Ocular Disease of the Aging Dog
World Small Animal Veterinary Association World Congress Proceedings, 2004
Ellen Bjerk s, DVM, PhD, DECVO
Norwegian School of Veterinary Science, Department of Companion Animal Clinical Sciences
Oslo, Norway

Older animals may suffer from ocular conditions that may be of slight discomfort, painful or vision threatening. The animals' quality of life relies in part on our skills in identifying and treating these conditions. Ocular disease in the aging dog may be divided into primary ocular disease, and ocular signs of systemic disease. Thus, it is important to identify and treat underlying conditions if present, and a general examination should always be included in the work-up of an ocular condition.


Orbital neoplasms in general occur in older animals, the mean age being approximately 9.5 years. In comparison, orbital abscesses most commonly occur at a younger age, with a mean age of about 4 years. Orbital neoplasms cause slowly progressive exophthalmos. Unless the tumor is positioned straight behind the globe, a deviation of the eye may be noted. Lateral deviation is most frequent, most often with a concurrent protrusion of the third eyelid. Neoplasms are not initially painful, in contrast to orbital inflammatory disease. Exophthalmos caused by orbital neoplasia must be distinguished from buphthalmos caused by glaucoma. Venous compression may lead to slightly elevated intraocular pressure in neoplasia-induced exophthalmos. In contrast, in glaucoma the globe itself is enlarged and the increase in intraocular pressure is usually more significant, the exception being concurrent uveitis where the intraocular pressure may be reduced even in buphthalmic eyes. Orbital ultrasound is useful in diagnosis, preferably combined with a fine-needle aspirate. Examination of the oral cavity should always be performed in dogs with space-occupying orbital lesions.

Primary glaucoma is a breed related disease, with bilateral clinical manifestation occurring in middle aged to older dogs. Several breeds may be affected, including the American Cocker Spaniel, Basset Hounds, Samoyed, Welsh and English Springer Spaniels, Bouvier des Flandres, Siberian Husky and Norwegian Elkhound.

In most breeds a congenital malformation of the drainage angle is present (goniodysgenesis) with further clogging of the angel with age.


Horner's syndrome is caused by an affection of the sympathetic nerve. The sympathetic nerve fibres arise from the hypothalamus, pass through the brainstem and follow the cervical spinal cord to synapse with preganglionic cell bodies in the gray matter. At the level of T1 to T3 the nerve leaves the spinal cord, extends along the thoracic sympathetic trunk and synapses in the cranial cervical ganglion near the tympanic bulla. Within the middle ear the sympathetic fibres join a branch of the glossopharyngeal nerve and cross the middle ear. From here the pupillomotor fibers enter the cavernous sinus and join the trigeminal nerve, pass through periorbita and enter the globe via the long ciliary nerve. In the dog, some sympathetic fibers may also innervate the smooth muscles in the eyelids and periorbita.

Clinical signs in Horner's syndrome include enophthalmos and drooping of eyelids (ptosis), in addition to miosis due to lack of tone in the extraocular smooth muscles. Idiopathic Horner's syndrome occurs in middle aged and old dogs with a breed predisposition in the Golden Retriever. A thorough examination to identify the primary cause is indicated. The level of injury can be diagnosed medically, by observing the time until pupil dilation after instillation of topical epinephrine. The result may, however, be difficult to interpret.

Severe pain may cause enophthalmos and miosis and is an important differential diagnosis to Horner's syndrome.

Changes in eyelids

Eyelid neoplasms occur most frequently in older dogs, with a mean age of 9-10 years. Tumors of glandular origin (adenoma or adenocarcinoma) are most common, followed by melanomas. A benignant: malignant ratio of 3:1 has been reported for eyelid tumors. In general, tumors of the upper eyelid produce most obvious clinical signs, as the upper eyelid is more involved in blinking and the third eyelid helps in protecting the cornea from tumors on the lower eyelid. An important differential diagnosis to tumors of the eyelid is chalazion. Chalazion is a granuloma formation at the rim of the eyelid caused by retained meibomian secretions and may be associated with chronic blepharitis.

Neoplasms of the eyelid should be resected surgically through a wedge-shaped incision and submitted for histopathology. Chalazion is treated by curettage followed by topical antibiotics. Based on the primary cause, topical steroids may be added.

Changes in tear film and distribution

Keratoconjunctivitis sicca is caused by lowered or absence of tear fluid. Although KCS can be seen in dogs of any breed, there is a certain breed predisposition. KCS can occur uni-or bilaterally, and is most often due to an immunologic reaction in the tear glands, but can also be connected with systemic disease and occur as a drug-related reaction (especially sulphonamides). Earlier surgical removal of prolapsed third eyelid gland (cherry eye) can predispose to later KCS.

The clinical signs vary according to the rate of progression with conjunctivitis, keratitis and corneal pigmentation. KCS is diagnosed by measuring tear production. Treatment for KCS includes cleaning of the eyes, artificial tears, and topical antibiotic treatment when a secondary infection is present, as well as topical cyclosporine. Recently, a similar drug, tacrolimus, has been suggested as treatment of KCS, tacrolimus being more potent than cyclosporine. Scientific data on the use in dogs is lacking, however. Some dogs will benefit from topical steroid treatment. 2-3 drops of 2% pilocarpine mixed in the feed is recommended by some to stimulate tear production. Corneal ulcers should be treated according to severity. If medication does not relieve the KCS situation, saliva can be used as tear substitute by transposition of the parotid gland duct to the conjunctiva.

Defective tear film may also be caused by a deficit in mucin produced from the conjunctival goblet cells. The mucinous part of the tear film normally covers the aqueous part and prevents desiccation and breaking of the tear film. With lack of mucin, the tear film breaks up more quickly, despite normal production from the tear glands. This condition is less common than KCS and is treated with daily rinsing and application of artificial tears.

Facial paralysis is associated with the dog being unable to blink, causing a desiccation of the cornea. The tear production may be reduced concurrently. Testing of menace response may be difficult to interpret, as the dog is not able to blink. Facial paralysis may occur as an idiopathic condition in old dogs, or may be associated with generalized neurological disease. A neurological examination should be included in the work-up.

Corneal change

Corneal dystrophies are most often seen in older dogs and are described according to localization within the cornea as basement membrane dystrophy, stromal dystrophy and endothelial dystrophy.

Basement membrane dystrophy

Persistent corneal erosions have been recognized primarily in the Boxer and Pembroke Welsh Corgi, but may also affect other dog breeds. There is no sex predisposition. The cause of these ulcers is a defect in the hemidesmosomes of the epithelial basement membrane, preventing adhesion of the epithelium to the underlying stroma. Other predisposing factors causing chronic corneal ulceration must be ruled out. The ulcer presents with characteristic loose edges of non-attached epithelium. Depending on the depth and duration of the ulcer there may also be signs of secondary wound healing, including corneal vascularization and formation of granulation tissue. Treatment consists of removing the loose epithelium followed by a grid pattern keratotomy, topical antibiotics, topical atropine and systemic NSAIDs.

The stromal dystrophies

Stromal dystrophies consist of lipid material, but the composition of the dystrophy varies. Cholesterol deposits have a crystalline appearance and may be aggregated into needle-like forms, while a more homogenous grayish opacity indicates non-crystalline lipids such as cholesterol esters, triglycerides and phospholipids. Usually both crystalline and non-crystalline lipids are present together, but their proportions may differ. The changes are seen as bilateral oval whitish glittering spots. The condition is not painful, and the changes will not be stained by fluorescein, as the epithelium is most often intact. Occasionally, however, the dystrophy may affect the epithelium, causing chronic corneal ulceration. This is most often seen in the Shetland Sheepdog, in which the disease may more correctly be classified as a degenerative or inflammatory keratopathy.

Endothelial dystrophy

Endothelial dystrophy presents as progressive corneal edema resulting from abnormal endothelial cells. The disease is diagnosed most frequently in the older Boston Terrier, but also in Chihuahuas and Dachshunds. Age of appearance of clinical signs vary from 5-9 years in the Boston Terrier to 8-13 years in the Chihuahua and Dachshund. Senile degeneration of the endothelial cells result in lowered cell number, while the cells still present become enlarged and irregular. Thus, they cannot maintain their pumping action, which results in increased water uptake in the corneal stroma. On examination the cornea shows a bluish-white irregular appearance with lack of corneal vascularization. The changes may initially be barely visible and although this is a bilateral disease, both eyes are not always symmetrically affected. In addition to corneal haziness the edematous cornea is predisposed to bullous keratopathy and corneal ulcerations. Vision is impaired in direct proportion to the severity of the corneal edema and the other corneal changes. Hyperosmotic preparations have been recommended, but have limited usefulness as they cause ocular irritation. Penetrating keratoplasty is the only definitive treatment, but the outcome may vary.

Iris and ciliary body

Iris atrophy is a common condition in the aged dog, especially in dogs of small breeds. The condition is most often bilateral, but the degree of changes may differ. Mild cases present with a slightly irregular pupil, while in more severe cases there may only be a thin peripheral rim of iris tissue left, or the iris may contain multiple perforations. Anisocoria (difference in pupil size) is a frequent finding, as is poor pupillary light reflex, as well as photophobia due to lack of iris tissue. A close examination will establish the diagnosis, revealing lack of the iris border or larger parts of the iris.

As already mentioned, glaucoma is most often a disease of the middle aged to older dog. With age, there is an increased deposit of glycosaminoglycans in the iridocorneal angle. Although many factors may be involved, obstruction of the drainage angle may be considered an important factor predisposing for glaucoma.


Lens fibres are formed as a continuous process throughout life, through elongation and transformation of lens epithelial cells in the equatorial region. Together with a gradual decrease in lens water content, the increased packing of lens fibres causes the lens to take on a bluish appearance in older dogs. This senile sclerosis must not be confused with cataract, which may also develop in old dogs. Directing a light beam through the pupil and observing the retroillumination from the tapetum can most easily differentiate the two conditions. In senile sclerosis there will be a tapetal reflex present, while in cataract this may be partially or totally lacking, darker areas covering parts of the visual field.


The vitreous body is loosely fastened to the back of the lens through small ligaments, while the attachment to the retina is more solid. The vitreous is normally transparent, but contains a few cells and may be site for inflammatory and degenerative reactions. Age-dependent changes include asteroid hyalosis, vitreous floaters, synchysis scintillans and vitreous syneresis. Vitreous syneresis represents irreversible change with liquefaction of the vitreous. This condition predisposes to retinal detachment. Asteroid hyalosis and synchysis scintillans may be difficult to differentiate clinically as both present as small particles floating in the vitreous in one or both eyes, however, asteroid hyalosis is by far the more common. The clinical significance is limited, as for vitreous floaters.


Inherited retinal degenerations (the PRAs) most often occur in older dogs of specific breeds. Retinal degeneration of non-hereditary nature can also be found in older dogs due to preceding ocular disease. PRA can be distinguished from these by the history, by PRA being breed-related with a known age of onset and with the retinal degeneration being bilateral symmetric.

Sudden acquired retinal degeneration (SARD) occurs sporadically in dogs of all breeds. The causal agent is not known, but a triggering of the photoreceptors causes sudden degeneration. SARD occurs in middle-aged dogs, females being slightly more often affected than males. Both eyes are affected equally. Since all photoreceptors degenerate simultaneously, the vision loss is complete, in comparison to PRA, which presents with initial night blindness. There is no known treatment.

Secondary ocular disease

Systemic diseases causing ocular disease in aging dogs primarily include tumor metastasis, diabetes mellitus (cataracts) and hypertension.

Diabetes mellitus is a common cause of rapid-onset bilateral cataracts. A high cataract incidence has been reported in diabetic dogs, even in animals apparently well regulated on insulin. Hypertensive retinopathy has been most commonly reported in cats but does occur in dogs with chronic renal failure as well. In early stages, there is constriction of retinal capillaries with later vessel rupture and hemorrhage. Rupture of retinal vessels causes posterior hemorrhage and retinal degeneration, while rupture of choroidal vessels causes retinal detachment or hyphema. The underlying cause should be diagnosed and corrected if possible.

Speaker Information
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Ellen Bjerk s, DVM, PhD, DECVO
Norwegian School of Veterinary Science
Department of Companion Animal Clinical Sciences
Oslo, Norway

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