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

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 Humors 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 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

Picture 1. Flow of Aqueous Humor

2.4 Pathophysiology of Glaucoma 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 6080 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 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 juxtacanalicularthe 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.

Picture 2. Open-Angle Glaucoma

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,
6

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 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.

Picture 3. Angle-Closure Glaucoma

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

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Congenital glaucoma is a rare condition that may be inherited, caused by incorrect development of the eyes 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 1021 mm Hg. The distribution is Gaussian, but with the curve skewed to the
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right. In the elderly, average intraocular pressure is higher, giving an upper limit of 24 mm Hg. In primary open-angle glaucoma, 3250% 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

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 1- 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 2-adrenergic agonist that decreases aqueous humor formation without effect
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on outflow. It is particularly useful for preventing rise of intraocular pressure after anterior 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 -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 125250 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

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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. 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 bomb 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
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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 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
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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). 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

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CHAPTER III CASE

A. Anamnesis Identity Name Sex Age Address Job Religion No. Mr : Mr. A : Male : 55 years old : Jln. Adi Sucipto Komp. Hanura Permai No. 23 : Driver : Moslem : 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.

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Family History: There are no families of patients who have the same illness or complaint.

B. Physical Examination Done on September 24th, 2012 General condition Awareness Blood pressure Pulse Respiratory rate Temperature : mild pain : Compos mentis : 140/ 100 mmHg : 76 x/minute : 16 x/minute : 36,6oC

Ophthalmologycal status Visual acuity OD OS : 6/20 : 1/60 Left eye Eye ball position (-), Palpebra Orthotropia Ptosis (-), lagoftalmos (-), edema(-) Redness (+), discharge (-), Conjungtiva injection (+), ulcer (-),

Right eye Orthotropia Ptosis (-), lagoftalmos edema (-) redness (-), discharge (-),

injection(-), ulcer (-), foreign body (-) Injection (-)

foreign body (-) Sclera Injection (-) Unclear, white cloudy, ulcer (-) Clear, hypopion (-), hyfema (-), shallow Iris colour : ash colored Pupil: circular, not reactive to light, pupil mydriatic

clear, edema (-), ulcer (-) Clear,hypopion (-), hyfema (-), shallow Iris colour : brown

Cornea

COA

Pupil: circular, isokor, reactive Iris and pupil to light, pupil myosis

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Lens clear

Lens

Clear

Can not be described with inspection Red reflex (+), CDR 1/3

Vitreous

Can not be described with inspection Red reflex (+), the optic disk looks pale. CDR

Fundus

Eye Movement:
+

OD +

OS + + +

Visual Field

OD + +

OS -

Intraocular pressure (tonometry) : OD 12 mmHg, OS 70 mmHg

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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

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b. Topikal Timolol 0,5% Polydex

Surgery : Trabeculectomy (Suggestion)

G. Complications Blindness

H. Prognosis OD a. Ad vitam b. Ad functionam c. Ad sanactionam : dubia Ad bonam : dubia Ad bonam : dubia Ad bonam

OS a. Ad vitam b. Ad functionam c. Ad sanactionam : dubia Ad bonam : malam : malam

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CHAPTER 4 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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