Current Concepts in Veterinary Ophthalmology
Dennis E. Brooks, DVM, PhD
University of Florida
What do dogs and cats see?
1. Small monocular visuals fields of peripheral vision in dogs and cats (~80°) as compared
to the horse (146°).
2. Large frontal binocular visual field of 85° in dogs and cats
3. Dogs have cones that are receptive at 429 and 555 nm and are dichromats. All evidence suggests that the cat is dichromat with vision similar to a human who is red-green color blind. Dogs and cats appear to respond to the blue and yellow short-wave length colors the best, but appear to have trouble with green and red. Dogs and cats are also rod- dominant animals. As rods do not function in daylight these animals are dependent on their few cones for spatial and temporal visual resolution, which probably means that their blue and yellow visual world is a fuzzy blue and yellow world. What appears red to us is simply dark to the dog and cat, and a part of the green spectrum is indistinguishable from white. Colors that would appear very rich to us a more pastel-like to the cat. The cat sees a green, grassy lawn as a whitish lawn, and a green rose-bush as a whitish bush with dark flowers.
4. Most dogs are emmetropic with a tendency for mild myopia in German Shepherds (-9.86D), Rottweilers (-1.77D) and Miniature Schnauzers (-0.66D). Myopia is associated with nuclear sclerosis in older dogs. Refractive errors are rare in cats, but when they do occur, they tend to be myopic.
5. Acuity is 30 cycles per degree (cpd) for humans, 18 cpd for horses, 12 cpd for dogs and 6 cpd for cats. Acuity in dogs in 0.4 times that of people, 0.67 times that of horses, and 2 times that of cats. Acuity in cats is 0.2 times that of people, 0.33 times that of horses, and 0.5 times that of dogs. If normal human vision is 20/20, then that of the dog is 20/50 and that of the cat is 20/100.
6. Aphakic condition in dogs is hyperopic. Streak retinoscopy for air or spectacle correction is +14D in the dog and +10.5D in humans. Pseudophakic emmetropia requires +41D intraocular lens to correct the hyperopic aphakic condition in the dog.
7. The preponderance of large diameter axons and large ganglion cells indicate that the dog should have good motion detection and high temporal contrast capabilities. Acuity is less than humans and horses, but greater than the cat. Dogs have few alpha ganglion cells (GC) in the temporal quadrants of the retina. Alpha GC have large receptive fields, large, fast-conducting axons, and are associated with motion detection. The effect of the loss of such cells to the binocular nasal visual fields of the dog is not known.
8. Siamese cats have fewer ganglion cells, little stereopsis, less acuity and too much crossing over of optic nerve axons at the optic chiasm. This results in misrouting and suppression of the visual input from the nasal visual fields at the LGN. Cross-eyedness may be an adaptation to move the nasal retinas (and temporal visual fields) more anteriorly, as the more esotropis that is present the more misrouting of axons that has occurred.
9. The vertical stenopaic slit pupil of the cat allows for maximum light control and optically decreases astigmatic scatter in the horizontal meridian.
10. The lens of dogs and cats has weak accommodative ability and therefore they have imited near focus capability. The corneal curvature of both species (u.9 mm in dog, 9.1 mm in cat) is much greater than the human (7.9mm) to compensate for this.
Common Ocular Disorders of Dogs and Cats
May result in enophthalmos, exophthalmos, or even complete proptosis or luxation of the eyeball. Infections, inflammation, blindness and/or strabismus may be sequelae. Brachycephalic breeds are at higher risk.
Pupils dilated ; guarded to unfavorable prognosis
Treatment for traumatic proptosis:
1. Keep the eye moist. Gently remove debris with copious sterile saline flushes.
2. Under general anesthesia replace the eye, performing canthotomy if necessary
3. Temporary tarsorrhaphy
4. Maintain medical treatment with systemic antiobiotics, topical antibiotic ointments and atropine. May use systemic anti-inflammatory drugs.
Ulcerative keratitis is the most common corneal disease in our practice. A corneal ulcer is a lesion in which epithelium and a variable amount of stroma have been lost. Small acute ulcers in normal cornea should heal rapidly.
Corneal ulcers classified by depth
Superficial Deep’ Descemetocele Iris Endophthalmitis
(simple)Ulceration Prolapse ulceration
Corneal ulcers classified by etiology.
Abrasions, Foreign bodies, Entropion, Eyelash disease,
Infectious, KCS Treatment the phases in treatment of a corneal ulcer are as follows:
Determine etiology : remove or eliminate specific cause (e.g. KCS, correction of entropion).
While most corneal ulcers are secondary, concurrent bacterial involvement must be treated by antimicrobial therapy.
Broad spectrum antibiotics are usually administered; culture and sensitivity tests can guide selection.
1. Acetylcysteine (5 percent) is used topically for its collagenase and protease
2. SERUM. Serum is thought to act when used topically or subconjunctivally because it contains an alpha-2 macroglobulin with antiocollagenase activity.
3. Topical atropine therapy (1 percent TID) is also instituted to relieve pain due to
secondary anterior uveitis, and to decrease the formation of synechiae from the miotic pupil (as a result of uveitis).
Provide corneal support: In the treatment of deep corneal ulceration, coverage with one of the various kinds of flaps should be maintained for 10-21 days. Types of conjunctival flaps: 360 ÌŠ, pedicle, and bridge.
Topical and Subconjunctival Corticosteroids are Contra-Indicated When the Cornea
Retains Fluorescein Stain (i.e. Corneal Erosion or Ulcer is Present).
Treatment of Deep Stromal Corneal Ulcers, Descemetoceles, Iris Prolapses, Corneal Lacerations
1. Aggressive therapy
2. Surgical repair is needed
3. Topical and systemic antiobiotics
4. Topical atropine
5. Conjunctival flap, corneoscleral transposition, or partial â€“ thickness corneal graft
Inward rolling of eyelid margin
Entropion is most common in dogs
Uncommon in cats (primarily in Persians)
Medical treatment: Ocular lubricant ointments “ Lacrilube, Dura Tears, or Duralube
Surgical treatment: Temporary vs. permanent
Sebaceous gland adenoma
Frequently found in older dogs
Should be removed
Frequently darkly pigmented
Early surgical resection is recommended
Squamous cell carcinoma
Rare in the dog
Most common lid tumor of cats, cows and horses
Early biopsy and wide surgical excision are imperative
Radiation therapy decreases the chance of recurrence
Keratoconjunctivitis sicca (KCS)
Keratoconjunctivitis sicca (KCS): aqueous deficiency of the precorneal tear film (PTF) causing progressive inflammatory changes of the cornea and conjunctiva.
Schirmer tear test
Normal 15-25 mm/minute
Suspicious 8-10 mm/minute
Low < 8 mm/minute
Breeds: English Bulldog, West Highland White Terrier, Lhasa Apso, Pug, Cocker Spaniel, Pekingese, Yorkshire Terrier Shih Tzu, Miniature Schnauzer, Boston Terrier
Acute: Blepharospasm, conjunctivitis, mucoid discharge, corneal ulcers, dry appearance
Chronic: owners frequently complain of â€œchronic eye infection,â€ copious, mucoid-mucopurulent discharge, dull cornea with neovascularization, pigmentation of cornea, improvement with any topical medication
Always attempt 1-2 months of medical treatment because the problem may be transient.
Owner compliance may be difficult.
Goals to remove pain and maintain vision:
o Replace tears Hypotears (Cooper Vision); Tears Naturale (Alcon), Lacrilube
(Allergen); Duratears (Alcon); Lacriserts (Merck)
o Stimulate production of tears with 2 percent cyclosporin (OPTIMUME); dose: 1
BID; may take 3-4 weeks before increasing tear production
o Control bacterial flora topical broad spectrum antibiotic (e.g. triple antibiotic
o Control inflammation topical corticosteriods, may combine with topical
antibiotic, use only if not ulcerated.
The eye gets red or has conjunctivitis in nearly all types of eye disease. The eye has limited
ways to react to injury!
STT routine on all conjunctivitis cases
Cytology topical anesthetic, spatula
Allergic frequent cause
Hypertrophy and Prolapse of Nictitans Gland (Cherry Eye)
1. Primarily seen in young dogs, less than two years
2. Most common in Beagles, American Cocker Spaniels, Pekingese
3. Gland protrudes above free border of the TE, becomes inflamed and enlarged. May see epiphora, mucoid discharge and conjunctival inflammation
4. Histologically plasma cell and lymphocyte infiltration
a. Medical physically replace gland, topical Corticosteroids
b. Surgical Repositioning of gland to normal location
Definition: Opacity of the lens or lens capsule. Lens fibers are disrupted.
Cataract Classification: to help evaluate etiology and prognosis. Classification of cataracts by degree of maturation:
Incipient: earliest lens changes
Immature: fundic reflex still present (usually present peripherally); vision is impaired to a variable extent
Mature: lens is totally opaque, the fundic reflex is absent, and vision is lost
Hypermature: wrinkling of the anterior lens capsule; this resorption may cause a lens-induced uveitis
Nuclear Sclerosis: Age related change due to compaction of the lens fibers. Not a true opacity therefore not a true cataract.
Surgical Techniques for Cataracts
Extracapsular cataract extraction (ECCE)
Phacofragmentation (preferred therapy at the moment)
Canine and Feline Glaucomas
Aqueous Humor Dynamics and Intraocular Pressure
By definition, glaucoma is increased IOP with associated visual deficits. In most cases in dogs and cats, glaucoma is caused by obstruction or stenosis of the aqueous humor outflow pathways.
Pathologic Effects of Glaucoma
All ocular tissues are eventually affected by the elevated IOP. The presence, individually or as a group, of a red eye, corneal edema, mydriasis, belepharospasm, blindness, and buphthalmos can be explained by the increased IOP. If the IOP cannot be reduced, an overall increase in the size of the globe may result (buphthalmos). This change may occur more rapidly in young dogs and cats. Zonular disinsertion results in lens luxation.
Types of Glaucoma
Primary glaucoma in dogs is a breed-related, hereditary condition. Predisposition to primary open-angle glaucoma in the Persian and Siamese cat breeds has also been noted, but in the author’s experience, domestic short-hairs are more often affected. In both dogs and cats, affected animals may present with only one eye involved, but the risk is very high for development of glaucoma in the other eye.
Secondary glaucoma is more commonly encountered than primary glaucoma in dogs and cats. The elevated IOP results from other disease processes within the eye. The glaucoma may be open or closed angle, and in some instances is associated with pupillary block. The condition tends to be unilateral without an inherited basis.
Clinical Signs of Acute and Chronic Glaucoma
The presentation of a patient with a painful, red eye requires that glaucoma be ruled out among the possible diagnoses of conjunctivitis, uveitis, or keratitis. The onset of clinical signs in cats is often insidious, as cats are less likely to demonstrate the acute intense corneal edema and episcleral congestion exhibited in dogs. Signs of chronic glaucoma are dramatic. The include combinations of the early signs with buphthalmos, lagophthalmos, exposure keratitis, luxated lens, corneal striae, optic nerve atrophy with cupping, and retinal atrophy.
IOP must be accurately measured to diagnose glaucoma. The normal canine and feline IOP is 15 to 25 mm Hg. An IOP greater than 30 mm Hg is considered pathologic and diagnostic for this condition.
Multiple drug therapy to decrease IOP by reducing production of aqueous humor and diminishing the resistance to aqueous humor outflow is the most effective approach. Carbonic- anhydrase inhibitors reduce ciliary-body production of aqueous humor independent of diuresis.
Topical parasympathomimetic drugs act primarily to cause ciliary muscle contraction, increasing the outflow of aqueous humor. Î’-adrenergic antagonists decrease production of aqueous humor.
Oral and intravenous hyperosmotic agents lower IOP rapidly and are used in the emergency treatment of acute glaucoma.
Cyclocryotherapy has been found to be effective in decreasing production of aqueous humor by the transcleral freezing of the ciliary body with nitrous oxide. The most effective surgical or medical therapy for glaucoma is the gonioimplant. Enucleation or evisceration with prosthetic silicone implants is indicated when vision is lost in uncontrolled glaucoma. The source of pain is removed, and no further medication is necessary. The cosmetic appearance of the prosthetic
implant is sometimes preferred to that of enucleation.
Inherited Retinal Disease
Collie Eye Anomaly
Congenital (present at birth)
A developmental anomaly of the choroids, + optic nerve and sclera
Inherited as a simple autosomal recessive, but probably is much more complex than this Stationary (non-progressive except for retinal detachments and intraocular hemorrhage)
Bilateral asymmetry of the signs
Collies (rough/smooth), Border Collie, Shetland Sheepdog
In USA approximately 85 percent of Collies are clinically affected but this number is declining (approximately 5-10 percent of Shelties). Obviously with a recessive condition this means that most normal dogs are carriers
o Choroidal hypoplasia: A pale area of varying size of depigmentation temporal
to superotemporal to the optic disc. This may be an area of RPE and choroidal
hypopigmentation, tapetal hypoplasia and choroidal dysplasia. Choroidal
hypoplasia is seen in all cases of CEA.
o Colobomas of posterior pole (often of optic nerve; seen in 30 percent of cases)
may be associated with visual deficit
o Retinal detachment (5-10 percent of cases)
o Retinal or vitreous hemorrhage of hyphema
o Blindness (3-4 percent of cases); many dogs with this disease show no visual
abnormalities, unless severe colobomas or retinal detachment are present. Other
anomalies seen in Collies may include retinal folds (vermiform streaks) and
subepithelial corneal opacities. These dogs are invariably microphthalmic.
Retinal dysplasia (folds) and corneal dystrophy may also be seen innormal-
eyed Collies; i.e. they are not necessarily part of the CEA syndrome. Tortuosity
of retinal vasculature is not per se a feature of the disease although may
Some dogs have only minor choroidal hypoplasia. These pale areas may become masked with pigment as the dog’s fundus matures. Thus by twelve months of age, although genotypically affected, may appear clinically normal and are termed go-normals.
Diagnosis can be made at 4-8 weeks of age. Severely affected puppies should be identified at this time. Due to the prevalence in the population, eradication is very difficult. Breeding minimally affected dogs does not necessarily avoid severely affected offspring.
Not really a specific disease an anatomic retinal abnormality that may occur alone or in conjunction with other ocular abnormalities. This is a separate entity from photoreceptor dysplasia seen in progressive retinal atrophy
Congenital “ seen in puppies
Stationary (non-progressive usually)
Can be inherited (recessive and maybe dominant forms) or acquired due to intrauterine inflammation and retinal necrosis (canine herpes virus or irradiation)
o Retinal folds seen as streaks, dots or Y or V shapes in the tapetal fundus, often
around the superior retinal vessels; may be green, grey or dark in color or grey or
black streaks in the nontapetal fundus
o Retinal rosettes: histiologic description of dysplasia
o Focal retinal degeneration
o Retinal detachments + hemorrhage, if dysplasia is extensive
o Blindness if dysplasia is sever Localized retinal dysplasia seen in American Cocker, Spaniel, English Springer Spaniel, Beagle, Labrador Retriever, Rottweiler, Samoyed, Golden Retriever and potentially in other breeds
In the Sealyham and Bedlington Terriers the disease is a vitreo-retinal dysplasia
In the Labrador Retriever at least one form of retinal dysplasia is associated with skeletal dysplasia
Diagnosis of retinal dysplasia at 4-8 weeks of age by ophthalmoscopy avoid breeding affected dogs.
Retinal Dysplasia with Multiple Ocular Anomalies
In the Australian Shepherd retinal dysplasia occurs with:
Microphthalmia + microcornea
Superficial cornea opacity
Similar abnormalities have been reported in the Great Dane, Merle Collies and Old English Sheepdogs
Inherited in the Merle Australian Shepherd. Etiology unknown in other breeds.
Progressive Retinal Atrophy (PRA)
Inherited retinal photoreceptor dysplasia (young animals) or degeneration (mature animals)
Usually not congenital
Not stationary (eventual blindness in some forms of the disease)
Generalized progressive retinal atrophy; blood tests becoming available for some dog breeds
o Inherited in most cases as simple autosomal recessive
o Progressive loss of vision night vision first, then day vision
o Breeds affected: Irish Setter, Collie, English/American Cocker Spaniel,
Miniature/Toy Poodle, Norwegian Elkhound, Afghan Hound, Border Collie,
Cardigan Welsh Corgi, Beagle, Borzoi, Dachshund, Cairn Terrier, English
Springer Spaniel, English/Gordon Setter, Greyhound, Labrador Retriever,
Miniature Pinscher, Pointer, Saluki, Siberian Husky, Samoyed, Swiss Hound,
Shetland Sheepdog, Tibetan Terrier
o Variable age of onset, e.g. in the Irish Setter and Collie PRA can be diagnosed by
ophthalmoscopy by 6-8 months of age. In Miniature Poodles PRA may develop
anywhere between 3 and 12 years of age. Other breeds tend to be in between
o Signs: Night blindness progressing to total blindness; slow and incomplete
pupillary light reflexes (maybe); tapetal hyper-reflectivity (retinal thinning);
nontapetal depigmentation and pigment clumping; retinal blood vessel narrowing
and loss, especially arterioles starting at the periphery; optic nerve atrophy;
cataracts form due to release of toxins from the diseased retina
o Diagnosis: behavioral signs, maze test, ophthalmoscopy, electroretinogram
o Etiology: in the dogs with early onset (Collies and Irish Setters) PRA, it is due to a deficiency of enzyme cGMP phosphodiesterase: allows accumulation of cGMP
which is toxic to photoreceptors. Other types of PRA are photoreceptor dysplasia
o No treatment at present
Sudden Acquired Retinal Degeneration (SARDS) or Silent Retina Syndrome
Sudden loss of vision (DDX optic neuritis, retinal detachment)
No ophthalmoscopic signs at first; later (months) see typical hyperreflectivity, etc., of retinal degeneration
ERG extinguished from the onset (hence silent retina)
Especially middle-aged, slightly obese female dogs that are also PU/PD (? Cushingoid);
seen in Poodles and Dachshunds
Etiology unknown, toxic degeneration or metabolic disorder; may be related to imbalances of MSH and ACTH and the resulting metabolic disturbances of the RPE; vitreal glutamate levels are high.
Dog Owners and Breeders Symposium
July 28, 2001
University of Florida
College of Veterinary Medicine