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

ANATOMY AND PHYSIOLOGY

Anatomy

The vitreous is a transparent elastic hydrogel (Figure 14-1). It occupies about 80% of the volume of the eye (Figure 14-2). During embryonic development, primary, secondary, and tertiary vitreous are formed and laid down (Figure 14-3). Their genesis is described in detail in Chapter 2. Briefly, the primary vitreous is associated with the hyaloid vascular supply system, which nourishes the lens during development. The secondary vitreous is laid down around the primary vitreous and forms the definitive (adult) vitreous, whereas the tertiary vitreous contributes to the formation of the lens zonules.

The vitreous body is divided into the following zones (Figure 14-4):

1.Anterior vitreous, located anterior to the ora ciliaris retinae (see Figure 14-4, area 5)

2.Posterior vitreous, located posterior to the ora ciliaris retinae (see Figure 14-4, area 7)

3.Cortex, which comprises the peripheral vitreous (see Figure 14-4, area 12), including:

a.Vitreous base, which is the attachment of the vitreous at the ora ciliaris retinae (see Figure 14-4, area 6)

b.Peripapillary vitreous, located adjacent to the optic disc (see Figure 14-4, area 10)

4.Central vitreous, including Cloquet’s canal (see Figures 14-3 and 14-4, area 13). Cloquet’s canal, which is a cleft in the vitreous where the hyaloid vasculature passed during embryonic development, is visible with the biomicroscope (see Figure 14-3, B and C).

Composition

Vitreous is a complex gel with the following constituents:

•Water (99%)

•Collagen fibers, which serve as a skeleton for the gel

•Cells (hyalocytes)

•Hyaluronic acid

Collagen fibrils form a meshwork internal to the retina (the vitreous cortex) and intermingle with the fibers of the internal limiting membrane of the retina, thus forming a firm attachment between the vitreous cortex and the retina (Figure 14-5).

Therefore anterior movement of the vitreous (such as occurs after lens luxation) may pull the retina off the retinal pigment epithelium (RPE) and cause traction retinal detachment. A potential space exists between the vitreous and the inner surface of the retina. Blood and exudates may accumulate in this space if the vitreous and retina separate, resulting in subhyaloid hemorrhage.

The collagen fibrils are also responsible for the numerous attachments of the vitreous to the adjacent structures—the posterior lens capsule, the ora ciliaris retinae (the vitreous base), and the optic nerve head (see Figure 14-4). Collagen fibrils are present in greater concentrations at the vitreous bases and around the optic disc, where attachment is the strongest.

The lens sits in a depression in the anterior face of the vitreous cortex, the hyaloid fossa (patella fossa). Collagen fibrils form attachments between the posterior lens capsule and the anterior vitreous. These attachments are especially significant in dogs. Removal of the posterior lens capsule, as in intracapsular lens extraction, results in loss of vitreous.

Hyalocytes are numerous within the vitreous and are more numerous near the cortex. The functions of these cells are unclear, but they may possess secretory and phagocytic capabilities as well as the potential for reversion to primitive fibroblasts able to form scar tissue. Mucopolysaccharides, containing a high proportion of hyaluronic acid, are intimately related to the collagen fibrils and hyalocytes and are present in higher concentration where hyalocytes are common. Hyaluronic acid provides the viscoelasticity of the vitreous body.

With the exception of collagen and hyaluronic acid, aqueous humor and vitreous are similar in composition, with free movement of many substances between them. The principles that govern entry of substances, including drugs, from the vascular circulation into the aqueous humor generally apply to the vitreous as well.

Function

The vitreous does not have a specific and clearly defined role in ocular physiology of the adult. It contributes to maintaining ocular volume and possibly the shape of the globe. It also helps maintain some ocular structures, notably the lens and retina, in their correct anatomic locations. Also, it forms part of the optical pathway that light must pass on its way to the retina. However, the vitreous does not have a significant role in refraction of this light, because its refractive index is similar to that of the lens.

FIGURE 14-1. Vitreous after dissection of the sclera, choroid, and retina. A band of dark tissue can be seen posterior to the ora ciliaris retinae, circling the dorsal two thirds of the vitreous. This is neural retina that was firmly adherent to the vitreous base and could not be dissected. The vitreous also remains attached to the anterior segment (ciliary body, iris, and lens). The vitreous is almost entirely gel and thus is solid, maintaining its shape even though situated on a surgical towel exposed to room air. (From Yanoff M, Duker JS [2004]: Ophthalmology, 2nd ed. Mosby, St. Louis).

Virtreous compartment

FIGURE 14-2. The vitreous body (SHADED AREA) occupies the posterior compartment of the eye. (Modified from Fine BS, Yanoff M [1979]: Ocular Histology. Harper & Row, New York.)

PATHOLOGIC REACTIONS

Because of its simple structure and lack of vascular and lymphatic supply, the vitreous has a limited range of pathologic reactions, as follows:

•Liquefaction: Because of its high water content, the vitreous gel may liquefy (syneresis) in response to many stimuli (e.g., infection, trauma, uveitis, senile changes). After liquefaction, the vitreous separates from the retina, encouraging retinal detachment from the underlying RPE. Liquified vitreous may also enter the subretinal space through retinal holes, predisposing to rhegmatogenous retinal detachment.

•Cicatrization: After inflammation of surrounding tissues or infection, scar tissue may form in the vitreous. These vitreous bands may contract and detach the retina (traction detachment).

•Proliferative vitreoretinopathy: This reaction occurs in association with retinal disease. In response to retinal disease, glial or RPE cells proliferate on the innermost retina or in the vitreous and form scars. Subsequently, these

Primary vitreous (hyloid artery)

A

Remains of primary vitreous (Cloquet’s canal)

Secondary (adult) vitreous

B

Tertiary vitreous (lens zonules)

Remains of primary vitreous (Cloquet’s canal)

C

Secondary (adult) vitreous

FIGURE 14-3. Stages of vitreous development. A, Primary vitreous and hyaloid vessels nourishing the embryonic lens. B, The secondary vitreous laid down around the primary vitreous, which condenses into Cloquet’s canal. The secondary vitreous will become the adult vitreous. C, Tertiary vitreous (lens zonules or ligaments) at the lens periphery. (Courtesy Dr. G.A. Severin.)

1, attachment of anterior zonular fibers to the lens; 2, attachment of posterior zonular fibers to the lens; 3, attachment of anterior vitreous face to posterior lens capsule; 4, anterior extremity of Cloquet’s canal (Mittendorf’s dot); 5, anteriormost attachment of vitreous base to mid pars plana; 6, region of vitreous “base”; 7, region of diminishing adherence of vitreous base to retinal surface; 8, vitreous-retinal attachment; 9, vitreousretinal attachment at margin of fovea centralis (ABSENT IN DOMESTIC ANIMALS); 10, attachment of posterior vitreous around optic disc; 11, posterior extremity of Cloquet’s canal (Bergmeister’s papilla); 12, cortical vitreous; 13, central vitreous. Density of lines indicates approximate relative degrees of strength of attachment. (Modified from Fine BS, Yanoff M [1979]: Ocular Histology. Harper & Row, New York.)

C

C

A B

FIGURE 14-5. The vitreous base near the peripheral retina. The Müller cells (A) have a basement membrane (B) that forms the inner limiting membrane of the retina. The collagen fibrils (C) of the vitreous base form a meshwork internal to the retina. These fibrils join the internal limiting membrane. (From Hogan MJ, et al. [1971]: Histology of the Human Eye. Saunders, Philadelphia.)

fibrotic membranes may form that pull on the retina, causing it to tear and detach.

•Vascularization: The vitreous has no blood supply, but blood vessels may grow into it from an inflamed or malformed retina (neovascularization). These vessels often are incomplete or fragile and are a source of vitreous hemorrhage (e.g., in the collie eye anomaly).

•Infection and inflammation: These reactions are discussed later.

•Elongation: Elongation of the vitreous body causes elongation of the axial length of the eye and, consequently, of the pathway that light must pass on its way to the retina. As a result, light that was previously focused on the retina is now focused in front of the retina, thereby causing shortsightedness (myopia). Such elongation occurs as a result of visual deprivation during the neonatal period. It may be induced by lid suturing and other deprivation techniques during the critical developmental period in animal models of myopia. It may also occur naturally, as a result of neonatal cataracts or corneal opacities that cause visual deprivation, resulting in neonatal myopia (as well as abnormalities in the visual cortex). This is another reason why congenital ocular opacities should be corrected as soon as possible, before irreparable changes occur in the eye, and why third eyelid flaps and tarsorrhaphies should be carefully considered in neonates.

CONGENITAL AND DEVELOPMENTAL ABNORMALITIES

Persistent Hyaloid Artery

The hyaloid artery is part of the embryonic vascular supply of the lens, which is described in Chapter 2. In most species, the hyaloid artery atrophies within a few weeks after birth (see Figure 14-3). An exception is ruminants, in which remains of the artery may be observed in a significant number of adults. However, persistent remnants of varying extent may be found in any species. The remnants of the artery origins on the surface

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of optic disc, which are surrounded by glial tissue, are called Bergmeister’s papilla (see Figure 14-4, area 11). These appear ophthalmoscopically, end-on, as red to white tufts originating from the optic disc and extending anteriorly a variable distance into the vitreous (see Figure 2-10, B, in Chapter 2). Similarly, at the distal end of the artery, remains of its attachment to the posterior lens capsule may be seen. The remains are known as Mittendorf ’s dot (see Figure 14-4, area 4). It does not interfere with vision, except for rare occasions when it induces focal, posterior cataracts. A persistent artery, however, may extend from the disc all the way to the posterior lens. Persistence of the hyaloid artery may be hereditary in the Doberman pinscher and Sussex spaniel. In rats, the hyaloid artery may bleed into the vitreous during normal atrophy.

A persistent hyaloid artery and its attachment to the posterior lens capsule must be differentiated from the following conditions by the following means:

•Posterior capsular and subcapsular cataracts: By accurate localization of the opacity. In the golden retriever and Labrador retriever, Mittendorf’s dot is differentiated from a cataract on the basis of its smaller size and location on the posterior lens capsule. The cataract is much larger and is usually triangular, and careful examination may determine that it is located in the posterior lens cortex, rather than capsule. Mittendorf’s dot usually has the anterior remnant of the hyaloid artery attached as a small white “tail” visible biomicroscopically.

•Normal lens sutures (especially in cattle and horses): By familiarity with the normal appearance

•Vitreous bands: By the linear appearance of the bands, which are usually located outside Cloquet’s canal as well as by the presence of other signs of injury or inflammation (see Acquired Disorders)

•Persistent tunica vasculosa lentis and persistent hyperplastic primary vitreous: By the more extensive nature of the opacity on the posterior lens capsule (see following sections)

Persistent Tunica Vasculosa Lentis

This condition is similar to persistent hyaloid artery, the difference being that it is the tunica vasculosa lentis (TVL), rather than the hyaloid artery, that has also failed to regress postnatally. The TVL is visible as a netlike opacity on the posterior surface of the lens. Because the opacity is usually a very fine matrix, it does not interfere with vision.

Persistent Hyperplastic Primary Vitreous

Unlike the former two disorders, which involve failure of the hyaloid artery and TVL to regress postnatally, this disorder involves fetal and postnatal hyperplasia of the hyaloid system, TVL, and primary vitreous. Therefore the resulting opacity (which varies in size) is usually more severe. The disorder may occur in cats and in most dog breeds, and it has been demonstrated to be hereditary in the Bouvier des Flandres, Staffordshire bull terrier, and Doberman pinscher. Extensive studies of PHPV in the Doberman pinscher in The Netherlands have shown it to be an autosomal incompletely dominant trait with variable expression.

Clinically PHPV appears as a white or fibrovascular plaque in the posterior pupil near the posterior lens capsule and anterior vitreous (Figure 14-6). Vessel ingrowth and frank hemorrhage

FIGURE 14-6. Persistent hyperplastic primary vitreous in a golden retriever. Note the fibrovascular opacity with patent vessels near the posterior lens capsule. The lesion is viewed in reflected light from the tapetum.

into the vitreous and lens substance, calcium deposits, posterior lenticonus, microphakia, lens coloboma, intralental pigmentation, progressive cataracts, and elongated ciliary processes may also be present. Surgery of cataracts associated with PHPV carries a guarded prognosis due to opacification of the posterior lens capsule, the possibility of a patent blood vessel, and the need to combine the surgery with anterior vitrectomy.

ACQUIRED DISORDERS

Vitreous Degeneration

Vitreous degeneration is separation of the fluid and solid constituents of the vitreous into segregate fractions, resulting in vitreal liquefaction (syneresis). The degeneration may occur naturally in elderly patients, or following inflammation, and may predispose the eye to retinal detachment. Degeneration of the vitreous is commonly demonstrated by ultrasonography in dogs with cataract as part of the preoperative screening of surgical candidates. In one study of 124 eyes degeneration was found in 50% of subjects with incipient cataract, 57% with immature cataract, 89% with mature cataract, and 100% with hypermature cataract. Eighty-six percent of eyes with lens-induced uveitis had vitreous degeneration, whereas 67% of those with cataracts but without uveitis were affected. The higher incidence of rhegmatogenous retinal detachments in eyes with hypermature cataracts may be associated with this increased incidence of vitreal degeneration.

Vitreous Hemorrhage

Because the vitreous does not have a vascular supply, vitreal hemorrhage is a relatively uncommon presentation (Figure 14-7). The source of the blood may be leakage from abnormally proliferating vessels, but it usually originates in retinal or uveal blood vessels due to the following:

•Hypertensive retinopathy in dogs and cats

•Clotting disorders (e.g., thrombocytopenia) and coagulopathies

•Ocular trauma

FIGURE 14-7. Hyphema and vitreal hemorrhage. The latter may be observed as a dark opacity in the posterior segment. (Courtesy David J. Maggs.)

•Severe retinitis and retinochoroiditis (e.g., canine ehrlichiosis, Rocky Mountain spotted fever, brucellosis, feline infectious peritonitis, feline leukemia virus; also— depending on geographic location—intraocular mycotic disease, including blastomycosis, coccidiomycosis, cryptococcosis, histoplasmosis)

•Collie eye anomaly

•As a sequel to intraocular surgery

•Severe anterior uveitis of many different causes

Small amounts of vitreal hemorrhage may resorb, but larger amounts may cause long-term visual disturbances. Whether a vitreous hemorrhage resorbs depends on the associated pathologic changes in adjacent tissues and on the location of the hemorrhage within the vitreous body. Resorption is infrequent in collie eye anomaly because neovascularization of the vitreous near the retina has occurred with rupture of some of the vessels. In hypertensive retinopathy, resorption may occur if the hypertension is controlled, but recurrent hemorrhage is common owing to the nature of the lesions, especially if the hypertension is not well controlled. In retinitis, retinochoroiditis, ocular trauma, and anterior uveitis, resorption is more likely if the underlying inflammation and vascular damage resolve.

Conservative treatment, consisting of antiinflammatory and mydriatic drugs, is recommended for recent hemorrhages. Vitreal membranes and traction bands may develop; these abnormalities may also cause secondary traction retinal detachments months after the primary cause of the hemorrhage has resolved (Figure 14-8). Therefore, if membranes and bands are seen, an intraocular injection of tissue plasminogen activator (TPA) may be advocated. The aim of the injection is to break down fibrin traction bands and thereby prevent vitreoretinal detachment. The ideal “time window” for such an injection is 3 to 4 days after the primary event. If the TPA is injected too early, the hemorrhage may recur (because the clots that sealed the vessels are also dissolved). The injection is ineffective if enough time has passed to allow fibrin organization.

Infection and Inflammation

Inflammation of the vitreous is called hyalitis or vitritis. Because of its lack of vasculature, primary inflammation per se

14-8. Ultrasound image of retinal detachment in a 6-year-old Samoyed with uveitis. The image shows the classic “seagull wings” sign, which is the detached retina adherent to the globe at the optic nerve head and the ora ciliaris retinae. The hyperechoic opacities anterior to the detached retina are fibrin strands that caused the detachment. (Courtesy Dr. I. Aizenberg.)

does not occur in the vitreous as in other tissues. However, the vitreous may be affected by inflammatory disorders of surrounding tissues (e.g., chorioretinitis, optic neuritis, anterior uveitis). The inflammation may cause opacification, hemorrhages, syneresis, and cellular exudation. Vitreous haze is common in inflammatory disorders of the posterior globe, and its disappearance is a valuable indicator of the efficacy of treatment. Reduction of this haze often improves vision. The treatment is similar to that of vitreal hemorrhage. The primary cause of the inflammation must be diagnosed and treated; the eye is treated symptomatically with cycloplegic and antiinflammatory drugs.

Infection of the vitreous by a variety of microorganisms is seen in penetrating injuries, systemic bacteremias, and ocular fungal infections. After the initial infection the surrounding vitreous liquefies and the infection spreads rapidly. Infections of the vitreous are associated with endophthalmitis (inflammation of all tissues of the eye except the sclera) and may progress to vitreous abscess. These infections must be treated aggressively with topical and systemic antibiotics or antifungal drugs. Severe cases are treated by intraocular injection of antimicrobial drugs, or surgically, by vitrectomy (see relevant section). Hyalocentesis (tapping of the vitreous) may be conducted for diagnostic purposes in cases that do not respond to medical therapy, with samples submitted for cytology, culture, serology, and pathology. The prognosis for these infections is usually very guarded.

The vitreous has also been implicated as a repository site for the antigens that cause the recurrent inflammation associated with equine recurrent uveitis (ERU). In particular, antigens of Leptospira, which are commonly associated with ERU, have been detected in the vitreous of affected horses. The involvement of the vitreous in the pathogenesis of ERU has led to the development of two novel treatment strategies. One consists of surgical removal of the vitreous (vitrectomy, discussed later). The other is based on the use of suprachoroidal implants for long-term release of cyclosporine, thereby suppressing the inflammatory reaction.

Vitreous Opacities (Floaters)

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probably represent degenerative changes in the vitreous. They may also appear following vitritis, especially in horses, in which case they usually contain blood or exudate. A focal light source with a binocular loupe or direct ophthalmoscope is adequate to demonstrate these opacities. Vitreous floaters are not responsible for the “fly-biting syndrome,” in which an affected animal appears to be biting at moving objects in the air. This syndrome is now believed to be due to seizures of the temporal or occipital lobe and responds to appropriate medication. Surgical treatment of vitreous floaters is not required.

Asteroid Hyalosis (Asteroid Hyalitis) and

Synchysis Scintillans

These are two pathologic conditions with a very similar presentation. Both are characterized by the appearance of numerous, small, refractile bodies scattered through the vitreous. Vision is not affected. The two conditions may occur spontaneously in older animals and also in association with chronic inflammatory and degenerative ocular disorders. In asteroid hyalosis the particles consist of calcium and phospholipids complexes (Figure 14-9). In synchysis scintillans the particles are composed of cholesterol. The two conditions can be distinguished clinically based on the mobility of the particles. In asteroid hyalosis the particles are attached to the collagen framework of the vitreous (Figure 14-10). Therefore they are fixed in the vitreous and move only with head or globe movements. In

14-9. Asteroid hyalosis in a dog. Note the numerous white particles scattered in the patient’s vitreous body. (From Rubin LF [1974]: Atlas of Veterinary Ophthalmoscopy. Lea & Febiger, Philadelphia.)

Floaters are small, mobile flakes that are seen in the vitreous. In most cases they are a benign finding in elderly patients and

14-10. Subretinal hematoma, vitreous hemorrhage, and asteroid hyalosis in a shih tzu. (Courtesy Dr. Ursula Dietrich.)

FIGURE 14-11. Ultrasound image of a vitreal mass, in this case a posterior luxated lens. (Courtesy Dr. I. Aizenberg.)

synchysis scintillans the bodies are mobile within the liquified vitreous. If the head is moved, the particles can be seen whirling like snowflakes in the vitreous, and then they slowly settle ventrally.

Vitreous Mass

The differential diagnosis of a mass in the vitreous includes the following entities:

•Retinal detachment (see Figure 14-8)

•Cataractous or normal, luxated lens (Figure 14-11)

•Intraocular neoplasm (usually by extension from the urea)

•Hemorrhage (acute or chronic) (see Figures 14-7 and 14-10)

•Foreign body

•PHPV

•Persistent hyaloid artery

•Traction band or fibrous tissue

•Vitreous abscess or endophthalmitis

•Parasites (e.g., Dirofilaria immitis, Toxocara canis larvae in dogs, Echinococcus spp., ophthalmomyiasis interna

[fly larvae])

•Cyst (from the pigmented epithelial layer of the ciliary body)

cause secondary glaucoma. Lens luxation is illustrated and discussed in detail in Chapter 13.

Aqueous Humor Misdirection Syndrome

Also known as “malignant glaucoma,” aqueous humor misdirection syndrome occurs in approximately 1% of cats older than 6 years presented to private practitioners for routine health care. In this disorder, aqueous humor is misdirected into the vitreous via minute breaks in the hyaloid membrane (perhaps during blinking or upon eyelid squeezing) rather than entering the posterior chamber. These breaks are suggested to act as one-way valves, trapping pools of aqueous humor in the vitreous, displacing the lens anteriorly (with intact lens zonules), dilating the pupil, and uniformly shallowing the anterior chamber. As the vitreal elements are compressed anteriorly it becomes much more difficult for aqueous humor to cross the hyaloid membrane. In some animals glaucoma may result. Therapy consists of suppressing aqueous humor production with topical carbonic anhydrase inhibitors or, in intractable cases, removal of the lens and anterior vitreous. Glaucoma is discussed in detail in Chapter 12.

Retinal Detachment

As noted, lens luxation may facilitate anterior prolapse (or movement) of the vitreous. Because of the attachment of the posterior vitreous to the inner retina, anterior movement of the vitreous may pull the retina off the choroid and cause traction retinal detachment. It is important to note that anterior vitreous prolapse may occur as a result of either anterior lens luxation (the lens pulls the vitreous forward) or posterior lens luxation (the lens being a “barrier” against vitreous movement, its posterior luxation may facilitate such prolapse). Traction retinal detachment may also occur following the formation of vitreal membranes or bands in the course of vitritis, infection, or hemorrhage. As the membranes and bands contract, they may pull the neuroretina off the RPE (see Figure 14-8).

The vitreous is also involved in the pathogenesis of rhegmatogenous retinal detachment. This kind of detachment is usually observed in elderly patients. Liquefied vitreous enters spontaneously occurring retinal holes and percolates into the subretinal space, causing detachment of the neuroretina from the RPE. Retinal detachment is discussed in detail in Chapter 15.

ROLE OF THE VITREOUS IN THE PATHOGENESIS OF OCULAR DISEASES

Vitreous and Lens Luxation

If lens zonules break, the lens may be partially or totally luxated. In the early stages, when small numbers of lens zonules rupture, vitreous may escape into the anterior chamber and may be visible as fine strands in the anterior chamber or near the pupillary margin. Pigment may be seen in this prolapsed vitreous and is a possible indicator of the presence of uveitis. As the number of ruptured lens zonules rises, the stability of the lens decreases, and it may be subluxated within the hyaloid fossa, in the plane of the iris. Due to gravity the lens settles ventrally; the part of the pupil that is no longer occupied by the lens is visible as an aphakic crescent dorsal to the visible lens border. As the lens becomes fully luxated, more vitreous may prolapse into the pupil or iridocorneal angle, obstruct the flow of aqueous, and

SURGICAL AND DIAGNOSTIC PROCEDURES

Hyalocentesis

Hyalocentesis is the removal of a small amount of liquefied vitreous for cytologic or microbiologic analysis. Indications for hyalocentesis include diagnosis of vitreous opacities suspected to be infectious or neoplastic in origin. The procedure is performed with the use of general anesthesia, after thorough preoperative preparation of the eye (see Chapter 5), and usually by an experienced veterinary ophthalmologist. Punctures must be accurately located in the pars plana ciliaris because more anterior punctures can strike the lens and result in cataract, or else they may penetrate the pars plicata ciliaris and result in severe intraocular hemorrhage (Figure 14-12 and Table 14-1). On the other hand, punctures made too posteriorly perforate the retina. A 22to 26-gauge needle is directed into the material of interest, while pointing toward the posterior pole to avoid the

lens. An equal volume of balanced salt or lactated Ringer’s solution is used to replace the liquefied vitreous removed.

Hyalocentesis is performed by an experienced veterinary ophthalmologist for the diagnosis of serious intraocular disorders. It carries the risk of intraocular hemorrhage.

FIGURE 14-12. Hyalocentesis. Precise location of the point of insertion of a 22to 26-gauge (0.70 to 0.45 mm) needle 5 to 7 mm posterior to the limbus, depending on the ocular quadrant and globe size as determined by calipers or ultrasonography, is of utmost importance to avoid intraocular trauma. (Modified from Boeve MH, Stades FC [1999]: Diseases and surgery of the canine vitreous, in Gelatt KN [editor]: Veterinary Ophthalmology, 3rd ed. Lippincott Williams & Wilkins, Philadelphia.)

Table 14-1 Location of the Pars Plana Ciliaris in the Dog

Modified from Smith PJ, et al. (1997): Identification of sclerotomy sites for posterior segment surgery in the dog. Vet Comp Ophthalmol 7:180.

A

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Vitrectomy

Vitrectomy is the removal of a portion of the vitreous body. Indications for vitrectomy include the following:

•Severe intraocular infection

•Prophylactic treatment of glaucoma, in cases where the vitreous presents in the anterior chamber following lens luxation or cataract surgery

•Surgical reattachment of a detached retina

•Recently vitrectomy has been advocated as surgical treatment for ERU, because the antigens that trigger the recurrent inflammation are postulated to be located in the vitreous.

In the course of anterior segment surgery (removal of cataracts and luxated lenses), small amounts of vitreous may present in the anterior chamber. These may be removed easily using sponges and scissors (Figure 14-13). When vitreous is removed it must not remain between wound edges, where it would interfere with wound healing, or in the anterior chamber, where it may lead to glaucoma. After lens luxation, syneresis is usually present. When syneresis or loss of vitreous is anticipated, use of hyperosmotic agents is advised to reduce the size of the vitreous body and risk of its subsequent loss.

More extensive vitrectomy is required in the treatment of ocular injuries and for treatment of retinal detachments and vitreal traction bands. The procedure requires more sophisticated instrumentation and surgical approaches to the posterior segment of the eye (see Figure 14-13, C and D). The incidence of postoperative complications is relatively high. Because of the intimate associations among the collagen framework of the vitreous body, lens capsule, and inner limiting membrane of the retina, removal of large amounts of vitreous carries a significant risk of postoperative retinal detachment.

Vitreous Replacement

If larger amounts of vitreous are removed, the physical deficit must be replaced. Vitreous replacements are especially useful in canine patients for maintaining retinal position after surgical correction of retinal detachment, because head shaking tends to disrupt the delicate retinal reattachments. Vitreous substitutes are also used to roll out folded retina before reattachment and to

FIGURE 14-13. Vitrectomy can be performed manually or using automated instruments. If small amounts of vitreous are present in the anterior chamber (e.g., following lens luxation or cataract surgery), these can be removed manually. The vitreous is pulled out with a sponge (A) and cut with scissors

B(B). Removal of large amounts of vitreous (e.g., during surgical reattachment of the retina or as glaucoma prophylaxis) is performed using a vitrector. The instrument may be inserted through the anterior chamber (C) or using a scleral port (D). Note that in all cases, the lens has been removed. (Modified from Deustch TA, Feller DB [1985]: Paton and Goldberg’s Management of Ocular Injuries. Saunders, Philadelphia.)

float pieces of dropped lens into the anterior chamber for removal during cataract extraction. Many different substances, including perfluorocarbons, silicone, and fluorosilicone, have been used. Complications from the toxicity of these substances include cataract formation, keratopathy, and glaucoma.

Advanced Vitreoretinal Surgical Techniques

Many surgical techniques have been developed for the reattachment and prevention of retinal detachments. Examples are laser and cryosurgical retinopexy, pneumatic retinopexy, scleral buckling procedures, and pars plana vitrectomy; most of these are applicable to the canine eye. For details of these methods, which are beyond the scope of this text, the reader is referred to a recent review (Vainisi and Wolfer, 2004). The scope and complexity of the surgery depends on the extent of the retinal detachment. Laser retinopexy and cryoretinopexy are used to “weld” the retina to the choroid in cases of retinal holes or partial detachment, in order to stop progression to full retinal detachment. More advanced techniques and specialized equipment are required to reattach a fully detached retina. Prognosis depends, to a large extent, on the duration of the detachment before reattachment, and it is accepted that retinas reattached within 4 weeks may regain some useful vision. A recent retrospective study of 500 canine cases reported restoration of some vision in 76% of patients.

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The retina is the organ responsible for transducing light into neuronal signals that are eventually perceived as a visual image. One might say that the entire purpose of the eye is to enable focused light to strike a functional retina.

More specifically, the light strikes the photoreceptors, a complex layer of specialized cells—the rods and cones—which contain photopigments that produce chemical energy on exposure to light. This energy is converted (transduced) into electrical energy, which is processed by the retina and transmitted by the optic nerve, via the optic chiasm, optic tracts, lateral geniculate body, and optic radiations, to the visual cortex.

The retina is a unique organ in that it can be studied noninvasively with the ophthalmoscope to show in vivo intricate details of pathologic processes that in most other organs are only visible histopathologically, or during invasive surgery. This enables the clinician to correlate clinical findings with histopathologic findings and may frequently allow specific, accurate diagnosis.

CELLULAR ANATOMY

Broadly speaking, the retina can be regarded as a three-neuron sensory unit, because photoreceptors relay the visual signal through bipolar cells and onto the ganglion cells (Figure 15-1). However, this is a gross simplification, and traditionally the retina is described as having 10 layers. The structure of these layers is summarized in Table 15-1, and their function is detailed below. From the outside (facing the choroid and sclera) to the inside (facing the vitreous) these layers are as follows (Figure 15-2):

1.Retinal pigment epithelium

2.Photoreceptor layer

3.External limiting membrane

4.Outer nuclear layer

5.Outer plexiform layer

6.Inner nuclear layer

7.Inner plexiform layer

8.Ganglion cell layer

9.Optic nerve fiber layer

10.Internal limiting membrane

The retinal pigment epithelium (RPE) (layer 1) is the outermost layer of the retina, facing the choroid. It is pigmented in the nontapetal part of the fundus of domestic animals and gives a homogenous brown-black color to this area. It is normally

unpigmented in the tapetal fundus and cannot be seen clinically; therefore it could be argued that the name RPE in this area is a misnomer, because the cells are nonpigmented retinal pigment epithelium. The lack of RPE pigment in the tapetal area allows incoming light that has not been absorbed by the photoreceptors to reach the tapetum. The tapetum acts as a mirror that reflects this light back toward the photoreceptor layer, thus increasing the probability that it will be absorbed by the photopigment and contribute to visual sensation in dim light (Figure 15-3).

Normal function of the pigment epithelium is essential to retinal integrity and function.

The RPE has two main functions. The first is to serve as metabolic interface between the photoreceptors and their choroidal blood supply, supplying metabolites and removing waste from the outer retina. The second function is to recycle the “used” (or bleached) photopigment of the photoreceptors. Discs containing the photopigment are continually synthesized and move from the base of the photoreceptor outer segment toward its distal end. After the photopigment absorbs the energy of the incoming light and transduces it into a neuronal signal, the disc is shed and phagocytized by the engulfing RPE (Figure 15-4). The recycling of the pigment by the RPE and the production of new discs by the photoreceptor outer segments are essential for the retina’s sensitive response to light. The RPE also has a phagocytic role in retinal inflammations (see later).

Layers 2 through 10 are collectively called the sensory retina or the neuroretina because they process the neuronal signal, or visual sensation (as opposed to the RPE, which has only a supporting role). It may be remembered from Chapter 2 that the neuroretina and the RPE originate from two different embryonic layers.

The photoreceptor layer (layer 2) is composed of the outer segments of the rods and cones, which contain the visual photopigments within discs stacked like a pile of coins (Figure 15-5). This is the site where vision is “initiated,” because it is here that the process of phototransduction, or the conversion of a visual stimulus into an initial neuronal signal, occurs (see Visual Photopigments). Therefore the previous statement, that the purpose of the eye is to enable focused light to strike the retina, could be refined—light should be focused precisely on the photoreceptor layer. As noted, a result of the phototransduction process is the bleaching and shedding of the photopigment by the outer segments, and its subsequent phagocytosis and recycling by the RPE.

NEURONAL CONNECTIONS IN THE RETINA

AND PARTICIPATING CELLS

Internal limiting membrane

Ganglion cell

External limiting membrane

Müller's fiber (glia)

Cone

Rod

FIGURE 15-1. Rods and cones relay a visual signal through bipolar cells onto ganglion cells. Amacrine and horizontal cells contribute to processing of the signal, while Müller’s cells provide structural support. (From Yanoff M, Duker JS [2004]: Ophthalmology, 2nd ed. Mosby, St. Louis.)

The external limiting membrane (layer 3) is formed by terminal processes joining the cell membranes of rods, cones, and Müller’s cells. Müller’s cells extend across the entire retina, from the external limiting membrane to the internal limiting membrane, and therefore serve as its structural “skeleton.” Small Müller’s cell processes pass between the outer limbs of rods and cones contributing to the formation of the outer limiting membrane

Internal limiting membrane

Nerve fiber layer

Table 15-1 Summary of Retinal Structure

(see Figures 15-5, A, and 15-6). The cells also perform important metabolic functions, such as energy storage and ionic regulation.

The outer nuclear layer (layer 4) consists of the nuclei of the rods and cones. The outer plexiform layer (layer 5) is a synaptic layer. Here, axonal extensions of the photoreceptors dilate to form synaptic expansions, which synapse with dendrites of bipolar cells as well as with adjacent photoreceptors. This is the site of the first synapse, which the neuronal visual signal must pass, and hence a potential site for its initial processing.

The inner nuclear layer (layer 6) contains the following four types of nuclei: (1) bipolar cells, (2) Müller’s cells, (3) horizontal cells, and (4) amacrine cells. Bipolar cells synapse with photoreceptor cells in the outer plexiform layer. Horizontal and amacrine cells are lateral communicating cells that modulate the neuronal activity and the visual signal.

The inner plexiform layer (layer 7) is the second synaptic layer, consisting of axons of bipolar, horizontal, and amacrine cells and dendrites of ganglion cells. Numerous synapses occur

Internal limiting membrane

Nerve fiber layer

Ganglion cell layer

Inner plexiform layer

Inner nuclear layer

Outer plexiform layer

Outer nuclear layer

External limiting membrane

Photoreceptor layer

Retinal pigment epithelium