Glaucoma in Dogs and Cats: Recognizing the Signs and Determining the Cause
World Small Animal Veterinary Association World Congress Proceedings, 2011
Gillian J. McLellan, BVMS, PhD, DVOphthal, DECVO, DACVO, MRCVS
School of Medicine & Public Health and School of Veterinary Medicine, University of Wisconsin - Madison, Madison, WI, USA


Glaucoma is not a single disease entity. "The glaucomas" represent a large, diverse group of disorders, unified in a final common pathway of characteristic optic nerve and retinal damage that results in loss of vision. The single most important risk factor for the development of glaucoma in animals is elevated intraocular pressure (IOP). Normal IOP is dependent on the equilibrium between production of aqueous humor by the ciliary body processes, and its unimpeded drainage. Outflow of aqueous proceeds through the pupil from the posterior to anterior chamber of the eye, and subsequently to the trabecular meshwork located within the irido-corneal angle and ciliary cleft, thence to collector channels in the episclera and sclera which are continuous with the episcleral and scleral vasculature. Perturbation of this normal route for aqueous outflow results in elevated IOP and glaucomatous damage.

Early recognition and prompt, appropriate therapy, are essential if vision is to be retained, as damage sustained by the optic nerve and retina rapidly becomes irreversible.

Recognizing the Signs

Clinical Signs

Clinical signs of glaucoma (outlined in Table 1) will vary depending on the speed of onset, duration and degree of IOP elevation, and age of the animal (the sclera of young animals is more compliant and distensible, so globe enlargement can be dramatic). Clinical signs in individual animals will also vary according to the underlying cause (e.g., signs of uveitis or an intraocular mass).

Ancillary Diagnostics

 Tonometry: Clinicians should be familiar with the normal range of IOP for the tonometer type available to them. Caution should be exercised in diagnosing glaucoma based solely on a single, elevated IOP reading. Elevated IOP in the absence of clinical evidence of glaucomatous optic nerve and retinal damage is termed "ocular hypertension", to distinguish it from overt glaucoma. IOP is influenced by age, positioning and manual restraint of the patient and breed of dog. Conversely, IOP may be normal, or even low, in animals with glaucoma, particularly in patients with chronic glaucoma, or animals with concurrent uveitis.

 Gonioscopy: This technique allows evaluation of the opening of the ciliary cleft and anterior-most portion of the trabecular meshwork. A contact lens applied to the corneal surface allows visualization of the pectinate ligament using focal illumination and magnification.

 High Resolution Ultrasonography: of the ciliary cleft.

Where's the Block?

When selecting a treatment strategy, it is important to determine the underlying mechanism of IOP elevation. As all cases of glaucoma in dogs and cats are caused by obstruction of aqueous humor outflow, determining the location of this obstruction should be a goal of the clinical examination. Note that aqueous outflow is often obstructed at multiple locations in individual patients The mechanisms proposed (Table 2) should not be considered mutually exclusive.

Table 1. Clinical signs of glaucoma in dogs.



- May be severe (squinting, tearing, rubbing, lethargy, inappetence)

Signs of Discomfort
- Variable
- Less frequent in cats

Episcleral Injection
- Often accompanied by conjunctival injection

Episcleral Injection
- May also see scleral thinning / staphyloma

Corneal Vascularization
- Deep 360° limbal "brush border"

Corneal Vascularization
- May be exposure keratitis, with ulceration, branching vascularization and pigment

Corneal Edema

Corneal Edema & Striae


Lens Subluxation
- Aphakic crescent
- Differentiate from primary lens luxation

Optic Disc Changes
- May be "cupped" or more often swollen in acute cases

Optic Disc Cupping & Atrophy

Loss of Vision
- Absent direct & consensual pupillary light reflex
- Absent menace response
- Absent dazzle reflex

Loss of Vision
- Usually complete, irreversible, with mydriasis


Buphthalmos or Phthisis Bulbi
- Enlarged, or end stage, shrunken globe

Table 2. Potential locations of obstruction to aqueous humor outflow.

Block at the ciliary body/ Posterior chamber/ Vitreous

"Crowding" of posterior chamber by:
- Intraocular neoplasia
- Cilio-vitreo-lenticular block (condensed anterior vitreous)
- Iridociliary cysts

Vitreous expanded or pushed forward ( "malignant" glaucoma):
- Posterior misdirection of aqueous
- Choroidal effusion

Pupil block

Obstruction to flow of aqueous through pupil by:
- Posterior synechiae / iris bombé (absolute block)
- Lens within pupil / lens and iris anatomically apposed (relative block) : posterior misdirection of aqueous, lens luxation/ subluxation, intumescent lens (phacomorphic), spherophakia
- Vitreous within pupil

Block at the level of the irido-corneal angle

Primary angle-closure
- Narrow-angle glaucoma
- Pectinate ligament dysplasia

Secondary angle closure
- Due to anterior "pull" by peripheral anterior synechiae or pre-iridal fibrovascular membrane
- Due to posterior "push" (e.g., by posteriorly misdirected aqueous humor or mass effect in the posterior chamber)

Trabecular meshwork obstructions

Primary malformation of the ciliary cleft
- Primary congenital glaucoma

Secondary to obstruction of a conformationally "open angle" by
- Inflammatory cells
- Neoplastic cells
- Pre-iridal fibrovascular membrane (iris neovasc.)
- Erythrocytes (both intact and "ghost cells")
- Vitreous
- Proteins including fibrin (uveitis) or globulin (hyperviscosity syndrome)

Post-trabecular block / Increased episcleral and/or scleral venous pressure

Inappropriate restraint
- e.g., tight neck collars or a stress response

Feline primary open-angle glaucoma
- Myxomatous change around vessels of outflow pathway

Orbital space occupying lesions
- Increasing episcleral venous pressure

Infiltration of the episclera and / or sclera
- Inflammatory
- Neoplastic

Adapted from: McLellan GJ, Miller PE. Feline glaucoma: a comprehensive review. Veterinary Ophthalmology (in press) 2011.

In summary, glaucoma may be considered either primary (occurring in the absence of other underlying ocular disease; and relatively common in purebred dogs) or secondary (most commonly associated with uveitis or intraocular tumors, particularly in cats, or with lens disease). However, this classification scheme is perhaps too simplistic. It is more important, when selecting treatment for glaucoma, that different mechanisms of aqueous humor outflow obstruction are identified and addressed.


Speaker Information
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Gillian J. McLellan, BVMS, PhD, DVOphthal, DECVO, DACVO, MRCVS
School of Medicine & Public Health and School of Veterinary Medicine
University of Wisconsin-Madison
Madison, WI, USA