Case Oculi

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    CHAPTER I

    INTRODUCTION

    A cataract is a clouding of the eye's natural lens, which lies behind the iris and the

    pupil. The lens works much like a camera lens, focusing light into the retina at the back of the

    eye. The lens also adjusts the eye's focus, letting us see things clearly both up close and far

    away.

    Aging is the most common cause of cataract (esp. persons over 65-70 years) but many

    other factors can be involved, including trauma, toxins, systemic disease, and heredity. Age

    related cataract is a common cause of visual impairment. Cataract usually happens in both

    eyes, but traumatic cataract may happen in only one eye. The sexes are equally affected.Cataracts also run in families. The condition is estimated to have blinded more than 25

    million people worldwide.

    The crystalline lens is implicated as a causative element in producing several forms of

    glaucoma. Etiologically they represent a diversity in the presentation of the glaucomatous

    process. These conditions include glaucoma related to: lens dislocation (ectopia lentis), lens

    swelling (intumescent cataract), classical pupillary block, aqueous misdirection - ciliary

    block, phacoanaphylaxis, lens particle, and phacolytic glaucoma. In normal eye, there is a

    balance between the production and outflow of the aqueous. When its blocked, the

    intraocular pressure increased leads to the damage of optic nerve.The management of

    elevated intraocular pressure often requires altering the intraocular relationship of anatomic

    structures surrounding the lens or lens removal. In glaucoma there is a weakness in eye

    function caused of the visual field decreased and anatomical damage and the degeneration of

    the optic disc which can resulting blindness.

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    CHAPTER II

    LITERATURE REVIEW

    Anatomy and Physiology of lensThe crystalline lens focuses a clear image on the retina. The lens is suspended by thin

    filamentous zonules from the ciliary body between the iris anteriorly and the vitreous

    humor posteriorly. Contraction of the ciliary muscle permits focusing of the lens. The

    lens is enclosed in a capsule of transparent elastic basement membrane. The capsule

    encloses the cortex and the nucleus of the lens as well as a single anterior layer of

    cuboidal epithelium. The lens has no innervation or blood supply. Nourishment comes

    from the aqueous fluid and the vitreous.

    The normal lens continues to grow throughout life. The epithelial cells continue to

    produce new cortical lens fibers, yielding a slow increase in size, weight, and density over

    the years. The normal lens consists of 35% protein by mass. The percentage of insoluble

    protein increases as the lens ages and as a cataract develops.

    Definition of CataractA cataract is any opacity or discoloration of the lens, whether a small, local opacity or

    the complete loss of transparency. Clinically, the term cataract is usually reserved foropacities that affect visual acuity because many normal lenses have small, visually

    opacities. A cataract is described in terms of the zones of the lens involved in the opacity.

    These zones of opacity may be subcapsular, cortical, or nuclear and may be anterior or

    posterior in location. In addition to of the nucleus and cortex, there may be a yellow or

    amber color change to the lens. A cataract also can be described in terms of its stage of

    development. A cataract with a clear cortex remaining is immature. A mature cataract

    has a totally opacified cortex.

    EpidemiologyAge-related cataract is responsible for 48% of world blindness, which represents

    about 18 million people, according to the World Health Organization (WHO). In many

    countries surgical services are inadequate, and cataracts remain the leading cause of

    blindness. As populations age, the number of people with cataracts is growing. Cataracts

    are also an important cause of low vision in both developed and developing countries.

    Even where surgical services are available, low vision associated with cataracts may still

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    metabolites can enter the cells of the lens nucleus via the epithelium and cortex occurs

    with a subsequent decrease in the rate of transport of water, nutrients, and antioxidants.

    Consequently, progressive oxidative damage to the lens with aging takes place,

    leading to senile cataract development. Various studies showing an increase in products of

    oxidation (eg, oxidized glutathione) and a decrease in antioxidant vitamins and the enzyme

    superoxide dismutase underscore the important role of oxidative processes in

    cataractogenesis.

    Another mechanism involved is the conversion of soluble low-molecular weight

    cytoplasmic lens proteins to soluble high molecular weight aggregates, insoluble phases,

    and insoluble membrane-protein matrices. The resulting protein changes cause abrupt

    fluctuations in the refractive index of the lens, scatter light rays, and reduce transparency.

    Other areas being investigated include the role of nutrition in cataract development,

    particularly the involvement of glucose and trace minerals and vitamins.

    6. StageIn clinical, senile cataract devided to 4 stage:

    1) Insipient CataractsIn this stadium opacity start from marginal equator to anterior and posterior cortex.

    This opacity can arised poliopia because refraction index is not same in the all of lens.

    2) Immature CataractsOpacity at a part of lens. In this stadium lens volume will increase and make osmotic

    pressure increase too. Subsequently, lens more convex and occure block pupil,finally can

    arise secunder glaucoma.

    3) Mature CatarctsOpacity can found in all of lens. This opacity can occure because there is calcium

    depotitions in the lens. Fluid in the lens will remove out so that lens will back at normal

    size, anterior chambers back at normal depth and there isnt iris image at the opaque lens

    so shadow test is negative.

    4) Hipermature CataractsMass lens move out from the lens capsule so lens becomes small,yellow colored and

    dry. In the examination seen anterior chamber is deep and there is lens capsule fold. If

    cataract process continued accompanied with thicken capsule so cortex degeneration can

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    not move out and can seen like a milk pack accompanied nucleus that concentrate in basal

    lens cortex. This condition called Morgagni Cataract.

    Symptoms and Signa. Symptoms

    Many patients complain of blurred vision, which is usually worse when viewing

    distant objects. If the patient is unable to read small print, the surgeon might suspect that

    other pathology, such as macular degeneration, could be present. One must bear in mind

    that some elderly patients say that they cannot read when it is found that they can read

    small print if carefully tested. It is a curious fact that when the cataract is unilateral, the

    patient can claim that the loss of vision has been quite sudden. Elucidation of the history

    in these cases sometimes reveals that the visual loss was noted when washing and

    observing the face in the mirror.

    When one hand is lowered before the other, the unilateral visual loss is noticed for the

    first time and interpreted as a sudden event. The history in cataract cases might be further

    confused by a natural tendency for patients to project their symptoms into the spectacles,

    and several pairs might be obtained before the true cause of the problem is found. In order

    to understand the symptoms of cataract, it is essential to understand what is meant byindex myopia. This simply refers to the change in refractive power of the lens, which

    occurs as a preliminary to cataract formation. Index myopia can also result from

    uncontrolled diabetes. If we imagine an elderly patient who requires reading glasses (for

    presbyopia) in the normal way but no glasses for viewing distant objects, the onset of

    index myopia will produce blurring of distance vision, but also the patient will discover to

    his or her surprise that it is possible to read again without glasses. In the same way, the

    hypermetropic patient will become less hypermetropic and find that it is possible to see

    again in the distance without glasses. The ageing fibres in the precataractous lens become

    more effective at converging light rays so that parallel rays of light are brought to a focus

    more anteriorly in the eye. A part from blurring of vision, the cataract patient often

    complains of monocular diplopia.

    Sometimes even a slight and subtle opacity in the posterior part of the lens can cause

    the patient to notice, for example, that car rear lights appear doubled, and this can be

    reproduced with the ophthalmoscope light. Monocular diplopia is suspect symptom, the

    suggestion being that if a patient continues to see double, even when one eye is closed,

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    then he or she might not be giving an accurate history. In actual practice nothing could be

    further from the truth and this is quite a common presenting feature of cataract. Glare is

    another common presenting symptom.

    Picture 2. Opaque areas in the lens can be seen clearly

    against the red reflex.

    The patient complains that he or she cannot see so well in bright light and might even

    be wearing a pair of dark glasses. Glare is a photographic term but here it refers to a

    significant reduction in visual acuity when an extraneous light source is introduced.

    Light shining from the side is scattered in the cataractous lens and reduces the quality

    of the image on the retina. Glare becomes an important consideration when advising

    an elderly cataractous patient on fitness to drive. The visual acuity might be within the

    requirements laid down by law (seeing a number plate at 20.5 m) but only when the

    patient is tested in the absence of glare.

    A consideration of all these factors makes itrelatively easy to diagnose cataract even

    before examining the patient. To summarise, a typical patient might complain that the

    glasses have been inaccurately prescribed, that the vision is much worse in bright

    sunlight, that sometimes things look double and that there is difficulty in recognising

    peoples faces in the street rather than difficulty in reading. Patients with cataracts

    alone do not usually complain that things look distorted or that straight lines look

    bent, nor do they experience pain in the eye. Rarely, cataracts become hypermature;

    that is to say, the lens enlarges in the eye and this in turn can lead to secondary

    glaucoma and pain in the eye. Urgent surgery might be needed under these

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    circumstances. In its late stages, acataract matures and becomes white, so that

    exceptionally a patient might complain of a white spot in the middle of the pupil.

    b. Signs1) Reduced Visual Acuity

    A reduction in visual acuity can, of course, be an early sign of cataract formation but this

    is not always the case. Some patients see surprisingly well through marked lens opacities, and

    the effect on visual acuity as measured by the Snellen test type depends as much on the

    position of the opacities in the lens as on the density of the opacities.

    2) Findings of OphthalmoscopyThe best way of picking up a cataract in its early stages is to view the pupil through the

    ophthalmoscope from a distance of about 50 cm. In this way, the red reflex is clearly seen.

    The red reflex is simply the reflection of light from the fundus and it is viewed in exactly the

    same manner that one might view a cats eyes in the headlamps of ones car or the eyes of

    ones friends in an illjudged flash photograph. In fact, such a flash photo could well show up

    an early cataract if an elderly relative were included in the photograph. When using the

    ophthalmoscope, the opacities in the lens are often seen as black spokes against the red

    reflex. It is important to focus ones eyes onto the plane of the patients pupil if the cataract isto be well seen, and it is preferable to dilate the pupil beforehand or at least examine in a

    darkened room. Typical age-related lens opacities are wedge shaped, pointing towards the

    centre of the pupil. At the same time, the central nucleus of the lens can take on a yellowish-

    brown colour, the appearance being termed lens sclerosis, and ultimately, the lens can

    become nearly black in some instances. After inspecting a cataract with the ophthalmoscope

    held at a distance from the eye, one must then approach closer and attempt to examine the

    fundus. Further useful information about the density of the cataract can be obtained in this

    way. It is generally true that if Cataract Opaque areas in the lens can be seen clearly against

    the red reflex. the observer can see in, the patient can see out. If there is an obvious

    discrepancy between the clarity of the fundus and the visual acuity of the patient, some other

    pathology might be suspected. Sometimes the patient might not have performed too well on

    subjective testing and such an error should be apparent when the fundus is viewed. Some

    types of cataract can be misleading in this respect and this applies particularly to those seen in

    highly myopic patients. Here, there is sometimes a preponderance of nuclear sclerosis, which

    simply causes distortion of the fundus while the disc and macula can be seen quite clearly.1

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    ManagementAt the present time, there is no effective medical treatment for cataract in spite of a

    number of claims over the years. A recent report has suggested that oral aspirin can delay the

    progress of cataract in female diabetics. Although this might be expected to have some effect

    on theoretical grounds, any benefit is probably marginal. Occasionally, patients claim that

    their cataracts seem to have cleared, but such fluctuation in density of the lens opacities has

    not been demonstrated in a scientific manner. Cataracts associated with galactosaemia are

    thought to clear under the influence of prompt treatment of the underlying problem. Cataract

    is, therefore, essentially a surgical problem, and the management of a patient with cataract

    depends on deciding at what point the visual impairment of the patient justifies undergoing

    the risks of surgery. The cataractoperation itself has been practiced since pre-Christian times,

    and developments in recent years have made it safe and effective in a large proportion of

    cases. The operation entails removal of all the opaque lens fibres from within the lens capsule

    and replacing them with a clear plastic lens. Common Eye Diseases and their Management In

    the early part of the last century the technical side of cataract surgery necessitated waiting for

    the cataract to become ripe.Nowadays no such waiting is needed and it is theoretically

    possible to remove a clear lens. The decision to operate is based on whether the patient will

    see better afterwards. Modern cataract surgery can restore the vision in a remarkable way and

    patients often say that theyhave not seen so well for many years. Indeed, many patients have

    quite reasonable vision without glasses but this cannot be guaranteed and, because the plastic

    lens implant gives a fixed focus, glasses will inevitably be needed for some distances.

    Probably the worst thing that can happen after the operation is infection leading to

    endophthalmitis and loss of the sight of the eye. Although this only occurs in about one out of

    a thousand cases, the patient contemplating cataract surgery needs to be aware of the

    possibility. Before the operation, it is now a routine to measure the length of the eye and the

    corneal curvature.Knowing these two measurements, one can assess the strength of

    lensimplant that is needed. When deciding on thestrength of implant, it is necessary to

    considerthe other eye. The aim is usually to make the two eyes optically similar because

    patients find it difficult to tolerate two different eyes.

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    b. When To Operate

    Even though the decision to operate on a cataract must be made by the ophthalmic

    surgeon, optometrists and the nonspecialist general practitioner need to understand the

    reasoning behind this decision. Elderly patients tend to forget what they have been told in the

    clinic and might not, for example, understand why cataract surgery is being delayed when

    macular degeneration is the main cause of visual loss. An operation is usually not required if

    the patient has not noticed any problem, although sometimes the patient can deny the

    problem through some unexpressed fear. The requirements of the patient need to be

    considered; those of the chairbound arthritic 80-year-old subject who can still read small print

    quite easily are different from the younger business person who needs to be able to see a car

    number plate at 20.5 m in order to drive. The visual acuity by itself is not always a reliable

    guide.Some patients who have marked glare might need surgery with a visual acuity of 6/9,

    whereas others with less visual demands might be quite happy with a vision of 6/12 or 6/18.

    Early surgery might be needed to keep a joiner or bus driver at work for which good

    binocular vision is needed.

    b. The Cataract Operation

    The definitive management for senile cataract is lens extraction. Over the years, various

    surgical techniques have evolved from the ancient method of couching to the present-day

    technique of phacoemulsification. Almost parallel is the evolution of the IOLs being used,

    which vary in ocular location, material, and manner of implantation. Depending on the

    integrity of the posterior lens capsule, the 2 main types of lens surgery are the intracapsular

    cataract extraction (ICCE) and the extracapsular cataract extraction (ECCE). Below is a

    general description of the 3 commonly used surgical procedures in cataract extraction,

    namely ICCE, standard ECCE, and phacoemulsification. Reading books on cataract surgeriesfor a more in-depth discussion of the topic, particularly with regard to technique and

    procedure, is also recommended.4

    1). Intracapsular cataract extraction

    Prior to the onset of more modern microsurgical instruments and better IOLs, ICCEwas the preferred method for cataract removal. It involves extraction of the entire

    lens, including the posterior capsule. In performing this technique, there is no need to

    worry about subsequent development and management of capsular opacity. The

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    technique can be performed with less sophisticated equipment and in areas where

    operating microscopes and irrigating systems are not available.

    However, a number of disadvantages and postoperative complications accompanyICCE. The larger limbal incision, often 160-180, is associated with the following

    risks: delayed healing, delayed visual rehabilitation, significant against-the-rule

    astigmatism, iris incarceration, postoperative wound leaks, and vitreous incarceration.

    Corneal edema is a common intraoperative and immediate postoperative

    complication.

    Furthermore, endothelial cell loss is greater in ICCE than in ECCE. The same is trueabout the incidence of postoperative cystoid macular edema (CME) and retinal

    detachment. The broken integrity of the vitreous can lead to postoperative

    complications even after a seemingly uneventful operation. Finally, because the

    posterior capsule is not intact, the IOL to be implanted must either be placed in the

    anterior chamber or sutured to the posterior chamber. Both techniques are more

    difficult to perform than simply placing an IOL in the capsular bag and are associated

    with postoperative complications, the most notorious of which is pseudophakic

    bullous keratopathy.5

    Although the myriad of postoperative complications has led to the decline inpopularity and use of ICCE, it still can be used in cases where zonular integrity is too

    severely impaired to allow successful lens removal and IOL implantation in ECCE.

    Furthermore, ICCE can be performed in remote areas where more sophisticated

    equipment is not available.

    ICCE is contraindicated absolutely in children and young adults with cataracts andcases with traumatic capsular rupture. Relative contraindications include high myopia,

    Marfan syndrome, morgagnian cataracts, and vitreous presenting in the anterior

    chamber.

    2. Extracapsular cataract extractionIn contrast to ICCE, ECCE involves the removal of the lens nucleus through an

    opening in the anterior capsule with retention of the integrity of the posterior capsule.

    ECCE possesses a number of advantages over ICCE, most of which are related to an

    intact posterior capsule, as follows:

    A smaller incision is required in ECCE, and, as such, less trauma to the cornealendothelium is expected.

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    Short- and long-term complications of vitreous adherence to the cornea, iris, andincision are minimized or eliminated.

    A better anatomical placement of the IOL is achieved with an intact posterior capsule.

    An intact posterior capsule also (1) reduces the iris and vitreous mobility that occurswith saccadic movements (eg, endophthalmodonesis), (2) provides a barrier

    restricting the exchange of some molecules between the aqueous and the vitreous, and

    (3) reduces the incidence of CME, retinal detachment, and corneal edema.

    Conversely, an intact capsule prevents bacteria and other microorganismsinadvertently introduced into the anterior chamber during surgery from gaining access

    to the posterior vitreous cavity and causing endophthalmitis.

    Secondary IOL implantation, filtration surgery, corneal transplantation, and woundrepairs are performed more easily with a higher degree of safety with an intact

    posterior capsule.

    The main requirement for a successful ECCE and posterior capsule IOL implantation

    is zonular integrity. As such, when zonular support is insufficient or appears suspect to

    allow a safe removal of the cataract via ECCE, ICCE or pars plana lensectomy should be

    considered.

    3.Standard ECCE and phacoemulsificationStandard ECCE and phacoemulsification are similar in that extraction of the lens

    nucleus is performed through an opening in the anterior capsule or anterior capsulotomy.

    Both techniques also require mechanisms to irrigate and aspirate fluid and cortical

    material during surgery. Finally, both procedures place the IOL in the posterior capsular

    bag that is more anatomical than the anteriorly placed IOL.

    Needless to say, significant differences exist between the 2 techniques. Removal of the

    lens nucleus in ECCE can be performed manually in standard ECCE or with an

    ultrasonically driven needle to fragment the nucleus of the cataract and then to aspirate

    the lens substrate through a needle port in a process termed phacoemulsification.

    The more modern of the 2 techniques, phacoemulsification offers the advantage of

    using smaller incisions, minimizing complications arising from improper wound closure,

    and affording more rapid wound healing and faster visual rehabilitation. Furthermore, it

    uses a relatively closed system during both phacoemulsification and aspiration with better

    control of intraocular pressure during surgery, providing safeguards against positive

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    vitreous pressure and choroidal hemorrhage. However, more sophisticated machines and

    instruments are required to perform phacoemulsification.

    Ultimately, the choice of which of the 2 procedures to use in cataract extraction

    depends on the patient, the type of cataract, the availability of the proper instruments, and

    the degree at which the surgeon is comfortable and proficient in performing standard

    ECCE or phacoemulsification

    GLAUCOMA

    A condition of increased fluid pressure inside the eye so it make the compression of the

    retina and the optic nerve then make the nerve damage end.

    Glaucoma can cause partial vision loss, with blindness as a possible eventual outcome

    one of the leading causes of blindness, is estimated to affect 1 of every 50 adults. This is

    the diagram of pathophysiology of glaucoma.

    There are some risk factor of glaucoma:

    Age Family History Drug consumption (steroid) Trauma Severe Hypermethrophya Other systemic disease (ex ; DM, Hypertension)

    The classification may include:

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    1. Open Angle Glaucoma2. Angle closure glaucoma3. Congenital Glaucoma4. Secondary glaucoma

    Glaucoma can be divided roughly into two main categories, "open angle" and "closed angle"

    glaucoma.

    Open Angle Glaucoma

    Primary open-angle glaucoma (POAG), the most common form of glaucoma, accounts

    for 6070% of all glaucomas and 9095% of primary glaucomas. POAG is a bilateral,

    chronic progressive condition that typically appears in individuals over 60 years of

    age.

    Symptoms

    a) asymptomatic (as moderately elevated IOP usually causes no symptoms but the IOP is

    still high enough to cause glaucomatous optic neuropathy)

    b) loss of part of their visual field cf tunnel vision

    c) blindness in one or both eyes (advanced optic nerve damage)

    Genetic factors are important and therefore the family history should be considered.

    Signs

    a) open angle

    b) elevated IOP

    c) glaucomatous optic nerve cupping

    d) may have visual field loss

    Mild glaucomatous cupping Advanced glaucomatous cupping

    The goal is to maintain IOP less than 21 mmHg and continued visual field loss should be

    minimal. In fact, medications have been shown to control IOP in 6080% of patients over

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    a five-year period. Various treatmentmodalities include medical treatment, laser

    therapy,and surgery. Patients will initially start with topical ocular drug therapy.

    Prognosis : If discovered early and treated adequately, the prognosis for POAG is excellent.

    Closure Angle Glaucoma

    Less than 5% of all primary glaucomas. Requires immediate attention within hours to

    avoid dramatic vision loss. In primary the pathophysiology is a shallow ocular anterior

    chamber so the angle between the cornea and iris become narrow.This creates a situation

    where pupil dilation can physically occlude the trabecular meshwork. And secondary

    angle-closure glaucoma results from any type of blockage throughout this drainage

    pathway.

    figure. Primary close angle glaucoma

    Diagnosis is determined by visualization of the angle by gonioscopy as well as provoking an IOP

    increase through mydriasis (dark room test) or by gravity (prone test).

    Treatment of angle-closure glaucoma

    Requires a rapid reduction in IOP to prevent a hypertensive event and ultimately preserve vision.

    For an acute hypertensive attack it can be given pilocarpine or secretory inhibitors (topical B-blockers, a2-agonists, CAIs). At IOPs greater than 60 mmHg, the iris becomes ischemic and may

    be unresponsive to pilocarpine even at high and frequent doses. An osmotic agent (oral glycerin,

    oral isosorbide, and intravenous Mannitol) is usually administered because of its rapid lowering

    of IOP. A peripheral iridectomy should be performed only when IOP is controlled.

    Normal-Tension Glaucoma

    Condition in which optic nerve damage and vision loss have occurred despite a normal pressure

    inside the eye (TIO< 21 mmHg). The patient has open, normal-appearing angles. In fact, the

    features of normal-tension glaucoma are similar to primary open-angle glaucoma.

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    The pathogenesis because of abnormal sensitivity to intraocular pressure caused by vascular or

    mechanically in the optical nerve

    Others sign & symptoms:

    Spasm of phertpheral vesselChepalgiaHipotension at nightDecrease of blood flow

    Primary Congenital Glaucoma

    Primary congenital glaucoma present at birth; however, but its manifestations may not be

    recognized until infancy or early childhood. The pathophysiology of primary congenital glaucoma

    is restricted to a developmental abnormality that affects the trabecular meshwork. Primarycongenital glaucoma estimated to affect fewer than 0.05% of ophthalmic patients. The disease is

    bilateral in approximately 75% of cases.

    Primary congenital glaucoma usually is diagnosed at birth or shortly thereafter, and most cases are

    diagnosed in the first year of life. Most cases are sporadic in occurrence and may be transmitted

    through an autosomal recessive pattern. Male patients are found to have a higher incidence of the

    disease, comprising approximately 65% of cases.

    The triad of manifestations of primary congenital glaucoma are epiphora,photophobia , and

    blepharospasm. Blepharospasm is a spasm and closure of the eyelids.

    Physically of congenital glaucoma there was:

    Changes within the cornea, especially within the first few years of life, provide strongadditional support for the diagnosis.

    Enlargement of the cornea The early presence of glaucoma may deepen the anterior chamber. Because of the

    frequent occurrence of iris abnormalities in many types of both primary and

    secondary childhood glaucomas, the iris and angles always should be studied

    carefully and with thorough gonioscopy.

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    The optic nerve head is usually abnormal. Variable cupping is present, usuallyannular in form, with nasalization of vessels and preservation of the well-vascularized

    rim. Pallor is first seen temporally when present at an advanced stage.

    The Treatment of Congenital Glaucoma

    Unlike adult glaucoma, the initial treatment for congenital glaucoma is often surgical. A

    drainageangle surgery is often recommended for congenital glaucoma.

    Secondary Glaucoma

    Glaucoma can occur as the result of an eye injury, inflammation, tumor or in advanced cases of

    cataract or diabetes. It can also be caused by certain drugs such as steroids. This form of

    glaucoma may be mild or severe.The type of treatment will depend on whether it is open-angle orangle-closure glaucoma.

    Pseudoexfoliative Glaucoma

    This form of secondary open-angle glaucoma occurs when a flaky, dandruff-like material peels

    off the outer layer of the lens within the eye. The material collects in the angle between the cornea

    and iris and can clog the drainage system of the eye, causing eye pressure to rise.

    Pseudoexfoliative Glaucoma is common in those of Scandinavian descent. Treatment usuallyincludes medications or surgery.

    Pigmentary Glaucoma

    A form of secondary open-angle glaucoma, this occurs when the pigment granules in the back of

    the iris (the colored part of the eye) break into the clear fluid produced inside the eye. These tiny

    pigment granules flow toward the drainage canals in the eye and slowly clog them, causing eye

    pressure to rise. Treatment usually includes medications or surgery.

    Traumatic Glaucoma

    Injury to the eye may cause secondary open-angle glaucoma. This type of glaucoma can occur

    immediately after the injury or years later.

    It can be caused by blunt injuries that bruise the eye (called blunt trauma) or by injuries that

    penetrate the eye.

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    In addition, conditions such as severe nearsightedness, previous injury, infection, or prior surgery

    may make the eye more vulnerable to a serious eye injury.

    Neovascular Glaucoma

    The abnormal formation of new blood vessels on the iris and over the eyes drainage channels can

    cause a form of secondary open-angle glaucoma.

    Neovascular glaucoma is always associated with other abnormalities, most often diabetes. It never

    occurs on its own. The new blood vessels block the eyes fluid from exiting through the trabecular

    meshwork (the eyes drainage canals), causing an increase in eye pressure. This type of glaucoma

    is very difficult to treat.

    Irido Corneal Endothelial Syndrome (ICE)

    This rare form of glaucoma usually appears in only one eye, rather than both. Cells on the back

    surface of the cornea spread over the eyes dra inage tissue and across the surface of the iris,

    increasing eye pressure and damaging the optic nerve. These corneal cells also form adhesions

    that bind the iris to the cornea, further blocking the drainage channels.

    Irido Corneal Endothelial Syndrome occurs more frequently in light-skinned females. Symptoms

    can include hazy vision upon awakening and the appearance of halos around lights. Treatment can

    include medications and filtering surgery. Laser therapy is not effective in these cases.

    Absolute Glaucoma

    Absolute glaucoma is the end stage of glaucoma (open angle/angle closure glaucoma). The

    clinical sign patien have total blindness. In absolute glaucoma, the cornea looks not clear, shallow

    of the chamber, athrofi of papil with excavation of glaucomatous, the eye become harder like a

    stone dan also painfull.

    The treatment of absolute glaucoma can by given beta light into ciliary body for compres the

    function of ciliarybody or doing the nucleation because the eye doesnt have function anymore so

    the eye cant painfull anymore.

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    CHAPTER III

    CASE REPORT

    1. Patient identityName : Mrs. S

    Sex : female

    Age : 84 years old

    Address : Kuala Secapah

    Job : housewife

    Religion : Moslem

    Patient was examined on January 21st, 2014

    2. Anamnesis Main complaint :

    Red eye, watery, blindness. History of desease :

    Patient complains blurry vision is affected in right eye. Blurry vision of the

    right eye since a few months ago, that become worse especially during this

    two weeks. Then, she told that her eye became redness until now. Not only

    red, but also pain and watery. Now, patient have cloudy in her eye (right eye),

    so patient really cant see anything from right eye. She also complaining the

    blurry vision at the left eye. Sometimes she had a headache. The

    manifestation of clinical from this patient : Headache (+), pain in the eyes (+),

    redness in the eye (+ right eye), itch feeling in the eyes (-), and traumatic

    history (-).

    Past clinical history :

    Hypertension (-) Diabetes Mellitus (denied) because patient never did clinical check. Glasses wearing (-) Traumatic history (-)

    Family history Hypertension (-) Diabetes Mellitus (-) Glasses wearing (-)

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    3. General Physical assestmentGeneral condition : Moderate

    Awareness : Compos mentis

    Vital sign :

    a. Blood Pressure : 130/90 mmHgb. RR : 18/minutec. Temperture : 36,5C

    4. Ophthalmological statusVisual acuity :

    a. OD : 0b. OS : 6/12c. Last glasses : the patient never use glasses

    OD OS

    Ortho Eye ball position Ortho

    Eye Movement

    Movement(+), ptosis (-),

    lagoftalmos (-)

    Palpebra Movement (+), ptosis (-),

    lagoftalmos (-)

    redness (+), discharge (-),

    degeneration plaque (-), foreign

    body (-), injection (-)

    conjungtiva redness (-), discharge (-),

    degeneration plaque (-), foreign

    body (-), injection (-)

    ulcer (-)

    arcus senilis (+)

    Cornea ulcer (-)

    arcus senilis (+)

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    Not clear Anterior chamber clear, deep impression

    Iris colour : brown, sinekia (-)

    Circular pupil, isochore

    Iris/pupil Iris colour : brown, sinekia (-)

    Circular pupil, isochore

    Milky Lense Cloudy

    - Shadow test +

    - Fundus -

    Shadow test : negatif (- right eye) , positive (+ left eye) Intra Ocular pressure (tonometry) : OD 26 mmHg, OS 15 mm Hg Funduscopy : - Visual field test: OD cannot be done, OS normal

    5. ResumeA woman, 84 years old, came to ophthalmologist with the complain of blurry

    vision in right eye since a few months ago, and become worse during this two weeks.

    She told that her eye became redness until now. Not only red, but also pain and

    watery. Now, patient have cloudy in her eye (right eye), so patient really cant see

    anything from right eye. She also complaining the blurry vision at the left eye.

    Sometimes she had a headache. The manifestation of clinical from this patient

    Headache (+), pain in the eyes (+), redness in the eye (+ right eye), watery (+), itch

    feeling in the eyes (-), and traumatic history (-).

    Visual acuity is 0 for OD, 6/12 for OS. Right lense seems milky. Left lense

    seems cloudy. Intraocular presure for OD 26mmHg, for OS 15 mmHg. Funduscopy

    cannot be done because of the lense opacity. Shadow test for left eye is positive.

    Confrontation test just be done at the left eye and the result is normal.

    6. DiagnosisDiagnose :

    a. OD : mature cataract with secondary glaucoma (absolute glaucoma)b. OS : immature cataract (senilis)

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    DDx :

    OD : hipermature cataract with absolute galucoma OS : -

    7. Plan for examinationa. Slit lamp

    b. Perimetric. Whole blood test and blood glucosed. Eyes USG

    8. Treatmenta. OD

    i. Pharmacological:1. Timolol2. Asetazolamide

    ii. Surgery : Extra Capsular Cataract Extraction

    b. OSi. Non-pharmacological

    1. Using eye protection

    ii. Surgery : Pachoemulsification + IOL9. Prognosis

    a. OD:i. Ad vitam : bonam

    ii. Ad functionam : malamiii. Ad sanactionam : dubia ad malam

    b. OS :i. Ad vitam : bonam

    ii. Ad functionam : dubia ad bonamiii. Ad sanactionam : dubia ad bonam

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    CHAPTER IV

    DISCUSSION

    A woman, 84 years old complained blurry vision clinic with complain redness,

    painfull, watery, even blindness in the right eye since a few months ago. The history before

    the eye became redness, patient had migrain at right part of head. The pain felt into her right

    eye. Then, she told that her eye became redness until now. Not only red, but also pain and

    watery. Now, patient have cloudy in her eye (right eye) , so patient really cant see anything

    from her right eye. There were no history of eye trauma.

    Visual acuity is 0 for OD, 6/12 for OS. Palpebra, conjunctiva, cornea and anterior

    chamber is inspected normally, while the right lens seems milky and the left eye seems

    blurry. No foreign body was found. Intra ocular pressure is 26 mmHg for OD, 15 mmHg for

    OS. Funduscopy cannot be done because of the lense opacity. Confrontation test for OD

    cannot be described, and for OS is normal, shadow test negative for right eye and positive for

    left eye.

    The abnormality found in physical examination is the opacity of the lens. We can get

    rid of inherited disorders because the patient is geriatric, and new phenomena arising in

    recent years. In addition, the symptoms that arise in these patients as well as typicalsymptoms of cataract, like the the visual loss is slowly, and there is a cloud on the view that

    closes the view. Beside the opacity of left lense, the shadow test results is positive.

    In lens assesment found that at the right eye the lens is totally opaque, milky

    appearance, funduscopy cant be done cause the light cant passes through the lens and it

    indicated that is mature cataract at the right eye and for the left eye the lens looks cloudy and

    shadow test is positive (+), show that it is an immature cataract at the left eye.

    These are some discussion about the clinical finding from the anamnesis and

    examination to the patient :

    Blurred vision is caused by the opacity of the lense, that can cause disrupting therefraction media and finally, it can hampered the light to retinal

    Vision slowly burred because of the progression of opacity in the lense (thickness ofopacity influence the degree of vision lost)

    VA : 0 for OD with good projection, 6/12 for OS opacity of OD is thicker thanOSso OD must be treated firstly

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    Based on the examination, known that the visual acuity for right eye is 0. The

    patient cant see at all, even with light perception.

    There are some specific symptoms that can lead to diagnose the condition of the

    right eye. The IOP level for right eye is measure 26 mmHg. It indicated the raised of

    IOP greater than normal range. Raised IPO is determine by the balance between

    aqueous production inside the eye and aqueous drainage of the eye through the

    trabecular meshwork. The resistance to outflow through the trabecular meshwork

    gradually increase, causing the damage to the nerve. Pressure on the nerve fibres and

    chronic ischaemia at the optic nerve head cause damage to the retinal nerve fibres that

    leads to rapid loss of vision. Once optic nerve damage is occured, it cannot be

    repaired. It indicated that is absolute glaucoma at the right eye.

    In mature cataract, there is degenerative lens capsule that cause the material out

    from the lens and enter the anterior chamber,stuck at the trabecular meshwork, block

    the drainage angle and cause the problem in excretion of aqueous humor. Type of

    glaucoma of this patient is absolute glaucoma indicated by the high level of IOP,

    visual acuity is 0, and the pain sensation inside the eye. So, the diagnosis of the right

    eye is absolute glaucoma e.c mature cataract

    Treatment to this patient is to lower the IOP. Common medical therapy that

    used in this condition are combination of beta-blocker and carbonic anhidrase

    inhibitor, such as timolol 0,5 % and asetazolamide. Both of them action on the

    secretion system, that result the decrease in producing aqueous from ciliary body.

    Definitive therapy for both eye is surgery. For the right eye should be treated by lens

    extraction. Medication that given to lower the IOP is aimed to controls the IPO and

    can minimize the symptoms. For the left eye with immature cataract the

    phacoemulsification is choosen as the therapy.

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    CHAPTER V

    CONCLUSION

    The diagnosis of this patient is Mature Cataract with Secondary right eye. And for

    the right eye is immature cataract. The therapy for OD is doing the treatment of glaucoma

    and surgery for the lens extraction.

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    BIBLIOGRAPHY

    1. Cynthia AB, basic ophthalmology For Medical Studens and Primary Care Residents,Seventh Edition, electronic book. American Academy Of ophthalmology, 1999.

    2. Ilyas, S.Ilmu Penyakit Mata. Edisi 3. Jakarta. Balai Penerbit FKUI. 20073. Galloway NR, Amoaku WMK, Galloway PH, Browing AC. Common Eye diseases and

    Their Management, electronic book.Springer-Verlag London, 2010

    4. Gnter K. Krieglstein, MD and friends.Glaucoma. Springer-Verlag Berlin Heidelberg.Germany.2008

    5. Olver, J. and Cassidy, L., 2005. Ophthalmology at a Glance. Australia: BlackwellPublishing Company

    6. Vaughan D. G, Asbury, T. Eva, P.R. Oftalmologi umum. EGC. Jakarta. 2000