CHAPTER I

INTRODUCTION

Worldwide more than 285 million people are affected by diabetes mellitus.

This number is expected to increase to 439 million by 2030 according to the

International Diabetes Federation.1

A cataract is present when the transparency of the lens is reduced to the

point that the patient’s vision is impaired. The term cataract comes from the Greek

word katarraktes (downrushing; waterfall) because earlier it was thought that the

cataract was a congealed fluid from the brain that had flowed in front of the lens.

Cataract is considered a major cause of visual impairment in diabetic patients as

the incidence and progression of cataract is elevated in patients with diabetes

mellitus. The association between diabetes and cataract formation has been shown

in clinical epidemiological and basic research studies. Due to increasing numbers

of type 1 and type 2 diabetics worldwide, the incidence of diabetic cataracts

steadily rises. Even though cataract surgery, the most common surgical

ophthalmic procedure worldwide, is an effective cure, the elucidation of

pathomechanisms to delay or prevent the development of cataract in diabetic

patients remains a challenge. Furthermore, patients with diabetes mellitus have

higher complication rates from cataract surgery. Both diabetes and cataract pose

an enormous health and economic burden, particularly in developing countries,

where diabetes treatment is insufficient and cataract surgery often inaccessible.2

CHAPTER II

LITERATURE REVIEW

1.1. Anatomy and Physiology of the Lens

The lens is one of the essential refractive media of the eye and focuses

incident rays of light on the retina. It adds a variable element to the eye’s total

refractive power (10 – 20 diopters, depending on individual accommodation) to

the fixed refractive power of the cornea (approximately 43 diopters).

The fully developed lens is a biconvex, transparent structure. The curvature

of the posterior surface, which has a radius of 6 mm, is greater than that of the

anterior surface, which has a radius of 10 mm. The lens is approximately 4 mm

thick , and its weight increases with age to five times its weight at birth. An adult

lens weighs about 220 mg.

The lens lies in the posterior chamber of the eye between the posterior

surface of the iris and the vitreous body in a saucer-shape d depression of the

vitreous body known as the hyaloid fossa. Together with the iris it forms an

optical diaphragm that separates the anterior and posterior chambers of the eye.

Radially arranged zonule fibers that insert into the lens around its equator connect

the lens to the ciliary body. These fibers hold the lens in position and transfer the

tensile force of the ciliary muscle

Pict 1. Anatomy of the lens

1.2. Definition of Cataract

Cataract is a opacity of the lens of the eye, which occurs when fluid gathers

between the lens fibres. The refractive index alters and causes light scatter with

resultant blurred vision.. 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.

Picture 2. Lens in Cataract

1.3. Epidemiology

In 2002, the World Health Organization calculated that the number of

visually impaired people worldwide was in excess of 161 million. Cataract is the

leading cause, accounting for 47.8% of all cases. The estimated global costs of

blindness and low vision in 2000 was estimated at US$42 billion. There are also

hidden costs of cataract blindness. Each person who is blind requires a caregiver,

placing demands on one tenth of their time so reducing their economic activity.

Over the next 20 years it is estimated that the world’s population will increase by

about one third, this growth occurring predominantly in developing countries.

During the same period, the number of people over the age of 65 years will more

than double. Therefore, there will be approximate doubling in the incidence of

cataract, visual morbidity, and need for cataract surgery. But questions remain,

such as, how much cataract is enough to warrant surgery, how should it be

performed and delivered, and how should it be paid for? In the developed world,

the threshold for cataract surgery is now 20/30 (6/9) or less, which has resulted in

a three- to fourfold increase in patients receiving surgery with an associated

increased need for resources and funding. The challenge is to determine at what

visual acuity level a government or insurer should pay for surgery, and how to

allocate resources appropriately.

1.4. Etiology

Cataract can be caused by many etiology that have manifestation in opacity

in lens, such as:

a. Age

b. Trauma

c. Systemic disorders (diabetes, galaktosemia)

d. Ocular diseases

e. Toxic causes (steroid, anticholinesterase)

f. Congenital (dominant, sporadic or part of a syndrome, abnormal

galactose metabolism, hypoglycaemia)

g. Associated with inherited abnormality (myotonic dystrophy,

h. Central nervous system disorders

1.5. Symptoms

Development of the cataract and its symptoms is generally an occult

process. Patients experience the various symptoms such as seeing only shades of

gray, visual impairment, blurred vision, distorted vision, glare or star bursts,

monocular diplopia, altered color perception, etc. to varying degrees, and these

symptoms will vary with the specific type of cataract.

Picture 3. Symptom Cataract

1.6. Classification

Cataracts may be classified according to time of occurence and maturity.

From classified by time, there are acquired cataract (senile cataract, cataract with

systemic disease, secondary and complicated cataract, traumatic and toxic

cataract) that cause 99% etiology of cataract and congenital cataract thta less than

1% of all cataract etiology.

a. Senile cataract

In the fourth decade of life, the pressure of peripheral lens fiber

production causes hardening of the entire lens, especially t he nucleus. The

nucleus takes on a yellowish brown color (brunescent nuclear cataract).This

may range from re ddish brown to nearly black discoloration of the entire

lens (black cataract). Because they increase t he refractive power of t he

lens, nuclear cataracts lead to lenticular myopia and occasionally produce a

second focal point in the lens with resulting monocular diplopia.

Nuclear cataracts are of ten associate d with changes in the lens cortex. It is

interesting to note that patients with cortical cataracts tend to have acquired

hyperopia in contrast to patients with nuclear cataracts, who tend to be

myopic.

b. Cataract with systemic disease

Diabetic cataract. The typical diabetic cataract is rare in young diabetic

patients. Transient metabolic decompensation promotes the occurrence of a

typical radial snowflake pattern of cortical opacities (snowflake cataract).

Transient hyperopia and myopia can occur. Diabetic cataract progresses

rapidly. Senile cataracts are observed about five times as often in older

diabetics as in patients the same age with normal metabolism. These

cataracts usually also occur two to three years earlier.

Galactosemic cataract. This deep posterior cortical opacity begins after

birth. Galactosemia is a rare cause of early cataract in children lacking an

enzyme required to metabolize galactose. The newborn receives ample

amounts of galactose in the mother’s milk . Due a lack of uridyl transferase,

or less frequently galactokinase, galactose cannot be metabolized to glucose,

and the body becomes inundated with galactose or with galactose and

galactose-1-phosphate. If the disorder is diagnosed promptly and the child is

maintained on a galactose-free diet, the opacities of the first few week s of

life will be reversible. Galactosemic cataract is the only form of cataract that

responds to conservative therapy.

Dialysis cataract. Hemodialysis to eliminate metabolic acidosis in renal

insufficiency can disturb the osmotic equilibrium of lens metabolism and

cause swelling of t he cortex of the lens.

Cataract with myotonic dystrophy. Opacities f irst occur between the ages

of 30 and 50, initially in a thin layer of the anterior cortex and later also in

the subcapsular posterior cortex in the form of rosettes. Detecting these

opacities is important for differential diagnosis as cataracts do not occur in

Thomsen’s disease (myotonia congenita) or Erb’s progressive muscular

dystrophy. Symptoms that confirm the diagnosis include cataract, active

signs of myotonia (delayed opening of the f ist), and passive signs of

myotonia (decreased relaxation of muscles in the extremities following

direct percussion of the muscle and absence of reflexes).

Tetany cataract. The opacity lies within a broad zone inferior to the

anterior lens capsule and consists of a series of gray punctate lesions.

Symptoms that confirm the diagnosis include low blood calcium levels, a

positive hyperventi-lation test, and signs of tetany: positive Chvostek,

Trousseau, and Erb signs.

Dermatogenous cataract. This may occur with chronic neurodermatitis, less

frequently with other skin disorders s uch as scleroderma, poikiloderma,and

chromic eczema. Characteristic signs include an anterior c rest-shaped

thickening of the protruding center of the capsule.

c. Complicated Cataracts

This form of cataract can occur as a complication of any protracted

intraocular inflammation, especially heterochromia, chronic iridocyclitis,

retinal vasculitis, and retinitis pigmentosa. The result is a pumice-like

posterior subcapsular cataract that progresses axially toward the nucleus.

This form of cataract produces extreme light scattering.

d. Cataract after Surgery

Cataracts usually develop earlier in the operated eye as compared to

the opposite, non-operated eye after intraocular surgery. This applies

especially to f iltering operations. A secondar y cataract will generally occur

following vitrectomy and silicone oil tamponade.

e. Traumatic Cataract

The incidence of these lens opacities is higher in men than in women due to

occupational and sports injuries.

Contusion cataract: Contusion of t he eyeball will produce a rosette-

shaped subcapsular opacity on the anterior surface of the lens. I t will

normally remain unchanged but will migrate into the deeper cortex over

time due to the apposition of new fibers

Infrared radiation cataract (glassblower’s cataract): This type of cataract

occurs af ter decades of prolonged exposure to the infrared radiation of fire

without eye protection. Characteristic findings include splitting of the

anterior lens capsule, whose edges will be observed to curl up and float in

the anterior chamber. Occupational safety regulations have drastically

reduced the incidence of t his t ype of cataract.

Picture 4. Radiation on eye

Electrical injury: This dense subcapsular cataract can be caused by

lightning or high-voltage electrical shock.

Then classified by maturity, there are insipient cataract, immature cataract,

mature cataract, and hypermature cataract.

a. Insipient Cataract

In 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.

b. Immature Cataract

Opacity at a part of lens. In this stadium lens volume will increase that

is caused by increased of osmotic pressure. Subsequently, lens become more

convex and can block the flow of aqueous humor and finally result on

secondary glaucoma.

Picture 5. Immature cataract

c. Mature Cataract

Opacity can found in all of lens. This opacity can occur 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 isn’t iris image at the opaque lens so shadow test is negative.

Picture 6. Mature Cataract

d. Hipermature Cataract

If a mature cataract progresses to the point of complete liquification of

the cortex, the dense brown nucleus will subside within the capsule. Its

superior margin will then be visible in the pupil as a dark brown silhouette

against the surrounding grayish white cortex. The pressure in the lens

capsule decreases. The contents of the limp and wrinkled capsular bag

gravitate within the capsule. This condition, referred to as Morgagni’s

cataract , is the final stage in a cataract that has usually develope d over the

course of two decades.

Picture 7. Hypermature Cataract

1.7. Pathogenesis of Diabetic Cataract

The enzyme aldose reductase (AR) catalyzes the reduction of glucose to

sorbitol through the polyol pathway, a process linked to the development of

diabetic cataract. Extensive research has focused on the central role of the AR

pathway as the initiating factor in diabetic cataract formation.

It has been shown that the intracellular accumulation of sorbitol leads to

osmotic changes resulting in hydropic lens fibers that degenerate and form sugar

cataracts. In the lens, sorbitol is produced faster than it is converted to fructose by

the enzyme sorbitol dehydrogenase. In addition, the polar character of sorbitol

prevents its intracellular removal through diffusion. The increased accumulation

of sorbitol creates a hyperosmotic effect that results in an infusion of fluid to

countervail the osmotic gradient. Animal studies have shown that the intracellular

accumulation of polyols leads to a collapse and liquefaction of lens fibers, which

ultimately results in the formation of lens opacities. These findings have led to the

“Osmotic Hypothesis” of sugar cataract formation, emphasizing that the

intracellular increase of fluid in response to AR-mediated accumulation of polyols

results in lens swelling associated with complex biochemical changes ultimately

leading to cataract formation.

Furthermore, studies have shown that osmotic stress in the lens caused by

sorbitol accumulation induces apoptosis in lens epithelial cells (LEC) leading to

the development of cataract. Transgenic hyperglycemic mice overexpressing AR

and phospholipase D (PLD) genes became susceptible to develop diabetic cataract

in contrast to diabetic mice overexpressing PLD alone, an enzyme with key

functions in the osmoregulation of the lens. These findings show that impairments

in the osmoregulation may render the lens susceptible to even small increases of

AR-mediated osmotic stress, potentially leading to progressive cataract formation.

The role of osmotic stress is particularly important for the rapid cataract

formation in young patients with type 1 diabetes mellitus due to the extensive

swelling of cortical lens fibers. A study performed by Oishi et al. investigated

whether AR is linked to the development of adult diabetic cataracts. Levels of AR

in red blood cells of patients under 60 years of age with a short duration of

diabetes were positively correlated with the prevalence of posterior subcapsular

cataracts. A negative correlation has been shown in diabetic patients between the

amount of AR in erythrocytes and the density of lens epithelial cells, which are

known to be decreased in diabetics compared to nondiabetics suggesting a

potential role of AR in this pathomechanism.

The polyol pathway has been described as the primary mediator of diabetes-

induced oxidative stress in the lens. Osmotic stress caused by the accumulation of

sorbitol induces stress in the endoplasmic reticulum (ER), the principal site of

protein synthesis, ultimately leading to the generation of free radicals. ER stress

may also result from fluctuations of glucose levels initiating an unfolded protein

response (UPR) that generates reactive oxygen species (ROS) and causes

oxidative stress damage to lens fibers. There are numerous recent publications that

describe oxidative stress damage to lens fibers by free radical scavengers in

diabetics. However, there is no evidence that these free radicals initiate the

process of cataract formation but rather accelerate and aggravate its development.

Hydrogen peroxide (H2O2) is elevated in the aqueous humor of diabetics and

induces the generation of hydroxyl radicals (OH–) after entering the lens through

processes described as Fenton reactions. The free radical nitric oxide (NO),

another factor elevated in the diabetic lens and in the aqueous humor, may lead to

an increased peroxynitrite formation, which in turn induces cell damage due to its

oxidizing properties.

Furthermore, increased glucose levels in the aqueous humor may induce

glycation of lens proteins, a process resulting in the generation of superoxide

radicals () and in the formation of advanced glycation endproducts (AGE). By

interaction of AGE with cell surface receptors such as receptor for advanced

glycation endproducts in the epithelium of the lens further  and H2O2 are

generated.

In addition to increased levels of free radicals, diabetic lenses show an

impaired antioxidant capacity, increasing their susceptibility to oxidative stress.

The loss of antioxidants is exacerbated by glycation and inactivation of lens

antioxidant enzymes like superoxide dismutases. Copper-zink superoxide

dismutase 1 (SOD1) is the most dominant superoxide dismutase isoenzyme in the

lens, which is important for the degradation of superoxide radicals () into

hydrogen peroxide (H2O2) and oxygen. The importance of SOD1 in the protection

against cataract development in the presence of diabetes mellitus has been shown

in various in vitro and in vivo animal studies.

In conclusion, a variety of publications support the hypothesis that the

initiating mechanism in diabetic cataract formation is the generation of polyols

from glucose by AR, which results in increased osmotic stress in the lens fibers

leading to their swelling and rupture.

1.8. Examination

a. 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 surpris-ingly

well through marked lens opacities, and the effect on visual acuity as

measured by the Snellen test type depends as much on the pos-ition of the

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

b. Findings of Ophthalmoscopy

The best way of picking up a cataract in its early stages is to view the

pupil through the ophthal-moscope 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. When using the ophthalmoscope, the opacities in the

lens are often seen as black spokes against the red reflex. It is important to

focus one’s eyes onto the plane of the patient’s pupil if the cataract is to 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.

Picture 8. Cataract in ofthalmoskop

1.9. Management

At the present time, there is no effective medical treatment for cataract.

Cataract extraction with the insertion of an intraocular lens is the treatment of

choice. Cataract extraction surgery can be divided into 2 form, that is

intracapsular cataract extraction and extracapsular cataract extraction.

Until the mid 1980s, intracapsular cataract extraction was the method of

choice. Today intracapsular cataract extraction is used only with subluxation or

dislocation of the lens. The entire lens is frozen in its capsule with a cryophake

and removed from the eye through a large superior corneal incision.

Picture 9. Intracapsular cataract extraction

Extracapsular cataract extraction with implantation of a posterior chamber

intraocular lens is now the method of choice. In this technique, the anterior

capsule is opened (capsulor rhexis). Then only the cortex and nucleus of the lens

are removed (extracapsular extraction); the posterior capsule and zonule

suspension remain intact. This provides a stable base for implantation of the

posterior chamber intraocular lens.

Picture 10. Extraocular Cataract Extraction

Today phacoemulsification (emulsifying and aspirating the nucleus of the

lens with a high-frequency ultrasonic needle) is the preferred technique for

removing the nucleus. Where the nucleus is very hard, the entire nucleus is

expressed or aspirated. Then the softer portions of the cortex are removed by

suction with an aspirator/ir rigator attachment in an aspiration/irrigation

maneuver. The posterior capsule is then polished, and an intraocular lens (IOL) is

implanted in the empty capsular bag. Phacoemulsification and IOL implantation

require an incision only 3 – 6 mm in length. Where a tunnel technique is used to

make this incision, no suture will be necessary as the wound will close itself.

Picture 11. Phacoemulsification surgery

CHAPTER III

CASE

1. Patient identity

Name : Mrs. M

Sex : Female

Age : 50 years old

Address : Jln Khatulistiwa Gg. Flora Batu Layang

Ethnic : -

Job : House wife

Religion : Islam

Patient was examined on April 8, 2014

2. Anamnesis

Main complaint :

Blur of vision in the right eye.

History of disease :

Patient came to opthalmologist with mayor complain blurred of vision in the

right eye from a year ago. At the first time, patient felt like there was cloudy in

his sight and then her vision become worse and more blurred than before.

Now, she claimed that her right eye cannot see everything properly. Patient

have had diabetes mellitus for two years and take the diabetic medication

routinely. There were no history of eye trauma and no complaint about pain in

the eyes. She did not consume any drug before to treat her eyes.

Past clinical history :

Patient claim that she has diabetes mellitus for two years and take the

diabetic medication routinely.

Family history :

She claim that no one of her family member has the eye symptom like her.

Her mother has diabetes mellitus also.

3. General Physical Assestment

General condition : good

Awareness : compos mentis, GCS= 15

Vital sign :

a. Blood Pressure : 140/90 mmHg

b. Heart rate : 68 x/ minute/ regular

c. RR : 18 x/minute

d. Temperature : 36,80 C

4. Ophthalmological status

Visual acuity :

a. OD : 1/60 good projection

b. OS : 6/6 f

OD OS

Ortho Eye ball position Ortho

Eye Movement

Movement (+), ptosis (-), lagoftalmos

(-), oedem(-)

Palpebra Movement (+), ptosis (-),

lagoftalmos (-), oedem (-)

redness (-), discharge (-), injection(-),

ulcer (-), foreign body (-)

Conjungtiva Redness (-), discharge (-), injection

(-), ulcer (-), foreign body (-)

Oedem (-), ulcer (-) Cornea Oedem (-), ulcer (-)

Clear, deep impression Anterior chamber Clear, deep impression

Iris colour : brown, direct light reflect

(+), indirect light refelct (+)

Circular pupil, isochore,

Iris/pupil Iris colour : brown, direct light

reflect (+), indirect light refelct (+)

Circular pupil, isochore,

Opacity (+) Lens Clear

Can not be described Vitreous Clear

Can not be described Fundus Optic disk and vaskular saw no

problem, there was not hemorragic

• Shadow test :

• OD : negatif

• OS : negatif

• Tonometri

• OD : normal (palpation)

• OS : normal (palpation)

• Eye field test (Confrontation test)

• OD : can not be examined

• OS : normal

5. Resume

Patient came to opthalmologist with mayor complain blurred of vision in

the right eye from a year ago. At the first time, patient felt like there was

cloudy in his sight and then her vision become worse and more blurred than

before. Now, she claimed that her right eye cannot see everything properly.

Patient have had diabetes mellitus for two years and take the diabetic

medication routinely. There were no history of eye trauma and no complaint

about pain in the eyes. She did not consume any drug before to treat her eyes.

In ophtalmology examination, visual acuity in the right eye is 1/60 with a

good projection and the left eye is 6/6 f. There is a high opacity on the right

eye and shadow test (-).

6. Diagnose

Working Diagnose:

OD : Diabetic cataract

OS : Normal

DDx:

OD : Senil Cataract, cataract traumatica, cataract complikata.

OS : -

7. Plan for examination

Hemotology,

Blood sugar in time, to know the etiology is diabetic or not

Routine hematology, bleding and cloting time to preparation surgery

Result:

Blood sugar in time: 220 ( Normal: 70-150)

Routine hematology : no result

8. Treatment

a.OD: Extracapsular cataract extraction with an implantation of posterior

chamber intraoculer lens.

b.OS: No treatment

9. Prognosis

OD:

a. Ad vitam : bonam

b. Ad functionam : dubia et bonam

c. Ad sanactionam : dubia et bonam

OS:

a. Ad vitam : bonam

b. Ad functionam : bonam

c. Ad sanactionam : bonam

CHAPTER IV

DISCUSSION

In this case Patient came to opthalmologist with mayor complain blurred

of vision in the right eye from a year ago. At the first time, patient felt like there

was cloudy in her sight and then her vision become worse and more blurred than

before. Now, she claimed that her right eye cannot see everything properly.

Patient have had diabetes mellitus for two years and take the diabetic medication

routinely. There were no history of eye trauma and no complaint about pain in the

eyes. She did not consume any drug before to treat her eyes. In ophtalmology

examination, visual acuity in the right eye is 1/60 with a good projection and the

left eye is 6/6 f. There is a high opacity on the right eye and shadow test (-).

From the data above, the diagnose for the right eye is mature cataract et

causa diabetes mellitus. This patient said that she has diabetes mellitus for two

years and began get the blurry in her right eye for the first time a year ago. This

diagnostic based on symptoms that patient had complaint with the same

characteristic with the symptoms of cataract such as: blurry vision with slowly

onset. In this case the most probably etiology is diabetes mellitus because she has

the diabetic history for 2 years, and she did not have traumatic history in the eyes

that can cause traumatic cataract or get radiation such as infrared or others.

From the examination, lens appeared opacity in all part of the lens. This

opacity can occur because there is ion calcium depositions in the lens. Opacity of

the lens will make disrupting the refraction media so the light can not focus to

retina, finally produce blurred vision. Vision slowly blurred because the

progression of lenses opacification (thickness of opacity influence the degree of

vision lost). Because of opacity of the lens, we can not see the fundus with

ofthalmoskop. This cataract classify to mature cataract because all of the lens was

clouded and from the shadow test is negatif that diffrent with immatur cataract.

From the result of laboratorium hematology test, patient had a bad control of

blood sugar, and has history for diabetes mellitus for 2 years, so cataract may

cause from diabetic mellitus she had.

The patogenesis of diabetic cataract is the enzyme aldose reductase (AR)

catalyzes the reduction of glucose to sorbitol through the polyol pathway, a

process linked to the development of diabetic cataract. Extensive research has

focused on the central role of the AR pathway as the initiating factor in diabetic

cataract formation.

It has been shown that the intracellular accumulation of sorbitol leads to

osmotic changes resulting in hydropic lens fibers that degenerate and form sugar

cataracts. In the lens, sorbitol is produced faster than it is converted to fructose by

the enzyme sorbitol dehydrogenase. In addition, the polar character of sorbitol

prevents its intracellular removal through diffusion. The increased accumulation

of sorbitol creates a hyperosmotic effect that results in an infusion of fluid to

countervail the osmotic gradient. Animal studies have shown that the intracellular

accumulation of polyols leads to a collapse and liquefaction of lens fibers, which

ultimately results in the formation of lens opacities. These findings have led to the

“Osmotic Hypothesis” of sugar cataract formation, emphasizing that the

intracellular increase of fluid in response to AR-mediated accumulation of polyols

results in lens swelling associated with complex biochemical changes ultimately

leading to cataract formation.

The treatment for the patient is surgery, becauase there was no effective

medical treatment for cataract. The definitive management for mature senile

cataract is lens extraction through surgery. The type of the surgery that

recommend for this patient is extracapsular cataract extraction (ECCE). we attend

to choose this type rather than intracapsular cataract extraction (ICCE) because

extracapsular cataract extraction maintains the integrity of the anterior and

posterior chambers of the eye, and the vitreous body cannot prolapse anterior as

after intracapsular cataract extraction. At 0.1 – 0.2 %, the incidence of retinal

detachment after extracapsular cataract extraction is about ten times less than after

intracapsular cataract extraction, which has an incidence of 2 – 3 %.

Prognosis cataract for patient after surgery may be good. Patient can see

clearly after removal the old lens and changed with syntetyc lens (Intra Ocular

Lens/ IOL). After surgery, eye’s patient had pseudofakhia from examination

ofthalmoskop. But then, because of the etiology for this case is diabetes mellitus,

the patient should control her blood sugar level in a good term to not make any

complication anymore.

CHAPTER V

CONCLUSION

From the case above, we can make a conclution about cataract are:

1. This patient suffer from diabetic cataract, because from the anamnesis and

examination it clearly pinpoint the cataract and also she has diabetes

mellitus for over 2 years.

2. A cataract is present when the transparency of the lens is reduced to the

point that the patient’s vision is impaired

3. Diagnostic of cataract based on anamnesis, examination, and laboratorium.

In anamnesis, we should to know abaout history of disease. In

examination, we have to see the opacity of lens and other examination. In

the laboratorium, we have to know abaut the etiology of cataract such as

diabetic that can see from blood sugar.

4. The efecctive tratment for catarac is surgery, there are many types of

surgery that can be used; extracapsular cataract extraction (ECCE) and

intracapsular cataract extraction (ICCE) but it was so rare to use nowdays.