Introduction

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.

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

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.