Outline

1.  Aqueous humor dynamics

2.  General glaucoma information

3.  Glaucoma classification

a.  Congenital

b.  Primary

c.  Secondary

4.  Clinical signs

5.  Diagnosis

6.  Treatment

1) Aqueous Humor Dynamics

Aqueous humor is produced by the ciliary body processes through active secretion, passive diffusion, dialysis, and ultrafiltration. Aqueous humor flows from the ciliary body processes into the posterior chamber, through the pupil, and into the anterior chamber. From the anterior chamber, aqueous humor exits the globe via two mechanisms: conventional and unconventional (i.e., uveoscleral) outflow.

Conventional outflow is through the iridocorneal angle to the scleral venous plexus. Uveoscleral outflow is across the ciliary body and iris to the suprachoroidal space and out the posterior choroidal circulation. In small animals, conventional outflow is the primary mechanism by which aqueous humor exits the globe. The iridocorneal angle is bordered by the peripheral cornea, anterior sclera, iris base, and anterior ciliary body. In small animals, aqueous humor flows through the pectinate ligament to enter the iridocorneal angle.

Aqueous humor production and outflow must remain in constant equilibrium. Glaucoma occurs when outflow of aqueous humor is obstructed and intraocular pressure (IOP) increases. Hypersecretory glaucoma (i.e., increased aqueous production with a normal drainage apparatus) is not known to occur in animals.

2) General Glaucoma Information

Glaucoma is a collection of ocular diseases and not a single entity. Most correctly, glaucoma is a group of diseases that lead to progressive optic nerve damage. In many cases, but not all, the optic nerve damage is mediated by (or associated with) an increased IOP. For practical clinical purposes in small animals, glaucoma is often defined as an IOP elevation beyond what is compatible with the health of ocular tissues. Elevated IOP leads to retinal ganglion cell and optic nerve damage by a multifactorial and poorly understood process, which includes: impaired axoplasmic flow, neurotropin deprivation, reduced blood flow/ischemia, biomechanical axonal stress, and excitotoxins.

3) Glaucoma Classification

Glaucoma can be classified into three major clinical groups: 1) congenital, 2) primary, and 3) secondary.

Congenital glaucoma occurs early in life and is the result of marked developmental anterior segment abnormalities affecting the aqueous humor outflow pathway and obstructing flow. In many cases, the outflow pathway fails to fully develop. It may be unilateral or bilateral. Congenital glaucoma is rare in small animals, is usually associated with a poor response to treatment, and rapidly leads to the development of buphthalmos.

Primary glaucoma is an inherited disease with a strong potential to be bilateral. The IOP increase occurs in the absence of antecedent disease. Primary glaucoma is the most common type of glaucoma in the dog and affects numerous breeds. The age of onset is generally between 4–10 years. Primary glaucoma results from a variety of poorly understood abnormalities that block aqueous outflow from the eye. This flow blockage might occur at the pupil, iridocorneal angle, or ciliary cleft. Primary glaucoma occurs infrequently in the cat.

Secondary glaucoma results from various insults to the ocular aqueous humor outflow mechanism. The most common etiologies of secondary glaucoma are: 1) chronic or severe uveitis; 2) intraocular hemorrhage; 3) intraocular neoplasia; and 4) lens luxation. Secondary glaucoma is not necessarily inherited or bilateral. Primary lens luxation is an exception; however, elevated IOP still occurs as a secondary event with lens luxation. Secondary glaucoma is the most common type of glaucoma in the cat and also occurs frequently in dogs.

4) Clinical Signs

The clinical signs associated with glaucoma depend on the stage of disease, level and duration of IOP elevation, and the type of glaucoma. In general, the clinical signs of glaucoma can be divided into acute and chronic signs with some overlap.

Clinical signs observed with acute glaucoma include blepharospasm, decreased activity level/appetite, epiphora, conjunctival hyperemia, episcleral vessel congestion, corneal edema, mydriasis, optic nerve head swelling, retinal edema, and reduced vision. Clinical signs that may also be seen with chronic glaucoma include buphthalmos, corneal striae, keratitis, corneal degeneration, scleral staphyloma, lens subluxation, cataract, retinal degeneration, optic nerve head cupping/atrophy, and blindness.

5) Diagnosis

The diagnosis of glaucoma in small animals is based upon the presence of compatible clinical signs and measurement of elevated IOP by tonometry. There are several types of tonometers used in veterinary medicine. Digital tonometry is generally not recommended as it is inaccurate, poorly reproducible, and qualitative only. Schiötz tonometers (an indentation tonometer) are inexpensive and relatively simple to operate; however, they can be difficult to use with uncooperative patients, require conversion charts, may damage the cornea, and are inaccurate/unreliable with low IOP or corneal disease. The TonoPen (an applanation tonometer) and TonoVet (a rebound tonometer) are precise, reliable, safe, and easy to use; however, they are relatively expensive to purchase.

Gonioscopy is an adjunct diagnostic technique that allows examination of the iridocorneal angle and ciliary cleft by application of a special viewing lens (goniolens) to the corneal surface. Glaucoma can then be classified based upon the anatomy of the filtration angle as open, narrow, closed, or goniodysgenesis. Gonioscopy may help distinguish primary and secondary glaucoma and be useful for determining prognosis; however, prognosis is highly variable between animals and gonioscopy is poorly predictive of future glaucoma development.

6) Treatment

When formulating a treatment strategy for glaucoma, one must determine what caused the glaucoma (i.e., primary or secondary) and if the eye is irreparably blind. If the cause is anything other than primary glaucoma, then treatment for the inciting condition must be undertaken concurrently with the glaucoma therapy. If the visual potential of the eye is unknown, the eye should be treated aggressively and then re-evaluated.

A variety of medical and surgical options are available to reduce IOP in animals with glaucoma. All glaucoma treatments work by one of 2 basic mechanisms: increase aqueous humor outflow or decrease aqueous humor production. There are 5 classes of drugs commonly or historically used for glaucoma therapy in small animals: cholinergics, adrenergics, osmotics, carbonic anhydrase inhibitors (CAIs), and prostaglandins. These medications are often used in combination.

Cholinergics include direct and indirect parasympathomimetic drugs. Adrenergics include β-blockers and α-agonists. These medications decrease aqueous humor production and/or increase outflow. They have weak IOP-lowering effects and should not be used alone to treat glaucoma. Cholinergics are contraindicated with most types of secondary glaucoma.

Osmotics (e.g., intravenous mannitol and oral glycerin) decrease vitreous volume and, to a lesser extent, reduce aqueous humor production. They have potent IOP-lowering effects, but are short acting and potentially toxic. They are contraindicated with dehydration, renal disease, and cardiac disease. Glycerin is contraindicated with diabetes mellitus. Use of osmotics is restricted to short-term emergency management of acute glaucoma.

Carbonic anhydrase inhibitors (CAIs) decrease aqueous humor production. Topical and systemic formulations are available. These medications have potent IOP-lowering effects and are relatively safe for long-term use. The topical CAIs are among the most common drugs used to manage glaucoma in small animals, are well tolerated, can be used for both primary and secondary glaucoma, and are effective across species. In most cases, systemic CAIs offer no advantages over the topicals and are associated with the potential for systemic toxicity.

Prostaglandins increase uveoscleral outflow and possibly decrease aqueous production. They are the most potent antiglaucoma drugs available for dogs and have largely replaced osmotics for emergency management of acute canine glaucoma. They are also used for long-term management of primary glaucoma in dogs. Prostaglandins have little effect on IOP in cats. Prostaglandins may cause extreme miosis and exacerbate uveitis, and are generally contraindicated for secondary glaucoma.

In all cases of primary glaucoma, the contralateral eye should be medically treated "prophylactically" to delay the onset of elevated IOP. Contraindicated treatments for glaucoma include anterior chamber paracentesis and mydriatics.

Surgical treatments for glaucoma either increase aqueous outflow (gonioimplants) or decrease aqueous production (cyclodestruction procedures). Multiple procedures can be combined and these are generally reserved for visual or potentially visual eyes. Gonioimplants involve insertion of a tube into the anterior chamber to allow aqueous to exit the eye via an alternative route. Cyclodestructive procedures involve the partial surgical destruction of the ciliary body epithelium, with a laser or cryotherapy, to decrease aqueous production.

End-stage glaucoma remains a painful condition and should not be ignored. The 3 primary options for permanently blind glaucoma eyes are enucleation, evisceration with intrascleral prosthesis, and chemical cycloablation. Enucleation is the procedure of choice for most cases of secondary glaucoma. Evisceration with intrascleral prosthesis and chemical cycloablation are more cosmetic options for primary glaucoma, but are associated with greater frequency of complications.