ArticlePDF Available

Nuggets in clinical approach to diagnosis of glaucoma

Authors:

Abstract

Having a high index of suspicion and comprehensive examination are key to success in early diagnosis of glaucoma. The diagnosis of glaucoma is many a time straight forward in mid or late stages, but becomes elusive in early stages. Once a diagnosis of glaucoma is made then the patient is to be treated ether by medical line of treatment or with surgical intervention or with lasers and the follow-up remains to be life-long. So, one has to be very astute in making a diagnosis of glaucoma. Glaucoma not only affects the quality of vision, but also the quality-of-life. We all know the glaucoma is an irreversible blindness so early diagnosis is of prime importance. Opportunistic screening at our clinics with comprehensive eye examination is very important. This article deals with importance history taking and diagnostics in case of glaucoma. Perfecting our basics makes our life easier for further management.
Journal of Clinical Ophthalmology and Research - Sep-Dec 2013 - Volume 1 - Issue 3 175
Access this article online
Website:
www.jcor.in
DOI:
10.4103/2320-3897.116865
Quick Response Code:
Department of Ophthalmology, Amina Hospital and ESIS Hospital,
Solapur, Maharashtra, India
Address for correspondence: Dr. Sayyed Mazhar, 158-A Railway Lines,
Parijat Complex, Solapur, Maharashtra, India. E-mail: drsmazhar@
gmail.com
Manuscript received: 12.02.2013; Revision accepted: 06.06.2013
Glaucoma is defined as chronic progressive optic neuropathy that
has common characteristic morphological changes at the optic nerve
head (ONH) and retinal nerve fiber layer (RNFL) in the absence of
other ocular disease and congenital anomalies. Progressive retinal
ganglion cell death and visual field (VF) losses are associated with
these changes. Intraocular pressure (IOP) is a definite risk factor.
Among the emerging causes of blindness glaucoma needs a special
attention. Prevalence of glaucoma is 4% in the population aged
above 30 years. In children, it is estimated to be 3%; hence, we should
sharpen our clinical skills for diagnosing and managing glaucoma.
The diagnosis of glaucoma is based on structural and
functional changes in the ONH. History, IOP, gonioscopy, central
corneal thickness (CCT) and newer diagnostic modalities are
complimentary to the diagnosis.
History
In any illness history, taking is a prospective aspect in making a
diagnosis, but in glaucoma it is a retrospective history, which plays
a major role in management of the case. Here is small acronym
for history taking.
A= Asthma, Arthritis, Allergy, Attacks in the past
In asthma non-selective beta blockers are to be avoided and
selective beta blockers are to be given with care.[1,2] Salbutamol can
precipitate an attack of angle closure (AC). Arthritis and allergies
are many times treated with the long-term use of steroids. Steroids
through any root of administration can cause an increase in IOP in
steroid responders. Allergy to sulphate has to be checked before
using carbonic anhydrase inhibitors (CAI). History of attacks in
the past suggesting the increase in IOP is very important when
we are dealing with a case of narrow angles.
B= Blood pressure, Breathlessness, Blood loss, Blow to the eye
In patients using systemic beta blockers, topical administration
of beta blockers may be less effective.[3] So also systemic beta
blockers are to be avoided at night times to prevent further dip of
IOP. Breathlessness may be a sign of cardio pulmonary problems so
care is to be advocated while administering mannitol and topical
beta blockers.[4] Blood loss either due to major surgery or accident
causing severer hypovolemia may show changes in ONH, which
mimic normal tension glaucoma (NTG). Blow to the eye (trauma)
can direct us to see angle recession and other correlated subtle
changes. No matter what the duration of trauma was or how
trivial it was.
C = Cardio vascular system (CVS): Blocks, arrhythmias, cardiac
failure, Central nervous system: Migraine, head injury
,
convulsions, depression, Calculus: Urinary.
Beta blockers adverse effects with CVS have already been
mentioned. Migraine history is important, especially in cases
of NTG. Head injury may cause optic disc pallor and one has to
carefully look for VFs for neurological defects. Convulsions and
depressions are important because of the type of drug being
taken, which is discussed later. Calculus-CAIs when used for a
long-term can precipitate renal calculus because higher urine
calcium levels.
D = Diabetes, Drugs-systemic/topical/local/inhalators.
Although Baltimore I study did not find any association of
diabetes with open angle glaucoma (OAG), but recent population
studies support an association with diabetes.[5] Drugs-use of
any current medications needs to be considered along with
certain specific past medications, including. Steroids-any route
of administration is associated with ocular hypertension (OHT)
and OAG, sometimes found in traditional medicines. Glaucoma
eye drops (prolonged use may increase the likelihood of
trabeculectomy failure) Anticholinergics/tricyclic antidepressants
can cause AC Anticonvulsants: Topiramate can cause acute
AC. Vigabatrin linked to nasal peripheral VF loss without disc
changes. Systemic beta-blockers/calcium channel blockers-
may interact with topical beta blockers. Alpha agonists are
contraindicated for patients taking monoamine oxidase inhibitors
Commissioned Article
Nuggets in clinical approach to diagnosis of glaucoma
Sayyed Mazhar
Having a high index of suspicion and comprehensive examination are key to success in early diagnosis of glaucoma.
The diagnosis of glaucoma is many a time straight forward in mid or late stages, but becomes elusive in early stages.
Once a diagnosis of glaucoma is made then the patient is to be treated ether by medical line of treatment or with
surgical intervention or with lasers and the follow-up remains to be life-long. So, one has to be very astute in making
a diagnosis of glaucoma. Glaucoma not only affects the quality of vision, but also the quality-of-life. We all know
the glaucoma is an irreversible blindness so early diagnosis is of prime importance. Opportunistic screening at our
clinics with comprehensive eye examination is very important. This article deals with importance history taking and
diagnostics in case of glaucoma. Perfecting our basics makes our life easier for further management.
Key words: Gonioscopy, history, perimetry
[Downloaded free from http://www.jcor.in on Wednesday, September 28, 2016, IP: 178.255.21.35]
176 Journal of Clinical Ophthalmology and Research - Sep-Dec 2013 - Volume 1 - Issue 3
Mazhar: Nuggets in glaucoma
(prescribed for depression, migraine prophylaxis, or Parkinson’s
disease) and in infants and children check for sulphur allergy
prior to using CIAs.
E = Endocrine (thyroid), Error of refraction, Economic status.
A more recent study confirmed the association of graves
diseases with primary open angle glaucoma (POAG) and NTG.[6]
Patient can be hypothyroid, euthyroid or hyperthyroid when the
eye problem begins. Other pituitary problems can be associated
with anomalies of angle or the lens. Refractory errors around
± 6D are not much significant, but high myopes are thought as
a risk factor for POAG and high hypermetropes are risk factors
for primary angle closure glaucoma (PACG). Economic status of
patients helps us to prescribe a drug according to the patient
life-style and needs and hence increasing compliance in glaucoma
management.
F = Family history of glaucoma, Family status.
Risk of developing POAG in the first degree relatives is 4-16%.
Rotterdam found the risk to be as high as 10 times.[7] Family status
regarding female patient a history of amenorrhea and lactation are
of prime importance as drugs can act on the fetus or the new born.
Slit Lamp Examination
Before we put our hands on to specific diagnostic tools of glaucoma,
a basic slit lamp examination is a must. Attention must be paid
to the following areas. Cornea and anterior chamber for central
and peripheral anterior chamber depth (Von-Herick test) presence
of keratic precipitates, haab’s striae and corneal dimensions. Iris
should be seen for reactions, which is slowly reacted after and
acute, attack. Other abnormalities in the iris to be look for are
rubeosis iridis, patchy atrophy, synechiae, ectropion of uveal
pigment, pseudoexfoliative material, transillumination defects,
iris nodules and displaced pupil with iris atrophy. Examination of
lens also reveals certain diagnostic clues such as pseudoexfoliation,
glaucoma fleckens, phacodonesis or abnormal lens shape.
Tonometry
Type-tonometers can be classified as:
a. Direct or indirect
b. Low displacement tonometer or high displacement tonometer
c. Contact and non-contact tonometer
d. Indentation tonometer or applanation tonometer
e. Dynamic contour matching tonometer.
Goldmann applanation tonometry (1954) until today is
considered as the gold standard.
Whom: Every OPD patient above the age of 40 years.
When: Every visit. If diurnal variation is required then at 8
am, 11 am, 2 pm, 6 pm.
Astigmatism: When above 3D turn the prism head to 90° and
take the average of horizontal and vertical meridians OR rotate
prism head at 45° corresponding to least curved meridian.[8]
Procedure: Performed under topical anesthesia, fluorescein
staining, blue light, set knob at 1 g, turn the knob until inner
borders of Fl rings touch each other at the midpoint of their
pulsations. Take the average of three readings. Calibration of
tonometer should be checked frequently [Figure 1].
Sterilizations: I wipe it with sterlium and then with normal
saline swab. Calibration-should be done monthly. The calibration
rod should be tested at (0, 20, 60) mm of Hg potential errors-
thin cornea, thick cornea, astigmatism more (>) three diopters,
inadequate fluorescein, too much fluorescein, irregular cornea,
tonometer out of calibration, elevating the eyes >15°, repeated
tonometry, pressing on the eyelids or globe, squeezing of the
eyelids, observer bias (expectations and even numbers).
Tips: After taking IOP turn over to normal light to examine if
prism head had made any damage to the cornea.
Gonioscopy should not be followed by tonometry, but it should
be vice versa.
CCT [9,10]
Goldmann tonometer is calibrated for average corneal thickness of
520 microns. Excessive thick or thin corneas either over estimate
or under estimate IOPs Normal CCT is 520 microns (Indians)
Correction factor is 2.5 mm of Hg for every 50 microns. Increase
or decrease target IOP by one standard deviation (SD) for every 1
SD of CCT. 1 SD of IOP = 3 mm of Hg 1 SD of CCT = 30 microns.
Whom: Ideally for all glaucoma patients on making a diagnosis
more important for OHT/NTG and resetting of target IOP when -
ideally ½ h after awakening.
Frequency: Once in 5 years.
Why: It is risk factor for progression. Thin corneas are a risk
factor for progression especially in case of raised IOP.
How: Ultrasonic pachymetry is gold standard.
Expression: Thin - <500 microns/average - 500-600 microns/
thick - >600 microns.[11]
Gonioscopy
It is biomicroscopic examination of the anterior chamber
angle of the eye.
Principal: The gonio lens eliminates the total internal reflection
Figure 1: Caliberation of applanation tonometer. Current glaucoma
practice from glaucoma society of india year 2002
[Downloaded free from http://www.jcor.in on Wednesday, September 28, 2016, IP: 178.255.21.35]
Journal of Clinical Ophthalmology and Research - Sep-Dec 2013 - Volume 1 - Issue 3 177
Mazhar: Nuggets in glaucoma
of the cornea by exceeding the critical angle of 46°.
When: Initially for all patients. Repeat more frequently for
patient with AC.
Which lens: To start learning single mirror after learning curve
shift to four mirrors [Table 1].
Indications [12]
Diagnostics
1. To study topography of the anterior chamber angle [Figure 2]
2. To assess degree of opening of anterior chamber angle recess
3. To assess risk of closure on dilatation of pupil
4. Visualization of congenital anomalies
5. Classification of glaucoma (primary/secondary)
6. To note the presence and extent of angle neovascularization
7. Assessment of abnormal angle pigmentation
8. Visualization of pseudoexfoliative material in the angle
9. To look for post-traumatic angle recession, cyclodialysis
10. Rule out foreign body in the angle after open globe injury
11. Neoplastic invasion into angle structures (ciliary body tumor)
12. Diagnosis of epithelial down-growth
13. To look for vitreous strands incarcerated in the surgical wound
14. To view copper deposition on Descemet’s membrane
15. To study patency of trabeculectomy fistula
16. To view a peripheral laser iridotomy
17. To visualize the internal ostium of glaucoma drainage device
18. To see orientation of haptics of an anterior chamber intraocular
lenses.
Therapeutic
1. Laser trabeculoplasty
2. Excimer laser trabeculotomy
3. Goniotomy/gonioplasty
4. Laser goniophotocoagulation
5. Reopening of a blocked trabeculectomy opening
6. Neodymium-doped yttrium aluminum garnet laser after deep
sclerectomy
7. Laser of suture tied around tube of a glaucoma drainage device
8. Indentation gonioscopy to break an acute attack of PACG.
How: Gonioscopy should be performed to look for iridotrabecular
contact. Gonioscopy needs to be performed in a dark room with a
small slit-lamp beam.
1. Minimal room illumination
2. Good anesthesia
3. Shortest slit practicable
4. High magnification
5. Dim slit illumination
6. Set slit lamp or upper cornea, beam off-center 30°-45° nasally
7. If necessary, elevate upper lid
8. Place lens gently on eye while looking through slit lamp (as if
you are doing tonometry) no gel needed with Zeiss-type lenses
9. Look through the upper mirror (inferior angle) as you place
lens on eye, stop pushing when you can see the iris
10. Move slit-lamp beam inferiorly (avoid pupil) to examine
superior angle
11. Turn beam 90° and move on axis
12. Move to Nasal side (temporal angle) then to temporal side
(nasal angle)
13. Record findings on goniogram
14. In the presence of appositional closure, indentation should
be performed to look for Peripheral Anterior ynechiae
15. It may be necessary to alter the position of the mirror or the
position of the gaze to look over a convex iris to visualize the
angle
16. In steep iris profile do manipulative gonioscopy (over the hill view)
17. Indentation gonioscopy is used to open up the angle and
differentiate between oppositional or synechial closure.
What can happen on indentation
a. Concave iris opening (oppositional)
b. Angle widens but synechial closure seen
c. Iris moved backwards peripherally, but role of iris bulges out
and doesn’t assume concave configuration (plateau iris)
d. Iris moves slightly backwards, but maintains its convex profile
(large/displaced lens).
What to see
1. Level of iris insertion
2. Shape of peripheral iris profile
3. Width of the angle recess
4. Degree of trabecular pigmentation
5. Areas of iridotrabecular apposition
6. Areas of iridocorneal synechiae.
Normal adult angle
1. Ciliary body band
2. Scleral spur
3. Schlemm’s canal
4. Pigmented trabecular meshwork
5. Non-pigmented trabecular meshwork
6. Schwalbe’s line.
Tips
1. Start form top mirror
2. Identify corneal wedge to locate Schwalbe’s line
3. Avoid folds in descemet’s membrane, which is a sign excessive
pressure
4. Avoid excess illumination
5. Avoid direct light on pupil.
Documentation
There are four angle grading systems:[13,14]
1. Shaffer
2. Spaeth
3. Scheie
Table 1: Comparison of Goldmann single mirror and zeiss
four mirror
Type of lens Goldmann single
mirror
Zeiss four
mirror
Diameter of corneal contact 12 mm 9 mm
Angle of mirror height 62° 64°
Radius of curvature 17 mm 12 mm
Coupling uid Required Nor required
Indentation gonioscopy Not possible Possible
[Downloaded free from http://www.jcor.in on Wednesday, September 28, 2016, IP: 178.255.21.35]
178 Journal of Clinical Ophthalmology and Research - Sep-Dec 2013 - Volume 1 - Issue 3
Mazhar: Nuggets in glaucoma
4. RPC classification (Dr. Rajendra Prasad Centre for ophthalmic
sciences.
Tip
Practically document what you see [Figure 3]:
Pigmentation ± (Trabecular Meshwork 1-4)
Iris shape - S/R/Q
S - Straight; R - Regular; Q - Queer.
ONH
ONH evaluation is gateway to diagnosis of glaucoma [Figure 4].
Structural damage of ONH and RNFL are first to occur in glaucoma.
30-50% of ganglion cells are lost before a change is observed on
w/w perimetry.
Why: It defines glaucoma.
When: At every visit.
What: Qualitative:
Neuroretinal rim (NRR)
Optic disk hemorrhage
Para papillary choroidal atrophy
Barred circum linear vessels (CLV)
Nerve fiber layer (NFL) defect.
Quantitative:
Vertical disk diameter
Vertical cup to disk ratio (C:D)
Rim to disk ratio (R:D) at thinnest portion of rim
NFL height optical coherence tomography (OCT).
Size-average: 1.5-2 mm. Classify discs as small/average/large.
Stereoscopic views with the slit lamp using indirect condensing
lens and considering magnification factor.
60 D × 0.88
78 D × 1.1
90 D × 1.3.
Welch Allyn ophthalmoscope smallest aperture casts an
illumination of 1.75 Sq. mm.
Does refractive status play a role. Up to 5 D to +5D - no
change seen. Hyperopes more than +5D - small discs. Myopes
more than 5D - large discs note-small discs need more attention.
Cup disc ratio
1. Vertical cup disc ratio is important
2. Stereoscopic view is required
3. Small discs have small C:D
4. Larger discs have large C:D
5. Change in C:D ratio indicates progression over period of time
6. Difference of 0.2 in C:D of two eyes is very significant
7. C:D changes super seed the perimetric changes
8. C:D of 0.7 is taken as cut off from healthy eye and glaucomatous
eye.
Rim discs ratio
It is designed by Spaeth. Takes into consideration the vertical
long axis where the rim is thinned. It makes more sense than C:D.
NRR
1. The rim is more important than the cup
2. Cardinal feature of G ON is a loss of tissue from inner edge of
rim
Figure 2: Peripheral Anterior Synechiae Gonioscopy a text and atlas
(Tanuja Dada)
Figure 3: Diagraming gonioscopy with concentric circles. Dianosis and
therapy of the glucomas (Becker-Shaffer’s)
Figure 4: Neuroretinal rim Diagnosis and management of glaucoma
(Jaypee Highlights) (Arvind Eye Care System) Auther – R.
Ramakrishnan, SR Krishnadas, Mona Khurana, Alan L Robin
[Downloaded free from http://www.jcor.in on Wednesday, September 28, 2016, IP: 178.255.21.35]
Journal of Clinical Ophthalmology and Research - Sep-Dec 2013 - Volume 1 - Issue 3 179
Mazhar: Nuggets in glaucoma
3. Check inferior superior nasal temporal (ISNT) rule-in majority
of eyes the rim is broadest in the inferior disc region followed
by the superior disc region, the nasal disc region and finally
a temporal disc region
4. ISNT rule is followed in 50-60% of cases
5. Early rim loss is manifested at superior temporal and inferior
temporal region[15]
6. Bared of circum linear vessel (CLV) is an early sign of NRR
thinning
7. Color - pallor more than cupping is suggestive of neurological
disc
8. Cataractous eye gives a hyperemic hue
9. Localized pallor of NRR may be seen after an acute attack.
RNFL[16]
Where: To be seen in superior and inferior are arcuate zone within
two disc diameter of the disc.
Appearance: RNFL are thickest in upper and lower poles hence
double hump seen in imaging.
Loss is of two types wedge shaped and diffuses loss. Apex of
wedge is on a disc margin and fans out in arcuate zone. Vessels
appear darker.
How to see: On slit lamp with green filter or fundus photograph
or on imaging technologies.
Difficult is to be seen in older persons and lens opacities.
Parapapillary atrophy (PPA) changes [17-20]
Beta zone-marked atrophy of retinal pigment epithelium (RPE)
leading to good visibility of large choroidal vessel and sclera.
It is seen besides or next to disc margin. Alpha zone-hyper or
hypo pigmentation of RPE. It is next to alpha zone. PPA has
high prevalence in glaucomatous eyes. PPA is a risk factor for
progression.[21] PPA is a useful in detection of glaucoma progression
in myopia.
Vascular signs of glaucoma
Disc hemorrhage
1. They are splinter shaped or flame shaped at the border of optic
disc
2. Important risk factor for glaucoma progression
3. Suggestive of ongoing damage to the ONH
4. Independent risk factor for development of glaucoma
5. In OHT disc hemorrhage presence increases conversion risk
by 6 times[22]
6. Recurrent hemorrhages increases risk by 3-4 times[23]
7. 70% hemorrhages are not glaucomatous.
Bayone ing of vessel
Bayonetting is rarely seen in normal discs even in presence of
large physiological cups.
Retinal arteriolar narrowing
The diameter of arteriole is narrower at the immediate region
around the optic disc compared with its diameter in more
peripheral region of retina. It is not specific of glaucomatous
change.
BCLV: A small branch of central retinal artery or vein recedes
from the inner disc margin as the cup enlarges. Barring of CLV
should prompt us to look for other signs of glaucoma.
Nasalization of vessel: Progressive nasalization may occur as
a result of progressive NRR loss.
Acquired pit of optic nerve (APON)[24]
The difference between notch and pit is that an APON is localized
loss of optic nerve tissue extending deep into lamina and disc
margin. Notch doesn’t extend deep into lamina.
Steps in clinical examination of ONH
Determine disc size
Check for unusual disc shape
Determine the vertical C:D
Determine cup and rim size in relation to disc size
Evaluate rim shape (which is the narrowest rim) and apply
the ISNT rule
Check RNFL (red free illumination)
Look for disc hemorrhages
Look for vascular changes: Bending of vessels, BCLV, collaterals,
anterior constriction
PPA (beta zone)
High myopia: Rule out glaucoma
Rule out non-glaucomatous causes of cupping
Correlate VFs with optic disc changes.
Documentation
Disc drawings using colored pencils
Disc photographs monoscopy
Disc photographs stereoscopy
• Newer imaging technologies like Heidelberg Retinal
Tomogram /Optical Coherence Tomography/Glaucoma
Diagnostics -Variable Corneal Compensator.
Features of non-glaucomatous optic atrophy
Pallor more than cupping
Marked asymmetry between fellow eyes
VF defects respect vertical meridian an are out of proportion
to degree of cupping
Visual acuity out of proportion to degree of cupping
Relative Afferent Pupillary Defect in presence of C:D <0.3
• Younger age
• Unilateral progression.
Perimetery
Why: Defines state of optic nerve function. Define visual
impairment.
When: When Glaucoma in suspected on examination.
Machine: Humphrey/octopus/medmont.
Which test: Central fields 30.2 threshold, 24.2 threshold.
Defects approaching fixation use macular program.
How to read: GRADES.
Foveal threshold: V/A should correspond.
Patient’s reliability decreases with age health and fatigue.
Take care of: Pupil size at least 3 mm.
Refractive correction ± 3 D.
G - General information
R - Reliability
[Downloaded free from http://www.jcor.in on Wednesday, September 28, 2016, IP: 178.255.21.35]
180 Journal of Clinical Ophthalmology and Research - Sep-Dec 2013 - Volume 1 - Issue 3
Mazhar: Nuggets in glaucoma
A - Abnormal/normal
D - Defect
E - Evaluate clinically
S - Subsequent evaluation.
Interpretation-1. Global indices
Mean deviation (MD) = generalized depression.
Pattern standard deviation (PSD) = localized loss
Glaucoma hemi field test (GHT) = early affected and most
sensitive in early disease process.
2. Anderson criteria to be satisfied.
Approach of interpretation of VF defects according to the stage
of glaucoma is given in Table 2.
Tips[25]
1. When we use decibels (dB) to express light sensitivity a high
dB value indicates dim light and low dB value indicates bright
light.
2. In the point pattern the bare area around the fixation spot is
a circle of 3° radius because the distance between the points
to the axis is 3°.
3. Raw data is strategy specific. Different strategies will have
different raw data hence for comparison same test strategy
should be used in the same patient.
4. Statistical Packagecalculates the P value for the points where
there is loss of sensitivity.
5. The pattern deviation plot is nothing but the total deviation
minus a generalized field defect worth of the dB value that
converts the 7th best sensitivity points of Total Deviation
Numerical Plot to 0 deviations.
6. During follow-up tests, the most important index to assess
field progression is MD index.
7. The increase in MD >0.08 dB/year should be considered
abnormal.
8. Never come to a conclusion of foveal split unless you see 0 dB
sensitivity in any four points on 1° circle around fixation point
of 10-2 raw data.
9. GHT is useful only in early cases.
Andersons criteria
At least two consecutive occasions GHTs outside normal limits.
Cluster of three or more non-edge points in location typical for
glaucoma, all of which are depressed on PSD at a P < 5% and one
of which is depressed P < 1% (P = Probability) PSD that occur in
<5% of normal individuals.
How many times elds should be done
1. At least twice/ideally thrice to establish base line field.
2. Two consecutive reproducible fields to establish progress.
3. Mild glaucoma-yearly.
4. Moderate glaucoma-6 monthly.
5. Severe Glaucoma with macular area threatened-quarterly.
Field progression
Event based-shows changes
Trend based-shows rate of change.
Programs
1. Overview printout
2. Glaucoma change analysis
3. Glaucoma change probability
4. VF index.
Conclusion
Glaucoma being an important cause of irreversible blindness, its
early detection and appropriate management goes a long way
in reducing the socio economic burden of the individual’s family
and this country
. Currently the optimal method for detection
of glaucoma at our clinic is comprehensive eye examination of
individuals attending our clinic for any reasons.
References
1. Murthy GV, Gupta SK, Bachani D, Jose R, John N. Current estimates
of blindness in India. Br J Ophthalmol 2005;89:257-60.
2. Neufeld AH, Bartels SP, Liu JH. Laboratory and clinical studies
on the mechanism of action of timolol. Surv Ophthalmol 1983;28
Suppl:286-92.
3. Schuman JS. E ects of systemic beta-blocker therapy on the e cacy
and safety of topical brimonidine and timolol. Brimonidine Study
Groups 1 and 2. Ophthalmology 2000;107:1171-7.
4. Jones FL Jr, Ekberg NL. Exacerbation of asthma by timolol. N Engl
J Med 1979;301:270.
5. Dielemans I, de Jong PT, Stolk R, Vingerling JR, Grobbee DE,
Hofman A. Primary open-angle glaucoma, intraocular pressure,
and diabetes mellitus in the general elderly population. The
Ro erdam Study. Ophthalmology 1996;103:1271-5.
6. Wiersinga WM, Smit T, van der Gaag R, Koornneef L. Temporal
relationship between onset of Graves’ ophthalmopathy and onset
of thyroidal Graves’ disease. J Endocrinol Invest 1988;11:615-9.
7. François J, Hein -De Bree C. Personal research on the heredity
of chronic simple (open-angle) glaucoma. Am J Ophthalmol
1966;62:1067-71.
8. Moses RA. The Goldmann applanation tonometer. Am J
Ophthalmol 1958;46:865-9.
9. Ehlers N, Bramsen T, Sperling S. Applanation tonometry and
central corneal thickness. Acta Ophthalmol (Copenh) 1975;53:34-43.
10. Tonnu PA, Ho T, Newson T, El Sheikh A, Sharma K, White E, et al.
The in uence of central corneal thickness and age on intraocular
pressure measured by pneumotonometry, non-contact tonometry,
Table 2: Approach of interpretation of visual elds based
on the stage of glaucoma
The point pattern - 30-2
or 24-2
Testing strategy-SITA
standard
Reliability indices-100%
perfect
Reproducibility-t he field
defect should be
reproduce d a minimum
of two times
Anderson’s criteria
should be fulfilled
Established glaucoma
Aim-to know the depth
and extent of the field
loss and its relation to
fovea
24-2 point pattern
Raw data
Total deviation
numerical plot
Total deviation
probability plot
MD index should be
looked at
Advanced glaucoma
Aim-to know the exact
residual retinal
sensitivity and foveal
status
10-2 point pattern and
raw data sho uld be
concentrated upon
Glaucoma Suspect
Aim-to know w hether
glaucoma is p resent or
not
[Downloaded free from http://www.jcor.in on Wednesday, September 28, 2016, IP: 178.255.21.35]
Journal of Clinical Ophthalmology and Research - Sep-Dec 2013 - Volume 1 - Issue 3 181
Mazhar: Nuggets in glaucoma
the Tono-Pen XL, and Goldmann applanation tonometry. Br J
Ophthalmol 2005;89:851-4.
11. Schaknow PN, Samples JR, editors. The Glaucoma Book:
A Practical, Evidence-Based Approach to Patient Care. Springer
(India); 2010. p. 79-90.
12. Gonioscopy a Text and Atlas. (Tanuja Dada). Table 1.1 indications
for gonioscopy. New Delhi, India: Jaypee Brothers Medical
Publishers; 2006. p. 4.
13. Spaeth GL. The normal development of the human anterior
chamber angle: A new system of descriptive grading. Trans
Ophthalmol Soc U K 1971;91:709-39.
14. Spaeth GL. Gonioscopy: Uses old and new. The inheritance of
occludable angles. Ophthalmology 1978;85:222-32.
15. Jonas JB, Fernández MC, Stürmer J. Pa ern of glaucomatous
neuroretinal rim loss. Ophthalmology 1993;100:63-8.
16. Tuulonen A, Airaksinen PJ. Initial glaucomatous optic disk and
retinal nerve ber layer abnormalities and their progression. Am
J Ophthalmol 1991;111:485-90.
17. Jonas JB, Fernández MC, Naumann GO. Parapapillary atrophy and
retinal vessel diameter in nonglaucomatous optic nerve damage.
Invest Ophthalmol Vis Sci 1991;32:2942-7.
18. Jonas JB, Naumann GO. Parapaillary chorioretinal atrophy in
normal and glaucoma eyes. II. Correlations. Invest Ophthalmol
Vis Sci 1989;30:919.
19. Jonas JB, Nguyen XN, Naumann Go. Parapaillary chorioretinal
atrophy in normal and glaucoma eyes I, Morphometric data. Invest
Opthalmol Vis Sci 1989;30:908
20. Jonas JB, Xu L. Parapapillary chorioretinal atrophy in normal-
pressure glaucoma. Am J Ophthalmol 1993;115:501-5.
21. Teng CC, De Moraes CG, Prata TS, Tello C, Ritch R, Liebmann JM.
Beta-Zone parapapillary atrophy and the velocity of glaucoma
progression. Ophthalmology 2010;117:909-15.
22. Siegner SW, Netland PA. Optic disc hemorrhages and progression
of glaucoma. Ophthalmology 1996;103:1014-24.
23. Kim SH, Park KH. The relationship between recurrent optic
disc hemorrhage and glaucoma progression. Ophthalmology
2006;113:598-602.
24. Radius RL, Maumenee AE, Green WR. Pit-like changes of the
optic nerve head in open-angle glaucoma. Br J Ophthalmol
1978;62:389-93.
25. Ramakrishnan R, Krishnadas SR, Khurana M, Robin AL. Diagnosis
and Management of Glaucoma. 1st ed. Interpretation of Visual
Fields. New Delhi (India): Jaypee Highlights Medical Publishers;
2013. p. 182-95.
Cite this article as: Mazhar S. Nuggets in clinical approach to diagnosis of
glaucoma. J Clin Ophthalmol Res 2013;1:175-81.
Source of Support: Nil. Con ict of Interest: None declared.
[Downloaded free from http://www.jcor.in on Wednesday, September 28, 2016, IP: 178.255.21.35]
... The interpretation of field OCT and disc examination can be imparted with training modules on the basics of interpretation and hands-on activity with case-based scenarios [ Tables 5-7]. [7] Trabeculectomy remains the gold standard and cost-effective surgical management for glaucoma. Surgical treatment of glaucoma may be a first-line management strategy in moderate cases and is essential for treating advanced and severe glaucoma. ...
Article
Full-text available
Clinical skills training in Glaucoma is an intergral for the Glaucoma specialist of tomorrow. We discuss the various modalities and resources for glaucoma skills training.
Article
Purpose: Guidelines for the screening, prognosis, diagnosis, management and prevention of glaucoma were released by the Australian National Health and Medical Research Council in 2010. Comparable guidance has been made available by respective bodies in the USA and UK at a similar time. Key to successful translation of guidelines into clinical practice includes clinicians having the necessary skills to perform required tests. Optometrists in Australia and New Zealand were invited to participate in an online survey exploring these aspects. The results provide insights for improving glaucoma diagnosis and management by optometric primary eye care practitioners. Methods: An online questionnaire was developed to investigate glaucoma assessment of optometrists as a function of demographic details, educational background and experience. Key points to ascertain compliance with current guidelines were the availability of equipment, procedural confidence in techniques, and preferences in visual field tests. Chi square statistics was employed to support similarity to national averages and highlight differences between the two countries. Multivariate linear regression analysis identified variables significantly associated with individual tests being available to optometrists and their confidence in applying them. Results: Thirteen per cent of all Australian and 36% of the New Zealand optometrists responded to the survey in 2013, which reflected the demographics/geography of the practising populations. Techniques considered essential or preferred for glaucoma assessment were widely available in both countries with the exception of gonioscopy and pachymetry. After correcting for availability, regression models highlighted therapeutic endorsement and knowledge of glaucoma guidelines as the main variables to maintain high diagnostic confidence. Correlations to number of years in optometric practice mirrored a changed emphasis in teaching and technology over the past 10-15 years. Conclusions: Australian and New Zealand optometrists were well equipped to perform glaucoma assessments with the possible exception of gonioscopy. Advanced imaging modalities were not yet fully integrated into optometric practice, although optical coherence tomography has shown use by 23-32% of optometrists. A marked increase in use, availability and procedural confidence of gonioscopy and other techniques with therapeutically endorsed optometrists demonstrates the advantage and importance of additional training.
Book
The Glaucoma Book is both a comprehensive academic work with evidence-based science and exhaustive bibliographies, and an everyday, pragmatic guide for general ophthalmologists, optometrists, and resident physicians who need immediate answers while examining patients. Its 92 chapters and 38 sidebar essays range from conventional topics (e.g., open angle glaucoma, pigmentary dispersion syndrome, pediatric glaucomas) to those that have not previously appeared in a glaucoma text (e.g., medical-legal aspects of glaucoma care, doing community-based glaucoma research). Diagnostic tests and instrumentation, current and possible future medical therapies, and traditional and cutting-edge surgical interventions are thoroughly explored. The contributors come from well-known academic institutions and high-volume community based glaucoma practices. Photos, illustrations, and tables are sprinkled liberally throughout the book. The Glaucoma Book embodies the art and science of caring for glaucoma patients. Unique features not found in other texts include: *extensive sidebar essays by experts exploring cutting-edge subtopics within chapters *latest laser treatments for glaucoma, including micro-diode and titanium sapphire trabeculoplasty, as well as external laser approaches and reduction of intraocular pressure by applying laser to the pars plana *comprehensive coverage of the optic nerve, including thorough discussion of the importance of the nerve fiber layer hemorrhages *neuro-ophthalmological considerations, diagnostic procedures (e.g., MRI, CT), and other optic neuropathies to consider when examining the glaucoma patient *combination of clinical science and basic science with expert commentary on the frontiers of future medical and surgical therapies that are likely to emerge for patient care *an integrated approach to neovascular glaucoma, merging treatment from the anterior segment to the retina, the use of new anti-VEGF drugs, and the use of tubes and shunts to achieve the best surgical outcome *exceptional advice on how to deal with the complications of various glaucoma surgeries by leading clinicians, as well as an outstanding chapter on trabeculectomy techniques for the general ophthalmologist *the best written overview of visual fields in glaucoma bar none *a complete description of a comprehensive office-based examination of the glaucoma patient, including clinical pearls (e.g., gonioscopy, visual field analysis, digital image analysis (OCT, GDx, HRT) , optic nerve photography) *contemporary issues and controversies about the importance of intraocular pressure (IOP) *the drug development process-what really goes on at the FDA to bring new glaucoma medications from the lab bench to clinical use-and how the community-based practices can participate. In short, this is the one book on glaucoma that no general eyecare physician who sees glaucoma patients can afford to be without. It is loaded with pearls and practical advice by expert, experienced clinicians and scientists, while firmly grounded in a scientific view of the disease. © Springer Science+Business Media, LLC 2010. All rights reserved.
Article
Beta-Zone parapapillary atrophy (PPA) occurs more commonly in eyes with glaucoma. Rates of glaucomatous visual field (VF) progression in eyes with and without beta-zone PPA at the time of baseline assessment were compared. Retrospective, comparative study. Two hundred forty-five patients from the New York Glaucoma Progression Study. Subjects with glaucomatous optic neuropathy and repeatable VF loss were assessed for eligibility. Eyes with a Heidelberg Retina Tomograph II (HRT) examination, at least 5 visual field tests after the HRT in either eye, optic disc photographs, and <6 diopters of myopia were enrolled. beta-Zone PPA was defined as a region of chorioretinal atrophy with visible sclera and choroidal vessels adjacent to the optic disc. Global rates of VF progression were determined by automated pointwise linear regression analysis. Univariate analysis included age, gender, ethnicity, central corneal thickness (CCT), refractive error, baseline mean deviation, baseline intraocular pressure (IOP), mean IOP, IOP fluctuation, disc area, rim area, rim area-to-disc area ratio, beta-zone PPA area, beta-zone PPA area-to-disc area ratio, and presence or absence of beta-zone PPA. The relationship between beta-zone PPA and the rate and risk of glaucoma progression. Two hundred forty-five eyes of 245 patients (mean age, 69.6+/-12.3 years) were enrolled. The mean follow-up was 4.9+/-1.4 years and the mean number of VFs after HRT was 9.3+/-2.7. beta-Zone PPA was present in 146 eyes (65%). Eyes with beta-zone PPA progressed more rapidly (-0.84+/-0.8 dB/year) than eyes without it (-0.51+/-0.6 dB/year; P<0.01). Multivariate regression showed significant influence of mean IOP (hazard ratio [HR], 1.11; P<0.01), IOP fluctuation (HR, 1.17; P = 0.02), and presence of beta-zone PPA (HR, 2.59; P<0.01) on VF progression. Moderate (0.5-1.5 dB/year; P = 0.01) and fast (>1.5 dB/year; P = 0.08) global rates of progression occurred more commonly in eyes with beta-zone PPA than in eyes without it. Thinner CCT (<525 microm) had a weak but significant correlation with presence of beta-zone PPA (kappa = 0.13). Eyes with beta-zone PPA are at increased risk for glaucoma progression and warrant close clinical surveillance.
Article
The goniolens has become increasingly important in the practice of ophthalmology, For example, the treatment of angle closure and neovascular glaucoma is most effective in the earliest stages of the diseases, even prior to the onset of symptoms. Routine gonioscopy is essential if patients are to be provided optimum care. The critical nature of pressure gonioscopy is reviewed. The use of the goniolens to examine the corneal endothelium is described and recommended. Characterization of the configuration of the angle recess demands description of at least three aspects: (1) the angular approach to the recess, (2) the peripheral curvature of the iris, and (3) the point of insertion of the iris onto the ciliary body or endothelial surface. The nature of these three considerations is reviewed, as is their frequency in a normal population, in a group of ten people with definite 1 degree angle-closure glaucoma, and in 95 relatives of the subjects with angle-closure glaucoma. Marked anterior convexity of the peripheral iris appears to be highly correlated with the development of 1 degree angle closure. The three aspects of the angle configuration appear to be independently inherited. Gonioscopy of relatives of cases with 1 degree angle-closure glaucoma is highly recommended.
Article
Six patients with open-angle glaucoma and acquired pit-like changes in the optic nerve head are presented. In 1 patient evolution of the pit-like defect is documented. In all 6 patients progression of associated visual field deficits is described. It is suggested that such pit-like changes in selected patients with glaucoma may not represent congenital lesions but rather local, progressive nerve head disease, occurring particularly in response to raised intraocular pressure. The management of patients with optic nerve head pitting and the pathogenesis of glaucomatous optic neuropathy are discussed with respect to this observation.
Article
Readings with the Goldmann applanation tonometer were made at various intraocular hydrostatic pressures and compared with central corneal thickness and radius in rabbit and in man. Linear correlations were established between hydrostatic pressure and applanation readings, with correlation coefficients close to 1.0. In rabbits the tonometer readings were generally too low. In human eyes with a normal corneal thickness tonometer readings and hydrostatic pressure coincided, with thick corneas the readings were too high, with thin corneas too low. The correlation between corneal thickness and the error of applanation tonometry (ΔP) was statistically highly significant (P < 0.001). No statistical correlation could be established between corneal radius and ΔP. Multiple regression, taking thickness as well as corneal radius into consideration, revealed only slightly higher correlation coefficients. It is concluded that the central corneal thickness is a parameter which should be taken into consideration when evaluating applanation tonometer readings. A Table is presented showing the correction to be added to the applanation reading at differing corneal thickness.
Article
Parapapillary chorioretinal atrophy and decreased retinal vessel diameter occur in glaucomatous eyes. To evaluate the frequency and degree of these signs in nonglaucomatous optic neuropathy, the authors evaluated morphometrically and compared 47 patients with nonglaucomatous optic nerve atrophy from extraocular causes with 292 patients with primary open-angle glaucoma and 179 normal subjects. Eyes with anterior ischemic optic neuropathy were excluded. The parapapillary atrophy was differentiated into a central zone (beta) with sclera and large choroidal vessels visible by ophthalmoscopy and a peripheral zone (alpha) with irregular pigmentation. Both zones did not differ significantly in the eyes with nonglaucomatous optic neuropathy and the normal eyes. In the glaucomatous eyes, they were significantly larger and occurred more frequently. The retinal vessel diameter was significantly smaller in both groups with optic nerve atrophy than in the normal group. It was concluded that decreased retinal vessel diameters unspecifically suggest optic nerve atrophy. Evaluation of parapapillary chorioretinal atrophy can be helpful in differentiating nonglaucomatous from glaucomatous optic neuropathy.
Article
We attempted to identify the initial glaucomatous changes of the optic disk and retinal nerve fiber layer and to analyze how these changes subsequently progressed. Of 61 eyes of 61 patients with ocular hypertension, 23 (38%) developed glaucoma during ten years of follow-up (range, five to 15 years). The initial sign of glaucomatous damage was diffuse enlargement of the optic disk cup in ten of 23 eyes or generalized thinning of the nerve fiber layer without localized changes in 12 of 23 eyes. We found localized optic disk damage in ten of 23 patients and localized retinal nerve fiber layer damage in 11 of 23 patients alone or in combination with diffuse damage. In 13 of 23 eyes, the cupping ended up in diffuse enlargement with even more profound thinning of the neural rim in the upper and lower temporal disk margins. There seems to be great variability in the appearance and progression of the initial glaucomatous optic disk and nerve fiber layer abnormalities in patients with increased intraocular pressure.
Article
The parapapillary chorio-pigment-epithelio-retinal atrophy in glaucomatous eyes is significantly larger than in normal eyes. In a previous study its area and frequency have been measured in 582 eyes of 321 patients with chronic primary open-angle glaucoma and in 390 eyes of 231 normal subjects. In the current study the parapapillary changes were correlated with intrapapillary morphometric data and with perimetric indices. The parapapillary chorioretinal atrophy was significantly correlated with the neuroretinal rim area, the horizontal and vertical cup/disc ratios, the quotient of horizontal to vertical cup/disc ratio, the retinal nerve fiber layer score, and the mean visual field loss. It was larger in the same sector where the neuroretinal rim loss was more marked. The correlation coefficients were generally higher for zone "Beta," characterized by complete chorioretinal atrophy with visible large choroidal vessels and sclera, than for zone "Alpha," which showed irregular hypo- and hyperpigmentation. The parapapillary chorioretinal atrophy was correlated in location and time with the intrapapillary glaucomatous changes. It deserves attention in glaucoma diagnosis and follow-up. Its evaluation is especially valuable in eyes with small optic nerveheads (disc size less than 1.6 mm2) in which the intrapapillary glaucomatous changes occur later than the parapapillary ones.