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.
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.
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