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Get an unprecedented view of corneal disease with Cornea Atlas by Jay H. Krachmer, MD and David A. Palay, MD. Hailed as the sharpest, most accurate collection of corneal images available, it is the only atlas that offers such an easy-to-understand, up-to-date review of clinical presentations and surgical techniques for all corneal and external eye disorders.
  • Sharpen your diagnostic and surgical skills for all corneal and external eye disorders - including tumors, dystrophic and degenerative disorders, inflammatory diseases, corneal manifestations of systemic disease, traumatic injuries, and therapeutic and reconstructive surgical procedures.
  • Rely on the expertise of internationally renowned ophthalmologists who have developed many innovative techniques for diagnosing and treating corneal and external eye diseases.



Publié par
Date de parution 04 juin 2013
Nombre de lectures 5
EAN13 9781455750054
Langue English
Poids de l'ouvrage 11 Mo

Informations légales : prix de location à la page 0,0798€. Cette information est donnée uniquement à titre indicatif conformément à la législation en vigueur.


Cornea Atlas
Third Edition

Jay H Krachmer, MD
Former Chairman, Department of Ophthalmology, University of Minnesota Medical School, Minneapolis, MN, USA

David A Palay, MD
Associate Clinical Professor, Department of Ophthalmology, Emory University, Atlanta, GA, USA
Table of Contents
Cover image
Title page
Tribute: Tuesdays with Jay
Chapter 1: Corneal Slit Lamp Techniques
Direct Illumination: Thin Slit Beam
Direct Illumination: Broad Oblique Beam
Indirect Illumination: Indirect Iris Lighting – Finding Darker Than Background
Indirect Illumination: Indirect Iris Lighting – Finding Lighter Than Background
Indirect Illumination: Sclerotic Scatter
Indirect Illumination: Adjacent Beam
Indirect Illumination: Red Reflex
Specular Reflection
Chapter 2: Diseases of the Lid: Anatomic Abnormalities
Floppy Eyelid Syndrome
Lower Lid Imbrication
Chapter 3: Diseases of the Lid: Tumors
Benign Lid Tumors
Malignant Lid Tumors
Chapter 4: Diseases of the Lid: Inflammatory (Blepharitis), Immunologic, Infectious, and Traumatic
Bacterial Infections
Viral Infections
Parasitic Infections
Allergic Inflammations
Foreign Body
Chapter 5: Disorders of Tear Production and the Lacrimal System
Dry Eye
Dacryoadenitis, Dacryocystitis, and Canaliculitis
Chapter 6: Conjunctival Disease: Tumors and Anatomic Abnormalities
Squamous Neoplasms of the Conjunctiva
Melanocytic Neoplasms and Other Pigmented Lesions of the Conjunctiva
Subepithelial Neoplasms and Other Lesions
Prolapsed Orbital fat
Chapter 7: Conjunctivitis
Clinical Features
Bacterial Conjunctivitis
Viral Conjunctivitis
Chlamydial Infections: Adult Inclusion Conjunctivitis
Ophthalmia Neonatorum
Parinaud’s Syndrome
Parasitic Conjunctivitis
Allergic Conjunctivitis
Vernal and Atopic Keratoconjunctivitis
Giant Papillary Conjunctivitis
Ocular Cicatricial Pemphigoid
Linear IgA Disease
Pemphigus Vulgaris
Stevens-Johnson Syndrome
Reiter’s Syndrome
Toxic Conjunctivitis
Theodore’s Superior Limbic Keratoconjunctivitis
Ligneous Conjunctivitis
Factitious Conjunctivitis
Chapter 8: Normal Anatomy and Developmental Abnormalities of the Cornea
Normal Anatomy
Developmental Corneal Opacities and Abnormalities of Size and Shape
Anterior Chamber Cleavage Syndromes
Chapter 9: Corneal Manifestations of Systemic Disease and Therapy
Metabolic Disorders
Skeletal Disorders
Inflammatory Bowel Disease
Nutritional Disorders
Hematologic Disorders
Endocrine Disorders
Dermatologic Disorders
Infectious Diseases
HIV-Related Disorders
Corneal Manifestations of Local and Systemic Therapies
Chapter 10: Lid, Conjunctival, and Corneal Manifestations of Chemical and Biological Warfare
Chapter 11: Corneal Dystrophies, Ectatic Disorders, and Degenerations
Anterior Membrane Dystrophies
Stromal Dystrophies
Posterior Membrane Dystrophies
Noninflammatory Ectatic Disorders
Secondary Ectasias
Iridocorneal Endothelial Syndrome
Conjunctival and Corneal Degenerations
Chapter 12: Corneal Infections
Bacterial Infections
Herpes Simplex Keratitis
Herpes Zoster Keratitis
Fungal Keratitis
Acanthamoeba Keratitis
Chapter 13: Interstitial Keratitis
Syphilitic Interstitial Keratitis
Nonsyphilitic Interstitial Keratitis
Chapter 14: Noninfectious Keratopathy
Recurrent Erosion Syndrome
Filamentary Keratitis
Thygeson’s Superficial Punctate Keratitis
Neurotrophic Keratopathy
Neurogenic Keratopathy
Exposure Keratopathy
Radiation Keratopathy
Factitious Disease
Chapter 15: Immunologic Disorders of the Cornea
Rheumatoid Arthritis
Nonrheumatoid Collagen Vascular Disease
Staphylococcal Disease
Mooren’s Ulcer
Chapter 16: Corneal Trauma
Foreign Body, Mechanical, Thermal, and Radiation Trauma
Surgical Trauma
Acid Burns
Alkali Burns
Chapter 17: Contact Lens Complications
Chapter 18: Disorders of the Sclera
Scleral Thinning
Chapter 19: Iris Tumors
Chapter 20: Anterior Uveitis
Fuchs’ Heterochromic Iridocyclitis
Behçet’s Disease
Vogt-Koyanagi-Harada Syndrome
Juvenile Rheumatoid Arthritis
Syphilitic Uveitis
HLA-B27-Related Uveitis
Chapter 21: Penetrating Keratoplasty
Preoperative and Postoperative Appearance
Intraoperative and Early Postoperative Complications
Late Complications
Rejection Reactions
High Astigmatism
Chapter 22: Deep Anterior Lamellar Keratoplasty
Preoperative, Intraoperative, and Postoperative Appearance
Intraoperative and Early Postoperative Complications
Late Complications
Rejection Reactions
Chapter 23: Endothelial Keratoplasty
Tissue Preparation
Preoperative, Intraoperative, and Postoperative Appearance
Intraoperative and Early Postoperative Complications
Late Complications
Rejection Reactions
Chapter 24: Therapeutic and Reconstructive Procedures
Scleral Contact Lenses
Conjunctival Flaps
Surgery for Pterygia
Surgery for Scleral Melt
Glue Application for Corneal Perforation
Superficial Keratectomy
Phototherapeutic Keratectomy (PTK)
Corneal Collagen Crosslinking
Keratolimbal Allograft (KLAL)
Surgery for Recurrent Erosions
Reconstructive Lamellar Keratoplasty
Anterior Segment Reconstruction
Temporary Keratoprosthesis
Permanent Keratoprosthesis
Chapter 25: Refractive Surgery
Incisional Refractive Surgery
Photorefractive Surgery: Photorefractive Keratectomy
Photorefractive Surgery: Laser-Assisted In Situ Keratomileusis (LASIK)
Photorefractive Surgery: Laser-Assisted Subepithelial Keratectomy (LASEK)
Intrastromal Rings
Thermal Keratoplasty
Phakic Intraocular Lenses

SAUNDERS is an imprint of Elsevier Inc.
© 2014, Elsevier Inc. All rights reserved.
First edition 1995
Second edition 2006
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: .
This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.
ISBN: 978-1-4557-4060-4
Ebook ISBN : 978-1-4557-5005-4

Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1
It was a pleasure for us to have the opportunity to write a third edition of our Cornea Atlas . We feel that this edition is a significant improvement over the previous book.
How does this edition differ from the previous editions?

•  Nearly all the figures from the previous editions have been edited with improvements.
•  Many figures have been eliminated or replaced.
•  There are 203 new figures.
•  In the first edition, 25% of the figures came from contributors. In the second edition 36% of our figures came from contributors. In this edition, 40% came from outside of our collections. Using the Internet, we were able to obtain contributions from Africa, Asia, Europe, and South America.
•  There are a total of 103 contributors, more than both previous editions.
•  There is a new chapter entitled “Corneal Slit Lamp Techniques”. This chapter, written by Jay Krachmer, is a summary of Jay’s observations and teaching points from a career that lasted more than 30 years.
•  There is a new chapter entitled “Deep Anterior Lamellar Keratoplasty”.
•  There is a new chapter entitled “Endothelial Keratoplasty”.
We hope that this edition is greatly improved but realize that we can still do better. As with the previous editions, we ask that readers let us know how we can make a future edition an even greater contribution.

Jay H Krachmer, MD

David A Palay, MD
We are extremely grateful to our many colleagues, associates, and friends who helped with the preparation of this book. We would like to credit and thank the following contributors for sending us materials:

Wallace L M Alward, Iowa City, Iowa (8.38, 11.142)
Haggay Avizemer, Tel Aviv, Israel (9.133, 11.68)
Jerry Barker, Winston-Salem, North Carolina (23.1)
William Basuk, Deceased (2.7)
Allen D Beck, Atlanta, Georgia (16.8)
Michael Belin, Merana, Arizona (11.130)
Erick Bothun, Minneapolis, Minnesota (9.15)
Mario Brunzini, Buenos Aires, Argentina (12.68)
J Douglas Cameron, Minneapolis, Minnesota (6.17, 11.122, 11.174)
Emmett Carpel, Minneapolis, Minnesota (11.137)
H Dwight Cavanagh, Dallas, Texas (8.5)
Naveen S Chandra, Walnut Creek, California (25.34)
Steven Ching, Rochester, New York (7.66, 7.67, 7.68, 7.69, 9.102, 9.103, 9.104, 11.177, 12.54, 22.2, 22.3, 22.4, 22.5, 22.6, 22.8, 22.9, 22.15)
Gary Chung, Federal Way, Washington (6.14, 6.15, 6.16, 17.9)
David Cogan, Deceased (13.11)
Elisabeth Cohen, New York City, New York (9.24, 9.25)
Michael Conners, Setauket, New York (25.37, 25.38)
Elizabeth Davis, Minneapolis, Minnesota (25.48)
Michael Diesenhouse, Tucson, Arizona (9.123, 18.11, 18.12)
Claes Dohlman, Boston, Massachusetts (24.53, 24.54, 24.57)
Fabio Dornelles, Porto Alegre, Brazil (1.27, 1.28, 4.8, 11.91, 11.147, 25.5, 25.6, 25.40)
Donald Doughman, Minneapolis, Minnesota (9.114)
Richard Eiferman, Louisville, Kentucky (4.34, 8.29, 9.86, 17.2, 18.1, 18.7, 21.53)
Robert S Feder, Chicago, Illinois (11.20, 11.21, 11.22, 11.37, 11.38, 11.56 (Lattice III))
Sandy Feldman, San Diego, California (9.55, 9.56)
Richard K Forster, Miami, Florida (7.32, 7.33, 10.5, 10.6)
Denise de Freitas, Sao Paulo, Brazil (1.11, 12.75, 25.35)
Juliana Freitas, Sao Jose de Rio Preto, Brazil (9.105, 9.106, 9.107, 9.108, 16.9)
Herb Friesom, Deceased (4.27, 4.28, 7.37, 7.51, 10.1, 10.2, 10.3, 10.4)
Lawrence Gans, Hazelwood, Missouri (19.5)
David Goldman, Palm Beach Gardens, Florida (23.13, 23.14, 23.15, 25.33)
Kenneth Goins, Iowa City, Iowa (22.1)
W Richard Green, Deceased (4.26)
Michael R Grimmett, Palm Beach Gardens, Florida (6.45)
Hans Grossniklaus, Atlanta, Georgia (3.5, 3.10, 3.15, 3.19, 3.18, 3.31, 3.34, 3.39, 3.41, 6.30, 6.58, 7.65, 8.14, 8.17, 8.28, 8.31, 8.41, 9.26, 11.3, 11.15, 11.32, 11.33, 11.34, 11.50, 11.61, 11.96, 11.99, 11.124, 11.165, 11.178, 12.85)
M Bowes Hamill, Houston, Texas (16.43, 16.65)
Stephen Hamilton, Atlanta, Georgia (9.42, 19.6, 24.55)
Kristen Hammersmith, Philidelphia, Pennsylvania (21.37)
David Hardten, Minneapolis, Minnesota (25.46)
Andrew Harrison, Minneapolis, Minnesota (2.4, 2.6, 3.4, 3.35, 3.36, 3.37, 9.85)
Koji Hirano, Nagoya, Japan (11.39, 11.40, 11.41, 11.56 (Lattice IV))
Lawrie Hirst, Graceville, Australia (16.6, 16.7, 24.8, 24.9)
Edward J Holland, Cincinnati, Ohio 3.40, 3.42, 5.23, 6.26, 6.46, 6.54, 7.38, 7.52, 7.81, 7.89, 7.90, 7.91, 9.94, 9.95, 9.96, 9.97, 9.128, 11.51, 11.52, 11.53, 11.56 (Granular II), 11.64, 11.65, 11.187, 12.11, 12.24, 12.34, 15.20, 15.21, 15.26, 16.84, 16.85, 18.5, 20.3, 20.7, 20.13, 20.14, 20.17, 20.18, 21.18, 21.32, 24.30, 24.31, 24.32, 24.33, 24.34, 25.3)
Andrew Huang, St. Louis, Missouri (7.53, 7.56, 9.35, 11.54, 11.55, 11.189)
Infect Dis Clin North Am, 1992 (9.120)
Int Ophthalmol Clin 29:98-104, 1989 (9.127)
Joe Iuorno, Richmond, Virginia (1.18, 6.3, 6.4, 6.34, 7.85, 9.138, 11.77, 11.108, 16.2, 16.10)
Timothy Johnson, Iowa City, Iowa (20.12)
David Jordan, Ottawa, Canada (5.26)
Muriel I Kaiser-Kupfer, Deceased (13.12)
Jack Kanski, London, England (8.35)
Stephen Kaufman, Minneapolis, Minnesota (6.21, 9.10, 9.11, 12.82, 16.90)
Kenneth Kenyon, Marion, Massachusetts (9.18, 9.34, 11.57)
William H Knobloch, Deceased (9.8)
David Knox, Baltimore, Maryland (9.52, 9.54)
Steven Koenig, Milwaukee, Wisconsin (16.12)
Regis Kowalski, Pittsburg, Pennsylvania (12.1, 12.2, 12.3 (A,C,D,E,F), 12.4)
Burton J Kushner, Madison, Wisconsin (3.8, 3.9)
Ethan Kutzscher, Walnut Creek, California (1.16, 12.86, 12.87, 25.24, 25.30)
Sergio Kwitko, Porto Alegre, Brazil (11.117, 11.188, 22.7, 22.10, 22.11, 22.12, 22.16, 23.3, 23.9, 24.56, 25.41, 25.42, 25.43, 25.44, 25.45 25.49)
Peter R Laibson, Philadelphia, Pennsylvania (7.12, 7.62, 7.77, 7.78, 7.83, 8.7, 11.2, 11.4, 11.19, 11.49, 11.56 (Thiel-Behnke), 11.155, 12.21, 12.25, 12.28, 12.35, 12.49, 12.58, 12.59, 13.6, 13.7, 14.3, 14.4, 14.7, 16.37, 16.82)
Ronald Laing, Sarasota, Florida (8.4)
Scott Lambert, Atlanta, Georgia (20.16)
Michael Law, Kuala Lumpur, Malaysia (11.6, 11.109, 11.118, 15.33, 16.96, 16.97, 16.98, 21.8, 23.10, 25.10)
Barry Lee, Atlanta, Georgia (2.14, 7.60, 8.16, 9.99, 11.115, 21.45, 21.46, 23.16)
Michael Lee, Minneapolis, Minnesota (9.151)
Michael Lemp, Lake Wales, Florida (5.1, 5.2, 5.3)
Mary Lynch, Atlanta, Georgia (8.32, 8.36, 8.37)
Marian Macsai, Chicago, Illinois (24.44, 24.45, 24.46, 24.52)
Mark Mandel, Hayward, California (16.88)
Mark J Mannis, Sacramento, California (4.3, 4.21, 5.20, 7.64, 11.69, 11.70, 21.15)
Daniel F Martin, Cleveland, Ohio (6.5, 19.19)
Darlene Miller, Miami, Florida (12.3 B)
Gioconda Mojica, Hayward, California (1.20, 6.66, 6.67, 7.23, 7.24, 8.22)
Andrew L Moyes, Kansas City, Missouri (4.20, 5.27)
Jeffrey Nerad, Cincinnati, Ohio (3.18)
David Park, Stillwater, Minnesota (25.47)
Rachana Patel, Jacksonville, Florida (9.32, 9.33)
Charles Pavlin, Toronto, Ontario (6.28, 6.29)
Louis Probst, Westchester, Illinois (25.12, 25.13, 25.16, 25.21, 25.22)
John J Purcell, St. Louis, Missouri (11.35, 11.36)
J Bradley Randleman, Atlanta, Georgia (25.36)
Christopher Rapuano, Philadelphia, Pennsylvania (11.23, 19.13, 23.11, 23.12, 24.13, 24.14, 24.21, 24.22, 24.41, 24.42, 25.17, 25.25, 25.27)
Merlyn Rodrigues, Bethesda, Maryland (11.87, 11.123, 11.169)
Roy Rubinfeld, Chevy Chase, Maryland (11.5, 24.23, 24.24, 24.25, 24.26, 24.27, 24.28, 24.29, 25.14, 25.15, 25.18, 25.19, 25.20, 25.23, 25.29, 25.31, 25.32)
Alan Sadowksy, Fridley, Minnesota (9.93, 9.98, 9.100)
Steven Schallhorn, San Diego, California (25.9, 25.11, 25.28)
Ivan Schwab, Sacramento, California (9.137)
Wendell J Scott, Springfield, Missouri (9.14)
Neal Shear, Minneapolis, Minnesota (1.19, 9.78, 9.79)
Roni Shtein, Ann Arbor, Michigan (11.12, 12.84)
Gilbert Smolin, Deceased (9.9, 9.12, 9.13, 9.81)
Tomy Starck, San Antonio, Texas (11.144)
Walter Stark, Baltimore, Maryland (21.58)
Alfred O Steldt, Minneapolis, Minnesota (16.62)
Alan Sugar, Ann Arbor, Michigan (11.97, 1198)
Joel Sugar, Chicago, Illinois (9.116, 9.117, 9.118, 9.119, 11.97, 11.98, 15.23)
Laurence Sullivan, East Melbourne, Australia (2.15, 7.42, 11.76, 17.8, 22.13, 22.14, 25.39)
C Gail Summers, Minneapolis, Minnesota (9.7, 9.16)
Survey of Ophthalmology 38:229, 1993 (9.115)
Hugh Taylor, Carlton, Australia (9.121, 9.122)
Thieme, New York, New York 1998 (24.19, 24.20)
Keith Thompson, Atlanta, Georgia (11.47, 25.1, 25.2)
Gregory L Thorgaard, Ottumwa, Iowa (14.22, 14.23)
Elias Traboulsi, Cleveland, Ohio (9.44)
David T Tse, Miami, Florida (2.16, 2.17)
Gary Varley, Cincinnati, Ohio (5.14, 12.19)
Arthur W Walsh, Lebanon, New Hampshire (9.143)
Keith Walter, Winston-Salem, North Carolina (7.8, 7.9, 24.49, 24.50)
Michael Ward, Atlanta, Georgia (24.1, 24.2)
George O Waring III, Atlanta, Georgia (6.23, 6.31, 8.9, 11.162, 24.58)
Michael Warner Hermiston, Oregon (6.1, 6.6, 6.20, 6.41, 6.43, 6.44, 6.61)
Robert Weisenthal, Dewitt, New York (11.94, 22.17, 22.18, 22.19)
John Wells III, West Columbia, South Carolina (9.49, 9.50)
Theodore Werblin, Princeton, West Virginia (25.4)
Jonathan Wirtschafter, Deceased (9.65, 9.66)
Ted H Wojno, Atlanta, Georgia (2.1, 2.2, 2.3, 2.5, 2.8, 2.11, 2.12, 3.13, 3.14, 3.16, 3.20, 3.21, 3.22, 3.23, 3.24, 3.25, 3.26, 3.29, 3.30, 3.32, 3.33, 3.38, 4.17, 6.48, 6.64, 6.65, 7.3, 9.101, 16.28)
Tom Wood, Memphis, Tennessee (6.11, 6.12, 6.13, 15.30, 15.31, 15.32)
Martha Wright, Minneapolis, Minnesota (11.143, 11.160, 11.161)
Sonia Yoo, Miami, Florida (23.17)
We would like to thank the staff at Elsevier/Saunders for their wonderful support. It was a pleasure working with them. Although many individuals were involved, it was Russell Gabbedy, Sharon Nash, and Caroline Jones who went to bat for us when we had ideas which might cost the publisher extra money but in the end would definitely be value-added.
With great love and appreciation, I dedicate this book to
my wife, Kathryn, our children, Edward, Kara, and Jill,
our parents, Paul and Rebecca Krachmer
and Louis and Gertrude Maraist

Jay H Krachmer
To my wife and best friend, Debbie, and my children Sarah and Matthew,
and my parents Sandra and Bernard.
Without their love and support this would not have been possible.
I dedicate this book in memory of my father, Bernard H. Palay MD.

David A Palay
Tribute: Tuesdays with Jay
I have had the honor and privilege to work with Jay on all three editions of the Cornea Atlas . The first edition was conceived during my cornea fellowship with Jay. Although the primary goal of the fellowship was to learn about diseases of the cornea, Jay’s fellowship was also a philosophical inquiry into how to live one’s life. It included discussions of science, research, politics, human relations, and ethics. So much of how I practice and live my life today was influenced by the time I spent with Jay. During my regular Tuesday conference call with Jay for this third edition, the book was discussed, but so too were many other life topics, cooking, movies, TV shows, politics, and the state of medicine just to name a few. My “Tuesdays with Jay” allowed me to relive the wonderful year I spent with him during my fellowship.
Jay achieves a level of perfection with his work that few will ever achieve. Similar to training with a great athlete, Jay pushes you to levels you didn’t realize were attainable.
Just one figure in this atlas took Jay over eight hours to construct. The lighting, color, and cropping must be perfect. The pathology must be highlighted in a way that is effortless for the viewer to discern. Most viewers will glance at the figure for a few seconds not realizing the dedication and time utilized to construct each figure. Cumulatively, this work represents hundreds of hours of work. It is often assumed that a third edition will take less time than a first or second edition. However, in this case each edition has taken more time to construct. The pursuit of perfection runs deeper with each subsequent edition.

“The slit lamp examination is a work of art. The examiner uses light like an artist uses a paintbrush; always looking for ways to see or demonstrate his/her view of the subject.” – Jay Krachmer.
Chapter 1 , Corneal Slit Lamp Techniques, is a summary of Jay’s observations and teaching points over a career that spanned more than 30 years. Jay has an innate power of observation; he is able to see things that most others miss. I remember showing a video at a conference of a difficult surgical case. The entire audience saw the surgical maneuvers in the video, only Jay noticed that the eye speculum I was using was highly unusual and it was a prototype of a new eyelid speculum. Every viewer was naturally drawn to the action in the center of the screen; only Jay saw the action in the center and the static speculum in the periphery of the screen.
It is with great appreciation and fondness that I write these words of thanks to Jay. He has guided me in my career to be an outstanding physician and human being and he has similarly served as a mentor to many fellows and residents. His teaching will live on: not only through this book but also with each generation of his students who will teach subsequent generations of students.
Thank you, Jay.

David Palay
Chapter 1
Corneal Slit Lamp Techniques

Except for some refinements, such as better optics and illumination, the current slit lamp is basically the same instrument Vogt used nearly 100 years ago. Ocular illustrations from that time were spectacularly detailed, indicating a degree of excellence rivaling today’s slit lamps. We hope that we will not go another 100 years without having a better instrument.
It is assumed that the reader is familiar with the mechanical use of the slit lamp and is therefore able to reproduce the techniques that will be discussed. The examiner uses one hand to control the light source (beam brightness, height, width, direction, color, and whether it is parfocal with the biomicroscope) and the other hand to focus the biomicroscope and change its magnification.

Points to Remember

•  Adjust the eye-pieces for your eyes. If you do not, you will miss a great deal of pathology.
•  Look at what is there – not what should be there.
•  Look for what is different – not what is the same.
•  Expand the number of parameters that you use to describe a finding.
•  Do not be too quick to label (name) what you see.
•  Use bright light.
•  Use the full range of slit lamp magnification.
•  Ask the patient to blink. Your attention will be drawn to what does not move (what is part of or attached to the cornea).
•  Findings have different appearances when different types of illumination are used.
•  Be sure that the thin slit beam is focused directly on an object for which you are determining depth.
•  Paint with light the way an artist uses a paintbrush.
•  Always focus on the tissue you want to examine.
•  Enjoy examining the cornea. It is a privilege.

Three Basic Forms of Illumination
Are you focusing the microscope directly within the light beam as it illuminates the cornea? If so, you are using a form of direct illumination. Or, are you not focusing the microscope within the beam on the cornea? If so, you are using a form of indirect illumination. A third form of illumination is the most difficult and will be described in its own category, specular reflection.

Examination Flow
To examine the cornea, first scan with a broad oblique beam. As you are doing so, vary the beam’s width and direction (from the left or right) and notice findings that come into view between the beam on the cornea and the beam falling on the iris. What you see between the corneal and iris beams will be out of focus. Therefore, you must constantly alternate focus from in the corneal beam to between the corneal beam and light falling on the iris. Remind the patient to blink. In that way, as you scan across the cornea, particles in the tear film will move and your attention will be drawn to that which does not move. When you are focusing in the corneal beam, you are using direct illumination. When you are not focusing in the corneal beam, you are using indirect illumination. Use a thin slit to determine the depth of pathology and corneal thickness. Other techniques, such as sclerotic scatter, adjacent beam, red reflex, and specular reflection are important but are used less frequently.
The two best forms of illumination for making observations are:

•  Broad oblique beam; or
•  Indirect illumination.

Order of Technique Presentation
Slit lamp techniques and illustrations follow in this order:

•  Direct illumination

•  Thin slit beam
•  Broad oblique beam
•  Indirect illumination

•  Indirect iris lighting – finding darker than background
•  Indirect iris lighting – finding lighter than background
•  Sclerotic scatter
•  Adjacent beam
•  Red reflex
•  Specular reflection.

Direct Illumination: Thin Slit Beam

Fig. 1.1 Thin slit beam. The thin slit beam has very specific purposes. Use it to determine the depth of findings or the shape of the cornea. Unfortunately, it is probably the most commonly used form of illumination and therefore the reason why so many features of the cornea are missed.

Fig. 1.2 Thin slit beam. A bright thin slit creates a cross section of the cornea demonstrating detailed anatomy. It is kind to the patient not to irritate them by having a bright light shining in their eye. It is unkind to the patient if important findings are missed.

Fig. 1.3 Thin slit beam. The bright, thin slit discloses the anterior–posterior location of this patient’s polychromatic proteinaceous deposits. They are at all depths, and even in the tear film.

Fig. 1.4 Thin slit beam. The thin slit is used to show the contour and thickness of the cornea. In this case, there is thinning with protrusion of the cornea above the thinning. This feature helps to distinguish this patient’s pellucid marginal degeneration from keratoconus, where the protrusion is in the area of thinning.

Direct Illumination: Broad Oblique Beam

Fig. 1.5 Broad oblique beam. Using a broad oblique beam, along with indirect illumination techniques, is both good and bad. The good news – you will observe ten times more corneal findings. The bad news – you will spend a lot more time wondering if what you see is normal or pathologic. The broad oblique beam makes a detail more obvious than a less angled beam. Imagine that you want to photograph a pimple on someone’s skin in a way to maximize its features. Would the lighting be better from the side (oblique) or straight on?

Fig. 1.6 Broad oblique beam. You can see that the beam is oblique by its curvature and that it is obviously broad. Whatever the findings are, there is no way to know their anterior–posterior location using this technique. This patient has keratoconus. The photo shows heavy white scars, thin white opacities which go away with pressure on the cornea because they are Descemet’s folds, and part of a ring of pigment (Fleisher ring) above the pupil (1).

Fig. 1.7 Thin slit beam of previous figure. The same cornea using a thin slit shows that the scars are anterior and the folds are posterior. The cornea is thin and protruding. This and the previous photo make a powerful combination. They furnish information that neither can disclose alone.

Fig. 1.8 Broad oblique beam. This very broad beam washing over the cornea shows the “big picture.” Shadows that are created make the findings stand out. Do not worry about naming it immediately. You need to know a lot more before doing that. A thin slit shows it is epithelial. It is also in the other eye and in family members. It is band-shaped and whorled microcystic dystrophy of the corneal epithelium.

Fig. 1.9 Broad oblique beam. This broad oblique beam shows the features of anterior membrane dystrophy. Notice the high magnification. Use it. That is what the biomicroscope is made for. You can see much more using high magnification and it is one of the many things that make the slit lamp examination more rewarding for you and the patient.

Indirect Illumination: Indirect Iris Lighting – Finding Darker Than Background

Fig. 1.10 Indirect iris lighting – finding darker than background. Subtle details are observed using indirect illumination. Light that is reflected or dispersed creates incredible detail.

Fig. 1.11 Indirect iris lighting – finding darker than background. The debris at the edge of an intrastromal ring is white as viewed with a broad oblique beam in direct illumination and is dark as viewed with indirect illumination off the iris. This figure demonstrates the principal that findings have different appearances when different types of illumination are used.

Fig. 1.12 Indirect iris lighting – finding darker than background. Backlighting off the iris exaggerates the crystalline appearance of protein recurrence in a corneal transplant in a patient with monoclonal gammopathy.

Fig. 1.13 Indirect iris lighting – finding darker than background. The corneal transplant suture infiltrate looks entirely different when viewed by direct illumination on the left versus indirect illumination off the iris on the right. Serially following translucency of the infiltrate using indirect illumination is a powerful method of following therapeutic response.

Indirect Illumination: Indirect Iris Lighting – Finding Lighter Than Background

Fig. 1.14 Indirect iris lighting – finding lighter than background. As you are moving across the cornea, varying the width of your broad oblique beam and at the same time finding opacities between the corneal and iris beams, you will notice that sometimes they are dark, as in the previous figures, and sometimes they are light, as in this group of figures.

Fig. 1.15 Indirect iris lighting – finding lighter than background. The cysts (1) in Meesmann’s dystrophy pop out off the edge of the iris beam against the dark pupil. Directly over the iris beam they are completely washed out (2).

Fig. 1.16 Indirect iris lighting – finding lighter than background. If the corneal beam were to fall directly on the post-LASIK (laser-assisted in situ keratomileusis) epithelial cysts, they would be washed out and barely visible. These structures were found while going across the cornea focusing directly in a broad oblique beam, but also noticing to see if anything appeared between the corneal and iris beams. When they were noticed, the joy stick was then moved to bring them into sharp focus. If the patient were asked to look slightly to the right (examiner’s left), the cysts might have been illuminated like the Meesmann’s cysts in the previous figure. Alternatively, they might have been beautifully featured using a red reflex. The slit lamp examination is a dynamic process. The examiner uses light like an artist uses a paintbrush; always looking for ways to see or demonstrate his/her view of the subject.

Indirect Illumination: Sclerotic Scatter

Fig. 1.17 Sclerotic scatter. Sclerotic scatter is a slit lamp technique, unlike the others, that requires an adjustment in the equipment. This illustration demonstrates the use of the Haag-Streit slit lamp. Because the light source is directed far from the area being examined, it must be decoupled from the microscope. In this case, the screw is loosened so the light beam can be angled off to the examiner’s left. The beam is then directed at the limbus while the examiner focuses on the cornea. If there are no corneal findings, the cornea will be dark. If there are findings, they will be seen, as in the figures to follow. Do not forget to tighten the screw when you are finished.

Fig. 1.18 Sclerotic scatter. Usually you will reduce the magnification to take advantage of being able to see the whole cornea. Focus anterior–posterior wherever there is pathology. Sclerotic scatter will not tell you that the findings (limbal stem cell deficiency in this case) are anterior. You will need a thin slit for that. Notice that the inferior cornea is not involved and is therefore dark.

Fig. 1.19 Sclerotic scatter. The entire cornea is involved in this case of benign monoclonal gammopathy.

Fig. 1.20 Sclerotic scatter. Sclerotic scatter nicely demonstrates the deposits in this patient with systemic amyloidosis.

Indirect Illumination: Adjacent Beam

Fig. 1.21 Adjacent beam. Placing the beam adjacent to an area of interest and then focusing on the area is a localized method of scattering light similar to sclerotic scatter. The light source and biomicroscope, however, do not usually need to be uncoupled.

Fig. 1.22 Adjacent beam. A broad oblique beam first identified these lesions in a patient with Wegener’s granulomatosis. The adjacent beam technique then enhanced the finding.

Fig. 1.23 Adjacent beam. Notice how clearly you can see the bubbles on the examiner’s side of the Bitot spot in this vitamin A deficiency patient. No other technique could work as well. Putting the beam right on the bubbles would wash them out.

Fig. 1.24 Adjacent beam. The cysts within the conjunctival cyst are seen using the adjacent beam method. The photo to the right, on the other hand, fails to demonstrate the tiny cysts because the more direct beam washes them out.

Indirect Illumination: Red Reflex

Fig. 1.25 Red reflex. Reflected light from the fundus can be in sharp contrast to corneal pathology and can sometimes be used to great advantage. When the pupil is well dilated, the light source and biomicroscope can be decoupled, as it is in sclerotic scatter, to move the direction of the light and biomicroscope further apart. Much more pathology can be seen at the same time that way.

Fig. 1.26 Red reflex. Descemet’s membrane and endothelial pathology are seen in sharp contrast to the red fundus reflex in this forceps injury patient.

Fig. 1.27 Red reflex. This patient has corneal edema. The pattern of Descemet’s folds over the entire cornea can be seen using good papillary dilation and the red reflex technique with uncoupling of the light source.

Fig. 1.28 Red reflex. Red reflex is the best slit lamp technique to show the extent of pigment loss in this patient with pigment dispersion syndrome.

Specular Reflection

Fig. 1.29 Specular reflection. Specular reflection is the most difficult slit lamp technique. Do not be discouraged if it takes some time and effort to see the very fine black lines at the border of each endothelial cell. Everyone is challenged by this technique.

Fig. 1.30 Specular reflection. In cornea guttata, each guttae is as large as many endothelial cells. The black borders of the cells can be seen surrounding the guttae in this patient.

Fig. 1.31 Specular reflection. Vesicular-like lesions are seen along with normal-appearing endothelial cells in this patient with posterior polymorphous dystrophy.
Chapter 2
Diseases of the Lid: Anatomic Abnormalities
The eyelids protect the eyes and redistribute the tear film over the ocular surface. Anatomic abnormalities of the eyelids are often associated with corneal exposure and, in severe cases, corneal ulceration.


Fig. 2.1 Involutional ectropion. This disorder is caused by laxity of the lid tissue associated with aging. It is almost always seen in the lower lids. The laxity specifically affects the lower lid retractors and/or canthal tendons.

Fig. 2.2 Cicatricial ectropion. This disorder is caused by scarring of the lid tissue or periocular skin. Eversion of the lid results from traction caused by the scar. In this case a burn injury to the skin resulted in lower lid ectropion.

Fig. 2.3 Paralytic ectropion. This disorder is caused by damage to the seventh cranial nerve. Weakness of the orbicularis muscle leads to an out-turning of the lower eyelid. This patient exhibits a paralytic ectropion and a poor Bell’s phenomenon caused by a seventh nerve palsy. Normal furrowing of the brow is absent. Exposure keratitis may occur, and these patients require aggressive topical lubrication and, occasionally, a tarsorrhaphy.

Fig. 2.4 Punctal ectropion. This disorder may occur in an otherwise normally positioned lid. In this example, the exposed palpebral conjunctiva is inflamed and erythematous. Repair may be needed in patients with symptoms of epiphora.

Fig. 2.5 Congenital ectropion. The arrow indicates the malposition of the lower eyelid (inset). This patient also has features of blepharophimosis syndrome, including telecanthus, epicanthus, ptosis, and a poorly developed nasal bridge.


Fig. 2.6 Involutional entropion. The lower eyelid is turned in and the eyelashes rub on the conjunctiva and cornea. It occurs with aging and is a result of laxity of the lower lid combined with weakness of the retraction complex.

Fig. 2.7 Cicatricial entropion. This disorder is caused by scarring of the palpebral conjunctiva, with resultant in-turning of the lid margins. In this case the conjunctival scarring resulted from trachoma. Other conditions in which cicatricial entropion is seen are Stevens-Johnson syndrome, ocular cicatricial pemphigoid, herpes zoster ophthalmicus, and severe burns.

Fig. 2.8 Epiblepharon. This is caused by an overriding of the skin and pretarsal muscle above the lid margin, which causes an in-turning of the lid margin and lashes. Epiblepharon usually resolves with aging and rarely requires treatment.


Fig. 2.9 Trichiasis. This is an acquired malposition of the eyelashes. In this patient the eyelashes rub on the superior cornea.

Fig. 2.10 Spastic entropion. This can be caused by acute ocular inflammation or irritation in a patient with a previously unrecognized involutional entropion. Here the lashes rub on the lower cornea and have caused a corneal erosion (inset).


Fig. 2.11 Distichiasis. In this rare condition an extra row of eyelashes exits from the meibomian orifices (inset). The eyelashes may rub on the conjunctiva or cornea.


Fig. 2.12 Lagophthalmos. This is the inability to appose the eyelids on attempted eyelid closure. In this case a left seventh nerve palsy has caused a lower lid paralytic ectropion and lagophthalmos.


Fig. 2.13 Ptosis. This patient has ptosis of the right upper eyelid with narrowing of the palpebral fissure. The right brow is elevated in an attempt to raise the abnormally low right upper eyelid. The abnormal lid position has induced astigmatism in the right eye. Results of keratometry in the right eye are 47.00 × 87/42.25 × 174; in the left eye, results are nearly spherical.

Floppy Eyelid Syndrome

Fig. 2.14 Floppy eyelid syndrome. This syndrome is associated with excessive laxity of the upper eyelid. The eyelid is easily everted with superior traction. Patients often complain of redness, irritation, and mucoid discharge. The symptoms are worse in the morning and may be related to nocturnal eversion of the eyelids leading to corneal exposure.

Fig. 2.15 Floppy eyelid syndrome. Eversion of the upper eyelid shows papillary hypertrophy.

Lower Lid Imbrication

Fig. 2.16 Eyelid imbrication syndrome. The upper eyelid rides over the lower eyelid. This syndrome shares many features with floppy eyelid syndrome, including redness, irritation, and a mucoid discharge. Nocturnal eversion of the eyelids may also occur.

Fig. 2.17 Eyelid imbrication syndrome. Keratinization of the upper palpebral conjunctiva (inset) and papillary conjunctivitis occur with lower lid imbrication. The keratinization is caused by chronic rubbing of the upper lid over the lower lid.
Chapter 3
Diseases of the Lid: Tumors
Patients with abnormal growths on their eyelids are often initially seen by the general practitioner. It is important to differentiate benign lid tumors from malignant lid tumors. Occasionally, a biopsy is needed to establish the diagnosis.

Benign Lid Tumors

Fig. 3.1 Amyloid deposits from systemic amyloidosis. These appear as elevated, waxy-yellow deposits in the skin. The deposits are usually bilateral and symmetric. They are occasionally associated with a superficial hemorrhage, as seen in this case.

Fig. 3.2 Xanthogranuloma deposits in the eyelid of an 8-year-old boy. Xanthogranuloma is a non-Langerhans histiocytic cell proliferation of unknown etiology. It usually occurs in childhood and is more common in males. The skin lesions usually resolve spontaneously in 3-6 years. Xanthogranulomas can also occur on the cornea (see Figure 6.59 ) and iris. Children with iris xanthogranulomas may initially present to the ophthalmologist with visual problems related to spontaneous hyphemas.

Fig 3.3 Nevus of the lids. Nevi may be congenital or acquired and pigmented or nonpigmented. This split nevus or “kissing nevus” occurs when the tumor involves both upper and lower eyelids.

Fig. 3.4 Intradermal nevus. The nevus cells are located exclusively within the dermis, as seen on the lower eyelid in this patient. These nevi are often nonpigmented and elevated.

Fig. 3.5 Histopathology of a compound nevus. Nests of nevus cells (1) are lined by clear melanocytes (2). Melanophages (3) are at the junction of the epidermis and dermis and in the dermis.

Fig. 3.6 Congenital oculodermal melanocytosis (nevus of Ota). This is a collection of melanocytes in the periocular skin associated with melanosis oculi (see Figure 3.7 ). It most commonly occurs in Asian and African-American patients.

Fig. 3.7 Melanosis oculi. Same patient as in Figure 3.6 . Melanocytes in the episclera and sclera are responsible for the slate-blue discoloration. The conjunctiva over these lesions is mobile. The risk of uveal malignant melanomas is increased in Caucasian patients with this lesion.

Fig. 3.8 Capillary hemangiomas of the lids, mouth, and temporal skin. These tumors are first seen several weeks after birth and grow rapidly during the first year of life. They often resolve spontaneously, but treatment is needed when severe disfigurement, anisometropia, strabismus, or amblyopia occurs.

Fig. 3.9 Capillary hemangiomas of the lids, mouth, and temporal skin. Same patient as in Figure 3.8 , after treatment with intralesional corticosteroids.

Fig. 3.10 Histopathology of a capillary hemangioma. Multiple small capillary channels lined with endothelial cells are seen.

Fig. 3.11 Capillary hemangioma of the lid. This is an isolated capillary hemagioma involving the eyelid margin in an adult.

Fig. 3.12 Cavernous hemangioma of the lid. Cavernous hemangiomas are more commonly found in the orbit and are rarely seen in the eyelid. When found on the skin, they are elevated lesions that are compressible with palpation.

Fig. 3.13 Dermoid cyst of the lid. The most common location is the lateral brow adjacent to the frontozygomatic suture. These cysts contain dermal appendages including sebaceous glands, sweat glands, and hair follicles. They are present at birth but enlarge in childhood as secretions from sebaceous glands and sweat glands fill the cyst cavity. Sudden rupture of the cyst can cause a severe inflammatory reaction.

Fig. 3.14 Seborrheic keratosis. This elevated, oily, crusted lesion appears to be stuck onto the surrounding skin. The lesion is common in older persons and is not premalignant.

Fig. 3.15 Histopathology of a seborrheic keratosis. A nodule of elevated epithelium is seen. Pseudocysts with keratin (1) are found within the lesion.

Fig. 3.16 Actinic keratoses. These flat, scaly lesions arise in sun-exposed areas. They are premalignant and may develop into basal or squamous cell carcinoma.

Fig. 3.17 Acrochordon (skin tag). Acrochordons are small skin-colored or lightly pigmented lesions that develop in areas of the body with multiple skin folds such as the eyelids. They are benign lesions that are usually asymptomatic, but occasionally may be associated with itching or discomfort. Simple excision is curative.

Fig. 3.18 A keratoacanthoma. This rapidly enlarging growth may be seen on the eyelids. There is a central crater filled with keratin. These lesions may spontaneously involute but are often excised for cosmetic concerns and to exclude the possibility of a malignant lesion.

Fig. 3.19 Histopathology of a keratoacanthoma. The central crater of keratin is buttressed by normal epithelium on both sides.

Fig. 3.20 Xanthelasma. These bilateral yellow plaques usually occur in the medial canthal regions. These lesions may be associated with hypercholesterolemia, particularly if they occur in a young patient. In addition, this patient has a probable intradermal nevus on the right upper eyelid margin.

Fig. 3.21 Varices. Varices composed of dilated venous channels are seen in the upper eyelid. They give a blue discoloration to the overlying skin.

Fig. 3.22 Neurofibromas. Composed of proliferating Schwann cells, they may be seen as elevated nodules and found on the skin anywhere in the body. Here the neurofibroma is on the lower lid margin.

Fig. 3.23 Cysts of Moll’s gland. These slow-growing tumors are usually found on the lower lid near the puncta.

Fig. 3.24 A myxoma. These are slow-growing, asymptomatic, and benign lesions. They may have a systemic association with Carney complex (autosomal dominant condition of atrial myxomas, hyperpigmentation of skin, and endocrine overactivity).

Malignant Lid Tumors

Fig. 3.25 Basal cell carcinomas. These slow-growing tumors are found in sun-exposed areas. They are the most common eyelid malignancy and are usually located on the lower eyelid.

Fig. 3.26 A large, nodular, basal cell carcinoma. The edges are raised and pearly, with a central ulceration.

Fig. 3.27 A large basal cell carcinoma. This lesion has invaded deep into the periorbital tissue. Basal cell carcinomas rarely metastasize but may exhibit extensive local invasion if neglected.

Fig. 3.28 Histopathology of a basal cell carcinoma. Basophilic nests of cells with peripheral palisading (1) are seen.

Fig. 3.29 A squamous cell carcinoma. This is a rare malignancy of the eyelids. It commonly arises in sun-exposed areas and may resemble other lesions of the eyelid, such as keratoacanthoma, basal cell carcinoma, and seborrheic keratosis. The inset shows pearly raised margins of a small squamous cell carcinoma.

Fig. 3.30 An extensive squamous cell carcinoma of the upper eyelid.

Fig. 3.31 Histopathology of squamous cell carcinoma. Eosinophilic cells with large cytoplasms are shown. Keratin pearls (1) and dyskeratotic cells (2) are seen within the lesion. Dyskeratotic cells have small, dark nuclei and produce keratin.

Fig. 3.32 A sebaceous cell carcinoma of the right eyelids. A unilateral or asymmetric chronic blepharitis in an older patient should always raise the suspicion of sebaceous cell carcinoma. This tumor is more common in women and usually located on the upper eyelid, but can be located on both eyelids as seen here.

Fig. 3.33 Lid margin in sebaceous cell carcinoma. It is thickened and erythematous and has extensive lash loss. This tumor is highly malignant and may spread by direct extension, lymphatics, or blood vessels. The mortality rate is as high as 28%.

Fig. 3.34 Histopathology of sebaceous cell carcinoma. Cells in nests and cords (outline) with vacuolated, foamy cytoplasms are shown. When the diagnosis is suspected, a full-thickness lid biopsy should be performed.

Fig. 3.35 Sebaceous cell carcinoma. Lash loss and thickening of the right upper eyelid are noted in this case.

Fig. 3.36 Sebaceous cell carcinoma. Same patient as seen in Figure 3.35 . Clinically, the tumor has spread into the superior bulbar conjunctiva and corneal epithelium. The spread of individual cells or nests of cells into all levels of the epidermis is termed “pagetoid spread”. With extensive pagetoid spread of tumor, exenteration is the recommended treatment.

Fig. 3.37 Sebaceous cell carcinoma. Histopathology of the case seen in Figures 3.35 and 3.36 . In this exenteration specimen, pagetoid spread of sebaceous cell carcinoma (1) is seen in the corneal epithelium.

Fig. 3.38 A nodular malignant melanoma of the lower eyelid. This extremely rare malignancy of the eyelid may arise de novo or from pre-existing nevi. The prognosis depends on the depth of tumor invasion. This tumor can spread hematogenously and through lymphatic channels.

Fig. 3.39 Histopathology of a malignant melanoma of the eyelid. Epithelioid cells with pleomorphic nuclei and eosinophilic nucleoli (1) are shown. Clumps of melanin are seen within the cytoplasm (2).

Fig. 3.40 Kaposi’s sarcoma of the eyelids. This lesion diffusely infiltrates the lid and has a reddish or purple discoloration. This tumor is found almost exclusively in immunocompromised patients.

Fig. 3.41 Histopathology of Kaposi’s sarcoma. There is proliferation of spindle cells with slit-like spaces between the cells. Erythrocytes (inset) can be seen within the slit-like spaces.

Fig. 3.42 Mycosis fungoides. This is a cutaneous T-cell lymphoma that occasionally involves the periocular skin. Early in the disease process the lesions are eczematoid; they later progress to indurated plaques.
Chapter 4
Diseases of the Lid: Inflammatory (Blepharitis), Immunologic, Infectious, and Traumatic
Infectious and inflammatory diseases of the eyelids are often associated with conjunctivitis and symptoms of ocular discomfort. These patients are commonly seen in clinical practice.


Fig. 4.1 Seborrheic blepharitis. This disorder is often associated with seborrheic dermatitis. Patients complain of redness, burning, and mattering of the eyelids. It is usually bilateral and often associated with meibomian gland dysfunction. The lashes are covered with yellow, greasy scales. The scales are translucent and easily removed (inset).

Fig. 4.2 Staphylococcal blepharitis. This disorder is associated with inflammation of the anterior lid lamella and is usually not seen with meibomian gland dysfunction. Erythema of the anterior lid margin, lash loss, misdirected lashes, and ocular discharge are common findings.

Fig. 4.3 A hordeolum (stye). This is an acute inflammation of the lid margin. An internal hordeolum originates in the meibomian glands, and an external hordeolum originates in Moll’s glands, Zeis’ glands, or lash follicles. This external hordeolum is on the upper eyelid.

Fig. 4.4 A chalazion. This is an acute inflammation of the eyelid caused by a localized obstruction of meibomian glands. The histopathology shows sebaceous secretions surrounded by a granulomatous reaction.

Fig. 4.5 A chalazion. Same patient as in Figure 4.4 . The lower lid is everted, and a focal nodular conjunctivitis is seen overlying the chalazion.

Fig. 4.6 Meibomitis. The lid margin is erythematous, and a loose, oily discharge is easily expressed from the meibomian orifices (inset). This condition is often associated with seborrheic blepharitis.

Fig. 4.7 Meibomitis. In contrast to Figure 4.6 , here the disorder is associated with thick, toothpaste-like secretions that plug the glands.

Fig. 4.8 Meibomitis. When there is plugging of the meibomian glands, the secretions can be expressed with moderate pressure on the lid margin.

Fig. 4.9 Rosacea. This is a chronic sebaceous gland dysfunction of the skin. This male patient exhibits rhinophyma, an enlargement of the nose secondary to sebaceous gland hypertrophy.

Fig. 4.10 Rosacea. It is often associated with blepharitis and meibomian gland dysfunction.

Fig. 4.11 Chronic rosacea. Corneal vascularization and scarring can result.

Fig. 4.12 Chronic rosacea keratitis. This patient has severe corneal scarring, vascularization, and lipid degeneration.

Fig. 4.13 Rosacea. Occurring with greater frequency in females, as in this patient, rosacea often involves erythema, telangiectasia, and acne as common skin findings.

Fig. 4.14 Rosacea. Same patient as in Figure 4.13 . The lid margins and conjunctiva are inflamed, and there is corneal pannus and scarring.

Fig. 4.15 Mixed anterior and posterior lid margin disease.

Fig. 4.16 Angular blepharitis. This is an inflammation of the lateral lid margins and canthal region. If it is infectious, it is often associated with bacterial infection from Moraxella or Staphylococcus species.


Fig. 4.17 Intratarsal keratinous cysts of the meibomian gland. These cysts may be solitary or multiple. They arise from the palpebral tarsus. Gradual slow growth and a lack of inflammation help distinguish these from chalazia. Complete excision of the cyst rather than incision and curettage is the treatment of choice. Immunohistochemical studies show monoclonal antibodies directed against cytokeratins and cell surface epithelial markers.

Bacterial Infections

Fig. 4.18 Preseptal cellulitis. This is an infection of the periorbital tissue anterior to the orbital septum. Visual acuity, pupil reactivity, and ocular motility are normal.

Fig. 4.19 Orbital cellulitis. This infection of the orbital tissues usually extends from an infection in the paranasal sinuses. Here an ethmoid sinusitis has extended into the orbital tissues. Clinical features that distinguish an orbital cellulitis from a preseptal cellulitis include fever, proptosis, severe chemosis, ocular motility disturbances, pupillary abnormalities, and decreased vision.

Viral Infections

Fig. 4.20 Multiple molluscum contagiosum lesions on the periocular lid. These small, elevated lesions with a central umbilicated core are caused by a poxvirus.

Fig. 4.21 Molluscum contagiosum. A higher magnification of a solitary lesion showing the central umbilicated core.

Fig. 4.22 Chronic follicular conjunctivitis from mucocutaneous molluscum contagiosum lesion. A small molluscum lesion (1) is the cause of a chronic follicular conjunctivitis (2). The lesion is small and solitary and could easily have been missed as the cause of this patient’s chronic follicular conjunctivitis.

Parasitic Infections

Fig. 4.23 Lid infestation with the crab louse ( Phthirus pubis ). Chronic conjunctivitis is seen in this patient’s right eye. Symptoms include itching, redness, and irritation.

Fig. 4.24 Phthirus pubis infestation of the eyelashes. The adult louse has six legs and appears transparent with direct illumination. The schematic (lower right) shows the outline of a louse.

Fig. 4.25 Nits. Ovoid eggs are seen attached to the eyelashes. They hatch 1 to 2 weeks after they are laid. The reddish-brown granular material on the lid seen here and in Figure 4.24 is feces from the lice.

Fig. 4.26 Lice. Two lice are seen after removal from the eyelid. The upper louse is clinging to cilia. Crab lice usually measure 2 mm or less, whereas head and body lice are usually 2–4 mm long.

Fig. 4.27 Leishmaniasis of lid. A healing pustule (1) is seen on the upper eyelid. Leishmaniasis is a protozoa transmitted between infected hosts (humans, rodents and canines) by the bite of the sandfly. The eyelid is an uncommon site of involvement due to the blinking action of the lid, which makes it more difficult for the sandfly to bite in this area. Most lesions are self-limiting, healing within 3 to 24 months.

Fig. 4.28 Leishmaniasis of face, lids, conjunctiva and cornea. A chronic form of leishmaniasis may cause psoriaform-plaques on the skin. This form is often resistant to therapy and may result in disfiguring scars on the face. Lid involvement (1) can result in cicatricial ectropion. Conjunctival and corneal involvement (2) can result in ulceration and scarring.

Allergic Inflammations

Fig. 4.29 Contact dermatitis. This may develop after prolonged use of a topical medication. Clinically, an eczematous reaction of the lid margin and redness of the periocular skin occur. Symptoms include itching and irritation. This patient developed a reaction to tape after several days of pressure patching a corneal abrasion.

Fig. 4.30 Hypersensitivity reaction. Thimerosal is believed to cause a type IV hypersensitivity reaction of the conjunctiva. Here the thimerosal was a preservative in a contact lens solution. It is now used less frequently in contact lens solutions because of this type of reaction.


Fig. 4.31 Alopecia. There is complete loss of all of the eyelashes. The underlying skin is hypopigmented and slightly erythematous.

Foreign Body

Fig. 4.32 Foreign body reaction. A retained foreign body may present as a localized area of eyelid inflammation. Here an occult wood foreign body was surgically removed.

Fig. 4.33 Foreign body. The wood foreign body was approximately 3.5 cm long.

Fig. 4.34 Thermal burns to right upper and lower lids.
Chapter 5
Disorders of Tear Production and the Lacrimal System
The tear film is composed of three layers: the mucous layer, the aqueous layer, and the lipid layer. The mucous layer is produced by conjunctival goblet cells and is in direct contact with the corneal epithelium. The aqueous layer is produced by the main lacrimal gland and the accessory lacrimal glands. The most anterior layer is the lipid layer, which is produced by the meibomian glands.

Dry Eye

Fig. 5.1 Normal tear film. In this example of a normal tear film, there is an adequate tear lake between the lower lid and the cornea. The cornea is clear and there are no staining irregularities of the corneal epithelium.

Fig. 5.2 Tear break-up. Rapid tear break-up time (BUT) is a sign of dry eye. To measure tear BUT, the patient is asked to blink, which evenly distributes the tear film across the cornea. As the tear film thins, dry spots (1) develop on the surface of the cornea. The time for this to occur is measured. Tear BUTs of 10 seconds or less are considered abnormal.

Fig. 5.3 Schirmer strip. To perform a Schirmer’s test, the inferior cul-de-sac is dried with a cotton swab. A standardized strip of filter paper is placed over the lateral third of the lower lid. This test can be performed with or without anesthesia. Schirmer’s test without anesthesia measures basal tear secretion and reflex tear secretion. Schirmer’s test with anesthesia measures only basal tear secretion by eliminating the irritation from the filter paper that causes reflex tearing. With anesthesia the interpretation is as follows: 0–5 mm of wetting, severe dry eyes; 5–10 mm of wetting, moderately dry eyes; 10–15 mm of wetting, mildly dry eyes; and >15 mm of wetting, normal tear function. Without anesthesia, wetting of <15 mm indicates dry eyes, and <5 mm indicates very severe dry eyes.

Fig. 5.4 Dry eye syndrome. This is often associated with lid margin disease. Dry eyes can occur as both a quantitative and a qualitative disorder of tear production. In this example, the upper lid margin is inflamed and shows lash loss. The corneal surface is dry, and there is an irregular light reflex. Mucus is evident on the corneal surface.

Fig. 5.5 Superficial punctate keratopathy. This is a common finding in patients with dry eye syndrome. The irregular epithelial surface can be appreciated without special stains.

Fig. 5.6 Superficial punctate keratopathy. Fluorescein staining in the same patient as in Figure 5.5 . Fluorescein is a water-soluble dye that stains in areas of missing epithelium.

Fig. 5.7 Rose bengal stain of conjunctival and corneal epithelial cells in dry eyes. Rose bengal stains conjunctival and corneal epithelial cells that have a disruption to the overlying mucin layer or damage to the epithelial cell wall.

Fig. 5.8 Dry eye syndrome. In addition to epithelial cells, rose bengal also stains mucous filaments (inset). Mucous does not stain well with fluorescein.

Fig. 5.9 Bilateral lacrimal gland enlargement from sarcoidosis. Enlargement of the lacrimal gland from sarcoidosis has caused inferior displacement of the lateral lid margins. The upper lid margins assume a characteristic S-shape.

Fig. 5.10 Lacrimal gland enlargement from sarcoidosis. The same patient as in Figure 5.9 . The lacrimal gland is inflamed and enlarged.

Fig. 5.11 Lacrimal gland tumor resulting in a dry eye. In this patient with pseudotumor of the lacrimal gland, the corneal surface is irregular (1) and there are mucous filaments (2).

Fig. 5.12 Dry eye syndrome. Mucous debris is stuck on the epithelium.

Fig. 5.13 Dry eye syndrome. Same patient as in Figure 5.12 . Several minutes after administration of 10% acetylcysteine (Mucomyst ® ), this was the appearance of the eye. Acetylcysteine is a mucolytic agent that is effective in the treatment of excessive mucous.

Fig. 5.14 Dry eye patient with an epithelialized ulcer. (A) White light without fluorescein suggests an ulcer (stromal tissue loss with an overlying epithelial defect). (B) Cobalt blue light with fluorescein apparently confirms an overlying epithelial defect. (C) White light with fluorescein apparently further confirms an overlying epithelial defect. (D) Clearing the pool of fluorescein with a cotton applicator reveals that there was pooling of the fluorescein simulating an active corneal ulcer. Active corneal ulcers with stromal thinning show fluorescein staining of the overlying epithelial defects whereas stromal thinning without ulceration may show pooling of fluorescein dye that simulates an active corneal ulcer.

Fig. 5.15 Severe dry eyes. Sterile ulceration can result.

Fig. 5.16 Dry eye syndrome. Slit beam examination of this patient’s cornea shows extensive tissue loss with a descemetocele.

Fig. 5.17 Dry eye syndrome. A fluorescein strip placed over the descemetocele indicates an active leak (positive Seidel’s test).

Fig. 5.18 Dry eye syndrome. A silicone punctal plug has been placed in the right inferior punctum. The plug increases the volume of the tear film by decreasing tear outflow.

Fig. 5.19 Dry eye syndrome. Silicone plugs can rub on the conjunctiva. Fluorescein stains an area of conjunctival erosion.

Fig. 5.20 Dry eye syndrome. Permanent punctal occlusion can be performed with cautery. The left lower punctum has been occluded, and fluorescein pools in the occluded area (inset).

Fig. 5.21 Dry eye syndrome. Familial dysautonomia (Riley-Day syndrome) causes systemic autonomic instability. Here the cornea is scarred from a previous corneal ulcer. Patients with this disease have corneal hypesthesia and severe dry eyes.

Fig. 5.22 Severe dry eye syndrome with graft-versus-host disease. Here a sterile corneal ulceration is seen.

Fig. 5.23 Dry eye syndrome with graft-versus-host disease. This patient has a severe dry eye and membranous conjunctivitis.

Dacryoadenitis, Dacryocystitis, and Canaliculitis

Fig. 5.24 Dacryoadenitis. This is an inflammation of the lacrimal gland. The superior temporal lid is erythematous, and the upper lid margin is S-shaped as a result of the underlying enlargement of the lacrimal gland.

Fig. 5.25 Dacryocystitis. This is an inflammation of the lacrimal sac. Here an acute infection is seen, with erythema and enlargement lateral to the nasal bridge. Mucopurulent conjunctivitis is also present.

Fig. 5.26 Dacryocystitis. In this case, a fistulous tract has developed from the lacrimal sac to the overlying skin. Purulent material is seen exiting the fistula.

Fig. 5.27 Canaliculitis due to Actinomyces israelli . The signs of canaliculitis include a chronic conjunctivitis and an inflamed pouting punctum. Canaliculitis and low-grade dacryocystitis are often overlooked as causes of chronic conjunctivitis.

Fig. 5.28 Canaliculitis due to Actinomyces israelli . When external pressure is placed on the puncta, a thick concretion with sulfur granules is expressed. The Actinomyces organism is often sequestered in diverticula within the canaliculus and treatment involves surgical opening and irrigation of the canaliculus.

Fig. 5.29 Canaliculitis due to Actinomyces israelli . Sulfur granules composed of branching filaments are found within the discharge. This organism was once thought to be a fungus due to the morphology of the branching filaments, but it is now known to be an anaerobic bacterium with variable Gram-positive and acid-fast staining characteristics.
Chapter 6
Conjunctival Disease: Tumors and Anatomic Abnormalities
Conjunctival tumors can be divided into squamous neoplasms, melanocytic neoplasms, and subepithelial neoplasms. It is often possible to differentiate benign lesions from malignant lesions based on the appearance of the lesion; however, in some cases a biopsy is necessary.

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