- Jul 1, 2002
Corneal diseases are collectively termed keratopathies. Keratopathies can be ulcerated or non-ulcerated, and infected or non-infected. Keratopathies can be rather benign diseases, or can be so severe that they result in corneal scarring and blindness if not properly diagnosed and treated.
Ocular eye trauma can vary widely. Trauma from whips, nails, buckets, light fixtures, plants, and tree branches can result in corneal/scleral lacerations.
Corneal lacerations in the horse are always accompanied by varying degrees of iridocyclitis (inflammation of the iris and ciliary body, also called anterior uveitis). The eye might be cloudy, red, and painful, and squinting and tearing are present with focal (localized) or generalized corneal edema (swelling). Slight droopiness of the eyelashes of the upper eyelid could be a subtle sign of corneal ulceration.
Full-thickness corneal/scleral perforations are usually associated with iris prolapse, a shallow anterior chamber, and hyphema (hemorrhage within the anterior chamber of the eye). If the corneal lesion extends to the limbus, the sclera should be carefully checked for perforation because the scleral wound can be obscured by conjunctival swelling and hemorrhage. Failure to detect a scleral tear will result in chronic, low intraocular pressure and shrinking of the eyeball (phthisis bulbi).
Fluorescein dye staining of the cornea will reveal the laceration, and might enter the anterior chamber. Leakage of clear aqueous humor from the anterior chamber into the fluorescein-stained tear film will be seen as a clearing of the fluorescein, and that positively identifies the location of the leak.
Small corneal lacerations can heal quickly if surgical and medical therapy is instituted quickly. Larger lesions are associated with more uveitis (inflammation of the uvea) and can heal more slowly. Medical therapy is similar to that used for ulcers and should be sufficient for cases of superficial, non-perforating (not making a full-thickness hole) lacerations. Topically applied antibiotics, atropine, serum, and systemic non-steroidal anti-inflammatory drugs (NSAIDs) are recommended. Systemic NSAIDs and broad-spectrum parenteral antibiotics are also indicated for full-thickness lesions.
Deep or irregular corneal lacerations require surgical support of the cornea and more aggressive therapy for anterior uveitis and infection. Direct corneal suturing and conjunctival flaps can be done to more rapidly restore corneal integrity. Both small and large full-thickness corneal perforations should be surgically repaired. Complications include infection, iris prolapse, anterior synechia (a disease of the eye in which the iris adheres to the cornea or the capsule of the crystalline lens), cataract formation, and persistent anterior uveitis. Both small and large corneal or scleral full-thickness defects can result in phthisis bulbi (eye atrophy) if left untreated.
A horse eye with a traumatic corneal perforation such that the eye contents have extensively prolapsed, severe hemorrhage within the eye, or evidence of bacterial infection should have the affected eye removed. Septic intrusion (infection) into the eye results in painful endophthalmitis (inflammation of the eye's internal structures); such infection can spread to surrounding soft tissues and requires removal of the eye.
Corneal Foreign Bodies
Foreign bodies, such as pieces of wood, metal, insects, or dirt, in the cornea cause varying degrees of keratitis and uveitis, and are common in horses. Superficial foreign bodies can be removed under topical anesthesia and the subsequent ulcer treated medically (see photo 1 on page 70). Deep corneal and penetrating foreign bodies can cause severe uveitis/endophthalmitis and require more aggressive care.
Burdock Pappus Bristle Keratopathy
In the northeastern United States, a bristle from the burdock pappus plant can become lodged in the horse's cornea and cause ulceration. Surgical removal of the bristle foreign body and surrounding tissue is recommended.
Endothelial Detachment Following Blunt Trauma
Profound, persistent corneal edema might be present following blunt trauma to the eye. Detachment of the endothelium is a proposed mechanism of this syndrome, and the prognosis for a return to normal eye function is poor. Hypertonic solutions (5% sodium chloride) administered topically might be beneficial in the early stages to reduce the amount of edema. Thermatokeratoplasty (a surgical technique where focal burns of the corneal epithelium allow the fluid trapped in the cornea to escape) might be necessary to reduce the edema in severe cases. Endothelial cell reattachment and cellular hypertrophy (overgrowth) might occur to resolve the condition in some horses.
The eosinophil is a type of white blood cell that responds to allergic and parasitic stimuli. When eosinophils invade the equine cornea, a disease called eosinophilic keratitis results. This disease is associated with eyelid squinting, conjunctival swelling and redness, a mucoid (resembling mucus) tear discharge, and corneal ulcers covered by raised, white superficial plaques of dead tissue (see photo 2 on page 70).
Diagnosis is based on clinical signs and corneal scrapings that contain numerous eosinophils and a few mast cells, lymphocytes, and plasma cells. Fungal, bacterial, allergic, parasitic, and neoplastic (new or abnormal growth of tissues) causes for this keratopathy must be considered in the diagnosis. It is possible that eosinophilic keratitis in the horse is an allergic, immune-mediated, or inflammatory result of parasitic microfilaria such as Onchocerca, but the specific cause of this disorder is not known.
Treatment can last several months. Topical corticosteroids are beneficial in the early stages, but medical therapy used in conjunction with surgery to remove the plaques significantly speeds healing. Topical antibiotics, corticosteroids, atropine, and phospholine iodide, in combination with systemic NSAIDs, can be beneficial.
Corneal opacities, whether multiple, superficial, white, focal, or linear, with or without fluorescein dye retention, can be associated with viral keratopathy (corneal disease) in the horse. Varying amounts of eye pain, conjunctivitis, and anterior uveitis are present. Some of these lesions will retain rose bengal stain when your veterinarian is diagnosing the problem. Equine herpesvirus-2 has been cultured from some lesions. Treatment with idoxuridine and trifluorothymidine has been successful, but recurrence is common. Multiple horses in a herd can be affected.
Linear white "bands" can be seen in the corneas of normal horses, in horses at risk of developing glaucoma, and in horses with glaucoma. They can occur after a blunt trauma, and can be single or multiple. The bands can be any thickness, and can be connecting or solitary (see photo 3 at left). They appear to be thin areas of Descemet's membrane rather than breaks in this basement membrane. Glaucoma is diagnosed when the intraocular pressure is elevated.
Calcific Band Keratopathy
This is a complication of anterior uveitis. These corneal lesions appear as dense, white bands in the central cornea (see photo 4 on page 70). When your veterinarian uses fluorescein dye for diagnosis, there might be scattered areas of dye retention.
In horses with calcific band keratopathy, calcium deposited in the corneal epithelial basement membrane accumulates and disrupts the epithelium to result in painful ulcers. Superficial keratectomy (removal of the outer part of the cornea) is generally necessary to remove the calcium deposits and eliminate the pain caused by the ulcers, but topically administered calcium chelating drugs that bind the calcium and help remove it from the eye can also be beneficial.
Superficial Corneal Erosions
Chronic superficial corneal ulcers (erosions) with a shiny grayish color and surprisingly faint retention of fluorescein dye are associated with a thin coating of broken-down protein on the surface of the ulcer site. These erosions are surrounded by a loose lip of epithelium, corneal blood vessels, and crystalline stromal deposits and are very slow to heal. The epithelium at the edge of the erosion is not attached to the deeper cornea. This failure to attach results in delayed healing. Blood vessels and other compounds (the "deposits") indicate slow healing. Superficial keratectomy and conjunctival graft placement are the treatments of choice, as epithelial migration to cover this erosion can take months.
The etiology of these superficial erosions is unknown. I have seen them develop secondary to acute corneal ulceration from rubbing of the silicone tubing of subpalpebral lavage medication systems. These ulcers are notoriously slow to heal.
Squamous Cell Carcinoma
Squamous cell carcinoma (SCC) is the most common tumor of the eye and surrounding tissues in horses. The way the tumor grows and spreads might be related to the ultraviolet (UV) component of solar radiation, periocular (around the eye) pigmentation, and an increased genetic susceptibility to tumor formation. The UV component is the most plausible carcinogenic agent associated with SCC, as it targets the tumor suppressor gene p53 that is altered in equine SCC.
The prevalence of SCC increases with age. Draft horses have a higher prevalence, followed by Appaloosas and Paints, with the least prevalence found in Arabians, Thoroughbreds, and Quarter Horses. White, gray-white, and palomino hair colors predispose horses to ocular SCC.
The cornea, conjunctiva, and limbus are commonly affected. These tumors are generally pink, fleshy masses that are raised or flat (see photo 5 on page 70). Diagnosis is by biopsy, and treatment selection depends on tumor location, tumor size, extent of tumor invasion, presence of vision or blindness, treatments available, and the owner's financial constraints. Untreated SCC in horses can invade local soft tissues, the bony orbit, sinuses, brain, and metastasize to regional lymph nodes, salivary glands, and the thorax.
Surgical excision of equine ocular SCC should be followed by either radiation, cryotherapy (cold therapy), hyperthermia (heat therapy), or intralesional chemotherapy to kill tumor cells not removed by surgery. Beta radiation is most beneficial in superficial SCC of the cornea and limbus following keratectomy. A CO2 laser can also be used effectively on the cornea after keratectomy. Topical 5-fluorouracil (1% 5-FU three times per day) might be effective for superficial SCC. Cisplatin or carboplatin can be used for chemotherapy of SCC.
Corneal perforation with iris prolapse (when some portion of the iris seeps out through a hole in the cornea) might follow traumatic insult to the globe or orbit, as well as infectious and non-infectious diseases of the cornea. Iris prolapse in the horse most frequently follows acute ocular trauma, particularly sharp, perforating corneal injuries or blunt injuries causing rupture of the cornea, limbus, and/or sclera. Corneal perforation can occur secondary to rapid enzymatic breakdown of stromal collagen due to infectious or non-infectious ulcerative keratitis (inflammation of the cornea).
Perforating corneal lacerations with iris prolapse that are confined to the cornea and measure 0.6 inches (15 mm) or less in length tend to have a favorable visual outcome after surgical repair. Conversely, iris prolapse with corneal lesions longer than 0.6 inches (15 mm) and extending beyond the limbus generally have a poor visual outcome and often require removal of the eye. Chances of retaining vision can also be substantially reduced if full-thickness corneal wounds are accompanied by anterior hemorrhage. Removal of the eye should be more seriously considered in cases with these clinical and surgical findings.
Perforating corneal ulcers and iris prolapse due to ulcerative keratitis that has lasted for more than two weeks, and/or iris prolapse due to melting ulcers and/or ulcers with accompanying fungal and bacterial infections, tend to have a poor visual outcome or result in eye removal in a majority of such cases.
This is an unusual corneal disease only seen in the southern United States. It is characterized by a non-ulcerated, pink-colored infiltrate involving the corneal stroma near the limbus (see photo 6 on page 70). These pink lesions are in the peripheral cornea only. The eyes are very painful, but no ulcer is present. Signs of anterior uveitis, including severe eye pain and squinting, are very prominent. This might be an immune-mediated disease, as no organisms have been cultured from the lesion sites or noted in biopsy specimens. This is likely to be an immune-mediated keratitis.
Treatment initially consists of topically administered corticosteroids and cyclosporine A. Radiation therapy and systemic NSAIDs such as flunixin meglumine (Banamine) or phenylbutazone (Bute) might be necessary. The pain in some cases can be so severe that the eye must be surgically removed.
Editor's note: This is the seventh in a series of eye articles by Dr. Brooks. See the first, "Eye Anatomy and Physiology," Article Quick Find #2797 at www.TheHorse.com, for more information on eye anatomy.
About the Author
Dennis E. Brooks, DVM, PhD, Dipl. ACVO, is a professor of ophthalmology at the University of Florida. He has lectured extensively, nationally and internationally, in comparative ophthalmology and glaucoma, and has more than 140 refereed publications. He is a recognized authority on canine glaucoma, and infectious keratitis, corneal transplantation, and glaucoma of horses.
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