Ординатура / Офтальмология / Английские материалы / Slatter's Fundemental of Vetrinary Ophthalmology 4th edition_Maggs, Miller, Ofri_2008

synechia (adherence of the iris to the anterior lens capsule) is a further complication of the anterior uveitis. It may lead to secondary glaucoma, and even if the adhesions resolve, residual iris pigment will usually be left on the anterior lens capsule.

Nutritional cataracts are caused by use of inappropriate milk-replacement formulas in young animals. In dogs and cats, such cataracts are due to a deficiency in essential amino acids in the formula. They do not progress to maturity and in fact may even regress. Most nutritional cataracts have a minimal effect on vision and do not require surgery. The opacities are located in the equatorial and posterior subcapsular regions. Similar cataracts have been observed in wolf cubs. Because the cataracts are thought to be most common if the pup is totally deprived of the dam’s milk or is fed replacement milk during the first week of life, it has been proposed that these cataracts can be controlled by limiting feeding of replacements and increasing the use of the dam’s milk during this first week of life.

Nutritional cataracts also develop in orphaned kangaroos and wallabies fed cow’s milk (Figure 13-17). These galactosemic cataracts form because of the animal’s inability to break down the galactose and lactose in the replacement cow’s milk. These molecules are therefore diverted into the sorbitol pathway (see later discussion of diabetic cataracts). Unlike the nutritional cataracts in dogs and cats, the resulting galactosemic cataracts progress to maturity, causing loss of vision. Furthermore, the surgical prognosis for these cataracts is poor owing to severe postoperative uveitis and opacification of the vitreous in affected animals.

Nutrition has also been implicated in cataracts that develop in fish raised in hatcheries, although other husbandry conditions (e.g., oxygen and light levels, excessive handling and agression) may also play a role in the pathogenesis. Another common cause of cataracts (in wild and farmed fish) is parasitic infection. Numerous species of fish throughout the world are affected by different species of trematode larvae that enter the lens and cause cataract. The fish is an integral part of the life cycle and is usually eaten by a bird in the next phase, so presumably the blindness increases the likelihood of the fish’s being caught and eaten by a bird. Infections have also been implicated in the pathogenesis of cataracts in poultry; spontaneous cataracts have been observed in turkeys and in chickens with avian encephalomyelitis and Marek’s disease. Encephalitozoa cuniculi infection has been implicated in the pathogenesis of cataract, and lens capsule rupture, in rabbits.

LENS 267

Radiated energy may cause cataracts by affecting dividing cells in the equatorial area. Use of megavoltage x-radiation to treat tumors of the nasal cavity caused cataracts in 28% of canine patients, whereas b-radiation radiotherapy treatment of intraocular tumors resulted in a 3% incidence of cataracts. Use of laser to treat glaucoma (cyclophotocoagulation) may also cause cataract in some patients.

Cataracts may also be caused by other insults to the dividing cells in the equator. These are usually due to toxicity, and numerous compounds and drugs have been shown (in toxicology studies) to cause cataracts in animals. However, most of these agents were used in high, nontherapeutic doses. An exception may be ketoconazole, which causes bilateral, progressive cataracts after long-term administration in dogs. Another type of possible “toxic” cataract is one that may result from concomitant retinal dystrophy. It has been postulated that toxic substances released by the degenerating retina cause cataracts in dogs, thus accounting for the common presentation of progressive retinal atrophy and cataract in the same patient. However, this pathogenesis, and the association between these two diseases, remains unproven and controversial in the dog, and it is possible that such eyes are affected by two separate diseases.

Senile Cataracts

Senile cataracts are part of the aging process and occur in both animals and humans. These lesions are frequently preceded by the formation of a dense nuclear sclerosis. Opaque streaks extend from the nucleus toward the cortical equator like spokes of a wheel. Opacification progresses to involve the entire lens, resulting in a mature cataract (see Figure 13-13). However, progression of senile cataracts is extremely slow, and it may take years for the cataract to reach total maturity.

A recent study reported that by age 13.5 years, all dogs examined had some degree of cataract. According to the authors, the age at which half the animals are affected by cataracts is 9.4 years in the dog, compared with 12.7 years in the cat and 28.3 years in the horse, thus demonstrating a correlation between prevalence of cataracts and longevity. However, it should be noted that senile cataracts are a controversial subject in veterinary ophthalmology, with some authorities claiming that they are in fact late-onset inherited cataracts. Other writers counter that the initial location of the opacity and the differences in the rate of progression distinguish these two entities. Largescale studies of elderly canine populations are needed to resolve the issue.

Diabetic Cataracts

lenticular cells, which leads to the formation and accumulation of sorbitol, fructose, and dulcitol in the lens. The resulting hyperosmolarity of the lens leads to fluid ingress. Initial changes include vacuole formation along the equatorial cortex that progresses to the anterior and posterior cortex (see Figure 13-12). As more fluid enters the lens and the cataract matures, it may swell dramatically, a phenomenon known as an intumescent cataract. The swollen lens may push the iris forward, resulting in a shallow anterior chamber and a narrowed iridocorneal angle, thus predisposing the animal to glaucoma. Because of the role of aldose reductase in the formation of diabetic cataracts, studies are underway to reduce their incidence and severity using aldose reductase inhibitors.

Diabetes is not an impediment to cataract surgery as long as the animal can withstand the anesthesia. Results of surgery in diabetic dogs are good, though postoperative medications (which usually include glucocorticosteroids) have to be replaced by nonsteroidal antiinflammatory drugs (NSAIDs).

Diabetic cataracts are rare in cats. This is because aldose reductase activity is significantly higher in cats younger than 4 years than in older cats. Because diabetes mellitus occurs primarily in older cats, the relatively low aldose reductase activity protects the lens of the elderly diabetic cat from cataract formation. Instead, diabetic cats may frequently suffer from retinal hemorrhages. However, these should not be confused with diabetic retinopathy, a complication of diabetes that leads to loss of vision in humans. The pathogenesis of the human disease involves retinal neovascularization that is not observed in cats.

Diagnosis

History

The extent of the visual deficits caused by cataract depends on the location and severity of the opacity. Small cataracts in the center of the visual axis interfere with vision through a small pupil but have less effect with a dilated pupil. Therefore owners of patients with centrally located cataracts often observe that the patient sees better under diminished light conditions (cloudy days, evenings, or inside buildings) than in bright sunshine. In diminished light the pupil dilates and the patient sees around the cataract.

The severity of the lens opacity also determines the effect on vision: Small vacuoles and opacities have minor effects. When the lens is diffusely opaque (immature cataract), sight is reduced. However, some vision is often maintained until both eyes are affected by mature cataracts. In most cases the patient is presented because the owner noted a change in behavior due to failing vision or total blindness (e.g., bumping into objects in unfamiliar surroundings, timidity or change in personality, inability to catch a ball). Such changes are more prominent when both eyes are affected (e.g., hereditary cataracts). In cases of unilateral disease (e.g., traumatic cataracts), behavioral visual deficits may be less obvious. Such patients may be presented due to a change in appearance of the eye itself (e.g., a white appearance that is more noticeable at night when the pupil is dilated).

It is also important to determine from the owner whether the animal has had poor night vision during cataract development. This feature may indicate that the patient is also suffering from progressive rod-cone degeneration. As noted previously, there is still a debate about whether such patients are suffering from two distinct hereditary diseases, or whether the cataract is

caused by noxious substances secreted by the degenerating retina. Breeds commonly affected by both cataracts and progressive rod-cone degeneration are the miniature poodle, Labrador retriever, and toy poodle. However, because the two diseases can occur in any breed, an assessment of retinal health cannot be made based on signalment and history. The retina must be examined ophthalmoscopically or electrophysiologically (see following sections) before cataract surgery. As mentioned, an “opposite history” (of poor daylight vision) occurs with an axial cataract and healthy retinas: The pupil becomes miotic in bright light, restricting light entrance through the small pupil to the opaque area of the lens.

Clinical Signs

Lens examination is part of a complete ophthalmic examination. The pupil must be dilated to enable adequate evaluation of the lens; if this is not done, peripheral cortical changes and capsular opacities near the equator may be overlooked. Pupil dilation also helps distinguish between nuclear sclerosis and “true” cataracts. Topical tropicamide (1%) administered immediately after the initial examination and repeated once in 5 to 10 minutes produces adequate mydriasis in most patients in 20 minutes. Both eyes must be examined, as each may be affected differently.

Routine evaluation can be adequately performed in a dark room using a focal examining light and binocular loupe. Light reflected back from the tapetum (retroillumination) is also most helpful, as any lens opacity will appear darker than the surrounding. In some dogs, slit-lamp examination reveals early and subtle changes that cannot be seen by a binocular loupe (see Table 13-2). Common sites for initial opacity development are at the equator, at anterior and posterior subcapsular areas, and along Y sutures (Figure 13-18). As noted, hereditary cataracts in each breed have a characteristic initial location as well as characteristic progression (e.g., from subcapsular opacities to nuclear involvement, or from equatorial vacuolation to cortical opacification). However, regardless of the location of the initial lesion, the opacity (with the exception of traumatic and secondary cataracts) most frequently will progress to immature and mature cataract (see Figures 13-11 to 13-13).

Nuclear

Lamellar

FIGURE 13-18. Classification of cataracts according to position within the lens. (Modified from Trevor-Roper PD [1984]: The Eye and Its Disorders. Blackwell Scientific, Oxford, England.)

Table 13-3 Cataract Prognosis in the Miniature

Schnauzer Based on Position of the Initial

Opacity

Modified from Gelatt KN, et al. (1983): Biometry and clinical characteristics of congenital cataracts and microphthalmia in the miniature schnauzer. J Am Vet Med Assoc 183:99.

Owners often ask how long it will take for the cataract to become mature and for total blindness to occur. With the exception of diabetic cataracts, which may progress rapidly to maturity (i.e., days to several weeks), this issue is most difficult to predict, although a rough estimate can sometimes be provided in breeds that have been thoroughly investigated (Table 13-3). This process may take months or longer.

As noted, breakdown and leakage of lens protein begins in mature cataracts but its extent is limited. The process is accelerated in hypermature cataracts. Signs of resorption are as follows:

•Small, shiny crystals and multifocal white plaques, resulting from protein breakdown, are visible in the lens.

•Deepening of the anterior chamber and a concave iris surface as the lens volume decreases; conversely, swelling of the lens in early cataract formation causes a shallow anterior chamber and a convex iris surface

•Decrease in lens diameter and thickness

•Corrugation of the anterior capsule

•Signs of LIU

The extent of the resorption varies with age. It will be limited in elderly patients and will rarely improve the patient’s vision. In young subjects it can be more extensive. As the lens becomes small, vision can be aided with mydriatics (1% atropine every 2 to 3 days). Complete resorption allows vision comparable to that after successful surgical lens removal (without IOL implantation). Lens removal is not performed in the presence of active uveitis or resorption.

LIU is a major cause of complications in cataract surgery. It can be assumed to be present in all patients with mature or hypermature cataract until proven otherwise. Early therapy for this uveitis and referral for treatment of the cataract are essential if optimal results are to be obtained.

Treatment

Medical Therapy

In the early stages of cataract, especially when the opacity lies on the visual axis, or in advanced stages of resorption, vision can be improved with the use of a mydriatic when required. Diabetic cataracts may be amenable to therapy with aldose reductase inhibitors. Studies have shown that both systemic and topical inhibitors can slow, halt, and perhaps reverse the progression of cataracts in diabetic patients. However, such drugs are still considered experimental.

As oxidation plays a role in the pathogenesis of cataracts, it has been proposed that antioxidants may halt and reverse pro-

LENS 269

gression of cataracts in dogs. Various systemic and topical agents, including selenium–vitamin E, orgotein (superoxide dismutase), zinc ascorbate, and carnosine, have been studied and marketed as “anticataract drugs,” most recently through Internet distributors. Many of these agents are marketed without supporting clinical and experimental data, whereas others have been evaluated only in vitro. The only clinical trial conducted to date in dogs has found a “marginal reduction” in lens opacity, which was clinically insignificant. Owners should not be misled into thinking that they can use drugs to cure their pet’s cataracts. On the contrary, such attempts at treatment will only delay professional care, thereby worsening any existing LIU and impacting gravely the prognosis of the inevitable surgery. While it is hoped that one day an effective medical treatment for cataracts will be discovered, at the time of writing all cataract patients should be referred for treatment of LIU and possible surgery.

Surgical Case Selection

Not all animals with cataract are suitable candidates for surgery. The following prerequisites should be fulfilled before cataract extraction is recommended:

1.The affected eye should have a significant visual deficit. Obviously the eye shown in Figure 13-11 does not require surgery. There is some debate among veterinary ophthalmologists regarding the stage (of maturity) at which surgery should be performed. Surgery in early stages of immaturity is technically easier, and there is less preoperative uveitis. However, if there are no significant visual deficits it is difficult to justify a complex and expensive surgical procedure that does not guarantee 100% success. On the other hand, it is inadvisable to wait until the cataract reaches advanced stages of maturity, as the concomitant development of LIU will affect the surgical prognosis. The success rate is higher for surgical removal of immature cataracts than for removal of mature cataracts.

2.Obviously, for the patient to regain vision, its retina must be healthy and functional. Ideally, the fundus should be examined by the surgeon early in the disease, when the cataract is not yet advanced and the retinal details are still visible. Alternatively, if the fundus cannot be examined thoroughly (because of the cataract), retinal function should be evaluated with electroretinography (ERG) to ensure that retinal degeneration is not present. ERG is described in Chapter 15. Because retinal degeneration can occur in any breed, an ERG evaluation is mandatory in bilaterally affected dogs in which the fundus cannot be examined. The owner must be carefully questioned about the relative onset of visual difficulty, cataract, and nyctalopia. However, patient history, signalment, and the speed of pupil contraction in response to light are not reliable indicators of the presence or absence of progressive rod-cone degeneration.

3.Any incipient LIU—indicated by ciliary injection, hypotony, miosis, aqueous flare, change in iris color, or resistance to mydriasis—must first be controlled by topical corticosteroids and/or NSAIDs under the supervision of the person who will perform the surgery. The incidence of shortand long-term complications is greater when uveitis is present preoperatively.

4.No other ocular pathologic process should be present. The eye must be examined by an experienced veterinary ophthalmologist. Any concurrent disease, such as keratitis or glaucoma, must be controlled before surgery. Older dogs or dogs affected with hypermature cataracts may have zonular instability. In many practices an ultrasound examination is performed before surgery to rule out vitreal/retinal detachment. In patients that are susceptible to postoperative retinal detachment (due to vitreous disease or breed susceptibility) some clinicians advocate prophylactic retinopexy (“fixating” the retina in its place), by either cryopexy or laser photocoagulation, at the time of cataract surgery.

5.The patient should be in good general health, should not suffer from any systemic diseases, and should undergo tests to ensure it is a suitable candidate for anesthesia.

6.The patient must be amenable to intensive handling, because frequent topical applications of medication are required in both the preoperative and postoperative periods. One cannot overemphasize the importance of postoperative treatment and its effect on the outcome. An excitable or fractious dog that cannot be handled and medicated is usually an unsuitable candidate. If there is doubt regarding the owner’s ability to medicate the dog postoperatively, topical medication should be provided preoperatively to determine the feasibility of drug application.

7.The owner must be prepared to sustain the cost and effort required to perform preoperative and postoperative treatment and to return for rechecks. Willingness to pay the bill is not enough. Long-term treatment to avoid uveitis, IOP monitoring for glaucoma, and frequent rechecks are mandatory for long-term visual success. An owner who cannot provide the required postoperative therapy and care should be counseled against surgery.

8.For an older dog, the owner must be counseled that senility, cognitive dysfunction, motor problems, and other aspects of old age may be as important in the dog’s behavior as the cataract, and that cataract removal, although technically successful, may not result in the improvement sought (the expectation often is that the dog will see and behave like a young dog again).

Surgical Correction

Once preexisting uveitis has been controlled, retinal function determined, and other tests completed, the patient is scheduled for surgery. Many surgeons prefer to perform bilateral surgery (assuming that both eyes are similarly affected), although some prefer to operate on one eye at a time.

The four methods of surgical correction commonly used are

(1) discission and aspiration, (2) extracapsular extraction,

(3) phacoemulsification, and (4) intracapsular extraction. Discission and Aspiration. Discission and aspiration con-

sists of opening the cornea and anterior lens capsule and using irrigation and aspiration to remove the contents from within the capsule (Figure 13-19). This method is restricted to young animals with liquid cataracts and animals with very small eyes (usually exotic pets) that will not accommodate regular ophthalmic instrumentation.

Extracapsular Extraction. In extracapsular extraction, a wide (180-degree) incision is made in the limbus and the anterior lens capsule, nucleus, and cortex are extracted manually, followed

Injection of flushing solution

Aspiration of liquid cortex + solution

B

13-19. Cataract extraction using dissection and aspiration. A, Rupture of lens capsule. B, Aspiration of contents via two-way cannula.

by rigorous flushing to remove any remaining lens particles (Figure 13-20). The posterior lens capsule, which is attached to the vitreous, remains intact. This method has largely been replaced by phacoemulsification.

Phacoemulsification. Surgery begins with a small incision at the limbus and tearing of the anterior lens capsule. A special probe is then used to shatter the lens with high-frequency ultrasonic waves, and the debris is removed via automated irrigation and aspiration (Figure 13-21). In fact, the technique for phacoemulsification is similar to that for discission, with the exception that a phacoemulsifier is used instead of cannulae. Phacoemulsification has the advantages of requiring a smaller limbal incision than extracapsular extraction (the incision has to accomodate only the probe) and allowing more complete removal of lens cortical material because the smaller incision results in faster surgery and healing, and because of the automated flushing system. The method has achieved widespread use because the smaller incision results in faster surgery and healing, and because the postoperative inflammation is more moderate, in comparison with extracapsular extraction. This results in fewer postoperative complications and less patient discomfort.

Intracapsular Extraction. Removal of the entire lens without opening or tearing the lens capsule is called intracapsular extraction. This method is restricted to the removal of luxated lenses, following tearing of the zonules (see following section). Because the capsular bag is not opened during surgery there is no leakage of lens protein, and the postoperative inflammation is minimal. However, surgery may lead to anterior movement of the vitreous body (and possible secondary retinal detachment or glaucoma), as the lens that normally separates the vitreous from the anterior chamber has been removed. Therefore some surgeons will combine this surgery with prophylactic vitrectomy (removal of the vitreous body). Others will implant a synthetic IOL fixed by sutures in the ciliary sulcus as a barrier against vitreous movement and to improve postoperative vision (see later).

Postoperative Vision and Intraocular Lens Implantation

After cataract extraction surgery the patient is severely hyperopic (farsighted) owing to the loss of the refractive power of the lens. This visual deficit can be corrected by implantation of an artificial lens (an IOL), which thus helps the patient achieve postoperative emmetropia (focused vision). With this aim in mind, veterinary ophthalmologists began implanting IOLs in their canine patients in the late 1980s (Figure 13-22). Subsequent studies have shown that the optical power of canine IOLs should

be approximately 41 D, and such lenses are now regularly implanted by veterinary ophthalmologists, with significant improvement in postoperative visual performance.

As stated earlier, however, the cornea is the major refractive organ of the eye, and the lens plays a less significant role in refraction and accommodation in animals. This means that contrary to popular belief, and to the owners’ puzzlement, vision

A

FIGURE 13-21. Phacoemulsification surgery to remove a cataract. Note the small incision (6 o’clock position) required to insert the tip of the phacoemulsifier into the eye. The instrument shatters the lens with ultrasound waves, and performs irrigation and aspiration. The second instrument (8 o’clock position) is used to rotate the lens pieces toward the phacoemulsification tip. (From Yanoff M, Duker JS [2004]: Ophthalmology, 2nd ed. Mosby, St Louis.)

caused by improper handling of the cornea leading to trauma, or by exposure to the energy emitted by the phacoemulsifier. Endothelial cell loss can be decreased by filling the anterior chamber with viscoelastic substances (sodium hyaluronate, methyl cellulose and its derivatives), which physically shield and protect the cells, and by keeping the duration of phacoemulsification to a minimum.

In both phacoemulsification and extracapsular extraction, the surgeon will try to avoid perforating the posterior lens capsule. Such perforation may allow vitreous to enter into the anterior chamber and cause secondary glaucoma. If the posterior lens capsule is torn during cataract surgery, the surgeon may perform vitrectomy to reduce the risk of glaucoma.

The major postoperative surgical complication is LIU. Because of the immunogenicity of the lens proteins, cataract surgery (which involves opening the lens capsule) inevitably results in uveitis. The inflammation is treated aggressively with mydriatics and various combinations of topical and systemic antiinflammatory drugs. Many surgeons begin treating their patients several days before surgery to ensure a dilated pupil during the operation (because the lens is removed through the pupil) and as prophylactic treatment for the uveitis. The treatment is intensified on the day of surgery, with many animals receiving intravenous, intramuscular, and/or subconjunctival antiinflammatory drugs, and the treatment is continued postoperatively according to the surgeon’s preference. Topical and/ or systemic antibiotics are usually provided, and some surgeons may add prophylactic glaucoma treatment because postoperative spikes of IOP (often temporary but blinding) have been reported. Frequent rechecks to monitor IOP and LIU are mandatory in the immediate postoperative period, and some surgeons may even hospitalize their patients for 1 to 2 days for evaluation. With time, the frequency of treatments and rechecks decreases, although occasional rechecks (once every 6 to 12 months) are warranted due to the insidious nature of LIU.

With improvement in surgical techniques and instrumentation, and with better understanding and treatment of the postoperative complications, the immediate postoperative

results of cataract surgery are excellent, and more than 95% of the patients regain useful vision. However, with time some of these patients may lose vision in one or both eyes. The reasons are the insidious nature of the uveitis, secondary complications, and failure of the owners to adhere to a long-term treatment and recheck schedule. Possible complications resulting from uveitis include secondary glaucoma, posterior synechia, and lens epithelial fibrous metaplasia and postoperative opacification. Retinal detachment, intraocular hemorrhage, infection, and suture failure are possible, though less common, complications.

Cataracts in Horses

Cataracts are less common in horses than in dogs. In some breeds, including Belgian and thoroughbred horses, cataracts have been demonstrated to be hereditary (dominant). Nonprogressive, nuclear cataracts that do not interfere with vision occur in Morgan horses. However, most cataracts of adult horses are secondary to trauma or equine recurrent uveitis. Senile cataracts causing visual impairment may occur in horses older than 20 years. Elderly horses are also affected by nuclear sclerosis, which, like the condition in the dog, does not affect vision. Cataracts (both hereditary and secondary) are a relatively common ocular defect in foals.

Foals and adult horses with visual impairment are suitable candidates for lens extraction, provided the horses are tractable and can be medicated postoperatively. In foals, early return of vision is important to development of higher visual centers. The workup, techniques, and complications of cataract removal are similar to those in the dog.

LENS LUXATION

Luxation occurs when all of the lens zonules are torn, leading to displacement of the lens from the hylaoid (patellar) fossa. Following the luxation, the lens may move anteriorly, posteriorly, or in the vertical plane of the eye. Lens luxation may be preceded by subluxation, resulting from tearing of some (but

not all) of the zonules, and leading to partial displacement of the lens from the hyaloid fossa.

Etiology

Lens luxation may be classified as primary (hereditary) or secondary. Primary lens luxation is most commonly seen in dogs. The luxation is due to weakened lens zonules that rupture early in life (up to 5 years of age). This condition is inherited in wirehaired fox, Sealyham, Manchester, Cairn, Jack Russell, Tibetan, and miniature bull terriers and miniature schnauzers. It is also common in poodles, but the hereditary nature is unconfirmed in this breed. Electron microscopy studies in the Tibetan terrier have shown that the insertions of the lens zonules into the lens capsule are abnormal. In such cases, luxation may follow minor trauma, which ruptures the weakened zonules. Primary congenital luxation, seen in multiple ocular anomalies, is rare in clinical practice.

Secondary luxation may be due to any of the following conditions:

•Blunt traumas (e.g., a violent strike to the orbital region) may cause secondary lens luxation (traumatic luxation). Trauma violent enough to cause lens luxation may also cause other severe ocular lesions (e.g., hyphema, retinal detachment, scleral rupture). Perforating traumas, such as cat claws, do not cause lens luxation, as they do not generate the mechanical forces needed to tear the zonules.

•Glaucoma: When the globe enlarges in chronic glaucoma the zonules may break, leading to lens subluxation and luxation. It is noteworthy that glaucoma may also be caused by lens luxation (see later), and when both diseases are present in an eye it may be difficult to determine which is the cause and which the effect.

•Uveitis: Alterations in the aqueous humor, and the presence of inflammatory mediators in the posterior chamber, may weaken the zonules.

•Intraocular tumors: As a tumor enlarges, it may displace the lens, creating a luxation or subluxation.

•Cataract: If a cataractous lens swells (intumescence), the zonules may break.

Clinical Signs and Diagnosis

In a normal eye, the iris rests on the anterior lens surface, which gives it its slightly convex curvature. If the zonules deteriorate or pull free from the lens, rapid eye movement causes the lens to oscillate back and forth in the hyaloid fossa. This oscillation causes iris vibration (iridodonesis). Iridodonesis is an early sign of impending lens displacement and becomes more evident as the lens continues to loosen from the zonules.

Increased lens movement causes the vitreous touching the posterior lens to separate from deeper vitreous, allowing more movement of the lens. Eventually the damaged vitreous liquefies and is replaced by aqueous. This process of liquefaction of the vitreous is referred to as syneresis (Figure 13-23). Therefore vitreous fibrils floating through the pupil in the aqueous are also a sign of zonule disruption and potential future luxation.

If the lens is subluxated in the equatorial plane, the iris is convex where it touches the lens and flat in the area of dislocation (compare the dorsal and ventral iris in Figure 13-23, B). As the subluxation progresses to luxation, the luxated lens usually sinks ventrally owing to the effect of gravity. The dorsal

LENS 273

A B

C D

FIGURE 13-23. Lens luxation and vitreous syneresis. A, Normal lens position. B, Zonules are ruptured dorsally but lens is held in place by the vitreous. C, Early liquefaction of the vitreous, which allows more lens movement. D, Lens motion accelerates syneresis, and the lens may sink ventrally. (Courtesy Dr. G.A. Severin.)

FIGURE 13-24. An aphakic crescent due to posterior lens luxation. The white lens is visible from the 4 to 9 o’clock positions because it luxated in a ventronasal direction (while maintaining its vertical orientation). Only the dorsotemporal part of the lens is visible; the rest of the lens is obscured by the iris. An aphakic crescent is visible between 9 o’clock and 4 o’clock, in the part of the pupil that has been vacated by the lens. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

edge of the lens becomes visible in the pupil. The dorsal area of the pupil where the lens is missing is called an aphakic crescent (Figure 13-24).

Syneresis may continue until most of the vitreous disappears. When this occurs, the lens may settle ventrally at the “bottom” of the eye and may disappear from the pupil (see Figure 13-23, D). This condition is called posterior luxation. In such cases, it is possible to observe the retinal blood vessels and optic disc without an ophthalmoscope, through the use of only a basic source of light.

Lens luxation causes changes in anterior chamber depth and iris (Figure 13-25). The clinician can best evaluate anterior chamber depth and iris position by observing the eye from the side rather than the front. The normal iris rests on the anterior surface of the lens and therefore is slightly convex (see Figure

A B

FIGURE 13-25. A, Lens luxation with anterior displacement of the iris (and possible pupillary blockage of aqueous passage): Anterior chamber is shallow. B, Luxation into the anterior chamber, which appears deep. Endothelial damage causes corneal edema where the lens capsule touches it. (Courtesy Dr. G.A. Severin.)

13-23, A). Initially the vitreous may swell, forcing the lens forward and resulting in a shallow anterior chamber and a more convex iris (see Figure 13-25, A). If the pupil dilates, the lens may luxate through the pupil into the anterior chamber (Figure 13-26). The luxation may be partial or complete.

When the lens is luxated, the depth of the anterior chamber will usually increase, regardless of the direction of the luxation (an exception is seen in Figure 13-25, A). In cases of anterior luxation the lens fills the anterior chamber, and therefore it physically pushes the iris posteriorly (see Figure 13-25, B). In cases of posterior luxation, the iris loses its posterior support and moves posteriorly (see Figure 13-23, D). In both cases the increase in anterior chamber depth is accompanied by a more concave position of the iris.

Anterior lens luxation is considered an ophthalmic emergency for the following reasons:

•Edema: Luxation into the anterior chamber brings the lens in contact with the corneal endothelium. This impairs the endothelial function, resulting in corneal edema. Furthermore, as the head of the animal moves the lens repeatedly strikes the corneal endothelium. This may cause permanent endothelial damage and irreversible corneal edema.

•Pain: Pain is caused by the striking of the inner cornea by the lens.

•Glaucoma: As the lens is luxated anteriorly, it may “pull” the vitreous behind it. The presence of vitreous in the pupil or in the anterior chamber impedes the flow of aqueous humor and causes an elevation in IOP. The presence of the lens in the anterior chamber further obstructs drainage of aqueous humor (see Figure 13-25, B). Glaucoma may also occur as a result of posterior lens luxation, because the “barrier” between the vitreous and the pupil disappears. As with anterior luxation, this may result in anterior movement of the vitreous, provided that it has liquefied or has become detached from its posterior attachment to the retina.

A clinician should suspect anterior lens luxation in cases of acute onset of severe pain, corneal edema, and/or glaucoma, especially when presented unilaterally and in susceptible breeds. The severe corneal edema, blepharospasm, and possible hyphema (in cases of traumatic luxation) that can accompany lens luxation may make it difficult to visualize the luxated lens or the changes in the depth of the anterior chamber and iris position. In these cases, ultrasound may be used to demonstrate the location of the lens in the eye (Figure 13-27).

Treatment

Some controversy exists regarding the treatment of subluxated lenses or posteriorly displaced lenses. Some surgeons prefer to remove them using intracapsular lens extraction techniques (in combination with vitrectomy) to prevent glaucoma. Others provide long-term miotic treatment to ensure that the luxated lens does not move anteriorly and educate the clients about signs of anterior luxation and glaucoma.

Because of the complications described in the previous section, there is no controversy surrounding the need to remove anteriorly luxated lens. These may be removed by intracapsular extraction or phacoemulsification. The major complication with extraction of luxated lenses (regardless of whether they luxated anteriorly or posteriorly) is glaucoma. Therefore many clinicians combine this procedure with vitrectomy, thus

FIGURE 13-26. Anterior lens luxation. Note that the entire lens equator can be seen and that the lens partially obscures the iris. (Courtesy University of Missouri Veterinary Ophthalmology Case Photo Collection.)

FIGURE 13-27. Ultrasonographic image of a posterior lens luxation. The lens, which could not be seen because of corneal edema, is visible as a hyperechoic mass in the posterior part of the eye (dashed line connecting the two asterisks). (Courtesy Dr. I. Aizenberg.)

reducing the risk of anterior vitreous movement. If glaucoma is present before the lens is removed, a lower success rate is achieved than if the lens is removed before glaucoma occurs. Placement of an IOL fixed by sutures has also been advocated after removal of luxated lenses in dogs. The IOL serves as a barrier to prevent anterior vitreal movement and improves postoperative vision.

In cases of anterior luxation where surgical removal is not feasible, the lens may be pushed from the anterior chamber back to the posterior part of the eye (reclination). This is a noninvasive procedure that may be facilitated by anesthesia (to reduce globe tension caused by the extraocular muscles) and by administration of hyperosmotic agents (to decrease the volume of the vitreous body). Following the procedure, permanent miotic therapy is instituted to ensure that the lens remains in the posterior part of the eye.

BIBLIOGRAPHY

Alpar JJ (1987): Use of Healon in different cataract surgery techniques: endothelial cell count study. Ophthalmic Surg 18:529.

Barnett KC (1985): Hereditary cataract in the miniature schnauzer. J Small Anim Pract 26:635.

Barnett KC (1980): Cataract in the golden retriever. Vet Rec 111:315. Barnett KC (1980): Hereditary cataract in the Welsh springer spaniel. J Small

Anim Pract 21:621.

Barros PS, et al. (2004): Blood and aqueous humour antioxidants in cataractous poodles. Can J Ophthalmol 39:19.

Barros PS, et al. (1999): Antioxidant profile of cataractous English cocker spaniels. Vet Ophthalmol 2:83.

Basher AW, Roberts SM (1995): Ocular manifestations of diabetes mellitus: diabetic cataracts in dogs. Vet Clin North Am Small Anim Pract 25:661.

Bayon A, et al. (2001): Ocular complications of persistent hyperplastic primary vitreous in three dogs. Vet Ophthalmol 4:35.

Beach J, Irby N (1985): Inherited nuclear cataracts in the Morgan horse. J Hered 76:371.

Bernays ME, Peiffer RL (2000): Morphologic alterations in the anterior lens capsule of canine eyes with cataracts. Am J Vet Res 61:1517.

Biros DJ, et al. (2000): Development of glaucoma after cataract surgery in dogs: 220 cases (1987-1998). J Am Vet Med Assoc 216:1780.

Bjerkas E, Haaland MB (1995): Pulverulent nuclear cataract in the Norwegian buhund. J Small Anim Pract 36:471.

Brainard J, et al. (1982): Evaluation of superoxide dismutase (Orgotein) in medical treatment of canine cataract. Arch Ophthalmol 100:1832.

Brightman AH (1986): Buyer beware—another medical “cure” for cataracts. J Am Vet Med Assoc 188:5.

Brightman AH, et al. (1981): Effect of aspirin on aqueous protein values in the dog. J Am Vet Med Assoc 178:572.

Buschmann W, et al. (1987): Microsurgical treatment of lens capsule perforations. Part I: experimental research. Ophthalmic Surg 18:731.

Colitz CM, et al. (2000): Histologic and immunohistochemical characterization of lens capsular plaques in dogs with cataracts. Am J Vet Res 61:139.

Colitz CM, et al. (1999): Telomerase activity in lens epithelial cells of normal and cataractous lenses. Exp Eye Res 69:641.

Curtis RC (1983): Aetiopathological aspects of inherited lens dislocation in the Tibetan terrier. J Comp Pathol 93:151.

Curtis RC, et al. (1983): Clinical and pathological observations concerning the aetiology of primary lens luxation in the dog. Vet Rec 112:238.

Davidson MG, et al. (2000): Effect of surgical technique on in vitro posterior capsule opacification. J Cataract Refract Surg 26:1550.

Davidson MG, et al. (2000): Ex vivo canine lens capsular sac explants. Graefes Arch Clin Exp Ophthalmol 238:708.

Davidson MG, et al. (1991): Phacoemulsification and intraocular lens implantation: a study of surgical results in 182 dogs. Prog Vet Comp Ophthalmol 1:4.

Davidson MG, et al. (1991): Traumatic anterior lens capsule disruption. J Am Anim Hosp Assoc 27:411.

DeCosta P, et al. (1996): Cataracts in dogs after long-term ketoconazole therapy. Vet Comp Ophthalmol 6:176.

Denis HM, et al. (2003): Detection of anti-lens crystallin antibody in dogs with and without cataracts. Vet Ophthalmol 6:321.

LENS 275

Dwyer WP, Smith CE (1988): Metacercariae of Diplostomum spathaceum in the eyes of fishes from Yellowstone Lake, Wyoming. J Wildl Dis 25:126.

Dziezyc J, et al. (1991): Use of phacofragmentation for cataract removal in horses: 12 cases (1985-1989). J Am Vet Med Assoc 198:1774.

Garcia-Sanchez GA, et al. (2005): Ahmed valve implantation to control intractable glaucoma after phacoemulsification and intraocular lens implantation in a dog. Vet Ophthalmol 8:139.

Gelatt KN, et al. (2003): Cataracts in the bichon frise. Vet Ophthalmol 6:3. Gelatt KN, Mackay EO (2005): Prevalence of primary breed-related cataracts

in the dog in North America. Vet Ophthalmol 8:101.

Gelatt KN, MacKay EO (2004): Secondary glaucomas in the dog in North America. Vet Ophthalmol 7:245.

Gemensky-Metzler AJ, Wilkie DA (2004): Surgical management and histologic and immunohistochemical features of a cataract and retrolental plaque secondary to persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous (PHTVL/PHPV) in a bloodhound puppy. Vet Ophthalmol 7:369.

Gilger BC, et al. (1998): Experimental implantation of posterior chamber prototype intraocular lenses for the feline eye. Am J Vet Res 59:1339.

Glaze M, Blanchard G (1983): Nutritional cataracts in a Samoyed litter. J Am Anim Hosp Assoc 19:951.

Glover TL, et al. (1995): The intracapsular extraction of displaced lenses in dogs: a retrospective study of 57 cases (1984-1990). J Am Anim Hosp Assoc 31:77.

Grahn BH, Cullen CL (2004): Iris to lens persistent pupillary membranes. Can Vet J 45:613.

Grahn BH, Cullen CL (2000): Equine phacoclastic uveitis: the clinical manifestations, light microscopic findings, and therapy of 7 cases. Can Vet J 41:376.

Gwin RM, et al. (1983): Effects of phacoemulsification and extracapsular lens removal on cornea thickness and endothelial cell density in the dog.

Invest Ophthalmol Vis Sci 24:227.

Harding JJ (1992): Physiology, biochemistry, and epidemiology of cataract. Curr Opin Ophthalmol 3:3.

Hardman C, et al. (2001): Phacofragmentation for morgagnian cataract in a horse. Vet Ophthalmol 4:221.

Jamieson V, et al. (1991): Ocular complications following cobalt 60 radiotherapy of neoplasms in the canine head region. J Am Anim Hosp Assoc 27:51.

Johnstone N, Ward DA (2005): The incidence of posterior capsule disruption during phacoemulsification and associated postoperative complication rates in dogs: 244 eyes (1995-2002): Vet Ophthalmol 8:47.

Kenny D, et al. (2003): Intracapsular lens removal in a Przewalski’s wild horse (Equus caballus przewalskii). J Zoo Wildl Med 34:284.

Lannek EB, Miller PE (2001): Development of glaucoma after phacoemulsification for removal of cataracts in dogs: 22 cases (1987-1997). J Am Vet Med Assoc 218:70.

Lazarus JA, et al. (1998): Primary lens luxation in the Chinese shar-pei: clinical and hereditary characteristics. Vet Ophthalmol 1:101.

Leasure J, et al. (2001): The relationship of cataract maturity to intraocular pressure in dogs. Vet Ophthalmol 4:273.

Ledbetter EC, et al. (2004): Microbial contamination of the anterior chamber during cataract phacoemulsification and intraocular lens implantation in dogs. Vet Ophthalmol 7:327.

Magrane WG (1969): Cataract extraction: a follow-up study (429 cases). J Small Anim Pract 10:545.

Magrane WG (1961): Cataract extraction: an evaluation of 104 cases. J Small Anim Pract 1:163.

Martin CL (1978): Zonular defects in the dog: a clinical and scanning electron microscopic study. J Am Anim Hosp Assoc 14:571.

Martin CL, Chambreau T (1982): Cataract production in experimentally orphaned puppies fed a commercial replacement for bitch’s milk.

J Am Anim Hosp Assoc 18:115.

Matthews AG (2004): The lens and cataracts. Vet Clin North Am Equine Pract 20:393.

Matthews AG (2000): Lens opacities in the horse: a clinical classification. Vet Ophthalmol 3:65.

Miller PE, et al. (1997): Mechanisms of acute intraocular pressure increases after phacoemulsification lens extraction in dogs. Am J Vet Res 58:1159.

Miller TR, et al. (1987): Phacofragmentation and aspiration for cataract extraction in dogs: 56 cases (1980-1984). J Am Vet Med Assoc 190:1577.

Millichamp NJ, Dziezyc J (2000): Cataract phacofragmentation in horses. Vet Ophthalmol 3:157.

Moore DL, et al. (2003): A study of the morphology of canine eyes enucleated or eviscerated due to complications following phacoemulsification. Vet Ophthalmol 6:219.

Murphy JM, et al. (1980): Sequelae of extracapsular lens extraction in the normal dog. J Am Anim Hosp Assoc 16:17.

Narfstrom K (1999): Hereditary and congenital ocular disease in the cat. J Feline Med Surg 1:135.

Narfstrom K, Dubielzig R (1984): Posterior lenticonus, cataracts and microphthalmia: congenital ocular defects in the Cavalier King Charles spaniel. J Small Anim Pract 25:669.

Nasisse MP, et al. (1995): Lens capsule opacification in aphakic and pseudophakic eyes. Graefes Arch Clin Exp Ophthalmol 233:63.

Nasisse MP, et al. (1995): Technique for suture fixation of intraocular lenses in dogs. Vet Comp Ophthalmol 5:146.

Nasisse MP, Davidson MG (1999): Surgery of the lens, in Gelatt KN (editor): Veterinary Ophthalmology, 3rd ed. Lippincott Williams & Wilkins, Philadelphia.

Nasisse MP, Glover TL (1997): Surgery for lens instability. Vet Clin North Am Small Anim Pract 27:1175.

Norton JH (1980): Cataracts in sows. Aust Vet J 56:408.

Ofri R, Horowitz I (1995): Spontaneous cataract resorption in an ostrich. Vet Rec 136:276.

Olivero DK, et al. (1991): Feline lens displacement—a retrospective analysis of 345 cases. Prog Vet Comp Ophthalmol 1:239.

O’Reilly A, et al. (2003): The use of transscleral cyclophotocoagulation with a diode laser for the treatment of glaucoma occurring post intracapsular extraction of displaced lenses: a retrospective study of 15 dogs (1995-2000). Vet Ophthalmol 6:113.

Ori JI, et al. (2000): Posterior lenticonus with congenital cataract in a shih tzu dog. J Vet Med Sci 62:1201.

Oz HH, et al. (1986): Bilateral cataract surgery in a Suffolk ewe. Vet Rec 118:512.

Paulsen ME (1986): The effect of lens-induced uveitis on the success of extracapsular cataract extraction—a retrospective study of 65 lens removals in the dog. J Am Anim Hosp Assoc 22:49.

Peiffer RL, Weintraub BA (1979): Clinical and histopathologic effects of lensectomy and anterior vitrectomy in the canine eye. J Am Anim Hosp Assoc 15:421.

Pollet L (1982): Refraction of normal and aphakic canine eyes. J Am Anim Hosp Assoc 18:323.

Ranz D, et al. (2002): Nutritional lens opacities in two litters of Newfoundland dogs. J Nutr 132:1688S.

Remillard R, et al. (1993): Comparison of kittens fed queen’s milk with those fed milk replacers. Am J Vet Res 52:901.

Richter M, et al. (2002): Aldose reductase activity and glucose-related opacities in incubated lenses from dogs and cats. Am J Vet Res 63:1591.

Rooks RL, et al. (1985): Extracapsular cataract extractions: an analysis of 240 operations in dogs. J Am Vet Med Assoc 190:1580.

Sanford SE, Dukes TW (1978): Acquired bilateral cortical cataracts in mature sows. J Am Vet Med Assoc 173:852.

Sato S, et al. (1998): Dose-dependent prevention of sugar cataracts in galactose-fed dogs by the aldose reductase inhibitor M79175. Exp Eye Res 66:217.

Sato S, et al. (1991): Progression of sugar cataract in the dog. Invest Ophthalmol Vis Sci 32:1925.

Sigle KJ, Nasisse MP (2006): Long-term complications after phacoemulsification for cataract removal in dogs: 172 cases (1995-2002). J Am Vet Med Assoc 228:74.

Slatter DH, et al. (1983): Hereditary cataracts in canaries. J Am Vet Med Assoc 183:872.

Slatter DH, et al. (1980): Cataracts and depressed galactose-1-phosphate uridyl transferase deficiency in a cus cus (Phalanger maculatus). Aust Vet J 56:141.

Smith PJ, et al. (1996): Ocular hypertension following cataract surgery in dogs: 139 cases (1992-1993). J Am Vet Med Assoc 209:105.

Stephens T, et al. (1974): Deficiency of two enzymes of galactose metabolism in kangaroos. Nature 248:524.

van der Woerdt A, et al. (1993): Ultrasonographic abnormalities in the eyes of dogs with cataracts. 147 cases (1986-1992). J Am Vet Med Assoc 203:838.

van der Woerdt A, et al. (1992): Lens induced uveitis in dogs: 151 cases (1985-1992). J Am Vet Med Assoc 120:921.

Warren C (2004): Phaco chop technique for cataract surgery in the dog. Vet Ophthalmol 7:348.

Williams DL, et al. (2004): Prevalence of canine cataract: preliminary results of a cross-sectional study. Vet Ophthalmol 7:29.

Williams DL, et al. (1996): Current concepts in the management of canine cataract: a survey of techniques used by surgeons in Britain, Europe and the USA and a review of recent literature. Vet Rec 138:347.

Williams DL, Munday P (2006): The effect of a topical antioxidant formulation including N-acetyl carnosine on canine cataract: a preliminary study. Vet Ophthalmol 9:311.