Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

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

.pdf
Скачиваний:
2
Добавлен:
28.03.2026
Размер:
44.54 Mб
Скачать

7 - Classification of the Glaucomas

Page 40 of 425

 

Selected Studies

 

 

Study (Reference)

Type of Blindness Evaluated, and Timing

Risk for Blindness, %

 

and Description

 

 

 

Hattenhauer et al., 1998 (178)a

 

 

 

100 Patients followed up after receiving a diagnosis of Monocular, at 20 y after 54

 

COAG in 1965-1980

COAG diagnosis

 

 

 

Binocular, at 20 y after

22

 

 

COAG diagnosis

 

 

191 Patients followed up and treated for OHT after

Monocular, at 20 y after 14

 

diagnosis in 1965-1980

OHT diagnosis

 

 

 

Binocular, at 20 y after

4

 

 

OHT diagnosis

 

Chen, 2003(179)a,b

186 Patients followed up at a glaucoma specialty clinic Monocular, at 15 y after 15

 

 

since receiving a diagnosis of COAG after 1975

COAG diagnosis

 

 

 

Binocular, at 15 y after

6

 

 

COAG diagnosis

 

Kwon et al., 2001 (180)

 

 

 

40 Eyes followed up at a glaucoma subspecialty clinic In study eye, at 22 y

19

 

after trabeculectomy surgery done in or after 1972

after surgery

 

aStudy sample included persons with exfoliation.

bStudy sample included persons with pigment dispersion. COAG, chronic open-angle glaucoma; OHT, ocular hypertension.

Outcomes from the long-term follow-up of cases are also helpful to estimate prognosis but must be used with caution because of limitations with generalizing from these studies to current patient care. In a community clinical practice in Olmstead County, Minnesota, the 20-year risk for blindness in individuals with newly diagnosed open-angle glaucoma between 1965 and 1980 was 22% in both eyes and 54% in one eye (178). In patients receiving treatment for ocular hypertension, the 20year risk for blindness was 4% in both eyes and 14% in one eye. A more recent clinical series of patients from a subspecialty glaucoma clinic who received a diagnosis of COAG after 1975 showed a 15-year risk for blindness due to glaucoma of 6.4% in both eyes and 14.6% in one eye (179) (Table 9.5). One of the difficulties in using these findings is that a patient with newly diagnosed disease today would be expected to do much better because of improvements in glaucoma care over the past three or four decades. Perhaps, the greatest difficulty in applying these figures to the care of a particular patient is that these clinical studies lump together newly diagnosed COAG of all levels of severity at the time of diagnosis. Consequently, patients with early glaucoma should fare much better overall, whereas those with advanced glaucoma should have an even poorer prognosis (Table 9.5).

Risk Factors for Blindness from COAG Advanced Stage

Rough general estimates of prognosis in glaucoma can be refined somewhat by the presence or absence of risk factors for glaucoma blindness, including advanced stage, young age, inadequate IOP control, and ongoing progression. Not only are more advanced stages of glaucoma further along in the process leading to blindness, but some evidence also suggests that more advanced glaucoma is more likely to progress than earlier stages of the disease and may require greater IOP lowering to halt

P.158

progression (181, 182, 183 and 184). However, other longitudinal studies have not found a more rapid progression in those with worse initial visual field scores (101, 180, 185).

Young Age

7 - Classification of the Glaucomas

Page 41 of 425

Onset of glaucoma at a younger age is another risk factor for blindness because the glaucoma is expected to have longer to progress. The median estimated duration of COAG in the United States is 13 years in whites, with 25% of cases beginning by age 64 and 50% by age 72 (1). In blacks, the median duration is estimated to be 16 years, with 25% of cases beginning by age 54 years and 50% by age 65 years (1). The onset of COAG before the median age of onset portends a longer duration of disease and a higher lifetime risk for blindness than the median; the onset of COAG in the earliest 25th percentile portends a considerably longer duration and higher level of risk. Furthermore, significant comorbidities may curtail life expectancy. The earlier onset and longer duration of COAG in black patients, compared with other patients, may largely account for the higher risk for glaucoma-related blindness among blacks in the United States (1), although other factors, such as decreased access to health care, may contribute (186, 187, 188, 189 and 190).

Inadequate Intraocular Pressure Control

It has long been standard clinical practice to treat glaucoma by safely lowering IOP below the level at which optic nerve damage occurred. Recent clinical trials have conclusively shown that failure to do so forfeits the benefit of IOP lowering and results in a higher risk of progression to blindness. Patient nonadherence to glaucoma-treatment regimens is one cause of inadequate IOP lowering and has been shown to increase the risk for blindness by a factor of 1.8 (179). Several studies have noted marked differences in individual susceptibility to IOP and have stressed the importance of additional IOP lowering in the face of ongoing progression (182, 191). This is supported by numerous studies showing that greater IOP reduction results in less progression (86, 192, 193, 194, 195 and 196). However, in blinding glaucoma, patients commonly progress to blindness despite IOP lowering to the mid to low teens (179, 191). It may be that heightened susceptibility to IOP damage or non-IOP-dependent mechanisms of damage may be more prominent in patients with blinding glaucoma, at least in the last stages of the disease.

High Rate of Progression Despite Treatment

A high rate of progression despite treatment is itself another risk factor for glaucoma blindness. The rate of visual field progression has been found to be 3 to 10 times more rapid in those eventually progressing to blindness than in ageand initial field-matched controls, although the IOP was actually lowered further in those progressing to blindness (191). Clinically, time to definite progression is often used as a practical indicator of progression rate. As one reference point, the median time to definite progression in treated COAG (mean initial IOP, 15.5 mm Hg after 25% IOP reduction) was about 6 years in the EMGT with the simple endpoint of significant progression of the same three or more points on a glaucoma change probability map (Humphrey 24-2) on three consecutive fields. However, even patients who take this long to show definite progression may eventually be blinded by glaucoma if they have advanced glaucoma; also, even slow progression may eventually lead to blindness in those with a long life expectancy or whose progression accelerates. COAG is often an asymmetric disease, and an aggressive clinical course in one eye may foreshadow the clinical course of the fellow eye (182, 197, 198). A strong family history of aggressive COAG may also put a patient at higher risk for significant vision loss. Prognosis for Blindness for Angle-Closure and Secondary Glaucomas

Although the foregoing discussion on risk factors for blindness in glaucoma relates to COAG, most of the risk factors discussed also apply to angle-closure glaucoma and secondary glaucoma. Prevalence surveys suggest that blindness is more common with angle-closure glaucoma and secondary glaucoma than with COAG. In cases of angle-closure glaucoma, estimates of glaucoma blindness in at least one eye range from 10% to 50% in Inuit and Chinese patients, and bilateral blindness in angleclosure glaucoma has been reported in 21% of cases in blacks in East Africa (31, 35, 40, 199). The corresponding figures for secondary glaucoma (neovascular, lens related, posttraumatic, and uveitic) with blindness in at least one eye were 71% in Chinese patients and for bilateral blindness were 25% in East Africans (31, 40). In each setting, the estimates given were higher than those for blindness due to COAG.

Undiagnosed Glaucoma

Prevalence surveys in primarily white populations from established market economies have consistently

7 - Classification of the Glaucomas

Page 42 of 425

shown that about 50% of cases of COAG in the population had not yet been diagnosed (46, 47, 49, 200). Among Chinese patients in Singapore, this percentage is 91% for COAG but only 29% for angle-closure glaucoma (40), presumably because the clinical course of angle-closure glaucoma is more likely to cause symptoms. Diagnosis of glaucoma has been found to be more likely in those with a history of other eye disease, a first-degree family history of glaucoma, and the use of one or more general medications.

A number of lines of evidence suggest that it is not just early glaucoma that is undiagnosed in the population. A series of 220 consecutive cases of newly diagnosed glaucoma from a hospital-based ophthalmology clinic in the United Kingdom reported that 50% had a visual field defect within 5 degrees of fixation (201, 202). Among patients with newly diagnosed COAG, between 6% and 10% were reported to be blind in at least one eye (178). In addition, 45% of new cases of glaucoma blindness registered on the Massachusetts Blindness registry between 1970 and 1980 were blind due to glaucoma in one or both eyes at the time of their glaucoma diagnosis, similar to earlier reports from the United Kingdom (203, 204). Risk factors for late presentation include lower socioeconomic status and time since last ocular examination (201).

P.159

Missed Opportunities for Diagnosing Glaucoma

Although delayed diagnosis may be due to a lack of ocular assessment, missed opportunities for diagnosis may also play an important role. In Sweden, a 5-year program ending in 1997 screened for glaucoma by using tonometry and fundus photography as an initial examination and identified 402 cases of undiagnosed open-angle glaucoma. Of these newly diagnosed cases, 67% of patients had previously seen an ophthalmologist and 17% had seen an ophthalmologist in the preceding 2 years (205). In Australia, 51% (36 of 70) of patients with undiagnosed glaucoma in the Melbourne Visual Impairment Project had seen an ophthalmologist, optometrist, or both in the preceding year (206). Some missed cases of COAG may have resulted from differing diagnostic criteria or from progression of disease between assessments. More probably, missed cases arose from less accurate assessment for glaucoma. In Sweden, among persons with newly identified openangle glaucoma after screening, 21% of those with an IOP less than 21 mm Hg had seen an ophthalmologist in the preceding 2 years, compared with 12% of those with a screening IOP of 21 mm Hg or greater (P < 0.001) (205). Similar findings have been reported from the Tierp Glaucoma Survey, also in Sweden. These reports suggest that the finding of a normal IOP decreases detection of COAG in routine eye care.

The nature of opportunities to improve diagnosis for glaucoma varies widely from setting to setting. In the United Kingdom, one study assessed practice patterns for glaucoma assessment and found that four of five optometrists could improve their detection of glaucoma by at least 50% by performing ophthalmoscopy and tonometry in all patients and perimetry in persons belonging to high-risk groups (207).

Nonadherence and Undertreatment

Suboptimal treatment may also significantly hamper efforts at preventing blindness due to glaucoma. Nonadherence to treatment and follow-up are a particular concern. In patients older than 65 years in the New Jersey Medicaid Program who were initiated on topical agent for the treatment of glaucoma, 23% never filled their prescription and the remainder missed an average of 30% of treatment days (208). In a managed care setting in Massachusetts, 25% of patients newly initiated on glaucoma therapy missed at least 20% of patient days of treatment (209). Adherence to treatment is notoriously difficult to predict but has been found to be several times more frequent in those seen only once in the 12 months after initiation of new treatment (209, 210). Models of care that focus on patient education in a supportive environment have the potential to enhance patient adherence (211).

Suboptimal treatment may also result from a failure to incorporate advances in management of glaucoma into practice. Currently, the data on quality of care for COAG are sparse. One study of U.S. working-age patients with COAG enrolled in managed care plans found that care was consistent with guidelines (212). However, one significant deficiency was that only 53% of patients with COAG

7 - Classification of the Glaucomas

Page 43 of 425

received an optic nerve drawing or photograph on initial examination (212). Given the expected delays in adopting new innovations, IOP may be undertreated in the United States and elsewhere in light of recent clinical trials.

CHALLENGES FROM GLAUCOMA IN THE DEVELOPING WORLD

In much of the developing world, the situation with glaucoma is entirely different. Eye-care services are limited, often severely so, and the amount of glaucoma in the general population that has been diagnosed is small; reports of 7% of COAG in India and 2% in Tanzania are typical (41). Glaucoma usually presents symptomatically with severe vision loss in one or both eyes, or a painful acute attack. Surgical trabeculectomy with or without antimetabolites is the treatment of choice except in cases of angleclosure glaucoma amenable to peripheral iridotomy or iridectomy. Ongoing follow-up is typically a hardship for patients and is often not possible. For most people with glaucoma in the developing world, the disease simply follows its natural course without detection or intervention, at least until symptoms develop and blindness encroaches.

Challenges to PreventinG Blindness: A Population Perspective

As the leading cause of irreversible blindness worldwide, affecting more than 6.6 million people, blindness due to glaucoma is a mounting problem of global public health importance. Glaucoma-related blindness is also largely preventable through timely diagnosis, effective treatment, and ongoing monitoring. Although this seems attainable in the developed world, glaucoma has proven itself a difficult adversary. The nature of most glaucomas is such that it typically evades detection until its final stages unless ocular assessment is done periodically to detect the disease early in its course; glaucoma is also unrelenting and takes advantage of any delays, lapses, or insufficiencies in treatment to destroy remaining axons. Consequently, a health services response sufficient to prevent blindness from glaucoma is resource intensive. Successful management of glaucoma typically requires long-term active involvement of the patient, except in the prevention of angle-closure glaucoma with iridotomy. From a clinical standpoint, determined efforts to detect glaucoma early and treat it effectively regularly meet with success in many patients, but even so, glaucoma has yet to be dislodged as a major cause of blindness in any country. Major deficiencies in the detection and treatment of glaucoma remain, even in developed countries.

STRATEGIES FOR PREVENTING BLINDNESS: IMPROVED EARLY DETECTION

There are numerous avenues to improve the prevention of blindness from glaucoma, but improved early detection offers the most potential. Undiagnosed glaucoma is probably the largest reservoir of preventable blindness in the developed

P.160

world and is second only to cataract overall in the developing world. The strategies for the identification of asymptomatic individuals at increased risk for glaucoma run the gamut from population screening to case finding. Population screening is the presumptive identification of individuals who might benefit from further diagnostic assessment of glaucoma by an ophthalmologist or optometrist; case finding involves testing for glaucoma as opportunities arise in the course of clinical care, such as during periodic eye evaluations. A blend of approaches for detecting glaucoma from this spectrum can complement one another and may offer the best hope of minimizing undiagnosed glaucoma.

Improving Coverage of Case Finding

In most developed countries, periodic comprehensive ocular assessments form the backbone of primary eye care and provide as one of their chief benefits an excellent vehicle for glaucoma case finding. In fact, rates of coverage are surprisingly good in some settings. In Australia, 81% of those 40 years and older had had an examination by an ophthalmologist or optometrist within the previous 5 years (206). An identical level of 5-year coverage was reported among persons without diabetes in a Canadian population aged 30 years and older (213). Eye examinations in both these populations occurred least frequently in younger men of lower socioeconomic status or without private insurance, and Australians in rural areas we less likely to undergo eye examinations (206, 213).

Coverage may be increased further by improving the provision of services to underserviced segments of

7 - Classification of the Glaucomas

Page 44 of 425

the population and targeting health promotion efforts to increase uptake of periodic ocular examinations in these groups (214). Changing population-wide use of preventive eye examinations is not an easy task, but even small percentage increases translate into a benefit to large numbers of individuals. An intensive use of this strategy in Australia, including targeted mailings and print and broadcast media announcements, successfully increased the use of retinal screening examinations in persons with diabetes from 55% to 70%. However, a targeted mailing campaign in the United States with the same objectives produced no sustained increase in retinal screening examinations (215).

Improving Accuracy of Case Finding

In clinical practice, the effectiveness of case finding for glaucoma in primary eye care may not be optimal (205, 206). This may be due to the limited extent of examination carried out and undue reliance on elevated IOP to trigger a complete evaluation for glaucoma (205, 207). In the U.S. context, the American Academy of Ophthalmology (AAO) has recommended the following elements for a comprehensive eye examination that pertain to improved detection of glaucoma (216): IOP, gonioscopy, slitlamp examination of the anterior segment, optic disc and nerve fiber layer evaluation with documentation of optic nerve appearance, and visual field examination. Alternatively, others suggest selective performance of visual field tests depending on risk factors and clinical findings (217). Similarly, routine gonioscopy may not be necessary in those who, on examination, have normal peripheral anterior chamber depth and normal IOP. Careful documentation of the optic nerve appearance at baseline examination, preferably with stereoscopic photos or other suitable imaging (such as optical coherence tomography or scanning laser ophthalmoscopy), is important to permit glaucomatous changes to be identified on follow-up. A good baseline evaluation for glaucoma is of particular importance in following higher-risk patients, such as glaucoma suspects and patients with ocular hypertension, but it is worth remembering that almost any patient can develop glaucoma. In one large population-based cohort study, 28% of persons with newly diagnosed glaucoma were not considered to be glaucoma suspects or to have ocular hypertension when examined 4 years earlier (58).

To maximize cost-effective glaucoma case finding, the frequency of periodic assessment should be adjusted to a patient's level of risk for glaucoma. One recommendation for the frequency of comprehensive eye examinations that reflects the risk for glaucoma comes from the AAO (Table 9.6): every 1 to 2 years for those 65 years and older, every 1 to 3 years for those 55 to 64 years of age, every 2 to 4 years for those between the ages of 40 and 54 years, and 5 to 10 years for those before 40 years of age. For persons with a first-degree relative with glaucoma or those who are of African descent (or who have other risk factors supported by good evidence [ Table 9.7]), the frequency may be increased and should be at least every 6 months to a year for patients 65 or older, every 1 to 2 years for those aged 55 to 64, every 1 to 3 years for those aged 40 to 54, and every 2 to 4 years for those younger than 40 years (216). Patient referral by primary care physicians to an eye specialist for periodic comprehensive eye examination is supported by the U.S. Preventive Services Task Force for those at increased risk for glaucoma (223).

Table 9.6Recommended Frequency of Comprehensive Medical Eye Examinations, according to Risk-Factor Status for Chronic Open-Angle Glaucoma

Age-Group

Frequency of Examinations

 

Adults with No Risk Factors

Adults with >1 COAG Risk Factor

<40y

5-10 y

Every 2-4 y

40-54 y

Every 2-4 y

Every 1-3 y

55-64 y

Every 1-3 y

Every 1-2 y

>65y

Every 1-2 y

Every 6-12 mo

aindividuals are considered to have a risk factor for COAG if they have elevated intraocular pressure or a family history of glaucoma, or are of African or Latino/Hispanic descent. COAG, chronic open-angle glaucoma.

7 - Classification of the Glaucomas

Page 45 of 425

Data from American Academy of Ophthalmology (AAO) Preferred Practice Patterns Committee. Preferred Practice Pattern Guidelines. Comprehensive Adult Medical Eye Evaluation. San Francisco, CA: AAO; 2005. Available at: http://www.aao.org/ppp.

P.161

Table 9.7 Variables with Good Evidence of Being Clinical Risk Factors for Chronic Open-Angle Glaucomaa

Variable

RRfor COAG

Best Evidence: References

Age (per decade >40 y)

2

3, 42, 50, 53

Black (white, referent)

4

29

Family history (first-degree relative)

2-4

78,80,82,218

IOP (<15 mm Hg, referent)b

 

58, 72, 82, 102

19-21 mm Hg

3

 

22-29 mm Hg

13

 

=30 mm Hg

40

 

Myopia

1.5-3

116-118,219

Exfoliation

5-10

82,102,118

Diastolic perfusion pressure (<55 mm Hg)

3

72,126,130,218

Central corneal thickness

1.4

129

Pigment dispersion syndrome

_c

220

aTable shows only those variables meeting the standard of “good”-level evidence, as graded according to method of the U Preventive Services Task Force (221). Display of risk-factor information modeled after Ref. 222.

bRelative risk data are from Ref. 53. For best evidence, see also Table 9.4 .

cThe estimated proportion of patients with pigment dispersion syndrome is 6% to 43%.

COAG, chronic open-angle glaucoma; IOP, intraocular pressure; RR, relative risk

The estimated proportion of patients with pigment dispersion syndrome is 6% to 43%. Screening for Chronic Open-Angle Glaucoma

Screening for undiagnosed glaucoma in high-risk populations (e.g., blacks, older adults, socioeconomically disadvantaged persons) may complement periodic ocular examination, particularly when targeting individuals who cannot or have not accessed care (224). In some respects, COAG is an ideal disease for population screening: It is of public health importance; detectable during its prolonged asymptomatic phase; and amenable to effective therapy to prevent blindness, particularly when diagnosed early. However, many obstacles to large-scale screening for COAG remain, including the lack of an entirely satisfactory screening test and the weakness of the economic argument to justify the resources required compared with other preventive interventions. Currently, population screening for COAG is, for the most part, carried out sporadically and on a modest scale by community and research groups (205).

The specifications for a suitable test for population screening for glaucoma are more exacting than the criteria for clinical use. One set of criteria for screening devices for COAG from Prevent Blindness America illustrates the difficult balance of specifications required: high accuracy (sensitivity, 85% for moderate to advanced glaucoma; specificity, 95%); ease of administration and transport, set up by minimally trained personnel; low cost and low maintenance; short testing and process time; and ease of

7 - Classification of the Glaucomas

Page 46 of 425

understanding and conduct for the patient. These criteria emphasize high specificity to reduce the large costs associated with false-positive referrals. For example, consider tonometry, the traditional screening modality for glaucoma. In the Baltimore Eye Survey, a screening IOP of more than 21 mm Hg detected only 47% of persons with COAG (i.e., sensitivity); using a criterion of IOP less than 21 mm Hg correctly identified 92% of persons without COAG (i.e., specificity) (29). For a prevalence of about 2%, such as in whites older than 39 years (Table 9.1), 9 of 100 persons would have a screening IOP greater than 21 mm Hg, of whom one would have COAG and eight would have false-positive results. If a different test were used with the same sensitivity but a higher specificity of 98%, then the number referred for definitive testing would be reduced to only 3 in 100, consisting of one person with COAG and two with false-positive results. This example illustrates the importance of high specificity in glaucoma screening. The fact that an IOP greater than 21 mm Hg detects only 50% of COAG also underlines the need for good sensitivity to avoid falsely reassuring those tested.

For varying reasons, none of the many useful diagnostic tests for glaucoma are completely satisfactory for population screening. Tonometry is now discouraged as a standalone method for screening because there is no IOP level that gives a reasonable balance between sensitivity and specificity (29). COAG screening by evaluation of the optic nerve head is limited by the cost of a highly trained clinician or of a suitable imaging device. The practicality of full threshold or thresholdrelated suprathreshold automated perimetry is limited by learning effects, the need for skilled interpretation, and relatively high costs. Frequency doubling perimetry may be one of the most promising psychophysical tests for population screening for glaucoma, although the cost remains significant and the specificity may be suboptimal unless adequate criteria are used to define an abnormal test (225).

Cost-Effectiveness of Screening for COAG

Population screening for COAG, although highly desirable, does not appear to be cost competitive with other preventive health care interventions (226, 227). The cost per year of vision saved by glaucoma screening appears to be many times the cost per year of life saved from such interventions as screening for breast cancer (226). In contrast, a 1983 analysis suggested that population screening for glaucoma would probably be cost-effective if subgroups at known higher risk for glaucoma were targeted (228). Glaucoma screening programs have typically also screened for visual impairment, leading causes of which include refractive error and cataracts, which are amenable to treatment. This major benefit of glaucoma screening has not been built in to cost-effectiveness analyses. In fact, it is probably more accurate to think of glaucoma screening as a component of a vision screening examination. Further screening innovations and updated economic

P.162

analyses will permit a stronger case to be made in the future for cost-effective screening for COAG, at least in high-risk segments of the population.

Screening for Angle-Closure Glaucoma

In Asian populations where angle-closure glaucoma is the predominant cause of morbidity from glaucoma, there is great potential for screening programs to prevent angle-closure glaucoma. In contrast to COAG, angle-closure glaucoma can be prevented by the bilateral laser iridotomies in individuals with occludable angles, a simple one-time intervention (229). Consequently, the cost of preventing angleclosure glaucoma is much less than that of providing long-term treatment for COAG. The risk for blindness is also much higher for angleclosure glaucoma than for COAG and therefore the benefit is greater for each case of angle-closure glaucoma prevented (31, 39, 40). As a result, population screening for angle-closure glaucoma in appropriate populations may be much more costeffective than population screening for COAG.

Numerous modalities have been suggested for population screening for occludable angles, including anterior chamber depth measurement, Van Herick test (or peripheral anterior chamber depth measurement), and the oblique flashlight test. However, the accuracy of the tests is not completely satisfactory for population screening and varies with the biometric characteristics of the population (40). For an acceptable sensitivity of about 85%, both anterior chamber depth measurement (<2.22 mm by

7 - Classification of the Glaucomas

Page 47 of 425

optical pachymetry) and Van Herick test (peripheral anterior chamber depth <15% peripheral corneal thickness) could achieve specificities of only 84% and 86%, respectively, for detecting occludable angles in a Mongolian population (40, 230).

A clinical trial is under way in Mongolia to determine whether population screening and prophylactic iridotomies for occludable angles will reduce the incidence of angle-closure glaucoma (231). The screening criteria of an anterior chamber depth of less than 2.53 mm (by ultrasonography) or an IOP greater than 24 mm Hg tagged almost one third of the screening population for a definitive evaluation including gonioscopy; 24% had occludable angles. Although appropriate for the purposes of a clinical trial, more specific tests or criteria would greatly improve the feasibility of large-scale screening for angle-closure glaucoma.

Strategies for Prevention in the Developing World

In much of the developing world, the tremendous scarcity of resources for eye care greatly limits the feasible interventions to prevent blindness from glaucoma. It has been suggested that the best workable option in much of the developing world may be to integrate glaucoma case finding into other blindness prevention efforts, such as cataract surgical programs, and to offer inexpensive and high-quality filtering surgery for those cases of surgical glaucoma identified (232) and peripheral iridotomy for those with occludable angles.

Teleglaucoma: Using Distance Technology to Improve Access to Care

Given progress in information technology, it is possible to obtain high-quality digital photographs of the optic nerve and transmit compressed images for storage, retrieval, and evaluation via Web-based platforms. Such an approach, with or without recommendations on management of patients, is referred to as teleglaucoma.

Given that camera systems are portable, and assuming that a high-speed Internet link exists, it should be possible to set up mobile units or multiple fixed centers, which facilitate access to eye examinations so that patients do not need to travel a great deal unnecessarily (233). These images can be stored and read from a distance, and patients can be triaged into healthy, suspect, or definite categories. Referral and treatment decisions can be made as appropriate and conveyed to the patient via trained ophthalmic personnel (e.g., nurse or technician). Compression can take place without altering the quality of images significantly, and digital images appear to provide comparable information for the purposes of grading glaucomatous optic nerve involvement as traditional stereo slide film (234, 235). More work is needed to assess whether two-dimensional images of the nerve convey adequate information, compared with stereoscopic images.

The deployment of advanced technologies can minimize the barriers of distance and geography to enhance access and facilitate the delivery of integrated health care (236). This is particularly important in areas with large underserved or rural populations or a limited number of ophthalmologists (237). SUMMARY

Glaucoma is the leading cause of irreversible blindness worldwide, and by 2020, the number of persons with glaucoma will almost double from the recent estimate of 67 million.

The prevalence of COAG and angle-closure glaucoma varies across different populations: COAG accounts for about 90% of all glaucoma in blacks, whites, and some Asian populations (e.g., Japanese); angle-closure glaucoma predominates in certain Asian populations (e.g., Inuit, Mongolian) and has a similar prevalence to COAG in others (e.g., Chinese in Singapore).

The age-specific prevalence of COAG (by population) is a useful starting point for clinicians to estimate the probability of COAG when beginning an initial assessment.

Clinical risk factors are useful to assess the risk of COAG, but only a small number are well supported by evidence: age, race (black), elevated IOP, family history (first-degree relative), myopia, exfoliation syndrome, and diastolic ocular perfusion pressure (<55 mm Hg).

The onset and progression of most glaucomas occur so slowly that careful documentation of baseline examination, including the optic nerve head appearance, is required to detect subtle changes.

7 - Classification of the Glaucomas

Page 48 of 425

The lifetime risk for blindness from COAG probably exceeds 5% on average; risk factors for blindness from COAG include

P.163

early age of onset, advanced stage, inadequate IOP control, and a high rate of progression despite treatment.

Undiagnosed COAG is probably the largest reservoirvoir preventable blindness in the world in that only 50% of COAG cases are identified, even in developed countries. A pressing need exists to complement this by developing cost-effective approaches for screening high-risk groups for COAG.

In some Asian populations, screening and treatment of occludable angles with laser iridotomy to prevent angle-closure glaucoma may soon be demonstrated to be effective and feasible.

REFERENCES

1.Quigley HA. Number of people with glaucoma worldwide. Br J Ophthalmol. 1996;80(5):389-393.

2.Thylefors B, Negrel AD, Pararajasegaram R, et al. Global data on blindness. Bull World Health Organ. 1995;73(1):115-121.

3.Friedman DS, Wolfs RC, O'Colmain BJ, et al. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol. 2004; 122(4):532-538.

4.Kobelt-Nguyen G, Gerdtham UG, Alm A. Costs of treating primary open-angle glaucoma and ocular hypertension: a retrospective, observational two-year chart review of newly diagnosed patients in Sweden and the United States. J Glaucoma. 1998;7(2):95-104.

5.Iskedjian M, Walker J, Vicente C, et al. Cost of glaucoma in Canada: analyses based on visual field and physician's assessment. J Glaucoma. 2003;12(6):456-462.

6.Calissendorff BM. Costs of medical and surgical treatment of glaucoma. Acta Ophthalmol Scand. 2001;79(3):286-288.

7.Quigley HA. (Inter)National cost of glaucoma. The Cost of Blindness Symposium. Toronto; January 31-February 1, 2004. Available at: http://www.costofblindness.org/presentations/quigley/quigley.htm.

8.Tielsch JM. Therapy for glaucoma: costs and consequences. In: Ball SF, Franklin RM, eds. Transactions of the New Orleans Academy of Ophthalmology. Amsterdam, the Netherlands: Kugler; 1993:61-68.

9.Gerdtham UG, HagaA, Karlsson G, et al. Observational costing study in open angle primary glaucoma in Sweden and the USA. EPI research paper no. 65666. Stockholm, Sweden: Stockholm School of Economics; 1996.

10.Coyle D, Drummond M. The economic burden of glaucoma in the UK. The need for a far-sighted policy. Pharmacoeconomics. 1995;7(6):484-489.

11.Glynn RJ, Seddon JM, Krug JH Jr, et al. Falls in elderly patients with glaucoma. Arch Ophthalmol. 1991;109(2):205-210.

12.Haymes SA, Leblanc RP, Nicolela MT, et al. Risk of falls and motor vehicle collisions in glaucoma. Invest Ophthalmol Vis Sci. 2007;48(3): 1149-1155.

13.Haymes SA, LeBlanc RP, Nicolela MT, et al. Glaucoma and on-road driving performance. Invest Ophthalmol Vis Sci. 2008;49(7):3035-3041.

14.McGwin G Jr, Xie A, Mays A, et al. Visual field defects and the risk of motor vehicle collisions among patients with glaucoma. Invest Ophthalmol Vis Sci. 2005;46(12):4437-4441.

15.Jampel HD, Frick KD, Janz NK, et al. Depression and mood indicators in newly diagnosed glaucoma patients. Am J Ophthalmol. 2007;144(2): 238-244.

16.Jayawant SS, Bhosle MJ, Anderson RT, et al. Depressive symptomatology, medication persistence, and associated healthcare costs in older adults with glaucoma. J Glaucoma. 2007;16(6):513-520.

17.Green J, Siddall H, Murdoch I. Learning to live with glaucoma: a qualitative study of diagnosis and the impact of sight loss. Soc Sci Med. 2002;55(2):257-267.

18.Mills RP, Janz NK, Wren PA, et al. Correlation of visual field with quality- of-life measures at

7 - Classification of the Glaucomas

Page 49 of 425

diagnosis in the Collaborative Initial Glaucoma Treatment Study (CIGTS). J Glaucoma. 2001;10 (3):192-198.

19.Jampel HD. Glaucoma patients' assessment of their visual function and quality of life. Trans Am Ophthalmol Soc. 2001;99:301-317.

20.Gutierrez P, Wilson MR, Johnson C, et al. Influence of glaucomatous visual field loss on healthrelated quality of life. Arch Ophthalmol. 1997;115(6):777-784.

21.Parrish RK II, Gedde SJ, Scott IU, et al. Visual function and quality of life among patients with glaucoma. Arch Ophthalmol. 1997;115(11): 1447-1455.

22.Sherwood MB, Garcia-Siekavizza A, Meltzer MI, et al. Glaucoma's impact on quality of life and its relation to clinical indicators. A pilot study. Ophthalmology. 1998;105(3):561-566.

23.Viswanathan AC, McNaught Al, Poinoosawmy D, et al. Severity and stability of glaucoma: patient perception compared with objective measurement. Arch Ophthalmol. 1999;117(4):450-454.

24.Nelson P, Aspinall P, Papasouliotis O, et al. Quality of life in glaucoma and its relationship with visual function. J Glaucoma. 2003;12(2):139-150.

25.Wilson MR, Coleman AL, Yu F, et al. Functional status and well-being in patients with glaucoma as measured by the Medical Outcomes Study Short Form-36 questionnaire. Ophthalmology. 1998;105 (11):2112-2116.

26.Barber BL, Strahlman ER, Laibovitz R, et al. Validation of a questionnaire for comparing the tolerability of ophthalmic medications. Ophthalmology. 1997; 104(2):334-342.

27.Lee BL, Gutierrez P, Gordon M, et al. The Glaucoma Symptom Scale. A brief index of glaucomaspecific symptoms. Arch Ophthalmol. 1998; 116(7): 861-866.

28.Kennedy GJ. The geriatric syndrome of late-life depression. Psychiatr Serv. 1995;46(1):43-48.

29.Tielsch JM, Sommer A, Katz J, et al. Racial variations in the prevalence of primary open-angle glaucoma. The Baltimore Eye Survey. JAMA. 1991;266(3):369-374.

30.Leske MC, Connell AM, Schachat AP, et al. The Barbados Eye Study. Prevalence of open angle glaucoma. Arch Ophthalmol. 1994; 112(6):821-829.

31.Buhrmann RR, Quigley HA, Barron Y, et al. Prevalence of glaucoma in a rural East African population. Invest Ophthalmol Vis Sci. 2000;41 (1):40-48.

32.Mason RP, Kosoko O, Wilson MR, et al. National survey of the prevalence and risk factors of glaucoma in St. Lucia, West Indies. Part I. Prevalence findings. Ophthalmology. 1989;96(9):1363-1368.

33.Rotchford AP, Kirwan JF, Muller MA, et al. Temba glaucoma study: a population-based crosssectional survey in urban South Africa. Ophthalmology. 2003; 110(2):376-382.

34.Quigley HA, West SK, Rodriguez J, et al. The prevalence of glaucoma in a population-based study of Hispanic subjects: Proyecto VER. Arch Ophthalmol. 2001;119(12):1819-1826.

35.Arkell SM, Lightman DA, Sommer A, et al. The prevalence of glaucoma among Eskimos of northwest Alaska. Arch Ophthalmol. 1987;105(4): 482-485.

36.Dandona L, Dandona R, Mandal P, et al. Angle-closure glaucoma in an urban population in southern India. The Andhra Pradesh eye disease study. Ophthalmology. 2000;107(9):1710-1716.

37.Dandona L, Dandona R, Srinivas M, et al. Open-angle glaucoma in an urban population in southern India: the Andhra Pradesh eye disease study. Ophthalmology. 2000;107(9):1702-1709.

38.Shiose Y, Kitazawa Y, Tsukahara S, et al. Epidemiology of glaucoma in Japan—a nationwide glaucoma survey. Jpn J Ophthalmol. 1991;35(2): 133-155.

39.Foster PJ, Baasanhu J, Alsbirk PH, et al. Glaucoma in Mongolia. A populationbased survey in Hovsgol province, northern Mongolia. Arch Ophthalmol. 1996;114(10):1235-1241.

40.Foster PJ, Oen FT, Machin D, et al. The prevalence of glaucoma in Chinese residents of Singapore: a cross-sectional population survey of the Tanjong Pagar district. Arch Ophthalmol. 2000; 118(8): 11051111.

41.Ramakrishnan R, Nirmalan PK, Krishnadas R, et al. Glaucoma in a rural population of southern India: the Aravind comprehensive eye survey. Ophthalmology. 2003;110(8):1484-1490.

42.Klein BE, Klein R, Sponsel WE, et al. Prevalence of glaucoma. The Beaver Dam Eye Study. Ophthalmology. 1992;99(10):1499-1504.

Соседние файлы в папке Английские материалы