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Optometric assessment of raised intraocular pressure: This article considers the underlying physiological factors relating to intraocular pressure and presents case studies to highlight patient examination and management.

Optometrists

Therapeutic opticians

Dispensing opticians

Introduction

A suspected diagnosis of glaucoma remains one of the most common reasons for referral to secondary care from optometric practice. (1,2) Determining the aetiology of raised intraocular pressure (IOP) is fundamental to successfully managing the patient. (3) Through this article we will explain some key physiological concepts in IOP assessment and present two cases to highlight areas for practitioners to focus their examination and decision making.

Aqueous production

The non-pigmented ciliary epithelial cells of the ciliary body pars plicata produce aqueous humour. The aqueous ionic concentration is very different to the plasma from which it is derived; this difference arises due to tight junctions between the non-pigmented epithelial cells of the ciliary body preventing passive diffusion of molecules. This, along with tight junctions in iris vasculature, is the blood-aqueous barrier. Breakdown of this barrier can be seen in numerous inflammatory and infective disorders where large proteins Teak' through into the anterior chamber causing it to become cloudier and 'plasma-like.' The non-pigmented epithelium actively transports ions into the posterior chamber, which then allows for the passive flow of water and the formation of aqueous humour.

The mean rate at which aqueous is produced ranges between 1.5 and 4.5 [micro]L/min and shows a normal distribution. This equates to 1-1.5% of the anterior chamber volume per minute. (4) The rate of production is highest in the mornings and lowest at night--a circadian rhythm. The rate of production is also influenced by adrenergic receptors in the ciliary epithelium. [beta]-antagonists, for example, Timolol, and [alpha]-2 agonists, such as brimonidine, both suppress aqueous production.

Once secreted into the posterior chamber, the aqueous passes between the iris and lens into the anterior chamber (see Figure 1). Here, a convection current, established by the relatively cooler anterior chamber being closer to the cornea, cycles the aqueous before it exits the eye at the anterior chamber 'drainage angle.'

Aqueous outflow

Outflow occurs via two pathways: the majority (70-90%) is via the trabecular meshwork and canal of Schlemm; and the remainder (10-30%) is via the uveoscleral outflow pathway. Trabecular outflow is dependent upon IOP (greater pressure = greater outflow) and episceral venous pressure (greater pressure = reduced outflow). Uveoscleral outflow is a constant at 0.3 [micro]L/min and is independent of IOP. (5) The trabecular meshwork is bound anteriorly by Schwalbe's line (termination of Descemet's membrane) and posteriorly by the scleral spur. It lies at the internal scleral sulcus. It is a sieve-like structure and is composed of three layers, inner to outer: uveal meshwork; corneoscleral meshwork; and juxtacanalicular meshwork. Trabecular meshwork cells have phagocytic properties that engulf debris that would otherwise 'clog-up' the trabecular meshwork and impede outflow. Aqueous passes through the trabecular meshwork and into Schlemm's canal. This, in turn is drained by the collector channels and aqueous veins, which empty into the conjunctival veins. As outlined above, the majority of outflow occurs via this 'conventional' pressure-dependent system.

The 'uncoventional' or uveoscleral route is a space between the ciliary muscle fibres and the suprachoroidal space. Aqueous then passes through the sclera in areas where vessels and nerves pierce the scleral substance.

Now that some key principles in how IOP is determined have been covered, this will be translated into a clinical context by use of case scenarios.

Case study 1

An asymptomatic 45-year-old Caucasian female presented for a routine sight test. Non-contact tonometry measurements were R36mmHg L35mmHg. She is hyperopic with a refraction of R +5.00DS VA 6/6 L +5.50DS VA 6/6. The visual fields were full, and optic discs appeared healthy. How would you manage this patient?

It is not uncommon for practitioners to find themselves in a situation similar to that above. Revised NICE Glaucoma guidelines, 2017, recommend referral for patients with IOP of 24mmHg or greater;6 this has increased from the previous threshold of greater than 21mmHg.

Essentially, the patient in this case study has raised IOP but no obvious glaucomatous damage. The choices, therefore, are to refer to eye casualty or to refer via the GP to a secondary care clinic. In most cases, the former approach would be entirely appropriate to ensure treatment is instigated promptly. However, the key question whenever we see such patients is to determine why the pressure is elevated. The answer often lies in assessment of the anterior chamber angle, which is why gonioscopic examination is of paramount importance and is a skill that could become a more routine undertaking for optometrists with the expansion of enhanced services.

Given that the patient is hyperopic it is likely she has narrow angles. It is good practice to assess the angles on hyperopic patients regularly in much the same way, as it is to perform dilated fundus examinations for highly myopic patients.

The fact that this patient is asymptomatic is very normal. Most patients with angle closure are asymptomatic, except of course in cases of acute primary angle closure. There is also poor correlation between symptoms of angle closure and clinical findings of angle closure. It is estimated that angle-closure glaucoma blinds five times more people than open angle glaucoma. (7)

The raised IOP in this case is explained by virtue of the fact that there is reduced aqueous outflow through the conventional route; this may be due to appositional contact with the iris and/or damage to the trabecular meshwork through contact with the iris, or, meshwork damage from elevated pressure. On gonioscopy, irido-trabecular-contact (ITC) would be observed; simply put, this is where the iris is in contact with the trabecular meshwork and so the only angle structures visible would be Schwalbe's line (see Figure 2).

The terms chronic and acute angle closure are also no longer used. A consensus group of the Association of Glaucoma Societies has put forward the following classification which is more prognostic and guides management: (8)

* Primary angle-closure suspect (PACS)--here there are two or more quadrants of ITC. However, IOP, visual fields and optic discs are normal. The risk of glaucomatous optic neuropathy may be around 30% at five years

* Primary angle-closure (PAC)--there are two or more quadrants of ITC and elevated IOP and/or peripheral anterior synechiae. Visual fields and optic discs are normal

* Primary angle-closure glaucoma (PACG)--ITC in two or more quadrants with evidence of glaucomatous optic neuropathy

* Acute primary angle-closure glaucoma (APAC)--this is acute angle closure. Patients present with reduced vision, nausea, and vomiting is common. Markedly elevated IOP, corneal oedema and mid-dilated nonreactive pupil are also likely to be observed. Often the fellow eye demonstrates features of PACS or PAC.

Once the cause has been established, the next question to ask is why there is ITC? The most likely scenario is that of relative pupillary block, that is to say, appositional closure between the posterior iris margin and anterior lens surface causing a failure of aqueous flow through the pupil. This leads to retention of aqueous in the posterior chamber and anterior bowing of the iris to cause appositional closure of the comeo-scleral angle, thus raising IOP. In this situation, a YAG peripheral iridotomy will relieve the posterior chamber pressure by creating an alternative pathway for aqueous flow into the anterior chamber and allow the iris to move away from the trabecular meshwork (given no permanent adhesions --peripheral anterior synechiae).

Other mechanisms which are beyond the remit of this article would be lens vault, plateau iris and phacogenic causes. However, even in these non-pupillary block I cases there is an element of pupil block that may need i treatment. In the case described here it is important, therefore, to determine which of these categories the patient would fall into; this can only be achieved by examining the angle, although it is likely that she has PAC. The relative merits of performing a peripheral iridotomy should then be considered. If this fails, the surgeon may proceed to cataract surgery to 'open' the angle. Indeed, the Effectiveness of early lens extraction for the treatment of primary angle-closure glaucoma (EAGLE) study randomised patients with angle closure to either a laser peripheral iridotomy (LPI) or clear lens extraction. (9) The study showed that lens extraction showed less need for drops and was more cost-effective than LPI as a first-line treatment for patients with PAC or PACG.

Case study 2

An asymptomatic 35-year-old man presented to clinic for a routine sight test. His refraction is R-7.00DS VA 6/6 L -8.00DS VA 6/6. lOPs using Goldmann applanation tonometry measured: R35mmHg L36mmHg. He had been to a gym class that morning. Visual fields were full and optic discs appeared healthy.

Again, this familiar scenario will resonate with practitioners. Often, the answer would be to send this patient to eye casualty as the IOP is significantly elevated. However, it is important to consider the reasons behind the raised pressure as this will help to manage the patient safely, appropriately, and allow for a more helpful discussion with the on-call ophthalmologist.

The patient here is moderately myopic and most likely to have a long axial length and unlikely to be anatomically predisposed to narrow angle pathology (see Figure 3). The differential diagnoses are between primary and secondary causes of open-angle glaucoma. When considering secondary causes for raised IOP and open angles it is still essential to perform gonioscopy. A useful classification system to use in this scenario is to consider the following causes for this presentation: pre-trabecular (membrane growing across the angle); trabecular (clogging-up); and post-trabecular (increased resistance from elevated episcleral venous pressure) (see Table 1). (10) Examination is, therefore, aimed at finding evidence for these causes. A comprehensive assessment would include examination of the:

* Conjunctiva--are there engorged episcleral vessels indicative of raised episcleral venous pressure? Is there circumcomeal injection indicating uveitis or keratitis?

* Cornea--is there evidence of anterior stromal scarring/haze or a new epithelial defect suggestive of viral keratitis? Examine for presence of endothelial pigmentary deposits (pigment dispersion syndrome (PDS)), keratic precipitates (hypertensive uveitis), or red blood cells (traumatic or neovascular)

* Anterior chamber--are there cells, pigment or red blood cells?

* Iris--is there sectoral iris atrophy (viral uveitis), mid-peripheral transillumination defect (PDS), iridodenesis or iridodialysis (previous trauma and angle recession), or polycoria/naevi (ICE)?

* Lens--is there pigment on the posterior lens surface, ruptured capsule, or leaking lens protein or phacodenesis (angle recession and previous trauma)?

In this case, the fact that the patient is myopic, aged 20-40, and has recently exercised, (11) prior to measuring a raised IOP, would point to a diagnosis of PDS. This is where posterior-bowing of the mid-peripheral iris rubs against the zonules releasing pigment granules which then lodge in the trabecular meshwork reducing outflow and elevating IOP. One theory of PDS is that there is a pressure differential between the anterior and posterior chambers generating 'reverse' pupillary block by bowing the iris backwards. Consequently, a possible treatment to reverse the posterior bowing is a YAG laser iridotomy, in much the same way as anterior bowing can be reversed in traditional pupillary block. However, a Cochrane review for laser in pigmentary glaucoma showed that there was no clear benefit in preventing loss of visual field and some low-quality evidence for lowering IOP. (12) This review suggested a need for better designed research studies to assess this concept further. Other non-gonioscopic examination features that would point to this diagnosis would be pigment on the corneal endothelium (Krukenberg spindle), mid-peripheral spoke-like iris transillumination, and pigment on the anterior lens surface.

Conclusion

This article has demonstrated the mechanisms leading to development of IOP and through each case has shown a rational and systematic approach to assessing a patient who has raised IOP; this can help practitioners consider potential causes and manage patients presenting with raised IOP.

Exam questions and references

Under the enhanced CET rules of the GOC, MCQs for this exam appear online at www.optometry.co.uk. Please complete online by midnight on 11 May 2018. You will be unable to submit exams after this date. Please note that when taking an exam, the MCQs may require practitioners to apply additional knowledge that has not been covered in the related CET article.

CET points will be uploaded to the GOC within 10 working days. You will then need to log into your CET portfolio by clicking on 'MyGOC' on the GOC website (www.optical.org) to confirm your points.

Visit www.optometry.co.uk, and click on the 'Related CET article' title to view the article and accompanying 'references' in full.

Course code: C-58976 Deadline: 11 May 2018

Learning objectives

Be able to explain the causes of raised intraocular pressure to patients (Group 1.2.4)

Be able to evaluate patients presenting with risk factors for glaucoma (Group 6.1.8)

Be able to assess patients presenting with raised intraocular pressure using appropriate techniques (Group 2.1.2)

Be able to explain the causes of raised intraocular pressure to patients (Group 1.2.4)

Understand the management of patients presenting with raised intraocular pressure (Group 8.1.3)

Dr Imran Jawaid is an ophthalmology registrar at Queen's Medical Centre, Nottingham. He was previously an optometrist. He has a keen interest in education for optometrists.

Richard Stead is a consultant ophthalmologist subspecialising in glaucoma at Queen's Medical Centre, Nottingham. He was previously an optometrist and has published a number of peer-reviewed papers.

Professor Anthony King is an internationally recognised consultant ophthalmologist subspecialising in glaucoma. He is an honorary professor of clinical ophthalmology and has published over 70 peer-reviewed papers.

Caption: Figure 1 Flow of aqueous from posterior chamber to anterior chamber. Image courtesy of Dr Samantha Strong

Caption: Figure 2 Demonstrating a narrow or occludable angle. Aqueous is produced but is unable to pass through the pupil due to apposition between the iris and lens. This increases pressure in the posterior chamber and makes the iris more convex, occluding the drainage angle. Image courtesy of Dr Samantha Strong

Caption: Figure 3 Demonstrating an open angle. There is free flow of aqueous from the posterior to the anterior chamber. There is easy access to the angle. However, resistance through the outflow structures may lead to raised IOP. Image courtesy of Dr Samantha Strong
Table 1 Classification of secondary causes of raised IOP
with open angles

Pre-trabecular
Neovascular glaucoma
Epithelial ingrowth
Irido-corneal-endothelial (ICE) syndrome

Trabecular
Pigmentary glaucoma
Red blood cells
Pseudoexfoliative material
Protein

Post-trabecular
Obstruction of superior vena cava
Carotid cavernous fistula
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Author:Jawaid, Imran; Stead, Richard; King, Anthony
Publication:Optometry Today
Date:Apr 1, 2018
Words:2400
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