case report absolute glaucoma
TRANSCRIPT
CHAPTER 1
INTRODUCTION
Glaucoma is an eye disease in which the optic nerve is damaged in a characteristic
pattern. It is a second to cataract as a leading cause of global blindness and is the leading cause
of irreversible visual loss. In 2002, 37 million individuals were blind worldwide, with glaucoma
accounting for 12.3% of these individuals. By the year 2020 it is estimated that there will be
almost 80 million people in the world with open-angle glaucoma and angle-closure glaucoma.1
The cause of glaucoma is associated with elevated intraocular pressure. The mechanism
of raised intraocular pressure in glaucoma is impaired outflow of aqueous resulting from
abnormalities within the drainage system of the anterior chamber angle (open-angle glaucoma)
or impaired access of aqueous to the drainage system (angle-closure glaucoma).1,2
Risk factors for open-angle glaucoma include increased age, African ethnicity, family
history, increased intraocular pressure, myopia, and decreased corneal thickness, but for angle
closure glaucoma include Inuit and Asian ethnicity, hyperopia, shallow anterior chamber, short
axial length, small corneal diameter, steep corneal curvature, shallow limbal chamber depth, and
thick, relatively anteriorly positioned lens.1
The symptoms of glaucoma depend on the type of glaucoma, such as severe pain in one
eye, nausea and vomiting, red eye, tearing, or may be see halos around lights. Goal for glaucoma
treatment is to reduce eye pressure and it is depends of the type of glaucoma. 3
1
CHAPTER 2
LITERATURE REVIEW
2.1 Definition
Glaucoma is a multifactorial optic neuropathy with characteristic acquired loss of optic
nerve fibres. Commonest cause of irreversible blindness in the world, affecting 2% of people
over 40 years of age, and 4% of people over 70 years. It is usually associated with elevated
intraocular pressure. In the majority of cases, there is no associated ocular disease (primary
glaucoma). 2,4
2.2 Epidemiology
Glaucoma is the second leading cause of blindness worldwide. The frequency of bilateral
blindness among persons with glaucoma varies across populations, with substantial bilateral
blindness from glaucoma observed in developing countries with poor access to eye care, and in
populations where angle-closure glaucoma predominates. In 2002, 37 million individuals were
blind worldwide, with glaucoma accounting for 12.3% of these individuals. By the year 2020 it
is estimated that there will be almost 80 million people in the world with open-angle glaucoma
and angle-closure glaucoma.1,3
2.3 Aqueous Humor’s Physiology
2.3.1 Composition of Aqueous
The aqueous is a clear liquid that fills the anterior and posterior chambers of the eye. Its
volume is about 250 L, and its rate of production, which is subject to diurnal variation, is about
2.5 L/min. The osmotic pressure is slightly higher than that of plasma. The composition of
aqueous is similar to that of plasma except for much higher concentrations of ascorbate,
pyruvate, and lactate and lower concentrations of protein, urea, and glucose.2
2.3.2 Formation & Flow of Aqueous
2
Aqueous is produced by the ciliary body. An ultrafiltrate of p lasma produced in the
stroma of the ciliary processes is modified by the barrier function and secretory processes of the
ciliary epithelium. Entering the posterior chamber, the aqueous passes through the pupil into the
anterior chamber and then to the trabecular meshwork in the anterior chamber angle. During this
period, there is some differential exchange of components with the blood in the iris.2
2.3.3 Outflow of Aqueous
The trabecular meshwork is composed of beams of collagen and elastic tissue covered by
trabecular cells that form a filter with a decreasing pore size as the canal of Schlemm is
approached. Contraction of the ciliary muscle through its insertion into the trabecular meshwork
increases pore size in the meshwork and hence the rate of aqueous drainage. Passage of aqueous
into Schlemm's canal depends on cyclic formation of transcellular channels in the endothelial
lining. Efferent channels from Schlemm's canal (about 30 collector channels and 12 aqueous
veins) conduct the fluid directly into the venous system. Some aqueous passes between the
bundles of the ciliary muscle into the suprachoroidal space and then into the venous system of
the ciliary body, choroid, and sclera (uveoscleral flow).2
2.4 Pathophysiology of Glaucoma
3
Picture 1. Flow of Aqueous Humor
The major mechanism of visual loss in glaucoma is retinal ganglion cell apoptosis,
leading to thinning of the inner nuclear and nerve fiber layers of the retina and axonal loss in the
optic nerve. The optic disk becomes atrophic, with enlargement of the optic cup.
The pathophysiology of intraocular pressure elevation whether due to open-angle or to
angle-closure mechanisms will be discussed as each disease entity is considered. The effects of
raised intraocular pressure are influenced by the time course and magnitude of the rise in
intraocular pressure. In acute angle-closure glaucoma, the intraocular pressure reaches 60–80
mm Hg, resulting in acute ischemic damage to the iris with associated corneal edema and optic
nerve damage. In primary open-angle glaucoma, the intraocular pressure does not usually rise
above 30 mm Hg and retinal ganglion cell damage develops over a prolonged period, often many
years. In normal-tensiol glaucoma, retinal ganglion cells may be susceptible to damage from
intraocular pressures in the normal range, or the major mechanism of damage may be optic nerve
head ischemia.2
2.5 Risk Factor of Glaucoma
There are some risk factor that can cause glaucoma5 :
a. Elevated internal eye pressure (intraocular pressure).
If intraocular pressure is higher than normal, it can increased risk of developing
glaucoma, though not everyone with elevated intraocular pressure develops the disease.
b. Age.
Everyone older than 60 is at increased risk of glaucoma.
c. Family history of glaucoma.
Glaucoma may have a genetic link, meaning there's a defect in one or more genes that
may cause certain individuals to be unusually susceptible to the disease. A form of
juvenile open-angle glaucoma has been clearly linked to genetic abnormalities.
d. Medical conditions.
Diabetes, hypertension and hypothyroidism increase risk of developing glaucoma.
e. Other eye conditions.
Severe eye injuries can result in increased eye pressure. Injury can also dislocate the
lens, closing the drainage angle. Other risk factors include retinal detachment, eye
4
tumors and eye inflammations, such as chronic uveitis and iritis. Certain types of eye
surgery also may trigger secondary glaucoma.
f. Nearsightedness.
Being nearsighted, which generally means that objects in the distance look fuzzy
without glasses or contacts, increases the risk of developing glaucoma.
g. Prolonged corticosteroid use.
Using corticosteroids for prolonged periods of time appears to put at risk of getting
secondary glaucoma. This is especially true if someone use corticosteroids eyedrops.
2.6 Types of Glaucoma
2.6.1 Open Angle Glaucoma6
In open-angle glaucoma, the aqueous humor has unimpeded access to the trabecular
meshwork in the angle of the anterior chamber, but there is abnormally high resistance to the
fluid flow through the trabecular meshwork (uveal, corneoscleral, and juxtacanalicular—the last
being the site of primary outflow resistance), into Schlemm's canal, and then into the scleral
venous plexus. The peripheral iris does notinterfere with the access of aqueous humor to the
draining angle structures.
a. Primary open-angle glaucoma (POAG) is the most common form of glaucoma. The
underlying abnormality in the trabecular angle tissue causing abnormal resistance to fluid
flow is not known. The disease is not secondary to another eye disease or condition.
POAG is a silent, surreptitious process. Usually there are no symptoms. Gradual loss of
peripheral vision occurs. Loss of central vision is usually the last to occur. Only actual
measurement of the IOP and inspection of the optic nerve head with an ophthalmoscope
can detect POAG in its early stages.
b. Secondary open-angle glaucoma occurs as a result of or in association with another eye
disease or condition such as uveitis or trauma, resulting in secondary blockage or damage
to the canals and collector channels.
5
Without treatment, open-angle glaucoma may progress insidiously to complete blindness.
If antiglaucoma drops control the intraocular pressure in an eye that has not suffered extensive
glaucomatous damage, the prognosis is good (although visual field loss may progress despite
normalized intraocular pressure). When the process is detected early, most glaucoma patients can
be successfully managed medically. Trabeculectomy is a good option in patients who progress
despite medical treatment.2
2.6.2 Angle Closure Glaucoma
In angle-closure glaucoma, the peripheral iris tissue covers the trabecular meshwork,
preventing access of the aqueous humor to the trabecular meshwork. This type of glaucoma is
often intermittent, with acute symptoms that are reversible when the peripheral iris is moved
away from draining angle structures. In pure angle-closure glaucoma, the trabecular meshwork
and Schlemm's canal angle tissue have inherently normal resistance to fluid flow. The IOP is
elevated only when the peripheral iris covers the trabecular meshwork, preventing egress of the
aqueous.
a. In primary angle-closure glaucoma, relative pupillary block is the mechanism of angle
closure. This means that there is relative resistance to fluid flow of aqueous humor
between the posterior iris surface and lens due to an abnormally close approximation at
the pupil. This tends to occur in eyes with small anterior segments or short axial length.
Relative pupillary block increases the pressure of aqueous in the posterior chamber,
forcing the peripheral iris forward over the trabecular meshwork. The state of relative
papillary block depends greatly on pupillary size and rigidity of the peripheral iris. For
6
Picture 2. Open-Angle Glaucoma
example, relative pupillary block may be increased and angle-closure glaucoma produced
by putting a patient in a dark room or by using dilating medications that move the pupil
into a middilated state. Drug-induced miosis may produce a very small pupil, blocking
posterior chamber aqueous passage and thus pushing the iris forward to close the angle.
Most eyes subject to possible angle-closure glaucoma can be recognized by the
shallowness of their axial anterior chamber depth.
b. Secondary angle-closure glaucoma occurs as a result of or in association with another
eye disease or condition, such as a swollen cataract or diabetic neovascularization
pushing or pulling the iris over the trabecular meshwork.
2.6.3 Normal Tension Glaucoma
Normal-tension glaucoma (NTG), also known as low tension or normal pressure
glaucoma, is a form of glaucoma in which damage occurs to the optic nerve without eye pressure
exceeding the normal range. In general, a "normal" pressure range is between 10-20 mm Hg. The
causes of NTG are still unknown. For some reason, the optic nerve is susceptible to damage from
even the normal amount of eye pressure.7
2.6.4 Congenital Glaucoma
7
Picture 3. Angle-Closure Glaucoma
Congenital glaucoma is a rare condition that may be inherited, caused by incorrect
development of the eye’s drainage system before birth. This leads to increased intraocular
pressure, which in turn damages the optic nerve.7
Symptoms of congenital glaucoma include enlarged eyes, cloudiness of the cornea, and
photosensitivity (sensitivity to light).
2.6.5 Absolute glaucoma
Absolute glaucoma is the end stage of all types of glaucoma. The eye has no vision,
absence of pupillary light reflex and pupillary response, and has a stony appearance. Severe pain
is present in the eye.
2.7 Glaucoma Symptoms
Acute onset of intense pain. The elevated intraocular pressure acts on the corneal nerves
(the ophthalmic nerve or first branch of the trigeminal nerve) to cause dull pain. This painmay be
referred to the temples, back of the head, and jaws via the three branches of the trigeminal nerve,
which can mask its ocular origin. Nausea and vomiting occur due to irritation of the vagus nerve
and can simulate abdominal disorders. The generalized symptoms such as headache, vomiting,
and nausea may dominate to the extent that the patient fails to notice local symptoms.
Diminished visual acuity. Patients notice obscured vision and colored halos around lights in the
affected eye. These symptoms are caused by the corneal epithelial edema precipitated by the
enormous increase in pressure. Prodromal symptoms. Patients report transitory episodes of
blurred vision or the appearance of colored halos around lights prior to the attack.
2.8 Clinical Assessment in Glaucoma
2.8.1 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. The normal range of intraocular
pressure is 10–21 mm Hg. The distribution is Gaussian, but with the curve skewed to the
8
right. In the elderly, average intraocular pressure is higher, giving an upper limit of 24
mm Hg. In primary open-angle glaucoma, 32–50% of affected individuals will have a
normal intraocular pressure when first measured. Conversely, isolated raised intraocular
pressure does not necessarily mean that the patient has primary open-angle glaucoma,
since other evidence in the form of a glaucomatous optic disk or visual field changes is
necessary for diagnosis. If the intraocular pressure is consistently elevated in the presence
of normal optic disks and visual fields (ocular hypertension), the patient may be observed
periodically as a glaucoma suspect.2
2.8.2 Genioscopy
The anterior chamber angle is formed by the junction of the peripheral cornea and the
iris, between which lies the trabecular meshwork. The configuration of this angle-ie,
whether it is wide (open), narrow, or closed-has an important bearing on the outflow of
aqueous. The anterior chamber angle width can be estimated by oblique illumination with
a penlight or by slitlamp observation of the depth of the peripheral anterior chamber, but
it is best determined by gonioscopy, which allows direct visualization of the angle
structures.
2.8.3 Visual Fields
Glaucomatous field loss is not in itself specific, since it consists of nerve fiber bundle
defects that may be seen in other forms of optic nerve disease; but the pattern of field
loss, the nature of its progression, and the correlation with changes in the optic disk are
characteristic of the disease. Peripheral field loss tends to start in the nasal periphery as a
constriction of the isopters. Subsequently, there may be connection to an arcuate defect,
producing peripheral breakthrough. The temporal peripheral field and the central 5-10
degrees are affected late in the disease. Central visual acuity is not a reliable index of
progress of the disease. In end-stage disease, there may be normal central acuity but only
5 degrees of visual field in each eye. In advanced glaucoma, the patient may have 20/20
visual acuity and be legally blind.
2.8.4 Optic Disk Assessment
9
The normal optic disk has a central depression the physiologic cup whose 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. Glaucomatous optic atrophy produces specific
disk changes characterized chiefly by loss of disk substance-detectable as enlargement of
the optic disk cup-associated with disk pallor in the area of cupping. Other forms of optic
atrophy cause widespread pallor without increased disk cupping.
The "cup disk ratio" is a useful way of recording the size of the optic disk in glaucoma
patients. It is the ratio of cup size to disk diameter, eg, a small cup is 0.1 and a large cup
0.9. In the presence of visual field loss or elevated intraocular pressure, a cup disk ratio
greater than 0.5 or significant asymmetry between the two eyes is highly suggestive of
glaucomatous atrophy.2,8
2.9 Treatment of Glaucoma
Although nerve damage and visual loss from glaucoma cannot usually be reversed,
glaucoma is a disease that can generally be controlled. That is, treatment can make the
intraocular pressure normal and, therefore, prevent or retard further nerve damage and visual
loss. Treatment may involve the use of eyedrops, pills (rarely), laser ,or surgery.9
2.9.1 Medical Treatment
a. Suppression of Aqueous Production
Topical beta-adrenergic blocking agents may be used alone or in combination with other
drugs. Timolol maleate 0.25% and 0.5%, betaxolol 0.25% and 0.5%, levobunolol 0.25% and
0.5%, metipranolol 0.3%, and carteolol 1% solutions twice daily and timolol maleate 0.1%,
0.25%, and 0.5% gel once daily in the morning are the currently available preparations. The
major contraindications to their use are chronic obstructive airway disease particularly
asthma and cardiac conduction defects. Betaxolol, with its relatively greater selectivity for
β1- receptors, less often produces respiratory side effects, but it is also less effective at
reducing intraocular pressure. Depression, confusion, and fatigue may occur with the topical
beta-blocking agents. The frequency of systemic effects and the availability of other agents
has reduced the popularity of the beta-adrenergic blocking agents.
Apraclonidine (0.5% solution three times daily and 1% solutionbefore and after laser
treatment) is an α2-adrenergic agonist that decreases aqueous humor formation without effect
on outflow. It is particularly useful for preventing rise of intraocular pressure after anterior
10
segment laser treatment and can be used on a short-term basis in refractory cases. It is not
suitable for long-term use because of tachyphylaxis (loss of therapeutic effect over time) and
a high incidence of allergic reactions. Epinephrine and dipivefrin have some effect on
aqueous production but are rarely used these days.
Brimonidine (0.2% solution twice daily) is an α-adrenergic agonist that primarily inhibits
aqueous production and secondarily increases aqueous outflow. It may be used as a first-line
or adjunctive agent, but allergic reactions are common.
Dorzolamide hydrochloride 2% solution and brinzolamide 1% (two or three times daily)
are topical carbonic anhydrase inhibitors that are especially effective when employed
adjunctively, although not as effective as systemic carbonic anhydrase inhibitors. The main
side-effects are a transient bitter taste and allergic blepharoconjunctivitis. Dorzolamide is
also available combined with timolol in the same solution.
Systemic carbonic anhydrase inhibitors acetazolamide is the most widely used, but
dichlorphenamide and methazolamide are alternatives are used in chronic glaucoma when
topical therapy is insufficient and in acute glaucoma when very high intraocular pressure
needs to be controlled quickly. They are capable of suppressing aqueous production by 40–
60%. Acetazolamide can be administered orally in a dosage of 125–250 mg up to four times
daily or as Diamox Sequels 500 mg once or twice daily, or it can be given intravenously (500
mg). The carbonic anhydrase inhibitors are associated with major systemic side effects that
limit their usefulness for long-term therapy.
Hyperosmotic agents influence aqueous production as well as dehydrate the vitreous
body.
b. Facilitation of Aqueous Outflow
The prostaglandin analogs bimatoprost 0.003%, latanoprost 0.005%, and travoprost
0.004% solutions, each once daily at night, and unoprostone 0.15% solution twice daily
increase uveoscleral outflow of aqueous. All the prostaglandin analogs may produce
conjunctival hyperemia, hyperpigmentation of periorbital skin, eyelash growth, and
permanent darkening of the iris (particularly in green-brown and yellow-brown irides). These
drugs have also been rarely associated with reactivation of uveitis and herpes keratitis and
can cause macular edema in predisposed individuals.
11
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 0.5–6%
solution instilled up to four times a day or as 4% gel instilled at bedtime.
c. Reduction of Vitreous Volume
Hyperosmotic agents render the blood hypertonic, thus drawing water out of the vitreous
and causing it to shrink. This is in addition to decreasing aqueous production. Reduction in
vitreous volume is helpful in the treatment of acute angle-closure glaucoma and in malignant
gaucoma when anterior displacement of the crystalline lens (caused by volume changes in
the vitreous or choroid) produces angle closure (secondary angle-closure glaucoma).
Oral glycerin (glycerol), 1 mL/kg of body weight in a cold 50% solution mixed with lemon
juice, is the most commonly used agent, but it should be used with care in diabetics.
Alternatives are oral isosorbide and intravenous urea or mannitol.
d. Miotics, Mydriatics, and Cycloplegics
Constriction of the pupil is fundamental to the management of primary angle-closure
glaucoma and the angle crowding of plateau iris. Pupillary dilation is important in the
treatment of angle closure secondary to iris bombé due to posterior synechiae. When angle
closure is secondary to anterior lens displacement, cycloplegics (cyclopentolate and atropine)
are used to relax the ciliary muscle and thus tighten the zonular apparatus in an attempt to
draw the lens backward.
2.9.2 Surgical Treatment
2.9.2.1 Laser Treatment
a. Laser iridotomy involves making a hole in the colored part of the eye (iris) to
allow fluid to drain normally in eyes with narrow or closed angles.
b. Laser trabeculoplasty is a laser procedure performed only in eyes with open
angles. Laser trabeculoplasty does not cure glaucoma but is often done instead of
increasing the number of different eyedrops or when a patient's intraocular
pressure is felt to be too high despite the use of multiple eyedrops (maximal
medical therapy). In some cases, it is used as the initial or primary therapy for
open-angle glaucoma. This procedure is a quick, painless, and relatively safe
12
method of lowering the intraocular pressure. With the eye numbed by anesthetic
drops, the laser treatment is applied through a mirrored contact lens to the angle
of the eye. Microscopic laser burns to the angle allow fluid to better exit the
drainage channels.
c. Laser trabeculoplasty is often done in two sessions, weeks or months apart.
Unfortunately, the improved drainage as a result of the treatment may last only
about two years, by which time the drainage channels tend to clog again. There
are two types of laser trabeculoplasty: argon laser trabeculoplasty (ALT) and
selective laser trabeculoplasty (SLT). ALT is generally not repeated after the
second session due to the formation of scar tissue in the angle. SLT is less likely
to produce scarring in the angle, so, theoretically, it can be repeated multiple
times. However, the likelihood of success with additional treatments when prior
attempts have failed is low. Thus, the options for the patient at that time are to
increase the use of eyedrops or proceed to surgery.
d. Lasercyclo-ablation (also known ciliary body destruction, cyclophotocoagulation
or cyclocryopexy) is another form of laser treatment generally reserved for
patients with severe forms of glaucoma with poor visual potential. This procedure
involves applying laser burns or freezing to the part of the eye that makes the
aqueous fluid (ciliary body). This therapy destroys the cells that make the fluid,
thereby reducing the eye pressure. This type of laser is typically performed after
other more traditional therapies have failed.9
2.9.2.2 Glaucoma Surgery
a. Trabeculectomy is a delicate microsurgical procedure used to treat glaucoma. In this
operation, a small piece of the clogged trabecular meshwork is removed to create an
opening and a new drainage pathway is made for the fluid to exit the eye. As part of this
new drainage system, a tiny collecting bag is created from conjunctival tissue. (The
conjunctiva is the clear covering over the white of the eye.) This bag is called a "filtering
bleb" and looks like a cystic raised area that is at the top part of the eye under the upper
lid. The new drainage system allows fluid to leave the eye, enter the bag/bleb, and then
pass into the capillary blood circulation (thereby lowering the eye pressure).
13
Trabeculectomy is the most commonly performed glaucoma surgery. If successful, it is
the most effective means of lowering the eye pressure.
b. Aqueous shunt devices (glaucoma implants or tubes) are artificial drainage devices
used to lower the eye pressure. They are essentially plastic microscopic tubes attached to
a plastic reservoir. The reservoir (or plate) is placed beneath the conjunctival tissue. The
actual tube (which extends from the reservoir) is placed inside the eye to create a new
pathway for fluid to exit the eye. This fluid collects within the reservoir beneath the
conjunctiva creating a filtering bleb. This procedure may be performed as an alternative
to trabeculectomy in patients with certain types of glaucoma.
c. Viscocanalostomy is an alternative surgical procedure used to lower eye pressure. It
involves removing a piece of the sclera (eye wall) to leave only a thin membrane of tissue
through which aqueous fluid can more easily drain. While it is less invasive than
trabeculectomy and aqueous shunt surgery, it also tends to be less effective.9
CHAPTER III
CASE
14
A. Anamnesis
Identity
Name : Mr. A
Sex : Male
Age : 55 years old
Address : Jln. Adi Sucipto Komp. Hanura Permai No. 23
Job : Driver
Religion : Moslem
No. Mr : 652917
Patient was examined on September 24th, 2012.
Chief Complaint: Blurred vision and eye pain
History of disease:
Patient complain blurred vision and eye pain on left eye since one month ago, his right eye also
blurred, but not really annoyed him. This day, he just complain headache and eye pain on left
eye, but not really severe. One month ago, patient felt headache suddenly on the left head and
pain suddenly on the left eye. He complained that he could not see well, his vision was very
blurred. Sometimes, when he look at the light, he saw a circle at the light. He did not complaint
for glare vision, swelling, itching, discharge, and watery. He said that he did not get a trauma
before. Patients admitted for treatment in clinic near his home, the doctor said that the pain due
to high blood, and doctors giving pain medication for reduce his headache.
Past Clinical History:
He never get these symtoms before, this is for the first time. He has not diabetes melitus, but he
has hypertension history.
Family History:
There are no families of patients who have the same illness or complaint.
15
B. Physical Examination
Done on September 24th, 2012
General condition : mild pain
Awareness : Compos mentis
Blood pressure : 140/ 100 mmHg
Pulse : 76 x/minute
Respiratory rate : 16 x/minute
Temperature : 36,6oC
Ophthalmologycal status
Visual acuity
OD : 6/20
OS : 1/60
Right eye Left eye
Orthotropia Eye ball position Orthotropia
Ptosis (-), lagoftalmos (-),
edema (-)Palpebra
Ptosis (-), lagoftalmos (-),
edema(-)
redness (-), discharge (-),
injection(-), ulcer (-),
foreign body (-)
Conjungtiva
Redness (+), discharge (-),
injection (+), ulcer (-),
foreign body (-)
Injection (-) Sclera Injection (-)
clear, edema (-), ulcer (-) CorneaUnclear, white cloudy, ulcer
(-)
Clear,hypopion (-),
hyfema (-), shallowCOA
Clear, hypopion (-),
hyfema (-), shallow
Iris colour : brown
Pupil: circular, isokor, reactive
to light, pupil myosis
Iris and pupil
Iris colour : ash colored
Pupil: circular, not reactive
to light, pupil mydriatic
16
++
+
+
+
+
+
+
++
+
+
+
+
+
+
OD OS
+
+
+
+
-
-
+
+
OD OS
Lens clear Lens Clear
Can not be described with
inspectionVitreous
Can not be described with
inspection
Red reflex (+), CDR 1/3 FundusRed reflex (+), the optic
disk looks pale. CDR ¾
Eye Movement:
Visual Field
Intraocular pressure (tonometry) : OD 12 mmHg, OS 70 mmHg
17
C. Resume
Male, 55 years old complain blurred vision and eye pain on left eye since one month ago,
his right eye also blurred, but not really annoyed him. One month ago, patient felt headache
suddenly on the left head and pain suddenly on the left eye. He complained that he could not see
well, his vision was very blurred. Sometimes, when he look at the light, he saw a circle at the
light. He has hypertension history.
From physical examination findings : his blood pressure 140/100, OS 1/60, OS TIO
70mmHg, left eye redness and injection conjungtiva, unclear, edema and white cloudy cornea,
shallow COA, ash coloured irish, pupil dilated and not respon with light, the optic disk looks
pale, CDR 3/4. Confrontation test suggests narrowing of the OS visual field.
D. Diagnosis
Working Diagnose:
OD : suspect presbiopy
OS : Glaucoma absolute
Hypertension
Differential Diagnose :
OS : - optic neuritis
- acute iritis
E. Plan of Examination
a. Repeat the visual acuity examination.
b. Genioscopy
F. Treatment
Medication :
a. Per oral
Mefenamat acid
Acetazolamid
Amylodipin
b. Topikal
18
Timolol 0,5%
Polydex
Surgery :
Trabeculectomy (Suggestion)
G. Complications
Blindness
H. Prognosis
OD
a. Ad vitam : dubia Ad bonam
b. Ad functionam : dubia Ad bonam
c. Ad sanactionam : dubia Ad bonam
OS
a. Ad vitam : dubia Ad bonam
b. Ad functionam : malam
c. Ad sanactionam : malam
CHAPTER 4
19
CASE EXPLANATION
Male, 55 years old complain blurred vision and eye pain on left eye since one month ago,
his right eye also blurred, but not really annoyed him. One month ago, patient felt headache
suddenly on the left head and pain suddenly on the left eye. He complained that he could not see
well, his vision was very blurred. Sometimes, when he look at the light, he saw a circle at the
light. He has hypertension history.
From physical examination findings : his blood pressure 140/100, OS 1/60, OS TIO
70mmHg, left eye redness and injection conjungtiva, unclear, edema and white cloudy cornea,
shallow COA, ash coloured irish, pupil dilated and not respon with light, the optic disk looks
pale, CDR 3/4. Confrontation test suggests narrowing of the OS visual field.
Based on the above data, this patient diagnosed absolute glaucoma oculi sinistra. the
specific finding is his visus 1/60, it is means the patient were blind which categorized by WHO.
In this patient the absolute glaucoma thought to be caused by acute primary glaucoma runs fast.
Commonly symptoms of galukoma is blurred vision, eye pain and headache.
Blurred vision is the most common visual symptom. It usually refers to decreased visual
acuity of gradual onset. Blurred vision has 4 general mechanisms: opacification of normally
transparent ocular structures (cornea, lens, vitreous) through which light rays must pass to reach
the retina, disorders affecting the retina, disorders, affecting the optic nerve or its connections,
and refractive errors. Headache in left head and pain in left eye in this patient due to the increase
in IOP which reached 70mmHg.
The examination that can do for this patient besides tonometry are such as visual fields
and funduscopy. The visual fields examination in absolute glaucoma may found peripheral field
loss tends to start in the nasal periphery as a constriction of the isopters. It suggest the damage of
the optic nerve. Funduscopy revealed larger the cup, the greater the possibility of a glaucomatous
optic nerve damage, but in this patient, i find hard to describe his fundus.
The glaucoma may threaten vision as a result of optic nerve damage, compromised blood
flow to the posterior segment, or corneal blood staining. So the treatment for this patient is to
reduce the IOP. Although absolute glaucoma is the end of stage, but it is still need drugs
medication. Drugs that can give for this patient such as timolol 0,5 % and polydex as a eyedrops,
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mefenamat acid, acetazolamid, and amylodipin. If the IOP not reduced, I recommend
trabuculectomy surgery for this patient.
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CHAPTER 5
SUMMARY
Male, 55 years old complain blurred vision and eye pain on left eye since one month ago,
his right eye also blurred, but not really annoyed him. One month ago, patient felt headache
suddenly on the left head and pain suddenly on the left eye. He complained that he could not see
well, his vision was very blurred. Sometimes, when he look at the light, he saw a circle at the
light. He has hypertension history.
From physical examination findings : his blood pressure 140/100, OS 1/60, OS TIO
70mmHg, left eye redness and injection conjungtiva, unclear, edema and white cloudy cornea,
shallow COA, ash coloured irish, pupil dilated and not respon with light, the optic disk looks
pale, CDR 3/4. Confrontation test suggests narrowing of the OS visual field.
The diagnosed for this patient is a absolute glaucoma. the treatment that can give such as
timolol 0,5 % and polydex as a eyedrops, mefenamat acid, acetazolamid, and amylodipin. If the
IOP not reduced, trabuculectomy surgery for this patient may be necessary.
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