or halt the disease. Certainly, if the IOP lowering has been very disappointing compared to the pressure before treatment, one need not wait until the disc and field deteriorate to reach the decision that a different approach is needed in an effort to lower the IOP even more. Notice again that the pressure readings do not need to be corrected for central corneal thickness (CCT) for this purpose [2]. The relative change in IOP may be more important than the actual CCT-corrected IOP (see Chap. 10 for full discussion of CCT and IOP). If the tonometer estimates an amount that is too high or too low, and the IOP is changed by a substantial amount with treatment, you will also have lowered the true IOP whether or not you corrected for CCT.

8.1.6  Treating the Risk of Developing

Glaucoma in the Future

A common and traditional question is, “at what level of IOP would one treat a patient who shows no evidence of damage to the optic nerve or loss of visual function?” The historical approach here is to lower the IOP simply because it is abnormal and it is a known risk factor. However, any pressure level cut-off is arbitrary and fails to take into account other contributions to the risk of glaucoma.

Indeed, as already noted, the risk of glaucomatous optic nerve damage rises progressively but gradually as IOP levels rise from within the normal range into the very elevated range. However, the variable susceptibility to harm indicates that other factors contribute to the risk of glaucoma. These factors can be divided into two groups.

1.Indicators of possible early damage that are of insufficient degree to be diagnostic. These factors include such things as cupping with a tendency toward thinning of the rim in the vertical sectors or variable and mild depressions of visual thresholds in characteristic locations that may correspond to areas of suspected nerve damage.

2.Indicators of risky circumstances without suggestion of early damage. This includes family history, ancestral heritage from certain gene pools, age, and possibly vascular status.

If the risk of glaucoma is high by virtue of either of these two types of factors, it makes sense to lower the IOP, just as it would make sense to lower the risk of glaucoma in an individual with very high IOP in the absence of any other risk factor. Calculating the risk of glaucoma is not yet perfected, and calculating the risk of developing mild glaucoma is not the same as calculating the risk of developing visual impairment before life ends.

Recent clinical trials confirm that even established glaucoma can be halted satisfactorily with adequate lowering of IOP, so delaying the treatment until vulnerability of the nerve becomes evident may be a practical approach. However economic analyses, which can take into account the dollar-value/face-value of such things as worry about going blind and relief from worry, even if not objectively justified, confirm that it does not make sense to treat all individuals with abnormal IOP [10, 11, 12]. Therefore, at present, the decision to lower IOP as prevention remains part of the art of medicine, which takes into account the personality, fears, socio-economic circumstances, and attitudes of patients toward preventative care as well as the prediction of medical outcome.

Summary for the Clinician

››IOP contributes to the development and progression of glaucoma.

››Non-IOP factors also contribute to the etiology of glaucoma and must be considered.

››IOP does not define glaucoma.

››For the diagnosis of glaucoma, the level of IOP is unimportant, although in equivocal cases an abnormal IOP makes the diagnosis of glaucoma more certain.

››There are individual differences in the magnitude of pressure-susceptibility.

››Based on the evidence that glaucomatous damage will either halt or slow when IOP is lowered, treatment is aimed at lowering the IOP.

››In monitoring a patient, the stability or change in the condition of the optic nerve and visual function is the prime criterion for whether therapy is adequate.

››Even if the future risk of glaucoma is based on non-IOP factors, the only modality we currently have available to reduce risk is to lower IOP.