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Review Article Equine Glaucomas F EQUINE VETERINARY EDUCATION / AE / JUNE 2010 299 Review Article Equine glaucomas F. Ollivier* and S. Monclin† Animal Eye Doctor, Meylan, and Clinique Vétérinaire Advetia, Paris, France; and †Rutland House Referrals, St. Helens, UK. Keywords: horse; glaucoma; intraocular pressure; laser; photocyclocoagulation; anti-glaucomatous medications Summary also been previously reported in Thoroughbred, Arabian and Standardbred foals but is relatively uncommon with no The glaucomas are diseases that lead to the destruction of breed predisposition (Gelatt 1973; Wilcock et al. 1991; retinal ganglion cells and their axons via a number of Barnett 1998; Lassaline and Brooks 2005). Active or mechanisms such as direct pressure damage, hypoxic quiescent iridocyclitis, age (>15 years) and breed and toxic injuries. The aim of this article is to present a (Appaloosas) represent risk factors for development of review of this condition in horses in order to have a glaucoma in horses (Wilcock et al. 1991; Miller et al. 1997; proactive attitude and to enable an early diagnosis to be Wilkie et al. 2001; Brooks and Matthews 2007). made in order to determine the most adequate prophylactic (on predisposed individuals) and therapeutic treatment. Physiology of the aqueous humour Introduction Aqueous humour fills the anterior and posterior chambers of the anterior segment of the eye and serves to carry The glaucomas are a group of diseases that lead to the nutrients to, and help remove waste from, the avascular destruction of retinal ganglion cells and their axons via a lens and cornea. As aqueous is formed by the ciliary body, number of mechanisms such as direct pressure damage, it accumulates in the posterior chamber and passed, hypoxic and toxic injuries (Wilcock et al. 1991; Wilkie and between the pupil and lens into the anterior chamber. In Gilger 2004; Lassaline and Brooks 2005). These diseases horses, as in many other animal species, its formation have been recognised in several domestic species, occurs via 3 separate processes: active secretion, including the horse and clinical presentations vary widely ultrafiltration and simple diffusion. Active secretion (primary between them. Equine glaucomas are usually slow to process) involves energy and carbonic anhydrase, an progress with discreet signs of pain and insidious loss of enzyme located in the nonpigmented ciliary body vision with an estimated incidence in the USA (Miller et al. epithelium that is constantly recycled. Only a small portion 1997; Wilkie et al. 2001; Brooks and Matthews 2007). of aqueous humour production arises from ultrafiltration of Following a review of the epidemiology and aetiology, this blood present in the ciliary body circulation. There are 2 article will present the physiology of the aqueous humour, main routes that aqueous may follow to exit the eye: the pathogenesis, clinical signs and various treatments for conventional and unconventional outflow pathways equine glaucomas. (Smith et al. 1986; Samuelson et al. 1989; De Geest et al. 1990; Glenwood et al. 2007). The conventional pathway Epidemiology and aetiology makes reference to aqueous outflow via the iridocorneal angle (ICA), which is delimited anteriorly by the peripheral Equine glaucoma usually represents a secondary ocular cornea and perilimbal sclera and posteriorly by the disease similarly to glaucoma in the cat. The initial insult peripheral iris and ciliary body (Fig 2). A stout pectinate that leads to its development is usually uveitis (Fig 1), ligament separates the anterior chamber from the ICA in although intraocular neoplasia, lens luxation and trauma the horse eye, and is visible at the limbus, medially and are also possible causes (Fig 1) (Gelatt 1973; Wilkie et al. laterally (Smith et al. 1986; Samuelson et al. 1989; De Geest 2001). Congenital glaucoma (i.e. goniodysgenesis) has et al. 1990; Barnett et al. 2004; Glenwood et al. 2007). Aqueous humour that exits the eye via the ICA reaches the corneoscleral and uveoscleral trabecular meshworks to *Corresponding author. Email: [email protected] ultimately access venous circulation via the vortex veins. © 2010 EVJ Ltd 300 EQUINE VETERINARY EDUCATION / AE / JUNE 2010 a) c) b) d) Fig 1: Main causes of secondary glaucoma in horses: (a, b) uveitis (fibrin clot and posterior synechiae can lead to secondary glaucoma) (c) intraocular neoplasm, in this case an iris melanoma (masses can interfere with the drainage of the aqueous and lead to glaucoma) (d) lens luxation. a route of aqueous clearance as prominent as the conventional outflow, whereas the latter is most important in small animals (Smith et al. 1986; Samuelson et al. 1989; De Geest et al. 1990; Barnett et al. 2004; Glenwood et al. 2007). Aqueous formation is balanced by its drainage from the eye and this equilibrium results in an intraocular pressure (IOP). A range of 15–30 mmHg is reported as being physiologically normal in the horse and a measurement above this range leads to the diagnosis of intraocular hypertension (Miller et al. 1990; Dziezyc et al. 1992; van der Woerdt et al. 1995; Knollinger et al. 2005; Lassaline and Brooks 2005). Sustained elevated intraocular hypertension will lead to the death of retinal ganglion cells (RGC) and this is termed glaucoma. However, an eye that suffers from glaucoma may present with no detectable vision loss Fig 2: Iridocorneal angle in the horse: The conventional pathway is during a period of normal IOP. Equally interesting is the fact the aqueous drainage through the iridocorneal angle (ICA). In the horse, a thick pectinate ligament separate the ICA from the that IOP in horses may be as high as 50 mmHg for several anterior chamber and is easily visible medially and laterally at the days with no detectable vision loss, which is unthinkable in limbus. other domestic animals such as dogs and cats. The examiner should be aware that several external factors This pathway is influenced by intraocular pressure. The influence IOP. If tonometry is performed without an unconventional pathway refers to the outflow of aqueous auriculopalpebral nerve block, it may result in a slight humour via the uveoscleral route, through which aqueous is overestimation of the IOP; if it is performed while the horse’s absorbed by the iris, ciliary body and sclera. This route is not head is lower than its heart, it may result in a 32% increase affected by intraocular pressure but by the state of the compared to when it is measured with the head held ciliary body. When the ciliary body is relaxed, outflow is higher; and, inversely, if performed on a horse under the enhanced. Although both pathways are important for effects of a sedative (i.e. xylazine) it may result in a 23–27% aqueous removal, interspecies differences exist. In the decrease in IOP reading (van der Woerdt et al. 1995; Garg horse, the unconventional outflow pathway is thought to be et al. 2005). © 2010 EVJ Ltd EQUINE VETERINARY EDUCATION / AE / JUNE 2010 301 Pathogenesis of glaucoma Glaucoma is not an uncommon ocular disease in horses but unfortunately little is know about the pathogenesis and development of equine glaucoma in comparison with other animal species. When glaucoma is secondary to uveitis, adhesions of the peripheral iris (i.e. peripheral synechiae) (Fig 1b) may lead to the partial closure of the ICA and adhesions of the pupil to the anterior lens surface may impede the free flow of aqueous into the anterior chamber, causing a pupil block glaucoma (Wilcock et al. 1991; Barnett et al. 2004). In addition, preiridal fibrovascular membranes may form and span the iridocorneal angle altering its ability to allow the passage of aqueous humour out of the eye. Debris composed of neoplastic cells; inflammatory cells and/or proteinaceous material may also be deposited in the iridocorneal angle, further blocking the exit of aqueous Fig 3: Optic nerve head ‘cupping’. Enlargement of the optic cupule (Figs 1a,b). Lastly, blockage of the iridocorneal angle is commonly seen in cases of chronic glaucoma due to the reduction of the number of axons, compression of the lamina and may be seen, in association with space occupying lesions enlargement of the scleral canal. These changes at the level of the in the eye (Wilcock et al. 1991; Wilkie et al. 2001; Wilkie lamina and the axons lead to a phenomenon of excavation and Gilger 2004). The obstruction of the pupil or the (cupping) of the optic nerve head. ICA can also be a result of anterior lens luxation and vitreal prolapse, common conditions seen in Appaloosas the processes described above, also affect the equine and Rocky Mountain Horses (Figs 1c,d) (Barnett et al. retina and optic nerve during the development and 2004). These processes, which mostly affect the progression of glaucoma (Wilcock et al. 1991; Brooks et al. conventional outflow, appear to be very relevant in the 1995; Wilkie and Gilger 2004), but more research is needed pathogenesis of secondary glaucoma in equids. to elucidate the pathogenesis of this disease in horses and Interestingly, the presence of a large ICA in the horse and its relationship with equine recurrent uveitis (ERU). the importance of the unconventional outflow in this species may, in part, explain the relative low incidence of Clinical signs glaucoma in this species when compared to dogs and man (Wilcock et al. 1991). Clinical signs of glaucoma in horses can be very subtle as An increase in IOP causes a compressive often only slight pupil dilation and very limited discomfort conformational distortion within the scleral lamina cribrosa may be present. In addition, the IOP variations in this (i.e. site where the RGC leave the retina to enter the optic species can be relatively large. These 2 facts make the nerve) with a collapse of the laminar pores and laminar diagnosis of equine glaucoma difficult to establish and channels such that optic nerve axoplasmic flow is reduced frequently repeating IOP measurements may be necessary and eventually blocked to cause RGC death (Brooks et al.
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