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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
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?
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:
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
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???
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
Classification
Diabetic retinopathy has been variously classified. Presently followed classification is as follows:
On the basis of severity of the above findings the NPDR has been further classified as under:
3. Severe NPDR. Any one of the following (4-2-1 Rule) (Fig. 11.14C):
4. Very severe NPDR. Any two of the following (4-2-1 Rule) (Fig. 11.14D):
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.
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).
IV. Idiopathic. About 50 percent cases are sporadic and of unknown etiology
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?
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