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INCIDENCE OF PERIPHERAL RETINAL LESIONS IN PATIENTS

ATTENDING OUTPATIENTS DEPARTMENT OF
Dr. B. R. AMBEDKAR MEDICAL COLLEGE HOSPITAL AND
K. C. GENERAL HOSPITAL, BANGALORE.
By
Dr. SUMEET PAL SINGH AHLUWALIA

Dissertation Submitted to the Rajiv Gandhi University of Health Sciences, Karnataka,

Bangalore, in partial fulfillment of the requirements for the degree of

M. S. (OPHTHALMOLOGY)
Under the guidance of
Dr. M. NARAYAN MS

DEPARTMENT OF OPHTHALMOLOGY
Dr. B. R. AMBEDKAR MEDICAL COLLEGE
BANGALORE.
2006

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES

DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation entitled “INCIDENCE OF PERIPHERAL
RETINAL LESIONS IN PATIENTS ATTENDING OUTPATIENTS
DEPARTMENT OF Dr. B. R. AMBEDKAR MEDICAL COLLEGE HOSPITAL
AND K. C. GENERAL HOSPITAL, BANGALORE” is a bonafide and genuine
research work carried out by me under the guidance of Dr. M. NARAYAN MS, Professor
and Head, Department of Ophthalmology, Dr. B. R. Ambedkar Medical College,
Bangalore.

Date:
Signature
of
the
Candidate
Place:

Name: Dr. SUMEET PAL SINGH AHLUWALIA

ii

CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled “INCIDENCE OF PERIPHERAL
RETINAL LESIONS IN PATIENTS ATTENDING OUTPATIENTS
DEPARTMENT OF Dr. B. R. AMBEDKAR MEDICAL COLLEGE HOSPITAL
AND K. C. GENERAL HOSPITAL, BANGALORE” is a bonafide work done by
Dr. SUMEET PAL SINGH AHLUWALIA in partial fulfillment of the requirement for
the degree of M. S. in Ophthalmology.

Signature of the Guide

Date:

Name: Dr. M. NARAYAN MS

Place:
Professor
and
Head,
Department
of
Ophthalmology
Dr. B. R. Ambedkar Medical College
Bangalore.

iii

ENDORSEMENT BY THE HOD/DEAN/

HEAD OF THE INSTITUTION

This is to certify that the dissertation entitled “INCIDENCE OF PERIPHERAL

RETINAL LESIONS IN PATIENTS ATTENDING OUTPATIENTS
DEPARTMENT OF Dr. B. R. AMBEDKAR MEDICAL COLLEGE HOSPITAL
AND K. C. GENERAL HOSPITAL, BANGALORE” is a bonafide research work
done by Dr. SUMEET PAL SINGH AHLUWALIA, under guidance of
Dr. M. NARAYAN MS Professor and Head, Department of Ophthalmology,
Dr. B. R. Ambedkar Medical College.

Seal and Signature of the HOD

Seal and Signature of the Principal

Dr. M. NARAYAN MS

Dr. N. GANDHI MD
Professor
&
Head,
Principal,

Department of Ophthalmology

Dr. B. R. Ambedkar Medical College,

Dr. B. R. Ambedkar Medical College

Bangalore.
Bangalore.
Date:

Date:
Place:
Bangalore

Place:
Bangalore

iv

COPYRIGHT
DECLARATION BY THE CANDIDATE

I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka
shall have the rights to preserve, use and disseminate this dissertation / thesis in print or
electronic format for academic / research purpose.

Date:
Signature
of
the
Candidate

Place:

Name: Dr. SUMEET PAL SINGH AHLUWALIA

© Rajiv Gandhi University of Health Sciences, Karnataka

ACKNOWLEDGEMENT
It is with great pleasure and pride that I attribute the success of my dissertation to
the guidance and support of many people to whom I am very grateful.

I am very much indebted and wish to express my earnest thanks to

Dr. M. Narayan MS, Professor and Head, Department of Ophthalmology,
Dr. B. R. Ambedkar Medical College, Bangalore for his valuable guidance, suggestions
and constant encouragement that motivated me throughout the course of this study.

I take this opportunity to express my sincere sense of gratitude to

Dr. Anant V. Joshi MS, Professor, Department of Ophthalmology and Medical
Superintendent, Dr. B. R. Ambedkar Medical College, Bangalore for his valuable
suggestion and encouragement throughout the course of this study.

I am extremely grateful and thankful

to
Associate
Professor
Dr. Kaushal Kumar MS, Assistant Professors Dr. K. S. Nagaraja MS,
Dr. Rani Sujatha MS and Lecturer Dr. M. B. Shanmukan DOMS, for their interest and
encouragement during my study.

I extend my heartfelt thanks to all other non-teaching Staff and my fellow

Postgraduates and Department of Ophthalmology, for their helping hand in completing this
study.

vi

I express my thanks and gratitude to Mrs. Jayashree Rao, Librarian and her
colleagues, Dr. B. R. Ambedkar Medical College, Bangalore, Mr. K. P. Suresh, Statistician
and Mr. A. S. Madhukeshwara for their time and patience in helping me to complete this
dissertation.

I thank all my patients for their cooperation without whom this study would not
have been possible.

I thank my family, without whose support this study would not have been possible.

And last but not the least, I would like to thank God Almighty for everything.

Date:
Signature
of
the
Candidate
Place:

Name: Dr. SUMEET PAL SINGH AHLUWALIA

vii

LIST OF ABBREVIATIONS USED

DD
→
Disc Diameter
ELM
→
External Limiting Membrane
ERG
→
Electroretinogram
ILM
→
Internal Limiting Membrane
mm
→ Millimeters
NFL
→ Nerve
Fiber
Layer
RPE
→
Retinal Pigmented Epithelium
SER
→
Smooth Endoplasmic Reticulum
WWP
→ White
With
Pressure

viii

ABSTRACT
BACKGROUND
The fundi of healthy subjects without eye complaints or history of eye disease
differ widely in morphology. The anatomical variations of normal peripheral fundus do not
impair visual functions by themselves. These are either non-progressive or very slowly
progressive with age. Alone, they do not cause pathological changes but some of them
constitute weak points & may give rise to retinal breaks later in life, when they combine
with other progressive senile changes or alterations that endanger the integrity of ocular
functions.

Degenerative conditions of retina comprise an important group of fundus diseases.

In contrast to dystrophies, which are usually bilateral & symmetrical, & have a hereditary
pattern, the degenerations are not necessarily bilateral or symmetrical & usually do not
have a hereditary tendency.
Ideally, fundus examination of all the patients should include detailed examination
of fundus periphery to exclude peripheral retinal degenerations.

ix

OBJECTIVES
•
Objective of the present study is to determine the incidence of peripheral retinal
lesions in the patients presenting in the outpatient department.

METHODS
Two hundred and thirty one patients attending the out patient department were
taken randomly for this study. The patients were of no specific age group. Patients with
hazy media impairing visualization of the fundus for example corneal opacity, healed or
active anterior uveitis, cataract, vitreous opacities etc. were excluded from the study.
Patients in whom dilatation of the pupil is contraindicated for example angle closure
glaucoma and small children were also excluded from the study.

RESULTS
The results of the study showed that cystoid degeneration is the most common
peripheral retinal degeneration present in all the eyes irrespective of age, sex and race.

White with pressure is the next most common lesion present in 29% of the eyes and
is bilateral in 38.8% of the cases.

INTERPRETATION AND CONCLUSION

All the peripheral retinal degenerations are more common in myopic patients
except retinoschisis, which is more common in hypermetropic patients.

All the patients have one or the other peripheral retinal degeneration. Therefore,
fundus examination of all the patients should include detailed examination of fundus
periphery to exclude peripheral retinal degenerations and fundus drawings of all the
patients should be maintained.

KEYWORDS
Peripheral retinal degeneration; Fundus; Ophthalmoscopy; Ora Serrata; Vitreous; Pars
plana; Fovea; Macula; Equator.

xi

TABLE OF CONTENTS
Page
No.
1. INTRODUCTION
1
2. OBJECTIVES

3
3. REVIEW
OF
LITERATURE
4
4. METHODOLOGY
75
5. RESULTS

87
6. DISCUSSION
97
7. CONCLUSION
99
8. SUMMARY
100
9. BIBLIOGRAPHY
102
10. ANNEXURES

• PROFORMA
109

• MASTER
CHART
112

•
KEY TO MASTER CHART
116

xii

LIST OF TABLES

Page Nos.
1.
Differentiating Retinal Detachment and Retinoschisis
42
2.
Inner layer breaks and detachments
46
3.
Outer layer breaks and detachments
47
4.
Developmental Variations of Peripheral Retina
72
5. Prevalence of Cystic retinal Tuft and Miscellaneous Peripheral Retinal
73
Findings
6.
Degenerations of Peripheral Retina
74
7.
Color Coding for Retinal Drawing
83
8.
Symbols used in retinal drawing
84
9. Sex
Distribution
86
10. Type of refractive error
87
11. Age distribution with sex
88
12. Age distribution according to type of refractive error
89
13. Incidence of Peripheral Retinal lesions
90
14. Incidence of peripheral retinal lesions according to type of refractive
91
error present
15. Percentage of bilateral lesions
92
16. Sex distribution of peripheral retinal lesions
93
17. Age distribution of peripheral retinal lesions
94

xiii

LIST OF FIGURES

Page
Nos.
1.
The two retinal walls
5
2.
Ophthalmoscopic view of retina
9
3.
Layers of Retina
13
4.
Outer plexiform layer
15
5.
Landmarks of retina
19
6. Meridonial
Fold
27
7.
Cystic retinal tuft
28
8.
Pearl of ora serrata
33
9.
Pars plana cyst
35
10. Cystoid
Degeneration
37
11. Paving stone degeneration near ora serrata
40
12. Degenerative
Retinoschisis
44
13. Multiple outer layer breaks in a case of degenerative retinoschisis
46
14. Congenital
Retinoschisis
49
15. White with pressure phenomenon
54
16. Lattice
lesion
containing
white crisscrossing wicker lines
57
17. Lattice
lesion
with
a
snail-track appearance
62
18. Lattice degeneration with atrophic holes
63
19. Horseshoe
retinal
tear
65
20. Indirect
ophthalmoscope
76
21. Indirect
Ophthalmoscopy
77
22. + 90D Lens
79
23. Indirect Slit-Lamp Biomicroscopy
80
24. Goldmann Triple Mirror Lens
80
25. Fundus
Drawing
86

xiv

INTRODUCTION
The fundi of healthy subjects without eye complaints or history of eye disease
differ widely in morphology. The anatomical variations of normal peripheral fundus do
not impair visual functions by themselves. These are either non-progressive or very
slowly progressive with age. Alone, they do not cause pathological changes but some of
them constitute weak points and may give rise to retinal breaks later in life, when they
combine with other progressive senile changes or alterations that endanger the integrity
of ocular functions.1

Various anatomical variations are present in peripheral fundus namely-variation

in oral bays and dentate process, granular tissue (cystic retinal tuft), pars plana cyst, ora
serrata pearls.2 Cystic retinal tuft is associated with 10% of retinal detachments
in general.3

Degenerative conditions of retina comprise an important group of fundus

diseases. In contrast to dystrophies, which are usually bilateral and symmetrical, and have
a hereditary pattern, the degenerations are not necessarily bilateral or symmetrical and
usually do not have a hereditary tendency.2 Findings that may exist in the normal eyes of
younger patients but that tend to progress markedly with age are:

•
Cystoid changes including cystoid degeneration, acquired retinoschisis and cyst of
pars plana ciliaris.
•
Chorioretinal degenerations.
•
Chorioretinal atrophy.1
1

Degenerative Retinoschisis is present in about 5% of the population over the age

of 20 years and is particularly present in hypermetropes and is nearly always
asymptomatic.4 A close relation between pars plana cyst, cystoid degeneration and
Peripheral retinoschisis has been noted.5

Vitreoretinal degenerations in peripheral fundus involves Lattice like

degeneration, Snail track degeneration and retinal erosions.1 Snail track degeneration is
suggested to be either a variant of or an early stage of lattice degeneration.6 In contrast to
other degenerations, lattice degeneration has a greater clinical significance. It is
especially important because of its relationship to rhegmatogenous retinal
detachment.2 Lattice degeneration occurs equally between both the sexes within an age
range of 3-80, the average being from 40-50.7

Paving stone degeneration is chronic slowly progressive disorder, which usually

does not produce any symptoms or complications. It is more commonly seen in later
years and is bilateral in one-third of the cases.2

A high prevalence of peripheral retinal degenerations was found in adult Chinese

high myopes. The presence of retinal holes was positively correlated with very high
myopia of an axial length of ≥ 30 mm.8

The present study has been aimed at finding the incidence of peripheral retinal
lesions in patients attending out patient department of Dr. B R Ambedkar Medical
College and K. C. General Hospital, Bangalore and study the distribution of various
peripheral retinal lesions in various age groups.

OBJECTIVES
•
Objective of the present study is to determine the incidence of peripheral retinal
lesions in the patients presenting in the outpatient department.
3

REVIEW OF LITERATURE
EMBRYOLOGY
The embryonal and foetal development of the human eye includes a series of
sequential events starting with the fertilization of the ovum and culminating in the birth
of a normal baby. Three main periods can be distinguished in the prenatal development of
the eye.

The first period called embryogenesis is characterized by the establishment of the

primary organ rudiments and ends at the end of the 3rd week with the appearance of the
optic sulci on both sides of the midline at the expanded cranial end of the still open neural
folds.

The second period called organogenesis includes the development of the primary
organ rudiments and extends till the end of the 8th week.

The third period involves the differentiation of each of the primitive organs into a fully or
partially active organ and is called differentiation.9

The developing eye appears in a 22 day embryo as a pair of shallow grooves on

each side of the forebrain with closure of the neural tube, these grooves form out
pocketing of the forebrain, the optic vesicle.10

The heterogeneous tissues that constitute the human eye are derived
embryonically from surface ectoderm, neural crest and mesodermal mesenchyme.11

Fig. 1: The two retinal walls. The inner retinal wall shows two zones—an inner, non-
nucleated layer and a deeper, nucleated layer.

Retina
The retina develops from the walls of the optic cup, an outgrowth of the forebrain.
The outer, thinner layer of optic cup becomes RPE, and the inner thicker layer
differentiates into multilayered neural retina.12

In the later developmental stages (6th to 9th week), apoptotic and mitotic cells
were observed in the neural retina.13

Neural retina
Differentiation of neuroectodermal layer of the retina commences early. At
26 days of gestation (embryo 4 mm) the inner layer of optic vesicle undergoes mitosis to
produce three or four compact rows of cells.
5

By 32-33 days of gestation (embryo 7 mm) the primordial retina consists of 5 or

6 rows of neuroepithelial cells. Thus, the inner 1/3 rd that faces the lens placode is devoid
of nucleus and has been termed the inner marginal layer.

Retinal maturation commences at the posterior pole and proceeds towards the
periphery. By 4-5 wks of gestation (embryo 12 mm), the neuroepithelium has become
organized into two distinct regions of neuroblastic cells: inner, towards the vitreous and
outer, adjacent to Retinal Pigment Epithelium.

Peripheral retina
The demarcation between the neural epithelium of the ciliary region and the retina
at the future ora serrata becomes apparent at about 4th month of gestation.

By 6th month the peripheral retina has only thin nerve fiber layer and the ora
serrata is established definitively.

Between the 8th and 9th months the development of this region is complete in the
temporal region and the indentation or serrated edge of the peripheral retina in other
regions of the globe continues to develop after birth. The zone between ora and the
equator enlarges in size until about 2 years of age.11

When proliferative activities were compared, the peripheral retina appeared to be

less mature than the central before the 9th week.14

Retinal Pigmented Epithelium

Upto 6th week of gestation (embryo 20 mm) the outer wall of the optic cup is
composed of mitotically active, pseudostratified columnar epithelial cells, the inner
surface of which are ciliated. The oval nuclei are located in mid region of the cells.
Melanogenesis begins at this time. The cilia disappear. Adjacent cells are already joined
by zonula occludens and zonular adherence complexes at their apical borders.

By 8 weeks (embryo 27-31 mm) the RPE has become organized as a single layer
of hexagonal shaped columnar cells posteriorly but remains pseudostratified at the
periphery.

During the 3rd and 4th month of gestation (embryo 77-83 mm) the cells become
tall cuboidal in shape and their nuclei spherical. There is an increase in cytoplasmic
organelles with more SER and a well developed golgi apparatus present. Most pigment
granules are mature or immature, but premelanosomes remain. The terminal web is well
established at the lateral apical borders and the inner border shows the beginnings of
apical process, which develop before the outer segments of the photoreceptors are
formed.

By the middle of the 4th month only a few premelanosomes persist and the apical
cell processes have become slender microvilli. At this stage the RPE is believed to be
fully functional.11

ANATOMY OF RETINA
Retina has two main components:
•
Sensory layer
•
Pigmented layer

The two layers are attached loosely to each other by the extracellular matrix that
fills the space between the apical villi of the pigment epithelium and the outer segments
of photoreceptors as well as inter photoreceptor space.

Topography
Retina is thin, delicate layer of nervous tissue that has a surface area of about
266 mm sq. The major landmarks of the retina are: the Optic Disc, the Retinal Blood
Vessels, the Area Centralis with fovea and foveola, the Peripheral Retina and the Ora
Serrata.

The retina is thickest near the optic disc, where it measures 0.56 mm. It becomes
thinner towards the periphery. The thickness reduces to 0.18 mm. at the equator and to
0.1 mm. at the ora serrata.

Fig. 2. Ophthalmoscopic view of retina

Optic Disc
It is circular to slightly oval structure that measures approximately 1.5 mm in
diameter. Centrally, it contains a depression, which is known as physiological cup.

Area Centralis
Area Centralis is divisible into the fovea and foveola, with a parafoveal and a
perifoveal ring around the fovea. This region of retina located in posterior fundus
temporal to the optic disc, is demarcated approximately by the upper and the lower
arcuate and temporal retinal vessels and has an elliptical shape horizontally.

The average diameter is about 5.5 mm, which represents approximately 150 of
visual field.

Fovea
It marks approximate centre of area centralis is located at the posterior pole of
globe, 4mm. temporal to the centre of the optic disc and about 0.8 mm below the
horizontal. It has a diameter of 1.85 mm, which represents 5 degree of the visual field.
9

Foveola
It measures 0.35 mm in diameter a represents only 10 of the visual field. It is
concave indentation cut in the centre of fovea. It is avascular in nature.

Macula Lutea
It is an oval zone of yellow coloration within the area centralis. It is a horizontally
oval zone, 3 mm in diameter, with the centre being the foveola. It is not easily discernible
on ophthalmoscopic examination of the living eye, but in red free light and darkly
pigmented individuals it is seen as a horizontally oval zone that includes the fovea.

In freshly enucleated eyes, the macula lutea appears as a greenish-yellow elliptical

region some 3mm in diameter, with the centre being the foveola, which itself is
colourless.

The yellow colouration probably derives from the presence of the carotenoid
pigment, xanthophylls, in the ganglion and bipolar cells.

The average diameter of macula is 5.5mm. and it represents central 15 degrees of

vision.

Within the area centralis two other regions are distinguished outside the fovea:
The parafovea (0.5 mm in width) and the perifovea (1.5 mm in width).

10

Peripheral retina
The peripheral retina increases the field of vision and is divided into four regions:
•
The near periphery
•
The mid – periphery
•
The far – periphery
•
The ora serrata

The near periphery occupies a circumscribed region of 1.5 mm. around the area
centralis, and the mid-periphery is a 3mm. wide zone around the near periphery.

The far – periphery is a region that extends from the optic disc, 9 – 10 mm. on the
temporal side and 16 mm. on the nasal side in the horizontal meridian. This asymmetry is
accounted for by the location of the optic nerve on the nasal side of the globe.

The most anterior region of retina is the Ora Serrata, which consists of a dentate
fringe, and which denotes the termination of the retina. It is 2.1 mm. wide temporally
0.7 – 0.8 mm wide nasally.

It is located 6.0 mm nasally and 7.0 mm temporally from the limbus, 6 – 8 mm.
from the equator and 25mm from the optic nerve on the nasal side.

The ora serrata marks the transition between the attenuated retina and the inner,
columnar, non-pigmented cells of the pars ciliaris retinae; the retinal pigment epithelium
continues anteriorly as the outer cuboidal cell layer of the ciliary body.11

11

At the ora serrata, a thin non-neural prolongation extends forwards over the
ciliary process and iris as the ciliary and iridal parts of retina, which consists of RPE and
columnar epithelial layers only.15

GENERAL ARCHITECTURE
As seen in cross section by light microscopy, the retina is represented by 10 layers.
From sclera to vitreous they are:

1.
Retinal Pigmented Epithelium
2.
Photoreceptors layer of rods and cones
3.
External Limiting Membrane
4.
Outer nuclear layer
5.
Outer plexiform layer
6.
Inner nuclear layer
7.
Inner plexiform layer
8.
Ganglion cell layer
9.
Nerve Fiber Layer
10.
Internal Limiting Membrane

12

Fig. 3. Layers of Retina

1.
Retinal Pigmented Epithelium: It consists of single layer of approximately five
million cells firmly attached to its basal lamina, the lamina vitrea of Bruch’s
membrane.
It continues forward as the pigmented layer of the ciliary epithelium. The
epithelial cells contain melanin granules. The apex of the cell makes contact with the
sensory retina through microvilli like processes. These villi of the RPE are involved in
phagocytosis of the outer segment discs and thus they promote the renewal of
photoreceptor cells.

It helps in recycling of Vitamin A, transport of nutrients and metabolites. It is also

involved in the absorption of scattered light.

13

2. Photoreceptor
Layer: This layer consists of rods and cones. Density of cones is
maximum at fovea. Density of cones is 40-50% greater on nasal aspect than on
the temporal aspect of retina. Rods are absent at fovea.

Average diameter of rod free area at fovea is 0.35 mm. Photoreceptors have a
morphologically distinct regions-outer segment and inner segment.

Purple pigment in rods allows scotopic vision whereas photopic vision originates
in the cones by the presence of trichromatic pigments. Its major function is conservation
of light energy to electrical impulses.

3.
External Limiting Membrane: It separates the layer of photoreceptors from
outer nuclear layer. It becomes continuous with the basal lamina between the
pigmented and non-pigmented portions of ciliary epithelium.

4.
Outer Nuclear Layer: It contains soma and nuclei of the photoreceptor cells.
Topographically the width of this layer varies, primarily because of the number of
rows of nuclei.

Nasal to disc the outer nuclear layer is 45 µ m. thick and has 8-9 rows of nuclei, at
the temporal disc only 4 rows of nuclei are present and the thickness is 22µm. In fovea 10
rows of cones nuclei increase the thickness to 50µm.

14

5.
Outer Plexiform Layer: It marks the junction of 1st and 2nd order neurons in
retina. The outer 2/3rd of this layer is composed of the inner fibers of
photoreceptors surrounded by the processes of Muller’s cells and the remaining
1/3rd consists of dendrites of the bipolar and horizontal cells as well as Muller cell
processes.

Outer plexiform layer is thickest at the macula and consists of predominantly of

oblique fiber that deviated from fovea. This layer is also known as Henle’s fiber layer.

Fig. 4: Outer plexiform layer

6.
Inner Nuclear Layer: It consists of 8-12 rows of closely packed nuclei of bipolar
cells, horizontal cell, amacrine cells, interplexiform cells and supportive Muller
cells. Four layers can be distinguished:
•
The outermost layer with horizontal cell nuclei

15

•
The outer intermediate layer with bipolar cell nuclei
•
The inner intermediate layer with Muller cell nuclei
•
The innermost layer with amacrine interplexiform cell nuclei

7.
Inner Plexiform Layer: It marks the junction of the 2nd Order neurons, the
bipolar cells with the third order neurons, the ganglion cells. It contains synaptic
connections among bipolar, ganglion amacrine and interplexiform cells.

It also contains processes of Muller cells, an abundant microvasculature and an

occasional displaced nucleus of a ganglion or an amacrine cells. It is absent at the fovea.

8.
Ganglion Cell Layer: It is composed mainly of the cell bodies of the third order
ganglion cells, although other elements such as process of Muller cells, other
neuroglia and branches of retinal vessels are present.

It forms a single layer in the peripheral retina, but two layers are formed at
temporal side of optic disc and 6 –8 layers at the edge of the foveola. At the foveola and
optic nerve head the ganglion cell layer is absent.

9.
Nerve Fiber Layer: It contains the axons (afferent fibers) of ganglion cells, glial
cells, a rich capillary bed and centrifugal fibers (efferent).

The axons remain unmyelinated until they reach the lamina cribrosa of the optic
nerve. It is thickest at the nasal edge of the disc where it measures 20-30µm. The

16

thickness decreases from optic disc to ora serrata, where the ganglion cell layer and the
NFL blend to form a single layer.
10.
Inner Limiting Membrane: - It forms innermost layer of the retina and outer
boundary of the vitreous. Both the retina and the vitreous contribute to formation
of this membrane, which consists of four elements:
•
Collagen fibrils
•
Proteoglycans
•
Basement membrane
•
The plasma membrane of Muller cells

At periphery of retina it is continuous with the basal lamina of the ciliary

epithelium. It continues uninterrupted at the fovea where it is thickest. With ageing, the
ILM becomes generally thicker and interrupted at the ora serrata.11

17

ANATOMICAL BOUNDARIES OF PERIPHERAL FUNDUS

Equatorial and Ora Serrata Regions
The fundus may be separated into central (posterior) and peripheral (anterior)
portions by a circle passing through the posterior edge of the scleral entrance of each
vortex vein. In addition, the peripheral fundus may be subdivided into two areas:

1.
An equatorial region: About 4 DD (5.83 mm) wide, extending approximately
2 DD (3 mm.) on either side of the anatomical equator.
2.
An ora serrata region or extreme fundus periphery: A zone about 3.0 DD
(4.73 mm) in width, extending on either side of the ora serrata.

The anatomical equator is located approximately 2 DD (3 mm) anterior to the

entrance of the scleral canals. Thus, the vortex veins become important landmarks in
separating the peripheral fundus from the posterior pole.

18
Fig. 5: Landmarks of retina

Horizontal and Vertical Fundus Landmarks

The fundus may also be divided by natural features into four quadrants, each of
which is limited by visible narrow landmarks that run horizontally and vertically within
the fundus. The long ciliary nerves and arteries form the horizontal boundary nasally and
temporal.

The vertical boundaries of the quadrants are made up of two poorly

vascularized meridonial strips, which are not pigmented and have indistinct borders.

19

These strips are most frequently located one-quarter hour nasal to the 6 ‘o’clock
position and one-quarter hour temporal to the 12 ‘o’clock meridian. They form
boundaries between two-vortex system, one belonging to the temporal and the other to
the nasal quadrant.

These vertical boundaries are found less often than the horizontal ones. However,
at least one short ciliary artery or nerve may sometimes be noted running along the
anatomical vertical meridian of the fundus.

Retinal Vessels
In the peripheral fundus it is often difficult or impossible to differentiate between
arteries and venules on the basis of size, color, or pattern. The most practical method of
identification is to trace the vessel back to the posterior fundus.

The retinal arterioles and the venules generally do not course together, but are
evenly distributed throughout the periphery. The majority becomes very small and
disappears before reaching a distance of ½ disc diameter from the ora serrata. The arteries
disappear first, whereas venules tend to extend closer to the ora serrata.
Ora Serrata
In the ora serrata region, the retina becomes opalescent and is often marked by
small rows of cystoid cavities. The underlying pigment epithelium is darker and more
granular in appearance than that seen posteriorly.

20

The sensory retina stops abruptly at the ora serrata and is continued by the non-
pigmented ciliary epithelium, which appears considerably thinner than the retina. The
pars plana ciliaris is more deeply pigmented than the peripheral retina and thus, the
choroidal pattern is obscured by that of the pigment epithelium.

The development of ora serrata is incomplete at birth and continues in early life.
In infants the ora serrata appears as a slightly wavy line, symmetrical all the way around
the fundus and situated closest to the posterior border of the ciliary crest.

During the early years of life, the pars plana ciliaris grows asymmetrically,
becoming wider temporally than nasally, and the nasal ora serrata forms scallops. The
concave side of each scallop is nearly always turned anteriorly.

Sometimes, however, the scallops appear inverted, with a slightly concave side
turned posteriorly. The teeth and bays formed by scalloping of the ora serrata become
obvious at about one-half hour temporal to the 12 ‘o’ clock meridian and extend nasally
to one half-hour on the nasal side of the 6 ‘o’clock meridian.

Vitreous Base
One of the most significant structures in the peripheral fundus is the vitreous base.
It is of clinical importance because retinal breaks frequently occur along its posterior
border, and, in the case of traumatic detachment, occasionally along the anterior border as
well.

21

The vitreous base involves the full circumference of the peripheral fundus and
measures approximately 3.20 mm. in width. It extends from the ora serrata anteriorly into
the pars plana for approximately 1DD (1.5 mm); posterior to the ora it varies in width
from 1.8 mm temporally to 3 mm nasally.

On occasion it migrates towards the equator. The vitreous base represents an area
in the fundus where the vitreous, sensory retina, and pigment epithelium are all firmly
adherent, one to the other.

The posterior border of the base is usually a smooth line paralleling the ora
serrata, and pigmentation is subtle, if present, in contrast to the more conspicuous
pigmentation of the ciliary portion of the vitreous base.

Pars plana
The pars plana is delineated at its posterior margin by the ora serrata. As
previously mentioned, there is a firm adhesion of vitreous base, sensory retina, and retinal
epithelium at the ora.

The sensory retina is continued into the pars plana as the non-pigmented ciliary
epithelium. Cells in the non-pigmented ciliary epithelium apparently contain acid
mucopolysaccharide. The vitreous base, which straddles the ora serrata, has its anterior
border in the pars plana, where it parallels the configuration of the ora serrata.

22

It is important to remember that breaks in the non-pigmented epithelium can

occur along this anterior border, especially after trauma, and can even, though their
location is anterior to the ora serrata, lead to rhegmatogenous retinal detachment.

Radial (or meridonial) striations are present in the pars plana. They line up with
the dentate processes and are directed between the ciliary processes.

Anteriorly the pars plana is delineated by the posterior margins of the ciliary
processes. The latter are about 73 in number, compared to the fewer dentate processes at
the ora serrata.

Thus, the width of the pars plana from the ora serrata to the posterior border of the
ciliary crest is on the average about 4mm, while the ciliary processes themselves measure
approximately 2 mm in length.2

23

DEVELOPMENTAL VARIATIONS IN THE FUNDUS PERIPHERY

Various types of developmental variations in fundus periphery are described –
•
Variation of bays and teeth of Ora Serrata
•
Meridonial retinal folds
•
Cystic retinal tufts
•
Non-cystic retinal tuft
•
Zonular tractional tuft
•
Pigment clumps
•
Pearls of ora serrata
•
Pars plana cyst

1.
Variation of Bays and Teeth of the Ora Serreta
Variation of size and shape include: deep bays, giant teeth, bifid teeth, ring teeth
and bridging teeth. Over 30% of normal subjects show at least one of these variations.
When multiple, they tend to occur adjacent to each other.

They are nearly always located near the horizontal meridian, close to or over the
course of a visible long ciliary artery and nerve. They are overwhelmingly more frequent
nasally than temporally.

a) Deep ora bays: They are at least six times more frequent than any other ora
serrata variation and have a significant tendency to bilateralism. The usual contour of a

24

bay is finely irregular and wavy, but in a deep bay the contour is perfectly smooth as if it
had been pulled taut.

A deep bay is two to four times wider and deeper than adjacent bays. As a rule the
teeth bordering a deep bay are larger than adjacent teeth. Deep bays are found singly, in
adjacent pairs, or in triplets. In about 25% of the cases showing deep bays, other
developmental variations are also present.

b) Giant teeth: These are oversize regular teeth. They extend beyond the middle
of the pars plana ciliaris and almost touch the ciliary processes.

Giant teeth are found exclusively in eyes with deep bays, but are much less
frequent than deep bays. All other variations in teeth are less frequent than giant teeth.

c) Bifid
tooth: It is larger than average and has a forked tip. A ring tooth
results from two adjacent teeth leaning towards each other and forming a ring enclosing a
bay. Ring teeth are also larger than average.

There are three stages of ring formation:

•
Open ring
•
Closed ring
•
Hole-in-the-tooth

In an open ring the tips of the adjacent teeth do not quite touch. In a closed ring
the tips of the adjacent teeth have joined, imprisoning an island of pars plana ciliaris.

25
Sometimes such an island is large in relation to the surrounding teeth and is easily
mistaken for a retinal break.

In a hole-in the-tooth the two adjacent teeth are merged into a singlewide tooth,
and a small punched out area of pars plana ciliaris forms an island in its base. This island
is much smaller than in a closed ring.

d) Bridging tooth is a cordlike structure extending from the peripheral retina to the
anterior portion of the pars plana ciliaris. Except for its anterior extremity, it is
detached from the ciliary epithelium and appears curved like a bow with its
convexity towards the centre of the globe.

It seems to be degenerated and cystic. A bridging tooth is seldom associated with

other variations of the ora serrata.

2)
Meridonial Retinal Folds
A meridonial retinal fold is a permanent fold of developmental origin. It is often
called “dry” because it is not accompanied by the retinal detachment. It measures 0.5 to
1.5 DD in length and involves all retinal layers.

As a rule, such a fold begins at the ora serrata and runs posteriorly in a meridonial
direction. The surface of a meridonial retinal fold appears irregular, lacks transparency,
and is finely wavy as though it were covered with microcysts. In most cases the
surrounding retinal area shows cystoid degeneration.

26
Meridonial folds are found in 25% of normal eyes and are bilateral in a
statistically significant number of instances. They are generally posterior extensions of
ora serrata teeth. The number of folds per eye varies from one to ten, one-fold being most
frequent.

Fig. 6: Meridonial Fold

A significant number of folds are associated with other developmental variations.

Meridonial retinal folds are found significantly more often nasally than temporally and in
the upper nasal quadrant more often than in lower. Their frequency near the nasal
horizontal meridian is notable.

27
The existence of meridonial folds does not increase the risk of a subclinical retinal
detachment develops in an eye with meridonial folds, the retinal breaks tend to be located
near the folds.1

3)
Cystic Retinal Tufts
It is a congenital developmental vitreoretinal abnormality associated with firm
vitreoretinal adhesions and can lead to acute tractional retinal tears at the time of an acute
posterior vitreous detachment.16

Fig. 7: Cystic retinal tuft

Histologically, it consists of a microcystic, elevated, peripheral retinal lesion

0.1 to 1.0 mm in diameter. Pigment is often found in the base, and trophic changes may
be present in the immediately adjacent retina. Vitreous condensations frequently are
visible at the surface of the lesion.

28

Degenerative changes in outer retinal layers (including the pigmented epithelium)

are usually present, and the larger tufts consistently show a lack of photoreceptor
elements.
Neuronal elements usually are replaced by microcyst and proliferating glial cells,
and a cap of glial cells with dense cytoplasm is a consistent finding on the surface of the
lesion.

Electron microscopy shows the vitreoretinal junction to be characterized by deep

crypt and microcyst formation, with extensive penetration of vitreous. The proliferating
glial cells processes around the microcysts are tightly packed and have extremely dense
cytoplasm.

Cystic retinal tufts may be avulsed by vitreous traction or without posterior

vitreous detachment. Topographically, lesions are found in the retrobasal zone and are
distributed equally in all quadrants of the retina. They are found in the eyes of newborn
infants and are represented equally in all age groups.

Clinically, the lesion is seen as a tiny discrete mound, sharply circumscribed,

rounded or ovoid, characteristically chalky white, and occasionally with pigment adjacent
to the lesion. On examination scleral indentation, it is slightly or moderately elevated,
with a broad base and borders that gradually slope and merge with the adjacent retina.

29

The lesion may sometimes be mistaken for a small-elevated flap of retina, but
because of its chalky white appearance, it does not show the translucency of a retinal
flap. Generally the lesion is found in the region of equator, is approximately 0.1 to
0.5 DD, and may show mirror symmetry with similar lesions in the fellow eye.

Cystic retinal tuft probably is associated with 10% of retinal detachments in

general. This makes it the second most important peripheral retinal degeneration in this
regard next to lattice degeneration, which is associated with approximately 30% of
detachments.

Because cystic retinal tuft is present in 5% of individuals in autopsy studies, it can

be calculated that the risk of retinal detachment is only about 0.28% (or 1 in 357persons
with cystic retinal tuft). Therefore, it is obvious that prophylactic treatment of such
lesions is not to be recommended.3

4)
Non-cystic Retinal Tuft
Non-cystic retinal tuft is a thin, slightly elevated wisp of retinal tissue, less than
0.1 mm in diameter at its base. Internally it contains Muller’s cell processes.

It is usually found in clusters within the vitreous base and without associated
cystic or pigmentary changes. It may degenerate, producing tiny floating spherical
fragments that probably represent decapitation of tufts by avulsion.

30
Non-cystic retinal tufts appear initially in the latter part of the first decade of life
and occur in about 1/3rd of adults. They are most prevalent nasally and are not associated
with retinal detachment.17

5)
Zonular Traction Tuft
Zonular traction tuft is a developmental abnormality in which there is a posterior
displacement of zonular attachments to the peripheral retina, resulting in an abnormal tuft
of tissue drawn from the surrounding retinal surface towards the ciliary body at an acute
angle, the anterior tip of which is either pointed or bulbous.

It is associated with trophic changes of adjacent retinal cystoid spaces, thinning,

and occasionally, full thickness retinal holes. Tractional changes may be seen in slightly
elevated retinal folds radiating posteriorly from the base, and rarely by rupturing of tuft,
or a full thickness retinal tear.3

Zonular traction tufts are statistically more frequent in males and are found in
15% of autopsied cases. 81% of these traction tufts are found in nasal quadrants, and they
are most prevalent in the inferonasal quadrant.

However, they occur independently of meridonial complexes, which are also

predominantly found on the nasal side. The bases of 4% of tufts have associated full-
thickness retinal holes.18

31

Zonular traction tufts account for 6% of tears, which are either flap tears (if the
tufts were partially avulsed) or tears with free opercula (if the tufts were completely
avulsed).

Retinal tears, if present, are almost always found within the vitreous base
(i.e. intrabasal) and can be recognized clinically by careful examination of the flap of the
tear or by the elongated shape of the operculum. Retinal detachment is uncommon from
this cause and is usually localized. Prophylactic treatment of zonular traction tuft is not
indicated.19

6)
Pigment Clumps
A clump of increased pigmentation without any other change around it is
frequently seen in the fundus.20 Pigment clumps are small, seldom being as large as the
disc. More clumps are found in the equatorial than in the oral region, but the difference is
not statistically significant. Clumps are rare in the posterior fundus.

The pigment sometimes invades the retina, raising the retinal surface overlying it.
Pigment granules may even be seen in the vitreous over the clump.

All quadrants appear equally involved, and age does not seem to be an important
factor. Even in normal eyes pigment clumps may be associated with a silent retinal break
or be surrounded by white-with pressure.
32

They may be related to granular tissue, or may result from a developmental

anomaly of the pigment epithelium, with benign proliferation into the retina. Pigment
proliferation is a frequent response to many stimuli such as traction or biochemical
irritation.

7)
PEARLS OF ORA SERRATA
Pearls of the ora serrata is a fitting descriptive term for a very interesting and
distinctive lesion seen in the far anterior periphery of the retina and always located
beneath a dentate process, either in line with or slightly anterior to the ora serrata.

An ophthalmoscopic examination, this lesion makes itself immediately and

strikingly apparent as a small glistening, bright yellow or opalescent sphere.

Fig. 8: Pearl of ora serrata

33
Histologically, these lesions appear to be drusen-like structures on the inner
surface of Bruch’s membrane and may be analogous to giant drusen of the retina.1

Clinically, they are found in 20% of individuals in all age groups and may occur
in any quadrant of eye. They tend to be bilaterally symmetric and increase significantly in
incidence with advancing age.

They have no known association with ocular disease are very useful as easily
found retinal landmarks to orient the position of other less obvious but important retinal
findings.21

8)
PARS PLANA CYST
A so-called cyst of pars plana ciliaris is clear cystoid space located between
pigmented and non-pigmented epithelium. The shape is generally oval but small cysts
tend to be irregular, kidney- or pear-shaped, or oblong, with somewhat lobulated walls.

The cysts observed in normal eyes range from 0.25 to 2.5 DD and are often
smaller than those seen in patients with retinal detachment, whose cysts are generally
smooth, round and distended.

Those in normal eyes often do not look distended, but appear like partially
inflated balloons. Since their inner wall is flabby and translucent, the underlying pattern
of the pigment epithelium is not visible through it.

34
The inner surface of undistended cyst is lusterless. In distended cysts the inner
wall is smooth, lustrous, and transparent, and the underlying pattern of the pigment
epithelium is easily recognized.

Fig. 9: Pars plana cyst

In the normal eyes cysts of the pars plana ciliaris are nearly always on the
temporal side.1 They usually appear after age 40 years and the prevalence increases
steadily with increasing age.22

Lesions (Degenerative Conditions) of Peripheral Retina

Degenerative conditions of retina compromise on important group of fundus
diseases. In contrast to dystrophies, which are usually bilateral and symmetrical, and have
a hereditary pattern, the degenerations are not necessarily bilateral or symmetrical and
usually do not have a hereditary tendency.1

35

The correlation between presence of a lesion and a longer axial length was always
significant, except with retinal detachment, pigmentary degeneration, retinal holes and
retinal tears.
The presence of lattice degeneration, paving stone degeneration, pigmentary
degeneration, white with or without pressure, retinal holes, tears, or both, retinal
detachment, and posterior vitreous detachment was reported. Paving stone degeneration
was significantly related to older age and white with or without pressure, retinal holes
and retinal tears to younger age.23

Increasing age is a significant factor in the incidence of pigmentary and paving

stone degenerations, whereas aging significantly reduced the prevalence of white without
pressure.24 Lasik does not cause any changes in peripheral retinal lesions.25

Incidence of various degenerations was studied. White without pressure was seen
in 11%. The incidence of formations predisposing to retinal breaks (lattice degeneration
and snail tracks 9.1%, round retinal holes 1.5%) was found.26

Evidence available suggests that most of the peripheral retinal degenerations

should not be treated except in rare, high-risk situations.27

1)
Cystoid Degenerations
Mild degenerative changes normally begin in a strip of approximately 0.25 to
0.5 DD posterior to the ora serrata, as early as neonatal period. In this area the retina
becomes opalescent and marked by one or three rows of small cystoid cavities.

36

The underlying pigment epithelium is definitely darker and more granular than
elsewhere. Retina affected by cystoid degeneration is thicker and less transparent than
usual.1

Histologically, two types of this lesion have been described, designated as

Typical involving the middle retinal layers and Reticular involving the superficial
retinal layers, but these two are not distinguishable on clinical examination.28

Fig. 10: Cystoid Degeneration

Individual cavities have such a thin inner wall that red choroidal reflex is easily
visible through their central portion. At periphery of each tiny cavity, the inner wall is
viewed more obliquely and therefore appears less transparent. Cystoid degeneration
forms accumulation of translucent red dots resembling frog’s eggs with indistinct,
whitish-grey boundaries.

Scleral depression, which gives an oblique view of the area, shows thickening of
affected retina. Viewed in profile, the inner walls of the cystoid cavities appear as

37

multiple small domes of translucent retina. The posterior of cystoid degeneration is best
seen by observation at an oblique angle.

The overlying vitreous remains clear and the inner surface of the involved retina
appears glossy except where the inner walls of the cystoid cavities are broken. Such
rupture occurs most often in fairly large cavities and is frequently noted in young
subjects.

When the inner wall of the single cavity is ruptured, it looks like a tiny retinal
break, usual with an oblique flap or with a group of fine grayish-white particles floating
in the overlying vitreous. Retinal detachment rarely begins around the ruptured cavity
because the rupture affects only the inner layer of the cystoid cavity, leaving the outer
layer intact.

The pigment epithelium underlying cystoid degeneration shows no sign of

disturbance except when other degenerative changes are superimposed, more frequently
in older subjects.

Cystoid degeneration is more marked temporally than nasally but the difference is
small in low degrees of the condition. However a marked preference for temporal side
becomes evident in extreme cystoid degeneration, particularly in the presence of acquired
retinoschisis.1

38

Both eyes of the same subject generally show same degree of cystoid
degeneration, which increases gradually with age in over 90% of the subjects; after age
40, females show significantly more advanced stages of cystoid degeneration than do
males.29
2)
Paving Stone Degeneration
This change has also been called “Chorioretinal Atrophy” of the retina.30 Pigment
proliferation, and migration into the retina, is present around the edges of the lesion, the
center of which is a pale, yellowish-gray.

Atrophy of the pigment epithelium and inner choroidal layer clearly exposes the
large choroidal vessels. When examined with scleral pressure, the inner retinal surface
appears depressed.

The size of the lesion varies and may reach 6 DD, the majority being about disc
size or smaller.

Males are affected about three times often than female. Two overwhelming
majority of the islands of atrophy are near the ora serrata. A few spots occur in the
equatorial region and an occasional area is seen either in the posterior fundus or in the
pars plana ciliaris.

39

Fig. 11: Paving stone degeneration near ora serrata

The upper nasal quadrant being most often immune and the lower temporal most
often affected. All age groups are involved, and the number of affected subjects over and
less than 40 years of age are about equal, although the changes often become more
extensive with age.1

The overlying vitreous is unchanged in the involved areas. Paving stone lesions
appear in about 22% of adults and bilateral in 38% of involved patients.

Clinically, paving stone degeneration presents no threat to vision and never

require prophylactic treatment. When found in eyes in which later detachment occurs, the
paving stone lesion generally provides an effective barrier to extension of the
detachment.30

40

Histological examination shows that thinning if the retina is due to a loss of the
photoreceptor and external limiting membrane. The pigment epithelium is absent in the
center of the lesion and has proliferated on its edges.

The inner layer of Bruch’s membrane shows damage and the choriocapillaries is
either absent or sparsely vascularized. The atrophy is apparently caused by a decreased
blood flow in the terminal arterial branches of the choriocapillaries.

Peripheral chorioretinal atrophy and peripheral chorioretinal degeneration, which

affect the same areas and often occurs together, are likely manifestations of the same
process - ischemia in the choriocapillaries.

When ischemia is localized and severe, circumscribed atrophy of the pigment

epithelium and of the external retinal layer occurs. At the same time hyperplasia of the
pigment epithelium is noted on the edges of the lesion. This is peripheral chorioretinal
atrophy. If ischemia is moderate but extensive, atrophy of the normal element is
accompanied by repair and pigment proliferation, and this is peripheral chorioretinal
degeneration.1

3)
Retinoschisis
Retinoschisis is the splitting (schisis) of the neural retinal layer, which is
embryologically derived from the inner layer of the optic cup.

41

Although retinoschisis resembles retinal detachment in that both show retinal

elevation in the ocular fundus, the latter is an actual separation of the neural retinal layer
from the pigment epithelium, which is derived from the outer layer of the optic cup.31

It is important to differentiate between retinoschisis and retinal detachment.

Table 1
Differentiating Retinal Detachment and Retinoschisis32
Characteristic Retinal
Detachment
Retinoschisis
Transparency Little
Much
Mobility Much
Immobile
Surface Folds
Smooth
Fluid Shift
Often present
Absent
Horseshoe tear, break with operculum
Common
Rare
Reaction to photocoagulation
Absent or faint
Whiten, rarely absent
Field defect
Sloping border
Sharp border
Ultrasonogram with scleral depression
Becomes shallow
Unchanged

Retinoschisis can be classified into three categories:

•
Acquired (senile, degenerative)
•
Congenital (juvenile, hereditary, development)
•
Secondary, in which splitting of the neural retina occurs as a result of, or in
association with, primary fundus disease or trauma.33

42
Acquired Retinoschisis
The most common type of retinoschisis is acquired retinoschisis, which is found
in 4 to 22% of the normal population older then 40 year and usually affects both sexes
equally.34

Splitting in acquired retinoschisis occurs in the outer plexiform layer, or

occasionally in the inner nuclear layer as a result of confluence of the area of cystoid
degeneration.35

Histological, two types of acquired retinoschisis are seen, one relatively flat,
which is called reticular cystoids degeneration, and the other bullous.

Because retinoschisis starts from the extreme peripheral fundus near the ora
serrata, usually in a lower temporal quadrant, patients commonly have no visual
symptoms except in the most advanced stages of the disease.32

Fig. 12: Degenerative Retinoschisis

43

Clinical Features
Ophthalmoscopically, early-acquired retinoschisis appears as a flat, smooth,
retinal elevation that is best appreciated when the area is viewed tangentially with a
binocular indirect ophthalmoscope using scleral depression.

The elevated retina, which represent an inner layer of the retinoschisis, always
contain retinal blood vessels, some of which appear white in the periphery as though they
were occluded.

A number of small, shiny, yellow white dots resembling snowflakes are observed
on the elevated retinal surface. These dots may represent the footstep of the pillars of the
Muller cells.
Retinoschisis usually remains stationary over many years; a spontaneous collapse
may occur, but this is rare.36 The presence of an outer layer of retinoschisis is
demonstrated by a white –with –pressure sign on indirect ophthalmoscopy with scleral
depression. The outer layer often has multiple, reddish, round spots that resemble cluster
of fish or frog eggs.

The inner layer also has a pitted appearance on its back, which is best appreciated
by slit-lamp examination with retroillumination. Cases in which retinoschisis reaches the
macula are rare.

44

Retinal detachment may develop in the eye with acquired retinoschisis as a

complication of the retinoschisis or as a result of a full –thickness retinal break located in
the area unaffected by retinoschisis.

The inner layer break(s) alone does not cause retinal detachment. A break or
breaks in the outer layer alone or in both layers may lead to retinal detachment. When the
retinoschisis is limited to the area anterior to the equator, usually no field defect is
detected.32

45
Table 2
Inner layer breaks and detachments32
No. of Inner layer breaks Detachment (%) No Detachment (%)
Total
1
16 (67)
8 (33)
24 (100)
2-4
30 (75)
10 (25)
40 (100)
5 or more
14 (100)
0 (0)
14 (100)
Total 60 18
78

Fig. 13: Multiple outer layer breaks in a case of degenerative retinoschisis

46

Table 3
Outer layer breaks and detachments32
No. of Inner layer breaks Detachment (%) No Detachment (%)
Total
1
27 (68)
13 (32)
40 (100)
2-4
26 (87)
4 (13)
30 (100)
5 or more
7 (88)
1 (12)
8 (100)
Total 60 18
78

Management
The management of acquired retinoschisis requires bilateral fundus drawing and
visual field plotting. The extent of retinoschisis should be marked in relation to the
adjacent fundus landmarks, such as branches of the retinal vessels or vortex ampulla.

If the retinoschisis is relatively flat without any break and is limited to the area
anterior to the equator, the examination is repeated in a year.

If the retinoschisis has a break or breaks in one of the layer or is already extended
posterior to the equator, reexamination is recommended in 3 to 6 month, depending on
the severity of the lesion; examination should take place sooner if the patient notices
symptoms such as floaters or visual disturbances.32

An outer layer break alone rarely causes full –thickness retinal detachment,
particularly if the break is round and trophic in nature, even though it can be large or
multiple.

47

Retinal detachment can be limited within the area of retinoschisis; this is actually
a detachment of the outer layer of retinoschisis from the pigment epithelium. Byer called
this condition schisis detachment, which can be followed up without treatment.37

A retinal detachment caused by breaks in both the outer and the inner layer of
retinoschisis often becomes extensive, sometimes total. Therefore retinoschisis with
breaks in both layers without retinal detachment deserves close follow –up than does one
involving an outer layer breaks alone.

There are two modes of treatment. The first is demarcation of the advancing edge
of retinoschisis by photocoagulation or cryo applications, or a combination of the two.
This method requires destruction of the normal retina at the edge of the retinoschisis,
which already may be so far advanced at the time of treatment. Therefore, the treatment
further increases the field defect.

The second mode is an attempt to collapse the inner layer by applying

photocoagulation or cryotherapy, or both, to the entire outer layer with or without
drainage of fluid from the cavity of the retinoschisis.32

Congenital Retinoschisis
In congenital retinoschisis retinal splitting usually occurs in the nerve layer. The
disease is usually transmitted by an X – linked recessive trait and is nearly always found
in males who are affected bilaterally, with the mother being an obligatory carrier. Rare
case of an autosomal type has been reported.

48
The retinal abnormality in these patients is probably present at birth; thus, it may
be called congenital. The disease affects whites, blacks, and Asians. The prevalence is
reported to be 1: 15,000 to 1:30,000, but the incidence appears to vary by region and
country.38

Fig. 14: Congenital Retinoschisis

Clinical feature
Because congenital retinoschisis frequently affected the macula or often causes
vitreous hemorrhage, the initial symptoms are poor vision, strabismus, or nystagmus.
Macular abnormalities are detected in virtually all cases and may be the only fundus
finding in congenital retinoschisis.32

49
Ophthalmoscopically visible peripheral retinoschisis is reported to occur in 71 to
85%.39

The most characteristic lesion outside of the macula is the ballooning elevation of
the inner layer with a large oval or hole, usually in the lower fundus.

Unlike acquired retinoschisis, which always originates from the ora serrata, the
anterior border of congenital retinoschisis seldom extends to the ora serrata, and the
posterior border of the congenital retinoschisis is usually convex.

Furthermore in congenital retinoschisis, the inner layer breaks are larger and
encountered more frequently then are the outer layer breaks, in contrast with acquired
retinoschisis in which the opposite is true.

The retinal blood vessels usually run in the inner layer or occasionally bridge the
inner and outer layer. Sheathing of retinal vessels is seen in the area of retinoschisis. In
some cases, the inner layer is so elevated that it can be seen behind the lens on slit –lamp
examination.

The inner layer holes can become quite large, almost as large as the retinoschisis
itself, and the retinal vessels and the attached flimsy retinal tissue bridge these holes. In
some cases the inner layer is missing and the retinal vessels may float free in the vitreous
cavity, a condition called a congenital vascular veil.

50

Retinoschisis in the periphery may be indistinct and may be detected as a very

low elevation of the inner layer only by viewing the fundus tangentially with a binocular
indirect ophthalmoscope with scleral depression.

Ophthalmoscopy without scleral depression often fails to detect vary shallow

retinoschisis in the periphery. Multiple small white dots usually more easily seen in
shallow acquired retinoschisis on scleral depression are also observed in low –grade
congenital retinoschisis.

These white dots, which have been referred as snowflakes, are pale in color, not
chalky white and difficult to see against the pale fundus in white patient.32

Hemorrhage, which can be the first symptom within retinoschisis cavity or

vitreous, is relatively common, and the rates of occurrence range from 4 to 40%. Vitreous
hemorrhage may be the initial sign of the disease.

The electroretinogram (ERG) in congenital retinoschisis is characteristic and

diagnostic. Because of the polymorphous fundus appearance in congenital retinoschisis,
diagnosis based on the fundus examination may be difficult. In such a case, the ERG may
help in the diagnosis.

The ERG in congenital retinoschisis is characterized by a disproportional decrease

of the b –wave amplitude compared with that of the a-wave. The b:a wave amplitude
ratio is especially reduced.32

51

Female heterozygote carriers usually have normal ophthalmoscopic and

electroretinographic findings, but some abnormalities have been reported to show
wrinkling of the internal limiting membrane around the fovea or peripheral retinal
alterations similar to those found in affected males, peripheral retinal degeneration and
gliosis. The majority of these abnormalities, however, appear to be nonspecific and not
consistent finding.40

Management
Congenital retinoschisis is typically stable, and slow progression may alternate
with spontaneous remission or collapsing of retinoschisis. Rapid progression of the
disease is likely to occur during the first decade of life. By age 20 years, most cases, with
few exceptions, stabilize in terms of the size of the retinoschisis.

Management of congenital retinoschisis requires careful fundus examination with

binocular indirect ophthalmoscopy, scleral depression, and a large fundus drawing.
Examination under general anesthesia is often necessary for infants and small children.

Visual field plotting is important but often unsatisfactory in the case of infants or
young children. We examine patient at intervals of every 3 month to 1 year, and at least
once in a year as long as no new signs and symptoms appear.

Because of the no progressive nature of congenital retinoschisis in most patients,

no treatment is indicated unless complications arise that impairs or threatens vision.

52

Secondary Retinoschisis
Splitting neural layers of the retina or retinoschisis can be found in association
with specific disease.

In such cases, the retinoschisis is usually considered a complication of the original

diseases, although cause and result relationship between the two or a mechanism by
which the retinoschisis develops is not entirely clear in some cases.

Conditions in which retinoschisis may develop include:-

•
Proliferative diabetic retinopathy
•
Regressed retinopathy of prematurity
•
Sickle –cell retinopathy
•
Occlusive vascular diseases
•
Aplastic anemia
•
Peripheral uveitis
•
Trauma
•
Tumors,
•
Phakomatoses
•
Long-standing retinal detachment (retinal cyst)
•
Optic pit
•
Good pasture’s syndrome

Although retinoschisis develops in the eye afflicted with these conditions, a

retinal detachment may also occur. In such a situation, it is often difficult to make a

53

distinction between retinoschisis and long-standing retinal detachment when one is

confronted with each clinical case.32
4)
WHITE WITH PRESSURE
This phenomenon refers to geographic areas of whiteness of the midperipheral
equator and peripheral retina. When the white appearance is observed by indirect
ophthalmoscopy without scleral depression, it is termed white without pressure. When a
white reflex is seen with scleral depression, it is termed white with pressure.

Fig. 15: White with pressure phenomenon

Eisner reported that all lesions internal to pigment epithelium have a whitish
appearance when viewed with scleral depression.

54

This was interpreted as resulting from variations in angle between the light beam
of indirect ophthalmoscope and structure being visualized.

Another possible explanation is that the phenomenon of white, with or without

pressure, is a light reflex occurring when the incident light is tangential to more dense
bundles of vitreous collagen.

Greater density of collagen is present at the vitreous base and in bundles that
insert into vitreous cortex at the equator and mid periphery. When the incident light is
tangential to such aggregates of collagen, one sees white. When the light is mostly
parallel with collagen fibers, no white reflex is seen.

Thus, when rolling the eye wall with scleral depression, one may alternately
visualize white and no white with pressure.41

White, with or without pressure, would therefore indicate a zone of greater

concentration of collagen fibers in cortical vitreous, but it does not necessarily imply that
there is more firm attachment of vitreous to retina.

This theory is inconsistent with migratory white without pressure. The cause of
migratory white without pressure is unknown, but it may be related to separation and
recreation of vitreo-retinal adhesions.42

White, with or without pressure, may be observed with coincidental posterior

vitreous detachment. Other than the incidental association white, with or without pressure

55

with posterior vitreous detachment and traction, the significance of these usual reflexes is
negligible.41

Early lattice degeneration always shows white with pressure along their borders.
An early retinoschisis sometimes become continuous with a band of white with pressure.
Some degree of white with pressure is found in over 30% of normal eyes, with a
strong tendency to bilaterality. Only 5% of the individuals under 20 years are affected,
where as two-thirds of those 70 years and over show white with pressure. The temporal
portion of the fundus tends to be most affected.43

5)
Lattice Degeneration
Lattice degeneration of the retina (equatorial degeneration, pigmentary
degeneration, retinal erosion) is the most commonly recognized vitreoretinal abnormality
of the peripheral fundus known to predispose to rhegmatogenous retinal detachment.
Approximately 30% patients with retinal detachment also have lattice degeneration.

Epidemiology
Lattice degeneration is a common disorder that is present in approximately 7 to
8% of the general population.44 The most-frequent peripheral retinal change is lattice
degeneration.45

This condition is bilateral in 42 to 45% of cases. Men and women appear to be

equally affected. It is present more frequently in black than in white patients.46 Patient
with lattice degeneration more frequently have myopia then the population in general.44

56

There is significant prevalence of open angle glaucoma in patients with retinal

lattice degeneration, especially in combination with myopia.47

Clinical features
Ophthalmoscopically, the lattice lesion is a sharply outlined round or oval, often
elongated area of retinal thinning or irregularity. It is the best seen with binocular indirect
ophthalmoscopy and scleral depression.44 A localized pocket of missing vitreous
invariably overlies lattice degeneration of the retina.48

Fig. 16: Lattice lesion containing white crisscrossing wicker lines

Vitreous liquefaction overlying the retinal thinning and vitreous attachment to its
edges, although consistently present, may be difficult to visualize without contact lens
biomicroscopy.
57

The majority of lesions is circumferential and is most frequently located slightly

posterior to the midpoint between the ora serrata and the equator. Two or more lesions
may be parallel and may overlap one another.

Oblique lesions and radial paravascular lesions may also be seen. Patches of
lattice degeneration vary in length from a fraction of a DD to more then 12 DD. The
width of most lesions is between one –quarter and two thirds of a DD, with an average of
one-half of a DD.

Lattice lesion are most commonly found in the 11 ‘o’ clock to 1 ‘o’ clock and the
5 ‘o’clock to 7 ‘o’ clock meridians, and the inferotemporal quadrant is most commonly
involved.

Variable clinically features include abnormally retinal or choroidal pigmentation,

yellow –white surface flecks, reddish patches, and branching white lines. Both are seen in
approximately 80% of patient with lattice degeneration.

Branching white lines, which represent occluded or sheathed retinal blood vessels,
are seen in 17% of patient. These white lines were once believed to be pathognomonic of
this disorder, and the term lattice degeneration is derived from the interlacing pattern of
these white vessels, even though they are now known to be present in just a fraction of
lesion.

The focal reddish areas within lattice lesions are zones of retinal thinning.
Atrophic retinal holes may result from progressive retinal thinning and are present in

58

about 25% of eyes with lattice degeneration. Traction retinal tears are less common
occurring in 1.0 to 2.4% of eyes with lattice degeneration.

Histological features
Light microscopy reveals the lack of internal limiting membrane, retinal thinning,
overlying vitreous liquefaction, vitreous condensation, and exaggerated vitreoretinal
adherence at the border of this lesion.

Retinal pigment epithelial abnormalities occurring in 92% of lesions include focal

loss of pigmentation, hyperplasia, and pigment migration into the retina, particularly
around retinal vessels.

Electron microscopy
The internal limiting lamina is consistently lacking over areas of lattice
degeneration. Glial cell processes may remodel the retinal surface and extend into the
vitreous cavity.

Clinical course
Most lattice lesions are present by the beginning of the second decade of life.
There is no age-related trend in morphologic characteristic or location of lattice lesions.
The degree of vitreoretinal adhesion and the prevalence of pigmentary changes, white
lines, retinal holes, posterior vitreous detachment, and retinal tears increase with time.44

59

Most lattice degenerations were accompanied by vitreous degeneration and

vitreoretinal traction. The disease progressed only slowly, though in a few cases it tended
to expand.49 Atrophic retinal holes and traction retinal tears, the two factor associated
with the risk of retinal detachment do increase with time.44

Heredity
The genetics of lattice degeneration have not been resolved. The prevalence of
lattice degeneration in first-degree relatives of patient with this condition is about 23% or
three times as high as in the general population.50

Lattice Degeneration and Retinal Detachment

The association between lattice degeneration and retinal detachment is well
known. Approximately 30% of patient who present with a retinal detachment will have
lattice degeneration on examination.

Because the prevalence of this condition is high in the general population, the risk
of development of a retinal detachment in any single patient with lattice degeneration has
been estimated at only 0.3% to 0.5 %.44

The incidence of lattice degeneration and full thickness retinal breaks is higher in
patients with pigment dispersion syndrome, and may be responsible for higher risk of
rhegmatogenous retinal detachment in these cases.51

60

Atrophic Round Holes

Beyer observed sub clinical retinal detachment caused by atrophic round holes in
6.7% of eyes with lattice degeneration that were followed up for many years. When
retinal detachment is produced by atrophic round holes, it is unrelated to posterior
vitreous detachment and almost always occurs in patient 30 years of age or younger.
These detachments may display multiple “high water mark” demarcation lines
(suggestion insidious progression) and have a good prognosis for successful surgical
repair.44

The risk of retinal detachment in lattice degeneration with atrophic holes is

estimated to be about 1 in 90 patients, and prophylactic treatment for this common
anomaly is not readily recommended.52

Traction Tears
In eyes with lattice degeneration strange vitreoretinal adhesions at the edges of
lattice lead to tears along the posterior border or at the end of lattice after posterior
vitreous detachment.
A traction retinal tear also occurs on ophthalmoscopically normal areas of retina
in eyes with lattice degeneration. Traction tears and the detachment they produce occur at
the time of posterior vitreous separation generally after 40 years of age.

61

Non-fellow Phakic Eyes

Lattice Degeneration without Retinal Breaks
Byers’ long –term natural history study reports a 1% risk of retinal detachment in
patient with lattice degeneration, with or without atrophic holes. Prophylactic therapy is
not indicated for this group.

Fig. 17: Lattice lesion with a snail-track appearance

Lattice Degeneration with Atrophic Holes

Although sub clinical retinal detachment is frequent among patient with atrophic
round holes in lattice degeneration, the incidence of clinical of progressive sub clinical
detachment is only about 2%.

Prophylactic therapy is not indicated for atrophic holes in lattice degeneration. If

sub clinical detachment caused by atrophic holes is present, treatment may be indicated,
particularly if the patient cannot be followed up at regular intervals on a long term basis.

62

Fig. 18: Lattice degeneration with atrophic holes

Lattice degeneration with retinal tears

Traction tears without acute symptoms are treated in (a) fellow eyes of patient
with retinal detachment, (b) patient with a strong family history of retinal detachment and
(c) aphakic eyes. Asymptomatic traction tears in patients with lattice degeneration do not
otherwise require treatment.

Prophylactic treatment is generally recommended for acute symptomatic tears on

both phakic and aphakic eyes. These eyes have a relatively high risk of progression to
retinal detachment.

Fellow eyes in lattice retinal detachment

The overall rate of retina detachment in untreated fellow eyes of patients with
lattice degeneration and lattice associated retinal detachment in the first eyes is
approximately 5.1%. In patients with myopia and lattice degeneration, it may be as high
as 24.6%.

63

Since lattice-associated retinal detachment has a good chance of successful

reattachment with conventional surgery, and since new tears are notoriously frequent in
ophthalmoscopically normal retina, controversies continues concerning the benefit of
prophylactic therapy in asymptomatic fellow eyes.44

6)
Snow Flake Degeneration
Snowflake degeneration is characterized by multiple minute whitish yellow-dots
resembling snow flakes, which appear primarily in peripheral retina. The numerous
granular-like deposits that provide the snowflake appearance are commonly 100-200µm
in size, are generally found in equatorial fundus, and focally thicken the retina.

They may be distributed evenly or localized predominantly in the inferior fundus.

These progressive retinal changes are frequently accompanied by an equally progressive
fibrillar condensation and liquefaction of the vitreous. According to the dominant features
of the fundus appearance, progression of fundus changes has been classified into 4 stages:

•
Stage 1- extensive white with pressure
•
Stage 2- snowflake degeneration
•
Stage 3- sheathing of retinal vessels and fundus pigmentation
•
Stage 4- further pigmentation and disappearance of peripheral retinal vessels

Snowflake degeneration is a hereditary vitreoretinopathy. Autosomal dominant

type of inheritance has been established. It is associated with retinal detachment. The
surgical success rate is less. Therefore it is generally agreed that liberal prophylactic

64
treatment should be given. If only snowflake-like lesion is present no treatment is
required.53

7)
Retinal Tear
Partial-thickness rental tear
A partial-thickness retinal tear involves the inner layers of the retina and results in
a thin flap or free operculum. Partial –thickness retinal tears are usually multiple and they
are classified into two types by distribution:
•
Paravascular tears occurring adjacent to peripheral retinal vessels.
•
Vitreous base tears aligned circumferentially along a segment of the posterior
border of the vitreous base.

Both forms, which sometimes exist concurrently in the same eye, reflect anatomic
feature and mechanisms that are of practical importance in ophthalmology.54

Fig. 19: Horseshoe retinal tear

65

Paravascular partial thickness retinal tears stem from exaggerated vitreoretinal

attachment at and immediately adjacent to peripheral arterioles and venules. These
relatively firm attachments often produce multiple, foci of cystic degeneration adjacent to
peripheral retinal vessels.

When posterior vitreous detachment occurs, the inner retinal layers at these foci
of paravascular rarefaction remain attached to the vitreous, and cluster of partial-
thickness retinal tears are formed. After this avulsion, microscopic studies of the retinal
show focal absence of varying amount of the inner retinal layers.55

Paravascular partial-thickness retinal tears occurs in 17% of adults, are bilateral in

27% of affected patients, and thus are present in 11% of adults eyes. Posterior vitreous
detachment is present in 100% of affected eyes. The superior quadrant is the area most
commonly involved, and the tears are always located posterior to the vitreous base.

On clinical examination by contact lens biomicroscopy, paravascular retinal

rarefaction is seen as a subtle irregularity of the retinal adjacent to peripheral retinal
vessels. Paravascular partial-thickness retinal tears are visible as small, usually multiple
retinal craters adjacent to peripheral retinal vessels.

These tears assume substantial clinical significance because of the occasional

association with retinal vessel avulsion.

The frequent association with partial-thickness vitreous base tears and full-
thickness retinal tears.

66

Avulsed base and full-thickness retinal tears frequently warrant treatment to

prevent recurrent vitreous hemorrhage or rhegmatogenous retinal detachment.

Vitreous base partial-thickness retinal tears develop in association with posterior

vitreous detachment as multiple flap tears aligned circumferentially along a segment of
the posterior border of the vitreous base. Inner retinal layers are partially avulsed and
attached to the detachment vitreous body.

Partial-thickness retinal tears at the posterior border of the vitreous base are
present in 12% of adults, are bilateral in 5% of affected patients, and thus are noted in 7%
of adult eyes. The process is equally prevalent in all quadrants, is always located at the
posterior margin of the vitreous base, and is invariably associated with posterior vitreous
detachment.

On clinical examination vitreous base partial-thickness tears are visible as

translucent shreds of tissue partially avulsed from the retina adjacent to the posterior
border of the vitreous base.

Like paravascular tractional lesion, vitreous base partial –thickness retinal tears
are clinically significant because of:
•
The occasional association with paravascular partial –thickness tears and vessel
avulsion.
•
The frequent association with full-thickness peripheral retinal tears.

67

Peripheral retinal vessel avulsion and full –thickness retinal tears often warrant
treatment in order to prevent recurrent vitreous hemorrhage and rhegmatogenous retinal
detachment.

Full-Thickness Retinal Tear

Full-thickness retinal tear is related to traction from either the zonule or the
vitreous. In autopsy eyes and clinical studies, full-thickness tears of the postural
peripheral retina are classified as:
•
Intranasal,
•
Juxtabasal,
•
Extrabasal

Each with a specific relation to vitreous base and with different antecedent
lesions.

Intrabasal Full-thickness retinal tear is located within the vitreous base and may
be of the flap or operculated type. The basic cause is zonulo-retinal traction, and the tear
results from partial or complete avulsion of a preexisting zonular traction tuft.

Juxtabasal Full-thickness retinal tear occurs at the posterior border of the

vitreous base and is almost always of the flap type. The most common type of full –
thickness retinal tear, juxtabasal tear, results from traction exerted by the posteriorly
detached vitreous on irregularities of the posterior vitreous base border.

68

Underlying cause of irregularities of the posterior border of the vitreous base

include development variation of the retina at the ora serrate and lesions of lattice
degeneration of the retina.

In some eyes, no underlying cause for vitreous base irregularities is evident, but
juxtabasal full –thickness retinal tear occurs on association with posterior vitreous
detachment.

Extrabasal Full-thickness tear in the peripheral retina is located posterior to the

vitreous base. Usually associated with posterior vitreous detachment, extrabasal retinal
tear results from vitreous retinal traction focally concentrated on a preexisting cystic
retinal tuft, a lesion of lattice degeneration or some other type of retinal abnormality.

In contour, full-thickness retinal tear is usually U or V shaped with the broad base
directed anteriorly, a tapered flap extending into the vitreous, and condensed vitreous
strands attached to the apex of this flap. In some cases flap is partially or completely
avulsed and can be identified as a free operculum in the overlying vitreous.

The free operculum retains its attachment to the vitreous body, and it is almost
always located anterior to the retinal tear. As time passes, the margins of the retinal tear
become smooth or rounded and the retinal flap becomes shrunken and degenerated. Seen
through the retinal break, the pigment epithelium often appears stippled or granular.

69

On histological examination, full-thickness retinal tears demonstrate vitreous

attachment to the degenerated retinal flap or free operculum, gliosis and degeneration
retinal flap or free operculum, gliosis and degeneration adjacent to the smooth, rounded
margins of the tear, a variable degree of the associated retinal detachment, and a
combination of cell breakdown and hyperplasia in the underlying retinal pigment
epithelium.

Excluding retinal tears at the ora serrata, full –thickness retinal tears are present at
autopsy in 3.3% of patients, are bilateral in 11.2% of affected patients, and thus are
present in 1.9% of eyes. These lesions are slightly more common in the inferior
quadrants. Topographically, tears are slightly more common temporally (58%) and
inferiorly (54%); and most tears (95%) are juxtabasal or extrabasal in location.

Of practical importance, full-thickness retinal tears occur significantly more

commonly in eyes with lattice degeneration, although only a minority of the tears directly
involves a lattice lesion. This could mean that lesions of lattice degeneration are too
subtle for detection by conventional means or those eyes with lattice degeneration contain
abnormal vitreoretinal that predispose to retinal tear formation.

Clinical identification of full-thickness retinal tears is particularly significant. In

the presence of posterior vitreous detachment, attention may be focused on abnormal
retinal areas by a free operculum, projecting retinal flap, hemorrhage, or localized retinal
pigment epithelium alteration. With or without these diagnostic clues, full-thickness
retinal tears are visible on contact lens biomicroscopy or on indirect ophthalmoscopy and

70

scleral depression. As the scleral depressor creates translucency in the adjacent sensory
retina, the tear is seen as a contrasting red area.

A retinal tear and a retinal hemorrhage may be differentiated by the fact that the
intensity of the contrasting red color of a tear varies with the position of the scleral
depressor, but the red color of a retinal hemorrhage is unaffected by movement of the
depressor.

These tears often warrant prophylactic therapy in an effort to prevent retinal

detachment and they require treatment when associated with rhegmatogenous retinal
detachment.54
Similar study was done by Bradley R. Straatsma, Robert Y. Foos and
Stephan S. Feman (Table-4).

They studied different anatomical variations in the peripheral retina.

71

Table 4
Developmental Variations of Peripheral Retina53
Patients With
Bilateral
Eyes With

Lesions
Lesions
Lesions
Variation
No. % No. % No. %
Meridonial folds
51/200
26
28/51
55
79/400
20
Meridonial Complex
31/200
16
18/31
58
49/400
12
Enclosed and Partially Enclosed 12/200
06 01/12 08
13/400
03
Oral Bays
Peripheral Retinal Excavation
21/200
10
09/12
43
30/400
08

According to this study Meridonial fold was the most common anatomical
variation present in the peripheral retina followed by meridonial complex, oral bays and
peripheral retinal excavation respectively.53
Norman E. Byer also studied the prevalence of anatomical variations and
degenerations in the peripheral retina (Table–5).

72

Table 5
Prevalence of Cystic retinal Tuft and Miscellaneous Peripheral Retinal
Findings3
Prevalence
Proportion of
Association of Lesion
in Adult
Detachments
Lesion or Finding
With Later Retinal
Population
Accounted for by
Detachment
(%)
This Lesion (%)
Cystic Retinal Tuft
5
0.28
10
Non-cystic Retinal Tuft
33
0
0
Zonular Tractional Tuft
15
Very rare
Nil
Meridonial Fold
26
Very rare
Nil
Enclosed Oral Bay
6
Very rare
Nil
Cystoid Degeneration
100
0
0
Paving Stone Degeneration
22
0
0
Pearl of Ora Serrata
20
0
0
Pars Plana Cyst
18
0
0
White-with-pressure Common
0
0

According to this study cystoid degeneration was the most common peripheral
retinal degeneration with 100% prevalence. None pf the peripheral retinal degeneration
studied was associated with retinal detachment. Of the entire anatomical variations only
cystic retinal tuft was associated with 10% cases of retinal detachment.

Bradley R. Straatsma, Robert Y. Foos and Stephan S. Feman conducted a study of

incidence of peripheral retinal degenerations. They also studied the lesions present
bilaterally (Table-6).

73

Table 6
Degenerations of Peripheral Retina53

Patients With

Bilateral Lesions Eyes With Lesions

Lesions
Variation
No.
%
No.
%
No.
%
Cystoid
Degeneration 1173/1173
100 1146/1146
100 2319/2319 100
Degenerative
12/1173 1 4/12 13 16/2319 0.70
Retinoschisis
Paving Stone
134/614 22 52/134 38 186/1223 17
Degeneration
Lattice Degeneration
86/800
10.7
39/81
48
125/1588
7.9
Paravascular Partial
Thickness Retinal
21/126 17 6/21 27 27/252 11
Tear
Vitreous Base Partial
Thickness Retinal
20/169 12 1/20 5 21/312 7
Tear
Full Thickness Retinal
80/2406 3.3 9/80 11.2 89/4812 1.9
Tear

According to this study cystoid degeneration was the most common peripheral
retinal lesion with incidence rate of 100%. Incidence of paving stone degeneration and
lattice degeneration were 22% and 10.7% respectively. Retinoschisis was present in only
1% cases. Cystoid degeneration was bilateral in 100% cases while retinoschisis, paving
stone degeneration and lattice degeneration were bilateral in 13%, 38% and 48% cases
respectively.

74

METHODOLOGY
231 patients (432 eyes) attending the Outpatient Department of Ophthalmology,
in Dr. B. R. Ambedkar Medical College and K. C. General Hospital, Bangalore, between
December 2004 and January 2006 were taken randomly for this study. The patients were
of no specific age group. Small children and patients with history of intra ocular surgery
in last six months were excluded from study. The main aim was to study the incidence of
Peripheral Retinal Lesions in these patients.

All the patients were subjected to the following tests.

•
Indirect Ophthalmoscopy with and without scleral depression.
•
Examination with Goldmann 3-mirror lens.
•
Examination with +78D lens.

EXAMINATION
Pupils of all the patients were dilated using mydriatic 1% tropicamide and 2.5%
phenylephrine hydrochloride drops, one drop of each in both eyes. Most patients’ pupil
dilated adequately after 20 to 30 minutes using this regimen. After complete dilatation
fundi of all the patients were examined using
•
Indirect Ophthalmoscope
•
Goldmann 3 mirror lens
•
+78D lens

The findings of the examination were recorded by fundus drawing.

75

1.
INDIRECT OPHTHALMOSCOPY: The principle of indirect ophthalmoscopy
is to make the eye highly myopic by placing strong convex lens in front of it.

This forms a real inverted image of the fundus in the air between the lens and the
observer. Such an image is always magnified. Condensing lens of various powers and
diameter are available.

The higher the power, the lower the magnification, the shorter the working
distance but the greater the field of view. A high quality 20-D spherical lens is most
widely used lens.

Fig. 20: Indirect ophthalmoscope

76
The technique is as follows:
Both the pupils should be well dilated and patient should be ideally supine. The
lens is held with the flat surface facing the patient should be held parallel to the patient’s
iris plane at all times.

Observer remains at 1 meter and observe the red reflex. Then he interposes the
condensing lens in the path of light close up to the patient’s eye and slowly moves the
lens from the eye towards himself until the image of the retina is seen clearly.

The patient is asked to move the head into optimal positions for examination.

•
In emmetropic eye the image is formed in the air at the principal focus of the lens,
between it and the observer eye.
•
In myopic eye the image is formed in the air within the focal length of lens,
between it and the observer eye.
•
In hypermetropic eye the image is formed in the air in front of its principal focus,
between it and the observer eye.

Fig. 21: Indirect Ophthalmoscopy

77

Scleral Indentation
It enhances the visualization of the peripheral retina anterior to the equator and
enables a dynamic fundus examination to be performed. The technique of depression was
originally suggested by Trantas. It is usually worn on the middle finger of the right hand.

The tip of the depressor is placed on the skin of the eyelid over the area of sclera
to be obtained. The eyelids should be closed, the depressor tip being applied to the upper
lid at the upper edge of the tarsus to examine upper fundus periphery. When the patient
looks up, the tip of the depressor slides easily under the orbital margin.

Lower fundus periphery is more difficult to see. The depressor tip should be
placed on the skin of lower lid about 2-3 mm from lid margin. With a gentle movement
of the depressor, lower lid and depressor can be made to slide together back and forth as
necessary for examination.

In order to depress the sclera at 3 ‘o’ or 9 ‘o’clock, in the palpebral fissure, it is

usually necessary to apply pressure directly to the bulbar conjunctiva. Some patients
tolerate this procedure well without topical anesthesia. With sensitive patients it is best to
anaesthetize the conjunctiva with 0.55 proparacaine eye drops. If topical anesthesia is
necessary, this portion of examination is performed last, since proparacaine may cause
oedema of the corneal epithelium and hazing the fundus view.

78

2.
INDIRECT SLIT-LAMP BIOMICROSCOPY: It is non-contact lens method
of Biomicroscopic retinal examination. This method utilizes high-power lenses
(+90D and +78D) designed to obtain a wide field of view.

The lenses are used in a similar manner to an ordinary ophthalmoscope lens and
the image is likewise vertically inverted and laterally reversed.

Fig. 22: + 90D Lens

Technique: Both the pupil should be well dilated. The slit beam is adjusted to
about one-quarter its full round diameter. The illumination angle is set co-axially with the
slit-lamp viewing system. The lens is interposed in the slit beam immediately in front of
the patient’s eye.

The red-reflex is identified, following which the microscope is pulled back, until
fundus comes into view. The fundus is scanned, executing horizontal and vertical
adjustments of the slit-lamp, while holding the lens still.

The width of the beam may be increased to obtain a larger field of view. The
magnification may be increased for greater detail as necessary.

79
Fig. 23: Indirect Slit-Lamp Biomicroscopy

To visualize peripheral retina patient is asked to assume appropriate portion of

gaze as with standard indirect ophthalmoscopy.

3.
GOLDMANN TRIPLE-MIRROR EXAMINATION: It is contact lens method
of biomicroscopic retinal examination.

Fig. 24: Goldmann Triple Mirror Lens

80

It consists of four parts:

•
Central part- provides 30° view of posterior pole.
•
Equatorial Mirror- (largest and oblong shaped) enables visualization from 30° to
equator.
•
Peripheral Mirror – (intermediate in size and square in shape) enables
visualization between the equator and ora serrata.
•
The Gonioscopy Mirror - (smallest and dome shaped) may be utilized for extreme
retinal periphery and pars plana.

It is therefore apparent that the smaller the mirror the more peripheral the view.
The central part affords an upright vertical image of the posterior pole with regard to
three mirrors:
•
The mirror should be positioned opposite the area of the fundus to be examined.
•
When viewing the vertical meridian, the image is upside down.
•
When viewing the horizontal meridian, the image is laterally reversed.

Technique
Topical anesthesia is instilled into lower fornix. A coupling fluid
(methylcellulose) is inserted into the cup of the lens but it should be no more than half
full.

The patient looks up and the inferior rim of the lens is inserted into the lower
fornix and then pressed quickly against the cornea so that the coupling substance does not
escape. The patient is then asked to gaze straight ahead with other eye.

81

The illumination column should always be tilted except when viewing the vertical
meridian. When viewing sectors of the peripheral retina the axis of the beam is rotated so
that it is always at right angle to the mirror.

To visualize the entire fundus the lens is rotated 360° using first the equatorial
mirror and then the peripheral mirror. To obtain a more peripheral view of any given
sector the lens is tilted to the opposite side.

The patient is asked to move the eyes to the same side for e.g. to obtain a more
peripheral view of 12 o’clock meridian (mirror at 6 o’clock) the lens is tilted down and
the patient looks up. The 6 o’clock meridian is viewed by placing the mirror at the
12 ‘o’clock position, with the illumination column tilted forward.

The horizontal meridian is viewed by placing the contact lens mirror at the
opposite end of the meridian- i.e., the 9 ‘o’clock area is viewed with the contact lens
mirror at 3 o’clock and vice versa.

The illumination – observation angle must be reduced to zero, the slit beam
oriented horizontally, and the illumination column tilted completely forward. The oblique
meridians are examined by placing the mirror of the contact lens at the opposite end of
the meridian examined. The slit beam must coincide with that meridian.
The illumination column should be on the same side of the biomicroscope as the
mirror in the contact lens when the mirror is located above the horizontal and on the

82

opposite side when the mirror is located below the horizontal. When the vicinity of the
horizontal meridian is examined, slit lamp and microscope should be coaxial.

Documentation of retinal findings

Detailed sketches of the fundus are made on durable drawing paper to document
the retinal pathologic condition. The location of a given lesion is drawn in reference to
the major retinal veins, the meridonial location of the lesion within the eye, and its
relative peripheral location.

The arteries are typically not drawn. By convention the 12 ‘o’clock meridian is
placed at the top of the retinal drawing because it represents the uppermost part of the
clock face.

Because the image seen with the indirect ophthalmoscope is vertically inverted
and laterally reversed, the top of the chart is placed towards the patient’s feet (upside
down). In this way the inverted position of the chart in relation to the patient’s eye
corresponds to the inverted image of the fundus.

83

TABLE 7
Color Coding for Retinal Drawing

Color Anatomic
Features
Red Retinal
arteries
Retinal hemorrhage
Microaneurysm
Blue Retinal
veins
Detached retina
Retinal Fold
Green Media
opacities
Black
Retinal or Choroidal hyperpigmentation
Brown
Pigment under detached retina
White Normal
Retina
Purple Flat
Neovascularization
Orange Elevated
Neovascularization
Yellow Retinal
edema

84

Table 8
Symbols used in retinal drawing

Symbols Interpretation
O
Optic Nerve Head
+ Fovea
X Exudate
D Drusen
C
Cotton Wool Patch
# Fibrous
Proliferation
Blue X’s
Peripheral Cystoid Degeneration
Blue line surrounding Blue X’s
Lattice Degeneration
Blue line surrounding Red Area
Retinal Break
Blue line surrounding Blue Cross Hatch
Retinoschisis
Blue line surrounding Red Cross Hatch
Thin Retina

85

Fig. 25: Fundus Drawing

Statistical methods
The Chi-square significant test and Fisher Exact test have been carried out to find
out the significance of difference of proportion of various parameters.

Statistical software
The Statistical software namely SPSS 10.0 and Systat 8.0 were used for the analysis
of the data and Microsoft Word and Excel have been used to generate graphs, tables, etc.
86

RESULTS
Study Design
A cross-sectional study consisting of 231 patients is undertaken to investigate the
incidence of various types of peripheral retinal lesions across the different age and sex.

Table 9
Sex Distribution

Sex
No. of patients
Male 109
Female 122

Female
n=122
Male
n=109
Sex

Out of 231 patients studied 109 patients were male and 122 were female.

87

Table 10
Type of refractive error

Refraction
No of patients
Myopia 83
Hypermetropia 65
Emmetropia 83

Emmetropia
Hypermetropia
n=83
n=65
Myopia
n=83
Refraction
Following examination of the eyes, patients were diagnosed of refractive error.
83 patients did not have any refractive error. 83 patients had myopia and 65 patients had
hypermetropia.

88

Table 11
Age distribution with sex
Age in years
Male (%)
Female (%)
Total (%)
0-20
21 (19.27)
22 (18.03)
43 (18.61)
21-40
27 (24.77)
35 (28.69)
62 (26.84)
41-60
34 (31.19)
36 (29.51)
70 (30.30)
> 60
27 (24.77)
29 (23.77)
56 (24.24)
Total
109 (100.00) 122 (100.00) 231 (100.00)

Figure 3
35
Male
30
Female
Total
25
e
s
20
tag
15
Percen
10
5
0
0-20
21-40
41-60
> 60

The patients were divided into four age groups. The age distribution of the
patients as analyzed showed a maximum number of patients in the age group 41-60 years
and minimum number of patients were in the age group of less than 20 years

89

Table 12
Age distribution according to type of refractive error

Age in years
Myopia
Hypermetropia Emmetropia
0-20
19 (23.17)
8 (12.50)
16 (19.28)
21-40
19 (21.95)
13 (18.75)
30 (36.14)
41-60
23 (28.05)
21 (32.81)
26 (31.33)
> 60
22 (26.83)
23 (35.94)
11 (13.25)
Total
83 (100.00)
65 (100.00)
83 (100.00)

40
Myopia
35
Hypermetropia
Emmetropia
30
25
20
Percentages
15
10
5
0
0-20
21-40
41-60
>60

Age distribution of refractive error showed that majority of myopics belonged to

age group 41-60 years and majority of hypermetropics belonged to age group more than
60 years.

90

Table 5
Incidence of Peripheral Retinal lesions
Lesions Total
Incidence
1.Cystoid degeneration
231/231 (100.00%)
2.Lattice degeneration
23/231 (9.96%)
3.Paving stone degeneration
48/231 (20.78%)
4.WWP 67/231
(29.00%)
5.Retinoschisis 9/231
(3.89%)
6.Partial thickness retinal tear
25/231 (10.82%)
7.Full thickness retinal tear
7/231 (3.03%)
100
Total Incidence
90
1.Cystoid degeneration
2.Lattice degeneration
80
3.Paving stone degeneration
4.WWP
70
5.Retinoschisis
6.Partial thickness retinal
e
60
tear
t
a
g
50
7.Full thickness retinal tear
Percen
40
30
20
10
0
1
2
3
4
5
6
7

Detailed fundus examination of all the patients was done and findings were
recorded. Cystoid degeneration was the most common peripheral retinal lesion present in
all the patients (100%), followed by WWP (29%), Paving stone degeneration (20.8%),
Partial thickness retinal tear (10.8%), Lattice degeneration (10%), Retinoschisis (3.9%)
and Full thickness retinal tear (3.3%).

91

Table 14
Incidence of peripheral retinal lesions according to type of refractive error present
Lesions
Incidence in Myopia
Incidence in
Incidence in
(%)
Hypermetropia
Emmetropia
(%)
(%)
1.Cystoid degeneration
83/83 (100.00%)
65/65 (100.00%)
83/83 (100.00%)
2.Lattice degeneration
11/83 (13.25%)
5/65 (7.69%)
7/83 (8.43%)
3.Paving stone degeneration
20/83 (24.09%)
12/65 (18.46%)
16/83 (19.28%)
4.WWP
26/83 (31.33%)
17/65 (26.15%)
24/83 (28.92%)
5.Retinoschisis
2/83 (2.41%)
4/65 (6.15%)
3/83 (3.61%)
6.Partial thickness retinal tear
11/83 (13.25%)
6/65 (9.23%)
8/83 (9.64%)
7.Full thickness retinal tear
3/83 (3.61%)
2/65 (3.08%)
2/83 (2.41%)

100
90
Incidence in
1.Cystoid degeneration
80
Myopia
2.Lattice degeneration
Hypermetropia
3.Paving stone degeneration
70
Emetropia
4.WWP
5.Retinoschisis
60
6.Partial thickness retinal
tear
50
7.Full thickness retinal tear
Percentage
40
30
20
10
0
1
2
3
4
5
6
7

The distribution of peripheral retinal lesions according to type refractive error

showed that all the lesions were more common in myopic patients except retinoschisis,
which was more common in hypermetropia.
92

Table 15
Percentage of bilateral lesions
Lesions Lesions
In
Bilateral Lesions
Lesions In eyes
patients
1.Cystoid degeneration
231/231 (100.00%) 231/231 (100.00%) 462/462 (100.00)
2.Lattice degeneration
23/231 (9.96%)
9/23 (39.13%)
32/462 (6.93%)
3.Paving stone degeneration
48/231 (20.78%)
17/48 (35.42%)
65/462 (14.07%)
4.WWP
67/231 (29.00%)
26/67 (38.81%)
93/462 (20.13%)
5.Retinoschisis 9/231
(3.89%)
1/9 (11.11%)
10/462 (2.16%)
6.Partial thickness retinal tear
25/231 (10.82%)
3/25 (12.00%)
28/462 (6.06%)
7. Full thickness retinal tear
7/231 (3.03%)
0/7 (0.00%)
7/462 (1.52%)

100
1.Cystoid degeneration
90
Lesions in patients
2.Lattice degeneration
Bilateral Lesions
80
3.Paving stone degeneration
Lesions in eyes
4.WWP
70
5.Retinoschisis
6.Partial thickness retinal
60
tear
7. Full thickness retinal tear
50
Percentage
40
30
20
10
0
1
2
3
4
5
6
7

The study showed that cystoid degeneration was 100% bilateral while lattice
degeneration; WWP and paving stone degeneration were bilateral in 39.13%, 38.81% and
35.42% cases respectively.

93

Table 16
Sex distribution of peripheral retinal lesions
Lesions
Lesion in Males Lesion on Females
1.Cystoid degeneration
109
122
2.Lattice degeneration
10
13
3.Paving stone degeneration
34
14
4.WWP 34
33
5.Retinoschisis 4
5
6.Partial thickness retinal tear
13
12
7. Full thickness retinal tear
3
4

140
1.Cystoid degeneration
Male
Female
2.Lattice degeneration
120
3.Paving stone degeneration
4.WWP
100
5.Retinoschisis
6.Partial thickness retinal
tear
80
7. Full thickness retinal tear
Number
60
40
20
0
1
2
3
4
5
6
7

The sex distribution of peripheral retinal lesions showed that all the lesions were
equally distributed except paving stone degeneration, which is more common in males.

94

Table 17
Age distribution of peripheral retinal lesions
Lesions
0-20yrs (%)
21-40 (%)
41-60 (%)
61and above
(%)
Cystoid degeneration
43/43
62/62
70/70
56/56
(100.0%)
(100.00%)
(100.00%)
(100.00%)
Lattice degeneration
4/43
6/62
7/70
6/56
(9.30%)
(9.67%)
(10.00%)
(10.71%)
Paving stone degeneration
9/43
13/62
15/70
11/56
(20.93%)
(20.97%)
(21.43%)
(19.64%)
WWP 2/43
18/62
20/70
27/56
(4.65%)
(29.03%)
(28.57%)
(48.21%)
Retinoschisis 0/43
0/62
5/70
4/56
(0.00%)
(0.00%)
(7.14%)
(7.14%)
Partial thickness retinal tear
5/43
6/62
8/70
6/56
(11.63%)
(9.67%)
(11.43%)
(10.71%)
Full thickness retinal tear
1/43
2/62
2/70
2/56
(2.33%)
(3.23%)
(2.86%)
(3.57%)

95

100
1.Cystoid degeneration
90
0-20 yrs
2.Lattice degeneration
21-40 yrs
3.Paving stone degeneration
41-60 yrs
80
4.WWP
61 yrs & Above
5.Retinoschisis
70
6.Partial thickness retinal
tear
7. Full thickness retinal tear
60
tage
50
Percen
40
30
20
10
0
1
2
3
4
5
6
7

Age distribution of peripheral retinal lesions showed that all the lesions were
equally distributed in all the age groups except retinoschisis and WWP. Retinoschisis is
present only in age group > 40 years. WWP is present in all age groups but is more
common in age group > 60years.Incidence of WWP increased with age.
96

DISCUSSION
The study undertaken included fundus examination of four hundred and sixty two
eyes of two hundred and thirty one patients attending out patient department of
Dr. B. R. Ambedkar Medical College and K. C. General hospital, Bangalore. A study of
various peripheral retinal lesions was done and incidence was calculated.

All the lesions were equally distributed in both sex except paving stone
degeneration, which is more common in males (M : F:: 2.5 :1). All the lesions were
present in all the age groups except retinoschisis, which was present in patients aged
more than forty years.

The present study shows that all the lesions were more common in myopic
patients except retinoschisis, which was more common in hypermetropes.

Cystoid degeneration was bilateral in all the cases. Lattice degeneration had
39.9% bilateral lesions while paving stone degeneration had 35.4% bilateral lesions and
WWP had 38.8% bilateral lesions.

This is similar to the results of study conducted by Norman E Byer3 and also
similar to the results of study conducted by Bradley R. Straatsma, Robert Y. Foos and
Stephan S. Feman.54

The results of study conducted by Bradley R. Straatsma, Robert Y. Foos and

Stephan S. Feman54 showed that cystoid degeneration is the most common peripheral

97

retinal degeneration present in 100% patients, paving stone degeneration is present in

22% of patients and lattice degeneration is present in 10.7% of patients.

Table
Comparison of incidence of peripheral retinal lesions in present study with the
study conducted by Bradley R. Straatsma, Robert Y. Foos and Stephan S. Feman54
Lesion Present
in
% Present
in % Significance
Patients (Earlier
Patients (Present
Study)
Study)
Cystoid
1173/1173 100 231/231 100 P>0.05
degeneration
Paving Stone
134/614 22 48/231 20.78
0.742
Degeneration
Lattice
86/800 10.7
23/231 9.96
0.730
Degeneration
There is no significant difference between earlier study and the
Inference
present study.

The results of this study also shows that cystoid degeneration is the most common
peripheral retinal degeneration, followed by WWP, paving stone degeneration, partial
thickness tear, lattice degeneration, retinoschisis and full thickness tear respectively

Hence it is important to maintain fundus drawings of all the patients so that

complications (like retinal detachment) of these degenerations can be prevented.

98

CONCLUSION
The results of this study show that in the periphery of the fundus cystoid
degeneration is the most frequent degeneration (100%), followed by WWP (29%), paving
stone degeneration (20.8%), partial thickness retinal tear (10.8%), lattice degeneration
(10%), Retinoschisis (3.9%) and full thickness retinal tear (3.3%). All the eyes examined
had one or the other degeneration.

Cystoid degeneration was present in all the eyes and was bilateral in all the cases.
Lattice degeneration had 39.9% bilateral lesions while paving stone degeneration had
35.4% bilateral lesions and WWP had 38.8% bilateral lesions.

All the lesions were more common in myopic patients except retinoschisis, which
was more common in hypermetropes.

Retinoschisis was present only in the patients’ aged 40 or more. All the lesions were
common in both the sexes except paving stone degeneration, which was more common in
male patients.

From this study I came to conclusion that all the patients in and around
Dr. B. R. Ambedkar Medical College and K. C. General Hospital have a high incidence
of peripheral retinal degenerations in their eyes. Therefore a detailed fundus examination
of all the patients attending the out patient department should be done. The fundus
drawings of all the patients should be maintained so that complications (like retinal
detachment) of these degenerations can be prevented.

99
SUMMARY
The study undertaken included fundus examination of four hundred and sixty two
eyes of two hundred and thirty one patients attending out patient department of
Dr. B. R. Ambedkar Medical College and K. C. General hospital, Bangalore. The
complete fundus examination of peripheral fundus was done. Findings of
ophthalmoscopy were recorded and following results are obtained.

The age and sex distribution showed that majority of the males and females
belonged to the age group of forty one to seventy years. Myopia was the more common
than hypermetropia. Most myopic patients belonged to age group forty-one to sixty
(27.7%), while most hypermetropic patients belonged to age group of sixty-one years and
above (35.4%). Most emmetropic patients belonged to age group twenty-one to forty
(36.1%).

The main parameter for this study was presence of any retinal lesion in the
peripheral retina of the patients examined, their incidence, bilateralism and their
association with refractive errors.

The peripheral retinal examination showed presence of one or the other retinal
lesion in all the patients. All the eyes showed presence of cystoid retinal degeneration.
Twenty nine percent of the patients showed WWP. Twenty percent of the patients
showed paving stone degeneration. Eleven percent of the patients showed partial

100

thickness retinal tear. Ten percent of the patients had lattice degeneration. Four and three
percent of the patients showed retinoschisis and full thickness retinal tear respectively.

The results of this study showed that cystoid degeneration is the most common
peripheral retinal degeneration, followed by WWP, paving stone degeneration, partial
thickness tear, lattice degeneration, retinoschisis and full thickness tear respectively.

All the lesions were more common in myopic patients except retinoschisis, which
was more common in hypermetropes. Cystoid degeneration was bilateral in all the cases.
Lattice degeneration had 39.9% bilateral lesions while paving stone degeneration had
35.4% bilateral lesions and WWP had 38.8% bilateral lesions.

All the lesions were equally distributed in both sex except paving stone
degeneration, which is more common in males (M : F:: 2.5 :1).All the lesions were
present in all the age groups except retinoschisis, which was present in patients aged
more than forty years.
101

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atrophic hole of lattice degeneration of the retina. Graefes Arch Clin Exp
Ophthalmol. 1983; 220 (4): 175-8.

107

53.
Stephen J. Ryan. Basic Science and Inherited Retinal Disease. Vol. 1. 2nd ed.
St. Louis, Mosby, 1994.

54.
William Tasman, Edward A Jaeger. Duane’s Clinical Ophthalmology. Vol. 3.
Philadelphia: Lippincott; 1989.

55.
Spencer LM, Foos RY. Paravascular vitreoretinal attachments: Role in retinal
tears. Arch Ophthalmol 1970; 84: 557.

108

PROFORMA
STUDY OF INCIDENCE OF PERIPHERAL RETINAL LESIONS IN PATIENT
ATTENDING OUTPATIENTS DEPARTMENT OF Dr. B. R. AMBEDKAR
MEDICAL COLLEGE HOSPITAL AND K. C. GENERAL HOSPITAL,
BANGALORE.

Name of the Patient:

Age:

Sex:
I. P No.:

O. No.:
Address:

•
Chief Complaint:

•
History of Presenting Illness:

•
Past Ocular History:

•
Vision:

Right eye

Left eye

•
Corrected Vision:

Right eye

Left eye

109

•
Refractive Error:

Right eye

Left eye

•
Slit Lamp Examination:
Right eye

Left eye

•
Intraocular Pressure:

Right eye

Left eye

•
Fundus Examination (Drawings):

Right eye

Left eye

•
Diagnosis:

Right eye

Left eye

110
111

MASTER CHART
Rt eye
Lt Eye
Sl. No.
Name
Pat.no.
Age
Sex
RE Lesion LE Lesion Combined Bilateral
correction correction
1
Shahina
433159
16
Female
M
M
CP
CP
CP
CP
2
Anuroopa
434586
19
Female
M
M
CP
C
CP
C
3
Vijay
434228
19
Male
M
M
CP
CP
CP
CP
4
Shabina
433877
23
Female
E
E
C
CF
CF
C
5
Nagaraju
431587
48
Male
M
M
CP
CW
CPW
C
6
Akbar
434499
41
Male
H
H
CP
CP
CP
CP
7
Mariyamma
434859
80
Female
M
M
CP
CPW
CPW
CP
8
Rehmathulla
433560
23
Male
M
M
C
CP
CP
C
9
Muniraj
425750
42
Male
M
M
CW
CW
CW
CW
10
John
433016
14
Male
M
M
CL
CL
CL
CL
11
Shahzadi Begum
433904
64
Female
E
E
CW
C
CW
C
12
Farida Khanumm
432544
63
Female
M
M
CP
CW
CPW
C
13
Makbul Jan
434457
55
Female
H
H
C
CP
CP
C
14
Shameen
434702
30
Female
E
E
CW
C
CW
C
15
K Veerbhadrappa
434345
57
Male
M
M
CW
CR
CRW
C
16
Suresh
433886
15
Male
M
M
C
CP
CP
C
17
Syed Jafar
422791
43
Male
M
M
C
C
C
C
18
Devrajamma
434434
62
Female
M
M
CR
C
CR
C
19
Syed Md
434046
61
Male
E
E
C
C
C
C
20
Krishnamurthy
435183
76
Male
H
H
CP
CP
CP
CP
21
Mustafa
431491
40
Male
H
H
CL
CW
CLW
C
22
Mohan Kumar
434624
58
Male
M
M
CW
CPW
CPW
CW
23
Malika
434451
45
Female
H
H
CW
CW
CW
CW
24
A S Kaleemulla
434200
76
Male
M
M
CP
CP
CP
CP
25
Tabassum
434084
35
Female
E
E
CW
CW
CW
CW
26
Mumtaz Begum
411558
65
Female
H
H
CW
CP
CPW
C
27
Goerge
431106
43
Female
M
M
CL
CL
CL
CL
28
Sharda
432837
14
Female
M
M
CL
CF
CFL
C
29
Kamrunissa
430638
50
Female
M
M
CL
CW
CLW
C
30
Hzeera
423922
33
Female
M
M
CW
CW
CW
CW
31
Praveen Taj
434331
61
Female
E
E
C
CW
CW
C
32
Sunadamma
429987
37
Female
H
H
C
CT
CT
C
33
Sunil
432326
15
Male
M
M
CT
C
CT
C
34
Ayesha Bee
434416
50
Female
H
H
CW
CR
CRW
C
35
Indrani
435145
73
Female
H
H
CW
CW
CW
CW
36
Shabana
431987
20
Female
M
M
C
CT
CT
C
37
Sunil
430541
18
Male
M
M
CW
CW
CW
CW
38
Ansar
434401
42
Male
H
H
CF
CR
CFR
C
39
Swaminadan
434472
65
Male
H
H
CW
CP
CPW
C
40
Sarasvati
393471
50
Female
E
E
C
C
C
C
41
Rajan
6963
62
Male
E
E
CW
CW
CW
CW
42
Gulzar
426446
32
Female
M
M
CL
C
CL
C
43
Rubiya
434888
75
Female
H
H
C
CW
CW
C
44
Shahnaz Banu
434717
15
Female
E
E
C
C
C
C
45
Vasantha
434326
45
Male
E
E
C
C
C
C
46
Abdul
434608
50
Male
E
E
C
C
C
C
47
Tabassum
427166
23
Female
M
M
C
CT
CT
C
48
Tanya
438337
65
Female
H
H
CW
C
CW
C
49
Gayulla
422281
45
Male
E
E
C
CW
CW
C
50
Bhagya
6939
55
Female
E
E
C
C
C
C
51
Rahim Beg
434207
61
Male
M
M
CPW
CW
CPW
CW
52
Pyari Jan
434741
65
Female
E
E
CW
CW
CW
CW
53
Azmal Pasha
430334
7
Male
E
E
C
CP
CP
C
54
Renuka
429443
27
Female
M
M
CW
CLW
CLW
CW
55
Anwar Pasha
431786
43
Male
M
M
CP
CP
CP
CP
56
Karim
434202
76
Male
M
M
CW
CW
CW
CW
57
Musibul Rehman
435163
10
Male
E
E
CP
CP
CP
CP
58
Rajeshwari
434414
45
Female
E
E
C
C
C
C
59
Bibijan
6599
70
Female
H
H
CW
CR
CRW
C
60
Ahmed
433998
72
Male
H
H
CR
CR
CR
CR
115

MASTER CHART
Rt eye
Lt Eye
Sl. No.
Name
Pat.no.
Age
Sex
RE Lesion LE Lesion Combined Bilateral
correction correction
61
Waheda Begum
431584
28
Female
M
M
C
C
C
C
62
Badrunissa
433075
46
Female
M
M
CP
C
CP
C
63
Pyari Jan
433989
57
Female
H
H
C
C
C
C
64
R nagaraj
434034
61
Male
E
E
CT
C
CT
C
65
Sathar Khan
366296
70
Male
M
M
CP
C
CP
C
66
Jayprada
435141
16
Female
E
E
C
CP
CP
C
67
Savithamma
433280
36
Female
E
E
C
C
C
C
68
Kamroon Hassan
433457
30
Female
E
E
C
C
C
C
69
Ajay
431030
25
Male
M
M
CT
C
CT
C
70
Balu
431570
45
Male
M
M
CP
CP
CP
CP
71
Saleema
434053
65
Female
M
M
CL
CL
CL
CL
72
Zarina
429415
38
Female
H
H
C
C
C
C
73
Nazeena
432133
30
Female
E
E
C
C
C
C
74
Anjum
431954
38
Female
E
E
C
C
C
C
75
Kumar
431485
32
Male
M
M
CW
CP
CPW
C
76
Shehzad
433698
48
Female
M
M
CP
CP
CP
CP
77
Rethi
434651
62
Female
E
E
C
CL
CL
C
78
Narayan Swami
6964
75
Male
H
H
C
C
C
C
79
LiyakatAli Khan
434487
41
Male
E
E
CW
C
CW
C
80
Leelavati
424235
45
Female
E
E
C
C
C
C
81
Rani
432182
28
Male
E
E
C
C
C
C
82
Abid
417019
11
Male
H
H
C
C
C
C
83
MukhtarPasha
432846
25
Male
M
M
CPW
CP
CP
CP
84
Khalid
433878
59
Male
H
H
CL
CL
CL
CL
85
Sather Khan
366290
76
Male
H
H
CL
CL
CL
CL
86
Sajjad
434006
62
Male
M
M
CL
CW
CLW
C
87
Shahana Begum
433904
64
Female
M
M
CT
CL
CLT
C
88
Sandhya
431736
35
Female
M
M
CW
C
CW
C
89
Khaleem Bee
403374
62
Female
H
H
CL
C
CL
C
90
Vivek
430139
15
Male
M
M
C
C
C
C
91
Rehana
426690
30
Female
H
H
C
C
C
C
92
Fathima Bano
434271
14
Female
E
E
C
C
C
C
93
Amanulla
6979
65
Male
E
E
CP
CW
CPW
C
94
Sudhanissa
433941
68
Female
M
M
CT
C
CT
C
95
Sardar
434402
25
Female
M
M
CP
CP
CP
CP
96
Manjula
433864
43
Female
H
H
C
CL
CL
C
97
Sahiba
420695
10
Female
H
H
C
C
C
C
98
Salman
434503
50
Male
E
E
C
CW
CW
C
99
Elvis
434521
42
Female
E
E
C
C
C
C
100
Gulzar
431675
35
Female
M
M
CP
CF
CFP
C
101
Srinivas
420428
50
Male
E
E
CW
CW
CW
CW
102
Rani
432463
22
Female
M
M
C
CP
CP
C
103
Nazia Begum
434747
18
Female
E
E
C
C
C
C
104
Shahid
434098
45
Male
H
H
CPW
CW
CPW
CW
105
Manik
421238
24
Male
H
H
C
C
C
C
106
Jayamma
415899
64
Female
M
M
CW
CW
CW
CW
107
Phool Kumari
434672
50
Female
E
E
C
C
C
C
108
Lingraju
424279
42
Male
E
E
CT
CT
CT
CT
109
Abbu
434133
30
Male
E
E
CW
CW
CW
CW
110
Kasif
423263
20
Male
H
H
C
C
C
C
111
Hina Parveen
433651
23
Female
E
E
C
C
C
C
112
Abdul Razzaq
434923
62
Male
E
E
CP
CW
CPW
C
113
Lalitha Naik
433890
85
Female
M
M
C
CF
CF
C
114
Rafiq Ahmed
424515
38
Male
H
H
CW
CW
CW
CW
115
Prabhakaran
430138
16
Male
M
M
C
C
C
C
116
Sarfunissa
434289
54
Female
E
E
CL
CL
CL
CL
117
Ziaulla Khan
433332
55
Male
H
H
C
CP
CP
C
118
Aftab Basha
434149
16
Male
E
E
C
C
C
C
119
Lakshmi
434154
38
Female
E
E
C
C
C
C
120
Md Zameer
434204
33
Male
E
E
C
CW
CW
C
115

MASTER CHART
Rt eye
Lt Eye
Sl. No.
Name
Pat.no.
Age
Sex
RE Lesion LE Lesion Combined Bilateral
correction correction
121
Shankar
421355
25
Male
M
E
CL
CLT
CLT
CL
122
Shamshad Begum
432768
50
Female
H
H
CT
C
CT
C
123
Hashim
434154
65
Male
H
H
CW
CW
CW
CW
124
Uma
428790
14
Female
H
H
CT
C
CT
C
125
Aslam
421328
38
Male
H
H
C
C
C
C
126
Imran
434323
17
Male
E
E
C
C
C
C
127
Ramesh
435121
65
Male
E
E
CP
CP
CP
CP
128
Lakshmi Devi
433261
74
Female
M
M
C
C
C
C
129
Rathma
417911
26
Female
M
M
C
C
C
C
130
Naszer Ahmed
428757
49
Male
M
M
CL
CL
CL
CL
131
Binu Joseph
433965
34
Female
E
E
C
C
C
C
132
Cecilia
427980
20
Female
H
H
C
C
C
C
133
Bee Bee
429000
51
Female
M
M
CT
CT
CT
CT
134
Soumya
434539
9
Female
E
E
C
C
C
C
135
Md Yusuf
430151
8
Male
M
M
C
C
C
C
136
Syed Azar
432777
45
Male
H
H
CT
C
CT
C
137
Abdul Gaffar
434799
65
Male
H
H
CW
CW
CW
CW
138
Pyaru
434607
54
Male
E
E
C
CL
CL
C
139
Haseena Bee
435142
62
Female
E
E
CR
C
CR
C
140
Syed Zakir
433504
32
Male
E
E
C
C
C
C
141
Mahalakshmi
434818
15
Female
E
E
C
C
C
C
142
Haseena
418446
35
Female
H
H
C
C
C
C
143
I Mercy
434583
29
Male
E
E
CP
CP
CP
CP
144
Noorjan
434311
39
Female
E
E
C
C
C
C
145
Salma
418048
22
Female
M
M
C
C
C
C
146
Asiya Beegum
428586
52
Female
M
M
CW
CW
CW
CW
147
Vijaylakshmi
432018
46
Female
H
H
C
C
C
C
148
Salma
429357
18
Female
M
M
C
C
C
C
149
Michael
433905
62
Male
M
M
CT
CT
CT
CT
150
Sheikh
434784
42
Male
E
E
CR
C
CR
C
151
Renuka
434898
18
Female
E
E
CLW
CL
CLW
CL
152
Mahadev
427945
45
Male
M
M
C
CT
CT
C
153
Rehmathulla
433560
23
Male
E
E
C
C
C
C
154
Rehman
427347
35
Male
M
E
CW
CW
CW
CW
155
Shahzadi Bee
431096
48
Female
H
H
C
C
C
C
156
Timothy
434779
45
Male
E
E
C
CP
CP
C
157
Syed Moin
428309
17
Male
M
M
C
C
C
C
158
Johnson
434518
21
Male
E
E
CP
CP
CP
CP
159
Lakshmi
434317
23
Female
E
E
C
C
C
C
160
Ramya
434802
14
Female
E
E
C
C
C
C
161
Anitha
438512
42
Female
M
M
CW
CW
CW
CW
162
Deendayal
433545
32
Male
E
E
C
C
C
C
163
Savir
433641
27
Male
E
E
C
C
C
C
164
Razia
428891
14
Female
M
M
C
C
C
C
165
Ghouzia shariff
428247
45
Female
M
M
C
C
C
C
166
Nawab
430288
55
Male
H
H
C
C
C
C
167
Rehmathunissa
355678
45
Female
H
H
C
C
C
C
168
Mohan Nathan
433904
82
Male
M
M
CW
C
CW
C
169
Mumtaz Ahmed
433898
72
Male
H
H
C
CF
CF
C
170
Zakira
425899
45
Female
M
M
C
C
C
C
171
Asma 428509
42
Female
M
M
CW
C
CW
C
172
Narayanamma
434387
30
Male
E
E
CW
CP
CPW
C
173
Upeksha
428695
12
Female
M
M
C
C
C
C
174
Ramachandra
434446
32
Male
E
E
CP
CW
CPW
C
175
Md Nasira
427386
38
Female
M
M
C
C
C
C
176
Joseph
433551
22
Male
E
E
C
C
C
C
177
Vasantha
430032
54
Female
H
H
C
C
C
C
178
Julia
429697
50
Female
H
H
C
C
C
C
179
Rishab
433514
75
Male
H
H
CT
C
CT
C
180
Dhanamma
428934
70
Female
M
M
CW
CW
CW
CW
115

MASTER CHART
Rt eye
Lt Eye
Sl. No.
Name
Pat.no.
Age
Sex
RE Lesion LE Lesion Combined Bilateral
correction correction
181
Shekhar
434308
22
Male
E
E
CT
CT
CT
CT
182
Mohan
427831
23
Male
M
M
C
C
C
C
183
Shreejith
434785
13
Male
E
E
C
C
C
C
184
Noorani
427615
45
Female
M
M
C
C
C
C
185
Md Salim
429493
45
Male
H
H
C
C
C
C
186
Sadiya
433411
70
Female
H
H
C
CT
CT
C
187
Muni Bai
433738
62
Female
M
M
CW
CW
CW
CW
188
Supriya
434479
22
Female
E
E
CT
C
CT
C
189
Asma Banu
422340
14
Female
M
M
C
C
C
C
190
Rashid
428601
42
Male
H
H
C
C
C
C
191
Vasanth
425369
42
Male
H
H
C
C
C
C
192
Raniamma
419313
65
Female
H
H
C
C
C
C
193
Manjunathan
382987
66
Male
M
M
C
CW
CW
C
194
Habeebunissa
433000
72
Female
H
H
C
C
C
C
195
Subhramaniyam
426767
48
Male
M
M
CT
C
CT
C
196
Mazibunissa
434943
50
Female
E
E
CP
CW
CPW
C
197
Yasmin
396820
24
Female
M
M
C
C
C
C
198
Abida
434502
30
Female
E
E
CL
CL
CL
CL
199
Maheshwari
435095
43
Female
E
E
CW
CW
CW
CW
200
Shahnaz
415806
15
Female
M
M
C
C
C
C
201
Gulab Jan
425631
50
Female
M
M
C
C
C
C
202
Raj
433822
24
Male
H
H
CP
C
CP
C
203
Basha Jan
434988
48
Male
E
E
CP
CP
CP
CP
204
Bebejan
433259
75
Female
H
H
C
C
C
C
205
Iqbal Ahmed
433521
65
Male
M
M
CW
C
CW
C
206
Naseema
434456
32
Female
H
H
C
CW
CW
C
207
Wasim Banu
426729
52
Female
E
E
C
CT
CT
C
208
Syedunissa
435010
50
Female
E
E
CT
C
CT
C
209
Khurshid
425927
50
Male
M
M
C
C
C
C
210
Abdul Rehman
415819
18
Male
M
M
C
C
C
C
211
Habeebunissa
433420
72
Female
M
M
C
C
C
C
212
Praveen
434319
34
Female
E
E
CW
C
CW
C
213
Amina Bee
434800
45
Female
E
E
C
CW
CW
C
214
Imran Pasha
433895
14
Male
H
H
CP
C
CP
C
215
Mushtaq Peer
6570
65
Male
H
H
CW
C
CW
C
216
Shahzadi Begum
6757
65
Female
M
M
C
C
C
C
217
Shabeer
432187
17
Male
H
H
C
CP
CP
C
218
Altaf
6999
45
Male
E
E
CP
CP
CP
CP
219
Tabassum
434075
25
Female
H
H
CW
CW
CW
CW
220
Azeem Ahmed
434614
26
Male
E
E
CP
C
CP
C
221
Lakshmi
434860
16
Female
E
E
C
CT
CT
C
222
Shabir Ahmed
392033
23
Male
E
E
CW
CLW
CLW
CW
223
Ranjan
434765
47
Male
E
E
CW
CP
CPW
C
224
Purshotam
435069
18
Male
E
E
CL
C
CL
C
225
Jayamma
433218
75
Female
H
H
C
C
C
C
226
Meera
434583
29
Female
H
H
CP
C
CP
C
227
Sarupamma
434829
55
Female
E
E
CR
CW
CRW
C
228
Fauzia
428071
11
Female
H
H
C
C
C
C
229
Vijay
434788
19
Male
E
E
CT
C
CT
C
230
Zakir
433111
76
Male
H
H
C
CW
CW
C
231
Syed Ataulla
358986
67
Male
H
H
C
C
C
C
115

KEY TO MASTER CHART

C
→ Cystoid
degeneration
E
→ Emmetropia
F
→
Full-thickness retinal tear
H
→ Hypermetropia
L
→ Lattice
degeneration
M
→ Myopia
P
→
Paving stone degeneration
R
→ Retinoschisis
T
→
Partial-thickness retinal tear
W
→ White
with
pressure

116