October 01, 1997
2 min read
Save

Glaucoma 101: Back to the basics

You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

When reflecting on my years of training at Pennsylvania College of Optometry I consider myself most fortunate. I was the benefactor of a progressive curriculum, modern clinical facilities, a diverse patient population and a gifted faculty. Furthermore, much of what I learned still holds true: myopes see better with minus, lid scrubs help with blepharitis and visually significant cataracts are surgically removed. Some things, however, have changed.

Indeed, it doesn’t seem long ago that glaucoma appeared as an entirely different disease. Its pathophysiology was explained solely on the basis of elevated intraocular pressure (IOP). Its diagnosis was predicated on tonometry, ophthalmoscopy and rudimentary visual fields. With respect to treatment, beta-blockers reigned supreme. While these basic tenets still hold true, glaucoma has become recognized and respected as a much more complex entity.

Conventional wisdom changing

Undoubtedly, the conventional wisdom behind treating glaucoma has been challenged in recent years. Consider, for instance, the prevailing thought on its pathophysiology. True, most cases of glaucoma are associated with an elevated IOP. However, is it due to aqueous hypersecretion, impaired flow dynamics or compromised trabecular or uveoscleral outflow? Certainly, a multifactorial etiology better explains varied responses to different therapeutic trials. Furthermore, the role of optic nerve perfusion in "normotensive" glaucoma challenges the prevailing assumption that IOP is always high.

Next, consider the recent advances in diagnosis and monitoring. We’re just entering the era in which more sophisticated visual field and optic nerve imaging technologies play an increasingly significant role in glaucoma management. Then there is the issue of treatment. Recognizing the limits of beta-blockers — efficacy, allergies, systemic side effects — it is only logical that other treatment strategies evolve. Today’s clinician can augment the mainstay therapy with topical carbonic anhydrase inhibitors (Trusopt [dorzolamide, Merck]), alpha agonists (Iopidine [apraclonidine, Alcon], Alphagan [brimonidine tartrate, Allergan]) and prostaglandin stimulators (Xalatan [latanoprost, Pharmacia & Upjohn]). And this is only the beginning as a variety of combination agents await Food and Drug Administration approval.

Finally, consider the multitude of surgical advances — argon laser trabeculoplasty, antimetabolite-assisted trabeculectomies and a variety of "shunt" devices — that are an integral part of the glaucoma surgeon’s practice.

The commonality of these issues is that of change. Whether an established practitioner or a new graduate, a veteran of glaucoma management or recently therapeutic pharmaceutical agent-certified, our challenge is one in the same: get educated! Do it for the intellectual stimulation, do it for the practice, but — most importantly — do it for the patients.