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OPHTHALMIC DISEASE AND ITS MANAGEMENT

Mary B. Glaze, DVM, MS

Few ophthalmic diseases are truly unique to the geriatric patient. Ocular lesions of the aging canine and feline eye are as likely to be the culmination of a lifetime of undiagnosed or ineffectively managed disease as they are to repre­sent a specific age-related phenomenon. Those disorders that do occur with increased frequency in the older dog and cat are the focus of this article.

SENILE OCULAR CHANGES

Iris Atrophy

Iris atrophy is a common aging change in both dogs and cats and is the single most common cause of sluggish and incomplete pupillary light responses. Pupils may appear dissimilar in size and shape, with an irregular or thread-like edge to the pupillary margin. Affected areas appear as translucent patches or openings within the iris when light is reflected from the tapetal fundus. Occa­sionally, atrophy will cause large holes within the iris stroma, resembling multi­ple pupillary openings. Although iris atrophy may occur in any breed, Toy and Miniature Poodles, Miniature Schnauzers, and Chihuahuas appear to have a higher incidence than other breeds. Vision is unaffected, but animals are some­times sensitive to bright light. Sunglasses and sunglass holders (Sunpups; Dog­works, Mill Valley, CA) may be beneficial in the rare case of extreme photopho­bia.

Lenticular Nuclear Sclerosis

Lenticular nuclear sclerosis generally begins in companion animals at 6 years of age. The nucleus of the lens becomes increasingly dense as newer fibers

From the Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME 27 • NUMBER 6 • NOVEMBER 1997 1505

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laid down at the lens equator compress the central fibers. A concurrent decrease in soluble protein contributes to the loss of lens clarity. When the pupil is dilated, the nucleus appears homogeneously opalescent, with smooth bound­aries separating it from the peripheral lens cortex (Fig. 1). The tapetal reflection can be easily seen through the opacity as can retinal detail. The increased translucency is more apparent when the eye is observed from the side. Nuclear sclerosis is unlikely to influence vision to a significant degree, although near and night vision may diminish slightly. If owners complain of vision loss in an animal with nuclear sclerosis in a quiet eye, the veterinarian should consider other causes of blindness, particularly retinal and optic nerve diseases.

ORBITAL NEOPLASIA

Most orbital neoplasms are aggressive, malignant tumors diagnosed in the advanced stages of development. In both dogs and cats, 90% of orbital tumors are malignant. Only 3 of 23 dogs in one retrospective study survived longer than 3 years from the time of diagnosis.U Mean survival in a series of 21 cats was only 1.9 months following diagnosis.5 Primary tumors predominate in dogs; secondary tumors are more common in cats. Primary neoplasms arise from an assortment of tissues within the orbit, including epithelium, bone, nerves, and vessels as well as connective, hemolymphatic, and glandular tissues. Secondary tumors extend from adjacent structures or metastasize from distant sites. Pri­mary and secondary orbital tumors reported include neurogenic sarcoma, rhab­domyosarcoma, osteogenic sarcoma, squamous cell carcinoma, zygomatic and lacrimal adenoma and adenocarcinoma, third eyelid gland adenocarcinoma, meningioma, undifferentiated sarcoma, optic nerve glioma, hidradenocarcinoma, undifferentiated carcinoma, pheochromocytoma, chondrosarcoma, hemangiosar-

Figure 1. Senile nuclear sclerosis is characterized by a homogeneous grayness in the central lens. The tapetal reflection can be easily visualized, and the fundus can still be examined. Impact on vision is negligible.

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coma, liposarcoma, lymphosarcoma, chondroma rodens, osteochondroma, multi­lobular osteochondrosarcoma, malignant melanoma, pituitary choristoma, mast cell tumor, reticulum cell sarcoma, schwannoma, neurofibrosarcoma, fibrosar­coma, fibrous histiocytoma, nasal carcinoma, and myeloproliferative disease.10

Gradual, painless exophthalmos is accompanied by periocular swelling, protrusion of the third eyelid, and deviation of the globe (Fig. 2). Secondary lagophthalmos may cause corneal drying, with secondary ulceration or superfi­cial keratitis. Compression of the globe can cause retinal detachment with subsequent pupillary abnormalities and blindness. Enophthalmos occasionally occurs as a consequence of orbital tissue destruction. Primary orbital neoplasia is typically unilateral, but metastatic disease may affect both orbits. The average age of dogs with orbital neoplasia is 8 years, ranging from 18 months to 15 years. Older cats are similarly at risk, with a median age of 9 years (range, 1-18 years) at diagnosis. Cats with primary tumors, including fibrosarcoma, undifferentiated carcinoma, and hemangioma, are generally younger (mean age, 5.7 years) than cats with secondary neoplasia such as squamous cell carcinoma or lymphosarcoma. Nevertheless, orbital lymphosarcoma and multicentric fi­brosarcoma have been reported in cats under 2 years of age.

The clinical suspicion of orbital neoplasia may be substantiated using radi­ography, orbital ultrasonography, computed tomography, or magnetic resonance imaging. Orbital aspirates may be obtained for cytologic evaluation from the anesthetized patient, first acknowledging the possibility of sampling error and inadvertent damage to ocular and orbital tissues. If ultrasound-guided biopsy is not available, the direction of deviation of the exophthalmic globe suggests the tumor's location and the site for needle entry. For example, lateral strabismus suggests a medial space-occupying mass. To reach the mass, the needle should be inserted medial to the third eyelid, penetrating the conjunctiva, and aspirating gently along the medial orbital wall. Other orbital quadrants may be sampled in a similar manner. For masses directly behind the eye, the lateral aspect of the

Figure 2. A 14-year-old Chihuahua demonstrates moderate exophthalmos and lateral strabismus associated with a retrobulbar adenocarcinoma.

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orbit should be surgically prepared, and the needle should then be inserted just posterior to the angle formed by the lateral orbital ligament and the zygomatic arch. Other diagnostics should include a complete physical examination and thoracic radiography. Patients requiring exploratory orbitotomy for confirmation should be referred to a veterinary ophthalmologist or surgeon.

Although orbitotomy and excision may be attempted in cases of circum­scribed primary tumors, early exenteration is the treatment of choice. Some tumor types may respond to adjunct chemotherapy or radiation therapy. Local recurrence and distant metastasis occur commonly, often within weeks to months following initial resection.

EYELID TUMORS

Tumors of the eyelid are routinely noted in aged animals, with a mean age of 9.6 years in affected dogs. The majority of canine eyelid tumors are benign. Adenomas, adenocarcinomas, benign and malignant melanomas, and papillo­mas are the most common eyelid tumors in the dog, with sebaceous adenomas accounting for 60% of canine eyelid neoplasms.19 In contrast, eyelid neoplasms in the cat are typically malignant and locally invasive if not distantly metastatic. Squamous cell carcinoma, basal cell carcinoma, fibrosarcoma, and mast cell tumor are the most common feline adnexal tumors.16

Although early excision of an eyelid tumor is the best means of eliminating potential irritation or enlargement, removal of small, asymptomatic, or slow­growing canine eyelid masses is considered elective due to the low incidence of malignancy. Although many canine eyelid tumors may be conservatively ob­served, those masses developing near a nasolacrimal punctum, enlarging rap­idly, or secondarily irritating the ocular surface should be removed. Feline masses should be completely and widely excised as soon as possible. In either species, tissue should be submitted for histopathologic examination.

For excision of a marginal eyelid neoplasm, a simple four-sided excision spares a greater proportion of the eyelid margin and provides a stable suture line when compared with the triangular wedge excision. The extent of the defect should not exceed one fourth to one third of the length of the lid; the latter is usually tolerated only in spaniels and hounds. A two-layer closure is recom­mended: simple continuous 6-0 absorbable sutures are placed in the tarsoconjunctiva and simple interrupted 4-0 to 6-0 nonabsorbable sutures are used to reappose skin/muscle. A permanent lateral canthotomy may be used to provide relief when removal of tissue compromises the length of the palpebral fissure. More extensive tumors generally require rectangular or square en bloc excisions followed by sliding skin grafts as in the modified H-plasty. Care must be taken to insure that the transposed tissue is lined by conjunctiva.

Ancillary treatments for eyelid neoplasms include cryotherapy, radiofre­quency hyperthermia, brachytherapy, radiation therapy, and laser resection. In geriatric patients, cryotherapy may be used to manage small masses using only local anesthesia. The site is clipped and cleansed with a topical antiseptic. Debulking prior to freezing provides adequate tissue for histopathologic exami­nation. A chalazion clamp placed around the mass compromises blood flow and facilitates the rapid freeze and slow thaw essential for successful cryotherapy. Two freeze-thaw cycles are performed with either liquid nitrogen or nitrous oxide, targeting a minimum peripheral temperature of - 25° C for most tumors and - 30° C for squamous cell carcinoma. Mild discomfort occurs for approxi­mately 12 hours following treatment. A tissue scab develops in a matter of

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days and then sloughs 10 to 20 days following the procedure. Secondary skin depigmentation usually resolves over a period of months, but whitening of the hair is permanent. Even in extensive lesions, cryotherapy characteristically causes minimal scarring or deformity.

ENTROPION

Enophthalmos secondary to depletion of retrobulbar fat, masticatory muscle atrophy, dehydration, or debilitating disease occurs with advanced age. Entro­pion is a common complication that may result in chronic conjunctivitis, corneal irritation, or ulceration, particularly in the cat. If the animal's systemic status precludes general anesthesia, local anesthesia is usually sufficient for placement of stay sutures to evert the eyelid margin. Permanent surgical repair should be considered in selected patients.

Entropion also occurs with some frequency in small-breed dogs involving the temporal superior eyelid. Secondary corneal ulceration results from contact of the eyelashes with the corneal surface. Surgical repair is a simple matter of removing a small ellipse of skin and muscle in the affected region and reappos­ing the skin with simple interrupted sutures to evert the eyelid margin.

LAGOPHTHALMOS

Facial nerve dysfunction occurs with increased frequency in geriatric dogs and cats, causing partial or complete loss of the blink response and alteration in lacrimal gland function.U Dryness of the cornea due to exposure or keratoconjunctivitis sicca results in chronic superficial keratitis and ulceration. Cocker Spaniels appear to be at highest risk, probably related to the incidence of otitis media/interna and surgical trauma in that breed. Affected animals may benefit from permanent lateral tarsorrhaphy to reduce the size of the palpebral fissure and minimize secondary exposure. The application of artificial tear oint­ment (Akwa Tears; Akorn, Abita Springs, LA) is also recommended to lubricate the ocular surface.

RECURRENT EPITHELIAL EROSIONS

A refractory superficial ulcer that persists, despite appropriate conventional therapy, suggests a healing disorder known as recurrent epithelial erosion. Synonyms include Boxer ulcer, rodent ulcer, and indolent ulcer. The dog may have a history of similar nonhealing ulcers. Clinical discomfort is usually charac­terized by intermittent squinting and tearing. The lesion is surrounded by a margin of edematous, scrolled, nonadherent epithelium, with diffusion of fluo­rescein dye beyond the defect margin. The adjacent cornea may demonstrate varying degrees of edema and vascularization but is often unremarkable. The problem occurs in any breed of dog and in either sex. Commonly affected breeds include the Boxer, Samoyed, Dachshund, Miniature Poodle, Welsh Corgi, and Wirehair Fox Terrier. Affected animals are usually over 5 years of age. Recurrent erosions are much less common in the cat.

The inciting cause of the erosion is frequently undetermined, but its refrac­tory nature is a consequence of abnormal adhesion between the corneal epithe­lium and stroma. Examination of the epithelium and basement membrane re­veals degeneration of the basal layer of epithelial cells, a misshapen basement

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membrane, and decreased density of hemidesmosomes.13 The animal is appar­ently unable to form a normal basement membrane to which the epithelial cells can adhere.

Treatment is preceded by topical anesthesia of the corneal surface with 0.5% proparacaine hydrochloride followed by mechanical debridement of the nonadherent marginal epithelium using a dry, sterile, cotton-tipped swab. The abnormal epithelium rubs off without effort when compared with healthy epi­thelium. The debrided area will be larger than the original epithelial defect and may encompass the entire corneal surface in some individuals.

Occasionally, debridement alone may stimulate healing. Epithelial adher­ence is more likely to follow when debridement is coupled with a punctate or grid keratotomy, however.2 This procedure creates multiple superficial defects in the stromal surface which serve as anchoring sites for the regenerating epithelium, probably by encouraging cellular infiltration within the stroma and elaboration of autologous growth factors. Owing to a less acute angle of needle placement, the grid keratotomy is more easily performed in the awake animal than is the punctate variety. Multiple superficial scratches are made 0.5 to 1 mm apart in a cross-hatched pattern using a 25-gauge needle held at a 45° angle to the corneal surface (Fig. 3). The scratches should extend approximately 1 mm into the normal cornea surrounding the erosion. Blepharospasm i s usually more apparent for 1 or 2 days following the procedure. Triple antibiotic solution is applied topically only two times daily to minimize manipulation which might disturb the vulnerable epithelium. Topical 1% atropine solution is indicated to effect if the pupil constricts. An Elizabethan collar is recommended to prevent self-trauma. Various medications and devices have been advocated in addition to this simple regimen, including antiproteases, replacement hormones, hyperos­motics, fibronectin, epidermal growth factor, aprotinin, polysulfated glycosami-

Figure 3. Linear scratches are apparent on the surface of the cornea after grid keratotomy to encourage epithelial adherence in a dog with recurrent epithelial erosion.

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noglycans, hydrophilic contact lenses, collagen shields, and third eyelid flaps. In most cases, the keratotomy decreases healing time significantly with resolution of the erosion occurring within 2 weeks. A recheck is advised 7 to 10 days following keratotomy. If epithelial lifting recurs, debridement is repeated at the first recheck. Keratotomy can be repeated at subsequent rechecks if the erosion persists. In rare circumstances, a superficial keratectomy or conjunctival graft may be necessary to effect healing. Clients should be informed of the inherent nature of the healing defect, the fact that subsequent debridement may be necessary, the potential for slow healing of the erosion, and the likelihood of recurrence.

CORNEAL STROMAL DEGENERATION

Corneal degeneration is characterized by loss of corneal clarity following deposition of lipid or mineral within the corneal stroma. The problem is rela­tively common in older dogs but is rare in cats. Refractory corneal ulceration, chronic corneal disease such as German Shepherd pannus, corneal exposure and drying secondary to lagophthalmos or keratoconjunctivitis sicca, prior excision of vascular masses such as dermoids, and previous episodes of episcleritis have all been associated with deposition of lipid or mineral within the cornea. Certain systemic diseases have also been implicated, including primary hyperlipidemia, hyperlipidemia associated with hypothyroidism, and hyperadrenocorticism pre­disposing to calcific degeneration or "band keratopathy."14 In many patients, the disorder occurs spontaneously with no known predisposing cause.

When located in the central cornea, the often symmetrical crystalline to dense yellow-white opacities may be indistinguishable from inherited corneal dystrophies. Lipid degenerations usually contain delicate white spicules seen best with magnification. Arcus lipoides, a ring-shaped opacity that develops in the perilimbal cornea and progresses centrally, has been linked to hypothyroid­induced hyperlipoproteinemia. Calcium has a more punctate, bright white, irreg­ular character. The surface also feels "gritty" when touched with a cotton­tipped applicator. Vascularization develops in long-standing lesions. A frequent complication of calcific degeneration is refractory corneal ulceration (Fig. 4).

Treatment for lipidosis is rarely indicated. In order to minimize progression, concurrent predisposing ocular disease should be treated appropriately. If serum lipid profiles are abnormal, dietary fat intake should be restricted. If endocrino­logic disorders such as hypothyroidism are confirmed, the primary disease should be treated. Progression of the infiltrate will likely cease with adequate control of the underlying disease, but resolution of the existing infiltrate is un­likely.

In patients with corneal ulceration secondary to calcific degeneration, topical treatment four to six times daily with chelating agents such as 1% to 4% disodium EDTA may reduce mineral accumulation and facilitate epithelializa­tion. In the face of persisting mineralization, superficial keratectomy should be considered to remove the deposits impeding normal corneal healing. Calcifica­tion may recur unless its underlying cause is corrected.

ENDOTHELIAL DYSTROPHY

Boston Terriers and Chihuahuas are afflicted with progressive, bilateral corneal edema secondary to a marked decrease in endothelial cell numbers and

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Figure 4. Calcific degeneration appears as a white, roughened opacity in the cornea of a 17-year-old Poodle. The pain of secondary ulceration caused the enopthalmos and third eyelid protrusion.

disorganization of the endothelium's normal mosaic arrangement. Female dogs 5 years of age and older are most commonly affected. Similar clinical signs have been described in the Boxer, Miniature Schnauzer, Miniature Poodle, and Dachshund. Progressive corneal edema can also occur in any geriatric patient secondary to natural endothelial senescence and accompanying loss of function.6

Corneal opacification usually begins temporally (Fig. 5) and then gradually spreads throughout the cornea. The fluid accumulation gives the cornea a bluish­white color and a stippled texture. The disorder is initially painless and devoid of inflammation, but extensive stromal and epithelial edema will ultimately result in recurrent corneal erosions. Corneal vascularization is usually absent. In the late stages of the disease, intraocular detail is obscured and vision is reduced to light perception. The entire process can take months to years. Endothelial dystrophy is presumptively diagnosed when bilateral corneal stromal edema is present without signs of uveitis, glaucoma, or anterior lens luxation. Any sec­ondary corneal ulceration is usually superficial and insufficient to generate the degree of stromal edema observed.

Treatment is palliative at best. Topical 5% sodium chloride ointment (Ak­NaCI; Akorn, Abita Springs, LA) may discourage development of corneal ero­sions but seldom results in significant corneal clearing. If epithelial erosions do occur, any nonadherent epithelium should be debrided and topical broad-spec­trum antibiotics should be administered four times daily as well as 1% atropine to effect. In the late stages of the disease, patients may be referred to an ophthalmologist for surgical options such as thermokeratoplasty.

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Figure 5. Bilateral corneal edema is the result of endothelial dystrophy in a 1 0-year-old Boston Terrier. An intense blue color, stippled corneal texture, and inevitable progression across the cornea are characteristic clinical features.

KERATOCONJUNCTIVITIS SICCA

Older animals, especially neutered female dogs, are predisposed to keratoconjunctivitis sicca.8 Although senile atrophy of the lacrimal glands has been traditionally blamed for the lack of tear production in older dogs, chronic inflammation due to autoimmune disease may be the real culprit.9

Clinical signs include sticky and mucopurulent discharge (frequently misdi­agnosed as bacterial conjunctivitis), conjunctival hyperemia, progressive corneal vascularization, and superficial pigmentation. Definitive diagnosis is by the Schirmer tear test, with affected animals measuring less than 10 mm wetting/ min. A variety of breeds are commonly affected, including the Cocker Spaniel, English Bulldog, Schnauzer, West Highland White Terrier, Yorkshire Terrier, and Beagle.

Topical cyclosporine has been shown to improve tear production and reduce corneal changes associated with the dry eye condition. This T-cell inhibitor is believed to counteract immune-mediated changes within the lacrimal gland, improving its function. Its efficacy in patients with keratoconjunctivitis sicca secondary to senile atrophy would be minimal, but a trial is nevertheless recom­mended in light of the current theory regarding pathogenesis in the geriatric patient. Twice-daily application of 0.2% cydosporine ointment (Optimmune; Schering-Plough, Kenilworth, NJ) is recommended initially. Because response is seldom seen before 2 weeks, adjunct therapy should be considered until tear production increases. Some dogs may be maintained on a once-daily application, although indefinite therapy is indicated. Tear production can drop precipitously if daily cydosporine is not continued. Animals that do not respond to

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cyclosporine ointment may respond to a 1% or 2% cyclosporine solution, which is available from compounding pharmacies. Owners should be informed that the cyclosporine solution represents an extralabel drug application.

Conventional medical therapy may be used while awaiting an initial re­sponse to cyclosporine or in patients that fail to respond to cyclosporine after an adequate trial period. Therapy combines acetylcysteine to break up the heavy mucus, an antibiotic/corticosteroid solution to control infection and inflamma­tion, and artificial tears to supplement the tear volume. This can be formulated and refrigerated in a single solution: 10% acetylcysteine (5 cc) and triple antibi­otic with 0.1% dexamethasone (10 cc) mixed with 15 cc artificial tears (Adsorbo­tear or Tears Naturale; Alcon, Fort Worth, TX). Frequency of application is dictated by the severity of the dryness and accompanying changes. The chronic use of topical ophthalmic corticosteroid preparations can lead to iatrogenic hyperadrenocorticism; thus, intermittent application is preferred. An artificial tear ointment (Akwa Tears; Akorn) may be applied as needed for added lubrica­tion especially at bedtime. Use of 1 to 2 drops of 2% pilocarpine twice daily in the food may also stimulate tear production. Parotid duct transposition may be considered in unresponsive patients.

UVEAL CYSTS

The majority of uveal cysts appear in middle-aged and older dogs as brown to black spherical masses, free-floating within the anterior chamber. Golden Retrievers, Labrador Retrievers, and Boston Terriers appear to be affected more commonly than other breeds. Uveal cysts typically arise from the posterior pigmented epithelium of the iris but may also develop from the ciliary body. Iris and ciliary cysts may be unilateral or bilateral and single or multiple. A collapsed iris cyst may leave an irregular vestige of pigment on the corneal endothelial surface or the anterior lens capsule.

The primary differential diagnosis is a uveal melanocytic neoplasm. Transil­lumination of the cyst easily differentiates it from a solid tumor. Ocular ultraso­nography may be used to document the cystic nature in equivocal cases such as those in which the cyst remains attached to the posterior iris. Therapy is rarely indicated.

Interestingly, male and female Golden Retrievers 8 years of age and older have been described with intractable glaucoma preceded by iris hyperpigmenta­tion, collapsed iris cysts, and posterior synechiae, without appreciable histopath­ologic evidence of inflammation. Periodic rechecks may be prudent if cysts are detected in this breed.

HYPHEMA

Intraocular hemorrhage is often attributed to trauma in companion animals, but in the older patient, it is more likely to signal an ocular tumor or retinal detachment. Animals presenting with recurrent bleeding or with blood that fails to clot in the anterior chamber should be evaluated for these primary ocular disorders in addition to systemic blood dyscrasias and systemic hypertension.

Symptomatic treatment may be used in an attempt to clear the blood and allow visualization of the intraocular structures. Topical corticosteroids may minimize uveal reaction to the free blood but should be used judiciously so as not to delay clot resolution. If intraocular pressures are normal, low-frequency

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atropine will minimize the likelihood of iris-to-lens adhesions and stabilize the blood-aqueous barrier. Large clots that threaten to compromise aqueous outflow by settling within the pupillary space may respond to intracameral tissue plas­minogen activator, an option provided by most veterinary ophthalmologists.

Retinal detachments are easily diagnosed using ultrasound if hemorrhage fails to clear sufficiently for intraocular examination. Intraocular tumors are not always evident in the early stages of development. Intraocular hemorrhage secondary to retinal detachment may be tolerable, but secondary glaucoma developed in over half of 17 dogs reported in one studyP Patients suspected of harboring an intraocular neoplasm should have the eye removed and submitted for histopathologic examination.

UVEAL NEOPLASIA

Intraocular neoplasms are relatively uncommon in the dog and cat. Of the primary neoplasms, anterior uveal melanoma is the most common in older dogs of 8 or more years of age.23 Tumor development appears to favor darkly pig­mented breeds such as the German Shepherd and the Boxer. Typically, there is a nodular, pigmented mass within the iris which alters pupillary shape as it enlarges. Site of origin, tumor size, and degree of pigmentation are common variables. For example, amelanotic masses can arise from the ciliary body and enlarge sufficiently to displace the iris and fill the pupil. Intraocular inflamma­tion and secondary glaucoma are common, although not inevitable, sequelae. Anterior uveal melanomas are potentially locally invasive and may metastasize hematogenously. Other primary uveal neoplasms in dogs include ciliary body adenoma, adenocarcinoma, medulloepithelioma, cavernous hemangioma, hem­angiosarcoma, and leiomyosarcoma.

Melanoma is a lso the most common primary intraocular tumor of cats. The neoplasm is likely to infiltrate the iris diffusely and insidiously rather than developing a distinct nodule. Iris color change is the usual presenting complaint. Early diagnosis is often complicated owing to the propensity of older cats to develop benign, age-related iris pigmentation or "freckles." Slit lamp examina­tion in patients with diffuse iris melanoma reveals pigmented cells floating within the aqueous and progressive iridal thickening, invasion of the iridocor­neal angle, and secondary glaucoma. The tumor spreads first to the regional lymph nodes and then to viscera, but clinical signs of metastasis may not be apparent for years. Owing to a reported metastatic rate of 63%, early enucleation is often recommended.18

Posttraumatic sarcoma has been described in cats with a mean age of 12 years.3 Most have a history of previous trauma or chronic uveitis. Severe lens changes are a c ommon factor, raising the suspicion that the neoplastic cells a re derived from lens epithelium. Tumors develop diffusely within the globe and are locally invasive, commonly extending through the optic canal.1 The majority of reported p atients have either died or been euthanized as a direct consequence of the tumor. Chronically inflamed or phthisical eyes, particularly in young cats, should be enucleated to reduce the likelihood of sarcoma formation. Other primary intraocular tumors that have been reported infrequently in cats include ciliary epithelial adenocarcinoma and astrocytoma.

Prior to any therapy, each patient should be screened for evidence of metastatic disease. Given the benign biologic behavior of most uveal neoplasms in dogs, conservative observation may be undertaken in selected p atients. The author has observed canine iris melanomas for years without evidence of sig-

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nificant ocular or systemic morbidity. Localized masses may be removed by sector iridectomy or transsclerally ablated by laser. Economic considerations and availability of instrumentation more often limit the therapeutic choices to enucleation or exenteration. Histopathology should be performed on all excised neoplasms or enucleated eyes to provide a diagnosis and, if possible, a progno­sis.

Secondary intraocular tumors spread to the globe hematogenously or extend directly from the adjacent adnexa, orbit, paranasal sinuses, or nasal cavity. The most common metastatic tumor to the canine and feline eye is lymphosarcoma. Diffuse uveal infiltration with neoplastic lymphocytes, perilimbal corneal and conjunctival infiltrates, hypopyon, hyphema, and retinal hemorrhages are com­mon signs of ocular lymphosarcoma. Orbital involvement also occurs with some frequency in cats. Aqueous paracentesis may recover neoplastic cells when cellular debris is present within the anterior chamber. Cats should be tested for feline leukemia virus if lymphosarcoma is suspected. Other metastatic neo­plasms include melanoma, hemangiosarcoma, seminoma, transmissible venereal tumor, transitional cell carcinoma, squamous cell carcinoma, neurogenic sar­coma, rhabdomyosarcoma, and anaplastic fibrosarcoma as well as adenocarci­noma of mammary, thyroid, sweat gland, and uterine origin.

Treatment of secondary neoplasms usually hinges on the animal's systemic status. The inflammation of ocular lymphosarcoma will often improve signifi­cantly with topical corticosteroids and systemic chemotherapy. In debilitated patients or those whose owners have declined therapy, euthanasia may be more appropriate than enucleation.

CATARACTS

Cataracts are particularly common in the dog but are comparatively infre­quent in the cat. Senile cataracts are defined as lens opacities that develop in animals over 6 years of age. Their cause is generally unknown, although changes in composition and metabolism of the aging lens may contribute to cataract development or render the lens more susceptible to cataractogenic stresses. Chronic uveitis or glaucoma, trauma, degenerative retinal diseases such as progressive retinal atrophy, or metabolic diseases such as diabetes mellitus may also produce cataracts in older patients. Inherited cataracts are also common in dogs but usually develop in young and middle-aged animals. If seen in the geriatric patient, they are no doubt of chronic duration. The most common cause of cataract in the aged cat is chronic uveitis. In either species, cataracts must be differentiated from senile nuclear sclerosis, a normal aging change produced by compression of central lens fibers.

Surgery has proved to be the only means of restoring sight; medical treat­ment for cataracts remains unsuccessful. Owing to the expense and potential risks of surgery as well as the ability of most visually handicapped animals to adjust to their home environment, cataract extraction should be considered an elective procedure. Proper selection of patients for cataract surgery is a critical . factor for success. The best candidates are those in good general health as· determined by a complete physical examination, including hematologic and chemical panels. The eye should have no other abnormalities such as uveitis, keratoconjunctivitis sicca, or glaucoma. This stipulation often excludes most cats from consideration as surgical candidates. Retinal function should be normal as determined by electroretinography and ocular ultrasound. The temperament of

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the animal must also be considered as well as the likelihood of owner compli­ance with postoperative management.

Early referral to an experienced veterinary ophthalmic surgeon is recom­mended. In general, the preferred surgical technique is phacoemulsification which fragments the lens nucleus by ultrasonic vibration and aspirates the particles through a small corneal incision. Residual cortical material is also aspirated to minimize postoperative immunologic reaction to lens protein. Re­ported success rates are as high as 95% at 1 month following surgery, 86% at 2 years, and 71% at 4 years.15 Intraocular lens (IOL) implants have been developed for use in the dog and cat, but considerable controversy still exists regarding their benefits to the patient. An animal without an implant usually functions well in its environment, despite its significant post-operative hyperopia. Although a successful IOL implant provides the animal with more normal post-operative vision, IOL implants have been linked with chronic, low-grade uveitis which compromises ocular clarity and vision.

LENS-INDUCED UVEITIS

Geriatric dogs with long-standing cataracts may develop lens-induced uve­itis (LIU), an inflammatory response of the uvea to lens protein. In one retrospec­tive study of 151 cases, the most commonly affected breeds were the Toy and Miniature Poodles and the Cocker Spaniel, no doubt reflecting the high incidence of cataracts in these breeds. The mean age was 7 years, with the poodles averaging 9 years of age. The interval between recognition of the cataract and diagnosis of the uveitis was from 1 to 2 years, with a mean of 17 months.21

Besides evidence of a hypermature cataract, patients with LIU usually demon­strate scleral injection, aqueous flare, decreased intraocular pressure, and poor response to topical mydriatic agents. More chronic uveitis results in synechiae, keratic precipitates, hypopyon, and iris hyperpigmentation (Fig. 6). Secondary glaucoma or phthisis bulbi may develop in the most severely or chronically inflamed eyes.

Treatment is directed at control of inflammation utilizing topical 1% predni­solone acetate (Pred Forte; Allergan, Irvine, CA) four to six times daily and 1% atropine sulfate ophthalmic solution to effect. Systemic prednisolone may be necessary in some patients. Maintenance therapy may be necessary indefinitely to prevent recurrence. Cataract surgery following control of LIU is less successful than that in patients without LIU. The 2- and 6-month success rates for LID­affected eyes were 78% and 39%, respectively, in 50 eyes.21

LENS LUXATION

Lens displacement may occur in older patients secondary to zonular weak­ness or rupture related to chronic LIU or capsular contracture of a hypermature cataract. Loss of lens support may also accompany age-related vitreous degener­ation. Miniature Poodles older than 11 years of age predominated in one report.4

The position of the lens and vitreous humor determine the accompanying clinical signs. Subluxated lenses may be relatively asymptomatic or may contribute to wide fluctuations in intraocular pressure, culminating in lesions typical of chronic glaucoma such as buphthalmos. Rarely will pressures elevate beyond the 30 to 45 mm Hg range unless complete anterior luxation has occurred.

In asymptomatic eyes, periodic evaluation of intraocular pressure is ad-

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Figure 6. Chronic lens-induced uveitis accompanies a hypermature cataract in a 12-year­old mixed-breed dog. Uveal reaction to lens protein leads to corneal opacity, aqueous turbidity, keratic precipitates posterior synechiae, and the threat of secondary glaucoma or phthisis bulbi.

vised. Medical therapy to reduce intraocular pressure is palliative but fails to address the underlying cause. For that reason, intracapsular lens extraction and vitrectomy are recommended in visual eyes. Unfortunately, retinal detachment occurs in approximately 15% of patients postoperatively. Medical therapy is not generally recommended in blind eyes due to the unpredictability of the lens position, the expense of long-term therapy and repeated re-evaluations, and the potential adverse side effects of systemic antiglaucoma agents. Preferable surgi­cal options are evisceration of the intraocular contents followed by implantation of an intrascleral silicone prosthesis or enucleation.

VITREOUS DEGENERATIONS

Asteroid Hyalosis

Asteroid hyalosis is an age-related degenerative process characterized by a collection of minute calcium-lipid complexes suspended within the vitreous humor. The opacities may move slightly with eye movement but usually do not interfere with vision.

Cholesterosis Bulbi

Cholesterosis bulbi or synchysis scintillans is a more severe, although less common, degenerative process which follows intraocular inflammation. In this disorder, vitreous liquefaction causes the cholesterol crystals to settle ventrally

OPHTHALMIC DISEASE AND ITS MANAGEMENT 1519

when the eye is at rest. This more advanced form of vitreous degeneration may influence lens and retinal stability, potentially predisposing the eye to lens luxation or retinal detachment.

RETINAL DISORDERS

Peripheral Cystoid Degeneration

Peripheral cystoid degeneration refers to single or multiple, nonpigmented, cystic structures that develop within the peripheral sensory retina near its junction with the posterior ciliary body. The cysts are most easily seen using indirect ophthalmoscopy in the maximally dilated eye. They are of no functional significance.

Retinal Detachment

Acute hypertension, either primary or secondary to renal disease, can result in unilateral or bilateral bullous retinal detachments (Fig. 7). The problem is less often recognized in the dog than in the geriatric cat, with the latter often having hyperthyroidism, cardiomyopathy, or chronic renal failure. If the condition is bilateral, the animal is frequently presented with an acute onset of blindness. Blood pressure elevation of a more chronic nature may result in retinal hemor­rhages alone.

If direct or Doppler measurement techniques are not available, the patient

Figure 7. An 11-year-old Domestic Shorthair cat demonstrates the classical signs of acute hypertensive retinopathy, with retinal detachment and hemorrhage.

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with retinal detachments or hemorrhages in an otherwise quiet eye should be referred for assessment. In general, therapy is advised if the indirect systolic pressure is greater than 170 mm Hg.7 The preferred treatment in cats is 0.625 mg of oral amlodipine (Norvasc) administered once daily. Oral propranolol (Inderal) has also been used in hypertensive cats at a dosage of 2.5 to 5.0 mg once or twice daily. Alternatively, captopril (Capoten), an angiotensin-con­verting enzyme inhibitor, may be used at a dosage of 6.25 to 12.5 mg twice daily. The prognosis for return of vision is best if blood pressure control is effectively established within 2 to 3 days of the onset of blindness. Unfortu­nately, retinal reattachment in some cats does not always result in restoration of vision.

Geriatric Miniature Poodles appear predisposed to spontaneous, bilateral retinal detachments resulting in irreversible blindness. Characteristically, the retina tears completely from its peripheral attachments, appearing as a gray veil of tissue resting on the floor of the vitreous cavity. The tapetal region appears hyperreflective and avascular, because the retina no longer overlies that portion of the fundus. It is unclear whether both eyes are affected simultaneously or whether the animal is presented only after the second eye is affected. The cause of the detachments is unknown. Surgical repair of giant retinal tears is possible, but experienced surgeons are few and prognosis for vision is guarded.20

Progressive Retinal Atrophy

Progressive retinal atrophy usually appears in young to middle-aged dogs, but owners may sometimes fail to recognize the slowly progressive loss of vision until the very late stages of the disease. Poodles and Labrador Retrievers are often presented in this fashion. Signs include progressive vision loss, first oc­curring in dim light and ultimately resulting in total blindness. Owing to the late presentation, owners may also complain of "green" or "yellow" eyes due to the reflection of the tapetum through the persistently dilated pupils. Ophthal­moscopic signs include retinal vessel attenuation and tapetal hyperreflectivity due to retinal thinning. Secondary cataract formation is common and may be incorrectly blamed for the vision loss. No treatment is available.

Sudden Acquired Retinal Degeneration

Sudden acquired retinal degeneration is reported to occur most commonly in dogs 6 to 11 years of age, with a mean age of 8.5 years.22 Seventy percent are female, with a breed predisposition favoring the Miniature Schnauzer and Dachshund. Affected dogs present with a history of rapid vision loss occurring over 24 hours to 1 month. Polyuria, polydipsia, polyphagia, obesity, and hepato­megaly are often noted. Pupillary light responses are absent in most dogs, but initial retinal appearance may be normal. Abnormalities in serum chemical profiles include increased levels of alkaline phosphatase and alanine aminotrans­ferase. Urine specific gravity is often below 1.025. Definitive diagnosis of sudden acquired retinal degeneration and differentiation from optic neuropathy is based on electroretinography. The affected patient will have an extinguished electroret­inogram. The cause is unknown, and the blindness is irreversible.

OPHTHALMIC DISEASE AND ITS MANAGEMENT 1521

CONCLUSIONS

A variety. of ocular disorders occur with some frequency in the aging canine and feline eye. The culmination of effects of long-standing ocular disease are often interspersed with the neoplastic and degenerative ailments common in older animals. Although cataracts and retinal disorders frequently account for vision loss, these and many of the other maladies are medically or surgically manageable. Veterinarians should not accept that poor vision inevitably accom­panies old age in their patients.

References

1. Barrett PM, Merideth RE, Alarcon FL: Central amaurosis induced by an intraocular, posttraumatic fibrosarcoma in a cat. JAm Anim Hosp Assoc 31:242, 1995

2. Champagne ES, Munger RJ: Multiple punctate keratotomy for the treatment of recur­rent epithelial erosions in dogs. JAm Anim Hosp Assoc 28:213, 1992

3. Dubielzig RR, Everitt J, Shadduck JA, et al: Clinical and morphologic features of post­traumatic ocular sarcomas in cats. Vet Pathol 27:62, 1990

4. Fischer CA: Geriatric ophthalmology. Vet Clin North Am Small Anim Pract 19:109, 1989

5. Gilger BC, McLaughlin SA, Whitley RD, et al: Orbital neoplasms in cats: 21 cases (1974-1990). JAVMA 201:1083, 1992

6. Gwin RM, Lerner I, Warren JK, et al: Decrease in canine corneal endothelial cell density and increase in corneal thickness as functions of age. Invest Ophthalmol Vis Sci 22:267, 1982

7. Henik RA: Diagnosis and treatment of feline systemic hypertension. Compend Contin Educ Pract Vet 19:163, 1997

8. Kaswan RL, Salisbury MA, Lothrop CD: Interaction of age and gender on occurrence of canine keratoconjunctivitis sicca. Progress in Veterinary and Comparative Ophthal­mology 1:93, 1991

9. Kaswan RL, Martin CL, Dawe DL: Keratoconjunctivitis sicca: Immunological evalua­tion of 62 canine cases. Am J Vet Res 46:376, 1985

10. Kern TJ: The canine orbit. In Gelatt KN (ed): Veterinary Ophthalmology, ed 2. Philadel­phia, Lea & Febiger, 1991, p 247

11. Kern TJ: Orbital neoplasia in 23 dogs. JAVMA 186:489, 1985 12. Kern TJ, Erb HN: Facial neuropathy in dogs and cats: 95 cases (1975--1985). JAVMA

191:1604, 1987 13. Kirschner SE: Persistent corneal ulcers. Vet Clin North Am Small Anim Pract 20:632,

1990 14. Lane IF, Roberts SM, Lappin MR: Ocular manifestations of vascular disease: Hyperten­

sion, hyperviscosity, and hyperlipidemia. JAm Anim Hosp Assoc 29:28, 1993 15. Miller TR, Whitley RD, Meek LA, et al: Phacofragmentation and aspiration for cataract

extraction in dogs: 56 cases (1980-1984). JAVMA 190:1577, 1987 16. Nasisse MP: Feline ophthalmology. In Gelatt KN (ed): Veterinary Ophthalmology, ed

2. Philadelphia, Lea & Febiger, 1991, p 533 17. Nelms SR, Nasisse MP, Davidson MG, et al: Hyphema associated with retinal disease

in dogs: 17 cases (1986-1991). JAVMA 202:1289, 1993 18. Patnaik AK, Mooney S: Feline melanoma: A comparative study of ocular, oral and

dermal neoplasms. Vet Pathol 25:105, 1988 19. Roberts SM, Severin GA, Lavach JD: Prevalence and treatment of palpebral neoplasms

in the dog: 200 cases (1975-1983). JAVMA 189:1355, 1986 20. Vainisi SJ, Packo KH: Management of giant retinal tears in dogs. JAVMA 206:491, 1995 21. van der Woerdt A, Nasisse MP, Davidson MG: Lens-induced uveitis in dogs: 151 cases

(1985- 1990). JAVMA 201:921, 1992

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22. van der Woerdt A, Nasisse MP, Davidson MG: Sudden acquired retinal degeneration in the dog: Clinical and laboratory findings in 36 cases. Progress in Veterinary and Comparative Ophthalmology 1:11, 1991

23. Wilcock BP, Peiffer RL: Morphology and behavior of primary ocular melanomas in 91 dogs. Vet Pathol 23:418, 1986

Address reprint requests to Mary B. Glaze, DVM, MS

Department of Veterinary Clinical Sciences School of Veterinary Medicine

Louisiana State University Baton Rouge, LA 70803

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