Clinical Ophthalmology Made Easy®

Clinical
Ophthalmology
Made Easy®
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Clinical
Ophthalmology
Made Easy®
A Samuel Gnanadoss
BD MS DO FIAMS
Dean and Professor of Ophthalmology
Aarupadaiveedu Medical College
Puducherry, India
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Clinical Ophthalmology Made Easy ®

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First Edition: 2009

ISBN 978-81-8448-611-7
Typeset at JPBMP typesetting unit
Printed at Ajanta
To
My wife Leela Samuel
Who stands by my side in everything in
my life
As she did so while I was writing
this book...
Preface
The basic clinical examination of eye and its adnexa

along with the diagnosis of some common ailments
are of importance to an ophthalmologist as well as to
general practitioners who, especially as family doctors,
have great responsibility to recognize the sight-
threatening problems and treat/refer them imme-
diately. Such basic eye examination, especially ocular
movements and pupil, is also a must for a neurologist
and physician—they are also aided by fundus study.
Such an examination commences with that of lids,
meanders through that of lacrymal apparatus and
eyeball, and ends with ocular movements. Sometimes,
the examination of a patient as a whole is called in—
more so if it is a case that requires neurology study.
Eye being window to the body cannot be ignored by
any physician/surgeon of any standing. Vision forming
90% of sensory input from external world underscores
the need for prompt diagnosis of any eye disease and
equally urgent therapy of such an ailment.
Needless to say, the first step is history elicitation,
which not only aids in the diagnosis but also helps in
eliminating unnecessary investigations (which have
nowadays become the fashion). Hence, this deserves
viii CLINICAL OPHTHALMOLOGY MADE EASY
our first attention before we go into clinical exami-

nation to basic details of common eye diseases and to
common instruments that are used in ophthalmology
which are asked in clinical examination.
This book is aimed at undergraduate students of
ophthalmology with an eye on their university exami-
nation. At the end are given certain common ques-
tions that are asked in the oral examination and
questions that have appeared frequently in university
theory examinations. But the need for basic ophthal-
mology knowledge for general practitioners and for,
to some extent, postgraduates is not lost sight of while
writing this book.
A Samuel Gnanadoss
Acknowledgements
I am grateful to Dr Kalavathy, Deputy Director of

Dr Joseph’s Eye Hospital, Trichy and Dr N Rajendran,
Professor of Ophthalmology, Tuticorin Medical
College for the excellent photographs they provided
for this book.
Dr Vidhyavathy, Associate Professor of Medicine,
helped me in writing the chapter on neuro-ophthal-
mology. My sincere thanks to her.
I must thank my Computer Operators, Sundara-
nathan and Arun, and technician Sundararaman for
their assistance.
Most of the line diagrams have been drawn by me.
They may lack the artistic touch. But it is my desire
that they should be scientifically accurate.
My gratitude to my wife Leela is great for putting
up with all the inconveniences I caused to her while
preparing this manuscript.
Last, but never the least, I am duty bound to thank
M/s Jaypee Brothers Medical Publishers (P) Ltd, New
Delhi especially Shri Jitendar P Vij (Chairman and
Managing Director), Mr Tarun Duneja (Director-Publi-
shing) and Mr Jayanandan (Chennai Branch) for their
useful suggestions and encouraging me to write this
book.
Contents
Introduction ............................................................ xiii

1. History Elicitation and Examination ................... 1
2. Lids ......................................................................... 15
3. Lacrymal Passage ................................................. 27
4. Conjunctiva ............................................................ 37
5. Cornea .................................................................... 65
6. Sclera ....................................................................... 95
7. Uveal Tract .......................................................... 103
8. Lens ....................................................................... 123
9. Glaucoma ............................................................. 149
10. Vitreous ................................................................ 175
11. Retina .................................................................... 183
12. Optic Nerve ......................................................... 209
13. Orbit ...................................................................... 223
14. Neuro-ophthalmology ....................................... 233
15. Squint .................................................................... 263
16. Ophthalmic Operations ...................................... 273
17. Instruments .......................................................... 299
18. Refraction ............................................................. 325
19. Dark Room Examinations ................................. 343
20. Ocular Therapeutics ........................................... 355
21. Community Ophthalmology ............................. 367
22. Frequently Asked Questions (FAQ)
in Oral Examinations.......................................... 391
23. Frequently Asked Questions (FAQ)
in Theory Examinations .................................... 401
Index ...................................................................... 407
Introduction
Ophthalmology is a subject which is easy to grasp and

the academic examination easy to get through. Proper
attention during theory classes and sincerity in clinical
postings can assure a pass in the examination. Devoting
just 30 minutes per day is enough to succeed in the
examinations without any last minute mugging up and
sweating.
THEORY
Stick to one standard book. Understandably books
vary in minor points. If needed supplement your
standard book by referring to other books. Going
through books on MCQ before examination will brush
up one’s knowledge of major points. Pay due attention
to photographs and diagrams in the standard textbook.
Do not underline and spoil the book. You may need it
later in life, or a poor junior may require it.
In written examinations, write in a neat and good
handwriting. Do not try to fill up pages. Write at least
20 to 25 lines per page. It is a good idea to answer
the questions first you know well. At the same time, it
is better you stick to the questions in the order in which
they are given in the question paper. Write clearly the
xiv CLINICAL OPHTHALMOLOGY MADE EASY
question numbers. Between two answers draw a line.

It is preferable to leave a small space after each answer
so that you can add later on any point you might have
missed. Draw diagrams wherever they are needed.
Highlight the important points but do not underline
too many points. Never use red pen/pencil anywhere
in your answer book (except in diagrams, if needed).
Remember – many examiners are “lazy”. So help them
to give you more marks.
CLINICAL AND ORAL

For clinical and oral examination, dress yourself well
and wear a clean doctor’s coat with the examination
register number attached to it.
In clinical examination, remember that you are
face- to-face with another human being (patient) for
the first time in your life in an examination. Spend a
few seconds establishing a rapport with him/her.
Never hurry into examining the patient. Ask for his/
her name, etc. and the complaints. Some patients who
have come for a few examinations before may not give
any reply unless you “take care of them”. You may
have to shell out some money (Author’s own expe-
rience about 40 years ago). Do not worry—anti-
corruption squad will not be around. Once paid, some
patients give the findings, diagnosis and even
treatment! (Again author’s experience).
It will be a good idea, during undergraduate oph-
thalmology examination, to shine the torch in the
patient’s eye in the beginning itself, to find out what
case you are given. Most of the time by such cursory
INTRODUCTION xv
examination you will be able to diagnose (If you cannot,

do not panic). This will help you in eliciting relevant
history and to decide whether general examination is
needed or not (in most of the cases it is not required).
When writing down, leave a small space after every
title (such as present history) so that you can add later
on what you think you have left out. But do not leave
a large space. The same is applicable while writing
down clinical findings. Do not make too many
alterations—it will look awful and the examiner is
liable to think that you got hints. Draw diagrams, if
needed.
Usually one long case and two short cases are given.
When you go to the examiner to present your cases,
you should remember the names of your patients, the
findings and the correct diagnosis for each one. Some
examiners get your paper and then ask you to present
the cases. When you are asked to give positive findings,
do not mention unwanted, normal, routine findings.
While presenting, keep going if you are not interrup-
ted. Stop only after you have given the provisional
diagnosis and treatment. Speak in a steady and uniform
speed. Do not keep looking at the examiner’s face after
mentioning every finding. This is a poor practice.
In orals you must be familiar and thorough with
ophthalmic instruments, the questions related to them
and certain other routine questions (all given at the
end of this manual). When instrument is given to you,
get it in your hand first and then answer. You must
have a good knowledge of refraction, especially if you
are wearing spects. You must have studied the answers
xvi CLINICAL OPHTHALMOLOGY MADE EASY
for the questions that were asked in your theory

question papers.
Do not forget the basic manners. Wish the
examiners first and get yourself seated only when you
are asked to. When you leave, thank the examiners—
even if they do not deserve it!
In clinical as well as oral if you do not know an
answer, it is better to use the statement, “Sorry sir, I
do not know,” rather than “Sorry Sir, I have for-
gotten”. Examiners know that you never knew the
answer, and not that you once knew it and forgotten
it. Also, if you do not know an answer say that instead
of keeping quiet and creating a deadly, uncomfortable
silence between you and the examiners.
If you are a student from another (linguistic) state,
it is better you learn the local language. In some busy
centers, you may get the interpreter late or may not.
After morning clinical exams, confirm the time
when orals are going to be. Do not leave the exami-
nation area immediately after orals. Very rarely you
may be called back.
1
History
Elicitation and
Examination
2 CLINICAL OPHTHALMOLOGY MADE EASY
HISTORY ELICITATION
As with other disciplines, examination of an eye patient

starts with the details of name, age and gender. Patient’s
religion is not so important. Trachoma is common
amongst Muslims especially if they pursue purdah habit.
Family history must be gone into when the case has a
hereditary basis or is a contagious one.
Patient’s domicile must be elicited to find out whether
the patient is from an endemic area for diseases such as
trachoma and leprosy. Nature of patient’s occupation is
equally important. Industrial workers and those
working with metals and glass are prone to injuries.
The socioeconomic status has some bearing on
conditions such as vitamin A deficiency, phlycten and
trachoma. So, patient’s socioeconomic status must be
elicited.
In undergraduate clinical examination, much of the
above details are not mentioned to examiner except
when specifically required. So much so many a time,
after ‘name, age and gender’, the candidate jumps to
patient’s complaints.
The patient’s complaints are recorded in chrono-
logical order and that too in patient’s own words. The
complaints alone are recorded first. Later, under “Pre-
sent history”, the complaints are elaborated – again in
chronological order. In clinical examination for under
graduates, the “Past history” is usually not mentioned
separately. It is clubbed with “Present history”.
The candidate must be careful in mentioning which
side eye he is talking about – right, left or both eyes—
while presenting “Complaints” and “Present history”.
HISTORY ELICITATION AND EXAMINATION 3
(The same concept must be applied when presenting

findings of ocular examination and when mentioning
diagnosis and treatment).
EXAMINATION
The clinical examination of an eye case starts with general

study of the patient. Attention must be directed towards
any congenital defects the patient has such as six fingers,
hypogenitalism, abnormal facial features and such other
abnormalities as preauricular skin tags. In general
examination signs of congenital and acquired syphilis,
of leprosy and tuberculosis must be looked for. One
should not miss examining nasal cavity, ear and sinuses.
The examination of eye begins with the face, eyebrows,
palpebral fissure and the eyeballs. Obvious squint
should not be missed. So also VII nerve paralysis. Quick
examination of eye can be done by three maneuvers:
(a) Pulling down the lower lid and pressing over the
lacrymal sac area (b) Everting upper lid (c) Keeping both
lids wide open. The last step facilitates study of anterior
segment, pupil, lens and checking of ocular movements
(Figs 1.1A to C). The illumination can be with torch
light. But better details are seen if examination of eyes
is carried out by oblique illumination along with loupe
(Fig. 1.2) or with slit-lamp (Fig.1.3).
In the anterior segment, the three essential points to
be looked for are (a) state of cornea, (b) pupil and (c)
depth of anterior chamber (A/C). It is not possible for a
beginner to assess anterior chamber depth accurately.
The eclipse test is useful— if light is shone from one side
into anterior chamber, if the chamber is shallow, the
Figs 1.1A to C: The three maneuvers for a quick examination of eye. In

the first step, the lower lid is pulled down to examine the inferior palpebral
conjunctiva and at the same time lacrymal sac area is pressed to check
for any regurgitation (Fig. 1.1A). In the next step, the upper lid is everted
to examine the upper palpebral conjunctiva (double eversion can be done
at this stage, if needed) (Fig. 1.1B). In the final step, the lids are kept
apart to examine the anterior segment of eye including pupil and lens
(Fig. 1.1C)
Fig. 1.2: The binocular loupe. It magnifies the image by two times
Fig. 1.3: Slit-lamp
other side half of the iris will be in shadow due to con-

vexity of iris. Pupil is studied for its size, shape, situation
and reaction to light – both for direct and consensual.
Patient’s vision should be recorded. The distance
vision is recorded with the help of Snellen’s chart
(Fig. 1.4). The illumination at chart should be at least
20 foot candles. The patient is seated 20 feet from chart.
The top letter of the chart is read by a person with
normal vision at a distance of 60 meters, the next line at
a distance of 36 meters and so on (3rd line at 24 meters
Fig. 1.4: Snellen’s chart for testing acuity of distance vision. Usually
there are seven lines (rows). The seventh line is 6/6 (The eighth line in
the chart is for 5 meter distance)
4th line at 18 meters, 5th line at 12 meters, 6th line at

9 meters and 7th line at 6 meters distance from chart). If
a person reads the 7th line at a distance of 6 meters,
then it is stated that he has a vision of 6/6, which is
normal vision. If one can read maximum, for instance,
only the 4th line at the same 6 meters distance then he
is said to be having a vision of 6/18. If at 6 meters if a
person is unable to read even the top line, then the
student shows his fingers from 5 meters to one meter
distance from the patient. If, for example, the patient

sees the finger at a distance of 3 meters, then he is said
to be having a vision of 3/60. If a patient is not able to
see the finger even at a distance of one meter, then he is
asked to count the fingers at 50 cm (written as CF 50
cm). Even if this vision is not present, observer’s hand
is moved across the eyes. If this is appreciated then it is
HM +. Finally, if even HM is not present, the patient is
asked if he can perceive a light thrown into his eyes. If
he can see light then projection of light is checked by
shining the light from all four quadrants. While
checking this, patient should be asked to look straight
ahead and not at the source of light.
Near vision is tested either with Roman test type
(notation used is N6, N8, N12, N18, etc.) or with Jaeger
chart (expressed as J7, J6, J5, etc) (Fig. 1.5).
Fig. 1.5: Near vision chart which is a hand held illuminated one.
But it is ideal that near vision is checked under usual room illumination
The refractive state of patient’s eye is tested

objectively by the procedure known as retinoscopy
using retinoscopy mirror and trial set. Instead of
retinoscopy mirror, many use streak retinoscope, which
is easier and has its own source of light.
Digital study of ocular pressure must be done. This is
carried out by keeping one index finger on the closed
upper lid of patient and with the other index finger
gently depressing the eye through the closed lid. The
fluctuation of globe under the lid is felt by the first index
finger (Fig. 1.6). This is very difficult to be appreciated
by a beginner. But with experience any change in ocular
pressure is appreciated. Tonometer such as Schiotz
tonometer (Fig. 1.7) or applanation tonometer (Fig. 1.8)
gives the correct value of intraocular pressure (Fig. 1.9).
Fig. 1.6: Assessing ocular pressure with fingers. One finger is stationary
and a gentle short pressure is applied to eye over the lid with the other
finger “to feel the pressure of the eye”
Fig. 1.7: Schiotz tonometer which is used for measuring the

intraocular pressure (IOP). It is one type of indentation tonometer
Fig. 1.8: Applanation tonometer

Fig. 1.9: Tonometry (procedure for measuring IOP)

with Schiotz tonometer
Checking the color vision may not be needed for the

undergraduates in the university examinations. But to
know it is essential for later life, especially if the student
takes up administrative post later on. Usually color
vision is checked with Ishihara chart (Figs 1.10A to F).
There are four sets of lettering in the chart:
1. In one set of charts the number in the chart can be
read by all.
2. In another set of charts the number is read differently
by persons with red-green blindness.
3. In certain other set of charts red-green blind cannot
read the numbers, which can be read by normal
persons.
4. In another series of charts the normal does not see any
number while the red green blind reads a number.
Figs 1.10A to F: Color vision chart (Ishihara). All the types

of charts are shown
Usually color blindness can be for red (protanopes

and protanomalous) or for green (deuteranopes and
deuteranomalous). If blindness for blue exists it is
known as tritanopes. The last condition is very rare (The
other methods of testing color vision are lantern test
using Edridge green lantern, Fransworth Munsell 100
hue test, Hologram’s wool test and Nagel’s anomalos-
cope).
Slit-lamp (biomicroscopy) study, fundus examination
(with indirect and direct ophthalmoscope or with 90
diopter lens) (Fig. 1.11), field analysis and other specia-
lized tests such as tonometry and gonioscopy to study
angle of anterior chamber are not usually required for
undergraduates.
Method of detailed examination of each part of the
eye and its adnexa, if needed, is dealt with in the
chapters dealing with them.
Fig. 1.11: + 90 D lens. Using this with slit-lamp one can

study the ocular fundus
2
Lids
Swellings of lids are usually kept for clinical exami-

nation. In theory examination, apart from swelling, tri-
chiasis and entropion or ectropion are asked.
Lids should be examined for any drooping, retrac-
tion, its normal shape, movements and for any swelling.
The lids can be in-turned or out-turned. The eye lashes
require the examiner’s attention for any absence, distor-
tion, discoloration (poliosis) or for the presence of scabs
or nits at their roots. Eversion of upper lid is to be done
to examine the upper palpebral conjunctiva. Shape of
the palpebral fissure should be studied.
ANATOMY
The eyelids have tarsal plates and muscles covered by

skin outside and conjunctiva inside. The enclosed mus-
cle is orbicularis oculi. In addition, upper lid has fibers
of levator palpebrae superioris (Fig. 2.1). Upper and
lower lids meet at canthi. Each lid has about
30 Meibomian (tarsal) glands which are modified
sebaceous glands, glands of Zeis (again modified seba-
ceous glands) and glands of Moll (which are modified
sweat glands). Each lid is supplied by medial and lateral
palpebral arteries. Motor nerves are from facial nerve,
oculomotor nerve and sympathetic. Sensory supply is
from trigeminal nerve.
The space between the two lids when the eye is open
is known as palpebral aperture.
The common diseases of lids are swellings and
inflammation.
LIDS 17
Fig. 2.1: Cross-section of upper lid. (A) Skin. (B) Cilia.

(C) Glands of Zeis and Moll. (D) Tarsal plate with embedded meibomian
gland. (E) Fibers of levator palpebrae superioris
SWELLINGS
The conditions that can frequently give rise to swellings

of lids are hordeolum externum (Fig. 2.2), hordeolum
internum and chalazion (tarsal cyst) (Fig. 2.3). Their
features and managements are given in Table 2.1 (If a
chalazion recurs repeatedly at the same site after
Fig. 2.2: Hordeolum externum with pus pointing to base of eye lash
Fig. 2.3: Chalazion. There is total absence of inflammatory

signs except for the swelling
LIDS 19
Table 2.1: Swellings of lids

H. externum H. internum Chalazion
Structure Glands of Zeis Meibomian Meibomian
affected and Moll (tarsal) glands (tarsal) glands
Etiology Infection Infection Low grade
(especially (especially inflammation
by staphylo), by Staphylo),
refractive refractive
errors, diabetes
errors, dia-
betes
Pathology Acute inflam- Acute inflam- Granulomatous
mation of the mation of
gland the glands
Onset and Sudden onset Sudden onset Insidious
duration with short with short onset and
duration duration chronic course
Symptoms Pain and Pain and Only swelling;
swelling of lids swelling of no pain
lids
Signs:
Swelling Nearer to skin Deep; more Deep; more
which is towards towards
adherent to it conjunctiva, conjunctiva,
Better seen skin can be skin can be
than felt pinched over pinched over
the swelling. the swelling.
Better felt Better felt than
than seen seen.
Pus To lid margin Towards Towards
pointing palpebral palpebral
conjunctiva conjunctiva
Contd...
Contd...
H. externum H. Internum Chalazion
Tenderness ++ ++ Nil
Manage- Local and Local and Surgery –
ment systemic systemic Incision and
antibiotics, antibiotics, Curettage
analgesics, analgesics, (I and C)
warm fomen- warm Capsule
tation and fomentation should be
drainage of and drainage removed.
pus (usually of pus No need for
by epilation) (by incision antibiotics
and drainage) Injection of
triamcinolone
into chalazion
curettage in an elderly person, one should think of

meibomian carcinoma).
INFLAMMATION OF LID MARGIN
It is called blepharitis. It is caused by infection

(especially staphylo), eye strain and parasites such as
demodex folliculorum (blepharitis acarica) and crab
louse (phthiriasis palpebrum) (Fig. 2.4).
Blepharitis is of two types (Table 2.2). Mixed type
can also occur.
For phthiriasis palpebrum, eserine is used locally.
POSITION OF LIDS
The lid may be abnormally turned, drooped or retracted.

Abnormal turning can be inwards (entropion) or
outwards (ectropion).
LIDS 21
Table 2.2: Types of blepharitis

Squamous Ulcerative
(Seborrheic)
Cause Metabolic; dandruff Infection, diabetes,
eye strain
Symptoms Discomfort; scales Itching, photophobia,
in lid margin; watering. Removal of
removal of scales— scales–Bleeding +
no bleeding
Features:
Lash No distortion Madarosis and
trichiasis +
Lid margin Normal Ulcers seen; tylosis
and yellow crusts+
Sequelae Nil Trichiasis, corneal
ulcer. Ectropion
Epiphora and eczema
of lid skin
Management Daily cleaning with Cleaning with 3%
baby shampoo; sodium bicarbonate.
treat cause; Deposits removed.
Good nutrition Antibiotic drops; treat
cause; treat sequelae
ENTROPION
Entropion can be: (a) cicatricial (due to scarring of pal-

pebral conjunctiva), (b) spastic (mostly lower lid is
affected; when Müller muscle or palpebral head of
inferior rectus degenerates; seen commonly in old age),
(c) involutional (in older individuals due to laxity of
posterior retractors of lid and canthal ligaments along
with atrophy of orbital fat). Entropion can be also
(d) congenital (due to tarsal plate abnormality or to
dysgenesis of lower lid retractors).
Fig. 2.4: Close-up of eye lashes showing the nits in a

case of phthiriasis palpebrum
Such an in-turning produces trichiasis, rubbing of

eyelashes on the cornea causing foreign body sensation,
epiphora and even corneal ulceration.
The in-turning may involve the posterior border of
lid upto the intermarginal strip or the whole lid margin
(in which cilia are also involved).
Management should be directed towards cause and
is mostly surgical correction, which differs according
to the etiological factors: (a) For cicatricial entropion
surgery such as modified Burrow’s or Jaesche-Arlt is
done to alter the direction of lashes or transplanting
the lashes. (b) Spastic entropion is managed by treating
the cause, using adhesive plaster, injection of botulinum
toxins and rarely surgery similar to that of senile
entropion and (c) For senile entropion, Wheeler’s or
Weiss operation is performed.
LIDS 23
ECTROPION
Ectropion is eversion of lid margin and eye lashes away

from eye. It is caused by: (a) scarring of skin of lid due
to trauma or burns (cicatricial), (b) laxity of suspensory
system of lower lid and of canthal ligaments (senile
ectropion), (c) paralysis of orbicularis oculi muscle
(paralytic), or (d) by mechanical factors. (e) Spastic is a
rare entity seen when lids are well supported.
The prominent symptom is watering from eye due
to punctal eversion from conjunctiva. Exposure keratitis
and dermatitis of lids are complications that can set in.
Management is mostly surgical. The procedures
employed are medial conjunctivoplasty (for senile type),
lateral tarsorrhaphy (for paralytic type), and V-Y
operation or Z plasty (for cicatricial type). Mechanical
and spastic ectropions are corrected by treating the
cause.
PTOSIS
Ptosis affects upper lid only and is due to paralysis of

levator palpebrae superioris or Müller’s muscle. It may
be unilateral or bilateral, partial or complete, congenital
or acquired. It is also classified according to the cause
into myogenic, neurogenic, mechanical and aponeu-
rotic. It is graded into mild, moderate and severe.
Apart from its cosmetic problem, a complete ptosis
produces amblyopia (defective vision) in the affected
eye. Pseudoptosis and Duane’s retraction syndrome
must be kept in mind. Horner’s syndrome and myas-
thenia gravis must be excluded.
Treatment is mostly surgery. Function of levator and
frontalis belly of occipito-frontalis, and presence of Bell’s
and jaw winking phenomena must be assessed before

operating, if there is need. Congenital ptosis is corrected
by Fasanella-Servat or by levator resection surgery.
Partial ptosis may not require correction, except for
cosmetic reason (Ptosis is not usually kept for under
graduate clinical examination).
LAGOPHTHALMOS
It is the inability to close the lids. (See Chapter 5 page 84)
TRICHIASIS
Trichiasis is inturning of eye lashes—a misdirection.

It is seen in trachoma, blepharitis and in any
condition that causes entropion of lids. Pemphigoid,
operations, severe local inflammation and burns are
other causes. Only one or a few lashes may be involved
(Fig. 2.5). In entropion the whole row of lashes may be
inturned.
Fig. 2.5: Trichiasis showing the in-turned lashes

LIDS 25
Symptoms are essentially that of lashes rubbing

against the cornea—foreign body sensation, pain,
watering and blepharospasm. Cornea is affected by
punctate keratitis, erosions or even by ulceration.
Management is by: (a) removing the concerned cilia
by epilation (may regrow) or (b) destruction of hair
follicle by eletrolysis or by diathermy and (c) Correction
of entropion, if it is present.
3
Lacrymal
Passage
Usually lacrymal gland is not for under graduate exami-

nations. Lacrymal sac and the nasolacrymal passage are
important for clinical and theory examinations.
Examination of lacrymal passage involves inspection
of sac area (for swelling), and pressure over it (for any
regurgitation of pus via punctum; pull down lower lid
for better view). Examine nasal cavity for hypertrophied
turbinate or for deviated nasal septum.
ANATOMY
Lacrymal sac is lodged inside lacrymal facia, which is

split periorbita. Sac is closely related to the two heads
of orbicularis and to angular vein. It lies in lacrymal
fossa. It has fundus, body and neck. The two canaliculi
empty in it separately or via a common canaliculus. Sac
empties into anterior region of inferior meatus through
nasolacrymal duct (NLD) (Fig. 3.1). The tear, secreted
Fig. 3.1 Anatomy of lacrymal passage: (A) Punctum, (B) Canaliculus,

(C) Common canaliculus, (D) Lacrymal sac, (E) Nasolacrymal duct.
Sometimes the two canaliculi may open independently into lacrymal sac
LACRYMAL PASSAGE 29
mainly by lacrymal gland, moistens the surface of

cornea and conjunctiva, enters canaliculus via punctum
and reaches sac. The orbicularis pumps the tear that is
in sac into NLD and then into nasal cavity. Tear film is
composed of three layers— mucus, aqueous and lipid.
The tear contains lysozyme.
Lacrymal sac can be involved in inflammatory
pathology—acute or chronic.
CONGENITAL DACRYOCYSTITIS
It is due to incomplete canalisation of lacrymal passage.
The obstruction is usually at the lower end of NLD. It is
prone to get infected. The parents notice watering from
eye one month after birth of the child. Cornea is of
normal size and there is no other ocular problem.
Watering is met with in ophthalmia neonatorum and
buphthalmos. In ophthalmia neonatorum watering
from eye occurs within 15 days of birth. In buphthalmos
watering from eye is met with one month or more after
birth and the cornea is large.
The management is by pressure over sac to empty
its content and application of antibiotic drops to eye.
This should be done three times a day and continued
for at least six months before giving up. Probing the
canaliculus and NLD is a one time cure. This must be
done carefully and it needs anesthetising the infant.
Syringing with antibiotic is also effective. Silicon tube
in NLD and kept for six months is another line of
treatment. If all fail, dacryocystorhinostomy (DCR) is
done.
CHRONIC DACRYOCYSTITIS
It is common in aged ladies and in poor people. It is

caused by obstruction to NLD by deviated nasal
septum, polyp or hypertrophied turbinate bone.
Majority of obstruction is at the valve of Krause and of
Hasner. Osteoma, bone fracture and calculi can also
cause block. Acute dacryocystitis may go onto chronic
stage.
The main complaint is watering from eye (chronic
catarrhal stage). Swelling over sac region is seen. Pressure
over it produces regurgitation of pus via canaliculus
and punctum or rarely through NLD. Probing reveals
the site of obstruction in some cases. If both entry and
exit of sac are blocked, the secretion accumulates inside
sac resulting in a considerable swelling (stage of lacrymal
mucocele). In this situation it can easily get infected
leading to infection of surrounding structures such as
cornea, or lead to acute dacryocystitis and abscess
(Chronic suppurative stage). Low grade infection repeated
over a long period of time results in small fibrous sac
(chronic fibrotic sac stage).
Dacryocystography with oil soluble radiopaque dye
shows the site of obstruction.
Management is by evacuation of sac by pressure and
local application of antibiotics in the eye. This may
succeed rarely. Repeated syringing (Fig. 3.2) with
antibiotics or probing may result in cure in some cases.
If these fail, either excision of sac (DCT) or DCR is done
(Fig. 3.3).
LACRYMAL PASSAGE 31
Fig. 3.2: Syringing the nasolacrymal passage. The direction of the

needle is at first vertical and then turned horizontally towards nose
Fig. 3.3: Dacryocystorhinostomy. An opening is made in the medial wall

of sac and in the lacrimal fossa (B) so that the tear goes straight into
nasal cavity from the sac bye passing the block (A)
DCT is done in: (a) Elderly (sac is atrophic; DCR is

difficult); (b) Shrunken sac; (c) Atrophic rhinitis (DCR
is difficult); (d) Sac being focus of infection such as
syphilis TB, trachoma and leprosy; (e) Tumors of sac,
and (f) Chronic dacryocystitis with ipsilateral corneal
ulcer or impending intraocular surgery. In some centers,
DCR is done instead of DCT for the last mentioned
indication. One should be very careful in rhinospori-
dium of sac, as there may be heavy bleeding during sur-
gery.
DCR is the surgery of choice in young patients.
Before DCR, the status of sac and NLD is assessed by
dacryocystography by linear tomography using oil
soluble dye.
Complications are ectropion, ulceration of cornea,
acute dacryocystitis and chronic conjunctivitis.
Intraocular surgery in an eye with ipsilateral chronic
dacryocystitis must be undertaken only after dealing
with the sac pathology.
ACUTE DACRYOCYSTITIS
A chronic dacryocystitis may get infected resulting in

acute dacryocystitis. The features are inflamed skin over
sac, pain, swelling over sac region along with reddening
of skin (Fig. 3.4). Some regurgitation via punctum occurs
on pressure over sac (if possible). There is tenderness if
sac region is pressed. It may form an abscess.
Complications are facial cellulitis, lid abscess,
inflammation of surrounding bone and corneal ulcera-
tion.
LACRYMAL PASSAGE 33
Fig. 3.4: Acute dacryocystitis
Management is by local and systemic antibiotics,

and analgesics. If there is abscess, it should be drained.
The condition either resolves or may result in
obstruction of NLD.
Remember
No need for antibiotics for chronic dacryocystitis; but
local investigations are needed. For acute dacryocystitis,
no local investigation; but antibiotic is needed and a
must.
WATERING FROM EYE
It can be epiphora (Normal secretion; but poor drainage)

or hypersecretion (Normal drainage; but excess tear
production).
Epiphora is due to obstruction to nasolacrymal

passage by dacryocystitis, scarring, stenosis or foreign
body. Obstructive cause can be at punctum, canaliculus,
sac or at NLD. It can be caused by malapposition of
punctum or by functional insufficiency of sac.
The course of dacryocystitis may be (Flow chart 3.1)
Flow chart 3.1: Dacryocystitis
Hypersecretory type is due to lacrymal gland

tumors (early stage), trichiasis, foreign body of conjunc-
tiva or cornea, conjunctivitis, scleritis, inflammation of
LACRYMAL PASSAGE 35
iris and ciliary body, glaucoma, psychogenic factors,

strong parasympathomimetic drugs or to orbital
cellulitis.
Constant wetting of lower lid due to epiphora may
produce skin excoriation, scarring and ectropion — The
last condition worsens the watering from eye and leads
to a vicious circle.
Before treatment is undertaken, patient should be
evaluated, the lacrymal passage checked for any
obstruction, the punctum for any eversion and the eye
for any factor which may result in hypersecretion.
Functional insufficiency is distinguished from anato-
mical cause by Jones dye test. In Jones primary test, fluo-
rescein is instilled into the conjunctival sac and its arrival
in inferior meatus is assessed by cotton kept in nose. If
negative, lacrymal passage is syringed (Jones secondary
test) and nasal cavity checked for any fluorescein.
Dacryocystography is also performed.
Treatment is directed mostly towards the causative
factor. If this does not relieve watering, DCR is done
for obstructive type when the problem is in NLD.
For hypersecretory type, the cause should be treated.
DRY EYE
Etiology
It may be due to deficiency of any of the three layers of
tear film. But the secretion of glands of conjunctiva is
more important than that of lacrymal gland.
1. Causes of lipid layer: Met with in chronic blepharitis.
2. Aqueous layer deficiency: Congenital or acquired
absence of tear secretion, Sjögren’s syndrome (Pri-

mary and secondary) and Riley Day’s syndrome.
3. Mucin layer defects: This is produced by hypovita-
minosis A, trachoma, conjunctival scarring, pemphi-
goid and burns of conjunctiva.
4. Improper lid closure as in lagophthalmos and ectro-
pion.
Features
Symptoms: Burning of eyes and foreign body sensation,
itching and dry feeling.
Signs: Dry eye is diagnosed by carrying out various tests,
which include rose Bengal staining, Schirmer’s test and
tear film break up time.
MANAGEMENT
Management of cause, if possible.
It is mainly symptomatic.
1. Preservation of any tear that may be present by using
protective glasses or by punctal occlusion.
2. Use of tear substitutes.
3. Use of hydrophilic bandage lenses.
ophthalmologyebooks.com
4
Conjunctiva
Conjunctival diseases are the cases that are frequently

kept in undergraduate clinical examinations. ACCO,
spring catarrh, trachoma, phlycten, pterygium, subcon-
junctival hemorrhage and Bitot’s spots are some of the
cases that are kept frequently for clinical examination.
In oral examination also many of the questions are
from this chapter. So, a good knowledge of conjunctival
diseases is a must for undergraduates (and for general
practitioners), since these diseases are seen so well and
alarm the patients so much.
The three maneuvers mentioned in chapter on
“Examination” facilitate study of conjunctiva. Eversion
of upper lid must be done. One should look for dryness,
scarring, adhesion, swelling, congestion and
discoloration. Follicles and papillae must be looked for.
ANATOMY
Conjunctiva joins globe to lids and has three portions—

palpebral (lining the inner side of lids), bulbar (which
is partly over the sclera) and the connecting fornix. Near
the inner canthus is plica semilunaris – remnant of
nictitating membrane of lower animals. Conjunctiva
joins cornea at limbus. At limbus conjunctiva, Tenon’s
capsule and episcleral tissue are firmly adherent.
Arterial supply is from arterial arcades of lids and
anterior ciliary arteries—former supply palpebral
conjunctiva, fornix and part of bulbar conjunctiva, and
the latter supply rest of bulbar conjunctiva around the
cornea through its anterior conjunctival branches. Nerve
supply of conjunctiva adjacent to cornea is from long
ciliary nerves and that of rest of conjunctiva is from first
division of trigeminal nerve.
CONJUNCTIVA 39
INFLAMMATION (CONJUNCTIVITIS)
Inflammation of conjunctiva due to any cause is called

conjunctivitis.
A simple classification is given in Flow chart 4.1.
Flow chart 4.1: Conjunctivitis—classification
They are the commonest affections. In these condi-

tions the secretion can be serous, mucopurulent or
purulent. The inflammatory reaction results in follicles
(in follicles cells are more and vessels are less), papilla
(wherein vessels are more and cells less), granuloma or
membrane. The symptoms range from foreign body
sensation to severe pain in eye.
Infective Conjunctivitis
Infective conjunctivitis may be acute or chronic. The
former is mainly classified into catarrhal (mucopuru-
lent), purulent and membranous.
The infective agents may come:

a. From outside by air, dust, water or fomites.
b. From surrounding structures such as lids and sac.
c. Very rarely via bloodstream.
ACUTE CATARRHAL CONJUNCTIVITIS (ACCO)
It usually has mucopurulent discharge. It is caused by

bacteria and rarely by virus (such as that of measles).
The common bacteria are Koch-Weeks, Staphylococcus
and Streptococcus. Organisms are from outside, from
surrounding structures or from an endogenous focus.
Patient complains of foreign body sensation (“sand
in the eye” feeling), sticking of lids together when
getting up from sleep and discharge near canthi and
over lid margin. Patient may give history of seeing
halos.
It can be either unilateral or bilateral. Lids are
swollen. The eye shows conjunctival type of congestion
(i.e. redness more at fornix) (Fig. 4.1) and matting of
eyelashes. Discharge is seen near medial canthus.
Petechial hemorrhages may occur. In viral conjunctivitis
the signs are less severe and the discharge is mostly
watery. It can lead to chronic conjunctivitis, marginal
corneal infiltration or frank corneal ulcer (if cornea gets
scratched).
Management
Management includes prevention of spread to other eye
(in unilateral case) or to other members of family.
Antibiotic drops are instilled into the unaffected eye.
CONJUNCTIVA 41
Fig. 4.1: Acute catarrhal conjunctivitis. The congestion is

mostly at the fornix and palpebral conjunctiva
The patient is isolated and other family members should

use local antibiotics.
Curative methods include washing the eye with
normal saline either with a cup (Fig. 4.2) or with an
undine (This washes away discharge and organisms).
Hourly antibiotic drops are used locally. Mostly genta-
micin, framycetin or ciprofloxacin is used. Silver nitrate
was once used. It acted (a) as antiseptic, (b) by increasing
local blood supply, and (c) by forming an eschar in
which the organisms got entangled and were removed.
It is better to avoid local cortisone. Decongestant such
as naphazoline locally gives relief and clears redness.
Ointment is applied before going to sleep to prevent
glueing of lids together when the patient gets up after
sleep.
Fig. 4.2: Cup. This is sometimes used to wash the eye. It is filled
with water (or saline), kept over the eye and the patient blinks
Purulent Type
This occurs in newborn (ophthalmia neonatorum) or
in adults (adult blenorrhea).
Ophthalmia Neonatorum
Ophthalmia neonatorum is due to N. gonorrhoea, Sta-
phylococcus, Pneumococcus, Streptococcus and virus.
Sometimes chemicals applied locally can cause this
condition. Latent period depends upon the causative
organism and it can be from three days (staphylococcus)
to two weeks (virus).
In newborn, infection may set in before birth (due
to premature rupture of membrane), during birth
(if eyes are open and birth canal is infected) or after
birth (from fomites and from dirty fingers of midwife,
CONJUNCTIVA 43
the doctors or relatives). As tear is not secreted unto

four weeks after birth, any watering from eye within
two weeks of birth should arouse suspicion.
Acute blenorrhea has three stages: In the first stage
(stage of infiltration) lids are swollen, conjunctiva is
chemotic and preauricular lymphadenitis is present.
General malaise is seen. There is watering from eyes.
As mentioned earlier, tears are produced one month
after birth only. Hence, any watering from eye within
two weeks of birth should alert the ophthalmologist/
pediatrician for the possibility of ophthalmia neo-
natorum.
In the next stage (Stage of blenorrhea) pus runs down
the cheek while other signs subside (Fig. 4.3).
If untreated the final stage of slow healing sets in with
complications.
Fig. 4.3: Ophthalmia neonatorum. Stage of blenorrhea

Complications are very dangerous. Cornea is easily

involved, as new born cornea is more prone for getting
infected. This is because (a) N. gonorrhoea penetrates
cornea even with intact epithelium, (b) Corneal
epithelial layers are less thick and (c) The conjunctival
chemosis at limbus jeopardises the nutrition to cornea.
The resultant corneal ulcer may lead to loss of eye and
the sight.
Xerosis and symblepharon are other complications.
Iritis and urethritis may be met with:
Adult Type
Adult type is almost the same as that of newborn except
for the mode of infection. There is more systemic
involvement such as endocarditis and septicemia.
Systemic therapy is also more relied upon in adult type.
Management in newborn includes prevention-
cleanliness before, during and after delivery, and proper
antenatal check-up. In suspected case, silver nitrate 1%
drops are used locally (silver nitrate is smeared over
the conjunctiva and then washed away. This is done
once in each eye. It should not touch the cornea. Crede’s
method). Locally erythromycin also can be used.
Once the disease has set in, management is by
frequent instillation of penicillin drops, ofloxacin, bac-
tricin, ciprofloxacin, tobramycin or moxifloxacin. Peni-
cillin drops (10,000 units/cc) is instilled once a minute
for 5 minutes, once in 5 minutes for 30 minutes, half
hourly for two hours and then second hourly for two
days (Sorsby’s method). While applying drops, cornea
should not be scratched. If there is response, it will be
CONJUNCTIVA 45
obvious by the end of two hours. Pus need not be

cleaned. Since penicillin resistant organisms are
appearing, systemic cefotaxime or norfloxacin is used.
In adults one injection of 1 g of cefotaxime or norfloxacin
1 g for 5 days is effective. Corneal problem must be
adequately dealt with. Chlamydial infection responds
well to tetracycline.
MEMBRANOUS CONJUNCTIVITIS
It is characterized by membrane formation over palpebral

conjunctiva. C. diphtheriae is the most feared causative
agent. The others are Staphylococcus, Streptococcus,
N. gonorrhoeae and virus. Most important source of the
organisms is nasal cavity. Burns—either chemical or
thermal—also produce membrane. The reaction may
range from minimal lid swelling, serous discharge and
peelable membrane over palpebral conjunctiva (mild
cases, pseudomembranous type) (Fig. 4.4) to brawny lids,
severe chemosis and membrane firmly adherent to
conjunctiva which, when peeled, leaves behind bleeding
points (true membranous type). The type of reaction (true
or pseudo membrane) has no relation to the etiological
agent. The disease process has three stages – infiltrative,
suppurative and cicatricial.
Complications
Complications are symblepharon, xerosis, and trichiasis.
More important is corneal ulcer. Cornea is involved
easily since (a) C. diphtheriae invades cornea even with
intact epithelium and (b) There is reduced nutrition to
cornea due to inflammation and chemosis of conjunctiva
at limbus.
Fig. 4.4: Membranous conjunctivitis. The membrane is

present over palpebral conjunctiva of lower lid
During treatment, one should not try to differentiate

pseudomembranous type from true membranous type.
This differentiation is only of academic interest and is
not absolutely needed. To differentiate between these
two types clinically, membrane should be peeled off.
If this is done in a true membranous type, the small
conjunctival vessels are torn. The exotoxin of
C. diphtheriae (if this is the etiological agent) might gain
access to circulation and affect the heart and kidney.
Starting the therapy should not wait for microbiological
report. To get this report takes around 48 hours and to
wait this long in a diphtheritic case is dangerous.
So, all cases of infective membranous conjunctivitis
must be considered as diphtheritic unless otherwise
proved. Local (10,000 units per cc every 30 minutes)
and systemic penicillin, and local hourly and systemic
CONJUNCTIVA 47
(20,000 units every 12 hours) antidiphtheritic serum are

administered. All cases of infective membranous con-
junctivitis, especially if diphtheritic, should be imme-
diately referred to a pediatrician.
Once the bacteriology report is negative for
C. diphtheriae, the treatment is changed to that of acute
catarrhal conjunctivitis.
ANGULAR CONJUNCTIVITIS
It is a chronic type caused by M. lacunata and rarely by

Staphylococcus. There are excoriation of skin of lids and
localized congestion of conjunctiva near canthi. The
proteolytic enzyme secreted by the organism causes
excoriation. There are suggestions that this condition is
also due to riboflavin deficiency.
Symptom
Symptom (discomfort) is minimal. Blepharitis and rarely
marginal or central corneal ulcer with or without
hypopyon are seen in long standing cases. Hyperemia
of lid margins and congestion of bulbar conjunctiva
along with excoriation of skin are seen near the canthi.
Treatment
Treatment is started with zinc eye drops, which
neutralizes the proteolytic enzyme produced by the
organism. With proteolytic enzyme neutralized there
is no more excoriation of skin. The organisms residing
amongst these dead skin scales are now exposed. If local
tetracycline ointment is used now, it is effective against
the ‘exposed’ bacteria.
Riboflavin (10 mg per day) is also given.
TRACHOMA
It is a chronic conjunctivitis caused by Chlamydazoa

trachomatis A, B and C strains. It is characterized by
follicles, scarring and complications.
It is known from ancient times. Trachoma is common
in Mediterranean countries, Central Asia, South
America and North India. It is said to be prevalent
amongst Muslims and economically backward society.
Flies, fingers and fomites transmit it.
Features
Conjunctiva shows redness, follicles and finally scarring.
The follicles, about 3 to 5 mm in size, are of lymphocytes
and other cells with minimal vessels (Fig. 4.5). Necrosis
occurs in them in late stage. Leber cells are seen. Follicles
Fig. 4.5: Case of trachoma (follicular stage)

CONJUNCTIVA 49
are seen in fornix, palpebral conjunctiva and sometimes

over plica, caruncle and, rarely, over bulbar conjunctiva.
Papillae (more of vessels and less of cells) are also seen.
Halberstaedter-Prowazek (HP) bodies are seen in the
epithelium. Scarring starts as stellate scars at line of Arlt
in upper palpebral conjunctiva (Fig. 4.6). Later the whole
conjunctiva is involved turning it into a parchment like
tissue.
The corneal epithelium is involved simultaneously
with conjunctiva and shows avascular superficial
punctate keratitis. This later on gets vascularized and
turns into pannus. In the early stage, the area of cellular
infiltration in cornea is in front of vessels (progressive
pannus). As disease subsides, the infiltration starts dis-
appearing and then the vessels are in front of the
infiltrated area (regressive pannus). The pannus may
completely resolve (except for empty vessels) or may
Fig. 4.6: Trachoma—early scarring

starting in the line of Arlt
leave behind corneal scar. Limbus shows follicle – like

infiltration (Herbert follicles). Herbert’s pits are scars at
limbus left behind by Herbert follicles.
Macallan first grouped the clinical features into
stages. WHO has put forth an alternate classification
(FISTO). Following table compares these two classifi-
cations (Table 4.1).
Third way of classification (Jones’ classification) is as
follows:
1. Blinding trachoma: It is caused by serotype A, B, Ba
and C. Secondary infection is seen.
2. Non-blinding trachoma: Same as above; but infective
element is absent. It is a mild form.
3. Paratrachoma: The infection is from genitals to eye. It
is caused by serotype D to K.
Complications of trachoma are (Table 4.2):
Diagnosis
Diagnosis is by microimmunofluorescence test, culture
on McCoy cells (costly) and by clinical features –
Follicles in upper palpebral conjunctiva, corneal scarring
in superior quadrant, pannus at the same site and limbal
follicles (Herbert pits). Presence of any two of these signs
is diagnostic.
Trachoma has to be differentiated from conditions
giving rise to follicles and from spring catarrh.
Treatment
It was once a prolonged one with sulpha drugs. Now
orally rifampicin, tetracycline (not for children and
Table 4.1: Staging of trachoma—a comparison
Macallan WHO Features Remarks
Stages Stages Conjunctiva Cornea
I. Infiltrative Immature SPK

follicle
II. Follicles
Follicles Florid follicle Pannus Properly treated at this
Intense (IIa) Papillae (Progressive) stage there is no
(IIb) scarring
III. Scarring Scarring Follicles along Pannus

with scarring (Regressive)
IV. (Complications) Trichiasis Scarring
complete Opacities cover
Opacities Complications pupillary area +
set in corneal scar
(Comparison of the above two methods of classification is schematic)
CONJUNCTIVA
51
Table 4.2: Complications of trachoma

Complications Causes
• Ptosis (a) Increase in weight of lid due to
follicles
(b) Destruction of elevators of lid
• Sinuous lid margin Softening and twisting of tarsal plate
• Entropion Contraction of conjunctival scar
• Trichiasis Entropion
• Corneal ulcer Trichiasis and corneal follicles
• Dry eye Destruction of conjunctival glands
• Symblepharon Inflammation; dry eye
• Chronic dacryocystitis Direct invasion by organism
pregnant ladies) or erythromycin (250 mg × qid) is given

for four weeks. Oral doxycycline (100 mg bid) for 3 to
5 weeks is curative. Locally erythromycin or tetracycline
(1%) applied four times a day combined with sul-
facetamide (20%) and used for six weeks gives equally
good result. Easier is azithromycin (1 gm) as a single
dose. These drugs eliminate the causative organism as
well as any secondary infection. Attention must be
directed towards complications.
Allergic Conjunctivitis
Allergic conjunctivitis is another group, which is impor-
tant. Vernal and phlycten are the important allergic
conjunctivitis.
VERNAL CONJUNCTIVITIS
It is otherwise known as spring catarrh or seasonal

allergic conjunctivitis. It is caused by exogenous aller-
CONJUNCTIVA 53
gen such as pollen. It is seen in young patients (5 to 15

years) and occurs mostly during summer. It may be
present throughout the year. Itching is the prominent
symptom. “No itching no spring catarrh” is an apt state-
ment. Photophobia and watering are present. Spring
catarrh is present either as palpebral form, bulbar form
or mixed form.
In palpebral form flat topped, milky white, large
(5 mm) papillae are seen mostly in upper palpebral
conjunctiva (Fig. 4.7). It appears like milk spilt upon
cobble stone. Bulbar form presents as discrete, white,
gelatinous thickenings at limbus. It may also be present
all around limbus like an epaulette. Discrete white
raised dots (Tranta’s dots) are seen at limbus.
These two forms can be associated with SPK or with
shield ulcers (Fig. 4.8) in upper part of cornea. The other
Fig. 4.7: Vernal conjunctivitis (palpebral form). The large cobble

stone like papillae with white hue are seen
Fig. 4.8: Shield ulcer. This is a rare complication of

vernal conjunctivitis
corneal sequelae are pseudogeronotoxon, subepithelial

scarring, corneal plaques and keratoconus. Mixed form
is also met with.
The secretion in all these three types is ropy, scanty,
acidic and contains plenty of eosinophils—the last one
indicates that this is IgE mediated type I hypersensitivity
reaction.
Management
Management is that of symptom—local steroid,
disodium cromoglycate (2%), antihistamine drops and
cold compress. Olopatadine is used twice a day. Compli-
cations of local steroid must be kept in mind. In severe
cases cyclosporine (1%) drops are used. Sticky mucus
CONJUNCTIVA 55
is relieved by local acetyl cysteine (10%). Rarely cryo or

beta radiation may be applied to papillae. Local
naphazoline reduces itching. Subtarsal injection of
triamcinolone is tried.
PHLYCTENULAR CONJUNCTIVITIS
In contrast to vernal conjunctivitis, this is caused by

endogenous allergen, which is mostly bacterial especially
of M. tuberculosis. Others are Staphylococcus and Morax-
Axenfeld. Long standing infection of tonsils or adenoids
is associated with this condition.
It is due to delayed hypersensitivity response (Type
IV). Affecting undernourished children, it is seen in
bulbar and rarely in palpebral conjunctiva as gray,
round, small nodule (Fig. 4.9). Congestion is seen
around the nodule. It may be single or multiple. Necrosis
or ulceration of the apex of the nodule occurs.
Fig. 4.9: Phlycten seen near the cornea

Recurrence is common. Pure conjunctival lesion has

very few symptoms such as irritation and watering.
It has no complication.
Limbal nodule can involve cornea resulting in fasci-
cular ulcer. In this type of ulcer, a leash of vessels runs
to the ulcer. The other types of corneal involvement are
miliary ulcers over whole of cornea, scrofulous ulcer
(shallow marginal ulcer at the limbus with no clear
cornea between it and limbus) and diffuse infiltrative
keratitis occurring in the middle of cornea which is
heavily vascularized from limbus. When miliary
phlycten heals up, it leaves behind scars, which are
known as Salzmann degeneration.
Treatment
Treatment is by local cortisone and wearing dark
glasses. Antibiotics and cycloplegics are called in if
cornea is involved. Opinion differs about use of anti-
tuberculous treatment and desensitization with
tuberculin. Any septic focus must be taken care of.
General nutrition must be attended to.
PINGUECULA
It is met with in the aged persons. It is seen as a trian-

gular patch in the conjunctiva over palpebral fissure
near the limbus; but not involving the cornea. It is yellow
in color. It is due to dust, sunlight and wind. It is hyaline
degeneration and elestotic changes in the submucous
tissue. It may grow over cornea as pterygium.
Treatment is not needed.
CONJUNCTIVA 57
PTERYGIUM
It is a subconjunctival degeneration caused by dust and

ultraviolet rays. Sometimes pinguecula may grow as
pterygium. Seen usually in persons above the age of 50
in both genders, its main symptom is cosmetic followed
by defective vision. The latter is due to astigmatism and
rarely to pterygium encroaching onto pupillary area,
causing mechanical obstruction to light rays. In very
large pterygium diplopia is met with and this is due to
restriction of ocular movements by the growth.
It is a triangular growth and has three parts—head
or apex over cornea, neck at limbus and the larger
portion, the body (Fig. 4.10). In the beginning pterygium
is fleshy and thick (progressive pterygium). When growth
ceases it appears as a fibrous tissue (regressive pterygium).
It is mostly seen over nasal side of cornea.
Fig. 4.10: Pterygium. It is seen here at the typical site—over palpebral

fissure. Since this is fleshy, it is of progressive type
It has to be differentiated from pinguecula (latter does

not encroach onto cornea) and pseudopterygium. Pseu-
dopterygium is a sequel of marginal corneal ulcer to
which the inflamed conjunctiva gets stuck up. Unlike
pterygium, it occurs at any age, involves any area of
limbus and it is stationery. A probe can be passed under
the growth at limbus (probe test).
Management
a. By releasing the head and body of pterygium and
excising them
b. By implanting the released head under the
conjunctiva or
c. After excision, covering the conjunctival defect with
graft. Pterygium is well-known to recur after sur-
gery. In such a case locally Mitomycin C drops, thio-
tepa (1: 2000) or beta radiation (1500 rads) is used
after surgery.
If the pterygium is extensive and encroaching onto
the pupillary area then a lamellar grafting is done after
freeing and excising the pterygium.
BITOT’S SPOTS
Bitot’s spots are associated with conjunctival xerosis.

The latter can be paranchymatous (as in scarring or long
exposure) or epithelial. Bitot’s spots occur in epithelial
xerosis (The term xerophthalmia usually denotes
dryness of eye and its sequelae caused by vitamin A
deficiency).
Bitot’s spots is mostly a manifestation of vitamin A
deficiency and is associated with dryness of conjunctiva.
CONJUNCTIVA 59
If the deficiency is not corrected it may lead to corneal

ulceration resulting in keratomalacia (corneal ulcer) and
blindness in children.
Bitot’s spots are seen temporal to cornea as
triangular aggregation of silvery white flakes with its
base towards cornea (Fig. 4.11). Amongst these flakes
is C. Xerosis producing gas resulting in foamy nature
of these spots (Fig. 4.12). Conjunctiva is dry and dusky.
The patient may have night blindness. It corresponds
to X1B of WHO Classification of vitamin A deficiency.
The treatment is with vitamin A 1,00,000/- units per
day for ten days. The causative factor for avitaminosis
A and nutrition must be attended to. While treating with
vitamin A the possibility of hypervitaminosis A must
be kept in mind. So also the possibility of oral vitamin
A being not absorbed must be borne in mind. Any
protein deficiency must be corrected.
Fig. 4.11: Bitot’s spots

Fig. 4.12: Bitot’s spots with pigmentation and frothy material
SYMBLEPHARON
It is adhesion of palpebral conjunctiva to bulbar conjunc-

tiva due to raw surfaces in them (Fig. 4.13). It follows
trauma, burns, trachoma, Stevens-Johnson and dry eye.
The adhesion may get fibrosed. Lagophthalmos with
its problems is seen in severe cases of symblepharon.
There are three types: The adhesion can be between lid
margin and limbus (anterior type), at fornix (posterior
type) or may involve whole of palpebral and bulbar
conjunctiva (total type) (Fig. 4.14).
Prevention is the best by using therapeutic bandage
lens. Treatment is by releasing the ahesion and covering
the raw areas with amniotic membrane, conjunctiva or
mucous membrane graft. A therapeutic contact lens is
useful in preventing re-adhesion. Result is not always
rewarding.
CONJUNCTIVA 61
Fig. 4.13: Case of symblepharon with pseudopterygium
Figs 4.14A to C: Types of symblepharon. (A) Total symblepharon.

(B) Anterior symblepharon. (C) Posterior symblepharon
SUBCONJUNCTIVAL HEMORRHAGE
It is a condition that alarms the patient. Except for this

fear factor, it has no symptom per se. The hemorrhage is
actually an intraconjunctival one and not really a
subconjunctival one (Fig. 4.15). It is caused by:
1. Trauma: Injury to eye or head injury involving
anterior or middle cranial fossa can cause this
condition. Hemorrhage due to these two conditions
should be differentiated (Table 4.3).
2. Increase in intrathoraccic pressure: Severe cough
(including whooping cough), lifting heavy weight
and heavy weight over chest as in building collapse.
3. Diseases of blood vessels: Arteriosclerosis.
4. Diseases of blood: Purpura, leukemia, aplastic anemia.
Fig. 4.15: Subconjunctival hemorrhage

CONJUNCTIVA 63
5. Severe conjunctivitis, especially Pneumococcal.

6. Systemic diseases: Hypertension, diabetes.
7. Acute fever: Malaria, diphtheria, measles.
8. Vicarious menstruation.
9. Idiopathic.
Management
Management is mainly that of cause. Local placebo is
recommended. Patient should be reassured. Cold
compress is applied. Subconjunctival hyaluronidase
may hasten the absorption of the hemorrhage.
FOLLICLES IN CONJUNCTIVA
Certain conditions are characterized by follicle forma-

tion in the conjunctiva (Fig. 4.16). They can be divided
Fig. 4.16: Case of follicular conjunctivitis

into acute, chronic and specific types. The etiological

factors are:
1. Acute type: It is seen in inclusion conjunctivitis,
pharyngoconjunctival fever, herpetic conjunctivitis,
New castle conjunctivitis, epidemic kerato-
conjunctivitis and Apollo conjunctivitis due to
Coxsakievirus.
2. Chronic type: In molluscum contagiosum, due to
prolonged application of topical medicine such as
eserine, pilocarpine and IDU, and in folliculosis of
children (which is part of generalized lymphoid
hyperplasia).
3. Specific: Trachoma and giant papillary conjunctivitis
(due to soft lens wear).
CONCRETIONS
They are also known as lithiasis.

They are seen in aged persons. They occur in
palpebral conjunctiva as hard, yellow spots. They are
inspissated mucus and epithelial cells which have
accumulated in Henle’s glands. The only symptom is
foreign body sensation.
They are removed with a needle.
OPHTHALMIA NODOSA
It is caused by caterpillar hair.

Semitransparent, yellowish or reddish nodule is seen
in conjunctiva (It may also be seen in cornea and iris).
The offending hair is seen in the excised lesion, which
is the treatment.
5
Cornea
Cornea is the most important structure as far as students

and practitioners are concerned. Pathology in this struc-
ture can result in severe pain, defective vision and also
can alarm the patient. Corneal ulcer and scar are the
common cases that are kept in undergraduate clinical
examination. In theory examination, ulcers of all types,
scars and rarely keratoconus are asked.
Cornea is best examined by oblique illumination
method or slit-lamp. Keratometry (to assess corneal
curvature), pachymetry (to measure corneal thickness)
and topography are some of the important specialized
tests. Staining with 2% fluorescein or Bengal rose is
employed in doubtful cases. The seven ‘S’ to be exami-
ned in a case of corneal ulcer are— situation, size, shape,
surface, stain, slough and sensation. Corneal surface
irregularity is best checked with placido disk which is
held in front of the cornea with source of light at the
level of patient’s ear on the same side.
ANATOMY
Cornea is developed from surface ectoderm (epi-

thelium) and from mesoderm (stroma and endothelium)
(Fig. 5.1).
Cornea is the transparent, avascular portion which
is the anterior 1/6th of globe circumference. It is 11 mm
in diameter and has a refractive power of +43 D. It is
one mm thick in periphery and 0.56 mm in the center.
It has five layers with substantia propria (stroma)
forming 90% of thickness. One anterior (Bowman’s) and
one posterior (Descemet’s) membranes are present.
Cornea is lined by epithelium (anterior) and a layer of
endothelium (posterior) (Fig. 5.2). If destroyed
CORNEA 67
Fig. 5.1: Development of cornea: (A) Epithelium. (B) Second wave of

neural crest (Keratocytes). (C) First wave of neural crest (endothelium).
(D) Future iris and pupil
Fig. 5.2: Layers of cornea: (A) Epithelium. (B) Bowman’s membrane.

(C) Stroma (substantia propria). (D) Descemet’s membrane.
(E) Endothelium
Bowman’s membrane is devoid of regeneration resul-

ting in some amount of corneal opacity. Cornea is richly
supplied by trigeminal nerve. It joins sclera (and
conjunctiva) at limbus.
Corneal lesions are mostly ulcer, scar, degeneration
and dystrophy.
Degeneration and dystrophy (except for kerato-
conus) are beyond the scope of this book – and under-
graduates.
Cornea, although exposed to atmosphere and
external irritants, is protected by its intact epithelium,
tear (mechanical wash and by its lysozyme) and by lids.
Good nutrition level of patient is equally important.
INFLAMMATION
Corneal inflammation is known as keratitis.
Flow chart 5.1: Classification of keratitis

CORNEA 69
The above division is based on the layer that is first

involved in the pathology. In almost all conditions, in
advanced stage, all the layers of cornea may be affected
by the lesion.
CORNEAL ULCER
It is purulent keratitis involving superficial layers of

cornea to begin with. It is caused by bacteria, fungus
and, rarely, by virus. Amongst bacteria, C. diphtheriae
and N. gonorrhoea are important as they are capable of
penetrating intact corneal epithelium.
The sources of organisms are exterior (such as dust,
injury), secondary (from contiguous surface such as
lacrymal sac and conjunctiva) and rarely from endo-
genous focus (which are mostly immunological).
Prolonged use of local steroids— and even antibiotics—
facilitates occurrence of corneal ulcer.
Corneal ulcer has three stages: (a) In progressive stage
the active ulcer is surrounded by edematous area
containing leukocytes. (b) In the next stage of regression,
line of demarcation forms, infiltration and edema
disappear and healing sets in with or without vasculari-
zation. Finally (c) stage of cicatrization occurs.
The symptoms are watering from eye, pain,
defective vision, redness of eye, photophobia (abolished
in dark) and blepharospasm (abolished by local
instillation of anesthetic agent). Ipsilateral headache is
present. These symptoms are sudden in onset and severe
in nature.
Signs (of bacterial ulcer) are edema of lids and
opacity (the ulcer) in cornea. Corneal opacity turns green
with local instillation of fluorescein 2% drops. Ciliary
congestion (circumcorneal congestion) is present and
Table 5.1: Differences between conjunctival

and ciliary congestion
Features Conjunctival Ciliary congestion
congestion (CCC)
Structure Conjunctiva Cornea, uveal tract,
affected glaucoma
Site At fornix Around cornea
Vessels Posterior Anterior conjunctival
conjunctival
Color Bright red Dull red
Branching Profuse, well seen Minimal; poorly seen
Blood flow From fornix to Away from cornea
cornea
Vasoconstrictor Blanching occurs No blanching
Mobility Moves with Conjunctiva moves
conjunctiva over it
Discharge Mucopurulent Watery
this has to be differentiated from conjunctival type of

congestion of conjunctivitis (Table 5.1).
Pus is seen in the ulcer floor which is surrounded
by infiltration. In later stage vessels may invade the
cornea.
In some infections (such as pneumococcal), the
bacterial toxin (and not organisms) seeps into anterior
chamber, irritates iris causing exudation of cells into
anterior chamber. This is sterile ‘pus’ which settles
down in anterior chamber with a horizontal upper
border. It is called hypopyon (Fig. 5.3). Its development
depends on the virulence of organisms and the
resistance of the patient. It changes position with the
change in the position of patient’s head. It usually does
CORNEA 71
Fig. 5.3: Case of hypopyon corneal ulcer
not need draining. It is absorbed when the ulcer heals.

It may cause rise in ocular pressure (controlled by oral
diamox). If raised ocular pressure cannot be controlled
and if the hypopyon is not showing signs of absorption,
then it is drained by paracentesis.
The pupil is small and sluggish due to iritis. Keratic
precipitates (KP), which are leucocytes settled on corneal
endothelium, may be seen if iris and ciliary body are
involved.
If untreated, improperly treated or ineffectively
treated a corneal ulcer may go in for complications.
They are:
I. Without perforation of ulcer:
1. Iritis: Mostly due to bacterial toxins. It subsides
promptly if ulcer is treated effectively.
2. Secondary glaucoma: It is usually seen with
hypopyon, which obstructs the outflow of aque-
ous through chamber angle.
Fig. 5.4: Case of corneal ulcer with descematocele
3. Descematocele (keratocele): If a small ulcer erodes

upto Descemet’s membrane, then this membrane
bulges like a transparent bleb into the ulcer due
to intraocular pressure (Fig. 5.4).
4. Keratectasia: When a larger ulcer erodes slowly
more than half the depth of cornea, the thinned
out ulcer floor bulges forwards.
5. Leucoma: Scar; not a complication but sequel
when ulcer heals up.
II. In the event of perforation:
1. Iris incarceration: Met with in a small, slowly
perforating ulcer which is usually in the center.
The incarcerated iris plugs the perforation and
anterior chamber reforms.
2. Iris prolapse: This is seen in slow perforation of a
large ulcer which is usually in the periphery.
CORNEA 73
3. Complicated cataract: When a large perforation

occurs, the lens comes in contact with cornea. If
this contact exists for a longer time, then lens opa-
city develops. It also occurs due to reduced nutri-
tion to lens caused by inflammatory debris in aque-
ous.
4. Pseudocornea: When a slow perforation occurs in a
larger ulcer, the prolapsed iris tissue is covered by
exudate and epithelium. The appearance is as
though the cornea is still there.
5. Endophthalmitis and panophthalmitis: When the
infection spreads into eye it produces abscess in
vitreous (endophthalmitis) or the whole interior
of eye is converted into a bag of pus (panophthal-
mitis).
6. Corneal fistula: When a very small perforation keeps
opening repeatedly the opening gets lined by
corneal epithelium. Then it does not close; but
remains permanently as a fistula.
7. Extrusion of intraocular contents: When a large ulcer
suddenly perforates, the lens and vitreous get
extruded (Fig. 5.5). Intraocular hemorrhage is
sometimes seen.
8. Adherent leucoma : A sequel of perforated ulcer.
9. Anterior staphyloma: A bulging pseudocornea
further gets invaded by fibrous tissue. This
contracts resulting in an ectatic mass which
resembles a bunch of grapes.
10. Phthisis bulbi: Shrunken, blind eye.
Management of corneal ulcer follows the general
surgical principles—local cleaning, control of infection,
rest to inflamed parts, protection of affected area and
relief from pain.
Fig. 5.5: Perforated corneal ulcer with impending lens extrusion
1. Before commencing treatment, focus of infection, espe-

cially that of lacrymal sac should be excluded.
Material from ulcer should be sent for microbiology
study.
2. The conjunctival sac is irrigated and cleaned of all
pus. The pus in the floor of ulcer is scraped off. The
ulcer is then cauterised with trichloracetic acid (10%)
or phenol (This should not be done in a case of per-
forated ulcer or for a very large ulcer with thin floor).
If needed the cauterization may be dispensed with.
3. The infection is controlled by local and systemic use
of antibiotics:
a. Locally, antibiotic is administered in the form of
drops or ointment. Hourly instillation of fortified
antibiotic eye drops has eliminated use of
CORNEA 75
subconjunctival route. Fortified drops are pre-

pared by mixing in the commercial eye drops the
injection variety of the same antibiotic, or it is
prepared from the systemic drug itself. Strength
of certain fortified antibiotic eye drops are:
Tobramycin (1.3%): Commercial drops + 2 ml
(80 mg) of tobramycin.
Cephazolin (5%): 500 mg cephazolin + 10 ml water
Vancomycin: 500 mg vancomycin + 10 ml sterile
water
b. Systemic antibacterial agents must be able to
cross blood—aqueous barrier since cornea is
avascular. The drugs preferred for systemic
administration are sulpha, chloramphenicol and
cephalosporin.
4. Rest is needed for intraocular mobile structures—
iris and ciliary body. Mydriatic—cycloplegic drugs
like atropine are used once a day. It also prevents
some of the dangerous problems associated with
iritis, should it occur. Local heat also gives good
relief.
5. Protection is offered by pad and bandage of eye. Since
hourly drops have to be instilled, dark glasses are
advised for smaller ulcers instead of pad and
bandage. Bandage contact lens can be used.
6. Pain is relieved by any analgesic such as paracetamol
(500 mg 8th hourly) or aspirin.
In larger ulcer threatening perforation, ulcer with
large hypopyon or in recently perforated ulcer, reduc-
tion of intraocular pressure is desirable. This is achieved
by oral acetazolamide 250 mg 8th hourly.
Small perforation can be sealed by glue.
A non-responding ulcer is best treated by pene-

trating grafting (Figs 5.6 and 5.7). The ulcer area must
be totally excised. The only treatment for total anterior
staphyloma (especially if it bleeds) is excision of eye.
Fig. 5.6: Recalcitrant corneal ulcer
Fig. 5.7: For case Figure 5.6, an 8 mm penetrating (therapeutic)

graft was done. Graft remained clear
CORNEA 77
Ulcus Serpens: Also called as “Typical hypopyon

ulcer”—occurs in adults and is caused by Pneumococcus.
It is a grayish white ulcer which starts at one side of
cornea and creeps across to the other side like a snake.
Grayish area with lines in it surrounds the ulcer.
Infiltration at Descemet’s level opposite to the ulcer
exists so much so perforation is common. Associated
virulent iritis and hypopyon are present. Treatment is
as that of bacterial corneal ulcer. If ulcer is over pupillary
area it is allowed to creep further as the scar at the site
where the ulcer stops is usually very dense.
Fungal corneal ulcer differs from bacterial in certain
aspects. The symptoms are minimal and inflammatory
signs are not marked. Ulcer is typical—usually central,
circular, pigmented one with satellite lesions (Fig. 5.8).
Fig. 5.8: Case of hypopyon corneal ulcer. The pigment in the ulcer
floor suggests it to be a fungal ulcer
Slough is dry and raised. Hypopyon is prominent. In

the diagnosis, for culture the pus must be obtained from
the depth of ulcer. In the treatment, antibiotic should
never be used; only anti fungal drugs such as natamycin
are employed.
(Note: In the theory examination if question is asked
about corneal ulcer, the student is advised to write only
on bacterial corneal ulcer).
Acanthamoeba Keratitis is due to an amoeba,
acanthamoeba. It invades cornea when unsterile water
or saline is used while using contact lens. Main
symptom is the severe pain. Other symptoms are that
of any corneal ulcer.
It starts as streaks of epithelial and subepithelial
lesions. Later on it assumes a ring shape and radial
keratoneuritis—the later involves the corneal nerves.
Dendritic ulcer also occurs.
Diagnosis is by observing the cysts stained with
lactophenol or calcofluor white.
Apart from treatment given to any infective corneal
ulcer, locally propamidine isethionate (1%), neomycin,
paramomycin or polyhexamethyle Biguanide (0.02%)
is used.Frequently therapeutic corneal grafting is
required.
NON-PURULENT SUPERFICIAL KERATITIS
It is seen usually with virus infection. The important

viruses are adenovirus, herpes simplex and herpes
zoster. In trachoma avascular superficial punctate
keratitis (SPK) occurs.
CORNEA 79
In herpes simplex of secondary type (which is

usually seen in adults), cornea is mostly involved. In
this there are superficial punctate keratitis (SPK) in rows
which heal well, only to recur. Pain and lacrymation
are met with. In some cases these may coalesce to form
dendritic ulcer – a branched ulcer with knobs at the tip
(Fig. 5.9). Epithelium around the ulcer is loose and takes
up rose Bengal stain. This may go onto amoeboid ulcer
(geographical ulcer) in a few cases (Fig. 5.10). Disciform
keratitis is also met with. Iritis is seen in some cases.
Treatment is by local use of IDU, Trifluridine (1%)
drops or acyclovir (3%) ointment 5 times per day. If
stroma also is involved cortisone with antiviral drops
are used. If epithelium is healthy and stroma only is
affected then cortisone alone is used locally. Recurrence
is managed by oral acyclovir (400 mg once in 12 hours).
Iodine cautery, which was once sheet anchor of
treatment, is not employed now.
Fig. 5.9: Dendritic ulcer due to herpes simplex

Fig. 5.10: Ameboid ulcer. This is usually due to desquamation of

epitheliolyzed cells found around a dendritic ulcer
Herpes zoster is seen in adults. There is usually

history of an attack of chickenpox in childhood. The
virus is in Gasserian ganglion. It reaches the target
organ–skin, nerves and eye- via ophthalmic division of
Trigeminal. If tip of nose is involved then eye is involved
(Hutchinson’s rule) since the innervation is common to
both—nasociliary nerve.
Herpes zoster ophthalmicus – a term used only if
eye is affected - is mostly a unilateral condition. Severe
pain over one side of face with redness followed by
eruptions (vesicles) of skin is seen. These may bleed or
suppurate. It lasts for three weeks during which or after
which eye signs appear. SPK (fine and, later, coarse),
nummular (disk-shaped) keratitis and dendritic ulcer
(it differs from that of herpes simplex in that it is actually
CORNEA 81
an elevated lesion and has no knobs) are the corneal

lesions. Cornea is anaesthetic. Iridocyclitis is present.
Associated scleritis, retinal necrosis and paralysis of
motor cranial nerves of eye (and VII nerve) may occur.
Post-herpetic neuralgia is sometimes so severe that some
patients may even commit suicide.
Management is with oral acyclovir (800/mg 5 times/
day × 10 days) at the early stage of disease. Antibiotic
ointment or calamine lotion is applied to skin lesions.
Antibiotic ointment to eye is employed. Antiviral eye
preparations are of no use except in scleritis and iritis
in which conditions local steroids are also added. Local
steroid is used for deep keratitis, scleritis and uveitis.
Systemic steroids are indicated if motor nerves are
affected. Analgesics are must and sometimes even
pethidine may be required.
One anothor superficial “ulcer” is Mooren’s ulcer
(Synom. Rodent ulcer, Chronic serpigenous ulcer). Exact
cause is unknown. It may be an autoimmune response
to conjunctival epithelium or to corneal antigen. Under-
lying ischemia is present. Usually it affects older persons
and is mostly unilateral. Males outnumber females by
four times. It starts as a semi-lunar ulcer in lower
quadrant of cornea and spreads tridimensionally (along
limbus, towards corneal center and towards sclera). The
central edge of ulcer is overhanging (Fig. 5.11).
Perforation is rare (10%). The floor is epithelialized and
vascularized. Pain is present. In younger patients, a
severe form is seen. In the final stage the whole cornea
becomes scarred and opaque,thinned and vascularized.
Fig. 5.11: Mooren’s ulcer. It is in the typical location.

The overhanging central edge can be seen
Management is by surgery. The usual procedure is

cutting the overhanging central edge of ulcer.
Conjunctiva adjacent to cornea is snipped off. Lamellar
keratoplasty is effective.
Fascicular ulcer is one type of phlyctenular keratits.
It is mostly seen in adults and mainly affects the epi-
thelium and superficial stroma. Photophobia is severe.
It starts as a grey nodule whose apex may ulcerate. It
invades cornea and is accompanied by a leash of parallel
vessels. Permanent scar is rare (Fig. 5.12).
Treatment is with local atropine, cortisone and
antibiotic if there is ulceration. Dark glasses are worn
for comfort.
CORNEA 83
Fig. 5.12: Healed-up phlyctenular keratitis. This is known as

Salzmann’s degeneration
PANNUS
It is lymphocytic infiltration with vascularization of

cornea. The infiltration is in between epithelium and
Bowman’s. After sometime Bowman’s membrane is
destroyed and stroma is invaded.
The types are:
1. Trachomatous:It may be progressive or regressive
2. Phlyctenular: Vascularization is less. It clears up well.
3. Degenerative: This is seen with absolute glaucoma,
chronic iridocyclitis and chronic inflammation of
cornea.
4. Lepromatous: Usually it is seen in superotemporal
quadrant of cornea.
NEUROTROPHIC KERATITIS
This is seen in paralysis of trigeminal nerve. It occurs

after alcohol injection to trigeminal ganglion, herpes
zoster, tumor near Gasserian ganglion, injury to this
ganglion, syphilis and leprosy. But all these cases do
not develop this. The exact cause is not known.
Disturbance of antidromic reflex is the most favored
factor.
The cornea turns dull, central epithelium gets
desquamated followed by the whole epithelium of
cornea. Later the stroma is involved breaking down into
a large ulcer. Eye is red; but there is no pain due to
corneal anesthesia.
The regular treatment for corneal ulcer may be tried.
Punctal closure is effective in many cases. Relapses
occur. Tarsorrhaphy is very effective. This should be
kept for at least one year.
EXPOSURE KERATITIS
It is seen in lagophthalmos wherein lids do not close

properly and the eye goes in for drying. Common
etiological factors are seventh nerve paralysis, coma,
very ill patients, gross symblepharon and marked
proptosis. Some persons sleep with eyes partially open
(nocturnal lagophthalmos) without any grave conse-
quence. Such exposed cornea is affected by external
noxious agents.
The condition starts as SPK just below the center of
cornea which later on ulcerates due to invasion by
organism. Management is by keeping eye lids closed
CORNEA 85
by lateral tarsorrhaphy (temporary or permanent). If

lagophthalmos is a temporary phenomenon cornea is
protected with antibiotic ointment.
INTERSTITIAL KERATITIS (IK)
It is an inflammation of corneal stroma caused by

bacteria (especially of syphilis, tuberculosis, leprosy),
virus, fungus and protozoa.
Syphilitic IK: It is met with in congenital and
occasionally in acquired syphilis. In congenital syphilis,
the condition appears by 2nd decade of life and stigmata
of congenital syphilis (including Hutchinson’s triad) are
seen. It is unilateral at a time, but finally affects both
eyes. Primary problem is iritis. It starts as scattered
infiltration in stroma at limbus and spreads to involve
whole of cornea (infiltrative stage). Later interstitial
vessels invade converting cornea into a pinkish tissue,
the appearance aptly called salmon patch (Florid stage).
Over months this resolves finally leaving behind vessels
empty of blood (ghost vessels) and scattered opacities
(regressive stage). Signs of iridocyclitis with its sequelae
are seen. This is an allergic reaction to bacterial protein
and not due to infection by T. pallidum.
Treatment is by local cycloplegic—mydriatic and
steroids. Anti-syphilitic treatment may be given; but has
no influence on the local pathology or occurrence of the
condition in the other eye later on. Local cortisone
should be continued for one year. If stopped earlier,
recurrence occurs.
IK due to acquired syphilis occurs about 10 years after
contact with the systemic problem. It is mostly unilateral
and can even be sectorial.
Tuberculous IK: It is also an allergic manifestation.

It is unilateral, sectorial and final clearing is not much.
ARCUS SENILIS
It is ring shaped opacity near the limbus with a clear

area between it and the limbus (Lucid interval of Vogt).
Cross section is like an hour glass—nearer to limbus at
epithelial and endothelial levels. It is due to lipid
infiltration.
It starts by 6th decade of life—first in upper and
lower quadrants of cornea. Border is sharp on the
periphery and indistinct towards corneal center. It starts
at lower quadrant of cornea and later forms a ring (Fig.
5.13). There may be two rings. Blood cholesterol level
has no bearing on it. If it occurs in younger individuals,
it is known as arcus juveniles. Treatment is not needed
for arcus senilis.
Fig. 5.13: Arcus senilis
CORNEA 87
CORNEAL SCAR
It occurs after corneal injury, operations on cornea and

corneal ulcer. Corneal opacity can also occur as a
congenital phenomenon.
The opacity is of four grades:
1. Facet: Not exactly an opacity. It is a depressed area
in cornea which is difficult to detect; but if centrally
situated it can cause considerable visual disturbance.
2. Nebula: Least dense opacity. It can cause marked
visual loss if centrally located.
3. Macula
4. Leucoma: Densest opacity.
Apart from cosmetic disfigurement, the main
symptom of corneal scar is defective vision. This is either
due to mechanical obstruction to rays of light if the
opacity is in the center of cornea, or due to astigmatism
if peripherally located. These opacities do not take up
stain with 2% fluorescein. If iris is adherent to the opacity
then the condition is called adherent leucoma. In this
condition the pupil is pear shaped and the anterior
chamber is irregularly shallow (Fig. 5.14).
Long standing cases may show clearing (very
minimal; starts as lines), pigmentation, degeneration or
atheromatous ulcer. Atheromatous ulcer results if an
atheroma (degenerative plaque) over the leucoma falls
off (Fig. 5.15). This carries with it the overlying epithe-
lium resulting in an ulcer. Usually such a leucoma is
heavily vascularized. The ulcer heals up slowly and well
if promptly treated. But it occurs again and again.
Keratoplasty is the only permanent treatment for this
condition.
Fig. 5.14: Case of adherent leucoma. The pear shaped pupil (and the
irregularly shallow anterior chamber) is diagnostic
Fig. 5.15: Atheroma in a long standing leucoma. The heavy

vascularization is typical. When these deposits fall off atheromatous ulcer
occurs
CORNEA 89
Management of corneal scar:

1. Medical therapy is useless. Dionine and yellow oxide
of mercury have been tried.
2. Glasses or contact lens are useful for peripheral scars
to correct the astigmatism.
3. If the eye has no vision then tinted contact lens can
be worn for cosmetic improvement.
4. Surgical:
a. Tatooing: The aim is to color the white scar so that
its color matches the color of iris behind. Gold
chloride (for brown iris) or platinum chloride (for
dark colored iris) is applied over the scar and is
reduced by hydrazine hydrate.
b. Keratectomy: In dense leucoma the excess scar
tissue is scraped off and the resultant “iatrogenic
ulcer” is treated carefully. Aim is to convert a
leucoma into a nebula. Visual improvement will
not be much.
c. Optical iridectomy: This is done for central scars.
A small, key hole shaped opening is made in iris
behind an area of clear cornea. It is usually in the
inferonasal quadrant so as to facilitate near vision
work.
d. Keratoplasty: The diseased portion of cornea (not
the whole cornea) is removed and replaced with
clear donor corneal piece (Figs 5.16 and 5.17).
Corneal grafting (keratoplasty): The donor material
for corneal transplantation is obtained within six hours
of donor’s death. The donor material is preserved by
short-term method (to be used within 48 hours) or long-
term method. Whole thickness of cornea (penetrating)
Fig. 5.16: Leucoma
Fig. 5.17: Postoperative appearance of case Figure 5.16 for which a

7.5 mm penetrating graft was done
CORNEA 91
or partial thickness of cornea (lamellar) is employed for

grafting depending on the depth of corneal lesion.
Usually not more than central 7 mm of cornea is
replaced. The whole cornea is not replaced. Suturing is
by 11/0 suture and the method may be continuous or
interrupted suturing.
Cortisone is given postoperatively for a month. Graft
rejection due to immune reaction is the common
problem. Other complications are vascularization,
infection, glaucoma, graft edema, iritis and anterior
synechia. Apart from optical purpose, corneal grafting
is indicated for therapeutic, cosmetic and tectonic (to
restore the thickness of cornea) purposes also. Best
results are obtained with avascular central leucoma,
keratoconus and corneal dystrophy.
KERATOCONUS
Otherwise known as conical cornea, it is a congenital

condition which manifests by second decade of life. It
may also occur after trauma, along with vernal con-
junctivitis and Down’s syndrome.
It produces defective vision due to irregular myopic
astigmatism. The cone is near the center of cornea in
inferonasal aspect (Fig. 5.18). Fleischer ring is seen at
the base of cone. When the patient looks down there is
‘depression’ in the lower lid (Munson’s sign). When a
pencil of light is shone from the side, the apex of the
triangular light reflex on the other side of cornea gets
focused (or not at all) beyond the limbus and not at the
limbus (as in normal cornea) (Rizzutti sign). Early
diagnosis is by placido disk (Fig. 5.19), keratometry,
Fig. 5.18: Keratoconus
Fig. 5.19: Placido’s disk. The image of rings reflected on a

conical cornea is distorted
CORNEA 93
distant direct ophthalmoscopy and by corneal topo-

graphy. In a few cases the cornea turns opaque due to
ingress of aqueous caused by Descemet’s rupture (acute
hydrops).
Management is with glasses or contact lens in early
stage and by keratoplasty (usually penetrating) in later
stages. Result of corneal grafting is very good.
6
Sclera
Scleritis, episcleritis and staphyloma (except equatorial

and posterior) are kept for clinical examination. These
are frequently asked short notes questions in theory
paper.
Sclera can be studied through conjunctiva only.
Swelling, thinning and discoloration are to be noted
down.
ANATOMY
Sclera is the fibrous protective coat of eyeball forming

posterior 5/6th of eye circumference. It is derived from
mesoderm. It joins cornea at limbus. On the outside it
has Tenon’s capsule and bulbar conjunctiva and on the
inside choroid. It is pierced by:
a. Apertures for ciliary vessels and nerves on its pos-
terior aspect,
b. Apertures (near equator) for vortex veins
c. Openings (4 mm from limbus) for anterior ciliary
vessels. It is almost avascular. Long ciliary nerves
supply it.
Since sclera is a fibrous tissue, inflammatory diseases
are rare. Such diseases can involve superficial (epis-
cleritis) or deep (scleritis) layer (Flow chart 6.1).
Flow chart 6.1: Inflammation of sclera and episcleral tissue
SCLERA 97
EPISCLERITIS
It is mostly an allergic manifestation to endogenous

toxin. It is seen with collagen diseases.
Young adults, mostly females, are affected. Pain may
or may not be present. Usually it occurs temporal to
cornea and has an acute onset. It is seen as red patch in
one or both eyes with mild tenderness (Fig. 6.1). It can
be either diffuse or nodular lesion. Nodule is about
3 mm in size, usually away from limbus and minimally
mobile. It recurs. Except for its recurrence and chroni-
city, the only other problem is the slate color scar to
which conjunctiva is adherent.
Fig. 6.1: Episcleritis
Treatment is difficult.
1. Mild to strong steroids are used locally.
2. Oral NSAID is useful. NSAID is also used locally
instead of steroids and this can avoid problems of
local steroids (Glaucoma, cataract and secondary
infection). Oral salicylate is sometimes used.
3. Cold compress applied locally gives relief from
symptoms.
SCLERITIS
It is like episcleritis; but involves cornea and deeper

tissue including iris. It is a bilateral, chronic granuloma-
tous condition. It is seen with connective tissue and
collagen disorders, metabolic disorders like gout,
syphilis, infection by bacteria such as staphylococcus,
ocular surgery and zoster.
It is present either in the anterior or posterior region.
Anterior scleritis, which is associated with above
disorders, can manifest as nodular, diffuse or necrotising
type. The last one may occur with or without inflamma-
tion—the latter is known also as scleromalacia perforens.
Scleromalacia perforens is seen in rheumatoid arthritis
patients. The lesion melts away leaving behind a
punched out area. Necrotizing scleritis with inflamma-
tion presents as red, painful eye with severe symptoms.
Scleral thinning, glaucoma, cataract and corneal melt
are seen. It is due to autoimmune disease.
Diffuse scleritis involves even a quadrant of sclera. It
is pink in color. Nodular scleritis is an elevated purple
nodule at limbus. If anterior nodular scleritis is present
all around the cornea then it is known as annular scleritis.
Anterior scleritis may spread to cornea as an avascular
SCLERA 99
tongue shaped opacity called sclerozing keratitis. This

clears up only partially. Ciliary staphyloma is another
complication.
Posterior scleritis is a local manifestation only and
produces decreased vision, reduced ocular movements,
choroidal folds, macular edema, retinal detachment and
proptosis. Pain may or may not be present. If pain is
absent the diagnosis can be missed. B scan and CT scan
assist in its diagnosis.
Management begins with thorough investigations
such as RF, Mantoux, ANA, ANF, ANCA, VDRL, TPI,
FM-ABS, X-ray and serum uric acid level.
Treatment
1. It is mainly systemic—NSAID, steroids and, if
needed, immunosuppressants. Ranitidine is given
along with this therapy.
2. Lubricant is a must for scleromalacia perforans.
Local steroids are ineffective.
3. If infective element is present, local and systemic
antibiotics are warranted.
4. If scleral perforation occurs, scleral patch graft is
done.
STAPHYLOMA
Staphyloma differs from scleral ectasia in that the

former is lined by uveal tissue. Except for anterior type,
the other types involve sclera in which scleral thinning
is a must. The thinning may be due to scleral inflamma-
tion, degeneration, surgery, trauma or stretching of eye
globe.
The various types of staphyloma are:

a. Anterior staphyloma: It is seen after a slow perforation
of a large corneal ulcer. The uveal tissue involved is
iris.
b. Intercalary staphyloma: It is seen in the sclera within
2 mm of limbus and the bulging sclera is lined by
root of iris and anterior part of ciliary body. Asso-
ciated angle closure glaucoma may occur.
c. Ciliary staphyloma: It is seen from 2 to 8 mm from
limbus and the incarcerated tissue is ciliary body. It
has a lobulated surface. Apart from the causes
mentioned above, absolute glaucoma can give rise
to this type of staphyloma (Fig. 6.2).
d. Equatorial staphyloma: This occurs 14 mm behind
limbus at the site of exit of vena vorticosae. It is lined
by choroid and is seen in high myopia also.
e. Posterior staphyloma: It is seen in high myopia, after
scleritis and injuries. The sclera is lined by choroid.
The diagnosis is by funduscopy (pale retina and
change in direction of retinal vessels). Floor of sta-
phyloma is focused by minus lens of ophthalmos-
cope. A crescentic shadow is seen near macula with
indirect ophthalmoscopy (Fig. 6.3).
Management
1. Prevention and treatment of factors causing scleral
thinning need attention.
2. Once it has occurred, local excision and repair with
scleral patch graft are called in.
3. Posterior staphyloma may require scleral support
procedure and myopic glasses.
4. Enucleation (or evisceration) is advised for bleeding
anterior staphyloma and for blind eye having large,
unsightly lesion.
SCLERA 101
Fig. 6.2: Staphyloma. Both intercalary and ciliary

staphylomata are seen in this case
Fig. 6.3: Schematic diagram showing the various types of staphylomata.

(A) Anterior staphyloma (sequel of perforated, large corneal ulcer).
(B) Intercalary staphyloma (within 2 to 3 mm of limbus. Lined by root of
iris). (C) Ciliary staphyloma (8 mm from limbus; lined by ciliary body).
(D) Equatorial staphyloma (14 mm from limbus; lined by choroid).
(E) Posterior staphyloma (Seen in high myopia). (L – Limbus)
7
Uveal Tract
Iridocyclitis is an important case kept for clinical exami-

nation. Along with sympathetic ophthalmia it is a
common question asked in the theory paper.
Proper examination requires study with oblique
illumination and slit-lamp study. Retroillumination is
sometimes employed. Gonioscopy study is done to exa-
mine the extreme periphery of iris.
Pupil is examined for direct and indirect (consensual)
reactions, size and shape.
ANATOMY
Uveal tract consists of iris, ciliary body and choroid. It

is the vascular coat of eye nourishing the latter.
Iris has pupil in the centre and periphery to it are
ridges and a collarette on its anterior surface. The latter
separates iris into two regions, viz pupillary zone and
ciliary zone. The sphincter muscle is near the pupil and
the dilator muscle is in the stroma periphery to colla-
rette.
Ciliary body has ciliary muscle. The latter has longi-
tudinal, circular and radial fibers which are embedded
in collagen connective tissue. It has an anterior pigment
epithelium and a posterior non-pigmented epithelium.
These two layers continue onto iris. Ciliary body has
two regions—posterior which is smooth (pars plana)
and anterior 2 mm which has finger like ciliary processes
(pars plicata). Ciliary processes are about 70 in number
and are the site of aqueous production.
UVEAL TRACT 105
Choroid has blood vessels arranged in three layers

lying in collagenous tissue. It extends from ora serrata
to optic disk. On the retinal side is the Bruch’s mem-
brane. Arterial supply to iris and ciliary body is from
long posterior and anterior ciliary arteries via circulus
arteriosus major and minor. Choroid derives its blood
supply from short posterior ciliary arteries (Figs 7.1
and 7.2).
The common pathology of uveal tract is inflamma-
tion. They are also affected by new growth.
Fig. 7.1: Blood supply to uveal tract. Co – Cornea. L – Lens. R – Retina.

CH – Choroid. M – Muscle. S – Sclera. ON – Optic nerve. AC – Anterior
ciliary artery. VV – Vena vorticosa. LPC – Long posterior ciliary artery
Fig. 7.2: Sclera from behind showing uveal tract blood vessels.
(A) Vena vorticosa. (B) Long posterior ciliary artery. (C) Optic nerve.
(D) Short posterior ciliary arteries
INFLAMMATION (UVEITIS) (FLOW CHART 7.1)
Flow chart 7.1: Inflammation of uvea

UVEAL TRACT 107
Anterior uveitis involves iris and ciliary body (Irido-

cyclitis); while posterior uveitis affects choroid
(choroiditis). Choroiditis usually involves the retina also
(chorioretinitis).
PURULENT UVEITIS
Panophthalmitis is an acute purulent inflammation of

whole uveal tract caused by purulent organisms which
gain entrance from outside or from surrounding tissues.
Patient has severe pain, proptosis and total loss of vision.
Cornea sloughs off and the whole eye ball is filled with
pus.
Management is by evisceration of eyeball, higher
antibiotics and analgesics. Some advise Pott’s frill
excision—a sort of partial enucleation. Enucleation is
never recommended as infection may spread along the
cut optic nerve via meningeal sheaths to brain.
NON-PURULENT ANTERIOR UVEITIS

(IRIDOCYCLITIS)
It is a condition of anterior uveal tract. It is mostly

caused by:
a. Immune related reaction to infection elsewhere or to
autoimmune disorder. The cause might be allergy
to airborne allergen or to microbial antigen of TB,
streptococcus. It is seen with anaphylactic reaction
such as serum sickness.
b. Infection: Bacterial, parasitic, viral or fungal. They

may invade either from outside or from contiguous
structure such as cornea and sclera, or from an
endogenous focus.
c. Some of the cases are caused by toxins which may
be bacterial, autotoxin, from ocular tissue or
chemical substance. These are from eye, from outside
or from some other point in body.
d. HLA B27 antigen is frequently associated with this
condition.
e. Rarely ocular trauma can cause this.
f. Certain conditions such as Behçet’s, arthritis, sarcoi-
dosis and brucellosis are associated with uveitis.
h. In some cases the cause is not known.
Although not totally accurate, the statement that
granulomatous type is due to infection and that non-
granulomatous type is due to hypersensitivity reaction
is almost true. There are definite exceptions to this
statement such as sympathetic ophthalmia.
Affecting any age group and any gender, the
intensity of symptoms varies between granulomatous
and non granulomatous types. The signs also depend
upon the reaction that the inflammation produces –
cellular, serous or purulent. The features of iridocyclitis
are (Table 7.1).
UVEAL TRACT 109
Table 7.1: Features of iridocyclitis

Features Features Mode/Cause
Mode/Cause
Symptoms:
1. Redness of eye Dilatation of anterior
conjunctival vessels
2. Pain in eye and ipsilateral Mediated through V cranial
headache (over forehead) nerve
3. Watering from eye Reflex phenomenon through
V nerve
4. Defective vision Corneal edema, cells in
anterior chamber, occlusio
pupillae, cataract, cyclitic
membrane, vitreous cells,
optic neuritis, macular
lesion, choroiditis, myopia,
secondary glaucoma
5. Photophobia and Through an arc from cranial
blepharospasm V nerve to cranial VII nerve
Signs: It can be divided into three groups.
I. Following signs are seen when there are more cells and
not much of exudate.
1. CCC (Ciliary congestion) Dilatation of anterior
conjunctival branches of
anterior ciliary arteries
2a. Corneal edema Inflammatory reaction
b. Keratic precipitates (KP)— Deposition of cells on the
mutton fat, white and red endothelium of cornea
KP (Old KPs have Deposited in a triangular
crenated margin) (Fig. 7.3) pattern (Arlt triangle) or all
over cornea
3. Aqueous flare Due to aqueous current.
Inflammatory protein in
aqueous from iris (seen
with narrow beam of slit-
lamp)
Contd...
Contd...
Features Mode/Cause
4. Hypopyon (Hyphema) Settling down of exudates
and cells
5. Alteration (loss) of iris Due to edema—the fluid
pattern and color changing the color of iris
(Muddy iris) and also filling up all iris
patterns
6. Complicated cataract Caused by defective
nutrition to lens due to
inflammatory materials in
aqueous. Cataract has
polychromatic lusture
7. Constricted, sluggish a. Increased weight of iris
pupil due to inflammatory
materials in it
b. The irritation of nerves of
both constrictor and dila-
tor muscles (Tone of cons-
trictor is stronger and
hence miosis)
c. Radial disposition of
vessels
8. Cells in vitreous Cells are from ciliary body
9. Choroiditis, optic neuritis Spread of inflammation
posteriorily
10. Hypertensive iridocyclitis Cells blocking the angle
resulting in secondary
glaucoma.
11. Iris nodule Due to inflammatory cells.
It can be Koeppe’s nodule (at
pupillary border) or
Busacca’s nodule (near
collarette)
Contd...
UVEAL TRACT 111
Contd...
Features Mode/Cause
II. The following signs are seen when there is sticky exudate in anterior
and vitreous chambers
1. Posterior synechiae (PS) The albuminous exudate
from iris sticking pupillary
border of iris to anterior
lens surface at various
points
2. Deep anterior chamber Due to pulling back of iris
by PS
3. Ring synechiae (RS) Posterior synechia
(Annular synechiae) involves whole pupillary
border—due to exudate
(This situation is known as
seclusio pupillae)
4. Iris bombe Due to seclusio pupillae the
aqueous stagnates in poste-
rior chamber as its circula-
tion is blocked by RS at
pupil. Aqueous pushes the
iris forwards like a bow
5. Peripheral anterior Due to iris bombe the
synechiae (PAS) peripheral iris is brought
into close apposition to
peripheral cornea and both
are glued together by the
purulent material
6. Total posterior synechiae Sticking of iris totally to lens
7. Ectropion of uveal Organized exudate over
pigment anterior surface contracting
pulling posterior iris
pigment around pupil
Contd...
Contd...
Features Mode/Cause
8. Secondary glaucoma Due to blockage of anterior
chamber angle by PAS and
by cells
9. Occlusio pupillae Condensation of exudate
(Figs 7.4 and 7.5) over pupillary area as a
thin film
10. Cyclitic membrane Condensation of exudate
(Pseudoglioma) material behind the lens
III. Iatrogenic Signs below occur when mydriatic is applied in a case
with posterior synechiae
1. Iris pigment over lens Occurs when PS is not very
capsule firm and is released by
mydriasis; but very small
portion of iris is torn
and is left over lens
2. Festooned pupil (Fig. 7.6) Seen when a few PS are very
firm and are not
released by mydriatic. Pupil
is irregular in shape
Fig. 7.3: Slit-lamp photo of cornea showing the keratic precipitates

UVEAL TRACT 113
Fig. 7.4: Thin exudate over pupillary area in a case of iritis
Fig. 7.5: Irregular pupil with early occlusio pupillae
Fig. 7.6: Festooned pupil in a case of iridocyclitis

for whom local mydriatric was applied
COMPLICATIONS
1. Glaucoma – either secondary or late onset.

2. Complicated cataract
3. Posterior segment involvement such as choroiditis,
papillitis.
4. Band shaped keratopathy
5. Cystoid macular edema
6. Phthisis bulbi
Acute iridocyclitis has to be differentiated from acute
conjunctivitis and acute angle closure glaucoma
(Table 7.2)
UVEAL TRACT 115
Table 7.2: Main differential diagnosis of iridocyclitis

Features Acute Acute Acute congestive
conjunctivitis iridocyclits glaucoma
1. Cause Infection Allergy, Angle closure
infection
2. Onset Sudden Sudden Sudden
3. Pain + ++ +++
4. Congestion Conjunctival Ciliary Ciliary
5. Vision Normal Reduced Markedly
reduced
6. Discharge ++ + (watery) + (watery)
7. Halos + _ +
8. Tenderness – ++ ++
9. Cornea Clear Clear or hazy Hazy
10. A/C depth Normal Variable Very shallow
11. Iris Normal Minimal No change
haziness +
12. Pupil Normal Small, Dilated;
sluggish sluggish
13. Media Clear Hazy Hazy
14. IOP Normal Variable Very much
raised
Note: The above table is also applicable if the question is on Red Eye.
IRIS NODULES
They may be present at pupillary border (Koeppe’s)

(Fig. 7.7) or at collarette (Bussaca’s).
The causative diseases are:
1. Tuberculous: It may be at pupil or collarette. The
nodule is an avascular, gray one which clears-up
well.
2. Syphilitic: Seen at both regions of iris. Minimally
vascularized yellowish red nodule and, on
disappearance, leaves behind an atrophic area in iris.
Fig. 7.7: Nodule at the pupillary border
3. Leprotic:At pupillary border. They are pale in color.

4. Sarcoid: Very vascular pinkish one and occurs
anywhere in iris. Mutton fat KPs are frequently
associated.
5. Melanotic: Seen anywhere in iris. They are brown or
black in color.
Management
Investigations for syphilis, TB, leprosy and arthritis,
HLA-B27, ANA, PTA-ABS, ACE, RPR and X-ray should
be carried out. These are usually ordered for bilateral
or recurrent non-granulomatous iritis and for granu-
lomatous type.
1. Treatment for the causative disease.
2. Specific treatment:
i. Pupillary dilatation with cyclopentolate 1%, homa-
tropine 2% (for milder case) or Atropine 1% twice
daily. These are useful by
a. Preventing or releasing PS
b. Reducing hyperemia
c. Keeping iris and ciliary muscles at rest.
UVEAL TRACT 117
If pupil fails to dilate with these drugs, mydricaine

is given subconjunctivally (Mydricaine is a
combination of atropine, adrenaline and procaine).
ii. Local corticosteroid: Beta-methasone or prednisolone
as drops, ointment or via sub-Tenon route is given
during acute stage. Fluoromethalone drop is used
when acute stage passes off.
iii. In cases where topical route is ineffective or in very
severe cases, systemic steroid or periocular methyl-
prednisolone is used. Occurrence of raised intra-
ocular pressure and cataract due to steroid must
be kept in mind.
iv. If there is no response with this therapy, systemic
immunosuppressant such as methotrexate is given.
v. Intravitreal triamcinolone and implants of
sustained release corticosteroids are used in
refractive cases.
vi. Subcutaneous interferon alpha (3 million units × 3
doses on alternate days) is also effective.
vii. Local warm application and oral aspirin to relieve
the pain. Former increases local circulation.
viii. Dark glasses.
ix. Treatment of complications such as glaucoma,
cataract.
Treatment is easier and better if one can differentiate
between granulomatous and non-granulomatous
iridocyclitis (Table 7.3).
Table 7.3: Differences between granulomatous and

non-granulomatous uveitis
Non-granulomatous Granulomatous
Cause (mostly) Immune reaction Infective element
Onset Acute Insidious
Course Short Chronic
Recurrence ++++ –––
Symptoms Acute Mild
Signs Cellular reaction Exudate and
(mostly) (Group synechiae are
I signs mentioned prominent.
above). Flare more (Group II and III
and synechiae less signs mentioned
above)
Posterior segment Usually escapes Involved
Sequelae and
complications Rare +++ : Loss of eye
possible.
(Posterior uveitis is inflammation of choroid known as
choroiditis)
SYMPATHETIC OPHTHALMIA (SO)
It is a granulomatous iridocyclitis; but has immune

etiology. It is a bilateral condition in which the sound
(sympathizing) eye suffers from uveitis when the other
(exciting) eye is injured. This is seen if the exciting eye
is injured especially over ciliary body area which is
known as the danger zone of eye (area between 2 and 4
mm from limbus), or rarely after an intraocular surgery.
It occurs more if uveal tissue is incarcerated in the
wound. SO does not occur if suppuration follows injury.
UVEAL TRACT 119
The cause was once thought to be infection (It may

be a modifying factor). It is now assumed that it is an
autoimmune T-cell mediated condition. The antigen is
uveal pigment. In both the eyes the uveal tract is heavily
infiltrated by lymphocytes and plasma cells. There is
proliferation of pigment epithelium (of iris and ciliary
body) forming Dalen-Fuchs nodules. Caseation is
absent.
The clinical picture is characterized by the non-
subsidence of uveitis in the exciting eye. There is reten-
tion of some vision in it. The onset is usually two weeks
after injury. If the injured eye is shrunken and blind,
irritation returns in it with the onset of SO. In the other
(sympathising) eye, photophobia and difficulty in near
vision are the earliest symptoms. The first signs are cells
in retrolental space and keratic precipitates. Tenderness
is present in both eyes. The full blown picture is that of
bilateral plastic (granulomatous) iridocyclitis. Vitritis
and papillitis are seen. Extensive exudation augurs poor
prognosis.
In the management, prevention is the best. The
penetrating wound must be treated- incarcerated tissue
released and wound properly sutured. Antibiotics and
cortisone are given. If the injured eye is to be removed
it should be done within a fortnight.
Once the disease has set in, if the exciting eye has no
vision, it should be removed in the early stage. If the
exciting eye has some vision it should be retained since,
after the disease subsides, the injured eye may
sometimes retain useful vision while sympathizing eye
will have none. The treatment is that for a granu-
lomatous iridocyclitis with special attention to systemic
steroid— intravenous to begin with. If steroids cannot

be given or ineffective, oral cyclosporine A is useful.
This drug can also be given along with steroids. It
should be remembered that local steroid must be used
for about 18 months—the normal duration of the
disease. If stopped early, SO recurs.
PHACOANAPHYLACTIC UVEITIS
It is another example of granulomatous uveitis caused

by immune reaction. The antigen is lens protein which
has come out of lens capsule due to extracapsular
cataract extraction, due to leak in a case of hypermature
cataract (leak of lens protein in Morgagnian cataract is
through posterior capsule) or to injury to lens.
Treatment is as that of any immune induced uveitis;
but the end result is not satisfactory.
SIDEROSIS BULBI
It is a post-traumatic condition in which an iron alloy

(iron is less than 85%) is retained inside the eye. The
iron ion combines with intraocular proteins causing
degeneration of ocular tissues (except epithelial). Dege-
neration of trabecular tissue gives rise to secondary
glaucoma.
In this condition the iris color changes to green and
then reddish brown.
Lens shows a rusty ring and cataract changes.
Management
It is early removal of the foreign body.
(Copper alloy produces chalcosis in which sunflower
cataract and Kayser- Fleischer ring of cornea are seen).
UVEAL TRACT 121
PUPIL
Students should know certain abnormal pupillary

reactions:
1. Amaurotic light reflex: Met with in lesions of retina or
optic nerve. Direct reflex on the affected side and
consensual reflex on the other (normal) side are
absent.
2. Argyll Robertson (AR) pupil: The light reflex is absent
but near reflex is retained in both eyes. The pupil is
small and reacts poorly to mydriatic. Lesion is in tec-
tum of midbrain.
3. Adie’s tonic pupil: Light reflex is absent and near reflex
is slow. It is unilateral and the affected pupil is large.
Even weak pilocarpine produces miosis.
4. Efferent pathway defect: Seen in pupillary sphincter
paralysis, III N paralysis and internal ophthalmop-
legia. Direct and consensual light reflexes and near
reflex are absent on the affected side, while both are
present on the normal side.
5. Relative afferent pathway defect (Marcus Gunn Pupil):
If a bright light is swung from one eye to the other
eye to and for (swinging flash light test), the pupil of
the affected eye dilates when the light is moved to
it. It is met with in optic neuritis, optic atrophy, CRA
and CRV occlusions and in retinal detachment.
6. Wernicke’s hemianopic pupil: When light is thrown
from one half of field (say, temporal of right eye and
nasal of left eye) light reflex is absent. But it is present
if the light is shone from the other half of field of
vision. It is seen in optic tract lesions.
IRIDODIALYSIS
It is the separation of iris from its root. It is usually due

to trauma— either injury or operative.
The patient may rarely complain of diplopia. He
may also have (in blue iris) cosmetic complaint. Glaring
is a rare symptom (Fig. 7.8).
Examination shows that the pupil is ‘D’ shaped. The
dialysed portion of the pupil is seen near the limbus
and it appears dark.
Treatment is usually not required. If symptom is
marked, the detached portion of the iris periphery can
be anchored to the root with 10/0 suture.
Fig. 7.8: Iridodialysis. The pupil is ‘D’ shaped and the dialysed
area is seen in the lower nasal quadrant
8
Lens
Diseases of lens—cataract, aphakia and even sub-

luxation —are commonly kept for clinical examination.
They are very important for the theory and oral
examinations. Hence it is mandatory that the student
has thorough knowledge of the diseases of lens as well
as the treatment procedures.
Lens is examined with diffuse illumination, oblique
illumination, slit-lamp, distant direct ophthalmoscopy
and direct ophthalmoscopy. Opacities of lens, if present,
must be carefully studied for its morphology.
ANATOMY
Human lens is a biconvex one with a capsule enclosing

cortex and, in the middle, nucleus. It has two surfaces
and an equator. It has epithelium under anterior capsule
Fig. 8.1: Development of lens. Lens vesicle (B) separates from

surface ectoderm (A) to form the lens
LENS 125
only. These cells grow into lens fibers throughout life.

These fibers condense as nucleus. Lens diameter is 10
mm. The refractive power is + 17 D. The refractive index
is 1.39%. It is suspended in front of vitreous by suspen-
sory ligaments from ciliary body.
CATARACT
It is classified into developmental and acquired—the

latter into senile and complicated. Usually develop-
mental is mostly partial and stationary; while acquired
is progressive.
Senile (Age-related) Cataract

The etiology is still obscure. Hereditary, performing
near work for a long time, sunlight and UV radiation
are implicated.
In senile cataract, there are three varieties— cortical,
nuclear and cupuliform—depending upon where the
opacity starts to develop. In nuclear cataract, sclerosis
of nucleus is the main change. Deposition of urochrome
and melanin may give it a dark brown (cataract brunes-
cens) or even black color (cataracta nigra). But, cortical
cataract formation goes through many stages. Initially
there are hydration and separation of lens fibers. Later
the lens fibers undergo denaturation. This lamellar
separation stage is followed by incipient stage wherein
wedge shaped opacities (lens striae) are seen in peri-
phery, first in lower nasal quadrant. They are in cortex
situated behind as well as in front of nucleus. In some
cases the hydration causes swelling of lens (intumescent
stage/cataract) resulting in shallowing of anterior
chamber. If the patient has pre existing shallow anterior

chamber then sometimes raised ocular pressure occurs
(phacomorphic glaucoma) which requires immediate
surgical intervention.
The next two stages are immature and mature cataract
stages (Fig. 8.2). Their differentiation is given below
(Table. 8.1).
Fig. 8.2: Case of mature (cortical) cataract. Iris shadow is absent.
Table 8.1: Differences between immature and mature

cataracts
Immature Mature
Clear lens fibers Seen in some areas No clear lens fibers
Iris shadow Present Absent
Color (Cortical) Grey Pearly white
Vision Some vision + Only PL +
Ophthalmoscopy Black shadow Only black shadow
in red reflex
(The above differences are for senile cortical cataract only).
LENS 127
The cause of iris shadow is the presence of a few clear

lens fibers between the capsule of lens and the
cataractous area (Fig. 8.3).
The final stage is hypermature one. In this stage the
hypermature cataract presents in various ways.
a. Morgagnian cataract: The cortex liquefies into a white
fluid in which the brown nucleus sinks down
(Fig. 8.4). It can lead to phacoanaphylatic uveitis and
glaucoma due to cortical matter that has leaked out.
Figs 8.3 A and B: Formation of iris shadow in a case of cataract. (A) Iris
shadow is present in an immature cataract due to presence of clear lens
fibers between capsule and cataractous area. (B) Iris shadow is not
present in mature cataract due to absence of clear lens fibers. (Dotted
line : Iris shadow, arrow : Light rays)
Fig. 8.4: Case of Morgagnian cataract. The milky white cortex in the
upper area and the brown sunken nucleus in the lower region are seen
b. The whole lens may shrink causing iridodonesis and

some amount of deepening of anterior chamber
(Fig. 8.5).
c. The lens may subluxate or dislocate due to degene-
ration of zonule fibers. It may result in secondary
glaucoma.
The prominent symptom is:
1. Defective distant vision which is more marked during
day time in nuclear cataract (pupil is small during
day time and lens opacity is in the middle). Vision is
better during night time. In cortical cataract the
situation is reversed—defect is more during the night
LENS 129
Fig. 8.5: Hypermature cataract with shrunken anterior capsule
time (pupil is dilated during night time and lens

opacity which is in the periphery comes into pupil-
lary area). As cataract advances, distance vision dete-
riorates still further finally ending in light perception
only. The other symptoms are:
2. Near vision has a different course. If the lens changes
cause myopic shift, then the presbyope the elderly
patient had before cataract formation gets “correc-
ted”. Because of this neutralization of hypermetropic
defect of presbyopia by lenticular myopia, he might
be able to read without the aid of near vision glasses
which he had been using. This is called “second
vision” or “second sight”.
3. Some patients complain of black, fixed spots in the
field of vision. This is due to entoptic phenomenon.
4. Another symptom is uniocular polyopia which is

present even with one eye closed. This is due to diffe-
rent refractive indices of the cataractous lens fibers
in cortical cataract.
5. Colored haloes are seen by a few. This can be differen-
tiated from haloes of glaucoma by Fincham’s test -
haloes of glaucoma remain intact while those due to
cataract break up when slit lamp beam is passed
across the lens.
6. Some experience a minimal red tinge in their vision.
This poses a problem for artists. This is seen more in
nuclear cataract.
7. Glare by light is the most discomforting symptom
with cortical and posterior subcapsular cataract.
8. Frequent change of glasses.
Management is mainly surgical:
1. Any medical treatment will not dissolve lens opacity.
(Only in diabetic cataract, and that too in hydration
stage, is reversability seen). Spectacles are useful in
early stages. Mydriatic may be used. In modern days
surgery is done even at (early) immature stage.
2. Surgery can either be intracapsular (ICCE) (whole
lens with capsule removed) or extracapsular (ECCE)
(Posterior capsule left behind in eye and rest of lens
portions removed) extraction.
Before surgery is taken up projection of light, two
light discrimination, color perception and Marcus-Gunn
pupillary response should be checked. General state of
patient must be assessed. Local and systemic focus of
infection must be looked for and eliminated.
Preoperatively, pupil is dilated, ocular pressure
lowered with acetazolamide, ocular massage done and
minimal sedation given.
LENS 131
The operation is done either under general or local

anesthesia. In the latter technique, facial and retrobulbar
blocks are used. Peribulbar is another method that is
employed. The last method does not require facial block.
In ECCE the lens cortical material and the nucleus are
removed after opening the anterior capsule. Iridectomy
usually is not done. There are so many variations in
surgery. ECCE is popular nowadays since it facilitates
placing intraocular lens (IOL) behind the iris at the end
surgery.
IOL is made of PMMA, acrylic or silicone. The IOL
may be placed at three places inside the eye: (a) Behind
iris (posterior chamber lens), (b) attached to iris (iris
clip on lens) (Fig. 8.6), or (c) in anterior chamber
(Fig. 8.7). The last mentioned site is not much preferred
because of the possibility of damage to corneal
endothelium resulting in corneal edema and bullous
keratopathy. For posterior chamber IOL (Fig. 8.8) to
remain in position inside the eye it should be supported
by posterior capsule of lens behind (which is possible
only with ECCE)— otherwise IOL will slip into vitreous.
Posterior chamber IOL has to be fixed to sclera when
there is no posterior capsule of lens after cataract
surgery. Use of foldable IOL (Fig. 8.9) or rollable IOL
has brought down the size of limbal incision to one mm.
Eye in which lens is removed/absent is known as
aphakia. Aphakic eye wih IOL is known as pseudophakia.
Multifocal IOL (Fig. 8.10) and accommodative IOL are
now available. The power of IOL that has to be used is
calculated before surgery for every case.
Fig. 8.6: Pseudophakia with Iris—clip-on IOL
Fig. 8.7: Case of anterior chamber intraocular lens (IOL). There is

danger of corneal damage with this type of IOL
LENS 133
Fig. 8.8: Posterior chamber IOL. The IOL may or may not
have the dialing holes
Fig. 8.9: Foldable IOL. When this lens is used, the limbal (or scleral)
incision can be very small
Fig. 8.10: Multifocal IOL. With the advent of this lens, there is no
need for separate postoperative near vision correction
Complications
1. Posterior capsule opacification (PCO) is a common
postoperative problem after ECCE. It is managed
by making an opening in it with Nd: YAG laser caps-
ulotomy. Sometime a hydrogel IOL can become
opaque necessitating exchange of IOL.
2. Hyphema: Usually gets absorbed. Rarely it may
require evacuation if it persists beyond seven days.
3. Striate keratitis: It is due to Descemet’s folds and is
commonly seen. It disappears by itself. If marked,
local sodium chloride (5%) is used.
LENS 135
4. Shallow chamber: It is caused by:

a. Pupillary block (local mydriatic and, if needed,
peripheral iridectomy done)
b. Wound leak (proper suturing is a must).
c. Choroidal detachment (acetazolamide and if it
persists for one week, drainage).
5. Infection: Prevention is the best.
6. Cystoid macular edema: More frequently seen with IOL
implantation.
7. Retinal detachment: It is common with ICCE.
Other complications such as severe iritis(Fig. 8.11),
wound leak, glaucoma, vitreous incarceration, which
were seen once before with cataract operations, are rare
nowadays.
The recent surgical techniques for cataract are small
Incision cataract surgery (SICS), manual phaco and
phacoemulsification.
Fig. 8.11: Postoperative iritis after cataract extraction

DEVELOPMENTAL CATARACT
Whether it occurs at birth or later, the etiology is mostly

obscure.
a. Virus, especially rubella.
b. Deficient oxygenation to fetus due to placental
hemorrhage.
c. Maternal malnutrition involving vitamin D.
d. Radiation given.
e. Hypocalcemia.
f. Storage disorders.
g. Infant malnutrition.
h. In some cases hereditary factor plays a role.
Most of developmental cataracts do not attract the
attention of patients as they do not cause defective
vision due to their peripheral location. So patients with
this peripheral type of congenital cataracts may not have
any visual problem. Symptoms are mostly present with
centrally located ones. They cause defective vision,
white opacity in pupillary area (leukocoria), nystagmus
and squint. Opacity may involve anterior capsule,
anterior cortex, nucleus, posterior cortex, posterior cap-
sule and even whole lens. It occurs as punctate cataract
(blue dot, sutural cataract (Fig. 8.12) or dots in the
nucleus), coronary cataract (in the periphery as club
shaped opacities), coralliform cataract, anterior cortical,
anterior pyramidal cataract, disk-shaped opacity in
posterior cortex, anterior and posterior polar (capsule)
cataract or as total cataract. The more important variety
is zonular cataract.
Zonular (Lamellar) cataract is the commonest (50%)
of all developmental cataracts (Fig. 8.13). It can either
LENS 137
Fig. 8.12: Congenital (sutural) cataract
Fig. 8.13: Lamellar cataract. The typical central disc

and riders are seen
be due to hereditary (dominant) factor or to malnu-

trition, especially vitamin D. The fibers that develop
during period of malnutrition are opaque, while fibers
that develop before and after this period are clear. So,
the opaque fibers are buried in the middle of clear lens
area. The opacity is seen as a disc shaped one (end on
view) with riders faning out. Associated transverse lines
on permanent incisors and canine teeth are present.
In the management of congenital cataract, preli-
minary detailed examination and investigations are
important. Latter include estimation of glucose, calcium
and phosphorus levels of serum.
Treatment is carried out only if vision is grossly
affected. If possible, in central cataract with clear peri-
phery, the surgery should be postponed till puberty.
The retention of accommodation plays a great role in
the decision to operate.
In lamellar cataract, operation should be deferred
till the child is at least two years old. Till then the pupil
can be kept dilated with local use of mydriatic. Earlier
surgery is done if pupil does not dilate; opacity involves
the whole lens and if there is nystagmus or squint. While
dealing with developmental cataract the following
points are important/should be remembered:
a. Fixation develops within four months after birth.
b. These cataracts are soft and can be aspirated through
a small incision.
c. Timing of surgery.
d. Rehabilitation needed.
e. Accommodation, binocular vision and amblyopia.
f. Type of IOL used and
g. Power of IOL used.
LENS 139
The techniques used are:

i. Lensectomy (No posterior capsular opacifi-
cation (PCO), but retinal detachment may
occur)
ii. Lens aspiration with anterior vitrectomy (Less
PCO; for children below two years).
iii. Simple lens aspiration (best for IOL implan-
tation).
ACQUIRED CATARACT
It can be due to diseases of eye, systemic condition or

to injury. Most of these cataracts have polychromatic
lusture.
Diseases of anterior segment of eye such as corneal ulcer
and iridocyclitis and those due to posterior segment
lesions such as choroiditis, retinal detachment, retinitis
pigmentosa can produce such a cataract. In the begin-
ning, anterior segment lesions produce opacities in
anterior subcapsular region and in the cortical fibers
which are in front of nucleus, and posterior segment
diseases cause opacities in posterior subcapsular (bread
crumb) region and in the cortex behind the nucleus.
The typical appearance is polychromatic lusture.
Presence of cataract is confirmed by distant direct or by
direct ophthalmoscopy. Vision is affected early and the
cataract is usually soft in type.
The systemic diseases associated with acquired
cataract are diabetes, hypoparathyroid, galactosemia,
Alport, Lowe’s, Down’s syndromes and skin diseases
(syndermatotic cataract).
In diabetics the cataract develops earlier and faster.

In young patients true diabetic cataract occurs rarely.
Fluid vacuoles appear and later on “snowflake like” opa-
cities are seen under the capsule. It is due to hydration
of the lens.
Hypoparathyroidism results in hypocalcemia leading
onto cataract. This cataract appears as multicolored
lamellar (children) or as flakes of opacities in cortex
away from capsule (adults). In myotonic dystrophy
“Christmas tree-like” subcapsular (anterior and pos-
terior) opacities are seen. Sunflower cataract is seen with
errors of copper metabolism (Lowe’s syndrome)
Trauma: Mechanical, chemical and radiational— and
toxic substances such as dinitrophenol, thalium, strong
miotics, steroids and cyanate can result in cataract
formation (Fig. 8.14).
Fig. 8.14: Traumatic cataract

LENS 141
Cataract due to infrared (heat) is seen in glass

workers. The heat is absorbed by iris pigment and
indirectly causes lens opacities. The lens capsule may
peel off and curl up. Radiation and powerful electric
current also cause cataract.
Treatment, except that for the causative factor, is
essentially similar to senile cataract.
AFTER CATARACT (SECONDARY CATARACT)

This type of cataract is usually met with after ECCE.
The various types are:
1. The commonest type is posterior capsular opacification
(PCO) in which the transparent posterior capsule
that is left behind after ECCE slowly becomes opaque
(Fig. 8.15). Vision is impaired.
2. If the remnant anterior capsule fringe gets stuck to
posterior capsule and if the peripheral anterior
subcapsular epithelium proliferates, the new formed
abnormal fibers are restricted to periphery by the
above adhesion. This forms a ring behind iris—ring
of Sommering. Vision is not impaired. Rarely the ring
may get subluxated and cause glaucoma.
3. In certain situation, the remnant epithelial cells form
balloon like cells instead of fibers. These occupy the
pupillary area like pearls (Elschnig’s pearls). Vision
may be impaired (Fig. 8.16).
4. The remnant anterior capsule may become opaque.
Vision is not much impaired.
5. In cataract extraction, (ICCE and ECCE), when there
are severe iritis and exudation, these may organize
forming a fibrous membrane in the pupillary area.
Vision is impaired.
Fig. 8.15: Case of after cataract (posterior capsular opacification). The

thickened capsule was opened with laser. The opening is seen
Fig. 8.16: Elschnig’s pearls after extracapsular cataract extraction

LENS 143
Management is by making an opening in the after

cataract by instrumental needling (using Ziegler knife),
by vitreous cutter or by Nd: YAG laser. This is needed
only if the vision is affected.
SUBLUXATION AND DISLOCATION OF LENS:

(ECTOPIA LENTIS)
A lens is said to be subluxated if some of zonules are

still attached to it. It is called dislocated if all the zonular
fibers are detached from it. The lens is not in its usual
anatomical position either completely or partially.
The causes are:
1. Congenital
2. Traumatic
3. Ocular conditions
4. Certain systemic conditions (Marfan’s, Weil-Mar-
chesani, homocystinuria and Ehlers-Donlos
syndrome) and
5. Couching.
Ocular conditions than can cause subluxation are high
myopia, buphthalmos, keratoglobus, aniridia, Reiger’s
anomaly, uveitis and degenerative status inside the eye
including hypermaturity of cataract.
Couching is the method used by itinerant mendicants
to treat cataract by depressing the lens with a needle
passed into eye through limbus or sclera. It is not seen
now a day due to government steps to eradicate cata-
ract. It is very rarely done even now in very old patient
not fit for anesthesia and who are also mentally
deranged.
Dislocation types are:

a. Anterior,
b. Posterior and
c. Incarceration in the pupil (Fig. 8.17).
In posterior dislocation, the lens may slide down into
vitreous so that its anterior surface still faces anteriorily
(sliding) or it may topple over so that its posterior
surface faces anteriorily, i.e. sclera (reclination)
(Fig. 8.18). The iris shows iridodonesis and anterior
chamber is deep. Lens either remains clear (difficult to
see) or becomes opaque. Due to trauma the lens may
sometimes dislocate outside the globe and come to lie
under conjunctiva. This is known as phacocele. Lens
removal in this last mentioned condition should be
undertaken with caution as vitreous loss may occur.
Fig. 8.17: Dislocated lens incarcerated in the pupil. It can cause

secondary glaucoma
LENS 145
Fig. 8.18: Posterior dislocation of lens into vitreous
In anterior dislocation, the lens remains clear and

resembles a globe of oil in anterior chamber with a
golden rim (Fig. 8.19). If a nuclear cataract subluxates
into anterior chamber, it may resemble blood staining
of cornea. In the latter, clear corneal periphery is seen
all around the stained area. This clear periphery is not
seen in the lower quadrant with anterior subluxation of
nuclear cataract. Sometimes the nucleus alone is
dislocated. Anterior subluxation results in secondary
glaucoma.
Symptoms of such a condition depends on:
a. The area of lens in pupil
b. Its tilt
c. Its clarity
Fig. 8.19: Anterior dislocation of lens nucleus. It leads

to increase in ocular pressure
d. Associated complications. In subluxation, there may

not be any symptoms. Or, defective vision, glare and
uniocular polyopia may occur.
Management of anterior dislocation and pupil incar-
cerated lens is surgical removal of it. The same is for
posterior dislocation if there is complication such as
iritis, glaucoma, retinal detachment or optic atrophy.
Otherwise spectacles are given for posterior dislocation.
The aphakic area is corrected.
APHAKIA
It is absence of lens from its normal position, i.e pupillary

area. The cause can be (a) congenital (Very rare cause),
or due to (b) trauma and (c) surgery.
LENS 147
Patient has defective vision for both distance and

near. The signs are deep anterior chamber, iridodonesis
(tremulousness of iris due to loss of normal support by
iris), jet black pupil (Fig. 8.20), high hypermetropia,
hypermetropic fundus and absence of 3rd and 4th
Purkinje’s images (First and second images are formed
at the cornea and the third and fourth images are formed
at the lens). Evidence of operation, iridectomy and after
cataract may be seen. Loss of accommodation is present.
In pseudophakia, IOL is seen. The anterior chamber is
normal in pseudophakic eye with posterior chamber
IOL.
Treatment is by spectacles, contact lens, IOL or
refractive surgery (if the power is low). Now aphakic
spectacle has been almost totally replaced by IOL.
Fig. 8.20: Aphakia with peripheral and sector iridectomies.

Pupillary area is jet black in color
Even with latter, near vision needs spectacle correction.

But multifocal IOL has obliterated the use of spectacle
completely. Table 8.2 compares these treatment modali-
ties.
Usual power needed for aphakic spectacle (if the
patient’s vision had been normal before the onset of
cataract) is: For distant vision it is +10.0 D with astig-
matism and for near vision it is +13.0 D.
Posterior chamber IOL power is around + 19 and
that of anterior chamber IOL is about +14.
Table 8.2: Comparison of certain aphakic correction

Aphakic Correction with
Spectacle Contact lens IOL
Discomfort ++ + (of cleaning) Nil
Increase in
image size 30% 8% 1%
Diplopia + No No
(if other eye
is normal)
Fields Restricted Normal Normal
Roving ring
scotoma + No No
Jack-in-box
phenomenon + No No
Pin cusion
effect + No No
Cosmetic
disfigurement + No No
Pin cushion effect is due to spherical aberration.

Roving scotoma is caused by prismatic aberration and
is seen between 50 to 65o of visual fields.
9
Glaucoma
Glaucoma cases are not kept for undergraduates in the

clinical examination. Questions on glaucoma are
frequently asked in theory examination and to a lesser
extent in orals. Recognition (or even suspecting its
presence) is important in a general practitioner’s clinical
practice.
Examination for a case of glaucoma requires many
instruments. Anterior segment should be examined
with slit-lamp, cornea with pachymeter and angle of
anterior chamber with gonioscopy. Fundus study is by
direct and indirect ophthalmoscope with or without
fluorescein angiography. Field study is by static
perimetry.
ANATOMY
Angle of anterior chamber (A/C) is formed by peri-

pheral posterior surface of cornea in front, and by root
of iris, part of ciliary body and trabecular meshwork
(TMW) behind (Fig. 9.1). This angle is from 20° (narrow)
to 40° (open; normal). TMW is a sieve-like structure in
many layers and has three parts—uveal, corneoscleral
and juxtacanalicular. Outside to it is Schlemm’s canal,
a circumferentially running channel into which aqueous
drains. Schlemm’s canal communicates with general
circulation via aqueous vessels.
Aqueous is secreted by ciliary body and is poured
into posterior chamber (posterior chamber is the space
between the iris in front, and zonules and lens behind).
From here aqueous goes into A/C via the pupil. It leaves
the eye mainly by two routes:
1. Trabecular route, which is via TMW and Schlemm’s
canal. About 90% of aqueous flows through this
route.
GLAUCOMA 151
Fig. 9.1: Anatomy of angle of anterior chamber. (A) Cornea.

(B) Schlemm’s canal. (C) Collector channels. (D) Ciliary body.
(E) Trabecular meshwork (TMW). (F) Lens
2. Uveoscleral route which is via ciliary body into

suprachoroidal space.
ETIOLOGY
The cause of glaucoma is obstruction to the outflow of

aqueous (at pupil, A/C angle or aqueous vein) or excess
secretion of aqueous. Such an increase in ocular pressure
presses on the whole of eyeball coat; but the weakest
point gives way—this point being optic disk. The disk
and the nerve fibers of retina are damaged. Apart from
mechanical damage to disk, such an increase in IOP re-
sults in reduction in blood flow to disc and dysfunction
of axoplasmic transport (which causes death of retinal
ganglion cells). These patients may also have inherent

susceptibility to increased IOP. The optic disk damage
can also occur even with normal IOP.
Normal intraocular pressure is 10 to 21mm Hg. This
is measured by Schiotz tonometer (which can give false
reading if there is change in scleral rigidity) or with
applanation tonometer (which gives more accurate
reading).
There are many classifications of glaucoma. The
simplest one is:
CONGENITAL GLAUCOMA
This includes developmental glaucoma, late onset

glaucoma and pediatric glaucomas. For undergraduate
purpose, congenital glaucoma specifies primary
congenital glaucoma which is otherwise known as
buphthalmos or hydrophthalmia.
GLAUCOMA 153
PRIMARY CONGENITAL GLAUCOMA
It is due to failure of iris to separate completely from

cornea so that A/C is not communicating with trabe-
cular meshwork. The idea that angle is covered by a
membrane (of Barkan) is not substantiated by histo-
logical studies. It has autosomal recessive inheritance.
Male: Female = 3:2. Glaucoma occurs within two years
of life. It is a bilateral (75%) condition. The parents notice
that the eye is larger, that cornea is hazy, and that the
child has photophobia and watering from eye (Fig. 9.2).
Examination shows increase in corneal diameter and
curvature. Corneal diameter of 13 mm and more is
significant (Fig. 9.3). Corneal haze and even lines of
corneal opacity (Haab striae), deep A/C, iridodonesis
and, later, thinning of sclera near limbus are other
Fig. 9.2: Case of congenital glaucoma
findings. The eye is myopic. Fundus shows increase in

optic disc cup. Gonioscopy reveals anterior insertion
of iris at angle (Fig. 9.4). At the end stage vision is totally
lost. Rarely it may not be lost.
Fig. 9.3: Close-up of cornea of case 10.2
Fig. 9.4: Goldman three mirror gonioprism. This is used to assess the
anterior chamber angle width and structures
GLAUCOMA 155
Treatment is surgical only. Goniotomy, trabeculo-

tomy or, if these two fail, trabeculectomy is recom-
mended.
In goniotomy, a knife (Barkan’s) is passed via limbus
and the opposite angle is incised for 180°. In trabeculo-
tomy, Schlemm’s canal is entered with a probe from
exterior through sclera. The angle is opened by rotating
the probe into A/C. Trabeculectomy is a filtering
surgery.
PRIMARY GLAUCOMAS
They are called so because they are not secondary to

any other ocular, systemic or traumatic causes. They
are of two types—narrow and open angle.
Narrow (Closed) Angle Glaucoma

In this condition, the A/C is shallow and its angle is
less than 20°, i.e. narrow (Fig. 9.5). It is more common
in females and in adults in 5th decade of life and after.
When the patient reaches the 5th decade of life or so,
the shallowness worsens due to increase in thickness of
lens. In such a situation, if pupil dilates due to any cause,
the iris gets bunched up at the angle. The angle gets
closed totally, aqueous gets stagnated in A/C and IOP
goes up. So, basically for this type of glaucoma to occur,
narrow angle and mydriasis both are needed.
In the evolution of narrow angle glaucoma there are
five stages. In the first stage (prodromal stage) persons
have discomfort now and then with colored haloes and
blurring of vision. These colored haloes, caused by fluid
Fig. 9.5: Composite diagram showing anterior chamber angle in

(A) Open angle eye (width 40°) and (B) in narrow angle eye (width 20°
and less)
in cornea, have red outside and violet inside. It is

differentiated from haloes due to cataract by Fincham’s
test—haloes of glaucoma remain intact while those due
to cataract break up when slit-lamp beam is passed
across the pupil.
Later on these symptoms recur constantly (stage of
constant instability). In such a case, when pupil dilates
due to any cause, an increase in IOP supervenes. This
passes off when patient sees a bright light, sleeps or
rests his eyes.
Acute congestive glaucoma is the third stage. It is seen
more in ladies above the age of 40. It is usually unilateral
at a time; but simultaneous bilateral occurrence is also
met with. The patient has shallow A/C and narrow
angle. When pupil dilates due to any cause such as local
application of mydriatic or patient being in a dark room,
the iris bunches up at the angle and obstructs out flow
of aqueous. The IOP goes up and acute attack super-
venes.
GLAUCOMA 157
Patient develops systemic symptoms such as fever,

pain abdomen and nausea. Severe eye pain, ipsilateral
headache and marked defective vision are constant
symptoms. Eye shows ciliary congestion, hazy cornea,
shallow A/C and dilated sluggish pupil. Vision is
reduced to light perception. IOP is raised to about 60
mm Hg (Normal is 10 to 21 mm Hg). Gonioscopy shows
closed angle. The disk initially shows edema and later
deepening widening of optic cup. The contralateral eye
has shallow A/C and narrow angle.
If untreated this acute stage goes onto the next stage-
chronic congestive stage—in which the angle is per-
manently closed for more than 1/3rd of the circum-
ference. The tension is constantly elevated. Disk damage
progresses.
The final stage is absolute glaucoma.
Management of acute congestive glaucoma is mainly
three-fold:
1. Constricting the pupil with local frequent application
of miotic such as pilocarpine or reducing the IOP with
local medication such as Timolol (0.5%) twice a day.
Pilocarpine may not act at higher ocular pressure.
2. Assisting reduction of IOP with systemic acetazo-
lamide (250 mg 8th hrly), or with intravenous urea
or mannitol.
3. Analgesics: Sometimes even opioid derivative is used.
Local cortisone drops is applied to reduce inflamma-
tion. Whether IOP comes down or not, case is usually
taken up for either laser iridotomy or for peripheral
iridectomy within 48 hours. If angle is occluded by more
than 1/3rd, then filtering surgery is needed.
Instillation of miotics to contralateral eye should

not be forgotten. Prophylactic laser iridotomy should
be done in the contralateral eye.
Left untreated, the condition goes onto chronic con-
gestive glaucoma stage. In chronic congestive glaucoma
stage only filtering surgery is effective.
Open Angle (Chronic Simple) Glaucoma

This is met with in adults of more than 50 years of age.
The angle and A/C are normal. The cause of obstruction
to aqueous outflow is at trabecular meshwork (TMW).
Its openings are reduced due to sclerosis and thus the
aqueous out flow to Schlemm’s canal is impaired. The
IOP goes up (compare this situation with raised blood
pressure due to sclerosis of blood vessel which reduces
its lumen resulting in impairment to smooth flow of
blood).
It is almost a symptomless disease. Patient may be
changing spectacles often— especially for reading. The
eye is normal; so also angle by gonioscopy.
The diagnosis depends on three signs:
1. Raised intraocular pressure (Figs 9.6 to 9.9): In the
beginning it may not be present throughout the day
and circadian variation is seen. If this variation is
more than 8 mm Hg between the highest and lowest
recorded IOP in a day, it is suspicious. The circadian
rise of IOP may occur once a day (monophasic) or
twice a day (biphasic) (Fig. 9.10). Later on IOP
remains constantly elevated and is around 30 mm
Hg. Measurement of corneal thickness is necessary
for correct assessment of IOP.
GLAUCOMA 159
Fig. 9.6: Schiotz tonometer
Fig. 9.7: Estimation of intraocular pressure with Schiotz

tonometer (tonometry)
Fig. 9.8: Applanation tonometer. It gives more accurate

measurement of ocular pressure
Fig. 9.9: Measuring intraocular pressure with applanation tonometer

GLAUCOMA 161
Fig. 9.10: Figure showing the possible circadian variation in

intraocular pressure. (A) and (B) Monophasic rise. (C) Biphasic rise.
Striations — normal intraocular pressure range.
2. Field of vision (Fig. 9.11)—scotoma (blind area) in the

central 1/3rd of field of vision as well as constriction
of peripheral field are seen. The scotoma in the
central field area starts near blind spot barring it first.
It then spreads like a comma above and below the
blind spot (Seidel’s sign). Later it curves around the
fixation point (arcuate or Bjerrum’s scotoma). The
upper and lower arucate scotomata meet at the
Fig. 9.11: Estimation of field of vision with computerized perimeter
opposite side of fixation point forming a ring scotoma.

This meeting point is not exact so that it shows a
step—Roenne’s nasal step (Fig. 9.12). Later on this ring
scotoma spreads centrally and peripherally - the
latter scotoma merging initially with peripheral field
defect (constriction) at superonasal aspect. This is
called superonasal breakthrough. The spread of
scotoma continues in all direction. In the penultimate
stage there is a seeing area around fixation point and
a kidney shaped seeing area in the inferotemporal
aspect of field. The rest of the field of vision is blind.
The patient has tubular vision. The patient’s acuity
GLAUCOMA 163
Figs 9.12A to F: Composite diagram showing the stages of progression

of visual field defects in glaucoma. (A) Baring of blind spot. (B) Seidel’s
sign. (C) Arcuate (Bjerrum’s) scotoma. (D) Ring scotoma with Ronne’s
nasal step. (E) Superonasal breakthrough of central field defect towards
(spreading) peripheral field defect (not shown). (F) Penultimate stage.
(Dotted areas—seeing regions)
of vision remains the same as before almost un-

affected upto this stage. The acuity of vision being
almost the same and this disease being a symptom-
less one, the patient may not be aware that he has
such a condition unless he is intelligent enough to
appreciate the constriction of fields.
3. Optic disc changes: To begin with, the site of central

retinal vessels in the disc shifts to nasal side. Later
on the cup—which normally occupies the central
1/3rd of disk— enlarges. The retinal vessels seem
to be cut off at the cup margin. Hemorrhages are
seen over the disk margin. Finally the cup margin
reaches almost the edge of disk. The color also pales
(Fig. 9.13). In the final stage the disc becomes papery
white in color (Glaucomatous optic atrophy).
Figs 9.13A to C: The progression of disk changes in glaucoma. 0.3—

Normal cup disk ratio. 0.7—the confirmative cup disk ratio of glaucoma.
0.8—glaucomatous cupping. The retinal vessels’ origin and emergence
from disk are shifted to the nasal side
GLAUCOMA 165
Management is mostly by drugs locally which lower

IOP (in various combinations and frequencies) with or
without oral acetazolamide. To begin with one kind of
drops is advised. If this is ineffective, it is changed to
another drug rather than adding one more. If a single
drug therapy in varying strength and frequencies fail,
then combination of drops is advocated. These drugs
can be combined with oral acetazolamide or metha-
zolamide (Table 9.1).
The drops used are pilocarpine, adrenergic and
prostaglandin analogues, and beta blockers. Beta
blockers lower IOP by reducing aqueous secretion and
most of them are equally effective. Some of the drugs
used are:
1. Timolol (0.25 to 0.5%; bid). It is contraindicated in
bronchial asthma.
2. Betaxolol (0.25% bid). This drug is safe in cardio-
pulmonary cases.
3. Carteolol (1% bid)
4. Levobunolol (0.2% bid)
5. Epinephrine (0.5 to 2%; bid) and
6. Latanoprost
Pilocarpine is not preferred because older persons
do not tolerate it well and in younger patients it causes
accommodation spasm. It lowers intraocular pressure
by opening spaces in TMW. Prostaglandin analogue,
Latanoprost, reduces IOP by increasing uveoscleral
flow. So it potentiates the effect of beta-blockers.
Adrenergic drugs include epinephrine (0.5 to 2%; bid;
lowers IOP by increasing outflow) and apraclonidine
(0.5 to 2%; bid; lowers IOP by decreasing aqueous
production).
Table 9.1: Drugs used in glaucoma

Drug Mechanism Dosage Onset Remarks
duration
Adrena- α and β 0.1- 2%
line or agonists
epine-
phrine
Timolol Beta -blocker 0.25 - 30 mts Allergy +
0.5% 12-24 can cause
hours systemic side
effect. Neuro-
protector
Carteolol Beta-blocker 1.0% 30 mts
12-24 hrs
Clonidine α2 adrener- 0.125% 8 hours Local
gic agonist bid application
lowers BP
caution with
CV disease
Apraclo- α2 adrenergic 0.5 -1% No effect on BP
nidine agonist if used locally
Tachyply-
laxis+
Brimo- α2 adernergic 0.5 -2% It is a neuro-
nidine agonist protector.
Allergy +++
No
tachyphylaxis
Pilocar- Muscarinic 1 - 4% 30 mts Systemic
pine agent 8 hrs effects +
Muscular
weakness +
Betaxolol Non-selective 0.25 - 30 mts Neuroprotec-
adrenergic 0.5% 12 - 24 tor can be used-
β-blocker hrs in pulmonary
cases
Contd...
GLAUCOMA 167
Contd...
Drug Mechanism Dosage Onset Remarks
duration
Carteolol β1 selective 1% 30 mts
adrenergic 12 - 24 hrs
blocker
Levo- Non-selective 0.25% - 30 mts
bunolol β-adrenergic 0.5% 12-24 hrs
antagonist
Dipive- Non-selective 0.1% 1 hr
frin adrenergic 12-24 hrs
agonist
Dorzo- Carbonic 2% 8 hours
lamide anhydrase 250 mg
Acetazo- inhibitors 8 hourly
lamide
When medicines fail to control the ocular pressure

and the disease is progressing, any one of the filtering
surgeries – popular one is trabeculectomy – is done. In
these operations a new communication is made between
A/C and subconjunctival space. (Compare it with
treatment for hydrocephalus). The aqueous that is
drained into subconjunctival space forms a bleb near
the limbus (Fig. 9.14).
Laser is also used to treat this condition. Argon laser
trabeculoplasty (diode laser also can be employed)
shrinks the TMW collagen thereby opening the pores
in TMW. Laser therapy is attended with transient rise
in ocular pressure, uveitis and hyphema.
ABSOLUTE GLAUCOMA
It is the end stage of all glaucomas. The cornea is hazy,

pupil dilated and fixed and iris is atrophic. IOP is raised
to about 60 mm Hg and optic disk shows glaucomatous

optic atrophy (Fig. 9.15). Vision is totally lost. The eye
is painful. The eye may finally become atrophic.
Fig. 9.14: A thin-walled bleb at limbus after a filtering surgery. The aqueous
bye passes its normal route through angle of anterior chamber and drains
into subconjunctival space
Fig. 9.15: Glaucomatous optic atrophy. Disk color is white and the
cup has enlarged almost up to the disk margin
GLAUCOMA 169
Management
It is mainly for the pain the patient has:
1. Cyclodestructive procedure is carried out to reduce
IOP and to relieve pain.
2. Retrobulbar alcohol injection may be given (it should
not enter the arterial circulation). It may be effective
for 2 to 4 weeks in relieving pain.
3. Enucleation if pain is not relieved by the above
methods.
PROVOCATIVE TESTS
These tests are not very popular now days and mostly
not performed.
In doubtful cases of glaucoma which are not yet full
blown cases, the eyes are “provoked” into glaucomat-
ous state. In narrow angle eyes, the provocation is by
dilating pupil (by applying homatropine or keeping the
patient in a dark room) or by increasing shallowness of
A/C (patient lies in prone position). These tests can be
combined.
In open angle eye, the provocation is by increasing
the aqueous secretion. This is done by asking the patient
to drink 500 ml of water in five minutes (Water drinking
test).
In all these tests, any variation of pressure of 8 mm
Hg or more from base level is positive. But a negative
test does not rule out occurrence of glaucoma later on.
Tonography when combined with these tests gives a
better clue.
CERTAIN OTHER GLAUCOMAS
Following glaucomas are some of the secondary

glaucomas.
Phacomorphic glaucoma is the one seen in shallow
chamber eye in which lens has swollen up (intumescent
stage of cataract formation). Anterior dislocation of lens
also is another cause. Management is by removing lens.
Phacolytic glaucoma is raised IOP due to blocking
of angle by macrophages loaded with lens protein. This
is seen with Morgagnian hypermature cataract. A/C is
deep in this case.
Dislocation of lens into anterior chamber (blocks
anterior chamber angle) (Fig. 9.16), a pupil incarcerated
Fig. 9.16: A dislocated lens into anterior chamber. This blocks the
angle of the anterior chamber and causes increase of ocular pressure
GLAUCOMA 171
lens (Fig. 9.17) and a posterior dislocated lens (irritates

ciliary body which results in increased aqueous
secretion) give rise to (secondary) glaucoma.
Hyphema is blood in anterior chamber (Fig. 9.18). It
can be due to iridocyclitis (especially gonococcal or
viral), trauma, or seen after operation. Spontaneous
occurrence is also met with.
Hyphema can cause secondary glaucoma. If
intraocular pressure is raised, it can result in blood
staining of cornea (Fig. 9.19). Such blood staining may
occur even with normal ocular pressure. Blood staining
affects the central cornea with clear corneal area all
around. It has to be differentiated from anterior dis-
location of nuclear cataract in which clear area is not
seen in the lower quadrant of cornea.
Fig. 9.17: Lens incarcerated in pupil. This gives

rise to secondary glaucoma
Fig. 9.18: Blood in anterior chamber (hyphema) due to trauma. Intra-

ocular pressure goes up due to blood cells blocking anterior chamber
angle. Sometimes, associated recession of chamber angle may also
contribute to raised ocular pressure
Fig. 9.19: Blood staining of cornea

GLAUCOMA 173
Hyphema mostly clears up well. Acetazolamide is

given. Otherwise draining the blood by paracentesis is
advised. Blood staining clears up over months. If it does
not, then keratoplasty may have to be done.
Hemorrhagic glaucoma is seen with cases of
neovascularization of iris (Fig. 9.20) and of angle of
anterior chamber. This is seen in chronic iritis, and in
those conditions of retina which give rise to retinal neo-
vascularization such as diabetic retinopathy.
Raised IOP is seen with local use of steroids, after
intraoculer hemorrhage, along with uveitis, pseudo-
exfoliation of lens capsule (Glaucoma capsulare),
aphakia and intraocular tumors.
Fig. 9.20: Neovascularization of iris in a case of chronic

iridocyclitis with consequent secondary glaucoma
10
Vitreous
Vitreous is never kept as a case for undergraduates.

Questions on vitreous are rarely asked in theory
examination.
ANATOMY
It is a gel like structure situated in vitreous chamber

behind the lens. It occupies 80% of eye volume. It is
avascular and transparent. Subhyaloid space is present
between internal limiting membrane of retina and
vitreous. It is attached to lens (by Weigert ligament), to
ora serrata and to optic disk. Vitreous base is attached
to Müller’s cells and to optic disk. Cloquet canal (pri-
mary vitreous) extends from lens to optic disk. Vitreous
gives form to eye and is a source of nutrient to retina
and lens.
VITREOUS OPACITIES
These opacities are divided into developmental and

degenerative.
Developmental
These opacities which are remnant of hyaloid system
are in the canal of Cloquet which runs in the middle of
vitreous.
Degenerative
a. Muscae volitantes: It is seen in elderly individuals.
Vitreous gets liquified and vitreous fibers condense
floating in the fluid vitreous. If one sees against a
VITREOUS 177
bright background like clear sky, floaters of various

shapes and sizes are seen. They may be caused by
remnant of hyaloid vasculature (physiological). This
may be experienced by younger individuals. This
needs no treatment. But sudden, marked increase in
the number and size of floaters requires thorough
study of fundus.
b. Synchisis scintilans: In this condition cholesterol is
deposited in the vitreous (and also in subretinal space
and anterior chamber also). Multiloculated, multico-
lored, glistening, gold dust like opacities floating in
the fluid vitreous are seen (Fig. 10.1). Any eye
movement causes a “shower of gold particles” in
vitreous. Except reassurance, treatment is not
needed.
Fig. 10.1: Synchisis scintilans

Fig. 10.2: Asteroid hyalosis
c. Asteroid hyalosis: Spherical, white, calcium contai-

ning, fixed opacities are seen in vitreous (Fig. 10.2).
Affecting both sexes it is mostly a unilateral condi-
tion seen in diabetes. It is associated with hyper-
cholesterolemia. Treatment is not needed unless the
opacities are very dense in which case vitrectomy
may be advocated.
d. Amyloid: This is seen along with systemic
amyloidosis. It is a bilateral condition. Apart from
linear vitreous opacities which are attached to retina
and lens, retinal hemorrhages and retinal exudates
are also seen. Treatment with vitrectomy may not
be satisfactory.
e. Other causes: Hemorrhages into vitreous, inflam-
matory cells due to cyclitis and retinal vasculitis and
neoplastic cells.
VITREOUS 179
VITREOUS HEMORRHAGE
Since it may cause sudden, painless loss of vision, it is

an alarming condition for the patient. This loss may be
preceded by floaters.
It can be detected by slit-lamp, ophthalmoscopy and
B scan. Hemorrhage can be in pre retinal (subhyaloid)
region or in vitreous itself. In the former the blood that
does not clot is boat shaped with horizontal upper
border. It moves freely. The hemorrhage is red in color;
but changes as time goes on. In very long standing cases
it settles down as white opaque mass.
Causes
1. Trauma: It may be due to concussion or perforating
injury. The bleeding is usually seen in vitreous.
2. Ocular Conditions: Diabetic retinopathy, central
retinal vein thrombosis (bleeding is from the delicate
new vessels), retinal neovascularization, retinal tear
(mostly in myopes) and posterior vitreous retraction.
Bleeding due to posterior vitreous detachment
occurs either in vitreous or in preretinal area. Pre-
retinal hemorrhage sinks down and appears like a
boat. It usually clears up well. Vitreous hemorrhages
are also seen in Eales’ disease which is vasculitis of
retinal vessels in young persons. It is characterised
by vitreous hemorrhage, vasoproliferation, new
vessels, soft exudates and retinal edema. Final pic-
ture is fibrous tissue proliferation in vitreous, reti-
nal detachment, secondary glaucoma and blindness.
3. Rupture of intracranial aneurysm (subarachnoid
hemorrhage).
Investigations
1. Detailed fundus study: If possible by direct ophthalmo-
scopy and distant direct ophthalmoscopy.
2. Biomicroscopic study.
3. B scan study: Free blood shows point – like echoes.
Settled down hemorrhage is seen as flat sheet of
echoes. B scan can detect retained foreign body also.
4. X- ray to rule out retained intraocular foreign body.
Management
1. Treatment of cause.
2. Bed rest with closure of eye (rest to the eye).
3. Closure of bleeding vessel by photocoagulation.
4. Vitrectomy if blood is not absorbed in 90-100 days.
PERSISTENT HYPERPLASTIC VITREOUS
It is a developmental anomaly in which primary

vitreous fails to regress.
It may affect the:
1. Anterior end nearer to lens giving rise to leukocoria,
or
2. Posterior end at optic disk in which persistent hya-
loid artery is seen at optic disk. Anterior one may be
associated with microphthalmos, glaucoma, cataract
and intraocular hemorrhage. Posterior type may get
complicated by tractional retinal detachment of
considerable size.
SURGERY ON VITREOUS
Vitreous was once considered as a hallowed site.

VITREOUS 181
The simplest intervention is intravitreal injection

of antibiotic or cortisone.
Vitrectomy
It is grouped into anterior vitrectomy, cone vitrectomy
and total vitrectomy depending on the amount and
position of vitreous that is to be removed. The entry is
through pars plana. Three sclerotomies are needed.
Vitrectomy instrument and endoilluminator are used.
Endophotocoagulation or endodiathermy with diode
laser can also be used. Vitrectomy is usually done along
with retinal surgery.
The indications for vitrectomy are:
a. To remove vitreous hemorrhages, tractional bands
and membrane over retina.
b. To treat abnormal retinal vessels.
c. To deal with retinal breaks by cryotherapy or
endophotocoagulation.
d. To drain sub-retinal fluid.
e. To inject silicon oil or gas into vitreous.
f. In endophthalmitis, to remove the infected tissue.
Types
It can be grouped into:
1. Open sky : It is done in trauma, vitreous touch, loss
of vitreous in cataract surgery and keratoplasty.
Dislocated lens can be removed by this route.
2. Closed Vitrectomy. Visual result of any vitrectomy
depends on so many factors.
11
Retina
Retinal pathology is not kept for undergraduate clinical

examination. Retina topics are frequently asked in
theory papers. Fundus examination is important for
physicians and neurologists.
Fundus is examined with indirect (Fig. 11.1) or direct
(Fig. 11.2) ophthalmoscopy. A+ 90 D lens using a slit-
lamp is also employed to see the ocular fundus. Each of
the former two methods have their own advantages and
disadvantages.
Fig. 11.1: Indirect ophthalmoscope
Fig. 11.2: Direct ophthalmoscope

RETINA 185
ANATOMY
Retina extends from optic nerve to ora serrata. It has

ten layers – the outermost pigment epithelium and the
inner nine neuronal layers. The layer of rods and cones
are deeply placed nearer to choroid (Fig. 11.3). The
acuity of vision depends on a 1.5 mm area called fovea
centralis situated in the middle of macula lutea. Macula
is about 2 disks diameter temporal to optic disk. This
area has only tightly packed cones. Ora serrata is the
anterior, peripheral, serrated edge of retina. Retina does
not reach upto ciliary body. Retina is supplied by central
Fig. 11.3: Layers of retina. (A) Inner limiting membrane. (B) Nerve fiber
layer. (C) Ganglion cell layer. (D) Inner plexiform layer. (E) Inner nuclear
layer. (F) Outer plexiform layer. (G) Outer nuclear layer. (H) Outer limiting
membrane. (I) Layer of rods and cones. (J) Pigment cell layer.
(1) Ganglion cell. (2) Nucleus of first order neurone. (3) Cones. (4) Rods
retinal vessels except for the outer layer which derives

its blood supply from choroid.
Of special importance to undergraduates are
disorders due to certain systemic diseases, retinal
detachment, dystrophy and tumor.
NORMAL FUNDUS
It has a pink color with uniform stippling. Medial to its

central point is the optic disk which is a little redder in
color. It is an oval structure with a depression (cup) in
its inner one-third. The central retinal artery emerges
from the cup and central retinal vein enters it to leave
the eye. In the center of retina and 3 mm temporal to
disk margin is macula lutea. In its center is fovea
centralis (Fig. 11.4). (Peripherally retina ends at the ora
serrata which is not visualized during the routine
fundus examination).
Fig. 11.4: Normal fundus showing the optic disk,

the retinal vessels and macula
RETINA 187
HYPERTENSIVE RETINOPATHY
Retinal vessels reflect the changes in systemic vessels

in hypertension. These changes in retina are divided
into four grades (Keith and Wagner 1939) (Fig. 11.5).
Grade I: There is narrowing of arterioles. Sclerosis is
present in them.
Grade II: The narrowing increases. Arterio venous (AV)
changes appear—the veins are deflected at AV cros-
sings. This is known as Salus’ sign. The light reflex on
the arterioles is exaggerated.
Grade III: The color of arterioles resembles that of copper
wire. The blood gets stagnated in veins distal to AV cros-
sing (Bonnet sign) with tapering of the veins on either
side (Gunn’s sign). Cotton-wool and hard exudates along
with superficial hemorrhages are seen (Fig. 11.6).
Fig. 11.5: Hypertensive retinopathy showing superficial hemorrhages

and soft exudate. Blurring of disk margin is seen
Fig. 11.6: Composite diagram showing the findings in hypertensive

retinopathy at various stages. (I) Grade I. (II) Grade II. (III) Grade III.
(IV) Grade IV. (A) Arteriolar narrowing. (B) Salus sign. (C) Flame shaped,
superficial hemorrhages. (D) Cotton wool exudates. (E) Banking (Bennet’s
sign) and “discontinuity” (Gunn’s sign) of venous blood column.
(F) Copper wire reflex. (G) Macular star. (H) Papilledema
Grade IV: The arterioles appear like fibrous thread (Silver

wire appearance). Edema of disk appears. Macular star
may be seen.
These changes occur in four situations:
1. In the absence of sclerosis (young patients). The signs
are minimal. Straightening and acute branching of
arterioles are seen. Soft exudates are seen; but never
hard ones.
2. In presence of involutionary sclerosis (older patients).
All signs of hypertensive retinopathy (except disk
edema) are present.
RETINA 189
3. In arteriolar sclerosis: This is also present in young

patients in whom kidney is also affected. This renal
retinopathy shows AV changes, hemorrhages and
plenty of exudates which form macular star. Vision
is affected permanently.
4. Malignant hypertension: In young patients. Edema is
prominent including that of optic disk.
PREGNANCY INDUCED HYPERTENSION
This is seen in eclampsia of pregnancy which occurs in

late months of pregnancy. The signs are marked
narrowing of arterioles—nasal ones to begin with and
cotton-wool exudates. Superficial hemorrhages appear
followed by exudates and macular star. AV crossing
changes are not seen. These signs are met with when
blood pressure goes above 180/110 mm Hg and there
is pedal edema. The appearance of exudative retinal
detachment is an indication for medical termination of
pregnancy.
DIABETIC RETINOPATHY
The retinopathy due to diabetes depends on duration

of systemic disease. The incidence is 7% in diabetic
patients of 10 years duration while it is 63% for 15 years
duration. The age at which the diabetes is detected also
is important in the development and prognosis of
retinopathy. It is basically a microvascular occlusion
which results in retinal ischemia. The latter leads to
retinal hemorrhages, microaneurysms (MA) and
exudates.
The stages in the development of retinopathy are:
Non-proliferative Diabetic Retinopathy (NPDR)

The fundus picture ranges from very mild condition to
very severe one. Microaneurysms and deep (dot and
blot) hemorrhages are seen. Both appear like red dots.
Hemorrhages are transient, while microaneurysm is
permanent. Yellowish white, hard exudates appear.
They may surround the macular area. Cotton-wool (soft)
exudates and larger hemorrhages appear later on.
Capillaries show occlusion and the arteries narrowing,
occlusion and sheathing. Venous beading, dilatation,
looping and occlusion are seen. Intraretinal micro-
vascular abnormalities (IRMA) involving capillaries
appear (Fig. 11.7).
Fig. 11.7: Non-proliferate diabetic retinopathy. Round (deep) and

superficial hemorrhages and hard exudates are seen
RETINA 191
Macula gets affected in this (and next) stage. There

are three ways this can happen:
1. The blood supply to macula is cut off resulting in
ischemia (Microaneurysm and hemorrhages at
macula with marked defective vision).
2. Hard exudates at macula in a circular pattern along
with microaneurysms and hemorrhages.
3. Leakage of fluid leading onto macular and retinal
edema. Exudates are very much less.
Proliferative Diabetic Retinopathy (PDR)

It is usually seen when diabetes has lasted for about 20
to 30 years. Along with signs of NPDR, neovas-
cularization is present. Presence of large blot hemorr-
hages temporal to macula, large areas of capillary
obstruction, eight or more cotton-wool spots and exten-
sive retinal hemorrhages are signs of impending
neovascularization. They are almost always seen in the
posterior fundus. Fibrous tissue invades. This is mostly
seen arising from optic disk, but it occurs also along
the course of retinal vessels (Fig. 11.8). Either they are
in the retrovitreal space, or invade the vitreous. Later
on fibrous tissue surrounds these vessels, contract and
lead to tractional retinal detachment. Vitreous
hemorrhage occurs. Vitreous shows contraction,
thickening and detachment of posterior hyaloid
membrane. These signs may be complicated by
neovascular glaucoma (Fig. 11.9).
Almost half the patients who are blind due to PDR
die within five years.
Management of diabetic retinopathy is mainly that
of systemic disease.
Fig. 11.8: Proliferative diabetic retinopathy. The fibrous tissue is seen
Fig. 11.9: Composite fundus picture showing the findings in the various
stages of diabetic retinopathy. BDR – Background diabetic retinopathy.
PPDR – Preproliferative diabetic retinopathy. PDR - Proliferative diabetic
retinopathy. (A) Dot (deep) hemorrhage. (B) Hard exudates.
(C) Microaneurysm. (D) IRMA. (E) Venous beading. (F) Cotton-wool
exudates. (G) Flame shaped hemorrhages. (H) Retinal detachment.
(I) Neovascularization. (J) Circinate retinopathy
RETINA 193
1. Clofibrate helps in absorption of exudates. This drug

has to be given for a long time and has no relation-
ship to visual improvement.
2. Calcium dobesilate has beneficial effect on abnormal
capillary permeability.
3. Flavinoid group of drugs helps in treating capillary
abnormality.
4. Pituitary ablation is effective in florid cases in main-
taining the vision and preventing blindness.
5. Aspirin may be effective.
6. Intravitreal triamcinolone (4 to 6 mg) is effective in
diabetic macular edema, especially if it is combined
with grid photocoagulation.
7. Laser application to retina destroying non-perfusing
portions of it is the important treatment method.
Laser is given:
a. At focal areas to destroy microvascular lesions.
b. Over large area of retina (at least 3 disk diameter
from macula) destroying some areas of the retina
so that the ischemic state is relieved (called pan-
retinal photocoagulation)
c. In a grid pattern over macular area when there is
severe macular edema. Either diode or Argon
laser is used. Laser is not used in macular ische-
mic state.
Laser should not be applied over macula or over
large retinal vessels.
8. In advanced cases surgery is undertaken for retinal
detachment and vitreous hemorrhage (vitrectomy).
RETINOPATHY OF PREMATURITY
(RETROLENTAL FIBROPLASIA)
This is seen when premature infant of less than 33 weeks

are weaned from the oxygen that was being given to it.
The oxygen concentration in such a situation is more
than 30%. There is neovascularization of retina
especially beyond equator. This is due to obliteration
of retinal arteries and veins. The temporal vessels which
are still developing are affected mainly. There is proli-
feration and then contraction of the vascular tissue in
the shunt area resulting in tractional detachment. The
changes undergo five stages:
a. Demarcation line between vascular and avascular
retinal regions.
b. The line is converted into a vascularized ridge.
c. Fibrovascular tissue develops at the ridge. Hemorr-
hages are seen.
d. Tractional retinal detachment.
e. Total retinal detachment and angle closure glaucoma.
Prevention is better.
Frequent observation is advised. Photocoagulation
is recommended for progressive disease. In late stage
vitrectomy and lensectomy are done; but the prognosis
is poor.
RETINITIS PIGMENTOSA (RP)
It is degeneration of rods (and cones) starting at equator.

Vascular, neurotrophic, abiotrophy and damage by light
are certain etiological suggestions for this condition.
These patients have hypersensitivity to retinal auto-
RETINA 195
antibody suggesting an autoimmune etiology. Its here-

ditary pattern is autosomal dominant (mild form),
recessive (severe form, early onset) and sex linked (less
frequent; poor prognosis).
Its symptoms include night blindness (nyctalopia) and
contraction of visual field. The vision is reduced by the
associated cataract that is present. In the penultimate
stage the field of vision is very much constricted so that
the patient has tubular vision. At this stage the patient
has difficulty in going about. The patient might go blind
by 7th or 8th decade of life.
Examination of anterior segment does not reveal any
abnormality except for posterior cortical cataract.
Fundus shows a few translucent floaters in vitreous. In
the retina bone corpuscle like black pigments are seen in
the equatorial region (to begin with) which are mostly
around veins and anterior to them. The retinal vessels
are attenuated. The disk goes in for consecutive optic
atrophy taking on a waxy yellow color (Fig. 11.10). High
percentage of myopia is met with. Cystoid macular
edema may occur. EOG is subnormal or even extin-
guished.
Field of vision shows ring shaped scotoma at equator.
Later the scotoma spreads peripherally as well as
centrally. In penultimate stage only a small seeing area
is present around the fixation point (tubular vision) (Fig.
11.11).
RP has certain variants:
RP sine pigmento (resembles RP; but pigments are
absent), retinitis punctata albescens (similar to RP; but
there are white spots instead of black pigments), inverse
RP (autosomal recessive; macula affected early),
Fig. 11.10: Fundus picture of retinitis pigmentosa. The disk shows

consecutive optic atrophy, the vessels are attenuated and there are bone
spicules—like pigments in the midperiphery
Fig.11.11: Field defect in retinitis pigmentosa. The ring scotoma in

midperiphery of field of vision results in tubular vision the patient
experiences. The ring scotoma does not have any (Ronne’s) nasal step
differentiating it from field defect due to glaucoma
RETINA 197
unilateral RP (one eye only is affected) and sectorial RP.

Secondary RP is due to retinitis and congenital syphilis.
RP is associated with microphthalmos, high
myopia, keratoconus, glaucoma (usually open angle),
Usher syndrome (deafness), Laurence-Moon-Bardet-
Biedl syndrome (hypogonadism, obesity, mental
retardation, polydactyly), Alstrom Hallgren syndrome
(Obesity, deafness and diabetes mellitus) and Refsum’s
syndrome (peripheral neuropathy and cerebellar
ataxia).
Treatment is ineffective. Placental extract, lateral
rectus tunneling, vasodilators and vitamin A have been
tried; but in vain. Genetic counseling should be given.
RETINAL DETACHMENT
A misnomer, it is retinal separation. It is separation of

nine neuronal layers from pigment layer. It may be
primary or secondary retinal detachment. There are
certain predisposing factors—age (common in older
persons), high myopia, retinal degeneration, trauma and
aphakia.
There are two types of detachments (Flow chart 11.1):
Flow chart 11.1: Retinal detachment
1. Primary (rhegmatogenous) detachment is seen

when there is a break in retina. This break involves
the neurosensory layers. The break can be a round
hole, horseshoe shaped, dialysis near ora serrata or
an irregular one. Through this break fluid vitreous
gets access into the layers of retina and a separation
of retinal layers occurs. These two factors—retinal
break and fluid vitreous - must be there for this type
of detachment to occur.
2. Secondary detachment is due to:
a. Push from behind: This may be fluid or solid like
neoplasm. Fluid cause is seen with toxemia of
pregnancy, hypertension, Harada’s disease and
central serous retinopathy.
b. Pull from in front (vitreous side): In this type, fibrous
tissue in vitreous contracts and pulls on the retina
causing detachment. It is seen in PDR, plastic
cyclitis.
Symptoms
Photopsia (flashes of light), micropsia, (smallness of
objects), macropsia (objects look larger), metamor-
phopsia (objects appear distorted) and muscae volitan-
tes (floaters in front of eye) are the main complaints of
the patient. Defective vision is met with when macula
is involved or when there is vitreous hemorrhage. When
these occur it may be sudden.
Signs
Visual field shows relative scotoma with sloping border
corresponding to detached area. Detachment at macula
shows up as gray reflex during retinoscopy. If it is a large
RETINA 199
detachment swinging flash light test shows ipsilateral

dilatation of pupil. Intraocular pressure is either reduced
(usual) or raised (rare).
Fundus shows the detached retina to be gray in color.
It is thrown into folds so that there is an apparent
“break” in retinal vessels over the folds. The vessels over
the detachment appear smaller and darker (optical
illusion). Faint white line may mark the edge of the
detachment. The retinal break or the causative condition
(in secondary type) is seen. The hole or retinal break is
red in color (Fig. 11.12). Anterior vitreous shows
pigment (Shaffer sign). When the retinal detachment
subsides the original edge of the detached area shows
pigmentation called ‘watermark’ (Fig. 11.13).
Fig. 11.12: Fundus picture of retinal detachment. The detached retina

has lost its pink color, thrown into folds, and the vessels appear attenuated
and appear cut off at folds edges. The dialysis which has produced this
detachment is seen as red area in the upper portion
Fig. 11.13: Case in which retinal detachment has subsided leaving

behind “water marks” which are seen in the figure
Management
It is mostly surgical. Thorough examination is a pre-
requisite for a successful outcome. If it is primary type,
all holes must be located and charted out. Medical therapy
(except: (a) where causative condition can be cured
medically and (b) the preoperative bed rest some
surgeons advocate) is not advised.
The aims of surgical treatment are to:
1. Close all the hole(s).
2. To bring the detached retina closer to choroid and
attaching the retina to choroid.
3. To drain the subretinal fluids. Closing the holes is
achieved by cryo, laser or even by cautery. Bringing
the detached retina and the choroid in close
RETINA 201
apposition is carried out by buckling the sclera (and

choroid) inwards towards retina using implants or
explants, or by pushing the retina towards sclera
(and choroid) from vitreous side using air, gases or
silicone oil. The subretinal fluid may or may not be
drained.
RETINOBLASTOMA
It is a tumor derived from neurosensory retina. Deletion

or mutation of q14 of chromosome 13 is seen. The
inheritance is dominant with variable gene penetration.
The hereditary cases are usually bilateral. Those due to
somatic mutation (non-hereditary) are commoner and
are mostly unilateral.
Features
It is mostly seen within first two years of life. It is
bilateral in 1/4th of cases. One fifth is unilateral and
hereditary. The rest of 55% are unilateral and non-
hereditary. The pupil shows a white (actually yellow)
reflex—so called leukocoria (Amauratic cat’s eye).
Sometimes squint and /or nystagmus may be present.
Its progress is divided into four stages:
Stage1 (Quiescent Stage)

Earliest stage, in which the condition is mostly unno-
ticed by the parents. The pupil shows a white reflex.
Fundus study shows the tumor mass. It has a cheesy
appearance and calcification—The latter is pathogno-
monic. Retinal vessels course through and over it.
Multiple tumor areas and retinal detachment are seen.
Stage 2 (Glaucomatous Stage)

The eye is congested. Child has pain in the eye. The
growth extends anteriorily. The iris-lens diaphragm is
shifted anteriorily. Its cells block angle of chamber.
These two factors increase intraocular pressure. If the
tumor bursts through the sclera the ocular pressure
comes down and pain is relieved. Sclera is the commo-
nest site for perforation.
Stage 3 (Extraocular Extension)

Extraocular spread sets in when the tumor bursts
through ocular coats or when the tumor extends via
the optic nerve. When the tumor bursts through cornea,
it is seen as fungating, bleeding mass with variegated
surface.
Stage 4 (Metastatic Stage)

It starts with metastasis in regional lymph nodes and,
later on, in the cranial bones, distal bones, spinal cord,
brain and, rarely, liver.
Pathology
The tumor consists of rosette-like formation of undiffe-
rentiated tumor cells which resemble rods and cones.
These may also be highly differentiated. The rosettes
are either Flexner-Wintersteiner (typical of retino-
blastoma) or Homer- Wright type (common in medullo-
blastoma; but rarely seen in retinoblastoma). Pseudo-
rosettes and fleurettes are also met with. The un-
differentiated cells have hyperchromatic nuclei and
RETINA 203
scanty cytoplasm. It has multicentric origin, i.e. the

multiple lesions that one might see in the retina have
independent origin and not by seeding. Areas of
calcification and necrosis are seen.
The tumor mass may spread along retina (glioma
planum), into vitreous (glioma endophytum) or through
sclera (glioma exophytum). Glioma exophytum causes
retinal detachment. The optic nerve spread shows skip
lesions, i.e. tumor areas in the optic nerve are intersposed
with normal optic nerve portions.
When the growth involves only the retina, it is
classified into five groups by Reese and Elisworth. The
prognosis and even treatment are based on this
classification.
Cases of retinoblastoma, if they survive, develop
“second” neoplasm later in life. The common ones are
osteogenic sarcoma, squamous cell carcinoma,
malignant melanoma and acute leukemia.
Differential Diagnosis
The various conditions that are to be differentiated from
retinoblastoma are grouped under the term pseudog-
lioma. All these show leukocoria. These can be prelen-
ticular (exudates over pupil), lenticular (congenital
cataract) and retrolenticular lesions. The retrolenticular
lesions are:
1. Cyclitis with vitreous inflammation
2. Retinopathy of prematurity
3. Persistent hyperplastic primary vitreous
4. Coats’ retinopathy
5. Exudative choroiditis, and
6. Toxocara infestation.
Investigations
X-ray orbit, ultrasonography, CT scan and aqueous
lactic dehydrogenase level estimation (which is raised).
Management
In the early stage of quiescence, the eye can be
enucleated especially if the condition is unilateral. If the
tumor is less than 6 mm in size without much elevation,
destructive procedures are carried out. The tumor can
be destroyed by radiotherapy. External supervoltage
radiation (total of 3600 to 4500 rads depending on the
stage of lesion) or cobalt 60 scleral plaque (especially
for recurrent large tumors and tumors involving
vitreous) is used. The lesion can also be destroyed by
photocoagulation with Argon laser or by cryo (–70° C).
In bilateral cases, the eye with more advanced tumor is
removed and the lesion in the other eye is treated by
radiation.
In stage II enucleation is the choice and radiotherapy
to orbital apex is applied if optic nerve is involved.
Along with this, cyclophosphamide (20 mg/kg), vincris-
tine (50 mg/kg) and Adriamycin (2 mg/kg) are given.
In stages III and IV exenteration is performed.
Orbital debulking is done with radiotherapy.
Treatment modality is usually guided by Reese and
Elisworth grading.
Prognosis
Treated early, patient may survive. In stage IV mortality
is cent percent. Spontaneous regression has been
RETINA 205
reported; but unfortunately this is very rare. Prognosis

depends upon cell pattern, optic nerve involvement and
presence of metastasis.
CENTRAL RETINAL VEIN OCCLUSION (CRVO)

It is due to:
1. Venous thrombosis.
2. Hyperviscosity causing venous stasis,
3. Pressure on vein by sclerotic retinal artery (just
behind lamina cribrosa).
It may be ischemic or non-ischemic type.
The patient gives history of marked defective vision.
Fundus in CRVO shows enormously engorged
retinal veins. There are plenty of retinal hemorrhages
(“angry looking” fundus). Papilledema and cystoid
macular edema are seen. Neovascularization appears
at the disk. Such a neovascularization in the retina can
be collateral vessels (Fig. 11.14). In later stages, pig-
mentary changes appear in the retina which is atrophic.
If a tributary alone is affected, these changes are seen in
the area drained by the tributary. In such a situation
the vision is partially affected and the macula may
escape. Sometimes, if superotemporal tributary is
occluded macula may be involved.
Management is by panretinal photocoagulation or
cryoapplication to prevent rubeosis iridis and neovas-
cular glaucoma. In complete obstruction treatment is
ineffective. Non-ischemic type has better prognosis than
ischemic type.
Fig. 11.14: Central retinal vein occlusion. Fundus appearance has been
aptly described as “angry looking fundus”— sheets of hemorrhages are
seen
Complication
Neovascularization of angle results in rise in intraocular
pressure. This is seen about three months after occlusion
(Hundredth day glaucoma). This complication is rarely
met with in tributary occlusion.
CENTRAL RETINAL ARTERY

OCCLUSION (CRAO)
It is due to embolism with or without central retinal

artery spasm. The source of embolus is common carotid
or heart valves. Systemic hypertension or arterio-
sclerosis is not a must. Thrombosis of retinal arteries
can also cause CRAO. Increased ocular pressure is a
rare cause.
RETINA 207
If the occlusion is not complete, patient may have

prodromal symptoms. If it is complete, patient has
sudden, painless loss of vision.
Fundus shows attenuated arteries. Veins are almost
normal. The retina is cloudy, edematous and white
(except at macula). Cherry red spot is seen at fovea as
choroid is visible at this site. Gentle pressure on globe
produces break up of venous blood column and cattle
truck appearance is seen.
Later, the retina regains its normal color. The vessels
are thin. The disk is atrophic. Pupil shows loss of direct
reflex. If cilioretinal vessel is present, some vision
persists; otherwise vision is completely lost.
Treatment should be immediate. Globe massage and
paracentesis may help. Inhalation of amyl nitrate may
relieve the spasm and the occlusion. IV mannitol has
been tried. Usually all attempts are futile.
COMMOTIO RETINAE
It is otherwise known as Berlin’s edema. It is caused by

blunt trauma to eye.
Patient complains of defective vision.
Signs include milky whitening of retina in the
posterior pole with cherry red spot at macula (Fig.
11.15). This is due retinal edema with choroid shining
through at macula. Retinal vessels are normal. One
should be careful in ruling out retinal detachment.
Fig. 11.15: Commotio retinae
Treatment
Specific treatment is not needed. Condition clears up
spontaneously. It may be followed by pigmentary
changes at macula in which case central vision comes
down.
12
Optic Nerve
Diseases of optic nerve are never kept for under-

graduates in clinical examination. Questions on optic
nerve are asked in theory (mainly) and in oral
examinations.
ANATOMY
Optic nerve consists of the second order neurons, that

of ganglion cells. It is about 55 mm in length. It has four
portions—intraocular, intraorbital, intracanalicular and
intracranial. Arterial supply to the nerve head is mainly
from posterior ciliary arteries and peripapillary
choroidal vessels. Its surface is supplied by capillaries
from retinal arterioles.
PAPILLEDEMA
It is a passive edema of optic disk (the nerve head) with-

out any inflammation. The exact mode of occurrence is
disputed. It is due to (a) compression of central retinal
vein, (b) blockage of axoplasmic transport due to
elevated cerebrospinal fluid pressure. It is usually
bilateral; but edema may be of different degrees in the
two eyes.
Causes
1. Raised intracranial pressure: Mostly due to tumors of
brain especially in the region of midbrain, parieto-
occipital area and cerebellum. Tumors of anterior
cranial fossa nearly always cause edema disk. The
other intracranial causes are thrombosis of cavernous
sinus, brain abscess, subarachnoid hemorrhage,
OPTIC NERVE 211
aneurysm, hydrocephalus, meningitis and pseudo-

tumor cerebri.
2. Systemic causes: Malignant hypertension, hypervita-
minosis A, tetracycline, nalidixic acid, excess steroid,
hypoparathyroidism and uremia.
3. Orbital causes: Tumors, inflammation.
4. Disk causes: Papillitis
(Some call disk edema caused by factors mentioned
under (1) above as papilledema. The edema due to
causes (2), (3) and (4) is called simply as disk edema.
Undergraduates need not make this differentiation).
Features
Symptoms, apart from that of causative lesion, are very
minimal or even absent. Transient blurring of vision
may occur. In the advanced stage, vision goes down.
Diplopia occurs due to VI nerve paralysis.
Fundus: Signs of papilledema are grouped into (a) early
and (b) established. There is blurring of disk margin.
To begin with, this is seen at upper and lower poles of
disk. Temporal margin is the last to be affected. Disk
becomes hyperemic and swells up. The optic cup is not
seen. Veins are congested and dilated. Spontaneous
venous pulsation is absent and even cannot be elicited
with pressure over globe. Arterioles over disk become
prominent giving the disk a striated appearance. The
disk swelling may measure upto +6 D with direct
ophthalmoscope (Fig. 12.1). Hemorrhages which are
mostly flame shaped, exudates and peripapillary retinal
folds appear. The last ones, when present near fovea,
take on a (macular) star appearance. The edema subsi-
Fig. 12.1: Papilledema. The disk is edematous. Margins are blurred.

Superficial hemorrhages are seen. Media is clear
des in all cases. But optic atrophy (post-papilledema)

sets in. Disk is grey in color and lamina cribrosa is not
seen. Pigmentary changes appear in retina.
Visual fields defects noticed, apart from that of causative
condition, are enlargement of blind spot and contraction
of the peripheral field.
Differential Diagnosis (Table 12.1)

1. Optic neuritis.
2. Pseudoneuritis: It is seen in hypermetropia.
3. Ischemic optic neuropathy.
4. Opaque nerve fibers: Sometimes myelin sheaths are
seen around the retinal nerve fibers adjacent to optic
nerve head and this may simulate the appearance
of papilledema (Fig. 12.2).
OPTIC NERVE 213
Table 12.1: Differential diagnosis

Papilledema Optic neuritis Pseudoneuritis
Laterality Usually Usually Bilateral
bilateral unilateral
Onset Slow Acute + Since birth
Afferent
pupillary – + –
defect
Vision
Fundus Normal Marked loss Reduced
Media Clear Hazy Clear
Disk swelling + 6D Less than Below + 3 D
+3D
Macular star + – –
Visual field Enlarged blind Central or Normal
spot centrocecal
Fluorescein
angio Leakage ++ Minimal leak Normal
Fig. 12.2: Opaque nerve fibers. These myelin sheaths of retinal nerve
fibers around the disk may mimic papilledema
Management is that of cause. Edema disk can be

brought down by decompression—making multiple
slits in the optic nerve sheath. Any intervention must
be carried out before peripheral constriction of fields
takes place.
OPTIC NEURITIS
Flow chart 12.1: Classification of optic neuritis
NON-PURULENT OPTIC NEURITIS
Etiology
1. Demyelinating diseases including neuromyelitis
optica. It is seen in multiple sclerosis.
2. Infective: This can be from a local focus or contiguous
spread such as endophthalmitis, orbital cellulitis,
sinusitis or from meninges. The organisms are
bacterial (TB, syphilis), viral (herpes zoster, CMV,
measles), fungus, protozoa (toxoplasma, malaria,
toxocara) or parasitic (cysticercus).
OPTIC NERVE 215
3. Immune mediated: Uveitis, sarcoidosis.

4. Metabolic: Diabetes, anemia.
5. Idiopathic.
Papillitis
Features
It is usually unilateral. Patient complains of sudden loss
of vision. There is orbital or retrobulbar pain. Tender-
ness over attachment of superior rectus and relative
afferent pupillary defect are met with. If vision is
present, there is color vision disturbance and a decrease
in contrast sensitivity. Central or centrocecal scotoma
is seen.
Fundus examination shows hazy medium due to cells
in vitreous. Disk is hyperemic, its margin blurred and
the disk itself is elevated by about 2 diopters. Scanty
peripapillary hemorrhages are seen. Exudates are
present over the disk. The end result is either normal
optic disk (in mild attack) or post-neuritic optic atrophy
(in severe attack).
Acute Retrobulbar Neuritis

The causative factors are the same as for papillitis. The
symptoms are similar to papillitis. The pupil shows ill
sustained contraction. Marcus Gunn pupil can be de-
monstrated and this is diagnostically significant. There
is tenderness over superior rectus insertion. Fundus is
normal. If at all there are any changes, they are disten-
tion of veins and attenuation of arteries. “Patient sees
nothing and doctor sees nothing” is an apt statement for
this condition. Finally optic atrophy sets in. Field of
vision, if it can be taken, shows peripheral loss. For color

it may show absolute or relative defects.
1. Ischemic optic neuropathy—anterior one resembles
papillitis and posterior mimics retrobulbar neuritis.
2. Papilledema.
3. Grade IV hypertensive retinopathy.
4. Leber’s hereditary optic neuropathy.
5. Space occupying lesion in orbit.
Investigations
Apart from field study, complete blood examination,
study of C reactive protein and X-ray orbit.
Treatment
1. Treatment of primary disease.
2. IV methylprednisolone (250 mg in 60 minutes)
followed by oral prednisolone with tapering dose is
advised for demyelinating disease. IV dexa-
methasone is also equally effective.
3. Large doses of B complex (methycobalamine).
TOXIC OPTIC NEUROPATHY

(TOXIC AMBLYOPIAS)
It is caused by many toxins. These etiological factors

can be divided into two groups based on the type of
field defects they produce initially—those that cause
centrocecal scotoma and those that cause peripheral
constriction. Some of these toxins are:
OPTIC NERVE 217
Tobacco
Ingestion of tobacco by smoking, chewing or absorption
of its dust in industry causes toxic neuropathy of optic
nerve. The cyanide in the smoke causes optic nerve
damage. It is triggered by Vitamin B12 deficiency. It
occurs in middle aged. The predominant symptom is
fogging of vision. Central vision is diminished and there
is scotoma to red. Centrocecal scotoma is seen. Treatment
is to avoid tobacco and take hydroxycobalamine
injection. Recovery is slow. Recurrence is uncommon,
even if tobacco habit is restarted.
Ethyl Alcohol
It is associated with the above condition. It is aggravated
by avitaminosis. Central scotoma is seen. Treatment is
to stop intake of alcohol and to take hydroxycobalamine.
Steroid is of no use. Prognosis is not as good as with
tobacco.
Methyl Alcohol
It is due to intake of spurious drink. It is of two types –
In acute form blindness occurs. In chronic form
progressive loss of vision is met with. Progressive optic
atrophy sets in. Initial disk margin blurring is replaced
by primary optic atrophy. Management of acute form is
by giving ethyl alcohol. Beyond certain stage recovery
is not seen.
Arsenic
Pentavalent preparation (atoxyl) can cause optic
atrophy which is usually total.
Lead
Nowdays it is mostly due to air pollution by exhaust
gas. Optic neuritis leads to post-neuritic optic atrophy.
Renal retinopathy is seen. Treatment is with calcium
EDTA, dimercaptol and D penicillamine. The noxious
agent must be excluded.
Chloroquine
Optic atrophy is consecutive to retinal condition in
which Bull’s eye retinal lesion is seen. Central scotoma
occurs. Daily dosage of drug is more important than
total amount given over a period of time. Pigmentary
retinopathy and optic atrophy are the irreversible end
results.
Quinine
Total blindness may result even with small dose in
sensitive patients. Disk edema followed by optic
atrophy is associated with extremely contracted vessels.
There is constriction of visual field resulting in tubular
vision. Deafness and tinnitus are met with.
OPTIC ATROPHY
It is the disk condition wherein the optic nerve dege-

nerates. The degeneration is from retina to lateral
geniculate body. It also follows extensive retinal damage
or to certain general diseases.
In total atrophy, pupil is dilated and fixed. In partial
atrophy some vision is present with field defects
(especially concentric contraction). The color of the disk
may not be an indication for extent of defective vision.
OPTIC NERVE 219
TYPES OF OPTIC ATROPHY
Primary Type
It is seen in second visual order neuron lesion with no
other fundus evidence or local problem. Primary optic
atrophy is caused by multiple sclerosis, syphilis, Leber’s
disease, exogenous poisons causing toxic optic
neuropathy and optic nerve compression in orbit.
Fundus shows “white disk on a normal fundus” (Fig.
12.3). The disk tint may be of various grades. Blue tint
is also seen. Lamina cribrosa shows stippling. Minimal
cupping may be present. Since the white color of disk is
due to loss of disk vessels, the color of disk may not be
congruous to amount of loss of vision —a patient with
white disk may even have normal acuity of vision.
Secondary Type (Postneuritic Type)

It follows papilledema and papillitis. The disk margins
are blurred, the floor has a dirty color and the cup is
filled up. Perivascular sheathing around attenuated
arteries is seen upto some distance from the disk and
beyond the first division of retinal vessels.
Glaucomatous
It is seen in final stage of any glaucoma. The disk is
white in color. The origin of central retinal vessels is
pushed nasally (Fig. 12.4).
Consecutive Type
It follows retinitis pigmentosa and extensive chorio-
retinitis. Fundus shows waxy yellow disk with sharp
borders. The vessels are narrowed (Fig. 12.5).
Fig. 12.3: Primary optic atrophy. The disk is papery white in color
Fig. 12.4: Glaucomatous optic atrophy. The cup is large

and disk is pale
OPTIC NERVE 221
Fig. 12.5: Case of consecutive optic atrophy due to retinitis

pigmentosa. The disk is yellow in color
Management of any optic atrophy is that of the

causative factor. For atrophy itself there is no treatment.
Large dose of vitamin B complex may be given; but in
vain.
13
Orbit
Orbit cases are not for undergraduates. Rarely proptosis

case may be kept. But some of its diseases may be asked
in theory examinations.
ANATOMY
Orbit is a quadrangular pyramid.

It has four walls and four borders. The size of orbit
is 40 mm in all dimensions. In its posterior part (apex)
is situated the optic foramen through which optic nerve,
ophthalmic artery and sympathetic plexus enter the
orbit. From adjacent to the optic foramen fan out
superior and inferior orbital fissures which convey the
motor nerves to extraocular muscles and certain vessels.
Extraocular muscles (except inferior oblique) and
levator palpebrae superioris take origin from the vicinity
of optic foramen. The orbit has four separate spaces –
the subperiosteal space, peripheral space (outside extra-
ocular muscles), central space (inside the muscle cone)
and sub-Tenon’s space (Fig. 13.1).
PROPTOSIS
It is abnormal protrusion of eyeballs. Exophthalmos also

means the same—but this term is reserved for pro-
trusion due to thyroid problem.
Proptosis can be unilateral or bilateral. It may be
pulsatile or non-pulsatile; static or progressive; constant
or intermittent. The direction of protrusion can be axial
or in any other direction.
ORBIT 225
Fig. 13.1: Spaces of orbit. (A) Subtenon space. (B) Central space.
(C) Peripheral space. (D) Subperiosteal space
Causes
1. Orbital inflammations such as orbital cellulitis, throm-
bophlebitis, panophthalmitis, gumma, tuberculoma
and sarcoidosis.
2. Vascular causes: Thrombosis of orbital veins and of
cavernous sinus, arteriovenous aneurysms and
orbital hemorrhage.
3. Accessory nasal sinus: Emphysema, mucocele.
4. Osseous: Reduced orbital volume due to oxycephaly,
rickets and leontiasis ossea.
5. Tumors:
a. Children: Optic nerve glioma, plexiform neurofib-
roma, leukemia, rhabdomyosarcoma, lymphan-
gioma, dermoid, teratoma, metastatic neuroblas-
toma and Wilms’ tumor.
b. Adults: Meningioma, Schwannoma, neurofib-
roma, lymphangioma, metastasis from lung,
breast, prostate and gastrointestinal tract.
Causes can also be grouped as below:
1. Space occupying lesion in orbit. It can be in (a) extra-
conal area and (b) intraconal area
2. Lacrymal gland tumors
3. Thyroid disease
4. Inflammatory
5. Trauma
6. Parasitic.
These space occupying lesions can also be grouped
into congenital, vascular, neural, mesenchymal,
hemophilic and metastasis.
Pseudoproptosis is seen in high myopia, extraocular
muscle paralysis, obesity and in stimulation of Müller’s
muscle.
The prominent symptom, apart from disfigurement,
is diplopia. Vision may be affected if optic atrophy
sets in.
Investigations
1. Exophthalmometry: It gives quantitative value of prop-
tosis which is useful in diagnosis and in assessing
the progress. It is measured by Hertel’s exophthal-
mometer. Normal values are from 12-21 mm and are
ORBIT 227
equal in both eyes. Any difference of more than

2 mm between the two eyes is diagnostic.
2. Plain X-ray: It shows bony problems, calcification
and shadows of soft tissue lesions. Water’s view and
posteroanterior views are contributive.
3. MRI and CT scan: They reveal the soft tissue patho-
logies. CT scan can be CAT and CCT. Nature, posi-
tion, shape and origin of the lesion are seen.
4. Ultrasound: Probe of 5 MHz is used. Soft tissue study
is possible.
5. Angiography: Carotid angiography, digital subtrac-
tion angiography, MR angiography (last two are 3
D) and orbital venography are some of the methods
employed.
6. Lab investigations for thyroid and hematological
study.
7. Fine needle aspiration is done to diagnose tumors
of orbit. It is done under CT scan.
Management
It is mainly that of causative lesion.
The cornea must be protected against exposure
keratitis.
THYROID
Excess Secretion
It causes Graves’ disease or goiter.
The important ocular signs are:
1. Dalrymple’s (Upper lid retraction)
2. Enroth’s (Edema of lower lid)
3. Gifford’s (Difficult eversion of the upper lid)

4. Griffith’s (Lower lid lags behind the globe on
upward gaze)
5. Grove’s (Upper lid resistance to downward trac-
tion)
6. Jellinek’s (Increased pigmentation of upper lid)
7. Kocher’s (Staring and frightened appearance)
8. Mobius (Weakness of convergence)
9. Stellwag’s (Infrequent blinking)
10. von Graefe’s (Upper lid lags on down gaze).
Thyrotropic Exophthalmos
This is due to excess of thyrotrophic hormone of anterior
pituitary. The features are:
1. Gradual proptosis of both eyes reaching severe deg-
ree. This may lead onto lagophthalmos and exposure
keratitis. Proptosis is due to increased orbital content
caused by swollen ocular muscles and edema of retro
orbital tissues.
2. Considerable edema of lids and conjunctiva.
3. External ophthalmoplegia—elevation is first affected
4. Engorged retinal veins and optic atrophy.
5. Residual ophthalmoplegia and proptosis after reso-
lution of the condition.
Diminished Secretion
It causes cretinism (children) or myxedema (adults).
Puffiness and edema of lids are seen.
ORBIT 229
ORBITAL CELLULITIS
It is a purulent inflammation of orbital cellular tissues.
Causes
External: Deep injuries, retained foreign body, septic
operations.
Secondary: From nasal sinuses, teeth, lids, face and eye
ball.
Endogenous: Pyemia, from abscess elsewhere and
thrombophlebitis of lower limb.
Features
Patient complains of severe pain, protrusion of eyeball,
diplopia and defective vision (Fig. 13.2).
Signs include general ones such as fever and cerebral
signs. Local signs are axial proptosis, lids swelling,
Fig. 13.2: Orbital cellulitis on the left side

conjunctival chemosis, restricted ocular movements,

engorged retinal vessels, disc edema, optic neuritis and
defective vision. If abscess forms it points either into
fornix of conjunctiva or along orbital margin.
Complications
• Panophthalmitis
• Optic atrophy
• Abscess formation.
• Cavernous sinus thrombosis
• Purulent meningitis and cerebral abscess.
Treatment
1. Broad spectrum antibiotics such as oxacillin or cefota-
xime by parenteral route.
2. Antiinflammatory agents.
3. Drainage of pus: Blind incision should be avoided.
Sub-periosteal abscess is drained by an incision at
super-medial aspect or orbital margin.
CAVERNOUS SINUS THROMBOSIS
Thrombus to cavernous sinus can be from many sources.

Knowledge of its various communications is needed for
understanding this aspect (Fig. 13.3).
The thrombus can be from face (via supraorbital and
inferior ophthalmic veins), middle ear (via inferior
petrosal sinus), from mastoid region (via lateral sinus –
superior petrosal sinus) and from the other side caver-
nous sinus (via transverse sinus).
ORBIT 231
Fig. 13.3: Connections of cavernous sinus (right side only is shown)

Anteriorily—superior and inferior (A) ophthalmic veins (Drain face and
nose). Medially—communicates with other cavernous sinus through
transverse sinus. (C) This is the reason for pathology spreading from
one cavernous sinus to the other. Posteriorily — superior (E) and inferior
(D) Petrosal sinuses (channels for spread of infection from middle ear
and mastoid). (F) Sigmoid sinus. (G) Transverse sinus. B—Sphenoparietal
sinus.
Symptoms
The patient complains of proptosis (one or both sides),
pain and defective vision. He might give history of
squeezing a furuncle which was there over “danger
zone of face”. General symptoms include vomiting,
fever, rigors and altered sensorium.
SIGNS
Conjunctival chemosis is present. Proptosis, which is
either unilateral or bilateral (50%) and edema of mastoid
region are present. Extraocular muscles paresis is seen.
Cornea is anesthetic and pupils are dilated (late stage).
Fundus shows disk edema (more in otitis origin) and in
a few cases engorgement of retinal veins. Fundus signs
develop late.
Management
1. Broad spectrum antibiotic by parenteral route. It
should be given early and in massive dose.
2. Anticoagulants.
3. Analgesic.
The differences between orbital cellulitis and
cavernous sinus thrombosis are shown in Table 13.1.
Table 13.1: Differences between orbital cellulitis and

cavernous sinus thrombosis
Orbital cellulitis Cavernous sinus
thrombosis
Cause Mostly infection Mostly thrombus
Laterality Unilateral Unilateral or bilateral
(50%)
Proptosis ++ +
Cornea Clear Clear
(early stage)
Ocular Limited Absent
movements
Fundus Disk edema and Disk edema and
engorged veins engorged veins
(late stage)
Vision Reduced Reduced
14
Neuro-
ophthalmology
Basic knowledge of the anatomy of ocular motor nerves

is needed for understanding the lesions of these nerves
(Fig. 14.1).
Fig. 14.1: Relations of ocular motor nerves to vessels of brain at their

origin: (A) Internal carotid artery. (B) Posterior communicating artery.
(C) Posterior cerebral artery (D) Superior cerebellar artery. (E) Basilar
artery. (F) Labyrinthine artery. (G) Anterior inferior cerebellar artery.
III, IV, VI, Oculomotor, trochlear and abducent nerves
OCULOMOTOR NERVE
The oculomotor nerve (3rd cranial) is entirely a motor

nerve, which supplies all the extraocular muscles except
lateral rectus and superior oblique. It also supplies the
intraocular muscles, namely sphincter pupillae and
ciliary muscle. It is divided into four parts:
NEURO-OPHTHALMOLOGY 235
a. Fascicular
b. Basilar
c. Intracavernous and
d. Intraorbital.
Causes of Third Nerve Paralysis

1. Vascular disease: Infarction of the central portion of
the nerve. This spares the pupil, since the pupillo-
constrictor fibers lie near the surface.
2. Diabetes and hypertension: They cause pupil sparing
with isolated third nerve palsy.
3. Trauma.
4. Aneurysm.
5. Miscellaneous causes like tumors, syphilis and tuber-
culosis.
6. Idiopathic.
The clinical features are:
1. Ptosis due to paralysis of the levator palpebrae
superioris (LPS) muscle.
2. Deviation: Eyeball is turned down, out and inturned.
Ocular movements are restricted due to paralysis of
muscle as follows:
• Adduction—due to medial rectus paralysis
• Elevation—due to superior rectus paralysis.
• Depression—due to inferior rectus paralysis
• Extorsion—due to inferior rectus and inferior
oblique paralysis.
Pupil is fixed and dilated due to paralysis of sphincter
pupillary muscle.
Crossed diplopia and loss of accommodation are
present.
Head posture: Head is turned to the opposite side,

chin is tilted towards the same side and is raised.
The features seen as per the site of lesions:

Nucleus
Unilateral nucleus damage results in unilateral III nerve
palsy with contralateral superior rectus palsy. There can
be pupil involvement. Cephalic nuclear lesion results
in bilateral III nerve palsy with spared LPS (with or
without pupil sparing). Bilateral ptosis is the result of a
lesion in caudal midline unpaired LPS nucleus
(midbrain ptosis). Bilateral medial rectus palsy is due
to injury. Medial longitudinal bundle may or may not
be affected. If affected, it causes inter nuclear ophthal-
moplegia.
Fascicle
Mostly due to vascular or neoplastic diseases.
a. Dorsal lesion (+ red nucleus and corticospinal tract):
Benedict’s syndrome (III nerve palsy with
contralateral ataxia and a static and intention
tremor).
b. Ventral lesion: Weber’s syndrome (III nerve palsy,
contralateral paresis of lower face, arm and leg).
c. Red nucleus also involved: Claude’s syndrome (III
nerve palsy with contralateral ataxia or tremor).
d. Fascicle and superior cerebellar peduncle involved: Nath-
nagel’s syndrome (III nerve palsy with ipsilateral
cerebellar ataxia).
Nerve Trunk
a. Interpeduncular: It can be caused by:
i. Basilar aneurysm (Rare; hemiparesis, ataxia,
nystagmus, homonymous hemianopia),
ii. Posterior communicating artery aneurysm
(Commonest; pupil involved since compres-
sion of III nerve by aneurysm involves the
pupils as pupilloconstrictor fibers lie on the
surface; acute onset; pain +).
iii. Trauma (Less common than IV and VI nerve
involvement. It is seen with closed head injury
and with basilar fracture. In mild injury III
nerve palsy can occur if the nerve is already
tethered by tumor). Nerve can be avulsed at
brainstem, contused or there can be intraneural
hemorrhage.
iv. Meningitis (other nerves are involved).
b. Intracavernous: Pupil fibers are more involved. Com-
pressive lesions often involve the other ocular motor
nerves and the ophthalmic branch of the trigeminal
nerve. Combined oculomotor paresis and sympa-
thetic denervation (small and poorly reactive pupil)
are virtually pathognomonic of a cavernous sinus
lesion. It can be due to carotid cavernous fistula,
Cavernous sinus thrombosis.
c. Superior orbital fissure: Tolosa-Hunt’s syndrome
(Superior orbital fissure syndrome; anterior
cavernous sinus syndrome). It is due to non-specific
granuloma at anterior cavernous sinus or at superior
orbital fissure. There is unilateral, acute, sudden pain
with diplopia and minimal proptosis. Spontaneous
recovery and recurrences are seen. Ocular muscles

are involved partially. Pupillary involvement is
variable. The lesions are generally partial with
involvement of IV and VI nerves.
d. Orbit: Trauma and tumor. Superior or inferior divi-
sion palsy (pupil affected in latter). Aberrant rege-
neration causes so varied ocular movements. They
include pseudo—Graefe phenomenon and seg-
mental pupillary reaction. Elevation of the lid on
downward gaze or on adduction. The pupil may be
fixed to light; but may respond to accommodation.
III nerve can be affected by HZ virus. In this it can
be partial or total.
III nerve paralysis with pupil sparing (with pain)
are seen in diabetes. Bilateral simultaneous, or multiple
unilateral palsies and aberrant regeneration are rare in
diabetes. III nerve palsy, pupil involvement, pain and
aberrant regeneration are features of aneurysm.
Oculomotor paresis with cyclic spasms: Ptosis, my-
driasis, ophthalmoparesis and decreased accommoda-
tion are cyclically interrupted by transient eyelid
elevation, globe adduction, pupil constriction and
increased accommodation. Cause can be congenital or
brainstem glioma.
TROCHLEAR NERVE
The trochlear (fourth cranial) nerve is entirely motor in

function and supplies only the superior oblique muscle.
It is the longest and thinnest of all cranial nerves and is
the only cranial nerve to cross completely on to the other
side. It is the only nerve to arise from the dorsal aspect
of brain. It is divided into four parts: Fascicular, pre-

cavernous; intracavernous and intraorbital.
Causes of IV nerve paralysis:
1. Idiopathic
2. Congenital
3. Trauma
4. Vascular, neurological
5. Tumors.
Clinical Features
Less frequent than III or VI nerve paralysis. It is the
commonest cause for sudden vertical diplopia.
1. Hyperdeviation: Involved eye is at a higher level as a
result of weakness of superior oblique muscle.
Bielschowsky’s head tilt test is useful in diagnosing
a fourth nerve palsy.
2. Ocular movements: Depression is restricted in adduc-
tion. Extorsion is also limited.
3. Diplopia is more in down gaze, especially when
coming down the stairs.
4. Abnormal head posture: Face is slightly turned to the
opposite side, chin is depressed and head is tilted
towards the opposite shoulder to avoid diplopia.

Nucleus
Occurs in closed head trauma. It is involved with fasci-
cular and nerve injury.
Fascicle
Bilateral palsy. It is due to impact of the decussation
against tentorial edge.
Nerve Trunk
a. Trauma: Impact against tentorium. Neurosurgery of
posterior fossa can also be a cause. (The nucleus and
fascicles are so close that differentiation is difficult).
b. Vascular and diabetic: Microvascular supply is affec-
ted. Spontaneous palsy and spontaneous recovery
are seen.
c. Cavernous sinus and superior orbital fissure: Usually
III nerve, V nerve, oculosympathetic and VI nerve
are also affected.
d. Herpes zoster: Isolated IV N is rare. Only 50% recover.
Superior oblique palsy can be diagnosed by the
following three features.
1. First is to determine which eye is higher. If the right
eye is higher, the right depressors or the left elevators
are weak.
2. The patient is asked to look to both sides. If the ima-
ges now appear further apart on left lateral gaze,
either the right superior oblique or the left superior
rectus is weak.
3. The patient is then asked to look up and down
toward the side where separation was greater. If this
maneuver elicits greater separation on down gaze,
the right superior oblique is the weak muscle.
Parinaud’s syndrome: There is bilateral upward gaze
paresis. When attempt is made to look up there is con-
vergence. Lid retraction or down gaze and mydriasis
are other features. It is seen in hydrocephalus and tumor
of pineal body.
Tensilon test, forced duction test, GTT, CT scan (rare)

and observation are advised in isolated IV nerve palsy.
ABDUCENT NERVE
The abducent (sixth cranial) nerve is a small, entirely

motor nerve which supplies the lateral rectus muscle.
It is divided into four parts: Fascicular, basilar,
intracavernous and intraorbital.
Isolated VI nerve palsy has no localizing value and
can never have nuclear cause.
Clinical Features
1. Deviation: In primary position eyeball is converged
because of unopposed action of medical rectus.
2. Ocular movements: Abduction is restricted due to
weakness of lateral rectus.
3. Diplopia: Uncrossed horizontal diplopia occurs.
4. Head posture: Face is turned towards the action of
paralysed muscle to minimize diplopia.

Nucleus
Nuclear lesion results in horizontal gaze palsy towards
the lesion (Not unilateral abduction palsy). Ipsilateral
VII nerve palsy and internuclear ophthalmoplegia are
seen. It can never be isolated VI nerve palsy.
Fascicle
a. If dorsolateral pons is affected, ipsilateral abduction
weakness (or gaze), VII nerve involvement, facial
analgesia (V nerve), Horner’s and deafness occur

(Foville’s syndrome).
b. Dorsal pons: The previous findings along with contra-
lateral hemiplegia (pyramidal tract affected)
(Millard-Gubler’s syndrome). Both these are usually
seen in elderly due to vascular cause. In pontine
lesion, ipsilateral VI nerve and contralateral
hemiparesis are seen (Raymond’s syndrome). The
above syndromes are seen in elderly patients with
diabetes or hypertension.
Nerve Trunk
a. Nasopharyngeal carcinoma: Many nerves are affected.
Hearing complaint is prominent. Hypo or hypertear
secretion is seen (Vidian nerve affected).
b. Chordomas: Very rare. VI nerve frequently affected.
Usually unilateral.
c. Increased intracranial pressure: VI nerve stretched
between brainstem and dural attachment. Tumor
can mimic this.
d. Petrous tip:
i. Gradenigo’s syndrome: VI nerve, VII nerve and
first branch of V nerve are involved. It is secon-
dary to ottitis media. Tumor can mimic this.
ii. Trauma results in bilateral VI and VII nerve
lesion and leaking of CSF from external ear
(Battle’s sign).
e. Inferior Petrosal sinus: In thrombosis and phlebitis.
f. Cavernous sinus: Cause can be carotid cavernous fis-
tula, and thrombosis or aneurysm (painful VI nerve
palsy), meningioma(III nerve and then VI nerve)
and Tolosa-Hunt’s syndrome.
g. Superior orbital fissure syndrome (same as Tolosa-

Hunt).
h. Orbit: No selective involvement of VI nerve. Thyroid,
orbital myositis and pseudotumor are the causes.
Isolated VI nerve palsy in children will develop
neurological signs within a few weeks.
In Mobius’ syndrome, there are bilateral VI and VII
nerves palsy, loss of horizontal movement with normal
pupil and Bell’s phenomenon. The cause is aplasia or
hypoplasia of nucleus of VI nerve (and other cranial
nerves). Common causes of bilateral VI nerve palsy are
congenital tumor, demyelinating disease, infection and
trauma. Vascular causes are rare in children; but
common in adults.
INTRACRANIAL TUMORS
They are relatively rare. Common intracranial tumors

are glioblastoma multiforme, astrocytoma, meningioma
of the cerebrum, adenoma and carcinoma of the
pituitary body, medulloblastoma of the cerebellum and
meningioma of the sphenoidal ridge.
They produce two sets of symptoms and signs.
1. General symptoms due to increased intracranial
pressure—headache, vomiting, convulsion and
bradycardia.
2. Ocular: Papilledema and occasionally paralytic
squint. Midbrain tumor is almost invariably asso-
ciated with papilledema of severe degree. Cerebellar
tumor is also accompanied by papilledema. Papille-
dema is not always present in cerebral neoplasms.
Ocular palsies due to increased intracranial

tension are relatively rare. Sixth nerve palsy may
sometimes be present in the early stage.
Above signs have no localizing value and hence
called “false-localizing signs”.
3. Focal signs are due to involvement of the structures
and vary with the location of the tumor (Fig. 14.2).
A. Prefrontal tumors: Sometimes, it produces atrophy
of the optic disk on the side of lesion due to direct
pressure and papilledema on the other side due
to increased intracranial tension (Foster- Kennedy
syndrome).
B. Chiasmal and pituitary tumors: Bitemporal hemia-
nopia is the characteristic field defect in these
tumours. Ocular palsies are seen occasionally.
Sixth nerve is more involved; but all the three
ocular motor nerves may be affected.
Gigantism or acromegaly is associated with
acidophil adenoma of the pituitary body. Other
pituitary adenomas are accompanied by signs of
hypopituitarism. X-ray of the skull shows balloo-
ning of the sella in pituitary tumors.
4. Temporal lobe tumors: It produces crossed upper
quadrantic hemianopia due to pressure on the optic
radiation. Visual hallucination is usually complained
of. Third nerve may, sometimes, be involved due to
downward extension of the neoplasm.
5. Occipital lobe tumors: There is typical homonymous
quadrantanopia or hemianopia of the opposite side.
Visual agnosia may occur in some cases.
6. Pineal body tumors: The characteristic sign is the loss
of conjugate upward movement of the eyes. Some-
Fig. 14.2: Field changes due to lesions of visual pathway. Lesion at (A)
Optic nerve (Ipsilateral blindness). (B) Proximal portion of optic nerve
(ipsilateral blindness and contralateral hemianopia). (C) Middle of chiasma
(Bitemporal hemianopia). (D) Optic tract (Homonymous hemianopia).
(E) Temporal lobe (Quadrantic homonymous hemianopia). (F) Optic
radiation (Homonymous hemianopia). (G) Occipital lobe (Homonymous
hemianopia with macular sparing)
times the downward gaze is also affected later on.

Both the third nerves are paralysed in some cases.
7. Tumor of the cerebral peduncle (midbrain): There is third
nerve palsy on the affected side together with contra-
lateral seventh nerve palsy and crossed hemiplegia
(Weber’s syndrome).
DEMYELINATING DISEASE
They include disseminated sclerosis, Devic’s disease of

neuromyelitis optica and Schilder’s disease.
Disseminated Sclerosis
There is patchy demyelination of the white matter of
the central nervous system. The symptoms start quite
suddenly. In the early stages, almost complete recovery
is the rule. It is more common in women between the
ages of twenty and forty.
The general symptoms and signs are weakness of the
limbs, ‘pins and needles’ sensation, scanning speech,
intentional tremor and signs of upper motor neuron
lesion.
Ocular Manifestations
In about 50 percent of cases, ocular symptoms appear
first.
a. Acute retrobulbar neuritis with profound loss of
vision in one eye and central scotoma in the other
eye are seen. Fundus is usually normal. Sometimes,
some degree of edema of the disk is present if the
lesion is situated immediately behind the globe.
Optic atrophy may occur as a sequel to a lesion in
the optic nerve, chiasma or optic tract.
b. Nystagmus is a common sign especially evident on

lateral rotation of the eyes. Inequality of the pupils
is quite common in this condition. Abnormal pupil-
lary reactions such as A-R pupil or reverse A- R pupil
may sometimes occur.
c. Ocular palsies are not very common. Sixth nerve
affection is more common than the others. Conver-
gence weakness and vertical gaze palsy are less
common. Lateral gaze palsy may occur in some
cases.
Neuromyelitis Optica (Devic’s Disease)

A condition characterized by bilateral optic neuritis and
transverse myelitis. Visual symptoms usually appear
earlier than those of myelitis, i.e. paraplegia. There is
sudden loss of vision in one eye followed by that of the
other within a day or two. Fundus usually shows mild-
to-moderate degree of papillitis with engorgement of
the retinal veins. Pupils are dilated and immobile.
Paraplegia usually appears 4 or 5 days after onset of
the visual symptoms. Demyelination commonly affects
the lumbodorsal region of the spinal cord.
Recovery occurs in some percentage of cases. Blind-
ness passes off and good vision is restored. Examination
of the visual fields always shows some residual
pericentral or paracentral scotoma. Unlike disseminated
sclerosis, Devic’s disease does not recur.
Schilder’s Disease (Encephalitis

Peri-axialis Diffusa)
Demyelination starts in the occipital lobes of the brain
and, later on, spreads to other parts of the cerebrum.
So, the condition starts with bilateral cortical blindness

with retention of the pupillary reactions. Papilledema
may develop due to raised intracranial tension caused
by diffuse cerebral edema. Optic neuritis, sometimes,
occurs due to direct involvement of the optic nerve.
The condition occurs in children under the age of 14
years. There is gradual paralysis of the limbs and the
child usually dies within a year.
PSEUDOTUMOR CEREBRI
Pseudotumor cerebri is also known as benign intra-

cranial hypertension.
It causes gross papilledema without any striking
neurological changes. It occurs mostly following intake
of certain drugs such as tetracycline, nalidixic acid, high
dose of vitamin A, steroids and oral contraceptives.
Presence of normal sized ventricles (as seen in CT scan)
and normal CSF study by lumbar puncture confirm the
diagnosis.
CEREBELLAR SYSTEM AND EYES
Isolated cerebellar damage is very rare. It is usually

cerebellum with brainstem.
The eye signs include cogwheel (saccadic) pursuit
movements, hypometric saccades, horizontal gaze
palsy, skew deviation, weakness of upward gaze, nys-
tagmus (up, down-beat, rebound, positional, horizon-
tal gaze—evoked and paretic), acquired pendular,
ocular dysmetria and flutter, opsoclonus and ocular
myoclonus. Oscillopsia occurs. If eye and head move-
ments do not match, the lesion is in flocculus. (In fact it

is duty of cerebellum to make a person adapt to new
glasses).
ANTERIOR ISCHEMIC OPTIC NEUROPATHY (AION)
It is segmental or generalized inflammation of anterior

part of the optic nerve caused by occlusion of short
posterior ciliary vessels.
It produces visual loss with altitudinal visual field
defect in the adults or elderly.
Causes
Atherosclerosis, giant cell arteritis, collagen vascular
diseases like systemic lupus erythematosis or poly-
arteritis nodosa.
Other causes are emboli, anemia and malignant
hypertension.
There are two types:
a. Non-arteritic AION
b. Arteritic AION
Non-arteritic AION
It is seen in elderly patient with systemic hypertension.
Visual loss is usually mono ocular, which is sudden and
painless without any premonitory symptoms. Visual
impairment is moderate to severe. The pathognomonic
visual field defect is altitudinal hemianopia which
includes the inferior half.
Fundus examination shows hyperemic disk (secto-

rial; upper part) which may be surrounded by splinter
hemorrhages.
Effective treatment is not available.
Arteritic AION
It occurs in one-fourth of elderly patients with untreated
giant cell arteritis. There is a sudden, profound and
permanent visual loss. The premonitory symptoms like
periocular pain and transient blurring of vision are seen.
Visual acuity is reduced to hand movements or counting
fingers. Systemic symptoms include headache, scalp
tenderness, jaw claudication, and pain and stiffness of
the proximal muscles.
Fundus examination shows a swollen white or pale
disk with splinter hemorrhages abound.
A high ESR, C- reactive protein and temporal artery
biopsy confirm the diagnosis.
Treatment includes heavy doses of systemic steroids
and then gradual reduction over a period of 3 months.
HEADACHE
Classification
Headache is classified into:
1. Vascular (Migraine, cluster, lower half, ophthal-
moplegic).
2. Muscle contraction (tension).
3. Combination of above two.
4. Others (Tractional, neuralgic, psychogenic, nasal,
ophthalmic).
(The other headaches are hypertensive head ache,

red wine headache, hangover headache, dialysis
headache, syphilitic headache, lower half headache,
neuralgic, arteritic, and rebound headaches. This
definitely is not an exhaustive list) (Table 14.1).
MIGRAINE
It is a unilateral, throbbing, periodic headache associated

with certain general symptoms. Women are more
affected. Familial occurrence is seen.
Susceptibility locus is on chromosome 19.
1. Classic: Short prodrome (visual, finger pricking,
aphasia, etc.), with or without head ache, which lasts
for a few hours accompanied by hyperosmia, photo-
phobia, hyperacousis, nausea and vomiting. It recurs
often within a month.
2. Common: It is seen in 8.5% of cases. Prodrome is not
a prominent feature. Headache lasts longer with
diuresis and diarrhea. It recurs once a year.
3. Basilar migraine: Brainstem symptoms predominate.
Etiology
It is divided into three phases: Brainstem origin, activation
of caudal nucleus of trigeminal with release of
vasoactive neuropeptides and vasomotor activation.
The extracranial vasodilatation and intracranial
vasoconstriction are secondary changes only.
Features
It is a unilateral, periodically recurring condition. It may
change the side of head. It is seen mostly in younger
Table 14.1: Common types of headaches 252
Age and Pain Trigger Cause Prognosis and
gender and other treatment
features
Migraine All ages, children Fronto Onset after Disturbance Cycles of several
with/without and young adults. temporal awakening; in cranial months to years.
aura Females more in unilateral/ quelled by circulation, Less frequent and
adults. Family bilateral; sleep. by neuro- less severe with
history + pulsating Trigger— kinin and aging. Avoid
Worse on external, substance P trigger
bending. physiologic Prophylaxis
Changes sides and psycho- and management
Duration: logic Photo- of attack (anti-
12 hours to phobia, nausea depressant, anti-
days and vomiting + convulsant and
anti-inflamma-
tory)
CLINICAL OPHTHALMOLOGY MADE EASY
Contd...
Contd...
features
Cluster 20-80 years. More Immense pain Periodic, Hypo- Decreases with
(Horton’s in men. No family (suicide unilateral thalamus ageing.Episodic
neuralgia; history headache) Caused by abnormality —chronic.
Vidian Boring, hard work, Narcotic
neuralgia; behind eye Alcohol, analgesic; beta-
Sluder’s Occurs in the perfume, blocker
neuralgia) morning weather Calcium
(Alarm clock changes and channel
headache) psychological blocker
Daily Ptosis, Septoplasty
Unilateral, watering of
shifts sides eye, face
Can recur blushing
within a day restlessness
Lasts for 15 Nausea not
minutes to much. Strange
NEURO-OPHTHALMOLOGY
3 minutes behaviour +
Remission + Chronic—no
253
remission
Contd...
Contd...
254
features
Tension All age; in young Radiates from Episodic or Brainstem. May even go on
(Muscle adults- females neck, back and chronic, lasts Serotonin, for months or
contraction) more eye. Constant, for 4-6 hours nitric oxide years. Cycles of
head being Trigger – Abnormal several
squeezed by Stress, CNS pain years. Sleep,
tight band hunger and processing analgesic
Bilateral eye strain Caffeine
Ocular Depends on Mild-to-severe Eye; radiates Refractive Management of
cause according to to head error, cause
cause Refreactive glaucoma,
error— more in corneal
evening causes,
iridocyclitis
Ictal Mild to very Along with Along with Anticonvulsants
severe (Suicide seizure epilepsy
headache); Unusual
bilateral thoughts and
experience
Contd...
Contd...
features
Pseudotumor Any age; any Worse in Nausea, diplopia Lumbar puncture
cerebri gender morning and papilledema+
Trigger —
Vitamin A
Brain tumor All ages; no Variable Interrupts sleep, Monophasic
gender unrelieved by illness lasting
difference sleep; weeks to months
Exacerbated by
orthostatic
changes; steadily
worsening pain;
may be preceded
by days to
weeks of nausea
and vomiting
NEURO-OPHTHALMOLOGY
Contd...
255
Contd...
256
features
Hemicrania Adults Continuous. Epiphra, Not known Indomethacin
continua (usually). Unilateral; rhinorrhea,
Women more moderate with ptosis, miosis
stabbing and photo-
pain phobia
Thunderclap Any age, any Worst of all Aneurysmal;
gender headaches, subarachnoid
sudden hemorrhage
Lumbar Over 10 years; Bifrontal and/ With jolting Lumbar Lasts for 3 - 4
puncture (LP) either sex or bioccipital pain; puncture days
orthostatic
Orgasmic Adult men more Base of skull. Lasts for a few Intercourse;
Goes to frontal minutes to few mastur
and behind eye; hours. Stiff bation
bilateral. neck; confusion
age group and in women. Head ache is in the front half

of head.
The visual disturbances are fortification spectra (Zig
Zag or flashes of light), visual blurring or even field
defect. They last for half an hour. Ipsilateral paralysis
of one or more extraocular muscles occurs. If basilar
artery is involved, formed visual hallucinations and
bilateral visual blurring or blindness can occur.
Other causes for headache must be ruled out. These
include refractive error, acute congestive glaucoma,
hypertension, tension headache, cluster headache,
trigeminal neuralgia and certain neurological conditions
such as raised intracranial tension, intracranial infarct,
cavernous sinus problem and intracranial bleeding.
Treatment
Prophylaxis
Avoidance of triggering agent and use of propranolol,
amitryptyline, NSAID, verapamil and anticonvulsant.
Symptomatic
1. Analgesics and mild sedatives.
2. Ergotamine, sumatriptan or acetaminophen
3. Opiates—last resort only.
OPHTHALMOPLEGIC MIGRAINE
It is a rare condition. Later on it may go onto migraine.

Cause is unknown. It occurs in children with positive
family history of migraine. Pain in eye, nausea,

vomiting, diplopia and paralysis occur in that order.
Optic nerve is normal. It subsides or recovery is partial.
Recurrence is seen.
INTERNUCLEAR OPHTHALMOPLEGIA
It is due to injury to medial longitudinal bundle. Lesion

is between nuclei of III and IV nerves. Bilateral one is
due to demyelinating disease (90% in young) and
multiple sclerosis. Ipsilateral eye adducts slowly or not
at all, while the contralateral eye shows nystagmus.
Convergence may be absent. Unilateral condition is due
to brainstem vascular disease.
HORNER’S SYNDROME
It is divided into acute and chronic types. This condition

is due to paralysis (loss) of sympathetic function.
Etiology
It may involve the first, second or third order neurons.
First Order Neuron

Stroke due to vertebrobasilar insufficiency or infarct,
tumor and severe osteoarthritis of neck.
Second Order Neuron

Tumors such as lung carcinoma or thyroid adenoma,
pan coast tumor, neuroblastoma and metastasis
Third Order Neuron

Internal carotid dissection, herpes zoster, otitis media,
Tolosa-Hunt’s syndrome and cluster migraine.
It may occur as a congenital condition.
Features
1. Enophthalmos of minimal degree
2. Lids—mild ptosis and lower lid elevation (“Reverse
ptosis”). Palpebral fissure is narrowed.
3. Iris—light color or heterochromia.
4. Pupil—anisocoria with a small pupil.
5. Increase in accommodation so that the reading
material is kept close to eye.
6. Unilateral absence of sweating.
Investigations
1. Cocaine test: Cocaine is instilled into both eyes (and
may be repeated after 15 minutes). The affected side
pupil will not dilate as much as the normal side
pupil.
2. Hydroxyamphetamine is instilled twice in both eyes
at one minute interval. In Horner’s due to 3rd order
neuron ipsilateral pupil may not dilate as much as
the fellow eye.
3. Computer tomography (CT) scans of lung apex.
4. MRI of brain and neck.
5. Carotid Doppler ultrasound.
6. Lymph node biopsy.
Management
1. Underlying cause is treated.
2. Ptosis surgery may be done.
MYASTHENIA GRAVIS
In this condition number and amplitude of acetylcholine

receptors are reduced. It is an autoimmune disease. The
incidence is 0.02%. Thyroid dysfunction may trigger it.
It is associated with thymoma or other autoimmune
disease such as multiple sclerosis. It has to be diffe-
rentiated from congenital myasthenic syndromes due
to gene mutation.
Features
It affects all age group.
Patient complains of weakness and diplopia. This is
more in the evening or when patient is tired.
Signs include drooping of upper lid and sustained
upward gaze. If the gaze is shifted from below to
primary position, the ptotic eyelid twitches (Cagorn’s
Lid twitch). Complete limitation of ocular movement
may be seen. The pupil is always normal. Intrinsic ocular
muscles are never involved.
Subtypes
Ocular
Ocular muscles are involved. Thymoma is rare.
Generalized
There are three subtypes.
Investigations
1. Tensilon test: If 0.2 ml (2 mg) of tensilon (edropho-
nium chloride) is given intravenously. The ptosis
disappears in one minute. If it does not, 8 mg is given
after 30 seconds.
2. Intramuscular neostigmine (2 mg) or oral pyridostig-
mine (60 mg) is given. This is another pharmacologist
test.
3. Estimation of acetyl choline receptor antibodies.
4. Mediastinal imaging.
5. Electromyographic study.
Treatment
1. Prism for diplopia.
2. Pyridostigmine.
3. Low dose of prednisolone (5 mg on alternative days).
4. Azathioprine or ocular muscle surgery is the last
resort.
5. Thymectomy is not recommended.
DUANE’S RETRACTION SYNDROME
It is a bilateral, congenital condition seen commonly in

girls. There are narrowing of interpalpebral aperture
(IPA), upshot of eye ball and globe retraction on
adduction and widening of the IPA on abduction.
There are three types:
I. IPA narrowing, globe retraction and limited
abduction.
II. Some as I; but adduction is limited

III. Adduction and abduction are limited. This is a rare
type.
The cause can be mechanical factors (fibrotic or
atrophic lateral rectus, posterior insertion of medial
rectus and muscles bound to orbital wall) and neural
causes (absent VI nerve nucleus).
Auricular, neural and skeletal system anomalies are
associated with this syndrome.
15
Squint
It is also known as strabismus in which one eye is

deviated relative to the other eye (Table 15.1).
Table 15.1: Comparison between comitant

and paralytic squints
Comitant squint Paralytic squint
Onset Gradual Sudden
Cause Poor vision or Paralysis of extra-
central problem ocular muscle(s)
Movements of eye Present Absent in one or
more direction
Angle of squint Same in all gaze/ Varies
directions
Secondary deviation Equal to primary Primary is less
Diplopia – +
False projection – +
Afferent pathway Defective Normal
Efferent pathway Normal Defective
Vision Normal Diminished
Systemic symptoms – Nausea and
vertigo in the
beginning
ARC + –
Amblyopia + –
It is divided into comitant and paralytic (incomitant

or restrictive) squints. The former is due to some fault
in the afferent pathway caused by poor vision or to
problem in central mechanism of fixation and fusion.
Latter, as the name implies, is due to paralysis of extra-
ocular muscle(s) (Fig. 15.1).
SQUINT 265
Fig. 15.1: Anatomy of extraocular muscles. (1) Levator palpebrae

superioris. (2) Superior rectus. (3) Medial rectus. (4) Lateral rectus.
(5) Inferior rectus. (6) Superior oblique. (7) Inferior oblique
COMITANT SQUINT
The factors that cause this type of strabismus are:

1. Defective vision in one eye of any cause from birth or
infancy. So fusion reflex at center is not developed.
2. Malinsertion or mal development of extraocular muscle
and congenital lateral rectus palsy wherein again the
fusion reflex is unable to develop.
3. Problems with accommodation (and thereby with
convergence) especially in hypermetropes. The con-
genital convergent type is seen with Mobius, Lang’s,
Ciancia and Duane’s retraction syndromes.
Comitant squint is divided into true and false. The
former is divided into eso and exo and each one further
into phorias and tropias. The squint that is obvious is
called tropias. The eyes may converge (estropia) or

diverge (exotropia). The former is common in hyper-
metropes and may diminish with age. The latter is
common in myopes and increases with aging. Tropias
are either congenital or acquired. Acquired esotropia
can be mainly accommodative and non-accommodative.
If the deviation is minimal, then it may be not be
obvious. This latent squint is known as phorias and is
made manifest by cover test.
Symptoms are minimal except for cosmetic problem
and lack of binocular vision. Diplopia, if it had been
present initially, is not present later on. The vision in
squinting eye goes down—amblyopia ex anopsia.
Investigations
1. Cover test: It differentiates
a. Uniocular and alternative squints.
b. Comitant and non-comitant squints.
c. True and pseudosquints.
2. Corneal reflex test. A light is shone into both eyes. The
light reflexes should be in the middle of the pupils.
One mm deviation from center indicates a squint
of 7°.
3. Prism reflex test
4. Worth four dot test to find out supperession.
5. Examination with synoptophore.
PARALYTIC SQUINT
Any lesion in midbrain or above results in paralysis of

gaze. In this the relative position of the eyes are main-
SQUINT 267
tained. If the lesion is lower down in nucleus, nerves or

muscles, it results in paralytic squint.
The chief complaints are:
1. Diplopia which is present when the patient looks in
the direction of paralytic muscle. Out of the two ima-
ges he sees, one is hazy (seen by squinting eye) and
other image is clear and sharp (seen by fixing eye).
It may be crossed or uncrossed diplopia.
2. The patient is also not able to correctly fix an object
in the direction of paralysis.
3. The head tilt: Face turned towards the direction of
action of the paralysed muscle.
4. If any effort is made to see in the direction of
paralyzed muscle, it can result in vertigo, nausea and
vomiting.
Diplopia charting is essential. The muscle that is
paralysed is correctly found out by charting with Hess
screen (Fig. 15.2).
Incomitant squint, apart from due to paralysis, is
caused by restriction of extraocular muscles. Forced
duction test confirms this condition.
1. Duane’s syndrome: Limited abduction (Type I),
adduction (Type II) or both (Type III) with globe ret-
raction and palpebral fissure narrowing on adduc-
tion.
2. Brown’s Syndrome: Mostly unilateral with limited
elevation in adduction.
3. Mobius syndrome: Unilateral or bilateral limitation of
horizontal eye movement with partial or complete
facial nerve palsy.
268
Fig. 15.2: Diplopia chart. It helps in diagnosing the extraocular muscles that are paralyzed
SQUINT 269
Fig. 15.3: Synoptophore. Used for investigation of a case of squint

and for giving orthoptic treatment
Management
1. The causative factor must be dealt with.
2. Minimal diplopia can be managed by prescribing
prisms.
3. One eye can be occluded as a temporary measure.
4. Operations on extraocular muscles.
5. Correction of refractive error with glasses.
6. Orthoptic treatment is the mainstay for comitant
squint. Synoptophore is mostly used (Fig.15.3). It is
used for:
a. Management of suppression.
b. Giving fusional exercises.
c. Treatment of amblyopia.
d. Treatment of abnormal retinal correspondence.
7. Management of amblyopia.
Surgery may precipitate diplopia. But this tends to

disappear. Surgery must be done before the age of
5 years.
AMBLYOPIA
It is unilateral (sometimes bilateral) defective vision

without any organic lesion. It develops mostly during
first decede of life and then does not deteriorate further.
The defective vision can be partial or total - the term
amaurosis is used for the latter.
Types
1. Anisometropic: Due to marked difference in refrac-
tive error in the two eyes. Usually the difference is
more than 4 diopter between the two eyes.
2. Strabismic: Caused by squint.
3 Ex anopsia: Deprivation of vision due to “closure” of
one eye.
4. Ametropic It is a result of high refractive error.
(Toxic amblyopia is nowadays called toxic neuro-
pathy).
Features
1. Gross defective vision in one (or both) eye which
cannot be improved by glasses.
2. Absence of organic lesion.
3. Individual letters can be read better than a whole
line.
4. Neutral density filter has no effect on the vision (This
differentiates amblyopia from defective vision due
to organic lesion).
5. In severe cases, mild afferent pupillary defect is seen.
SQUINT 271
Treatment
Treatment should be carried out before the age of
10 years.
1. Appropriate spectacle correction
2. Total occlusion of better eye (for one weak per year
of age). This is called conventional occlusion.
3. Alternate occlusion of better and amblyopic eye.
Occlusion is carried out till the vision is equalized
or when there is no further improvement with
occlusion.
In children older than 10 years of age, prognosis for
visual improvement with treatment is poor.
16
Ophthalmic
Operations
Only a few operations of importance to students and

general ophthalmologists are dealt with here.
ANESTHESIA
General Anesthesia
It is usually not needed for most of the eye surgeries. It
is mainly indicated in:
1. Operations of long duration.
2. Children.
3. Apprehensive patients.
4. Patients who specifically desire it.
5. Injuries especially if the injury to globe is an open one.
6. Patient who are sensitive to local anesthetic drugs.
While giving general anesthesia it should be
remembered that:
1. There should be good relaxation of muscles.
2. It should lower the ocular pressure.
3. There should not be any retching during intubation,
or nausea/vomiting during recovery period.
The special advantages and uses of general anes-
thesia are:
1. Useful in apprehensive patients, patients who refuse
regional anesthesia and children.
2. No risk of any local complication to globe.
3. When surgery is going to be a prolonged one.
4. In injury to eye with open globe.
5. No chance of myotoxicity (and neurotoxicity).
General anesthesia is not advisable in:
1. Patients who are on anticoagulants or MAO inhi-
bitors.
OPHTHALMIC OPERATIONS 275
2. Patients with certain muscular diseases, hemoglo-

binopathies, diabetics and difficult airway. Patients
who refuse general anesthesia.
General anesthesia usually reduces IOP. But
agents like trichlorethylene and ketamine increase
IOP. Halothane produces reduction in IOP. Hyp-
notics, barbiturates and tranquilizers cause reduction
in IOP. But oral chloral hydrate solution does not
affect IOP.
Among premedication drugs, agents such as
succinylcholine (administered intravenously) and
suxamethonium produce transient rise in IOP due to
vasodilatation and extraocular muscle contraction.
Diazepam prevents IOP elevation during intubation.
The anesthetist should be aware that it is preferable
for the surgeon to measure the IOP as early as possible
during the induction of general anesthesia.
At the same time, during the induction of anesthetic,
airway management is of tantamount importance and
the surgeon must defer to the judgment of the anes-
thetist as to when IOP measurements can be taken
safely.
Regional Anesthesia
This is the method for most of the eye operations. The
eye should be anesthetic, devoid of movements
(akinesia) and the lids should not close.
1. In order to anesthetize the eye ball and to achieve
akinesia the following methods are employed:
A. Retrobulbar (ciliary) block: About 1.5 ml of ligno-
caine (2%) mixed with adrenaline and hyalase is
injected into central space of orbit. The injection

is made through the lower lid at the junction of
lateral 1/3rd and medial 2/3rd. Needle is
directed superomedially (Fig. 16.1).
Ciliary block results in
a. Anesthesia of interior of eye ball
b. Akinesia (absence of ocular movements)
c. Dilatation of pupil
d. Lowering of intraocular pressure and
e. Minimal ptosis.
Peribulbar block: Instead of above method, peribulbar
block is given. About 5 ml of 2% lignocaine is injected
into the peripheral space of orbit. The solution seeps
into central space as well as to lids. Separate facial block
Fig. 16.1: Ciliary (retrobulbar) block. The needle enters near inferior orbital
margin at the junction of medial 2/3rd and lateral 1/3rd. The needle is
then directed posteriorily, medially and upwards. The patient looks straight
ahead
is not needed. Effect begins from 5 to 15 minutes. The

bogginess of lids may be considered by some surgeons
as a disadvantage. The akinesia is also not as good as
with retrobulbar block.
B. Local drops: One drop of 4% lignocaine is instilled
once a minute for five times. This alone produces
enough anesthesia to perform any eye surgery -
intraocular and of conjunctiva. It lasts for about
15 minutes. Lack of akinesia is the main problem.
C. Sub-Tenon’s and subconjunctival injections are
equally effective.
Complications of ciliary block:
a. Sensitivity to drug.
b. Retrobulbar hemorrhage: If this occurs the surgery
is to be postponed and to be taken up after about
a week.
c. Increased ocular pressure: Globe massage for about
a minute is recommended. Massage should be
intermittent and gentle. Pressure over closed lids
with a balloon is also recommended.
d. Scleral penetration by needle: This is more common
with myopes. It can occur with intraconal and
periconal methods.
e. Brainstem anesthesia: This is due to spread along
meningeal pathway by the agent and is seen in
intraconal block. Patient is mildly confused,
shivering or even goes for convulsions. Apnea
and cardiovascular problems can also occur. This
complication is very rare.
f. Retinal vascular occlusion: It is due to trauma to
central retinal vessels or compression by the
injected agent.
g. Oculocardiac reflex: It is seen when larger gauge

needle is used. A retro bulbar hemorrhage can
precipitate this. In fact an orbital block can prevent
oculocardiac reflex occurring during eye surgery
done under general anesthesia.
2. Facial Nerve Block
This paralyses the facial nerve temporarily. There are
four ways by which this can be achieved.
A. O’Brien method: About 5 ml of lignocaine (2%) is injec-
ted at the point where the facial nerve crosses the
neck of mandible. This paralyses all the branches of
facial nerve. It is painful (Fig. 16.2) .
B. In Van Lint technique: The injection is made in a V
shaped manner just outside the lateral canthus. Only
the upper division of facial nerve is paralysed. When
O’ Brien method fails, Van Lint’s technique is resor-
ted to.
C. Atkinson’s method is another way of achieving
paralysis of upper division of facial nerve. An injec-
tion of 2% lignocaine is made in a horizontal manner
just below the lateral half of the lower lid for about
5 cm.
D. In Nabat technique, the injection is made at the point
where the facial nerve leaves the stylomastoid
foramen. It is a painful injection (Fig. 16.3).
This author tried acupuncture with the help of a spe-
cialist. But, it failed to anesthetise.
Advantages of regional anesthesia:
a. Lesser postoperative retching and pain.
b. Patient is conscious during surgery.
c. No complication that is seen with general
anesthesia.
d. Oculocardiac reflex is abolished.
Fig. 16.2: Facial block. About 4 ml of lignocaine (2%) is given near

neck of mandible (O’Brien’s method)
Fig. 16.3: Sites of various facial block methods. (A) O’ Brien’s method.
(B) Van Lint’s method. (C) Alkinson’s technique. (D) Nabat’s method
It is not advised in:

a. Mentally retarded and/or agitated patients.
b. Patients who refuse for injection.
c. Head movements or tremors.
d. General conditions such as arthritis, neurological
problems.
e. Patient who had problem with regional anes-
thesia in the contralateral eye.
f. Eye injuries with open globe.
Complications of facial block:
1. Permanent facial nerve paralysis has been reported
with O’ Brien method.
2. In Nadbath technique, difficulties in swallowing and
airway obstruction caused by vagus and gloso-
pharyngeal block are met with. In this technique hya-
luronidase should be avoided.
Regional anesthesia is mostly given by ophthal-
mologist. But now the involvement of anesthetist has
increased. He is called in especially if the number of
surgeries done is more.
Short acting sedative such as barbiturate is given
prior to regional anesthesia. But some do not prefer this.
Even if the operation is performed under regional
anesthesia, patient must be on empty stomach and facility
for conversion to general anesthesia must be available.
LOCAL ANESTHETIC AGENTS (TABLE 16.2)
They can be ester-linked agents such as cocaine and

procaine, or amide linked agents like lignocaine,
bupivacaine and mapivacaine. The duration of action

of former group is short (30 to 60 minutes), while that
of the latter group is long (Bupivacaine duration can
last anywhere from 3 to 10 hours). These agents are
weak bases, poorly soluble in water and as such may
not be useful. So they are prepared as water soluble salts
of hydrochloric acid.
Adverse Effects
1. Allergy: This is mostly seen with ester linked group.
It is due to its breakdown product, para-amino
benzoic acid. Sometimes the preservative used in it
such as sodium metabisulphite might be the cause.
2. Tissue toxicity especially of nerves and muscles occur
in high concentration
3. Systemic toxicity mainly affecting cardiovascular and
central nervous system.
4. Neurotocity: This is seen mostly with ester linked
agents. It is more if sodium metabisulphite is added
to an agent with low pH. The nerve can be damaged
by the needle or pressure ischemia if intraneural
injection is made. This is not of great importance in
ophthalmology.
5. Of greater importance is myotoxicity which is seen
in higher concentration. This may affect the extra-
ocular muscles leading to even permanent paralysis.
ADJUVANTS
Adrenaline
By its vasoconstriction effect it delays absorption and
increases duration of action of anesthetic agent. The
concentration should be 5 mg/ml (1:200,000) and the
total amount should be less than 0.2 mg. It must be
remembered that adrenaline may reduce blood supply
to globe and lower perfusion pressure in eye. It is
avoided in patients taking tricycline antidepressant.
Hyaluronidase
It spreads the injected agent across connective tissue
barrier by hydrolyzing the hyaluronic acid of the tissues.
The recommended concentration is 15 turbidity units/
cc. It might reduce the effective duration of the anes-
thetic agent. But this is countered by mixing adrenaline.
It has to be kept in fridge. It has myotoxicity.
Sodium Bicarbonate
Onset and penetrance of an agent is governed by its
pH. These are facilitated by addition of sodium bicarbo-
nate. Its usefulness is questionable.
Certain agents used for regional anesthesia in
ophthalmology are given below (Table 16.1):
Table 16.1: Regional anesthetic agents

Lignocaine Bupivacaine Mapivacaine
(Xylocaine) (Marcaine)
Concentration 1 to 2 % 0.25 to 0.75%
Onset Fast Intermediate Fast
Duration of 1-2 hours 3-10 hours 2-4 hours
action
Maximum dose 250 mg 150 mg 300 mg
Adrenaline Prolongs Prolongs No effect
action action
Metabolised by Liver Liver Liver
Others Vasodilator Cardiogenic No topical

effect + motor block effect; less
vasodila-
tation
(Maximum dose can be higher, if adrenaline is mixed)
Topical anesthetic is a must in ophthalmology.

Cataract surgery was once done with these agents alone
and this technique has come back.
STERILIZATION
The word sterilization brings to one’s mind the asepsis

of the operation theatre and its related materials. But,
sterilization for an ophthalmic surgery starts even
earlier (Flow chart 16.1).
Table 16.2: Common topical anesthetic agents 284
Cocaine Lignocaine Amethocaine Proparcaine
Composition Ester linked Amide linked Ester lined Ester linked
Concentration 1-4 4 0.5 0.5
Duration 20 min 15 min 15 min 15 min
Dose 1- 2 mg /kg 3 mg/kg 5 mg 10 mg
Corneal toxicity ++; ulcer + + + ?+
Others Vasoconstriction Antibacterial Antibacterial Stinging ?+
Mydriasis Sting Hyperemia + Contact
Euphoria + Least toxic Sting + dermatitis
Dysrhythmia + Dysrhythmias
Toxic
Flow chat 16.1: Classification of sterilization methods
Patient
Any source of infection must be eliminated, especially
lacrymal passage. Preoperative conjunctival swabs for
microbiological assessment and use of antibiotic solu-
tion to eye must be carried out. Just before operation,
skin around the eye should be cleaned with 10% povi-
done – iodine pyrolidone and the conjunctival sac irri-
gated with 5% povidone- iodine. Proper draping which
covers even the eye lashes is important.
Instruments
Sterilization by boiling is almost on the way out. Moist
heat is effective. It denatures and coagulates enzymes
and proteins. (1) Autoclaving: It may be vertical or
horizontal equipment. The material (cloth and blunt
instruments) are cleaned, packed and kept for 30
minutes at 120° C at a pressure of 15 lbs per square inch.
In between surgery quick sterilization can be done with
flash (134°C to 5 minutes) or high speed autoclave
(120oC at 15 pounds per square inch for 15 minutes).
The other forms of dry heat sterilization such as
flaming and incineration are inefficient and do not merit
any mention here. Hot air is employed to sterilize sharp
instruments and glass materials.
Chemical Sterilization
Gases like ethylene oxide or solutions like glutarald-
ehyde (cidex), dettol or savlon is used. Instruments are
kept in these agents for 30 minutes. The chemical agent
must be washed out before using the instrument.
Cetrimide is not used nowadays as it is ineffective
against gram negative organisms. Cidex destroys
spores. Spirit does not kill viruses.
Laser lenses are sterilized by ethylene oxide for one
hour at a temperature of 55°C. They should not be steam
autoclaved or boiled.
OCULAR SURGERIES
Cataract
Ciliary and facial block (or) peribulbar block are used.
Locally 2% lignocaine drops are instilled.
Extracapsular Cataract Extraction (ECCE)

This method is used:
1. For patients below 40 years of age.
2. When posterior chamber IOL implantation is plan-
ned.
3. In patients with pathological myopia with degene-
rative changes.
4. For patients who had postoperative retinal detach-
ment in the other eye.
The superior rectus suture is applied (not manda-
tory). The conjunctiva is cut at limbus in the upper
quadrant and reflected back. Bleeding points secured.
Anterior chamber is entered with the tip of blade at
limbus. Viscoelastic is injected into anterior chamber.
The anterior capsule of lens is cut open in a circular
fashion with the help of bent 24 G needle. The limbal
incision is extended to a length of 3 to 5.2 mm (or, the
incision is made away from limbus in sclera and
tunneled into anterior chamber). The cut circular ante-
rior capsule piece removed. The rest of capsule is
separated from the cortex with fluid (hydrodissection).
The epinucleus is also separated from nucleus by
injecting fluid (hydrodelineation). By the latter proce-
dure the nucleus becomes free so that it can be easily
rotated. The nucleus is divided with phaco , emulsified
and aspirated. The cortex that remains is also aspirated.
After hydrodissection, the nucleus can also be expressed
out with pressure and counter pressure and the
remaining cortex aspirated. Iridectomy is not a must.
The IOL is introduced into capsular bag and rotated so
that the haptic (supporting arm) is in horizontal position.
The limbal wound is closed with 10/0 suture. Perfor-

ming iridectomy is not a must (Fig. 16.4) . With the
advent of rollable or foldable IOL the size of the (limbal)
incision has come down to one mm. (There are so many
modifications in ECCE).
Figs 16.4A to F: Extracapsular cataract extraction. (A) Small limbal

incision made. (B) Anterior capsule of lens opened with a bent 26 G
needle (Canopener method). (C) Nucleus expressed out by pressure
and counter pressure. (D) Cortical matter aspirated with Simcoe cannula.
(E) IOL inserted. (F) IOL haptics placed in horizontal position and limbal
wound closed
Intracapsular Cataract Extraction (ICCE) (Fig. 16.5)

Nowadays it is done (1) for subluxated or dislocated
lens and (2) in cases where the other eye had developed
severe phacoanaphylactic glaucoma or phacogenic
uveitis. After superior rectus suture application, a
limbal based conjunctival flap is reflected. Limbus is
opened for 120° and a peripheral iridectomy done. The
lens is removed in toto by cryo (Fig. 16.6) , intracapsular
forceps, vectis (in subluxated lens) or by erysiphake. In
hypermature cataract tapping at 6 o’ clock position with
Figs 16.5A to D: Steps of intracapsular cataract extraction. (A) After

reflecting limbal based conjunctival flap, the incision is made at limbus
and anterior chamber (A/C) entered. (B) Peripheral iridectomy is
performed. (C) The lens is removed in toto using cryoprobe. (D) Limbal
and conjunctival wounds closed
Fig. 16.6: Cryo equipments. Using these equipments, the cataractous

lens is removed in toto. The other instruments that can be used to remove
the cataractous lens in toto are intracapsular forceps, vectis and
erysiphake
counter pressure at 12 o’ clock position expresses out

the lens (Smith-Indian method). Limbal wound is closed
with 10/0 suture. The conjunctival wound closed with
continuous suture.
Complications
Complications of anesthesia:
1. Reaction to drug
2. Retrobulbar hemorrhage (does not occur with peri-
bulbar block).
3. Perforation of globe.
Operative:
1. Expulsive hemorrhage
2. Vitreous loss (in ICCE)
3. Capsular rupture (in planned ECCE).
Postoperative:
1. Iris prolapse: Not seen with modern day technique.
2. Shallow chamber: Due to wound leak, pupillary block
or cilio choroidal detachment.
3. Retinal detachment: Seen in cases with retinal dege-
neration as in high myopia and in cases that had
vitreous loss. This is common with ICCE.
4. Corneal edema: It is due to corneal endothelial damage
caused during surgery or later by vitreous touching
back of cornea.
5. After cataract: Commonly seen after ECCE.
Complications associated with IOL:
1. Malposition of IOL: It may be decentered (this is
mostly due to faulty technique), or may move up or
down due to subluxation.
2. Corneal endothelial damage: More common with A/C
IOL.
3. Cystoid macular edema.
4. Dislocation of IOL into vitreous.
5. Swinging of IOL: Seen with small IOL with haptics
placed vertically.
GLAUCOMA
The surgeries for glaucoma can be grouped into:

Flow chart 16.2: Surgeries for glaucoma
Enucleation is done for absolute glaucoma with

intractable pain.
Cyclodialysis (Fig. 16.7)

It is indicated in aphakic glaucoma and in failed
filtration procedures. Conjunctiva is cut for 5 mm about
10 mm from limbus at superotemporal quadrant.
A 3 mm cut is made in sclera 7 mm away and parallel
to limbus. Cyclodialysis spatula inserted via this incision
into suprachoroidal space till the tip of spatula appears
in anterior chamber. The spatula is rotated up and down
so that ciliary body is detached for about 180o and a
communication is established between anterior
Figs 16.7A and B: Cyclodialysis. (A) Classical method in which the

cyclodialysis spatula is introduced via a scleral incision into anterior
chamber and scleral spur detached by turning the spatula outwards.
(B) In the modified procedure, the cyclodialysis spatula is introduced
into anterior chamber through a vertical, limbal incision. The scleral spur
separated by rotating the spatula towards the angle
chamber and suprachoroidal space. Conjunctival

wound closed (Fig. 16.7A).
In another modification, conjunctiva is incised as for
cataract surgery. Radial incision is made at limbus and
cyclodialysis spatula introduced into anterior chamber.
The ciliary body is separated from scleral spur by
sweeping the spatula from anterior chamber. In this
modification iridectomy or iridotomy can be performed
(Fig. 16.7B).
Trabeculectomy
It is indicated when medical treatment has failed in open
angle glaucoma and in infants when goniotomy has
failed. After application of speculum and superior
rectus suture, conjunctiva is cut 6 mm from limbus and
Figs 16.8A and B : Peripheral iridectomy. (A) Small limbal opening

made. (B) Peripheral iridectomy performed
a limbal based conjunctival flap is reflected down.

(Fornix based flap also is employed). The sclera is dissec-
ted off the Tenon’s capsule. A square (4 × 4 mm) partial
thickness limbus based scleral flap is reflected upto and
beyond the limbal blue line. A 3 mm long and 2 mm
broad limbal tissue containing deeper sclera and
trabecular meshwork is removed. Peripheral iridectomy
is done. Superficial scleral flap and conjunctival flap
sutured (Fig. 16.9) . (The superficial scleral flap can be
triangular also). Scleral flap suture, if needed, can be
releasable.
Scheie’s Operation
This surgery was once popular. It is indicated in
uncontrolled glaucomas. Under a limbal based 4 mm
conjunctival flap, the limbal tissue is incised for 3 mm
to 1/3rd depth. The posterior lip of wound cauterized.
The cut deepened still more minimally and posterior
lip again cauterized. This is repeated till A/C is entered.
Peripheral iridectomy done and conjunctival wound
Figs 16.9A to C: Trabeculectomy. (A) Limbal based conjunctival flap

reflected down. Incision (4 × 4 mm) made in superficial sclera. (B)
Superficial scleral flap reflected down and a block of limbal tissue (2 mm
broad) containing trabecular meshwork and Schlemm’s canal excised.
(C) Peripheral iridectomy performed and superficial scleral flap and
conjunctival wounds closed.
Figs 16.10A and B: Scheie’s operation. (A) The limbal incision is made
step by step. Each time the posterior lip alone is cauterized. This is done
till A/C is entered. (B) Peripheral iridectomy done and conjunctival wound
closed (Limbal wound is not sutured)
closed with running suture. Limbal wound is not

sutured (Fig. 16.10) .
Sac Surgeries
Dacryocystectomy (DCT)
It is done for chronic dacryocystitis in older individuals,
with ipsilateral impending intraocular surgery or
ipsilateral corneal ulcer, when sac is focus infection such
as of trachoma or tuberculosis, and in tumors of sac.
Anesthesia is by infiltration of the sac region. Skin
over sac is incised for about 1" starting 2 mm above the
medial palpebral ligament and 3 mm medial to inner
canthus. Orbicularis oculi and periostium over sac
incised. The exposed sac is dissected free and removed.
The nasolacrymal duct curetted. Wound is closed in two
layers.
Dacryocystorhinostomy (DCR)
It is done for chronic dacryocystitis especially in youn-
ger patients and in congenital dacryocystitis when other
methods have failed. (It should be avoided for children
below 3 years of age).
The anesthesia is same as above. In addition, the
nasal mucosa is anesthetized with spray and ipsilateral
nasal cavity packed with gauze. The incision is same as
for DCT. After exposing and isolating the lacrymal sac,
the lacrymal bone (of lacrymal fossa) is punched out.
The nasal mucosa is seen. The exposed nasal mucosa
and medial wall of sac are opened to form an “I” shaped
flaps. The flaps (or only the anterior flaps) of sac and
nasal mucosa are sutured together through the opening
in the lacrymal fossa (Fig. 16.11). The skin wound closed
in layers. Nasal pack is removed the next day. Syringing
Fig. 16.11: Dacryocystorhinostomy. Openings are made in the medial

wall of sac and in the lacrimal fossa (B). The nasal mucosa is opened in
an I-shaped manner. The nasal and sac mucosa are sutured together.
The tear now goes straight into nasal cavity from the sac bye passing
the block (A)
with antibiotic is done the next day and after one week.
If DCR fails, conjunctivorhinostomy may be performed.
In canalicular block, canaliculodacryocystorhinostomy
is done.
In DCT, epiphora is not relieved. In DCR epiphora
is cured. In acute dacryocystitis, surgery of any type
(except incision and drainage of abscess) is not
undertaken.
ENUCLEATION
Although it can be done under regional anesthesia, yet

it is better to perform this surgery (and evisceration)
under general anesthesia. After inserting the eye
speculum, conjunctiva is cut all around out side the
limbus. The Tenon’s capsule is cut 3 mm behind limbus.

The six extraocular muscles are detached. The eyeball
lifted up with enucleation spoon and the optic nerve
cut with scissors as far behind as possible. The separated
globe removed. Hemostasis obtained. Conjunctival and
Tenon’s wounds closed with or without an implant in
the empty orbit (Plastic implant such as Allen’s can be
buried in the orbit and Tenon’s and conjunctiva closed
over it separately).
EVICERATION
After speculum insertion, the cornea is cut all around

at just inside the limbus and the intraocular contents
scooped out. It is important that all uveal tissue is com-
pletely removed. Hemostasis obtained. Tenon’s capsule
and conjunctiva wounds are closed separately (Some
surgeons do not close these wounds).
Lasers
Apart from incisional surgeries mentioned above,
LASERS are used for treating certain ocular conditions.
They are used for photocoagulation of retinal lesions,
for iridotomy/capsulotomy, to lyse sutures, for trabe-
culoplasty and gonioplasty.
17
Instruments
Identification of common ophthalmic instrument is very

important for students since the (afternoon) oral exami-
nation starts with this and proceeds. If the student is
unable to identify the given instrument, then the oral
exam comes to an uncomfortable stand still.
When an instrument is given, the student must:
a. Get it in his own hand from examiner.
b. Look at it, and then.
c. Mention its name. Some candidates do not even get
the instrument in their hands, but mention name off
hand to examiner. This should be avoided.
Universal Eye Speculum

It is used for separating the eyelids during all extra-
ocular operations like foreign body removal, excising
pterygium, squint surgeries, evisceration and enu-
cleation of eyeball. It is called universal because it can
be used for both eyes (Fig. 17.1).
Fig. 17.1: Universal eye speculum

INSTRUMENTS 301
Wire Speculum
This is also used for the above purposes. It is preferred
because of its lightweight. It may be used in cataract
operations (Fig. 17.2).
Fig. 17.2: Wire speculum
Desmarre’s Lid Retractor

To open eyelids carefully:
a. While examining children, in noncooperative adults,
in severe blepharospasm, when there is danger of
corneal perforation or in severe edema lids.
b. For double eversion.
c. It may be used while removing sutures of eye globe
or any foreign body of cornea and conjunctiva
(Fig. 17.3).
Fig. 17.3: Desmarre’s lid refractor

Müller’s Self-retaining Hemostatic

Lacrymal Retractor
To retract the lips of the skin wound in operations on
sac like DCT and DCR. It acts as hemostat as well as
retractor of lips of wound (Fig. 17.4).
Fig. 17.4: Müller’s self-retaining hemostatic lacrymal retractor
IIndications for DCT and DCR

1. DCT done in:
a. Chronic dacryocystitis (CD) in old age.
b. When CD is associated with ipsilateral corneal
ulcer.
c. CD of an eye with impending intraocular sur-
gery.
d. Tumors of sac
e. When sac is focus of infection such as trachoma,
syphilis, leprosy.
2. DCR: It is done for chronic dacryocystitis in young.
Dastoor’s Superior Rectus Forceps

It is used to hold superior rectus tendon while applying
suture under it. This suture gives control over globe in
surgeries such as cataract, glaucoma, keratoplasty.
It enables surgeon to rotate the eye ball down. Eyeball
is rolled down since most of the eye surgeries are done
in the upper quadrant of globe (Fig. 17.5).
INSTRUMENTS 303
Fig. 17.5: Dastoor’s superior rectus forceps
Fixation Forceps (Graffe)

Useful in fixing the globe at limbus at 6 o’clock position
while making incision at the limbus in cataract surgery,
paracentesis, antiglaucoma operations and discision
and in forced duction test.
Globe is held at limbus since it is the site where
conjunctiva and sclera are adherent. So a firm grip can
be obtained (Fig. 17.6).
Fig. 17.6: Fixation forceps (Graffe)
Iris Forceps (HESS)

The iris is held with this instrument while cutting the
former during iridectomy (Fig. 17.7).
Fig. 17.7: Iris forceps (HESS)

Types of Iridectomy and their Indications

a. Peripheral iridectomy: Along with corneal grafting,
cataract and glaucoma surgeries and in first three
stages of narrow angle glaucoma.
b. Complete (sector) iridectomy: Along with cataract
surgery, for extensive posterior synechiae, retinal
detachment in the other eye, possible long-term
miotic therapy, sphincter rigidity and in iridencleisis,
c. Broad basal iridectomy: Prophylaxis for hemorrhagic
glaucoma.
d. Optical (key hole) iridectomy: Central leukoma and
central, stationary, congenital cataract.
e. Iris excision: Impacted foreign body in iris (especially
chemically active one), infected iris prolapse and
tumors of iris (amount of iris excised depends upon
the size of the pathology).
Various Types of Iridectomy (Fig.17.8)
Fig. 17.8: Various types of iridectomy

INSTRUMENTS 305
A. Peripheral (button hole) iridectomy.

B. Complete (sector) iridectomy.
C. Broadbasal iridectomy.
D. Optical iridectomy.
Arruga’s Intracapsular Forceps

Useful in holding the lens at 12 o’ clock or at 6 o’ clock
position and delivering it in intracapsular cataract
extraction (ICCE). It is also used to remove capsular
remnant after rupture of lens in ICCE. It has a cup at its
tip. For intracapsular extraction, lens can also be
removed by using:
a. Cryo equipment
b. Vectis
c. Erysiphake
d. Smith-Indian technique (in hypermature cataract)
was once employed (Fig. 17.9).
Fig. 17.9: Arruga’s intracapsular forceps
Epilation Forceps (Fig. 17.10)

To remove eyelash in trichiasis, stye, after electrolysis
of eye lash and when eyelash is lodged in punctum.
Fig. 17.10: Epilation forceps

Chalazion Clamp (or Forceps)

Useful in fixing the chalazion mass before incision. Flat
surface of the instrument should be on the skin side and
fenestrated one on the conjunctival aspect. Vertical
incision is made to prevent cutting other neighboring
ducts as well as blood vessels—both run in vertical
direction (Fig. 17.11).
Fig. 17.11: Chalazion clamp
Its role in the operation: It forms a base for operation,

prevents bleeding, helps in everting the lid, protects the
eye and steadies the lesion (In an older person, if
chalazion recurs at the same site after surgery, one has
to consider meibomian carcinoma).
Lid Clamp (Snellen)

Used in lid operations such as entropion. It acts as hemo-
stat, protects the globe and forms a base for surgery
(Fig. 17.12 ).
Fig. 17.12: Lid clamp (Snellen)

INSTRUMENTS 307
Erysiphake
It acts by suction—the cup gets attached to anterior
lens capsule by vacuum. It is used for removing lens
in ICCE. It is useful in intumescent cataract removal
(Fig. 17.13).
Fig. 17.13: Erysiphake
Conjunctival Scissors
a. Used for cutting the conjunctiva for limbal based
conjunctival flap for cataract extraction (ab externo)
or glaucoma surgery.
b. Pterygium excision.
c. Suture removal.
d. Squint surgery.
e. Detachment surgery and.
f. Gunderson’s flap (Fig. 17.14).
Fig. 17.14: Conjunctival Scissors
De Wecker’s Iris Scissors

Uses
a. To cut (and excise) the iris as in foreign body in iris,
cyst in iris, in traumatic prolapse of iris which is
infected, various types of iridectomies like peripheral
(button-hole), sector, broad basal and optical (key
hole) iridectomy.
b. To cut iris at the sphincter.
c. In certain antiglaucoma operations.
(Indications for each type of iridectomy - see under
“iris forceps”) (Fig. 17.15).
Fig. 17.15: De Wecker’s iris scissors
Iris Repositor (Dastoor)

Used to replace the iris into anterior chamber:
a. Dduring eye operations.
b. In early traumatic iris prolapse if it involves the lower
quadrant and is free of dense infiltration.
c. For paracentesis (Fig. 17.16).
INSTRUMENTS 309
Fig. 17.16: Iris repositor (Dastoor)
Von Graefe’s Cataract Knife

Uses
a. In cataract surgery section.
b. Paracentesis, (for evacuation of large, fluid, persis-
tent hypopyon or hyphema, in threatening corneal
ulcer perforation, CRA occlusion).
c. Chalazion incision, abscess incision.
d. Fuchs’ 4 dot iridotomy.
e. Saemichs’ section for corneal ulcer.
f. In certain antiglaucoma operations.
g. To make a scleral opening at pars plana for lensec-
tomy.
h. Elschnig’s operation of capsulo iridectomy (occlusio
pupillae) (Fig. 17.17).
Fig. 17.17: Von Graefe’s cataract knife
Bent or Angled Keratome

Uses
a. For limbal section in cataract, glaucoma surgery
b. For paracentesis
c. For optical iridectomy

d. Currette evacuation
e. Wilmer’s operation (capsuloiridectomy for occlusio
pupillae). Angle of bend is 60° (Fig. 17.18).
Fig. 17.18: Bent or angled keratome
Ziegler’s Needle
Used for needling congenital cataract, after cataract and
traumatic cataract (Fig. 17.19).
Fig. 17.19: Ziegler’s Needle
Lens Hook or Lens Expressor

It is employed to:
a. Apply pressure and rupture the zonules of lens in
the lower part in the intra capsular cataract surgery.
b. Express the nucleus (and cortex) out in extra capsular
cataract extraction.
c. Apply light pressure in the lower part of limbus
during modified Smith Indian intracapsular surgery.
d. Hold extraocular muscles during enucleation of
eyeball.
e. It may be used in squint operations (Fig. 17.20).
INSTRUMENTS 311
Fig. 17.20: Lens Hook or lens expressor
Simcoe Cannula
Employed to:
a. Separate epinucleus from nucleus.
b. Aspirate out the cortical matter in extracapsular
cataract extraction (Fig. 17.21) .
Fig. 17.21: Simcoe cannula
Sinskey Lens Hook

Used for rotating the IOL after the latter is placed inside
the capsular bag (Fig. 17.22).
Fig. 17.22: Sinskey lens hook

Muscle Hook
Helps in holding the extra ocular muscles during squint,
enucleation and retinal detachment operations (Fig.
17.23).
Fig. 17.23: Muscle hook
Cyclodialysis Spatula
Used in cyclodialysis for aphakic glaucoma—to sepa-
rate scleral spur. Angle of bend is at 100° and length of
bent portion is 15 mm (Fig. 17.24).
Fig. 17.24: Cyclodialysis spatula
INSTRUMENTS 313
Lacrimal Dissector with Curette (Lang)

Dissector is used to dissect and isolate sac during
dacryocystectomy (DCT) and dacryocystorhinostomy
(DCR). Curette is used to curette the nasolacrimal duct
in DCT. It can be used to open nasolacrymal duct. The
epithelial remnant is scooped out after DCT with this
instrument (Fig. 17.25).
Fig. 17.25: Lacimal dissector with curette
Lens Loop (Levies)

To remove subluxated or dislocated lens. Irrigation type
is used in extracapsular cataract surgery (This instru-
ment is also known as vectis) (Fig. 17.26).
Fig. 17.26: Lens loop (Levies)

Nettleship’s Punctum Dilator

To dilate the punctum:
a. Before syringing the nasolacrimal passage.
b. Before probing in dacryocystitis.
c. In congenital atresia of punctum.
d. It may be used as a marker for retinal detachment
and squint surgeries (Fig. 17.27).
Fig. 17.27: Nettleship’s punctum dilator
Lacrymal Probe (Bowman)

a. To probe the lacrymal passage in congenital dacryo-
cystits.
b. To investigate the site of obstruction in chronic
dacryocysitis.
c. To identify sac during DCR and DCT (Fig. 17.28).
INSTRUMENTS 315
Fig. 17.28: Lacrymal probe (Bowman)
Chalazion Curette
To curette out the contents of chalazion after incision
(Fig. 17.29).
Fig. 17.29: Chalazion Curette
Corneal trephine (Castroviejo)

To trephine corneal button in keratoplasty—of both
donor and recipient cornea. Different sizes of trephine
are available— from 5.0 to 0.11 mm (Fig. 17.30).
Fig. 17.30: Corneal trephine
Enucleation Spoon (Wells)

It is used during enucleation of the eyeball. Indications
for enucleation: Retinoblastoma and malignant
melanoma stages I and II, in sympathetic ophthalmia,
blunt trauma with total dissolution of eye, painful blind
eye such as absolute glaucoma, bleeding anterior
staphyloma, for eye bank purposes, phthisis bulbi, long
standing total retinal detachment with severe photopsia.
Contraindication: Panophthalmits.
Role of this instrument during the surgery: To pull
up eyeball (so as to perform long stem enucleation), to
protect eyeball while cutting optic nerve and to steady
eyeball while cutting optic nerve (Fig. 17.31).
Fig. 17.31: Enucleation spoon
Enucleation Scissors
It is a curved, long, comparatively heavy scissors used
for cutting optic nerve during enucleation. It has blunt
tips (17.32).
INSTRUMENTS 317
Fig. 17.32: Enucleation scissors
Evisceration Scoop (Mule)

Used for scooping out the contents of eye ball in evis-
ceration after excising the cornea. Indications for evis-
ceration: Panophthalmitis, expulsive hemorrhage and
bleeding anterior staphyloma (Fig. 17.33).
Fig. 17.33: Evisceration scoop
Caliper
To measure distances. It is used in squint and retinal
detachment operations (Fig. 17.34).
Fig. 17.34: Caliper
Bone Punch (Adler)

Used in making an opening in the lacrimal bone in DCR
(Fig. 17.35).
Fig. 17.35: Bone punch

INSTRUMENTS 319
Cataract Set (Fig. 17.36)
1. Barraquer Wire Speculum 10. Barraquer Needle Holder,

2. Hess Iris Forceps Micro
3. St. Martin Forceps 11. Hartman Mosquito Forceps,
4. Jalfe Tying Forceps Straight
(Straight) 12. Hartman Mosquito Forceps,
5. Me Pherson Forceps, Curved
Angled 11 mm 13. Dastoor Iris Retractor,
6. Superior Rectus Forceps Straight
7. Vannas Capsulotomy 14. Koman Nair Iris Spatula
Scissors, Curved 15. Lewis Lens Loop, Small
8. Castroviejo Corneal 16. Barraquer Cataract Knife,
Scissors, Universal Sliding
9. De-Wecker’s Iris Scissors 17. Bard-Parker Handle
Fig. 17.36: Cataract set
SICS (Bluementhol) Set (for Cataract Surgery)

(Fig. 17.37)
1. AAI025 Kratz Barraquer Wire Speculum, Big. 2. AA1465 Sinskey II

Lens Manipulating Hook, Angled. 3. AA 1597 Akahoshi Nucleus Sustainer.
4. AA1682 Castroviejo Cyclodialysis Spatula, 0.50 mm Wide. 5. AA1817
Shepard Fixation Ring. 6. AA1993 Agarwal’s Phaco Chopper 1 mm
Fully Cutting Edge. 7. AA 2075 Castroviejo Caliper, Straight. 8. AA3145
Lim’s Corneoscleral Forceps, 0.12 mm, 1x2 Teeth. 9. AA3255 Bishop-
Harmon Tissue Forceps, Delicate, 0.8 mm. 10. AA3340 Dastoor Superior
Reclus Forceps, 1 x 2 Teeth. 11. AA3742 Appasamy Lens Folder.
12. AA3744 Appasamy Lens Inserting Forceps. 13. AA3790 Mc Pherson
Tying Forceps. Long Handle. 14. AA3855 Utrata Capsulorhexis Forceps,
Flat Handle. 15. AA3906 Dodick Nucleus Cracker. 16. AA3914 Akahoshi
Prechop Forceps, Curved Shanks. 17. AA3945 Baby Jones Towel Clap.
18. AA3950 Serrefine Small. Straight. 19. AA4040 Castroviejo Corneal
Scissors, Small Blades. 20. AA4180 Westcott Stitch Scissors. 21.
AA4275 Vannas Capsulotomy Scissors, Ang. Forward, 11 mm Blade.
22. AA4510 Eye Scissors. Straight, 4½" Length. 23. AA5020 Kalt Needle
Holder, Straight. 24. AA5145 Barraquer N.Holder, Short Model, M.Jaws,
Cur. w/o Lock. 25. AA5500 Keratome Blade. 26. AA5510 Slit Blade. 27.
AA5520 Slit Enlarging Blade. Blunt. 28. AA5530 Super Sharp Blade. 29.
AA7105 Rycrolt Air Injection Cannula, 23G. 30. AA7145 Anterior Chamber
Washout Cannula, 16G. 31. AA7205 Pearce Hydrodissection Cannula,
35 Degree Ang. 25G. 32 . AA7215 Gimbel ‘U’ Shaped Hydrodissector.
25G. 33. AA7230 Kellan Hydrodelineation, Curved Bevel Tip. 25G. 34.
AA7420 Simcoe I/A Cannula, 23G, ‘Direct’
Fig. 17.37: SICS set
INSTRUMENTS 321
Chalazion Set (Fig. 17.38)
1. AA1740 Jaeger Lid Plate

2. AA1875 Meyerhoefer Chalazion Curette, Size 0, 1.50 mm dia
4. AA 1877 Meyerhoefer Chalazion Curette, Size 2, 2.25 mm dia
6. AA4515 Eye Scissors, Curved, 4.5" Length
7. AA3275 St Martin Suturing Forceps, 1 x 2 Teeth
8. AA3630 Hunt Chalazion Forceps, 12 mm dia
9. AA3625 Desmarres Chalazion Forceps, 13 mm/20 mm dia
10. AA5090 Castroviejo Needle Holder, Curved with lock
11. AA5560 Bard-Parker Blade #11.AA 5561 #15
12. AA5465 Bard-Parker Handle, # 3 Round Handle
Fig. 17.38: Chalazion set
Lacrymal set (Fig. 17.39)
1. AA1200 Stevenson Lacrimal Sac Retractor, 3x3 Blunt Prongs.

2. AA1220 Knapp Lacrimal Sac Retractor, Blunt 3. AA 1260 Desmarres
Lid Retractor, Size 0 4. AA3275 St.Martin Suturing Forceps, 1x2 Teeth
5. AA3460 Wills Hospital utility Forceps 6. AA3925 Hartman Mosquito
Forceps, Curved 7. AA3930 Halsted Mosquito Forceps. Straight.
8. AA4180 Westcott Stitch Scissors 9. AA4510 Eye Scissors, Straight, 4
1/2" Length. 10. AA4535 Stevens Tenotomy Scissors, Curved. 11. AA5020
Kalt Needle Holder, Straight. 12. AA5145 Baraquer N.Holder Micro Jaws,
w/o Lock. 13. AA5405 Castroviejo Blade Breaker and Holder, Big.
14. AA 6010 Kerrison Bone Nibbling Ronguer, Size 0. 15. AA6030 Beyer
Ronguer, Single Action. 16. AA6040 Nasal Speculum, Infant. 17. AA6100
West Lacrimal Chisel, Straight. 18. AA6110 West Bone Gauge.
19. AA6120 Mallet for DCR. 20. AA6130 Freer Periosteal Elevator.
21. AA6140 Traquair Periosteal Elevator. 22. AA6150 Pigtail Probe with
Suture Holes. 23. AA6175 Bowman Lacrimal Probe, Malleable Stainless
Steel. 24. AA6440 Castrovejo Lacrimal Dialator (Double End). 25. AA
7040 West Lacrimal Cannula, Curved. 26. AA1185 Mueller’s Lacrimal
Sac Retractor. 27. AA3790 Me Pherson Tying Forceps. 28. AA3300
Fixation Forceps
Fig. 17.39: Lacrymal set
INSTRUMENTS 323
Schiotz tonometer
To measure intraocular pressure. This is an indentation
type tonometer. The reading can be affected by scleral
rigidity (Fig. 17.40).
Fig. 17.40: Schiotz tonometer

18
Refraction
GENERAL
A normally developed eye acts as a convex lens with a

power of + 60 D. The two major components are cornea
(+ 43D) and lens (+17 D).
In normal eye, the parallel rays of light are brought
to a focus on the retina while accommodation is at rest
(unaccommodated). This refractive state is known as
emmetropia. When a child is born, the axial length of
eyeball is smaller, i.e. eye is hypermetropic. When the
child grows up the length of eye ball increases so that
by the age of 4 or 5 years it reaches the normal length of
24 mm and the eye becomes emmetropic.
If all parallel rays are not brought to a focus on the
retina in all meridians while accommodation is at rest
then it is known as ametropia.
TYPES OF AMETROPIA
1. Myopia
2. Hypermetropia (Hyperopia)
3. Astigmatism
4. Aphakia
5. Presbyopia
CAUSES OF AMETROPIA
Axial
All emmetropic eyes have an axial length of about 24
mm. If there is any change in this length, it produces
ametropia. A change of one mm in length results in
ametropia of 3 diopter.
REFRACTION 327
Curvature
If curvature of cornea (mostly) and lens is altered then
ametropia occurs.
Index
If the refractive index of any one or more media of eye
is altered then ametropia is seen. Change to higher index
results in myopia and to a lower index in hyperopia.
Position of Lens
Tilting of lens forwards causes myopia, while backward
causes hypermetropia.
MYOPIA (TABLE 18.1)
It is a condition in which while the eye is at rest (i.e. not

accommodated) parallel rays of light are brought to a
focus in front of the retina (Fig. 18.1).
Etiology
Axial
In this condition the anteroposterior length of the eye
ball is more than the normal 24 mm.
Curvature
The curvature of cornea and, sometimes, lens is
increased and this results in myopia.
Figs 18.1A to C: Path of light rays in a case of myopia. (A) Normal eye.
(B) Myopic eye. The light rays come to a focus in front of retina. (C) The
defect is corrected with concave lens
Index
This is seen in opacification of the lens which produces
change in the refractive index of the lens.
REFRACTION 329
Lens Position
If the lens is tilted forward it will cause myopia.
Excess Accommodation
Table 18.1 : Varieties of myopia
Features Simple Congenital Pathological
Condition Normal Large defect Normal
at birth
Increase of Minimal Minimal Gross
error
Final power About – 6 D Around – 20 D Around –20 to
25 D
Fundus Nil Very minimal Extensive
changes
There are three varieties of myopia:

In simple myopia (also called as school myopia) the child
is born with usual +2 or +4 “error”; but, the physiolo-
gical increase in the length over shoots and the patient
lands with a final refractive error of –4 to –6.
In congenital myopia the child is born with a high error
(around – 15); but the increase during life is minimal so
that the patient finally has a defect of around –20
diopter.
Myopia of prematurity is seen in premature children.
The error fluctuates between – 10 to – 20 diopter. The
refractive state of eye is normal at the end of one year.
In pathological myopia the child is born almost with a
near normal eye; but the defect increases markedly. It
runs in families and is more common in girls. The final
refractive error will be around –20 to –25 diopter. It is
hereditary and racial.
Myopia can also be classified into primary and

secondary.
Symptoms
The patient has defective vision for distance. He will be
comfortable with near vision work. In pathological
myopia, some amount of “Night blindness” is present.
If he develops cataract (especially in pathological
myopia) the defect in vision worsens. Floaters in front
of eye is one other complaint especially in pathological
myopia.
Signs
The eye looks larger (pseudoproptosis). The anterior
chamber is comparatively deep. Pupil is larger. In
pathological myopia, visual field may show ring sco-
toma. The lens shows complicated cataract.
The fundus changes are observed mostly in patho-
logical myopia. Herein the vitreous shows floaters. The
optic disk looks larger with a large cup. There may be
posterior staphyloma in which the retinal vessels appear
to dip into the staphyloma area. The macula shows
hemorrhagic spots known as Foster-Fuchs spots. Dege-
nerative changes are observed in the retina (cystoid) and
choroid (Fig. 18.2) . Retinal detachment occurs in some
cases especially after trauma to the head. Peripapillary
crescent is seen in later stage.
Pseudomyopia is seen in hypermetropic children who
over accommodate. Thus they may cross emmetropic
point and become myopic.
REFRACTION 331
Fig. 18.2: Myopic fundus. Degenerative changes are seen
Treatment
1. Correction with spectacles—the minimum accep-
table power should be prescribed.
2. Correction with contact lens.
3. Refractive surgeries—radial keratotomy (Fig. 18.3).
photorefractive keratectomy, LASIK (Fig. 18.4) and
LASEK and epiLASEK, intrastromal corneal ring,
corneal inlay technique and lenticular surgery (Clear
lens removal in cases with – 20 D error).
4. Phakic intraocular lens.
5. Nutrition status must receive attention.
Fig. 18.3: Myopic eye for which radial keratotomy

(RK) has been done. The incisions are seen
Fig. 18.4: LASIK for myopia. Under hinged-epithelial flap (raised in the
diagram), portion of central stroma is removed with laser beam (red in
diagram)
REFRACTION 333
6. Genetic counseling should be given to patients with

pathological myopia. Consanguinous marriage must
be discouraged.
Complications
1. Cataract
2. Retinal detachment
3. Vitreous hemorrhage
4. Amblyopia.
HYPERMETROPIA (HYPEROPIA)
It is that condition in which, while the eye is at rest,

parallel rays of light are brought to a focus behind the
retina (Fig. 18.5).
Etiology
Axial
As stated already, all children are born with hyperopic
eye which lengthens to the normal axial length. If this
does not happen, then axial type occurs.
Curvature
Astigmatism is the usual condition that occurs due to
problems in the curvature of cornea. Pure spherical
hyperopia due to this cause is rare. It is seen in cornea
plana, microphthalmos, microcornea and after injury.
Index Type
Index type is met with in cataract. Aphakia is another
example.
Figs 18.5A to C: Diagram of hypermetropic (hyperopic) eye is which the

rays of light are focused behind the retina. (A) Normal eye. (B)
Hypermetropic eye. The rays of light have come to a focus behind the
retina. (C) The error is corrected with convex lens
Lens Tilt
Lens tilt backwards produces hyperopia.
The clinical varieties of hyperopia are:
Simple hypermetropia: Common form which represents
the normal variation.
Pathological: It is seen with posteriorily placed lens,
cortical sclerosis, consecutive hyperopia (over correc-
tion of myopia) and aphakia.
REFRACTION 335
Functional: In accommodation paralysis.

The components of hypermetropia are:
Latent hypermetropia: The amount that is corrected by
the normal tone of ciliary muscle. This decreases with
ageing.
Manifest hypermetropia: Hyperopia which is in excess of
latent one. It has two components:
a. Facultative: This can be corrected by patient himself.
b. Absolute: The manifest portion which cannot be over
come by patient.
Total: It is manifest and latent hypermetropia put
together.
Facultative + absolute = Manifest + Latent = Total
hypermetropia.
Symptoms are eye strain and defective vision. The
defective vision is more for near vision (in mild cases),
or it is present for both near and distance vision (cases
with high error). The persistent effort to accommodate
gives rise to frontal head ache, watering from eye and
tired eye. In low degrees of error, there may not be any
symptom. Recurrent stye and blepharitis may be comp-
lained of. Convergent squint is seen.
Signs include small eye and shallow anterior
chamber. Fundus shows pseudoneuritis and shot silk
appearance of retina.
Pseudomyopia may occur.
Complications
1. Occurrence of angle closure glaucoma.
2. Convergent squint in children.
3. Problems of eye strain such as hordeola and

blepharitis.
4. Amblyopia.
Treatment
1. Spectacles: Convex lens is recommended. This should
be prescribed only after refraction with cycloplegics.
2. Contact lens.
3. Refractive surgeries: Laser thermoplasty, photo-
refractive keratectomy, LASIK and phakic intra-
ocular lens.
ASTIGMATISM
In this condition, while the eye is at rest, parallel rays of

light cannot be brought to a point focus at retina.
The causes are:
1. Congenital defect in the curvature of refractive media
of the eye, especially cornea and to some extent of
lens.
2. Tilt of lens can result in astigmatism.
Rarely it can arise due to:
3. Obliquity of retina.
4. Trauma.
5. Index: This is caused by variable refractive indices
of lens. It is rare.
The main symptoms are eye strain and in very high
astigmatism defective vision. The former is due to ciliary
muscles trying to overcome the defect. Objects may
appear elongated. Rarely these patients develop torti-
collis.
REFRACTION 337
Types (Flow chart 18.1)
Flow chart 18.1: Types of astigmatism
I. In regular astigmatism the two principle meridia

which are at 90° to each other are affected. Based on
this, regular astigmatism can be:
a. With the rule astigmatism: Out of the two meridia
the vertical one is more curved than the horizon-
tal. So concave cylinder will be required at hori-
zonal meridian (its axis of power). If small, this
is not prescribed.
b. Against the rule astigmatism: Herein the vertical
meridian is flatter than horizontal one. So
concave cylinders axis of power will be in vertical

meridian direction.
II. Oblique astigmatism: Here the two principle meridia
are placed in oblique direction and at least 20o away
from vertical or horizontal axis.
III. When considering the image relationship to retina
position, the astigmatism can be:
i. Simple regular astigmatism. One meridian is
ametropic while the other meridian is defec-
tive—either myopic or hypermetropic.
ii. In compound type, both meridia are out of
focus—either myopic or hyperopic.
iii. Mixed type is like compound; but one meridian
is myopic while the other one is hyperopic.
These five situations can be best understood if
Sturm’s conoid is studied (Fig. 18.6).
Fig. 18.6: Sturm’s conoid. This composite diagram represents all the
five types of astigmatism. If the retina is at (A) the patient has compound
hypermetropic astigmatism. If it is at (B), then the patient has simple
hypermetropic astigmatism (rays of light of one plane have come to a
focus; those of other plane are still converging). If retina is at (C) there
occurs mixed astigmatism (myopia + hypermetropia). Retina at position
(D) results in simple myopic astigmatism (rays of one plane have come
to focus while of other plane have started diverging). If retina is at (E),
then the patient is said to be having compound myopic astigmatism (In
both the planes, the eye is myopic)
REFRACTION 339
Treatment
1. Optical correction. Cylindrical lenses are prescribed.
These may be given as spectacle or as contact lens.
Toric contact lenses are used for astigmatism of more
than 3 D. Irregular astigmatism is best corrected with
contact lens.
2. Refractive surgery.
PRESBYOPIA
If a person has to look at a near object (for practical

purpose, within 33 cm) when his eye is already focused
for a distance object, he exerts Accommodation. This is
brought about by the action of ciliary muscle so that
the lens becomes more convex especially its anterior
curvature.
When this capacity fails at the age of 40 and above,
due to hardening of lens or to weakness of ciliary
muscle, he is unable to see clearly near objects, i.e. within
33 cm. This is known as presbyopia. It is a condition of
failing near vision due to reduction in the accommo-
dative capacity of the eye. This may set in earlier if the
person is already hypermetropic, has general debility,
develops early open angle glaucoma, has premature
sclerosis of lens or he is doing excess near work, e.g.
watch repairer.
The symptom is that of difficulty in focusing near
objects such as reading, writing, etc.
Treatment
Convex lens is advised. Normally +1 D is prescribed
for 40 to 45 years old patient and increased by +0.5 for
every five years of age thereafter. The maximum power

required is around +3 D for any patient.
While prescribing reading glasses, following points
must be kept in mind.
a. Each patient should be assessed for near vision
correction and not empirically.
b. Each eye should be checked separately for the power
that is needed for near work.
c. Near vision correction is complementary to any
distance vision correction the patient requires.
d. Near vision correction should be done at the distance
that is required for his profession.
e. Some may require a mid distance correction also,
e.g. pianist, typist.
ACCOMMODATION
It is the ability of eye to see a near object when it is

already focused to a distant scene. It is brought about
by increase in anterior curvature of lens by the action
of ciliary muscle, i.e. contraction. Such a contraction
relaxes the ciliary ring, the zonules suspending the lens
bcomes lax and the convexity of the lens increases. When
the convexity increases the converging power of the lens
goes up (Fig. 18.7).
This ability may be insufficient or excess in certain
conditions.
Accommodation Insufficiency
It is caused by:
a. Systemic weakness due to prolonged illness or fatigue.
b. Prodromal stage of open angle glaucoma.
REFRACTION 341
Fig 18.7: Accommodation. When the eye is not accommodating the

ciliary muscles (A) are relaxed and the zonules (B) are tight. This results
in “thinning” of lens (C). When the eye is accommodating the ciliary
muscle (D) Contracts. The zonules (E) are relexed and the “thickness”
of lens is increased (F). This causes increase in convexity of lens and its
power on hypermetropic side
c. Due to sclerosis of lens (reason for presbyopia).

d. Paralysis of accommodation caused by III nerve
paralysis.
e. Iatrogenic (use of cycloplegics locally), contusion
injury and in diabetes.
g. Undercorrected hypermetropia or over corrected
myopia.
h. Nystagmus.
i. Aphakia.
Symptom is visual. If patient is already myopic it may
go unnoticed. This depends upon the myopic power.
If he is ametropic, near vision is affected. If he is already

hyperopic then both distance and near vision are
affected.
Treatment is that of cause. Some (e.g. Iatrogenic) may
pass off. Correction with spectacles is advised for
permanently affected persons.
Accommodation Spasm
It is seen with:
a. local use of miotics.
b. Spontaneous spasm is seen with constant near vision
work in dim light, with bad reading position or with
mental stress.
Management is by cycloplegics. The causative agent
must be treated which may include psychotherapy.
19
Dark Room
Examinations
OBLIQUE ILLUMINATION (FOCAL ILLUMINATION

OR LATERAL ILLUMINATION)
Purpose
To examine the anterior segment of eye and adnexa.
Requirements
Dark room, source of light, + 13 diopter lens, loupe.
Method
Light is placed at some distance in front, on the same
side of the eye to be examined and more or less at the
eye level. Light is condensed by means of a large convex
lens (usually +13 D) and brought to a focus on the part
to be examined. The lens is held about 8 cm from the
eye which is the focal length of the +13 D lens. Fine
details in the eye may be examined by using a binocular
loupe, whose magnification is 2 times. Corneal loupe
(+ 41 D) gives a better magnification of 10 X.
Advantages
1. High degree of illumination.
2. Light is focused to a small area leaving the surroun-
ding area comparatively dark.
3. Light can be focused exactly on the part of the eye to
be examined.
4. Aids convergence.
DARK ROOM EXAMINATIONS 345
DISTANT DIRECT OPHTHALMOSCOPY
Purpose
Diagnosis and location of opacities in the media of the
eye can be made by this examination.
Requirements
Dark room, source of light, plane mirror.
Method
This is done in a dark room with a plane mirror at a
distance of 22 cm. Light is kept above and behind the
patient’s head. Pupillary area appears red by
transmitted light.
1. Any opacity in the media appears as a black body
upon the red back ground. Its position can be
detected by its apparent displacement with the
movement of the eyeball:
Corneal opacity : Moves in the
same direction
Anterior lenticular : No movement
opacity
Posterior lenticular : Moves in the
opacity and that in opposite direction
solid vitreous
Opacities in fluid : Moves independently
vitreous
2. Recognition of dislocated lens and coloboma of the
lens. The edge of the lens appears black due to the
total internal reflection of the light rays.
3. Recognition of the detached retina or tumor arising

from the retina.
4. To differentiate between black spot on the surface
of iris, mole and hole in iris.
5. Malignant melanoma of the ciliary body and iris can
be examined.
RETINOSCOPY
(SHADOW TEST OR SKYASCOPY)
Purpose
To estimate the refraction of the eye objectively.
Requirements
Dark room, plane mirror (Fig. 19.1), concave mirror,
source of artificial light, trial lenses (Fig. 19.2) and trial
frame.
Method
The light is kept on the same side of the eye to be
examined, above and behind the head of the patient.
Observer is seated at a distance of one meter from the
patient. Trial frame is put on the patient’s face. Patient
Fig. 19.1. Retinoscope mirror (plane mirror)

Fig. 19.2: Trial set. It is used both for objective and subjective
examinations of refractive error. The central two pairs of rows have
cylindrical lenses. On the left side is the pair of rows of concave lenses
(for myopia) and on the right two rows of convex lenses (for
hypermetropia)
is directed to see at a distance in the direction of the

observer’s opposite ear. With the plane mirror, observer
directs the light into the patient’s eye and tilts mirror
vertically and horizontally (Fig. 19.3).
The movement of the shadow in the patient’s eye
when the mirror is tilted is noted. Appropriate lenses
are placed in the trial frame till the neutral point is
obtained. Patient’s refraction is corrected for one meter
distance by reducing one diopter. If this refraction is
estimated under the cycloplegic, further one diopter is
reduced for correction of ciliary muscle tone. With plane
mirror movement of shadow in the same direction as
Fig. 19.3: Retinoscopy procedure. The source of light is above and behind
the patient’s head and on the same side as the eye to be examined. The
examiner is seated one meter from the patient
mirror movement means hypermetropia, emmetropia

or myopia less than one diopter. Movement in the oppo-
site direction means myopia of more than one diopter.
No movement of shadow means myopia of one diopter.
When concave mirror is used the above derivation of
movements is opposite.
The one meter distance is the best bargain between
convenient distance to change lenses in trial frame and
ease of calculation.
Autorefractometer, which is a computerised instru-
ment, is one by which objectively refractive error is
estimated (Fig. 19.4). Keratometer is useful in determining
corneal curvature and astigmatism.
Fig. 19.4: Autorefractometer. This eliminates the need for

retinoscopy and is quick
DIRECT OPHTHALMOSCOPY
Purpose
1. To study the fundus details.
2. To study refraction.
3. To measure the elevation or depression in the retina
and disk.
Requirements
Dark room, artificial source of light and small tilted
concave mirror.
Method
Light is kept on the side of the eye to be examined
behind the patient’s head. Mirror is adjusted so that the
tilt of the mirror is towards the nose of the patient. The

observer stands on the right side of the patient (if it is
right eye), holds the ophthalmoscope with the right
hand, he goes close to the right eye of the patient and
looks into the patient’s right eye. To examine the left
eye of the patient, the light is kept on the left side,
observer stands on the left side, holds the ophthal-
moscope in the left hand and looks into the left eye of
the patient with his own left eye.
Nowadays the direct ophthalmoscope instrument
has totally replaced the above procedure. The image
with this instrument is virtual.
Advantages of Direct Ophthalmoscopy

Larger magnification, minute details like hemorrhages,
new vessels, holes, macular star, etc. can be studied
easily, estimation or confirmation of refraction is possi-
ble, elevation or depression in fundus can be seen and
an approximate estimate of their dimensions can be
made and any opacity in the different media of the eye
can be located.
INDIRECT OPHTHALMOSCOPY
It was introduced in 1864 by Nigel.

It is called indirect ophthalmoscopy because the
observer does not see a direct image of the fundus but
an inverted one formed by the convex lens somewhere
between it and the observer’s eye.
Principle
The eye is made myopic by interposing a convex lens
of + 13 Diopter lens, by means of which all the emergent
rays from the retina could be gathered into a single focus
to form a real image between the lens and the observer.
Purpose
To view the posterior segment of the eye and to study
the refraction of eye.
Requirements
Dark room, artificial source of light, large concave
mirror and convex lens of + 13 D.
Method
The light is kept behind and above the patient’s head.
The observer stands in front of the patient at a distance
of less than an arm’s length. If the observer is amme-
tropic, it is corrected with proper lens. With the large
concave mirror he directs the light into the patient’s
pupil and illuminates the retina. The patient is asked to
look towards the observer’s opposite eye. A + 13 diopter
lens is placed in front of the patient eye about 2 inches
away. By moving his head backwards or forwards, or
slightly altering the position of the lens the observer
succeeds in seeing the image of the fundus between the
lens and his eye—a real, inverted and five times
magnified image. Magnification of image depends on
lens used. The lens is taken further away from the
patient—no change in size of image means emmetropia.
Increase in size means myopia. Decrease in size means

hypermetropia. Change in shape means astigmatism.
Advantages
1. Used extensively to study the fundus in detachment
of the retina because:
a. Large area of fundus is seen at a time.
b. As the normal and detached areas are seen at the
same time in the same field the contrast in color
can be appreciated especially in shallow detach-
ment of retina.
c. Peripheral part of the fundus is seen easily.
2. To study the fundus by direct method in cases of
high myopia one has to go very near the patient’s
eye. In such cases indirect method has the advantage.
3. If the patient has contagious disease of the face, the
indirect method is better.
4. With the indirect method it is possible to study the
fundus even when the media are hazy.
Direct method Indirect method

i. Magnification 15 times 5 times
ii. Nature of image Erect Inverted
iii. Extent of fundus Small area Larger area
visualized
iv. Comparable to High power Low power
microscope
Table 19.1: Summary of dark room examinations
Points Oblique illumin. Retinoscopy Indirect oph. Direct oph.
1. Aim Anterior segment Refraction Fundus and Fundus,
study refraction refraction,
measure of
elevation or
depression
or disk
2. Position of Front side at Above and Above and Side of the
light the level of the behind the pt’s behind the pt. behind
eye head pt’s head and at the
level of eye
3. Instruments + 13 D lens, Plane mirror, Large con- Small tilted
loupe trial frame, cave mirror, concave
trial lenses + 13 D lens mirror
4. Observer In front 1 meter Arm’s Side of the
position length patient
5. Observer eye Both eyes Rt. eye Rt. eye Rt. or Lt.
DARK ROOM EXAMINATIONS
353
20
Ocular
Therapeutics
Pharmacology is science of study of drugs. The student

should know the basic of certain important drugs used
in ophthalmology.
MYDRIATICS
These drugs dilate the pupil. Phenylephrine (2.5%) is

the most commonly used one. Mydriatics are of special
use in the study of fundus and in improving vision in
certain cataract cases. Some of the mydriatics such as
atropine and homatropine paralyse the ciliary muscle
also (cycloplegia). So there is some amount of defective
distant vision and gross reduction in near vision
(reading). Cycloplogic-mydriatics are used for treating
corneal ulcer, iridocyclitis, to check vision in children
and in certain postoperative conditions.
These drugs may be grouped into short acting (tro-
picamide and cyclopentolate) and long acting (atropine
and homatropine) compounds.
Side effects of these drugs include stinging, glaring
and defective vision. When applying atropine (and
homatropine), the lacrymal sac area should be pressed
for one minute so that the drug does not get absorbed
via nasal mucosa and produce systemic problems. These
drugs should never be used in a narrow angle glaucoma
case.
MIOTICS
They cause constriction of pupil and contraction of the

ciliary muscle. These result in improvement of vision
(in visual field) and reduction in ocular pressure. Miotics
OCULAR THERAPEUTICS 357
are used to constrict pupil during refraction after it is

dilated, in glaucoma cases and in certain accommo-
dative squints. Examples of certain miotics are pilo-
carpine, physostigmine and carbachol.
CHEMOTHERAPY
Chemotherapy is the use of drugs to kill or to inhibit

the growth of infectious organisms or cancerous cells.
(This topic deals only with those drugs which act against
infectious agents).
Antibacterial Agents
They can be bacterocidal or bacterostatic. They are
obtained from soil microbes or by chemical synthesis.
Sulfa
It was discovered in 1935 as a bye product of dye indus-
try. The various sufas that are in use are Mafenide, slver
sulfadiazine (both for burns cases), sulfacetamide (for
eye infection), sulfamethizole and sulfamethoxazole (for
urinary tract infections) .
Sulfa drugs act against synthesis of folic acid from
PABA—so they are mainly bacterostatic only. In trime-
thoprim—sulfamethoxazole combination, the former
inhibits dihydrofolate reductase and thereby prevents
conversion of folic acid to folinic acid (so bactericidal)
and the latter inhibits PABA forming folic acid (hence
bacterostatic).
They are effective against all cocci (except
Streptococcus), certain bacilli (B coli, C diphtheriae,
Claustradium), fungus (nocardia, actinomyces), virus

(PLT) and Toxoplasma gondii. Sulfones and diamox are
certain derivatives.
Adverse reactions: Agranulocytosis (vitamin B 6 is
administered), hematuria, anuria, nausea, vomiting,
cyanosis, Stevens-Johnson syndrome, polyarteritis
nodosa and drug fever. Prolonged use can result in
macrocytic anemia.
Antibiotics
They can be classified as follows:
A . Beta Lactam group
a. Penicillin: Penicillinase sensitive and resistant
b. Cephalosporins.
a. Penicillin: Penicillin was discovered by Alexander
Fleming (1929) and first used clinically by Henry
Florey (1948). It is obtained from penicillium mould.
It can be grouped into:
1. First generation: They mainly act against gram-
positive organisms and Neisseriaceae. These can
be:
i. Penicillinase sensitive—they are destroyed
by acid, alkalis, metals and rubber. They are
penicillin G and penicillin V.
ii. Penicillinase resistant—they are cloxacillin,
methicillin and oxacillin.
2. Second generation: Penicillinase sensitive. Effective
against gram-negative and gram-positive orga-
nisms. Examples are amoxicillin and ampicillin.
3. Third generation: They are also penicillinase sensi-
tive and are effective against Pseudomonas and
Proteus. Carbenicillin is one drug of this group.
4. Fourth generation: Against Pseudo, Proteus and

Klebsilla. Penicillinase sensitive. Sodium ingestion
is less. Piperacillin belongs to this group.
Clavulanic acid inhibits penicillinase. It has
been combined with amoxycillin.
Adverse effects include allergy (serious),
nausea, rashes and diarrhoea. In very high doses
it can produce convulsions.
Ampicillin in chronic lymphatic leukemia can
cause rashes due to interaction with abnormal
lymphocytes.
Third generation penicillin can produce
sodium or potassium excess (sodium in the drug)
and is dangerous in cardiac patients.
Chloramphenical and tetracycline are incom-
patible with penicillin.
b. Cephalosporins: Discovered in 1945 from a sewage of
Sardinia Island. It has B-lactase ring (like penicillin).
They interfere with bacterial cell wall synthesis.
Mostly for gram-negative bacteria. They are
bacteriocidal. They are mainly useful for patients
with penicillin allergy and for certain gram-negative
infections. Cephalosporinase breaks down cephalos-
porin molecule.
They are given either orally (cephalaxin, cepha-
droxil, cefdinir, cefaclor) or parenterally.
The side effects include hypersensitivity (lesser than
penicillin), nephrotoxicity (more with aminogly-
cosides) and false positive Benedict’s and Coomb’s
test. Intravenous injections can produce local inflam-
mation or phlebitis. Oral route can cause gastro-
intestinal upset.
B. Aminoglycosides
Streptomycin, the first aminoglycoside, was isolated
from chicken throat and from heavily manured field
by Wakeman in 1943. Drugs of this group include
amikacin, gentamicin, streptomycin, kanamycin and
neomycin.
They get attached to ribosomes of bacterium
causing inhibition of protein synthesis. It is poorly
absorbed from Gastrointestinal tract (so IV or IM)
and excreted almost unchanged in urine.
They are used mainly against Gram-negative
bacilli. They are bacteriocidal.
Adverse reactions: Orally, they cause nausea, vomiting
and diarrhea. By injection, they cause nephrotoxicity
and (temporary) ototoxicity. Albuminuria and
oliguria may occur. Deafness may become
permanent if used for longer period. Others are
malar paresthesia, contact dermatitis (with strep-
tomycin) and drug fever.
It causes neuromuscular block—so general
anesthesia can cause respiratory arrest during
surgery due to diaphragmatic paralysis. Combi-
nation with cephalosporin increases nephrotoxicity.
C. Tetracyclines
They were first isolated by Duggar and Subba Rao
(1947). First one to be isolated was chlortetracycline.
The others are oxytetracycline, doxycycline, tetra-
cycline, demeclocycline and minocycline.
They are bacteriostatic by preventing protein
synthesis—but also involve the host causing anabolic
effect. They are useful against gram-positive and
gram-negative infections and of special use in
rickettsiae and V. cholera.
Adverse reactions: Thrush, moniliasis, sore throat due to

suppression of normal flora. (B complex given). Dental
enamel hypoplasia and pigmentation due to chelation
of calcium of teeth (forming calcium orthophosphate).
These drugs are not advised for children. Effect on bone
growth is very minimal. Rarely, intracranial hyper-
tension and liver and pancreatic damage. Photosen-
sitivity occurs with dimethylchlorotetracycline. Fan-
coni’s syndrome (Polyuria, proteinuria and acidosis)
when outdated products are used.
D. Macrolides
Erythromycin was the first one to be introduced.
Azithromycin, clarithromycin, spiromycin and
roxithromycin are others.
They are available as estolate, succinate, stearate
and glucoheptanate. They are destroyed by gastric
acidity. Hence they are enteric coated.
These drugs are very useful against Staph,
Strepto, Pneumo, Corynebacterium and Treponema.
Adverse reactions: They are very minimal and include
nausea, vomiting and diarrhea. The may cause
cholestatic hepatitis.
E. Polypeptides
This group includes polymyxin, bacitracin, tryco-
thricin. They are effective only against gram-nega-
tives.
Adverse reactions: They can cause gastrointestinal
tract upset, ototoxicity and neurotoxicity.
F. Lincosamide
They inhibit bacterial protein. The drugs are clindo-
mycin and lincomycin. They are effective against
gram +/– and anaerobic gram-negative organisms.
Adverse reactions: Stomatitis, glossitis, anorexia,

metallic taste, angioedema, vertigo, tinnitus, aplastic
anemia (with rapid Intravenous administration),
cardiac arrest and hypotension, colitis and jaundice.
G. Quinolones and fluoroquinolones
They are bactericidal agents. They are effective
against Staph, Entero, Pseudomonas, hemophilus and
Neisseriaceae organisms. They are less active against
Strepto and inactive against anaerobic bacteria.
The members are nalidixic acid, ciprofloxacin, per-
floxacin and ofloxacin.
Nitrofurantoin
Used in urinary tract infection. Oral dose is 100 mg QID.
Adverse reactions are gastrointestinal tract upset,
neuritis, anemia and allergic reaction (which can result
even in pulmonary edema).
Fortified Drops
Sometimes, especially in corneal ulcers, the amount of
antibiotic concentration in the drops should be more.
For this, fortified drops are prepared. These drops are
to be applied once in 2 minutes for 30 minutes and then
½ hourly. The concentrations are:
Gentamicin 14 mg/ml (80 mg to 5 ml
commercial; latter is 3 mg/ml)
Tobramicin 10 mg/ml
Cephalosporidine 32 mg/ml (2 ml saline to 500
mg +13 ml tear sub)
Penicillin G 333000 U/ml
Vancomicin 31 mg/ml
Antifungal agents can be polyene antibiotics (such

as nystatin, pimaricin) or non antibiotic compounds
such as imidazoles and triazoles. Most of them act on
the fungal cell wall rupturing it.
Antivirals suppress the viral multiplication. They
are purine or pyrimidine derivatives. Adenine
arabinoside (3% ointment), acyclovir and ganciclovir are
purine derivaties. Idoxyuridine (0.1%) drops and
Trifluorothymidine (1% drops) are pyrimidine com-
pounds. Zidovidine is used against HIV virus. They are
of special use, as local agents, in herpes simplex and
herpes zoster cases. Some of them like Acyclovir can be
given by systemic route also.
CORTICOSTEROIDS
They are useful in inflammatory conditions. If the

inflammation is due to infection, the latter should be
controlled before corticosteroids are used. Commonly
used steroids are cortisone (1%), hydrocortisone (1.5%),
betamethasone (0.5%), prednisolone (1%) and
fluoromethalone (1%). Corticosteroids (cortisones) are
combined with antibiotics in certain preparations used
locally in eye. Indiscriminate use of local cortisone can
result in cataract, rise in ocular pressure (glaucoma),
overgrowth of bacteria, fungus or virus, delayed healing
and lowering of resistance to infection.
V. NSAIDs
These are also anti-inflammatory agents which do not

belong to cortisone family. These are safer than
cortisones. They include diclofenac, flurbiprofen and

ketorolac. They can be used for a long time without
many side effects.
ANESTHETICS
(See under “Operations)
ANTIMETABOLITES
They are used to reduce the local fibroblastic activity

formation of fibrous tissue. The two important drugs
are:
1. Mitomycin C: Daily use of it is advised as 0.4 mg/ml
after pterygium excision to prevent recurrence. In
antiglaucoma operation 0.4 mg/ml is placed for two
minutes at the operation site.
2. 5 fluorouracil: In glaucoma surgery 50 mg/ml is
placed under the conjunctiva during operation.
These two drugs are dangerous ones and must be
handled and used with care and caution.
ANTIGLAUCOMA DRUGS
See under “Glaucoma”
OTHERS
Mast call stabilizers such as cromoglycate and olopata-

dine are effective against symptoms of itching and
redness. They prevent release of histamine. They are of
special use in vernal conjunctivitis.
Decongestants reduce redness of eye and give relief

from irritation. They constrict the conjunctival vessels.
Naphazoline is the most common decongestant.
Lubricants are useful in symptoms of dryness of eye.
Preservative free drugs are preferred. They basically
contain methyl cellulose.
Dyes are used to stain certain ocular structures.
Locally used ones are fluorescein (2%), rose bengal and
congo red. They are used to study the fundus, lacrimal
passage and to assess the intraocular pressure by
applanation method (fluorescein), iris (Indocyanine
green).
ROUTES OF ADMINISTRATION
Medication for eye has to cross three main barriers

depending on the route of administration: Corneal
epithelium, blood-brain and blood-aqueous barriers.
Topical
These are ointment, drops or inserts applied directly to
the conjunctival sac. The drops do not stay in the eye
for long and so require hourly applications. The oint-
ments stay for longer time; but cause minimal blurring.
Inserts are like wafers and the drugs in it may be
released even as long as a week. Many of them which
are soluble act for a few hours to one day only.
Local Injections
The injection can be made under the conjunctiva, into
the vitreous or outside the globe (retrobulbar or peri-
ocular).
Systemic Route
This route is employed if the disease is outside the eye
in the orbit or lacrymal passage. It is also used to
supplement the local therapy if needed. Entry into the
eye by drugs by this method depends on the molecular
size and its lipid solubility.
21
Community
Ophthalmology
Community ophthalmology deals with identification of

common causes of ocular morbidity in different regions,
assessing the needs of the population, selecting appro-
priate intervention strategies, planning education
programs and analysing the utilization patterns. It
denotes the use of appropriate strategies to reduce the
burden of eye diseases in the community and the conse-
quences of ocular ill health, while striving to ensure the
best possible ocular health status for a major proportion
of the community.
Magnitude of Visual Problem

According to World Health Organization (WHO) defini-
tion, blindness is visual acuity < 3/60 in the better eye.
The number of people with visual impairment
worldwide in 2002 was in excess of 161 million, of whom
about 37 million were blind and 124 million people had
low vision. It is estimated that 7 million people become
blind every year and the number of blind people are
increasing by 1-2 million per year.
In India a survey done in 2001-2002 revealed an
overall prevalence of blindness to be 1.1% but in >50
years age group it rose to 8.5%.
Causes of Blindness (Fig. 21.1)

Cataract remains the leading cause of blindness in all
regions of the world except for the most developed
countries. Associated with ageing, it is even more
significant as a cause of low vision. Age -related cataract
is responsible for 48% of world blindness, which
represents about 18 million people. Although cataracts
COMMUNITY OPHTHALMOLOGY 369
Fig. 21.1: Global Causes of blindness as a proportion of

total blindness in 2002
can be surgically removed, yet it remains the leading
cause of blindness. In India, cataract is the commonest
cause of blindness contributing to 63.7% of blindness.
In unilateral blindness, cataract is the cause in 45.7%
and it is responsible for 24.5% of cases of low vision.
Glaucoma is the second leading cause of blindness
globally as well as in most regions. Worldwide the num-
ber of persons estimated to be blind as a result of pri-
mary glaucoma is 4.5 million.
Posterior segment pathology including age-related macu-
lar degeneration(AMD): Globally, AMD ranks third as a
cause of visual impairment with a blindness prevalence
of 8.7%.
The 4th cause of blindness globally (5.1%). Corneal
blindness is one of the major causes of visual deficiency.
Trachoma is responsible for nearly 4.9 million blind,
mainly as a result of corneal scarring and vasculariza-

tion. Corneal opacity accounts for 0.9% of blindness in
India. Under the age of 5 years, 92 million suffer from
xerophthalmia. Every year some 40,000 go blind due to
vitamin A deficiency. Now this has started coming
down.
Refractive Error: Severe refractive errors have been
estimated to account for about 5 million blind people
worldwide. According to WHO, there are an estimated
124 million people in the world with low vision. In India
the second most common cause of blindness is
uncorrected refractive errors with 27.7% of cases of
blindness attributed to it and 12.6% of unilateral
blindness. However, the proportion of low vision due
to uncorrected refractive error is highest at 71.9%.
EPIDEMIOLOGY
Age
Visual impairment is unequally distributed across age
groups. More than 82% of all people who are blind are
50 years of age and older, although they represent only
19% of the world’s population. In India almost one-third
of the blind are said to lose their sight before the age of
20 years and many before the age of 5. The risk factors
and causes in different age groups vary with younger
age groups mainly affected by refractive error,
conjunctivitis, trachoma and vitamin A deficiency.
In the middle aged cataract, glaucoma, refractive error
and diabetic retinopathy are more common whereas
accidents and injury affect all age groups; but 20-40
years are more at risk.
Sex
Available studies consistently indicate that in every
region of the world (including India), and at all ages,
females have a significantly higher risk of being visually
impaired than males. This is probably due to higher
prevalence of conjunctivitis, cataract and trachoma and
vitamin A deficiency in females.
Malnutrition
This is more a problem of the developing countries
where protein energy malnourishment (PEM) is more
common. Vitamin A deficiency is one of the major form
of malnutrition that causes blindness through corneal
ulceration and keratomalacia. PEM also makes the child
more vulnerable to diseases such as measles and diarr-
hea and they in turn precipitate malnutrition which
leads to vitamin A deficiency. This problem is usually
seen in younger age groups of 6 months to 5 years.
Social Class
There is a close relationship between social class and
incidence of blindness. Lower people belonging to lower
socioeconomic strata have twice the prevalence rate of
blindness than those belonging to the higher socio-
economic class. The factors that contribute are igno-
rance, poverty, low level of personal hygiene and inade-
quate eye care services. Inadequate services may also
mean loss of eyesight by meddling by quacks for people
who cannot afford to go to a qualified practitioner.
Occupation
Some occupations are more likely to result in eye injury
due to varied reasons ranging from factories and
workshops where injury occur due to dust, flying
objects, radiation, etc. to health care settings where
injury occurs due to X-rays and ultraviolet rays.
PREVENTION AND CONTROL STRATEGIES
The five levels of prevention and intervention methods

adopted are:
Positive Health Promotion

It is done through health education, environmental
hygiene and healthy dietary nutritional practices.
Specific Prevention of Diseases

This can be achieved by providing vitamin A supple-
mentation to children and pregnant women as well as
immunization against childhood diseases specially
measles that has the tendency to precipitate vitamin A
deficiency.
Early Diagnosis and Treatment

Conditions such as cataract and refractive error are more
amenable to this approach where blindness can be
identified at an early stage and cured through the help
of spectacles and/or surgery.
Disability Limitation
This is done by monitoring cases and treating them as
in glaucoma and diabetic retinopathy where complete
cure is not possible but the extent of disability can be
reduced to a considerable extent. It has to be combined
with health education and awareness campaign for full
utilization of existing services.
Rehabilitation
It is needed for absolute and irreversibly blind cases
that need social and economical support. This helps the
blind people by their capacity building in various
aspects of life so that they can live a socially and econo-
mically productive life.
PROGRAMS FOR BLINDNESS PREVENTION AND

CONTROL
It is estimated that 80% of blindness is avoidable, i.e.

preventable like xerophthalmia, or curable like cataract.
Recognizing this, the WHO Program for the Prevention
of Blindness was created in 1978 following a resolution
adopted by the World Health Assembly in 1975. The
global target is to ultimately reduce blindness preva-
lence to less than 0.5 % in all countries, or less than 1 %
in any country. In 1999 the WHO launched Vision 2020:
The Right to Sight.
I. Vision 2020: The Right to Sight

It is a collaborative effort between the WHO and
International Agency for Prevention of Blindness (IAPB)
and other Non-Governmental Organizations (NGOs)

and professional bodies.
Mission
To eliminate the main causes of avoidable blindness in
order to give all the people in the world, particularly
the millions of needlessly blind the right to sight.
Goal
To eliminate avoidable blindness by 2020.
Strategies:
1. Cost effective disease control interventions.
2. Human Resource Development (training and moti-
vation).
3. Infrastructure development (facilities, appropriate
technology, consumables and funds).
Guiding principles: (ISEE)
1. Integrated to existing health-care systems.
2. Sustainable in terms of money and other resources.
3. Equitable care and services available to all, not only
the wealthy.
4. Excellence, i.e. a high standard of care throughout.
Vision 2020 provides technical guidance and support
to countries that adopt it. At the national level, a strong
partnership between the Ministry of Health, National
and International Organizations that work in eye care,
professional organizations and civil society groups
should be established. They should work together
towards Vision 2020 goal of eliminating blindness
through implementation of effective and efficient eye
care services.
Vision 2020: The Right to Sight – India (Fig. 21.2)

India has committed itself to the global initiative to
reduce avoidable blindness and the plan of action for
the country has been developed with following main
features:
1. Target diseases are cataract, refractive errors, child-
hood blindness, corneal blindness, glaucoma and
diabetic retinopathy.
2. Human resource development as well as infra-
structure and technology development at various
levels of health system. The proposed four tier struc-
Fig. 21.2: Proposed structure for Vision 2020

tures include Centers of Excellence(20), Training

Centers(200), Service Centers (2000) and Vision
Centers (20,000).
The significance of this initiative is that its concept
centers on rights issues—recognition of sight as a
fundamental human right by all countries. It can be an
important factor in propelling the Program for
Prevention and Control of Blindness forward to achieve
its goal of elimination of avoidable blindness by 2020.
II. National Program for Control of

Blindness (NPCB)
India launched the program in 1976 as a 100% centrally
sponsored one with the support of DANIDA. It incor-
porated the earlier Trachoma control program which
was started in 1968. Now India has adopted the Vision
2020. It started with the goal of reducing prevalence of
blindness to 0.3% from 1.4%. Target of the 10th plan
was to reduce prevalence to 0.8%.
Objectives
1. To reduce the backlog of blindness through identi-
fication and treatment of the blind.
2. To develop eye care facilities in every district.
3. To develop human resources for providing eye care
services.
4. To improve quality of service delivery.
5. To secure participation of voluntary organizations
in eye care.
Strategies
Five main strategies for the program were:
a. Strengthening service delivery.
b. Developing human resources for eye care.
c. Promoting out reach services and public awareness.
d. Developing institutional capacity and to.
e. Establish eye care facilities for every 5,00,000
persons. Besides these, there are revised strategies
which aim to:
1. Make NPCB more comprehensive by strengthening
services for other causes of blindness like corneal
blindness (requiring transplantation of donated
eyes), refractive errors in school children, im-
prove follow-up services of cataract operated per-
sons and treating other causes of blindness like
glaucoma.
2. To shift from the eye camp approach to fixed
facility surgical approach and from conventional
surgery to intraocular lens implantation for better
quality of postoperative vision.
3. To expand the World Bank project activities like
construction of dedicated eye operation theaters,
eye wards at district level, training of eye
surgeons in modern cataract surgery, and supply
of ophthalmic instruments to the whole country.
4. To strengthen participation of voluntary organi-
zations, to earmark geographic areas to NGOs
and Government hospitals to avoid duplication
and to improve the performance.
5. To enhance the coverage of eye care services in
tribal and other under served areas.
Organizational Structure
The apex institute is the National Institute of Ophthal-
mology at All India Institute of Medical Sciences called
the Dr Rajendra Prasad Centre for Ophthalmic Services.
There are 10 other regional institutes for manpower
development, research and referral services. In addition
82 medical colleges have been upgraded and 39 desig-
nated as training centers for paramedical ophthalmic
assistants. The country has 166 eye banks in the
government and non-government sectors.
Administration
Central Ophthalmology Section, Director General
of Health Services, Ministry of Health and
Family Welfare, New Delhi
State State Ophthalmic Cell, Directorate of
Health Services, State Health services
District District Blindness Control Society
Service Delivery and Referral System

Tertiary level Regional Institutes of Ophthalmology
and Centers of Excellence in Eye Care
Secondary level District Hospital and NGO Eye Hospi-
tal
Primary level Sub-district Level Hospitals, Commu-
nity Health Centers, Mobile Ophthal-
mic units, Upgraded Primary Health
Care Centers, Link Workers/Pan-
chayats
Plan of Action and Activities

1. Extension of eye case services: Eye camp approach is
the main aim. State and district mobile units were
established. They deal with treatment of common
eye diseases, detection of refractive error in children,
general morbidity survey and rehabilitation of
visually handicapped persons.
2. Establishment of permanent infrastructure: It is in three
tier system:
a. At primary health center by strengthening its
equipments.
b. At district level to deal with cataract, glaucoma,
lid lesion and emergency care of eye injuries.
c. Central institution to deal with retinal detach-
ment, corneal grafting and glasses treatment
(tertiary eye care). It is in medical colleges and in
regional institutes of ophthalmology
Intensification of health education: Health education is the
most important wing of NPCB. It:
a. Makes the public realize the importance of preven-
tive aspects of blindness such as vitamin A defi-
ciency, use of irritants to eye and injury to eye.
b. Imparts to the people the basic concepts of various
eye problems such as the cataract, glaucoma, etc.
c. It educates the people to utilize the various schemes
of Government.
d. It is able to clear many wrong concepts and super-
stitions about eye and its problems. In Health
Education, the Questions “when, where, to whom,
by whom and how” arise. To answer these queries:
Health education can be given whenever an

opportunity for it arises— during eye camps, school and
public screening programes, as part of school education
and even in movie theaters during interval.
Nobody is exempt. Even general physician and
surgeons may not be aware of many a thing in
ophthalmology. Politicians, policy makers and planners
must be aware of certain facts such as vitamin A.
Health education is given usually by medical and
paramedical personnel of eye department. Parents and
teachers (who are well informed) are very ideal persons.
The health education itself can be done through TV,
radio, newspapers, bit notices, stickers, movie slides and
documentaries, direct lectures with slides and OHP and
classes. The method to be used depends upon the type
of audience and the place. For example, the methodo-
logy for lay people may not be applicable to school
children. It can be carried out by:
a. Lectures
b. Group discussions
c. Panel discussion
d. Symposium
e. Workshop
f. Institutional Meetings and
g. Demonstrations.
The health education itself can be to:
a. Individuals
b. groups, and
c. Mass.
There are barriers to health education:
• Physiological (Deaf, Blind)
• Psychological (Neurosis)
• Environmental (Noise, Invisibility)

• Cultural (Religion, customs, beliefs). These have to
be overcome.
III. Other Specific Programs

1. Trachoma Control
Endemic trachoma and associated infections are a major
cause of preventable blindness in the developing
countries especially in North India and Mediterranean
countries. Early diagnosis and treatment will cure
trachoma. On this basis, SAFE strategy has been a global
initiative to eliminate trachoma. GET 2020 (Global
Elimination of Trachoma) was launched under WHO’s
leadership in 1997. Through this program control
activities are instituted through primary health centers.
These follow the evidence-based “SAFE” strategy. This
consists of:
• Surgery on lid (S)
• Antibiotics to treat the community pool of infection
(A)
• Facial cleanliness (F)
• Environmental changes (E)
Trachoma control program was launched in India
in 1963 and is now incorporated into the NPCB.
2. School Eye Health Services

Six to 7% of children aged between 10 and 14 years have
problems with their eye sight affecting their learning at
school. Children are first screened by trained teachers
for refractive errors, squint, trachoma, etc. Children
suspected to have problems are confirmed by ophthal-
mic assistants. Corrective spectacles are prescribed or

provided free of cost to the poor students. Health edu-
cation is an important part of the school health services.
Students should be taught to practice the principles of
good posture, proper lighting, avoidance of glare, etc.
3. Vitamin A prophylaxis
Children are most vulnerable to this form of malnourish-
ment. It is one of the main causes of childhood blindness
especially in the developing countries. Measures to
prevent this type of blindness entail vitamin A supple-
mentation, immunization against measles, nutrition
education and avoidance of harmful traditional
practices. Under the vitamin A distribution scheme in
India 200,000 IU of vitamin A is given orally to all
children between the ages of 1 to 6 years every 6 months.
4. Occupational Eye Health Services

This program helps to prevent/treat eye hazards in
industries. It entails:
a. Education on the prevention of occupational eye
hazards.
b. The use of protective devices.
c. Improving safety features of machines and equip-
ments.
d. Proper illumination of the work area.
e. Proper pre-placement examination to identify and
select workers with requisite expertise and good
vision.
DISTRICT BLINDNESS CONTROL SOCIETIES

(DBCS)
The concept of District Blindness Control Societies was

born in with a need to decentralize National Program
for Control of Blindness (NPCB) for the implementation
of the program. District Blindness Control Societies have
been set up in 522 districts of the country as nodal
agency for implementing NPCB. Members of the society
include District Administration, Health, Education,
Social Welfare, Media, Community Leaders, NGOs and
Private Sector. These societies receive funds from
Government of India for various activities. The concept
is to establish a bottom up approach in dealing with
blindness through multisectoral and coordinated
efforts.
Main objectives of the District Blindness Control
Society shall be:
1. To achieve the goal of 0.3% level of prevalence of
blindness
2. To achieve excellence in eye care services by high
quality patient care.
Composition of DBCS
The DBCS may have a maximum of 15 members,
consisting of not more than 8 ex-officio and 7 other
members. While the District Collector or Magistrate is
the Chairman of the DBCS, the Chief Medical Officer
(CMO) will be the Vice Chairman. As the District
Collectors/Magistrates have various responsibilities
and may not be able to find time for regular monitoring,
the CMO will be responsible for close monitoring of
the program, under the guidance of and in accordance

with the instructions issued by the Chairman.
The 3 tier system is followed in DBCS. Primary
Health Centers (PHC) play very prominent role. PHC
medical officers and ophthalmic assistants carry out the
basic functions such as diagnosis, treatment of minor
ailments, refraction, health education, helping in eye
camps, school screening and door to door survey. Com-
plicated cases are referred to higher centers (of the
3 tier system, i.e. district hospital and central institution).
Mobile units are the backbone of DBCS (and NPCB).
They function at district level and at central level (of
3 tier system). If needed personnel are down from
medical colleges.
Main Functions of DBCS

• To assess the magnitude and spread of blindness in
the district by means of active case finding, door to
door survey. The findings are to be recorded and
maintained in Blind Registers. India is the first coun-
try to launch a sentinel surveillance system for trac-
king blindness and ocular morbidity.
• Based on data available, to organize the screening
camps amongst the public for identifying those
requiring cataract surgery.
• To plan logistics needed for screening of cataract
patients and transferring of patients.
• To assess the status of available facilities and resources
in the district such as infrastructure (buildings, beds,
equipments) and manpower (existing and potential).
• To prepare an annual plan of action indicating the
location and calendar of events including follow-up
camps/visits.
• To ensure distribution of prophylactic vitamin A

through the health functionaries of the district to
prevent blindness due to vitamin A deficiency
among children. This is part of Child Survival and
Safe Motherhood Program.
• To prepare a list of voluntary agencies and private
hospitals/practitioners and actively involve them in
the programe. DBCS should co-ordinate activities
of the Government, Non-Governmental and private
sectors in the field of eye care in the district.
• To organise screening of school and preschool children
for eye defects by involving District Education
officer/Inspector of schools, parents, teachers and
other functionaries.
• To periodically review and monitor the implemen-
tation of the District Action Plan. To assess whether
the objectives of of National Program for Control of
Blindness is being attained or not. This includes up
gradation of the knowledge and skills of the service
providers through training programs. They are
sponsored and sent to various conferences/
workshops within India. Publicity/advertisement of
the various programes of District Blindness Control
Society, their activities and usefulness is made so
that the public will come to know about it and be
benefitted.
In implementing the objectives of DBCS, government
and Non-Government Organizations (NGOs) work
together. It is well-known that NGO do better than
government organization. The reasons for better
performance by NGO are as follows:
1. NGO starts the work in a small scale and works it

up slowly. As they gain momentum they acquire
experience and organize better. In government,
any plan is in a vast scale with not much thought
about its immediate feasibility.
2. The follow-up service is good with NGO.
3. In its growth, NGO establishes good co-ordination
and co-operation of the public.
4. NGO also studies the actual need. As the NGO
belongs to the locality, it is able to assess the real
ophthalmic requirement of the people of that
locality. Morbidity survey of the prevalence of
various eye diseases helps NGO its scheme. But
Government has a single scheme for all areas
which may not work in certain areas.
5. Since it is a local affair, every one in that area takes
up health education or propaganda. It reaches the
far corners of the area.
6. Selection of Staff by NGO for the various schemes
is done keeping in mind the actual need and the
capability of the staff that are selected. So much
so, one sees ideal persons at all levels of
management in an NGO. This is not possible with
the Government urgency.
7. As there are no restrictions, international assistance
and local financial help are obtained by NGO.
Government agency cannot obtain monitory help
from donors so easily.
8. Flexible aim is another strong point for NGO. If an
aim is found to be unsuitable or unattainable du-
ring implementation of a program it is altered/
changed to suit the actual needs. This flexibility is
not possible with the government.
9. Sincerity amongst NGO. There blooms a man to

man relationship between the NGO and the
“targets”. The beneficiaries themselves become
active participants in the future programs of NGO.
10. Another field in which NGO is better off is rehabi-
litation. Rehabilitation is very important and the
Government has almost neglected this.
ORGANISATION OF EYE CAMPS
a. Preparatory phase: Finalising the camp site and getting

permission for it, finalising the team, publicity and
collecting materials.
b. Intensive phase: It is the first three days of camp
during which operations are performed. Health edu-
cation is also imparted.
c. Consolidation phase: It is in the second half of the eye
camp. Postoperative care and running an OPD are
the main activities. Surveys are carried out.
d. Retrieval phase: Last day of camp. Patients are
discharged.
e. Follow up phase: It takes place about 6 weeks after
the closure of camp. Glasses are prescribed and
sutures are removed (nowadays IOL is used).
VARIOUS VOLUNTARY ORGANISATIONS
Following are the various voluntary organizations:

a. NSPB: National Society for Prevention of Blindness.
b. Rotary International
c. Royal Commonwealth Society for the Blind (Sight
Savers)
d. Lions International
e. Helpage India
f. Christofell Blenden Relief Mission (CBM): A west
German Christian Mission
g. International Agency for Prevention of Blindness
(IAPB)
h. Helen Keller International
i. Danish International Development Assistance
(DANIDA)
BLIND REHABILITATION
Blindness has been defined, classified and grouped in

various ways by many, including World Health
Organization. One such is grouping is Mohan Nomen-
clature.
Mohan Nomenclature
• Grade I (of WHO). Low vision of Mohan (LV)— 6/
18 to 6/60.
• Grade II. Economic Blindness (E) – 6/60 to 3/60.
• Grade III. Social Blindness (S)—3/60 to 1/60.
• Grade IV. Manifest blindness (M) – 1/60 to PL and
PrL +.
• Grade V. Absolute blindness.
Blind rehabilitation is one field in blindness
programme that is usually not given due attention
especially by Government. It is the NGOs who are now
putting their major efforts in this area.
The blind rehabilitation can be grouped into three
headings:
1. Orientation and mobility training: When a person
knows that he has incurable blindness, he becomes
an extreme introvert. He feels that he has become a

burden to the society. To overcome this, he is to be
up and about and mobile.
It is at this juncture that he is given orientation
and mobilization training so that he is able to move
around freely in his own house, surrounding area
and, if possible, to distant places. The use of cane
and use of seeing—eye dog come under this cate-
gory.
2. Vocational training: Once the incurably blind has
recovered his composure after mobilization and
orientation training, he is given vocational training
so that he can earn his own livelihood, become an
useful member of the community and regain his own
confidence and dignity. So many are self employed
by this vocational training.
Usual occupations taught are cane work, wea-
ving and tailoring. But blind are employed by many
companies nowadays and the work of Orbit in this
field is laudable. Managing of telephone booths is a
useful occupation for the blind.
Another vocational training is teaching the
Braille letters. With many books being published in
Braille nowadays, “reading” for pleasure as well as
for business has become possible for the blind.
3. Normalization: It is the final stage of rehabilitation.
Once the blind has regained his self by orientation
and mobility training and his confidence and inde-
pendence by his vocational training, he is now fit to
become a normal citizen of this community. Home
training is instituted at this stage so that his family
and society accept him as a useful, normal citizen.
22
Frequently
Asked
Questions
(FAQ)
in Oral
Examinations
1. Causes of night blindness:

a. Vitamin A deficiency
b. Retinitis pigmentosa and its variants
c. Fundus albipunctatus
d. Siderosis bulbi
e. Myopia—pathological
f. Senile cortical cataract
g. Syphilitic chorioretinitis
h. Congenital stationary night blindness
i. Choroideremia
j. Oguchi’s disease
k. Advanced glaucoma
l. Drugs—chloroquine, quinine
m. Gyrate atrophy
n. Small pupil
2. Causes for day blindness (Hamarlopia):
a. Nuclear cataract
b. Central small leucoma
c. Central vitreous opacity
d. Congenital cone dystrophy
3. Causes of Xerophthalmia:
a. Vitamin A deficiency
b. Trauma, especially chemical burns
c. Trachoma
d. Pemphigus
e. Disease of lacrymal gland and its nerve connec-
tions
f. Iatrogenic
4. Causes for cherry red spot at macula:
a. CRA occlusion
b. Berlin’s edema (commotio retinae)
FAQ IN ORAL EXAMINATIONS 393
c. Nieman- Pick’s disease

d. Tay-Sach’s disease
5. Uses of atropine in ophthalmology:
a. Corneal ulcer
b. Iridocyclitis
c. Postoperative medication
d. Refraction in children
e. In management of certain congenital cataract
f. Amblyopia treatment
6. Uses of eserine:
a. Refraction—to constrict pupil after dilatation
with homatropine
b. In glaucoma
c. In phthiriasis palpebrum
7. Uses of pilocarpine in ophthalmology:
a. Refraction—to constrict pupil after dilatation
with phenylephrine
b. In glaucoma
8. Uses of fluorescein in ophthalmology:
a. To stain corneal lesion
b. For deep staining of cornea
c. For double staining of cornea
d. To study patency of lacrymal passage
(Jones test)
e. For Siedel’s test
f. For fluorescein angiography
g. For applanation tonometry
9. Causes for red eye:
I. Conjunctival congestion
– Conjunctivitis
II. Ciliary congestion
– Corneal ulcer
– Iridocyclitis
– Acute congestive glaucoma
III. Others
a. Blepharitis
b. Angular conjunctivitis
c. Subconjunctival hemorrhage
d. Phlcyten
e. Episcleritis
f. Scleritis
10. Causes of sudden loss of vision:
I. Painless
a. CRA and CRV occlusion
b. Vitreous hemorrhage
c. Retinal detachment
d. Ischemic optic neuropathy
e. Optic neuritis
f. Toxic amblyopia—especially methyl
alcohol
II. Painful
a. Acute angle closure glaucoma
b. Corneal ulcer
c. Injuries to eye—chemical or mechanical
11. Causes of slow loss of vision:
I. Painless
a. Cataract—developmental, complicated
and senile
b. Refractive error
c. Open angle glaucoma
d. Chronic retinal disease
e. Chronic corneal disease—degeneration
and dystrophy
f. Optic neuropathy
g. ARMD
h. Diabetic retinopathy
II. Painful
a. Optic neuritis
b. Uveitis
c. Corneal ulcer
12. Causes for halos around light:
a. Cataract
b. Angle-closure glaucoma
c. Corneal edema
d. Acute catarrhal conjunctivitis
e. Drugs
13. Causes for watering from eye:
a. Dacryocystitis
b. Nasolacrymal duct obstruction
c. Conjunctivitis
d. Foreign body in conjunctiva and cornea
e. Congenital glaucoma
14. Causes for papillae:
a. Vernal conjunctivitis
b. Giant papillary conjunctivitis
c. Trachoma
d. Exposed suture
e. Superior limbic conjunctivitis
15. Causes for spots in front of eye:
a. Synchisis scintilans
b. Lens opacity
c. Vitreous hemorrhage
d. High myopia
16. Causes for diplopia:
I. Uniocular
a. Cataract
b. Double pupil
c. Subluxated lens
d. Keratoconus
B. Binocular
a. Paralytic squint
b. After correction for squint with ARC (para-
doxical diplopia)
c. Anisometropia
d. Blow out fracture of orbital floor
e. Myasthenia gravis
f. Diabetes
g. Thyroid disorders
17. Causes for flashes of light: Occur due to traction on
retina in following conditions:
a. Posterior vitreous detachment
b. Prodromal symptom of retinal detachment
c. Vitreous traction bands
d. Sudden appearance of flashes and floaters is a
sign of retinal tear
e. Retinitis
18. Causes of Itching, burning and foreign body sensation
in the eyes:
a. Vernal conjunctivitis
b. Simple allergic conjunctivitis
c. Dry eye
d. Trachoma and other conjunctival inflamma-
tions
e. Trichiasis and entropion
19. Uses of cryo in ophthalmology:
a. In cryo extraction (ICCE) of lens
b. For destroying ciliary body (cyclocryotherapy)
c. To seal retinal holes

d. To destroy large papillae in Trachoma
e. Cryotherapy for lid wart and basal cell
carcinoma
f. To preserve corneal buttons (freezing)
20. Uses of laser in ophthalmology:
a. In retinal condition such as diabetic retino-
pathy, ARMD, Eales’ disease and coats
disease
b. To create an opening in after cataract
c. Laser trabeculoplasty, iridotomy, goniopunc-
ture and for ciliary body destruction
d. Refractive surgeries.
21. Causes for small pupil:
a. Local miotics applications
b. Iridocyclitis
c. Horner’s syndrome
d. A–R pupil
e. Side effect of morphia
f. Pontine hemorrhage
g. Poisoning by barbiturates, organophospho-
rous, alcohol
h. During sleep
i. Hyperpyrexia
j. Old age
22. Causes for large pupil (mydriasis):
a. Topical application of mydriatic
b. Acute congestive glaucoma
c. Absolute glaucoma
d. Retinal detachment (total)
e. Optic atrophy
f. Third nerve paralysis

g. Coma
h. Internal ophthalmoplegia
i. Adie’s pupil
23. Causes for various field defects (site of lesions):
I. Homonymous hemianopia
a. Optic tract
b. Lateral geniculate body
c. Optic radiation
d. Occipital cortex (macular sparing is seen)
II. Bitemporal hemianopia
Optic chiasma (middle) (Caused by cranio-
pharyngioma, glioma of 3rd ventricle, supra-
sellar aneurysms and meningioma, pituitary
gland tumors)
III. Binasal hemianopia
a. Distension of III ventricle
b. Atheroma of carotid or posterior communi-
cating arteries
c. Lateral chiasmal lesions.
IV. Altitudinal hemianopia (Horizontal hemi-
anopia)
a. Upper half—sellar tumors (pressure on
chiasma)
b. Lower half—suprasellar tumors (pressure
on chiasma)
(Due to internal hydrocephalus or III ven-
tricle lesion)
c. Ischemic optic neuropathy
V. Quadrantic hemianopia
a. Homonymous upper—Temporal lobe
lesions
b. Homonymous lower—Parietal lobe
(anterior) lesions
VI. Enlargement of blind spot.
a. Primary open angle—glaucoma
b. Papilledema
c. Drusen on disk
d. Juxtapapillary choroiditis
e. Medullated nerve fibers.
VII. Central scotoma.
a. Optic neuritis
b. Ischemia or compression of ON
VIII. Centrocoecal
a. Toxic neuritis
b. AION
c. Optic pit and optic disc drusen
d. Glaucoma.
Optic Tract
Complete or incomplete homonymous hemianopia
which is denser above.
Parietal Lobe
Congruous homonymous hemianopia, which is com-
plete or denser below.
Cortex
1. Congruous homonymous hemianopia.
2. Congruous homonymous hemianopic scotoma.
3. (1) with sparring of the temporal crescent.

4. Monocular field defect sparring the temporal cres-
cent.
5. Checker board field defect (superior in one eye and
Inferior in the other eye).
6. Bilateral homonymous hemianopia with macular
sparring (this resembles tubular field).
Cortical Blindness
Two phenomena occur:
a. Anton’s syndrome (Denial of blindness)
b. Riddoch phenomenon (Dissociation of perception of
kinetic and ststic stimuli)). This can occur in lesions
of other parts of visual pathway also.
Visual information from BOTH right and left
occipital cortex is transmitted to Left parietal lobe for
processing (from right it goes to left side by corpus
callosum). So corpus callosum lesion produces alexia
(inability to read), object agnosia (touch recognition +)
and agraphia (inability to write). These are seen in
parietal lobe lesions also (here homonymous hemi
anopia +).
23
Frequently
Asked
Questions
(FAQ) in
Theory
Examinations
1. Discuss etiology, clinical features and management

of acute iridocyclitis.
2. Etiology, signs, symptoms and management of
chronic iridocyclitis.
3. Discuss the clinical signs and management of acute
congestive glaucoma.
4. A middle aged lady of 45 years comes with history
of seeing halos. Discuss the differential diagnosis
and management of any one condition.
5. Discuss the etiology, clinical features and
management of chronic glaucoma (Open-angle
glaucoma).
6. Enumerate the etiological causes for cataract;
describe the signs, symptoms and treatment of
senile cataract.
7. Define myopia. Describe the different types of
myopia and modes of treatment of myopia.
8. Enumerate the viral infections affecting the eye;
describe the signs, symptoms and their treatment.
9. Describe the etiology, signs, symptoms and
management of hypopyon corneal ulcer.
10. Enumerate the ocular manifestations of diabetes
mellitus.
11. Describe the signs, symptoms and treatment of
retinoblastoma.
12. Discuss the differential diagnosis of ‘red eye’ and
its management .
13. A 40-year-old female complains of redness, pain,
watering and diminution of vision in the left eye
of a week’s duration. Discuss the differential diag-
nosis and management.
FAQ IN THEORY EXAMINATIONS 403
14. Discuss the etiology, clinical features, compli-

cations and treatment of phlyctenular conjunc-
tivitis.
15. Describe the features and management of chronic
Dacryocystitis.
16. A 65-year-old patient comes to your clinic with
history of slow, progressive and painless loss of
vision in both eyes. Discuss the differential diag-
nosis. How will you manage the patient?
17. Optic atrophy—classification, features and
treatment.
18. Discuss the etiology, differential diagnosis and
management of retinal hemorrhages.
Short Notes Questions

1. Blepharitis
2. Ectropion
3. Trichiasis
4. Chalazion
5. Lagophthalmos
6. Epiphora
7. Phlycten
8. Symblepharon
9. Xerosis
10. Angular conjunctivitis
11. Nodule at the limbus
12. Ophthalmia neonatorum
13. Pterygium
14. Spring catarrh
15. Subconjunctival hemorrhage
16. Corneal opacities
17. Keratoplasty
18. Keratomalacia
19. Keratoconus
20. Pannus
21. Keyser-Fleischer ring
22. Hypopyon
23. Episcleritis
24. Scleritis
25. Sympathetic ophthalmia
26. Keratic precipitates
27. Occlusio pupillae
28. Granulomatous uveitis
29. Iridodialysis
30. Ectopia lentis
31. Complicated cataract
32. Pseudophakia
33. Lamellar cataract
34. Phacoemulsification
35. After cataract
36. Disadvantages of aphakic glasses
37. Zonular cataract
38. Traumatic cataract
39. Trabeculectomy
40. Papilledema
41. Papillitis
42. Primary optic atrophy
43. Fundus picture in central retinal vein occlusion
44. Hypertensive retinopathy
45. Berlin’s edema
46. Cherry red spot
47. Diabetic retinopathy
FAQ IN THEORY EXAMINATIONS 405
48. Retinoblastoma
49. Presbyopia
50. Myopia
51. Astigmatism
52. Organization and functions of District Blindness
Control Society
53. Causes of preventable blindness in children
54. Vision 2020
55. NPCB—DBCS
56. Three tier system of control of blindness
57. Carbonic anhydrase Inhibitors
58. Legal blindness
59. Enucleation
60. YAG Laser
61. Tests for color vision
62. Atropine
63. Orbital cellulitis
64. Colored haloes
65. Antifungal agents
INDEX
A Atheromatous ulcer 87, 88

Atropine 75
Acanthamoeba 78 Autorefractometer 348
Accommodation 340-342
Acetyl cysteine 55
B
Acupuncture 278
Adherent leucoma 3, 87 B scan
Adjuvants Vitreous hemorrhage 179
for anesthesia 282 Barkan membrane 153
Amblyopia 266, 270 Benign intracranial tension 248
Ametropia 326 Beta radiation
Amyloid 178 pterygium 58
Anesthesia vernal 55
general 274, 275 Binocular loupe 5
complications 291 Bitot’s spots 58-60
regional 275, 278 Blenorrhea 42, 43
agents 283, 284 Blepharitis
Angular conjunctivitis 47 causes 20, 47
Anterior ischemic optic differentiation 21
neuropathy 249, 250 treatment 24
Anterior staphyloma 73, 100 Blindness
Antibiotics 358, 363 causes 368, 369
fortified 75 epidemiology 370, 371
Antifungal 363 magnitude 368
Antimetabolites 364 prevention 372
Antiviral 363 NGO 385-387
Aphakia 146-148 rehabilitation 388, 389
Aqueous flare 109
Arcus juvenilis 86 C
Arcus senilis 86 Cataract 125-143
Arlt line 49 acquired 139, 140
triangle 109 after cataract 142, 143
Astigmatism 326, 339 complicated 73, 110
developmental 136-139 membranous 45-47

lamellar (zonular) 136 phlyctenular 55, 56
senile 125-134 pseudomembranous 45
immature 126 purulent 42-45
mature 126 trachoma 48-52
hypermature 127 vernal 52-55
Morgagnian 126 Contact lens 89, 93
management 130 therapeutic bandage 76
snow flake 140 Cornea
sunflower 140 anatomy 66-68
syndermatotic 139 blood staining 145
varieties 125 examination 66
Cavernous sinus, anatomy 231 fistula 73
thrombosis 230-232 scar 72, 87-91
differential diagnosis 232 grades 87
Central retinal artery occlusion ulcer
206, 207 atheromatous 87, 88
Central retinal vein occlusion complications 71-73
205, 206 dendrite 79, 80
Cerebellum and eye 248 fascicular 56
Chalcosis 120 features 70
Chlamydazoa trachomatis 45, 48 fungal 77
Chalazion 17-20 rodent (Mooren’s) 81
Chemotherapy 357-362 stages 69
Cherry red spot 207 typical hypopyon 77
Ciliary block 275 Crede’s method 44
Color vision 215 Cryo 289, 290
examination 12 vernal 55
Commotio retinae 207, 308 Cup, eye 41, 42
Community ophthalmology Cycloplegic 75
367-389 Cyclosporine
Concretion 64 in vernal 54
ciliary and conjunctival 70
Conjunctiva
D
anatomy 8 DBCS 383-387
congestion DCR 32
differentiation 70 DCT 30, 32
Conjunctivitis Dacryocystitis
ACCO 40-42 acute 32
angular 47 chronic 30, 32
classification 39 congenital 29
INDEX 409
Dacryocystography 30, 31 F
Dalen Fuchs nodules 119
Facial block 278-280
Danger zone of eye 119
complications 280
Dark room examination 343-353
Festooned pupil 112
Decongestant 365
FISTO 50
Degeneration
Fleurettes 202
Salzmann 56, 83
Focal illumination 344
Demyelinating disease 246-248
Follicles, etiology 64
Descematocele 72
Herbert’s 50
Deuteranope 13
trachomatous 48
Devic’s disease 247, 248
Fortified eye drops 75, 362
Diabetes 139
Foster-Fuchs spots 330
Diplopia 148 Fundus, normal 186
Direct ophthalomoscopy
349, 350, 353 G
Distant direct ophthalmoscopy
Glands
345, 346
Meibomian 16
Dry eye 35, 52
Moll 16
Dyes 365
Zeis 16
Glaucoma
E absolute 157, 167, 168
ECCE 130, 131, 287, 288 angle anatomy 150
Ectopia lentis 143-146 classification 152
Ectropion 23 congenital 152-154
Elschnig’s pearls 141 hundredth day 206
Emmetropia 326 etiology 151
Encephalitis periaxialis primary
diffusa 247 narrow angle 155-158
Endophthalmitis 73 open angle 158-167
Entropion 23-25 drugs in 165-167
Enucleation 100 secondary
Epilation 20, 25 dislocated lens 170
Episcleritis 97, 98 hemorrhagic 173
Epiphora 34 phacolytic 170
Evisceration 100 phacomorphic
Eye camps 387 124, 126, 170
Examination surgery 158, 167,292-297
ocular 3-13 Glue 75
Exophthalmos, thyrotropic 228 Ghost vessels 85
Glioma 203 Internuclear ophthalmoplegia

Gonioscopy 154 241, 258
Graves’ disease 227 Iridectomy 303, 304
Iridocyclitis 107-115
H causes 85, 107, 108
complications 114
Haab striae 153
differential diagnosis 115
Hallberstaedter -Prowazek bodies
features 109-112
49
management 116, 117
Haloes 130,156
types, differences 118
Headache 250
Iridodialysis 122
differentiation 252-256
Iris
Health education 379, 380
anatomy 104
Herbert’s pits 50
bombe 111
Herpes, simplex 79
neovascularization 173
zoster 80, 81, 98
nodules 110, 115, 116
History, elicitation 2, 3
Ishihara chart 11, 12
Hemorrhage
subconjunctival 62, 63
hyaluronidase 63
J
Hordeolum, externum 19, 20 Jack-in-box effect 148
internum 19, 20 Jone’s classification (trachoma) 50
Hutchinson’s triad 85 Jones’ dye test 35
rule 80
Hyaluronidase 63 K
Hypermetropia (Hyperopia)
Kayser-Fleischer ring 120
333-336
Keratic precipitate 71, 109, 116
Hyphema 110, 134, 167,171-173
Keratitis 68
Hypopyon 70,110
acanthamoeba 78
typical 78
disciform 79
Hypervitaminosis A 59
classification 68
exposure 23, 84, 228
I herpes 79
ICCE 130, 289, 290 interstitial 85, 86
complications 291 neurotrophic 84
I & C 28 nummular 80
IOL 131-133 sclerosing 99
Indirect ophthalmoscopy striate 134
350-352 Keratectasia 72
Instruments (description) Keratocele 72
299-323 Keratometry 348
INDEX 411
Keratoconus 54, 91-93 Muscae volitantes 176,198
Keratoneuritis 78 Myasthenia gravis 260, 261
Keratoplasty 87-93, 173 Mydriatic 75, 356
Mydricaine 117
L Myopia 327-333
Lacrymal passage
anatomy 28, 29
N
examination 28 NPCB 376-381
Lagophthalmos 24, 36, 85,228 NSAID 363
nocturnal 85 Near vision 8, 9
Lasers 158, 167,193,298 Nebula 87
LASIK 331, 332 Neuromyelitis optica 247
Lateral illumination 344 Nodules
Leber cells 48 Dalen-Fuchs 119
Lens iris 110, 115-117
anatomy 124, 125
cataract dislocation 128, O
143-146
Oblique illumination 344
+ 90 D 13
Occlusio pupillae 112
Leukocoria 136, 180, 201
Occupational eye health 382
Leucoma 73, 87
Ocular pressure, digital study 9
Lids
Oculomotor nerve 234-238
anatomy 16, 17
anatomy 234
examination 16
lesions 236-238
with cyclic spasm 238
Line of Arlt 49
Opaque nerve fibers 212
Loupe 3, 5
Ophthalmia neonatorum 42-44
Lithiasis 64
Ophthalmia nodosa 64
Lucid interval of Vogt 86
Ophthalmoplegic migraine 257
Operation
M Burrows 22
Macallan staging 50, 51 cyclodestructive 169
Maneuvers, for examination 3 cyclodialysis 292, 293
Membranous conjunctivitis enucleation 168, 297, 293
45-47 evisceration 298
Migraine 251, 257, 258 extracapsular cataract
Miotics 157, 356-357 130, 131,287, 288
Mitomycin C complications 134, 291
pterygium 58 Fasanella-Servat 24
Mohan nomenclature 388, 389 goniotomy 155
intracapsular cataract Papillitis 119

130, 289, 290 Persistent hyperplastic vitreous
complications 134, 135, 180
141, 142, 291 Papillae 49
iridectomy 157 Pemphigoid 24, 36
Jaescha-Arlt 22 Peribulbar block 276
peripheral iridectomy 294 Phacocele 144
Pott’s full excision 107 Phlyctenular conjunctivitis 55, 56
radial keratotomy 331 Phthisis bulbi 73, 114
refractive surgeries 331, Pinguecula 56
336, 339 Placido disk 66,92
sac surgeries 30-32, 296, Placental extract 197
297
Polyopia 130
Scheie 294, 295
Presbyopia 129, 339, 340
tarsorrhaphy 85
Proptosis 224-227
trabeculectomy 167, 293,
causes 225
294
investigation 226
trabeculoplasty 167
management 227
V-Y operation 23
Protanope 13
Weiss 22
Wheeler 22 Provocative tests 169
Z plasty 23 Pseudocornea 73
Optic atrophy 212, 215, 218-221 Pseudogeronotoxon 54
Optic nerve Pseudoglioma 112, 202, 203
anatomy 210 Pseudomyopia 330
neuritis 214-216 Pseudoproptosis 226
neuropathy, toxic 216-218 Pseudomembranous conjunctivitis
Orbit 45
anatomy 224 Pseudopterygium 58
cellulitis 229, 230 Pseudotumor cerebri 248
differential diagnosis 232 Pterygium 57, 58
Ptosis
P causes 23
classification 23
PCO 141
Pachymetry 66
treatment 23, 24
Panophthalmitis 73, 230
Pupil
Pannus 49, 51, 83
Papilledema 210-212, 243 abnormal 121
differential diagnosis festooned 112
212 Marcus Gunn 121,130, 215
INDEX 413
R patch graft 99, 100
Red eye, differentiation 115 posterior 99
Refraction 325-342 Scleromalacia perforans 98
Refractive surgeries 331,336,339 Scotoma
Retina Bjerrum’s 161
anatomy 185 ring 162, 196, 330
Retinopathy roving 148
diabetic 189-193 Seclusio pupillae 111
hypertensive 187-189 Second vision (sight) 129
pregnancy induced 189 Shadow test 346-348
of prematurity 194 Siderosis bulbi 120
Retinal detachment 197 Sign
features 197, 198 Battle’s 242
management 200, 201 Bonnet’s 187
types 197, 198
Gunn’s 187
Retinitis pigmentosa 194-197
Munson’s 91
variants 195
Graves’ 227
Retinoblastoma
Riziutti 91
features 201 Salus’s 187
pathology 202 Shaffer’s 199
stages 201, 202 Skyascopy 346-348
treatment 204, 205 Slit lamp 3, 6
Retinoscopy 9, 346-349 Snellen’s chart 6, 7
Retrobulbar neuritis 215, 216 Sorsby method 44
Riboflavin 47 Spring catarrh 52
Ring of Sommering 141 Squint
Rodent ulcer 81 comitant 265, 266
Roenne’s nasal step 162 differentiation 264
Rosette paralytic 266, 267
Flexner-Wintersteiner 202 differentiation 267
Homer-Wright 202 Staphyloma 99-101
Sturm’s conoid 338
S Sterilization 283-286
SPK 53,78-80 Strabismus 264-271
Salmon patch 85 Striate keratitis 134
Schilder’s disease 246 Subconjunctival hemorrhage
School eye health 381 62, 63
Sclera Sympathetic ophthalmia 118-120
anatomy 96
Symblepharon 44, 45, 60, 61
anterior 98, 99
Synchisis scintilans 177
Syndrome T
Alport’s 139
Therapeutics 355, 366
Alstrom-Hallgren’s 197
Tonometer 10, 11, 159
Anton’s 400
Benedict’s 236 Tatooing 89
Tear
Brown’s 267
deficiency 35
Claude’s 236
Down’s 139 layers 35
Three tier system 379-381
Duane’s 261, 262, 267
Thyroid 227, 228
Ehlers Danlos’ 143
Fanconi’s 361 Test
Bielschowsky’s head tilt 239
Foster-Kennedy 244
cocaine 259
Foville’s 242
Gradenigo’s 242 cover 266
eclipse 3
Horner’s 258-260
Fincham’s 130,156
Lowe’s 139
Laurence-Moon-Biedl-Bardat forced duction 267
Jones 35
197
probe 58
Marfan’s 143
Mobius 243, 265, 267 provocative 169
Schirmer’s 36
Millard-Gubler’s 242
swinging flash light 121
Nathnagel’s 236
Parinaud’s 240 tensilon 261
water drinking 169
Raymond’s 242
Toxic amblyopia (Toxic optic
Refsum’s 197
Riley-Day’s 36 neuropathy)
Sjögren’s 36 ethyl alcohol 217
Stevens-Johnson 60 arsenic 217
Superior orbital fissure 237, chloroquine 218
243 lead 218
Tolosa-Hunt 237, 242 methyl alcohol 217
Usher’s 197 quinine 218
Weber’s 236, 246 tobacco 217
Weill-Marchesani 143 Thiotepa and pterygium 58
Synechia Trachoma 24, 36, 48-52, 60
peripheral anterior 111 Trachoma control 381
posterior 111 Tranta’s dots 53
ring 111 Trichiasis 24, 25
total posterior 111 Trochlear nerve
Synoptophore 269 lesions 238-241
INDEX 415
Tumors Vision
intracranial 243 near 8
pituitary 244 recording 6-8
second (second sight) 129
U tubular 162,195
Vision 2020 373-376
Ulcer Vitamin A 36, 58, 59,197,382
amoeboid 79 Vitreous
atheromatous 87, 88 anatomy 176
corneal (Sec cornea, Ulcer) hemorrhage 179, 180
fascicular 56, 82 opacities 176-178
geographical 79 Vitrectomy 178, 180, 181, 193,
miliary 56 194
Mooren’s 81, 82 Voluntary organisations 387
scrofulous 56
W
shield 53
Ulcus serpens 77 WHO classification of trachoma
50, 51
Uveal tract
vitamin A deficiency 58, 59
anatomy 104, 105
Watering from eye 33-35
uveitis 106-118 causes 34
anterior 107-115 treatment 35
phacoanaphylactic 120 Weigert ligament 176
purulent 107
X
V Xerophthalmia 58
Vernal conjunctivitis 52-55 Xerosis 44, 45, 58

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What are the different branches of Jaypee Brothers Medical Publishers mentioned?

What are the different branches of Jaypee Brothers Medical Publishers mentioned?

What are some of the eye diseases discussed in the document?

What are some of the eye diseases discussed in the document?

Clinical

Accompanying Photo CD ROM is playable only in Computer

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Clinical Ophthalmology Made Easy ®

First Edition: 2009

The basic clinical examination of eye and its adnexa

our first attention before we go into clinical exami-

I am grateful to Dr Kalavathy, Deputy Director of

Introduction ............................................................ xiii

Ophthalmology is a subject which is easy to grasp and

question numbers. Between two answers draw a line.

CLINICAL AND ORAL

examination you will be able to diagnose (If you cannot,

for the questions that were asked in your theory

As with other disciplines, examination of an eye patient

(The same concept must be applied when presenting

The clinical examination of an eye case starts with general

Figs 1.1A to C: The three maneuvers for a quick examination of eye. In

Fig. 1.3: Slit-lamp

other side half of the iris will be in shadow due to con-

4th line at 18 meters, 5th line at 12 meters, 6th line at

distance from the patient. If, for example, the patient

The refractive state of patient’s eye is tested

Fig. 1.7: Schiotz tonometer which is used for measuring the

Fig. 1.8: Applanation tonometer

Fig. 1.9: Tonometry (procedure for measuring IOP)

Checking the color vision may not be needed for the

Figs 1.10A to F: Color vision chart (Ishihara). All the types

Usually color blindness can be for red (protanopes

Fig. 1.11: + 90 D lens. Using this with slit-lamp one can

Swellings of lids are usually kept for clinical exami-

The eyelids have tarsal plates and muscles covered by

Fig. 2.1: Cross-section of upper lid. (A) Skin. (B) Cilia.

The conditions that can frequently give rise to swellings

Fig. 2.3: Chalazion. There is total absence of inflammatory

Table 2.1: Swellings of lids

curettage in an elderly person, one should think of

INFLAMMATION OF LID MARGIN

It is called blepharitis. It is caused by infection

The lid may be abnormally turned, drooped or retracted.

Table 2.2: Types of blepharitis

Entropion can be: (a) cicatricial (due to scarring of pal-

Fig. 2.4: Close-up of eye lashes showing the nits in a

Such an in-turning produces trichiasis, rubbing of

Ectropion is eversion of lid margin and eye lashes away

Ptosis affects upper lid only and is due to paralysis of

and jaw winking phenomena must be assessed before

It is the inability to close the lids. (See Chapter 5 page 84)

Trichiasis is inturning of eye lashes—a misdirection.

Fig. 2.5: Trichiasis showing the in-turned lashes

Symptoms are essentially that of lashes rubbing

Usually lacrymal gland is not for under graduate exami-

Lacrymal sac is lodged inside lacrymal facia, which is

Fig. 3.1 Anatomy of lacrymal passage: (A) Punctum, (B) Canaliculus,

mainly by lacrymal gland, moistens the surface of

It is common in aged ladies and in poor people. It is