Chapter 11 Uvea
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 blood-aqueous 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.
(Modified from Fine BS, Yanoff M : Ocular Histology. Harper & Row, New York.)
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:
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.
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 11-4 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. : Histology of the Human Eye. Saunders, Philadelphia.)
(Courtesy Dr. Richard R. Dubielzig.)
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).
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. : Histology of the Human Eye. Saunders, Philadelphia.)
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.
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).
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.)
Figure 11-8 Posterior aspect of the canine iris and ciliary body (with the lens removed) showing the arrangement of the numerous bladelike ciliary processes. In this golden retriever multiple small ciliary cysts are also present at the tips of these processes.
(Courtesy Dr. Richard R. Dubielzig.)
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. : 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. : Histology of the Human Eye. Saunders, Philadelphia.)
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 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:
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.)
Figure 11-13 Degree of development of the ciliary body musculature among mammalian iridocorneal angles in the ungulate (top), carnivore (middle), and ape (bottom). Development is most pronounced in primates (ape) and least pronounced in herbivorous species (ungulate), with carnivore development between. The size of the iridocorneal angle and its cilioscleral cleft or sinus (CC) is inversely large or most pronounced in the ungulate.
(Modified from Samuelson DA : Ophthalmic anatomy, in Gelatt KN [editor]: Veterinary Ophthalmology, 3rd ed. Lippincott Williams & Wilkins, Philadelphia, p. 77; which was drawn after Duke-Elder S : System of Ophthalmology, Vol 1: The Eye in Evolution. Henry Kimpton, London.)
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).
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 numerous small capillaries, which appear as small focal dark spots (the stars of Winslow) when viewed end-on with the ophthalmoscope. The arteries and nerves to the anterior parts of the eye pass forward through the choroid. The choroid receives its main arterial supply from the following vessels:
Figure 11-14 Choroidal blood supply and innervation, and Bruch’s membrane. The retina is located at the bottom and the sclera at the top of the drawing. The retinal pigment epithelium (a) is in close contact with Bruch’s membrane (b). The choriocapillaris (c) forms an intricate network along the inner choroid. Bruch’s membrane is very thin in some domestic species. In the superior fundus the tapetum lies between the branching vessels in the choroid and the single layer of the choriocapillaris under the retina. Venules (d) leave the choriocapillaris to join the vortex system (e). The short ciliary artery is shown at f, before its branching (g) to form the choriocapillaris. A short ciliary nerve enters the choroid at h and branches into the choroidal stroma (i). j, Superchoroidea.
(Modified from Hogan MJ, et al. : Histology of the Human Eye. Saunders, Philadelphia.)
In herbivores the tapetum is fibrous in nature (tapetum fibrosum), whereas in carnivores the tapetum is cellular and composed of reflective crystals (tapetum cellulosum) (Figure 11-15). The reflective properties of the tapetum, and not the presence of pigments, causes the distinctive color of the fundi of different animals and is the reason an animal’s eyes “shine” in the dark. This color varies with thickness of the tapetum, breed, age, and species. Reflecting light through the retina a second time improves the animal’s ability to function in dim light.
The uveal tract plays a key role in maintaining the blood-ocular barrier (Figure 11-16). Diseases involving the uveal tract frequently cause a breakdown of this barrier, which leads to exudation of excessive amounts of proteins or cells into the aqueous humor, vitreous, or subretinal space. The blood-ocular barrier is composed primarily of a blood-retinal barrier and a blood-aqueous barrier. The blood-retinal barrier is formed at the level of the retinal capillary vascular endothelium, which is nonfenestrated and has tight junctions, and the retinal pigment epithelium, which also has tight junctions and separates the relatively leaky choroidal blood vessels from the overlying retina. The blood-aqueous barrier is formed by tight junctions at the level of the nonfenestrated iridal vascular endothelium and between cells constituting the nonpigmented ciliary body epithelium. Most large molecules, especially proteins, are unable to pass through or between the cells in this barrier system. The exact anatomic location of the barrier is probably different for different substances (e.g., capillary endothelial cells, endothelial basement membrane, and intercellular junctions). By limiting the amount of protein and other large molecules that may scatter light in the aqueous and vitreous humor, these barriers serve to create a more optically perfect media. They are, however, frequently disrupted by inflammation or other disease processes.
Figure 11-16 A, Blood-ocular barrier. The barrier normally prevents large molecules and cells from leaving the blood vessels and entering the eye, thereby maintaining clarity of the aqueous humor and vitreous. B, Aqueous flare in a cat with uveitis. This finding, which represents breakdown of the blood-aqueous barrier, is a hallmark of anterior uveitis.
(A from Gilger B : Equine Ophthalmology. Saunders, St. Louis.)
Because of the continuity between the various parts of the uvea, aqueous humor, and vitreous, however, uveal inflammation often involves many ocular structures. The retina and choroid are adjacent, with no major barriers between, so they are frequently inflamed together. Consequently, the following terms are often preferable:
The uvea is an immunologically competent tissue that behaves as an accessory lymph node. Intraocular antigens may enter the systemic circulation and stimulate distant lymphoid organs. In 5 to 7 days sensitized B and T lymphocytes migrate toward the antigen within the eye, enter the uvea, and engage in antibody formation or cell-mediated immune reactions, which may create intraocular inflammation. Subsequent exposure to the same antigen results in a faster and greater (anamnestic) response.
The uvea is often secondarily inflamed when other parts of the eye are inflamed (e.g., secondary anterior uveitis frequently accompanies keratitis). Although such reactions are commonly beneficial in resolution of the primary disease (e.g., production of immunoglobulins and sensitized lymphocytes), excessive secondary uveitis may irreparably damage the eye.
Autoimmune phenomena also occur in the uvea. Preceding tissue damage (e.g., previous inflammation) releases tissue-specific retinal or uveal antigens that are normally intracellular or otherwise immunologically isolated. Hence one cause of uveal inflammation (e.g., trauma, infection by various organisms) may subsequently lead to a secondary, immune-mediated mechanism that results in persisting or recurring inflammation. Such a response may be involved in recurrent equine uveitis. Immune-mediated inflammation may also occur after exposure to lens proteins that have been immunologically isolated by the lens capsule before birth (e.g., lens-induced uveitis) or in response to antigens associated with uveal melanocytes (e.g., uveodermatologic syndrome).
Corectopia (which is congenital) must be distinguished from a pupil pulled out of shape by synechia (which is acquired). In synechiation the pupil is distorted by adhesions between the lens and iris. Pupillary abnormalities are rarely significant by themselves, but they may be an important indication of other abnormalities.
During development the pupillary membrane (anterior portion of the tunica vasculosa lentis) spans the pupil from one portion of the iris collarette to another and supplies nutrients to the developing lens (see Chapter 2). In dogs this membrane is usually resorbed during later fetal development and the first 6 weeks of life, leaving a clear pupillary aperture. It is not uncommon, however, for remnants to remain for several months or longer. In general small remnants spanning from one portion of the iris to another (iris-to-iris persistent pupillary membranes [PPMs]) have no visual consequences, although visual impairment may occur if strands contact the cornea (iris-to-cornea PPMs) or lens (iris-to-lens PPMs) and create an opacity within the visual axis (Figure 11-17).
Figure 11-17 Persistent pupillary membranes (iris to cornea) in a young Saint Bernard dog. Unlike postinflammatory anterior synechia, these iridal strands originate near the iris collarette region. Anterior synechia would originate at the pupillary border or in the far periphery of the iris, near the iridocorneal angle.
(Courtesy University of Wisconsin–Madison Veterinary Ophthalmology Service Collection.)
PPMs occur in a large number of dog breeds, most notably the basenji, in which they are recessively inherited (see Appendix I). A genetic basis is also likely in many other dog breeds, but the mode of inheritance is probably not simply mendelian. PPMs may span from one region of the iris to another (sometimes crossing the pupil) or they may extend to the cornea or lens, creating opacities in these structures. PPMs can usually be differentiated from inflammatory anterior or posterior synechia on the basis of their origin near the iris collarette region (versus an origin at the pupillary margin for synechia) and their presence at birth. It usually is possible to see the membrane extending from the iris collarette region to the cornea or lens, although occasionally the membrane may have broken free and the cornea or lens opacity (often pigmented) is all that remains. Therapy is not typically required or possible. The best method of preventing the disorder is to examine breeding stock and breed only animals that are free of PPMs. Slit-lamp biomicroscopy is essential for the examinations.
A coloboma is a defect in the eye resulting from incomplete closure of the embryonic fissure. Typical colobomas occur in the inferomedial portion of the iris or choroid or adjacent to the optic disc (Figure 11-18). Colobomas of the sclera also occur in the collie eye anomaly. Although the embryonic fissure is not involved, coloboma is also applied to lid defects and to sector defects in the iris and lens.
Anterior segment dysgenesis is an autosomal recessive trait in the Doberman pinscher characterized by variable degrees of microphthalmia, corneal opacity, lack of anterior chamber, undifferentiated iris and ciliary body, hyaloid artery remnants, absence of or rudimentary lens, retinal dysplasia and separations, and congenital blindness. There is no treatment for this disorder.
Anterior segment dysgenesis syndrome occurs frequently in Rocky Mountain horses and has two distinct ocular phenotypes: (1) large cysts originating from the temporal ciliary body or peripheral retina (Figure 11-19) and (2) multiple anterior segment anomalies, including ciliary cysts, iris hypoplasia, iridocorneal adhesions and opacification, nuclear cataract, and megalocornea (Figure 11-20). This condition may be codominantly inherited, so that ciliary cysts are seen in heterozygous animals and multiple anterior segment anomalies are seen in homozygous animals.
Figure 11-20 Anterior segment dysgenesis in a Rocky Mountain horse presumed to be homozygous for the responsible gene. The iris is smooth, dark, and histologically hypoplastic. The pupil resists dilation, presumably owing to defects in the iris musculature. This horse had other anterior segment anomalies, including ciliary cysts, iris hypoplasia, iridocorneal adhesions and opacification, nuclear cataract, and megalocornea.
Heterochromia refers to variations in iris coloration. Both eyes, one eye only, or only part of an iris may be affected, and often there are concurrent variations in coat color (Table 11-1). Heterochromia iridis refers to variations in pigmentation of different regions of the iris in the same eye (Figure 11-21), and heterochromia iridium refers to variations in coloration between the two eyes of the same animal. Although heterochromia may be normal, blue iridal tissue has also been associated with iris hypoplasia, iris coloboma, and corectopia as well as with absence of or a small tapetum and lack of pigmentation of the nontapetal fundus. An association between congenital deafness and heterochromia has also been recognized in blue-eyed white cats and in the Dalmatian, Australian cattle dog, English setter, Australian shepherd, Boston terrier, Old English sheepdog, and English bulldog.
|Burmese||Variable iris hypopigmentation|
|Abyssinian||Variable iris hypopigmentation|
|Persian||Variable iris hypopigmentation|
|Dog||Australian cattle dog||Dappling|
|Collie||Merling (autosomal dominant)|
|Great Dane||Harlequin coat (autosomal dominant)|
|Long-haired dachshund||Harlequin coat (autosomal dominant)|
|Dalmatian||Dappling (autosomal dominant)|
|Old English sheepdog||Heterochromia iridis|
|Siberian husky||Dappling (autosomal dominant)|
|Weimaraner||Iris hypopigmentation varies|
|Horse||Pinto, appaloosa, white and gray horses||Variable heterochromia|
|Cattle||Hereford, shorthorn||Albinism, subalbinism|
In dogs, heterochromia is due to incomplete maturation or absence of pigment granules in the iris stroma or anterior pigmented layer. Heterochromia iridis is proposed to be due to decreased availability of tyrosine hydrolase, necessary for the synthesis of melanin, as follows:
|TYPE OF ALBINISM||FEATURES|
|Partial||Iris blue and white centrally, brown peripherally|
|Hair color normal|
|Incomplete||Iris light blue, gray, and white|
|Hair color white|
|Some brown sectors in iris, and some colored hair patches|
|Nontapetal fundus incompletely pigmented and choroidal vasculature visible|
|Complete||Iris very pale blue or white|
|Hair pure white|
|Variable fundus colobomas and tapetal hypoplasia|
Iris nevi (Figure 11-22) are most commonly observed in cats and dogs. They may consist of focal spots of hyperpigmentation. They must be differentiated from neoplasms that require surgical treatment. Iris nevi do not protrude above the surface of the iris and do not enlarge. Nevi have a low malignant potential and show an increase in the number of cells or greater pigmentation of existing cells. They must be observed carefully for changes, especially in cats, in which they may transform into the early stages of diffuse malignant iris melanoma.
Waardenburg’s syndrome consists of deafness, heterochromia iridis, and white coat color. Although this hereditary syndrome occurs most commonly in blue-eyed white cats, it also occurs in dogs (especially the Australian cattle dog, Great Dane, and Dalmatian), mice, and humans. Not all blue-eyed white cats are affected. In the cat, the syndrome is inherited as a dominant trait with complete penetrance for the white coat and incomplete penetrance for deafness and blue irides.
Aqueous flare is due to breakdown of the blood-aqueous barrier with increased permeability of vessels in the iris and ciliary body, resulting in release of protein into the aqueous. Keratic precipitates (KPs) are accumulations of inflammatory cells (neutrophils, lymphocytes, or macrophages) that adhere to the corneal endothelium. In large numbers these cells form a white layer in the anterior chamber called hypopyon (Figure 11-23). KPs may be small and scattered (in feline infectious peritonitis) or large and yellow (“mutton-fat” KPs) in granulomatous diseases. Miosis may be due to iridal edema or spasm of the iridal sphincter muscle. As the inflammation subsides, synechiae may form, causing an irregularly shaped pupil (Figure 11-24) or a scalloped appearance on dilation, with pigment remnants on the anterior lens capsule. If posterior uveitis is present, the vitreous may become hazy, and retinal edema, exudates, or detachments may be seen.
Figure 11-23 Hypopyon in the ventral anterior chamber in a dog that had suffered a penetrating ocular injury. Unless the cornea has been perforated, the anterior chamber is usually sterile in most patients with hypopyon.
Posterior synechiae occur when fibrinous adhesions form between the lens and iris, with fibrovascular organization occurring later (see Figure 11-24). Formation of synechiae is more likely when aqueous protein content is high. If synechiae form around the entire circumference of the pupil, iris bombé occurs, preventing aqueous flow to the anterior chamber, and secondary glaucoma almost invariably follows. An irregularly shaped pupil is frequently caused by synechiae. If blood or exudate organizes in the anterior chamber, a connective tissue membrane may occlude or obliterate the pupil.
Adhesions may form between the iris and trabecular mesh-work or between the iris and cornea. Swelling, iris bombé, and cellular infiltrates may reduce drainage of aqueous through the iridocorneal angle early in uveitis, but once peripheral anterior synechiae have formed, an alternative route for drainage must be provided, because the angle is held closed by the synechiae.
Cataract (opacity of the lens) occurs frequently after uveitis. It is probably caused by altered composition of the aqueous that interferes with lens nutrition. When an animal with a cataract and signs of uveitis is examined, determination must be made as to whether the cataract caused the uveitis or the uveitis caused the cataract.
IOP is usually lowered during uveitis because an inflamed ciliary body makes less aqueous humor and endogenous prostaglandins may increase uveoscleral outflow. If IOP is normal or increased in the presence of active inflammation, it is likely that aqueous humor outflow via the trabecular meshwork is impaired in one of the following ways:
Intractable secondary glaucoma due to lens-induced uveitis is a common entity, especially in dogs. This condition may be seen after penetrating injuries to the lens, in patients with long-standing cataracts undergoing lens resorption, and sometimes after cataract extraction.
The iris and ciliary body atrophy as the stroma is replaced by fibrous tissue. Defects may appear in the iris. Atrophy of areas of the choroid frequently results in atrophy of the overlying retina, which is visible ophthalmoscopically. Severe atrophy of the ciliary body causes hypotony (lowered IOP). In some animals the color of the iris becomes darker after uveitis. In severe cases the entire globe may shrink, a condition called phthisis bulbi.
In some animals with chronic anterior uveitis new blood vessels and fibrous membranes form on the anterior surface of the iris. These may result in eversion of the pupillary margin, called ectropion uveae, or glaucoma as they cover the trabecular meshwork.
A cyclitic membrane is a band of fibrovascular tissue extending from the ciliary body across either the pupil or the anterior face of the vitreous. It consists of fibrous tissue and blood vessels and may severely obstruct vision.
Sympathetic ophthalmia is a rare immune-mediated disorder in humans, and perhaps in animals, in which unilateral intraocular inflammation liberates previously immunologically isolated antigens. The resulting immune response to these ocular antigens leads to damage of the previously normal other eye.
Anterior uveitis is distinguished from conjunctivitis, superficial keratitis, and glaucoma, the other causes of the red-eye syndrome (Table 11-3). The uvea is involved in numerous systemic disorders (Table 11-4). Such diseases usually affect other parts of the eye in addition to the uvea and are discussed in Chapter 18. Once uveitis is detected, every effort should be made to identify a specific cause of the inflammation so that the most effective therapy may be started. A thorough history and complete physical examination are essential for the proper diagnosis as to the cause of the inflammation in a given patient.
|CAUSE||MOST COMMONLY AFFECTED SPECIES|
|Histiocytic proliferative disease||Dog|
|Miscellaneous primary intraocular tumors||Any|
|Miscellaneous metastatic tumors||Any|
|Diabetes mellitus (lens-induced uveitis)||Dog|
|Systemic hypertension||Cat, dog|
|Cataracts (lens-induced uveitis)||Any|
|Lens trauma (phacoclastic uveitis)||Any|
|Uveodermatologic syndrome (Vogt-Koyanagi-Harada–like syndrome)||Dog|
|Septicemia/endotoxemia due to any cause||Any|
|Leptospira spp.||Dog, horse|
|Bartonella spp.||Dog, cat|
|Borrelia burgdorferi||Dog, horse|
|Brucella spp.||Dog, horse|
|Escherichia coli||Cattle, horse|
|Listeria monocytogenes||Sheep, cattle|
|Ehrlichia canis or Ehrlichia platys||Dog|
|Yeasts and Fungi|
|Aspergillus spp.||Chickens, turkeys, cat|
|Blastomyces spp.||Dog, cat|
|Cryptococcus spp.||Dog, cat|
|Histoplasma capsulatum||Dog, cat|
|Canine adenovirus types 1 and 2 (immune-mediated)||Dog|
|Canine distemper virus||Dog|
|Coronavirus (feline infectious peritonitis)||Cat|
|Feline leukemia virus||Cat|
|Feline immunodeficiency virus||Cat|
|Herpesvirus (Marek’s disease)||Chickens, turkeys|
|Feline herpesvirus 1||Cat|
|Canine herpesvirus 1||Dog|
|Equine herpesvirus 1 and 2||Horse|
|Ovine herpes virus 2 (MCF)||Cattle|
|Alcelaphine herpes virus 1 (MCF)||Cattle|
|Equine viral arteritis||Horse|
|Parainfluenza type 3||Horse|
|Taenia multiceps||Sheep, dog|
|Echinococcus granulosis||Horse (rare)|
|Onchocerca cervicalis||Horse (equine recurrent uveitis)|
|Diptera spp. (ophthalmomyiasis interna)||Various|
|Toxocara spp., Baylisascaris spp. (ocular larval migrans)||Dog, cat|
|Pilocarpine, carbachol other parasympathomimetics||Any|
|Prostaglandin derivatives (latanoprost)||Any|
|Endotoxemia from any systemic source||Any|
|Infectious keratitis with bacterial toxin production||Any|
|Blunt or penetrating injuries||Any|
|Corneal foreign bodies||Any|
|Ulcerative keratitis of any cause||Any|
|Deep necrotizing or nonnecrotizing scleritis||Dog|
MCF, Malignant catarrhal fever.
Numerous uveitis classification schemes have been proposed, including those based on the tissues affected (anterior uveitis, posterior uveitis, panuveitis), on the presumed histologic nature of the disorder (suppurative, nonsuppurative, granulomatous, nongranulomatous), on whether the cause starts inside the eye or from its surface (endogenous versus exogenous), and on a specific etiology (see Table 11-4). Although each of these schemes has its own advantages and disadvantages, classification into granulomatous or nongranulomatous and then by specific etiology is probably the most useful method in a clinical setting, because it also helps guide specific therapy (Table 11-5). This scheme, however, is plagued by the presence of a large percentage of patients having idiopathic uveitis in which the cause remains obscure and therapy can be only nonspecific and directed at controlling inflammation and preventing further damage to the eye. Presumably, most of these cases are immune-mediated or involve microorganisms that are not yet recognized as pathogenic. It is hoped that over time the percentage of patients with idiopathic uveitis will decline as our understanding of the causes of this disorder improves.
|Acute onset||Gradual onset|
|Short course||Chronic or recurrent|
|No keratic precipitates||Keratic precipitates/greasy exudate on lens surface|
|No synechiae||Posterior synechiae|
|No iris nodules||Iris nodules may be present|
|Primarily anterior uveitis||Posterior uveitis may also be present|
These criteria are useful but not absolute and are interpreted along with other clinical signs.
Although classification as granulomatous or nongranulomatous uveitis is based on a histologic classification scheme, the criteria in Table 11-5 can also be used to make reasonable clinical inferences about the histologic nature of the inflammation and to allow for prioritization of the diagnostic tests to be performed. Most cases of granulomatous uveitis are associated with microorganism or foreign material stimulation of a chronic immune response, whereas nongranulomatous uveitis is often associated with physical, toxic, or allergic causes. After determining whether a specific animal has granulomatous or nongranulomatous uveitis, the clinician should consider specific tests to try to determine the exact cause (e.g., serum titer measurement for Toxoplasma). In general the following specific categories of uveitis should be considered: