Restricted Access

You must be logged in to view this content.

Visual field defects and glaucoma

$currentPage/@nodeName

Dr Jack Phu
BOptom (Hons) BSc

 

CASE REPORT

HC is an 87-year-old Chinese woman who first presented to the practice on 13 August 2013 for routine eye examination. The patient complained of blurry vision with her old spectacles. She had no other complaints of red, sore or itchy eyes. The patient had had cataract surgery with posterior capsular intraocular lenses in the left eye in Australia about three years previously. She had a systemic history of type 2 non-insulin dependent diabetes mellitus, hypertension, hyperlipidaemia, cardiac arrhythmia, and gastroesophogeal reflux disease, and was taking medications for these conditions. The patient reported no history of asthma, renal disease or any medical allergies. There was no family history of vascular or ocular disease.

Best corrected visual acuities were 6/45 at distance and 6/45 at near OD and 6/18 at distance and 6/12 at near OS with manifest refraction of +0.25 DS OD and +0.25 DS OS. Pupils were equal, round, reactive to light and with no afferent pupillary defect OU. Extraocular motilities were smooth, accurate, full and extensive OU. Anterior examination showed open angles with deep anterior chambers OU. Corneas were clear OU. There were grade 2+ pterygia on the bulbar conjunctiva OU, and grade 3+ meibomian gland dysfunction OU. There was grade 3+ mixed cataract OD. The posterior chamber intraocular lens was clear OS. Intraocular pressures measured by Goldmann applanation tonometry were 15 mmHg OU at 5:36 pm.

Dilated fundus examination with Superfield lens showed cup-disc ratios of 0.95 with deep cupping OU. Neuroretinal rims were notched superior and inferior OU, and there was a Drance haemorrhage at 10:30 on the disc OD. There were grade 2+ epiretinal membranes OU, and numerous dot-blot haemorrhages and microaneurysms in the fundus OU. Vitreous body was clear OU. Confrontation visual fields showed slight restriction of temporal and nasal fields OU.

The patient was asked to come back in one week for automated perimetry and OCT imaging.

The patient was seen on 21 August 2013 for glaucoma assessment. Automated perimetry (M700 Automated Perimeter, Medmont Pty Ltd, VIC Australia) results were reliable and showed superior scotoma, nasal defects and enlarged blind spot with possible inferior defect OD though it was difficult to separate the cataractous defects (Figure 1), and very restricted visual fields OS (Figure 2).

976 Figure 1 Right Eye Visual Field Result - F

Figure 1. HC’s right visual field result. Reliability indices were mostly reliable except for high false negatives which may have been due to poor understanding of the task. It shows a superior scotoma with nasal defects, and enlarged blind spot with possible inferior defect.

976 Figure 2 Left Eye Visual Field Result - F

Figure 2. HC’s left visual field result. Reliability indices were better compared with right eye. The raw data shows severe restriction of the visual field inferior more than superior. The pattern deviation shows a similar arcuate defect inferior more than superior; however, such a defect could possibly be due to poor understanding of the task.

Colour fundus photography showed notching and pallor of the superior and inferior neuroretinal rims with adjacent peripapillary atrophy right more than left (Figure 3). The microaneurysms and dot-blot haemorrhages were also seen. The Drance haemorrhage OD was still present. Spectral-domain OCT (3D OCT-1 Maestro, Topcon, Device Technologies, Australia) was unreliable in the right eye due to cataracts but showed corresponding thinning of the nerve fibre layers superior and inferior OU (Figure 4). Intraocular pressures measured by applanation were 15 mmHg OD and 16 mmHg OS at 12:25 pm. Gonioscopy (Sussman G4 goniolens, Volk, Designs For Vision, Australia) showed angles open to the ciliary body OU with no synechiae and light pigmentation of trabecular meshwork. Central corneal thicknesses were 498 um OD and 480 um OS by ultrasound pachymetry (Pachmate DGH55, DGH Technology, Inc PA, USA).

976 Figure 3b RIGHT Eye - F 976 Figure 3a LEFT Eye - F

Figure 3. HC’s colour fundus photos. (Left) Right eye fundus photo, slightly blurred due to cataract. Despite blurriness, the notching of the neuroretinal rim, inferior more than superior, is easily detected. There is also a small Drance haemorrhage visible at 10:30 o’clock on the disc. (Right) Left eye fundus photo, much clearer with intraocular lens implant. There is also significant thinning and pallor of the neuroretinal rims superiorly and inferiorly with loss of retinal nerve fibre layer. The small microaneurysms are easily seen in the left macula.

Differential diagnoses for this patient included compressive optic neuropathy and secondary glaucoma. Signs of secondary glaucomas such as inflammation, exfoliation, and pigmentation were all absent. In light of classical cupped appearance, rather than diffuse pallor, age, and pattern of visual field defect, neuroimaging was not performed for compressive optic neuropathy.

With clear correlation of optic nerve head appearance, visual fields and OCT imaging, HC was diagnosed with advanced glaucoma OU and moderate non-proliferative diabetic retinopathy OU. She was referred to a local ophthalmologist for glaucoma co-management. Because the ophthalmologist was fully booked for the next proceeding weeks, she was started on latanoprost 0.005% (Xalatan, Pfizer, Australia) nocte to both eyes to at least lower the pressure to slow progression of the disease. An appointment was scheduled for three months ahead to discuss the treatment and to ensure that she was compliant and agreed with the management plan. She was to repeat visual field tests after six months. Based on these findings, the ophthalmologist agreed with the diagnosis. The post-treatment IOP was 10 mmHg, which is a 30 per cent reduction from baseline.

976 Figure 4- F

Figure 4. HC’s OCT result. Right OCT result was artifactual, but the thickness maps in both eyes show definitive correlated thinning of the nerve fibre layer. The nerve fibre layer is much thinner inferiorly compared with superiorly in the right eye, which is correlated with its disc appearance. The left eye result also showed corresponding thinning of both superior and inferior nerve fibre layers. The symmetry graph shows that the right eye appears more severely affected than the left, correlated with disc appearance.

Management of glaucoma with significant visual field defects presents a challenge to both the optometrist and the ophthalmologist. There are numerous methods of staging glaucoma. One uses the Bascom-Palmer method, or Glaucoma Staging System (GSS).1 Based on this scoring system, HC has moderate-advanced defect from this visual field result.

Different studies suggest different target IOP for normal-tension glaucoma. The Collaborative Normal-Tension Glaucoma Study group refers to a target IOP of 30 per cent;2 the Early Manifest Glaucoma Trial reported a resultant pressure reduction of 25%;3 and the Advanced Glaucoma Intervention Study and similar studies suggest a reduction of 50 per cent, or to 10 mmHg.4,5 Controversy still exists regarding the recommended target IOP for patients with NTG.6 however, a recent study showed any reduction in IOP is beneficial for the patient in helping to preserve visual function and should be titred according to severity of disease.7 This should be further refined from the individual’s rate of progression.

Studies of topical ophthalmic anti-glaucoma drops show that a reduction of about 20-30 per cent is expected with prostaglandin analogue medications in patients with NTG. Because HC’s baseline IOP was 15 mmHg, the resultant IOP is expected to be 10-12 mmHg. A prostaglandin analogue was selected as first-line therapy due to its ease of dosing—once at night, 24-hour maintenance of IOP reduction, its minimal systemic side-effects, and long-term sustained effect.8 In comparison to timolol, latanoprost has a superior 24-hour IOP reduction profile and is more favourable towards ocular perfusion pressure.7,9

However, prostaglandin analogues have a number of well-documented ocular side-effects, including conjunctival hyperaemia, hypertrichosis, iris and eyelid pigmentation, and prostaglandin-associated periorbitopathy.10 To a lesser extent, prostaglandin analogues have also been linked to inflammatory disease such as uveitis, recurrent ocular herpes and cystoid macular oedema.10 These need to be monitored closely. In addition to topical treatment, HC was counselled on the importance of blood sugar, cholesterol and hypertensive control, as vascular comorbidities may be associated with progression of glaucomatous disease.11,12

Advanced glaucoma with normal-range IOP can present a challenge to the optometrist and ophthalmologist as reduction in IOP alone may be insufficient to prevent progression of glaucomatous disease. Ocular perfusion pressure should be considered in these cases.6 Such a late presentation requires regular follow-up with disc assessment, IOP measurements, and trend analysis by perimetry and optic nerve imaging.

 

  1. Mills RP, Budenz DL, Lee PP, Noecker RJ, Walt JG, Siegartel LR, Evans SJ, Doyle JJ. Categorizing the stage of glaucoma from pre-diagnosis to end-stage disease. Amer J Ophthalmol 2006; 141: 24-30.
  2. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Amer J Ophthalmol 1998; 126: 487-497.
  3. Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson B, Hussein M, for the Early Manifest Glaucoma Trial Group. Reduction of intraocular pressure and glaucoma progression. Archives Ophthalmol 2002; 120: 1268-1279.
  4. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Amer J Ophthalmol 2000; 130: 429-440.
  5. Aoyama A, Ishida K, Sawada A, Yamamoto T. Target intraocular pressure for stability of visual field loss progression in normal-tension glaucoma. Japanese J Ophthalmology 2010; 54: 117-123.
  6. Mozaffarieh M, Flammer J. New insights in the pathogenesis and treatment of normal tension glaucoma. Current Opinion Pharmacology 2013; 13: 43-49.
  7. Cheng J-W, Cai J-P, Wei R-L. Meta-analysis of medical intervention for normal tension glaucoma. Ophthalmology 2009; 116: 1243-1249.
  8. Ang A, Reddy MA, Shepstone L, Broadway DC. Long term effect of latanoprost on intraocular pressure in normal tension glaucoma. Brit J Ophthalmol 2004; 88: 630-634.
  9. McKibbin M, Menage MJ. The effect of once-daily latanoprost on intraocular pressure and pulsatile ocular blood flow in normal tension glaucoma. Eye 1999; 13: 31-34.
  10. Digiuni M, Fogagnolo P, Rossetti L. A review of the use of latanoprost for glaucoma since its launch. Expert Opinion Pharmacology 2012; 13: 5: 723-745.
  11. Yanagi M, Kawasaki R, Wang JJ, Wong TY, Crowston J, Kiuchi Y. Vascular risk factors in glaucoma: a review. Clinical Exp Ophthalmol 2011; 39: 252-258.
  12. Anderson DR, Drance SM, Schulzer M, Collaborative Normal Tension Glaucoma Study Group. Factors that predict the benefit of lowering intraocular pressure in normal tension glaucoma. Amer J Ophthalmology 2003; 136: 820-829.


Like us on Facebook




Subscribe to our News RSS Feed

Latest Tweets




Recent Comments