Canine Uveitis

Alexandra Van Der Woerdt, New York, New York

Uveitis is defined as inflammation of the vascular uveal tract within the eye. Anterior uveitis is inflammation of the iris and ciliary body. Chorioretinitis is inflammation of the choroid and the adjacent retina. Isolated choroiditis without involvement of the retina is rare. Panuveitis refers to inflammation that affects the entire uveal tract. Anterior uveitis and chorioretinitis are common ocular diseases in dogs and often are present at the same time. There are numerous causes of uveitis in dogs, and they include both systemic diseases and localized ocular diseases. Proper diagnosis and investigation of possible underlying diseases is important for the management of both the eye and the dog. This chapter provides a brief description of uveal anatomy and physiology, followed by a discussion of clinical signs, differential diagnoses, and treatment of uveitis in dogs.

Anatomy and Physiology

The uvea consists of the iris, ciliary body, and choroid. The uvea has many functions, including production of aqueous humor, regulation of the amount of light that enters the eye through constriction and dilation of the pupil, and supply of nutrients and oxygen to the nonvascularized or poorly vascularized portions of the eye. The uvea also is responsible for maintenance of the blood-aqueous barrier that protects the eye from toxins, infectious organisms, and exuberant inflammation. Inflammation starts either within the eye itself or in reaction to a disease process elsewhere in the body. Microorganisms or damaged tissue release inflammatory mediators such as histamine, serotonin, prostaglandins, and leukotrienes, which result in vasodilation and increased vascular permeability. This leads to breakdown of the blood-aqueous barrier. These inflammatory mediators also cause leukocyte activation and migration. Antigens are transported through the bloodstream to the spleen or other lymphoid tissues, which results in activation of T and B lymphocytes. These activated T and B lymphocytes are transported back to the eye through the bloodstream to the uveal tract. Uveitis resolves when inhibitory cytokines eliminate the inflammatory response and the initial offending antigen is removed. Chronic inflammation may occur when the initial offending antigen cannot be removed or the inflammatory response is not adequately suppressed.

Diagnosis

Clinical signs of anterior uveitis include blepharospasm, conjunctival hyperemia, corneal edema, aqueous flare, hypopyon, swelling of the iris, rubeosis iridis (neovascularization of the iris in chronic uveitis), decreased intraocular pressure (IOP), decrease or loss of vision, and miosis. Table 249-1 lists the differential diagnoses for the various clinical signs associated with anterior uveitis. Blepharospasm is a sign of ocular pain associated with spasm of the ciliary body musculature and intraocular inflammation. Conjunctival hyperemia is a nonspecific sign associated with many ocular diseases and cannot be used to rule in or rule out uveitis. Corneal edema is caused by temporary malfunction of the endothelial cells resulting in decreased removal of fluid from the cornea. Breakdown of the blood-aqueous barrier results in the leakage of protein and inflammatory cells into the aqueous humor. The anterior chamber is best evaluated for the presence of aqueous flare by illumination using a bright pinpoint or slit-beam light source held in close proximity to the cornea in a dark room. A normal eye shows a white light beam on the cornea, no light reflection from the aqueous humor, and a white light beam on the iris-lens. An eye with uveitis has increased protein and cells in the aqueous humor, which can be seen as light reflecting between the beam on the cornea and the beam on the iris-lens. Severe breakdown of the blood-aqueous barrier may result in the presence of white blood cells in the anterior chamber, a condition called hypopyon. These often settle at the bottom of the anterior chamber. It is important to remember that the presence of hypopyon does not necessarily indicate intraocular infection but is pathognomonic for intraocular inflammation. Inflammation of the iris and ciliary body causes a decrease in IOP because of a decrease in the production of aqueous humor and an increase in the removal of aqueous humor through the inflamed iris. Miosis results from elevated levels of prostaglandins in the aqueous humor that stimulate contraction of the iris sphincter muscle. Blepharospasm, corneal edema, aqueous flare, and miosis all may contribute to a decrease in vision.

TABLE 249-1

Clinical Signs of Anterior Uveitis with Common Differential Diagnoses

Clinical Sign	Differential Diagnoses	Diagnostic Tests and Other Clinical Signs to Help Differentiate Diagnoses
Blepharospasm	Corneal ulceration Glaucoma Lens luxation Blepharitis Entropion	Thorough ophthalmic examination Measurement of IOP
Conjunctival hyperemia	Glaucoma Conjunctivitis Allergic Keratoconjunctivitis sicca Corneal ulceration	Schirmer tear test Measurement of IOP Fluorescein staining
Corneal edema	Corneal ulceration Glaucoma Anterior lens luxation Endothelial cell degeneration	Fluorescein staining Measurement of IOP Evaluation of lens position
Aqueous flare	Lipid-laden aqueous humor	Biochemistry profile with evaluation of cholesterol and total lipids
Hypopyon	Focal area of depigmentation in iris	Comfortable eye with no other signs of inflammation
Iris swelling	Normal iris crypts Major arterial circle visible at base of iris Neoplastic infiltration	No other signs of inflammation present with normal iris crypts
Rubeosis iridis	Major arterial circle may appear as a red vessel at base of iris in eyes with a light-colored iris	Circular, irregular vessel at base of iris
Miosis	Neurologic disease Use of miotic agents (i.e., latanoprost, pilocarpine)
Low intraocular pressure	Advanced age	Absence of other clinical signs of uveitis in an older dog
Decreased or loss of vision	Severe corneal disease Cataract Lens luxation Retinal degeneration Sudden acquired retinal degeneration Optic neuritis Retinal detachment	Mydriasis usually present in the following: Retinal degeneration Sudden acquired retinal degeneration Optic neuritis Retinal detachment Difficult to evaluate intraocular details in severe corneal disease