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 35–38% 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 (Horton’s 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.
• The prevalence of retinal detachment with emmetropia :
severe myopia > S-10D = 0.2 % : 7%
 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 neurosensory retina and
the retinal pigment epithelium.
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 patient’s 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 AIDS-
associated 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 cotton-wool
spots.
• Cytomegalovirus retinitis occurs in 20–40% 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