Glaucoma is an optic neuropathology. The disease leads to the death of neurons - the retinal ganglion cells (RGC) and their axons. In humans, this disease can be presented without an elevation in intraocular pressure, but with progressive optic neuropathy. Eventually, elevation of intraocular pressure will persist. This normal tension glaucoma has not been documented in animals. Therefore, in humans, elevation of intraocular pressure is only one factor leading to blindness. In animals, however, elevation of intraocular pressure is the primary risk factor for blindness.
In eyes, the fluid known as the aqueous humour is produced at a constant rate by the epithelium of the ciliary body at the posterior chamber of the eye. The aqueous humour circulates via the pupillary opening and through the filtration angle draining into the vascular plexus of the choroid. The filtration angle is a sieve-like network located between the base of the iris and the cornea. Normal intraocular pressure, between 15 to 25mmHg, is achieved by stable production and filtration of the aqueous humour. In animals, when the aqueous humour cannot exit the eye through the filtration angle at an appropriate rate, the intraocular pressure will rise. Generally speaking, RGC will be affected when the pressure is above 30mmHg and corneal oedema (cloudiness) will be noticed when the pressure is above 40mmHg.
In both human and veterinary medicine, glaucoma is categorised into two groups: primary and secondary. Primary glaucoma can be further categorised into open and closed angle primary glaucoma. The former type is rare in dogs. Closed angle primary glaucoma is due to abnormal embryological development of the filtration angle, a general term known as goniodysgenesis. In secondary glaucoma, the filtration angle is affected, damaged or blocked by another ocular disease such as uveitis, lens luxation, pigment deposition, blood clots or neoplasia.
Diagnosis of glaucoma by veterinary eye specialist is based on clinical history, clinical findings, tonometry and gonioscopy. Intraocular pressure can be measured by either applanation tonometer or rebound tonometer. There are slight differences in accuracy between these instruments, and it is important that one instrument is used consistently for comparison pressure measurements in the same eye. A rebound tonometer must be held parallel to the floor for accurate measurement. Iatrogenic pressure elevation can occur by having excessive pressure around the patient’s neck or the globe.
Gonioscopy allows direct assessment of the status of the filtration angle. If there is goniodysgenesis, the unaffected eye is predisposed to glaucoma at a later time.
Apart from high intraocular pressure, other clinical signs of glaucoma include deep limbal vascularisation, dilated iris, nonresponsive pupillary light reflex, cornea oedema if the pressure is above 40mmHg, buphthalmia, cupped optic disc, lens subluxation, Haab Striae (breaks in the endothelium) and non-responsive menace and dazzle reflexes.
Buphthalmia, conjunctival hyperaemia, corneal oedema and medical lens subluxation resulting in aphakic crescent.
Once a diagnosis of glaucoma is made, depending on the clinical findings, appropriate therapy will be initiated on the glaucomatous eye. There are two broad types of medication available to treat glaucoma- drugs that suppress production of aqueous humour, and drugs that assist in improving the outflow of aqueous humour. Carbonic anhydrase inhibitor (Cosopt/ Trusopt) and beta blockers (Timolol) are medications that reduce the production of aqueous humour. Parasympathomimmetics (Pilocarpine) and prostaglandin analogues (Xalatan, Lumigan) are medications that are commonly used and may help to improve outflow of the aqueous humour. However, pilocarpine can be quite irritating to the eye. In most glaucomatous cases, a combination of drugs to suppress aqueous humour production and assist aqueous humour outflow are used. In addition therapy to resolve the primary ocular disease that resulted in secondary glaucoma should be pursued. In most instances, medical therapy can only temporarily alleviate high intraocular pressure.
Surgery is generally advocated in cases when the intraocular pressure cannot be reduced with maximum medical therapy. Surgical therapy for glaucoma can be divided into vision-saving procedures such as gonioshunt implantation and cyclophotocoagulation (transcleral or endoscopic laser), or surgeries to alleviate pain such as intrascleral prosthesis (ISP) or enucleation. Vision-saving surgery will be considered when the eye still retrains vision but the intraocular pressure cannot be controlled with maximum antiglaucoma medication. Enucleation surgery or ISP is only considered when intraocular pressure cannot be reduced and the eye is permanently blind.
The prognosis for eyes that receive vision-saving procedures is generally good, but it is not a permanent solution to the eye at this point in time. Obstruction of the gonioimplant can occur over time, usually in 2 to 4 years. Regrowth of the ciliary epithelium that has been destroyed by cyclophotocoagulation can occur, usually several weeks to months. The goal of treatment in humans as well as animals is to delay the complete loss of vision for as long as possible. Therefore, early diagnosis, appropriate therapy, regular re-evaluation and timely surgical intervention are important in the treatment of glaucoma. therapy, regular re-evaluation and timely surgical intervention are important in glaucoma.
Dr. Derek Wai Yee Chow
BVSc (HONS), DACVO, DAiCVO, MANZCVS, MRCVS Specialist in Veterinary Ophthalmology
Diplomate of the American College of Veterinary Ophthalmologists
Diplomate of the Asian College of Veterinary Ophthalmologists