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Chapter 220 – Primary Open-Angle Glaucoma

Chapter 220 – Primary Open-Angle Glaucoma

 

RAYMOND ZIMMERMAN

DARIN SAKIYALAK

THEODORE KRUPIN

LISA F. ROSENBERG

 

 

 

 

 

DEFINITION

• A chronic, bilateral, often asymmetrical disease in adults, featuring acquired loss of optic nerve fibers and abnormality in the visual field with an open anterior chamber angle.

 

KEY FEATURES

• Progressive death of retinal ganglion cells.

• Thinning of the neuroretinal rim.

• Visual field loss.

 

ASSOCIATED FEATURES

• Elevated intraocular pressure, over 21?mmHg (2.8?kPa).

 

 

 

INTRODUCTION

A characteristic pattern of optic nerve and visual field damage defines glaucoma. The collection of conditions called glaucoma is categorized into open- or closed-angle forms, and is divided further into primary and secondary forms. Although separation into open- and closed-angle and congenital types is fundamental for appropriate clinical management, division into primary and secondary levels is arbitrary. All kinds of glaucoma are actually an end stage or secondary to some abnormal inciting event(s). As such, glaucoma is a final common pathway of many disorders that affect the eye.

Primary open-angle glaucoma (POAG) is a chronic, bilateral, and often asymmetrical disease in adults in whom acquired loss of optic nerve fibers and abnormality in the visual field occurs with an open anterior chamber angle of normal appearance, and an intraocular pressure (IOP) often over 21?mmHg (2.8?kPa). A definitive pathophysiological description of the processes that cause death of retinal ganglion cells by apoptosis (a form of cell suicide)[1] still needs to be established. An alternative classification of glaucoma takes into account the stages of the disease process and is more amenable to diagnostic and therapeutic advances in cellular and molecular biology, genetics, and optic nerve regeneration.[2] In this scheme, an unknown precipitating event (stage 1) results in obstruction of aqueous outflow (stage 2) and abnormal IOP (stage 3), which causes death to retinal ganglion cells and cupping of the optic nerve (stage 4) and, finally, loss of vision (stage 5). Idiopathic open-angle glaucoma is a better term than POAG, which ultimately has one or several causes. In the same vein, the term secondary is replaced according to the systemic or ocular condition associated with the glaucoma.

EPIDEMIOLOGY AND PATHOGENESIS

Review of Risk Factors for Primary Open-Angle Glaucoma

A risk factor represents an inherited characteristic, environmental exposure, or aspect of personal behavior that influences the probability that an individual develops a given condition. It is important to differentiate causal risk factors from associated, or noncausal, risk factors. Some of the risk factors that predict glaucoma are both causal and changeable (e.g., IOP) and, therefore, lend themselves to intervention. On the other hand, epidemiological data may demonstrate a strong association between a factor and disease and, thus, serve as an inference related to risk. Although statistically this is calculated as a risk factor, it clearly is not causal. Other risk factors for POAG (e.g., race, age, family history) are not subject to change but may still influence risk and are, therefore, useful in the identification of individuals for whom close ophthalmic supervision is indicated. The distinction between causal and noncausal factors is important to understand the disease process (diagnosis and pathogenesis) and to plan management.

Five-year findings of the Ocular Hypertensive Treatment Study (OHTS)[3] [4] shed important evidence-based data on risk factors for POAG. This prospective, randomized, multicenter clinical trial evaluated the safety and efficacy of topical IOP-lowering medications in preventing or delaying the onset of visual field loss or optic nerve damage in patients with ocular hypertension at moderate risk of developing POAG.

Intraocular Pressure

After Leydhecker et al.[5] characterized IOP in 20,000 presumably normal eyes using Schiøtz tonometry, IOP became the defining parameter of glaucoma; they measured a mean (±SD) IOP of 15.5 ± 2.6?mmHg (2.1 ± 0.3?kPa). Using a gaussian distribution, Leydhecker et al. declared that eyes having IOP of 20.5?mmHg (2.7?kPa; two standard deviations above the mean) are highly suspect for glaucoma, and those having IOP 24?mmHg or more (=3.2?kPa; three standard deviations above the mean) must have the disease. Although subsequent population-based studies using more reliable tonometric techniques have confirmed these values, IOP does not follow a gaussian distribution—it is skewed toward higher pressure.[6] [7] Therefore, statistically, values beyond two standard deviations of the mean do not necessarily imply abnormality.

Clinically, the contribution of IOP to the development and management of glaucoma is best considered a continuum. The division between health and disease cannot be based solely on IOP, as exemplified by the debate as to whether the terms low-pressure or normal-tension glaucoma (glaucomatous nerve damage despite pressures <21?mmHg [<2.8?kPa]) and ocular hypertension (glaucoma suspect; pressure >21?mmHg [>2.8?kPa] without optic nerve or visual field damage) are separate entities or represent opposite poles of a disease spectrum in which IOP plays an important role and other factors contribute to the pathogenesis. The important feature of glaucomatous damage in this context lies in the individual susceptibility of the retinal ganglion cell or optic nerve head to IOP-related damage. Variation occurs in the degree of harm caused by a given IOP level, as well as variation in the level of IOP that is tolerated without harm. In any case, raised IOP is the most important risk factor, but it is not the disease per se.

 

The causal role of IOP in optic nerve damage is evidenced by experimental production of high pressure in primates that results in

 

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glaucomatous damage.[8] Among population-based studies, the prevalence of POAG increases with increasing IOP.[9] [10] [11] That IOP level and glaucoma development follows a dose–response pattern is indicated in cross-sectional studies; individuals who have pressures of 15–20?mmHg (2.0–2.7?kPa) have a low prevalence of nerve damage,[12] whereas the prevalence of damage is higher among individuals who have pressures of 25–30?mmHg (3.3–4.0?kPa).[13] [14]

Central Corneal Thickness

The applanation tonometer described by Goldmann and Schmidt[15] assumes a central corneal thickness (CCT) of 500?µm. Although they recognized that CCT would influence applanation readings, they believed that variations in CCT occurred rarely in the absence of corneal diseases. However, it has become apparent that CCT in clinically normal individuals is more variable than Goldmann and Schmidt recognized. Many patients with ocular hypertension have little more than thickened corneas, resulting in erroneous elevated IOP readings. In the OHTS, 24% of subjects had CCT greater than 600?µm.[16] In this study, subjects with a CCT of 555?µm or less had a threefold greater risk of developing POAG than participants with a CCT over 588?µm.[4] CCT may be a valuable test in assessing patients with elevated IOP.

Optic Nerve

An enlarged cup (=0.5 cup-to-disc ratio) on initial optic nerve examination is suspicious either for the presence of glaucoma or for a greater risk for the development of glaucoma.[4] [10] [17] [18] Acquired, progressive thinning of the neuroretinal rim (or progressive enlargement of the cup) is the essence of POAG ( Box 220-1 ). An enlarged cup may represent a normal physiological variant and, as such, contains the normal number of nerve fibers, so the patient may not be at increased risk for glaucoma. Jonas[19] has reported on the characteristic configuration of the neural rim in normal eyes The width of the rim is greatest in the inferior quadrant, followed by the superior, nasal, and temporal quadrants. This relationship may be remembered using the mnemonic ISN’T (inferior, superior, nasal, and temporal quadrants), and this anatomy is largely independent of disc size, cup size, cup-to-disc ratio, or neural rim area. Alternatively, an enlarged cup may be inherently more susceptible to glaucomatous damage by virtue of its anatomy (e.g., features of the lamina cribrosa). Also, an enlarged cup may be damaged already, and if tests of sufficient sensitivity could reveal a functional abnormality, glaucoma could be diagnosable. It is impossible to differentiate which is the case in a given individual at a given time, so patients who have “suspicious” discs must be observed closely (photographs of the optic nerve or computerized analysis of the optic nerve or retinal nerve fiber layer) for the development of clinically detectable glaucoma damage.

Importance of stereoscopic optic disc photographs was confirmed in the OHTS study.[3] Photographic glaucomatous progression of the optic disc without the onset of visual field damage

 

 

Signs That Suggest Acquired Disc Damage

Progressive thinning of neuroretinal rim (most specific)

 

Vertical elongation of the cup

 

Notching

 

Splinter disc margin hemorrhage

 

Asymmetry between the two cups of =20% in discs of equal size

 

Deep cup (excavation)

 

Baring of circumlinear vessels

 

Saucerization of cup

 

Laminar dots

 

Nasalization of vessels

 

Loss of normal striations in nerve fiber layer

 

 

 

 

was the first POAG end point in 18 of 36 (50.0%) subjects in the medication group (n = 817) and in 51 of 89 (57.3%) subjects in the observation (no therapy) group (n = 819).

Age

The prevalence (number of cases in a given population at a given time) of POAG increases substantially with age.[4] [10] [17] [20] [21] [22] The proportion of patients affected by optic disc damage and vision loss rises from approximately 1% in people under 40 years of age to prevalence estimates 3–8 times higher in patients over 70 years of age. One possible explanation for this relationship may be that older people have had elevated IOP for a longer time compared with younger people. Alternatively, the optic nerve may become more susceptible to damage not only from an elevated IOP, but from microvascular perfusion defects, or changes in connective tissue integrity in older compared with younger individuals.

Race

The prevalence of POAG is 3–4 times higher in black than in white populations.[21] [23] [24] Optic nerve damage tends to occur at least a decade earlier in blacks, is more severe at the time of diagnosis, and is more refractory to medical and surgical management. [25] Higher IOPs, vascular abnormalities of the optic nerve, and optic nerve size are factors proposed to account for the increased risk of development of glaucoma in this group. However, race in the OHTS was statistically not significant as a baseline factor associated with developing POAG.[4] The black population in the OHTS had larger mean baseline vertical cup-to-disc ratio and thinner central corneal measurement compared with other study participants. Adjustment for these factors in the multivariate analysis eliminated race as a statistically significant predictor.

Major differences in POAG exist between Japanese and Western populations. Approximately 75% of Japanese with open-angle glaucoma have IOPs below 21?mmHg. [26] This is considerably higher than the 25–30% observed in United States population-based studies.[22] These findings also emphasize the limited utility of IOP as an indicator of glaucomatous disease.

Family History

Familial factors play a role in the underlying susceptibility to POAG.[17] [27] The association is stronger if a sibling has glaucoma (odds ratio, 3.69) than if a parent (odds ratio, 2.17) or child (odds ratio, 1.12) has POAG.[28] Family history was not a significant predictor in the OHTS; 42% of all participants reported a positive family history of glaucoma (8.5% of participants who developed glaucoma compared with 7.3% who did not).[4] The risk of a positive family history of POAG does not weigh as heavily as the factors described above.

Genetic factors that influence POAG are complex. Although at least six genes have been identified with POAG, only one genetic locus, (GLC1A) on chromosome 1q that is associated with juvenile-onset open-angle glaucoma, has been reported in patients with adult-onset POAG. A gene that produces the protein myocilin (TIGR) resides within this interval, and myocilin mutations occur in up to 4.6% of patients with adult-onset POAG. [29] Myocilin is expressed in multiple tissues throughout the eye and in many other organs. In the trabecular meshwork, the production of myocilin can be induced by application of topical corticosteroids.[30]

Myopia

Evidence that supports the association between myopia and POAG is derived from the observation of an increased prevalence of myopia among patients with glaucoma compared with the general population.[31] [32] It has been postulated, but not confirmed, that the occurrence of elevated IOP in myopic individuals may be an important contribution to the development of

 

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glaucoma in this group of patients. Shared alterations in collagen and other components of the extracellular matrix of the optic nerve also may be contributory factors in myopia and POAG. However, in the OHTS, myopia was not predictive of POAG.[4]

Vascular Disease

Abnormalities in vascular function, such as arterial hypertension, diabetes mellitus, and migraine, have been associated with POAG, although the relationships are not well characterized. It seems logical to assume systemic vascular disease has a potential impact on POAG, because compromised microcirculation of the optic disc is a possible mechanism for nerve damage. Migraine seems to be most closely associated with open-angle glaucoma and pressures in the normal range.[33] Nevertheless, the results of retrospective and population-based studies on the relationships of vascular disease and POAG are unclear.[4]

DIFFERENTIAL DIAGNOSIS

Conditions that may masquerade as POAG exhibit a similar optic nerve appearance or characteristic visual field abnormality. Patients who have POAG may demonstrate wide diurnal pressure variation and, unless frequent pressure measurements are obtained at various times during the day, higher pressure levels may not be detected. Such information has an impact on the target pressure level chosen for glaucoma therapy. Careful gonioscopic visualization of the anterior chamber angle differentiates patients who suffer subacute angle-closure glaucoma. The presence of peripheral anterior synechiae, anterior chamber-angle pigment, or blood in Schlemm’s canal may point to a diagnosis other than POAG ( Box 220-2 ).

 

 

 

Gonioscopic Features**

 

NORMAL ANTERIOR CHAMBER ANGLE BLOOD VESSELS

Do not cross scleral spur

 

Do not branch

 

Have stromal sheath

 

Travel radially or circumferentially

 

• Radial iris vessels

• Arterial circle of ciliary body

• Vertical vessels of the anterior ciliary body

 

SEVEN CAUSES OF PERIPHERAL ANTERIOR SYNECHIAE

Blunt trauma

 

Penetrating trauma

 

Primary angle-closure glaucoma

 

Inflammation

 

Rubeosis iridis

 

Posterior pressure on iris–lens diaphragm

 

Iridocornoendothelial syndrome or epithelial downgrowth

 

 

DIFFERENTIAL DIAGNOSIS OF ANTERIOR CHAMBER ANGLE PIGMENT

Ciliary body tumor

 

Pigment dispersion or glaucoma

 

Pseudoexfoliation

 

Malignant glaucoma

 

Trauma

 

Surgery

 

Inflammation

 

Hyphema

 

Angle-closure glaucoma

 

 

BLOOD IN SCHLEMM’S CANAL

Artifactual from compression on goniolens

 

Elevated episcleral venous pressure

 

Hypotony

 

Idiopathic uveal effusion syndrome

 

 

*These help differentiate primary open-angle glaucoma from other forms of glaucoma.

 

 

 

Patients who have glaucomatous appearing optic nerves or visual field defects but normal IOP may have had elevated IOP in the past, but for a finite period. Such scenarios occur in patients who had IOP elevation from long-term corticosteroid use, transient uveitis, or pigmentary glaucoma that subsided with increased pupillary block and decreased pigment liberation.

Certain retinal conditions cause visual field defects that may mimic typical glaucomatous defects. Careful retinal examination reveals retinal detachment, chorioretinitis, arterial or venous branch vascular occlusion, retinoschisis, or retinal photocoagulation scars, as some examples.

Congenital optic nerve conditions and ischemic or compressive optic neuropathies may mimic glaucomatous cupping. Methanol toxicity is a very unusual cause of cupping.[34] A careful history elicits sudden visual loss (ischemic optic neuropathy), headache, neurological signs, or hormonal abnormalities (compressive lesion); discriminating stereoscopic examination of the optic nerve differentiates these entities (e.g., pallor greater than cupping) from glaucomatous optic neuropathy. The diagnosis of POAG must be reevaluated at each visit to eliminate other possible causes for progressive visual field loss and change in the appearance of the optic nerve.

PATHOLOGY

Although the anterior chamber angle appears clinically normal in patients who have POAG, it is dysfunctional. The site of resistance

 

 

 

 

Figure 220-1 Retina. A, Histological section of the nasal retina shows that only an occasional ganglion cell remains, instead of the normally seen continuous single layer. The atrophic inner neural retinal layers are still identifiable, unlike the neural retina following central retinal artery occlusion, where the inner layers appear as a homogeneous scar. I, internal limiting membrane; A, atrophic nerve fiber and ganglion cell layers; RC, rods and cones; RPE, retinal pigment epithelium; C, choroid. B, Another case shows more marked glaucomatous atrophy of the inner layers (compare with the inner nuclear layer in A). (A–B, From Yanoff M, Fine BS. Ocular pathology, ed 5. St. Louis: Mosby; 2002.)

 

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to aqueous humor outflow is postulated to lie in the juxtacanalicular portion of the trabecular meshwork. Several alterations in the meshwork ultrastructure have been described but cannot be differentiated from nonspecific changes observed with normal aging.

Loss of retinal ganglion cells and thinning of the nerve fiber layer occurs, while the outer layers of the retina are preserved for the most part ( Fig. 220-1 ). The optic disc appears excavated because of the extensive loss of nerve fiber substance ( Fig. 220-2 ). The lamina cribrosa is displaced posteriorly.

TREATMENT

The challenge of glaucoma management lies in maintaining low IOP for the life of the patient. Because glaucoma is chronic and often asymptomatic, therapy often demands multiple and expensive medications which must be used frequently and often cause unwanted side effects (see Chapter 233 ) or surgical remedies which carry risk. Also to be considered in the decision on therapy is the patient’s age (life expectancy), physical condition, and social situation, because these impact the high level of compliance required for successful management. Management, therefore, varies among patients but has as its universal goal the greatest potential benefit for preservation of vision at the lowest risk, cost, and inconvenience to the patient.

The incidence of visual field damage is small, even if all risk factors are present, for a patient who at initial examination has no nerve damage and normal visual fields.[10] Most patients with ocular hypertension (glaucoma suspects) do not require IOP-lowering therapy, because the probability of developing POAG (optic nerve damage or visual field loss) has been estimated to be only 0.5–1.0% per year.[35] [36] These estimates are probably low, considering the OHTS report that 24% of patients with ocular hypertension have CCT greater than 600?µm.[16] This finding underestimates the true conversion to POAG, because many glaucoma suspects with thick CCT have “corrected” IOPs that are within normal range (i.e., misclassified as having ocular hypertension). Cumulative probability of developing POAG in the OHTS was 4.4% in the medication group and 9.5% in the observation group. These probabilities also are higher than prior reports based on the high percentage (approximately 50%) of conversion determined by stereoscopic disc photograph alterations without development of visual field damage. Multivariate analysis of the OHTS identified baseline factors that were predictive of developing POAG as older age, larger vertical or horizontal cup-to-disc ratio, higher IOP, and thinner CCT.

 

 

Figure 220-2 Glaucoma cupping. The optic nerve head is deeply cupped. Atrophy of the optic nerve is determined by comparing the diameter of the optic nerve at its internal surface and posteriorly, where it should double in size. Here it is the same because of a loss of axons and myelin, which also causes an increase in size of the subarachnoid space and a proliferation of glial cells, resulting in an increased cellularity of the optic nerve. (From Yanoff M, Fine BS. Ocular pathology, ed 5. St. Louis: Mosby; 2002.)

Therapy, with its attendant cost and potential for side effects, is not justified for all patients with ocular hypertension. In the OHTS, 90.5% of the observation group did not develop glaucomatous optic nerve or visual field changes during the 5 years of study. On the other hand, one report on a small number of eyes has described loss of retinal nerve fibers prior to clinically detectable optic nerve damage or visual field loss, thus advocating the initiation of tolerable glaucoma therapy in patients with ocular hypertension.[37] We are unable to identify with a high level of certainty which combination of risk factors in a given patient with ocular hypertension increases the likelihood that glaucoma damage will develop. Considerations in the decision to treat these patients include useful vision in only one eye, inability to obtain reliable visual field determinations, inadequate visualization of the fundus, other vision-threatening ocular disorders, an IOP consistently higher than 30?mmHg, or the patient’s request for treatment.

It is difficult to identify accurately early glaucoma changes. Short-wavelength automated perimetry (SWAP; blue-on-yellow perimetry) can detect visual field loss earlier than standard white-on-white perimetry.[38] Additional studies are needed to determine if frequency-doubling technology (FDT) perimetry and computerized analysis of the optic nerve or retinal nerve fiber layer will be additional parameters that prove useful in the early detection of optic nerve damage.[39] The ongoing multicenter OHTS will provide important information on the value of these tests.

The goal of treatment must be individualized for every patient—no specific IOP level avoids visual loss in all patients. Similarly, in the glaucoma suspect, no specific IOP level exists that demands treatment; the level also must be individualized according to other risk factors and the comfort of the ophthalmologist who monitors the patient. For example, a patient who has an IOP as high as 30?mmHg (4.0?kPa) may be monitored (e.g., visual fields and optic disc stereoscopic photographs or computerized analysis) carefully without glaucoma therapy in the absence of disc damage, visual field loss, or other important risk factors. So long as the physician and patient are comfortable with an established follow-up plan, the patient is spared not only the cost and inconvenience incurred from treatment, but also the psychological impact that may occur when a chronic and potentially blinding disorder is diagnosed.

To detect acquired disc damage is even more of a challenge in high myopia with tilted discs, anomalous optic nerve heads, and symmetrically enlarged (i.e., >0.5 cup-to-disc ratio) cups. Again, in these patients therapy is individualized; generally, it is advised if the patient is young, but an elderly patient may be monitored conservatively without medication.

Results published by the multicenter Early Manifest Glaucoma Trial [40] have confirmed the clinical impression that therapy is indicated when optic nerve or visual field damage has occurred. The goal in such cases is to prevent progressive optic nerve and functional vision loss for the remainder of the patient’s lifetime. Management is to lower IOP, the only risk factor amenable to management, to a safer level such that further optic nerve damage is unlikely. The target IOP varies among patients and may also vary within the same patient during the course of the disease. The chosen IOP, in time, may prove to be inadequate such that progressive damage occurs despite the degree of IOP reduction; alternatively, the desired IOP reduction may be achieved, but with the induction of intolerable ocular or systemic effects. Variable amounts of IOP reduction may be required to stabilize similar degrees of optic nerve damage. For example, a young myope who has cupping and visual field loss within or close to fixation and whose highest IOP is in the low 20–22?mmHg (2.7–2.9?kPa) range may need IOP reduced to 13–15?mmHg (1.7–2.0?kPa), or lower, to stabilize the condition.

The multicenter Advanced Glaucoma Intervention Study (AGIS) was established to determine whether laser trabeculoplasty or trabeculectomy was the best management in medically uncontrolled open-angle glaucoma.[25] [41] Recent AGIS reports

 

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have analyzed visual field progression according to the level of IOP maintenance. [42] Patients with an average IOP greater than 17.5?mmHg had significantly more field progression than patients with an average IOP less than 14?mmHg. Visual field worsening was greater after 7 years than after 2 years following initiation of the study. Finally, eyes with an IOP less than 18?mmHg on all study visits had no significant change in visual field defect score, while eyes with this level of pressure control on only 50% of the visits had significant worsening of their visual field. Ten-year study results are similar.

The AGIS study indicates that an IOP greater than 18?mmHg is not acceptable in eyes with glaucomatous optic nerve damage. This impacts the concept of target IOP, selection of an IOP range that will halt or slow progressive ocular damage. Selection has utilized a variety of clinical benchmarks, such as the severity of optic nerve damage, the IOP level at which damage occurred, the rapidity with which damage occurred, and the presence of other risk factors. In general, the more advanced the damage, the lower the desired target IOP. The IOP range chosen in each case is somewhat arbitrary and based on clinical experience. A spectrum or range of IOPs exists for a given patient and extends from the ideal pressure, to acceptable pressure, to borderline pressure, and at the furthest end unacceptable pressure. Finally, just as not all patients respond equally to a given anithypertensive therapy, not all disease halts at a given IOP level. The protective effect of lowered IOP is not absolute, and relentless deterioration may continue in some patients despite IOP reduction. It is believed that in these patients additional factors, other than IOP, must play an important role in the disease process.

COURSE AND OUTCOMES

In the long term, the decision as to whether the achieved IOP level is sufficient is based on whether progressive disc and field damage has halted. Findings from stereoscopic examination of the optic nerves with pupil dilatation are compared with baseline stereoscopic photographs every year. Computer analysis of the optic nerve head and retinal nerve fiber layer are additional anatomical measurements that are used to assess stability of the glaucomatous process. Kinetic or static visual field examinations are obtained 2–4 times per year, and IOP measurements are carried out 3–4 times a year. Factors that alter the length and constitution of follow-up interval include severity of disease (more frequent for more severe disease), range of achieved IOP lowering, stability of optic nerve and visual field damage, and duration of glaucoma control ( Table 220-1 ).

Change of the optic nerve or visual field must be verified and correlated with the ocular physical examination. For example, is the new visual field defect present on repeated tests with proper test parameters? Does the change represent progressive glaucomatous cupping? Could the change in disc appearance represent ischemic optic neuropathy? Could the change in field represent a retinovascular insult? If the clinical change indeed represents progressive glaucomatous damage, then more aggressive IOP reduction

 

TABLE 220-1 — RECOMMENDED GUIDELINES FOR FOLLOW-UP

Target Intraocular Pressure Achieved

Progression of Damage

Duration of Control (Months)

Follow-up Interval (Days)

Optic Nerve Evaluation (Months)

Visual Field Evaluation (Months)

Yes

No

<6

30–180

6–12

6–18

Yes

No

>6

90–365

6–18

6–24

Yes

Yes

Not applicable

7–90

3–12

2–6

No

No

Not applicable

7–90

3–12

2–6

No

Yes

Not applicable

1–30

3–12

2–6

Adapted from American Academy of Ophthalmology: Primary open-angle glaucoma preferred practice pattern. San Francisco: American Academy of Ophthalmology; 1996.

 

 

is needed. Another indication for escalation of glaucoma therapy is the return of IOP to a level that previously caused damage. Other indications for adjustment of therapy are noncompliance with the prescribed medication or occurrence of ocular or systemic side effects.

The patient who has advanced glaucoma on initial examination with deeply excavated optic nerves and visual field defects that involve fixation is of particular concern. In such a patient, it is more difficult to recognize further changes in disc or field. A suggested guideline is to set a goal of IOP 50% lower than at diagnosis or an IOP less than 15?mmHg (2.0?kPa), whichever is less. If the IOP is decreased to this level, the patient’s course is followed carefully. If this IOP goal cannot be achieved with medical or laser therapy, filtration surgery is recommended.

Progressive optic disc damage may be impossible to detect in eyes in which extensive disc damage has resulted in a nerve that has a completely excavated appearance. The best assessment of the nerve is obtained using stereophotography. Computerized optic disc analysis may provide different useful measures of the optic nerve (see Chapter 216 ). Visual fields, although limited, may be more important in the long-term assessment of such patients.

The subjective nature of the visual field examination limits its usefulness in uncooperative patients. Moreover, it is difficult to monitor for progressive deterioration when extensive visual field loss approaches or involves fixation or takes the form of a severely contracted island of vision (5–10°). It is helpful to enlarge the standard automated test object to size V, to make sure the patient’s pupil is at least 3?mm in diameter, and to utilize the central 10° field program in automated perimeters (see Chapter 214 ). Goldmann kinetic perimetry is frequently the best method to follow visual fields in these patients. Sometimes IOP and visual acuity are the only parameters to follow in patients who have extensive optic nerve and visual field abnormalities.

 

Clinical monitoring has several limitations. Diurnal IOP variations are much greater in patients who have POAG, compared with those in the normal population. Particularly in patients who demonstrate progressive damage at seemingly normal IOPs, attempts must be made to schedule IOP measurement at different times of the day, toward the end of a dosage interval, or just before instillation of the next medication dose to characterize a profile of pressure fluctuation as a possible factor in suboptimal glaucoma control.

Poor medication compliance is common in a large proportion of patients, a particularly significant phenomenon given the many medical options now available to manage glaucoma. Consideration of the lifestyle implication of multiple medications is critical. It is essential to prescribe (and that the patient use) only those drugs proved to lower eye pressure effectively in an individual patient. One-eyed therapeutic trials are helpful in this regard (see Chapter 233 ).

Management options (medical therapy, laser trabeculoplasty, filtration surgery with or without antifibrotic therapy) are made on individual basis and with regard to attendant risks (e.g., side effects, loss of vision) and benefits. Achievement of adequately

 

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lowered IOP to prevent further glaucomatous damage serves most patients well. The proof of glaucoma control can be obtained retrospectively only, by examination of the optic nerve and visual field.

 

REFERENCES

 

1. Kerrigan LA, Zack DJ, Quiglet HA, et al. TUNEL-positive ganglion cells in human primary open-angle glaucoma. Arch Ophthalmol. 1997;115:1031–5.

 

2. Shields MB, Ritch R, Krupin T. Classification of the glaucomas. In: Ritch R, Shields MB, Krupin T, eds. The glaucomas. St Louis: Mosby–Year Book; 1996:717–25.

 

3. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:701–13.

 

 

4. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertensive Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:714–20.

 

5. Leydhecker W, Akiyama K, Neumann HG. Der intraokulare Druck gesunder menschlicher Augen. Klin Monatsbl Augenheilkd 1958;133:662–70.

 

6. Armaly MF. On the distribution of applanation pressure. I. Statistical features and the effect of age, sex, and family history of glaucoma. Arch Ophthalmol. 1965; 73:11–8.

 

7. Hollows FC, Graham PA. Intraocular pressure, glaucoma, and glaucoma suspects in a defined population. Br J Ophthalmol. 1966;50:570–86.

 

8. Quigley HA, Addicks EM, Green RW. Chronic experimental glaucoma in primates. II. Effect of extended intraocular pressure elevation on optic nerve head and axonal transport. Invest Ophthalmol Vis Sci. 1980;19:137–52.

 

9. Pohjanpelto PEJ, Palva J. Ocular hypertension and glaucomatous optic nerve damage. Acta Ophthalmol (Copenh). 1974;52:194–200.

 

10. Armaly MF, Krueger MF, Maunder L, et al. Biostatistical analysis of the collaborative glaucoma study. I. Summary of the risk factors for glaucomatous visual-field defects. Arch Ophthalmol. 1980;98:2163–71.

 

11. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open-angle glaucoma among white and black Americans. The Baltimore Eye Survey. Arch Ophthalmol. 1991;109:1090–5.

 

12. Cartwright MJ, Anderson DR. Correlation of asymmetric damage with asymmetric intraocular pressure in normal-tension glaucoma (low-tension glaucoma). Arch Ophthalmol. 1988;106:898–900.

 

13. Anderson DR. The management of elevated intraocular pressure with normal optic discs and visual fields. I. Therapeutic approach based on high risk factors. Surv Ophthalmol. 1977;21:479–89.

 

14. Sommer AI. Intraocular pressure and glaucoma. Am J Ophthalmol. 1989;107:186–8.

 

15. Goldmann H, Schmidt T. über Applanationstonometrie. Ophthalmologica. 1957;134:221–42.

 

16. Brandt JD, Beiser JA, Kass MA, et al. Central corneal thickness in the Ocular Hypertensive Treatment Study (OHTS). Ophthalmology. 2001;108:1779–88.

 

17. Hart WM Jr, Yablonski M, Kass MA, et al. Multivariate analysis of the risk of glaucomatous visual field loss. Arch Ophthalmol. 1979;97:1455–8.

 

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2 comments on “Chapter 220 – Primary Open-Angle Glaucoma

  1. At which poing people start claiming that Catholics aren’t Christian….

  2. If you ever wish to listen with the reader’s suggestions, We price this with regard to 4/5. Good data, however We have to see which darn windows live messenger to see the skipped items. Thanks, anyways

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