come together in a way that has exceeded our expectations.

Editing a project like this can be trying; the big benefit comes from having the material to read as part of the editorial process. We learned a lot about glaucoma as we went through the individual chapters, and trust that the readers will likewise benefit. The chapters were written by authors recognized for their clinical and research expertise, particularly in their subject areas: Drs Toris and Yablonski (two of the world’s experts in fluorophotometry) from the University of Nebraska (with wonderful artwork by Richard Temesis) on aqueous humor dynamics, Ron Fellman on gonioscopy, Gustavo Gamero from Tarpon Springs, Florida with Rob Fechtner from the University of Medicine and Dentistry of New Jersey, Newark, New Jersey on the optic nerve (Rob was one of the first people in the world to work with scanning laser polarimetry), Jennifer Weizer and Paul Lee from Duke University (an expert in epidemiology as well as glaucoma) on primary open angle glaucoma, Jonathan Meyers and L Jay Katz from the Wills Eye Hospital in Philadelphia, Pennsylvania, on secondary glaucoma, Jeff Liebman and the group from the New York Eye and Ear Infirmary on the angle closure glaucomas (pioneering experts on ultrasound biomicroscopy), Lou Cantor and the group from the University of Indiana on normal tension glaucoma, Alon Harris on ocular blood flow, Carlo Traverso from the University of Genoa, Italy, on developmental glaucoma and its treatment (Carlo’s experience with the subject while in Saudi Arabia is staggering, where he saw something like 300 cases of congenital and developmental glaucoma in a three-year period!), Paul S Lee, Donna Gagliuso, and Janet Serle from Mount Sinai School of Medicine, New York, NY on medical treatment (new to the Second Edition, welcome!),

Rick Hill from the University of California, Irvine (who has done outstanding work in laser sclerostomy and ciliodestruction), on laser therapy, Jeffrey Henderer and Rick Wilson from the Wills Eye Hospital in Philadelphia on filtering surgery (Rick was one of Dr Choplin’s mentors on the art of trabeculectomy), Anne Coleman and JoAnn Giaconi from the University of California, Los Angeles on aqueous shunts (Anne was one of the original investigators for the Ahmed Glaucoma Valve, and was the senior author on the first published paper dealing with the device), and Mark Sherwood and co-workers from the University of Florida, Gainesville (superb clinicians and experienced glaucoma researchers), on the co-management of cataract and glaucoma. As times have changed since the publication of the First Edition, we have added two new very exciting chapters in this Second Edition: Ike Ahmed on nonpenetrating filtering surgery, and Chris Bowd, Lindal Zangwill, and Bob Weinreb from the University of California, San Diego, on scanning laser imaging. It was in Dr Weinreb’s laboratory that scanning laser polarimetry was ‘born’.

Having a diversity of authors makes for a diversity of styles. Although the editors wielded a broad editorial pen, attempting to maintain a consistent style throughout the book, the reader will note that each chapter has its own unique character. Some chapters have much text and few illustrations, while others are almost exclusively graphical, with extensive legends written to bring out the teaching point of the picture. Hopefully, the material, no matter how it is presented, will add to the readers’ knowledge of glaucoma, as it has for ours.

Disclaimer

The editors are former active duty medical officers in the United States Navy, now both retired from active service. Neither of us have any further official relationship with the United States Navy (except as ‘retirees’), and this book, as the First Edition, was not written as part of any official duties.

xiii

xiv Foreword

Notwithstanding, the views and opinions expressed

or device mentioned in this book, while Dr Choplin

in this work are ours or those of the individual

is a paid consultant to Carl Zeiss Meditec, Inc., and

authors, and should not be construed as official

has received travel funds and honoraria from most of

opinions of the Department of the Navy, the

the major ophthalmic pharmaceutical companies.

Department of Defense, or of the United States gov-

 

ernment. Dr Lundy has no financial or proprietary

Neil T Choplin

interest in any company, product, drug, machine,

Diane C Lundy

Preface

It was once said to me that there is no specialty in the field of medicine that deals with only one disease. I suppose there are endocrinologists who specialize in treating only patients with diabetes mellitus, making them ‘diabetologists’, but there may not be any other ‘one disease doctors’ except for the ophthalmologists who specialize in the diagnosis and management of patients with glaucoma, and these specialists may be termed ‘glaucomologists’. However, if it is true that ‘diabetologists’ treat only one disease, it is not true that ‘glaucomologists’ treat only one disease, simply because glaucoma is not one disease. In fact, at this point in time, it is hard to say exactly what glaucoma is. What is becoming clear is that glaucoma is a spectrum of clinical entities that encompasses many ocular and systemic conditions. It may be a primary eye disease, or a manifestation of some other ocular or systemic disease.

It was while contemplating some aspect of a lecture to be given (or thinking about one just given, I can’t remember which) that it occurred to me that in my day-to-day clinical practice I’m really not doing anything the way I was trained over 20 years ago. As I continued to reflect on this it became apparent that nothing in glaucoma is what it was. Indeed, this gave way to a lecture called ‘Current Concepts in Glaucoma: Nothing is What it Was’. Indeed, the change in the definition of glaucoma from a pressure disease to an optic neuropathy, intraocular pressure as a risk factor rather than the cause of glaucoma, new methods for early detection and diagnosis of glaucoma (‘pre-perimetric’), and a solid scientific basis for approaches to treatment (based upon a number of landmark clinical studies) are all different from what they were when I was a glaucoma fellow.

Around the time of the publication of the First Edition, ophthalmologists had begun to recognize that glaucoma is an optic nerve disease, with ‘characteristic’ progressive structural changes leading to loss of visual function in a ‘characteristic’ way. The use of intraocular pressure levels to define the disease has pretty much gone away, and now pressure is used to gauge the risk of having, or developing, glaucoma. Does that mean that the 65-year-old patient with ‘cupped out’ optic nerves, central and temporal islands in the

visual fields, and an untreated intraocular pressure of 12 mmHg has glaucoma, while the 45-year-old myopic male with pigment dispersion syndrome and an initial intraocular pressure of 52 mmHg in each eye with normal optic nerves and visual fields doesn’t? The former patient may be in the ‘burned out’ stage of glaucoma or may have suffered visual loss from anterior ischemic optic neuropathy, while the latter may be in the early stages of glaucoma or may have simply had a transient rise in pressure following a brisk walk. To try to describe multiple disease, conditions, and scenarios in a widely disparate group of patients with a single term ‘glaucoma’ is subject to frustration. ‘Glaucomologists’ do not deal with a single disease.

Comprehension of glaucoma’s pathophysiology is improving, but there is much we don’t know. We are well into a new era in glaucoma research, focusing on the cellular mechanisms responsible for the death of optic nerve axons. The research is proceeding on many different fronts: genetic, biochemical, and cellular biological, to name but a few. New ideas are emerging. Perhaps intraocular pressure (in some people) is the initiating event that damages a handful of neurons, with the bulk of the damage then done by the propagation of environmental toxins released when those cells die. Perhaps glaucoma is the genetically predetermined self-destruction of the optic nerve, with similar genetically determined mechanisms in the trabecular meshwork responsible for the observed increase in intraocular pressure, with no causal relationship between intraocular pressure and optic nerve damage. Perhaps glaucoma is a condition in which the blood flow to the optic nerve is insufficient for its nutritional requirements, leading to its ultimate demise. How different these ideas are from the concept that ‘glaucoma is a disease in which the intraocular pressure rises and this causes optic nerve damage’.

This book illustrates what we know about ‘glaucoma’ today. It encompasses a wide variety of subjects, as one would expect for a disease that encompasses a wide variety of clinical conditions, syndromes, and findings.

Neil T Choplin, MD

xv

Acknowledgments

Thank you to our co-workers, spouses, and families, and to our residents and former residents for keeping us on our toes and advancing our knowledge as we attempted to advance theirs. We would also like to acknowledge the hard work and effort put forth by the contributors and their co-workers, without whom this book would not have been possible. We remain extremely grateful to Alan Burgess, the

commissioning editor for the First Edition, for his help, advice, and constant encouragement. Lastly, this project might not have been seen through to completion were it not for the diligence, persistence, badgering (always in a nice way), and encouragement of Oliver Walter, whose names we have finally got in the correct order. Thank you, Oliver.

xvii

1 Introduction to glaucoma

Diane C Lundy, Neil T Choplin

INTRODUCTION

Glaucoma is a diagnosis that may be readily and perhaps too frequently made, based upon a variety of clinical findings by different eye-care professionals. It is not a single disease, but rather a group of diseases with some common characteristics (see Chapter 2). The hallmarks of glaucoma are typical, often progressive, optic nerve head changes and visual field loss (Figure 1.1) or the potential for them. Optic nerve damage (discussed in Chapters 6 and 7), and its corresponding visual field loss (discussed in Chapter 8), is often, but not always, reached in the setting of intraocular pressure deemed to be too high for the affected eye (Chapters 3, 4, 9 and 12). All glaucomatous disease may have a common end point, that being irreversible loss of visual function and even blindness. Since ‘glaucoma’ is not a single disease, there is no typical ‘glaucoma patient’ or single best ‘glaucoma treatment’.

Figure 1.1 Optic disc and corresponding visual field from a patient with glaucoma. Note the thinning of the temporal rim of this left optic disc with extension of the cup to the inferior rim. The visual field shows a superior altitudinal hemianopia, corresponding to the loss of the inferior rim.

THE SPECTRUM OF GLAUCOMA

The manifestations of glaucoma are protean regardless of which parameter is considered. At one end of the clinical spectrum is the white, quiet, painless eye of a patient with primary open-angle glaucoma (POAG) who may, in fact, be unaware of the presence of the disease (Chapter 9). At the other extreme is the patient with acute angle closure glaucoma who is distraught with eye pain, decreased vision, and possibly even systemic symptoms such as nausea and vomiting (Chapter 11). The age of the glaucoma patient at the time of clinical presentations is likewise variable. Congenital glaucoma (Chapter 14) presents in the newborn, while typical patients with glaucoma due to the exfoliation syndrome (Chapter 10) are usually in their seventh or eighth decade of life. Although the glaucomas share a common end point, their proximal etiologies range from acute macroscopic mechanical closure of the outflow structures, as in acute angle closure, to a macroscopically open angle with increased resistance to outflow at the microscopic and cellular level, as in POAG. In some patients with glaucoma, intraocular pressure may have nothing to do with the observed damage. Newer evidence points towards a possible role of neurotoxins as a distal part of the route to glaucomatous optic neuropathy and field loss.

The differing manifestations of glaucoma are reflected in the clinical examination findings, which can range from the normal-appearing anterior segment of the POAG patient to the markedly abnormal findings in the patient with uveitic glaucoma or iridocorneal endothelial syndrome (ICE). (Consider the appearance of the eye of a patient with Rieger’s syndrome shown in Figure 1.2.) Intraocular pressure may be quite elevated, as in the case of acute angle closure, or well within the ‘average’ range (Chapter 12). The visual field examination of the glaucoma patient may likewise represent a spectrum

1