Ophthalmology PDF - Wendy M. Townsend

Ophthalmology 8 CHA P TE R Wendy M. Townsend...

Ophthalmology 8 CHA P TE R Wendy M. Townsend II. Basic ocular anatomy EXAMINING THE EYE A. Eyelids I. Diagnostic tests 1. Protect the globe A. The Schirmer tear test I (STTI): Allows quantifica- 2. Distribute the tear film tion of the production of the aqueous tear phase 3. Produce the lipid layer of the tears 1. Measures basal plus stimulated tear 4. Drainage of the tear film production B. Third eyelid (nictitating membrane, nictitans) 2. Must be performed before the application of 1. T-shaped cartilage skeleton any drops or topical anesthetic 2. Nictitans gland produces part of the aqueous 3. Measure how far tears travel along the strip portion of tears from the notch in 1 minute C. Tear film 4. Normal results can range from 15 to 1. Oily outer layer produced by meibomian 25 mm/minute glands 5. Less than 10 mm/minute is suspicious of re- 2. Aqueous layer (main portion) produced by lac- duced tear production rimal and nictitans glands 6. Less than 5 mm/minute is diagnostic of 3. Inner mucoid layer produced by conjunctival dry eye goblet cells B. The Schirmer tear test II D. Drainage of the tears 1. Measures basal tear production 1. Lacrimal puncta at medial canthus of upper 2. Performed after anesthetizing the cornea with and lower eyelids proparacaine and drying the excess fluid from 2. Canaliculi from puncta to lacrimal sac the conjunctival sac 3. Nasolacrimal duct empties into the nose at the 3. Performed as for STTI nasal ostium 4. STTII reading 艐 50% of STTI reading E. Globe: The wall of the globe itself consists of C. Fluorescein staining three main tunics (layers) 1. Administer from sterile, single-use impregnated 1. The outer fibrous wall (cornea and sclera) paper strips (or single-use vials) 2. A middle vascular coat: The uveal tract (iris, 2. Moisten the strip with artificial tears or sterile ciliary body, choroid) saline and apply a small amount over the dor- 3. An inner neuroepithelial layer (retina  retinal sal bulbar conjunctiva pigment epithelium  neurosensory retina) 3. Do not touch the cornea to avoid misleading stain deposition DISEASES OF THE ORBIT 4. Flush eye with sterile saline to prevent a false impression of stain uptake I. Anatomy of the orbit 5. In the presence of an epithelial defect, fluores- A. Bony structure cein stains the stroma bright green 1. Maxillary, frontal, lacrimal, zygomatic, sphe- D. Measurement of intraocular pressure (IOP) noid, and palatine bones 1. Normal is 15 to 25 mm Hg 2. Herbivores have “closed” orbit with bone 2. Digital assessment of IOP: Very unreliable and 360 degrees around orbital circumference inaccurate 3. Dogs, cats, and others have “open” orbit with 3. The Schiφtz tonometer: Operates on the supraorbital ligament at lateral aspect principle that the amount of indentation of a B. Extraocular muscles given area of the cornea is proportional to 1. Dorsal, medial, ventral, and lateral rectus the IOP muscles 4. Applanation tonometers measure the pressure 2. Dorsal and ventral oblique muscles required to flatten a given area of the corneal 3. Retractor bulbi muscles surface (this pressure is proportional to the II. Conditions that affect the orbit IOP). The most commonly used applanation to- A. Abcesses and cellulitis nometer is the Tonopen 1. Acute onset unilateral exophthalmos 84  CHAPTER 8 Ophthalmology 85 2. Pain is apparent on opening of mouth B. Districhiasis: More than one hair emanates from a 3. Causes: Trauma, foreign body, fungal or para- meibomian gland opening sitic infections, tooth-root abscess, sinus infec- C. Ectopic cilia: Hair erupts through the palpebral tion, inflammation of zygomatic salivary gland conjunctiva (often associated with a mucocele) D. Trichiasis: Hair in normal location but misdi- 4. Diagnostics: Complete blood cell count (CBC), rected toward the globe serum chemistry. Orbital ultrasound. Dental III. Blepharitis: Inflammation of the eyelids examination with or without radiographs. Fine A. Bacterial: Most commonly Staphylococcus needle aspiration (FNA) through oral mucosa intermedius behind last molar B. Parasitic: Mites (e.g., Demodex or Sarcoptes in 5. Treatment: Drain abscess  systemic antibiotics young dogs, Notoedres in cats, face flies and hab- B. Orbital neoplasia ronemiasis in horses) 1. Presentation: Gradual onset, slowly progres- IV. Neoplastic eyelid diseases sive exophthalmos A. Canine 2. Usually nonpainful when manipulating mouth 1. Benign a. Occassionally enophthalmos 2. Meibomian gland adenoma most common b. Older animals B. Feline 3. 90% are malignant 1. Malignant 4. Diagnostics: Ultrasound, orbital computed to- 2. Squamous cell carcinoma most common mography (CT) or magnetic resonance imaging C. Equine (MRI), and FNA with cytology 1. Sarcoid: Locally invasive and fibroblastic 5. Treatment: Surgical excision often enucleation neoplasm. Usually affect horses younger than with extenteration of the orbit or partial or 7 years of age complete orbitectomy is required 2. Squamous cell carcinoma: Predilection for 6. Prognosis: Poor horses with light circumocular pigmentation C. Orbital trauma: Traumatic proptosis D. Bovine: Squamous cell carcinoma, the most com- 1. Presentation: Eyelids trapped behind the equa- mon eyelid neoplasm of cows tor of the globe 2. Treatment DISORDERS OF THE CONJUNCTIVA a. Globes deemed nonreplaceable should be enucleated I. Anatomy and physiology b. Globes to be replaced should be replaced A. The conjunctiva is a mucous membrane that lines with a temproary tarsorraphy under general the posterior aspects of the eyelids, the nictitat- anesthesia ing membrane, and the sclera before terminating 3. Prognosis at the limbus (corneoscleral junction) a. 20% to 30% chance of vision following pro- B. Functions of the conjunctiva ptosis 1. Protective covering of the eye and adnexa b. 50% to 60% chance of globe replacement 2. A source of the mucus portion of the tear film with or without vision (via goblet cells) 3. First line of defense against potential patho- gens (via conjunctival associated lymphoid DISORDERS OF THE EYELIDS tissue) I. Structural or functional abnormalities II. Congenital abnormalities: Dermoid (a choristoma) A. Agenesis (coloboma): A congenital defect in cats normal elements of skin in an abnormal location and horses A. Aberrant dermis affecting conjunctiva and/or cor- 1. Cats: Upper temporal eyelid (lateral 1/3 to 2/3) nea (sometimes also eyelids) fails to develop B. Appears as an elevated, often pigmented mass, 2. Absence of eyelids results in secondary trichia- usually bearing hairs sis and exposure keratoconjunctivitis C. Surgical excision is curative B. Ankyloblepharon: Adhesion of the eyelid margins III. Neonatal disease. Neonatal conjunctivitis (ophthal- to each other mia neonatorum) C. Dermoid: A choristoma (normal tissue in an ab- A. Infection before lid separation; often bacterial in normal location) puppies and viral or chlamydial in kittens D. Entropion: Inversion of the eyelid margin (usually B. Treatment: Separate lids, flush with sterile saline, results in secondary trichiasis) apply broad-spectrum antibiotic ointment four 1. Causes hairs to rub on cornea (secondary times daily in dogs, tetracycline in kittens trichiasis) C. Sequelae: Symblepharon (conjunctival adhesion 2. Correct surgically with a modified Hotz-Celsus to adjacent tissues), corneal perforation, fibrosis, excision blindness E. Ectropion: Eversion of the eyelid margin IV. Conjunctivitis II. Eyelash abnormalities A. Canine conjunctivitis A. Distichiasis: Cilia arise from meibomian gland 1. Bacterial: Rare openings 2. Secondary causes 86 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE a. Conformational lid abnormalities (e.g., en- 3. Basement membrane tropion, ectropion, trichiasis, lid tumors) 4. Stroma b. Spread of infection from elsewhere (e.g., 5. Descemet membrane: Does not take up fluores- skin, ears, lips) cein stain c. Tear film abnormalities: Keratoconjunctivitis 6. Endothelium sicca (dry eye) B. Corneal response to insult d. Irritants: Chemicals, dust 1. Edema: Loss of epithelial or endothelial layers 3. Viral: Canine distemper lead to edema. Fluid accumulation 4. Allergic or hypersensitivity 2. Vacularization: Normal cornea does not have B. Feline conjunctivitis blood vessels 1. Feline herpesvirus 1 (FHV-1) is the most com- 3. Pigmentation: It can arise from chronic corneal mon cause irritation 2. Chlamydophila felis may cause conjunctivitis as C. Keratitis: Inflammation of the cornea well. Treat with tetracycline or doxycycline II. Keratoconjunctivitis sicca (KCS; dry eye) 3. Mycoplasma felis: Opportunistic. Treat with A. Inflammation of the cornea and conjunctiva as a topical tetracycline result of low aqueous component of the tear film B. Causes 1. Immune-mediated destruction of the tear- DISORDERS OF THE NICTITATING producing glands: Most common cause MEMBRANE (usually bilateral) I. Anatomy 2. Congenital: Gland aplasia (unilateral or A. T-shaped cartilage bilateral) B. Nictitans gland at base 3. Iatrogenic: Excision of nictitans gland (unilat- C. Responsible for 30% to 40% of aqueous tears eral or bilateral) plus later loss of lacrimal D. Movement is passive protrustion gland function II. Abnormalities 4. Drug induced: Sulfa drugs, etogesic (usually A. Eversion or inversion of the cartilage bilateral) 1. Most common in large breeds 5. Trauma: Often follows prolpase or proptosis of 2. Scroll-like curling of the cartilage the globe (usually unilateral) B. Prolapsed gland of the third eyelid (Figure 8-1) 6. Neurogenic: Interference with nerve supply to 1. Weak connective tissue glands (usually unilateral) 2. Replace by tacking to orbital rim or pocket 7. Following infection: Distemper in dogs, herpes- technique virus in cats (unilateral or bilateral) 3. Do not remove or risk decreased tear production C. Clinical signs of KCS 1. Ocular irritation or pain 2. Conjunctivitis DISEASES OF THE CORNEA 3. Ocular discharge I. Anatomy 4. Keratitis A. Layers of the cornea D. Diagnosis of KCS 1. Tear film 1. Clinical signs (see above) 2. Epithelium 2. Schirmer tear test readings E. Treatment of KCS 1. Reduce immune destruction of tear producing glands: Cyclosporine 2. Stimulate tear production: Oral pilocarpine 3. Parotid duct transposition: Moving the parotid duct so that it opens into the lower conjuncti- val fornix III. Ulcerative keratitis A. Investigation of corneal ulcer 1. Fluorescein stain: Show presence of ulcer and demonstrate extent 2. Judge depth of ulcer. Note: Descemet's mem- brane does not stain with fluorescein 3. Swab from edge of ulcer crater for culture (bacterial, or fungal in some cases) 4. Smear from edge of ulcer for cytology B. Superficial corneal ulcers Figure 8-1 Cherry eye in a 2-year-old American cocker spaniel. Note 1. Treat initially with a broad-spectrum antibiotic the intumescent, hyperemic appearance of the gland, which can be seen 2. Typically, superficial ulcers heal within 3 to through the bulbar surface of the third eyelid conjunctiva. (From Dziezyc J, 5 days. If the ulcer has not resolved in 3 to Millichamp NJ. Color Atlas of Canine and Feline Ophthalmology. St Louis, 5 days 2005, Saunders.) a. The cause for the ulcer is still present  CHAPTER 8 Ophthalmology 87 b. The ulcer is infected (see below) c. An indolent ulcer is present (see below) 3. Slow-healing (indolent) ulcers in dogs. These are common in dogs and are due to a failure of the epithelium to adhere to the basement membrane. Management: a. Debridement and grid keratotomy: First line of treatment b. If ulcer does not heal in 2 to 3 weeks, repeat c. If ulcer does not heal, can do a superficial keratectomy (1) Requires general anesthesia and magni- fication (2) Surgical removal of superficial layer of cornea includes removal of epithelium, basement membrane, and very thin layer of corneal stroma Figure 8-2 Fungal plaque in the left eye of an 11-year-old American 4. Slow healing (indolent) ulcers in cats Quarter horse gelding being treated medically for fungal keratitis. The yellowish plaque is raised, and blood vessels are approaching the lesion a. Often associated with feline herpesvirus in- from the temporal aspect. Mild corneal edema can be noted surrounding fection the plaque. (From Gilger BC. Equine Ophthalmology. St Louis, 2006, b. Do not perform grid keratotomy, which may Saunders.) lead to corneal sequestrum formation 5. Slow healing (indolent) ulcers in horses a. Often superficial fungal infections b. Antifungal preparations b. Do not perform a grid keratotomy; debrid- (1) Fluconazole, miconazole, silver ing loose epithelium is acceptable sulfadiazine, natamycin C. Midstromal corneal ulcer (2) Miconazole: Intravenous (IV) preparation 1. Potentially more serious c. Topical atropine 1% drops aiming to dilate 2. Watch carefully the pupil 3. Perform culture and cytology d. Systemic nonsteroidal antiinflammatory 4. Antibiotics should be given frequently if ulcer drugs (NSAIDs) are given to help suppress is infected (e.g., initially every 2 hours) the uveitis 5. 1% atropine to dilate the pupil as needed but e. Surgery may be required not more than 4 times daily IV. Nonulcerative keratitis D. Deep ulcers or descemetoceles A. Chronic superficial keratitis (pannus) 1. Perforation can occur, so treat as an 1. Bilateral disease emergency 2. German shepherd, greyhound, border 2. Usually require surgical repair collie a. Conjunctival pedicle flap is preferred tech- 3. Immune mediated, exposure to ultraviolet nique. It provides a blood supply to the de- (UV) light a trigger fect for healing and physical protection to 4. Clinical signs seal the defect a. Raised pink swelling of the conjunctiva adja- b. If surrounding cornea is healthy and not in- cent to the ventrolateral limbus fected or melting, a corneoscleral transposi- b. Vascularization to produce a granulation tion can be performed tissue appearance that spreads across the E. Herpesvirus keratitis (FHV-1) cornea 1. Common in cats c. Pigmentation often accompanies the 2. Conjunctivitis with or without corneal ulcer vascularization 3. Symblepharon conjunctival adhesions are com- d. Not painful mon sequelae 5. Treatment 4. Treatment a. Topical cyclosporine a. Topical antiviral medication (idoxuridine or b. Topical corticosteroids trifluridine; Viroptic) c. Subbulbar conjunctiva injections of b. Topical -interferon has questionable depo corticosteroid preparations (e.g., efficacy Depo-Medrol) c. L-lysine orally administered may help re- d. Keratectomy duce frequency of recrudescence e. -irradiation F. Corneal fungal infection (mycosis) (Figure 8-2) f. Once inflammation is controlled mainte- 1. Common in horses nance treatment is necessary: 2. Ulcer or stromal abscess (1) Owners need to monitor dogs consis- 3. Aspergillus and Fusarium spp. tently for recurrence 4. Management (2) Limit UV light exposure, keep indoors, a. Subpalpebral lavage fit with Doggles (www.doggles.com) 88 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE B. Eosinophilic keratoconjunctivitis 13. Secondary glaucoma 1. A unique condition of cats III. Treatment of uveitis 2. Corneal lesions are pink and raised with white A. Topical steroids or topical nonsteroidal adherent material ophthalmic solutions 3. Not painful B. Topical atropine to relieve ciliary spasm and 4. Diagnosis miosis a. Appearance C. Systemic steroids or systemic NSAIDs b. Surface scrapings for cytology reveal D. Identify and treat underlying cause eosinophils E. Topical treatment treats only the anterior uvea 5. Treatment IV. Infectious diseases that cause anterior uveitis in a. Attempt topical steroids. the dog b. Megestrol acetate (Ovaban) A. Tick-borne disease C. Corneal sequestrum (corneal mummification) 1. Rickettsia rickettsii 1. A condition unique to cats 2. Ehrlichia canis 2. Commonest in brachycephalic breeds (e.g., 3. Borrelia burgdorferi Persians, Himalayans) B. Fungal disease 3. Cause: Chronic irritation to the cornea 1. Blastomycosis 4. Appearance: Light brown to black lesion on 2. Cryptococcosis corneal surface 3. Coccidiomycosis 5. Management 4. Histoplasmosis a. Leave alone to slough; can cause perfora- C. Bacterial disease tion of cornea 1. Bacteremia or sepsis b. Keratectomy 2. Leptosporosis 3. Brucellosis D. Protozoal DISEASES OF THE ANTERIOR UVEA 1. Toxoplasmosis I. Anatomy of the anterior uvea 2. Leishmaniasis A. Iris E. Viral 1. Ciliary zone 1. Infectious canine hepatitis due to canine 2. Pupillary zone adenovirus type-1 3. Iris sphincter muscle 2. Distemper 4. Iris dilator muscle V. Noninfectious causes of anterior uveitis in the dog B. Ciliary body A. Immune mediated 1. Produces aqueous humor 1. Lens-induced uveitis 2. Pars plicata 2. Immune-mediated thrombocytopenia 3. Pars plana 3. Uveodermatologic syndrome 4. Zonular fibers of lens attach here a. Affects pigmented areas of both the eyes II. Effects of inflammation on the anterior uveal tract and skin A. Increased vascular permeability b. Immune-mediated disorder whereby B. Breakdown of blood-aqueous barrier melanocytes are targeted by cytotoxic C. Clinical signs T-lymphocytes 1. Hypotony: Decreased production of aqueous c. Predisposition exists in the Akita, Samoyed, humor Siberian husky, and Shetland sheepdog 2. Flare: Protein in the anterior chamber B. Corneal ulceration 3. Cell: Inflammatory cells in the anterior C. Neoplastic chamber 1. Primary Intraocular tumors 4. Hypopyon: White cells (pus) in the anterior a. Uveal melanoma: Most common primary in- chamber traocular tumor in dogs 5. Hyphema: Blood in the anterior chamber b. Ciliary body neoplasia 6. Keratic precipitates: Aggregates of cells and 2. Secondary intraocular tumors: Lymphosar- inflammatory debris that stick to the corneal coma most common endothelium 3. Trauma 7. Miosis: Prostaglandin F-induced ciliary muscle VI. Agents associated with feline uveitis spasm A. Viral 8. Cataracts 1. Feline leukemia virus (FeLV) 9. Posterior synechia: Iris adhered to the 2. Feline immunodeficiency virus (FIV) anterior lens capsule 3. Feline infectious peritonitis (FIP) 10. Preiridal fibrovascular membrane: Fibrovascu- B. Protozoal toxoplasmosis lar membrane on the surface of the iris C. Fungal: Same agents as dogs 11. Iris bombe: A 360-degree circumferential pos- VII. Uveitis in the horse: Equine recurrent uveitis (ERU), terior synechia that results in pupillary block “moonblindness” glaucoma A. Possible causes 12. Lens luxation 1. Leptospirosis  CHAPTER 8 Ophthalmology 89 2. Onchocerca cervicalis 1. Buphthalmos 3. Trauma 2. Corneal changes B. Bacterial sepsis especially in neonates a. Corneal vascularization b. Exposure keratitis c. Corneal (Haab's) striae: Gray, linear GLAUCOMA streaks that represent breaks in Descemet I. Pathology membrane A. Impairment of the aqueous humor outflow system 3. Scleral thinning B. Elevation of pressure within the eye 4. Decreased evidence of pain C. Damages the axoplasmic flow in the optic nerve 5. Episcleral vascular engorgement head resulting in retinal degeneration and a loss 6. Subluxated or luxated lens of vision 7. Iris degeneration D. Glaucoma is a leading cause of blindness in the 8. Ciliary body degeneration middle-aged dog 9. Cataract II. Anatomy and physiology 10. Funduscopic lesions A. Production of aqueous humor a. Cupped optic disc: Posterior bowing of the 1. Nonpigmented ciliary body epithelium lamina cribrosa 2. Energy-dependent ionic transport, energy- b. Retinal degeneration: Thinning of the independent hydrostatic and colloid osmotic retina, increased tapetal reflectivity and gradients retinal vascular attenuation 3. An important enzyme in the active secretory c. Optic nerve atrophy (energy-dependent) process is carbonic V. Treatment of glaucoma anhydrase A. Medical B. Normal outflow of aqueous humor 1. Osmotic diuretics (mannitol IV 20%, glycerol 1. Corneoscleral outflow (conventional outflow, 50% oral solution) 85% in dogs, 97% in cats). Aqueous passes into a. Action: Dehydrates the vitreous humor and the iridocorneal angle, between the fibers of causes a rapid drop in IOP. Water must be the pectinate ligament through the trabecular withheld for 2 to 3 hours after administra- meshwork, into the angular aqueous plexus, tion or the osmotic effect is lost scleral venous plexus, and ultimately into b. Contraindications: Compromised cardiovas- systemic vascular circulation through the cular or renal function, dehydration, pneu- vortex veins and episcleral veins monia, cerebrovascular hemorrhage 2. Uveoscleral outflow (nonconventional, 15% in c. Side effects: Severe hypovolemia, fulminant dogs, 3% in cats). Aqueous humor passes pulmonary edema, renal failure through the trabecular meshwork and passes 2. Carbonic anhydrase inhibitors (CAIs) (meth- into the iris stroma or between the ciliary mus- azolamide, acetazolamide, dorzolamide hydro- cle fibers to reach the supraciliary and supra- chloride 2% topical) choroidal spaces where it is absorbed by the a. Action: Decreases aqueous humor produc- vessels of the iris, ciliary body, and choroid tion by decreasing the formation of bicar- III. Classification of glaucoma bonate ions A. Primary glaucoma b. Side effects: Hypovolemia, metabolic 1. Common in dogs acidosis and hypokalemia (panting, 2. Abnormal formation of the iridocorneal angle vomiting, diarrhea, anorexia, behavioral (goniodysgenesis) changes, and rarely KCS) B. Secondary glaucoma: Any disease process can 3. Miotics, applied topically (pilocarpine 2% solu- interfere with aqueous outflow and result in tion, phospholine iodide). Action: Increase secondary glaucoma aqueous humor outflow 1. Primary lens luxation 4. Sympatholytic drugs (-blockers) (timolol male- 2. Iridocyclitis ate, betaxolol hydrochloride, levobunolol HCl) 3. Intumescent cataract a. Action: Reduce aqueous production by an 4. Trauma unknown mechanism 5. Hyphema b. Contraindications: Hypotension; may influ- 6. Retinal detachment (chronic) ence cardiac function during anesthesia 7. Neoplasia 5. Adrenergic drugs (sympathomimetics) (dipive- 8. Ocular melanosis frin hydrochloride, epinephrine bitartrate). Ac- IV. Clinical signs of glaucoma tion: Increases aqueous outflow (-receptors) A. Acute glaucoma with grossly elevated IOP and decreases aqueous humor production 1. Severe pain (-receptors) 2. Episcleral and conjunctival vascular injection 6. Prostaglandin analogues (latanoprost, 3. Corneal edema travaprost, bimatoprost) 4. Pupillary dilation a. Action: Increases uveoscleral outflow and 5. Loss of vision causes miosis B. Chronic glaucoma b. Can cause marked lowering of IOP 90 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE B. Surgical Treatment 1. Procedures to reduce aqueous production: Cyclodestruction a. Cyclocryosurgery b. Transscleral cyclophotocoagulation (laser ciliary body ablation) c. Intravitreal injection of cyclodestructive drug (pharmacologic ablation of ciliary body) (1) Gentamicin (2) Destroys retina: Use only in blind eyes 2. Surgical production of alternative drainage pathways: Drainage implant 3. Removal of the globe (enucleation) or evisceration a. Evisceration and intraocular silicone prosthesis b. Enucleation with or without orbital prosthesis Figure 8-3 Mature cataract. (From Dziezyc J, Millichamp NJ. Color Atlas DISORDERS OF THE LENS of Canine and Feline Ophthalmology. St Louis, 2005, Saunders.) I. Anatomy A. Capsule 4. Cause B. Cortex a. Heritable or genetic: One of the most com- C. Nucleus mon causes of cataracts in dogs D. Lens sutures b. Metabolic: Diabetes mellitus E. Zonular fibers (1) Hyperglycemia overwhelms normal II. Lens aging (nuclear sclerosis) metabolic pathways in lens: Hexokinase A. Lens fibers produced throughout life enzyme saturated so aldose reductase B. Central portions become compressed enzyme shunts sugars to sorbitol C. Hardening (sclerosis) of lens nucleus pathway D. Can still see the fundus (2) Production of nonsoluble sugar alcohol III. Cataracts: Any opacity within the lens (sorbitol) creates osmotic gradient with A. Classification of cataracts influx of fluid into lens 1. Age of animal at onset (3) Disruption of lens fiber membranes a. Congenital: Present at birth leads to protein precipitation and cata- b. Juvenile: Occurs in young dogs ract formation c. Senile: A cataract that develops at 6 years c. Associated with other ocular abnormalities of age and older (1) Ocular malformations 2. Stage of maturation (2) Intraocular disease such as a. Incipient: The very smallest opacity. Less (a) Secondary to uveitis than 15% of the lens is opaque (b) Glaucoma b. Immature: A tapetal reflection is still visible (c) Lens luxation c. Mature: A solid opacity of the lens and ab- (d) Secondary to retinal degeneration sence of a tapetal reflection. (Figure 8-3) (e) Senile d. Intumescent: The lens has imbibed water (f) Traumatic: Perforating injury to the and is “swollen” cornea and lens (i.e., cat claw) e. Hypermature: Liquefaction of lens cortex 5. Others begins and the cortex begins to clear a. Nutritional: Canine and feline milk replacers f. Morgagnian: Liquefaction of the cortex leav- (arginine, tryptophan deficiency) ing a nuclear remnant that sinks b. Electric shock: Anterior subcapsular (puppy 3. Location within the lens that bites an electric cord) a. Capsular: Opacity confined to the lens c. Radiation: Causes ↓ epithelial cell mitosis— capsule young animals more susceptible b. Subcapsular: Most of opacity involves cor- d. Toxic: Disophenol for hookworms tex directly beneath lens capsule B. Treatment (cataract surgery) c. Cortical: Opacity of the lens cortex (may be IV. Abnormalities of the zonular fibers (lens anterior or posterior cortical) displacement) d. Nuclear: Opacity primarily in center of the A. Degree of dislocation lens (nucleus) 1. Subluxation: Lens remains in the patellar fossa e. Equatorial: Opacity is primarily in the area behind the iris of the lens equator 2. Luxation f. Polar and axial: Within the pupillary axis. a. Complete displacement of the lens from the Usually a focal, central opacity patellar fossa  CHAPTER 8 Ophthalmology 91 b. Anterior luxation predisposes to glaucoma 2. Retinal dysplasia (RD) due to pupillary blockade by the lens and a. Abnormal development of the retina accompanying vitreous b. Vary in severity from lesions that have no B. Direction of dislocation effect on vision to blindness 1. Anterior c. Three categories of RD a. Lens anterior to the plane of the iris (in the (1) Multifocal RD anterior chamber) (2) Geographic RD b. Lens usually touching the axial cornea: May (3) Total RD cause corneal edema (a) In the Labrador retriever and Samo- 2. Posterior: Lens in the vitreous cavity yed, RD is associated with skeletal C. Cause dysplasia and the syndrome is 1. Primary luxation called oculoskeletal dysplasia a. Degeneration of lens zonular fibers (b) The skeletal abnormalities result in b. Breeds predisposed: Terriers dogs with shortened legs with joint c. Usually anterior luxation deformities. Oculoskeletal dysplasia 2. Secondary to ocular disease in the two breeds is dominant with a. Iridocyclitis (inflammatory zonulysis), espe- incomplete penetrance cially in cats C. Acquired inherited abnormalities: Progressive ret- b. Chronic glaucoma or buphthalmos inal atrophy (PRA) are bilateral and progressive, c. Cataracts leading to eventual blindness D. Treatment: Intracapsular lens extraction 1. Rod-cone dysplasia (rcd): Animals are typically blind by between 1 and 3 years of age 2. Rod-cone degeneration: Onset is at 2 to 4 years DISEASES OF THE VITREOUS AND FUNDUS of age, and blindness occurs sometime later I. Vitreous 3. Diagnosis: Electroretinogram (ERG) A. Anatomy and physiology D. Acquired noninherited abnormalities 1. Vitreous occupies ¾ of the volume of 1. Sudden acquired retinal degeneration (SARDs) the eye a. Signalment: Overweight, middle-aged female 2. Composition: 98% water dogs, usually smaller breeds 3. Collagen fibrils as skeleton for gel b. History: Sudden onset of vision loss (hours B. Pathology or diseases of the vitreous to days) 1. Asteroid hyalosis c. Clinical signs: Sudden onset of blindness, a. Punctate, calcium-lipid complex absent or depressed pupillary light reflexes b. Commonly seen in geriatric animals (PLRs). The retina initially appears normal. c. No treatment necessary After several days to weeks, the retina will 2. Synchysis scintillans (liquified vitreous): Cho- degenerate, resulting in tapetal hyperreflec- lesterol deposits suspended in a liquefied vitre- tivity, vascular attenuation, and a pale optic ous (vitreous syneresis) nerve 3. Vitreous hemorrhage d. Diagnosis: Extinguished ERG. This disease a. Serious event affects only the rods and cones of the retina b. Possible causes: Coagulopathy, retinal de- e. Treatment: None tachment, infectious disease, hypertensive 2. Feline central retinal degeneration (FCRD) retinopathy, trauma, and metastatic or pri- a. Dietary taurine deficiency (historically seen mary neoplasia should be considered in cats fed food formulated for dogs) 4. Vitritis: Occurs secondary to inflammation of b. Lesions are bilaterally symmetrical surrounding (pars plana, retina, uvea) ocular c. They start as elliptical lesions dorsal and tissues temporal to the optic papilla (involving area II. Fundus centralis) and may progress to horizontally A. Anatomy linear hyperreflective bands above the pa- 1. Outermost layer  sclera pilla and even total degeneration of the 2. Middle layer  choroid, part of uveal tract, tapetal fundus very vascular, special reflective layer 3. Retinitis-chorioretinitis  tapetum a. Active: Dull gray area with indistinct mar- 3. Innermost layer  retina composed of retinal gins between normal and affected retina pigment epithelium and neurosensory retina b. Inactive: Hyperreflectivity of the tapetal fun- B. Congenital anomalies dus; hyperpigmentation of the tapetal fun- 1. Collie eye anomaly dus (usually focal and may be in the center a. Choroidal hypoplasia lateral to the of a hyperreflective area) optic disc c. Causes: Mycoses (blastomycosis, histoplas- b. Coloboma: “Pits” in the wall of the eye mosis, cryptococcosis, coccidiomycosis; c. Retinal detachment bacterial-septicemia; viral-distemper; d. Intraocular hemorrhage toxoplasmosis; hypertension; neoplasia- e. Tortuosity of retinal vasculature lymphoma; parasitic migration; FIP, 92 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE FeLV-lymphoma, FIV, toxoplasmosis in cats, NEURO-OPHTHALMOLOGY Streptococcus equi in horses, thromboembolic meninogoencephalitis (TEME), bluetongue, I. Cranial nerves (CN) with ophthalmic implications hog cholera, scrapie in food animals A. CN II optic: Carries the axons for vision and 4. Retinal hemorrhage the PLR a. Thrombocytopenia or thrombocytopathy B. CN III oculomotor b. Coagulopathy 1. Motor to the dorsal, medial, and ventral rectus c. Vasculitis muscles and the ventral oblique muscle d. Hypertension 2. Motor to the levator palpebrae superioris e. Anemic retinopathy 3. Parasympathetic innervation to the pupillary f. Hyperviscosity syndrome and ciliary constrictor muscles g. Radiation-induced C. CN IV trochlear: Motor to the dorsal oblique h. Metastatic neoplasia: Hemangiosarcoma muscle most common. D. CN V trigeminal i. Senile 1. Ophthalmic branch: Corneal and conjunctival 5. Retinal detachment or separation sensation and skin sensation of the medial a. Separation of the neural retina from the region of the eyelids retinal pigment epithelium (RPE) 2. Maxillary branch: Skin sensation of the lateral b. Causes: Inflammatory choroiditis with region of the eyelids subretinal exudates, infectious diseases E. CN VI abducens such as mycoses, trauma, congenital 1. Motor to the lateral rectus muscle and retrac- (collie eye, dysplasia), immune-mediated, tor bulbi muscles (not present in primates and hyperviscosity, hypertension, neoplastic, birds) idiopathic 2. Sympathetic innervation to the muscles of the c. Treatment cat’s third eyelid (1) Treat underlying cause F. CN VII facial (2) Symptomatic treatment for noninfec- 1. Motor to the orbicularis oculi muscle (closes tious disease the eyelids) 6. Equine peripapillary retinopathy (butterfly 2. Parasympathetic innervation to the lacrimal lesions). glands a. Postinflammatory scars resulting in depig- G. CN VIII vestibulocochlear mentation around the optic disc 1. Sensory information for hearing, balance, and b. Some cases may be manifestations of ocular motility equine recurrent uveitis 2. Position with regard to gravity 3. Detection of linear or rotational stimuli of the head DISEASES OF THE OPTIC NERVE 4. Postural and ocular motility reflexes generated I. Optic nerve hypoplasia: Congenital malformation of by these positional changes the optic nerve II. The visual pathway II. Papilledema A. Photon of light A. Edema of the optic papilla B. Hits retina B. Causes include increased intracranial pressure C. Relayed along optic nerve (hydrocephalus), neoplasia of the optic nerve, or- D. Crosses at optic chiasm (about 65% in the cat; bital space–occupying masses (abscesses, neo- 75% in the dog; up to 90% in cows, horses, plasms, hemorrhage), neoplasia resulting in com- sheep and pigs; and 100% in most fish, birds, pression of the optic nerve fibers, vitamin A and reptiles) deficiency in steers E. Optic tracts III. Optic neuritis or papillitis F. Lateral geniculate nucleus: Approximately 20% of A. Animal presents with no PLRs and blindness of the fibers diverge from the optic tracts before the affected eye(s) reaching the lateral geniculate nucleus and are in- B. Causes include trauma, orbital abscess-neoplasia, volved in generating the pupillary light reflex (see metastatic neoplasia, granulomatous meningoen- section below). Therefore the pupillary light re- cephalitis (reticulosis) or infectious causes flex is not a test for vision (distemper, blastomycosis, cryptococcus, G. Optic radiations toxoplasmosis, FIP), idiopathic H. Visual cortex of the occipital lobes of the IV. Optic atrophy: Usually the result of postinflamma- cerebrum tory disease, glaucoma, trauma or proptosis, post- III. Ocular reflexes papilledema, or massive blood loss or cranial trauma A. PLRs (II and III): In simplistic terms, PLR or visual in the horse pathway lesions will have the following character- V. Coloboma: Pits or excavations of the optic disc or istics: peripapillary region caused by incomplete closure of 1. Afferent arm: Vision loss and direct PLR deficit the embryonic fissure present  CHAPTER 8 Ophthalmology 93 2. Efferent arm: No vision loss; direct or consen- sual deficit present 3. Cortical: Vision loss, no PLR deficit B. The menace response (II and VII) 1. Make a menacing gesture with your hand to- ward the eye while covering the contralateral eye. The animal should blink in response to the stimulus 2. This is a learned response, not a reflex, and is frequently absent in young animals C. The dazzle reflex (II and VII). Technique: Direct a high intensity light into the animal’s eye. This re- flex does not mean that the animal “sees,” but it does mean there is some function to the retina, optic nerve, and visual tract D. Palpebral reflex (V and VII). Technique: Touch the Figure 8-4 Presenting signs of Horner syndrome (autonomic denervation) animal at the medial canthus and lateral canthus include a quadrad of ocular signs in small animals. In this cat with Horner and evaluate for a blink response to the stimulus syndrome of the right eye, the classic signs (MEPP) of miosis, enophthal- E. Corneal reflex (V and VII). Technique: Before ap- mos, protrusion of the third eyelid, and ptosis are present. (From Dziezyc J, plying topical anesthetic to the cornea, use a few Millichamp NJ. Color Atlas of Canine and Feline Ophthalmology. St Louis, wisps from a cotton ball or cotton swab (or an 2005, Saunders.) aesthesiometer) to touch the surface of the cor- nea and monitor for a blink response F. Vestibulo-ocular reflex (VIII and III, IV, and VI). 3. Postganglionic Technique: Move the head back and forth and ob- a. Otitis media or interna (small animals), tu- serve that the eyes move equally in the opposite mors direction of the head movement b. Orbital tumors IV. Horner syndrome c. Guttural pouch disease (horses) A. Definition: Loss of sympathetic innervation to 4. Horner syndrome: Often (i.e., in more than 50% the eye of cases) idiopathic in dogs and cats B. Anatomy of the sympathetic innervation to the E. Localization of the lesion eye: three components 1. Clinical signs: Suggestive 1. Central neuron: From hypothalamus to T1-T3 2. Pharmacologic testing of spinal cord a. Differentiates preganglionic vs. postgangli- 2. Preganglionic neuron: Brachial plexus, anterior onic Horner syndrome mediastinum, the neck along with the jugular b. 10% phenylephrine ophthalmic solution: To vein and carotid artery, ending just caudome- evaluate for denervation hypersensitivity dial to the tympanic bullae and confirm the presence of Horner 3. Postganglionic neuron: From the cranial cervi- syndrome cal ganglion, through the middle ear and cav- ernous sinus, to the orbit to innervate the iris Supplemental Reading dilator muscle C. Signs of Horner syndrome (Figure 8-4) Gelatt KN. Veterinary Ophthalmology, 3rd ed. Baltimore, 1. Miosis: Loss of dilator muscle function 1999, Lippincott Williams & Wilkins. 2. Ptosis: Mueller muscle paralysis Gilger BC. Equine Ophthalmology. St Louis, 2005, 3. Enophthalmos: Loss of tone from muscularis Saunders. orbitalis Maggs DJ, Miller PE, Ofri R. Slatter’s Fundamentals of 4. Protrusion of nictitans: From loss of smooth Veterinary Ophthalmology, 4th ed. St Louis, 2007, muscle tone to nictitans and enophthalmos Saunders. 5. Increased sweating over affected side of face in Peiffer RL, Petersen-Jones SM. Small Animal Ophthalmol- horses, decreased sweating in cattle (the ipsi- ogy: A Problem-Oriented Approach, 4th ed. St Louis, lateral nostril will be dry) 2008, Saunders. D. Causes of Horner syndrome Petersen-Jones SM, Crispin SM. BSAVA Manual of Small 1. Central (usually associated with other signs) Animal Ophthalmology, 2nd ed. Gloucester, UK, 2002, a. Injury (spinal) BSAVA. b. Neoplasia Riis RC. Small Animal Ophthalmology Secrets, c. Embolic infarct, disk compression Philadelphia, 2002, Hanley & Belfus. 2. Preganglionic a. Brachial plexus avulsion b. Anterior mediastinal lymphosarcoma (cats) c. Neck injuries (misplaced injection in horses)