The Glaucoma is one of the most important causes of blindness in both humans and dogs. Usually, it is associated with an increase of the intraocular pressure (IOP); however, the better understanding of the disease have changed this concept. Recent definition of glaucoma refers to the most important damage observed during the disease, which is the progressive death of the retinal ganglion cells (RGCs) and their axons. Therefore, glaucoma could be defined as a progressive optic neuropathy associated with a level of IOP non-compatible with a normal function of RGCs and the optic nerve head (ONH).

There are several reasons for glaucoma to be one of the most common causes of blindness but the difficult to make early diagnosis and low response to therapy probably are the most important. Early diagnosis is really difficult since first changes are often not recognized by general practitioners. In addition, the exact value of IOP that begins the damage is not known for each individual.

The most used classification for canine glaucoma includes a combination of two schemes: the possible cause and the gonioscopic appearance of the entrance of the ciliary cleft. Based on this, glaucoma may be primary or secondary, and primary glaucoma in its turn, is divided in open and narrow/closed angle glaucoma. It is important to know that narrow/closed angle primary glaucoma is the most common in dogs, it is hereditary and a bilateral condition. In man, the open angle primary glaucoma represents the largest clinical presentation group, which means that most of the medical therapy is indicated for this kind of glaucoma but not for canine's one. This explains in part, why medical therapy is often not effective in the dog.

The diagnosis of glaucoma is based in clinical signs, tonometry and gonioscopy. The earlier clinical signs are not easily recognized by owners and general practitioners because they are related to changes in the ONH. These changes can be evaluated on the ONH neuroretinal rim and cup by using direct and indirect ophthalmoscopy, but this is not usual in a dog until an acute increase of IOP is present. Other clinical signs such as episcleral congestion, mydriasis, corneal edema and buphthalmia are easier to recognize but indicate a late moment to reach some success with treatment. In other words, the most common clinical situation is to receive a patient with high IOP in one eye, but this case should be considered as a glaucomatous patient and both eyes must be thoroughly examined. The management of this patient should include an accurate therapy for the hypertensive eye and the follow up of the other eye considering it as a "suspicious" eye.

Control of the suspicious eye includes gonioscopy to classify the glaucoma as primary or secondary, and a study of its IOP including diurnal variations. Diurnal variations have been reported in the dog, with higher levels in the morning and the lowest in the evening. The gap between these values is larger in glaucomatous dogs than in normal dogs. Diurnal variations in systolic pressure can also be studied because they are related to perfusion of the optic nerve.

Recent advances in therapy

Medical and surgical therapy may be used in glaucomatous patients. Many drugs can be indicated but we are going to consider here the newest and more effective for the dog.

1.  Prostaglandins: Aqueous humor is drained by two pathways; in the dog, approximately 15 to 20% is eliminated trough the uveoscleral outflow which begins in the ciliary cleft but continues between fibers of ciliary muscle to the posterior pole. Topical prostaglandins (PGs) reduce IOP by increasing uveoscleral outflow trough an enzymatic mechanism. There are four PGs available for using in dogs: latanoprost, unoprostone, bimatoprost and travoprost. PGs are the most effective hypotensive agentes and clinical experience shows that they are the first choice drugs for canine glaucoma.

2.  Neurodegeneration and neuroprotection: recent advances in the study of the effects of IOP in glaucoma leaded to understand the process by which RGCs degenerate. This process, called neurodegeneration, consists of several biochemistry changes that finish with cellular death. Theories for the adverse effects of IOP include a combination of two mechanisms: the mechanical and the ischemia effects.

a.  The mechanical effect is an alteration of the scleral laminar cribrosa channels and impairment of the axoplasmic flow of the optic nerve axons. Neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are transported by axoplasmic flow to the RGC.

b.  The ischemic mechanism affects choroidal, retinal, and ONH circulation producing high levels of glutamate. This is an excitotoxic amino acid that produces high levels of intracellular nitric oxide (NO).

Both processes lead RGC to death by apoptosis. Neurodegeneration begins due high IOP but continues independently of it.

Neuroprotection is a new concept in glaucoma therapy that reduces the effects of neurodegeneration. Some drugs are been evaluated such as glutamate inhibitors, NO inhibitors, and calcium channels blockers.

Regarding surgical treatment, several devices called gonioimplants have been used in dogs. These are tubing devices that communicate the anterior chamber with the subconjunctival space where aqueous can be easily absorbed and drained. Gonioimplants may be valved or non-valved, and good results were obtained by using simplified implants. Considering that the most common cause of failure of these tubular implants is their obstruction, a new concept of non-tubular implants has been recently reported.

Conclusions

An accurate management of a glaucoma patient should consider:

1.  Early diagnosis and follow up of a suspicious patient.

2.  Reduction and control of IOP in a "safe" level. Medical and/or surgical therapy must be used.

3.  Neuroprotection

References

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2.  Brooks, D.E., García, G.A., Dreyer, E.B., Zurakowsky, D., Franco-Bourland, R. (1997): Vitreous body glutamate concentrations in dogs with glaucoma. Am. J. Vet. Res. 58(8): 864-867

3.  Neufeld, A.H., Hernandez, M.R., Gonzalez, M.(1997): Nitric oxid synthase in the human glaucomatous optic nerve head. Arch. Ophthalmol. 115: 497-503

4.  García, G.A., Brooks, D.E., Gelatt, K.N., Kubilis, P.S., Gil, F., Whitley, R.D. (1998): Evaluation of valved and nonvalved gonioimplant in 83 eyes of 65 dogs with glaucoma. Anim. Eye Res. 17(1-2): 9-16

5.  Herrera, H.D. (1998): Surgical treatment of canine glaucoma with nonvalved simplified gonioimplants. Proc. ISVO/SOLOVE/WSAVA Congress. Buenos Aires, 5 - 6 de Octubre.

6.  Gelatt, K.N., Brooks, D.E. (1999): The canine glaucomas. En: Gelatt, K.N. (Ed): Veterinary Ophthalmology (third edition), Lippincott Williams & Wilkins. Philadelphia, 701-754

7.  Herrera, H.D., Bruhl Day, R., Martinez, M.E., Gomez, N.V. (2000): Variaciones diurnas de la presión intraocular y la presión sanguínea en caninos normales. Congreso AVEPA Madrid (España), octubre.

8.  Herrera, H.D. (2001): Gonioimplante intraescleral no tubular como tratamiento quirúrgico de glaucoma en un canino. Congreso AMMVEPE Morelia (México), junio.

9.  Gelatt, K.N., MacKay, E.O. (2001): Effect of different dose schedules of latanoprost on intraocular pressure and pupil size in the glaucomatous Beagle. Vet. Ophthalmol. 4(4): 283-288.