Incidence And Management Of Amblyopia In School Children

INCIDENCE AND MANAGEMENT OF AMBLYOPIA IN SCHOOL CHILDREN

INTRODUCTION

Amblyopia is the commonest vision defect in children, resulting in abnormal sight in one or both eyes. The conditions are sometimes called ‘lazy eye’. The condition affects an many as ‘one to five’ percent of children but the rate is different in various part of the world.¹

The disorder is caused by any condition that sends the brain abnormal or unequal visual input during infancy or childhood. These conditions can include an imbalance in he positioning of the eyes, such as strabismus, in which the eyes are crossed inward (esotropia) or turned outward (exotrcpia). Amblyopia also can result from a major difference in refractive error between the two eyes, such as myopia, hypermetropia or astigmatism. Less common causes of amblyopia are cornea and lens diseases and injury to the eye of a young child.^2,10-16 The results reported in this study do not include amblyopia from these less common causes.

Amblyopia has been subdivided in terms of the major disorders that may be responsible for its occurrence. They are stimulus deprivation amblyopia, strabismic amblyopia and anisometropic amblyopia.³

The treatment of amblyopia involves (1) Eliminating, if possible, any obstacle to vision such as a cataract (2) correcting the refractive error & (3) forcing the use of the poorer eye by limiting the use of the better eye by means of occlusion or penalization.^5,14 Part time occlusion and penalization are of ancillary value but cannot be considered equal in effectiveness to constant occlusion.⁶

It has been commonly thought that the best time to correct amblyopia was during infancy or early childhood before the eyes and the entire visual system including the brain, have fully matured.⁴

Amblyopia is responsible fro more unilaterally reduced vision of childhood onset than all other caused combined. This fact is particularly distressing because in principle, nearly all amblyopic visual loss is preventable or reversible with timely detection and appropriate intervention.

In our country there is no effective screening system to detect amblyopia and prompt effective treatment. Illiteracy, lack of awareness, limited availability of ophthalmic care personnel and scant health funds all these contribute to the tragedy of visual loss due to amblyopia.

This study is to find out the incidence of amblyopia in school children and effectiveness of treatment modalities in children 5-11 years old.

AIMS AND OBJECTIVES

General Objectives:

To find out the incidence of amblyopia is school children and improvement of visual acuity after appropriate treatment.

Specific Objectives:

To assess the incidence and resolution rates of amblyopia in children age 5-11 years.
The time course of visual acuity improvement.
To evaluate the effectiveness of treatment modalities and rate of resolution or improvement of amblyopia.

REVIEW LITERATURE

Historical Background and Context

Probably the first known description of amblyopia and its treatment was given during the Dark Ages by Paulus Sextineus in AD 783. Its more modern description by Comte de Buffon in 1743 included the first description of the use of occlusion therapy. It is important to note that even during that primitive era the value of occlusion was recognized as being helpful in overcoming or ameliorating the condition, clearly separating it from other forms of visual impairment for which no treatment existed. In 1803, Erasmus Darwin, the grandfather of Charles, recommended the use of differing forms of occluders on the sound eye for differing levels of amblyopia. Its first mention in the English language literature displayed a clear indication of the level of sophistication of clinical thinking about the condition at that time:

If the squinting has not been confirmed by long habit, and one eye be not much worse than the other, a piece of gauze stretched on a circle of whalebone, to cover the best eye in such a manner as to reduce the distinctness of vision of the eye to a similar degree of imperfection with the other, should be worn some hours every day, or the better eye should be totally darkened by a tin cup covered with black silk for some hours daily (Darwin E, 1801).

In the specialty of ophthalmology, practically none of the therapeutic^, modalities used to treat common eye conditions are the same as those in use 3 or even 2 decades ago. An almost unique exception to this is the use of occlusion therapy for the treatment of ambyopia. This might suggest that occlusion is a fully satisfactory therapy requiring no change or critical analysis. Clinicians who treat amblyopia in children (where it is most commonly detected), parents, and children themselves know otherwise. The truth is that there is no common agreement among clinicians as to the best way to treat amblyopia – even to the extent of questioning whether patching of the sound eye is the best way to treat the condition. A significant minority of clinicians eschew the patch and opt instead for the use of some form of blurring, optical or pharmacologic, to treat amblyopia. The situation presents a unique opportunity to determine the answer to the question in a systemic way by carrying out a randomized clinical trial.

Epidemiology

Amblyopia is among the top three causes of monocular visual loss in the adult age group from 18 to 85 years. This is a disconcerting finding, as these are the ages where the bilateral diseases of the older ages – cataract, macular degeneration, diabetic retinopathy, glaucoma – take their toll. It suggests that the condition persists well beyond the childhood years, resistant to therapy and leaving its victims vulnerable to the above mentioned disease in later life.

PART II

BASIC ASPECTS AND PATHOPHYSIOLOGY

Definition of Amblyopia:

The Greek word amblyopia refers to a dimness or dullness of vision. Amblyopia is a real diminution of vision usually, but not exclusively in one eye, for which no appropriate structural cause exits that is either visible ophthalmoscopically or found in the afferent visual pathway. It is caused by abnormal visual experience early in life. Although classic definition stress that amblyopia is visual loss with no associated organic defect, in fact there is always an abnormality, be it strabismus, or Isoametropia, anisometropia, media opacity which predisposes the eye or eyes to become amblyopic. Amblyopia is primarily a defect of central vision; the peripheral visual field nearly always remains normal.

Neurophysiology of vision

The retino-geniculo-cortical pathway that provides the neural substrate for visual perception consists of :

Magno and parvo cells of retinal ganglion cell layer
Lateral geniculate body (LGB)
Primary visual cortex (Brodmann’s area 17)

Magnocellular (M) and parvooellular (P) systems

Theses are the main systems in retino-geniculo cortical pathway

Magnocellular System:

Magnocellular retinal cells have large soma with large dendritic fields and large axons.
Magnocellular cells are rare in foveal area and increase in number towards periphery
Synapse with magnocellular neurons in LGB. The Magnocellular geniculate axons terminate in striate cortex layer IV C?.
The Magnoceilular system is sensitive to moving stimuli and relatively insensitive to color.

Parvocellular System:

Parvocellular retinal ganglion cells have small soma and small dendritic fields.
Relatively high density in fovea and decreases in number as retinal eccentricity increases.
The Parvocellular retinal ganglion cells synapse with the Parvocellular LGB cells,
The Parvocellular geniculate axons terminate I layer IV C? of striate cortex
The Parvocellular system gives a slow tonic response to visual stimulation and carries high resolution information about object’s borders and color contrast and is important for shape perception and the ability to see standing objects in detail.

Lateral Geniculate Boby (LGB)

The lateral geniculate body consists of six purely monocular laminae (four dorsal Parvocellular and two ventral mangocelluiar laminae)
Geniculate laminae 1(Parvo), 4 (parvo) and 6 (Magno) receive axons from contralateral nasal retina; laminae 2 (Parvo), 3 (Parvo) and 5 (Magno) receive axons from temporal retina.
The LGB is the principal thalamic visual nucleus linking the retina and the striate cortex.

Striate Cortex

The striate cortex performs the basic analysis of geniculate input and then transmit its essence to higher peristriate cortical areas for further interpretation. The monocular separation through the lateral geniculate laminae continues into the striate cortex (VI), where the geniculate axon terminal from the right and left eye are segregated into a system of alternating parallel stripes called ocular dominance columns.

NEUROPHYSILOGIC MECHANISM OF AMBLYOPIA

Understanding of different neurophysiologic mechanisms that underlie amblyopia is still far from complete. The studies of experimental modification of visual experience in animal and laboratory testing of amblyopic humans have provided some insights.

When a young child experiences abnormal visual experience, there may be a loss of visual function that persists even after the optical or ocular problems are corrected. Amblyopia or “lazy eye” often develops when unequal refractive power (anisometropia) or misalignment of the visual axis (Strabismus) of the two eyes interferes with focused and balanced binocular vision early in development. This leads to a condition in which information from the affected eye is not processed properly because of binocular competition and visual acuity is reduced relative to the normal eye. Thus amblyopia is a disease of the development of the central visual system.

Animal models have revealed that a variety of profound disturbances of visual system neuron function may result from abnormal early visual experience. In the striate cortex, monocular visual deprivation caused the ocular dominance columns of the deprived eye to appear radially warred. The cells in the cortex lose their innate ability to respond to stimulation and if remains responsive may show significant functional deficiencies.

Minor shrinkage of both Magno and Parvo cells of lateral geniculate laminae receiving input from deprived eye also occurs but these cells respond briskly to visual stimulation, implying that a defect in the LGB is not likely to account for amblyopia. Evidence concerning involvement at the retinal level remains inconclusive, if present,, changes in the retina make at most a minor contribution to}`.the overall visual defect.

Several findings from both animals and humans, such as increased spatial summation and lateral inhibition when light detection thresholds are measured using different-sized spots, suggest that the receptive fields of neurons in the amblyopic visual system are abnormally large. This disturbance may account for the crowding phenomenon (also known as contour interaction), whereby Snellen letters or equivalent symbols of a given size become more difficult to recognize if they are closely surrounded by similar forms, such as a full line or chart of letters. The crowding phenomenon sometimes causes the measured “linear” acuity of an amblyopia eye to drop several lines below that measured with isolated letters.

Aetiology

Amblyoria is caused by inadequate stimulation of the visual system during the critical period of visual development in early childhood (<8 years). This is most marked under the age of two years. Amblyopia may be unilateral or bilateral and the cause may be any or a combination of the following factors.

Light deprivation: Light fails to enter into the eye (eg. Cataract, Ptosis etc.) and cannot stimulate the retina.

Form deprivation: The retina receives a defocused image as with refractive errors,

Abnormal binocular interaction: Non-fusible images fall on each fovea as with strabismus.

The prognosis for achieving good visual acuity decreases when more than one of these factors present together in one case.

PATHOGENESIS

Perhaps the best definition of amblyopic available is that of Levi: “Amblyopia is a developmental defect of spatial vision, the chief symptom of which is loss of visual acuity.” It is almost always associated with the presence of strabismus, anisometropia, a combination of both, or from deprivation early in life. The loss may be monocular or binocular. The emphasis in this definition is on “developmental defect”, for the condition occurs during the cascade of events recent neuroscience and psychophysical studies have describe as “visual development”.

In contrast to the auditory system, where sound acuity thresholds are adult levels at birth (after the external canals have been cleared of amniotic fluid), the visual system thresholds in a newborn are several log units below adult levels, in spite of optics that have 20/20 clarity. The auditory system is “hard wired” at birth. The visual system, although hard wired in its basic plan at birth, requires visual experience and especially the competitive interaction between the visual pathways of the two eyes in the visual cortex to develop adult levels of vision. As the study of the development of the visual nervous system has progressed in the last 2 decades, it has become clear that there are many critical periods. The concept of plasticity and continuing visual development over a long span of time has arisen to challenge the old orthodoxies. The best evidence is that a severe insult is required to produce a level of deprivation, such as that of a dense axial monocular cataract or corneal leukoma that will lead to an irremediable defect in an eye’s visual thresholds.

Types of Amblyopia

Amblyopia has been subdivided in terms of the major disorders that may be responsible for its occurrence.

Stimulus deprivation amblyopia : this type of amblyopia results from vision deprivation and is usually caused by congenital or early acquired media opacities or severe ptosis. It may be unilateral or bilateral. Amblyopic visual loss resulting from a unilateral lack of form vision tends to be worse than that produced by bilateral deprivation of similar degree because in.terocular effects add to the direct developmental impact of severe image degradation.
5trabismic amblyopia: It results from abnormal binocular interaction where there is continued monocular suppression of the deviating eye. It is characterized by an impairment of vision which is present even when the eye is forced to fixate.

Features of Typical Strabismic Amblyopia

i) Grating acuity

This is the ability to detect patterns composed of uniformly spaced stripes. In strabismic amblyopia grating acuity is often reduced considerably less than snellen acuity. Apparently the affected eyes see forms in a twisted or distorted manner that interferes more with letter recognition than with a simpler task of determining whether a grating pattern is present.

ii) Neutral – density filter effect

When illumination is reduced the acuity of an eye with strabismic amblyopia tends to decline less sharply than that of an originally diseased eye. This phenomenon is called the neutral density filter effect after the device classically used to demonstrate it.

iii) Anisometric amblyopia :

This type of amblyopia is caused by a difference in refractive error of even as little as 1.0 D sphere. It results from abnormal binocular interaction from the superimposition of focused and unfocused images or from the superimposition of large and small images (aniseikonia). There may also be an element of form vision deprivation as one eye constantly receives a blurred image. It is frequently associated with microstrabismus and may coexist with strabismic amblyopia.

Relatively mild degrees of hyperopic or astigmatic anisometropia (1-2 D) can induce mild amblyopia. Mild Myopic anisometropia (<-3D) usually does not cause amblyopia, but unilateral high myopia (-6D) often results in severe amblyopic visual loss.

iv) Meridional amblyopia: It results from form vision deprivation in one meridian. It can be unilateral or bilateral and is caused by uncorrected astigmatism. The degree of cylindrical ametropia necessary to produce meridional amblyopia is not known but most ophthalmologists recommend correction of greater than 2.00 D of cylinder

v) Ametropic amblyopia: Bilateral amblyopia, which is the result of a high degree of uncorrected bilateral refractive error. Hyperopia exceeding about 5D and myopia in excess of 10D carry a risk of inducing bilateral amblyopia.

vi) Occlusion amblyopia: It is a form of deprivation amblyopia caused by excessive therapeutic patching.

Investigations for Amblyopia

Case history: Early-onset, unilateral, constant strabismus with long duration without treatment predisposes to strabismic amblyopia. Congenital ocular pathology such as cataract and ptosis predispose to stimulus deprivation amblyopia.

Visual acuity: If possible it is better to use a linear test type. The patient may demonstrate the crowding phenomenon where reduced visual acuity is detected on linear testing, despite better visual acuity on single optotype. This is due to additional stimulation from contours of adjacent letters in a linear test type which produces confusion.

Refraction: Anisometropia, high astigmatism and bilateral high refractive errors are aetiological factors.

Cover test: There may be unilateral constant strabismus. By observing fixatation and reaction to occlusion and estimate of visual acuity can be obtained.

Visuscope: Fixation may be eccentric or wandering, in a parafoveal, parama,ular or peripheral retinal area.

Neutral density: This test makes use of the fact that amblyopic eyes perform relatively well under condition of low illumination. The visual acuity, when tested with the filter, is not significantly reduced in thIq amblyopic eye when compared with visual acuity of the normal eye. This test differentiates between amblyopia and reduced visual acuity due to organic defects, as organic amblyopia will have further reduction in visual acuity under poor illumination.

Ocular Examination: Detailed ocular examination including fundus examination should be done to exclude any ocular pathology that may reduce vision.

Visual Acuity Assessment in Children

Testing in preverbal children

An estimation of the comparative vision between the two eyes can be gained from simple examination and observation of the child.

Occlusion of one eye: If strongly objected to by the child, indicates poorer acuity in the other eye.
‘Hundred and thousands’ sweet test is a gross test which is seldom performed. In principle, if the child is able to see and pick up small sweets at 33 cm, visual acuity is at least 6/24.
Perferential looking test can be used from early infancy: They are based on the fact that infants prefer to look at a pattern rather than a homogenous stimulus. The infant is exposed to a stimulus and the examiner observes the eyes for fixation movement. Two example are teller acuity cards, which consists of black stripe5 of varying thickness, and Cardiff acuity cards, which consists of shapes with variable outlines.
Optokinetmc nystagmus may provide an estimation of visual acuity dependent on the size of the stripes used.

Testing in verbal children

At age 2 years, most children will have sufficient language skills to undertake a picture – naming test such as the kay pictures.
At age 3 years, most children will be able to undertake jh matching of single-letter optotypes as in the Sheridan-Gardiner test. This test has the disadvantage of overestimating acuity in the amblyopic eye as it eliminates the crowding phenomenon. The keeler Log MAR crowded test is more accurate in amblyopia as it requires the child to match one letter out of a group of optotypes, which relates more accurately to Snellen acuity.
At age 4 years, most children will be able to perform a linear Snellen acuity test.

Assessment of Visual Acuity in Children

Below 2 years	Occlusion of one eye Hundreds and thousands sweet test Fixation test Teller acuity cards test Cardiff acuity cards test Optokinetic nystagmus
At age 2 years	Kay pictures test
At age 3 years	Sheridan-Grandiner test Keller LogMAR crowded test
At age 4 years & above	Kelfer LogMAR crowded test Linear Snellen acuity test

Log MAR Crowded Test

The Log MAR crowded test has been designed by Paul Mc Graw and Barry Winn to include features which should allow change in letter acuity to be detected in pre-school children especially those undergoing vision therapy training. However, the cards are useful fT~ the measurement of letter acuity in all patients in both clinical and domiciliary environments.

The Log MAR crowded test is usually performed at a test distance of 3 m in an evenly well illuminated room. Six letters are used in the test and they are – X V 0 H U Y. Each line on the chart represents changes of 0.1 Log unit in the acuity level and snellen equivalent value is provided for each line.

The Log MAR crowded test is an appropriate method for assessing visual acuity in children, particularly for the management of Amblyopia.

LogMAR score and snellen equivalent on each line : Linec” Snellen (UK) Snellen (USA) LogMAR Line 1 6/38 20/127 0.8

Line 2 6/30 20/100 0.7

Line 3 6/24 20/80 0.6

Line 4 6/19 20/63 0.5

Line 5 6/15 20/50 0.4

Line 6 6/12 20/40 0.3

Line 7 6/9.5 20/32 0.2

Line 8 6/7.5 20/25 0.1

Line 9 6/6 20/20 0.0 21

Prevention of Amblyopia

The literature on prevention of Amblyopia is sparse. Ingram has published on the early detection of high refractive errors, particularly hypermetropia & amisometropia in children through school screening programs. He has reached the conclusion that it does not prevent emblyopia.

Others ( Atkinson et al) have come to the conclusion that the early detection & treatment of high hypermetropia (>3D) ref. errors can prevent accommodative strabismus, one of the precursor conditions of amblyopia.

Treatment of Ambryopra

Effective treatment is done during the sensitive period in humans. The sensitive period during which amblyopia can be reversed is upto 7-8 years in strabismic amblyopia and longer (upto 11-12 years) for anisometropic amblyopia.

Optical Correction:

Correction of significant refractive error is an essential preparation for active amblyopia treatment visual acuity may respond when the correction prescription is worn as in cases of ametropic amblyopia. Occlusion:

The grandfather of Charles Darwin was one of the first to introduce occlusion therapy. Even today a patch over the better sighted eye remains the mainstay of active treatment for Amblyopia. Naturally all media opacities are cleared if possible before the initiation of occlusion. If strabismus is present then amblyopia must first be severed with occlusion therapy prior to any surgical treatment.

Regimen of occlusion:

Occlusion regimen may be full time or part time.

Full time total occlusion:

Full time total occlusion of the sound eye is the most powerful means of treating amblyopia by enforced use of the defective eye. This treatment is usually done with commercially available adhesive patches. The patch can either left in place at night ~removed at bed time. Spectacle mounted occluderor 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. In general total full time occlusion should not be prescribed in excess of 1 week of occlusion per year of age. A 4 years old child for instance should be given 4 weeks of occlusion therapy.

Part time occlusion:

Part time occlusion is defined as occlusion for 1-6 hours per day. The relative duration of patch on and patch off interval should reflect the degree of amblyopia for moderate to sever deficits, at least b hours per day is preferred. The child undergoing part time occlusion should be kept as visually active as possible when the patch is in place, but no specific visual exercises have been proved to be of particular benefit.

Penalizatien :

Atropine treatment of the sound eye with distance correction may encourage use of the amblyopic eye for near task. Alternatively the sound eye may be corrected for near fixation ,and the amblyopic eye for distance. Best results are obtained in high hyperopes in the amblyopic eye

Oral Levodopa and Carbidopas :

The neurotransmitter dopamine is present in retinal amacrine and interplexiform cells and is probably involved in the brains processing of information. Low dose of levodopa alone and together with carbidopa have been shown to augment the effect of occlusion therapy, even in children over 12 years of age. The drugs mechanism of action is unknown.

MATERIALS AND METHODS

Type of study : Prospective (randomized controlled trial)

Place of study : National Institute of Ophthalmology and Hospital, Sher-E-Bangla Nagor, Dhaka.

Period of study : 15^th April, 2007 to 15^th October, 2007.

Study Design :

A. Sampling:

i. Sample Source : Four primary school, 2 in the rural and 2 in the urban area. Children were detected initially by screening test of visual acuity. The amblyopic children and children with reduced visual acuity were further studied and selected for management.

ii. Inclusion Criteria:

A. For incidence –

i. Primary school children, Age – 5 to 11 years

ii. Patients with anisometropic, ametropic and meridional amblyopia were included in the study.

B. For management –

i. Primary school children, Age –5 to 11 years.

ii. A difference in Best corrected visual acuity 6/12 or less.

iii. Exclusion Criteria:

a. Children below age 5 years and above as 11 years

b. Presence of anterior and posterior segment pathology as corneal opacity, cataract pathological myopia etc as well as patients with presence of strabismus were excluded. Patients with prior history of amblyopic treatment were also excluded from the study.

iv. Sample Size:

2000 children from 4 primary school were screened out, total number of 58 amblyopic children detected. Children from urban primary school and outpatient department of NIOH were included in the study.

B. Parameters to be evaluated:

· Demographic variables:

o Age

o Sex

o Socio-economic status

· Clinical variables (outcome measures):

o Detection of amblyopia to find out the incidence rate in school children age 5-11 years

o Effectiveness of treatment of amblyopia

Grouping of study population:

· The study population was divided into two groups according to age 5 to 8 years and 9 to 11 years.

Methods:

After preliminary study of the problem, a protocol was made, the proforma contained the following information: Name, age, sex, parents’ name, address, presenting complaints, full ocular & systemic examinations including refraction and follow-up.

All the children in the schools visited were included in the study. Visual acuity was measured by the linear Snellen ‘E’ chart at a 20′ foot testing distance, and cover testing conducted with the child fixating both near and distant targets. Detail history taking and ocular examination was performed in all cases. The suspected amblyopic children underwent a detailed anterior and posterior segments evaluation by slit lamp biomicroscopy & stereoscopic evaluation of the macula of both eyes. Refraction with cycloplegia by 1% cyclopentolate was done for every patient.

Best corrected visual acuity of6/12 or worse or two lines difference in visual acuity of the eyes were the diagnostic criteria apart from others. The protocol comprised two consecutive phases, first (‘pretreatment’) phase where subjects’ were enrolled, full examination and refraction done. On entering this phase, the previously prescribed spectacles were worn for the first time. Corrected acuity was recorded.

Amblyopia therapy : At this point subject progressed to the second (‘treatment’) phase of the trial in which they were prescribed 4 weeks of direct, unilateral occlusion for 4 to 10 hours per day according to severity, during the waking hours. Every patient was advised for maximum use of the amblyopic eye by watching TV/Computer games, Studying books or drawing colour pictures as appropriate for the patient.

Ensuring the compliance with occlusion or penalization:

As research has shown that understanding by the patient in key areas of the disease and treatment has a significant effect on the level of compliance. And also that the extent of parents’ knowledge is important as they are responsible for the implementation of the treatment by occlusion on their child, special care was taken in this regard.

The Patients as well as their parents or guardians were explained fully about the rationale of the treatment and the details of treatment regimen to maximize compliance. They were also warned of the consequence of not occluding the unaffected eye.

Time was taken to explain to the parents about the details of pathogenesis of amblyopia as well as the treatment rationale in simple language and they were encouraged to ask questions back and was again cross-questioned to check their understanding & apprehension of the matter.

Follow-up: While undergoing occlusion therapy, subjects returned at 4 weekly intervals for visual performance assessment and an appraisal of the occlusion acuity was measured on same illumination and in the same snellen chard. Feedback was provided to parents as to the extent of treatment compliance and, where necessary, encouragement given to comply with the treatment regimen.

Occlusion was carried out 6 month or until no further improvement was found on two consecutive visits or 6 / 6 vision was attained. Thereafter, patching was withdrawn after 14 days patient was followed up checking visual acuity.

Follow-up Schedule and Work-Up:

Schedule A Work-up

(Pre treatment phase )

1st post enrolment visit 1. Spectacle use alone starts

(2 weeks after enrolment) 2. Patient and Parents’ education Every two weeks until visual 1. Visual acuity

acuity is stable, thereafter patient

enters schedule-B.

Schedule B

(treatment phase )

Occlusion or penalization therapy starts

1. Visual acuity

2. Patient and Parents education

3. Any adverse effects of patching

Follow-up every 4 weeks As above

Occlusion or penalization ends as patients visual acuity is stable for 2 consecutive visits, But follow-up continuous for 3 more months to rule out reversion of Amblyopia.

Data Collection:

Data was collected in a pre-designed data collection sheet (Appendix-1).

DATA COLLECTION SHEET

Particulars of the patient

Patient’s Name Age Sex

Fathers Name Educational Profession

Qualifications

Mother’s Name Educational Profession

Qualifications

Mailing Address

Presenting Complains:- a)

History of Present illness:

General Examination:

Appearance:- Body Build:

Pulse:- Temp:- Anaemia:

Heart:- Liver:- Lymph nodes:

Lungs:- Spleen:- Dehydration:

Systemic Examination:

Respirator system:

Cardiovascular:

Nervous:

G.I. Tract:

Locomotors systems:-

	Right Eye	Left Eye
Visual acuity Unaided Optotype With pinhole With correction
Eye lids
Conjunctiva
Cornea Transparency Diameter
Anterior Chamber
Pupil
Iris
Lens
IOP
Posterior Segment

OBSERVATION AND RESULTS

Two thousands school children was examined out of 1034 male and 966 female. In which 58 (2.9%) children were amblyopic. Among the students 30(51.72%) male and 28(48.28%) female with an almost equal number of both the sexes. We had 40(68.97%) unilateral 18 (31.03%) bilateral cases. Total 50 patients finally enrolled for the study of amblyopia management we had 26 male and 24 female student. There were 34 (68%) unilateral and 16(32%) bilateral amblyopia cases. In the age group 5-8 years there were 20 unilateral and 10 bilateral amblyopia in the age group of 9-11 years 14 were unilateral and 6 were bilateral cases. There were 34 cases of unilateral amblyopia and 16 cases were bilateral amblyopia thus a total of 66 eyes studied. Half of the unilateral cases and all bilateral cases studied for occlusion therapy. Half of the unilateral cases studied for penalization.

Table-I

Total number of children examined between 5-11 years age group.

Total	Boys		Girls
	Total No.	Percentage	Total No.	Percentage
2000	1034	51.72%	966	48.3%

Above table shows total of 2000 students out his 1034 (51.7%) were boys and 966 (48.3%) were girls. So boys and girls almost equal number.

Table-II

Percentage of amblyopia according to sex age of 5-11 years.

Boys			Girls			Total
No of students	No of amblyopia	%	No of students	No of amblyopia	%	No of students	No of amblyopia	%
1034	30	2.9%	966	28	2.89%	2000	58	2.9%

Observation: Total 2000 school students were examined out of which 58 were amblyopic. So the incidence rates is 2.9%.

Table-III

Distribution of screened out amblyopia according to laterality

Laterality	Total number	Percentage	Total
Unilateral	40	68.97%	58
Bilateral	18	31.03%	58

Table-IV

Distribution of studied amblyopic patients according to sex and laterality (n-50).

Laterality	Boys		Girls		Total 50 pt.
	Total No.	%	Total No.	%
Unilateral	18	69.23%	16	66.67%	34(68%)
Bilateral	8	30.77%	8	33.33%	16(32%)

Observation: Unilateral cases are more in number. Boys and girls were almost equally affected.

Table-V

Laterality was amblyopic eyes showing refractive error if any (for unilateral cases only).

5 -8 years age group:

No. Amblyopic eye Refraction RE Refraction LE

1 Left + 2.50 + 4.00/+ 1.00×90 °

2 Right + 2.00 + 4.50/ + 1.00 x 100 °

3 Left Plano + 2.50 x 90 °

4 Right + 3.50 / + 1.50 x 70 ° Plano

5 Left – 2.00/ – 0.50 x 180 ° – 9.00 / – 1.00 x 180 °

6 Left Plano -3.25

7 Right -4.50 -0.50

8 Right +4.50 +0.50

9 Left Plano -5.00

10 Left -1.50 – 9.00/ – 3.00 x 110 °

11 Right – 9.00/ – 2.00 x 150 ° – 1.75

12 Left – 1.25 – 8.00 / – 1.00 x 180 °

13 Right – 0.50 / – 3.50 x 150 ° – 0.50 x 30 °

14 Left Plano +4.00

15 Right + 3.00 + 0.50

16 Left Plano + 6.00/ + 0.50 x 20 °

17 Left – 1.00/ – 0.50 x 160′ – 9.00 / 2.00 x 20 °

18 Right – 6.00 / -1.00 x,, 180⁰ -1.00

19 Left – 3.00/ – 1.00 x 20 ° – 10.00 / – 4.00 x 150 °

20 Left -2.00 – 8.00/ – 5.00 x 160 °

Table-VI

Laterality was amblyopic eyes showing refractive error if any (for unilateral cases only).

5 -9 years age group:

No. Amblyopic eye Refraction RE Refraction LE

1. Right +1.00/ – 5.00×180⁰ -1.25

2. Left -1.00 +3.00

3. Left Plano +2.50×180

4. Right +8.00/+1.00×180⁰ +1.00

5. Left + 2.50 + 4.00/+ 1.00×90 °

6. Right + 2.00 + 4.50/ + 1.00 x 100 °

7. Left Plano + 2.50 x 90 °

8. Right + 3.50 / + 1.50 x 70 ° Plano

9. Left – 2.00/ – 0.50 x 180 ° – 9.00 / – 1.00 x 180 °

10. Left Plano -3.25

11. Right -4.50 -0.50

12. Right +4.50 +0.50

13. Left Plano -5.00

14. Left -1.50 – 9.00/ – 3.00 x 110 °

Table-VII

Visual outcome in unilateral amblyopia age 5-8 years received occlusion therapy (n-10)

Type of refractive error	Refractive of the amblyopic eye	Distant visual acuity				Lines of improvement
		On 1^st visit	After spectacle correction	Before occlusion	After occlusion
Hyper metropia ± astigmatism	+4.00	3/60	6/36	6/18	6/9	2
	+1.00×90⁰
	+4.50	3/60	6/18	6/18	6/9	2
	+1.00×100⁰
	+2.50×90⁰	6/60	6/24	6/18	6/6	3
	+3.50	3/60	6/36	6/24	6/12	2
	+1.50×70⁰
Myopia ± astigmatism	-9.00	2/60	6/60	6/12	6/12	0
	-1.00×180⁰
	-5.25	3/60	6/24	6/12	6/6	2
	-4.50	3/60	6/36	6/12	6/9	1
	-9.00	2/60	6/60	6/36	6/36	0
	-3.00×110⁰
	-9.00	3/60	6/60	6/36	6/36	0
	-2.00×150⁰
	-9.00	3/60	6/36	6/18	6/9	2
	-1.00×180⁰

Observation: In the 5-8 years group with unilateral amblyopia out of 10 patients 1 had improved 3 lines, 5 had 2 lines and 1 had 1 line improvement. 4 patients did not improved.

Table-VIII

Visual outcome in unilateral amblyopia age 9-11 years received occlusion therapy (n-7)

Type of refractive error	Refractive of the amblyopic eye	Distant visual acuity				Lines of improve-ement
		On 1^st visit	After spectacle correction	Before occlusion	After occlusion
Hyper metropia ± astigmatism	+4.00	4/60	6/60	6/36	6/12	3
	+3.00	4/60	6/24	6/24	6/12	2
	+6.00	2/60	6/60	6/36	6/18	2
	+1.50×20
Myopia ± astigmatism	-9.00	3/60	6/24	6/24	6/24	0
	-2.50×20⁰
	-9.00	3/60	6/60	6/36	6/24	1
	-2.00×150⁰
	-9.00	3/60	6/36	6/18	6/9	2
	-1.00×180⁰
	-0.50	4/60	6/24	6/24	6/24	0
	-3.50×150⁰

Observation: Out of 7 patients 9-11 age group with unilateral amblyopia, 1 patient improved 3 lines, 3 patients improved 2 lines and 1 patient improve 1 line, 3 patients not improved at all.

Table-IX

Visual outcome in bilateral amblyopia age 5-8 years received occlusion therapy (n-10)

Type of refractive error	Refractive		Distant visual acuity						Lines of improve-ement
			On 1^st visit		After pretreatment with spectacle		After occlusion
	R/E	L/E	R/E	L/E	R/E	L/E	R/E	L/E	R/E	L/E
HM ± astig.	+2.00	+1.00	6/36	6/24	6/18	6/12	6/9	6/9	2	1
	+1.75×90⁰	+1.50×85⁰
	+2.50	+2.50	6/60	6/36	6/24	6/12	6/24	6/9	0	1
	+2.00×45⁰	+3.00×90⁰
Myopia ± astig.	-2.00	-2.50	6/60	5/60	6/36	6/24	6/24	6/24	1	0
	-5.00×90⁰	-3.50×45⁰
	-3.50×180⁰	-1.50×180⁰	6/60	6/24	6/9	6/9	6/6	6/6	1	1
	-9.00	-3.00	3/60	6/60	6/18	6/18	6/18	6/18	0	0
		-1.50×45⁰
	-4.00	-6.50	5/60	3/60	6/24	6/24	6/12	6/12	2	2
	-5.00×175⁰	-2.50×5⁰
	-8.00	-3.50	3/60	6/60	6/36	6/24	6/36	6/18	0	1
	-1.25×90⁰	-0.5×160⁰
	-3.00×180⁰	-2.00×180⁰	6/60	6/36	6/36	6/24	6/36	6/18	0	1
	-5.00×175⁰	-3.00×90⁰	3/60	6/60	6/60	6/60	6/24	6/36	2	1
Mixed	+3.50	+1.50	5/60	6/60	6/36	6/36	6/24	6/24	1	1
	-4.00×180⁰	-3.00×180⁰

Observation: In bilateral 10 cases and 20 eyes there were 2 lines of improvement in 4 eyes and 1 line of improvement in 10 eyes. 6 eyes showed no improvement.

Table-X

Visual outcome of bilateral amblyopia recived occlusion therapy (9-11 years)

(n-6)

Type of refractive error	Refractive		Distant visual acuity						Lines of improve-ement
			On 1^st visit		After pretreatment with spectacle		After occlusion
	R/E	L/E	R/E	L/E	R/E	L/E	R/E	L/E	R/E	L/E
HM ± astig.	+1.00	+2.00	6/36	6/24	6/18	6/12	6/9	6/9	2	1
	+1.75×90⁰	+1.50×90⁰
	+2.50	+2.50	6/60	6/36	6/24	6/12	6/24	6/9	0	1
	+2.00×145⁰	+3.00×180⁰
Myopia ± astig.	-1.00	-2.50	6/60	5/60	6/36	6/24	6/36	6/18	0	1
	-6.00×90⁰	-3.50×45⁰
	-3.50×180⁰	-1.50×180⁰	6/60	6/24	6/9	6/9	6/6	6/6	1	1
	-9.00	-3.00	3/60	6/60	6/18	6/18	6/18	6/12	0	1
		-1.50×45⁰
	-4.00	-6.50	5/60	3/60	6/24	6/24	6/12	6/24	2	0
	-5.00×175⁰	-2.50×5⁰

Observation: In 6 cases and 12 eyes there were 1 line of improvement 6 eyes, 2 line of improvement 2 eyes. 4 eyes showed no improvement.

Table-XI

Visual outcome of unilateral amblyopia studied under

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