Cataracts may occur at any age and in any location in the lens. Location may predict progression risk. Cataracts partially or completely block tapetal reflection and fundic examination and are often classified by stage of maturation and cause.

• Incipient (Figure 1): <15% lens volume. Tapetal reflection is minimally obstructed. Visual deficits are not apparent.
• Immature (Figure 2): 15% to 99% lens volume. Tapetal reflection is still visible but varies with the degree of cataractous lens. Visual impairment is variable, from minimal to near-complete blindness. Note that partial tapetal reflection and vision may be restored during cortical resorption in hypermature cataracts. This can confound the distinction between hypermature and immature cataracts.
• Mature (Figure 3): 100% lens volume with no resorption. No tapetal reflection is visible. Eyes are blind but retain dazzle reflex and pupillary light reflexes (PLRs) if the retina is functional.
• Hypermature (Figure 4): Resorption is present and produces a wrinkled anterior lens capsule with white plaques and multifocal sparkling. Phacolytic uveitis is common.
• Morgagnian: Resorption and liquefaction of lens cortex with ventrally positioned (ie, dependent) nucleus. Vision may return.

Primary cataracts have a genetic basis and occur without exogenous insult or metabolic disease. They frequently occur bilaterally and are typically symmetrical. Clinicians should consult the literature for specific appearance in at-risk breeds and inform breeders of suspected primary cataracts to prevent perpetuating the heritable condition.

Heritable cataracts are the most common presentation in dogs and may occur in juvenile or adult dogs of many breeds. Bilaterally symmetrical cataracts with a hallmark, breed-related appearance and/or location in a young-to-middle-aged purebred dog are diagnostic. Progression varies among breeds and individual patients. Few breeds have proven mechanisms of inheritance or genetic tests available. Consulting the literature is recommended, as is examination of the patients parents and littermates when possible.

Some congenital cataracts are primary and inherited, as exemplified in some breeds (eg, miniature schnauzer, Boston terrier). Parents and littermates should be examined when possible.

These cataracts occur secondary to exogenous insult or concurrent disease processes (ocular or systemic). Categories include diabetic, uveitic, hypocalcemic, degenerative, traumatic, nutritional, radiation-induced, and toxic.

Diabetic cataracts are the second most common cataracts in dogs. With hyperglycemia, sorbitol accumulates in the lens and causes osmotic draw and disruption of lens fibers. Diabetic cataracts begin as vacuoles at the equator and are most easily visible following pharmacologic dilation, then progress quickly and become swollen. They can produce visible Y sutures and phacolytic uveitis and create risk for lens capsule rupture. In a historical or undiagnosed diabetic patient, acute-onset blindness with eyes concurrently clouding over is a classic presenting complaint. Most diabetic dogs (75%) develop cataracts within 6 to 12 months of disease onset, even when regulated.³ Dogs with acute cataract development should be screened for diabetes mellitus.

Intraocular inflammation of any cause can result in cataract development. All cataracts, regardless of cause, may cause phacolytic uveitis. This can make it difficult to determine whether a cataract is the cause or result of uveitis. If uveitis preceded cataractogenesis, systemic diagnostics are warranted. It is important to rule out neoplastic, infectious, and inflammatory diseases.

Hypocalcemic cataracts commonly occur secondary to metabolic disease (eg, primary hypoparathyroidism) rather than nutritional deficiency. These cataracts present as classic multifocal white pinpoints or as a field of stars within the lens cortices. In 1 study, cataractogenesis occurred in 32% of hypocalcemic dogs with primary hypoparathyroidism.⁴ Care should be taken not to mistake asteroid hyalosis in the vitreous for hypocalcemic cataracts, as both are multifocal and star-like.

As in humans, age-related cataracts develop in dogs. Appearance and progression of degenerative cataracts is variable, and diagnosis is based on exclusion and signalment. Differentiation between genetic and degenerative cataracts is rarely possible. For large breeds, degenerative cataracts should be suspected in patients 6 years of age; for small breeds, degenerative cataracts should be suspected in patients >10 years of age.¹

Cataracts can result from penetrating trauma from a sharp object (eg, cat claw, plant thorn). Severe uveitis secondary to blunt trauma, corneal trauma, or foreign material in the anterior chamber can also cause cataract development. A small rent in the lens capsule can cause a focal cataract and then self-seal with no or minimal progression. However, in some animals, severe uveitis may occur after a period of quiescence. This indicates septic implantation syndrome, which occurs when bacteria are implanted in the lens during the initial injury. A large lens capsule tear may occur with sharp penetrating trauma, most commonly a cat claw. This often results in severe, intractable (ie, phacoclastic) uveitis and often necessitates enucleation. Cataracts can also result from electrocution secondary to a lightning strike or chewing wires.

When fed exclusively, inappropriate milk replacers that are amino acid-deficient may cause cataracts in puppies. Because of their neonatal onset, nutritional cataracts are most often isolated to the nucleus, at least initially. Thorough history and littermate examination is essential. Supplementation with dams milk or appropriate puppy milk replacer can prevent cataract formation and progression. Once the puppy is on a balanced puppy food diet, nuclear cataracts will often condense as new lens fibers are laid down.

If eyes are in the exposure field during radiation therapy, cataracts may form 6 to 12 months after insult.⁷ A thorough history is essential. Other signs (eg, conjunctivitis, keratoconjunctivitis sicca [KCS], keratitis, retinopathy) may also occur secondary to radiation.

During retinal degeneration, progressive retinal atrophy (PRA), and retinal detachment, dying photoreceptor cells are hypothesized to produce toxic aldehyde metabolites that progressively damage the lens.⁸ However, in at-risk breeds, concurrent cataracts and PRA may represent 2 separately inherited diseases occurring together. Certain medications (eg, ketoconazole administered at high doses,⁹ dimethyl sulfoxide used long-term¹⁰) may cause lenticular damage. Identifying retinal degeneration is difficult when fundic examination is impaired. Thus, pre-operative screening with an electroretinogram is essential before cataract surgery, as phacoemulsification will not restore vision without a functional retina.

Cataract location within the lens may provide clues about cause and risk for progression. Accurately describing a cataracts location in medical records also helps track progression over time.

• Subcapsular: Within the cortex, adjacent to the anterior or posterior lens capsule. These cataracts are frequently heritable and variably progressive.
• Cortical: Within the anterior or posterior cortex, potentially both. Progressive cataracts in any location eventually expand into the cortex.
• Equatorial: At the lens periphery, closest to the lens zonules. Typically progressive, as lens growth is active at the equator. Diabetic cataracts begin as equatorial vacuoles.
• Nuclear: Within the lens nucleus. Almost always congenital or neonatal (primary or secondary). Nuclear cataracts rarely progress.