Pembahasan Pemicu 1

Penginderaan
 Mata tenang Penurunan visus 12. Anisometropi
perlahan : 13. Diplopia
1. Retinopati diabetikum 14. Keratokonus
2. Katarak 15. Strabismus
3. Miopia 16. Retinitis pigmentosa
4. Hipermetropi
5. Presbiopi
6. Glaukoma
7. Astigmatisme
8. Ambliopia
9. Buta senja
10. Degenerasi makula
11. Hipertensi retinopati

LI 4
 GANGGUAN REFRAKSI
• Presbiopia trtentu,biasanya:
– Gg akomodasi pd usia lanjut 1. S +1 D u/ usia 40 thn
dpt terjadi akibat : 2. S+ 1.50 D u/ usia 45 thn
a) Kelemahan otot akomodasi 3. S+2.00 D untuk usia 50 thn
b) Lensa mata tidak kenyal 4. S+ 2.50 D untuk usia 55 thn
/berkrg elastisitasnya akibat 5. S+ 3.00 D untuk usia 60 thn
sklerosis lensa
• -akibat gg akomodasi maka pd • Krn jarak baca biasanya 30 cm
ps berusia > dari 40 thn maka adisi S+ 3.00
mberikan keluhan stlh dipotrilensa + terkuat
mmbaca ( mata lelahmberair
& sering terasa pedas) • Px adisi untuk membaca perlu
• Pd presbiopia kacamata/adisi disesuaikan dengan kebutuhan
diperlukan untuk mmbaca jarak kerja ps pd wktu
dkat yg berkekuatan mmbaca
 Correction of Presbyopia
• Lens extraction, either to treat that one eye (usually the dominant) is
cataract or for purely refractive optimized for clear uncorrected distance
purposes. vision and the other for near or
– Acronyms used include : intermediate vision, in order to
• clear lens exchange (CLE), facilitate both good distance and near
• refractive lens exchange (RLE) and vision when the eyes are used
presbyopic lens exchange (PreLEx). together.
• Much research effort is being applied to the
development of effective accommodating
prosthetic lenses.
• Conductive keratoplasty evidence
• Implantation of a multifocal, bifocal or of multifocal functionality to the
‘accommodating’/ cornea
pseudoaccommodative intraocular
lens implant (IOL) can optically : • Laser induced monovision refers to
– Restore some reading vision; reading
the use of laser refractive surgery ( to
glasses commonly still have to be used for optimize 1 eye for distance & the
some tasks. fellow for near /intermediate vision)
– Although many recipients of multifocal • Corneal multifocality  laser
IOLs are very happy with the visual procedure to alter the shape of the
outcome cornea ( bifocal/transitional effect )
• dissatisfaction occurs in a significant
minority mainly due to nocturnal glare
and reduced contrast sensitivity.
• Monovision consists of the targeting
of IOL-induced refractive outcomes so
• Scleral expansion surgeryinconsistent &
unpredictable
• Intracorneal inlays substansial benefit in
presbyopia ( complication extrusion)
• Laser modification of the natural lensuse of
femtosecond laser to modulate crystalline lens
elasticity
 Ametropia
• Keseimbangan dlm pmbiasan prubahan panjang ( lbh
ditentukan oleh dataran depan & pnjang,lbh pendek ) bola mata
kelengkungan kornea & panjang mka sinar normal tdk dpt
bola mata terfokus pd retina
• Kornea pnya daya pmbiasan
sinar terkuat dibanding bag mata – Keadaan ini disebut :
lainnya miopia,hipermetropia,astigmat
• Lensa mmegang peranan • Ametropiakeadaan pmbiasan
mmbiaskan sinar trutama pd saat mata dgn panjang bola mata yg
melakukan akomodasi/bila tdk seimbang
melihat benda yg dkat. – Trjd krn kelainan kekuatan
pmbiasan sinar media
pnglihatan /klainan bntuk bola
• Bila trdpt kelainan pmbiasan mata
sinar oleh kornea ( mendatar
,mencembung) /adanya
 Jenis ametropia
• Ametropia aksial
– Terjadi akibat sumbu optik bola mata lbh panjang/lbh pendek shingga
bayang benda difoksukan didpn /diblakang retina
– Pd miopia aksialfokus akan terletak didpn retina ( bola mata lbh
pnjang ) dn sbaliknya pd hipermetropia
• Ametropia refraktif kelainan sistem pmbiasan sinar didlm mata
– Bila daya bias kuat maka byangan bnda trltak didpn retina ( miopia)
/bila daya bias kurang maka bayangan benda akan terletak di blakang
retina ( hipermetropia refraktif)
Ametropia Lensa koreksi Kausa
– Kausa Ametropia
Miopia Lensa - Refraktif aksial
Hipermetropia Lensa + Bias kuat Bola mata panjang
Bias lemah Bola mata pendek
Astigmata regular Kacamata silinder Kurvatur 2 meridian
tegak lurus
Astigmata iregular Lensa kontak Kurvatur kornea
iregular
 Miopia
• Pd miopia panjang bola mata anteroposterior dpt trlalu besar
/kekuatan pmbiasan media refraksi trlalu kuat.
• Dikenal bbrp bntk miopia spt :
– Miopia refraktif  ber+ indeks bias media pnglihatan spt terjdi pd
katarak intumesen dimana lensa mnjd cembung shingga pmbiasan lbh
kuat
• Sma dgn miopia bias /miopia indeks ( miopia yg terjd akibat pmbiasan media
pnghlitan kornea dan lensa yg trlalu kuat)
– Miopia aksial miopia akibat panjangnya sumbu bola mata dgn
kornea & lensa yg normal
• Mnurut drajat beratnya miopia dlm :
a) Miopia ringan 1-3 dioptri
b) Miopia sedang  3-6 dioptri
c) Miopia berat/tinggi > 6 dioptri
• Mnurut perjalanan miopia dikenal bntuk :
a) Miopia stasioner miopia yg mnetap dewasa
b) Miopia progresif miopia yg ber+ terus pd usia dewasa akibat ber+ panjangnya
bola mata
c) Miopia malignamiopia yg berjalan progresif yg dpt mngakibkan ablasi retina &
kebutaan /sma dgn miopia pernisiosa=miopia maligna =miopia degeneratif

• Miopia degeneratif /miopia maligna biasanya bila miopia > dr 6 dioptri

– (disertai kelainan pd fundus okuli & pd pnjangny bola mata smpai trbntuk stafiloma
postikum ( yg trletak pd bag temporal papil disertai dgn atrofi korioretina)

– Stlh terjadi atrofi sklera akan terjadi atrofi retina & kadang terjadi ruptur pd membran Bruch
mrangsang neovaskularisasi subretina
– Pd miopia terjd bercak Fuch biperplasi pigmen epitel & perdarahan ,atrofi lapis sensoris
retina luar & dewasaterjdi degenerasi papil saraf optik

• Ps dgn miopia akan mnyatakan mlihat jelas bila mlihat dkat ( dibanding jauh
)rabun jauh
 Miopia
• S/s:skit kepala sering disertai julih & makula & degenerasi retina bag perifer)
celah klopak yg smpt
• Biasanya sering mnyipitkan matanya • T/: pngobatan mberkan kacamata sferis
untuk mncegah aberasi sferis/untuk – terkecil yg mberikan ktamajan
mndapat efek pinhole ( lubang kcil) pnglihatan maks
• Ps miopia mmpunyai pungtum – c/: bila ps dikoreksi dgn -3 mbrikan tjam
remotum yg dkat mata slalu pnglihatan 6/6 & jg -3.25 sbaiknya
dalam/berkedudukan konvergensi diberikan lensa koreksi -3 ( u/mberikan
astenopia konvergensia istirahat mata dgn baik)
– Jika dibiarkan ps akan trlihat juling
kedalam ( esotropia) • Komplikasi: ablasi retina & juling (
esotropia biasanya) krn mata
konvergensi terus terus
• Pd px funduskopi miopik kresen (
gmbaran bulan sabit yg terlihat pd
polus posterior fundus mata miopia • Jika juling keluarterdapat ambliopia
,sklera oleh koroid

• Miopia minus bsa jg terdapat

kelainan pd fundus okuli ( degenerasi
 Correction of Myopia
• Surface ablation procedures can correct low– the iris
– Complications include subluxation or
moderate degrees of myopia. dislocation due to dislodgement of one or
• Laser in situ keratomileusis (LASIK ) both attachments an oval pupil, endothelial
– Can correct moderate to high myopia cell loss, cataract, pupillary-block glaucoma
• depending on initial corneal thickness, and retinal detachment.
but for very high refractive errors one • Phakic posterior chamber implant
of the intraocular procedures below is implantable contact lens, ICL) is inserted
necessary behind the iris and in front of the lens and
• Refractive lenticule extraction supported in the ciliary sulcus.
– The lens is composed of material derived from collagen
– newer technique for the correction of (Collamer) with a power of −3 D to −20.50 D.
myopia and myopic astigmatism.
• Clear lens exchange gives very good visual – Visual results are usually very good but complications
results include uveitis, pupillary block, endothelial cell loss,
cataract formation and retinal detachment.
– but carries a small risk of the
• Radial keratotomy is now predominantly of
complications of cataract surgery
historical interest.
particularly retinal detachment in high
myopes.
• Iris clip (‘lobster claw’) implant is attached to
 Hipermetropia
• rabun dkat mrupakan keadaan gg mrupakan kelainan refraksi krn
kekuatan pmbiasan mata dimana bola mata pendek /sumbu
sinar sjajar jauh tdk cukup anteroposterior yg pendek
dibiaskan shingga titik fokusnya – Hipermetropia
trletak diblakang retina. kurvaturkelengkungan
kornea/lensa lemah bayangan
• Hipermetropisinar difokuskan difokuskan diblakang retina
diblakang makula lutea – Refraktifindeks bias yg lemah –
• Trdpt 3 bntuk hipermetropia : pd mata
1.kongenital: bola mata pendek /kecil
2.simple: lanjutan hipermetropia anak • Tingkatan pd hipermetropi berdasar
yg tdk ber- pd perkembanganya besarnya dioptri:
jarang me> 5 dioptri 1.ringan: spheris +0.25D s/d Spheris +
3.didapat: stlh bedah pengeluaran lensa 3.00 D
pd katarak ( afakia) 2.sedang: spheris +3.25 D s/d Spheris
• E/: + 6.00
– Hipermetropia sumbu/aksial: 3.berat: > spheris 6.00 D
 Jenis hipermetropia
• Manifes: tnpa siklopegik ( yg dpt • lokal: laten & manifes yg ukurannya
dikoreksi dgn kacamata+ maks didapatkan sesudah diberika siklopegia
mberikan tjam pnglihatan normal) (
absolut + fakultatif_ • Gejala : pd anak tdk mberikan keluhan
• Manifes absolut : kelainan refraksi tdk – Keluhan yg dit: pnglihatan dkat & jauh
dpt diimbangi dgn akomodasi & perlu kabur,skit kepala,silau,rasa juling /lihat
kacamata + ganda
• Manifes fakultatif: klainan yg dpt • Matanya mudah lelah & skit (krn terus2
diimbangi dgn akomodasi / kcamata + berakomodasi )u/ melihat/mfokuskan
– Ps akan mlihat normal tnpa kacamata tp bayangan yg terletak diblakang makula
jika diberikan kacamata + mberikan agar trletak di makula luteaastenopia
pnglihatan normal otot akomodasi akan akomodatif mata melakukan
istirahat konvergensijuling ke dalam/esotropia
• Laten: tnpa siklopegia ( /obat yg
melemahkan akomodasi)diimbangi dgn
akomodasi
– Mkin tua seseorang  kelemahan
akomodasi shingga hipermetropia
latenfakultatifabsolut
 Hipermetropia
• Mata dgn hipermetropia sering akan pnglihatnan maks
mprlihatkan ambliopia akibat mata tnpa C:bila ps +3.00 /dgn +3.25 mberikan
akomodasi tdk prnah mlihat objek dgn & ktajaman pnglihatan 6/6 diberikan
jelas kacamata +3.25 hal ini dgn tujuan u/
– Jika trdpt perbedaan kekuatan mberikan istirahat pd mata
hipermetropia akan trjd ambliopi pd
slh 1 mata ( mata ambliopia sering ke
temporal)
– t/ : diberikan koreksi manifes dimana
tnpa siklopegia didapatkan ukuran lensa
+ maks mberikan tjam pnglihatan
(6/6)
– Jika trdpt juling ke dlm /esotropia
kacamata koreksi hipermetropia total
• Jika juling ke luarkoreksi + krg
– Sbaikanya: kacamata sferis + trkuat
/lensa + tsbesar yg mberikan tjam
• Ps muda klo hipermetropi tdk kacamata sferis + trkuat
akan mberikan kluhan krn pnglihatan maks
matanya msh mampu
melakukan akomodasi kuat u/ – Komplikasi: esotropia(Krn
mlihat bnda dgn jelas ps slamanya melakukan
• Pd ps yg bnyak akomodasi ) & glaukoma (
baca/mmprgunakan matanya ( hipertrofi otot siliar pd
trutama ps usia badan siliar yg akan
lanjut)mberikan kluhan mmprsempit sudut bilik
kelelahan stlh baca ( kluhan mata)
tsb brupa : skit kepala,mata
terasa pedas,tertekan)
– Pd ps ini diberikan
 Correction of hypermetropia (hyperopia)

• Surface ablation procedures can correct low degrees of hypermetropia.

• LASIK can correct up to 4 D.
• Conductive keratoplasty (CK) involves:
– the application of radiofrequency energy to the corneal stroma and can
correct low–moderate hypermetropia and hypermetropic astigmatism.
– . CK may also be helpful for presbyopia. Complications are infrequent.
• Laser thermal keratoplasty with a holmium laser can correct low
hypermetropia.
 AFAKIA
• Keadaan dimana mata tdk mmpunyai – Pusat lensa yg dipakai letaknya
lensa hipermetropia tinggi tpt pd tmptnya
• Pasien perlu pemakaian lensa yg – Jarak lensa dgn mata cocok u/
tebalmka akan mberikan keluhan pmakaian lensa afakia
pd mata tsb berikut: – Bag tepi lensa tdk mnggangu
– Benda yg dilihat mnjadi lbh > lapang pandang
25% dibanding normal – Kacamata tdk terlalu berat
– Efek prisma lensa tebal benda
tmpak melengkung
• Pnglihatan spt badut dlm
kotak/fenomaena jack in the box (
bag yg jelas terlihat hnya pd sentral
,tp tepi kabur)

• Pd ps afakia diberikan kacamata yg:

 Astigmatisme
• Berkas sinar tdk difokuskan pd 1 titik dgn tajam
pd retina tp pd 2 garis titik yg sling tgak lurus • Bentuk astigmat:
– Krn kegagalan kelengkungan permukaan – Regular: kkuatan biasan bertambah/ber-
korna prlahan scara teratur dri 1 meridian ke
• Bayi yg baru lahir ( biasanya mmpnyai kornea yg meridian brikutnya
bulat/sferis dlm perkembangannya • Byangan yg terjdi pd astigmatisme
astigmatisme with the rule ( lazim) reguler: garis ,lonjong /lingkaran
– Brarti kelengkungan kornea pd bidang – Ireguler: yg terjadi tdk mmpunyai 2 meridian
vertikal ber+ /lbh kuat/jari2nya lbh pndek sling tegak lurus
dibanding jari2 yg horizongtal • Kelengkungan kornea pd meridian yg
– Perlu lensa silinder – dgn sumbu 180degree sma beda shingga byagan mnjd iregular
• Usia prtengahan kornea mnnjd lbh sferis kmbali • Dpt terjdi krn : infeksi kornea
shingga astigma mnjadi against the rule: trauma,distrofi/kelainan pmbiasan pd
• Astigmatistme against the rulekeadaan kelainan meridian lensa yg beda
refraksi astigmat ( dimana koreksi dgn silinder -)
dilakukan sudut tegak lurus (60-120 drajat) / dgn
silinder + sumbu horisontal ( 30-150 drajat)
– Trjadi akibat kelengkungan kornea pd
meridian horizontal lbh >> ( sering pd usia
lanjut)
 Astigmatisme
• Gejala : pnglihatan • T/koreksi px astigmat
buram,menengok u/ lbh px astigmt (px mata dgn
jelas,mmbaca lbh dkat sentris pd prmukaan
kornea)
• Pngeobatan dgn lensa
kontak keras bila epitel • Juling/kipas astigmat
tdk rapuh /lensa kontak garis berwrna hitam yg
lmbek bila disebabkan disusun radial dgn bntuk
infeksi,trauma dan dsitrofi smisirkular dgn dasar yg
untuk mberikan lbh dkeat putihdigunakan untuk
• Pd ps plasidoskopi px subjektif & besarnya
gmbaran yg ireguler kelainan refraksi astigmat
 Correction of astigmatism
• Limbal relaxing incisions/arcuate keratotomy involves:
– making paired arcuate incisions on opposite sides of the cornea in
the axis of the correcting‘plus’cylinder (the steep meridian).
• • PRK and LASEK can correct up to 3 D.
• • LASIK can correct up to 5 D.
• Lens surgery involves using a ‘toric’ intraocular implant
incorporating an astigmatic correction
• Postoperative rotation of the implant away from the desired
axis occurs in a small minority of cases.
• Conductive keratoplasty (see ‘Correction of
hypermetropia’
 Diplopia
• Double vision has many causes from
benign entity of an incorrect spectale – Monocularif double vision/even mor
• Ocular,orbital ,intracranial,generalized than 2 image ( is present when the
neurological ,systemic diseasecan all patient is viewing with only 1 eye) (
whether it is just with one eye /with
present with double vision each alone
• The visual disturbance is not due to
• TRIAGE ocular misalignment likely to be due
refractive error,lens opacity/possibly
– IN Oculomotor nerve palsy there macular disease
may be clues from associated ptosis or
pupillary abnormality • Every episode of double vision has an
– Otherwise ,unless pattern of double acute onset ( because double vision is
eiteher pres ent /not
vision (reported b the ps )leads to
identifacation of specific entity
• An ocular motor cranial nerve palsy is
abducens nerve palsy ( n6) diagnosed it is essential to determine
– In general ,ps with multive cranial whether is is isolated/multiple cranial
nerve palsies/other neurologic features nerve dysfunction
severe headache,associated sytemic
ilnness • In oculomotor nerve palsy the presence
of pupillary dysfunction,eaither
• Clinical assesment anisocoria /particulary impaired
– Double vision is usually due to ocular respolnse to light provides importan
misalignment,but 1st step evaluation is clue of possibility of a compressive
lesion ( posterior communicationg
to determine wheteher it is artery anereusym)
monocolura/binocular
 Diplopia
• Specific eye movement abnormalities provide
precise anatomical localitation.
– Internuclear opthalmoplegia  there is impairment
of adduction of 1 /both eyes , localizes to the
medial longitudinal fasciculus within the
brainstem)
– Horizontal gaze plalsy (there is loss of conjugate
horizontal gaze to 1/both sides ) ( localizes to the
pons)
– Vertical gaze palsymidbrain
 Diplopia binokuler
• Istilah diplopia berasal dari bahasa yunani:
diplous, artinya ganda, and ops, artinya mata.
• Diplopia adalah penglihatan ganda disebabkan
oleh kerusakan fungsi otot-otot ekstraokuler
atau gangguan nervus yang menginervasi otot-
otot tersebut. Diplopia binokuler atau diplopia
sejati adalah kerusakan kemampuan nuntuk
memfusikan bayangan dari sistem binokular.
• Diplopia binokuler hanya terjadi • Masalah-masalah tersebut
jika kedua mata bekerja bersama. termasuk:
Pada diplopia jenis ini, • StrabismusKerusakan saraf yang
penglihatan ganda pasien mengontrol otot-otot ekstraokuler:
menghilang jika salah satu mata – kerusakan ini bisa dikarenakan
ditutup dan diuji sendiri-sendiri. infeksi, stroke, trauma kepala atau
• Diplopia Binokuler adalah suatu tumor otak
kondisi yang berkaitan dengan • Infark mikrovaskuler pembuluh
gangguan kesejajaran dari mata, darah yang memperdarahi
dan dapat disebabkan oleh semua persarafan otot-otot mata.
masalah yang mengenai satu atau • Myasthenia gravisGrave's disease
lebih dari otot-otot ektraokuler. (suatu bentuk hyperthyroidism)
• Trauma pada otot-otot mata
 Pemeriksaan fisik
• Anamnesis • Melakukan pemeriksaan
– Gejala terpenting: apakah ketajaman visual dari
diplopianya horizontal (2 masing-masing mata
bayangan berdampingan) /
vertical (2 bayangan terlihat • Evaluasi lapangan pandang
menumpuk atas bawah). dengan uji konfrontasi.
– Oblique diplopia (2 bayangan
terpisah baik vertikal maupun
horizontal) harus dianggap
sebagai manifestasi dari
vertical diplopia.
– onset (cepat atau lambat),
keparahan, durasi, lokasi,
gejala-gejala terkait, dan
faktor-faktor yang
memperparah dan
memperlemah gejala.
• Evaluasi fisiologis aspek motoris :
• Evaluasi anatomis
• Tentukan adanya kisaran normal
pergerakan okuler. meliputi inspeksi,
• Tentukan bahwa masing-masing mata palpasi, perkusi dan
mampu addusi dan abduksi
sepenuhnya dan mampu elevasi dan auskultasi
depresi selagi abduksi dan adduksi
sepenuhnya (sebagaimana mata
bergerak seperti huruf "H")
• Tentukan apakah diplopia memburuk
jika otot-otot mata menjadi lelah
• Tentukan apakah fungsi motoris
normal.
 Tatalaksana
• Konservatif: • KIE :
• Menutup satu mata untuk • pasien dengan diplopia
mencegah diplopia harus menghindari
• Prisma Fresnel mengemudi atau
• pengobatan myasthenia mengoperasikan mesin.
gravis
• Surgical Care:
• Hummelsheim surgery
• Pembedahan otot obliq
superior Knapp
 Management
• Isolated ocular motor cranial nerve palsy in ps >
50 are due to ischemic ( microvascular disease)
• In isolated oculomotor nerve palsy suspicion of
posterior communicating artery aneurysm due
papillary involvment

• Initial treatment with prism

• In ps with myasathenia gravis it is important to
establihsh whether there is non –ocular weakness
 generalized diseases ( impairment of
breathing/swallowing )
 Amblyopia
• Keadaan mata dimana tajam pnglihatan tdk sensitif
mncapai optimal sesuai dgn usia &
intelegensinya wlau sdh dikoreksi kelainan – Bratnya ambliopia berhub dgn lamanya
refraksinya. mngalami krgnya rangsangan u/ prkembangan
pn’glihatan makula
• Pd ambliopia trjdi pnurunan tjam pnglihatan
unilateral/bilateral ( krn kehilangan pngenalan • Jika ank di<6 thn msh dpt dilakukan latihan
bntuk ,interaksi binokular abnormal /ke2 nya u/ prbaikan pnglihatan
)(dimana tdk dit kausa organik pd px fisik mata
& pd kasus keadaan baik ,dpt dikembalikan • e/: anisometropia,juling,oklusi & katarak
fungsinya dgn pngobatan.
• 2 faktor diduga pnyebab trjdinya ambliopia
• Dpt terjd tnpa kelainan organik & dpt pula dgn supresi & non use
kelainan organik – Non use: akibat tdk dipergunakannya elemen
visual retino kortikal pd saat kritis
perkembangannya sblm 9 thn
• e/ dr ambliopia biasanya kurangnya rangsangan
– Supresi ( terjdi akibat krn proses kortikal
u/ mningkatkan perkembangan pnglihatan mngakibatkan terjdinya skotoma absolut
pnglihatan binokular )
– e/ ekstraneural yg mnyebabkan mnurunnya tajam
pnglihatan ( katarak,astigmat,strabismus/kelainan
refraksi unilateral/bilateral yg tdk
dikoreksimmicu pnurunan fungsi visual pd org
 Tanda pd mata ambliopia
• Berkurang pnglihatan 1 mata
• Mnnuruannya tajam pnglihatan ( fenomena crowding)
• Hilangnya sensitivitas kornea
• Mata mudah mnglami fiksasi eksentrik
• Adanya anisokoria
• Tdk pngaruh pd pnglihatan wrna
• Daya akomodasi turun
• ERG & EEG slalu norma ( yg berarti tdk ada kelainan
organik pd retina /korteks serebri)

• Pencegahan pd anak usia < 5 thn perlu px tajam

pnglihatan ( trutama bila anak juling)
 Px ambliopia
• Px & mngetahui prkembangan • Uji densiti filter netral
tajam pnglihatan sjak bayi -9 thn – Jika pd mata ambliopia
( u/ mcengah kterlambatan) dilakukan dgn uji pnglihatan
• Px kedudukan mata & reaksi intensitas sinar yg direndahkan
pupil slain px fundus terjdi pnurunana tajam
pnglihatan
• Uji crowding phenomena ( u/
tau ada ambliopia)
– Ps suruh baca huruf snelen
• Uji worth’s four dot ( u/ fusi &
smpai huruf terkecil yg dibuka pnglihatan stereosis )
1 persatu/yg diisolasi ,kemudian – Uji u/ liat pnglihatan binokular
isolasi huruf dibuka & ps suruh ( fusi,korespondensi ,retina
melihat sbaris huruf yg sama abnormal ,supresi pd 1 mata &
• Klo ada pnurunan tajam juling)
pnglihatan dari huruf isolasi ke – Baca hal 267 FKUI
huruf dalam baris fenomena
crowding pd mata tsb brarti
ada ambliopia
 Classification
• Strabismic amblyopia results from – It may be unilateral or bilateral and is
abnormal binocular interaction typically caused by opacities in the
where there is continued monocular media (e.g. cataract) or ptosis that
covers the pupil.
suppression of the deviating eye.

• Bilateral ametropic amblyopia results

• Anisometropic amblyopia is caused from high symmetrical refractive errors,
by a difference in refractive error usually hypermetropia.
between the eyes and may result from a
difference of as little as 1 dioptre.It is • Meridional amblyopia results from image
frequently associated with blur in one meridian.
microstrabismus and may coexist with – It can be unilateral or bilateral and is caused by
uncorrected astigmatism (usually >1 D) persisting
strabismic amblyopia. beyond the period of emmetropization in early
childhood.

• Stimulus deprivation amblyopia results

from vision deprivation.
Ambliopia Ambliopia strabismik Ambliopia Ambliopia Ambliopia
fungsional refraktif anisometropik ametropik

: dpt terjdi : trjdi akibat juling Ambliopia pd mata -krn kelainan -mnurunya tajam
kongenital/didapat lama (biasanya eso) ametropia/anisome refraksi ke 2 mata pnglihatan dgn
dgn tajam trjd supresi pd mata tropi yg tdk yg berbedas jauh
u/ mncegah diplopia
kelainan refraksi
pnglihatan – tnpa :kedudukan bola mata
dikoreksi & mata berat yg tdk
kelainan organik ( tdk sejajar shingga dgn isometropia ( -krn anisometropik dikoreksi (
yg tdk dpt hnya 1 mata yg pd hipermetropia bayangan benda pd hipermetrop/astig
diperbaiki dgn diarakan benda yg dalam /miopia ke2 mata tdk sama matisme (biasa)
kacamata) dilihat berat ) besar jdnya
bayangan pd retina -pd ke2 mata tdk
Resiko anak2 Fiksasi silang: (liat Ambliopia yg terjd diluar fokus (
kekanan pake mata
mncapai
Smpai usia 6-7 thn kiri & sbalikny)
pd mata dgn shingga mata akan pnglihatan 5/5
resiko trhdp antiuji ambliopia kelainan refraksi fokus melihat dgn biasany
ambliopia strabismmik dalam tdk 1 mata) pnglihatan
fungsional dikoreksi /kelainan hipermetropi tinggi
Pngobatan: mmnutup refraksi pd ke2 Beda refraksi yg (+7.0d) /astigmat
Pengobatan mata yg sehat & rujuk mata ( >> trbentuk tinggi(3.0 D) krn
ambliopia meliputi (dpt pulih kmbali pd anisometropia) bayangan kabur pd ps tdk mlihat
anak <9thn)
: oklusi ,penalisasi komplikasi: diplopia
1 mata byangan jelas
Yg pling efektif: Pnglihatan mnjadi Mata tdk dpt
oklusi mata baik stlh bbrp berfusi krn adanya T: mberikan
bulan pake perbedaan refraksi kacamata yg baik
kacamata koreksi
Ambliopia Ambliopia Ambliopia histeria Ambliopia organik
eksanopsia intoksikasi
:trjdi krn pnglihatan : intoksikasi krn : lapang pndang yg : terjdi akibat
terganggu pd saat pmakaian tmbakau
perkembangan bayi
mnciut konsentris & krusakan fovea
,alkohol yg lbh karakteristik kongenital shingga
:e/krn supresi /proses
aktif dari otak u/ menekan : gmbaran sprti mnggangu ps
kesadaran melihat Timah/bahan toksik
spiral slama
Dpt terjd pd katarak Biasanya tnd neuritis dilakukan px lapang Tdk reversibel
kongenital,ptosis,kruh optik toksik krn pandang
kornea keracunan disertai ada
-jika ank krg dari 4 thn tnda2 lapang pnadang
mnderita pnglihatan dpt
Gejala lain:
>> buruk
yg berubah2 blefarospasme,mem
ajkan mata &
Disebabkan jg krn mata Hilangnya tjam
lakrimasi
tdk dipergunakan dgn pnglihatan sentral
baik(biasanya krn juling bilateraldiduga
kedalam) kracunan metilalkohol Reaksi pupil normal
/gizi buruk
Tx: mnutup mata sehat
stlh mata skit dibersihkan
kekeruhannya
Katarak dpt mnimbulkan
komplikasi: nistagmus &
strabismus
 Diagnosis
• In the absence of an organic lesion, a difference in best
corrected VA of two Snellen lines or more (or >1 log unit) is
indicative of amblyopia.

• Visual acuity in amblyopia is usually better when reading

single letters than letters in a row.
• This ‘crowding’ phenomenon occurs to a certain extent in normal individuals but is
more marked in amblyopes and must be taken into account when testing preverbal
children.
 Treatment
• It is essential to examine the fundi on the age of the patient and the density of
amblyopia.
– diagnose any visible organic – The younger the ps the >> rapid
disease prior to commencing improvement but greater risk ( inducing
treatment for amblyopia amblyopia in the normal eye)
– If no improvement after 6 months effective
• The sensitive period during which oclusion( further treatment is unlikely to be
acuity of an amblyopic eye can be fruitful)
improved  usually up to 7–8 years • Penalizationwhich vision in the
in strabismic amblyopia and may be normal eye is blurred with atropin
longer (into the teens) for – Work best in the treatment of moderate
anisometropic amblyopia where good ambylopia (6/24)
binocular function is present. – Patch occlusion is likely to produce a quicker
response than atropine
• Occlusion of the normal eye, to
encourage use of the amblyopic eye, is
the most effective treatment.
– The regimen, full-time or part-time, depends
 Tatalaksana Ambliopia
• Sifatnya reversibel & trgantung dkat dgn mmberi lensa +2.5 D
pd saat mulai & lamanya sdg mata yg baik diberi atropin)
– Saat rentan: bayi pd umur 6 bln – Penalisasi jauhmata yg
pr 1 & ambliopia tdk akan terjdi ambliopi suruh ngeliat jauh dgn
ssdh usia > 5 thn mmberi atropin pd mata yg baik
– Bila ditmukan pd usia di< 6 thn lalu diberi lensa +2.5 D
msh dpt dilakukan latihan u/ – Latihan ortoptik klo juling
perbaikan pnglihatan – Pncegahan ambliopiapd anak
usia < 5 thn prlu px tajam
pnglihatan trutama bila
• Pengobatan dpt dgn : mmprhatikan tnada juling
– Pngobatan antisupresi aktif
myingkirkan faktor
ambliopiagenik
– Oklusi mata sehat
– Penalisasi dkat ( mata
ambliopia dibiasin suruh ngeliat
 Diabetic Retinopathy
BACA FK UI JG HAL 230-234
• Risk Factor
– Duration of diabetes is the most important risk factor. In patients diagnosed with diabetes < the age of 30
years the incidence of DR after 10 years is 50%, and after 30 years 90%.
– Poor control of diabetes.
• shown that tight blood glucose control, particularly when instituted early, can prevent or delay the development or
progression of DR.
• Raised HbA1c is associated with an increased risk of proliferative disease.
• Predicating factors include greater pre-pregnancy severity of retinopathy, poor pre-pregnancy
control of diabetes, control exerted too rapidly during the early stages
– risk of progression is related to the severity of DR in the first trimester.
• Diabetic macular oedema usually resolves spontaneously after pregnancy and need not be treated if it
develops in later pregnancy.

• Hypertension, which is very common in patients with type 2 diabetes, should be rigorously
controlled (<140/80 mmHg).
– Tight control appears to be particularly beneficial in type 2 diabetics with maculopathy.
– Cardiovascular disease and previous stroke are also predictive.
• Nephropathy, if severe, is associated with worsening of DR.
.
• • Other risk factors include hyperlipidaemia, smoking, cataract surgery, obesity and anaemia.
 Pathogenesis
• DR is predominantly a microangiopathy  which
small blood vessels are particularly vulnerable to
damage from high glucose levels.

• Direct hyperglycaemic effects on retinal cells are

also likely to play a role.

• Many angiogenic stimulators and inhibitors have

been identified; vascular endothelial growth
factor (VEGF) appears to be of particular
importance in the former category.
 Classification
• Background diabetic retinopathy – PPDR indicates progressive retinal
(BDR) is characterized by ischaemia, with a heightened risk of
microaneurysms, dot and blot progression to retinal
haemorrhages and exudates. neovascularization.
– These are generally the earliest signs
of DR, and persist as more advanced • • PDR is characterized by
lesions appear. neovascularization on or within one
disc diameter of the disc (NVD)
• Diabetic maculopathy strictly and/or new vessels elsewhere (NVE)
refers to the presence of any in the fundus.
retinopathy at the macula, but is
commonly oedema and ischaemia.
• Advanced diabetic eye disease is
• Preproliferative diabetic characterized by tractional retinal
retinopathy (PPDR) manifests detachment, significant persistent
– with cotton wool spots vitreous haemorrhage and
– venous changes neovascular glaucoma.
– intraretinal microvascular anomalies
(IRMA) and often deep retinal
haemorrhages.
 Signs
a) Microaneurisma localized outpouchings, into the retina as a result of breakdown in
mainly saccular, of the capillary wall that the blood–retinal barrier, or may thrombose.
may form: They tend to be the earliest sign of DR
– either by focal dilatation of the • Signs.: Tiny red dots, often initially
capillary wall where pericytes are temporal to the fovea (Fig. 13.3A); may be
absent, or by fusion of two arms of a indistinguishable clinically from dot
capillary loop haemorrhages.
– Loss of pericytes may also lead 
endothelial cell proliferation with the • Fluorescein angiography (FA) allows
formation of ‘cellular’ microaneurysms differentiation between dot haemorrhages
• Microaneurysms  leak plasma constituents and non-thrombosed microaneurysms.

(A) Microaneurysms and dot/blot

haemorrhages at the posterior pole;
 Signs
Exudates
• Hard exudates caused by chronic • Waxy yellow lesions with relatively distinct
localized retinal oedema: they develop at margins arranged in clumps and/or rings at
the junction of normal and oedematous the posterior pole, often surrounding leaking
retina microaneurysms.
• composed of lipoprotein and
lipid-filled macrophages located • With time the number and size tend to
mainly within the outer plexiform increase, and the fovea may be involved.
layer . • When leakage ceases, exudates absorb
• Hyperlipidaemia may increase the spontaneously over a period of months,
likelihood of exudate formation. either into healthy surrounding capillaries or
Signs by phagocytosis.

more extensive exudates,

some associated with exudates involving the
microaneurysms fovea, including central crystalline cholesterol deposition
 Sign
Cotton wool spot
• accumulations of neuronal debris post-equatorial retina, where the
within the nerve fibre layer. nerve fibre layer is of sufficient
– Cause from ischemic disruption of nerve thickness to render them visible.
axons ,swollen ends ( cytoid bodies)
– As cotton wool spots heal debris is • FA shows focal hypofluorescence due to local
removed by autolysis & phagocytosis ischaemia and blockage of background choroidal
• Signs. fluorescence.
– Small fluffy whitish superficial lesions that
obscure underlying blood vessels.
– they are clinically evident only in the

red-free photography showing differing

appearance of cotton wool spots and
haemorrhages, the
latter appearing black – the smaller well-
defined white
lesions are exudates
 Sign
Venous changes
• Venous changes
• Venous anomalies seen in ischaemia
– consist of generalized dilatation and tortuosity, looping, beading (focal
narrowing and dilatation) and sausage-like segmentation.

• The extent of the retinal area exhibiting venous changes

correlates well with the likelihood of developing proliferative
disease.
 Proliferative retinopathy
• Preretinal new vessels may arise anywhere in the retina
– most commonly seen at the posterior pole.
– Fibrous tissue, initially fine, gradually develops in association as vessels
increase in size.
• New vessels at the disc (NVD) describes neovascularization on or
within one disc diameter of the optic nerve head
• New vessels elsewhere (NVE) describes neovascularization further
away from the disc ; it may be associated with fibrosis if long-standing.
• New vessels on the iris (NVI), also known as rubeosis iridis, carry a high
likelihood of progression to neovascular glaucoma
 TREATMENT
GENERAL
• Patient education is critical, including regarding the need to comply
with review and treatment schedules in order to optimize visual outcomes.

• Diabetic control should be optimized. Other risk factors, particularly

systemic hypertension (especially type 2 diabetes) and hyperlipidaemia
should be controlled in conjunction with the patient’s diabetologist.

• Fenofibrate 200 mg daily has been shown to reduce the progression of

diabetic retinopathy in type 2 diabetics and prescription should be
considered; the decision is independent of whether the patient already takes
a statin.
• Smoking should be discontinued, though this has not been definitively
shown to affect retinopathy.
• Other modifiable factors such as anaemia and renal failure should be
addressed as necessary.
 Mata tenang Penurunan Visus 7. Neuritis optic
Mendadak: 8. Ambliopia toksik
1. Vitreous Hemorrage 9. Atrofi optik
2. Retinal Detachment /ablasio 10. Migraine
retina 11. Uveitis posterior
3. RAOD,RVOD
4. Amaurosis Fugax
5. Cntral Serous
chorioretinopathy
6. Papil edema

LI 5
 Retinal Hemorrhage
• Retinal nerve fibre layer haemorrhages arise from the larger
superficial pre-capillary arterioles and assume their characteristic shape
because of the architecture of the retinal nerve fibre layer.

• Intraretinal haemorrhages arise from the venous end of capillaries and are
located in the compact middle layers of the retina with a resultant red
‘dot/blot’ configuration .

• Deeper dark round haemorrhages represent haemorrhagic retinal infarcts

and are located within the middle retinal layers .

• The extent of involvement is a significant marker of the likelihood of

progression to PDR.
 Retinal vein occlusive disease
• Branch retinal vein occlusion (BRVO) arteriolosclerotic thickening of a branch
retinal arteriole is associated with compression of a venule at an arteriovenous
crossing point.
– changes that include endothelial cell loss, turbulent flow and thrombus formation

– Venous occlusion occurredelevation of venous & capillary pressure (with stagnation of

blood flow) retinal hypoxia  damage to capillary endothelial cells ,extravasation of
blood constituent & mediators ( VEGF)
• Risk Factor
– Age : over 50% occur in ps > 65 years
– Hypertension
– Hyperlipidemia
– DM
– Glaucoma
– Oral contraceptive pill
– Smoking
– Uncommon : dehydration,myeloproliferative disorder,thrombophilia,inflammatory
disease associated with occlusive periphlebitis ,orbital disease & chronic renal failure
 OVRS
• Penyumbatan vena retina yg • E/:
mengakibatkan gg perdarahan dlm – Krn kompresi dr luar trhdp vena tsb
bola mata – Pnyakit pd p.d vena sndiri (
• Trletak dimana sj pd retina ( akan fibrosklerosis/endoflebitis)
ttp lbh sering didpn lamina kribosa) – Hambatan aliran darah dlm pmbuluh
vena tsb ( viskositas darah,diskrasia
• Pnyumbatan vena dpt terjd pd suatu darah/spasme arteri retina yg
cbang kecil/pmbuluh vena utama ( berhubungan)
vena retina sentral)
• Pnyumbatan cabang vena retina lbh • Tjam pnglihatan sentral trgg bila
sering ada di daerah temporal atas perdarahan mngenai daerah makula
/temporal bwh lutea
• Pnyumbatan vena retina – Ps biasany mngeluh pnurunan tajam
sentralmdh trjd pd ps dgn pnglihatan sentral/perifer mendadak (
glaukoma,DM,hipertensi,kelainan mmburuk tinggal persepsi cahaya)
darah,arteriosklerosis – Gk ada rasa sakit & mngenai 1 mata
–
 OVRS
• Pd px funduskopi: mngalami hipoksia
– Vena yg berkelok2 • Steroid diberi jika pnyumbatan
– Edema makula & retina disebabkan o/ flebitis
– Perdarahan brupa titik ( trutama bila • Pnyumbatan akan terjd gg fungsi
trdpt pnyumbatan vena yg tdk smpurna)
pnglihtan tajam pnglihatan ber-
• Pd retina dan makulaedema & – Bsa dipertimbangkan u/ fotokoagulasi
bercak wol yg ada diantara bercak
perdarahan • Pnyulit oklusi vena sentral:
– Prdarahan masif ke dlm retina ( trutama
pd serabut saraf retina & tnda iskemia
• Papil yg merah & mnonjol disertai retina)
pulsasi vena hilang
• Pnciutan lapang pandang /skotoma – Pmbuluh darah baru yg dpt ditemukan
diskitar papil.iris & diretina (rubeosis
sentral & defek iregular iridis)
– Rubeosis iridis dpt terjdi nya glaukoma
• Pngobatan: mncari pnyebab & sekunder
mngobati,antikoagulasi &
fotokoagulasi daerah retina yg
 OARS
symptom
• Symptoms. corresponding to the area of
– Sudden and profound ischaemia.
painless altitudinal or – One or more occluding
sectoral visual field loss. emboli may be seen,
– VA is variable. especially at bifurcation
points.
• Fundus signs may be – The affected artery is likely
subtle to remain attenuated.
– Attenuation of arteries and • Review in 3 months is
veins with sludging and
segmentation of the blood warranted to review the
column (‘cattle trucking/ appearance of the fundus,
boxcarring’). the visual fields,
– Cloudy white oedematous
(ground glass) retina
 Oklusi arteri retina sentral
• Trdpt pd usia tua/pertengahan dgn pucat krn edema & gg nutrisi
kluhan pnglihatan kabur yg hilang
timbul ( amaurosis fugaks) tdk
disertai rasa skit & gelap mnetap • Trdpt gmbaran bntuk sosis pd arteri
retina krn pngisian arteri yg tdk
• E/ temporal arteritis & nonarteritik ( merata
emboli) • Lalu retina akan tmpak pucat ,keruh
• Pnurunan visusserangan berulang abu2 (Disebabkan edema lapisan
dpt disebabkan o/ pnyakit spasme dlm retina & lap sel
p/d /emboli berjalan ganglion)cherry red spot pd
• Pnyumbatan arterikeluhan makula lutea )disebabkan krn tdk
pnglihatan tiba2 gelap tnpa adanya lap ganglion dimakula
terlihatnya kelainan pd mata luar )makula mmprtahankan wrna
• Reaksi pupil mnjd lemah dgn pupil aslinya
anisokor

• Pd px funduskopi: retina berwarna

 OARS
• Pnyumbatan dpt disebabkan o/: • Vasodilator+ bersama antikoagulan
– Radang arteri & diberikan steroid bila diduga
– Trombus ada pradangan
– Embolus • Ps dgn OARS harus diberi O2
– Spasme pmbuluh darah )krn scapatnya
trlambatnya aliran pd
– Tmpt trsumbatnya arteri retina • Pnyulit”
sentral biasanya didaerah lamina – Glaukoma neovaskular(trgntung pd
kribosa letak & lamanya oklusi )
• Emboli  pnybab pnyumbatan – Kdg visus bs kmbali normal tp
arteri retina sentral yg pling sering lapang pandang smpit
• Pnybab spasme pmbuluh lainnya:
migren,kracunan alkohol ,tmbakau
• Pngobatan dini mnurunkan
tkanan bola mata dgn mngurut bola
mata & asetazolamid /parasentesis
bilik mata dpn
 TREATMENT
• Retinal artery occlusion  is an emergency because it causes irreversible visual loss
unless the retinal circulation is re-established prior to the development of retinal
infarction

• .The following treatments may be tried in patients with occlusions of less than 24–48
hours.
– Adoption of supine positionimprove ocular perfusion
– Ocular massage improve perfusion & potentially dislodge an embolus /thrombus
– Anterior chamber paracentesis ( povidone iodine 5% & topical antibiotic) instilled a few minutes
prior to procedure
– Topical apraclonidine 1% ,timolol 5% & IV acetazolamid 500 mg lowering TIO
– Sublingual isosorbide dinitratinduce vasodilation
– Breathing high oxygen 95%
– Hyperosmotic agentmanitol /glycerol hve been use for their possibly rapid IOP lowering effect
as well intravascular vol
– Transluminal ND /Embolectomy
– Thrombolysis