Normal Eye with Sudden

Vision Loss
Dofi Pebriadi & Yusuf Harkian
I11109068 I11109097

Normal Eye with Sudden Vision Loss

Sudden loss of vision associated with
eye pain or headache in the white
non-inflamed eye needs urgent
attention as it may be due to sight
or even life-threatening illness.

Topic
Optic Neuritis

OPTIC NEURITIS

Optic Neuritis
An inflammation of the optic nerve
that may occur within the globe
(papillitis) or posterior to it
( retrobulbar optic neuritis).
Most frequently in adults between the
ages of 20 and 45.
20-40 % of all patients with optic
neuritis develop diffuse encephalitis
(multiple sclerosis).

 Papilitis anterior part, nerve is

inflammed, optic disc will appear
swollen.
Retrobulbar neuritis behind the
globe (i.e. the retrobulbar part of the
nerve), sometimes didnt look
inflamation

Etiologi
Papillitis.
Inflammatory processes: Lyme disease, malaria, and syphilis,
and manifestations in the optic nerve of inflammation of the
orbit, paranasal sinuses, or base of t he sk ull.
Autoimmune disorders: lupus erythematosus, polychon-dritis,
regional enteritis (Crohns disease), ulcerative c olitis, nodular
panarteritis, and Wegeners granulomatosis.
Toxic damage due to agents such as methanol, l ead,
Myambutol (ethambu-tol hydrochloride), and chloramphenicol.
In 70 % of these cases, the cause is not determined .

Retrobulbar optic neuritis.

The primary causes: demyelinating diseases of the central
nervous system such as dif fuse encephalitis.

Symptom
The cardinal symptom is sudden
loss of vision, which may
occasionally be accompanie d by
fever ( Uhthof f symptom).
Pain that increases in extreme
positions of gaze when pressure is
applied to the globe.
Reduced perception of color intensity.

 The field of vision is typically

impaired by a central scotoma,
paracentral scotomas, a
centrocecal scotoma involving the
macula and blind spot, and wedgeshaped visual field defects up to and
including complete blindness.

Diagnosis

 Papillitis include edema and

hyperemia of the head of the optic
nerve. This flat-tens the optic cup
and obscures the margin of the
optic disk. Bleeding at the margin of
the optic disk may or may not be
present.
The optic disk will appear normal
in retrobulbar optic neuritis.

Treatment
Papilitis and neuritis retrobulbar have
a same medication
Corticosterioid.
Abtibiotik to treat infection as a
cause.

RETINAL DETACHMENT

 Separation of the neurosensory retina from the

underlying retinal pigment epithelium, to which
normally it is loosely attached.
This can be classified into 4 types:
Rhegmatogenous retinal detachment results from a tear,
i.e., a break in the retina. Presdipotition in trauma and
myopic.
Tractional retinal detachment results from traction, i.e., from
vitreous strands that exert tensile forces on the retina
Exudative retinal detachment is caused by fluid. Blood,
lipids, or serous fluid accumulates between the neurosensory
retina and the retinal pigment epithelium. Coats disease is a
typical example.
Tumor-related retinal detachment.

Symtoms
Retinal detachment can remain asymptomatic for a
long time.
In the stage of acute posterior vitreous detachment
flashes of light (photopsia) and floaters,
black points that move with the patients gaze.
Blood from this vessel will then enter the vitreous body.
black rain, numerous slowly falling small black dots .
Dark shadow in the visual field. The patient will perceive
a falling curtain or a rising wall, depending on whether
the detachment is superior or inferior.
A break in the center of the retina (macula is involved )
sudden and significant loss of visual acuity

Diagnostic
Ofthalmoscope : retina white and edematous and will lose
its transparency.
Rhegmatogenous, a bright red retinal break will also be visible.
The tears in rhegmatogenous retinal detachment usually occur in
the superior half of the retina in a region of equatorial
degeneration.
Tractional retinal detachment, the bullous detachment will be
accompanied by preretinal gray strands.
Exudative retinal detachment, massive fatty deposits and often by
intra retinal bleeding.
The tumor-related retinal detachment secondary retinal
detachment over the tumor or at some distance from the tumor in
the inferior peripheral retina.

Ultrasound studies can help confirm the diagnosis where

retinal findings are equivocal or a tumor is suspected.

Rhegmatogenous

Exudate

Tractional

Treatment
Retinal breaks with minimal circular
retinal detachment can be treated
with argon laser coagulation.
Extensive retinal detachments are
usually treated with a retinal
tamponade with an elastic silicone
sponge that is sutured to the outer
surface of the sclera, a so called
budding procedure.

 Rhegmatogenous RD use
reattachment surgery: laser, cryotherapy plus explant or internal
surgery with vitrectomy.
Exudative and solid RD establish
and treat the cause.
Tractional RD relieve traction by
vitreoretinal surgery

RETINAL VEIN OCCLUSION

 Vein occlusion occurs as a result of

circulatory dysfunction in the central
vein or one of its branches.
Retinal vein occlusion is the second
most frequent vascular retinal
disorder after diabetic retinopathy
and glaucoma.

Etiology
Local thrombosis at sites where
sclerotic arteries compress the veins.
In central retinal vein occlusion, the
thrombus lies at the level of the
lamina cribrosa in branch retinal
vein occlusion, it is frequently at an
arteriovenous crossing.

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

Diagnostic
Linear or punctiform hemorrhages are seen to
occur in all four quadrants of t he retina.
In branch retinal vein occlusion, intraretinal
hemorrhages will occur in the area of vascular
supply; this bleeding may occur in only one
quadrant or in two quadrants (hemispheric
vein occlusion).
Cotton-wool spots and retinal or optic disk
edema.
Chronic occlusions may also be accompanied by
lipid deposits.

Treatment
In the acute stage of vein occlusion,
hematocrit should be reduce d to 35 38 %
by hemodilution.
Laser treatment is performed in ischemic
occlusion that progresses to
neovascularization or rubeosis iridis.
Focal laser treatment is performed in branch
retinal vein occlusion with macular edema
when visual acuity is re duce d to 20/40 or
less within three months of occlusion.

RETINAL ARTERIAL
OCCLUSION

 Retinal infarction due to occlusion of

an artery in the lamina cribrosa or a
branch retinal artery occlusion.

Etiology
Emboli are frequently the cause of
retinal artery and branch retinal
artery occlusions.
Less frequent causes include
inflammatory processes such as
temporal arteritis (Hortons arteritis).

Symptoms
Patient generally complains of
sudden, painless unilateral blindness.
In branch retinal artery occlusion, the
patient will notice a loss of visual
acuity or visual field defects.

Diagnostic
In the acute stage of central retinal artery
occlusion , the retina appears grayish white
due to edema of the layer of optic nerve
fibers and is no longer transparent.
Fovea centralis, remains visible as a
cherry red spot because the red of the
choroid shows through at this site.
Atrophy of the optic nerve will develop in
the chronic stage of central retinal artery
occlusion

Treatment
Medications that reduce intraocular pressure,
or paracentesis are applied in an attempt to
drain t he embolus in a peripheral retinal
vessel.
Calcium antagonists or hemodilution are
applie d in an attempt to improve vascular
supply.
Lysis therapy is no longer performed due to
the poor prognosis (it is not able to prevent
blindness) and the risk to vital tissue involved

VITREOUS HEMORRHAGE

 Bleeding into the vitreous chamber

or a space created by vitreous
detachment.

Etiology
Bleeding from normal retinal vessels as can
occur as a result of mechanical vascular
damage in acute vitreous detachment or retinal
tear.
Bleeding from retinal vessels with abnormal
changes as can occur as a result of retinal
neovascularization in ischemic retinopathy or
retinal macroaneurysms.
Influx of blood from the retina or other sources
such as the subretinal space or the anterior s
egments of the eye.

 More frequent causes of vitreous hemorrhage

include:
Posterior vitreous detachment with or without retinal
tears ( 38 %).
Proliferative diabetic retinopathy (32 %).
Branch retinal vein occlusion ( 11 %).
Age-related macular degeneration (2 %).
Retinal macroaneurysm (2 %).

Less frequent causes of vitreous hemor rhage

include:
Arteriosclerosis.
Retinal periphlebitis.

Symptoms
Patients often report the sudden
occurrence of black opacities that they
may describe as swarms of black
bugs or black rain .
Severe vitreous hemorrhage can
significantly reduce visual acuity
Approximately 10 l of blood are sufficient
to reduce visual acuity to perception of
hand movements in front of the eye.

Diagnostic
Hemorrhages into the vitreous body
itself do not exhibit any
characteristic limitations but spread
diffusely (the blood cannot form a
fluid meniscus in the gelatinous
vitreous body) and coagulation
occurs quickly.

Treatment
Patients with acute vitreous hemorrhage
should be placed in an upright resting
position.
Next the cause of the vitreous
hemorrhage should be treated, for
example a retinal tear may be treate d
with a laser.
Vitrectomy will be require d to drain any
vitreous hemorrhage that is not absorbed.

ANTERIOR ISCHEMIC
OPTIC NEUROPATHY
(AION)

Anterior Ischemic Optic Neuropathy

(AION)
The following forms of anterior
ischemic optic neuropathy (AION) are
distinguished according to the cause
of the disorder:
1. Arteriosclerotic anterior ischemic
optic neuropathy.
2. Arteritic anterior ischemic optic
neuropathy.

1. Arteriosclerotic anterior ischemic

optic neuropathy.
An acute disruption of the blood supply to
the optic disk, i.e., optic disk infarction,
resulting from vascular changes in
arteriosclerosis.
Epidemiology: Arteriosclerotic AION is a
common cause of sudden loss of visual
acuity. The greatest incidence of this
disorder is between the ages of 60 and 70.
In contrast to arteritic AION, it can also
occur in adults below the age of 60.

 Etiology: The causes of the disorder

lie in acute disruption of the blood
flow through the lateral branches of
the short posterior ciliary arteries
and the ring of Zinn in the setting of
severe arteriosclerosis.

 Symptoms: Patients report a sudden

unilateral loss of visual acuity. This is due to
segmental or complete infarction of the
anterior portion of the optic nerve.
Severity is variable. The patient may present
with wedge-shaped visual field defects or
horizontal visual field defects that correlate
with segmental nerve fiber edemas.
However, severe concentric defects
progressing to total blindness can also occur.

 Diagnostic considerations: The

patient will frequently have a history
of hypertension, diabetes mellitus, or
hyperlipidemia.
Ophthalmoscopy will reveal edema of
the optic disk, whose margin will be
accordingly obscured.

 Treatment: Examination by an internist and Doppler

ultrasound studies of the carotid artery may be
helpful because the diagnosis of the underlying
cause is important
Underlying disorders such as diabetes mellitus or
arterial hypertension should be treated.
Anterior ischemic optic neuropathy is nearly
impossible to treat. Attempted methods include
hemodilution (pentoxifylline infusions, acetylsalicylic acid, and bloodletting depending on
hematocrit levels) and systemic administration of
steroids to control the edema.

 Prognosis: The prognosis is usually

poor even where therapy is initiated
early. Isolated atrophy of the optic
nerve will appear within three weeks,
complex atrophy of the optic nerve is
less frequent but may also be
observed.

2. Arteritic Anterior Ischemic Optic

Neuropathy
An acute disruption of the blood supply to
the optic disk due to inflammation of
medium-sized and small arterial branches.
Epidemiology: The annual incidence is
approximately three cases per 100000.
The disorder occurs almost exclusively
after the age of 60. Women are affected
slightly more often than men, accounting
for 55% of all cases.

 Etiology: Giant cell arteritis is a frequently

bilateral granulomatous vasculitis that
primarily affects the medium-sized and
small arteries.
Common sites include the temporal
arteries, ophthalmic artery, short posterior
ciliary arteries, central retinal artery, and
the proximal portion of the vertebral
arteries, which may be affected in varying
combinations.

 Symptoms: Patients report sudden unilateral

blindness or severe visual impairment. Other
symptoms include headaches, painful scalp
in the region of the temporal arteries,
tenderness to palpation in the region of the
temporal arteries, pain while chewing (a
characteristic sign), weight loss, reduced
general health and exercise tolerance.
Patients may have a history of amaurosis
fugax or polymyalgia rheumatica.

 Diagnostic considerations: The

ophthalmoscopic findings are the same as
in arteriosclerotic AION.
Other findings include a significantly
increased erythrocyte sedimentation
rate/ESR (precipitous sedimentation is
the most important hematologic finding),
an increased level of C-reactive
protein/CRP, leukocytosis, and irondeficiency anemia.

 The temporal arteries are prominent ,

painful to palpation, and have no
pulse. The diagnosis is confirmed by
a biopsy of the temporal artery.

 Treatment: Immediate high-dosage systemic

steroid therapy (initial doses up to 1000 mg of
intravenous prednisone) is indicated. Steroids
are reduced as the erythrocyte sedimentation
rate decreases, C-reactive protein levels drop,
and clinical symptoms abate.
However, a maintenance dose will be required
for several months. Vascular treatment such
as pentoxifylline infusions may be attempted.

 Prognosis: The prognosis for the

affected eye is poor even where
therapy is initiated early. Immediate
steroid therapy is absolutely
indicated because in approximately
75% of all cases the fellow eye is
affected within a few hours and
cerebral arteries may also be at risk.

CENTRAL SEROUS
CHORIORETINOPATHY

Central Serous
Chorioretinopathy
Serous detachment of the retina
and/or retinal pigment epithelium.
Etiology: Serous detachment occurs
through a defect in the outer blood
retina barrier (tight junctions in the
retinal pigment epithelium).

 Epidemiology: The disorder primarily

affects men in the third and fourth
decade of life.
Symptoms: Patients present with a
loss of visual acuity, a relative
central scotoma (dark spot), image
distortion, or perception of objects as
larger or smaller than they are
(macropsia or micropsia).

 Diagnostic considerations: Ophthalmoscopy

will reveal a serous retinal detachment,
usually at the macula. In chronic cases, a
fine brown and white pigment epithelial scar
will develop at the site of the fluid effusion.
Swelling in the central retina shortens the
visual axis and produces hyperopia.
The site of fluid effusion can be identified
during the active phase with the aid of
fluorescein angiography

 Treatment: Usually no treatment is

required for the first occurrence of
the disorder. Retinal swelling resolves
spontaneously within a few weeks.
Recurrences may be treated with
laser therapy provided the site of
fluid effusion lies outside the fovea
centralis.

 Clinical course and prognosis: The

prognosis is usually good. However,
recurrences or chronic forms can
lead to a permanent loss of visual
acuity.

CHOROIDITIS

Choroiditis
Epidemiology: There are few epidemiologic
studies of choroiditis. The annual incidence is
assumed to be four cases per 100 000 people.
Etiology:
o Toxoplasmosis
o Syphilis
o Behets disease
o Trauma
o Immunodeficiency
o Post-surgery

 Symptoms: Patients are free of pain, although

they report blurred vision and floaters.
Diagnostic considerations: Ophthalmoscopy
reveals isolated or multiple choroiditis foci. In
acute disease they appear as ill-defined white
dots. Once scarring has occurred the foci are
sharply demarcated with a yellowish-brown
color. Occasionally the major choroidal
vessels will be visible through the atrophic
scars.

 Treatment: Choroiditis is treated

either with antibiotics or steroids,
depending on its etiology.
Prognosis: The inflammatory foci will
heal within two to six weeks and
form chorioretinal scars. The scars
will result in localized scotomas that
will reduce visual acuity if the macula
is affected.

Thank You