Core Messages

››IOP contributes to the damage of the optic nerve in glaucoma, but an elevated IOP is not itself the defining feature of glaucoma.

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

››Current treatment of glaucoma is aimed at lowering IOP based on evidence from clinical trials.

››Non-IOP factors may explain cases of progressive glaucoma with low IOP.

››The prime criterion that determines whether or not therapy is adequate is the stability of the optic nerve and visual function, not IOP levels.

8.1  Why is Intraocular Pressure Important in Diagnosing and Treating Glaucoma?

8.1.1  High IOP Can Cause Glaucoma (and Other Harm to the Eye) Although High IOP Itself

is Not Glaucoma

In patients with a pathophysiologic condition of the optic nerve that makes it susceptible to glaucomatous damage it appears that the level of IOP affects the rate

D. R. Anderson

Bascom Palmer Eye Institute, University of Miami, Miller School of Medicine, Clinical Research Building (LOC C-209), 1120 NW 14 Street, Room 1560G, Miami, FL 33136-2107, USA e-mail: danderson@med.miami.edu

at which that damage occurs. Clinical trials published in the last three decades have confirmed that if IOP is lowered an eye with ocular hypertension is less likely to develop glaucoma, that established glaucoma with abnormal IOP is slowed or halted in its progression, and that eyes with normal tension glaucoma also suffer less progression of field loss [1, 5, 8]. The proportion of individuals with glaucomatous damage increases with increasing levels of IOP. Although the proportion of those with “normal” pressure who have glaucoma is small, individuals with normal pressure make up between one-third and one-half of all cases of glaucoma [3], perhaps simply because normal pressures are more common than “abnormal” pressure. Therefore, the level of IOP in itself is a poor means to detect glaucoma.

8.1.2  Glaucoma Can Be Diagnosed

Independently of IOP

The characteristics of glaucomatous damage involve changes to the optic nerve and visual function. This pathologic process can occur at any level of intraocular pressure. Glaucoma is recognized by the tendency of the loss of tissue that occurs at the superior and inferior poles of the disc [6, 7, 9] through clinical examination and with the help of the emerging optic nerve and retinal nerve fiber layer imaging technologies. If the anatomy appears pathological, visual field tests can help to confirm the diagnosis. It is not unusual, however, for a damaged optic nerve to be associated with an entirely normal visual field. Sometimes the ability to note a change in structure or function from previous examinations is more useful in determining the presence of glaucoma than being able to recognize an obviously glaucomatous appearance on a single examination than

recognizing an abnormal optic nerve, which can result from other causes [4, 12].

8.1.3  Non-IOP Factors May also Be Involved in the Pathogenesis of Glaucoma

Individual variation in the magnitude of pressure-­ susceptibility is evident from the fact that some individuals suffer little harm from an abnormally high IOP (ocular hypertension), while others have damage when IOP is higher than extraocular venous pressure but within the normal population range (normal pressure glaucoma). However, it appears that most or all eyes will develop glaucomatous excavation if the pressure is extremely high; they may also suffer other problems aside from cupping if the pressure is extremely high. While the pathophysiologic process of glaucomatous cupping is not understood, a working hypothesis is that it results from interplay between IOP and various physiological processes that vary from one person to another. For example, vasoconstriction may be an etiologic factor in glaucoma. The amount of vasoconstriction an individual­ experiences with exposure to cold varies greatly from one individual to the other. To the degree that such a variation in physiologic response participates in the pathophysiologic process of glaucoma, it is logical that if a person has glaucoma with a lower level of IOP, he may be more likely to be at one extreme of the spectrum of the relevant pathophysiologic processes than a person with “high-pressure” glaucoma. Stated differently, without the fundamental disease being different, the non-IOP contributing factors may be more conspicuous in patients with a normal IOP.

8.1.4  The Decision to Initiate Treatment by Lowering IOP

In patients with established glaucoma, treatment is to lower IOP. Usually, the goal of treatment is not just to lower IOP, but to lower it by some significant amount from the level at which damage has occurred (or presumably occurred), with a particular target pressure in mind. Although the baseline level of IOP may be a

consideration when deciding on a target pressure, the degree of damage to the optic nerve already manifest is a stronger guide. For example, some cases of glaucoma with a relatively high starting IOP may be stabilized –24 mmHg may be satisfactory if the pretreatment IOP was 45 mmHg. Other cases may require the IOP to be at the lower end of the normal range (12 mmHg instead of 19 mmHg). In the future, as imaging technology becomes more sophisticated in detecting progression, it may become feasible to withhold treatment for a while in order to gauge the rate of damage as a guide to the necessary aggressiveness of treatment.

8.1.5  Use of IOP in Monitoring a Patient

with Glaucoma

The IOP measurement is a surrogate or short-term predictor of what the future likely holds. One expects that if IOP is substantially lower than it was before treatment, the course of events will be better than if treatment had not been undertaken. Because IOP fluctuates from one time to another, as a guide to therapy, obtaining several baseline readings to get an average (for comparison to a future set of readings rather than a single reading) is more important than correcting the tonometric reading for corneal thickness.

However, office measurements of IOP are not truly representative of the IOP that an eye experiences – for example, considerable variation in IOP is not detected at the random times of office pressure measurements, or the patient may not take medications regularly but may on the day of an office visit. The initial goal set for IOP lowering may not have been set adequately low and with time, despite a seemingly satisfactory IOP, the glaucoma progresses. The IOP goal needs to be set lower. For these reasons, IOP measurements alone are not enough to monitor a patient with glaucoma. What the IOP measurements do provide is some short-term gauge about what to expect long-term, even though the future cannot be accurately predicted.

It is useful to keep track of IOP readings during the initial months of treatment, which may later be the basis for setting a new, lower future IOP goal, if unexpected progression occurs. Intraocular pressure measurements are immediately useful when a target IOP goal has been set with the expectation that meeting that goal will slow