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Ketebalan retina
Anatomi
retina
Pemeriksaan
Funduskopi dg:
Oftalmoskop direk
Oftalmoskop indirek
Lensa kontak goldmann
USG
Foto fundus
Fluoresence angiography
Fundus normal
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
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.
PDR
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.
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.
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
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
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.
Prophylaxis
Excluding or initiating prompt therapy of
predisposing underlying systemic disorders is
crucial.
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.
Prophylaxis
Regular blood pressure monitoring
Ophthalmoscopic examination of the fundus
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.
Perdarahan vitreus
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
Treatment
Retinal breaks with minimal circular
retinal detachment argon laser
coagulation
Scleral buckle
Vitrectomy wih silicon oil tamponade
or gas tamponade
argon laser
photocoagulation
Prophylaxis
High-risk patients:
age > 40 with a positive family history and severe
myopia examined once a year.
Etiology
physical or psychological stress
Epidemiology
men in the 3rd and 4th decade of life.
Symptoms
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
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.
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.
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.
Symptoms
glare,
night blindness,
progressive visual field defects,
loss of visual acuity, and
color vision defects.
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.
chronically progressive.
lead to blindness.
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.
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.
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
Korioretinitis CMV
TERIMA KASIH