Vous êtes sur la page 1sur 82

RETINA

Dr. Mandiri Nindiasari, SpM,


MSc

Ketebalan retina

Anatomi
retina

Pemeriksaan
Funduskopi dg:
Oftalmoskop direk
Oftalmoskop indirek
Lensa kontak goldmann

USG
Foto fundus
Fluoresence angiography

Fundus normal

Wall reflex di makula remaja

RETINOPATI DIABETIK
Diabetic retinopathy is an ocular
microangiopathy
Epidemiology:
the main causes of acquired
blindness in the industrialized
countries.
90% diabetic patients have
retinopathy > 20 yrs

Pathogenesis and individual stages


of diabetic retinopathy
Diabetes mellitus can lead to changes in
almost every ocular tissue.
These include symptoms of
keratoconjunctivitis sicca, xanthelasma,
mycotic orbital infections, transitory
refractory changes, cataract, glaucoma,
neuropathy of the optic nerve, oculomotor
palsy.
90% of all visual impairments in diabetic
patients are caused by diabetic retinopathy.

Symptoms
asymptomatic for a long time.
Only in the late stages with macular involvement or
vitreous hemorrhage will the patient notice visual
impairment or suddenly go blind.

Diagnostic considerations
stereoscopic examination of the fundus with the
pupil dilated (gold standard)
Fluorescein angiography : if laser treatment is
indicated.
slit-lamp examination : rubeosis iridis +/-

Treatment
Clinically significant macular edema focal laser
Proliferative diabetic retinopathy scatter
photocoagulation (3-5 sessions)

Prophylaxis
regular ophthalmologic screening examinations
type II diabetics : upon diagnosis of the disorder
once a year / more often
type I diabetics: within 5 years of the diagnosis
Pregnant patients: once every trimester.

Clinical course and


prognosis
Optimum control of blood glucose can
prevent or delay retinopathy.
However, diabetic retinopathy can occur
despite optimum therapy.
The risk of blindness due to diabetic
retinopathy can be reduced by optimum
control of blood glucose, regular
ophthalmologic examination, and timely
therapy, but it cannot be completely
eliminated.

Retinopati diabetik (NPDR


sedang)

PDR

PDS high risk

PDR, pre & post laser

Retinal vein occlusion


Vein occlusion occurs as a result of circulatory
dysfunction in the central vein or one of its
branches.

Epidemiology
the second most frequent vascular retinal
disorder after diabetic retinopathy.
The most frequent underlying systemic disorders
are arterial hypertension and diabetes mellitus
The most frequent underlying ocular disorder is
glaucoma.

Etiology
Occlusion due to local thrombosis at sites
where sclerotic arteries compress the veins.
In CRVO: the thrombus lies at the level of
the lamina cribrosa
In BRVO: at an arteriovenous crossing.

Symptoms
a loss of visual acuity if the macula or optic
disk are involved.

Diagnostic considerations and


findings
CRVO: hemorrhages in all four quadrants of the retina
BRVO: hemorrhages in the area of vascular supply;
this bleeding may occur in only one quadrant
Cotton-wool spots and retinal or optic-disk edema
Chronic occlusions: lipid deposits.
One differentiates between non-ischemic and
ischemic occlusion depending on the extent of
capillary occlusion.
Ischemic occlusion is diagnosed with the aid of
fluorescein angiography.

Differential diagnosis
diabetic retinopathy
An internist should be consulted

Treatment
In acute : hematocrit to 3538% by
hemodilution.
Laser treatment: in ischemic occlusion
Focal laser treatment: in BRVO with macular
edema when VA < 20/40 within 3

Prophylaxis
Early diagnosis and prompt treatment of
underlying systemic and ocular disorders is
important.

Clinical course and prognosis

VA in 1/3 patients
remains unchanged in 1/3
worsens in 1/3 despite therapy.
Complications: preretinal neovascularization,
retinal detachment, and rubeosis iridis with
angle closure glaucoma

CRVO

BRVO

Retinal Arterial Occlusion


Retinal infarction due to occlusion of
an artery in the lamina cribrosa or
a branch retinal artery occlusion.

Epidemiology
Retinal artery occlusions occur
significantly less often than vein
occlusions.

Etiology
Emboli
inflammatory processes such as
temporal arteritis (Hortons arteritis).

Symptoms
CRAO: sudden, painless unilateral
blindness.
BRAO: a loss of visual acuity or visual
field defects.

Diagnostic considerations
Ophthalmoscopy
acute stage of CRAO: grayish white
fovea centralis: cherry red spot
The column of blood will be seen to be
interrupted.
optic nerve atrophy : in chronic stage of CRAO
BRAO: a retinal edema in the affected area of
vascular supply

Perimetry (visual field testing)


a total visual field defect in CRAO
a partial defect in BRAO

Treatment
Emergency treatment is often unsuccessful even
when initiated immediately:
Ocular massage
medications that reduce intraocular pressure
Paracentesis
to drain the embolus in a peripheral retinal vessel.

Calcium antagonists or hemodilution to


improve vascular supply.

Prophylaxis
Excluding or initiating prompt therapy of
predisposing underlying systemic disorders is
crucial.

Clinical course and


prognosis
The prognosis is poor because
irreparable damage to the inner layers
of the retina occurs within one hour.
Blindness usually cannot be prevented
in CRAO.
The prognosis is better where only a
branch of the artery is occluded
unless a macular branch is affected.

CRAO

BRAO

Hypertensive Retinopathy
Arterial changes in hypertension are
primarily caused by vasospasm

Pathogenesis
High blood pressure breakdown of the
blood-retina barrier or obliteration of
capillaries intraretinal bleeding,
cotton-wool spots, retinal edema, or
optic disk swelling

Symptoms
Patients with high blood pressure
Headache or eye pain.
Impaired vision or loss of VA in stage
III or IV

Diagnostic considerations
diagnosed by ophthalmoscopy,
preferably with the pupil dilated

Differential diagnosis
other vascular retinal disorders such
as diabetic retinopathy.

Treatment
Treating the underlying disorder is
crucial
Blood pressure < 140/90mm Hg.

Stages of hypertensive vascular changes (as


described by Keith,Wagener, and Barker)

The WHO distinguishes between HT


retinopathy (stages I and II) and malignant
HT retinopathy (stages III and IV)

Prophylaxis
Regular blood pressure monitoring
Ophthalmoscopic examination of the fundus

Clinical course and complications


vascular changes (retinal artery and vein occlusion)
and macroaneurysms vitreous hemorrhage.
Papilledema t atrophy of the optic nerve severe
loss of visual acuity.

Prognosis
In some cases, the complications described above are
unavoidable despite well controlled blood pressure.

Retinopati HT gr.III

Retinal detachment
(ablasio retina)
the separation of the neurosensory retina
from the underlying retinal pigment
epithelium, to which normally it is loosely
attached.
Rhegmatogenous retinal detachment results
from a tear
Tractional retinal detachment results from
traction
Exudative retinal detachment is caused by fluid.
Tumor-related retinal detachment.

Epidemiology
Rhegmatogenous retinal detachment (most
frequent form)
7% of all adults have retinal breaks.
The incidence with advanced age.
The peak incidence is 5th -7th decades of life (PVD
/
posterior vitreous detachment (separation of the
vitreous body from inner surface of the retina;
also age-related)
The annual incidence : 1/10 000 persons
The prevalence : 0.4% in the elderly.
There is a known familial disposition, and retinal
detachment also occurs in conjunction with
myopia.

Etiology
Rhegmatogenous retinal detachment.
This disorder develops from an existing break
in the retina, usually in the peripheral retina
Round breaks: A portion of the retina has been
completely torn out due to a posterior vitreous
detachment.
Horseshoe tears: The retina is only slightly torn.

Retinal break liquified vitreous body


separates vitreous humor penetrates
beneath the retina through the tear retinal
detachment

Tractional retinal detachment.


tensile forces exerted on the retina by
preretinal fibrovascular strands especially
in proliferative retinal diseases such as
diabetic retinopathy.
Exudative retinal detachment.
the breakdown of the inner or outer
blood retina barrier, usually as a result of
a vascular disorder.
Subretinal fluid with or without hard
exudate accumulates between the

Perdarahan vitreus

Tumor-related retinal detachment.


Either the transudate from the tumor
vasculature or the mass of the tumor
separates the retina from its underlying
tissue.

Symptoms
asymptomatic for a long time.
acute stage posterior vitreous detachment: flashes
of light (photopsia) and floaters, black points
that move with the patients gaze.
PVD a retinal tear avulsion of a retinal vessel
Blood enter the vitreous body: black rain,
dark shadow in the visual field: a falling curtain
or a risingwall
A break in the cente: sudden and significant loss of
visual acuity, which will include
metamorphopsia (image distortion) if the macula
is involved.

Diagnostic considerations
diagnosed by ophtalmoscopy with
the pupil dilated.

Differential diagnosis
Degenerative retinoschisis
choroidal detachment.

Treatment

Retinal breaks with minimal circular


retinal detachment argon laser
coagulation
Scleral buckle
Vitrectomy wih silicon oil tamponade
or gas tamponade

Treatment
Retinal breaks with minimal circular
retinal detachment argon laser
coagulation
Scleral buckle
Vitrectomy wih silicon oil tamponade
or gas tamponade

argon laser
photocoagulation

Vitrektomi pars plana

Penggunaan gas pada


vitrektomi

Penggunaan minyak silikon pd


vitrektomi

Prophylaxis
High-risk patients:
age > 40 with a positive family history and severe
myopia examined once a year.

Clinical course and prognosis


about 95% of RRD : successfully with surgery.
if macular involvement a loss of visual acuity will
remain.
The prognosis for the other forms of retinal
detachment is usually poor, and they are often
associated with significant loss of visual acuity.

Central serous retinophathy


Serous detachment of the retina
and/or retinal pigment epithelium

Etiology
physical or psychological stress

Epidemiology
men in the 3rd and 4th decade of life.

Symptoms

A loss of visual acuity,


a relative central scotoma (dark spot),
image distortion (metamorphopsia), or
perception of objects as larger or smaller than they are
(macropsia or micropsia).

Diagnostic considerations
Ophthalmoscopy : a serous retinal detachment, at the macula
Hyperopia
fluorescein angiography

Treatment
no treatment
resolves spontaneously within a few
weeks.
Recurrences laser therapy
Corticosteroid therapy is
contraindicated

Clinical course and


prognosis
The prognosis is usually good.
recurrences or chronic forms a
permanent loss of visual acuity.

Central serous retinophathy

Age-Related Macular
Degeneration
Progressive degeneration of the macula in elderly patients.

Epidemiology
the most frequent cause of blindness beyond the age of 65 years.
Pathogenesis
Drusen develop in the retinal pigment epithelium due to
accumulation of metabolic products.
Symptoms
a gradual loss of visual acuity.
macular edema image distortion (metamorphopsia),
macropsia, or micropsia.

Findings and diagnostic considerations


Ophthalmoscopic examination

Differential diagnosis
BRVO
Malignant melanoma

Treatment
No effective medical therapy is available.
Laser therapy : in exudative stage involving the
fovea centralis.
Use hand magnifier or binocular magnifier.

Clinical course and prognosis


chronic progressive loss of visual
acuity.
Laser therapy: in exudative stage
Stages of age-related macular degeneration
(ARM)

Age-related macular degeneration

Perdarahan subhialoid

Retinitis Pigmentosa
a heterogeneous group of retinal
disorders that lead to progressive loss
of visual acuity, visual field defects,
and night blindness.

Epidemiology
Incidence: 1/35000 1/70000 persons.
incidence of mutated alleles: 1/80
persons.

autosomal recessive (60%),


autosomal dominant (up to 25%),
X-linked (15%).

Symptoms

glare,
night blindness,
progressive visual field defects,
loss of visual acuity, and
color vision defects.

Findings and diagnostic


considerations
Ophthalmoscopy
Bone-spicule
gradually spread toward the center and farther
peripherally
loss of visual acuity
gradual progressive loss of visual field
color vision defects
disturbed contrast perception
Atrophy of the optic nerve
The arteries will appear narrowed
the fundus reflex will be extremely muted

Differential diagnosis
pseudoretinitis pigmentosa
Posttraumatic changes.
Postinflammatory or postinfectious
changes
Tumors.
Medications, such as chloroquine,
Myambutol (ethambutol), and
thioridazine.

Treatment
The causes of the disorder cannot be
treated.
Edge-filtered eyeglasses (eyeglasses with
orange or blue colored lenses that filter
out certain wavelengths)
magnifying near vision aids

Prophylaxis
No prophylaxis is possible.

Clinical course and


prognosis

chronically progressive.
lead to blindness.

Posterior Uveitis Due to


Toxoplasmosis
Focal chorioretinal inflammation caused by
infection

Epidemiology
this clinical syndrome is encountered frequently.

Pathogenesis
Toxoplasma gondii, is transmitted by ingestion of
tissue cysts in rawor undercooked meat or by
oocysts from cat feces.
In congenital toxoplasmosis, the child acquires the
pathogen through transplacental transmission.

Symptoms and diagnostic


considerations
grayish white chorioretinal focal lesions
surrounded by vitreous infiltration
In congenital toxoplasmosis: a macular scar
that significantly impairs visual acuity
secondary strabismus.
Intracerebral involvement hydrocephalus
and intracranial calcifications.
acquired form: visual acuity is impaired
only where the macula is involved.

Differential diagnosis
Chorioretinitis with tuberculosis,
sarcoidosis, borreliosis (Lyme disease), or
syphilis

Treatment
combination of pyrimethamine,
sulfonamide, folinic acid, and steroids

Prophylaxis
Avoid raw meat and cat feces.

Clinical course and


prognosis
heals without severe loss of visual
acuity where the macula is not
involved.
recur at any time.
no cure for the congenital form.

toksoplasmosis

AIDS-Related Retinal
Disorders
Retinal disorders
in AIDS involve either AIDSassociated microangiopathy or infection.

Epidemiology
Up to 80% of all AIDS patients have retinal
disorders

Pathogenesis
The pathogenesis of microangiopathy is still
unclear. Opportunistic infections are
frequently caused by viruses.

Diagnostic considerations
Ophthalmoscopic findings: hemorrhages,
microaneurysms, telangiectasia, and cottonwool spots.
Cytomegalovirus retinitis occurs in 2040% of
older patients.
Peripheral retinal necrosis
intraretinal bleeding
Vascular occlusion is rare.
Secondary rhegmatogenous retinal detachment
AIDS is confirmed by positive serum cultures
and by resistance testing.

Differential diagnosis
Inflammatory retinal changes due to other
causes should be excluded by serologic
studies.

Treatment
Microangiopathy does not require treatment.
Viral retinitis is treated with ganciclovir or
foscarnet.
Herpes simplex and varicella-zoster viruses are
treated with acyclovir.

Prophylaxis
Ophthalmologic screening

Clinical course and prognosis


The prognosis for microangiopathy is
very good.
Infectious retinitis will lead to blindness
if left untreated.
Visual acuity can often be preserved if
a prompt diagnosis is made.

Korioretinitis CMV

TERIMA KASIH