Surgery is the only proven and reliable, effective way to restore vision lost due to cataracts. For clinical anatomy, it is useful to think of the lens like a peanut M&M: composed of the “candy shell” capsule, the “chocolate” cortex, and the “peanut” dense nucleus. The lens cells are elongate, spanning from the front to the back of the lens, meeting at the “sutures.” After being produced at the equator, lens cells are sequentially compressed in to the lens center by new growth, making the nucleus denser with age (nuclear sclerosis). Lens protein is highly antigenic. The lens focuses images on the retina. To do that, it must be transparent and in the proper position: suspended in place (behind the iris and centered in the pupil) by the lens zonules. A cataract is any opacity within the lens. Such opacities occur due to disruption of the normally orderly lamellar arrangement of the lens cells, and, in varying degrees, cause blurred vision or blindness when severe. Despite this potential visual impairment, even with a complete cataract, the pupil should have normal resting size and react normally to light. Retro-illumination is useful to evaluate for subtle or posterior cataracts. While in the dark, from arm’s distance away with a focal light source, use the tapetal or red reflex to backlight the lens. Lens opacities will block the reflex and appear as dark lesions. Evaluation with a slit beam (creating an optic cross section) may further localize a cataract within the lens. Cataracts maybe classified by etiology, size, location within the lens, and age of onset. Bilateral nuclear sclerosis with senile incipient equatorial cortical cataracts in left > right eye.Photos courtesy Kathryn A. Diehl Common etiologies Inherited/genetic is the most common cause of cataracts in dogs. They occur in many breeds, some with a classic appearance. One common example is triangular incipient posterior polar cataracts of retrievers, as well as many other large-breed dogs. Diabetes mellitus is a common cause of canine cataracts; while it is rare in diabetic cats. Diabetic cataracts are usually bilateral, complete, develop rapidly, and cause vision loss. In a hyperglycemic state, normal glucose metabolism by hexokinase is overwhelmed and is shifted to the enzyme aldose reductase and a pathway that produces sorbitol. Sorbitol is a large, osmotically active molecule, and its accumulation in the lens cells leads to swelling and rupture, with associated lens opacity, and sometimes intumescence or even capsule rupture. Uveitis/vitritis of any cause (systemic or ocular) is the most common cause of cataracts in cats and horses. Additionally, significant cataracts may actually cause (phacolytic) uveitis via aberrant exposure of the eye to antigenic lens protein. It is important to look for hallmarks of inflammation, including anterior chamber flare, posterior synechiae (adhesions of the iris to the lens), and iris hyperpigmentation. Eyes with cataracts in this category are poorer candidates for cataract surgery due to increased risk of post-operative complications. Trauma may cause cataracts through uveitis. Sharp trauma causes cataracts via direct lens fiber disruption. For cataracts caused by penetrating trauma, capsule integrity must also be considered as lens capsule tears larger than about 1.5 mm pose an additional problem. These generally will not self-seal, and this can lead to severe lens-induced uveitis that is refractory to treatment (phacoclastic). Treatment is, therefore, more urgent cataract surgery; not only to address the lens opacity, but also, and almost more importantly, to remove the inflammatory-inciting leaking lens material from the eye before secondary complications occur. In cats, lens capsule damage is associated with the risk of post-traumatic sarcoma, thus, especially with sharp traumatic cataracts, long-term close monitoring and ultimately possibly enucleation over cataract surgery is warranted. Nutritional cataracts may occur in orphaned or nutritionally supplemented puppies (as well as some other species) fed milk replacer due to amino acid deficiency. Some ophthalmologists advocate adding beef or liver baby food to the milk replacer to reduce this risk. Milk replacer-related cataracts typically occur bilaterally at the nuclear-cortical junction, and, fortunately, usually don’t progress. Senile/degenerative cataracts are incredibly common in older dogs with cumulative damage to the lens cells (by UV light radiation, free radicals, etc.), but fortunately rarely affect vision and, thus, are often benignly neglected. They are often wedge-shaped and located at the equatorial cortex. Toxic cataracts may occur after exposure to certain drugs, most notably though infrequent and not well described, ketoconazole. Toxic cataracts may also occur secondary to exposure to “natural” toxins, such as those in the aqueous humor with uveitis, or in the vitreous from posterior uveitis, or dying retinal cells. The latter is common in dogs with progressive retinal atrophy (PRA) and is important to recognize, as these patients are not good surgical candidates. This cause of cataracts is one major reason for performing electroretinograms to assess retinal function before cataract surgery is performed. If the function is abnormally low, surgery may not be indicated to remove the opaque lens because the visual impairment is also (without treatment options available), retinally based. Aberrant retention of fetal vasculature that normally regresses by soon after birth (which may be inherited or a random developmental “hiccup”), may result in cataracts (usually congenital) if it contacts the lens. Examples include iris to lens persistent pupillary membranes (ppms) anteriorly and persistent hyaloid artery (potentially with bleeding into the lens) posteriorly. Infection within the lens may occur via septic implantation during penetrating trauma. This may result in cataract formation and progression even years after the inciting incident. The most common example of this scenario is after penetrating cat scratch trauma. In rabbits, Encephalitozoon cuniculi (usually through intrauterine transplacental vertical transmission though spore ingestion or even inhalation is possible) or Pasteurella may infect the lens and or iris forming an abscess/granuloma and associated cataract, as well as uveitis. E. cuniculi lens abscessation and cataract has also been described in cats (rare). Left: Incomplete cataract, notice the yellow tapetal refex. Right: Complete cataract. Size Cataracts may be incipient: involving less than 10 percent of the lens volume and not typically affecting vision; incomplete (immature): involving greater than 10 percent of the lens volume but not the entire lens—sometimes further subdivided into early and late incomplete cataracts and variably affecting vision; or complete (mature): involving the entire lens and almost always associated with visual impairment. Resorbing (hypermature) cataracts are starting to liquefy. Cataract resorption often occurs with chronicity but also in very rapid-onset and progressive cataracts. Hallmarks of resorbing cataracts include a sparkly appearance, wrinkling of the anterior lens capsule, a deep anterior chamber and sometimes-decreased lens thickness. As lens resorption and leakage of lens proteins through the lens capsule often causes phacolytic lens-induced uveitis, other signs to look for are those associated with intraocular inflammation. Intumescent cataracts are those where the lens physically swells. This shallows the anterior chamber and may cause intraocular pressure elevation. It can also result in rupture of the lens capsule and then phacoclastic uveitis. This type of cataract is most commonly associated with diabetes (rapid onset osmotic cataract). Location within the lens Penetrating traumatic cataract with uvetis. Note: there is a penetrating corneal wound with edema laterally. The pupil has been pharmcologically dilated. An incomplete or smaller cataract can occupy a focal region within the lens. During examination, the location of lens opacities is best determined using a slit beam to create an optic cross section, highlighting the anterior and posterior lens capsule with bright, convex and concave, respectively, lines of light, and then assessing relative depth and position of lesions. Cataracts may be capsular, cortical, or nuclear. Age of onset Cataracts may be congenital (present at birth), juvenile (commonly inherited), or senile (occurring after about 6 to 10 years of age). Nuclear sclerosis is normal age-related “opacification” of the nucleus associated with increased density due to lens fiber growth around and compressing it throughout life. In dogs and cats, this starts to be visible at around age eight to 10 years, and gets denser with further age. In humans, it begins at around age 40 and results in decreased accommodative ability and presbyopia. In veterinary patients with different vision and visual demands, nuclear sclerosis should be differentiated from true cataract, which is possible unless the nuclear sclerosis is very advanced. With nuclear sclerosis, vision is not usually affected, the tapetal reflex is still present, and the fundus can be visualized. Additionally, differentiating nuclear sclerosis from cataract is often easier with pupil dilation, which allows visualization of the clear(-er) cortical halo around the dense central nucleus. Medical therapy There have been some aggressively marketed topical therapies touted to “melt away” cataracts. These are generally antioxidants, specifically N-acetyl carnosine and other ocular health vitamin supplement agents. In controversial studies, some did decrease lens opacity of nuclear sclerosis. However, they do not slow progression of significant cataracts that actually warrant treatment due to their visual impact. Ocu-GLO might be a more worthwhile oral nutraceutical containing a combination of ocular and immune health antioxidant ingredients and formulated specifically for dogs and cats. It is probably most indicated to potentially delay progression of degenerative retinal diseases (e.g., PRA), and will not reduce existing lens opacities but might delay progression of such. A more promising potential medical therapy is aldose reductase inhibitors, which delay onset and severity of diabetic cataracts. Unfortunately, these drugs are not commercially available for use at this time. Cataract surgery Surgery is the only proven and reliable, effective way to restore vision lost due to cataracts. Surgery employs advanced training, an ophthalmic operating microscope and instrumentation, and phacoemulsification or ultrasound energy to break up the opaque lens. The most important potential complications of surgery include retinal detachment and glaucoma. Other possible issues include infection; corneal ulceration, chronic and refractory uveitis; and especially in young dogs, lens fiber regrowth. Postoperative therapy is as important as what happens in surgery—it entails initially intense, slowly tapered topical and systemic anti-inflammatory medications, and frequent monitoring. Because the inflammatory response of dogs to cataract surgery is dramatic, afterwards months are spent controlling it. Many patients remain on some level of topical therapy and monitoring long term. Cataract surgery may not be elected or the patient may not be a candidate, etc. In these cases, it is still indicated to monitor and treat any lens-induced uveitis to decrease the risk of discomfort. In terms of visual impairment, if only one eye is affected, most veterinary patients function well. Fortunately, even most blind dogs adapt well, especially when their vision loss is gradual or given time to adjust when it is rapid. Ideally, their environments should be kept as stable as possible to help them adjust and cope. THE PERFECT PATIENT The ideal veterinary candidate for cataract surgery: Is systemically healthy or at least regulated/stable (diabetes, allergies, periodontal disease, etc.). Is a manageable patient; intensive post-operative medical therapy and follow-up are vital to success. The patient, client, and veterinary ophthalmologist must be able to tolerate this! Has vision affected by cataract/is impaired or functionally blind at least in the affected eye(s), making the potential benefit/gain of surgery worth the cost/risks. Has a healthy ocular surface (tear film and cornea) and normal intraocular pressure. Does not have uveitis, or it is controlled. Previous or refractory intraocular inflammation poses an increased risk of post-operative complication(s). Has no significant lens resorption; this significantly increases the risk of retinal detachment. Has a normal electroretinogram (ERG) (assessing retinal function) and ocular ultrasound (normal lens shape and capsule), non-degenerate vitreous (as when present slightly increases the risk of retinal detachment), and no pre-existing retinal detachment. Direct examination to evaluate the vitreous and fundus/retina would be precluded by the cataract. Kathryn A. Diehl MS, DVM, DACVO, earned her master’s and veterinary degrees at the Ohio State University, then completed a small animal rotating internship at the University of Georgia. She went on to complete a residency in comparative ophthalmology and cellular biology fellowship at the University of Wisconsin. Subsequently, Dr. Diehl worked in academia at the University of Minnesota and Auburn University, as well as in private specialty practice. She is currently an associate professor of comparative ophthalmology at the University of Georgia.
