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Glaucoma diagnosis goes well beyond IOP
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As an optometry student, I still remember the first time I picked up Becker-Shaeffer’s Diagnosis and Therapy of the Glaucomas (CV Mosby Co., 1976). Authored by Drs. Allan Kolker and John Hetherington Jr., the 4th edition was heralded as the bible of glaucoma, providing everything from classification to surgical management of this dreaded disease.
Having skimmed through the preface and table of contents, I turned to chapter 1, which began with, “Glaucoma is an eye disease in which the complete clinical picture is characterized by increased intraocular pressure, excavation and degeneration of the optic disc, and typical nerve fiber bundle damage, producing defects in the field of vision.” Later in the same paragraph they summarized it all by stating, “A definite diagnosis of glaucoma cannot be made unless the increased intraocular pressure has produced damage to the optic nerve.” Having no real conceptual basis for glaucoma, I remember highlighting those two sentences and reading them again ... and again. Increased IOP. Optic nerve damage. Loss of field of vision. Got it.
At the time, I found Kolker and Hetherington’s statements both simple and far reaching. Somehow, they seemed to have simplified glaucoma to a level even a first semester optometry student could understand. Unfortunately, for me and my classmates, that was page 3 ... of a 500-page book. As it turns out, glaucoma was not so simple. Not then and not now.
As optometrists, we have the great fortune of being part of a dynamic profession. Granted, the stakes are high, as preserving vision is a tremendous responsibility. However, we are also the benefactors of an ever-evolving discipline, one in which there are continual advances in our understanding of the underlying pathophysiology, risk factors, comorbidities, diagnosis and treatment of so many clinical conditions. Perhaps this is no more evident than in glaucoma. While we remain grounded in our beliefs of IOP control, optic nerve assessment and protecting visual function, we have also come to realize there is so much more. In many respects, there is so much more beyond the eye.
Humbled by the reality that glaucoma can progress at a variety of IOP levels – some of which are quite normal – we have begun to look beyond this time-honored metric. Fueled by the theory that suboptimal optic nerve perfusion, increased oxidative stress and aberrant axoplasmic transport may well be intertwined in the pathophysiology of glaucoma, we are now looking outside of the eye. Could it be that orthostatic hypotension, nocturnal dipping or sleep apnea are the drivers behind poor perfusion? Can a genetically predisposed, anatomically susceptible lamina play a role in compromised axoplasmic flow? Do certain systemic inflammatory biomarkers correlate with an increased risk of glaucoma? These are complex questions with no easy answers – and, certainly, not the answers one finds on page 3 of the textbook.
In this month’s Primary Care Optometry News, our feature article “Researchers, clinicians continue to determine driving force behind glaucoma” provides a thought-provoking look at glaucoma well beyond IOPs. Our contributors, each with a wealth of knowledge and experience, offer sage advice on unraveling the complexities of glaucoma, sometimes by looking beyond the eye.
I am sure you will agree it is a worthy read – and proof that the final chapter on glaucoma has yet to be written.