STEP 7

1. Bagaimana anatomi dan fisiologi lensa, retina dan koroid?

Vitreous humour is an inert, transparent, jelly-like structure that fills the posterior four-fifth of the
cavity of eyeball and is about 4 ml in volume. It is a hydrophilic gel that mainly serves the optical
functions. In addition, it mechanically stabilizes the volume of the globe and is a pathway for nutrients
to reach the lens and retina.

Structure. The normal youthful vitreous gel is composed of a network of randomly-oriented collagen
fibrils interspersed with numerous spheroidal macromolecules of hyaluronic acid. The collapse of this
structure with age or otherwise leads to conversion of the gel into sol. The vitreous body can be divided
into two parts: the cortex and the nucleus (the main vitreous body).
1. Cortical vitreous. It lies adjacent to the retina posteriorly and lens, ciliary body and zonules anteriorly.
The density of collagen fibrils is greater in this peripheral part. The condensation of these fibrils form a
false anatomic membrane which is called as anterior hyaloid membrane anterior to ora serrate and
posterior hyaloid membrane posterior to ora. The attachment of the anterior hyaloid membrane to the
posterior lens surface is firm in the young and weak in the elderly whereas posterior hyaloid membrane
remains loosely attached to the internal limiting membrane of the retina throughout life. These
membranes cannot be discerned in a normal eye unless the lens has been extracted and posterior
vitreous detachment has occurred.

2. The main vitreous body (nucleus). It has a less dense fibrillar structure and is a true biological gel. It
is here where liquefactions of the vitreous gel start first. Microscopically the vitreous body is
homogenous, but exhibits wavy lines as of watered silk in the slit-lamp beams. Running down the centre
of the vitreous body from the optic disc to the posterior pole of the lens is the hyaloid canal (Cloquets
canal) of doubtful existence in adults. Down this canal ran the hyaloid artery of the foetus.

Attachments. The part of the vitreous about 4 mm across the ora serrata is called as vitreous base,
where the attachment of the vitreous is strongest. The other firm attachments are around the margins
of the optic disc, foveal region and back of the crystalline lens by hyloidocapsular ligament of Wieger.
Retina, the innermost tunic of the eyeball, is a thin, delicate and transparent membrane. It is the most
highly-developed tissue of the eye. It appears purplish-red due to the visual purple of the rods and
underlying vascular choroid.

Gross anatomy

Retina extends from the optic disc to the ora serrata. Grossly it is divided into two distinct regions:
posterior pole and peripheral retina separated by the so called retinal equator.

Retinal equator is an imaginary line which is considered to lie in line with the exit of the four vena
verticose.

Posterior pole refers to the area of the retina posterior to the retinal equator. The posterior pole of
the retina includes two distinct areas: the optic disc and macula lutea. Posterior pole of the retina is
best examined by slit-lamp indirect biomicroscopy using +78D and +90D lens and direct
ophthalmoscopy.

Optic disc. It is a pink coloured, well-defined circular area of 1.5-mm diameter. At the optic disc all the
retinal layers terminate except the nerve fibres, which pass through the lamina cribrosa to run into the
optic nerve. A depression seen in the disc is called the physiological cup. The central retinal artery and
vein emerge through the centre of this cup.
Macula lutea. It is also called the yellow spot. It is comparatively deeper red than the surrounding
fundus and is situated at the posterior pole temporal to the optic disc. It is about 5.5 mm in diameter.
Fovea centralis is the central depressed part of the macula. It is about 1.5 mm in diameter and is the
most sensitive part of the retina. In its centre is a shining pit called foveola (0.35-mm diameter) which
is situated about 2 disc diameters (3 mm) away from the temporal margin of the disc and about 1 mm
below the horizontal meridian. An area about 0.8 mm in diameter (including foveola and some
surrounding area) does not contain any retinal capillaries and is called foveal avascular zone (FAZ).
Surrounding the fovea are the parafoveal and perifoveal areas.

Peripheral retina refers to the area bounded posteriorly by the retinal equator and anteriorly by the
ora serrata. Peripheral retina is best examined with indirect ophthalmoscopy and by the use of Goldman
three mirror contact lens.

Ora serrata. It is the serrated peripheral margin where the retina ends. Here the retina is firmly attached
both to the vitreous and the choroid. The pars plana extends anteriorly from the ora serrata.
Bruch's Membrane

The basal portion of the RPE is attached to Bruch's membrane, which has S layers. Starting with the
innermost, these are

basement membrane of the RPE

inner loose collagenous zone
middle layer of elastic fibers
outer loose collagenous zone
basement membrane of the endothelium of the choriocapillaris

Throughout life, lipids and oxidatively damaged materials build up within Bruch's membrane. Some
disease states, such as pseudoxanthoma elasticum, are associated with increased frag ility of Bruch's
membrane, presumably due to abnormali ties within its collagen or elastic portions. Patients with
pseudoxanthoma elasticum may develop breaks or cracks within Bruch's membrane that radiate from
the optic nerve and form angioid streaks, named after their vessel-like appearance.

2. Hubungan mata pasien semakin buram dengan riwayat penyakit DM dan hipertensi dari kedua
orang tuanya?

Conditions Associated With Potential Visual Loss From Diabetic Retinopathy

Potential visual loss in patients with diabetic retinopathy can be associated with the fol
lowing conditions:
Macular edema (capillary leakage) caused by increased intraretinal vascular
permeability. Blood-retinal barrier breakdown contributes to macular edema,
which occurs in over 25% of people with diabetes and correlates highly with
visual impairment in people with diabetic retinopathy.
 macular ischemia (capillary occlusion)
sequelae from ischemia-induced neovascularization

American Academy of Ophthalmology. 2011. Retina and Vitreous

Gabriele E. Lang, Ulm. 2007. Diabetic Retinopathy

DIABETIC RETINOPATHY
The exact cause of diabetic microvascular disease is unknown. It is believed that exposure to
hyperglycemia over an extended period results in a number of biochemical and physiologic changes
that ultimately cause endothelial damage. Specific retinal capillary changes include selective loss of
pericytes and basement membrane thickening, which favor capillary occlusion and retinal non
perfusion, as well as decompensation of the endothelial barrier function, which allows serum leakage
and retinal edema to occur. A large number of hematologic and biochemical abnormalities have been
correlated with the prevalence and severity of retinopathy:

increased platelet adhesiveness

increased erythrocyte aggregation
abnormal serum lipids
defective fibrinolysis
abnormal levels of growth hormone
up regulation of vascular endothelial growth factor (VEGF)
abnormalities in serum and whole blood viscosity
However, the precise role of these abnormalities-individually or in combination-in the pathogenesis of
retinopathy is not well defined.

Retinopati Diabetika:

Terdapat 4 proses biokimiawi yang terjadi pada hiperglikemia kronis yang diduga berhubungan dengan
timbulnya retinopati diabetik, antara lain:

- Akumulasi Sorbitol
Hiperglikemi kronis peningkatan aktv enzim aldose reduktase (pada jarringan saraf, retina,
lensa, glomerolus dan dinding pembuluh darahakumulasi dari sorbitol. Sorbitol merupakan
suatu senyawa gula dan alkohol yang tidak dapat melewati membrana basalis sehingga akan
tertimbun dalam jumlah yang banyak dalam sel. Kerusakan sel terjadi akibat akumulasi sorbitol
yang bersifat hidrofilik sehingga sel menjadi bengkak akibat proses osmotik.
- Pembentukan protein kinase C (PKC)
o Hiperglikemiapeningkatan sintesis de novo dari diasilgliserol aktivitas PKC di retina
dan sel endotel vaskular meningkat,
o PKC diketahui memiliki pengaruh terhadap agregasi trombosit, permeabilitas vaskular,
sintesis growth factor dan vasokonstriksi. Peningkatan PKC secara relevan meningkatkan
komplikasi diabetika, dengan mengganggu permeabilitas dan aliran darah vaskular
retina.
o Peningkatan permeabilitas vaskularterjadinya ekstravasasi plasma viskositas darah
intravaskular meningkat disertai dengan peningkatan agregasi trombosit yang saling
berinteraksi menyebabkan terjadinya trombosis.
o Selain itu, sintesis growth factorpeningkatan proliferasi sel otot polos vaskular dan
matriks ekstraseluler termasuk jaringan fibrosa,penebalan dinding vaskular, ditambah
dengan aktivasi endotelin-1 yang merupakan vasokonstriktorlumen vaskular makin
menyempit. Seluruh proses tersebut terjadi secara bersamaan, hingga akhirnya
menyebabkan terjadinya oklusi vaskular retina.
- Pembentukan Advanced Glycation End Product (AGE)
o Glukosa mengikat gugus amino membentuk ikatan kovalen secara non enzimatik. Proses
tersebut pada akhirnya akan menghasilkan suatu senyawa AGE. Efek dari AGE ini saling
sinergis dengan efek PKC dalam menyebabkan peningkatan permeabilitas vaskular,
sintesis growth factor, aktivasi endotelin 1 sekaligus menghambat aktivasi nitrit oxide
oleh sel endotelakan meningkatkan risiko terjadinya oklusi vaskular retina.
o AGE terdapat di dalam dan di luar sel, berkorelasi dengan kadar glukosa. Akumulasi AGE
mendahului terjadinya kerusakan sel. Pada pasien DM, sedikit saja kenaikan glukosa
maka meningkatkan akumulasi AGE yang cukup banyak, dan akumulasi ini lebih cepat
pada intrasel daripada ekstrasel.
- Pembentukan Reactive Oxygen Speciesi (ROS)
o ROS dibentuk dari oksigen dengan katalisator ion metal atau enzim yang menghasilkan
hidrogen peroksida (H2O2), superokside (O2-).
 o Pembentukan ROS meningkat melalui autooksidasi glukosa pada jalur poliol dan
degradasi AGE. Akumulasi ROS di jaringan akan menyebabkan terjadinya stres oksidatif
yang menambah kerusakan sel.

Pandelaki K. 2007. Retinopati Diabetik dalam Buku Ajar Ilmu Penyakit Dalam. Edisi IV Jilid
III. Editor: Aru W. Sudoyo dkk. Departemen ilmu penyakit dalam Fakultas Kedokteran Universitas
Indonesia: Jakarta

Arterosklerosis arteriosclerosis dan patfis katarak dan retinopati diabetikum!

Arteriosclerosis literally means hardening of the arteries; it is a generic term reflcting

arterial wall thickening and loss of elasticity. Three distinct types are recognized, each with
different clinical and pathologic consequences:
Arteriolosclerosis affects small arteries and arterioles and may cause downstream
ischemic injury. The two variants, hyaline and hyperplastic arteriolosclerosis, were
described above in relation to hypertension.
Mnckeberg medial sclerosis is characterized by the presence of calcifi deposits in
muscular arteries, typically in persons older than 50. The lesions do not encroach on the
vessel lumen and usually are not clinically significant.
Atherosclerosis is characterized by the presence of intimal lesions called atheromas (or
atheromatous or atherosclerotic plaques). Atheromatous plaques are raised lesions
composed of soft grumous lipid cores (mainly cholesterol and cholesterol esters, with
necrotic debris) covered by fibrous caps
Kumar, Abbas. 2013. Robbins Basic Pathology 9th Edition. Saunders, an imprint of Elsevier Inc

3. Apa hubungan pasien mengguankan kacamata sejak 15tahun yang lalu?

Merupakan faktor resiko dari myopia ddlm lensa dan katarak akan mengabsorbsi cairan lensa
cembung daya refraksi meningkat, penderita retina lebih mudah melihat dekat drpda mlihat
jauh. Akibat absorbs semakin banyaklensa mencembung bayangan jatuh didpn retina.
Pemakian kacamata yang lama dapat menyebabkan penurunan visus secara mendadak???

4. Bagaimana hubungan keadaan lensa dengan usia pasien?

Seiring dengan pertambahan usia, lensa akan mengalami penuaan juga. Keistimewaan
lensa adalah ia terus menerus tumbuh dan membentuk serat lensa dengan arah
pertumbuhannya yang konsentris. Tidak ada sel yang mati ataupun terbuang karena lensa
 tertutupi oleh serat lensa. Akibatnya, serat lensa paling tua berada di pusat lensa
(nukleus) dan serat lensa yang paling muda berada tepat di bawah kapsul lensa (korteks).
Dengan pertambahan usia, lensa pun bertambah berat, tebal, dan keras terutama bagian
nukleus. Pengerasan nukleus lensa disebut dengan nuklear sklerosis. Selain itu, seiring
dengan pertambahan usia, protein lensa pun mengalami perubahan kimia. Fraksi protein
lensa yang dahulunya larut air menjadi tidak larut air dan beragregasi membentuk protein
dengan berat molekul yang besar. Hal ini menyebabkan transparansi lensa berkurang
sehingga lensa tidak lagi meneruskan cahaya tetapi malah mengaburkan cahaya dan lensa
menjadi tidak tembus cahaya.

5. Apa interpretasi px VOD 6/60 dengan s-1,75 jadi 6/12 NBC, VOS 6/48 dengan s-1.50 jadi 6/9,6
NBC, addisi S+1,50 J4, segmen anterior tenang dengan lensa keruh tidak merata?
VOD: dapat melihat jarak 6meter dikoreksi6/12: dapat melihat 6meter sedangkan org
normal 12
VOS: 6/48 dikoreksi menjadi 6/9,6
Diberi lensa koreksi + 1,50 dapat melihat J4

6. Apa macam-macam penyakit lensa yang dapat mengakibatkan kebutaan ?

1. Katarak : kekeruhan pd lensa akibat hidrasi pada lensa
Etiologi : radiasi, trauma
Dari dalam : nuclear katarak ,pranuklear,subkapsuler,kapsuler(bagian luarnya)
Table dan hasil px!

Classification

Diabetic retinopathy has been variously classified. Presently followed classification is as follows:

1. Non-proliferative diabetic retinopathy (NPDR)

a. Mild NPDR
b. Moderate NPDR
c. Severe NPDR
d. Very severe NPDR
2. Proliferative diabetic retinopathy (PDR)
3. Diabetic maculopathy
4. Advanced diabetic eye disease (ADED)

Non-proliferative diabetic retinopathy (NPDR)

Ophthalmoscopic features of NPDR include:

Microaneurysms in the macular area (the earliest detectable lesion).

Retinal haemorrhages both deep (dot and blot haemorrhages) and superficial haemorrhages
(flame-shaped).
Hard exudates-yellowish-white waxy-looking patches are arranged in clumps or in circinate
pattern. These are commonly seen in the macular area.
 Retinal oedema characterized by retinal thickening.
Cotton-wool spots (if > 8, there is high risk of developing PDR).
Venous abnormalities, beading, looping and dilatation.
Intraretinal microvascular abnormalities (IRMA).
Dark-blot haemorrhages representing haemorrhagic retinal infarcts.

On the basis of severity of the above findings the NPDR has been further classified as under:

1. Mild NPDR (Fig. 11.14A).

At least one microaneurysm or intraretinal hemorrhage.

Hard/soft exudates may or may not be present.

2. Moderate NPDR (Fig. 11.14B)

Moderate microaneurysms/intraretinal hemorrhage.

Early mild IRMA.

Hard/soft exudates may or may not present.

3. Severe NPDR. Any one of the following (4-2-1 Rule) (Fig. 11.14C):

Four quadrants of severe microaneurysms/ intraretinal hemorrhages.

Two quadrants of venous beading.

One quadrant of IRMA changes.

4. Very severe NPDR. Any two of the following (4-2-1 Rule) (Fig. 11.14D):

Four quadrants of severe microaneurysms/ intraretinal hemorrhages.

Two quadrants of venous beading.

One quadrant of IRMA changes.

Proliferative diabetic retinopathy (PDR)

Proliferative diabetic retinopathy (Figs. 11.14 E&F) develops in more than 50 percent of cases after
about 25 years of the onset of disease. Therefore, it is more common in patients with juvenile onset
diabetes. The hallmark of PDR is the occurrence of neovascularisation over the changes of very severe
non-proliferative diabetic retinopathy. It is characterised by proliferation of new vessels from the
capillaries, in the form of neovascularisation at the optic disc (NVD) and/or elsewhere (NVE) in the
fundus, usually along the course of the major temporal retinal vessels. These new vessels may
proliferate in the plane of retina or spread into the vitreous as vascular fronds. Later on condensation of
connective tissue around the new vessels results in formation of fibrovascular epiretinal membrane.
Vitreous detachment and vitreous haemorrhage may occur in this stage.

Types. On the basis of high risk characteristics (HRCs) described by diabetic retinopathy study (DRS)
group, the PDR can be further classified as below:
1. PDR without HRCs (Early PDR) (Fig. 11.14E), and

2. PDR with HRCs (Advanced PDR). High risk characteristics (HRC) of PDR are as follows (Fig. 11.14F):

NVD 1/4 to 1/3 of disc area with or without vitreous haemorrhage (VH) or pre-retinal
haemorrhage (PRH)
NVD < 1/4 disc area with VH or PRH
NVE > 1/2 disc area with VH or PRH

Katarak

Definition
The crystalline lens is a transparent structure. Its transparency may be disturbed due to
degenerative process leading to opacification of lens fibres. Development of an opacity in the
lens is known as cataract.
Classification
A. Etiological classification
a. Congenital and developmental cataract
b. Acquired cataract
1. Senile cataract
2. Traumatic cataract (see page 405)
3. Complicated cataract
4. Metabolic cataract
5. Electric cataract
6. Radiational cataract
7. Toxic cataract e.g.,
a. Corticosteroid-induced cataract
b. Miotics-induced cataract
c. Copper (in chalcosis) and iron (in siderosis) induced cataract.
8. Cataract associated with skin diseases (Dermatogenic cataract).
9. Cataract associated with osseous diseases.
10. Cataract with miscellaneous syndromes e.g.,
a. Dystrophica myotonica
b. Down's syndrome.
c. Lowe's syndrome
d. Treacher - Collin's syndrome
B. Morphological classification (Fig. 8.4)
a. Capsular cataract. It involves the capsule and may be:
i. Anterior capsular cataract
ii. Posterior capsular cataract
b. Subcapsular cataract. It involves the superficial part of the cortex (just below
the capsule) and includes:
ii. Anterior subcapsular cataract
iii. Posterior subcapsular cataract
c. Cortical cataract. It involves the major part of the cortex.
d. Supranuclear cataract. It involves only the deeper parts of cortex (just outside
the nucleus).
e. Nuclear cataract. It involves the nucleus of the crystalline lens.
Clinical presentations
Common
Change in visionreduced acuity, contrast sensitivity, or color appreciation, glare,
monocular diplopia, or ghosting.
Change in refractiontypically a myopic shift due to nuclear sclerosis.
Change in fundus viewclinicians may have difficulty looking in long before the patients
feel they have difficulties looking out. This may be a problem when trying to monitor or
treat posterior segment disease such as diabetic retinopathy or macular degeneration.
Uncommon
Phacomorphic glaucoma
The large cataractous lens may cause anterior bowing of the iris with secondary angle
closure. Presentation may occur as acute angle closure with high IOP, shallow AC, and fixed
semi dilated pupil. Phacomorphic glaucoma can be distinguished from primary angle closure
glaucoma by the presence of an ipsi lateral swollen cataractous lens and contralateral open
angle with deep AC.
Phacolytic glaucoma
The hypermature cataract loses soluble lens proteins through the anterior capsule, causing
trabecular obstruction and subsequent secondary open angle glaucoma. Note raised IOP, lens
protein in a deep AC (may form a pseudohypopyon), open angles, and hypermature cataract.
Phacoanaphylactic uveitis (i.e., phacoantigenic, lens-induced granulomatous uveitis)
Phacoanaphylactic uveitis is a misnomer, as the inflammatory response is not a type I
phacoanyphylactic response but a granulomatous inflammatory response to lens proteins.
This condition usually follows traumatic capsular rupture or postoperative retention of lens
material (it must be distinguished from endophthalmitis). The IOP may be high, normal, or low.
Khurana, K. A. (2007). Comprehensive Ophthalmology 4th Edition. New Delhi: New
Age International (P) Ltd.

7. Apa etilogi dari scenario?

Risk factors associated with occurence of DR are:

1. Duration of diabetes is the most important determining factor. Roughly 50 percent of
patients develop DR after 10 years, 70 percent after 20 years and 90 percent after 30
years of onset of the disease.
2. Sex. Incidence is more in females than males (4:3).
3. Poor metabolic control is less important than duration, but is nevertheless relevant to
the development and progression of DR.
4. Heredity. It is transmitted as a recessive trait without sex linkage. The effect of
heredity is more on the proliferative retinopathy.
5. Pregnancy may accelerate the changes of diabetic retinopathy.
6. Hypertension, when associated, may also accentuate the changes of diabetic
retinopathy.
7. Other risk factors include smoking, obesity and hyperlipidemia.

Etiology
Exact etiology is not known. Some factors which have been associated with certain types
of cataracts are described below:
I. Heredity. Genetically-determined cataract is due to an anomaly in the chromosomal
pattern of the individual. About one-third of all congenital cataracts are hereditary. The
mode of inheritance is usually dominant. Common familial cataracts include: cataracta
pulverulenta, zonular cataract (also occurs as non-familial), coronary cataract and total
soft cataract (may also occur due to rubella).

II. Maternal factors

1. Malnutrition during pregnancy has been associated with non-familial zonular cataract.
2. Infections. Maternal infections like rubella are associated with cataract in 50 percent of
 cases. Other maternal infections associated with congenital cataract include
toxoplasmosis and cytomegalo-inclusion disease.
3. Drugs ingestion. Congenital cataracts have also been reported in the children of
mothers who have taken certain drugs during pregnancy (e.g., thalidomide,
corticosteroids).
4. Radiation. Maternal exposure to radiation during pregnancy may cause congenital
cataracts.

III. Foetal or infantile factors

1. Deficient oxygenation (anoxia) owing to placental haemorrhage.
2. Metabolic disorders of the foetus or infant such as galactosemia, galactokinase
deficiency and neonatal hypoglycemia.
3. Cataracts associated with other congenital anomalies e.g., as seen in Lowe's
syndrome, myotonia dystrophica and congenital icthyosis.
4. Birth trauma.
5. Malnutrition in early infancy may also cause developmental cataract.

IV. Idiopathic. About 50 percent cases are sporadic and of unknown etiology

8. Apa faktor resiko dari scenario?

Risk factors associated with occurence of DR are:

1. Duration of diabetes is the most important determining factor. Roughly 50 percent of
patients develop DR after 10 years, 70 percent after 20 years and 90 percent after 30
years of onset of the disease.
2. Sex. Incidence is more in females than males (4:3).
3. Poor metabolic control is less important than duration, but is nevertheless relevant to
the development and progression of DR.
4. Heredity. It is transmitted as a recessive trait without sex linkage. The effect of
heredity is more on the proliferative retinopathy.
5. Pregnancy may accelerate the changes of diabetic retinopathy.
6. Hypertension, when associated, may also accentuate the changes of diabetic
retinopathy.
7. Other risk factors include smoking, obesity and hyperlipidemia.

Khurana, K. A. (2007). Comprehensive Ophthalmology 4th Edition. New Delhi: New Age
International (P) Ltd.
9. Apa diagnosis dan dd? Mata tenang visus turun!!
Olver, Jane. 2014. Ophthalmology at a glance. Blackwell Science Ltd
10. Apa pemeriksaan penunjang yang dilakukan untuk menegakkan diagnosis?

Yanoff, Myron. 2014. Opthtalmic Diagnosis and Treatment 3rd Edition

11. Apa penatalaksannan dari scenario?

Treatment aims
To stabilize vision or decrease the rate of visual loss
To decrease macular edema
To achieve regression of proliferative retinopathy
To release traction if macula is threatened
To clear vitreous hemorrhage if present greater than or equal to 2 months.

Prognosis
Depends on the severity of the disease
 Follow-up and Management
Yearly screening dilated fundus examinations should be performed on all diabetic
patients.
If diabetic retinopathy is detected, followup examinations may be as frequent as every
23 months to observe the rate of progression.

Complications
Cataracts
Neovascular glaucoma secondary to ischemia with iris or angle neovascularization (see
Pharmacologic Treatment)
Tractional retinal detachment
Vitreous hemorrhage
Preretinal hemorrhage
Macular edema
Optic nerve damage

Cataract surgery indications

Role of Quality of Life
Cataract/IOL surgery improves quality of life better than any other medical procedure known to
mankind. Cataract surgery is indicated when the patient's quality of life is being affected by
visual impairment, when there is a diminution in vision if the patient is exposed to light or
at night, and when the preoperative evaluation indicates that the potential for restoration
of sight is good. How much a patient's quality of life is impaired from a cataract is relative,
varying with the patient's occupation and age. The key factor is not to wait until a nuclear
cataract becomes hard. With time, the lens fiber density becomes a hard nuclear brunescent
cataract. With most modern phacoemulsification techniques it may become increasingly
difficult to perform surgery if the lens becomes extremely dense or brunescent.
Waiting too long may require that the surgeon operate on dense nuclear cataracts, which
increases the risk of posterior capsule tears, whether we perform planned extracapsular or a
phacoemulsification. This complication may lead to other rather serious problems such as
dislocated nucleus, retinal detachment, macular edema, bullous keratopathy and
inflammation.
The Role of Visual Acuity
There are very few strict criteria for recommending cataract surgery. In the United States,
however, many professional review organizations have indicated that the reduction of Snellen
distance acuity to 20/40 or worse as a result of cataract is sufficient indication in and of
itself for cataract surgery. This is generally the minimum standard for driving. In some of
the advanced, developed countries, being unable to obtain a driver's license may seriously affect
a person's life because he/she may be disqualified to drive to the market or shop to purchase food
and other materials essential to daily existence. However, in many cases surgery may be
indicated without reduction of visual acuity to the level of 20/40 if the patient has difficulty
performing activities of daily living. Because patients have varying occupational and
recreational needs, some patients may need cataract surgery prior to having their vision reduced
to 20/40 by standard tests. In addition, near vision in some cases may be compromised more than
distance acuity particularly in the case of central posterior subcapsular cataracts. The trend
toward early removal of cataract offers the advantage of operating on a younger age group, many
of whom are still productive members of society. Their need for early return to their usual
lifestyle is extremely important.
The older population, often living alone, also benefits from early visual recovery. These high
expectations and needs require that the ophthalmic surgeon perform superior surgery to obtain
excellent postoperative visual acuity and early visual rehabilitation.
As emphasized by Gimbel, symptoms of cataracts include complaints of a yellowing of vision,
glare, halos, decreased night vision, and generally blurred vision in adults. Nuclear sclerosis
which is a typical form of age-related cataracts may also induce a myopic shift and patients may
give a history of having changed their glasses several times within a short period of time. In
children cataracts may present as leukocoria and may result in strabismus and/or
amblyopia if not treated promptly.

Yanoff, Myron. 2014. Opthtalmic Diagnosis and Treatment 3rd Edition

Kelainan sitem saraf dan media refraksi dan pencegahannya

Lensa dan retinopati dan refraksi anomali