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Setting target intraocular pressure

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Dr Jennifer Fan Gaskin
FRANZCO MD
Glaucoma clinician, Royal Victorian Eye and Ear Hospital and Centre for Eye Research Australia

 

The concept of target intraocular pressure (IOP) dates back as least as far as Paul Chandler’s lecture series in the 1950s.

The notion was reinforced by a post hoc analysis from the Advanced Glaucoma Intervention Study (AGIS) that led to the conclusion that if IOP was kept below 18 mmHg at all visits or at a mean of 12.3 mmHg, then glaucoma progression could be halted (Figure 1).1

 

33-OL Gaskin Figure-1

Figure 1. Associative analysis from the Advanced Glaucoma Intervention Study1

 

Soon afterwards, the American Academy of Ophthalmology and other ophthalmic organisations began encouraging clinicians to identify their therapeutic goals and advocated the term ‘target IOP’, defining it as a range of intraocular pressure adequate to stop progressive pressure-induced injury.2-4

There are various methods by which target IOP can be derived. Most glaucoma trials aim for a percentage reduction of 25-30 per cent as such a percentage drop is likely to be statistically significant and exceed the normal fluctuations of IOP.

A percentage reduction also individualises the target somewhat for each patient, rather than arbitrarily setting a target of 8 mmHg for every patient, which would also prevent progression but undoubtedly would lead to overtreatment of a large number of patients.

Alternatively, several complicated formulae have been derived to assist us in setting a target IOP, incorporating patient factors such as age, race, corneal thickness, refractive error, amount of visual field loss and nerve damage. However, none of these has been shown to be practically applicable or demonstrated any accuracy or effectiveness in clinical studies.

On the surface, target IOP seems like a good idea. We all know that glaucoma is a challenging disease; the condition is incurable and associated with progressive and irreversible damage. Additionally, glaucoma is notorious for ‘breeding complacency’.

In the busy, relentless practice of the modern-day ophthalmic practitioner, not only do we need to check the IOP, examine for optic disc changes and assess visual fields for deterioration, there is also an increasing number of devices emerging to assist us in monitoring for glaucoma progression. Optical coherence tomography (OCT) of the retinal nerve fibre layer (RNFL), Heidelberg Retina Tomography (HRT) of the optic disc, and analysis of the ganglion cell complex are some of the technologies in the armamentarium of the glaucoma clinician.

Invariably, at least one piece of information among the above will contradict the rest, and it is easy to deem the tests ‘unreliable’ or ‘inconclusive’ and continue the patient on the same regimen, with a plan to repeat the tests again in six months. The same scenario is just as likely to recur six months later.

Because lowering IOP is the only proven treatment for reducing glaucoma progression, it makes sense to set a target IOP early in the patient’s disease and alter the treatment when the measurement deviates from the target. Similarly, if the other parameters progress despite the fact that target IOP is met, then a lower target should be set and treatment adjusted accordingly.

There are IOP thresholds above which all clinicians would recommend treatment, even without current evidence of disc cupping, visual field loss or nerve fibre layer thinning. For example, when a patient presents with acute angle closure and an IOP of > 50 mmHg, responsible clinicians would recommend treatment because it is recognised that an IOP of 50 mmHg is incompatible with long-term retinal ganglion cell survival.

There are also patients who go blind from glaucomatous optic disc damage without ever having elevated IOP. It is easy to overlook the fact that blindness results from damage to the optic disc and its axons, not from elevated IOP. IOP is, at most, a risk factor and at other times simply a surrogate measure of the disease.

The limitation of monitoring a patient by a surrogate measure such as IOP is that it may or may not be consistent with the actual parameters of interest, such as the RNFL, optic nerve head or visual function. If the RNFL, optic nerve head and visual function worsen despite an IOP within target, it may be that the target IOP was not set at an appropriate level, or it may be that there are other factors causing optic disc damage.

The patient’s blood pressure can influence glaucoma progression, both in the form of uncontrolled systemic hypertension and nocturnal hypotension due to over-treated hypertension. Lack of compliance is also well-recognised among glaucoma patients and can account for disease progression despite seemingly adequate in-office IOPs. Additional, less well-understood factors also exist, such as blood flow, genetic factors and neuronal susceptibility, and these may not correlate with IOP but can account for worsening of disease.

There are inherent flaws in IOP itself. We rely on one diurnal IOP measurement every six months to reflect the true IOP across the entire period when we know in reality that IOPs fluctuate significantly throughout 24 hours and this fluctuation is further influenced by factors such as body position.5,6 IOP can increase by more than 3-4 mmHg when lying down compared to sitting. We still do not have an adequate means of measuring 24-hour IOP. Additionally, we do not understand which element of IOP (the peak IOP, mean IOP, fluctuation in IOP) has the biggest influence on glaucoma progression.

Benefit versus risk

Glaucoma care, as with all areas of medicine, involves the careful balance of the benefit versus the risks of treatment and unfortunately, the definition of target IOP does not take into account risks or side-effects of treatment.7

While seasoned clinicians may adjust the target IOP based on the potential risks associated with the treatment required to reach the target, this flexibility is not understood within the definition itself.

There is also some evidence that there may be overall diminishing returns in progressive IOP lowering, such that the benefit derived from lowering the IOP from 20 mmHg to 18 mmHg may be higher than reducing the IOP from 12 mmHg to 10 mmHg.8,9 Therefore with decreasing potential benefits, the balance tips towards potential risks when attempting to achieve lower IOPs (Figure 2).

 

33-OL Gaskin Figure-2

Figure 2. The therapeutic goal of glaucoma management: balancing risks and benefits7

As an extreme example, an elderly, low-risk patient with mild glaucoma, who is systemically unwell and unable to reach target IOP, generally should not undergo glaucoma filtration surgery as it is recognised that the side-effects and potential risks of the procedure outweigh the benefits in this situation. Strictly following target IOPs can lead to the trap of treating a number and not a patient, and inadvertently placing patients at risk by setting inappropriate IOP targets.

The subtleties of glaucoma management cannot be overemphasised. It is a challenging disease that is still one of the leading causes of blindness in the world. While the practice of setting target IOPs may simplify a clinician’s life, it does not necessarily improve patient care.

A target IOP may be a useful surrogate marker of treatment, but rather than adhering strictly to a single number, setting a target IOP range may be more practically useful. The clinician should also be mindful that IOP lowering is not an end in itself but a strategy to prevent the patient from glaucoma-induced disability, that all treatment should be a careful balance of benefit versus risks, and they need to look beyond the slitlamp and consider the whole patient.

 

1. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. The AGIS Investigators. Am J Ophthalmol 2000; 130: 4: 429-440.

2. Gaasterland DE, Allingham RR, Gross RL et al. Preferred Practice Patterns Committee Glaucoma Panel. Primary open-angle glaucoma preferred practice pattern. San Francisco, CA: American Academy of Ophthalmology, 2006.

3. European Glaucoma Society Terminology and Guidelines for Glaucoma, 3rd ed. Savona, Italy: DOGMA; 2008 (cited 2008 12 October)Available from: http://www.eugs.org/ebook.asp.

4. Damji KF, Behki R, Wang L. Canadian perspectives in glaucoma management: setting target intraocular pressure range. Can J Ophthalmol 2003; 38: 3: 189-197.

5. Sit AJ, Liu JH, Weinreb RN. Asymmetry of right versus left intraocular pressures over 24 hours in glaucoma patients. Ophthalmology 2006; 113: 3: 425-430.

6. Liu JH, Sit AJ, Weinreb RN. Variation of 24-hour intraocular pressure in healthy individuals: right eye versus left eye. Ophthalmology 2005; 112: 10: 1670-1675.

7. Singh K, Shrivastava A. Medical management of glaucoma: principles and practice. Indian J Ophthalmol 2011; 59: 7: 88.

8. Lichter PR, Musch DC, Gillespie BW et al. Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology 2001; 108: 11: 1943-1953.

9. Heijl A, Leske MC, Bengtsson B et al. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol 2002; 120: 10: 1268-1279.

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