PEMICU 1

PENGINDERAAN
Cindy Claudia
405140139
LI 1
Anatomi MATA
Moore Clinical Oriented Anatomy
Eyelids & Lacrimal APPARATUS
Moore Clinical orieted anatomy
Innervation of
Lacrimal gland
Layers of eyeball
 Eyeball
 Occupies most of the anterior portion of
the orbit, suspended by six extrinsic
muscles that control its movement,
and a fascial suspensory apparatus.
 It measures approximately 25 mm in
diameter.
 The connective tissue layer is composed
: 2. Vascular layer (middle coat), consisting
 posteriorly of the fascial sheath of the
eyeball (bulbar fascia or Tenon
capsule) which forms the actual
socket for the eyeball & anteriorly of
bulbar conjunctiva.
 A very loose connective tissue layer
the episcleral space (a potential space)
lies between the fascial sheath and the
outer layer of the eyeball, facilitating
movements of the eyeball within the
fascial sheath.
The three layers of the eyeball are the
1. Fibrous layer (outer coat), consisting of
the sclera and cornea.
of the choroid, ciliary body, and iris.
3. Inner layer (inner coat), consisting of the
retina, which has both optic and non-
visual parts.
Extraocular Muscle of the orbit
Nerves of the orbit
 The optic nerves begin at the lamina cribrosa of the sclera, where the
unmyelinated nerve fibers pierce the sclera and become myelinated, posterior
to the optic disc exit canal optic
 the optic nerves are surrounded by extensions of the cranial meninges and
subarachnoid space,the latter occupied by a thin layer of CSF.

 optic nerve (CN II), the nerves of the orbit include those that enter through the
superior orbital fissure and supply the ocular muscles: oculomotor (CN III),
trochlear (CN IV), and abducent (CN VI) nerves). A memory device for the
innervation of the extra-ocular muscles moving the eyeball is similar to a
chemical formula: LR6SO4AO3
Vasculature of the Orbit
Veins of orbits
LI 2
Histologi MATA
Difiore Atlas of Histology
Junquiera Basic Histology TEXT & Atlas 13th edition c
Junquiera Basic
Histology TEXT &
Atlas 13th edition c
Junquiera Basic Histology TEXT & Atlas 13th edition c
IRIS

Junquiera Basic
Histology TEXT &
Atlas 13th edition c
Retina / Tunika Neuralis
 Dari sisi luar yg brbatasan dgn koroid dalam :
 Epitel pigmen
 Lapis batang & krucut
 Mmbran limitan luar
 Lapis inti luar
 Lapis pleksiform luar
 Lapis inti dalam
 Lapis pleksiform dalam
 Lapis sel ganglion
 Lapis serat nervus optikus
 Membran limitan dalam
Diverse function of Pigmented
Epithelium
■■ The pigmented layer absorbs scattered light that passes through the neural layer,
supplementing the choroid in
this regard.
■■ With many tight junctions, cells of the pigmented epithelium form an important part of the
protective blood-retina
barrier isolating retina photoreceptors from the highly vascular choroid and regulating ion
transport between
these compartments.

■■ The cells play key roles in the visual cycle of retinal regeneration, having enzyme systems
that isomerize
all-trans-retinal released from photoreceptors and produce 11-cis-retinal that is then transferred
back to the photoreceptors.
■■ Phagocytosis of shed components from the adjacent photoreceptors and degradation of this
material occurs in these epithelial cells.
■■ Cells of pigmented epithelium remove free radicals by various protective antioxidant
activities and support the neural retina by secretion of ATP, various polypeptide growth
factors, and immunomodulatory factors.
Accessories structure of the eye
LI 3
FISIOLOGI MATA
Phsyiology Laurelee sherwood
Proses Refraksi
Phototransduction by retinal cells (
convert light stimuli  neural signals)
1. An outer segment, which lies closest to the eye’s exterior,
facing the choroid. It detects the light stimulus.

2. An inner segment, which lies in the middle of the

photoreceptor’s length. It contains the metabolic machinery
of the cell.

3. A synaptic terminal, which lies closest to the eye’s interior,

facing the bipolar cells. It transmits the signal generated in the
photoreceptor on light stimulation to these next cells in the
Visual pathway.
Visual Pathway
Ganong
Review of Medical Phsyiology
COLOR VISION
LI 4
Penurunan visus perlahan : 9. Buta senja
1. Retinopati diabetikum 10. Degenerasi makula
2. Katarak 11. Hipertensi retinopati
3. Miopia 12. Anisometropi
4. Hipermetropi 13. Diplopia
5. Presbiopi 14. Keratokonus
6. Glaukoma 15. Strabismus
7. Astigmatisme 16. Retinitis pigmentosa
8. Ambliopia
Keratoconus
 is a progressive disorder in which central or paracentral
corneal stromal thinning occurs, accompanied by apical
protrusion and irregular astigmatism.
 Approximately 50% of normal fellow eyes will progress to
KC within 16 years.
 It can be graded by the highest axis of corneal power on
keratometry as
 mild (<48 D)

 moderate (48–54 D)

 severe (>54 D)
Keratoconus
 Diagnosis
 Symptoms. Unilateral impairment of vision due to progressive
myopia and astigmatism; occasionally, initial presentation is with
acute hydrops.
 Signs :
 Direct ophthalmoscopy shows a fairly well delineated ‘oil
droplet’ reflex
 Retinoscopy shows an irregular ‘scissoring’ reflex.
 Slit lamp biomicroscopy shows very fine, vertical, deep
stromal stress lines, which disappear with pressure on the
globe.
 Epithelial iron deposits, best seen with a cobalt blue filter, may
surround the base of the cone (Fleischer ring)
 Progressive corneal protrusion in a cone configuration, with
thinning maximal at the apex.
 Treatment
 LASIK is contraindicated
 patients should be screened for KC prior to corneal refractive surgery.
 Eye rubbing should be avoided.
 Spectacles or soft contact lenses are generally sufficient in early
cases.
 Rigid contact lenses, sometimes scleral, are required for higher
degrees of astigmatism.
 Corneal collagen cross-linking (CXL), using riboflavin drops to
photosensitize the eye followed by exposure to ultraviolet-A light,
may stabilize or even reverse ectasia.
 Intracorneal ring segment implantation using laser or
mechanical channel creation
 Keratoplasty, either penetrating or deep anterior lamellar
(DALK), may be necessary in patients with severe disease.
Anisometropia
 Anisometropia is a difference in refractive error between the
two eyes
 major cause of amblyopia because the eyes cannot
accommodate independently and the more hyperopic eye is
chronically blurred
 Refractive correction of anisometropia is complicated by
differences in size of the retinal images (aniseikonia)
 Correction
 Spectacle  difference in retinal image size of
approximately 25%, which is rarely tolerable
 Contact lens  difference in image size to approximately
6%, which can be tolerated
 Intraocular lens  difference of less than 1%
AGE-RELATED MACULAR
DEGENERATION
 is a degenerative disorder
affecting the macula.  Risk factors :

 It is characterized by the  Age

presence of specific clinical  Race
findings, including drusen and
RPE changes, in the absence of  Heredity
another disorder.  Smoking

 Later stages of the disease are  Dietary factors.

associated with impairment of  Aspirin

vision.
 The prevalence increases with
age and symptoms are rare in
patients under 50 years of age.
 Pathogenesis
 degeneration of the retinal pigment epithelium, linked to oxidative stress
 Changes in the adjacent extracellular matrix of Bruch's membrane and the
formation of subretinal deposits
 diffuse thickening of Bruch's membrane 

 oxygen diffusion into retinal pigment epithelium and photoreceptors ↓ 

 release of growth factors and cytokines 

 growth of choroidal new vessels 
 grow through into the subretinal space 
 choroidal neovascular membrane 
 new vessels leak serous fluid and/or blood  distortion and reduction of
clarity of central vision 
 progression of the degenerative process to cell death and atrophy of the
retinal pigment epithelium  visual loss
Classification
 Conventionally, AMD has been divided into two main
types:
 Dry (non-exudative, non-neovascular) AMD is the most
common form, comprising around 90% of diagnosed
disease.
 Geographic atrophy (GA) is the advanced stage of dry
AMD.
 Wet (exudative, neovascular) AMD is much less common
than dry, but is associated with more rapid progression to
advanced sight loss.
Early Age-Related Macular Degeneration
Late Age-Related Macular Degeneration
Prophylactic Therapy
 Recommended daily supplementation based on AREDS2:
 Vitamin E (400 IU).
 Vitamin C (500 mg).
 Lutein (10 mg).
 Zeaxanthin (2 mg).
 Zinc (25–80 mg)
 Copper (2 mg).
 A liberal green leafy vegetable intake confers a lower risk of
AMD.
 Cessation of smoking should be advised.
 Protective measures against exposure to excessive sunlight
should be considered.
 Treatment of Neovascular Age-Related Macular
Degeneration
 Conventional retinal laser Bevacizumab
photocoagulation  Surgery (part of clinical trial)
 photodynamic therapy  surgical removal of the
 anti-VEGF therapy choroidal neovascular
 Pegaptanib (intravitreal membrane, macular
injection every 6 weeks) translocation, and retinal
pigment epithelial
 binds the major pathogenic
transplantation
isoform of vascular
endothelial growth factor,
VEGF165
 Ranibizumab
 able to bind all isoforms of
VEGF
Katarak
 Stiap keadaan kekeruhan lensa
yg dpt terjadi akibat hidrasi (
pe+ cairan) lensa,denaturasi
protein lensa atau ke2 nya
 Kekeruhan mengenai ke2 mata
& berjalan progresif /dpt tdk
mengalami prubahan dlm wktu
yg lama
 Pnyakit pd usia lanjut (
umumnya)
 E:
 Bahan toksik (kimia /fisik)
 Kracunan bbrp jenis obat :
kortikosteroid ,ergot
eserin,antikolinesterase topikal
 Kelainan sistemikyg dpt
mnimbulkan katarak :
DM,galaktosemi,distrofi
miotonik
 Ktarak jg dpt ditemukan dlm
keadaan tnpa adanya kelainan
mata /sistemik
 Fisik
 Kimia
 Pnyakit predisposisi
 Genetik & gg perkembangan
 Infeksi virus saat janin
 Usia
FKUI
ILMU PENYAKIT MATA
 Gejala:
 Psien dgn katarak mngluh
pnglihatan berasap &
tajam pnglihatan mnurun  Klasifikasi katarak:
progresif
 Lensa keruhlensa tdk
transparan pupil bsa
berwarna putih /abu
 Px yang dilakukan pd
psien katarak : px slit
lamp ,funduskopi pd ke2
mata bila
mungkin,tonometri
 Berdasarkan usia katarak
dpt diklasifikasikan dlm:
 Katarak
kongenitalkatarak yg
terjdi pd usia dibwh 1 thn
 Katarak juvenilkatarak yg
terjdi > 1 thn
 Katarak sensil katarak
stlh usia 50 thn
Katarak Senil
 Kekeruhan lensa yg terdapat
pd usia lanjut ( diatas 50
thn)
 Serat lensa:
 Prubahan lensa pd usia
lanjut :
 Kapsul
 Menebal & krg elastis ( ¼
dibanding anak2)
 Mulai presbiopia
 Bentuk lamel kapsul
berkurang
 Trlihat bahan granular
 Epitel makin tipis
 Sel epitel pd ekuator
bertambah besar dan berat
 Bengkak dan vakuolisasi
mitokondria yg nyata
 Lbh ireguler
 Pd kortek jelas kerusakan
serat sel
 Brown sclerotic nucleus ,sinar
uv lama kelamaan mrubah
protein nukleus ( histidin dll)
lensa
 Korteks tdk berwrna karena:
kadar a.askorbat tinggi &
mnghalangi fotooksidasi
 Sinar tdk bnyak mngubah
protein pd serat muda
Acquired cataract
 Age Related Cataract
a) Subcapsular Cataract
 Anterior subcapsular cataract lies directly  Nuclear sclerotic cataract is characterized by
under the lens capsule
 associated with fibrous metaplasia of the
lens epithelium.
 Posterior subcapsular opacity lies just in
front of the posterior capsule and has a
granular or plaque-like appearance typically  Cortical cataract may involve the anterior
appears black and vacuolated
(retroilumination)
 Common symptom : glare & reduced vision
under bright lighting condition symptoms
are increased by:
 miosis, such as occurs during near visual
activity and in bright sunlight.
b) Nuclear sclerotic cataract :
 Nuclear cataract is an exaggeration of
normal ageing change
 associated with myopia due to an increase in
the refractive index of the nucleus.
a yellowish hue
 due to the deposition of urochrome pigment,
(best assessed with an oblique slit lamp beam)
c) Cortical Cataract :
/posterior lens cortex.
 The opacities start as clefts and vacuoles
between lens fibres due to cortical
hydration
 Opacification result inwedge shaped
/radial spoke like opacities ( inferonasal
quadrant
Kanski Clinical Opthalmology
Vaughan & Ashbury
Fig. 9.2 Age-related cataract. (A) Cortical;
 Cataract Maturity
Cataract maturity
• Immature cataract is one in which the
lens is partially opaque.

• Mature cataract is one in which the lens

is completely opaque

• Hypermature cataract has a shrunken

and wrinkled anterior capsule ( due to
leakage of water out of the lens.
• Morgagnian cataract is a hypermature
cataract in which liquefaction of the
cortex has allowed the nucleus to sink
inferiorly
 Cataract in Systemic Disease
a) Diabetes Mellitus b) Atopic dermatitis
 Hyperglycaemia is reflected in a high level of  About 10% of patients with severe atopic
glucose in the aqueous humour  diffuses into dermatitis develop cataracts
the lens.
 glucose is metabolized into sorbitol, which  these are often bilateral and may mature
accumulates within the lens, resulting in secondary quickly.
osmotic overhydration.
 may affect the refractive index of the lens with
consequent fluctuation of refraction  Shield-like dense anterior subcapsular
 Cortical fluid vacuoles develop and later evolve plaque that wrinkles the anterior capsule is
into frank opacities. characteristic.
 Classic diabetic cataract, which is actually rare,
consists of snowflake cortical opacities.
Secondary Cataract
A secondary (complicated) cataract develops as a
result of other primary ocular disease.
 Chronic anterior uveitis is the most common cause

of secondary cataract, the incidence being related to

the duration and intensity of inflammation.
 High myopia

 Acute congestive angle closure

Management
 Operasi katarak ekstrakapsular
 Dilakukan pngeluaran isi lensa dgn memcah /mrobek
kapsul lensa anterior shingga masa lensa dan korteks lensa
dpt keluar
 Trmsk: ekstraksi linear,aspirasi &irigasi
 Pnyulit yg dpt timbul: katarak sekunder

 Operasi katarak intrakapsular:

 P’mbedahan dgn mngeluarkan sluruh lensa bersama kapsul
 KI  tdk boleh dilakukan pd ps krg dari 40 thn
 Pnyulit: astigma,glaukoma,uveitis,endoftalmitis dan
perdarahan
Glaukoma
 Glaukoma berarti hijau
kebiruan yg mmberikan kesan
wrna pd pupil ps glaukoma
 Kelainan mata glaukoma
ditandai dgn mningkatnya
tekanan bola mata,atrofi papil
saraf optik & mnciutnya lapang
pandang
 Pnyakit yg ditandai dgn
pninggian tekanan intraokular
ini disebabkan o/
 Ber+ produksi cairan mata oleh
bdn siliar
 br – nya pngeluaran cairan mata
didaerah sudut bilik
mata/dicelah pupil ( glaukoma
hambatan pupil)
 Pd glaukoma akan ada
lemahnya fungsi mata dgn cacat
lapang pandang & krusakan
anatomi ( brupa ekskavasi serta
degenerasi papil saraf optik
)kebutaan
 Luas /dlmnya ekskavasi (
pnggaungan) pd glaukoma
kongenital dipakai sbg indikator
progresifitas glaukoma
FKUI
ILMU KESEHATAN MATA
Klasifikasi Glaukoma
 Klasifikasi Vaughen:
 Glaukoma primer
 Glaukoma sudut terbuka
 Glaukoma sudut smpit
 Glaukoma kongenital
 Primer /infantil
 Mnyertai kelainan kongenital lain
 Glaukoma sekunder:
 Prubahan lensa Fig. 10.51 Moderate to marked glaucoma.
 Kelainan uvea
 Trauma
 Bedah
 Steroid
 Pathophysiology of Glaucoma
 Major mechanism of visual loss
in glaucoma retinal ganglion
cell apoptosis thinning of the
inner nuclear & nerve fiber layers
of retina & axonal loss in optic
nerves
 In primary open angle glaucoma
 Optic disc becomes atrophic ,with
enlargment of optic cup
 The effect of raised TIO are
influenced by the time course &
magnitude of the rise TIO
 In acute angle closure glaucoma
TIO reache 60-80 mmhg (
resulting in acute ischemic
damage to the iris with corneal
edema & optic nerve damage)
 The TIO does not usually rise
above 30 mmHg & retinal
ganglion cells may susceptible to
damage ( from TIO pressure in
the normal range) /major
mechanism of damage  optic
nerve head ischemia .
Vaughan & Ashbury
Clinical opthalmology
Primary open angel glaucoma
 Primary open-angle glaucoma
(POAG) is a commonly bilateral
disease of adult onset.
It is characterized by:
 IOP >21 mmHg at some stage.
 Glaucomatous optic nerve
damage.
 An open anterior chamber angle.
 Characteristic visual field loss
as damage progresses.
 Absence of signs of secondary
glaucoma or a nonglaucomatous
cause for the optic neuropathy.
 RISK FACTOR:
 IOP higher the IOP ,the
greater glaucoma ( IOP of 4
mmhg or more)
 Race :4x more common develop
at earlier age
 Family history of POAG
 DM
 Myopia ( speculated that this
may be due to mechanical
factors ( optic disk)
 Contraceptive pill  long term
oral contraceptive pill
 Vascular disease (ex
,hypertension,poor ocular
perfusion )
 Translaminar pressure gradiant
 Optic disc area
 Ocular perfusion presure
Pathogenesis of glaucomatous
optic neuropathy
 Retinal ganglion cell
death in glaucoma occurs
predominantly through
apoptosis (programmed
cell death)
 After injury cascade of
proliferation in astrocyte
& glial cell ,matrix
extracellular &
remodelling
 Common pathways of
 One or both of the
following mechanisms
may be involved:
 Direct mechanical
damage to retinal nerve
fibres at the optic nerve
head.
 Ischaemic damage,
possibly due to
compression of blood
vessels supplying the optic
nerve head.
damage.
DIAGNOSIS
 History  Visual acuity
 Visual symptoms  Pupils

 Previous opthalmic history  Colour vision

 Family history  Slit lamp

 Past medical history  Tonometry

 Current medication  Gonioscopy

 Social history including  Optic disc examination

smoking & alcohol intake
 Allergies

 Examination:
 Treatment Goals
Treatment goals
 Proportional reduction. An alternative
strategy is to aim for a reduction in IOP
by a certain percentage – often 30% – and
then monitor, aiming for a further
reduction if progression occurs.
 Response to progression
Medical Therapy
Commencing medical therapy
○ Any drug chosen should be prescribed in the  Surgery trabeculectomy
lowest concentration consistent with the
desired therapeutic effect, and
administered as infrequently as possible.
 Ideally the drug with the fewest potential
side effects should be used.
 Initial treatment is usually with one type
of medication, typically a prostaglandin
analogue or beta-blocker.
 N/review after starting medication 4-8
weeks
 Response to the drug against the target
IOP
 If the response satisfactory asses set
further 3-6 months
 PROGNOSIS
 Ps will not become blind in their lifetime
 POAG the lifetime chance of blindness in
both eyes has historically been 5–10%;
 Primary Angle Closure Glaucoma
 angle closure’ refers to occlusion of the
trabecular meshwork by the peripheral iris
(iridotrabecular contact – ITC) obstructing
aqueous outflow.
 Classification
 Primary angle closure suspect (PACS)
 Gonioscopy (shows posterior meshwork ITC in 3/
more quadrant)
 Normal IOP,optic disc & visual field
 Pigment smudging /narrow angle approach (20
degree/less)

 Primary angle closure ( PAC)

 Gonioscopy shows 3 /more quadrant of ITC with
raised IOP /excessive pigment smudging
 Normal optic disc & field
 Primary angle closure glaucoma
 ITC in 3/more quadrant
 Optic nerve damage from an episode of severe IOP
elevation
Mechanism
 Mechanism involved can be categorized according anatomical level
:
 Relative pupilary block
 Failure of aquos flow throw pupil lead to a pressure differential between
anterior & posterior chamber resulting anterior bowing of the iris
 Relieved by iridotomy ( equalize anterior & posterior chamber pressure)
 non pupillary block
 Associated with deeper anterior chamber
 Ptient with non pupillary block (particulary those with plateau iris)
 Plateau irisuncommon condition which CAO depth is normal but anterior
chamber angle is very narrow becausee of anterior position of ciliary
procesuss
 Reduced aqueous outflow
 Appositional obstruction of iris
 Risk Factors
 Age (relative pupillary block
about 60 years )
 Gender ( Female>>)
 Race (far eastern )
 Family history
 Refraction eyes with “
pure” pupillary block are
typically hypermetropic
 Axial length ( short eyes
tend to have shallow AC)
 Diagnosis
 Symptoms
 Asymtomatic (include
intermittenly/chronic
elevated IOP)
 Intermittent mild symptoms
of blurring (“smoke filled
room) & haloes ( rainbow
around light) ( due corneal
epithelial edema)
 Acutely with decrease
vision,redness,headache
 Precipitating factor:
 Watch tv in dark room
 Pharmacological
mydriasis
 topiramate
 Sign:
 Acute primary angle closure
 VA 6/60
 IOP usually high ( 50-100
mmhg)
 Conjunctival hyperami
with circumcorneal
injection
 Corneal epithelial edema
 Anterior chamber
shallow
 Unreactive mid-dilated
vertically oval pupil
Investigation
 Anterior Segment OCT :
ultrasound biomicroscopy
 Anterior chamber depth
measurement
 Biometry
 Posterior segment USG
 Provocative test
 THERAPY
 PACS laser iridotomy
 APAC
 Acetazolamid 500 mg is
given IV if IOP > 50 mmhg &
orally if IOP <50 mmhg
 If treatment IV an additional
oral dose of acetazolamid (
may be given ps is not low
body weight)
 KI: sulfonamid allergy &
angle closure secondary to
topiramat
 Apraclonidine 0,5%-1%
,timolol 0,5 % & prednisone
1% /dexamethasone 0,1%
affected eye ( leaving 5
minutes each)
 Pilocarpine 2-4 % ( one drop
to affected eye ,repeated after
half an hour)
Normal Tension Glaucoma
is characterized by:
 IOP consistently equal to or
less than 21 mmHg.
 Signs of optic nerve damage in
a characteristic glaucomatous
pattern.
 An open anterior chamber
angle.
 Visual field loss as damage
progresses
 No features of secondary
glaucoma or a non-
glaucomatous cause for the
neuropathy.
 RISK Factors:
 Age
 Gender
 Race
 Family history
 CCT (lower in ps with NTG)
 Abnormal vasoregulation
 Systemic hypotension
 Obstructive sleep apnea
 Autoantibody level
 Ocular perfusion pressure ( may
be lower in POAG)
 Myopia
Retinopati Diabetikum
 Kelainan retina ( retinopati) yg
ditemukan pd penderita DM
 Retinopati akibat DM brupa
aneurismata,melebarnya vena
,perdarahan & eksudat lemak
 Retinopati mrupakan gejala DM
utama pd mata:
 Mikroaneurisma
 Perdarahan dlm bntuk
titik,garis,bercak yg biasanya
trletak dkat mikroaneurisma di
polus posterior
 Dilatasi p.d balik dgn lumenny
ireguler dan berkelok2
 Hard exudate infiltrasi lipid
ke dlm retina (ireguler
)(kekuningan)
 Soft exudate cotton wool
patches (iskemia retina)
 Pmbuluh darah baru pd retina
biasanya trletak dipermukaa
jaringan
 Neovaskularisasi ( proliferasi sel
endotel pmbuluh darah)
 Edema retina dgn tanda
hilangnya gmabaran retina
trutama daerah makula (shingga
gg tajam pnglihatan)
 Hiperlipidemia
 Biasany dit bilateral,simetris &
progresif 3 bntk:
 Mikroaneurisma,prdarahan bercak
,edema
 Makulopati: edema retina & gg fungsi
makula
 Proliferasi: vaskularisasi retina & bdn
kaca
 Klasifikasi retinopati diabetes :
 Derajat 1 : mikroanerisma dgn /tnpa
eksudat lemak pd fundus okuli
 Derajat 2 : mikroaneurisma ,perdarahan
bintik dan bercak dgn /tnpa eksudat lemak
pd fundus okuli
 Derajat 3 mikroaneurisma ,perdarahan
bintik danb ercak trdpt neovaskularisasi &
proliferasi pd fundus okuli

dot and blot haemorrhages;

(D) deep dark haemorrhages
Retinopati Hipertensi
 Kelainan retina & pmbuluh darah retina  Bila kelainan brupa sklerosis dpt tmpak
& pmbuluh darah retina akibat tekanan sbg:
darah tinggi  Copper wire refleks
 Hipertensimmberikan kelainan pd  Silver wire
retina brupa retinopati hipertensi,dgn  Lumen p,d yg iregur
arteri yg besarnya tdk teratur,eksudat
 Fenomena crossing :
pd retina,edema retina dan prdarahan
 Elevasi
retina
 Deviasi
 Kelainan pmbuluh darah dpt  Kompresi
brupapnyempitan umum/stempat
,prcabangan pmbuluh darah yg tajam
 Retinopati hipertensi dpt berupa
 Pnyempitan /spasme pmbuluh darah perdarahan/eksudat retina yg pd daerah
tmpak: makula dpt mmberikan gmbaran spt
 Pmbuluh darah ( a.retina) pucat bintang
 Kaliber pmbuluh yg mnjd lbh kecil atau
iregular
 Percabangan arteriol yg tajam
 Eksudat retina b’btk :
 Cotton wool patches ( edema serat saraf retina krn mikroinfark sesudah pnyumbatan arteriole)
 Eksudat yg tersebar
 Eksudat putih pd daerah yg tak tertentu & luas
 Prdarahan retina dpt terjdi primer krn oklusi arteri/sekunder akibat arteriosklerose

 Klasifikasi retinopati hipertensi :

 Grade 1 penyempitan arteri retina ringan
 Grade 2 pnyempitan focal arteri & arterivena terjepit,tmpak gambaran kabel pd dinding arteri
 Grade 3 grade 2 + perdarahan retina ( dot,blot),eksudat ( edema (deposisi dari hard exudate skitar
fovea “ macular star) & cotton wool spot
 Grade 4 grade 3 + pmbengkakan optic disc

copper wiring’; grade 3 retinopathy with macular star; Grade 4 hypertensive retinopathy
Strabismus
 Suatu keadaan dimana kedudukan kedua bola mata tidak ke
satu arah.
 Pada strabismus, sumbu bola tidak berpotongan pada satu titik
benda yang dilihat.
 Pasien dgn strabismus akan mengeluh mata lelah atau
astenopia, penglihatan kurang pada satu mata, lihat ganda
(diplopia), & sering menutup sebelah mata.
 Faktor resiko : Riwayat keluarga , kelainan refraksi & kondisi
medis.
 Penyulit supresi dini : terjadinya ambliopia & fiksasi
eksternal.
Klasifikasi Strabismus
1. Apparent squint atau pseudostrabismus
2. Latent squint (Heterophoria)
3. Manifest squint (Heterotropia)
Pseudostrabismus
 Pasien kadang-kadang terlihat seperti juling tetapi dengan
pemeriksaan tidak terdapat tanda” juling.
 Mungkin disebabkan adanya epikantus  mengakibatkan
bagian nasal sklera tidak terlihat jelas.
 Pasien terlihat seperti ada juling ke dalam.
 Kelainan ini merupakan gambaran karakteristik pada pas. dgn
ras Mongol.
Heteroforia
 Keadaan kedudukan bola mata yg normal namun akan timbul
penyimpangan (deviasi) apabila refleks fusi terganggu.
 Macam-macam heteroforia berdasarkan bidang
penyimpangannya :
 Bidang horizontal : esoforia & eksoforia
 Bidang vertikal : hipo atau hiperforia
 Bidang frontal : insiklofori & eksiklofori
 Penyebab : akibat tidak seimbangnya atau insufisiensinya otot
penggerak mata.
 75-90% penduduk yg menderita heteroforia, biasanya tanpa
keluhan.
 Esoforia
 Suatu penyimpangan sumbu
penglihatan ke arah nasal yg
tersembunyi oleh karena masih
adanya refleks fusi.
 Esoforia yg punya sudut
penyimpangan lebih besar pada saat
melihat jauh dibandingkan melihat
dekat disebabkan o/ suatu
insufisiensi divergen.
 Esoforia yg punya sudut
penyimpangan lebih kecil pada
waktu melihat dekat disebabkan oleh
suatu ekses konvergen.
 Sudut penyimpangan sama besar
saat melihat jauh & dekat = basic
type.
 Terapi :
 Memberikan koreksi
hipermetropia u/ ↓ rangsang
akomodasi berlebihan.
 Memberikan miotika u/
menghilangkan akomodasinya.
 Memberikan prisma base out yg
dibagi sama besar mata kanan &
kiri.
 Tindakan operasi
Eksoforia / Strabismus Divergen Laten
 Suatu tendensi penyimpangan
sumbu penglihatan ke arah
temporal.
 Pada eksoforia akan terjadi
deviasi ke luar pada mata yg
ditutup atau dicegah
terbentuknya refleks fusi.
 Eksoforia kecil tanpa keluhan
sering terdapat pada anak”.
 Eksoforia besar sering sering
akan memberikan keluhan
astenopia
 Bila sudut penyimpangan pada
saat melihat jauh lebih besar 
disebabkan oleh ekses divergen.
Bila sudut penyimpangan pada
waktu melihat dekat lebih besar
 disebabkan oleh kelemahan
akomodasi.
Pengobatan secara umum:
 Bila ada kelainan refraksi 
dikoreki.
 Bila mungkin diberikan
latihan ortoptik
 Bila tidak berhasil, bisa
diberikan prisma base in
Hiperforia / Strabismus Sursumvergen
Laten
 Suatu tendensi penyimpangan sumbu penglihatan ke arah atas.
 Umumnya disebabkan o/ kerja berlebihan atau kelemahan
otot-otot rektus inferior & obliqus superior.
 Pengobatan dengan kacamata prisma & puncak di atas
(vertical base down) di depan mata yg sumbu penglihatannya
lebih tinggi.
 Dapat juga dilakukan operasi pada otot” rektus superior dan
inferior.
 Heterotropia
 Keadaan penyimpangan sumbu
bola mata yg nyata di mana kedua
sumbu penglihatan tidak
berpotongan pada titik fiksasi.
 Dapat disebabkan oleh kelainan :
 Herediter
 Anatomik, kelainan otot luar,
kelainan ronggan orbita.
 Kelainan refraksi
 Kelainan persarafan, sensori
mototrik, keadaan yang
menggagalkan fusi.
 Bentuk” heterotropia berdasarkan
kedudukan penyimpangannya :
 Bidang horizontal : eksotropia
& esotropia
 Vertikal : hipertrofi
 Sagital : insiklotropia (kornea
jam 12 berputar ke arah nasal)
& esiklotropia
 Pemeriksaan untuk menentukan
adanya heterotropia : uji tutup
mata, uji refleks korena
Hisrchberg, uji Krimsky, uji
Maddox rod.
 Esotropia / Strabismus Konvergen
Manifes
 Penyimpangan sumbu penglihatan  Faktor refleks dekat, akomodatif
dimana salah satu sumbu estropia.
penglihatan menuju titik fiksasi  Hipertoni rektus medius
sedangkan sumbu penglihatan lain kongenital.
menyimpang pada bidang
 Hipotoni rektus lateral akuisita
horizontal ke arah medial.
 ↓ fungsi penglihatan satu mata
 Bentuk” esotropia
pada bayi & anak.
 Esotropia konkomitan (sudut
 Pengobatan:
penyimpangan sama besar pada
semua arah pandangan)  Memberikan lensa koreksi untuk
mengatas keadaan miopinya.
 Esotropia nonkomitan (besar
sudut penyimpangan beda” pada  Tindakan operatif

arah pandang berbeda-beda)

 Penyebab :
 Eksotropia / Strabismus divergen
manifes
 Penyimpangan sumbu  Anatomi, kelainan rongga
penglihatan dimana salah satu orbita mis: pada penyakit
sumbu penglihatan menuju titik Crouzon
fiksasi sedangkan sumbu yg lain  Pengobatan dgn koreksi refraksi
menyimpang pada bidang pada ekstropia harus dilakukan
horizontal ke arah lateral. dengan hati-hati.
 Bentuk: Eksotropia konkomitan  Operasi pada eksotropia
& nonkomitan tergantung pada jenis
 Penyebab : eksotropianya, biasanya
 Herediter dilakukan resesi otot rektus
lateral & reseksi otot rektus
 Inervasi tapi tidak terdapat
medial mata yg sama pada yg
abnormalitas yg berarti dalam
berdeviasi.
bidang sensorimotor
 LI 5
Penurunan Visus Mendadak: chorioretinopathy
1. Vitreous Hemorrage 6. Papil edema
2. Retinal Detachment 7. Neuritis optic
/ablasio retina 8. Ambliopia toksik
3. RAOD,RVOD 9. Atrofi optik
4. Amaurosis Fugax 10. Migraine
5. Cntral Serous 11. Uveitis posterior
Ambliopia toksik
 Pd keracunan bbrp obat dpt terjd kbutaan
mendadak
 Neuritis optik toksik dpt terjdi keracunan
alkohol/tmbakau timah dan bahan toksis lainnya
 Biasanya tanda lapang pandang berubah
 Pd uremia dpt tejrdi amblopia uremik dimana
pnglihatan akan brkg
 Brkgnya pnglihatan akibat keracunan
alkoholamblopia alkohol
Amaurosis fugax
 Buta sekjap satu mata yg total & dpt mrupakan gejala dini
berulang obstruksi arteri retina sentral
 Gelap sementara slama 2-5 dtk  Amaurosis fugax mrupakan
yg biasanya hnya mngenai 1 tanda yg paling sering pd insuf
mata pd saat serangan dan arteri karotis/trdptnya emboli pd
normal kembali ssdh bbrp mnit arteri oftalmik retina
/jam disertai dgn gg segmental  Tdk ditemukan kelainan fundus
tnpa rasa sakit dan trdptnya krn pendeknya serangan
gejala sisa
 DD: TIA
 Monokular amaurosis fugax dpt
terjdi akibat hipotensi
ortostatik,spasme p.d
,aritmia,migren ,anemia,arteritis
& koagulopatia
 Hilangnya pnglihatan jarang