·Bibliometric
Research·Current
Issue· ·Achieve· ·Search Articles· ·Online Submission· ·About IJO· PMC
Critical
pathway for primary open angle glaucoma diagnosis
Alejandro R. Allocco, Julia A. Ponce, Maria J. Riera, Mauricio G.
Magurno
Instituto Santa Lucía Paraná, Alameda de la Federación 493, Paraná 3100,
Entre Ríos, Argentina
Correspondence to: Alejandro R. Allocco. Alameda de la
Federación 493, Paraná 3100, Entre Ríos, Argentina. ale_allocco@outlook.com
Received:
2016-11-08
Accepted: 2017-02-07
AIM: To develop a
critical pathway for primary open angle glaucoma (POAG) diagnosis intended to
be efficient, to unify criteria, reduce resource use and minimize costs to the
health system.
METHODS: We performed a
systematic search on PubMed, Cochrane, Embase and ClinicalTrials.org databases
and classified the quality of evidence from level I through III.
RESULTS: A critical
pathway was designed by setting a key-decision step by step model on the basis
of the best current evidence.
CONCLUSION: A critical
pathway, evidence-based guideline, may be a useful tool intended to reduce
costs while maintaining or even improving the quality of care for diagnosing a
highly prevalent pathology such as open angle glaucoma.
KEYWORDS: glaucoma; diagnosis;
critical pathway; guideline
DOI:10.18240/ijo.2017.06.21
Citation: Allocco AR, Ponce JA,
Riera MJ, Magurno MG. Critical pathway
for primary open angle glaucoma diagnosis. Int J Ophthalmol 2017;10(6):968-972
Glaucoma
affects more than 60 million people and represents the second leading cause of
blindness worldwide. Primary open angle glaucoma (POAG) is the most frequent
type of glaucoma, affecting almost 45 million people over the globe. Blindness
caused by glaucoma affects 8.4 million people nowadays, and this number is
estimated to rise up to 11 million people for the year 2020[1-2].
Prompt
diagnosis and treatment of ocular hypertension (OH) and glaucoma can diminish
the permanent visual field loss and optic nerve head (ONH) damage observed in
these patients[2-4]. This
highlights the significance of reckon on with an effective diagnosis strategy
that allows to optimize resources and, mainly, gain time. Glaucoma is commonly
diagnosed using several ancillary tests and in fact there is no unique
screening method that has proven to be totally effective by its own[2]. This explains several situations of delayed
diagnosis seen on these patients, which finally leads to permanent and
irreversible visual loss.
Critical
pathway guidelines have emerged as improving proposals for making decisions,
applied for both diagnosis and treatment of specific pathologies. Particularly,
critical pathways have been successfully applied for emergency pathologies in
order to optimize time and resources, unifying medical criteria for making
decisions[5]. Considering the high prevalence of
POAG and its irreversible consequence, we thought to be necessary to have a
step by step model of taking decisions on the basis of the best current
evidence.
The purpose of
this paper is to develop a critical pathway for POAG diagnosis intended to be
efficient, to unify criteria, reduce resource use and minimize costs to the
health system.
Critical
pathway was designed by setting a key-decision step by step model on the basis
of the current evidence. We performed a systematic search on PubMed, Cochrane,
Embase and ClinicalTrials.org databases using the following search terms:
“primary open angle glaucoma”, “critical pathway”, “ocular hypertension”,
“IOP”, “glaucoma epidemiology”, “glaucoma diagnosis”, “gonioscopy”, “visual
field in glaucoma”, “pachymetry”, “glaucoma progression”.
The aim of a
critical pathway is to reach efficiency, to minimize treatment variability
among clinicians, to shorten times and to minimize the resources and costs.
Therefore, critical review and proper classification of the quality of the
evidence is crucial to support this model. Thus, articles were classified
according to their scientific quality from level I through III following the
guidelines of the Preferred Practice Patterns of the American Academy of
Ophthalmology[3,6]. Briefly,
level I included evidence obtained from at least one properly conducted, well
designed, randomized and controlled clinical trial, as well as Meta-analysis
including this type of studies. Level II, well-designed, controlled trials
without randomization and cohort or control-case studies. Finally, level III
included descriptive studies, case reports and expert consensus.
Inclusion
criteria for critical pathway were patients that reach to ophthalmologic
examination for the first time and also those patients followed up for other
ocular pathologies different than POAG. Exclusion criteria were patients with
established diagnosis of POAG, patients under glaucoma treatment or patients
with other types of glaucoma different that POAG.
A total of 37
papers were selected that meet our standards of inclusion criteria. In all, we
found 9 level I, 14 level II and 14 level III papers, basing each step of the
pathway on the highest quality evidence possible. The critical pathway is shown
in Figure 1.
Figure 1 Critical
pathway for POAG diagnosis.
Roughly, first
clinical examination should be focused on detecting glaucoma suspect patients
that are going to be studied throughout the pathway. Patients that do not
fulfill criteria for glaucoma suspect could be regularly followed up according
to Table 1. Gonioscopy is a key element for splitting decision while it aims to
differentiate open anterior chamber angle from other types of glaucoma like
closed angle or patients with other angle alterations. After OH is confirmed,
qualitative and quantitative analysis of ONH and retinal nerve fiber layer
(RNFL) plus abnormalities in computerized visual field (CVF) represents major
key steps for making decisions through the diagnosis process. This step by step
model of making decisions proposed by the critical pathway ensure prompt
diagnosis for POAG patients and reduce costs to the health system.
Table 1
Regular follow up
Age (a) |
With risk factors |
Without risk factors (a) |
≥65 |
6-12mo |
1 |
55-64 |
1-2d |
1-3 |
40-54 |
1-3d |
2-4 |
<40 |
2-4d |
5-10 |
Even though
some guidelines for open angle glaucoma diagnosis have been published, we
believe that applying a step by step model is the best way for unify medical
criteria and to reach cost-effectiveness.
Initial
examination should include all the components of the comprehensive eye
examination. Because screening methods for glaucoma in general population are
not cost-effective, only patients considered glaucoma suspect should be studied
deeper[2-3]. For
instance, glaucoma suspect patients are those with biomicroscopy abnormalities,
high intraocular pressure (IOP) levels, abnormal appearance of the ONH and
those with family history of glaucoma. Besides that, older age, type 2
diabetes, myopia, thinner central cornea, corneal hysteresis (CH) and corneal
resistance factor, pseudoexfoliation material, low ocular perfusion pressure,
African ancestry and Latino ethnicity are also known risk factors for glaucoma
and should be assessed as well[3,6-13]. Patients that not fulfill criteria to be considered
glaucoma suspect are considered normal and can be followed up according to the
regime showed in Table 1.
During first
ophthalmological examination, detailed biomicroscopy and pupillary dilatation
should be performed looking for anterior segment abnormalities, with special
consideration in the presence of pseudoexfoliation syndrome (PXFS). PXFS is
known to be a strong independent risk factor for glaucoma progression in
patients with OH[11]. Recent studies showed that
after a mean of 8.7y without treatment, glaucoma conversion rate was twice as
high in patients with OH and PXFS as in control patients (OH without PXFS)[12]. Exfoliative glaucoma (XFG) affects up to 6 million
people worldwide and is known to have higher IOP levels and greater 24h IOP
fluctuations, with worse response to medical and surgical treatment and worse
overall prognosis[13].
Older age and
ethnicity are well-known risk factors for glaucoma. Several epidemiological
studies demonstrated a direct relationship between increasing age and the
higher prevalence of glaucoma[3,6].
In addition to this, POAG is three-fold times more frequent among Africans
Americans and Hispanics ancestry compared with non-Hispanic Whites[1,14]. Furthermore, blindness from
glaucoma reaches six times more Africans Americans than Caucasian Americans
patients, although there is no clear evidence if this difference lies in the
individual predisposition or it represents difficulties in the access to the
health system[15].
Family history
is another risk factor for glaucoma. For instance, the Rotterdam Eye Study, the
Baltimore Eye Survey and the Los Angeles Latino Eye Study demonstrated that
individuals with first-degree relatives with confirmed POAG have higher odds of
having glaucoma[6,10,14].
Interestingly, the odds of developing glaucoma increases as does the number of
relatives with confirmed POAG.
High IOP level
is a major risk factor for glaucoma. Several population-based studies provided
strong evidence to consider IOP as a key element for glaucomatous optic nerve
damage progression[11,15-17]. Because there is great inter-individual variation in
the susceptibility of the optic nerve to IOP-related damage, defining an IOP
cutoff measure for screening and diagnosing glaucoma remains arbitrary.
Nevertheless, most studies support the fact that IOP levels higher than 21 mm
Hg represent a higher risk for glaucoma development and so it seems reasonable
to accept that value as standard cutoff[6,16-17].
Measurement of
central corneal thickness (CCT) is an important element for glaucoma diagnosis
because it represents not only an independent risk factor but also it helps the
interpretation of IOP readings when corneal thickness is too distant from
normal values[3,6,10,18]. Population-based studies showed that Latinos or
African Americans, whom mean CCT is 546 and 534 μm respectively, have higher
glaucoma prevalence than Caucasian Americans or Asians with mean CCT of 556 and
552 μm, respectively. Hence, CCT is considered an independent risk factor for
glaucoma development[18-19].
On the other hand, IOP readings could be under or overestimated when CCT are
too thin or too thick, and despite some correcting-formulas have been
published, there are still none universally accepted. Finally, because IOP
readings from Goldmann applanation tonometry (GAT) depends on corneal
resistance to indentation and stiffness, patients with abnormal corneas like
those following keratorefractive surgery, keratoconus or Fuchs endoteliopathy
should be measured by methods less influenced by corneal thickness like
pneumotonometry. However, it should be noted that pneumotonometry
measurements are known to overestimate IOP readings when compared to GAT and
those overestimations are higher as the IOP level increases[19].
CH and corneal
resistance factor, two previously unmeasured corneal biomechanical
characteristics, have gained importance referring to glaucoma diagnosis and
follow-up. It has been suggested that changes in corneal biomechanical factors
are associated with the development and progression of glaucoma, especially in
normal tension glaucoma[10,20-21]. Recent studies demonstrated that low CH
is directly associated with progressive glaucomatous optic neuropathy[20]. Thus, CH can be used not only for screening and
diagnosis purpose but also as one of the prognostic factors for glaucoma
progression, independent of corneal thickness or IOP.
Patients with
axial myopia are prone to develop glaucoma. Several large cross-sectional
epidemiological studies showed evidence that persons with myopia have a higher
prevalence of POAG than normal patients. Hypothetically, patients with axial
myopia have weaker scleral support, which finally increases ONH susceptibility
to glaucomatous ONH damage[6,22-24].
Gonioscopy
represents a key-decision test for glaucoma suspect patients. With gonioscopy,
physicians would differentiate patients with open anterior chamber angle that
will continue throughout the pathway from alternative diagnosis like
angle-closure glaucoma and those patients with structural abnormalities like
angle recession, peripheral anterior synechiae, angle neovascularization,
pigment dispersion, and inflammatory precipitates who will need specific
treatments and follow up[25].
Patients with
several risk factors for glaucoma but constantly normal IOP readings during
medical examinations should be further assessed. Several ocular, hemodynamic
and neurohormonal factors determine circadian variations in IOP readings in
normal patients and, even more, these variations where found to be greater in
patients with suspected or confirmed glaucoma[26-27]. Measurements made with GAT during office
hours capture the IOP at specific moments and therefore do not reflect IOP
fluctuations over a 24h period. Thus, glaucoma suspect patients with IOP levels
below 21 mm Hg need to be studied with a Diurnal Pressure Curve (DPC) in order
to detect, if any, IOP peaks during the entire day[27].
Rebound tonometry as developed by iCare (Tiolat, Helsinki, Finland) emerged as
a complement for self-monitor IOP, and clinical studies have demonstrated high
agreement between GAT and iCare results[28-31]. The instrument is easy to use for IOP
measurements at home, and the results are reliable after a short period of
instruction and practice. Thus, iCare represents a good alternative for IOP
readings after office when DPC is not practicable. In case DPC is normal
(no IOP peaks are detected) and patients have no visual field or ONH
alterations, glaucoma diagnosis is dismissed. If a patient has a normal DPC but
there are signs of visual field or ONH alterations, normal tension glaucoma
and/or neurological disease should be ruled out. Finally, those patients with
abnormal DPC have confirmed OH and should continue through the critical
pathway.
CVF evaluation
with static treshold perimetry remains the gold standard test for glaucoma
detection and follow up[2,6]. It
is important to mention that testing strategies should be individualized to
patients degree of vision loss by using specific programs that evaluate the
central threshold sensitivity at 24 degrees, 30 degrees, and 10 degrees, and by
varying stimulus size[6,32]. On
the other hand, ONH and RNFL evaluation with both qualitative and quantitative
imaging test should be performed[2,33].
Stereoscopic disc photograph is the preferred method for evaluation and follow
up, whereas confocal scanning laser ophthalmoscopy, optical coherence
tomography (OCT), and scanning laser polarimetry showed similar results to
detect glaucomatous patients[33-37].
Nevertheless, physicians should be encouraged to always use computer-based
quantitative imaging test as complementary tests and evaluate the patients full
context after making decisions.
The next step
for splitting decisions in a glaucoma suspect patient relies on the results of
both CVF and ONH. Those patients with normal CVF and ONH are considered OH
patients and the decision for treating and/or follow up depends on several
factors that are beyond the purpose this pathway. By the other side, those
patients with OH, normal CVF but abnormal ONH are diagnosed as pre-perimetric
glaucoma and should be treated[6].
In the case of
patients with high IOP readings and abnormal CVF but non glaucomatous optic
nerve damage should be referred to neurologist to rule out neurological
diseases. Finally, patients with OH, abnormal visual field and alteration of
ONH and RNFL are diagnosed as perimetric glaucoma and should be treated[35,37].
Even though
there is no universally accepted consensus regarding glaucoma diagnosis due to its
multifactorial etiology and clinical presentation, we believe that this
evidence-based step by step model of making decisions improves the quality of
medical attention and unify criteria.
A critical pathway, evidence-based guideline, may be a
useful tool intended to reduce costs while maintaining or even improving the
quality of care in the diagnosis of a highly prevalent pathology such as open
angle glaucoma.
We would like to express our deepest gratitude to Dr.
Carlos Bantar for his valuable collaboration in the preparation of the
manuscript.
Conflicts of Interest: Allocco AR, None; Ponce JA, None; Riera MJ, None; Magurno
MG, None.
1 Quigley HA, Broman AT. The number of people with
glaucoma worldwide in 2010 and 2020.<ii> Br J Ophthalmol
</ii>2006;90(3):262-267. [CrossRef] [PMC free article] [PubMed]
2 Ahmed S, Khan Z, Si F, <ii>et al</ii>.
Summary of glaucoma diagnostic testing accuracy: an evidence-based
Meta-analysis. <ii>J Clin Med Res</ii> 2016;8(9):641-649. [CrossRef] [PMC free article] [PubMed]
3 Prum BE Jr, Lim MC, Mansberger SL, Stein JD, Moroi
SE, Gedde SJ, Herndon LW Jr, Rosenberg LF, Williams RD. Primary Open-Angle
Glaucoma Suspect Preferred Practice Pattern (<supsup>®</supsup>)
Guidelines.<ii> Ophthalmology </ii>2016;123(1):P112-P151. [CrossRef] [PubMed]
4 Gugleta K, Polunina A, Kochkorov A, Waldmann N,
Portmann N, Katamay R, Flammer J, Orgul S. Association between risk factors and
glaucomatous damage in untreated primary open-angle glaucoma. <ii>J
Glaucoma </ii> 2013;22(6):501-505. [CrossRef] [PubMed]
5 Pearson SD, Goulart-Fisher D, Lee TH. Critical
pathways as a strategy for improving care: problems and potential.
<ii>Ann Intern Med </ii> 1995;123(12):941-948. [CrossRef]
6 Prum BE Jr, Lim MC, Mansberger SL, Stein JD, Moroi
SE, Gedde SJ, Herndon LW Jr, Rosenberg LF, Williams RD. Primary Open-Angle
Glaucoma Suspect Preferred Practice Pattern (<supsup>®</supsup>) Guidelines.
<ii>Ophthalmology</ii> 2016;123(1):P41-P111. [CrossRef] [PubMed]
<no>7 Fallon M, Valero O, Pazos M, Antón A.
Diagnostic accuracy of imaging devices in glaucoma: a meta-analysis.
<ii>Surv Ophthalmol</ii> 2017.pii:S0039-6257(16)30197-7.</no>
8 The Advanced Glaucoma Intervention Study (AGIS): 7.
The relationship between control of intraocular pressure and visual field
deterioration. The AGIS Investigators. <ii>Am J Ophthalmol </ii>
2000;130(4):429-440. [CrossRef]
9 Chopra V, Varma R, Francis BA, Wu J, Torres M, Azen
SP; Los Angeles Latino Eye Study Group. Type 2 diabetes mellitus and the risk
of open-angle glaucoma: the Los Angeles Latino Eye Study.
<ii>Ophthalmology </ii>2008;115(2):227-232.e1. [CrossRef] [PMC free article] [PubMed]
10 Carbonaro F, Hysi PG, Fahy SJ, Nag A, Hammond CJ.
Optic disc planimetry, corneal hysteresis, central corneal thickness, and
intraocular pressure as risk factors for glaucoma. <ii>Am J Ophthalmol
</ii> 2014;157(2):441-446. [CrossRef] [PubMed]
11 Miglior S, Bertuzzi F. Exfoliative glaucoma: new
evidence in the pathogenesis and treatment. <ii>Prog Brain Res
</ii>2015;221:233-241. [CrossRef] [PubMed]
12 Teekhasaenee C, Suwan Y, Supakontanasan W,
Tulvatana W, Ritch R. The clinical spectrum and a new theory of pathogenesis of
true exfoliation syndrome. <ii>Ophthalmology </ii>
2016;123(11):2328-2337. [CrossRef] [PubMed]
13 Holló G, Katsanos A, Konstas AG. Management of
exfoliative glaucoma: challenges and solutions. <ii>Clin Ophthalmol
</ii> 2015;9:907-919. [CrossRef] [PMC free article] [PubMed]
14 Varma R, Ying-Lai M, Francis BA, Nguyen BB, Deneen
J, Wilson MR, Azen SP; Los Angeles Latino Eye Study Group. Prevalence of
open-angle glaucoma and ocular hypertension in Latinos: the Los Angeles Latino
Eye Study. <ii>Ophthalmology </ii> 2004;111(8):1439-1448. [CrossRef] [PubMed]
15 Kass MA, Heuer DK, Higginbotham EJ, Johnson CA,
Keltner JL, Miller JP, Parrish RK 2nd, Wilson MR, Gordon MO. The Ocular
Hypertension Treatment Study: a randomized trial determines that topical ocular
hypotensive medication delays or prevents the onset of primary open-angle
glaucoma. <ii>Arch Ophthalmol </ii>2002;120(6):701-713; discussion
829-830. [CrossRef] [PubMed]
16 Ederer F, Gaasterland DA, Dally LG, Kim J,
VanVeldhuisen PC, Blackwell B, Prum B, Shafranov G, Allen RC, Beck A; AGIS
Investigators. The Advanced Glaucoma Intervention Study (AGIS): 13. Comparison
of treatment outcomes within race: 10-year results. <ii>Ophthalmology</ii>
2004;111(4):651-664. [CrossRef] [PubMed]
17 Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson
B, Hussein M; Early Manifest Glaucoma Trial Group. Reduction of intraocular
pressure and glaucoma progression: results from the Early Manifest Glaucoma
Trial. <ii>Arch Ophthalmol </ii> 2002;120(10):1268-1279. [CrossRef] [PubMed]
18 Wang SY, Melles R, Lin SC. The impact of central
corneal thickness on the risk for glaucoma in a large multiethnic population.
<ii>J Glaucoma</ii> 2014;23(9):606-612. [CrossRef] [PMC free article] [PubMed]
19 Brandt JD, Beiser JA, Kass MA, Gordon MO. Central
corneal thickness in the Ocular Hypertension Treatment Study (OHTS).
<ii>Ophthalmology </ii> 2001;108(10):1779-1788. [CrossRef]
20 De Moraes CV, Hill V, Tello C, Liebmann JM, Ritch
R. Lower corneal hysteresis is associated with more rapid glaucomatous visual
field progression.<ii> J Glaucoma </ii> 2012;21(4):209-213. [CrossRef] [PubMed]
21 Medeiros FA, Meira-Freitas D, Lisboa R, Kuang TM,
Zangwill LM, Weinreb RN. Corneal hysteresis as a risk factor for glaucoma
progression: a prospective longitudinal study. <ii>Ophthalmology
</ii>2013;120(8):1533-1540. [CrossRef] [PMC free article] [PubMed]
22 Hsu CH, Chen RI, Lin SC. Myopia and glaucoma:
sorting out the difference. <ii>Curr Opin Ophthalmol </ii>
2015;26(2):90-95. [CrossRef] [PubMed]
23 Miki A, Ikuno Y, Asai T, Usui S, Nishida K. Defects
of the lamina cribrosa in high myopia and glaucoma. <ii>PLoS One
</ii> 2015;10(9):e0137909. [CrossRef] [PMC free article] [PubMed]
24 Chang RT, Singh K. Myopia and glaucoma: diagnostic
and therapeutic challenges. <ii>Curr Opin Ophthalmol</ii>
2013;24(2):96-101. [CrossRef] [PubMed]
25 Mallick J, Devi L, Malik PK, Mallick J. Update on
normal tension glaucoma. <ii>J Ophthalmic Vis Res</ii>
2016;11(2):204-208. [CrossRef] [PMC free article] [PubMed]
26 Kim SH, Lee EJ, Han JC, Sohn SW, Rhee T, Kee C. The
effect of diurnal fluctuation in intraocular pressure on the evaluation of risk
factors of progression in normal tension glaucoma. <ii>PLoS
One</ii> 2016;11(10):e0164876. [CrossRef] [PMC free article] [PubMed]
27 Gautam N, Kaur S, Kaushik S, Raj S, Pandav SS.
Postural and diurnal fluctuations in intraocular pressure across the spectrum
of glaucoma. <ii>Br J Ophthalmol</ii> 2016;100(4):537-541. [CrossRef] [PubMed]
<no>28 Pahlitzsch M, Brünner J, Gonnermann J,
Maier AB, Torun N, Bertelmann E, Klamann MK. Comparison of ICare and IOPen vs
Goldmann applanation tonometry according to international standards 8612 in
glaucoma patients. <ii>Int J Ophthalmol
</ii>2016;9(11):1624-1628.</no>
29 Gandhi NG, Jones SK, Freedman SF. Icare ONE home
tonometry in children with and without known glaucoma. <ii>J Glaucoma
</ii> 2016;25(2): e66-e69. [CrossRef] [PubMed]
30 Mudie LI, LaBarre S, Varadaraj V, Karakus S, Onnela
J, Munoz B, Friedman DS. The Icare HOME (TA022) Study: performance of an
intraocular pressure measuring device for self-tonometry by glaucoma patients.
<ii>Ophthalmology </ii> 2016;123(8):1675-1684. [CrossRef] [PubMed]
31 Borrego Sanz L, Morales-Fernandez L, Martínez
de-la-Casa JM, Sáenz-Francés F, Fuentes M, García-Feijóo J. The Icare-Pro
rebound tonometer versus the hand-held applanation tonometer in congenital
glaucoma. <ii>J Glaucoma </ii> 2016;25(2):149-154. [CrossRef] [PubMed]
32 Comparison of glaucomatous progression between
untreated patients with normal-tension glaucoma and patients with
therapeutically reduced intraocular pressures. Collaborative Normal-Tension
Glaucoma Study Group. <ii>Am J Ophthalmol </ii>
1998;126(4):487-497. [CrossRef]
33 Chong GT, Lee RK. Glaucoma versus red disease:
imaging and glaucoma diagnosis. <ii>Curr Opin Ophthalmol
</ii>2012;23(2):79-88. [CrossRef] [PubMed]
34 Wu H, de Boer JF, Chen TC. Diagnostic capability of
spectral-domain optical coherence tomography for glaucoma. <ii>Am J
Ophthalmol </ii>2012;153(5):815-826.e2. [CrossRef] [PMC free article] [PubMed]
35 Gracitelli CP, Abe RY, Medeiros FA. Spectral-domain
optical coherence tomography for glaucoma diagnosis. <ii>Open Ophthalmol
J </ii> 2015;9:68-77. [CrossRef] [PMC free article] [PubMed]
36 Abe RY, Gracitelli CP, Medeiros FA. The use of
spectral-domain optical coherence tomography to detect glaucoma progression.
<ii>Open Ophthalmol J </ii> 2015;9:78-88. [CrossRef] [PMC free article] [PubMed]
37 Bussel II, Wollstein G, Schuman JS. OCT for
glaucoma diagnosis, screening and detection of glaucoma progression.
<ii>Br J Ophthalmol </ii> 2014;98 Suppl 2:ii15-9. [CrossRef] [PMC free article] [PubMed]