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Headaches in optometric practice part 3: Asthenopia or angle closure?

Kirit Patel describes a case where asthenopic symptoms were discovered to be related to angle closure glaucoma requiring urgent referral

In practice, we regularly deal with patients who have been referred by friends or professional colleagues for an eye examination. These patients invariably have to wait a few weeks for an appointment due to our booked clinics. They are mostly booked in at the end of the day where there is always time pressure to finish the clinics and, typically, these patients have a list of concerns and problems. As a clinician, one has to be focused and treat every patient equally, whether known to one or not.

Case study

A 58-year-old male attended for his first appointment after the recommendation of his sister and mother who had been patients at the practice for 10 years. His mother had been referred by the author a few years ago with a diagnosis of pseudoexfoliative glaucoma. He had previously been assessed by his optometrist near to his workplace for a number of years, and had a long and persistent history of tiredness and soreness of the eyes associated with prolonged computer use.

His reported symptoms at presentation were, again, tired eyes on a daily basis and extreme sensitivity to light. This was particularly noticeable when using a tablet in the evening and when at the desktop computer during the daytime. For the last 12 to 18 months he had changed his working pattern, starting work at 7am and finishing at 3pm, in order to give his eyes a rest. He preferred to go into work early so that he could do his work with the overhead lights switched off. He had a history of migraine. He had an anti-glare coating on his spectacles and there had been no alteration in his prescription for the past two years.

Refraction

(6/9) R: +1.00DS / -0.50 DC X 180 (6/6) ADD +2.00 (N5)

(6/9) L: +1.25DS / -0.25 DC X 175 (6/6) ADD +2.00 (N5)

There was no change in his spectacle prescription on this occasion,

Intraocular pressures were R: 19mmHg and L: 18mmHg (Perkins @ 17.15).

Fundus examination revealed no suspicious cupping of the disc and his fundus appeared healthy, with no signs of optic nerve inflammation or vascular abnormalities.

Anterior assessment

It would have been easy to reassure the patient that his symptoms were probably related to his use of computers and tablets and to dispense a pair of suitable spectacles in an attempt to reduce eye fatigue and eye strain.

Slit-lamp examination revealed no corneal, anterior chamber or crystalline lens abnormality. Van Herick’s technique, however, revealed very narrow, virtually closed angles both nasally and temporally in both eyes (Figure 2). The Van Herick method uses a narrow slit beam at 60 degrees onto the cornea just anterior to the limbus to evaluate the anterior chamber depth. The patient was very sensitive to all drops and gonioscopy proved to be a no-go as the patient closed his eyes as soon as the gonio lens was brought towards to the eye. I have however, attempted to simulate the gonioscopy view of the angle using examples from other patients (see Figures 1 and 2).

Figure 1: Schwalbe’s line (SWL) is the anterior edge of the trabecular meshwork. 2 represents non-pigmented anterior and pigmented posterior trabecular meshwork (TM). 3 represents the scleral spur (SSP) and 4 ciliary body band (CB). Open angle as 4 structures seen

OCT assessment

OCT examination of the anterior eye revealed closed angles in both eyes and the narrowing was such that the region from Schlemm’s canal through to the edge of Descemet’s layer was fully obstructed (Figure 2). Corneal thicknesses were R: 572 microns and L: 575 microns. OCT retinal nerve fibre and ganglion cell assessment revealed no signs of nerve fibre or ganglion cell loss.

Figure 2: Schwalbe’s line (SWL) is now covered by the iris as the angle narrows. Similarly, the trabecular meshwork (TM) is also occluded by the closing angle. There is no way the fluid is going to track through the Schlemm’s canal (SC). We cannot see the scleral spur (SSP) and ciliary body (CB). The middle image shows a very narrow angle with Van Herick. The final image is the gonioscopy showing the wedge and the Schwalbe’s line but none of the four structures. This is VH grade one – nearly closed angle.

Action taken

The patient had my findings explained to him in a calm and reassuring manner. He was told that he would be referred to the ophthalmologist urgently to prevent an acute attack of glaucoma. He was also advised to avoid darkness where possible prior to his hospital assessment as this could precipitate pupil dilation and further increase the risk of an acute attack of glaucoma. He did report coloured haloes around lights but it is possible his glare symptoms were induced by corneal oedema. A letter was written that evening and he took this the next morning for the local eye clinic.

Ophthalmologists examination

He was seen at the eye clinic that afternoon and (unfortunately or fortunately) had his pressures taken after a misjudged dilation. As soon as the ophthalmologist saw him 40 minutes later, his pressures had risen to nearly 50mmHg and alarm bells rang out. He was immediately put on pilocarpine drops (3x), Ganfort (1x), Alphagan (3x) and Diamox tablets (250mg, 2x) to reduce the pressures. He was then booked in to have YAG laser iridotomies to both eyes some five days later.

Discussion

Firstly, this case underlines just how important it is to listen to patient’s symptoms, and not to jump to any conclusion immediately without due consideration of all the facts. Time must always be flexible enough in a clinic to give due regard to assimilating all information. OCT now enables optometrists to assess the patients angles non-invasively and is a must in diagnosing narrow or moderately narrow angles. In our patient’s case the symptoms were primarily fatigue in nature and only through delving deeper was it possible to ascertain the cause of his symptoms.

In bright light I believe he was being troubled by haloes and misty vision and switching the lights off only served to prolong his pupil dilation and elevation of pressures. It was a vicious cycle pupil dilation – raised pressures – corneal oedema – misty vision – eye fatigue and headaches. He was fortunate not to suffer an acute attack of angle closure glaucoma. His retinal nerve fibres and ganglion cells revealed no loss.

Narrow angles or moderately narrow angles do not cause any symptoms in 90% of patients, but in 10% any pupil dilation can lead to pain and/or haloes around lights due to corneal oedema. Our patient was a primary angle closure suspect with an anatomically narrow angle. The peripheral iris was located close to, but not touching, the posterior pigmented trabecular meshwork. He also had normal IOP, normal nerve fibre layer and full visual fields. If trabecular obstruction by the peripheral iris occurs, such as with the formation of peripheral anterior synechiae, the IOPs will rise and this is described as a definite primary angle closure.

Primary angle closure glaucoma is diagnosed when there is irido-trabecular contact present in three or more quadrants, together with optic nerve damage and visual field loss. Sometimes it is better to induce angle closure glaucoma within the clinical setting, so that the patient can be referred and treated immediately. If it happens in the night at home, the patient may not register the symptoms immediately and any delay could lead to loss of sight.

Primary closed angle glaucoma is thought to be less common in Caucasians compared to Asians and high hypermetropia (greater than +5.00DS) is a major risk factor. In our practice we are finding more instances of narrow angles in Caucasians and this could be a result of using slit-lamp biomicroscope and OCT’s regularly to look at the angles.

Pathology

Primary angle closure glaucoma is the result of blockage of the angle by a dilated pupil preventing flow of fluid from posterior chamber to the anterior chamber and consequently causing a sudden rise in intra ocular pressure due to obstruction of the trabecular meshwork. The risk of pupillary block is highest with a mid-dilated pupil causing maximum contact between the iris and the lens. A narrow angle is the main contributor to this condition, especially when the pupil is dilated by stress and sympathetic autonomic activity, drugs or low light levels and the risk factors are listed in Table 1. Our patient was unfortunate in having shallow anterior chamber.

Table 1

Risk factors for primary angle closure glaucoma

  • Ethnicity: Asians are at a greater risk (1 in 100 compared to 1 in 1,000 in Caucasians). This could be related to smaller eyes in Asians compared to Caucasians.
  • Gender: Females are four times more likely than males.
  • Shallow anterior chambers – often seen in hypermetropes (>+5.00DS) and individuals where the crystalline lens is positioned anteriorly in the eye.
  • Age – lens growth as well as thickening of lens following cataract leads to iris encroachment upon the anterior chamber. This is a major predisposing factor.
  • Pupillary dilation – in darkened rooms
  • Stress – during periods of stress or excitement pupils can dilate leading to acute attack
  • Drugs – in predisposed individuals, certain drugs can induce acute attack. These include;

– Anti-histamines.

– Anti-depressants.

– Cold and flu medication.

– Asthma medications, such as ipratropium.

– Stomach ulcer medication such as ranitidine, cimetidine and chlorpheniramine.

– Anti-nausea medication such as phenothiazine.

Acute attack of glaucoma causes sudden rise in pressure with patient suffering pain, redness, blurred vision, coloured haloes around lights as well as nausea, headaches and abdominal pain. Signs of acute glaucoma are dilated pupil, circumciliary injection, corneal oedema and very high intra ocular pressures.

Drug treatment

The aim of medical treatment for acute angle closure glaucoma is to firstly lower the IOP, reduce pain and clear any corneal oedema in preparation for subsequent iridotomy. The medications used are summarised in Table 2

Table 2

Drugs used in the treatment of angle closure glaucoma

Topical
– Beta blockers
– Selective alpha agonists
– Carbonic anhydrase inhibitors

Miotics
– 2% pilocarpine to break early angle closure.
Systemic
– Oral Diamox (acetazolamide 250mg) gives maximum IOP reduction within two to four hours and lasts for six to eight hours.

Osmotic Agents
– Intravenous 15%-20% solution of mannitol lowers IOP of 30mmHg or more within 30 minutes of administration.

Iridotomy

Peripheral laser iridotomy is a safe and effective first line treatment and allows tiny holes to be made at the base of the iris by a YAG laser. It is used in patients at risk presenting with subacute glaucoma as opposed to full surgical iridectomy which involves removal of a portion of the iris. Incisional iridectomy (Figure 3) may be necessary in cases of significantly cloudy corneas. This allows the free flow of aqueous from the posterior chamber to the anterior chamber which then drains out through the trabecular meshwork.

Figure 3: Image on the left shows a laser iridotomy which is the treatment of choice for narrow angles. The middle image shows incisional iridectomy used in patients where the cornea is cloudy and inaccessible to laser. The image on the right shows a typical gonioscopy view of an angle with pigment accumulation

As well as its ease of application, the other advantage of a peripheral iridotomy is the lower risk of inducing cataracts when compared with invasive surgery. An untreated fellow eye has a 50% chance of developing an acute primary angle closure attack over the next five to 10 years and therefore, it is imperative to treat the fellow eye. Forty-five per cent of laser iridotomies will develop some lenticular opacification but rarely full blown cataract. Nine per cent of YAG iridotomies may close up some two to three years after the procedure and therefore may need further laser applications and regular follow ups. YAG laser is used for patients with lighter eyes whereas argon laser may be more appropriate for patients with darker irises.

Conclusion

Here we had a lot of mitigating circumstances – end of the day, patient exhibiting asthenopic type symptoms, normal pressures, normal retina and the perennial problem of underpayment by the NHS? It would be easy to put it down to work symptoms but remember if we do not delve deeper we are unlikely to find the pearls. I hope colleagues would also be enlightened by the angle structures seen through a goniolens and relate this to the angle scans acquired through the OCT.

Kirit Patel works in independent practice in Radlett, Hertfordshire.

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