Aqueous flare is the hallmark of uveitis and is visible when proteins are in the anterior chamber, indicating a breakdown of the blood-ocular barrier. These proteins scatter light, making the aqueous humor appear cloudy. Hyperemia of the conjunctival vessels and aqueous flare are characteristic, but anterior uveitis can also manifest as corneal edema, hyphema, hypopyon, iris color change (usually to a darker shade), keratic precipitates (deposition of inflammatory cells on the corneal endothelium), miosis, and pain.¹

Decreased IOP occurs when the ciliary body becomes inflamed, decreasing aqueous humor production and increasing perfusion through the posterior vascular pathway. In acute uveitis, blepharospasm, enophthalmos, and elevation of the third eyelid are common. With chronic uveitis, these manifestations of ocular pain may no longer be present. Patients with chronic uveitis may also present with posterior synechiae. Iris bombé and glaucoma can occur, as seen in this cat.

Work-up for feline uveitis

Initially test any cat with uveitis of unknown cause for FIV and FeLV infections, and ask the owner about travel, trauma history, vaccination status, and whether the cat goes outdoors. Additional diagnostic tests when systemic causes are suspected include a complete blood count, a serum chemistry profile, and a urinalysis. Fungal antibody titers and antibody titers against Toxoplasma gondii also may be useful. Anterior chamber paracentesis with PCR and culture of the aqueous humor for Bartonella species, coronavirus, T. gondii, and Cryptococcus species are helpful. A Western blot may be performed to look for Bartonella species.⁵ Even with an exhaustive diagnostic work-up, a definitive cause may not be found.⁶

This patient had anterior uveitis and developed secondary iris bombé, glaucoma, and finally blindness. This progression illustrates the importance of early recognition and treatment of uveitis. When inflammation compromises the integrity of the blood-ocular barrier, proteins, fibrin, and blood leak into the aqueous humor and the vitreous. Synechiae and glaucoma can follow. Glaucoma can also occur when inflammatory mediators affect the trabecular endothelium and physically obstruct the filtration angle or block aqueous flow through the pupil.²

Treating uveitis

When uveitis is recognized, administer atropine to dilate the pupil to avoid synechiae and administer topical (e.g. diclofenac) and systemic anti-inflammatory medications to avoid complicating sequelae. Anti-inflammatory medications are the mainstay of treatment for uveitis. The treatment goals for any uveitis case are to block prostaglandin formation and other mediators of inflammation, reduce painful ciliary spasm, dilate the pupil to prevent synechiae and secondary glaucoma, and restore the blood-aqueous and blood-retinal barriers.¹²

Thoughtful use of atropine is important because overuse can decrease tear production and cause glaucoma. The idea is to keep the pupil moving; do not simply administer atropine twice daily but rather wait until the pupil begins to constrict before repeat dosing. Glaucoma results when mydriasis further reduces the outflow of aqueous humor due to the accumulation of red blood cells and inflammatory cells together with a dilated iris.¹⁷

Iridotomy

Laser iridotomy was performed in this cat to control the IOP in the right eye. The potential complications associated with iris surgery include hemorrhage, the iridotomy sites resealing, and iris bombé recurrence.¹⁰ Gonioscopy was not performed to document that the angles were opened postoperatively; however, the IOP in the right eye stabilized and eventually decreased, and the iris bombé resolved after the procedure was performed. Because the right eye was already blind, these results were considered successful.