Focus on Ophthalmology Inside the Eye of the Horse

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1 Proceedings of the American Association of Equine Practitioners - Focus Meeting Focus on Ophthalmology Inside the Eye of the Horse Raleigh, NC, USA 2012 Next Focus Meetings: August 4-6, Focus on Dentistry Charlotte, NC, USA September 5-7, Focus on the Foot Fort Collins, CO, USA Reprinted in the IVIS website with the permission of the AAEP

2 Diagnosis and Treatment of Glaucoma in the Horse Brian C. Gilger, DVM, MS, Diplomate ACVO Author s address: College of Veterinary Medicine, North Carolina State University, Raleigh, NC; bgilger@unity.ncsu.edu. 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 humans 1 (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. 82

3 Fig. 1. Horse with glaucoma in the left eye. Fig. 2. Diffuse corneal edema typical of glaucoma. 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 mm anterior to posterior) and lens subluxation can also occur late in the disease. Table 1. Clinical Signs of Glaucoma in Horses Secondary Glaucoma Primary Glaucoma Early in disease process: Early in disease process: Unrelenting corneal edema Focal or diffuse corneal edema Severe discomfort Minimal discomfort Signs of chronic uveitis Minimal other ocular signs Vision loss/blindness None or minimal vision loss Chronic disease: Chronic disease: Diffuse corneal edema Diffuse corneal edema Enlarged eye Corneal striae Signs of chronic uveitis Mydriatic pupil Vision loss/blindness Enlarged eye Retinal/optic nerve degeneration Mild to moderate ocular discomfort Vision loss/blindness Diagnosis of Equine Glaucoma A tonometer is essential for the diagnosis of equine glaucoma. Indentation tonometers, such as the schiotz tonometer cannot be used in horses because of the horse s thick cornea and because the horse s cornea cannot be positioned horizontally. Therefore, applanation tonometers must be used. The most practical and portable applanation tonometer is the Tonopen (Tonopen 83

4 Tonometer, Medtronic, Jacksonville, FL) or TonoVet (Acrivet, Salt Lake City, UT) tonometer (Fig. 3). For accurate tonometry, auriculopalpebral nerve blocks should be performed because tension on the eyelids may artificially elevated the intraocular pressure. 4 In addition, tranquilization may artificially lower the intraocular pressure. 4 The pressure measurement should be taken from the most normal, least edematous location of the cornea if possible. Fig. 3. Tonovet tonometer. A thorough and complete ophthalmic examination should also be done to help differentiate the cause of the glaucoma and to rule out other causes of corneal edema, such as keratitis. With glaucoma, the cornea is edematous, but rarely is there yellow or creamy cellular infiltrate, epithelial loss (i.e., corneal ulceration) or diffuse vascularization. These findings are more common with primary corneal disease. The complete ophthalmic examination will also determine if the glaucoma is primary or secondary. Glaucoma secondary to intraocular disease other than uveitis is rare, but is possible with intraocular tumors and luxation of the lens. Treatment of Equine Glaucoma Ideally, glaucoma should be treated by increasing the outflow of the fluid from the eye. This theoretically can be accomplished by medical or surgical methods. Because the outflow pathways of aqueous humor from the equine eye is primarily through the uveal-scleral pathway, traditional medications to increase outflow through the iridocorneal angle, such as miotic medications, are not useful in horses. 5 Because the uveo-scleral outflow pathway is not well characterized and treatment modalities have not been developed specifically for horses, medications designed to increase the uveo-scleral outflow in humans and dogs (i.e., prostaglandin analogs) have not proven beneficial in horses. 6 Surgical methods to increase outflow (i.e., glaucoma shunts or valves, drainage surgeries such as sclerostomies or iridectomies) have not been evaluated in horses and may not be successful because of the horse s high inflammatory response to intraocular surgery and their propensity to develop fibrin and scarring in the eye. Therefore, treatment options for equine glaucoma have centered around two main categories: treatment of the underlying inflammation and decreasing the production of aqueous humor. Systemic anti-inflammatory medications, such as flunixin meglumine, should be used initially in 84

5 all cases of glaucoma to help control intraocular inflammation. Topical therapy to decrease aqueous humor should also be used. I initially recommend topical timolol 0.5% (1 drop or 0.2 ml) twice a day. If there is poor control with this therapy (after 7-10 days), the next choice is a combination of timolol 0.5% and dorzolamide HCL (1%) (1 drop or 0.2 ml every 8 hours). If there continues to be poor intraocular pressure control and there is potential for vision, then laser cycloablation 7 (laser destruction of the ciliary body) is indicated. Trans-Scleral Diode Laser Cycloablation Prior to considering laser therapy, existing uveitis must be controlled and if uveitis is active, then intraocular inflammation must be controlled prior to laser treatment. Also, other intraocular disease such as neoplasia (i.e., perform ultrasound) should be ruled out. If significant corneal ulcers are present (i.e., larger than small bulla formation from edema), then treat with antibiotics, debridement, etc. to attempt to heal prior to laser. Laser surgery is most indicated if there is a consensual pupillary light response i.e., chance for vision in glaucomatous eye. Blind, painful globes should be removed or a cosmetic prosthesis done. Laser can be done to help control the pressures in these chronic eyes, but with poorer response than less chronic cases. Prior to considering laser therapy, the veterinarian should determine that there is no clinical response to antiglaucoma medications. Surgical procedure: General anesthesia is usually required, although some horses can be adequately treated standing using a retrobulbar lidocaine block. We will generally use a triple drip anesthesia in the recovery stall since aseptic surgery is not required. Too high of energy use or too many treatment spots may result in ocular hemorrhage or subsequent hypotony resulting in decreased vision in the eye. Not enough laser application may result in the inability to control the glaucoma. Therefore, the amount of laser therapy applied should be adjusted for each case. Topical proparacaine is given immediately prior to laser application and diode laser settings are mw power; 5000 ms Duration; Repeat interval 0 (visual eye 40 laser sites; blind eye laser spots). The laser energy is delivered through the sclera by placing the laser probe at 5-7 o clock (ventrally) 4 mm posterior to the limbus and 10-1 o clock (dorsally) 4 to 6 mm posterior to the limbus. 8 Aqueocentesis is usually performed, either before or after laser applications, and ml of aqueous humor is removed through the limbus with a 25 to 27 gauge needle. Postoperative laser treatment: The intraocular pressure should be checked approximately 2 hours and 24 hours after surgery. Intraocular pressure will usually still be elevated, but less than prior to surgery. The pressure should be measured again 1 week later, then monthly if pressures are low. Antiglaucoma medications are generally required after surgery (usually indefinitely). Systemic anti-inflammatory medications, such as flunixin meglumine, should be continued for 7-10 days after laser therapy. Many eyes need to be treated again in 6-12 months. A recent review of efficacy of diode laser therapy in horses revealed 64% of the eyes treated with laser remained sighted but 90% required topical antiglaucoma medication. 9 Use of endoscopic cyclophotocoagulation, or endoscopic visualization of the laser procedure, has been evaluated in normal horses. 10 Because the surgical technique and laser parameters remain to be determined in glaucoma patients and because of cataract complications, much more work is needed on this technique prior to recommendation for use in clinical patients

6 Discussion Glaucoma, by definition, is an increase in the intraocular pressure to a level that is incompatible with the health of the eye. An increased intraocular pressure is always the result of a decrease in outflow of aqueous humor, while an decreased intraocular pressure is always the result of a decrease in production of aqueous humor (uveitis). Primary glaucoma is not associated with any other ocular disease and there is no antecedent cause. Horses with primary glaucoma are unfortunately predisposed to bilateral involvement. Therefore if you are presented with a unilateral primary glaucoma it is essential that the other eye is evaluated and closely monitored. In addition to routine monitoring, the unaffected eye requires preventive therapy in the form of either systemic medication given to treat the affected eye, which will also treat the predisposed eye, or topical medication administered to the predisposed eye. Suggest repeated measurements of the intraocular pressure in the predisposed eye every 3-4 months for life or until the eye becomes glaucomatous. In secondary glaucoma, some other event in the eye occurs that results in a decrease in aqueous humor access to the outflow pathways. It is essential to determine the cause for the glaucoma as therapy will vary according to etiology; however, the most common cause in horses is equine recurrent uveitis. There is no predisposition to bilateral involvement in horses with secondary glaucoma unless the horse has bilateral recurrent uveitis. Equine practitioners should consider glaucoma as the cause of any unexplained corneal edema or ocular cloudiness and in cases of severe unrelenting ocular inflammation. Accurate measurement with a portable tonometer is essential to make the definitive diagnosis and to monitor the response to therapy. Table 2. Treatment of Equine Glaucoma Secondary Glaucoma Initial therapy Treat primary uveitis Systemic NSAIDS +/- atropine topically +/- corticosteroids topically Treat glaucoma Timolol XE 0.5% q12 hrs Poor response or Reevaluate uveitis increasing intraocular pressure Determine vision prognosis If good, treat as with primary glaucoma Continued poor response If poor, consider enucleation Determine vision prognosis If good, consider laser cycloablation If poor, consider enucleation Primary Glaucoma Timolol XE 0.5% q12 hrs Systemic NSAIDS Timolol (0.5%)/ dorzolamide (1%) combination (generic Cosopt ) q8 hours Systemic NSAIDS Determine vision prognosis If good, consider laser cycloablation If poor, consider enucleation 86

7 References 1. Smith PA, Samuelson DA, Brooks DE. Aqueous drainage pathways in the equine eye: scanning electron microscopy. J of Morphology 1988;198: Wilkie DA, Gilger BC. Equine glaucoma. Vet Clin N Am Equine Pract 2004;20: Lassaline ME, Brooks DE. Equine Glaucoma. In: Gilger BC, ed. Equine Ophthal 1 st ed. St. Louis: Elsevier Science, 2005; van der Woerdt A, Gilger BC, Wilkie DA, et al. Effect of auriculopalpebral nerve block and intravenous administration of xylazine on intraocular pressure and corneal thickness in horses. Am J Vet Res 1995;56: van der Woerdt A, Gilger BC, Wilkie DA. Effect of topical pilocarpine on pupil size and intraocular pressure in horses. Am J Vet Res 1998;59: Willis AM, Diehl KA, Hoshaw-Woodard S, et al. Effects of topical administration of 0.005% latanoprost solution on eyes of clinically normal horses. Am J Vet Res 2001;62: Whigham HM, Brooks DE, Andrew SE, et al. Treatment of equine glaucoma by transscleral neodymium:yttrium aluminum garnet laser cyclophotocoagulation: a retrospective study of 23 eyes of 16 horses. Vet Ophthal 1999;2(4): Miller TM, Willis AM, Wilkie DA, et al. Description of ciliary body anatomy and identification of sites for transscleral cyclophotocoagulation in the equine eye. Vet Ophthalmol 2001;4: Annear MJ, Wilkie DA, Gemensky-Metzler AJ. Semiconductor diode laser transscleral cyclophotocoagulation for the treatment of glaucoma in horses: a retrospective study of 42 eyes. Vet Ophthal 2010;13: Harrinton, JT, McMullen RJ, Cullen J. Diode laser endoscopic cyclocoagulation in the normal equine eye. Am J Vet Res 2012 (Submitted). 87