Ophthalmic Epidemiology, 15:176182

ISSN: 0928-6586 print / 1744-5086 online

Copyright

c 2008 Informa Healthcare USA, Inc.
DOI: 10.1080/09286580801977668

Childhood Blindness in a Rural Population

of Southern India: Prevalence and Etiology
Syril K. Dorairaj,1,2 Parasappa Bandrakalli,3 Chandrashekar Shetty,3 Vathsala R,3 Dominic Misquith,4,5
and Robert Ritch2,5
1 Beth Israel Medical Center, New York, New York, USA
2 Einhorn Research Center, Department of Ophthalmology, The New York Eye and Ear Infirmary, New York, New York, USA
3 Regional Institute of Ophthalmology, Minto Ophthalmic Hospital, Bangalore, India
4 St. Johns Medical College, Bangalore, India
5 New York Medical College, Valhalla, New York, USA

ABSTRACT
Purpose: To determine the prevalence and etiology of childhood blindness in a rural popula-
tion in southern India through a population based study. Methods: A cross sectional, house-to-
house survey to screen for childhood blindness included 14,423 children <16 years. Blindness
was defined as best corrected visual acuity <3/60 in the better eye. The first stage of screen-
ing for blindness was done by interns under supervision of ophthalmology residents. Senior
residents examined the referred cases from the first stage. Those detected to be blind were
brought to a tertiary care hospital for detailed examination. Results: Fifty-four children were re-
ferred after first stage of screening of 13,241 children. Of these 14 were bilaterally blind giving
a prevalence of 1.06/1000 (95% confidence interval (CI), 0.50 to 1.61); 6 (42.9%) had lens and
related complications, 4 (28.6%) had globe anomalies (2 Microphthalmos and 2 Anophthalmos),
2 (14.3%) had retinal dystrophy and 1 (7.1%) each of glaucoma and optic atrophy. Among the
parents of blind children, 71.4% (p = 0.002) had consanguineous marriage (83.3% in cataract
blind children). Conclusions: More than half of the blindness detected was potentially avoidable.
Genetic counseling, early identification and access to tertiary care would reduce the burden of
childhood blindness in the local community.

INTRODUCTION blindness have been conducted in blind schools in the UK,4

Childhood blindness is a priority of Vision 2020The Right
to Sight a global initiative for the elimination of avoidable
blindness. There are 1.4 million blind children in the world,
2/3 of whom live in Asia and Africa. Although their number
is less than the estimated number of blind adults (45 million),
a blind child has a lifetime of blindness ahead, whereas most
adults become blind late in life.13 Recent studies on childhood
Received September 4, 2006; accepted February 3, 2008.
Keywords: Childhood, blindness, prevalence, censanguinity
Correspondence to:
Robert Ritch, M.D.
Professor and Chief, Glaucoma Services
The New York Eye and Ear Infirmary
310 East 14th Street
New York, NY 10003
USA.
email: ritchmd@earthlink.net
The study protocol adhered to the tenets of the Declaration of
Helsinki and approval was obtained from the Institutional Ethics
Committee of Bangalore Medical College, Bangalore, India.
Hong Kong,5 Ethiopia,6 Indonesia,7 Malaysia,8 China,9 and
India.1012 Other studies in Sweden,13 Finland,14,15 Turkey,16
the UK,17,18 and Saudi Arabia19 have assessed causes of visual
impairment in children using hospital and community based pe-
diatricians records, and national registers.
In many developing countries like India, strategies to fight
blindness need to be formulated based on data from community-
based studies in the absence of a registration system for the
blind.20 However, such studies have been relatively rare and
not much data is available on prevalence and causes of child-
hood blindness. Although attempts have been made to study the
pattern of blindness present in the blind schools,1012 not all
children have access to them and only those with severe visual
disability may have been included, also children with multiple
disabilities may not have been admitted.
Population based data on childhood blindness have been re-
ported from studies conducted in the southern Indian states of
Andhra Pradesh and Tamil Nadu using trained field workers.
In Andhra Pradesh study, questionnaires were used for primary
screening and only children suspected of having poor vision or
eye problems were examined21 although in a recent study, ma-
jority of eligible children received complete eye examination.22

176 MayJune 2008 Ophthalmic Epidemiology

Visual acuity was not tested in children less than 6 years in the
Tamil Nadu study.23
The present population based study on childhood blindness
was conducted in a rural population in the state of Karnataka in
southern India. Karnataka is the 8th largest state, both in terms
of area (5.8%) and population (53 million, 2001 census) with a
literacy rate of 67% and life expectancy of 66 years.
MATERIALS AND METHODS
The sampling frame for this cross sectional study consisted
of all the 127 villages of a single Hobli, (the smallest adminis-
trative unit of the Indian Government) that are associated to the
tertiary care center of the Regional Institute of Ophthalmology,
Bangalore (Kasaba Hobli, Nelamangala taluk, Bangalore Rural
District, Karnataka). The area is representative of rural south-
ern India in demographic patterns and healthcare utilization, but
may differ from other regions of India. All children from birth to
15 years, whose parents had resided in the study area for at least
6 months before the study, were included. The villages surveyed
had 8,222 households with a total population of 40,336 of which
14,423 (35.7%) were children aged <16 years. Enumeration of
the study area was done with the assistance of the local village
health guide/worker to ensure coverage of all households.
The study protocol adhered to the guidelines of the Decla-
ration of Helsinki and approval was obtained from the Insti-
tutional Ethics Committee of Bangalore Medical College. All
efforts were made to maximize response rate including prior in-
formation to the villagers and treatment for common ailments to
enhance community participation. Primary screening was con-
ducted during the school vacation period (April and May) in the
morning hours to ensure presence of both parents and children at
home. Informed consent for examination was verbally obtained
as a significant percent of the population is illiterate. All children
present at home were examined.
Children were retested and further evaluation of the anterior
segment was done in instances where visual acuity could not be
assessed during our first visit. History was taken from the parents
of absent children or from the neighbor for locked households
and three specific questions were asked: 1) Does the child have
any problem with eyes? 2) Does he/she see things as his/her peer
group? 3) Do they have any apprehension towards the vision of
any of the eyes of their child? If the answer to any of these
questions was yes, this particular household was revisited to
examine the child again.
The survey team in each village consisted of two medical
interns who were supervised by an ophthalmology resident. Ex-
tensive training was provided to the interns on the proper admin-
istration of the survey questionnaire, standardized procedures to
enter information, assessment of visual acuity and the usage of
correct test instrument. The survey method, questionnaire and
the performance of the interns were assessed in a pilot survey in
a village located outside the study area.
Definitions: Visual impairment: Best corrected visual acuity
of less than 6/18, but equal to or better than 3/60 in the better
eye, Blindness: Best corrected visual acuity <3/60 in the better
eye (World Health Organization (WHO) classification).24 Stra-
Ophthalmic Epidemiology
bismus: Any misalignment of the eyes.25 Vitamin A Deficiency:
History of night blindness, Bitots spots or corneal xerosis 26
Measurement of visual acuity:27,28 (1) in children aged 515
years: Snellens tumbling E chart at 6 meters (m); the child had
to read all the letters in order to pass a line up to 6/18. (2) in chil-
dren aged 34 years: Snellens equivalent picture chart at 6 m,
(3) in children aged <3 years: Examination with a flash light and
assessment of the ability to fix and follow the light. Cover tests
were done to rule out strabismus. A refractionist was present at
the village for performing cyclopegic refraction and retinoscopy
(objective retinoscopy in younger children).
Each primary screening team was provided with a flashlight
and a 6 meter tape. The following information was recorded
at each household: total number of persons, their religion; the
number of children, their sex and age (<3 years, 34 years and
515 years) and whether they were present or absent. History of
consanguinity and additional disabilities were enquired.
Two interns examined the anterior segment of the eye of each
child, to determine strabismus and xerophthalmia and measured
the visual acuity. The interns were guided to check each eye in-
dividually for visual assessment, followed by both eyes together.
For children aged <3 years, interns were trained to determine
the ability to fix and follow a light when shown from a dis-
tance of half a meter and recorded the following: (1) Does the
child fix on the light steadily? (2) Is the corneal reflex centered?
(3) Is the fixation maintained as the light is moved through a
short distance? If all these are normal, the vision is recorded
as CSM (central, steady and maintained). Fixation pattern was
subsequently correlated with visual acuity (see Table 1).29
The ophthalmology residents examined every positive and
every ambiguous finding of the primary screening teams. Along
with clinical assessment, serological tests [Toxoplasma gondii,
rubella, cytonegalovirus, and herpes simplex virus (TORCH)]
for microphthalmus and cataract were done. B-scan was per-
formed where needed. Visual Evoked Potential was done for a
case of developmental cataract with cerebral palsy. All children
with a visual acuity <6/18 in at least one eye were referred to
the second stage.
Temporary arrangements were made for refraction and fun-
dus examination by the senior ophthalmology resident and
refractionist. They examined the referred children and filled
the following details in the questionnaire: relevant ophthalmic
history; general and ophthalmic examination; visual acuity
Table 1. Correlation of Fixation Pattern with Visual Acuity
Visual Acuity Fixation pattern
5/60 Gross eccentric fixation or affixation
6/100 Unsteady central fixation
6/246/60 Central steady fixation, but will not hold fixation when
cover is removed
6/96/18 Central steady fixation, will hold with deviating eye but
prefers fixation with the other eye
6/6 (BE) Alternates spontaneously, holds well with both eyes,
cross fixation, homonimous fixation
BE=Better Eye
MayJune 2008 177

Open Households: 7141
(13241 children)
Children not examined: 4557
(Screened though parental history)
Children referred to Stage II: 1
Children referred to Hospital: 1
Children confirmed blind: 1
Figure 1.
assessment; category of visual impairment; presence of any ab-
normalities; anatomical and etiological cause of visual impair-
ment, and action required.30 The causes of visual impairment
were classified based on the WHO system.3,31
All children with a visual acuity <3/60 in the better eye were
referred to the Regional Institute of Ophthalmology. They were
examined by consultant ophthalmologists and relevant inves-
tigations were conducted. The WHO Prevention of Blindness
(PBL) eye examination record for children with blindness and
low vision was completed.32
Data management and statistical analysis
The data collection process was monitored by the principal
investigator and discussions with clinical and field teams were
held at regular intervals. Consistency checks were performed on
the data at the study headquarters at Regional Institute of Oph-
thalmology. Prevalence rates and 95% confidence intervals were
calculated using Poisson distribution33 assumption for preva-
lence <1% and normal approximation of the binomial distribu-
tion for prevalence 1%.
RESULTS
During the first stage of primary screening, the medical in-
terns visited 7,141 (86.8%) households having 13,241 children.
The number of children examined was 8,684 (65.6%). A his-
tory of believed sighted or believed blind was elicited from the
parents for the 4,557 (35.4%) children who were absent. Of the
178 MayJune 2008
127 Villages
8222 households
Locked Households: 1081
(1182 children);
none reported blind by neighbors
Children examined: 8684
Children referred to Stage II: 53 Children not referred: 8634
Children referred to Hospital: 13 Children not referred: 40
Children confirmed blind: 13
absent children, only one was referred with history of blindness
and none were reported to be visually impaired. Another 1081
households with 1182 children were locked, though none were
reported blind by neighbors. The data on locked households was
not included in the survey results. (see Figure 1)
Fifty-three children were referred to the second stage and ex-
amined by ophthalmology residents, 25 of them had monocular
and 28 had binocular visual impairment. One child not present
during initial screening, but referred with a history of blindness
was examined and confirmed blind. The worse eye improved
with refraction in 4 children with monocular visual impairment
(4/25). In children with binocular visual impairment, refraction
of the better eye resulted in 6 children (6/29) having no visual
impairment and vision in 2 children improved to low vision
from the category of blind. Fourteen children were referred to
the third stage, they were examined by ophthalmologists at the
Regional Institute of Ophthalmology and confirmed blind. The
prevalence rate of childhood blindness is 1.06/1000 children
including those screened by examination and those screened
by history (14/13241, 95% CI, 0.501.61). The prevalence rate
when excluding those screened by history is 1.50/1000 (13/8684,
95% CI, 0.682.31)
The age range of blind children was 315 years with a me-
dian age of 10. A high proportion of the blind children were
female (13/14, 92.9%). Five children had a history of visual im-
pairment from birth and nine since the age of one year. The ex-
amination/response rate was higher in younger children (80.5%,
<3 yrs and 72.7%, 34 yrs) as they were more likely to be at
home compared to older children (60.7%, 515 yrs). Similarly,
Ophthalmic Epidemiology
 Table 2. Children referred from the various age groups:

Age (y)
Children <3 34 515
Method of Fix and Snellens Equivalent Snellens
Examination Follow picture chart Tumbling E chart Total
Examined
Female 875 687 2942 4504(67.8)
Male 847 653 2680 4180(63.3)
Total 1722(80.5) 1340(72.7) 5622(60.7) 8684(65.6)
Not Examined (Screened used parental history)
Female 215 236 1682 2133
Male 202 268 1954 2424
Total 417(19.5) 504(27.3) 3636(39.3) 4557
Total
Female 1090 923 4624 6637
Male 1049 921 4634 6604
Total 2139(100) 1844(100) 9258(100) 13241(100)
1st Stage Referral (method)
Female 1(0.09) 3(0.30) 26(0.56) 30(0.45)
Male 1(0.09) 3(0.30) 20(0.43) 24(0.36)
2nd Stage Referral (method)
Female 0 2(0.21) 11(0.23) 13(0.19)
Male 0 0 1(0.02) 1(0.01)

Data presented as number of persons. Percent data in brackets refers to children within a particular age-group
that were examined and not examined (sums to 100% for each age-group).

68.7% of the female children were available while only 63.3% child, operated in one eye, had Pseudophakia with PCO and
of the male children could be examined. (see Table 2) an unoperated cataract in the other eye; anterior segment was
Lens and related complications accounted for 42.9% (6/14) of unaffected with clear non-enlarged cornea.
the childhood blindness. Four children had un-operated cataracts Congenital anomalies such as Anophthalmos (14.3%, 2/14)
and two had undergone surgery with unsuccessful visual recov- and Microphthalmos (14.3%, 2/14) were responsible for 28.6%
ery <3/60. One child had two eyes operated, one was phthisical of blindness. Optic atrophy was responsible for 7.1% (1/14)
and the other had Posterior Capsular Opacity (PCO). Another and disorganized globe with a previous history of congenital
glaucoma confirmed by records accounted for 7.1% (1/14) of
the total blindness. (see Table 3). Among the parents of blind
Table 3. Prevalence and Etiology of Childhood Blindness. children, 71.4% had consanguinity (10/14, p = 0.002) (see
Table 4).
No. of Prevalence Based on examination, 25 children had monocular visual im-
Site of Abnormality Blind (%) (95% Cl) pairment giving a prevalence of 2.88/ 1000 children (25/8684,
Total Lens 6(42.9) 0.45 (0.090.82) 95% CI 1.75 to 4.01). Corneal scarring was the commonest cause
Cataract (unoperated) 4(28.7) of blindness in children >5 years (16%, 4/25) and globe abnor-
Aphakia (after cataract) & Phthisis 1(7.1)
malities in children <5 years (12%, 3/25). Among additional
following surgery
Pseudophakia & Posterior capsular 1(7.1) disabilities, mental retardation was seen in 28 children.
opacification
Total Whole Eye 5(35.7) 0.38(0.120.88)
Microphthalmos 2(14.3)
Table 4. Consanguinity among parents of children surveyed.
Anophthalmos 2(14.3)
Disorganized globe (Glaucoma) 1(7.1)
No. of Blind No. of Non-Blind Total
Total Retina 2(14.3) 0.15(0.020.55)
Hereditary Cone Dystrophy Consanguinity 10 4000 4010
Total Optic Nerve 1(7.1) 0.08(00.42) Uncle/niece 4 1855 1859
Optic Atrophy First cousin 4 1499 1503
Total 14 (100) 1.06(0.51.61) Second cousin 2 646 648
No consanguinity 4 9227 9231
Data presented as number of persons (%). Total 14 13227 13241
Values are expressed as prevalence per 1000. Values in parentheses
are 95% CI. Data presented as number of persons.

Ophthalmic Epidemiology MayJune 2008 179

 DISCUSSION
In the absence of a registration system for the blind in India,
the present study of a well-defined community, conducted using
trained medical interns and ophthalmology residents for initial
screening, provides valuable insight into the causes and magni-
tude of childhood blindness. The prevalence rate of 1.06/1000
when including children screened by examination as well as
parental history is similar to the recent study by Rakhi Dandona22
(1.0/1000). The earlier study by Lalit Dandona estimated lower
prevalence (0.65/1000).21
The high proportion of female blind children (92.8%) was
also seen in the study by Rakhi Dandona (85.7%).22 Blindness
was higher in females of all ages considered together in an-
other southern Indian state.34 The root cause may be discrim-
ination towards the girl child resulting in less medical care. It
has been noted that in developing countries, a large proportion
of children die within a few years of becoming blind either from
systemic complications of the condition causing blindness or be-
cause poor parents have more difficulty caring for them than for
their sighted siblings. Female children may receive even lesser
medical attention.
Lens and related complications and globe anomalies were
the leading cause of blindness in prior studies (see Table 5).21,22
While cone dystrophy in two siblings was the cause for reti-
nal involvement in our study, retinopathy of prematurity (ROP),
retinoblastoma, vascular abnormalities and chorioretinal scars
were the causes reported in the study by Lalit Dandona21 and
retinal degeneration due to congenital cataract in the study by
Rakhi Dandona.22 We did not find any corneal related blindness,
however it was seen in 25.0% in the study by Rakhi Dandona.22
Certain studies especially in developed world have reported ROP
as an important cause of childhood visual impairment,35,36 how-
ever it was not seen in this study. With little or no access to
neo-natal facilities in rural areas, incidence of ROP is low since
children at high risk of premature lung development are more
likely to die (see Table 5).
Incidence of blindness among children born to parents
with consanguineous marriages was 0.25% (10/4010) as com-
pared to 0.04% (4/9231) in children born to parents with non-
consanguineous marriages. (Relative Risk: 5.75 (0.25%/0.04%),
95% CI: 1.818.3). Hereditary diseases such as autosomal
recessive retinal dystrophy (14.3%) and autosomal dominant
Table 5. Causes of Childhood Blindness: Comparison with other
Population-based studies in India
Site of Present Dandona L Dandona R
Abnormality Study et al Study et al Study
Lens 6(42.9%) 11(15.3%) 2(25.0%)
Whole eye 5(35.7%) 21(29.0%) 2(25.0%)
Retina 2(14.3%) 16(22.2%) 2(25.0%)
Optic Nerve 1(7.1%) 12(16.7%) None
Cornea None None 2(25.0%)
Data presented as number of persons (%).
180 MayJune 2008 Ophthalmic Epidemiology
hereditary cataract (14.3%), both preventable by genetic coun-
seling, caused 28.6% of the blindness. Significant among the
treatable causes were cataract (42.8%) and congenital glaucoma
(7.1%).
Etiologies of childhood cataract can be either genetic or infec-
tions like toxoplasmosis, rubella, cytomegalovirus, and herpes.37
Among children with cataract, 83.3% (5/6) had parents with con-
sanguineous marriages (2: 1st degree and 3: 2nd degree) sug-
gesting the importance of hereditary factors. The World Bank-
assisted Cataract Control Program38 has primarily focused on
age related cataract; however the study findings also underscore
the importance of allocating resources for congenital cataract,
since its management is more complex.
Earlier studies have reported that congenital anomalies were
responsible for 20% of the blindness in south India, 8.8% in Chile
and 8.5% in West Africa.39 We found 28.7% of blindness due to
congenital anomalies (16.7%, Rakhi Dandona).22 The etiology
of anophthalmos and microphthalmos could not be determined
definitely although the causes could be factors operating in the
prenatal period,40 consanguinity was seen in 25% of the parents
(1/4, 2nd degree). Retinal dystrophy, a hereditary cone dystrophy
is known to have autosomal dominant inheritance with variable
penetrance, however the pedigree analysis of affected children
suggested an autosomal recessive inheritance, both children had
consanguineous parents (1st degree). High proportion of retinal
dystrophies in consanguineous marriages were seen in a Uzbek-
istan study.41 Other Indian studies have also shown that blind-
ness due to early onset retinal dystrophies,12,42 primary congen-
ital glaucoma,43 and anophthalmos and microphthalmos12,44 are
more prevalent in consanguineous progeny.
Blindness due to Vitamin A deficiency was not seen in this
study, though it was a probable cause in earlier studies (12.5%,
Rakhi Dandona),22 possibly due to government efforts such as
Vitamin A prophylaxis and mid-day meal programs being im-
plemented since the last decade. Primary screening data showed
a lower prevalence of signs of Vitamin A deficiency (1% Bitot
spots, night blindness and corneal xerosis).
The total examination rate was 65.6% despite efforts to im-
prove response and may be partially due to public apathy toward
health events. More measures such as free follow-up care need
to be designed to generate interest and improve participation.
Screening through parental history is likely to underestimate the
actual number of those visually impaired. Repeat screening of a
sample of absent children who were believed to be sighted as per
parental history could provide an estimate of the underestima-
tion. Though 19.8% of the children screened through examina-
tion were < 3 years of age, this age group only accounted for 4%
of children referred to the next stage. This may be due in some
part to the difficulty in measuring visual acuity in field settings.
The assessment using fix and follow method has some concerns
of intra-observer reliability, however it is important to recog-
nize that even in clinical settings, the results of tests designed
for younger children and infants are typically less accurate than
results based on tests designed for adults.
Also, results of visual acuity testing have been shown to be
related to a young childs daily activities and the way the child
interacts with the environment.45 The most successful way to 9.
assess their visual acuity has been using acuity card procedure
through observation of the visual systems electrophysiologi-
cal responses or eye movement responses to repetitive grating 10.
(striped) or checkerboard patterns. However, this strategy of as-
sessing an infants resolution acuity rather than his or her recog-
nition acuity may underestimate the depth of some visual acuity 11.
deficits (e.g., amblyopia). Also the results depend on the in-
tegrity of the tester in remaining masked to the location of the 12.
gratings on the cards during their presentation (the purpose of
remaining masked is to ensure that an unbiased assessment of
visual acuity status is obtained). The cards must be kept free of 13.
dirt and smudges that could attract the infants attention away
from the grating target. In children >3 years, the testing distance 14.
was 6 meters which increases the rate of successful testing. The
rate of visual loss may be higher vs. studies where the testing
distance had been 3 meters and a symbols chart designed for 15.
use at that distance had been used, however it is unlikely to have
changed the estimate of blindness. 16.
Since the majority of blindness in this study was from pre-
ventable and treatable causes, appropriate prevention measures, 17.
early identification and surgical intervention are crucial. By de-
tailing the etiology of blindness, a regional prevalence study 18.
helps in formulating appropriately targeted measures. Such stud-
ies should be the first priority in the context of Vision 2020.3
19.
ACKNOWLEDGMENTS 20.
The authors thank the Ophthalmology residents, interns, and
staff of Minto Ophthalmic Hospital in helping to conduct the
study; Jamima Devasena for assistance with the statistical anal- 21.
ysis; and all the local residents of Nelamangala, Kasaba Hobli,
for the active participation and contribution to the study.
22.
23.
REFERENCES
1. WHO. Preventing blindness in children, Report of WHO/IAPB sci-
entific meeting, WHO/PBL/0.77. Geneva: World Health Organiza- 24.
tion, 2000.
2. Dandona L, Gilbert CE, Rahi JS, et al. Planning to reduce child- 25.
hood blindness in India. Indian J Ophthalmol. 1998; 46:11722.
3. Steinkuller PG, Du L, Gilbert C, et al. Childhood blindness. J AA-
POS. 1999; 3:2632. 26.
4. Alagaratnam J, Sharma TK, Lim CS, et al. A survey of visual im-
pairment in children attending the Royal Blind School, Edinburgh
using the WHO childhood visual impairment database. Eye. 2002; 27.
16:557561.
5. Fan DS, Lai TY, Cheung EY, et al. Causes of childhood blindness
in a school for the visually impaired in Hong Kong. Hong Kong Med 28.
J. 2005; 11:859.
6. Kello AB, Gilbert C. Causes of severe visual impairment and blind-
ness in children in schools for the blind in Ethiopia. Br J Ophthalmol. 29.
2003; 87:52630.
7. Sitorus R, Preising M, Lorenz B. Causes of blindness at the Wiyata
Guna School for the Blind, Indonesia. Br J Ophthalmol. 2003; 30.
87:10651068.
8. Reddy SC, Tan BC. Causes of childhood blindness in Malaysia: re-
sults from a national study of blind school students. Int Ophthalmol. 31.
2001; 24:5359.
Ophthalmic Epidemiology
Hornby SJ, Xiao Y, Gilbert CE, et al. Causes of childhood blind-
ness in the Peoples Republic of China: Results from 1131 blind
school students in 18 provinces. Br J Ophthalmol. 1999; 83:929
932.
Hornby SJ, Adolph S, Gothwal VK, et al. Evaluation of children in
six blind schools of Andhra Pradesh. Indian J Ophthalmol. 2000;
48:195200.
Titiyal JS, Pal N, Murthy GV, et al. Causes and temporal trends of
blindness and severe visual impairment in children in schools for
the blind in North India. Br J Ophthalmol. 2003; 87:9415.
Rahi JS, Sripathi S, Gilbert CE, et al. Childhood blindness in India:
Causes in 1318 blind school students in nine states. Eye. 1995;
9:54550.
Blohme J, Tornqvist K. Visually impaired Swedish children. The
1980 cohort studyAspects on mortality. Acta Ophthalmol Scand.
2000; 78:560565.
Rudanko SL, Fellman V, Laatikainen L. Visual impairment in chil-
dren born prematurely from 1972 through 1989. Ophthalmology.
2003; 110:16391645.
Rudanko SL, Laatikainen L. Visual impairment in children born at
full term from 1972 through 1989 in Finland. Ophthalmology. 2004;
111:23072312.
Cetin E, Yaman A, Berk AT. Etiology of childhood blindness in Izmir,
Turkey. Eur J Ophthalmol. 2004; 14:5317.
Flanagan NM, Jackson AJ, Hill AE. Visual impairment in childhood:
Insights from a community-based survey. Child Care Health Dev.
2003; 29:493499.
Rahi JS, Cable N; British Childhood Visual Impairment Study
Group. Severe visual impairment and blindness in children in the
UK. Lancet. 2003; 362:13591365.
Tabbara FK, El-Sheikh HF, Shawaf SS: Pattern of childhood blind-
ness at a referral center in Saudi Arabia. Ann Saudi Med. 2005;
25:1821.
Hereditary disease as a cause of childhood blindness: Regional
variation. Results of blind school studies undertaken in countries
of Latin America, Asia and Africa. Ophthalmic Genet. 1995; 16:
110.
Dandona L, Williams JD, Williams BC, et al. Population-based as-
sessment of childhood blindness in southern India. Arch Ophthal-
mol. 1998; 116:5456.
Dandona R, Dandona L. Childhood blindness in India: a population
based perspective. Br J Ophthalmol. 2003; 87:263265.
Thulasiraj RD, Nirmalan PK, Ramakrishnan R, et al. Blindness and
vision impairment in a rural south Indian population: The Aravind
Comprehensive Eye Survey. Ophthalmol. 2003; 110(8):14918.
WHO. International statistical classification of dseases and related
health problems: Tenth revision. Geneva: WHO; 1992:456457.
Wright W. Kenneth, Peter H. Spiegel. Pediatric ophthalmology
and strabismus, 2nd edition. Los Angeles: Springer; 2002:210
1112.
Rahi JS, Sripathi S, Gilbert CE, et al. Childhood blindness due to
vitamin A deficiency in India: Regional variations. Arch Dis Child.
1995; 72:3303.
Gilbert CE, Foster A. Epidemiology of childhood blindness, (Taylor
D. ed.) In: Paedriatric ophthalmology 2nd edition. Oxford: Blackwell
Science, 1997:112.
Kalikivayi V, Naduvilath TJ, Bansal AK, et al. Visual impairment
in school children in southern India. Indian J Ophthalmol. 1997;
45:12934.
Peyman GA, Sanders DR, Goldberg HF. Principles and practices
of ophthalmology. 1987, 1st edition. New Delhi: Jaypee Brothers;
17801810, 1987.
Abrahmsons JH. An introduction to epidemiological studies:
Survey methods in community medicine., 15th ed. Edinburgh:
Churchill Livingston; 1218, 1979.
WHO. WHO coding instructions for WHO/ PBL eye examination
record for children with blindness and low vision. Geneva: WHO.
MayJune 2008 181
32. Rosner J., Rosner J.. Measurement of visual acuity in children,
Paediatric optometry, 2nd ed., 1990, Stoneham, UK: Butterworth;
4577.
33. Rosner B. Fundamentals of biostatistics, 5th ed. Pacific Grove, CA:
Thomson Learning; 2000; 106,19497.
34. Dandona L, Dandona R, Srinivas M, et al. Blindness in the Indian
state of Andhra Pradesh. Invest Ophthalmol Vis Sci. 2001; 42:908
16.
35. Gilbert CE, Rahi J, Eckstein M, et al. Retinopathy of prematurity in
middle-income countries. Lancet 1997; 350:1214[Medline].
36. Hoyt CS, Good WV. The many challenges of childhood blindness
(editorial). Arch Dis Child. 2001; 85:4523.
37. Thylefors B, Negrel AD, Pararajasegaram R, et al. Global data on
blindness. Bull World Health Organ. 1995; 73:11521.
38. Jose R, Bachani D. World Bank-assisted cataract blindness control
project. Indian J Ophthalmol. 1995:43:3543.
39. Gilbert CE, Canovas R, Hagan M, et al. Causes of childhood blind-
ness: Results from West Africa, south India and Chile. Eye. 1993;
7(Pt 1):1848.
182 MayJune 2008 Ophthalmic Epidemiology
40. Rahi JS, Sripathi S, Gilbert CE, et al. The importance of prena-
tal factors in childhood blindness in India. Dev Med Child Neurol.
1997; 39:44955.
41. Rogers NK, Gilbert CE, Foster A, et al. Childhood blindness in
Uzbekistan. Eye. 1999; 13(Pt 1):6570.
42. Kumaramanickavel G, Joseph B, Vidhya A, et al. Consanguinity
and ocular genetic disease in South India: Analysis of a five-year
study. Commun Genet. 2002; 5:1825.
43. Panicker SG, Reddy ABM, Mandal AK et al. Identification of
novel mutations causing familial primary congenital glaucoma
in Indian pedigrees. Invest Ophthal Vis Sci. 2002; 43:1358
66.
44. Hornby SJ, Dandona L, Foster A, et al. Clinical findings, consan-
guinity and pedigrees in children with anonphtalmos in southern
India. Dev Med Child Neurol. 2001; 43:3928.
45. Katsumi, O, Chedid, SG, Kronheim, JK, et al. Correlating prefer-
ential looking visual acuity and visual behavior in severely visually
handicapped children. Acta Ophthalmol Scand. 1995; 73(5), 407
413.