Eye Disease in Geriatric Horses

Eye Disease in Geriatric Horses

W0613-15.qxd 11/16/05 01:26 PM Page 173 C H A P T E R 15 Eye Disease in Geriatric Horses Keith J. Chandler, Andrew G. Matthews ittle is known a...

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C H A P T E R

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Eye Disease in Geriatric Horses Keith J. Chandler, Andrew G. Matthews

ittle is known about senile ophthalmic changes in equine animals, although in humans certain ophthalmic pathologic conditions become more common with increasing age, including vitreous degeneration (liquefaction), asteroid hyalosis, synchysis scintillans, senile retinal hyperpigmentation, and chorioretinal degeneration (cobblestone degeneration).1 Among horses and ponies older than 15 years of age, more than 80 percent have eye lesions, although these lesions are not all agerelated.2 There are several equine ocular conditions, however, that are reportedly more common with advancing age, and these include senile retinopathy,3 proliferative optic neuropathy,4,5 and vitreal degeneration.6 In a study on the health of horses in the United Kingdom, only 1 percent of horse owners reported that their animals suffered from ocular disorders.7 This may indicate that elderly animals are coping well with poor sight. The fact that so many elderly animals have ophthalmic lesions suggests that the lesions, and the potential visual disturbance, are not significant to the survival of aging domesticated horses. In wild horses, there are a number of limiting factors to longevity, including dental disease, but it would not be unreasonable to assume that deterioration in sight may also be a limiting factor. There are no published data on the prevalence of ocular pathologic conditions in younger horses, so it is difficult to compare the prevalence in geriatric equine animals with the remainder of the equine population. Comparing lesions in old and young animals gives a cross-sectional indication of aging changes within the eye, but this method does not provide a direct measure-

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ment of senescence in individuals, since differences between age groups may be due to age-cohort effects. However, to qualify whether the lesions are true ageing changes, it would be necessary to repeatedly examine the same individual as it becomes older. These types of longitudinal studies in which the animals are drawn from a similar birth cohort are not usual in veterinary medicine because they are very time-consuming and costly.

Cornea and Ocular Surface The ocular surfaces are continuously challenged, both by minor physical insults and by overgrowth of potential microbial pathogens, including bacteria and fungi, which make up the normal commensal population of the external eye. The health of the ocular surfaces, including the cornea, in the face of such challenge is to a large extent dependent on the ocular surface defense mechanisms. Most superficially, these include the physical and biochemical integrity of the tear film. The tear film mucin lysozyme, possibly the most potent of the tear film bacteriolytic agents, has been shown to decrease with age in humans. A nonspecific, innate immunity is present on the ocular surface. Innate immunity has no immunologic memory and comprises both phagocytic cells such as natural killer cells and leukocytes and serum-derived macromolecules such as defensins, complement components, and creative protein. These latter cells enter the tear film via increased capillary permeability after surface insult. In laboratory animals, the recruitment and phagocytic 173

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activity of polymorphonuclear leukocytes on the ocular surface is significantly reduced with age. Similarly, specific surface immunity driven by T cells and based on cellmediated immunity is believed to become impaired in aging animals. The result of age-based compromise of ocular surface defense mechanisms is seen in the increased risk of microbial disease, in particular keratomycosis, in older horses. In addition, these diseases may be more difficult to treat in older animals and, in general, carry a more guarded prognosis. Other clinical considerations arising from this include the imperative to select bacteriocidal over bacteriostatic antibiotics in treating bacterial ulceration in older animals, and in electing to use topical corticosteroids only with considerable circumspection. Age is only one of a number of risk factors in microbial disease of the ocular surface, in particular of the cornea. Others include geographic and seasonal variation in the prevalence of potential keratopathogens among the microflora of the external eye,the liability to minor injury of the corneal surface, and the protracted or inappropriate use of topical antibiotics and corticosteroids.

Figure 15-2 Senile retinopathy.

Retina The incidence of so-called senile retinopathy, a form of retinal degeneration, has been shown to increase with age (Fig. 15-1).2 The retinopathy is characterized ophthalmoscopically by a generalized depigmentation and linear or branching hyperpigmentation in the nontapetal fundus and, in some cases, by attenuation of the peripapillary retinal blood vessels (Figs. 15-2 and 15-3). In advanced cases, there may be hyper-reflectivity in the non-tapetal fundus. Histologically, this condition is characterized by disruption of the of the retinal pigment epithelium, loss of photoreceptors, and cystic degenera-

Figure 15-3 Senile retinopathy. Note the blood vessel attenuation.

percentage affected

80 70 60 50 40 30 20 10 0 15-19

20-24

25-29

30 +

age groups

Figure 15-1 The prevalence of senile retinopathy in each age group of geriatric equine animals. Senile retinopathy is significantly more prevalent in older age groups (P = .0007).

tion of the inner layers of the neurosensory retina,3 causing functional injury to the neurosensory retina and inevitably resulting in some degree of visual disruption.5 The extent of any visual disability in affected horses is notoriously difficult to assess. Ophthalmoscopy has limitations, and electroretinography and visually evoked responses are not particularly accurate or practical.5,8 Horses have the largest globe among domestic animals,9 but the visual field of the direct ophthalmoscope corresponds to approximately 2 percent of the visually receptive fundus, permitting examination of only 15 percent to 20 percent of the retina through a maximally dilated

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pupil. As a result, lesions that appear large on ophthalmoscopic examination may represent only a small and possibly inconsequential defect.5 However, there is little doubt that senile retinopathy does affect vision, particularly under poor lighting conditions.The visually attributable behavioral changes noted by the owners of affected animals include avoiding standing inside darkened stables and clumsiness in failing light.The photoreceptor and ganglion cell geography of the rod-rich equine retina permits a high degree of sensitivity to movement and changes in luminosity in dim light, but at the expense of visual acuity and point discrimination,10 which may partly explain why disruption in photopic vision is commonly the first indication of visual disability. However, many geriatric animals are no longer working at a competitive level, and reduced or impaired vision may be less important. Retired animals are often managed in such a way that owners may miss cues to disturbances in vision; these animals are often kept in familiar surroundings and on a regular daily routine. Other fundic lesions, such as focal chorioretinopathy (Fig. 15-4), affect up to 10 percent of the equine population in the United Kingdom.11 Focal chorioretinopathy is found commonly in older horses, but it is likely that the initial inflammatory insult occurred some time before, most probably as a result of equine herpes virus infection.The resultant chorioretinal pathologic condition is present for the rest of the animal’s life.

Optic Nerve Optic nerve disease is more common in older horses. Optic atrophy is the end stage of ischemic injury to the nerve and in animals of any age can result from head trauma, optic neuritis, and, rarely, septic embolism. In older animals, optic atrophy may be associated with local perineural or infiltrative pathologic conditions such as orbital space-occupying lesions, tumors of the diencephalon, midbrain, meninges, or the optic nerve itself, and from sphenopalatine sinusitis. Affected eyes are invariably blind and may appear ophthalmoscopically normal in the early stages of the disease. Subsequently, the optic disc becomes pale and may have a granular appearance as the lamina cribrosa of the sclera foramen is exposed. There is profound attenuation of the retinal vasculature, and ischemic retinopathy may be evident. The condition may be found coincidentally with senile retinopathy. Proliferative optic neuropathy is also reported to be more common in older horses; however, it is likely to be present in less than 2 percent of geriatric eyes.2 This is a discrete, nonprogressive, whitish-pink lobular lesion located at the edge of the optic disc (Fig. 15-5) that does not appear to affect vision.5,12 Histologically, the lesion



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Figure 15-4 Focal chorioretinopathy.

typically consists of extruded glial tissue with lipid-filled cytoplasm vesicles, and in one case has been described as a schwannoma.

Vitreous The vitreous occupies the greater part of the ocular volume and has a number of functions, including metabolic support of the neuroretina, maintenance of the spatial and geographic integrity of the neuroretina, removal of

Figure 15-5 Proliferative optic neuropathy.

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metabolic waste, and the unhindered transmission of light to the retina. In humans,the consistency and optical clarity of the vitreous changes throughout life, and with increasing age liquefaction (syneresis) and collapse of the vitreal body occurs.13 In horses, the uniformly low-density vitreal hydrogel probably does not undergo true age-related liquefaction until extreme old age.However,progressive dilution of the hydrogel throughout life appears to convey the clinical impression of liquefaction from a relatively early age, usually evident in the movement of intravitreal “floaters” with ocular saccades. Pathologic liquefaction arising from posterior segment inflammatory disease may also commonly contribute to the apparent vitreal liquefaction in relatively young horses. The cumulative effect of apparent liquefaction and the appearance of inflammatory or other cellular debris is referred to as vitreal degeneration and begins to affect horses from the age of 6 years.6 Inflammatory debris in the vitreous can result from diseases such as equine recurrent uveitis. Vitreal degeneration may affect up to half of all equine animals older than 15 years of age,2 and these vitreal changes may be even more common in areas where there is a high prevalence of recurrent uveitis, such as in continental Europe, where uveitis affects up to 15 percent of that equine population.14 Vitreous degeneration is best visualized using direct ophthalmoscopy or slit-lamp biomicroscopy. Typically, there is clouding or discoloration of the vitreous gel, and particulate, membranous, or cellular debris may be suspended within the vitreal body. These changes are rarely severe enough to adversely affect vision, but in some cases direct ophthalmoscopic examination of retinal detail may be markedly hindered. Synchysis scintillans, or cholesterosis bulbi (Fig. 15-6), is a rare condition in horses and is reportedly more common in older animals. It manifests as highly refractile, golden particles floating freely within the vitreous.These particles are made up of cholesterol crystals and usually reflect previous hemorrhage within the vitreous, which in most instances is likely to be secondary to head trauma. Asteroid hyalosis (Fig. 15-7) is a very rare finding in old horses. It appears as relatively large whitish or refractile particles enmeshed in the vitreous gel structure. The particles probably consist of lipid-mineral complexes and typically remain suspended in the vitreous body, although some movement is provoked by ocular saccades.Their origin is unknown.

Lens Cataracts are the loss of optical homogeneity of the lens, and they are common in older horses.15,16 As horses and ponies age, there is increased risk of cataract development

Figure 15-6 Synchysis scintillans in a 38-year-old pony.

percentage of animals affected

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70% 60% 50% 40% 30% 20% 10% 0% 15-19

20-24

25-29

30+

age groups

Figure 15-7 The prevalence of lens lesions in each age group of geriatric equine animals. The prevalence of lens lesions is significantly higher in older age groups (P = .0048).

(Fig. 15-8). Senile cataracts are age-dependant opacities found commonly in animals older than 18 years. It is unclear how senile cataracts develop in the horse. They may represent true senescence of the lens but in most cases are more likely to be associated with an age-determined susceptibility of the lens to autocrine or oxidative injury associated with subclinical intraocular pathologic conditions. Senile cataracts typically involve the posterior nuclear suture lines and anterior or posterior cortex (Fig. 15-9). Complete and occasionally hypermature cataracts occur in some animals,with the animal losing the pupillary light response in advanced cases. Posterior capsular cataract is found in association with posterior uveitis and, on occasion, with vitreal degeneration. This type of cataract becomes increas-

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Figure 15-10 Posterior capsular cataract with incidental anterior cataract. Figure 15-8 Unilateral asteroid hyalosis.

Glaucoma

Figure 15-9 Senile cataract with posterior suture condensations.

ingly common with age and appears as an irregular diffuse opacity of the posterior lens (Fig. 15-10).This type of cataract may be progressive and can hinder ophthalmoscopic examination of the posterior segment. Nuclear sclerosis has not been definitively described in equines. In extreme old age, however, horse lenses commonly show an enhanced nuclear delineation, which may be associated with senile cataracts and, rarely, brunescence of the lens. Vision is unlikely to be affected by these types of lens changes. Aged animals with senile cataracts are likely to be a poor surgical risk and are not suitable candidates for lensectomy.

Glaucoma is relatively uncommon in horses and ponies. Animals older than 15 years are at an increased risk, however, particularly if they have been previously or are currently affected by anterior segment inflammatory disease, including equine recurrent uveitis (Figs. 15-11 and 1512).17 Appaloosas are at particular risk from the disease. Clinical signs in the early stages of equine glaucoma are often subtle, and ocular pain may not be apparent. Corneal opacity is a common and early presenting sign, either as diffuse “ground glass” opacity or as branching striate opacities arising from dehiscences in Descemet’s membrane caused by elevations in intraocular pressure. As the condition progresses, other signs, including cataract and posterior synechiae, may become apparent. Diagnosis is based on clinical signs and tonometric measurement of intraocular pressure. However, intraocular pressure rises may be transient, and some glaucomatous eyes may be normotonic at the time of examination.Treatment of the condition is directed at reducing intraocular pressure using topical carbonic-anhydrase inhibitors such as dorzolamide and topical beta blockers such as timolol maleate. In addition, some horses will respond to treatment of underlying uveitis with topical corticosteroids and systemic antiinflammatory medication. Topical prostaglandins, as used in the management of some human glaucomas, are contraindicated in the horse. All glaucoma cases in the horse are difficult to manage medically over the long term, and surgical options including cyclodestruction or enucleation should be considered.

Ocular Neoplasia Squamous cell carcinoma is the most common tumor of the eye, and there is an increased prevalence with age: an

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Squamous cell carcinoma primarily affects the limbal conjunctiva and the third eyelid. Some cases are quite subtle and manifest as a persistent nonresponsive conjunctivitis, although closer inspection may reveal roughening of the surface of the conjunctiva by tumor formation. Diagnosis is based on history and, ultimately, biopsy results. Excision or radiotherapy is effective, and the prognosis is favorable if the tumor is removed at an early stage. Metastasis is uncommon. Melanomas are usually found in older gray horses, although they rarely cause more than local affects such as protrusion of the third eyelid. Periorbital sarcoids tend to affect young adult horses and do not commonly appear for the first time in geriatric animals. REFERENCES

Figure 15-11 Uveitic glaucoma, note incidental anterior capsular cataract.

Figure 15-12 Acute uveitic glaucoma.

11-year-old horse is 2.4 times more likely to develop squamous cell carcinoma than a 2-year-old.18 With advancing age comes long-term exposure to carcinogens, in this case ultraviolet light. However, there may be age-related biochemical or immunologic factors that influence the risk of development of these neoplasms.

1. Naumann GOH, Apple DJ: Pathology of the Eye. New York, SpringerVerlag, 1986. 2. Chandler KJ, Billson FM, Mellor DJ: Ophthalmic lesions in 83 geriatric horses and ponies.Vet Rec 153:319, 2003. 3. Barnett KC:The ocular fundus of the horse. Equine Vet J 4:17, 1971. 4. Rebhun WC: Equine retinal lesions and retinal detachments. Equine Vet J Suppl 2:86, 1983. 5. Matthews AG, Crispin SM, Parker J:The equine fundus III: Pathological variants. Equine Vet J Suppl 10:55, 1990. 6. Gellat KN: Equine ophthalmology. In Essentials of Veterinary Ophthalmology. Philadelphia: Lippincott, Williams & Wilkins, 2000, pp 337–377. 7. Mellor DJ, Love S,Walker R, et al: Sentinel practice-based survey of the management and health of horses in northern Britain. Vet Rec 149:417, 2001. 8. Crispin SM, Matthews AG, Parker J:The equine fundus I: Examination, embryology, structure and function. Equine Vet J Suppl 10:42, 1990. 9. Davidson MG: Equine ophthalmology. In Gellat KN, editor:Veterinary Ophthalmology. Philadelphia: Lea & Febiger, 1991, pp 576–611. 10. Ehrenhofer MCA, Deeg CA, Reese S, et al: Normal structure and agerelated changes in the equine retina. Vet Ophthalmol 5:39, 2002. 11. Slater JD, Ellis MA, Froesch N, et al: Herpesvirus chorioretinal lesions. In Proceedings of the 40th British Equine Veterinary Association Congress, 2001, pp 169–170. 12. Rebhun WC: Equine retinal lesions and retinal detachments. Equine Vet J Suppl 2:86, 1983. 13. Sebag J:The vitreous. In Hart WM, editors: Alders Physiology of the Eye, 9th edition. London, Butterworth, 1992, pp 268–348. 14. Deeg C: Equine recurrent uveitis:An inflammatory disease mediated by organ-specific autoimmunity. In Proceedings of the 40th British Equine Veterinary Association Congress, 2001, pp 167–168. 15. Matthews AG: Lens opacities in the horse: a clinical classification. Vet Ophthalmol 3:65, 2000. 16. Matthews AG: Classification, diagnosis and prognosis of equine cataracts. In Proceedings of the 40th British Equine Veterinary Association Congress, 2001, pp 173–175. 17. Miller TR, Brooks DE, Smith PJ, et al: Equine glaucoma: clinical findings and response to treatment in 14 horses.Vet Comp Ophthalmol 5:170, 1995. 18. Dugan SJ, Curtis CR, Roberts SM, et al: Epidemiological study of ocular/adnexal squamous cell carcinoma in horses. J Am Vet Med Assoc 198:251, 1991.