Ophthalmology: A Short Textbook PDF

I Ophthalmology A Short Textbook Gerhard K. Lang, M. D. Professor and Chairman Department of Ophthalmology and...

I Ophthalmology A Short Textbook Gerhard K. Lang, M. D. Professor and Chairman Department of Ophthalmology and University Eye Hospital Ulm Germany With contributions by J. Amann, M. D. O. Gareis, M. D. Gabriele E. Lang, M. D. Doris Recker, M. D. C. W. Spraul, M. D. P. Wagner, M. D. 305 Illustrations Thieme Stuttgart · New York 2000 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  II Library of Congress Cataloging-in-Publica- Important Note: Medicine is an ever- tion Data changing science undergoing continual development. Research and clinical Lang, Gerhard K. experience are continually expanding our [Augenheilkunde. English] knowledge, in particular our knowledge of Ophthalmology : a short textbook / proper treatment and drug therapy. Insofar Gerhard K. Lang ; with contributions by as this book mentions any dosage or appli- J. Amann... [et al.]. p. ; cm. Includes biblio- cation, readers may rest assured that the graphical references and index. authors, editors, and publishers have made ISBN 3131261617 every effort to ensure that such references 1. Eye-Diseases. 2. Ophthalmology. are in accordance with the state of knowl- I. Amann, J. (Josef) II. Title. edge at the time of production of the book. [DNLM: 1. Eye Diseases. Nevertheless this does not involve, WW 40 L269a 2000a] imply, or express any guarantee or RE46.L3413 2000 responsibility on the part of the publishers 617.7–dc21 00-032597 in respect of any dosage instructions and forms of application stated in the book. Every user is requested to examine care- Student contributors: fully the manufacturers’ leaflets accom- Christopher Dedner, Tübingen panying each drug and to check, if neces- Uta Eichler, Karlsruhe sary in consultation with a physician or Heidi Janeczek, Göttingen specialist, whether the dosage schedules Beate Jentzen, Husberg mentioned therein or the contraindications Mathis Kayser, Freiburg stated by the manufacturers differ from the Kerstin Lipka, Kiel statements made in the present book. Such Maren Molkewehrum, Kiel examination is particularly important with Alexandra Ogilvie, Munich drugs that are either rarely used or have Patricia Ogilvie, Würzburg been newly released on the market. Every Stefan Rose, Oldenburg dosage schedule or every form of applica- tion used is entirely at the user’s own risk Translated by John Grossman, Berlin, and responsibility. The authors and pub- Germany lishers request every user to report to the publishers any discrepancies or inaccura- This book is an authorized translation of the cies noticed. German edition published and copyrighted 1998 by Georg Thieme Verlag, Stuttgart, Some of the product names, patents, and Germany. registered designs referred to in this book are in fact registered trademarks or pro- Drawings by Markus Voll, Fürstenfeldbruck prietary names even though specific refer- ence to this fact is not always made in the text. Therefore, the appearance of a name ! 2000 Georg Thieme Verlag without designation as proprietary is not to Rüdigerstraße 14 be construed as a representation by the D-70469 Stuttgart, Germany publisher that it is in the public domain. Thieme New York, 333 Seventh Avenue This book, including all parts thereof, is New York, N. Y. 10001 U.S.A legally protected by copyright. Any use, exploitation, or commercialization outside Typesetting by Druckhaus Götz GmbH, the narrow limits set by copyright legisla- Ludwigsburg tion, without the publisher’s consent, is Printed in Germany by illegal and liable to prosecution. This Appl, Wemding applies in particular to photostat reproduc- tion, copying, mimeographing or duplica- tion of any kind, translating, preparation of ISBN 3-13-126161-7 (GTV) microfilms, and electronic data processing ISBN 0-86577-936-8 (TNY) 1 2 3 4 5 and storage. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  III The Concept of the Book in Brief... Definition: The concept behind this book was to organize content and layout according to a uniform structure. This enhances the clarity of the presenta- tion and allows the reader to access information quickly. Each chapter has its own header icon, which is shown on every page of the chapter. Figure headings summarize the key information presented in the respective figure, eliminating the need for the reader to read through the entire legend. Epidemiology: In the absence of precise epidemiologic data, the authors state whether the disorder is common or rare wherever possible. Etiology: This section usually combines information about the etiology and pathogenesis of a disorder and in so doing helps to illuminate important rela- tionships. Symptoms and diagnostic considerations: These items are usually dis- cussed separately. The section on symptoms includes only the phenomena with which the patient presents. How and by which methods the examiner proceeds from these symptoms to a diagnosis is only discussed under diag- nostic considerations. Sections highlighted with an exclamation mark contain important facts. These may be facts that one is often required to know for exami- nations, or they may be practical tips that are helpful in diagnosing and treating the disorder. Differential diagnosis: Wherever possible, this section discusses not only other possible diagnoses but also important criteria for differentiating the disorder from others. Treatment: This section goes beyond merely documenting all possible ther- apeutic options. It also explains which therapeutic measures are advisable and offer a prospect of success. The discussion of medical treatment occa- sionally includes dosage information and examples of preparations used. This is done where such information is relevant to cases students will encounter in practice. The trade names specified do not represent a comprehensive listing. Prognosis and clinical course: The further development of the book depends in no small measure on your criticism. We are happy to receive any suggestions for improvements as this will help us tailor the next edition to better suit yor needs. Please use the enclosed postcard. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  IV Authors Gerhard K. Lang, M. D. Professor and Chairman, University Eye Hospital, Ulm, Germany J. Amann, M. D. Research assistant, University Eye Hospital, Ulm O. Gareis, M. D. Senior physician, University Eye Hospital, Ulm Gabriele E. Lang, M. D. Director, Department of Medical Retina and Laser Surgery, University Eye Hospital, Ulm Doris Recker Orthoptist, University Eye Hospital, Ulm C. W. Spraul, M. D. Senior physician, University Eye Hospital, Ulm P. Wagner, M. D. Chief of medical staff, University Eye Hospital, Ulm Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  V Preface When my coworkers and I first took up the task of writing a textbook of ophthalmology that was aimed at medical students but would also be suita- ble for interns and ophthalmology residents, we did not know exactly what we were getting ourselves into. The next four years were devoted to intensive study of this subject. We did not merely intend to design a book according to the maxims “understand it in medical school,” “learn it for the examination,” and “use it during your internship.” Our broader goal was to give students a textbook that would kindle their interest and indeed their enthusiasm for a “small” specialty like ophthalmology and that would sustain this enthusiasm all the way through a successful examination. In an age in which teaching is undergoing evaluation, we felt this was particularly important. In pursuing this admittedly ambitious goal, we were able to draw upon many years of teaching experience. This experience has shaped the educational concept behind this book and manifests itself in details such as the layout, which is characterized by numerous photographs and illustrative drawings. We have placed special emphasis on the figures in particular. These illustrations make ophthalmology come alive and hopefully will be able to imbue the reader with some of the enthusiasm that the authors themselves have for their specialty. I would like to take this opportunity to offer my heartfelt thanks to my teacher, Prof. Dr. Dr. hc G. O. H. Naumann, Erlangen, Germany, for his sugges- tions and for the slides from the collection of the Department of Ophthal- mology and University Eye Hospital, Erlangen. I would also like to offer special thanks to my coauthors, Dr. Josef Amann, Dr. Oskar Gareis, Prof. Dr. Gabriele E. Lang, Doris Recker, Dr. Christoph Spraul, and Dr. Peter Wagner for their harmonious cooperation and exceptional initiative in writing this book. I also thank Dr. Eckhard Weingärtner for his assistance in compiling the Appendix. I would also like to extend special thanks to Dr. Jürgen Lüthje and Sabine Bartl of Georg Thieme Verlag, whose professionalism and active and tireless support were a constant source of inspiration to us all. I would again like to thank Markus Voll, Fürstenfeldbruck, Germany, for his splendid illustrations. Ulm, Germany, Summer 2000 Gerhard K. Lang Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  VI Table of Contents 1 The Ophthalmic Examination... 1 (Gabriele E. Lang, Gerhard K. Lang) 1.1 Equipment... 1 1.2 History... 3 1.3 Visual Acuity... 4 1.4 Ocular Motility... 5 1.5 Binocular Alignment... 6 1.6 Examination of the Eyelids and Nasolacrimal Duct... 7 1.7 Examination of the Conjunctiva... 7 1.8 Examination of the Cornea... 10 1.9 Examination of the Anterior Chamber... 11 1.10 Examination of the Lens... 12 1.11 Ophthalmoscopy... 13 1.12 Confrontation Field Testing... 14 1.13 Measurement of Intraocular Pressure... 15 1.14 Eyedrops, Ointment, and Bandages... 15 2 The Eyelids... 17 (Peter Wagner, Gerhard K. Lang) 2.1 Basic Knowledge... 17 2.2 Examination Methods... 19 2.3 Developmental Anomalies... 20 2.3.1 Coloboma... 20 2.3.2 Epicanthal Folds... 21 2.3.3 Blepharophimosis... 21 2.3.4 Ankyloblepharon... 22 2.4 Deformities... 22 2.4.1 Ptosis... 22 2.4.2 Entropion... 24 2.4.3 Ectropion... 28 2.4.4 Trichiasis... 30 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  Table of Contents VII 2.4.5 Blepharospasm... 30 2.5 Disorders of the Skin and Margin of the Eyelid... 30 2.5.1 Contact Eczema... 30 2.5.2 Edema... 31 2.5.3 Seborrheic Blepharitis... 33 2.5.4 Herpes Simplex of the Eyelids... 34 2.5.5 Herpes Zoster Ophthalmicus... 35 2.5.6 Eyelid Abscess... 36 2.5.7 Tick Infestation of the Eyelids... 37 2.5.8 Louse Infestation of the Eyelids... 37 2.6 Disorders of the Eyelid Glands... 38 2.6.1 Hordeolum... 38 2.6.2 Chalazion... 39 2.7 Tumors... 40 2.7.1 Benign Tumors... 40 2.7.1.1 Ductal Cysts... 40 2.7.1.2 Xanthelasma... 40 2.7.1.3 Molluscum Contagiosum... 42 2.7.1.4 Cutaneous Horn... 42 2.7.1.5 Keratoacanthoma... 42 2.7.1.6 Hemangioma... 43 2.7.1.7 Neurofibromatosis (Recklinghausen’s Disease)... 44 2.7.2 Malignant Tumors... 45 2.7.2.1 Basal Cell Carcinoma... 45 2.7.2.2 Squamous Cell Carcinoma... 47 2.7.2.3 Adenocarcinoma... 47 3 Lacrimal System... 49 (Peter Wagner, Gerhard K. Lang) 3.1 Basic Knowledge... 49 3.2 Examination Methods... 52 3.2.1 Evaluation of Tear Formation... 52 3.2.2 Evaluation of Tear Drainage... 53 3.3 Disorders of the Lower Lacrimal System... 57 3.3.1 Dacryocystitis... 57 3.3.1.1 Acute Dacryocystitis... 57 3.3.1.2 Chronic Dacryocystitis... 60 3.3.1.3 Neonatal Dacryocystitis... 60 3.3.2 Canaliculitis... 61 3.3.3 Tumors of the Lacrimal Sac... 61 3.4 Lacrimal System Dysfunction... 62 3.4.1 Keratoconjunctivitis Sicca... 62 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  VIII Table of Contents 3.4.2 Illacrimation... 64 3.5 Disorders of the Lacrimal Gland... 64 3.5.1 Acute Dacryoadenitis... 64 3.5.2 Chronic Dacryoadenitis... 65 3.5.3 Tumors of the Lacrimal Gland... 66 4 Conjunctiva... 67 (Gerhard K. Lang, Gabriele E. Lang) 4.1 Basic Knowledge... 67 4.2 Examination Methods... 68 4.3 Conjunctival Degeneration and Aging Changes... 69 4.3.1 Pinguecula... 69 4.3.2 Pterygium... 69 4.3.3 Pseudopterygium... 71 4.3.4 Subconjunctival Hemorrhage... 72 4.3.5 Calcareous Infiltration... 72 4.3.6 Conjunctival Xerosis... 72 4.4 Conjunctivitis... 74 4.4.1 General Notes on the Causes, Symptoms, and Diagnosis of Conjunctivitis... 74 4.4.2 Infectious Conjunctivitis... 82 4.4.2.1 Bacterial Conjunctivitis... 82 4.4.2.2 Chlamydial Conjunctivitis... 83 4.4.2.3 Viral Conjunctivitis... 93 4.4.2.4 Neonatal Conjunctivitis... 95 4.4.2.5 Parasitic and Mycotic Conjunctivitis... 98 4.4.3 Noninfectious Conjunctivitis... 98 4.5 Tumors... 104 4.5.1 Epibulbar Dermoid... 104 4.5.2 Conjunctival Hemangioma... 104 4.5.3 Epithelial Conjunctival Tumors... 105 4.5.3.1 Conjunctival Cysts... 105 4.5.3.2 Conjunctival Papilloma... 106 4.5.3.3 Conjunctival Carcinoma... 107 4.5.4 Melanocytic Conjunctival Tumors... 108 4.5.4.1 Conjunctival Nevus... 108 4.5.4.2 Conjunctival Melanosis... 108 4.5.4.3 Congenital Ocular Melanosis... 112 4.5.5 Conjunctival Lymphoma... 113 4.5.6 Kaposi’s Sarcoma... 113 4.6 Conjunctival Deposits... 114 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  Table of Contents IX 5 Cornea... 117 (Gerhard K. Lang) 5.1 Basic Knowledge... 117 5.2 Examination Methods... 120 5.2.1 Slit Lamp Examination... 120 5.2.2 Dye Examination of the Cornea... 120 5.2.3 Corneal Topography... 121 5.2.4 Determining Corneal Sensitivity... 121 5.2.5 Measuring the Density of the Corneal Epithelium... 121 5.2.6 Measuring the Diameter of the Cornea... 124 5.2.7 Corneal Pachymetry... 125 5.2.8 Confocal Corneal Microscopy... 125 5.3 Developmental Anomalies... 125 5.3.1 Protrusion Anomalies... 125 5.3.1.1 Keratoconus... 125 5.3.1.2 Keratoglobus... 127 5.3.2 Corneal Size Anomalies (Microcornea and Megalocornea)... 127 5.4 Infectious Keratitis... 127 5.4.1 Protective Mechanisms of the Cornea... 127 5.4.2 Corneal Infections: Predisposing Factors, Pathogens, and Pathogenesis... 128 5.4.3 General Notes on Diagnosing Infectious Forms of Keratitis... 130 5.4.4 Bacterial Keratitis... 130 5.4.5 Viral Keratitis... 132 5.4.5.1 Herpes Simplex Keratitis... 132 5.4.5.2 Herpes Zoster Keratitis... 134 5.4.6 Mycotic Keratitis... 134 5.4.7 Acanthamoeba Keratitis... 136 5.5 Noninfectious Keratitis and Keratopathy... 137 5.5.1 Superficial Punctate Keratitis... 138 5.5.2 Exposure Keratitis... 140 5.5.3 Neuroparalytic Keratitis... 141 5.5.4 Problems with Contact Lenses... 141 5.5.5 Bullous Keratopathy... 143 5.6 Corneal Deposits, Degenerations, and Dystrophies... 145 5.6.1 Corneal Deposits... 145 5.6.1.1 Arcus Senilis... 145 5.6.1.2 Corneal Verticillata... 145 5.6.1.3 Argyrosis and Chrysiasis... 146 5.6.1.4 Iron Lines... 146 5.6.1.5 Kayser-Fleischer Ring... 146 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  X Table of Contents 5.6.2 Corneal Degeneration... 146 5.6.2.1 Calcific Band Keratopathy... 146 5.6.2.2 Peripheral Furrow Keratitis... 147 5.6.3 Corneal Dystrophies... 148 5.7 Corneal Surgery... 150 5.7.1 Curative Corneal Procedures... 152 5.7.1.1 Penetrating Keratoplasty (Fig. 5.18 a)... 152 5.7.1.2 Lamellar Keratoplasty (Fig. 5.18 b)... 153 5.7.1.3 Phototherapeutic Keratectomy (Fig. 5.18 c)... 154 5.7.2 Refractive Corneal Procedures... 155 5.7.2.1 Photorefractive Keratectomy (Fig. 5.18 d)... 155 5.7.2.2 Radial Keratotomy (Fig. 5.18 e)... 155 5.7.2.3 Photorefractive Keratectomy Correction of Astigmatism... 156 5.7.2.4 Holmium Laser Correction of Hyperopia... 156 5.7.2.5 Epikeratophakic Keratoplasty (Epikeratophakia)... 156 5.7.2.6 Excimer Laser In Situ Keratomileusis (LASIK)... 156 6 Sclera... 157 (Gerhard K. Lang) 6.1 Basic Knowledge... 157 6.2 Examination Methods... 157 6.3 Color Changes... 157 6.4 Staphyloma and Ectasia... 158 6.5 Trauma... 158 6.6 Inflammations... 158 6.6.1 Episcleritis... 159 6.6.2 Scleritis... 161 7 Lens... 165 (Gerhard K. Lang) 7.1 Basic Knowledge... 165 7.2 Examination Methods... 168 7.3 Developmental Anomalies of the Lens... 169 7.4 Cataract... 170 7.4.1 Acquired Cataract... 173 7.4.1.1 Senile Cataract... 173 7.4.2 Cataract in Systemic Disease... 179 7.4.3 Complicated Cataracts... 180 7.4.4 Cataract after Intraocular Surgery... 180 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  Table of Contents XI 7.4.5 Traumatic Cataract... 180 7.4.6 Toxic Cataract... 182 7.4.7 Congenital Cataract... 182 7.4.7.1 Hereditary Congenital Cataracts... 183 7.4.7.2 Cataract from Transplacental Infection in the First Trimester of Pregnancy... 185 7.4.8 Treatment of Cataracts... 185 7.4.8.1 Medical Treatment... 185 7.4.8.2 Surgical Treatment... 185 7.4.8.3 Secondary Cataract... 192 7.4.8.4 Special Considerations in Cataract Surgery in Children... 192 7.5 Lens Dislocation... 195 8 Uveal Tract (Vascular Pigmented Layer)... 199 (Gabriele E. Lang, Gerhard K. Lang) 8.1 Basic Knowledge... 199 8.1.1 Iris... 199 8.1.2 Ciliary Body... 201 8.1.3 Choroid... 201 8.2 Examination Methods... 201 8.3 Developmental Anomalies... 202 8.3.1 Aniridia... 202 8.3.2 Coloboma... 203 8.4 Pigmentation Anomalies... 206 8.4.1 Heterochromia... 206 8.4.2 Albinism... 206 8.5 Inflammation... 208 8.5.1 Acute Iritis and Iridocyclitis... 208 8.5.2 Chronic Iritis and Iridocyclitis... 212 8.5.3 Choroiditis... 213 8.5.4 Sympathetic Ophthalmia... 214 8.6 Neovascularization in the Iris: Rubeosis Iridis... 215 8.7 Tumors... 216 8.7.1 Malignant Tumors (Uveal Melanoma)... 216 8.7.2 Benign Choroidal Tumors... 217 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  XII Table of Contents 9 Pupil... 219 (Oskar Gareis, Gerhard K. Lang) 9.1 Basic Knowledge... 219 9.2 Examination Methods... 221 9.2.1 Testing the Light Reflex (Table 9.1)... 221 9.2.2 Evaluating the Near Reflex... 223 9.3 Influence of Pharmacologic Agents on the Pupil (Table 9.2)... 224 9.4 Pupillary Motor Dysfunction... 226 9.4.1 Isocoria with Normal Pupil Size... 227 9.4.2 Anisocoria with Dilated Pupil in the Affected Eye... 228 9.4.3 Anisocoria with a Constricted Pupil in the Affected Eye... 229 9.4.4 Isocoria with Constricted Pupils... 230 9.3.5 Isocoria with Dilated Pupils... 231 10 Glaucoma... 233 (Gerhard K. Lang) 10.1 Basic Knowledge... 233 10.2 Examination Methods... 238 10.2.1 Oblique Illumination of the Anterior Chamber... 238 10.2.2 Slit-Lamp Examination... 238 10.2.3 Gonioscopy... 238 10.2.4 Measuring Intraocular Pressure... 240 10.2.5 Optic Disk Ophthalmoscopy... 244 10.2.6 Visual Field Testing... 246 10.2.7 Examination of the Retinal Nerve Fiber Layer... 250 10.3 Primary Glaucoma... 251 10.3.1 Primary Open Angle Glaucoma... 251 10.3.2 Primary Angle Closure Glaucoma... 265 10.4 Secondary Glaucomas... 270 10.4.1 Secondary Open Angle Glaucoma... 271 10.4.2 Secondary Angle Closure Glaucoma... 271 10.5 Childhood Glaucomas... 273 11 Vitreous Body... 279 (Christoph W. Spraul, Gerhard K. Lang) 11.1 Basic Knowledge... 279 11.2 Examination Methods... 281 11.3 Aging Changes... 282 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  Table of Contents XIII 11.3.1 Synchysis... 282 11.3.2 Vitreous Detachment... 282 11.4 Abnormal Changes in the Vitreous Body... 284 11.4.1 Persistent Fetal Vasculature (Developmental Anomalies)... 284 11.4.1.1 Mittendorf’s Dot... 284 11.4.1.2 Bergmeister’s Papilla... 285 11.4.1.3 Persistent Hyaloid Artery... 285 11.4.1.4 Persistent Hyperplastic Primary Vitreous (PHPV)... 285 11.4.2 Abnormal Opacities of the Vitreous Body... 287 11.4.2.1 Asteroid Hyalosis... 287 11.4.2.2 Synchysis Scintillans... 287 11.4.2.3 Vitreous Amyloidosis... 287 11.4.3 Vitreous Hemorrhage... 287 11.4.4 Vitritis and Endophthalmitis... 290 11.4.5 Vitreoretinal Dystrophies... 293 11.4.5.1 Juvenile Retinoschisis... 293 11.4.5.2 Wagner’s Disease... 293 11.5 The Role of the Vitreous Body in Various Ocular Changes and Following Cataract Surgery... 293 11.5.1 Retinal Detachment... 293 11.5.2 Retinal Vascular Proliferation... 293 11.5.3 Cataract Surgery... 294 11.6 Surgical Treatment: Vitrectomy... 294 12 Retina... 299 (Gabriele E. Lang, Gerhard K. Lang) 12.1 Basic Knowledge... 299 12.2 Examination Methods... 304 12.2.1 Examination of the Fundus... 304 12.2.2 Normal and Abnormal Fundus Findings in General... 308 12.2.3 Color Vision... 311 12.2.4 Electrophysiologic Examination Methods (electroretinogram, electrooculogram, and visual evoked potentials; see Fig. 12.2 a)... 312 12.3 Vascular Disorders... 314 12.3.1 Diabetic Retinopathy... 314 12.3.2 Retinal Vein Occlusion... 318 12.3.3 Retinal Arterial Occlusion... 320 12.3.4 Hypertensive Retinopathy and Sclerotic Changes... 323 12.3.5 Coats’ Disease... 325 12.3.6 Retinopathy of Prematurity... 326 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  XIV Table of Contents 12.4 Degenerative Retinal Disorders... 328 12.4.1 Retinal Detachment... 328 12.4.2 Degenerative Retinoschisis... 333 12.4.3 Peripheral Retinal Degenerations... 334 12.4.4 Central Serous Chorioretinopathy... 335 12.4.5 Age-Related Macular Degeneration... 337 12.4.6 Degenerative Myopia... 339 12.5 Retinal Dystrophies... 340 12.5.1 Macular Dystrophies... 340 12.5.1.1 Stargardt’s Disease... 340 12.5.1.2 Best’s Vitelliform Dystrophy... 341 12.5.2 Retinitis Pigmentosa... 343 12.6 Toxic Retinopathy... 345 12.7 Retinal Inflammatory Disease... 346 12.7.1 Retinal Vasculitis... 346 12.7.2 Posterior Uveitis Due to Toxoplasmosis... 348 12.7.3 AIDS-Related Retinal Disorders... 349 12.7.4 Viral Retinitis... 351 12.7.5 Retinitis in Lyme Disease... 351 12.7.6 Parasitic Retinal Disorders... 352 12.8 Retinal Tumors and Hamartomas... 353 12.8.1 Retinoblastoma... 353 12.8.2 Astrocytoma... 355 12.8.3 Hemangiomas... 356 13 Optic Nerve... 359 (Oskar Gareis, Gerhard K. Lang) 13.1 Basic Knowledge... 359 13.1.1 Intraocular Portion of the Optic Nerve... 360 13.1.2 The Intraorbital and Intracranial Portion of the Optic Nerve... 361 13.2 Examination Methods... 362 13.3 Disorders that Obscure the Margin of the Optic Disc... 363 13.3.1 Congenital Disorders that Obscure the Margin of the Optic Disc... 363 13.3.1.1 Oblique Entry of the Optic Nerve... 363 13.3.1.2 Tilted Disc... 364 13.3.1.3 Pseudopapilledema... 364 13.3.1.4 Myelinated Nerve Fibers... 365 13.3.1.5 Bergmeister’s Papilla... 366 13.3.1.6 Optic Disc Drusen... 366 13.3.2 Acquired Disorders that Obscure the Margin of the Optic Disc... 367 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  Table of Contents XV 13.3.2.1 Papilledema... 368 13.3.2.2 Optic Neuritis... 370 13.3.2.3 Anterior Ischemic Optic Neuropathy (AION)... 374 13.3.2.4 Infiltrative Optic Disc Edema... 379 13.4 Disorders in which the Margin of the Optic Disc is Well Defined... 380 13.4.1 Atrophy of the Optic Nerve... 380 13.4.2 Optic Nerve Pits... 383 13.4.3 Optic Disc Coloboma (Morning Glory Disc)... 385 13.5 Tumors... 385 13.5.1 Intraocular Optic Nerve Tumors... 385 13.5.2 Retrobulbar Optic Nerve Tumors... 387 14 Visual Pathway... 389 (Oskar Gareis, Gerhard K. Lang) 14.1 Basic Knowledge... 389 14.2 Examination Methods... 391 14.3 Disorders of the Visual Pathway... 394 14.3.1 Prechiasmal Lesions... 394 14.3.2 Chiasmal Lesions... 396 14.3.3 Retrochiasmal Lesions... 400 15 Orbital Cavity... 403 (Christoph W. Spraul, Gerhard K. Lang) 15.1 Basic Knowledge... 403 15.2 Examination Methods... 405 15.3 Developmental Anomalies... 409 15.3.1 Craniofacial Dysplasia... 409 15.3.1.1 Craniostenosis... 409 15.3.2 Mandibulofacial Dysplasia... 410 15.3.2.1 Oculoauriculovertebral Dysplasia... 410 15.3.2.2 Mandibulofacial Dysostosis... 410 15.3.2.3 Oculomandibular Dysostosis... 410 15.3.2.4 Rubinstein–Taybi Syndrome... 410 15.3.3 Meningoencephalocele... 410 15.3.4 Osteopathies... 411 15.4 Orbital Involvement in Autoimmune Disorders: Graves’ Disease... 411 15.5 Orbital Inflammation... 413 15.5.1 Orbital Cellulitis... 414 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  XVI Table of Contents 15.5.2 Cavernous Sinus Thrombosis... 415 15.5.3 Orbital Pseudotumor... 416 15.5.4 Myositis... 416 15.5.5 Orbital Periostitis... 417 15.5.6 Mucocele... 417 15.5.7 Mycoses (Mucormycosis and Aspergillomycosis)... 417 15.6 Vascular Disorders... 418 15.6.1 Pulsating Exophthalmos... 418 15.6.2 Intermittent Exophthalmos... 419 15.6.3 Orbital Hematoma... 419 15.7 Tumors... 420 15.7.1 Orbital Tumors... 420 15.7.1.1 Hemangioma... 420 15.7.1.2 Dermoid and Epidermoid Cyst... 420 15.7.1.3 Neurinoma and Neurofibroma... 420 15.7.1.4 Meningioma... 420 15.7.1.5 Histiocytosis X... 421 15.7.1.6 Leukemic Infiltrations... 421 15.7.1.7 Lymphoma... 421 15.7.1.8 Rhabdomyosarcoma... 421 15.7.2 Metastases... 421 15.7.3 Optic Nerve Glioma... 422 15.8 Orbital Surgery... 422 16 Optics and Refractive Errors... 423 (Christoph W. Spraul, Gerhard K. Lang) 16.1 Basic Knowledge... 423 16.1.1 Uncorrected and Corrected Visual Acuity... 423 16.1.2 Refraction: Emmetropia and Ametropia... 423 16.1.3 Accommodation... 425 16.1.4 Adaptation to Differences in Light Intensity... 428 16.2 Examination Methods... 429 16.2.1 Refraction Testing... 429 16.2.2. Testing the Potential Resolving Power of the Retina in the Presence of Opacified Optic Media... 431 16.3 Refractive Anomalies (Table 16.2)... 432 16.3.1 Myopia (Shortsightedness)... 432 16.3.2 Hyperopia (Farsightedness)... 436 16.3.3 Astigmatism... 440 16.3.4 Anisometropia... 444 16.4 Impaired Accommodation... 445 16.4.1 Accommodation Spasm... 445 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  Table of Contents XVII 16.4.2 Accommodation Palsy... 446 16.5 Correction of Refractive Errors... 447 16.5.1 Eyeglass Lenses... 447 16.5.2 Contact Lenses... 451 16.5.2.1 Advantages and Characteristics of Contact Lenses... 451 16.5.3 Prisms... 455 16.5.4 Magnifying Vision Aids... 455 16.5.5 Aberrations of Lenses and Eyeglasses... 456 17 Ocular Motility and Strabismus... 459 (Doris Recker, Josef Amann, Gerhard K. Lang) 17.1 Basic Knowledge... 459 17.2 Concomitant Strabismus... 465 17.2.1 Forms of Concomitant Strabismus... 467 17.2.1.1 Esotropia... 467 17.2.1.2 Abnormal Accommodative Convergence/Accommodation Ratio... 470 17.2.1.3 Exotropia... 471 17.2.1.4 Vertical Deviations (Hypertropia and Hypotropia)... 471 17.2.2 Diagnosis of Concomitant Strabismus... 471 17.2.2.1 Evaluating Ocular Alignment with a Focused Light... 471 17.2.2.2 Diagnosis of Infantile Strabismic Amblyopia (Preferential Looking Test)... 472 17.2.2.3 Diagnosis of Unilateral and Alternating Strabismus (Unilateral Cover Test)... 473 17.2.2.4 Measuring the Angle of Deviation... 474 17.2.2.5 Determining the Type of Fixation... 476 17.2.2.6 Testing Binocular Vision... 476 17.2.3 Therapy of Concomitant Strabismus... 477 17.2.3.1 Eyeglass Prescription... 477 17.2.3.2 Treatment and Avoidance of Strabismic Amblyopia... 477 17.2.3.3 Surgery... 479 17.3 Heterophoria... 480 17.4 Pseudostrabismus... 481 17.5 Ophthalmoplegia and Paralytic Strabismus... 481 17.6 Nystagmus... 494 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  XVIII Table of Contents 18 Ocular Trauma... 497 (Gerhard K. Lang) 18.1 Examination Methods... 497 18.2 Classification of Ocular Injuries by Mechanism of Injury... 498 18.3 Mechanical Injuries... 498 18.3.1 Eyelid Injury... 498 18.3.2 Injuries to the Lacrimal System... 499 18.3.3 Conjunctival Laceration... 499 18.3.4 Corneal and Conjunctival Foreign Bodies... 503 18.3.5 Corneal Erosion... 505 18.3.6 Blunt Ocular Trauma (Ocular Contusion)... 506 18.3.7 Blowout Fracture... 507 18.3.8 Open-Globe Injuries... 514 18.3.9 Impalement Injuries of the Orbit... 515 18.4 Chemical Injuries... 517 18.5 Injuries Due to Physical Agents... 523 18.5.1 Ultraviolet Keratoconjunctivitis... 523 18.5.2 Burns... 523 18.5.3 Radiation Injuries (Ionizing Radiation)... 524 18.6 Indirect Ocular Trauma: Purtscher’s Retinopathy... 525 19 Cardinal Symptoms... 527 (Gerhard K. Lang) Index... 563 Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1 1 The Ophthalmic Examination Gabriele E. Lang and Gerhard K. Lang 1.1 Equipment The basic equipment for the ophthalmic examination includes the following instruments: ❖ Direct ophthalmoscope for examining the fundus (Fig. 1.1). ❖ Focused light (Fig. 1.1) for examining the reaction of the pupil and the ante- rior chamber. ❖ Aspheric lens (Fig. 1.1) for examining the anterior chamber. ❖ Eye chart for testing visual acuity at a distance of 5 meters (20 feet) (Fig. 1.2). Basic diagnostic instruments for the fundus, pupil, and anterior chamber. Fig. 1.1 From left to right: direct ophthalmoscope, aspheric lens, and focused light. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2 1 The Ophthalmic Examination Eye charts for testing visual acuity at a distance of 5 meters. Fig. 1.2 From left to right: Snel- len letter chart, Arabic number chart, E game, Landolt broken rings, children’s pictograph. ❖ Binocular loupes for removing corneal and conjunctival foreign bodies. ❖ Desmarres eyelid retractor and glass rod or sterile cotton swab for eyelid eversion (Fig. 1.3). Foreign-body needle for removing superficial corneal foreign bodies (Fig. 1.3). Recommended medications: ❖ Topical anesthetic (such as oxybuprocaine 0.4% eyedrops) to provide local anesthesia during removal of conjunctival and corneal foreign bodies and superficial anesthesia prior to flushing the conjunctival sac in chemical injuries. ❖ Sterile buffer solution for primary treatment of chemical injuries. ❖ Antibiotic eyedrops for first aid treatment of injuries, sterile eye compresses, and a 1 cm adhesive bandage for protective bandaging. An ophthalmologist should be consulted following any emergency treatment of eye injuries. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1.2 History 3 Basic diagnostic equipment for removing corneal foreign bodies and eyelid eversion. Fig. 1.3 From left to right: Foreign body needle, glass spatula, and Des- marres eyelid retractor. 1.2 History A complete history includes four aspects: 1. Family history. Many eye disorders are hereditary or of higher incidence in members of the same family. Examples include refractive errors, stra- bismus, cataract, glaucoma, retinal detachment, and retinal dystrophy. 2. Medical history. As ocular changes may be related to systemic disorders, this possibility must be explored. Conditions affecting the eyes include diabetes mellitus, hypertension, infectious diseases, rheumatic disorders, skin diseases, and surgery. Eye disorders such as corticosteroid-induced glaucoma, corticosteroid-induced cataract, and chloroquine-induced maculopathy can occur as a result of treatment with medications such as steroids, chloroquine, Amiodarone, Myambutol, or chlorpromazine (see table in Appendix). 3. Ophthalmic history. The examiner should inquire about corrective lenses, strabismus or amblyopia, posttraumatic conditions, and surgery or eye inflammation. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  4 1 The Ophthalmic Examination 4. Current history. What symptoms does the patient present with? Does the patient have impaired vision, pain, redness of the eye, or double vision? When did these symptoms occur? Are injuries or associated generalized symptoms present? 1.3 Visual Acuity Visual acuity, the sharpness of near and distance vision, is tested separately for each eye. One eye is covered with a piece of paper or the palm of the hand placed lightly over the eye. The fingers should not be used to cover the eye because the patient will be able to see between them (Fig. 1.4). The general practitioner or student can perform an approximate test of visual acuity. The patient is first asked to identify certain visual symbols referred to as optotypes (see Fig. 1.2) at a distance of 5 meters or 20 feet (test of distance vision). These visual symbols are designed so that optotypes of a cer- tain size can barely be resolved by the normal eye at a specified distance (this standard distance is specified in meters next to the respective symbol). The eye charts must be clean and well illuminated for the examination. The sharpness of vision measured is expressed as a fraction: Examining visual acuity. Fig. 1.4 The palm of the hand is placed lightly over the eye to cover it to allow testing of the distance and near vision in the opposite eye. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1.4 Ocular Motility 5 actual distance ! visual acuity. standard distance Normal visual acuity is 5/5 (20/20), or 1.0 as a decimal number, where the actual distance equals the standard distance. An example of diminished visual acuity (see Fig. 1.2): The patient sees only the “4” and none of the smaller symbols on the left eye chart at a distance of 5 meters (20 feet) (actual distance). A normal-sighted person would be able to discern the “4” at a distance of 50 meters or 200 feet (standard distance). Accordingly, the patient has a visual acuity of 5/50 (20/200) or 0.1. The ophthalmologist tests visual acuity after determining objective refraction using the integral lens system of a Phoroptor, or a box of individual lenses and an image projector that projects the visual symbols at a defined distance in front of the eye. Visual acuity is automatically calculated from the fixed actual distance and is displayed as a decimal value. Plus lenses (convex lenses) are used for farsightedness (hyperopia or hypermetropia), minus lenses (concave lenses) for nearsightedness (myopia), and cylindrical lenses for astigmatism. If the patient cannot discern the symbols on the eye chart at a distance of 5 meters (20 feet), the examiner shows the patient the chart at a distance of 1 meter or 3 feet (both the ophthalmologist and the general practitioner use eye charts for this examination). If the patient is still unable to discern any symbols, the examiner has the patient count fingers, discern the direction of hand motion, and discern the direction of a point light source. 1.4 Ocular Motility With the patient’s head immobilized, the examiner asks the patient to look in each of the nine diagnostic positions of gaze: 1, straight ahead; 2, right; 3, upper right; 4, up; 5, upper left; 6, left; 7, lower left; 8, down; and 9, lower right (Fig. 1.5). This allows the examiner to diagnose strabismus, paralysis of ocular muscles, and gaze paresis. Evaluating the six cardinal directions of gaze (right, left, upper right, lower right, upper left, lower left) is sufficient when examining paralysis of the one of the six extraocular muscles. The motion impairment of the eye resulting from paralysis of an ocular muscle will be most evident in these positions. Only one of the rectus muscles is involved in each of the left and right positions of gaze (lateral or medial rectus muscle). All other directions of gaze involve several muscles. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  6 1 The Ophthalmic Examination Evaluating the nine diagnostic positions of gaze. Fig. 1.5 This examination allows the examiner to diagnose strabismus, paralysis of ocular muscles, and gaze paresis. 1.5 Binocular Alignment Binocular alignment is evaluated with a cover test. The examiner holds a point light source beneath his or her own eyes and observes the light reflec- tions in the patient’s corneas in the near field (40 cm) and at a distance (5 m). The reflections are normally in the center of each pupil. If the corneal reflection is not in the center of the pupil in one eye, then a tropia is present in that eye. Then the examiner covers one eye with a hand or an occluder (Fig. 1.6) and tests whether the uncovered eye makes a compensatory movement. Compen- satory movement of the eye indicates the presence of tropia. However, there will also be a lack of compensatory movement if the eye is blind. The cover test is then repeated with the other eye. If tropia is present in a newborn with extremely poor vision, the baby will not tolerate the good eye being covered. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1.7 Examination of the Conjunctiva 7 Evaluation of binocular alignment. Fig. 1.6 The ex- aminer covers one eye of the patient with the hand to test if the uncovered eye makes a compensatory movement indi- cating presence of tropia. 1.6 Examination of the Eyelids and Nasolacrimal Duct The upper eyelid covers the superior margin of the cornea. A few millimeters of the sclera will be visible above the lower eyelid. The eyelids are in direct con- tact with the eyeball. Stenosis of the nasolacrimal duct produces a pool of tears in the medial angle of the eye with lacrimation (epiphora). In inflammation of the lacrimal sac, pressure on the nasolacrimal sac frequently causes a reflux of mucus or pus from the inferior punctum. Patency of the nasolacrimal duct is tested by instilling a 10% fluorescein solution in the conjunctival sac of the eye. If the dye is present in nasal mucus expelled into paper tissue after two minutes, the lacrimal duct is open (see also p. 53). Due to the danger of infection, any probing or irrigation of the nasolacrimal duct should be performed only by an ophthalmologist. 1.7 Examination of the Conjunctiva The conjunctiva is examined by direct inspection. The bulbar conjunctiva is directly visible between the eyelids; the palpebral conjunctiva can only be examined by everting the upper or lower eyelid. The normal conjunctiva is smooth, shiny, and moist. The examiner should be alert to any reddening, secretion, thickening, scars, or foreign bodies. Eversion of the lower eyelid. The patient looks up while the examiner pulls the eyelid downward close to the anterior margin (Fig. 1.7). This exposes the conjunctiva and the posterior surface of the lower eyelid. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  8 1 The Ophthalmic Examination Examination of the lower eyelid and inferior fornix. Fig. 1.7 The lower eyelid must be everted for this examination. The patient looks up while the ex- aminer pulls the eyelid downward close to the ante- rior margin. Eversion of the upper eyelid. Simple eversion (Fig. 1.8). The patient is asked to look down. The patient should repeatedly be told to relax and to avoid tightly shutting the opposite eye. This relaxes the levator palpebrae superioris and orbicularis oculi muscles. The examiner grasps the eyelashes of the upper eyelid between the thumb and forefinger and everts the eyelid against a glass rod or swab used as a fulcrum. Eversion should be performed with a quick levering motion while applying slight traction. The palpebral conjunctiva can then be inspected and cleaned if necessary. Examination of the upper eyelid (simple eversion). Fig. 1.8 The patient relaxes and looks down. The examiner places a swab superior to the tarsal region of the upper eyelid, grasps the eyelashes of the upper eyelid between the thumb and forefinger, and everts the eyelid using the swab as a fulcrum. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1.7 Examination of the Conjunctiva 9 Full eversion with retractor. To expose the superior fornix, the upper eyelid is fully everted around a Desmarres eyelid retractor (Figs. 1.9 a and b). This method is used solely by the ophthalmologist and is only discussed here for the sake of completeness. This eversion technique is required to remove for- eign bodies or “lost” contact lenses from the superior fornix or to clean the conjunctiva of lime particles in a chemical injury with lime. Examination of the upper eyelid and superior fornix (full eversion with retractor). Figs. 1.9 a and b In this case, the ex- aminer everts the eyelid around a Des- marres eyelid retractor. In contrast to simple eversion, this procedure allows examination of the superior fornix in addition to the palpebral conjunctiva. a b Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  10 1 The Ophthalmic Examination Blepharospasm can render simple and full eversion very difficult especially in the presence of chemical injury. In these cases, the spasm should first be eliminated by instilling a topical anesthetic such as oxy- buprocaine hydrochloride eyedrops. 1.8 Examination of the Cornea The cornea is examined with a point light source and a loupe (Fig. 1.10). The cornea is smooth, clear, and reflective. The reflection is distorted in the pres- ence of corneal disorders. Epithelial defects, which are also very painful, will take on an intense green color after application of fluorescein dye; corneal infiltrates and scars are grayish white. Evaluating corneal sensitivity is also important. Sensitivity is evaluated bilaterally to detect possible differences in the reaction of both eyes. The patient looks straight ahead during the exami- nation. The examiner holds the upper eyelid to prevent reflexive closing and touches the cornea anteriorly (Fig. 1.11). Decreased sensitivity can provide information about trigeminal or facial neuropathy, or may be a sign of a viral infection of the cornea. Examination of the anterior portion of the eye. Fig. 1.10 The examiner evalu- ates the eye using a focal light source and loupe magnification. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1.9 Examination of the Anterior Chamber 11 Evaluation of corneal sensitivity. Fig. 1.11 Corneal sensitivity can be evaluated with a distended cotton swab. The patient looks straight ahead while the examiner holds the upper eyelid and touches the cornea anteriorly. 1.9 Examination of the Anterior Chamber The anterior chamber is filled with clear aqueous humor. Cellular infiltration and collection of pus may occur (hypopyon). Bleeding in the anterior cham- ber is referred to as hyphema. It is important to evaluate the depth of the anterior chamber. In a cham- ber of normal depth, the iris can be well illuminated by a lateral light source (Fig. 1.12). In a shallow anterior chamber there will be a medial shadow on the iris. The pupillary dilation should be avoided in patients with shallow ante- rior chambers because of the risk of precipitating a glaucoma attack. Older patients with “small” hyperopic eyes are a particular risk group. Dilation of the pupil with a mydriatic is contraindicated in patients with a shallow anterior chamber due to the risk of precipitating angle closure glaucoma. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  12 1 The Ophthalmic Examination Evaluation of the depth of the anterior chamber. Illuminated area Shadow a b Fig. 1.12 a Normal anterior chamber depth: the iris can be well illuminated by a lateral light source. b Shallow anterior chamber: a medial shadow is visible on the iris. 1.10 Examination of the Lens The ophthalmologist uses a slit lamp to examine the lens. The eye can also be examined with a focused light if necessary. Direct illumination will produce a red reflection of the fundus if the lens is clear and gray shadows if lens opacities are present. The examiner then illuminates the eye laterally with a focused light held as close to the eye as possible and inspects the eye through a +14 diopter loupe (see Fig. 1.10). This examination permits better evaluation of changes in the conjunctiva, cornea, and anterior chamber. With severe opacification of the lens, a gray coloration will be vis- ible in the pupillary plane. Any such light-scattering opacity is referred to as a cataract. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1.11 Ophthalmoscopy 13 1.11 Ophthalmoscopy Indirect ophthalmoscopy is usually performed by the ophthalmologist (see p. 306) and produces a laterally reversed image of the fundus. Less experienced examiners will prefer direct ophthalmoscopy. Here, the oph- thalmoscope is held as close to the patient as possible (Fig. 1.13; see also Figs. 12.4 b and c). Refractive errors in the patient’s eye and the examiner’s eye are corrected by selecting the ophthalmoscope lens required to bring the retina into focus. The examiner sees an erect, 16 power magnified image of the ret- ina. The examination should be performed in a slightly darkened room with the patient’s pupils dilated. Students should be able to identify the optic disk. In a normal eye, it is sharply defined structure with vital coloration (i.e., yel- lowish orange) at the level of the retina and may have a central excavation. The central vein lies lateral to the artery; venous diameter is normally 1.5 times greater than arterial diameter. Each vascular structure should be of uni- form diameter, and there should be no vascular constriction where vessels overlap. A spontaneous venous pulse is normal; an arterial pulse is abnormal. Younger patients will have a foveal and macular light reflex, and the retina will have a reddish color (see Fig. 12.8). An ophthalmologist should be con- sulted if there are any abnormal findings. Ophthalmoscopy. Fig. 1.13 A direct ophthalmoscope produces an erect image of the fundus. The ex- aminer views the patient’s right eye with his or her own right eye so that their noses do not interfere with the examination. The examiner’s right hand rests on the dial of the ophthalmoscope to bring the retina into focus. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  14 1 The Ophthalmic Examination 1.12 Confrontation Field Testing Confrontation testing provides gross screening of the field of vision where perimetry tests are not available (see p. 391). The patient faces the examiner at a standard distance of 1 m with his or her eyes at the same level as the examiner’s (Fig. 1.14). Both focus on the other’s opposite eye (i.e., the patient’s left eye focuses on the examiner’s right eye) while covering their contralateral eye with the palm of the hand. The examiner moves an object such as a pen, cotton swab, or finger from the periphery toward the midline in all four quadrants (in the superior and infe- rior nasal fields and superior and inferior temporal fields). A patient with a normal field of vision will see the object at the same time as the examiner; a patient with an abnormal or restricted field of vision will see the object later than the examiner. Confrontation testing is a gross method of assessing the field of vision. It can be used to diagnose a severely restricted field of vision such as homonymous hemianopsia or quadrant anopsia. Confrontation field testing. Fig. 1.14 Confrontation test: the patient faces the examiner at a distance of 1 m with his or her eyes at the same level as the examiner’s. Each focuses on the other’s opposite eye while covering their contralateral eye with the palm of the hand. The examiner moves a pen from the periphery toward the midline in all four quadrants in the nasal and temporal fields and in the superior and inferior fields. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  1.14 Eyedrops, Ointment, and Bandages 15 Measurement of intraocular pressure. Fig. 1.15 The examiner uses both index fin- gers to palpate the eye through the upper eyelid. 1.13 Measurement of Intraocular Pressure With the patient’s eyes closed, the examiner places his or her hands on the patient’s head and palpates the eye through the upper eyelid with both index fingers (Fig. 1.15). The test is repeated on the contralateral eye for comparison. A “rock hard” eyeball only occurs in acute angle closure glaucoma. Slight increases in intraocular pressure such as occur in chronic glau- coma will not be palpable. 1.14 Eyedrops, Ointment, and Bandages Eyedrops and ointment should be administered posterior to the everted lower eyelid. One drop or strip of ointment approximately 1 cm long should be administered laterally to the inferior conjunctival sac. To avoid injury to the eye, drops should be administered with the patient supine (Fig. 1.16) or seated with the head tilted back and supported. The person administering the medi- cation places his or her hand on the patient’s face for support. Bottles and tubes must not come in contact with the patient’s eyelashes as they might otherwise become contaminated. Allow the drops or strip of ointment to drop into the conjunctival sac. Eye ointment should not be administered following ocular trauma as this may complicate subsequent examination or surgery. Dilation of the pupils with a mydriatic in unconscious patients should be avoided as this complicates neurologic examination. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  16 1 The Ophthalmic Examination Administration of eyedrops with the patient supine. Fig. 1.16 Eye- drops should be administered posterior to the everted lower eyelid. Eye bandage. A sterile swab or commercially available bandage (two oval layers of bandage material with a layer cotton between them) may be used. Care should be taken to avoid touching the side in contact with the eye. The bandage is fixed to the forehead and cheek with strips of adhesive tape. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  17 2 The Eyelids Peter Wagner and Gerhard K. Lang 2.1 Basic Knowledge Protective function of the eyelids: The eyelids are folds of muscular soft tissue that lie anterior to the eyeball and protect it from injury. Their shape is such that the eyeball is completely covered when they are closed. Strong mechanical, optical, and acoustic stimuli (such as a foreign body, blinding light, or sudden loud noise) “automatically” elicit an eye closing reflex. The cornea is also protected by an additional upward movement of the eyeball (Bell’s phenomenon). Regular blinking (20 – 30 times a minute) helps to uni- formly distribute glandular secretions and tears over the conjunctiva and cor- nea, keeping them from drying out. Structure of the eyelids: The eyelids consist of superficial and deep layers (Fig. 2.1). ❖ Superficial layer: – Thin, well vascularized layer of skin. – Sweat glands. – Modified sweat gland and sebaceous glands (ciliary glands or glands of Moll) and sebaceous glands (glands of Zeis) in the vicinity of the eye- lashes. – Striated muscle fibers of the orbicularis oculi muscle that actively closes the eye (supplied by the facial nerve). ❖ Deep layer: – The tarsal plate gives the eyelid firmness and shape. – Smooth musculature of the levator palpebrae that inserts into the tarsal plate (tarsal muscle). The tarsal muscle is supplied by the sympathetic nervous system and regulates the width of the palpebral fissure. High sympathetic tone contracts the tarsal muscle and widens the palpebral fissure; low sympathetic tone relaxes the tarsal muscle and narrows the palpebral fissure. – The palpebral conjunctiva is firmly attached to the tarsal plate. It forms an articular layer for the eyeball. Every time the eye blinks, it acts like a windshield wiper and uniformly distributes glandular secretions and tears over the conjunctiva and cornea. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  18 2 The Eyelids Sagittal section through the upper eyelid. Orbicularis oculi muscle Orbital septum Orbital fat Levator palpebrae muscle Accessory lacrimal gland Superior M. tarsalis Müller palpebral furrow Accessory lacrimal gland Meibomian gland Palpebral conjunctiva Gland of Moll Gland of Zeis Eyelash Fig. 2.1 The superficial layer of the eyelid consists of the skin, glands of Moll and Zeis, and the orbicularis oculi and levator palpebrae muscles. The deep layer consists of the tarsal plate, tarsal muscle, palpebral conjunctiva, and meibomian glands. – Sebaceous glands (tarsal or meibomian glands), tubular structures in the cartilage of the eyelid, which lubricate the margin of the eyelid. Their function is to prevent the escape of tear fluid past the margins of the eyelids. The fibers of Riolan’s muscle at the inferior aspect of these sebaceous glands squeeze out the ducts of the tarsal glands every time the eye blinks. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.2 Examination Methods 19 The eyelashes project from the anterior aspect of the margin of the eyelid. On the upper eyelid, approximately 150 eyelashes are arranged in three or four rows; on the lower eyelid there are about 75 in two rows. Like the eyebrows, the eyelashes help prevent dust and sweat from entering the eye. The orbital septum is located between the tarsal plate and the margin of the orbit. It is a membranous sheet of connective tissue attached to the margin of the orbit that retains the orbital fat. 2.2 Examination Methods The eyelids are examined by direct inspection under a bright light. A slit lamp may be used for this purpose. Bilateral inspection of the eyelids includes the following aspects: ❖ Eyelid position: Normally the margins of the eyelids are in contact with the eyeball and the puncta are submerged in the lacus lacrimalis. ❖ Width of the palpebral fissure: When the eye is open and looking straight ahead, the upper lid should cover the superior margin of the cornea by about 2 mm. Occasionally a thin strip of sclera will be visible between the cornea and the margin of the lower lid. The width of the palpebral fissure is normally 6 – 10 mm, and the distance between the lateral and medial angles of the eye is 28 – 30 mm (Fig. 2.2). Varying widths of the gaps between the eyelids may be a sign of protrusion of the eyeball, enophthal- mos, or eyeballs of varying size (Table 2.1). ❖ Skin of the eyelid: The skin of the eyelid is thin with only a slight amount of subcutaneous fatty tissue. Allergic reaction and inflammation can rapidly cause extensive edema and swelling. In older patients, the skin of the upper eyelid may become increasingly flaccid (cutis laxa senilis). Occa- sionally it can even hang down over the eyelashes and restrict the field of vision (dermatochalasis or blepharochalasis). Dimensions of the normal palpebral fissure. Fig. 2.2 The width of the palpebral fissure is an important in- 2 mm 3 mm dicator for a num- 9 mm ber of pathologic changes in the eye (see Table 2.1). 28–30 mm Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  20 2 The Eyelids Table 2.1 Possible causes of abnormal width of the palpebral fissure Increased palpebral fissure Decreased palpebral fissure ❖ Peripheral facial paresis ❖ Congenital ptosis (lagophthalmos) ❖ Ptosis in oculomotor nerve palsy ❖ Grave’s disease ❖ Ptosis in myasthenia gravis ❖ Perinaud’s syndrome ❖ Sympathetic ptosis (with Horner’s syndrome, ❖ Buphthalmos see pp. 23 – 24) ❖ High-grade myopia ❖ Progressive ophthalmoplegia (Graefe’s sign) ❖ Retrobulbar tumor ❖ Microphthalmos ❖ Enophthalmos ❖ Shrinkage of the orbital fat (as in senile enophthalmos) The palpebral conjunctiva is examined by simple eversion of the upper eye- lid (see Figs. 1.7 and 1.8). The normal palpebral conjunctiva is smooth and shiny without any scar strictures or papilliform projections. Full eversion of the upper eyelid with a Desmarres eyelid retractor (see Fig. 1.9, p. 9) allows examination of the superior fornix (for normal appear- ance, see palpebral conjunctiva). 2.3 Developmental Anomalies 2.3.1 Coloboma Definition A normally unilateral triangular eyelid defect with its base at the margin of the eyelid occurring most often in the upper eyelid (Fig. 2.3). Epidemiology and etiology. Colobomas are rare defects resulting from a reduction malformation (defective closure of the optic cup). They are only rarely the result of an injury. Diagnostic considerations: The disorder is often accompanied by additional deformities such as dermoid cysts or a microphthalmos. Congenital defects of the first embryonic branchial arch that can result in coloboma include Franceschetti’s syndrome (mandibulofacial dysostosis) or Goldenhar’s syn- drome (oculoauriculovertebral dysplasia). Depending on the extent of the coloboma, desiccation symptoms on the conjunctiva and cornea with incipient ulceration may arise from the lack of regular and uniform moisten- ing of the conjunctiva and cornea. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.3 Developmental Anomalies 21 Congenital coloboma. Fig. 2.3 The tri- angular eyelid de- fect with its base at the margin of the eyelid results from a reduction malformation during closure of the optic cup in the embryonic stage. Treatment: Defects are closed by direct approximation or plastic surgery with a skin flap. 2.3.2 Epicanthal Folds A crescentic fold of skin usually extending bilaterally between the upper and lower eyelids and covering the medial angle of the eye. This rare congenital anomaly is harmless and typical in eastern Asians. However, it also occurs with Down’s syndrome (trisomy 21 syndrome). Thirty per cent of newborns have epicanthal folds until the age of six months. Where one fold is more pro- nounced, it can simulate esotropia. The nasal bridge becomes more pro- nounced as the child grows, and most epicanthal folds disappear by the age of four. 2.3.3 Blepharophimosis This refers to shortening of the horizontal palpebral fissure without patho- logic changes in the eyelids. The palpebral fissure, normally 28 – 30 mm wide, may be reduced to half that width. Blepharophimosis is a rare disorder that is either congenital or acquired (for example, from scar contracture or aging). As long as the center of the pupil remains unobstructed despite the decreased size of the palpebral fissure, surgical enlargement of the palpebral fissure (by canthotomy or plastic surgery) has a purely cosmetic purpose. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  22 2 The Eyelids 2.3.4 Ankyloblepharon This refers to horizontal shortening of the palpebral fissure with fusion of the eyelids at the lateral and medial angles of the eye. Usually, the partial or total fusion between the upper and lower eyelids will be bilateral, and the palpebral fissure will be partially or completely occluded as a result. Posterior to the eyelids, the eyeball itself will be deformed or totally absent. Ankylo- blepharon is frequently associated with other skull deformities. 2.4 Deformities 2.4.1 Ptosis Definition Paralysis of the levator palpebrae muscle with resulting drooping of one or both upper eyelids (from the Greek ptosis, a falling). The following forms are differentiated according to their origin (see also Etiology): ❖ Congenital ptosis (Fig. 2.4). ❖ Acquired ptosis: – Paralytic ptosis. – Sympathetic ptosis. – Myotonic ptosis. – Traumatic ptosis. Epidemiology. On the whole ptosis is a rare disorder. Etiology: Ptosis may be congenital or acquired. Congenital ptosis. Fig. 2.4 Con- genital ptosis of the levator palpe- brae muscle causes the upper eyelid to droop; usually the de- formity is uni- lateral. Ambly- opia will result if the center of the pupil is covered. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.4 Deformities 23 Congenital ptosis. The disorder is usually hereditary and is primarily auto- somal dominant as opposed to recessive. The cause is frequently aplasia in the core of the oculomotor nerve (neurogenic) that supplies the levator palpe- brae muscle; less frequently it is attributable to an underdeveloped levator palpebrae muscle (myogenic). Acquired ptosis: ❖ Neurogenic causes: – Oculomotor palsy (paralytic ptosis). – Lesions in the sympathetic nerve (sympathetic ptosis) is Horner’s palsy (ptosis, miosis, and enophthalmos). ❖ Myogenic ptosis: myasthenia gravis and myotonic dystrophy. ❖ Traumatic ptosis can occur after injuries. Symptoms. The drooping of the upper eyelid may be unilateral (usually a sign of a neurogenic cause) or bilateral (usually a sign of a myogenic cause). A characteristic feature of the unilateral form is that the patient attempts to increase the palpebral fissure by frowning (contracting the frontalis muscle). Congenital ptosis (Fig. 2.4) generally affects one eye only; bilateral symptoms are observed far less frequently (7%). Diagnostic considerations: Congenital ptosis. The affected eyelid in general is underdeveloped. The skin of the upper eyelid is smooth and thin; the supe- rior palpebral furrow is absent or ill-defined. A typical symptom is “lid lag” in which the upper eyelid does not move when the patient glances down. This important distinguishing symptom excludes acquired ptosis in differential diag- nosis. In about 3% of all cases, congenital ptosis is associated with epicanthal folds and blepharophimosis (Waardenburg syndrome). Congenital ptosis can occur in varying degrees of severity and may be com- plicated by the presence of additional eyelid and ocular muscle disorders such as strabismus. Congenital ptosis in which the upper eyelid droops over the center of the pupil always involves an increased risk of amblyopia. Acquired ptosis: ❖ Paralytic ptosis in oculomotor palsy (see also Chap. 17) is usually unilateral with the drooping eyelid covering the whole eye. Often there will be other signs of palsy in the area supplied by the oculomotor nerve. In external oculomotor palsy, only the extraocular muscles are affected (mydriasis will not be present), whereas in complete oculomotor palsy, the inner ciliary muscle and the sphincter pupillae muscle are also affected (internal oph- thalmoplegia with loss of accommodation, mydriasis, and complete loss of pupillary light reflexes). ❖ Myasthenia gravis (myogenic ptosis that is often bilateral and may be asymmetrical) is associated with abnormal fatigue of the striated Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  24 2 The Eyelids extraocular muscles. Ptosis typically becomes more severe as the day goes on. ❖ Sympathetic ptosis occurs in Horner’s palsy (ptosis, miosis, and enophthal- mos). Rapidly opening and closing the eyelids provokes ptosis in myasthenia gravis and simplifies the diagnosis. Treatment: ❖ Congenital ptosis: This involves surgical retraction of the upper eyelid (Fig. 2.5 a – c), which should be undertaken as quickly as possible when there is a risk of the affected eye developing a visual impairment as a result of the ptosis. ❖ Acquired ptosis: Treatment depends on the cause. As palsies often resolve spontaneously, the patient should be observed before resorting to surgical intervention. Conservative treatment with special eyeglasses may be suffi- cient even in irreversible cases. Because of the risk of overcorrecting or undercorrecting the disorder, several operations may be necessary. Prognosis and complications: Prompt surgical intervention in congenital ptosis can prevent amblyopia. Surgical overcorrection of the ptosis can lead to desiccation of the conjunctiva and cornea with ulceration as a result of incomplete closure of the eyelids. 2.4.2 Entropion Definition Entropion is characterized by inward rotation of the eyelid margin. The margin of the eyelid and eyelashes or even the outer skin of the eyelid are in contact with the globe instead of only the conjunctiva. The following forms are differ- entiated according to their origin (see Etiology): ❖ Congenital entropion (Fig. 2.6). ❖ Spastic entropion (Fig. 2.7). ❖ Cicatricial entropion. Epidemiology: Congenital entropion occurs frequently among Asians but is rare among people of European descent, in whom the spastic and cicatricial forms are more commonly encountered (see also Chap. 18). Etiology: ❖ Congenital entropion: This results from fleshy thickening of the skin and orbicularis oculi muscle near the margin of the eyelid. Usually the lower eyelid is affected. This condition may persist into adulthood. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.4 Deformities 25 Methods of surgical retraction of the upper eyelid. Fig. 2.5 a The Fasanella-Servat pro- cedure, indicated for correction of minimal ptosis, involves resec- tion of a portion of the tarsus (2 mm or less) to vertically shorten the eyelid. b The amount of muscle removed in a levator resection de- pends on levator func- tion (ranging from ap- a proximately 10 mm with slight ptosis, up to 22 mm with mod- erate ptosis). c Where levator function is poor (less than 5 mm), the upper eyelid can be connected to tissue in the eyebrow region. The frontalis suspen- sion technique may employ autogenous fascia lata or plastic suture. b c Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  26 2 The Eyelids Congenital entropion. Fig. 2.6 Con- genital inward ro- tation of the mar- gins of the upper and lower eyelids is a frequent find- ing in Asian populations and is usually asymp- tomatic. Spastic entropion. Fig. 2.7 Dis- placed fibers of the orbicularis oculi muscle cause the eye- lashes of the lower eyelid to turn inward. Sur- gical intervention is indicated to correct the laxity of the lower eye- lid. ❖ Spastic entropion: This affects only the lower eyelid. A combination of several pathogenetic factors of varying severity is usually involved: – The structures supporting the lower eyelid (palpebral ligaments, tarsus, and eyelid retractor) may become lax with age, causing the tarsus to tilt inward. – This causes the fibers of the orbicularis oculi muscle to override the normally superior margin of the eyelid, intensifying the blepharospasm resulting from the permanent contact between the eyelashes and the eyeball. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.4 Deformities 27 – Senile enophthalmos, usually occurring in old age as a result of atrophy of the orbit fatty tissue, further contributes to instability of the lower eyelid. ❖ Cicatricial entropion: This form of entropion is frequently the result of postinfectious or post-traumatic tarsal contracture (such as trachoma; burns and chemical injuries). Causes can also include allergic and toxic reactions (pemphigus, Stevens-Johnson syndrome, and Lyell’s syndrome). Symptoms and diagnostic considerations (see also etiology): Constant rubbing of the eyelashes against the eyeball (trichiasis) represents a per- manent foreign-body irritation of the conjunctiva which causes a blepharo- spasm (p. 93) that in turn exacerbates the entropion. The chronically irritated conjunctiva is reddened, and the eye fills with tears. Only congenital entropion is usually asymptomatic. Treatment: ❖ Congenital entropion: To the extent that any treatment is required, it con- sists of measured, semicircular resection of skin and orbicularis oculi muscle tissue that can be supplemented by everting sutures where indi- cated. ❖ Spastic entropion: Surgical management must be tailored to the specific situation. Usually treatment combines several techniques such as shorten- ing the eyelid horizontally combined with weakening or diverting the pre- tarsal fibers of the orbicularis oculi muscle and shortening the skin verti- cally. ❖ Cicatricial entropion: The surgical management of this form is identical to that of spastic entropion. An adhesive bandage may be applied to increase tension on the eyelid for temporary relief of symptoms prior to surgery. Prognosis and complications: Congenital entropion is usually asymptomatic and often resolves within the first few months of life. ❖ Spastic entropion: The prognosis is favorable with prompt surgical inter- vention, although the disorder may recur. Left untreated, spastic entropion entails a risk of damage to the corneal epithelium with superin- fection which may progress to the complete clinical syndrome of a serpigi- nous corneal ulcer (see p. 29). ❖ Cicatricial entropion: The prognosis is favorable with prompt surgical intervention (i.e., before any corneal changes occur). Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  28 2 The Eyelids 2.4.3 Ectropion Definition Ectropion refers to the condition in which the margin of the eyelid is turned away from the eyeball. This condition almost exclusively affects the lower eye- lid. The following forms are differentiated according to their origin (see also Etiology): ❖ Congenital ectropion. ❖ Senile ectropion. ❖ Paralytic ectropion. ❖ Cicatricial ectropion. Epidemiology: Senile ectropion is the most prevalent form; the paralytic and cicatricial forms occur less frequently. Congenital ectropion is very rare and is usually associated with other developmental anomalies of the eyelid and face such as Franceschetti’s syndrome. Etiology: ❖ Congenital ectropion: See Epidemiology. ❖ Senile ectropion: The palpebral ligaments and tarsus may become lax with age, causing the tarsus to sag outward (Fig. 2.8). ❖ Paralytic ectropion: This is caused by facial paralysis with resulting loss of function of the orbicularis oculi muscle that closes the eyelid. ❖ Cicatricial ectropion: Like cicatricial entropion, this form is usually a sequela of infection or injury. Senile ectropion. Fig. 2.8 The structures supporting the eyelid are lax, causing the lower eyelid sag out- ward. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.4 Deformities 29 Symptoms and diagnostic considerations: Left untreated, incomplete clo- sure of the eyelids can lead to symptoms associated with desiccation of the cornea including ulceration from lagophthalmos. At the same time, the ever- sion of the punctum causes tears to flow down across the cheek instead of draining into the nose. Wiping away the tears increases the ectropion. This results in chronic conjunctivitis and blepharitis. Treatment: ❖ Congenital ectropion: Surgery. ❖ Senile ectropion: Surgery is indicated. A proven procedure is to tighten the lower eyelid via a tarsal wedge resection followed by horizontal tightening of the skin. ❖ Paralytic ectropion: Depending on the severity of the disorder, artificial tear solutions, eyeglasses with an anatomic lateral protective feature, or a “watch glass” bandage (Fig. 2.9) may be sufficient to prevent desiccation of the cornea. In severe or irreversible cases, the lagophthalmos is treated surgically via a lateral tarsorrhaphy. ❖ Cicatricial ectropion: Plastic surgery is often required to correct the eyelid deformity. Prognosis: The prognosis is favorable when the disorder is treated promptly. Sometimes several operations will be required. Surgery is more difficult where scarring is present. Watch glass bandage for paralytic ectropion. Fig. 2.9 In patients with lagoph- thalmos resulting from facial paraly- sis, a watch glass bandage creates a moist chamber that protects the cornea against desiccation. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  30 2 The Eyelids 2.4.4 Trichiasis Trichiasis refers to the rare postinfectious or post-traumatic inward turning of the eyelashes. The deformity causes the eyelashes to run against the con- junctiva and cornea, causing a permanent foreign-body sensation, increased tear secretion, and chronic conjunctivitis. The eyelash follicles can be oblit- erated by electrolysis. The disorder may also be successfully treated by cryo- cautery epilation or surgical removal of the follicle bed. 2.4.5 Blepharospasm Definition This refers to an involuntary spasmodic contraction of the orbicularis oculi muscle supplied by the facial nerve. Etiology: In addition to photosensitivity and increased tear production, blepharospasm will also accompany inflammation or irritation of the anterior chamber. (Photosensitivity, epiphora, and blepharospasm form a triad of reactive clinical symptoms.) Causes of the disorder include extrapyramidal disease such as encephalitis or multiple sclerosis. Trigeminal neuralgia or psy- chogenic causes may also be present. Symptoms: Clinical symptoms include spasmodically narrowed or closed palpebral fissures and lowered eyebrows. Treatment: This depends on the cause of the disorder. Mild cases can be con- trolled well with muscle relaxants. Severe cases may require transection of the fibers of the facial nerve supplying the orbicularis oculi muscle. The disorder may also be successfully treated with repeated local injections of botulinum toxin. Prognosis: The prognosis is good where a cause-related treatment is possible. Essential blepharospasm does not respond well to treatment. 2.5 Disorders of the Skin and Margin of the Eyelid 2.5.1 Contact Eczema Epidemiology: Light-skinned patients and patients susceptible to allergy are frequently affected. Etiology: Contact eczema is caused by an antigen – antibody reaction in patients with intolerance to certain noxious substances. Cosmetics, adhesive bandages, or eyedrops and eye ointments are often responsible, particularly the preservatives used in them such as benzalkonium chloride. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.5 Disorders of the Skin and Margin of the Eyelid 31 Contact eczema. Fig. 2.10 This disorder is frequently caused by preservatives such as those used in eyedrops. They cause typical reddening, swelling, and lichenifica- tion of the skin of the eyelid. Symptoms: Reddening, swelling, lichenification, and severe itching of the skin of the eyelid occur initially, followed by scaling of the indurated skin with a sensation of tension (Fig. 2.10). Treatment: This consists of eliminating the causative agent. (Allergy testing may be necessary.) Limited use of corticosteroids usually brings quick relief of symptoms. Prognosis: The prognosis is good if the cause can be identified. 2.5.2 Edema Definition This refers to swelling of the eyelid due to abnormal collection of fluid in the subcutaneous tissue. Epidemiology: Edema is a frequently encountered clinical symptom. Etiology: The skin of the eyelid is affected intensively by infectious and aller- gic processes. With the upper eyelid’s relatively thin skin and the loose struc- Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  32 2 The Eyelids ture of its subcutaneous tissue, water can easily accumulate and cause edema. Symptoms: Depending on the cause (Table 2.2), the intensity of swelling in the eyelid will vary. The location of swelling is also influenced by gravity and can vary in intensity. For example, it may be more intense in the early morn- ing after the patient rises than in the evening (Fig. 2.11). Fig. 2.2 Differential diagnosis of edema Criteria Inflammatory edema Noninflammatory edema Symptoms ❖ Swelling ❖ Swelling ❖ Reddening ❖ Pale skin ❖ Sensation of heat ❖ Cool skin ❖ Painful ❖ Painless ❖ Usually unilateral ❖ Usually bilateral Possible causes ❖ Hordeolum (p. 38) ❖ Systemic disorder: ❖ Abscess (p. 36) – heart ❖ Erysipelas – kidneys ❖ Eczema (p. 104) – thyroid gland ❖ Associated with: ❖ Allergy such as Quincke’s – paranasal sinus disorders edema – orbital cellulitis – dacryoadenitis – dacryocystitis Edema. Fig. 2.11 With its relatively thin skin and its sub- cutaneous tissue that contains little fat, the upper eyelid is particularly sus- ceptible to rapid fluid accumula- tions from patho- logic processes. Lang, Ophthalmology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.  2.5 Disorders of the Skin and Margin of the Eyelid 33 Table 2.2 shows the causes and differential diagnosis for inflammatory and noninflammatory edemas. Treatment: This depends on the cause of the disorder. Clinical course and prognosis: This depends on the underlying disorder. 2.5.3 Seborrheic Blepharitis Definition This relatively frequent disorder is characterized by scaly inflammation of the margins of the eyelids. Usually both eyes are affected. Etiology: There are often several contributing causes. The constitution of the skin, seborrhea, refractive anomalies, hypersecretion of the eyelid glands, and external stimuli such as dust, smoke, and dry air in air-conditioned rooms often contribute to persistent chronic inflammation. Symptoms and diagnostic considerations: The margins of the eyelids usu- ally exhibit slight inflammatory changes such as thickening. The eyelashes adhere due to the increased secretion from the glands of the eyelids, and scaly deposits form (Fig. 2.12