In: 49th Annual Convention of the American Association of Equine Practitioners, 2003, New Orleans,
Louisiana, (Ed.)
Publisher: American Association of Equine Practitioners, Lexington KY
Internet Publisher: Publisher: International Veterinary Information Service (www.ivis.org), Ithaca, New York,
USA.
How to Diagnose and Treat Glaucoma in the Horse (21-Nov-2003)
B. C. Gilger
Equine Ophthalmology Service, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
1. 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 with 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.
2. Materials and Methods
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 mm Hg), 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.
Figure 1. Secondary glaucoma in a horse with chronic equine recurrent uveitis. These eyes have high
intraocular pressure (40 - 80 mm Hg), diffusely edematous corneas, and signs of chronic intraocular
inflammation, such as posterior synechia (adhesions), a miotic pupil, and cataract formation. - To view
this image in full size go to the IVIS website at www.ivis.org . 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 mm Hg. 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; Fig. 2). In general, however, the horse tends to lose vision much later in the disease process
compared with 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.
Figure 2. Primary equine glaucoma. Horses with primary glaucoma most commonly present with partial
or diffuse corneal edema (A). With chronic primary glaucoma (B), vision decreases, the cornea
becomes diffusely edematous, and other signs of chronic glaucoma may become evident (diffuse
corneal edema, corneal striae, retinal and optic nerve degeneration). - To view this image in full size go
to the IVIS website at www.ivis.org . -
Table 1. Clinical Signs of Glaucoma in Horses
Secondary Glaucoma
z
z
Early in disease process
{ Unrelenting corneal edema
{ Severe discomfort
{ Signs of chronic uveitis
{ Vision loss/blindness
Chronic disease
{ Diffuse corneal edema
{ Enlarged eye
{ Signs of chronic uveitis
{ Vision loss/blindness
Primary Glaucoma
z
z
Early in disease process
{ Focal or diffuse corneal edema
{ Minimal discomfort
{ Minimal other ocular signs
{ None or minimal vision loss
Chronic disease
{ Diffuse corneal edema
{ Corneal striae
{ Mydriatic pupil
{ 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 schiotiz 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 (Fig. 3) [a]. For accurate tonometry, auriculopalpebral nerve blocks should be performed because tension on the
eyelids may artificially elevate 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.
Figure 3. Tonopen applanation tonometer. The most practical applanation tonometer for measurement
of the intraocular pressure in horses is the portable tonophen. - To view this image in full size go to the
IVIS website at www.ivis.org . 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 uveoscleral 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 (Table 2). Systemic anti-inflammatory medications, such as
flunixin meglumine, should be used initially in 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% [b] (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 5% and
dorzolamide HCl [c] (1 drop or 0.2 ml, q 8 h). 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.
Table 2. Treatment of Equine Glaucoma
Secondary Glaucoma
z
Initial therapy
z
z
Poor response or
increasing
intraocular
pressure
z
z
Continued poor
response
Treat primary uveitis
{ Systemic NSAIDS
{ + atropine topically
{ + corticosteroids topically
Treat glaucoma
{ Timolol XE 0.5% [c] q 12 h
Re-evaluate uveitis
Determine vision prognosis
{ If good, treat as with primary
glaucoma
{ If poor, consider enucleation
Determine vision prognosis
{ If good, consider laser
cycloablation
{ If poor, consider enucleation
Primary Glaucoma
z
z
z
z
z
Timolol XE 0.5% [c] q 12 h
Systemic NSAIDS
Timolol/dorzolamide combination
(Cosopt) [d] q 8 h
Systemic NSAIDS
Determine vision prognosis
{ If good, consider laser
cycloablation
{ If poor, consider enucleation
Diode Laser Cycloablation - Before considering laser therapy, existing uveitis must be controlled, and if uveitis is active,
intraocular inflammation must be controlled before 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 treatment with antibiotics, debridement, etc. to attempt to heal before laser surgery is necessary. 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 and an intraocular silicone prosthesis 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. Before 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 because 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 not be effective in controlling the glaucoma. Therefore, the
amount of laser therapy applied should be adjusted for each case. Topical proparacaine [d] is given immediately before laser
application [e], and diode laser settings are 1200 - 1500-mW power; 5000-ms duration; repeat interval 0 (visual eye 40 laser
sites; blind eye 40 - 50 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 - 6 mm posterior to the limbus [8] (Fig. 4).
Aqueocentesis is usually performed, either before or after laser applications, and 0.25 - 0.5 ml of aqueous humor is removed
through the limbus with a 25- to 27-gauge needle.
Figure 4. Diode laser cycloablation of the ciliary body. 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. - To view this image in full size go to the IVIS website at
www.ivis.org . -
Postoperative Laser Treatment
The intraocular pressure should be checked approximately 2 and 24 h after surgery. Intraocular pressure will usually still be
elevated, but less than before surgery. The pressure should be measured again 1 wk later, and then monthly if pressures are
low. Antiglaucoma medications are generally required after surgery (usually indefinitely). Systemic anti-inflammatory
medications, such as flunixin meglumine [f] should be continued for 7 - 10 days after laser therapy. Many eyes need to be
treated again in 6 - 12 mo. 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].
3. 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 a 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 mo 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 because 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.
Footnotes
[a] Tonopen Tonometer; Medtronic, Jacksonville, FL, 32216.
[b] Timolol Maleate Ophthalmic Solution 0.5%; Major Pharmaceuticals, Livonia, MI, 48150.
[c] Cosopt; Merck & Co., Inc., West Point, PA, 19486.
[d] Alcaine; Alcon Laboratories, Fort Worth, TX, 76134.
[e] Diovet laser; Iris Medical, Mountain View, CA, 94041.
[f] Banamine; Schering-Plough Animal Health, Kenilworth, NJ, 07083.
References
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