Case study
Patient initials: BW
DOB: 09/02/57
Condition: primary open angle glaucoma
Presentation: 09/01/2017
Patient had been seen for a routine eye examination in December 2016 and had been referred by a colleague for a formal Glaucoma Refinement appointment. At original examination a simple change in prescription had been identified and glasses were updated.
Ocular history
Iritis early 1990s in the right eye but with no recurrence. No other issues.
General health
Heart double bypass in 2010
High blood pressure and cholesterol – last check 6/12
Medication
- Aspirin
- Bisoprolol
- Furosemide
- Atorvastatin
- Omeprazole
- Candesartan
Family history
No systemic issues
Mother had closed angle glaucoma diagnosed in her 70s – controlled with drops
Lifestyle
Technician
Drives
Computer seven hours per day
Plays golf
Clinical features as described in referral from colleague
Concern due to asymmetry in IOP and RE inferior NRR loss. Reports that previous splinter haemorrhage described in this location in 2014 but IOPs and fields normal in 2014. Fields unreliable at this visit.
Clinical investigation at refinement appointment
Tonometry
Goldmann Applanation Tonometry (GAT)
R 23mmHg L 15mmHg
Slit lamp
External eye and adnexae – Healthy R&L
Anterior Chamber – Grade IV VH R&L
Anterior Chamber Depth – 2.6mm (Smith’s Method)
Figure 2: Gonioscopy recording chart
Iris – Grey even colour– no apparent atrophy or synechiael damage from previous iritis R&L
Cornea – Clear – no KPs /PDS R&L
Sclera – Healthy R&L
Gonioscopy using Goldmann 4 Mirror goniolens (figures 1-2)
Angle Wide Open – Grade IV Schaeffers.
No evidence of secondary causes (pigment dispersion, pseudoexfoliation, peripheral anterior synaechiae)
Dilated ophthalmoscopy (figures 3 and 4)
Figures 3 and 4: Left fundus and right fundus
Volk Superfield general examination & Super 66D for Disc / Macula
Lens – Clear R&L
Vitreous – Mild Syneresis – normal for age R&L
Vessels – Healthy AV 2:3 – No nipping / tortuosity R&L
Macula – Healthy – normal reflex R&L
Periphery – Healthy R&L
Disc Assessment (figure 5)
Figure 5: Right and left disc under magnification
Humphrey 24-2 SITA Fast with +3.00DS R&L (figures 6 and 7)
Figure 7: Left eye fields; left first attempt and right second attempt
Fields unreliable but correlated well with fields from initial examination
- RE Mean Deviation on 1st attempt -7.46dB 2nd attempt -7.78dB
- LE Mean Deviation on 1st attempt +1.25dB 2nd attempt +0.79dB
Despite poor reliability there was a marked difference between performance R+L.
Both RE fields showed evidence of a right nasal step, development of an early inferior arcuate defect and superior paracentral defects respecting the horizontal midline. The field plots are consistent with glaucoma, but the degree of RE inferior neuroretinal rim loss would be expected to produce more noticeable superior defect.
LE fields unreliable but not glaucomatous.
Baseline OCT scans
These show a significant loss of both ganglion cell complex and retinal nerve fibre layer in the inferior field of the RE with subtle superior rim changes also being apparent (figure 8).
Figure 8: OCT scan data for both eyes
Differential diagnosis
A right glaucomatous optic neuropathy is the most likely diagnosis for BW, though had the field loss been solely inferior rather than superior, an alternative could have been a right non-arteritic ischaemic optic neuropathy, especially as the left eye is fine.1
There are a range of glaucomatous conditions that you would consider with such a unilateral presentation. All the occlusive conditions would be ruled out by the normal gonioscopic appearance which showed open angles and no evidence of secondary causes (pigment dispersion syndrome, pseudoexfoliation, peripheral anterior synaechiae). There are several glaucomas implicated in uveitis due to trabecular meshwork damage and blockage by debris and proteins, with a prevalence of 10 to 20%.2
The patient has consistently high IOPs; an established risk factor for the development and progression of glaucoma.3,4 The patient had symmetrical central corneal thicknesses (CCTs) which could allow a downwards correction factor though there is limited evidence for its use in COAG. A thinner than average CCT is a recognised risk for progression of ocular hypertension (OHT) to COAG.5
The right optic nerve head was highly suggestive of glaucoma with inferior focal loss, non-concentric cupping, nasalisation of vessels and pronounced lamina cribrosa pores. Superior NRR showed some thinning and possible early bearing of vessels. Of note is the reference made to a splinter haemorrhage in the inferior position in 2014’s otherwise normal examination – splinter haemorrhages are a significant risk factor, especially in normal tension glaucoma. However, their transient nature often means they are not present if a patient is referred to secondary care.
The right visual fields plots were consistent with optic nerve head damage.
The OCT scans also show evidence of inferior loss of the NRR and ganglion cell complex (GCC) reduction in the same zone which would also support the measured visual field loss. GCC loss has been shown to precede visual field loss in patients who went on to develop glaucoma.6
Tentative diagnosis
RE Chronic open angle glaucoma. LE Normal at this stage
Management plan
Patient was advised they were likely to have RE chronic open angle glaucoma in the RE and that I would be referring them for confirmation of diagnosis by a consultant ophthalmologist. I issued the College of Optometrists information leaflet on glaucoma and also advised the patient that, if diagnosed, they should inform both their immediate family due to the increased risks presented to them as well as the DVLA.
Therapeutic management*
In line with NICE guidelines on glaucoma, a topical prostaglandin analogue (PGA) hypotensive agent was presented as the first line of therapy with the aim of establishing a target IOP of 16 to 17mmHg, which is reduction of 30% of that at diagnosis.7
PGA drugs reduce IOP by promoting the outflow of aqueous humour via the uveoscleral route. A monotherapy with a PGA could realistically be expected to reduce the IOP to this level.8 Future reviews will establish whether further reduction in IOP is required by reference to visual field and optic nerve head changes.
BW reports no allergies or previous reactions to drugs. It was decided to commence him on generic latanoprost 50microgram per 1ml at a dose of RE 1 drop nocte. I explained the likely side effects of thickened, lengthened eyelashes, as well as pigment changes to the lashes and possibly iris.
He was made aware that irritation and mild redness may also occur. A specialist glaucoma nurse undertook a medication competency training session to ensure ability and compliance. She also underlined the lifelong management and treatment required and consequences of uncontrolled glaucoma. The patient was informed of the need to advise the DVLA of their diagnosis.
A standard NHS prescription was written for latanoprost 50 microgram per 1ml 1gt RE only for the patient. A letter was sent to the patients GP advising him of the diagnosis and need for repeat prescriptions.
The patient was placed on a 1/12 recall to ensure that a target IOP was being achieved as well as to repeat visual fields. The patient was advised to contact us sooner should serious adverse effects be suspected.
Reflection
I was also careful to point out the slightly increased risk of a recurrence of the iritis or the development of cystoid macula oedema from the PGA prescribed. The BNF notes that PGA should be used with caution in patients with a history of iritis,9 but as BW had no current systemic association with systemic inflammatory disease I felt the risk posed by using a PGA was justified in pursuit of the best control of the RE glaucoma. A home Amsler grid was issued with instructions.10
Consideration was given as to whether a carbonic anhydrase inhibitor or alpha agonist should be offered as first line therapy to remove the induced asymmetry of lash colour and morphology. However, the patient decided he wanted a simple regime and was not worried about cosmesis.
I am surprised at the rapid development of glaucoma, but noted a one year recall was requested in 2014 due to the splinter haemorrhage and that the patient did not make a return visit until late 2016.
The normal LE would make me highly suspicious that the RE was the eye that had experienced the iritis, though the lack of visible changes in the angle and anterior chamber would not absolutely support this, and close monitoring of the LE would be essential at future visits.
I would also hope that, with practice and suitable training, the patient’s visual fields would become more reliable and allow better monitoring of disease progression.
* The latter sections describe the management as a therapeutic optometrist working under the local glaucoma ophthalmologist.
Andy Bitton is an optometrist and co-director of Specsavers Haverfordwest in South Wales.
References
1 Hayreh SS & Zimmerman B. 2005. Visual field abnormalities in nonarteritic anterior ischemic optic neuropathy – Their pattern and prevalence at initial examination. Archives of Ophthalmology, 123, 1554-1562.
2 Stainer L & Masood I. 2017. Glaucoma: definitions, epidemiology and pathyophysiology. Optometry in Practice, 18, 17-26.
3 Heijl A, Leske MC, Bengtsson B, Hyman L, Hussein M & Early Manifest Glaucoma Trial, G. 2002. Reduction of intraocular pressure and glaucoma progression – Results from the early manifest glaucoma trial. Archives of Ophthalmology, 120, 1268-1279.
4 Kass MA et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002 Jun;120(6):701-13; discussion 829-30.
5 Sng CCA, Ang M & Barton K. 2017. Central corneal thickness in glaucoma. Current Opinion in Ophthalmology, 28, 120-126.
6 Cennamo G, Montorio D, Romano MR, Cardone DM, Minervino C & Reibaldi M. 2016. Structure-Functional Parameters in Differentiating Between Patients With Different Degrees of Glaucoma. Journal of Glaucoma, 25, E884-E888.
7 Van Veldhuisen, P. C., Ederer, F., Gaasterland, D. E., Sullivan, E. K., Beck, A., Prum, B. E., Cyrlin, M. N., Weiss, H. & Inv, A. 2000. The advanced glaucoma intervention study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. American Journal of Ophthalmology, 130, 429-440.
8 Doucette, L. P. & Walter, M. A. 2017. Prostaglandins in the eye: Function, expression, and roles in glaucoma. Ophthalmic Genetics, 38, 108-116.
9 BNF. BNF - Latanoprost [Online]. https://bnf.nice.org.uk/drug/latanoprost.html: NICE - National Institute of Health and Clinical Excellence. [Accessed 20th May 2017 2017].
10 Horsley, M. B. & Chen, T. C. 2011. The Use of Prostaglandin Analogs in the Uveitic Patient. Seminars in Ophthalmology, 26, 285-289.