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Primary Open-Angle Glaucoma

Kimberly V. Miller, MD; Joel S. Schuman, MD, FACS; Rachel L. Anderson, MD; and David L. Epstein, MD, MMM

GENERAL CONSIDERATIONS

Primary Versus Secondary

The overriding fundamental distinction is between open-angle and angle-closure glaucomas. These are both often called primary when there is no apparent ocular or systemic cause and secondary when there is an identifiable initiating ocular or systemic mechanism. Because there is likely more than one mechanism of primary open-angle glaucoma (POAG), the disease entity should likely be termed the POAGs. (Similarly, primary angle-closure glaucoma is usually due to pupillary block, but plateau iris, an uncommon condition, is also often called a form of primary angle-closure glaucoma.) In some ways, these terms are not that important except for clinical categorization, because they reflect that we understand some mechanisms but not others. For example, it is common for a patient with apparent POAG to later be discovered to have pseudoexfoliation, at which time the diagnosis is changed to that of a secondary open-angle glaucoma (because we believe we now understand the mechanism of that glaucoma; see Chapter 21).

Also, by analogy, secondary forms of angle-closure glaucoma can involve the same mechanism for iris occlusion of the trabecular meshwork (TM) as primary causes. For example, an increase in posterior segment volume (eg, acute central retinal vein occlusion) may move the crystalline lens forward and result in pupillary block by this means. Thus, there are common final mechanisms for all the glaucomas, whether primary or secondary.

POAG is so called because it occurs spontaneously, without evident antecedent or related disease and with no known basis other than genetic or hereditary predisposition. This is the most common variety of glaucoma in some parts of the world.

Other types of open-angle glaucoma differ from the so-called primary type by the fact that they characteristically occur in conjunction with specific abnormalities or diseases of the eye that can be considered causative of the associated glaucoma. Such types of secondary open-angle glaucoma include pseudoexfoliation with open-angle glaucoma, amyloidosis with open-angle glaucoma, pigmentary glaucoma, and, in special instances, glaucoma after trauma and glaucoma due to intraocular inflammation. These glaucomas are discussed in detail under separate headings in this chapter. However, much of what is to be said concerning the treatment of POAG can be applied equally well to other open-angle glaucomas, except those involving active intraocular inflammation.

POAG itself is a clinically well-defined disease, having moderate variation in its characteristics. A small proportion of cases is extraordinary and fall into subcategories.

PRIMARY OPEN-ANGLE GLAUCOMA IS REALLY A DISEASE OF EXCLUSION (OF SECONDARY CAUSES)

POAG is a diagnosis of exclusion. In all cases, no matter how deep the anterior chamber looks on slit-lamp examination, gonioscopy must be performed. One may be surprised by the observation of heretofore unsuspected angle recession; pigment dispersion or exfoliation; fine, new blood vessels in the angle; partial angle closure; or inflammatory precipitates. In diabetes, neovascularization can occur in the angle before the iris is involved. Any abnormal pigment in the angle warrants investigation to identify a cause (eg, pigmentary glaucoma, exfoliation, iris or ciliary body cysts, melanoma). Chronic silent angle-closure glaucoma may masquerade as POAG.

The diagnosis of POAG is usually made by routine tonometry and inspection of the optic nerve heads. The importance of the latter cannot be overemphasized. The IOP at a given examination may be in a normal phase, but abnormality of the disc should arouse immediate suspicion. If the disc is normal and routine tonometry reveals an IOP at the upper limit of normal, further testing may be warranted, such as visual field testing, scanning laser polarimetry, confocal scanning laser topography, or optical coherence tomography (OCT; see Chapter 9). Once the ophthalmologist is suspicious of potential glaucoma, he or she is bound to keep the patient under close observation. If the patient does in fact have early glaucoma, it will ultimately become apparent in subsequent examinations.

An IOP of 22 mm Hg or more with the Goldmann applanation tonometer (Haag-Streit) should trigger suspicion of glaucoma. Screening of all close relatives of a patient with glaucoma will reveal a higher incidence of glaucoma than in the general population.

Many cases of apparent POAG can be diagnosed by inspection of the optic disc. If the optic disc shows changes consistent with glaucoma, even if IOP is normal, further investigation will usually lead to a definite diagnosis. One learns in time to recognize the earliest glaucomatous appearance of the optic disc (see Chapter 8), so that even if the IOP is well within normal limits, one may be sufficiently suspicious to go on to additional subsequent examinations to detect the presence of POAG (or other forms of open-angle glaucoma, eg, normal-tension glaucoma).

Asymmetry of the physiologic cup between the 2 eyes is a significant finding in early detection of open-angle glaucoma. Even when both cups appear physiologic and do not reach the disc margin throughout, if the cup in one eye is definitively different from the cup in the other eye, the ophthalmologist should suspect POAG. This assertion holds even if the IOP is equal in the 2 eyes and well within the normal limits. If the cup is definitely larger in one eye than in the other, the patient should be followed as a glaucoma suspect. In a large number of patients, asymmetry of the physiologic cups is characteristic of early open-angle glaucoma.

As a personal illustration, when the son of Dr. Grant was in medical school and was practicing on his father with the ophthalmoscope, he remarked that the optic disc in one eye looked different from that in the other. Dr. Grant confirmed the fact that the physiologic cup was a little wider in the left eye than in the right. IOP was 18 mm Hg in both eyes. Facility of outflow was normal and equal in the 2 eyes on several occasions, but 5 years later, obstruction to outflow became measurable in the eye with the larger cup, and the IOP elevated to a glaucomatous level.

In addition to optic disc asymmetry, other early changes in the cup of the optic disc that portend a diagnosis of glaucoma include:

• A cup that reaches the disc margin at any point, but most commonly inferiorly
  
• A slight bending of all vessels at the margin
  
• An appearance (difficult to describe) of little or no bending of vessels at the margin that gives the impression that the whole disc has a shallow saucer-like depression to the margins, which might be called saucerization of the disc (see Figures 8-8 and 8-12)

Many times we have suspected glaucoma from a slight bending of the vessels at the margin of the disc, or this appearance of saucerization, and the diagnosis has later been confirmed. In normal eyes, the neuroretinal rim generally obeys the ISNT rule: the inferior (I) rim of the optic nerve is the thickest, followed sequentially by the superior (S) rim, nasal (N) rim, and temporal (T) rim. Deviation from this pattern should arouse further suspicion of glaucomatous damage. One must practice looking at optic discs very critically, and eventually, one will become expert at picking out those that should arouse suspicion of early glaucoma. While the instrumentation described in Chapter 9 helps the clinician with the diagnosis, such optic nerve sleuthing is not obsolete, and the clinician is still obliged to identify even the subtlest disc abnormalities.

The characteristic progressive changes of the discs in glaucoma are described in greater detail, with diagrams, in Chapter 8.

An exception to be remembered is that, in high myopia, it may be extremely difficult to diagnose early glaucoma by the appearance of the optic disc, whereas it is easier to diagnose it in the average eye. In trying to determine whether glaucoma is present in a case of considerable myopia, special care is necessary.

Another special condition of the optic nerve head that is suggestive of glaucoma is occlusion of the central retinal vein in one eye. In such a case, both eyes should be studied carefully for open-angle glaucoma (especially pseudoexfoliation) because a high percentage of patients having occlusion of the central vein in one eye turn out to have open-angle glaucoma in both eyes, either frankly present then or diagnosed later. After occlusion of the central retinal vein, the fellow eye is usually the better eye for vision, so it should receive special attention and early treatment for elevated IOP.

An increase in IOP of 8 to 10 mm Hg after rapid ingestion of a quart of water strongly suggests glaucoma, but a negative test does not rule it out. Tonography plus a water-drinking test may reveal an abnormality in cases in which either test alone is inconclusive. Although theoretically useful, we have, in truth, only rarely performed a water-drinking test in recent years and do not recommend it for routine use. On the other hand, some investigators recently have found this test to be of use.1 In the absence of a rigorous and widely available method of 24-hour IOP measurement, the water-drinking test may provide a useful “stress test” to evaluate the ability of the outflow system to cope with transient increases in IOP, and some studies have noted that the peak IOPs induced by this test correlate with peaks throughout the day.² Further work in this arena, and particularly prospective studies, would be useful in delineating the circumstances under which this test provides a meaningful clinical benefit.

Time

Once glaucoma is suspected, either on the basis of IOP or a suggestive disc, the patient should be kept under observation indefinitely. If glaucoma is developing, eventually, one will find definite elevation of IOP or definite glaucomatous changes in the disc. Stereo disc photographs as well as visual field testing and structural imaging are important baseline measurements.

The ophthalmologist sees the patient several times a year. If the patient does have glaucoma, sooner or later, unequivocally elevated IOP and/or optic disc changes will occur. Of course, during this time, close monitoring of the optic nerve appearance and visual fields is essential to be sure that no appreciable change is occurring. Such a leisurely approach is justified only in patients in whom the optic nerve heads have no more than physiologic cupping. If there is pathologic cupping, atrophy, or field loss with initial equivocal IOP measurements, one must examine the problem more intensively and not wait unduly to initiate antiglaucoma therapy. The IOP might be in a normal phase of diurnal fluctuation, or the patient might have a form of normal-tension glaucoma (see Chapter 20).

DIFFERENTIAL DIAGNOSIS

If IOP is definitely elevated or the disc shows definite changes characteristic of glaucoma, one must determine whether the glaucoma is POAG, angle-closure glaucoma, or some form of secondary glaucoma.

Gonioscopic exam can rule out angle closure; if the angle is open throughout at the time of IOP elevation, the diagnosis is not angle-closure glaucoma, even if the angle is narrow. If the IOP is normal because the patient is already under treatment when gonioscopy is carried out, the finding of a narrow but open angle is inconclusive. Treatment must then be discontinued to allow the IOP to increase, and gonioscopy should be repeated. If the angle is still open throughout, the diagnosis is open-angle glaucoma. On the other hand, if one finds closure of the angle consistent with the degree of elevation of IOP (see Chapters 23 and 25), the diagnosis is angle-closure glaucoma. Sometimes, it is difficult to be sure whether a portion of the angle is closed or almost closed, and repeated examination may be necessary, especially in cases in which the IOP without treatment is only moderately elevated. Ultrasound biomicroscopy or anterior segment OCT can be helpful to discern whether or not the angle is closed in these cases. If IOP without treatment rises to greater than 35 mm Hg, it is usually not difficult to determine whether there is sufficient closure to account for the elevated IOP. If IOP without treatment increases only to 28 or 30 mm Hg, little of the angle needs to be closed to account for such a moderate elevation of the IOP. It is particularly in these cases that the differential diagnosis between open-angle glaucoma with a narrow angle and angle-closure glaucoma is most difficult.

Beta-blockers, alpha-2 agonists, and carbonic anhydrase inhibitors, due to their suppression of aqueous formation, cause some widening of the angle. One may be deceived as to the true width of the angle. In cases in which the angle appears narrow but open while the patient is using these drugs, it may appear narrower or partially closed after the drugs are discontinued.

One must always rule out secondary glaucoma before deciding on a diagnosis of POAG. The possibility that the glaucoma may be secondary to some other abnormality of the eye is one of the many good reasons why one should never omit gonioscopy in any case of glaucoma, no matter if it seems obvious from the appearance at slit-lamp examination that the angle must be wide and open. Unexpected gonioscopic findings that may be present in the setting of a normal slit-lamp examination and that suggest a secondary cause of glaucoma include anterior synechiae, abnormal vessels, abnormal pigmentation, exudates (KP) on the uveal or corneoscleral meshwork, tumors in the angle, and disruption of the angle from trauma. These abnormal findings in the angle are discussed more fully in chapters on the individual secondary glaucomas.

Finding glaucoma in only one eye while the other eye is completely normal is strongly discordant with a diagnosis of POAG and indicates that one is probably dealing with some other type of glaucoma. However, it is not unusual to have POAG advanced to a more severe stage in one eye than in the other eye, and one must have good tonographic measurements or IOP curves to be sure whether an eye in question is normal. Differential diagnosis of glaucoma restricted to one eye is discussed in Chapter 41.

NORMAL VERSUS ABNORMAL INTRAOCULAR PRESSURE

By general convention, IOPs above 22 mm Hg are considered to be either abnormal or suspicious of being abnormal. Population studies generated this statistic; the mean IOP of normal individuals was measured, and IOPs greater than 2 or 3 standard deviations from this normal mean were defined as abnormal. However, there are several flaws in the logic of this approach to defining normal IOP.

In population studies, patients with frank glaucomatous optic nerve changes and field loss may have a normal IOP, especially if only one measurement is made.^3–6 As mentioned in Chapter 1, our clinical methods of detecting early optic nerve damage or unequivocal visual field loss from glaucoma are not adequately sensitive. Even with the most sophisticated imaging techniques, it can be difficult to discriminate very early glaucoma damage from normal morphology. Therefore, categorizing people as “normal” presents a challenge. Finally, the same logic, if applied to systemic hypertension, would result in patients at risk not receiving what is regarded as necessary therapy; with age, systemic hypertension increases in prevalence to seemingly affect as many as one-third of the older population (with notable risk of future end-organ damage).^7–10 Yet, if one surveyed an older population and calculated the mean blood pressure and only considered abnormality as being a certain number of standard deviations from the mean, one would mislabel many patients who have systemic hypertension as being normal. Statistical methods of identifying normality are useful only for establishing general guidelines rather than distinct criteria, especially when it is usual or normal for a disease to have a higher prevalence in a certain population.

In many ways, the glaucomas share characteristics with other diseases of aging. Although it may be normal to age, as physicians, we want to intervene to stabilize and prevent further development of aging processes. (Death itself can be considered normal for a certain age group!)

We also know that progressive low-tension glaucoma (normal-tension glaucoma) is a real entity that in the vast majority of patients has some IOP-sensitive component (see Chapter 20). In low-tension glaucoma, there is something substantially wrong with the optic nerve that we do not fully understand. Ultimately, we need to develop intervention remedies that correct or treat this susceptibility of the optic nerve to glaucomatous damage. However, there is a large body of clinical evidence obtained over long periods that substantiates the clinical impression that decreasing IOP, especially to a very low level, does alter the natural history of this disease in a favorable way. Perhaps controlled clinical trials may ultimately disprove this opinion, but at the present time the available clinical information strongly suggests the need to decrease IOP in low-tension glaucoma.¹¹ The clinical implications of this are that IOP below 22 mm Hg, even if repeatable, may not be normal and, therefore, still can encompass glaucomatous disease.

The original Chandler–Grant tenet,¹² the notion that an optic nerve damaged by glaucoma commonly requires a lower-than-normal IOP, has now achieved generally wide acceptance. Therefore, for patients with known glaucoma, an IOP simply in the normal range is not necessarily adequate to prevent further progression of the disease.¹³

What then is the clinician to do with the IOP data? What is an abnormal IOP? The diseases of glaucoma behave clinically as if individual eyes (or pairs of eyes) have an individual susceptibility to a given level of IOP that can only be determined for that patient by long-term follow-up. A significant goal in the clinical practice of glaucoma is to better understand the reasons for this individual susceptibility. We have some guidelines, but the key to the detection of glaucoma is not simply the measurement of IOP but also the simultaneous evaluation of the optic nerve and visual field (the methods for which have their own uncertainties in sensitivity and accuracy).

Glaucoma screenings should therefore involve not only IOP measurements but also ophthalmoscopic evaluation of the optic nerve appearance, and preferably structural imaging and functional testing as well. In any suspect patient, we should obtain stereo disc photographs because, in the progression of glaucoma, the appearance of the cup of the optic nerve will change. Structural imaging will provide an objective, quantitative measure that can be compared to the healthy population and followed for change. In the long-term care of patients with glaucoma or suspicion of glaucoma, it is remarkable how often we wish we had baseline photographs and quantitative imaging data from previous years to assist our clinical judgment. It is excellent ophthalmologic care to obtain stereo disc photo graphs and structural imaging on any patient with a suspicion of glaucoma or a future risk of developing glaucoma.

ELEVATED INTRAOCULAR PRESSURE ABOVE 22 MM HG

We have so far dealt with the clinical fact that a statistically normal IOP does not by itself indicate the absence of glaucoma. How about the opposite question: Does the presence of an IOP above 22 mm Hg indicate an abnormal condition, that is, the presence of glaucoma?

For this question also, there is surprising uncertainty and varying opinions that have changed over time. Clinically, a great number of patients exist whose optic nerves (and visual fields) seem to tolerate IOPs in the mid-to upper 20s without apparent damage. However, the key word is “seem.” Our clinical methods to detect early axonal death in the optic nerve are not very sensitive, though they are improving. Structural imaging provides a more sensitive and quantitative, objective measure than simple optic disc examination alone. Glaucoma for the ophthalmologist is truly the “curse” of long-term follow-up, and such observations have led many to realize that elevated IOP is not as benign as once thought. Studies14–16 have indicated that there is a protective effect of lowering IOP in patients who initially had no apparent glaucomatous damage. Probably (although not with certainty until our methods can truly detect early damage), there are individuals with IOP elevated into the 20s who will never suffer clinically detectable optic nerve damage, but it is impossible to identify all such individuals.

One can view this in terms of relative risk. There are risk factors¹⁷ that increase the chances for optic nerve damage, such as the degree of IOP elevation, having large or asymmetrical cups, thin retinal nerve fiber layer, abnormal tonographic outflow,¹⁴ the presence of myopia,¹⁸ a strong family history, Black race,¹⁹ the presence of disc hemorrhages, or below-average central corneal thickness.²⁰

However, we know that by treating even patients not considered clinically to be at excessive risk, the risk of developing end-organ damage is reduced.^14–16 In the Boston study,¹⁴ it was clinically sobering to realize that such a protective effect was not apparent at 2 years of follow-up, but only after longer time periods. In the Ocular Hypertension Treatment Study (OHTS),²¹ it was clear that the protective effect of treatment increased over time. In those whose treatment was withheld and then started years later, while they developed a parallel risk of developing glaucoma compared to those treated at the outset, they always had a higher risk of manifesting the disease.²¹ Early treatment is key, even in glaucoma suspects.

There are strong analogies to a similar clinical question in the treatment of asymptomatic mild systemic hypertension, where controlled studies have indicated the protective effect of early treatment,²² and therefore the clinical implication has been to treat all patients with mild elevation of blood pressure, even those without additional risk factors. Yet, a critical examination of the data on which this is based indicates that internists have chosen to treat perhaps a majority of such patients who seemingly will not develop end-organ damage to protect a minority who will, because they cannot prospectively identify those individuals who will develop clinical disease.

We face the same question and dilemma in treating (or not) asymptomatic elevation of IOP. (Glaucoma and systemic hypertension are not totally unrelated diseases from an epidemiologic point of view; see Chapter 4.²³) Although one could argue to wait to treat elevated IOP until clinical damage is evident, we also know (from long-term clinical observations) that once a disc is damaged, it commonly requires a progressively lower IOP to prevent further damage. IOP elevation results in damage not only to axons, but to the supporting structures of the optic nerve itself, the cells of the lamina cribrosa, and the extracellular matrix.^24,25 One could hypothesize that a disc damaged by elevated pressure is more susceptible to further damage due to the changes in the substance of the optic nerve head. The implication of this is that earlier preventative treatment could make the subsequent glaucoma less difficult to treat. (Although this latter statement has never been proven, it is the logical deduction from the clinical observation that a disc, once damaged, requires a lower-than-usual IOP for stability.)

We return again to this problem in glaucoma of individual susceptibility of the optic nerve of a given patient, in which general rules or statistical considerations are probably not as meaningful as the detailed clinical observation of the individual patient, using all the clinical means that we have available to document what is present, so that we can accurately detect future change. This individual susceptibility and variability is what makes it impossible to precisely define a normal or abnormal IOP (except for very high IOP levels. However, it is curious how this was defined 25 years ago as IOP in the 40s, where now it is regarded as IOP in the 30s).

A further complicating factor was mentioned in Chapter 1: although the measurement of IOP is usually (but not always) an accurate data point, it is just a snapshot in time. Due to diurnal and seasonal fluctuation in IOP, we are not yet able to determine the true representative (eg, mean, median, time integrated) IOP of any given patient.

WHEN TO TREAT (WHEN THERE IS NO OBVIOUS END-ORGAN DAMAGE)

A few decades ago, the prevailing clinical opinion was that IOPs below a certain cut-off, usually in the 30- to 33-mm Hg range, did not require antiglaucoma therapy unless there was evidence of optic nerve damage or visual field loss (for which the IOP would be vigorously treated!). There was a belief among some that elevated IOP (to even higher levels than the low 30s) could be a benign separate condition that was sometimes labeled ocular hypertension. Regardless, most glaucoma clinicians likely did have an IOP cut-off in the 30-mm Hg range. Today, there is probably general consensus that a separate benign condition of ocular hypertension does not exist (or at least cannot be prospectively distinguished from early POAG), and the threshold for treating asymptomatic elevated IOP has been lowered for most clinicians to somewhere in the 20s. Historically, when IOP was elevated from some secondary cause, the threshold of IOP for treatment was in many cases lower than for POAG. We practiced as if elevated IOP in POAG was somehow less damaging than in secondary causes. There is no reason to believe this is true.

The early prospective randomized clinical studies of Epstein et al14 and Kass et al¹⁵ had different protocols but reached the same conclusion (based on surprisingly similar unexpectedly high rates of clinical failure): lowering the IOP (with a beta-blocker) is protective against end-organ damage. More recently, in the landmark OHTS,¹⁶ topical medical therapy with the aim of reducing IOP by 20% was found to significantly decrease the risk of developing glaucomatous visual field or optic nerve damage.

All clinical studies should be judged by this criterion: does it change the way one practices? A related question involves treating one’s patients as one would want his or her own eyes to be treated. OHTS and earlier studies^14,15 indeed changed clinical practice for many physicians; OHTS generated a number of key clinical insights:

• In patients with “elevated” IOP (24 to 32 mm Hg) and no obvious end-organ damage (optic nerve or abnormalities in the visual field), lowering the IOP by a mean of 22.5% is protective against developing end-organ damage as measured by a reproducible visual field defect or reproducible optic disc deterioration attributable to POAG.
  
• The overall risk of developing progression to glaucoma decreased from 9.5% in the observation group to 4.4% in the treatment group.
  
• The highest risk of conversion to glaucoma occurred in patients with higher IOP measurements and thinner central corneal thickness measurements.
  
• Patients with larger vertical cup-to-disc ratios were more likely to convert to glaucoma than those with smaller cup-to-disc ratios.

The Boston study,¹⁴ OHTS,¹⁶ the earlier study by Kass et al,¹⁵ and further clinical observation have convinced us that moderate elevation of IOP is not as benign a condition as formerly thought. Although exact cut-offs await further studies, we do generally treat patients (except perhaps older adults) with IOPs of 25 mm Hg or higher with significant risk factors for development of glaucoma but without identifiable disc or visual field damage. If there are large (even deemed physiological) cups, slight asymmetry of the cups or IOP, thin corneas, severely impaired outflow facility, if the patient is myopic or has a strong family history of POAG, or if he or she is a Black patient, treatment for IOPs of 23 mm Hg or higher may be initiated. Obviously, this is modified by individual factors for individual patients, such as their age (because these studies show that damage occurs over years, elevated IOP is therefore a greater risk to younger patients) and side effects from medications (in the absence of obvious end-organ damage, prophylactic therapy should not disable the patient; if medications cannot be tolerated, the balance of benefits to risks can redirect the approach to treatment to consider laser trabeculoplasty or a strategy of close observation). An additional factor to be considered in myopic eyes with POAG is the possibility for the initial field loss to extend close to or actually involve central fixation.

What if the patient without apparent end-organ damage is on therapy, but the IOP exceeds these guidelines? For the patient on maximally tolerated medical therapy already, a decision for surgical intervention usually should require (in the absence of evidence of end-organ damage) very high IOPs (eg, upper 30s or greater). What is known and what is not known should be discussed with the patient, who should have input with his or her philosophical wishes (eg, therapeutic activism vs nihilism).

GENERAL PRINCIPLES IN TREATMENT

The goal of treatment in POAG is to prevent loss of visual function. If we prevent loss of function, our treatment is adequate. All of our treatment is designed to lower the IOP, either by increasing the facility of outflow, by suppressing formation of aqueous humor, or both. It is humbling to realize that we have no specific treatment for the outflow abnormality of POAG because the cause is still largely unknown.

There is no absolute level of IOP necessary and sufficient to ensure successful treatment in all cases. In some eyes with normal optic nerves, if treatment maintains IOP at a level in the mid- or low 20s, no loss of function occurs and the treatment may be considered successful. On the other hand, in cases of advanced glaucoma, IOP must usually be maintained at much lower levels to prevent continued loss of function.¹³ In far advanced glaucoma, IOP in the low teens or lower is required (see next section). The intensity of treatment required may therefore be considerably influenced by the stage of the disease, as evidenced by the condition of the optic nerve and the visual field.

A patient with extensive cupping and considerable field loss, having an initial IOP of 20 mm Hg, should be treated just as vigorously as a patient with a normal disc and IOP in the 40s. Occasionally, one sees a patient of this sort whose IOP is 20 to 22 mm Hg and in whom the IOP can be reduced to less than 15 mm Hg by intensive treatment. Thus, the mere fact that an occasional patient with advanced cupping and field loss does not have a very high IOP does not mean that one should treat him or her with only single-agent antiglaucoma therapy.

A high initial IOP, such as the 40s to the 50s, in patients with little or no field change indicates that the patient has an extremely poor facility of outflow. In such cases, we expect large fluctuations in IOP, often a considerable elevation during a particular portion of the day or night. A slight change in the rate of formation of aqueous humor in such an eye is reflected in a large change in IOP.

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