The Cornea

Congenital Abnormalities

Comeal Opacities. The cornea of the newborn puppy or kitten is a light blue color; or at least the cornea is less clear than that of the adult. In 2 to 4 weeks, corneal clearing is sufficient to permit ophthalmoscopic examination. It is not unusual to observe multifocal or diffuse faint white opacities in the corneas of young puppies and kittens. The opacities represent superficial foci of edema, and most are self-limiting. The cause of these opacities is unknown. Therapy is not necessary unless the opacities are accompanied by a mucopurulent discharge, in which case topical ophthalmic antimicrobial preparations may be applied. Animals born with their eyelids open often have diffuse corneal edema that clears in 14 to 18 days. Because reflex lacrimation is absent at birth, the exposed cornea is subject to desiccation and infection and can be avoided by frequent application of a broad-spectrum antimicrobial ointment every 3 or 4 hours until the animal is 10 to 12 days old.

Cats with lysosomal storage diseases may develop corneal opacities related to the accumulation of polysaccharides within the endothelial cells and fibroblasts of the cornea. Fine granular deposits in the corneal stroma may give the eye a ground-glass appearance as early as 8 weeks of age. Corneal clouding or stippling may occur in kittens with GM, gangliosidosis, in cats of Siamese ancestry with mucopolysaccharidosis I and mucopolysaccharidosis VI, and in Persians with a-mannosidosis.

Deep corneal opacities are usually associated with remnants of embryonic pupillary membranes (persistent pupillary membranes) that adhere to the inner corneal surface (). The tissue strands, which arise from the anterior iris face, should be differentiated from post-inflammatory synechiae extending from the pupillary margin. Therapy is not indicated in most cases, and on occasion the corneal opacity may diminish over several weeks or months.

Dermoid. Owners often notice a skin-like appendage soon after the animal’s eyelids separate (). The dermoid usually involves the temporal cornea and conjunctiva in both puppies and kittens. Saint Bernards, German shepherds, dachshunds, and Dalmatians and the Birman and Burmese cats have an increased incidence of dermoids. If the dermoid contains no hair, any signs of squinting and ocular discharge may be minimal. Therapy consists of superficial keratectomy, usually performed around 12 to 14 weeks of age. Complete excision is essential, or regrowth may occur.

Acquired Abnormalities

Symblepharon. An infectious conjunctivitis and keratitis that develop before eyelid separation may result in adhesion of the conjunctiva to the cornea (symblepharon). A similar situation also may follow chronic conjunctivitis associated with upper respiratory infection in cats. Ophthalmic examination shows a thin vascu-Iarized membrane overlying the cornea (). Occasionally, the overlying tissue can be partially elevated from the corneal surface with topical anesthesia and a small-toothed forceps. Prompt medical therapy of external eye disease minimizes symblepharon formation. Surgical repair is difficult, and re-adherence following surgery is common.

Dystrophies. Corneal dystrophies are familial, bilaterally symmetric corneal opacities that can affect any layer of the cornea. Stromal dystrophies in dogs are characterized by deposition of triglycerides, phospholipids, and neutral fat within the cornea; the cat more often demonstrates stromal edema and ulceration. Most stromal dystrophies appear after 1 year of age, but occasionally dogs may demonstrate mild corneal changes before 6 months of age. The Siberian husky dog is best known for its corneal dystrophy, which appears in the central cornea as a round or horizontally oval opacity as early as 5 months of age. The affected corneas ultimately show a homogeneous gray haze but in the early stages may only contain fine, highly retractile crystals in the stroma (). The inherited trait is recessive, with variable expressivity. Although the corneal opacities seldom become dense enough to affect vision, the use of affected dogs in breeding programs is not recommended. There is no treatment.

An axial dystrophy occurs in Airedale terriers as early as 6 months of age. Stromal deposition of triglycerides and neutral fats results in marked subepithelial opacification. The terrier’s vision deteriorates as the axial dystrophy progresses. Multifocal 1- to 3-mm opacities may occur in the central superficial corneas of Shetland sheepdogs at 6 months of age. These sheepdogs at 3 to 4 years of age develop epithelial erosions overlying the corneal opacities. A progressive corneal dystrophy occurs in stumptailed Manx cats. Early signs of axial outer stromal edema are noticed at approximately 4 months of age. The cornea progressively deteriorates, with accumulation of fluid-filled vesicles within the stroma (bullous keratopathy). Eventually, breakdown of both the epithelium and stroma occurs. An autosomal recessive pattern of inheritance is suspected.

Melanosis. Superficial corneal pigmentation is common in young brachycephalic dogs, notably the Chinese pug, Shih Tzu, Lhasa apso, and Pekingese. The pigmentation occurs most often in the nasal corneal quadrant, sometimes involving the adjacent conjunctiva. Therapy is directed at correcting adnexal abnormalities such as medial entropion and canthal trichiasis, which promotes additional pigmentation.

Sequestra. A recognizable corneal degeneration occurs in the cat that is characterized by formation of a brown to black superficial plaque in the cornea (). A breed predisposition has been identified in the Persian and Siamese. The corneal degeneration is often accompanied by corneal ulceration and superficial vascularization. The discolored plaque should be differentiated from corneal pigmentation by its sparing of the peripheral cornea. The sequestrum is excised by superficial keratectomy.

Injuries. Small corneal perforations are accompanied by pain, perilesional corneal edema, anterior uveitis, and sometimes hyphema. If the depth of the anterior chamber is comparable with that of the unaffected eye, the perforation may have sealed itself and require no more than restricted activity, topical and systemic antimicrobial agents, and topical atropine. Ophthalmic ointments should be avoided in the perforated eye because the oil base of the ointment causes a severe reaction when introduced into the anterior chamber. Larger corneal perforations and lacerations require prompt surgical repair. These injuries have more severe corneal edema and uveitis; prolapsed iris tissue may also extend above the corneal surface (). Preoper-tive examination should be minimal to prevent any further damage to the eye. The surgical techniques and reparative capability of the cornea are similar to those in the adult animal.

Foreign Objects. After application of topical anesthesia, superficial corneal foreign objects may be removed with a moistened sterile cotton-tipped swab, a 2 5-gauge needle, or a slightly blunted ophthalmic instrument known as a foreign body spud. Deeper foreign objects require general anesthesia and surgical extraction. After removal, a broad-spectrum antimicrobial solution is applied four to six times daily to prevent infection. Topical atropine is used as needed to dilate the pupil.

Ulceration. Corneal ulceration exists when there is a loss of epithelium and some portion of the corneal stroma. Most corneal ulcers are caused by traumatic insult, either from another animal or from such endogenous factors as low tear production or eyelid abnormalities. Secondary bacterial infection may occur once the corneal surface has been disrupted. Although corneal ulcers associated with feline herpesvirus infection are well characterized, such ulcers are uncommon in kittens younger than 6 months of age. The fluorescein dye test can be used to determine epithelial integrity after the eyelids have been completely separated in puppies and kittens. If the epithelium is disrupted, the stroma will absorb the dye and the ulcerated area will appear bright green. Fluorescein staining is to be performed after a Schirmer’s tear test and corneal culture have been completed.

Superficial corneal ulcers in which only epithelium and superficial stroma are missing may heal in just a few days. Corticosteroids are not recommended in the treatment of corneal ulcers because they slow epithelial healing and potentiate destructive enzymatic activity within the corneal lesion. If the animal rubs the eye, use of an Elizabethan collar or other protective device is indicated. When corneal healing is delayed, ectopic cilia or other adnexal abnormalities should be pursued. Tear production should also be evaluated, and corneal culture and cytology should be done to rule out an infectious cause.

Deep corneal ulcers are more likely to have an infectious cause; bacterial culture and sensitivity testing should be performed. Tear production should also be evaluated. Brachycephalic dog breeds are predisposed to the development of deep ulcers and descemetoceles, probably related to traumatic insult or corneal exposure (). These dogs also may develop collagenase-associated ulcers that are characterized by a melting, gelatinous appearance in the affected cornea. Epithelial cells, inflammatory cells, and various bacteria, especially Pseudomonas, produce the collagenase responsible for the rapid corneal breakdown. An antimicrobial agent with activity against Pseudomonas species should be instilled hourly until culture results are obtained. Acetylcysteine solution, diluted to 5% to 10% with artificial tears, is also applied hourly until collagenolysis stops. Topical 1% atropine solution is used for the concurrent anterior uveitis. Deep ulcers with impending corneal rupture necessitate surgical intervention, such as a third eyelid flap, temporary apposition of the eyelids (tarsorrhaphy), conjunctival flap, or corneoscleral transposition.

Keratoconjunctivitis Sicca. The early stages of inadequate tear production are frequently characterized by conjunctivitis, varying amounts of tenacious mucopurulent discharge, and a dull, irregular appearance to the cornea. As inadequate tear production persists, gradual vascularization and pigmentation of the cornea occur, and corneal ulcers may appear. Eventually, total corneal pigmentation is noted. Diagnosis is confirmed by determination of tear production using the Schirmer’s tear test. A standardized strip of absorbent paper is creased, inserted over the lower eyelid into the conjunctival sac, and left for 1 minute. Values below 10 mm/min are indicative of inadequate tear production, regardless of the animal’s age.

The causes of inadequate tear production in puppies and kittens are varied. Congenital lacrimal gland abnormalities may be present, resulting in delayed separation of the eyelids and early signs of corneal disease. Dogs with canine distemper and cats with acute or chronic upper respiratory tract infection may develop inadequate tear production. Traumatic insult to the nictitans gland or its nerve supply also reduces tear production. Tear production may improve with once or twice daily topical application of 2% cyclosporine formulated for ophthalmic use. Alternatively, an artificial tear, broad-spectrum antimicrobial agent, and corticosteroid are combined for topical application as frequently as possible in the nonulcerated eye. A mucolytic such as acetylcysteine may be added at a concentration of 5% if mucopurulent discharge is excessive. The resulting solution requires refrigeration. Artificial tear ointment at bedtime should minimize overnight drying. Improvement should occur within 6 to 8 weeks of applied topical regimen.


Selections from the book: “Veterinary pediatrics: dogs and cats from birth to six months”. Johnny D. Hoskins. (2001)