SIGNS AND SYMPTOMS
Patients with uveitic glaucoma will present with a unilateral red, painful, photophobic, lacrimating eye. Acuity will be moderately decreased. There will be corneal edema and folds in Descemet's membrane, but the epithelium should be intact. There will be a profuse anterior chamber reaction, possibly with hypopyon. There are frequently posterior synechiae. There will be injection of the conjunctival and episcleral vessels. The angle may be closed with peripheral anterior synechiae (PAS). Intraocular pressure (IOP) may range from 30 to 80mm Hg.
The patient with glaucomatocyclitic crisis will present with a recurrent, unilateral red eye with very mild discomfort, or possibly no discomfort at all. Acuity will be mildly reduced; this is often the chief complaint. The cornea will be mildly edematous, but the anterior chamber will be remarkably clear. Often, the only signs of anterior chamber inflammation will be a rare cell or two in the chamber or, more commonly, a few keratic precipitates on the endothelium. Intraocular pressure can range from 30 to 70mm Hg, but the patient will not be in acute distress.
In uveitic glaucoma the patient first develops uveitis, either due to trauma, systemic disease or idiopathically. The ensuing inflammation results in a rise in IOP through several mechanisms.
Often, the inflammatory cells physically block the trabecular meshwork, decreasing aqueous outflow, with the angle remaining open. Occasionally, the inflammatory cells and fibrous protein will form a connective bridge between the peripheral iris and cornea, pulling these structures into apposition, and resulting in an angle closure with PAS formation.
Because the inflammatory cells and protein in the anterior chamber form adhesions between the posterior iris and anterior lens, posterior synechiae commonly form. This will lead to iris bombé, secondary angle closure and peripheral anterior synechiae formation. There may also be a combination of mechanisms that increases IOP. Untreated, the patient will eventually experience glaucomatous optic atrophy, or possibly central retinal artery occlusion.
In glaucomatocyclitic crisis, there is an idiopathic inflammation of the trabecular meshwork that reduces this structure's ability to actively drain aqueous. Due to prostaglandin release, it is theorized that there may also be a concurrent overproduction of aqueous. Despite the elevated IOP, this condition is only mildly symptomatic, and is usually self-limiting. However, the recurrent nature of the attacks predisposes the patient to developing glaucomatous optic atrophy.
Successful management of uveitic glaucoma involves prompt and aggressive measures. In any inflammatory glaucoma, you must treat the inflammation first and the IOP secondarily. Initiate strong cycloplegia in the form of atropine 1% BID immediately to put the uveal tissue at rest and begin healing. Have the patient use a steroid such as Vexol (rimexolone), Pred Forte (prednisolone acetate) or fluorometholone acetate (Flarex, Eflone) every 15 minutes for the first several hours, then taper to every hour.
If any posterior synechiae have formed, prescribe phenylephrine 10% BID. Quelling the inflammation will temporize the IOP rise. To further reduce the IOP, use a topical beta-blocker BID or the topical carbonic anhydrase inhibitor Trusopt TID, provided there are no medical contraindications to any of these drugs. Avoid pilocarpine and other miotics in these patients. Follow the patient every 24 hours and gradually taper the medications as the condition improves.
Management of glaucomatocyclitic crisis is nearly identical to that described above for uveitic glaucoma, with the following two exceptions:
(1) It is acceptable to use a slightly weaker cycloplegic such as scopolamine (hyoscine 0.25%) or homatropine 5% BID.
(2) The patient should instill a topical steroid hourly rather than every 15 minutes.
Avoid pilocarpine and other miotics in inflammatory glaucoma. Miotics will induce ciliary spasm and increase inflammation, fostering both posterior and peripheral anterior synechiae. We have seen many cases of inflammatory glaucoma improperly treated with pilocarpine; all patients worsened considerably and one ultimately resulted in enucleation.
Steroids are absolutely necessary to manage inflammatory glaucoma. However, practitioners tend to be hesitant to prescribe steroids for patients with elevated IOP for fear of a concomitant steroid-induced pressure rise. One must realize that steroids will not increase IOP for at least two weeks, and this pressure rise only occurs in one-third of the population. In fact, steroids will actually reduce IOP by quelling the inflammation. Withholding steroids in inflammatory glaucoma is extreme mismanagement.
Strong cycloplegia is necessary in managing uveitic glaucoma. The use of tropicamide, cyclogel or other weak cycloplegic agents is considered poor management.
Avoid the prostaglandin analog latanoprost (Xalatan) since, as in any inflammatory condition, there will already be copious amounts of prostaglandins in the anterior chamber and Xalatan will not provide any benefit.
Remember: treat the inflammation first and the IOP secondarily!