Approach to a glaucoma

1. Approach to a
Patient with
Glaucoma
By Dr Lakshmi K S
Moderator: Dr Rajani Kadri

2.  Glaucoma is defined as a group of
disorders characterized by a progressive
optic neuropathy resulting in a
characteristic appearance of the optic disc
and a specific pattern of irreversible visual
field defects that are associated frequently
but not invariably with raised intraocular
pressure (IOP).

3. Proforma for examination
 PRILIMNARY DATA
• Name:
• Age:
• Sex:
• Occupation:
• Address:
 HISTORY TAKING
• Chief complaints:
• History of presenting
complaints:
• Past history:
• Personal history:
• Family History:
 EXAMINATION
• General Physical
Examination:
• Systemic Examination:
 OCULAR EXAMINTION
• VISUAL ACUITY
 ANTERIOR SEGMENT
EXAMINATION:
• EYE LIDS
• CONJUNCTIVA
• CORNEA
• SCLERA
• ANTERIOR CHAMBER
• IRIS
• PUPIL
• LENS
• FUNDUS
• IOP
• ANGLE OF ANTERIOR
CHAMBER
 VISUAL FIELD TESTING
 NEWER
TECHNOLOGIES

4. PRILIMNARY DATA
 Name: identification and familiarisation
 Age: POAG=40-60 yrs, NTG>60 yrs, ACG
with pupillary block- 60 yrs, ACG without
pupillary block-40-50 yrs.
 Sex: OHT- males, OHT→POAG- males,
NTG- females, PACG- females
 Occupation: Lower levels of occupation-
increased visual morbidity
 Address: POAG- European and African
ethnicity, NTG- Japanese, PACG-Indians

5. Chief Complaints
Symptoms depend upon:
1. Onset of disease—acute and chronic
2. Age of patient- higher the age, greater is the risk of visual loss
3. Rise of IOP
• How fast- acute rise- acute symptoms, chronic raise- may be
asymptomatic
• How much- PACG and Pseudoexfoliative Glaucoma- VF
change correlation with IOP high, POAG- VF change
correlation is less
• Duration of raised tension- longer the duration, more is the
glaucomatous damage and larger is the field defect
4. Associated ocular diseases: cataract, uveitis, trauma,
retinopathy and vascularisation

6. 1. No symptoms
2. Visual
(a) Diminished distant vision
• Sudden—acute glaucoma, both primary or
secondary
• Gradual—all chronic glaucomas with moderate
rise of tension
(b) Diminished near vision: Early onset of presbyopia and frequent
change of presbyopic glasses is seen in chronic simple glaucoma
(c) Loss of field—Unless there is extensive loss of field, it may go
unnoticed; however patient with good central vision and constricted
peripheral field may complain of tubular vision
(d)Photophobia is seen in congenital glaucoma due to rupture of
Descemet’s membrane
(e)Colored haloes are seen in sudden, moderate to high, rise of IOP.
Common causes are prodromal stage of primary angle closure
glaucoma, acute secondary glaucoma and epidemic dropsy glaucoma

7. 3 . Lacrimation is prominent feature of congenital glaucoma and acute
glaucomas
4. Pain is seen in acute rise of tension, both primary and secondary. In
acute congestive glaucoma, it is a very prominent feature, a
throbbing ocular pain with peri orbital tenderness associated with
nausea/vomiting. Unexplained pain in uveitis and corneal ulcer may
raise the suspicion of glaucoma.
5. Redness of eye
(a) Circumciliary congestion is seen in acute congestive glaucoma,
chronic congestive glaucoma and some secondary glaucomas
(b) Episcleral congestion is seen in absolute glaucoma and raised
episcleral pressure

8. History of Presenting illness
 Previous attack of acute glaucoma
 Treatment taken for any glaucoma
 Trauma, surgery, uveitis, retinopathy
 Diabetes, hypertension, dysthyroid
condition, epidemic dropsy
 Local or systematic use of steroid
 Coloured haloes

9.  Past history: diabetes, hypertension,
asthma, seizures
 NTG associated systemic diseases-
migraine headache, raynauds disease, MI,
nocturnal hypotension, autoimmune
diseases, shock syndromes, anaemias,
DM, sleep aopnea syndrome
 Family history: glaucoma, diabetes,
Hypertension
• Risk is increased by x2 if parent has POAG
• Risk is increased x4 if sibling has POAG
 Personal history: smoking, alcohol

10. General examination
 Systemic diseases associated with Glaucoma
1. autoimmune diseases-JRA, Ankylosing spondylitis
2. Infections- congenital Rubella, Leprosy, Syphillis
3. Vascular and hematologic disorders(NVG)- sickle cell anemia,
vessel occlusions
4. Neoplasias- metastatic CA of breast an d lung
5. when the glaucoma and systemic disorder are parts of a
syndrome- Phakomatoses, Axenfeld Reiger Syndrome, Marfans
dyndrome, Weil Marchesaani syndrome
6. when the glaucoma and systemic disease are frequently seen in
the same patient but there is noestablished cause-and-effect
relationship- systemic hypertension, hypothyroidism, migraine
headaches, nocturnal hypotension, sleep apnea, and silent
myocardial infarction

11. OCULAR EXAMINATION
 Visual acuity:
(a) Without glasses—will give the extent of visual loss
(b) With pinhole—will indicate the limit to which vision can be salvaged
with treatment
(c) With spectacle—will show the type of error of refraction, the patient
is suffering from. Myopes are more often associated with POAG
while PNAG is commonly seen in hypermetropia. Many a times,
patient may not be aware of diminished vision especially if it is
uniocular

12. In some patients, vision deteriorates with treatment of glaucoma:
 Miotics will
(a) Reduce vision in cases associated with central nuclear cataract,
central corneal opacity and macular lesion
(b) Cause diminished night vision
(c) Reduce field of vision
(d) Produce difficulty in near vision
 Carbonic anhydrase inhibitors may produce transient myopia
 Anti-glaucoma surgery may produce:
• Troublesome astigmatism
• Persistent hypotony

13. Coloured haloes
 DDs: acute mucopurulent conjunctivitis, ACG, Incipient
cataract
 Fincham’s test is done using the staenopic slit to differentiate
the colored haloes caused by cataract (lenticular) from that
caused by glaucoma (corneal). Staenopic slit is moved across
patient’s eye while the patient looks at a bright point source of
light which gives rise to halo. The halo caused by
cataract breaks into a fan the blades of which seem to
move whereas the halo caused by glaucoma
remains unchanged or just becomes a little faint. This is
caused by peculiar disposition of the lens fibers which cause
diffraction of light parallel to them.

14. Anterior Segment Examination
 Eye Lids: congested and
edematous in an acute attack of
angle closure glaucoma
 Conjunctiva
(i) Circumciliary congestion is seen
in acute
congestive glaucoma, chronic
congestive
glaucoma and absolute glaucoma
(ii) Episcleral congestion is seen in
raised episcleral pressure.
Typical corkscrewing of vessels
seen. d/d CCF

15. Cornea
(i) Rupture in Descemet’s membrane and Haab’s
striations are seen in congenital glaucoma
(ii) Corneal oedema is seen in acute rise of tension
(iii) Krukenberg spindle is sometimes seen in
Pigment dispersion glaucoma
(iv) KP may be present following acute rise of
tension, or uveitis
(v) Band keratopathy is seen in long-standing
glaucoma
(vi) Diminished corneal sensation is seen with acute
rise of tension
(vii) Bullous keratopathy is seen in absolute
glaucoma
(viii) Vascularisation may be present in the absolute
stage

16. Sclera
(i) Thinning and stretching of sclera is very common in congenital
glaucoma
(ii) Scleral ectasia is seen in congenital glaucoma and sometimes in
absolute glaucoma
Anterior chamber depth
(i) Normal—in chronic simple glaucoma and some secondary
glaucomas
(ii) Shallow—in NAG, lens-induced glaucoma and malignant glaucoma
(iii) Deep—buphthalmos, aphakic glaucoma, trauma and pseudo-
phakic glaucoma

17. Measurement of anterior
chamber depth
(a) By oblique illumination
(b) Comparing corneal thickness to anterior
chamber depth - Van Herick’s grading
(c) Shadow of temporal iris
(d) Pachymetry
(e) A Scan
(f) B Scan
ANGLE DEPTH
Grade 4 angle AC depth =corneal thickness
Grade 3 angle AC depth= ¼ to ½ corneal thickness
Grade 2 AC depth= ¼ corneal thickness
Grade 1 angle AC depth= less than ¼ corneal
thickness
Slit angle AC depth=slit like (extremely shallow)
Closed angle Absent peripheral anterior chamber

18. UBM
 Helps in differentiating open and closed
angle glaucoma
 Diagnosis of
• Plateau iris syndrome
• Angle recession glaucoma
• Lens induced glaucoma
• Cysts and tumors of angles causing
glaucoma

19. Iris(i) Loss of pattern is due to oedema or
iris; it is commonly seen in acute
congestive attack of glaucoma,
both primary and secondary
(ii) Atrophic patches are seen following
iritis glaucomatosa, chronic
congestive glaucoma and absolute
glaucoma- segmental iris atrophy
in ACG and herpes simplex uveitis
and diffuse in OAG, Senility,
Chronic uveitis.
(iii) Posterior synechiae—sudden high
rise of intraocular tension, anterior
uveitis, iritis and glaucomatosa
result in posterior synechiae
(iv) Peripheral anterior synechiae are
seen following unrelieved tension
in acute congestive glaucoma,
chronic uveitis and neo-vascular
glaucoma

20. (v) Neovascularisation—
thrombotic glaucoma
(vi) Coloboma—surgical,
laser and trauma
(vii) Holes—(positive trans-
illumination) are seen in
essential iris atrophy,
mesodermal dys-genesis
of anterior chamber,
glaucomatocyclitic uveitis,
heterochromic uveitis,
pigment dispersion
syndrome and herpes
zoster
(viii) Flakes are seen in
pseudo-exfoliation
syndrome

21. Pupil
 A large, sluggish pupil with fairly good vision, without a history of
use of mydriatic, in a person past 40 years should raise the
possibility of increased intraocular tension unless proved otherwise
 An afferent pupillary defect in glaucoma denotes unilateral
advanced glaucomatous change in the optic disc
 A Mid-dilated, sluggish, vertically oval pupil in a congested eye
means acute narrow-angle glaucoma due to the nerve endings
being concentrated on superior and inferior poles and vessel
bundles being concentrated on the horizontal poles
 A constricted pupil should invite enquiry about the instillation of a
miotic, its strength and frequency. All small pupils should be
examined to exclude iritis
 Distorted pupil is seen in trauma, uveitis, chronic congestive
glaucoma and absolute glaucoma

22. Lens
 Cataract: Mature /
Hypermature (Lens Induced
Glaucoma)
 Pseudoexfoliation material
 Glaucomflecken (with patchy
iris atrophy and mid dilated
non reacting pupil forms the
vogt’s triad of ACG)
 Pigments on lens
 Posterior synechae
 Complicated cataract-
chronic glaucoma

23. Fundus
Media
clear
Glaucoma
evaluation
Hazy
cataract
Fundus Changes in
glaucoma
 Glaucomatous damage
results in characteristic
signs involving
 (a) the optic nerve head,
 (b) the peripapillary area
 (c) the retinal nerve fibre
layer

24. Optic Nerve Head
 Cup Disc Ratio: Normal is 0.3-0.5
 The appearance and pattern of disc damage
may correlate with subtypes of glaucoma and
provide clues as to the pathogenic mechanisms
involved. Four ‘pure’ glaucomatous disc
appearances have been described, although the
majority of discs are unclassifiable
1. Focal ischaemic discs are characterized by
focal superior and/or inferior polar notching
2. Myopic disc with glaucoma refers to a tilted
(obliquely inserted), shallow disc with a
temporal crescent of parapapillary atrophy,
together with features glaucomatous damage
3. Senile sclerotic discs are characterized by a
shallow, saucerized cup and a gently sloping
NRR, variable peripapillary atrophy and
peripheral visual field loss
4. Concentrically enlarging discs (verified by
serial monitoring) are characterized by uniform
NRR thinning

25. Non-specific signs of
glaucomatous damage
 Baring of circumlinear blood vessels is a sign of early thinning
of the NRR. It is characterized by a space between a superficial
blood vessel that runs from the superior or inferior aspects of the
disc towards the macula, and the disc margin
 ‘Overpass cupping’, in which there is loss of NRR underlying
vessels, leaving space between the bridging vessels and the
remaining nerve tissue, is similar.
 Bayoneting is characterized by double angulation of a blood
vessel With NRR loss, a vessel entering the disk from the retina
may angle sharply backwards into the disk and then turn towards
its original direction to run across the lamina cribrosa.

26.  Size of the disc: 1.5-1.7mm is normal size. Vertical diameter is
measured on slit lamp biomicroscopy. Larger discs are more
amenable to glaucoatous damage.
 Collaterals between two veins at the disc
 Loss of nasal NRR is a sign of moderately advanced damage;
a space may develop between the NRR and the central retinal
vasculature. Does not follow ISNT rule. Highly sensitive but not
specific.
 Lamina dot sign occurs in advancing glaucoma. The gray dot-
like fenestrations in the lamina cribrosa become exposed as
the NRR recedes
 Disc haemorrhages (Drance Haemorrhagea) often extend
from the NRR onto the retina, most commonly inferotemporally
 ‘Sharpened edge’ or ‘sharpened rim’ is a sign of advancing
damage. As NRR is lost adjacent to the edge of the disc, the

27. (A) Inferior baring of circumlinear blood vessels; (B) inferior
bayoneting; (C) collaterals; (D) loss of nasal neuroretinal rim;
(E) lamellar dots; (F) disc haemorrhage

28. Disc Damage Likelyhood Scale
 The disc damage likelihood scale (DDLS) was devised
by Spaeth et al in 2002 to incorporate the effect of disc
size and focal rim width into a clinical grading scale
 Disc size can be measured using a fundus lens at the
slit-lamp
 A 66D gives the exact measure from the graticule.
Correction factors for the other lenses are
Volk
60D-0.88
78D-1.2
90D-1.33

29.  DDLS advocates measurement of the width of
the thinnest part of the rim.
 This forces the examiner to evaluate the rim
throughout its entire circumference in order to
identify the area of greatest thinning. The
measurement is expressed in rim:disc. Where
there is no rim present at the thinnest point the
value is 0. The circumferential extent of rim
absence is then measured in degrees.

31. Peripapillary changes
 Peripapillary atrophy surrounding
the optic nerve head may be of
significance in glaucoma and may
be a sign of early damage in
patients with ocular hypertension.
 Alpha (outer) zone is
characterized by superficial retinal
pigment epithelial changes. It
tends to be larger and possibly
more common in glaucomatous
eyes.
 Beta (inner) zone is
characterized by chorioretinal
atrophy. It is larger and more
common in glaucoma.

32. Retinal nerve fibre layer
 In glaucoma subtle retinal nerve
fibre layer (RNFL) defects precede
the development of detectable optic
disc and visual field changes; their
onset often follows disk
haemorrhages. Two patterns occur:
 (a) localized wedge-shaped defects
 (b) diffuse defects that are larger
and have indistinct borders
Red-free (green) light increases the
contrast between normal retina and
defects on slit-lamp biomicroscopy and
typically makes identification easier

33.  Retinal nerve fibre layer
Nerve fiber layer dropout
 Optic nerve head
1. Focal notching of neuroretinal rim - Thining of
infero-temporal Rim (ISNT rule is not
preserved)
2. Vertical elongation of cup
3. Asymmetry of cupping between 2 eyes
 Non specific signs of glaucomatous damage
1. Baring of circumlinear blood vessels
2. Splinter haemorrhages

34.  Optic nerve head
1. Generalized enlargement of cup
2. Vertical elongation of cup
3. Asymmetry of cupping between 2 eyes
 Peripapillary changes
 Non specific signs of glaucomatous damage
1. Exposure of lamina cribrosa
2. Bayoneting (double angulation of blood
vessel)

35. Intra Ocular Pressure
 IOP is the oncotic pressure exerted by the
contents of the eyeball on the coats of the
eyeball to maintain the integrity of the eye
ball. The normal intraocular pressure is
between 10 mm Hg and 21 mm Hg.
 Goldman’s applanation tonometer is the
gold standard instrument for IOP
measurement

36. (a) More than 21 mm
 Established glaucoma
 Ocular hypertension
(b) Less than 21 mm
 Normal
 Glaucoma suspect
 Glaucoma under treatment
 Normal tension glaucoma

37. Central Corneal Thickness
 The CCT is undoubtedly of value in management of
both glaucoma and glaucoma suspects, especially
occur hypertension.
 Thicker corneas produce falsely higher reading while
thinner corneas produce falsely lower readings.
However, corneal thickening due to edema causes a
falsely lower reading.
 A meta-analysis of many different populations
deduced 2.5 mm Hg for every 50 µ increase in CCT
 An average error is 0.5-0.7 mm Hg per 10 microns of
deviation from the mean of 520 microns.
 Patients with less than 555 U had 3 times greater risk
of POAG

38. CCT importance to predict
glaucoma risk (OHTS)

39.  Conditions which influence IOP
i. Diurnal variation
ii. Postural variation
iii. Exertional influences
iv. Lid and eye movement
v. Intraocular conditions
vi. Systemic conditions
vii. Environmental conditions
viii. General anesthesia
ix. Food and drugs

40. In an eye suspected to have glaucoma, if
any of the following is present then the eye
should be subjected to fundus, field and
gonioscopy examination.
1. If there is difference in IOP more than 7
mm between the two eyes
2. Diurnal variation—positive
3. Provocative test—positive

41. There are four types of diurnal variation curves.
They are:
i. Falling type: maximal at 6–8 am followed by a continuous decline
ii. Rising type: maximal at 4–6 pm
iii. Double variation type: with 2 peaks 9–11 am and 6 pm
iv. Flat type of curve.
 The most common pattern is that the IOP is maximum in the
morning and decreases as day progresses and becomes minimum
in the evening. It once again starts to rise as the night progresses.
The variation is about 3 to 6 mm Hg in normal individuals. The
variation is about 10 mm Hg or more in a glaucomatous eye.
 It is due to cyclic fluctuation of blood levels of adrenocortical
steroids. Maximum IOP is reached 3 to 4 hours after the peak of
plasma cortisol. The night time elevated IOP is due to the supine
position along with the fluctuating cortisol levels.

42. The various provocative tests include:
i. Mydriatic test
ii. Dark room test
iii. Prone test
iv. Prone dark room test
v. Phenylephrine-pilocarpine test
vi. Triple test.

44. Examination of Angle of
Anterior Chamber
Angle of anterior chamber is formed by the anterior and posterior
borders of anterior chamber
Through the angle, AC communicates with extracellular spaces of iris,
ciliary body and trabecular meshwork.
Volume of AC= 220micro liter
AC depth= 3.15mm (2.6-4.4)
AC diameter=11.3-12.4mm

45. GONIOSCOPY
Biomicroscopic examination of the anterior
chamber
Works on the principle of prevention of total
internal reflection of rays reflected from far
peripheral iris, angle recess, and trabecular
meshwork, by using a contact lens to
eliminate the air cornea interface.

46. Total internal reflection occurs because angle of
incidence of rays of from the angle structures is
greater than the critical angle of cornea-air interface
(46 degrees)
Gonioscopic contact lenses have refractive index
similar to cornea, hence eliminate the optical effect
of the front corneal surface.
Ziess 4 mirror contact lens is most commonly used
goniolens for gonioscopy

47. A- structures normally seen on gonioscopy in an open angle
B-CBB is light grey and TM is heavily pigmented. The thinner
pigmented line above the meshwork is the Schwalbe's line
C-iris processes
D- reflux of blood in schlemm’s canal is helpful in identifying the
pigmented TM

48. SHAFFER GRADING
GRAD
E
ANGLE
WIDTH
CONFIGURA
TION
CHAN
CE OF
CLOS
URE
STRUCTURES
VISIBLE ON
GONIOSCOPY
IV 30-40 WIDE OPEN NIL SCHWALBE’S LINE
TO CILIARY BODY
III 20-30 OPEN NIL SCHWALBE’S LINE
TO SCLERAL SPUR
II 20 MODERATE
LY NARROW
POSSI
BLE
SCHWALBE’S LINE
TO TRABECULAR
MESHWORK
I 10 VERY
NARROW
HIGH SCHWALBE’S LINE
ONLY
0 0 CLOSED CLOS
ED
NONE

49. Tests for visual fields
 Kinetic perimetry: manual confrontation
method, goldmann’s perimeter, listers
perimetry
 Static perimetry: capimetry (tangent
screen testing), Humphry’s perimeter

50. Confrontation method
 First test the binocular visual field and
then test each eye separately. A
defect is detected by the absence of a
patient response to the showing of a
target, when the target is visible to
you.
 Testing to confrontation with both
eyes open
 Testing each eye to confrontation

51. Humphry’s Visual fields in
glaucoma
 Glaucomatous visual field loss commonly occours
in the arcuate area in the sup and inf hemifields
 These areas arch around the fovea, starting from
optic disc and extending nasally to end at the
horizontal raphe.
 A relative decrease in retinal sensitivity (relative
scotoma) in this rea is usually the first evidance of
glaucoma. These scotomas tend to occur nasally
and there is significant asymmetry bet sup and inf
visual fields.

52.  Localised field defects- hallmark of
glaucoma but are frequently associated
with overall reduction in sensitivity.
 A pure generalised reduction in sensitivity-
more likely to be due to media opacities.

53. Characteristics of glaucomatous
defects
 Asymmetrical across the horizontal midline.
 Located in the mid-periphery (5-25 degrees from
fixation)
 Reproducible
 Not attributable to other pathology.
 Localised
 Correlating with the appearance of the optic disc
and the neighbouring areas.

54. Diagnosis of glaucoma
 Anderson’s criteria is commonly used to define
abnormality in visual fields.
 As per this criteria,presence of a cluster of three or
more nonedge points on the pattern deviation
probability plot deviating at p<5% with
1. One of these points deviating at p< 1%;
2. Pattern standard deviation(PSD) having a value
(p<5%)
3. Glaucoma hemifield test (GHT) outside normal limits
Two out of these three should be present for diagnosis of
glaucoma.

56. Visual function in glaucoma
 Testing of visual field is the primary method of
assessing visual function in glaucoma patients and
glaucoma suspects.
 Because central visual function is lost late in
glaucoma, central visual acuity is a poor test of visual
function in glaucoma.
 Visual field testing in used in 3 distinct ways in
glaucoma evaluation and management:
1. Diagnosis
2. Assessment of severity
3. Determination of progression.

57. Specific glaucomatous visual
field defects
 a nasal step defect obeying the horizontal meridian
 a temporal wedge defect
 the classic arcuate defect, which is a comma-shaped extension of the blind
spot
 a paracentral defect 10–20° from the blind spot
 an arcuate defect with peripheral breakthrough
 generalised constriction (tunnel vision)
 temporal-sparing severe visual field loss
 total loss of field.

58. Progression of glaucoma
 Compare to selected baseline
 Discard learning fields from baseline.
 Recognise false progression.
Learning curve
Long term fluctuations
Artefacts
Patient factors
Pupil size

59. Glaucoma Progression Analysis
 GPA™ is now in clinical use
 Change is based on the pattern deviation plot
 Compatible with both SITA and full threshold

60. New technologies and the
future
 Other technologies are available and being developed in
the hope that formal visual field testing will become
easier, more reliable, more affordable, and more
widespread – using equipment that can detect glaucoma
earlier than standard perimetry. These emerging
technologies include:
 short-wavelength (blue–yellow) automated perimetry
(SWAP)
 frequency doubling technology (FDT) perimetry
 motion displacement perimetry (MDP

61. Optic nerve imaging
technologies
Although other technologies exist for the
evaluation of the optic nerve and nerve fiber,
the following are the major technologies with
the greatest installed user base in 2015.
 Disc Photography- baseline for progression
assessment
 Confocal Scanning Laser Ophthalmoscopy
 Scanning Laser Polarimetry
 Optical Coherence Tomography

62. QUANTITATIVE IMAGING
Principles Clinical Parameters Measured
HRT Confocal Scanning Laser Optic Disc Tomography
Ophthalmoscopy
GDx Scanning Laser Retinal Nerve Fiber Layer Thickness
Polarimetry/Birefringence
OCT Interferometry Retinal Nerve Fiber Layer Thickness

63. IOP
High
Unilateral
Rule out
secondary
glaucomas
Uveitic
Steroid
induced
Lens induced
Neovascular
Bilateral
Glaucoma
suspect
glaucoma
Normal
Disc changes
resembling
glaucoma
NTG
Old female>60
yrs, associated
with risk factors
like hypotension
and migraine,
specific changes
in disc and
visual fields.
Other
causes-
congenital
deep cup,
myopic disc-
large disc
with large
cup, optic
colobomas
VF changes resembling
glaucomatous defects
NTG
Other causes of VF
changes- tilted disc,
myelinated nerves, ONH,
peripheral retinal
degenerations, extensive
PRP

64. Glaucoma/glaucoma suspect
Accurate IOP measurement-
tonometer used, central corneal
thickness, diurnal variation
Disc
evauation
Early change
Difficulties
like large
disc and
small disc
and NRR
evaluation.
Late changes
Fundus
photography
No changes
Visual field
evaluation
Glaucomatous Non
glaucomatou
s
Undetected POAG-
detected on SWAP,
frequency doubling
perimetry, motion detection
perimetry.
Angle
assessment
Open
Closed

65. NTG suspicion
 Diagnosis of exclusion
 Specific characteristics- history, fundus, visual fields
 Investigations for systemic conditions associated with
NTG
• 24 hr BP monitoring
• 24 hr ECG monitoring
• Blood tests- CBC, Lipid profile, CRP, blood sugars,
autoimmune markers, thyroid status
• Polysomnography and other sleep studies
• Ocular blood flow and carotid doppler

66. Conclusion
 Systematic approach helps in the accurate
and timely diagnosis of glaucoma

67. References
 Clinical ophthalmology-Kanski
 Text book of OphthalmologyYanoff
 Clinical examination- mukherjee
 FAQs in Ophtahlmology- Aravind
 Textbook of glaucoma- Shields
 Optic Nerve and Retinal Nerve Fiber Imaging-
Aaron M Miller
 Visual field testing for glaucoma – a practical
guide- David C Broadway

68. THANK YOU