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CASE REPORT: Remember, examine the optic nerve head


Figure 1. Right and left optic nerves. The red arrow highlights the location of the inferior rim thinning in the right eye. No nerve fibre layer defect is noticeable with red-free viewing.


Alex Petty
Tauranga, New Zealand


A 62-year-old English woman of Indian descent presented to my practice as she had been noticing flashes in the temporal periphery of her vision of the left eye for the previous month.

These flashes were occurring only in the evening and more so when she rotated her head to the left. There was no history of trauma and she was not noticing any floaters, blind spots in her vision or decreased acuity.

The patient had emigrated from the United Kingdom several years before and remembered that at her previous eye test she had been told one of her eyes looked a little unusual; however, treatment was not discussed. She got by using a pair of over-the-counter +2.00 reading glasses.

Our patient’s general health was fine, although she did have some deafness from a severe bout of chicken pox when she was in her 30s. She had no diabetes or high blood pressure and she took no regular medications. As far as she knew, no-one in her family had any eye issues.

Suspecting a posterior vitreous detachment, I carried out a pre-dilation work-up. Unaided visual acuity was 6/5 in each eye with a refraction showing R +0.50/-0.50 x 35 (6/5), L +0.50/-0.50 x 95 (6/5), add +2.25. Pupils were equal, round and regular and no afferent defect was present. Ocular motility revealed no restrictions and in my chair the patient reported no flashes or discomfort on left gaze. The anterior eye was unremarkable with open angles (AC/C ratio of 0.6 with Van Herrick estimation) and clear cornea and crystalline lens. There was no obvious iris trans-illumination. Tonometry revealed some intraocular pressure asymmetry with R 25 mmHg, L 21 mmHg. Her corneae were on the thin side at R 512 microns and L 519 microns.

Following dilation with 1% tropicamide in both eyes, the mobile posterior vitreous face could be seen in the left eye although no free pigment was noticeable behind the crystalline lens. The retina was intact in each eye with no holes, tears, blood or traction seen, and there were no obvious vitreous floaters close to the retina. A diagnosis of posterior vitreous detachment in the left eye was made and the patient was reassured and given warnings in case her symptoms changed.

Optic nerve

Examination of the optic nerves during this posterior investigation revealed the unusual appearance that was alluded to in the history. Asymmetry was present between the two eyes with the right eye’s inferior neuro-retinal rim appearing notched and pale (Figure 1). The left eye, in contrast, was relatively normal with a medium size and a 0.45 cup/disc ratio. The patient was asked to return for a glaucoma work-up the following week.

After further questioning on our patient’s return, she admitted that she noticed tingling at the tips of her fingers from time to time. She mentioned that she had had some blood loss during her chicken pox illness; however, this was likely to have been related to her skin lesions and was not relevant.

Intraocular pressures were again higher in the right eye (R 23 mmHg, L 18 mmHg, Goldmann applanation). Gonioscopy showed normal open angle structures and no sign of any pseudo-exfoliative material or pigment.

Visual field testing was performed well by the patient (Medmont M700 Glaucoma Test) and unsurprisingly, showed a superior arcuate field defect. The right inferior field and the left field were relatively normal (Figure 2).



Figure 2. Visual field plots of the right eye (top) and left eye (bottom) showing the superior arcuate defect in the right eye


OCT testing (Nidek RS-3000) was carried out and confirmed an inferior retinal nerve fibre layer (RNFL) defect in the right eye. Surprisingly, the superior RNFL in the right eye is also flagged as being markedly thin (Figure 3). The left eye RNFL was within normal limits.



Figure 3. OCT showing thinning of the RNFL superiorly and inferiorly in the right eye


Analysis of the ganglion cell layer (GCL) showed an expected defect of the inferior macula (Figure 4); however, the superior macula GCL was relatively normal. Given that the superior rim of the right ONH appeared healthy and the inferior visual field was normal, this brings into question the validity of the flagged superior RNFL loss in this eye. The left eye GCL was within normal limits.



Figure 4. OCT macula analysis of the ganglion cell layer shows thinning inferiorly in the right eye. Note the wedge defect of this layer in the colour representation as shown by the red arrow.


After consideration of these findings and the patient’s risk factors, a diagnosis of unilateral primary open-angle glaucoma in the right eye was made. The patient was concerned about the prospect of life-long topical glaucoma medication as she had apparently reacted to eye-drops in the past. As a result, she was referred for consideration of selective laser trabeculoplasty (SLT).


This case is a classic example of a patient needing our services for one issue and having an unrelated condition diagnosed in the process. It highlights the importance of being on the look-out for other signs of ocular disease when carrying out routine investigations.

This patient had a number of risk factors for glaucoma:1 advancing age, higher IOP in one eye, thin corneae and potential Raynaud’s disease.

It is unclear in the literature if people of Indian descent are more or less likely to develop POAG, although according to one group, glaucoma was responsible for 12 per cent of the blindness in Hyderabad, India,2 a figure similar to that in the UK and USA.1

Raynaud’s disease is a condition which is characterised by cold fingers and toes, loss of skin colour in these areas and a prickly feeling or stinging pain during recovery. In Raynaud’s disease, arteries to the extremities go into vasospasm when exposed to cold or stress, narrowing and temporarily limiting blood supply. It is thought that this decreased perfusion could suggest a vascular disorder compromising blood flow to the optic nerve and increasing the risk of glaucoma.

Other conditions with poor ocular perfusion include sleep apnoea, migraine headaches and patients with a nocturnal drop in blood pressure. Patients with these conditions may also have a higher risk of glaucoma.3

When making the initial diagnosis of glaucoma, as practitioners we have to be careful to consider other masquerade conditions. Compressive optic neuropathy, ocular ischaemic syndrome, anterior ischaemic optic neuropathy and even methanol poisoning may cause glaucoma-like cupping of the optic nerve head.4

This patient has a number of clinical signs of glaucoma: a notched optic nerve head, a higher IOP in the eye, thin corneae, visual field changes in the expected location and OCT scanning confirming RNFL loss and ganglion cell layer loss. In this case, it is highly unlikely another condition is responsible.

When considering treatment options, it is useful to be mindful of the patient’s stage in life. Glaucoma is a condition that requires treatment for life and it carries significant financial and social burdens for the patient. Our patient is in her early 60s and may have another three to four decades of life ahead of her.

It is important her treatment gives her the best chance of retaining her vision in the future. Laser treatment such as SLT can be useful as an initial treatment for POAG as it is equally efficacious as the typical front-line glaucoma medication latanoprost, decreasing intraocular pressure by around 30 per cent.5 SLT treatment also avoids the risks of non-compliance with medical treatment. Research with electronic eye-drop monitoring revealed only 76 per cent to 86 per cent eye-drop compliance in glaucoma patients, and evaluation of prescription claims showed patients had glaucoma eye-drops available to use 69 per cent of the time.6

SLT is not a magic bullet as it is well known that the IOP-lowering effect of SLT decreases over time. The mean survival time (time taken for 50 per cent of eyes to no longer have pressure reduction of >/= 20 per cent) is around two years,7 although some patients may still retain good pressure control after five years.8

In the end, the patient opted to start with medical treatment (Xalatan nightly to both eyes) for her POAG, despite being offered SLT by the ophthalmologist in order to avoid allergy. Apparently the prospect of a laser was more confronting than the idea of using eye-drops each night. She was to be followed up in our clinic after two months to assess her pressure control.


With optometry’s increasing scope of practice, it is important for practitioners to remain highly vigilant when examining even routine cases. All optometrists should be comfortable detecting, diagnosing and managing glaucoma. Management may include referral to other optometry or ophthalmology colleagues who regularly treat glaucoma, commencing the patient on medical treatment yourself, or recommending SLT treatment as a first-line therapy in order to avoid eye-drops and increase compliance. Be comforted that patients with POAG will not go blind overnight but they will require your care and expertise for many years into the future.


1.         Kanski J. Clinical Ophthalmology: A Systematic Approach. 6th ed. Philadelphia: Butterworth Heinemann Elsevier; 2007.

2.         Dandona L, Dandona R, Naduvilath TJ et al. Is current eye-care-policy focus almost exclusively on cataract adequate to deal with blindness in India? Lancet 1998; 351: 1312–1316.

3.         What is the relationship of conditions like sleep apnea and Raynaud’s to glaucoma? (Accessed 30/6/16)

4.         Choudhari NS, Neog A, Fudnawala V, George R. Cupped disc with normal intraocular pressure: the long road to avoid misdiagnosis. Indian J Ophthalmol 2011; 59: 6: 491–497.

5.         McIlraith I, Strasfeld M, Colev G, Hutnik CM. Selective laser trabeculoplasty as initial and adjunctive treatment for open-angle glaucoma. J Glaucoma 2006; 15: 2: 124–130.

6.         Schwartz GF, Quigley HA. Adherence and persistence with glaucoma therapy. Surv Ophthalmol 2008; 53 (Suppl 1): S57–S68.

7.         Leahy K, White A. Selective laser trabeculoplasty: current perspectives. Clin Ophthalmol 2015; 9: 833–841.

8.         Lai JS, Chua JK, Tham CC, Lam DS. Five-year follow up of selective laser trabeculoplasty in Chinese eyes. Clin Exp Ophthalmol 2004; 32: 4: 368–372.

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