After an 18-month absence, a 71-year-old female patient presented back to the office for a progress examination related to her “glaucoma suspect” status. Since last being seen, she had lost her husband to cardiovascular issues and had been spending time with her family out of the area. She has been a patient of mine for approximately 10 years and was followed regularly as a glaucoma suspect, due to family history and disc cupping asymmetry. She was always diligent in her care, and I was surprised it had been 18 months since she was last seen. Given the specifics of her case, she had been seen once every six months.

When initially seen, and through subsequent follow up visits, her Intraocular pressure averaged approximately 18mm Hg to 19mm Hg OD and OS. Pachymetry readings were 536µm OD and 544µm OS. The optic discs were of average size, but the asymmetry in the cupping was pronounced. She had optic nerves characterized by cupping judged to be 0.6 x 0.65 OD and 0.3 x 0.4 OS, and these estimates were supported by HRT 3 imaging. Her overall systemic health was reasonably good, and she was currently medicated with Cymbalta (duloxetine, Eli Lilly) 60mg QD, Zyrtec (cetirizine, Johnson & Johnson) QD, Ditropan (oxybutynin, Janseen) 10mg HS and had recently discontinued Prozac (fluoxetine, Eli Lilly) QD. She reported allergies to sulfa-based medications.

Blue laser image of the right optic disc and perioptic region. Note the disc hemorrhage between 6 o’clock and 7 o’clock as well as the RNFL wedge defect in the adjacent tissue.

Best-corrected visual acuities when initially seen were 20/20 OD, OS, OU through hyperopic astigmatic and presbyopic correction. Visual acuities have gradually declined over the period in which she was seen, primarily due to the development of age-consistent nuclear and cortical cataracts. Pupils were equal, round and reactive to light and accommodation with no afferent pupillary defect.

After the 18-month hiatus, a slit lamp examination of the anterior segments was entirely unremarkable. IOPs were 20mm Hg OD and 19mm Hg OS at 11:15am. Her anterior chamber angles were well formed and deep, as estimated by von Herrick angle estimation and confirmed on gonioscopy. There was normal trabecular pigmentation and no angle abnormalities visible on gonioscopy OU over the entire period she was seen. Her crystalline lenses were characterized by nuclear and cortical cataracts consistent with her best-corrected visual acuity of 20/30+ OD and 20/30- OS.

Through dilated pupils, there were bilateral PVDs noted. Stereoscopic evaluation of the optic nerves demonstrated similar neuroretinal rim appearances as described above, along with the new finding of a small disc hemorrhage in the right eye at 6:30. There appeared to be a small RNFL wedge defect in the area contiguous with the disc hemorrhage, which was not noted previously. Both maculae were characterized only by fine RPE granulation, consistent with her age. 

The retinal vascular examination was characterized by mild arteriosclerotic retinopathy, with no crossing changes noted. Her peripheral retinal examination was unremarkable in both eyes.

The patient underwent HRT 3 imaging of the optic nerves, as well as OCT imaging of the perioptic RNFL and macular regions. There was demonstrable change in the inferotemporal segment of the right eye in the HRT 3 scan compared with previous visits and her baselines, which were obtained 10 years earlier. There was similar RNFL loss inferotemporally to the right eye on the OCT study, compared with baseline images obtained five years earlier that was also not noted in previous scans.


Given the noted changes to the structure of the right neuroretinal rim—tissue loss, disc hemorrhage and RNFL loss in the same area—it was evident that the patient had converted from a glaucoma suspect in the right eye to a patient with structural damage consistent with glaucomatous optic neuropathy. The left eye did not show any changes on the HRT3 or OCT studies and was currently deemed stable. As such, the patient was asked to return for threshold visual field testing, stereo optic nerve imaging and anterior segment angle OCT.

The patient returned for follow up as directed. At this visit, applanation tensions were 18mm Hg OD and OS at 10:00am. Threshold visual fields employing the Flicker Defined Form strategy demonstrated a pronounced arcuate defect superiorly to the right eye, which was significantly different (progressed) compared with earlier visual field studies. The field in the left eye was unremarkable, and both fields were obtained with good reliability indices. Multimodal disc and macular images were obtained using the Spectralis Multi Color Image Acquisition system, which clearly showed the RNFL wedge defect inferotemporally in the right eye. 

Anterior segment OCT imaging of the anterior chamber angles demonstrated normal iris approach to the angle with no subtle plateau iris configuration.

Threshold HEP (Heidelberg Edge Perimeter) FDF field studies demonstrating the development of a superior arcuate defect in the right eye as compared with the previous study. Click image to enlarge.


While the evidence in this case strongly suggests that the patient converted from a glaucoma suspect in the right eye to a patient with both structural and functional defects consistent with glaucoma in the right eye, it is striking that this conversion occurred during the time the patient was unable to obtain her maintenance care. There were no significant medication changes in her history and no personal health changes that could have reasonably played a role in the conversion to glaucoma—other than the possible effects from personal life stressors. 

There was no previous trauma or angle abnormalities that would precipitate an abrupt conversion. It simply just happened.

Conversion Happens

When it happens can depend on several things: IOP, the patient’s overall cardiovascular health, angle abnormalities, nocturnal hypotension and fragility of the neuroretinal rims, to name a few. In some individuals—for example those with narrow angles that occlude—the conversion can be abrupt and, frankly, expected. But in the majority of open angle glaucoma cases, the conversion occurs gradually and, most importantly, can happen at any time.

And therein lies the difficult position in which we find ourselves—walking that fine line in determining the frequency of follow up visits for the patient who we determine is a patient at risk for developing glaucoma. How much is too much? How little is too infrequent? Neither too much nor too little is desired. But the frequency of care and follow up is based on our clinical judgment. In general, in those patients where we consider the risk of conversion to be great, we see them more frequently than those patients that we’ve determined have a low risk to convert. Fortunately, we have a plethora of studies that help guide us in shedding light on who is more likely to convert and what factors are involved in their conversion. And we have some tremendous technology available to help us determine subtle changes in both structure and function that shed light on conversion. But, at the end of the day, we really don’t know when conversion will occur. So we see the patient every year and torture them with visual field studies, bright lights and drops.

Visual field and corresponding optic nerve sector representation of the structure and function deficits found in this patient.

Naturally, patients can become disaffected with the follow up visits, and some may ask why they should continue since “nothing has happened so far.” It then becomes a challenge for us to relay the importance of continuing care to the patient. 

But what happens when the doctor begins to doubt the necessity of the follow up care and stretches the time between visits? While on one hand that may be prudent (only if a thorough evaluation has been made of the patient’s risk and it was deemed to be low), this case highlights what happens all the time in glaucoma management: there is never any convenient time for patients  to convert. 

Like in mutual fund investing, the caveat “past performance is no guarantee of future results” applies. Just because the patient hasn’t converted in 10 years doesn’t mean it won’t happen. It can and does. That’s why we need to be continually vigilant in our management of the patient.