Clinical Signs of Anterior Uveitis

FIGURE 1 Diffuse corneal edema, conjunctival hyperemia, episcleral congestion, and decreased intraocular detail. Classic clinical signs of acute uveitis in a dog, including significant aqueous flare in the anterior chamber. Intraocular pressure was 4 mm Hg, and vision was reduced (assessed with menace response). Fluorescein dye had been recently applied.

FIGURE 2 Well-organized fibrin clot in the anterior chamber. Well-organized fibrin clot in the inferior anterior chamber in a cat. The clot was initially larger and less organized, but it decreased in size after treatment with topical anti-inflammatory medications. Fibrin clots can form secondary to severe anterior uveitis and may require treatment with an intracameral tissue plasminogen activator.

FIGURE 3 Frank hyphema, corneal neovascularization, corneal edema, and decreased intraocular detail. RBCs in the anterior chamber in a dog. Anterior uveitis resulted from breakdown of the blood–aqueous barrier, allowing blood components to enter the eye. Significant aqueous flare was also present.

FIGURE 4 Iridal lymphoid nodules and incomplete cataract. Multifocal, gray iridal nodules most likely composed of lymphocytes and plasma cells and consistent with lymphocytic-plasmocytic idiopathic uveitis in a cat.² This presentation of anterior uveitis is most common in cats.

FIGURE 5 Fibrin clot containing blood in the anterior chamber. Anterior chamber with a large fibrin clot mixed with hemorrhage and a significant degree of aqueous flare in a cat 

FIGURE 6 Iris bombe, complete cataract, hyphema, and decreased intraocular detail. Clinical signs of iris bombe (ie, 360-degree attachment of the iris margin to the anterior lens capsule [360-degree posterior synechiae]) in a dog. Hyphema, rubeosis iridis (increased vascularization of the iris surface), and a complete cataract were also present. Decreased intraocular detail was secondary to severe anterior chamber aqueous flare. Eyes with iris bombe commonly have elevated intraocular pressure due to occlusion of the pupil and blockage of aqueous outflow, leading to secondary glaucoma. The iris tissue body can curve toward the posterior surface of the cornea, creating an anterior chamber with uneven depth.

FIGURE 7 Multifocal posterior synechiae, incomplete cataract, and iridal hyperpigmentation. Clinical signs of chronic anterior uveitis (eg, multifocal posterior synechiae that likely caused the incomplete cataract) in a dog. The iris can darken over time (ie, iridal hyperpigmentation) if anterior uveitis persists.

FIGURE 8 Posterior synechiae, resorbing cataract, iridal hyperpigmentation, and episcleral congestion. Clinical signs of anterior uveitis secondary to advanced cataract formation (ie, multifocal posterior synechiae, isolated multifocal regions of pigmentation of the anterior lens capsule with marked episcleral congestion) in a dog. The lens capsule appeared wrinkled, and the anterior lens cortex contained multifocal, hyperrefractile structures, supporting a diagnosis of resorbing cataract. Anterior uveitis caused iridal hyperpigmentation in this case.

FIGURE 9 Hypopyon, corneal edema, and corneal infiltrate with keratomalacia. Hypopyon (ie, visible WBCs in the anterior chamber) settled in the inferior half of a canine eye due to gravity. Hypopyon is usually associated with severe aqueous flare. Severe anterior uveitis was secondary to a deep, infected corneal ulcer that caused an irregular corneal surface. Corneal infiltrate was visible in the temporal section of the cornea.