The optically clear and avascular lens consists of (from anterior to posterior) the anterior lens capsule, anterior cortex, nucleus, posterior cortex, and very thin posterior lens capsule. The lens is formed early in the development of the eye and coated with its basement membranes (anterior and posterior lens capsules), which insulate the lens proteins from the later-developing immune system. Hence in later life, if the lens capsule barrier is compromised by trauma or surgery, the immune system “attacks” the foreign lens material. The sole function of the lens is to allow unaltered passage of light and images to the retina. Diseases of the lens involve changes in its transparency.
Cataracts are an opacity of the lens or its capsule and should be differentiated from the minor lens imperfections in young dogs (seen on slit-lamp biomicroscopy ) and the normal increase in nuclear density (nuclear sclerosis) that occurs in older animals. Cataract formation and cataract surgery in people and dogs have many similarities, but dogs experience more postoperative anterior uveitis. Cataract surgery is highly effective (95%) in people and is performed with advanced nuclear sclerosis and the failure of missing two lines on the Snellen eye acuity test. Cataracts usually are classified by their age of onset (congenital, juvenile, senile), anatomic location, cause, degree of opacification (incipient, immature, mature, hypermature), and shape. Most cataracts can be detected by dilating the pupil and examining the pupillary region against the retroillumination of the tapetal fundus. Slit-lamp biomicroscopy permits optimal direct examination of the lens. Cataracts (often inherited) are more common in dogs than in other species (see Table: Inherited Cataracts in Domestic Animals Inherited Cataracts in Domestic Animals The optically clear and avascular lens consists of (from anterior to posterior) the anterior lens capsule, anterior cortex, nucleus, posterior cortex, and very thin posterior lens capsule. The... read more ), and vary by age of onset, rate of progression, and original site of cataract formation. Other causes include diabetes mellitus (the second most frequent group of cataract surgeries in the dog), malnutrition, radiation, inflammation, and trauma. In cats and horses, most cataracts are secondary to anterior uveal inflammation. Most reported inherited cataracts in cats are in young animals. Population studies on cataracts in cattle, rabbits (laboratory and pet), and guinea pigs suggest spontaneous cataracts occur not infrequently, but these species infrequently become blind.
In dogs, cataracts that are secondary related to diabetes mellitus are increasingly common; these cataracts represent the second largest group of cataracts operated on in dogs in the USA. The increased blood glucose causes intralenticular sorbitol to accumulate, which increases the osmotic forces of the lens, causing the lens to imbibe water and result in fiber swelling, rupture, and death. Typically, these cataracts develop rapidly and can occasionally rupture the equatorial or posterior lens capsule. Cataract surgery appears to yield the same success rate as for inherited cataracts in dogs. Other ocular sequelae of diabetes mellitus in dogs are occasional small retinal hemorrhages, presumed corneal neuropathy, and reduced corneal sensitivity. Cats seem quite resistant to diabetic cataract formation, perhaps associated with lower aldose reductase activity than in dogs.
Sight may be regained in some young dogs, cats, and horses when cataracts undergo sufficient spontaneous resorption; congenital nuclear cataracts in young animals may reduce in size with growth of the lens to permit restoration of vision as the animal matures. Animals with immature and incomplete cataracts may benefit from topical ophthalmic atropine 2–3 times/wk, which allows vision around a central or nuclear cataract. However, the only definitive therapy for cataracts is surgical removal of the lens. In dogs and horses, cataract extraction, often by phacoemulsification and with intraocular lens implantation, yields best results when performed before cataract maturation is complete and lens-induced uveitis (due to leakage of lens material) is established. Lens-induced uveitis is intensified by cataract surgery and contributes substantially to postoperative complications. In animals in which cataract surgery is not performed, continued clinical monitoring is important. The secondary lens-induced anterior uveitis often requires longterm monitoring and repeated tonometry, with occasional corticosteroid and mydriatic therapy. Secondary glaucoma and phthisis bulbus formation are possible complications.
Lens displacement (subluxation, anterior or posterior luxation) occurs in all species but is common as a primary inherited defect associated with the ADAMTS17 mutation in several terrier breeds. Complete displacement into the anterior chamber produces acute signs and frequently is accompanied by glaucoma and corneal edema. Treatment is surgical removal by phacoemulsification or intracapsular lens extraction. Posterior displacement into the vitreous cavity is asymptomatic or associated with ocular inflammation or glaucoma. Subluxated lenses are recognized by an aphakic crescent and trembling or instability of the iris (iridodonesis) and lens (phacodonesis). The decision to remove subluxated lenses is based on the severity of ocular disease that can be attributed to the lens displacement. Lens displacements also can be produced by trauma, enlargement of the globe with glaucoma, and degenerative zonular changes with hypermature cataracts. Procedures to remove the lens for lens displacement are associated with higher levels of postoperative complications of glaucoma and retinal detachment.