by Noelle La Croix, DVM, Dip. ACVO
Canine (not human) Glaucoma
It can be very difficult for clients to understand their dog’s loss of vision when caused by glaucoma. Clients tend to associate ‘glaucoma’ with the disease of their affected parents or grandparents. Glaucomatous humans typically receive medications and regular ocular pressure checks, but do not usually develop complete blindness. However, canine glaucoma is quite different than human glaucoma.
Glaucoma is the progressive dysfunction and death of retinal ganglia. A retinal ganglion is a nerve cell that receives visual information from the retina which it transfers through the optic nerve to the midbrain. Retinal ganglia can be killed by increases in ocular pressure. The mechanism by which this occurs remains unclear. Cell death may result from restricted axoplasmic flow, from physical pressure, or via secondary ischemia. There are also toxic factors (e.g., glutamate) released during pressure spikes that can contribute to retinal ganglia death. Once a retinal ganglion cell has died it cannot normally be regenerated.
The main risk factor for retinal ganglion cell death is elevated intraocular pressure (IOP). To understand an increase in canine IOP, one must first understand the role of aqueous humor. The aqueous humor supplies nutrition and oxygen to the avascular tissues of the eye (lens, anterior vitreous, posterior cornea, and trabecular meshwork). This fluid is secreted by the ciliary body, flows between the lens and iris, and then travels through the pupil into the anterior chamber (Figure 1). The fluid is drained from the eye by two pathways described as conventional (trabecular) and non-conventional (uveoscleral) outflow. In conventional outflow, aqueous humor flows through the trabecular meshwork, angular aqueous plexus, and intrascleral plexus before exiting through episcleral veins. The majority of canine aqueous humor outflow is conventional. In non-conventional outflow the fluid flows through ciliary muscle bundles and the supraciliary and suprachoroidal spaces, before draining through the sclera.
Glaucoma can be a primary (inherited) defect or the result of secondary factors including intraocular hemorrhage, lens displacement, uveitis, intraocular cancer, intumescent cataract formation, and complications following intraocular surgery.
Primary glaucomas are typically described as either “open angle” or “closed angle.” The majority of human glaucomas are open angle. In open angle glaucoma the opening to the trabecular meshwork, or drainage angle, is open to the flow of aqueous humor. However, the flow through the meshwork is compromised by an accumulation of debris, a loss of trabecular endothelia, a decrease in meshwork pore size, or changes in trabecular vacuoles. To simplify, the opening of the trabecular meshwork is similar to a drain, whereas the meshwork itself is piping leading away from the drain. In open angle glaucoma the drain is open but the plumming is clogged. Therefore, open angle glaucoma typically progresses gradually, without significant pain, as the drain slowly clogs. With gradual increases in IOP, pressure-induced ischemia of the optic nerve can often be prevented by autoregulatory vasodilation. These common human glaucomas do not generally lead to a complete loss of vision.
Unfortunately, most canine primary glaucomas are classified as closed angle. In closed angle glaucoma the iris is positioned so that access to the opening (drainage angle) of the trabecular meshwork is severely restricted. In our plumbing analogy, the drain itself is malformed and has smaller drainage holes. Certain dog breeds (e.g., American Cocker Spaniel, Bassett Hound, Chow Chow, English Cocker Spaniel, and Siberian Husky) are associated with goniodysgenesis or pectinate ligament dysgenesis that decreases the size of the drain. However, the malformation of the drainage angle is not the only factor predisposing a dog to developing closed angle glaucoma.
Breeds with goniodysgenesis do not usually develop glaucoma when they are very young. The first incidence of glaucoma is typically between 5 and 6 years of age. In the young dog, the anterior chamber can compensate for iris dilation without angle closure. However, intraocular lenses increase in size and volume with age. Larger lenses cause the iris to bow forward decreasing anterior chamber depth. A small anterior chamber repositions the iris so that its movement during dilation blocks the drainage angle. This can lead to an acute entrapment of aqueous fluid behind the iris increasing IOP rapidly (Figure 2). This pressure increase is extremely painful and death of retinal ganglia quickly follows (there is little time for autoregulation to protect the retina). In this way, the common canine closed angle glaucoma is often blinding.
Most primary canine glaucomas are closed angle and associated with an acute loss of vision. In contrast, most human glaucomas are open angle and not associated with acute drastic changes in vision. Hopefully this article will help you explain to your clients why their dog’s glaucoma is so different from that of their human relatives. In the dog, acute glaucoma should always be treated as an emergency to minimize damage to the retina. If you have any questions about canine glaucoma, please feel free to ask your veterinary ophthalmologist.
Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006
Figure 1: The normal canine lens (L), iris (I), cornea (C), anterior chamber (A), posterior chamber (P), and drainage angle (D) (diagram courtesy of Paul Miller, DVM, Dip. ACVO).
Figure 2: Canine angle closure glaucoma. The iris prevents fluid from moving past the pupil (1) causing closure of the drainage angle (2) (diagram courtesy Paul Miller, DVM, Dip. ACVO).