When confronted with acute hypertensive uveitis associated with elevated IOP, physicians should consider an infection, such as herpes simplex virus (HSV), cytomegalovirus (CMV), varicella zoster virus (VZV), toxoplasmosis, or rubella. Posner-Schlossman syndrome and Fuchs' hetrerochromic cyclitis are syndromes that probably are caused by these same infectious agents. Trabeculitis has been considered a possible mechanism.
San Francisco-When confronted with acute hypertensive uveitis associated with elevated IOP, physicians should consider an infection, such as herpes simplex virus (HSV), cytomegalovirus (CMV), varicella zoster virus (VZV), toxoplasmosis, or rubella. Posner-Schlossman syndrome and Fuchs’ heterochromic cyclitis are syndromes that probably are caused by these same infectious agents. Trabeculitis has been considered a possible mechanism. Todd Margolis, MD, PhD, discussed elevated IOP associated with acute inflammation.
“Elevated IOP with acute inflammation is almost always an infectious condition. The most common infectious agents are Toxoplasma gondii, HSV, and VZV,” Dr. Margolis emphasized. He is professor of ophthalmology and director, F. I. Proctor Foundation and Department of Ophthalmology, University of California, San Francisco.
The clinical features of toxoplasmosis are granulomatous keratic precipitates, classic vitreoretinal findings such as headlight-in-the-fog, T gondii seropositivity, and T gondii DNA in ocular fluids. The primary treatments are anti-toxoplasmosis drugs and corticosteroids, he explained.
In the acute phase of toxoplasmosis, IOP-lowering medications are usually not required, because the IOP usually decreases within about 48 hours of the initiation of topical corticosteroid treatment.
“Unless the IOP is dangerously high I don’t prescribe an anti-glaucoma medication, although I will follow the patients closely,” Dr. Margolis said.
Patients with HSV or VZV iritis have similar clinical findings. Patients might have evidence of previous interstitial keratitis, decreased corneal sensation, diffuse pleomorphic granulomatous keratic precipitates, patchy or focal iris atrophy, and abnormal pupillary responses, he commented.
Diagnostic testing for HSV or VZV includes evaluation for decreased corneal sensation and local immune responses in the aqueous, and polymerase chain reaction (PCR) for DNA in the aqueous. Finally, clinicians can perform a therapeutic challenge with acyclovir.
“Acyclovir is relatively inexpensive with few side effects. Acyclovir can be administered with a small amount of a topical corticosteroid to see if there is any improvement,” he instructed.
“An advantage of this is that the elevated IOP will drop dramatically within 2 days of adding a topical corticosteroid, even if the IOPs are in the high 30s. Unless the patients’ IOPs are in the danger zone, I don’t [use] additional agents,” he said.
Zoster without skin eruptions (zoster sine herpete) does occur.
“Don’t be fooled by this. Just because there is no cutaneous eruption doesn’t mean that the patients don’t have ocular VZV. VZV iritis without corneal involvement, and chronic and recurrent VZV, also exist,” Dr. Margolis cautioned. Some of these older notions are disappearing because of molecular diagnostics, which are much more sensitive than the old very insensitive cultures, he explained further.
HSV and VZV are best managed with systemic anti-viral drugs because higher drug levels are achieved in the aqueous, Dr. Margolis said. Topical corticosteroids can be prescribed but rarely are needed more frequently than four times daily.
CMV iritis can occur in patients who are immunocompetent. The disease, which tends to occur unilaterally in patients between the ages of 20 and 50, is characterized by the presence of small gray or brown keratic precipitates, with or without endotheliitis, with or without iris heterochromia, and viral DNA detected by PCR.
“CMV iritis begins to look like the ICE (iridocorneal endothelial) syndrome, with atrophy and changes in the endothelium. And it raises the question about virus involvement in the ICE syndromes,” he commented.
Treatment for CMV iritis is systemic valganciclovir. Intravitreal and topic ganciclovir can be administered. However, corticosteroids are stopped or reduced.
Dr. Margolis pointed out that two syndromes must be considered: Posner-Schlossman and Fuchs’ heterochromic cyclitis. These are not etiologic diagnoses, but syndromes, he emphasized.
The former, Posner-Schlossman syndrome, is an intermittent, unilateral syndrome that occurs in patients aged 20 to 50 years. The episodes last from hours to weeks with quiescence between episodes. A few keratic precipitates can be seen, minimal cells, and very high IOPs ranging from the 40s to 60s.
“Most of these cases are caused by the herpesviruses, i.e., HSV, VZV, or CMV. I treat these patients prophylactically with anti-viral drugs to help reduce the recurrences,” he noted.
The second syndrome, Fuchs’ heterochromic cyclitis, is frequently characterized by the presence of CMV DNA or rubella RNA in the aqueous, as well as a localized immune response to these agents in the aqueous.
“In cases of acute iritis with elevated IOP, diffuse keratic precipitates are frequently found,” Dr. Margolis said and advised clinicians to think about an infection, i.e., HSV, CMV, VZV, toxoplasmosis, and rubella. Posner-Schlossman and Fuchs’ heterochromic cyclitis are syndromes that are probably the result of the same infectious agents. We do not know the mechanism, he noted, but trabeculitis has been a consideration.
Dr. Margolis has no financial interest in this subject matter.
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