Glaucoma: Treat to restore vision and comfort in horses


Treatment of glaucoma depends on the athletic needs and use of the individual ...

Glaucoma is an emerging disease in horses. Until recently it was thought to be quite rare, but better and more available methods to measure intraocular pressure (IOP) demonstrate that glaucoma is not so uncommon.

Prevalence has been estimated between 0.07 and 0.5 percent. Glaucoma is progressive and debilitating and results in destruction and death of retinal neurons, and is both painful and blinding. Vision loss occurs late and chronically due to IOP elevation, effecting retinal blood flow and killing neurons over a period of days to months depending on severity. If IOP is reduced and stabilized, vision may be preserved for prolonged periods.

Photo 1: Generalized corneal edema secondary to elevated intraocular pressure. Glaucoma was secondary to uncontrolled uveitis.

Management of glaucoma requires control of both IOP and any underlying process, either by chronic use of topical or systemic drugs or surgery. Damage from glaucoma does not immediately halt with IOP reduction. The neurosensory retina is a delicate nine-layer sheet that contains photoreceptors, other short connecting nerves that collate and modify photoreceptor output and signal the retinal ganglion cells (RGCs), which chemically transmit perception of light to the midbrain and visual centers of the cortex.

RGC death

Glaucoma results in malfunction and death of RGCs in particular. All RGCs are not equally susceptible, and those with larger axons die early. Greater losses of RGCs diminish vision but central RGCs are more important than those peripherally. The pathogenesis of death involves release of chemical mediators (glutamate) and inadequate blood flow. Destruction spreads as toxic mediators are released from decaying neurons, injuring adjacent cells.

In horses, glaucoma secondary to uveitis is by far the most common (Photo 1). Precipitating causes are chronic low grade or recurrent uveitis, including equine recurrent uveitis (ERU) and acute traumatic uveitis. Uveitis precipitated 85 percent of glaucoma cases in one report. Obstruction of the drainage angle and pupil with inflammatory membranes and synechiae results from accumulating protein precipitates, blood cells and anterior chamber debris. Chronic complications are cataract, retinal detachment and optic nerve atrophy. Horses are remarkable in that retinal function and vision may be somewhat sustained despite chronically elevated IOP, chemical mediators and globe enlargement (photo 2, p. 2E). Thus, although early intervention will be the most successful, light detection and vision may be retained despite chronicity of quite evident pathology.

Photo 2: Prolonged ocular hypertension results in globe enlargement and partial thickness breaks in Descemet's membrane termed striae. Note the corneal edema. IOP was 43mmHg.

If aggressive therapy is desired and pursued, and the uveitis becomes contained, vision may be restored despite substantial retinal damage and sequelae. The prognosis is certainly poorer if uveitis cannot be brought into remission. It is imperative that both globes are fully evaluated prior to selecting a therapeutic plan. Perception of light as a dazzle response or consensual PLR to the contralateral eye are encouraging. If in doubt, a treatment trial is warranted. After two weeks, if vision remains absent or IOP cannot be controlled, comfort and quality of life become primary goals.

Evaluate options

Options are continued topical therapy, but compliance is often poor with a blind eye, especially in stoic individuals that show few signs despite clearly substantial disease. Alternative surgical approaches are placement of an ocular prosthesis (intrascleral or hydroxyapatite shell conformer) or more simply by globe removal. Occasionally, intravitreal injection of 25-40 mg of gentamicin is performed under general anesthesia to induce ciliary ablation. This procedure is blinding and unpredictable, with potential complications including persistent uveitis, hyphema, phthisis and endophthalmitis. Ablation forces an IOP reduction but is a poor choice if IOP is not elevated because it is unlikely to improve comfort.

Complete hyphema (Photo 3) induces the most troublesome glaucoma because intense obstruction of the anterior chamber with blood rapidly results in high IOPs, inflammatory membrane formation and intense pain. Aggressive anti-inflammatories (topical steroids, oral NSAIDs) are the key, with close monitoring of IOP and in select cases more aggressive intraocular procedures to minimize sequelae and attempt to salvage vision. The prognosis remains guarded, and the possibility of globe rupture should be investigated.

Primary glaucoma appears to be uncommon, although it may be over represented in certain Warmbloods. No predisposing causes are identified, and all clinical signs relate to the glaucoma itself. These cases are likely to be much more difficult to identify, but surgical success should be better in the absence of uveitis. Aqueous humor outflow in horses is predominantly by the uveal tract and sclera not through the drainage angle. This raises some unique differences in glaucoma pathology and management in the horse.

Classic clinical signs of moderate or severe glaucoma are generalized corneal opacity (edema if IOP >40mmHg), conjunctival hyperemia and episcleral injection, incomplete or slow PLRs, reduced vision or apparent blindness, and blepharospasm, epiphora and guarding of the effected eye. Chronically, clear lines appear deep within the cornea as fractures of Descemet's membrane, suggesting IOP elevation and globe stretching (Photo 4, p. 4E). Such striae may be present without pathology, in which case they are termed band keratopathy. Complications of uveitis are very common and include iris discoloration, corpora nigra atrophy, extensive synechiae, cataract, sequestered pupil, yellow-discolored vitreous and retinal detachment depending on severity.

Photo 3: Traumatic hyphema in a polo pony. Glaucoma associated with hyphema is extremely problematic to deal with, and immediate referral is indicated if the globe appears intact and attempts to save vision are desired. IOP was >60 mmHg.

There is often diminished ability to examine intraocular structures due to opacification. If the fundus is visible, optic nerve atrophy is recognized as a pale disc with prominently criss-crossing fibers. The retina may exhibit inactive chorioretinitis as linear and geographic discolored bands, particularly below the optic disc. Milder forms of glaucoma may be more covert, with merely episcleral injection, reduced or variable vision, slower PLRs and diminished dazzle, midrange pupil, and perhaps few striae to alert the attentive clinician. Signs may fluctuate with IOP, potentially requiring repeated measurements to confirm the diagnosis. Ideally, IOP is measured and if uveitis is present, IOP is re-measured when it is controlled.

Measure it

If glaucoma is suspected, measurement of IOP is the definitive diagnosis The Tonopen [Dan Scott & Associates, (888) TONOPEN] is a robust and reliable IOP instrument in horses with a relatively brief learning curve. It is readily portable and accurate independent of globe position. Topical desensitization with proparacaine or tetracaine reduces blinking. It is important to avoid globe distortion from forceful squinting or eyelid opening, or the IOP will appear elevated. Ideally, the auriculopalpebral nerve is temporarily blocked to completely open the palpebral fissure (ointment is administered afterward). Sedation facilitates the ocular examination and IOP measurement but may substantially reduce IOP and falsely make a glaucomatous globe appear to have normal IOP. Normal IOP ranges from 20-28 mmHg. It is not uncommon to record IOPs up to 30mmHg, and if symmetric without clinical complaints, this is likely to be normal. Glaucoma is suspected when the IOP is above 32 mmHg. Asymmetry of 5 mmHg between globes prompts remeasuring, and scrutiny to determine which globe has pathology. Uveitis-induced glaucoma will have a high IOP, a variable or distorted pupil, decreased vision and an obstructed intraocular view.

Differential diagnoses of corneal edema are blunt trauma or primary uveitis with endothelial damage, or age-associated decompensation reducing endothelial cell density and pumping efficiency. These conditions permit edema without increased IOP. Endothelial cells contain Na/K-ATPase pumps that ensure corneal clarity by maintaining relative dehydration (deturgescence). Uveitis increases fluid accumulation because inflammatory mediators make cellular tight junctions leaky. In more severe uveitis, accumulations of keratic precipitates on the endothelium cause further damage. Generalized edema raises suspicion of glaucoma, but is not pathognomonic.

Photo 4: Chronic uveitis resulted in synechiae, a sequestered pupil, cataract and glaucoma. Note the opacified and obstructed drainage angle, the iris hyperpigmentation and atrophied corpora nigra. IOP was over 40mmHg, but corneal edema was absent.

Globe enlargement is termed buphthalmia, or preferably hydrophthalmos, and occurs after prolonged high IOP stretches the scleral tunic and distorts the globe. Enlargement in foals is rapid, but slower in adults, and does not always render the eye blind. With therapy, size may normalize and vision return. The horse appears more capable of withstanding IOP fluctuations by scleral elasticity and distortion. Deep corneal striae never resolve and are a reminder to consider glaucoma in globes that have apparently innocuous branching refractile lines.

Assess the situation

Treatment of glaucoma depends on the athletic needs and use of the individual, together with its age, pre-existing conditions, degree of vision loss, personality, and the client's expectations and desires. The severity of glaucoma at the time of diagnosis strongly dictates what is possible. Vision may be a very attainable goal if there is a strong commitment to therapy, and it may permit a prolonged athletic career in individuals who must be visual to compete.

Initially, medical management is begun to attempt immediate relief from discomfort, and attenuate retinal damage from elevated IOP. Timolol 0.5% is a beta-blocker that mildly reduces IOP. Dorzolamide 2% (Trusopt(r)) is a carbonic anhydrase inhibitor (CAI), and is more potent. Preferably, combination therapy is administered BID-TID and is available pre-mixed (Cosopt(r)). Ophthalmic solutions are dosed at 0.15-0.2 mL per eye in horses. This combination reduces IOP modestly in normal horses and mild/moderate glaucoma cases. Uncommonly, oral acetazolamide (3-4mg/kg PO TID) may be used, but it is poorly bioavailable and does have systemic effects. In other species, combining oral and topical CAIs is not significantly different than one route alone in most individuals. Control of uveitis is evidently a critical step to controlling glaucoma. Topical corticosteroids and oral NSAIDs are aimed at reducing active inflammation.

Atropine has been advocated to treat glaucoma in horses, but its effects on IOP are unpredictable. It is most useful when uveitis is active concurrently. Atropine frequency may be fine-tuned while monitoring IOP to balance uveitis control and uveoscleral outflow. Xalatan is a highly effective ocular hypotensive in many species but is not recommended in horses. The Ohio State University (OSU) reported an IOP reduction of 5-17 percent in normal horses (more in mares than geldings), but with a side-effect profile that largely negated its value. It may potentiate miosis and uveitis, and worsen ocular pain. It still can be useful in selected individuals who respond insufficiently to other therapy. If medications do not control IOP, or athletic competition rules preclude chronic administration, surgical intervention may be highly effective.

Photo 5: Laser cyclophotocoagulation results in a rise in IOP, being reduced by aqueouscentesis. Centesis is not recommended for medical control of glaucoma in horses.

Surgical treatment

Surgical control of glaucoma and IOP may be attempted by reducing aqueous production (partial ciliary ablation) or by increasing outflow (implanting a drainage device). Gonioimplants are performed rarely in horses to date. Controlled ciliary ablation is best attained with a laser, a procedure termed trans-scleral cyclophotocoagulation (TSCPC). Recent work from OSU detailed the equine ciliary body anatomy that permits highly accurate lasering to maximize ablation of fluid-producing cells with minimal peripheral damage. Preferred sites are 4-6mm posterior to the limbus avoiding the nasal quadrants and the ciliary arteries. Immediately post-surgical, the IOP may elevate and require centesis (photo 5, p. 4E), and this may recur for several days because of increased uveitis. IOP begins to drop as inflammation subsides and aqueous-production decreases. The University of Florida retrospectively analyzed 23 eyes of 16 horses treated by Nd:YAG laser. Preoperative IOP was 51 (+17) mmHg, and declined post surgery into the low 20s (+9) until beyond five months. Vision was present in 60 percent of eyes compared to 52 percent at presentation. Achieving stable IOPs <30 mmHg declined from 93 percent at 24 hours to 70 percent at five months.

Diode lasers are now more commonly used, and OSU reported 64 percent of 27 horses retained vision at an average three years, although 90 percent required concurrent medication. Laser TSCPC may be performed under general anesthesia or after sedation and retrobulbar blockade. Morbidity, surgery duration and cost are all reduced as a result, making the procedure conveniently possible as outpatient hospital therapy, with follow-up performed at the barn. Post-operative therapy is aimed at uveitis control and IOP maintenance in the short term, and may be weaned subsequently. Laser TSCPC may need to be repeated periodically in some individuals if the ciliary body regenerates.

Options for glaucoma control in horses


Glaucoma results in corneal opacification, reduced vision and discomfort and is now recognized more commonly than ever. IOP measurement is easier and more accurate with the Tonopen, and therapeutic success is improved with better monitoring. Early medication maintains vision and limits complications from primary inflammation. Control of uveitis may eliminate the need for specific IOP medications. Laser surgery has very good success for individuals with vision and minor complications, and still may restore partial vision in more advanced cases. Laser TSCPC may be performed standing with retrobulbar blockade and typically has a short recovery time of two to three weeks.

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