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Diagnosis and Treatment of Glaucoma in the Horse
B.C. Gilger
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Take Home Message
Equine glaucoma is a frustrating disease that is different in clinical appearance, pathogenesis, and response to treatment compared to canine and human glaucoma. It is very important for the equine clinician to recognize early signs of glaucoma, be able to measure the intraocular pressure of horses, and use appropriate anti-glaucoma therapy.
Introduction
Aqueous humor, which acts to supply metabolic needs of intraocular structures, is produced constantly by the ciliary body of the equine eye. The fluid must also drain constantly from the eye through the iridocorneal and uveoscleral outflow pathways. Obstruction of this outflow of fluid can be the result of an abnormally developed drain (i.e., primary glaucoma) or through damage to the drain from scarring, vascularization, or accumulation of debris (i.e., secondary glaucoma). The result of this obstruction is retention of aqueous humor and subsequent increase in the pressure within the eye. The pathologic disease state associated with elevated intraocular pressure is called glaucoma.
Horses have a much greater percentage of aqueous humor outflow through the uveoscleral outflow compared to dogs and humans1 (the species in which most glaucoma research has centered) where the outflow is primarily through the iridocorneal angle. Therefore, the causes, clinical findings, and treatments are different for horses with glaucoma. Because of these differences and the fact that few veterinarians have a suitable tonometer (e.g., instrument to measure intraocular pressure) for horses, glaucoma is not commonly recognized and therefore frequently not treated appropriately in many horses. The purpose of this paper is to describe the clinical features, diagnosis, and appropriate therapy for glaucoma in horses.
Clinical Features of Equine Glaucoma
The most common cause of glaucoma in horses is chronic or recurrent uveitis (a type of secondary glaucoma).2 Historically, these horses have multiple episodes of intraocular inflammation followed by a severe unrelenting bout of ocular cloudiness and discomfort (as a result of the development of glaucoma) that does not respond to traditional uveitis therapy. These eyes have high intraocular pressures (40-80 mmHg), diffusely edematous corneas (Fig. 1), and signs of chronic intraocular inflammation, such as posterior synechia (adhesions), a miotic pupil, and cataract formation (Table 1). These eyes may appear enlarged or normal sized.
Horses with primary glaucoma most commonly present with partial or diffuse corneal edema (Fig. 2). These eyes may or may not be painful. Early in the disease process vision and the pupil size may be normal. Intraocular pressure can range from 35 to 80 mmHg. With chronic primary glaucoma, vision decreases, the cornea becomes diffusely edematous, and other signs of chronic glaucoma may become evident (e.g., diffuse corneal edema, corneal striae, retinal and optic nerve degeneration) (Table 1). In general however, the horse tends to lose vision much later in the disease process compared to dogs and humans.3 An increased size of the eye (greater than 40-45 mm anterior to posterior) and lens subluxation can also occur late in the disease.
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