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

FIGURE 10-45. Corneal sequestrum in a cat. Note also the surrounding corneal edema and vascularization. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

ment of the ulcer and secondary uveitis with topical antibiotics and atropine, respectively, along with antiviral therapy if herpesvirus is believed to be the initiating cause should be provided until sloughing occurs. Corticosteroids should not be used for sequestra. However, most animals exhibit signs of marked ocular pain during this period, and removal of the plaque by keratectomy is preferred as it shortens this period of discomfort. Associated keratitis should be controlled before keratectomy is performed. Manual removal of sequestra should not be attempted, because some sequestra extend to Descemet’s membrane and globe rupture is possible. After keratectomy, most ophthalmologists graft the corneal defect with conjunctiva or corneoconjunctival transposition. Recurrences after treatment may occur, but results are normally excellent.

Feline sequestra are painful and may take many months to slough. Keratectomy hastens healing and resolves discomfort.

Bullous Keratopathy

Bullous keratopathy is a nonspecific diagnosis that describes the formation of small vesicles in the epithelium and stroma of an edematous cornea (Figure 10-46). These vesicles ultimately coalesce to form larger bullae. The surrounding epithelium and stroma are edematous and often vascularized, either in response to the bullae or as a result of the underlying corneal disorder. Rupture of the bullae with subsequent ulceration is expected once they become severe.

Treatment relies on resolution of the underlying condition, although this is often not possible. Symptomatic therapy with hyperosmotic sodium chloride ointment may reduce the edema and limit rupture of bullae. Topical antibiotics should be applied if bullae rupture and fluorescein is retained by the exposed stroma. In intractable, progressive bullous keratopathy, thermokeratoplasty may be used. In this technique the cornea is treated carefully with focal application of heat. A scar forms in treated areas, and the associated tissue contraction “squeezes” out stromal fluid and limits further stromal distention. Alternatively, complete corneal coverage with a very thin, 360-degree conjunctival graft may reduce bullae formation. The patient is best referred to an ophthalmologist for these treatments. The prognosis for mild bullous keratopathy is good, especially if the

A

B

FIGURE 10-46. Bullous keratopathy. A, Frontal view; B, profile.

underlying cause can be cured. Extensive bullous keratopathy has a poor prognosis.

“Florida Keratopathy” or “Florida Spots”

Small, usually multifocal, white corneal stromal opacities unique to tropical and subtropical climates have been described in both dogs and cats. These opacities, called Florida keratopathy or Florida spots, are not associated with inflammation or pain, do not respond to any therapy, and are apparently self-limiting. Their cause is unknown.

Infectious Bovine Keratoconjunctivitis

Infectious bovine keratoconjunctivitis (IBK), one of the most common diseases of cattle, is of major economic importance in beefand milk-producing areas throughout the world. Synonyms include “pink eye” and “New Forest eye.” M. bovis is considered the causative agent as well as one of very few organisms considered to be a primary corneal pathogen—that is, one that can attach to and penetrate through intact corneal epithelium. In fact, M. bovis is the only bacterium of veterinary importance that can initiate corneal ulceration. Piliated M. bovis organisms adhere to the corneal epithelium and produce cytotoxins, epithelial detachment factor, and hemolysins, which, together with collagenases from host cells, cause necrosis of epithelium and stroma. Other organisms, including Mycoplasma bovoculi, infectious bovine rhinotracheitis virus (BHV-1),

Box 10-2 Microbial, host, and environmental or husbandry factors involved in the pathogenesis of infectious bovine keratoconjunctivitis

Microbial Factors

•Pili

•Hemolysins

•Epithelial detachment factor

•Cytotoxins

•Presence of other infectious organisms:

•Infectious bovine rhinotracheitis virus (BHV-1)

•Mycoplasma spp.

•Ureaplasma spp.

•Ability to use iron bound by lactoferrin

Host Factors

•Genetics (Bos indicus less susceptible)

•Age

•Periocular pigmentation?

Environmental or Husbandry Factors

•Ultraviolet radiation

•Herding animals together

•Infectious bovine rhinotracheitis vaccination

•Dust

•Fly vectors:

•Musca autumnalis

•Musca domestica

•Stomoxys calcitrans

•Heavy snowfall

•Transport stress

•Dry tall weeds?

Ureaplasma spp., and adenoviruses, have been isolated from field outbreaks of IBK and are likely also involved in the pathogenesis of some outbreaks. Other microorganisms and environmental and host factors are also critical in the pathogenesis of IBK; these cofactors are listed in Box 10-2.

In herds with no previous outbreaks, young and older animals are equally severely affected. After the initial occurrence, however, younger animals are more frequently and severely affected. Affected animals possess some immunity that becomes less effective after 1 or 2 years, frequently allowing reinfection. The effectiveness of this immunity depends directly on the severity of the initial disease. Unfortunately, attempts to produce either live or killed vaccines against M. bovis have been disappointing. Recent commercial vaccines using pili antigens require further field evaluation before their true value is known. Peak outbreaks usually occur in summer, especially when ultraviolet radiation, flies, and dusty conditions prevail.

The initial lesion is severe, ulcerative keratoconjunctivitis (Figure 10-47) associated with intense epiphora, blepharospasm, and marked corneal edema. There is a usually central corneal opacity due to stromal cell infiltration, which enlarges, ulcerates, and vascularizes. Secondary (so-called reflex) uveitis is marked. Ulceration may progress to involve the stroma, and descemetocele formation with perforation and subsequent panophthalmitis may occur. At the peak of disease, the animal is in considerable pain, may be totally blind, and may have difficulty walking and finding food and water. Such animals are often dangerous for farm staff to handle, and extensive weight losses and reduced

FIGURE 10-47. Infectious bovine keratoconjunctivitis. Note the central ulceration with stromal white blood cell infiltration along with diffuse edema and deep corneal vascularization.

milk yields may occur. In less severe cases recovery takes 1 to 3 weeks, with vascularization and clearing from the limbus toward the center of the cornea. Some residual scar formation is expected. However, the bovine cornea possesses remarkable reparative properties, and many extensively scarred corneas are completely healed a year later, especially in young animals. Nevertheless, severe scarring does remain in a proportion of affected eyes.

If possible, affected animals should be segregated to limit spread of the disease and provided with shade. Attempts to reduce the vector fly population may be instituted. Individual animals may be treated with injections of procaine penicillin G beneath the bulbar conjunctiva. In a study in which penicillin was injected into the superior palpebral conjunctiva of naturally infected calves, the therapy did not shorten healing time, proving that site of injection is critical. A single systemic dose of repository oxytetracycline (20 mg/kg) followed by 10 days of oral oxytetracycline has been shown to be superior to 300,000 U procaine penicillin G injected subconjunctivally and to no treatment and may be used if withholding regulations are followed. Florfenicol, given once subcutaneously (40 mg/kg) or twice 2 days apart intramuscularly (20 mg/kg) to experimentally infected calves, also significantly reduced healing times compared with that in untreated calves. This finding was subsequently verified in a natural outbreak. Finally, a single dose of ceftiofur injected subcutaneously into the pinnae has also shown to be a useful therapy. Severe lesions can be protected by a temporary tarsorrhaphy (see Figure 10-29) or third eyelid flap.

Control measures include genetic selection, elimination of carrier animals, and good fly control. After an outbreak or in newly introduced animals, carrier status can be shortened by two systemic injections of long-acting tetracycline (20 mg/kg). The use of vaccines cannot be recommended to prevent IBK, although decreased prevalence and severity have been reported when vaccination is performed 6 weeks before the expected onset of the disease season. Calves are vaccinated at 21 to 30 days of age with a second vaccination 21 days later. Powders and sprays are contraindicated in the treatment of IBK because they provide suitable antibiotic concentrations only for short periods and are irritating.

Infectious Bovine Rhinotracheitis

Infectious bovine rhinotracheitis (IBR) is due to bovine herpesvirus. In affected animals, conjunctivitis is more

prominent than keratitis (see Chapter 7). However, peripheral corneal edema, ulceration, and vascularization are occasionally present. Keratitis due to IBR virus must be distinguished from corneal lesions of malignant catarrhal fever (bovine malignant catarrh), IBK, and squamous cell carcinoma.

Malignant Catarrhal Fever

Malignant catarrhal fever (MCF) is discussed more fully in Chapter 18. The corneal signs only are emphasized here. Ocular lesions are typically seen in the “head and eye” form of the disease. Lesions begin in the central cornea and move toward the limbus. If the cornea remains clear, signs of uveitis, including aqueous flare, cells, fibrin, miosis, and iris swelling, may be observed. MCF is suspected when nasal, oral, and ocular lesions occur with persistent pyrexia, enlarged lymph nodes, and encephalitis. The presence of ocular lesions differentiates MCF from rinderpest, bovine viral diarrhea mucosal disease, infectious stomatitis, and calf diphtheria. IBR is distinguished by its infectious nature, respiratory signs, recovery rate, and predominance of conjunctivitis rather than endophthalmitis. Ocular signs arise from the necrotizing effect of the virus on vascular tissues and vary according to the form of the disease.

Infectious Canine Hepatitis

Infectious canine hepatitis due to infection with canine adenovirus type 1 causes hepatic and renal disease in dogs and is discussed in Chapter 18. The major ocular effect is corneal edema, leading to its lay name “blue-eye.” The corneal edema is due, in part, to anterior uveitis, which can be extremely marked and can even lead to secondary glaucoma. However, corneal edema also arises from endothelial cell death or dysfunction as a direct result of viral replication as well as antigen-antibody complex deposition within corneal endothelial cells themselves (Figure 10-48). If endothelial damage is temporary, corneal edema usually resolves in 1 to 2 weeks, but some animals have permanent partial or total corneal opacity.

Treatment is directed at limiting permanent endothelial cell death or dysfunction, anterior uveitis, and secondary glaucoma. In the acute stages, topical corticosteroids, sometimes in combination with topical NSAIDs, should be used to control uveitis. Systemic administration of corticosteroids or NSAIDs may also be necessary. Frequent reexaminations with regular measurements of IOP are advisable. Topical atropine should be applied if IOP is not elevated. Topical hyperosmotic sodium chloride ointment may be used to limit edema or bullae formation, but its effect is mild and transitory. If response is not evident in 4 to 5 weeks, permanent corneal edema is likely. Once glaucoma has occurred, intraocular prosthesis or enucleation is necessary.

SCLERAL DISORDERS BELIEVED TO BE INHERITED

Colobomatous Defects

Colobomatous or notch defects in the sclera most commonly occur toward the equator or posterior pole of the globe. Their clinical appearance varies greatly according to location, but in both situations the areas of scleral absence (coloboma) or thinning (ectasia) are associated with protrusion of the underlying uveal tract through the affected sclera. At the equator the protrusion appears as a black or blue bulge often almost completely hidden by the eyelids in most normal positions of gaze (Figure 10-49). Unless they are large and cause significant weakening of the globe, such protrusions can be monitored. Repair involves a scleral or other tectonic grafting procedure and requires referral to a veterinary ophthalmologist. At the posterior pole, scleral thinning or absence typically involves the optic nerve as well as the choroid. If it is severe, the overlying retina may detach. This is a common feature of collie eye anomaly, which is discussed in the chapter on retinal disease (see Chapter 15).

ACQUIRED SCLERAL DISORDERS

Scleritis/Episcleritis

Anteriorly, the sclera is overlaid by a loose connective tissue called the episclera, which connects it to the bulbar conjunctiva. At the limbus, the sclera is confluent with the cornea. Posteriorly, the sclera overlies the choroid and retina and externally it is adjacent to the orbital tissues. Because all of these layers are so

FIGURE 10-48. Diffuse marked corneal edema due to endotheliitis and anterior uveitis in association with infectious canine hepatitis virus. (Courtesy University of Missouri, Columbia, Veterinary Ophthalmology Service Collection.)

FIGURE 10-49. Equatorial scleral coloboma with associated staphyloma. (Courtesy University of Missouri, Columbia, Veterinary Ophthalmology Service Collection.)

intimately related anatomically and physiologically, inflammation of the sclera and episclera inevitably involves adjacent tissues and therefore can lead to chorioretinitis (and potentially retinal detachment), orbital cellulitis, keratitis, conjunctivitis, and blepharitis in any combination. Partly because of this variation in clinical involvement, the terms scleritis, episcleritis, episcleroconjunctivitis, episclerokeratitis, and episclerokeratoconjunctivitis have become somewhat jumbled in the literature. Here the term episcleritis is used with the acknowledgment that the neighboring tissues are almost inevitably involved to varying degrees.

Episcleritis has been broadly divided into necrotizing and nodular variants. In the necrotizing form, there is inflammation, necrosis, and thinning and loss of sclera and surrounding tissues. In the nodular form, there is granulomatous thickening of the sclera and/or episclera. The latter has commonly been called nodular granulomatous episclerokeratoconjunctivitis

(NGE). Regardless of their histologic and clinical nature, this group of diseases is believed to be immune-mediated and is typically treated with immunomodulation. Some of the disorders are remarkably resistant to therapy, frequently recur, and often require prolonged treatment.

Typically, NGE appears as a single or sometimes multiple, raised, tan to red subconjunctival mass(es) at the limbus (Figure 10-50). Occasionally there is a more diffuse thickening of a broader region of episclera. The dorsolateral limbus is most commonly affected, but other limbal regions and even the third eyelid are occasionally affected. There is associated conjunctivitis and often the cornea becomes affected as the lesion advances into the corneal stroma. Crystalline opacities (presumably cholesterol or triglycerides) and corneal edema are the classic lesions. The syndrome occurs predominantly in collies, but many other breeds may be affected. Commonly used synonyms are nodular fasciitis, fibrous histiocytoma, limbal granuloma, and collie granuloma. The etiology is unknown. Lesions may be bilateral but are usually not symmetrical. Although clinical appearance is usually highly suggestive, histologic analysis is required to definitively confirm the diagnosis and differentiate this syndrome from neoplastic diseases such as squamous cell carcinoma and amelanotic limbal melanoma. The lesions consist of masses of histiocytes and fibrocytes.

FIGURE 10-50. Nodular granulomatous episclerokeratoconjunctivitis in a dog. Note extension into the neighboring corneal stroma. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

Because of the alleged immune-mediated nature of the condition, long-term immunomodulatory treatment is usually necessary for its control, although some cases regress completely. Without treatment, the condition is usually slowly progressive. Immunomodulatory therapy must be provided at the maximum level tolerated by the animal and the minimum level that causes some regression of the lesion. Frequency of application as well as concentration or dose of medications should be tapered as rapidly as possible as the patient improves. Additionally, medication type and route can be altered so as to cause the minimum of side effects as the disease regresses.

Recommended therapies and routes of administration are as follows:

•Corticosteroids:

•Systemic

•Subconjunctival

•Intralesional

•Topical (dexamethasone or prednisolone only)

•Topical cyclosporine (1% or 2 %)

•Systemic tetracycline and niacinamide (not niacin):

•For dogs weighing less than 10 kg: 250 mg of each drug q8h

•For dogs weighing 10 kg or more: 500 mg of each drug q8h

•Systemic azathioprine

•Surgical removal/debulking

•Cryotherapy

•B-Irradiation

Scleral Trauma

Blunt or sharp trauma to the sclera may result in thinning or rupture of the sclera with subsequent protrusion of the underlying uveal tract—a traumatic staphyloma. As with corneal perforations, prognosis depends largely on the extent of damage to the intraocular structures. Hyphema, iris prolapse, vitreous hemorrhage, lens capsule rupture, lens luxation, and retinal detachment are all possible and obviously indicate a poor prognosis. For simple uncomplicated penetrating wounds, surgical closure along with control of postoperative uveitis with corticosteroids and prostaglandin inhibitors is often successful. Systemic antibiotics and antiinflammatory agents should also be administered. For more extensive injuries, referral to an ophthalmologist for more sophisticated procedures (e.g., lens removal, vitrectomy, scleral allografting) may be indicated.

Severe blunt or concussive injuries can also cause scleral rupture, usually with even more devastating intraocular consequences than those of sharp trauma. In such instances, the eye usually ruptures adjacent to and concentric with the limbus (Figure 10-51). This situation is particularly common in the horse, especially when kicked by another horse. These ruptures may vary in size from a few millimeters in length to involvement of almost the entire circumference, with prolapse of lens, vitreous, iris, and ciliary body. Less extensive ruptures should be referred for primary closure and control of uveitis. The prognosis for extensive ruptures depends on damage to intraocular structures but is always guarded to poor. Damage to the ciliary body frequently leads to phthisis bulbi, and enucleation is recommended.

Penetrating and concussive scleral injuries are often associated with phthisis, especially when hyphema is marked.

FIGURE 10-51. Corneoscleral rupture with uveal prolapse in a dog.

Limbal Neoplasia

Primary scleral and corneal tumors are rare. In fact, rather than being a site of neoplastic origin, the sclera and cornea are important barriers, typically preventing spread of intraocular neoplasms to other parts of the body and intraocular spread of adnexal or orbital tumors. However, intraocular neoplasms may leave the eye via the optic nerve, ciliary and vortex veins, and intrascleral nerve canals.

In contrast to the cornea and sclera proper, the corneoscleral limbus is a relatively common site of origin for neoplasms. Perhaps this is because it is a region of very high mitotic activity and, particularly dorsolaterally, experiences notable exposure to ultraviolet light. The most frequently observed tumors are hemangioma/hemangiosarcoma (particularly in dogs and horses), limbal melanoma (dogs), and squamous cell carcinoma (horses and cattle). Squamous cell carcinomas are discussed in Chapter 7, because they almost always extend caudally from the limbus to involve the conjunctiva in addition to or instead of the cornea.

Limbal (Epibulbar) Melanocytoma

Limbal melanocytomas are relatively common in dogs. They arise from melanocytes in the superficial tissues near the limbus but often invade the adjacent corneal stroma or, less frequently, extend posteriorly into the sclera (Figure 10-52). Outward growth such that the tumor protrudes from the ocular surface is common, but intraocular penetration of the sclera and invasion of the iris or ciliary body is uncommon. When it does occur, intraocular extension makes differentiation of a melanocytic tumor of limbal origin from one of anterior uveal origin challenging. Although they are sometimes referred to as “limbal melanomas,” these tumors have a low metastatic potential and are often slow growing, especially in older dogs. Therefore they are best called limbal melanocytomas because of their biologic behavior. In younger dogs or when there is rapid growth, these tumors may be surgically debulked and treated with cryosurgery or with en bloc resection followed by a corneoscleral allograft. The prognosis for survival is excellent, and vision can also frequently be saved. Reduction in tumor size can also be achieved by laser photocoagulation; however, a 25% recurrence rate has been recorded for this approach.

FIGURE 10-52. Limbal (or epibulbar) melanoma in a dog. Note extension into the neighboring corneal stroma. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

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The uvea plays an important role in ocular physiology, and disorders of this tissue are common in veterinary practice. The iris controls the amount of light entering the eye, and the ciliary body alters the focal power of the lens, produces aqueous humor that supplies nutrition to ocular structures, and aids in regulating intraocular pressure (IOP). Together they also form a bloodaqueous barrier so as to maintain the clarity of the aqueous humor and vitreous. The choroid plays a major role in providing nutrition to the retina. Because of these diverse roles, uveal disorders are frequently associated with alterations in vision and IOP.

ANATOMY AND PHYSIOLOGY

The eye consists of the following basic layers (Figure 11-1):

•Fibrous (outer) layer—the sclera and cornea

•Vascular (middle) layer—the uvea, or uveal tract

•Neuroectodermal inner layer—the retina and optic nerve

The uveal tract has three parts: the iris and the ciliary body, which together form the anterior uvea, and the choroid, which is also known as the posterior uvea.

Iris

The iris controls the amount of light entering the eye by varying the size of the pupil. Reduction in the size of the pupil also increases the depth of field for near objects and reduces certain optical aberrations. To accomplish this goal, the iris has two sets of muscles:

•Musculus constrictor pupillae: A circular band of muscle fibers concentric with the pupil. These fibers have predominantly parasympathetic innervation (Figure 11-2).

•Musculus dilator pupillae: Radially oriented fibers passing from near the root of the iris toward the pupillary margin. These fibers have predominantly sympathetic innervation.

Viewed from the anterior surface, the iris has two zones, the pupillary zone (Figures 11-3 and 11-4) and the ciliary zone. A variable thickening of the iris at the junction of these two zones is called the collarette. The anterior surface of the iris is covered by a modified layer of stromal cells, the anterior border layer (Figure 11-5). The remaining parts of the iris are the stroma and sphincter muscle, the anterior epithelium and dilator muscle, and the posterior pigmented epithelium and

pigment ruff. The posterior pigmented epithelium is continuous with the nonpigmented epithelium covering the ciliary body and eventually with the retina.

The bulk of the iris is stroma, which consists of fibrous connective tissue with bundles of collagen, pigmented and nonpigmented cells, and blood vessels in a mucopolysaccharide matrix. Variations in iris color are due to variations in pigmentation of the stroma and posterior pigmented epithelium and in the arrangement of the anterior border layer (Figure 11-6).

The temporal and nasal long ciliary arteries enter the iris near its root (see Figure 11-3) and form the major arterial circle, which may be incomplete. The vascular supply of the iris of domestic animals greatly exceeds that of the human iris. Therefore surgical procedures near the iris root in animals often result in profuse hemorrhage if the major arterial circle is transected.

The dilator pupillae muscle extends as a continuous sheet in front of the anterior epithelium (see Figure 11-4) and is intimately related with it. The constrictor pupillae muscle is a flat ring of smooth muscle surrounding the pupil in the posterior iris stroma (see Figure 11-5).

In horses, cattle, sheep, and goats, which have a horizontally elliptical pupil, black masses suspended from the superior and occasionally the inferior rim of the pupil are termed corpora nigra (e.g., in horses) or granula iridica (e.g., in ruminants). These masses aid in further control of light entering the pupil and should not be mistaken for tumors or cysts.

Ciliary Body

The ciliary body lies immediately posterior to the iris. On its posterior surface the ciliary body has numerous folds known as the ciliary processes (Figures 11-7 and 11-8). This area of the ciliary body, termed the pars plicata (folded part), merges posteriorly into a flat area (pars plana), which joins the retina. The zonular fibers, which support the lens, originate from the pars plana and between the ciliary processes (Figures 11-9 and 11-10).

Viewed in section, the ciliary body is triangular, with one side joining the sclera, one side facing the vitreous body, and the base giving rise to the iris and iridocorneal angle (Figure 11-11). The ciliary body is covered with two layers of epithelium, the inner layer of which is nonpigmented and the outer layer of which is pigmented. It is continuous with similar epithelium on the posterior surface of the iris and the pigment epithelium of the retina (Figure 11-12). The smooth muscle fibers of the ciliary muscle (parasympathetic innervation) together with blood

FIGURE 11-1. The three layers of the eye. CB, Ciliary body; Ch, choroid; Co, cornea; ON, optic nerve; R, retina; S, sclera. (Modified from Fine BS, Yanoff M [1972]: Ocular Histology. Harper & Row, New York.)

Dilator pupillae muscle (sympathetic)

Constrictor pupillae muscle (parasympathetic)

j

c

i

e

c

h e

f

FIGURE 11-2. Control of pupil size. The arrangement of the constrictor fibers varies among domestic species, but the principles are similar.

FIGURE 11-4. Pupillary portion of the iris. The dense, cellular anterior border layer (a) terminates at the pigment ruff (b) in the pupillary margin. The sphincter muscle is at (C). The arcades (d) from the minor circle extend toward the pupil and through the sphincter muscle. The sphincter muscle and the iris epithelium are close to each other at the pupillary margin. Capillaries, nerves, melanocytes, and clump cells (e) are found within and around the muscle. The three to five layers of dilator muscle

(f) gradually diminish in number until they terminate behind the midportion of the sphincter muscle (arrow), leaving low, cuboidal epithelial cells (g) to form the anterior epithelium to the pupillary margin. Spurlike extensions from the dilator muscle form Michel’s spur

(h) and Fuchs’s spur (i) (these spurs are not commonly described in domestic animals). The posterior epithelium (j) is formed by columnar cells with basal nuclei. Its apical surface is contiguous with the apical surface of the anterior epithelium. (From Hogan MJ, et al. [1971]: Histology of the Human Eye. Saunders, Philadelphia.)

FIGURE 11-3. Clinical anatomy of the iris. The pupillary zone of the iris is typically darker than the surrounding, lighter-colored ciliary zone. The junction between the two zones is termed the iris collarette (solid arrow). Persistent pupillary membranes, if present, typically originate at the iris collarette region. The sinuous posterior ciliary artery enters the iris near the limbus at the 3 and 9 o’clock position (open arrows). From there it divides into superior and inferior branches to form the major vascular circle of the iris.

FIGURE 11-5. Structure of the iris. A, Anterior border layer; B, stroma; C, constrictor muscle; D, dilator muscle; E, posterior epithelium. (Courtesy Dr. Richard R. Dubielzig.)

FIGURE 11-6. Surfaces and layers of the iris. Clockwise from the top the iris cross-section shows the pupillary (a) and ciliary (b) portions, and the surface view shows a brown iris with its dense, matted anterior border layer. The blue iris surface shows a less dense anterior border layer and more prominent trabeculae. Arrows indicate circular contraction furrows. c, Fuchs’s crypts; d, pigment ruff; e, major arterial circle. Radial branches of arteries and veins extend toward the pupillary region. The arteries form the incomplete minor arterial circle (f), from which branches extend toward the pupil, forming capillary arcades. (Note: The incomplete minor arterial circle is variable or absent in many animals.) g, Circular arrangement of the sphincter muscle; h, radial processes of the dilator muscle; i, radial contraction furrows; j, structure folds of Schwalbe; k, pars plicata of the ciliary body. (Modified from Hogan MJ, et al. [1971]: Histology of the Human Eye. Saunders, Philadelphia.)

FIGURE 11-7. Dissecting microscope view of the relationship between the iris, ciliary body, and iridocorneal angle. C, Endothelial surface of the cornea; CP, ciliary processes; I, iris at pupil margin; PL, pectinate ligament; TM, trabecular meshwork. (Courtesy Dr. Mitzi Zarfoss.)

i

h

a

g

f

e

b

e

d

c

FIGURE 11-9. Posterior aspect of the ciliary body, showing pars plicata (a) and pars plana (b). The junction between ciliary body and retina is at c, and the retina at d. In primates this junction is scalloped with bays (e), dentate processes (f), and striae (g) (ora serrata), but in most domestic species it is a straight line (ora ciliaris retinae). (From Hogan MJ, et al. [1971]: Histology of the Human Eye. Saunders, Philadelphia.)

FIGURE 11-10. Anterior view of ciliary processes showing zonules attached to the lens: a, lens zonules; b, ciliary process; c, d, and e, attachment of zonules to lens capsule; f, radial folds in iris; g, circular folds in iris. The precise arrangement of the lens zonules with the lens capsule varies considerably among species. (From Hogan MJ, et al. [1971]: Histology of the Human Eye. Saunders, Philadelphia.)

B

FIGURE 11-12. A, Normal ciliary body of a cat: CC, region of the ciliary cleft; CP, ciliary processes; I, iris; PL, pectinate ligament, PP, pars plana; SVP, scleral venous plexus. B, The ciliary body epithelium is bilayered, with the innermost layer being nonpigmented and the outer layer containing pigment. (Courtesy Dr. Richard R. Dubielzig.)

Pars plana

Pectinate ligaments

Scleral venous sinuses

Triangular outline

of ciliary cleft

Triangular outline of ciliary body

Sclera

FIGURE 11-11. Parts of the ciliary body.

vessels, connective tissue, and nerves occupy a large portion of the ciliary body (Figure 11-13). The muscle fibers originate near the apex of the triangle and insert into the region of the ciliary cleft and trabecular spaces of the iridocorneal angle. Contraction of the ciliary muscle causes the following:

•Relaxation of lens zonules and change in shape or position of the lens to allow for near vision

•Increased drainage of aqueous via the trabecular meshwork

Inflammation of the ciliary body often leads to spasm of the ciliary muscle, which in turn causes ocular pain. Pain relief may be achieved by use of a cycloplegic drug (e.g., atropine), which relaxes the ciliary body. Although drugs that dilate the pupil (mydriatics) may also relax the ciliary muscle (atropine), not all do so (e.g., epinephrine).

Choroid

The choroid is a thin, variably pigmented, vascular tissue forming the posterior uvea. It joins the ciliary body anteriorly and lies between the retina and sclera posteriorly. The choroid is extremely vascular, with its capillaries arranged in a single layer on the inner surface to nourish the outer retinal layers (Figure 11-14). In species with limited retinal vasculature (e.g., horse, rabbit, guinea pig) the retina depends to a large extent on the choroidal blood supply. The choroidal stroma typically contains numerous melanocytes, which form a dark optical background to the retina. In most domestic mammals except the pig, a reflective layer—the tapetum lucidum—lies within the inner capillary layer. In large animals the tapetum is penetrated by