The term glaucoma refers to a group of neurodegenerative diseases characterized by polymorphic clinical signs caused by an increase in intraocular pressure, capable of triggering a chain of events at the optic nerve and at retinal level that result in damage to the integrity and function of the ocular structures that persists even if the pressure returns within normal limits.
In the eye, the equilibrium between the production and drainage of aqueous humour is responsible for keeping the intraocular pressure within the normal values of 22.2+/-5.2 mm/Hg, with the presence of variations linked to the circadian rhythm.
The aqueous humour is produced by the ciliary bodies mostly through secretion and active transport mechanisms and to a lesser degree through passive diffusion and ultrafiltration. The aqueous humour moves from the posterior chamber to the anterior chamber passing between lens and iris through the pupillary aperture. In the anterior chamber it is drained through the iridocorneal angle, where the pectinate ligaments are found between the base of the iris and the cornea. It penetrates through the spaces of Fontana delimited by these ligaments and insinuates itself into the trabecular meshwork, which is a zone of resistance to the aqueous humour flow. Crossing the trabecular meshwork, the aqueous humour finally reaches the venous system through the conventional and unconventional outflow pathways. In the cat, the unconventional pathways are considered responsible for only around 3% of this outflow.
Even though to all appearances the anatomical structures assigned to aqueous humour filtration in the dog and cat are roughly similar, slight differences between the two species can be found. In the cat, the anterior chamber is considerably deeper than in the dog. The fibres of the pectinate ligament appear more slender, longer and less numerous. The trabecular meshwork is richer in fibres and the corneoscleral cribriform ligament (trabeculo-corneoscleral) has pores of larger diameter. The scleral venous plexus is more developed and the trabecular veins are more numerous. These differences might explain the inferior incidence of feline glaucoma compared to canine glaucoma.
The diagnosis of glaucoma must be carried out based on the physical examination and measurement of intraocular pressure. The observation of the iridocorneal angle through gonioscopic examination is also important.
CLASSIFICATION
From the classification standpoint, the criteria followed may take into consideration the disease causing the glaucoma, and in this case it is differentiated into primary, when pre-existing diseases are not present, and secondary, when intraocular diseases responsible for the glaucomatous crisis have occurred. The primary form can be congenital.
Considering instead the state of the iridocorneal angle, the differentiation is between open angle and narrow/closed angle glaucoma, with the presence of pectinate ligament dysplasia. The classification in acute or chronic, on the other hand, is prompted by the time of onset of the disease.
In the feline species, the majority of glaucoma cases are of secondary origin and, given the subtle onset, chronic in nature. Males are more frequently affected than females. There is a certain preponderance of incidence in crossbreed cats compared to purebreds.
Initially, ocular hypertension is especially critical at the level of the optic disc, due to mechanisms that are in part known and in part still under study and in-depth examination. Later on, under the hypertensive stimulus, also the retina becomes affected by degenerative phenomena.
Secondary glaucoma is mainly ascribed to inflammatory/infective, traumatic and systemic neoplastic diseases. In the case of intraocular tumours, the cause of the increase in pressure is linked to the mechanism of compression and/or invasion of the iris stroma, of the iridocorneal angle and of the trabecular apparatus by the neoplastic tissue and/or cellularity. Diffuse iris melanoma is the most common primary neoplasm. Lymphosarcoma is the most common form among the secondary neoplasms.
With regard to infective/inflammatory conditions, it can be stated that any systemic disease capable of causing uveitis in cats may also potentially cause glaucoma. Iridocyclitis causes breaking of the haemato-aqueous barrier with an increase in proteins and cellularity of the aqueous humour; hypopyon and hyphaema may form and, as a result, cause an increase in the viscosity of the aqueous humour and a decrease in the filtration coefficient. Fibrin deposits may be present on the iris surface, in the pupillary aperture and on the iridocorneal angle, with formation of pre-iridal fibrovascular membranes. Anterior or posterior synechiae can be formed, with pupillary seclusion and severe impediment to the circulation of the aqueous humour. There can be an iris bombè with consequent closure of the iridocorneal angle. The miosis associated with uveitis creates an additional obstacle to the circulation of aqueous humour. Dislocation of the lens can ensue from the inflammatory event due to a degenerative process in the zonular fibres. The displacement of the crystalline lens can lead to a pupillary block with consequent obstruction to the outflow of aqueous humour through the pupillary aperture, or more frequently the movement of the lens towards the anterior chamber is responsible for an altered outflow at the iridocorneal angle (Fig. 1). As a result of lens dislocation, a prolapse of the vitreous body at pupillary level with consequent pupillary block can occur.
The predisposing element for a glaucoma secondary to traumatism is haemorrhage starting from the anterior uvea with hyphaema and altered drainage by the iridocorneal angle and the consequences of the inflammatory phenomenon secondary to the trauma itself (Fig. 2). If the trauma is caused by a puncture wound, the breaking of the lens capsule with the onset of phacoclastic uveitis may be observed.
A particular form of feline glaucoma is linked to an altered flow-direction of the aqueous humour, a condition similar to malignant glaucoma in humans. In this case, the aqueous humour tends to flow towards the vitreous body, imbibing it and causing an anterograde displacement of the lens and of the iris with closure of the iridocorneal filtration angle (Fig. 3).
CLINICAL SIGNS
In the cat, the signs and symptoms of glaucoma are similar to those seen in the dog, even though quite often the clinical signs start in a more subtle and less striking way, especially in the initial phase. Not infrequently, cats are belatedly referred with blindness and buphthalmia associated with the other clinical symptoms typical of the disease (Fig. 4). Along with the above-mentioned symptoms there can be the presence of epiphora, dilated and fixed pupil or a pupil not very responsive to light stimulus, changes in iris colour and, in advanced forms, excavation of the optic disc, which is not easy to detect due to the poor myelination of the papilla, which appears darker, and retinal degeneration manifested by tapetal hyperreflectivity and vascular attenuation. The presence of pain with blepharospasm, conjunctival hyperaemia, scleral injection and corneal oedema, which is usually not pronounced, are less frequently present.
TREATMENT
The treatment of feline glaucoma is often extremely frustrating as the subject is often brought to the visit with advanced symptomatology. The treatment can be medical (specific and nonspecific) and surgical.
The specific medical treatment makes use of drugs that work on the vitreous body by dehydration (mannitol and glycerol), by reducing the production of aqueous humour (topical carbonic anhydrase inhibitors) and by facilitating the outflow of aqueous humour (beta-blockers). The nonspecific treatments involve the use of anti-inflammatory agents, corneal lubricating products and antibiotics.
The surgical therapeutic possibilities of feline glaucoma are similar to those of canine glaucoma and they are used when the intraocular pressure cannot be controlled with medical treatment. If visual function is maintained, it is possible to act on the aqueous humour drainage pathways through cyclodialysis, iridencleisis, subconjunctival implants or with cyclocryotherapy and cyclophotocoagulation. In the absence of vision, the epithelium of the ciliary body can be destroyed and the production of aqueous humour can be reduced via the pharmacological ablation of the ciliary bodies. Evisceration with insertion of an endobulbar prosthesis for aesthetic purposes is another therapeutic possibility. It should however be considered that all these operations expose the operated subject to the risk of the possible onset of a post-traumatic fibrosarcoma, a diseases which is infrequent but well documented in literature.
With reference to what is described above, in the feline species in the absence of visual function enucleation is quite often the most correct surgical treatment for resolving a glaucoma not controlled by medical treatment.
Suggested readings
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- Olivero DK,Riis RC,Dutton AG,Murphy CJ,Nasisse MP,Davidson MG.(1991). Feline lens displacement:a retrospective analysis of 345 cases. Prog Vet Comp Ophthalmol 1:239-244
- Dietrich U.(2005) Feline glaucomas. Clin Tech Small Anim Pract. 2005 May;20(2):108-16.
- Brooks DE.(1990) Glaucoma in the dog and cat. Vet Clin North Am Small Anim Pract. 1990 May;20(3):775-97.
- Ridgway MD,Brightman AH. (1989) Feline glaucoma:a retrospective study of 29 clinical cases. Journal of the American Animal Hospital Association September/October vol 25 485-490
- Jacobi S.,Dubielzig R.R. (2008) Feline primary ocular glaucoma. Vet Ophthalmol. 2008 11 (3):162-165.