NAVLE Special Senses

Canine Glaucoma Study Guide

Glaucoma is defined as a group of optic neuropathies characterized by progressive retinal ganglion cell death and optic nerve degeneration, typically associated with elevated intraocular pressure (IOP).

Overview and Clinical Importance

Glaucoma is defined as a group of optic neuropathies characterized by progressive retinal ganglion cell death and optic nerve degeneration, typically associated with elevated intraocular pressure (IOP). It is one of the leading causes of irreversible blindness in dogs, affecting approximately 0.9% of purebred dogs in North America. Glaucoma is also a major cause of ocular pain and is the most common reason for enucleation in dogs.

Understanding glaucoma pathophysiology, classification, clinical signs, and treatment options is essential for the NAVLE examination. The disease represents a true ophthalmic emergency when presenting acutely, as irreversible vision loss can occur within hours of IOP elevation.

Parameter Normal Range Clinical Significance
Normal IOP (dogs) 15-25 mmHg Decreases with age; varies by breed
Glaucoma threshold Greater than 25-30 mmHg With compatible clinical signs
Emergency IOP Greater than 40-50 mmHg Requires immediate treatment
Asymmetry between eyes Greater than 10 mmHg difference Suspicious for unilateral glaucoma

Aqueous Humor Dynamics and Pathophysiology

Aqueous humor is a transparent fluid produced by the ciliary body epithelium that provides nutrients to the avascular lens and cornea while maintaining IOP and globe shape. Understanding aqueous humor production and drainage is fundamental to understanding glaucoma.

Production and Flow

Aqueous humor is produced by the ciliary processes through active secretion (80%) and ultrafiltration (20%). The fluid flows from the posterior chamber, through the pupil, into the anterior chamber. It circulates in the anterior chamber, supplying the metabolic requirements of the lens and cornea, before draining through the iridocorneal angle (ICA).

Drainage Pathways

  • Conventional (trabecular) outflow: 85% of drainage in dogs. Aqueous flows through the pectinate ligaments, trabecular meshwork, and into the angular aqueous plexus and scleral venous plexus.
  • Unconventional (uveoscleral) outflow: 15% of drainage. Aqueous diffuses through the iris root and ciliary body into the suprachoroidal space.
High-YieldGlaucoma is ALWAYS caused by decreased aqueous outflow, NOT overproduction. The obstruction can occur at the level of the pectinate ligaments, trabecular meshwork, or ciliary cleft.

Normal Intraocular Pressure Parameters

High-Risk Breeds Associated Features
American Cocker Spaniel Highest prevalence (5.5%); PACG with PLD; female predisposition
Basset Hound PACG with PLD; female predisposition (1.7:1)
Siberian Husky, Samoyed PACG; Northern breeds commonly affected
Chow Chow, Shar-Pei PACG; Asian breeds commonly affected
English Springer Spaniel PACG with documented PLD heritability
Beagle Primary open-angle glaucoma (POAG); ADAMTS10 mutation
Boston Terrier PACG with narrow angle morphology

Classification of Canine Glaucoma

Glaucoma is classified based on cause (congenital, primary, or secondary) and iridocorneal angle status (open, narrow, or closed). This classification has important implications for treatment and prognosis.

Congenital Glaucoma

Develops early in life (less than 1 year of age) due to severe abnormalities in iridocorneal angle development. Puppies present with unilateral or bilateral rapidly enlarging globes. The young sclera is highly elastic, accounting for marked buphthalmos. Prognosis for vision is typically poor.

Primary Glaucoma

Occurs without antecedent ocular disease, resulting from inherited anatomical abnormalities of the drainage angle. Primary angle-closure glaucoma (PACG) is the most common form in dogs, comprising approximately 87% of primary glaucoma cases. It is strongly associated with pectinate ligament dysplasia (PLD), a developmental abnormality where sheets of tissue replace the normal thin, widely separated pectinate ligaments.

NAVLE TipPrimary glaucoma is ALWAYS bilateral, but clinical onset is typically asymmetric. When one eye is diagnosed, the contralateral eye is at high risk and requires prophylactic treatment. On average, the second eye develops clinical glaucoma within 8 months.

Breed Predispositions for Primary Glaucoma

Secondary Glaucoma

Results from physical obstruction of aqueous outflow caused by another ocular disease. Secondary glaucoma is 2-3 times more common than primary glaucoma in dogs. May be unilateral or bilateral depending on the underlying cause.

Common Causes of Secondary Glaucoma

High-YieldSecondary glaucoma MAY be curable if the underlying cause is successfully treated (e.g., lens extraction for anterior luxation). However, once trabecular meshwork damage occurs, glaucoma may persist despite treating the primary cause.
Cause Mechanism and Clinical Notes
Anterior Uveitis Most common cause. Inflammatory debris, protein, and cells clog trabecular meshwork. Posterior synechia can cause iris bombe with pupillary block.
Anterior Lens Luxation Lens physically blocks pupil (pupillary block) or ICA. Common in terrier breeds. Miotics CONTRAINDICATED (worsen pupillary block).
Intraocular Neoplasia Tumor cells or associated inflammation obstruct outflow. Melanoma most common primary intraocular tumor in dogs.
Hyphema Blood cells and fibrin obstruct trabecular meshwork. Trauma, coagulopathy, or systemic disease.
Lens-Induced Uveitis (LIU) Associated with hypermature cataracts. Lens protein leakage causes chronic uveitis leading to glaucoma.
Post-Surgical (Phacoemulsification) Inflammation, fibrin, or hemorrhage post-cataract surgery. IOP monitoring critical postoperatively.

Clinical Signs

Clinical signs are classically divided into acute and chronic presentations, though most cases of acute glaucoma are superimposed on underlying chronic changes.

Acute Glaucoma - The Red, Painful Eye

NAVLE TipIf IOP has been greater than 50 mmHg for more than 3 days, the potential for vision recovery is negligible. The dazzle reflex and consensual PLR are critical prognostic indicators - their presence suggests retinal function and potential for vision recovery.

Chronic Glaucoma - End-Stage Disease

High-YieldBuphthalmos is an EXCLUSIVE sign of chronic glaucoma and indicates irreversible blindness. Do NOT confuse with exophthalmos (orbital disease). In buphthalmic eyes, IOP may actually normalize or decrease as the ciliary body becomes atrophic - but the eye remains blind and often painful.
Clinical Sign Description and Pathophysiology
Ocular Pain Blepharospasm, photophobia, behavioral changes (hiding, decreased appetite, lethargy). Dogs may appear nauseous or vomit.
Episcleral Congestion Marked engorgement of episcleral vessels giving "red eye" appearance. Due to impaired drainage of blood from scleral venous plexus.
Diffuse Corneal Edema Bluish-white hazy appearance. IOP greater than 40 mmHg overcomes endothelial pump function. Makes fundic exam difficult.
Mydriasis Fixed, dilated pupil. IOP-induced ischemia causes iris sphincter muscle dysfunction. Sluggish to absent PLR.
Vision Loss Absent menace response, absent dazzle reflex. May be reversible if treated promptly within hours.
Elevated Third Eyelid Often prominent due to pain and globe enlargement.

Diagnosis

Tonometry

Measurement of IOP is ESSENTIAL for diagnosis. All patients presenting with a red, painful eye should have tonometry performed. The two primary methods used in veterinary practice are:

  • Applanation tonometry (Tono-Pen): Measures pressure required to flatten corneal surface. Requires topical anesthesia. Accurate when used correctly with perpendicular, light contact.
  • Rebound tonometry (TonoVet): Measures probe rebound characteristics. Does NOT require topical anesthesia. Probe must be held horizontally. Equally accurate and increasingly popular.
NAVLE TipSources of falsely elevated IOP: pressure on neck or jugular vein, pressure on eyelids, excited patient, head below heart level. ALWAYS compare both eyes and use proper technique.

Gonioscopy

Visualization of the iridocorneal angle using a special goniolens placed on the cornea. Essential for:

  • Classifying angle status (open, narrow, closed)
  • Identifying pectinate ligament dysplasia (PLD)
  • Assessing the contralateral eye of patients with unilateral glaucoma
  • Screening at-risk breeds
Clinical Sign Description
Buphthalmos Globe enlargement from stretching of sclera and cornea. Indicates chronic, irreversible disease and permanent blindness.
Haab's Striae Linear breaks in Descemet's membrane appearing as white/gray lines in cornea. PATHOGNOMONIC for glaucoma.
Secondary Lens Luxation Zonular breakdown from stretching. Must differentiate from PRIMARY lens luxation causing secondary glaucoma.
Optic Nerve Atrophy/Cupping Atrophied, cupped optic disc. Retinal ganglion cell death and axonal loss.
Retinal Degeneration Tapetal hyperreflectivity, vascular attenuation from chronic ischemia.
Exposure Keratitis Lagophthalmos from enlarged globe leads to corneal ulceration and scarring.

Treatment

Treatment goals depend on whether vision is salvageable:

  • Visual eye: Rapidly reduce IOP to preserve or restore vision
  • Blind eye: Control pain and provide comfort (surgery of comfort)

Emergency Medical Treatment

NAVLE TipALWAYS check for anterior lens luxation BEFORE giving latanoprost! The intense miosis caused by prostaglandin analogs can trap an anteriorly luxated lens and worsen pupillary block, increasing IOP further.

Maintenance Medical Therapy

High-YieldProphylactic treatment of the normotensive contralateral eye in dogs with primary glaucoma delays onset of clinical disease from 8 months to 31 months. Use timolol 0.5% or betaxolol 0.5% q12-24h plus topical anti-inflammatory.

Surgical Treatment

Surgery is indicated when medical therapy fails or when IOP remains greater than 25 mmHg despite maximum medical management. Surgical options depend on whether vision is present.

Vision-Sparing Procedures

Surgeries of Comfort (Blind, Painful Eyes)

  • Enucleation: Removal of the globe. Most definitive procedure. Submit for histopathology (rule out neoplasia).
  • Evisceration with intrascleral prosthesis: Cosmetic alternative. Remove intraocular contents and place silicone sphere within scleral shell.
  • Intravitreal gentamicin injection: Chemical ablation of ciliary body (25 mg gentamicin + 1 mg dexamethasone). Requires only sedation. NOT recommended for cats (risk of malignant ocular tumors).
Drug Dose/Route Mechanism Key Notes
Mannitol 20% 1-2 g/kg IV over 30-45 min Osmotic diuretic; dehydrates vitreous Effect in 30-60 min, lasts 6-10 hrs. Withhold water 4 hrs. AVOID in CHF, renal failure, diabetes.
Latanoprost 0.005% 1 drop topically Prostaglandin analog; increases uveoscleral outflow 45% IOP reduction in 20 min. Causes miosis. CONTRAINDICATED with anterior lens luxation!
Dorzolamide 2% 1 drop q8-12h topically Carbonic anhydrase inhibitor; decreases AH production Safe in all glaucoma types. May cause transient stinging.

Prognosis

Prognosis depends on the type of glaucoma, timing of diagnosis, and response to treatment:

  • Primary glaucoma: Guarded to poor. Disease is bilateral and progressive. Most dogs eventually become blind despite treatment.
  • Secondary glaucoma: Variable. May be curable if underlying cause is treatable (e.g., lens extraction for anterior luxation).
  • Acute glaucoma treated within 24-48 hours: Better prognosis for vision recovery.
  • Chronic glaucoma with buphthalmos: Vision permanently lost. Treatment focused on comfort.
Drug Class Examples Mechanism Clinical Notes
Prostaglandin Analogs Latanoprost, travoprost, bimatoprost Increase uveoscleral outflow via remodeling of ciliary body Most effective in dogs. BID dosing. Avoid in uveitis/lens luxation. Ineffective in cats.
Topical CAIs Dorzolamide, brinzolamide Inhibit carbonic anhydrase; decrease AH production TID dosing. Safe in all glaucoma types. Effective in dogs and cats.
Beta-Blockers Timolol 0.5%, betaxolol Reduce blood flow to ciliary body; decrease AH production Modest effect alone. Used for prophylaxis. Caution: bradycardia in small dogs/cats.
Combination Products Cosopt (dorzolamide/timolol) Combined mechanism More effective than either alone. BID dosing. Available as generic.
Systemic CAIs Methazolamide 2-4 mg/kg PO q8-12h Systemic inhibition of AH production Side effects: panting, GI upset, hypokalemia. Use when topical therapy fails.
Procedure Description and Outcomes
Endoscopic Cyclophotocoagulation (ECP) Diode laser destroys ciliary processes under direct visualization. IOP controlled in 90% at 1 year, vision maintained in 63% at 1 year. Safer than TSCP due to direct visualization.
Transscleral Cyclophotocoagulation (TSCP) Diode laser applied transclerally to destroy ciliary body. IOP controlled in 67% at 1 year, vision in 53%. Higher complication rate than ECP.
Ahmed Valve Gonioimplant Shunt diverts aqueous from anterior chamber to subconjunctival space. 89% visual success at 1 year. Eventually fails due to scar tissue formation.
Combined TSCP + Gonioimplant Reduces AH production AND improves outflow. Better long-term IOP control than either alone.

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