Prevalence and treatment pattern of Glaucoma

A Project on
Prevalence and treatment pattern of Glaucoma
B. PHARM THESIS
(A dissertation submitted to the Department of Pharmacy)
It has being submitted for partial fulfillment of the requirements for the degree of
B.Pharm (Honors) in Southeast University, Banani, Dhaka.
Submitted by:
ID: 2015000300008
Batch: Spring 2018
Department of Pharmacy
Southeast University

APPROVAL
The project paper, entitled “Prevalence and treatment pattern of Glaucoma” submitted by
ID: 2015000300008, summer 2018, Department of Pharmacy, Southeast University, has been
accepted as satisfactory for the partial fulfillment of the requirement for the degree of B.
Pharm. (Honors.) and approved as to its style and contents.
………………………………
Abdullah Al Hasan
(Supervisor)
Department of Pharmacy
Southeast University

ABSTRACT
Aim: Aim of the study was to estimate prevalence of diagnosis & treatment pattern of
glaucoma disease in Dhaka city with the determination of related factors affecting this
condition in different aspects.
Study design: A questionnaire survey was done among 100 Glaucoma patients across three
study centers in Dhaka city.
Place & duration of study:
The cross sectional study was conducted in three hospitals in Dhaka city. On around 100
patients from Dhaka medical college hospital, Ispahani Islamia Eye Institute and Hospital and
BIRDEM General Hospital from March to December 2018.
Methodology:
A cross-sectional, cluster-sample survey was carried out in randomly selected rural and urban
populations across Dhaka city. Patients who were admitted in that hospital and non-
hospitalized were interviewed through a well designed questionnaire form and data were
collected from them. From the collected data the prevalence and treatment pattern of the
Glaucoma disease were studied in selected area in Dhaka city.
Result:
Among a total of 100 surveyed patients had Glaucoma were diagnosed by the trained
research team doctors. The sensitivity and specificity of the disease was diagnoses made by
local hospital. The most number of patients suffered from Halos around lights (75%), sudden
onset of visual disturbance (74%).Other studied symptoms were Gradual loss of peripheral
vision, Tunnel vision, severe eye pain, Nausea and vomiting, Blurred vision & Reddening of
the eye. The majority of patients were affected with age range above 48 years (35%) and least
number was between 30-35 years (15%). The rate of the main modalities drug used for the
management of this disease was as follows: highest prescribed drug was Hyperosmotic agents
(72%) and least prescribed drug was Prostaglandin analogues (32%). Data was analyzed by
using Microsoft Excel. A graphical presentation of the data was developed on the basis of
different perspective of collected information.
Conclusion:
The Glaucoma is still in high mark in Bangladesh and the risk was assessed at several
multilevel factors. Therefore, prevention of glaucoma disease should be given top priority as
a major public health intervention and awareness should be developed in the patients about
the episode, diagnostic protocol & medication prospectus of this disease.

TABLE OF CONTENTS
2 Literature Review 26-40
Chapter-01: Introduction
Si.no. Topic Page
no.
1 Introduction 1
1.2 Signs & Symptoms 2-3
1.3 Causes of glaucoma 3-5
1.4 Dietary of glaucoma 5-7
1.5 Ethnicity 7
1.6 Genetics 7-8
1.7 Pathophysiology 8
1.8 Diagnosis 9-11
1.9 Glaucoma has been classified into specific types 11-13
1.10 Types of Glaucoma 13-15
1.11 Other Types of Glaucoma 15-17
1.12 Disease 17-18
1.13 Risk Factors 18
1.14 Epidemiology 19
1.15 Glaucoma Screening 19-20
1.16 Treatment 20-25
Chapter-02: Literature Review

3 Purpose of the study 41
4 Methods 42-47
5.1.1 PERSONAL HISTORY 48-49
5.1.2 BIOPHYSICAL CHARACTERISTICS 50
5.1.3 INVESTIGATION OF GLAUCOMA PATIENTS 51-56
6 Discussion 57
7 Conclusion 58
6 References 59-65
Chapter-03: Purpose of the study
Chapter-04: Materials & Methods
Chapter-05: Results
Chapter-06: Discussion
Chapter-07: Conclusion
Chapter-08: References

Chapter-1 Introduction
1 Prevalence and treatment pattern of Glaucoma
1.1 Introduction:
Glaucoma is a group of eye diseases which result in damage to the optic nerve and vision
loss. The most common type is open-angle glaucoma with less common types including
closed-angle glaucoma and normal-tension glaucoma. Open-angle glaucoma develops slowly
over time and there is no pain. Peripheral vision may begin to decrease followed by central
vision resulting in blindness if not treated. Closed-angle glaucoma can present gradually or
suddenly. The sudden presentation may involve severe eye pain, blurred vision, mid-dilated
pupil, redness of the eye, and nausea. Vision loss from glaucoma, once it has occurred, is
permanent.
Risk factors for glaucoma include increased pressure in the eye, a family history of the
condition, and high blood pressure. For eye pressures a value of greater than 21 mmHg or 2.8
kPa is often used with higher pressures leading to a greater risk. However, some may have
high eye pressure for years and never develop damage. Conversely, optic nerve damage may
occur with normal pressure, known as normal-tension glaucoma. The mechanism of open-
angle glaucoma is believed to be slow exit of aqueous humor through the trabecular
meshwork while in closed-angle glaucoma the iris blocks the trabecular meshwork. Diagnosis
is by a dilated eye examination. Often the optic nerve shows an abnormal amount of cupping.
Figure 1.1: This figure show the glaucoma
If treated early it is possible to slow or stop the progression of disease with medication, laser
treatment, or surgery. The goal of these treatments is to decrease eye pressure. A number of
different classes of glaucoma medication are available. Laser treatments may be effective in

both open-angle and closed-angle glaucoma. A number of types of glaucoma surgeries may
be used in people who do not respond sufficiently to other measures. Treatment of closed-
angle glaucoma is a medical emergency.
About 6 to 67 million people have glaucoma globally. The disease affects about 2 million
people in the United States. It occurs more commonly among older people. Closed-angle
glaucoma is more common in women. Glaucoma has been called the "silent thief of sight"
because the loss of vision usually occurs slowly over a long period of time. Worldwide,
glaucoma is the second-leading cause of blindness after cataracts. The word "glaucoma" is
from Ancient Greek glaukos which means blue, green, or gray. In English, the word was used
as early as 1587 but did not become commonly used until after 1850, when the development
of the ophthalmoscope allowed people to see the optic nerve damage.
1.2 Signs & Symptoms
The most common types of glaucoma—open-angle and angle-closure—have completely
different symptoms.
1.2.1 Symptoms of Open-Angle Glaucoma
Most people who develop open-angle glaucoma don’t experience any noticeable symptoms at
first. That’s why it’s critical to have regular eye exams, so that your eye doctor can detect
problems early on.
Symptoms of open-angle glaucoma are:
Gradual loss of peripheral vision, usually in both eyes
Tunnel vision in the advanced stages
See how the progression of glaucoma may affect your vision.
1.2.2 Symptoms of Acute Angle-Closure Glaucoma
Acute angle-closure glaucoma is a medical emergency and must be treated immediately or
blindness could result in one or two days.
Acute angle-closure glaucoma signs and symptoms include:
Severe eye pain

Nausea and vomiting (accompanying the severe eye pain)
Sudden onset of visual disturbance, often in low light
Blurred vision
Halos around lights
Reddening of the eye
1.2.3 Symptoms of Chronic Angle-Closure Glaucoma
This type of glaucoma progresses more slowly and can damage the optic nerve without
symptoms, similar to open-angle glaucoma.
Similarly, people with normal-tension glaucoma will not experience any symptoms until they
begin to lose peripheral vision.
1.3Causes of glaucoma
Elevated pressure in the eye is the main factor leading to glaucomatous damage to the eye
(optic) nerve. Glaucoma with normal intraocular pressure is discussed below in the section on
the different types of glaucoma. The optic nerve, which is located in back of the eye, is the
main visual nerve for the eye. This nerve transmits the images we see back to the brain for
interpretation. The eye is firm and round, like a basketball. Its tone and shape are maintained
by a pressure within the eye (the intraocular pressure), which normally ranges between 8
millimeters (mm) and 22 mm of mercury. When the pressure is too low, the eye becomes
softer, while an elevated pressure causes the eye to become harder. The optic nerve is the
most susceptible part of the eye to high pressure because the delicate fibers in this nerve are
easily damaged either by direct pressure on the nerve or decreased blood flow to the nerve.
The front of the eye is filled with a clear fluid called the aqueous humor, which provides
nourishment to the structures in the front of the eye. This fluid is produced constantly by the
ciliary body, which surrounds the lens of the eye. The aqueous humor then flows through the
pupil and leaves the eye through tiny drainage channels called the trabecular meshwork.
These channels are located at what is called the drainage angle of the eye. This angle is where
the clear cornea, which covers the front of the eye, attaches to the base (root or periphery) of

the iris, which is the colored part of the eye. The cornea covers the iris and the pupil, which
are in front of the lens. The pupil is the small, round, black-appearing opening in the center of
the iris. Light passes through the pupil, on through the lens, and to the retina at the back of
the eye. Please see the figure, which is a diagram that shows the drainage angle of the eye.
Figure 1.3: This diagram of the front part of the eye is in cross section to show the filtering,
or drainage, angle. This angle is between the cornea and the iris, which join each other right
where the drainage channels (trabecular meshwork) are located. The arrow shows the flow of
the aqueous fluid from the ciliary body, through the pupil, and into the drainage channels.
This figure is recreated from Understanding and Treating Glaucoma, a book by Tim Peters
and Company Inc., Gladstone N.J.
In most people, the drainage angles are wide open, but in some individuals, they can be
narrow. For example, the usual angle is about 45 degrees, whereas a narrow angle is about 25
degrees or less. After exiting through the trabecular meshwork in the drainage angle, the
aqueous fluid then drains into tiny blood vessels (capillaries) into the main bloodstream. The
aqueous humor should not be confused with tears, which are produced by the lacrimal glands
under the upper eyelid outside of the eyeball itself.

This process of producing and removing the fluid from the eye is similar to that of a sink with
the faucet always turned on, producing and draining the water. If the sink's drain becomes
clogged, the water may overflow. If this sink were a closed system, as is the eye, and unable
to overflow, the pressure within the sink would rise. Likewise, if the eye's trabecular
meshwork becomes clogged or blocked, the intraocular pressure may become elevated. Also,
if the sink's faucet is on too high, the water may overflow. Again, if this sink were a closed
system, the pressure within the sink would increase. Likewise, if too much fluid is being
produced within the eye, the intraocular pressure may become too high. In either event, since
the eye is a closed system, if it cannot adequately remove the increased fluid, the pressure
builds up and optic-nerve damage may result.
1.4 Dietary of glaucoma
Many people often wonder whether there are any diet or lifestyle changes they can make in
order to take better care of themselves and their glaucoma. This article explores the current
research concerning caffeine, alcohol, antioxidants, supplements, and more.
It is important to note that, at this juncture, the only proven method to treat glaucoma is to
lower eye pressure. Also, when considering the population-based studies mentioned below
that have examined the question of diet and glaucoma, they are primarily addressing whether
dietary factors play a role in the development and diagnosis of glaucoma, and not whether
they can help slow the progression of the disease.
1.4.1 Caffeine and Alcohol
An often asked question is whether caffeine affects eye pressure and glaucoma. It is known
that caffeine can cause a several point rise in eye pressure that lasts for at least 90 minutes.
However, whether that increase is of concern is best addressed between the patient and their
eye doctor. A good rule of thumb is to exercise moderation with caffeine consumption. One
cup of coffee is unlikely to cause any harm, but if you like to drink large amounts of coffee
consider switching some of that consumption to decaffeinate. With regard to alcohol
consumption, it is known that alcohol can lower eye pressure in the very short term, but there
is no data to suggest that drinking alcohol reduces the risk of developing glaucoma or
prevents its progression. As with almost everything, moderation is a good idea.

1.4.2 Antioxidants
As oxidative stress is thought to be an important feature of glaucoma, there have been several
studies examining the relationship between antioxidant intake and glaucoma. In one
prospective study,* no relationship was found between antioxidant intake, such as
carotenoids, vitamin C, vitamin E, and the risk of developing glaucoma. However, there are
other large studies that have shown a possible relationship between the consumption of foods
rich in antioxidants, such as green leafy vegetables like kale and collards, and decreased
glaucoma risk. In African-American women, there was a decreased risk of glaucoma with
higher intake of certain fruits and vegetables high in vitamin A, vitamin C, and carotenoids. It
has certainly been shown that increased consumption of fruits and vegetables and a heart-
healthy diet will help decrease risk of heart disease and diabetes, and this is what I often
recommend to my patients who ask about diet and glaucoma. More research needs to be
done, however, to determine specific recommendations about antioxidants and glaucoma
progression.
1.4.3 Dietary Nitrates (Green Leafy Vegetables)
Intake of dietary nitrates, derived mainly from green leafy vegetables, was associated with a
20 to 30 percent lower risk of primary open-angle glaucoma in two large studies examining
the relationship between nutrition among other factors and various chronic diseases in men
and women (the Nurses’ Health Study and the Health Professionals Follow-up Study).
Interestingly, in patients with early visual field loss that was close to the central vision, the
association was even stronger (40 to 50 percent lower risk). Again, it is important to note that
this association was examining the risk of glaucoma diagnosis, not progression or worsening
of existing glaucoma. Nevertheless, the advice to eat green leafy vegetables is probably a
good one!
1.4.4 Omega Fatty Acids
A recently published prospective study found that a diet with a high omega 3:6 ratio intake,
and thus low in omega 6, was associated with a higher risk of glaucoma. However, more
studies are needed in order to determine whether recommending a diet with a lower omega
3:6 ratio is justified, especially since both omega-3 fatty acids and omega-6 fatty acids are
important for heart health and other diseases. Omega-3 fatty acids are typically found in
vegetable oils, green vegetables such as kale, and fatty fish such as salmon. Omega-6 fatty

acids are found in many types of vegetable oils and can help lower LDL cholesterol. Thus, at
this juncture, it would not be recommended to modify your omega-3 and omega-6
consumption since both have been shown to be associated with many health benefits.
1.4.5 Supplements
Another common question is whether there are any supplements that can be taken to reduce
the risk of glaucoma or to treat glaucoma. Currently, there is no convincing data that
supplementation can help in preventing or treating glaucoma. Due to the fact that
supplements are made by many different suppliers and there is no legal or regulatory
standardization in the United States, and that they can be expensive, I usually advise patients
not to take additional “eye” supplements other than a standard multivitamin, which was
demonstrated by a randomized controlled trial.
Please note that there is a specific supplement intervention, however, that could delay and
possibly prevent intermediate age-related macular degeneration from progressing to the
advanced stage. It is very important to ask your ophthalmologist if this supplement would be
beneficial to you if you have macular degeneration.
1.5 Ethnicity
Many people of East Asian descent are prone to developing angle closure glaucoma due to
shallower anterior chamber depths, with the majority of cases of glaucoma in this population
consisting of some form of angle closure. Other Asians such as South Asians are also prone
to developing angle closure glaucoma. Higher rates of glaucoma have also been reported for
Inuit populations, compared to white populations, in Canada and Greenland
1.6 Genetics
Positive family history is a risk factor for glaucoma. The relative risk of having primary
open-angle glaucoma (P.O.A.G.) is increased about two- to four-fold for people who have a
sibling with glaucoma. Glaucoma, particularly primary open-angle glaucoma, is associated
with mutations in several genes, including MYOC, ASB10, WDR36, NTF4, TBK1, and
RPGRIP1, although most cases of glaucoma do not involve these genetic mutations. Normal-
tension glaucoma, which comprises one-third of POAG, is also associated with genetic
mutations (including OPA1 and OPTN genes).

Various rare congenital/genetic eye malformations are associated with glaucoma.
Occasionally, failure of the normal third-trimester gestational atrophy of the hyaloid canal
and the tunica vasculosa lentis is associated with other anomalies. Angle closure-induced
ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies,
and has been modelled in mice.
1.7 Pathophysiology
The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its
exact etiology. However, the major risk factor for most glaucomas and the focus of treatment
is increased intraocular pressure. Intraocular pressure is a function of production of liquid
aqueous humor by the ciliary processes of the eye, and its drainage through the trabecular
meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber,
bounded posteriorly by the lens and the zonules of Zinn, and anteriorly by the iris. It then
flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris
and anteriorly by the cornea. From here, the trabecular meshwork drains aqueous humor via
the scleral venous sinus (Schlemm's canal) into scleral plexuses and general blood
circulation.
In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork, due to the
degeneration and obstruction of the trabecular meshwork, whose original function is to
absorb the aqueous humor. Loss of aqueous humor absorption leads to increased resistance
and thus a chronic, painless buildup of pressure in the eye.
In close/narrow-angle, the iridocorneal angle is completely closed because of forward
displacement of the final roll and root of the iris against the cornea, resulting in the inability
of the aqueous fluid to flow from the posterior to the anterior chamber and then out of the
trabecular network. This accumulation of aqueous humor causes an acute increase in pressure
and pain.
The inconsistent relationship of glaucomatous optic neuropathy with increased intraocular
pressure has provoked hypotheses and studies on anatomic structure, eye development, nerve
compression trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor,
retinal ganglion cell/axon degeneration, glial support cell, immune system, aging mechanisms
of neuron loss, and severing of the nerve fibers at the scleral edge

1.8 Diagnosis
Screening for glaucoma is usually performed as part of a standard eye examination performed
by optometrists and ophthalmologists. Testing for glaucoma should include measurements of
the intraocular pressure via tonometry, anterior chamber angle examination or gonioscopy,
and examination of the optic nerve to look for any visible damage to it, or change in the cup-
to-disc ratio and also rim appearance and vascular change. A formal visual field test should
be performed. The retinal nerve fiber layer can be assessed with imaging techniques such as
optical coherence tomography, scanning laser polarimetry, and/or scanning laser
ophthalmoscopy (Heidelberg retinal tomogram).
Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as
Goldmann tonometry should be augmented with pachymetry to measure the central corneal
thickness (CCT). A thicker-than-average cornea can result in a pressure reading higher than
the 'true' pressure whereas a thinner-than-average cornea can produce a pressure reading
lower than the 'true' pressure.
Because pressure measurement error can be caused by more than just CCT (i.e., corneal
hydration, elastic properties, etc.), it is impossible to 'adjust' pressure measurements based
only on CCT measurements. The frequency doubling illusion can also be used to detect
glaucoma with the use of a frequency doubling technology perimeter.
Examination for glaucoma also could be assessed with more attention given to sex, race,
history of drug use, refraction, inheritance and family history
Your eye doctor has a variety of diagnostic tools which aid in determining whether or not you
have glaucoma -- even before you have any symptoms. Let us explore these tools and what
they do.
1.8.1 The Tonometer
The tonometer measures the pressure in your eye. Your doctor places a numbing eye drop in
your eye. Then you sit at a slit-lamp, resting your chin and forehead on a support that keeps
your head steady. The lamp, which lets your doctor see a magnified view of your eye, is
moved forward until the tonometer, a plastic prism, barely touches the cornea to measure
your IOP. The test is quick, easy and painless

1.8.2Ophthalmoscopy
Using an instrument called an ophthalmoscope, your eye doctor can look directly through the
pupil at the optic nerve. Its color and appearance can indicate whether or not damage from
glaucoma is present and how extensive it is. This technique remains the most important in
diagnosing and monitoring glaucoma
1.8.3 Perimetry (visual field test)
Perimetry is a visual field test that produces a map of your complete field of vision. This test
will help a doctor determine whether your vision has been affected by glaucoma. During this
test, you will be asked to look straight ahead and then indicate when a moving light passes
your peripheral (or side) vision. This helps draw a "map" of your vision.
Do not be concerned if there is a delay in seeing the light as it moves in or around your blind
spot. This is perfectly normal and does not necessarily mean that your field of vision is
damaged. Try to relax and respond as accurately as possible during the test.
Your doctor may want you to repeat the test to see if the results are the same the next time
you take it. After glaucoma has been diagnosed, visual field tests are usually done one to two
times a year to check for any changes in your vision.
1.8.4 Gonioscopy
Your doctor may perform a gonioscopy to closely examine the trabecular meshwork and the
angle where fluid drains out of the eye. After dilating and numbing the eye with anesthetic
drops, the doctor places a special type of hand-held contact lens, with mirrors inside, on the
eye. The mirrors enable the doctor to view the interior of the eye from different directions. In
this procedure, the doctor can determine whether the angle is open or narrow. Individuals
with narrow angles have an increased risk for a sudeen closure of the angle, which can cause
an acute glaucoma attack. Gonioscopy can also determine if anything, such as abnormal
blood vessels or excessive pigment, might be blocking the drainage of the aqueous humor out
of the eye.

1.8.5 The Pachymeter
The pachymeter measures central corneal thickness (CCT). Like the tonometer, your doctor
will first anesthetize your eyes. Then a small probe will be placed perpendicular to the central
cornea.
CCT is an important measure and helps your doctor interpret your IOP levels. Some people
with thin central corneal thickness will have pressures that are actually higher than when
measured by tonometry. Likewise, those with thick CCT will have a true IOP that is lower
than that measured. Measuring your central corneal thickness is also important since recent
studies have found that thin CCT is a strong predictor of developing glaucoma in patients
with high IOP.
1.8.6 Optic nerve assessment
The optic nerve, which connects your eye to your brain, can become damaged in glaucoma,
so an assessment may be carried out to see if it's healthy.
For the test, eye drops will be used to enlarge your pupils. Your eyes are then examined using
either:
a slit lamp (a microscope with a bright light)
optical coherence tomography – a type of scan where special rays of light are used to scan the
back of your eye and produce an image of it
The eye drops used to widen your pupils could temporarily affect your ability to drive, so
you'll need to make arrangements for getting home after your appointment.
1.9 Glaucoma has been classified into specific types
1.9.1 Primary glaucoma and its variants
Primary glaucoma
Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple
glaucoma, glaucoma simplex
High-tension glaucoma

Low-tension glaucoma
Primary angle closure glaucoma, also known as primary closed-angle glaucoma, narrow-
angle glaucoma, pupil-block glaucoma, acute congestive glaucoma
Acute angle closure glaucoma (aka AACG)
Chronic angle closure glaucoma
Intermittent angle closure glaucoma
Superimposed on chronic open-angle closure glaucoma ("combined mechanism" –
uncommon)
Variants of primary glaucoma
Pigmentary glaucoma
Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare
Primary juvenile glaucoma
1.9.2 Primary angle closure glaucoma is caused by contact between the iris and trabecular
meshwork, which in turn obstructs outflow of the aqueous humor from the eye. This contact
between iris and trabecular meshwork (TM) may gradually damage the function of the
meshwork until it fails to keep pace with aqueous production, and the pressure rises. In over
half of all cases, prolonged contact between iris and TM causes the formation of synechiae
(effectively "scars").
These cause permanent obstruction of aqueous outflow. In some cases, pressure may rapidly
build up in the eye, causing pain and redness (symptomatic or so-called "acute" angle
closure). In this situation, the vision may become blurred, and halos may be seen around
bright lights. Accompanying symptoms may include a headache and vomiting.
Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to
light, cornea edematous (cloudy), reduced vision, redness, and pain. However, the majority of
cases are asymptomatic. Prior to the very severe loss of vision, these cases can only be
identified by examination, generally by an eye care professional.

Once any symptoms have been controlled, the first line (and often definitive) treatment is
laser iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some
cases by conventional incisional surgery. The goal of treatment is to reverse and prevent,
contact between the iris and trabecular meshwork. In early to moderately advanced cases,
iridotomy is successful in opening the angle in around 75% of cases. In the other 25%, laser
iridoplasty, medication (pilocarpine) or incisional surgery may be required.
1.9.3 Primary open-angle glaucoma is when optic nerve damage results in a progressive
loss of the visual field. This is associated with increased pressure in the eye. Not all people
with primary open-angle glaucoma have eye pressure that is elevated beyond normal, but
decreasing the eye pressure further has been shown to stop progression even in these cases.
The increased pressure is caused by trabecular meshwork blockage. Because the microscopic
passageways are blocked, the pressure builds up in the eye and causes imperceptible very
gradual vision loss. Peripheral vision is affected first, but eventually the entire vision will be
lost if not treated.
Diagnosis is made by looking for cupping of the optic nerve. Prostaglandin agonists work by
opening uveoscleral passageways. Beta-blockers, such as timolol, work by decreasing
aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from
ciliary processes in the eye, thus decreasing the formation of Aqueous humor.
Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the
passageway and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both
decrease fluid production (via. inhibition of AC) and increase drainage.
1.10 Types of Glaucoma
There are several types of glaucoma. The two main types are open-angle and angle-closure.
These are marked by an increase of intraocular pressure (IOP), or pressure inside the eye.
1.10.1Open-Angle Glaucoma
Open-angle glaucoma, the most common form of glaucoma, accounting for at least 90% of
all glaucoma cases:
Is caused by the slow clogging of the drainage canals, resulting in increased eye pressure

Has a wide and open angle between the iris and cornea
Develops slowly and is a lifelong condition
Figure 1.10.1: This figure show the open angle glaucoma
Has symptoms and damage that are not noticed.
“Open-angle” means that the angle where the iris meets the cornea is as wide and open as it
should be. Open-angle glaucoma is also called primary or chronic glaucoma. It is the most
common type of glaucoma, affecting about three million Americans.
1.10.2 Angle-Closure Glaucoma
Angle-closure glaucoma, a less common form of glaucoma:
Figure 1.10.2: This figure show the angle-closure glaucoma

Is caused by blocked drainage canals, resulting in a sudden rise in intraocular pressure
Has a closed or narrow angle between the iris and cornea
Develops very quickly
Has symptoms and damage that are usually very noticeable
Demand immediate medical attention.
It is also called acute glaucoma or narrow-angle glaucoma. Unlike open-angle glaucoma,
angle-closure glaucoma is a result of the angle between the iris and cornea closing.
1.10.3 Normal-Tension Glaucoma (NTG)
It is also called low-tension or normal-pressure glaucoma. In normal-tension glaucoma the
optic nerve is damaged even though the eye pressure is not very high. We still don't know
why some people’s optic nerves are damaged even though they have almost normal pressure
levels.
1.10.4 Congenital Glaucoma
This type of glaucoma occurs in babies when there is incorrect or incomplete development of
the eye's drainage canals during the prenatal period. This is a rare condition that may be
inherited. When uncomplicated, microsurgery can often correct the structural defects. Other
cases are treated with medication and surgery.
1.11Other Types of Glaucoma
Most other types of glaucoma are variations of open-angle or angle-closure types. These
types can occur in one or both of your eyes.
1.11.1Secondary Glaucoma
Secondary glaucoma refers to any case in which another disease causes or contributes to
increased eye pressure, resulting in optic nerve damage and vision loss.
Secondary glaucoma can occur as the result of an eye injury, inflammation, tumor, or in
advanced cases of cataract or diabetes. It can also be caused by certain drugs such as steroids.

This form of glaucoma may be mild or severe. The type of treatment will depend on whether
it is open-angle or angle-closure glaucoma.
1.11.2 Pigmentary Glaucoma
Pigmentary Glaucoma is a form of secondary open-angle glaucoma. It occurs when the
pigment granules that are in the back of the iris (the colored part of the eye) break into the
clear fluid produced inside the eye. These tiny pigment granules flow toward the drainage
canals in the eye and slowly clog them. This causes eye pressure to rise. Treatment usually
includes medications, laser surgery, or conventional surgery.
1.11.3Pseudoexfoliative Glaucoma
This form of secondary open-angle glaucoma occurs when a flaky, dandruff-like material
peels off the outer layer of the lens within the eye. The material collects in the angle between
the cornea and iris and can clog the drainage system of the eye, causing eye pressure to rise.
Pseudoexfoliative Glaucoma is common in those of Scandinavian descent. Treatment usually
includes medications or surgery.
1.11.4 Traumatic Glaucoma
Injury to the eye may cause secondary open-angle glaucoma. Traumatic glaucoma can occur
immediately after the injury or years later. It can be caused by blunt injuries that bruise the
eye (called blunt trauma) or by injuries that penetrate the eye.
In addition, conditions such as severe nearsightedness, previous injury, infection, or prior
surgery may make the eye more vulnerable to a serious eye injury.
1.11.5 Neovascular Glaucoma
The abnormal formation of new blood vessels on the iris and over the eye's drainage channels
can cause a form of secondary open-angle glaucoma.
Neovascular glaucoma is always associated with other abnormalities, most often diabetes. It
never occurs on its own. The new blood vessels block the eye's fluid from exiting through the
trabecular meshwork (the eye's drainage canals), causing an increase in eye pressure. This
type of glaucoma is very difficult to treat.

1.11.6 Irido Corneal Endothelial Syndrome (ICE)
This rare form of glaucoma usually appears in only one eye, rather than both. Cells on the
back surface of the cornea spread over the eye's drainage tissue and across the surface of the
iris, increasing eye pressure and damaging the optic nerve. These corneal cells also form
adhesions that bind the iris to the cornea, further blocking the drainage channels.
Irido Corneal Endothelial Syndrome occurs more frequently in light-skinned females.
Symptoms can include hazy vision upon awakening and the appearance of halos around
lights. Treatment can include medications and filtering surgery. Laser therapy is not effective
in these cases.
1.11.7 Congenital Glaucoma (Childhood Glaucoma)
Childhood Glaucoma refers to the presence of glaucoma in a child, and occurs in 1 out of
every 10,000 births in the United States. Congenital glaucoma is the common term used for a
glaucoma diagnosed in infancy or early childhood.
This glaucoma is caused by abnormal intraocular fluid drainage from the eye as a result of a
blocked or defective trabecular meshwork (the mesh-like drainage canals in the eye).
Congenital glaucoma may be due to an hereditary defect or abnormal development during
pregnancy.
In other cases, an abnormal drainage system may be the result of some other disease in the
eye which results in secondary glaucoma. In these cases, the glaucoma may be associated
with recognizable iris (the colored part of the eye), corneal, or other eye problems.
In an uncomplicated case of congenital glaucoma, microsurgery can often correct the
structural defects. Other cases are treated with medication and surgery.
1.12 Disease
Glaucoma is the most common optic neuropathy in the adulthood. Glaucoma is defined as an
optic neuropathy associated in most cases with elevated intraocular pressure (although
pressure may be within the normal range), with or without anatomic predisposing factors in
the anterior chamber (open angle vs angle closure). The American Academy of
Ophthalmology has defined Glaucoma as " a multifactorial optic neuropathy with a

characteristic acquired loss of optic nerve fibers" which is usually (but not necessarily)
identified in visual field exam and retinal fiber OCT. This cluster of diseases is progressive
without appropriate treatment, and unfortunately the damage is irreversible. Primary Open
Angle Glaucoma is the most common form of this cluster of diseases and so is the main focus
of this article.
1.13 Risk Factors
Glaucoma is a multifactorial disease and there are several risk factors that are associated with
the development of this entity.
1.13.1 Age: age by itself is a risk factor. In the Baltimore Eye Studi, patients in their 70s had
x 3.5 times the risk for developing glaucoma than those patients in their 40's
1.13.2 Race: Black individuals have 3-4 times more risk than whites to develop glaucoma;
and hispanics have 1-2 times more risk than whites to develop glaucoma. The cause of this
race variation is unknown.
1.13.3 Intraocular Pressure (IOP): Increased intraocular pressure is a risk factor for the
development of glaucoma. It should be taken into account that the IOP has a diurnal
variation, and so even if one measurement is within the normal range, high peaks of IOP may
still be present causing optic nerve damage. And so it is recommended that the time of IOP
measurement be recorded along with IOP. Most subjects have a peak of IOP during the night
(because of the body position)
1.13.4 Family History: people with first degree relatives with glaucoma are at higher risk for
developing glaucoma
1.13.5 Corneal thickness: patients with thinner corneas have a greater risk for developing
the disease (besides the influence on the IOP measurement). It has been thought that thinner
corneas may be related to increased biomechanical susceptibility of the lamina cribrosa and
peripapillary sclera.
Myopia and Diabetes Mellitus: they are thought to be related but no hard evidences exists yet
to show a relation.

1.14 Epidemiology
The estimated prevalence of Primary Open Angle Glaucoma in patients older than 40 years of
age is 1.86%, which means that almost 2.22 million Americans are diagnosed with this
disease. The fact that the data takes into account patients with the diagnosis (with visual field
loss and other factors), this number probably underestimates the real prevalence due to the
fact that does not contemplate the complete spectrum of the disease.
It is a potentially blinding disease, considered the most frequent cause of non-reversible
blindness in blacks in the US. It estimated that it is the third leading cause of blindness
worldwide (following cataract and river blindness)
1.15 Glaucoma Screening
There has been emphasis on glaucoma screening, since most of the times there is an insidious
start of the disease (with no clear start point, POAG), and progression may be slow and
unnoticed to the patient. In addition to that, there is a recognized stage of the disease in which
patients are apparently in a pre-perimetric (before loss of the visual field is present) stage,
bringing a challenge to the diagnosis and screening techniques.
The purpose of glaucoma screening tests is to detect those with early stage disease, so that
these patients can be treated to reduce the risk of visual field loss.
For patients with pre-perimetric glaucoma, screening tests are limited to the evaluation of the
optic nerve and the NFL. Optic nerve and retinal nerve fiber layer imaging is used to find
anatomic alterations. Probably one of the imaging systems most commonly used is the OCT
of the optic nerve; the new spectral domain OCT has been used to screen for loss of the
retinal fiber layer in glaucoma. However clinical evaluation is paramount, the increase in
vertical cup/disc ratio, the appearance of cup notching or hemorrhages in the disc are taken as
a positive screening for glaucoma. It is recommended that stereoscopic pictures of the optic
nerve be taken with some regularity, and is considered as the most sensitive early detection
method. Caution must be taken due to the fact that there is certain variability between
observers, and to the fact that there is no gold standard unique test for the diagnosis of
glaucoma, but rather a set of factors that all together lead to the diagnosis.

The recommendation for screening is complex, and several issues should be taken into
account. Every patient during a regular ophthalmologic visit is checked for visual acuity,
intraocular pressure and cup/disc ratio as part of the optic nerve assessment. If any of those
key points raises suspicion such as decreased visual acuity (with no other apparent cause),
high or borderline intraocular pressure, or a characteristic glaucomatous vertical optic nerve
excavation or disc hemorrhages studies are ordered for a more detailed evaluation of the optic
nerve fibers and visual function.
The usual studies that are taken are corneal pachymetry, optic nerve head OCT and a 24:2
visual field. The OCT and visual field are helpful not only to screen or diagnose glaucoma,
but to have a starting point to compare the patient through a time lapse. Care must be taken
however for the interpretation of the studies, since they are not absolute values or diagnostic
tools; especially the visual field, where it may take a patient several times to perform
correctly on the exam.
The rate of progression through a time lapse should also be registered since it fundamental
for diagnostic and treatment decisions.
There are several countries that are pioneering in the field of ophthalmologic telemedicine.
Perhaps in the near future patients that are seen in the ER or in another branch of medicine
could be taken IOP with an "easy to use" tonometer (Tonopen or icare ) and have a fundus
photograph taken and sent to an ophthalmologist, for screening and early referral if needed.
1.16 Treatment
The modern goals of glaucoma management are to avoid glaucomatous damage and nerve
damage, and preserve visual field and total quality of life for patients, with minimal side-
effects. This requires appropriate diagnostic techniques and follow-up examinations, and
judicious selection of treatments for the individual patient. Although intraocular pressure
(IOP) is only one of the major risk factors for glaucoma, lowering it via various
pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment.
A review of people with primary open-angle glaucoma and ocular hypertension concluded
that medical IOP lowering treatment slowed down the progression of visual field loss.
Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have
prompted studies on various neuroprotective therapeutic strategies, including nutritional

compounds, some of which may be regarded by clinicians as safe for use now, while others
are on trial.
1.16.1 Medication
Intraocular pressure can be lowered with medication, usually eye drops. Several classes of
medications are used to treat glaucoma, with several medications in each class.
Each of these medicines may have local and systemic side effects. Adherence to medication
protocol can be confusing and expensive; if side effects occur, the patient must be willing
either to tolerate them or to communicate with the treating physician to improve the drug
regimen. Initially, glaucoma drops may reasonably be started in either one or in both eyes.
Wiping the eye with an absorbent pad after the administration of eye drops may result in
fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid.
Poor compliance with medications and follow-up visits is a major reason for vision loss in
glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their
prescriptions the first time, and one-fourth failed to refill their prescriptions a second time.
Patient education and communication must be ongoing to sustain successful treatment plans
for this lifelong disease with no early symptoms.
The possible neuroprotective effects of various topical and systemic medications are also
being investigated.
Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral
outflow of aqueous humor. Bimatoprost also increases trabecular outflow.
Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol,
decrease aqueous humor production by the epithelium of the ciliary body.
Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual
mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.
Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production
through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma.
Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due
to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork,
which is responsible for absorption of aqueous humor).

Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the
ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the
aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic
glaucoma.
Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower
secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.
1.16.2 Laser
Argon laser trabeculoplasty (ALT) may be used to treat open-angle glaucoma, but this is a
temporary solution, not a cure. A 50-μm argon laser spot is aimed at the trabecular meshwork
to stimulate the opening of the mesh to allow more outflow of aqueous fluid. Usually, half of
the angle is treated at a time. Traditional laser trabeculoplasty uses a thermal argon laser in an
argon laser trabeculoplasty procedure.
A newer type of laser trabeculoplasty uses a "cold" (nonthermal) laser to stimulate drainage
in the trabecular meshwork. This newer procedure, selective laser trabeculoplasty (SLT), uses
a 532-nm, frequency-doubled, Q-switched Nd:YAG laser, which selectively targets melanin
pigment in the trabecular meshwork cells. Studies show SLT is as effective as ALT at
lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT
can usually be repeated only once.
Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected
by angle closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser
energy is used to make a small, full-thickness opening in the iris to equalize the pressure
between the front and back of the iris, thus correcting any abnormal bulging of the iris. In
people with narrow angles, this can uncover the trabecular meshwork. In some cases of
intermittent or short-term angle closure, this may lower the eye pressure. Laser iridotomy
reduces the risk of developing an attack of acute angle closure. In most cases, it also reduces
the risk of developing chronic angle closure or of adhesions of the iris to the trabecular
meshwork.
Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory
ciliary epithelium

1.16.3 Surgery
Both laser and conventional surgeries are performed to treat glaucoma. Surgery is the primary
therapy for those with congenital glaucoma. Generally, these operations are a temporary
solution, as there is not yet a cure for glaucoma.
1.16.4 Canaloplasty
Canaloplasty is a nonpenetrating procedure using microcatheter technology. To perform a
canaloplasty, an incision is made into the eye to gain access to the Schlemm's canal in a
similar fashion to a viscocanalostomy. A microcatheter will circumnavigate the canal around
the iris, enlarging the main drainage channel and its smaller collector channels through the
injection of a sterile, gel-like material called viscoelastic. The catheter is then removed and a
suture is placed within the canal and tightened.
By opening the canal, the pressure inside the eye may be relieved, although the reason is
unclear, since the canal (of Schlemm) does not have any significant fluid resistance in
glaucoma or healthy eyes. Long-term results are not available.
1.16.5 Trabeculectomy
The most common conventional surgery performed for glaucoma is the trabeculectomy.
Here, a partial thickness flap is made in the scleral wall of the eye, and a window opening is
made under the flap to remove a portion of the trabecular meshwork. The scleral flap is then
sutured loosely back in place to allow fluid to flow out of the eye through this opening,
resulting in lowered intraocular pressure and the formation of a bleb or fluid bubble on the
surface of the eye.
Scarring can occur around or over the flap opening, causing it to become less effective or lose
effectiveness altogether. Traditionally, chemotherapeutic adjuvants, such as mitomycin C
(MMC) or 5-fluorouracil (5-FU), are applied with soaked sponges on the wound bed to
prevent filtering blebs from scarring by inhibiting fibroblast proliferation. Contemporary
alternatives to prevent the scarring of the meshwork opening include the sole or combinative
implementation of nonchemotherapeutic adjuvants such as the ologen collagen matrix, which
has been clinically shown to increase the success rates of surgical treatment.

1.16.6 Glaucoma drainage implants
Professor Anthony Molteno developed the first glaucoma drainage implant, in Cape Town in
1966. Since then, several types of implants have followed on from the original, the Baerveldt
tube shunt, or the valved implants, such as the Ahmed glaucoma valve implant or the ExPress
Mini Shunt and the later generation pressure ridge Molteno implants. These are indicated for
glaucoma patients not responding to maximal medical therapy, with previous failed guarded
filtering surgery (trabeculectomy). The flow tube is inserted into the anterior chamber of the
eye, and the plate is implanted underneath the conjunctiva to allow a flow of aqueous fluid
out of the eye into a chamber called a bleb.
The first-generation Molteno and other nonvalved implants sometimes require the ligation of
the tube until the bleb formed is mildly fibrosed and water-tight.This is done to reduce
postoperative hypotony—sudden drops in postoperative intraocular pressure.
Valved implants, such as the Ahmed glaucoma valve, attempt to control postoperative
hypotony by using a mechanical valve.
Ab interno implants, such as the Xen Gel Stent, are transscleral implants by an ab interno
procedure to channel aqueous humor into the non-dissected Tenon's space, creating a
subconjunctival drainage area similar to a bleb. The implants are transscleral and different
from more other ab interno implants that do not create a transscleral drainage, such as iStent,
CyPass, or Hydrus.
The ongoing scarring over the conjunctival dissipation segment of the shunt may become too
thick for the aqueous humor to filter through. This may require preventive measures using
antifibrotic medications, such as 5-fluorouracil or mitomycin-C (during the procedure), or
other nonantifibrotic medication methods, such as collagen matrix implant,or biodegradable
spacer, or later on create a necessity for revision surgery with the sole or combinative use of
donor patch grafts or collagen matrix implant.And for glaucomatous painful blind eye and
some cases of glaucoma, cyclocryotherapy for ciliary body ablation could be considered to be
performed.
1.16.7 Laser-assisted nonpenetrating deep sclerectomy
The most common surgical approach currently used for the treatment of glaucoma is
trabeculectomy, in which the sclera is punctured to alleviate intraocular pressure.

Nonpenetrating deep sclerectomy (NPDS) surgery is a similar, but modified, procedure, in
which instead of puncturing the scleral bed and trabecular meshwork under a scleral flap, a
second deep scleral flap is created, excised, with further procedures of deroofing the
Schlemm's canal, upon which, percolation of liquid from the inner eye is achieved and thus
alleviating intraocular pressure, without penetrating the eye. NPDS is demonstrated to have
significantly fewer side effects than trabeculectomy. However, NPDS is performed manually
and requires higher level of skills that may be assisted with instruments.[citation needed] In
order to prevent wound adhesion after deep scleral excision and to maintain good filtering
results, NPDS as with other non-penetrating procedures is sometimes performed with a
variety of biocompatible spacer or devices, such as the Aquaflow collagen wick, ologen
Collagen Matrix, or Xenoplast glaucoma implant.
Laser-assisted NPDS is performed with the use of a CO2 laser system. The laser-based
system is self-terminating once the required scleral thickness and adequate drainage of the
intraocular fluid have been achieved. This self-regulation effect is achieved as the CO2 laser
essentially stops ablating as soon as it comes in contact with the intraocular percolated liquid,
which occurs as soon as the laser reaches the optimal residual intact layer thickness.

Chapter-2 Literature
Review
Literature Review
2.1 Loss of foxc1 in zebrafish reduces optic nerve size and cell number in the ganglion
cell layer.
Umali J et al. has found study that, Mutation of FOXC1 causes Axenfeld-Rieger Syndrome
(ARS) with early onset or congenital glaucoma. They assessed retinal ganglion cell (RGC)
number in zebrafish due to CRISPR-mediated mutation and antisense inhibition of two-
forkhead box transcription factors, foxc1a and foxc1b. These genes represent duplicated
homologues of human FOXC1. Using a CRISPR induced null mutation in foxc1b, in
combination with antisense inhibition of foxc1a, they demonstrate reduced cell number in the
retinal ganglion cell layer of developing zebrafish eyes. As early as 5 days post fertilization
(dpf), fewer RGCs are found in foxc1b homozygous mutants injected with foxc1a
morpholinos, and a thinner optic nerve results. their data illustrates that foxc1 is required for
the expression of atonal homolog 7 (atoh7), a gene that is necessary for RGC differentiation.
As markers of differentiated RGCs (pou4f2) are downregulated in foxc1b-/- mutants injected
with foxc1a morpholinos and no cell death is observed, their results are consistent with
defects in the differentiation of RGCs leading to reduced cell number, as opposed to
increased cell death of RGCs or off targets effects of morpholino injection. their zebrafish
model demonstrates that aberrant regulation of RGC number could act in concert with other
known glaucoma risk factors to influence the development of congenital and early onset
glaucoma due to FOXC1 mutation.
2.2 Meibomian glands dysfunction and ocular surface in black people
J Fr Ophtalmol et al. has found study that, Meibomian gland dysfunction is the leading cause
of evaporative-type dry eye syndrome. their goal was to determine the epidemiological and
clinical features of meibomian gland dysfunction as well as its impact on the ocular surface in
elderly black patients in Cameroon. They performed a cross-sectional analysis from January
2 through May 31, 2017 in the ophthalmology department of Laquintinie Hospital in Douala,
including blacks aged 50 years and older. The examination focused on the Meibomian
glands, Tear film Break Up Time and Schirmer I test for qualitative and quantitative
assessment of tears. The relationship between the quantitative and qualitative variables and
meibomian gland dysfunction was determined by linear regression tests. They enrolled 340
elderly black patients. The mean age was 62±9 years. The prevalence of meibomian gland

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dysfunction was 71.8 % and did not increase with age. The hypoproductive clinical form was
the most frequent (47.9 %). The prevalence of asymptomatic Meibomian gland dysfunction
was 19.7 %. Evaporative dry eye disease was the most frequent (34.7 %). Aside from
advanced age, Meibomian gland dysfunction was associated with high blood pressure
(P=0.020), cataract surgery (P=0.034), long-term glaucoma medication (P=0.041) and
alcohol consumption (P=0.043).Meibomian gland dysfunction is very common in elderly
black patients in Cameroon.
2.3 XEN® Gel Stent for management of chronic open angle glaucoma: A review of the
literature.
Buffault J et al. has found study that, The purpose of this study was to analyze the change in
intraocular pressure (IOP) and glaucoma medications using the XEN®
Gel Stent as a solo
procedure or in association with phacoemulsification in patients with chronic open angle
glaucoma (OAG).We included cohort studies with at least one year of follow-up in patients
with primary open angle glaucoma (POAG), pseudo-exfoliative glaucoma (PXG) or
pigmentary glaucoma (PG) who received a XEN®
gel stent. The main outcome measure was
IOP reduction at 12 months follow-up. Secondary outcomes were the decrease in glaucoma
medications 12 months after surgery, frequency and type of postoperative interventions and
complication rate.A total of 8 case series published between 2016 and 2018 were included;
six were prospective studies, and two were retrospective. There was no randomized
controlled trial. The data concerned a total of 958 eyes of 777 patients. The various studies
showed a mean IOP at 12 months between 13 and 16mmHg, which represented an IOP
reduction between 25 and 56% (mean: 42%). This decrease was associated with a reduction
in glaucoma medications in all studies. The decrease in IOP was significantly greater in
XEN®
implantation as a stand-alone procedure (44%) than in combined surgery (32%)
(P<0.05). Transient hypotony (< 1 month) (3%), choroidal detachment or choroidal folds
(1.5%), hyphema (1.9%), bleb leak (1.1%) and shallow anterior chamber (1.1%) were the
most frequent complications. As for severe complications, four cases of malignant glaucoma
(0.4%) and one case of retinal detachment have been reported. In the follow-up period,
needling has been required in 32% of cases, and a total of 55 eyes (5.7%) required repeat
filtering surgery or cyclodestructive procedure.XEN®
Gel Stent appears effective for
reducing IOP and the number of medications in OAG patients within 1 year postoperatively

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with an acceptable safety profile. However, vigilant postoperative follow-up and frequent
postoperative maneuvers are required.
2.4 An Artificial Intelligence Approach to Detect Visual Field Progression in Glaucoma
Based on Spatial Pattern Analysis.
Wang M et al. has found study that, they selected 12,217 eyes from 7360 patients with at
least five reliable 24-2 VFs and 5 years of follow-up with an interval of at least 6 months.
VFs were decomposed into 16 archetype patterns previously derived by artificial intelligence
techniques. Linear regressions were applied to the 16 archetype weights of VF series over
time. They defined progression as the decrease rate of the normal archetype or any increase
rate of the 15 VF defect archetypes to be outside normal limits. The archetype method was
compared with mean deviation (MD) slope, Advanced Glaucoma Intervention Study (AGIS)
scoring, Collaborative Initial Glaucoma Treatment Study (CIGTS) scoring, and the
permutation of pointwise linear regression (PoPLR), and was validated by a subset of VFs
assessed by three glaucoma specialists.In the method development cohort of 11,817 eyes, the
archetype method agreed more with MD slope (kappa: 0.37) and PoPLR (0.33) than AGIS
(0.12) and CIGTS (0.22). The most frequently progressed patterns included decreased normal
pattern (63.7%), and increased nasal steps (16.4%), altitudinal loss (15.9%), superior-
peripheral defect (12.1%), paracentral/central defects (10.5%), and near total loss (10.4%). In
the clinical validation cohort of 397 eyes with 27.5% of confirmed progression, the
agreement (kappa) and accuracy (mean of hit rate and correct rejection rate) of the archetype
method (0.51 and 0.77) significantly (P < 0.001 for all) outperformed AGIS (0.06 and 0.52),
CIGTS (0.24 and 0.59), MD slope (0.21 and 0.59), and PoPLR (0.26 and 0.60).The archetype
method can inform clinicians of VF progression patterns.
2.5 Protective effects of hypercapnic acidosis on Ischemia-reperfusion-induced retinal
injury.
Lin LT et al. have found study that,Ischemia-reperfusion (I/R) injury is associated with
numerous retinal diseases, such as diabetic retinopathy, acute glaucoma, and other vascular
retinopathies. Hypercapnic acidosis (HCA) has a protective effect on lung, myocardial, and
central nervous system ischemic injury models. However, no study has evaluated its
protective effects in an experimental retinal I/R injury model. In this study, retinal I/R injury
was induced in Sprague Dawley rats by elevating the intraocular pressure to 110 mmHg for

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60 minutes. HCA was induced before and after the injury. After 24 hours, the terminal dUTP
nick end labeling assay was performed. Moreover, the ratios of cleaved caspase-3/total
caspase-3, phosphorylated IκB/IκB, and phosphorylated p38 were measured through Western
blotting. After 7 days, the rats' aqueous humor was analyzed. In addition, electroretinography
and retinal thickness measurement were performed in the rats. Moreover, the retinal neural
cell line RGC-5 was exposed to 500 μM H2O2 for 24 hours to induce a sustained oxidative
stress in vitro. The effects of HCA were evaluated by comparing oxidative stress, MAPK
signals, NF-κB signals, survival rates, and apoptosis rates in the RGC-5 cells before and after
H2O2 exposure. They further investigated whether the potent I/R-protective heat shock
protein (HSP) 32 contribute to protective effects of HCA. Their results indicated that HCA
has protective effects against retinal I/R injury both in vivo and in vitro, at multiple levels,
including antiapoptotic, anti-inflammatory, antioxidative, and functional retinal cell
protection. Further research clarifying the role of HCA in retinal I/R injury prevention and
treatment is warranted.
2.6 Changes in glaucoma medication numbers after cataract and glaucoma surgery: A
nationwide population-based study.
Chen HY et al. have found study that, To determine whether cataract or glaucoma and
combined cataract and glaucoma surgery (CGS) affect glaucoma medication usage.We
recruited patients who received new diagnoses of glaucoma, either primary open-angle
glaucoma (POAG) (International Classification of Diseases, Ninth Revision, Clinical
Modification [ICD-9-CM] code 365.1) or primary angle-closure glaucoma (PACG) (ICD-9-
CM code 365.2), between 1998 and 2011 and had undergone cataract surgery alone (CS),
glaucoma surgery alone (GS), or CGS under the National Health Insurance program in
Taiwan. CS, GS, and CGS in all the patients were performed after the glaucoma diagnosis
date. The patients were subdivided into CS, CGS, and GS groups. The number of glaucoma
medications, including prostaglandin analogs, β-blockers, carbonic anhydrase inhibitors, α-
agonists, pilocarpine, and a combination of drugs, in each prescription, were compared before
and after surgery.The mean number of glaucoma medications in each prescription before the
surgery increased from approximately 0.5/1 (CS/CGS + GS) to a peak of 1.75/3 within 3
months before the index date. The mean number of glaucoma medications in each
prescription reduced to 0 (CS group) and to approximately 0.5 (CGS and GS) at the end of
the 3-year follow-up period. The mean number of glaucoma medications in each prescription

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significantly reduced at the time points within 6 months, between 6 months and 2 years, and
during 2 to 3 years after surgery in each group. At the end of the 3-year period, the reduction
effect was most evident in the CS group. Similar trends were also observed in the POAG and
PACG group.CS, GS, and CGS significantly reduced the number of glaucoma medications
used by the glaucoma patients.
2.7 Comparing the long-term impact on health care resources utilization and costs due
to various single-piece acrylic monofocal intraocular lens implantation during cataract
surgery: a cost-consequence analysis for the United Kingdom, Italy, and Denmark.
Dhariwal M et al. have found study that, The objective of this study was to estimate the cost
impact of neodymium-doped yttrium aluminum garnet (Nd:YAG) laser capsulotomy and its
complications due to single-piece acrylic monofocal intraocular lenses (IOLs) in the
healthcare setting of United Kingdom, Italy, and Denmark.A hypothetical cost-consequence
model was developed to estimate economic burden of Nd:YAG laser capsulotomy due to
different single-piece acrylic monofocal IOLs. Cumulative incidence of Nd:YAG laser
capsulotomy at 3 years after cataract surgery with five single-piece monofocal acrylic IOLs
was sourced from retrospective data analysis of electronic medical records of cataract patients
in the United Kingdom. Risk probability of post-Nd:YAG laser complications, ie, retinal
detachment, glaucoma, and cystoid macular edema at 3 years was derived using published
literature. Unit costs were taken from publicly available sources with all costs converted to
euro (€). Number of cataract procedures per year for each country was sourced from Eurostat
statistics.For the estimated cataract procedures carried out nationally every year, single-piece
monofocal hydrophobic AcrySof IOL was associated with substantially lower cases of
Nd:YAG laser capsulotomy procedures and subsequent complications in 3 years after
cataract surgery when compared to other single-piece monofocal acrylic IOLs. The total cost
savings with the use of AcrySof over other IOLs in countries assessed ranged from €0.5 to
€4.7 million (vs AMO Tecnis) and €2.1 to €17.9 million (vs Rayner C-/Super-flex).Incidence
of Nd:YAG capsulotomy due to the choice of IOL could significantly affect healthcare
budgets in the post-cataract surgery period. Our analysis indicates that single-piece
monofocal AcrySof IOLs is the most cost-saving treatment option for health care systems
when compared to other acrylic single-piece IOLs.

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2.8 Risk assessment of sudden visual loss following non-penetrating deep sclerectomy in
severe and end-stage glaucoma.
Leleu I et al. have found study that, To assess the risk of immediate sudden visual loss
("wipe-out" phenomenon) following non-penetrating deep sclerectomy (NPDS) for end-
stages glaucoma within the first 6-months postoperative period.Monocenter database study.
We reviewed the results for 73 eyes with severe or end-stage glaucoma that underwent
NPDS. End-stage glaucoma (stage 5) was defined by the inability of patients to perform the
Humphrey visual field test or by a visual acuity <20/200 due to glaucoma, according to the
Glaucoma Staging System classification. Severe glaucoma (stage 4) was defined by a mean
deviation (MD) <-20 dB by the preoperative 24-2 Humphrey visual field assessment. All eyes
had a severe defect on the central 10° visual field: only a central island of vision remained.
"Wipe-out" was defined as the permanent postoperative reduction of visual acuity to <20/200
or to "counting fingers" or less if preoperative visual acuity was <20/200.The mean age was
60 years (range 22-86). Before surgery, the average MD (Humphrey 24-2) was -
25.6 ± 3.8 dB, the MD (Humphrey 10-2) -19.9 ± 7.0 dB, and the VFI 24.6 ± 13%. There were
no cases of postoperative flat anterior chamber. No patients experienced "wipe-out" within
the first 6 months following surgery. At the six-month visit, intraocular pressure (IOP) had
decreased significantly from 22.0 ± 8.8 to 13.5 ± 4.5 mmHg (P<0.001). There were no
significant changes in mean visual acuity after 6 months (P = 6).In our study, NPDS provided
considerable IOP decrease with no occurrences of "wipe-out" and few other complications.
Consideration of NPDS in end-stage and severe glaucoma is advisable given its low risk of
intraoperative and postoperative complications and the low risk of wipe out. This surgery
should probably be offered with less apprehension about the risk of "wipe-out" in end-stages
glaucoma.
2.9 Relationship between macular vessel density and central visual field sensitivity at
different glaucoma stages.
Shin JW et al. have found study that, To evaluate the relationship between macular vessel
density (mVD) and central visual field sensitivity (cVFS) at different stages of glaucoma and
to compare this relationship with that between the thickness of the macular ganglion cell-
inner plexiform layer (mGCIPLT) and cVFS.The mVD and mGCIPLT were measured by
optical coherence tomography angiography in 139 patients with glaucoma. The cVFS was

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defined as the average of 12 central points on 24-2 visual field (VF) testing. Vasculature-
function and structure-function relationships were analysed by comparing mVD and
mGCIPLT with cVFS in eyes with early and moderate-to-advanced glaucoma.Global and
regional mVD-cVFS associations were statistically significant in eyes with moderate-to-
advanced (all p<0.05), but not early stage (all p>0.05) glaucoma. The global association
between average mVD and cVFS was significantly stronger than that between average
mGCIPLT and cVFS in eyes with moderate-to-advanced glaucoma (p=0.049). Reduced mVD
was independently associated with cVFS loss after adjusting for age and mGCIPLT in eyes
with moderate-to-advanced glaucoma.The macular vasculature-function relationship using
mVD was stronger than the structure-function relationship using mGCIPLT in eyes with
moderate-to-advanced glaucoma. The mVD may be useful in monitoring cVFS in advanced
glaucoma.
2.10 The effects of corneal cross-linking on intraocular pressure measurement in
keratoconus
Badri S et al. have found study that, Cross-linking (CXL) is a technique whose design aims to
achieve a specific goal: to harden the corneal tissue of eyes with a progressive form of
keratoconus. Other indications are being investigated, such as treatment of infectious keratitis
and prevention of corneal ectasia post corneal ablative refractive surgery. Hardening the
cornea means changing its biomechanical properties. The existence of true corneal hardening
after CXL would inevitably result in an increase in measured intraocular pressure (IOP). This
would have a considerable impact in the screening and follow-up of glaucoma patients who
have undergone cross-linking because of the central role of IOP measurement in
glaucomatous pathology.
2.11 Substances of Interest That Support Glaucoma Therapy.
Saccà SC et al. have found study that, Glaucoma is a multifactorial disease in which pro-
apoptotic signals are directed to retinal ganglion cells. During this disease the conventional
outflow pathway becomes malfunctioning. Aqueous humour builds up in the anterior
chamber, leading to increased intraocular pressure. Both of these events are related to
functional impairment. The knowledge of molecular mechanisms allows us to better
understand the usefulness of substances that can support anti-glaucoma therapy. The goal of
glaucoma therapy is not simply to lower intraocular pressure; it should also be to facilitate the

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survival of retinal ganglion cells, as these constitute the real target tissue in this disease, in
which the visual pathway is progressively compromised. Indeed, an endothelial dysfunction
syndrome affecting the endothelial cells of the trabecular meshwork occurs in both normal-
tension glaucoma and high-tension glaucoma. Some substances, such as polyunsaturated fatty
acids, can counteract the damage due to the molecular mechanisms - whether ischemic,
oxidative, inflammatory or other - that underlie the pathogenesis of glaucoma. In this review,
we consider some molecules, such as polyphenols, that can contribute, not only theoretically,
to neuroprotection but which are also able to counteract the metabolic pathways that lead to
glaucomatous damage. Ginkgo biloba extract, for instance, improves the blood supply to
peripheral districts, including the optic nerve and retina and exerts a neuro-protective action
by inhibiting apoptosis. Polyunsaturated fatty acids can protect the endothelium and
polyphenols exert an anti-inflammatory action through the down-regulation of cytokines such
as TNF-α and IL-6. All these substances can aid anti-glaucoma therapy by providing
metabolic support for the cells involved in glaucomatous injury. Indeed, it is known that the
food we eat is able to change our gene expression.
2.12 Carbonic Anhydrase Inhibitors of Different Structures Dilate Pre-Contracted
Porcine Retinal Arteries.
Eysteinsson T Carbonic anhydrase inhibitors (CAIs), such as dorzolamide (DZA), are used as
anti-glaucoma drugs to lower intraocular pressure, but it has been found that some of these
drugs act as vasodilators of retinal arteries. The exact mechanism behind the vasodilatory
effect is not yet clear. Here they have addressed the issue by using small vessel myography to
examine the effect of CAIs of the sulfonamide and coumarin type on the wall tension in
isolated segments of porcine retinal arteries. Vessels were pre-contracted by the prostaglandin
analog U-46619, and CAIs with varying affinity for five different carbonic anhydrase (CA)
isoenzymes found in human tissue tested. They found that all compounds tested cause a
vasodilation of pre-contracted retinal arteries, but with varying efficacy, as indicated by the
calculated mean EC50 of each compound, ranging from 4.12 µM to 0.86 mM. All compounds
had a lower mean EC50 compared to DZA. The dilation induced by benzolamide (BZA) and
DZA was additive, suggesting that they may act on separate mechanisms. No clear pattern in
efficacy and affinity for CA isoenzymes could be discerned from the results, although
Compound 5, with a low affinity for all isoenzymes except the human (h) CA isoform IV,
had the greatest potency, with the lowest EC50 and inducing the most rapid and profound

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dilation of the vessels. The results suggest that more than one isozyme of CA is involved in
mediating its role in controlling vascular tone in retinal arteries, with a probable crucial role
played by the membrane-bound isoform CA IV.
2.13 Orthostatic blood pressure variability is associated with lower visual contrast
sensitivity function: Findings from the Irish Longitudinal Study on Aging.
Bhuachalla BN et al. found IN study that, Hypertension is established to cause vascular end-
organ damage. Other forms of dysregulated blood pressure (BP) behaviour, such as
orthostatic hypotension have also been associated with cardiovascular (CV) events. The eye
is potentially vulnerable to dysregulated systemic BP if ocular circulation autoregulation is
impaired. they investigated whether phenotypes of abnormal BP stabilisation after
orthostasis, an autonomic stressor, had a relationship with contrast sensitivity (CS), an
outcome measure of subtle psychophysical visual function.This was a cross-sectional study
from wave 1 of The Irish Longitudinal Study on Ageing (TILDA). From beat-to-beat
orthostatic BP (BP), measured by digital photoplethysmography during active stand, 4
phenotypes have been defined 1) normal stabilisation 2) orthostatic hypotension, 3)
orthostatic hypertension 4) BP variability. Contrast sensitivity was measured using a
Functional Visual Analyzer. Multivariable linear regression models investigated the
relationship between orthostatic BP phenotypes and contrast sensitivity in 4289 adults aged
≥50 years adjusting for, demographics, cardiovascular risk factors, self-reported eye
pathologies, objective hypertension and antihypertensives. A sensitivity analysis adjusted for
age-related macular degeneration, glaucoma, diabetic retinopathy and maculopathy identified
on retinal photographs. Finally models were compared, adjusting for alternative measures of
cataract versus not, to examine the potential effect of cataract on any associations.Systolic
orthostatic BP variability was associated with worse contrast sensitivity, in the primary and
the sensitivity analysis. Adjusting for alternative measures of clinical cataract attenuated the
association by 18%.Orthostatic BP variability is associated with worse contrast sensitivity,
independent of hypertension and retinal pathology and may be a cardiovascular biomarker of
early ocular pathology.

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2.14 Potential Biomarkers for Primary Open-Angle Glaucoma Identified by Long
Noncoding RNA Profiling in the Aqueous Humor.
Xie L et al. found IN study that, This study aimed to identify potential biomarkers for
primary open-angle glaucoma (POAG) diagnosis. First, lncRNA and message RNA (mRNA)
expression profiles in the aqueous humor (AH) from 10 POAG and 10 control patients were
accessed by microarray analyses. Moreover, coding-non-coding gene co-expression networks
were drawn to predict potential lncRNA functions. LncRNAs-T267384, ENST00000607393,
and T342877 expression were further tested by quantitative real-time PCR in AH from 29
POAG and 30 cataract patients, in iris tissues from 16 POAG patients and 10 controls, and in
plasma from 49 POAG patients and 55 healthy controls. Finally, ENST00000607393
function was characterized in an in vitro model of cell calcification. Three-thousand six-
hundred and twenty-seven lncRNAs and 2,228 mRNAs in the AH of POAG patients were
significantly up-regulated and 1,520 lncRNAs and 820 mRNAs were significantly down-
regulated. Seven lncRNAs showed positive correlation with glaucoma associated gene, bone
morphogenetic protein 2. Moreover, RT-qPCR confirmed that T267384, ENST00000607393,
and T342877 expression were significantly higher in the AH from a different cohort of
POAG patients. In addition, ENST00000607393 was also significantly higher in the iris and
plasma of POAG patients. Last, ENST00000607393 knockdown alleviated calcification of
primary human trabecular meshwork cells in vitro. Therefore, lncRNA-T267384,
ENST00000607393, and T342877 may be potential biomarkers for POAG diagnosis.
ENST00000607393 might be a new therapeutic target for trabecular meshwork calcification.
2.15 The diagnostic and prognostication of glaucoma.
Sakhnov SN et al. found IN study that, The glaucoma is a leading cause of irreversible
blindness in all countries. In the nearest years an increasing of patients with the given
pathology is prognosticated. Nowadays, development of disease is related to alteration of
interleukin profile in lacrimal fluid. however, diagnostic significance of interleukins is
studied insufficiently. The purpose of study. To determine diagnostic significance of
interleukins on a local level for amelioration of diagnostic and prognostication of
development of glaucoma. The content of interleukins in lacrimal fluid was analyzed in 80
patients with glaucoma stage II and 45 healthy individuals using technique of sandwich-
linked enzyme-linked immunosorbent assay with calculation of informativeness of indices of

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immunity. The results. The analysis established high diagnostic significance of IL-2, IL-17,
IL-8 for verification of glaucoma. They are proposed to be applied in laboratory diagnostic
and prognostication of disease. The developed regression model ensures with high accuracy
prognostication of development of glaucoma in case of increased level of IL-2, IL-17, IL-8.
2.16 Recurrent Exposure of XEN Gel Stent Implant and Conjunctival Erosion.
Arnould L et al. has found study that, To report a case of recurrent conjunctival erosion and
XEN Gel Stent exposure after implantation in a primary open-angle glaucoma patient.
Minimally invasive glaucoma surgery (MIGS) is a new approach in glaucoma surgery and
there is a lack of published data regarding management of postoperative ocular surface
complications.Case report of a patient with a persistent corneal erosion after XEN Gel Stent
implantation. A standalone MIGS surgery was planned for both eyes in this case of refractory
glaucoma. Despite a first surgical revision, the patient was suffering from a chronic leaking
bleb, an exposed XEN Gel Stent and severe hypotonia in the left eye.A free conjunctival
autografting technique covered with a complementary amniotic membrane graft was
performed under local anesthesia. One month following bleb revision, the intraocular
pressure was 13mm Hg on medical treatment and slit lamp examination showed a well-
formed moderate bleb with no leakage.This is the first described case of the use of a free
conjunctival autograft to treat a persistently leaking bleb after XEN Gel Stent implantation.
This case highlights the potential complication of conjunctival erosion due to XEN Gel Stent
implantation. It emphasizes the management of complicated filtration blebs after MIGS
surgery.
2.17 Screening Glaucoma With Red-free Fundus Photography Using Deep Learning
Classifier and Polar Transformation.
Lee J et al. has found in study that, To develop novel software to determine whether there is a
retinal nerve fiber layer (RNFL) defect in a given fundus image using deep learning classifier
and, if there is, where it presents.In the deep learning classifier, the bottleneck features were
extracted, followed by application of the softmax classifier, which outputted the glaucoma
probability. For localization of RNFL defect, an image processing algorithm was
implemented as follows: (1) the given image was normalized to enhance the contrast; (2) the
region of interest (ROI) was set as the circumferential area surrounding the optic disc
(internal diameter: 2 disc diameters [DD], external diameter: 3 DD), and converted to a polar

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image; (3) blood vessels were removed and the average curvatures were calculated. If the
local maximum curvature was greater than the cut-off value, the sector was considered to be
an RNFL defect.The images of 100 normal healthy controls and 100 open-angle glaucoma
patients were enrolled. Maximum curvatures and area under receiver operating characteristic
curve (AUC) were compared to determine the diagnostic validity.There were no significant
differences in age or gender (P=0.275, P=0.479, respectively) between the two groups. In the
glaucoma group, the mean deviation was -4.9±5.4dB. There was a significant difference of
maximum curvature (14.37±5.13 in control group, 20.67±10.56 in glaucoma group,
P<0.001). AUCs were 0.939 in deep learning classifier and 0.711 in maximum curvature.The
proposed software can be an effective tool for automated detection of RNFL defect.
2.18 Congenital Refractory Glaucoma: a New Ophthalmic Association of Kabuki
Syndrome and its Management with Glaucoma Drainage Devices.
Bravetti GE et al. has found in study that, Kabuki syndrome (KS) is a rare congenital and
polymalformative condition, traditionally associated with mental retardation, unusual facial
features and skeletal abnormalities. They hereby describe a case of bilateral congenital
glaucoma associated with MLL2-mutation Kabuki Syndrome. To the best of our knowledge,
this is the first association of KS with congenital glaucoma.The patient was a 3 year-old male
of North-African ethnicity diagnosed with KS and bilateral congenital glaucoma at the age of
3 months and the first child of a non-consanguineous healthy couple, with no known genetic
conditions within the family. The patient was referred to our tertiary glaucoma centre with
uncontrollable intraocular pressures (IOP) between 50-60mmHg in both eyes. Past
ophthalmic history included bilateral trabeculectomies and right retinal detachment with
phthisis bulbi. They performed left lensectomy combined with Baerveldt tube insertion in the
vitreous cavity, revealing extensive posterior synechiae. Postoperatively, he developed
intense inflammation with fibrin and vitreous strand formation, requiring subsequent
surgeries and subconjunctival injections of betamethasone. Despite these complications, IOP
stabilized between 3-6mmHg.This case confirms congenital glaucoma as a rare association of
Kabuki Syndrome, and highlights the potential high-risk nature of such cases. In their
opinion, the presence of high levels of inflammation peri- and post-operatively is an
indication for primary glaucoma drainage device surgery given the high risk of bleb scarring
resulting in recurrent surgical revisions. In view of these observations, we also advocate the
use of intensive post-operative anti-inflammatory therapy.

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2.19 Postoperative Complications of Ab-Interno Gelatin Microstent.
Rooney DM et al. has found in study that, To report 4 previously undescribed postoperative
complications in 4 cases of ab-interno XEN45 Gel Stent (XEN) implantation following
uncomplicated surgeries.Case 1 is an 86-year-old woman who suffered a suprachoroidal
hemorrhage and associated rhegmatogenous retinal detachment following XEN implantation.
One month after sclerotomy drainage and pars plana vitrectomy repair, an amputated XEN
was found to have eroded through the conjunctiva. Case 2 is a 68-year-old man with
persistent elevated IOP due to recurrent Tenon's capsule fibrosis who developed complete
XEN retraction into the subconjunctival space. Cases 3 and 4 are a 68-year-old man and a 78-
year-old woman who developed occlusion of the microstent's internal ostium by a partially
detached Descemet's membrane. Case 3 maintained normal IOP on timolol, whereas case 4
resulted in bleb failure, despite Nd:YAG laser lysis of the occluded XEN internal
ostium.While the XEN45 Gel Stent is a promising new surgical option for the management of
primary open-angle glaucoma, it can present unique postoperative challenges that are still
being elucidated. Timely intervention or prevention of these complications can be improved
by early surgeon recognition and effective communication with co-managing
ophthalmologists.
2.20 A Comparison of Deep Sclerectomy Trainer versus Trainee Outcomes.
Karaconji T et al. has found in study that, The aim of this study was to compare the results of
Deep Sclerectomy (DS) and combined Deep Sclerectomy with phacoemulsification (phaco-
DS) performed by clinical fellows with those by an experienced glaucoma surgeon and DS
trainer.This is a retrospective non-randomised study of two hundred sixty-six eyes of 226
consecutive patients who had DS or phaco-DS between March 2014 and December 2016
which were included from a database of all glaucoma surgery performed in our department.
A minimum of 9 months follow up was required. The cases were recorded as to whether a
fellow or consultant performed the entire procedure. Overall, 114 surgeries were performed
by the consultant and 164 surgeries were performed by the fellow, in which 91 cases received
no assistance from the consultant. Intraocular pressure (IOP) success criteria were: (A)
IOP<22mmHg and/or 20% decrease from baseline off any glaucoma medications and (B)
IOP <16mmHg and/or 30% drop from baseline off any glaucoma medications.No statistically
significant difference was noted by any criteria (P<0.05) between the two groups. The

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Kaplan-Meir IOP success rates at two years with criteria B (IOP<16mmHg without
medications) were 64% for consultant, 76% for independent surgeries done by a fellow and
72% for surgeries with assistance from the consultant trainer (P=0.15). There were no
significant differences between measured IOPs at any time after surgery. Intra-operative
perforation of trabeculo-Descemet's membrane (TDM) was noted in 4 cases (3.5%) done by
the consultant and 12 cases (7.3%) performed by fellows (Fisher Exact P=0.19).IOP
outcomes of DS and phaco-DS were not adversely affected if fellows performed surgery,
whether under supervision or independently.
2.21 Anterior Chamber XEN Gel Stent Movements: The Impact on Corneal Endothelial
Cell Density.
Gillmann K et al. has found in study that, While there are several examples of glaucoma
drainage devices dislocations in the literature, the movement of XEN gel stents is scarcely
documented and the impact of such displacements on the corneal endothelium remains
unknown. In light of the recent global market withdrawal of the CyPass micro-stent over
concerns regarding endothelial cell loss, we present a case of XEN gel stent dislocation into
the anterior chamber, with localized corneal damage.They describe the case of a 64-year old
female patient who underwent bilateral XEN gel stent implantation for normal tension
glaucoma. While right eye surgery was uneventful, intraocular pressure increased in the left
eye, and examination revealed a flat filtration bleb with no microstent visible through the
conjunctiva. A 3mm segment of the XEN stent was visible within the anterior chamber, with
corneal contact during eye movement and blinking. Endothelial cell density was measured
twice one month apart before the XEN gel stent was replaced.
2.22 A Case Report of Complete Blockage of a Baerveldt Glaucoma Implant Following
Insertion of a 3-0 Supramid Suture.
Lee RMH et al. has found in study that, The aim of this study was to present a case of a
Baerveldt glaucoma implant lumen being completely occluded with a 3-0 Supramid stent
suture.The patient underwent Baerveldt glaucoma implant surgery with placement of an
intraluminal 3-0 Supramid stent suture that acts to restrict flow across the device and reduce
the risk of postoperative hypotony. Following suturing of the implant to the sclera, the device
was flow tested. No flow was observed through the device tube and a significant ballooning
of the tube diameter occurred with increased pressure on the device. The device was

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explanted from the eye and replaced with a different implant without further post-operative
complication. The explanted device was assessed using custom microfluidic equipment in an
in vitro environment.This phenomenon occurred despite using several different batches of the
3-0 Supramid stent suture and the device had to be removed and replaced with another device
without complication. In vitro microfluidic assessment of the device demonstrated no flow
across the device tube despite over 150mmHg of pressure being exerted on the device. They
hypothesize that the blockage occurred at the junction between the device tube and plate and
that the ballooning phenomenon observed was due to a defect in the tube wall. This case
highlights the importance of flow testing all glaucoma drainage devices before insertion
given the variation in manufacturing conditions to avoid the risk of intra-operative
complications.

Chapter-3 Purpose
of study
3.1 Purpose of study
The core objective of this study was to known the awareness among the patient as well as
creates awareness among this patient and different occupational people.
The most significant objective of this study are given blew:
 To identify patient at risk of developing Glaucoma disease.
 To accurately diagnosis glaucoma disease of diverse origins.
 To improve the quality of care rendered to patients glaucoma disease.
 Initiate appropriate treatment for glaucoma disease.
 To find which drugs were prescribed more in Bangladesh for glaucoma.
 To find out proper ways to get medications for glaucoma disease.
 To reduce the potentially adverse effects of Glaucoma disease.
 Suggesting measures for preventing glaucoma.

Chaoter-4 Methods
4.1 Methods
Number of study center: 03
Number of patients: 100
Study site: Study center 1: Dhaka Medical Collage Hospital, Address: Secretariate Road,
Dhaka 1000, Bangladesh
Study center 2: Ispahani Islamia Eye Institute and Hospital, Address: Sher e Bangla Nagar,
Farmgate, Dhaka 1215
Study center 3: BIRDEM General Hospital, Address: 122 Kazi Nazrul Islam Ave, Dhaka
1000
Duration of Study: 3 Months.
Study Type: Glaucoma, All the patients who underwent glaucoma treatment at the Dhaka
Medical Collage hospital, Ispahani Islamia Eye Institute and Hospital and BIRDEM General
Hospital, during the study period where studied. Any patient who was affected in any stage of
glaucoma was included.
Operational Modality: Indoor & outdoor patients of glaucoma from Dhaka Medical
Collage Hospital, Ispahani Islamia Eye Institute and Hospital and BIRDEM General
Hospital ,were studied. Information like age, sex, biophysical characteristics, signs &
symptoms, cause, type of glaucoma, treatment pattern, drugs prescribed to treat glaucoma,
duration of treatment, hospital cost, family history were analyzed by using Microsoft word
and Microsoft Excel software.

Chaoter-4 Methods
Survey Work
4.2 Data Collection Form
1. IDENTIFICATION
1.1 ID CODE:
1.2 NAME:
1.3 FATHER NAME:
1.4 SEX:
1.5 DATE OF BIRTH:
1.6 RELIGION:
1.7 PRESENT ADDRESS:
1.8 PERMANENT ADDRESS:
2. PERSONAL HISTORY
2.1 AREA OF RESIDENCE: Please tick as appropriate(s)
2.2 IMPRESSION ABOUT SOCIAL CLASS:
3. BIOPHYSICAL CHARACTERISTICS
3.1 AGE:
3.2 WEIGHT:
3.3 PULSE:
3.4 TEMPERATURE:
3.5 HEIGHT:
Rural
Urban
s-urban
others
Rich
Upper Middle
Middle
Lower Middle
Poor

Chaoter-4 Methods
4. INVESTIGATION OF GLAUCOMA PATIENTS
4.1 AGE DISTRIBUTION:
4.2 SIGNS & SYMPTOMS:
No. SIGNS & SYMPTOMS TICK
MARK
1 Gradual loss of
peripheral vision
2 Tunnel vision
3 Severe eye pain
4 Nausea and vomiting
5 Sudden onset of visual
disturbance
6 Blurred vision
7 Halos around lights
8 Reddening of the eye
9 Others
4.3 TYPES OF GLAUCOMA (ACCORDING TO UNDERLYING CAUSE):
NO TYPES OF
CONJUNCTIVITIS
TICK
MARK
1 Open-Angle
Glaucoma
2 Acute Angle-
Closure Glaucoma
3 Chronic Angle-
Closure Glaucoma
4 Others
AGE GROUP
(MONTHS)
TICK
MARK
0-5
6-11
12-17
18-23
24-29
30-35
36-41
42-47
48-up

Chaoter-4 Methods
4.4TYPES OF DRUG:
TYPES OF DRUG TICK
MARK
BRAND NAME
β-Blockers (e.g., timolol)
Carbonic anhydrase
inhibitors (e.g., Diamox)
Prostaglandin analogues
(latanoprost, bimatoprost,
travoprost, tafluprost)
Alpha-2 agonists
Cholinergic agonists
Hyperosmotic agents
(mannitol)
Artificial tears
Others
4.5 CONDITION OF PATIENT:
4.7 DURATION OF HOSPITAL SUPERVISION:
HOSPITALIZED NON-
HOSPITALIZED
DAYS TICK MARK
1-3
4-6
7-9
10-12
13-15
16-18
19-21

Chaoter-4 Methods
4.8 HOSPITAL COST:
5. FAMILY HISTORY (if any)
INVESTIGATED BY
NAME:
SIGNATURE:
DATE:

Chaoter-4 Methods
4.3 Study Protocol:
For pediatric and Geriatric Patients:
At first, we selected tertiary care hospital for study and applied for permission from the Authorized
Body (Director/Chairman) of the child/adult Department of the Hospital to conduct the research work.
From collected data the types of glaucoma problems were studied in Bangladesh and its treatment
pattern.
Then data were analyzed by using Microsoft Excel.
Then we select patient whom were admitted in those hospitals and data were collected from them.

Chapter-5 Results
5.1 Results
In my study 100 patients who were suffering from Glaucoma, were randomly selected from
three study centers during three months study period to method discussed earlier.
5.1.1. PERSONAL HISTORY
5.1.1.1 AREA OF RESIDENCE:
I asked 100 people about their area of resident; than I found 30 % patients are from Rural,
50% from any Urban Area, 15 % from any s-urban and 5% from others
Area of resident of Glaucoma patients are shown as follow:
Resident of Patient No of Patient Prevalence (%)
Rural 30 30%
Urban 50 50%
s-urban 15 15%
others 5 5%
Table 5.1.1.1: Area of resident of Glaucoma patient
Fig 5.1.1.1: Area of resident of Glaucoma patient
Rural
30%
Urban
50%
s-urban
15%
others
5%
Area of resident of Glaucoma patient

Chapter-5 Results
5.1.1.2 IMPRESSION ABOUT SOCIAL CLASS:
I asked 100 people about their SOCIAL CLASS, than I found 28 % patients SOCIAL CLASS is Rich
20 % Upper Middle, 30 % Middle, 15 % Lower Middle 7 % Poor.
SOCIAL CLASS of Glaucoma patients are shown as follow:
SOCIAL CLASS of
Patient
No of Patient Prevalence (%)
Rich 28 28%
Upper Middle 20 20%
Middle 30 30%
Lower Middle 15 15%
Poor 7 7%
Table 5.1.1.2: SOCIAL CLASS of Glaucoma patient
Figure 5.1.1.2: SOCIAL CLASS of Glaucoma patient
28%
20%30%
15%
7%
Social class of patient
Rich Upper Middle Middle Lower Middle Poor

Chapter-5 Results
5.1.2 BIOPHYSICAL CHARACTERISTICS
5.1.2.1Weight Distribution of Glaucoma patient
I asked 100 people about the Weight of Glaucoma patients, than I found 18% patients weight
are51-60 , 61-70 are 69%, Up to 70 are 13%.
The prevalence of Glaucoma disease patient according to weight was presented and graph as
follow:
Weight(Kg) Number of patient(n=100) Prevalence(%)
51-60 18 18%
61-70 69 69%
Up to 70 13 13%
Table 5.1.2.1: Weight Distribution of Glaucoma patient
Figure 5.1.2.1: Weight Distribution of Glaucoma patient
18%
69%
13%
Weight Distribution of Galucoma patient
51-60 61-70 up to 70

Prevalence and treatment pattern of Glaucoma

Prevalence and treatment pattern of Glaucoma

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