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INTRODUCTION
Glaucoma is a disease of the major nerve of vision, called the optic nerve.
The optic nerve receives light-generated nerve impulses from the retina and
transmits these to the brain, where we recognize those electrical signals as vision.
Glaucoma is characterized by a particular pattern of progressive damage to the
optic nerve that generally begins with a subtle loss of side vision (peripheral
vision). If glaucoma is not diagnosed and treated, it can progress to loss of central
vision and blindness.1
Glaucoma is usually, but not always, associated with elevated pressure in
the eye (intraocular pressure). Generally, it is this elevated eye pressure that leads
to damage of the eye (optic) nerve. In some cases, glaucoma may occur in the
presence of normal eye pressure. This form of glaucoma is believed to be caused
by poor regulation of blood flow to the optic nerve.1
The glaucoma is the leading cause of blindness in North America and
affects approximately 1 in 100 Canadians over the age of 40.3 It has been
estimated that this condition is only detected in one half of patients who have it.
This remaining 50% of patients are unaware of this potentially blinding disease
because they do not experience symptoms and therefore do not seek treatment.2
In fact, as many as 6 million individuals are blind in both eyes from this
disease. In the United States alone, according to one estimate, over 3 million
people have glaucoma. As many as half of the individuals with glaucoma,
however, may not know that they have the disease. The reason they are unaware is
that glaucoma initially causes no symptoms, and the subsequent loss of side vision
(peripheral vision) is usually not recognized.1
Population-based studies are the gold standard for measuring the
prevalence of eye diseases, and many have been conducted specifically to test for
glaucoma. Study techniques and definitions of glaucoma have not been uniform
CHAPTER II
LITERATURE REVIEW
2.1. Glaucoma
2.1.1.
Definition
Glaucoma is a chronic, degenerative optic neuropathy that can be
Epidemiology
Glaucoma is the second leading cause of blindness worldwide. The
2.1.3.
significantly higher than the average tissue pressure in almost every other
organ in the body. Such a high pressure is important for the optical
imaging and helps to ensure several things:5
pigmented
Epithelium on Bruchs membrane, which is normally taut and smooth.
2.1.4.
Clasification
Glaucoma classified according to etiology, could be divided in 4
1. Primary Glaucoma
2. Cogenital Glaucoma
3. Secondary Glaucoma
4. Absolute glaucoma
Glaucoma classified according to mechanisme of intraocular
pressure rise, could be divided in 2 type, there are Open-Angle Glaucoma
and Angle-closure Glaucoma.
lying flat.
Intermittent elevations of intraocular pressure, such as in subacute angle
closure.
Underestimation of intraocular pressure due to reduced corneal
thickness.
Other causes of optic disk and field changes, including congenital disk
abnormalities, inherited optic neuropathy, and acquired optic atrophy
due to tumors or vascular disease.
Among
patients
diagnosed with
normal-tension
glaucoma,
progressive visual field loss, but this may not be achieved with medical
therapy. Glaucoma drainage surgery with an antimetabolite may be
required. The possibility of a vascular basis for normal-tension glaucoma
has led to the use of systemic calcium channel blockers, but definite
benefit from this intervention has yet to be demonstrated.
3. Acute Angle Closure
Acute angle closure ("acute glaucoma") occurs when sufficient iris
bomb develops to cause occlusion of the anterior chamber angle by the
peripheral iris. This blocks aqueous outflow, and the intraocular pressure
rises rapidly, causing severe pain, redness, and blurring of vision. Angle
closure develops in hyperopic eyes with preexisting anatomic narrowing of
the anterior chamber angle, usually when it is exacerbated by enlargement
of the crystalline lens associated with aging. The acute attack is often
precipitated by pupillary dilation. This occurs spontaneously in the
evenings, when the level of illumination is reduced. It may be due to
medications with anticholinergic or sympathomimetic activity (eg,
atropine
for
preoperative
medication,
antidepressants,
nebulized
10
2.1.5.
Diagnostic
1. Tonometry
Tonometry is measurement of intraocular pressure. The most
widely used instrument is the Goldmann applanation tonometer, which
is attached to the slitlamp and measures the force required to flatten a
fixed area of the cornea. Corneal thickness influences the accuracy of
measurement. Intraocular pressure is overestimated in eyes with thick
corneas and underestimated in eyes with thin corneas. This difficulty
may be overcome by the Pascal dynamic contour tonometer. Other
applanation tonometers are the Perkins tonometer and the Tono-Pen,
both of which are portable, and the pneumatotonometer, which can be
used with a soft contact lens in place when the cornea has an irregular
surface. The Schiotz tonometer is portable and measures the corneal
indentation produced by a known weight.
The normal range of intraocular pressure is 1021 mm Hg. The
distribution is Gaussian, but with the curve skewed to the right. In the
elderly, average intraocular pressure is higher, giving an upper limit of
11
12
Large myopic eyes have wide angles, and small hyperopic eyes
have narrow angles. Enlargement of the lens with age narrows the angle
and accounts for some cases of angle-closure glaucoma.
3. Optic Disk Assessment
The normal optic disk has a central depressionthe physiologic
cupwhose size depends on the bulk of the fibers that form the optic
nerve relative to the size of the scleral opening through which they must
pass. In hyperopic eyes, the scleral opening is small, and thus the optic
cup is small; the reverse is true in myopic eyes. Glaucomatous optic
atrophy produces specific disk changes characterized chiefly by loss of
disk substance-detectable as enlargement of the optic disk cupassociated with disk pallor in the area of cupping. Other forms of optic
atrophy cause widespread pallor without increased disk cupping.
In glaucoma, there may be concentric enlargement of the optic
cup or preferential superior and inferior cupping with focal notching of
the rim of the optic disk. The optic cup also increases in depth as the
13
14
2.1.6.
Treatment
1. Medical Treatment
15
16
17
permanent darkening of the iris (particularly in green-brown and yellowbrown irides). These drugs have also been rarely associated with
reactivation of uveitis and herpes keratitis and can cause macular edema
in predisposed individuals.
Parasympathomimetic agents increase aqueous outflow by
action on the trabecular meshwork through contraction of the ciliary
muscle. Pilocarpine is not commonly used since the advent of
prostaglandin analogs but can be useful in some patients. It is given as
0.56% solution instilled up to four times a day or as 4% gel instilled at
bedtime. Carbachol 0.753% is an alternative cholinergic agent.
Parasympathomimetic agents produce miosis with dimness of vision,
particularly in patients with cataract, and accommodative spasm that may
be disabling to younger patients. Retinal detachment is a serious but rare
occurrence.
Epinephrine, 0.252% instilled once or twice daily, increases
aqueous outflow with some decrease in aqueous production. There are
several external ocular side effects, including reflex conjunctival
vasodilation, adrenochrome deposits, follicular conjunctivitis, and
allergic reactions. Dipivefrin is a prodrug of epinephrine that is
metabolized intraocularly to its active state. Neither epinephrine nor
dipivefrin should be used in eyes with narrow anterior chamber angles.
Both agents have an adverse effect on the outcome of subsequent
glaucoma drainage surgery.
18
19
Laser Trabeculoplasty
Application of laser (usually argon) burns via a goniolens to the
trabecular meshwork facilitates aqueous outflow by virtue of its effects
on the trabecular meshwork and Schlemm's canal or cellular events that
enhance the function of the meshwork. The technique is applicable to
many forms of open-angle glaucoma, and the results are variable
depending on the underlying cause. The pressure reduction usually
allows decrease of medical therapy and postponement of glaucoma
surgery. Treatments can be repeated (see Chapter 24). Laser
trabeculoplasty may be used in the initial treatment of primary openangle glaucoma. In most cases, the intraocular pressure gradually returns
to the pretreatment level 25 years later. The outcome of subsequent
glaucoma drainage surgery may be adversely affected.
Cyclodestructive Procedures
Failure of medical and surgical treatment in advanced glaucoma
may lead to consideration of laser or surgical destruction of the ciliary
body to control intraocular pressure. Cryotherapy, diathermy, thermal
mode neodymium:YAG laser, or diode laser can all be used to destroy the
ciliary body. Treatment is usually applied externally through the sclera,
but endoscopic laser application systems are available.
21
Definition
Chronic open-angle glaucoma typically is associated with an
elevated intraocular pressure (IOP). Total population surveys show that 1030% of patients newly diagnosed with glaucoma have IOPs that are and
remain normal. Although the relative risk for the development of
glaucomatous optic neuropathy increases with an increase in IOP, the
numerical majority of normotensive individuals ensures that the small
percentage who have open-angle glaucoma constitute a significant
proportion of the whole open-angle glaucoma population. The traditional
therapy for primary open-angle glaucoma is to lower IOP to within the
normal range, but this approach becomes more difficult when the initial
IOP is normal.2
2.1.2.
22
Ocular Manifestasion
No characteristic features exist, other than level of IOP that
23
24
25
Diagnostic
Confirmation of the diagnosis requires:
26
2.1.5.
Diagnosis Differential
Traetment
Treatment is indicated for patients with progressive disease. Few
patients become legally blind from this disease. Many patients are elderly
at diagnosis and have a sufficiently slow rate of change that, even without
treatment, clinically significant loss of vision does not occur. Significant
visual loss may cause social restriction, such as the loss of a driving
license. Trend or event analysis that uses commercially available software
will identify progression. Cluster or point-wise analysis is more likely to
identify progression than analyses that rely on the identification of a global
27
unaltered.
Reversal of Circulatory Deficiencies at the Optic Nerve Head
Reversal of Circulatory Deficiencies at the Optic Nerve Head
can be done by :
a. Vasospasm. Central vasospasm may be indicated by an abnormal
(vasoconstrictive) response of finger circulation to cold, which may
be reversed by calcium channel blockers and carbon dioxide
rebreathing. Theoretically, a carbonic anhydrase inhibitor also should
have a beneficial effect.
b. Nocturnal hypotension. Patients who take drugs to lower blood
pressure and some patients who have NTG exhibit an excessive fall
in systolic and diastolic blood pressures while asleep (dips). Such
changes may reduce ocular perfusion pressure unless the IOP also
falls. All patients must be questioned about systemic hypotensive
(antihypertensive) medication, and any patient who uses such
medication must be checked for such falls in blood pressure.
c. Carotid insufficiency. Patients who have asymmetrical NTG may
show significant (> 50%) lumen reduction in the common carotid
artery, which results in reduction of turbulence and reduction of
volume flow. The end arteries of the ophthalmic artery (and
particularly those in the laminar region of the optic nerve) may suffer
as a result of reduced flow.
28
To date, the best hope for those patients who have progressive
disease is to reduce IOP by 25% or more, to reverse vasospasm using a
calcium channel blocker, and to correct any drug-induced nocturnal
dips.
twice a year.
Therapeutic Intervention
Medical management to lower IOP that fails to maintain a 25%
reduction is unlikely to affect the course of the disease. A trial of
medical management may be justified in patients with progressive
disease, but failure to achieve this reduction should mean a
recommendation for fistulizing surgery, rather than waiting for further
progression to occur.
Glaucoma surgery designed to lower IOP by 30% from a
starting level of, say, 17 mmHg runs a significant risk of postoperative
hypotony. This will convert the frequently asymptomatic patient into
one with symptoms of fluctuating and progressively deteriorating sight.
It is essential, therefore, to have identified progressive disease correctly
and to have discussed with patients the effect of their rate of visual loss
on their vision before asking them to undergo fistulizing surgery. Most
patients with NTG are elderly and their disease progresses slowly, so
that the surgical option is not resorted to frequently.
Neuroprotection
29
Prognosis
Many patients are in their seventh and eighth decade of life at
diagnosis and, with slow disease progression, they do not notice any visual
change. Progression for other patients is more rapid, and they suffer severe
visual loss. No progression has been seen in some patients monitored for
10 years or more by the author, while other patients have demonstrated
rates of loss at individual retinal locations of up to and exceeding 5 db per
year. Similarly, patients who have one normal visual field initially may
show no signs of visual field loss in the second eye for more than 10 years,
even though the appearance of the optic disc suggests glaucoma. The
identification of change, either by the patients symptoms or by visual
performance, is an indication that IOP must be lowered by 25% or more.
To maintain this reduction in IOP for the necessary decades may be
difficult, but if this is not carried out the visual loss may be slowed only
and not halted. Finally, neuroprotective agents, such as calcium channel
blockers, may come to play a pivotal role in the management of this
condition. To date, the only two approaches shown to affect the course of
the disease are the lowering of IOP and the use of calcium channel
blockers.3
30
CHAPTER III
CASE
A. ANAMNESIS
Identity
Name
: Mrs. Fn
Sex
: Femal
Age
: 41 years old
Address
: Suka Bangun, Ketapang
Occupation : Housewife
Religion
: Islam
Tribe/ Ethnic : Malay
Date of consult: 15 February 2012
Major Complaint
Blurry vision in her right eyes
Current Medical History
At the beginning of 2009 the patient's left eye feels like intruding trash,
and then treated with bought eye drops in the store, over time the patient's left
eye become so blurred, so that patients wear glasses. After the patient was
wearing glasses there is no change in his left eye and now the patient is not
able to see again. Since 2 years ago the patients right eye felt the same
complaint as previous left eye, and now the patient's right eye blurred. Patients
do not feel dizzy, pain in both eyes, red eyes or itching and no complaints of
dirt in both of eyes.
Past Medical History
Patient dont have diabetes melitus, hypertension, and
history.
Family Medical History
Two sisters from her mother have a blinded history.
B. PHYSICAL EXAMINATION
General condition
Awareness
: good
: compos mentis
31
traumatic
+
+
+
+
+
+
+
+
Vital Sign
+
+
+
+
BP : 120/80 mmHg
RR : 18 x/minute
HR : 76 x/minute
Ophthalmologycal Status
Visual acuity :
1 /2
OD
: 60
OS
:0
Eye ball position : ortho
Eye movement :
OD
OS
+
+
Inspection
OD
Movement(+),
OS
ptosis
(-), Palpebra
(-),
discharge
Movement
(+),
ptosis
(-),
redness
(-),
discharge
(-),
body (-)
body (-)
Cornea
Anterior
chamber
Iris colour : brown, synechia(-)
Iris/pupil
Circular pupil, isochore, reflect
pupil (+)
32
Clear
Lens
Clear
Clear
Vitreous
Not done
Fundus
Not done
C. RESUME
A female 41 years old, came to opthalmologic clinic to cure his right
eye, which is feel blurry vision. Patient feel blurry in her right eye since 2 years
ago when her left eye still look but have blurrid vision. But now, her left eye
getting lost of vision and her right eye which is feel blurry vision getting
worse. For the first time the symptom of her both of eyes is same, there are
like intruding the weste suffer her left eye first and then her right eye. In her
left eye do the corection by glasses but no chage and her left eye has blinded
now. Now her right eye still have a vision but the patient feel bulrry. No history
about hypertension, diabetes melitus and trauma, pain in the eyes, discharge,
redness or itching history , but in family history two of her mothers sister have
blinded.
33
Visual acuity is
1/2
/60 for OD and 0 for OS. Her left eyes no reflect pupil.
Her right eye examination by funduscopy the Cup Disk Ratio is 0,9 -1,0 and by
Tonometry OD is 9 mmHg and OS is 10 mmHg and the result of perimetri on
her right eye seen only a little remaining visual field still good.
D. DIAGNOSIS
Working Diagnosis :
OD
: Normo Tension Glaucoma
OS
: Blinded
E. PLAN OF EXAMINATION
Gonioscopy
F. TREATMENT
Timolol 5% 2x1
Drozol 3x1
G.
PROGNOSIS
Ad vitam
Ad functionam
Ad sanationam
: ad dubisan
: ad dubisan
: ad dubisan
34
CHAPTER IV
CASED EXPLANATION
A female, 41 years old, came to the eye centre with the major
complaint blurry vision in her right eye since 2 years ago, but 1 last years
her right eye vision getting worse. Blurry vision is one of the symptom
which is no spesific symptom of glaucoma, so the patient need to do some
anamnesis and examination to find the disease that she has.
The patient did not complain of headache, pain in the eyeball, and
vomiting. This indicates that the absence of high eye pressure in her right
eye, it was supported by the results of tonometry examination on the
patient's right eye the result is 9 mmHg in OD and 10 mmHg in OS. The
pathogenesis why in the normal intraocular pressure can make patient
become glaucma is an abnormal sensitivity to intraocular pressure because
of vascular or mechanical abnormalities at the optic nerve head, or this
may be a purely vascular disease.
The patient have familial history that two sisters of her mother have
blinded like her. The familial history is predisposition of glaucoma. A few
families with normal tension glaucoma have an abnormality in the
optineurin (OPTN) gene on chromosome 10. OPTN was reported to be
responsible for up to 16% of heritable normal tension glaucoma, but others
have reported that this gene is responsible for only a minor fraction of
POAG. Optineurin is expressed in a variety of ocular tissues, including the
ciliary body, TM, and retina, but its role in glaucoma pathogenesis is still
unclear.
In right eyes inspection didnt fine any signs like red eyes, itching,
injection and no trauma history on her right eye. This is indicates that no
sign of the eye infection diseases.
In the right eyes cup disk ratio of the patient is 0,9-1,0 and IOP 9
mmHg. It maybe can conclude that has happend normal tension glaucoma.
Normal tension glaucoma happen because in the patient the nerve cell so
fragile and sensitive. So without the increase of IOP the nerve cell still can
damage. The damage of the nerve cell can see trought cupping papil.
35
Cupping the papil optic nerve that we see in increasing of cup disk ratio.
The cupping begin in the central because in that place the nerve cell more
sensitive than the other place.
Based on the result of perimetry, the patient has large loss of vision.
The patient need to do the perimetry test because of the wide variation in
the appearance of the optic disc, it is often difficult to be certain that a
patient has glaucoma based on a single observation of the disc in time.
Even patients with a cup-to-disc ratio of 0.9 may not have glaucoma.
Changes in the optic disc appearance in the form of focal or diffuse loss of
neuroretinal rim resulting in an increase in cup, while diagnostic for
glaucoma, generally take years to develop and it is difficult to document
this change without serial stereoscopic photographs of the optic disc. The
perimetry measure how severe of visual field getting loss. The severity of
visual field defects can be used to judge the severity of functional damage
to the visual system from glaucoma. This is important to determine the
aggressiveness of initial therapy (the worse the visual field, the greater the
IOP lowering) and to assess the success of ongoing treatment (patients
who go from moderate to severe visual field defect under treatment, for
example, might require more aggressive therapy).
Visual acuity patient in OD is 1/2/60 and OS is 0. In OS patient the
vision is 0 because the optic nerve of the patient had been damaged, it can
caused by the normo tension glaucoma that she has. In OD a vision acuity
is
1/2
/60 it can indicate that had been lost of vision by glaucoma, we know
36
BIBILIOGRAPHY
1. Schwartz, L.J
Treatment.
2010.
Available
from
37
China.Elsevier. 2009
Kwon Y.H et al. Primary Open-Angle Primary. The New England
Journal
of
Medicine.
2009.
Available
http://www.nejm.org/doi/full/10.1056/NEJMra0804630
from
visited at
2006.
Available
38
from