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A S I A PA C I F I C
Asia Pacific Glaucoma Guidelines
Glaucoma Guidelines
SEAGIG
2004
ISBN 0-9751692-0-3
www.seagig.org
Cover
20/11/03
9:21 AM
Page 2
DISCLAIMER
These guidelines for clinical practice are based on the best available evidence at the
time of development. They are not intended to serve as standards of medical care.
The use of these recommendations is the decision of each clinician, who is ultimately
responsible for the management of his/her patient. The South East Asia Glaucoma
Interest Group (SEAGIG) and the Asian-Oceanic Glaucoma Society (AOGS), together with
the contributors, reviewers, sponsor and publisher, disclaim responsibility and liability
for any injury, adverse medical or legal effects resulting directly or indirectly from the
use of these Guidelines. All clinical diagnoses, procedures and drug regimens/doses must
be independently verified. All products mentioned in this publication should be used in
accordance with the manufacturers instructions or prescribing information.
Printed in Singapore
ISBN 0-9751692-0-3
A S I A PA C I F I C
Glaucoma Guidelines
Foreword
By increasing awareness and knowledge of glaucoma across the Asia
Pacific region, these Guidelines aim to reduce glaucomatous visual
disability and to provide a rational basis for glaucoma management.
The establishment of best-practice methodologies throughout the Asia
Pacific region represents a unique challenge, given our diverse healthcare
service systems and wide range of available resources. To address this
need, the South East Asia Glaucoma Interest Group (SEAGIG), with the
support of the Asian-Oceanic Glaucoma Society (AOGS), convened an
Asia Pacific Glaucoma Guidelines Working Party to develop comprehensive
Glaucoma Guidelines for the Asia Pacific region.
The members of the Working Party collaborated during a series of
meetings to compile information and recommendations to assist
comprehensive ophthalmologists, general healthcare and eye care
professionals, as well as healthcare policy makers to deliver effective
glaucoma management to their communities. An extensive Review
Committee assessed the results and made significant contributions to
the final manuscript.
As these Guidelines rely on direct medical experience and, wherever
possible, on published evidence, they are as up-to-date as possible.
The Asia Pacific Glaucoma Guidelines Working Party is committed to
providing updates to the Guidelines on a regular basis.
Critical to the development of the Asia Pacific Glaucoma Guidelines has
been the support of the AOGS, and a generous educational grant from
then Pharmacia Corporation (now Pfizer Inc.). This sponsorship permitted
the Working Party to meet and to produce, publish and distribute these
Guidelines.
Contributors
Gus Guzzard (UK)
Ching Lin Ho (Singapore)
ii
iii
ACKNOWLEDGEMENT
iv
Contents
Page
Foreword
Acknowledgement
iv
Introduction
Section 1
1.1 Patient Assessment
11
25
Section 2
2.1 Initiation of Treatment
31
33
41
2.4 Surgery
51
Section 3
3.1 Follow-up
59
Case Detection
67
Appendices
75
88
Definition of Terms
89
Index
91
List of Appendices
Appendix
vi
Page
76
Tonometry mires
77
3a
Gonioscopy
78
3b
Goniogram/gonioscopic chart
79
3c
80
81
82
83
7a
84
7b
85
86
87
Introduction
Introduction
In 1996, with the support of the American Glaucoma Society, the American
Academy of Ophthalmology produced its Preferred Practice Pattern for
Primary Open-Angle Glaucoma,1 followed four years later by an update2
and two additional volumes on Primary Angle Closure3 and Primary OpenAngle Glaucoma Suspect.4 These guidelines identify characteristics and
components of quality eye care commensurate with present knowledge
and resources this translates into guidance for state-of-the-art patterns
of practice, which should be helpful in the care of most patients, rather
than any particular individual. Where data permits, these guidelines are
firmly evidence-based; otherwise they rely on consensus opinion. Similarly,
the European Glaucoma Society published its Terminology and Guidelines
for Glaucoma in 1998,5 with the aim of improving the mutual
understanding of this disease in addition to providing a rational approach
to the diagnosis and management of glaucoma. This year a Second Edition
has been released.6 These projects have set out to complement existing
scientific literature, and involved input from many glaucoma sub-specialists.
The resulting publications have proven useful for, and thus popular with,
comprehensive ophthalmologists around the world. They have also been
useful in communications with allied eye healthcare professionals, as well
as governmental agencies and non-governmental organizations.
Over the past 20 years, increasing epidemiological data from across the
Asia Pacific region has highlighted the varying prevalence and incidence
rates, diagnostic types and behavior of different glaucoma disease patterns
encountered by the ophthalmological community. With the availability of
this information, the need for similar guidelines relevant to our region can
now be met. Such guidelines must be sensitive to the wide variations in
human, structural and equipment resources available throughout the
region, as well as the ethnic diversity of our communities. What is
applicable in one country or location may not be in another.
These Guidelines have been developed during a time of rapidly expanding
medical technology, knowledge and skills in a changing environment.
As public awareness and expectations increase, and as the population ages
(even in less developed societies), there is an increasing demand for
high-level care for a greater number of people over extended periods of
time. However, available resources have been unable to expand
proportionally. As cost containment is an inescapable reality, every
treatment or investigation that is undertaken reduces the capacity to
implement another intervention that could benefit another patient.
Therefore, what we, as clinicians, do for our patients needs to be
demonstrated to be effective. If not, it must at least be recognized to
be only partly proven or as yet unproven. Guided by this knowledge, our
lines of enquiry can be channeled appropriately.
References
1 American Academy of Ophthalmology. Preferred Practice Pattern: Primary Open-Angle
Glaucoma, 1996.
2 American Academy of Ophthalmology. Preferred Practice Pattern: Primary Open-Angle
Glaucoma, 2000.
3 American Academy of Ophthalmology. Preferred Practice Pattern: Primary Angle
Closure, 2000.
4 American Academy of Ophthalmology. Preferred Practice Pattern: Primary Open-Angle
Glaucoma Suspect, 2000.
5 European Glaucoma Society. Terminology and Guidelines for Glaucoma, 1998, Italy:
Dogma.
6 European Glaucoma Society. Terminology and Guidelines for Glaucoma, IInd Edition,
2003, Italy: Dogma.
Incidence of
symptomatic,
acute angle
closure
Glaucoma
blindness
Risk factors
for
glaucoma
Advancing age is the single most consistent risk factor for all types of
glaucoma.4,5,7,10,1216 A positive family history is also a risk factor for
glaucoma.17,18 Female gender is recognized as a major predisposing factor
toward the development of PACG.7,13,16 There is little clear evidence to
support a gender difference in POAG. Those of Chinese ethnic origin are
at a higher risk of developing angle closure than those of Malay descent
and South Indian people.4,5 Raised intraocular pressure (IOP) is a risk factor
for glaucomatous optic neuropathy in Chinese people.19
5
References:
1.
2.
Foster PJ, Johnson GJ. Glaucoma in China: how big is the problem? Br J Ophthalmol
2001;85:12771282.
3.
4.
Seah SKL, Foster PJ, Chew PT, et al. Incidence of acute primary angle-closure
glaucoma in Singapore. An Island-Wide Survey. Arch Ophthalmol
1997;115:14361440.
5.
Wong TY, Foster PJ, Seah SKL, et al. Rates of hospital admissions for primary angle
closure glaucoma among Chinese, Malays, and Indians in Singapore. Br J Ophthalmol
2000;84:990992.
6.
Baasanhu J, Johnson GJ, Burendei G, et al. Prevalence and causes of blindness and
visual impairment in Mongolia: a survey of populations aged 40 years and older. Bull
World Health Organization 1994;72:771776.
7.
Foster PJ, Oen FT, Machin DS, et al. The prevalence of glaucoma in Chinese residents
of Singapore. A cross-sectional population survey in Tanjong Pagar district. Arch
Ophthalmol 2000;118:11051111.
8.
9.
Tso MOM, Naumann GO, Zhang S. Editorial Studies of the prevalence of blindness
in the Asia-Pacific region and the worldwide initiative in ophthalmic education. Am J
Ophthalmol 1998;126:582585.
10. Dandona L, Dandona R, Naduvilath TJ, et al. Is current eye-care-policy focus almost
exclusively on cataract adequate to deal with blindness in India? Lancet
1998;351:13121316.
11. Thulasiraj RD, Nirmalan OK, Ramakrishnan R, et al. Blindness and vision impairment
in a rural south Indian population: the Aravind Comprehensive Eye Survey.
Ophthalmology 2003;110:14911498.
12. 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;107:17101716.
13. Foster PJ, Baasanhu J, Alsbirk PH, et al. Glaucoma in Mongolia A population-based
survey in Hvsgl Province, Northern Mongolia. Arch Ophthalmol
1996;114:12351241.
14. Wensor MD, McCarty CA, Stanislavsky YL, et al. The prevalence of glaucoma in the
Melbourne Visual Impariment Project. Ophthalmology 1998;105:733739.
15. Mitchell P, Smith W, Attebo W, et al. Prevalence of open-angle glaucoma in Australia.
The Blue Mountains Eye Study. Ophthalmology 1996;103:16611669.
16. Shiose Y, Kitazawa Y, Tsukuhara S, et al. Epidemiology of glaucoma in Japan A
nationwide glaucoma survey. Jpn J Ophthalmol 1991;35:133155.
17. Leske MC, Connell AM, Wu SY, et al. Risk factors for open angle glaucoma. The
Barbados Eye Study. Arch Ophthalmol 1995;113(7):91824.
18. McNaught AI, Allen JG, Healey DL, et al. Accuracy and implications of a reported
family history of glaucoma: experience from the Glaucoma Inheritance Study in
Tasmania. Arch Ophthalmol 2000;118(7):900904.
19. Foster PJ, Machin D, Wong TY, et al. Determinants of intraocular pressure and its
association with glaucomatous optic neuropathy in Chinese Singaporeans: the
Tanjong Pagar Study. Invest Ophthalmol Vis Sci 2003;44(9):38853891.
20. Trnquist R. Shallow anterior chamber in acute angle-closure. A clinical and genetic
study. Acta Ophthalmol 1953;31(Suppl. 39):174.
21. Okabe I, Taniguchi T, Yamamtoo T, et al.. Age-related changes of the anterior
chamber width. J Glaucoma 1992;1:100107.
22. Foster PJ, Alsbirk PH, Baasanhu J, et al. Anterior chamber depth in Mongolians.
Variation with age, sex and method of measurement. Am J Ophthalmol
1997;124:5360.
23. Mitchell P, Hourihan F, Sandbach J, et al. The relationship between glaucoma and
myopia. The Blue Mountains Eye Study. Ophthalmology 1999;106:20102015.
24. Krishnadas R, Nirmalan PK, Ramakrishnan R, et al. Pseudoexfoliation in a rural
population of southern India: the Aravind Comprehensive Eye Survey. Am J
Ophthalmol 2003;135:8307.
Section 1
10
Patient Assessment
Why assess?
What to
assess?
Understand the natural history of the glaucomas in your region. The initial
assessment can be divided into two phases:
1. History
2. Examination/investigations
History
Key points:
Most glaucomas, including angle closure glaucoma (ACG), are
asymptomatic until advanced
Assess medical and social factors that will affect treatment decisions
Older age and family history of glaucoma are particularly important
Younger age means a longer exposure to glaucoma and its treatment
11
Cardiovascular
12
Patient Assessment
Endocrine
Central
nervous system
Musculoskeletal
Urogenital
Ocular trauma
Pregnancy and
lactation
Medication
Use of any current medication needs to be considered, along with
certain specific past medications, including:
a) Steroids any route of administration is associated with ocular
hypertension, open angle glaucoma. Sometimes found in
traditional medicines
b) Glaucoma drops (prolonged use may increase trabeculectomy failure)
c) Anticholinergics/tricyclic antidepressants can cause angle closure
d) Anticonvulsants (vigabatrin) linked to nasal peripheral field loss
without disc changes
e) Systemic -blockers/calcium channel blockers may interact with
topical -blockers
13
Social history
Consider:
How regularly can the patient attend?
Can the patient afford and comply with treatment?
How will having glaucoma affect the patients life/work/family (disease
and treatment)?
Family history
Consider:
What is the disease type and course in the family? (See Epidemiology).
14
Patient Assessment
Slit lamp
examination
tonometry
How to
Why?
perform
Goldmann
What?
tonometry?
Intraocular pressure (IOP) is the only modifiable risk factor for glaucoma.
When?
Every visit.
How to
perform
Goldmann
tonometry?
Central corneal
thickness
Blood pressure
Age
Exercise
Lifestyle
Posture
15
Anterior segment
When examining the anterior segment, look for:
Globe surface:
episcleral blood vessels
follicles.
16
Patient Assessment
Anterior chamber:
pigment on corneal endothelium (pigment dispersion)
peripheral anterior chamber depth (van Herick technique)
central anterior chamber depth
evidence of inflammation (e.g., keratic precipitates).
Iris:
mid-dilated poorly reactive (post angle closure attack)
isolated zones of patch atrophy or spiraling
rubeosis
synechiae
configuration in relation to lens
pseudoexfoliation material on pupil edge
pigment deposit on anterior surface
transillumination defect.
Lens:
pseudoexfoliation material
lens thickness and opacity
phacodonesis
glaukomflecken.
Gonioscopy
Why?
What to look
for?
When?
How to
perform
gonioscopy?
17
Place lens gently on eye while looking through slit lamp (as if you are
doing tonometry) no gel needed with Zeiss-type lenses.
Look through the upper mirror (inferior angle) as you place lens on eye,
stop pushing when you can see the iris.
Move slit lamp beam inferiorly (avoid pupil) to examine superior angle
Then turn beam 90 degrees and move on axis.
Move to nasal side (temporal angle) then to temporal side (nasal angle).
Record findings on goniogram.
(see Appendix 3b: Goniogram/Gonioscopic chart)
Tip: If you cannot find the angle structures, use a bright wide slit (parallel to the mirror)
at low magnification. Once you have found the angle structures, turn the illumination
down, shorten and narrow the slit and look for the change in iris/angle configuration.
You may need to wait a minute or so.
NO
Do indentation gonioscopy
Any synechiae?
YES
Grade: Record findings
Open angle
YES
Grade: Record findings
NO
IOP raised?
PAC (synechiae)
YES
Grade: Record findings
NO
Grade: Record findings
PAC (apposition)
PACS
18
Patient Assessment
Optic nerve
head and
retinal
nerve fiber
layer
Why?
Defines glaucoma.
What to look
for?
Disc size.
Neuroretinal rim.
Disc hemorrhage.
Nerve fiber layer defect.
Peripapillary atrophy (PPA).
Vascular pattern.
When?
Every visit.
How to
perform disc
examination?
Consider:
Non-glaucomatous optic neuropathies. Differentiate anterior ischemic
optic neuropathy (AION) from glaucoma especially giant cell arteritis.9,10
Both cause pale cupped disc and field loss.
Slit lamp.
Very thin, bright beam for disc measurement.
Dimmer beam for clearer/artificial lenses.
Indirect slit lamp lens (6090D).
Stereoscopic view (best when dilated recommended if safe).
Red-free (green) illumination may help assessment of nerve fiber layer.
Direct ophthalmoscopy or slit lamp view through undimpled Koeppe
lens if pupil small and not able to be dilated.
Figure 1.5: Disc examination flowchart
Can you see disc?
No
Follow vessels to disc
Yes
Look for peripapillary signs and disc rim
Measure vertical disc diameter
Can you identify rim?
Yes
Record findings
No
Follow vessels
Ensure stereoscopy
Try green light
19
Table 1.6: Normal vertical cupdisc ratios for vertical disc diameter 11
Disc diameter
1.0
1.2
1.4
1.6
1.8
2.0
95%
0.20
0.32
0.39
0.45
0.50
0.53
CI
0.32
0.34
0.39
0.45
0.50
0.57
Disc recording
Draw optic disc (large), rim, key vessels that define rim and peripapillary
signs.
Draw notches, shelving, loss to rimclock hours.
Record whether nerve fiber layer is visible and assess for wedge or slit
defects.
Record vertical cupdisc ratio in the narrowest part of the rim. Consider
recording the rimdisc ratio at key parts of the rim.
Record disc hemorrhages, baring of circumlinear blood vessels, blood
vessels bayoneting.
Tip: Disc margin is INSIDE the peripapillary scleral ring of Elschnig.
Appropriate lens magnification correction: Superfield 1.5x, 90D 1.3x, 78D 1.1x, 66D 1.0x.
Disc size
Disc size is extremely variable, large discs have large cupdisc ratios
even though the area of the neuroretinal rim is normal. Therefore,
a large cupdisc ratio may not necessarily be pathological.
Conversely, pathological rim loss can be missed in a small disc
especially if generalized.
Disc size can also be measured by using the small size spot of a
direct ophthalmoscope. This spot size can be used to estimate
whether a disc is larger or smaller than average.
Disc size can also be evaluated using more conventional
photographic means with an overlay grid, as well as by optic nerve
head analysis.
20
Patient Assessment
ISNT rule
Normally, the thickest to thinnest parts of the neuroretinal rim of the
optic disc are Inferior Superior Nasal Temporal (ISNT). Any variation
from this may help to detect glaucomatous damage.
21
Quantitative
Direct ophthalmoscopy
Visual field
examination
Why?
What?
Automated perimetry.
When?
How?
22
Patient Assessment
References:
1.
Drance SM. The visual field of low tension glaucoma and shock-induced optic
neuropathy. Arch Ophthalmol 1977;95:13591361.
2.
Drance SM. Some factors in the production of low tension glaucoma. Br J Ophthalmol
1972;56:229242.
3.
Drance SM, Sweeney VP, Morgan RW, et al. Studies of factors involved in the
production of low tension glaucoma. Arch Ophthalmol 1973;89:457465.
4.
Drance SM. Some studies of the relationships of haemodynamics and ocular pressure
in open angle glaucoma, Trans Ophthalmol Soc UK 1968;88:633640.
5.
Rochtchina E, Mitchell P, Wang JJ. Relationship between age and intraocular pressure:
the Blue Mountains Eye Study. Clin Experiment Ophthalmol 2002;30:173175.
6.
Foster PJ, Machin D, Wong TY , et al. Determinants of intraocular pressure and its
association with glaucomatous optic neuropathy in Chinese Singaporeans: the
Tanjong Pagar Study. Invest Ophthalmol Vis Sci 2003;44:38853891.
7.
Lee JS, Lee SH, Oum BS, et al. Relationship between intraocular pressure and systemic
health parameters in a Korean population. Clin Experiment Ophthalmol
2002;30:237241.
8.
Whitacre MM, Stein R. Source of errors with use of Goldmann-type tonometers. Surv
Ophthalmol 1993;38(1):130.
9.
Danesh-Meyer HV, Savino PJ, Sergott RC. The prevalence of cupping in end-stage
arteritic and nonarteritic ischemic optic neuropathy. Ophthalmology
2001;108:593598.
10. Hayreh SS, Jonas JB. Optic disc morphology after arteritic anterior ischemic optic
neuropathy. Ophthalmology 2001;108:15861594.
11. Healey PR, Mitchell P, Smith W, et al. Relationship between cup-disc ratio and optic
disc diameter: the Blue Mountains Eye Study. Aust N Z J Ophthalmol 1997;25(Suppl
1):S99101.
12. Shields MB. The Optic Nerve Head and Peripapillary Retina. In: Textbook of
Glaucoma, 1998, 4th Ed, pp.72107, Baltimore: William & Wilkins.
23
24
What
are the
categories?
25
Less important:
steroid responder, steroid users
myopia, peripapillary atrophy (PPA)
diabetes mellitus
uveitis
systemic hypertension.
Other risk factors
Genetic risk factors:
family history
ethnicity
Vascular risk factors:
hypertension
reduced perfusion pressure
nocturnal hypotension
Myopia
Diabetes mellitus
Vasospasm
migraine
Raynauds phenomenon
Sleep apnea
When?
Each visit.
How?
Objective
Stage of disease
Use the four treatment categories above.
Severity of RFs
Modifiers of goals
Life expectancy.
Ability to attend follow-up.
Diseases that prevent accurate disc or field assessment.
IOP control
IOP landmarks
Presenting (untreated) IOP.
IOP in fellow normal eye in unilateral secondary glaucoma.
Population mean and standard deviation IOP for normal eyes.
Target IOP
Target IOP is based on the pressure reduction required to slow or
halt disease progression
When the target is achieved, the patient needs continued
monitoring for structural and functional changes
Target IOP needs to be individualized
The benefits of further pressure reduction need to be weighed
against the risks
27
Goals in Group 2
Target pressure reduction of at least 20%.47
Goals in Group 3
Monitor closely for change.
Treat if risk(s) increase(s) with target pressure reduction of at least 20%.47
Group 4
Monitor, no treatment.
References:
1. The Collaborative Normal-Tension Glaucoma Intervention Study Group. The
effectiveness of intraocular pressure reduction in the treatment of normal-tension
glaucoma. Am J Ophthalmol 1998;126:498505.
2. Tezel G, Siegmund KD, Trinkaus K, et al. Clinical factors associated with progression of
glaucomatous optic disc damage in treated patients. Arch Ophthalmol
2001;119(6):813818.
3. Gordon MO, Beiser JA, James MS, et al. The ocular hypertension study: baseline factors
that predict the onset of primary open-angle glaucoma. Arch Ophthalmol
2002;120:714720.
4. Leske MC, Heijl A, Hussein M, et al. Factors for glaucoma progression and the effect of
treatment: the early manifest glaucoma trial. Arch Ophthalmol 2003;121:4856.
5. The AGIS Investigators. The advanced glaucoma intervention study (AGIS): 7. The
relationship between control of intraocular pressure and visual field deterioration. Am
J Ophthalmol 2000; 130(4):42940.
6. Kass MA, Heuer DK, Higginbotham EJ, et al. The ocular hypertension treatment study:
a randomized trial determines that topical ocular hypotensive medication delays or
prevents the onset of primary open-angle glaucoma. Arch Ophthalmol
2002;120:701713.
7. Heijl A, Leske C, Bengtsson B, et al. Reduction of intraocular pressure and glaucoma
progression: results from the early manifest glaucoma trial. Arch Ophthalmol
2002;120:12681279.
28
Section 2
29
30
Initiation of Treatment
What
should be
treated?
When to
treat?
31
How to
treat?
References:
1. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and
primary open angle glaucoma among white and black Americans. The Baltimore Eye
Survey. Arch Ophthalmol 1991;109(8):10901095.
2. The AGIS Investigators. The advanced glaucoma intervention study (AGIS): 7. The
relationship between control of intraocular pressure and visual field deterioration.
Am J Ophthalmol 2000; 130(4):429440.
32
Medical Treatment
What?
Table 2.1: Efficacy, safety and dosing frequency of various drug classes
Side effects
Daily
Dosage
Efficacy
Adrenergic
agonists
2x to 3x
-blockers
Drug class
Local
Systemic
++ to +++
++
+ to ++
1x to 2x
+++
+ to +++
Topical
2x to 3x
++
++
0 to ++
Systemic
2x to 4x
++++
++ to ++++
Cholinergics
3x to 4x
+++
++++
0 to ++
Hyperosmotic
agents
Stat
dose(s)
+++++
++ to +++++
Prostaglandins
and other lipid
receptor
agonists*
1x
++++
+ to ++
BB + CAI
2x
+++ to ++++
++
+ to +++
BB + PG
1x
++++ to +++++
+ to ++
+ to +++
BB + Pilo
2x
++++
++++
+ to +++
Carbonic
anhydrase
inhibitors
Proprietary fixed
combinations
0 rare
PG Prostaglandins
BB -blockers
Pilo Pilocarpine
*excluding unoprostone
33
Mechanism of action
Drug class
Adrenergic agonists
Preparations
Brimonidine
Apraclonidine
Non-selective
Timolol
-blockers
Levobunolol
Carteolol
1-selective
Reduction of
aqueous inflow
Betaxolol
Systemic
Acetazolamide
Methazolamide
Carbonic anhydrase
inhibitors
Dichlorphenamide
Topical
Dorzolamide
Brinzolamide
Cholinergics
Increase trabecular
outflow
Increase in
aqueous outflow
Prostaglandins
and other lipid
receptor agonists
Increase uveoscleral
outflow
34
Pilocarpine
Carbachol
Latanoprost
Travoprost
Bimatoprost
Unoprostone
Relatively
contraindicated in
bronchial asthma,
chronic obstructive
pulmonary disease,
bradycardia, heart
block, cardiac failure
To be used
cautiously in cardiac
failure
Absolutely
contraindicated in
bronchial asthma,
chronic obstructive
pulmonary disease,
bradycardia, heart
block
As for non-selective
-blockers with wider
safety margin
Systemic -blockers,
calcium channel
blockers
CNS depressants
(alcohol, barbiturates,
opiates, sedatives, or
anesthetics), tricyclic
antidepressants
Common drug
interactions
Betaxolol
-blockers
(selective)
Timolol
Levobunolol
Carteolol
Metipranolol
-blockers
(non-selective)
Monoamine oxidase
inhibitor therapy
Adrenergic agonists
Brimonidine
Apraclonidine
Contraindications*
Preparations by class
Burning, stinging,
photophobia, itching,
tearing, decreased
corneal sensitivity,
hyperemia, punctate
epithelial keratopathy
Burning, stinging,
blurring, foreign-body
sensation, itching,
hyperemia, follicular
conjunctivitis
As for non-selective
-blockers with wider
safety margin
Bronchospasm,
hypotension,
bradycardia, heart
block, mask
hypoglycemia,
adversely affects lipid
profile (except
carteolol), loss of
libido, fatigue,
aggravation of
myasthenia gravis,
depression, memory
impairment, reduced
exercise tolerance,
increased falls
in the elderly
Oral dryness,
headache, fatigue,
drowsiness
Medical Treatment
35
36
Sulfonamide allergy,
renal stones/failure,
respiratory/metabolic
acidosis, hypokalemia
Carbonic anhydrase
inhibitors
(systemic)
Aqueous misdirection
syndrome
Post-drainage surgery
Steroids, diuretics,
digoxin
Common drug
interactions
Pilocarpine
Carbachol
Cholinergics
Acetazolamide
Methazolamide
Dichlorphenamide
Uveitic, neovascular
and lens induced
glaucomas
Relatively
contraindicated with
compromised corneal
endothelium,
sulfonamide allergy
Carbonic anhydrase
inhibitors
(topical)
Dorzolamide
Brinzolamide
Contraindications*
Preparations by class
Fatigue, lethargy,
anorexia,
gastrointestinal upset,
weight loss,
paresthesia, taste
disturbance, StevensJohnson Syndrome,
blood dyscrasias, renal
stones, hypokalemia
Headache, salivation,
lacrimation, urinary
frequency, diarrhea,
abdominal cramps
Bitter taste
Transient myopia
Burning, stinging,
itching, punctate
epithelial keratopathy,
blepharoconjuctivitis
Caution following
complicated
intraocular surgery
Relatively
contraindicated in
the presence of active
inflammatory ocular
conditions, cystoid
macular edema
Blurred vision,
burning, stinging,
conjunctival
hyperemia,
foreign-body
sensation, itching,
increased
iris/periorbital skin
pigmentation, lash
growth, punctate
epithelial keratopathy,
cystoid macular
edema, reactivation
of herpetic infection
NA
Chronic pilocarpine
use may reduce
efficacy of these
agents
Common drug
interactions
Proprietary fixed
combinations
Latanoprost
Travoprost
Bimatoprost
Unoprostone
Prostaglandins and
other lipid receptor
agonists
Caution with
hypertension
Heart failure,
pulmonary edema,
renal failure
Hyperosmotic agents
Mannitol
Contraindications*
Preparations by class
Headaches,
unpleasant taste,
heart failure,
pulmonary edema,
death
Medical Treatment
37
How?
38
Medical Treatment
Suggested reading:
1.
European Glaucoma Society. Treatment principles and options. In: Terminology and
Guidelines for Glaucoma, IInd edition, 2003, pp.3-13-45. Italy: Dogma.
2.
Ritch R, Shields MB, Krupin T. The Glaucomas Glaucoma Therapy,1996, vol III, 2nd
Ed, Missouri: Mosby.
3.
Hoyng PFJ, van Beek LM. Pharmacological Therapy for Glaucoma. Drugs
2000;59:411434.
4.
5.
6.
Kass MA, the Ocular Hypertension Treatment Study Group. The ocular hypertension
treatment study. A randomized trial determines that topical ocular hypotensive
medication delays or prevents the onset of primary open-angle glaucoma. Arch
Ophthalmol 2002;120:701713.
7.
8.
9.
Susanna R Jr, Medeiros FA. The pros and cons of different prostanoids in the medical
management of glaucoma. Curr Opin Ophthalmol 2001;12(2):149156.
10. Herkel U, Pfeiffer N. Update on topical carbonic anhydrase inhibitors. Curr Opin
Ophthalmol 2001;12(2):8893.
11. Mauger TF, Craig EL. Haveners Ocular Pharmacology, 1994, 6th Ed, St. Louis: Mosby.
39
Drug 1
Maximize compliance
Reaches target?
Side effects none
/ tolerable?
NO
Ineffective
Stop
Hold in reserve
Reaches target?
Side effects none
/ tolerable?
Discard
Drug 2
Maximize compliance
NO
Ineffective
Stop
Hold in reserve
YES
Reaches target?
Side effects none
/ tolerable?
Discard
Drug 3 or more
(if appropriate)
Maximize compliance
NO
Ineffective
Stop
Hold in reserve
Reaches target?
Side effects none
/ tolerable?
Discard
NO
Continue treatment
and monitor
40
Laser or surgery
Laser Treatment
Laser
trabeculoplasty
Why?
Relatively effective.
Relatively non-invasive.
What?
When?
How?
Pre-laser management
Explain the procedure.
To reduce post-treatment intraocular pressure (IOP) spike or
inflammation, consider 1% apraclonidine1 or 0.2% brimonidine2 and/or
24% pilocarpine and/or -blocker and/or steroid drops before the
procedure.
Topical anesthesia.
Laser
Lens*
Goldmann gonioscopy lens.
Ritch trabeculoplasty lens.
CGA LASAG CH.
*should be coated to minimize reflection and hazard to observers
41
Number of burns: 3050 spots evenly spaced over 180 degrees. Treat the
remaining 180 degrees sequentially, or at the same time, as required.
Complications
Post-laser management
Continue any current medical treatment.
Especially if IOP spike prevention treatment is not available, re-check
IOP at 16 hours after laser and again 2448 hours.
Topical steroid qid for 414 days (consider omitting with SLT).
Closer monitoring is suggested in certain cases
Repeat treatment
Initial treatment may not be long lasting. Laser trabeculoplasty can be
repeated especially in eyes that have shown a prolonged response to
previous treatment 3.
42
Laser Treatment
Iridotomy
Why?
Effective.
Relatively non-invasive.
Preferable to surgical iridectomy.
What?
When?
Angle closure.
Angle closure glaucoma.
Occludable angle (absolute):
angle closure in the fellow eye
confirmed family history of angle closure glaucoma.
Occludable angle (relative):
need for repeated dilated examinations
poor access to regular ophthalmic care.
How?
Pre-laser management
Explain the procedure.
Instill 2% or 4% pilocarpine .
To reduce post-treatment IOP spike/inflammation, consider
1% apraclonidine1 or 0.2% brimonidine2 and/or -blocker and/or oral
carbonic anhydrase inhibitor and/or steroid drops before the procedure.
Topical anesthesia.
Topical glycerin, if the cornea is edematous.
Superior 1/3 of iris (beneath upper lids) desirable.
Laser:
Nd-YAG.
Argon or krypton.
Laser parameters for Nd-YAG laser
Energy: 25 mJ, use minimum energy, 13 pulses per burst
(lens damage possible above 2 mJ per pulse)
Focus the beam within the iris stroma rather than on the surface
of the iris
Choose an iris crypt or an area of thin iris
Can be effectively combined with Argon laser
To facilitate penetration of a uniformly thick iris, Argon laser
pretreatment can:
coagulate
stretch
thin the target area
43
Complications
Temporary blurring of vision.
Corneal epithelial and/or endothelial burns with Argon (latter
aggravated by bubble formation and contact with endothelium).
Intra-operative bleeding with Nd-YAG.
IOP spikes.
Post-operative inflammation.
Posterior synechiae.
Closure of iridotomy.
Failure to penetrate.
Localized lens opacities.
Rarely: retinal damage, cystoid macular edema, malignant glaucoma,
endothelial decompensation.
44
Laser Treatment
Post-laser management
Particularly if IOP spike prevention treatment is not available, re-check
IOP at 16 hours after laser and again at 2448 hours.
Topical steroid at least 46 times/day for 414 days depending on
inflammation.
Verify the patency of the peripheral iridotomy (PI).
Repeat gonioscopy.
Pupillary dilatation to break posterior synechiae when suspected.
Iridoplasty
(gonioplasty)
Why?
Reasonably effective.
Relatively non-invasive.
Adjunct to peripheral iridotomy.
What?
When?
How?
Pre-laser management
Procedure
Argon green or bluegreen.
Diode laser.
Lens
CGI LASAG CH.
Goldmann 3-mirror lens.
Placement of laser spot: aim at the most peripheral location, avoid
corneal arcus.
45
Laser parameters
Power:
Spot size:
Duration:
Number of burns:
Endpoint
Iris contraction with peripheral anterior chamber deepening and more
visible angle in line with the laser applications.
Complications
Mild iritis.
Corneal endothelial burns.
IOP spikes.
Peripheral anterior and/or posterior synechiae.
Post-operative treatment
If IOP spike prevention treatment is not available, check IOP within
16 hours and then 2448 hours depending on the status of the patient.
Topical corticosteroids 46 times/day for 7 days or more depending on
the post-laser inflammation.
Repeat gonioscopy to evaluate the anterior chamber angle and identify
any other mechanism(s) of angle closure that might necessitate further
intervention.
Pupillary dilatation to break posterior synechiae when suspected.
Cyclophotocoagulation
Why?
What?
When?
How?
Pre-laser management
Explain procedure.
Topical and sub-Tenons or retro/peri-bulbar anesthesia.
General anesthesia when indicated.
46
Laser Treatment
Techniques
Transpupillary.
Transscleral.
Endolaser.
Conservative, incremental applications avoiding 3 and 9 oclock
positions.
Endolaser
Diode endoscopic laser.
Argon or krypton laser.
Laser parameters
Depends on laser system used, consult the instruction manual and
clinical updates
47
Complications
Pain.
Persistent inflammation.
Loss of visual acuity.4,5
Hypotony.6
Scleral thinning.7,8
Macular edema.
Retinal detachment.9
Aqueous misdirection syndrome.10
Phthisis.11
Sympathetic ophthalmia.12
Failure to control IOP multiple procedures may be needed.
Post-operative management
Analgesia.
Continue any current treatment.
Check IOP after 2448 hours.
Topical corticosteroids 46 times/day for 14 days or more depending on
post-laser inflammation.
Cycloplegia 24 times/day for 714 days.
References:
48
1.
Robin AL. Argon laser trabeculoplasty medical therapy to prevent the intraocular
pressure rise associated with Argon laser trabeculoplasty. Ophthalmic Surg 1991
Jan;22(1):3137.
2.
Barnes SD, Campagna JA, Dirks MS, et al. Control of intraocular pressure elevations
after Argon laser trabeculoplasty: comparison of brimonidine 0.2% to apraclonidine
1.0%. Ophthalmol 1999 Oct;106(10):20332037.
3.
Jorizzo PA, Samples JR, Van Buskirk EM. The effect of repeat Argon laser
trabeculoplasty. Am J Ophthalmol 1988 Dec 15;106(6):682685.
4.
5.
Schuman JS, Bellows AR, Shingleton BJ, et al. Contact transscleral Nd:YAG laser
cyclophotocoagulation. Midterm results. Ophthalmol 1992 Jul;99(7):10891094;
discussion 1095.
6.
Maus M, Katz LJ. Choroidal detachment, flat anterior chamber, and hypotony as
complications of neodymium: YAG laser cyclophotocoagulation. Ophthalmol 1990
Jan;97(1):6972.
7.
Fiore PM, Melamed S, Krug JH Jr. Focal scleral thinning after transscleral Nd:YAG
cyclophotocoagulation. Ophthalmic Surg 1989 Mar;20(3):215216.
Laser Treatment
8.
Bhola RM, Prasad S, McCormick AG, et al. Pupillary distortion and staphyloma
following trans-scleral contact diode laser cyclophotocoagulation: a
clinicopathological study of three patients. Eye 2001 Aug;15(Pt 4):453457.
9.
10. Hardten DR, Brown JD. Malignant glaucoma after Nd:YAG cyclophotocoagulation.
Am J Ophthalmol 1991 Feb 15;111(2):245247.
11. Trope GE, Ma S. Mid-term effects of neodymium:YAG transscleral
cyclophotocoagulation in glaucoma. Ophthalmol 1990;97(1):7375.
12. Lam S, Tessler HH, Lam BL, et al. High incidence of sympathetic ophthalmia after
contact and noncontact neodymium:YAG cyclotherapy. Ophthalmol
1992:99(12):18181822.
49
50
Surgery
2.4 Surgery
Open angle glaucoma
Outflow enhancement: penetrating and non-penetrating filtering
surgery.
Glaucoma drainage device.
Childhood glaucoma
Angle surgery: goniotomy and trabeculotomy.
Outflow enhancement: trabeculectomy with or without trabeculotomy.
Glaucoma drainage device.
Why?
Reasonably effective.1,2
Reasonably safe.
Widely available.
What?
Childhood surgery
Goniotomy (primary treatment to be performed at specialist centers).
Trabeculotomy (primary treatment to be performed at specialist centers).
When?
How?
Pre-operative assessment
Surgical technique
Select appropriate technique.
Enhancement of surgery
Use of anti-fibrotic agents:
intra-operative4
post-operative4,6,7
Use of anti-inflammatory agent:
systemic corticosteroids8,9
other agents (e.g., NSAIDs)
Use of laser suture lysis or releasable sutures10
Post-operative management
52
Surgery
Use of antifibrotics in
surgery
Why?
What?
When?
For high risk of failure following standard filtering surgery. This includes
repeat surgery, neovascular glaucoma, glaucoma in uveitis, glaucoma in
aphakia, younger age, black race.
In primary surgery, especially where a lower target pressure is
required.11, 12
To increase the success rates with artificial drainage devices.
With needling of a failed filter.
In these instances, the enhanced success rates with anti-fibrotics may make
the complications associated with their use more acceptable.
How?
B. Post-operative application:
5-FU is also used as post-operative injections of 5 mg/0.1 mL for up to
4 post-operative weeks. The injection may be given alongside or behind the
bleb, or sometimes 90 to 180 degrees away using preferably a 30 gauge
needle. The number of injections is titrated according to the appearance of
the bleb. Care is taken to avoid spillage on the cornea. The conjunctiva
53
over the area of injection may be tamponaded with a cotton bud for
about 1 minute after the injection.
Note: The use of anti-fibrotic agents can be associated with sight threatening
complications and they must be used with caution. Use of an algorithm developed by
those experienced in the use of such agents is desirable.15
Glaucoma
drainage
implants
Why?
What?
When?
How?
54
Surgery
Cataract and
glaucoma
surgery
Cataract and glaucoma are both common conditions and which often
co-exist. A recent review has assessed current surgical management.20
Table 2.4: Evidence for surgical management of cataract and glaucoma20
Review comments
Evidence
Evidence grades:
A strong
B moderate
C weak
I insufficient
For the surgical management of coexisting cataract and glaucoma, there is
some evidence of efficacy for using MMC.
*Extracapsular cataract extraction.
55
References:
1.
2.
Jay JL, Murray SB. Early trabeculectomy versus conventional management in primary
open angle glaucoma. Brit J Ophthalmol 1988;72:881889.
3.
4.
Ritch R, Shields MB, Krupin T. Glaucoma Surgery. In: The Glaucomas Glaucoma
Therapy ,1996, vol III, 2nd ed, pp.16331652. Missouri: Mosby.
5.
6.
Weinreb RN. Adjusting the dose of 5-fluorouracil after filtration surgery to minimize
side effects. Ophthalmol 1987;94(5):564570.
7.
8.
Araujo SV, Spaeth GL, Roth SM, et al. A ten-year follow-up on a prospective,
randomized trial of postoperative corticosteroids after trabeculectomy. Ophthalmol
1995;102(12):17531759.
9.
Starita RJ, Fellman RL, Spath GL, et al. Short- and long-term effects of postoperative
corticosteroids on trabeculolectomy. Ophthalmol 1985;92(7):938946.
10. Kolker AE, Kass MA, Rait JL. Trabeculectomy with releasable sutures. Arch
Ophthalmol 1994;112(1):6266.
11. Ramakrishnan R, Michon J, Robin AL, et al. Safety and efficacy of mitomycin C
trabeculectomy in southern India. A short-term pilot study. Ophthalmology 1993;
100(11):16191623.
12. Lamba PA, Pandey PK, Raina UK et al. Short-term results of initial trabeculectomy
with intraoperative or postoperative 5-FU for primary glaucomas. Ind J Ophthalmol
1996;44:157160.
13. Mardelli PG, Lederer CM Jr, Murray PL, et al. Slit-lamp needle revision of failed
filtering blebs using mitomycin C. Ophthalmology 1996;103(11):19461955.
14. Khaw PT. Advances in glaucoma surgey: evolution of antimetabolite adjunctive
therapy. J Glaucoma 2001;10(Suppl 1): S81S84.
15. Khaw PT, Chang L, Wong TTL, et al. Modulation of wound healing after glaucoma
surgey. Opin Ophthalmol 2001;12:143148.
16. Ellingham RB, Morgan WH, Westlake W, et al. Mitomycin C eliminates the short-term
intraocular pressure rise found following Molteno tube implantation. Clin Experiment
Ophthalmol 2003;31(3):191198.
17. Minckler DS, Heuer DK, Hasty B, et al. Clinical experience with the single-plate
Molteno implant in complicated glaucomas. Ophthalmology 1988; 95:11818.
18. Molteno ACB. Use of Molteno implants to treat secondary glaucoma. In: Glaucoma,
Cairns JE eds, Vol 1, 1986, pp 21138, Grune & Stratton: London.
19. Goldberg I. Management of Uncontrolled Glaucoma with the Molteno System. Aust
NZ J Ophthalmol 1987;15:97.
20. Jampel HD, Friedman DS, Lubomski LH, et al. Effect of technique on intraocular
pressure after combined cataract and glaucoma surgery: An evidence-based review.
Ophthalmology 2002; (12):22152214.
56
Section 3
57
58
Follow-up
3.1 Follow-up
Why?
What?
The follow-up process starts with the management plan made at the
initiation of therapy. At the follow-up visits the doctor should:
briefly discuss the patients subjective well being and visual function
reassess risk factors: especially intraocular pressure (IOP) and
gonioscopic change(s)
reassess structure and function of the optic nerve
estimate rate of (any) progression
identify adverse effect(s) of treatment
assess compliance
identify change(s) in current medical and ophthalmological problems
discuss quality of life issue(s)
reinforce appropriate patient information:
revise management
plan follow-up.
When?
The more severe the damage, the worse the risk factors, the sooner should
be the follow-up.
Patients
subjective
wellbeing
and visual
function
Patients will often wish to tell the doctor how they feel their condition
has (or has not) changed.
This discussion helps build a good doctorpatient relationship.
Subjective changes in vision with glaucoma are rare, but in advanced
disease, changes in the following qualities of vision may indicate a
deterioration of glaucomatous optic neuropathy (GON):
night vision
dark adaptation
glare
stereopsis
acuity (high and low contrast)
missing pieces of vision.
59
Reassess the
risk factors
Gonioscopic changes
Maintain baseline examination conditions.
Perform gonioscopy regularly in patients with angle closure and
periodically in patients with open angles.
Look for increased appositional and/or synechial closure.
Pupil size changes have dynamic effects on the angle.
Look for change in angle width, synechiae, and pigmentation.
60
Follow-up
Reassess
structure
and
function of
the optic
nerve
Optic disc
Progression of GON usually occurs over a long period, which can make the
detection of change difficult.
The occurrence of the following indicate GON progression (refer to
Appendix 8: Glaucomatous optic neuropathy):
disc hemorrhage
focal rim notching
change in vessel position
wedge-type nerve fiber layer defects
generalized rim thinning
increased cupdisc ratio.
Where baseline optic disc photographs and serial photography are
available, detection of these changes is substantially enhanced.
If photographs are not available, the pupil should be dilated (if it is not
possible to do this safely, consider prophylactic iridotomy/iridoplasty) to
obtain an adequate view of the disc.1
Visual field
Change is frequent in perimetry. Usually only a small proportion is owing
to GON progression.
Causes of change
Learning field performance usually improves over the first few
attempts.
Reliability changes, poor concentration may cause general
depression, look for false negatives.
False negative errors may indicate progression. False positive errors
reflect poor reliability and may mask progression. Fixation losses
may reflect poor reliability and mask progression, or may reflect
technical errors.
Progression of disease.
Cataract causes generalized depression2,3 and masks relative
scotomas.4
Pupil size changes miosis causes generalized field depression;
minimum 3 mm recommended.
Retinal disease (e.g., vein occlusion, macular degeneration,
significant diabetic retinopathy).
Retinal laser.
Miscellaneous artifacts.
Change in measurement strategy (Fastpac vs. Full Threshold vs. SITA).
61
Detecting progression
Progression is characterized by:
widening or deepening of an existing scotoma
development of a new glaucomatous scotoma
occasionally generalized field depression (although this is usually caused
by media opacity or miosis).
(Refer to Appendix 9: Field progression print-outs).
Changes in visual field should be confirmed by at least one or more
repeat tests.
There is a close correlation between glaucomatous changes in structure of
the optic disc and consequent visual field loss.5, 6 However, there may be
considerable variation in morphology of a normal disc, and in patients
ability to perform visual field tests adequately.
Changes should be regarded skeptically until the deviation exceeds the
standard deviation of serial measurements.
62
Identify
adverse
effects of
treatment
Quality of
life issues
The patients quality of life (QOL) should be estimated and the impact
of the glaucoma management on QOL assessed.
This forms part of the assessment of burden of disease and burden of
treatment.
Follow-up
Disease status
Risk
Stable
Uncertain
Progressing
Increased
++
+++
Uncertain
Reassess risk
Reassess both
++
Stable
Reassess disease
Risk factors*
The following factors confer a higher risk of loss of vision from glaucoma:
high or rising IOP
any appositional angle closure
any peripheral anterior synechiae (PAS), or an increase in PAS, if seen
before
longer life expectancy.
*The more risk factors there are, the higher the risk. Therefore, add + for every
additional risk factor.
Disease progression
Stable disease indicates no change in optic disc or visual field status
Uncertain disease status indicates a change in visual field that is not
consistent with the status of the disc.
Progressing disease indicates changes consistent with glaucoma in the
optic disc and visual field.
Add + if the rate of progression appears rapid.
63
Increasing damage
50
High
risk
factors
Medium risk
factors
100
Diagnosis
Death
64
Follow-up
Follow-up timing
The target pressure is the IOP at which it is believed the patient can retain
vision for the rest of his/her life. However this needs to be checked from
time to time.
Follow-up timing is determined by the treatment regime if this has
changed. If the patient is stable the timing is determined mainly by the
extent of damage: for glaucoma suspect, 624 months; for mild damage,
612 months; moderate damage, 46 months; severe damage, 14 months.
References:
1.
Kirwan JF, Gouws P, Linnell AET, et al. Pharmacological mydriasis and optic disc
examination. Br J Ophthalmol 2000;84:894898.
2.
Budenz DL, Feuer WJ, Anderson DR. The effect of simulated cataract on the
glaucomatous visual field. Ophthalmology 1993;100:511517.
3.
Lam BL, Alward WL, Kolder HE. Effect of cataract on automated perimetry.
Ophthalmology 1991;98:10661070.
4.
Smith SD, Katz J, Quigley HA. Effect of cataract extraction on the results of
automated perimetry in glaucoma. Arch Ophthalmol 1998;115:15151519.
5.
Quigley HA, Katz J, Derick RJ, et al. An evaluation of optic disc and nerve fiber layer
examinations in monitoring progression of early glaucoma damage. Ophthalmology
1992;99:1928.
6.
Yamagishi N, Antn A, Sample PA, et al. Mapping structural damage of the optic disk
to visual field defect in glaucoma. Am J Ophthalmol 1997;123:667676.
65
66
Case Detection
Case Detection
Why
case detect
or screen?
67
What is the
best
strategy?
Case detection
How to
screen or
detect?
68
Detecting early glaucoma is ideal, but requires a sensitive test that leads
to many false positives. For screening, a test should have a reasonably
high sensitivity with as high specificity as possible. Prevent Blindness
America suggests 9598% specificity and 85% sensitivity for moderate-tosevere glaucoma.4
Case Detection
Automated
perimetry
Sensitivity
Specificity
92.4%5
97%6
84%6
Comments
Poor sensitivity and specificity
Half of the patients with
POAG have IOPs <22 mmHg
at a single screening
Test can be made more
specific or sensitive
Time-consuming and laborious
Frequency
doubling
perimetry
Disc and nerve
fiber layer
examination
9094%79*
9196%79*
Rapid
Relatively inexpensive
Cupdisc ratio of
0.55 cut off:
59%10
73%10
69
Recommend
-ations
Population-based screening
This is not recommended as a strategy. Population-based screening is
especially inappropriate for developing countries without an adequate
infrastructure. Adequate infrastructure here implies the availability of
expertise (trained ophthalmologists), time and instrumentation required
to confirm the diagnosis among test positives in an appropriate manner.
It also means the availability of expertise (trained surgeons) and
instrumentation to treat appropriately those in whom the diagnosis is
confirmed. The operative word is appropriate and implies modern
preferred practice. The requirements for diagnosis and management are
covered in the relevant sections.
Each country will need to make a decision on population-based screening
based on an assessment of the ground reality. Thus, more developed
countries may opt to target high risk groups for screening.
Case detection
Any person over the age of 35 who seeks ophthalmic attention for any
reason should have a comprehensive ophthalmic examination. As far as
the diagnosis of glaucoma is concerned, this would include the following.
70
Case Detection
Test
Ideal
Acceptable
Tonometry
Applanation
tonometry
Tonopen
Dilated
evaluation of
the optic disc
Dilated
stereoscopic
evaluation by
slit lamp biomicroscopy,
fundus
photography
Direct
ophthalmoscope
Slit lamp
biomicroscopy
and van Herick
test
NA
NA
Less than
ideal
Comments
Pneumotonometer
or Schitz
tonometer
NA
Gonioscopy
Indentation
gonioscopy
using a Sussman,
Zeiss or Posner
lens
Goldmann
single or two
mirror with
manipulation
Visual field
examination (if
the IOP is >21
mmHg and/or
the disc is
suspicious)
A full threshold
test (includes
SITA) using a
calibrated
white-on-white
automated
perimeter or
Goldmann
perimetry
Frequency
doubling
perimeter
(FDP),
Hensons
visual field
screener, or a
Bjerrum
screen
71
Definitions
Screening
Case detection
(opportunistic
screening)
Prevalence
Sensitivity
Specificity
Positive
predictive value
Negative
predictive value
50
Prevalence (%)
72
100
Case Detection
With a low prevalence of glaucoma, most of those who test positive will in
fact be false positives.
In order to increase the effectiveness of all tests, the prevalence of
glaucoma in the population to be tested must be reasonably high. The
prevalence of glaucoma can be increased by targeting high-risk groups
such as the elderly, persons with family history of glaucoma, diabetics,
hypermetropes (angle closure) and myopes (open angle).
References:
1.
Wilson JMG, Jungner F. Principles and practice of screening for disease. Geneva:
WHO, 1968, Public Health Papers No 34.
2.
Sackett DL, Haynes RB, Guyatt GH, et al. Early diagnosis. In: Clinical Epidemiology:
A basic science for clinical medicine, 1991, pp.153170. Boston: Little Brown and Co.
3.
Sackett DL, Haynes RB, Guyatt GH, et al. The Clinical Examination. In: Clinical
Epidemiology: A basic science for clinical medicine, 1991, pp.1949. Boston: Little
Brown and Co.
4.
5.
6.
7.
8.
Patel SC, Friedman DS, Varadkar P, et al. Algorithm for interpreting the results of the
Frequency Doubling Perimeter. Am J Ophthalmol 2000;129:323327.
9.
10. Quigley HA, Katz J, Derick RJ, et al. An evaluation of optic disc and nerve fiber layer
examinations in monitoring progression of early glaucoma damage. Ophthalmology
1992; 99:1928.
11. Tielsch JM, Sommer A, Witt K, et al. Blindness and visual impairment in an American
urban population. The Baltimore Eye survey. Arch Ophthalmol 1990;108:286290.
12. Kahn HA. The Framingham eye study. Am J Epidemiol 1977;106:1732.
13. Congdon N, Wang F, Tielsch JM. Issues in the epidemiology and population based
screening of primary angle closure glaucoma. Surv Ophthalmol 1992;36:411423.
14. Congdon N, Quigley HA, Hung PT, et al. Screening techniques for angle-closure
glaucoma in rural Taiwan. Acta Ophthalmol Scand 1996;74:113119.
15. Thomas R, George T, Braganza A, et al. The flashlight test and van Hericks test are
poor predictors for occludable angles. Aust NZ J Ophthalmol 1996;24(3):251256.
16. Foster PJ, Baasanhu J, Alsbirk PH, et al. Glaucoma in Mongolia, a population-based
survey in Hovsgol province, northern Mongolia. Arch Ophthalmol
1996;114:12351241.
73
74
Appendices
75
Figure B
Figure A
1
6
0
Figure C
6. Slowly twirl the circular dial clockwise until the head rocks forwards. Note the tension
reading on the dial: it should be 2023 mmHg.
7. Slowly twirl the circular dial counter-clockwise until the head rocks backwards. The
tension on the dial should read 1720 mmHg.
8. Remove the rod and holding bracket from
the tonometer and reposition the bracket so
that it is aligned exactly with the most
forward mark on the rod furthest away
from you (Figure D).
9. Replace the rod in its bracket in the
tonometer receptacle. The tonometer head
should rock backwards, towards you.
6
Figure D
10. Slowly twirl the dial clockwise until the head rocks forwards. The tension should read
6064mm Hg.
11. Slowly twirl the dial counter-clockwise until the head rocks backwards the tension
should read 5660mm Hg.
Comments:
The three threshold tension levels being used to test the tonometers calibration are at 0,
20 and 60 mmHg. At each of these thresholds, you can gently twirl the dial backwards
and forwards, reading the tension as the head responds: these points should bracket the
threshold level evenly the higher the level being tested, the greater the interval is likely
to be.
(Figures A, B and D Courtesy of Haag-Streit AG and Mandarin Opto-Medic Co Pte Ltd)
76
77
Methods
Gonioscopic contact lens permits the angle to be seen.
1. Direct gonioscopy
Place the Koeppe goniolens on an anesthetized cornea with the
patient supine. Fill the space between the lens and the cornea with
a contact fluid (e.g., saline or methylcellulose). View the angle with
a handheld biomicroscope and an illuminator.
2. Indirect gonioscopy
At the slit lamp, place a mirrored lens (e.g., Goldmann-type or
four-mirror indentation) on the cornea.
78
Iridocorneal contact
Grade I
Grade II
Grade 0
II
III
IV
closed
10
20
30
40
Schwalbes
line is
not visible
Schwalbes
line is
visible
Anterior TM
is visible
Scleral
spur
is visible
Ciliary
band
is visible
C. Spaeth
1. Iris insertion
Anterior to Schwalbes line or TM
Behind Schwalbes line
Centered at scleral spur
Deep to scleral spur
Extremely deep/on ciliary band
2. Angular width
slit
10
20
30
40
3. Peripheral iris configuration
queerly concave
regular
steep
4. TM pigment
0 (none) to 4 (maximal)
Reference:
Stamper RL, Lieberman, MF, Drake MV. Clinical Interpretation of Gonioscopic Findings. In: Becker-Shaffers
Diagnosis and Therapy of the Glaucomas, 1999, 7th Ed, p101113, St. Louis: Mosby.
Spaeth GL. The normal development of the human anterior chamber angle: a new system of descriptive
grading. Trans Ophthalmol Soc UK 1971;91:709739.
79
From PJ Foster and GJ Johnson. Chapter 16. Classification and Clinical Features, pp.148,
Figure 16.2. In: Fundamentals of Clinical Ophthalmology: Glaucoma, 2000, Ed Hitchings,
London: BMJ Books. (Reproduced with permission from BMJ Books)
80
Do not abandon the patient during the test have your technician return
regularly and frequently to supervise.
Reassure and encourage the patient during the test.
Restart the test if the performance is proving unreliable. Try to identify
and to rectify the cause of the problem. Do not disparage or blame the
patient.
Consider rescheduling the test if the patient cannot cope.
Be patient, more patient, and then even more patient.
81
82
Strategy
Anti-inflammatories
-blockers; 2-agonists;
Carbonic anhydrase inhibitors
Site two: anteriorly rotated ciliary processes that push the iris
forward and/or thick peripheral iris plateau iris configuration
83
About 100 equally spaced laser spots (diameter 50 microns) each for 0.1
seconds are applied over 360 degrees of trabecular meshwork, often in
two sessions of 180 degrees, separated by 12 weeks. Ideally the spots
should be applied over Schlemms canal, avoiding the iris root: at the
junction of the anterior 1/3 and posterior 2/3 of the meshwork. The energy
level should be set to induce a reaction from a slight transient blanching
of the treated area, to small bubble formation.
84
85
Advanced glaucomatous
optic neuropathy
Neuroretinal rim thinning
The cup extends to the disc rim
Circumlinear blood vessel
baring
Bayoneting of the blood vessels
Peripapillary atrophy
86
87
88
Definition of Terms
Angle neovascularization
Glaucomatous optic
neuropathy (GON)
Occludable angle
Peripheral anterior
synechiae (PAS)
Definition of Terms
90
Pigment dispersion
syndrome (PDS)
Posner-Schlossman Syndrome
Pseudoexfoliation
syndrome (PXFS)
Index
A
Adrenergic agonists, 33,34,35
factors influencing treatment,12
Angle closure
incidence, 5
mechanisms, 31, Appendix 6
signs of, 18
surgery, 51
Anterior chamber
depth, risk factor for glaucoma, 6
examination, 17
Anti-fibrotics
use in surgery, 53
B
-blockers, 33,34,35
factors influencing treatment, 13
C
Cataract
cause of blindness, 5
and glaucoma surgery, 55
Carbonic anhydrase inhibitors
factors influencing treatment, 12
Gonioscopic changes
assessment at follow-up, 60
Gonioscopy, 17
corneal wedge diagram, Appendix 3c
goniogram, Appendix 3b
methods, Appendix 3a
tool for case detection, 71
H
Hyperosmotic agents, 33,37
I
Intraocular pressure
causes of change at follow-up, 60
factors influencing, 15
targets, 27
Iridoplasty
laser, 45
modifiers of treatment goals, 27
Iridotomy
laser, 43
modifiers of treatment goals, 27
Iris examination, 17
ISNT rule, 21
Cholinergics, 33,34,36
Cupdisc ratio, 20
Cyclophotocoagulation, 46
L
Lens
examination, 17
extraction, 27
D
Disc haemorrhage, Appendix 8
treatment category, 25
N
Neuroretinal rim, 21
Double DOT, 39
Occudable angles
treatment category, 25
Ocular hypertension
treatment category, 25
G
Glaucoma drainage implants, 54
Glaucoma life story, 64
Glaucomatous optic neuropathy,
Appendix 8
indications of progression, 61
91
Index
P
Perimetry
automated, 22
frequency doubling, 23, 71
how to optimize patient performance,
Appendix 4
minimum acceptable resources for
examination, 14
tool for case detection, 71
Peripapillary atrophy, 18
treatment category, 25
Pigment dispersion syndrome
treatment category, 25
Posner-Schlossman syndrome
past ophthalmic history of, 12
Primary open angle glaucoma
epidemiology, 5, 69
surgery, 51
Primary angle closure glaucoma
epidemiology, 7, 65
surgery, 50
Prostagladins and other lipid receptor
agonists, 33, 34, 37
Pseudoexfoliation syndrome
treatment category, 25
R
Retinal nerve fiber layer examination, 19
Risk factors
reassessment at follow-up, 60
reduction, 26
S
Scotoma, 62, Appendix 9
SEAGIG decision square, 63
Secondary glaucoma
cause of uniocular blindness, 5
principles of management, Appendix 5
92
Surgery, 51
penetrating filtering, 51
non-penetrating, 51
use of anti-fibrotics, 53
Slit lamp
examination, 15, 16
minimum acceptable resources for
examination, 14
tool for case detection, 71
Synechiae
peripheral anterior, 18
risk factor for progression, 63
treatment category, 25
T
Tonometry
tool for case detection, 71
Goldmann-style applanation
tonometry, 15
how to test calibration, Appendix 1
measurement errors, 16, Appendix 2
minimum acceptable resources for
examination, 14
Tonopen, 15
Perkins tonometer, 15
Trabeculoplasty
laser, 41, Appendix 7a
V
van Herick technique, 17
tool for case detection, 70, 71
Visual field
causes of change in, 61
characteristics of glaucomatous
defects, 23
examination, 23
treatment categories, 25
Cover
20/11/03
10:35 AM
Page 1
A S I A PA C I F I C
Asia Pacific Glaucoma Guidelines
Glaucoma Guidelines
SEAGIG
2004
ISBN 0-9751692-0-3
www.seagig.org