Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010

screening, then there is a high rate of false-positive and false-negative results for COAG. Skilled optic nerve examination is good but not always practical. Standard automated perimetry (SAP) can detect glaucomatous defects, but by the time a defect is detected, a substantial loss of axons has often occurred (29, 30). A number of studies have demonstrated that defects on short-wavelength automated perimetry (SWAP) and frequency doubling technology (FDT) perimetry can precede development of SAPdetected defects in patients with elevated IOP. Table 10.4 provides a comparative summary of these types of perimeters (31). Imaging devices may also be useful in the early detection of glaucoma. (These are covered in greater detail in Chapter 4 and below.)

Table 10.3 High-Risk Glaucoma Suspects

High-risk glaucoma suspects include patients who have one or more of the following:

IOP consistently >30 mm Hga

Thin central corneal thickness (dependent on ethnicity)3

Vertical cup-to-disc ratio >0.7a

Older agea

Abnormal visual field, e.g., increased pattern standard deviation on Humphrey Visual Field testa

Presence of exfoliation or pigment dispersion syndrome

Disc hemorrhagea

Family history of glaucoma or known genetic predisposition

Fellow eye of patient with severe unilateral glaucoma (excluding secondary unilateral glaucoma)

Additional ocular (e.g., suspicious disc appearance, myopia, low optic nerve perfusion pressure, steroid responder) or systemic risk factors that might increase the likelihood of developing glaucomatous nerve damage (e.g., African ancestry, sleep apnea, diabetes mellitus, hypertension, cardiovascular disease, hypothyroidism, myopia, migraine headache, vasospasm)

a These factors were identified as significant risk factors for development of chronic open-angle glaucoma in the Ocular Hypertension Treatment Study and the European Glaucoma Prevention Study. P.170

Table 10.4 Comparison of Advantages and Limitations of Manual Perimetry, SAP, SWAP, and

FDT Perimetry

Favorable patient acceptance

a Some limitations to all techniques include a lack of consensus on what constitutes a defect or progression; relatively crude reliability indices; poor acceptance by patients; and relatively long duration for threshold tests, even with fast techniques.

FDT, frequency doubling technology; SAP, standard automated perimetry; SITA, Swedish interactive thresholding algorithm; SWAP, short-wavelength automated perimetry.

Modified from Canadian Ophthalmological Society evidence-based clinical practice guidelines for the management of glaucoma in the adult eye. Can J Ophthalmol. 2009;44(suppl 1):S7-S93.

According to the American Academy of Ophthalmology, the best method to detect early glaucoma is a comprehensive eye evaluation, which includes assessment of the IOP, optic nerve, and visual field (see Chapter 9). Guidelines for frequency of screening for glaucoma are listed in Table 10.5 (4).

Intraocular Pressure and Pachymetry

To detect any change in IOP, optic nerve, or visual field status (i.e., early progression with structural or functional damage evident), it is essential to obtain good baseline documentation. In the case of IOP, it is worthwhile to measure central corneal thickness (CCT) with a pachymeter (Fig. 10.1). Patients classified as glaucoma suspects have been reported to have a higher CCT than individuals with COAG or healthy individuals (32, 33 and 34), with 42% of glaucoma suspects having a CCT of greater than 585 µm (34). This is significant because the Goldmann a pplanation tonometer was calibrated for a CCT of approximately 530 |µm (35, 36). Any significant dev iation from this induces an artifact of measurement. It has been estimated that 30% to 57% of elevated IOPs in glaucoma suspects are actually artifacts of measurement (33, 37, 38).

There is no universally accepted formula, however, that can be applied to ‘correct’ the IOP measurement

for any given CCT. Based on a review of various correction-factor approaches, the range probably falls between 2.5 and 3.5 mm Hg per 50 |µ of difference f rom normal (39). Hence, if a patient's CCT measured 650 |µ (in the absence of any visible corn eal pathology), then the ‘true’ IOP would likely be several millimeters of mercury less than measured. To avoid confusion, however, when sharing patient information with other practitioners, it is recommended that IOP should always be communicated as the measured IOP rather than a ‘corrected’ IOP.

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Table 10.5 Recommended Guidelines for Follow-up of a Glaucoma Suspect, American Academy of

IOP, intraocular pressure; N/A, not applicable; ONH, optic nerve head; VF, visual field. Modified from American Academy of Ophthalmology. Primary Open-Angle Glaucoma Suspect,

Preferred Practice Pattern.

San Francisco, CA: American Academy of Ophthalmology, 2005. Available at: http://www.aao.org/ppp. Slitlamp Biomicroscopy and Gonioscopy

Baseline documentation requires precise slitlamp examination and gonioscopy to exclude secondary causes of glaucoma. This includes angle closure and other secondary causes, such as angle recession, pigment dispersion, and inflammatory forms of glaucoma. After dilation, the anterior lens capsule should be examined for the presence of exfoliation.

Fundus Examination

In the posterior segment, it is important to document the appearance of the optic nerve head with careful drawings or stereo optic nerve head photos. Optic nerve head imaging devices (e.g., confocal laser scanning tomography) may also be useful. It is also worth studying the disc rim carefully for small hemorrhages, because these can precede visual field loss and future optic nerve damage. Similarly, the appearance of the nerve fiber layer (NFL) can be noted using red-free (green) light. It is important to document the presence or absence of NFL defects. Additional tools to document the NFL include laser polarimetry with the nerve fiber analyzer, scanning laser ophthalmoscopy, and optical coherence tomography (OCT) (see Chapter 4).

Figure 10.1Proper technique for measuring CCT, with probe placed perpendicular to central cornea. A structurally thick cornea can artifactually raise measured applanation IOP

Visual Fields

An attempt should be made to obtain two or three baseline visual fields. Our preferred options include

one or more of the following: (a) 24-2 Swedish interactive threshold algorithm (SITA) standard on Humphrey field analyzer II perimeter, (b) 24-2 full threshold white-on-white Humphrey perimetry or equivalent program on a different automated perimeter, (c) FDT (matrix preferred) or SWAP.

If an abnormality is found, it needs to be confirmed on repeated visual field examination. This was dramatically illustrated in OHTS (40). Over a 5-year period, 21,603 visual fields were obtained from 1637 OHTS participants. When follow-up visual field results were outside the normal limits on the Glaucoma Hemifield Test, the Corrected Pattern Standard Deviation, or both, follow-up visual fields were obtained to confirm the abnormality. Results of 748 visual fields were abnormal; of these, 703 (94%) were abnormal and reliable, and 45 (6%) were abnormal and unreliable. On retesting, abnormalities were not confirmed for 604 (85.9%) of the originally abnormal and reliable visual fields. Hence, most visual field abnormalities in OHTS participants were not verified on repeated testing and were probably due to the learning curve or long-term variability in the visual field.

Imaging of the Optic Nerve and Nerve Fiber Layer

Photographic assessment of the optic nerve head remains a mainstay in the diagnosis and management of glaucoma suspects. However, there are imaging tools capable of

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documenting the topographic features of the optic nerve head and measuring the thickness of the retinal NFL that can be useful adjuncts in the management of glaucoma suspects. These tools are reviewed in Chapter 4 and include the confocal scanning laser ophthalmoscope (manufactured as Heidelberg retinal tomography [HRT]), OCT, and scanning laser polarimetry (e.g., the GDx nerve fiber analyzer with variable corneal compensator [GDx-VCC]). Each of the technologies has good reproducibility and provides objective and quantitative analysis of ocular structure. An evidence-based medicine review of these technologies by the American Academy of Ophthalmology (41) came to the following conclusion: The [optic nerve head] and [retinal] NFL imaging devices provide quantitative information for the clinician. Based on studies that have compared the various available technologies directly, there is no single imaging device that outperforms the others in distinguishing patients with glaucoma from controls The information obtained from imaging devices is useful in clinical practice when analyzed in conjunction with other relevant parameters that define glaucoma diagnosis and progression.

Ocular Blood Flow

Whether blood flow to the optic nerve is reduced in glaucoma suspects and may be an early finding in the course of COAG remains to be proven. However, in one study using laser Doppler flowmetry, optic nerve head blood velocity, volume, and flow in four quadrants of the nerve were compared in patients with COAG, glaucoma suspects, and healthy participants (42). In the eyes of glaucoma suspects, flow was significantly lower in the superotemporal rim (16% lower), the cup (35% lower), and the inferotemporal neuroretinal rim (22% lower), compared with that in the controls. No significant difference between glaucoma suspect and control eyes was seen in the inferonasal rim or superonasal rim, and no significant difference was detected at any location between glaucoma suspect eyes and eyes with COAG. Further data are needed to clarify whether a reduction in blood flow to the optic nerve head plays a significant role in early damage to some optic nerves.

RISK FACTORS

The risk for glaucoma increases with the number and strength of risk factors. Studies that have evaluated risk factors in this context include longitudinal population studies and randomized, controlled trials comparing treatment with no treatment in persons with ocular hypertension (43).

Longitudinal population studies, such as the Barbados Incidence Study of Eye Diseases (BISED), the Melbourne Visual Impairment Project (Melbourne VIP) and the Rotterdam Eye Study (RES), provide information on risk factors that are involved in progression from normal to COAG. The most relevant risk factors consistently found in all three studies are older age at baseline and an approximately 1-mm Hg increase in IOP at baseline. BISED and RES reported a 4% and 6% risk, respectively, of developing glaucoma for persons 1 year older versus baseline (baseline mean, 56.9 years in BISED and 65.7 years in RES). In all three studies, there was a 10% to 14% increased risk among persons with a baseline IOP

1 mm Hg or more higher than the average for the population of developing COAG over the following 5 to 9 years. Other risk factors in these studies include a family history of COAG, a thinner CCT, and lower ocular perfusion pressures (systemic blood pressure minus IOP) in BISED; the use of systemic calcium-channel blockers for the treatment of systemic hypertension in the RES; and exfoliation, large cup-to-disc ratios of the optic discs, or use of systemic a- agonist blockers in VIP.

High-quality studies examining the risk for progression from normal to glaucoma in those with ocular hypertension include the OHTS and the European Glaucoma Prevention Study (EGPS) (22, 44). In OHTS, 1636 patients, aged 40 to 80 years, with no evidence of glaucomatous damage and with IOP between 24 and 32 mm Hg in one eye and between 21 and 32 mm Hg in the other eye were randomly assigned to either observation or treatment with topical medication. The goal in the medication group was to reduce the IOP by 20% or more and to reach an IOP of 24 mm Hg or less. In EGPS, 1081 patients aged 30 years or older with an IOP between 22 and 29 mm Hg were enrolled. Patients were randomly assigned to treatment with dorzolamide or placebo. Open-angle glaucoma in both studies was defined as the development of reproducible visual field abnormality or reproducible finding of optic nerve deterioration. Factors consistently identified in both studies as predictive of COAG development included elevated IOP, large cup-to-disc ratio, older age, thinner CCT, and higher pattern standard deviation values on the Humphrey automated perimeter. The EGPS also found vertical cup-to-disc asymmetry to be an important predictive factor (45). Other longitudinal studies have also shown suspicious disc appearance, myopia, and family history of glaucoma to be risk factors for the development of glaucomatous optic neuropathy and visual field loss (46, 47 and 48). In OHTS and EGPS, predictive factors that occurred after baseline were a higher mean IOP during followup, a smaller IOP reduction from baseline, and optic disc hemorrhages (43). In addition, in EGPS the use of systemic diuretics to treat systemic hypertension during follow-up increased the risk for COAG. Interestingly, long-term fluctuation in IOP and diurnal fluctuation in IOP have not been associated with the development of COAG (44, 46).

Risk Calculators

The risk for COAG in patients who are considered glaucoma suspects on the basis of elevated IOP can be estimated with risk calculators (49). The most recent risk calculators are available online and incorporate data from OHTS; EGPS; and another longitudinal study, the Diagnostic Innovations in Glaucoma Study (DIGS). This pooled analysis, which provides the 5-year risk for COAG in one eye in a patient aged 40 years with ocular hypertension, has narrowed the 95% confidence limits for prediction and strengthened the generalizability of the results.

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Given the studies that risk calculators are based on, calculations may not apply to patients who are younger than 40 years, nonwhite or of African descent, and do not have an IOP of 22 mm Hg or higher. Risk calculators also do not provide critical information that may guide therapy, such as life expectancy and psychological and social factors. The calculators may provide supplementary information for the physician and the patient, but caution needs to be exercised, as the clinical decision to treat is complex and involves taking the best available evidence and tailoring it to the individual patient.

WHEN TO TREAT

Whether to begin treatment in a glaucoma suspect is a complex decision that involves consideration of many factors, including visual, physical, medical, psychological, and social circumstances (50). Every attempt should be made to engage the patient in the decision-making process, because potentially exposing the patient to long-term therapy when there is no definite evidence of glaucomatous optic nerve damage is a major decision.

If the IOP is elevated, we suggest first stratifying the patient into low, moderate, or high risk for progression (Table 10.3 and Table 10.6). The OHTS and EGPS results should be kept in mind for identifying high-risk groups. In the OHTS, for those with a mean baseline IOP greater than 25.75 mm Hg, the risk for glaucomatous optic nerve damage at 5 years was 36% if the patient had a thin or average (555 |µ m) cornea, and 13% with a CCT of 565 to 588 |µ m. For a cup-to-disc ratio of more than 0.3, the

risk for those with a thin or average cornea was 24%, and for those with a thickness of 565 to 588 µ m was 16%.

Patients at high risk for progression warrant treatment to prevent optic nerve damage, whereas those at low risk can be observed at periodic intervals (51). If there is a moderate risk for progression, then a decision can be made to treat or observe at more frequent intervals than patients at low risk. If the IOP is not elevated and the disc or visual field is suspicious, there is no compelling evidence to guide clinicians regarding whether to treat or to simply observe.

Table 10.6Making the Decision to Treat in Glaucoma Suspects with Elevated IOP

Stratify patients into low, moderate, or high risk for progression (based on best available evidence and clinical judgement):

High risk: Suggest treatment be initiated

Moderate risk: Can initiate treatment if appropriate, or monitor closely

Low risk: Monitor IOP as well as optic nerve structure and function, and treat if evidence of progression

Carefully consider these factors when deciding whether to treat:

Greater age and life expectancy

Psychological factors

Convictions (patient and physician)

Social environment

Availability for follow-up

Pregnancy

The results of the OHTS indicate that reducing IOP by at least 20% (and to <24 mm Hg) in patients with elevated IOP and no evidence of glaucomatous damage can reduce the risk for COAG by more than half over a 5-year period (from 9.5% in the observation group to 4.4% in the medication group). However, although topical hypotensive medication was effective in delaying or preventing the onset of COAG in this group of patients, the results do not imply that all patients with borderline or elevated IOP should receive medication. In fact, most cases of elevated IOP did not progress to glaucoma over the 5- year follow-up. Furthermore, results of the EGPS suggest that patients treated with dorzolamide progressed at the same rate as patients receiving a placebo. However, this result is controversial and may relate to selective dropout of treated and untreated patients with higher IOPs and to the failure to achieve sufficient lowering of IOP (52).

If there is evidence of damage to or deterioration of the optic nerve or visual field in one or both eyes, then the patient's diagnosis changes to early COAG, and treatment should commence according to the principles outlined in Chapters 27 and 35. Kass (53) also suggests a lower threshold for treatment in patients with only one functional eye, where it is not possible to obtain reliable visual fields, or in patients in whom the optic disc cannot be visualized.

In its 2005 Preferred Practice Pattern, the American Academy of Ophthalmology recommends that, when deciding whether therapy is warranted, a risk-benefit analysis should be done, and the likelihood of development of glaucomatous optic nerve damage should be carefully weighed against the risks of treatment (4). The decision should be individualized, taking into account the rate at which glaucomatous optic nerve damage and visual impairment are likely to occur, the patient's life expectancy, and the patient's tolerance for effective treatment.

APPROACH TO TREATMENT

If a decision is made to treat, the choice of treatment should be governed by selecting a topical medication that will likely achieve the target IOP range (see discussion in Chapter 27)

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with the least risk to ocular or systemic health and quality of life for the patient. Cost and convenience may also enter into this decision. Patients should be educated about the disease process and the rationale and goals of therapy, so that they can participate meaningfully in the development of an optimal treatment plan.

Whether laser trabeculoplasty has a role in early treatment of glaucoma suspects remains controversial. In our opinion, laser trabeculoplasty may be indicated, and it can be a useful adjunct in decreasing IOP by 20% to 25% if the target IOP range cannot be achieved with use of one or two medications.

Surgery is rarely, if ever, indicated as first-line therapy in a glaucoma suspect. However, trabeculectomy or other surgical approaches may be indicated if the patient has an extremely high, uncontrolled IOP (corrected for pachymetry) that the physician believes is certain to cause glaucomatous damage (i.e., 40 to 50 mm Hg). Additional factors such as poor adherence to medical therapy, inability to tolerate medical therapy (e.g., benzalkonium chloride sensitivity), quality of life, and longevity of the patient may need to be considered when deciding which IOP-lowering approach is best for the patient. GUIDELINES FOR FOLLOW-UP

Follow-up of the glaucoma suspect is necessary to determine whether there is a change in the IOP, optic nerve head, or visual field status over time.

The frequency of follow-up visits depends on several factors: whether the patient is receiving medical therapy, whether the target IOP range has been achieved, and the number of risk factors for COAG the patient has. We believe that follow-up of glaucoma suspects should occur at least every 6 to 12 months, and more frequently in high-risk patients, especially those on treatment in whom the target IOP has not been achieved. There are no hard and fast rules on this subject, although the American Academy of Ophthalmology has developed some guidelines that represent the consensus of an expert panel and are listed in Table 10.5(4).

At each visit, the IOP should be assessed, and the clinician should document whether the appearance of the optic nerve head has changed since baseline. Visual fields should be obtained once every 6 to 18 months and compared with the baseline measurement. Gonioscopy should be repeated if there is a suspicion of angle closure or other angle abnormality. Gonioscopy should also be considered if the patient is given a miotic agent, because this type of treatment can induce pupillary block and formation of peripheral anterior synechiae.

KEY POINTS

The term ‘glaucoma suspect’ is typically used when the patient has an IOP greater than 21 mm Hg with normal discs and visual fields, or an appearance of the optic nerve head, NFL, or visual field that is suggestive of but not definitive for glaucoma. It can also be used when the optic nerve or visual field is suspicious for optic nerve damage.

The physician should document good baseline data, including IOP, pachymetry, optic nerve head, NFL, and visual fields, so as to have a benchmark to assess whether progression has occurred on follow-up visits. The CCT should be measured routinely to assess the level of risk of these patients.

Baseline factors that consistently predict the development of COAG in major prospective studies include older age, larger vertical or horizontal cup-to-disc ratio, higher IOP, greater pattern standard deviation, and thinner CCT. These criteria can be used to stage the glaucoma suspect into low, moderate, or high risk for progression.

The decision to initiate therapy in a glaucoma suspect should be based on the patient's risk for developing visual loss; his or her systemic, psychological, and social health; and his or her preference.

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