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 and the normal increase in nuclear density (nuclear sclerosis) that occurs in older animals.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 Ophthalmology: Inherited Cataracts in Domestic Animals). Other etiologies include diabetes mellitus, 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.

Nuclear sclerosis, dog

Cataract, American Cocker Spaniel

Cataract, rat

Cataracts, guinea pig

Table 2
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Inherited Cataracts in Domestic Animals Breed Age of Onset Initial Localization Mode of Inheritance Dogs Afghan Hound 6–12 mo Equatorial/posterior cortex Autosomal recessive American Cocker Spaniel 1–6 yr Posterior/anterior cortex Autosomal recessive polygenetic Australian Shepherd 2–4 yr Posterior cortex Autosomal dominanta Bichon Frise Cataract, Bichon Frise 2–6 yr Posterior/anterior cortex Autosomal recessive Boston Terrier Congenital or juvenile Late onset Posterior sutures/ nuclear Equatorial/anterior cortex Autosomal recessivea Autosomal recessive Chesapeake Bay Retriever ≥1 yr Nuclear/cortex Incomplete dominant Entelbucher Mountain Dog 1–2 yr Posterior cortex Autosomal recessive German Shepherd ≥ 8 wk Posterior sutures/ cortex Incomplete dominant Golden Retriever Cataract, Golden Retriever ≥ 6 mo Posterior subcapsular (triangular) Incomplete dominant Labrador Retriever ≥ 6 mo Posterior subcapsular (triangular) Incomplete dominant Havanese 2–6 yr Posterior/anterior cortex Possible autosomal recessive Congenital cataract, Miniature Schnauzer Miniature Schnauzer Congenital ≥ 6 mo Nuclear/posterior cortex Posterior cortex Autosomal recessive Autosomal recessive Norwegian Buhund ≥1 yr Nuclear/cortex Autosomal dominant Old English Sheepdog Congenital Nuclear/cortex Autosomal recessive Rottweiler ≥10 mo Posterior polar/complete Unknown Siberian Husky Cataract, Siberian Husky ≥ 6 mo Posterior subcapsular/ posterior sutures Autosomal recessive Staffordshire Bull Terrier ≥ 6 mo Posterior sutures/ cortex Autosomal recessivea Standard Poodle ≥1 yr Equatorial cortex Autosomal recessive Welsh Springer Spaniel Congenital Nuclear/posterior cortex Autosomal recessive West Highland White Terrier Congenital Posterior sutures Autosomal recessive Horses Belgian Congenital Nuclear/cortex Autosomal dominant Morgan Congenital Nuclear Autosomal dominant Cattle Holstein-Friesian Congenital Nuclear/cortex Autosomal recessive Jersey Congenital Nuclear Autosomal recessive Sheep New Zealand Romney Congenital Anterior/posterior cortex Autosomal dominant a Associated with mutations in HSF4 gene. a Duplicate figures represent different reports for that species. Inherited Cataracts in Domestic Animals Breed Age of Onset Initial Localization Mode of Inheritance Dogs Afghan Hound 6–12 mo Equatorial/posterior cortex Autosomal recessive American Cocker Spaniel 1–6 yr Posterior/anterior cortex Autosomal recessive polygenetic Australian Shepherd 2–4 yr Posterior cortex Autosomal dominanta Bichon Frise Cataract, Bichon Frise 2–6 yr Posterior/anterior cortex Autosomal recessive Boston Terrier Congenital or juvenile Late onset Posterior sutures/ nuclear Equatorial/anterior cortex Autosomal recessivea Autosomal recessive Chesapeake Bay Retriever ≥1 yr Nuclear/cortex Incomplete dominant Entelbucher Mountain Dog 1–2 yr Posterior cortex Autosomal recessive German Shepherd ≥ 8 wk Posterior sutures/ cortex Incomplete dominant Golden Retriever Cataract, Golden Retriever ≥ 6 mo Posterior subcapsular (triangular) Incomplete dominant Labrador Retriever ≥ 6 mo Posterior subcapsular (triangular) Incomplete dominant Havanese 2–6 yr Posterior/anterior cortex Possible autosomal recessive Congenital cataract, Miniature Schnauzer Miniature Schnauzer Congenital ≥ 6 mo Nuclear/posterior cortex Posterior cortex Autosomal recessive Autosomal recessive Norwegian Buhund ≥1 yr Nuclear/cortex Autosomal dominant Old English Sheepdog Congenital Nuclear/cortex Autosomal recessive Rottweiler ≥10 mo Posterior polar/complete Unknown Siberian Husky Cataract, Siberian Husky ≥ 6 mo Posterior subcapsular/ posterior sutures Autosomal recessive Staffordshire Bull Terrier ≥ 6 mo Posterior sutures/ cortex Autosomal recessivea Standard Poodle ≥1 yr Equatorial cortex Autosomal recessive Welsh Springer Spaniel Congenital Nuclear/posterior cortex Autosomal recessive West Highland White Terrier Congenital Posterior sutures Autosomal recessive Horses Belgian Congenital Nuclear/cortex Autosomal dominant Morgan Congenital Nuclear Autosomal dominant Cattle Holstein-Friesian Congenital Nuclear/cortex Autosomal recessive Jersey Congenital Nuclear Autosomal recessive Sheep New Zealand Romney Congenital Anterior/posterior cortex Autosomal dominant a Associated with mutations in HSF4 gene. a Duplicate figures represent different reports for that species.

In dogs, cataracts that are secondary related to diabetes mellitus are increasingly common. The elevated blood glucose causes intralenticular sorbitol to accumulate, which increases the osmotic forces of the lens, causing the lens to imbibe water and resulting in fiber swelling, rupture, and death. Typically, these cataracts develop rapidly and can occasionally rupture the 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.

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, 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, and 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 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.

Lens subluxation, dog

Anterior lens luxation, dog

Last full review/revision July 2011 by Kirk N. Gelatt, VMD