The Role of OCT i n [606335]

2020

The Role of OCT i n
the Diagnosis and Maintenance
of Glaucoma Patients

Asadi Ali

Discipline: Ophthalmology

Coordinator – Dr. Stefanescu -Dima Alin -Stefan
Thesis Advisor – Dr. Olaru Andrei

The Role Of OCT In
The Diagnosis And Maintenance
Of Glaucoma Patients

A thesis submitted to the
University of Medicine and Pharmacy of Craiova
in partial fulfillment of requirements for the
degree of Medical Doctor – M.D.

2020
Craiova

Table of Contents
Page
1. Introduction 5
1.1 Glaucoma 5
1.1.1 Definition 5
1.1.2 Physiology 5
1.1.2.1 Aqueous Humour 5
1.1.2.2 Intraocular Pressure (IOP) 6
1.1.2.3 The Anterior Chamber Angle 6
1.1.2.4 The Trabecular Meshwork 7
1.1.2.5 The Ciliary Bodies 7
1.1.3 The Retina 8
1.1.3.1 The fovea 10
1.1.3.2 The Macula 10
1.1.3.3 The Optic Nerve 10
1.1.3.4 Pathophysiology of Glaucomatous Optic Nerve Damage 12
1.1.3.5 The Optic D isc 13
1.1.3.5.1 Optic Disc Cupping 13
1.1.3.5.2 Optic Disc Edema 14
1.1.4 Primary Open Angle Glaucoma (POAG) 14
1.1.4.1 POAG Risk Factors and Epidemiology 14
1.1.4.2 Diagnosis 15
1.1.5 Secondary Open Angle Glaucoma 16
1.1.5.1 Forms of SOAG 16
I. Exfoliation glaucoma 16
II. Pigmentary glaucoma 16
III. Corticosteroid -Induced G laucoma 17
IV. Inflammatory glaucoma 17
V. Phacolytic glaucoma 17
VI. Aphakic and Pseudophakic G laucomas 17
VII. Post-Traumatic G laucoma 18
VIII. Ghost Cell Glaucoma 18
1.1.6 Primary Angle Closure Glaucoma (PACG) 19
1.1.6.1 Classification by Anatomi c Level 19
1.1.6.2 Epidemiology 19
1.1.6.3 Etology 20
1.1.6.4 Risk F actors 20
1.1.6.5 Clinical Presentation 20
1.1.6.6 Diagnosis 21
1.1.7 Secondary Angle Closure Glaucoma 22
1.1.7.1 Etiology 22
1.1.7.2 Diagnosis 22

1.2 Optical Coherence Tomography – OCT 23
1.2.1 Definition 23
1.2.2 Time Domain OCT 23
1.2.3 Spectral Domain OCT 23
1.2.4 Swept Source OC T 24
1.2.5 Interpretation 24

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1. Introduction
1.1 Glaucoma
1.1.1 Definition
Glaucoma itself is not a specific disease. It is a group of diseases and a damage to the optic
nerve that is illustrated by a distinctive impairm ent and damage to the optic disc for which the
pressure inside the eye – Intra Ocular Pressure – is a variable risk factor. This group of
diseases can eventually promote diminished visual acuity, visual field deterioration and
possibly blindness. There are many forms of Glaucoma but mainly it can be classified into
two major schemes: open angle glaucoma and closed angle glaucoma , with the first being the
forms of glaucoma in which t he aqueous humor can access the trabecular meshwork without
obstruction, while the latter is comprised by the forms of glaucoma in which the irido -corneal
angle is obstructed and the aqueous humor can‟t reach the trabecular meshwork. Both of the
two major categories are characterized by progressive optic neuropathy with deterioration of
the visual field and distinctive structural changes, inclusive of thinning of the retinal nerve
fiber layer and excavation of the optic nerve head. Glaucoma can‟t be defined by a change in
the intra -ocular pressure, some patients who have glaucoma may also have normal IOP
values same as values seen in normal people. The dynamics of the aqueous humor what‟s
most important in the pathophysiology of glaucoma. The anatomical stru ctures which are
associated with it are the ciliary body, especially the pars plicata part of it, the irido -conreal
angle, and the aqueous humor‟s outflow pathway.
1.1.2 Physiology
1.1.2.1 Aqueous Humour
The aqueous humo r is a transparent non colour ed, BSS that resembles plasma. It is produced
by the ciliary body . It occupies a hugely important role providing nutrition to the lens and the
cornea and structural integrity to the eye. When compared to plasma we find that it is lower
in glucose and prote in levels while at the same time it‟s higher in ascorbate. The aqueous
formation rate is close to 2.5 microliter/minute, this rate is made up 70% by active secretion,
20% by ultrafiltration and10% osmosis. The active secretion engages into sustaining and
altering the trans -epithelial potential by the Na+K+ pump, ion transport by symports and
antiports (including the important Na+/K+/2Cl− symport), calcium – and voltage -gated ion
channels, and carbonic anhydrase .
– Aqueous drainage: The majority of the aqueous humor exits the eye passing through the
trabecular route which is passive pressure sensitive. A big portion of the outflow resistance is
owed to the trabecular meshwork itself (about 75%), with the most signi ficant element being
the outermost (juxtacanalicular) section of the trabecular meshwork. This consists of several
layers of endothelial cells embedded in ground substance which appears to function as a
filter, which is continually cleaned by endothelial c ell phagocytosis. Further movement into

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Schlemm‟s canal is obtained by pressure dependent transcellular channels and paracellular
pores. After that the aqueous gets to the episcleral veins through collector channels and from
there ends up in the general ve nous circulation.
There‟s also an other option for the humor to exit the eye which is through the root of the iris
specifically through the interstitial spaces between the ciliary muscle bundles, and then it
keeps moving towards the superchoroidal space wh ere it will be transferred to the venous
system, this pathway is called the uveoscleral outflow pathway.
1.1.2.2 Intraocular Pressure (IOP)
The intracellular pressure (IOP) is the pressure that the fluid inside the eye – the aqueous
humor – exerts on the internal surface area of the anterior eye. Theoretically the IOP can be
determined by the Goldmann equation, IOP = (F/C) + P , in which F means the rate of the
aqueous outflow rate, while C the aqueous outflow and finally P the episcleral v enous
pressure. Any change to either of the values can cause an elevation or a decrease in the IOP.
The IOP is a major risk factor for both the development and progression of glaucoma, it even
plays a role in progressive optic nerve damage in normal tensio n glaucoma in which the IOP
does not exceed 21 mmHg.
1.1.2.3 The Anterior Chamber Angle
The anterior Chamber Angle is the angle formed by the converging of the anterior (scleral)
wall with the posterior wall of the iris in a curved part composed of the inner area of the
ciliary body. The angle houses some important features of the eyeball which are the
Schwalbe‟s line, the trabecular meshwork (overlying Schlemm‟ s canal), and the scleral spur.
Schwalbe‟s line signs the termination of the corneal endotheli um.

Source: Figure 1 –16 Vaughan & Asbury‟s General Ophthalmology -McGraw -Hill (2017) – Paul Riordan -Eva, James J. Augsburger –
Page 35

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1.1.2. 4 The Trabecular Meshwork
The trabecular meshwork is made of beams of collagen and elastic tissue covered by
trabecular cells that comes into being a filter with a pore that decreases in dimension
advancing towards the canal of Schlemm. Increasing the pore size is achieved by the
contraction of the ciliary muscle through its insertion into the trabecular meshwork, which in
turn increases the rate of the aqueous drainage. The access of aqueous humor into the
Schlemm‟s relies on cyclic formation of transcellular channels in the endoth elial lining. The
aqueous humor is directly conducted into the venous system by efferent channels from
Schlemm‟s canal (approx. 30 collector channels and 12 aqueous veins).

Source: Figure 11 -1 Vaughan & Asbury‟s General Ophthalmology -McGraw -Hill (2017) – Paul Riordan -Eva, James J. Augsburger –
Page 524

1.1.2. 5 The Ciliary Bodies
The Ciliary body spreads forward from the anterior end of the choroid to the root of the iris
(~6mm). It comprises of two main parts: the pars plicata (2mm) which is the corru gated
anterior area of the ciliary body and from which the ciliary process emerges, and the pars
plana which is the flat area (4mm). The ciliary epithelium is divided into two layers: a non –
pigmented layer internally, representing the anterior extension of the neuro -retina, and a
pigmented layer externally, representing the extension of the retinal pigment epithelium. The
ciliary epithelium that covers the ciliary processes and the ciliary processes are accountable
for forming the aqueous humor. Longitudina l, radial and circular fibers combined form the
ciliary muscle. The circular fibers are responsible for contracting and relaxing the zonular
fibers which originate in the valleys between the ciliary processes. This action can change the
tension on the lens ‟ capsule, providing it with a modifiable focus for close by and far away

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objects in the visual field. The longitudinal fibers of the ciliary muscle are connected to the
trabecular meshwork to modify its pore size.

Source: Figure 1-12 Vaughan & Asbury‟s General Ophthalmology -McGraw -Hill (2017) – Paul Riordan -Eva, James J. Augsburger – Page 32

1.1.3 The Retina
The retina is a structure that originally developed from the embryonic forebrain, it‟s role is to
collect the light coming towards the eyes and transform the information to an electrical signal
(transduces), then broadcast it through the optic nerve to some areas in the brain responsible
for processing it. Embryologically, it came from the optic vesicle (neuroectoderm) , with an
outer wal l which is goes on to become the retinal pigment epithelium, a potential space
(becomes the subretinal space) and an inner wall that transforms in the end to be the neural
retina. From a histological point of view, the following nine layers comprise the re tina
(ordered from outermost to innermost):
1. Layer of the outer and inne r segment of the photoreceptors.
2. External limiting membrane.
3. Outer nuclear layer .
4. Outer plexiform layer .
5. Inner nuclear layer.
6. Inner plexiform layer.
7. Ganglion cell layer.

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8. Nerve fiber layer.
9. Internal limiting membrane .
The layers mentioned above work one with the other aiming to transform the light images
into neuronal signals to allow the brain to process it as vision. The rod and cone cells of the
retina are co ntained in layers 1 -4 which are in the deepest levels of the retina. Approximately
we have 100 million retinal rod cells and five million retinal cone cells in the human eye. The
outer segments of these of these photoreceptor cells in the first layer accom modate visual
pigment stacked on dis c membranes. These light sensitive pigments get hyperpolarized and
start to transduce the light energy into a neuronal signal when they absorb at least one light
photon. The rod cells are more sensitive to light and abso rb photons more than the cones do,
this is probably owing to the fact that rods contain more visual pigment rhodopsin, but on the
other hand they are also insensitive to color and have lower special acuity. The villous
processes of the retinal pigment epit helium surrounding the rods and cones support the latter
duo. The rods and cons‟ inner segments contain protein synthesis and metabolic machinery
for that photoreceptor cell also gives them support. The outer and the inner segments rest
distal to the exter nal limiting membrane (layer 2). Nuclei of the retinal cone and rod cells
make up the outer nuclear layer (layer 3). The 4th layer (the outer plexiform layer) contains
the proximal ends of the photoreceptor cells. And in this layer the connection between t he
horizontal cells, bipolar cells, and second -order neurons to complete the transduction of light
energy to neurological signals exist through glutamate neuro -synaptic junctions. The
interneurons of the outer retina are the horizontal cells. They admit in put from certain
photoreceptor terminals, pass laterally, and reconnect to other photoreceptors terminals.
Nuclei of bipolar cells, amacrine cells and interplexiform cells are found in the 5th layer (the
inner nuclear layer). The conduction of signals from photoreceptors to ganglion cells in is
executed by the bipolar cells in the 6th layer (the plexiform layer). The amacrine cells are
horizontal cells found in the inner nuclear level and they are able to conduct signals between
ganglion cells and other amacrine cells. Bipolar cells are further divided into two forms:
depolarizing and hyperpolarizing. The basis for the on and off ganglion cell receptive field is
formed by these cells. Various ne urotransmitters are employed by the amacrine cells, they
include peptides, gamma amino butyric acid (GABA), glycine, acetylcholine, and dopamine .
The discovery of the interplexiform cells happened relatively recently, their role is likely to
transfer the i nformation opposite to the direction of most signals in the retina, from the inner
retinal to the outer retinal. The ganglion cells with the axons extending from the retinal to the
brain are found in the 7th layer (the ganglion cell layer) and they embo dy the final common
pathway of light transduction from the retinal photoreceptors to the brain.
The axons from the ganglion cells which go to the brain are unmyelinated in the retina as
myelination stops at the lamina cirbrosa in embryologic development and t hey are found in
the 8th layer (the nerve fiber layer). Rarely we may find axons that appear as myelinated in
the retina.
The internal limiting membrane (9th layer) is the innermost layer of the retina. It‟s made of
basal lamina of Muller cells. It is thicker posteriorly –the posterior fundus – with progressive
thinning travelling anteriorly .

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1.1.3.1 The Fovea
The fovea is a circular area of the retina stret ching about 1.5mm in diameter and found
approximately 17 ° (4500 -500mm) temporally to the optic nerve. The fovea has the best
visual acuity and it‟s accountable for the central and color vision. It‟s centre is called the
foveal pit or the umbo. The fovea co ntains only cone cells with various color opsin pigments
and an area of 400mm named the foveal avascular zone that does not contain any retinal
capillaries. This area is probably vascularized before birth but the vascularization stops a
short time before t he birth. The retina has some special characteristics in the foveal pit area
mainly that it is especially thin, with an absence of neurons in it. The size of the cone cells in
this area is minimal and their shape is hexagonal while their density is notably elevated as it‟s
approximately 200,000 cells per mm2. The absence of the blue cones in this area is most
likely due to their large size, their susceptibility to chromatic aberration from the lens, and
also their low visual acuity potential. Rods are also absent he due to their low visual acuity
potential. Around the foveal margin exists a belt 0.5mm wide surrounding it. Here the retina
has 4 -6 layers of ganglion cells an d 7-11 layers of bipolar cells. Around the parafovea we will
find the perifovea wich surround the former and is about 1.5mm wide. It presents a number of
layers of ganglion cells and six layers of bipolar cells.
1.1.3.2 The Macula
The macula is the central area of the retina and it‟s made of the umbo, foveola, fovea,
parafovea and peri fovea all together. It can be distinguished from extra -areal periphery by
looking at ganglion cell layer which will be several cells thick in the central area compared
with only being one cell thick in the extra -areal periphery. The macula is approximately
5.5mm in diame ter as it is the sum of the its contents as follows: The diameter of the fovea +
twice the width of the parafovea + twice the width of the perifovea:
1.5mm + 2 × 0.5mm + 2 × 1.5mm = 1.5mm + 1mm + 3mm = 5.5mm.

Source: Figure 6-1-7 Ophthalmology, Fourth Editi on- Myron Yanoff & Jay S. Duker – Page 421
1.1.3.3 The Optic Nerve
The optic nerve is the second of the cranial nerves. It is an afferent sensory nerve responsible
for transferring the visual input from the eye to the occipita l cortex. It originates in the retinal
nerve fiber layer and is made up of an average 1.2 million axons . The optic nerve is different

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from the other CN by being a part of th e CNS and that it devel ops from the d iencephalon.
Surrounding the optic nerve are m eninges of the optic nerve sheath and it‟s myelinated by
oligodendrocytes . The diameter of the optic nerve changes due to the myelin nerve sheath –
responsible for protecting and insulating it -, from being approximately 1.5mm to being
around 3.5mm posteri orly to the lamina cribrosa. The total length of the optic nerve is around
45-50mm made of four segments:
▪ The intraocular segment : found inside the eye and it is myelinated, it is supplied by the shirt
posterior ciliary arteries that come from the ophthalmic artery. The intraocular segment is
about 1mm long and is also called the op tic nerve head (t he optic disc ).
▪ The intraorbital segment: this segment is thicker than the previous due to myelination as the
optic nerve becomes myelinated posterior to the lamina cribrosa. Supplying this 25mm
segment that‟s extending from the posterior part of the globe until the optic canal is the
ophthalmic artery.
▪ The intracanalicular: This part of t he optic nerve passes in the optic canal accompanied by
the symp athetic pl exus and the ophthalmic artery. It spans around 9mm. The supply of this
segment is provided by the ophthalmic artery.
▪ The intracranial segment: it is the part of the optic nerve that starts from the optic canal until
the optic chiasm. Several a rteries supply the intracranial segment those arteries are the
internal carotid, anterior cerebral, and the anterior communicating arteries.
At the level of the optic chiasm the two optic nerves meet and separate into the optic tracts,
which extend to the lateral geniculate nucleus (LGN) and the brains‟ visual cortex. The optic
chiasm is the point where the medial (nasal side of each retina) nerve fibers cross to the
opposite side‟s optic tract . Though the lateral nerve fibers (the temporal) do not cross a nd
pass on th e same each of them is. The visual information reaches the lateral g eniculate body
in the mid brain from the optic tracts. The optic radiation then carries visual input to the optic
radiation and after that to the occipital visual cortex. A low number of fibers for ocular and
pupillary reflexes pass directly to the pretectal nucleus and superior colliculus avoiding the
latera l geniculate body.

Source: Figure 9-14 Ganong‟s Review of Medical Physiology 24th edition – Page 189

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1.1.3.4 Pathophysiology of Glaucomatous Optic Nerve Damage
The production and turnover of the extracellular material in the lamina cribrosa becomes
abnormal in the primary open angle glaucoma. Because of the lamina cribrosa becomes
unable to carry out all of its functions (mechanical resistance and elasticity) properly and
efficiently. This consequently leads to glaucomatous damage by the increasing mechanical
lamina cribrosa and the stress of the axons running through it, especially at the superior and
inferior poles of the optic nerve head as the laminar pores there are bigger and thus possibly
have higher vu lnerability to mechanical damage. Intra ocular pressures‟ rising halts at the
lamina cribrosa the axonal transport processes because of the increase of the gradient of the
translaminar pressure which is the difference between the intraocular pressure and t he liquor
pressure (the pressure which is present behind the eye). The result of this is the blockage of
the orthograde transport , which means that the intracellular organelles produced in the cell
body of the RGCs (e.g., mitochondria) will lose the abilit y to move forward along the long
axon. In turn, this causes energy supply shortage. Meanwhile, the retrograde transport is also
getting halted (the neurotrophic factors that the brain produces aren‟t able to get to the
ganglion cell body), which will lead to apoptosis -mediated lethal damage of the RGCs. The
ophthalmic artery is the artery that supplies the optic nerve head mainly by the short posterior
and ciliary arteries. This arterial scheme is segmented and is coordinated separately for each
optic nerve head layer with quite small amount of communi cation between them . Branches of
the central retinal artery are what mainly supply the RNFL. Direct branches of the short
posterior ciliary arteries and an intrascleral vascular structure around the optic nerve head
called the Zinn -Haller circle supply the prelaminar part of the ONH. While the short posterior
ciliary arteries hold the role of supplying the laminar segment. Direct choroidal assistance to
the prelaminar an d laminar segments‟ blood supply is minimal. Failure to regulate the arterial
blood supply of the ON head causes provisional vasoconstriction superseded by
vasorelaxation , leading to a number of localized ischemia -reperfusion damages throughout a
period of years. This may lead to the RGCs apoptosis, just like the low ocular perfusion
pressure and fluctuating low ocular perfusion pressure. The failure in regulating the systemic
blood pressure causes the ophthalmic artery to have low or provisionally low effective
arterial pressure which in turn leads to low ocular perfusion pressure. In the short posterior
ciliary artery, this combines with vascular dysregulation. The low ocular perfusion pressure
can occur due to excessive treatment of the systemic arterial hypertension, especially at night
when the intra ocular pressure is typically high and even untreated blood pressure is usually
low. Gl aucomatous optic neuropathy can be aided also by some immunological mechanisms.
The pathophysiological alterations mentioned above are often combined for the same eye. As
per our current knowledge, apoptosis is the last mechanism of RGC damage in all
patho mechanisms resulting in glaucomatous optic neuropathy. It is an intrinsic self –
destruction mechanism, which is coded genetically, that eventually leads to cell death. To
elaborate more we can say that the glutamate toxicity, lack of neurotrophic factors, a nd the
reduced supply of energy might be highly responsible for the RGCs apoptosis. Lately, it was
discovered that in glaucoma the whole visual pathway get s damaged as the ON gets thinner
and the layers of the geniculate body which the RGC axons of the eye s of glaucoma patients

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appear to be notably shrank. These last few statements furthermore prove that glaucoma
affects the entire visual pathway.
1.1.3.5 The Optic Disc
The optic disc is a portion of the optic nerve that spans from the retinal surface all the way
until just behind the sclera, where the myelinated part of the optic nerve begins. The optic
nerve is made of 1.2 million axons originating from the retinal ganglion cell laye r. It can be
found nasally and a small way superior to the macula. It is a group of fibers of the retinal
nerve fiber layer leaving the intraocular space via the sclera forming what we know as the
optic nerve. When they enter the optic nerve, the retinal g anglion axons bend and separate
into approximately 1000 fascicles. Afterwards pass through some holes that perforate the
lamina cribrosa. The central retinal artery carries the important role of supplying the optic
disc with blood but travelling posteriorl y we find that this carrying this role shifts towards
branches of the ophthalmic artery. On average, the optic dis c is 1mm in diameter measuring
anterior to posterior, while it averages 1.5mm horizontally and finally 1.8mm vertically.
These numbers are the average but we still find big dimensional variations in normal people.
Located centrally in the optic dis c exists physiological cup (central depression), which is
normally sized about a fourth to a third of the optic discs width. The size of this cup can vary
from person to person ranging from a small or even to not existing in individuals with small
optic discs to being larger in individuals with larger optic discs and it is normal in both of the
cases. Typically the ratio between the diameter of the cup and the diameter of the optic disc is
used as a standard way to exa mine the optic discs appearance.

1.1.3.5.1 Optic Disc Cupping
Alterations to the intraocular pressure can have a noticeable effect on the optic disc.
Elevation in the IOP value can may lead to glaucomatous optic atrophy which is represented
by an increase in the optic discs cups‟ size progressively or over a period of time. This
cupping may develop as concentric cupping or can also be more localized alteration
accompanied with focal not ching of the optic disc s rim (consequently the ISNT rule). The
ISNT rule indicates that the rim width is usually shown in a specific gradual thinning manner
as the Inferior rim is the widest of all followed by the superior then the nasal and finally the
temporal rim which should be the thinnest of all. Each rim should be as thick of thicker than
the following (I ≥ S ≥ N ≥ T). The superior and inferior rims are especially more prone to
glaucomatous damage that might lead to their relative thinning, that is w hy any deviation
outside the ISNT rule should draw our attention to the possibility of glaucoma existing in the
patient. Pallor can also be present without the disc cupping increasing in other types of optic
atrophy. The optic disc‟s thinning may also be due to a physiologic cause. It is the
mechanical theory states that the damage might be due to the pressure forces which act on the
lamina cribrosa, which is not supported well at the superior and inferior edges of the disc.
However, microcirculatory irregularities can also facilitate the glaucoma‟s development.

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1.1.3.5.2 Optic Disc Edema
This phenomenon appears when the transfer of materials required for maintaining the axons
of the optic nerve is hindered. Multipl e abnormalities can be linked to the optic disc edema;
Ocular hypotony, intracranial pressure, elevated IOP, tumors, or central retinal vein
occlusion. Unclear optic disc margins, reduced cup size or even loss of the cup, venous
congestion, hemorrahages (p apillary and peripapillary) and optic disc hyperemia can all be
clinical signs of optic disc edema.
1.1.4 Primary Open Angle Glaucoma (POAG)
POAG is a progressive optic neuropathy characterized by cupping of the optic nerve, elevated
intraocular pressure (IOP) without a clear reason, and open anterior chamber angle
gonioscopically. At the basis of the POAG is the progressive loss of retinal ganglion ce lls
along with their axons, and the intraocular pressure being an important risk factor. Glaucoma
can lead to blindness overtime if left untreated as it‟s a progressive condition.
1.1.4.1 POAG Risk Factors and Epidemiology
patient‟s eyes that manifest elevated ocular pressure are more prone to developing POAG,
with the risk of it occurring is reaching until six times higher when comparing with people
who do not show any of the glaucoma‟s ris k factors. According to Ocular Hypertension
Treatment Study (OH TS), patients with high intraocular pressure have 1 -2% risk of
developing PAOG per year or approximately 10% per 10 years, can rise up to 9.5% for 5 year
period. The risk increases with the IOP values increasing, notably when the IOP values are
over 24 mmH g, and especially above 30 mmHg. Normal tension glaucoma is the presence of
glaucoma with normal IOP values, this type of glaucoma is more prevalent in Japan and
China where it is present in over 80% of the open angle glaucoma cases. Meanwhile in the
weste rn countries this percentage is closer to 30% of the patients. Glaucoma cases in the
Western countries were generally determined by IOP elevation not by visual field nor optic
disc criteria, for this reason the normal tension glaucoma is possibly one of th e contributors in
the under -diagnosis of glaucoma there. In spite of the fact the NTG does not meet the
standards for being classified as „elevated IOP‟, the IOP in these patient‟s eyes is likely to be
higher than it should, that‟s why lowering the IOP val ues may help slowing down glaucoma‟s
advancement. Risk factors can range between age, genetic predisposition, positive family
history and race. Meanwhile thin corneas can also lead to underestimating of the IOP values
by the Goldmann tonometry (Imbert -Fick principle: P = F/A ). By itself the intraocular
pressure fluctutation can be risk factor a iding in glaucoma‟s progression. Regardless of the
before mentioned info, age is considered to be the most influential independent risk factor for
glaucoma devel opment as people who passed the 60 years old mark being at risk of
developing glaucoma seven times more than those under 40 years old. Other factors that are
considered as POAG risk factors can be myopia, diabetes, hypertension and vascular
conditions like migraine and vasospasm. Regarding epidemiology, we find that Glaucoma is
more prevalent in those of Hispanic and African descent, and at the same time those of
African descent tend to be younger , possess higher IOP values, show more advanced optic

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neuropa thy at the initial diagno sis, and their disease is less responsive to treatment and has
worse prognosis when comparing with whites.

1.1.4.2 Diagnosis
In order to establish a POAG diagnosis we must evaluate the IOP values, the condition of the
anterior chamber angle (by Gonioscopy), the optic disc and its associated structures such as
the retinal nerve fiber layer and the visual field.
– Assessment of the intra ocular pressure: The IOP has some normal value variations during
the day and in glaucoma it ge ts amplified. Normally the IOP is measured by Goldmann
applanation tonometry. When measuring the IOP this way we should pay close attention to
the patients‟ corneal thickness as it can cause changes to the results of the test, in patients
with thicker than normal corneas there is a risk of overestimating the IOP meanwhile in
patients with thinner corneas the risk is of underestimating the IOP this happens because the
Goldmann tonomet ry assumes a central corneal thickness of 550 µm. This point is also
crucial when examining patients who underwent laser refractive surgeries or were diagnosed
with NTG or ocular hypertension.
– Assess ment of the iridocorneal angle: The angles‟ structures can be evaluated directly with
Gonioscopy. The angle is considered open if the doctor was able to see the trabecular
meshwork fully, the scleral spur and the iris processes. We have a narrow angle if we are
capable of observing only Schwalbe‟s line or a l ittle part of the trabecular meshwork. On the
other hand the angle is considered closed if viewing Schwalbe‟s line is not possible.
– Assessment of the Optic Disc: We must evaluate the optic disc to check for the presence of
glaucomatous cupping. In practi ce, if might be challenging to differentiate a glaucomatous
optic disc from a normal one due to the wide range of normal disc morphology which can
overlap with the glaucomatous appearance notably in the early stages of glaucoma. Assessing
structural abnorm alities or alterations is usually obtained via optic disc stereophotography
and RNFL observation by red -free fundoscopy or photography, disc photography is still
widely used too. New emerging technologies like scanning laser tomography, scanning laser
polarimetry and OCT – optical coherence tomography – carry some especially useful
algorithms aiding in identifying glaucomatous morphology. Thinning of the RNFL in the area
around the optic disc is the foremost sign of glaucoma. Some distinct disc modification s are
observed due to glaucomatous optic atrophy, it is mainly characterized by disc substance loss,
appearing as an enlargement of the optic disc cup, and pallor in the cupping zone. Some
forms of optic atrophy lead to extensive pallor without increased d isc cupping.
– Assessment of the visual field: Visual field examinations are crucial for the diagnosis of
glaucoma and also for follow -up. Visual field loss is not specific from itself as it‟s made up
of nerve fiber bundle defects which can be found in oth er kinds of optic nerve diseases;
what‟s specific and characteristic is the pattern in which this visual field loss happens, the
nature of its progression and above all the correlation between the field loss and optic disc
changes. Reproducible visual field flaw on standard automated perimetry is sufficient to
confirm a suspicion of a glaucomatous optic disc. The defect in the visual field and the area

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which we think is abnormal on the optic disc should correspond with each other. A defect on
„white -on white‟ visual field test is not normally one of the first signs of glaucoma but it is
still a fundamental test in glaucoma diagnosing.
1.1.5 Secondary Open Angle Glaucoma
This type of glaucoma is made of many conditions where the I OP levels increase as a result
to different mechanisms other than the trabecular meshwork primary dysfunction. The cause
of the intra ocular levels incre ase is generally identifiable. In this type of glaucoma the reason
for the intra ocular pressure levels rising can typically be distinguished. The expression
“Glaucoma” can be seen utilized also in cases where we don‟t observe any optic nerve
damage. This glaucoma is typically portrayed by adding the description of the IOP elevation
cause. A more simple cla rification can be that the relations between the structures of the
aqueous flow route – root of the iris, trabecular meshwork, and peripheral cornea – are not
damaged but on the other hand the trabecular meshwork is congested for some reason and the
outflo w and drainage rate is diminished due to increased resistance.

1.1.5.1 Forms of SOAG
I. Exfoliation glaucoma
amorphous acellular material form deposits spread throughout the anterior chamber which
leads to congestion of the trabecular meshwok . In numerous societies exfoliation syndrome is
one of the most frequent causes of SOAG. Signs of exfoliation syndrome are found in over
20% of patients in Iceland and Finland, which accounts for more than half of the glaucoma
patients in the before mentio ned countries, in addition to that, a strong connection with the
exfoliation syndrome can be observed in patients from the more northern populations and it is
especially common in Scandinavian countries. LOXL1 is a gene that has recently been
identified as the responsible for an increased risk of acquiring pseudo -exfoliation glaucoma.
In exfoliation syndrome when inspecting the anterior lens capsule a grayish -white flaky
material is usually found. There is a chance that we also find it on the margin of the pupil,
corneal endothelium, trabecular meshwork, zonular fibers, and ciliary body. It can also be
found on the posterior capsule, intraocular lens , and vi treous face following a cataract
extraction procedure. As a result of this abrasive exfoliation materi al formation on the
anterior lens capsule, some pigment gets released from the posterior iris surface. Some
preipupillary transillumination abnormalities and pigmented ruff loss may be apparent. This
pigment disposition can be observed throughout the anter ior chamber and the iridocorneal
angle. It is believed that the exfoliation materials and the pigment that are on the trabecular
meshwork are the causing source of the elevated IOP levels that‟s related to the exfoliation
syndrome. It is believed that the exfoliation materials and the pigment that are on the
trabecular meshwork are the causing source of the elevated IOP levels that‟s related to the
exfoliation syndrome.
II. Pigmentary glaucoma.
in This form of SOAG pigment granules from the pigmentary e pithelium of the iris are
released and go on to block and congest the trabecular meshwork. It usually affects younger

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males who suffer from myopia.
III. Corticosteroid -Induced G laucoma
Corticosteroid in any shape or form can cause open angle glaucoma de velopment. It has been
proved that the levels of IOP increases in patients who use topical, periocular, inhalational
and systemic steroids also accompanying increased endogenous steroid in adrenal hyperplasia
and Cushing‟s syndrome.
In patients who have used steroids in the past we may observe that they suffered from normal
tension glaucoma as they present with optic nerve damage and defects in the visual field
which may have happened whilst they were using the steroids in the increased IOP levels
period in that time and their IOP levels decreased back to normal values when the use of the
steroids was halted. It was also found that Tropical steroid s affect the levels of the IOP more
than their systemic counterpart . With more powerful steroids and bigger do ses we observe a
stronger and more frequent IOP elevation. Elevated IOPs usually appear after 2 -6 weeks from
the beginning of steroids administration. Primary open angle glaucoma patients manifest a
more frequent and severe IOP elevation as a result of ste roid administration. Another thing
that happens as a result of corticosteroids is that glycosaminoglycans accumulate on and
congest the trabecular meshwork, which leads to lowering the outflow rate. There is more
than one theory to explain why that accumul ation occurs including increased production and
also reduced clearance, either by the means of nuclear steroid receptors or by membrane
stabilization.
IV. Inflammatory glaucoma
intraocular inflammation can cause an elevation in the IOP as it changes the dynamics of the
aqueous humo r. The acute inflammations cause the aqueous secretion to be reduced and at
the same time increase the aqueous outflow rate. These changes lead to lowering the IOP
rather than elevate it, but on the other hand inflammatory mat erial – white blood cells,
macrophages, and proteins – accumulate and congest the trabecular meshwork leading to
lower outflow rate and increase in the IOP values. There are 2 mechanisms that play a role in
elevating the IOP:
A. The aqueous humor viscosity rises due to proteins coming from the vessels of the inflamed
iris.
B. Inflammatory cells and cellular debris accumulate on the trabecular meshwork obstructing
it.
V. Phacolytic glaucoma
Phacolytic Glaucoma is an acute glaucoma associated with mature a nd hyper mature
cataracts. As a result of the cataract, denatured lens proteins travel through the intact lens
capsule heading inside the anterior chamber and is phagocytized . Protein -binding
macrophages and proteins accumulate on the trabecular meshwork and congest it obstructing
the aqueous outflow.
VI. Aphakic and Pseudophakic G laucomas
One of the common issues which may arise after cataract removals is the issue of an elevated
IOP level. Documented cases might differ from each other, based on the siz e and techniques
involved; in extracapsular cataract extraction and phacoemulsification the rate in which we

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observe this IOP elevation is lower than in intracapsular extractions. Varying etiologies may
be responsible for a postoperative elevation in the IOP levels and it‟s better to take them into
consideration by onset time. Many of the materials that get scattered during the operation can
cause an elevation in the IOP values in the first week. In the first two days following removal
of intracapsular cataracts, alphachymotrypsin might often lead to a reduction in the outflow
rate. In the first day after the operation v iscoelastic material that is left can also congest and
obstruct the trabecular meshwork. There is no variation in the incidence rate of the IOP
elevation in any of the viscoelastics as all can present it. During the surgery, careful removal
can help lower the risk of this happening after it. Also Hyphema can case an o bstruction,
reduce the outflow rate and increase the IOP. Other reasons from debris, inflammation, to
trabecular edema can also lead and aid in having a high intraocular pressure after an
operation. The severity and frequence of the acute IOP pressure elev ations post -operations
are raised in case of a pre -existing glaucoma.
VII. Post-Traumatic G laucoma
Nearly every eye trauma leads to glaucoma, while mostly the type of trauma determines the
specific eye injuries. Anterior -to-posterior eye compression a longside secondary equatorial
stretching are often times associated with non -penetrating eye injuries due to blunt trauma.
Sphincter ruptures, iridodialysis, angle recession, cyclodialysis, trabecular dialysis, zonules
disruption and retinal detachment or dialysis are all possible outcomes to the above
mentioned stretching. Disruption of the major arterial circle of the iris and the ciliary body‟s
venous and arterial connections can occur due to injuries in the face of the ciliary body,
which mostly happen between the circular and the longitudinal muscles, these disruptions
may eventually lead to hyphema. The hyphema severity can vary ranging from
microhyphema all the way to total hyphema , with the first requiring a slit lamp microscope to
access the blood presence in the anterior chamber and the latter being when blood fills fully
both the anterior and posterior chambers. After injury, based on the balance of several
factors, IOP may be i ncreased or decreased. The aqueous product ion can be severely
diminished; a separation of the longitudinal ciliary muscle fibers from the scleral spur –
cyclodialysis – can increase the uveoscleral outflow; an inflamed and damaged trabecular
meshwork can g et obstructed by blood. Normally erythrocytes are able to move through the
trabecular meshwork‟s pores, but large amounts of erythrocytes and debris alongside an acute
inflammation and swelling of the trabec ular meshwork can overload its ability to work
properly.
VIII. Ghost Cell Glaucoma
Long term presence of red blood cells in the vitreous leads them to degenerate and form what
is known as ghost cells. These degenerated erythrocytes lost most of their hemoglobin
content. The hemoglobin which exited the erythrocytes and got degenerated, travel and
accumulate on the inner cell walls in form of Heinz bodies. The r esulting spherical cells lack
the ability to pass via the trabecular meshwork in the in tertrabecular spaces due to its lower
flexibility. When co mpared with normal erythrocytes, ghost cells cause the IOP to elevate
easier and quicker. Sequestration of erythrocytes in the vitreous for multiple weeks is needed
to form ghost cells. Regardless of the source of the hemorrhage: Bleeding from diabetic

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neovascularization of the retina, hemorrhage caused by a trauma or a hyphema occurring due
to surgery with spill -over into the vitreous through a compromised vitreous fa ce can lead to
the appearance of secondary glaucoma. The degenerated cells travel throu gh a defect in the
vitreous face – whether it was surgical or traumatic – and enter the anterior chamber, then it
goes on towards the trabecular mes hwork congesting i t and constricting the outflow.

1.1.6 Primary Angle Closure Glaucoma (PACG)
Angle -closure glaucomas represent a complex group of conditions that are characterized by
the iris invasion to the trabecular meshwork which in turn leads to blockage to the aqueous
outflow pathway mechanically, a gradual dysfunction of the trabecular meshwork, synechial
closure, and elevated levels of IOP resulting in optic nerve damage and vision impairment.
One or more of the following can lead to angle closure:
I. Irregularities in the anterior segment structures‟ relative sizes or positions.
II. Irregulari ties in anterior segment structures ‟ absolute sizes or positions.
III. Irregular forces acting on the posterior segment resulting in a change in the anatomy of
the anterior segment .
Primary acute angle closure is characterized by an elevation i n the IOP levels alongside acute
symptoms, while intermittent primary angle closure is accompanied by Intermittent
symptoms. On the other hand chromnic primary angle closure is characterized by a synechial
closure, generally lacking the traditional clinical symptoms, except where extreme GON –
glaucomatous optic neuropathy – manifists .

1.1.6.1 Classification by Anatomic Level
Angle closure glaucoma can be classified into four distinct categories depending on the
anatomic location of the blocks‟ cause, described according to the structure which is causing
the “forces” leading to the block, facilitates understanding of the different mechanisms , and
thus the treatment to each situation is decided logically accordingly . The four categories of
the block, ordered from the anterior most to the posterior:
I. Iris.
II. Ciliary body.
III. Lens.
IV. Posterior to the lens.
Progressing through the levels can mean a more complex treatment path as each of the levels
can also contain elements of any of the prior levels which will need to be treated as well.

1.1.6.2 Epidemiology
One in every one thousand people over 60 years old develops it. When comparing between
the genders, the incidence is triple in females than i t is in males. The Inuit ethnic group is the
most affected, and black people rarely develop it.

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1.1.6.3 Etiology
The most prominent underlying reason behind primary angle closure and angle closure
glaucoma is relative pupil obstruction. The trans -pupillary aqueous flow resistance rises,
accompanied by forward bowing of the peripheral iris and iridotrabecular contact with
occlusion of the anterior chamber angle as a result of an anatomic predisposition.
With age the crystalline lens‟ thickness rises a nd it starts to shift forward which inreases the
iridolenticular contact and also rises the resistance for the aqueous trans -pupillary movement,
these changes are lens -block mechanisms and they can contribute to this phenomenon.
Fast and
The iridal apposi tion to the trabecular meshwork a severe and fast elevation in the IOP levels
in case of an acute angle closure. In comparison, the clinical symptoms are usually more
moderate in intermittent angle closure due to the fact that the iris‟ apposition to the t rabecular
meshwork is brief and terminates spontaneously. Acute angle closure can develop sometimes
and turn into a chronic angle closure if synechial closure persists. Chronic angle closure may
also evolve if the angle closes slowly overtime accompanied b y the development of
peripheral anterior synechiae – PAS (the peripheral iris adheres with structures of the anterior
chamber angle) -. Pupillary block and plateau iris are mechanisms that are thought to play a
role in this form of angle closures.

1.1.6.4 Risk F actors
– Epidemio logical risk factors:
People over 40 years old are at a bigger risk of developing PACG, with a mean age of
diagnosis of ± 60. When comparing between the genders it appears that females have higher
risk than males. PACG is most ab undant in Inuit people, Chinese, South East Asians.
– Anatomical Pupil block mechanism:
The risk of developing PACG increases in p eople who have anatomically narrower angles,
shallow AC, relatively anterior iris -lens diaphragm, large lens (older, cataract), smaller
corneal diameter, short axial length; risk increases with increasing lens thickness to axial
length ratio.
The aqueous flow from the posterior chamber towards the anterior chamber is hindered by
the iris‟ apposition to the lens in pupill ary block, which in turn puts pressure behind the iris,
causing bowing of the peripheral iris anteriorly followed by angle closure.
– Plateau iris mechanism:
A. Plateau iris configuration aids in developing PACG (patients present with relatively
anteri or ciliary body apposing the peripheral iris to the trabeculum; normal depth of the
anterior chamber centrally, but shallow peripherally along with flat iris plane).
B. Mild cases of plateau iris are susceptible to pupil block, a more serious plateau ir is can
lead to developing plateau iris syndrome. In this case, the peripheral iris block the trabeculum
directly. According to this, regardless of the patent PI, angle closure can develop.

1.1.6.5 Clinical Presentation
Patients with acute primary angle closure present with pain in one of the eyes – unilateral –

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and headache, the patients‟ eyes are red, the pupils are lightly dilated and non -reactive, iris
bombé , photophobia, lowered visual acuity and halos, nausea, vomiting, disc edema, and
splinter hem orrhages, some of the patients also present with abdominal cramps and
palpitations.
Patients with primary angle closure usually have symmetric small anterior segments, a
shallower than normal anterior chamber, a short axial length and may have hyperopia to o. A
high suspicion of secondary angle closure presence is associated with the asymmetry of the
anterior chamber depth.
Typically patients who present with intermittent angle closure have recurrent periods of
blurred vision, halos, and light pain caused by the increase in the intraocular pressure. Unlike
acute angle closure, in intermittent angle closure these symptoms resolve spontaneously,
mostly during sleep, which is why they are misdiagnosed sometimes and mistaken for
headaches or migranes. The intra o cular pressure may return to its normal values in between
these recurrent periods. Signs of previous attacks can be present otherwise, including a
permanently fixed, mid -dilated pupil, sector iris atrophy, pigmentary dusting of the corneal
endothelium, anterior subcapsular lens opacities (so -called glaukomflecken), PAS –
Peripheral anterior synechiae -, and the development of GON – glaucomatous optic
neuropathy -.
Chronic angle closure can develop from the intermittent angle closure. It is usually
asymptomat ic. It can cause the levels of the IOP to rise mildly to moderately leading
progressively to glaucomatous optic nerve neuropathy and visual field defects associated with
the GON.

1.1.6.6 Diagnosis
Gonioscopy is typically the test used to check for angl e closures, dynamic Gonioscopy is
recommended as it allows us to differentiate between appositional angle closure and
peripheral synechiae.
In primary angle closure, t hrough Gonioscopy we can identify if there is a narrowing in the
affected eye and the other eye also; a substantial difference in the anterior chambers‟ depth
can be an indicator to secondary angle closure glaucoma.
PAS may be observed using dynamic Gonios copy in chronic angle closures in patients with a
moderate IOP escalations and GON .
Using ultrasound on the anterior segment we may be able to determine if some additional
structural alterations of the peripheral iris or ciliary body are present.
IOP eleva tions are detected by tonometry. In identifying different forms of angle closure and
angle closure glaucoma; Biomicroscopy with careful and detailed examination of the anterior
and posterior chambers is required and mandatory. An inquiry about the prior me dical,
ocular, family history alongside subjective symptoms must be performed in case the patient
has intermittent or acute angle closures as this inquiry aids in confirming prior episodes.
The diseases‟ stage should be also assessed by carrying out a visu al field test, RNFL
evaluation, and optic disc imaging.

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1.1.7 Secondary Angle Closure Glaucoma
All forms of angle -closure glaucoma which develop in the presence of a second ocular
disease are considered secondary angle -closure. They develop in associati on with diseases
such as i ris neovascularization, uveitis, trauma, or lens disease related conditions.

1.1.7.1 Etiology
Mechanisms of angle closure can contain cases where the peripheral iris and the trabecular
meshwork or the peripheral cornea are in a close proximity. Two main mechanisms can cause
this kind of apposition; the anterior mechanism which is the situation in which the peripheral
iris gets pulled into its position and the posterior mec hanism in which the peripheral iris is
pushed rather than pulled. An irregular tissue spans and connects the iridocorneal angle then
it contracts and pulls the peripheral iris with it towards the angle. Posterior mechanism relies
on pressure that is exerted behind the iris, lens or vitreous which can lead t o pushing the iris
towards the iridocorneal angle, this process can happen whether in the presence or the
absence of pupillary block. Fibrovascular membreane, an endothelial layer accompanied by a
Descemet -like membrane, and inflammatory p recipitates are e xamples of the contracting
tissue. The peripapillary iris apposition with the lens causes the resistance of the aqueous
flow towards the anterior chamber to rise, which in turn leads to an elevation in the pressure
inside the posterior chamber and to the p eripheral iris bowing in patients with pupillary block
glaucoma . Genetically based anterior ocular segment configuration is the cause of the
functional apposition in the before mentioned patients. A different reason for this locational
convergence involving the lens and iris is the forward movement of the lens in the
intumescent cataract or subluxated lens for example. In synechia that is related to an
inflammation of the anterior segment of the eye can also lead to a blockage of the pupil. In
the before mentioned cases, elevated levels of pressure in the posterior chamber of the eye
and a forward bowing deformation of the peripheral iris moving it towards the iridocorneal
angle are all a result of an apposition involving the iris and the lens, intr aocular lens, and the
aqueous humour normal flow en route to the anterior chamber being altered and obstructed.
The angle closure posterior mechanism involves the lens-iris or vitreous -iris being driven
forward by an abnormal elevation in t he posterior seg ment of the eye. In malignant (ciliary
block) glaucoma, plateau iris syndrome, intraocular tumors, cysts of the iris and ciliary body,
and contracture of retro -lenticular tissue this phenomenon can be observed.
1.1.7.2 Diagnosis
The ability to differentiat e between the two cases discussed above is very crucial and a
precise cautious clinical test must be performed and must include slit -lamp biomicroscopy,
indirect binocular funduscopy, and an accurate and cautious gonioscopy. Alongside a
thorough history of the patient (particularly in patients who had undergone an intraocular
surgery before) the diagnosis can be evidently clear. In case of a need to perform further tests,
the ophthalmologist can perform the standard A -mode and B -mode ultrasound ecography in
order to be able to eliminate the possibility of a tumor presence and to measure the axial
length and lens thickness. Another test that is available and can be of a significant amount of

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help is the high -resolution ultrasound biomicroscopy (UBM), the UBM can help us in
judging the relationship between the anterior segment structures (the chamber angle, iris,
ciliary body, and lens). The ultrasound biomicroscopy plays a crucial role in differentiating
between primary iris en plateau syndrome and secondary a ngle closure due to iris ciliary
body cysts. On the basis of the findings further tests should be also performed (i.e., specular
microscopy in patients with presumed I CE syndrome) .
1.2 Optical Coherence Tomography – OCT
1.2.1 Definition
Optical coherence tomography is a technology of imaging the interior microstructure of
biological tissues , based on the principle of optical reflectometry, which uses echoes of
backscattered light in order to provide and create high resolution, cross sectional, an d three
dimensional volumetric imaging. The imaging process can be done in situ and in real time,
delivering images with resolutions of 1–15 mm, one to two orders of magnitude finer than
conventional ultrasound. OCT can be seen used in a varying multitude of clinical specialties
and also in essential fundamental sci entific and biological research. OCT works by measuring
the intensity and echo time delay of light waves that are sent to and scattered from the tissues
we are investigating. A source of broadban d light emits light waves which are further divided
into two arms, one is a reference arm and the other is a sample arm, which is in turn reflected
back of structures found at diversified depths within the posterior ocular pole.
The light that is scattered back can be detected by a couple of ways:
I. Time domain (TD) detection
II. Fourier domain (FD) detection – which contains in itself two main aspects:
A. Spectral domain (SD)
B. Swept Source (SS)
1.2.2 Time Domain OCT
Time domain optical coherence tomography scans work by reading, processing and
combining numerous „A-scans‟. The A -scans are obtained through emitting light from the
reference arm towards the tissue where it gets reflected back and undergoes interference; over
a perio d of time this interference is then utilized to create an A-scan. The subject tissue is
then moved and the process is rep eated in order to create more A -scans which finally get
combined together creating a cross sectional linear image known as a linear sca n or simply,
B-scan. Time domains OCT scanning speed is composed of the number of A -scans created
every second, which is approximately 400 scans per second.
1.2.3 Spectral Domain OCT
In this type of OCT an array detector is used in order to collect simu ltaneously the spectral
interference pattern involving the reference and sample beams which got dispersed by a
spectrometer. After gathering the simultaneous data, an inverse Fourier transform is put in
motion in granting us with an A scan. Much more rapid scanning speeds averaging from
18,000 A scans per second and reaching up to 70,000 A scans per second are made available

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by the spectral domain OCT devices on the market as a result of this simultaneous
information acquisition compared to the speeds we we re getting from the more conventional
time domain optical coherence tomography instruments which averaged at 400 A scans per
second and used an interferometer that must be moved mechanically in order to acquire the
necessary data required over time. One of the enemies and challenges of OCT imaging eye
movement during the process especially in patients with inadequate ability to control or fixate
the eye, this problem is minimized in spectral domain OCT thanks to the fast acqui sition
speeds . These speeds also ensure a better quality results with a significant upgrade in
resolution, a higher sampling density of the macula, improving the chances of finding
pathologies if present, the capability of producing three dimensional OCT s cans. Hardware
and software enhancements are available and are capable of permitting an accurate
registration of the acquired image s which in turn leads a boost in the reliability of the
comparison between results from different visits. Commercially availa ble spectral domain
OCT devices are enjoys broader light sources that aid in acquiring images with a notable
axial resolution elevation leading to a superior visualization of the retinal anatomy.
1.2.4 Swept Source OCT
This type of OCT works by reading over a period of time the acquired spectral interference
patterns detected by a few receivers. The spectral interference patterns are the result of light
emitted from a light source that is being rapidly swept in wavelength – hence the name swept
source -. An A -scan is then generated by performing a reverse Fourier Transform to the
information acquired in the previously mentioned process. Here we can also observe the
advantages of the fast scanning speeds, denser sampling and better registration. Other
bene fits of the swept source OCT are that it is less prone to roll -off with depth, which assures
a more fine end result and an improved visualization of the retina and deep structures.
1.2.5 Interpretation
Interpreting the OCT results (final B -scans) can be achieved via multiple different methods.
False -colour B -scans tend to display tissues with higher reflecting ability as reddish white
and the tissues with less reflecting ability appear more as a bluish black in colour. Another
way to interpret the result s is displaying it as an image with 256 shades of grey, structures
will assigned a corresponding shade of grey depending on its optical reflectivities. Identifying
the structures on the result B -scan can be done using the previous two methods as different
structures have different optical reflectivities with the inner, outer nuclear layers and ganglion
cell layer being typically hyporeflective and the inner, outer plexiform layers and the nerve
fibre layer being hyperreflective. Circular hyperreflective foc i accompanied with underlying
„shadowing‟ appearing in the inner retina on the OCT represent the larger retinal vessels.
Multiple hyperreflective bands can also sometimes be seen in the outer retina, usually they
contain the external limiting membrane, the ellipsoid zone – which represents the the
photoreceptor inner segment – outer segment junction area -, and the retinal pigment
epithelium. The choroid and the CSJ (choroid -sclera junction) can also be seen and evaluated
but specialized scanning protocols are needed in order to achieve that. Special circular OCT

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scanning protocols are performed in case of a patient presenti ng with glaucoma, these
protocols provide a single circular B -scan, centered on the optic disc and measuring 3.4mm in
diameter. Evaluation of the peripapillary retinal nerve fiber layer can be done by
segmentation of the inner and outer boundaries of the r etinal nerve fiber layer. By comparing
the results to normative databases we can then determine if a glaucomatous thinning of the
retinal nerve fiber layer exists or not.

Source: Figure 2.3 Oxford Handbook of Ophthalmology 3rd edition – Page 73

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Vaughan & Asbury‟s General Ophthalmology -McGraw -Hill (2017) – Paul
Riordan -Eva, James J. Augsburger – Pages 526, 527, 528, 529 .
1.1.5 Ophth almology – Gerhard K. Lang, M. D. – Page 271 .
Atlas of Glaucoma Third Edition – Edited by Neil T. Choplin Carlo E. Traverso
– Page 127 .
1.1.5.1 Ophthalmology – Gerhard K. Lang, M. D. – Page 271 .
Atlas of Glaucoma Third Edition – Edited by Neil T. Choplin Carlo E. Traverso
– Page s 128-130, 1 32, 133, 135 , 136 .

1.1.6 Atlas of Glaucoma Third Edition – Edited by Neil T. Choplin Carlo E. Traverso –
Page 143 .
1.1.6.1 Atlas of Glaucoma Third Edition – Edited by Neil T. Choplin Carlo E. Traverso
– Page 143 .
1.1.6.2 Ophthalmology – Gerhard K. Lang, M. D. – Page 265
1.1.6.3 Enclopedia of Ophthalmology – Ursula Schmidt -Erfurth & Thomas Kohnen –
Page 1435 .
1.1.6.4 Oxfor d Handbook of Ophthalmology 3rd edition – Page 358
1.1.6.5 Enclopedia of Ophthalmology – Ursula Schmidt -Erfurth & Thomas Kohnen –
Page s 1435 & 1436 .
1.1.6.6 En clopedia of Ophthalmology – Ursula Schmidt -Erfurth & Thomas Kohnen –
Page 1436 .
1.1.7 En clopedia of Ophthalmology – Ursula Schmidt -Erfurth & Thomas Kohnen –
Page 1611 & 1612 .
1.1.7.1 Enclopedia of Ophthalmology – Ursula Schmidt -Erfurth & Thomas Kohnen –
Page 1612 .
1.2
1.2.1 Optical Coherence Tomography: Technology and Applications – Wolfgang
Drexler & James G. Fujimoto – Page 3.
Handbook of Retinal OCT – Jay S. Duker, Nadia K. Waheed, Darin R. Goldman –
Page 2
1.2.2 Handbook of Retinal OCT – Jay S. Duker, Nadia K. Waheed, Darin R. Goldman
– Page 2
1.2.3 Handbook of Retinal OCT – Jay S. Duker, Nadia K. Waheed, Darin R. Goldman
– Page 2
1.2.4 Handbook of Retinal OCT – Jay S. Duker, Nadia K. Waheed, Darin R. Goldman
– Page 3
1.2.5 Oxfor d Handbook of Ophthalmology 3rd edition – Pages 72 & 73.