The anterior uvea consists of the iris, ciliary body, and anterior chamber (or iridocorneal) angle. The iris provides most of the eye color as well as an aperture (pupil) to regulate the amount of light that enters the eye and posterior segment. Pupil shape varies widely among animal species, including circle, vertical slit, horizontal oval, square, or even multiple pupils. The ciliary body provides most of the aqueous humor to nourish the anterior segment and remove its metabolic wastes, as well as the outflow channels (anterior chamber angle) for aqueous humor to reenter the venous system. The ciliary body also regulates lens curvature (accommodation), which is more limited in animals than in people. The ciliary body continues posteriorly as the choroid, and diseases of the iris and ciliary body also often involve the choroid. Diseases of the anterior uvea are common in domestic animals.
Persistent pupillary membranes are remnants of the normal prenatal vascular network that fills the pupillary region. Persistence of pigmented strands across the pupil from one area of the iris to another, or to the lens or cornea, is not uncommon in dogs and occurs occasionally in other species. In Basenjis, the condition is inherited.
Atrophy of the iris is common in older dogs and may involve the pupillary margin or the stroma. Atrophy of the pupillary margin creates a scalloped border and a weakening of the sphincter muscle, which is manifest as a dilated pupil(s) or by sluggish pupillary light reflexes. Stromal atrophy results in dramatic holes in the iris and, often, displacement of the pupil. Neither form of atrophy appears to affect vision. Animals lacking a functional iridal sphincter may show increased sensitivity to bright light.
Iridic cysts are seen in dogs, cats, and horses. In dogs, they usually are free-floating, pigmented spheres in the aqueous humor within the pupil and anterior and posterior chambers. Although innocuous in most breeds of dogs, anterior uveal cysts (iris and ciliary body) in Golden Retrievers are associated with exfoliation of pigmented cells, chronic uveitis, glaucoma, and cataract formation. In cats, the cysts frequently are attached at the pupillary margin. In horses, they are present in the stroma of the iris and more frequently involve blue irides. Therapy is rarely necessary, but aspiration or laser-induced deflation can be performed. Transillumination will usually demonstrate their cystic nature and differentiate them from neoplasms. Enlarged and cystic dorsal corpora nigra may impair vision and mimic iridic melanomas in horses. Surgical excision or aspiration may be indicated.
Iris colobomas are rare in animals but occur occasionally in Australian Shepherds. They are usually in the upper iris, mainly in heterochromic irides, and cause an irregularity to the pupil. Viewed closely, the defect involves the iridal anterior stroma and apparently the sphincter muscle, but the pigment layer is present.
Anterior uveitis or iridocyclitis, when acute, is manifest by miosis, increased protein and cells in the anterior chamber (aqueous flare), low intraocular pressure, bulbar conjunctival hyperemia, iridal swelling, photophobia, and blepharospasm. Secondary glaucoma, cataract, and corneal opacification may be complications. Concurrent posterior uveitis or choroiditis is frequent. Causes of anterior uveitis can be separated into exogenous and endogenous. Penetrating and nonpenetrating trauma and, rarely, intraocular neoplasms or intraocular helminths are causes of unilateral uveitis. Common causes of bilateral uveitis include immune-mediated diseases and infectious diseases such as infectious canine hepatitis, feline infectious peritonitis, feline leukemia, feline immunodeficiency, feline toxoplasmosis, systemic mycoses in dogs and cats, canine brucellosis, leptospirosis in horses, bovine malignant catarrhal fever, infectious bovine rhinotracheitis, equine viral arteritis, classical swine fever, canine ehrlichiosis, and neonatal bacterial infections (joint, navel, and gut) of calves, lambs, kids, and foals. Recurrent uveitis that is at least in part immune-mediated affects horses (periodic ophthalmia or recurrent uveitis) and dogs (panuveitis with dermal depigmentation or uveodermal syndrome). A thorough history, examination of the cornea for injuries, physical examination, serum -serology, and centesis of the aqueous for culture, serology, and cytology aid in diagnosis.
Nonspecific therapy consists of topical mydriatics to maintain pupillary dilation and movement, topical corticosteroids (if nonbacterial), a darkened environment, and prostaglandin inhibitors (such as aspirin, flunixin meglumine, or phenylbutazone). If bacterial in origin, topical, systemic, and perhaps intraocular antibiotics are indicated. Treatment of immune-mediated processes may require systemic or subconjunctival as well as topical corticosteroids and oral azathioprine.
Hyphema or hemorrhage in the anterior chamber has several clinical appearances, including the following: 1) small, focal blood clots that are suspended within the anterior chamber or adhered to the posterior cornea, iris, or anterior lens capsule; 2) diffuse, unclotted hemorrhage throughout the entire anterior chamber occluding deeper eye examination and vision; and 3) multiple layers of recurrent or chronic unclotted hemorrhage (the oldest is a purple or black layer in the bottom of the anterior chamber and the most recent hemorrhage is the dorsal bright red layer). Causes of hyphema include uveitis, trauma, intraocular neoplasia, systemic hypertension, coagulation factor abnormalities, platelet disorders, hyperviscosity, congenital ocular anomalies, anterior segment neovascularization, and glaucoma. Resolution of hyphema requires exit of intact RBC through the aqueous humor outflow channels.
Acute hyphema generally has a good prognosis provided the cause is identified and treated. Recurrent and/or chronic hyphema has a poor to guarded prognosis because secondary glaucoma or phthisis bulbus is likely. No drugs have been proved to facilitate resolution of hyphema, but in-tracameral tissue-plasminogen activator (TPA) can dissolve fibrin that is <10–14 days old and release the entrapped RBC within the anterior chamber. TPA does not prevent future fibrin formation, but topical and systemic corticosteroids may.
Last full review/revision July 2011 by Kirk N. Gelatt, VMD