A 63-year-old white female, who had recently moved to the area, presented as a new patient in 2011. She reported that she had been followed on a six-month basis because of “borderline eye pressures.” She presented with a copy of her previous optometrist’s records, which confirmed this.
She was not medicated for ocular hypertension, but her systemic medications included low-dose (81mg) aspirin q.d., Crestor (rosuvastatin calcium, AstraZeneca), doxycycline, triamterene and Zoloft (sertraline HCl, Pfizer) h.s.
She had no visual complaints on the initial visit, though she did mention that she was bothered cosmetically with her sagging eyelids.
Diagnostic Data
At the initial visit, entering visual acuity was 20/25 O.D. and O.S., and 20/20-2 O.U. Best-corrected visual acuity was 20/20-1 O.D. and 20/20-2 O.S., which did not improve with pinhole or refraction. Pupils were equal, round and reactive to light and accommodation with no afferent defect. Confrontation fields were full in both eyes. Extraocular motilities were full in all diagnostic positions of gaze. Slit lamp examination of her anterior segments was unremarkable, except for moderate dermatochalasis that did not appear to affect her superior fields.
Intraocular pressure measured 22mm Hg O.D. and 24mm Hg O.S., which was consistent with those noted in her record.
Upon dilation, her crystalline lenses showed mild nuclear sclerosis in both eyes, consistent with her slightly reduced visual acuity. Stereoscopic examination at the slit lamp showed cup-to-disc ratios of 0.35 x 0.35 O.D. and 0.40 x 0.40 O.S. Both discs were somewhat tilted vertically with a relatively flat contour to both inferotemporal neuroretinal rims, and adjacent peripapillary atrophy in the inferotemporal quadrants of each nerve. Retinal vasculature was characterized by mild arteriolar sclerosis, consistent with her hyperlipidemia. Her peripheral retinal examination was normal, with several areas of microcystoid O.U.
We obtained stereo photographs and asked her to return for threshold visual fields and Heidelberg Retina Tomograph-3 (HRT-3, Heidelberg Engineering) imaging of her optic nerves.
1. Notice the lack of a white-on-white defect in the pattern deviation plot as well as on the outer ring of the structure-function map.
2. In the same patient, flicker defined form perimetry clearly shows the field defect in the pattern deviation plot as well as on the structure-function map.
Three weeks later, the patient presented for the requested testing. Given her complaints of cosmetically bothersome dermatochalasis, as well as for her ocular hypertension, we tested her with a 24-2 standard field. But she had no field defects associated with glaucomatous optic neuropathy, nor was there significant loss due to the dermatochalasis. These fields were consistent with those in her record.
We asked her to return on a six-month basis for field studies, IOP readings and nerve evaluations, which she did.
Then in March 2012, during one of her regularly scheduled follow-up visits, she presented with a disc hemorrhage at the inferotemporal portion of the neuroretinal rim in the right eye. IOPs measured 24mm Hg O.D. and 25mm Hg O.S.
Discussion
Her record indicates no prior evidence of a disc hemorrhage in either eye. Nevertheless, a disc hemorrhage on the neuroretinal rim in the context of glaucoma certainly calls into question the stability of the health of the optic nerve. So, does this warrant a change in her management?
Specifically, should we initiate therapy?
Interestingly, the patient was scheduled for Heidelberg Edge Perimetry (HEP) at this visit, instead of standard perimetry. The HEP’s flicker-defined form stimulus targets functional assessment of the M ganglion cells, the first cells believed to be damaged in glaucoma.1 Sure enough, this patient’s HEP visual field studies demonstrated an arcuate defect in the eye with the disc hemorrhage, strongly suggestive of glaucomatous field loss in that eye.
Now, did the hemorrhage contribute to this field defect by compromising the neuroretinal rim, or did the field defect exist earlier in the care of this patient and it was simply not seen or appreciated, as all previous studies involved standard white-on-white (WOW) threshold perimetry? Either scenario is as likely to be correct.
No matter what, the patient now has documented visual field loss consistent with glaucoma, and therapy should be initiated. Accordingly, I prescribed Lumigan h.s. O.D.
Follow-Up
On a follow-up visit in August 2012, we ran WOW field studies on this patient that showed no defects in either eye (figure 1). While this does not answer the question of whether her glaucoma has existed for a long time or whether she converted due to functional changes as a result of the disc hemorrhage, it does point out the utility of the HEP’s flicker-defined form stimulus in identifying glaucomatous visual field defects earlier than standard white-on-white field studies (figure 2).
Disclaimer: Dr. Fanelli has no financial interest in Heidelberg Engineering.
1. Quaid PT, Flanagan JG. Defining the limits of flicker defined form: effect of stimulus size, eccentricity and number of random dots. Vision Res. 2005 Apr;45(8):1075-84.
