Small Animal Ophthalmology: A Problem-Oriented Approach

We dedicate this book to our families, our pets, and our patients. For Elsevier: Commissioning Editor Joyce Rodenhuis D...

Author: Robert L. Peiffer Jr. DVM PhD DACVO | Simon M. Petersen-Jones DVetMed PhD DVOphthal DipECVO MRCVS

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We dedicate this book to our families, our pets, and our patients.

For Elsevier: Commissioning Editor Joyce Rodenhuis Development Editor Louisa Welch Project Manager Morven Dean/Jane Dingwall Designer Erik Bigland Illustration Manager Kirsteen Wright

© 2009, Elsevier Limited. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without either the prior permission of the publishers or a licence permitting restricted copying in the United Kingdom issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1T 4LP. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, USA: phone: (+1) 215 238 7869, fax: (+1) 215 238 2239, e-mail: [email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’. First published 1989 Second edition 1996 Third edition 2001 Fourth edition 2009 ISBN: 978-0-7020-2861-8

British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Knowledge and best practice in this ﬁeld are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. 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 the practitioner, relying on their own experience and knowledge of the patient, 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 author assumes any liability for any injury and/or damage. The Publisher

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Contributors

Peter GC Bedford BVetMed PhD DVOphthal DipECVO FRCVS GBDA Professor of Canine Medicine and Surgery Royal Veterinary College Hatﬁeld, UK Ellen Bjerkås DVM PhD DipECVO Professor Department of Companion Animal Clinical Sciences Norwegian School of Veterinary Sciences Oslo, Norway Cynthia S Cook DVM PhD DipACVO Veterinary Vision San Carlos, CA, USA Björn Ekesten DVM PhD Professor of Clinical Neurophysiology Department of Clinical Sciences Swedish University of Agricultural Sciences Uppsala, Sweden Bruce H Grahn DVM Diplomate ABVP ACVO Professor of Veterinary Ophthalmology Department of Small Animal Clinical Sciences Western College of Veterinary Medicine University of Saskatchewan Saskatoon, Saskatchewan, Canada R Gareth Jones BVSc CertVOphthal MRCVS The Park Veterinary Group Leicester, UK Olivier Jongh DMV Clinique Vétérinaire du Val de Saône Neuville sur Saône, France

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CONTRIBUTORS

Mary L Landis MS VMD Resident in Ophthalmology Bucks County Animal Ophthalmology Doylestown, PA, USA Sebastien Monclin DVM Resident of Ophthalmology University of Liège Belgium Domenico Multari DVM SCMPA PhD Centro Veterinario Oculisto ‘Fontane’ Treviso, Italy Kristina Narfström DVM PhD DipECVO Professor of Veterinary Ophthalmology Department of Veterinary Medicine & Surgery University of Missouri Columbia, MO, USA Robert L Peiffer Jr DVM PhD DipACVO Bucks County Animal Ophthalmology Doylestown, PA, USA Simon M Petersen-Jones DVetMed PhD DVOphthal DipECVO MRCVS Assistant Professor of Comparative Ophthalmology Department of Small Animal Clinical Sciences Veterinary Medical Center Michigan State University East Lansing, MI, USA Peter W Renwick MA VetMB DVOphthal MRCVS Willows Referral Service Shirley, Solihull, UK Serge G Rosolen DVM PhD Eye Veterinary Clinic Asnières, France Robin Stanley BVSc(Hons) FACVSc Animal Eye Care East Malvern, Victoria, Australia

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Wendy M Townsend DVM MS DipACVO Assistant Professor of Comparative Ophthalmology Small Animal Clinical Sciences Veterinary Teaching Hospital Michigan State University East Lansing, MI, USA

Mike Woods MVB CertVOphthal MRCVS Practice Principal & Ophthalmologist Primrose Hill Veterinary Hospital Dun Laoghaire, Co Dublin, Ireland

CONTRIBUTORS

Joe Wolfer DVM DipACVO Veterinary Ophthalmologist Animal Eye Clinic Toronto, Ontario, Canada

ix

Preface to First Edition

Ophthalmology has blossomed and matured as a recognized, valued specialty of veterinary medicine and surgery; ophthalmic exposure is generally emphasized in the professional curriculum; the competency and sophistication of the general practitioner is continually improving; and several excellent contemporary comprehensive textbooks are available on the subject. Then why this text? We have recognized a need by the general practitioner for an informative source that he or she can turn to as a guide to the management of a particular problem. Appropriate management implies two inseparable principles – accurate diagnosis and adequate therapy. We have attempted to address each with equal emphasis. We perceive a need by the student for a text that condenses a large amount of information into a ‘friendly’ manual that emphasizes problem solving rather than memorization and that provides more usable information than lecture notes without the depth of a reference text. We hope this manual meets these needs. Why these authors? The profession and the specialty are evolving and changing. Although I am somewhat reluctant to classify myself as ‘mature’ as a clinical ophthalmologist, I cannot help but be impressed by the energy, enthusiasm, and ideas of a younger generation of amazingly well-trained ophthalmologists. All of the contributors ﬁt this mold, and I hope that they and their colleagues who follow will continue to probingly question the established as well as addressing unsolved problems. Experience is almost always tainted by dogmatism, which in turn can cloud truth; I have encouraged Drs Cook, Leon, Cottrell, and Petersen-Jones to express their ideas and philosophies without unwarranted respect for sacred cows. The product is exciting. We have attempted not to reproduce a comprehensive text but to produce a clinical manual; references are not included. As conditions may present with more than one presenting sign, there is some repetition; conditions are discussed in detail under their most obvious or signiﬁcant sign. We have discussed in detail only those surgical procedures that are likely to be routinely performed by the practitioner, and details of these procedures are described with their pictorial presentation rather than in the text. Emphasis is placed on techniques that have proven to be most valuable and effective for the authors, and readers should recognize that there may indeed be quite acceptable alternative approaches to clinical problems. We do hope that this

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PREFACE TO FIRST EDITION

xii

handbook will prove a ready and valuable reference to the general practitioner presenting with a challenging ophthalmic case and when reviewed in its entirety will provide a practical overall approach to small animal ophthalmology. Bob Peiffer Chapel Hill 1989

Preface to Fourth Edition

When the ﬁrst edition of Small Animal Ophthalmology: a Problem-Oriented Approach was published in 1989 I would not have foreseen struggling with the Preface to the Fourth Edition almost two decades later. The children have grown and moved away, and a German Shorthair and Redbone Coon Hound have been replaced by a pair of Labrador Retrievers. The cat, I suspect, is reincarnate of his predecessors, and the Pennsylvania winters are a bit longer and colder than those in the South. I have been fortunate to have Simon Petersen-Jones to share the labor from the second edition onward and both myself and the text have beneﬁted from his diligence and insight. While the world has changed, the scope and intent of the text remain constant – to provide the student or general practitioner with a practical reference that condenses an ever-expanding base of knowledge in small animal ophthalmology into an affordable user-friendly clinical manual that emphasizes problem-solving in dealing with patients that present with ophthalmic signs. This was a novel approach at the time, and the fact that the book has been translated into Japanese, Spanish, and French, and oft mimicked since, speaks to its utility. We have maintained the theme of recruiting accomplished contributors who provide broad, contemporary, and international perspectives. All share a commitment to excellence in the management of their patients that is reﬂected in the quality of their work. As I compare their contributions to those in the ﬁrst edition I realize that progress is made in small steps; successful management of canine glaucoma is still largely an exercise in frustration in spite of new potent drugs and the contemporary technologies of laser and implants. Treatment of tear ﬁlm deﬁciencies still requires long-term management and a motivated and educated pet owner, although the lacrimostimulants have obviated the necessity of parotid duct transposition in many. Technologies and methodologies in imaging, cataract surgery, and retinal detachment repair have remarkably enhanced outcomes for many of our patients. The potential of molecular medicine beckons from a seemingly distant horizon. Practicing ophthalmology during these times has been an adventure and a privilege indeed. We are grateful for the competence and professionalism of the Elsevier staff who have provided encouragement, guidance, and the occasional nudge that

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PREFACE VERSO TO FOURTH RUNNING EDITION HEAD

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these projects seem to require. The opportunity to include a CD-Rom allows us to expand the visual impact of observation to formulate differential diagnoses. We will be content with our labors if readers emerge from their study more proﬁcient in the management of their ophthalmic cases. Bob Peiffer Doylestown, Pennsylvania. 2008

I am delighted to join with Bob again to help edit another edition of Small Animal Ophthalmology: a Problem-Oriented Approach. I well remember over 20 years ago writing a chapter for the ﬁrst edition. I was an ophthalmology resident visiting Dr Peiffer (as have many aspiring young ophthalmologists before and after me) when he asked if I would be interested to write a chapter for the book he was developing. I jumped at the opportunity, never suspecting that I would join Bob to edit the subsequent editions. Veterinary ophthalmology has a rapidly expanding knowledge base but the problem-oriented approach still works well. Our patients present to us with certain clinical signs that fall into the broad categories of the chapters in the book, rather than with a diagnosis of, for example, retinal detachment or distichiasis. It is our job to identify the clinical signs and through a systematic and thorough eye examination reach a diagnosis. The aim of the book is to help practitioners achieve this goal. In this latest edition we have added a CD-Rom that allows for case presentations – we hope that this will be useful and educational for our readers. Simon Petersen-Jones East Lansing, Michigan. 2008

Clinical basic science Cynthia S. Cook, Robert L. Peiffer, Jr and Mary L. Landis

OCULAR EMBRYOLOGY

1

The ocular primordia appear during the ﬁrst weeks of gestation as bilateral evaginations of the neural ectoderm of the forebrain. These optic sulci gradually enlarge and approach the surface ectoderm as optic vesicles connected to the forebrain by the optic stalks. Thickening of the overlying surface ectoderm to form the lens placode (Fig. 1.1A,B) occurs as a result of inductive inﬂuences by the optic vesicle. Invagination of the lens placode occurs concurrently with that of the optic vesicle to form a hollow lens vesicle within a bilayered optic cup (Fig. 1.1C,D), the inner layer of which will form the stratiﬁed layers of the neural retina and the inner epithelial layer of the iris and ciliary body; the outer layer becomes the cuboidal monolayered retinal pigment epithelium, the outer pigmented epithelial layer of the iris and ciliary body, and, in the dog and cat, the pupillary sphincter and dilator muscles (the only muscles in the body of neural ectodermal origin). The potential space between the two apposed layers becomes formed and ﬂuid-ﬁlled in retinal detachment and uveal cysts. The stalk attaching the lens vesicle to the surface ectoderm atrophies through a combination of cell death and active migration of cells out of the stalk (Fig. 1.1E,F). Invagination to form the optic cup occurs eccentrically, with formation of a slit-like opening called the optic (choroid) ﬁssure located inferiorly (Fig. 1.1F). The vascular supply to the embryonic eye, the hyaloid artery (or primary vitreous), enters the optic cup through this opening and arborizes extensively around the lens to form the tunica vasculosa lentis. Embryonic remnants of this vascular structure may persist as insigniﬁcant posterior capsular opacities (including Mittendorf’s dot, located inferior to the suture junction), persistent tunica vasculosa lentis, or, more signiﬁcant clinically, persistent hyperplastic primary vitreous (PHPV). The term persistent embryonic vasculature, or PEV, encompasses the entire spectrum. Failure of the optic ﬁssure to close normally may result in congenital defects anteriorly (iridial coloboma) or posteriorly (chorioretinal or optic nerve coloboma). Microphthalmos or anophthalmos may occur as a result of deﬁciencies in the early formation of the optic sulcus or vesicle, or from incomplete closure of the optic ﬁssure with failure to establish early intraocular pressure (Fig. 1.2).

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SMALL ANIMAL OPHTHALMOLOGY

2

A

B

C

D

E

F

The posterior lens epithelial cells elongate, forming primary lens ﬁbers that obliterate the space within the lens vesicle. Secondary lens ﬁbers are formed by elongation of cells at the equator (lens bow); these ﬁbers pass circumferentially around the embryonal lens nucleus. Note that the sutures are associated only with the fetal and adult lens ﬁbers. This marvellous differentiaton of the young posterior epithelial cells accounts for the unchanging 3–6 μm thick posterior capsule (the bane of the cataract surgeon) compared to the more robust anterior capsule, which progressively thickens with age as basement membrane produced by the lens epithelial cells accumulates. Thickening of the future neural retina occurs with segregation into inner and outer neuroblastic layers. Cellular proliferation takes place in the outer neuroblastic layer, with migration to form the inner layer. The ganglion cells are the ﬁrst to achieve ﬁnal differentiation, extending axons that form the nerve ﬁber layer and collectively form the optic nerve. The horizontal, amacrine, and

Fig. 1.2 Microphthalmia in a merle Australian Shepherd pup. This genetic syndrome (merle ocular dysgenesis) occurs in dogs with a predominantly white coat color. Microphthalmia occurs through multiple mechanisms including hypoplasia of the optic vesicle.

CLINICAL BASIC SCIENCE

Fig. 1.1 Sequential development of ocular structures. These scanning electron micrographs are of mouse embryos on days 10 and 11 of gestation, corresponding to days 17–24 of gestation in the dog. The sequence in most mammals is quite similar. (A) On external examination the invaginating lens placode can be seen (arrow). Note its position relative to the maxillary (Mx) and mandibular (Mn) prominences of the ﬁrst visceral arch. (B) Embryo of the same age as that in (A). Frontal fracture through the lens placode (arrow) illustrates the associated thickening of the surface ectoderm (E). Mesenchyme (M) of neural crest origin is present adjacent to the lens placode. The distal portion of the optic vesicle concurrently thickens as the precursor of the neural retina (NR), while the proximal optic vesicle becomes a shorter, cuboidal layer which is the anlage of the retinal pigment epithelium (PE). The cavity of the optic vesicle (V) becomes progressively smaller. (C) The epithelium of the lens placode continues to invaginate (L). There is an abrupt transition between the thicker epithelium of the placode and the adjacent surface ectoderm, which is not unlike the transition between the future neural retina (NR) and the future pigmented epithelium (PE) (periodic acid–Schiff). (D) As the lens vesicle enlarges, the external opening, or lens pore (arrow), becomes progressively smaller. The lens epithelial cells at the posterior pole of the lens elongate to form the primary lens ﬁbers (L). NR = anlage of the neural retina; PE = anlage of the pigmented epithelium (now a very short cuboidal layer) (magniﬁcation ×221). (E) External view of the lens pore (arrowhead) and its relationship to the maxillary prominence (Mx). (F) Frontal fracture reveals the optic ﬁssure (*) where the two sides of the invaginating optic cup meet. This forms an opening in the cup allowing access to the hyaloid artery (H), which ramiﬁes around the invaginating lens vesicle (L). The former cavity of the optic vesicle is obliterated except in the marginal sinus (S), at the transition between the neural retina (NR) and the pigmented epithelium. E = surface ectoderm. Arrowhead = stalk of separating lens vesicle. (Reprinted with permission from Vet. Comp. Ophthalmol. (1995) 5: 109–123.)

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SMALL ANIMAL OPHTHALMOLOGY

Müller cells also differentiate in the inner neuroblastic layer. The bipolar cells and photoreceptors develop in the outer neuroblastic layer and form the inner and outer nuclear layers in the adult. Retinal dysplasia may result from disorganized development of the neural retina, with formation of rosettes. The retinal pigment epithelium is the determining factor for the differentiation of the layers on each side, namely the retina and the choroid and sclera. Following detachment of the lens vesicle from the surface ectoderm, development of the anterior chamber structures progresses. A specialized population of the neural ectoderm called the neural crest cells migrate between the surface ectoderm and lens vesicle to form the corneal endothelium, which secretes its basement membrane, Descemet’s membrane. Additional neural crest cells form the corneal stroma between the surface epithelium and endothelium. The pupillary membrane and anterior iris stroma develop from neural crest cells migrating onto the anterior surface of the optic cup; persistence or dysplasia of the pupillary membrane results in uveal attachments between the iris and lens and/or cornea (Figs 1.3 & 1.4). Neural crest cells also form the outer two coats of the posterior globe, the choroid (including the tapetum) and sclera.

OCULAR ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY Orbit The orbit in the cat and dog is formed by contributions of the frontal, palatine, lacrimal, maxillary, zygomatic, and presphenoid bones. The bony orbit is incomplete superotemporally, where it is bridged by the dense orbital ligament spanning the frontal process of the zygomatic bone and the zygomatic process of the frontal bone. The lacrimal gland lies superiorly, under this orbital ligament. The orbital contents are covered by a connective tissue layer, the periorbita, which is ﬁrmly attached to the orbital margins rostrally. Seven extraocular muscles innervated by the third, fourth, and sixth cranial nerves

4

Fig. 1.3 Peter’s anomaly in a cat. Note the persistent pupillary membranes attached to the anterior lens capsule with associated anterior subcapsular opacity.

A C D

CLINICAL BASIC SCIENCE

B

Fig. 1.4 Schematic of components of Peter’s anomaly (anterior segment dysgenesis) which result from incomplete or delayed separation of the lens vesicle from the surface ectoderm. (A) Persistent pupillary membranes; (B) corneal opacity with absence of endothelium and Descemet’s membrane; (C) iris hypoplasia; (D) anterior lenticonus and anterior polar cataract associated with anterior capsular defects. (Courtesy of Farid Mogannam.)

control movement of the globe. There is a variable amount of fat between the periorbita and the bony wall and surrounding the extraocular muscles. The zygomatic salivary gland is located inferotemporally, deep to the zygomatic arch, and may be a site of infection or mucocele formation. The wall of the bony orbital wall is thinner medially and may allow extension of infectious or neoplastic processes originating in the nasal cavity or periorbital sinuses. Infectious processes involving the roots of the molar teeth may also extend to involve the orbit. Space-occupying orbital lesions include both inﬂammatory and neoplastic etiologies. Due to the incomplete nature of the bony orbit, both inferiorly and superotemporally, a space-occupying process may become quite advanced before exophthalmos and/or deviation of the globe is noted. Diagnosis and management of such conditions are discussed in subsequent chapters.

Eyelids The eyelids form the initial barrier to mechanical damage to the eye. They also serve to distribute the tear ﬁlm and, through the meibomian glands, provide an oily secretion to slow tear evaporation. The eyelids consist of: 1. An outer layer of thin, pliable skin 2. A small amount of loose connective tissue containing modiﬁed sweat glands and the circumferential ﬁbers of the orbicularis oculi muscle (innervated by branches of the facial nerve) 3. The more rigid ﬁbrous connective tissue of the tarsal plate 4. The radial ﬁbers of the levator palpebrae superioris (innervated by the oculomotor nerve) and Müller’s (sympathetic innervation via branches of the trigeminal nerve) muscles 5. The palpebral conjunctiva containing goblet cells.

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SMALL ANIMAL OPHTHALMOLOGY

Cilia are found on the margin of the upper lid; posterior to these follicles are the openings of the sebaceous (meibomian) glands; these gland oriﬁces are found along the eyelid margin (Figs 1.5 & 1.6). Dysplasia or metaplasia of these glands results in formation of aberrant hair follicles (distichia or ectopic cilia), which may contact the cornea and result in epiphora and, rarely, keratitis. Surgical manipulations of the eyelids require delicate handling to minimize swelling and careful apposition of surgical or traumatic wound margins. Particular attention should be paid to maintenance of a smooth eyelid margin. Closure of full-thickness defects should utilize a two-layer pattern; the tarsal plate has the greatest strength and should be included in the subcutaneous layer.

Lacrimal system The precorneal tear ﬁlm consists of three distinct layers: 1. A mucous layer located closest to the cornea and produced by the conjunctival goblet cells 2. A thick aqueous layer 3. An outer oily layer produced by the meibomian glands of the eyelids. The aqueous portion of the tear ﬁlm is the combined product of the orbital lacrimal gland and a gland located at the base of the third eyelid. The major lacrimal gland is located in the superotemporal area of the orbit beneath the orbital ligament and supraorbital process of the frontal bone; its secretions gain access to the conjunctival sac from numerous small ducts in the superior fornix. The tears are distributed over the surface of the cornea through the action of the eyelids and exit through the nasolacrimal puncta. These two openings are located nasally, superior, and inferior to the medial canthus, just inside the eyelid margin (see Fig. 1.5). The puncta open into two canaliculi joining to form the nasolacrimal duct, which passes through a bony canal in the maxilla to open ventrolaterally in the nasal cavity.

Pupil Dorsal (superior) punctum Medial (nasal) canthus Ventral (inferior) punctum Third eyelid

6

Cilium Limbus Lateral (temporal) canthus Conjunctiva

Iris

Fig. 1.5 External appearance of the canine eye depicting the adnexal structures. With the exception of the pupillary shape, the feline eye is identical.

CLINICAL BASIC SCIENCE

Orbicularis oculi m.

Levator palpebrae superioris m.

Palpebral conjunctiva

Müller’s m. Fornix

Bulbar conjunctiva Tarsal plate Gland of Zeis and Moll

Zonules

Cilium A

Retinal vessels

Meibomian gland

Tapetum Lens

Pupil Optic nerve

Anterior chamber Iris

Myelinated fibers

Iridocorneal angle Ciliary body

Optic disk

B

A Stroma

Endothelium

Epithelium

Descemet’s membrane

B Nerve fiber layer Ganglion cell layer Inner plexiform layer Inner nuclei layer Outer plexiform layer Outer nuclei layer Rods and cones Pigment epithelium Choroid Sclera Fig. 1.6

Inner limiting membrane Ganglion cell Ganglion cell axons forming optic nerve Bipolar cell Outer limiting membrane Nuclei of photoreceptors

Schematic anatomy of the canine and feline eye.

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SMALL ANIMAL OPHTHALMOLOGY

Conjunctiva and third eyelid The conjunctiva is a mucous membrane that covers the globe between the fornix and the cornea, the third eyelid, and the inner surface of the eyelids (see Fig. 1.6). Over the surface of the globe, the conjunctiva blends with Tenon’s capsule, which attaches ﬁrmly to the limbus. The conjunctiva is a highly vascular, delicate tissue containing many mucus-secreting goblet cells. The vascularity and mobility of the conjunctiva can be used to the surgeon’s advantage to act as a graft for corneal defects. The stroma is rich in lymphatics and the conjunctiva is a site of localization of lymphocytes, and provides a reservoir of immunocompetent cells for the globe, playing an important role in the inﬂammatory responses of the avascular cornea. The third eyelid is a mobile, semi-rigid structure located inferonasal to the globe (see Fig. 1.5). It is covered on both palpebral and bulbar surfaces by conjunctiva. The third eyelid owes its rigidity to a T-shaped piece of hyaline cartilage located within its substantia propria. At the base of the cartilage is a seromucoid lacrimal gland that produces approximately one third of the precorneal tear ﬁlm. Poorly deﬁned connective tissue attaches the gland and base of the cartilage to the sclera and periorbita inferiorly. Inadequacy of these attachments with prolapse of the gland occurs not uncommonly, particularly in the American Cocker Spaniel and English Bulldog breeds. Removal of the gland in such cases is contraindicated as it may predispose to future development of keratoconjunctivitis sicca; the gland should be repositioned and ﬁxated as described in Chapter 4 (pp. 88–90).

Cornea

8

The cornea is the transparent, avascular, anterior portion of the outer ﬁbrous coat of the eye (see Fig. 1.6A). The cornea consists of surface epithelium, collagenous stroma, and Descemet’s membrane, which is the basement membrane produced by the inner endothelial monolayer. As the cornea is avascular, its oxygen and nutritional needs are met by diffusion externally from the precorneal tear ﬁlm and internally from the aqueous humor; the peripheral cornea is also oxygenated by the limbal capillary plexus. Corneal transparency is a product of several factors unique to corneal physiology. Relative dehydration of the cornea is maintained by an active Na+-K+ ATPase-associated pump mechanism within the endothelial monolayer. The regular arrangement of the collagen ﬁbrils in the corneal stroma minimizes scattered light and thus enhances transparency. The normal absence of pigment and blood vessels in the stroma is also a requirement for optical transparency. The cornea has remarkable healing capabilities. Simple epithelial defects are covered by a combination of sliding of adjacent cells and mitosis to restore normal architecture. Wounds that extend into the stroma heal ﬁrst by reepithelialization, with a longer period of time required to ﬁll the stromal defect. Corneal scarring is a result of the irregular pattern created by replacement collagen ﬁbrils. Vascularization is expected to accompany any corneal injury or inﬂammatory condition that persists longer than 7–10 days and contributes to the granulation tissue that initially ﬁlls a deep corneal wound. Descemet’s membrane is elastic and tends to resist tearing during an injury. Wounds extending to Descemet’s membrane (descemetocele) and full-thickness lacerations are indications for immediate surgical management. Some regen-

Iris and ciliary body The iris and ciliary body comprise the anterior portion of the middle, vascular coat of the eye, called the uvea (see Fig. 1.6). The iris creates a pupillary opening of variable diameter to adjust the quantity of light that is able to pass through the lens to reach the photosensitive retina. This variable aperture is maintained by the sympathetically supplied radial dilator muscle and the parasympathetically supplied circumferential sphincter muscle. Both muscles are located on the posterior side of the iris, adjacent to the pigmented epithelial layer. The iris anterior to these muscles consists of a loose, vascular connective tissue that is variably pigmented. Full-thickness corneal wounds often seal with prolapsed iris tissue, which must be replaced into the anterior chamber (if viable) or excised. Surgical manipulations of the iris are frequently accompanied by hemorrhage that may complicate postoperative healing. The ciliary body is the posterior continuation of the iris and consists of an anterior portion called the pars plicata (with the ciliary processes) and a posterior portion called the pars plana. The ciliary body is lined by a bilayered epithelium of which only the inner layer is pigmented. Aqueous humor is produced by the ciliary epithelium through a combination of passive ultraﬁltration and active secretion involving carbonic anhydrase. The passive production of aqueous humor is inﬂuenced by mean arterial blood pressure. Inﬂammation of the anterior uvea will result in reduced active aqueous secretion and thus lowered intraocular pressure. The stroma of the ciliary body contains the smooth ﬁbers of the parasympathetically innervated ciliary muscle, which is important in accommodation of the lens for near vision. Aqueous humor circulates from the ciliary processes into the posterior chamber of the eye, through the pupil, to exit via the trabecular meshwork within the iridocorneal angle. During this process, metabolites are exchanged with the avascular lens and cornea. Morphologic or physiologic barriers to aqueous circulation and outﬂow are responsible for elevations in intraocular pressure (glaucoma).

CLINICAL BASIC SCIENCE

erative properties are attributed to the canine endothelium, fewer to the feline.

Lens The lens is a transparent, biconvex structure anchored equatorially to the ciliary body by collagenous zonular ﬁbers (see Fig. 1.6). Contraction of the ciliary muscle alters the degree of curvature of the lens, thereby changing its optical power. The lens is surrounded by an outer capsule; deep to the anterior portion of the capsule is a monolayer of cuboidal epithelium. These epithelial cells are metabolically active and undergo mitosis throughout life. As the cells multiply they migrate to the equator of the lens where they elongate and gradually lose their nucleus and other organelles to form the lens ﬁbers. These ﬁbers are added in a circumferential arrangement so that older ﬁbers are within the deeper portion of the lens. The ﬁber ends meet anteriorly at the upright Y suture and posteriorly at the inverted Y suture. The anterior epithelial cells utilize glucose, which diffuses into the lens from the circulating aqueous humor and is broken down anaerobically to lactic acid.

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SMALL ANIMAL OPHTHALMOLOGY

Saturation of the normal pathways for glucose metabolism occurs in diabetes mellitus and results in accumulation of sorbitol within the lens. Sorbitol accumulation causes the lens to imbibe water by osmosis, which leads to the formation of a clinically observable cataract that usually progresses rapidly.

Retina The retina (see Fig. 1.6) is a complex photosensory structure consisting of ten layers: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Pigment epithelium Photoreceptors (rod and cone outer segments) External limiting membrane (Müller cell processes) Outer nuclear layer (photoreceptor nuclei) Outer plexiform layer Inner nuclear layer (nuclei of Müller; amacrine, horizontal, and bipolar cells) Inner plexiform layer Ganglion cell layer Nerve ﬁber layer (axons of ganglion cells) Inner limiting membrane (Müller cell processes).

The principal neuronal connections of the retina involve the photoreceptors, which synapse with the bipolar cells that then synapse with the ganglion cells in the inner plexiform layer. The axons of the ganglion cells form the nerve ﬁber layer and join to make up the optic nerve at the posterior pole. The amacrine and horizontal cells form internal connections between bipolar cells and may thus exert a regulatory inﬂuence. Müller cells are a non-neuronal constituent that forms a supporting matrix and the barriers of the inner and outer limiting membranes. Inherited retinal degenerative processes and sudden acquired retinal degeneration (SARD) initially involve the photoreceptors, either rods or cones, or both. With time the condition usually progresses to involve the other retinal layers, and diffuse thinning and blindness results.

Tapetum The tapetum is a modiﬁcation of the choroid located deep to the pigment epithelium and choriocapillaris. It is composed of a highly organized arrangement of cells containing zinc and riboﬂavin, which results in a reﬂective appearance. The color of the tapetum ranges from green to blue to yellow and varies with the species, breed, and age. Thinning of the overlying retina (as occurs in retinal degeneration) results in a hyper-reﬂective appearance of the tapetum.

Optic nerve and central visual pathways

10

The optic nerve consists of combined axons of the ganglion cells and is surrounded by all three meningeal layers of the central nervous system. The optic disk is the origin of the optic nerve within the globe; its irregular triangular appearance in the dog is a result of the variable quantity of myelin surrounding the nerve ﬁbers of the optic disk (see Fig. 1.6). The optic nerve exits the orbit at the optic foramen. The right and left optic nerves meet at the optic chiasm, located rostral to the pituitary gland. In cats and dogs, the majority (65–75%)

Visual fields:

L

R

L

CLINICAL BASIC SCIENCE

of nerve ﬁbers cross in the chiasm to travel as the optic tracts to the contralateral lateral geniculate nucleus. This decussation is responsible for coordinated bilateral vision as well as the occurrence of a consensual pupillary light reﬂex (Fig. 1.7). The majority of axons in the optic tracts terminate in the lateral geniculate nucleus, synapsing on neurons whose axons form the optic radiations and terminate in the occipital cortex. This pathway is responsible for conscious visual perception. The remaining optic tract axons bypass the lateral geniculate nucleus and terminate in the rostral colliculus of the pretectal area. Parasympathetic axons originating here synapse in the oculomotor nucleus of the midbrain, origin of the oculomotor nerves, whose axons synapse in the ciliary ganglion prior to entering the globe as the short ciliary nerves to the pupillary sphincter muscles. This pathway is responsible for the direct and consensual pupillary light responses. The cat has two short ciliary nerves whereas the dog has several.

R Constrictor

Retina

Dilator Optic nn.

Ciliary ganglion Optic tract Oculomotor nerve Lateral geniculate nucleus

Chiasm Forebrain

Midbrain Oculomotor nucleus

Cervical spinal cord

Optic tract

Middle ear

Cranial cervical ganglion

Cervical sympathetic trunk

Thoracic spinal cord T1–T3

Fig. 1.7

Pupillary reﬂex pathways.

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SMALL ANIMAL OPHTHALMOLOGY

Sympathetic control of the pupillary dilator muscle originates in the hypothalamus, the axons from which synapse with preganglionic neurons in the ﬁrst three or four segments of the thoracic spinal cord. These axons join the sympathetic trunk terminating in the cranial cervical ganglion. Postganglionic ﬁbers travel to the eye after crossing the roof of the middle ear cavity and are distributed to the ciliary muscle, pupillary dilator, third eyelid, and the Müller’s muscle of the upper lid. Compromise of sympathetic innervation to the globe and adnexa results in the classic signs of Horner’s syndrome: ptosis (drooping of the upper lid), miosis (pupillary constriction), and protrusion of the third eyelid.

OCULAR PATHOLOGY The systematic examination of surgical and necropsy-obtained ocular tissue is essential for optimal patient management, the career-long educational process, and enhancing understanding of ocular disease in animals. Maximal beneﬁt is obtained from optimally ﬁxed tissues; in almost all cases, immersion ﬁxation in 10% formalin is adequate. Fixation should be expedient as the retina, especially, undergoes rapid autolysis; trimming of periocular tissues enhances penetration of ﬁxatives, and injection of 0.5 ml of the ﬁxative into the vitreous cavity with a 27-gauge needle at the equator will minimize neurosensory retinal separation artifact. Otherwise, submit globes intact so that the pathologist can appreciate the intertissue relationships. Use adequate volumes of ﬁxative (at least 100 ml for dog and cat eyes), and allow 72 h for ﬁxation to occur.

Ocular response to disease A detailed discussion of ocular pathology would ﬁll a text of its own; principles and concepts of importance to clinicians are discussed with particular disease processes throughout the following chapters. Three related features warrant note: 1. The propensity of the ocular tissues (especially the epithelium of lens, uvea, and retina, but also the corneal endothelium and uveal vasculature) to undergo reactive changes of hypertrophy, hyperplasia, and metaplasia (in the case of feline ocular sarcomas, perhaps neoplasia as well) 2. In contrast to the above, the fact that many of the specialized ocular tissues are post-mitotic, with limited regenerative potential 3. Because of the dependence of the ocular tissues on tissue transparency and intertissue relationships for normal function, the devastating effect that these changes can have on vision. A focus of hepatitis may resolve with scarring and minimal, if any, functional signiﬁcance, while a comparable process in the eye may lead to blindness.

12

Fibroplasia in the cornea, for example, will result in scarring and opaciﬁcation. In the anterior chamber, peripheral anterior and posterior synechia and membranes are associated with secondary glaucoma. Iris neovascularization, also known as rubeosis irides or pre-iridal ﬁbrovascular membrane, is a common cause of intraocular hemorrhage and secondary angle closure glaucoma.

CLINICAL BASIC SCIENCE

Hypertrophy, hyperplasia, and metaplasia of lens epithelium are an integral part of cataractogenesis, and the bane of the cataract surgeon who has to deal with postoperative capsular ﬁbrosis. Vitreous detachment, ﬁbrosis, and neovascularization lead to cyclitic membranes and their dire consequences of retinal detachment and phthisis bulbi. The clinical ophthalmologist wages a relentless pharmacologic battle against these processes with anti-inﬂammatories and antimetabolites, and new approaches will likely play an important role in the future management of ocular disease.

13

SMALL ANIMAL OPHTHALMOLOGY

Diagnostics Serge G. Rosolen, Domenico Multari, Mike Woods and Olivier Jongh

INTRODUCTION

2

The ophthalmic examination, combined with history and signalment, provides the foundation for obtaining an accurate diagnosis. Ophthalmic diagnosis is achieved by a combination of basic knowledge, the mastering of simple instrumentation, and critical observation. The former includes an understanding of anatomy, physiology, and disease mechanisms. Instrumentation facilitates critical observation. Basic equipment and simple techniques, including a magnifying loupe, bright focal illumination, Schirmer tear test strips, diagnostic dyes, cytology, direct ophthalmoscopy, and Schiøtz tonometry should be readily available in any practice, and in experienced hands will be adequate to manage the great majority of ophthalmic cases. More expensive and sophisticated instrumentation and technologies, including the slit-lamp biomicroscope, indirect ophthalmoscope, applanation tonometry, electrophysiology, gonioscopy, ultrasonography, and other imaging modalities, ﬂuorescein angiography, keratoscopy, and retinoscopy represent the next level of diagnostics and are available to specialists or to those with a particular interest in the ﬁeld. A systematic approach to examination should be followed and modiﬁed for each individual case based upon the history and signs. Technical competency in diagnostics is achieved simply by practice; making an ophthalmic examination a part of every routine physical examination will hone skills for the occasion upon which they are more urgently required.

INSTRUMENTS AND BASIC DIAGNOSTIC TECHNIQUES Magnifying loupe A binocular magnifying loupe of ×2 to ×4 magniﬁcation and a focal length of 15–25 cm is useful not only for diagnostics but also for surgery; it allows freedom of both hands for manipulation and a loupe-mounted diffuse illuminator facilitates observation.

Focal illumination 14

A transilluminator provides an excellent light source for external eye examination and to evaluate the pupillary light reﬂexes (PLRs). For the latter, it is

Schirmer tear test (STT)

DIAGNOSTICS

important to use a narrow beam of bright light with a constant source of energy (such as a rechargeable handle) directed toward the posterior pole. One of the most common causes of abnormal PLRs is a dim light source.

This test is used quantitatively to evaluate the aqueous component of the tear ﬁlm and thus aid in the diagnosis of keratoconjunctivitis sicca (KCS). The STT is indicated in all patients with external ocular disease. Individually wrapped sterile ﬁlter paper test strips may be dye impregnated to facilitate reading; these strips are typically 5 mm wide and 50 mm in length. If performing a STT, it should be undertaken before any other procedures or tests; if there is discharge in or around the eye, dry cotton swabs should be used gently to clean the area, avoiding irritation and reﬂex lacrimation. The strips have a notch near one end where they are folded prior to use; fold the strip without touching it with ﬁngers while it is still in the overwrap. Then open the package and, grasping the strip from the end opposite the notch with ﬁngers or forceps, place it into the lower conjunctival sac approximately midway between the medial and lateral canthus with the short folded end in the fornix and the notch on the eyelid margin (Fig. 2.1). The lower lid can be rolled outward with the thumb to facilitate insertion, but care should be applied not to compress the eye, which may likewise elicit reﬂex lacrimation. The lids may be maintained in an open position, or closed by gentle pressure on the upper lid if blinking and retention of the strip becomes a problem. After 1 min, the moistened distance from the notch in the longer part is measured. Normal values in the dog are 15–25 mm/min; values lower than 10 mm/min are suggestive of a deﬁcit in aqueous tear production. Most clinical cases of KCS have a wetting of less than 5 mm; cats have slightly lower and more variable normal values. There is a wide range of normal readings, and results should be interpreted in association with clinical signs. Increased aqueous tear production may occur if conditions causing ocular irritation are present.

Fig. 2.1

Schirmer tear test being performed in a feline patient.

15

SMALL ANIMAL OPHTHALMOLOGY

Diagnostic stains Fluorescein stain Fluorescein is a water-soluble dye; owing to its lipid insolubility, it does not penetrate intact corneal epithelium. Epithelial erosions or ulcers, which expose the hydrophilic stroma, allow penetration and retention of the dye. The barrier to penetration in the healthy eye resides in the outermost cells of the corneal epithelium. As Descemet’s membrane does not retain ﬂuorescein, descemetoceles will not stain. Fluorescein is available as impregnated paper strips or as a solution; the solution may become contaminated with multiple usage, and individually wrapped strips are preferred. Fluorescein staining is indicated in all patients with ocular pain or observable corneal lesions. The tip of the ﬂuorescein-impregnated strip is moistened with a drop of sterile saline and gently applied to the superior bulbar conjunctiva. If the patient exhibits severe blepharospasm, local anesthetic can be instilled but may result in a mild diffuse positivity that is usually readily discernible from signiﬁcant retention. Blinking will distribute the dye over the corneal surface. The excess dye is immediately ﬂushed with a sterile saline rinse and the eye is then examined with a focal light and magniﬁcation (Fig. 2.2). A cobalt blue ﬁlter will facilitate detection of subtle lesions. To evaluate nasolacrimal patency, apply the ﬂuorescein as described above, but do not rinse the eye. If the ipsilateral nostril shows dye within 5 to 10 min, the nasolacrimal drainage system on that side is patent; the absence of dye passage, however, does not necessarily mean the contrary, and negative passage is followed by cannulation and irrigation. Dye may be seen in the nasopharynx related to alternative duct openings. Biomicroscopic observation of the ﬂuorescein-stained tear ﬁlm while holding the lids open enables evaluation of the tear break-up time (BUT) as an indirect method of evaluating the non-aqueous components of the tear ﬁlm; mucus deﬁciency will result in shortening of the BUT from the 20–30 s normally encountered.

Rose bengal and lissamine green These dyes stain cells of the cornea and conjunctiva that are not covered by mucin; usually these are degenerating cells. The stains are taken up by neoplastic cells as well and may be useful in deﬁning the extent of epithelial neo-

16

Fig. 2.2 Fluorescein uptake by the corneal stroma associated with a boxer ulcer.

DIAGNOSTICS

plasia of the cornea and conjunctiva. The dyes are available as solutions or impregnated strips; as with ﬂuorescein, the latter are preferred. Rose bengal may cause irritation upon instillation and persists somewhat longer than ﬂuorescein. It is useful in highlighting dendritic intraepithelial erosions caused by herpesvirus, which may be difﬁcult to detect with ﬂuorescein, and in the diagnosis of tear ﬁlm abnormalities involving the lipid or mucin components of the tear ﬁlm (Fig. 2.3). Application techniques are identical to those described for ﬂuorescein.

Cytology, culture, and additional diagnostic procedures Cytologic examination is increasingly utilized in small animal ophthalmology; over the last decades, it has emerged as a reliable tool in facilitating diagnosis in a minimally invasive way. Techniques of sampling of a smear are outlined for each of the ocular structures. On the other hand, the microscopic interpretation of a smear is beyond the scope of this chapter. Routine dermatologic techniques can be utilized to obtain scrapings from the eyelid skin for parasitic and fungal detection. Fine needle aspiration may prove useful for characterizing proliferative lesions (by using a 23-G needle and a 5 ml syringe). Impression smears can be obtained from ulcerated lesions (Figs 2.4 & 2.5), notably in cats with suspected squamous cell carcinoma. If necessary, biopsy of skin lesions is performed to evaluate tissue architecture with histopathology. Conjunctival cytologic evaluation is useful: 1. In the differential diagnosis of acute conjunctivitis (the cellular response associated with speciﬁc conjunctivitis is helpful when performed early in inﬂamed conjunctivas, and Gram stain can provide guidelines for antibiotic selection) 2. In the identiﬁcation of inclusion bodies (chlamydial, mycoplasma, canine distemper, and leishmania inclusions) 3. To facilitate the diagnosis of conjunctival tumors including lymphosarcoma, mast cell tumor, melanoma, and squamous cell carcinoma.

Fig. 2.3 Rose bengal positivity in a punctate pattern was evident in this 6-year-old Shih Tzu with a vascularized cornea due to keratoconjunctivitis sicca.

17

SMALL ANIMAL OPHTHALMOLOGY Fig. 2.4 A middle-aged mixed breed presented with ulcerated lesions of both eyelids.

Fig. 2.5 Impression smears obtained from these ulcerated lesions revealed a neoplastic population formed by lymphoid cells (Giemsa, original magniﬁcation ×400). Mycosis fungoides was conﬁrmed with partial-thickness biopsy of the eyelid lesions.

18

Cells from the conjunctival surface may be harvested using a sterilized spatula (i.e. Kimura spatula), the blunt end of a sterile surgical blade, or a small nylon cytology brush; moist sterile cotton swabs are less likely to capture as many cells. Sterile swabs may be utilized for culture of potentially pathogenic microorganisms (bacterial and fungal), and a cytology brush is preferred for the detection of the presence of herpesvirus, calicivirus, or Chlamydia (Chlamydophila) by polymerase chain reaction (PCR). Unﬁxed and unstained slides may be submitted for immunoﬂuorescent antibody (IFA) studies. The scraping should be made from the area most severely involved. A topical anesthetic may not be necessary in most cases if the animal’s head is ﬁrmly restrained, but greatly facilitates the procedure and is unlikely to affect culture results. Mucus and exudate are removed prior to scraping. It requires gentle but ﬁrm manipulation to collect an adequate sample (the conjunctiva should blanch but should not bleed). Collected cells are immediately transferred to a glass microscope slide; gentle spreading will avoid fracturing nuclear

Fig. 2.6 Aspiration of aqueous humor with a 25-G hypodermic needle in a cat.

DIAGNOSTICS

membranes. The material is air dried and ﬁxed and can be stained with the routine stains of value such as Giemsa, Gram, or Wright’s. Corneal cytology is often a rewarding diagnostic method for characterization of exudative lesions (keratomalacia, keratomycosis) and may aid in the differentiation of proliferative lesions (eosinophilic keratitis or nodular episclerokeratitis). Topical anesthesia is usually applied prior to obtaining the sample. Care must be taken not to rupture deep ulcers with pressure. Special stains for fungi (periodic acid–Schiff) may be useful. Cells can also be harvested by using a cellulose strip that is gently applied on the corneal surface (‘impression cytology’). Aspiration of aqueous humor may be undertaken with topical or general anesthesia, with a 25–27-G hypodermic needle, inserted just anterior to the limbus, bevel up and parallel to the iris surface (Fig. 2.6). Approximately 0.1–0.2 ml of ﬂuid can be collected and is generally safe; remove the barrel from the tuberculin syringe and allow the ﬂuid to collect by pressure differential rather than aspiration. Centrifugal cytology (‘cytospin’) is particularly well suited for the preparation of small sample volumes and dilute cell suspensions. Aqueous humor cytology may allow distinction between nongranulomatous and granulomatous uveitis, and protein-laden macrophages are encountered with phacolytic or phacoclastic uveitis. Lymphosarcoma and feline melanoma cells may exfoliate into the aqueous; if cells are seen with the biomicroscope, aqueocentesis with cytology may conﬁrm the diagnosis. Aqueous humor samples can also be collected for culture, PCR, and antibody level determination. Tumors of the anterior uvea are candidates for trans-corneal ﬁne needle aspiration, best performed by those familiar with the technique. Aspiration is accomplished as described above for aqueous humor as a microsurgical procedure with the needle positioned over the tumor and an attempt made to aspirate surface cells. Alternatively the needle may be directed into the tumor. Technical challenges include obtaining an adequate sample and interpretation may be problematic. Potential complications of hemorrhage, lens trauma, and tumor seeding temper the decision to pursue this modality.

19

SMALL ANIMAL OPHTHALMOLOGY

20

Cytology of vitreous or sub-retinal ﬂuid is indicated for both diagnostic and therapeutic reasons, the former where other diagnostic options have been exhausted, the latter for intravitreal pharmacologic cycloablation or in the management of retinal detachments by pneumatic retinopexy. The procedure is performed transsclerally, usually with general anesthesia and a 25-G needle. For vitreous aspiration, the needle penetrates the eye 5–6 mm posterior to the limbus (entering through the pars plana but avoiding the lens) and is directed toward the posterior pole; a volume of 0.5 ml liqueﬁed vitreous can be aspirated. For withdrawal of subretinal ﬂuid, the needle is gently introduced through the sclera overlying the bullous retinal detachment. Assessment of orbital disorders using ﬁne needle (23 or 24 G) aspiration remains a reliable method that can facilitate diagnosis for the clinician, provided that localization of the lesion allows for accurate sampling. Exophthalmos results from a space-occupying lesion in the orbit (benign or malignant neoplasm, orbital inﬂammation, cystic disease). Palpation, imaging, and the direction of globe displacement may be used to determine the site of the orbital lesion. Ultrasound guidance provides optimal assurance of a representative sample. Several routes for ﬁne needle aspiration biopsy are available, dependent upon location: through the eyelids, conjunctiva, the mucosa caudal to the last upper molar, or, in the case of posterior orbital lesions, transdermally at the posterior junction of the orbital ligament and zygomatic arch (Fig. 2.7).

Fig. 2.7 Fine needle aspiration biopsy through the mucosa caudal to the last upper molar in a dog.

To evaluate the structure and function of the lacrimal puncta, lacrimal canaliculi, lacrimal sac, and nasolacrimal duct, topical anesthesia, sedation, or general anesthesia may be required in dogs, dependent on the nature of the patient. In cats, general anesthesia is usually required; the lacrimal puncta are smaller and less accessible. A curved stainless steel lacrimal cannula may be utilized; 22–23 G works well in dogs, 26 G in cats. Its rigidity allows the operator easily to identify and enter the opening of the nasolacrimal duct in the lacrimal bone after having entered the lower punctum and nasolacrimal sac. The disadvantage of a rigid cannula is that of possible damage to the mucous membranes if the animal is not adequately restrained and anesthetized, or if the procedure is not performed gently; alternatively a Teﬂon intravenous catheter works almost as well. The cannula should be mounted on a 2.5–3.0 ml syringe ﬁlled with sterile saline, or a small saline-ﬁlled compressible bottle. The cannula is inserted into the upper punctum, located 4–5 mm from the medial canthus, stretching the upper lid superiorly with the index ﬁnger to immobilize and straighten the canaliculus and facilitate cannula penetration. After the lacrimal punctum is entered, the system is ﬂushed; saline will exit from the lower punctum. Smooth movements are then used to pass through the lacrimal sac and locate and enter the opening of the nasolacrimal duct. At this point, the lower punctum is closed with ﬁnger pressure on the adjacent lid. The nasolacrimal duct is ﬂushed and keeping the nose of the animal angled downward, the ﬂuid should ﬂow from the ipsilateral nostril. Cannulation with monoﬁlament nylon suture can be used to localize and attempt to dislodge obstructions. Radiographs can be helpful in diagnosing nasolacrimal cysts or obstructions occurring secondary to sinus disorders. Contrast media may be injected through the upper puncta (dacryocystorhinography) to localize obstructive lesions.

DIAGNOSTICS

Evaluation of the lacrimal drainage system

Direct ophthalmoscopy The ophthalmoscope has a light source which is directed into the patient’s eye so that the beam is nearly parallel with the line of sight of the examiner. A rheostat controls the light intensity while the dimension and the characteristics of the beam may be varied with a series of colored ﬁlters (blue to excite ﬂuorescein, green to help differentiate pigment from retinal hemorrhage), a slit (to help evaluate the elevation of lesions), and a grid (to project onto the fundus in order to measure lesions). A selection of lenses ranging from + (black) 40 D to – (red) 25 D (diopters) is assembled on a rotating wheel which adjusts the depth of focus into the eye (Table 2.1). Thorough examination of the fundus of the eye can be performed only in a dark room through a well-dilated pupil; 1–2 drops of 1% tropicamide should be applied 15–20 min prior to examination. Observation with a setting of around 0 to +1 or +2 D and the instrument held 30–60 cm from the eye allows critical evaluation of the fundus reﬂex. The fundus is then observed from a distance of 2–5 cm and starting with a setting of 0, altered to achieve optimal focus. Direct ophthalmoscopy provides magniﬁcation of fundic features by 14 to 15 times. The disk is located and evaluated initially, the major vessels are traced to the periphery, and each quadrant is evaluated systematically to obtain a mental panorama. The main disadvantages of direct compared with indirect

21

SMALL ANIMAL OPHTHALMOLOGY

examination are the small ﬁeld of vision, limited to about 4–5 mm of the fundus, and the risks due to the close proximity to the muzzle of uncooperative patients! There are notable intra- and inter-species differences in the ophthalmoscopic anatomy of the fundus including color and extent of the tapetum, intensity of retinal pigment epithelium (RPE) pigment in the non-tapetum, degree of myelination of the optic disk, location of the disk in relation to the tapetal/nontapetal junction, and vascular patterns (Fig. 2.8).

Hand lens monocular indirect ophthalmoscopy The most economical way to perform indirect ophthalmoscopy is by using a 14–30 D hand-held lens and a focal light source such as the Finoff transillumiTable 2.1 Ophthalmoscope settings for examination of normal canine eyes.

22

Structure

Ophthalmoscope settings (diopters)

Cornea

+15 to +20

Iris

+12 to +15

Anterior capsule of lens

+12 to +15

Posterior capsule of lens

+8 to +12

Vitreous

+2 to +8

Optic disk and fundus

+2 to −2

A

Fig. 2.8 Variations in normal fundus appearance. (A) The fundus of a sandcoated retriever with a richly myelinated optic disk.

DIAGNOSTICS

B

C

Fig. 2.8 Variations in normal fundus appearance. (B) An Australian Shepherd fundus: the tapetum is aplastic, which allows visualization of the underlying choroidal vessels and sclera. (C) This Siamese cat fundus exempliﬁes the non-myelinated optic disk characteristic of felines. There is absence of pigment in the non-tapetal retinal pigment epithelium and choroid to reveal the radial choroidal vasculature.

nator. Relatively inexpensive glass Nikon or Volk lenses or even less inexpensive +10 to +20 magnifying lenses, 30–55 mm in diameter, can be utilized. After dilatation of the pupil and in a dark room, the observer should stand in front of the animal at arm’s length, holding the transilluminator in front of the observer’s own nose and the lens 5–6 cm in front of the patient’s cornea (an assistant is required to restrain the patient’s head and retract the lids). The fundus image is made to ﬁll the entire lens by moving the lens toward or away from the cornea.

23

SMALL ANIMAL OPHTHALMOLOGY

24

Indentation tonometry Tonometry is the assessment of intraocular pressure (IOP). Digital tonometry is a very crude technique; two-ﬁnger ballottement of the globe through the upper lids can detect a discrepancy between the two eyes, but should not be used without additional objective measurement. Instrumental tonometry may be performed by indentation or applanation methods. Indentation tonometry is based on the measurement of the extent of indentation of the cornea obtained with a Schiøtz tonometer. It is a relatively inexpensive instrument which consists of a plunger that glides through a cylindrical chamber stabilized by a bracket handle, and a footplate that conforms with and is placed on the anesthetized corneal surface. The plunger can be charged with different weights (5.5 g, 7.5 g, 10.0 g). The depth of indentation is reﬂected by movement of a lever, which allows a scale reading to be converted to an estimation of IOP. Theoretically, the curvature and rigidity of the human cornea differ from those of the small animal cornea, so species-speciﬁc conversion tables are required for optimal quantitative accuracy; practically, indentation tonometry only estimates IOP and it is not critical whether the table with human data that comes with the instrument or a veterinary scale is used. Normal values should be less than 25 mmHg. As a rule of thumb, with the 5.5 g weight, scale values between 3 and 7 on the Schiøtz scale represent normal pressure in the dog; normal values in the cat are 2–6. Readings of less than 2–3 suggest an elevated IOP and those greater than 7 a hypotensive eye. Size of the eye (smaller eyes give values higher than actual IOP), age-related differences in scleral rigidity (young eyes are more elastic and give higher values as well), and corneal lesions (edematous corneas will indent more, scarred corneas less) can affect accuracy of results. Before each patient evaluation, the instrument should be calibrated on the convex steel test block; the indicator should read 0. The patient is given a few drops of topical anesthetic and the instrument is applied to the eye. Because the plunger is gravity driven, it is essential that the tonometer be held as close to perpendicular as possible and that its components are well cleaned and free moving. The footplate is applied to the cornea, positioning the head of the dog by elevating the nose toward the ceiling. It is important not to occlude the jugular veins in order not to artifactually increase the IOP, or to compress the globe while retracting the eyelids, for the same reason. Occasionally it is easier to restrain the dog on its back, with the head held perpendicular to the body axis with the cornea in the horizontal plane. The measurement should be repeated several times in order to obtain three readings within 1–2 scale units of each other. The instrument should be placed as centrally as possible on the corneal surface, as the sclera has a different rigidity. The curved surface of the footplate should be in perfect and complete contact with the cornea. No force should be applied on the handle, which should be held gently to allow the instrument to rest freely on the corneal surface. Readings should be regarded as estimations of IOP rather than precise determinations. The main disadvantage is that the technique is demanding and requires practice to master. Suggestions for reliable use include: • Calibrate the tonometer before each use • Ensure that the cornea is well anesthetized; most systemic anesthetics and sedatives alter blood pressure and thus IOP, and are ideally avoided

DIAGNOSTICS

• Do not compress the jugular veins or the globe • Keep the cornea horizontal, the tonometer vertical and in the center of the cornea; avoid the limbus and the sclera as well as the third eyelid (you can slip the footplate beneath the third eyelid if it protrudes) • Make several measurements (3–5) • Always evaluate both eyes • Interpret readings in conjunction with other clinical signs • After each use, disassemble and clean the instrument • Make tonometry a part of your routine physical/ophthalmic examination to build conﬁdence in your technique.

ADVANCED DIAGNOSTICS To appreciate fully the anatomic details and pathologic changes of the eye, special examination techniques and more sophisticated equipment may be necessary to reﬁne preliminary observation and pursue differential diagnoses.

Slit-lamp biomicroscope The slit-lamp biomicroscope allows deﬁnition and precise localization of lesions within the adnexa, cornea, anterior chamber, lens, anterior vitreous and, using an interposed biconvex lens, the posterior segment. These structures can be examined with high magniﬁcation; the beam of light can be controlled to appear diffuse, pinpoint (to detect subtle ﬂare and cells), or a slit, and may be colored by inserting various ﬁlters. Observations of reﬂected and/or transmitted light provide a magniﬁed three-dimensional view of the various ocular structures.

Indirect ophthalmoscope The monocular hand lens method, already described, can be replaced by a more sophisticated and expensive instrument, the binocular indirect ophthalmoscope, which emits a bright light from a unit on the examiner’s head that is directed into the eye of the animal; the emergent rays are converged by a 14– 30 D biconvex condensing lens placed in the same fashion as described for monocular indirect ophthalmoscopy. The image is inverted and magniﬁed less than with direct ophthalmoscopy, dependent upon the dioptric power of the lens utilized. The indirect ophthalmoscope has three major advantages: both hands can be used to manipulate the patient’s head and eyelids while the examiner is at arm’s length from the animal; it is possible to obtain a panoramic (although inverted) view of the ocular fundus; and bright illumination can penetrate translucent ocular media. The technique is easily mastered with practice.

Applanation tonometry In contrast to Schiøtz indentation tonometry, applanation tonometry enables measurement of the variable force necessary to ﬂatten a constant small area of the cornea. The ‘Tono Pen’® and the ‘Tono Vet’® are hand-held tonometers with several advantages over the Schiøtz tonometer, but are much more expensive. Readings are not as subject to the inﬂuences of rigidity and other tissue characteristics as with indentation tonometry although readings are sensitive

25

SMALL ANIMAL OPHTHALMOLOGY

to artifacts induced by manual lid retraction, which yields spuriously high measurements.With the ‘Tono Pen’®, the stainless probe contains a solid-state strain gauge which converts intraocular pressure to an electrical signal. Every touch on the anesthetized cornea produces a waveform that is translated into a number on the digital display indicating the IOP expressed in mmHg. Every four valid readings the device sounds a prolonged beep and the mean IOP is displayed. The tip of the instrument has to be covered with a disposable latex protective membrane to ensure sterility and prevent exposure to the preocular ﬂuids. The device is light and ﬁts comfortably in the user’s hand and can be used regardless of the position of the animal’s cornea, so minimal restraint is needed.

Gonioscopy The iridocorneal angle and outﬂow pathways are not directly visible without using a refractory lens placed on the corneal surface. In most cases, gonioscopy can be performed with topical anesthesia. Many different lenses are used in small animal ophthalmology, with the Franklin, Barkan, and Koeppe lenses the most popular direct goniolenses; an indirect (mirror) lens facilitates 360° examination simply by rotation of the lens. The interface between lens and cornea is maintained with saline or 1.0% methylcellulose solutions. A coaxial light source and some magniﬁcation are needed for optimal observation (the biomicroscope is ideal); an otoscope can be satisfactorily used. The technique is indicated to evaluate glaucoma patients; when the glaucoma is unilateral, the presence of goniodysgenesis in the contralateral eye is an important risk factor, as well as suggesting the pathogenesis of the glaucoma in the involved eye. Cross-sectional and gonioscopic anatomy of the outﬂow pathway is depicted in Figure 2.9. Parameters of interpretation are summarized in Table 2.2.

Retinoscopy Retinoscopy, also called skiascopy, is a technique by which the refractive state of the eye can be determined objectively by observing characteristic light reﬂections that are created by illuminating the retina with a band or circular beam of light emitted from the retinoscope. The nature of these reﬂexes and how they are inﬂuenced both by the properties of incoming light and by refractive lenses placed between the eye and the retinoscope indicates the refractive power of the eye. This technique has been used to deﬁne the normal, pathologic, and surgically induced refractive state of the eye in dogs. It is necessary to provide basic deﬁnitions of refractive properties of the eye and refraction.

26

• Emmetropia is an eye without refractive error where the plus power of the cornea and lens refracts light to a point source on the plane of the retina. • Ametropia is an eye with a refractive error, generally from variations in axial length of the eye, astigmatism, or a shift in position or absence of the crystalline lens. • Myopia is ametropia due to relatively excessive refractive power, generally due to a longer than normal axial length; images are formed in front of the plane of the retina.

DIAGNOSTICS

A

c svp pl

tm

cc

i

cbol

cbil

B

a b c d

e

f

g

a. Corneal dome b. Superficial band of pigment zone – varies in density c. Deep band of pigment zone d. Individual fibers of the pectinate ligament e. Ciliary cleft (space of Fontana) containing the uveal trabecular meshwork f. Iris g. Pupil

Fig. 2.9 Anatomy of the outﬂow pathways is depicted schematically in cross-section in (A) and gonioscopically in (B). The normal gonioscopic appearance of the canine (C) and feline (D) outﬂow pathway is shown. Key for (A): c: cornea; i: iris; pl: pectinate ligment; cc: ciliary cleft containing uveal trabecular meshwork; cbil: inner leaﬂet of ciliary body; cbol: outer leaﬂet of ciliary body; tm: scleral trabecular meshwork; svp: scleral venous plexus. (Courtesy of R.L. Peiffer.)

• Hyperopia is a refractive error caused by relatively inadequate refractive power, generally due to a shorter than normal axial length; images are formed behind the plane of the retina. • Astigmatism is an eye with aspherical ametropia caused when the refractive surfaces of the eye have different radii of curvature in different meridians, generally caused by differences in corneal curvature, such that an eye has two focal points. • A meridian is an imaginary line on the surface of a spherical body; a corneal meridian is a line formed by the intersection with the corneal surface of an anteroposterior plane passing through the apex of the cornea and can be horizontal or vertical.

27

SMALL ANIMAL OPHTHALMOLOGY C

D

Fig. 2.9 For caption see previous.

• Refraction is the bending of light rays; minus lenses (concave) diverge light rays and plus lenses (convex) converge light rays. • Diopters are a measure of lens power, deﬁned by the inverse of the focal length in meters. • Optical inﬁnity is any distance greater than 6 m.

28

A retinoscope is characterized by a light projection system and an examiner observation system. The projection system has a bulb that projects a linear band or streak of light into the patient’s eye. The observation system is an aperture that allows the examiner to view emergent light rays from the eye. When performing retinoscopy, refracting lenses from a trial lens may be used;

Scheme for classiﬁcation of gonioscopic observations.

Iridocorneal angle • Open (approximately 2 mm)

DIAGNOSTICS

Table 2.2

• Narrow • Closed (pectinate ligament, ciliary cleft, inner and outer pigment zones not visible with iris root in contact with peripheral cornea) Pectinate ligament • Normal • Goniodysgenesis (pectinate ﬁbers shortened/thickened to imperforate; ﬂow holes reduced in number and size; anterior insertion displaced axially) Ciliary cleft and trabecular meshwork • Normal • Compressed • Collapsed (iris root apposed to inner pigment zone; pectinate ligament not visible) • Obstructed (with inﬂammatory or neoplastic inﬁltrates)

veterinary patients are generally refracted with a skiascopy bar or rack, which contains a series of spherical plus and minus lenses in increments of 0.5 D to 1.0 D. The optimal distance to perform retinoscopy is 66 cm between the patient’s and observer’s eyes; at this distance it is necessary to use a (+)1.5 D working lens to optimize neutralization of the emergent light rays. Emerging light rays reﬂecting from an illuminated retina leave an emmetropic eye as parallel rays, from a myopic eye as converging rays with a reﬂex moving opposite to or against the motion of the streak, and from a hyperopic eye as diverging rays with a reﬂex moving with the motion of the streak. Some reports have documented a tendency for the canine population mean toward a slight hyperopia, especially for large breeds, while other reports suggest a tendency toward slight myopia, especially for small- and medium-size dogs.1,2

Computerized topography of the cornea (keratoscopy) This examination of the curvature of the corneal surface involves projecting onto it concentric rings of light (Placido’s rings), the reﬂected image of which is analyzed by a computer which measures the distance between these rings. Optical measurement of corneal curvature is termed keratometry. The results are reported in millimeters or diopters; for the dog eye mean corneal curvature in diopters is 39.94 ± 2.61; mean radius of curvature in mm is 8.46 ± 0.55.3 Mean curvature for large breed dogs is less than that for dogs of medium size or small breeds, indicating a ﬂatter cornea in larger dogs. This technique allows evaluation of astigmatism and is requisite for refractive procedures on the cornea.3

29

SMALL ANIMAL OPHTHALMOLOGY

Specular microscopy The specular microscope allows in vivo observation of the corneal endothelium; endothelial cells of the dog and cat form a regular monolayered mosaic of hexagonal cells at a normal density of about 2000 cells/mm2 (Fig. 2.10).4,5

Ultrasonography Ocular ultrasonography in two-dimensional B-mode with a 10 MHz probe is ideal but very adequate studies can be performed with a 7.5 MHz probe, which is generally more readily available to practitioners (Fig. 2.11A). The technique

Fig. 2.10 Specular microscopic appearance of the normal canine corneal endothelium demonstrates a monolayer of regular hexagonal cells.

A

30

Fig. 2.11 Ultrasonography. (A) Normal eye (7.5 MHz probe). (B) Pathology. I Exophthalmos/orbital abscess/cellulitis (10 MHz probe). II Orbital abscess/cellulitis (7.5 MHz probe) (Courtesy of Dr A. Bertoldi.)

DIAGNOSTICS

BI

BII Fig. 2.11 For caption see opposite.

31

SMALL ANIMAL OPHTHALMOLOGY CI

CII Fig. 2.11 Ultrasonography. (C) Persian cat, iris melanoma: the iris is completely pigmented, irregular, and thicker than normal (20 MHz probe).

32

provides the ability to image the inner structures of the eye if alterations (corneal edema, intraocular hemorrhage, cataract) of the normally transparent tissues prevent direct intraocular observation. It also allows an evaluation of the soft and bony tissues of the orbit, making it of particular value in cases of exophthalmos (Fig. 2.11B). Suspected intraocular disease in the presence of opaque media, uveal neoplasia, orbital diseases, and retinal detachment are the major indications for ultrasonography (Fig. 2.11C,D,E). One-dimensional (A-mode) ultrasonography can be used to determine biometric parameters of corneal thickness, anterior chamber depth, lens thickness, and axial length

DIAGNOSTICS

(20.43 ± 0.48 mm), which are useful in the study of the physiologic optics of the eye (Fig. 2.11F). Most dogs and cats tolerate ultrasound examination very well with only topical anesthesia (e.g. proparacaine hydrochloride 0.05%); in some uncooperative patients sedation is necessary. Recently, very high frequency ultrasound with probes ranging from 20 MHz to 60 MHz has enabled images of very high detail and resolution to be obtained (Fig. 2.11G).

Radiology Radiology is used in small animal ophthalmology as a preliminary for other imaging techniques (ultrasound, CT scan, MRI), which generally provide more sensitive information. Orbital bone, sinus, and skull evaluation are the main indications. Dacryocystorhinography allows evaluation of the nasolacrimal duct.

Computed tomography (CT) A CT scan is recommended when critical evaluation of the orbit is required. Detailed imaging of the orbital contents, including globe, extraocular muscles, and optic nerve, as well as the adjacent bony skull and sinuses, is invaluable in the diagnosis and localization of orbital neoplastic, inﬂammatory, or traumatic disease.

Magnetic resonance imaging (MRI) This technology magnetizes and determines the concentration of protons in tissues and offers enhanced projection and resolution of soft tissues compared with a CT scan. It is of particular value in neurophthalmology.

Electroretinography (ERG) and visual evoked response (VER) (Fig. 2.12) The ERG records the total response of the retina to a short light stimulus by measuring the difference in potential between the retina and cornea through surface electrodes at the cornea and the lateral canthus. The VER simultaneously records the activity of the visual cortex and reﬂects the integrity of the entire afferent visual pathway. Two major waves characterize the ERG: 1. The initial negative a-wave reﬂects the activity of the photoreceptors (rods and cones) 2. The following b-wave reﬂects the activity of the Müller cells/ON bipolar cells complex. Other minor waves are elicited, depending upon the conditions of stimulation and recording. The oscillatory potentials (OPs) are a component of the b-wave that reﬂect the activity of the amacrine cells in the inner nuclear layer. The i-wave,6 a positive deﬂection following the b-wave, likely reﬂects the activity of ganglion cell and/or optic nerve activity. Furthermore, in speciﬁc experimental conditions, in addition to the a-, b-, and i-waves, there is a slower second positive deﬂection, the c-wave, which is more prolonged and probably arises from the RPE. ERG must be conducted under general anesthesia and care must be taken in electrode positioning to avoid third eyelid protrusion.7 ERG protocols can be designed to evaluate the individual photoreceptor populations (rods or

33

SMALL ANIMAL OPHTHALMOLOGY DI

DII

34

Fig. 2.11 Ultrasonography. (D) Mixed breed dog, iris melanoma: the iris is pigmented, irregular, and thicker than normal (20 MHz probe).

cones) by manipulating the parameters of stimulus and patient status in regard to dark or light adaptation, stimulus spectral composition, stimulus intensity, and stimulus frequency.8 Patterned stimuli can be projected onto the retina to assess ganglion cell activity or localized retinal activity (multifocal ERG) if prior refraction has been performed and corrected. This ensures that the stimulus is projected onto the retina.9 Waveforms are evaluated by amplitude and temporal relationship to the stimulus; anesthesia may affect both of these parameters. The electro-oculogram (EOG) measures the standing potential of the RPE and to date has not proven to be of great value in veterinary ophthalmology because verbal cooperation of the patient is not possible with animals! Record-

DIAGNOSTICS

E Fig. 2.11 Ultrasonography. (E) Dog: retinal detachment and vitreous hemorrhage are visible (10 MHz probe).

F Fig. 2.11 Ultrasonography. (F) Normal biometry using a 10 MHz probe.

ing of ERGs during dark adaptation can provide insights into functional alterations of the RPE. The VER is in essence a localized electroencephalogram (EEG) that utilizes active scalp electrodes placed over the occipital lobe and signal averaging to evaluate the conduction of impulses from the ganglion cells of the retina to the visual cortex along the optic nerve, optic chiasm, optic tract, lateral geniculate body, and the optic radiation. Flash or pattern stimuli (evoked in the same conditions that were previously described for ERGs) can be used to differentiate between peripheral (retinal) and central processes that cause visual dysfunction. It is important to note that the amplitude of the VER signal ranges from 5 to 10 microvolts while the amplitude of the ERG signal is generally greater than 100 microvolts. The VER responses are challenging to record and results may be difﬁcult to interpret.

35

SMALL ANIMAL OPHTHALMOLOGY G Fig. 2.11 Ultrasonography. (G) Dog: glaucoma, goniodysplasia (GD). Note increased contact of the iris with the anterior lens capsule (35–50 MHz probe). (Courtesy of Dr J. Sapienza.)

Electrophysiology is indicated when critical assessment of the retinal components and pathways is required and may be a more sensitive indicator of retinal health than ophthalmoscopy. Differentiation between peripheral and more central causes of visual impairment may also be accomplished. ERG is useful in the detection of inherited retinal degenerations, to evaluate retinal function in the presence of opaque media that precludes critical direct evaluation, and to study drug effects on retinal function.

Fluorescein angiography (Fig. 2.13) The ocular vascular system and the integrity of the blood–ocular barriers can be observed by direct ophthalmoscopy using an exciting wavelength of light (blue) and the appropriate barrier ﬁlters (yellow) following the intravenous injection of ﬂuorescein dye (0.1 ml/kg of a 10% solution). The technique is useful to evaluate neovascular or inﬂammatory changes. Serial photography provides the ability to observe sequentially the choroidal and retinal arteriovenous ﬁlling. Hypoﬂuorescence can result from a masking defect (hemorrhage, exudate, or pigment) or a ﬁlling defect (vascular occlusion). Hyperﬂuorescence can develop because of a window defect of the tapetum or RPE, or result from incompetency of the blood–ocular barriers due to inﬂammation or neovascularization.10 Scanning laser ophthalmoscopy (SLO) 36

This contemporary technology utilizes illumination with two laser beams (red and argon) which facilitate detailed and dynamic image recording of the fundus;

B

M

R

H

C

As

G

Am

Conduction (VEPs)

Post-receptoral (ERG)

Receptoral (ERG)

Pre-receptoral (EOG: basal membrane)

a

OP2

OP3

b OP4

i

Fig. 2.12 Electroretinography. (A) On left, retinal histologic section; on right, retinal functional aspect. Electroretinogram (ERG) reﬂects the activity of photoreceptors (a-wave) and the bipolar cell/Müller cell complex (b-wave). Visual evoked cortical potentials (VEPs) reﬂect the activity of the visual pathways from the ganglion cells to the primary visual cortex.

A

Nerve fiber layer

Ganglion cell layer

Inner plexiform layer

Inner nuclear layer

Outer plexiform layer

Photoreceptor cell bodies

Photoreceptor outer segments

Retinal pigment epithelium

DIAGNOSTICS

37

SMALL ANIMAL OPHTHALMOLOGY

α : a-wave implicit time

Flash onset

Amplitude (microvolts)

OP3 200

OP4

b

β : b-wave implicit time γ : Photopic Negative Response

OP2

100 0

i

a α

0

β

Bandpass 0.1-70 Hz Baseline

γ

50 Time (milliseconds)

100

B Fig. 2.12 Electroretinography. (B) The parameters and measurements of the ﬂash ERG in diurnal species. The ﬁrst negative deﬂection following the ﬂash onset (ﬂash onset is represented by the red arrow) is the a-wave. It corresponds to the hyperpolarization of the photoreceptors due to the closing of the sodium channels. This negative deﬂection is followed by a positive wave known as the b-wave (corresponding to the activity of the bipolar and Müller cells). Oscillatory potentials (OPs) are found on the ascending limb of the b-wave; the exact origin of these OPs remains unclear and their number can vary between one and three depending on the intensity of the stimulation used. Approximately 20 milliseconds later, a second positive wave appears which is known as the i-wave (corresponding to the function of the ganglion cells and/or of the prechiasmatic optic nerve). Each wave is characterized by amplitude (in microvolts), peak latency, and implicit time, calculated from the ﬂash onset. The amplitude of the a-wave is calculated from the baseline to the peak of the a-wave, whereas the b-wave is calculated from the peak of the a-wave to the positive peak of the b-wave. The distance that separates the baseline from the negative peak of the b-wave is known as the photopic negative response. It corresponds to the response of ganglion cells and to the parts of their axons that are still unmyelinated.

it can be performed through a small pupil or when media opacities obscure ophthalmoscopic detail. Digital image analysis is utilized to study vascular, inﬂammatory, or degenerative disorders of the retina and optic nerve.11

Ocular coherence tomography (Fig. 2.14) Ocular coherence tomography (OCT) is a contemporary high-resolution (10 μm) non-invasive imaging technique12 that produces cross-sectional images without the use of any radiation or contact. The precision of images obtained by this device is ‘histologic’. This technique is useful to evaluate the junction of the vitreous and the retina and to characterize intraretinal changes.

EXAMINATION OF THE EYE 38

The ﬁrst step in ophthalmic diagnosis is to collect a thorough history; while doing this, the animal should be observed so that an impression of alertness,

DIAGNOSTICS

-3.39 log cd.s.m-2 -3.09 log cd.s.m-2

b i

0.81 log cd.s.m-2

a 50 μV 25 ms -3.39 log cd.s.m-2

0 min of dark adaptation 2 min of dark adaptation 5 min of dark adaptation 10 min of dark adaptation 15 min of dark adaptation

100 μV

30 min of dark adaptation

25 ms C

Fig. 2.12 Electroretinography. (C) On left: representative ERG obtained in photopic conditions in dogs. The averaged responses to 15 ﬂashes at progressively increasing intensities (from −4.89 log cd.s/m2 to 0.81 log cd.s/m2) delivered at 1.3 Hz were taken at the onset (vertical arrow) in photopic constant background. On right: representative ERG obtained in scotopic conditions in dogs. The averaged responses to three standard ﬂashes (intensity: −3.39 log cd.s/m2) delivered at 0.1 Hz were taken at the onset (vertical arrow) of the dark adaptation process (t0) and at regular time intervals thereafter (t2, t5, t10, t15, and t30 minutes). Note the gradual gain in amplitude and in lengthening in the timing of the b-wave of the ERG. The progressive increase in the amplitude of the b-wave during dark adaptation is supposed to reﬂect the function of the neural–retinal pigment epithelium junction.

39

SMALL ANIMAL OPHTHALMOLOGY

1

2 3

4

AI

1 3 2

AII

40

Fig. 2.13 Angiography. (A) Normal angiogram of a dog. I Fundus photography. 1: Tapetal fundus; 2: arteriole; 3: venule; 4: non-tapetal fundus. II Arterial phase. 1: Retinal arteriole ﬁlled with ﬂuorescein; 2: venule; 3: choroidal ﬂuorescence.

DIAGNOSTICS

2

1 3

AIII

1

4

2

3

AIV Fig. 2.13 Angiography. III Arteriovenous phase. 1: Laminar ﬁlling; 2: choroidal ﬂuorescence; 3: intervascular area. IV Venous phase. 1: Retinal arteriole; 2: venule totally ﬂuorescent; 3: intervascular area; 4: choroidal ﬂuorescence.

41

SMALL ANIMAL OPHTHALMOLOGY

2

1

BI

2

1

BII

42

Fig. 2.13 Angiography. (B) Pre-retinal masking of hypoﬂuorescence by hemorrhage (arrow). I Fundus photography. 1: A hemorrhage is visible; 2: venule in proximity to hemorrhage. II Arterial phase. 1: A non-perfused retinal vessel emerging over choroidal hypoﬂuorescent area (2).

DIAGNOSTICS

BIII

BIV Fig. 2.13 Angiography. III Arteriovenous phase. IV Venous phase.

43

SMALL ANIMAL OPHTHALMOLOGY CI

CII Fig. 2.13 Angiography. (C) Hyperﬂuorescence by window effect and leakage into a tissue (staining). I Fundus photography. Retinal pigment epithelium dystrophy. Note abnormal pigment in tapetum lucidum (arrow). II Arterial phase. Window effect with visualization of choroidal vessels (arrow).

44

DIAGNOSTICS

CIII

CIV Fig. 2.13 Angiography. III Arteriovenous phase. Note leakage from a retinal vessel (arrow). IV Venous phase. Leakage into retina (arrows).

45

SMALL ANIMAL OPHTHALMOLOGY

V

A

a Cc

NR b Sc

B Fig. 2.14 Ocular coherence tomography. Vitreo-retinal junction in cat: fundus photography reveals a vitreo-retinal junction abnormality (A). OCT examination (B): between the sclera (Sc) and the vitreous (V), the neuroretina (NR) is detached from chorio-capillaris (Cc). Two spaces (a & b) are visible and arrows show vitreo-retinal connections.

visual acuity, and behavior is registered. Ocular examination should be conducted routinely as a part of the general physical examination. A systematic standard approach is suggested for a quick but complete eye examination, ﬁrst in ambient light, then in a dark room.

Examination with ambient illumination

46

• The gross appearance of the eye and surrounding structures is observed to determine the presence of periorbital swelling, lacrimation, abnormal discharge, and the size and position of the eye. Examination of the anterior segment of the eye follows. Both eyes must always be considered, even if only one is obviously affected. In such instances it is preferable to examine the normal (or less obviously affected) eye ﬁrst. A magnifying loupe and focal illumination are used to assess the adnexa and anterior segment structures. The STT, if indicated, is performed before additional manipulations or applications are performed. • Pupil light reﬂex (PLR), menace response, blinking, and ocular and periocular sensation should then be evaluated. PLR can be tested in ambient light; repeat the procedure in a darkened room prior to the instillation of dilating agents if abnormalities are noted. First each eye is

•

•

•

•

•

DIAGNOSTICS

•

directly stimulated with a bright focal light and the completeness and briskness of PLR is noted. This is the direct reﬂex, while the pupil of the opposite eye constricts due to the consensual reﬂex. For anatomic reasons in non-primates, the consensual pupil may not constrict to exactly the same size as the pupil of the stimulated eye. The menace response should be tested next, paying attention not to cause air movement toward the patient’s eye and a consequent blink (mediated by the trigeminal nerve). Bear in mind that absence of the menace response is normal in very young animals and problematic to interpret in cats. Manipulate the head and neck to evaluate ocular motility. Critically evaluate globe size and position, observe the symmetry of the globes from above, palpate around the orbital rim and the orbital fossa, and retropulse both globes simultaneously. Distinction between exophthalmos and globe enlargement is critical. Then consider the eyelids, third eyelid, conjunctiva, sclera, and cornea, and anterior chamber, iris, lens, and anterior vitreous, using the magnifying loupe and the focal light. If the adnexa is inﬂamed and there is discharge, STT is indicated, and cytology and culture should be considered. If a serous discharge is bilateral without evidence of inﬂammation, or the discharge is concentrated on the medial aspect and the hyperemia is particularly evident in the medial canthus, the lacrimal drainage system should be investigated, with a suspicion of obstruction and/or dacryocystitis. In these cases palpation over the lacrimal sac may be painful and induce the expression of exudates through the punctae. If the patient exhibits blepharospasm, look for corneal ulcers, a foreign body, entropion, or ectopic cilia, and stain with ﬂuorescein. Chronic disorders of the cornea manifested by neovascularization and melanosis may be associated with trichiasis, distichiasis, lagophthalmos, lacrimal secretory disorders, or immune-mediated disease. If intraocular disease is suspected, based on the presence of episcleral/ scleral injection, corneal edema, aqueous cells or ﬂare, or abnormal PLRs, tonometry is a requisite. Congestion of episcleral vessels may be differentiated from conjunctival injection by applying one drop of phenylephrine; in cases of conjunctivitis the hyperemic pattern will almost completely disappear. Episcleral injection is an indication of episcleritis, glaucoma, or uveitis. Because pupillary dilatation is necessary for the remainder of the ophthalmic exam, one drop of 1.0% tropicamide should be applied to each eye at this point; perform the rest of the general physical examination in the interim. Gonioscopy is optimally performed prior to mydriasis.

Dark room examination • When the pupils are completely dilated as an effect of the previously instilled mydriatic, the lens, vitreous, and the ocular fundus may be carefully examined. The lens can be examined by moving the transilluminator to the right and to the left from the frontal position in

47

SMALL ANIMAL OPHTHALMOLOGY

such a way as to shift the incident light and better visualize any opacity with the magniﬁcation loupe. • Using the direct ophthalmoscope with a lens setting between 0 and +2 D and the eye examined from arm’s length it is possible to evaluate the fundus reﬂex as a relatively sensitive indicator of opacities within the media, which appear as a dark shadow when using this technique of distant direct ophthalmoscopy. The fundus should then be examined using the indirect or direct ophthalmoscope. During all steps of the examination, all data should be recorded in the patient’s permanent record and, in case of consultation, transmitted to the veterinary ophthalmologist. Most importantly, ocular disease should always be approached from the ‘whole animal’ perspective. Detecting unsuspected ocular conditions in their early stages during the course of a routine examination, or simply reassuring a client of the inevitability and insigniﬁcance of nuclear sclerosis, will elevate the quality of your service. Ocular signs such as cataracts of rapid onset in an unlikely breed or vitreous hemorrhage should alert the astute clinician to rule out diabetes mellitus or systemic hypertension, respectively. Only in the eye can one directly observe the central nervous system (optic nerve) and the peripheral vasculature (retinal arterioles and venules). Ocular function draws from a signiﬁcant component of the nervous system and this association should be kept in mind.

REFERENCES

48

1. Gaiddon, J., Bouhana, N. and Lallement, P.E. (1996) Refraction by retinoscopy of normal, aphakic and pseudophakic canine eyes: advantage of a 41 diopters intraocular lens? Vet. Comp. Ophthalmol. 2: 121– 124. 2. Davidson, M.G. (1997) Clinical retinoscopy for the veterinary ophthalmologist. Vet. Comp. Ophthalmol. 2: 128–137. 3. Rosolen, S.G., Ganem, S., Gross, M. et al. (1995) Refractive corneal surgery on dogs: preliminary results of keratomileusis using a 193 nanometer excimer laser. Vet. Comp. Ophthalmol. 5: 18– 24. 4. Stapleton, S. and Peiffer, R.L. (1980) Specular microscopic observations of the clinically normal canine endothelium. J. Am. Vet. Med. Assoc. 176: 249–251. 5. Peiffer, R.L., DeVanzo, R. and Cohen, K.L. (1981) Specular

microscopic appearance of the normal feline endothelium. Am. J. Vet. Res. 42: 854–855. 6. Rosolen, S.G., Rigaudière F., Le Gargasson, J.-F. et al. (2004) Comparing the photopic ERG i-wave in different species. Vet. Opthalmol. 7(3):189–192. 7. Rosolen, S.G., Rigaudière, F., Lachapelle, P. (2002) A practical method to obtain reproducible binocular electroretinograms in dogs. Doc. Ophthalmol. 105: 93– 103. 8. Narfström, K., Ekesten, B., Rosolen, S.G. et al. (2002) Guidelines for clinical electroretinography in the dog. Doc. Ophthalmol. 105: 83– 92. 9. Lescure, F. (1998) Evaluation of the angiograms – semeiology. In: Fluorescein Angiographic Atlas of the Small Animal Ocular Fundus. Pratique Médicale et Chirurgicale des Animaux de Compagnie, Paris, pp. 75–105.

angiography for clinical and toxicological studies on animals. Invest. Ophthalmol. Vis. Sci. 40: 1461 [ARVO abstract]. 12. Puliaﬁto, C.A., Hee, R.H., Schuman, J.S. and Fujimoto, J.G. (1996) Optical Coherence Tomography of Ocular Diseases. Slack Inc., Thorofare.

DIAGNOSTICS

10. Rosolen, S.G., Gautier, V., SaintMacary, G. et al. (2000) Eye fundus images with confocal scanning laser ophthalmoscope on dog, monkey and minipig. Vet. Ophthalmol. 4: 41–45. 11. Rosolen, S.G., LeGargasson, J.-F. and Saint-Macary, G. (1999) SLO

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SMALL ANIMAL OPHTHALMOLOGY

Therapeutics Bruce H. Grahn and Joe Wolfer

INTRODUCTION

50

3

The eye is a delicate and complex organ which is affected by a variety of diseases; successful medical management of ocular disease is based not only on an accurate diagnosis but also on in-depth knowledge of pharmacology and therapeutics. The purpose of this chapter is to enhance the veterinarian’s understanding of ocular therapeutics by reviewing the pharmacokinetics and indications for medications that are commonly prescribed for ocular disorders by topical, subconjunctival, and/or systemic routes. The eye may be medicated topically, systemically, or by injection into the subconjunctival, intraocular, or orbital tissues. There are several compartments in the eye, separated by semi-permeable barriers. Delivery of systemic medications to the cornea via the circulatory system is limited to diffusion from the perilimbal vasculature, and those agents secreted in the tears or that penetrate the blood–ocular barriers enter the anterior chamber and pass through the corneal endothelium; topical or subconjunctival medications are appropriate for most corneal diseases. Diseases of the anterior segment may be medicated topically, subconjunctivally, or systemically, while most posterior segment, orbital, and eyelid diseases require systemic medications. Intraocular and intraorbital injections have inherent risks, are indicated in speciﬁc ophthalmic diseases, and should be performed by an ophthalmologist; these injections will not be discussed in detail in this chapter. When an animal is to be medicated at home, owner compliance is an important and often forgotten factor. The owner must have the time and ability to medicate the eye during the speciﬁed treatment period and a sense of what to expect in terms of improvement or deterioration in the condition. Treatment instructions should be given to the owner verbally and in written form. Consider the following with regard to owner compliance: topical solutions are usually easier to apply than ointments but they require more frequent application. Is the animal manageable by the owner alone and, if not, will an assistant be available to restrain the animal during medication? Will painful orbital or ocular inﬂammation preclude or reduce the frequency of administration of medications? If the medications are used for an extended period of time, has the most economical formulation been selected? Are systemic side effects going

PHARMACOKINETICS OF OPHTHALMIC MEDICATIONS

THERAPEUTICS

The most commonly used route for ocular therapy is topical. The ocular penetration of a topical medication is dependent on the concentration and kinetics within the conjunctival cul-de-sac, corneal permeability, and the rate of elimination of the medication from the conjunctival sac.1 Tear ﬂow and space within the conjunctival fornix have a dynamic effect on topical ophthalmic medications. Commercial droppers deliver 25–50 μl/drop of solution or suspension and immediate reﬂex tearing occurs after a drop of medication is placed on the eye. The non-blinking eye will retain approximately 10–25 μl (varies with species) of additional ﬂuid in the conjunctival fornix and tear ﬁlm, after which immediate overﬂow occurs.2 Application of more than one drop at a time will not increase the amount of available medication because this volume will overﬂow into the nasolacrimal duct or onto the eyelid.3 It is important to wait at least 5 min between the applications of consecutive topical medications. Only 20% of topically applied medications will remain on the ocular surface after 5 min.2 This rapid reduction is the result of drainage through the nasolacrimal system and absorption of the medication through the cornea and conjunctiva. Therefore, if increased concentrations of topically applied medication within the cornea and the anterior chamber are desired, an increased frequency of application is useful provided the applications are at least 10 min apart. Most of the intraocular penetration of topically applied medications occurs via the cornea.4 The cornea has a thick hydrophilic stroma which is enveloped by two thin lipophilic structures: the epithelium and the endothelium. Factors such as solubility, ionization, and molecular size affect absorption of all pharmaceuticals. Membrane factors including weakness or absence of portions of the cornea (the epithelial barrier is not present in corneal ulcers, enhancing permeability) are also important.5 The intact epithelium is a signiﬁcant barrier for hydrophilic medications, while the underlying stroma is a signiﬁcant barrier for lipophilic agents, which consequently accumulate in the epithelium. In order to penetrate the intact cornea adequately, topical medications require both hydrophilic and lipophilic characteristics. Protein binding of pharmaceuticals in the tear ﬁlm, aqueous humor, and vitreous also inﬂuence the availability of medications.6 The protein concentrations in these ﬂuids will increase during inﬂammation due to disruption of the blood–ocular barriers and signiﬁcant protein binding may occur.7 Topical ophthalmic pharmaceuticals are available as solutions, emulsions or suspensions, and ointments. Emulsions and ointments have slightly prolonged contact times compared to solutions and therefore require less frequent administration to achieve therapeutic concentrations. However, emulsions have the disadvantage of being less stable and ointments are more difﬁcult to apply, result in blurred vision, and may elicit rubbing and self-induced trauma. For a more complete review of pharmacokinetics and corneal penetration of topically applied ophthalmic pharmaceuticals, the reader is referred to reports by Shell8 and Burstein and Anderson.9

51

to be induced by the long-term topical ophthalmic medications and is the owner adequately informed and prepared for these effects?

SMALL ANIMAL OPHTHALMOLOGY

52

Treatment compliance is dependent on provision of accurate and thorough instructions to the owner, and a demonstration is worth a thousand words. Bottles of ophthalmic solutions and suspensions should be kept at a safe distance from the eye during medicating in order to avoid contamination of the bottle and injury to the eye. Instruct the owner to rest their hand holding the medication on the animal’s forehead, use the other hand to stablilize head and retract the eyelids, and to come from behind and above to place one drop onto the ocular surface at a safe distance. Gentle occlusion of the lower puncta for a few minutes after medications are applied will increase the total available medication by decreasing drainage into the nasolacrimal duct. When ointments are being applied, it is preferable to place a 5 mm strip on a clean ﬁngertip, and then use the lid margin to scrape the medication onto the lower palpebral conjunctival surface. This prevents contact and contamination of the ointment tube and corneal and conjunctival injury. Alternately, the upper or lower lid can be retracted and the medication applied directly to the conjunctival surface. Subconjunctival injection of medications can be a valuable adjunct to topical therapy. It is important that the practitioner understands the indications and limitations of their use. Medications, including some of the antibiotics, enjoy enhanced ocular penetration with bulbar subconjunctival injections.10 Depot formulations provide prolonged therapy, and in fractious or aggressive patients subconjunctival injection under sedation may be the only means of therapy. The pharmacokinetics of subconjunctival injections are not well understood and likely vary considerably between classes of pharmaceuticals and their formulations. Medications injected into the subconjunctival space are thought to enter the ciliary circulation, thereby gaining access to the anterior segment. However, some of the injected medication simply leaks through the puncture site in the conjunctiva and is absorbed directly through the cornea.11 In the case of subconjunctival corticosteroids, transscleral penetration has also been reported.12 Direct absorption of medication from the subconjunctival injection site bypasses the epithelial barrier and increases intraocular drug availability by avoiding tear dilution.13 The use of subconjunctival medications at surgery minimizes the need for some of the topical medications during the immediate postoperative period. Other advantages include increased intraocular concentration of medications that penetrate the cornea poorly, and ensured presence of the therapeutic agent when owner compliance is poor.14 Subconjunctival injections require the utmost care. Topical anesthesia is required and occasionally sedation or general anesthesia is necessary to ensure accurate bulbar subconjunctival injection. A subconjunctival injection is performed by manually retracting the upper eyelid and gently grasping the superior bulbar conjunctiva with small tissue forceps (i.e. Bishop Harmon). A 25 G needle (attached to a 1 ml syringe) is inserted bevel up through the tented bulbar conjunctiva. Up to 0.5 ml of medication may be slowly injected to form a subconjunctival bleb. The dosage will vary with the ocular condition and medication but the total volume per injection site should not exceed 0.5 ml. Long-lasting (depot) medications should be avoided unless they are required as they are irritating and may predispose to granuloma formation.15 Subconjunctival injections of solutions including antibiotics and atropine need to be repeated every 24 h; the repetition rate will vary depending on the response to therapy and the frequency of topical and systemic medications. Subconjunctival injections of long-lasting steroids, e.g. betamethasone valerate, need to be

THERAPEUTICS

repeated every 7–10 days. There are inherent risks associated with the use of subconjunctival injections; complications include irritation at the injection site, granuloma formation, an inability to withdraw medications if necessary, and rarely inadvertent intraocular injections. Many medications are irritating and should not be administered subconjunctivally, especially when similar approved topical medications are available. Systemic medications may be administered orally, intramuscularly, intravenously, or subcutaneously for therapy of glaucoma, and eyelid, orbital, posterior segment, and optic nerve diseases. Systemic anti-microbials, corticosteroids, non-steroidal anti-inﬂammatory drugs (NSAIDs), hypotensive agents, and carbonic anhydrase inhibitors are commonly so administered for these conditions. The blood–ocular barriers are composed of tight junctions of the endothelium of the iris and retinal blood vessels and the ciliary and retinal pigment epithelium. These barriers are only penetrated by a few lipophilic medications of low molecular weight (e.g. chloramphenicol). However, with inﬂammatory eye conditions the blood–ocular barriers are compromised, which allows most systemic medications to reach the anterior and posterior segments. Antibiotics should be selected initially on the basis of cytologic evaluation of scrapings or ﬁne needle aspirates from the eye, eyelid, or orbit and re-evaluated when bacterial cultures and sensitivities are available. Systemic corticosteroids are indicated in most inﬂammatory conditions of the posterior segment. Prednisone, prednisolone, dexamethasone, and ﬂumethasone are common choices for severe posterior segment, optic nerve, or orbital inﬂammation. Systemic NSAIDs are frequently administered to control inﬂammation of the posterior segment or orbit. Examples include ﬂunixin, carprofen, aspirin, ketoprofen, and indometacin. Contraindications for NSAIDs include platelet disorders, coagulopathies, some hepatic and renal insufﬁciencies, and speciﬁc hypersensitivities to these drugs. Systemic carbonic anhydrase inhibitors decrease the production of aqueous humor by the non-pigmented ciliary epithelium and are indicated for treatment of acute glaucoma and prophylactic treatment of primary glaucoma; examples of these agents include methazolamide, dichlorphenamide, and acetazolamide. These medications are contraindicated when acidosis or hypokalemia is present as they will aggravate these conditions. Clinical manifestations of acidosis and hypokalemia include panting, vomiting, diarrhea, and collapse. Because of these adverse effects, the availability of topical carbonic anhydrase inhibitors has largely obviated their use. Numerous ﬁxed ratio topical ophthalmic medications are available and frequently prescribed by veterinarians. It is our opinion that many of these medications (usually an antibiotic and steroid combination) are overused, often because of a lack of a speciﬁc diagnosis. Topical or systemic corticosteroid therapy does not require the addition of antibiotics, and vice versa. If both are required for separate purposes then separate formulations are usually more appropriate to deliver adequate concentrations of each.

Antimicrobials Topical antimicrobials (antibiotics, antifungals, and antivirals) (see Appendix, Tables 1 & 2) Topical antibiotics may be categorized, based on their intended use, into primary, secondary, and tertiary types. Primary antibiotics are used to treat bacterial conjunctivitis and simple corneal ulcers. The bacterial ﬂora of the

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54

normal surface of dogs and cats are a mixed population of predominantly Gram-positive organisms.16,17 Therefore, broad-spectrum antibiotics including triple antibiotics (neomycin, polymyxin B, bacitracin), gentamicin, or chloramphenicol are appropriate for bacterial conjunctivitis or simple corneal ulcers. Triple antibiotics and gentamicin are bactericidal. Chloramphenicol is bacteriostatic but penetrates the eye rapidly and achieves high intraocular concentrations. Secondary categories of topical ophthalmic antibiotics are indicated for speciﬁc anterior segment conditions. An example is tetracycline, which is the topical antibiotic of choice for feline Chlamydia or Mycoplasma conjunctivitis. It is bacteriostatic and achieves an adequate concentration in the cornea and conjunctiva. The tertiary category of antibiotics should be reserved for septic conditions including melting corneal ulcers and panophthalmitis. Examples include some ﬂuoquinolones and aminoglycosides which are bactericidal and effective against most antibiotic-resistant Gram-negative bacteria including Pseudomonas. Prudent selection of tertiary antibiotics is encouraged and should be based on culture and sensitivities. Indiscriminate usage of any antibiotic is discouraged as development of bacterial resistance is common. Bacterial infections of the conjunctiva, cornea, or anterior segment require a minimum of one drop QID with antibiotic solutions or emulsions for 7 days or until the infection is resolved. When ointments are prescribed, a 5 mm strip is applied to the conjunctiva a minimum of three times per day until the infection is resolved. Fusidic acid, a viscid topical antibiotic drop, is now available in North America; this slow-release viscid suspension may be applied only twice a day and still produce inhibitory antibacterial drug levels.18 Ointments are contraindicated when the cornea is perforated because they are irritating to the uvea.3 Topical gentamicin and tobramycin should be avoided when the cornea is perforated as toxic effects on the corneal endothelium and the retina and ciliary epithelium were found when those tissues were exposed to high concentrations of aminoglycosides.19,20 Most antivirals are nucleoside analogs that are similar in structure to nucleosides and when they are incorporated into viral DNA or RNA they alter or disrupt the viral replication. Idoxuridine, adenine arabinoside, and triﬂuridine are topical antivirals that have been used to treat feline herpetic keratitis and conjunctivitis. Idoxuridine mimics thymidine, thereby altering virus metabolism. It is available as a solution or ointment and should be applied frequently (q2 h for 2 weeks) and q6 h for 4 weeks. Adenine arabinoside inhibits virus DNA polymerase. It is available as an ointment and should be applied q4 h for several weeks to be effective. Triﬂuridine inhibits viral DNA synthesis and is available as a solution which is applied q4 h for at least 3 weeks. Triﬂuridine has the highest in vitro activity against feline herpesvirus. Bromovinyldeoxyuridine is a pyrimidine analog of nucleoside thymidine and, although it is selective for human herpes simplex 1, it is ineffective against feline herpes virus 1 (FHV-1).21 Vidarabine is a nucleoside analog of adenosine and has been used topically to treat FHV-1; however, it is no longer available commercially. Ganciclovir is an acyclic analog of guanosine and in vitro potency studies have suggested it may be useful in treating FHV-1 infections.22 Valganciclovir is a prodrug of ganciclovir. Penciclovir is similar to aciclovir structurally and a moderately high anti-feline herpesvirus 1 activity has been demonstrated in

THERAPEUTICS

vitro; and further in vitro studies are required.22 Famciclovir is a prodrug of penciclovir. Cidofovir is an acyclic analog of cytosine and its in vitro efﬁcacy suggests that it may be as potent as idoxuridine; however in vivo efﬁcacy has not been established and topical usage resulted in stenosis of the nasolacrimal duct in rabbits and humans.22,23 Foscarnet is a non-nucleoside replication inhibitor of herpesviruses that has been investigated for in vitro anti-feline herpesvirus activity, and unfortunately is not effective.22 Fungal infections of the dog and cat eye are uncommon and are usually limited to the cornea (with the exception of systemic mycotic disease with ocular involvement). Topical antifungal ophthalmic medications including amphotericin B, natamycin, miconazole, clotrimazole, silver sulfadiazine, ketaconazole, itraconazole, ﬂuconazole, econazole, thiabendazole, ﬂucytosine, or povidone–iodine may be required. Natamycin is the only available commercial topical ophthalmic antifungal and is administered as a solution q6 h until the corneal fungal infection is eliminated. Miconazole solutions may be administered topically or subconjunctivally. Clotrimazole and silver sulfadiazine are available as dermatologic ointments which may be applied topically onto the eye.24 Dilute (1 : 25) povidone–iodine solution has also been reported as a useful and readily available topical ophthalmic antifungal agent.24 There are many complexities that affect the development of ocular mycoses, accurate diagnosis, and the management of effective fungal therapy. Therefore referral of affected animals and consultation with a veterinary ophthalmologist is strongly encouraged.

Subconjunctival antimicrobials Antibiotic or antifungal solutions may be injected under the bulbar conjunctiva as adjunct therapy for bacterial or fungal infections of the anterior segment. Medications inadvertently placed under the palpebral conjunctiva are not considered as useful since the blood circulation is away from the eye in this location. Gentamicin, penicillin, or cephalosporins are appropriate antibiotics for subconjunctival injections. Miconazole solution can be administered as an antifungal agent. These injections increase the anterior segment concentration of the drug by absorption into the anterior ciliary circulation and across the cornea from the injection site. The contraindications for these forms of therapy include known hypersensitivities. Conjunctival and episcleral irritation are commonly observed with this form of therapy.

Systemic antimicrobials Bacterial infections of the eyelid, orbit, anterior and posterior uvea require systemic antibiotic therapy. Ideally these antibiotics are chosen on the basis of culture and sensitivity results; however these are seldom available at the critical stage of early infection. Cytologic evaluations of ﬁne needle aspirates from the infected intraocular or orbital tissues should be performed and aerobic and anaerobic cultures collected as early as possible in the course of disease. Thorough examination of cytologic specimens from the ocular surface may aid the clinician in identiﬁcation of the potential bacteria and assist in the selection of an appropriate antibiotic. Bactericidal antibiotics that are effective against aerobic and anaerobic bacteria are appropriate for most of these infections. Beta-lactams including ampicillin, amoxicillin, or cephalosporins are

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recommended and they may be administered via oral, intravenous, intramuscular, or subcutaneous routes. The antibiotic initially selected should be reconsidered after cultures and sensitivities are available. The prognosis for maintenance of vision is dependent on prompt control of intraocular or orbital infections. Intravenous therapy is recommended to establish immediate tissue concentrations. Intramuscular or oral therapy should be continued until the clinical signs of the infection are gone. It is worth repeating that most systemic antibiotics will penetrate inﬂamed intraocular tissues well. Systemic antifungals (including amphotericin B, ketoconazole, ﬂucytosine, itraconazole, thiabendazole) have been reported in the therapy of blastomycosis, coccidioidomycosis, cryptococcosis, candidiasis, aspergillosis, and histoplasmosis. For a review of the systemic antifungal therapy of ocular and systemic mycosis, the reader is referred to Noxon et al.25 and Ford.26 Aciclovir is a systemic antiviral drug that has been administered to cats with FHV-1 conjunctivitis and keratitis. Aciclovir is a thymidine kinase substrate which interferes with viral DNA synthesis. This medication is administered orally at a dose of 2 mg/kg for 21 days. The effectiveness of this medication against feline herpes is controversial.27,28 Interferon α may be effective in controlling feline herpesvirus infection and has synergistic activities in vitro with aciclovir.29,30 However, clinical trials have not been reported to date. L-lysine has also recently been recommended as an oral supplement, 250 mg orally every 12 h. This amino acid has been reported to reduce the severity of recrudescent FHV-1 infection and virus shedding in experimental cats;31,32 however, its clinical efﬁcacy has not been demonstrated. Valaciclovir is the L-valy ester of aciclovir. Although it is more readily absorbed, it induces bone marrow suppression and hepatic necrosis in cats and has no treatment value in cats.33 Famciclovir at a dosage of 31.25–62.5 mg twice daily for 7–14 days has been reported empirically to be safe and effective, but scientiﬁc clinical studies have not been performed. Systemic antivirals theoretically might be advantageous in minimizing recurrences. Nonetheless feline herpetic ocular disorders are difﬁcult to treat and veterinarians are encouraged to consult with veterinary ophthalmologists regarding effective systemic and topical FHV-1 therapy.

Anti-inﬂammatory medications Topical anti-inﬂammatories Topical corticosteroids and NSAIDs are commonly used to control anterior segment inﬂammation and are often used in combination for severe intraocular inﬂammation. However, indiscriminate use of these potent anti-inﬂammatories is discouraged.

Topical ophthalmic corticosteroids (see Appendix, Tables 3 & 4)

56

Corticosteroids inhibit phospholipase which alters the arachidonic acid metabolic pathway and minimizes inﬂammation. Corticosteroids decrease vasodilatation, capillary permeability, leukocyte inﬁltration, and release of inﬂammatory mediators from cells. They also inhibit ﬁbroblasts and collagen formation. Corticosteroids are derived from cholesterol and are available in several forms. The acetate forms are generally more lipophilic which allows for better corneal penetration when compared to succinates or phosphates. Dexamethasone and

THERAPEUTICS

prednisone are excellent selections for control of anterior segment inﬂammation and are available as suspensions, solutions, or ointments. Less potent corticosteroids are also available, the most common of which is hydrocortisone which is often combined with an antibiotic in a solution or ointment form. Topical corticosteroids are contraindicated when corneal ulceration is present. Local immunosuppression predisposes to or exacerbates infectious disease, notably fungal and viral infections. Continuous topical corticosteroid therapy may induce adrenal gland suppression via conjunctival absorption, and continuous use is recommended only if other options are not available for preservation of vision.

Topical NSAIDs (see Appendix, Table 5) These medications inhibit the cyclo-oxygenase pathway and reduce intraocular inﬂammation. Their inhibition of cyclo-oxygenase and endoperoxide isomerase decreases the production of prostaglandins, which cause miosis, altered blood– aqueous barrier, vasodilatation, and increased vascular permeability. NSAIDs also inhibit leukocyte chemotaxis and movement,34 and are commonly used to treat ocular inﬂammation today. Topical ophthalmic NSAIDs are indicated to control most anterior segment inﬂammation; there are several preparations available including ﬂurbiprofen, ketorolac, diclofenac, and suprofen. They should be used with caution when corneal ulceration is present as delayed epithelial healing, stromal inﬁltrates, punctate keratitis, and collagenolysis may develop concurrent to their usage.35–37 Topical NSAIDs may be contraindicated in animals with some forms of glaucoma as they may increase the intraocular pressure. They should be avoided or used with caution in animals with platelet dyscrasias, as they may decrease platelet aggregation and promote intraocular hemorrhage. However, despite these cautions, topical NSAIDs remain an important class of pharmaceuticals that the veterinarian should consider to control anterior segment inﬂammation. Topical mast cell stabilizers and antihistamines Cromolyn sodium solution is a topical mast cell stabilizer which prevents the release of inﬂammatory mediators from mast cells. It is useful in the treatment of inﬂammatory conjunctival diseases where mast cells predominate, such as allergic conjunctivitis. However, conjunctivitis associated with inhalant or food allergies are very uncommon in the dog and cat. When allergic conjunctivitis is conﬁrmed with cytology or biopsy it may be controlled in the acute stages with any one of several topical human antihistamines that are available commercially including antazoline, pheniramine maleate, and pyrilamine, as well as cromolyn sodium.

Subconjunctival anti-inﬂammatory drugs Subconjunctival corticosteroids are indicated to control progressive, poorly responsive, anterior segment inﬂammation. They provide anti-inﬂammatory effects to the anterior segment via the ciliary circulation, and by seepage of the medication onto the cornea through the bulbar conjunctival injection site. Subconjunctival corticosteroid injections are contraindicated when corneal ulceration is present. Conjunctival and episcleral inﬂammation and granulomas occur frequently after long-acting corticosteroid injections and their usage

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should be discouraged. Prednisone, dexamethasone, or betamethasone sodium phosphate may be recommended as adjunctive therapy for non-responsive immune-mediated anterior segment inﬂammation.

Systemic anti-inﬂammatories Systemic corticosteroids may be required to control severe anterior and posterior segment inﬂammation. Similar to antibiotics they readily concentrate intraocularly when the blood–ocular barrier has been compromised. They are contraindicated when corneal ulcers are present as they delay epithelialization and healing. Prednisone and dexamethasone are the most frequently prescribed. They may be administered orally, subcutaneously, intramuscularly, or intravenously at immune suppressive doses for prednisone (2 mg/kg) and dexamethasone (0.5 mg/kg) or anti-inﬂammatory doses for prednisone (1 mg/kg) and dexamethasone (0.125 mg/kg) in the dog and cat. The commonly used systemic NSAIDs include ﬂunixin meglumine, aspirin, carprofen, meloxicam, phenylbutazone, aspirin, ketorolac, etodolac, deracoxib, and ketoprofen. They may be administered intravenously (carprofen, ﬂunixin meglumine, meloxicam, ketoprofen, ketorolac) or orally (aspirin, etodolac, deracoxib, carprofen, meloxicam, phenylbutazone, ketoprofen). Flunixin meglumine is often administered to dogs prior to intraocular surgery. It should not be administered for longer than 3 days.38 Aspirin, carprofen, ketorolac, etodolac, deracoxib, or ketoprofen may also be administered to control intraocular inﬂammation. The recommended dosage for aspirin is 10 mg/kg BID in the dog and 10 mg/kg q72–96 h in the cat. The recommended dosage for carprofen in the dog is 2 mg/kg q12 h and 4 mg/kg SQ in cats. The recommended dosages for ketorolac in dogs is 0.5 mg/kg IV, and for cats is 0.25 mg/kg IM, etodolac 15 mg/kg orally, and deracoxib 4 mg/kg orally in dogs. The recommended dosage for ketoprofen in the dog and cat is 1 mg/kg q24 h. Systemic NSAIDs are contraindicated in patients with bleeding disorders, impaired renal function, or pre-existing hypersensitivities and they predispose the animal to gastrointestinal ulceration.39 Systemic steroids and NSAIDs are commonly used and provide excellent anti-inﬂammatoriy activity. They deserve consideration in most severe ocular inﬂammations when contraindications are not present.

Ocular hypotensive medications These medications lower the intraocular pressure by reducing the rate of production of aqueous humor, by increasing the rate of outﬂow of aqueous humor by conventional (trans-trabecular) or uveoscleral pathways, or via a combination of these actions. They are useful in the emergency management of acute glaucoma, as adjunctive medical therapy to surgical procedures, and as prophylactic medications to slow the onset of primary glaucoma. They are available in topical and systemic formulations, and as intravitreal injections.

Topical ocular hypotensives (see Appendix, Table 6) Parasympathomimetics

58

Parasympathomimetics may be direct acting (i.e. have their effect directly on cholinergic receptors) or be indirect acting and inhibit acetylcholinesterase. These medications lower the intraocular pressure by altering the ﬁltration angle which increases the outﬂow of aqueous humor.

THERAPEUTICS

Direct acting parasympathomimetics Pilocarpine has been commonly used in the past to lower the intraocular pressure. Pilocarpine is a potent miotic and is available as a solution or gel. Pilocarpine should be administered 3–4 times/ day and is usually used in combination with other antiglaucoma drugs including beta-adrenergic blockers, adrenergics, and systemic carbonic anhydrase inhibitors. Pilocarpine is seldom used today as an ocular hypotensive agent because it irritates the ocular surface and induces uveitis, and more effective medications are readily available. Pilocarpine is also contraindicated in uveitis and secondary glaucoma because its miotic effect may predispose to posterior synechiae and pupillary occlusion. A frequently observed side effect after prolonged use is conjunctival hypersensitivity which warrants dilution of the pilocarpine or discontinuance of this drug. Despite its diminished usage in the therapy of glaucoma in the dog and cat, topical pilocarpine is still used occasionally in the therapy of neurogenic keratoconjunctivitis sicca, and in the pharmacologic diagnosis of some parasympathetic ocular neuropathies. Indirect acting parasympathomimetics Cholinesterase inhibitors are categorized into reversible and irreversible agents. Physostigmine salicylate is a reversible cholinesterase inhibitor with a short duration of activity which limits its use to a diagnostic agent for parasympathetic disorders. Demecarium bromide is an irreversible carbamate inhibitor that is available as a topical solution. It is a potent cholinesterase inhibitor that lowers the intraocular pressure and has a duration of action of approximately 12–48 h. Isoﬂurophate and echothiophate iodide are irreversible cholinesterase inhibitors. They are also longacting, potent organophosphates that lower the intraocular pressure and are only occasionally administered today on a q12–48 h basis in the dog. In general, most parasympathomimetics are irritating to the eye and may produce painful spasms of the ciliary and iridial muscles. Systemic toxicity may also develop and the clinical signs include salivation, vomiting, diarrhea, and abdominal cramps. These drugs should be used with caution and avoided when systemic anticholinesterases are being administered.

Adrenergics Epinephrine and dipivefrin are adrenergic agents that lower the intraocular pressure in the dog and cat. Their mechanism of action is not completely understood. However, the outﬂow facility has been shown to increase and the aqueous humor formation may decrease.40 Epinephrine and dipivefrin solutions are administered q8 h. Contraindications include known sensitivities to adrenergic medications and predisposition to arrhythmias. Alpha-adrenergic agonists Alpha-adrenergic agonists, notably apraclonidine hydrochloride and brimonidine, lower IOP by decreasing aqueous production in humans and rabbits; the effect is transient and a 1.0% solution may be of value in the dog in managing the IOP elevations that may occur following surgical procedures, including cataract extraction and cyclocryosurgery.

Adrenergic antagonists Numerous topical adrenergic antagonists are available for treating glaucoma, and betaxalol and timolol maleate are the most commonly used in veterinary medicine. Limited studies are available regarding their therapeutic efﬁcacy in the dog or cat. The beta-blocker timolol maleate has been shown to reduce aqueous humor production in the dog signiﬁcantly,41 and more so in the cat,

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by up to 71%.42 Timolol decreases the rate of aqueous humor production by reduction of blood ﬂow through the ciliary processes. It is available as a solution and may be administered topically, one drop q12 h in dogs and cats. Betaxalol is a selective β-1 blocker and has been used as a prophylactic to delay the onset of primary glaucoma in the contralateral eye.43 These drugs are contraindicated in animals with known sensitivities to beta-blockers, including some cardiovascular and respiratory diseases.

Prostaglandin analogs Several prostaglandin pro-ester topical anti-glaucoma medications are available. Latanaprost, unoprostone, and travoprost are currently popular examples of these prostaglandin analogs. They exert potent and relatively long-lasting hypotensive effects after topical ocular application in the dog. Latanaprost is available as a 0.005% solution, travoprost is available as a 0.004% solution, and unoprostone as a 0.12% solution. These may be applied q12–24 h. These prostaglandin analogs induce miosis and increase uveoscleral outﬂow of aqueous humor, and may decrease aqueous humor production. Long-term clinical studies are not yet available in dogs. These medications are not as effective in cats.44,45

Carbonic anhydrase inhibitors Topical carbonic anhydrase inhibitors include dorzolamide hydrochloride, a 2% solution that should be applied q8 h, brinzolamide, a 1% solution that may be administered q8 h, and a dorzolamide (2%)–timolol (0.5%) solution that may be administered q8–12 h. Topical application avoids the potential acidotic side effects associated with systemic carbonic anhydrase medications and their use is encouraged over oral agents. These medications decrease the intraocular pressure by reducing production of aqueous humor and, aside from topical hypersensivity which is uncommon, there are no other contraindications in dogs.

Systemic ocular hypotensive medications

60

Systemic medications that reduce intraocular pressure include carbonic anhydrase inhibitors, mannitol, and glycerine. Carbonic anhydrase inhibitors reduce the intraocular pressure by decreasing the rate of aqueous humor production. Examples of carbonic anhydrase inhibitors include dichlorphenamide, acetazolamide, and methazolamide. Dichlorphenamide is currently the carbonic anhydrase of choice as it effectively lowers the intraocular pressure and has the fewest side effects. Carbonic anhydrase inhibitors are contraindicated in dogs or cats with a predisposition to or concurrent acidosis. Topical carbonic anhydrase inhibitors are now available and are aimed at avoiding the systemic side effects of these drugs. Intravenous mannitol solution and oral glycerine paste reduce the vitreous volume by osmosis and lower the intraocular pressure. They are indicated in the emergency management of some cases of canine glaucoma. Water should be restricted for 1 h after administration to attain maximum effect. Glycerine is contraindicated in the vomiting patient and both are contraindicated in patients with congestive heart failure, hypertension, or renal failure.46 Their use in the diabetic patient is controversial.3,46,47 Since the emergence and success of topical prostaglandins in the emergency management of primary

Intravitreal hypotensive injections Intravitreal injections of cyclotoxic agents have been utilized as a last resort therapy for blind glaucomatous eyes where other forms of therapy have failed and surgical therapy (enucleation or evisceration and intraocular silicone prosthesis) are not applicable due to signiﬁcant anesthetic risk or ﬁnancial considerations. Gentamicin when injected into the vitreous at a dose of 10–25 mg is toxic to the ciliary epithelium and decreases aqueous humor production;48,49 cataract and phthisis are frequent sequelae. More recently, intravitreal injections of the antiviral agent cidofovir (350–500 μg) have been used in dogs with more predictable cosmetic results.50 However, intravitreal injections for the treatment of glaucoma in the dog or cat carry signiﬁcant risk to the eye and therefore should be used only when all other alternative therapies have been considered.

THERAPEUTICS

glaucoma in dogs, oral glycerine and intravenous mannitol are seldom required today.

Mydriatics and cycloplegics Mydriasis is dilatation of the pupil, and cycloplegia is paralysis of the ciliary muscle which results in a loss of accommodative function. Parasympatholytics paralyze the iris sphincter muscle and cause mydriasis. Cycloplegia may develop depending on the type of parasympatholytic administered. Sympathomimetics stimulate the adrenergic receptors of the dilator muscle and may cause mydriasis.

Parasympatholytics Tropicamide is available as a topical ophthalmic solution. Tropicamide has minimal effect on the ciliary muscles, has a rapid onset of action (20 min), is short acting (2–4 h) and is the mydriatic of choice for intraocular examinations. Atropine has a slow onset of action (45 min) and the pupillary dilatation is accompanied by cycloplegia. Atropine is available as a topical ophthalmic solution or ointment and as a systemic medication which can be administered subconjunctivally. Topical or subconjunctival atropine is recommended for mydriasis and cycloplegia when uveitis is diagnosed in the dog and cat. Atropine may be required as often as every 6 h to maintain comfort by control of the ciliary spasm or as needed on a daily basis when the uveitis is mild. Salivation is a common side effect of these drugs as they are bitter tasting, reaching the mouth via drainage through the nasolacrimal duct; this may be a signiﬁcant problem in cats that is minimized by the use of ointments rather than solutions. Systemic side effects of atropine include tachycardia, decreased gastrointestinal motility, and reduced tear production.

Sympathomimetics Phenylephrine and epinephrine are examples of sympathomimetics. They are available as topical ophthalmic solutions which have a synergistic effect with parasympatholytics. This synergistic activity is useful in cases of resistant miosis associated with severe uveitis. Dilute solutions of epinephrine and phenylephrine are useful for differentiation of pre- and post-ganglionic Horner’s syndrome. Intracameral injections of sterile dilute solutions of epinephrine or phenylephrine are also administered during intraocular surgery to maintain

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mydriasis and control capillary bleeding. Adrenergics are contraindicated in patients with a predisposition to cardiac arrhythmias or known sensitivities to these drugs.

Indirect acting sympathomimetics Cocaine and hydroxyamfetamine are indirect acting sympathomimetics which may be administered topically to diagnose Horner’s syndrome. These medications are the drugs of choice for conﬁrming the diagnosis of Horner’s syndrome and differentiating central and pre-ganglionic from post-ganglionic lesions.51 However, the availability and need for strict control of these potentially addictive drugs has limited their use in veterinary medicine.

Lacrimomimetic drugs and artiﬁcial tears Ciclosporin is a potent immunosuppressive drug that is very useful in the treatment of immune-mediated keratoconjunctivitis sicca (KCS) in the dog. It is a T-cell suppressor which decreases lacrimal gland inﬂammation. In addition this drug has a direct lacrimomimetic effect and it also reduces corneal inﬂammation. It is available commercially as a 0.2% ophthalmic ointment and has been compounded as a 1% and 2% solution and as a 1% emulsion. A quarter of an inch strip of the ointment or one drop of the solution or emulsion is applied to the cornea every 12 h and, if instituted early in the course of immune-mediated keratoconjunctivitis sicca, will reverse the low tear production in the majority of patients with restoration of normal Schirner values in 6 weeks. Topical ciclosporin is poorly absorbed through the cornea and has minimal systemic effects. It may be used when corneal ulcers are present and it remains the drug of choice for dry eye in the dog.52 In addition it has been reported as an effective agent in the control of chronic superﬁcial keratitis in the dog.53 The contraindications for topical ophthalmic ciclosporin include keratomycosis and known hypersensitivities to ciclosporin or its carriers. Recently, other calcineurin inhibitors similar to ciclosporin have been utilized to treat KCS in dogs. These include tacrolimus and sirolimus. However, most of the information reported at this time regarding these potentially carcinogenic topical medications is anecdotal and only two conﬂicting studies are reported.54,55 Before these medications are utilized further, placebocontrolled pharmaceutic studies need to be completed and their safety thoroughly assessed. Pilocarpine has been reported to be an effective lacrimomimetic drug in the treatment of neurogenic KCS.56 Oral pilocarpine can be toxic and should be administered with caution to dogs. Signs of toxicity include vomiting and diarrhea. These clinical signs are often used to ensure an adequate dosing and, if the tear production is not increased at that time, the pilocarpine is discontinued.

Tear replacements

62

Numerous tear supplements are available. These include hypertonic, isotonic, and hypotonic tear solutions. In addition, tear replacements are available as ointments which provide a longer duration of effect compared to the solutions. Artiﬁcial tears, hydroxymethylcellulose, and polyvinyl alcohols should be administered frequently and are usually required in excess of q4 h to prevent corneal dehydration. Hyaluronic acid solutions increase the duration of tear

MISCELLANEOUS TOPICAL DRUGS

THERAPEUTICS

contact and stabilize the tear ﬁlm, and they are useful adjunctive agents in the treatment of qualitative and quantitative tear ﬁlm abnormalities in the dog and cat.

(see Appendix, Table 7) Proparacaine and tetracaine are topical anesthetics that are required prior to tonometry and to facilitate the ocular examination. Topical anesthetics are toxic to the corneal epithelium and repetitive or prolonged use is strongly discouraged as it may lead to severe corneal ulceration, or even perforation. The preservatives that are present are reported to interfere with bacterial cultures.57 Ideally laboratory submissions including bacterial, fungal, and viral cultures, and cytologic samples should be collected prior to application of any topical solutions, emulsions, or ointments. Fluorescein and Rose bengal are stains which are routinely used in ocular examinations. Fluorescein is a water-soluble dye which readily penetrates the conjunctival submucosa or the corneal stroma when the lipophilic epithelium has been disrupted. It is applied topically during the ophthalmic examination to conﬁrm corneal ulceration. It is available as an impregnated strip or solution. Rose bengal is available as an impregnated strip. It is a supravital dye that is used to detect devitalized epithelium. These stains will interfere with bacterial and viral cultures and immunocytology, and therefore those laboratory submissions should be completed before these stains are applied.58,59

REFERENCES 1. Mishima, S. (1981) Clinical pharmacokinetics of the eye. Invest. Ophthalmol. Vis. Sci. 21: 504–541. 2. Peiffer, R.L. and Stowe, C.M. (1981) Veterinary ophthalmic pharmacology. In: Gelatt, K.N. (ed) Veterinary Ophthalmology. Philadelphia: Lea & Febiger, pp. 160–205. 3. Regnier, A. and Toutain, P.L. (1991) Ocular pharmacology and therapeutic modalities. In: Gelatt, K.N. (ed) Veterinary Ophthalmology, 2nd edn. Philadelphia: Lea & Febiger, pp. 162–194. 4. Doane, M.G., Jensen, A.D. and Dohlman, C.H. (1978) Penetration routes of topically applied eye medications. Am. J. Ophthalmol. 85: 383. 5. Schoenwald, R.D. (1990) Ocular drug delivery. Pharmacokinetic

considerations. Clin. Pharmacokinet. 18: 255–269. 6. Mikkelson, T.J., Chrai, S.S. and Robinson, J.R. (1973) Competitive inhibition of drug–protein interaction in eye ﬂuids and tissues. J. Pharm. Sci. 62: 1942–1945. 7. Mikkelson, T.J., Chrai, S.S. and Robinson, J.R. (1973) Altered bioavailability of drugs in the eye due to drug–protein interaction. J. Pharm. Sci. 62: 1648–1653. 8. Shell, J.W. (1982) Pharmacokinetics of topically applied ophthalmic drugs. Surv. Ophthalmol. 26: 207–218. 9. Burstein, N.L. and Anderson, J.A. (1985) Review: Corneal penetration and ocular bioavailability of drugs. J. Ocular Pharmacol. 1: 309–326. 10. Bartlett, J.D. and Cullen, A.P. (1989) Clinical administration of ocular

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drugs. In: Bartlett, J.D. and Jaanus, S.D. (eds) Clinical Ocular Pharmacology. Toronto: ButterworthHeinemann, pp. 29–66. 11. Wine, N.A., Gonall, A.G. and Basu, P.K. (1964) The ocular uptake of subconjunctivally injected C14 hydrocortisone. I. Time and major route of penetration in a normal eye. Am. J. Ophthalmol. 58: 362–366. 12. McCartney, H.J., Drysdale, I.O., Gornall, A.G. et al. (1965) An autoradiographic study of the penetration of subconjunctivally injected hydrocortisone into the normal and inﬂamed rabbit eye. Invest. Ophthalmol. Vis. Sci. 4: 297–302. 13. Lapalus, P. and Garraffo, R.G. Ocular pharmacokinetics. In: Hockwin, O., Green, K.G. and Rubin, L.F. (eds) Manual of Oculotoxicity Testing. New York: Gustav Fischer, pp. 119–136. 14. Fraunfelder, F.T. and Hanna, C. (1974) Ophthalmic drug delivery systems. Surv. Ophthalmol. 18: 292–298. 15. Fisher, C.A. (1979) Granuloma formation associated with subconjunctival injection of a corticosteroid in dogs. J. Am. Vet. Med. Ass. 174: 1086–1088. 16. Murphy, C.M., Lavach, J.D. and Severin, G.A. (1978) Survey of conjunctival ﬂora in dogs with clinical signs of external eye disease. J. Am. Vet. Med. Ass. 172: 66–68. 17. Gerding, P.A., McLaughlin, S.A. and Troop, M. (1988) Pathogenic bacteria and fungi associated with external ocular diseases in dogs: 131 cases (1981–1986). J. Am. Vet. Med. Ass. 193: 242–244. 18. Van Bijsterveld, O.P., Andriesse, H., Nielsen, B.H. (1987) Fusidic acid in tear ﬁlm: pharmokinetic study of fusidic acid viscous eye drops. Eur. J. Drug Metab. Pharmokinet. 12: 215–218. 19. Petroutsos, G., Savoldelli, M. and Pauliquen, Y. (1990) The effect of gentamicin on the corneal endothelium. Cornea 9: 62–65.

20. Moller, I., Cook, C., Peiffer, R.L. et al. (1986) Indications for and complications of the pharmacological ablation of the ciliary body for the treatment of chronic glaucoma in the dog. J. Am. Anim. Hosp. Ass. 22: 319–326. 21. Nasisse, M.P., Guy, J.S., Davidson, M.G. et al. (1989) In vitro susceptibility of feline herpesvirus-1 to vidarabine, idoxuridine, tridﬂuridine, acyclovir, or bromovinlydeoxyuridine. Am. J. Vet. Res. 50: 58–60. 22. Maggs, D.J. and Clark, H.E. (2004) In-vitro efﬁcacy of ganciclovir, cidofovir, pencyclovir, foscarnet, idoxuridine, and acyclovir against feline herpesvirus 1. Am. J. Vet. Res. 65: 399–403. 23. Sandmeyer, L.S., Keller, C.B. and Bienzle, D. (2005) Effects of cidofovir on cell death and replication of feline herpesvirus-1 in cultured feline corneal epithelial cells. Am. J. Res. 66: 217–222. 24. Severin, G.A. (1995) Severin’s Veterinary Ophthalmology Notes, 3rd edn. Fort Collins: Design Pointe Communications, pp. 88–89. 25. Noxon, J.O., Monroe, W.E. and Chinn, D.R. (1986) Ketaconazole therapy in canine and feline cryptococcosis. J. Am. Anim. Hosp. Ass. 22: 179. 26. Ford, M.M. (2004) Antifungals and their use in veterinary ophthalmology. In: Moore, C.P. (ed) Ocular Therapeutics. Vet. Clin. North Am. 34: 669–691. 27. Nasisse, M.P. (1991) Feline Ophthalmology. In: Gelatt, K.N. (ed) Veterinary Ophthalmology, 2nd edn. Philadelphia: Lea & Febiger, pp. 539–541. 28. Weiss, R.C. (1989) Synergistic antiviral activities of acyclovir and recombinant human leukocyte (alpha) interferon on feline herpes virus replication. Am. J. Vet. Res. 50: 1672– 1677. 29. Weiss, R.C. (1989) Synergistic antiviral activities of acyclovir and recombinant human leukocyte (alpha)

tracts of dogs. Am. J. Vet. Res. 51: 1131–1138. 39. Giuliano, E.A. (2004) Nonsteroidal anti-inﬂammatory drugs in veterinary ophthalmology. In: Moore, C.P. (ed) Ocular Therapeutics. Vet. Clin. North Am. 34: 707–723. 40. Gwin, R.M., Gelatt, K.N., Gum, G.G. et al. (1978) Effects of topical epinephrine and dipivalyl epinephrine on intraocular pressure and pupil size in the normotensive and glaucomatous beagle. Am. J. Vet. Res. 39: 83–86. 41. Gumm, G.G., Larocca, R.D., Gelatt, K.N. et al. (1991) The effect of topical timolol maleate on intraocular pressure in normal beagles and beagles with inherited glaucoma. Prog. Vet. Comp. Ophthalmol. 1: 141–149. 42. Lui, H.K., Chiou, G.C.Y. and Gorg, L.L. (1980) Ocular hypotensive effects of timolol in cat eyes. Arch. Ophthalmol. 98: 1467–1469. 43. Miller, P.E., Schmidt, G.M., Vainisi, S.J. et al. (2000) The efﬁcacy of topical prophylactic antiglaucoma therapy in primary closed angle glaucoma in dogs: a multicenter clinical trial. J. Am. Anim. Hosp. Assoc. 36: 431–438. 44. Studer, M.E., Martin, C.L. and Stiles, M.J. (1998) The effect of latanaprost 0.005% on intraocular pressure in normal feline and canine eyes. Proc. Am. Coll. Vet. Ophthalmol. 29: 45. 45. Willis, A.M. (2004) Ocular hypotensive drugs. In: Moore, C.P. (ed) Ocular Therapeutics. Vet. Clin. North Am. 34: 755–776. 46. Dugan, S.J., Roberts, S.M. and Severin, G.A. (1989) Systemic osmotherapy for ophthalmic disease in dogs and cats. J. Am. Vet. Med. Ass. 194: 115–118. 47. Adams, R.E., Kirschner, R.J. and Leopold, I.H. (1963) Ocular hypotensive effect of intravenously administered mannitol. Arch. Ophthalmol. 69: 55–58. 48. Moller, I., Cook, C.S., Peiffer, R.L. et al. (1986) Indications for and complications of pharmacological

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interferon on feline herpesvirus replication. Am. J. Vet. Res. 50: 1672–1677. 30. Sandmeyer, L.S., Keller, C.B. and Bienzle, D. (2005) Effects of interferon-α on cytopathic changes and titers for feline herpesvirus-1 in primary cultures of feline corneal epithelial cells. Am. J. Res. 66: 210–216. 31. Collins, B.K., Nasisse, M.P. and Moore, C.P. (1995) In vitro efﬁcacy of L-lysine supplementation on ocular shedding rate of feline herpesvirus type 1. Proc. Am. Coll. Vet. Ophthalmol. 26: 141. 32. Maggs, D.J. and Nasisse, M.P. (1997) Effects of L-lysine supplementation on ocular shedding rate of herpesvirus (FHV-1) in cats. Proc. Am. Coll. Vet. Ophthalmol. 28: 101. 33. Nasisse, M.P., Dorman, D.C., Jamison, K.C. et al. (1997) Effects of valcyclovir in cats infected with feline herpesvirus 1. Am. J. Vet. Res. 58: 1141–1144. 34. Gayles, B.I. and Fiscella, R. (2002) Topical non-steroidal antiinﬂammatory drugs for ophthalmic use: a safety review. Drug Saf. 25: 233–250. 35. Hendrix, D.V.H., Ward, D.A. and Barnhill, M.A. (2002) Effects of antiinﬂammatory drugs and preservatives on morphologic characteristics and migration of canine corneal epithelial cells in tissue culture. Vet. Ophthalmol. 5: 127–135. 36. Lin, J.C., Rapuano, C.J., Laibson, P.R. et al. (2000) Corneal melting associated with use of topical nonsteroidal anti-inﬂammatory drugs after ocular surgery. Arch. Ophthalmol. 118: 1129–1132. 37. Flach, A.J. (2001) Corneal melts associated with topically applied nonsteroidal anti-inﬂammatory drugs. Trans. Am. Ophthalmol. Soc. 99: 205–212. 38. Dow, S.W., Rosychuk, R.A., McChesney, A.E. et al. (1990) Effects of ﬂunixin and ﬂunixin plus prednisone on the gastrointestinal

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ablation of the ciliary body for the treatment of chronic glaucoma in the dog. J. Am. Anim. Hosp. Assoc. 1986; 22: 319–326. 49. Bingaman, D.P., Lindley, D.M., Glickman, N.W. et al. (1994) Intraocular gentamicin and glaucoma: a retrospective study of 60 dog and cat eyes (1985–1993). Vet. Comp. Ophthalmol. 4: 113–119. 50. Peiffer, R.L. and Harling, D.E. (1998) Intravitreal cidofovir (Vistide) in the management of glaucoma in the dog and cat. Proc. Am. Coll. Vet. Ophthalmol. 29: 29. 51. Scagliotti, R.H. (1998) Neuroophthalmology. In: Gelatt, K.N. (ed) Veterinary Ophthalmology, 3rd edn. Philadelphia: Lea & Febiger, pp. 1307–1400. 52. Kaswan, R.L., Salisbury, M.A. and Ward, D.A. (1989) Spontaneous canine keratoconjunctivitis: a model for human keratoconjunctivitis sicca – treatment with cyclosporine eye drops. Arch. Ophthalmol. 107: 1210. 53. Jackson, P.A., Kaswan, R.L., Meredith, R.E. et al. (1991) Chronic superﬁcial keratitis in dogs: a placebo controlled trial of topical cyclosporine treatment. Prog. Vet. Comp. Ophthalmol. 1: 269–275.

54. Berdoulay, A., English, R.V., Nadelstein, B. et al. (2003) The effect of 0.02% tacrolimus aqueous suspension on the tear ﬁlm in dogs with keratoconjunctivitis sicca. Proc. Am. Coll. Vet. Ophthalmol. 34: 33. 55. Adkins, E.A., Hendrix, D.V.H., Stufﬂe, J.L. et al. (2003) An investigation of the safety and efﬁcacy of topical ophthalmic application of tacrolimus in dogs. Proc. Am. Coll. Vet. Ophthalmol. 34: 39. 56. Rubin, L.F. and Aguirre, G.D. (1969) Clinical use of pilocarpine for keratoconjunctivitis in dogs and cats. J. Am. Vet. Med. Ass. 151: 313. 57. Kleinfeld, J. and Ellis, P.P. (1966) Effects of topical anesthetics on growth of microorganisms. Arch. Ophthalmol. 76: 712–715. 58. Roat, M.E., Romanowski, E., Araullo-Cruz, T. et al. (1987) The antiviral effect of rose bengal and ﬂuorescein. Arch. Ophthalmol. 105: 1415–1417. 59. da Silva Curiel, J.M.A., Nasisse, M.P., Hook, R. et al. (1991) Topical ﬂuorescein dye: effects on immunoﬂuorescent antibody tests for feline herpesvirus keratoconjunctivitis. Prog. Vet. Comp. Ophthalmol. 1: 99–104.

Abnormal appearance Wendy Townsend, Peter Bedford, and Gareth Jones

4

The conditions discussed in this chapter are those in which an alteration in the gross appearance of the eye is the primary presenting clinical feature. Other signs of disease may also be present and the reader should refer to other chapters in this book in cases where visual impairment, ocular pain, or ocular discharge is the most signiﬁcant presenting sign. The ﬁrst part of this chapter describes the normal appearance of the eye and adnexa (Figs 4.1 & 4.2). Abnormal appearance is discussed in the second part of the chapter.

NORMAL APPEARANCE Selective breeding, particularly in dogs, has resulted in a wide variation in skull shape, globe position, and adnexal conformation. Many of these traits may be considered ‘normal’ for a particular breed. Examples include the exophthalmos (globe prominence) and lagophthalmos (failure to blink completely) noted frequently in brachycephalic animals. In all cases the clinician must decide if the noted attribute is an incidental ﬁnding or associated with ocular disease.

The globe The size of the globe, shape and length of the palpebral ﬁssure, and depth of the orbit all contribute to the external appearance of the eye. Brachycephalic animals have shallow orbits and large palpebral ﬁssures resulting in a very prominent globe. In contrast, dolicocephalic dogs have the globe positioned deeper within the orbit resulting in a much less prominent globe. In all animals the globe should be centrally positioned within the orbit and freely mobile. The extraocular muscles provide globe movement and maintain a centrally directed gaze. Sympathetic innervation of the orbital smooth muscle (muscularis orbitalis) maintains positive tone within the orbit and thereby an anterior position of the globe. The retractor bulbi muscles function to retract the globe.

The eyelids The appearance and position of the eyelids are determined by a number of factors including the length of the palpebral ﬁssure, physical support by the

67

SMALL ANIMAL OPHTHALMOLOGY Fig. 4.1 The normal appearance of the eye and adnexa in the dog. Right eye.

Fig. 4.2 The normal appearance of the eye and adnexa in the cat. Right eye.

68

presence of the globe, and tension at the medial and lateral canthi. The shape of the cranium and mass of facial skin can alter this relationship, leading to conformational differences between the breeds. An example of an abnormality required by breed standards is the ‘diamond eye’ conformation in breeds like the St Bernard and the Bloodhound, where central lower ectropion and third eyelid exposure can be responsible for chronic conjunctivitis. Similarly Shar Peis have excess facial skin that frequently contributes to entropion. In normal animals the eyelids rest on the globe and follow its contour. The eyelid margins are hairless and distinct. In dogs two to four rows of cilia are present along the upper eyelid. Varying amounts of sclera are exposed depending upon breed and facial conformation. Cats have little exposed sclera and no true cilia.

ABNORMAL APPEARANCE

The eyelids protect the globe, remove debris from the ocular surface, and distribute the tear ﬁlm. The eyelids should move freely and fully across the corneal surface. The superior eyelid is the most mobile. Regular blinking is an essential feature. Dogs blink three to ﬁve times per minute; cats one to ﬁve times per minute. Brachycephalic animals blink less frequently and less completely (lagophthalmos) due to their exophthalmos and decreased corneal sensitivity. Cats normally demonstrate complete and incomplete blinks. Elevation of the upper eyelid occurs primarily through the action of the levator palpebrae superioris muscle that is innervated by cranial nerve III, assisted by the smooth muscle ﬁbers of Müller’s muscle. The orbicularis oculi muscle innervated by cranial nerve VII is responsible for closure of the eyelids.

The third eyelid The third eyelid (membrana nictitans) arises as a fold of ventromedial conjunctiva and lies against the anteromedial aspect of the globe. A T-shaped cartilage stabilizes the third eyelid. The top of the T runs across the free edge and the base runs through the center to end in the gland of the third eyelid. The leading edge of the third eyelid may or may not be pigmented (Figs 4.3 & 4.4). When lacking pigment, the third eyelid appears more prominent. The position of the third eyelid is inﬂuenced by globe size, position of the globe within the orbit, orbital depth and contents, and length of the palpebral ﬁssure. Movement of the third eyelid is passive in dogs. Retraction of the globe will result in protrusion of the third eyelid. In cats, smooth muscle contributes to movement of the third eyelid and sympathetic stimulation can cause the third eyelid to move slightly.

The conjunctiva/sclera The conjunctiva is the transparent mucous membrane that lines the eyelids (palpebral conjunctiva) and covers the membrana nictitans and the anterior sclera (bulbar conjunctiva). There is little variation between species and breeds.

Fig. 4.3 The normally pigmented leading edge of the membrana nictitans in a 2-yearold German Shepherd Dog. Left eye.

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SMALL ANIMAL OPHTHALMOLOGY Fig. 4.4

Left eye of a dog with a non-pigmented leading edge to the third eyelid.

Fig. 4.5 eye.

Comparison of the bulbar, palpebral, and membrana conjunctival surfaces. Left

Pigmentation may be normal, especially within the palpebral ﬁssure, and is usually diffuse and irregular. It is important to appreciate the differences in normal appearance across the conjunctival sac. The bulbar conjunctiva is loosely bound to the globe and it appears mainly white due to the color of the sclera beneath. Blood-ﬁlled capillaries impart a salmon pink color. Elements of the underlying episcleral vasculature are not very prominent in the normal dog but are more readily seen in the cat. In contrast, the palpebral conjunctiva is ﬁrmly attached and its deep pink appearance is that of the underlying tarsal tissues (Fig. 4.5). The conjunctiva within the fornix has a similar coloration but is loosely attached.

The cornea 70

The normal cornea is transparent with a glossy and smooth anterior surface. The junction between the cornea and sclera is the limbus. The corneal diameter

ABNORMAL APPEARANCE

varies from 12.5 mm in the dog to 18.0 mm in the cat. The radius of curvature is approximately 8 mm. Multiple layers comprise the cornea. The tear ﬁlm is the outermost later which overlies a multilayered epithelium and creates a smooth optical surface. The thickest corneal layer, the stroma, is predominantly collagen ﬁbrils in regularly arranged lamellae that provide optical clarity. Descemet’s membrane is the basement membrane of the innermost layer, a single layer of endothelium. In order to allow transparency, the cornea is avascular; nutrition is supplied via the aqueous and to a lesser extent by the precorneal tear ﬁlm, limbal scleral circulation, and conjunctival vasculature. The stroma must be maintained in a relative state of dehydration for transparency and both the epithelium and endothelium are involved in this process. The epithelium presents a barrier to water in the tear ﬁlm while an active endothelial pump mechanism regulates ﬂuid exchange with the aqueous. In puppies and kittens, it is common for the cornea to appear cloudy immediately after the palpebral ﬁssure ﬁrst opens and before the endothelial ‘pump’ becomes fully functional.

The aqueous and the anterior chamber The aqueous is a modiﬁed ultraﬁltrate of blood and is normally transparent due to a low protein and cell content. It is produced by the ciliary processes, released into the posterior chamber, and ﬂows forward between the iris and lens through the pupil into the anterior chamber. The aqueous circulates thermodynamically within the anterior chamber and drains into the scleral vasculature through the 360° of the iridocorneal angle. In domestic species, the angle extends into the ciliary body as the ciliary cleft. The entrance to the cleft is spanned by ﬁbers of the pectinate ligament and the cleft contains the trabecular meshwork. The pectinate ligament may be visualized with the naked eye in the cat because of the considerable depth of the anterior chamber. In the dog, the use of a goniolens is required to examine the iridocorneal angle (see Fig. 2.9). Individual variation exists in both the amount of pigmentation in the scleral shelf and the physical structure of the pectinate ligament. Those individuals with a wider pigmentary zone are more difﬁcult to examine. The pectinate ligament should always be visible. Intraocular pressure (IOP) is maintained by homeostatic mechanisms resulting in equilibrium between the rates of aqueous production and outﬂow. The normal IOP ranges from 13 to 24 mmHg.1 In the dog this value can fall to below 10 mmHg with age.

The iris The iris rests on the anterior surface of the lens, imparting an anterior bow to the iris. Loss of this lenticular support results in ﬂattening of the iridal surface, a deepened anterior chamber, and iridodonesis (trembling of the iris) with ocular movement. The iris is divided into two areas by the collarette (the area where the iris changes from a lighter to a darker color): the ciliary zone (peripherally) and the pupillary zone (centrally). The pupillary ruff is the edge of the iris that forms the pupil. The major arterial circle is the prominent circular vessel within the ciliary zone; this vessel is especially easy to visualize in cats with blue irides. The anterior iris is deﬁned by a condensation of melanocytes and a pigmented epithelium lines its posterior surface. The stroma of the iris

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contains two muscles: the iris dilator (longitudinal muscle) and the iris constrictor (circular muscle located in the pupillary zone). The iris regulates the amount of light entering the eye via the constrictor and dilator muscles. Iris coloration is related to the density of coat and skin pigmentation and consequently demonstrates considerable variation between both species and breeds. Darker coated breeds of dog will have a dark brown iris while in the subalbinotic breeds the iris is often blue (Fig. 4.6). Yellow, green, and blue iris coloration can all be seen in cats (Fig. 4.7). Heterochromia iridis describes a difference in color within the same iris and heterochromia irides describes a difference in color between the two irides of the same individual.

Fig. 4.6 A blue iris demonstrating the difference in color density between the ciliary and pupillary zones in a 4year-old Siberian Husky. Left eye.

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Fig. 4.7

Blue iris color in a 2-year-old cat.

The pupil The pupil is round in the dog and a vertical ellipse when constricted in the cat. A slight exposure of the darkly colored iris pigment epithelium may occur at the pupillary rim. Abnormal prominence of the iris pigment epithelium may occur with cystic hypertrophy due to chronic uveitis. Eversion of the pupillary margin (ectropion uveae) may occur secondary to formation of pre-iridal ﬁbrovascular membranes (rubeosis iridis). The pupil should move freely with maximal dilatation in the dark and brisk constriction in bright light; this movement is observed when assessing the direct and consensual pupillary light responses. Senile iris atrophy may cause an irregular scalloped pupillary margin and incomplete constriction in bright light. Posterior synechia (adhesions between the iris and anterior lens capsule) may also distort the pupillary margin and prevent free pupillary movement.

ABNORMAL APPEARANCE

Senile iris atrophy can result in a lace-like appearance demonstrable by transillumination or retroillumination using reﬂection of light from the fundus to highlight the thinned iris. Atrophy of the sphincter muscle results in pupil irregularities and reduced pupillary constriction.

The lens The lens is a transparent biconvex structure enclosed within its own capsule. Nutrition is via ﬂuid exchange with the aqueous across the lens capsule. The lens is normally positioned between the posterior iridal surface and the vitreous body. Without the use of mydriatic drugs to dilate the pupil, only the axial portion of the lens is visible. With mydriasis a complete examination of the lens including the equatorial regions can be performed. Lens transparency is attributed to the absence of blood vessels and the precise arrangement of the proteins within the lens ﬁbers. New cortical ﬁbers are formed throughout life by the equatorially positioned lens epithelial cells. The anterior Y and posterior inverted Y suture lines mark the meeting of the ends of lens ﬁbers. In young animals increased prominence of the tips of these suture lines may be present. The continuous cortical lens ﬁber formation causes compression of the central nuclear material which results in altered refraction through the nuclear region noted clinically as nuclear sclerosis. Nuclear sclerosis is a normal aging change which can be differentiated from a true cataract using indirect ophthalmoscopy, distant direct ophthalmoscopy, or distant examination with a transilluminator. The tapetal reﬂex and detail of the fundus can be observed through a sclerotic nucleus.

The posterior segment The fundus is divided into tapetal and non-tapetal areas. The non-tapetal area occupies the greater part of the fundus and this area is usually darkly colored due to pigment within the retinal pigment epithelium and the underlying choroid. The retinal pigment epithelium, which overlies the reﬂective brightly colored tapetum, is non-pigmented. Tapetal color varies, but most commonly is yellow, orange, green, or blue (Fig. 4.8). The tapetum may be small or completely absent, particularly in the toy breeds. A ‘red’ reﬂex is normal in subalbinotic breeds which may lack a tapetum in addition to having reduced or absent pigment within the retinal pigment epithelium and choroids (Fig. 4.9). Edema and/or inﬁltrates within the vitreous, retina, or sub-retinal space will

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SMALL ANIMAL OPHTHALMOLOGY

Fig. 4.8 A yellow-green tapetal reﬂex in a 4-yearold crossbred dog.

Fig. 4.9 The red tapetal reﬂex due to subalbinism in a 2-year-old Old English Sheepdog.

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reduce the intensity of the tapetal reﬂex. Where the retina is degenerate or absent due to complete detachment, tapetal reﬂectivity will be considerably increased. In the presence of extensive retinal degeneration there will be a loss of the pupillary light reﬂex, which enhances the appearance of the increased reﬂection from the affected eye. In dogs the optic disk is circular to triangular in shape, the variation due to varying degrees of myelination. The disk may reside in the tapetal or nontapetal fundus as the size of the tapetum varies greatly between individuals.

ABNORMAL APPEARANCE

The dark gray spot in the center of the disk represents the physiologic pit. Three to four large retinal venules anastomose in an incomplete venous circle over the optic disk. Fifteen to 20 arterioles, lighter in color and more tortuous than the venules, radiate away from the periphery of the optic disk. In cats the optic disk is unmyelinated which accounts for its perfectly circular and dark salmon to grey coloration. The disk is always located in the tapetal fundus. The feline tapetum is more brightly reﬂective than that of the dog. Three to ﬁve main pairs of retinal arterioles and venules are present. The venules do not traverse the surface of the optic disk.

ABNORMAL APPEARANCE The eye should never be examined in isolation. The ocular examination should be systematic. The most signiﬁcant changes in appearance are listed in Table 4.1. Each clinical sign listed in Table 4.1 will be discussed in terms of investigation, diagnosis, and treatment.

The globe Changes in globe size Abnormally small globe Microphthalmos is the presence of a congenitally small globe. Microphthalmos may be seen alone or in association with multiple ocular anomalies including nystagmus, persistent pupillary membranes, colobomata, cataract, and retinal dysplasia. Associated cataracts are usually non-progressive. The degree of visual impairment depends upon the extent of the abnormalities. Penetrating sharp trauma or perforation of a corneal ulcer through Descemet’s membrane may lead to collapse of the globe. A careful ophthalmic examination should be performed to assess damage while preventing further trauma to the globe. Prompt repair can be successful depending upon the extent of intraocular damage. The prognosis for vision following globe rupture from blunt trauma is usually poor due to more pronounced intraocular damage. Phthisis bulbi is a previously normal globe that has become irreversibly damaged, hypotensive, and shrunken. Phthisis bulbi is a common sequela to severe injury, chronic uveitis, or long-standing glaucoma. Phthisical eyes are non-visual. If the eye is a chronic source of discomfort, enucleation is indicated. In phthisical feline globes, post-traumatic sarcomas have developed. These sarcomas are very aggressive and often metastasize.2 Therefore enucleation of blind traumatized feline globes is recommended.

Enlarged globe Buphthalmos is the acquired enlargement of a globe, typically associated with glaucoma. Buphthalmos must be differentiated from exophthalmos (rostral displacement of the globe within the orbit). The cardinal signs of glaucoma are a dilated non-responsive pupil, episcleral congestion, corneal edema, and an elevated IOP. Degenerative corneal changes may occur with chronic glaucoma. Linear breaks in Descemet’s membrane (Haab’s striae) also indicate increased globe size (Fig. 4.10). Buphthalmic globes are usually blind due to the associated ganglion cell degeneration and optic nerve atrophy; exceptions include the

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Table 4.1 Abnormal appearance. Globe Small globe

Globe rupture, microphthalmos, phthisis bulbi

Enlarged globe

Glaucoma, neoplasia

Exophthalmos

Arteriovenous ﬁstula (rare), orbital fracture, retrobulbar space-occupying lesion (e.g. masticatory myositis, extraocular polymyositis, neoplasia, retrobulbar abscess/cellulites, zygomatic mucocele), temporomandibular osteopathy, traumatic proptosis

Enophthalmos

Horner’s syndrome, loss of retrobulbar fat (debility, senility), orbital fracture, severe ocular pain, temporal muscle atrophy, contracture of extraocular muscles

Eyelids Alopecia

Bacterial pyoderma, immune-mediated disease, mycoses, nutritional disease, parasitic infestation, seborrhea

Swellings/masses

Abscess, allergy, epibulbar dermoid, neoplasia, ophthalmia neonatorum, trauma

Shape of palpebral ﬁssure

Coloboma, ectropion, entropion, combined entropion/ectropion (diamond eye), laceration, symblepharon, dermoid, ankyloblepharon, Horner’s syndrome

Membrana nictitans Prominence

Anterior segment pain, dysautonomia, Horner’s syndrome, retrobulbar lesion, sedation, ‘Haw’s syndrome’, symblepharon, systemic disease (e.g. tetanus)

Distortion

Prolapse of the nictitans gland, scrolling of the cartilage

Masses

Lymphoid follicles, neoplasia, plasma cell inﬁltration

Conjunctiva/sclera

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Redness

Conjunctivitis (superﬁcial), ciliary ﬂush/episcleral congestion, episcleritis (deep), subconjunctival hemorrhage

Swelling

Allergy, conjunctivitis, diffuse neoplasia

Masses

Cyst, neoplasia, nodular episcleritis

Cornea Opacity

Cellular inﬁltration (white/gray), edema (white/ blue), pigmentation (black), scarring (blue/gray), vascularization (red)

Masses

Dermoid, granulation tissue, inclusion cysts, abscess, inﬁltrative neoplasia

Vascularization

Superﬁcial and deep keratitis, corneal inﬁltration and degeneration, eosinophilic keratitis, healing ulcer, herpes keratitis, immune-mediated disease, sequestrum, trauma

Inﬁltration

Calcareous degeneration, corneal ‘melting’ ulcer, lipidosis (dystrophy, degeneration, and inﬁltration), neoplasia

Change in contour

Bullous keratopathy, corneal abscess, corneal laceration, descemetocele, inclusion cyst, iris prolapse

Loss of tissue

Laceration, ulceration, post-corneal nigrum slough

ABNORMAL APPEARANCE

Table 4.1 continued

Anterior chamber Turbidity

Lipid-laden aqueous, uveitis (ﬂare/hypopyon, keratic precipitates, hyphema)

Masses

Foreign body, lens luxation, neoplasia, uveal cyst

Hyphema

Blood dyscrasias, chronic glaucoma, congenital lesions, hypertension, neoplasia, retinal detachment, trauma, uveitis

Iris Discoloration

Chronic uveitis (pigmentation), rubeosis iridis (vascularization)

Masses

Neoplasia, uveal cysts

‘Strands’

Persistent pupillary membrane, synechiae

Pupil Dilated

Coloboma, dysautonomia, glaucoma, iris atrophy, oculomotor nerve lesion, optic neuropathy, retinopathy, pharmacologic agents, fear

Constricted

Uveitis, Horner’s syndrome, pharmacologic agents

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Table 4.1 continued Distorted

Synechiae, coloboma, iridodonesis, ‘D’-shaped pupil, iris atrophy

Lens Opaciﬁcation

Cataract, uveitis (anterior capsular pigment), nuclear sclerosis, persistent pupillary membrane, persistent hyperplastic primary vitreous

Shape

Lenticonus, coloboma

Position

Luxation, subluxation

Posterior segment

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Leukocoria (white pupil)

Cataract, intraocular foreign body, neoplasia, persistent hyperplastic primary vitreous, retinal detachment, vitreous abscess

Increased reﬂectivity (+ dilated pupil)

Retinal degeneration, retinal detachment with disinsertion

Decreased reﬂectivity

Posterior uveitis (vitreal haze), bullous retinal detachment

Fig. 4.10 Haab’s striae in chronic glaucoma. Right eye, 6-year-old Norwegian Elkhound.

ABNORMAL APPEARANCE

globes of young animals where the elastic sclera can allow for globe enlargement with some degree of vision remaining. A similar ﬁnding is occasionally found in dogs where the IOP is only moderately elevated. For permanently blind eyes options to improve patient comfort include enucleation or evisceration and implantation of an intrascleral silicone prosthesis. An alternative approach is to destroy part of the ciliary body to reduce IOP. Techniques include cyclocryotherapy, cyclophotocoagulation, and pharmacologic ablation using intravitreal gentamicin or cidofovir.3 In every instance the etiology of the glaucoma should be determined in order to rule out the presence of an intraocular tumor resulting in secondary glaucoma.

Changes in globe position Exophthalmos (globe protrusion) Exophthalmos is the rostral displacement of a normal sized globe within the orbit (Fig. 4.11). This displacement will cause widening of the palpebral ﬁssure and may prevent complete eyelid closure. The induced lagophthalmos may result in exposure keratitis (drying and ulceration of the central cornea) to develop. A comparison of the position of each globe, particularly when viewed from above, helps to distinguish exophthalmos from buphthalmos. Resistance of the globe to retropulsion is also helpful to conﬁrm exophthalmos. The direction of displacement of the globe can be helpful in localizing the site of the mass lesion. The third eyelid is often passively elevated due to displacement by a spaceoccupying lesion. Intraconal lesions (within the endorbital muscle cone) often have minimal protrusion of the nictitating membrane as compared to extra-

Fig. 4.11 A retrobulbar neoplasm causing exophthalmos in a 1-year-old Springer Spaniel.

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80

conal lesions (outside the endorbital muscle cone but within the soft tissue conﬁnes of the orbit).4 Historical information concerning chronicity, progression, and association with trauma may assist in ranking differential diagnoses. The presence of pain, particularly upon opening the mouth, is highly suggestive of a retrobulbar abscess, orbital fracture, or masticatory muscle myositis. One must perform a careful oral examination with particular attention paid to the area caudal to the last upper molar where extension of retrobulbar neoplasia, the draining sinus of a retrobulbar abscess, or distension due to zygomatic mucocele formation may be observed. Radiography may only reveal non-speciﬁc soft tissue swelling although an occlusal view of the nasal cavity is important in the investigation of nasal tumors, which can erode through the orbital wall. Periosteal changes may be seen in craniomandibular osteopathy. Dental radiographs may reveal fractured tooth roots and lytic areas along the maxilla. Ultrasonographic examination can conﬁrm the presence as well as the location of a retrobulbar mass and may give some indication of the tissue type based on the echo texture.5 Imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) can be invaluable.6 A ﬁne needle aspirate may allow for a cytologic diagnosis.7 An exploratory orbitotomy may be necessary to conﬁrm the exact nature and extent of the orbital pathology. Orbital abscesses or cellulitis are common, especially in young dogs that chew on sticks. The lesions are typically acute and unilateral. Marked pain is often present upon opening the mouth. Upon oral examination a ﬂuctuant swelling and/or mucosal hyperemia are often noted caudal to the ipsilateral last molar (see Ch. 6). Extraocular polymyositis typically occurs in young Golden Retrievers and causes a bilateral, non-painful exophthalmos with reduced ocular movement (Fig. 4.12). Minimal spongy resistance to retropulsion is detected. Ultrasonographic examination or CT will demonstrate the swollen extraocular muscles. The inﬂammation must be suppressed with systemic corticosteroids and, if

Fig. 4.12 Extraocular polymyositis in a Golden Retriever. Note the marked exophthalmos but no third eyelid protrusion. (Courtesy of Dr D. Ramsey.)

ABNORMAL APPEARANCE

required, azathioprine. If untreated, ﬁbrosis and contracture of the muscles may cause the development of strabismus and enophthalmos.8 The prognosis for orbital neoplasia is dependent on the nature of the tumor; the majority of these lesions are primary and malignant. Animals are usually older with a slowly progressive, non-painful exophthalmos. Only rarely can a tumor be removed via an orbitotomy without an enucleation. Usually exenteration (removal of the globe and orbital contents) is required and in many patients even this is not curative. Lateral orbitotomy enables extirpation of the zygomatic salivary gland when mucocele formation is the cause of the exophthalmos.

Enophthalmos (globe recession) Enophthalmos is the recession of a normal sized globe into the orbit. There is associated elevation of the third eyelid and variable narrowing of the palpebral ﬁssure. Retraction of the globe as a result of pain is a common cause. If enophthalmos follows trauma, the clinician should check to see if the globe has been perforated or ruptured, or if there are periorbital fractures. A ruptured globe will be hypotensive. Ultrasonographic examination may be required to demonstrate the presence of a posterior scleral rupture. Enophthalmos may also result from loss of retrobulbar fat in cachexic states, the presence of retrobulbar scar tissue, post-inﬂammatory contracture of the extraocular muscles or chronic, post-masticatory muscle myositis muscle wasting. The history and clinical signs should make the diagnosis obvious and the treatment is addressed to the cause. Horner’s syndrome is a common cause of enophthalmos. The other cardinal signs of Horner’s syndrome are ptosis, relative miosis, and elevation of the third eyelid (Fig. 4.13). As the pain associated with a corneal ulcer or anterior uveitis can cause similar clinical signs, staining with ﬂuorescein dye and a complete ocular examination are indicated. Pharmacologic testing with phenylephrine

Fig. 4.13 Third order Horner’s syndrome following bullous osteotomy in a 4-year-old domestic short-haired (DSH) cat. The signs of ptosis, miosis, enophthalmos, and membrana nictitans protrusion are present in the right eye.

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can conﬁrm the presence of Horner’s syndrome and give an indication as to whether the lesion is central (ﬁrst order), preganglionic (second order), or postganglionic (third order).9 Pupillary dilatation and third eyelid retraction within 20 min following topical application of 10% phenylephrine is suggestive of third order Horner’s syndrome; responses greater than 20 min suggest ﬁrst or second order lesions. Common causes of Horner’s syndrome include middle ear disease, iatrogenic damage sustained during total ear canal ablations, and trauma to the neck. Less common causes include polyneuropathy, neoplasia, and brachial plexus avulsion. A complete physical examination focusing upon the tympanic membrane, middle ear, cervical, and thoracic regions is indicated. In many instances the etiology remains obscure and clinical signs resolve after 60–90 days. The incidence of idiopathic Horner’s syndrome appears to be increased in the Golden Retriever.10

Proptosis Traumatic proptosis occurs when a sudden forward displacement of the globe traps the eyelid margins behind the globe’s equator (Fig. 4.14). Minor trauma such as scrufﬁng or dog ﬁghts may result in proptosis in the brachycephalic breeds. Proptosis in the dolicocephalic breeds or cats requires considerable trauma. Various criteria including the absence of the pupillary light reﬂex and the degree of ocular damage are used to determine the prognosis for vision.11 Often the eye is blind due to the accompanying optic neuropraxia or damage. If three or more rectus muscles are torn, the optic nerve has been transected; if the cornea or sclera is ruptured, the globe should be enucleated. In those eyes deemed salvageable, the cornea must be kept moist until the animal is stable for general anesthesia. Under anesthesia a lateral canthotomy to enlarge the palpebral ﬁssure will facilitate globe replacement. A temporary tarsorrhaphy is then performed to maintain the globe in situ. The tarsorrhaphy is maintained until the orbital swelling subsides and lid movement is noted; the sutures are then removed in a staggered fashion. Lateral (divergent) strabismus is a

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Fig. 4.14 Traumatic proptosis of the right eye in a 5-year-old Cavalier King Charles Spaniel. Complete avulsion of the optic nerve has occurred.

Changes in primary gaze Strabismus Strabismus is a deviation in the position of the globe that can be due to a congenital anomaly, a neurologic lesion, or abnormality of the extraocular muscles. Congenital esotropia (bilateral medial strabismus) is seen in Siamese cats. Acquired strabismus may result from traumatic proptosis or retrobulbar lesions. Lesions of cranial nerves III, IV, and VI will produce speciﬁc deviations. A progressive, restrictive ventromedial strabismus has been reported in young dogs, particularly Shar Peis, that appears to result from post-inﬂammatory changes to the extraocular muscles (Fig. 4.16).12

ABNORMAL APPEARANCE

common sequela due to oculomotor nerve damage or avulsion of the medial rectus muscle (Fig. 4.15).

Fig. 4.15 Acquired strabismus following traumatic proptosis in a 3-year-old Tibetan Spaniel. Rupture of the medial rectus muscle has occurred. Left eye.

Fig. 4.16 Ventromedial strabismus due to progressive extraocular muscle ﬁbrosis in a 2year-old Chow Chow dog.

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Nystagmus Nystagmus is an involuntary oscillatory movement of the eyes that consists of alternating slow and fast phases. During the slow phase the eyes move away from the primary gaze position (straight ahead), followed by the fast phase which recenters the eyes. Normal nystagmus can be induced as a response to movement of the head, for example in the oculocephalic reﬂex. Abnormal nystagmus is associated with central or peripheral vestibular disease and in some cases only occurs when the animal’s head is moved to a particular position (positional nystagmus). It may be present without changing head position (spontaneous nystagmus). Animals with multiple congenital ocular abnormalities (e.g. microphthalmos, persistent pupillary membranes, and cataract), or conditions resulting in a very early onset of blindness, often show abnormal eye movements of an oscillatory or wandering nature which are described as a searching nystagmus. Cerebellar disease can also result in oscillatory eye movements.

The eyelids Congenital/neonatal eyelid conditions A coloboma is a congenital absence of tissue within the eye or its adnexa. In the cat, colobomas usually involve the lateral part of the upper eyelid and are bilateral. The absence of the eyelid margin is obvious and haired skin will be seen fused to the bulbar conjunctiva obliterating most of the dorsal conjunctival fornix. Eyelid closure is not complete and exposure keratitis results. The associated trichiasis also results in keratitis and discomfort (Fig. 4.17). Blepharoplastic techniques are necessary to correct the deformity, but success in producing an adequate blink response depends on the amount of normal eyelid present. An epibulbar dermoid (choristoma) is a congenital mass of haired skin in an abnormal location. The dermoid may involve the eyelid, the conjunctiva, the cornea, or all three. The temporal limbus is the most common site of involvement (Fig. 4.18). Treatment is by resection, keratectomy, or blepharoplastic repair depending upon the location.

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Fig. 4.17 A lateral upper eyelid coloboma (eyelid agenesis) in a 2year-old DSH causing trichiasis, corneal vascularization, and elevation of the third eyelid. Right eye.

ABNORMAL APPEARANCE Fig. 4.18 Temporal limbal dermoid in a 6month-old Shih Tzu dog. Left eye.

Fusion of the eyelids (ankyloblepharon) is normal in kittens and puppies up to 10–14 days of age. On occasion it may persist beyond this time, necessitating surgical separation of the fused lids. Ophthalmia neonatorum is the development of a purulent conjunctivitis prior to eyelid opening which results in a swelling of the fused lids. Early intervention is required to avoid corneal damage and loss of the eye. The eyelids must be opened, the material collected for culture, and the conjunctival sac irrigated. Broad-spectrum topical antibiotics are then applied to control bacterial infection and keep the ocular surface moist until tear production is established. Abnormalities of eyelid conformation are common and often breed related. An inward rolling of the eyelid margin is called entropion while an eversion is termed ectropion. In entropion the resultant trichiasis can result in superﬁcial keratitis and corneal ulceration. Surgical intervention is required to correct the eyelid deformity (see Ch. 6). Ectropion causes chronic exposure of the ventral conjunctival sac which may lead to permanent conjunctival changes. Several techniques involving eyelid shortening and lateral canthoplasty are available for the correction of ectropion should this prove to be necessary.13 Many patients can be managed using daily irrigation with sterile saline and periodic use of lubricating ointments. A combination of ectropion and entropion associated with overly long eyelids and a weak lateral canthal ligament is seen in breeds that select for a diamond-shaped palpebral ﬁssure. Surgical correction is challenging and several procedures have been devised to shorten and lift the palpebral ﬁssure.14

Acquired eyelid lesions Traumatic eyelid lacerations require careful surgical repair with minimal debridement and treatment of any secondary infection. In particular accurate apposition of the eyelid margin is required for a satisfactory result. Blepharitis has a number of possible causes including bacterial pyoderma, immune-mediated disease, mycotic infection, parasitic infestation, and sebor-

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86

rhea. Obtaining a speciﬁc diagnosis depends on skin scrapings, bacteriologic culture, and/or biopsy. Treatment is with systemic antibiotics, antifungals, corticosteroids, and antiparasitic drugs as indicated. The initial blepharitis is often exacerbated by self-trauma. Measures should be taken to control selftrauma as part of managing this condition. Swellings or masses of the eyelids may be due to abscess formation (stye or hordeolum), chalazion, allergy, epibulbar dermoid, neoplasia, ophthalmia neonatorum, and trauma. Hordeola (styes) result from bacterial abscesses involving the meibomian gland or the glands of Zeiss or Moll. Treatment requires the use of systemic antibiotics, hot compresses, and surgical drainage. A chalazion results from the retention or blockage of the oily secretions within a meibomian gland, which ruptures into the surrounding eyelid tissue inciting an inﬂammatory response; in dogs they are most commonly encountered associated with meibomian adenomas. Chalazia are ﬁrm, nodular, non-painful, yellow-gray masses when viewed on the conjunctival surface. Treatment requires curettage and application of a topical antibiotic and corticosteroid solution. Eyelid tumors in the dog are usually benign. The most common tumor is the meibomian gland adenoma. Benign tumors involving up to approximately one-fourth of the eyelid length can be treated successfully by wedge resection and direct two-layer closure. Removal of larger tumors often requires more elaborate reconstructive procedures. Eyelid tumors in cats are more commonly malignant and include squamous cell carcinoma and ﬁbrosarcoma (Fig. 4.19). Facial paralysis results in a loss of the palpebral reﬂex and thereby possible exposure-induced damage to the ocular surface. If the initial portion of the facial nerve is affected, the parasympathetic innervation to the lacrimal gland and gland of the third eyelid may be disrupted, resulting in reduced tear production. Unilateral facial nerve paralysis may be idiopathic or associated with erosive middle ear disease. Bilateral lesions may be idiopathic although systemic endocrinopathies, such as hypothyroidism, which may be associated with

Fig. 4.19 Upper eyelid mast cell tumor with a small central area of erosion in a 4-year-old DSH. Left eye.

ABNORMAL APPEARANCE

neuropathies, should be considered. Brachycephalic dogs with their prominent globes and shallow orbits are most likely to develop severe exposure keratopathy as a result of facial paralysis. In all cases topical tear replacement should be applied frequently. If the third eyelid does not adequately spread the tear ﬁlm during attempted blinks, a temporary tarsorrhaphy can be performed until normal eyelid movement is restored. If the condition cannot be corrected, a permanent canthoplasty may be required to provide adequate corneal coverage. The epiphora-induced staining of facial hair at the medial canthus indicates excessive lacrimation, poor tear drainage, or both (Fig. 4.20). Excessive lacrimation is suggested by Schirmer tear test values greater than 25 mm of wetting per minute. The clinician must determine the cause of excessive lacrimation to correct the overﬂow of tears. Entropion, distichiasis, and trichiasis are all irritating and can thereby induce excessive lacrimation. Epiphora due to an inability to drain the normal tear ﬁlm volume may involve a congenital lesion or acquired blockage or occlusion of the nasolacrimal system. Management of epiphora is discussed in Chapter 7.

The third eyelid Prominence of the third eyelid Prominence of the third eyelid is commonly caused by anterior segment pain. Treatment is thus directed towards the cause (see Ch. 6). Other causes of protrusion include sedation, dehydration, ‘Haw’s’ syndrome in cats (often associated with diarrhea), retrobulbar lesions, symblepharon, Horner’s syndrome (see above), dysautonomia, and systemic disease (e.g. tetanus).

Scrolling of the third eyelid The third eyelid may be distorted by a scrolling of its cartilage resulting in the free margin of the membrane rolling outwards (Fig. 4.21). There may be epiphora due to an inability to pool tears in the medial lacrimal lake and to

Fig. 4.20

Marked facial hair staining due to epiphora in a 2-year-old Burmese cat.

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Fig. 4.21 Scrolling of the third eyelid cartilage in a 1-year-old Bernese Mountain Dog. Left eye.

complete the blink. Correction requires resection of the scrolled portion of the cartilage while leaving the cross-bar of the T-shaped structure intact.

Prolapse of the nictitans gland The base of the third eyelid is enveloped by the nictitans gland which produces up to 50% of the aqueous portion of the precorneal tear ﬁlm. In dogs with a genetic predisposition (Beagle, American Cocker Spaniel, English Bulldog, Boston Terrier) and rarely in cats (Burmese), the nictitans gland can prolapse subconjunctivally between the posterior surface of the third eyelid and the cornea. The gland appears as a smooth, ellipsoidal mass at the medial canthus (Fig. 4.22). Diagnosis is straightforward. Treatment requires surgical repositioning of the gland either by anchoring it to the ventromedial orbital rim or by performing a ‘pocketing’ procedure (Fig. 4.23).15 Gland excision should be avoided as this may adversely affect the precorneal tear ﬁlm.

Other third eyelid conditions

88

Other conditions altering the appearance of the third eyelid include lymphoid follicle hyperplasia, plasmacytic conjunctivitis, and neoplasia. It is normal for the bulbar surface of the third eyelid to have a roughened appearance due to the conjunctival lymphoid tissue overlying the nictitans gland. Proliferation of lymphoid follicles tends to occur in young dogs, apparently as a non-speciﬁc immune response, and is often accompanied by mild irritation and a mucoid discharge. If the irritation does not improve after a course of topical antibiotics and corticosteroids, careful debridement of the hyperplastic lymphoid follicles with dry gauze placed over a cotton-tipped applicator may relieve the irritation. Plasmacytic conjunctivitis (plasmoma) is most common in the German Shepherd Dog and may present as the solitary component of the disease complex or accompany chronic superﬁcial keratitis. Plasma cells and lymphocytes inﬁltrate the nictitating membrane. The third eyelid becomes thickened, develops

ABNORMAL APPEARANCE

Fig. 4.22

Prolapse of the nictitans gland in a 4-month-old Bulldog. Left eye.

an irregular border, and may become depigmented. A seromucoid discharge may be present. Topical corticosteroids or ciclosporin effectively control this immune-mediated condition. Tumors involving the nictitating membrane include squamous cell carcinoma, ﬁbrosarcoma, adenomas or adenocarcinomas, and hemangiomas or hemangiosarcomas. Treatment often requires surgical excision of the third eyelid and associated nictitans gland in their entirety.

The conjunctiva/sclera Conjunctivitis is speciﬁcally inﬂammation of the conjunctiva. Causes of conjunctivitis include allergy, eyelid lesions, foreign bodies, immune-mediated disease, infection, irritation, precorneal tear ﬁlm deﬁciencies, and trauma (see Ch. 7). Conjunctival tissues may become edematous. Marked chemosis (swelling) may obscure visualization of the cornea (Fig. 4.24). Differential diagnoses for a ‘red eye’ include conjunctivitis, uveitis, glaucoma, episcleritis, and neoplasia. Conjunctivitis is a common misdiagnosis. A complete ophthalmic examination is indicated in every animal with a ‘red eye’. Differentiation between conjunctival hyperemia and episcleral hyperemia/ injection is of tremendous importance as episcleral injection is often associated with serious intraocular disease. Several key features assist in differentiation. The conjunctival vasculature is bright red in color, branches extensively, is freely mobile as it moves with the conjunctiva over the surface of the globe, and readily blanches with the application of topical phenylephrine. The episcleral vasculature in contrast is dark red in color, straight, runs at 90° to the limbus, is not mobile, and does not blanch when phenylephrine is applied topically (Fig. 4.25). Episcleritis is an immune-mediated inﬂammatory disease of the episclera that occurs most commonly in dogs. Episcleritis may be a distinct raised pink lesion (nodular form) or more diffuse (Fig. 4.26). The lesion often involves the adjacent cornea. Episcleritis is usually treated with corticosteroids, systemic tetra-

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90

A

B

C

D

Fig. 4.23 Diagram showing correction of prolapse of the nictitans gland by suturing the orbital rim. (A) An Allis tissue forceps is gently applied to the periphery of the free margin of the third eyelid, which is pulled across the eye. An incision is made in the medioventral conjunctival fornix (at the base of the third eyelid) using scissors. Blunt dissection allows access to the periosteum of the medioventral orbital rim. A ﬁrm bite of periosteum along the orbital rim is taken using 3/0 polydioxanone swaged (PDS, Ethicon) or monoﬁlament nylon suture with a swaged-on needle introduced through the previously made incision. It can be difﬁcult to obtain a bite of periosteum and bring the needle out through the incision, because access to the area is limited. (B) The needle is then passed through the original incision dorsally towards the prolapsed gland so as to emerge from the gland at its most prominent point of prolapse. (C) With the third eyelid everted, the needle is passed back through the exit hole in the gland to take a horizontal bite from the most prominent part of the gland. (D) Finally the needle is passed back through the last exit hole to emerge through the original incision in the conjunctival fornix, thus encircling a large portion of the gland. The suture ends are tied. This creates a suture loop through the gland which anchors it to the periosteum of the orbital rim, preventing it from re-prolapsing. The conjunctival incision can now be repaired using 6/0 polyglactin (Vicryl, Ethicon) or it may be left unsutured. Postoperatively, topical antibiotic cover is given. Redrawn with permission from BSAVA: Petersen-Jones, S.M. (1993) Conditions of the eyelid and nictating membrane. In: Petersen-Jones, S.M. and Crispin, S.M. (eds) BSAVA Manual of Small Animal Ophthalmology. Quedgeley: BSAVA Publications, pp. 65–90.

ABNORMAL APPEARANCE

Fig. 4.24 Marked chemosis of the palpebral conjunctiva of the upper eyelid in a 5year-old Beagle. Right eye.

Fig. 4.25 Acute glaucoma demonstrating episcleral congestion in a 4-year-old Welsh Springer Spaniel. Right eye.

Fig. 4.26 Raised area of episclera at the lateral limbus with associated lipid deposition in the adjacent cornea in a 2-year-old mixed breed dog.

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cycline and niacinamide, or, if necessary, immunosuppressive drugs such as azathioprine. An uncommon conjunctival disease, membranous or ligneous conjunctivitis, has been seen in Dobermann Pinschers and Golden Retrievers.16 The ocular lesion appears as a bilateral yellow-green membrane lining any or all of the conjunctival surfaces. Removal of the membrane leaves a roughened and ulcerated epithelial surface. Exfoliative cytology reveals inﬂammatory cells with a prominent eosinophilic component. The membrane is composed of epithelial cells and a proteinaceous exudate. Variably associated systemic signs include proteinuria and ulcerative lesions of the skin and other mucous membranes, particularly within the oral cavity. The condition can be controlled in most cases with topical corticosteroids in conjunction with systemic corticosteroids and/or azathioprine. Conjunctival adhesions (symblepharon) are a sequela of severe conjunctivitis. In cats the most common cause is infection with feline herpesvirus-1 (FHV1). The chemotic, ulcerated conjunctiva may adhere to itself, the third eyelid, or the cornea, and may obliterate the conjunctival fornices, interfere with tear drainage, or obscure vision (Fig. 4.27). Recurrent bouts of inﬂammation due to recurrences of the herpesvirus infection are possible. Surgery to break down the adhesions and reconstruction of fornix and limbus is best reserved for the most severely affected animals (e.g. those with visual impairment) as adhesions will often reform after surgery. This tendency to reform adhesions can be decreased by the postoperative application of a bandage contact lens for 3–4 weeks. The most common congenital conjunctival mass is the dermoid. Acquired masses include neoplasia (squamous cell carcinoma, limbal melanocytoma, conjunctival malignant melanoma, and hemangioma), conjunctival cysts, and nodular episcleritis. Ocular melanosis, a familial condition in Cairn Terriers, is characterized by the development of darkly pigmented scleral/episcleral patches, diffuse proliferation of pigmented cells, and pronounced thickening of the anterior uvea leading to secondary (melanocytic) glaucoma (Fig. 4.28).

Fig. 4.27 Extensive symblepharon obscuring the cornea and causing functional blindness of the affected eye in a 1year-old DSH cat. Right eye.

ABNORMAL APPEARANCE Fig. 4.28 The development of darkly pigmented scleral and episcleral patches in melanocytosis. Nineyear-old Cairn Terrier. Left eye. (Courtesy of Dr S. Petersen-Jones.)

Limbal melanocytomas and staphylomas may affect the sclera as well as the cornea and are discussed within the corneal pigmentation section of this chapter.

The cornea Loss of corneal transparency is readily diagnosed and may result from ﬂuid accumulation, pigmentation, vascularization, symblepharon, endothelial deposits, or stromal lipid deposition.

Congenital corneal opacities When puppies’ eyelids open there is usually some degree of corneal opacity that normally clears over the subsequent few weeks. Sometimes there is delayed corneal clearing usually resulting in a central geographic gray appearance to the superﬁcial stroma. This will usually clear with time. With some congenital ocular malformations corneal opacities may be present and persist; examples include anterior segment dysgenesis and the insertion of persistent pupillary membrane on the corneal endothelial surface.

Corneal edema Corneal edema occurs if there is a break in the anatomic or functional integrity of the corneal epithelium or endothelium. It is commonly seen within an area of corneal ulceration as the loss of epithelium allows the exposed stroma to imbibe ﬂuid from the tear ﬁlm (Fig. 4.29). Canine adenovirus I infection (or, historically, use of live CAV I vaccine) can result in corneal edema due to immune complex deposition (a type III hypersensitivity reaction) along the corneal endothelium (Fig. 4.30). The immune complexes prevent normal functioning of the corneal endothelial pumps that maintain dehydration of the corneal stroma. Corneal edema may also be seen in association with anterior uveitis or glaucoma. Therefore, when evaluating a patient with corneal edema,

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Fig. 4.29 Ulcerative keratitis and corneal edema due to epithelial dystrophy in a 4-year-old Boxer. Left eye.

Fig. 4.30 Blue eye. Dense corneal edema due to CAV I infection. Right eye.

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a complete intraocular assessment including tonometry and gonioscopy should be performed. Severe corneal edema may limit one’s ability to visualize intraocular structures and ultrasonography may be helpful to assess intraocular changes. The treatment of corneal edema is directed toward resolution of the underlying cause. The edema may be transient and resolve completely if the underlying cause is successfully treated, but with severe damage the edema can be permanent as endothelial cells have minimal regenerative capabilities, especially in older animals. Corneal edema may also result from inherited endothelial dystrophy. This condition occurs in Boston Terriers, Chihuahuas, Dachshunds, English Springer

ABNORMAL APPEARANCE

Spaniels, Miniature Poodles, and occasionally other breeds. Usually middleaged or older animals are affected. The condition is typically bilateral and begins in the dorsotemporal or central regions of the cornea. The progressive edema eventually involves the entire cornea (Fig. 4.31). In severely affected patients, ﬂuid-ﬁlled bullae may form and rupture to form superﬁcial corneal ulcers that are painful and often slow to heal. Topical hyperosmotic agents such as 5% sodium chloride ointment or solution may decrease bullae formation although they will not completely resolve the corneal edema. The results of penetrating keratoplasty for this condition may be disappointing due to the lack of a suitable pool of corneal donors or rejection. The use of a thin conjunctival ﬂap or thermokeratoplasty may be palliative in selected cases. In the cat an idiopathic severe focal edema with formation of large bullae has been described and is termed ‘bullous keratopathy’. Some cases have been associated with a congenital endothelial dysplasia, while others have been associated with anterior uveitis. Third eyelid ﬂaps are often beneﬁcial in treating cats with acute bullous keratopathy.

Corneal pigmentation Acquired pigmentation is often common in dogs and results from the migration of melanocytes from the limbus; it is often accompanied by superﬁcial vascularization. The pigment typically arises in response to chronic corneal irritation or inﬂammation (Fig. 4.32). Common causes include chronic superﬁcial keratitis (pannus), deﬁciencies in the precorneal tear ﬁlm, lagophthalmos, and trichiasis from entropion or corneal contact with the nasal folds. Brachycephalic breeds are commonly affected. Therapy is directed at correction of the underlying cause. Corneal sequestrum is a disease peculiar to cats and is the cause of the majority of cases of brown or black corneal lesions in cats. The characteristic lesions range from faint brown discoloration of the central cornea to the formation of a variably sized, dense black plaque (Fig. 4.33). The sequestrum consists of necrotic corneal stroma and is often surrounded by a ring of inﬂammatory cells. The condition may be unilateral or bilateral. The amount of pain associated

Fig. 4.31 Diffuse corneal edema due to corneal endothelial dystrophy in a 9-yearold Dachshund. Right eye.

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SMALL ANIMAL OPHTHALMOLOGY Fig. 4.32 Extensive corneal pigmentation and ﬁbrosis secondary to trichiasis, medial canthal entropion, and lagophthalmos in a 3-year-old Shih Tzu.

Fig. 4.33 Corneal sequestrum in a 4-yearold Burmese cat. Right eye.

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with the condition varies with the intensity of the inﬂammatory response. Very dense plaques will often slough which may leave a full-thickness corneal defect. The etiopathogenesis remains open to speculation, but infection with feline herpesvirus may play a role.17 Sequestra frequently form in areas of longstanding corneal ulceration. Performing a grid keratotomy in cats has also been shown to induce sequestrum formation.18 In Persians and Himalayans, corneal exposure due to lagophthalmos is likely a contributing factor; therefore the likelihood of the condition developing bilaterally is greatly increased. While faint sequestra may respond to therapy with topical lubricating ointments,

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dense sequestra are often removed by keratectomy and, if the lesion is deep, repaired with a conjunctival pedicle ﬂap or lamellar corneal graft. Limbal melanocytomas may inﬁltrate the cornea as well as the sclera and appear as raised black lesions which tend to be slow growing (Fig. 4.34). They must be differentiated from intraocular melanomas that have extended through the sclera. Their behavior is usually benign. Progressive lesions usually respond to treatment by excision with or without a graft, laser excision, or cryosurgery. Staphylomas are the protrusion of uveal tissue through thinned cornea or sclera. Staphylomas may initially appear black or slightly brown due to a covering of ﬁbrin. Subsequent granulation and scar formation mutes the color to a vascular gray. Staphylomas may be congenital, traumatic, or secondary to severe scleritis or chronic glaucoma.

Corneal vascularization Corneal vascularization is a common feature of corneal disease. Whenever corneal vascularization is present, the possibility of precorneal tear ﬁlm deﬁciency or concurrent corneal ulceration should be considered. Therefore a Schirmer tear test and staining the cornea with ﬂuorescein dye are essential parts of the complete ophthalmic examination. It should be remembered that vascularization will occur as a normal component of stromal healing and should not be inappropriately suppressed. Once the stimulus for vascularization is resolved, the corneal vessels will narrow and no longer transmit blood, and are observed as faint gray lines (‘ghost vessels’) upon close examination of the cornea. Corneal vascularization is a common pathologic reaction to a number of different insults. These include precorneal tear ﬁlm deﬁciency, eyelid abnormalities, trauma, infection, chemical irritants, immune-mediated disease, and diseases involving adjacent structures such as episcleritis, scleritis, anterior uveitis, and glaucoma. Differentiation between superﬁcial and deep corneal vascularization is helpful to determine the underlying cause for the vascularization. The presence of deep vessels typically indicates intraocular involvement. Deeper vessels tend to branch less, are darker in color, and their origins from scleral vessels are obscured by the scleral overhang at the limbus. In

Fig. 4.34 Limbal melanoma and associated lipid keratopathy in a mixed breed dog.

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contrast, superﬁcial vessels branch frequently, are lighter red in color, and can be seen crossing the limbus as they arise from the conjunctival vessels. Chronic superﬁcial keratitis (CSK, pannus) is an immune-mediated condition characterized by progressive, superﬁcial, densely vascularized corneal inﬂammatory lesions. CSK occurs bilaterally with the lesions ﬁrst developing in the ventrolateral quadrant of the cornea. Lymphocytes and plasma cells inﬁltrate the superﬁcial stroma accompanied by vascularization. The lesions progress at a variable rate to produce a thick, superﬁcial, corneal granulation tissue which may eventually involve the entire cornea resulting in severe visual impairment or blindness. There is a variable degree of pigmentation of the lesions and in long-standing cases corneal ﬁbrosis (scar tissue) and/or corneal lipid degeneration is present (Fig. 4.35). Exposure to ultraviolet light is a known predisposing factor for CSK. Therefore dogs that reside at high elevations are often more difﬁcult to treat. Treatment consists of topical immunosuppression with corticosteroids and/ or topical ciclosporin.19,20 Subconjunctival depot corticosteroids are useful in more severe cases or those in which the owners have difﬁculty applying medication. Owners should be aware of the need for lifelong treatment and the likelihood of periods of exacerbation. Treatment with beta radiation may be useful in severe cases. Limiting exposure to ultraviolet light, either by keeping the dog indoors during peak ultraviolet light levels or using sunglasses (Doggles®), can be of beneﬁt as well. Performing a superﬁcial keratectomy may reduce extensive irreversible corneal changes that limit vision. As the cornea vascularizes quite rapidly following keratectomy, topical ciclosporin should be continued during the healing phase. Eosinophilic keratitis, a condition unique to the cat, is a progressive, superﬁcial, corneal inﬂammatory lesion with a surface deposit of a white ‘cottage cheese-like’ material (Fig. 4.36). While any part of the cornea may be involved, the lesions are often noted dorsotemporally. Exfoliative cytology of the lesion

Fig. 4.35 Chronic superﬁcial keratitis in an 8-year-old German Shepherd Dog. The marked corneal vascularization and pigmentation indicate chronicity. Left eye.

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Fig. 4.36

Eosinophilic keratoconjunctivitis in a 4-year-old cat.

typically reveals multiple eosinophils as well as mast cells, neutrophils, lymphocytes, and plasma cells. The etiopathogenesis remains unknown, but infection with feline herpesvirus-1 has been implicated.17 The disease is controlled by administration of topical mast cell stabilizers, topical corticosteroids, or topical ciclosporin. As FHV-1 may be involved, the possibility of causing reactivation of latent herpetic infections should be discussed with the owners when employing topical corticosteroids in the treatment regimen. Occasionally systemic megestrol acetate therapy is utilized, but the clinician must be aware of the potential side effects, including inducing diabetes mellitus, when using this drug in the cat. Lesions often resolve completely with treatment, although recurrence is common. Symblepharon is another cause of corneal opacity in which a vascularized whitish/gray membrane of conjunctival origin is adherent to the corneal surface. It has been discussed above with conditions causing abnormal appearance of the conjunctiva.

Corneal lipid and calcium deposition Lipid keratopathy is the deposition of lipid within the corneal stroma. The lipid deposition may be due to corneal dystrophy or degeneration or systemic hyperlipidemia (hyperlipoproteinemia, dyslipoproteinemia).21 If the deposition is marked or progressive, the animal should be investigated for hyperlipoproteinemia and/or endocrinopathy. Crystalline stromal dystrophy is a genetic, bilateral (although not always comcurrent or symmetric) condition characterized by discrete subepithelial crystalline refractile opacities, usually in an oval or circular pattern, imparting a ‘ground glass’ appearance, in an otherwise normal cornea (Fig. 4.37). Lesions may slowly alter in size, but generally have no effect on vision and require no

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Fig. 4.37 Crystalline stromal dystrophy in a 3-year-old Miniature Dachshund.

Fig. 4.38 Lipid keratopathy in a Shetland Sheepdog. The lesion developed 6 months following cataract extraction. (Courtesy of Dr S.M. Petersen-Jones.)

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treatment. A number of dog breeds are affected and the condition has been shown to be familial in some breeds. Siberian Huskies suffer from a more severe manifestation of the condition with lipid deposition also occurring deeper in the cornea.22 In Shelties corneal dystrophy may be associated with focal thinning of corneal stroma and overlying recurrent erosions. Corneal lipid deposition can occur as a degenerative process secondary to corneoscleral diseases such as keratitis, episcleritis, and limbal melanocytoma. Lipid leakage from blood vessels causes the lipid deposition (Fig. 4.38). The appearance of the lipid deposit is more variable than with dystrophies; it may be a diffuse white color or appear as a granular deposit or refractile ‘ﬂakes’.

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Lipid deposition as a circumferential ring in the perilimbal cornea is known as arcus lipoides and in such cases the possibility of a predisposing systemic condition should be investigated. Lipid crystals may occasionally erode through the corneal epithelium causing ulceration and pain (Fig. 4.39). Management of lipid keratopathy involves treatment for a possible underlying hyperlipidemia. If the lesion is extensive, progressive, or painful, a keratectomy may be required. Calcareous degeneration is characterized by the presence of dense white, often needle-shaped, chalky, stromal deposits (Fig. 4.40). These lesions frequently will ulcerate causing discomfort and may become vascularized. This condition often affects older dogs. Cushing’s disease or uremia may be predisposing factors. Topical 1–5% disodium ethylenediamine tetra-acetic acid (EDTA) may assist in resolution of the lesions by chelating the calcium present within the corneal stroma. Keratectomy may be indicated if the lesion causes discomfort or is extensive, but healing may be complicated.

Corneal endothelial deposits Roundish, usually yellow to gray foci on the corneal endothelial surface are known as keratic precipitates (KPs) (Fig. 4.41). The keratic precipitates form as a result of anterior uveitis and represent the deposition of inﬂammatory cells on the endothelial surface. The KPs tend to be deposited inferiorly and may be concealed by an elevated third eyelid. Keratic precipitates are seen more commonly in cats with chronic anterior uveitis than in dogs, where they most commonly accompany lens-induced uveitis. The KPs will slowly resolve as the underlying uveitis is treated but may leave a focal endothelial scar.

Fig. 4.39 Crystalline stromal dystrophy and associated vascularization in a 6-year-old Shetland Sheepdog. Left eye.

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Fig. 4.40 Calcareous degeneration of the cornea in an elderly crossbred dog. (Courtesy of Dr S.M. Petersen-Jones.)

Fig. 4.41 Keratic precipitates associated with toxoplasmosis in a 2-yearold DSH cat. Right eye.

A slowly progressive thin pigment deposit involving the corneal endothelium and originating from the limbal region is sometimes observed. The pigment is presumed to be due to migration or slow proliferation of limbal pigment. No therapy is required. Occasionally iris cysts (see below) rupture against the corneal endothelium leaving an adherent donut-shaped deposit of pigmented tissue.

Alteration of corneal contour 102

A profound accumulation of ﬂuid in the cornea may cause distortion of the corneal proﬁle, the appearance of which is referred to as keratoconus. Other

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possible causes of a misshapen corneal contour include corneal abscesses and inclusion cysts. Both of these conditions are rare and necessitate keratectomy. Corneal abscesses are typically painful and consist of a usually central yellowish stroma opacity with indistinct borders and associated focal edema. They are typically accompanied by vascularization and conjunctival inﬂammation. Corneal inclusion cysts are typically non-painful and are ﬁlled with a thick, cream or tan colored material composed of desquamated epithelial cells; they occur as a sequel to ulceration or trauma, which may be surgical as well as accidental (Fig. 4.42). Minimal inﬂammation is present although a few superﬁcial corneal blood vessels may be present. A deep corneal ulceration will often cause an obvious concavity within the corneal contour. If such a lesion does not retain ﬂuorescein dye at the base, this indicates the presence of a descemetocele (see pp. 221–223). A corneal ulceration that involved the loss of corneal stroma can heal leaving an epithelialized indentation (corneal facet). A corneal laceration usually causes an obvious alteration in the corneal contour. Corneal laceration, with or without iris prolapse, requires surgical repair of the wound, reformation of the anterior chamber, and medical treatment to control possible infection and anterior uveitis.

The anterior chamber and anterior uvea Congenital lesions of the iris include colobomas, persistent pupillary membranes, and iris cysts. Colobomas of the iris are rare. Their presence may create an irregular or false pupil (Fig. 4.43). In older individuals, colobomas must be distinguished from senile iris atrophy (discussed in the normal iris section of this chapter). Persistent pupillary membranes (PPMs) are single or multiple strands of iris tissue that arise from the iris collarette. The strands may be free ﬂoating, insert onto the corneal endothelium (iris to cornea PPM) (Fig. 4.44), span the iris (iris to iris PPM) (Fig. 4.45), or attach to the anterior lens capsule (iris to lens PPM). Non-progressive focal opacities of varying extent are associated with the corneal attachments. The lenticular attachments often result in focal cataract formation (see pp. 127–128).

Fig. 4.42 Epithelial inclusion cyst in a 12year-old Yorkshire Terrier.

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Fig. 4.43 Appearance of polycoria due to an iridal coloboma in a 1-year-old Siberian Husky. Note that an iris to iris persistent pupillary membrane is present as well.

Fig. 4.44 Persistent pupillary membrane (PPM) with corneal attachment in a 12week-old Afghan Hound.

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Fig. 4.45 Iris to iris persistent pupillary membranes (PPM) in a 2year-old Labrador Retriever.

Anterior uveitis is inﬂammation of the iris and ciliary body (see Ch. 6). Acute anterior uveitis is typically painful. Animals with a low-grade, chronic uveitis are often less noticeably painful and may present because the owner has noticed a change in the appearance of the eye. Clinical signs can include episcleral congestion; corneal changes such as edema, vascularization, and keratic precipitates; hypopyon (white blood cells) or ﬁbrin within the anterior chamber, iris color changes, pupillary abnormalities, and lens changes such as posterior synechia and cataract formation. The potential etiologies of chronic uveitis are similar to those described for acute uveitis (see Table 6.5 and pp. 245–247).23 Typically, the iris color change consists of darkening with a loss of normal surface detail, although animals with a blue iris may develop a yellow hue to the iridal stroma. In some forms of uveitis, predominantly uveodermatologic syndrome, iris depigmentation occurs. A reddening of the iris (rubeosis iridis) may develop and is most easily noted in animals with a light-colored iris, typically cats. Rubeosis iridis is due to neovascularization of the iridal surface. The inﬂammation may result in adhesions between the iris and the anterior lens capsule (posterior synechiae). These adhesions limit pupillary movement and often distort the pupillary shape. Extensive posterior synechiae will block aqueous passage through the pupil causing the iris to bulge anteriorly (iris bombé) and leads to secondary glaucoma as a result of iridocorneal angle collapse. Lenticular changes include pigment deposits on the anterior capsule due to transient adhesion of the iris to the lens capsule or adherent pigment containing macrophages, and cataract formation. Secondary lens luxation may occur, particularly in cats with chronic uveitis. Uveodermatologic syndrome is a speciﬁc form of immune-mediated uveitis seen in dogs, most commonly Akitas and the Arctic breeds. Melanocytes are the immune system’s target in uveodermatologic syndrome. Therefore severe anterior and posterior uveitis and a characteristic poliosis (whitening of the hair) and vitiligo (depigmentation of the skin) around the eyes and muzzle are seen. Control of the uveitis is challenging; retinal detachment and degeneration and secondary glaucoma are common sequelae.

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Anterior uveitis

Blood-ﬁlled anterior chamber (hyphema) Hyphema may result from inﬂammatory disease, systemic disease such as clotting disorders or hypertension, or ocular disease such as persistence of embryonic blood vessels, neoplasia, retinal detachment, and trauma. Investigation of hyphema requires a thorough ocular and systemic examination, ultrasonography (to investigate the possible presence of intraocular neoplasia or retinal detachment), hematology, biochemistry, clotting proﬁles, and blood pressure measurement. Spontaneous hyphema is often associated with preiridal ﬁbrovascular membrane formation (rubeosis iridis) as the new vessels on the iris surface are very fragile and hemorrhage easily. Chronic uveitis, long-standing retinal detachment, intraocular neoplasia, and chronic glaucoma can all incite formation of pre-iridal ﬁbrovascular membranes. In older animals for which no other ocular or systemic cause of hyphema can be identiﬁed, retinal detachment should be strongly considered.24 Non-speciﬁc therapy for hyphema includes decreased activity to discourage re-bleeding, the use of topical corticosteroids to control any concurrent uveitis, and topical atropine

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to prevent signiﬁcant adhesions. Intraocular pressure should be monitored and increased pressure treated as necessary. Uncomplicated hyphemas will usually resorb over several weeks; those associated with intraocular disease may persist indeﬁnitely.

Mass lesions in the anterior chamber Mass lesions are readily visualized within the anterior chamber given adequate corneal transparency. In patients with uveitis, organized ﬁbrin, hypopyon, and other inﬂammatory products may be seen as strands or masses adherent to the corneal endothelium, anterior lens capsule, or iris. Anterior chamber foreign bodies are usually accompanied by corneal or scleral damage and a uveitic response (Fig. 4.46). The iris cyst is typically a spherical, often free-ﬂoating, structure of variable size in the anterior chamber (Fig. 4.47). On occasion its origin from the iridal pigment epithelium or ciliary epithelium is indicated by a connecting strand.25 The thin walls typically transilluminate, but occasionally the pigment density renders the cyst totally opaque. Iridal cysts are usually of no clinical signiﬁcance although on occasion their size and/or number are such that vision may be obscured. In such cases deﬂation by needle aspiration or laser puncture is indicated. The presence of a luxated lens anterior to the iris is usually heralded by the sudden onset of corneal edema and glaucoma, particularly in the dog (see Ch. 6). Occasionally in the dog and routinely in the cat, the presence of the lens in the anterior chamber does not cause glaucoma. However, contact of the lens with the corneal endothelium can still incite corneal edema. Lens luxation is discussed further within this chapter under the abnormal appearance of the lens. Uveal tumors may be primary or secondary (Fig. 4.48). The primary tumors include melanoma, adenoma, adenocarcinoma, and medulloepithelioma. The diagnosis of uveal neoplasia depends on the demonstration of a solid mass

Fig. 4.46 A linear foreign body (a thorn) and attendant anterior uveitis in a 4-year-old crossbred dog. Left eye.

ABNORMAL APPEARANCE Fig. 4.47 Multiple anterior uveal cysts demonstrating their appearance on transillumination in a 10year-old Dobermann. Right eye.

Fig. 4.48 Posterior iridal and ciliary body mass extending through the pupil into the anterior chamber in a 5-year-old Newfoundland dog. Right eye.

involving the iris or ciliary body. Histopathologic conﬁrmation is often not performed until the eye has been enucleated.26 Most primary ocular tumors in the dog are benign, but ultimately the eye will be destroyed by the resultant glaucoma. In an eye that is otherwise normal, owners may request local resection, although this is a skilled procedure and in many cases enucleation is eventually performed. Laser photocoagulation has been used to treat uveal tumors with some success.27 In cats primary tumors are more often malignant. A cat with diffuse iris melanoma may present due to iridal pigmentation changes as opposed to the observation of a distinct mass within the anterior chamber. Metastasis of diffuse iris melanoma is not infrequent.28 Although any metastatic tumor embolus may locate in the eye, the most common secondary uveal tumor is lymphoma. The ocular manifestations of lymphoma vary considerably and may not be speciﬁc for neoplasia. Clinical signs such as anterior uveitis, glaucoma, and/or intraocular hemorrhage may

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be the initial presenting features.29 For the treatment of secondary tumors, palliative enucleation, chemotherapy, or euthanasia of the terminal patient represent the treatment options.

Pupillary abnormalities Ophthalmic patients may present with anisocoria, a difference in size between the two pupils (Fig. 4.49). The clinician must determine which is the abnormal pupil by comparing relative sizes in light and dark conditions, checking the direct and consensual pupillary light responses, and performing visual tests. Possible causes of an abnormally dilated pupil include unilateral iris atrophy, glaucoma, oculomotor and parasympathetic nerve lesions, mydriatic application, dysautonomia, severe unilateral retinal disease, and optic neuropathy. Causes of the unilaterally constricted pupil include anterior uveitis, synechiae formation, Horner’s syndrome, miotic usage, and organophosphate poisoning. Cranial trauma may result in anisocoria. The prognosis is poor if the anisocoria progresses to dilated non-responsive pupils. If bilateral mydriasis or miosis is present the differential diagnoses should similarly consider all those causes listed for anisocoria. A ‘D’-shaped or reverse ‘D’-shaped pupil or spastic pupil syndrome (a static anisocoria) may be seen in cats infected with feline leukemia virus.30 The prognosis for long-term survival is poor.

The lens Changes in the appearance of the lens most commonly result from a loss of transparency or because of dislocation from its normal position in the posterior chamber. Gross opaciﬁcation is obvious, but magniﬁcation or the use of slitlamp biomicroscopy may be necessary to detect small lesions and identify the position of the opacity within the lens. Distant direct ophthalmoscopy makes it easy to differentiate between the opacity of cataract and the translucency of nuclear sclerosis. Cataract results in a black shadow against the reﬂection from the fundus whereas nuclear sclerosis presents no barrier to the fundus reﬂection. Nuclear sclerosis is a normal aging feature due to the compaction of the nuclear region of the lens. It has little or no effect on vision, but the blue-gray appearance of the lens often prompts a misdiagnosis of cataract. Cataract is simply deﬁned as opacity of the lens and/or its lens capsule (Figs 4.50 & 4.51). There are a number of possible causes including genetic defects, congenital anomalies, diabetes mellitus, trauma, and accompanying other ocular conditions (e.g. uveitis, glaucoma, lens luxation, and retinal degeneration). With inherited cataract, the predominant reason for cataract formation in dogs, the age of onset and the appearance of the opacity are often speciﬁc

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Fig. 4.49 Anisocoria in a 4year-old Persian cat.

ABNORMAL APPEARANCE Fig. 4.50 Posterior polar and equatorial cataract in a 7-year-old Labrador Retriever. Left eye.

Fig. 4.51 Cortical ‘spoke wheel’ cataract in a 9-yearold Boston Terrier. Left eye.

for the breed. Lens opacity may also be due to the attachment of posterior synechiae and any associated pigment migration, the presence of pupillary membranes, or the persistence of elements of the primary vitreous. The reason for presentation of the cataract patient may be the abnormal appearance of the eye as the owner may be unaware of the degree of visual impairment. If the cataract is progressive or has a signiﬁcant effect on vision then the patient should be assessed for possible surgery. This assessment should involve a complete systemic and ophthalmic examination together with electroretinography and ocular ultrasonography to determine if other ocular disease if present and to assess the integrity and functionality of the retina.

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There is no medical treatment for cataract. Surgical extraction can successfully restore sight. Phacoemulsiﬁcation is the most commonly performed procedure with a success rate for vision of 90–95%.31 Primary lens luxation most commonly occurs in the terrier breeds. The lens may move posteriorly into the vitreous cavity if vitreal liquefaction is present or, more commonly, anteriorly into or through the pupil into the anterior chamber (Fig. 4.52). Its position within the pupil or the anterior chamber together with adherent vitreous produces interference with the transpupillary ﬂow of aqueous, and acute secondary glaucoma is the usual presenting feature in the dog; the cat’s deeper anterior chamber is somewhat protective against pupillary block and acute IOP elevation (see Ch. 6). Diagnosis is usually straightforward as one visualizes the lens in the anterior chamber. The elevated IOP should be relieved followed by emergency lens extraction.32 A posteriorly luxated lens does not necessarily require removal, although in some patients the lens repeatedly moves between the anterior chamber and the vitreous, causing glaucoma each time it is in the anterior chamber. Conservative longterm management may be possible using long-acting miotics to maintain the lens within the vitreous cavity. Secondary lens luxation occurs in both dogs and cats as a result of conditions such as uveitis, hypermature cataract formation, and glaucoma. Spontaneous lens luxation occurs infrequently in aged animals, particularly Siamese cats. An anteriorly luxated lens may become cataractous. Contact between the anteriorly luxated lens and the corneal endothelial surface may result in pain and an area of corneal edema.

The posterior segment Leukocoria is deﬁned as white appearance to the pupil. The differential diagnoses include cataract, neoplasia, persistent hyperplastic primary vitreous, vitreous abscess, posterior uveitis, and retinal detachment. Persistent hyperplastic primary vitreous is a congenital cause of leukocoria in which stromal ﬁbrovascular and posterior capsular plaques render the pos-

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Fig. 4.52 Primary anterior lens luxation in a 5-year-old Jack Russell Terrier. Left eye.

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terior lens opaque.33,34 The lesions may range from small ﬁbrovascular dots that minimally impair vision to severe retrolental and lenticular changes that markedly impair vision. Cortical cataract may also be present. The problem may be sporadic although it is inherited in some breeds, notably the Dobermann and Staffordshire Bull Terrier. The presence of retrolenticular vasculature is diagnostic, although ocular ultrasonography may be needed to demonstrate the full extent of the involvement, particularly when cortical and capsular cataract is extensively present. In visually impaired individuals, treatment is difﬁcult because it involves the removal of the lens and the anterior vitreous. Hemorrhage can be a severe complication. Animals with this condition should not be used for breeding. Severe retinal dysplasia with retinal non-attachment or detachment may result in congenital leukocoria due to contact of the retina with the posterior surface of the lens. Cataract formation may also be present. This condition is discussed further on pages 136–141. Labrador Retrievers and Samoyeds are affected by another inherited condition, oculoskeletal dysplasia. The condition is inherited as an autosomal recessive trait.35 Homozygotes demonstrate skeletal and ocular abnormalities including cataracts and complete retinal detachment in association with retarded growth of the radius, ulna, and tibia resulting in a chondrodysplastic appearance. Heterozygotes do not develop the skeletal abnormalities and the ocular lesions are less severe, manifesting often as multiple retinal folds. Animals with bilateral retinal detachment will often present with blindness, but if the condition is unilateral and the retina is occupying the anterior vitreous or there is vitreal hemorrhage, the resulting abnormal appearance or anisocoria may be the reason for presentation.36 Generally, the prognosis for vision in retinal detachment is poor due to the late presentation of many of these cases. The treatment is discussed on pages 155–160. Hypertensive retinopathy is now recognized commonly in older animals, particularly cats. Hypertensive retinopathy may cause retinal detachment and intraocular hemorrhage (Figs 4.53 & 4.54). The retinal vasculature may appear tortuous. Feline patients presenting with this problem should be investigated for underlying cardiac, renal, and thyroid disease. Treatment with a calcium channel blocker such as amlodipine besylate can offer rapid and effective hypotensive therapy preventing the development of further retinal pathology and allowing retinal reattachment. If the detachment occurred recently, then at least partial restoration of vision is possible.37 As hypertensive retinopathy is fairly common, the systolic blood pressure should be evaluated in all cases of serous retinal detachment. Alterations in the quality of the tapetal reﬂex may be the reason for presentation. A ‘glassy’ appearance or ‘glare’ may be the layperson’s description of the pupil due to tapetal hyperreﬂectivity following retinal degeneration or retinal detachment with disinsertion. The loss of the pupillary light response exacerbates the appearance. The funduscopic changes resulting from retinal degeneration are described on pages 144–147 and 182–186. Alterations noted upon examination of the posterior segment may include asteroid hyalosis, tapetal hyporeﬂectivity, tapetal hyperreﬂectivity, retinal vascular tortuosity or attenuation, retinal hemorrhage, and optic neuritis. Asteroid hyalosis is an innocuous degenerative change of the vitreous. Minute,

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SMALL ANIMAL OPHTHALMOLOGY Fig. 4.53 Complete retinal detachment resulting from hypertensive retinopathy associated with hyperthyroidism in a 13-year-old DSH cat. Left eye.

Fig. 4.54 Multiple preretinal, intraretinal, and subretinal hemorrhages due to hypertensive retinopathy in an 8-yearold DSH cat.

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spherical, lipid opacities are suspended throughout the vitreous. The condition is frequently noted in geriatric animals, but may also occur in association with ciliary body epithelial tumors and previous episodes of inﬂammation. Areas of tapetal hyporeﬂectivity indicate areas of thickened neural retina or subretinal inﬁltrates. Causes of tapetal hyporeﬂectivity include retinal edema, retinal dysplasia, retinitis, and separation of the sensory retina from the retinal pigment epithelium by subretinal ﬂuid or a cellular inﬁltrate. Areas of tapetal hyperreﬂectivity indicate thinning or absence of the neural retina. Causes include retinal atrophy, retinal degeneration, and dysinsertion retinal detachment. The retinal vasculature may appear tortuous due to systemic hypertension, hyperviscosity syndrome, polycythemia, and inﬂammation. The retinal vasculature may appear thin or attenuated with anemia, progressive retinal atrophy, chronic sudden acquired retinal degeneration, and chronic glaucoma. Retinal hemorrhages may occur at different levels in the sensory retina. The hemorrhages may be pre-retinal (between the sensory retina and vitreous),

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within the nerve ﬁber layer, intraretinal, or subretinal. Causes of retinal hemorrhage include vasculitis, thrombocytopenia, thrombocytopathy, coagulopathy, hypertension, anemia, and polycythemia. Optic neuritis causes the optic nerve head to appear swollen with indistinct margins. Peripapillary hemorrhage is often present. Causes include inﬂammation and neoplasia. For further discussion of the differential diagnoses and treatment options for the above ﬁndings, see Chapter 5.

REFERENCES 1. Gelatt, K. and Mackay, E. (1997) Distribution of intraocular pressure in dogs. Trans. Am. Coll. Vet. Ophthalmol. 28: 13. 2. Dubielzig, R.R. (2002) Feline ocular sarcomas. In: Peiffer, R. and Simons, K. (eds) Ocular Tumors in Animals and Humans. Ames: Iowa State Press, pp. 283–288. 3. Bingaman, D., Lindley, D., Glickman, N. et al. (1994) Intraocular gentamicin and glaucoma: a retrospective study in 60 dog and cat eyes (1985–1993). Vet. Comp. Ophthalmol. 4: 113–119. 4. Ramsey, D.T. and Fox, D.B. (1997) Surgery of the orbit. Vet. Clin. North Am. Small Anim. Pract. 27(5): 1215–1264. 5. Dziezyc, J., Hager, D.A. and Millichamp, N.J. (1987) Twodimensional real-time ocular ultrasonography in the diagnosis of ocular lesions in dogs. J. Am. Anim. Hosp. Assoc. 23(5): 501–508. 6. Morgan, R.V., Ring, R.D., Ward, D.A. et al. (1996) Magnetic resonance imaging of ocular and orbital disease in 5 dogs and a cat. Vet. Radiol. Ultrasound 37(3): 185–192. 7. Boydell, P. (1991) Fine needle aspiration biopsy in the diagnosis of exophthalmos. J. Small Anim. Pract. 32(11): 542–546. 8. Ramsey, D., Hamor, R., Gerding, P. et al. (1995) Clinical and immunohistochemical characteristics of bilateral polymyositis of dogs. Proc. Am. Coll. Vet. Ophthalmol. 26: 130–132.

9. Kern, T.J., Aromando, M.C. and Erb, H.N. (1989) Horner’s syndrome in dogs and cats: 100 cases (1975– 1985). J. Am. Vet. Med. Assoc. 195(3): 369–373. 10. Boydell, P. (1995) Idiopathic Horner’s syndrome in the Golden Retriever. J. Small Anim. Pract. 36(9): 382– 384. 11. Gilger, B.C., Hamilton, H.L., Wilkie, D.A. et al. (1995) Traumatic ocular proptoses in dogs and cats: 84 cases (1980–1993). J. Am. Vet. Med. Assoc. 206(8): 1186–1190. 12. Allgoewer, I., Blair, M., Basher, T. et al. (2000) Extraocular muscle myositis and restrictive strabismus in 10 dogs. Vet. Ophthalmol. 3(1): 21–26. 13. Gelatt, K. and Gelatt, J. (2001) Small animal ophthalmic surgery: practical techniques for the veterinarian. New York: Butterworth Heinemann, pp. 74–123. 14. Bedford, P.G.C. (1998) Technique of lateral canthoplasty for the correction of macropalpebral ﬁssure in the dog. J. Small Anim. Pract. 39(3): 117–120. 15. Morgan, R.V., Duddy, J.M. and McClurg, K. (1993) Prolapse of the gland of the third eyelid in dogs: a retrospective study of 89 cases (1980 to 1990). J. Am. Anim. Hosp. Assoc. 29(1): 56–60. 16. Ramsey, D.T., Ketring, K.L., Glaze, M.B. et al. (1996) Ligneous conjunctivitis in four Doberman Pinschers. J. Am. Anim. Hosp. Assoc. 32(5): 439–447. 17. Nasisse, M.P., Glover, T.L., Moore, C.P. et al. (1998) Detection of feline

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herpesvirus 1 DNA in corneas of cats with eosinophilic keratitis or corneal sequestration. Am. J. Vet. Res. 59(7): 856–858. 18. La Croix, N.C., van der Woerdt, A. and Olivero, D.K. (2001) Nonhealing corneal ulcers in cats: 29 cases (1991– 1999). J. Am. Vet. Med. Assoc. 218(5): 733–735. 19. Jackson, P.A., Kaswan, R.L., Merideth, R.E. et al. (1991) Chronic superﬁcial keratitis in dogs: a placebo controlled trial of topical cyclosporine treatment. Prog. Vet. Comp. Ophthalmol. 1(4): 269–275. 20. Clerc, B. (1996) The treatment of immune-mediated and auto-immune ocular diseases in dogs and cats using cyclosporine A ointment. (A literature review and personal experience). Pratique Médicale et Chirurgicale de l’Animal de Compagnie 31(1): 73–81. 21. Crispin, S. and Barnett, K.C. (1983) Dystrophy, degeneration, and inﬁltration of the canine cornea. J. Small Anim. Pract. 24: 63–83. 22. MacMillan, A., Waring, G., Spangler, W. et al. (1979) Crystalline corneal opacities in the Siberian Husky. J. Am. Vet. Med. Assoc. 175: 829– 832. 23. Crispin, S. (1988) Uveitis in the dog and cat. J. Small Anim. Pract. 29: 429–447. 24. Nelms, S.R., Nasisse, M.P., Davidson, M.G. et al. (1993) Hyphema associated with retinal disease in dogs: 17 cases (1986–1991). J. Am. Vet. Med. Assoc. 202(8): 1289–1292. 25. Spiess, B.M., Bolliger, J.O., Guscetti, F. et al. (1998) Multiple ciliary body cysts and secondary glaucoma in the Great Dane: a report of nine cases. Vet. Ophthalmol. 1(1): 41–45. 26. Dubielzig, R.R., Steinberg, H., Garvin, H. et al. (1998) Iridociliary epithelial tumors in 100 dogs and 17 cats: a morphological study. Vet. Ophthalmol. 1(4): 223–231. 27. Nasisse, M.P., Davidson, M.G., Olivero, D.K. et al. (1993) Neodymium : YAG laser treatment of

primary canine intraocular tumors. Prog. Vet. Comp. Ophthalmol. 3(4): 152–157. 28. Kalishman, J.B., Chappell, R., Flood, L.A. et al. (1998) A matched observational study of survival in cats with enucleation due to diffuse iris melanoma. Vet. Ophthalmol. 1(1): 25–29. 29. Krohne, S.G., Henderson, N.M., Richardson, R.C. et al. (1994) Prevalence of ocular involvement in dogs with multicentric lymphoma: prospective evaluation of 94 cases. Vet. Comp. Ophthalmol. 4(3): 127–135. 30. Nell, B. and Suchy, A. (1998) ‘Dshaped’ and ‘reverse-D-shaped’ pupil in a cat with lymphosarcoma. Vet. Ophthalmol. 1(1): 53–56. 31. Sigle, K.J. and Nasisse, M.P. (2006) Long-term complications after phacoemulsiﬁcation for cataract removal in dogs: 172 cases (1995– 2002). J. Am. Vet. Med. Assoc. 228(1): 74–79. 32. Glover, T.L., Davidson, M.G., Nasisse, M.P. et al. (1995) The intracapsular extraction of displaced lenses in dogs: a retrospective study of 57 cases (1984–1990). J. Am. Anim. Hosp. Assoc. 31(1): 77–81. 33. Boeve, M.H., Stades, F.C., van der Linde-Sipman, J.S. et al. (1992) Persistent hyperplastic tunica vasculosa lentis and primary vitreous (PHTVL/PHPV) in the dog: a comparative review. Prog. Vet. Comp. Ophthalmol. 2(4): 163–172. 34. Gemensky-Metzler, A.J. and Wilkie, D.A. (2004) Surgical management and histologic and immunohistochemical features of a cataract and retrolental plaque secondary to persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous (PHTVL/PHPV) in a Bloodhound puppy. Vet. Ophthalmol. 7(5): 369–375. 35. Pellegrini, B., Acland, G.M. and Ray, J. (2002) Cloning and characterization of opticin cDNA: evaluation as a candidate for canine oculo-skeletal

37. Van de Sandt, RROM, Stades, F.C., Boeve, M.H. et al. (2004) Arterial hypertension in the cat: a pathophysiological and clinical overview with the emphasis on ophthalmic aspects. Eur. J. Comp. Anim. Pract. 14(1): 47– 55.

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dysplasia. Gene 282(1/2): 121– 131. 36. Hendrix, D.V., Nasisse, M.P., Cowen, P. et al. (1993) Clinical signs, concurrent diseases and risk factors associated with retinal detachment in dogs. Prog. Vet. Comp. Ophthalmol. 3(3): 87–91.

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Visual impairment Ellen Bjerkås, Björn Ekesten, Kristina Narfström, and Bruce Grahn

EVALUATION OF VISUAL FUNCTION

5

This chapter deals with visual impairment and concerns both diseases primarily related to the eyes as well as eye diseases occurring secondary to systemic conditions. When an animal is examined because of visual impairment, careful questioning of the owner is of utmost importance and may often give an indication as to the nature of the disease. Essential information to be obtained from the owner is listed in Table 5.1.

Ophthalmic history Age Congenital conditions or malformation are more likely to be diagnosed in younger animals than in older ones. Puppies and kittens may also be prone to general infection, which may include ophthalmia neonatorum with accumulation of exudate underneath the fused eyelids in puppies, and upper respiratory and ocular infection caused by feline herpesvirus-1 in kittens. Both of these conditions may have deleterious effects on vision if concurrent keratitis is severe. Degenerative diseases, like hereditary rod–cone degeneration (generalized progressive retinal atrophy, PRA) and primary glaucoma show breed-speciﬁc age of onset of clinical signs and most often become evident in older animals.

Breed Many diseases show a breed-related incidence, and knowledge of such diseases often makes it easier to establish a diagnosis. However, incidence of breedrelated diseases varies in different parts of the world, which makes local knowledge essential.

General health and other clinical signs

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Visual impairment may occur as part of a systemic disease, and a general physical examination should always be performed in connection with the ocular examination. Examples of systemic diseases causing visual impairment are diabetes mellitus, which causes cataract frequently in dogs, occasionally in cats; malignant lymphoma with uveal inﬁltration of neoplastic cells and secondary uveitis; hypertension causing retinal hemorrhage and/or detachment, especially

• Age • Breed • General health

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Table 5.1 Essential information to acquire from the owner.

• Other clinical signs • Onset (sudden or gradual) • Known etiology (e.g. injury, accident) • Initial clinical signs • Pain/no pain • Vision in daylight/poor light • Duration

in the cat; and diseases affecting the central nervous system which may impair the conduction or interpretation of the visual impulse.

Onset The onset of impaired vision may be sudden, as in injuries, acute glaucoma, hypertensive retinopathy, and certain inﬂammatory retinal conditions, or gradual, as in chronic keratitis, most forms of cataracts and progressive retinal degenerations (the PRAs). In congenital conditions, the animal may have been born with reduced vision, or vision loss may develop secondary to the malformation. Examples of the latter would include retinal detachment or intraocular hemorrhage caused by collie eye anomaly (CEA), glaucoma related to dysplasia of the pectinate ligament, or progression of congenital cataract caused by persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous (PHTVL/PHPV or more readily referred to as persistent embryonic vasculature (PEV)).

Known etiologic factors The owner is usually able to provide information about the occurrence of an ocular injury. Useful information may also be vaccination status, as corneal edema (blue eye) may occur, although very rarely nowadays, after vaccination with live modiﬁed hepatitis virus (canine adenovirus-1) in dogs. In addition to the risk of direct infection, introduction of a new animal into a household or a change in environment may impair an animal’s immune balance. This is seen in cats with subclinical infection of feline herpesvirus-1 and may result in exacerbation of keratitis.

Initial clinical signs Initial signs may vary from ocular hyperemia and discomfort to acute vision loss, dependent on speciﬁc cause. Accidents and injuries most often cause uni-

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lateral problems. Early stages of keratoconjunctivitis sicca may present with only moderate signs with conjunctivitis and mucoid discharge, while in chronic cases dryness of the cornea causes chronic keratitis with neovascularization and pigment deposits. In early stages of lens subluxation, obvious clinical signs may be moderate with just some ocular hyperemia, while in acute uveitis the clinical signs may be more obvious with the animal showing severe discomfort. One should remember that animals in their usual surroundings may apparently function more or less normally even though visually impaired. Thus, the owner may not have noticed vision loss until the animal is introduced to an unfamiliar environment. A unilaterally blind animal often shows no noticeable evidence of blindness until the second eye becomes affected.

Pain Assessment of pain may sometimes be difﬁcult for the owner. However, if a condition is painful, the animal will usually try to avoid examination and keep the eyelids partly closed. More subtle signs of pain or discomfort may be lethargy, inappetence, or otherwise altered behavior including bad temper and reluctance to play or take part in other types of activity. Most congenital conditions as well as retinal degenerations are not painful, while glaucoma, uveitis, and large corneal ulcers may cause severe pain. Cataracts are rarely painful unless secondary lens-induced uveitis is present.

Vision in daylight and in dim light This information is important when dealing with diseases of the retina. The PRAs cause initial night blindness, with a later reduction of day vision, while hemeralopia presents with day blindness. In sudden acquired retinal degeneration (SARD) both day and night vision are acutely and simultaneously impaired. Animals with axially positioned cataracts may have better vision in dim light than in daylight, due to pupil dilatation.

Examination of the patient General examination This should be an assessment of the animal’s general condition including examination of cardiovascular circulation, respiration, mucous membranes, and peripheral lymph nodes. The owner should be questioned about appetite, thirst, and changes in the animal’s behavior. Information on the diet should be obtained; for example, cats fed dog food may develop a taurine-related retinopathy. Medication may inﬂuence the clinical signs: certain sulfonamides may be responsible for the development of keratoconjunctivitis sicca, systemic treatment with high doses of enroﬂoxacin may cause retinal degeneration in cats, and atropine drops impair pupillary light reﬂexes. In many cases diagnostic work-up is required, including hematology, serum biochemistry, urine analysis, sampling (bacteriology, cytology, polymerase chain reaction, serology), blood pressure measurements, diagnostic imaging, and electroretinography.

Neurologic examination

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If a condition affecting the central nervous system (CNS) is suspected, a full neurologic examination should be performed.1,2 Common causes of blindness of CNS origin are presented in Table 5.2. The general physical examination may already have revealed CNS signs, such as reduced vision, nystagmus,

Some causes of blindness of CNS origin.

• Optic neuritis • Trauma to optic nerves • Hydrocephalus (juvenile or acute, decompensating)

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Table 5.2

• Hepatic encephalopathy • Lysosomal storage diseases and other CNS degenerative diseases • Brain tumors (meningioma, lymphoma, pituitary tumors, reticulosis) • Encephalitis (canine distemper, feline infectious peritonitis, toxoplasmosis) • Meningitis (bacterial, viral, fungal, or algal) • Cerebrosvascular accident (cats) • Brain trauma • Toxicity (lead, ivermectin, levamisole) • Parasites (migrating larvae)

hearing loss, paresis of facial muscles, head tilt, changes in behavior, or ataxia. A neurologic examination should at least include testing of the cranial nerves, the postural reactions, and the spinal reﬂexes. Cranial nerves II (optic) and III (oculomotor) affect the pupillary light reﬂexes, while III, IV (trochlear), and VI (abducens) control ocular position and movements. It should be noted that the trigeminal nerve (V) in addition to containing sensory ﬁbers from the cornea and the skin of the face also has a motor branch to the masticatory muscles. The facial nerve (VII) is responsible for the motor function of the facial muscles including most of the muscles of the eyelids. The trigeminal and facial nerves are tested together by tapping or pricking each side of the face. The sympathetic nerve supply, which leaves the spinal cord in the T1–T3 region, is responsible for pupil dilatation and for the tone of the smooth muscles in the periorbital fasciae and eyelids (Müller muscles).

Testing vision Obstacle course The easiest way of testing an animal’s vision is to set up an obstacle course in unfamiliar surroundings and carefully observe the animal’s movements through the area. The test should be performed both in normal and in dim light to assess day (photopic) and night (scotopic) vision. An obstacle course can be set up with almost anything; a set of small buckets put upside down can be moved around to create new paths; if unaltered, an animal may learn the path after one or two attempts, which may lead the examiner to draw the wrong conclusions. An obstacle course is a very crude way of testing vision, especially in

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younger animals that are easily distracted. Most cats are reluctant to walk an obstacle course, however, and will usually choose to hide under the nearest table instead. It may be noted that dogs with reduced vision tend to use their nose more eagerly, whereas cats tend to feel with their paws.

Cotton ball An additional way of vision testing is to hold up a cotton ball, attract the animal’s attention to it, and then drop the ball. The ball may be dropped both in front of the animal and to its sides to assess central and peripheral vision. Most animals will follow the movement of the cotton ball, even if vision is reduced. However, puppies, lethargic animals, and some cats may show little interest in the procedure. These animals may be tested by dragging a noiseless object, like a cotton ball tied to a string, along the ﬂoor.

Swinging light In a darkened room the examiner watches for corresponding head or eye movements while the light beam from a penlight is swept across the visual axis. Visual ﬁeld defects are difﬁcult to assess in animals, but an attempt can be made by repeating the procedures in various planes and with one eye blindfolded.

The optic nerve The optic nerve is the afferent path for both vision and pupillary light reﬂexes. At the chiasm, optic nerve ﬁbers decussate to different degrees amongst species. As a rule, the more laterally the eyes are placed in the skull, the greater the degree of decussation. In the cat about two-thirds, and in the dog about threequarters, of the optic nerve ﬁbers cross in the optic chiasm to the opposite side of the brain. Temporal nerve ﬁbers from the nasal visual ﬁeld remain uncrossed in the optic tract on the same side, while nasal ﬁbers from the temporal visual ﬁeld cross to the opposite optic tract (i.e. the visual ﬁeld from one side of the body projects to the opposite visual cortex). This knowledge is important when assessing visual ﬁeld defects in humans, but of less importance in animals, where visual ﬁeld defects are difﬁcult to evaluate. In the optic tract, 80% of the nerve ﬁbers project via the lateral geniculate nucleus to the visual cortex of the cerebrum, whereas 20% go to the midbrain. The midbrain structures handle reﬂex vision, like dazzle reﬂex and pupillary light reﬂexes, and also visual input for balance and gaze ﬁxation. The function of the optic nerve can be tested in many ways. Practical testing includes: • • • •

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Menace reaction Visual placing reaction Pupillary light reﬂexes Dazzle reﬂex.

Note the difference between reactions and reﬂexes: a reaction involves higher (cortical) function, whereas reﬂexes are not dependent upon cortical function and may even be present in an animal with abnormal visual perception associated with higher lesions. The menace reaction A normal menace reaction requires a normal visual pathway – the sensory pathway – as well as normal facial innervation – the motor pathway (Fig. 5.1). The visual pathway consists of the retina, the optic

Cortex

Facial nerve

VISUAL IMPAIRMENT

Nucleus (thalamus)

Optic nerve Optic chiasm Fig. 5.1 The menace reaction. A sudden movement in front of the eye produces a rapid blink. The menace reaction requires normal visual pathways to the visual cortex as well as normal motor pathway to the eyelids.

nerve, the optic chiasm, the optic tract, the lateral geniculate nucleus in the thalamus, the optic radiation, and the visual cortex. The motor pathway involves the connection from the visual cortex to the facial nucleus and the facial nerve (VII). The menace reaction is a way of testing whether the animal is visual, as a positive response (usually expressed by a blink) tells that an image has been formed in the visual cortex. The animal is threatened by suddenly moving a hand into its visual ﬁeld or by opening a clenched ﬁst in front of the eye. It is, however, important to note that the menace reaction is absent in young puppies, and can also be absent in animals with cerebellar or facial nerve lesions, without the animal being blind. Seriously ill animals may also react poorly to the stimulus. The visual placing reactions Normal visual placing reactions require normal visual pathways to the cerebral cortex, communication from the visual cortex to the motor cortex, and intact motor pathways to the lower motor neurons (ﬁnal common pathway) of the forelimbs. Testing in small dogs and cats can be performed by holding the animal in front of a table. The animal is allowed to see the table surface when moved towards the table edge. Normal animals reach for the surface before the carpus touches the table. Some cats and dogs that are accustomed to being carried around may ignore the table and animals with neurologic deﬁcits may perform the test poorly. Peripheral visual ﬁelds can be tested by making a lateral approach to the table. Larger dogs can be led over a curb or a step. The dazzle reﬂex This is a stimulation of the optic nerve by the examiner suddenly shining a bright light into the eye of the patient. Normally, this will make the animal blink. The dazzle reﬂex (or the retinal light reﬂex) is not a reaction, i.e. it is subcortical, mediated by reﬂex centers in the midbrain with ﬁbers to the facial nucleus. The pupillary light reﬂexes Most important in the evaluation of visual function is the assessment of the pupillary light reﬂexes (PLRs) (Fig. 5.2). The

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1 6

2

3

4

5

Fig. 5.2 The pupillary light reﬂex arc. Shining light into one eye produces constriction of the pupil in the stimulated eye (direct pupillary light reﬂex) as well as in the contralateral eye (indirect pupillary light reﬂex). 1: optic nerve (II); 2: optic chiasm; 3: lateral geniculate nucleus; 4: parasympathetic nucleus of cranial nerve III; 5: visual cortex; 6: oculomotor nerve (III).

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afferent, or sensory, pathway involves the retina, the optic nerve (II), and the optic chiasm to the optic tract, where the majority of the ﬁbers continue the visual pathway to the lateral geniculate nucleus. However, about 20% leave the optic tract before the lateral geniculate nucleus and course towards the midbrain, where they synapse in the pretectal nuclei. From the pretectal nuclei, ﬁbers are distributed to the parasympathetic nuclei of the oculomotor nerve (III). The efferent or motor pathway extends via the parasympathetic ﬁbers of the third cranial nerve through the ciliary ganglion (in which the ﬁbers synapse) to the ciliary body and iris sphincter muscle. Pupillary constriction and dilatation is essentially a balance between parasympathetic and sympathetic control. The constrictor muscle of the iris, inner-

VISUAL IMPAIRMENT

vated by the parasympathetic ﬁbers of the oculomotor nerve (III), is a sphincter muscle located at the pupillary border and is more powerful than the dilator muscle, which runs along the peripheral iris in a radial fashion. The dilator muscle is innervated by sympathetic nerves. These nerves leave the spinal cord in the ﬁrst three thoracic segments and run along the neck in the vagosympathetic trunk, through the middle ear cavity and through the superior orbital ﬁssure before entering the eye. Before testing the pupillary light reﬂexes, it is important to evaluate the size of both pupils, and to note any difference in pupil size – anisocoria. A dim light is directed from below and any changes in pupil size noted. When evaluating anisocoria, it must be remembered that, because sympathetics dilate the pupils, a sympathetic lesion will be most noticeable in the dark, as a small pupil stays small. Conversely, the parasympathetics constrict the pupils. Therefore, in parasympathetic lesions, as the pupil stays dilated, the difference in pupillary size will be greater in the light. Also remember that an anxious or excited animal may have widely dilated pupils due to sympathetic stimulation, and that re-evaluation of pupil size after the animal has relaxed may be necessary. Pupillary light reﬂexes in very young animals may be sluggish and incomplete, probably related to the stage of maturational myelination of the optic nerve. Testing of direct and consensual pupillary light reﬂexes In a darkened room, a bright light is shone into one eye. Normally this causes a rapid and complete constriction of the pupil in the stimulated eye, the direct PLR. The constriction in the other eye, the consensual (or indirect) PLR, is slightly slower. The indirect PLR is produced because of the decussation of nerve ﬁbers in the optic chiasm as well as the contralateral connections in the nuclei of the midbrain. By evaluating the direct and consensual PLRs it is possible to localize defects along the reﬂex arcs, as well as to evaluate the function of the retina and optic nerve in an eye where more anterior lesions do not allow inspection of intraocular structures. The PLRs are independent of cortical vision but do still provide useful information on the integrity of the components of the afferent and efferent pathways. As the pupillary light reﬂexes do not involve higher (cortical) structures, a positive reﬂex does not necessarily infer that the animal has normal vision. It may be noted that blindness with an abnormal PLR localizes the lesion rostral to the lateral geniculate body, while blindness with a normal PLR reveals the lesion to involve the lateral geniculate body, optic radiation, or visual cortex.

Refraction The optical properties of the eye probably play an important role in visual discrimination in small animals, as well as in people. Refractive errors, e.g. myopia and hyperopia, are known in dogs and may be breed related.3 Although refractive errors may be suspected from the behavior of the patient, the refractive state of the eye can be objectively determined using a retinoscope and a series of lenses. The technique is called retinoscopy or skiascopy. Retinoscopy is easily performed in most dogs and cats. Lenses that correct for the refractive error and therefore enhance visual performance of the patient can be used to verify the diagnosis, and contact lenses can be used to adjust visual acuity. Long-term use of contact lenses to correct refractive errors may be used in small

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animals and contact lenses for aphakic (with no lens) dogs are now commercially available.

Electrophysiology Electrophysiologic testing becomes invaluable in animals with visual dysfunction.4 Different procedures can be performed depending on the site of a suspected lesion, such as the retina, optic nerve, or the visual cortex. To examine visual function clinically, the recording of two types of response is recommended. The electroretinogram (ERG) allows a rapid and objective examination of the outer and inner retina while the visual evoked potential (VEP) depends on normal optic nerve function and therefore reﬂects the conduction of the retinal signal all the way to the brain. Because the area centralis region is magniﬁed in the optic nerve and brain response, the VEP also provides some insight into potential visual acuity. ERG The ERG is a technique for observing the changes of electrical potential that occur when the eye is stimulated by light. These voltage changes, generated in the retina, reﬂect the responses of several types of neuron summed across the retina. They are critically dependent on the function of the retinal photoreceptors, i.e. the rods and cones. The ERG is usually recorded by means of a corneal contact lens electrode in response to a deﬁned ﬂash of light or repeated ﬂashes (ﬂicker) and displayed on an oscilloscope or on a computer screen. General anesthesia, intubation, and continuous monitoring of the patient are recommended during the procedure. In veterinary ophthalmology the ERG mainly has two broad applications: the easiest and most straightforward simply tests whether or not a standard stimulus elicits an ERG response. An example of this application is in an animal with complete cataracts. An ERG is indicated before proceeding to cataract surgery in order to ascertain that the retina is functional and not affected by PRA. The second and more sophisticated application is the study of rod and cone function as a part of research projects or in the early diagnosis of hereditary retinal dystrophies. A complex set of processes, PI, PII, and PIII, ﬁrst described by Granit,5 collectively comprise the ERG response, with its a-, b-, and, in some types of recording, c-waves. Grossly, the a-wave reﬂects the membrane current of photoreceptors and thus reﬂects their activity directly. The b-wave is generated as a complicated interaction, involving potassium movement between the bipolar and Müller cells, in response to input from the photoreceptors. The cwave is generated mainly through hyperpolarization of the apical membrane of the pigment epithelium and thus reﬂects retinal pigment epithelial cell function. The rod photoreceptors mainly function under scotopic conditions, and the cones mainly under photopic conditions. ERG recordings thus represent various combinations of rod and cone responses depending on the speciﬁc lighting used as background and/or stimulus. Therefore, it is important that a ﬁxed protocol is used to obtain meaningful ERGs. In order to interpret the ERG responses successfully it is, moreover, recommended that a technique be used that allows for the direct separation of rod and cone contributions to the ERG. Recommendations regarding how to perform diagnostic ERGs in dogs have recently been published.6

VISUAL IMPAIRMENT

The waveform of the ERG together with the amplitude and implicit times of the a- and b-waves is most often used when evaluating ERGs in a clinical situation. Comparisons are made of the observed responses with those of normals or controls. It should be noted that there are species, breed, and age-related variations in ERG parameters, so comparisons have always to be made with breed and age-matched animals. VEP Using active scalp electrodes, VEPs can be recorded in anesthetized animals using stroboscopic ﬂashes of light and averaging techniques.7 VEPs are cone dominated and reﬂect activity in a small part of the central area of the retina. Fibers from the central area of the retina are projected onto the surface of the occipital cortex, whereas ﬁbers from the peripheral areas are projected to deeper parts of the cortex and are not readily recorded. Apart from the central area of the retina, VEP mainly tests function of the post-retinal structures such as the optic nerve and the visual cortex. The waveform of the VEP consists of three major positive waves, the P1, P2, and P3. The characteristics of the VEP recording depend on a complex array of spatial and temporal conditions of light stimulation including luminance, contrast, and rate of stimulation. Depth of consciousness, age, visual acuity, and degree of light adaptation also inﬂuence the VEP. The VEP is currently used most often for research purposes, but the technique certainly has evolving clinical applications in the assessment of disease affecting the optic nerve and central visual systems. VEPs and ERGs can, moreover, be recorded simultaneously in the anesthetized animal, which makes it possible to evaluate visual function electrophysiologically in a more complete fashion.

Other Ultrasonography indicated to deﬁne space-occupying lesions, foreign bodies, scleral tears, and retinal detachment, especially in cases where the fundus cannot be visualized. Fluorescein angiography is a specialized technique used to assess the retinal and choroidal vasculature. It requires a ﬂuorescein fundus camera with ﬁlters that are placed in both the illuminating beam and the observing beam. The exciter ﬁlter in the illuminating beam transmits blue-green light at the peak excitation wavelength for ﬂuorescein, thus making it ﬂuoresce. The barrier ﬁlter (in the pathway for the observing beam) transmits yellow light at ﬂuorescein’s peak emission range. Fluorescein is delivered by an intravenous bolus and serial photographs are taken of the various stages of ﬁlling and emptying of retinal and choroidal vessels.

CONGENITAL DISEASE AND MALFORMATIONS Anophthalmia, nanophthalmia, and microphthalmia In anophthalmia, the globe is not present. This is a rare condition caused by a defect in the formation of the optic vesicle from the neuroectoderm, and may be unilateral or bilateral. Histologic examination of tissue from the orbital region may often reveal traces of rudimentary optic structures. Microphthalmia is relatively common in the dog, and may present as a small but otherwise normal globe; this form of microphthalmia is termed nanophthalmia. The term microphthalmia, however, is usually used to describe a small

125

SMALL ANIMAL OPHTHALMOLOGY

and abnormal globe, the result of retarded or aberrant development of the optic vesicle with associated ocular anomalies that may include cataract, persistent pupillary membrane, retinal dysplasia, and colobomas. Microphthalmia is seen more frequently in certain breeds, including the Collie breeds, English Cocker Spaniel, Saint Bernard, and Dobermann Pinscher, but may occur spontaneously in dogs of any breed. Teratogenic agents as well as hereditary factors may cause malformations of the eyes. Microphthalmia may occur unilaterally or bilaterally, and one or more littermates may be affected.

Clinical ﬁndings Anophthalmic or grossly microphthalmic eyes should not be difﬁcult to recognize. Mild cases of microphthalmia or nanophthalmia may cause diagnostic problems, however, especially if the condition occurs bilaterally. In certain breeds, like the Collie and the Shetland Sheepdog, the breed standard demands small eyes, making differentiation between normal and microphthalmic eyes difﬁcult. The following features may be of help when comparing a unilaterally microphthalmic eye to its fellow normal eye. • Compare both eyes by inspection from above and in front of the animal and observe differences in the palpebral ﬁssure, recession of the microphthalmic eye into the orbit (enophthalmia), and protrusion of the third eyelid. • Note the exposure of the sclera and the diameter of the cornea. • Closer examination may reveal abnormalities including persistent pupillary membranes, abnormal pupil shape (dyscoria), cataracts, and multifocal retinal dysplasia or retinal detachment. • Colobomas may be present, but are more rarely diagnosed. • There are often abnormal eye movements such as a ‘searching’ nystagmus or a ﬁne oscillatory nystagmus, which indicates that the visual pathways are not fully developed.

Differential diagnoses Difference in iris pigmentation between two otherwise normal eyes (heterochromia irides) is not uncommon and should not be confused with abnormalities of the eyes. Phthisis bulbi (shrinkage of the eye) occurs as a result of severe trauma or as an end-stage of intraocular inﬂammation. This condition is commonly preceded by a history of red eye and ocular pain, whereas microphthalmia is painless. Microphthalmia as a congenital condition is usually detected in the young animal, while phthisis bulbi may occur in animals of any age.

Prognosis and treatment

126

Abnormal development of the eye cannot be treated and the prognosis depends on the degree of visual impairment and whether the condition is unilateral or bilateral. Secondary cataracts may develop as may chronic conjunctivitis due to poor conﬁguration of eyelids and globe. The conjunctivitis may need daily cleansing to remove accumulated discharges. Cataract surgery in microphthalmic eyes may be rewarding if no other malformations are present. Enucleation may be recommended if the microphthalmic eye is blind and causes discomfort

Persistent pupillary membrane (PPM) During the embryonal phase before the pupil is formed, the area is covered by a vascular membrane, the pupillary membrane. The membrane is formed during development of the eye by anastomoses between the tunica vasculosa lentis, which branches from the hyaloid artery and forms a meshwork around the lens, and vascular loops from the annular vessel in front of the lens. Normally, regression of the pupillary membrane starts about 2 weeks before birth, with the membrane no longer present by 2–4 weeks after birth. Minute remnants of the membrane are frequent in animals and are usually of no signiﬁcance. These remnants may be seen as tissue strands originating from the collarette of the iris. The strands may extend from iris to iris across the pupil, from iris to lens or to cornea or to both, or there may be sheets of tissue in the anterior chamber extending between iris, lens, and cornea. Where attached to the lens, there may be concurrent cataract formation, and attachment to the inside of the cornea may cause focal corneal opacities and edema. A variant of PPM may be seen as an area of pigmented ﬂecks on the anterior lens capsule.

VISUAL IMPAIRMENT

to the animal. The use of the animal for future breeding is not advised, particularly in those breeds where the condition is suspected to be inherited.

Clinical ﬁndings PPM is congenital and may therefore be diagnosed in the young animal. The condition is not painful and there is no history of previous injury to the eye. With corneal involvement the opacity does not stain with ﬂuorescein, as it affects the endothelium and the stroma. A genetic disposition has been described in the Basenji8 and has been suggested in the English Cocker Spaniel and the Collie.9 More than one puppy in a litter is often affected.

Treatment and prognosis There is no effective treatment for this congenital condition, but, unless the changes are extensive, vision is not impaired. Severely affected dogs from breeds where a hereditary disposition is suspected should not be used for breeding.

Congenital lens disorders These disorders are usually part of other developmental abnormalities of the eye and may be due to a chance error in embryogenesis. In some cases, however, the abnormalities have a hereditary background. Congenital developmental abnormalities of the lens, which often occur in combination with other malformations of the eye, such as persistence of the hyaloid vessels or microphthalmia, include: • Aphakia – the total absence of the lens or the presence of only rudimentary lens tissue. This is a rare condition. • Microphakia – smaller than normal lens equatorial diameter. Elongated ciliary processes can be seen surrounding the lens, and the lens borders are clearly visible when the pupil is dilated. The condition may be breed related, as in the Miniature Schnauzer, where it is associated with congenital cataract.

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SMALL ANIMAL OPHTHALMOLOGY

• Spherophakia – an abnormal spherical shape to the lens which is usually microphakic as well. • Coloboma – where the lens has an equatorial notching (Fig. 5.3). The zonular ﬁbers are either deﬁcient or absent in the affected area. This condition may be associated with congenital cataract and colobomas of the iris and ciliary body. • Lenticonus/lentiglobus – a thinning of the lens capsule permitting the cortex to bulge. This causes a conical malformation, most commonly at the posterior pole. Lentiglobus is more severe than lenticonus. The capsule in the affected area may show dysplastic or degenerative changes that inﬂuence lens metabolism and result in cataract development. Spontaneous rupture of the posterior capsule may occur. The abnormality is most often diagnosed in connection with abnormalities of the posterior hyaloid system, as described in persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic Primary vitreous (PHTVL/PHPV) in the Dobermann Pinscher,10 or in connection with microphthalmia and cataract. A congenital defect of the lens including cataract, posterior lenticonus, and sometimes also microphthalmia has been described in the Cavalier King Charles Spaniel (Fig. 5.4).11 • Cataracts – nuclear and sometimes posterior and/or anterior cortical opaciﬁcation with or without capsular involvement is observed in litters of several breeds. This type of congenital cataract has been described speciﬁcally in the English Cocker Spaniel.9 In the West Highland White Terrier a speciﬁc type of posterior suture line cataract has been described, as well as congenital complete cataracts.12

Persistent hyaloid artery (PHA) The hyaloid artery is present in fetal life, but will normally undergo regression during the ﬁrst postnatal weeks. Remnants of the obliterated hyaloid artery

128

Fig. 5.3 Congenital malformations of the lens in a 1-year-old Samoyed dog: unilateral lens coloboma and cataract.

VISUAL IMPAIRMENT

Fig. 5.4 Posterior lenticonus, with rupture of the posterior lens capsule, and bilateral congenital cataract in the eye of a 12-week-old Cavalier King Charles Spaniel.

which persist without any other abnormalities are referred to as PHA.13 The artery can remain as a curvilinear structure, still containing blood, between the optic disk and the lens. Usually, however, only a small connective tissue strand remains.

Clinical ﬁndings The persistent hyaloid artery can be seen as a white strand adherent to the posterior lens capsule, below the posterior pole. The vessel remnants extend back into the vitreous body and move with the eye movements. Occasionally, the hyaloid vessel arises from an anomalous superﬁcial retinal vessel. Small vessel remnants do not affect vision, but at the site of adherence to the lens there may be a focal opacity (Mittendorf’s dot). Secondary cataracts may develop in this area. The condition may occur unilaterally or bilaterally and is occasionally seen in the dog. A familial disposition has been suspected in the Sussex Spaniel.

Persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous (PHTVL/PHPV) or persistent embryonic vasculature (PEV) In this disorder, parts of the hyaloid system and primitive vitreous become hyperplastic and remain postnatally instead of undergoing normal regression.10,14 Embryologic alterations occur in the eye cup, the primary vitreous, the hyaloid artery, and the tunica vasculosa lentis. The hyperplasia and lack of normal regression are considered to be caused by a disharmony between growth factors and inhibitors within the eye. In severe cases, secondary cataracts develop. The condition may be unilateral or bilateral and may occur sporadically in any animal. In the Dobermann Pinscher primarily, but also in other

129

SMALL ANIMAL OPHTHALMOLOGY

breeds such as the Staffordshire Bull Terrier and Standard Pinscher,15,16 the disorder occurs bilaterally, and appears to be inherited by an incomplete dominant mode of inheritance in the Dobermann Pinscher.

Clinical ﬁndings In the mildest form of PEV, tiny punctuate opacities, residual tissue from the vascular network, are found on the axial posterior lens capsule. These lesions do not progress and do not detectably affect vision. They are only seen by use of a slit-lamp biomicroscope, and may be difﬁcult to diagnose in puppies because of small eye size. The severe forms occur bilaterally and often lead to visual impairment. A plaque of white ﬁbrovascular tissue may be identiﬁed on the posterior capsule. In addition, large remnants of the hyaloid system can persist and may be accompanied by pigment or blood in and around the lens, lenticonus, or other lens malformations (Figs 5.5 & 5.6). PHTVL may also be seen as vascular loops anterior to the lens. In the most severe forms, secondary cataracts are either present at birth or develop early in life.

Diagnosis and differential diagnosis Since the condition is congenital and can be diagnosed in the puppy, a scoring system depending on the severity of the disorder has been suggested. The disease does not include persistent pupillary membranes as described earlier, but small loops of the tunica vasculosa lentis system may be seen adjacent to the anterior capsule of the lens. Differential diagnoses include congenital cataract and retinal detachment.

Therapy and prognosis In severely abnormal eyes, lens extraction (see cataract therapy) can be performed together with posterior capsulorhexis and vitrectomy. The prognosis

130

Fig. 5.5 PHTVL/PHPV in a 9-month-old Dobermann Pinscher. Fibrovascular tissue and pigmentation are seen on the posterior lens capsule as well as posterior lenticonus.

VISUAL IMPAIRMENT

Fig. 5.6 Intralenticular bleeding and low-grade uveitis is seen in conjunction with PHTVL/ PHPV in this 1-year-old Dobermann Pinscher.

for the operation is less favorable than in uncomplicated lens extraction, because of the increased incidence of intraoperative and postoperative complications. Dobermann Pinscher puppies can be screened for PHTVL/PHPV at about 7–8 weeks of age. Severely affected animals should not be used for breeding, while dogs expressing only multifocal pin-point posterior capsular opacities may be bred to normal-eyed animals.

Congenital vitreous opaciﬁcation Vitreous opaciﬁcation is uncommon and is usually due to hemorrhage associated with congenital retinal abnormalities. These may result from rupture of blood vessels in a detached retina or from retinal neovascularization. The congenital diseases most commonly connected with blood in the vitreous are: • Collie eye anomaly (CEA) in collie breeds. The hemorrhage usually occurs sporadically in the young dog, most often before 2 years of age. • Total retinal dysplasia with non-attachment, as seen sporadically in many breeds and as an inherited condition in the Labrador Retriever, Sealyham Terrier, Bedlington Terrier, and occasionally the English Springer Spaniel. • Multiple congenital ocular anomalies may be the result of mating of two merle-colored dogs and does also occur in the Australian Shepherd Dog. • Other conditions including preretinal arteriolar loops and vascular malformations.

Clinical ﬁndings Hemorrhage in the vitreous is diagnosed unilaterally or bilaterally as blood seen behind the lens. The blood may also pass forward into the anterior segment of the eye. The condition is usually non-painful unless occurring secondary to

131

SMALL ANIMAL OPHTHALMOLOGY

a painful ocular disease. One should remember that acquired vitreal hemorrhage is not an uncommon condition and will be discussed later in this chapter.

Diagnosis Examination of the fellow eye, if unaffected, may reveal congenital anomalies of types that may cause vitreous hemorrhage. The breed incidence is also important to consider.

Differential diagnosis Intralenticular hemorrhage may be seen in connection with PHTVL/PHPV. The hemorrhage in this disorder, however, is within the retrolental plaque of tissue and sometimes also within the lens (see Fig. 5.6). Breed incidence must be considered. Hyphema (blood in the anterior chamber) may resemble vitreous hemorrhage, and may occur from the same disorder (e.g. CEA), but will most often represent a different condition, like trauma, uveitis, or neoplasia. While hyphema is seen in front of the lens, hemorrhage from hyaloid vessel remnants is seen behind the lens. Hyperviscosity of the blood is usually associated with monoclonal gammopathies and plasma cell producing tumors, and may lead to vessel rupture and hemorrhage. A thorough clinical examination should be performed. This disease, however, is usually diagnosed in older animals.

Treatment and prognosis Surgical removal (vitrectomy) of congenital intravitreal hemorrhage is rarely indicated. The condition is serious because it usually indicates a severe disorder of the posterior segment or an underlying systemic disease. This is especially true if the blood remains unclotted, indicating continuous bleeding. The hemorrhage may seemingly clear if the dog is inactive for a period, but will return as soon as the dog is exercised. If, however, the hemorrhage should clear permanently, the vitreous may undergo degenerative changes which may lead to traction on the retina with subsequent detachment. More uncommonly, secondary glaucoma or uveitis may develop.

Congenital malformations of the retina and the optic nerve The retina can be congenitally malformed in several ways including involvement of all layers of the neuroretina, such as in retinal dysplasia, or speciﬁc cells in the retina being affected, such as rod–cone dysplasia or retinal pigment epithelial cell dystrophy. In certain defects structures posterior to the retina are malformed, as well as in posterior segment colobomata. Congenital malformations are often caused by hereditary factors but some are also induced by maternal infection or X-irradiation, such as retinal dysplasia (see below), or may occur as a spontaneous malformation. See Table 5.3 for a summary of hereditary retinal disease affecting speciﬁc cells of the neurosensory retina in the dog and cat.

General treatment 132

There is usually no effective treatment for congenital malformations of the posterior segment of the eye. If the defect is known to be hereditary, preventive

AR AR

Rod–cone dysplasia/rcd1

Rod–cone dysplasia/rcd2

Rod–cone dysplasia/rcd3

Rod dysplasia/rd

Early rod degeneration/erd

Photoreceptor degeneration/pd/type A PRA

Cone–rod dystrophy/crd1

Cone–rod dystrophy/crd2

Early cone–rod dystrophy

Cone–rod dystrophy

Cone–rod dystrophy

Irish Red & White Setter

Rough Collie

Cardigan Welsh Corgi

Norwegian Elkhound

Norwegian Elkhound

Miniature Schnauzer

Pit Bull Terrier

Pit Bull Terrier

Shorthaired Dachshund

Longhaired Dachshund

Wirehaired Dachshund

AR

AR

AR

AR

AR

AR

AR

AR

AR

AR

Rod–cone dysplasia/rcd1

Irish Setter

Mode of inheritance

Disease/Gene symbol

1.5–3.0 y

0.5 y

1.5–3.0 y

0.4–0.5 y

0.4–0.5 y

1.5–5.0 y

0.75–1 y

0.5–1.5 y

0.3 y

0.3 y

0.3 y

0.3 y

Diagnosis by ophthalmoscopy

Summary of some clinically characterized hereditary primary photoreceptor disorders of dog and cat breeds.

Breed of dog

Table 5.3

5 wk

6 wk

5 wk

7 wk

7 wk

6 wk

5 wk

6 wk

3 wk

6 wk

6 wk

6 wk

Diagnosis by ERG

VISUAL IMPAIRMENT

133

Disease/Gene symbol

Cone degeneration/achromotopsia

Cone degeneration/achromotopsia

X-linked progressive retinal degeneration/XL PRA1

X-linked progressive retinal degeneration/XL PRA1

X-linked progressive retinal degeneration/XL PRA2

Dominant progressive retinal atrophy (rhodopsin mutant dog)

Dominant progressive retinal atrophy (rhodopsin mutant dog)

Progressive rod–cone degeneration/prcd

Breed of dog

Alaskan Malamute

German Shorthaired Pointer

Siberian Husky

Samoyed

Mixed breed

Old English Mastiff

Bull Mastiff

Toy and Miniature Poodle

Table 5.3 continued

134 0.5–1.0 y

3.0–5.0 y

AR

0.5–1.0 y

1–2 y

3.0–5.0 y

2.0 y

–

–

Diagnosis by ophthalmoscopy

AD

AD

X-linked

X-linked

X-linked

AR

AR

Mode of inheritance

9 mo

<14 mo

<14 mo

6 wk

0.5 y

0.5 y

6 wk

6 wk

Diagnosis by ERG

SMALL ANIMAL OPHTHALMOLOGY

Progressive rod–cone degeneration/prcd

Progressive rod–cone degeneration/prcd

Progressive rod–cone degeneration/prcd

Progressive retinal atrophy

Progressive retinal atrophy

Progressive retinal atrophy

American Cocker Spaniel

English Cocker Spaniel

Portuguese Waterdog

Tibetan Terrier

Papillon

Akita

Rod/cone dysplasia

Rod/cone dysplasia

Abyssinian

Persian

AD, autosomal dominant; AR, autosomal recessive

Progressive rod cone degeneration

Abyssinian

Breed of cat

Progressive rod–cone degeneration/prcd

Labrador Retriever

AR

AD

AR

AR

AR

AR

AR

AR

AR

AR

8 mo 5w 5w

<0.3 y <0.3 y

1.5–2.0 y

9 mo-1.5 y

10 mo

1.5 y

2.0–3.0 y

9 mo

1.5 y

1.0–2.5 y

1.0–3.0 y

1.2–5.0 y

1.0–1.5 y

3.0–6.0 y

3.0–8.0 y

2.5–3.0 y

3.0–6.0 y

VISUAL IMPAIRMENT

135

SMALL ANIMAL OPHTHALMOLOGY

measures need to be taken in the breeding program. The rule of thumb is not to use affected individuals for breeding. Breeders are also recommended not to use known carriers of the defect in their breeding, as for example the parents of an affected animal and the affected animal’s offspring in an autosomal recessive disorder. There are currently a number of breed-speciﬁc molecular genetic tests available, which should make control or even eradication of speciﬁc diseases possible. For a summary of DNA-based tests for hereditary retinal and neurodegenerative diseases in the dog, see Table 5.4.

Retinal dysplasia (RD) Focal RD and multifocal RD, geographic RD, and diffuse RD are ocular anomalies caused by an intrinsic abnormality of neural retinal differentiation.33 Morphology includes folding and rosette formation mainly of the neuronal retinal cells with or without retinal detachment/non-attachment. Retinal folds are included in the deﬁnition of focal/multifocal RD. The disease is believed to be inherited as an autosomal recessive trait in the breeds of dog that have been described genetically so far. Diffuse RD has been described in the Sealyham and Bedlington Terrier breeds, the Labrador Retriever, the Australian Shepherd Dog, and the English Springer Spaniel. Dogs affected with focal or multifocal RD include the Labrador Retriever, American Cocker Spaniel, English Springer Spaniel, Beagle, Cavalier King Charles Spaniel, Rottweiler, and the Golden Retriever. Multifocal RD has also been observed in the cat. Geographic RD has been recognized in breeds such as the Cavalier King Charles Spaniel and the Golden Retriever. It appears that the geographic form of RD is not always congenital, i.e. may appear at or later than the age of 8 months in some breeds of dog.34 Inherited RD in combination with hyperplastic primary vitreous has recently been described in the Miniature Schnauzer dog.35 Affected dogs have generalized changes in the retina observed as thickened areas or complete retinal detachment, as seen by ophthalmoscopy. Vitreous opaciﬁcations are concurrently observed, as well as small white posterior lens capsule plaques. The white primary vitreous masses may extend from the lens to the Bergermeister’s papilla on the optic disk.

Clinical ﬁndings The ophthalmoscopic appearance of RD is typical but may, in some cases, be difﬁcult to differentiate from focal scarring. In diffuse RD most or all of the neuroretina is detached (or non-attached). In multifocal RD, vermiform streaks or spots are seen typically around the large retinal blood vessels superior to the optic disk. The lesions are most often bilateral but the extent of the retinal changes may vary between the eyes. In diffuse RD the eye is blind, while in multifocal RD vision is usually unaffected. Nystagmus may be present in blind puppies. Cataracts and skeletal abnormalities in conjunction with RD have been described in the homozygously affected Labrador Retriever and Samoyed breeds of dog, as non-allelic defects. The diseases in both breeds have been termed dwarﬁsm with retinal dysplasia.36

Speciﬁc treatment and prognosis 136

Blindness is permanent in eyes with detached neural retinas and affected eyes may develop neovascular glaucoma and intraocular hemorrhage. Euthanasia

Mutation detection Mutation detection Mutation detection Mutation detection

Mutation detection Mutation detection

Gene on chromosome 9∗ Gene on chromosome 9∗ Gene on chromosome 37∗ Gene on chromosome 9∗

Gene on chromosome 37∗ RPE65

Rhodopsin PDE6A

arPRA – prcd

arPRA – prcd

CEA-CH

arPRA – prcd

CEA-CH

Congenital stationary night blindness/retinal dystrophy

adPRA

arPRA – rcd3

American Eskimo Dog

Australian Cattle Dog

Australian Shepherd

Australian Stumpy Tail Cattle Dog

Border Collie

Briard

Bull Mastiff

Cardigan Welsh Corgi

Mutation detection

Mutation detection

Mutation detection

Type of test

Gene on chromosome 9∗

Gene

arPRA – prcd

Disease

American Cocker Spaniel

Retina

Breed

Table 5.4 DNA-based tests for hereditary retinal and neurodegenerative diseases in the dog.

21, 22

20, www.optigen.com

19

18, www.optigen.com

17, www.optigen.com

18, www.optigen.com

17, www.optigen.com

17, www.optigen.com

17, www.optigen.com

Reference

VISUAL IMPAIRMENT

137

Mutation detection Mutation detection

Mutation detection Mutation detection Mutation detection Mutation detection Mutation detection Mutation detection

Gene on chromosome 9∗ Gene on chromosome 9∗ Gene on chromosome 9∗

Gene on chromosome 9∗ CNGB3 PDE6B Gene on chromosome 9∗ Gene on chromosome 37∗ Gene on chromosome 9∗

arPRA – prcd

arPRA – prcd

arPRA – prcd

arPRA – prcd

CD

arPRA – rcd1

arPRA – prcd

CEA-CH

arPRA – prcd

arPRA – type A

Chinese Crested

English Cocker Spaniel

Entlebucher Sennenhund (Swiss Mountain Dog)

Finnish Lapphund

German Shorthaired Pointer

Irish Setter

Labrador Retriever

Lancashire Heeler

Miniature Poodle

Miniature Schnauzer†

Phosducin

Mutation detection

Gene on chromosome 9

arPRA – prcd

Chesapeake Bay Retriever

Mutation detection

Mutation detection

∗

Gene

Disease

Type of test

27

17, www.optigen.com

26, www.optigen.com

17, www.optigen.com

24, 25

23

17, www.optigen.com

17, www.optigen.com

17, www.optigen.com

17, www.optigen.com

17, www.optigen.com

Reference

SMALL ANIMAL OPHTHALMOLOGY

Breed

Table 5.4 continued

138

Mutation detection

RPGR‡

xlPRA

CEA-CH

xlPRA

arPRA

Samoyed

Shetland Sheepdog

Siberian Husky

Sloughi

Smooth Collie

Toy Poodle

Brain and retina

Mutation detection

Gene on chromosome 37∗

CEA-CH

Rough Collie

Mutation detection Mutation detection Mutation detection Mutation detection

RPGR‡ PDE6B Gene on chromosome 37∗ Gene on chromosome 9∗

CEA-CH

arPRA – prcd

Gene on chromosome 37

Mutation detection

Mutation detection

Gene on chromosome 9∗

arPRA – prcd

Portuguese Water Dog

∗

Mutation detection

Rhodopsin

adRPA

Mutation detection

Old English Mastiff

Gene on chromosome 9∗

arPRA – prcd

Nova Scotia Duck Tolling Retriever

17, www.optigen.com

18, www.optigen.com

29

28

28, www.optigen.com

18, www.optigen.com

17, www.optigen.com

20, www.optigen.com

17, www.optigen.com

VISUAL IMPAIRMENT

139

NCL

NCL

NCL

American Bulldog

Border Collie

English Setter

Mutant gene has been discovered but not published at time of writing † an additional form of PRA exists in this breed ‡ mutations in RPGR in Siberian Husky and Samoyed are different arPRA = autosomal recessive progressive retinal atrophy adPRA = autosomal dominant progressive retinal atrophy CD = cone degeneration (achromatopsia) CEA-CH = choroidal hypoplasia manifestation of collie eye anomaly CLN5 & CLN8 = respective genes encoding for NCL CNGB3 = cyclic nucleotide-gated channel beta-subunit gene CTSD = cathepsin D gene NCL = neuronal ceroid lipofuscinosis PDE6A = gene encoding the alpha subunit of rod cyclic GMP phosphodiesterase PDE6B = gene encoding the beta subunit of rod cyclic GMP phosphodiesterase prcd = progressive rod–cone dysplasia rcd1 = rod–cone dysplasia type 1 rcd3 = rod–cone dysplasia type 3 RPGR = RP GTPase regulator xlPRA = X-linked progressive retinal atrophy

∗

Disease

Breed

Table 5.4 continued

140 Type of test Mutation detection Mutation detection Mutation detection

Gene CTSD CLN5 CLN8

32

31

30

Reference

SMALL ANIMAL OPHTHALMOLOGY

Secondary (non-inherited) RD Abnormal retinal differentiation with formation of retinal folds and rosettes occurs spontaneously in dogs and cats. Causes may be maternal infection, intrauterine trauma, vitamin A deﬁciency during pregnancy, irradiation, and idiopathic. Clinical signs are similar to those above. Other ocular signs often accompany the secondary type of retinal dysplasia such as cataracts, uveitis, and synechia formation.

VISUAL IMPAIRMENT

is recommended in bilaterally affected puppies. In multifocal RD vision is often unaffected and will most often stay so throughout life. An exception is multifocal RD in the Springer Spaniel in which slowly progressive multifocal atrophic areas of the retina can result in severe visual impairment (Fig. 5.7).

Serous retinopathy/retinal pigment epithelial dysplasia This is a unique multifocal hereditary disease of the outer retina, speciﬁcally the retinal pigment epithelium, described in the Great Pyrenees dog.37,38 Retinal lesions develop approximately at the age of 11 weeks, gradually over several years in the peripheral fundus but more quickly centrally, as peripapillary lesions. The latter are serous retinal detachments, seen as blocked ﬂuorescence and subretinal pooling of ﬂuorescein upon angiography. There appears to be no signiﬁcant progression of retinal degeneration over time.

Optic nerve hypoplasia and aplasia This refers to an abnormal differentiation of the ganglion cell and nerve ﬁber layers of the retina resulting in a paucity of axons in the optic nerve and optic chiasm. This uncommon condition is either unilateral or bilateral. Histologi-

Fig. 5.7 Multifocal retinal dysplasia may sometimes be severe and cause reduction in visual capacity as seen in this 4-year-old English Springer Spaniel.

141

SMALL ANIMAL OPHTHALMOLOGY

cally it is seen as a reduction in the number of ganglion cells and thinning of the nerve ﬁber layer in the retina. The defect has been reported in several breeds and is believed to be hereditary in some.39,40

Clinical ﬁndings The clinical ﬁndings depend on the severity of the defect. If bilateral, the animal is usually blind, but if unilateral the problem is often not noticed by the owner. The pupils are typically dilated and the pupillary light reﬂexes are depressed to absent. In cases of unilateral hypoplasia the affected eye may still show an indirect (or consensual) response. Ophthalmoscopically the disk is abnormally small and dark, often gray in appearance.

Treatment There is no treatment. In cases of a suspected hereditary background, affected individuals should not be used for breeding.

Posterior segment colobomas A coloboma is a congenital tissue defect manifested by a pit, hole, ﬁssure, or notch. A posterior segment coloboma may affect the retina, choroid, and sclera, and often affects the optic disk. Colobomas in the Collie breeds are part of the Collie eye anomaly complex, and hereditary optic disk colobomas have been reported in the Basenji dog. In cats colobomas of the choroid have been described with a hereditary background and may be seen associated with eyelid agenesis. Very extensive colobomas may cause blindness, while small ones cause no obvious visual problems.

Collie eye anomaly (CEA) CEA is a common defect with a frequency of over 90% in the Rough Collie in the USA 25–30 years ago. The prevalence in most countries today is signiﬁcantly lower. The disease is a congenital inherited ocular anomaly originally considered to be inherited as a simple autosomal recessive trait.41 Etiologic factors include the failure of normal closing of the fetal ﬁssure during development of the eye. The defect results in bilateral changes of variable severity that may affect the retina, choroid, sclera, and/or optic disk.42 The essential lesion is choroidal hypoplasia which may or may not be accompanied by other defects (Fig. 5.8). Affected breeds are the Rough Collie, Smooth Collie, Shetland Sheepdog, Australian Shepherd, Border Collie, and the Lancaster Heeler.26 Linkage studies of the primary CEA locus was shown on canine chromosome 37.18 Recently the gene responsible for choroidal hypoplasia was identiﬁed (www.optigen.com), although the information has not yet been published in the scientiﬁc literature.

Clinical ﬁndings and signiﬁcance Funduscopic manifestations of CEA are variable, even within a single litter, and often the lesions in the two eyes are dissimilar in severity or distribution. One or more of the following signs can be observed in conjunction with CEA:

142

1. Choroidal hypoplasia. This is a lesion found temporal to the optic disk. It is an area with lack of pigment and tapetum, exposing sclera and abnormal choroidal vessels. The lesion is bilateral although the extent

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may vary between eyes. Choroidal hypoplasia in its mildest form may have little or no effect on vision, but major defects may cause some reduced vision due to absence of photoreceptors and reduced numbers of ganglion cells and thinning of the nerve ﬁber layer of the retina.43 Minor chorioretinal changes found on examination before 3 months of age can be masked by later pigmentation. Affected dogs in which this phenomenon masks previous lesions are called ‘go normals’, and the condition is prevalent in a signiﬁcant number of animals.44 2. Colobomas. This defect is usually found at or in the vicinity of the optic disk. It is seen as a gray and/or white defect, either small and difﬁcult to detect or larger with vessels dipping down over the rim. Small colobomas do not cause visual problems, but large ones, usually the size of the disk or more, may cause defective vision or blindness. Large colobomas involving the whole optic disk may predispose to retinal detachment. 3. Retinal detachment. The neural retina has partially or completely detached and can be observed ﬂoating in the vitreous. Large peripheral retinal tears are present. Detachment usually occurs at an early age, before 7 weeks, but can also occur later in life, although usually before the age of 1 year. Vision is always severely affected with resultant blindness if complete and bilateral. Intraocular hemorrhage is common in conjunction with retinal detachment. Euthanasia is usually recommended in the most severe forms of CEA, i.e. dogs bilaterally blind because of large colobomas or retinal detachments.

Speciﬁc treatment There is no effective treatment for CEA. It is important to induce preventive measures for the genetic defect. With a genetic test now available the frequency of the disease can be signiﬁcantly reduced on a worldwide basis. However,

Fig. 5.8 Choroidal hypoplasia and coloboma of the optic nerve head, as seen in this young Collie, are signs of Collie eye anomaly (CEA).

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recommendations in regard to regulatory procedures will most probably vary in different countries.

Early-onset photoreceptor dystrophies The forms of progressive retinal atrophy (PRA) due to photoreceptor dysplasias have an early onset. See Table 5.3.

Rod–cone dysplasia (rcd) Rod–cone dysplasia is an early-onset retinal cell dystrophy, characterized by retarded differentiation of the rod and cone photoreceptors, followed by subsequent degeneration. Affected breeds are the Irish Setter, Rough Collie, and the Cardigan Welsh Corgi. In the three dog breeds, speciﬁc biochemical abnormalities are present that result in elevated retinal cGMP, due to deﬁcient retinal cGMP-PDE (cyclic guanosine monophosphate-phosphodiesterase) activity.45 The defects have been shown to be inherited in a simple recessive mode, although the diseases are caused by genes at different loci. The gene defect causal for rod–cone dysplasia type 1 (rcd-1) in the Irish Setter has been identiﬁed,46,47 and a DNA-based diagnostic test for the presence of the gene mutation has been developed.46,48 The test can be used to distinguish between dogs that are normal, heterozygous carriers, or homozygously affected at the rcd-1 gene locus.49 The gene mutation responsible for early-onset PRA in the Collie (rcd-2) has not been identiﬁed.50 The gene for rcd-3 in the Cardigan Welsh Corgi has been identiﬁed and is one of the cGMP-PDE subunits.51 A DNA-based test has been developed for this form of PRA.22 In cats rod–cone dysplasia has been described in two speciﬁc breeds: a strain of English Abyssinian cats52 and Persian cats.53 The mode of inheritance for the defect had been shown to be autosomal dominant in the Abyssinian rod– cone dysplasia cats, while the disease is due to an autosomal recessive defect in the Persian cat breed.

Clinical ﬁndings These include initial night blindness followed by a progressive loss of day vision as well. Clinical signs are apparent early, usually at 6–12 weeks in dogs, somewhat earlier in cats (2–3 weeks). Blindness is apparent by 1–2 years in the dog and 12–16 weeks in the cat. Ophthalmoscopically the tapetal fundus is hyperreﬂective, starting peripherally and spreading centrally. Within months there is a completely atrophic fundus with severe vascular attenuation. In the cat, nystagmus and sometimes a slight lateral strabismus may be observed at an early age in affected animals. Early diagnosis of rod–cone dysplasia is performed by ERG, abnormalities being detectable by 4–6 weeks of age. In affected animals there are severely reduced, or a lack of, rod and cone responses.

Rod dysplasia (rd) This disease is characterized by a defective development of the rod photoreceptors with secondary degeneration of the cone system. The only breed in which the disease has been described so far is the Norwegian Elkhound.54

Clinical ﬁndings 144

Initial night blindness (nyctalopia) is detected in affected puppies at 2–3 months, while day vision is normal at this time. Day and night vision deteriorates successively and affected dogs are blind at the age of 3–6 years. Ophthalmoscopi-

Early retinal degeneration (erd)

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cally a granular and discolored appearance of the tapetal fundus is observed at 6–12 months progressing to tapetal hyperreﬂectivity and vascular attenuation within a few years. Electroretinography at 6 weeks is diagnostic for the disease, with a lack of rod responses and normal to slightly reduced cone responses in affected dogs. A recessively inherited retinal dystrophy has been described in the Norwegian Elkhound.55 Morphologically there is an abnormal development of both rod and cone photoreceptors.

Clinical ﬁndings Affected puppies are night-blind at 6 weeks and completely blind at 1–1.5 years. Ophthalmoscopic signs of the disease may be observed at about 6 months and there is a retinal atrophy at the age of 1 year. Speciﬁcally the photoreceptor synaptic terminals are abnormal. ERG enables diagnosis of the disease by 6 weeks of age: there is an a-wave dominated response which becomes nonrecordable with age.

Photoreceptor dysplasia (pd) A progressive retinal atrophy has been described in the Miniature Schnauzer dog and deﬁned as a photoreceptor dysplasia.56 The disease is characterized by unique morphologic and functional deﬁcits during rod and cone development. The ophthalmoscopic diagnosis is practicable only very late in the disease process. Morphologically, however, changes are observed early in the photoreceptor outer segment layer as an area of short proﬁles of disorganized and disoriented disk membranes. The mode of inheritance for the gene defect is autosomal recessive.

Clinical ﬁndings Retinal changes are not seen by ophthalmoscopy until 2–5 years of age. ERG can, however, provide evidence of disease by the age of 8 weeks. Affected puppies demonstrate signiﬁcantly reduced dark-adapted b-wave response amplitudes to red or white light. There is no treatment for the defect except preventive measures taken through the breeding program.

Hemeralopia Day blindness (hemeralopia) is an uncommon disease in the dog, initially described in the Alaskan Malamute.57 Recently, the German Shorthaired Pointer was found to be affected by the same genetic defect.58 Day blindness in the Miniature Poodle59 as well as in some sporadic cases60 showed typical clinical characteristics.

Clinical ﬁndings Clinical signs include blindness or clumsiness in bright, outdoor sunlight, but normal vision in darkness, often noticed at 2–6 months of age. ERGs are diagnostic at an early age with abnormal cone responses, including ﬂicker recordings, while the rod responses are normal. The disease in the Alaskan Malamute has an autosomal recessive inheritance. It is caused by a partial or total failure in development of cone photoreceptors. Usually the fundus of affected dogs has a lifelong normal appearance.

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Cone–rod dystrophy This is a heterogeneous group of diseases, characterized by simultaneous involvement of cones primarily, then rod photoreceptors. Pit Bull Terriers are affected by the disease61 as well as Wirehaired Dachshunds.62

Clinical ﬁndings In both breeds there are abnormal pupillary light reﬂexes as initial ﬁndings in most affected dogs. Ophthalmoscopic ﬁndings vary in their time of appearance in the two breeds; in the former funduscopic changes are observed by 3–6 months of age, while in the latter the appearance of changes is more variable and may not be observed until 3 years of age. Fundus changes are generalized in both breeds but in the Shorthaired Dachshund the non-tapetal fundus appears to become affected unusually early, with a severely mottled appearance. Test breeding of affected Pit Bull Terriers has shown two variants of the disease that are non-allelic. In the Longhaired Dachshund, a disease initially described as rod–cone dystrophy63 has been further characterized. Clinically ophthalmoscopic changes were observed at age 6 months, although there was a marked variation in age of onset and progression of the disease. ERGs have recently shown that the cone system is affected prior to that of the rod system in the disease process, and the disease is now categorized as a cone–rod dystrophy.64

Congenital retinal dystrophy (RPE65 gene defect) This is a hereditary and congenital disease of Briard dogs with a simple autosomal recessive inheritance.65 The gene defect was elucidated and found to be a 4-base pair deletion in the RPE65 gene.19 Morphologic studies have shown changes in the retinal pigment epithelium with an accumulation of large vacuoles, so-called lipoid inclusion bodies. Ultrastructurally there is also disorganization of the rod photoreceptor outer segments at an early age with a successive involvement of the cone photoreceptors a few years later.

Clinical ﬁndings

146

Affected Briards are congenitally night-blind and usually have reduced or severely reduced daylight vision as well. Some affected dogs are both night- and day-blind. Ophthalmoscopically the fundus appears normal until the dogs are at least 3–4 years old. Subtle changes in tapetal color and a slight vascular attenuation are initial changes that appear. Then some gray-white specks may be observed that spread peripherally with increasing age. The disease has an extremely slow progression and deterioration of vision is difﬁcult to detect clinically even through long-term studies (up to 7 years). Low-amplitude or non-recordable rod ERG responses are found with markedly reduced cone responses in affected puppies as young as 5 weeks of age. A 4-base pair deletion has been described in the RPE65 gene, which encodes for a 61 kD protein, preferentially expressed in the retinal pigment epithelium. The protein is involved in the retinoid cycle and, in the RPE65 null mutation, 11-cis retinal is not formed, which then results in a lack of rhodopsin.66 Treatment for this speciﬁc gene defect has been performed and shown amazing results, using gene therapy in affected dogs.67,68 Further studies by two independent groups have shown long-term visual improvement.69,70 These exciting

Malformation of the central nervous system associated with blindness This may include any disorder affecting the visual pathways. Examination of the visual pathway has been discussed earlier in this chapter. Detailed descriptions of these disorders are beyond the scope of this book; however, a brief overview of hydrocephalus is included.

VISUAL IMPAIRMENT

results provide evidence that treatment for hereditary retinal disease is possible when a precise gene defect is known.

Hydrocephalus Hydrocephalus may be deﬁned as a dilatation of the normally small, ﬂuid-ﬁlled cavities and spaces (ventricles inside and subarachnoid space outside) of the brain with an increase in the volume of cerebrospinal ﬂuid. In the dog, the most common form of hydrocephalus occurs as a congenital, compensated condition with normal intracranial pressure in breeds with dome-shaped skulls. However, congenital hydrocephalus may be seen in other breeds as well. Often, few clinical signs are observed in this condition. The hydrocephalus may, however, become decompensated with subsequent increased intracranial pressure. The affected animal may be ataxic and show loss of higher functions such as vision, hearing, and mental capacity. Acquired hydrocephalus may develop secondarily to brain tumors, trauma, encephalitis, or meningitis in any breed of dog or cat. An animal with hydrocephalus may present with few clinical signs obvious to the owner, as little cortical function is demanded for maintenance of basal functions in a non-working breed of dog. Should, however, the disorder affect the visual cortex, visual impairment may result. Involvement of the brainstem may compromise the optic nerve(s) as well as the other cranial nerves necessary for normal function of the eyes.

Clinical ﬁndings The puppy may present only with the complaint of visual impairment. The pupils are dilated and direct and indirect pupillary light reﬂexes are usually absent. The menace response is absent, but this may be difﬁcult to evaluate even in normal puppies. A ‘wandering’ nystagmus with rolling of the eyes in no speciﬁc pattern may be present. A thorough neurologic examination usually reveals additional neurologic abnormalities. Open fontanelles and small skull bones are usually present in hydrocephalic puppies, especially of miniature breeds, and the anterior part of the brain may protrude between the bones.

Diagnosis A neurologic examination will support the diagnosis, as will the shape of the head and the breed of the affected animal. CT scan or other imaging techniques can be used to conﬁrm the diagnosis.

Treatment and prognosis Prognosis in animals with neurologic signs is poor: corticosteroid therapy or placement of a ventriculoperitoneal shunt have been beneﬁcial in isolated cases. The prognosis for regaining vision in a congenitally blind animal is highly unlikely.

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ACQUIRED VISUAL IMPAIRMENT – ACUTE ONSET Acute visual impairment is an occurrence that often makes both the patient and the owner distressed. Although the interest is, understandably, focused only on the eyes, a detailed history should be taken and a thorough general physical examination of the patient performed, to rule out the presence of preceding or concurrent systemic disease and/or medication. It must also be remembered that, even if the owner considers the visual impairment to be of sudden onset, the condition may have developed insidiously over a longer period of time.

Acute glaucoma Acute glaucoma (see also Ch. 6) is in many ways the ‘epitome of evil’ among eye diseases; it starts suddenly and unexpectedly, the course is accompanied by pain, and the condition progresses irreversibly and promptly to blindness, if not treated. Different pathogenic mechanisms causing the high intraocular pressure (IOP) in acute glaucoma produce similar clinical signs and a thorough examination is necessary to establish the cause of the condition.

Clinical signs The pathologically elevated IOP produces obvious clinical signs in dogs, whereas the clinical signs in cats are less prominent. Signs of pain (e.g. blepharospasm, moderate epiphora, and altered behavior), engorged episcleral vessels, corneal edema, and a ﬁxed, mid-sized, or dilated pupil can be observed. The anterior chamber often appears shallower than normal, although this feature may be difﬁcult to appreciate without experience. The iridocorneal angle and entrance to the ciliary cleft usually appear closed when gonioscopy is performed. Retinal vessels are compressed, whereas changes in the optic nerve head are usually not detectable clinically in acute cases of glaucoma. The globe may be enlarged relatively early in the course of the disease, especially in young animals. The IOP is considerably elevated and tonometry readings of 50 mmHg or higher are common.

Diagnosis The diagnosis of acute glaucoma is made on the basis of ocular signs, an elevated IOP being the most important. The ﬁrmness of the globe caused by the high IOP can usually be detected by palpation, but this is an inaccurate and unreliable method of estimating IOP. Use of a tonometer is therefore strongly recommended both to verify the diagnosis and to have an IOP value to compare with when therapy has been initiated (see Ch. 2). Gonioscopy should always be performed to evaluate the appearance of the iridocorneal angle (pp. 26–28, 229–230), although corneal edema may obscure the gonioscopic view. In patients with unilateral glaucoma, gonioscopy should also be performed on the normotensive eye as part of the attempt to establish the etiology of the glaucoma.

Differential diagnosis 148

Episcleritis causes the eye to appear red with prominent vessels; in conjunctivitis, the conjunctiva is diffusely pink or reddish and the individual vessels are not prominent. Furthermore, the conjunctival vessels are easily movable, unlike

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the episcleral ones, and discharge is more prominent in conjunctivitis. Orbital disease or episcleritis may cause episcleral injection but intraocular disease is usually not present. However, orbital disease may cause pupillary abnormalities, and uveitis may occur with episcleritis. Corneal edema is seen in several other diseases (e.g. ulcerative keratitis, endothelial dystrophy, and uveitis), but neither dilatation of the pupil nor elevation of the IOP is present in these diseases. Iris atrophy causes the pupil to appear dilated. Dilated pupils, unresponsive to light stimulus, can be seen in several other diseases, including advanced stages of retinal degeneration and optic neuritis. Retinal degeneration also causes attenuation of retinal vessels, which looks similar to the vessel compression in acute glaucoma. Occasionally, the IOP is slightly elevated for a long period of time, sometimes years, causing very subtle clinical signs that are often neglected by the owner. In advanced stages of this form of glaucoma, the ciliary cleft is likely to collapse, which causes a sudden increase in the IOP mimicking acute glaucoma. The possibility of an insidious, chronic glaucoma preceding the acute, severe elevation in IOP should be considered in patients where signs of an acute glaucoma and unexpected ﬁndings indicative of chronic glaucoma are seen simultaneously.

Treatment and prognosis Acute glaucoma is an emergency. The treatment should aim at retrieving vision, but in cases where vision is already lost, the aim is to keep the animal comfortable and pain free. Medical treatment should be initiated immediately to lower the IOP to a physiologic level. If the glaucoma is secondary to another disease, the primary cause has to be treated as well. Repeated tonometry is essential to evaluate the response to the therapy. If IOP is not lowered sufﬁciently or returns to pathologic levels, surgical treatment is necessary at an early stage. The animal should not leave the clinic before the IOP is controlled. A combination of medical and surgical treatments is often more likely to be succesful long-term. In patients with unilateral primary glaucoma, it is important to treat the unaffected eye prophylactically and to inform the owner of the bilateral potential of the disease. Correct diagnosis and successful lowering of the IOP very early in the course of the condition are essential for a favorable outcome. Markedly elevated IOP (greater than 50 mmHg) may cause permanent visual loss within 24 h, and moderate elevation (30–50 mmHg) results in more gradual loss of vision. Despite rapid diagnosis and considerable efforts to obtain and stabilize the IOP within the normal range, vision is often impaired. Unfortunately, it is not uncommon that maintaining the IOP under 40 mmHg, a level at which several animals show signs of pain if exceeded, may prove to be difﬁcult long-term. In these patients, the main goal is to keep them pain free, which may require enucleation.

Intraocular hemorrhage Intraocular hemorrhage can be caused by several different pathogenic mechanisms. The extent of blood within the eye, as well as the location of the hemor-

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rhage, may vary considerably. Several conditions causing neovascularization and/or the leakage of blood from intraocular vessels can be listed: • Hemorrhage in the anterior chamber – trauma – pre-iridal ﬁbrovascular membranes – anterior uveitis – intraocular neoplasia – coagulation factor disorders or platelet disorders – retinal detachment – PHTVL/PHPV • Hemorrhage in the lens or in a retrolental plaque – PHTVL/PHPV • Hemorrhage in the vitreous cavity or in the retina – chorioretinitis – coagulation factor disorders or platelet disorders – systemic lupus erythematosus – hyperviscosity syndrome – diabetes mellitus – hypertensive retinopathy – retinal detachment – PHTVL/PHPV.

Clinical signs Hemorrhage in the anterior chamber, hyphema, is easily detectable (Fig. 5.9). In complete hyphema, the blood turns bluish-black after approximately 1 week. This is often referred to as eight-ball hyphema (from the color of ball number 8 in pool). Hemorrhage in the posterior part of the eye may often require use of a slitlamp biomicroscope or ophthalmoscope to be clearly visualized. The location

150

Fig. 5.9 Blunt trauma to the eye of this dog caused hyphema, traumatic uveitis, and the development of iris bombé.

Diagnosis The owners should be asked if the pet may have ingested toxic substances, e. g. rodenticides containing anticoagulants, or if abnormal bleeding has been noticed previously. Recurrent hemorrhages are often indicative of a neoplastic or congenital origin. Breed disposition (e.g. CEA in Collies and PHTVL/PHPV in Dobermann Pinschers), concurrent systemic diseases (e.g. feline viral leukemia and immune-mediated thrombocytopenia), and the age of the patient (congenital diseases) should be considered. A general clinical examination including the testing of hematologic parameters should always be performed. Coagulation screening can be used to rule out coagulopathies. Examination of littermates may give clues to the cause when excessive hemorrhage is found in young animals. IOP should be measured because excessive hemorrhage in the anterior chamber may impair aqueous drainage and cause secondary glaucoma. Ultrasonography may be useful to detect intraocular neoplasia, vitreal hemorrhage, and retinal detachment in blood-ﬁlled eyes.

VISUAL IMPAIRMENT

of the hemorrhage within the retina can be established ophthalmoscopically by shape and color. Furthermore, it is valuable to establish whether the blood is clotted or not. Clotted blood in the anterior chamber is often seen when the cause is anterior uveitis or trauma, whereas hemorrhage caused by coagulation disorders is unclotted.

Treatment and prognosis The treatment depends on the cause of the intraocular hemorrhage. Some suggestions on treatment of hyphema are given below: • Treatment of concurrent uveitis is essential in hyphema to avoid inﬂammatory sequelae. Non-steroidal anti-inﬂammatory drugs should be used cautiously as these drugs may interfere with thrombocytic function. Furthermore, mydriatics should be used with caution in excessive hyphema; mydriatics may contribute to impairment of aqueous humor outﬂow in these cases. IOP should be monitored when mydriatics are used. If a secondary glaucoma is elicited, mydriatics should be discontinued immediately and medical treatment to lower the IOP should be started. • Surgical intervention in hyphema is rarely indicated in patients with excessive hyphema and elevated IOP; removal of blood elements by irrigation of the anterior chamber may be advantageous. Intracameral injection or addition of ﬁbrinolytic agents71 to the irrigation solution will lyze clots and enhance their physiologic removal. The prognosis for intraocular hemorrhage depends on the cause and the extent of the intraocular lesions. It is often advisable not to give a prognosis until resorption of the blood allows inspection of the intraocular structures in cases where severe hemorrhage obscures the view.

Toxic retinopathy Assessment of retinal integrity is a routine and essential component in drug safety evaluations. Several compounds are known to have ocular adverse effects. Typical for these is that they are characterized by bilateral symmetry. There is often a relationship between administration of a toxic compound and

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the onset of clinical signs. The following are some well-known drug-related retinotoxic compounds: • • • • • • • •

Azalide72 Chlorochine73 Closantel74 Hydroxypyridinethione75 Rafoxanide76 Thiram77 Quinine73 Speciﬁcally in the cat, enroﬂoxacin has been shown to cause toxic retinopathy, especially if administered at higher than recommended dosages (recommended dosage: 5 mg/kg/24 h). Within days after initiation of oral administration clinical signs of a generalized retinal degeneration may occur as well as systemic and neurologic effects.78

SARD SARD (sudden acquired retinal degeneration) is a retinal degenerative disease that occurs acutely in adult dogs. The cause of the disease is unknown.79 Although initially the fundus appearance in affected animals is normal (Fig. 5.10), there are marked morphologic changes; a rapid loss of photoreceptor outer segments is seen (Fig. 5.11) followed by degeneration of the other retinal layers. No breed is particularly susceptible and crossbreeds have also been affected by the disease. Most often, the affected animal is of middle age and appears to be in good general health. In some instances there has been a history of polyphagia, polyuria, and polydipsia, together with elevations in the levels of serum alkaline phosphatase (SAP), serum alanine aminotransferase (SAAT), serum cholesterol, or serum bilirubin. It has been speculated that these changes

152

Fig. 5.10 The fundus appearance is normal in this acutely blind (for about 4 weeks) 4-year-old Dachshund with sudden acquired retinal degeneration (SARD).

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Fig. 5.11 Electron micrograph of the outer retina of the dog in Fig. 5.10. Obvious degenerative changes are observed in the photoreceptor outer and inner segment layer. (Magniﬁcation: ×2080.)

may be indicative of the physiologic stress associated with the unidentiﬁed retinotoxic factor.

Clinical ﬁndings Affected dogs lose their vision completely and irreversibly within 1–2 weeks. Clinical examination shows moderately to widely dilated pupils which are more or less unresponsive to light stimuli. The fundus appearance is normal, but the ERG is non-recordable. After several weeks or months there is ophthalmoscopic evidence of a generalized retinal degeneration.

Differential diagnosis SARD can be differentiated from optic neuritis by the totally extinguished ERG. It might, in the late stage of the disease, be more difﬁcult to differentiate

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SARD from generalized retinal degeneration of other causes, such as hereditary rod–cone degeneration, in which the ERG is also non-recordable. Another differential diagnosis is CNS neoplasia, in which sudden-onset blindness may occur. However the ERG is not often extinguished in such cases.

Treatment There is no effective treatment for SARD.

Retinal detachment Retinal detachment is a rather common ﬁnding, resulting from a separation of the neural retina from the retinal pigment epithelium, through maldevelopment (as in CEA or RD), vitreal traction, exudation, or transudation (as in chorioretinitis and hypertension), or associated with retinal tears or holes that may occur with a hereditary predisposition in brachycephalic breeds, as sequelae to trauma or atrophy, or as a complication of cataract or lens luxation surgery. Detachments due to tears or holes are referred to as rhegmatogenous. In severe cases the neural retina may be separated over its whole area, remaining attached only at the optic disk and at the ora ciliaris retinae. When the latter attachment is completely separated, a veil of retinal tissue may hang loosely down from the optic disk (Fig. 5.12). Separation of the photoreceptors from the choriocapillaris and retinal pigment epithelium causes photoreceptor degeneration.

Clinical ﬁndings Acute onset of severe visual impairment or blindness is a common sequela of retinal detachment. In partial detachments there are usually no obvious clinical signs due to the detachment. Pupillary light reﬂexes are abnormal to

154

Fig. 5.12 Complete retinal detachment and disinsertion in a 2-yearold Tibetan Terrier. The hyperreﬂective and avascular fundus (without neural retina) might be confused with complete retinal atrophy.

VISUAL IMPAIRMENT Fig. 5.13 Partial retinal detachment with a neuroretinal hole and elevation of large areas of the neural retina in conjunction with hypertension in a 12-yearold Persian cat.

normal depending on extent and duration of the lesion. Ophthalmoscopically, a grayish veil-like structure is seen ﬂoating in the vitreous, with clearly visible retinal vessels. If the retina is only partly detached, areas become elevated as ﬂat or bullous regions that are out of focus compared to normal areas and the optic disk. There may be accompanying signs of systemic disease (Fig. 5.13).

Differential diagnosis An important differential diagnosis in retinal detachment is end-stage retinal atrophy. When the retina is completely detached and not fastened at the ora ciliaris retinae, the neural tissue may not always be easily seen by the examiner, who might only observe the hyper-reﬂective tapetal fundus without retinal vessels (see Fig. 5.12).

Treatment and prognosis Treatment of early cases and especially partial retinal detachment is sometimes successful, depending on etiology. Chorioretinitis cases have the most favorable prognosis where treatment consists of anti-inﬂammatory medication as well as treatment directed towards the primary cause. Mild to moderate serous detachments often respond to a combination of diuretics and systemic corticosteroids. Surgical treatment of rhegmatogenous retinal detachments is attempted less frequently in small animals compared to humans because most cases in animals are not diagnosed early enough. Recently, however, specialized veterinary ophthalmologists perform surgeries very similar to those performed by human vitreo-retinal surgeons. Methods of surgical treatment include cryopexy of holes and tears, drainage of subretinal ﬂuid, application of a scleral buckle, and ﬁlling the posterior segment with

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156

air, gas, or silicone oil. Prognosis for large and complete retinal detachments in the dog is poor.

THERAPEUTIC OPTIONS FOR RETINAL DETACHMENT IN DOGS AND CATS To understand therapeutic options for retinal detachments in dogs and cats veterinarians need a basic understanding of ocular embryology and the pathophysiology of retinal detachments. The retina and the retinal pigment epithelial interface forms when the optic vesicle, which is composed of neuroectoderm, invaginates; the inner layer (destined to be retina) is then juxtaposed to the outer layer (retinal pigment epithelium). There are no cellular connections between these layers and the tight junctions of the retinal pigment epithelium (RPE) and external limiting membrane of the retina maintain the blood–ocular barrier in this photoreceptor region. The apposition of the rod and cone outer segments to the retinal pigment epithelium is essential for maintenance of photoreceptors and vision. Retinal detachment develops when these layers are separated, and when the detachment is complete the affected eye becomes blind. The outer retina, deprived of its nutrition from the choriocapillaris and the metabolic support of the RPE, degenerates progressively after detachment; the rate of retinal degeneration is dependent on many factors including but not limited to the etiology and type of retina (anangiotic, paurangiotic, merangiotic, and holangiotic). Poorly vascularized and anangiotic retinas will become necrotic and degenerate very rapidly after detachment and, if anangiotic retinal reattachment is to be sight restoring, therapy would need to be achieved within hours of detachment. However, dog and cat retinas are holangiotic and the photoreceptor external and inner segments usually degenerate relatively slowly over several weeks. Determining the time of onset of retinal detachment is imprecise at best. Careful examination by an ophthalmologist and an accurate history are required to establish potential viability when considering appropriate therapy, and general practitioners are encouraged to refer animals with retinal detachments promptly. As a general rule successful reattachment and return of vision is achievable if the retina is reattached within a few weeks, preferably within 1 month of detachment in most dogs. Retinal detachments are diagnosed with direct or indirect ophthalmoscopy. When the detachment is focal, the raised area of the retina or a hole within the retina is usually obvious (Fig. 5.14). When the retina is completely detached and torn at the periphery it will be draped over the optic disk (Fig. 5.15). Retinal detachment is common and there are many etiologies including trauma (Fig. 5.16), septic and immune-mediated uveitis, neoplasia, vitreous degeneration and hyalitis, genetic mutations (Fig. 5.17), and numerous others. Despite a multitude of etiologies the pathogenesis of retinal detachment is limited to three basic mechanisms: disruption of the blood–ocular barrier with leakage of ﬂuid into the photoreceptor–RPE interface (exudative detachment) (Fig. 5.18); vitreous ﬁbrosis that pulls the retina off the RPE as contraction occurs (tractional detachments); and retinal holes or tears that allow ﬂuid to seep under the retina and induce the detachment (rhegmatogenous detachment) (see Fig. 5.14).

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Fig. 5.14 Peripheral retinal tear and focal detachment in a small mixed breed dog.

Fig. 5.15 A complete retinal detachment with giant peripheral tears in a dog. Note the retina is draped over the optic disk.

The therapy of retinal detachment is selected based on these pathogeneses. Exudative and serous retinal detachments (Fig. 5.18) are usually treated by medical therapy that is focused on treating the etiology and reducing the uveitis and stabilizing the blood–ocular barriers, usually systemic corticosteroids. When the uveitis is controlled and the blood–ocular barrier is restored, the cellular pumps in the RPE and the Müller cells within the retina remove the subretinal ﬂuid and the retina will spontaneously reattach. Functional vision will usually be regained once the retina is reattached.80,81 Partial or focal detachments induced by small retinal tears (see Fig. 5.14), colobomas, and geographic retinal dysplasia are commonly treated by trans-

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Fig. 5.16 A ventral retinal detachment that developed secondary to trauma and hemorrhage in a mature terrier cross dog.

Fig. 5.17 Multiple focal retinal detachments that are inherited in Coton de Tulear dogs.

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corneal barrier diode laser retinopexy (Figs 5.19 & 5.20). The diode laser induces chorioretinal scars as the laser energy passes through the clear cornea, aqueous humor, and vitreous, and is absorbed by the RPE and choroidal pigment, inducing focal necrosis and creating focal chorioretinal scars which seal the hole and prevent further retinal detachment.82,83 Large or complete retinal detachments caused by retinal dysinsertion (dialysis) at the ora ciliaris retinae (see Fig. 5.15) develop presumably secondary to vitreous traction bands and holes. Veterinary retinal surgeons have been successful with vitrectomy and surgical reattachment of relatively acute (1–6

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Fig. 5.18 Serous retinal detachment in a middle-aged German Shepherd cross dog. The other eye was similar in appearance and the dog was blind. These retinal detachments are exudative rather than rhegmatogenous and will reattach over several days with restoration of vision with immunosuppressive therapy. This is an idiopathic condition that develops most commonly in large breed dogs.

Fig. 5.19 A focal retinal detachment in this English Springer Spaniel developed secondary to an area of geographic retinal dysplasia. A transcorneal diode laser barrier retinopexy was completed to scar the retina to the choroid and prevent further detachment.

weeks) retinal detachments in dogs and cats.84,85 After the affected animal is anesthetized the affected globe is proptosed and draped. The sclera is exposed and three ports are placed through the pars plana (for ﬂuid, light, and manipulation) and the vitreous is removed. The detached retina is reattached by injection of perﬂuorocarbon liquid which has a speciﬁc gravity that is heavier than water; this expands and ﬂattens the retina and tamponades it against the RPE.

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Fig. 5.20 This mixed breed dog’s retina was reattached after a vitrectomy, perﬂuorocarbon gas tamponade, diode laser endopexy, and silicone oil transfer. Multiple chorioretinal scars are present around multiple retinal tears and holes that were detected during the surgery. This eye regained functional vision and had minimal postoperative complications.

The edges of the torn retina are then sealed by chorioretinal scars induced by a diode laser or cryotherapy. The perﬂuorocarbon is then replaced with silicone oil and the pars plana ports sutured closed. Vision is often restored even when detachments have been present for a signiﬁcant amount of time.86 Complications are not uncommon and include uveitis, glaucoma, and occasionally retinal slippage. Complications related to retinal detachment approach 95% with or without medical therapy. These globe-threatening complications usually develop because pre-iridal ﬁbrovascular membranes develop secondary to the release of ﬁbrovascular inducing cytokines from the hypoxic retina. These membranes are fragile, and secondary uveitis and glaucoma that ensue are difﬁcult, if not impossible, to treat medically;87 intractable glaucoma that develops after chronic retinal detachment may best be treated by enucleation or evisceration and intrascleral prosthesis.

Hypertensive retinopathy Hypertensive retinopathy is not an uncommon disease in small animal practice and occurs most often in older cats.88 In addition to acute blindness or severe visual impairment, affected animals usually have an elevated systolic arterial blood pressure (often greater than 200 mmHg), elevated blood urea nitrogen and creatinine levels, and in some cases cardiac abnormalities as well. It is often difﬁcult to evaluate which disease process comes ﬁrst: a primary renal disease, which may cause hypertension, or primary hypertension causing secondary cardiac and renal abnormalities (Fig. 5.21). Hyperthyroidism is a common potential cause in older cats.

Clinical ﬁndings

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The typical presenting complaint is acute vision loss. Ophthalmoscopically there are often bilateral severe retinal changes, such as retinal and vitreal hemorrhage, elevation or detachment of all or parts of the neural retina, and retinal vascular tortuosity.

VISUAL IMPAIRMENT Fig. 5.21 Bullous retinal detachment seen through the pupil in a 10-year-old Border Collie with primary renal disease and hypertension.

Treatment and prognosis Therapy is directed towards treatment of the primary disease. Hypotensive therapy is initiated and, in some cases, diuretics. Early treatment of less severe retinal lesions gives return of vision in some cases although the longterm prognosis is poor. Most cases of hypertensive retinopathy are advanced when diagnosed and treatment is unlikely to be successful. Prognosis for general health depends on the severity of the underlying systemic abnormalities and their response to treatment.

Optic neuritis Optic neuritis is an inﬂammation of the optic nerve, either at the level of the globe or closer to the brain. The potential causes include speciﬁc infections, such as toxoplasmosis, extension of inﬂammation from adjacent tissues, neoplasia, the inﬂuence of toxins, and trauma. Immune-mediated causes are often suspected although the majority of such cases are categorized as idiopathic.

Clinical ﬁndings Affected animals usually present with bilateral acute-onset blindness. The pupils are widely dilated and the pupillary light reﬂexes are absent. Ophthalmoscopically the disk may appear swollen and indistinct, and sometimes small hemorrhages are observed at or in the vicinity of the disk (Fig. 5.22). The adjacent retina may also be affected. The ERG is usually only somewhat reduced or may be normal. In some cases of optic neuritis, with inﬂammatory lesions closer to the brain, the fundus appears normal.

Differential diagnosis SARD is an important differential of optic neuritis, although in SARD the ERG is non-recordable and PLRs may be present but sluggish. Central blindness is another differential. In such cases PLRs are often normal, the animal has other CNS symptoms, and the fundus and optic disk are often normal-

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Fig. 5.22 Optic neuritis in a 4-year-old Bichon Frisé with acute-onset blindness.

appearing. Reticulosis (see below) is a further differential. In papilledema, there is a non-inﬂammatory swelling of the optic disk, usually associated with compression of the retrobulbar part of the optic nerve by tumor or associated with systemic hypertension. Vision is not impaired by the simple presence of papilledema, and pupillary light reﬂexes and ERG are normal; however when caused by optic nerve compression the central transmission of visual information may be impaired.

Treatment and prognosis Optic neuritis is treated by systemic corticosteroids at high doses initially (2–3 weeks), then as long-term treatment at lower levels, every other day for up to several months. The underlying cause should be treated if possible. In speciﬁc infections, broad-spectrum antimicrobials are indicated. The prognosis is guarded with recurrence of the disease and progression to optic atrophy is a common sequel.

Central blindness

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Central blindness describes visual impairment with normal ocular ﬁndings in which the lesion can be localized to the visual pathway within the brain. On neurologic examination signs other than visual disturbance are often present. Apparent blindness is, however, often the ﬁrst sign noted by the owner. In managing a neurologic problem, the ﬁrst step is localization of the disease process. The disorder may be categorized as focal and affecting only one part of the CNS, multifocal, or diffuse. Some conditions may initially appear as focal disease but progress to affect other structures. Examples of multifocal signs involving the visual pathway are brainstem lesions involving cranial nerves and cerebral lesions affecting the visual cortex. The major disease categories producing multifocal signs are degenerative, metabolic, neoplastic, nutritional, inﬂammatory, and toxic disorders.

This is a malignant inﬂammatory condition seen in the dog and rarely in the cat. The condition is now considered to be part of the granulomatous meningoencephalomyelitis disease. Reticulosis predominantly involves the white matter and may inﬁltrate the optic nerves causing diffuse or focal lesions, including atrophy or swelling of the optic disk, depending on the degree of involvement. White matter of the brainstem, cerebellum, and upper cervical spinal cord may also be affected. The disease may affect dogs of all ages.

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Reticulosis (granulomatous meningoencephalomyelitis)

Clinical ﬁndings Acute or gradual vision loss in one or both eyes is the main clinical sign when the optic nerves are affected. The condition does not seem to cause pain unless the upper cervical spinal cord is involved. Lesions in this area will produce neck stiffness. In the ocular form of reticulosis, the pupil is dilated and the menace reaction as well as direct and consensual pupillary light reﬂexes are absent. The ERG shows normal retinal function.

Differential diagnosis The most important differential diagnosis is optic neuritis, which clinically is indistinguishable from reticulosis of the optic nerve. In fact, reticulosis may be considered one form of optic neuritis, while not all cases of optic neuritis are reticulosis. Sudden acquired retinal degeneration (SARD) also causes acute vision loss. In this case, the ERG is non-recordable. SARD will not improve on corticosteroid therapy, in contrast to reticulosis.

Treatment and prognosis The disease responds to treatment with corticosteroids, but long-term treatment with high doses of steroids or other immunosuppressive agents may be necessary. Recurrence of signs usually occurs when steroid doses are reduced below therapeutic levels. Thus, the prognosis is considered guarded.

Encephalitis Inﬂammation of the brain tissue is referred to as encephalitis and inﬂammation of the meninges covering the brain as meningitis. When both occur simultaneously, the disease is termed meningoencephalitis. The condition is caused by several infectious agents, both viral and bacterial. In cats, the most important is feline infectious peritonitis (FIP), usually of the non-effusive (‘dry’) form, causing pyogranulomatous inﬂammation in the CNS. Ocular signs, notably intraocular inﬂammation (uveitis, often with keratitic precipitates), may accompany the CNS ﬁndings. In dogs distemper must be included in the differential diagnosis of any dog with neurologic signs. Accompanying ocular signs of distemper may include conjunctivitis, keratoconjunctivitis sicca (KCS), optic neuritis, and retinitis, as well as Horner’s syndrome (ptosis, miosis, enophthalmos, and protrusion of the third eyelid) due to lesions of the sympathetic innervation to the eye and adnexa.

Clinical ﬁndings Depending on the site of the lesion within the brain, neurologic signs vary. There is usually evidence of CNS damage. In lesions involving the visual cortex, central blindness may develop. If the lower parts of the visual pathway are

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intact, clinical ﬁndings may include lack of menace reactions, but with pupillary light reﬂexes present. Signs develop over a few days in most infections, but in FIP onset may be insidious. There is often a slight elevation of body temperature.

Differential diagnosis Any other multifocal brain disease may produce similar signs. Examination of cerebrospinal ﬂuid as well as blood biochemistry and serology are important factors in establishing a diagnosis.

Treatment Broad-spectrum antibiotics should be used when a bacterial infection is suspected. A normal blood–brain barrier may be difﬁcult to penetrate for many types of antibiotic. When inﬂammation is present, however, the barrier is broken down, permitting penetrance of several antibacterial agents. Symptomatic supportive treatment will also be necessary.

Intoxicants CNS signs can result from endogenous (produced within the body) as well as exogenous (ingested, inhaled, absorbed through the skin) toxins. Hepatic encephalopathy is described later as an effect of an endogenous toxin. A history of exposure to a toxic agent is the most important factor establishing the diagnosis in cases of exogenous poisoning. Therefore, the owner must be questioned carefully in an attempt to ﬁnd a possible source. CNS signs other than central blindness might be more obvious in exogenous intoxications. For identiﬁcation of toxic agents, treatment, and prognosis, the reader is referred to textbooks on this topic.

ACQUIRED VISUAL IMPAIRMENT – CHRONIC PROGRESSIVE ONSET A chronic progressive onset of visual impairment is often difﬁcult to detect by the owner. It is not uncommon that blinding disorders of this type are elucidated by chance in conjunction with examination or treatment of an animal for reasons other than ophthalmic problems. Several disease processes of this type are breed-related and in many cases hereditary. Many potentially blinding disorders of chronic progressive onset are revealed when animals are screened for hereditary eye diseases.

Phthisis bulbi Phthisis bulbi – a degenerated, shrunken eye – can develop secondary to severe damage to the ciliary body with decreased aqueous humor production and resultant hypotension. There is commonly a history of severe ocular trauma or chronic uveitis. The condition develops over a long period of time, usually months, and the end-stage is a globe of considerably smaller size than normal, with disorganized contents (Fig. 5.23).

Clinical signs 164

The globe is considerably smaller than normal, the cornea is opaque, and neovascularization with pigmentation is present in variable degrees. Phthisis bulbi

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Fig. 5.23 A middle-aged English Springer Spaniel with phthisis bulbi of the right eye.

is usually unilateral and the size of the globe diminishes gradually over months. Signs of intraocular inﬂammation may be noticed when the cornea is still transparent. Vision is lost when the globe has become phthisical.

Differential diagnosis Microphthalmos is a differential diagnosis to phthisis bulbi. Microphthalmos is a congenital condition that develops without preceding ocular trauma or intraocular inﬂammation.

Treatment Chronic intraocular inﬂammation may cause discomfort. The relationship between the eyelids and the globe is disturbed, and recurrent conjunctivitis is a common problem. Furthermore, the cosmesis of a phthisical globe is usually poor. Enucleation is often the best solution for the animal, but in patients where the globe is maintained, palliative treatment of conjunctivitis with irrigation and topical medications is necessary. A relationship between primary ocular sarcomas and concurrent chronic uveitis, which may cause phthisis bulbi, has been suggested in cats.89,90 Thus, enucleation is a preferred option in this species.

Corneal disease The transparency of the cornea is necessary for normal vision. This transparency is due to the cornea’s state of relative dehydration, avascularity, and lack of pigmentation, and the regular arrangement of stromal collagen ﬁbrils. In order for the cornea to remain healthy, the eyelids must be normal in shape and function, and the tear ﬁlm must be normal. In chronic corneal diseases, the cornea gradually changes appearance. This may be caused by edema, neovascularization, granulation tissue formation, scarring, and pigmentation. A thorough description of corneal diseases is given in Chapter 4; however, chronic diseases leading to visual impairment are brieﬂy mentioned here. These include

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keratoconjunctivitis sicca, pigmentary keratitis, chronic superﬁcial keratitis, punctate keratitis, corneal dystrophies, and endothelial dystrophy.

Keratoconjunctivitis sicca (KCS) The condition is caused by a tear deﬁciency, most often associated with a presumed immune-mediated lacrimal adenitis.91 Acute tear deﬁciency may cause corneal ulceration and perforation. More common, however, KCS is a chronic disease with progressive deterioration in vision due to corneal changes.

Clinical ﬁndings Typically, there is a history of chronic conjunctivitis with an accumulation of tenacious mucus on and around the eye. Conjunctivitis and keratitis develop when the ocular surface dries and desiccates. Abnormal hypertrophy of the inﬂamed conjunctiva causes redundant pleating folds. Opportunistic bacteria can be cultured from the ocular discharge, but their abundance is secondary to the effect of KCS. Corneal changes include vascularization, scarring, and pigmentation, which may progress to involve the entire cornea. If the cornea has normal sensory innervation, marked discomfort is present. However, the corneal nerves are usually damaged and insensitive in canine KCS, thus the condition is not associated with severe pain. A Schirmer tear test will reveal subnormal values. Treatment is discussed in Chapter 7, but usually includes daily cleaning, tear replacement therapy, and/or topical instillation of ciclosporin.

Pigmentary keratitis This condition is a corneal response to chronic irritation. Exophthalmic breeds are most susceptible and several factors can be responsible for the pigmentation: • KCS – even moderately lowered tear production may produce clinical signs, as a large portion of the globe is exposed in brachycephalic dogs. In addition, the quantitative tear ﬁlm disorders, conditions altering the quality of the tear ﬁlm, for instance making the tear ﬁlm unstable and frequently leaving parts of the cornea uncovered, may add to a low-grade corneal inﬂammation. • Lagophthalmos – the animal is not able to close the eyelids completely. On close questioning, an owner may state that the animal sleeps with the eyelids only partly closed. A reduced blinking frequency with poor distribution of the tears may also be present. • Trichiasis – hairs from the area adjacent to the eye rub on the cornea.

Treatment Treatment of pigmentary keratitis includes management of the initiating cause. Medial canthoplasty is effective in dogs with lagophthalmos and/or medial trichiasis. Medical treatment may include topical ciclosporin, topical application of tear-substituting eye drops, and in some cases also corticosteroids, depending on the cause of the condition.

Chronic superﬁcial keratitis (CSK) 166

Several names have been used for this disease, including keratitis pigmentosa, pannus, and Überreiter’s disease. The main cause appears to be an immuno-

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logic reaction in the cornea, with exposure to sunlight triggering the disease and aggravating the clinical signs.92 The disease may occasionally be seen in dogs of any breed, but the majority of the cases are diagnosed in the German Shepherd and related breeds.93 A genetic predisposition is considered likely. The condition occurs bilaterally in middle-aged dogs, with males and females equally affected. A chronic inﬂammation of the nictitating membrane, termed plasmacytic conjunctivitis, is often also present in dogs affected with CSK.

Clinical signs Corneal changes include cellular inﬁltration, extensive vascularization, and formation of granulation tissue, which may be heavily pigmented. Initial changes are often seen in the ventrolateral parts of the cornea, in untreated cases progressing to involve the whole cornea. Schirmer tear test values are normal or elevated because of irritation. The surface of the nictitating membrane, especially near the border, may have a cobblestone-like appearance.

Treatment Treatment is lifelong and consists mainly of topical application of ciclosporin, occasionally in combination with steroids. Protection of the eyes from sunlight may be of beneﬁt. The results of treatment may be remarkably successful, but the condition will recur if treatment is discontinued.

Superﬁcial punctate keratitis The term describes a multifocal, ulcerative keratitis that is recurrent, bilateral, and symmetric (Fig. 5.24).94 The condition affects mainly the long-haired dachshund, but dogs of other breeds may also be affected sporadically. The disease is considered to be immune mediated, although the pathogenesis is not completely understood.

Fig. 5.24 Punctate keratitis causing severe bilateral corneal cloudiness and partial pigmentation in a 6-year-old Longhaired Dachshund.

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Clinical ﬁndings The condition may be acute and painful with bilateral epiphora and blepharospasm. More chronic onset, however, is not uncommon. A number of small gray spots that may be ﬂuorescein positive in the initial stage are seen in the cornea, and some edema may be present. After some days, neovascularization develops as an attempt at healing of the cornea. As the condition becomes chronic, a combination of punctate ulcers, vascularization, and pigmentation can be observed. The changes gradually progress to involve the whole cornea. Acute episodes with pain and deeper ulcers may occur and occasional descemetoceles and melting ulcers may aggravate the situation.

Treatment and prognosis Treatment is lifelong and consists mainly of topical ciclosporin, if required combined with topical steroids, plus antibiotics topically if secondary bacterial infection is present. Deep or perforated ulcers may demand surgical treatment.

Corneal lipid dystrophy and degeneration Corneal stromal dystrophy is a non-inﬂammatory, most often bilateral, condition which may be caused by accumulation of lipid within the cornea.95 The term dystrophy is usually reserved for the forms thought to have an inherited basis. Degenerations may occur secondary to chronic inﬂammatory disease, such as episcleritis or chronic superﬁcial keratitis, or to hypercholesterolemia, which is frequently associated with hypothyroidism. The deposits are most commonly present in the central parts of the cornea, in the outer stromal layers. The epithelium is usually not involved. Typically vision is unaffected, but in certain patients the entire cornea may be involved with defects in the corneal epithelium and ingrowth of blood vessels. Arcus lipoides corneae, where the lipid is located in the periphery, occurs more rarely.

Clinical ﬁndings The dystrophic area may present as a reﬂective, fairly well demarcated zone in the middle area of the cornea. Lipid crystals may resemble tiny needles, but in degenerations they may be denser and occasionally the epithelium will ulcerate, with associated signs of discomfort. If the overlying epithelium is intact, the condition is not painful.

Treatment If secondary to other disease, this should be identiﬁed and treated. Accumulations in the stroma not impairing vision do not require treatment. Deposits affecting the corneal epithelium with recurrent erosions may require lamellar keratectomy.

Corneal edema and endothelial dysfunction

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Corneal edema in the absence of other ﬁndings may be due to a dysfunction of the endothelial cells.96 The corneal endothelium is a single cell layer and, if injured, the cells have little regenerative capacity. To compensate, they will stretch to cover a large area. Endothelial dystrophy has been described as a familial disorder in the Boston Terrier (Fig. 5.25), the Chihuahua, and the

VISUAL IMPAIRMENT

Fig. 5.25 Endothelial dystrophy in an 8-year-old Boston Terrier.

Dachshund, and probably also occurs in the Airedale Terrier and English Springer Spaniel. It is seen sporadically in older dogs of all breeds. Corneal edema may also result from other ocular diseases, such as glaucoma, uveitis, and ulcerative keratitis. A hazy cornea mimicking corneal edema may occur in metabolic disorders in the cat.

Clinical ﬁndings The edematous cornea is opaque, complicating examination of the inner structures of the eye. The cornea is gray to light blue with a spongy appearance. If not associated with other painful ocular diseases, the condition itself is painless. There may or may not be scleral injection, and the cornea is ﬂuorescein negative. Bullous keratopathy may complicate the disease in advanced stages and cause painful and persistent ulceration. If bilateral, vision may be impaired.

Treatment and prognosis If secondary to another eye disease, the primary disease must be diagnosed and treated properly. Topical osmotic agents have been used to try to desiccate the cornea, but with little effect. Thermal keratoplasty or the placement of permanent thin conjuctival ﬂaps may be of value. Full-thickness corneal transplantation (corneal grafts) will restore vision, but rejection of donor tissue usually occurs. The prognosis for restoration of vision must therefore be considered guarded.

Chronic uveitis and its sequelae Uveitis is an inﬂammation of the vascular tunics of the eye, which can be subdivided into iritis, cyclitis, and choroiditis depending on the part of the uvea that is affected. Anterior uveitis or iridocyclitis refers to an inﬂammation of both the iris and the ciliary body. Multiple etiologies are capable of causing uveitis in cats and dogs (see Ch. 6). Chronic uveitis is a potential threat to both

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vision and eye. Cats are more commonly presented with the condition than dogs.

Aspects of the pathogenesis The pathogenesis of chronic and recurrent uveitis is still poorly understood, but immunologic reactions are involved. Alterations of the vascular structure and/or permeability of uveal blood vessels may persist after the acute stages of an extensive, uncontrolled inﬂammation. A subsequent tendency for circulating immune complexes to be deposited in vessels with increased permeability has been reported. Furthermore, the property of the vitreous body in acting as a reservoir for antigens and persisting sensitized lymphocytes may be of importance.

Intraocular tumors causing uveitis Neoplastic uveitis is more commonly seen in cats than in dogs. Diffuse iridal melanomas followed by primary ocular (or trauma-associated) sarcomas are the most common tumors causing uveitis in the cat. Primary and metastatic uveal neoplasms are less frequent. Feline leukemia virus may cause anterior uveitis both directly and indirectly. Diffuse iridal melanomas often involve multiple, enlarging areas of the iris, where the amount of pigmentation slowly increases. The shape and function of the pupil may become abnormal. Secondary anterior uveitis and secondary glaucoma are not uncommon. Uveitis, intraocular hemorrhages, secondary glaucoma, and visible masses may be observed in cats with primary ocular sarcomas. Distant metastases are relatively commonly seen in cats with diffuse iridal melanomas or primary ocular sarcomas.

Clinical signs of uveitis The condition may be unilateral or bilateral. Bilateral involvement is commonly seen in patients with systemic infectious or autoimmune diseases, whereas unilateral chronic uveitis may initially be caused by severe trauma to the eye or unilateral lens disease. Unilateral uveitis may also be the most evident clinical sign in cats with primary ocular or trauma-associated sarcomas or in patients affected by other tumors involving the uvea. The clinical signs of acute uveitis include pain and discomfort, ciliary ﬂush, miosis, aqueous ﬂare, precipitates of cells or ﬁbrin on the corneal endothelial surface and anterior lens capsule, spongy swollen iris, and lowered IOP (Fig. 5.26), but will vary depending upon intensity, distribution (anterior vs. posterior segment), and duration of the inﬂam-mation. Vitreous inﬁltrates, chorioretinitis, and exudative retinal detachment may accompany posterior uveitis. Additional clinical signs in chronic uveitis may include:

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• Neovascularization of the iris with or without engorgement of the iris vessels. Pre-iridal ﬁbrovascular membranes or rubeosis iridis can be observed as randomly organized vessels compared to the normal iris vessels that are arranged in a radial fashion. Neovascularization is usually more prominent in cats than in dogs. • Changes in iris pigmentation. The iris is usually diffusely hyperpigmented in the affected eye. Dispersed pigment may be observed on the anterior lens capsule. Pupillary marginal cysts may develop. Iridal lymphocytic

VISUAL IMPAIRMENT Fig. 5.26 Acute uveitis as a result of a corneal foreign body of 1 week’s duration in a 3year-old Pekinese. As well as the corneal defect there is corneal edema, hypopyon, small and irregular pupil, and obvious swelling of the iris. The intraocular pressure is lowered.

nodules appearing as circular reddish-brown to gray lesions with a diameter of 1–2 mm are common in chronic uveitis in cats. • Secondary iris atrophy. • Various sequelae including corneal changes, intraocular adhesions (synechiae), intraocular membranes, secondary cataracts, secondary retinal diseases, or glaucoma. • Partial visual impairment or blindness.

Sequelae A number of vision-threatening conditions may be caused by uveitis (Fig. 5.27). Thus, early diagnosis and proper treatment of the initial inﬂammation is essential to prevent or reduce the development of potentially harmful sequelae. • Corneal changes. Uveitis may interfere with the water-pumping ability of the corneal endothelium causing corneal edema. Furthermore, keratitis with pigmentation and neovascularization is not uncommon. • Intraocular adhesions form when the inﬂamed iris adheres to other structures in the eye. The initial ﬁbrinous adhesions are followed by ﬁbrovascular organization. Adhesions between iris and cornea peripherally (peripheral anterior synechiae) may impair aqueous outﬂow. Posterior synechiae (adhesions between iris and lens) are commonly seen at the edge of the pupil. Posterior synechiae affecting only parts of the circumference of the pupil may cause distortion of the pupil. If the posterior synechiae affect the entire circumference of the pupil (seclusio pupillae) aqueous humor is trapped in the posterior segment of the eye.

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SMALL ANIMAL OPHTHALMOLOGY Fig. 5.27 Sequelae of chronic uveitis in a 13-year-old cat: ﬁbrovascular membranes, cataracts, and lens luxation.

•

• •

•

•

•

172

This implies that the IOP will be higher in the posterior segment than in the anterior chamber, which results in forward ballooning of the iris (iris bombé) (see Fig. 5.9). Exudates or blood in the pupil may cause formation of tissue membranes across the pupil (from iris to iris). Membranes covering the entire pupil will cause an occlusion of the pupil. High aqueous protein levels, e.g. due to protein exudation or intraocular hemorrhage, increase the risk of synechiae formation. Cyclitic membranes are ﬁbrovascular membranes extending from the ciliary body across the pupil and/or across the anterior face of the vitreous body. Secondary cataracts may form, probably as a result of alterations in the aqueous humor. Lens luxation may occur in eyes with chronic uveitis. Decrease in strength and subsequent rupture of the lens zonules have been proposed to be a sequel to intraocular inﬂammation, especially in cats. Secondary glaucoma may arise from several different mechanisms in conjunction with uveitis. Impaired aqueous ﬂow due to inﬂammatory cells and debris in the outﬂow pathways, peripheral anterior synechiae, and seclusion or occlusion of the pupil may cause elevation of IOP. Secondary retinal degeneration may be caused by extension of choroiditis to involve both the choroid and the retina (chorioretinitis) or by inﬂammatory effects on the choriocapillaris and/or RPE. Exudative retinal detachment may be seen in patients with choroiditis, where the retina is elevated by subretinal ﬂuid, or secondary to traction by intravitreal or cyclitic membranes caused by intraocular inﬂammation or hemorrhage.

Diagnosis The diagnosis of uveitis is based on history and clinical ﬁndings. General physical examination, blood biochemistry, hematology, and serology may be of value, although the etiology is often difﬁcult to establish. It must be remembered that the uveitis may have developed secondarily to some other primary ocular disease. Aqueous, vitreous, or subretinal paracentesis may be indicated for cytology and microbial isolation. Results are often non-speciﬁc and the procedure may even cause exacerbation of the inﬂammation. However, results of diagnostic value are most likely to be found in eyes with visible exudates or in lymphosarcoma suspects. The risk of hemorrhage must be considered before vitreous paracentesis is performed.

VISUAL IMPAIRMENT

• Phthisis bulbi. Chronic uveitis may cause severe ciliary body atrophy with decreased aqueous humor formation and pathologically lowered IOP.

Differential diagnosis Conjunctivitis causes the eye to look red, but in conjunctivitis the conjunctiva is pink or reddish and the underlying individual episcleral vessels are not prominent. Furthermore, the conjunctival vessels are easily moved, in contrast to the straight perilimbal anterior ciliary vessels, which cause the ciliary ﬂush seen in uveitis. Corneal edema is seen in several other diseases, such as ulcerative keratitis, endothelial dystrophy, and glaucoma. In chronic anterior uveitis, however, there are other signs of chronic inﬂammatory intraocular disease. Primary iris atrophy can be distinguished from iris atrophy secondary to chronic uveitis by the presence of other clinical signs of intraocular inﬂammation in the latter condition. Cataracts may cause secondary lens-induced uveitis. The history, breed, and age of the patient and thorough examination of the lenses of both eyes may yield useful information about the cause of the cataract. Progressive retinal atrophy is a differential diagnosis to chorioretinitis. In progressive retinal atrophy the changes are always bilateral and symmetrical and there are no signs of inﬂammatory disease.

Treatment and prognosis The primary disease must be treated if the underlying cause of the uveitis can be established. Otherwise, symptomatic treatment (corticosteroids and/or nonsteroidal anti-inﬂammatory drugs and mydriatic–cycloplegic drugs) is indicated. The treatment usually has to be continued for a long period of time, often months. In some cases it is advisable to maintain topical anti-inﬂammatory treatment lifelong to avoid recurrence of the uveitis and limit the risk of additional complications. Immunosuppressive drugs, e.g. azathioprine, have mainly been used in cases unresponsive to conventional therapy, such as uveodermatologic syndrome in dogs.97,98 In cats with neoplastic uveitis, enucleation combined with exenteration, if involvement of the optic nerve or orbital tissues is suspected, should be performed early if no signs of metastatic disease can be detected.

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The prognosis depends on the cause and degree of damage to the tissues. Long-term therapeutic success should not be expected in most cases. The prognosis is generally grave in cases with glaucoma secondary to uveitis.

Chronic glaucoma The condition arises when the earlier signs of glaucoma are neglected or unnoticed or when therapeutic efforts have been insufﬁcient. The damage to the eye is usually considerable. Signs of pain may not be obvious and chronic glaucomatous eyes often seem to be reasonably well tolerated by the patient, although attitude and behavior frequently improve following therapy.

Clinical signs Chronic glaucomas share several clinical signs, although various initial causes of the glaucoma are possible. The clinical signs are often less prominent in cats compared to dogs. Pain is usually not conspicuous in chronic stages of glaucoma and the eye is held open. However, concurrent uveitis may cause discomfort. The most obvious sign is usually enlargement of the globe, buphthalmos. Ocular enlargement takes months to develop in adults, but may develop in less than a week in puppies and kittens. It is sometimes difﬁcult to appreciate slight enlargement of the globe in cats. Episcleral blood vessels may or may not be congested, and IOP may vary from normal to elevated. Distended episcleral vessels and normal IOP are most commonly seen in dogs, where the IOP has been considerably elevated for a long time. Corneal changes including haziness and edema caused by corneal stretching as well as white irregular linear opacities, or Haab’s striae, are common. Buphthalmos with or without lagophthalmos can cause keratitis and corneal ulcers. The cornea may also be enlarged (megalocornea) in patients with buphthalmos. Gonioscopy usually shows a collapsed ciliary cleft or closed iridocorneal angle. Development of secondary cataracts and subluxation or luxation of the lens may be present. The possibility of an anteriorly luxated lens should be borne in mind in patients with dense corneal edema. Visible changes in the posterior part of the eye include liquefaction of the vitreous body, various degrees of retinal degeneration, and cupping and atrophy of the optic nerve head. Atrophy and cupping of the optic nerve head is not an obvious feature in cats, because of their normal lack of myelin in the optic nerve.

Diagnosis Chronic glaucoma is easily diagnosed because the clinical signs are obvious and easily recognized. The initial cause of glaucoma is often impossible to identify because of abundant secondary changes within the eye. The possibility of concurrent chronic uveitis or ocular neo-plasia, the two most common causes of secondary glaucoma in cats,99 must be considered.

Treatment and prognosis

174

The aim of treatment in most chronic cases is to keep the animal comfortable and pain-free. Lowering the IOP to less than 30 mmHg is usually sufﬁcient to avoid pain and enlargement of the globe. If some vision is still present, it is advisable to try to keep the IOP very low, probably less than 15 mmHg, to maintain vision, and surgical options may be considered. If primary glaucoma

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is suspected to be the cause of unilateral chronic glaucoma, it is recommended that the unaffected eye should be treated prophylactically.100 Furthermore, the owner should be advised to monitor the remaining normotensive eye thoroughly and immediately report signs of (acute) glaucoma. Exposure keratitis, corneal ulcerations, and mechanical injuries as well as concurrent, often low-grade, uveitis must be treated symptomatically. Buphthalmic eyes rarely respond well to medical treatment. Procedures reducing aqueous humor production – cyclocryotherapy, laser ablation of the ciliary body, or intravitreal injection of gentamicin or cidofovir – may be necessary. Radical surgical procedures, for example enucleation or evisceration, should be considered in eyes with marked buphthalmos. Pharmacologic ablation and the use of evisceration and intraocular prosthesis should not be used in cats because of the risk of development of ocular sarcoma.101 Chronic glaucomatous eyes are usually blind and buphthalmos is a poor visual prognosticator. The prognosis for vision is generally poor when buphthalmos develops, except in young animals, in which the condition develops rapidly. Perception of light is sometimes present in patients with advanced chronic changes, and cats and some canine breeds, such as the Norwegian Elkhound, seem to be more resistant to glaucomatous damage than others.

Cataract The lens is a clear structure of ectodermal origin, constantly growing throughout life, as new ﬁbers are formed by elongation of equatorial epithelial cells. The oldest ﬁbers form the nucleus, while the cortex consists of younger cells. The lens ﬁbers meet at the poles, in dogs and cats forming an upright Y anteriorly and an inverted Y posteriorly. The lens is avascular, which precludes typical inﬂammatory reactions. In general, pathologic changes in the lens include hydropic swelling of lens ﬁbers, lysis of ﬁbers, and attempted ﬁber regeneration resulting in epithelial hyperplasia and capsular thickening. The term cataract is derived from the Greek word katauraktes (waterfall). As a medical term, cataract deﬁnes every non-physiologic opaciﬁcation of lens ﬁbers and/or the capsule, regardless of the etiology. Cataracts are most easily diagnosed by retroillumination through a dilated pupil. The lens opacity will present as a dark and more or less opaque area against the brighter fundus reﬂex. More thorough examination of the lens demands the use of a slit-lamp biomicroscope. Cataracts can be classiﬁed according to stage of development, appearance, localization, and etiology. The stages of development are termed incipient, immature, mature, and hypermature: • Incipient cataract describes focal opaciﬁcations(s) of the lens and/or its capsule. Vision is not notably impaired. This cataract may or may not progress. • Immature cataract. The opacity is more or less diffuse, but the fundus can still be examined. Vision may or may not be impaired. • Mature cataract. The fundus cannot be inspected, as the opaciﬁcation is complete and dense. Vision is severely impaired. If a mature cataract undergoes ﬂuid uptake and swelling it is referred to as intumescent. • Hypermature cataract. Lens proteins may liquefy; leakage through an intact capsule can lead to shrinkage and a wrinkling and dimpling of the

175

SMALL ANIMAL OPHTHALMOLOGY

lens capsule. The nucleus will dissolve to a lesser extent and may migrate inferiorly in the capsular bag to form what is termed a Morgagnian cataract. If a cataract is present at birth it is considered congenital. Cataracts developing after the eighth week are termed developmental. Senile cataracts may occur in aged animals, but should not be confused with nuclear sclerosis, which is a normal aging process of the lens. Cataracts are caused by several factors, some of which are: • • • • • • • •

Congenital anomalies Genetic factors Toxins Radiation Trauma Other ocular diseases Systemic diseases Aging.

Cataracts are also described according to localization within the lens. In animals cataracts are classiﬁed as nuclear, anterior or posterior cortical or subcapsular, equatorial, or capsular. Nuclear cataracts most frequently occur in the congenital form. Pulverulent cataract, where the nucleus has a ‘cotton candy/candy ﬂoss’ appearance, is occasionally seen. The condition most often does not progress to disturb vision.

Hereditary cataract Primary hereditary cataracts are the most commonly encountered cataracts in dogs; they have been described in many breeds and the list is continually growing.102 Depending on the gene pool in different countries, the incidence of hereditary cataracts within a breed may differ signiﬁcantly. Hereditary cataracts are far rarer in cats, but are suspected in the Persian, Birman, and Himalayan.103 Hereditary cataracts may be congenital or developmental. It may be difﬁcult to determine whether a cataract should be considered hereditary or not. However, the more of the following criteria that are met in conjunction with an affected animal, the greater is the likelihood that the cataract is hereditary: • Hereditary cataract has previously been described in the breed • The cataract occurs bilaterally (exceptions may occur) • The age of appearance and the localization of the lens changes correspond to those described for the breed • The cataract is progressive, although slowly in certain cases. Other criteria, including breed incidence and increase in incidence within a breed over a period of time, are also taken into consideration. The problem arises when suspected hereditary forms of cataract are diagnosed in a ‘new’ breed. Examination of the parents, littermates, and offspring should be performed. 176

Congenital hereditary cataract In congenital hereditary cataract, the nucleus and perinuclear cortex are most often affected. Congenital cataracts conﬁned to the nucleus are generally non-

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progressive: cortical involvement is a poor prognosticator. Congenital cataract may occur in combination with other congenital eye abnormalities, such as microphthalmia, retinal dysplasia, PPM, posterior lenticonus/lentiglobus, and PHTVL/PHPV. Primary congenital cataracts not associated with malformations of the eye may be seen in breeds like the Staffordshire bull terrier, the West Highland white terrier, and the Boston terrier. Congenital cataract associated with microphthalmia is diagnosed, among others, in the Miniature Schnauzer, English Cocker Spaniel, Cavalier King Charles Spaniel, West Highland White Terrier, and Old English Sheepdog. In the Cavalier King Charles Spaniel, congenital cataract often occurs in combination with lenticonus or lentiglobus. The mode of inheritance has been established in only a few breeds, and genetic testing is available for the French Bulldog and the Staffordshire Bull Terrier. It is important to note that not all congenital bilateral cataracts are inherited. Inherited developmental cataract Most developmental cataracts begin in the cortex and may progress to involve the whole lens, including the nucleus. The rate of progression varies, from barely noticeable to rapidly progressing changes. The triangular posterior polar cataract seen in the Golden and Labrador Retrievers as well as other breeds including Rottweiler and Belgian Sheepdog is considered developmental as it occurs after 6 months of age in most cases (Fig. 5.28). The list of breeds with proven or suspected inherited developmental cataract is long, with local variations. Further information on hereditary or suspected hereditary cataracts is summarized in Table 5.5.39,40,104

Lens-induced uveitis Cataract is a common cause of uveitis and may accompany both cataract formation and resorption. While intensity of lens-induced uveitis is reversible105 in rapidly progressing and in hypermature cataracts, clinically signiﬁcant uveitis may be present. This is most often a chronic condition with episcleral

Fig. 5.28 Posterior polar cataracts (bilateral) in a 2-year-old dog with minor visual problems, according to the owner.

177

Recessive

German Shepherd

Congenital to 4 mos

Recessive

Recessive

Recessive

Recessive

Dominant

Miniature Schnauzer

Old English Sheepdog

Staffordshire Bull Terrier

Welsh Springer Spaniel

Beagle

4 mos

Congenital to 4 mos

Congenital to 4 mos

Congenital to 2 yr

Congenital

Golden Retriever (type 1)

Congenital to 2–3 mos

Congenital to 4 mos

Recessive

Boston Bull Terrier (type 1)

Age of onset Congenital

Mode of genetic transmission

Clinical features of inherited canine cataracts.

American Cocker Spaniel (type 1)

Breed

Table 5.5

178 Posterior axial opacities

Cortical

Nuclear and cortical

Nuclear and cortical

Nuclear and cortical

Nuclear and cortical

Posterior cortical/suture line vacuoles; extension to nucleus and cortex

Nuclear and cortical

Nuclear and cortical

Characteristic early appearance

Non-progressive

Progressive; mature by 1.5–2 years

Slowly progressive; mature by 2 years

Progressive

Slowly progressive; mature by 2 years

Slowly progressive

Progressive; equatorial cortex spared

Slowly progressive; mature by 2 years

Slowly progressive

Biologic behavior

SMALL ANIMAL OPHTHALMOLOGY

Incomplete dominant

Incomplete dominant

Golden Retriever (type 2)

Labrador Retriever

9–18 mos

9–18 mos

Congenital to 2 yr

9–18 mos

Recessive

Standard Poodle

6 mos to 2 yr

Belgian Sheepdog

Recessive

Siberian Husky

4 mos to 2 yr

9–18 mos

Recessive

Irish Setter

4 mos to 2 yr

Large Munsterlander

Recessive

Afghan Hound

Axial posterior subcapsular triangular opacity

Axial posterior subcapsular triangular opacity

Axial posterior subcapsular triangular opacity

Axial posterior subcapsular triangular opacity

Equatorial

Posterior axial subcapsular opacity ± cortical vacuoles

Cortical

Equatorial vacuoles

Usually progressive

Usually non-progressive

Usually non-progressive

Usually non-progressive

Progressive; mature by 1–3 years

Very slowly progressive

Rapidly progressive

Rapidly progressive

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179

Recessive

Recessive

Standard Poodle

West Highland Terrier

Congenital

1+ yr

Congenital

2–10 yr

Dominant

Recessive

Miniature and Toy Poodles

6 mos to 8 yr

Norwegian Buhund

Recessive

American Cocker Spaniel

Variable

4–12 yr

Dominant with incomplete penetrance

Chesapeake Bay Retriever

Age of onset

Boston Bull Terrier (type 2)

Mode of genetic transmission

Breed

Table 5.5 continued

180 Posterior suture

Equatorial cortex

Fetal nucleus

Radiating cuneiform (wedgelike) cortical opacities

Cortical

Cortical

Posterior subcapsular, axial or equatorial

Characteristic early appearance

Usually non-progressive

Progressive

Non-progressive

Very slowly progressive

Progressive

Often asymmetric; stable or slowly progressive for months to years, then rapid progression to maturity

Slowly progressive

Biologic behavior

SMALL ANIMAL OPHTHALMOLOGY

Traumatic cataract

VISUAL IMPAIRMENT

hyperemia and moderate discomfort. The iris is not markedly swollen, but the chronic condition will eventually result in a darkening of the iris color. The pupil is slightly constricted and resistant to mydriatics, and the IOP is moderately lowered. A granulomatous variant seen most commonly in association with diabetic cataracts is characterized by prominent keratic precipitates and may be refractory to therapy. Traumatic cataract can develop as a result of blunt trauma or a perforating wound with or without rupture of the lens capsule. Small perforations of the capsule may seal with ﬁbrin and posterior synechiae, with a resultant non-progressive cataract. Blunt trauma or perforating larger wounds may cause more extensive changes, progressing to complete cataracts. Rupture of the lens capsule with release of lens proteins into the aqueous humor usually results in intense uveitis.

Toxic cataract

Several toxic substances can cause cataracts.106 These include mitotic agents, enzyme inhibitors, and certain metals. Cataract formation after long-term therapy with ketoconazole has also been described. A brand of commercial milk substitute produced cataracts in orphaned puppies, although this type of cataract might be better classiﬁed as a nutritional type.107

Cataract secondary to other ocular diseases In a number of other eye diseases, cataract can develop as a secondary entity. Progressive retinal atrophy (PRA) in dogs (not in cats) often results in secondary cataract, obscuring the primary disease. Questioning the owner about onset and vision in daylight and under reduced lighting conditions, as well as considering the age and the breed of the dog, is essential to establish a diagnosis. ERG should always be performed before cataract surgery if the retina cannot be visualized ophthalmoscopically. Uveitis, lens luxation, and glaucoma frequently lead to cataract formation, especially in the cat. These cataracts are caused by an altered composition of the aqueous humor, which is responsible for lens nutrition.

Cataract secondary to systemic diseases Diabetes mellitus is a common cause of cataracts and most diabetic dogs eventually develop lens changes.108,109 The cataracts are bilateral, rapidly progressive, and involve the entire lens. A typical ﬁnding in diabetic cataracts is broad and clearly marked suture line separation; rarely, spontaneous rupture of the lens capsule may occur. The cause of cataract is the increase in glucose entering the lens from the aqueous. The excess glucose is metabolized via the aldose reductase pathway, resulting in an increased concentration of sorbitol. Sorbitol acts as an osmotic agent, drawing water into the lens cells, thus causing swelling of the ﬁbers and loss of transparency. Excess glucose also affects the lens proteins directly by altering their structure, which causes scattering of light through the lens.

Treatment of cataract Despite anecdotal reports, no effective medical treatment for cataract has been conﬁrmed. However, continuous studies on the effect of systemic and/or topical

181

SMALL ANIMAL OPHTHALMOLOGY

administration of antioxidants are being carried out, as oxidative damage is considered an essential factor in cataract development. There are presently also studies carried out on the effect of aldose reductase inhibitors and its future use in the prevention of diabetic cataracts. Surgical treatment with lens extraction provides predictable restoration of functional vision. The general condition of the patient as to health and behavior should be considered. Cataract surgery should be left to veterinarians with special interest in ophthalmology and experience in lens extractions. There are three basic techniques for removal of a cataractous lens: intracapsular lens extraction, extracapsular lens extraction, and phacoemulsiﬁcation. In intracapsular extraction the lens is removed in toto. That is, the zonular ﬁbers are broken and the lens is removed from the vitreous. There is a high risk of complications, and the method is not used in cats and dogs except in cases of lens luxation. In extracapsular extraction an opening is made in the anterior capsule and the lens contents are removed. The nucleus of the lens is taken out via the corneal incision, with subsequent cleaning of the capsular bag by irrigation and aspiration of residual cortical material. In phacoemulsiﬁcation, the lens material is fragmented by ultrasound and aspirated. The equipment for phacoemulsiﬁcation is expensive, but the technique is advantageous in terms of incision size and risk of secondary complications. Both phacoemulsiﬁcation and extracapsular lens extraction, however, require careful evaluation before surgery, as well as close follow-up after surgery. Postoperative medication is indicated for several months. An aphakic (without a lens) animal is strongly hyperopic (far-sighted) and the use of intraocular lenses in cataract surgery has gained increased popularity. If placement of an intraocular lens is not possible, corneal contact lenses for aphakic dogs are also commercially available. The success rate of extracapsular lens extractions varies, depending on the type of cataract, the skill of the surgeon, the method used, and the cooperation of the patient; in general, in experienced hands a high success rate should be anticipated. Frequent, but usually insigniﬁcant, complications after cataract surgery are focal posterior synechiae and capsular ﬁbrosis. Glaucoma, retinal detachment, corneal edema, and endophthalmitis are critical complications that may occur.

Inherited retinal degeneration Generalized progressive retinal atrophy (PRA)

182

Classical PRA has been described in a great number of dog breeds as well as in a few cat breeds.39,40 The condition has been further clariﬁed through clinical, biochemical, morphological, and electrophysiological studies in several breeds of dog and cat.56 Further, through molecular genetic studies speciﬁc gene defects have been described in many canine breeds (see Table 5.4). It is now clear that classic PRA groups together several diseases at the cellular level although the clinical manifestations are more or less similar. In these diseases it is the photoreceptor layer that is primarily involved. The age of onset and rate of progression of PRA may vary between breeds. PRA has been grossly divided into two main disease types: PRA of early onset and usually rapid progression (such as rod–cone, rod, or cone dysplasia), and late-onset PRA, usually with a slow progression of the retinal degenera-

VISUAL IMPAIRMENT

tion. In the latter type of PRA, the photoreceptors show normal development, but degenerate after the time of retinal maturation, which occurs at about 8 weeks in the dog.110 A common ﬁnding in all types of PRA is that the disease process is always bilateral and always leads to blindness. Most of the retinal degenerative diseases in dog and cat breeds have an autosomal recessive mode of inheritance. In recent years, however, retinal degenerative diseases with Xlinked and autosomal dominant modes of inheritance have also been discovered. See Table 5.3 for a summary of speciﬁc inherited retinal diseases in dog and cat breeds.

Progressive rod–cone degeneration In the Miniature Poodle, classic generalized PRA has been further speciﬁed as progressive rod–cone degeneration.111 Morphologically, signs of disease are observed in the Poodle by electron microscopy at the age of 14.5 weeks and at the age of 30 weeks by light microscopy. A reduced renewal rate of outer segment lamellae has been reported as well as abnormal relative concentrations of phospholipids and free fatty acids in rod outer segments. The retinal degenerative disease in at least 12 breeds of dog has been described as having a mutation at the same gene locus, among which are the Toy and Miniature Poodle, English and American Cocker Spaniel, the Portuguese Water Dog and the Labrador Retriever. In a press release dated June 1, 2005, Optigen LLC (www.optigen.com) announced that the gene causing prcd has been identiﬁed, although at the time of writing the actual mutation had not been published. The Abyssinian cat is also affected by an autosomal recessively inherited progressive rod–cone degenerative disease112 with similarities to the miniature poodle model described above. Further studies of this speciﬁc disease have shown a signiﬁcant reduction in interphotoreceptor retinol binding protein (IRBP) in affected individuals compared to normals, before signs of retinal degeneration are observed by morphology.113 It is not clear yet whether this is a primary or secondary defect in the photoreceptor disease process. Clinical ﬁndings Regardless of the speciﬁc underlying cause and the age of onset of progressive rod–cone degeneration/generalized PRA, the clinical manifestations tend to be rather similar in affected animals of different breeds. Clinical signs include an initial reduction of night vision, followed by a progressive loss of day and night vision. The end-stage is always complete blindness. Early ophthalmoscopic signs are seen as a discoloration of the tapetal fundus (brown to grayish changes most obvious peripherally) with an altered tapetal reﬂectivity and a slight vascular attenuation between the age of 3 and 5 years in the Poodle, somewhat earlier in the American Cocker Spaniel, and somewhat later in the English Cocker Spaniel. In the Labrador Retriever there is a great variation in timing of appearance of early retinal changes, between the age of 2 and 6 years (Fig. 5.29). Progression of disease is variable, but a bilateral retinal atrophy is usually observed after another 2–4 years in the affected breeds. ERG is diagnostic between the age of 6 and 9 months in the poodle and not until 1.5 years or later in the English Cocker Spaniel and Labrador Retriever breeds. Electrophysiologic ﬁndings include low-amplitude rod and cone responses, rod responses being more reduced than cone responses initially.

183

SMALL ANIMAL OPHTHALMOLOGY Fig. 5.29 Early signs of hereditary rod–cone degeneration (generalized progressive retinal atrophy, PRA) in a 4-year-old Labrador Retriever. The dog had slight visual problems at night, but normal daylight vision still. Funduscopic changes were minimal, but ERG was non-recordable.

184

In the affected Abyssinian cat early clinical signs include changes in tapetal reﬂectivity and grayish lesions centrally near the optic disk and in the peripheral tapetal fundus, usually observed between the age of 1.5 and 2.0 years. The fundic lesions progress to a generalized atrophic fundus with severely attenuated retinal vessels at the age of 3–5 years (Fig. 5.30). ERG is diagnostic of the disease after the age of 8 months with signiﬁcantly reduced rod responses, while cone responses are still more or less normal. Secondary cataracts are usually found in dog breeds affected with progressive rod–cone degeneration/generalized PRA, but not in the cat. Differential diagnosis Generalized retinopathy of inﬂammatory origin is an important differential diagnosis. In most inﬂammatory retinopathies, however, the retinal changes are not bilaterally symmetrical as in progressive rod–cone degeneration. Furthermore, the ERG is often still recordable but is reduced or of low amplitude. Drug-induced retinopathy is, however, difﬁcult to differentiate since retinal changes are often bilateral and symmetric, and there is often a non-recordable ERG. Another differentic, is SARD. In this disease the onset of clinical signs is acute, with a normal-appearing fundus and a non-recordable ERG. However several months or years after the onset of SARD it is impossible to differentiate this disease clinically from progressive rod–cone degeneration/generalized PRA. Treatment There is to date no effective treatment for progressive rod–cone degeneration/generalized PRA in the dog and cat. Preventive measures need to be taken in breeding programs. Affected animals should not be used for breed-

VISUAL IMPAIRMENT

Fig. 5.30 Advanced stage of hereditary rod–cone degeneration (PRA) in a 4-year-old Abyssinian cat.

ing nor should known carriers of the defect (i.e. for the autosomal recessive disorders, parents of the affected individual and its offspring are in general not used for breeding purposes). Blood testing can be performed, based on knowledge of speciﬁc gene defects.

X-linked progressive retinal atrophy Two breeds of dog have been shown to be affected by this disease, namely the Siberian Husky114 and the Samoyed.28 Clinical signs in both breeds are similar and include initial night blindness and funduscopic signs of classic PRA, although at different ages. The disease in the latter is more severe than in the former. Interestingly, carrier female dogs for both diseases show clinical signs also. In the former breed multifocal areas of complete loss of photoreceptor cells were described, while in the latter female carriers developed a generalized retinal degeneration. A mutation-based DNA test is available for XLPRA (see Table 5.4).

Dominant progressive retinal atrophy A very speciﬁc retinal disease has recently been found in the Old English Mastiff and in the Bullmastiff. Through test breeding an autosomal dominant mutation was found and it was subsequently shown that a mutation in the rhodopsin gene was causative.20,115 At a young age affected dogs are normal appearing. However, by 6 months a variably sized and located area of retinal thinning in the central fundus is observed by ophthalmoscopy. ERGs show severely reduced b-waves at 12–18 months. A non-uniform degeneration of photoreceptors was veriﬁed by histology in affected dogs. A striking ﬁnding is that environmental light appears to contribute to the regional variation of early retinal disease. It was shown by clinical studies and morphology that modest

185

SMALL ANIMAL OPHTHALMOLOGY

light levels accelerated the retinal degeneration in dogs affected with this mutation.115 There is a DNA-based test available for the defect.

Retinal pigment epithelial cell dystrophy (RPED) In this disease the primary defect is in the pigment epithelial cell layer of the retina. The essential morphologic lesion is hypertrophy of the RPE with accumulation of lipopigments. The defect causes secondary photoreceptor degeneration and retinal atrophy. Because of the clinical appearance of the disease, with pigment accumulation and retinal degenerative changes most prevalent in the central part of the retina, this disease was formerly called central progressive retinal atrophy (CPRA).116 The disease has been described in several dog breeds, particularly the Briard,117 Labrador Retriever, and the Collie. The disease is still widely recognized as having a hereditary basis although there are recent indications that other factors may play a signiﬁcant role in the development and/or expression of the disease. Speciﬁcally, lack of antioxidants, such as vitamin E, plays a part in the pathogenesis of RPED.

Clinical ﬁndings Affected dogs usually lose central vision before peripheral vision, with the result that moving objects may still be seen while stationary objects are not. Ophthalmoscopic retinal alterations may be seen from as early as 18 months of age but in some dogs they are not present until much later in life. They appear as light-brown pigment foci within the tapetal fundus, usually ﬁrst developing temporal to the optic disk. With progression of disease the foci become more numerous and may coalesce with areas of hyperreﬂectivity developing between them. With advancing disease there is vascular attenuation, more severe retinal atrophy, and development of some changes in the non-tapetal fundus such as depigmentation and mottling. The presence or absence of non-tapetal changes appears to vary between affected breeds. Secondary cataract is a common but not consistent ﬁnding in older dogs. Usually the changes are bilaterally more or less symmetric. Affected dogs become severely visually impaired and some become blind. ERG is not diagnostic in RPED. At moderately advanced and advanced stages low-amplitude, barely recordable, or non-recordable ERGs are found.

Differential diagnosis Chorioretinitis can give similar funduscopic changes, although usually not as bilaterally symmetric as in RPED. In neuronal ceroid lipofuscinosis the fundus appearance may be similar to that of RPED, although in the former disease neurologic symptoms are usually found as well. Vitamin E deﬁciency will produce ophthalmoscopic lesions similar to those of RPED.

Treatment There is no available treatment to date for RPED. Further studies are needed to elucidate the speciﬁc environmental and/or dietary factors that play a role in the disease process. Also the hereditary basis for the disease needs to be clariﬁed. Until this has been done affected individuals should not be used for breeding purposes. 186

Neuronal ceroid lipofuscinosis (NCL) This disease entity comprises a group of recessively inherited progressive neurodegenerative disease of many species, including humans, dogs, and

VISUAL IMPAIRMENT

cats.118,119 The defect is an inborn error of metabolism that causes an accumulation of lipopigments in the brain and, in some breeds, also in the retina. The retinal lesions are associated with increasing accumulation of autoﬂuorescent and periodic acid–Schiff-positive particles of lipopigment in RPE, photoreceptors, cells of the inner nuclear layer, and ganglion cells. The term ceroid lipofuscinosis is derived from the histochemical and ﬂuorescent properties of pigment that accumulates in neuronal cells. The central nervous system appears to be the main focus of the pathogenic defect, however.120 The association between lipopigment storage, cell dysfunction, and cell death has not yet been elucidated. Clinically affected individuals have neurologic abnormalities including central blindness, tremors, seizures, and premature death. Visual impairment and blindness is due to either central nervous effects, retinal degeneration, or both. NCL has been described in several breeds of dog (for a review see: www.caninegeneticdiseases.net), most of which have variable clinical signs. Several genes have been implicated in the disease.30–32 For a summary of known causative genetic neurodegenerative defects in dog breeds, see Table 5.4.

Clinical ﬁndings Blindness, ataxia, and mental disturbances develop at an early age, usually around the age of 1 year or earlier. The appearance and development of ophthalmoscopic changes vary between breeds. In the Polish Owczarek Nizinny (PON)121 funduscopic alterations are obvious at the age of 1–2 years (Fig. 5.31), while in the English Setter ophthalmoscopically detectable lesions are absent. Results of ERG recordings vary depending on species and age at examination, from normal to non-recordable ERGs. The most severely affected breed of dog is the English Setter, in which the disease leads to death within a few years.

Differential diagnosis RPED is the main differential, with ophthalmoscopic lesions rather similar to the ones observed in neuronal ceroid lipofuscinosis in some breeds, such as in

Fig. 5.31 Retinal pigment epithelial dystrophy-like lesions in the fundus of a 4-year-old Polish Owczarek Nizinny with neuronal ceroid lipofuscinosis.

187

SMALL ANIMAL OPHTHALMOLOGY

the PON. Vitamin E deﬁciency will also produce ophthalmoscopic lesions similar to RPED and neuronal ceroid lipofuscinosis in some breeds, such as the PON.

Treatment and prognosis There is no treatment for affected individuals and the prognosis is poor. The breeding of affected individuals and known carriers of the defect should be avoided.

Nutritional retinal degeneration Vitamin E deﬁciency Vitamin E is an antioxidant which functions to stabilize cell membranes by the prevention of lipid peroxidation. Deﬁciency of this vital vitamin in animals may result in pathologic changes in the retina, central nervous system, reproductive tract, and skeletal muscle. Dogs experimentally fed a diet deﬁcient in vitamin E from weaning developed night blindness, ophthalmoscopic fundus changes, and non-recordable ERGs within 4 months.122 Histologically there was an accumulation of autoﬂuorescent pigment within the RPE and, at later stages, in all retinal layers. Secondary photoreceptor damage was observed with successive development of retinal atrophy. There are obvious similarities between RPED and vitamin E deﬁciency, which suggests a common etiologic factor.

Vitamin A deﬁciency Vitamin A is important for normal visual function. A deﬁciency is characterized by night blindness in most animals since vitamin A is a precursor of the visual pigment rhodopsin. Vitamin A deﬁciency is seldom diagnosed in the clinical situation, although deﬁciency may develop as a result of systemic diseases that cause impaired fat absorption. Early changes are characterized by an alteration in color of the tapetal fundus; in a more chronic deﬁciency there is complete retinal atrophy.

Taurine deﬁciency retinopathy Taurine deﬁciency will cause retinal degeneration (and cardiomyopathy) in the cat.123 Research has established that taurine, which is a sulfur-containing amino acid, is essential for the cat, which has a daily requirement of 35–56 mg.124 Taurine content is high in milk, liver, and shellﬁsh, but has been present in low levels in most dog foods. It is not yet clear if all cases of feline central retinal degeneration (FCRD), the classic name of the disease, are caused by a primary taurine deﬁciency. It could be that other factors are also involved, such as individual sensitivity to taurine deﬁciency or problems with absorption of taurine or other required nutrients.

Clinical ﬁndings

188

Ophthalmoscopic evidence for the disease develops after the cat has been on a deﬁcient diet for several months. The signs include bilaterally symmetric dark grayish lesions in the area centralis. The discolored region enlarges and the center becomes hyperreﬂective. With progression the lesion becomes streak-like and is observed along the areas with a high cone density, on both sides of the optic disk (Fig. 5.32). Further progression includes a generalized retinopathy with changed reﬂectivity and vascular attenuation, and the end-stage is complete retinal atrophy. The ERG shows reduced amplitudes and increased

VISUAL IMPAIRMENT

Fig. 5.32 A 3-year-old European domestic short-haired (DSH) male cat with a moderate to advanced stage of feline central retinal degeneration (FCRD).

implicit time of the cone-derived responses early in the disease. With progression of the disorder, the ERG is non-recordable.

Differential diagnosis Generalized retinal atrophy of other causes, such as inﬂammatory or hereditary, is the main differential to advanced cases of FCRD. The disease cannot be differentiated at this stage since in both cases the animal is blind, pupillary light reﬂexes are sluggish or absent, and the ERG is non-recordable. Earlier cases of FCRD can be differentiated from chorioretinitis or related disease. In chorioretinitis the lesions are often arbitrarily spread in the fundus and not so typically located as in FCRD.

Treatment and prognosis Treatment of the disease includes correcting the taurine-deﬁcient diet. If this is done before there is a generalized retinopathy there will be no progression of the disorder; once developed, generalized retinal atrophy is not reversible.

Posterior segment inﬂammatory disease The retina has an exceptionally high metabolic rate and is nourished from the choriocapillaris and the retinal vasculature. Many disease processes may result in decreased circulation and tissue hypoxia. After hypoxia begins, death of retinal cells follows, intracellular and extracellular edema occurs, and neural elements disintegrate with resultant atrophy and gliosis of the retina. The retina has limited regenerative capacity. Changes in the photoreceptor or other neural elements are often irreversible, limiting the possibilities of treatment of many disorders to prevention of further damage. Lesions of photore-

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190

ceptors result in secondary loss of inner retinal structures as well as of the retinal vasculature. Trans-synaptic degeneration is less marked in the opposite direction. Chronic lesions of the optic nerve, however, cause degeneration and atrophy of the nerve ﬁber and ganglion cell layers. Inﬂammatory and infectious processes in tissues and structures surrounding the retina, such as vitreous and choroid, may result in severe retinal damage. Examples are autoimmune disorders, and bacterial and viral infections, as well as neoplastic disorders of the choroid. The retinal structures react to disease processes as other neural tissues do. In conjunction with inﬂammation there is an inﬁltration of inﬂammatory cells and edema primarily; thereafter degenerative changes prevail, followed by atrophic changes. Ophthalmoscopically these changes appear different depending on fundal area, retinal structures affected, and stage of the inﬂammatory process. Acute inﬂammatory lesions in the tapetal fundus appear indistinct, grayish, or dark brown if the neural retina is primarily affected (Fig. 5.33). More chronic alterations at this level give a more distinct dark gray or brown color change with or without hyperreﬂective regions (Fig. 5.34). Long-standing alterations with atrophy of neural retinal structures result in a hyperreﬂective tapetal fundus. Acute inﬂammatory changes in the non-tapetal fundus appear as indistinct, grayish or whitish lesions if the neural retina is affected. In chronic changes there is mainly depigmentation and mottling of the non-tapetal fundus. Inﬂammatory changes affecting the retinal pigment epithelium look somewhat different in that there are always black or dark brown to gray spots in conjunction with the above described alterations. More chronic alterations affecting the retinal pigment epithelium in the tapetal fundus result in well demarcated

Fig. 5.33 Active stage of toxic retinopathy in a young laboratory cat. Inﬂammatory lesions in the tapetal fundus are grayish. The folding of the neural retina in the peripheral areas is indicative that the inﬂammation has subsided and that the lesions may be under organization.

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pigmented lesions, often in combination with grayish and/or hyperreﬂective rings around the lesion (see Fig. 5.34). If the retinal pigment epithelium of the non-tapetal fundus is affected chronically the lesions appear as depigmented areas. In conjunction with generalized atrophic changes and lack of neural retinal cell tissue, there is always an effect on retinal vasculature, starting with a slight beading of vessels. In generalized disease processes such as in generalized retinopathies of inﬂammatory or hereditary origin, there is a marked or complete attenuation of retinal vessels.

Chorioretinitis and related conditions Inﬂammations affecting the posterior structures of the eye usually involve both choroid and retina concurrently, the choroidal contribution often being predominant. There are several known causes of chorioretinitis and related conditions including bacterial, fungal, and viral agents, trauma, neoplasia, and foreign bodies. More speciﬁcally for the dog some of the recognized causes are: distemper, toxoplasmosis, leishmaniasis, toxocariasis, brucellosis, protothecosis, and oculomycosis (blastomycosis, histoplasmosis, cryptococcosis, coccidiomycosis, and geotrichosis). For the cat identiﬁed causes of chorioretinitis and related conditions are feline infectious peritonitis, feline leukemia virus, feline immunodeﬁciency virus, tuberculosis, toxoplasmosis, and oculomycosis. Nevertheless, many cases of chorioretinitis are idiopathic. Some causes of retinochoroiditis and chorioretinitis are of public health signiﬁcance.125 Toxoplasmosis, caused by Toxoplasma gondii, is recognized as a cause of retinal disease in several species, including humans.126 In this proto-

Fig. 5.34 Scarring of the tapetal fundus, an incidental ﬁnding in a 5-year-old Poodle. The lesion to the left is a focal region of inﬂammation that still may be somewhat active, while the lesion to the right is an inactive lesion with central pigmentation surrounded by hyperreﬂectivity, i.e. pigment epithelial hypertrophy with a rim of neural retinal atrophy.

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zoan disease the oocysts are produced by cats and the organism has an intraintestinal cycle that occurs in mammals and birds. Toxocaral retinochoroiditis is caused by visceral larval migrans of an ascarid nematode that is an important intestinal parasite in the dog, and is of public health signiﬁcance on account of the possible migration of larvae in humans.

Diagnosis and clinical ﬁndings A general physical examination and laboratory work-up is important in all cases of chorioretinitis and related conditions. Affected animals are usually sighted; impaired vision usually results only if the inﬂammatory processes are bilateral and generalized. Pupillary light reﬂexes and the result of ERG recordings may be normal in chorioretinitis and related conditions. The ophthalmoscopic appearance of the fundus is indicative of an inﬂammatory process. It is not unusual, in conjunction with routine ophthalmoscopic screening for hereditary retinal disease, to ﬁnd chronic focal lesions in the fundus (retinal scars) (see Fig. 5.34), sequelae to low-grade chorioretinitis, with no clinical signiﬁcance to the animal.

Differential diagnosis An important differential to chorioretinitis is RPED. In the latter disease, retinal lesions are generalized and bilateral, which is not always the case with chorioretinitis. Another differential is multifocal RD, in which the lesions may be difﬁcult to differentiate from chorioretinitis. In the former disease, however, the lesions are most often found centrally in the tapetal fundus, often along or in the vicinity of the larger superior vessels. In multifocal RD, the funduscopic lesions are, furthermore, often curvilinear or small and circular, while in chorioretinitis the changes are often larger and more darkly pigmented, and with hyperreﬂective areas or circles around a darkly pigmented spot. The end-stage of generalized retinal atrophy may also be difﬁcult to differentiate from generalized chorioretinitis lesions. Most often the former is bilaterally symmetric, while the latter rarely is. Histopathology may help to provide the correct diagnosis in such cases.

Treatment The primary cause should be treated. The administration of systemic antimicrobials is useful in most instances while corticosteroids may be contraindicated in cases of active infection. Diuretics may be of value in severe retinal edema or detachments.

Optic nerve disease The optic nerve consists of the myelinated axons of the retinal ganglion cells. As the axons come together to exit from the globe through the cribriform plate of the sclera, they gain a myelin sheath and form the optic nerve head. The optic nerve may be affected by developmental abnormalities, either inherited or non-inherited, trauma, neoplasia, and inﬂammatory processes in the nerve or its adnexa. Primary chronic lesions of the optic nerve, which often result in atrophic changes in the nerve, also cause retrograde changes such as degeneration and atrophy of the nerve ﬁber and ganglion cell layers of the retina. 192

Papilledema Papilledema is a non-inﬂammatory swelling of the optic disk and is usually caused by increased pressure on the optic nerve. This occurs in conjunction

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with brain tumors in the region of the optic chiasm (Fig. 5.35)127 and sometimes also in systemic hypertension. Papilledema itself does not impair vision and pupillary light reﬂexes are present; the ERG is normal. Ophthalmoscopically the optic disk appears enlarged but there are no inﬂammatory components. If the papilledema is not controlled through treatment of the primary disease, the optic nerve head will atrophy, which results in blindness.

Chronic neurologic disorders causing blindness This group of diseases rarely has visual impairment as the only clinical sign, although apparent blindness may be the only indication of disease noted by the owner. A general and neurologic examination usually reveals other signs of abnormal function. Localization of the site of the deﬁcit in the visual pathway should be attempted. For a thorough description of neurologic diseases causing blindness, the reader is recommended to read textbooks on neurology. However, the most important diseases will be brieﬂy mentioned here.

Hepatic encephalopathy Hepatic encephalopathy is an endogenous intoxication, a complex metabolic disorder resulting from liver dysfunction. The condition may develop either because of advanced liver damage, or secondary to portosystemic venous shunts, which divert portal blood past the liver into the caudal vena cava or other systemic vessels.128 Potentially toxic products absorbed in the gastrointestinal tract are normally detoxiﬁed in the liver, but in the present condition they enter the systemic circulation instead. These toxic products include ammonia, which is produced by bacteria in the colon and normally converted to urea in the liver, as well as dietary amino acids usually metabolized in the liver. Ammonia and certain amino acids may act as neurotoxins to the brain.

Fig. 5.35 Papilledema in a 2-year-old acutely blind Norwegian Elkhound. The dog had no other clinical signs. Autopsy revealed a tumor in the optic chiasm.

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Clinical ﬁndings and diagnosis Clinical signs are most confusing in young animals with congenital portosystemic shunts. The animals may present apparently blind, especially shortly after a protein-rich meal. Other signs, such as excitation or confusion, may also be present. Diagnosis is established by blood chemistry, urinalysis, and imaging techniques for liver tissue and vessels.

Treatment and prognosis In chronic liver damage, supportive treatment, including a low-protein diet, is recommended. If the condition is caused by vascular abnormalities, identiﬁcation and closing of the shunting vein(s) before secondary liver disease develops is the recommended treatment.

Lysosomal storage diseases

These rare conditions are often genetic and may affect both dogs and cats.129 The condition in the Polish Owczarek Nizinny is described earlier in this chapter. Lysosomal storage diseases include diseases in which the absence of a speciﬁc enzyme leads to the accumulation of its substrates with subsequent cell damage, or diseases that may be a direct result of the metabolic disturbance. Many enzymes in cells are contained within small organelles called lysosomes. The enzymes are involved in a variety of catabolic processes and in tissue or substrate turnover (mainly degradation) pathways in the CNS. Because the retina and retinal pigment epithelium are of neuroectodermal origin, they can also be involved in these diseases. Fundus changes, due to accumulation of degraded material, followed by degeneration, may be diagnosed. Lysosomal enzyme deﬁciencies fall into several groups: glycogen storage diseases, glycolipid catabolism diseases, ceroid-lipofuscin storage diseases, and mucopolysaccharidoses.

Clinical ﬁndings Onset of clinical signs is usually in the ﬁrst months of life. The diseases are slowly progressive in nature, most often leading to the death of the animal. The degenerative changes are diffuse and, as in other CNS diseases, blindness may be the initial complaint. In cats, other ﬁndings, including facial abnormalities and corneal cloudiness, may accompany the CNS signs.

Treatment No treatment exists for these diseases. As most of them are recessively inherited, affected animals, including offspring and parents, should not be used for breeding.

Neoplasms

194

Melanomas are the commonest primary neoplasms of the globe, most often arising from the anterior uvea, but tumors originating from other tissues within the eye are also reported.130 Melanocytic neoplasms are locally expansive with low metastatic potential in the dog, while in cats they may be highly malignant. While malignant lymphoma is the most common metastatic neoplasm that involves the eye, any malignant tumor may metastasize to the eye. Intraocular neoplasms cause blindness by virtue of secondary uveitis and glaucoma; extraocular neoplasms do so by compression or destruction of the optic nerve, chiasm, or tracts, or central visual pathway. Visual pathway abnor-

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malities are often helpful for localizing intracranial neoplasms. Neoplasms affecting the visual pathways may be primary or metastatic. Primary tumors usually grow slowly, but the vision loss may appear to be rather acute. This happens because tumors are space occupying and may grow to a certain size before clinical signs develop. Edema of surrounding tissues is also frequent. Neoplasms may arise within the tissue of the visual pathway itself, or may be space-occupying lesions from adjacent structures, compressing vital tissue. Metastatic neoplasms may have a more acute progression than primary tumors and may be multifocal.

Clinical ﬁndings Many animals may have demonstrated vague signs, such as behavioral changes, for some time before showing more obvious neurologic signs. When blindness related to the CNS is suspected, a thorough neurologic examination should be performed, in particular testing of all ocular reﬂexes and reactions. In addition to signs related to the localization of the lesion, signs related to an increase in intracranial pressure are frequently present, resulting in head pressing and altered behavior. Papilledema may be seen in some animals but if mild can be difﬁcult to appreciate, especially in dogs, because of the great variation in myelination of the optic nerve head. Pituitary tumors may compress the optic nerves, as well as other cranial nerves. Brainstem tumors are characterized by abnormal gait and cranial nerve signs, including the cranial nerves associated with vision, eye reﬂexes, and eye movements. Behavioral changes and seizures do not usually result from tumors of the brainstem until the mass affects the reticular activating system (the reticular formation dorsal to the brainstem sending impulses to the cerebral cortex) or alters intracranial pressure. Ocular abnormalities associated with brain tumors may present as nystagmus, anisocoria (difference in pupil size), central blindness, pupillary light reﬂex abnormalities, or abnormal eye movements.

Therapy and prognosis The signs accompanying brain neoplasms are often temporarily relieved by corticosteroid and/or anticonvulsant therapy, and some animals with slowly growing neoplasms may be kept relatively free of clinical signs for several months with such therapy. Radiation therapy and surgery, when possible, may provide therapeutic options, but the prognosis is often grave.

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72. Fortner, J.H., Milisen, W.B., Lundeen, G.R. et al. (1993) Tapetal effect of an azalide antibiotic following oral administration in beagle dogs. Fund. Appl. Toxicol. 21: 164–173. 73. Rubin, L.F. (1974) Atlas of Veterinary Ophthalmoscopy. Philadelphia: Lea & Febiger. 74. Entee, K.M., Grauwels, M., Clerc, B. et al. (1995) Closantel intoxication in a dog. Vet. Hum. Toxicol. 37: 234–236. 75. DeLahunt, C.S., Stebbins, R.B., Anderson, J. et al. (1962) The cause of blindness in dogs given hydroxypyridinethione. Toxicol. Appl. Pharmacol. 4: 286–291. 76. Brown, W.R.L., Rubin, M., Hite, M. et al. (1971) Experimental papilledema induced by a salicylanilide. Toxicol. Appl. Pharmacol. 27: 532–541. 77. Maita, K., Tsuda, S. and Shirasu, Y. (1991) Chronic toxicity studies with thiram in Wistar rats and beagle dogs. Fund. Appl. Toxicol. 16: 667–686. 78. Ford, M.M., Dubielzig, R., Giuliano, E. et al. (2007) Ocular and systemic manifestations of high-dose oral enroﬂoxacin in cat. Am. J. Vet. Res. 68(2): 190–202. 79. van der Woerdt, A., Nasisse, M.P. and Davidson, M.G. (1991) Sudden acquired retinal degeneration in the dog: clinical and laboratory ﬁndings in 36 cases. Prog. Vet. Compar. Ophthalmol. 1:11–18. 80. Andrew, S.E., Abrams, K.L., Brooks, D.E. et al. (1997) Clinical features of steroid responsive retinal detachments in twenty-two dogs. Vet. Comp. Ophthalmol. 7: 82–87. 81. Gwin, R.M., Wyman, M., Ketring, K. et al. (1980) Idiopathic uveitis and exudative retinal detachment in the dog. J. Am. Anim. Hosp. Assoc. 16: 163–170. 82. Vainisi, S.J., Peyman, G., Wolf, D. et al. (1989) Treatment of serous retinal detachment associated with optic disc pits in dogs. J. Am. Vet. Med. Assoc. 195: 1233–1236.

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Dachshund. Vet. Ophthalmol. 10: 69–75. 63. Curtis, R. and Barnett, K.C. (1993) Progressive retinal atrophy in Miniature Longhaired Dachshund dogs. Br. Vet. J. 149: 71–85. 64. Turney, C., Chong, N.H.V., Alexander, R.A. et al. (2006) Pathological and electrophysiological features of a canine cone-rod dystrophy in the miniature longhaired dachshund. Investig. Ophthalmol. Vis. Sci. 48: 4240– 4249. 65. Narfström, K., Wrigstad, A., Ekesten, B. et al. (1994) Hereditary retinal dystrophy in the Briard dog: clinical and hereditary characteristics. Prog. Vet. Compar. Ophthalmol. 4: 85–92. 66. Redmond, T.M., Yu, S., Lee, E. et al. (1998) RPE65 is necessary for the production of 11-cis-vitamin A in the retinal visual cycle. Nat. Genet. 20: 344–351. 67. Acland, G.M., Aguirre, G.D., Ray, J. et al. (2001) Gene thereapy restores vision in a canine model of childhood blindness. Nat. Genet. 28: 92–95. 68. Narfström, K., Katz, M.L., Ford, M. et al. (2003) In vivo gene therapy in young and adult RPE65 -/- dogs produces long-term visual improvement. J. Hered. 94: 31– 37. 69. Narfström, K., Vaegan, X., Katz, M.L. et al. (2005) Assessment of structure and function over a 3-year period after gene transfer in RPE65 -/- dogs. Doc. Ophthalmol. 111: 39–48. 70. Acland, G.M., Aguirre, G.D., Bennett, J. et al. (2005) Long-term restoration of rod and cone vision by single dose rAAV-mediated gene transfer to the retina in a canine model of childhood blindness. Mol. Ther. 12: 1072–1082. 71. Martin, C., Kaswan, R., Gratzek, A. et al. (1993) Ocular use of tissue plasminogen activator in companion animals. Prog. Vet. Compar. Ophthalmol. 3: 29–36.

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83. Grahn, B.H., Szentimrey, D., Pharr, J.W. et al. (1995) Ocular and orbital porcupine quills in the dog: a review and case series. Can. Vet. J. 36: 488–493. 84. Vainisi, S.J. and Packo, K.H. (1995) Management of giant retinal tears in dogs. J. Am. Vet. Med. Assoc. 206: 491–495. 85. Dziezyc, J., Wolf, D.E. and Barrie, K.P. (1986) Surgical repair of rhegmatogenous retinal detachments in dogs. J. Am. Vet. Med. Assoc. 188: 902–904. 86. Vainisi, S.J. and Wolfer, J.C. (2004) Canine retinal surgery. Vet. Ophthalmol. 7: 291–306. 87. Peiffer, R.L., Wilcock, B.P. and Yin, H. (1990) The pathogenesis and signiﬁcance of pre-iridal ﬁbrovascular membrane in domestic animals. Vet. Pathol. 27: 41–45. 88. Crispin, S.M. and Mould, J.R. (2001) Systemic hypertensive disease and the feline fundus. Vet. Ophthalmol. 4: 131–140. 89. Peiffer, R.L., Monticello, T. and Bouldin, T.W. (1988) Primary ocular sarcomas in the cat. J. Small Anim. Pract. 29: 105–116. 90. Dubielzig, R.R., Everitt, J., Shadduck, J.A. et al. (1990) Clinical and morphologic features of posttraumatic ocular sarcomas in cats. Vet. Pathol. 27: 62–65. 91. Kaswan, R.L., Bounous, D. and Hirsh, S.G. (1994) Diagnosis and medical management of keratoconjunctivitis sicca. In: Cyclosporine: Veterinary Application in Ophthalmic Disease. Trenton, NJ: Veterinary Learning Systems, pp. 21–30. 92. Chavkin, M.J., Roberts, S.M., Salman, M.D. et al. (1994) Risk factors for development of chronic superﬁcial keratitis in dogs. J. Am. Vet. Med. Assoc. 204: 1630–1634. 93. Clerc, B. (1994) Chronic superﬁcial keratitis in German Shepherd dogs. In: Cyclosporine: Veterinary Application in Ophthalmic Disease.

Trenton, NJ: Veterinary Learning Systems, pp. 48–54. 94. Clerc, B. and Jegou, J.P. (1994) Superﬁcial punctate keratitis. In: Cyclosporine: Veterinary Application in Ophthalmic Disease. Trenton, NJ: Veterinary Learning Systems, pp. 67–71. 95. Crispin, S.M. (1993) Ocular manifestations of hyperlipoproteinaemia. J. Small Anim. Pract. 34: 500–506. 96. Crispin, S.M. (2002) The cornea. In: Petersen-Jones, S.M. and Crispin, S.M. (eds) BSAVA Manual of Small Animal Ophthalmology. Cheltenham: BSAVA Publications, pp. 134–154. 97. Morgan, R.V. (1989) VogtKoyanagi-Harada syndrome in humans and dogs. Compendium of Continuing Education 11: 1211– 1218. 98. Yamaki, K., Takiyama, N., Itho, N. et al. (2005) Experimentally induced Vogt-Koyanaga-Harada disease in two Akita dogs. Exp. Eye Res. 80: 273–280. 99. Wilcock, B.P., Peiffer, R.L., Jr. and Davidson, M.G. (1990) The causes of glaucoma in cats. Vet. Pathol. 27: 35–40. 100. Slater, M.R. and Erb H.N. (1986) Effects of risk factors and prophylactic treatment on primary glaucoma in the dog. J. Am. Vet. Med. Assoc. 188: 1028– 1030. 101. Peiffer, R.L. Jr. (1994) Intraocular gentamicin in glaucoma. Vet. Comp. Ophthalmol. 4: 166 (Letter). 102. Gelatt, K.N. and MacKay, E.O. (2005) Prevalence of primary breedrelated cataracts in the dog in North America. Vet. Ophthalmol. 8:101–111. 103. Hoskins, J.D. (1995) Congenital defects of cats. Compendium of Continuing Education 17: 385– 405. 104. Petersen-Jones, S.M. (2002) The lens. In: Petersen-Jones, S.M. and Crispin, S.M. (eds) BSAVA Manual

Abyssinian cats homozygous for hereditary rod-cone degeneration. Cell Tissue Res. 278: 291–298. 114. Acland, G.M., Blanton, S.H., Hershﬁeld, B. et al. (1994) XLPRA: a canine retinal degeneration inherited as an X-linked trait. Am. J. Med. Genet. 52: 27–33. 115. Cideciyan, A.V., Jacobson, S.G., Aleman, T.S. et al. (2005) In vivo dynamics of retinal injury and repair in the rhodopsin mutant dog model of human retinitis pigmentosa. Proc. Natl. Acad. Sci. USA 102: 5233–5238. 116. Barnett, K.C. (1965) Canine retinopathies. III. The other breeds. J. Small Anim. Pract. 6: 185–196. 117. Bedford, P.G.C. (1984) Retinal pigment epithelial dystrophy (CPRA): study of the disease in the Briard. J. Small Anim. Pract. 25: 129–138. 118. Armstrong, D., Koppang, N. and Nilsson, S.E. (1982) Canine hereditary ceroid lipofuscinosis. Eur. Neurol. 21: 147–156. 119. Koppang, N. (1992) English Setter model and juvenile ceroidlipofuscinosis in man. Am. J. Med. Genet. 42: 599–604. 120. Rider, J.A., Dawson, G. and Siakotos, A.N. (1992) Perspective of biochemical research in the neuronal ceroid-lipofuscinosis. Am. J. Med. Genet. 42: 519–524. 121. Wrigstad, A., Nilsson, S.E.G., Dubielzig, R.R. et al. (1995) Neuronal ceroid lipofuscinosis in the Polish Owczarek Nizinny (PON) dog. A retinal study. Doc. Ophthalmol. 91: 33–47. 122. Riis, R., Sheffy, B.E., Loewe, E. et al. (1981) Vitamin E deﬁciency retinopathy of dogs. Am. J. Vet. Res. 42: 74–86. 123. Schmidt, S.Y. (1980) Biochemical and functional abnormalities in retinas of taurine-deﬁcient cats. Fed. Proc. 39: 2706–2708. 124. Burger, I.H. and Barnett, K.C. (1982) The taurine requirement of the adult cat. J. Small Anim. Pract. 23: 533–537.

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of Small Animal Ophthalmology. Cheltenham: BSAVA Publications, pp. 204–218. 105. Krohne, S.G. and Krohne, D.T. (1995) Use of laser ﬂaremetry to measure aqueous humor protein concentrations in dogs. J. Am. Vet. Med. Assoc. 206: 1167– 1182. 106. Martin, C.L., Christmas, R. and Leipold, H.W. (1972) Formations of temporary cataracts in dogs given a dispophenol preparation. J. Am. Vet. Med. Assoc. 161: 294–301. 107. Glaze, M.B. and Blanchard, G.L. (1983) Nutritional cataracts in a Samoyed litter. J. Am. Anim. Hosp. Assoc. 19: 951–953. 108. Bagley, L.H. and Lavach, J.D. (1994) Comparisons of postoperative phacoemulsiﬁcation results in dogs with and without diabetes mellitus: 153 cases (1991–1992). J. Am. Vet. Med. Assoc. 205: 1165–1169. 109. Basher, A.W.P. and Roberts, S.M. (1995) Ocular manifestations of diabetes mellitus: diabetic cataracts in dogs. Vet. Clin. North Am. (Small Anim. Pract.) 25: 661–676. 110. Gum, G.G., Gelatt, K.N. and Samuelsson, D.A. (1984) Maturation of the retina of the canine neonate as determined by electroretinography and histology. Am. J. Vet. Res. 45: 1166–1171. 111. Aguirre, G.D. and O’Brien, P. (1986) Morphological and biochemical studies of canine progressive rod-cone degeneration. Investig. Ophthalmol. Vis. Sci. 27: 635–655. 112. Narfström, K. (1985) Retinal degeneration in a strain of Abyssinian cats: a hereditary, clinical, electrophysiological and morphological study. PhD thesis, Linköping University and Swedish University of Agricultural Sciences. 113. Wiggert, B., van Veen, T., Kutty, G. et al. (1994) An early decrease in interphotoreceptor retinoid-binding protein gene expression in

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125. Curtis, R., Barnett, K.C. and Leon, A.L. (1991) Diseases of the canine posterior segment. In: Gelatt, K.N. (ed) Veterinary Ophthalmology, 2nd edn. Philadelphia: Lea & Febiger, pp. 461–526. 126. Frenkel, J.K., Dubey, J.P. and Miller, N.L. (1970) Toxoplasma gondii in cats: fecal stages identiﬁed as coccidian oocysts. Science 167: 893–896. 127. Palmer, A.C., Malinowski, W. and Barnett, K.C. (1974) Clinical signs including papilledema associated with brain tumors in twenty-one

dogs. J. Small Anim. Pract. 15: 359–386. 128. Vulgamott, J. (1985) Portosystemic shunts. Vet. Clin. North Am. (Small Anim. Pract.) 15: 229– 242. 129. Jolly, R.D., Palmer, D.N., Studdert, V.P. et al. (1994) Canine ceroidlipofuscinoses: a review and classiﬁcation. J. Small Anim. Pract. 35: 299–306. 130. Dubielzig, R.R. (1990) Ocular neoplasia in small animals. Vet. Clin. North Am. (Small Anim. Pract.) 20: 837–848.

Orbital and ocular pain Peter W. Renwick and Simon M. Petersen-Jones

6

Pain is a common and important feature of many ocular and orbital diseases. The resulting clinical signs depend on the severity of the pain and include blepharospasm, increased lacrimation, pawing or rubbing of the eyes, and, in more severe cases, even depression and inappetence. Some of the differentials to consider when an animal presents with a painful eye are listed in Table 6.1.

ORBITAL DISEASE AS A CAUSE OF PAIN The orbit of cats and dogs is only partially enclosed by bone meaning that: • Opening the mouth is painful in animals with orbital inﬂammatory disease due to pressure from the vertical ramus of the mandible on orbital contents. • Infection and foreign bodies from the oral cavity may reach the orbit. • The orbit may be accessed for the drainage of retrobulbar abscesses via the mouth (Fig. 6.1) or for ultrasound-guided ﬁne needle aspiration of orbital tumors. • Orbital tumors may reach a large size before noticeably displacing the globe. Careful examination of an animal with painful orbital disease should guide the veterinarian to the correct diagnosis. Rostral displacement of the globe (exophthalmos) is a common feature of several orbital disorders.1,2 Exophthalmos is most readily appreciated by viewing the head from above and comparing the position of the corneas in relation to the medial canthi (also valuable in distinguishing exophthalmos from globe enlargement due to glaucoma). A comparison of the degree to which the globes can be repelled into the orbit is helpful in deciding if an orbital swelling or space-occupying lesion is present (retropulsion of the globe will be painful for animals with orbital inﬂammation). The presence and direction of any globe deviation can be useful in trying to localize the site of the swelling, for example a medial orbital mass will tend to deviate the globe laterally. The doll’s head reﬂex can be utilized as a method to evaluate ocular motility, which can be compromised with a

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Table 6.1

Differential diagnoses of the painful eye.

Orbital disease • Orbital cellulitis/retrobulbar abscess • Orbital trauma • Eosinophilic myositis • Advanced orbital neoplasm Eyelid abnormalities • Entropion • Blepharitis/eyelid abscessation • Trauma to the eyelids • Ectopic cilia • Other cilia abnormalities Ocular surface disease • Trauma • Conjunctivitis • Conjunctival sac foreign body • Corneal ulceration Intraocular disease • Acute uveitis • Endophthalmitis • Glaucoma (especially acute) • Anterior lens luxation • Ocular trauma • Penetrating wounds/foreign bodies

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Investigation of orbital disease A thorough physical examination involving visual inspection of the head, palpation of the superﬁcial orbital area, and close inspection of the oral cavity should be completed. Several imaging techniques can be used to investigate orbital disease. Ultrasonography is useful and is usually performed through the globe (with the probe placed on the cornea) or by using a lateral approach through the skin dorsal to the zygomatic arch. Ultrasound-guided ﬁne needle aspirates of orbital lesions can help in reaching a diagnosis. Radiography is useful only when sinus or bony changes have developed, where a radio-opaque foreign body is present, or where the disease has originated from adjacent structures such as the nasal chambers, frontal sinus or dental arcade. Computed tomography (CT) is informative in many cases but magnetic resonance imaging (MRI) provides superior detail of the orbital soft tissues. Nonetheless skull radiographs should be considered an important component of the initial diagnostic work-up of orbital disease.

ORBITAL AND OCULAR PAIN

space-occupying orbital lesion. The presence or absence of protrusion of the third eyelid helps to distinguish between masses within the ﬁbrous sheath that encloses the extraocular muscle cone from those outside the muscle cone; intraconal masses cause exophthalmos with little or no third eyelid protrusion, examples being extraocular polymyositis or tumors involving the optic nerve, whereas extraconal lesions tend to cause exophthalmos accompanied by protrusion of the third eyelid.

Orbital cellulitis/retrobulbar abscess Orbital infection may result from penetrating wounds (e.g. via the conjunctival sac, eyelids, or mouth), extension from adjacent structures such as tooth roots or frontal sinus, or possibly hematologic spread. The following signs may result: • Rapid onset of exophthalmos • Pain, especially on opening mouth (inappetence and depression may result) • Pyrexia, often accompanied by neutrophilia with a left shift • Variable facial and adnexal swelling, possibly accompanied by discharging tracts • Protrusion of the third eyelid • Conjunctival swelling (chemosis) and hyperemia • Hyperemia and swelling of the oral mucosa caudal to last molar tooth on the affected side.

Investigation The clinical features are often diagnostic but a complete blood count (CBC) may be useful in suggesting the presence of infection. Ultrasonography of the orbit is useful and may enable localization of abscesses. Radiography may be unrewarding but should be undertaken if an orbital foreign body is suspected, or if there are signs that structures adjacent to the orbit are involved. Examination of the oral cavity for dental disease, areas of inﬂammation, penetrating wounds, or foreign bodies should be performed, although the pain induced by opening the mouth may necessitate the use of sedation or general anesthesia.

205

SMALL ANIMAL OPHTHALMOLOGY A

B Fig. 6.1 (A) A cat with a retrobulbar abscess resulting in exophthalmos, third eyelid protrusion, and conjunctival hyperemia/congestion and swelling. (B) Draining of the retrobulbar abscess in the same cat after blunt dissection to the orbit via the oral mucosa caudal to the last upper molar tooth.

Orbital swelling typically results in ﬁlling or bulging of the space caudal to the last upper molar.

Treatment

206

Retrobulbar abscesses may be drained via a stab incision through the oral mucosa behind the last molar tooth followed by careful blunt dissection dorsally towards the orbit. Discrete abscesses are not always found, but when present samples should be collected for culture and sensitivity. A course of broad-spectrum systemic antibiotic is provided and the choice of antibiotic is reviewed once the bacterial sensitivity results are available. Cellulitis is similarly treated with broad-spectrum antibiotics. If there is a lack of response to medical treatment or recurrence of signs, the possibility of the presence of an abscess

Masticatory muscle myositis Myositis of the masticatory muscles (eosinophilic myositis) is com-monest in young dogs in breeds such as the German Shepherd and Weimaraner. It initially results in painful swelling of the masticatory musculature. Exophthalmos may develop due to swelling of the temporal and pterygoid musculature and is often bilateral. It is accompanied by protrusion of the third eyelid and a reduced range of jaw movement.

ORBITAL AND OCULAR PAIN

requiring drainage, a foreign body necessitating exploratory surgery, or persistent infection of the roots of the upper dental arcade should be considered.

Investigation The signalment and clinical signs in acute cases helps in reaching a diagnosis. In chronic cases atrophy of the musculature occurs with resulting enophthalmos as well as further restriction of jaw movement. The blood count in some dogs reveals a mild leukocytosis, neutrophilia, and eosinophilia, and serum creatinine kinase may be moderately elevated. Histologic examination of muscle biopsies (the temporalis muscle is readily accessed) aid in the diagnosis. MRI will reveal swelling of the involved muscle groups.

Treatment The acute condition is treated with immunosuppressive doses of corticosteroids or other immunosuppressive agents.

Traumatic orbital disease Injuries affecting the orbit and orbital contents may result from blunt or sharp trauma. There may be associated fractures or penetration of foreign bodies. Proptosis of the globe, which is deﬁned as a forward displacement of the globe beyond the plane of the eyelids, may result from trauma and is considered on pp. 82–83.

Investigation A full clinical examination is mandatory, as other injuries may be present. Skull radiographs may be necessary depending on the degree of trauma, or if a radioopaque foreign body is suspected.

Treatment The treatment required depends on the extent and severity of the lesions.

EYELID ABNORMALITIES AS A CAUSE OF OCULAR PAIN OR IRRITATION Abnormal eyelid position Entropion

Entropion3 is an inward turning of the eyelid leading to contact between the hairy eyelid skin and the ocular surface with resultant irritation or pain and, potentially, corneal damage. It is relatively common in dogs (Fig. 6.2) but less so in cats (Fig. 6.3). It may result from anatomic abnormalities of eyelid and eyelid/globe relationship or it may develop secondarily to blepharospasm due to painful ocular surface disorders. Anatomic predisposition is often breed

207

SMALL ANIMAL OPHTHALMOLOGY Fig. 6.2 Entropion in a Shar Pei. Although the lids are being held open the tendency for the lower eyelid to turn in can be clearly seen. Note the superﬁcial ulceration and vascularization resulting from the abrasion of eyelid hair.

Fig. 6.3 Lower eyelid entropion in a cat.

208

related and the resultant entropion usually develops in puppies or juveniles. In the Shar Pei entropion may occur in young puppies and is related to excessive facial skin folds. As the puppies grow the tendency towards entropion decreases. In such cases a temporary eversion of the eyelids using tacking sutures may be all that is necessary (Fig. 6.4).4

B

C

ORBITAL AND OCULAR PAIN

A

Fig. 6.4 Temporary eversion of the lower eyelid to treat entropion in a puppy. (A) The lower eyelid is exhibiting entropion. (B) and (C) Two or three temporary everting sutures are placed and tightened sufﬁciently to correct the entropion.

Entropion in juvenile or young adult dogs such as that seen in retrievers, pointers, and setters usually requires permanent correction. If the degree of entropion is mild and the puppy still has quite a lot of growth anticipated it is possible that a temporary eversion will sufﬁce. The opinion of some breeders that young dogs with entropion should not have the entropion corrected until they have reached maturity is not to be encouraged. Delaying surgery can result in the development of permanent corneal damage, coupled in some cases with an increased turning in of the lids due to blepharospasm, to say nothing of the prolongation of the discomfort the condition results in. For these reasons, at least a tacking procedure should be performed. Entropion in most young dogs can be readily corrected by everting blepharoplasty. While more complicated procedures are described in the literature, for the majority of cases a straightforward Hotz–Celsus procedure will sufﬁce. This technique involves removing a strip of skin or skin/muscle parallel to and about 3–4 mm from the inverted eyelid margin (Fig. 6.5). When assessing the degree of correction required (this is performed before sedation or anesthesia), care should be taken to avoid pulling on the skin of the head and thus altering the eyelid position. It is also useful to apply a topical anesthetic to the cornea to relieve the blepharospastic component, thus allowing a more accurate assessment of the degree of correction required to reverse the anatomic deformity. When entropion accompanies more severe lid conformational deformities, such as the ‘diamond eye’ conformation, where a combination of entropion and ectropion may be present associated with an overlong palpebral ﬁssure, a more elaborate blepharoplastic procedure with lateral canthal tightening may be required.5 Entropion may also result from scarring (cicatricial entropion) and recurrence of entropion may be seen in some middle-aged dogs such as Chow Chows and Shar Peis where it appears that the rolling in of the eyelids in middle-aged dogs results from deposition of subcutaneous fat under skin folds around the eyes.

Atonic entropion/trichiasis This condition is most commonly seen in middle-aged and older English Cocker Spaniels. It results from a loss of elasticity of the skin on the head, a slipped facial mask and a rolling in of the upper eyelids so that the eyelashes are in

209

SMALL ANIMAL OPHTHALMOLOGY

A

B

C

D

Fig. 6.5 Diagram of skin–muscle resection for lower eyelid entropion. (A) The degree of correction has been assessed in the conscious, unsedated animal. Forceps can be used to ‘tent up’ a ridge of skin corresponding to the amount to be excised. (B) and (C) A strip of skin about 3 mm from the eyelid margin is excised and corresponds to the length of eyelid that is turning in. The width of skin that needs to be removed is governed by the amount that the eyelid turns in. (D) 6/0 sutures are used to repair the skin; the knots should be directed away from the cornea.

210

Fig. 6.6 Upper eyelid entropion/trichiasis in a middle-aged English Cocker Spaniel. Abrasion from the upper eyelid cilia has caused an area of ulcerative keratitis.

Blepharitis/eyelid abscessation Abscessation of the eyelid skin and acute suppurative blepharitis can cause considerable discomfort (Fig. 6.8). These conditions may result from trauma or bite wounds, but in some cases there is no obvious cause. The latter cases are often due to staphylococcal infections (probably with some accompanying immune reaction to staphylococcal toxins) and may involve the glands of the eyelid that are associated with the follicles of the cilia, the glands of Zeis and Moll. Blepharitis is discussed further in Chapter 4.

ORBITAL AND OCULAR PAIN

contact with the corneal surface (Fig. 6.6). The more severely affected dogs also have a marked lower eyelid ectropion. The condition is often accompanied by chronic changes including blepharitis, conjunctivitis, and keratitis, and even corneal ulceration. A reduction in tear production may also develop and contributes to the ocular surface pathology and the general discomfort. Surgical correction is required and the technique described by Stades gives consistently good results (Fig. 6.7).6

Treatment of blepharitis Abscesses should be treated by drainage, warm compresses, and systemic broad-spectrum antibiotics. Staphylococcal blepharitis is also treated by warm compresses and an extended course of beta-lactamase-resistant broad-spectrum antibiotic combined with systemic corticosteroids. Fitting of an Elizabethan collar to prevent self-inﬂicted trauma should also be considered.

A

B

C

Fig. 6.7 Correction of upper eyelid trichiasis/entropion using the technique described by Stades.6 (A) A skin incision is made 1 mm dorsal to the meibomian gland openings so as to include all the hair-bearing skin and extending 3–4 mm lateral to the medial canthus to 5–10 mm past the lateral canthus. The ends of the incision are joined by a second, more dorsally positioned, incision creating a strip of skin approximately 15– 20 mm wide. This strip of skin is removed and any remaining hair follicles excised. (B) The upper skin edge is pulled part way across the wound to approximately the base of the meibomian glands and sutured into place. (C) A continuous suture pattern ﬁnishes the repair. The uncovered portion of the wound heals by second intention and creates a narrow strip of hairless skin adjacent to the upper eyelid helping to prevent recurrence of the trichiasis.

211

SMALL ANIMAL OPHTHALMOLOGY Fig. 6.8

Staphylococcal blepharitis in a Bichon Frisé.

Abnormalities involving cilia Distichiasis The presence of cilia emerging from the eyelid margin is known as distichiasis. This is a very common ﬁnding in dogs, particularly of certain breeds, but is rare in cats. The vast majority of dogs with distichiasis show few signs of irritation. Corneal damage and accompanying pain may occur in a few affected individuals with thick cilia that are directed onto the cornea. The management of distichiasis is described on pp. 267–268.

Ectopic cilia (Fig. 6.9)

212

Ectopic cilia are less common than distichia. Similarly to distichia they arise from follicles in or adjacent to the meibomian glands. However, in the case of ectopic cilia they emerge through the palpebral conjunctiva, most commonly singly and typically midway along the upper eyelid. They almost invariably cause marked discomfort and often shallow, vertically elongated ulcers. Usually they occur in young dogs although they may develop in mature dogs, possibly due to metaplasia of the meibomian gland epithelium. When they occur in middle-aged dogs it is not uncommon to ﬁnd multiple ectopic cilia and associated cysts, particularly in breeds such as the Shih Tzu. Magniﬁcation is usually required to see the ectopic cilium and even then it may be hard to visualize, particularly if non-pigmented. Treatment consists of removal or destruction of the originating follicle. Destruction may be achieved by cryosurgery or electrolysis; alternatively the follicle may be removed by excising a small block of partial-thickness eyelid tissue surrounding the cilium as shown in Figure 6.10.

ORBITAL AND OCULAR PAIN

A

B Fig. 6.9 Ectopic cilia in an English Cocker Spaniel. (A) Blepharospasm and lacrimation are present indicating ocular pain. (B) A superﬁcial corneal ulcer is present. (C) An ectopic cilium is emerging through the palpebral conjunctiva of the upper eyelid.

213

SMALL ANIMAL OPHTHALMOLOGY C Fig. 6.9 For caption see p. 213.

Fig. 6.10 Excision of an ectopic cilium. A chalazion clamp immobilizes and everts the upper lid and reduces hemorrhage. A square of partial-thickness eyelid tissue containing the offending cilium and follicle is removed and the wound left unsutured.

Other cilia abnormalities

214

Trichiasis, where facial hairs are misdirected resulting in contact with the cornea, may result in pain, but usually only when the hairs cause superﬁcial corneal damage. Nasal fold trichiasis and the presence of medial canthal hairs commonly cause a chronic low-grade superﬁcial keratitis (usually pigmentary) in brachycephalic breeds but may occasionally result in corneal ulceration and

ORBITAL AND OCULAR PAIN

pain. If treatment for nasal fold trichiasis is required simple excision of the nasal folds can be performed, although the owners should be made aware of the altered facial appearance that this will cause. Caruncular hairs (hairs arising from the caruncle at the medial canthus) can cause a medial pigmentary keratitis, occasional ulcers, or a bothersome tear overﬂow due to a wick effect. They may be treated by excision of the dermal tissue; this is often performed as part of a medial canthoplasty procedure employed to address the medial canthal entropion and macropalpebral ﬁssure that is often present in the affected breeds (see Ch. 7, Fig. 7.18). Trichiasis can also result from eyelid scarring or eyelid agenesis; these abnormalities are treated by an appropriate blepharoplastic procedure. Trichiasis resulting from entropion is considered above.

OCULAR SURFACE LESIONS AS A CAUSE OF PAIN Corneal ulceration A corneal ulcer is deﬁned as a full-thickness loss of corneal epithelium. Ulcers may be superﬁcial, i.e. just involving the epithelium, or deeper with stromal loss and even progression down to Descemet’s membrane (a descemetocele), or may lead to corneal penetration, often with iris prolapse. The anterior cornea is well supplied with sensory nerve endings and therefore superﬁcial ulcers may actually be more painful than deeper more serious ulcers. The pain from ulcers is usually manifest as blepharospasm and increased lacrimation. There are a number of potential causes of corneal ulceration as listed below:7 • Trauma • Chemicals – alkalis, acids, detergents • Infection – bacterial (possibly following initial trauma) – viral infection (e.g. cats with feline herpesvirus infection) – fungal infection (rare) • Tear ﬁlm abnormalities (see pp. 283–291) • Cilia abnormalities • Exposure keratopathy – brachycephalics with prominent globe/shallow orbit and poor lid closure – facial nerve paralysis. Most mesocephalic and dolicocephalic breeds can retract their globes sufﬁciently to result in a complete spread of tears across the cornea by the third eyelid, thus keeping the cornea healthy. Tear spreading by the third eyelids in brachycephalics is usually inadequate – trigeminal nerve lesions. Reduced or absent corneal sensation invariably results in a keratitis affecting the area of cornea exposed within the palpebral ﬁssure (neurotrophic keratopathy). • Corneal epithelial basement membrane disease; this results in recurrent epithelial erosions, indolent ulcers, and superﬁcial chronic corneal epithelial defects (Fig. 6.11). • Rupture of epithelial bullae in edematous corneas (e.g. those with endothelial dystrophy – Figure 6.12; also see pp. 94–95 and 168)

215

SMALL ANIMAL OPHTHALMOLOGY A

B Fig. 6.11 The use of ﬂuorescein dye to demonstrate corneal ulceration. (A) A cat with a painful eye; an area of corneal roughening can be seen. (B) The ulcer is clearly demonstrated after application of ﬂuorescein.

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ORBITAL AND OCULAR PAIN

Fig. 6.12 A corneal ulcer in an English Springer Spaniel with corneal endothelial dystrophy. The ulcer has resulted from rupture of a corneal epithelial bulla.

• Epithelial erosion by corneal cholesterol or calcium deposits in patients with lipid keratopathy (Fig. 6.13) or corneal calcareous degeneration (Fig. 6.14; also see pp. 101–102)

Investigation of corneal ulceration Eyes with deeper ulcers, ruptured ulcers, or corneal penetration should be treated very gently to avoid exacerbating the problem. For all ulcers as complete an ocular examination as can be safely performed should be carried out with the aim of identifying any predisposing factors. The eyelid conformation should be noted and attention paid to the frequency of blinking and the extent of eyelid closure. The tear ﬁlm should be assessed early in the investigation and a Schirmer tear test performed before any ﬂuid is applied to the ocular surface (see p. 15). This test is not performed if the ulcer is seen to be deep or the cornea penetrated; in such cases tear production is best evaluated once the cornea has healed. Palpebral and corneal sensation should be assessed by inducing the palpebral and corneal blink reﬂexes respectively; this also enables the extent of eyelid movement to be observed. Magniﬁcation is useful when examining corneal lesions and the use of a slit-lamp biomicroscope is particularly helpful for judging the depth of ulcers. When this instrument is not available a magnifying loupe or direct ophthalmoscope (with a high positive diopter setting) can be used. Particular attention should be paid to the depth and extent of the ulcer, the presence or absence of stromal inﬁltrate, and the state of the stroma; the presence of liquefaction is considered a serious ﬁnding.

Use of ophthalmic dyes in investigating corneal disease Ophthalmic dyes are useful in the investigation of corneal pathology. Fluorescein is the most commonly used dye (see Fig. 6.11):

217

SMALL ANIMAL OPHTHALMOLOGY Fig. 6.13 A corneal ulcer in a young Bulldog associated (secondary) to an area of corneal lipid deposition. Circulating lipid levels should be investigated in such cases.

Fig. 6.14 Corneal ulcer in an elderly crossbred dog secondary to calcareous corneal degeneration.

218

Rose bengal is less commonly used in veterinary ophthalmology; it has the following features:

ORBITAL AND OCULAR PAIN

• Apply ﬂuorescein from single-dose vial or from impregnated paper strips • Wash excess dye from ocular surface using sterile saline to prevent false impression of staining • Dye will stain corneal stroma if epithelial defects are present • Fluorescein does not stain Descemet’s membrane (useful for determining whether a descemetocele is present) • Dye will spread to stain the stroma beneath non-adherent epithelium (see non-healing superﬁcial ulcers below).

• Vital dye – stains dead/damaged cells and mucus • Demonstrates presence of superﬁcial corneal epithelial damage • It is useful for staining epithelial defects in cats due to feline herpesvirus infection (dendritic ulcers) • Can be irritating.

Laboratory investigation of corneal ulceration Laboratory investigations are aimed at identifying the presence of causal or complicating corneal infection and are usually reserved for the more serious ulcers (deeper, deepening, or with stromal liquefaction). As it takes several days to get results from culture and other techniques to identify the presence of microorganisms (immunoﬂuorescence and polymerase chain reaction, PCR), direct examination of smears is recommended and is often performed when a serious or complicated ulcer is present.

Swabs for culture • Swab ulcers where bacterial infection is suspected or the ulcer is progressing • Use of local anesthetic is required to allow active edge of ulcer to be safely sampled • Swabs for feline herpesvirus culture must be transported to the laboratory in the appropriate transport medium • When submitting samples for PCR analysis contact the diagnostic laboratory for instruction on sampling, handling, and shipping.

Scrapes/smears for histopathology • Sample edge of ulcer with cotton-tipped swab, cytology brush, or sterile spatula after local anesthesia – aiming to collect some material but being very careful not to damage the cornea further • Gently smear on at least two clean microscope slides (alcohol washed) • Dry • Stain – Diff-Quik® (Dade Behring) provides a rapid in-house stain and is useful for both cytology and identifying the presence of bacteria. The results of a Gram stain help in the selection of an appropriate antibiotic until culture and sensitivity results are available.

Management of corneal ulcers Superﬁcial uncomplicated ulcers Simple minor ulcers will normally heal within a few days and topical broadspectrum antibiotic cover is all that is required.

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SMALL ANIMAL OPHTHALMOLOGY

Indolent or non-healing ulcers (superﬁcial chronic corneal epithelial defects) Ulcers involving only epithelium that have been present for more than 2 weeks are considered to be non-healing or indolent (Fig. 6.15; see Fig. 4.29) (also known as superﬁcial chronic corneal epithelial defects – SCCED, recurrent epithelial erosions, or boxer ulcers). These are common in dogs and usually require intervention to facilitate healing. They are thought to be due to abnormalities of adherence of epithelium to the basement membrane and of the basement membrane itself.8–10 These ulcers have the following characteristics: • • • •

They are superﬁcial and involve only epithelium There may or may not be a history of minor trauma There is little tendency to heal; can persist for months They are surrounded by a zone of non-adherent epithelium (ﬂuorescein passes under this, staining the stroma beyond the apparent edge of the ulcer) • There is a variable extent of accompanying corneal edema and vascularization. Similar non-healing ulcers are occasionally seen in cats and may be associated with feline herpesvirus infection; they are usually managed in a different manner to the indolent canine corneal ulcer. Several methods of managing canine non-healing ulcers have been advocated. One of the simpler and more effective methods is ﬁrst to remove all loose epithelium surrounding the ulcer and then to create shallow stromal wounds in a punctate or grid fashion (Fig. 6.16).11,12 A cotton-tipped swab or spatula is used to remove non-adherent epithelium, which may cover a large area of the cornea. Multiple shallow anterior stromal punctures or linear wounds in a grid pattern are then made over the new extent of exposed stroma using a 25-gauge hypodermic needle. To limit the depth of the penetration of the needle into the stroma it may be clamped in a hemostat with just the tip protruding or alternatively a commercially avail-

220

Fig. 6.15 A superﬁcial non-healing ulcer. This has been stained with ﬂuorescein. Note the characteristic staining beyond the edge of the epithelial defect. This is due to non-adherence of the surrounding epithelium.

B

ORBITAL AND OCULAR PAIN

A

Fig. 6.16 Treatment for a superﬁcial non-healing ulcer. (A) All surrounding loose epithelium is removed using a dry swab, a spatula, or a scalpel blade. (B) A punctate keratotomy is performed using a hypodermic needle to make multiple superﬁcial wounds into the anterior corneal stroma.

able device can be used. To perform a grid keratotomy the needle is used to score the anterior stroma in a crosshatch pattern with about 0.5–1 mm between the lines. This procedure can be performed in most patients under topical anesthesia and has a 70–80% success rate. A bandage contact lens can be placed to make the eye more comfortable. If the cornea does not re-epithelialize within 2–3 weeks the procedure may be repeated. Superﬁcial keratectomy is a very effective method of managing these ulcers and almost invariably leads to their resolution;13 however, as general anesthesia and magniﬁcation are required, this technique is usually reserved for those cases where other procedures have failed.

Deep corneal ulcers Deeper ulcers (Fig. 6.17) may potentially lead to corneal perforation. Liquefaction of the collagen-rich corneal stroma due to the action of proteolytic enzymes released from bacteria or neutrophils can result in devastating, rapidly progressive, or melting ulcers. Animals with such ulcers usually require hospitalization and intensive medical and possibly surgical therapy. Swabs and scrapes should be taken to investigate possible bacterial infection. Potential corneal pathogens include coagulase-positive staphylococci, β-hemolytic streptococci, Pseudomonas aeruginosa (notorious as a cause of melting ulcers), and other Gram-negative bacteria. For progressive or melting ulcers intensive treatment with an appropriate antibiotic should be started. For example, for Pseudomonas aeruginosa infections gentamicin, tobramycin, or a ﬂuoroquinolone (ciproﬂoxacin or oﬂoxacin) is a useful antibiotic. The ﬂuoroquinolones can also be a good choice for staphylococcal infections. When streptococcal infection is suspected a topical cephalosporin such as cefazolin has been advocated; a suitable preparation may be made by adding cefazolin for intravenous use to an artiﬁcial tear preparation to a ﬁnal concentration of 33 mg/ml.14 In most

221

SMALL ANIMAL OPHTHALMOLOGY

222

Fig. 6.17 A deep ulcer in a Pug. Note the red appearance of the eye and the corneal edema. The clearer center to the ulcer suggests that it deepens to the level of Descemet’s membrane and is at risk of perforating.

instances where corneal melting is not a problem the use of a commercial broad-spectrum topical antibiotic is sufﬁcient. When liquefaction of the corneal stromal is occurring application of topical agents to suppress the action of collagenases and proteases may be considered; a variety of agents have been used including acetylcysteine, doxycycline, EDTA solution (e.g. obtained by adding a small amount of sterile saline to a blood collection tube), and autologous serum (kept sterile and refrigerated). Autologous serum is readily available and has gained popularity in the treatment of melting ulcers. However, there are no published studies proving the efﬁcacy of these agents in small animals. The antibiotic and anticollagenase solution may be applied hourly in the initial stages of treating the more serious melting type of ulcer. Topical atropine (as a 1% ophthalmic solution initially q6 h) is also applied for its cycloplegic and therefore pain-relieving effects. Suturing the third eyelid across the eye (preferably to the bulbar conjunctiva rather than through the upper eyelid) remains a mode of therapy utilized by some veterinary practitioners. The major disadvantage of this technique is that the cornea cannot be observed, so deepening of the ulcer will not be apparent until perforation occurs. If the technique is used, care should be taken to ensure that the sutures do not abrade the cornea. When the ulcer is deeper than approximately one-half the thickness of the cornea a conjunctival ﬂap or pedicle graft is preferable. A variety of conjunctival ﬂaps have been described. These have the advantage of providing protection and support for the weakened cornea. The blood supply provided directly to the ulcer site aids in corneal healing and has an antibacterial and antiprotease action that can help control bacterial infection and corneal liquefaction. The pedicle ﬂap (Figs 6.18 & 6.19) is useful for the treatment of deep ulcers, descemetoceles, and even ulcers that have perforated (Fig. 6.19).15,16 The placement of sutures into the cornea is a microsurgical technique requiring the necessary expertise, magniﬁcation, and instrumentation.

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Alternative methods of managing deeper ulcers include techniques such as corneoscleral lamellar transposition and corneal lamellar grafting (donor cornea stored frozen in gentamicin solution can be used),17 or using graft material of non-ocular origin such as lyophilized porcine submucosa (Biosist®).18 For perforated corneas a combination of a graft material and a conjunctival pedicle graft can be utilized. Application of corneal tissue glue (butylcyanoacrylate) can be effective in treating ulcers with stromal involvement although this is not recommended where there is progressive melting of the ulcer. To utilize this technique the ulcer is carefully debrided to remove necrotic material and then dried thoroughly. The tissue adhesive is painted on in thin layers using a 25–30-gauge hypodermic needle. The aim is to coat the bed of the ulcer but not to have excess glue protruding from the surface, as this will cause further irritation. For obvious reasons the adhesive must be allowed to dry before allowing blinking. The presence of the tissue glue will result in corneal vascularization which aids in healing the corneal defect.

Corneal wounds and foreign bodies Sharp trauma to the eye will often carry a better prognosis than blunt trauma. Corneal or scleral ruptures as a result of blunt compressive trauma carry a poor prognosis as they are usually accompanied by intraocular hemorrhage and extrusion of ocular contents. Ocular ultrasonography can be useful in assessing eyes where direct visualization of the intraocular structures is not possible. The ultrasound examination may reveal changes such as displacement of the lens, retinal detachments, intraocular hemorrhage, and, in some instances of compressive blunt trauma, a split in the posterior sclera adjacent to the optic nerve head. Where there is an obvious corneal wound or split an ultrasound examination should be avoided as it may place pressure on the globe and could also introduce ultrasound gel into the defect. The prognosis for sharp trauma to the cornea depends on the extent of the injury and the involvement of intraocular structures. Simple corneal lacerations are usually sealed by prolapse of the iris following the initial collapse of the anterior chamber. Early specialist treatment usually results in a favorable outcome. Replacement of the prolapsed iris following thorough irrigation and the stripping off of adherent ﬁbrin layers, followed by an accurate water-tight corneal repair, will usually result in a sighted eye. Careful evaluation of the eye to rule out lens or posterior segment involvement or the presence of a foreign body should be performed. The repair is best carried out under an operating microscope with microsurgical instrumentation. Viscoelastic agents can be a useful tool in keeping the anterior chamber formed and avoiding iris to cornea contact during the surgical repair. If a water-tight corneal repair cannot be achieved an overlay of a conjunctival pedicle graft can be used. When penetrating wounds also involve the lens the prognosis is poorer. Large lacerations of the lens capsule necessitate lens removal at a very early stage, otherwise a phacoclastic uveitis will result. This form of uveitis is severe and will typically lead to loss of the eye. Small lens capsule punctures may seal spontaneously leaving a focal cataract, although development of a progressive cataract is also possible. Corneal foreign bodies require removal. Superﬁcial ones are often easy to remove, but care must be taken not to push them deeper into the cornea.

223

224 SMALL ANIMAL OPHTHALMOLOGY

A

C

D

B

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Fig. 6.18 Application of a conjunctival pedicle ﬂap for treatment of a deep corneal ulcer. (A) An initial paralimbal incision has been made and the bulbar conjunctiva is being undermined by blunt and sharp dissection with scissors. The bulbar conjunctiva is translucent, allowing the scissors to be clearly visualized. Dissection is continued towards the fornix. Two divergent incisions are then made towards the fornix. Once these incisions have been made and the bulbar conjunctival pedicle has been freed from the underlying episclera, it is possible to achieve a substantial length of pedicle. A lateral canthotomy has been performed in this diagram. (B) The conjunctival pedicle graft has been advanced to overlie the recipient ulcer bed. The base of the pedicle is usually at the conjunctival fornix. It is necessary to loosen or remove the eyelid retractors to allow the pedicle graft to be advanced onto the ulcer site without undue tension. (C) The ventromedial, ventral, and ventrolateral borders of the pedicle graft are sutured to the recipient ulcer bed with 7.0 or 8.0 absorbable suture. (D) One blade of a pair of scissors is slid beneath the non-adherent pedicle bridge when the pedicle bridge is to be sectioned 4–6 weeks postoperatively. Steven’s tenotomy scissors are ideal as the ends are slightly blunted, thereby reducing the risk of corneal damage if the animal moves suddenly while the pedicle bridge is cut. (Redrawn with permission from Habin, D. (1995) Conjunctival pedicle grafts. In Practice 17: 61–65.)

A Fig. 6.19A A ruptured corneal ulcer in a Boston Terrier. The anterior chamber has collapsed.

225

SMALL ANIMAL OPHTHALMOLOGY B Fig. 6.19B The same eye following repair using a conjunctival pedicle graft. The graft has now been trimmed. The dog had good vision around the residual graft.

Using a 25-gauge needle to pry them out of the cornea can be helpful if there is not enough of the foreign body protruding from the corneal surface to grasp with ﬁne forceps. If the foreign body has penetrated into the anterior chamber a ﬁbrin clot adherent to the intraocular portion of the foreign body will often develop. Eyes with foreign bodies that penetrate through the cornea into intraocular structures such as lens or iris hold a guarded prognosis and require urgent specialist management.

Feline herpesvirus keratitis

226

Classic feline herpesvirus ulcers are superﬁcial branching (dendritic) epithelial defects (Fig. 6.20) that are readily demonstrated by Rose bengal staining. Herpesvirus infection may also be associated with geographic-shaped ulcers and with some indolent ulcers in cats. Less commonly a more extensive keratitis may develop characterized by a marked corneal cellular inﬁltrate (Fig. 6.21), and in some cases may lead to serious ulceration (probably contributed to by secondary pathogens). Antiviral therapy using topical triﬂuorothymidine or idoxuridine may be effective. Recombinant interferon is suggested to improve the action of some antiviral agents and is often given topically to cats with herpesvirus infection. Aciclovir, a drug that is effective in treating herpes simplex virus infections in humans, has been shown to have poor action against feline herpesvirus in vitro,19,20 although its efﬁcacy may be improved by concurrent application of topical interferon.21 Oral L-lysine at a dose rate of 250– 500 mg q12 h to impede viral replication has been advocated as a potential long-term therapy.22,23 Recently, there has been a report of canine herpesvirus-1 corneal infections in dogs.24

ORBITAL AND OCULAR PAIN

Fig. 6.20

Dendritic ulcers in a cat with herpesvirus infection.

Fig. 6.21

Stromal keratitis in a cat with herpesvirus infection.

GLAUCOMA AS A CAUSE OF OCULAR PAIN Glaucoma is a pathologic increase in intraocular pressure (IOP) which causes optic nerve and retinal damage and subsequent blindness. When the IOP increases rapidly, pain is often a major presenting sign. The reference range of IOP in dogs is approximately 7–24 mmHg,25 but it is worth noting that obtaining reliable results when performing tonometry requires practice. It is possible to obtain artifactually high readings especially by over-zealous restraint of the patient, e.g. by putting pressure on the jugular veins or forcing the eyelids open.

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SMALL ANIMAL OPHTHALMOLOGY

Sclera

Ciliary cleft Drainage angle

Pectinate ligament

Ciliary processes

Iris

Anterior chamber Cornea Lens

Fig. 6.22 Aqueous is produced by the ciliary processes, passes from the posterior chamber through the pupil to the anterior chamber, and then leaves the eye via the drainage apparatus situated in the iridocorneal angle.

228

The results of IOP assessment should therefore be interpreted against the background of the clinical ﬁndings. Measurement of IOP is considered in further detail on pp. 25–26. Aqueous humor is continually produced by the ciliary body, enters the posterior chamber, passes through the pupil, and ﬂows into the anterior chamber. It then exits the anterior chamber through the drainage apparatus that lies within the iridocorneal angle (Fig. 6.22). Under normal circumstances the balance of aqueous production and drainage equilibrates to achieve a physiologic IOP. Glaucoma arises as a result of impaired passage of aqueous humor from the eye; the defect in the drainage pathway may lie at the level of either the pupil or the iridocorneal angle. Glaucoma may be primary, i.e. arise in the absence of any antecedent ocular condition, or it may be secondary to other ocular disease (Table 6.2). Primary glaucoma in dogs is most commonly associated with the presence of a congenitally abnormal sheet of tissue at the site of the pectinate ligament (goniodysgenesis), often with associated narrowing of the entrance to the ciliary cleft (Figs 6.23 & 6.24).25–30 Examination of the iridocorneal angle is described on p. 26. Goniodysgenesis/narrow angle glaucoma occurs with increased frequency in several breeds of dog (Table 6.3). Differing degrees of severity of goniodysgenesis are encountered. Dogs with the most severe deformities are very likely to develop glaucoma, typically in middle age (although in some breeds it may occur at a younger age),31 whilst those with milder abnormalities may escape the disease altogether. Glaucomatous attacks in affected dogs tend to be acute and result in very high IOPs causing severe pain and loss of vision in the affected eye. The fellow eye is frequently affected months or even years after glaucoma develops in the ﬁrst eye. The predisposing goniodysgenesis is known to be heritable, so prior to breeding from dogs known to be at risk from

Causes of glaucoma.

Primary

• goniodysgenesis/narrow angle • primary open angle glaucoma

Secondary

• • • •

• • • • • •

primary lens luxation – terrier breeds, border collie uveitis, including lens-induced uveitis neoplasia extension of a pre-iridal ﬁbrovascular membrane over the opening into the ciliary cleft – secondary to retinal detachment, neoplasia, or uveitis intraocular hemorrhage intumescence (swelling) of a cataractous lens ocular melanosis (Cairn terriers) – formerly described as pigmentary glaucoma multiple iris cysts and uveitis – golden retrievers vitreous prolapse after surgical lens extraction obstruction of the entrance to the ciliary cleft by membranes formed by proliferation and metaplasia of residual lens epithelial cells following cataract surgery

ORBITAL AND OCULAR PAIN

Table 6.2

Fig. 6.23 Goniophotograph showing a narrow opening to the ciliary cleft and pectinate ligament dysplasia (goniodysgenesis) of an eye predisposed to primary glaucoma. The dog’s other eye has already developed glaucoma.

this form of glaucoma, screening by gonioscopy should be considered. Those animals with moderate or severe drainage angle abnormalities should not be used for breeding.32 Chronic open angle glaucoma, the commonest form of primary glaucoma in humans, is much less common in dogs than goniodysgenesis/narrow angle glaucoma. It results in glaucoma with a gradual and insidious onset which typically affects both eyes to a similar degree. The presenting sign in this

229

SMALL ANIMAL OPHTHALMOLOGY Fig. 6.24 Goniophotograph showing a very narrow opening to the ciliary cleft. The dog’s other eye has already developed glaucoma. Table 6.3 Breed incidence of primary glaucoma associated with goniodysgenesis/ narrow angle. Breed incidence of goniodysgenesis/narrow angle (breed incidence differs between countries) American Cocker Spaniel English Cocker Spaniel Welsh Springer Spaniel English Springer Spaniel Basset Hound Great Dane Dandie Dinmont Terrier

Siberian Husky Flat Coated Retriever Golden Retriever Labrador Retriever Samoyed Shar Pei Bouvier des Flandres

condition is often the development of an altered appearance due to globe enlargement rather than the presence of obvious pain and visual loss.

Clinical signs of glaucoma33,34 When considering clinical signs, glaucoma may be divided into acute and chronic forms.

Acute glaucoma (also see pp. 148–149)

230

Acute-onset cases tend to present with signs of a painful eye, i.e. blepharospasm, epiphora, and head-shyness. At very high IOPs (e.g. over 60 mmHg) the pain may be so severe as to cause yelping, lethargy, and anorexia. Blindness may develop rapidly and at higher IOPs can become irreversible in a matter of hours. Corneal edema is often seen due to the accumulation of ﬂuid from the aqueous that has not been cleared from the cornea. The edema generally affects

ORBITAL AND OCULAR PAIN

Fig. 6.25 Corneal edema in a Dandie Dinmont Terrier with primary glaucoma due to goniodysgenesis. Rupture of a corneal epithelial bulla has resulted in a small corneal ulcer.

Fig. 6.26 Episcleral and conjunctival vascular congestion in a 7-year-old Basset Hound with glaucoma. Note the early development of perilimbal corneal neovascularization.

the entire cornea and may range in severity from a subtle, ‘steamy’ appearance through to marked opacity which may render detailed visual inspection of the intraocular structures impossible (Fig. 6.25). The degree of ﬂuid accumulation can be so marked as to result in the development of bullous keratopathy and resultant ulcer formation (see Fig. 6.25). Episcleral (and associated conjunctival) congestion is a major presenting sign in both acute and chronic glaucoma cases (Fig. 6.26). This ‘red eye’ presentation can also result from a range of ocular diseases from which glaucoma must be differentiated (see p. 91). These include conjunctivitis, episcleritis, corneal disease, uveitis, Horner’s syndrome, and orbital disease. The key feature for differentiation of these conditions from

231

SMALL ANIMAL OPHTHALMOLOGY

glaucoma is measurement of the IOP. It is worthy of note that a small percentage of patients develop acute but transitory elevation of the IOP which may be sufﬁcient to cause temporary pain and visual impairment (or even permanent blindness). However, the IOP may have returned to within normal limits by the time of presentation. Such IOP spikes can be difﬁcult to detect and diagnose, and if the clinician is in doubt then referral to a specialist should be considered. Increased IOP (especially over 40 mmHg) leads to paralysis of the iris sphincter muscle, and the pupil tends to become mid-dilated and poorly mobile. However, it is important to appreciate that not all patients with glaucoma will present with a dilated pupil – for example, the development of adhesions of the iris to the lens in some cases of uveitis may prevent pupillary dilatation if secondary glaucoma develops. Acute-onset glaucoma most commonly results from goniodysgenesis, lens luxation, or uveitis.

Chronic glaucoma With chronicity the signs of pain may become less obvious, but the capacity for glaucoma to cause discomfort should never be underestimated. Chronic cases may exhibit some or all of the signs associated with acute disease, but often to a lesser degree. In addition, the globe enlarges (hydrophthalmos or buphthalmos) and this may lead to lens subluxation or occasionally luxation, breaks in Descemet’s membrane which are seen as gray streaks in the cornea known as Haab’s striae (Fig. 6.27; see also Fig. 4.10), and, rarely, staphyloma formation (blue swelling at the equator of the globe). The cornea may become vascularized (Fig. 6.28) and pigmented, and with globe enlargement an exposure keratitis and ulceration may develop. Secondary cataracts may form in long-standing cases and intraocular hemorrhage is another possible sequel. Fundus changes which may be seen include cupping and atrophy of the optic disk and retinal degeneration (Fig. 6.29). The affected optic disk

232

Fig. 6.27 Gross enlargement of the globe in this Labrador Retriever with primary glaucoma has led to breaks in Descemet’s membrane also known as Haab’s striae. These are visible as multiple gray streaks in the cornea.

ORBITAL AND OCULAR PAIN

Fig. 6.28 A Basset Hound with gross globe enlargement due to primary glaucoma. Secondary corneal neovascularization has developed.

Fig. 6.29 Fundic changes in a Golden Retriever with primary glaucoma. There are signs of tapetal hyperreﬂectivity and retinal vascular attenuation. The optic disk is dark and cupped. The view is hazy due to clouding of the ocular media.

appears circular, darker than normal, and is depressed below the surface of the surrounding retina. Retinal degeneration manifests as zones of tapetal hyperreﬂectivity and accompanying superﬁcial retinal blood vessel attenuation. Primary open angle glaucoma, glaucoma secondary to neoplasia, and some cases resulting from uveitis are most likely to present as insidious, chronic disease. Cats commonly present with chronic glaucoma secondary either to

233

SMALL ANIMAL OPHTHALMOLOGY Fig. 6.30 Bilateral glaucoma secondary to chronic uveitis in a 2-year-old DSH cat. Both globes are grossly enlarged, the pupils are dilated, and dark keratic precipitates can be seen on the ventral endothelium of both corneas.

low-grade chronic uveitis (Fig. 6.30) or intraocular neoplasia.35 They rarely present with primary glaucoma of any type.

Management

234

Therapy may be medical or surgical. Glaucoma often carries a guarded outlook for vision and all too often results in loss of the globe. Early diagnosis and aggressive therapy are generally required if vision is to be preserved for a signiﬁcant period. Acute glaucoma (such as that resulting from goniodysgenesis/ narrow angle complex) with elevation of the IOP resulting in blindness is an emergency and the pressure must be reduced to the normal range rapidly if there is to be any chance of saving vision. Initially hospitalization is required and treatment is generally commenced with topical prostaglandin analogs (see below). Should the IOP fail to return to normal within the ﬁrst 30–60 min then the use of osmotic diuretics should be considered. Provided that the IOP returns to normal, treatment is continued with a combination of topical prostaglandin analogs and carbonic anhydrase inhibitors, plus or minus other combinations of topical medication. The patient should remain hospitalized while the response to therapy is assessed. Despite maximal medical therapy a signiﬁcant proportion of cases may require surgery in an attempt to keep the IOP within the normal range. The prognosis for vision in such cases is guarded. Long-term anti-glaucoma medication (e.g. with topical carbonic anhydrase inhibitors) for the second, predisposed but normotensive eye should be undertaken after a dog presents with primary closed angle glaucoma in one eye. There is evidence that prophylactic therapy may delay the onset of glaucoma in the second eye of such cases.36 Chronic open angle glaucoma is much more amenable to medical treatment in its early stages than the goniodysgenesis/narrow angle glaucomas, although later in the disease acute rises in IOP may occur. Management of the secondary glaucomas very much depends on the etiology of the problem. Therapy may range from removal of the lens in cases of primary anterior lens luxation to enucleation for those secondary to an intra-

ORBITAL AND OCULAR PAIN

ocular tumor. In all cases of glaucoma, investigations should be undertaken to identify the initiating disease. These should include a detailed ophthalmic examination, including assessment of the other eye. Gonioscopy should be performed on the affected eye if possible, although this may prove difﬁcult in the presence of signiﬁcant corneal edema. In addition, gonioscopy should be carried out in the fellow eye as this may provide vital information in determining whether the glaucoma in the presenting eye is likely to be due to goniodysgenesis/narrow angle complex or secondary to some other disease process. Ocular ultrasonography may be indicated if the ocular media of the presenting eye are clouded and the cause of the glaucoma is in doubt. Where the globe can potentially be saved, treatment must be directed at controlling the raised IOP in addition to whatever therapy is indicated for management of the underlying cause. In view of the requirements for (a) accurate IOP measurement, (b) the use of advanced diagnostic techniques such as gonioscopy, and (c) potential indications for specialist surgical techniques in glaucoma management, referral to a veterinary ophthalmologist should always be considered. This is especially important where there is the possibility of preserving vision or where the fellow eye may be involved in the underlying disease process.

Medical treatment (also see pp. 58–61 and Appendix Table 6) Osmotic diuretics Mannitol 10–20% solution, 1–2 g/kg given i.v. over 20 min may be used for rapid reduction of IOP. It acts by dehydrating the vitreous body; water should be withheld over the initial period to maintain this effect. Care should be taken with its use in elderly or sick patients. Glycerol (50%) given orally at a dose of 1–2 ml/kg can be used for emergency at-home treatment for dogs known to be predisposed to primary glaucoma, although this may induce emesis, and emergency treatment in the home may be better accomplished with the use of prostaglandin analogs (see below).

Prostaglandin analogs Latanoprost, travaprost, and bimatoprost are prostaglandin analogs that are now available for topical treatment of glaucoma. They act by increasing uveoscleral outﬂow, a drainage route responsible for 15% of aqueous drainage in normal dogs, and they also cause a profound reduction in the production of aqueous, at least in normal dogs.37 As a result of their rapid onset of action and marked effect on the IOP in many patients they are frequently used for emergency treatment in cases with acute-onset glaucoma. They are usually applied twice daily, and carbonic anhydrase inhibitors may also be used concurrently as adjunctive therapy. Prostaglandin analogs cause signiﬁcant miosis and may exacerbate underlying uveitis. They should therefore be used with care in cases with pre-existing inﬂammation or where prolapsed vitreous may become entrapped in the pupil and lead to pupil block. In view of both the potency of the prostaglandin analogs, and the miosis which they cause, their use tends to be reserved for ﬁrst-line therapy in severe acute cases or in instances where other medical therapy (such as the use of topical carbonic anhydrase inhibitors) is proving ineffective. This class of drugs has been shown to be ineffective in reducing the IOP of normal cats.38

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SMALL ANIMAL OPHTHALMOLOGY

Carbonic anhydrase inhibitors Carbonic anhydrase inhibitors remain one of the mainstays of medical therapy for glaucoma in dogs and cats. They act by inhibiting aqueous production.39 Various drugs are available (Table 6.4 and Appendix Table 6). Adverse effects to systemic therapy include diuresis, gastrointestinal disturbances, hypokalemia, and metabolic acidosis. The topical application of carbonic anhydrase inhibitors avoids these systemic side effects and is therefore generally the preferred route of administration. This beneﬁt of topical use is particularly applicable to elderly or sick dogs and also cats, as these individuals may be especially susceptible to the side effects of systemic carbonic anhydrase inhibitor use.

b-adrenergic blockers

β-blockers applied topically result in reduced aqueous production. They may be a useful adjunct to therapy, but their effect is insufﬁcient to warrant their sole use. Timolol maleate and metipranolol applied q12 h to q8 h are the most commonly used agents.

Miotics Where the drainage apparatus is still open, topical miotics such as pilocarpine (1% or 2% q12 h to q8 h) and demecarium bromide (0.125% or 0.25% q24 h to q12 h) cause a reduction in IOP. Their use is questionable when the ciliary cleft is collapsed or completely obscured, as is true of most longer-standing glaucoma cases. Where the use of a miotic may be indicated it is generally preferable to use a prostaglandin analog, at least in dogs.

Neuroprotective therapy The systemic use of calcium channel blockers (e.g. diltiazem 1 mg/kg q8 h per os) in glaucoma cases may have a neuroprotective effect by reducing the rate of retinal ganglion cell death caused by an excessive inﬂux of calcium.40

Table 6.4

Carbonic anhydrase inhibitors.

Drug

Dosage

Topical Dorzolamide hydrochloride

2% q8 h

Oral

236

Ethoxzolamide

4 to 7.5 mg/kg q12 h to q8 h per os

Methazolamide

5 to 10 mg/kg q12 h to q8 h per os

Dichlorphenamide

5 to 10 mg/kg q12 h to q8 h per os

Acetazolamide

10 to 25 mg/kg q12 h per os

Surgery aimed at preserving vision is not infrequently indicated in the management of primary glaucoma and also in some cases of secondary glaucoma, especially those caused by primary lens luxation. Surgery may be directed at decreasing the production of aqueous or increasing its outﬂow.

Cyclodestructive techniques Partial destruction of the ciliary body can be achieved using transscleral cryotherapy,41,42 laser therapy,43 or chemical ablation with an intravitreal injection of gentamicin or cidofovir.44 Of these, laser therapy is the technique of choice, especially where vision is to be preserved. Chemical ablation offers unpredictable results, both in terms of IOP control and cosmesis – its use should be reserved only for blind, painful eyes in which enucleation or evisceration is not a viable option for management.

ORBITAL AND OCULAR PAIN

Surgical treatment

Drainage procedures Scleral trephination combined with peripheral iridectomy is a simple method of temporarily increasing aqueous outﬂow.45 Drainage implants of various types are currently preferred as they reduce the risk of failure due to scar tissue formation which prevents resorption of aqueous (Fig. 6.31).46,47 The technique may be combined with laser cyclophotocoagulation.48 Fibrosis around the periocular portion of drainage implants impairs their long-term success, although methods of managing this complication are under development.49

Enucleation or evisceration with intraocular prosthesis Some blind, painful, glaucomatous eyes cannot be successfully managed by the techniques outlined above. In these cases, enucleation or evisceration with insertion of a silicone sphere may be the best option available.

Fig. 6.31 A drainage device has been implanted in this eye to drain aqueous to the periocular tissues. A plastic tube can be seen in the anterior chamber.

237

SMALL ANIMAL OPHTHALMOLOGY

238

LENS LUXATION AS A CAUSE OF OCULAR PAIN Dislocation (luxation) of the lens may occur as a primary or a secondary event.

Primary lens luxation Primary lens luxation is seen most commonly in middle-aged terrier breeds, and may also occur in other breeds such as the Shar Pei, Border Collie, Lancashire Heeler, and Italian Spitz.50–52 An abnormality of the lens zonule is believed to lead to a progressive breakdown of the zonular ﬁbers, resulting in subluxation and eventual luxation of the lens.50,53 Pain is often a major presenting feature of anterior lens luxation. The lens may be visible in the anterior chamber and is most easily recognized by the presence of a bright, refractile ring which represents the lens equator (Fig. 6.32). Sub-central corneal edema may result from the luxated lens contacting the cornea. Prior to complete luxation the unsupported iris may be seen to tremble (iridodonesis) and prolapsed vitreous may be seen as grayish strands in the anterior chamber (Fig. 6.33). The extent of zonular breakdown may be seen more readily after dilating the pupil (Fig. 6.34). Secondary glaucoma commonly results from lens luxation due to blockage of the pupil by the lens or vitreous, or as a result of obstruction of the drainage angle by vitreous. Blindness may rapidly ensue due to optic nerve damage. Early diagnosis is therefore paramount if the condition is to be successfully managed; any terrier or other predisposed breed presenting with a red eye should be speciﬁcally assessed for the possible presence of lens luxation and elevation of the IOP. Glaucoma secondary to anterior lens luxation is uncommon in cats, probably due to the depth of the feline anterior chamber. Treatment involves rapidly reducing the IOP (see p. 235) followed by intracapsular lens extraction combined with anterior vitrectomy as required,

Fig. 6.32 Primary lens luxation in a Parson Jack Russell Terrier. The lens is positioned in the anterior chamber and can be recognized by the refractile ring of the lens equator.

ORBITAL AND OCULAR PAIN Fig. 6.33 Vitreous protruding through the pupil of a Jack Russell Terrier with impending primary lens luxation.

Fig. 6.34 Lens subluxation (readily seen after the pupil was dilated) due to lens zonule breakdown in a Tibetan Terrier with primary lens luxation.

239

SMALL ANIMAL OPHTHALMOLOGY

providing that there is potential for preserving vision. The surgery is not without risks of signiﬁcant complications, e.g. retinal detachment, intraocular hemorrhage, and postoperative glaucoma. Optimal results are obtained using microsurgical techniques and the procedure should be performed by veterinarians who are expert in performing intraocular surgery. Careful postoperative management is required, and patients should be monitored at regular intervals for life in order to optimize the long-term outcome. In animals where the lens of the second eye has not yet luxated, lentectomy at that stage is considered preferable to leaving the eye until the lens luxates, especially if it can be removed by small incision surgery (phacoemulsiﬁcation). In cases of posterior lens luxation the use of miotics (e.g. prostaglandin analogs) to retain the lens in the posterior segment has been advocated. There is the ongoing risk of acute glaucoma development in such cases, however, as a result of either pupil block due to vitreous prolapse or inadvertent escape of the lens into the anterior chamber, e.g. due to medication errors.

Secondary lens luxation The lens may dislocate due to damage to the zonular attachments resulting from antecedent ocular disease. The commonest primary event is glaucoma, which then causes enlargement of the globe and stretching of the zonular ﬁbers, typically resulting in lens subluxation (Fig. 6.35) and the appearance of an aphakic crescent, or less commonly complete luxation (Fig. 6.36). Secondary lens luxation may also result from uveitis,54 the development of a hypermature cataract (Fig. 6.37), or severe trauma. Where lens luxation is secondary to other ocular disease, especially glaucoma, lens extraction is infrequently indicated.

240

Fig. 6.35 Lens subluxation in a dog with primary glaucoma resulting in globe enlargement and tearing of lens zonular ﬁbers.

ORBITAL AND OCULAR PAIN

Fig. 6.36 Secondary lens luxation in a dog with glaucoma and globe enlargement. The lens is within the anterior chamber and has become cataractous.

Fig. 6.37

Luxation of a hypermature cataract in a 13-year-old crossbred dog.

Efforts should ﬁrst be directed towards control of the underlying problem before considering surgical intervention.

ACUTE ANTERIOR UVEITIS AS A CAUSE OF OCULAR PAIN Anterior uveitis constitutes inﬂammation of the iris and the ciliary body.55,56 Acute uveitis can cause intense ocular pain, mainly as a result of ciliary and iris muscle spasm. Chronic uveitis is dealt with on pp. 169–174. Causes of anterior uveitis include infection (Table 6.5), trauma (Fig. 6.38), corneal insult, intraocular neoplasia, and immune-mediated disease (including

241

SMALL ANIMAL OPHTHALMOLOGY

Table 6.5

Infectious causes of uveitis. DOG

CAT

Viral

Canine adenovirus Rabies

FIP FeLV FIV ? Herpesvirus

Bacterial

Leptospirosis Borreliosis (Lyme disease) Brucellosis Miscellaneous infections (pyometra, tooth root abscess, etc.)

? Bartonella spp. Tuberculosis Miscellaneous infections

Fungal

Blastomycosis Cryptococcosis Histoplasmosis Coccidioidomycosis

Cryptococcosis Histoplasmosis Blastomycosis Coccidioidomycosis

Protozoal

Toxoplasmosis Leishmaniasis

Toxoplasmosis

Parasitic

Toxocariasis Diroﬁlariasis Angiostrongylus vasorum Migrating ﬂy larvae (ophthalmomyiasis interna)

Rickettsial

Ehrlichiosis Rocky Mountain spotted fever

Algal

Protothecosis

FeLV = feline leukemia virus FIP = feline infectious peritonitis FIV = feline immunodeﬁciency virus

the uveo-dermatologic syndrome – pp. 106–107), and lens-induced uveitis57 due to lens trauma or cataract. Less commonly it may be associated with granulomatous meningoencephalitis, hyperviscosity syndrome, or hypertension. There is a marked geographic difference in incidence of some of the infectious causes of uveitis, particularly those caused by fungi, protozoa, rickettsia, and algae. Posterior uveitis may or may not accompany anterior uveitis.

Clinical signs Acute anterior uveitis may cause combinations of the following signs:

242

• Evidence of pain – Blepharospasm, enophthalmos (active retraction of the globe), photophobia, increased lacrimation and epiphora, protrusion of the third eyelid

ORBITAL AND OCULAR PAIN Fig. 6.38 Acute traumatic uveitis in the left eye of a cat. A limbal wound has resulted in hemorrhage, iris swelling, posterior synechia formation with consequent pupil distortion, and the development of a ﬁbrin clot within the aqueous.

Fig. 6.39 Episcleral hyperemia in an English Springer Spaniel with acute-onset uveitis. The episcleral vessels are most engorged where they overlie the ciliary body.

• • • • • • • • •

Episcleral and conjunctival hyperemia (Figs 6.39 & 6.40) Miosis (constricted pupil) Aqueous ﬂare (protein) and cells in the anterior chamber (Fig. 6.40) Hypopyon (white blood cells in the anterior chamber) (Fig. 6.41) Hyphema (red blood cells in the anterior chamber) (Fig. 6.42) Corneal edema (Fig. 6.41) Deep corneal vascularization Iris swelling and vascular congestion (Fig. 6.41) Lowered IOP.

243

SMALL ANIMAL OPHTHALMOLOGY Fig. 6.40 Marked aqueous ﬂare in a 10-year-old Labrador Retriever with anterior uveitis secondary to intraocular lymphosarcoma. Moderate episcleral congestion is also present.

Fig. 6.41 Hypopyon, intraocular hemorrhage, intense iris congestion, and corneal edema in a cat with acute anterior uveitis.

With chronicity other signs may develop (see also pp. 169–174):

244

• With granulomatous uveitis, keratic precipitates may form on the corneal endothelium – especially ventrally (Figs 6.30 & 6.43) • Iris neovascularization (pre-iridal ﬁbrovascular membranes) (Fig. 6.43) • Inﬂammatory cell nodules on the iris (especially in cats) (Fig. 6.43) • Iris pigmentary changes (Fig. 6.44) • Synechiae formation (adhesions between iris and lens or cornea) (Figs 6.38 & 6.45) • Iris bombé (360° posterior synechiae with resultant bowing forward of the iris and secondary glaucoma) (Fig. 6.46)

ORBITAL AND OCULAR PAIN Fig. 6.42 An Old English Sheepdog with acute uveitis. The normally hypochromic iris of this patient is severely hyperemic and shows intra-stromal hemorrhage. In addition there is blood in the anterior chamber (hyphema).

Fig. 6.43 Iris neovascularization and iris inﬂammatory cell nests in a cat with chronic anterior uveitis.

• Secondary glaucoma, either as a result of iris bombé (see above) or resulting from pathologic changes within the drainage angle.

Diagnosis The diagnosis of anterior uveitis depends upon assessment of signalment and history (especially important as associated systemic disease may be present), and is particularly reliant upon a careful ophthalmic examination. Some signs

245

SMALL ANIMAL OPHTHALMOLOGY Fig. 6.44 A 2-year-old Labrador Retriever with cataract of the right eye and resultant lens-induced uveitis. This has led to darkening of the iris.

Fig. 6.45 Posterior synechiae (adhesions of iris to anterior lens capsule) have occurred at numerous points around the pupil margin in this Japanese Akita with uveodermatologic syndrome.

246

of acute uveitis, such as aqueous ﬂare and keratic precipitates, may be subtle and are best detected in a darkened room using a focal light source and good magniﬁcation, e.g. a slit-lamp biomicroscope. The use of tonometry is important in the assessment of suspected cases of anterior uveitis as (a) lowered IOP may be an early indicator of the disease and (b) glaucoma may develop as a complication of the underlying inﬂammation. Diagnosis of the cause of uveitis may involve extensive laboratory work-up and thorough investigation of the case for evidence of systemic disease,58–61 the latter including a full clinical examination. In many instances, however, the cause of uveitis will not be identiﬁed, despite thorough investigation.62 Numerous diseases may mimic the signs of anterior uveitis, especially where redness of the ocular coats is a feature.63 Most notably these include glaucoma

ORBITAL AND OCULAR PAIN

Fig. 6.46 Iris bombé and secondary glaucoma in a cat. The iris is extremely stretched and almost completely obliterates the anterior chamber.

(which may itself arise secondary to underlying uveitis), episcleritis, keratitis, conjunctivitis, and retrobulbar cellulitis. In addition, miosis, enophthalmos, and conjunctival vascular injection are features common to both uveitis and Horner’s syndrome (see pp. 81–82).

Management The main aims are to remove any underlying cause, control inﬂammation, and relieve pain.

Anti-inﬂammatory therapy (Table 6.6)64 Corticosteroids may be used topically and systemically in the treatment of anterior uveitis. The risks of using systemic steroids in the face of possible systemic infection should be borne in mind when treating cases of uveitis; it may be prudent in selected instances to withhold systemic steroid use until the results of laboratory investigations have been obtained. Prednisolone acetate or dexamethasone applied topically both exhibit good intraocular penetration. Surface-acting topical steroids such as prednisolone sodium phosphate and betamethasone should be avoided when treating anterior uveitis. Topical steroids will not achieve sufﬁciently high drug levels in the posterior segment to be effective in the treatment of any concurrent posterior uveitis. Non-steroidal anti-inﬂammatory drugs (NSAIDs) may also be used systemically and topically for treatment of uveitis. Topical treatment is particularly useful not only before and after intraocular surgery but also for cats, in which topical steroids carry a greater risk of inducing recrudescent herpesvirus infection than do NSAIDs. Some of the drugs available for systemic use are indi-

247

SMALL ANIMAL OPHTHALMOLOGY

cated in Table 6.6 (availability and data sheet details vary between countries). When underlying infection may be present, systemic NSAID therapy has the advantage, by comparison to systemic steroid treatment, of not compromising the patient’s immune response. In severe cases, and once infectious causes of uveitis have been eliminated, anti-inﬂammatory therapy may be supplemented with the use of immunosuppressive agents. The drug most commonly employed is azathioprine (giving 2 mg/kg q24 h for 5 days and then reducing the dose). It is important that the patient’s hematologic parameters and liver function are regularly monitored during treatment.

Mydriatic cycloplegics These agents act by (a) dilating the pupil (mydriasis) which reduces the likelihood of posterior synechiae formation and (b) decreasing iris and ciliary muscle spasm (cycloplegia) which relieves pain. Topical 1% atropine is generally used

Table 6.6 Anti-inﬂammatory drugs. Drug

Dosage

Topical

Prednisolone acetate 1% Dexamethasone 0.1%

q6 h to q4 h initially (more often in severe cases)

Systemic

Prednisolone Methylprednisolone

0.5 to 1 mg/kg/day initially (or higher doses in severe or autoimmune cases)

Topical

Ketorolac trometamol 0.5% Flurbiprofen 0.03% Diclofenac sodium 0.1% Suprofen 1%

Various human data sheet dosage schedules for perioperative use

Systemic – dogs

Carprofen Meloxicam Flunixin meglumine

2 to 4 mg/kg/day initially 0.2 mg/kg q24 h initially 0.25 to 0.5 mg/kg q24 h 3 days max. 4 mg/kg q24 h 3 days max.

Corticosteroids

Non-steroidals

Tolfenamic acid Systemic – cats

Carprofen

Ketoprofen Tolfenamic acid Meloxicam

248

2 to 4 mg/kg/day initially (long-term use is unlicensed in cats) 1 mg/kg q24 h 5 days 4 mg/kg q24 h 3 days max. 0.3 mg/kg by single injection initially (longer term oral use at a dose of 0.1 mg/kg q24 h is unlicensed)

ORBITAL AND OCULAR PAIN

q6 h initially. Where severe miosis or iris bombé is present, 10% phenylephrine may be used for its additive action. Mid-dilatation of the pupil is desirable as maximal dilatation may compromise aqueous drainage and lead to an increase in IOP. When managing uveitis cases, the dosage/frequency of medication is gradually reduced over a period of several weeks or months in order to reduce the likelihood of relapse; an episode of recrudescence can be more difﬁcult to control than the original bout of inﬂammation. Careful monitoring, including regular measurement of the IOP, is required during this period, and therapy should be adjusted as indicated.

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Schiotz tonometry conversion tables in clinically normal dogs. J. Am. Vet. Med. Assoc. 201: 1021–1025. 26. van der Linde-Sipman, J.S. (1987) Dysplasia of the pectinate ligament and primary glaucoma in the Bouvier des Flandres dog. Vet. Pathol. 24: 201–206. 27. Renwick, P.W. (2002) Glaucoma. In: Petersen-Jones, S.M. and Crispin, S. M. (eds) BSAVA Manual of Small Animal Ophthalmology, 2nd edn. Quedgeley: BSAVA Publications, pp. 185–203. 28. Ekesten, B. (1993) Correlation of intraocular distances to the iridocorneal angle in Samoyeds with special reference to angle-closure glaucoma. Prog. Vet. Comp. Ophthalmol. 3: 67–73. 29. Read, R.A., Wood, J.L. and Lakhani, K.H. (1998) Pectinate ligament dysplasia (PLD) and glaucoma in Flat Coated Retrievers. I. Objectives, technique and results of a PLD survey. Vet. Ophthalmol. 1: 85–90. 30. Bjerkas, E., Ekesten, B. and Farstad, W. (2002) Pectinate ligament dysplasia and narrowing of the iridocorneal angle associated with glaucoma in the English Springer Spaniel. Vet. Ophthalmol. 5: 49–54. 31. Cottrell, B.D. and Barnett, K.C. (1988) Primary glaucoma in the Welsh Springer Spaniel. J. Small Anim. Pract. 29: 185–199. 32. Wood, J.L., Lakhani, K.H. and Read, R.A. (1998) Pectinate ligament dysplasia and glaucoma in Flat Coated Retrievers. II. Assessment of prevalence and heritability. Vet. Ophthalmol. 1: 91–99. 33. Barnett, K.C., Sansom, J., Heinrich, C. et al. Glaucoma. In: Barnett, K.C. (ed.) Canine Ophthalmology, 1st edn. London: Saunders, pp. 99–108. 34. Barnett, K.C. and Crispin, S.M. (1998) Aqueous and glaucoma. In: Barnett, K.C. and Crispin, S.M. (eds) Feline Ophthalmology: An Atlas and Text, 1st edn. London: Saunders, pp. 104–111. 35. Wilcock, B.P., Peiffer, R.L., Jr. and Davidson, M.G. (1990) The causes of

complications of pharmacological ablation of the ciliary body for the treatment of chronic glaucoma in the dog. J. Am. Anim. Hosp. Assoc. 22: 319–326. 45. Bedford, P.G.C. (1977) The surgical treatment of canine glaucoma. J. Small Anim. Pract. 18: 713–730. 46. Bedford, P.G.C. (1989) A clinical evaluation of a one-piece drainage system in the treatment of canine glaucoma. J. Small Anim. Pract. 30: 68–75. 47. Gelatt, K.N., Brooks, D.E., Miller, T.R. et al. (1992) Issues in ophthalmic therapy: the development of anterior chamber shunts for the clinical management of the canine glaucomas. Prog. Vet. Comp. Ophthalmol. 2: 59–64. 48. Bentley, E., Miller, P.E., Murphy, C.J. et al. (1999) Combined cycloablation and gonioimplantation for treatment of glaucoma in dogs: 18 cases (1992–1998). J. Am. Vet. Med. Assoc. 215: 1469–1472. 49. Cullen, C.L. (2004) Cullen frontal sinus valved glaucoma shunt: preliminary ﬁndings in dogs with primary glaucoma. Vet. Ophthalmol. 7: 311–318. 50. Curtis, R. (1990) Lens luxation in the dog and cat. Vet. Clin. North Am. (Small Anim. Pract.) 20: 755–773. 51. Foster, S.J., Curtis, R. and Barnett, K.C. (1986) Primary lens luxation in the border collie. J. Small Anim. Pract. 27: 1–6. 52. Lazarus, J.A., Pickett, J.P. and Champagne, E.S. (1998) Primary lens luxation in the Chinese Shar Pei: clinical and hereditary characteristics. Vet. Ophthalmol. 1: 101–107. 53. Morris, R.A. and Dubielzig, R.R. (2005) Light-microscopy evaluation of zonular ﬁber morphology in dogs with glaucoma: secondary to lens displacement. Vet. Ophthalmol. 8: 81–84. 54. Olivero, D.K., Riis, R.C., Dutton, A.G. et al. (1991) Feline lens displacement: a retrospective analysis of 345 cases. Prog. Vet. Comp. Ophthalmol. 1: 239–244.

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glaucoma in cats. Vet. Pathol. 27: 35–40. 36. Miller, P.E., Schmidt, G.M., Vainisi, S.J. et al. (2000) The efﬁcacy of topical prophylactic antiglaucoma therapy in primary closed angle glaucoma in dogs: a multicenter clinical trial. J. Am. Anim. Hosp. Assoc. 36: 431–438. 37. Ward D.A. (2004) Effect of latanoprost on aqueous humor ﬂow rate in normal dogs. Proceeding of the 36th Annual Meeting of the American College of Veterinary Ophthalmologists. 38. Studer, M.E., Martin, C.L. and Stiles, J. (2000) Effects of 0.005% latanoprost solution on intraocular pressure in healthy dogs and cats. Am. J. Vet. Res. 61: 1220–1224. 39. Regnier, A. (1999) Ocular pharmacology and therapeutics: Part 2. Antimicrobial, anti-inﬂammatory agents and antiglacuoma drugs. In: Gelatt, K.N. (ed.) Veterinary Ophthalmology. 3rd edn. Philadelphia: Lippincot, Williams and Wilkins, pp. 297–336. 40. Brooks, D.E., Komaromy, A.M. and Kallberg, M.E. (1999) Comparative optic nerve physiology: implications for glaucoma, neuroprotection, and neuroregeneration. Vet. Ophthalmol. 2: 13–25. 41. Roberts, S.M., Severin, G.A. and Lavach, J.D. (1984) Cyclocryotherapy. I. Evaluation of a liquid nitrogen system. J. Am. Anim. Hosp. Assoc. 20: 823–827. 42. Roberts, S.M., Severin, G.A. and Lavach, J.D. (1984) Cyclocryotherapy: II. Clinical comparison of liquid nitrogen and nitrous oxide cryotherapy on glaucomatous eyes. J. Am. Anim. Hosp. Assoc. 20: 828–833. 43. Nasisse, M.P., Davidson, M.G., English, R.V. et al. (1990) Treatment of glaucoma by use of transscleral neodymium : yttrium aluminum garnet laser cyclocoagulation in dogs. J. Am. Vet. Med. Assoc. 197: 350–354. 44. Moller, I., Cook, C.S., Peiffer, R.L., Jr. et al. (1986) Indications for and

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55. Hakanson, N. and Forrester, S.D. (1990) Uveitis in the dog and cat. Vet. Clin. North Am. (Small Anim. Pract.) 20: 715–735. 56. Crispin, S.M. (2002) The uveal tract. In: Petersen-Jones, S.M. and Crispin, S.M. (eds) BSAVA Manual of Small Animal Ophthalmology, 2nd edn. Quedgeley: BSAVA Publications, pp. 162–184. 57. Van Der W.A., Nasisse, M.P. and Davidson, M.G. (1992) Lens-induced uveitis in dogs: 151 cases (1985–1990). J. Am. Vet. Med. Assoc. 201: 921–926. 58. Davidson, M.G., Nasisse, M.P., English, R.V. et al. (1991) Feline anterior uveitis: a study of 53 cases. J. Am. Anim. Hosp. Assoc. 27: 77– 83. 59. Hopper, C. and Crispin, S.M. (1992) Differential diagnosis of uveitis in cats. In Pract. 14: 289–297.

60. Lappin, M.R., Marks, A., Greene, C.E. et al. (1992) Serologic prevalence of selected infectious diseases in cats with uveitis. J. Am. Vet. Med. Assoc. 201: 1005–1009. 61. Lappin, M.R. and Black, J.C. (1999) Bartonella spp infection as a possible cause of uveitis in a cat. J. Am. Vet. Med. Assoc. 214: 1205–1207. 62. Massa, K.L., Gilger, B.C., Miller, T.L. et al. (2002) Causes of uveitis in dogs: 102 cases (1989–2000). Vet. Ophthalmol. 5: 93–98. 63. Petersen-Jones, S.M. (1993) Differential diagnosis of the “red eye” in small animals. In Pract. 15: 55– 64. 64. Regnier, A. (1999) Clinical pharmacology and therapeutics: antiinﬂammatory agents. In: Gelatt, K.N. (ed.) Veterinary Ophthalmology, 3rd edn. Philadelphia: Lippincot, Williams and Wilkins, pp. 308–318.

Ocular discharge Simon Petersen-Jones and Robin Stanley

7

Ocular discharge is a common clinical presentation in veterinary practice. Discharge from the eye can result from an overﬂow of tears, or epiphora, as a consequence of nasolacrimal drainage obstruction or excess production in response to irritation. It may also or be inﬂammatory in nature, and characterized as mucoid, mucopurulent, or purulent. A systematic approach is required to investigate the cause of the discharge. In this chapter, tear ﬁlm anatomy and physiology will be considered followed by methodology for routine examination of the lacrimal and nasolacrimal systems, and subsequently consideration of conditions causing ocular discharge and their management.

THE NORMAL TEAR FILM – ANATOMY AND PHYSIOLOGY The lacrimal and nasolacrimal system comprises the structures that produce tears, the tear ﬁlm itself, and those structures that drain tears from the ocular surface. The precorneal tear ﬁlm is trilaminar, with an outer lipid layer (from meibomian glands), middle aqueous layer (from lacrimal and nictitans glands), and an inner mucous layer (predominantly from conjunctival goblet cells).

Structures that produce the tear ﬁlm • Meibomian glands (lipid layer). These are positioned within the tarsal plate of the upper and lower eyelids and empty their secretions at the eyelid margin. • Lacrimal gland (aqueous layer). The lacrimal gland lies under the orbital ligament on the dorsolateral surface of the globe. The lacrimal excretory ducts (the lacrimal ducts, not to be confused with the nasolacrimal duct) open into the superior conjunctival sac. • Third eyelid gland (aqueous layer). This gland sits at the base of the third eyelid and provides a signiﬁcant contribution to the aqueous phase of the precorneal tear ﬁlm.1 Its ducts open onto the bulbar aspect of the third eyelid amongst lymphoid tissue that gives a roughened appearance to that region of the nictitans. Clinically the third eyelid gland can prolapse

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(‘cherry eye’). Prolapsed third eyelid glands should be surgically replaced to preserve glandular function. • Conjunctival goblet cells (mucous layer). Goblet cells are at highest density in the conjunctival fornices.

Function of tears The precorneal tear ﬁlm is vitally important for the health of the cornea. It provides nutrition to the normally avascular cornea and removes waste products. It also protects the cornea by washing away debris, providing some degree of buffering against noxious substances, and transporting leukocytes, immunoglobulins such as secretory IgA, enzymes, and immunoproteins. Tears also provide a smooth optical surface to the cornea and lubricate the passage of the eyelids across the eye. One of the commonest abnormalities involving the tear ﬁlm of dogs is a lack of the aqueous portion of the tear ﬁlm. This results in pathologic changes of the ocular surface (a condition known as keratoconjunctivitis sicca). Ocular disease also results from abnormalities of distribution of the tear ﬁlm (such as inadequate eyelid closure during blinking), or can result from a reduction in the lipid or mucous components of the tear ﬁlm (conditions often referred to as qualitative tear ﬁlm disorders).

Lacrimation or tearing The normal process of lacrimation or tearing occurs as follows: • A continuous function of lacrimal glands – the basal rate of lacrimation • A reﬂex action in response to stimulation (e.g. light, wind, cold, foreign body, nasal and ocular irritation or pain) – reﬂex lacrimation.

Tear drainage (Fig. 7.1) The tear drainage system consists of:

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• Nasolacrimal puncta. There are two openings into the nasolacrimal duct system in most domestic species: upper and lower. They are usually positioned in the medial aspect of the eyelids just within the eyelid margin. A failure of the punctal openings to develop, known as imperforate puncta, is seen in some puppies and is discussed further below. • Nasolacrimal canaliculi and lacrimal sac. The canaliculi are small ducts that join the puncta to the lacrimal sac. In cats, they are of clinical signiﬁcance because they can be easily scarred closed as a result of feline herpesvirus conjunctivitis. They can also be quite easily ruptured if excessive force is used to ﬂush the nasolacrimal duct. The lacrimal sac is a slight dilatation at their conﬂuence at the origin of the nasolacrimal duct. • Nasolacrimal duct. The nasolacrimal duct runs from the lacrimal sac at the medial canthus of the eye to the nasal cavity, penetrating through the lacrimal bone to open at the nasal ostium. This duct may have considerable variations in its diameter, and in some brachycephalic breeds there may be an accessory opening into the pharynx. • Nasal ostium. This is the distal opening of the nasolacrimal duct and is usually positioned ventral to the basal lamina of the maxilloturbinate scrolls. In large breed dogs it is possible to cannulate the nasolacrimal duct via the nasal ostium, allowing for a retrograde nasolacrimal duct

Lacrimal ducts Canaliculi

OCULAR DISCHARGE

Lacrimal gland

Nasolacrimal puncta

Meibomian glands Gland of the third eyelid Nasolacrimal duct Nasal ostium Fig. 7.1 Anatomy of the lacrimal and nasolacrimal system. (Reproduced with premission from Maggs, D., Miller, P. and Ofri, R. (2007) Slatter’s Fundamentals of Veterinary Ophthalmology, 4th edn. Saunders/Elsevier.)

ﬂush which may be helpful if the system cannot be ﬂushed via the nasolacrimal puncta. A proportion of the tear ﬁlm is lost from the ocular surface by evaporation; the remainder drains down the nasolacrimal duct system. At any one time a large portion of the tears is in the lacrimal lake. This can be seen with the naked eye as a meniscus at the medial and lateral canthus and where the lower eyelid margin is adjacent to the cornea. From studies in humans it is known that the entrance of tears from the lacrimal lake through the lacrimal puncta into the nasolacrimal duct system is the result of blinking, capillary attraction, and gravity. When the eyelids close the lacrimal sac walls tense, creating a vacuum within the sac, which then draws tears in as the lids open. This mechanism is called the lacrimal pump.

Examination of the tear ﬁlm A visual assessment of the tear ﬁlm forms part of every ophthalmic examination. The reﬂection of the examining light from the cornea should be clean and even. Close examination should reveal a tear meniscus between the lower eyelid margin and corneal surface. At the medial canthus there is a slightly deeper accumulation of tears (the medial canthal lake) and often at this site there is an accumulation of mucus. The Schirmer tear test is used to measure aqueous tear production (Fig. 7.2). A Schirmer tear test should be performed whenever there is any abnormal ocular discharge, or when corneal or conjunctival disease is present. The test is performed by placing standardized strips of absorbent paper between the corneal surface and the lower eyelid to measure both the basal and reﬂex tears produced in 1 min (this is known as a Schirmer tear test I; STTI). In most normal dogs there is over 15 mm of wetting and in cats more than 10 mm. This test should be performed early in the examination before adding any ﬂuid to

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SMALL ANIMAL OPHTHALMOLOGY Fig. 7.2 A Schirmer tear test being performed on a cat. The ﬁlter paper strip is positioned between the lower lid and the cornea where it stimulates lacrimation. The paper is marked with a scale and has a dye impregnated in it so the measurement can be easily read.

Fig. 7.3

Epiphora in a dog. The overﬂowing tears have stained the facial hair brown.

the eye or unduly manipulating the eye. A Schirmer tear test II is used in some instances to measure basal tear secretion (see pp. 283–284). Specialized methods can be used to assess the lipid and mucous phases of the tear ﬁlm. These are considered further on pages 298–300.

WATERY OCULAR DISCHARGE (THE WET EYE)

256

An overﬂow of tears, often known as epiphora, is a common clinical presentation. Chronic epiphora can result in unsightly tear staining of the hair ventral to the medial canthus (Fig. 7.3).

Investigating a ‘wet eye’ Complete eye examination A history of blepharospasm may be helpful in distinguishing conditions associated with ocular irritation from those due to nasolacrimal outﬂow obstruction. The adnexa, eyelid position, ocular surface, and conjunctival fornices should be examined. Conditions such as medial lower eyelid entropion, medial caruncular hairs, nasal fold irritation, and trichiasis can contribute to a watery ocular discharge. Additionally, an intraocular examination should be performed because conditions such as uveitis and glaucoma can cause ocular discharge.

OCULAR DISCHARGE

A wet eye may result from an increase in tear production (usually in response to irritation) or from inadequate drainage of tears, or a combination of the two. A careful and thorough eye examination can help to identify the cause of a watery ocular discharge.

Examination using magniﬁcation Good illumination is required; to detect some lesions that can cause ocular irritation and to examine the openings into the nasolacrimal duct system, magniﬁcation is also useful. The biomicroscope slit-lamp (expense tends to limit it to specialist use), a Welch Allyn LumiView (a headband-mounted binocular microscope which is useful as it leaves the hands free for manipulations), loupes, or a direct ophthalmoscope with a high positive diopter setting can be used. The eyelid margin should be examined for distichia and the conjunctival surface of the eyelids for ectopic cilia. The external portion of the nasolacrimal drainage apparatus, the puncta, is inspected by retracting the lid margins at the medial canthus. Abnormalities that may be detected by examining the puncta include punctal atresia, micropunctum, and abnormal punctal position. If palpation of the lacrimal sac is painful and results in the expression of exudates from the puncta, dacryocystitis should be considered.

Fluorescein dye – corneal staining and assessment of nasolacrimal drainage Fluorescein can by used to help detect corneal ulcers and also to monitor tear drainage (Jones test). To test for corneal ulceration a small drop of ﬂuorescein dye is placed in the conjunctival sac, using a ﬂuorescein-impregnated paper strip to which a drop of saline is added. Excess ﬂuorescein is ﬂushed from the ocular surface using sterile eyewash. This is important to avoid excess dye in the tear ﬁlm giving a false impression of corneal uptake of dye. In eyes with a lack of tear production copious irrigation may be required to remove the excess dye. The cornea is examined to see if there is retention of ﬂuorescein stain indicating the presence of a corneal ulcer which could be the cause of increased lacrimation. Examination using a blue light enhances the ﬂuorescence of ﬂuorescein. To evaluate nasolacrimal tear drainage ﬂuorescein is applied to the conjunctival sac and the ipsilateral nostril is examined for appearance of the ﬂuorescein dye indicating patency of the nasolacrimal duct system (Fig. 7.4). It may take several minutes before the dye appears at the nostril. Negative results do not necessarily indicate that there is an abnormality in the nasolacrimal duct

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Fig. 7.4 Fluorescein has been applied to the conjunctival sac of both eyes of this dog. The ﬂuorescein has failed to come through the right nasolacrimal duct to the nostril. The next step in investigating this problem would be to ﬂush the duct.

system; in some brachycephalics, the nasolacrimal duct can have accessory openings such that ﬂuorescein drains posteriorly and does not appear at the nostril. The back of the tongue should be examined to help identify drainage of tears to the nasopharynx.

Examination under the nictitans In any eye with evidence of irritation it is important to examine the recesses of the conjunctival fornices as well as behind the third eyelid for the presence of foreign bodies or other lesions. This is readily performed after application of a topical anesthetic and manipulation with a cotton swab or appropriate instrument.

Flushing the nasolacrimal duct system Irrigation of the nasolacrimal duct is useful to evaluate patency where a ﬂuorescein passage (Jones) test is negative. It should also be considered where there is a chronic mucopurulent ocular discharge in the presence of normal tear production because dacryocystitis is a differential for a mucopurulent discharge that is refractory to topical medication.

Equipment for examining and cannulating the lacrimal drainage system

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• Magniﬁcation, e.g. Welch Allyn LumiView, Optivisor, or loupes • Lacrimal cannulas: these can be purchased, or you can use a 20- to 22-gauge plastic sleeve from an i.v. catheter – these are easiest to use if trimmed to about 5–10 mm in length and the end bevelled • Monoﬁlament 3/0 to 2/0 nylon that can be used to cannulate the duct • Small forceps, e.g. Bishop-Harmon, to handle the eyelid • Nettleship dilators of different sizes. These can be used to dilate the puncta, and to probe the canaliculi • 5 ml syringe ﬁlled with ﬂushing solution, e.g. sterile eyewash (visualization can be improved by adding ﬂuorescein dye), or if lushing a system with dacryocystitis povidone–iodine solution (not the scrub, which contains detergent) diluted 1 : 50 with saline can be used

Technique (Figs 7.5 & 7.6) For all small dogs and cats it is preferable to perform the nasolacrimal ﬂush under sedation or a light general anesthetic. The punctal openings in these animals are quite small and could be damaged if the animal struggles. For larger dogs the system may be ﬂushed just under topical anesthesia, although, if the animal will not keep still, light sedation may be advantageous. Position the head in such a way that the nose is lower than the eye, so that the irrigating solution will run out of the nostril. A metal or plastic cannula, 20–22-gauge for dogs, or 25-gauge for cats, attached to a 5 ml syringe, is inserted into the upper punctum, and the nasolacrimal duct irrigated with sterile saline or diluted povidone–iodine. If the lower punctum is patent, a vigorous stream of saline should emerge through it. The lower punctum is then occluded with ﬁnger pressure (see Fig. 7.5). The saline stream should then exit from the nasal ostium and thus the nostril. Irrigation by cannulating the lower punctum and occluding the upper punctum (by ﬁnger pressure) is then carried out. Again, a vigorous stream should exit from the nostril. If there is resistance to ﬂushing, undue pressure should not be used as it is possible to rupture the duct or propel a foreign body that is occluding ﬂow further along the duct system.

OCULAR DISCHARGE

• Fine hemostats or needle holders that can be used to hold the nylon suture material during cannulation.

Cannulation of the nasal ostium In larger breed dogs it is often possible to cannulate and ﬂush from the nasal ostium. This can be attempted when it is not possible to ﬂush the nasolacrimal duct from the eye. The dog is anesthetized and the nasal ostium visualized using a speculum to dilate the nostrils (a vaginal speculum of the size used for small animals is suitable if the tips of the instrument are used) and a small focal light source. The nasal ostium is usually positioned on the ﬂoor of the nasal cavity (Fig. 7.7). There may be more than one opening. An irrigating cannula can be introduced into the opening, and the nasolacrimal duct ﬂushed. If required, it may be possible to cannulate the nasolacrimal duct system by introducing a piece of monoﬁlament nylon into the nasal ostium, and gently feeding this up until it emerges from the upper punctum of the eyelid. This will establish the patency of the nasolacrimal duct, after which irrigation may be carried out. Additionally, if placement of an indwelling catheter is required this can be fed over the nylon (see p. 282).

Interpreting the nasolacrimal ﬂush • Exit of saline via the non-cannulated punctum but not the nose suggests that the lacrimal canaliculi are patent but the nasolacrimal duct is blocked. • Expelling mucopurulent material from the nose or punctum suggests the presence of infection (dacryocystitis). • Saline readily exits from the nose, without resistance, but passage of ﬂuorescein has been slow or absent. This shows that the system is patent but the physiologic process involved in allowing tears to enter the duct system and drain along it is inadequate. This situation is common in breeds such as Poodles and Maltese Terriers (see below and Figs 7.3 & 7.9).

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A

B

260

Fig. 7.5 Method for testing the patency of the nasolacrimal duct system. Cannulation of the upper punctum, shown in (A) allows one to observe exit of ﬂuid (saline) from either the lower punctum or the nose. The latter is shown in (B); note that ﬁnger pressure is applied to the lower punctum to force the ﬂuid along the nasolacrimal duct. (Redrawn with permission from the Post Graduate Foundation and Ms Rosemary Craig, from Blogg, J.R. and Stanley, R.G. (1990) Discharging eye. In: Common Eye Disease, Proceedings 158. Post Graduate Committee in Veterinary Science, University of Sydney, pp. 223–236.)

OCULAR DISCHARGE

Fig. 7.6 A metal nasolacrimal cannula has been introduced into the upper canaliculus via the punctum to irrigate the nasolacrimal system.

Fig. 7.7 Forceps spreading the left nostril to expose the nasal ostium of the nasolacrimal duct. In the dog, the nasal ostium is located caudal to the opening of the external nares near the junction of the lateral wall and the ﬂoor of the nostril. It is similarly located in the cat, but, owing to the size of the external nares, it is difﬁcult to observe.

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SMALL ANIMAL OPHTHALMOLOGY

Dacryocystorhinography This technique can be used to investigate blockage of the nasolacrimal duct system. It can indicate the site of blockage and may outline any foreign bodies present. Contrast material is injected into the nasolacrimal apparatus to make the system visible on radiographs. General anesthesia is required, the upper punctum is cannulated, the lower punctum occluded, and radiographs taken immediately the contrast media is injected. Care should be taken to avoid the overﬂow of contrast media onto the face as this can obscure the view of the duct systems on the radiographs. Lateral and oblique views are recommended as in the dorsoventral view the teeth may overlie the nasolacrimal duct making it more difﬁcult to examine.

Epiphora associated with impaired tear drainage Table 7.1 indicates conditions that are associated with impaired tear drainage.

Congenital anomalies of the nasolacrimal drainage system Congenital absence of the puncta, canaliculi, and/or nasolacrimal duct results in epiphora. Golden Retrievers and English and American Cocker Spaniels are commonly affected by punctal atresia, most typically of the lower punctum. Affected puppies present with marked epiphora that is typically noted from several weeks or months of age (although the defect is developmental, epiphora is not usually noted in younger puppies). Examination of the eye with the aid of magniﬁcation reveals that the lower opening to the nasolacrimal duct is absent; usually the upper punctum is present. A cystic swelling may be evident deep to the occluded punctum.

Surgery for punctal atresia (Fig. 7.8) The patent punctum is cannulated with a 20–22-gauge cannula. Pulse ﬂushing from the patent punctum causes mucosa overlying the other canaliculus to ‘tent’. A punctum can be created in a number of ways: a #11 blade or small scissors can be used to incise through the mucosa overlying the canaliculus and ﬁne iris scissors used to create a punctum as shown in Figure 7.8; or the mucosa can be punctured with a 25-gauge needle and a Nettleship dilator used to enlarge the new opening. It is unusual for the newly created punctum to close over, but if that occurs it may be necessary to recreate the opening and place an indwelling cannula. Alternatively, gelatin plugs or punctal plugs can be inserted into the newly created punctum. Enlargement of a micropunctum A small punctum can be enlarged by dilatation with a Nettleship dilator. This probe is placed into the punctum and is gently twisted to enlarge the opening.

Correcting a misplaced punctum A misplaced punctum can be enlarged with a Nettleship dilator with the aim of improving tear ﬂow.

Tear staining syndrome (Fig. 7.9) 262

This is a common complaint in dog breeds such as Maltese Terriers and Poodles, and also in Persian cats. Animals with a white coat develop an

Epiphora – causes associated with impaired tear drainage.

Disease or lesion causing epiphora

Prominent accompanying signs and result of ﬂuorescein passage test*

Diagnostic aids

Atresia of nasolacrimal puncta

Negative ﬂuorescein passage

Examine site of nasolacrimal puncta with magniﬁcation

Micropunctum

Negative or slow ﬂuorescein passage

Examine site of nasolacrimal puncta with magniﬁcation

Displaced lower punctum

Negative or slow ﬂuorescein passage

Examine site of nasolacrimal puncta with magniﬁcation

Inadequate passage of tears into or through nasolacrimal duct system

Often associated with medial canthal entropion, prominent globe, and tight lower lid with shallow medial canthal lake and trichiasis from hairs on the caruncle

Examination of eyelid and globe positioning. It is possible to ﬂush through the duct

Blocked nasolacrimal duct

Negative ﬂuorescein passage

It will not be possible to ﬂush through the duct

Dacryocystitis

Mucopurulent ocular discharge, often profuse

Mucopurulent or purulent material can be expressed out of the lower punctum by digital pressure on the medial canthal skin over the lacrimal sac

OCULAR DISCHARGE

Table 7.1

* This category refers to signs other than epiphora

unsightly brown staining of the hair ventral to the medial canthus. This is usually a cosmetic problem and the constant wetness of the skin does not often result in a moist dermatitis. In many animals with this condition there is no obvious sign of irritation and the nasolacrimal duct system is found to be patent. It appears that the rate of tear entry into the nasolacrimal duct system is not sufﬁcient to drain the lacrimal lake rapidly enough and a tear overﬂow results. Possible contributory factors include: • Caruncular hairs acting to ‘wick’ tears onto the face • Prominent eye with a shallow lacrimal lake • Medial lower eyelid entropion – results in suboptimal positioning of the lower punctum.

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B

A

Fig. 7.8 Method of correcting punctal atresia. The upper punctum is cannulated and when ﬂushed ‘tenting’ or ballooning of the mucosa over the lower canaliculus is evident, as shown in (A). The mucosa overlying the lower canaliculus can then be opened; note that incising the mucosa with scissors, as shown in (B), is not the only means of opening the punctum.

Fig. 7.9 Epiphora in a Poodle. There is brown tear staining of the hair medial and ventral to the right eye. Fluorescein has been placed in the conjunctival sac and has run onto the tear-stained periocular hairs.

Management

264

Correction of any contributory abnormalities detected such as medial canthal entropion may be of beneﬁt. Some veterinarians advocate the use of tetracyclines, tylosine, or metronidazole given orally (generally at sub-therapeutic dosage) to reduce the brown staining. However, indiscriminate use of antibiotics for this typically cosmetic problem is not recommended.

• Acquired blockage of the nasolacrimal duct system may be due to aggregation of exudate within the duct or the presence of foreign bodies. Exudates may be due to inﬂammatory or infectious processes and grass seed foreign bodies are a common cause. • In cats obstruction of the proximal portion of the system can be the result of symblepharon formation following feline herpesvirus infection (Fig. 7.10). • Lacerations of the medial eyelids or the canthal area may involve the nasolacrimal system. Whenever possible an indwelling cannula should be kept in place until the eyelid has healed in order to preserve tear drainage. • Inﬂammatory disease in the nose or facial area such as tooth root infections, dacryocystitis, facial osteomyelitis, rhinitis, and sinusitis. • Neoplasms impinging on the nasolacrimal drainage system such as eyelid tumors involving the medial canthal region and nasal or maxillary sinus tumors.

OCULAR DISCHARGE

Decreased tear drainage: acquired problems

Creating an artiﬁcial nasolacrimal duct In animals with absence of portions of the nasolacrimal duct system or an irreversible lack of tear drainage it is possible to create an alternative tear drainage pathway. When the system is patent from the puncta to the lacrimal sac a passageway for drainage of tears from the lacrimal sac to the nasal cavity can be created (dacryocystomaxillorhinostomy) and kept patent while healing by an indwelling catheter.2 Two techniques have been described to create a tear drainage pathway from the conjunctival sac. These procedures should only be considered when epiph-

Fig. 7.10 Adhesions (symblepharon) resulting from a previous feline herpesvirus infection. The third eyelid is ﬁxed partly across the eye and the lower conjunctival fornix is partly obliterated, leading to epiphora.

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Table 7.2 Epiphora – painful or irritating conditions associated with increased tear production. Disease or lesion causing epiphora

Prominent accompanying signs*

Diagnostic aids

Trichiasis

Signs of irritation, possibly keratitis

Examine eye and adnexa with aid of magniﬁcation

Distichiasis

Variable: from no obvious signs to signs of irritation, possibly keratitis

Examine eyelid margins with aid of magniﬁcation

Ectopic cilia (see Ch. 6)

Keratitis, conjunctival hyperemia, corneal ulcer

Evert lid edge and examine with magniﬁcation

Eyelid margin lesions: injuries, inﬂammatory and neoplastic lesions

May be associated with keratitis, conjunctival hyperemia, and possibly a corneal ulcer

Evert lid edge and examine with magniﬁcation

Entropion

Signs of irritation, possibly keratitis

Assess eyelid position while animal is minimally restrained

Conjunctivitis

Superﬁcial conjunctival hyperemia

Retract lid and look for thickened conjunctiva in fornices

Irritation from third eyelid

Inﬂammatory inﬁltration of third eyelid

Examine under third eyelid for follicles, inﬁltration, or foreign body

Corneal ulcer (see Ch. 6)

Corneal edema, rough area of denuded epithelium, with chronicity corneal vascularization

Examine corneal surface with magniﬁcation, ﬂuorescein dye test, and examine under blue light

Perforating corneal wounds† (see Ch. 6)

Leakage of aqueous humor out of the wound, formation of secondary aqueous showing as strands or clots of ﬁbrin on the cornea

Apply ﬂuorescein; leaking aqueous humor will stain an intense green (Seidel test)

Acute glaucoma (see Ch. 6)

Red eye, semi-dilated pupil, increased intraocular pressure

Tonometry

Anterior uveitis (see Ch. 6)

Red eye, miotic pupil

Use oblique light to detect aqueous ﬂare

Orbital spaceoccupying lesions (see Ch. 6)

Exophthalmos

Compare position or globes from above, check degree to which globe can be retropulsed into orbit

266 * This category refers to signs other than epiphora † Epiphora in this case is an overﬂow of tears and aqueous humor

Conjunctivorhinostomy A new duct is created by making an opening into either the maxillary sinus or the nasal cavity. Polyethylene or Silastic tubing is placed into the new outﬂow tract for 6–8 weeks to keep the duct open.3–5

OCULAR DISCHARGE

ora is resulting in a clinical problem as results can be quite variable and disappointing.

Conjunctivobuccostomy A tunnel is bluntly dissected from the ventral conjunctival sac downwards until the oral mucosa can be entered between the lip and upper dental arcade. The tunnel is then cannulated with polyethylene tubing to ensure epithelialization and permanent ﬁstulization.

Epiphora associated with ocular irritation Table 7.2 lists potential causes of increased tear production due to ocular irritation or pain.

Irritation from eyelid abnormalities Abnormalities involving the contact of cilia with the ocular surface, such as distichiasis, ectopic cilia, trichiasis, and entropion, are common causes of epiphora. Other sources of irritation that cause epiphora include eyelid neoplasia, lacerations, and marginal blepharitis.

Distichiasis Distichiasis is very common in dogs. Distichia originate from follicles within or between the meibomian glands and exit from the eyelid along the eyelid margin, either through or adjacent to the meibomian gland oriﬁces (Fig. 7.11). Many dogs have distichiasis without showing clinical signs because either the distichia do not contact the ocular surface, or they are ﬁne and ﬂoat in the precorneal tear ﬁlm. In some cases where the distichia are thick and stiff, even a single distichium can irritate the eye producing epiphora, focal keratitis, and

Fig. 7.11 Distichiasis in a Shetland Sheepdog.

267

SMALL ANIMAL OPHTHALMOLOGY Fig. 7.12 Distichia at the medial lower eyelid that can be seen rubbing on the cornea. Can be a cause of epiphora and in this case a perforated corneal ulcer.

even corneal ulceration (although distichia by themselves are a rare cause of ulcerative keratitis) (Fig. 7.12). Treatment consists of destruction or removal of the offending follicles. Destruction is achieved by excision, electrolysis, or cryoepilation.6

Ectopic cilia Ectopic cilia are less common than distichia but when present they invariably cause irritation or pain. In contrast to distichiasis, corneal ulceration is a common association. They are discussed in more detail on pages 212–214.

Trichiasis

268

Trichiasis is a condition in which normally positioned hairs are misdirected to contact the cornea. Facial hair may act as an irritant in breeds such as the Pekinese, Poodle, and Lhasa Apso. Trichiasis from the nasal fold (Fig. 7.13) is common in breeds such as the Pekinese. Affected dogs often develop a medial pigmentary keratitis. Application of petroleum jelly to the hair of the nasal fold may be used temporarily to redirect the hairs that are contacting the cornea. In severely affected dogs the nasal fold can be surgically excised, either partially or completely (Fig. 7.14). Removal of nasal folds is quite straightforward: once the surgical site is clipped the fold requiring removal is obvious. Owners should be warned of the change in appearance that results. Hairs at the medial canthus that contact the cornea may be due to medial lower eyelid entropion (Fig. 7.15) or from hairs originating from the caruncle (Fig. 7.16). These abnormalities are commonest in breeds such as Lhasa Apso, Shih Tzu, and the brachycephalic breeds; discharge may be due to irritation or a ‘wicking’ effect of the hairs. A hairy caruncle can be surgically excised or the hair roots destroyed by cryoepilation. Medial canthal entropion can be treated by everting the medial lower eyelid in a similar manner to a conventional

OCULAR DISCHARGE

Fig. 7.13

Oblique view to show the corneal contact from nasal fold hair in this Pekinese.

Fig. 7.14 Surgical excision of nasal folds. The site is prepared for surgery. A preparation such as dilute povidone–iodine is used to prepare the skin – as this is close to the eye avoid detergents or alcohols that could damage the corneal surface. The entire nasal fold or a portion of the nasal fold is excised. The defect may be closed with simple interrupted sutures or a mattress suture pattern as shown in the diagram. Care must be taken to keep knots away from the eye.

entropion correction (Fig. 7.17). Some cases are better managed by a medial canthoplasty, in particular in dogs that have an overlong palpebral ﬁssure and develop a progressive medial pigmentary keratitis. For a medial canthoplasty a thin strip of the margins of the upper and lower eyelids at the medial canthus is excised and the mucosa at the medial canthus also excised (including hairbearing tissue of the caruncle). The defect is closed in a two-layer repair and will result in a narrowed palpebral ﬁssure (Fig. 7.18). Care is taken not to

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SMALL ANIMAL OPHTHALMOLOGY

Fig. 7.15 Medial lower eyelid entropion. This can result in malpositioning of the lower puncta and epiphora.

Fig. 7.16 Long caruncular hairs in a Shih Tzu. These may cause a medial keratitis and contribute to tear overﬂow.

damage the nasolacrimal puncta. This surgery should be performed with the aid of magniﬁcation and referral to an ophthalmologist is recommended.

Entropion Entropion results in contact between eyelid hair and the cornea causing irritation, lacrimation, and blepharospasm (Fig. 7.19). See pages 207–211 for further consideration of entropion. Entropion at the medial canthus typically involves the lower eyelid and is considered above (see Figs 7.15 and 7.17).

Conditions involving the third eyelid 270

Hyperplasia of the superﬁcial lymphoid tissue on the bulbar aspect of the third eyelid occurs as a non-speciﬁc response to chronic antigenic stimulation and

OCULAR DISCHARGE

A

B

C

Fig. 7.17 Correction of lower eyelid medial canthal entropion. (A) The medial lower eyelid has entropion. (B) A roughly triangular piece of skin is excised. (C) As the defect is repaired it everts the medial portion of the lower eyelid. (From Petersen-Jones, S.M. and Crispin, S.M. (eds) (2002) BSAVA Manual of Small Animal Ophthalmology, 2nd edn. Quedgeley: BSAVA Publications.)

271

SMALL ANIMAL OPHTHALMOLOGY

272

can cause mild irritation. Third eyelid deformities such as prolapse of the third eyelid gland and eversion of the third eyelid cartilage (Fig. 7.20) can also be accompanied by tearing (see p. 87).

ABNORMAL OCULAR DISCHARGE IN THE PRESENCE OF NORMAL TEAR PRODUCTION Investigation of an eye with an ocular discharge should include a complete eye examination as previously described.

Fig. 7.18 Diagram of a medial canthoplasty. (A) The affected eye has medial lower eyelid entropion and a hairy caruncle. The nasolacrimal puncta are identiﬁed and cannulated to avoid inadvertent damage during the surgery. (B & C) A strip of eyelid margin is excised from the upper lid and the incision continued around the medial canthus to include the caruncle and along the lower lid. (D & E) The defect is repaired in two layers. This results in a shortening of the palpebral ﬁssure. (From Petersen-Jones, S. M. and Crispin, S.M. (eds) (2002) BSAVA Manual of Small Animal Ophthalmology, 2nd edn. Quedgeley: BSAVA Publications.)

OCULAR DISCHARGE

Fig. 7.19 Entropion in a dog that had epiphora. Note the entropion involving the lower lateral eyelid resulting in contact of eyelid hair with the cornea.

Fig. 7.20 Scrolling of the cartilage of the nictitans leading to eversion. This can result in epiphora.

Mucoid discharge Mucus is a normal component of the tear ﬁlm. Increased mucus production may result from any ocular surface irritation. Accumulations of mucus appear as gray jelly-like discharge. When infection is involved the discharge may become mucopurulent. Some dogs, e.g. Dobermanns, have deep-set globes resulting in a deep ‘pocket’ at the medial canthus that accumulates mucous secretions (Fig. 7.21). This is a normal build-up of discharge and just requires regular cleaning. This should not be confused with conjunctivitis and medications are NOT usually required.

Mucopurulent or purulent discharge Purulent or mucopurulent discharge can result from a number of conditions.

273

SMALL ANIMAL OPHTHALMOLOGY

Fig. 7.21 Deep medial canthal pocket in a Dobermann. This tends to accumulate mucus.

Conjunctival abnormalities Signs of inﬂammation of the conjunctiva are the same as those of other tissues: vascular dilatation (hyperemia), tissue edema (chemosis), and exudation. The exudate results from vascular stasis, cellular exudation, and leakage of ﬂuid containing ﬁbrin and immunoglobulins from the involved blood vessels. According to its main component the exudate may be described as serous, mucoid, purulent, or any combination, such as mucopurulent. Conditions may be acute, subacute, or chronic. Additional changes can include conjunctival hemorrhage in severe cases and with chronicity follicle formation (the conjunctiva is rich in lymphatics). If the condition causes pruritus, alopecia and excoriation of the eyelids and surrounding skin may develop.

Investigation of conjunctival disease

274

Diagnosis of conjunctivitis is made from the history, clinical ocular examination, and the general physical examination. Laboratory investigations are only usually performed in severe infections, chronic disease, or when required to conﬁrm the diagnosis or etiology. The conjunctiva may be readily sampled for culture, collection of cells (for cytology, polymersase chain reaction tests, and immunoﬂuorescent tests), and small tissue samples (for histopathology or polymerase chain reaction tests). Samples for culture Bacterial culture in dogs with severe conjunctivitis or chronic conjunctivitis that does not respond to initial treatment should be undertaken. When sampling for bacteriology avoid contacting the eyelid skin or eyelid margin as these sites have a different bacterial ﬂora to the conjunctival sac. It is useful, when trying to assess the signiﬁcance of the results, to ﬁnd out from the laboratory how heavy the bacterial growth was. Cats are more often sampled for Chlamydophila culture or herpesvirus isolation. Transport of samples for Chlamydophila culture or virus isolation must be made in the appropriate medium. Samples for polymerase chain reaction tests Polymerase chain reaction (PCR)-based tests are becoming more widely available. They can be particularly sensitive at detecting the presence of the DNA of the target microorganism. PCR assays are available for detecting the presence of Chlamydophila and feline herpesvirus DNA.7–12 These assays require that cells or small tissue

Fig. 7.22 Conjunctival cytology smear stained with Diff-Quik (Dade Behring) showing conjunctival epithelial cells, goblet cells, and stained mucus.

OCULAR DISCHARGE

samples are collected. The laboratory conducting the assay should be contacted for advice about sample collection and transport. Conjunctival smears Investigation of conjunctival surface cytology by collecting surface smears or scrapes and staining with a Romanowski-type stain and Gram stain can be very useful13 (Fig. 7.22). It is advisable ﬁrst to clean the discharges from the eye using a sterile eyewash solution. Topical anesthesia can be used if required. Cells may be collected by a sterile swab, a cytology brush, a sterile Kimura spatula, or even the handle end (i.e. not the cutting surface) of a sterile disposable scalpel blade. The collected material is gently transferred onto a clean microscope slide so as not to damage the collected cells. Several slides should be made if different stains are to be used. Diff-Quik (Dade Behring) is a quick in-house Romanowski-type stain that is useful for cytology and indication of the presence of bacteria. When bacteria are seen on the DiffQuik-stained slide one of the other slides should be stained with Gram stain to further characterize the bacteria. Early in the disease process cytology may show inclusion bodies suggestive of Chlamydophila (cytoplasmic) or feline herpesvirus (intranuclear) and may indicate the presence of Mycoplasma spp (seen on the surface of epithelial cells). Cytology is also useful in the conﬁrmation of eosinophilic keratoconjunctivitis in cats and plasma cell inﬁltration of the third eyelid in dogs (although the appearance of the latter is usually pathognomonic). However, in conjunctivitis caused by other etiologies typically by the time smears are taken the inﬂammation is chronic with a resultant mixed inﬂammatory cell reaction that does not point to any particular etiology. Conjunctival smears may also be sent for immunoﬂuorescent antibody tests, e.g. immunoﬂuorescent antibody staining to detect canine distemper virus,14 feline herpesvirus, and Chlamydophila felis.15 Always check with the laboratory offering the service to ﬁnd out what they require for these tests for optimum results.

275

SMALL ANIMAL OPHTHALMOLOGY

Conjunctival biopsies Biopsies may be taken when more detailed histopathologic information is required. Following repeated application of a topical anesthetic over the period of a few minutes, small conjunctival biopsies may be taken. Fine forceps and sharp iris scissors can be used, taking care not to crush the tissues. It is useful to place the sample conjunctival surface uppermost onto a piece of paper before ﬁxation; this prevents it from curling up. It should be remembered that the normal conjunctival morphology differs between different portions of the conjunctival sac. Additional laboratory investigations Serology may be useful in the investigation of some cases. Titers for feline herpesvirus and Chlamydophila may be an adjunct to the previously mentioned tests, depending on the vaccination status of the cat.

Conjunctival disease in dogs There are many possible causes of conjunctivitis in dogs.

Canine conjunctivitis associated with infection (Figs 7.23 & 7.24) Conjunctivitis is characterized by irritation, hyperemia, and a mucopurulent discharge. Bacterial conjunctivitis may result either from overgrowth of bacteria normally found in the conjunctival sac or from contamination from the surroundings including transfer of organisms from other infected sites (e.g. in animals with ear or labial fold infections). Gram-positive bacteria are most commonly involved and there is often a predisposing factor that allows the bacteria to resist the ocular surface defense mechanisms and infect the tissue. Investigation of a dog with conjunctivitis should include an examination for any such predisposing factors, for example a Schirmer tear test and examining the fornix and under the third eyelid for foreign bodies such as grass awns. Most cases of conjunctivitis are self-limiting, although treatment with broadspectrum antibiotics may expedite resolution. A few cases become chronic;

276

Fig. 7.23 Chronic bacterial conjunctivitis in a dog. Coagulase-positive staphylococci and diphtheroids were present in large numbers.

OCULAR DISCHARGE Fig. 7.24 Staphylococcal blepharoconjunctivitis in a dog.

these should be re-examined for predisposing factors and sampled for bacterial culture and antibiotic sensitivity testing. Rickettsial diseases are seen in some parts of the world and subconjunctival petechial hemorrhages may be a feature, for example with ehrlichiosis and Rocky Mountain spotted fever. Viral diseases such as canine distemper and canine adenoviruses may cause chemosis and seromucoid to mucopurulent discharges. Distemper can also cause a reduced tear production. Fungal conjunctivitis is not common. In Asia parasitic conjunctivitis caused by Thelazia spp has been reported.16 Treatment Mild bacterial conjunctivitis in dogs is usually self-limiting and is generally treated by application of a broad-spectrum topical antibacterial preparation. In chronic or severe cases when cultures have been performed initial antibacterial therapy can be chosen based on the Gram staining of smears while awaiting culture and sensitivity results. Suitable broad-spectrum preparations include a ‘triple antibiotic pre-paration’ containing neomycin, polymyxin B, and either gramicidin or bacitracin. Gentamicin, tobramycin, and ciproﬂoxacin also have a broad spectrum of action against Gram-positive and -negative organisms, but are of particular use in the treatment of pseudomonal infections (often associated with progressive corneal ulcers). Where staphylococci are involved a drug such as fusidic acid (where available) can be effective. Long-term application of antibiotics in the absence of evidence of actual infection should be avoided since it may lead to antibiotic resistance or overgrowth of organisms outside the spectrum of activity of the drug.

Hypersensitivity and immune-mediated canine conjunctival disease Plasmacytic conjunctivitis (plasma cell inﬁltration of the third eyelid; plasmoma) is a chronic, probably immune-mediated, inﬂammatory condition of the exposed areas of the third eyelid conjunctiva. It may be accompanied by a seromucoid discharge. It is most prevalent in the German Shepherd Dog and

277

SMALL ANIMAL OPHTHALMOLOGY

may occur in conjunction with chronic superﬁcial keratitis – pannus (see pp. 97–99 and 166–167). The condition usually improves, and sometimes completely resolves, after treatment with topical ciclosporin or corticosteroids, although it may recur if treatment is stopped. In dogs affected with the pemphigus group of diseases, eyelid margin lesions are accompanied by a mucopurulent conjunctivitis. Dogs with atopy may present with epiphora and mild signs of conjunctival inﬂammation. Atopy is a type I hypersensitivity reaction and is initiated by inhalation of pollens, house dust, and other allergens. Follicular conjunctivitis, seen as hypertrophied lymphoid follicles scattered on the surface of the nictitans and the conjunctival fornices, occurs with chronic antigenic stimulation or even apparently chronic mechanical irritation in some cases.17 It usually affects young dogs and seems commoner in certain breeds such as the Weimaraner. The presence of multiple follicles appears to cause mild irritation and discharge even after the initial stimulus has gone. Management consists of treating any predisposing factors and then administering a topical corticosteroid preparation. If this does not relieve the irritation, debriding the follicles may be necessary. A blade used in a sideways brushing movement to scrape the follicles from the conjunctival surface followed by application of a steroid/broad-spectrum antibiotic preparation is usually curative.

Canine conjunctival neoplasia and proliferation Neoplasia of the canine conjunctiva is uncommon. Reported tumor types include melanoma, squamous cell carcinoma, papillomas, ﬁbrosarcoma, lymphosarcoma, lipoma, adenoma, histiocytoma, hemangioma, hemangiosarcoma, angiokeratomas, angioendotheliomatosis, and mast cell tumors.18 Occasionally inﬂammatory masses can develop in the perilimbal conjunctiva, most commonly this is nodular granulomatous episclerokeratitis.19

Conjunctival disease in cats Infective feline conjunctivitis

278

Feline herpesvirus infection Feline herpesvirus 1 (FHV-1) is a common cause of upper respiratory tract and ocular surface infection, typically in young cats. Sneezing, accompanied by nasal discharge and seromucoid to mucopurulent ocular discharges, typiﬁes the early stages (Fig. 7.25). There is bilateral conjunctivitis and chemosis, and in severe cases sloughing of the conjunctival epithelium may occur with resultant symblepharon formation20 (see Fig. 7.10) and there may also be corneal involvement, especially in young kittens. Secondary bacterial infection may complicate the picture. Chronic carrier states are possible, with recrudescence occurring during periods of stress. A diagnosis of FHV-1 infection may be suggested by the clinical signs (when seen, dendritic corneal ulceration is very strongly suggestive of a herpes infection) and conﬁrmed by viral isolation, immunoﬂuorescent test, or polymerase chain reaction test. The suggested treatment depends on the severity of the infection. In kittens with mild infections careful nursing and application of broad-spectrum antibiotics are all that is required. In more severe cases topically applied antiviral preparations are used. In vitro studies suggest that triﬂuridine is the most effective topical agent, followed by idoxuridine, vidarabine, bromovinyldeoxyuridine, and lastly aciclovir.21 However, clinical

OCULAR DISCHARGE

Fig. 7.25 Kitten with a unilateral conjunctivitis caused by a feline herpesvirus infection. Note the hyperemia, chemosis, and seromucoid ocular discharge.

studies have not shown any speciﬁc antiviral preparation to be superior and results in general were poor.22 Currently idoxuridine and triﬂuridine are commonly used antivirals in treating feline herpesvirus infection. Assessment of other antivirals is underway.23–25 Oral antivirals such as aciclovir and famciclovir may be safe and efﬁcacious but currently only antecdotal reports are available. Alpha-interferon has shown some efﬁcacy in human patients with ocular herpesvirus infection and has been used topically in cats with feline herpesvirus infection as an adjunctive therapy. Recently in vitro studies showed that both human and feline recombinant alpha-interferon reduced the cytopathic effect of feline herpesvirus infection.26,27 Some ophthalmologists recommend topical alpha-interferon at a dose of 25 IU/ml several times daily, although this is a much lower dose than has been used in humans and there are no published clinical trials to show its efﬁcacy. Orally applied interferon has also been used in the management of feline herpesvirus infection; a dose of 30 IU/cat given into the mouth daily for 7 days on and 7 days off in repeating cycles is suggested.28 Oral L-lysine may be useful to inhibit replication of feline herpesvirus.29 At a dose of 400 mg in food once daily L-lysine was found to reduce viral shedding in latently infected cats in response to stress.30 Chlamydophila felis infection Chlamydophila felis (previously Chlamydia psittaci) is another common pathogen of cats. It primarily causes a conjunctivitis without respiratory infection. The condition often starts unilaterally but typically becomes bilateral. It results in chemosis (Fig. 7.26) and initially a copious serous discharge which becomes mucopurulent with chronicity.31 Conjunctival lymphoid follicle formation may also be a feature of chronic disease (Fig. 7.27). In cats, Chlamydophila infections are best treated with systemic doxycycline. Doxycyline can be used to eradicate Chlamydophila from the eye as well as from the respiratory and urogenital tracts, which may be sites of

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SMALL ANIMAL OPHTHALMOLOGY

Fig. 7.26 Cat with chemosis and conjunctival hyperemia and ocular discharge as a result of a Chlamydophila felis infection.

Fig. 7.27 Cat with follicular conjunctivitis caused by chronic Chlamydophila felis infection.

280

latent infection. Azithromycin has been suggested, but in a clinical trial proved to be less efﬁcacious in clearing chronic infection than doxycycline.32 Using a topical tetracycline alone will only treat the eye, and in some cases recurrences can be expected. To eradicate Chlamydophila from carrier cats doxycycline at up to 10 mg/kg/day33 for up to 4–6 weeks32 may be required. It is important to treat all the cats in the immediate environment because latent carrier infections can occur. Mycoplasma felis and Mycoplasma gatae infection may result in epiphora, conjunctival follicle proliferation, chemosis, and pseudomembrane formation. Hypersensitivity and immune-mediated feline conjunctival disease Eosinophilic keratoconjunctivitis (see pp. 98–99) is a disease peculiar to cats (although a similar condition occurs in horses). The condition is characterized by a proliferative lesion affecting the conjunctiva and/or cornea with an adherent,

Dacryocystitis: infection of the nasolacrimal system Inﬂammation of the lacrimal sac (the part of the nasolacrimal duct lying within the orbit) is called dacryocystitis. This condition is characterized by a chronic mucopurulent ocular discharge, which is often profuse, and may also be associated with irritation and conjunctivitis. Pressing on the medial canthus of an affected animal usually elicits discomfort and displaces mucopurulent discharge from the puncta (Fig. 7.28). Always consider the possibility of an underlying dacrocystitis in patients with refractory ocular discharge. Dacryocystitis can be confused with a primary mucopurulent conjunctivitis.

OCULAR DISCHARGE

whitish, ﬂocular surface discharge.34 Characteristically eosinophils are seen in scrapings from the lesions. Feline conjunctival masses and neoplasms Neoplasia reported involving the feline conjunctiva includes squamous cell carcinoma, lymphoma, and melanoma.

Etiology Dacryocystitis is commonly the result of the presence of a foreign body in the nasolacrimal system.

Management Treatment is aimed at removing any foreign material and irrigating the system. Usually the upper punctum is cannulated and sterile saline gently irrigated through it; some of the purulent material ﬂushed out should be collected for culture and sensitivity (Fig. 7.29). Care must be taken not to force any foreign bodies into the less accessible portions of the nasolacrimal duct. Enlarging the punctal opening by cutting open the conjunctival wall of the canaliculus (one blade of a pair of iris scissors is inserted into the punctum and the canaliculus wall is cut) may facilitate removal of foreign material in the lacrimal sac.

Fig. 7.28 Dacryocystitis in an English Springer Spaniel. Mucopurulent discharge could be expressed from the nasolacrimal duct system by digital pressure over the medial canthus.

281

SMALL ANIMAL OPHTHALMOLOGY Fig. 7.29 Flushing further discharge from the lower punctum of the dog in Figure 7.28. A metal nasolacrimal cannula is in the upper punctum.

Repeated ﬂushing of the nasolacrimal system with an appropriate antibiotic solution or dilute (1 : 50) povidone–iodine solution may help control the infection. In non-responsive cases nasolacrimal catheterization is useful and has the added advantage of maintaining patency of the system. Catheterization is performed by passing monoﬁlament nylon (0 or 2/0), the end of which has been blunted in a ﬂame, from the upper punctum to the nasal ostium. Some manipulation may be required to encourage the monoﬁlament nylon to exit from the nasal ostium. Retrograde cannulation from the nasal ostium may be possible in larger dogs. Polyethylene tubing (PE 50 or PE 90) of the required length is threaded over the monoﬁlament nylon and hemostats are used to grasp the nylon at either end. Gentle traction is applied to the distal hemostat and the tubing pulled through the system. Once the nasolacrimal system is catheterized the monoﬁlament nylon is withdrawn and the ends of the tubing are sutured at either end to the skin adjacent to the medial canthus and nares. The tubing is removed after about 3 weeks. In some unresponsive cases it may be necessary to consider contrast radiographs of the nasolacrimal duct. This may help to identify the location of an obstruction. Surgical approach to the site of blockage may be required if the system cannot be cannulated.2,35

Dacryocystitis in rabbits

282

Dacryocystitis is a common and sometimes frustrating problem in rabbits. Affected rabbits present with a copious, thick, white, purulent discharge. Pasteurella spp are commonly isolated from affected rabbits.36 Topical medication is not often successful in these cases. Some instances of dacryocystitis appear to be due to an osteodystrophy and abnormal growth of the roots of the molars associated with nutritional hyperparathyroidism as a result of a low calcium diet.37,38 The roots of the teeth impinge on the nasolacrimal duct. Radiographs may be indicated to investigate the possibility of concurrent dental disease. The condition is managed by repeated ﬂushing of the nasolacrimal duct system. Antibiotic solutions can be used as the irrigating solution. When ﬂushing the nasolacrimal duct it must be remembered that

Foreign bodies Conjunctival sac foreign bodies are a common cause of ocular irritation and increased lacrimation. If the foreign body has been present for some time or has penetrated through the conjunctiva the affected animal is likely to have a chronic mucopurulent discharge. Exploration of the conjunctival sac for a discharging sinus should be performed. Signs of orbital swelling may also be present. Exploration of the orbit for a migrating foreign body can be challenging and imaging studies to accurately localize the lesion should be performed.

OCULAR DISCHARGE

rabbits have only one nasolacrimal punctum, which is located at the medial canthus between the third eyelid and the lower eyelid.

Sinus, dental, and orbital disease causing inﬂammatory discharge Retrobulbar or dental abscessation and orbital cellulitis will often cause marked conjunctival hyperemia, chemosis, and a copious mucopurulent discharge. Zygomatic salivary gland mucocele is another potential cause of orbital swelling and globe displacement. Ultrasonography, computed tomography (CT), or magnetic resonance imaging (MRI) is useful in the diagnosis and localization of orbital swellings. Ultrasound or CT-guided biopsies of affected tissue can be performed (see pp. 79–81). Extension of infection and neoplasia from the sinuses may give a similar presentation to retrobulbar abscessation. Retention mucoceles in the frontal sinus can cause erosion of the frontal bone leading to recurrent drainage of accumulated secretions via the conjunctival sac. The discharge in such cases may be profuse. Imaging studies help reach a diagnosis in such cases. Treatment is dependent on the etiology.

Other problems causing ocular discharge Keratitis, either ulcerative, proliferative, or infectious, is a common cause of ocular discharge. Problems that cause blepharitis may have conjunctival involvement. Immune-mediated diseases in dogs such as the pemphigus group and the uveodermatologic syndrome can result in mucoid to mucopurulent ocular discharge. An ocular discharge may also accompany intraocular disease.

REDUCED OR ALTERED TEAR PRODUCTION The commonest condition resulting from alterations in the tear ﬁlm is a reduction in production of the aqueous phase of the tear ﬁlm (resulting in dry eye – keratoconjunctivitis sicca, KCS). Alterations in the lipid and mucous layer can also result in ocular surface disease.

Dry eye – keratoconjunctivitis sicca (KCS) Clinical signs and diagnosis KCS in the dog is most commonly a chronic progressive disorder. It may be unilateral or bilateral. Dogs with a moderately lowered tear production may present with a chronic or recurrent conjunctivitis and minimal corneal involvement. The diagnosis is not always obvious at this stage and a Schirmer tear test (STT) should be performed on all dogs with this presentation. The normal canine STT reading is in excess of 15 mm/min39 while that of the normal feline exceeds 10 mm/min.40 If the results of the STT are not conclusive then a

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SMALL ANIMAL OPHTHALMOLOGY

Schirmer tear test II (STTII) can be performed. This test measures basal tear production. Following a regular STT (known as a Schirmer tear test I – STTI) a topical anesthetic is applied to the eye and the conjunctival sac dried with a sterile cotton-tipped applicator. A Schirmer tear test (STTI) is then performed. STTII levels should normally be one half or greater those of STTI levels. As tear production decreases, accumulations of sticky mucoid or mucopurulent discharge tend to build up (Figs 7.30 & 7.31). The discharge clings to the conjunctival fornices and corneal surface and in more severe cases may stick

Fig. 7.30 Severe KCS in a West Highland White Terrier. The corneal surface is very dry and has adherent mucopurulent discharge.

284

Fig. 7.31 Dog with KCS. Note the profuse adherent mucopurulent ocular discharge coating the ocular surface. Corneal vascularization can be visualized through the discharge.

OCULAR DISCHARGE

the eyelids together. The conjunctiva becomes hyperemic, thickened, and possibly pigmented. There is a lack of corneal luster accompanied by a variable degree of superﬁcial vascularization, pigmentation, and scarring (Fig. 7.32). Some animals also have a dry nostril on the affected side. Animals with KCS tend to exhibit signs of mild irritation or discomfort. Corneal ulceration develops in some cases, particularly those with an acute onset, and this results in increased discomfort. The ulceration may be progressive or slow to heal because the dry ocular surface is not an ideal environment for corneal healing. Some animals may even develop descemetoceles or corneal perforations (Fig. 7.33). Secondary bacterial involvement exacerbates the problem.

Fig. 7.32 Severe KCS in a West Highland White Terrier. The cornea is heavily pigmented and there is adherent ocular discharge.

Fig. 7.33 Severe KCS in a West Highland White Terrier. A deep corneal ulcer has developed and there is extensive keratitis and an adherent ocular discharge.

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SMALL ANIMAL OPHTHALMOLOGY

There is a marked breed incidence for KCS and predisposed breeds include West Highland White Terrier, Cocker Spaniel, Shih Tzu, Lhasa Apso, Cavalier King Charles Spaniel, Bull Terrier, Bulldog, Miniature Schnauzer, Dachshund, Chihuahua, and Pekinese. The frequency of KCS within each breed appears to vary from country to country. A positive correlation between age and gender on occurrence of KCS exists.41 Older dogs are more predisposed than younger ones and neutered animals are more predisposed than intact males and females. Keratoconjunctivitis sicca also occurs in the cat, albeit far less commonly. In contrast to the dog, the resultant ocular discharge tends to be less, and corneal changes develop much more slowly.

Etiology of keratoconjunctivitis sicca

286

• Glandular aplasia or hypoplasia. This results in congenital KCS. In some instances tear production can increase to normal levels suggesting that there was perhaps a delayed maturation of the glandular tissue. • Autoimmune adenitis of glandular tissue.42 The majority of cases of canine KCS probably fall into this category. Histopathologic examination of the lacrimal gland reveals break-up of glandular structure with duct dilatation and epithelial cell loss, mononuclear cell inﬁltration, and ﬁbrosis. • Trauma. KCS due to trauma may be the result of damage to the parasympathetic supply to the lacrimal glands. In some instances normal lacrimal secretion may return over 1–2 months. • Neurogenic KCS results from denervation of the tear-producing glands. Causes include trauma, infection, neoplasia, and surgical intervention. The ipsilateral nostril may also be dry. Lesions that also involve the motor branch of the facial nerve (VII) result in facial paralysis, including an inability to blink. • Iatrogenic causes include glandular damage induced by administration of sulfa drugs, e.g. sulfadiazine, sulfasalazine,43 and trimethoprim/ sulfamethoxazole.44 Although only certain dogs appear to be at risk of dry eye with sulfa drug administration, STT levels should be monitored on all dogs prescribed longer courses of sulfa drugs. Atropine and atropine-like substances reduce tear production45 and local and general anesthesia results in decreased tear volume.46 Acute KCS may therefore follow a surgical procedure where atropine and general anesthesia have been given. Etodolac administration has been reported to be associated with KCS in some dogs.47 Surgical removal of the nictitans gland as a treatment for prolapsed nictitans gland (cherry eye) has been associated with KCS later in life.48 • KCS secondary to chronic conjunctivitis with obstruction of secretory ductules. A common example of this is the older English Cocker Spaniel with upper lid entropion/trichiasis and chronic keratoconjunctivitis. Correction of the eyelid disorder, with treatment for KCS, usually leads to a marked improvement in lacrimal function. KCS in the cat sometimes follows feline herpesvirus infection. • Distemper-associated KCS.49 Distemper can cause a dacryoadenitis with resultant destruction of the glandular tissue.

Dry eye is more responsive to therapy whilst there is still some functional lacrimal and third eyelid gland tissue present. Eyes that present with an initial STT of 5 mm/min or more, and those who have had dry eye for less than 6 months, have a much better prognosis as they are more likely to respond to medical therapy. Management of KCS consists of medications to reduce immune destruction of lacrimal and nictitans glandular tissue, to stimulate tear production, to reduce ocular surface pathology, and to replace tears combined with nursing care to remove discharges. If the medical approach fails to control the condition then surgical options can be considered.

OCULAR DISCHARGE

Management of KCS

Immune modulators and anti-inﬂammatories in the treatment of KCS The topical immunomodulator ciclosporin has been used in the management of immune-mediated KCS in dogs for several years.50 In addition to modulating T-helper cells and thus reducing immune destruction of lacrimal and nictitans glandular tissue, ciclosporin also acts to stimulate tear production possibly through prolactin receptors. Tacrolimus51 and pimecrolimus52 are similar drugs that have more recently been shown to be effective in the management of KCS and have a similar mode of action to ciclosporin. Ciclosporin is available as a commercial ointment and as various preparations through compounding pharmacies while tacrolimus and pimecrolimus are available through compounding pharmacies. The preparations are initially given twice daily and will often result in an improvement in Schirmer tear test levels. In addition to the action on the lacrimal and nictitans glands their action directly on the cornea may also help to reduce the degree of keratitis in affected dogs. Topical corticosteroids have also been advocated for use in KCS and help to reduce inﬂammation in the tear-producing glands and reduce the degree of keratitis and conjunctivitis. However, in view of the risk of corneal ulceration in KCS corticosteroids should be used with care. Parasympathomimetic drugs (e.g. pilocarpine) have been used in the treatment of dry eye to stimulate tear production. They are given orally but only seem to be effective in animals with neurogenic dry eye, where presumably the glandular tissue is more responsive to the effects of parasympathomimetics due to denervation hypersensitivity. Usually pilocarpine 1% drops are mixed in food at an empirical rate of 1 to 4 drops twice daily depending on body size. Tear production should be monitored for signs of improvement and the animal observed for systemic signs of pilocarpine toxicity (hypersalivation, vomiting, diarrhea, bradycardia).

Tear substitutes Dry eye is a common problem in people so there are many different artiﬁcial tear preparations available. In selection of a tear substitute it is important to consider the severity of the dry eye, the likely duration of corneal contact time of the preparation, and the frequency of administration that is feasible for the client. Preparations come as aqueous artiﬁcial tears, gels, and ointments. The more viscous preparations tend to be of beneﬁt in animals. Common ingredients of the aqueous and gel preparations include hypromellose, polyvinyl alcohol, polyethylene glycol, and propylene glycol. More recently hylauronate-

287

SMALL ANIMAL OPHTHALMOLOGY

containing preparations have been introduced. Hylauronate is a viscoelastic agent that has a prolonged corneal contact time and seems a useful addition to the range of available products. Artiﬁcial tear ointments (such as those containing lanolin or petrolatum) are useful for veterinary patients because of their long corneal contact time. They can be applied last thing at night or when the animal is to be left untreated for a while. Many preparations contain preservatives and frequent application of preparations containing preservatives may be detrimental to the corneal epithelium. In view of this, and potential hypersensitivity to preservatives, some preparations that are preservative free (usually as single-dose preparations) or contain a ‘vanishing’ preservative are available. It may be necessary to try a few different preparations before ﬁnding one that seems to suit the individual animal the best.

Surgical options for managing dry eye disease Parotid duct transposition Parotid duct transposition is reserved for chronic KCS that has not responded to intensive medical therapy and despite treatment remains uncomfortable with progression of corneal changes. In general a parotid duct transposition should not be performed if the Schirmer tear test I level is greater than 1 or 2 mm/min. In the majority of cases it results in an improvement in comfort level and over time a reduction in the degree of corneal vascularization and pigmentation (if these changes had developed). Dogs with excessive saliva production tend to have more complications, including mineral deposits around the eyes that can result in blepharitis (Figs 7.34 & 7.35). Regular cleaning of the face and keeping the facial hair short can help to prevent the development of blepharitis. Corneal mineral deposition that results in discomfort or irritation can be more difﬁcult to manage. Topical EDTA application may help dissolve mineral deposits.

288

Fig. 7.34 A dog with KCS that has had a parotid duct transposition. Salivary deposits coat the periocular region.

OCULAR DISCHARGE Fig. 7.35 Blepharitis resulting from overﬂow of saliva in a dog that has had a parotid duct transposition.

For the eyes with excessive salivary secretions surgery can be performed to narrow the parotid duct. This is best left to those with experience in dealing with this complication. Punctal occlusion Punctal plugs are commonly used in humans who develop dry eye. The aim of a punctal plug is to impede the drainage of tears from the eye. They are made out of silicone, and are removable. In absolute dry eye they will only help by reducing the run-off of artiﬁcial tears that have been applied to the eyes. This may reduce the frequency with which artiﬁcial tears will need to be applied.53 Permanent surgical punctal closure has also been advocated. Shortening the palpebral ﬁssure Shortening the palpebral ﬁssure by medial or lateral canthal closures helps to reduce corneal exposure and improve the stability of the precorneal tear ﬁlm. Medial canthal closure can also be helpful by reducing irritation to the already dry cornea by removing the medial caruncular hairs, correcting any medial entropion that is present, and also by preventing nasal fold trichiasis when present.

Ocular surface disease resulting from inadequate distribution of the tear ﬁlm Inadequate tear ﬁlm distribution may result from the anatomic characteristics of the animal, from exophthalmos, as a result of congenital or acquired eyelid deformity, or as a result of reduced blinking due to sensory or motor deﬁcits. Factors that contribute to inadequate spreading of the tear ﬁlm include: • A wide palpebral ﬁssure can reduce effective eyelid closure, so that the spreading of the tear ﬁlm and stability of the tear ﬁlm between blinks is impaired. • It is common for brachycephalic breeds to have an overlong palpebral ﬁssure, prominent globe, and limited third eyelid movement.

289

SMALL ANIMAL OPHTHALMOLOGY

• Exophthalmos due to orbital space-occupying lesions can result in an inability to close the eyelids leading to corneal pathology. • Colobomatous congenital eyelid defects and acquired eyelid defects can also prevent adequate corneal coverage by the lids. Cicatricial contraction of eyelid wounds can lead to keratitis in a deﬁned area. Iatrogenic eyelid dysfunction is commonest as a result of overzealous entropion repair. Surgical correction of such deformity is usually successful. • A lack of blink due to impaired facial nerve (cranial nerve VII) function may be of central or peripheral origin. Lesions of the facial nerve proximal to the genu of the facial canal may also involve the parasympathetic supply to the lacrimal gland resulting in KCS in addition to potentially impaired tear distribution by the lack of movement in the outer eyelids.54 The maintenance of a healthy cornea, in the presence of facial paralysis but normal tear production, relies upon the effectiveness of the third eyelid in spreading the tear ﬁlm. Where the nictitans has limited movement (brachycephalics, exophthalmos, reduced retractor oculi muscle function, or innervation), discharge, corneal clouding, and possibly even severe ulceration will result. • Inadequate corneal sensation due to lesions involving the ophthalmic division of the trigeminal (V) nerve typically results in ulceration of the portion of cornea exposed within the palpebral ﬁssure. This is partly due to reduced blinking and therefore to inadequate spreading of the tear ﬁlm. These factors can by themselves result in a rapid break-up of the tear ﬁlm over the central cornea with dry spot formation, epithelial damage, and the development of an exposure keratopathy. They also exacerbate the effects of a reduced tear production.

Qualitative tear ﬁlm disease

290

As well as disease resulting from inadequate production of aqueous tears or inadequate distribution of the produced tears, changes in either the lipid or mucous phases of the tear ﬁlm can also cause ocular surface disease. These conditions are rarely diagnosed. A deﬁciency of goblet cells leads to instability of the tear ﬁlm.55 This results in a superﬁcial keratitis in the presence of adequate aqueous tears. There is also a notable lack of mucus associated with the ocular discharge. An assessment of the tear break-up time (BUT) will determine adequacy of tear ﬁlm mucins.56,57 The tear BUT is assessed by holding the lids open after applying ﬂuorescein to the tear ﬁlm and observing the eye under a cobalt blue light looking for the ﬁrst sign of tear break-up, which is seen as the formation of a dark spot. Normal BUT is approximately 20 s. Mucin-deﬁciency BUT is less than 5 s.55,57 Conjunctival biopsy will show markedly reduced goblet cell numbers. The fornix should be sampled as this is the region that normally has the greatest ratio of goblet cells to epithelial cells. The number of goblet cells is compared to the number of epithelial cells.56 The normal goblet cell index is 0.30, i.e. three goblet cells for every ten epithelial cells. In affected animals the index is 0.05 or less.55 Chronic eyelid disease such as marginal blepharitis and meibomian gland inﬂammation may reduce production of the lipid phase of the tear ﬁlm resulting

OCULAR DISCHARGE

in tear ﬁlm instability and ocular surface disease. Lipid layer assessment requires specialist equipment (polarized light biomicroscopy) that is not widely available but suspicion increases with lid margin disease or meibomian adenitis where acini are blocked with white oily secretion.

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screen for feline herpesvirus-1 and Chlamydophila spp. in mucosal swabs from cats. New Microbiol. 27: 287–292. 10. Stiles, J., McDermott, M., Bigsby, D. et al. (1997) Use of nested polymerase chain reaction to identify feline herpesvirus in ocular tissue from clinically normal cats and cats with corneal sequestra or conjunctivitis. Am. J. Vet. Res. 58: 338–342. 11. Dean, R., Harley, R., Helps, C. et al. (2005) Use of quantitative real-time PCR to monitor the response of Chlamydophila felis infection to doxycycline treatment. J. Clin. Microbiol. 43: 1858–1864. 12. Stiles, J., McDermott, M., Willis, M. et al. (1997) Comparison of nested polymerase chain reaction, virus isolation, and ﬂuorescent antibody testing for identifying feline herpesvirus in cats with conjunctivitis. Am. J. Vet. Res. 58: 804–807. 13. Lavach, J.D., Thrall, M.A., Benjamin, M.M. et al. (1977) Cytology of normal and inﬂamed conjunctivas in dogs and cats. J. Am. Vet. Med. Assoc. 170: 722–727. 14. Valencia, M. (1987) Contribution to the study of canine distemper. 1. Direct immunoﬂuorescence and detection of inclusion bodies in live animal smears. Medicina Veterinaria 4: 211–218. 15. Nasisse, M.P., Guy, J.S., Stevens, J.B. et al. (1993) Clinical and laboratory ﬁndings in chronic conjunctivitis in cats: 91 cases (1983–1991). J. Am. Vet. Med. Assoc. 203: 834– 837. 16. Peng, C.G. and Jiang, J.S. (1983) Treatment of ocular thelaziasis in dogs. Chin. J. Vet. Med. 9: 18–19.

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17. Glaze, M.B. (1991) Ocular allergy. Sem. Vet. Med. Surg. (Small Anim.) 6: 296–302. 18. Hendrix, D.V. (1999) Diseases and surgery of the canine conjunctiva. In: Gelatt, K.N. (ed.) Veterinary Ophthalmology, 3rd edn. Philadelphia: Lippincott, Williams & Wilkins, pp. 619–634. 19. Paulsen, M.E., Lavach, J.D., Snyder, S.P. et al. (1987) Nodular granulomatous episclerokeratitis in dogs: 19 cases (1973–1985). J. Am. Vet. Med. Assoc. 190: 1581–1587. 20. Nasisse, M.P. (1982) Manifestations, diagnosis and treatment of ocular herpesvirus infection in the cat. Comp. Cont. Educ. Pract. Vet. 4: 962–970. 21. Nasisse, M.P., Guy, J.S., Davidson, M.G. et al. (1989) In vitro susceptibility of feline herpesvirus-1 to vidarabine, idoxuridine, triﬂuridine, acyclovir, or bromovinyldeoxyuridine. Am. J. Vet. Res. 50: 158–160. 22. Stiles, J. (1995) Treatment of cats with ocular disease attributable to herpesvirus infection: 17 cases (1983– 1993). J. Am. Vet. Med. Assoc. 207: 599–603. 23. Maggs, D.J. and Clarke, H.E. (2004) In vitro efﬁcacy of ganciclovir, cidofovir, penciclovir, foscarnet, idoxuridine, and acyclovir against feline herpesvirus type-1. Am. J. Vet. Res. 65: 399–403. 24. van der Meulen, K., Garre, B., Croubels, S. et al. (2006) In vitro comparison of antiviral drugs against feline herpesvirus 1. BMC Vet. Res. 2: 13. 25. Sandmeyer, L.S., Keller, C.B. and Bienzle, D. (2005) Effects of cidofovir on cell death and replication of feline herpesvirus-1 in cultured feline corneal epithelial cells. Am. J. Vet. Res. 66: 217–222. 26. Siebeck, N., Hurley, D.J., Garcia, M. et al. (2006) Effects of human recombinant alpha-2b interferon and feline recombinant omega interferon on in vitro replication of feline herpesvirus-1. Am. J. Vet. Res. 67: 1406–1411.

27. Sandmeyer, L.S., Keller, C.B. and Bienzle, D. (2005) Effects of interferon-alpha on cytopathic changes and titers for feline herpesvirus-1 in primary cultures of feline corneal epithelial cells. Am. J. Vet. Res. 66: 210–216. 28. Stiles, J. (2000) Feline herpesvirus. Vet. Clin. North Am. (Small Anim. Pract.) 30: 1001–1014. 29. Stiles, J., Townsend, W.M., Rogers, Q.R. et al. (2002) Effect of oral administration of L-lysine on conjunctivitis caused by feline herpesvirus in cats. Am. J. Vet. Res. 63: 99–103. 30. Maggs, D.J., Nasisse, M.P. and Kass, P.H. (2003) Efﬁcacy of oral supplementation with L-lysine in cats latently infected with feline herpesvirus. Am. J. Vet. Res. 64: 37–42. 31. Sykes, J.E. (2005) Feline chlamydiosis. Clin. Tech. Small Anim. Pract. 20: 129–134. 32. Owen, W.M., Sturgess, C.P., Harbour, D.A. et al. (2003) Efﬁcacy of azithromycin for the treatment of feline chlamydophilosis. J. Feline Med. Surg. 5: 305–311. 33. Sparkes, A.H., Caney, S.M., Sturgess, C.P. et al. (1999) The clinical efﬁcacy of topical and systemic therapy for the treatment of feline ocular chlamydiosis. J. Feline Med. Surg. 1: 31–35. 34. Pentlarge, V.W. (1991) Eosinophilic conjunctivitis in ﬁve cats. J. Am. Anim. Hosp. Assoc. 27: 21–28. 35. Pope, E.R., Champagne, E.S. and Fox, D. (2001) Intraosseous approach to the nasolacrimal duct for removal of a foreign body in a dog. J. Am. Anim. Hosp. Assoc. 218: 541– 542. 36. Petersen-Jones, S.M. and Carrington, S.D. (1988) Pasteurella dacryocystitis in rabbits. Vet. Rec. 122: 512–514. 37. Harcourt-Brown, F.M. (1995) A review of clinical conditions in pet rabbits associated with their teeth. Vet. Rec. 137: 341–346. 38. Harcourt-Brown, F.M. and Baker, S.J. (2001) Parathyroid hormone,

48. Morgan, R.V. (1993) To excise or not to excise. Prog. Vet. Comp. Ophthalmol. 3: 109–110. 49. Martin, C.L. and Kaswan, R.L. (1985) Distemper-associated keratoconjunctivitis sicca. J. Am. Anim. Hosp. Assoc. 21: 355–359. 50. Kaswan, R.L., Salisbury, M.A. and Ward, D.A. (1989) Spontaneous canine keratoconjunctivitis sicca. A useful model for human keratoconjunctivitis sicca: treatment with cyclosporine eye drops. Arch. Ophthalmol. 107: 1210–1216. 51. Berdoulay, A., English, R.V. and Nadelstein, B. (2005) Effect of topical 0.02% tacrolimus aqueous suspension on tear production in dogs with keratoconjunctivitis sicca. Vet. Ophthalmol. 8: 225–232. 52. Nell, B., Walde, I., Billich, A. et al. (2005) The effect of topical pimecrolimus on keratoconjunctivitis sicca and chronic superﬁcial keratitis in dogs: results from an exploratory study. Vet. Ophthalmol. 8: 39–46. 53. Williams, D.L. (2002) Use of punctal occlusion in the treatment of canine keratoconjunctivitis sicca. J. Small Anim. Pract. 43: 478–481. 54. Scagliotti, R.H. (1999) Neuroophthalmology. In: Gelatt, K.N. (ed.) Veterinary Ophthalmology, 3rd edn. Philadelphia: Lippincott, Williams & Wilkins, pp. 1307–1400. 55. Moore, C.P. and Collier, L.L. (1990) Ocular surface disease associated with loss of conjunctival goblet cells in dogs. J. Am. Anim. Hosp. Assoc. 26: 458–466. 56. Moore, C.P., Wilsman, N.J., Nordheim, E.V. et al. (1987) Density and distribution of canine conjunctival goblet cells. Invest. Ophthalmol. Vis. Sci. 28: 1925–1932. 57. Moore, C.P. (1990) Qualitative tear ﬁlm disease. Vet. Clin. North Am. (Small Anim. Pract.) 20: 565–581.

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haematological and biochemical parameters in relation to dental disease and husbandry in rabbits. J. Small Anim. Pract. 42: 130–136. 39. Rubin, L.F., Lynch, R.K. and Stockman, W.S. (1965) Clinical estimation of lacrimal function in dogs. J. Am. Vet. Med. Assoc. 147: 946–947. 40. Veith, L.A., Cure, T.H. and Gelatt, K.N. (1970) The Schirmer tear test in cats. Mod. Vet. Pract. 51: 48–49. 41. Kaswan, R.L., Salisbury, M.A. and Lothrop, C.D. (1991) Interaction of age and gender on occurrence of canine keratoconjunctivitis sicca. Prog. Vet. Comp. Ophthalmol. 1: 93–97. 42. Kaswan, R.L., Martin, C.L. and Dawe, D.L. (1985) Keratoconjunctivitis sicca: immunological evaluation of 62 canine cases. Am. J. Vet. Res. 46: 376–383. 43. Slatter, D.H. and Blogg, J.R. (1978) Keratoconjunctivitis sicca in dogs associated with sulphonamide administration. Aust. Vet. J. 54: 444–446. 44. Morgan, R.V. and Bachrach, A. (1982) Keratoconjunctivitis sicca associated with sulphonamide therapy in dogs. J. Am. Vet. Med. Assoc. 180: 432–434. 45. Ludders, J.W. and Heavner, J.E. (1979) Effect of atropine on tear formation in anesthetized dogs. J. Am. Vet. Med. Assoc. 175: 585–586. 46. Vestre, W.A., Brightman, A.H., Helper, L.C. et al. (1979) Decreased tear production associated with general anaesthesia in the dog. J. Am. Vet. Med. Assoc. 174: 1006–1007. 47. Stiles, J. (2004) Warning of an adverse effect of etodolac. J. Am. Vet. Med. Assoc. 225: 503.

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Appendix: ophthalmic formulary B.H. Grahn and J. Wolfer

Table 1 Topical ophthalmic antibiotics and their formulations. Antibiotic

Formulation

Bacitracin, neomycin, polymyxin B

Bacitracin zinc 400 IU, neomycin sulfate 3.5 mg, & polymyxin B 5000 IU/g ointment Neomycin 3.5 mg, polymyxin B sulfate 10 000 IU, & bacitracin zinc 400 IU/g ointment Polymyxin B sulfate 10 000 IU, neomycin sulfate 5 mg, & bacitracin zinc 400 IU/g ointment

Bacitracin, neomycin

Bacitracin 500 IU & neomycin 5 mg/g ointment

Bacitracin, polymyxin B

Bacitracin 500 IU & polymyxin B 10 000 IU/g ointment

Chloramphenicol

Chloramphenicol 10 mg/g ointment Chloramphenicol 4 mg/ml solution Chloramphenicol 5 mg/ml or 25 mg/ml solution

Chlortetracycline hydrochloride

Chlortetracycline hydrochloride 10 mg/g ointment

Ciproﬂoxacin

Ciproﬂoxacin hydrochloride 3.5 mg/ml solution

Erythromycin

Erythromycin 5 mg/g ointment

Framycetin

Framycetin sulfate 5 mg/ml solution Framycetin sulfate 15 mg/g ointment

294

Fusidic acid

Fusidic acid 10 mg/ml slow-release solution

Gentamicin

Gentamicin sulfate 3 mg/ml solution

Antibiotic

Formulation Gentamicin 3 mg/g ointment

Neomycin, polymyxin B, gramicidin

Neomycin 75 mg, polymyxin B 10 000 IU, & gramicidin 0.025 mg/ml solution Polymyxin B sulfate 10 000 IU, gramicidin 0.025 mg, & neomycin sulfate 2.5 mg/ml solution

Neomycin, polymyxin B

Neomycin 3.5 mg, polymyxin B sulfate 10 000 IU/ml solution

Nitrofurazone

Nitrofurazone 2 mg/g powder

Norﬂoxacin

Norﬂoxacin 3 mg/ml solution

Oﬂoxacin

Oﬂoxacin 3 mg/ml solution

Oxytetracycline, polymyxin B

Oxytetracycline 5 mg & polymyxin B 10 000 IU/g ointment

Quixin

Levoﬂoxacin 0.5% solution

Sulfacetamide

Sulfacetamide sodium 10 mg/ml solution

APPENDIX: OPHTHALMIC FORMULARY

Table 1 continued

Sulfacetamide sodium 100 mg/g ointment Tetracycline

Tetracycline 10 mg/g ointment

Tobramycin

Tobramycin 3 mg/g ointment Tobramycin 3 mg/ml solution

Vigamox

Moxiﬂoxacin 0.5% solution

Zymur

Gatiﬂoxacin 0.3% solution

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Table 2 Topical antiviral ophthalmic medications and their formulations. Antiviral

Formulation

Aciclovir

Aciclovir 30 mg ointment

Idoxuridine

Idoxuridine 1 mg/ml solution

Triﬂuridine

Triﬂuridine 10 mg/ml solution

Vidarabine

Vidarabine 30 mg/g ointment

Table 3 Topical ophthalmic steroids and their formulations. Dexamethasone

Dexamethasone sodium phosphate 0.5 mg/g or 1 mg/g ointment Dexamethasone sodium phosphate 1.0 mg/ml solution Dexamethasone sodium phosphate 1 mg/ml suspension

Fluorometholone

Fluorometholone acetate 1 mg/ml solution Fluorometholone 1 mg/ml or 2.5 mg/ml solution Fluorometholone acetate 1 mg/g ointment

296

Medrysone

Medrysone 10 mg/ml solution

Prednisolone

Prednisolone acetate 1 mg/ml or 1.25 mg/ml solution, or 10 mg/ml suspension

Rimexolone

Rimexolone 10 mg/ml solution

Chloramphenicol 10 mg, polymyxin B sulfate 10 000 IU, & hydrocortisone acetate 5 mg/g ointment Chloramphenicol 10 mg & prednisolone acetate 2.5 mg/g ointment Framycetin sulfate 5 mg, gramicidin 0.05 mg/ml, & dexamethasone 0.5 mg/ml solution Gentamicin 3 mg/ml & prednisolone acetate 6 mg/ml suspension

Choramphenicol, prednisolone

Framycetin, gramicidin, dexamethasone

Gentamicin, prednisolone

Neomycin sulfate 3.5 mg, polymyxin B sulfate 10 000 IU, bacitracin 400 IU, & hydrocortisone acetate 10 mg/g ointment

Bacitracin zinc 400 IU, neomycin sulfate 5 g, polymyxin B 5000 IU, & hydrocortisone acetate 10 mg/g ointment

Bacitracin 400 IU, neomycin 3.5 mg, polymyxin B sulfate 10 000 IU, & hydrocortisone 10 mg/g ointment

Chloramphenicol, polymyxin B sulfate, hydrocortisone acetate

Bacitracin, neomycin, polymyxin B, hydrocortisone acetate

Bacitracin zinc 400 IU, neomycin sulfate 3.5 g, polymyxin B 5000 IU, & hydrocortisone 10 mg/g ointment

Bacitracin, neomycin, polymyxin B, hydorcortisone

Bacitracin zinc 400 IU, neomycin sulfate 5 mg, polymyxin B sulfate, 5000 IU, & hydrocortisone 10 mg/g ointment

Formulation

Antibiotic/steroid

Table 4 Ophthalmic antibiotic/steroids and their formulations.

APPENDIX: OPHTHALMIC FORMULARY

297

Formulation

Neomycin 5 mg & isoﬂupredone 1 mg/g ointment Neomycin 3.5 mg, polymyxin B sulfate 10 000 IU, bacitracin 400 IU, & hydrocortisone 10 mg/g ointment Neomycin 3.5 mg, polymyxin B sulfate 10 000 IU, & hydrocortisone 10 mg/g ointment Neomycin 3.5 mg, polymyxin B sulfate 10 000 IU, bacitracin 400 IU, & hydrocortisone acetate 10 mg/g ointment Neomycin 3.5 mg, polymyxin B sulfate 6000 IU, & dexamethasone 1 mg/ml solution

Neomycin, isoﬂupredone

Neomycin, polymyxin B, bacitracin, hydrocortisone

Neomycin, polymyxin B sulfate, hydrocortisone

Neomycin, polymyxin B, bacitracin, hydrocortisone acetate

Neomycin, polymyxin B, dexamethasone

Neomycin sulfate 3.5 mg, polymyxin B sulfate 10 000 IU, & dexamethasone 1 mg/ml solution

Neomycin sulfate 3.5 mg, polymyxin B sulfate 6000 IU, & dexamethasone 1 mg/g ointment

Neomycin 3.5 mg, polymyxin B 10 000 IU, & dexamethasone 1.0 mg/g ointment

Gentamicin 3 mg & betamethasone 1 mg/ml solution

Gentamicin 3 mg/ml & prednisolone acetate 10 mg/ml ointment

SMALL ANIMAL OPHTHALMOLOGY

Gentamicin, betamethasone

Antibiotic/steroid

Table 4 continued

298

Oxytetracycline hydrochloride 5 mg/ml & hydrocortisone acetate 15 mg/ml suspension Sulfacetamide sodium 10 mg/ml & ﬂuorometholone 1 mg/ml solution Sulfacetamide sodium 10 mg/ml & prednisolone acetate 2 mg/ml solution

Oxytetracycline hydrochloride, hydrocortisone acetate

Sulfacetamide sodium, ﬂuorometholone

Sulfacetamide, prednisolone

Tobramycin, dexamethasone

Neomycin 3.5 mg, polymyxin B sulfate 10 000 IU, & ﬂumethasone 0.10 mg/ml solution

Neomycin, polymyxin B sulfate, ﬂumethasone

Tobramycin 3 mg & dexamethasone 1 mg/ml suspension

Tobramycin 3 mg & dexamethasone 1 mg/ml solution

Tobramycin 3 mg & dexamethasone 1 mg/g ointment

Sulfacetamide sodium 10 mg/ml & prednisolone acetate 2.5 mg/ml solution

Sulfacetamide sodium 10 mg/ml & prednisolone acetate 5 mg/ml solution

Neomycin 3.5 mg, polymyxin B sulfate 10 000 IU, & prednisolone acetate 5 mg/ml solution

Neomycin 3.5 mg & dexamethasone 1 mg/ml solution

Neomycin 3.5 mg & dexamethasone 0.5 mg/g ointment

Neomycin, polymyxin B, prednisolone

Neomycin, dexamethasone

APPENDIX: OPHTHALMIC FORMULARY

299

SMALL ANIMAL OPHTHALMOLOGY

Table 5 Topical non-steroidal ophthalmic medications and their formulations. Medication

Formulation

Flurbiprofen

Flurbiprofen 0.3 mg/ml solution

Ketorolac

Ketorolac tromethamine 5 mg/ml solution

Diclofenac

Diclofenac sodium 1 mg/ml solution

Table 6 Topical anti-glaucoma medications and their formulations. Medication

Formulation

Apraclonidine

Apraclonidine hydrochloride 5 mg/ml or 10 mg/ml solution

Betaxolol

Betaxolol hydrochloride 2.8 mg/ml or 5 mg/ml solution Betaxolol hydrochloride 2.5 mg/ml suspension

300

Brimonidine

Brimonidine tartrate 2 mg/ml solution

Brinzolamide

Brinzolamide 10 mg/ml solution

Demecarium bromide

Demecarium bromide 1.25 mg/ml or 2.5 mg/ml solution

Dipivefrine

Dipivefrine hydrochloride 1 mg/ml solution

Dorzolamide

Dorzolamide hydrochloride 20 mg/ml solution

Echothiophate iodide

Echothiophate iodide 0.3 mg/ml, 0.6 mg/ml, 1.25 mg/ml, or 2.5 mg/ml solution

Epinephrine

Epinephrine 5 mg/ml, 10 mg/ml, or 20 mg/ml solution

Epinephryl

Epinephryl borate 5 mg/ml or 10 mg/ml solution

Isoﬂurophate

Isoﬂurophate 0.25 mg/ml solution

Latanaprost

Latanaprost 50 μg/ml solution

Levobunolol

Levobunolol hydrochloride 2.5 mg/ml or 5 mg/ml solution

Lumigan

Bimatoprost 0.03% solution

Physostigmine

Physostigmine sulfate 0.25% ointment

Medication

Formulation

Pilocarpine

Pilocarpine hydrochloride 2.5 mg/ml, 5 mg/ml, 10 mg/ml, 20 mg/ml, 30 mg/ml, 40 mg/ml, 50 mg/ml, 60 mg/ml, 80 mg/ml, or 100 mg/ml solution Pilocarpine hydrochloride 40 mg/ml gel

Pilocarpine, epinephrine

Pilocarpine 10 mg/ml, 20 mg/ml, 30 mg/ml, 40 mg/ml, or 60 mg/ml & epinephrine 5 mg/ml solution

Timolol maleate

Timolol maleate 2.5 mg/ml or 5 mg/ml solution

Timolol, pilocarpine

Timolol maleate 5 mg/ml & pilocarpine hydrochloride 20 mg/ml or 40 mg/ml solution

Travatan

Travoprost 0.004% solution

Xalacom

Latanaprost/timolol (0.5%)

APPENDIX: OPHTHALMIC FORMULARY

Table 6 continued

Table 7 Miscellaneous topical medications including tear stimulants, mydriatics, miotics, anesthetics, and mast cell stabilizers and their formulations. Medication

Formulation

Atropine

Atropine sulfate 5 mg/ml or 10 mg/ml solution Atropine sulfate 10 mg/g ointment

Carbachol

Carbachol 0.1 mg/ml or 15 mg/ml solution

Cyclopentolate

Cyclopentolate hydrochloride 5 mg/ml, 10 mg/ml, or 20 mg/ml solution Cyclopentolate hydrochloride 2 mg/ml & phenylephrine hydrochloride 10 mg/ml solution

Ciclosporin A

Ciclosporin A 2 mg/g ointment

Homatropine

Homatropine bromide 20 mg/ml or 50 mg/ml solution Homatropine 20 mg/ml or 50 mg/ml solution

Lodoxamide

Lodoxamide 1 mg/ml solution

Olaptadine

Olaptadine nitrate 1 mg/ml solution

Phenylephrine

Phenylephrine hydrochloride 25 mg/ml solution Phenylephrine hydrochloride 1.2 mg/ml or 25 mg/ml solution

301

SMALL ANIMAL OPHTHALMOLOGY

302

Table 7 continued Medication

Formulation Phenylephrine hydrochloride 50 mg & tropicamide 8 mg/ml solution

Proparacaine

Proparacaine hydrochloride 5 mg/ml solution

Sodium chloride

Sodium chloride 50 mg/ml solution

Tropicamide

Tropicamide 5 mg/ml or 10 mg/ml solution

Tropicamide, hydroxyamfetamine

Tropicamide 2.5 mg/ml & hydroxyamfetamine hydrobromide 10 mg/ml solution

Index

A Abscesses corneal, 103 eyelid, 211 retrobulbar/orbital, 80, 205–206 Abyssinian cat, 135, 144, 183, 184, 185 Acetazolamide, 236 Aciclovir, 56, 226, 296 Adenine arabinoside, 54 Adenocarcinoma, uveal, 106–107 Adenoma, uveal, 106–107 Adhesions, intraocular see Synechiae Adrenergic agents, 59 Adrenergic antagonists, 59–60 Afghan Hound, 179 Age, 116 Akita, 135 Alaskan Malamute, 134, 145 Alopecia, 76 Alpha-adrenergic agonists, 59 American Bulldog, 140 American Cocker Spaniel cataracts, 178, 180 punctal aplasia, 262 retinal disorders, 135, 136, 137, 183 American Eskimo Dog, 137 Ametropia, 26 Aminoglycosides, 54 Amlodipine besylate, 111 Amoxicillin, 55–56 Ampicillin, 55–56 Anatomy, ocular, 4–12 Angiography, ﬂuorescein, 36, 40–45, 125 Angle, iridocorneal see Iridocorneal angle Anisocoria, 108, 123 Ankyloblepharon, 85

Anophthalmia (anophthalmos), 1, 125–127 Anterior chamber, 7 abnormal appearances, 77, 103–108 embryology, 4 hemorrhage see Hyphema mass lesions, 77, 106–108 normal appearance, 71 Anterior segment dysgenesis (Peter’s anomaly), 4, 5 Anterior uvea abnormal appearances, 103–108 tumors, 106–108 Anterior uveitis, 105 acute, 105, 241–249 clinical signs, 242–245 diagnosis, 245–247 management, 247–249 chronic, 105, 169–174 corneal edema, 93–94 epiphora, 266 keratitic precipitates (KPs), 101 see also Uveitis Anti-glaucoma medications see Ocular hypotensive medications Anti-inﬂammatory medications, 56–58 anterior uveitis, 247–248 keratoconjunctivitis sicca, 287 Antibiotic/steroid combination preparations, 53, 297–299 Antibiotics, 53–56, 297–299 conjunctivitis, 277 corneal ulcers, 221–222 subconjunctival, 52, 55 systemic, 53, 55–56 tear staining syndrome, 264

303

INDEX

304

topical, 53–55, 294–295 triple preparations, 54, 294, 295 Antifungals, 55, 56 Antihistamines, 57 Antimicrobials, 53–56 subconjunctival, 55 systemic, 55–56 topical, 53–55, 294–296 Antioxidants, 182 Antiviral agents feline herpes virus infections, 226, 278–279 systemic, 56 topical, 54–55, 296 Aphakia, 127, 182 Appearance, ocular, 67–115 abnormal, 75–113 normal, 67–75 Apraclonidine, 59, 300 Aqueous (humor), 9, 228 cytology, 19 drainage procedures, 237 ﬂare, 243, 244 normal appearance, 71 Arcus lipoides corneae, 101, 168 Artiﬁcial tears, 62–63, 287–288 Aspirin, 58 Asteroid hyalosis, 111–112 Astigmatism, 27, 29 Atopy, 278 Atropine, 61, 301 ocular side-effects, 118, 286 subconjunctival, 52, 61 uveitis, 248–249 Australian Cattle Dog, 137 Australian Shepherd Dog, 136, 137, 142 Australian Stumpy Tail Cattle Dog, 137 Azalide, 152 Azathioprine, 173, 248 Azithromycin, 280 B Bacitracin, 294, 297, 298 Bacterial infections, 53–54, 55–56 Basenji, 127, 142 Beagle, 136, 178 Bedlington Terrier, 136 Belgian Sheepdog, 179 β-adrenergic blockers (beta-blockers), 59–60, 236 Betamethasone, 58, 298 Betaxolol, 59–60, 300 Bimatoprost, 235, 300 Biochemistry, ocular, 4–12

Biometry, ultrasonic, 32–33, 35 Biomicroscope, slit-lamp, 25 Biopsy, 17, 276 Blepharitis, 85–86, 211, 212 after parotid duct transposition, 288, 289 tear ﬁlm problems, 290–291 Blepharoplasty, everting, 209, 210 Blepharospasm, 47 Blindness see Visual impairment Blinking, 69 Blood hyperviscosity, 132 Blood–ocular barrier, 53 Bloodhound, 68 Border Collie, 137, 140, 142 Boston Terrier, 94–95, 168–169, 178, 180 Boxer ulcers, 16, 220–221 Brachycephalic dogs, 67, 69 corneal pigmentation, 95, 166 corneal ulceration, 215 nasal fold trichiasis, 214–215 tear ﬁlm problems, 289 Brain tumors, 194–195 Brainstem tumors, 195 Breed, 116 Briard, 137, 146–147, 186 Brimonidine, 59, 300 Brinzolamide, 60, 300 Bromovinyldeoxyuridine, 54 Bull Mastiff, 134, 137, 185–186 Bullous keratopathy, 95, 169, 231 Buphthalmos, 75–79, 174, 175, 232 C Cairn Terrier, 92, 93 Calcareous corneal degeneration, 101, 102, 217, 218 Calcium channel blockers, 111, 236 Canine adenovirus (CAV 1) infections, 93, 94, 277 Canine herpesvirus-1, 226 Carbachol, 301 Carbonic anhydrase inhibitors, 236 systemic, 53, 60, 236 topical, 60, 236 Cardigan Welsh Corgi, 133, 137, 144 Carprofen, 58, 248 Caruncular hairs, 215, 268, 270 Cataracts, 13, 108–110, 175–182 congenital, 128, 176–177 developmental, 176, 177 diabetic, 10, 181 electroretinography, 124 hereditary, 176–177, 178–180

Chronic superﬁcial keratitis (CSK) (pannus), 98, 166–167 Ciclosporin, 62, 98, 287, 301 Cidofovir, 55, 61, 237 Cilia, 6 abnormalities, 212–215 ectopic, 212, 213–214, 266, 268 Ciliary body, 7, 9 destructive surgery, 237 embryology, 1 Ciliary cleft, 27, 29, 71 Ciliary ganglion, 11 Ciliary muscle, 9 Ciproﬂoxacin, 294 Clinical basic science, 1–13 Closantel, 152 Clotrimazole, 55 Coagulopathies, 151 Cocaine, 62 Collie breeds, 126, 127, 142, 186 Collie eye anomaly (CEA), 131, 142–144 DNA-based tests, 137–139 Colobomas, 1, 126, 128 eyelid, 84 iris, 103, 104 posterior segment, 142, 143 Combination medications, ﬁxed ratio, 53, 297–299 Compliance, owner, 50–51, 52 Computed tomography (CT), 33, 205 Computerized topography of cornea, 29 Cone–rod dystrophy, 133, 146 Congenital disease/malformations, 116, 117, 125–147 Congenital retinal dystrophy (RPE65 gene defect), 137, 146–147 Conjunctiva, 8 abnormal appearances, 76 biopsies, 276 bulbar, 7, 69, 70 cytology, 17, 19, 275 diagnostic stains, 16–17 goblet cells, 254, 290 hyperemia, 243 masses/neoplasia, 76, 92–93, 278, 281 normal appearance, 69–70 palpebral, 5, 7, 69, 70 pedicle grafts, 222, 224–226 redness/hyperemia, 76, 89 sampling methods, 17–19, 274–276 swelling (chemosis), 76, 89, 91 Conjunctivitis, 89, 274–281 allergic (hypersensitivity), 57, 277–278, 280–281

INDEX

hypermature, 175–176 immature, 175 incipient, 175 lens-induced uveitis, 173, 177–181 lens luxation, 240, 241 mature, 175 in microphthalmia, 126–127, 177 nuclear, 176 pulverulent, 176 secondary, 172, 181, 232 senile, 176 surgical techniques, 182 toxic, 181 traumatic, 181 treatment, 181–182 Cavalier King Charles Spaniel, 128, 129, 136, 177 Cefazolin, 221 Central blindness, 162–164 Central nervous system (CNS) disorders causing blindness, 119, 162–164, 193–194 malformations causing blindness, 147 tumors, 195 Central progressive retinal atrophy (CPRA) see Retinal pigment epithelial cell dystrophy Central visual pathways, 10–12 Cephalosporins, 55–56 Chalazion, 86 Chemosis (conjunctival swelling), 76, 89, 91 Cherry eye see Nictitans gland prolapse Chesapeake Bay Retriever, 138, 180 Chihuahua, 94–95, 168–169 Chinese Crested, 138 Chlamydophila felis (Chlamydia psittaci) conjunctivitis, 279–280 diagnosis, 274, 275, 276 treatment, 54, 279–280 Chloramphenicol, 54, 294, 297 Chlorochine, 152 Chlortetracycline, 294 Cholinesterase inhibitors, 59 Chorioretinitis, 172, 191–192 differential diagnosis, 186, 192 retinal detachment, 154, 155 Choristoma, epibulbar, 84 Choroid, 4 Choroidal hypoplasia, 142–143 Choroiditis chronic, 169–174 sequelae, 172 Chow Chow, 209

305

INDEX

306

bacterial, 53–54, 276–277, 279–280 cats, 278–281 chronic, 68, 126, 166, 286 differential diagnosis, 173 dogs, 276–278 epiphora, 266 feline herpetic see Feline herpes virus 1 (FHV-1) infection follicular, 278, 280 immune-mediated, 277–278, 280–281 infectious, 276–277, 278–280 investigation, 274–276 membranous/ligneous, 92 in microphthalmia, 126 phthisis bulbi, 165 plasmacytic (plasmoma), 88–89, 167, 277–278 Conjunctivobuccostomy, 267 Conjunctivorhinostomy, 267 Contact lenses, 123–124, 182 Cornea, 8–9 abnormal appearances, 77, 93–103 abscesses, 103 anatomy, 7, 8 calcareous degeneration, 101, 102, 217, 218 chronic diseases causing blindness, 165–169 computerized topography, 29 contour alterations, 77, 102–103 cytological examination, 19 diagnostic stains, 16–17 embryology, 4 foreign bodies, 223–226 inclusion cysts, 103 lacerations, 103 lipid deposition, 99–101, 168, 217, 218 normal appearance, 70–71 penetration of topical medications, 51 perforation, 222, 223, 225, 266 pigmentation, 95–97, 166 sequestrum, 95–97 wound healing, 8–9 wounds, 223–226 Corneal curvature, 29, 71 Corneal edema, 93–95, 168–169 acute uveitis, 243, 244 chronic uveitis, 171 differential diagnosis, 149, 173 glaucoma, 93–94, 174, 230–231 ulcer development, 215, 217 Corneal endothelial dystrophy, 94–95, 168–169 corneal ulcers, 215, 217

Corneal endothelium, 30, 71 deposits, 101–102 dysfunction, 168–169 Corneal epithelial basement membrane disease, 215 Corneal epithelial defects see Corneal ulcers Corneal epithelium, 16 Corneal facet, 103 Corneal grafts, 169, 223 conjunctival pedicle ﬂap, 222, 224–226 Corneal lipid dystrophy, 99–100, 168 Corneal opacities, 77, 93–102 congenital, 93 Corneal stroma, 8, 71 Corneal (crystalline) stromal dystrophy, 99–100, 101, 167 Corneal ulcers, 103, 215–223 deep, 221–223, 224–225 dendritic, 226, 227 epiphora, 266 feline herpesvirus, 226, 227 glaucoma, 174, 175, 231 indolent or non-healing, 220–221 investigation, 16, 217–219 keratoconjunctivitis sicca, 285 management, 219–223 melting, 54, 221–222 ruptured, 222, 223, 225 simple (superﬁcial uncomplicated), 53– 54, 219 superﬁcial chronic (boxer ulcers), 16, 220–221 Corneal vascularization, 77, 97–99 acute uveitis, 243 chronic glaucoma, 232, 233 Corticosteroids, 297–299 antibiotic combination preparations, 53, 297–299 chronic superﬁcial keratitis, 98 keratoconjunctivitis sicca, 287 subconjunctival, 52–53, 57–58 systemic, 53, 58 topical, 56–57, 296 uveitis, 247, 248 Cotton ball test, 120 Cranial nerves, 119 Cromolyn sodium, 57 Crystalline stromal dystrophy, 99–100, 101, 168 Culture, microbiological, 17–20, 274 Cushing’s disease, 101 Cyclitic membranes, 172 Cyclitis see Anterior uveitis

D Dacryocystitis, 263, 281–283 diagnosis, 257, 258, 259 management, 281–282 in rabbits, 282–283 Dacryocystomaxillorhinostomy, 265 Dacryocystorhinography, 21, 33, 262 Dark room examination, 47–48 Day blindness see Hemeralopia Dazzle reﬂex, 121 Demecarium bromide, 59, 236, 300 Dental disease, 282, 283 Deracoxib, 58 Dermoid conjunctival, 92 epibulbar, 84, 85 Descemetocele, 8, 103, 215 treatment, 222–223 Descemet’s membrane, 4, 8, 71 breaks in see Haab’s striae Dexamethasone, 248, 296, 297 systemic, 58 topical, 56–57, 298–299 Diabetes mellitus, 10, 116, 181 Diagnostics, 14–49 advanced, 25–38 basic, 14–25 Diamond eye, 68, 209 Dichlorphenamide, 60, 236 Diclofenac, 57, 248, 300 Diff-Quik® stain, 219, 275 Diltiazem, 236 Diopters, 28 Dipivefrine, 59, 300 Discharge, ocular, 47, 253–293 mucoid, 273 mucopurulent/purulent, 273–283 with normal tear production, 272–283 watery, 256–272 Distemper, 163, 277, 286 Distichiasis, 212, 266, 267–268 DNA-based tests, 137–140 Dobermann Pinscher, 111, 128, 129–130, 131, 273, 274 Dolicocephalic dogs, 67 Doll’s head reﬂex, 203–205 Dorzolamide, 60, 236, 300 Dorzolamide–timolol, 60

Doxycycline, 279–280 Drugs see Medications Dry eye see Keratoconjunctivitis sicca E Early retinal degeneration (erd), 133, 145 Echothiophate iodide, 59, 300 Ectropion, 85 Ectropion uveae, 73 Ehrlichiosis, 277 Electro-oculogram (EOG), 34–35 Electrophysiology, 33–36, 124–125 Electroretinography (ERG), 33–36, 37– 39, 124–125 Embryology, 1–4 Emmetropia, 26, 29 Emulsions, 51 Encephalitis, 163–164 English Cocker Spaniel, 127, 128, 262 atonic entropion/trichiasis, 209–211 retinal disorders, 135, 138, 183 English Setter, 140, 187 English Springer Spaniel, 136, 141 Enophthalmos, 76, 81–82 Enroﬂoxacin, 118, 152 Entlebucher Sennenhund, 138 Entropion, 85, 207–211 atonic, 209–211 cicatricial, 209 epiphora, 266, 270, 273 management, 208–209, 210 medial lower eyelid, 263, 264, 268–270, 271 Enucleation, 237 Eosinophilic keratoconjunctivitis, 98–99, 280–281 Eosinophilic myositis, 207 Epinephrine, 59, 61–62, 300, 301 Epinephryl, 300 Epiphora, 87, 253, 256–272 impaired tear drainage, 262–267 investigations, 257–262 ocular irritation, 267–272 Episcleral injection/hyperemia, 47, 89, 91 acute anterior uveitis, 243, 244 glaucoma, 174, 231–232 Episcleritis, 89–92, 148–149 Episclerokeratitis, nodular granulomatous, 278 Erythromycin, 294 Esotropia, congenital, 83 Ethoxzolamide, 236 Ethylenediamine tetra-acetic acid (EDTA), 101

INDEX

Cyclodestructive surgery, 237 Cyclopentolate, 301 Cycloplegia, 61 Cycloplegics, 61–62, 248–249 Cytology, 17–20

307

INDEX

308

Etodolac, 58, 286 Evisceration, 237 Examination eye see Ophthalmic examination patient, 118–125 Exophthalmos, 76, 79–81 brachycephalic dogs, 67 diagnostic evaluation, 20, 31, 32 painful, 203–205 tear ﬁlm problems, 290 Exposure keratopathy, 79, 87 chronic glaucoma, 174, 175 corneal ulceration, 215 Extraocular polymyositis, 80–81 Eyelashes see Cilia Eyelids, 5–6 abnormal appearances, 76, 84–87 abnormal position, 207–211 abscessation, 211 acquired lesions, 85–87 coloboma, 84 congenital/neonatal conditions, 84–85 defects causing tear ﬁlm problems, 290–291 fusion, 85 lacerations, 85, 265 normal appearance, 67–69 painful/irritating disorders, 207–215, 266, 267–270 skin scrapings, 17 swellings/masses, 76, 86 tumors, 86 see also Third eyelid F Facial nerve paralysis, 86–87, 215, 286, 290 Famciclovir, 55, 56 Feline central retinal degeneration (FCRD), 188–189 Feline herpes virus 1 (FHV-1) infection, 278–279 corneal ulcers, 219, 220 diagnosis, 274–275, 276, 278 keratitis, 99, 226, 227 symblepharon, 92, 265 treatment, 54–55, 56, 278–279 visual impairment, 116 Feline infectious peritonitis (FIP), 163, 164 Feline leukemia virus, 108, 170 FHV-1 see Feline herpes virus 1 Fine needle aspiration, 17, 19–20, 205 Finnish Lapphund, 138

Fixatives, tissue, 12 Flumethasone, 299 Flunixin meglumine, 58, 248 Fluorescein angiography, 36, 40–45, 125 corneal ulcer staining, 16, 216, 217–219 nasolacrimal drainage assessment, 257–258 stain, 16, 63 Fluorometholone, 296, 299 Fluoroquinolones, 54 Flurbiprofen, 57, 248, 300 Focal illumination, 14–15 Foreign bodies anterior chamber, 106 conjunctival sac, 283 corneal, 223–226 nasolacrimal duct system, 265, 281 orbital, 203 Formulary, 294–302 Foscarnet, 55 Framycetin, 294, 297 Fundus examination, 21–22, 23, 25, 48 normal appearances, 22, 23, 73–75 photography, 36, 40 Fungal infections, 55, 56, 277 Fusidic acid, 54, 277, 294 G Ganciclovir, 54 Gatiﬂoxacin, 295 Gaze, changes in primary, 83–84 Gene therapy, 146–147 Genetic (DNA-based) tests, 137–140 Gentamicin, 54, 237, 294–295 intravitreal injections, 61 steroid combinations, 297–298 German Shepherd, 98, 167, 178, 277–278 German Shorthaired Pointer, 134, 138, 145 Glaucoma, 227–237 acute, 148–149, 230–232, 234, 266 buphthalmos, 75–79, 174 chronic, 174–175, 232–234 clinical signs, 230–234 corneal edema, 93–94, 174, 230–231 gonioscopic evaluation, 26, 27, 28, 29 Haab’s striae, 75, 78 lens luxation, 240, 241 management, 234–237 medical therapy see Ocular hypotensive medications narrow angle see Goniodysgenesis

H Haab’s striae, 75, 78, 174, 232 ‘Haw’s’ syndrome, 87 Health, general, 116–117 Hemeralopia, 118, 145 Hemorrhage anterior chamber see Hyphema intralenticular, 131, 132, 150 intraocular, 149–151 Hepatic encephalopathy, 193–194 Herpes virus, feline see Feline herpes virus 1 Heterochromia irides, 72, 126 Heterochromia iridis, 72 History, ophthalmic, 116–117 Homatropine, 301 Hordeola, 86

Horner’s syndrome, 12, 81–82 distemper, 163 sympathomimetics, 61, 62 Hotz–Celsus procedure, 209, 210 Hyaloid artery, 1, 128 persistent (PHA), 128–129 Hyaluronate solutions, 62–63, 287–288 Hydrocephalus, 147 Hydrocortisone, 57, 297, 298, 299 Hydrophthalmos, 232 see also Buphthalmos Hydroxyamfetamine, 62, 302 Hydroxypyridinethione, 152 Hyperlipidemia, 99 Hyperopia, 27, 29 Hypersensitivity, conjunctival, 277–278, 280–281 Hypertension, 116–117, 160 retinal detachment, 154, 155 Hypertensive retinopathy, 111, 112, 160–161 Hyperthyroidism, 160 Hyphema, 77, 105–106, 150 acute uveitis, 243, 245 differential diagnosis, 132 eight-ball, 150 treatment, 151 Hypopyon, 105, 243, 244 Hypotensives, ocular see Ocular hypotensive medications Hypothyroidism, 86–87, 168 I Idoxuridine, 54, 278–279, 296 Illumination, 14–15, 46–47 Immunosuppressive drugs, 173, 248, 287 Impression cytology, 19 Impression smears, 17, 18 Infections acute uveitis, 242 antimicrobial therapy, 53–56 conjunctivitis, 276–277, 278–280 corneal ulceration, 215, 219, 221–222, 226 eyelid, 211, 212 orbital, 203, 205–207 Inﬁnity, optical, 28 Inﬂammatory disease, posterior segment, 189–193 Inﬂammatory retinopathy, 184 Instruments, diagnostic, 14–25 Interferon α, 56, 226, 279 Intoxicants, 164 Intralenticular hemorrhage, 131, 132, 150

INDEX

primary, 228–230 primary open angle, 229–230, 233– 234 secondary, 12, 229, 234–235 chronic uveitis, 172, 233–234, 244–245, 247 hyphema, 151 lens luxation, 110, 238 retinal detachment, 160 surgical treatment, 237 ultrasonography, 36 Globe abnormal appearances, 75–84 abnormally small, 75, 76 enlarged, 75–79 normal appearance, 67 penetrating trauma, 75 position changes, 79–83 protrusion see Exophthalmos recession see Enophthalmos rupture, 75, 81 size changes, 75–79 Glycerine/glycerol, 60–61, 235 Goblet cells, conjunctival, 254, 290 Golden Retriever, 80, 136, 177, 178, 179, 262 Goniodysgenesis, 26, 29, 228–229, 230 Goniodysplasia, 36 Gonioscopy, 26, 27, 28, 29 Gram stain, 17, 275 Gramicidin, 295, 297 Granulomatous meningoencephalomyelitis (reticulosis), 162, 163 Granulomatous uveitis, 244 Great Pyrenees, 141

309

INDEX

310

Intramuscular administration, antibiotics, 56 Intraocular hemorrhage, 149–151 Intraocular injections, 50 Intraocular lens, 182 Intraocular pressure (IOP) acute glaucoma, 148, 149 assessment, 24–26, 227–228 chronic glaucoma, 149, 174 medications lowering see Ocular hypotensive medications normal values, 24, 71 transitory elevations, 232 Intraorbital injections, 50 Intravitreal hypotensive injections, 61 IOP see Intraocular pressure Iridal melanoma, 32, 34, 107, 170 Iridocorneal angle, 7, 71, 228 gonioscopic evaluation, 26, 29 Iridocyclitis see Anterior uveitis Iridodonesis, 71, 238 Iris, 7, 9 abnormal appearances, 77 colobomas, 103, 104 coloration, 72 congestion, uveitis, 243, 244 cysts, 102, 106, 107 discoloration, 77 embryology, 1, 4 inﬂammatory cell nodules, 170–171, 244, 245 masses, 77, 106–108 neovascularization see Rubeosis iridis normal appearance, 71–73 pigmentary changes, 170–171, 244, 245, 246 prolapse, 223 ‘strands’, 77, 127 ultrasonography, 32, 34 Iris atrophy, 149 secondary to uveitis, 171, 173 senile, 73 Iris bombé, 105, 150, 172, 244, 247 Iris constrictor (sphincter) muscle, 9, 72, 122–123 atrophy, 73 embryology, 1 glaucoma, 232 neural control, 11, 12 Iris (pupillary) dilator muscle, 9, 72, 123 embryology, 1 Irish Red & White Setter, 133 Irish Setter, 133, 138, 144, 179 Iritis see Anterior uveitis

Irritation, ocular epiphora, 257, 266, 267–272 eyelid abnormalities, 207–215, 267–270 Isoﬂupredone, 298 Isoﬂurophate, 59, 300 J Jones test, 257–258 K KCS see Keratoconjunctivitis sicca Keratectomy, superﬁcial, 221 Keratitic precipitates (KPs), 101, 102, 244 Keratitis chronic superﬁcial (pannus), 98, 166–167 chronic uveitis, 171 eosinophilic, 98–99, 280–281 feline herpetic see Feline herpes virus 1 ocular discharge, 283 pigmentary, 95–97, 166 pigmentosa see Keratitis, chronic superﬁcial superﬁcial punctate, 167–168 Keratoconjunctivitis sicca (KCS), 283–289 clinical signs/diagnosis, 15, 17, 118, 166, 283–286 congenital, 286 etiology, 286 iatrogenic, 286 management, 62, 287–289 neurogenic, 286 Keratoconus, 102–103 Keratometry, 29 Keratoscopy, 29 Keratotomy, punctate or grid, 220–221 Ketoconazole, 181 Ketoprofen, 58, 248 Ketorolac, 57, 58, 248, 300 L Labrador Retriever cataracts, 177, 179 retinal disorders, 135, 136, 138, 183, 184, 186 Lacrimal drainage system see Nasolacrimal drainage system Lacrimal gland, 4, 6, 8, 253 aplasia or hypoplasia, 286 autoimmune adenitis, 286

Lodoxamide, 301 Longhaired Dachshund, 133, 146, 167 Loupe, magnifying, 14 Lumigan see Bimatoprost Lymphoma, 107–108, 116, 194 L-Lysine, 56, 226, 279 Lysosomal storage diseases, 194 M Magnetic resonance imaging (MRI), 33, 205 Magnifying loupe, 14 Mannitol, 60–61, 235 Mast cell stabilizers, 57, 301–302 Masticatory muscle myositis, 207 Medial canthal entropion, 263, 264, 268–270, 271 Medial canthoplasty, 269–270, 272 Medial canthus, 6 closure, 289 Medications, 50–66 adverse ocular effects, 118, 151–152, 286 combination, 53, 297–299 owner compliance, 50–51, 52 pharmacokinetics, 51–63 routes of administration, 50 Medrysone, 296 Medulloepithelioma, uveal, 106–107 Megalocornea, 174 Megestrol acetate, 99 Meibomian glands, 6, 7, 253 adenoma, 86 inﬂammation, 290–291 Melanocytomas, limbal, 93, 97 Melanoma, 194 iris, 32, 34, 107, 170 uveal, 106–107 Melanosis (melanocytosis), 92, 93 Meloxicam, 248 Membrana nictitans see Third eyelid Menace reaction, 47, 120–121 Meningitis, 163 Meningoencephalitis, 163 Meningoencephalomyelitis, granulomatous (reticulosis), 162, 163 Meridian, 27 Merle ocular dysgenesis, 3, 131 Methazolamide, 236 Methylprednisolone, 248 Metipranolol, 236 Miconazole, 55 Microphakia, 127

INDEX

Lacrimal lake, 255 Lacrimal sac, 254 Lacrimal system, 6, 253–254, 255 inﬂammation see Dacryocystitis trauma, 265, 286 Lacrimation, 254 increased, 87, 266, 267–272 reduced, 166, 283–289 Lacrimomimetic drugs, 62 Lagophthalmos brachycephalic dogs, 67, 69 corneal pigmentation, 95, 96, 166 exophthalmos, 79 Lancashire Heeler, 138, 142 Large Munsterlander, 179 Laser therapy, 158, 159, 237 Lashes see Cilia Latanaprost, 60, 235, 300, 301 Lateral canthus, 6 Lateral geniculate nucleus, 11, 120 Lens, 7, 9–10, 175 abnormal appearances, 78, 108–110 coloboma, 128 congenital disorders, 127–128 dislocation see Lens luxation embryology, 1, 2, 3 examination, 47–48 extraction techniques, 182 hemorrhage within, 131, 132 induced uveitis, 173, 177–181 normal appearance, 73 nuclear sclerosis, 73, 108 opaciﬁcation, 78, 108–110 position change, 78 shape change, 78 Lens capsule, 2 lenticonus, 128, 129 traumatic puncture, 223 uveitis, 105, 170 Lens luxation, 110, 238–241 anterior, 106, 110 primary, 238–240 secondary, 172, 240–241 Lenticonus, 128, 129, 130 Lentiglobus, 128 Leukocoria, 78, 110–111 congenital, 111 Levator palpebrae superioris muscle, 5, 7, 69 Levobunolol, 300 Levoﬂoxacin, 295 Limbus, 6, 70 Lipid keratopathy, 99–101, 168, 217, 218 Lissamine green, 16–17

311

INDEX

312

Microphthalmia (microphthalmos), 75, 125–127 cataracts, 126–127, 177 differential diagnosis, 165 mechanisms, 1, 3 Micropunctum, 262, 263 Miniature Poodle, 134, 138, 145, 180, 183 Miniature Schnauzer, 127, 133, 136, 138, 145, 178 Miotics, 236, 301–302 Mittendorf’s dot, 1, 129 Moll, gland of, 7 Monoclonal gammopathies, 132 Mouth opening, pain on, 80, 203, 205 Moxiﬂoxacin, 295 Mucoceles, 283 Mucopurulent discharge, 273–283 Mucus, tear ﬁlm, 273, 290 Müller’s muscle, 5, 7 Mycoplasma infections, 54, 275, 280 Mycoses, ocular, 55, 56 Mycosis fungoides, 18 Mydriasis, 47, 61 Mydriatics, 61–62, 248–249, 301–302 Myopia, 26, 29 Myositis, masticatory muscle, 207 N Nanophthalmia, 125–127 Nasal folds surgical excision, 268, 269 trichiasis, 214–215, 268, 269 Nasal ostium, 254–255 cannulation, 259, 261 Nasolacrimal canaliculi, 6, 254 Nasolacrimal drainage system, 254–255 congenital anomalies, 262 disorders, 262–267 evaluation, 21, 257–259 ﬂushing, 258–259, 260–261, 282–283 inadequate passage of tears, 263 neoplasms, 265 traumatic injuries, 265 Nasolacrimal duct, 6, 254, 255 blocked, 263, 265, 281 creating an artiﬁcial, 265–267 evaluating patency, 16, 21, 257–259 Nasolacrimal puncta, 6, 254, 255 atresia, 262, 263, 264 examination, 257 misplaced, 262, 263 small (micropunctum), 262, 263 therapeutic occlusion, 289 Natamycin, 55

Neomycin, 294, 295, 297, 298–299 Neoplasms see Tumors Neural crest cells, 3, 4 Neural retina detachment see Retinal detachment dysplasia see Retinal dysplasia embryology, 1, 2–4 tapetal hyperreﬂectivity, 112 Neurologic disorders, causing blindness, 119, 162–164, 193–194 Neurologic examination, 118–119 Neuronal ceroid lipofuscinosis (NCL), 140, 186–188 Neuroprotective therapy, 236 Neurotrophic keratopathy, 215 Nictitans (third eyelid) gland, 253–254 Nictitans gland prolapse (cherry eye), 8, 88, 89, 253–254 sequelae of surgery, 272 surgical correction, 88, 90 Nictitating membrane see Third eyelid Night blindness, 118 hereditary disorders, 144, 146, 185 nutritional deﬁciencies, 188 Nitrofurazone, 295 Nodular granulomatous episclerokeratitis, 278 Non-steroidal anti-inﬂammatory drugs (NSAIDs) systemic, 53, 58 topical, 56, 57, 300 uveitis, 247–248 Norﬂoxacin, 295 Norwegian Buhund, 180 Norwegian Elkhound, 133, 144, 175 Nova Scotia Duck Tolling Retriever, 139 Nutritional retinal degeneration, 188–189 Nyctalopia see Night blindness Nystagmus, 84, 126, 147 O Obstacle course, 119–120 Ocular coherence tomography (OCT), 38, 46 Ocular hypotensive (anti-glaucoma) medications, 58–61, 234, 235–236 intravitreal injections, 61 systemic, 53, 60–61 topical, 58–60, 300–301 Ocular surface disease painful, 215–226 reduced/altered tear production, 283–291 Oculomotor nerves, 11

P Painful eye, 118, 203–252 acute anterior uveitis, 241–249

differential diagnosis, 204 eyelid abnormalities, 207–215 glaucoma, 227–237 lens luxation, 238–241 ocular surface lesions, 215–226 orbital disease, 203–207 Palpebral ﬁssure abnormal shape, 76 shortening, 289 wide, tear ﬁlm problems, 289 Pannus (chronic superﬁcial keratitis), 98, 166–167 Panophthalmitis, 54 Papilledema, 162, 192–193, 195 Papillon, 135 Parasympathetic nerve supply, 9, 11, 122–123 Parasympatholytics, 61 Parasympathomimetics, 58–59, 287 Parotid duct transposition, 288–289 Pathology, ocular, 12–13 Pectinate ligament, 27, 29, 71 dysplasia see Goniodysgenesis Pemphigus, 278, 283 Penciclovir, 54–55 Perﬂuorocarbon tamponade, 159–160 Periorbita, 4 Persian cat, 135, 144 Persistent hyaloid artery (PHA), 128–129 Persistent hyperplastic tunica vasculosa lentis/primary vitreous (PHTVL/ PHPV) or persistent embryonic vasculature (PEV), 1, 110–111, 129–131, 132 Persistent pupillary membranes (PPM), 4, 5, 103, 104, 127 Peter’s anomaly, 4, 5 Phacoemulsiﬁcation, 182 Pharmacokinetics, 51–63 Phenylephrine, 61–62, 249, 301–302 Photography, fundus, 36, 40 Photopic vision, testing, 119–120 Photoreceptor dysplasia (pd), 133, 145 Photoreceptor dystrophies, early-onset, 133–135, 144–147 Photoreceptors, 10 Phthisis bulbi, 75, 126, 164–165, 173 Physiology, ocular, 4–12 Physostigmine, 59, 300 Pigmentary keratitis, 95–97, 166 Pilocarpine, 59, 62, 236, 287, 301 Pimecrolimus, 287 Pit Bull Terrier, 133, 146 Pituitary tumors, 195

INDEX

Oculoskeletal dysplasia, 111 Oﬂoxacin, 295 Ointments, 51, 52 Olaptadine, 301 Old English Mastiff, 134, 139, 185–186 Old English Sheepdog, 178 Ophthalmia neonatorum, 85, 116 Ophthalmic examination, 14, 38–48 ambient illumination, 46–47 dark room, 47–48 Ophthalmic history, 116–117 Ophthalmoscopy binocular indirect, 25 direct, 21–22 hand lens indirect, 22–23 Optic chiasm, 10–11, 120 tumors, 193 Optic cup, 1, 2–3 Optic disk, 7, 10 chronic glaucoma, 232–233 coloboma, 143 normal appearance, 74–75 Optic ﬁssure, 1, 2–3 Optic nerve, 10–12 aplasia, 141–142 congenital malformations, 132–147 disease, 192 embryology, 2 hypoplasia, 141–142 testing function, 120–123 Optic neuritis, 113, 161–162, 163 Optic tracts, 11, 120 Optic vesicle, 1, 2–3 Optical inﬁnity, 28 Orbicularis oculi muscle, 5, 7, 69 Orbit, 4–5 Orbital cellulitis/retrobulbar abscess, 80, 205–206 Orbital disease exophthalmos, 80–81, 203 investigations, 20, 31, 32, 33, 205 ocular discharge, 283 painful, 203–207 space-occupying lesions, 5, 203–205, 266 Orbital neoplasia, 81, 203 Orbital trauma, 82–83, 207 Oscillatory potentials (OPs), 33, 38 Osmotic diuretics, 60–61, 235 Oxytetracycline, 295, 299

313

INDEX

314

Placido’s rings, 29 Plasma cell producing tumors, 132 Plasmacytic conjunctivitis (plasmoma), 88–89, 167, 277–278 Poliosis, 105 Polish Owczarek Nizinny (PON), 187, 194 Polymerase chain reaction (PCR), 274–275 Polymyositis, extraocular, 80–81 Polymyxin B, 294, 295, 297, 298, 299 Portuguese Waterdog, 135, 139 Posterior segment abnormal appearances, 78, 110–113 colobomas, 142, 143 congenital malformations, 132–147 decreased reﬂectivity, 78, 112 hemorrhage, 150–151 increased reﬂectivity, 78, 112 inﬂammatory disease, 189–193 normal appearance, 73–75 Posterior synechiae, 73, 105, 171–172, 243, 244, 245 Povidone–iodine solution, 55 Pre-iridal ﬁbrovascular membranes see Rubeosis iridis Prednisolone, 247, 248, 296, 297, 299 Prednisone, 57, 58 Progressive retinal atrophy (PRA) cataracts, 181 central (CPRA) see Retinal pigment epithelial cell dystrophy differential diagnosis, 173, 192 DNA-based tests, 137–139 dominant, 137, 139, 185–186 early-onset, 133–135, 144–147, 182–183 generalized, 182–185 history taking, 117, 118 inherited, 182–186 late-onset, 182–183 X-linked, 139, 185 Progressive rod–cone degeneration (prcd), 183–185 Proparacaine, 63, 302 Proptosis, 82–83, 207 Prostaglandin analogs, 60, 235 Prosthesis, intraocular, 237 Puncta, nasolacrimal see Nasolacrimal puncta Pupil, 7, 9 abnormal appearances, 77–78, 108 constricted, 77, 243 constriction, 122–123 dilatation, 47, 122–123

dilated, 77, 232 distorted, 78 normal appearance, 73 white see Leukocoria Pupillary dilator muscle see Iris dilator muscle Pupillary light reﬂexes (PLR), 121–123 examination, 46–47, 123 pathways, 11, 122 testing equipment, 14–15 Pupillary membrane, 4, 127 persistent see Persistent pupillary membranes Pupillary sphincter muscle see Iris constrictor muscle Purulent discharge, 273–283 Q Quinine, 152 Quixin, 295 R Radiography, 205 Radiology, 33, 205 Rafoxanide, 152 Red eye, 89, 231–232 Refraction, 28, 123–124 Refractive errors, 123–124 Reticulosis, 162, 163 Retina, 10 anatomy, 7, 10 congenital malformations, 132–147 embryology, 1, 2–4 inﬂammatory processes, 189–190 scars, 191, 192 Retinal degenerations, 111 chronic glaucoma, 232–233 chronic uveitis, 172 detached retina, 156 early (erd), 145 early-onset photoreceptor dystrophies, 134–135, 144–147 feline central (FCRD), 188–189 history taking, 117, 118 inherited, 182–188 nutritional, 188–189 sudden acquired see Sudden acquired retinal degeneration see also Progressive retinal atrophy Retinal detachment, 13, 154–160 clinical ﬁndings, 154–155 Collie eye anomaly, 143 complete, 154, 156, 157, 158–160 complications, 160

Rough Collie, 133, 139, 142, 144 RPE65 gene defect, 137, 146–147 RPED see Retinal pigment epithelial cell dystrophy Rubeosis iridis (iris neovascularization), 12 anterior uveitis, 105, 170, 244, 245 ectropion uveae, 73 S Samoyed, 134, 136, 139, 185 Sarcoma post-traumatic, 75 primary, 165, 170 SARD see Sudden acquired retinal degeneration Scanning laser ophthalmoscopy (SLO), 36–38 Schiøtz tonometer, 24 Schirmer tear test (STT), 15, 255–256, 283–284 Sclera abnormal appearances, 76 embryology, 4 normal appearance, 69–70 Scotopic vision, testing, 119–120 Scrapings, 17, 18–19, 219, 275 Sealyham Terrier, 136 Seclusio pupillae, 171–172 Serology, 276 Serous retinopathy, 141 Serum, autologous, 222 Shar Pei, 68, 83, 208, 209 Sheltie, 100 Shetland Sheepdog, 126, 139, 142 Short ciliary nerves, 11 Shorthaired Dachshund, 133, 146 Siberian Husky, 100, 134, 139, 179, 185 Signs, initial clinical, 117–118 Silver sulfadiazine, 55 Sinus disease, 283 Sirolimus, 62 Skiascopy see Retinoscopy Slit-lamp biomicroscope, 25 Sloughi, 139 Smears, 17, 18, 219, 275 Smooth Collie, 139, 142 Sodium chloride, 302 Solutions, ophthalmic, 51, 52 Sorbitol, 10, 181 Specular microscopy, 30 Spherophakia, 128 St Bernard, 68 Stades technique, 211

INDEX

differential diagnosis, 155 focal or partial, 156, 157–158, 159 hyphema, 105 leukocoria, 111, 112 pathogenesis, 156 prognosis, 155–156 rhegmatogenous, 154, 155, 156 serous and exudative, 156, 157, 159, 172 treatment, 155–156, 157–160 ultrasonography, 32, 35 Retinal dysplasia (RD), 4, 136–141 diffuse, 136 focal, 136 geographic, 136, 157–158 leukocoria, 111 multifocal, 136, 141, 192 secondary (non-inherited), 141 speciﬁc breeds, 133–135 total, with non-attachment, 131 Retinal dystrophy, congenital (RPE65 gene defect), 137, 146–147 Retinal folds, 136 Retinal hemorrhages, 112–113, 150–151 Retinal light reﬂex, 121 Retinal pigment epithelial cell dystrophy (RPED), 186 differential diagnosis, 186, 187, 192 ﬂuorescein angiography, 44 Retinal pigment epithelial dysplasia, 141 Retinal pigment epithelium (RPE), 156 embryology, 1, 2–3 inﬂammatory processes, 190–192 normal appearance, 73 Retinal tears, 157–158 Retinal vasculature abnormal appearances, 112 inﬂammatory lesions, 191 Retinopexy, transcorneal diode laser, 158, 159, 160 Retinoscopy, 26–29, 123–124 Retrobulbar abscess/orbital cellulitis, 80, 205–206 Rickettsial diseases, 277 Rimexolone, 296 Rocky Mountain spotted fever, 277 Rod–cone degeneration, progressive, 183–185 Rod–cone dysplasia (rcd), 133, 135, 144 Rod degeneration, early (erd), 133, 145 Rod dysplasia (rd), 133, 144–145 Romanowski-type stain, 275 Rose bengal, 16–17, 63, 219 Rottweiler, 136

315

INDEX

316

Staffordshire Bull Terrier, 111, 130, 178 Stains, diagnostic, 16–17 Standard Pinscher, 130 Standard Poodle, 179, 180 Staphylococcal infections, 211, 212, 277 Staphylomas, 93, 97, 232 Steroids see Corticosteroids Strabismus, 83 Styes, 86 Sub-retinal ﬂuid cytology, 20 Subconjunctival injections, 50, 52–53 anti-inﬂammatories, 57–58 antimicrobials, 55 mydriatics and cycloplegics, 61 Sudden acquired retinal degeneration (SARD), 10, 152–154 clinical ﬁndings, 118, 153 differential diagnosis, 153–154, 161– 162, 163, 184 Sulfacetamide, 295, 299 Sulfonamides, 118, 286 Sunglasses, 98 Superﬁcial chronic corneal epithelial defects (SCCED) (boxer ulcers), 16, 220–221 Superﬁcial punctate keratitis, 167–168 Suprofen, 57, 248 Suspensions, ophthalmic, 51, 52 Sussex Spaniel, 129 Swabs, 18, 219 Swinging light test, 120 Swiss Mountain Dog, 138 Symblepharon, 92, 99, 265 Sympathetic nerve supply, 12, 119, 122–123 Sympathomimetics, 61–62 Synechiae (intraocular adhesions), 171– 172, 244 peripheral anterior, 171 posterior see Posterior synechiae Systemic disease, visual impairment, 116–117 Systemic medications, 50, 53 anti-inﬂammatories, 58 antimicrobials, 55–56 mydriatics and cycloplegics, 61–62 ocular hypotensives, 60–61 T Tacrolimus, 62, 287 Tapetal reﬂex, 73–74, 111 Tapetum, 10 hyperreﬂectivity, 78, 111, 112, 190 hyporeﬂectivity, 78, 112

inﬂammatory lesions, 190–191 normal appearance, 73–74 Tarsal plate, 5, 6, 7 Taurine deﬁciency retinopathy, 188–189 Tear break-up time (BUT), 16, 290 Tear ﬁlm, 6, 71, 253–256 examination, 255–256 inadequate distribution, 289–290 layers, 6, 253 qualitative disease, 290–291 structures producing, 253–254 Tear production see Lacrimation Tear staining syndrome, 262–264 Tear stimulants, 301–302 Tears artiﬁcial, 62–63, 287–288 drainage see Nasolacrimal drainage system function, 254 Tenon’s capsule, 8 Tetracaine, 63 Tetracycline, 54, 280, 295 Thelazia spp, 277 Therapeutics, 50–66 Thiram, 152 Third eyelid, 8 abnormal appearances, 76, 87–89 conditions causing epiphora, 266, 270–272 distortion, 76 examination behind, 258 in exophthalmos, 79–80 gland see Nictitans gland lymphoid follicle hyperplasia, 88 masses, 76, 88–89 normal appearance, 69, 70 plasma cell inﬁltration see Plasmacytic conjunctivitis prominence, 76, 87, 205 scrolling of cartilage, 87–88, 272, 273 suturing across corneal ulcers, 222 Tibetan Terrier, 135 Timolol, 59–60, 236, 301 Tissue glue, corneal, 223 Tobramycin, 54, 295, 299 Tolfenamic acid, 248 Tono Pen®, 25–26 Tono Vet®, 25–26 Tonometry, 24–26 applanation, 25–26 digital, 24 indentation, 24–25 Topical anesthetics, 63, 301–302

U Überreiter’s disease see Chronic superﬁcial keratitis Ultrasonography, 30–33, 34, 35, 36, 125 ocular trauma, 223 orbital disease, 31, 32, 205 Ultraviolet light exposure, 98 Unoprostone, 60 Uremia, 101 Uvea, 9 anterior see Anterior uvea Uveal tumors, 106–108 Uveitis acute see under Anterior uveitis anterior see Anterior uveitis chronic, 169–174 clinical signs, 170–171, 244– 245 diagnosis, 173 differential diagnosis, 173 pathogenesis, 170 sequelae, 171–173, 233–234 treatment and prognosis, 173– 174 granulomatous, 244 lens-induced, 173, 177–181 neoplastic, 170, 173 phacoclastic, 223 retinal detachment, 157 Uveodermatologic syndrome, 105, 173, 283 V Valaciclovir, 56 Valganciclovir, 54 Vidarabine, 54, 296 Vigamox, 295 Visceral larva migrans, 192 Vision in daylight and dim light, 118 evaluation, 116–125 testing, 119–125 Visual evoked potentials (or response) (VEP or VER), 33–36, 37, 124, 125 Visual ﬁeld defects, 120 Visual impairment, 116–202 acquired, 148–195 acute onset, 148–164 chronic progressive, 164–195 congenital disease/malformations, 125–147 evaluation, 116–125

INDEX

Topical medications, 50 anti-inﬂammatories, 56–58 antimicrobials, 53–55 application technique, 52 ﬁxed ratio combination, 53 formulary, 294–302 miscellaneous, 63 mydriatics and cycloplegics, 61 ocular hypotensives, 58–60 pharmacokinetics, 51–52 tear supplements, 62–63 Toxic cataracts, 181 Toxic central nervous system disorders, 164 Toxic retinopathy, 151–152, 190 Toxocaral retinochoroiditis, 192 Toxoplasmosis, 102, 192–193 Toy Poodle, 134, 139, 180 Trabecular meshwork, 27, 29, 71 Trans-corneal ﬁne needle aspiration, 19 Transilluminator, 14–15 Transscleral ﬁne needle aspiration, 20 Trauma acute uveitis, 241, 243 cataracts, 181 corneal, 223–226 eyelid lacerations, 85, 265 keratoconjunctivitis sicca, 286 nasolacrimal system, 265, 286 orbital, 82, 207 penetrating, 75 retinal detachment, 158 Travatan see Travoprost Travoprost, 60, 235, 301 Trichiasis, 214–215 atonic entropion, 209–211 corneal pigmentation, 95, 96, 166 epiphora, 266, 268–270 nasal fold, 214–215, 268, 269 Triﬂuridine, 54, 278–279, 296 Trigeminal nerve lesions, 215, 290 Triple antibiotic preparations, 54, 294, 295 Tropicamide, 47, 61, 302 Tumors causing blindness, 194–195 causing uveitis, 170 ﬁne needle aspiration, 19 glaucoma secondary to, 233–234 Tunica vasculosa lentis, 1 persistent see Persistent hyperplastic tunica vasculosa lentis/primary vitreous

317

INDEX

318

Visual pathways central, 10–12 neoplasms affecting, 194–195 testing, 120–123 Visual placing reactions, 121 Vitamin A deﬁciency, 188 Vitamin E deﬁciency, 186, 188 Vitiligo, 105 Vitrectomy, 158–159, 160 Vitreous cytology, 20 hemorrhage, 35, 131–132, 150 opaciﬁcation, congenital, 131–132 persistent hyperplastic primary see Persistent hyperplastic tunica vasculosa lentis/primary vitreous

W Welsh Springer Spaniel, 178 West Highland White Terrier, 128, 180, 284, 285 Wet eye, 256–272 see also Epiphora White pupil see Leukocoria Wirehaired Dachshund, 133, 146 X Xalacom see Latanaprost Z Zeis, gland of, 7 Zygomatic salivary gland, 5 mucocele, 283 Zymur, 295