7 common mistakes in managing uveitic glaucoma

Glaucoma is a relatively common complication of uveitis, occurring in about 20% of affected eyes and arising through several different mechanisms.

Emmett T Cunningham Jr., MD, PhD, MPH, reviewed seven common mistakes clinicians make in evaluating and managing elevated intraocular pressure (IOP) in eyes with uveitis during the Glaucoma Symposium CME at the 2016 Glaucoma 360 meeting.

Dr. Cunningham is director, Uveitis Service, California Pacific Medical Center, San Francisco; adjunct clinical professor of ophthalmology, Stanford University, Stanford, CA; research associate at The Francis I. Proctor Foundation, University of California-San Francisco; and a partner at West Coast Retina Medical Group, San Francisco. 

Mistake #1: Failure to recognize masquerades

Dr. Cunningham described two issues-failure to distinguish leukocytes from pigment and failure to recognize acute angle closure.  As an aid in distinguishing leukocytes from pigment, he reminded ophthalmologists to look for hallmark signs of inflammation.

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“If there is pigment release, you should not see keratic precipitates or posterior synechiae,” he said.

Dr. Cunningham noted that acute angle closure is typically not too difficult to distinguish. Although there can be cells, corneal edema and elevated IOP are the predominant findings and the fellow eye will show the narrow angle.

Mistake #2: Failure to recognize inflammatory ocular hypertension syndrome (IOHS)

IOHS is a strong predictor of infectious uveitis, and when the infection is treated appropriately, the IOP will go down. “When you see an acute elevation of IOP in eyes with uveitis, think about and look for infection,” Dr. Cunningham said.

The most common cause of IOHS is herpes virus infection. “About 30% to 40% of herpetic eyes have IOHS, and the dictum is, IOHS is herpetic until proven otherwise,” Dr. Cunningham said.

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Presence of cutaneous manifestations of herpetic infection can provide a diagnostic clue to herpes related-IOHS, as will sectoral iris atrophy, which is virtually pathognomic for herpes zoster or herpes simplex infection, Dr. Cunningham said.

Other infections associated with IOHS include toxoplasmosis and syphilis. Ocular hypertension can also occur with sarcoidosis, which has not been linked definitively to infection, but suspicion for an infective cause remains, and with Posner-Schlossman syndrome, which is widely thought to be form fruste herpetic anterior uveitis.

Mistake #3

Mistake #3: Failure to recognize Fuchs uveitis syndrome

Dr. Cunningham said the finding of cells in the anterior chamber with elevated IOP is not that uncommon in eyes with Fuchs Uveitis Syndrome (formerly called Fuchs Heterochromic Iridocyclitis), but the IOP tends to increase over time secondary to progressive angle damage rather than acutely. Although treatment of mild anterior chamber inflammation is usually not needed in these eyes, it is important to be aware that the angle vessels are abnormal and have a tendency to bleed during surgery (Amsler sign).

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Clues to the diagnosis of Fuchs uveitis syndrome include iris atrophy or heterochromia-light irides turn dark and dark irides turn light-characteristic, diffusely distributed, stellate keratic precipitates, and small iris nodules over the pupillary sphincter muscle.

Mistake #4: Failure to identify and treat the cause for angle closure

In this situation, treatment of the anterior chamber inflammation alone does not resolve elevated IOP because the anti-inflammatory treatment has not addressed the angle closure. Pupillary seclusion is one cause for angle closure, and it particularly occurs in uveitides associated with heavy fibrin deposition, such as HLA-B27-associated and sarcoidosis.

Dr. Cunningham noted that treatment for pupillary seclusion varies by country. In the United States, it is addressed by creating two, generous iridotomies, whereas sector iridectomy is performed more often in the United Kingdom, particularly when the inflammation is severe.

Other mechanisms of uveitis-related angle closure include iris bombé and uveal effusion. Anterior ciliary body rotation accounts for the second situation, and it is seen specifically in eyes with diffuse choroidal inflammation, particularly Vogt–Koyanagi–Harada disease, sympathetic ophthalmia, and scleritis.

Mistake #5

Mistake #5: Tapering the corticosteroid too quickly in eyes with corticosteroid-induced ocular hypertension

When corticosteroid treatment for uveitis causes IOP elevation, prompt withdrawal of the corticosteroids is the wrong thing to do, said Dr. Cunningham. Rather, the corticosteroid should be maintained while adding medication to control IOP. Treatment with corticosteroids should be continued until the inflammation is controlled, as defined by ≤ 1+ cells.

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“If you can’t count the cells, the inflammation is not controlled,” he said. “Don’t taper the corticosteroid until the inflammation is controlled, and in the meantime, deal with the elevated IOP by any means necessary,” he stated.

Dr. Cunningham noted that corticosteroid-induced ocular hypertension occurs more often with more potent corticosteroids, such as difluprednate, which he uses routinely when treating uveitis. “Corticosteroid-sparing immunosuppressive agents can also be used to control inflammation, but these agents typically take many weeks to achieve efficacy,” he added.

Mistake #6: Using the wrong IOP-lowering medication

Dr. Cunningham said that because they are not pro-inflammatory, either a beta-blocker or a carbonic anhydrase inhibitor is typically his treatment of choice for IOHS, assuming that there is no contraindication for these medications.

“Avoid the alpha adrenergic agonists (brimonidine, apraclonidine), epinephrine, dipivefrin, or pilocarpine to treat elevated IOP because they are pro-inflammatory,” Dr. Cunningham said.

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Although prostaglandin analogues have been said to cause inflammation, prostaglandin analogue-induced uveitis appears to be uncommon. Therefore, Dr. Cunningham noted that he often uses one of the prostaglandin analogues for ocular hypertension in eyes with uveitis.

Dr. Cunningham highlighted two exceptions-herpetic uveitis, because there are reports associating use of a prostaglandin analogue with viral reactivation; and chronic unilateral uveitis, where a prostaglandin analogue can induce periorbitopathy with fat atrophy that can result in cosmetically unacceptable oculofacial asymmetry.

Mistake #7

Mistake #7: Failure to adequately monitor and refer

Dr. Cunningham noted that it can be easy to overlook the need to monitor eyes with uveitis and ocular hypertension for angle damage and to check for visual field loss because these cases tend to be so complex and because the primary focus is on controlling the inflammation.

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For that reason, and because he expects a need for more aggressive intervention to control IOP, Dr. Cunningham prefers to involve a glaucoma specialist early on in the course of treatment.

“I anticipate that a high proportion of these patients will need a procedure, which is typically surgery,” Dr. Cunningham said. “I want the glaucoma specialist to be ready when the time comes.”

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Emmett T Cunningham Jr., MD, PhD, MPH

E: emmett_cunningham@yahoo.com

Dr. Cunningham has no relevant financial interests to disclose.