Case study II

By- Dr. Tyson Xu

An 82-year-old Caucasian female visited to the ophthalmologist.

Reason for visit: Noticed her RE wasn’t as clear as her LE, even with
optical correction from a year ago.
General History: Controlled hypertensive and migraine sufferer.
Treatment History: Multiple drugs, but no steroidal medication.
Past History: Bilateral pseudophakia for the last 6 years. Was initially
diagnosed at the time with glaucoma by the ophthalmologist but was lost
to follow up.
Family History: No history of glaucoma.

Clinical History

Assessment

Best corrected visual acuity (BCVA): RE: Plano/-0.75×100 (6/7.5-

1)

LE: +0.25/-1.00×80 (6/6)

Pupils: PERRL (Pupils equal, round, reacting to light) and no RAPD
(Relative afferent pupillary defect).

IOP: RE: 11mmHg

LE: 11mmHg @ 11:10am

Pachymetry (Measurement of corneal thickness) :

RE: 474µm and LE: 495µm

Anterior eye:
  Angles open
 No signs of pigment dispersion or pseudoexfoliation syndrome.
 Intraocular lens clear and central.

Dilated fundus examination:

 Maculae flat with no evidence of epiretinal membrane nor

vitreomacular traction.
 Right optic nerve: Focal rim thinning inferiorly (notch) with
correlating retinal nerve fibre layer (RNFL) wedge defect and
thinning of ganglion cell layer (GCL) inferiorly (Figure 1).
 Left optic nerve: RNFL and GCL within normal limits (Figure 2).
 OCT 3D disc analysis showing marked disc asymmetry (Figure
3).

Figure 1. 3D wide report of RE showing RNFL and GCL thinning

 Figure 2. 3D wide report of LE showing RNFL and GCL within
normal limits

Figure 3. 3D disc report showing disc asymmetry

Automated perimetry:
  Repeatable paracentral visual field defect in the RE in the
superior nasal quadrant – this correlate to the inferior temporal
thinning of the ganglion cell layer (Figures 4 and 5).

Amsler grid:

 Absolute scotoma superonasal to fixation in the RE. LE normal.

Figure 4. Visual field from a year ago showing a paracentral defect

in the RE
 Figure 5. Visual field from most recent presentation showing a
repeatable paracentral defect in the RE

Diagnosis & Management

Differential diagnosis:

 Normal-tension glaucoma
 Secondary open-angle glaucoma
 Angle-closure glaucoma
 Physiological disc asymmetry
 Optic atrophy

Diagnosis: Normal-tension glaucoma

Management:
  Patient was advised that the RE’s central vision wasn’t as good
due to the absolute scotoma caused by loss of ganglion cells
from glaucoma.
 Patient was referred to a local glaucoma specialist for
management as well as to Glaucoma Australia to help facilitate
understanding and encourage compliance with treatment and
reviews.
 She was also advised to encourage her family members to get
their eyes checked.

Discussion

Normal-tension glaucoma (NTG) is a form of primary open-angle

glaucoma in which IOP is less than 21mmHg and is one of the most
common forms of glaucoma in Australia, Japan, Western Europe and
the US. Compared to other forms of glaucoma, NTG has a relatively
slower average rate of progression with reported mean deviation visual
field loss of 0.36dB-0.41dB / year as opposed to 3.13dB / year in
pseudoexfoliative glaucoma and 1.31dB / year in hypertensive
glaucoma. However, NTG visual field defects tend to be more localised,
dense and closer to fixation. In this patient’s case, it has affected her
central vision in the RE, and she is now symptomatic.

Risk factors for progression of VF defects include female gender,

migraines and disc haemorrhages. Disc haemorrhages are also very
characteristic of NTG as well as inferotemporal rim thinning and
notching.

Since ophthalmological assessment, the patient’s IOP has been

controlled with prostaglandin analogue eyedrops (Xalatan, latanoprost
0.005%) and she is being reviewed on a six-monthly basis.