Symposium

Natural history of glaucoma

Ying Pan, Rohit Varma

Purpose: To present an overview of the recent observations and research that shed light on the understanding
of open and closed angle glaucoma. Methods: Literature review. Results: Glaucoma is a major eye problem
afflicting millions of people worldwide. As the population increases, the number of people with glaucoma
also increases, with glaucoma becoming an increasing public health concern. This paper presents the
natural history of open angle and angle closure glaucoma. We examine the glaucomatous progression in
terms of changes in optic disk morphology and visual fi elds as well as the risk factors for progression.
Conclusions: This present review highlights the magnitude of glaucoma globally and the need for a greater
understanding of this disease and its natural progression.

Key words: Angle closure glaucoma, natural history definition of glaucoma, open angle glaucoma

Indian J Ophthalmol: 2011;59 Suppl 1:S19-23

DOI: 10.4103/0301-4738.73682 PMID: ***

Open and closed angle glaucoma are leading causes of blindness. however, IOP is the only modifiable risk factor that can be used
With aging of the population, the number of people with glaucoma to prevent progressive optic neuropathy.
is expected to rise, posing a substantial public health challenge
worldwide. Understanding the natural history of glaucoma is Magnitude of Glaucoma Worldwide
essential to our clinical practices
Glaucoma is the leading cause of irreversible blindness
The manifestations of glaucoma range from mechanical worldwide, and the second most common cause of blindness
angle closure of outflow structures in patients with angle after cataracts. [1,2] It is responsible for 14% of blindness
closure glaucoma (ACG), who typically present with ocular worldwide.[3] It afflicts almost 70 million people, of whom 10%
pain and acute visual loss, to increased resistance of outflow are believed to be bilaterally blind.[2]
in patients with open angle glaucoma (OAG), who are often
asymptomatic. Although glaucoma embodies a diverse group Several population-based studies have contributed to our
of diseases, all these diseases share common characteristics, the understanding of the incidence and prevalence of OAG within
hallmarks of which include progressive irreversible damage defined populations in the United States and other countries.
to the optic nerve head and the retinal ganglion cells with In the Baltimore Eye Survey, the prevalence of OAG was
corresponding visual field loss. significantly higher in blacks (4.7%) than in whites (1.3%).[4]
The Los Angeles Latino Eye Study[5] found that Latinos in the
Primary OAG is defined as a chronic optic neuropathy United States have a prevalence of OAG of 4.7%. The prevalence
with characteristic changes in the optic disc and visual field. of OAG in Asians varies widely, perhaps in part because the
Risk factors for OAG include older age, black race, family term Asian encompasses broad racial and ethnic categories.
history (first-degree relative), thinner central corneal thickness, Rudnicka et al. documented OAG rates in Asia to range from
myopia and elevated intraocular ocular pressure (IOP). ACG 1 to 4%,[6] whereas Ramakrishnan et al. found the prevalence
is characterized by the opposition of the iris to the trabecular of OAG in India to be 1.7%.[7]
meshwork, resulting in blockage of the aqueous outflow. Risk
factors for developing angle closure include Asian race, female In Asian populations, ACG is the main cause of morbidity
gender and advanced age. Anatomic features predisposing to from glaucoma. ACG blinds 10-times more people than OAG
angle closure are hyperopia, anterior iris insertion and shallow does, and the worldwide incidence of ACG is growing.[8] While
anterior chamber. ACG represents only 10–15% of all glaucomas in the black and
white populations, it accounts for a significant percentage of
It is important to note that the definition of glaucoma has glaucomas that occur in Asian populations. The rate of ACG
evolved from a disease of eye pressure to a disease of optic among Chinese is three-times that of OAG.[1] Approximately
neuropathy. An elevated IOP in the affected eye is now seen 91% of bilateral blindness in China is due to ACG.[9] Vijaya
as a risk factor for glaucoma rather than its cause. Presently, et al. found that 2.75% of the population had angle closure and
0.88% had ACG.[10] The Andhra Pradesh Eye Disease Survey in
south India suggests that 0.7% of the population over 30 years
Doheny Eye Institute, University of Southern California, Los Angeles, of age has ACG.[11]
CA, USA
Glaucomatous Morphology of the Optic
Correspondence to: Dr Rohit Varma, Doheny Eye Institute, 1450 San
Pablo Street, Los Angeles, CA 90033, USA. E-mail: rvarma@usc.edu Nerve
Manuscript received: 28.02.10; Revision accepted: 14.10.10 Glaucoma damages the ganglion cell and its respective axons,
S20 Indian Journal of Ophthalmology Vol. 59 Suppl. 1

which comprise the retinal nerve fiber layer (rNFL). This visual fields and/or localized visual field defects. In these
results in progressive and asymmetric changes in the optic earlier stages, peripheral changes in visual fields may be the
cup, with corresponding visual field loss. Typically, structural only detectable abnormality. Increasing scatter and fluctuation
changes occur before functional loss. Up to 40% of the retinal is often noted. Isolated defects tend to occur in the superior
nerve fibers may be destroyed before detectable changes in half of the visual field because of the susceptibility of the
visual field. The morphology of these rNFL defects follows the inferior poles of the optic nerve in early glaucomatous damage.
normal structural pattern of the rNFL in the retina. Normally, Although central vision is preserved during the early course
rNFL has a striated appearance, radiating from the optic disk, of glaucoma, defects can involve the fixation point. Isolated
and is thickest in the superior and inferior poles, compared paracentral defects can appear as the initial glaucoma defect
with the nasal and the temporal poles. Glaucomatous rNFL in 41% of the patients.[16]
changes can present as focal wedge-shaped defects of varying
Progression in visual fields can occur in a variety of ways.
width radiating from the optic nerve head or as diffuse loss
There can be gradual but steady decrease in retinal sensitivity
of the striations in rNFL.[12] Because glaucoma tends to afflict
affecting the field uniformly. Initial defects that were shallow
the superior and inferior nerve fibers preferentially, focal loss
can coalesce, extend, deepen and enlarge into nasal steps,
is often detected in these areas.
arcuate scotomas or complete altitudinal defect. New defects
Disc changes present with a variety of characteristic can also appear with further progression. For example, in
patterns. As ganglion cells and their axons are destroyed, the advanced glaucoma, arcuate scotomas can manifest superiorly
neural rim begins to thin. Typically, localized thinning in early and inferiorly, forming a double arcuate scotoma. This double
glaucoma can lead to focal atrophy of the neural rim, known arcuate scotoma comes together nasally at the horizontal
as focal notching. This tends to occur in the inferotemporal meridian, creating the central and temporal islands seen in
region of the optic nerve head because of preferential loss of advanced glaucoma. With the destruction of the remaining
the inferior nerve fibers. This is followed, to a lesser extent, by areas of the macular fibers and the nasal retina, these islands
focal neural loss and atrophy in the superotemporal region. continue to disappear until they are extinguished. Temporal
As a result, the optic cup usually enlarges in a vertical or islands may be more resistant and may persist after central
oblique fashion. As the glaucomatous process progresses, the islands are lost. However, these too can be destroyed, leaving
temporal rim becomes involved. The nasal quadrant is the last patients with complete visual loss.
to be affected. Early glaucomatous damage can also lead to
progressive, generalized and concentric expansion of the nerve Natural History of Open Angle Glaucoma
cup. In some cases, early glaucomatous optic atrophy presents The lack of symptoms in OAG plays a large role in delaying its
with deepening of the cup, exposing the underlying lamina detection and diagnosis. Typically, OAG is slowly progressive,
cribrosa. In other cases, early glaucoma can be evidenced by remaining asymptomatic until late. By the time OAG becomes
saucerization of the disc, in which shallow sloping and cupping symptomatic, severe and irreversible damage has usually
extend to the margins of the disk. Progressive glaucoma results occurred to the visual field in one or both eyes. The rate
in axonal loss and backward bowing of the lamina cribrosa, of progression of the visual field defect varies in patients,
leading to enlargement and/or excavation of the cup. Loss of all and treatment of the glaucoma may not completely halt the
neural rim tissue with exposure of the laminar pores can be seen visual field loss.[17] Some patients progress despite aggressive
in advanced glaucoma. Complete cupping with undermining therapy.[18]
of the neural rim produces a bean pot appearance, with a pale
disc and vessels that bend at the margins of the disc. The incidence of blindness 20 years after the initial diagnosis
of OAG has been estimated at 27% for one eye and 9% for both
Vascular signs of glaucomatous optic atrophy include eyes in a primarily white population.[19] Data from population-
splinter hemorrhages that result due to loss of axons at the optic based, cross-sectional studies revealed that for patients with
nerve head and reflect progressive rNFL damage. They occur OAG, the mean change in visual field testing for European-
more commonly in patients with normal-tension glaucoma derived, Hispanic, African-derived and Chinese was −1.12,
(NTG) than those with primary OAG, with a cumulative −1.26, −1.33 and −1.56 dB/year, respectively. The differences
incidence of 35.3% and 10.3%, respectively.[13] The most common in the mean deviation (MD) were not statistically significant
location for these hemorrhages is the temporal rim, followed by ethnicity. Because some participants were treated, the data
by the inferior and superior rim. Rarely, splinter hemorrhages cannot be used to represent the natural history of OAG.[20]
occur nasally. They are most often seen in the early to middle
The Ocular Hypertension Treatment Study elucidated the
stages of glaucoma and are a prognostic sign of progressive
natural history of OAG by identifying the rate of conversion
disease. The hemorrhages leave behind a focal area of rNFL
from ocular hypertension to primary OAG and the impact of
defect, focal notching and a corresponding visual field
treating IOP (decreasing IOP more than 20% from baseline)
defect. [14,15] The disappearance of neural rim can lead to
on the development of OAG. After 60 months of follow-up,
overpassing vessels. The bending of the retinal vessels
conversion to OAG from ocular hypertension was 4.4% in the
along the edge of a disappearing rim is termed bayoneting.
treated group as compared with 9.5% in the untreated group.
Circumlinear vessels may be also bared from the margin of
Thus, a protective effect of 54% was seen with treatment.
the cup. In advanced glaucoma, the central vessels can be
However, over 90% of the untreated subjects did not develop
nasally displaced.
visual field or disc changes consistent with OAG during
this time. To prevent one patient with ocular hypertension
Glaucomatous Visual Field Progression
from developing glaucoma, 19 would need to be treated
Early glaucoma can create mild, diffuse depression in the unnecessarily if the risk factors were ignored. Baseline factors
 Pan and Varma: Natural history of glaucoma
Glaucoma Supplement S21

associated with the conversion to OAG included advanced a more aggressive disease, with a mean progression rate
age, elevated IOP, central corneal thickness thinner than the corresponding to full-field blindness within 10 years. In
study mean, increased cup-to-disc ratio and increased pattern addition, glaucoma patients with higher IOP are more likely
standard deviation on the visual field.[21,22] to progress rapidly than those with IOP <21. NTG patients
progressed more slowly and had a lower risk of rapid evolution
Data from individuals in the Early Manifest Glaucoma Trial
to blindness. Therefore, the immediacy and aggressiveness of
(EMGT) randomized to the no-treatment group shed light on
therapy for these patients may be less than that for patients with
the natural course of newly detected OAG and can be used to
HTG and PXEG. That being said, high intragroup variability
predict the likelihood of visual loss from glaucoma. After 4
exists and, therefore, treatment should be guided by individual
years of follow-up, 49% of the individuals without treatment
presentation.
progressed, compared with 30% with treatment (an average
IOP lowering of 25%).[23,24] After 6 years of follow-up, 68% of The EMGT and the CNTG are the only two prospective
the untreated patients showed definite visual field progression, studies that studied large groups of people with glaucoma
with an overall median time to progression of 42.8 months. without treatment. These two studies have provided important
The study also revealed a very large variation in time to data on the natural course of OAG and on its risk factors for
progression among the subjects. Some progress rapidly, with progression. Patients need to be monitored carefully after
a deterioration in the MD index of greater than 10 dB per year; being diagnosed with glaucoma to determine the rapidity of
others did not progress at all, even after lengthy follow-up. Of glaucoma progression. Individualized treatment plans must be
those individuals in the high-tension glaucoma (HTG) group tailored to patients and to their rate of progression.
(with elevated IOP ≥21 mm Hg), 74% had progressed, with
a median time to progression of 44.8 months, while 56% of Natural History of Angle Closure Glaucoma
those individuals with NTG progressed, with a median time to Although OAG is more common worldwide, ACG causes more
progression of 61.1 months. Of the pseudoexfoliation patients serious loss of vision than OAG.[9] ACGs are characterized
(PXEG), 93% progressed, with a median time to progression by apposition of the peripheral iris against the trabecular
of 19.5 months. Thus, the visual field loss progressed for meshwork, resulting in obstruction of the aqueous outflow.
most of these patients; the majority progressed slowly, but a The main mechanisms of closure are pupillary block, plateau
minority progressed rapidly. Specifically, in the PXEG group, iris, lens-related and retrolenticular causes. The most common
the MD on automated visual field testing was −3.13 dB/year.
cause is pupillary block.
The perimetric MD for the NTG group and the HTG group
was −0.36 dB/year and −1.31 dB/year, respectively.[25] Large ACG may be divided into acute, subacute and chronic ACG.
variations existed between the rates of progression in visual Although they represent different clinical manifestations, they
field for HTG, NTG and PXEG as well as among subjects within can occur at different times in the same person. In acute ACG,
each group. closure of the angle occurs suddenly, resulting in rapid rise in
IOP. The affected person may present with dramatic symptoms
This variability in clinical course was also found by the
of severe ocular pain, nausea, vomiting, headache and blurred
Collaborative Normal Tension Glaucoma Study (CNTGS).
vision. Subacute or intermittent ACG occurs when episodes of
Similar to the EMGT, the CNTGS documented the natural
pupillary block resolve spontaneously and can recur repeatedly
course of untreated NTG.[26] The study specifically focused on
over time. Chronic ACG develops when the angle narrows
patients with glaucomatous optic nerve damage and visual
slowly and results in scarring between the peripheral iris and
field loss accompanied by IOP in the normal range. While some
the trabecular meshwork.
believe that NTG represents a distinct variety of glaucoma from
primary OAG, the two most likely represent a continuum of The natural history of ACG has been subdivided into three
glaucomas. After 5–7 years of follow-up, progression of the stages: (1) an anatomically narrow angle without elevated IOP,
visual field defect was noted in 60% of those individuals with abnormal visual fields or peripheral anterior synechia (primary
untreated glaucoma with optic nerve damage, visual loss and angle closure suspect [PAC]), (2) development of peripheral
IOP under 21 mmHg. Treatment targeting IOP lowering of anterior synechia or a closed angle with elevated IOP, labeled
>30% decreased the progression rate to 20%.[26] Most cases PAC and (3) development of an anatomical angle closure with
progressed slowly, requiring several years to demonstrate glaucomatous optic nerve and visual field changes, termed
progression; in other cases, deterioration manifested within 1 primary angle closure glaucoma (PACG).[27]
year. The mean estimated slope of the MD index deterioration
Although the prevalence and pattern of disease varies across
for all untreated subjects was −0.41 dB/year. However, the MD
different parts of the world, the majority of those with ACG
index ranged from −0.2 dB/year to −2 dB or more/year. This 10-
will be Asian due to their anatomical predisposition. Data
fold range reflects the broad range in the rates of deterioration.
on the natural history of ACG are limited. Large population-
Because the course of glaucomatous progression is highly based data on the disease progression are nonexistent. In one
variable, identifying factors that predict progression can help small study, 22% of the normal patients with narrow angles
guide clinical practice and patient treatment and monitoring. developed synechial angle closure (64%) or appositional
In the EMGT, faster and greater progression was noted in angle closure (36%) over a period of 5 years.[28] Of 28 subjects
older patients (≥68 years of age) when compared with younger who were identified as having PAC, eight progressed to
patients. Frequent disc hemorrhages predict faster progression, PACG within 5 years. Only one of the nine participants who
as did bilateral disease and greater visual field loss at initial underwent laser peripheral iridotomy (LPI) progressed
diagnosis, as measured by perimetric MD. PXEG glaucoma, compared with seven of 19 subjects who refused the laser
when compared with NTG and HTG, was also noted to be iridotomy.[28] Publications on response to treatment provide
S22 Indian Journal of Ophthalmology Vol. 59 Suppl. 1

important insight into the natural history of angle closure. 9. Foster PJ, Johnson GJ. Glaucoma in China: how big is the problem?
The first-line treatment of LPI relieves the relative pupillary Br J Ophthalmol 2001;85:1277-82.
block element. The response to LPI and the long-term course 10. Vijaya L, George R, Arvind H, Baskaran M, Ve Ramesh S, Raju P,
of PACG appears to vary by race. Studies found that LPI in et al. Prevalence of primary angle closure disease in an urban south
Caucasian subjects with ACG were more likely to effectively Indian population and comparision with a rural population. The
Chennai Glaucoma Study. Ophthalmology 2008;115:655-60.
prevent the subsequent need for surgical intervention than
LPI in Asian subjects. Intraocular pressure was controlled 11. Dandona L, Dandona R, Mandal P, Srinivas M, John RK, McCarty
with LPI alone in 65–76% of eyes, with only 0–13% of the CA, et al. Angle closure glaucoma in an urban population
in Southern India. The Andhra Pradesh eye disease study.
eyes requiring subsequent filtering surgery. [29-33] In Asian
Ophthalmology 2000;107:1710-6.
populations, however, Alsagoff et al. found that the majority of
12. Tuulonen A, Airaksinen PJ. Initial glaucomatous optic disk and
eyes with established ACG required antiglaucoma medications
retinal nerve fiber layer abnormalities and their progression. Am
or filtering surgery, despite undergoing treatment with J Ophthalmol 1991;111:485.
LPI.[34] The disease in Asians appears to be more aggressive.
13. Hendrickx KH, van den Enden A, Rasker MT, Hoyng PF.
Even after laser iridotomy for eyes with narrow angles, the Cumulative incidence of patients with disc hemorrhages in
rates of progression to ACG can be significant. A decade after glaucoma and the effect of therapy. Ophthalmology 1994;101:1165.
treatment for acute PAC, 47.8% of the patients developed
14. Jonas JB, Xu L. Optic disk hemorrhages in glaucoma. Am J
glaucomatous optic neuropathy.[35] Aung et al. found that Ophthalmol 1994;181:1-8.
several years after the initial attack of acute angle closure in
15. Shihab ZM, Lee PF, Hay P. The significance of disc hemorrhage in
Asian subjects, 17.8% were blind in the affected eye and half open-angle glaucoma. Ophthalmology 1982;89:211-3.
had blindness caused by the advanced glaucoma.[35] Thus,
16. Choplin NT. Psychophysical and electrophysiological testing in
Asian patients are at a higher risk of further glaucomatous
glaucoma. In: Choplin NT, Lundy DC, editors. Atlas of glaucoma.
damage even after patent LPI and would benefit from long- 2nd ed. Boca Raton, FL: Taylor and Francis; 2007. p. 89-115.
term follow-up.
17. Leske MC, Heijl A, Hyman L, Bengtsson B, Komaroff E. Factors for
progression and glaucoma treatment: the Early Manifest Glaucoma
Glaucoma Screening and Prevention Trial. Curr Opin Ophthalmol 2004;15:102-6.
As the number of people with glaucoma is expected to grow, 18. Oliver JE. Hattenhauer MG, Herman D, Hodge DO, Kennedy
glaucoma will become an increasing public health problem in R, Fang-Yen M, et al. Blindness and glaucoma: A comparision of
the coming decade. Undiagnosed glaucoma could underlie a patients progressing to blindness from glaucoma with patients
potentially large number of cases of preventable blindness. maintaining vision. Am J Ophthalmol 2002;133:764-72.
Using risk factors for glaucoma to provide guidelines for 19. Hattenhauer MG, Johnson DH, Ing HH, Herman DC, Hodge
targeting at-risk groups, to improve early glaucoma detection DO, Yawn BP, et al. The probability of blindness from open-angle
glaucoma. Ophthalmology 1998;105:2099-104.
and treatment are currently the most powerful tools for
preventing blindness and low vision in this predominantly 20. Broman AT, Quigley HA, West SK, Katz J, Munoz B, Bandeen-Roche
K, et al. Estimating the rate of progressive visual field damage in
asymptomatic disease in its early stages.
those with open-angle glaucoma, from cross-sectional data. Invest
Ophthalmol Vis Sci 2008;49:66-76
References
21. Gordon MO, Beiser JA, Brandt JD, Heuer DK, Higginbotham EJ,
1. Quigley HA. Number of people with glaucoma worldwide. Br J Johnson CA, et al. The Ocular Hypertension Treatment Study:
Ophthalmol 1996;80:389-93. baseline factors that predict the onset of primary open-angle
2. Congdon N, O’Colmain B, Klaver CC, Klein R, Munoz B, Friedman glaucoma. Arch Ophthalmol 2002;120:714-20.
DS, et al. Causes and prevalence of visual impairment among adults 22. Kass MA, Heuer DK, Higginbotham EJ, Johnson CA, Keltner
in the United States. Arch Ophthalmol 2004;122;477-85. JL, Miller JP, et al. The Ocular Hypertension Treatment Study:
3. Thylefors DS, Negrel AD, Pararajasegaram R, Dadzie KY. Global a randomized trial determines that topical ocular hypotensive
data on blindness. Bull World Health Organ 1995;73:115-21. medication delays or prevents the onset of primary open-angle
glaucoma. Arch Ophthalmol 2002;120:701-13.
4. Sommer A, Tielsch JM, Katz J, Quigley HA, Gottsch JD, Javitt J,
et al. Relationship between intraocular pressure and primary open- 23. Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson B, Hussein
angle glaucoma among white and black Americans: The Baltimore M; Early Manifest Glaucoma Trial Group. Reduction of intraocular
Eye Survey. Arch Ophthalmol 1991;109:1090-5. pressure and glaucoma progression: results from the Early
Manifest Glaucoma Trial. Arch Ophthalmol 2002;120:1268-79.
5. Varma R, Ying-Lai M, Francis BA, Nguyen BB, Deneen J, Wilson
MR, et al. Prevalence of open-angle glaucoma and ocular 24. Leske MC, Heijl A, Hyman L, Bengtsson B. Early Manifest
hypertension in Latinos: the Los Angeles Latino Eye Study. Glaucoma Trial: design and baseline data. Ophthalmology
Ophthalmology 2004;111:1439-48. 1999;106:2144-53.
6. Rudnicka AR, Mt-Isa S, Owen CG, Cook DG, Ashby D. Variations 25. Heijl A, Bengtsson B, Hyman L, Leske MC, Early Manifest
in primary open-angle glaucoma prevalence by age, gender, and Glaucoma Trial Group. Natural history of open-angle glaucoma.
race: a Bayesian meta-analysis. Invest Ophthalmol Vis Sci 2006;47: Ophthalmology 2009;116:2271-6.
4254-61. 26. The effectiveness of intraocular pressure reduction in the treatment
7. Ramakrishnan R, Nirmalan PK, Krishnadas R, Thulasiraj RD, of normal-tension glaucoma. Collaborative Normal Tension
Tielsch JM, Katz J, et al. Glaucoma in a rural population of southern Glaucoma Study Group. Am J Ophthalmol 1998;126:498-505.
India: the Aravind comprehensive eye survey. Ophthalmology 27. American Academy of Ophthalmology. Primary angle-closure.
2003;110:1484-90. In: Caprioli J, Gaasterland DE, Gross RL, Jampel H. Kolker AE,
8. Foster PJ. The epidemiology of primary angle closure and Lampin KA, et al. editors. San Francisco: American Academy of
associated glaucomatous optic neuropathy. Semin Ophthalmol Ophthalmology; 2000.
2002;17:50-8. 28. Thomas R, Parikh R, Muliyil J, Kumar RS. Five-year risk of
 Pan and Varma: Natural history of glaucoma
Glaucoma Supplement S23

progression of primary angle closure to primary angle closure: a 1979;63:17-22.

population-based study. Acta Ophthalmol Scand 2003;81:480-5. 34. Alsagoff Z, Aung T, Ang LP, Chew PT. Long-term clinical course
29. Robin AL, Pollack IP. Argon laser peripheral iridotomies in the of primary angle-closure glaucoma in an Asian population.
treatment of primary angle closure glaucoma. Long-term follow- Ophthalmology 2000;107:2300-4.
up. Arch Ophthalmol 1982;100:919-23. 35. Aung T, Friedman DS, Chew PT, Ang LP, Gazzard G, Lai YF, et al.
30. Gieser DK, Wilensky JT. Laser iridectomy in the management of Long-term outcomes in Asians after acute primary angle closure.
chronic angle-closure glaucoma. Am J Ophthalmol 1984;98:446-50. Ophthalmology 2004;111:1464-9.
31. Buckley SA, Reeves B, Burdon M, Moorman C, Wheatcroft S,
Edelsten C, et al. Acute angle close glaucoma: Relative failure of
YAG iridotomy in affected eyes and factors influencing outcome. Publication of the supplement was not supported by any external funding. The
Br J Ophthalmol 1994;78:529-33. Editors, Authors and others involved with the journal did not get any financial
or non-financial benefit from any sponsors, unless specified otherwise in the
32. Krupin T, Mitchell KB, Johnson MF, Becker B. The long-term effects Source of Support at the end of individual articles. I confirm that none of the articles
of iridectomy for primary acute angle-closure glaucoma. Am J appearing in the Glaucoma Supplement are sponsored articles.
Ophthalmol 1978;86:506-9.
33. Playfair TJ, Watson PG. Management of acute primary angle-
closure glaucoma: A long-term follow-up of the results of Source of Support: Nil, Conflict of Interest: None declared.
peripheral iridectomy used as an initial procedure. Br J Ophthalmol