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Specialist relates pearls for diagnosing, treating uveitis
Treatment options include a local/systemic approach, a sustained-release implant or a combination of the two.
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Uveitis is difficult to diagnose, particularly when there is an obstructed view of the posterior segment; however, there are several sensible approaches to detection and treatment, according to one expert.
When approaching a new patient with posterior segment inflammatory disease, it is important to consider potential infectious causes, Thomas A. Albini, MD, an associate professor of ophthalmology at Bascom Palmer Eye Institute, told Ocular Surgery News. However, occasionally an inflamed eye will present without any views of the posterior segment due to massive vitritis or a hypopyon in the anterior segment. A cataract may also shield the physician’s view.
“In these eyes, ultrasound can be very helpful in excluding retinal detachment and provide a sense of the degree of inflammation in the posterior segment,” Albini said.
Differential diagnosis
One differential diagnosis to consider in uveitis patients is acute retinal necrosis. This requires immediate and aggressive treatment with systemic anti- viral medications because the disease can move rapidly to retinal detachment and optic nerve involvement and can render the patient blind, according to Albini.
Thomas A. Albini
A polymerase chain reaction (PCR) test from an anterior chamber tap can be used to confirm diagnosis.
“The sensitivity of the PCR is very high, over 90%,” Albini said.
Syphilis and toxoplasmosis are two other common infectious etiologies that must be evaluated by means of serology and/or PCR and antibody tests from ocular fluid.
Some uveitis patients present with endogenous endophthalmitis (either bacterial or fungal). In these cases, a good history from the patient is critical. Red flags include recent hospitalizations and surgeries, intravenous drug use and any other risk factors for immunosuppression, such as chronic treatment for rheumatic diseases or AIDS.
“A vitrectomy may be essential in establishing the diagnosis and allowing a view to the posterior segment,” Albini said.
Another possible etiology for severe vitritis is intraocular lymphoma, especially in older patients who have an intraocular cellular burden that is out of proportion to the inflammatory signs in the eye, Albini said.
“This presents as a quiet, white eye, with very little scarring, but with a great degree of cellular infiltration, most often in sheets of cells throughout the vitreous,” he said.
In addition, these eyes may have deposits of cells under the retinal pigment epithelium.
The most important test to immediately schedule for suspected intraocular lymphoma is a brain MRI.
“Mortality in these patients is a consequence of associated central nervous system lymphoma,” Albini said.
Once the MRI scan is obtained, the clinician can then conduct a lumbar puncture to identify cancer cells from the cerebral spinal fluid. Cancer cells may also be detected in vitrectomy samples.
Visualizing the retina
If infectious and neoplastic etiologies are not suspected, a trial of systemic steroids is often helpful to decrease inflammation to the point where the retina can be visualized, according to Albini. Once visibility is achieved, a full armamentarium of imaging modalities, such as fundus photography, fluorescein angiography, indocyanine green (ICG) angiography and optical coherence tomography, can be enlisted.
“Each modality is important, not only to differentiate among the different types of posterior segment disease, but also to help provide objective quantification of the inflammation, so that you can monitor response to treatment,” Albini said.
Three commonly used markers for the degree of inflammation are cystoid macular edema, vascular leakage seen on fluorescein angiography and choroidal infiltrate seen on ICG angiography.
Treatment
Albini said the protocol for treating uveitis can be either local or systemic. For systemic treatment, Albini recommended starting with steroids, usually prednisone, at 1 mg/kg a day until the inflammation is controlled, followed by tapering over 2 to 3 months.
“The goal is to get the patient on 10 mg or less of prednisone daily within about 2 months,” Albini said.
If the inflammation cannot be adequately controlled with that dosing schedule, or if the inflammation recurs once the prednisone is lowered, a steroid-sparing agent, such as an antimetabolite, can be added.
“These agents can be used for long-term treatment, most typically for 2 years, then withdrawn,” Albini said. However, the use of these antimetabolite drugs requires monitoring of liver function and blood counts on a routine basis.
With this overall protocol, inflammation resolves in 80% to 90% of these patients; however, in some cases two agents are needed — for example, a T-cell inhibitor or an anti-tumor necrosis factor-alpha biologic, according to Albini.
An intravitreal sustained-release implant is a local therapy option. Retisert (Bausch + Lomb) is a fluocinolone acetonide implant that is surgically implanted and lasts 2.5 years.
“We know from the Multicenter Uveitis Steroid (MUST) trial that there is a non-inferiority of the implant relative to standard systemic therapy for visual acuity outcomes for uveitis, plus there was a tendency to have better control of inflammation with the implant,” Albini said.
Despite Retisert’s advantages, there are local complications, foremost the need for all patients to undergo cataract surgery, and 30% will require glaucoma surgery, according to Albini.
“I typically use Retisert on patients who cannot tolerate or do not desire systemic treatments, or on patients who require complicated systemic immunosuppression with two or more agents,” Albini said.
A third alternative is to use a combination approach: a single immunosuppressive systemic agent in conjunction with Ozurdex (Allergan), a 6-month dexamethasone biodegradable implant. – by Bob Kronemyer