BUTA MENDADAK /

ACUTE VISION LOSS

Dr. R. HANDOKO PRATOMO, SpM

PATHOPHYSIOLOGI

Opacification of normally transparent structures

through which light rays pass to reach the retina (eg,
cornea, vitreous)

Retinal abnormalities

Abnormalities affecting the optic nerve or visual

pathways
ETIOLOGY
Vascular occlusions of the retina (central retinal
artery occlusion, central retinal vein occlusion)

Ischemic optic neuropathy (often in patients with

temporal arteritis)

Vitreous hemorrhage (caused by diabetic

retinopathy or trauma)
 Causes of Acute Visual Loss
Painful Painless
Keratitis Vitreous hem

Acute A. C. glaucoma RD
Uveitis Retinal vascular Occlusions

X
Lens Optic neuritis +
Ischemic optic neuropathy
CVA
Functional
 Some Causes of Acute Vision Loss

Cause Suggestive Findings Diagnostic Approach

Arteritic ischemic optic Sometimes headache, ESR

neuropathy (usually in jaw or tongue
patients with giant cell claudication, temporal Temporal artery biopsy
[temporal] arteritis) artery tenderness or
swelling, pale and
swollen disk with
surrounding
hemorrhages, occlusion
of retinal artery or its
branches

Sometimes proximal
myalgias with stiffness
(due to polymyalgia
rheumatica)
Cause Suggestive Findings Diagnostic Approach

Functional loss of vision Normal pupillary light Clinical evaluation

reflexes, positive
optokinetic nystagmus, If diagnosis is in doubt,
no objective ophthalmologic
abnormalities on eye evaluation and visual
examination evoked responses

Often inability to write

name or bring
outstretched hands
together

Sometimes indifferent
affect despite severity
of claimed loss of vision

Macular hemorrhage due Blood within or deep to Clinical evaluation

to neovascularization in retina in and around the
age-related macular macula
degeneration
Cause Suggestive Findings Diagnostic Approach

Nonarteritic ischemic Optic disk edema and ESR

optic neuropathy hemorrhages
Consideration of
Sometimes loss of temporal artery biopsy
inferior and central to exclude giant cell
visual fields arteritis

Risk factors (eg,

diabetes, hypertension,
hypotensive episode)

Ocular migraine Scintillating scotomata, Clinical evaluation

mosaic patterns, or
complete loss of vision
lasting usually 1060 min
and often followed by
headache

Often in young patients

Cause Suggestive Findings Diagnostic Approach

Retinal artery occlusion Nearly instantaneous ESR to exclude giant cell

onset, pale retina, arteritis
cherry-red fovea,
sometimes Hollenhorst
plaque (refractile object
at the site of arterial
occlusion)

Risk factors for vascular

disease

Retinal detachment Recent increase in Clinical evaluation

floaters, photopsias
(flashing lights), or both

Visual field defect,

retinal folds

Risk factors (eg, trauma,

eye surgery, severe
myopia; in men,
Cause Suggestive Findings Diagnostic Approach

Retinal vein occlusion Frequent, multiple, widely Clinical evaluation

distributed retinal
hemorrhages

Risk factors (eg, diabetes,

hypertension, hyperviscosity
syndrome, sickle cell
anemia)
Transient ischemic Bilaterally symmetric Consideration of
attack or stroke (homonymous) field
defects, no effect on visual MRI or CT
acuity in the intact parts of
the visual field (bilateral Carotid ultrasonography
occipital lesions are the
exception and are ECG
uncommon but can occur
due to basilar artery Continuous monitoring
occlusion) of cardiac rhythm

Risk factors for

atherosclerosis
Cause Suggestive Findings Diagnostic Approach

Vitreous hemorrhage Previous floaters or Possible ultrasonography

spider web in vision to assess retina

Risk factors (eg,

diabetes, retinal tear,
sickle cell anemia,
trauma)
Acute angle-closure Halos around lights, Immediate
glaucoma nausea, headache, ophthalmologic
photophobia, evaluation
conjunctival injection,
corneal edema, shallow Gonioscopy
anterior chamber,
intraocular pressure
usually > 40
Cause Suggestive Findings Diagnostic Approach

Corneal ulcer Ulcer visible with fluorescein Ophthalmologic

staining, slit-lamp evaluation
examination, or both

Risk factors (eg, injury,

contact lens use, herpetic
[painful vesicular] rash in V1
distribution)

Endophthalmitis Floaters, conjunctival Immediate

injection, decreased red ophthalmologic
reflex, hypopyon, or a evaluation with cultures
combination of anterior chamber and
vitreous fluids
Risk factors (such as history
of traumatic ruptured globe
or intraocular foreign body
[eg, after hammering metal
on metal], injury during eye
surgery)
Cause Suggestive Findings Diagnostic Approach

Optic neuritis (usually Mild pain with eye Gadolinium-enhanced

painful but not always) movement, afferent MRI to diagnose multiple
pupillary defect (occurs sclerosis
early)

Central or peripheral
visual field defects

Abnormal color vision

testing results

Sometimes optic disk

edema
EVALUASI
History: History of present illness should
describe loss of vision in terms of onset,
duration, progression, and location (whether it
is monocular or binocular and whether it
involves the entire visual field or a specific part
and which part). Important associated visual
symptoms include floaters, flashing lights, halos
around lights, distorted color vision, and jagged
or mosaic patterns (scintillating scotomata).
The patient should be asked about eye pain and
whether it is constant or occurs only with eye
movement.
 Review of systems should seek extraocular symptoms of
possible causes, including jaw or tongue claudication,
temporal headache, proximal muscle pain, and stiffness
(giant cell arteritis); and headaches (ocular migraine).

Past medical history should seek known risk factors for eye
disorders (eg, contact lens use, severe myopia, recent eye
surgery or injury), risk factors for vascular disease (eg,
diabetes, hypertension), and hematologic disorders (eg,
sickle cell anemia or disorders such as Waldenstrm
macroglobulinemia or multiple myeloma that could cause a
hyperviscosity syndrome).

Family history should note any family history of migraine

headaches.
TREATMENT
Causative disorders are treated. Treatment should usually
commence immediately if the cause is treatable. In many
cases (eg, vascular disorders), treatment is unlikely to
salvage the affected eye but can decrease the risk of the
same process occurring in the contralateral eye or of a
complication caused by the same process (eg, ischemic
stroke).
KEY POINTS
Diagnosis and treatment should occur as rapidly as possible.

Acute monocular loss of vision with an afferent pupillary defect

indicates a lesion of the eye or of the optic nerve anterior to the
optic chiasm.

Optic nerve lesion, particularly ischemia, is considered in patients

with acute monocular loss of vision or afferent pupillary defect and
in those with or without optic nerve abnormalities on
ophthalmoscopy but no other abnormalities on eye examination.

Corneal ulcer, acute angle-closure glaucoma, endophthalmitis, or

severe anterior uveitis is considered in patients with acute
monocular loss of vision, afferent pupillary defect, eye pain, and
conjunctival injection.
Acute Angle Closure Glaucoma
Aims of Acute ACG
management :

Decrease IOP

Prevent future attacks in OU

TERIMA KASIH