RETINAL DISEASES

Marliyanti N. Akib
CONGENITAL AND
DEVELOPMENTAL
DISORDERS
CLASSIFICATION

1. Anomalies of the optic disc. These include crescents, situs inversus,

congenital pigmentation, coloboma, drusen and hypoplasia of the
optic disc.

2. Anomalies of the nerve fibres e.g., medullated

(opaque) nerve fibres.

3. Anomalies of vascular elements, such as persistent hyaloid artery

and congenital tortuosity of retinal vessels.
4. Anomalies of the retina proper. These include

albinism, congenital night blindness,

congenital day blindness, Oguchis disease,

congenital retinal cyst, congenital retinal

detachment and coloboma of the fundus.

5. Congenital anomalies of the macula

aplasia, hypoplasia and coloboma.

Medulated nerve fiber layer
 INFLAMMATORY
DISORDERS
RETINITIS

I. Non-specific retinitis.
OF THE RETINA
It is caused by pyogenic organisms and may

be either acute or subacute.

1. Acute purulent retinitis

2. Subacute retinitis of Roth

II. Specific retinitis bacterial (tuberculosis,

leprosy, syphilis and actinomycosis), viral

(cytomegalic inclusion disease, rubella, herpes

zoster), mycotic, rickettsial or parasitic in origin.

 Fundus photograph showing typical
cytomegalovirus (CMV) retinitis in
a patient with AIDS.
Note white necrotic retina
associated with retinal
haemorrhages

Toxoplamosis congenital
RETINAL VASCULITIS

inflammation of the retinal vessels may be primary, exp

(Eales disease) or secondary to uveitis.

Eales disease
idiopathic inflammation of the peripheral retinal veins. It is
characterised by recurrent vitreous haemorrhage; so also
referred to as primary vitreous haemorrhage
Note venous congestion,
perivascular exudates and sheets of
haemorrhages pr-esent near the
affected veins.
 VASCULAR DISORDERS OF
RETINA
Retinal artery occlusions

Retinal vein occlusions

Diabetic retinopathy

Hypertensive retinopathy

Sickle cell retinopathy

Retinopathy of prematurity

Retinal telengiectasias

Ocular ischaemic syndrome

Others : retinopahty leucemia, trombocytophenia

anemia
Fundus normal
Papil normal
RETINOPATHY
 DIABETIC RETINOPATHY

Frequent cause of blindness in USA,

aged 20 to 64 years
Indonesia blindness due to D.R. increase
PATHOGENESIS
The exact cause is still unclear
It is believed :
Hiperglycemia over an extended period results in a
number biochemical and physiologic changes ---
endothelial damage.
Retinal vascular changes : loss of pericyte
basement membrane thickening---compromises
capillary lumen--- decompensation of endothelial
barrier function
Hematologic and biochemical abnormalities
Increased platelet adhesiveness
Increaser erythrocyte aggregation
Abnormal serum lipids
Defective fibrinolysis
Abnormal levels of growth hormone : ex
vascular endothelial growth factor (VEGF)
Abnormalities in serum and whole blood
viscosity
CLASSIFICATION
Non proliferative diabetic retinopathy (NPDR) =
back ground diabetic retinopathy :
Mild
Moderate
Severe
Very severe

Proliferative Diabetic Retinopathy :

Early
High risk
Advanced

Macular edema
NPDR : Retinal microvasculer changes
limited to the retina
Micro aneurysme
Dot & blot hemorrhage
Retinal edema
Hard exudates
Dilatation & bleading of the vein
Intraretinal micro vascular abnormalites (IRMA)
Nerve fiber layer infarct (cotton wool spot)
Areas of capillary non perfussion
RD : mikroaneurisma + hard exudate
RD 1: cotton wool + Flame shaped
Affect visual function through
Capillary disease ischemic
Vascular permeability edema
Diabetic macular edema
The most common :
Cause of VA
Proliferative diabetic retinopathy
(PDR)
Extra retinal fibrovascular
proliferation extends beyond the
ILM
 NPDR

Ischemic retina

Release of vaso poliferative factors

Neovascularization of the retina

optic nerve head, anterior segment
 PDR
Neovascularisation at disc
 PDR
Neovascularisation elsewhere
 COMPLICATION
Reduced of visual acuity
Vitreous hemorrhage
Traction retinal detachment
Neurovascular glaucoma
 TREATMENT

Regulation of blood glucose level

Laser photocoagulation
Vitrectomy
HYPERTENSIVE RETINOPATHY

Effect of systemic arterial hypertension to

chronic retinal vascularization
Hypertensive retinopathy
Hypertensive choroidopathy
Hypertensive opticneuropathy
HYPERTENSIVE RETINOPATHY
(HR)

Hypertensive vascular changes & arterio

sclero vascular disease
express in HR.
Classification of HR, the modified scheir.
Grade 0 : No change (a/v 2 : 3)
Grade 1 : barely table arterial
narrowing a : v = 1 : 2
CLASSIFICATION OF HR
Grade 2 : obvious arterial narrowing with
focal irregularities.
Copper wire arteries
Silver wire arteries
Banking sign
Salus sign
Gunn Sign
Gunn phenomen
Gunn Phenomen
 Classification. cont

Grade 3 : grade 2 + retinal hemorrhages

and/or exudate

Grade 4 : grade 3 + disc swelling

HYPERTENSIVE
CHOROIDOPATHY

Typically occur in young patients : with

acute hypertension ex :
Preeclampsia, eclampsia
Pheochromacytoma
Acute renal failure
Retinopathy Hypertensive pada
Hipertensi Renal
Retinopathy Hypertensive pada
Hipertensi Renal + edem papil
Hypertensive Optic Neuropathy
Flame-shaped hemorrhages around the
disc
Blurring of the disc margin
Congestion of the retinal vein
Secondary macular exudates
Retinopati angiospastik : cotton wool + flame shaped +
dot hemorrhage
OKLUSI VENA RETINA SENTRALIS
Hambatan aliran darah vena dari retina

Etiologi :
- arteriosklerosis & hipertensi
- trombus peny jantung, DM
- perubahan viskositas darah

Gambaran fundus khas berupa dilatasi dan

berkelok-keloknya p. drh vena, edema papil
N.optik, perdarahan intraretina dan edema
retina.
Etiology
1. Pressure on the vein by a sclerotic retinal
artery
2. Hyperviscosity of blood as in polycythemia,
hyperlipidemia and macroglobulinemia.
3. Periphlebitis retinae which can be central or
peripheral.
4. Raised introcular pressure.
5. Local causes are orbital cellulitis, facial
erysipelas and cavernous sinus thrombosis.
Klasifikasi
1. noniskemik (venous stasis retinopathy), btk ringan
kadang dikenal sbg partial, perfused atau retinopati venus
statis.

2. Iskemik (haemorrhagic retinopathy), khas plng sdkt

area yg terkena 10 DD
Mekanisme
Diduga terjadi trombosis di posterior pada lamina
kribrosa menyebabkan turbulensi, kerusakan endotel dan
pembentukan thrombus
NONISKEMIK

- Pembuluh darah dilatasi ringan dan

berkelok-kelok pd semua cabang
V.Retina sentralis

- perdarahan retina bentuk dot dan

flame shape di semua kuadran.

- edema makula dgn penurunan visus

dgn atau tanpa edema papil.

- jarang terjadi neovaskularisasi di

segmen anterior
ISKEMIK
perdarahan lbh ekstensif di 4 kuadran dan edema retina.
ada dilatasi vena dan cotton wool spot.
prognosis biasanya jelek.
neovask. iris > 60%, tjd 3 5 bln sesudah onset.
Gambaran klinik:

Subyektif : - visus tiba-tiba atau bertahap

Obyektif :

Flame shape hemorrhage

Vena retina kongesti & berkelok- kelok

Perdarahan pd membran hyaloid & vitreus

Neovaskularisasi di sekitar n.optik & iris

Defek lapang pandang sesuai cabang oklusi

CRVO NON-ISCHAEMIC

CRAO - ISCHAEMIC

BRVO
Diagnosis
Anamnesis : KU, riwayat penyakit sistemik
Gejala klinik : - funduskopi
- FFA
Lab mendukung peny sistemik

Evaluasi : - TIO
- Gonioskopi
- FFA
Penanganan :
Kausal, tdk ada R/ efektif utk noniskemik OVRS.
Fotokoagulasi utk neovaskularisasi & edema makula.
Kortikosteroid & terapi utk me(-) adhesi platelet.
Komplikasi
Trombotik glaukoma (glaukoma sekunder)
Retinal detachment
Prognosis
Komplikasi jelek
OKLUSI ARTERI RETINA SENTRALIS

Marliyanti N. Akib

Bagian Ilmu Kesehatan Mata

Fakultas Kedokteran Unhas

Hambatan aliran darah ke retina
A. retina sentralis
cab I a. oftalmika
msk ke dlm n. optik 8
15 mm di belakang
bola mata
2/3 lapisan bgn dalam
retina

Daerah yang paling

sering mengalami
obstruksi lamina
cribrosa
Etiologi
Atherosklerosis trombosis penyebab terbanyak
Hipertensi
Emboli
Penyakit jantung
Carotid artery disease
Penyakit sistemik (DM)
Hiperviskositas darah
Trauma (fraktur tulang panjang emboli lemak)
Gejala :
Tajam penglihatan secara tiba-tiba
Tidak nyeri
Amaurosis fugax
CENTRAL RETINAL ARTERY OCCLUSION (CRAO)

Oftalmoskopi

Retina pucat iskemi

Cherry red spot refleks merah dr p. drh koroid di bwh

fovea
tiny thread like pembuluh darah kolaps,
mengecil seperti benang & halus
boxcar phenomenon arteri sangat menciut,
mengempes tanpa darah, kadang terputus-
putus
BRANCH RETINAL ARTERY OCCLUSION (BRAO)

Retina di bagian distal dari okluasi menjadi

edem dengan penyempitan arteriol

Lama kelamaan daerah yang terkena akan

menjadi atrofi dan terjadi defek lapangan
pandang sektoral
 CRAO: milky white

BRAO supero temporal

Kerusakan irreversibel terjadi dlm 90 100 mnt

Setelah beberapa minggu :

edem menghilang
atrofi papil dgn batas tegas

neovaskularisasi iris tjd pd 18%

1-12 mgg setelah serangan

rata2 : 4 - 5 mgg
Diagnosis berdasarkan :
- anamnesis
- gambaran klinik

Penanganan:
Blm memuaskan masih dipertanyakan
Tujuan mengembalikan aliran darah secepat
mungkin
Menurunkan TIO :
Massage bola mata emboli lepas
Parasentesis BMD
Acetazolamide

Vasodilator pd daerah retrobulbar

Prognosis

Tergantung :
kausa
derajat obstruksi
lamanya oklusi menetap

Komplikasi :

Glaukoma neovaskuler
Retinopathy of Prematurity
 Pathogenesis
In the normal foetus, vascular development of the
retina occurs in two phases.
Fase 1 : True vasculogenesis : 8-21 weeks of foetal
development
Fase 2 : Angiogenesis : 22 to 40 weeks of development :
VEGF dependant
Physiologic angiogenesis
Pathologic angiogenesis (ROP pathogenesis)
 Risk Factors
Crucial risk factors :
Birth weight
Gestational age
Number of days oxygen administered

Other risk factors :

Multiple births
Blood transfusions
Respiratory Distress Syndrome (RDS)
Sepsis
Intra Ventricular Hemorrhage (IVH)
Intra Uterine Growth Retardation (IUGR)
Vit E deficiency
Anemia
Seizures.
Screening criteria in Indonesia

BW < 1500 gr or GA < 34 minggu

Pemeriksaan pada bayi dengan berat lahir lebih atau usia

gestasi lebih dapat diminta oleh neonatologis atau dokter anak
tergantung keparahan faktor risiko seperti tingginya saturasi
O2 selama lebih dari 1 minggu, transfusi berulang

Bayi dengan usia gestasi 37 mgg atau lebih tidak perlu

pemeriksaan ROP
 When to screen ??

Jika usia gestasi > 30 mgg, diperiksa 2-4 mgg setelah

kelahiran

Jika usia gestasi kurang atau sama dengan 30 mgg,

diperiksa 4 mgg setelah kelahiran

Setidaknya satu kali pemeriksaan sebelum pulang dari

rumah sakit
Stage 1 : Demarcation line
Stage 2 : Ridge
Stage 2 : Ridge
Stage 3 : Extraretinal fibrovascular
proliferation
Stage 3 : Extraretinal fibrovascular
proliferation
Stage 3 : Extraretinal fibrovascular
proliferation
Stage 4 : Partial retinal
detachment
Stage 4 : Partial retinal
detachment
Stage 5 : Total retinal
detachment
 How to treat ?
Principle is ablation of the ischemic peripheral retina
stops release of angiogenic factors
Cryotherapy
Laser photocoagulation
Surgical treatment
Scleral buckling
Lens sparing vitrectomy for stage 4
Lensectomy + vitrectomy
Open sky vitrectomy for stage 5
Other types of retinopathy
Leukemia retinopathy

Thrombocytopenia retinopathy

Anemia retinopathy
Trombositopenia
Hemofilia
Leukemia akut
 RETINAL
DETACHMENT
EMBRIOLOGY OF THE EYE

SUBRETINAL SPACE

83
 RETINAL
DETACHMENT
Separation of the sensory part of the retina from

the retinal pigment epithelium (RPE).

There is an accumulation of fluid in the space

between the neural retina and the RPE known as

Subretinal fluid.
 Pathogenesis
There is an embryological explanation for retinal
detachment in that the separating layers open up a
potential space that existed during the early development
of the eye.
The inner lining of the eye develops as two layers.

The outer of the two layers remains as a single layer of

pigmented cells, known as the pigment epithelium. The
inner of the two layers becomes many cells thick and
develops into the
sensory retina.
 CLASSIFICATION

Rhegmatogenous Retinal Detachment

Tractional Retinal Detachment

Exudative Retinal Detachment

 Rhegmatogenous
Retinal Detachment
This is the most common form of
retinal detachment, caused by the
recruitment of fluid from the
vitreous cavity to the subretinal
space
via a full-thickness discontinuity (a
retinal break) in the sensory
retina.
Etiology
Retinal degeneration of peripheral retina (lattice degeneration in high
myopia >>>.
Vitreous change ( posterior vitreous detachment/PVD. Vitreous
traction).
Trauma
 Vitreus
traction

prediposes to
retinal breaks
Tractional
Retinal Detachment

This form of retinal

detachment develops as a
result of tractional forces
within the vitreous gel
pulling on the retina, causing
the retina to be tented up
from the RPE. No retinal
breaks.
Etiology
The retinal detachment can be pulled away by the contraction of
fibrous
bands in the vitreous, advanced proliferative diabetic retinopathy is
the common cause of tractional retinal detachment.
Exudative
Retinal Detachment

The fluid gains access to the subretinal space through an

abnormal choroidal circulation can be found from a choroidal
malignant melanoma or, rarely, secondary to inflammation of the RPE or
deeper layers of the eye (e.g., scleritis).
Signs and Symptoms Retinal Detachment

Flashes (Photopsiae)
Floaters
Shadow
Ophthalmoscopy :

- Grey retinal bullous seen in

the part of retinal
detachment. Retinal
vasculatures were join the
bullous retina. In
rhegmatogenous RD, retinal
break can be identified.
Tractional ret. Detachment in PDR
Large retinal tears
 MANAGEMENT
Rhegmatogenous retinal detachment
Prophylaxis

Retinal tears without significant subretinal fluid

can be sealed by means of light coagulation. A
powerful light beam from a laser is directed at
the surrounds of the tear.

Laser spots

Retinal tears
Retinal Surgery
Modern retinal reattachment surgery is carried out using either the
cryobuckling or vitrectomy technique. Addition treatment are
unrarely performed with scleral buckling/vitrectomy are internal
drainage, endolaser photocoagulation, or gas/silicon intravitreal
injection.
Cryobuckle
This involves the sewing of small inert pieces of material,
usually silicone rubber, onto the outside of the sclera in
such a way as to make a suitable indent at the site of the
tear.
This is combined with cryopexy to the break.
It is often necessary to drain off
the subretinal fluid and inject air
or gas into the vitreous. In more
difficult cases, the eye can be
encircled with a silicone strap to
provide allround support to a
retina with extensive
degenerative changes.
 Scleral
buckling
Vitrectomy

The detached retina is reattached from within the

vitreous cavity.

Cannula infusion is inserted to the

globe for maintaining the intraocular
pressure.

A light probe is used to illuminate the

operative field

Vitrectomy cutter is used to remove

the vitreous,
hence relieving the abnormal vitreous
adhesions that produced the retinal
tear in the first instance
Infusion cannula

light port

vitrectomy cutter port

Injecting air or
gas into the
vitreous.
Cutting fibrous membrane Laser endophotocoagulation
Tractional Retinal
Detachment
Fibrous tissues pulling retinal layer
are cut away till retinal re-attach.
Sometime combined with silicon
injection or endolaser
photocoagulation.
Serous Retinal
Detachment
Depend on the cause of the retinal
detachment.
Prognosis
The retina can now be successfully reattached by one
operation in about 85% of cases.

Those in which the macular region was affected by the

retinal detachment do not achieve a full restoration of
their central
Vision.
The main cause of failure of surgery is proliferative
vitreoretinopathy.This is characterised by excessive
scarring following initial retinal reattachment surgery

When retinal surgery has failed, further surgery might be

required and for a few patients a series of operations is
necessary.
Thank you...