Equine Glaucoma (Secondary to Uveitis) – NAVLE Study Guide

Overview and Clinical Importance

Glaucoma is a multifactorial neurodegenerative ocular disease characterized by elevated intraocular pressure (IOP) that leads to progressive loss of retinal ganglion cells and optic nerve damage, ultimately resulting in blindness. In horses, glaucoma is most commonly secondary to equine recurrent uveitis (ERU), making it a critical sequela to recognize and manage. The prevalence of equine glaucoma is reported between 0.07% and 0.5%, though it is likely underdiagnosed because clinical signs are often subtle and easily confused with ongoing uveitis.

Understanding the pathophysiology, clinical presentation, and management of glaucoma secondary to uveitis is essential for the NAVLE, as horses with ERU represent a significant proportion of equine ophthalmology cases encountered in general practice.

Anatomy and Physiology of Aqueous Humor Dynamics

Aqueous humor is produced by the ciliary body epithelium through both active secretion (involving carbonic anhydrase and Na+/K+ ATPase) and passive ultrafiltration. This clear fluid provides nutrients to the avascular lens and cornea while removing metabolic waste products.

Aqueous humor outflow in horses occurs through two pathways:

• Conventional pathway: Through the iridocorneal angle (trabecular meshwork)
• Uveoscleral (unconventional) pathway: Through the iris vasculature, ciliary body, and supraciliary space

Key species difference: Horses have a significantly greater percentage of aqueous humor drainage through the uveoscleral pathway compared to dogs and humans. This may explain why severe glaucoma is relatively less common in horses despite the high prevalence of ERU and extensive anterior segment damage.

Etiology and Classification

Classification of Equine Glaucoma

Pathophysiology of Secondary Glaucoma

In horses with ERU, chronic or recurrent inflammation causes structural damage to aqueous outflow pathways through several mechanisms:

• Pre-iridal fibrovascular membrane formation: Obstructs the iridocorneal angle
• Posterior synechiae: Adhesions between iris and lens cause pupillary block
• Peripheral anterior synechiae: Adhesions closing the drainage angle
• Inflammatory debris accumulation: Cells, fibrin, and protein clog trabecular meshwork
• Descemetization of pectinate ligaments: Found in 83% of histopathologic cases

Breed Predisposition and Risk Factors

Clinical Signs and Presentation

Key concept: Clinical signs of equine glaucoma are often more subtle than in other species, and horses can maintain vision despite significantly elevated IOP for longer periods than dogs or humans. This makes early detection challenging but critical.

Clinical Signs by Disease Stage

Haab's Striae (Corneal Striae)

Haab's striae are linear, branching opacities in the deep cornea that represent breaks or ruptures in Descemet's membrane caused by elevated IOP and globe stretching. They often extend from limbus to limbus and are found in approximately 70% of histopathologic cases. Note that similar linear opacities can occur in normal horses ('band keratopathy') and may not be pathognomonic for glaucoma.

Signs Specific to Secondary Glaucoma from ERU

When glaucoma develops secondary to ERU, additional signs of chronic uveitis will be present: posterior synechiae (adhesions between iris and lens), iris hyperpigmentation or depigmentation, aqueous flare, cataracts (often posterior cortical), vitritis, and potentially lens subluxation or luxation. The pupil is frequently miotic (constricted) due to synechiae rather than dilated as seen in primary glaucoma of other species.

Diagnosis

Tonometry - The Gold Standard

Measurement of intraocular pressure (IOP) is essential for diagnosing glaucoma. Prior to the 1980s, equine glaucoma was considered rare because tonometers were not readily available for horses.

Tonometry Technique in Horses

• Perform auriculopalpebral nerve block: MANDATORY before tonometry to prevent artificially elevated readings from eyelid tension
• Apply topical anesthesia: 0.5% proparacaine for applanation tonometry
• Use appropriate tonometer: Applanation (TonoPen) or rebound (TonoVet) tonometers are suitable for horses
• Head position: Keep head at normal elevation; IOP increases significantly when head is below heart level
• Sedation considerations: IV xylazine and detomidine significantly LOWER IOP; account for this effect when interpreting results

Complete Ophthalmic Examination

A thorough examination should include:

• Neuro-ophthalmic examination: Menace response, pupillary light reflexes (direct and consensual), dazzle reflex
• Schirmer tear test: Rule out concurrent keratoconjunctivitis sicca
• Biomicroscopy (slit lamp): Evaluate cornea (edema, striae), anterior chamber (depth, flare), iris (synechiae), lens (cataract, position)
• Indirect ophthalmoscopy: After mydriasis with tropicamide; evaluate optic nerve (pallor, cupping), retina
• Gonioscopy: Visualize iridocorneal angle to assess drainage pathway patency
• Ocular ultrasonography: Useful when media opacity prevents fundic examination; can measure globe size, detect lens luxation, retinal detachment

Treatment

Treatment goals are to: (1) reduce IOP to levels compatible with optic nerve and retinal health (less than 20-25 mmHg), (2) control underlying inflammation, (3) maintain comfort, and (4) preserve vision when possible.

Medical Management

Atropine Use - Controversial

In most species, atropine is contraindicated in glaucoma because mydriasis can worsen angle closure. However, in horses, atropine may actually lower IOP in some cases due to the unique aqueous humor dynamics. Use cautiously on a case-by-case basis when tonometry is consistently available and uveitis is the underlying cause.

Surgical Treatment

Prognosis

The prognosis for maintaining vision in equine glaucoma is guarded to poor, even with aggressive treatment. Key prognostic factors include:

• Type of glaucoma: Congenital (poor), secondary to ERU (guarded), primary (better if caught early)
• Vision status at presentation: 52% visual at presentation; 60% visual at 20+ weeks post-TSCP (not significantly different)
• Breed: Appaloosas have a particularly aggressive form poorly responsive to therapy
• Early detection: Horses can maintain vision longer than dogs with similar IOP elevations
• Ongoing medical therapy: 100% of horses require continued topical medication even after TSCP

Memory Aids

Mnemonic: "GLAUCOMA" - Risk Factors in Horses

• G - Globe trauma history
• L - Lens luxation
• A - Appaloosa breed (8x risk!)
• U - Uveitis (ERU) - most common cause
• C - Chronic inflammation
• O - Older horses (greater than 15 years)
• M - Melanoma (intraocular neoplasia)
• A - Angle closure from synechiae

Remember: "Cosopt is TOP choice"

Cosopt (dorzolamide/timolol combination) is the TOP medical choice for equine glaucoma. Prostaglandins are NOT effective in horses!