Lecture: What is Glaucoma? (1 Slide in 5 Mins)

Dr. Kahook: Welcome to a new series called “1 Slide in 5 Minutes” where we will present no more than one content slide and will always keep it at 5 minutes or less. The first question to start with is maybe a bit too ambitious, “What is Glaucoma?” The answer is intended to be appropriate for patients, medical students and residents.
Glaucoma is a general or “umbrella” term that we use to cover a group of diseases that share the common clinical picture of characteristic optic nerve “cupping” with distinctive patterns of visual field loss. The optic nerve ”cupping” is an expansion of the internal optic nerve head void that occurs secondary to the loss of ganglion cell axons (think of them as straws that extend from cells on the retina) that leave the eye through the opening in the sclera in the back of the eye. We diagnose glaucoma though optic nerve head exam looking at the size of the cup and width of the neuroretinal rim as well as other features of the optic nerve (see the 5Rs lecture on www.keogt.com). We also utilize optical coherence tomography (or OCT) to objectively measure the thickness of the retinal nerve fiber layer and other features of the back of the eye (macula and more recently OCT-A). OCT allows for measuring RNFL thickness as well as many features of the nerce (size, neuroretinal rim, etc) and also allows for macular scans that can be a piece to the puzzle when diagnosing and following progression of glaucoma. Visual field testing to look for the distinct visual field defects that are characteristic of glaucoma (including nasal steps (with superior nasal steps most common, arcuate scotomas and, unfortunately, in some cases paracentral and central scotomas. The pattern of the HVF scotoma follows the pattern of the ganglion cell loss giving glaucoma the characteristic defects that are part of the definition of the disease. (see the HVF chapter in www.KEOGT.com). It should be noted that the findings between ONH exam, HVF and OCT are frequently asynchronous and HVF deficits may lag findings on ONH exam and RNFL OCT in which case we refer to the stage of disease as “pre-perimetric” glaucoma meaning it has not manifested on the more subjective HVF perimetry but can be identified objectively by examination.
In the distant past, glaucoma was thought to be a disease of elevated pressure in the eye (or intraocular pressure-IOP), however, we now know that glaucoma can happen at what was thought to be “normal” pressure (10-21mmHg) and we no longer use IOP as part of our definition of glaucoma. About 75% of my patients in Colorado have “normal pressure”.
Still, intraocular pressure is an important risk factor for glaucoma and is the only modifiable risk factor that we can do something about. We treat glaucoma with drops that decrease fluid production (beta blockers and carbonic anhydrase inhibitors) or increase outflow of fluid from the eye (like the prostaglandin analogs and rho kinase inhibitors). Our goal with treatment is to decrease pressure by 25-30% from baseline as a simple rule. We can also use oral medications (like acetazolamide and methazolamide) to decrease IOP. Lasers can be used to increase outflow (laser trabeculoplasty-SLT) or decrease inflow (like mpCPC and CPC). Finally, we can use various surgical approaches to decrease pressure when needed (see www.KEOGT.com for a full discussion of surgical interventions).
When measuring IOP, it is important to take diurnal (day time) and nocturnal (night time) fluctuations into account. Pressure is highest in the early morning hours and many patients might have higher pressures outside of normal office hours (making us believe the IOP is within normal range when it often is not). There are other factors that contribute to glaucomatous optic neuropathy (for example age, ethnicity, myopia, genetics, family history) that should be taken into account. Research continues to explore the effects of IOP independent factors such as immunologic causes as well as ocular blood flow connections to advancing disease (despite what appears to be well controlled IOP) all of which remain poorly characterized to date. In summary, glaucoma is a disease of the optic nerve that results in loss of ganglion cells and thinning of the optic nerve neuroretinal rim (producing cupping). The neve damage leads to characteristic patterns of visual field loss usually sparing the central visual field until advanced disease stages. Treatment is focused on lowering IOP but many other “pressure independent factors” are at play and we continue to research other ways to preserve vision with potential for both neuroprotection as well as aspirational hopes to reverse diseased nerves in the future. Thank you for your time.