SAFII RAHMI

R. HANDOKO PRATOMO

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 Unilateral or less commonly, bilateral
reduction of best corrected visual acuity that
can not be attributed directly to the effect of
any structural abnormality of the eye or the
posterior visual pathway. Defect of central
vision

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 Resulting from one of following:

A. Strabismus
B. Anisometropia or high bilateral refractive
error (Isoametropia)
C. Visual deprivation

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 Prevalence: 2%-4% in the North American
population
Commonly unilateral
Nearly all amblyopic visual loss is
preventable or reversible with timely detection
and appropriate intervention.
Children with amblyopia or at risk for
amblyopia should be identified at a young age
when the prognosis for successful treatment
is best.
Role of screening is important
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 Amblyopia is primarily a defect of central
vision.
There is a critical period for sensitivity in
developing amblyopia.
The time necessary for amblyopia to occur
during critical period is shorter for stimulus
deprivation than for strabismus or
anisometropia.

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Neurophysiology:

Cells of the primary visual cortex can completely

lose their innate ability or show significant
functional deficiencies

Abnormalities also occur in neurons in the lateral

geniculate body

Evidence concerning involvement at the retinal level

remains inconclusive

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Classification:

1. Strabismus Amblyopia
2. Anisometropia Amblyopia
3. Amblyopia Due to bilateral high refractive
error (isometropia)
4. Deprivation Amblyopia

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Strabismus Amblyopia
The most common form of amblyopia
Strabismic amblyopia is thought to result
from competitive or inhibitory interaction
between neurons carrying the nonfusible
inputs from the tow eye.
Which leads to domination of cortical vision
centers by the fixating eye and chronically
reduced responsiveness to the nonfixating
eye input.

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Anisometropia Amblyopia

Second in frequency
It develops when unequal refractive error in the tow
eyes causes the image on the one retina to be
chronically defocused.
This condition is thought to result:
Partly from the direct effect of image blur in the
development of visual acuity.
Partly from intraocular competition or inhibition

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 Mild hyperopic or astigmatic anisometropia
(1-2D) mild amblyopia
Mild myopia anisometropia (less than -3D)
usually doesn't cause amblyopia
unilateral high myopia (-6D) sever
amblyopia visual loss.
The eye s of a child with anisometropic
amblyopia look normaly to the family and
primary care physician.

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 Amblyopia Due to bilateral high
refractive error (isometropia)
isometropia amblyopia result from large,
approximately equal, uncorrected refractive
error in both eyes of a young child.
Hyperopia exceeding 5D & myopia excess of
10 D risk bilateral amblyopia

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 Merdional amblyopia:
Uncorrected bilateral astigmatism in early
childhood may result in loss of resoling
ability limited to chronically blurred
meridians.

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Deprivation Amblyopia

It is usually caused by congenital or early

acquired media opacity.
This form of amblyopia is the least common
but most damaging and difficult to treat.
In bilateral cases acuity can be 20/200 or
worse.

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 In children younger than 6 years, dons
congenital cataract that occupy the central 3
mm. or more of the lens must be considered
capable of causing sever amblyopia.
Similar lens opacities acquired after 6 years
are generally less harmful.

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 Small polar cataracts & lamellar cataracts
may cause mild to moderate amblyopia or
may have no effect on visual development.

Occlusion amblyopia is a form of deprivation

caused by excessive therapeutic patching.

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Diagnosis
Characteristics of vision alone cannot be used
to reliably differentiated amblyopia from
other form of visual loss.
The crowding phenomenon is typical for
amblyopia but not uniformly demonstrable.
Afferent pupillary defect are Characteristic of
optic nerve disease but occasiinally appear to
be present with amblyopia

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 Multiple assessment using a variety of tests or
performed on different occasions are
sometime required to make a final judgment
concerning the presence and severity of
amblyopia.

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 Binocular fixation pattern:
It is a test for estimating the relative level of
vision in the tow eyes for children with
strabismus who are under the age of about 3.
This test is quite sensitive for detecting
amblyopia but results can be falsely positive.
Showing a strong preference when sision is
equal or nearly equal in the tow eyes,
particularly with small angle strabismic
deviations.

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 The modified Snellen technique directly
measures acuity in children 3-6 years old.
Often, however, only isolated letters can be
used, which may lead to under estimated
amblyopia visual loss.
Croding bar may help alleviate this problem.

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 E O
Crowding bar, or contour interaction bars, allow the
examinator to test the crowing phenomenon with
isolated optotype. Bar surrounding the optotype
mimic the full of optotype to the amblyopia child.

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Treatment

Treatment of amblyopia involves the

following steps:
Eliminating (if possible) any obstacle to
vision such as a cataract
Correcting refractive error
Forcing use of the poorer eye by limiting use
of the better eye.

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Cataract removal
Cataracts capable of producing amblyopia require
surgery without unnecessary delay.
Removal of significant congenital lens opacities
during the first 2-3 months of life is necessary for
optimal recovery of vision.
In symmetrical bilateral cases, the interval between
operations on the first and second eyes should be no
more than 1-2 weeks.
Acutely developing severe traumatic cataracts in
children younger than 6 years should be removed
within a few weeks of injury, if possible.
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Refractive correction

In generally, optical prescription for

amblyopic eyes should correct the full
refractive error as determined with
cyclopagic.

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Occlusion and optical degradation
Full time occlusion of the sound eye:
Defined as occlusion for all or all but one waking
hour.
It is the most powerful means of treating of
amblyopia by enforced use of the defective eye.
The patch can either be left in place at night or
removed at bedtime.
Spectacle-mounted occluser or special opaque
contact lenses can be used as an alternative to full-
time patching if skin irritation or poor adhesion
proves to be a significant problem

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 Full time patching should generally be used
only when constant strabismus eliminates any
possibility of useful binocular vision because
full time patching runs a small risk of
perturbing binocularity.

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 Part-time occlusion:
Defined as occlusion for 1-6 hours per day.
The children undergoing part time occlusion
should be kept as visually active as possible
when the patch is in place.
Compliance with occlusion therapy for
amblyopia declines with increasing age.

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 Penalization:
A cyclopagic agent (usually atropine 1% or
homatropine 5% ) once daily to the better
eye
This form of treatment has recently been
demonstrated to be as effective as patching
for mild to moderate amblyopia.

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Complication of therapy
Full time occlusion carries the greatest risk of this
complication and requires close monitoring,
especially in the younger child.
The first follow up visit after initial treatment should
occur within 1 week for an infant and after interval
corresponding to 1 week per year of age for the
older child.
Part time occlusion & optical degradation methods
allow for less frequent observation but regular
follow up is still critical

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 The time required for completion of
treatment depends on the following:
1. Degree of amblyopia
2. Choice of therapeutic approach
3. Compliance with the prescribed regimen
4. age of the patient

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Unresponsiveness
Complete or partial Unresponsiveness to treatment
occasionally affect younger children but must often
occurs in patients older than 5 years.
Primary therapy should generally be terminated if
there is a lock of demonstrable progress over 3-6
months with good compliance.
Refraction should be carefully rechecked and the
macula and optic nerve critically inspected for
subtle evidence of hypoplasia or other malformation
that might have been previously overlooked.

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 Recurrence

When amblyopia treatment is discontinued after fully

or partially successful completion, approximately half
of patients show some dgree of recurrence,
Maintenance therapy:
Patching for 1-3 hours per day
Optical penalization with spectacles
Pharmacologic penalization with atropine 1 or 2 day
per week.
This may require periodic monitoring until age 8-10.

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