Diseases of the Lens

Chapter 135 Diseases of the Lens



David A. Wilkie



ANATOMY


The normal canine and feline lens is composed of an outer capsule, epithelial cells beneath the anterior capsule, and lens fibers formed by the migration of epithelial cells to the lens equator, where the cells elongate and create a regular arrangement of fibers. The regular arrangement of these fibers accounts for the transparency of the lens. The lens is posterior to the iris, anterior to the vitreous to which it is attached, and suspended by zonules, which arise from the ciliary body and attach to the lens capsule at the equator (see Fig. 131-1).



CONGENITAL ANOMALIES



Etiology


Lens development takes place early in embryogenesis and is complete in the dog by day 30 of gestation. Any genetic abnormality affecting lens development or any insult to the bitch or queen early in gestation, including infectious, nutritional, chemical, or drug related, can result in congenital lens anomalies. These abnormalities are often associated with other congenital ocular anomalies, including microphthalmia (small globe), persistent pupillary membranes, persistent hyaloid artery, retinal dysplasia, retinal detachment, posterior coloboma or staphyloma, and optic nerve hypoplasia.



Clinical Signs


Examples and features of congenital lens anomalies include the following:



• Microphakia (small lens)—With the pupil dilated, the equator of the lens and fine zonules, attaching at the equator and originating from elongated ciliary processes, are visible. The lens may also be luxated.

• Coloboma (notch defect)—With the pupil dilated, a notch defect may be visible in any quadrant of the equatorial zone, with or without zonular attachments.

• Cataract—See the cataract discussion in this chapter.

• Lens luxation—Often associated with microphakia (see discussion in this chapter).


Diagnosis



• Clinical signs (see previous section).

• Present at birth. Microphakia and coloboma are always congenital. Cataract and lens luxation, unless associated with microphakia, may not be congenital. An accurate history and early examination are helpful in differentiating congenital from acquired abnormalities.


Treatment



• Determine concomitant ocular anomalies and their significance to vision.

• Microphakia and coloboma alone require no treatment.

• Cataract, if impairing vision, may be amenable to surgical removal once the integrity of the retina and optic nerve has been ascertained by fundic examination, electroretinogram, ocular ultrasound, and visual-evoked potential.

• Remove a luxated lens if it is inciting uveitis and/or glaucoma, impairing vision, or interfering with corneal endothelial cell function.


Prevention


Congenital anomalies are not necessarily inherited anomalies. Careful inquiry into affected littermates and prevalence of problems in previous matings may raise the suspicion for an inherited defect. If the cause of the abnormality cannot be determined, discourage the use of this and related animals for breeding.



CATARACT



Etiology


Cataract is an opacity of the lens resulting from pathologic changes in lens protein composition or disruption of lens fiber arrangement.




Key Point


Cataract must be distinguished from nuclear sclerosis. Nuclear sclerosis is a normal aging change seen in all dogs and cats 6 years of age or older, produced by compression of central lens fibers.


Etiologies of cataract development include the following:



• Hereditary—This is the most common cause of cataract in the dog (Table 135-1). Location, progression, and mode of inheritance of cataracts vary among breeds. The majority of inherited cataracts are bilateral but often asymmetrical in onset and progression.

• Inflammatory—This is a common cause of cataract in the cat. Because the lens needs the aqueous and vitreous humors for nutrition and removal of metabolic wastes, intraocular inflammation can result in capsular and cortical opacities. Posterior synechia from anterior uveitis can result in anterior capsular cataracts.

• Metabolic—Diabetes mellitus in dogs frequently results in rapid (days to weeks) onset of bilateral cataracts because of a shift in metabolic pathways, an accumulation of sorbitol causing an osmotic gradient, and a subsequent disruption of lens fibers. The cataracts are irreversible.

• Degenerative—Cataracts may occur secondary to chronic retinal degeneration or chronic glaucoma.

• Traumatic—Severe blunt trauma to the eye can result in cataract formation from concussive effects or can be secondary to inflammation and/or lens luxation. Penetrating injuries that puncture the anterior lens capsule (e.g., cat claw injuries) result in a focal or diffuse cataract, depending on the severity of the capsular tear. Uveitis may occur secondary to rupture of the lens capsule.

• Nutritional—Puppies and kittens hand fed exclusively milk-replacement formula that is deficient in required amino acids, the most frequently cited being arginine, can develop bilateral cataracts.

• Toxic—Electric shock, radiation therapy involving the ocular region, and certain drugs have been reported to cause cataracts.


Table 135-1 BREED LIST OF INHERITED OR FAMILIAL CATARACTS IN THE DOG


Data from: Rubin LF: Inherited Eye Diseases in Purebred Dogs. Baltimore: Lippincott Williams & Wilkins, 1989.


Afghan hound


Alaskan malamute


Beagle


Bedlington terrier


Belgian Tervuren


Bernese mountain dog


Bichon frisé


Border collie


Border terrier


Borzoi


Boston terrier


Bouvier des Flandres


Cairn terrier


Cavalier King Charles spaniel


Chesapeake Bay retriever


Cocker spaniel


Collie


Curly-coated retriever


Dachshund


English cocker spaniel


English springer spaniel


English toy spaniel


Field spaniel


French bulldog


German shepherd


German shorthaired pointer


Giant schnauzer


Golden retriever


Great Dane


Ibizan hound


Irish setter


Irish water spaniel


Irish wolfhound


Italian greyhound


Keeshond


Kerry blue terrier


Labrador retriever


Lakeland terrier


Lhasa apso


Manchester terrier


Miniature pinscher


Miniature schnauzer


Norfolk terrier


Norwegian elkhound


Norwich terrier


Old English sheepdog


Papillon


Pembroke Welsh corgi


Pointer


Pomeranian


Poodle (toy, miniature, standard)


Puli


Rhodesian ridgeback


Rottweiler


Saint Bernard


Samoyed


Schipperke


Scottish terrier


Siberian husky


Silky terrier


Staffordshire bull terrier


Standard schnauzer


Tibetan terrier


Welsh springer spaniel


Welsh terrier


West Highland white terrier


Whippet


Wirehaired fox terrier


Yorkshire terrier



Clinical Signs and Diagnosis




Key Point


For a thorough examination of the lens, mydriasis is mandatory because some of the most significant changes occur in the extreme periphery (equatorial zone) or posterior cortex of the lens. Topical tropicamide 1% (Mydriacyl, Alcon) results in mydriasis in 15 to 20 minutes and lasts 6 to 8 hours. An inexpensive, monocular biomicroscope will facilitate examination of the lens and aid determination of location and depth of lesion (see Chapter 131).

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Diseases of the Lens

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