Sunday, December 9, 2007

4.2 So you have high IOP

First, some pictures of the optic disc:

(POAG with large cupping occupying 90% of the disc area)

(Normal optic disc with no cupping)

Glaucoma in adults actually has many different types. It most commonly refers to POAG, primary open-angle glaucoma, which can be familial. In Asia, we often see acute angle-closure glaucoma in a hospital ER. It is a true medical emergency, which also can be a consequence of chronic narrow-angle glaucoma. Then we have secondary glaucomas from neovascularization (e.g., rubeosis in diabetes), pigmentary dispersion, phacolysis, pseudoexfoliation, uveitis, or trauma. And of course, there is this somewhat mysterious normal-tension glaucoma (NTG) in which, as the name indicates, the intraocular pressure (IOP) is actually within the normal range and the angle is open as well. Interestingly, NTG seems to be more common among the Japanese and it is often associated with migraines and cold hands/feet.

This "angle" refers to the junction between the cornea and the root of the iris where the intraocular fluid drains, into the trabecular meshwork and then into Schlemm's Canal and the venous system.

Acute angle-closure is a condition where an adhesion between the back of the iris and the front of the crystalline lens causes a forward bulging of the iris proper (see picture below). Chronic narrow-angle is similar but without the iris-lens interaction. In both cases, the angle closes or narrows. The fluid can no longer drain properly, resulting in an elevated IOP. The solution is, in the acute case, to reduce the IOP pronto, followed by laser iridotomy - after the pressure is under control. And in the chronic case, medical control of the pressure as in POAG or laser treatment. The purpose of laser iridotomy is to open a hole in the iris proper to allow a direct fluid flow from the posterior aqueous chamber into the angle. It can be and probably should be done on a prophylactic basis.

(Modified from najafimd.com)
Here, we'll touch upon the most recent advances in diagnosis and treatment of POAG. Indeed the evaluation of POAG is now heavily technology-driven and the wide availability of efficacious anti-glaucoma agents is astounding.

First, the diagnosis. In the not so distant past, IOP is used as the primary if not the sole index of POAG. To this day, patients still request a "glaucoma test" which is essentially a pressure check using a gauge (i.e., a tonometer). Now it is known that a high IOP does not always lead to POAG and the pressure readings must be corrected based on corneal thickness. For example, patients after LASIK thinning of the cornea will have a falsely low IOP. And the same applies to people with thin corneas. The corrected IOP, if high, must still be complemented with an evaluation of the optic disc for evidence of "cupping" (see pictures at top of page) and nerve fiber defects, followed by a visual field test for any losses. A definitive diagnosis of POAG (and NTG) must be based on all three. The "cupping" is a depression or excavation of the optic nerve head caused by elevated IOP, which also damages the retina and the optic nerve leading to the visual field loss (see below: from A to D, progressive loss of visual fields indicated in black).
(from www.aafp.org)
The corneal thickness is measure with a pachymeter. The angle and the optic disc can both be imaged with OCT (Optic Coherence Tomography). And the visual fields plotted with perimeters of various designs. The treatment of POAG and NTG is fairly straightforward. Anti-glaucoma drugs now include the following:

Prostaglandins: We now have Xalatan and Travatan (both esters) and Lumigan, an amide. One drop a day can reduce the IOP by 30%.

Beta-Blockers: There are a few of them, Betagan, Betoptic, Timoptic, Betimol, and Istalol. It is well-known that beta-blocked must not be used on patients with respiratory illnesses, such as asthma, or cardiac issues such as congestive heart failure - or risk death.

Alpha-adrenergic agonists: Alphagan is an example - to be used as a second line drug if the first line drugs, prostaglandins and timolol, are not tolerated by the patient .

Carbonic anhydrase inhibitors (CAIs): CAIs can only reduce the IOP by 15%, so a daily dosing of 2 to 3 times maybe needed. We now have Azopt and Trusopt that are often used together with timolol.

Indeed, proper diagnosis, optimal dosing, patient compliance, and vigilant follow-ups can prevent vision loss in almost all cases of POAG and NTG.

Of course, there are cases of recalcitrant glaucoma, especially that of neovascular origin (as a complication of diabetes or hypertension), which cannot be controlled by medicine. Surgical intervention as that for congenital glaucoma is then performed. The outcome is somewhat guarded, however.

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