How to Diagnose and Manage Horses With Glaucoma - · PDF fileHow to Diagnose and Manage Horses...

How to Diagnose and Manage Horses WithGlaucoma

Erica L. Tolar, DVM, Diplomate ACVO*; andAmber 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 WestHazelwood Drive, Urbana, IL 61802; e-mail: [email protected] (Labelle). *Corresponding andpresenting author. © 2013 AAEP.

1. Introduction

Glaucoma is a painful ocular disease that often resultsin vision loss and can be frustrating to treat.1–4 Equineglaucoma is most often secondary to chronic, recurrentepisodes of intraocular inflammation as occur withequine recurrent uveitis (ERU).1–8 Diagnosis of glau-coma requires tonometry, or measurement of the in-traocular pressure (IOP). Many types of portable,affordable tonometers are available to the veterinarypractitioner, and tonometry is becoming more widelyused in equine practice. Once a diagnosis of glau-coma has been established, therapy options rangefrom topical and oral medications to advanced surgicalprocedures. Referral to a veterinary ophthalmologistis appropriate for all cases of equine glaucoma. De-termining the cause of the glaucoma and deciding onan appropriate treatment plan is crucial to obtain theultimate goal of maintaining a comfortable and visualeye. When vision has been lost and IOP is uncon-trolled, surgical procedures to ensure long-term com-fort, including enucleation, should be considered.

2. Anatomy and Pathophysiology of Glaucoma

Knowledge of normal ocular anatomy allows thepractitioner to recognize abnormalities in the equine

eye and pathologic changes associated with glau-coma. Immediately posterior to the iris is the cili-ary body, which is hidden from view by the iris faceeven when the pupil is fully dilated. The ciliarybody processes produce aqueous humor, the clearintraocular fluid that provides metabolic support tothe posterior cornea and the internal structures ofthe eye. Aqueous humor flows from the posteriorchamber, through the pupil, into the anterior cham-ber, and drains from the eye through the uveoscleralor iridocorneal outflow pathways (Fig. 1).9 The iri-docorneal angle is visible as an intraocular mesh-work at the temporal and nasal limbus, withpectinate ligaments extending from the iris root tothe corneoscleral junction (Fig. 2).10,11 Horses areunique in that up to 50% of their aqueous humordrainage is through the uveoscleral (also called “un-conventional”) outflow pathway.12,13

Intraocular pressure is a balance of aqueous hu-mor production and aqueous humor outflow. Glau-coma is a series of intraocular pathologic eventsculminating in IOP elevation, optic nerve damage,and vision loss. Elevated IOP results in decreasedblood flow and optic nerve axoplasmic flow, ulti-mately resulting in retinal cell death, compression of

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NOTES

the optic nerve, and blindness.14 In humans, formsof glaucoma are recognized that result in optic nervedegeneration, retinal degeneration, and vision losswithout elevation in IOP. Similar forms of glau-coma have not been documented in the horse; eleva-tion in IOP is thought to be the most important riskfactor for glaucomatous optic nerve damage inequine patients.14,15 Intraocular pressure eleva-tion typically results from obstruction of the aque-ous humor outflow pathway. Aqueous humoroverproduction has not been reported in any domes-tic animal species and is not considered to be a causeof glaucoma in the horse.

Glaucoma in the horse is often divided into threecategories: primary, secondary, and congenital.

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, bilateralcondition that results from abnormal functioning ofthe aqueous humor outflow system. Primary glau-coma is infrequently reported in the horse. Glau-coma in horses is most often secondary to aconcurrent ocular disease such as ERU, intraocularneoplasia, 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 bywhich ERU leads to secondary glaucoma is poorlyunderstood.4

3. Examination Techniques

The minimum equipment necessary for any equineophthalmic examination includes a Finhoff transil-luminator, magnification head loupe, fluoresceinstain, a tonometer, tropicamide,a and a retinoscope(such as a direct ophthalmoscope or hand lens).If possible, the horse should be observed navigatingin its environment before sedation. An obstaclecourse can be created with the use of large objects inthe barn (such as trash cans and poles on theground) to allow the practitioner to more criticallyassess vision. Menace responses and dazzle re-flexes should also be observed before sedation.Ophthalmic examination should be performed in adimly lit location to maximize detection of subtlelesions. Sedation with detomidine hydrochlorideb

or xylazine hydrochloridec and an auriculopalpebralblock are important for completion of a completeexamination. Butorphanol tartrated is not recom-mended because it tends to result in jerky, sponta-neous head movements.

Tonometry is recommended for all horses withclinical signs of ophthalmic disease. Whereas seda-tion with �-2 agonists can decrease IOP readings, anauriculopalpebral block has no effect on IOP.18,19

Head position does have a critical effect on IOP;lowering the head below the heart causes significantelevations in IOP.20 It is important to maintain ahead position level with or above the heart whileperforming 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. Anyexcessive 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 amagnetic probe that is projected at the cornea.The rebound tonometer is handheld, battery-oper-ated, and does not require daily calibration. Thenoise emitted from the machine while taking therequired six readings is very quiet and not likely todisturb the horse, even if not sedated. The read-ings are averaged within the machine and displayed

Fig. 1. The equine aqueous humor pathway. Aqueous humor isproduced in the ciliary body (shaded), flows into the posteriorchamber, through the pupil into the anterior chamber, and thendrains through the iridocorneal angle or uveoscleral outflowpathway.

Fig. 2. Photograph of a normal equine eye. The iridocornealangle is visible just axial to the limbus (white arrow). Normalpectinate ligaments are visible as a meshwork.

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in an easily viewed window opposite the probe. Top-ical anesthesia is not required. The mean intraocularpressure with the use of a TonoVet is 22.1 � 5.9 mmHg, with a range from 10 to 34 mm Hg.23

Multiple applanation tonometers are commer-cially availablef,g (Fig. 4). Applanation tonometersdiffer from the rebound tonometer in that they mea-sure the force required to flatten the corneal surface.All of the devices are handheld and portable. Ap-planation tonometers require a latex cover to protectthe tip of the device. Both of the listed applanationtonometers require use of topical anesthesia to ob-tain accurate readings. One advantage of an ap-planation tonometer is that it can be used with thepatient in any position, unlike the rebound tonome-ter, which must remain perpendicular to the patientwith the magnetic probe parallel to the ground.The mean intraocular pressure with the use of aTono-Pen is 21.0 � 5.9 mm Hg, with a range from 9to 33 mm Hg.23

4. Clinical Signs of Glaucoma

The clinical signs of glaucoma vary.1–3,7,8,17,24 Manyhorses with glaucoma do not exhibit the classic signs ofocular pain, including blepharospasm and epiphora.Acute signs often differ from chronic signs (Table 1).

Glaucomatous horses exhibit variable pupillarylight reflex deficits. Glaucoma generally results ina mydriatic pupil caused by effects on the opticnerve and iris sphincter muscle, but horses withconcurrent intraocular inflammation may have mi-otic pupils instead. Dyscoria, an abnormallyshaped pupil, may result from posterior synechiae(adhesions between the iris and the lens capsule)(Fig. 5). Posterior synechiae may result in pupilsize being discordant with concurrent ocular disease(ie, a miotic pupil in an end-stage glaucoma eye).

Fig. 3. Photograph of rebound tonometry being performed in apatient with glaucoma. Note that the tonometer is held perpen-dicular to the ground, and the practitioner is using caution toavoid excessive digital pressure on the globe.

Fig. 4. Photograph of applanation tonometry being performed ina patient with glaucoma. Note that the tonometer can be held inany plane, and the practitioner is using caution to avoid excessivedigital pressure on the globe.

Table 1. Clinical Signs of Equine Glaucoma

Acute signsVision lossEpiphoraBlepharospasmCorneal edemaConjunctival hyperemiaMydriasis

Chronic signsVision lossEpiphoraBlepharospasmBuphthalmosCorneal edemaDescemet’s striaeCorneal ulcersLens luxationMydriasisChanges in the appearance of drainage angle (collapse,

fibrosis)Retinal degenerationOptic nerve cupping

Fig. 5. Photograph of the right eye of a horse with end-stageERU. Note the small globe size, corneal fibrosis, dyscoria causedby posterior synechiae, and cataract. This eye is not visual andhas no potential to regain vision.



Conjunctival hyperemia and episcleral injection iscommon in glaucomatous horses. Mild to severediffuse corneal edema is observed frequently. Cor-neal edema may be focal or begin as a vertical stripeacross the cornea, then progress to diffuse edema(Fig. 6). Edema results from dysfunction of theendothelium and physical distortion of corneal stro-mal fibers. Descemet’s striae (also termed “cornealstriae” or “Haab’s striae”) are areas of discontinuityin Descemet’s membrane and may later appear atthese sites of linear edema traversing the cornea(Fig. 7). Severe corneal edema may be associatedwith fluid-filled subepithelial blisters or bullae.Bullae may rupture and result in corneal ulceration.

Corneal vascularization may be superficial, peril-imbal, and extend several millimeters from the lim-bus toward the axial cornea. Keratic precipitates(pinpoint conglomerates of fibrin and inflammatorycells) may be present on the corneal endothelium.

Keratic precipitates are often difficult to visualizewithout magnification.

The diffuse corneal edema, frequently present inhorses with glaucoma, makes intraocular examina-tion challenging. Performing the exam in a darkarea and directing a light source across the anteriorchamber from limbus to limbus facilitates visualiza-tion of intraocular structures. Common intraocu-lar exam findings may include clinical signs seenwith ERU, including iridal hyperpigmentation, at-rophy of the corpora nigra, posterior synechiae, dys-coria, aqueous flare, and cataract. The iridocornealangle is most visible laterally, in which the openingof the trabecular meshwork is visible just axial tothe limbus. Pectinate ligaments are visible as ameshwork traversing the opening of the iridocornealangle. Abnormal iridocorneal angles may be scle-rotic, with a band of white fibrous tissue replacing thenormal pectinate ligaments, or narrowed (Fig. 8).Appearance of the iridocorneal angle has not beencorrelated with the onset of glaucoma or prognosis inhorses. Lens subluxation or luxation is usually a re-sult of chronic expansion of the glaucomatous globe(termed “buphthalmos”) and subsequent zonularstretching and degeneration (Fig. 9).

In the early stages of glaucoma, the appearance ofthe retina may be normal. With time, the opticnerve may become atrophic, pale, and “cupped” inappearance, as if the center of the optic nerve was

Fig. 8. Photograph of the left eye of a horse with chronic glau-coma. The iridocorneal angle is collapsed with marked fibrosis(white arrow).

Fig. 6. Photograph of the left eye of a horse with glau-coma. Note the diffuse corneal edema and bullae (fluid-filledvesicles or “blisters” that can be present with severe cornealedema).

Fig. 7. Photograph of the left eye of a horse with chronic glau-coma. Descemet’s striae are visible, traversing the cornea aswhite curvilinear lines.



being pushed away from the viewer. Retinal bloodvessels may appear absent or attenuated. Chronicelevations in IOP may lead to expansion in the sizeof the globe, termed buphthalmos.

5. Treatment of Glaucoma

The goal of glaucoma treatment is maintaining IOPin a range that prevents continuing optic nerve andretinal damage. The “ideal” IOP is unknown, butmost clinicians agree that �25 mm Hg would beacceptable. Because IOP is a balance of aqueoushumor production and drainage, all glaucoma treat-ments are aimed at one of two targets: reducingaqueous humor production or increasing IOP drain-age. Glaucoma treatment can be divided into med-ical and surgical therapies; medical therapy istypically the first-line treatment. The underlyingcauses of glaucoma, such as ERU, may also requireconcurrent treatment. In addition to topical anti-glaucoma medications, such cases may also needtopical and systemic anti-inflammatories. The useof atropine in cases of concurrent ERU and glau-coma is controversial because atropine may be asso-ciated with elevations in IOP.3,25,26 Atropineshould only be used in cases of glaucoma when IOPcan be closely monitored.

Medical therapy is generally the first line of treat-ment for glaucoma.27 Drug classes that reduceaqueous humor production include �-adrenergic an-tagonists and carbonic anhydrase inhibitors (CAIs).�-Adrenergic antagonists, also called �-blockers, in-hibit cAMP activity in the ciliary body. Timololmaleate 0.5%h is the most commonly used drug inthis class. It has been shown to reduce IOP inclinically normal horses.28 Other commerciallyavailable �-adrenergic agonists include betaxolol,levobunolol, and metipranolol. These drugs arewidely used and have not been evaluated in horses.�-Adrenergic agents should be applied every 8 to 12hours.28

Carbonic anhydrase inhibitors inhibit carbonicanhydrase, an enzyme in the ciliary body epithelium

that is required for aqueous humor production.Commercially available CAIs include brinzolamide1%i and dorzolamide 2%.j Both have been demon-strated to reduce IOP in clinically normal horses,although brinzolamide results in slightly greater re-duction.29,30 Generic dorzolamide is affordable andwidely available, which has made it more popularfor the treatment of equine glaucoma in the UnitedStates. Dorzolamide 2% and timolol 0.5% solutionis also available as a combination drug. The effi-cacy of a dorzolamide/timolol combination versusdorzolamide alone versus brinzolamide alone hasnot been evaluated in horses with glaucoma. Top-ical CAIs should be administered every 8 to 12hours.29,30 Acetazolamide, an oral CAI, is fre-quently used as a potassium-wasting diuretic inhorses with hyperkalemic periodic paralysis at dosesof 2 to 3 mg/kg PO every 12 hours.31 The efficacy ofthis drug in decreasing IOP is unknown; however, itis available as an oral formulation. This makes itadvantageous for use in patients in which topicaladministration of a solution is not possible.

Few drugs are available for increasing IOP out-flow. Prostaglandin analogues include lantano-prost 0.005%k and travaprost 0.004%.l This drugclass results in miosis and increased IOP outflow inother species but is not consistently effective in thehorse.32 Complications are reported with use ofprostaglandin analogues, including increased ocularpain and intraocular inflammation.32 A high rateof complications, including increased ocular pain, isreported. This drug class should be used with greatcaution in horses with glaucoma associated withERU.

Surgical therapy for glaucoma can either increaseaqueous outflow or decrease production. The mostcommon surgical procedure is cyclophotocoagulation(laser ablation of the ciliary body epithelium), whichresults in decreased aqueous humor produc-tion.1,3,33–36 The procedure can be performed tran-sclerally or endoscopically with the use of a diodelaser that preferentially targets pigmented tissuesuch as the ciliary body epithelium. Complicationsof cyclophotocoagulation include corneal ulcer-ation, uveitis, hyphema, cataract formation, and ret-inal detachment. Continued topical medicationsare often necessary despite surgical intervention.1

Surgical therapies for glaucoma were previouslylimited to those decreasing aqueous humor outflow.Recent evidence supports the use of drainage im-plants that direct aqueous humor subconjunc-tivally.37 Ahmed valved shunts have been placedexperimentally with good success. Clinical trialsare underway evaluating the use of this type ofdrainage implant in clinical glaucoma patients.37

When glaucoma therapy fails, the patient is leftwith a painful, blind globe, and eliminating ocularpain is essential for the welfare of the horse. Enu-cleation is one therapy to eliminate glaucoma painin a blind eye. Surgical alternatives to enucleationinclude placement of a cosmetic intraocular or in-

Fig. 9. Photograph of the left eye of a horse with chronic glau-coma. Note the complete anterior lens luxation of a cataractouslens with a mydriatic pupil.



traorbital prosthesis.38,39 Chemical ciliary bodyablation can be used to decrease aqueous humorproduction and induce shrinkage of the globe (phthi-sis bulbi).40 Intravitreal injection of 50 to 75 mg ofgentamicin sulfate results in necrosis of the ciliarybody with long-term reduction of IOP. Intravitrealinjection can be performed in the sedated horse withthe use of topical anesthesia; a retrobulbar blockmay be necessary. After the application of topicalanesthesia, a 22- to 25-g needle should be positioned10 to 12 mm posterior to the dorsolateral limbus andaimed toward the optic nerve (Fig. 10). Ensuringthe appropriate angle of the needle is essential toavoid lacerating the posterior lens capsule duringintravitreal injection, because intractable uveitisprobably will result. If IOP is elevated at the timeof injection, aqueous paracentesis should be per-formed first to lower IOP into a normal range andprevent further IOP elevation. Tonometry shouldbe performed after injection, and, if the IOP is stillelevated, the aqueous paracentesis should berepeated.

References and Footnotes1. Annear MJ, Wilkie DA, Gemensky-Metzler AJ. Semicon-

ductor diode laser transscleral cyclophotocoagulation for thetreatment of glaucoma in horses: a retrospective study of 42eyes. Vet Ophthalmol 2010;13:204–209.

2. Cullen CL, Grahn BH. Equine glaucoma: a retrospectivestudy of 13 cases presented at the Western College of VeterinaryMedicine from 1992 to 1999. Can Vet J 2000;41:470–480.

3. Miller TR, Brooks DE, Gelatt KN, et al. Equine glaucoma:clinical findings and response to treatment in 14 horses. VetComp Ophthalmol 1995;5:170–182.

4. Wilcock BP, Brooks DE, Latimer CA. Glaucoma in horses.Vet Pathol 1991;28:74–78.

5. Gilger BC, Wilkie DA, Clode AB, et al. Long-term outcomeafter implantation of a suprachoroidal cyclosporine drug de-livery device in horses with recurrent uveitis. Vet Ophthal-mol 2010;13:294–300.

6. Peiffer RL Jr, Wilcock BP, Yin H. The pathogenesis andsignificance of pre-iridal fibrovascular membrane in domesticanimals. Vet Pathol 1990;27:41–45.

7. Barnett KC, Cottrell BD, Paterson BW, et al. Buphthalmosin a Thoroughbred foal. Equine Vet J 1988;20:132–135.

8. Gelatt KN. Glaucoma and lens luxation in a foal. Vet MedSmall Anim Clin 1973;68:261.

9. Samuelson DA. Ophthalmic anatomy. In: Gelatt KN, edi-tor. Veterinary Ophthalmology. 4th edition. Ames, Io-wa: Blackwell Publishing; 2007:37–148.

10. Samuelson D, Smith P, Brooks D. Morphologic features ofthe aqueous humor drainage pathways in horses. Am J VetRes 1989;50:720–727.

11. Smith P, Samuelson D, Brooks D. Aqueous drainage pathsin the equine eye: scanning electron microscopy of corrosioncast. J Morphol 1988;198:33–42.

12. Sedacca K, Samuelson D, Lewis P. Examination of the an-terior uveoscleral pathway in domestic species. Vet Oph-thalmol 2012;15(Suppl 1):1–7.

13. Smith PJ, Samuelson DA, Brooks DE, et al. Unconventionalaqueous humor outflow of microspheres perfused into theequine eye. Am J Vet Res 1986;47:2445–2453.

14. Brooks DE, Blocker TL, Samuelson DA, et al. Histomor-phometry of the optic nerves of normal horses and horseswith glaucoma. Vet Comp Ophthalmol 1995;5:193–210.

15. De Geest JP, Lauwers H, Simoens P, et al. The morphologyof the equine iridocorneal angle: a light and scanning elec-tron microscopic study. Equine Vet J Suppl Sept 1990;(10):30–35.

16. Latimer CA, Wyman M. Neonatal ophthalmology. VetClin North Am Equine Pract 1985;1:235–259.

17. Davidson HJ, Blanchard GL, Wheeler CA, et al. Anterioruveal melanoma, with secondary keratitis, cataract, and glau-coma, in a horse. J Am Vet Med Assoc 1991;199:1049–1050.

18. McClure JR Jr, Gelatt KN, Gum GG, et al. The effect of par-enteral acepromazine and xylazine on intraocular pressure inthe horse. Vet Med Small Anim Clin 1976;71:1727–1730.

19. van der Woerdt A, Gilger BC, Wilkie DA, et al. Effect ofauriculopalpebral nerve block and intravenous administra-tion of xylazine on intraocular pressure and corneal thicknessin horses. Am J Vet Res 1995;56:155–158.

20. Komaromy AM, Garg CD, Ying GS, et al. Effect of headposition on intraocular pressure in horses. Am J Vet Res2006;67:1232–1235.

21. Andrade SF, Kupper DS, Pinho LF, et al. Evaluation of thePerkins handheld applanation tonometer in horses and cat-tle. J Vet Sci 2011;12:171–176.

22. Dziezyc J, Millichamp NJ, Smith WB. Comparison of appla-nation tonometers in dogs and horses. J Am Vet Med Assoc1992;201:430–433.

23. Knollinger AM, La Croix NC, Barrett PM, et al. Evaluationof a rebound tonometer for measuring intraocular pressure indogs and horses. J Am Vet Med Assoc 2005;227:244–248.

24. Frauenfelder HC, Vestre WA. Cryosurgical treatment ofglaucoma in a horse. Vet Med Small Anim Clin 1981;76:183–186.

25. Herring IP, Pickett JP, Champagne ES, et al. Effect oftopical 1% atropine sulfate on intraocular pressure in normalhorses. Vet Ophthalmol 2000;3:139–143.

26. Mughannam AJ, Buyukmihci NC, Kass PH. Effect of topi-cal atropine on intraocular pressure and pupil diameter inthe normal horse eye. Vet Ophthalmol 1999;2:213–215.

27. Wilkie DA. Equine glaucoma: state of the art. Equine VetJ Suppl March 2010;37:62–68.

28. Van Der Woerdt A, Wilkie DA, Gilger BC, et al. Effect ofsingle- and multiple-dose 0.5% timolol maleate on intraocularpressure and pupil size in female horses. Vet Ophthalmol2000;3:165–168.

29. Willis AM, Robbin TE, Hoshaw-Woodard S, et al. Effect oftopical administration of 2% dorzlamide hydrochloride or 2%dorzlamide hydrochloride-0.5% timolol maleate on intraocu-lar pressure in clinically normal horses. Am J Vet Res 2001;62:709–713.

Fig. 10. Photograph of a chemical ciliary body ablation per-formed on the left eye of a horse with vision loss and elevated IOPsecondary to chronic glaucoma.



30. Germann SE, Matheis FL, Rampazzo A, et al. Effects oftopical administration of 1% brinzolamide on intraocularpressure in clinically normal horses. Equine Vet J 2008;40:662–665.

31. Beech J, Lindborg S. Prophylactic efficacy of phenytoin, ac-etazolamide and hydrochlorothiazide in horses with hyper-kalaemic periodic paralysis. Res Vet Sci 1995;59:95–101.

32. Willis AM, Diehl KA, Hoshaw-Woodard S, et al. Effects oftopical administration of 0.005% latanoprost solution on eyesof clinically normal horses. Am J Vet Res 2001;62:1945–1951.

33. Harrington JT, McMullen RJ Jr, Cullen JM, et al. Clinicaland histopathologic effects of diode laser endoscopic cyclopho-tocoagulation in the normal equine eye. American College ofVeterinary Ophthalmologists, 42nd Annual Conference.Hilton Head, SC. 2011:100.

34. Miller TL, Willis AM, Wilkie DA, et al. Description of ciliarybody anatomy and identification of sites for transscleral cy-clophotocoagulation in the equine eye. Vet Ophthalmol2001;4:183–190.

35. Morreale RJ, Wilkie DA, Gemensky-Metzler AJ, et al.Histologic effect of semiconductor diode laser transscleralcyclophotocoagulation on the normal equine eye. Vet Oph-thalmol 2007;10:84–92.

36. Whigham HM, Brooks DE, Andrew SE, et al. Treatment ofequine glaucoma by transscleral neodymium:yttrium alumi-num garnet laser cyclophotocoagulation: a retrospective

study of 23 eyes of 16 horses. Vet Ophthalmol 1999;2:243–250.

37. Townsend WM, Langohr IM, Mouney MC. Feasibility ofaqueous shunts as therapy for equine glaucoma. Interna-tional Equine Ophthalmology Consortium. Sterling, Scot-land. 2012.

38. Meek LA. Intraocular silicone prosthesis in a horse. J AmVet Med Assoc 1988;193:343–345.

39. Michau TM, Gilger BC. Cosmetic globe surgery in thehorse. Vet Clin North Am Equine Pract 2004;20:467–484.

40. Utter ME, Brooks DE. Glaucoma. In: Gilger BC, editor.Equine Ophthalmology. 2nd edition. Maryland Heights,Missouri: Elsevier Saunders; 2011:350–366.

aMydriacyl, Alcon Laboratories, Fort Worth, TX 76134.bDormosedan, Orion Corporation, Espoo, Finland.cRompun, Bayer Animal Health Division, Shawnee, KS 66216.dTorbugesic, Fort Dodge Animal Health, Fort Dodge, IA 50501.eTonoVet, Icare Finland Oy, Helsinki, Finland.fTono-Pen XL, Reichert, Depew, NY 14043.gTono-Pen AVIA, Reichert, Depew, NY 14043.hTimolol maleate, Bausch & Lomb Pharmaceuticals Inc,

Tampa, FL 33637.iAzopt, Alcon Laboratories, Fort Worth, TX 76134.jTrusopt, Merck, West Point, PA 19454.kTravatan, Alcon, Irvine, CA 92618.lXalatan, Pfizer, New York, NY 10017.



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