The glaucomas are generally related to reduced outflow of aqueous humor through the trabecular meshwork of the anterior chamber or iridocorneal angle (conventional outflow, about 85%), and through the uveoscleral network (through the ciliary body and subscleral space, about 15%). Excessive production of aqueous humor in people appears to be rare as a cause of glaucoma and has not been reported in animals. Changes in the composition of aqueous humor have been reported recently in human and animal glaucomas and appear important in the disease genesis and progression.
The glaucomas represent a group of diseases characterized by increased intraocular pressure with resultant retinal and optic disk destruction. Low-tension glaucoma, characterized in people by normal levels of intraocular pressure and progressive optic disk damage, has not been documented in domestic animals. In dogs, the primary (inherited) and secondary glaucomas occur in ~1.7% of the canine population in North America. The frequency of bilateral primary breed-predisposed glaucomas in purebred dogs is the highest of any animal species, except people (0.9%). In cats, the glaucomas are predominately secondary to anterior uveitis and neoplasms; however, primary open-angle glaucoma occurs in the Siamese breed. In horses, the glaucomas appear underdiagnosed because applanation tonometry is not routinely done; they appear most frequently in older animals, Appaloosas, and with concurrent anterior uveitis. In cattle, the glaucomas have been associated with congenital iridocorneal anomalies and anterior uveitis.
Diagnostic procedures essential to manage the glaucomas include tonometry, ophthalmoscopy (direct and indirect), and gonioscopy (visualization of the iridocorneal angle and anterior ciliary cleft). Newer electrophysiologic techniques, such as pattern electroretinograms and visual evoked potentials, estimate damage to the retinal ganglion cells and their axons, and appear to be sensitive indicators of glaucoma-related destruction of these cells. New clinical high-resolution imaging techniques, including ultrasound biomicroscopy for anterior segment changes and optical coherence tomography for retinal and optic nerve head changes, permit noninvasive detailed intraocular examinations. In small animals, the Schiotz indentation tonometer has been replaced by newer and more accurate applanation tonometers used to estimate intraocular pressure; in horses and cattle, only applanation-type tonometers can be used.
Intraocular pressure is reasonably consistent in most species (see Ophthalmology: Intraocular Pressure (IOP) by Applanation Tonometry), and diurnal variations have been documented in dogs, cats, rabbits, and non-human primates. Ophthalmoscopy permits detection of the intraocular pressure-related damage to the retina and optic disk. Gonioscopy is the basis for classification of all glaucomas; it detects iridocorneal and sclerociliary cleft opening outflow changes as the glaucoma progresses and helps determine the most appropriate medical and surgical treatments. Ultrasound biomicroscopy (50–100 MHz) permits further examination of the anterior chamber angle and the entire sclerociliary cleft.
Clinical signs are traditionally divided into acute and chronic; in reality, most cases of acute glaucoma are superimposed on chronic glaucoma rather than occurring as singular events. Most dogs with early to moderate chronic glaucoma are not taken to the veterinarian because the early clinical signs—sluggish to slightly dilated pupils, mild bulbar conjunctival venous congestion, and early enlargement of the eye (buphthalmia or megaloglobus)—are so subtle. To detect early glaucoma, tonometry should be routinely performed on high-risk breeds of dogs as part of the annual general physical examination. The clinical signs of acute and often markedly increased levels of intraocular pressure are a dilated, fixed, or sluggish pupil; bulbar conjunctival venous congestion; corneal edema; and a firm globe. With prolonged increases of intraocular pressure, secondary enlargement of the globe, lens displacement, and breaks in Descemet's membrane (corneal striae) result. Pain usually is manifest by behavioral changes and occasional periorbital pain, rather than by blepharospasm.
Classification of the glaucomas assists in the optimal plan for clinical management and preservation of vision. The choice of medical or surgical treatment, or most frequently a combination of both, is based on the progressive iridocorneal angle closure that occurs in most of the glaucomas. For open-angle glaucoma in dogs, short- and longterm management is by treatment with miotics, topical and systemic carbonic anhydrase inhibitors, prostaglandins, osmotics, and β-blocking adrenergics. These same treatments are used for initial control of narrow and closed-angle glaucoma, but short- and longterm management often requires supplemental surgery, eg, filtering procedures, anterior chamber shunts, cyclocryotherapy, or laser transscleral cyclophotocoagulation. Short- and longterm management of end-stage glaucoma with buphthalmia and blindness in dogs also requires surgery, eg, intrascleral prosthesis, enucleation, cyclocryothermy, or intravitreal gentamycin (10–25 mg) combined with 1 mg dexamethasone. Surgical procedures in dogs have traditionally provided only short-term resolution because the filtering fistulas eventually scar over and fail. More recently, anterior chamber shunts, with and without valves, offer improved results. Antifibrotic drugs, such as mitomycin C and 5-fluorouracil, may delay or prevent scarring of the alternate aqueous outflow channels and prolong their function. In cats, medical therapy is usually the mainstay and consists of topical β-blocking adrenergics (caution in small cats), topical carbonic anhydrase inhibitors, and for those glaucomas associated with anterior uveitis, topical and/or systemic corticosteroids. In horses, single and/or repeated laser transscleral cyclophotocoagulation is most effective.
Last full review/revision July 2011 by Kirk N. Gelatt, VMD