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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