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The size of the nearly round to oval cornea (vertical/horizontal) varies by animal species: dog (8.5 × 9.5 mm), cat 8.4 × 8.9 mm), horse (16.6 × 17.9 mm), and cow (15.2 × 16.4 mm). The animal cornea consists of the superficial epithelium and basement membrane, large and relatively acellular stroma, deeper Descemet's membrane, and deep single layer endothelium. The cornea maintains a strong and durable barrier between the eye and environment, as well as a transparent medium to permit passage of light and images into the posterior segment. Corneal diseases are common in most animal species, and fortunately can be treated successfully by medical, surgical, or a combination of these methods. The accessibility of the cornea permits several detailed and non-invasive diagnostic techniques.
Superficial keratitis is common in all species and is characterized by corneal vascularization and opacification, which may be due to edema, cellular infiltrates, pigmentation, or fibroplasia. If ulceration is present, pain—manifest by epiphora and blepharospasm—is an outstanding sign. Unilateral keratitis frequently is traumatic in origin. Mechanical factors, such as lid conformational defects and foreign bodies, should always be eliminated as possible causes, because improvement will not occur until they are resolved. Ulcerative keratitis may be complicated by secondary invasion by bacteria and, in horses, by saprophytic fungi. Bilateral superficial keratitis may be immune-mediated or associated with a lack of tears, eyelid conformational defects, or infectious agents.
Pannus or Uberreiter's disease is a specific, bilateral, progressive, proliferative, chronic, superficial keratitis that begins laterally at the limbus and eventually extends from all quadrants to cover the cornea. This immune-mediated keratitis is common in German Shepherds, Belgian Tervurens, Border Collies, Greyhounds, Siberian Huskies, and Australian Shepherds. Specific therapy consists of topical antibiotics, antiviral or antimycotic agents when appropriate, removal of any mechanical irritants, tear replacement when deficient, and corticosteroids or cyclosporin A (or both) when immune-mediated. The latter may need to be continued indefinitely and the frequency varied depending on the response.
Interstitial keratitis is a deep involvement of the corneal stroma that is present with all chronic and many acute cases of anterior uveitis. The corneal vascularization is less branching, finer, and deeper than in superficial keratitis; if the endothelium has been disrupted, corneal edema is often marked. Systemic diseases, such as infectious canine hepatitis, bovine malignant catarrhal fever, systemic mycoses in many species, and neonatal septicemias that localize in the eye, can cause bilateral or unilateral interstitial keratitis. Therapy is directed at the anterior uveitis, the systemic infection, or both. A specific, nonulcerative, peripheral, stromal keratitis and persistent anterior uveitis (keratouveitis) occurs in horses; prognosis and response to treatment are poor.
Ulcerative keratitis may be superficial, deep, deep with descemetocele, or perforating. Pain, corneal irregularity, edema, and eventually vascularization are signs of ulceration. A dense, white infiltrate at the ulcer margin indicates strong leukotaxis and bacterial involvement. To detect small ulcers, topical fluorescein may be required. In dogs and horses, most ulcers are mechanical in origin; in cattle, sheep, goats, and reindeer, infectious agents and mechanical causes are important; in cats and horses, herpesvirus infection is a frequent cause. All ulcers have the potential for secondary bacterial contamination as well as endogenous proteinase “melting” of the stroma. Therapy for superficial ulcers is usually medical and consists of topical broad-spectrum antibiotic(s), correction of any mechanical factors, and topical atropine for iridocycloplegia and reduction of ocular pain. Adverse effects of atropine-induced reduced tear production in all species and colic in horses must be considered. Antiproteinase therapy for melting stromal ulcers includes topical serum and other drugs.
Syndromes of very slow-healing and recurrent superficial ulcers occur in dogs, cats, and horses; in dogs, they may be due to basement membrane disease causing faulty attachment of the corneal epithelium, while in cats and horses, herpesvirus should be suspected. Initial therapy is ulcer debridement followed by topical antibiotics and atropine. For refractory cases in dogs, multiple punctures or cross-hatching (punctate and grid keratotomies) of affected corneas with a 22-gauge needle stimulates most indolent ulcers to heal within 7–10 days. Early reports suggest these keratotomies in cats may predispose to corneal sequestration and should be used with great care. Nictitating membrane flaps (or soft contact lenses or collagen shields) act as a pressure bandage and often are therapeutic for shallow ulcers. Medical treatment of deep ulcers is similar to that of superficial ulcers, but many deep ulcers also require conjunctival grafts to strengthen and maintain the integrity of the cornea.
Corneal sequestration and keratitis appear to be unique to the cat. There is a painful, central to paracentral, brown to black opacity composed of necrotic stroma, vascularization, and surrounding inflammation. Treatment consists of superficial keratectomy and, with deeper lesions, conjunctival grafts.
Corneal stromal abscesses in horses may be sequelae of healing corneal ulcers or defects and the trapping of bacteria or fungal organisms (or both) within the stroma after re-epithelialization. A variable, white to yellow, stromal infiltrate is surrounded by an intense stromal keratitis and vascularization, and a variable but sometimes intense anterior uveitis. Treatment consists of intensive topical and occasional systemic antibiotics (and if indicated, antifungals), iridocycloplegics, NSAID, and often surgical removal of the abscess with conjunctival and tectonic corneal grafts.
Corneal degeneration and dystrophies occur in dogs, cats, and horses. Corneal degenerations are often unilateral and usually secondary to ocular or systemic diseases. Corneal stromal dystrophies are bilateral; appear inherited or breed-predisposed in dogs; and often consist of triglyceride, cholesterol, and calcium deposits within the corneal stroma. Treatment is not usually necessary.
Corneal dystrophy may also involve the corneal endothelium. It primarily affects Boston Terriers, Chihuahuas, and Dachshunds. Female Boston Terriers are affected more frequently than males, and the mean age is ~7.5 yr. With the dystrophic and degenerating endothelium, progressive but painless corneal edema develops. With extensive and full-thickness corneal edema, corneal epithelial bullae may develop and are quite painful. Treatment of early cases before complete corneal involvement consists of topical hyperosmotics (2–5% sodium chloride or 40% glucose) applied frequently and, for advanced cases, thermokeratoplasty (Salaras procedure) or full-thickness (penetrating) keratoplasty.
Last full review/revision July 2011 by Kirk N. Gelatt, VMD
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