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E-Book, Deutsch, Englisch, 271 Seiten

Stades / Wyman / Boevé Ophthalmology for the Veterinary Practitioner


2. Revised Auflage 2010
ISBN: 978-3-89993-095-5
Verlag: Schlütersche
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Deutsch, Englisch, 271 Seiten

ISBN: 978-3-89993-095-5
Verlag: Schlütersche
Format: PDF
Kopierschutz: 1 - PDF Watermark



Recognized as a standard work, this new, completely revised and expanded edition contains: • All important eye diseases encountered in daily practice • Coverage of pet animals, horses, birds and farm animals

• Practical tips for effective diagnosis
• The latest drugs, diagnostic and therapeutic methods
• Step-by-step surgical procedures
• First-class color photographs and instructive drawings to illustrate symptoms and techniques

The book’s structure follows the steps of a clinical investigation. It is a reliable and indispensable handbook both for the novice in veterinary ophthalmology and the general practitioner.

Stades / Wyman / Boevé Ophthalmology for the Veterinary Practitioner jetzt bestellen!

Weitere Infos & Material


1;Contents;6
2;Authors;11
3;Abbreviations;12
4;Origin of Plates and Figures;13
5;1 Introduction;14
6;2 Clinical and Differential Diagnostic Procedures;18
6.1;2.1 Description of the patient;18
6.2;2.2 Patient history;18
6.3;2.3 Animal handling, equipment, and instruments;21
6.3.1;2.3.1 Restraint and sedation;21
6.3.2;2.3.2 Materials and instruments;21
6.4;2.4 Examination of the eye and its adnexa;21
6.4.1;2.4.1 Head, skull, and orbital area;21
6.4.2;2.4.2 Tear film and tear production;22
6.4.3;2.4.3 Ocular discharge;23
6.4.4;2.4.4 Eyelids (palpebrae);23
6.4.5;2.4.5 Conjunctiva;24
6.4.6;2.4.6 Globe (bulbus);25
6.4.7;2.4.7 Sclera;26
6.4.8;2.4.8 Cornea;26
6.4.9;2.4.9 Anterior and posterior chambers;26
6.4.10;2.4.10 Pupil and iris;27
6.4.11;2.4.11 Lens;27
6.4.12;2.4.12 Vitreous;27
6.4.13;2.4.13 Fundus;27
6.4.14;2.4.14 Additional and specific examinations;28
6.5;2.5 Differential diagnosis;29
6.5.1;2.5.1 Introduction;29
6.5.2;2.5.2 The “red” eye;29
6.5.3;2.5.3 Epiphora without distinct blepharospasm;29
6.5.4;2.5.4 Blepharospastic / painful eye (Schirmer tear test not decreased);29
6.5.5;2.5.5 Protrusion of the nictitating membrane with enophthalmos;29
6.5.6;2.5.6 Exophthalmos;29
6.5.7;2.5.7 The “blue-white” cornea;30
6.5.8;2.5.8 The “pigmented” eye;30
6.5.9;2.5.9 The “blind” eye;30
7;3 Diagnostics and Therapeutics for Eye Diseases;32
7.1;3.1 Introduction;32
7.1.1;3.1.1 Into the conjunctival sac;32
7.1.2;3.1.2 Subconjunctival;34
7.1.3;3.1.3 Retrobulbar;34
7.1.4;3.1.4 Intraocular;34
7.1.5;3.1.5 General rules;35
7.2;3.2 Ocular therapeutic agents;35
7.2.1;3.2.1 Vasoconstrictors;35
7.2.2;3.2.2 Antihistamines (nowadays mostly replaced by corticosteroids);35
7.2.3;3.2.3 Antiglaucoma agents;36
7.2.4;3.2.4. Mydriatics;36
7.2.5;3.2.5 Antimicrobial agents;37
7.2.6;3.2.6 Corticosteroids;38
7.2.7;3.2.7 Non-steroidal anti-inflammatory drugs (NSAIDs);38
7.2.8;3.2.8 Local anesthetics;39
7.2.9;3.2.9 Vitamins, epithelializing agents,;39
7.2.10;3.2.10 Collyria;39
7.2.11;3.2.11 Other “drugs” for ocular use;39
7.2.12;3.2.12 Radiation;40
7.2.13;3.2.13 Protective devices;40
7.3;3.3 Surgical possibilities;40
7.3.1;3.3.1 Anesthesia;40
7.3.2;3.3.2 Preparation of the operative field;41
7.3.3;3.3.3 Positioning on the operating table;41
7.3.4;3.3.4 Draping;41
7.3.5;3.3.5 Magnification equipment;41
7.3.6;3.3.6 Surgical equipment;41
7.3.7;3.3.7 Suture material;41
7.3.8;3.3.8 Hemostasis;42
7.3.9;3.3.9 Cryosurgery;42
7.3.10;3.3.10 Laser techniques;42
8;4 Ocular Emergencies;44
8.1;4.1 Introduction;44
8.2;4.2 Luxation and proptosis of the globe;44
8.3;4.3 Chemical burns;47
8.4;4.4 Blunt trauma;47
8.4.1;4.4.1 Orbital fractures;47
8.4.2;4.4.2 Contusion of the globe;48
8.5;4.5 Penetrating or perforating trauma;50
8.5.1;4.5.1 Lid lacerations and conjunctival sac wounds;50
8.5.2;4.5.2 Conjunctival lacerations;52
8.5.3;4.5.3 Corneal lacerations;53
9;5 Orbital and Periorbital Structures;60
9.1;5.1 Introduction;60
9.2;5.2 Congenital abnormalities;61
9.3;5.3 Trauma;61
9.4;5.4 Enophthalmos;61
9.4.1;5.4.1 Enophthalmos due to loss of support;61
9.4.2;5.4.2 Enophthalmos due to Horner’s syndrome;62
9.5;5.5 Exophthalmos;62
9.5.1;5.5.1 Exophthalmos due to swelling of the temporal muscles;63
9.5.2;5.5.2 Exophthalmos due to retrobulbar processes;63
9.5.3;5.6 Enucleation of the globe including the conjunctiva;66
9.5.4;5.7 Evisceration of the globe;69
9.5.5;5.8 Enucleation of the globe;69
9.5.6;5.9 Exenteration of the orbit;69
9.5.7;5.10 Orbitotomy;69
10;6 Lacrimal Apparatus;72
10.1;6.1 Introduction;72
10.2;6.2 Keratoconjunctivitis sicca (KCS);74
10.3;6.3 (Sialo)dacryoadenitis;77
10.4;6.4 Tear stripe formation;78
10.4.1;6.4.1 Micropunctum or stenosis of the lacrimal punctum;78
10.4.2;6.4.2 Atresia and secondary closure of the punctum;79
10.5;6.5 Dacryocystitis;80
10.6;6.6 Lacerations;83
10.7;6.7 Cysts and neoplasia;83
11;7 Eyelids;86
11.1;7.1 Introduction;86
11.2;7.2 Ankyloblepharon;87
11.3;7.3 Aplasia palpebrae;87
11.4;7.4 Dermoids / dysplasia of the lid;89
11.5;7.5 Distichiasis;89
11.6;7.6 Entropion;91
11.6.1;7.6.1 Entropion in sheep and horses;99
11.7;7.7 Ectropion and / or oversized palpebral fissure (macroblepharon) (Ect / OPF);99
11.7.1;7.7.1 Shortening of the lower palpebral conjunctiva;100
11.7.2;7.7.2 V-Y Method;100
11.7.3;7.7.3 Simple wedge resection;100
11.7.4;7.7.4 Kuhnt-Szymanowski method, Blaskovic’s modification15;100
11.7.5;7.7.5 Kuhnt-Szymanowski method16;100
11.7.6;7.7.6 Z-plasty / free transplants;101
11.7.7;7.7.7. Total fissure shortening methods;101
11.8;7.8 Trichiasis;102
11.8.1;7.8.1 Nasal fold trichiasis;102
11.8.2;7.8.2 Upper eyelid trichiasis;103
11.8.3;7.8.3 Caruncle trichiasis and trichiasis in other locations;104
11.9;7.9 Blepharophimosis;107
11.10;7.10 Oversized / overlong palpebral fissure;107
11.11;7.11 Injuries;107
11.12;7.12 Ptosis;107
11.13;7.13 Lagophthalmos;108
11.13.1;7.13.1 Medial canthoplasty;108
11.13.2;7.13.2 Lateral canthoplasty;108
11.14;7.14 Blepharitis;108
11.14.1;7.14.1 Non-specific blepharitis;108
11.14.2;7.14.2 Chronic blepharitis;108
11.14.3;7.14.3 Specific blepharitis;109
11.15;7.15 Neoplasia of the eyelids;112
11.15.1;7.15.1 Sarcoids in horses;116
12;8 Conjunctiva and Nictitating Membrane;118
12.1;8.1 Introduction;118
12.2;8.2 Non-pigmented margin of the nictitating membrane;119
12.3;8.3 Dermoid;119
12.4;8.4 Ectopic cilia;119
12.5;8.5 Protrusion of the nictitating membrane;120
12.6;8.6 Cysts;121
12.7;8.7 Eversion / inversion of the nictitating membrane;121
12.8;8.8 Hyperplasia / hypertrophy of the gland of the nictitating membrane (“cherry eye”);123
12.9;8.9 Subconjunctival hemorrhages;126
12.10;8.10 Injuries;126
12.11;8.11 Conjunctivitis;126
12.11.1;8.11.1 Catarrhal (or serous) conjunctivitis;127
12.11.2;8.11.2 Purulent conjunctivitis;127
12.11.3;8.11.3 Follicular conjunctivitis;129
12.11.4;8.11.4 Plasmacellular conjunctivitis;129
12.11.5;8.11.5 Papillary / nodular / granulomatous conjunctivitis;130
12.11.6;8.11.6 Conjunctivitis neonatorum;130
12.11.7;8.11.7 Infectious bovine / ovine keratoconjunctivitis (pinkeye);131
12.12;8.12 Eosinophilic granuloma;132
12.13;8.13 Allergic conjunctivitis;132
12.14;8.14 Conjunctival adhesions;132
12.14.1;8.14.1 Symblepharon;132
12.14.2;8.14.2 Conjunctival stricture in the rabbit;133
12.15;8.15 Neoplasia of the conjunctiva;135
13;9 Globe;138
13.1;9.1 Introduction;138
13.2;9.2 Exophthalmos, enophthalmos;138
13.3;9.3 Pseudo-exophthalmos / pseudo-enophthalmos;138
13.4;9.4 Setting sun phenomenon;139
13.5;9.5 Strabismus;139
13.6;9.6 Nystagmus;139
13.7;9.7 Anophthalmia, cyclopia, microphthalmia;140
13.8;9.8 Phthisis bulbi;140
13.9;9.9 Macrophthalmia;141
13.10;9.10 Buphthalmos / hydrophthalmia;141
13.11;9.11 Endophthalmitis, panophthalmitis;141
14;10 Cornea and Sclera;142
14.1;10.1 Introduction;142
14.1.1;10.1.1 Symptoms of corneal disease;142
14.1.2;10.1.2 Localization and causes of corneal abnormalities;145
14.1.3;10.1.3 Corneal regeneration;145
14.1.4;10.1.4 Retardation of healing;146
14.2;10.2 Microcornea;146
14.3;10.3 Persistent pupillary membrane (PPM);146
14.4;10.4 Dermoid;146
14.5;10.5 Trauma;147
14.6;10.6 Keratitis;147
14.6.1;10.6.1 Superficial keratitis (without ulceration);147
14.6.2;10.6.2 Deep or interstitial keratitis or keratitis profunda (without defects);149
14.6.3;10.6.3 Ulcerative keratitis;150
14.6.4;10.6.4 Corneal sequestration / cornea nigrum / corneal necrosis / corneal mummification;160
14.6.5;10.6.5 Keratitis punctata;162
14.6.6;10.6.6. Keratitis herpetica;163
14.6.7;10.6.7 Infectious bovine / ovine keratoconjunctivitis;163
14.6.8;10.6.8 Corneal cysts;163
14.6.9;10.6.9. Corneal abscess;163
14.7;10.7 Dystrophic / degenerative deposits in the cornea;164
14.7.1;10.7.1 Corneal dystrophies;164
14.7.2;10.7.2 Local degenerative crystal deposits;166
14.7.3;10.7.3 Deposits resulting from systemic diseases;166
14.7.4;10.7.4 Corneal edema in the Manx cat;166
14.7.5;10.7.5 Mucopolysaccharidosis;167
14.7.6;10.7.6. GM1 and GM2 gangliosidosis;167
14.8;10.8 (Epi)scleritis;167
14.9;10.9 Neoplasms;168
15;11 Intraocular Pressure and Glaucoma;170
15.1;11.1 Introduction;170
15.2;11.2 Glaucoma;172
15.2.1;11.2.1 Etiology;172
15.2.2;11.2.2 Irido-corneal angle abnormalities;174
15.2.3;11.2.3 Conditions of the drainage angle;174
15.2.4;11.2.4 Length of time of development and progression of glaucoma;174
15.3;11.3 Clinical aspects of glaucoma;175
15.3.1;11.3.1 Acute glaucoma;175
15.3.2;11.3.2 Chronic glaucoma;177
15.3.3;11.3.3 Therapeutic possibilities in glaucoma;178
15.4;11.4 Secondary glaucoma;181
15.4.1;11.4.1 Secondary glaucoma associated with the lens or vitreous;181
15.4.2;11.4.2 Secondary glaucoma associated with uveal changes;181
15.4.3;11.4.3 Secondary glaucoma associated with trauma;182
15.4.4;11.4.4 Secondary glaucoma associated with intraocular neoplasia;182
15.4.5;11.4.5 Secondary glaucoma associated with medication;182
15.4.6;11.4.6 Secondary glaucoma associated with ocular surgery;182
15.5;11.5 Phthisis bulbi;182
16;12 Uvea;184
16.1;12.1 Introduction;184
16.1.1;12.1.1 Iris;184
16.1.2;12.1.2 Ciliary body;185
16.1.3;12.1.3 Choroid;186
16.2;12.2 Persistent (epi)pupillary membrane;186
16.3;12.3 Coloboma;187
16.4;12.4 Acorea / aniridia;188
16.5;12.5 Heterochromia of the iris;188
16.6;12.6 Blue iris / white coat;188
16.6.1;12.6.1 Oculocutaneous albinism and deafness;188
16.6.2;12.6.2 Partial oculocutaneous albinism;188
16.7;12.7 Acquired color differences in the iris;188
16.8;12.8 Iris cysts;189
16.9;12.9 Hyphema;189
16.9.1;12.9.1 Dysplastic abnormalities;189
16.9.2;12.9.2 Trauma;189
16.9.3;12.9.3 Leaking of vessels;189
16.9.4;12.9.4 Coagulation disorders;189
16.9.5;12.9.5 Uveitis;190
16.9.6;12.9.6 Neoplasms;190
16.10;12.10 Uveitis (anterior);190
16.10.1;12.10.1 Traumatic uveitis;192
16.10.2;12.10.2 Metabolic uveitis;192
16.10.3;12.10.3 Infections;192
16.10.4;12.10.4 Immune reactions;193
16.10.5;12.10.5 Idiopathic uveitis;194
16.10.6;12.10.6 Pseudo-uveitis caused by neoplasia;194
16.10.7;12.10.7 Equine recurrent (chronic) uveitis (ERU);195
16.11;12.11 Iris atrophy;196
16.12;12.12 Dysautonomia or pupil dilatation syndrome (Key-Gaskell Syndrome);197
16.13;12.13 Horner’s syndrome;197
16.14;12.14 Other pupillary abnormalities;197
16.15;12.15 Neoplasia;197
16.16;12.16 Posterior Uvea;199
17;13 Lens and Vitreous;202
17.1;13.1 Introduction;202
17.1.1;13.1.1 Ontogenesis;202
17.1.2;13.1.2 Anatomy and physiology;203
17.1.3;13.1.3 Vitreous;204
17.2;13.2 Developmental disorders of the lens;205
17.3;13.3 Cataract;206
17.4;13.4 Lens luxation or ectopic lens;214
17.5;13.5 Vitreous floaters, asteroid hyalosis, and synchysis scintillans;219
17.5.1;13.5.1 Vitreous floaters;219
17.5.2;13.5.2 Asteroid hyalosis;219
17.5.3;13.5.3 Synchysis scintillans;219
17.6;13.6 Hemorrhages and / or exudates in the vitreous;219
17.7;13.7 Retinal detachment and intraocular neoplasms;220
18;14 Fundus and Optic nerve;222
18.1;14.1 Introduction;222
18.1.1;14.1.1 Ontogenesis;222
18.1.2;14.1.2 Retina;222
18.1.3;14.1.3 Optic nerve or tract;224
18.1.4;14.1.4 Vascular supply;226
18.1.5;14.1.5 Choroid (vascular membranes);227
18.2;14.2 Symptoms, pathologic changes, and reaction patterns of the fundus;227
18.3;14.3 Aplasia;231
18.4;14.4 Micropapilla and hypoplastic papilla;231
18.5;14.5 Coloboma;231
18.6;14.6 Retinal dysplasia (RD);232
18.7;14.7 Collie eye anomaly (CEA);232
18.8;14.8 Inherited enzyme deficiencies;234
18.9;14.9 Hereditary (progressive) retinal dysplasias / atrophy / degeneration (PRA);234
18.10;14.10 Hemorrhages and other vascular abnormalities;237
18.11;14.11 Trauma;238
18.12;14.12 Intoxications;238
18.13;14.13 Abnormalities of nutritional origin;238
18.14;14.14 Posterior uveitis / chorioretinitis / retinitis;240
18.15;14.15 Retinal detachment;241
18.16;14.16 Hypertensive Retinopathy;242
18.17;14.17 Non-hereditary degenerative abnormalities;243
18.18;14.17.1 Feline central retinal degeneration (FCRD);243
18.19;14.18 Papilledema;243
18.20;14.19 Papillitis, optic neuritis;244
18.21;14.20 Neoplasia;244
18.22;14.21 Amblyopia / amaurosis;245
19;15 Breed Predispositions and Hereditary Eye Diseases;250
20;15.1 Introduction;250
21;15.2 Modes of inheritance;250
22;15.3 Is the abnormality inherited?;251
23;15.4 Breed predispositions and inherited eye abnormalities;253
24;16 Glossary of Terms Relating to the Eye;260
25;Index;264


(p. 237)

15.1 Introduction
During routine examinations, particularly of young animals, the clinician may be confronted with eye abnormalities which are presumed or are known to have a genetic cause. In addition to the eventual treatment of the patient, it is important for the owner, the breeder, and the breed association to know what the consequences are for the affected animal, its littermates, its parents, and the breed population (prognosis, whether or not to use the animals for breeding, spreading within the population, etc.).

Inherited abnormalities are in general caused by one or more "abnormal" genes (mutations) in the inheritance pattern (genotype) of the animal. These abnormal factors (also called alleles, defined as any alternative form of a gene responsible for a specific phenotype that can occupy a particular homolog chromosomal locus) are often suppressed or influenced by the rest of the genes of the animal (rest genotype).There are also influences from non-inheritable factors in the environment, for example, the food or housing. The genes and the environment together determine the individual’s ultimate appearance (phenotype).

Half of the genes of an individual are received from one parent and half from the other. The number of abnormal genes and the manner in which they are transmitted lead to certain patterns of inheritance. Once the pattern of inheritance is known or presumed, most affected animals and also, eventually, the carriers can be detected. Moreover, then it is often possible to determine the means by which the disease can be eradicated. It also should be noted that a disease which has a simple mode of inheritance (especially dominant) can generally be eliminated more efficiently than a disease that has a multiple mode of transmission.

15.2 Modes of inheritance

15.2.1 Simple inheritance
In this mode of inheritance only one gene plays a role in transmitting the disease. This gene can be expressed in a number of ways.

15.2.1.1 Autosomal dominant (not sex-linked)
In this mode of inheritance, the disease is caused by a gene mutation (D) that suppresses or is dominant over the corresponding gene for the normal characteristic. The gene for the 15 normal characteristic that is suppressed is called the recessive gene (d). If the animal receives the "D" gene from both parents, then it has the genotype "DD" and will show the disease (affected). If the animal receives the "D" gene from one parent (this parent must therefore have the "D" gene itself) and the "d" gene from the other parent, its genotype is "Dd" and it will also show the abnormality. If the animal is "dd", it is normal and does not inherit the abnormality. Diseases with complete simple dominant inheritance occur, unfortunately, only sporadically. Unfortunate, because in these diseases the carriers are also directly recognizable and thus prevention of the disease by means of breeding rules is greatly simplified. These types of diseases will present in every generation, and genotypically affected animals will also be phenotypically affected. Exclusion of all affected animals from breeding will eliminate the disease.


The authors

All authors are well experienced in theory and practice since ages. They are one of the well respected Ophthalmologists in Europe and the USA.

Frans C. Stades, DVM, PhD, Dip. ECVO
Associate Professor of Veterinary Ophthalmology
Department of Clinical Sciences of Companion
Animals
Faculty of Veterinary Medicine
Utrecht University, The Netherlands

Milton Wyman, DVM, MS, Dip. ACVO
Professor of Veterinary Clinical Sciences
Ohio State University College of Veterinary
Medicine
Professor of Ophthalmology
Ohio State University College of Medicine
Columbus, Ohio, USA

Michael H. Boevé, DVM, PhD, Dip. ECVO
Associate Professor of Veterinary Ophthalmology
Department of Clinical Sciences of Companion Animals
Faculty of Veterinary Medicine, Utrecht University,
The Netherlands
Honorary Professor of Veterinary Ophthalmology, Stiftung
Tierärztliche Hochschule Hannover, Germany

Willy Neumann, DVM, Dip. ECVO
Specialist for Veterinary Surgery, Veterinary Ophthalmology
Am Drosselschlag 25
Giessen-Heuchelheim, Germany

Bernhard Spiess, DVM, PhD, Dip. ACVO/ECVO
Department for Small Animals, Ophthalmology Unit
Vetsuisse Faculty
University of Zurich, Switzerland



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