Om Namh Sivai 4.0.0 0

Kheni Sweta Vinodray[2nd year M.
Optometry] 5
“OPTICAL COHERENCE TOMOGRAPHY MEASUREMENT OF
MACULAR AND NERVE FIBRE LAYER THICKNESS IN NORMAL AND
GLAUCOMATOUS HUMAN EYES.”
SUBMITTED BY:
SWETA VINODRAY KHENI
( 2 nd YEAR, M.OPTOMETRY)
UNDER THE GUIDANCE OF:
DR. MAHENDRASINH D. CHAUHAN
(M.S. OPHTHAL, D.O.M. S, Ph.D.)
DR.CHETNA PATEL
(M.S. OPHTHAL)
THESIS SUBMITTED TO:
SHREE BHARATIMAIYA COLLEGE OF OPTOMETRY AND PHYSIOTHERAPY, SURAT
AFFILIATED TO
VEER NARMAD SOUTH GUJARAT UNIVERSITY, SURAT GUJARAT
YEAR 2020-2021
Kheni Sweta Vinodray[2nd year M.Optometry] 6

“OPTICAL COHERENCE TOMOGRAPHY MEASUREMENT OF MACULAR AND NERVE
FIBRE LAYER THICKNESS IN NORMAL AND GLAUCOMATOUS HUMAN EYES.”
A DISSERTATION SUBMITTED TO THE
VEER NARMAD SOUTH GUJARAT UNIVERSITY, SURAT
In partial fulfillment of the regulations for the award of
THE DEGREE OF MASTER OF OPTOMETRY
BY
(2nd Year, M.OPTOMETRY)
Under the guidance of

DR.MAHENDRASINH D.CHAUHAN
(M. S. OPHTHAL, D. O.M. S, Ph. D.)
DR.CHETNA PATEL
(M. S. OPHTHAL)
SHREE BHARATIMAIYA COLLEGE OF OPTOMETRY AND

PHYSIOTHERAPY, SURAT
Affiliated to
VEER NARMAD SOUTH GUJARAT UNIVERSITY, SURAT
YEAR 2020-2021

CERTIFICATE
This is to certify that enclosed work on the subject “OPTICAL COHERENCE

TOMOGRAPHY MEASUREMENT OF MACULAR AND NERVE FIBRE LAYER
THICKNESS IN NORMAL AND GLAUCOMATOUS HUMAN EYES” is done by kheni
sweta vinodray (2nd Year, M. Optometry) herself under my supervision and guidance
towards the fulfillment of requirement of degree of “Master of Optometry” from the
Shree Bharatimaiya College of Optometry and Physiotherapy, Surat.
------------------------------------- -----------------------------------
Dr. Mahendrasinh D. Chauhan Dr. Chetna Patel
(M. S. OPHTHAL, D.O.M.S, Ph.D.) (M.S.OPHTHAL)
(Principal) (Vice principal)
Shree Bharatimaiya College of Shree Bharatimaiya College of
Optometry and Physiotherapy. Optometry and Physiotherapy.
Date: Date:

ACKNOWLEDGEMENT
There are a number of people to whom I would like to express my heartfelt gratitude for
helping me with my thesis.
I am highly indebted to Shree Bharatimaiya College of Optometry And Physiotherapy, Surat;
Principal Dr. Mahendrasinh D. Chauhan (M.S Ophthalmology, D.O.M.S., and Ph.D.), Vice
Principal Dr. Chetna Patel (M.S Ophthalmology), Assistant professor Optom. Ankit
Varshney (M.Optom. FIACLE, FASCO), Assistant professor Optom. Keyur Sharma
(M.Optom. FIACLE, FASCO) and Assistant professor Optom. Krutarth Desai (M.Optom.)
without whose constant support, guidance and constructive criticism this study would not
have been possible.
My whole hearted thanks to Dr. ANIMESH DHRUVA (M.S Ophthal), for his constant
support and guidance.
I am thankful to my parents, my friends and my classmates who have been a constant source
of inspiration and support throughout my academic career.
Last, but not the least special thanks to all my subjects who have cooperated with me for the
study without whom it wouldn’t have been possible.

ABBREVIATIONS
 RNFL- Retinal nerve fiber layer

 POAG- Primary open angle glaucoma
 PACG-Primary angle closure glaucoma
 OHT- Ocular hypertension
 NTG-Normal tension glaucoma
 GS- Glaucoma suspect
 WNL-Within normal limits
 OCT-Optical coherence tomography
 IOP- Intra ocular pressure
 GAT-Goldmann applanation tonometry
 UBM-Ultrasound biomicroscopy
 NRR- Neuroretinal rim
 VFI-Visual field index
 MD-Mean deviation
 PSD- Pattern standard deviation
 LV-Loss variance
 RE- Right eye
 LE- Left eye
 ST- Subjective test
 SD- Standard deviation

INDEX
SR.NO. CHAPTER PAGE NO.
1 ABSTRACT
2 INTRODUCTION
3 AIM AND OBJECTIVE
4 BASIC CONSIDERATIONS
5 REVIEW OF LITERATURE
6 MATERIALS AND METHODOLOGY
7 OBSERVATIONS AND RESULTS
8 DISCUSSION
9 CONCLUSION
10 RECOMMENDATION AND LIMITATIONS
11 BIBLIOGRAPHY

ABSTRACT
TITLE : Optical coherence tomography measurement of macular and nerve fibre layer
thickness in normal and glaucomatous human eyes.
AIM & OBJECTIVE : To evaluate the hypothesis that macular thickness and nerve fibre
layer thickness correlate with the diagnosis of glaucoma.
MATERIAL AND METHOD : All subjects underwent anterior segment slitlamp
examinations, Goldman applanation tonometry ,Gonioscopy and fundus examination with
plus 90D lens or indirect ophthalmoscope. we will use optical coherence tomography (oct) to
measure macular and nerve fibre layer (NFL) thickness and analyze their correlation with
each other and with normal and glaucoma status.
RESULT : In all over 100 eyes of total 56 patients, 50 eyes of control group and 50 eyes of
glaucoma groups were analyzed. The average RNFL measurement were significantly thinner
in glaucoma group with compared normal group (p= 0.03,). Mean average RNFL thickness in
control group was (89.56±10.67) which difference significantly from that of the glaucoma
group (83.18±15.99). Mean macular thickness in normal group was (251.96±14.33) which
difference significantly from that of the glaucoma group (229.84±41.28), (p=0.0003). Four
quadrant RNFL thicknesses were analyzed between normal group and glaucoma group. This
was statistically highly significant. Superior quadrant RNFL thickness among two group were
(109.64±17.67) and (99.84±22.71)μm respectively, (p=0.009), inferior quadrant RNFL
thickness among two groups were (114±21.94) and (64.72±36.051)μm respectively, (p=<
0.05), temporal quadrant RNFL thickness among two groups were (61.46±8.32) and
(56.18±14.37) μm respectively, (p= 0.013) and nasal quadrant RNFL thickness among two
groups were (73.1±11.76) and (66.6±11.65) μm respectively, (p= 0.01). It was observed that
there is a statistically significant mean difference in all four quadrants RNFL thickness
between the two groups.
CONCLUSION: OCT detected significant quantitative differences in RNFL and macular
thickness between normal and glaucoma groups. RNFL average thicknesses in four quadrants
and macular thickness in glaucomatous patients were significantly decreased compared with
control groups. Thus, OCT is prior in early detection of glaucoma as well as in keeping an
eye on progression of glaucoma.
Keywords: - Optical coherence tomography (OCT), Retinal nerve fibre layer (RNFL)

INTRODUCTION
Glaucoma is considered to be the second leading cause of blindness in the world after
cataract and refractive error.(9)Glaucoma is a term describing a group of ocular disorders with
multi-factorial aetiology united by a clinically characteristic raised intraocular pressure-
associated progressive optic neuropathy resulting in a characteristic appearance of the optic
disc and irreversible visual field defect. Primary Open Angle Glaucoma (POAG) is more
prevalent than Primary Angle Closure Glaucoma (PACG). (9) In the early stages the disease is
largely asymptomatic, and it is estimated that only half of glaucoma patient are aware that
they have the disease. (12)
Globally, there are more than 80 million cases of glaucoma in 2020. (9) And it will increase by
111.8 million in 2040. (12) The prevalence of glaucoma is 2.65% in people above 40 yrs. (9)
Glaucoma is the most common cause of irreversible blindness globally. More than 3
million people are blind because to glaucoma. (9) In India, more than 11.2 million individuals
above 40 yrs. and older suffer from glaucoma. POAG is estimated to affect 6.48 million
people. PACG is estimated to affect 2.54 million whereas PACG could comprise 27.6 million
people. (10)
The diagnosis of glaucoma depends on visual field loss (VF) or the appearance of the
disc, measurement of IOP or changes in the retinal nerve fiber layer (RNFL). (12)
In other words, Glaucoma is the chronic progressive optic neuropathy which is caused
by typical optic disc and retinal nerve fiber layer (RNFL) change with correcting visual field
defects where in IOP is major risk factor. The common sign among them all is an increase in
the pressure inside the eye. When the pressure is too high, damage occurs to the optic nerve.
The optic nerve is made up of a bundle of nerve fibers which sends signals to the brain. Any
damage to the optic nerve can initially cause blind spot at the outer edges of the field of
vision called peripheral or side vision, which is the main sign of glaucoma. As damage to
optic nerve worsens, the visual field can shrink leading to tunnel vision or even loss of central

vision affecting a patient’s ability to read. Fortunately, this occurs only in patients with a very
severe disease.
Optical Coherence Tomography (OCT) is a promising technology that has been

developed to examine tissue thickness in vivo, such as that of the retinal nerve fiber layer
(RNFL) and macular thickness. As there is considerable evidence that RNFL loss precedes
visual field loss and optic nerve head defects in patients with glaucoma.12
OCT is widely used for measurement of the RNFL thickness and macular thickness in
normal, glaucoma suspect, and glaucomatous eyes. The recently introduced Stratus OCT has
better resolution than the older versions by virtue of acquiring increased number of A-scans
and it has also amalgamated the new feature of probability of likelihood of abnormality after
comparison with an internal normative database.12
Circumpapillary retinal nerve fiber layer RNFL thickness, measured using OCT, is the
primary structural assessment strategy used in glaucoma diagnosis. However, because
glaucomatous damage involves progressive loss of retinal ganglion cells RGCs, observation
of macular changes has additionally been considered for structural assessment of
glaucoma. The macula is the retinal area concerned with central vision and contains
approximately 50% of all RGCs. Therefore, macular thickness measurement can be a good
target for assessment of glaucomatous structural damage. 1
Numerous studies have reported difference in OCT measured RNFL and macular
thickness among normal eyes and glaucomatous eyes that may differentiate between healthy
eye and those with early glaucomatous damage before other technique. (12)
In this study, we aim to determine the pattern of RNFL loss and macular thicknesss by
comparing across the groups and detect structural changes by measuring the thickness of
peripapillary nerve fiber layer and macular thickness in subjects of Glaucoma with the help of
Optical Coherence Tomography (OCT).

AIM AND OBJECTIVE
AIM: -
To evaluate retinal nerve fiber layer thickness and macular thickness in glaucoma
group and normal control group.
OBJECTIVE: -
 To evaluate retinal nerve fiber layer thickness and macular thickness

in glaucoma patients.
 To evaluate retinal nerve fiber layer thickness and macular thickness

in normal patients.
 To compare the average and in four quadrant ( superior ,inferior,

nasal and temporal) nerve fiber layer thickness between
glaucomatous and normal eye.
 To compare the central macular thickness in glaucomatous and

normal eye.

GENERAL CONSIDERATION
DEFINITION OF GLAUCOMA
It is difficult to define glaucoma precisely, partly because the term encompasses a
diverse group of disorders. All forms of the disease have in common a characteristic
potentially progressive optic neuropathy that is associated with visual field loss as damage
progresses, and in which IOP is a key modifiable factor.
Figure 1: Risk factors of glaucoma

Classification
Glaucoma may be congenital (developmental) or acquired. Open-angle and angle-closure
types are distinguished based on the mechanism by which aqueous outflow is impaired with
respect to the AC angle configuration. Distinction is also made between primary and
secondary glaucoma; in the latter a recognizable ocular or non-ocular disorder contributes to
elevation of IOP.
Epidemiology
Glaucoma affects 2–3% of people over the age of 40 years; 50% may be undiagnosed.
Primary open-angle glaucoma (POAG) is the most common form in white, Hispanic/Latino
and black individuals; the prevalence is especially high in the latter. On a worldwide basis,

primary angle closure (PAC) constitutes up to half of cases, and has a particularly high
prevalence in individuals of Asian descent, although with improved assessment such as the
routine performance of gonioscopyin a darkened rather than a bright environment, PAC is
known to be more prevalent in Caucasian individuals than previously realized.
SIGNS AND SYMPTOMS

Open-angle glaucoma is painless and does not have acute attacks, thus the lack of
clear symptoms make screening via regular eye check-ups important. The only signs are
gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio
on fundoscopic examination).
About 10% of people with closed angles present with acute angle closure
characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular
pressure (>30 mmHg), nausea and vomiting, suddenly decreased vision, and a fixed, mid-
dilated pupil. It is also associated with an oval pupil in some cases. Acute angle closure is an
emergency.(3)
Figure 2: - Symptoms of glaucoma

Figure 3: - Cause of glaucoma
OCULAR HYPERTENSION
Definition
In the general population the mean IOP is 16 mmHg; two standard deviations either
side of this gives a ‘normal’ IOP range of 11–21 mmHg. It is estimated that 4–10% of the
population over the age of 40 years have IOP >21 mmHg without detectable glaucomatous
damage: ‘ocular hypertension’ (OHT). An absence of angle closure is implicit, and there
should be no detectable cause of secondary glaucoma, though sometimes the term OHT is
used to describe raised IOP in these contexts. These patients should be carefully monitored
by an ophthalmologist and should be treated as cases of POAG in the presence of high-risk
factors.
GLAUCOMA SUSPECT
Definition
It is defined as an adult having normal open angle on gonioscopy and anyone of the
following signs in at least one eye.
 Elevated IOP, consistently more than 21 mm of Hg by applanation tonometry
 Suspicious disc changes in the form of asymmetric cup-disc ratio (difference >0.2), notching,
or narrowing of Neuroretinal rim, or a disc haemorrhage.
 Visual field consistent with glaucomatous damage.
Risk factors for developing glaucoma in OHT

The Ocular Hypertension Treatment Study (OHTS) was a multicenter longitudinal
trial. In addition to looking at the effect of treatment in ocular hypertensive (IOP <32
mmHg), invaluable information was gained about the effect of a range of putative risks for

conversion from OHT to glaucoma; the percentage of OHT patients likely to develop
glaucoma taking key factors into account is set out in Tables 1.1 and 1.2; median follow-up
was 72 months. Additional considerations are discussed below. Limitations included the
possibility that early glaucomatous damage was already present in some of the patients
classified as having OHT.
Table 1.1 Risk of developing glaucoma according to IOP (intra ocular pressure) and
CCT (central corneal thickness)
Mean IOP >25.75mmHg 36% 13% 6%
Mean IOP>23.75TO<25.75mmHg 12% 10% 7%
Mean IOP<23.75 mmHg 17% 9% 2%
CCT< 555µm CCT>555 µm CCT>588µm
to 588 µm
Table 1.2 Risk of developing glaucoma according to vertical C/D ratio and CCT.
C/D ratio>0.50 22% 16% 8%
C/D ratio >0.30 to 26% 16% 4%
<0.50
C/D ratio <0.30 15% 1% 4%
CCT<555 µm CCT>555µm to <588 CCT>588 µm
µm
The following factors were significant on multivariate analysis:

1. Intraocular pressure. The risk of developing glaucoma increases with increasing IOP.
2. Age. Older age is associated with greater risk.
3. Central corneal thickness (CCT). The risk is greater in eyes with low CCT and lower in
eyes with higher CCT. This is probably due to resultant under- and over-estimation of IOP
although it has been proposed that associated structural factors, perhaps at the lamina
cribrosa, might also be important.
4. Cup/disc (C/D) ratio. The greater the C/D ratio the higher the risk. This may be because an
optic nerve head with a large cup is structurally more vulnerable, or it may be that early
damage is already present.

5. Pattern standard deviation (PSD). A greater PSD result represented a significant risk. It is
possible that this signified early glaucomatous field change. The following factors were
significant on univariate analysis only; they were not significant in isolation but were over-
ridden when the factors considered above were taken into account.
African-American race was associated with a higher glaucoma risk.

1. Gender. Males were more likely to convert.
2. Heart disease was found to be significant. Factors examined in the OHTS but not found to
be significant are listed below.
3. Myopia, although it is suspected that myopic discs are more susceptible to glaucomatous
damage at a lower IOP than Emmetropic discs.
4. Diabetes. An apparent protective effect of diabetes was initially found, but later analysis with
refreshed data did not confirm this.
5. Family history of glaucoma was not found to be a risk factor for conversion. Other factors
that were not examined in the OHTS but may be important include retinal nerve fibre defects
(though the presence of these may be taken to indicate pre-perimetric glaucoma) and specific
peripapillary atrophic changes.
Clinical evaluation
History and examination should be carried out as for glaucoma. Of particular note,
consideration should be given to whether any systemic medication is being taken that might
be influencing IOP, either upwards (e.g. steroids) or downwards (e.g. beta-blockers).
Pre-perimetric glaucoma
This concept refers to glaucomatous damage, usually manifested by a suspicious optic
disc and/or the presence of retinal nerve fiber layer defects, in which no visual field
abnormality has developed. The field-testing modality for this purpose is usually taken as
standard achromatic automated perimetry.
Management

In the OHTS, untreated patients with ocular hypertension had a 9.5% cumulative risk of
developing POAG after 5 years; treatment (which aimed to reduce IOP by 20% or more and
to reach 24 mmHg or less) reduced this to 4.4%. Hence, when deciding on whether to start
treatment it is important to take into account that it will be necessary to treat a large number
of patients in order to prevent the development of glaucoma in a single individual. Various
guidelines exist, but there is a high level of disagreement even between glaucoma specialists.
 In general, only those at higher risk should be treated, although patient preference may be a
decisive factor.
 Age, and so life expectancy, is a key point to consider. Most practitioners would treat every
patient with an IOP of 30 mmHg or more (>40% 5-year risk of glaucoma). The decision to
treat in patients with varying risk profiles is commonly less than straightforward, and has to
be made on an individual basis.
 OHT almost certainly increases the risk of retinal venous occlusion, an additional point to
take into account when considering whether to start treatment.
 Treatment options are the same as for POAG, although a less aggressive pressure-lowering
approach is frequently taken, e.g. alternate day prostaglandin dosing and low intensity
selective laser trabeculoplasty have been proposed; filtration surgery is only occasionally
indicated. Cataract surgery commonly results in a significant IOP reduction.
 Careful monitoring is a reasonable alternative in many circumstances: baseline visual fields
and RNFL/disc imaging should be performed.
PRIMARY OPEN-ANGLE GLAUCOMA
Definition
Primary open-angle glaucoma (POAG) is a commonly bilateral disease of adult onset. It
is characterized by:
 IOP >21 mmHg at some stage.
 Glaucomatous optic nerve damage.
 An open anterior chamber angle.
 Characteristic visual field loss as damage progresses.

 Absence of signs of secondary glaucoma or a non-glaucomatous cause for the optic
neuropathy.
POAG is the most prevalent type of glaucoma in individuals of European and African
ethnic origin, in a meta-analysis of those older than 70 years of age having a prevalence of
6% in white populations, 16% in black populations and around 3% in Asian populations. It
affects both genders equally.
Risk factors
 IOP. The higher the IOP, the greater the likelihood of glaucoma. Asymmetry of IOP of 4
mmHg or more is also significant.
 Age. POAG is more common in older individuals.
 Race. It is significantly (perhaps four times) more common, develops at an earlier age and
may be more difficult to control in black individuals than in whites.
 Family history of POAG. First-degree relatives of patients with POAG are at increased risk.
An approximate risk to siblings is four times and to offspring twice the normal population
risk, though surveyed figures vary.
 Diabetes mellitus. Many studies suggest a correlation between diabetes and POAG.
 Myopia is associated with an increased incidence of POAG and myopic eyes may be more
susceptible to glaucomatous damage. it is speculated that this may be due to mechanical
factors, particularly the region of the optic disc.
 Contraceptive pill. Recent research suggests that long-term use of the oral contraceptive pill
may substantially increase the risk of glaucoma, perhaps by blocking a protective oestrogen
effect.
 Vascular disease. A range of systemic conditions linked to vascular compromise may be
associated, though clear-cut relationships have proved difficult to demonstrate consistently.
Systemic hypertension, cardiovascular disease, diabetes and vasospastic conditions such as
migraine have all been implicated. Poor ocular perfusion may be a risk factor for glaucoma
progression.
 Translaminar pressure gradient. Studies suggest that a difference in the levels of IOP and
orbital CSF pressure may increase the likelihood of the development and progression of
glaucomatous damage, perhaps due to associated deformation of the lamina cribrosa.

 Optic disc area. Large discs may be more vulnerable to damage, again with some
commentators speculating that causation may be linked to mechanical factors associated with
laminar deformation.
 Ocular perfusion pressure. is the difference between the arterial BP and the intraocular
pressure (IOP), and has been shown in population studies to be linked to increased risk for
the development and progression of glaucoma?
Screening
Universal population screening for glaucoma has not been demonstrated to be cost-
effective, and current practice restricts screening to high-risk groups, such as older
individuals, those over the age of 40 with a history of POAG in a close family member, and
people of black ethnicity. In these groups, screening tends to be performed sporadically via
routes such as commercial optometric eye examinations, which may lead to the relative
exclusion of underprivileged economic groups. Population screening with tonometry alone is
unsatisfactory, since it will label as normal a significant number of cases with other features
of POAG such as cupping and visual field loss, and routine screening eye examinations
should include visual field assessment as well as tonometry and ophthalmoscopy.
DIAGNOSIS
History
 Visual symptoms will usually be absent, unless damage is advanced. Sometimes
symptomatic central field defects may occur at an early stage, in the presence of a relatively
normal peripheral field.
 Previous ophthalmic history. Specific enquiry should be made about:
1. Refractive status as myopia carries an increased risk of POAG, and hypermetropia of primary
angle-closure glaucoma (PACG).
2. Causes of secondary glaucoma such as ocular trauma or inflammation; previous eye surgery,
including refractive surgery, may affect IOP readings.
 Family history
1. POAG or related conditions such as OHT.
2. Other ocular disease in family members.
 Past medical history. Asking specifically about the following may be indicated.

1. Asthma, heart failure or block, peripheral vascular disease: contraindications to the use of
beta-blockers.
2. Head injury, intracranial pathology including stroke: may cause optic atrophy or visual field
defects.
3. Vasospasm: migraine and Raynaud phenomenon.
4. Diabetes, systemic hypertension and cardiovascular disease may increase the risk of POAG.
5. Oral contraceptive pill for several years may be associated with an increased risk of
glaucoma.
 Current medication
1. Steroids including skin cream and inhalants.
2. Oral beta-blockers may lower IOP.
 Social history including smoking and alcohol intake, especially if toxic/nutritional optic
neuropathy is suspected.
 Allergies, particularly to any drugs likely to be used in glaucoma treatment, e.g.
sulfonamides.
EXAMINATION
 Visual acuity is likely to be normal except in advanced glaucoma.
 Pupils. Exclude a relative afferent papillary defect (RAPD); if initially absent but develops
later, this constitutes an indicator of substantial progression.
 Colour vision assessment such as Ishihara chart testing if there is any suggestion of an optic
neuropathy other than glaucoma.
 Slit lamp examination. Exclude features of secondary glaucoma such as pigmentary and
pseudoexfoliative.
 Tonometry prior to pachymetry, note time and date of the day.
 Gonioscopy.
 Optic disc examination for glaucomatous changes should always be performed with the
pupils dilated, provided gonioscopy does not show critically narrow angles. Red-free light
can be used to detect RNFL defects.
INVESTIGATION
 Pachymetry for CCT.

 Perimetry should usually be performed prior to clinical examination. Perimetry to detect the
visual field defects.
 Imaging of the optic disc, peripapillary RNFL and/or ganglion cell complex, e.g. red-free
photography, stereo disc photography, OCT, confocal scanning laser ophthalmoscopy and/or
scanning laser polarimetry.
 Tonometry. Applanation tonometry should be preferred over Schiotz tonometry
 Diurnal variation test is especially useful in detection of early cases
 Gonioscopy. It reveals a wide-open angle of anterior chamber. Its primary importance in
POAG is to rule out other forms of glaucoma.
 Documentation of optic disc changes is of utmost importance
 Slit-lamp examination of anterior segment to rule out causes of secondary open angle
glaucoma.
 Nerve fibre layer analyzer (NFLA) is a recently introduced device which helps in detecting
theglaucomatous damage to the retinal nerve fibres before the appearance of actual visual
field changes and/or optic disc changes.
 Provocative tests are required in border-line cases. The test commonly performed is water
drinking test. Other provocative tests not frequently performed include combined water
drinking and tonography, bulbar pressure test, prescoline test and caffeine test.
Water drinking test. It is based on the theory that glaucomatous eyes have a greater
response to water drinking. In it after 8 hours fast, baseline IOP is noted and the patient is
asked to drink one litre of water, following which IOP is noted every 15 min. for 1 hour. The
maximum rise in IOP occurs in 15-30 min. and returns to baseline level after 60 minutes in
both normal and the glaucomatous eyes. A rise of 8 mm of Hg or more is said to be
diagnostic of POAG.
SYMPTOMS
 The disease is insidious and usually asymptomatic, until it has caused a significant loss of
visual field. Therefore, periodic eye examination is required after middle age.
 Patients may experience mild headache and eye ache.
 Occasionally, an observant patient may notice a defect in the visual field.

 Reading and close work often present increasing difficulties owing to accommodative failure
due to constant pressure on the ciliary muscle and its nerve supply. Therefore, patients
usually complain of frequent changes in presbyopic glasses.
 Patients develop delayed dark adaptation, a disability which becomes increasingly disturbing
in the later stages.
 Significant loss of vision and blindness is the end result of untreated cases of POAG.
SIGNS
 Anterior segment signs. Ocular examination including slit-lamp biomicroscopy may reveal
normal anterior segment. In late stages pupil reflex becomes sluggish and cornea may show
slight haze.
 Intraocular pressure changes. In the initial stages the IOP may not be raised permanently,
but there is an exaggeration of the normal diurnal variation. Therefore, repeated observations
of IOP (every 3-4 hour), for 24 hours is required during this stage (Diurnal variation test). In
most patients IOP falls during the evening, contrary to what happens in closed angle
glaucoma. A variation in IOP of over 5 mm Hg (Schiotz) is suspicious and over 8 mm of Hg
is diagnostic of glaucoma. In later stages, IOP is permanently raised above 21 mm of Hg and
ranges between 30 and 45 mm of Hg.
 Optic disc changes. optic disc changes, usually observed on routine fundus examination,
provide an important clue for suspecting POAG. These are typically progressive, asymmetric
and present a variety of characteristic clinical patterns. It is essential, therefore, to record the
appearance of the nerve head in such a way that will accurately reveal subtle glaucomatous
changes over the course of follow-up evaluation.
Examination techniques. Careful assessment of disc changes can be made by direct

ophthalmoscopy, slit lamp biomicroscopy using a + 90D lens, Hruby lens or Goldmann
contact lens and indirect ophthalmoscopy.
The recording and documentation techniques include serial drawings, photography and
photogrammetry. Confocal scanning laser topography (CSLT) i.e., Heidelberg retinal
tomography (HRT) is an accurate and sensitive method for this purpose. Other advanced

imaging techniques include optical coherence tomography (OCT) and scanning laser
polarimetry i.e., Nerve fibre analyser (NFA).
Glaucomatous changes in the optic disc can be described as early changes, advanced changes
and glaucomatous optic atrophy.
Figure 4: - stage of glaucoma

 Early glaucomatous changes should be suspected to exist if fundus examination reveals one
or more of the following signs:
1. Vertically oval cup due to selective loss of neural rim tissue in the inferior and superior poles.
2. Asymmetry of the cups. A difference of more than 0.2 between two eyes is significant.
3. Large cup i.e., 0.6 or more (normal cup size is 0.3 to 0.4) may occur due to concentric
expansion.
4. Splinter haemorrhages present on or near the optic disc margin.
5. Pallor areas on the disc.
6. Atrophy of retinal nerve fibre layer which may be seen with red free light.
 Advanced glaucomatous changes in the optic disc

1. Marked cupping (cup size 0.7 to 0.9), excavation may even reach the disc margin, the sides
are steep and not shelving (c.f. deep physiological cup).
2. Thinning of Neuroretinal rim which occurs in advanced cases is seen as a crescentric shadow
adjacent to the disc margin.
3. Nasal shifting of retinal vessels which have the appearance of being broken off at the margin
is an important sign (Bayonetting sign). When the edges overhang, the course of the vessels
as they climb the sides of the cup is hidden.
4. Pulsations of the retinal arterioles may be seen at the disc margin (a pathognomic sign of
glaucoma), when IOP is very high.
5. Lamellar dot signs the pores in the lamina cribrosa are slit-shaped and are visible up to the
margin of the disc.
 Glaucomatous optic atrophy.
As the damage progresses, all the neural tissue of the disc is destroyed and the optic
nerve head appears white and deeply excavated.
Pathophysiology of disc changes. Both mechanical and vascular factors play a role in the
cupping of the disc.
1. Mechanical effect of raised IOP forces the lamina cribrosa backwards and squeezes the nerve
fibres within it meshes to disturb axoplasmic flow.
2. Vascular factors contribute in ischemic atrophy of the nerve fibres without corresponding
increase of supporting glial tissue. As a result, large caverns or lacunae are formed
(cavernous optic atrophy).
 Visual field defects. Visual field defects usually run parallel to the changes at the optic nerve
head and continue to progress if IOP is not controlled. These can be described as early and
late field defects.
Anatomical basis of field defects. For better understanding of the actual field defects, it is
mandatory to have knowledge of their anatomical basis.
A. Distribution of retinal nerve fibres
1 Fibres from nasal half of the retina come directly to the optic disc as superior and inferior
radiating fibres.
2 Those from the macular area come horizontally as papillomacular bundle (pmb).
3 Fibres from the temporal retina arch above and below the macula and papillomacular bundle
as superior and inferior arcuate fibres with a horizontal raphe in between

B. Arrangement of nerve fibres within optic nerve head Those from the peripheral part of the
retina lie deep in the retina but occupy the most peripheral (superficial) part of the optic disc.
While fibres originating closer to the nerve head lie superficially in the retina and occupy a
more central (deep) portion of the disc.
The arcuate nerve fibres occupy the superior and inferior temporal portions of optic nerve
head and are most sensitive to glaucomatous damage; accounting for the early loss in the
corresponding regions of the visual field. Macular fibres are most resistant to the
glaucomatous damage and explain the retention of the central vision till end.
 Progression of field defects. Visual field defects in glaucoma are initially observed in
Bjerrum’s area (1025 degree from fixation) and correlate with optic disc changes. The natural
history of the progressive glaucomatous field loss, more or less, takes the following
sequence:
1. Isopter contraction. It refers to mild generalized constriction of central as well as peripheral
field. It is the earliest visual field defect occurring in glaucoma. However, it is of limited
diagnostic value, as it may also occur in many other conditions.
2. Baring of blind spot. It is also considered to be an early glaucomatous change, but is very
non-specific and thus of limited diagnostic value. Baring of the blind spot means exclusion of
the blind spot from the central field due to inward curve of the outer boundary of 30° central
field
3. Small wing-shaped paracentral scotoma It is the earliest clinically significant field defect.
It may appear either below or above the blind spot in Bjerrum's area (an arcuate area
extending above and below the blind spot to between 10o and 20o of fixation point).
4. Seidel’s scotoma. With the passage of time paracental scotoma joins the blind spot to form a
sickle shaped scotoma known as Seidel’s scotoma
5. Arcuate or Bjerrum’s scotoma. It is formed at a later stage by the extension of Seidel’s
scotoma in an area either above or below the fixation point to reach the horizontal line.
Damage to the adjacent fibres causes a peripheral breakthrough.
6. Ring or double arcuate scotoma. It develops when the two arcuate scotomas join together.
7. Roenne's central nasal step. It is created when the two arcuate scotomas run in different
arcs and meet to form a sharp right-angled defect at the horizontal meridian

8. Peripheral field defects. These appear sometimes at an early stage and sometimes only late
in the disease. The peripheral nasal step of Roenne's results from unequal contraction of the
peripheral isopter.
9. Advanced glaucomatous field defects. The visual field loss gradually spreads centrally as
well as peripherally, and eventually only a small island of central vision (tubular vision) and
an accompanying temporal island are left. With the continued damage, these islands of vision
also progressively diminish in size until the tiny central island is totally extinguished. The
temporal island of the vision is more resistant and is lost in the end leaving the patient with
no light perception.
MANAGEMENT
Baseline evaluation and grading of severity of glaucoma. The aim of treatment is to lower
intraocular pressure to a level where (further) visual loss does not occur.
The management thus requires careful and regular periodic supervision by an
ophthalmologist. Therefore, it is important to perform a good baseline examination with
which future progress can be compared. The initial data should include: visual acuity, slit-
lamp examination of anterior segment, tonometry (preferably with applanation tonometer);
optic disc evaluation (preferably with fundus photography), gonioscopy and visual field
charting.
Therapeutic choices include:
 Medical therapy,
 Argon or diode laser trabeculoplasty, and
 Filteration surgery.
NORMAL-TENSION GLAUCOMA
Introduction
Normal-tension glaucoma (NTG), also referred to as low-tension or normal-pressure
glaucoma, is usually regarded as a variant of POAG. It is characterized by:
 IOP consistently equal to or less than 21 mmHg.
 Signs of optic nerve damage in a characteristic glaucomatous pattern.
 An open anterior chamber angle.
 Visual field loss as damage progresses, consistent in pattern with the nerve appearance.

 No features of secondary glaucoma or a non-glaucomatous cause for the neuropathy.
The distinction between NTG and POAG is based on an epidemiologically derived range of
normal IOP. It is essentially an arbitrary division that may not have significant clinical value,
though it is possible that a spectrum exists in which, towards the NTG end, IOP-independent
factors are of increasing relative importance. Up to two-thirds of Japanese patients and 30%
of Caucasians with OAG may have normal IOP at initial assessments.
Pathogenesis
Any an etiological factor distinct from those in POAG have not been conclusively
determined, although various mechanisms have been postulated including anomalies of local
and systemic vascular function, structural optic nerve anomalies and autoimmune disease.
With the introduction of widespread central corneal thickness (CCT) assessment, NTG in
some patients has been explained by very low CCT, and overall CCT in patients with NTG is
lower than in POAG. A small proportion of NTG patients have been found to have marked
nocturnal IOP spikes, sometimes only detected on testing in the supine position.
Risk factors
 Age. Patients tend to be older than those with POAG, though this may be due to delayed
diagnosis.
 Gender. Some studies have found a higher prevalence in females.
 Race. NTG occurs more frequently in people of Japanese origin than in European or North
American Caucasians.
 Family history. The prevalence of POAG is greater in families of patients with NTG than in
the normal population. Mutations in the OPTN gene coding for optineurin have been
identified in some patients with NTG, though also in patients with POAG.
 CCT is lower in patients with NTG than POAG.
 Abnormal vasoregulation, particularly migraine and Raynaud phenomenon, has been found
more commonly in NTG than POAG by some investigators; others have found abnormalities
just as commonly in POAG. Other systemic diseases associated with vascular risk, such as
diabetes, carotid insufficiency, hypertension and hypercoagulability, may also be important.
 Systemic hypotension including nocturnal blood pressure dips of >20%, particularly in those
on oral hypotensive medication.

 Obstructive sleep apnoea syndrome may be associated, perhaps via an effect on ocular
perfusion.
 Autoantibody levels have been found to be higher in some groups of NTG patients by some
investigators.
 Translaminar pressure gradient. This may on average be larger than in POAG.
 Ocular perfusion pressure may be relatively lower than in POAG.
 Myopia is associated with a greater likelihood of glaucoma and of its progression.
 Thyroid disease may be more common.
DIFFERENTIAL DIAGNOSIS
 Angle closure should always be ruled out by meticulous dark-room gonioscopy.
 Low CCT leading to underestimation of IOP; suspicion has also been raised that a thin
posterior ocular wall may increase mechanical stress in the region of the lamina cribrosa.
Prior refractive surgery and corneal ectasia also lead to falsely low IOP readings, sometimes
dramatically so.
 POAG presenting with apparently normal IOP because of wide diurnal fluctuation. Plotting a
diurnal IOP curve over an 8-hour period (phasing) during office hours may detect daytime
elevation, but detection of nocturnal IOP spikes requires substantial resource commitment.
 Previous episodes of raised IOP may have occurred as a result of ocular trauma, uveitis or
local or systemic steroid therapy.
 Masking by systemic treatment such as an oral betablocker, commenced after
glaucomatous damage has already been sustained.
 Spontaneously resolved pigmentary glaucoma. The typical examination features of
pigmentary glaucoma tend to become less evident with increasing age. The IOP in some
cases of POAG may also spontaneously normalize over time.
 Progressive retinal nerve fibre defectsnot due to glaucoma such as may occur in myopic
degeneration and optic disc drusen.
 Congenital discanomalies simulating glaucomatous cupping, such as disc pits and
colobomas.
 Neurological lesions causing optic nerve or chiasmal compression can produce visual field
defects that may be misinterpreted as glaucomatous, and neuroimaging should be performed

if there is any suspicion; some practitioners routinely perform a cranial MRI in all cases of
NTG.
 Previous anterior ischaemic optic neuropathy (AION) may give rise to a disc appearance
and visual field defect consistent with glaucoma. Non-arteritic AION often occurs in a
‘crowded’ disc, and the fellow eye should be examined for this; prior retinal vascular
occlusion should also be considered.
 Previous acute optic nerve insult such as hypovolaemic or septicemic shock, or head injury.
 Miscellaneous optic neuropathies including inflammatory, infiltrative and drug-induced
pathology will often be clinically obvious, but can occasionally masquerade as NTG.
Clinical features
History and examination are essentially the same as for POAG but specific points
warrant attention.
 History
1. Migraine and Raynaud phenomenon.
2. Episodes of shock.
3. Head or eye injury.
4. Headache and other neurological symptoms (intracranial lesion).
5. Medication, e.g. systemic steroids, beta-blockers.
 IOP is usually in the high teens, but may rarely be in the low teens. In asymmetrical disease
the more damaged disc typically corresponds to the eye with the higher IOP.
 Optic nerve head
1. The optic nerve head may be larger on average in NTG than in POAG.
2. The pattern of cupping is similar, but acquired optic disc pits and focal nerve fibre layer
defects may be more common.
3. Peripapillary atrophic changes may be more prevalent.
4. Disc haemorrhages may be more frequent than in POAG, and are associated with a greater
likelihood of progression.
5. Pallor disproportionate to cupping should prompt a suspicion of an alternative diagnosis.
 Visual field defects are essentially the same as in POAG although there is some evidence
that they tend to be closer to fixation, deeper, steeper and more localized. In probably more
than half of patients, field changes are non-progressive over a period of 5 years or more
without treatment. However, perhaps because of delayed diagnosis, patients tend to present

with more advanced damage than in POAG. A high level of suspicion for a deficit pattern
suggesting a lesion posterior to the optic nerve is important.
 Other investigations are as for POAG although in selected patients the following can be
considered.
1. Assessment of systemic vascular risk factors.
2. Blood pressure measurement can be used to calculate ocular perfusion pressure; 24-hour
ambulatory monitoring will exclude nocturnal systemic hypotension in selected patients.
3. Blood tests for other causes of non-glaucomatous optic neuropathy such as vitamin B12, red
cell folate, full blood count, erythrocyte sedimentation rate/C-reactive protein, treponemal
serology including Lyme disease, serum angiotensin-converting enzyme level, plasma protein
electrophoresis and autoantibody screen.
4. Cranial MRI.
5. Carotid Duplex imaging.
6. Ocular blood flow assessment (e.g. laser flowmetry) may have useful clinical potential.
Treatment
Further lowering of IOP is effective in reducing progression in many or most patients.
However, as a large proportion of untreated patients will not deteriorate (approximately 50%
at 5 years), in many cases progression should be demonstrated before commencing treatment.
Exceptions include advanced glaucomatous damage, particularly if threatening central vision,
and young age. Regular assessment including perimetry should be performed at 4–6 monthly
intervals initially.
 Medical treatment. The alpha-2 agonist brimonidine may have a neuroprotective effect on
the retina and optic nerve in addition to its IOP-lowering effect and may be superior to beta-
blockers. Carbonic anhydrase inhibitors, particularly dorzolamide, may improve ocular
perfusion. Prostaglandin derivatives tend to have a greater ocular hypotensive effect, which
may be an over-riding consideration. Topical beta-blockers can have a dramatic effect on BP
in a minority, and may contribute to nocturnal dips, though selective blockade (e.g.
Betaxolol) may actually have a beneficial effect on optic nerve perfusion.
 Laser trabeculoplasty, particularly SLT, is a reasonable option to achieve IOP targets.

 Surgery may be considered if progression occurs despite IOP in the low teens; antimetabolite
enhancement of trabeculectomy is likely to be indicated in order to achieve a satisfactorily
low pressure.
 Control of systemic vascular disease such as diabetes, hypertension and hyperlipidaemia
may be important, in order theoretically to optimize optic nerve perfusion.
 Systemic calcium-channel blockers to address vasospasm have been advocated by some
authorities.
 Antihypotensive measures. If significant nocturnal dips in BP are detected, it may be
necessary to reduce antihypertensive medication, especially if taken at bedtime. Non-
selective topical beta-blockers in particular may cause a profound drop in systemic blood
pressure in some individuals. Selected patients might be encouraged to increase their salted
food intake, in consultation with the patient’s cardiovascular physician.
 Neuroprotective agents of proven benefit are not yet available; memantine is used to retard
neuronal death in some CNS disorders, and its use has been adopted in glaucoma by some
practitioners. Ginkgo biloba (40 mg three times daily) or an antiplatelet agent may confer
some benefit in selected cases.
INVESTIGATION
 TONOMETRY
 Goldmann tonometry
Principles
Goldmann applanation tonometry (GAT) is based on the Imbert–Fick principle, which
states that for a dry thin-walled sphere, the pressure (P) inside the sphere equals the force (F)
necessary to flatten its surface divided by the area (A) of flattening (i.e. P = F/A).
Theoretically, average corneal rigidity (taken as 520 µm for GAT) and the capillary attraction
of the tear meniscus cancel each other out when the flattened area has the 3.06 mm diameter
contact surface of the Goldmann prism, which is applied to the cornea using the Goldmann
tonometer with a measurable amount of force from which the IOP is deduced. The tonometer
prism should be disinfected between patients and replaced regularly in accordance with the
manufacturer’s instructions. Disposable tonometer prisms and caps have been introduced to
address concerns of infection from reusable prisms.

(B)
Figure 5: - Goldmann tonometry. A) physical principles B) tonometer (courtesy of

salmon -fig B)
Technique

o Topical anesthetic (commonly proxymetacaine 0.5%) and a small amount of fluorescein are
instilled into the conjunctival sac.
o The patient is positioned at the slit lamp with his or her forehead firmly against the headrest
and instructed to look straight ahead (often at the examiner’s opposite ear) and to breathe
normally.
o With the cobalt blue filter in place and illumination of maximal intensity directed obliquely
(approximately 60°) at the prism, the prism is centered in front of the apex of the cornea.
o The dial is preset at 1 (i.e. 10 mmHg).
o The prism is advanced until it just touches the apex of the cornea.
o Viewing is switched to the ocular of the slit lamp.
o A pattern of two green semicircular mires will be seen, one above and one below the
horizontal midline, which represent the fluorescein-stained tear film touching the upper and
lower outer halves of the prism. Mire thickness should be around 10% of the diameter of its
total arc Care should be taken to horizontally and vertically center the mires so that as far as
practically possible two centralized semicircles are observed.
o The dial on the tonometer is rotated to vary the applied force; the inner margins of the
semicircles align when a circular area of diameter precisely 3.06 mm is flattened.
o The reading on the dial, multiplied by 10, gives the IOP; a version is available that shows
IOP on a digital display.

Figure 6: - Applanation tonometry. (A) contact between the tonometer prism and the
cornea; (B) fluorescein-stained semicircular mires-the diagram at right show the correct
end-point using mires of appropriate thickness.
Sources of error
 Inappropriate fluorescein pattern. Excessive fluorescein will result in the mires being too
thick, with consequent overestimation of IOP; insufficient will make the semicircles too thin,
with consequent underestimation.
 Pressure on the globe from the examiner’s fingers, eyelid squeezing or restricted extra
ocular muscles (e.g. thyroid myopathy) may give an anomalously high reading.
 Central corneal thickness (CCT). Calculations of IOP by GAT assume that central corneal
thickness is 520 µm, with minimal normal variation. If the cornea is thinner, an
underestimation of IOP is likely to result, and if thicker, an overestimation. Corneas tend to
be thicker than average in individuals with ocular hypertension, and thinner in normal-tension
glaucoma (NTG); following refractive surgery procedures the cornea is both thinner and
structurally altered such that IOP is likely to be underestimated. Some methods of IOP
measurement may reduce the effect of structural confounding variables. Other corneal
mechanical factors may also be important but are less well defined.
 Corneal oedema may result in artificial lowering of IOP, hypothesized to be due to a boggy
softening; the associated increased CCT seems to be more than offset.
 Astigmatism, if significant, may give distorted mires as well as leading to mechanically
induced errors. If over 3 diopters, the average reading of two can be taken with the prism
rotated 90° for the second, or optimally the prism is rotated so that the red line on the
tonometer housing is aligned with the prescription of the minus axis.
 Incorrect calibration of the tonometer can result in a false reading, and calibration should
optimally be checked before each clinical session using the manufacturer’s calibration arm.
 Wide pulse pressure. It is normal for there to be a small oscillation of IOP in concert with
the rhythm of ocular perfusion. If this ‘pulse pressure’ is substantial, either the midpoint or
the highest level observed may be taken.
 Repeated readings over a short period will often be associated with a slight fall in IOP due
to a massaging effect on the eye.
 Other factors include a tight collar and breath-holding, both of which obstruct venous return
and can raise IOP.

Figure 7: - Portable tonometers. (A) Keeler pneumotonometer; (B) Perkins applanation
tonometer; (C) Tono-Pen®; (D) iCare® (Courtesy of Mainline Instruments Ltd – fig. D)
GONIOSCOPY
Gonioscopy is a method of evaluating the AC angle, and can be used therapeutically
for procedures such as laser trabeculoplasty and goniotomy.
Other means of angle assessment such as anterior segment optical coherence tomography
(OCT) and high-frequency ultrasound biomicroscopy (UBM) offer advantages in some
aspects of angle analysis, but current clinical opinion suggests they should supplement rather
than replace visual gonioscopy analysis.
Principle:
The anatomy of the eye is such that the angle recess is not visualized by routine
instrumentation due to total internal reflection of rays emerging from the angle recess.
gonioscope interferes with total internal reflection.
procedure:
 Disinfect the lens and fill the lens surface with viscous coupling solution.
 Anaesthetize both eye
 Align the biomicroscope illumination and observation system.
 Insert the gonio lens and wipe away excess solution.

 Rotate the gonio lens through 360 degree to establish a good seal.
 Place the thumbnail mirror at 12 o'clock on the cornea to view the inferior angle first.
 Identify the most posterior structure observable.
 Position the slit lamp beam horizontally to view the lateral and medial sides and vertically to
view the inferior and superior side.
 Examine all quadrants in a systematic manner.
 Remove the lens by simply releasing from contact with the cornea.
Indication:
 Narrow anterior chamber angle
 Closed angle glaucoma
 POAG
 SOAG
 Risk of angle recession
 Risk of angle neovascularization
 Risk of intraocular foreign body
 Congenital or acquired structural anomalies of iris and anterior chamber
 Post laser peripheral iridotomy to assess effect of on angle depth.
Contraindication:
 Recent ocular trauma in presence of hyphema.
 Recent intra ocular surgery.
Grading of angle width
In practice, the angle is graded by many practitioners simply according to the number of
structures visible, together with qualifying comments relating to the width of the iris
approach; many angles are narrowest superiorly, though this difference may be reduced by
decreasing the ambient illumination.

Figure 8: - Grading of angle width according to number of visible structures.
Shaffer system
The Shaffer system records the angle in degrees between two imaginary lines tangential to
the inner surface of the trabeculum and the anterior surface of the iris about one-third of the
distance from its periphery.
The system assigns a numerical grade to each quadrant of the angle.
 Grade 4 (35–45°) is the widest angle, characteristic of myopia and Pseudophakia; the ciliary
body can be visualized without tilting the lens.
 Grade 3 (25–35°) is an open angle in which the scleral spur is visible.
 Grade 2 (20°) is an angle in which the trabeculum but not the scleral spur can be seen.
 Grade 1 (10°) is a very narrow angle in which only the Schwalbe line and perhaps the top of
the trabeculum can be identified.
 Slit angle is one in which there is no obvious iridocorneal contact but no angle structures can
be identified.
 Grade 0 (0°) is closed due to iridocorneal contact.
 Indentation will distinguish appositional from synechial angle closure.
OPHTHALMOSCOPY:
Ophthalmoscopy is used to examine the inside of the eye, especially the optic nerve.
In a darkened room, this test is performed to check the fibers in your optic nerve by means of
ophthalmoscopy which enables him or her to look directly through the pupil to the back of
your eye. this can reveal slight changes that may indicate the beginnings of glaucoma. this
helps the doctor look at the shape and color of the optic nerve.
Evaluation of the optic nerve head includes assessment of:
 The size and shape of the optic disc
 Size and shape of the neuron retinal rim, which is the intrapapillary equivalent of the optic
nerve fibers
 Size of the optic cup in relation to the area of the disc

 Configuration and depth of the of the optic cup
 Position of the exit of the central retinal vessel trunk on the lamina cribrosa surface
 Presence and location of splinter-shaped hemorrhages
 Occurrence, size, configuration and location of peripallarychorioretinal atrophy
 Occurrence of diffuse and /or focal decrease of the diameters of the retinal arterioles and
 Visibility of the retinal nerve fiber.
EVALUATION OF THE OPTIC NERVE HEAD
Normal optic nerve head
Neuroretinal rim
The Neuroretinal rim (NRR) is the orange-pink tissue between the outer edge of the
cup and the optic disc margin. The inferior rim is the broadest followed by the superior, nasal
and temporal (the ‘ISNT’ rule); this has high sensitivity for glaucoma but is not very specific,
i.e. eyes without glaucoma often do not respect the rule.
Figure 9: - Normal disc that obeys the ‘ISNT’ rule.

Cup/disc (C/D) ratio
The C/D ratio indicates the diameter of the cup expressed as a fraction of the diameter of the
disc; the vertical rather than the horizontal ratio is generally taken. Small diameter optic discs
have small cups (Fig. A) and vice versa (Fig B); only 2% of the population have a C/D ratio
greater than 0.7. In any individual, asymmetry of 0.2 or more between the eyes should also be
regarded with suspicion, though it is critical to exclude a corresponding difference in overall
disc diameter.

Figure 10: - Normal discs. (A) Small disc with a low cup/disc ratio; (B) larger disc with
a proportionally larger cup.
Optic disc size

Optic disc size is important in deciding if a cup/disc (C/D) ratio is normal, and is also a
prognostic indicator. Large discs are believed to be more likely to sustain damage,
particularly in NTG. This may be the result of the larger diameter conferring relative
mechanical weakness and hence greater vulnerability to IOP-induced displacement of the
lamina cribrosa; the lamina cribrosa has been found to be thinner in eyes with NTG. Disc size
varies on average between racial groups, and is largest in black individuals. Imaging can
objectively measure disc area, but vertical diameter is the parameter most frequently used
clinically; normal median vertical diameter (for non-glaucomatous discs) is 1.5–1.7 mm in a
white population.
 A narrow-slit beam is focused on the disc using a fundus lens.

 The height of the beam is adjusted until it matches the distance between the superior and
inferior limits of the NRR (not the scleral rim surrounding the neural tissue), and the diameter
in millimeter’s is read from the slit lamp graticule.
 A correction factor may be necessary, depending on the lens used. Refractive error affects
measurement only minimally, although myopia above −8 diopters may distort the result.

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 disc haemorrhages.
Two patterns occur: localized wedge-shaped defects and diffuse defects that are larger and
have indistinct borders. Defects are sometimes evident following disc haemorrhages. Red-
free (green) light increases the contrast between normal retina and defects on slit lamp
biomicroscopy or fundus photography and typically makes identification easier. OCT and
scanning laser polarimetry are highly effective means of quantifying the RNFL.
It should be noted that RNFL defects are not specific to glaucoma, and can be seen in a range
of neurological disease, as well as apparently normal individuals.
Figure 11: - Retinal nerve fibre layer defects. (A) Superotemporal wedge-shaped defect
associated with a disc margin haemorrhage; (B) red-free photograph of the same eye
IMAGING IN GLAUCOMA
Pachymetry
Pachymetry, the measurement of corneal thickness, in recent years has become an
essential part of the assessment of glaucoma patients.

Method of pachymetry
 Contact method
1. Optical pachymetry
2. Ultrasonic pachymetry
 Non- contact method
1. Pachycam
2. Orbscan
3. pentacam
Normal corneal thickness:
 central corneal thickness: 500 to 575 microns.
 Peripheral corneal thickness: 700 to 900 microns.
Pachymetry is generally used for the following:

 To determine if the patient’s corneal thickness is appropriate for LASIK or should he/she opt
for another variety of treatment
 In routine eye exams when the doctor suspects any corneal abnormality
 As an essential part of the glaucoma examination
 To manage /treat various corneal diseases e.g. Fuch’s dystrophy, bullous keratopathy &
keratoconus.
Procedure of pachymetry:
The method for using the non-contact specular microscope Topcon SP-2000 pachymetry was
as follows:
 The subject’s head was positioned against the head band and chin rest, and they were then
instructed to look straight ahead into the fixation targets.
 Pictures were captured of the central cornea area using the automatic mode low flash
intensity.
 Each image was taken after proper positioning of the alignment dot, circle, and bar on the
screen.
 The images were printed with the analysed data.
Corneal thickness and glaucoma

The thickness of your corneal may significantly impact reading of your intraocular
pressure. if you have thin corneas, your eye pressure will read artificially low (falsely low).
Similarly, if you have a thicker cornea, you may register as having a higher intraocular
pressure, leading your eye doctor to conclude that you have glaucoma and start you on course
of treatment when you actually have no risk.
Stereo disc photography
Stereo photography has historically been regarded as the reference standard in optic
disc imaging, and remains a valuable option. The images are taken by repositioning slightly
between shots, either manually or using a stereo separator built into the camera.
Optical coherence tomography
OCT has Diagnostic test that allows for imaging and measurement of various ocular
structures. (6) OCT has become a routine part of the management of macular and other retinal
disease; the same machine can be used for the assessment of glaucoma and has been widely
adopted for this purpose. Sensitivity and specificity utilizing comparison with a normative
database are as high as 90%.
Peripapillary retinal nerve fibre layer (RNFL). This involves the acquisition of a
circular scan of the retina around the optic nerve head. Retinal thickness is compared with
normal.
Principle:
It works based on the principle of low coherence interferometry.
Types of OCT
Based on area of examination
1. Anterior segment OCT (AS-OCT)
2. Posterior segment OCT (PS-OCT)
 anterior segment OCT (AS-OCT)

Anterior segment OCT is used to assess anterior segment. (anterior chamber depth, angle
width, iris thickness, angle opening distance, trabecular space area. etc.)
 posterior segment OCT(PS-OCT)

It is used to assess
macula, retinal
nerve fiber layer
thickness and
optic nerve head
region.
Figure 12 : -
optovue
OCTRTVu e
Model -
RT100
PROCEDURE
 Switch on the machine.
 Dilate the pupil.
 Seat the patient comfortably and ask to look into the target light and also instruct the patients
not to blink during procedure.
 Protocol selected as per case requirement.
 OCT machine provide different type of scanning protocol.
RETINAL NERVE FIBER LAYAR (RNFL) SCANNING PROTOCOL
 3D reference
 ONH
 RNFL 3.45
MACULAR THICKNESS PROTOCOL
 3D macular

COLOUR CODES IN OCT
Brighter colour (red and yellow) Highly reflective ocular structures
Green Intermediate reflective ocular structures
Blue and black Low reflective ocular structures
Limitations of OCT
 Mydriasis may sometimes be necessary
 Dioptric media must be somewhat transparent
 Exploration typically limited to posterior pole
 Good lacrimal film necessary (4)
Indications for OCT

 Helpful for diagnosing retinal disorder such as macular hole retinal detachment etc.
 Glaucoma diagnosis and monitoring.
 Evaluation of optic nerve disorders.
 High myopia
 Intraretinal haemorrhages.
 To examine the retina and its sub-layers – Atrophy, Edema, Traction, Subretinal fluid, RPE
irregularity – ARMD, CME, CSME, CSR
 To monitor progression
 To aid in treatment planning
 To monitor response to therapy
 To examine the retina and its sub-layers – Extent of retinal defects or abnormalities –
Detailed measurements. (4)
OCT Advantage
 Enhanced visualization of pathological process
 Aided in determining optimal treatment
 Postoperative OCT showed resolution
 Quantified morphological abnormality
 Showed failure to respond to original laser treatment

 Showed improvement with adjunctive intravitreal therapy
 Effectively demonstrates the layers involved in the pathological process
 Reveals structural defect that is difficult to identify ophthalmoscopically. (4)
Optic nerve head.

Radial cross-sectional scans permit an objective and repeatable assessment of disc
morphology, with reasonable discriminatory value. This function has tended to be less
commonly used than RNFL analysis in practice.
Ganglion cell complex (GCC)

GCCanalysis involves measurement of retinal thickness at the macula in an attempt to detect
early stage glaucomatous damage. Using older time domain OCT, it was found to be regarded
as inferior to assessment of other parameters such as peripapillary RNFL assessment; with
newer OCT technology interest in GCC analysis has been renewed and it is regarded as
comparable and supplementary.
Progression analysis software has been introduced on several machines, providing a
computed assessment of the extent of damage over time presented in graphical form.
PERIMETRY
Definitions
The visual field can be represented as a three-dimensional structure akin to a hill of
increasing sensitivity. The outer aspect extends approximately 50° superiorly, 60° nasally,
70° inferiorly and 90° temporally. Visual acuity is sharpest at the very top of the hill (i.e. the
fovea) and then declines progressively towards the periphery, the nasal slope being steeper
than the temporal. The ‘bottomless pit’ of the blind spot is located temporally between 10°
and 20°, slightly below the horizontal.
PROCEDURE
 Patient education
 Before starting the procedure, examiner should explain indention and method of examination
in detail.

 Entering patient information: which include
 Name
 Age
 Sex
 Date of birth
 Visual acuity
 Refractive error
 Patient preparation
 Occlude the eye not to be examined
 Select appropriate trial lens and put it in the lens holder.
 For spherical correction > +/-8.00 it is better to use contact lens for reducing field defect due
to optical aberrations.
 Instrument alignment
 Perimeter is adjusted for patient height.
 Chin rest should be adjusted until the tested eye is centered at the cross hire of eye screening
monitor.
 Lens holder is adjusted to place the lens as close as possible.
 Patient instruction
 Instruct the patient to fixate at yellow light at the center. Ask the patients to press
buzzer in the hand every time when he/she see a spot of light random location.
TESTING PATTERNS
Glaucoma
 Importance of central area. Most important defects in glaucoma occur centrally –
within a 30° radius from the fixation point – so this is the area most commonly tested.
 24-2 is a glaucoma-orientated pattern used routinely. ‘24’ denotes the extent in
degrees to which the field is tested on the temporal side (to 30° on the nasal side). The
number after the hyphen (2) describes the pattern of the points tested. 30-2 is an alternative.
 10-2 is used to assess a central area of radius 10°. Glaucomatous defects here may
threaten central vision; the 10-2 pattern facilitates more detailed monitoring of the extent of

damage, especially in advanced glaucoma.
Peripheral field. Patterns that include central and peripheral points are typically limited to
the assessment of neurological defects.
Binocular field testing (e.g. Esterman strategy) is used to assess statutory driving entitlement
in many jurisdictions.
Analysis
SAP provides the clinician with an array of clinically relevant information via monitor
display or printout. The patient’s name and age are confirmed and a check made that any
appropriate refractive error compensation was used. General information should be reviewed,
such as the type of algorithm performed, the time taken for the test and the order in which the
eyes were tested;in some cases, these must be interpreted to discern likely learning or fatigue-
induced effects.
Reliability indices
Reliability indices reflect the extent to which the patient’s results are reliable, but it is
important to note that there is relatively little research-based evidence in this area, with
limited absolutes in branding a field as clearly reliable or unreliable. With SITA strategies,
false negatives or false positives over about 15% should probably be regarded as highly
significant, and with full-threshold strategies, fixation losses over 20% and false positives or
negatives over 33%. In patients who consistently fail to achieve good reliability it may be
useful to switch to a supra threshold strategy or kinetic perimetry.
 Fixation losses indicate steadiness of gaze during the test. Methods of assessment
include presentation of stimuli to the blind spot to ensure no response is recorded, and the use
of a ‘gaze monitor’.
 False positives are usually assessed by decoupling a stimulus from its accompanying
sound. If the sound alone is presented and the patient still responds, a false positive is
recorded. With a high false-positive score the grey scale printout appears abnormally pale. In
SITA testing, false positives are estimated based on the response time.
 False negatives are registered by presenting a stimulus much brighter than threshold
at a location where the threshold has already been determined. If the patient fails to respond,

a false negative is recorded. A high false-negative score indicates inattention, tiredness or
malingering, but is occasionally an indication of disease severity rather than unreliability. The
grey scale printout in individuals with high false-negative responses tends to have a clover
leaf shape.
Sensitivity values
 A numerical display gives the measured or estimated (depending on strategy)
threshold in dB at each point. In a full-threshold strategy, where the threshold is rechecked
either as routine or because of an unexpected (>5 dB) result, the second result is shown in
brackets next to the first.
 A grey scale represents the numerical display in graphical form and is the simplest
display modality to interpret: decreasing sensitivity is represented by darker tones – the
physiological blind spot is a darker area in the temporal field typically just below the
horizontal axis. Each change in grey scale tone is equivalent to a 5 dB change in sensitivity at
that location.
 Total deviation shows the difference between a test-derived threshold at a given
point and the normal sensitivity at that point for the general population, correcting for age.
Negative values indicate lower than normal sensitivity, positive values higher than normal.
 Pattern deviation is derived from total deviation values adjusted for any generalized
decrease in sensitivity in the overall field (e.g. lens opacity), and demonstrates localized
defects.
 Probability value plots of the total and pattern deviation are a representation of the
percentage (<5% to <0.5%) of the normal population in whom the measured defect at each
point would be expected. Darker symbols represent a greater likelihood that a defect is
significant.
SUMMARY VALUES
Summary values represent distilled statistical information,taking into account age-matched
normal data, and are principally used to monitor progression of glaucomatous damage rather
than for initial diagnosis.
 Visual field index (VFI) in the HFA is a measure of the patient’s overall visual field
function expressed as a percentage, the normal age-adjusted value being 100%.

 Mean deviation (MD) on the HFA (mean defect on the Octopus) gives an indication
of the overall sensitivity of the field. It is derived from averaging the total deviation values.
 Pattern standard deviation (PSD) is a measure of focal loss or variability within the
field taking into account any generalized depression in the hill of vision. An increased PSD is
therefore a more specific indicator of glaucomatous damage than MD.
 Loss variance (LV) is a summary measure on the Octopus perimeter similar to PSD.
 Probability values. Abnormal summary values are followed by a probability value,
representing the percentage likelihood that an abnormal value of this level will occur in a
normal subject; the lower the P value, the more likely the result is abnormal.
 The glaucoma hemi field test (GHT) used with some HFA testing patterns assesses
the visual field for damage conforming to a pattern commonly seen in glaucoma.
Sources of error
 Inexperienced or unskilled perimetrist. Though less important with SAP than
manual perimetry, correctly setting up the test, explaining the procedure to and reassuring the
patient, and monitoring performance are fundamental to obtaining an accurate field.
 Incorrect patient details. The patient’s date of birth must be entered correctly to
facilitate appropriate normative database matching.
 Poor patient performance.
 Uncorrected refractive error can cause a significant decrease in central sensitivity.
If a hypermetropia patient who usually wears contact lenses is tested wearing spectacles, this
will have the effect of magnifying and enlarging any scotomas as compared with contact
lenses. Most perimetry is performed with a stimulus at approximately reading distance, so a
near correction should be used for presbyopic patients.
 Spectacle rim artefact. Spectacles can cause rim scotomas if small aperture lenses
are used or if incorrectly dispensed. Narrow-aperture trial frame lenses are unsuitable for
perimetry.
 Miosis decreases sensitivity in the peripheral field and increases variability in the
central field in both normal and glaucomatous eyes. Pupils less than 3 mm in diameter should
therefore be dilated prior to perimetry; a consistent mydriatic should be used for serial tests.
 Media opacities (usually cataract) can have a profound effect, exaggerated by miosis.

 Ptosis, even if mild, can suppress the superior visual field. Similar effects result from
dermatochalasis, prominent eyelashes and deeply set eyes.
 Inadequate retinal adaptation may lead to error if perimetry is performed soon after
ophthalmo1scopy.

REVIEW OF LITERATURE
Optical coherence tomography measurement of macular and nerve fiber layer thickness
in normal and glaucomatous human eyes study was done byViviane Guedes, Joel S
Schuman, Ellen Hertzmark, Gadi Wollstein, Anthony Correnti and their team. In this study
367 subjects (534 eyes), including 166 eyes of 109 normal subjects, 83 eyes of 58 glaucoma
suspects, 196 eyes of 132 early glaucoma patients, and 89 eyes of 68 advanced glaucoma
patients. All NFL parameters both in prototype and commercial OCT units were statistically
significantly different comparing normal subjects and either early or advanced glaucoma (P <
0.001). Inner ring, outer ring, and mean macular thickness both in prototype and commercial
OCT devices were found to be significantly different between normal subjects and advanced
glaucomatous eyes (P < 0.001). The outer ring was the only macular parameter that could
significantly differentiate between normal and early glaucoma with either the prototype or
commercial OCT unit (P = 0.003, P = 0.008, respectively). The area under the receiver
operator characteristic (AROC) curves comparing mean NFL thickness between normal and
advanced glaucomatous eyes was 1.00 for both the prototype and commercial OCT devices
for eyes scanned on both machines on the same day. The AROC comparing mean macular
thickness in normal and advanced glaucomatous eyes scanned on both machines on the same
day was 0.88 for the prototype OCT device and 0.80 for the commercial OCT.(5)
Analysis of macular volume in normal and glaucomatous eyes using optical coherence
tomographystudy done by David E Lederer, Joel S Schuman, Ellen Hertzmark, James
Heltzer, Leonardo J Velazques, James G Fujimoto, Cynthia MattoxThe authors assessed 272
eyes of 164 subjects as part of an institutional study at New England Eye Center in Boston
Using repeated measures regression, macular volume in normal (2.37 +/- 0.11 mm(3))
glaucoma suspect (2.33 +/- 0.16 mm(3)), and early glaucoma eyes (2.27 +/- 0.13 mm(3)) was
significantly greater than in eyes with advanced glaucoma (2.12 +/- 0.23 mm(3), P =.0001, P
=.0001, and P =.0008, respectively). Macular volume in normal eyes was significantly greater
than in early glaucoma eyes (P =.01). (4)

Retinal nerve fiber layer and macular inner retina measurements by spectral domain
optical coherence tomograph in Indian eyes with early glaucoma study was done byH L
Rao , J G Babu, U K Addepalli, S Senthil, C S GarudadriR1 this study was aimed, 125 eyes
of 64 normal subjects and 91 eyes of 59 early glaucoma patients underwent RNFL and MIR
imaging with SD-OCT.RNFL parameters ranged from 0.537 for the temporal quadrant
thickness to 0.821 for the inferior quadrant RNFL thickness. AUCs for the MIR parameters
ranged from 0.603 for the superior minus inferior MIR thickness average to 0.908 for
ganglion cell complex focal loss volume (GCC-FLV). AUC for the best MIR parameter
(GCC-FLV) was significantly better (P<0.001) than that of the best RNFL parameter (inferior
quadrant thickness). The sensitivities of these parameters at high specificity of 95%,
however, were comparable (52.7% vs58.2%). Evaluation of the LRs showed that outside
normal limits results of most of the RNFL and MIR parameters were associated with large
effects on the post-test probability of disease. (6)
Mapping of Macular Substructures with Optical Coherence Tomography for Glaucoma

Diagnosisstudy was done by OuTanPhDGisèleLiMDAke Tzu-HuiLuPhDRohitVarmaMD,
MPHDavidHuangMD, PhDAdvanced Imaging for Glaucoma Study Group. This study aimed
One hundred forty-nine participants in the Advanced Imaging for Glaucoma Study, divided
into 3 groups: normal (N) perimetric glaucoma (PG), and glaucoma suspect and preperimetric
glaucoma (GSPPG) with 44, 73, and 29 persons, respectively.The Zeiss Stratus OCT system
(Carl Zeiss Meditec, Inc., Dublin, CA) was used to map the macula over a 6-mm diameter
and to scan the circumpapillary nerve fiber layer (cpNFL).The mNFL, mGCL, mIPL, and
mINL were significantly (P<0.001) thinner in both the GSPPG and PG eyes than in the N
eyes. In PG eyes, mNFL, mGCL, and mIPL thinning was most severe (approximately 20%),
mINL thinning was intermediate (7%), and mORL thinning was minimal (3%). The
repeatability (coefficient of variation and intraclass correlation) of thickness measurements
was improved by combining the mNFL, mGCL, and mIPL measurements as the inner retinal
layer (mIRL). The mIRL was the best macular parameter for glaucoma diagnosis and had
discriminant power comparable with that of the cpNFL. The fractional loss of mIRL
thickness was most severe in the inferior perifoveal region for both the PG and GSPPG
groups. (7)

Comparative analysis of macular and peripapillary retinal nerve fiber layer thickness in
normal, glaucoma suspect and glaucomatous eyes by optical coherence tomography
study was done by Mita Saha, Sabyasachi Bandyopadhyay, Debabrata Das, Sourav Ghosh
and their team. In this study macular and peripapillary RNFL scans were performed in one
eye of 70 controls, 35 glaucoma suspects and 70 glaucoma patients by TD-OCT. The
discriminating power of each parameter between the groups was determined by area under
the receiver operating characteristic (AROC) curve. The correlation of macular thickness and
RNFL thickness parameters with global field indices were also performed. P-value of less
than 0.05 was considered statistically significant. The differences in all the macular thickness
parameters between the groups were statistically significant (pless than 0.05) except foveal
thickness (FT) and nasal inner (NI) quadrant thickness. The temporal outer (TO) macular
quadrant produced largest AROC curve of 0.90 between controls and glaucoma patients. The
differences in all the RNFL thickness parameters were highly significant between the groups
(pless than 0.001). The AROC curve between control group and glaucoma patients for RNFL
average thickness was 0.99. (16)
Macular retinal and nerve fiber layer thickness in early glaucoma: clinical correlations
study was done by Vassiliki Arvanitaki, Miltiadis K Tsilimbaris, Aristofanis Pallikaris and
their team. In this study examines RT and RNFLT using standard scanning protocols in early
glaucoma. In this prospective, nonrandomized case series, 95 eyes of 95 patients were
evaluated, including 29 nonglaucomatous subjects (control group), 34 glaucoma suspects,
and 32 early manifest glaucoma patients. RT and RNFLT were measured using scanning fast
macular thickness map and Fast RNFLT (3.4) protocols on a 1.70 mm radius around the
macular center (respectively) in all four quadrants. The fast RNFLT (3.4) protocol was
transposed on the macula from the peri-papillary area. Data were statistically analyzed for
differences between groups, and for correlations between parameters. P<0.5 was statistically
significant. Both early manifest glaucoma patients and glaucoma suspects had significantly
lower RT than controls in all quadrants. RNFLT differences in all quadrants were not
statistically significant (P>0.05). RT was significantly inversely correlated with axial length
in early manifest glaucoma patients and glaucoma suspects but not in controls. (17)

MATERIALS AND METHODOLOGY
Materials:-
Vision charts, trial set, retinoscope, autorefractometer, slit lamp, ophthalmoscope,
applanation tonometer, perimeter, gonio lens, pachymeter, optical coherence tomography.
Methodology: -
 It was a prospective, non-randomized, observational cross section study which carried
out from November 2020 to May 2021at dhruva eye hospital. In this study comprised
100 eyes independent of any gender with glaucomatous eye and non-glaucomatous
eye age group more than 40 years were included.
 After the registration of patients, the regular routine of an ocular examination was
carried out, it which consist of chief complain, ocular history, family history and
systemic history.
 All of subjects were examination by optometrists and senior medical staff.
 The visual acuity was checked with Snellen’s latter chart and dot chart for illiterates.
Refractive error was first measured with autorefractometer and then the best corrected
visual acuity was obtained by performing subjective refraction. Cycloplegic refraction
was done.
 Anterior segment examination was performed with the use of slit lamp
biomicroscopy. Intra ocular pressure was measured using applanation tonometer.
 Posterior segment examination was performed using by indirect ophthalmoscope.
 Once it was found out that patient was factor of glaucoma, which is raised IOP,
special investigation carried out to confirm the diagnosis.
 Glaucoma workup included IOP measurement by means of Goldmann applanation
tonometer, central corneal thickness evaluation by means of TOPCON SP2000P
specular microscope, angle structure measurement by means of gonioscope, visual
field assessment by means of Humphrey perimeter. Retinal nerve fiber layer thickness
evaluation by mean of optovueOCT.
 The four quadrants (superior, inferior, temporal and nasal) average RNFL thickness
was measured. The differences in RNFL thickness measured between the two groups
glaucomatous and non-glaucomatous.

Inclusion criteria:-
 Age group above 40 years of age.
 Patients with systemic illness.
 Refractive error of <+/- 4 diopters
 Patient having glaucomatous eye and normal eye
 No gender preference
Exclusion criteria: -
 Primary angle closure glaucoma.
 Secondary glaucoma
 Age less than 40 years
 History of prior ocular disease
 History of intraocular surgery
 previous ocular trauma
 Other ocular disease except glaucoma
optovue OCTRTVue Model -RT100
 Retinal nerve fiber layer thickness was measure using optovueOCT.

CT report

For Macular thickness
Optic nerve head analysis

Retinal nerve fibre layer

ANNRXURE
NAME: -
OPD.NO: -
AGE/SEX: -
HISTORY: -
RIGHT EYE LEFT EYE

VISIONWITHOUT GLASS
VISION WITH GLASS
I.O TENSION
SUBJECTIVE REFRACTION: -
DIST.VN SPH CYL AXIS VA
RIGHT EYE
LEFT EYE
NEAR VN NEAR. ADD NEAR VA

RIGHT EYE
LEFT EYE
OBJECTIVE REFRACTION: -
RE WD LE
SPH. CYL. AXIS.

RIGHT EYE
LEFT EYE

RIGHT EYE LEFT EYE
SLIT LAMP EXAMINATION
FUNDUS EXAMINATION
APPLANATION TONOMETRY
PACHYMETRY
GONIOSCOPY
PERIMETRY
DIAGNOSIS
TREATMENT
RNFL THICKNESS:-
SUPERIOR INFERIOR TEMPORAL NASAL AVERAGE
RIGHT EYE
LEFT EYE
MACULAR THICKNESS:-
SUPERIOR INFERIOR TEMPORAL NASAL CENTRAL
RIGHT EYE
LEFT EYE

OBSERVATIONS AND RESULTS
STATISTICAL ANALYSIS
T-test": Two sample assuming unequal variance

Using sample data, find the standard error, degrees of freedom, test statistic, and the P-value
associated with the test statistic.
 Standard error. Compute the standard error (SE) of the sampling distribution.

SE = sqrt [ (s12/n1) + (s22/n2)]
where s1 is the standard deviation of sample 1, s2 is the standard deviation of sample 2, n 1 is
the size of sample 1, and n2 is the size of sample 2.
 Degrees of freedom. The degrees of freedom (DF) is:

DF = (s12/n1 + s22/n2)2 / {[ (s12 / n1)2 / (n1 - 1)] + [ (s22 / n2)2 / (n2 - 1)]}
If DF does not compute to an integer, round it off to the nearest whole number. Some texts
suggest that the degrees of freedom can be approximated by the smaller of n 1 - 1 and n2 - 1;
but the above formula gives better results.
 Test statistic. The test statistic is a t statistic (t) defined by the following equation.
t = [ (x1 - x2) - d] / SEwhere x1 is the mean of sample 1, x2 is the mean of sample 2, d is the
hypothesized difference between population means, and SE is the standard error. (13)

Table 1: t-Test Two-Sample Assuming Unequal Variances for comparison
of average RNFL thickness between control and glaucoma group.
t-Test: Two-Sample Assuming Unequal Variances

Variable 1 Variable 2
Mean 83.18 89.56
Variance 255.7832653 113.9657
Observations 50 50
Hypothesized Mean
1Difference 0
Df 85
t Stat -2.346130626
P(T<=t) one-tail 0.010648459
t Critical one-tail 1.6629785
P(T<=t) two-tail 0.021296919
t Critical two-tail 1.988267868
H0: There is no significant difference between average RNFL thickness of normal and
glaucoma group.
TStat -2.346130626 < tcritical1.988267868
hypothesis is rejected so there is significant difference between average RNFL thickness of

normal and glaucoma group.

Table 2: t-Test Two-Sample Assuming -Unequal Variances for comparison
of temporal RNFL thickness between control and glaucoma group.

Mean 56.18 61.46
Variance 206.7628571 69.27388
Observations 50 50
Hypothesized Mean Difference 0
Df 79
t Stat -2.247167701
P(T<=t) one-tail 0.013709662
P(T<=t) two-tail 0.027419324
H0: There is no significant difference between average temporal RNFL thickness of normal
and glaucoma group.
T Stat -2.247167701 < t critical1.99045017
hypothesis is rejected so there is significant difference between average temporal RNFL

thickness of normal and glaucoma group.

of nasal RNFL thickness between control and glaucoma group.

Mean 66.6 73.1
Variance 135.9183673 138.4184
H0:
Observations 50 50
There Hypothesized Mean is
no Difference 0
df 98
t Stat -2.774957757
P(T<=t) one-tail 0.003306208
P(T<=t) two-tail 0.006612416
significant difference between average nasal RNFL thickness of normal and glaucoma group.
T Stat-2.774957757 < t critical1.984467404
hypothesis is rejected so there is significant difference between average nasal RNFL


of superior RNFL thickness between control and glaucoma group.

Mean 99.84 109.64
Variance 515.8514286 312.3167
Observations 50 50
Hypothesized Mean
Difference 0
Df 92
t Stat -2.407974105
P(T<=t) one-tail 0.009018101
P(T<=t) two-tail 0.018036201
H0: There is no significant difference between average superior RNFL thickness of normal
and glaucoma group.
T Stat-2.407974105<t critical1.986086272
hypothesis is rejected so there is significant difference between average superior RNFL


of inferior RNFL thickness between control and glaucoma group.

Mean 64.72 114
Variance 678.6546939 481.7551
Observations 50 50
Hypothesized Mean
Difference 0
df 95
t Stat -10.2293964
P(T<=t) one-tail 2.6746E-17
P(T<=t) two-tail 5.3492E-17
H0: There is no significant difference between average inferior RNFL thickness of normal
and glaucoma group.
T Stat-10.2293964<t critical1.985250956
hypothesis is rejected so there is significant difference between average inferior RNFL


of macular thickness between control and glaucoma group.
Mean 229.84 251.96
Variance 1704.749388 205.4269
Observations 50 50
Hypothesized Mean Difference 0
Df 61
t Stat -3.578766766
P(T<=t) one-tail 0.00034196
P(T<=t) two-tail 0.000683919
H0: There is no significant difference between macular thickness of normal and glaucoma
group.
T Stat-3.578766766 < t critical1.999623567
hypothesis is rejected so there is significant difference between macular thickness of normal

and glaucoma group.

Table 7 : Distribution of patient by gender.
Gender glaucoma normal

male 33 29
female 17 21
35
30
25
20 male
female
15
10
0
glaucoma normal
Out of 50 eyes of normal group 58% (29 eyes) were male and 42% (21 eyes) were female.
Out of 50 eyes of glaucoma group 66% (33 eyes) were male and 34% (17 eyes) were female.

Table 8: Distribution of patients by age group.
AGE Glaucoma Normal

40-50 17 26
50-60 14 11
60-70 15 10
70-80 4 3
DISTRIBUTION OF PATIENT BY AGE

GROUP
30
25
20
15
10
5
0
40-50 50-60 60-70 70-80
Glaucoma normal
This graph shows distribution eyes by age group at the time of ophthalmological diagnosis
normal and glaucoma group.

Table 9 : Comparison of average CD ratio in control group and glaucoma
group.
Average C/D
group Ratio
glaucoma 0.6442
normal 0.5804
Average C/D Ratio
0.66
0.64
0.62 Average C/D Ratio
0.6
0.58
0.56
0.54
glaucoma normal
Average CD ratio analysed by OCT finding in control group and glaucoma group. The graph
shows that average CD ratio in control group was (0.58±0.08). The average CD ratio in
glaucoma group was (0.64±0.09).

Table 11: Comparison of Intra Ocular Pressure in control and type of
glaucoma group.
GROUP GLAUCOMA NORMAL

IOP 16.34 14.88
IOP
16.5
16
15.5
15
14.5
14
GLAUCOMA NORMAL
IOP was analysed in control group and glaucoma group. The graph reveled that mean IOP in
control group was (14.88±3.60). The mean IOP in glaucoma group was (16.34±3.32).

Table 13: Comparison of four quadrant RNFL thickness in normal and
glaucoma group.
RNFL GLAUCOMA NORMAL
AVERAGE 83.18 89.56
TEMPORA 56.18 61.46

L
SUPERIOR 99.84 109.64
NASAL 66.6 73.1
INFERIOR 64.72 114
120
100
80
60
40 GLAUCOMA
NORMAL
20
0
NORMAL
E L GLAUCOMA
RAG RA OR L
AV
E P O
ERI A SA IO
R
M P N R
TE SU FE
IN
Here, graphical demonstration of RNFL thickness comparison in control and glaucoma

group. In control group superior quadrant RNFL thickness is (109.65±17.67) μm, inferior
RNFL thickness is (114±21.94) μm, temporal RNFL thickness is (61.46±8.32) μm and in
nasal it was (73.1±11.76) μm. In glaucoma group superior quadrant RNFL thickness is
(56.18±14.37) μm, inferior RNFL thickness is (64.72±26.05) μm, temporal RNFL thickness
is (56.18±14.37) μm and in nasal it was (66.6±11.65) μm.

DISCUSSION
Glaucoma is considered to be the second leading cause of blindness in the world so the main
goal of glaucoma management is to diagnose this disease when it is asymptomatic. Visual
field testing is essential in the diagnosis and monitoring of glaucoma. However, it is known
that standard perimetry cannot detect VF defects until 20-40% of ganglion cells have been
lost. Nowadays RNFL defects have been objectively demonstrated earlier than VF defects
with new investigative technologies. Measuring RNFL thickness by OCT enables an
objective and quantitative assessment of glaucomatous structural loss.(2)
In this study total 100 eyes of 56 subjects were taken which are attended in OPD of dhruva
eye hospital with diagnosis of glaucoma. They consented for their case history to be
reviewed, anonymized, summarized and that information to be used in this study.
50 eyes of 29 subjects were included in glaucoma group and 50 eyes of 27 subjects were
included in normal group.
It was observed that Out of 50 eyes of normal group 58% (29 eyes) were male and 42% (21
eyes) were female. Out of 50 eyes of glaucoma group 66% (33 eyes) were male and 34% (17
eyes) were female.
In this study the mean age ± standard deviation (SD) was (56.53±9.79) years (range,40-80
years) were analysed for both with glaucoma and control group.
Comparison of RNFL thickness was done between control group and glaucoma group.
Similer study done by study was done by Viviane Guedes, Joel S Schuman, Ellen
Hertzmark, Gadi Wollstein, Anthony Correnti and their team. In this study 367 subjects (534
eyes), including 166 eyes of 109 normal subjects, 83 eyes of 58 glaucoma suspects, 196 eyes
of 132 early glaucoma patients, and 89 eyes of 68 advanced glaucoma patients. All NFL
parameters both in prototype and commercial OCT units were statistically significantly
different comparing normal subjects and either early or advanced glaucoma (P < 0.001).
Inner ring, outer ring, and mean macular thickness both in prototype and commercial OCT
devices were found to be significantly different between normal subjects and advanced

glaucomatous eyes (P < 0.001). The outer ring was the only macular parameter that could
significantly differentiate between normal and early glaucoma with either the prototype or
commercial OCT unit (P = 0.003, P = 0.008, respectively). The area under the receiver
operator characteristic (AROC) curves comparing mean NFL thickness between normal and
advanced glaucomatous eyes was 1.00 for both the prototype and commercial OCT devices
for eyes scanned on both machines on the same day. The AROC comparing mean macular
thickness in normal and advanced glaucomatous eyes scanned on both machines on the same
day was 0.88 fr the prototype OCT device and 0.80 for the commercial OCT .(5)
In this study,RNFL thickness were analysed in normal group and glaucoma group. Mean
average RNFL thickness in control group was (89.56±10.67) which difference significantly
from that of the glaucoma group (83.18±15.99) respectively, (p= 0.03) this data shows table
no.1, mean macular thickness in normal group was (251.96±14.33) which difference
significantly from that of the glaucoma group (229.84±41.28) respectively, (0.0003) this data
shows table no.6. From t-Test: Two-Sample Assuming Unequal Variance test for RNFL
thickness and macular thickness it was observed that there is a statistically significant mean
different between average RNFL thickness and macular thickness between the two groups.
In present study, four quadrant RNFL thickness were analyzed between control group and
glaucoma group. This was statistically highly significant. Superior quadrant RNFL thickness
among two group were (109.64±17.67) and (99.84±22.71) μm respectively, (p=0.009) this
data shows table no 3 , inferior quadrant RNFL thickness among two groups were
(114±21.94) and (64.72±36.051)μm respectively, (p=< 0.05)this data shows table no 5,
temporal quadrant RNFL thickness among two groups were (61.46±8.32) and (56.18±14.37)
μm respectively, (p= 0.013) this data shows table no 2. and nasal quadrant RNFL thickness
among two groups were (73.1±11.76) and (66.6±11.65) μm respectively, (p= 0.01)this data
shows table no 4. From t-Test: Two-Sample Assuming Unequal Variance test for RNFL
thickness it was observed that there is a statistically significant mean difference in all four
quadrants RNFL thickness between the two groups.
In current study we found that RNFL average thicknesses in four quadrants and macular
thickness in glaucoma were significantly decreased compared with normal group.

CONCLUSION
OCT is an important instrument part of the imaging in glaucoma is the monitoring for
progression. OCT evaluation results suggest that RNFL parameters and macular thickness for
glaucoma During diagnostic assessment of patients are highly effective.
We suggest initiating an early treatment for the patients who show structural change in OCT
in one or more quadrant so as to prevent the likely damage to optic nerve head in future.
Treatment may also be initiated in the patients without structural changes in OCT in presence
of risk factor. OCT can be used as a helpful tool in glaucomatous patients for measurement of
structural loss which precedes functional loss alerting ophthalmologist to start early treatment
especially in presence of risk factor and contributes to quality of life.
RNFL average thicknesses in four quadrants and macular thickness in glaucomatous patients
were significantly decreased compared with control groups.
OCT is useful and prior in early detection of glaucoma as well as in keeping an eye on
progression of glaucoma.

RECOMMENDATIONS AND LIMITATIONS
 There are several limitations to this study. The sample size in two diagnostic groups
was small and the participants were not age matched, so generalizations about these
measurements should be made with caution. Despite the small sample size, significant
differences among study groups for OCT RNFL thickness were found.
 Study can be also done by comparing central corneal thickness.
 Study can be also done with RNFL thickness and visual field defects.

BIBLIOGRAPHY
1. C bowd, R N weinreb, J M williams, Lm zangwill. (jan,2000). the retinal nerve fiber
layer thickness in ocular hypertensive ,normal, and glaucomatous eyes with optical coherence
tomography.JAMA Ophthalmology ,118(1): P-22-26.
2. Dipak Patel1*, Poonam Rana1,siddharth dua,roshni patel. (26 February 2018). Retinal
nerve fiber layer thickness analysis in normal,ocularhypertensive and primary open angle
glaucoma : an optical coherence tomography study. international journal of research in
medical sciences .
3. Ferri, Fred F. (2010). Ferri's differential diagnosis: a practical guide to the differential
diagnosis of symptoms, signs, and clinical disorders (2nd ed.). Philadelphia, PA:
Elsevier/Mosby. p. Chapter G. ISBN 0323076998.
4. David E Lederer et al. Am j ophthalmol.2003 jan PMID : 12788124 Analysis of

macular volume in normal and glaucomatous eyes using optical coherence tomography
5. Viviane Guedes PMID : 12511364 Optical coherence tomography measurement of

macular and nerve fiber layer thickness in normal and glaucomatous human eyes
Opthalmology volume 110, issue 1,jan2003, pages177-189
6. H L Rao etal.eye (Lond) PMID : 22079964 Retinal nerve fiber layer and macular
inner retina measurements by spectral domain optical coherence tomograph in Indian eyes
with early glaucoma 2012 JAN
7. Ou Tan et al. Ophthalmology.2008janMapping of Macular Substructures with

Optical Coherence Tomography for Glaucoma Diagnosis
8. Hilary Wilson (M.D.). (November 2,2008).OCT Bootcamp: The basic of retina

OCT.GUSET USER(2015).

9. Rohit saxena,Digvijay singh,Praveen vashist. (2013). Glaucoma: An emerging peril.
indian journal of community medicine , 135-137.
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disease.Journal of glaucoma volume-19, Issue 6-P 391-397.
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(june 16,2018). A comparision of retinal nerve fiber layer thickness by spectral Domain
Optical coherence tomography in primary open angle glaucoma, normotensive glaucoma and
glaucoma suspect. open access journal of opthalmology.
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A.Quigley ,MD Tin Aung, FRCS (Ed),PhD, Ching-Yu Cheng,MD,PhD. (November,2014).
Global prevalence of glaucoma and projections of glaucoma burden through 2040. American
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7th edition
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Ophthalmol 2016 jul Comparative analysis of macular and peripapillary retinal nerve fiber
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Kheni Sweta Vinodray[2nd year M.

SWETA VINODRAY KHENI

UNDER THE GUIDANCE OF:

DR. MAHENDRASINH D. CHAUHAN

(M.S. OPHTHAL, D.O.M. S, Ph.D.)

THESIS SUBMITTED TO:

SHREE BHARATIMAIYA COLLEGE OF OPTOMETRY AND PHYSIOTHERAPY, SURAT

VEER NARMAD SOUTH GUJARAT UNIVERSITY, SURAT GUJARAT

Kheni Sweta Vinodray[2nd year M.Optometry] 6

A DISSERTATION SUBMITTED TO THE

VEER NARMAD SOUTH GUJARAT UNIVERSITY, SURAT

In partial fulfillment of the regulations for the award of

THE DEGREE OF MASTER OF OPTOMETRY

Under the guidance of

SHREE BHARATIMAIYA COLLEGE OF OPTOMETRY AND

Kheni Sweta Vinodray[2nd year M.Optometry] 7

This is to certify that enclosed work on the subject “OPTICAL COHERENCE

Dr. Mahendrasinh D. Chauhan Dr. Chetna Patel

(M. S. OPHTHAL, D.O.M.S, Ph.D.) (M.S.OPHTHAL)

(Principal) (Vice principal)

Shree Bharatimaiya College of Shree Bharatimaiya College of

Optometry and Physiotherapy. Optometry and Physiotherapy.

Kheni Sweta Vinodray[2nd year M.Optometry] 8

SWETA VINODRAY KHENI

Kheni Sweta Vinodray[2nd year M.Optometry] 9

 RNFL- Retinal nerve fiber layer

Kheni Sweta Vinodray[2nd year M.Optometry] 10

3 AIM AND OBJECTIVE

6 MATERIALS AND METHODOLOGY

7 OBSERVATIONS AND RESULTS

10 RECOMMENDATION AND LIMITATIONS

Kheni Sweta Vinodray[2nd year M.Optometry] 12

Kheni Sweta Vinodray[2nd year M.Optometry] 13

Kheni Sweta Vinodray[2nd year M.Optometry] 14

Optical Coherence Tomography (OCT) is a promising technology that has been

Kheni Sweta Vinodray[2nd year M.Optometry] 15

 To evaluate retinal nerve fiber layer thickness and macular thickness

 To evaluate retinal nerve fiber layer thickness and macular thickness

 To compare the average and in four quadrant ( superior ,inferior,

 To compare the central macular thickness in glaucomatous and

Kheni Sweta Vinodray[2nd year M.Optometry] 16

Figure 1: Risk factors of glaucoma

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SIGNS AND SYMPTOMS

Figure 2: - Symptoms of glaucoma

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Risk factors for developing glaucoma in OHT

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The following factors were significant on multivariate analysis:

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African-American race was associated with a higher glaucoma risk.

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Examination techniques. Careful assessment of disc changes can be made by direct

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Figure 4: - stage of glaucoma

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