Ocular Hypertension and the lost suspect

Erik Greve

Ocular Hypertension is a well defined condition, or is it? The criteria are based on statistical IOP data from population studies. IOPs lower than mean + 2 SD are considered normal. However we are not so much interested in the absolute level of IOP (unless it is high) as in the relative raised IOP. It is the raised IOP (relative to the original) that is considered a risk factor for the development of glaucomatous damage. The probability that an IOP of more than mean + 2 SD is a raised IOP is substantial (if corrected for CCT). The probability, however, that an IOP of less than mean + 2SD is raised is CONSIDERABLE.

A raised IOP can easily be present within the statistically normal range of IOP. An original IOP of 12 mmHg may rise by as much as 50% to 18 mmHg and still be considered normal. A comparable 50% rise from an original IOP of 18 mmHg would lead to an abnormal IOP of 27 mmHg. Unfortunately, we are unable to measure the relative rise of IOP. This means that we are unable to find a sizable number of ocular hypertensives (defined as persons with a raised IOP). This is in agreement with the fact that as much as 50% of the glaucomas found in population studies do not have an IOP of over mean + 2SD. It also means that a good percentage of so-called normal pressure glaucomas are 'simply' raised pressure glaucomas. Many NPGs have their IOPs in the upper teens.

As mentioned above, Ocular Hypertension is a risk factor for the development of glaucoma, because the IOP is most probably a raised IOP. Similarly, a raised IOP within the statistical normal range is a risk factor, however, one we cannot identify. Of course studies on tonographic outflow with or without provocation have tried to approach this problem but have not reached clinical popularity. As long as we do not have a good measure for raised IOP, we will miss a sizable proportion of glaucoma suspects: the lost suspects.

In these cases we will have to rely on the detection of the earliest damage or even better the earliest change of damage. This could be done by conventional functional and structural testing or by potentially earlier techniques that visualize retinal cells in vivo (if proven to be realistic). It still is not detection in the risk stage, but of early damage.
Little attention is given to the lost suspect, even though it concerns a very large group. Time to redirect our research?

Issue 8-1

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