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Reflections on Central Corneal Thickness

Douglas Anderson

Central corneal thickness (CCT) was identified in the Ocular Hypertension Treatment Study (OHTS) as a risk factor for the development of glaucomatous damage in patients with intraocular pressure (IOP) outside the normal range.¹ It has since been debated whether thin corneas predict the risk only because the IOP is underestimated by tonometry when the cornea is thin or additionally because a thin cornea represents a general weakness of ocular support structures that makes the eye more vulnerable to harmful effects of IOP.

In an effort to discover whether CCT affects the course of established glaucoma in the same way it affects ocular hypertension, several investigators have reviewed clinical records of patients with glaucoma, sometimes uncovering an apparent relationship between CCT and the rate of glaucomatous progression or severity.^2-4 It would seem that in principle if the treating physician strives to lower the IOP by a certain percentage, there is only a slight difference between lowering the IOP by 25% or lowering the tonometer reading by 25%, even when CCT is abnormal. The potential bias in the reported results is that despite nominally striving for a percentage drop of IOP, the clinician may accept a lower percentage lowering when the IOP under treatment has entered the normal range than when the tonometer suggests the IOP is still borderline or slightly abnormal. In other words, assertiveness of treatment may have been influenced by false readings produced by abnormal CCT.

What should we make of the reported evidence?

First, we should notice that the thickness of the cornea is only one risk factor. Corneal thickness does not over-ride or eliminate other features of the case that may lead you to an estimate of risk, but simply increases or decreases your estimate based on other factors. In fact, there may be features that are so compelling in assigning a risk that you find corneal thickness to be irrelevant. A strong family history of blindness from glaucoma, or an already observed rapid progression may signal danger that is little diminished by noting that the cornea is abnormally thick. Long standing ocular hypertension without glaucomatous damage may signal low risk, even if the cornea is thin.

We should also consider why the cornea is thicker or thinner than average in a particular individual. If we believe that the OHTS findings result from false tonometric readings, it should be noted that thick corneas likely have a normal composition, but are simply thicker than average, and therefore stiffer, resisting indentation or flattening by the tonometer. By this mechanism a high tonometric reading arises when the IOP is not high. However, a cornea that is thickened by edema due to endothelial disease is soft and will give a falsely low tonometer reading. On the other hand, if we believe from the OHTS data that support structures of the optic nerve are weak in eyes with naturally thin corneas, it would not be expected that the structure of the optic nerve would be affected by acquired alteration of the corneal thickness. For example, if the cornea is thin by virtue of LASIK, the optic nerve is not made weaker, nor is it stronger if the cornea is thickened by edema or by scarring. Such acquired corneal changes may affect the tonometric readings, but not the sturdiness of the optic nerve.

How do we use the reported data and the concepts?

The purest setting for use of the CCT information duplicates the clinical circumstance of subjects who participated in OHTS, that is, a patient who has just been discovered to have high tonometer readings, without apparent disc damage or visual field loss. The CCT may moderate your assessment of risk in conjunction with age, level of tonometer reading, family history, and other factors you feel affect the patient's risk.

The use of CCT information may be different in cases of newly discovered glaucoma, in contrast to newly discovered ocular hypertension. The fact is that whether the cornea is thick or thin, the eye has become glaucomatous by virtue of the cumulative effect of whatever risk factors exits, including the CCT. The evidence that corneal thickness affects the rate of further glaucomatous damage is not as firm for cases of glaucoma as it is for ocular hypertension. Until we know more, the severity of existing damage, family history, and age likely remain the main guides to choosing a percentage of pressure of IOP lowering you would like to achieve. It would seem that the severity of damage largely incorporates the net cumulative risk that results from all contributory predictors, such as age, family history, sturdiness of ocular structures, and level of IOP, and includes whatever predictive contribution the CCT makes. At the time of initial diagnosis, we do not know the duration of the glaucoma, however, or the rate at which damage has been occurring. It is possible, but not known with certainty, that CCT is an accurate indication of the rate of damage or a reliable guide to setting the target IOP.

It may also be noted that risk assessment at the time that either ocular hypertension or glaucoma is first discovered is not the same as assessing the risk of a patient who has been monitored for several years. As time goes on, the clinical course to date gradually takes an increasingly dominant role in risk assessment and decision making. Therefore, if the eye shows progressive cupping or field loss at an unacceptable rate, the decision to lower the pressure is unaffected by CCT. Similarly, long term stability may be taken as evidence of adequate treatment, no matter how thick or thin the cornea may be.

There are times when CCT may be helpful in cases that have been monitored for several years. For example, if there is progressive damage in a case of normal tension glaucoma despite a tonometer reading of 10 or 11 mmHg, it may encourage more aggressive lowering of IOP if it is found that the cornea is so thin that the true IOP may be 14 mmHg, for example. The finding of a very thin cornea in such a case may convince the clinician that there is potential help from further efforts to lower the IOP, rather than have him conclude that the nerve damage in this case is pressure-independent, so further treatment is futile.

In summary

CCT has been identified as a contributing predictive factor for glaucoma development in cases of recently discovered ocular hypertension. The basis for its ability to predict (inaccurate tonometry or weakness of ocular structures) is not known. In some analyses, CCT also seems to affect the likelihood or rate of further progression in cases of glaucoma.

References

1. Gordon MO, Beiser JA, Brandt JD, Heuer DK, Higginbotham EJ, Johnson CA, Keltner JL, Miller JP, Parrish RK 2nd, Wilson MR, Kass MA. 2002. Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 120: 714-720
2. Medeiros FA, Sample PA, Zangwill LM, Bowd C, Aiharaa M, Weinreb R. 2003. Corneal thickness as a risk factor for visual field loss in patients with pre-perimetric glaucomatous optic neuropathy. Amer J Ophthalmol 136: 805-813
3. Kim JW, Chen PP. 2004. Central corneal pachymetry and visual field progression in patients with open-angle glaucoma. Ophthalmology 111: 2126-2132
4. Herndon LW, Weizer JS, Stinnett SS. 2004. Central corneal thickness as a risk factor for advanced glaucomatous damage. Arch Ophthalmol 122: 17-21