HOW-TO SESSION: OPHTHALMOLOGY How to Diagnose and Manage Horses With Glaucoma Erica L. Tolar, DVM, Diplomate ACVO*; and Amber L. Labelle, DVM, MS, Diplomate ACVO Authors’ addresses: Bluegrass Veterinary Vision, 2563 Todd’s Point Road, Simpsonville, KY 40067; e-mail: [email protected] (Tolar); University of Illinois Urbana-Champaign, 1008 West Hazelwood Drive, Urbana, IL 61802; e-mail: [email protected] (Labelle). *Corresponding and presenting author. © 2013 AAEP. 1. Introduction eye and pathologic changes associated with glau- Glaucoma is a painful ocular disease that often results coma. Immediately posterior to the iris is the cili- in vision loss and can be frustrating to treat.1–4 Equine ary body, which is hidden from view by the iris face glaucoma is most often secondary to chronic, recurrent even when the pupil is fully dilated. The ciliary episodes of intraocular inflammation as occur with body processes produce aqueous humor, the clear equine recurrent uveitis (ERU).1–8 Diagnosis of glau- intraocular fluid that provides metabolic support to coma requires tonometry, or measurement of the in- the posterior cornea and the internal structures of traocular pressure (IOP). Many types of portable, the eye. Aqueous humor flows from the posterior affordable tonometers are available to the veterinary chamber, through the pupil, into the anterior cham- practitioner, and tonometry is becoming more widely ber, and drains from the eye through the uveoscleral used in equine practice. Once a diagnosis of glau- or iridocorneal outflow pathways (Fig. 1).9 The iri- coma has been established, therapy options range docorneal angle is visible as an intraocular mesh- from topical and oral medications to advanced surgical work at the temporal and nasal limbus, with procedures. Referral to a veterinary ophthalmologist pectinate ligaments extending from the iris root to is appropriate for all cases of equine glaucoma. De- the corneoscleral junction (Fig. 2).10,11 Horses are termining the cause of the glaucoma and deciding on unique in that up to 50% of their aqueous humor an appropriate treatment plan is crucial to obtain the drainage is through the uveoscleral (also called “un- ultimate goal of maintaining a comfortable and visual conventional”) outflow pathway.12,13 eye. When vision has been lost and IOP is uncon- Intraocular pressure is a balance of aqueous hu- trolled, surgical procedures to ensure long-term com- mor production and aqueous humor outflow. Glau- fort, including enucleation, should be considered. coma is a series of intraocular pathologic events culminating in IOP elevation, optic nerve damage, 2. Anatomy and Pathophysiology of Glaucoma and vision loss. Elevated IOP results in decreased Knowledge of normal ocular anatomy allows the blood flow and optic nerve axoplasmic flow, ulti- practitioner to recognize abnormalities in the equine mately resulting in retinal cell death, compression of NOTES 174 2013 ր Vol. 59 ր AAEP PROCEEDINGS HOW-TO SESSION: OPHTHALMOLOGY Congenital glaucoma is present at birth and is un- likely to respond to therapy.7,8,16 Primary glau- coma in small-animal species is a heritable, bilateral condition that results from abnormal functioning of the aqueous humor outflow system. Primary glau- coma is infrequently reported in the horse. Glau- coma in horses is most often secondary to a concurrent ocular disease such as ERU, intraocular neoplasia, corneal perforation, or lens luxation.2–4,17 Although ERU is widely regarded as the most com- mon cause of glaucoma in horses, the mechanism by which ERU leads to secondary glaucoma is poorly understood.4 3. Examination Techniques The minimum equipment necessary for any equine ophthalmic examination includes a Finhoff transil- luminator, magnification head loupe, fluorescein stain, a tonometer, tropicamide,a and a retinoscope Fig. 1. The equine aqueous humor pathway. Aqueous humor is produced in the ciliary body (shaded), flows into the posterior (such as a direct ophthalmoscope or hand lens). chamber, through the pupil into the anterior chamber, and then If possible, the horse should be observed navigating drains through the iridocorneal angle or uveoscleral outflow in its environment before sedation. An obstacle pathway. course can be created with the use of large objects in the barn (such as trash cans and poles on the ground) to allow the practitioner to more critically 14 assess vision. Menace responses and dazzle re- the optic nerve, and blindness. In humans, forms flexes should also be observed before sedation. of glaucoma are recognized that result in optic nerve Ophthalmic examination should be performed in a degeneration, retinal degeneration, and vision loss dimly lit location to maximize detection of subtle without elevation in IOP. Similar forms of glau- lesions. Sedation with detomidine hydrochlorideb coma have not been documented in the horse; eleva- or xylazine hydrochloridec and an auriculopalpebral tion in IOP is thought to be the most important risk block are important for completion of a complete factor for glaucomatous optic nerve damage in d 14,15 examination. Butorphanol tartrate is not recom- equine patients. Intraocular pressure eleva- mended because it tends to result in jerky, sponta- tion typically results from obstruction of the aque- neous head movements. ous humor outflow pathway. Aqueous humor Tonometry is recommended for all horses with overproduction has not been reported in any domes- clinical signs of ophthalmic disease. Whereas seda- tic animal species and is not considered to be a cause tion with ␣-2 agonists can decrease IOP readings, an of glaucoma in the horse. auriculopalpebral block has no effect on IOP.18,19 Glaucoma in the horse is often divided into three Head position does have a critical effect on IOP; categories: primary, secondary, and congenital. lowering the head below the heart causes significant elevations in IOP.20 It is important to maintain a head position level with or above the heart while performing tonometry. Consistency is recom- mended when performing serial IOP measurements, with the use of the same sedation, nerve block, tonometer, and examiner each time to achieve max- imal comparability between measurements. Care- ful attention to technique is also important. Any excessive pressure on the globe may artificially in- crease IOP. Two types of tonometers are commercially avail- able for use in the horse: rebound and applana- tion.21–23 The rebound tonometere (Fig. 3) uses a magnetic probe that is projected at the cornea. The rebound tonometer is handheld, battery-oper- ated, and does not require daily calibration. The noise emitted from the machine while taking the Fig. 2. Photograph of a normal equine eye. The iridocorneal required six readings is very quiet and not likely to angle is visible just axial to the limbus (white arrow). Normal disturb the horse, even if not sedated. The read- pectinate ligaments are visible as a meshwork. ings are averaged within the machine and displayed AAEP PROCEEDINGS ր Vol. 59 ր 2013 175 HOW-TO SESSION: OPHTHALMOLOGY Table 1. Clinical Signs of Equine Glaucoma Acute signs Vision loss Epiphora Blepharospasm Corneal edema Conjunctival hyperemia Mydriasis Chronic signs Vision loss Epiphora Blepharospasm Buphthalmos Corneal edema Descemet’s striae Fig. 3. Photograph of rebound tonometry being performed in a Corneal ulcers patient with glaucoma. Note that the tonometer is held perpen- Lens luxation dicular to the ground, and the practitioner is using caution to Mydriasis avoid excessive digital pressure on the globe. Changes in the appearance of drainage angle (collapse, fibrosis) Retinal degeneration in an easily viewed window opposite the probe. Top- Optic nerve cupping ical anesthesia is not required. The mean intraocular pressure with the use of a TonoVet is 22.1 Ϯ 5.9 mm Hg, with a range from 10 to 34 mm Hg.23 Multiple applanation tonometers are commer- 4. Clinical Signs of Glaucoma cially availablef,g (Fig. 4). Applanation tonometers The clinical signs of glaucoma vary.1–3,7,8,17,24 Many differ from the rebound tonometer in that they mea- horses with glaucoma do not exhibit the classic signs of sure the force required to flatten the corneal surface. ocular pain, including blepharospasm and epiphora. All of the devices are handheld and portable. Ap- Acute signs often differ from chronic signs (Table 1). planation tonometers require a latex cover to protect Glaucomatous horses exhibit variable pupillary the tip of the device. Both of the listed applanation light reflex deficits. Glaucoma generally results in tonometers require use of topical anesthesia to ob- a mydriatic pupil caused by effects on the optic tain accurate readings. One advantage of an ap- nerve and iris sphincter muscle, but horses with planation tonometer is that it can be used with the concurrent intraocular inflammation may have mi- patient in any position, unlike the rebound tonome- otic pupils instead. Dyscoria, an abnormally ter, which must remain perpendicular to the patient shaped pupil, may result from posterior synechiae with the magnetic probe parallel to the ground. (adhesions between the iris and the lens capsule) The mean intraocular pressure with the use of a (Fig. 5). Posterior synechiae may result in pupil Tono-Pen is 21.0 Ϯ 5.9 mm Hg, with a range from 9 size being discordant with concurrent ocular disease to 33 mm Hg.23 (ie, a miotic pupil in an end-stage glaucoma eye). Fig. 4. Photograph of applanation tonometry being performed in Fig. 5. Photograph of the right eye of a horse with end-stage a patient with glaucoma. Note that the tonometer can be held in ERU. Note the small globe size, corneal fibrosis, dyscoria caused any plane, and the practitioner is using caution to avoid excessive by posterior synechiae, and cataract. This eye is not visual and digital pressure on the globe. has no potential to regain vision. 176 2013 ր Vol. 59 ր AAEP PROCEEDINGS HOW-TO SESSION: OPHTHALMOLOGY Fig. 6.