CASE 1: OCULAR HYPERTENSION
A patient has elevated IOP, normal visual fields, and a normal optic nerve—a classic presentation of ocular hypertension (OHT). The superior neuroretinal rim may be somewhat thin but not enough to be diagnostic. Over a 13-year period, visual fields have remained essentially unchanged, but the superior rim has become thinner, which is evidence of damage and continued loss (Figure 1).
At this point, the patient would be better defined as having mild glaucoma, that is, normal, standard whiteon- white Humphrey visual fields (Carl Zeiss Meditec, Inc., Dublin, CA), but with evidence of change in the optic nerve attributable to glaucoma.
CASE 2: GLAUCOMA SUSPECT
A 59-year-old man has a family history of glaucoma and elevated IOP, which was never treated. His medical history was not contributory. Visual acuities were 20/20 OU, angles were open, and on initial examination, his pressure was 26 mm Hg OU. We measured his IOPs on a modified diurnal curve, early morning, late afternoon, and in between. His pressures fluctuated between 22 mm Hg and 28 mm Hg during that time. His initial visual field was normal in the right eye. We observed a large amount of cupping of the optic nerves (Figure 2), but the neuroretinal rim was intact. It followed the “ISNT” rule, with the inferior rim the thickest, followed by the superior, nasal, and temporal rims. This patient was a glaucoma suspect, with a normal field and what may be an optic nerve that is normal for him.
We observed this patient for 8 years. His medical history, visual fields, and optic nerves were unchanged; his vision remained good, and his pressures ranged from 22 mm Hg to 29 mm Hg. During this time, we learned of the importance of central corneal thickness (CCT) and noted this patient's CCT was somewhat thick, which could explain why his pressure was elevated.
The patient moved to another state and returned 5 years later. On examination, his pressure was 28 mm Hg. His visual field (Figure 3) shows what appears to be a definite defect on the inferior arcuate distribution; it is relatively mild but certainly present. As we know, by the time a field defect is present, the optic nerve has likely changed. Comparing the optic nerve to where it was 5 years previously, we see evidence of neuroretinal rim loss, probably more profound superiorly than inferiorly, but a definite change from where it was before.
Treating OHT
What is the best treatment for OHT? Is it medication, laser trabeculoplasty, possibly no treatment, depending on the individual patient's risk, or should we begin to consider one of the newer surgeries, such as canaloplasty (iScience Interventional, Menlo Park, CA) or Trabectome (NeoMedix Corp., Tustin, CA)?
When we decide to treat a patient who has OHT, medication is typically our first line, given the patient's acceptance and risk profile. Laser trabeculoplasty is rarely an option, as it is restricted to the patient with OHT who has a very high risk profile, specifically, thin corneas, high pressures, and older age.
The idea of not treating these patients is important. The decision should result from a discussion centering on risk between the clinician and the patient. Typically, these patients are in one of two categories. First is the patient who says, “If there's anything you can do to decrease my risk of developing glaucomatous damage, I want it.” For these patients, treatment is appropriate. Conversely, a patient may say, “If I absolutely have to have a medication, I will take it, but I would rather you monitor my status, and when the risk outweighs the potential benefits of not treating me, I am willing to take the medication.” I have had patients with a high risk for OHT opt for no treatment. This is acceptable as long as the patient understands the risks and is willing to return for appropriate follow-up. We must remember that a person with OHT does not have definitive damage, and we are trying to prevent that from occurring.
The newer surgeries that avoid formation of a bleb may have a much better side effect profile than trabeculectomy, 1 but they may not be advisable to use in a patient without manifest damage.
Determining structural or functional damage
If we are going to observe and not treat patients who are at risk for development of glaucomatous damage, we must be able to identify progression if it occurs. How do we determine if the patient has true structural or functional damage? Should we look for atrophy of the remaining neuroretinal rim, focal thinning of the neuroretinal rim, asymmetry between the superior and inferior hemifields on visual field testing, or a retinal nerve fiber layer distribution of the visual field defect?
Atrophy of the intact neuroretinal rim does not occur in glaucoma. When cupping occurs, you can expect atrophy or paleness of the optic nerve within that cup, but the remaining neuroretinal rim is not pale. If it is, then some other etiology of nonglaucomatous optic nerve damage should be investigated.
Focal thinning of the neuroretinal rim is expected and common. Typically, there are two types of progression: focal thinning of the neuroretinal rim or a generalized increase in cupping associated with generalized thinning of the rim tissue.
In my second case, an inferior arcuate defect was distinct from what was found in the superior hemifield. Asymmetry between the superior and inferior hemifields is assessed in the glaucoma hemifield test on the Humphrey Visual Field Analyzer (Carl Zeiss Meditec, Inc., Dublin, CA) and can be useful in determining if a subtle defect is true damage or just scatter.
Finally, we must remember that perimetry measures only the visual field, not the glaucomatous visual field. When a visual field defect is present, we must be sure it is consistent with an intrinsic defect in the retinal nerve fiber layer and in the optic nerve and not indicative of some other disease, such as central etiology from a tumor.
- 1. Mosaed S, Dustin L, Minckler DS. Comparative outcomes between newer and older surgeries for glaucoma. Trans Am Ophthmolol Soc. 2009;107:127-133.
