Clinical Examination in Ophthalmology PDF

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CLINICAL EXAMINATION
IN OPHTHALMOLOGY
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CLINICAL EXAMINATION
IN OPHTHALMOLOGY
P.K. Mukherjee, MS
Former Dean, Professor and Head
Department of Ophthalmology
Pt. J.N.M. Medical College
Raipur, India
ELSEVIER
A division of
Reed Elsevier India Private Limited
Clinical Examination in Ophthalmology, 2/e
Mukherjee
ELSEVIER
A division of
Reed Elsevier India Private Limited
Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann and

Hanley & Belfus are the Health Science imprints of Elsevier.
© 2006 Elsevier
All rights are reserved. No part of this publication may be reproduced,

stored in a retrieval system, or transmitted in any form or by any means,
electronic, mechanical, photocopying, recording or otherwise, without the
prior permission of the publisher.
ISBN-13: 978-81-312-0335-4
ISBN-10: 81-312-0335-2
Medical knowledge is constantly changing. As new information becomes

available, changes in treatment, procedures equipment and the use of drugs
become necessary. The authors, editors, contributors and the publishers have,
as far as it is possible, taken care to ensure that the information given in this
text is accurate and up-to-date. However, readers are strongly advised to
confirm that the information, especially with regard to drug dose/usage,
complies with current legislation and standards of practice.
Published by Elsevier, a division of Reed Elsevier India Private Limited,

Sri Pratap Udyog, 274, Captain Gaur Marg, Sriniwaspuri,
New Delhi – 110065, India.
Printed and bound in India at

To my teachers who ignored my ignorance
and
To my students who were ignorant of my ignorance
P REFACE
Whenever a new book is published, the most often asked question is, “Yet another book, but
why?”
Robert Hutchison the author of Hutchison’s Clinical Methods in 1897 answered it very well,
“It is not intended as a treatise upon clinical diagnosis. On that subject there are already suffi-
ciency of good works in existence.”
The present author also subscribes to this statement more than a century after Hutchison.
In fact there is no shortage of textbooks in ophthalmology, many of which are written in a
superb fashion. Most of these books, generally concise, contain a chapter on examination of
the eye, which is not sufficient for an undergraduate student. Hence this book. However, the
author does not claim to have produced a book that answers all questions which come to the
minds of the students nor is this book the last word in examination of the eyes.
Having been a teacher and an examiner for many years, the author has realized that both
undergraduates and postgraduates may be able to form a diagnosis but fumble miserably when
asked, how? or why? A resident is known to order a battery of costly investigations to prove his
theoretical knowledge without bothering to do simple outdoor procedures like recording of
vision, use of pin-hole, cover test or listen carefully to the complaints of the person, which may
in fact lead to diagnosis and provide a clue to appropriate investigations.
The book is addressed primarily to undergraduate students; however this book will be a
good foundation for postgraduates too.
The book has not been written in the Queen’s English deliberately. It has been written in
English that is spoken in the third world.
The book includes general information regarding signs, symptoms and terminology. Each
chapter is devoted to a system of the eye. There are some repetitions in various chapters, prima-
rily in order to emphasize the importance of certain key facts. For details of sophisticated and
specialized investigations and their interpretations, the postgraduates are advised to consult
standard references on such subjects. Management of various diseases is out of this book’s limit,
hence has not been included.
In spite of the author’s best efforts, it is unlikely that this book is free from inaccuracies like
typographic errors, statistical ambiguities, etc. Feedback from teachers and students will be
most welcome in order to remove them and improve the book.
P.K. Mukherjee
ACKNOWLEDGEMENT
I am thankful to my students who for years have been urging me to publish my notes in a book
form. It is their desire that has prompted me to put my thoughts on examination of eyes in
a book form.
I am thankful to Elsevier, a division of Reed Elsevier India Private Limited, for publishing
the book. I am thankful to their officers especially Shri Tanveer Ahmad, Shri Rajiv Banerji,
Ms. Shabina Nasim and other members of the staff for their cooperation and help in getting
this book published.
I profusely thank members of the upgraded Department of Ophthalmology, Pt. J.N.M.
Medical College, Raipur for the help that they have rendered to me. Prof. S.L. Adile,
Prof. A.K. Chandrakar, Dr. M.L. Garg, Associate Professor, Dr. Nidhi Pandey, Assistant
Professor, Dr. Subhash Mishra and Dr. B.K. Das of the Mobile Unit have been generous
enough to give me books and journals for reference. I thank them profusely. I am also thank-
ful to Dr. Dilip Agrawal, Plastic Surgeon, Raipur, Dr. Alka Das, Ophthalmic Consultant,
Raipur and Dr. Madan Kumar Deshpande, Ophthalmic Consultant, Bilaspur, for permitting
me to use the photograph of their patients from their collection. I am thankful to Dr. K. Appa
Rao, Dr. Sunil Gupta, Dr. Santhosh Patel. I am thankful to Dr. Manik Chatterjee, Assistant
Anatomy, Dr. Preeti Gupta, Consultant Ophthalmologist and Dr. B.P. Sharma, Consultant
Ophthalmologist, Bhilai, for having provided me with their personal books. I am thankful to
Padmashree Dr. A.T. Dabke for helping me in collecting the photographs of my patient over
the years.
The real inspiration behind this book remains my wife, Protima. My daughters, Protibha
and Preeti kept on pestering me to keep to the time schedule and even permitted their respective
spouses Satyadeep and Abir to spend their holidays in typing the manuscript and rearranging
them many a time. They also laboured very hard in drawing and re-drawing the figures. They all
deserve thanks.
I am thankful to Shri Maneesh Dandekar of HyperSoft Computers, Raipur for typing of
the book.
P.K. Mukherjee
C ONTENTS
Preface vii
Acknowledgement ix
Chapter 1 Symptomatology and History Taking 1
Chapter 2 Examination of Vision and Recording of Visual Acuity 14
Chapter 3 Examination of Eyes Under Diffuse Light 37
Chapter 4 Examination of Eyes Under Focal Illumination 42
Chapter 5 Examination of the Lid 49
Chapter 6 Evaluation of a Case of Ptosis 65
Chapter 7 Examination of the Lacrimal System 74
Chapter 8 Examination of the Conjunctiva 81
Chapter 9 Examination of the Globe, Cornea and Sclera 100
Chapter 10 Evaluation of an Eye with Disorder of Tear Film 127
Chapter 11 Examination of Anterior Chamber 134
Chapter 12 Examination of Iris, Ciliary Body and Choroid 141
Chapter 13 Examination of Lens and Evaluation of an Eye for Lens Extraction 158
Chapter 14 Measurement of Intraocular Tension 173
Chapter 15 Examination of Eyes with Abnormal Intraocular Tension 180
Chapter 16 Examination of the Eyes Requiring Optical Correction 213
Chapter 17 Examination of a Case of Squint 232
Chapter 18 Neurological Examination of the Pupil 278
Chapter 19 Examination of the Orbit and Radiology of Ophthalmic Interest 285
Chapter 20 Examination of Retina and Macula 309
Chapter 21 Examination of Vitreous 343
Chapter 22 Examination of the Optic Nerve and the Visual Pathway 349
Chapter 23 Examination of Eyes in Paediatric Age 365
Bibliography 372
Index 379
■■■ CHAPTER 1
S YMPTOMATOLOGY AND
H ISTORY TAKING
Symptoms comprise complaints of the person regarding the disease he or she is suffer-
ing from and signs are clinical features that an examiner notices or elicits.
Some of the symptoms are signs by themselves, e.g. deviation of eye in a particular
direction. This is an obvious complaint of the patient but is also a sign, which requires
further examination to find out if it is paralytic or non-paralytic, if it is a simple deviation
or is associated with diminished vision, and if the diminished vision can be improved.
Redness around the cornea is an important sign that patients first notice and report.
Many times symptoms provide an important clue towards diagnosis, e.g. if a per-
son of forty years complains of difficulty in reading but has no difficulty in distant
vision, the obvious diagnosis is presbyopia. An adult with gradually diminishing night
vision is most probably a case of retinitis pigmentosa.
It is important to listen carefully to what the patient has to say in his or her own words.
SYMPTOMS IN OPHTHALMIC DISORDERS
Symptoms in ophthalmic disorders are as follows:

A. Ocular
B. Non-ocular
Ocular Symptoms
Ocular symptoms can be:
1. Visual
2. Non-visual
3. Mixed
Visual Symptoms of Ocular Disorders

● Diminished distant vision
● Diminished near vision
● Diminished distant as well as near vision
● Diminished night vision
● Diminished day vision
● Diminished colour vision
● Diminished field of vision
2 CLINICAL OPHTHALMOLOGY
● Diminished vision in bright light

● Diplopia
● Polyopia
● Metamorphopsia
● Photopsia
● Chromatopsia
● Coloured haloes
● Glare
● Photophobia
● Frequent change of glasses
Visual symptoms are brought about by:
● Errors of refraction
● Anomalies of accommodation
● Opacities in media
● Pathology in optic pathway, retina and choroid
● Disturbance of ocular motility
● Neurological
● Amblyopia
Diminished distant vision Diminished distant vision is the commonest visual symp-
tom for which a person seeks help. It surpasses all other symptoms. Diminished distant
vision can be unilateral or bilateral. It is seldom equal in both eyes. Differences may vary
from slight to severe. It could be gradual or sudden in onset. It could be associated with
non-visual symptoms like pain, redness, watering or could just be gradual without any
other symptoms. Again, gradual painless diminished distant vision surpasses other painful
symptoms.
Causes of gradual painless diminished distant vision are:
(a) Errors of refraction
(b) Gradually developing opacities in ocular media
(c) Chronic optic neuropathy
● Chronic glaucomas, primary or secondary, produce diminished distant vision when they are
well advanced
● Heredofamilial optic neuropathy
● Consecutive optic atrophy
● Secondary optic atrophy
● Drug-induced neuropathy
(d) Chronic maculopathy

● Macular degenerations and dystrophies
● Cystoid macular oedema
● Diabetic maculopathy
● Chronic macular oedema, secondary to vascular lesion, inflammation, trauma or drug
induced
(e) Chronic retinopathy
● Diabetic retinopathy
● Hypertensive retinopathy
● Branch artery occlusion
● Branch vein occlusion
● Sub-retinal neovascularisation
SYMPTOMATOLOGY AND HISTORY TAKING 3
(f) Amblyopia
● Anisometropic
● Strabismic
● Ex anopsia (form vision deprivation)
(a) Errors of refraction are myopia, hypermetropia and astigmatism

(b) Ocular media are cornea, aqueous, lens and vitreous
● Most frequent gradually increasing opacity in ocular media is immature cataract, followed
by opacities of cornea, which may be post-traumatic and post-infective, vascularisation of

cornea, degenerations, dystrophies and deposits on the cornea
● Aqueous is not capable of being opaque.Vitreous opacities are common but do not produce
visual loss unless they are very large or present in front of and near macula
(c) Chronic optic neuropathy
(d) Chronic maculopathy
In amblyopia, gradual painless unilateral diminished vision may go unnoticed by the
patient especially in the absence of other symptoms like squint, corneal opacity, etc. It
is detected either on routine checkup or when the patient closes the seeing eye and for
the first time realises diminished vision in the other eye. It is generally due to errors of
refraction developing after six or seven years of age, or small angle tropias or faint cen-
tral corneal opacities. These eyes are generally not capable of improvement.
Sudden loss of distant vision can be painful or painless.
Causes of sudden painful loss of distant vision are:
1. Trauma
2. Corneal ulcer
3. Herpes zoster ophthalmicus
4. Interstitial keratitis
5. Acute iridocyclitis
6. Acute congestive glaucoma
7. Endophthalmitis
Causes of sudden painless loss of distant vision are:
1. Central artery occlusion
2. Retinal vein thrombosis
3. Vitreous haemorrhage in front of macula
4. Macular haemorrhage
5. Retinal detachment
6. Central serous retinopathy
7. Acute ischaemic optic neuropathy
8. Cortical blindness
9. Malingering
All the above causes are generally unilateral. For a bilateral sudden loss of vision, the
lesion is generally vascular involving both the visual pathways.
Causes of bilateral sudden loss of vision are:
1. Cortical blindness
2. Hysterical patient sometimes report bilateral sudden painless loss of distant vision
3. Malingering
4. Uraemia
5. Methyl alcohol poisoning
6. Quinine toxicity
Diminished near vision It could be gradual or sudden. Generally, gradual dimin-
ished near vision is bilateral and equal. It is universal after 45 years of age. If a person
after age of 45 years does not develop diminished near vision then there are only two
possibilities, i.e. he is myope or does not have to undertake near work at usual near
distance of 30 cm.
Causes of gradual diminished near vision are:
1. Presbyopia
2. Posterior capsular cataract
3. Posterior polar cataract
4. Macular degeneration
5. Bilateral large corneal opacity on the nasal side
Causes of sudden diminished near vision are:
1. Instillation of cycloplegic for therapeutic or diagnostic purpose. It can be accidental or psychogenic
(cycloplegia with atropine may last as long as fortnight)
2. Internal ophthalmoplegia
3. Total ophthalmoplegia
4. Spasm of accommodation
5. Iatrogenic
(a) Aphakia
(b) Pseudophakia
(c) Over correction of myopia
(d) Under correction of hypermetropia
(e) Systemic parasympatholytic drug administration
Diminished distant as well as near vision It is seen in uncorrected aphakia, pseudo-
phakia, advanced cataract, macular degeneration, corneal degeneration and dystrophy,
and uncorrected errors of refraction.
Diminished night vision By far the commonest cause of diminished night vision
is vitamin A deficiency followed by retinal dystrophy. It should be remembered that:
➤ If a child under five years of age presents with diminished night vision, it is most
probably due to vitamin A deficiency and will improve with therapeutic dose of vitamin A
➤ An adult with night blindness is most probably suffering from retinitis pigmentosa
and will not improve with administration of vitamin A
Diminished colour vision This is commonly known as colour blindness.

However, as there is no change in visual acuity due to the diminished colour sense, it
is not appropriate to designate it as blindness.
The commonest cause of this defect is genetic, seen almost exclusively in males.
About 4–8% of male population have colour vision defects not amenable to treatment,
and patients are generally unaware of the defect unless it is specifically tested for, or
causes social embarrassment in the form of choice of dress.
Other causes of diminished colour vision are acquired, e.g. immature cataract, optic
neuritis and macular degeneration.
Diminished field of vision (scotoma) Loss of field is called scotoma. It could be cen-
tral or peripheral, unilateral or bilateral, simultaneous or one may follow the other. One
eye may have more advanced scotoma than the other. A scotoma is said to be positive
if the person is aware of its presence and negative when the person is not aware of it. Blind
spot is a physiological negative scotoma. In the long-run positive scotomas can become
negative, while the reverse is not possible. A scotoma is called relative when its density or
shape changes with illumination or colour. In case of relative scotoma the patient seems
to see through a haze. Patients describe scotoma in various terms. Patients may complain
that they have to move their head to see an object on one side. Hemianopias are generally
spoken of as diminished vision. Central field defects are also reported as diminished vision.
Causes of central scotoma are:
1. Optic neuritis
2. Retrobulbar neuritis
3. Macular lesions
Peripheral scotomas are produced by lesions of retina, optic nerve and optic pathway.
Causes of peripheral scotoma are:
1. Advanced glaucoma, mostly primary
2. Retinal dystrophy, retinitis pigmentosa and related conditions
3. Choroidal dystrophy
6. Pituitary tumours
7. Post-papilledematous optic atrophy
8. Drug induced
9. Lesions of chiasma, optic tract and optic radiation
Scotoma can be congruous or incongruous; it can be homonymous or heteronymous.
Congruous field defects are those defects where the edges of the scotoma in each eye are
symmetrical. Homonymous field defects are those defects that are situated on the same
side of visual field, e.g. right nasal and left temporal. Heteronymous field defects are
those that are situated on the same position, e.g. right temporal defect and left tempo-
ral defect of right and left eye, respectively.
Diminished vision in bright light (diminished day vision) Patients complain that
they have good vision in the evening or at night, but in bright light their vision is
greatly reduced.
Common causes of diminished vision in bright light are:
1. Posterior polar cataract
2. Central nuclear cataract
3. Macular lesions
4. Central corneal opacity
Diplopia (seeing double) The patient sees two images of a single object. The main
image has a sharp outline. The second image is fainter, may partially overlap the first
image or may be separated by a gap. It may be displaced horizontally or vertically, may

be tilted, the distance between the two images may change in different gazes and may
disappear with compensatory change in head posture. Both the images may be on the
same side or may cross over mid-line. If diplopia disappears by closing one of the eyes,
it is known as binocular diplopia. If diplopia disappears by obstructing the affected eye,
it is called uniocular diplopia.
The commonest cause of binocular diplopia is paralytic squint, other causes being
restrictive strabismus, dysthyroid oculopathy, blow out fracture of the orbit, post-
operative entrapment of muscles in retinal surgery, myasthenia gravis, retrobulbar
growth, and trauma to muscles.
Uniocular diplopia is relatively rare.
Causes of uniocular diplopia are:
1. Recent corneal opacity
2. High astigmatism
3. Subluxated lens
4. Iridodialysis
5. Displaced IOL
Polyopia (seeing multiple) The patient complains of seeing multiple images of

linear or crescent-shaped lights, commonly moonlight and streetlight. It is seen in
incipient stages of immature cataract.
Metamorphopsia (distorted vision) In metamorphopsia objects look distorted.
They may look smaller—micropsia or larger—macropsia. Lines may look wavy.
Metamorphopsia may be seen in retinal detachment, macular oedema, macular degen-
eration, and central serous retinopathy.
Photopsia (flashes of light) The patient complains of flashes of light in the periph-
ery of field of vision. These are transient and recurrent, and are best appreciated in the
dark. They imply retinal or cerebral irritation. They may be a warning symptom of
impending retinal detachment. They are also seen in posterior vitreous detachment.
Chromatopsia (coloured vision) The patient complains that light-coloured objects
like whitewashed wall, white clothes, etc. seem to be tinged. If the tinge is blue, which is
very common, it is called cyanopsia, if the tinge is red it is called erythropsia, and yellow is
xanthopsia.
Coloured haloes around lights Rainbow-like haloes are seen around artificial
lights in dark surroundings. They could be unilateral or bilateral. They are caused by
the splitting of white light into seven colours due to the prismatic effect of fluid in the
cornea or lens. They are seen in prodromal stage of acute congestive glaucoma, corneal
oedema and incipient stage of cataract. In acute mucopurulent conjunctivitis, mucus
shreds on cornea may have prismatic effect and produce coloured haloes that disap-
pear with the removal of mucus.
Glare (discomfort of bright light) The patient does not like bright light. This is
to be differentiated from photophobia.
Glare is seen in:

1. Large pupil
2. Myopia
3. Use of mydriatic and cycloplegic
4. Immature cataract
5. Recent aphakia
6. Large iridectomies
7. Albinism
Photophobia (intolerance to light) The patient is not able to tolerate light and
may close the eye or move the head away from the source of light. This is associated
with forceful closure of lids. Photophobia can be unilateral or bilateral. Photophobia
is more marked in children.
Causes of photophobia are:
1. Trauma to the cornea
2. Embedded foreign body in the cornea
4. Rupture in the Descemet’s membrane
5. Phlyctenular keratoconjunctivitis
7. Chemical burn
8. Ultraviolet light exposure (welding, snow blindness)
Frequent change of glasses Change of power every year or alternate year is com-
mon. A myopic child requires increased power every year. A presbyope may require a
change every second or third year. If a person feels uncomfortable with glasses and
requires change frequently, this should receive attention.
Causes of frequent change of glasses are:
1. Keratoconus
2. Central nuclear cataract
3. After cataract
4. Chronic simple glaucoma
5. Hypoglycaemia
6. Hyperglycaemia
7. Macular oedema
8. Retrobulbar growth
9. Hypotony
10. Subjective prescription of glasses in children
Visual agnosia: Inability to recognise familiar object by sight, for example the patient
may not be able to recognise a watch but can identify it with its sound or by touch.
Visual hallucinations: They may be formed or unformed. Formed hallucinations
represent objects, persons and animals that are not actually present. Unformed hallucina-
tions represent vague forms, lights and colours.
Dyslexia: Impaired ability to comprehend the written words (reading difficulty) in the
presence of good vision and hearing, generally seen in children who may be stigmatised as
dull or mentally retarded. Dyslexia in milder form may persist in adults, and go unnoticed.
Non-Visual Symptoms of Ocular Disorders

Like visual symptoms, the list of non-visual symptoms is also very long, which may be
associated with visual symptoms as well. They are:
(a) Redness
(b) Watering
(c) Discharge
(d) Dryness
(e) Itching
(f) Pain in and around the eye
(g) Change in appearance of the eye
(h) Growth of the eye and its adnexa
(i) Change in colour of the cornea
(j) Change in colour of the pupil
(k) Change in colour of the lids
(l) Whitening of eyebrow and lashes
(m) White spot on the conjunctiva (Bitot’s spot)
Redness of the eye This is a very common symptom. It can be associated with pain
or may be painless. It can be unilateral or bilateral, generalised or localised. It may be
associated with watering discharge, displacement of globe, diminished vision, etc.
Causes of redness of the eye are:
1. Conjunctivitis—infective or allergic
2. Trauma
3. Sub-conjunctival haemorrhage
4. Keratitis
5. Iridocyclitis
6. Acute and chronic congestive glaucoma
7. Episcleritis and scleritis
8. Pterygium
9. Conjunctival growth
Causes of redness of the eye with pain are:
1. Trauma
3. Keratitis
4. Corneal ulcer
5. Herpes zoster
8. Endophthalmitis
Causes of redness of the eye without pain are:
1. Simple allergic conjunctivitis
2. Spring catarrh
3. Phlycten (conjunctival)
4. Pterygium
5. Non-traumatic sub-conjunctival haemorrhage
6. Angular conjunctivitis
7. Trachoma
8. Chronic dacryocystitis
➤ Unilateral redness of eye is seldom conjunctivitis

➤ Other causes of redness should be looked for
➤ Bilateral redness of eyes need not be conjunctivitis always
Watering from the eye Normal eyes are always wet; however an average person
is not aware of the wetness. A person becomes aware when either there is excessive pro-
duction of tear or there is normal tear production with inadequate drainage. Tradi-
tionally, the former is called lacrimation and latter epiphora. Recently, it has become
common practice to use epiphora for both; and lacrimation is only referred to as reflex
epiphora.
Lacrimation is always due to irritation of the fifth nerve in the eye, adnexa or sur-
rounding structure. It can also be psychological in nature.
Causes of lacrimation are trauma, foreign body, allergy, infective conjunctivitis,
corneal ulcer, keratitis, lagophthalmos, proptosis, entropion, trichiasis and ectropion.
Causes of epiphora are coloboma of lower lid, lagophthalmos, ectropion of lower lid
and puncta, obstruction of puncta and canaliculi, chronic dacryocystitis, absence of
sac, and nasolacrimal duct blockage.
➤ Acute watering is generally lacrimation

➤ Prolonged watering is invariably epiphora
Discharge from the eye Discharge from the eye may be from the conjunctiva,
lacrimal sac or orbital sinus. Conjunctival causes of discharge can be mucopurulent
conjunctivitis, or purulent due to ophthalmia neonatorum, gonococcal conjunctivitis
in adults. Ropy discharge is characteristic of spring catarrh.
Chronic dacryocystitis may be associated with mucopurulent or purulent discharge
on pressing the sac. A discharging sinus of orbit or paranasal sinus may open in the
conjunctival sac.
Blood discharge is seen in cases of trauma, membranous and pseudo-membranous
conjunctivitis, papilloma of the conjunctiva, haemangioma of conjunctiva, oculo-
sporidiosis, blood dyscrasia and haemorrhagic conjunctivitis.
Dryness of the eye (scanty tear formation) Generally the patient does not com-
plain of reduced tear formation but complains about irritation, pain and redness,
which are produced by scanty tears. When dryness of the eye is pointed out to the
patient, then the patient may come forward with the information that even during
crying, there is either very little or no water. Causes of dry eye are grouped under dry
eye syndromes (see Chapter 11).
Itching of the eye Itching of the eye is very common in children; it is generally
bilateral and seasonal. It may also be seen in adults and may be perennial.
Causes of itching of the eye are spring catarrh, acute allergic conjunctivitis, seasonal
allergic conjunctivitis, perennial allergic conjunctivitis, giant papillary conjunctivitis,
systemic allergy, chronic follicular conjunctivitis, blepharitis and drug-induced aller-
gic conjunctivitis.
➤ Trachoma, pterygium and phlycten do not cause itching per se
Pain in and around the eye Causes of pain in the eyeball are trauma, iritis, irido-
cyclitis, acute and chronic congestive glaucoma, corneal ulcer, herpes zoster, episcleri-
tis, scleritis, endophthalmitis and absolute glaucoma.
Causes of tenderness in the eyeball are iritis, iridocyclitis and retrobulbar neuritis.
Causes of pain on movement of the eye are retrobulbar neuritis, optic neuritis and
myositis.
Causes of pain around the eye are stye, infected chalazion, lid abscess, acute dacry-
ocystitis, dacryoadenitis, orbital cellulitis, superior orbital fissure syndrome, cavernous
sinus thrombosis, lid abscess, fracture of orbit, sinusitis, herpes zoster and trigeminal
neuralgia.
Causes of tenderness in periocular structures are trauma, stye, infected chalazion, lid
abscess, acute dacryocystitis, acute dacryoadenitis, sinusitis and fractured orbit.
➤ White eyes are generally not painful

➤ Yet all red eyes need not be painful
Change in appearance of the eye Causes of change in appearance of the eye are:
1. Narrow palpebral aperture: Ptosis, pseudoptosis and soft eye
2. Wide palpebral aperture: Lagophthalmos and lid retraction
3. Proptosis and exophthalmos
4. Squint
5. Pterygium, growth of conjunctiva, corneal opacity and staphyloma
6. Loss of eyebrow: Idiopathic, senile, hypothyroidism, leprosy and burns
7. Loss of eyelashes: Idiopathic, senile, blepharitis, trachoma and burns
Growth of the eye and its adnexa Intraocular growths go unnoticed until they
produce other symptoms of loss of vision, pain, redness, etc. Extraocular growths are
prominent. They can arise from lid, lacrimal gland, conjunctiva and orbit. They can
be benign or malignant, primary or secondary.
Change in colour of the cornea This may be due to corneal opacity or corneal
ulcer, blood staining of cornea, blood in anterior chamber and tattooing.
Change in colour of the pupil This may be due to congenital cataract, traumatic
cataract, senile cataract, retinoblastoma or other diseases simulating retinoblastoma.
Change in colour of the lids If the colour of lid turns white, it may be due to
albinism, vitiligo, leprosy, burns, scar, sympathetic ophthalmia and Vogt Koyanagi
syndrome.
If the colour of lid turns dark, it may be due to birthmark, haemangioma, neuro-
fibromatosis, nevus, black eye, spring catarrh or idiopathic.
Whitening of eyebrows and lashes The causes are physiological, sympathetic

ophthalmia, Vogt Koyanagi syndrome and albinism.
Mixed Symptoms of Ocular Disorders

There are many conditions where both visual and non-visual symptoms coexist. Some
examples are errors of refraction and squint, squint and amblyopia, pterygium and
diminished vision. There can be many such combinations.
Non-Ocular Symptoms
The commonest non-ocular symptom with which the patient comes to the ophthal-
mologist is headache followed by vertigo. Most frequent non-ocular symptom with
which a patient is referred to ophthalmic checkup is also headache. Acute headaches
without ocular signs are most often not related to eye. Ocular causes of headache con-
stitute a small group of causes.
Some of the important ocular causes of headache are:
1. Uncorrected error of refraction: Large errors of refraction are less likely to cause headache.
Myopia causes headache less frequently than hypermetropia. Astigmatism is a very common
causes of ocular headache; oblique axis causes more trouble than vertical or horizontal axis.
2. Wrong glasses: Hypermetropic children may be prescribed myopic glasses
Presbyopia: Uncorrected, over or under corrected
3. Accommodation and convergence disparity
4. Muscle imbalance: Both phorias and tropias can cause headache. Paralytic squint can cause
headache, or headache may be due to raised intracranial tension, hypertension or diabetes.
Muscle imbalance for near can especially cause headache
Headache radiated to the distribution of the fifth nerve on the same side can be due to
iritis, iridocyclitis, acute and chronic congestive glaucoma, absolute glaucoma, endoph-
thalmitis, panophthalmitis, proptosis, Tolosa Hunt syndrome, oculomotor palsy due to
posterior communicating artery aneurysm or diabetes, chronic granuloma of orbit and
post-herpetic neuralgia.
➤ Posterior uveitis and retinitis do not produce headache or pain in the eye
➤ Spectacles will not relieve headache unless it is due to asthenopia
➤ Headache may be independent of error of refraction
HISTORY TAKING IN OCULAR DISORDERS
History of a disease is the keystone that binds subsequent diagnosis in all branches of
medicine; ophthalmology is no exception. It is rewarding to take a proper history and cor-
relate it with the symptoms. Some of the symptoms and their clinical presentation may
directly lead to a diagnosis. For example, a school going child finds it difficult to see the
letters on the blackboard in the classroom but has no difficulty in reading his books.
Obviously this child is suffering from an error of refraction, most probably myopia. In
contrast to this, a grandfather who has been using glasses for reading finds that, of late,
he can read his newspaper without glasses, although his distant vision has diminished
considerably. This indicates that he is suffering from central nuclear sclerosis. There are
numerous instances where history directly leads to diagnosis. A patient may use local jar-
gon or a term that may mean different symptoms to different persons especially the cli-
nician. A patient may report that he has night blindness. On questioning it is revealed
that he actually finds it difficult to read at night due to dim illumination. In fact he is suf-
fering from presbyopia.
Pain is a very personal sensation. Threshold of pain varies among individuals; chil-
dren have better tolerance for pain but are more apprehensive about the mode of treat-
ment. Many adjectives are prefixed to pain, e.g. mild, severe, dull, throbbing, bursting,
boring, etc.
However, history alone is not always sufficient in clinical ophthalmology. It should
be backed by clinical signs, symptoms, usual clinical procedures, routine investigations
and special investigations.
History should be elicited under following heads:
1. History of present illness
2. Past history of ocular and non-ocular diseases and treatment taken
3. Allergy and drug reaction
4. Family history
5. Occupation
6. Personal history
History of Present Illness

History of present illness should give information regarding the onset of disease, whether
sudden or gradual, acute exacerbation on chronic disease and recurrence of a treated
disease. In acute cases patient may be able to state not only the date of onset but also the
hour of onset. In chronic cases the patient is not very sure of the date and time.
Unilateral or bilateral: If bilateral, did the other eye get involved simultaneously or
was there a gap of some days, and if the condition is equal in both eyes.
Symptoms: Visual, non-visual or combination of both. Is it painful or painless. The
exact location of pain or tenderness. Does it radiate? Is there an improvement with
treatment? Has it remained the same? Has it worsened?
Treatment: Has the patient taken any treatment, may be a home remedy, or prescribed
by a general practitioner or a specialist. Details of medicine, its dose and frequency
should be noted.
Trauma: Trauma is one of the major causes of ocular morbidity. A child may pre-
fer to hide history of trauma, while in a medico-legal or labour dispute, the patient
may try to overplay the role of trauma.
Past History
Past History of Ocular Disease
It may be related to the present disease, e.g. history of blunt injury leading to the
development of cataract, hyphaema or even rupture of globe and retinal detachment.
Stye, chalazion and infective conjunctivitis in childhood cannot be correlated to
cataract or glaucoma in later life but a child who has been under treatment for spring
catarrh by steroids may develop diminished vision due to steroid-induced cataract,

glaucoma or both. A patient may have a disease in the other eye, which is not related
to the present disease or a similar disease may develop in other eye later. Common
examples are iridocyclitis, episcleritis, scleritis, myopic retinal detachment and age-
related macular degeneration.
Past history of surgery: Common instances are a patient of amblyopia who has had
squint correction, a patient of retinal detachment with a history of lens removal, or
someone with hypotony following glaucoma surgery. Question should be asked
regarding the age at which the surgery was done? Was it followed by another opera-
tion? Did the vision improve following surgery? (The patient may not be able to state
the exact nature of surgery performed.)
Spectacles: It should be ascertained whether the glasses are for distance, near or both;
age at which the glasses were prescribed for the first time and the purpose of it. Has
the power changed since then and if so how often and how much? Could the patient
read the last line in the vision chart when last prescribed? Were they prescribed by
a qualified optometrist, optician or ophthalmologist or by a non-qualified person?
Past History of Systemic Disease

(a) Infective diseases—tuberculosis, syphilis, leprosy, gonorrhoea, diptheria and meningitis
(b) Metabolic disorders—diabetes and dysthyroid state
(c) Autoimmune diseases—rheumatoid arthritis, Reiter’s disease and Still’s disease
Allergy and Drug Reaction

(a) Exogenous: Dust, fume, pollen, husk, fur, nylon, wool and food
(b) Endogenous: Patient may not be able to state
(c) Drug: Local instillation of antibiotics, atropine, pilocarpine, iodine containing drops and skin
lotion, local anaesthetics or systemic anaesthetics. Acetazolamide, sulpha drugs, analgesics and
antibiotics
Family History
Many ocular disorders have a strong genetic background, which becomes more pertinent
in cases of consanguinity among parents, e.g. errors of refraction, squint, glaucoma,
cataract, dystrophies, abiotrophies, diabetic retinopathy and hypertensive retinopathy.
Infective disease, both acute and chronic, may inflict members of a family or society—
trachoma, acute epidemic conjunctivitis, tuberculosis and sometimes leprosy. Some
maternal infections are passed to the child, e.g. rubella, syphilis, gonorrhoea and AIDS.
Occupation
Some occupations pose a threat to vision, e.g. blast furnace workers, glass blowers and
people employed in the drug industry. People working on lathe machines are prone to
foreign bodies in the eye, both intraocular and extraocular.
Personal History
Smoking and drinking may lead to chronic retrobulbar neuritis and toxic amblyopia.
■ ■ ■ CHAPTER 2
E XAMINATION OF V ISION AND
R ECORDING OF V ISUAL ACUITY
From Chapter 1 it is obvious that ocular symptoms outnumber non-ocular symptoms.

Out of ocular symptoms, visual complaints are far more common than non-visual symp-
toms. Hence, evaluation of visual status of a patient is of extreme importance in the
clinical examination of an eye. Visual evaluation should get priority over the rest of
the examination; this should be first, followed by others.
The visual evaluation comprises the following:
A. Distant vision
B. Near vision
C. Colour vision
D. Field of vision
E. Night vision
In a given patient all of these need not be subnormal, various combinations are possible
in the same patient and same eye.
➤ Recording of vision is not only of diagnostic, therapeutic and prognostic value, it has
tremendous legal value that should not be overlooked in clinical ophthalmology
There are individual variations in recording of vision. Each ophthalmologist has his/her
own style and follows a particular school of training.
It is customary to record distant and near vision in the following order.
Vision without glasses is noted in the right eye first and then the left, followed by both
the eyes together. Binocular vision is better than uniocular vision which was recorded
separately, unless one eye is not fixing, may be amblyopic, or blind. Recording of vision
with glasses is followed by examination without glasses in the same order. Next step,
one should find out if the glasses used are for distance, near, or both, their type and
power.
Most widely used method to examine distant vision is to use Snellen’s chart (Fig. 2.1)
in the language of the literate patient.
For illiterate persons various types of modification like E chart (Fig. 2.2), Landolt’s
broken C (Fig. 2.3), Allen picture chart (Fig. 2.4), and dots are available. Landolt’s C and
E charts are most accurate, they are better than alphabets of Snellen’s charts. STYCAR
(Snellen’s test for young children and retarded, Figs 2.5 and 2.6) is used for children.
The charts are generally used at a distance of 6 m or 20 ft from the patient and kept
straight.
EXAMINATION OF VISION AND RECORDING OF VISUAL ACUITY 15
Snellen’s charts consist of clearly inscribed black letters on white background. There
are 28 letters arranged in seven rows. First line has a single and largest letter, seventh
has the smallest letters. Size of the letters gradually diminishes in a ratio of 10 : 6 : 4 : 3 :
2 : 1.5 : 1, i.e. the topmost letter is 10 times larger than the letters in seventh row. The
number of letters increases as size diminishes in successive lines.
60 H
A L
E
36 60
T N C E
E
24 36
O L H A E E
E
18
24
E C T N O E E
E E
E
12 18
9 C L O H N A
E E
E
E
12
6 A E L O H C T
E E E
E
E
E
9
5 H T N E L A C O
E
6
E
E E
E
E
E
4 A E C O H N T L
Fig. 2.1 | Snellen’s chart. Fig. 2.2 | E test types.
c
c c
c
c
c
c
c
c
c
c
c
c
c
c
c c
c
c
c
c
c c
c
c
c
c
Fig. 2.3 | C chart. Fig. 2.4 | Allen pictures.

The charts are of two types:

1. Self-illuminated rotatory drums, which can be revolved round either a vertical or a horizontal
axis manually or electrically. The panels of these drums are actually fitted in rectangular boxes
and are translucent
2. Letters written on opaque white boards that are externally illuminated
H
LX
V T A U
V
A
C H T
X 0 T
X U L
T O H H C
A X O L
Fig. 2.5 | STYCAR (Snellen’s test for young children and retarded) chart (left) to be used at 6 m. Small card
(right) to be held by child to point out to the matching letter.
F N P R Z
60
metres
200 1-0
(feet )
48
(160)
E Z H P V 0.9
38
(125)
D P N F R 0.8
30
(100)
R D F U V 0.7
24
(80 )
U R Z V H 0.6
19
(63 )
H N D R U 0.5
15 (50)
Z V U D N 0.4
12 (40) V P H D E 0.3
9 .5 (32) P V E HR 0.2
7.5 ( 25) E H V D F 0.1
6 ( 20) N U Z F E Log MAR 0
4 . 0 :161 U H N Z R
3 0 ( 12.8 ) D N E F P
3 . 0 ( 10 ) P U E P I
Fig. 2.6 | Minimal angle of resolution in minute is MAR. Bailey–Lovie Log MAR chart for distant and near vision.
If there is shortage of space, then instead of 6 m, 3 m distance is used with changed

position of drum in relation to the patient. The patient sits under a reversed chart and
looks at a plain mirror in front, fixed at a distance of 3 m. As the patient looks into
the mirror he gets a virtual, erect, laterally reversed view of the chart that seems to be
at 6 m of distance. In still smaller places two plane mirrors and one usual chart is used
with suitable adjustment of mirrors. A proportionately reduced smaller distance chart
is also available, which is good for home visits, non-ambulatory patients, school surveys
and mass screening. As rays arising from 3 m are slightly divergent, a person may use
accommodation or may move a little forward resulting in wrong assessment of vision,
especially in children. Letters of the Snellen’s chart can be projected on a suitable screen
as well.
Method of Recording of Vision

The patient sits comfortably in front of a vision drum kept at 6 m away in a nor-
mally illuminated room. The right eye is tested first. The other eye is occluded com-
pletely without exerting pressure on the globe. Various methods of occlusion are given
below:
1. Occluder
2. Hand-held occluder
3. Palm of the patient
In children, it is better to close the eye with the palm of the examiner. Otherwise they
try to peek over the occluder.
Trial frame (Fig. 2.7): These are spectacle frames in which lenses and other optical
devices like occluder, pin hole, stenopeic slit, Maddox rod and prisms can be put and
removed at ease. They have an adjustable nose bridge and a pair of sidebars. The rims
are open on the upper side and have slots for multiple devices. The fronts of the rims
have axis of cylinder etched on their faces. The numbering is done according to uni-
versal convention where zero is marked on temporal side of right eye and nasal side of
left eye, 180⬚ on nasal side of right eye and temporal side of left eye, 90⬚ is vertically
down in mid position. The axis is marked at an interval of 5⬚, which is sufficient for
usual clinical work. The trial frame should be light and well fitted with provision to
adjust intrapupillary distance. They are generally available in two sizes, adult and
child. They may also be hand held or fixed to a headband.
A very sophisticated trial frame is incorporated in refraction unit.
0 Rt 180 0 Lt 180
45 135 45 135
90 90
Fig. 2.7 | Notation in a trial frame.

CONSTRUCTION OF LETTERS IN SNELLEN’S CHART
Vision denotes the smallest retinal image, which can be appreciated correctly at a given
distance. This depends upon the intensity of light, spectrum of light and distance.
Area of retina-stimulated plays a very important part in visual acuity. Vision is maxi-
mum at the fovea and falls sharply at the periphery. Vision on the retinal periphery is
one-tenth of foveal vision in the normal eye, and that is why a patient with a small
macular lesion may not be able to read more than two lines on a Snellen’s chart, while
a patient with extensive peripheral lesions and unaffected macula may have very good
vision. It is customary to state that parallel rays form a pinpoint image on the macula
to give good vision. In clinical practice it is presumed that a pencil of rays form a
minute circle of clear vision, called circle of least diffusion. The larger the circle of least
diffusion, the poorer the vision. Diameter of an ideal circle of least diffusion is
0.04 mm. This forms the basis of construction of the Snellen’s chart.
In a typical Snellen’s chart, the letters are so constructed that one line of each letter
forms a square, which forms an angle of 5 min on the fovea at a specific distance. For
example the top letter forms an angle of 5 min at a distance of 6 m; this angle will
enlarge if the letter is moved nearer to the patient, and diminish if it is moved away,
making it blurred (Figs 2.8–2.10).
Each square is divided into 25 smaller squares of equal size. Each square forms an angle
of 1 min on the fovea. An angle less than 1 min which is equal to 0.04 mm, is not visible
to the eye. This is the diameter of ideal circle of blur or minimal separable distance that
can be differentiated by fovea.
➤ One degree ⴝ 1/360th of a circle. 1/60 degree ⴝ 1 min

➤ Thus each arm of a letter should form an angle of 1 min to be visible at a given
distance
5 min
5 min
1 min
1 min 1 min
Fig. 2.8 | Construction of Snellen’s letter and Landolt’s ring.

6/36 6/26 6/12
H C E
Fig. 2.9 | H, C and E subtend an angle of 5 min at 36, 24 and 12 m, respectively.

E E E 12 m
24 m
36 m
Fig. 2.10 | Letter of same size when brought nearer subtends larger angle.
In MAR chart (Fig. 2.6), optotypes of subsequent lines differ by a logarithmic differ-
ence. The charts are larger than usual Snellen’s chart and are used at 4 m. In Snellen’s
chart, the size of the letters (optotypes) changes by half octave after 6/36 and is noted
as 6/60, 6/36, 6/24 and 6/18, etc.
If a person cannot see the top letter, following options are available:
1. Increase the size of the letter till it becomes visible
2. Reduce the distance between the chart and the patient
The first option is not practical. However with letters projected on a screen in place
of the usual charts, the size of a letter may be changed at will. The second option is
used to record vision if the top letter is not visible.
HOW TO RECORD LEVEL OF DISTANT VISION
Vision is recorded as a fraction in which the denominator denotes the distance at

which the letter should be visible and the numerator indicates distant at which the let-
ter is visible.
The top letter in a standard vision chart should be visible at a distance of 60 m in
a normal eye. If it is visible at 6 m it is written as 6/60, similarly 6/36 means that the
letter that should be visible at 36 m is visible at 6 m. The same fraction can be written as
6/60 ⫽ 1/10 ⫽ 0.1 or 20/200, where 200 stands for distance in feet. A normal eye should
be able to read the seventh line at a distance of 6 m and it should be written as 6/6.
If the patient cannot make out the top letter at 6 m on a standard chart, the patient
is moved by 1 m at a time until the top letter becomes clear.
If it is visible at 5 m it is noted as 5/60, at 4 m as 4/60 and then 3/60, 2/60 and
1/60, respectively, as the patient is moved by 1 m at a time.
A patient with 5/60 vision may be able to read the second or third line, i.e. he can
read 6/36 or 6/24 line, if moved by 1 m towards the chart, e.g. 4 m from it. It will be
inappropriate to write 5/60 as 4/36 or 4/24.
If the patient cannot see the top letter at a distance of 1 m then attempts to record
vision on the vision chart are given up and the patient is asked to count fingers of the
examiner at various distances. This is noted as FC or finger counting. The distance at
which the patient can count fingers is noted. For example, counting fingers at a distance
of half a meter is noted as FC half meter. A single finger count may be guesswork by
the patient. At least three accurate counts should be taken as correct.
Finger count can be roughly translated into Snellen’s factor, since thickness of the
adult finger is almost the same as that of a single line of the top letter. A patient with
6/60 vision should be able to count fingers at a distance of 6 m. Therefore 6/60 ⫽ FC
6M, 5/60 ⫽ FC 5M, 1/60 ⫽ FC 1M roughly.
If the patient is unable to count fingers at 1 m, the examiner moves his palm in
front of the eye and asks if the patient can see something moving. If a patient appre-
ciates the movement of the hand, it is noted as hand movement and recorded as HM.
While eliciting the ability to count fingers or ability to appreciate movement of the
hand, the examiner’s finger or hand is used as an object and not the patient’s; even a
blind person can say if his own hand is moving or not. If a patient’s vision is less than
hand movement, his ability to perceive light is tested and recorded as perception of
light (PL).
How to Test Perception of Light

To test PL one eye is completely closed so that no light reaches it. Light is then flashed
in the uncovered eye and the patient is asked if he can sense this light. If the patient
fails to do so, vision is recorded as no perception of light or NO PL.
While recording the vision of a person, it is the maximum vision present that should
be noted, e.g. a patient, who can read the top letter from 6 m (6/60) will surely be able
to do so from 5 and 4 m. The patient will have FC, as well as HM, but it should be
noted as 6/60 and not as 6/60 with CF, hand movement and PL. Absence of light per-
ception should be recorded as NO PL and not blind.
➤ Perception of light is the ability to perceive light anywhere on the retina.

It is not a macular function test. A patient may have an extensively scared
macula but will retain perception, while other macular functions may be
absent or faulty
Causes of loss of perception of light

Causes are total disruption of optic nerve, trans-section of optic nerve, avulsion of
optic nerve, primary, secondary and glaucomatous optic atrophy, central retinal artery
occlusion, extensive retinal lesion and total retinal detachment.
➤ Any amount of opacity of media may it be corneal, lenticular or vitreous with intact
retina and optic nerve will not produce loss of perception of light. Perception of light
once lost is lost forever
Projection of Light
So far the methods employed were used for recording central vision. It has already
been noted that peripheral vision is less than central or foveal vision. However, in the
presence of a good central vision, the periphery may be extensively defective and vice
versa. It is of extreme importance that both peripheral and central vision be noted for
complete evaluation of visual status of an eye.
➤ Projection of light denotes gross retinal function at the periphery

➤ Central vision denotes function of cones
➤ Peripheral vision shows function of rods
How to Examine Projection of Light

Projection of light is the ability to perceive light at the retinal periphery. To examine
the projection of light, the patient is asked to look straight and the other eye is closed.
A small beam of light is thrown from various directions. The patient is asked to state
the direction of light, the direction is noted down, projection of light is recorded as
PR and the direction is noted along with it. Presence of projection of light is denoted
as ⫹ and absence as ⫺. For example PR ⫹ ⫹ ⫹ ⫹ means projection from all quadrant,
PR ⫹ ⫹ means projection from two quadrants. The quadrant in which projection
is present is noted as superior, lateral, inferior and medial. When the patient can see
light coming from the temporal side his nasal retina is stimulated and tested, similarly
if the patient can see light from the nasal side then his temporal retina is stimulated
and tested.
It is generally believed that projection should be tested only when vision is reduced to
perception of light and not with any other level of vision. In case of retinal detachment
of lower part, the patient may have 6/36 or better vision with faulty projection infe-
riorly. Similarly a patient with advanced chronic simple glaucoma may have HM and
faulty projection. Hence, it should be a routine practice to test projection of light with
every level of visual acuity noted.
Causes of faulty projection are:
2. Long-standing glaucoma
3. Advanced retinal dystrophy
4. Central artery obstruction
5. Post-papilledematous optic atrophy
Points to Remember in Recording Distant Vision

1 First examine the right eye
2. Close the left eye while testing right eye
3. Record maximum vision
4. If there is no perception, write it as NO PL and not as blind
5. Test projection with every level of vision
6. Repeat it in the left eye
7. Record vision in both eyes together
8. Take every possible care while recording vision in eyes of children, as they may
memorise Snellen’s Chart, see through the other eye or peek over the occluder
Method of Documenting Distant Vision

Vision in the right eye is preceded by the abbreviation RE and left by LE. If abbrevi-
ation RE and LE are not inscribed then vision appearing on the left side of the paper
or on the top is taken as belonging to the right eye, e.g.
1. RE 6/60 LE 6/36 or 6/60 6/36
2. RE 6/60 6/60
LE 6/36 6/36
Vision in both eyes together is preceded by the abbreviation BE.
The other method is using letters OD, OS and OU standing for RE, LE and BE,
respectively.
Letters OD mean oculus dexter, OS mean oculus sinister, and OU mean oculus
uterque or unitas.
Recording of Near Vision

In a normally illuminated room, the patient is given a near vision chart of Snellen’s or
Jaeger’s to read at his normal working distance. Though near vision is tested in both
eyes simultaneously, the more scientific method would be to test it in the two eyes sep-
arately. While testing near vision, distant vision should be tested first it as there may be
difference in vision in the two eyes. In presbyopic age, a patient with uniocular myopia
uses the myopic eye for near and the emmetropic or hypermetropic eye for distance
and does not require a near correction.
The near vision charts may have letters rather than sentences, dots, Landolt’s broken
C or E to read. The size of the letters gradually reduces from bottom towards top. They
are designated between 5 and 48, each prefixed by the letter N or J depending on the
type of chart used, e.g. N5, N6, etc.
Causes of diminished near vision
Commonest cause of diminished near vision is presbyopia followed by uncorrected
facultative hypermetropia and aphakia. If the patient uses glasses for near vision,
power of glasses should also be recorded.
Examination of Spectacles of the Patient

After recording the distant vision attention should be directed towards the patient’s
spectacle or spectacles.
Each pair of spectacles should be examined to find out if it is for distance, near or for
both. Is it bifocal, unifocal, multi-focal or progressive? While examining spectacles the
patient should be asked if he/she is using any other magnifier for near as well as distant
vision, e.g. low vision aids or contact lenses. The next step is to find out the type and
power of the lenses in the patient’s spectacles.
Procedure to examine spectacles (Plates 2.1 and 2.2)
1. Hold the spectacle by the frame and not by the lens
2. The lenses should be very close to the eyes of the examiner
3. Look at a distant object
Plate 2.1 | Correct method to find out type and power of a given glass. Hold the glass very near the eye and
see shape, size and movement of a distant object.
Plate 2.2 | Wrong method. Holding glasses away from the eye and looking at a near object.
4. Move the lenses from side to side, up and down and rotate to note the movement and the
size of the object and any distortion
Spectacle Lenses
A lens is an optical device, which has at least one curved surface. Optical lenses are of
two types:
1. Convex or converging lenses
2. Concave or diverging lenses
Divergence is also known as negative convergence. For calculation and reconstruction
of images the rays are always presumed to travel from left to right. Those lenses in which
parallel rays are brought to focus on the right side of the lens are plus or converging
lenses, while those in which rays come to focus on the left-hand side of the lens are
divergent or negative lenses.
Biconvex Plano-convex Concavo-convex Biconcave Plano-concave Convexo-concave
Fig. 2.11 | Types of lenses.
Fig. 2.12 | Movement of image in a plus sphere.

Based on shape lenses can be plano-convex or plano-concave, when one surface is plane
and other surface is convex or concave, respectively. It could be biconvex or biconcave.
It could be concavo-convex or convexo-concave; the last word denoting the type of lenses
(Fig. 2.11).
A lens can be spherical, cylindrical or sphero-cylinder. The first two can either be plus
or minus sphere or plus and minus cylinder. Sphero-cylinders are those lenses that have
both spherical and cylindrical components. They could be of the same type, e.g. plus
sphere with plus-cylinder or minus-sphere with minus-cylinder; these are called com-
pound sphero-cylinder. The next combination is the combination of sphere and cylinder
of opposite signs and they are called mixed sphero-cylinders, where the value of the cylin-
der is always more than that of the sphere and opposite in sign.
To find out the type of lens, it should be held between the thumb and index finger
by the edge and not the substance and is kept as near as possible to the eye of the exam-
iner. A distant object is seen through the lens. The lens is then moved by the following
three movements:
1. Move side to side
2. Move up and down
3. Rotate between thumb and index finger
4. Do not focus a near object
5. Do not move the lens in anterio-posterior direction
These rules are applicable for spectacle lenses also.
Characteristics of plus sphere (Fig. 2.12 and Table 2.1)
1. The image moves opposite to the direction of movement of the lens, i.e. if the lens is moved
to the right, the image moves to the left
2. Movement is equal in all directions

3. There is no distortion of the image on rotating the lens
4. There is magnification of the image
5. Thickness of the lens is maximum at the centre
Characteristics of minus sphere

1. The image moves in the direction (Table 2.1) of the lens, i.e. if the lens moves to the right the
image also moves towards the right
2. The movement is equal in all directions
3. There is no distortion of the image on rotation of the lens
4. There is minification of the image
5. Thickness of the lens is minimum at the centre
A spherical lens is part of a sphere, hence it has equal power in all meridians and
parallel rays are brought to a pinpoint on the focal point.
A cylindrical lens is part of a cylinder, it has power in one meridian and parallel rays
are brought to focus as a line at the focal plane.
Characteristics of a plus cylinder
1. The image moves against in one direction
2. There is no movement at right angles to this meridian
3. The image is elongated at right angles to the axis and shortened in the direction of the axis
4. When the cylinder is rotated, there is distortion of image (Fig. 2.13)
Characteristics of a minus cylinder

1. The image moves with one direction
2. There is no movement at right angles to this meridian
3. The image is elongated along the axis of the cylinder and shortened at right angles to the axis
4. When the cylinder is rotated, there is distortion of the image
Table 2.1 Comparison between characteristics of plus and minus sphere (Fig. 2.13)
Characteristics Plus (Convex) Minus (Concave)
Movement of image Against With

Distortion on rotation Nil Nil
Size of image Magnified Minified
Thickness of lens Maximum at the centre Minimum at the centre
Edge of lens Thin Thick
AV
AH AH
AV
Fig. 2.13 | Changes in the size and shape of the image due to alignment of axis in plus cylinder. AH ⫽ hori-
zontal axis; AV ⫽ vertical axis.
Method to Find Out Power of a Lens

Hand neutralisation To neutralise a lens, the first step is to find out whether it is
convex, concave or mixed lens. Next, find out whether it is a sphere, a cylinder or a
sphero-cylinder. Start putting spherical lenses of the opposite sign very close to the
lens and observe the movement of the image. Keep on adding lenses until one meridian
is neutralised. In spherical lenses, a single sphere of the opposite sign neutralises all
meridians. In cylindrical lenses, a sphere of the opposite sign will neutralise only one
axis; the other axis will show opposite movement equal to the cylindrical value.
To neutralise a plus one cylinder if a minus one sphere is used, it will neutralise the
cylindrical value but will add an equal amount of cylindrical value of the opposite sign
at right angles to the cylinder. It would be best to use a cylinder of the opposite sign
and same power, in the same axis, to neutralise a cylinder.
To neutralise a compound sphere, first neutralise the sphere with a sphere of the
opposite sign and then add a cylinder of the opposite sign in the appropriate axis.
A lensometer is an optical device that is used to find out the power of a lens. There
are two types of lensometers: fully optical and computerised automatic.
The optical lensometer consists of a small telescope mounted on a stand, which
looks like a clinical microscope. The image of a target, which is in-built, is focussed
by a standard lens. The unknown lens is now inserted in the system and the target is
focussed again. The difference between these two readings gives the power of lens at
particular axis. The instrument can also be used to find out:
1. Power of the sphere
2. Power of the cylinder
3. Axis of the cylinder
4. Optical centre of the lens
5. Value of the presbyopic addition
Automated computerised lensometer The basic principle is the same as any other
lensometer. This gives a quick and more accurate reading and digital print-out is also
available.
Power of an optical lens is measured in dioptre. This is a unit of measurement of
converging power (positive or negative) of a lens. It is the reciprocal of focal length in
metres. A lens of one diopter will have focal length of 1 m. The more the converging
power of a lens, the less is its focal length (Table 2.2).
Table 2.2 Relation between dioptre and focal length
Dioptre Focal length (cm)
10 10
5 20
4 25
2 50
1 100
0.5 200
Table 2.3 Type of spectacle lens and their uses
Type of lens Error of refraction
Plus sphere Hypermetropia, presbyopia and aphakia

Minus sphere Myopia
Plus sphero-cylinder Compound hypermetropic astigmatism
Minus sphero-cylinder Compound myopic astigmatism
Single plus cylinder Simple hypermetropic astigmatism
Single minus cylinder Simple myopic astigmatism
Mixed sphero-cylinder Mixed astigmatism and pseudophakia
Uses of lens in ophthalmology Lenses can be used either for therapeutic purposes,
i.e. to improve subnormal vision or in an instrument used for diagnostic purposes.
The former is in the form of spectacles, contact lenses, low vision aids or IOLs.
The latter is in the form of instruments of routine and special investigation, e.g.
ophthalmoscope, slit lamp, synaptophore, etc. (Table 2.3).
Prisms
Prisms are composed of two refractive surfaces that are inclined to each other. The line
at which the two surfaces meet is called apex, while the surface opposite to apex is
called base. The angle formed by two surfaces is called the refracting angle. Light pass-
ing through a prism is deviated towards the base and broken into seven colours, i.e.
VIBGYOR. As the emerging rays bend towards the base, the object seems to move
towards the apex. Thus, if two prisms of equal strength are put base together and apex
away, light will converge towards the base. If two prisms of the same strength are put
apex together and base away, the rays will diverge. Thus, two prisms with base against
each other will act as a convex lens and two prism with apex against each other will
act as concave lens. This principle is the basis of optics of lenses. A lens is said to be a
combination of multiple prisms. If two prisms of equal strength are kept base to apex,
they will act as a plate of glass (Figs 2.14 and 2.15).
Nomenclature of Prism
For all practical purposes, strength of a prism is measured in prism dioptre. It denotes
1 cm displacement of an image towards the apex when the object is kept at a distance
of 1 m from the prism.
Identification of a Prism
Identifying a single thick prism is not difficult as in single prism or prism bar. For
optical purposes, the prisms used are thin and low powered, and most of them are
incorporated into spectacle lenses or pasted on their surface, e.g. Fresnel prisms.
To find out if a given lens has prismatic value or not, hold the lens in the same fash-
ion as any other lens near the eye and look at a straight line at a distance. If a device has
a prism, the image of the line will move towards the apex and parallel with the base.
O
A
O
B
A I
B I
B B
O O
Fig. 2.14 | Identification of prism. A ⫽ apex, BB ⫽ base, OO ⫽ object, I ⫽ image.
(A) (B)
Fig. 2.15 | Optics of (A) convex lens and (B) concave lens.
Now rotate the prism by 90⬚, there will be no deviation of the image. Now add prisms
base to apex till there is no shift in first position, this will neutralise the prism (Fig. 2.14).
Uses of Prisms
1. Therapeutic uses: Prisms by themselves do not correct errors of refraction. They are used to
relieve diplopia and relax or reinforce convergence. In muscle imbalance they are prescribed as
base in, base up or down. The base may rarely be oblique.
2. The diagnostic instruments that contain prisms are:
(a) Maddox double prism
(b) Riddley’s rotating prism
(c) Synaptophore
(d) Direct ophthalmoscope
(e) Indirect ophthalmoscope
(f) Gonioscope
(g) Microscope
Types of Spectacle Lenses

Toric lenses: These lenses are curved lenses and curvatures are different, different in
meridians and in two surfaces. It is like a section through a teaspoon or an automobile
tyre. One meridian is more curved than the other. The meridian at right angles to the
steepest is flatter than the other meridians. Numerically lower value is called base curve.
In toric lenses, meridians of maximum and minimum curvature are at right angles to
each other. Toric lenses can be plus, minus or combination of both. They can be plano-
cylindrical. Toric lenses produce least distortion (Fig. 2.16).
Fig. 2.16 | Torus. Fig. 2.17 | Myodisc.
Fig. 2.18 | Lenticular lens. Fig. 2.19 | Aspherical lens.
Meniscus: Front surface is more curved than back surface. Power in all meridians is
the same.
Myodisc: These are high myopic lenses where peripheral part is devoid of power, the
peripheral surfaces are parallel, central 25–30 mm have corrective power. They are
used to reduce the overall weight of the lens (Fig. 2.17).
Lenticular: These are high plus lenses where central portion is thick and has correc-
tive power while peripheral surfaces are parallel; it gives an appearance of bull’s eye
(Fig. 2.18).
Aspherical lenses: In an aspherical lens, the inner curve is circular and spherical. The
outer curve is parabolic and aspherical (Fig. 2.19).
Coloured Lenses
White lenses (transparent) allow not only the visible spectrum of light between 380
and 760 nm but also some of ultraviolet, less than 360 nm and infrared, i.e. more
than 760 nm to enter the eye. Some of the ultraviolet and infrared lights are absorbed
by the lens. Both ultraviolet and infrared have harmful effects. Ultraviolet rays have
ionising effect on ocular tissues, specially cornea, conjunctiva and lens. Infrared rays
have a thermal effect. To avoid these effects of light, protective glasses are prescribed.
Unfortunately these coloured glasses are worn more for cosmetic reason than thera-
peutic value. Coloured or tinted glasses are also used to reduced glare in large pupils,
e.g. myopia, mydriasis, coloboma of iris and albinism. Therapeutic effect of tinted
glasses depends directly upon their ability to absorb ultraviolet and infrared part of
the spectrum. Various types of tinted glasses are available. A good tinted glass should
absorb all ultraviolet, and infrared, and 60–80% of visible light. These are made out
of glass as well as plastic. They are of two types. One which has a tint that does not
change with illumination. These are the usual goggles used for cosmetic purpose. The
second type of tint changes in intensity with varying illumination; brighter the light
darker the tint. Darkening occurs very quickly but lightening takes sometime. They
are known as photosun and photogrey. Special tinted glasses are prescribed in indus-
trial workers, e.g. welders, steel furnace workers and glass blowers.
EXAMINATION OF COLOUR VISION
Colour vision is a property of cones. Rods have very little colour sense. Colour vision
depends upon three factors; hue, saturation and intensity. Hue depends upon wave-
length, saturation depends upon its proportion to white, and intensity is brightness.
Hues are violet, blue, green, yellow, orange and red. Violet is nearer 380 nm while red
is nearer to 760 nm.
Colour blindness may be congenital or acquired. Congenital can be dichromatopsia
which is common colour blindness or achromatopsia, a rare form with subnormal
vision and nystagmus that is not seen in other types of colour blindness.
Dichromatopsia (Partial colour blindness) The three subgroups of this type are as
follows:
● Protanopia—Single-colour defect, confuse red with blue, green.
● Deuteranopia—Two-colour defect confuses blue and green with purple.
● Tritanopia—Confuses yellow and blue.
Normal persons are called trichromats, while those with colour defects are called
anomalous trichromats. They can recognise all bright and saturated colours and they
will call a leaf green and a ripe tomato red, but will not be able to match colours of var-
ious hues of red or blue. The different type of anomalous trichromats are protanom-
alous, deuteranomalous and tritanomalous.
➤ Colour vision defect is not true blindness because it does not produce diminished
vision. It may, however, be associated with defective vision
Monochromatism is rare. Blue blindness is generally acquired.
Why Should Colour Vision Defect Be Tested?

Some jobs require the ability to differentiate between coloured signals, like pilots,
locomotive drivers, electricians, weavers and artists. Dress designers also require good
colour sense. In some of these jobs people are disqualified due to defective colour
sense. It is better to screen colour defects in a child and let the child know about it to
plan for the future and save from embarrassment and disappointment in later life.
Acquired colour vision defect is seen in diseases of the macula and optic nerve.
Immature cataract also interferes with normal colour vision.
Various methods for testing colour visions are:
(a) Pseudo isochromatic plates (Plates 2.3 and 2.4)
(i) Ishihara plates
1 2
3 4
5 6
Plate 2.3 | Sample of Ishihara plate.

Person with Person with
Fig Normal person red-green total colour
deficiency blindness
1 12 12 12
2 29 70 X
3 5 2 X
4 6 X X
5 7 X X
6 X 5 X
The mark X shows that the plate cannot be read
Plate 2.4 | Corresponding index of Ishihara plate.

(ii) Hardy Rand Rittler plates
(iii) Stilling plates
(b) Farnsworth-Munsell: 100 hue test
Farnsworth-Munsell: D-15 test
(c) Edridge Green lantern
(d) Nagel’s anomaloscope
Ishihara plates—These are most commonly used devices. It is useful to detect red green
defect but not for blue yellow defects. The plates are made up of dots of primary colours
printed on background of similar dots of confusing colour. Primary coloured dots are
arranged in such a way that they form a number, which is visible to normal trichro-
mats. The person with colour vision defects will read them as some other number. To
test colour blindness the person is given an Ishihara plate to read and his answers are
noted down, which are later matched with a list attached to the plate at the end and
the type of colour vision defect is noted.
Examination of the Visual Field

When an eye fixes an object, it is not only the point of fixation that is visible but also
a large area around the point of fixation. All the area that is visible at a given time
around a point of fixation is the field of vision for that eye in that gaze. Visual field is
restricted superiorly by the superior orbital rim, medially by the bridge of the nose and
inferiorly by the maxilla. As there is no obstruction on the lateral side, hence this field
is widest. Visual fields of the two eyes put together is larger than that of a single eye.
Field of vision has been defined as—an island of vision in a sea of blindness. The peak
of the island represents maximum visual acuity, i.e. fovea. The optic disc which has no
vision acts as bottomless pit and represents, the blind spot. The visual field, besides patho-
logical defects, depends upon the size of the object, the intensity of light and colour of
the object. Coloured objects give less stimuli than a white object of the same size.
The visual field examination gives the following information:
1. Location of lesion, e.g. retina, optic nerve, chiasma and optic tract and radiation
2. Congruence
3. Side
4. Homonymous/heteronymous
Test object: Size of the test object is expressed in fractions. This represents the size
of the object used to plot the contour in relation to distance at which test is per-
formed. For example in a Lister perimeter that has a radius of 33 cm, the distance of
eye from the target is 33 cm ⫽ 330 mm. If an object of 3 mm in diameter is used, the
test object will be 3/330. These are also called test targets. The commonest colour is
white, but they can be any colour.
While recording field of vision the following should be noted—name of the patient,
eye tested, vision in the eye, size of test object used, and distance and colour of the
target. Size of the target varies between 1 and 50 mm.
Various methods of testing visual field are:
1. Confrontation method
2. Amsler grid: For papillo-macular defect within 10⬚
3. Perimeters: Arc perimeter and bowl perimeter. Perimeters are used mostly for peripheral field
but central field can also be recorded
4. Tangent screen: For 30⬚ central field
5. Multiple pattern field analyser
6. Automated perimeters
Confrontation method This is one of the most useful methods of charting both
central as well as peripheral field of vision. It can also give information regarding
colour field if tested with a coloured object like a small coloured medicine vial, small
white and coloured pins etc.
The patient and the examiner sit face to face 1 m away from each other, the eyes of
both are at the same level. To examine the right eye of the patient, the left eye is closed.
The observer closes his right eye. The patient is asked to fix the left eye of the examiner.
Now the observer moves his index finger of left hand from periphery to centre and the
patient is asked to say yes as soon as the finger becomes visible. This is repeated all around.
If the observer and patient’s area of visibility are same, the patient has normal field.
The other method is to ask the patient to count fingers of the observer in different
quadrants after the other eye has been closed. A medicine vial with a coloured cap can
be used to give coloured field, when moved in the same fashion. The field changes
shown on confrontation are gross and must be confirmed by other methods.
Amsler grid (Fig. 2.20) This consists of a 10 cm ⫻ 10 cm square that is divided

into 400 small squares, each 5 mm ⫻ 5 mm (Fig. 2.20A). The squares are printed on a
dull background, the lines being generally white. Any graph paper will also serve the pur-
pose. The outer square forms an angle of 20⬚ and each small square forms an angle of 1⬚.
The chart is held 30 cm from the eye under usual indoor illumination. The presbyope
should use reading glasses. When the chart is kept at a usual reading distance, it occupies
the central 10⬚ of the field and the blind spot is outside the chart. Thus the chart can be
used to locate field changes of 10⬚ round point of fixation, which is the geometrical cen-
tre of the chart. The chart is used to plot central and centrocecal field defects, both absolute
and relative and find out if there is any metamorphopsia. Thus, this can differentiate
between optic neuropathy and maculopathy. Any defect on the periphery of the chart could
be part of a larger field defect that should be tested and confirmed on the Bjerrum screen
(Fig. 2.20E).
How to use the Amsler grid: One eye is tested at a time, the other eye is closed. The
patient keeps the chart at usual reading distance and fixes the central point. The
patient is asked:
1. Can he see the central point? If the answer is no, the patient has an absolute central scotoma.
The patient is then asked to state the extent of scotoma. He may be asked to draw it
(Fig. 2.20B)
A B C
. . .
D E F
Fig. 2.20 | Interpretation of Amsler grid test.

2. If he can see the central point, is it as clear as the surrounding area? If it is duller than the sur-
rounding area, the patient has a relative scotoma (Fig. 2.20C)
3. Does the patient see blank spaces or holes away from the point of fixation? In this case, the
patient has a paracentral scotoma (Fig. 2.20D)
4. Are all the corners of the grid intact or is one of the corners or side missing? The patient has
a large scotoma that is extending beyond 10⬚ (Fig. 2.20E)
5. Are the lines are straight or wavy; a wavy outline means metamorphopsia (Fig. 2.20F)
Tangent screen or bjerrum screen (Fig. 2.21) This inexpensive device can be fixed
on a wall and does not require any electric supply or additional space. It is used to
chart central field defect within 308 around the point of fixation. It can be made on
a dull rigid cork or hard board. There is a prominent central point of fixation, and
around this point of fixation are drawn inconspicuous concentric circles at a difference
of 58. Six such circles are drawn so that the diameter of outer circle is 1m. There can
be a screen twice this size where the outer diameter is 2m. The former is used at a dis-
tance of 1m, the latter at a distance of 2m. Advantage of the large screen is that the
scotomas are enlarged, hence are easily detected. Each circle is again divided by radial
lines of 58 separation. The blind spots are marked on each side of point of fixation on
the horizontal line that divides the circle into two equal upper and lower parts. The
blind spot extends 58 horizontally and 88 vertically. It is vertically oval in shape. It lies
between 138 and 188 horizontally.
The test objects vary from 1 to 50 mm circular discs, generally white in colour and can
be of different colours. The targets are mounted on one end of black, non-reflecting
pointers. The patient sits at a distance of 1 m from the screen in front of it. The eye looks
straight ahead and at level with the point of fixation. One eye is tested at a time, the other
eye is patched and the patients head is kept erect and straight without any tilt or turn.
The examiner moves the target from the periphery towards the centre and when the
target just becomes visible, the patient promptly indicates so. A dull-coloured pin is
inserted at this point on the screen and left there till all the defects are charted. Blind
spot is charted first because this gives a feeling of non-seeing area to the patient. Once
all the defects have been lined by pins they are transferred on a paper chart that serves
as a permanent record that can be compared on subsequent visits.
LB RB
Fig. 2.21 | Bjerrum’s chart. LB ⫽ left blind spot; RB ⫽ right blind spot.
Fig. 2.22 | Perimetry chart for peripheral field (right eye).
Each chart should have patient’s name, reference number and date of examination,
vision, size and colour of target and distance.
Bjerrum screen is used to chart:
1. Blind spot for size and shape
2. Arcuate scotomas
3. Altitudinal field defects
4. Central, centrocecal and paracentral scotomas
5. Generalised peripheral constriction
6. Hysterical field defects.
Arc perimeter (Fig. 2.22) There are many models; most commonly used are
Lister’s and Aimark. These are made up of an arc of 33 cm radius, the arc is generally
made of metal and this can be rotated round a central axis by 360⬚. The arc is marked
in degrees; there is a central point of fixation. The target can be moved along the arc
from the point of fixation to extreme periphery and vice versa.
The target is generally in the form of a stud, the size and colour of which can be
changed. It could also be a circular beam of light that can be projected on the arc.
When such projected lights are used as targets, the perimeter is called projection
perimeter. There is a chin rest in front of the point of fixation at a distance of 33 cm,
and there is a headband to fix the head of the patient. The patient keeps his chin on
the chin rest and forehead on the headband. One eye is tested at a time, the other eye
is occluded. The patient fixes the fixation point and the target is moved from the
periphery towards the centre in various meridians at an interval of 5–10⬚. As soon as
the patient can see the object he indicates this by sound. The examiner punches the
point on the perimeter chart. This could be automatic or drawn separately.
Bowl perimeters—Goldmann or Tubinger The working principle of a bowl perime-

ter is the same as Lister’s perimeter. The arc is replaced by an opaque hemispherical dome
of 30 cm. This forces the eye to see only the inner surface of the bowl, which is uniformly
illuminated, though the illumination can be changed. The target is projected on the
hemisphere as a spot of light, the size and colour of which is changeable. The patient
Fig. 2.23 | Multiple pattern field analyser.

sits in front of the instrument with chin in the chin rest, head strapped to the head-
rest and hands suitably placed on the table on which the perimeter is kept. One eye is
tested at a time and the other eye is occluded. Fixation of the patient is observed
through a telescope mounted just behind the point of fixation by the observer who is
not visible to the patient. These perimeters are used for both kinetic and static perime-
try. They can be used for peripheral as well as central field, though central field record-
ing in these perimeters requires more patience. Static perimeter is more accurate and
uses test object of varying illumination. It produces a vertical section or profile of the
field (for more details refer Chapter 16).
Multiple pattern field analyser (Fig. 2.23) Almost all common field changes in
both centre and periphery can be detected. It contains ten cards with distinct pattern
printed in fluorescent material. Each card has a central point of fixation. The patient
is asked to fix this point. The card is exposed to ultraviolet light for quarter of second,
the patient is asked to tell the shape and number of figures on a given chart. The fig-
ures that are omitted represent field defects. The method is inexpensive and portable.
It is useful to screen fields in large numbers in a short time.
■■■ CHAPTER 3
E XAMINATION OF E YES U NDER
D IFFUSE L IGHT
After the symptoms have been noted, history is heard and vision is noted. It is time to
examine the eyes for any disorder, its location and pathology, and cause of the pathology.
OCULAR EXAMINATION
Ocular examination is done under the following heads:

1. Examination in diffuse light
2. Examination under focal illumination and magnification
3. Detailed examination of various parts with specific instruments
4. Special investigations
5. Systemic examination
These divisions are not absolute; there may be overlap between two groups.
EXAMINATION IN DIFFUSE LIGHT
The patient is seated comfortably in a normally illuminated room roughly 1 m from

the observer and the following points are noted:
1. Is the patient in agony, or is apprehensive or anxious?
2. Can the patient reach his seat unaided?
3. Head posture
4. Symmetry of the face
5. Eyebrow and forehead
6. Inter-palpebral aperture
7. Proptosis and exophthalmos
8. Squint
9. Nystagmus
Agony and Apprehension

A patient who is in agony has a severely painful condition. It may be trauma, post-
operative infection, corneal ulcer threatening to perforate, acute congestive glaucoma,
lens-induced glaucoma, orbital cellulitis, acute dacryoadenitis, cavernous sinus throm-
bosis, herpes zoster or trigeminal neuralgia.
Apprehensive or anxious patients are those who have lost an eye either following a sim-
ilar episode or know that such symptoms may lead to loss of vision. Diseases evoking
such anxiety generally include retinal detachment in myopia or aphakia, central artery
and central vein thrombosis (fortunately these are generally unilateral), dysthyroid
oculopathy, acute ischaemic optic neuropathy and methyl alcohol poisoning.
Locating the Examination Seat

If the patient cannot locate his seat, he should be assisted to reach and sit in the exami-
nation chair. The examiner should then find out if the patient’s hearing is all right, and
whether he can understand the examiner’s language. A child with mental retardation with
good vision may not be able to follow such simple instructions as to take his seat.
Inability to locate the examination seat may be due to gross visual loss in both eyes,
diminished scotopic vision, grossly restricted visual field of both eyes, loss of lower
visual field or the patient malingering.
Head Posture
Once the patient is seated comfortably, start talking to the patient (the subject need
not be very specific) like his job, address, number of children, etc. While the patient
is settling down, the observer notes the following things regarding his head posture.
Normal Head Posture

It is erect, looking straight without any turn, tilt, elevation or depression of chin or
abnormal movements of the head.
A shy child may keep his chin tucked on the chest; he has to be coaxed to look straight.
Abnormal head posture consists of :
1. Turning of the head towards right or left
2. Elevation of the chin
3. Depression of the chin
4. Tilting of head towards the left or right shoulder
5. Combination of turning, tilting and changed chin position
Turning of head towards left or right implies:

● Restriction of movement of horizontal muscles, which could be paralytic or restrictive, or
● Loss of corresponding visual field
Abnormal turning, tilting and altered chin posture means involvement of cyclover-
tical muscles, possibly due to congenital anomaly, paralysis of extra-ocular muscle,
myopathy, restrictive pathology, e.g. dysthyroid oculopathy, fracture orbit, etc.
Causes of elevation of chin are:
1. Ptosis and pseudoptosis
2. Paralysis of elevators of the eyeball
3. Overaction of depressors
4. Loss of the upper lid
EXAMINATION OF EYES UNDER DIFFUSE LIGHT 39
5. High ametropia with correction:

● Spectacle corrected aphakia
● High myopia
6. Double elevator palsy

Causes of depression of chin are:
1. Paralysis of depressors of the eyeball
2. Overaction of elevators of the eyeball
3. Loss of lower field of vision
4. Double depressor palsy
➤ Abnormal chin position without turning or tilting is due to ptosis, loss of field or high
ametropia
➤ Abnormal chin position with tilting and turning of the head is due to abnormality of
cyclovertical muscles
Symmetry of the Face

Human face looks almost symmetrical on each side of the midline, which is in fact not
so. A normal face should have:
1. Eyebrows evenly and smoothly spread out from the midline with a gentle curve upwards, and
taper laterally
2. Space between the two lids is symmetrical and equal on each side
3. Naso-orbital creases are equal on each side
4. Naso-labial folds are symmetrical on each side
5. When the patient speaks or smiles, the angle of the mouth moves equally on each side
Causes of asymmetry of face are:
1. Congenital anomaly
2. Trauma—cranio-facial anomaly, burns, post-maxillectomy
3. Facial nerve palsy
4. Ptosis
5. Hamartomas of the face, eyes, lids and orbit:
● Sturge Weber syndrome
● Neuro-fibromatosis
● Facial haemangiomas
Eyebrows and Forehead

Eyebrows are a symmetrically spread out collection of hair along the supra-ciliary arch
of orbit. They have a smooth upwards convexity and are wide medially, and gradually
taper to a point laterally a few millimetres above the outer canthus.
1. Eyebrows are flat in paralysis of orbicularis
2. They are raised in ptosis, pseudoptosis and hysteria
Eyebrows are scanty in the new born, in childhood, old age, hypothyroidism and in lep-
rosy. Localised loss of eyebrows is seen following trauma, fungal infections of the skin
and scar ring. They may be totally absent in generalised alopecia. Luxuriant eyebrows do
not indicate any local or systemic condition.
Poliosis (grey eyebrows), especially unilateral, is seen in vitiligo, Vogt Koyanagi

Harada syndrome and sympathetic ophthalmia. In leprosy, not only are the eyebrows
lost on both sides, but the skin may be hypopigmented and show nodular appearance
with loss of sensation.
Forehead is examined for:
1. Any lesion like haemangioma, neurofibroma, birthmark, port wine stain, Café-au-lait and scars
2. Forehead creases are lost in facial palsy, paralysis of the orbicularis and in burns
3. Forehead furrows are accentuated in ptosis, pseudoptosis and hysteria
Inter-Palpebral Aperture
Inter-palpebral aperture is a conch-shaped space between upper and lower lid. It is
widest in the middle. Junctions of the two lids are called medial and lateral canthus,
respectively. Medial canthus is rounded while the lateral canthus is angular. While
examining the inter-palpebral aperture, the following points are noted.
1. Slant
2. Width
3. Length
Slant: Generally, the inter-palpebral aperture is horizontally parallel to the ground; all
canthi are in the same level. However the aperture may be slanted downwards or
upwards, the lateral canthus being lower or higher, respectively. If the lateral canthus is
higher, it is called mongoloid obliquity and the reverse is called anti-mongoloid obliquity.
Mongoloid obliquity is a normal feature of oriental (Chinese) eyes. Other causes of
mongoloid obliquity are Down syndrome, Laurence Moon Biedl syndrome, V esotropia
and A exotropia.
The outer canthus is displaced downwards in fracture of the malar bone.
Causes of anti-mongoloid obliquity are congenital facial hemiatrophy, Crouzon’s syn-
drome, mandibulofacial dysostosis and maxillofacial dysostosis.
Width (Fig. 3.1): The upper lid covers 2 mm of normal upper cornea, while the lower
lid just touches the lower limbus. The normal intra-palpebral aperture (IPA) is roughly
10 mm wide in front of the cornea. The interpalpebral fissure is called narrow if the
upper lid covers more than 2 mm of the upper cornea.
Causes of narrow inter-palpebral aperture (Fig. 3.2):
1. Causes in lid: ptosis, congenital or acquired, oculomotor palsy, Horner’s syndrome, myasthenia
gravis, senile ptosis. Pseudoptosis: oedema of lid, growth in the lid, blepharochalasis, ankyloble-
pharon, blepharophimosis and tarsorrhaphy
2. Causes in globe: anophthalmos, microphthalmos, microcornea, hypotony, phthisis and perforated
globe
3. Causes in orbit: enophthalmos, eviscerated socket, enucleated socket, blow out fracture of the
orbit and loss of orbital fat
If the sclera is visible above and below the cornea, the inter-palpebral fissure is called wide.
Causes of wide inter-palpebral fissure (Fig. 3.3):
● Causes in lid: facial palsy, paralysis of orbicularis, coloboma of lid and lid retraction
EXAMINATION OF EYES UNDER DIFFUSE LIGHT 41
2 mm
Fig. 3.1 | Normal width of IPA. Upper lid

covering 2 mm of upper cornea
Fig. 3.2 | Narrow IPA. Upper lid
covering more than 2 mm
Fig. 3.3 | Wide IPA. Sclera is visible
above and below the cornea.
and lower lid touching lower of upper cornea.
border of cornea.
● Causes in globe: buphthalmos, large anterior staphyloma and annular ciliary staphyloma
● Causes in orbit: dysthyroid orbitopathy and proptosis
Length: Normal IPA is about 35 mm in length in adults. It is smaller in newborns. By 10
years of age, the IPA acquires almost full adult length. IPA may look short in the presence
of epicanthus. It is reduced in blepharophimosis, which may be primary or associated with
ptosis; it is reduced in length following lateral tarsorrhaphy, burns and plastic repair.
Proptosis and Exophthalmos

These are two types of protrusion of the globe. Exophthalmos is exclusively used for
dysthyroid orbitopathy where the main pathology is in the extraocular muscles and there
are no clearcut deposits or mass in the retrobulbar space. It is an active process due to
poorly understood causes. In proptosis, the globe is pushed forward due to a mass in
the retrobulbar space, or the orbit is too small for the growing eyeball. A fully developed
proptosis presents no problem in diagnosis. The relatives are first to notice the abnor-
mal appearance or the patient may be aware of it. It could be unilateral or bilateral,
symmetrical or asymmetrical, painful and painless (for details refer Chapter 21).
Squint
It is surprising that on many occasions the patient is not aware even of large angle squint
not to talk of small deviations, especially when it is alternating squint with fairly good
vision. A patient is never aware of latent squint. Children do not complain of squint; par-
ents notice the deviation and bring the child for treatment. Adults are more likely to pres-
ent with acute squint that is invariably paralytic. Non-paralytic squint in adults usually has
a long history. They generally come for cosmetic purposes (for details refer Chapter 19).
Nystagmus
Nystagmus is a complete involuntary to and fro movement of the eyes. Horizontal
nystagmus is the commonest, vertical nystagmus is less common and torsional nystag-
mus is the least.
Causes of nystagmus
It could be physiological, ocular or secondary to motor imbalance (neurological).
E XAMINATION OF E YES U NDER
F OCAL I LLUMINATION
Examination under diffuse illumination is good enough for gross lesions, but may not
be sufficient to delineate subtle signs. The first requirement for focal examination is a
good source of light that can be focused to pinpoint. The most commonly used appli-
ance is a flashlight (torch), either battery-operated or electrical. Most widely used are
three-celled battery-operated torches. They are handy, easy to carry and operate without
electricity. Halogen bulbs fitted with fibre optical system can also be used. It is a good
idea to have a cobalt blue filter fitted to the source of light to examine fluorescein stain.
Oblique illumination: This effective method of illumination has been replaced by
the simple torchlight, though sometimes this is a very useful method especially when
pinpoint focus is not available by torchlight.
In this method, parallel rays from a distant source (not sun rays) are focused on the
eye by a condensing lens (Plate 4.1). By moving the lens towards the eye or away from the
eye, the diameter of the illuminated circle can be changed. Thus this can be used for a
pinpoint illumination or diffuse illumination. It is used to see corneal opacities, ulcers,
KP and synechia. It is generally used along with a corneal loupe that acts as magnifier
(Plate 4.1). Combined use of corneal loupe and condensing lens requires practice.
FOCAL ILLUMINATORS USED IN OPHTHALMOLOGY
1. Flash light
● Battery-operated, dry cell/rechargeable
● Electrically-operated through step down transformer
2. Fibre optic device

3. Biomicroscopic (slit lamp)
4. Ophthalmoscope
● Direct
● Indirect
5. Gonioscope
● Direct
● Indirect
6. Retinoscope
7. Trans-illuminator
8. Endo-illuminator
EXAMINATION OF EYES UNDER FOCAL ILLUMINATION 43
Plate 4.1 | Uniocular corneal loupe, condensing lens and operating telescope.
Plate 4.2 | Binocular corneal loupe in use.
MAGNIFIERS USED IN OPHTHALMOLOGY
1. Uniocular corneal loupe

2. Binocular corneal loupe (Binomag) (Plate 4.2)
3. Operating loupes and telescope
4. Slit lamp
5. Operating microscope
6. Direct ophthalmoscope
7. Indirect ophthalmoscope
The first three magnifiers (Plate 4.1) mentioned above are useful only in the exami-
nation of anterior segment of the eye.
Slit lamp and operating microscope are generally used for the anterior segment.
With appropriate attachments, they can be used for posterior segment examination
as well.
A
b
f B
N
Fig. 4.1 | Optics of uniocular corneal loupe (N ⫽ nodal point of ⫹40 lens, f ⫽ focal length of the lens 2.5 cm,
AB ⫽ object kept between f and N, ab ⫽ virtual image of AB, erect and 10⫻ magnified).
Ophthalmoscopes are meant for examination of the posterior segment. They can
be used as illuminators for examination of the anterior segment as well. Some direct
ophthalmoscopes have in-built devices by which cornea, AC, iris and lens can be exam-
ined. These ophthalmoscopes are called bifocal ophthalmoscopes.
UNIOCULAR CORNEAL LOUPE
This is a versatile, inexpensive, easy-to-use magnifier that gives an excellent magnifi-

cation of 10⫻.
It consists of a case with cover and two plano-convex lenses of ⫹20 D, each fitted in the
case so that their plane surfaces are parallel, while convex surfaces face outwards. There is
a gap of 2–3 mm between the two lenses. This arrangement of lenses reduces spheri-
cal, prismatic and chromatic aberrations. Total diopteric value of two lenses becomes
⫹40 D with focal length of 2.5 cm and magnification of 10⫻. For a clear image,
objects of interest should be within the focal length of the device, i.e. ⬍2.5 cm. By
moving the lens back and forth, magnification can be changed within a limited range.
The image is virtual, magnified and erect, and on the same side as the object. As the
device is not self-illuminated, a separate source of illumination, e.g. a flashlight or con-
densing lens, is required, which engages both hands of the examiner. Due to the short
focal length of the loupe, the examiner has to move very close to the patient (Fig. 4.1).
BINOCULAR CORNEAL LOUPES
These give less magnification than uniocular corneal loupes, but offer stereopsis and a
longer working distance. They also requires an extra source of illumination that engages
one hand while the other hand is free to manipulate the lid. The device is fitted with a
headband that is worn over the forehead by the examiner. The optical part hangs in
front of the eyes, a little away from the anterior focal plane of the examiner’s eye.
It comprises of ⫹6 D lenses fitted in the frame one in front of each eye. The focal
length is 17 cm and magnification is 1.5⫻. By increasing the diopteric value of the lenses
magnification can be increased. The optics of the binocular loupe are same as those of
the uniocular loupe. The object has to be within the focal length of the lenses. These give
less magnification than uniocular corneal loupes, but offer stereopsis and a longer work-
ing distance. In the more expensive model of the binocular loupe, 6 PD prism base is
added to give comfortable convergence to the observer. Instead of headband mounted
binocular loupes, it can be in the form of spectacles as well. As hands are free, these can
be used as moderate magnifiers in ocular surgery with additional pedestal operating light.
OPERATING TELESCOPES
These are expensive magnifiers, which are in fact binoculars mounted on a spectacle
frame. The spectacle frame can be used for distant correction of the observer. It has a com-
bination of lenses and the magnification achieved varies between 4⫻ and 6⫻. The more
the magnification, the lesser the working distance and smaller the field of vision. Distance
between the two telescopes can be adjusted as per inter-pupillary distance of the exam-
iner. Angle between the two telescopes is also adjustable. They are good for the examina-
tion of the anterior segment, and surgery where much magnification is not required.
BIOMICROSCOPE (SLIT LAMP)
As the name suggests, this is a horizontally placed clinical microscope (Plates 4.3 and
4.4). Parts of a slit lamp are:
1. Optical
● Magnifier (microscope)
● Illuminator
2. Mechanical: table, base and device to adjust

● Angulation between the microscope and the illumination system
● Height of the slit beam
● Width of the slit beam
● Angulation of the slit beam
● Chin rest and head rest for patients
Slit lamp is a binocular microscope where distance between the two eyepieces can be
adjusted and the power of the eyepieces is changeable. The microscope is horizontally
placed and can be moved in various directions. Magnification varies between 5⫻ and
50⫻. Commonly used magnifications are 10⫻, 16⫻ and 25⫻.
A good biomicroscope should have brightness, choice of magnification, high reso-
lution, comfortable working distance and arrangement for accessories. The micro-
scope should also have stereopsis, large field of vision and good depth of field.
Illumination
The illumination system consists of electrically operated gas bulb of low voltage,
which works on mains through a step-down transformer. The light from the bulb
Plate 4.3 | Slit lamp biomicroscope.
Plate 4.4 | Slit lamp in use.

passes through a system of collecting lenses, prisms and an adjustable slit whose
length, width, height and axis are adjustable. Appropriate colour filters can be super-
imposed on the slit. The microscope and illumination system can be coaxial or angu-
lated to one another.
Various modes of examination of anterior segment by slit lamp (Figs 9.7, 9.8, 9.11–9.13):
1. Diffuse illumination
2. Direct illumination
3. Retro illumination
4. Sclerotic illumination
5. Oscillatory illumination
6. Specular reflection
7. Depth measurement
8. Photography
Observations with Accessories of the Slit Lamp

Filters
A commonly used filter is the cobalt blue filter with high transmission between 450
and 500 nm. This is used in examination where fluorescein sodium is employed, for
example to stain epithelial defects, Goldmann applanation tonometry, contact lens fit-
ting, tear film study and examination of leaking wounds. Red free (green) filter is used
rarely to see fine vessels on conjunctiva and cornea.
Gonioscope
The single mirror is exclusively used for the examination of the angle of the anterior
chamber, while the three-mirror gonioscope is used to examine the fundus; (both central
as well as peripheral) and the angle of the anterior chamber (for details see Chapter 17).
Fundus Examination
The slit lamp can focus up to anterior vitreous without additional optical attachments.
To see the fundus the far point of the eye under observation should be brought within
the focus of the objective of the microscope. This can be achieved by interposing either a
minus Hruby lens, Goldmann three mirror contact lens or a plus El Bayadi type lens between
the cornea and the slit lamp.
Concave lens Hruby lens is a plano-concave lens with diopteric value of ⫺58.6 D.
The original Hruby lens had ⫺55 D power. It is attached to the slit lamp in such a
way that it can be easily interposed between the microscope and the eye. It is kept at a
constant distance of 15 mm in front of the cornea with the plane surface towards the
cornea. It gives an upright virtual image of the fundus that is formed in the anterior
vitreous. It can examine the posterior pole up to 30⬚ all around. With a widely dilated
pupil, the lateral field is extended to 60⬚. By putting a high minus near the cornea, the
power of the cornea is neutralised and the slit lamp acts as a telescope giving a magni-
fied view.
Convex lens El Bayadi and Volk: These lenses produce an inverted real magnified
view of the posterior pole. To see the image, the slit lamp must be moved away from
the eye. Convex lenses give a wide field of view. Plus lenses are suitable in high myopic
eyes. The power of these plus lenses varies between ⫹60 and ⫹90.
Curvature of cornea is measured by a keratometer, which is not attached to a slit lamp.

Some of the slit lamp microscopes can be modified to accommodate a keratometer by
removing the microscope objective.
Measurement of Corneal Thickness and Depth of

Anterior Chamber by Slit Lamp Microscope
Until the development of ultrasonic pachymetry and ultrasonic depth measurement
device, these two measurements were done by the slit lamp with special attachments.
Trans-Illumination of the Eye

Before binocular indirect ophthalmoscope became popular and ultrasonic examination
was in its infancy, the only method of detecting peripheral raised lesions, e.g. retinal
detachment, ciliary body tumours, cysts and foreign bodies, was by trans-illumination
(Plate 20.1). Even today when binocular indirect ophthalmoscopy or ocular ultrasonog-
raphy are not available, trans-illumination is the only method of localising peripheral
mass lesions and defects in the iris. For trans-illumination, the patient is made to sit in
a dark room. The pupil is widely dilated. A trans-illuminator that is available as acces-
sory with many direct ophthalmoscopes (Pentoscope Keeler) or a bright small source of
light is put in contact with the anaesthetised conjunctiva. In a normal eye the pupil
stands out as a pink circular glow, if the media are transparent. Growth of ciliary body
stands out as black dome-shaped shadow in the pupillary area, edge of the subluxated
lens also becomes clearly visible as a dark crescent. Holes in iris transmit pink glow.
■■■ CHAPTER 5
E XAMINATION OF THE L ID
Lids are multi-layered ocular adnexa and have a protective function. They comprise of
the following layers (Fig. 5.1).
1. Skin
2. Muscles—orbicularis
● Levator palpebral superioris
● Muller’s muscles
3. Adeno fibrous layers—tarsal plate

4. Conjunctiva
Disorders of lids are generally confined to one of the layers. However, involvement of more
than one layer is not unusual e.g. congenital defects, trauma, neoplasm and allergy.
Lid margin is a junction of the skin and conjunctiva with an inter-marginal strip
in between, in which lashes grow and meibomian ducts open. This makes it suscepti-
ble to disorders not only of the skin, but also of the conjunctiva.
Examination of the lid involves examination of:
1. Skin
2. Lid margin
3. Orbicularis
4. Levator
5. Tarsal conjunctiva
6. Lashes
7. New growths
SKIN
Colour of Skin
1. Normal
2. Hyper-pigmented
3. Hypo-pigmented
There may be a generalized hyper-pigmentation of the lids in some persons. It appears
as dark circles around the eye, which may be familial and do not require any treatment.
Other causes of hyper-pigmentation are spring catarrh and loss of orbital fat. Localised
hyper-pigmentation is seen in moles and naevi (Plates 5.1 and 5.2).
Hypo-pigmentation is seen in vitiligo, leprosy, scars, burns, fungal infections and
xanthelasma.
LPS
Skin Krause’s gland
Wolfring gland
Orbicularis
Meibomian gland in
tarsal plate
Sulcus subtarsalis
Lash
Opening of
Meibomian gland
Gland of Zeiss and Moll Intermarginal strip
Fig. 5.1 | Diagram showing anatomy of upper lid. Plate 5.1 | Hairy naevus involving both the lids.
(Courtesy Dr. Dilip Agarwal.)
Plate 5.2 | Same patient after repair. The eye has some vision
but is amblyopic. (Courtesy Dr. Dilip Agarwal.)
Plate 5.3 | Diffuse oedema of lids due to renal
pathology.
In case of injury to frontal scalp and orbit, there may be accumulation of blood in the
lid. Initially it is red, gradually becoming dark and later gives an appearance of black eye.
Oedema
1. Diffuse (Plate 5.3)
2. Localised
EXAMINATION OF THE LID 51
Plate 5.4 | Oedema of the right lower lid

due to insect bite.
Plate 5.5 | Severe diffuse oedema due to acute
mucopurulent conjunctivitis.
Diffuse Oedema
Diffuse oedema may be limited to one eye or may be bilateral. It may be associated
with generalised puffiness of the face.
Causes of diffuse oedema are allergy, insect bite (Plate 5.4), nephrotic syndrome,
hypo-proteinaemia, myxoedema, cellulitis of the lid, lid abscess, post-surgical, puru-
lent conjunctivitis (Plate 5.5), endophthalmitis, panophthalmitis, emphysema and
trauma.
Localised Oedema
Growth of lid may be benign or neoplastic, chalazion, cyst or stye.
Eruption of Vesicles
Eruption of vesicles is seen in chicken pox, measles, herpes zoster, primary herpes
simplex and molluscum.
LID MARGIN
Lid margin is examined for:

1. Coloboma
2. Misdirection of lid margin
3. Misdirection of lashes
4. Absence of lashes
5. Thickening of lid margin
6. Growth of lid margin

7. Adhesion
8. Inflammation: blepharitis, stye and chalazion
9. Parasites
Coloboma
Coloboma can be
1. Congenital
2. Acquired: traumatic—accidental and surgical
Congenital coloboma of the upper lid is generally seen on medial side, while that of
lower lid is seen in the lateral third (Fig. 5.2).
Traumatic coloboma can be surgical or accidental. In accidental injury the whole
lid may be lost. Tissue loss may be full thickness, or partial thickness or the coloboma
may just be a notch. Coloboma of the lower lid produces more symptoms than that
of the upper lid.
Misdirection of Lid Margin

1. In turning—entropion (Fig. 5.3C, Plate 5.6)
2. Out turning—ectropion (Fig. 5.3D, Plate 5.7)
Entropion
Entropion can be acquired or very rarely congenital.
Acquired entropion may be cicatricial or spastic
Full thickness upper lid

Notch coloboma, cornea exposed
coloboma
upper lid Notch coloboma Iower lid
Fig. 5.2 | Congenital coloboma.
(A) Normal lid margin,

anterior border rounded,
(B) Trichiasis (C) Entropion (D) Ectropion (E) Madarosis (F) Tylosis (G) Distichiasis
Iashes in normal position,
inner margin sharp
Fig. 5.3 | Deformity of lid margin.

Plate 5.6 | Spastic entropion of right lower lid. Plate 5.7 | Ectropion of left lower lid following maxillectomy.
Causes of cicatricial entropion are:

1. Stage four of trachoma
2. Leprosy
3. Acid and alkali burn of conjunctiva
4. Ocular pemphigus
5. Severe membranous conjunctivitis
6. Stevens Johnson syndrome
Causes of spastic entropion are:
1. Loss of orbital fat
2. Senile
3. Enophthalmos
4. Enucleated socket
5. Tight bandage
Symptoms of entropion depend upon its extent, duration and corneal involvement.
Symptoms are lacrimation, epiphora (entropion of lower lid produce both epiphora
and lacrimation), foreign body sensation, pain, redness and diminished vision.
Signs of entropion are deformity of lid margin, rounding of inner lid margin, in-
rolling of lid margin, chronic conjunctivitis, corneal erosion, corneal ulceration,
corneal opacity and superficial vascularisation.
Ectropion
Ectropion of lid can be paralytic or cicatricial and both are generally seen in the lower
lid. Upper lid is not capable of going into paralytic ectropion or spastic entropion.
Ectropion of upper lid is always cicatricial, caused by scarring of the skin of upper lid.
Causes of paralytic and non-cicatricial ectropion are:
1. Paralysis of orbicularis—leprosy and local trauma (Plate 5.8)
2. Facial palsy
Plate 5.8 | Bilateral orbicularis palsy; note retained Bell’s

phenomenon. (Courtesy Dr. Dilip Agarwal.)
Plate 5.9 | Burn involving both the lids.
(Courtesy Dr. Dilip Agarwal.)
3. Senile
4. Idiopathic
Causes of cicatricial ectropion are:
The causes are localised on the skin surface of lid.
1. Infective
2. Traumatic: chemical or thermal burn of lids (Plate 5.9), badly repaired lid and facial wounds and
radiation
Symptoms of ectropion: watering is the most prominent symptom. It is mostly epi-
phora, but if the conjunctiva or cornea is exposed it can be lacrimation as well. There
may also be foreign body sensation.
Signs of ectropion include eversion of the lid margin, chronic conjunctivitis, keratini-
sation of conjunctiva, corneal exposure, corneal ulcer, corneal opacity and vascularisation
of cornea.
Misdirected Lashes
Misdirection of lashes is called trichiasis. It can be misdirection of a single lash or
many lashes (Fig. 5.3B).
Distichiasis is the presence of an additional row of lashes in place of meibomian
opening (Fig. 5.3G).
Causes of trichiasis are:
1. Trachoma
2. Leprosy
3. Ulcerative blepharitis
4. Herpes zoster
5. Trauma
6. Chemical burn
7. Idiopathic
Symptoms of trichiasis are lacrimation, foreign body sensation and redness.
Signs of trichiasis are misdirected lash or lashes, chronic conjunctivitis, keratitis,
corneal ulcer, corneal vascularisation and corneal opacity.
Trichiasis can be seen alone or with entropion.
Absence of Lashes
Absence of lashes is called madarosis. There may be a total loss of lashes in one or both
lids or the problem may be localised (Fig. 5.3E).
Causes of madarosis are:
1. Trachoma (madarosis is mostly confined to the lower lid)
3. Leprosy
4. Burn—thermal or chemical
5. Idiopathic
6. Congenital
Symptoms of madarosis are mostly cosmetic. The only sign of madarosis is the loss of
lashes, partial or total.
Thickening of Lid Margin

Thickening of lid margin is called tylosis (Fig. 5.3F). This is generally associated with
madarosis. The lid margin is diffusely oedematous, hyperaemic and rounded.
Causes of tylosis are:
2. Squamous blepharitis
3. Leprosy
Inflammation of the Lid Margin

1. Blepharitis (generalised)
2. Meibomian (tarsal) gland: Chalazion (Fig. 5.4)
3. Zeis and Moll (Lash) glands: Stye (Fig. 5.4)
Inflammation of the lid margin is called blepharitis. It is generally chronic and

bilateral. The two types are squamous and ulcerative (Table 5.1).
Chalazion
This is a chronic granuloma of tarsal gland and commonly seen in children and young
adults. As there are more and larger tarsal glands in upper lids, chalazia are more common,
and larger, in upper lids. There may be single or multiple chalazia in any or both the
Chalazion
Stye
Blepharitis
Fig. 5.4 | Inflammation of the lid margin.

Table 5.1 Comparison between squamous and ulcerative blepharitis
Feature Squamous Ulcerative
Scale Fine, dry and white like dandruff Yellowish, wet and matted
Ulceration Absent Present, seen on removal of scales
Bleeding Nil Small pin point on removal of scales
Madarosis Less common More common, extensive
Trichiasis Nil May be present
Complication Rare Blepharoconjunctivitis,
recurrent keratitis and tarsitis
lids at a given point of time. They may be recurrent. They are painless and the swelling
develops gradually.
Predisposing factors for chalazion are:
1. Familial
2. Errors of refraction
3. Acute exanthematous condition
4. Idiopathic
Symptoms are a painless and gradually increasing swelling in any eye and any lid. The
swelling is self-limiting, and usually subsides after a while, but another one may crop up.
Signs are a diffuse, round swelling, away from lid margin; non-tender; skin can be
moved over the swelling, on eversion of the lid; the conjunctiva over the chalazion
appears bluish. The growth may erode the conjunctiva and protrude on the conjunc-
tival surface like a sessile mass.
When a chalazion develops acute bacterial infection, it is called hordeolum inter-
num. It is a very painful condition and mimics a stye. Recurrent chalazia in adults
should be suspected to be adenocarcinoma of tarsal gland and investigated as such.
Stye
This is an acute infection of the glands of Zeis and Moll. Infection limited to the
gland of Moll is called hidradenitis (Table 5.2).
Styes are equivalent to boils on the skin, and are common in children and young
adults. They are painful, seen on the lid margin, pink in colour and tender to touch.
There may be a pus point at the base of the infected lash, accompanied by a diffuse
swelling of the lid. Pre-auricular lymph glands are frequently enlarged. Adults with
stye should be investigated for diabetes.
Symptoms are—painful and tender swelling on the lid margin.
A well-formed stye may be visible on inspection (Plate 5.10). If the examiner’s
index finger is moved slowly over the affected lid margin from one end to other, the
patient complains of pain as soon as the finger passes over the stye. Pre-auricular lymph-
nodes are enlarged.
Table 5.2 Comparison between stye and chalazion (Fig. 5.4)
Features Stye Chalazion
Age Children and young adults Children and young adults

Sex Equal in both sexes Equal in both sexes
Family history May be present May be present
Bilaterality Common, both lids may be involved Common, both lids may be
involved
Number Single or multiple Single or multiple
Pain Painful and tender Painless, non-tender
Skin Cannot be moved over the lesion Can be moved over the lesion
Position Lid margin Away from lid margin
Pre-auricular lymphnodes Enlarged Not enlarged
Complications Cellulitis lid, lid abscess, May produce astigmatism
cavernous sinus thrombosis
Plate 5.10 | Stye of left upper lid.

Growth of Lid Margin

As the lid consists of many types of tissues, various forms of inflammation and neo-
plasia are possible. The growths may be small and confined to the lid margin. They
may spill over the lid margin to spread towards the skin or conjunctiva, or both. They
may start in the substance of the lid and grow to involve the margin.
Benign Growths
1. Warts
2. Burst chalazion
3. Foreign body granuloma
4. Molluscum
5. Cornu cutaneum
6. Xanthelasma
7. Tarsal cyst
Plate 5.11 | Hemangioma of lower lid.
Plate 5.12 | Kissing naevus.

8. Neuro fibroma
9. Haemangioma (Plate 5.11)
10. Naevus (Plates 5.12 and 5.13)
Malignant Tumours of the Lid

1. Basal cell carcinoma (Plates 5.14 and 5.15)
2. Squamous cell carcinoma
3. Meibomian cell carcinoma
4. Malignant melanoma
5. Xeroderma pigmentosa (Plate 5.16)
Adhesion
Adhesion of lid margin could be congenital ankyloblepharon or acquired tarsorrhaphy
(Fig. 5.5, Plate 5.17).
Parasites of the Lid Margin

Commonest parasites seen on the lid margin are body lice—phthiriasis. There may beac-
tual lice of their nits. The lice cling to the skin of the lid margin, while nits are seen on
the shaft of the lashes. They cause itching and redness of the lid margin and the patient
may actually complain of having lice. They are difficult to eradicate. Other parasites are
pediculus and demodex.
EXAMINATION OF THE ORBICULARIS
The orbicularis is primarily protective in function. It narrows the inter-palpebral

fissure, closes the lid and keeps it closed.
Plate 5.13 | Benign naevus. Plate 5.14 | Basal cell carcinoma of lower lid.
Plate 5.15 | Basal cell carcinoma involving both

the lids and eroding into the orbit.
(Courtesy Dr. Madan Deshpande.) Plate 5.16 | Xeroderma pigmentosa involving lids,
conjunctiva, face and chest.
Middle tarsorrhaphy
Median tarsorrhaphy Lateral tarsorrhaphy
Fig. 5.5 | Various types of tarsorrhaphy. Plate 5.17 | Ankyloblepharon filiformis.

Orbicularis is involved either by its paralysis or spasm.
Paralysis of orbicularis produces lagophthalmos or inability to close the lid. In pare-
sis of the orbicularis, there is partial closure.
Lagophthalmos
1. There is widening of the IPA
2. Ectropion of the lower lid
3. Epiphora
4. In an attempt to close the lids, it fails to close but the eyeball rolls up.This phenomenon is called
Bell’s phenomenon
5. There is exposure conjunctivitis; there may be keratinisation of the conjunctiva
Plate 5.19 | Bilateral severe blepharospasm.
Plate 5.18 | Bilateral lagophthalmos and madarosis.
6. Exposure keratitis, mostly in the lower half

7. There may be corneal ulceration
8. There is flattening of the supra ciliary furrows and the naso-labial fold
Lagophthalmos can be uniocular or binocular. The lesion could be direct trauma to
orbicularis, bells palsy or infra-nuclear seventh nerve palsy.
Leprosy is the commonest cause of bilateral lagophthalmos (Plate 5.18). Another
cause is Melkersson Rosenthal syndrome.
Evaluation of Orbicularis
Strength of the orbicularis is measured by asking the patient to close the lids tightly
against resistance offered by examiner’s index finger and thumb. The power is graded
between 1 and 4.
Spasm of Orbicularis
It could be:
1. Blepharospasm due to ocular cause (simple blepharospasm)
2. Blepharospasm due to neurological cause (essential blepharospasm)
Simple blepharospasm is involuntary closure of lids, generally bilateral (Plate 5.19). It is
associated with lacrimation and photophobia. Blepharospasm is more marked in children.
Causes of blepharospasm are:

1. Buphthalmos: primary or secondary
3. Fascicular ulcer
4. Corneal ulcer
6. Chemical burn
7. Exposure to ultraviolet rays
8. Exposure to welding
9. Hysteria
Essential Blepharospasm
This is relatively rare bilateral neurological disorder of unknown origin. The patient
goes into episodes of involuntary closure of both eyes for a variable period of time,
with variable intervals.
EXAMINATION OF LEVATOR PALPEBRAL SUPERIOR (LPS)
Function of the LPS is to elevate the upper lid from normal or closed position. It is
antagonist to the orbicularis and its agonist is Muller’s muscle.
Abnormal LPS function manifests as its underaction resulting into drooping of the
upper lid. Spasm of LPS is almost unknown. Underaction of LPS results in:
1. Drooping of the upper lid (Plates 5.20 and 5.21)
2. Narrowing of the inter-palpebral aperture
3. Loss of horizontal crease in the upper lid
4. Reduced excursion of the upper lid
Plate 5.20 | Drooping of left upper lid.

To examine the LPS, the patient is asked to look straight. Action of frontalis is obliter-
ated by pressing it with the thumb of the examiner against the frontal bone (Plate 5.22).
The patient is now asked to look up. Excursion of the lid from its previous position is
measured in millimetres (see Chapter 6).
EXAMINATION OF MULLER’S MUSCLE
Muller’s muscle is supplied by cervical sympathetic. Underaction of Muller’s muscle pro-

duces mild drooping and Horner’s syndrome, while overaction produces lid retraction.
There is no specific test to evaluate underaction of Muller’s muscle except the presence
of mild ptosis.
Lid Retraction
Normal upper lid covers upper 2 mm of cornea. If sclera is visible above the cornea,
it is the characteristic of lid refraction. The eye has a staring look. It can be unilateral
or bilateral. It can be symmetrical or one eye may have more retraction than the
other. In pseudo-retraction of lid the Muller’s muscle is normal, but the eyeball is
mechanically pushed forward, exposing the sclera, e.g. in proptosis. Generally there is
underaction of orbicularis in such cases. The commonest cause of lid retraction is dys-
thyroid oculopathy, which is due to overaction of Muller’s muscle. Action of Muller’s
muscle is enhanced by instilling 10% phenylephrine. In a normal person, this does
not produce lid retraction, but if there is overaction of Muller’s muscle, lid retraction
is seen.
Plate 5.21 | Partial unilateral ptosis. Plate 5.22 | Examination

of frontalis.
of LPS function after obliterating action
Lid lag
Normally when the eyeball looks down, the upper lid follows and keeps the upper part
of cornea covered and no bare sclera is visible. In lid lag, the upper lid fails to move
downwards. While the commonest cause is dysthyroid oculopathy, the other cause is
when the upper lid is tucked up either following trauma or post-inflammatory scar.
CONGENITAL ANOMALIES OF LIDS
Ptosis
Ptosis is one of the commonest congenital anomalies of the lid. It can be unilateral or
bilateral, partial or total. It is generally due to hypoplasia of the levator (see Chapter 6).
Coloboma
This is rare. It can be present in upper or lower lid, or both (Fig. 5.2). Upper lid colobo-
mas are generally seen at the junction of medial one-third with lateral two-thirds. Less
common is the absence of the middle third of the upper lid. This requires early repair to
prevent corneal exposure. Lower lid colobomas are seen at the outer third. They do not
produce exposure but epiphora. They are more common in mandibulo-facial dysostosis.
Ankyloblepharon
This is congenital fusion of the upper lid margin with the lower lid. The adhesion is
more common on the lateral side. It can be a few millimetres wide or may be a thin,
filament-like structure (Plate 5.17).
Epicanthus
This is a skin-fold, appears on the nasal side of the eye, and is continuous with the
upper lid. It is generally bilateral. Epicanthus is the commonest cause of convergent
pseudo-squint. This may be associated with ptosis and blepharophimosis.
Telecanthus
The orbits are set apart wider than normal, increasing the distance between the medial
canthi of the two eyes.
Blepharophimosis
Length and width of the IPA is reduced, giving a slit-like appearance. It may be asso-
ciated with ptosis.
Distichiasis
Normal lids have three to four rows of lashes. The tarsal ducts open behind the last row.
There is a strip of lid margin between the last row and opening of the tarsal glands. In
distichiasis, there is an extra row of lashes that springs at the opening of tarsal glands.
Numbers of such lashes vary. They rub against the cornea and conjunctiva in the same
way as simple trichiasis (Fig. 5.3G).
■■■ CHAPTER 6
E VALUATION OF A
C ASE OF P TOSIS
The word ptosis denotes the lowering of any organ (tissue) from its normal position and
prefixed with name of the organ, e.g. visceroptosis means sagging of viscera. Similarly,
drooping of lid is known as blepharoptosis. However, the word Ptosis been used to denote
blepharoptosis for years and has been a common term in clinical ophthalmology. Lower
lid is not capable of drooping; however, elevation of the lower lid margin is called upside
down ptosis. The commonest feature of ptosis is cosmetic blemish. It can be very small and
go unnoticed if it is equal and symmetrical in both the eyes, or it may be severe enough
to cover the pupil and cause diminished vision. It may be associated with diplopia.
PTOSIS
Ptosis can be of the following types (Table 6.1):

1. Congenital (75%) or acquired (25%)
2. Unilateral or bilateral
3. Complete or partial
4. Symmetrical or asymmetrical
5. Ptosis is said to be complete when there is no action of levator palpebral superior
Congenital Anomalies Associated with

Congenital Ptosis
1. Epicanthus
2. Blepharophimosis
Table 6.1 Symptoms of ptosis and their causes
Symptoms Causes
Drooping of upper lid Underaction of LPS or Muller’s muscle

Narrowing of IPA Underaction of LPS or Muller’s muscle
Inability to lift upper lid Underaction of LPS or Muller’s muscle
Raised eyebrow Overaction of frontalis
Prominent forehead furrow Overaction of frontalis
Elevation of chin Attempt to increase upper field
Jaw winking Aberrant third nerve. Congenital misdirection of fifth nerve
Diminished vision Covering of pupil and astigmatism and amblyopia
Diplopia Paralysis of other extra-ocular muscles
3. Superior rectus underactions

4. Jaw winking
Drooping of upper lid can be broadly divided into:
A. Pseudo-ptosis
B. True ptosis—fault may be in:
1. Levator palpebrae superioris:
(a) muscle
(b) aponeurosis
2. Neurogenic, due to paralysis of:
(a) Third cranial nerve
● Upper division
● Complete
(b) Cervical sympathetic: Horner’s syndrome

Myogenic causes of ptosis, other than congenital, are:
1. Myasthenia
2. Progressive external ophthalmoplegia
3. Dysthyroid myopathy
4. Myotonic dystrophy
5. Prolonged use of steroids
Aponeurotic causes of ptosis are:
1. Congenital
2. Senile
3. Trauma to aponeurosis
4. Post-operative
● Cataract
● Squint
● Retinal detachment
Causes of bilateral ptosis are:

1. Congenital
2. Myasthenia
5. Supranuclear lesion
6. Senile ptosis
7. Prolonged use of steroids
Causes of pseudo-ptosis are:
1. Lid
(a) Oedema
● Allergic
● Infective
● Nephrotic syndrome
(b) Ecchymosis
(c) Growth
● Neurofibromatosis (Plate 6.1)
● Sturge Weber syndrome (Plates 6.2 and 6.3)

EVALUATION OF A CASE OF PTOSIS 67
● Lacrimal gland tumour

● Epidermoid carcinoma
● Adenocarcinoma
● Tarsal cyst
2. Globe
(a) Anophthalmos
(b) Microphthalmos (Plate 6.4)
(c) Eviscerated socket
(d) Enucleated globe
(e) Small prosthesis
Plate 6.1 | Neurofibroma of right upper lid. Plate 6.2 | Sturge-Weber syndrome.
Plate 6.3 | Sturge-Weber syndrome with secondary

glaucoma. (Courtesy Prof. S.L. Adile.)
Plate 6.4 | Microphthalmos causing narrowing of inter-
palpebral aperture. (Courtesy Dr. Dilip Agarwal.)
(f) Hypotony
(g) Phthisis
(h) Perforated globe
(i) Ipsilateral hypertropia
(j) Contra lateral lagophthalmos
3. Orbit
(a) Enophthalmos (fracture orbit)
(b) Loss of orbital fat
EXAMINATION OF PTOSIS (FLOWCHART 6.1)
History
1. Onset: congenital and acquired
Acute: ocular palsy and myasthenia
Gradual: progressive external ophthalmoplegia, senile, drug-induced and myasthenia
2. Diplopia if present: look for other extra-ocular muscle palsy. If absent: raise upper lid and see if
patient complains of diplopia, this denotes other extra-ocular muscle palsy
In case of absent diplopia, test vision; try to find out cause of gross diminished vision.
1. Error of refraction
2. Fundus lesion
If no cause of diminished vision is detected, presence of amblyopia should be suspected.

Causes of absent diplopia in ptosis are:
1. Only levator is involved
2. Pupil is covered by lid
3. Amblyopia
4. Ipsilateral gross loss of vision
5. Contralateral gross loss of vision
Examination of ptosis should also be studied under the following heads:

1. Relation to exercise: diplopia becomes worse and ptosis increases, most probable cause is
myasthenia
2. Vision to exclude amblyopia
3. Fundus: (a) exclude raised intracranial tension, (b) exclude other causes of diminished vision—
lesions of optic nerve, macula and opacity in media
4. Head posture: chin is elevated both in ptosis and pseudo-ptosis
5. Width of IPA (Table 6.2)
6. Function of LPS
7. Pupil
8. Corneal sensation
9. Bell’s phenomenon
10. Other extra-ocular muscle
11. Tensilon test
Ptosis
Pseudo-ptosis True ptosis
Neurogenic Congenital Myogenic
Exercise
Oculomotor nerve Cervical
involvement sympathetic
Increased No change
Horner's diplopia in diplopia
syndrome
Tensilon test Progressive

Only external
Oculomotor and other ophthalmoplegia
oculomotor nerves involved
Positive
E.M.G
Upper division Myasthenia
L.P.S. + S.R. Both
involved divisions
Examine pupil
Pupil involved Pupil spared (Diabetic)
Flowchart 6.1 | Steps for examination of a case of ptosis.
Table 6.2 Estimation of grades of ptosis
Visible Cornea (mm) Drooping (mm) Grade
7 2 Mild ptosis
6 3 Moderate ptosis
5 4 Severe ptosis
12. EMG
13. Urine examination for sugar
14. Neurological evaluation
15. Tear film status
A
2 mm AE = 11.0 mm, diameter of cornea
B
AB = 2.0 mm, distance of normal upper
Iid from upper limbus
D BE = Width of interpalpebral aperture
11 mm 9 mm D = Central corneal light reflex
BD = Distance between upper lid and
corneal light reflex
E
Fig. 6.1 | Normal position of lid in relation to the cornea.

A
AB = 2 mm, distance of normal upper
2 mm Iid from upper limbus
B D = Central corneal light reflex
C AC = Distance of drooping lid from
D upper limbus
11 mm 9 mm CE = 7 mm, width of palpebral
aperture
AC-AB = 2 mm is ptosis
E
Fig. 6.2 | Measurement of ptosis (margin limbus distance).
➤ While examining a case of ptosis, it should be clearly determined if

it is congenital or acquired. A congenital ptosis may be under
corrected if it is operated as acquired and vice versa
EXAMINATION OF INTERPALPEBRAL APERTURE IN PTOSIS
1. Normal lid covers 2 mm of upper part of cornea. Normal vertical diameter of cornea is
1 1 mm.Visible cornea is 9 mm (Fig. 6.1)
2. Ask the patient to look up and measure visible cornea from lower limbus. This is known as
margin limbus distance or MLD (Fig. 6.2)
MEASURING MARGIN REFLEX DISTANCE
MRD-I (Fig. 6.3)

1. Bring the eyes of the patient and the observer to the same level
2. Ask the patient to fix a distant object
3. Bring a fixation light in between the patient and the observer
4. Note the position of the corneal reflex
5. Measure the distance between the corneal light reflex and centre of the upper lid.This meas-
urement is called positive (Fig. 6.3B)
1. Normal lid covering 2 mm of upper cornea

Ptotic lid margin M
MRD-I
positive
Corneal light reflex R
2. Ptotic lid covering 4 mm of upper cornea

M
MRD-I
negative
R
Ptotic upper lid
R MRD-II
Lower lid margin
Fig. 6.3 | Measurement of MRD-I and II.

6. If the corneal light reflex is obstructed by the drooping lid, note the position of the drooped
lid and elevate it until the corneal light reflex becomes visible and this distance is measured as
negative (Fig. 6.3C)
MRD-II
MRD-II is the distance between the corneal light reflex and lower lid at the primary
position (Fig. 6.3).
MRD-III
MRD-III is the distance between the corneal light reflex and the upper lid in up gaze.
ASSESSMENT OF LPS FUNCTION (FIG. 6.4)
Normal excursion of upper lid is about 12 mm, i.e. the difference between the level of
upper lid in down and up gaze. Range between 8 and 12 is considered as good LPS
function. Excursion of 5–7 mm denotes moderate LPS action and less than 4 mm is
poor function.
LPS Function Test (Plate 5.22)
1. Ask the patient to look down, put a vertical scale in front of the lower lid so the zero of the
scale is at the level of the margin of the lower lid
10
5 Cornea in primary position

Ptotic lid in primary position
0
Ptotic lid margin in down gaze
10
5 Ptotic lid margin in up gaze
Corneal margin in up gaze

0
Fig. 6.4 | Measurement of ptosis in down gaze and up gaze.

2. Measure the distance from zero to the upper lid margin
3. Keep the scale in the same position
4. Ask the patient to look up
5. Measure the position of lid margin in millimetres in the raised position. This is normal excur-
sion of the upper lid
JAW WINKING
This represents a very common synkinetic movement of the lid with movement of the
jaw, generally in congenital ptosis. Otherwise it may be an independent phenomenon
without ptosis. Movements of jaw that produce a change in the width of the IPA are
either mastication or moving the jaw from side to side. In most of the cases IPA
becomes wider on opening the mouth, but the reverse is also possible.
EXAMINATION OF THE PUPIL
In congenital ptosis the pupil is generally normal. The pupil is spared in diabetic third
nerve palsy. In Horner’s syndrome the pupil is miotic. In mass lesions affecting third
nerve, the pupil is dilated.
Corneal sensation and Bell’s phenomenon have prognostic importance in surgical cor-
rection of ptosis. Surgery is contraindicated if corneal sensation is subnormal. Absent
Bell’s denotes paralysis of SR; in such cases if the ptosis is corrected, there is always a
chance of corneal exposure and ulceration.
Schirmer’s test II The basic Schirmer’s test should be 3 mm or more in 5 min.
Eyes with less than 3 mm Schirmer II should not be over corrected. All cases of dry
eye are relative contraindications for ptosis surgery.
Tensilon test This is a diagnostic test to confirm myasthenia and differentiate it

from other causes of ptosis. However, this test is not much help in early cases. It is pos-
itive when ptosis is present. In a suspected case of myasthenia, there is no ptosis. It is
precipitated by asking the patient to look up and down for few times or to take a brisk
walk for a few minutes. The test is an outdoor procedure, and resuscitation facilities
should be available.
The procedure is explained to the patient, i.e. 0.4 mg atropine I.M. is given 15 min
before the actual test is started. This abolishes the untoward cholinergic side effects,
but not the effect on the neuromuscular junction.
Tensilon (edrophonium hydrochloride) is available in single dose ampoule of 1 cc
containing 10 mg of the drug. The drug is given intravenously. It is better to put a
scalp vein needle in a suitable vein of forearm.
1. The drug is drawn in 1 cc tuberculin syringe and kept aside.
2. A second syringe is filled with 10 cc normal saline.
3. One cc of normal saline is injected in the vein and the reaction is observed. There should be
no change in ptosis.
4. 0.2 ml of Tensilon is injected in the scalp vein and the drug is flushed with 1 cc of normal saline
and patient is observed for the next 1 min. In a sensitive patient, slight improvement would be
seen. If there is no response, remaining 0.8 ml of drug is injected fast and washed with 1 ml
saline.The three possible results are given below.
(a) Improvement of ptosis, reduction of diplopia, reduction of tropia; and this confirms
myasthenia
(b) Worsening of ptosis and tropia
(c) Reversal, i.e. ptosis develops in the other eye. If there is ptosis in other eye it becomes
worse, right hypertropia becomes left.
The last two above-mentioned results are seen in non-myasthenic patients.
E XAMINATION OF THE
L ACRIMAL S YSTEM
The lacrimal system consists of (Fig. 7.1):

1. Secretary system
● Lacrimal gland
● Accessory lacrimal gland
● Conjunctival glands
● Meibomian glands
● Zeis and Moll glands
2. Spreading system
● Normally functioning lids
● Intact lid margin
● Normal blink reflex
● Normal tear film
3. Draining system
● Upper puncta
● Lower puncta
● Upper and lower canaliculi
● Lacrimal sac
● Nasolacrimal
EXAMINATION OF LACRIMAL GLAND
Normally, lacrimal glands are neither visible nor palpable as they are situated deep
under the superior-lateral part of the orbit in the fossa of lacrimal gland. Sometimes,
normal accessory lacrimal glands are visible on everting the upper lid on the lateral part
Upper canaliculus Upper puncta

Lacrimal sac
Lacrimal gland
Accessory lacrimal gland

Nasolacrimal duct
Lower canaliculus Lower puncta
Fig. 7.1 | Diagrammatic representation of the lacrimal system.

EXAMINATION OF THE LACRIMAL SYSTEM 75
of the lid above the lateral canthus. The commonest disorder of lacrimal glands is
swelling due to infection, inflammation or neoplasm, which pushes the eyeball forward
and downward. In acute infection, the gland is enlarged and painful. In chronic
inflammation, it is swollen without pain, as is the case in neoplasia. Inflammation of
the lacrimal gland is called dacryoadenitis.
Causes of dacryoadenitis are:
1. Acute: mumps (commonest), influenza, erysipelas and trauma
2. Chronic
(a) Sequel to acute adenitis
(b) Chronic granuloma:
● Tuberculosis
● Syphilis
● Sarcoid
● Pseudo granuloma
3. Neoplasm: mixed tumour

4. Dacryops: retention cyst
5. Parasitic cysts
Causes of bilateral enlargement of lacrimal gland are:
1. Mikulicz syndrome
2. Sarcoidosis
EXAMINATION OF LACRIMAL GLAND SWELLING
Swelling of the lacrimal gland pushes the eyeball down and medially. It also pushes the
eye forward, so there is moderate proptosis down and in. One cannot insinuate a fin-
ger between the swelling and the orbital wall. There is an S-shaped curve of the lid
margin which droops.
Examination of spreading system is essentially examination of lids and tear film
(see Chapter 10).
Examination of Draining System

Puncta—Look for its presence.
Size pinpoint or normal. It should be remembered that the lower punctum and
canaliculus drain 75% of tears. Actually, the lower punctum is more important than
the upper punctum.
To see the lower punctum, press the medial side of the lower lid near the medial
canthus. This will evert the lower lid along with the punctum alternatively, the medial
end of the lower lid may be pulled down to see the punctum. Inspection of the upper
punctum is more difficult, especially in children. The upper punctum becomes visible
on lifting the medial side of the upper lid and asking the patient to look down.
Examination of canaliculi is performed indirectly by performing the regurgitation test
and syringing. Regurgitation of fluid from puncta in presence of chronic dacryocystitis
Plate 7.1 | Acute dacryocystitis in an infant of five days.
means patent canaliculi and punctum. In the absence of chronic dacryocystitis patency
can be ascertained by syringing only (see evaluation of nasolacrimal duct patency).
Examination of Lacrimal Sac

Lacrimal sac is situated under the medial palpebral ligament, and normally it is nei-
ther visible nor palpable. The sac becomes visible and palpable only when it is either
distended due to accumulation of fluid, or harbours a growth.
Causes of distended sac: chronic dacryocystitis, pyocele of sac, mucocele of sac and
encysted mucocele of the sac. In acute dacryocystitis, inflammation of peri-cystic tis-
sues overshadows distension of the sac. The area over the sac is tender, warm and red.
The wall of the sac is thickened in granuloma of the sac and neoplasm of the sac.
Common granulomas of the sac are rhinosporidiosis, tuberculoma and gumma.
Neoplasm of the sac is very rare.
The enlarged sac presents as a diffuse, oval swelling between the medial canthus and
lateral wall of the nose at the level of medial canthus. The swelling is subcutaneous, thus
the skin moves freely over it. Restriction of movement of skin occurs in acute dacry-
ocystitis (Plate 7.1) lacrimal fistula, or following surgery on the sac.
Regurgitation test (RT) is the single most important test to demonstrate patency of
the drainage passage. This is done by pressing the sac with the index finger of the
examiner against the lacrimal fossa. If there is regurgitation of fluid, mucoid or puru-
lent, through the puncta, it means that:
● The sac is full of fluid
● The nasolacrimal duct is blocked
● The canaliculi and puncta are open. If there is regurgitation from only one punctum, this denotes
obstruction of the other canaliculus or punctum
Non-compressibility of the sac without regurgitation means encysted mucocele of the

sac where there is accumulation of fluid in the sac but the canaliculi and nasolacrimal
duct are simultaneously blocked. The sac is also non-compressible in cases with growth
of the sac wall. Compressible sac without regurgitation means that:
● The nasolacrimal duct is patent or passage of DCR is open
● The sac is fibrosed
● The sac is absent—the commonest cause of absent sac is its surgical removal, congenital
absence of sac being extremely rare
EVALUATION OF PATENCY OF LACRIMAL DRAINAGE PASSAGE
Lacrimal passage consists of two puncta, two canaliculi, a common canaliculus, a

lacrimal sac and a nasolacrimal duct.
A disorder blocking of any one of these or a combination thereof will produce
epiphora, regurgitation, chronic medial conjunctivitis or swelling of the sac depending
upon the level of obstruction.
Symptoms of lacrimal drainage obstruction are:
● Epiphora
● Mucoid discharge
● Swelling between the medial canthus and lateral wall of the nose
● Positive regurgitation test
Tests Done to Evaluate Lacrimal Drainage

1. Regurgitation test
2. Taste test
3. Dye recovery test
4. Lacrimal syringing
5. Dacryocystography
6. Lacrimal scintillography or scintigraphy
Regurgitation Test (RT)

Gentle pressure over the distended sac will cause regurgitation of mucoid or purulent
discharge from the lower punctum and occasionally from both the puncta, denoting
obstruction of the nasolacrimal duct. This does not give any indication of the position
of block in the nasolacrimal duct. Regurgitation from upper punctum and not from
the lower indicates block in the lower canaliculus or punctum along with nasolacrimal
duct obstruction. Regurgitation from lower punctum only means block in the upper
canaliculus or punctum.
Pressure over the sac area with no regurgitation may imply any of these:
1. Patent nasolacrimal duct
2. Absent sac
3. Patent DCR or intubation of NLD/sac

4. Encysted mucocele of sac
5. Recently emptied sac
Absent sac and DCR will be obvious by history and surgical scar.
Characteristics of encysted mucocele of the sac:
(a) Distended, non-tender and tense sac
(b) Non-compressible swelling
(c) No regurgitation from any puncta
(d) No epiphora
Taste Test
Lacrimal sac communicates with the conjunctiva on one end and the nasopharynx on
the other. Any fluid instilled in the conjunctiva is bound to trickle down the throat
and the patient can taste this fluid. Many fluids are used in this simple test:
● 5% sodium chloride drop (common salt)
● 5% glucose saline
● Any bitter antibiotic eye drop, most commonly Chloramphenicol eyedrops
If the block is suspected to be unilateral, any of the drops is put in the ipsilateral
conjunctival sac. The patient is asked to indicate as soon as the taste of the drug is felt
at the back of the tongue. Absence of taste denotes NLD block on the same side. The
test is positive when the lacrimal passage is open. It is also positive in cases of partial
NLD block with positive regurgitation.
If bilateral block is suspected, one side is tested first and the other side is tested after
48 h.
If taste is not felt after 15–20 min, a complete block is diagnosed. This test should
be preceded by the regurgitation test.
Dye Recovery Test

Jones I test
1. Inferior turbinate is anaesthetised by 4% Xylocaine
2. One drop of 2% fluorescein is instilled in the conjunctiva
3. After 1 min, a cotton tipped applicator is introduced under the inferior turbinate and with-
drawn after sometime. Staining of cotton indicates patent NLD. If the first inspection does not
show positive stain the applicator is introduced and examined after every minute for 5 min.
Absence of stain means NLD obstruction. Any other medical stain like mercurochrome can
also be used
Jones II test
1. Anaesthesia of inferior turbinate and instillation of fluorescein is done as in test I
2. The conjunctival sac is cleaned of residual dye
3. The sac is flushed with normal saline by a lacrimal canula and syringe
4. If stained fluid is recovered from the nose after syringing, it means there is a functional block of
the NLD
➤ Jones I and II can be modified by asking the patient to blow the nose on a white
piece of gauze. If the gauze is sprinkled with drops of fluorescein fluid there is no
block in NLD
Lacrimal Syringing
The test is performed to find out:
1. Patency of NLD
2. Patency of DCR
3. Patency of lacrimal fistula
4. To open partially blocked NLD
Procedure
1. Conjunctival sac is anaesthetised with 4% Xylocaine.This will anaesthetise puncta as well as the
canaliculi
2. Lower punctum and canaliculus are dilated by punctum dilator
3. Lacrimal canula is introduced through the dilated punctum and canaliculus
4. Lacrimal canula is attached to a saline filled 5 cc syringe
5. The plunger is slowly pushed down and the following observations are made:
(a) Patient feels the saline in the throat and swallows it. NLD is patent
(b) Saline is felt in the throat under pressure. NLD is partially blocked
(c) Saline is not felt in the throat and regurgitates through upper puncta—NLD is completely
blocked and upper canaliculus and punctum are open
(d) Saline regurgitates through lower puncta by the side of lacrimal canula—NLD, upper
canaliculus and punctum are blocked
(e) Saline trickles through an opening on the skin—Lacrimal fistula
(f) Distension of sac without regurgitation and slight trickle down the throat is suggestive of
rhinosporidiosis of the sac
The test is contra indicated in acute dacryocystitis.
Dacryocystography (DCG)
Principle of DCG is same as that of syringing. Instead of using a clear watery fluid, a
radio-opaque dye is injected in the sac.
The dye can be watery, viscous or oily. Aqueous solutions are easy to inject but flow
out quickly.
Commonly used dyes are:
1. Conray 280
2. Neohydroil
3. Diagonal viscous
4. Lipiodol in water or oil
5. Dionosil
There are basically two types of dacryocystography:
1. Plain DCG
2. Macrodacryocystography
Plain DCG: The dye is injected. The lacrimal canula is removed, and a lateral and
AP X-rays of the orbit are taken, avoiding shadow of the petrous bone is taken.
Macrodacryocystography This consists of keeping the sac distended with dye
throughout the procedure without removing the lacrimal canula and taking magnified
view of the sac, canaliculi and NLD. A small well-focused beam of X-ray is used.
X-ray film is kept 18 in. away from head of patient in contrast to plain DCG where
the skull is almost in contact with the cassette. The lacrimal canula is attached to a long
polythene tube that connects to a 10 ml syringe containing dye. The dye is injected to
distend the sac. Anterio-posterior X-rays are taken immediately and repeated after 15
and 30 min.
Lacrimal scintillography (Dacryoscintigraphy)

This is a lesser used method to evaluate anatomical as well as functional block of lacrimal
passage because it requires a specially designed gamma camera. Drops containing radio
tracer are instilled in the conjunctival sac in both eyes. Commonly used tracers are TC
99m or sulphur colloid. Pictures with gamma camera are taken at an interval of 5 min
for 40 min. In patent NLD the tracer is visualised in the nasal cavity after outlining
the canaliculi, sac and NLD. Retained tracer in the sac indicates NLD block.
■■■ CHAPTER 8
E XAMINATION OF THE
C ONJUNCTIVA
Conjunctiva spreads from the intermarginal strip of the lid to the limbus. It acts as a
protective membrane over the sclera and part of the extra-ocular muscles. It is transpar-
ent, and is rich in blood vessels and lymphoid tissue. It is firmly attached over the tarsal
plate and at the limbus. It is very loose at the fornices. It can be lifted with ease from the
bulbar conjunctiva or distended with fluid. It cannot be peeled off from the tarsal plate.
The conjunctiva that covers the tarsus is called palpebral or tarsal conjunctiva and the
part that overlies the sclera is called bulbar conjunctiva (Fig. 8.1).
The conjunctiva is most lax between the tarsal and bulbar conjunctiva at the fornices.
Upper fornix is the most spacious and its upper limit is not visible for inspection. Top of
the upper fornix is about 15 mm from the superior limbus and the lower fornix is almost
half in depth. The lateral fornix is situated at the junction of lids under the lateral canthus
and its maximum depth is 5 mm. Medial fornix is occupied by caruncle which is a
3 mm ⫻ 3 mm raised epithelised nodule situated between the two lids in the medial can-
thus. There may be very fine hair growing over the caruncle. It represents the vestigial
third lid. It does not have any known function but is involved in diseases of the con-
junctiva. Lateral to the caruncle is a semi-lunar fold of conjunctiva with concavity towards
the cornea and is called plica semilunaris. The conjunctiva is highly vascularised. In the
Upper fornix
Skin
Tarsal conjunctiva
Lashes Bulbar conjunctiva
Lower fornix
Fig. 8.1 | Various parts of conjunctiva.

Circumciliary congestion Conjunctival congestion
Episcleral congestion
Fig. 8.2 | Types of congestion.

normal eye, only a few blood vessels are visible as red streaks against the white sclera. The
conjunctival vessels travel centripetally from the periphery to the centre (Fig. 8.2).
The thinness, profuse blood supply and abundant nerve supply allow conjunctival
wounds to heal quickly. Small gaps in conjunctiva heal on their own due to sliding of
the epithelium from each end of the wound, without scar formation. Large wounds
should be stitched without incarcerating Tenon’s capsule or pouting of the conjuncti-
val edges; otherwise a thick scar and cyst will be formed.
Irritation of the conjunctiva will lead to conjunctival congestion and lymphoid prolifer-
ation, leading to conjunctival papillae and follicle formation. The conjunctiva supplies
mucous to the tear film and binds the lacrimal secretion to the cornea. Conjunctiva reacts
to allergens, both endogenous and exogenous, in various ways that may be acute or
chronic. As the conjunctiva is continuous with the skin of the lid and nasopharynx (via
the nasolacrimal duct), it is vulnerable to spread of infections from skin, nose or throat.
Conjunctival epithelium is continuous with the corneal epithelium. While spread
of infection from the conjunctiva to cornea is very common, vice versa is rare. Except
for the first few days after birth, the conjunctiva is never sterile. Organisms that are
commonly seen in conjunctiva are diphtheroid, pneumococci and staphylococci. Some
fungi may be dormant in the conjunctiva without any ill effects as long as the defence
mechanisms are in order.
PROCEDURE OF EXAMINATION OF THE CONJUNCTIVA
Conjunctiva is best examined by inspection. Palpation has a limited role, limited to find-
ing out its consistency and eliciting tenderness. Conjunctiva should be inspected in:
1. Diffuse illumination
2. Focal illumination with magnification
(a) Examination under diffuse illumination is done with any handy bright flashlight with good
focus. After the interpalpebral aperture has been examined for its width, proptosis and obvi-
ous squint, the lower lid is pulled down and the patient is asked to look up.This exposes the
lower tarsal and bulbar conjunctiva from canthus to canthus, lower punctum, lower half of
cornea, AC and iris for inspection. After these parts have been examined the following
steps are carried out
(b) The upper lid is raised and the patient is instructed to look down. This exposes the upper
bulbar conjunctiva up to mid-corneal line in a horizontal plane, the upper cornea, and the
upper part of AC and iris
EXAMINATION OF THE CONJUNCTIVA 83
(c) The patient then turns her eye medially, exposing the lateral bulbar conjunctiva up to
the outer canthus, and then laterally, exposing the medial bulbar conjunctiva, caruncle
and plica
(d) Once the bulbar conjunctiva has been examined without much discomfort, the patient
relaxes and permits examination of the upper tarsal conjunctiva by eversion of the
upper lid
Eversion of the lid is done by asking the patient to look down, the lashes are grasped
between the thumb and index finger and pulled down and everted over the pulp of
the index finger. This exposes the tarsal conjunctiva from one end to the other end up
to a few millimetres above the superior border of the tarsus. It takes some practice to
evert the lid. It is difficult to evert the lid in small children, lid oedema, blepharospasm,
advanced trachoma, wet and oily lashes, madarosis and growth of lid. In the presence
of painful conditions like stye, internal hordeolum, lid abscess, eversion of lid should
not be done. In ophthalmia neonatorum and membranous conjunctivitis eversion is
best avoided.
(e) In blepharospasm instillation of a few drops of a local anaesthetic agent in both the eyes
will permit the patient to open them for examination and permit eversion of upper lid
(f) Upper fornix is not visible for examination. To examine the upper fornix the lid has to be
everted twice, which is called double eversion. Double eversion of the upper lid is done by
anaesthetising the conjunctiva, evertion of lid is done in the manner. Grasping the tarsal con-
junctiva and upper part of the palpebral conjunctiva between thumb and index finger and
everting again. This will expose the upper part of palpebral conjunctiva and the upper part of
fornix
In case of uncooperative patients, severe blepharospasm, severe oedema of lid, ophth-
almia neonatorum, the eye cannot be examined without the use of lid retractor and lid
hook. Most commonly used lid retractor is Desmarre’s retractor. It is available in two
sizes: adult and child. It can be used without local anaesthesia but it is better to use
local anaesthesia as that abolishes the associated blepharospasm (Plate 8.1).
A lid hook or a smaller retractor can be used simultaneously for the lower lid. Care
should be taken not to press the globe while using a retractor especially if there is his-
tory of injury, or in the presence of a large corneal ulcer or keratomalacia. Sometimes
a child may have to be examined under short-term general anaesthesia administered
by a qualified anaesthetist.
METHOD OF EXAMINING ANTERIOR SEGMENT OF

A CHILD’S EYE
The child is made to lie down on the thigh of an attendant with head on the lap
of the examiner. The attendant holds the child, restraining movement of hands
and body. The examiner restricts the movement of the head by gently pressing
between the observers thighs. This virtually immobilises the child with no discomfort,
leaving both hands of the examiner free to use the flash light and to separate the lids
(Plate 8.2).
Plate 8.1 | Use of Desmarre’s retractor. Plate 8.2 | Examination of anterior segment of a non-cooperative child.
CONJUNCTIVA IS EXAMINED UNDER FOLLOWING HEADINGS
1. Transparency
2. Change of colour
3. Congestion
4. Oedema
5. Discharge
6. Membrane formation
7. Follicles
8. Papillae formation
9. Nodules
10. Dryness
11. Injury
12. Foreign body (Plate 8.3)
13. Bleb
14. Degeneration
15. Concretion
16. Ulcer
17. Growth/cyst
18. Parasites
19. Bleeding from conjunctiva
20. Sub-conjunctival haemorrhage
21. Symblepharon
Transparency of Conjunctiva
Conjunctiva is transparent enough to make the underlying sclera and tarsal glands visi-
ble. Through the transparent conjunctiva any change in the white colour of the sclera,
localised or generalised, is visible. The tarsal glands are visible through the conjunctiva
as bluish translucent lines (Fig. 8.3).
Lid margin with lashes and

meibomian opening
Visible tarsal glands
Plate 8.3 | Foreign body upper tarsal conjunctiva. Fig. 8.3 | Everted upper lid.
Almost all diseases of the conjunctiva compromise transparency. The causes of loss
of transparency are congestion, oedema, membrane formation, follicles, papillae, sub-
conjunctival haemorrhage, xerosis, Bitot’s spots, pterygium, pinguecula and growths.
Change in Colour of Conjunctiva

The conjunctiva does not have any colour of its own. Any change in colour of con-
junctiva is due to change in colour of the sclera, blood vessels, deposition of melanin and
sub-conjunctival drug depot (steroid).
Pallor—conjunctiva becomes pale in anaemia, instillation of vasoconstrictors and
chemical burn.
Xanthosis (yellow) is seen in jaundice. Jaundice should always be seen in natural light.
Cyanosis (blue) is always associated with generalised cyanosis. Blue colouration is
also seen in blue sclera.
Red—pink to bloodshot is seen in congestion of conjunctiva, circumciliary conges-
tion, episcleritis, scleritis, sub-conjunctival haemorrhage and haematoma.
Black—this is due to deposit of melanin, benign or malignant melanoma or scleral
staphyloma.
White—these are due to sub-conjunctival injection of depots steroid, scleral
explants and Bitot’s spots. The last is seen over the conjunctiva, while the others are
under it.
Conjunctival Congestion
Conjunctiva is a highly vascular structure (Table 8.1). Normally the vessels are visible
as red tortuous branching lines against the white scleral background. There are three
types of congestion that are seen in the conjunctiva: congestion of conjunctival ves-
sels, congestion of ciliary vessels and congestion of episcleral vessels (Fig. 8.2).
Conjunctival congestion can be:
1. Active arterial congestion also known as conjunctival injection or
2. Passive venous congestion
Table 8.1 Difference between various types of conjunctival congestion
Features Conjunctival Ciliary Episcleral
Site Peripheral conjunctiva Around the cornea Peripheral sub-conjunctival

Colour Bright red Purple Bright red, vessels move
away from each other
Movement Move with bulbar Do not move Conjunctiva moves
conjunctiva. Do not over the vessel
move in tarsal
conjunctiva
Vessels
Direction Centripetal Centrifugal Centripetal
Size Moderate, individual Fine. Difficult Large individual vessels
vessels can be seen to differentiate stand out prominently.
individual vessels
Caput Medusae Nil Nil Vessels may anastomose
with each other and track
back away from limbus
called Caput Medusae
Effect of weak Blanch immediately Do not blanch Blanch with strong vaso
vasoconstrictor with rebound immediately, may constrictor
congestion blanch after few drops
Discharge Muco purulent Watery Nil
Anterior chamber Absent Present Present/absent
reaction
Cause Conjunctivitis Keratitis, iridocyclitis Absolute glaucoma and
and acute glaucoma raised episcleral pressure
Active conjunctival congestion is due to dilatation of conjunctival vessels following

any injury—mechanical, chemical, allergic or microbial. It can be localised or gener-
alised, unilateral or bilateral. It could be acute or chronic. Conjunctival congestion is
more marked in the fornices and gradually fades towards the limbus. The blood vessels
move with the conjunctiva (Table 8.2).
Passive congestion is due to obstruction of the venous flow in the orbit, cranium,
neck or thorax. It is seen in orbital tumours, dysthyroid oculopathy, cavernous sinus
thrombosis, varices of the orbital veins, neck glands and compressive lesions over the
superior vena cava.
Ciliary congestion is also known as cirumciliary or circumcorneal congestion. It is
due to dilatation of anterior ciliary vessels. It is seen in:
1. Corneal infection and inflammation
2. Anterior uveitis
Episcleral congestion is due to dilatation of episcleral vessels. It is seen in late stages
of chronic congestive and absolute glaucoma, and dysthyroid orbitopathy.
Causes of generalised conjunctival congestion are various types of microbial conjunc-
tivitis (Plate 8.4), some forms of allergic conjunctivitis and chemical injury.
Causes of localised congestion are circumciliary congestion, phlycten, scleritis,
episcleritis, pterygium, angular conjunctivitis lateral side, new growth, chronic dacryo-
cystitis and pinguecula granuloma (Fig. 8.4).
Table 8.2 Various types of localised conjunctival congestion, their site and causes (Fig. 8.4)
Site Causes
Circumciliary Keratitis, anterior uveitis, acute glaucoma and endophthalmitis

Localised near limbus Phlycten and spring catarrh
Away from limbus Episcleritis and scleritis
Outer canthus Angular conjunctivitis
Medial canthus Chronic dacryocystitis
Between medial canthus Pinguecula
and limbus
From medial canthus Pterygium
up to cornea
Tarsal Spring catarrh and follicular conjunctivitis
Anywhere Acute and chronic conjunctivitis, trauma and sub-conjunctival
haemorrhage
Spring catarrh Circumciliary congestion
Episcleritis Pterygium
Angular
Pinguecula
conjunctivitis
Lacrimal
conjunctivitis
Phlycten
Plate 8.4 | Severe conjunctival congestion and Fig. 8.4 | Various sites of localised conjunctival congestion.
sub-conjunctival haemorrhage in
acute mucopurulent conjunctivitis.
Note prominent arcus.
Causes of bilateral conjunctival congestion

Common causes of bilateral conjunctival congestion are various types of infective
and allergic conjunctivitis, degenerations and chemical injuries. They are purulent
conjunctivitis, muco purulent conjunctivitis, membranous conjunctivitis, phlyctenu-
lar conjunctivitis, spring catarrh, trachoma, chronic follicular conjunctivitis, epidemic
conjunctivitis, pterygium, angular conjunctivitis, chemical injury and blast injury.
Causes of unilateral conjunctivitis
All the above causes can start as unilateral conjunctival congestion, soon to become
bilateral within 24–48 h. A congestion that remains confined to one eye is rarely con-
junctival and other causes should be sought for it.
➤ Unilateral redness of eye is seldom conjunctivitis, other causes should be excluded

Plate 8.5 | Sub-conjunctival haemorrhage in blunt injury.
Conditions that Present as Unilateral Redness of Eye

1. Trauma—foreign body in tarsal plate, cornea, upper fornix, corneal abrasion, laceration of
conjunctiva, traumatic sub-conjunctival haemorrhage (Plate 8.5)
2. Keratitis—corneal ulcer
3. Uveitis—acute and chronic anterior uveitis and endophthalmitis
4. Glaucoma—acute and chronic congestive glaucoma both primary and secondary,
unilateral buphthalmos
6. Facial palsy
7. Unilateral pterygium
8. Pseudo-pterygium
9. Granuloma
10. Neoplasm
➤ Posterior uveitis alone and chronic simple glaucoma never produce congestion
Chemosis or Oedema of Conjunctiva

A lax and vascular conjunctiva predisposes to the accumulation of fluid underneath.
Most of the time it is a transudate from the conjunctival vessels. It is mostly seen
in bulbar conjunctiva. The fornices may be so much chemosed as to bulge in the IPA.
It does not occur in tarsal conjunctiva as it is firmly adherent to the tarsus. It can be
produced artificially by injecting fluid, e.g. antibiotic or anaesthetic agents.
Other causes of chemosis of conjunctiva are acute infections of conjunctiva, oph-

thalmia neonatorum, membranous conjunctivitis, angio-neurotic oedema, drug reac-
tion, hay fever conjunctivitis, orbital surgery and obstruction to lymphatic drainage.
The chemosed conjunctiva looks water laden, translucent and details of the underlying
sclera are obscured. It may be localised or generalised. In severe form, the conjunctiva
protrudes through the interpalpebral aperture. If chemosed conjunctiva remains exposed
outside the lid, it dries up, gets keratinised, may even ulcerate, e.g. in thyrotoxicosis.
Membrane Formation on the Conjunctiva

Membrane formation over the conjunctiva is peculiar to some forms of severe bacter-
ial and less commonly, viral conjunctivitis. All severe conjunctivitis do not result in
membrane formation.
➤ If pus is formed no membrane results
It is due to coagulation of fibrin-rich transudate from the conjunctival vessels. It has

been divided into to two types: severe—true membrane and milder—pseudo-membrane.
A true membrane is difficult to peel off and on peeling there is profuse bleeding
from the conjunctiva. The coagulum involves whole of the conjunctival tissue, which
is generally associated with pharyngeal diphtheria.
➤ As diphtheria is the commonest cause of membrane formation, all membranes of

conjunctiva should be considered as diphtheritic unless proved otherwise
Causes of pseudo-membrane formation are:

● Bacterial—streptococcus, staphylococcus, pneumococcus, meningococcus and Koch-Weeks
bacilli
● Viral—epidemic kerato conjunctivitis and herpes simplex
● Drugs and autoimmune disorders—Stevens-Johnson syndrome and benign ocular pemphigoid.
Sometimes the membrane is localised to the tarsal conjunctiva only
Follicles
Follicle formation in conjunctiva is a lymphoid reaction to insult of the conjunctiva, e.g.
bacterial, viral, irritant and drugs. Follicles are small hemispherical raised spots; there
is no vessel in the follicle. It mostly comprises of lymphoid tissue, with vessels either
surrounding the follicles or underneath them.
Causes of follicles are trachoma, chronic follicular conjunctivitis and drug reaction.
They are generally seen in the lower fornix. In trachoma they are seen in the palpebral
conjunctiva also (Tables 8.3 and 8.4).
Papillae Formation
These are flat topped polygonal elevations in the conjunctiva that are separated from
each other by a narrow gap. A papilla consists of a tuft of vessels covered by epithe-
lium and surrounded by fibrous septa (Tables 8.3 and 8.4).
Table 8.3 Comparison between papillae and follicles
Features Papillae Follicles
Age Any age, generally after Not seen before 3 months of age
the conjunctiva has been
exposed to exogenous allergen
Aetiology Exogenous allergy Infection, viral, trachoma, toxin and idiopathic
Location Common in upper tarsal Common in lower fornix
conjunctiva
Size Larger than 1 mm, may be as 0.5–2 mm
large as 5 mm in giant papillary
conjunctivitis
Shape Polygonal with flat top Small oval with round top
Symptoms Generally itching Mild irritation
Histopathology Central core of blood vessel Accumulation of lymphoid tissue in the
surrounded by inflammatory cells epithelium
Table 8.4 Differential diagnosis of follicles in conjunctiva
Features Follicular conjunctivitis Trachoma Spring catarrh
Age Children and young adult Children and young adult Rare after 20 years
Sex Equal in both sexes Slightly more in girls More in boys
Location Lower palpebral Upper palpebra Tarsal conjunctiva
conjunctiva and fornix conjunctiva and limbus
Arrangement In rows Irregular Cobblestone
Seasonal variation Nil Nil Mostly in summer
Symptoms Watering, redness Watery discharge Itching and ropy
and mucopurulent unless secondarily discharge
discharge infected. No itching
Cells in conjunctival Non-contributory Non-contributory Eosinophil
scrapping
Pannus Absent Very common May develop
There are two types of papillae:

● Simple papillae: 1–2 mm in size, seen in the upper tarsal conjunctiva. They are seen in spring
catarrh and atopic conjunctivitis
● Giant papillae:These are larger than 2 mm in diameter.They are seen in contact lens users, eyes
using ocular prosthesis or where round nylon sutures are left following various surgeries
Discharge from the conjunctiva—It consists of tears, mucous, inflammatory cells,
fibrin, organisms and pus.
It could be:
● Watery in allergic conjunctivitis
● Mucoid in chronic dacryocystitis
● Mucopurulent in acute mucopurulent conjunctivitis
● Purulent in gonococcal conjunctivitis
● Ropy in spring catarrh
Plate 8.6 | Laceration of conjunctiva.
Bleeding from Conjunctiva

Bleeding from the conjunctiva is seen in trauma (Plate 8.6), acute haemorrhagic con-
junctivitis, haemangioma, membranous conjunctivitis, papilloma, rhinosporidiosis of
conjunctiva, malignancy of sac and conjunctiva.
Sub-Conjunctival Haemorrhage
Sub-conjunctival haemorrhage is accumulation of blood under the conjunctiva. Fresh
sub-conjunctival haemorrhage has a bright red colour. Old haemorrhage becomes
black. It may be in a large patch or as small dots. Large sub-conjunctival haemorrhages
are seen in trauma, direct or indirect, to the eye, orbital trauma and fracture base
of skull (Table 8.5). In children, whooping cough is the most common cause of sub-
conjunctival haemorrhage.
Other causes are purpura, leukaemia, diabetes, hypertension and telangiectasia.
Small multiple haemorrhages are seen in pneumococcal conjunctivitis and acute
haemorrhagic conjunctivitis.
➤ If outer edge of the sub-conjunctival haemorrhage cannot be traced, it is due

to injury to either the orbit or the skull
Degenerations of the Conjunctiva

Two common degenerations of the conjunctiva are:
1. Pinguecula
2. Pterygium
Table 8.5 Comparison between traumatic sub-conjunctival haemorrhage due to cranio-

orbital fracture and due to non-cranio-orbital fracture (Fig. 8.5)
Features Cranio-orbital fracture Without cranio-orbital fractures
Onset 12–24 h after injury Immediate, following direct trauma

to the conjunctiva
Type of injury Blunt trauma to forehead, Mild-to-moderate trauma to
orbit or base of the skull conjunctiva
Spread of haemorrhage Fornix to cornea Does not spread much, may
spread in all directions
Visibility of outer Not visible Visible
border of haemorrhage
Location True sub-conjunctival. Inter-conjunctival haemorrhage.
Conjunctiva can be moved Moves with the conjunctiva
over the haemorrhage
Extension to the lids Ecchymosis is common No ecchymosis
Colour Dark and changes from Bright red
red to black
Surgical emphysema May be present Absent
Proptosis May be present Absent
Traumatic neuropathy May be present Absent
Petechial haemorrhage Large haemorrhage, periphery

due to conjunctivitis not visible—head or orbital injury
Moderate haemorrhage,
periphery visible—local
trauma or systemic
non-traumatic
Fig. 8.5 | Various kinds of sub-conjunctival haemorrhages.

Pinguecula
Pinguecula develops in adults. It is a painless nodule, not encroaching on the cornea.
It is not to be confused with phlycten. It is familial and said to be a precursor of
pterygium.
Pterygium
Pterygium (Plates 8.7 and 8.8; Table 8.6) is a degenerative condition of the cornea and
conjunctiva. It is the most common cause of localised conjunctival congestion on the
medial side in IPA. It is more common in adult males and is general bilateral. It is a
triangular fold of the conjunctiva with its apex over the cornea. The apex has a tendency
to move from the periphery towards the centre of the cornea. No probe can be passed
under the pterygium. Bilateral pterygia are more common. Unilateral pterygium without
involvement of the other eye is not degenerative.
Plate 8.7 | Pterygium lateral side. Plate 8.8 | Nasal pterygium.

(Courtesy Prof. A.K. Chandrakar.)
Table 8.6 Comparison between pterygium and pseudo-pterygium
Features Pterygium Pseudo-pterygium
Age Generally after 40 years Any age

Sex More in males Equal in both sexes
Family history May be present Absent
Location Always in IPA Anywhere
Spread Spreads from canthus to limbus Not specific
Aetiology Degenerative Post-traumatic
Probe test Probe cannot be passed under Probe can be passed
the pterygium
Progress May progress Does not progress
Recurrence following surgery Common Nil
Pseudo-Pterygium
Pseudo-pterygium is less common than pterygium (Table 8.6). It is mostly post-
inflammatory or post-traumatic. It is unilateral, may develop anywhere on the conjunc-
tiva and resembles a pterygium in appearance. A probe can be passed under the growth.
It does not grow towards the cornea. Its apex is stationary.
Nodules of the Conjunctiva

Nodules of varied aetiology, shape and size are common. Most of them are conjunc-
tival in origin. Conjunctival nodules move with the conjunctiva. Conjunctiva can
be moved over scleral and episcleral nodules. Nodules can develop anywhere on the
conjunctiva depending upon their cause. Limbus is the most common site and tarsal
conjunctiva the rarest (Fig. 8.6).
Causes of nodules in conjunctiva are:
● At or near the limbus: (1) phlycten (Plate 8.9), (2) pingucecula, (3) limbal dermoid (Plate 8.10) (4)
spring catarrh, (5) foreign body granuloma, (6) filtering bleb (Plate 8.14), (7) intra-epithelial
epithelioma of Bowen, (8) papilloma and (9) epidermoid carcinoma (Plate 8.11)
Filtering bleb
Spring catarrh
Pinguecula
Papilloma
Limbal dermoid
Phylcten
Intra-epithelial epithelioma
Fig. 8.6 | Nodules at and near the limbus.
Plate 8.9 | Phlycten in an adult.
Plate 8.10 | Bilateral dermoid at limbus.

Plate 8.12 | Bilateral dermolipoma.
Plate 8.11 | Epidermoid carcinoma at the limbus

in a case of xeroderma pigmentosa.
Plate 8.13 | Conjunctival

lower lid.
non-specific granuloma of Plate 8.14 | Filtering bleb, left eye.
● Away from the limbus: (1) episcleritis, (2) scleritis, (3) dermolipoma (Plate 8.12), (4) Granuloma
(Plate 8.13) and (5) new growth (Table 8.7)
Dryness of the Conjunctiva

Normally conjunctiva is a wet, shining and transparent structure. It remains moist due
to tears. Occasionally, due to defects in the tear film, dry spots develop on the con-
junctiva. A dry conjunctiva becomes lustreless. Normal conjunctiva does not wrinkle
on lateral gaze. A dry conjunctiva is thrown into vertical folds when the patient looks
Table 8.7 Comparison between phlycten and episcleritis
Features Phlycten Episcleritis
Age Children under 15 years Adults

Location At or near the limbus Away from the limbus
Number Single or multiple Generally single
Blepharospasm Generally present when at the limbus Absent
Tenderness Non-tender Tenderness frequent
Conjunctiva Moves with conjunctiva when present Conjunctiva moves
in bulbar conjunctiva over the nodule
Conjunctivitis Mucopurulent conjunctivitis is common Nil
Corneal involvement Fascicular ulcer and keratoconjunctivitis No involvement
Recurrence At other location Same location
to the lateral side. The folds may vary between 1 and 3 to 4, and the conjunctiva looks
dry. The dry spots stain with rose bengal but not with fluorescein.
Bitot’s spot This is deposition of a foamy substance on the conjunctiva in a trian-
gular fashion. It is generally present on the lateral side, between the limbus and outer
canthus. The apex always points laterally. The accumulated material can be wiped off,
only to reappear again. It stains black with kajal and surma, does not stain with rose
bengal or fluorescein.
Causes of dryness and conjunctival xerosis are:
1. Vitamin A deficiency
2. Exposure
Coloboma of lid
(a) Lagophthalmos
(b) Ectropion of lid
(c) Exophthalmos
(d) Proptosis
3. Dry eye syndromes
4. Systemic condition
(a) Stevens-Johnson’s syndrome, ocular pemphigus
(b) Sjogren syndrome
Symblepharon
Normal bulbar and palpebral conjunctiva do not adhere to each other. If they get
stuck together, it is called symblepharon. It can be localised as a small adhesion or two
large surfaces can get fused. Adhesion between palpebral and bulbar conjunctiva is
called anterior symblepharon. Obliteration of fornix is called posterior symblepharon.
Causes of symblepharon are:
1. Chemical injury
2. Simultaneous loss of bulbar and palpebral conjunctiva
3. Burns
4. Stevens-Johnson’s syndrome
Concretion (conjunctival lithiasis)—Contrary to the name, they are not minute

stones. They are not even calcified as their appearance would suggest. They are raised,
yellowish-white, hard granules that develop in tarsal conjunctiva, either singly or in
clusters. They are composed of dried mucous in which epithelial cells get entangled. They
can be scrapped off the conjunctiva with a needle or a blade without bleeding. They are
commonly seen following chronic inflammation or atrophia or in old age.
Granulomas of conjunctiva These can be:
1. Infective
2. Foreign body
3. Neoplastic
Infective Granuloma
The most common cause is a burst chalazion. This is very frequent in the upper tarsal
conjunctiva.
Other causes are:
1. Tubercular
2. Syphilitic
3. Rhinosporidiosis (Plates 8.15 and 8.16)
Granulomas can develop anywhere on the conjunctiva. Depending upon these sites,
they can be sessile or pedunculated, round or flat. Sessile and round granulomas are
seen in the IPA. Sessile and flat granulomas are seen arising from the tarsal conjunctiva.
Compression of lid over the globe makes the tarsal granuloma flat.
Pedunculated and flat granulomas arise from the fornices.
Small haemangiomas, papillomas, dermoids and epidermoid carcinomas may be
mistaken as granulomas.
Plate 8.15 | Rhinosporidiosis conjunctiva—lower

fornix. (Courtesy Prof. A.K. Chandrakar.)
Plate 8.16 | Rhinosporidiosis upper fornix.
(Courtesy Dr. M.L. Garg.)
Plate 8.17 | Non-specific conjunctival cyst.
Plate 8.18 | Twin cysticercosis cysts removed from the sub-conjunctival space.
Cysts of the Conjunctiva
Cysts could be congenital, implantation and parasitic. Congenital cysts are dermoid
and dermolipoma.
Implantation cysts are generally post-traumatic, surgical or accidental (Plate 8.17).
Parasitic cysts—cysticercosis and hydatid cyst. The former are more common.
Parasitic cysts are more often seen in the left eye and medial side is more often involved
than the lateral side (Plate 8.18).
A conjunctival cyst on the left side is considered to be cysticercosis unless proved
otherwise.
The cyst can be translucent or may look solid. Parasitic and implantation cysts are
generally translucent.
Plate 8.20 | Malignant melanoma conjunctiva. (Courtesy Prof. S.L. Adile.)
Plate 8.19 | Epidermoid carcinoma of conjunctiva.

Ulcers of conjunctiva Conjunctival ulcers are relatively rare. The most common
cause is conjunctival phlycten. Other causes are tuberculosis and basal cell carcinoma of
conjunctiva, herpes simplex, mucous membrane pemphigus, trauma and burns.
New growths of conjunctiva Neoplasms of conjunctiva can be benign or malignant.
The former are more common. Benign tumours can be—dermoid, dermolipoma,
papilloma, haemangioma, nevus and neurofibroma.
Malignant tumours are—adenocarcinoma (Plate 8.19), basal cell carcinoma and
malignant melanoma (Plate 8.20).
Bowen’s disease is a pre-cancerous condition called carcinoma in situ. It develops
near the limbus and invades the cornea in adults.
E XAMINATION OF THE G LOBE ,
C ORNEA AND S CLERA
EXAMINATION OF THE GLOBE
The globe of the eye consists of two parts:

1. Transparent, more curved, highly pain sensitive, small optical part—cornea
2. Opaque, less curved, poorly pain sensitive, larger, non-optical, more of a supporting structure
than anything else—sclera
Examination of the globe consists of:

1. Overall assessment of its presence, size, curvature, shape and position
2. Examination of cornea
3. Examination of sclera
Overall Assessment of the Globe

Causes of absent globe are:
A. Congenital—anophthalmos: the term anophthalmos is used only in those rare cases where
there is a complete failure of development of the optic vesicle and not in cases of enophthal-
mos or microphthalmos, which are more common
B. Surgical removal
1. Complete
(a) Enucleation
(b) Exenteration
2. Partial—evisceration
C
24 mm
11 mm
P A normal globe
S–S : Maximum diameter of globe, 24 mm
C C–C : Diameter of cornea, 11 mm
S P : Pupil, 2.5 mm
Fig. 9.1 | Dimensions of normal globe.

EXAMINATION OF THE GLOBE, CORNEA AND SCLERA 101
S S
C C
24 mm
13 mm
24 mm
9 mm
C
C
S S
Fig. 9.2 | Buphthalmos. Fig. 9.3 | Microphthalmos (all dimensions are reduced;
may have coloboma of uvea).
Size: normal size of adult globe is 23–24 mm in diameter. Due to the increased curva-
ture of cornea, the anterio-posterior diameter is slightly more than the other dimensions.
Length of the globe of the new born normal child is 16–17 mm. Volume is 2.8 cc as
compared to the adult volume of 7.1 cc (Fig. 9.1).
Size of the globe is increased in (Fig. 9.2):
1. Buphthalmos
2. Megalocornea
3. Congenital myopia
4. Scleral staphyloma
Size of the globe is decreased in (Fig. 9.3):
1. Microphthalmos
2. Phthisis bulbi
3. Atrophic bulbi
4. Perforated globe
5. Nanophthalmos
Signs of small eyes are:
1. Lid:
● Narrow palpebral aperture (Plate 6.4)
● Loss of curvature of lid
● Increased lid crease
● Absence of eyeball may cause entropion and trichiasis
● Pseudoptosis
2. Globe: On inspection the globe looks smaller than the fellow globe if the abnormality is
uniocular
3. Vision: Vision is subnormal in a small globe. Generally microphthalmic eyes have small, flat
cornea. Absent or very shallow AC associated with coloboma of iris. Size of the microphthalmic
eye may be as low as 3–4 mm
4. Curvature: Curvature of the globe is generally reduced in microphthalmos, phthisis and perfo-
rated globe
5. Shape: Shape of the globe is distorted in microphthalmos, phthisis and perforated globe; the
distortion is least in microphthalmos. In phthisis and hypotony, the cornea may become hori-
zontally oval due to pressure of the lids (Fig. 9.4). In phthisis, the scleral shape may become dis-
torted to an irregular quadrilateral, with depressions at the site of attachment of the four recti
(Fig. 9.5)
6. Position of globe: Position of the normal globe is such that it has freedom of movement, can be
compressed in the orbit considerably, protrudes slightly anteriorly to give a convex curvature to
Fig. 9.4 | Soft eye—horizontally oval globe,

cornea and pupil.
Fig. 9.5 | Phthisis bulbi.
the lid but does not protrude beyond the superior border of the orbit. It is fully covered by
the lids on lid closure.When open, the upper lid covers the superior 2 mm of cornea, while the
lower lid just touches the lower limbus.The small eye is a deep set eye with a negative reading
on exophthalmometer, and showing pseudoptosis
Abnormal positions of globe in relation to the orbit are:
1. Proptosis
2. Exophthalmos
3. Enophthalmos
Proptosis: This is active protrusion of the globe forward due to causes other than dys-
thyroid oculopathy. It can be unilateral or bilateral, symmetrical or asymmetrical. It
can occur at any age. There is widening of the IPA without true lid retraction, the apex
of cornea bulges beyond the superior orbital border and exophthalmometry reading is
more than 18 mm (for details see examination of proptosis).
Exophthalmos: This term is exclusively used to denote passive displacement of the
globe due to exophthalmos producing substance in dysthyroid condition. This is due to
multiple systemic factors which are generally bilateral, but a unilateral bulge does not
exclude exophthalmos. It is generally associated with lid retraction, wide IPA, lid lag
and restrictive strabismus. Exophthalmometric reading are more than normal.
Enophthalmos: This is withdrawal of globe deep into the orbit. Common causes are:
1. Loss of orbital fat—old age, starvation and prolonged illness
2. Blow out fracture of orbit
3. Horner’s syndrome
4. Contracture of orbital tissue due to chronic orbital inflammation or some secondaries that pro-
duce shrinkage of the orbital structures
In enophthalmos, there is narrowing of IPA, pseudoptosis and loss of lid contour. It

could be misdiagnosed as contralateral proptosis (see enophthalmos).
EXAMINATION OF THE CORNEA
Cornea is examined under the following headings:

1. Recording of vision
2. Examination of cornea proper is done in the following order—shape, size, curvature, thickness,
transparency, sensation, vascularisation, deposits and encroachment from limbus
Recording of vision should precede all other examinations due to its diagnostic,
prognostic and legal value.
Cornea is examined by:
(a) Focal illumination
(b) Focal illumination with magnification
● Corneal loupe: uniocular or binocular
● Slit-lamp biomicroscopy
(c) Special techniques utilised in corneal examination are:

● Sensation
● Staining
● Keratometry
● Pachymetry
● Keratoscopy and corneal topography
3. Examination of corneal scraping

4. Examination of the tear film
5. Examination of ocular adnexa
(a) Lid margin
(b) Conjunctiva
(c) Lacrimal sac
6. Recording of intraocular pressure
(a) Skin disorders
(b) Autoimmune disorders
(c) Systemic infections
(d) Metabolic disorders
Focal Illumination
Examination of cornea under diffuse illumination is unsatisfactory. It is best examined
using the slit lamp, in the absence of which a good flashlight with bright illumination
that can be brought to a pinpoint focus should be used.
Lister’s lamp is a very handy appliance. It can either be operated on mains through
a step down transformer or on a rechargeable battery. Generally it gives a circular
beam of light that can be brought to a pinpoint focus by interposing a strong convex
lens that is attached to it in front of the bulb. A cobalt blue filter can be attached over
the light; in some models there is also arrangement for a slit (Plate 9.1).
Hand-held slit lamp is a convenient instrument that has a bright source of light,
arrangement to alter beam width and shape, cobalt blue filter and moderate magnifi-
cation. It is very useful for the recumbent patient, in eye camps and school survey.
Focal Illumination with Magnification

Cheapest and most effective magnifier for corneal examination is the corneal loupe.
Uniocular corneal loupe (Fig. 4.1) gives 10⫻ magnification, whereas the binocular
one gives only 1.5⫻ magnification. Hence cornea should be examined with the unioc-
ular loupe when the slit lamp is not available. However, it requires some practice to
master the use of a uniocular loupe.
Plate 9.1 | Lister’s lamp with step down transformer.
A. Normal corneal and scleral B. Buphthalmos: Curvatures C. Keratoconus. Only corneal

curvature of both cornea and sclera curvature is increased, scleral
are increased. Corneo- curvature is normal. Corneo-
scleral sulcus is obscured scleral sulcus is normal
D. Pellucid corneal degeneration. E. Corneal (anterior) staphyloma

Curvature of lower cornea is
increased
Fig. 9.6 | Changes in corneal curvature.

Slit-lamp biomicroscopy
A modern slit-lamp biomicroscope allows examination of the cornea under various modes
of illumination so that minute defects stand out prominently. The different modes of
illumination are direct and indirect.
Direct Illumination
1. Focal (diffuse): A wide moderately intense beam is used to examine the cornea under low
magnification (Fig. 9.7)
2. Narrow beam: A narrow beam is focussed on the lesion in an angular fashion with moderate
magnification (Fig. 9.8)
Path of light
Path of light
Fig. 9.7 | Diffuse illumination—a wide beam and

low magnification.
Fig. 9.8 | Direct illumination—a narrow beam
is focussed on the lesion in an angular
fashion with moderate magnification.
E
A
F
B
H
D G
(A) If both surfaces of cornea C

were straight and parallel, (B) Both surfaces of (C) ABCD, Anterior band
it would look like a cornea are curved EFGH, Posterior band
rectangular block and not parallel
Fig. 9.9 | Optical section of cornea.
1
Epithelium
2
Stroma
Descemet’s 3
membrane
4
Endothelium
Fig. 9.10 | Lesions at various levels of the cornea.
3. Optical section (Figs 9.9 and 9.10): An intense, narrow beam of illumination gives a linear cut
of the cornea without illuminating the surrounding. In this mode various levels of cornea are
available for inspection at the same time by changing the angulation between the light source,
the microscope and the distance between the cornea and the microscope (Fig. 9.11)
Anterior Posterior
corneal surface corneal surface
Lens
Light beam
Aqueous flare
Fig. 9.11 | Examination of aqueous flare with a narrow circular beam.

M
Microscope focussed centrally
Light leaves
cornea on Angled beam of
opposite light focussed
limbus on the limbus
S1 S
Fig. 9.12 | Retro-illumination (light is reflected

back either from iris or lens).
Fig. 9.13 | Scleral scatter (no light is seen by microscope if
the cornea is clear, but any opacity will stand
out prominently).
4. Specular reflection: It uses the principle of reflection of light by a polished surface. The princi-
ple states that when light falls on a mirror it is reflected. The angle of incidence and angle of
reflection are same, therefore, to see the source of light, the eye should be in the line of reflec-
tion. This method is the most widely used mode of examination of endothelium of the cornea.
Epithelium can also be seen by this method
Specular microscopy is a specialised biomicroscopy to examine the corneal
endothelium.
Confocal microscope is used mostly to detect organisms like fungi and microsporidia
during slit-lamp examination.
Indirect Illumination
This mode of illumination enhances contrast during visualisation of defects at various
levels of the cornea. Indirect modes of illumination are retro-illumination (Fig. 9.12)
and sclerotic scatter (Fig. 9.13; see slit-lamp biomicroscope).
Points To Be Noted During Biomicroscopy of the Cornea

In biomicroscopy various structures of the cornea can be seen. Lesions which are not visi-
ble on diffuse illumination and low magnification stand out prominently in optical
section. Occasionally more than one mode of examination has to be employed. The
examiner should examine one structure at a time instead of wandering haphazardly.
Following order should be considered while examining the patient: epithelium, Bowman’s
membrane, stroma, Descemet’s membrane and endothelium.
Epithelium—Look for: erosion, ulcer, oedema, filament, punctate epithelial kerati-
tis, foreign body, opacity and ghost images.
Erosions: These are depressed grey, white spots that stain brightly with fluorescein (better
seen under cobalt blue filter) and poorly with rose bengal. Superior erosions are caused by
tarsal foreign bodies, concretions, superior limbic keratopathy and vernal catarrh. Lid
pathology like lagophthalmos, trichiasis, entropion and blepharo-conjunctivitis cause
erosion of the lower cornea. Erosion of interpalpebral cornea is caused by exposure to
ultraviolet light, as in exposure to welding, snow blindness, and by neuroparalytic keratitis.
Ulcer: In erosion there is no breach in continuity of corneal epithelium, which is
the hallmark of an ulcer. Corneal ulcers present as grey white irregular areas sur-
rounded by infiltration and having a margin and a floor. The ulcer stains brightly with
fluorescein and the edges stain better than the floor.
Oedema: Appears like empty spaces in the epithelium that may be converted into
actual bullae, which are 1–2 mm in size. Bullae are vesicle-like structures laden with
fluid, which on rupture produce severe pain. They are found in acute congestive glau-
coma, endothelial decompensation, trauma, following IOL implantation, vitreous
touching the endothelium following ICC extraction, Fuch’s endothelial dystrophy,
long-standing interstitial keratitis and keratoconus.
Filaments: They represent peeled-off epithelium that remains attached to the
cornea. The loose ends hang over the cornea and move with the movement of the lid,
staining brightly with rose bengal. They are seen in recurrent idiopathic corneal ero-
sion, traumatic keratalgia, keratoconjunctivitis sicca and neurotropic keratitis.
Punctate epithelial keratitis: These are small white spots that stain poorly with fluores-
cein and better with rose bengal. They are seen in viral keratoconjunctivitis. Sometimes
it becomes difficult to differentiate between erosion and punctate keratitis.
Staining of Cornea (Plates 9.2 and 9.3)

Normal cornea does not stain with any stain. Stain only discolours the tear film that
passes off in due course or may be washed off. Many chemicals have been used to stain
the cornea, but all have not proved to be as useful as fluorescein and rose bengal. Both
are vital stains that resemble each other in structure, both are available as dark crystals,
soluble in water, and used as 1% drops. Fluorescein stains the damaged corneal epithe-
lium bright green, best seen under cobalt blue and ultraviolet light. Rose bengal stains the
devitalised corneal and conjunctival epithelium. The drawback with rose bengal is its sting.
It produces intense burning when instilled. Eyes may be anaesthetised before the use of
rose bengal with a local anaesthetic agent, e.g. proparacaine. Xylocaine should be avoided
as it produces desquamation of the epithelium. Both stains should be used either as
freshly made solutions or in the form of sterilised strips. Excess stain is washed with water.
Lissamine green is another stain, which has the staining properties of rose bengal.
It stains the cell nucleus dark. Vacuoles in mucus threads remain unstained but mucus
strands and dead and degenerated cells are stained.
Plate 9.2 | Fluorescein and rose bengal strips.
Plate 9.3 | Diffuse fluorescein stain in a case of chemical injury.

Uses of fluorescein in clinical ophthalmology are as follows:
1. To detect breach in continuity of corneal epithelium
2. Contact lens fitting
3. Applanation tonometry
4. Test for leaking wound (Seidel test)
5. Patency of nasolacrimal duct
6. Fluorescein angiography
7. Diagnosis of lacrimal fistula
8. Treatment of pediculosis
2
3
1. Nebula_not deeper than Bowman’s membrane

2. Macula_depth up to anterior stroma
3. Leucoma_depth up to posterior stroma
4. Adherent leucoma_an opacity in which iris is incarcerated
or was incarcerated
Fig. 9.14 | Grades of corneal opacity.
Clinical uses of rose bengal Rose bengal has limited role in staining corneal ulcers
or abrasions. It stains dead and damaged cells and mucus, without penetrating the
epithelial defect or intercellular space. It also stains conjunctiva in dry eye. Punctate
epithelial keratitis stains bright red (magenta) with rose bengal but poorly with fluo-
rescein, which stains erosion better. Both stains can be used simultaneously for differ-
ential staining of the cornea.
Opacities These are the due to replacement of transparent keratocytes by fibro-
cytes, accumulation of fluid in various layers, infiltration, deposits on the cornea or
vascularisation of the cornea.
Opacities are the end results of trauma, infection, inflammation, degeneration or dys-
trophy. They can be congenital or acquired. They can develop in any layer of the cornea.
Multiple layers may be involved at the same time, in one or both eyes. Opacities can be
single or multiple superficial or deep. Iris can get incarcerated. Foreign bodies are
known to be embedded in corneal opacities. They may be transient or permanent. Fully
healed opacities do not stain. Sensation over the opacity is generally absent or poor.
Opacities have been categorised into following four groups according to density
and incarceration of iris into it (Fig. 9.14).
Nebula, macula, leucoma and leucoma adherent—The lightest is nebula, which is
hardly perceptible while leucoma is a prominent white opacity that is visible even in
diffuse illumination, and a macula is in between. Any opacity in which iris is or was
incarcerated is called leucoma adherent.
Bowman’s membrane: This has a shorter diameter than the other layers of cornea. It
stops short of the periphery by almost a millimetre all round, and is a common site for
deposits.
Deposits: Various chemical can be deposited in healthy or diseased cornea. They are
generally either in Bowman’s membrane or superficial stroma, but other layers may
also be involved. The deposits are calcium in band keratopathy, hemosiderin—in blood
staining, copper in Kayser–Fleischer ring and iron in Fleischer ring in keratoconus.
Stroma While examining the stroma look for oedema, infiltrates and vascularisation.
Stromal oedema: This is a generalised or local thickening of the stroma due to accu-
mulation of fluid. The oedematous area looks like an empty space in the stroma. It
may be associated with infiltrate and seen in disciform keratitis, Fuch’s dystrophy, and
sometimes in keratoconus.
Stromal infiltrates: These are leucocytes that get into the stroma either through
limbal blood vessels or via a break in the epithelium. Infiltrates always denote active
inflammation.
Stromal vascularisation: Normal cornea is avascular except for a few limbal vessels on
the peripheral 1 mm; presence of vessels on or in the cornea denotes corneal pathology.
Vascularisation could be:
1. Superficial
2. Deep
3. Intercorneal
4. Retrocorneal
Superficial corneal vascularisation is called pannus where vessels along with fibrocytes
invade the cornea between the epithelium and the Bowman’s membrane. Commonest
site of superficial vascularisation is the upper part of cornea.
Some of the causes of superficial vascularisation are trachoma, leprosy, spring catarrh,
phlycten, superior limbic keratitis and contact lens use. Vascularisation of lower part
of the cornea is due to lagophthalmos, trichiasis, entropion, ectropion and proptosis.
Generalised vascularisation is seen in chemical burns, phlycten, spring catarrh and
riboflavin deficiency.
Deep vascularisation is due to entry of anterior ciliary vessels at the level of the stroma.
Deep vascularisation is seen in interstitial keratitis, disciform keratitis and chemical burns.
Vessels may grow in the substance of cornea in case of oblique wound of the cornea
near the limbus or under lamellar keratoplasty. New vessels grow on the posterior sur-
face of the cornea in case of epithelial down growth or rubeosis of iris (Fig. 9.18).
Descemet’s membrane: Common defects in Descemet’s membrane are breaks, splits
and folds. Breaks are seen in congenital glaucoma, trauma and keratoconus. Rupture
of Descemet’s membrane produces Haab’s striation in congenital glaucoma. Split is
seen in trauma, mostly surgical manipulation of the cornea: IOL insertion, glaucoma
surgery and lamellar keratoplasty. Folds are seen in a soft eye.
Endothelium: Examination of endothelium requires special skill, high magnification
i.e. 25⫻, and bright illumination. It can be seen either in the optical section or by spec-
ular microscopy. In specular microscopy photographs are taken to study the density and
characteristics of cells. Other observations in examination of endothelium show—fine
KPs (large KPs are visible with a uniocular corneal loupe) fibrin deposits, vascularisation
and vitreous touch.
Keratometry
Gross corneal curvature can be assessed by looking at the cornea from temporal side.
This is sufficient to tell if corneal curvature is grossly increased as in keratoconus or
flat as in a soft eye and micro-cornea. This information does not suffice for contact
lens fitting where the exact curvature of the optical zone should be determined. This
is made possible by using the keratometer which functions on the principle of image
formation by a convex mirror. Though cornea acts as a strong convex lens in the opti-
cal system of the eye, its anterior surface acts as a convex mirror, which forms a vir-
tual, erect small image, i.e. the first Purkinje Sanson image. If the size of the object,
its distance from the mirror, and size of the image formed is known, the curvature of
the mirror can be calculated. The curvature is measured in millimetres or in dioptre.
It is calculated by the formula D ⫽ (n ⫺ 1)/r, where D is the refractive power of
cornea, n is the refractive index and r is the radius of curvature of the cornea.
The disadvantage of the keratometer is that it measures curvature of cornea only in
the central 3 mm of the optical zone that is almost spherical. The range varies between
36 D and 52 D, which corresponds to 9.38–6.49 mm. This range is sufficient for
contact lens fittings, but in high degree of keratoconus a ⫹1.25 D lens is fitted with a
suitable adopter so that a reading of up to 61 D can be recorded.
Pachometry (Pachymetry)
Corneal thickness is not uniform throughout. It is thicker on the periphery and
thinnest in the centre. This is due to unequal radii of curvature of the two surfaces.
The posterior surface is more curved than anterior. Corneal thickness varies in various
diseases of cornea. In keratoconus and keratectaria, corneal thickness decreases while
in corneal scar and in hydration of cornea it increases. Increased corneal thickness
reflects malfunction of the endothelium. In refractive corneal surgery (RK, LASIK,
and keratoplasty), knowledge of corneal thickness is very important. There are two
types of pachometry:
1. Optical
2. Ultrasonic
Optical pachometer is attached to any standard slit lamp and uses one of the two
modes:
● Optical doubling
● Optical focussing
In the former, the pachometer splits the cornea into two optical sections. One half
moves in front of the other thus creating “doubling”. This doubling is adjusted so that
the posterior surface of the forwardly displaced image is in line with the anterior sur-
face of the other image; difference between the two gives corneal thickness which can
be read off directly.
Optical focussing is possible with the specular microscope when the endothelium
is focussed. Thickness of the cornea is automatically displayed digitally.
Ultrasonic pachometer is the most commonly used device to measure the corneal
thickness and has virtually replaced the optical one. It uses the same principle that is
utilised to measure the axial length of the eye by ultrasound. An ultrasonic probe can
be used in the sitting or supine position. It measures the thickness of cornea all over.
Average thickness of normal stroma in the centre is 0.52 mm. Value greater than this
indicates endothelial malfunction. It is useful in the diagnosis of subtle oedema in
various types of corneal disease.
Keratoscopy and Corneal Topography

The cornea acts as a convex mirror, and any change in its surface will produce a change
in the shape of the image. It is common knowledge that if a person looks at an object,
an observer standing in front can see the miniature mirror image of the object on the
cornea of the observed person. This observation has been used in eliciting:
1. Window reflex test
2. First Purkinje image
3. Keratoscope
4. Keratometer
Window reflex If a person stands a few feet away from an open window, an
observer stationed in front and slightly on one side with back towards the window, can
see the image of the window frame and bars as a miniature replica on the cornea. If
there is any distortion on the surface of the cornea, the window bars will either show
a break in continuity or give a wavy pattern. When there is a haze or opacity of the
cornea, outline of the image will be blurred and distorted.
First Purkinje image First Purkinje image is a small erect virtual image of a
light on the anterior surface of cornea that moves with the movement of light. This
principle forms the basis of any keratoscope. Common types of keratoscopes are
explained below.
Placido disc (Fig. 9.15): This comprises of a circular disc of 10 inches diameter with
a central hole through which the cornea can be seen. Around this hole are concentric
rings of increasing diameter and equal width. The rings are of white and black colours,
alternating with each other. It has a handle for holding. The central peephole has
a ⫹2 D sphere lens attached to it to relax the accommodation of the observer (Plate 9.4).
The rings of Placido disc are externally illuminated. To see the cornea with the
Placido disc: the patient sits with her back towards a source of light. The light falls on
the rings of the disc and the observer looks through the peephole and moves closer to the
cornea until the rings become visible. The eye of the observer, the peephole and centre
of the observed cornea should be in the same line perpendicular to the cornea. In a nor-
mal cornea, concentric white and black rings spaced at regular intervals will be visible.
Causes of distorted rings are:
1. Astigmatism
2. Keratoconus
3. Pterygium
Fig. 9.15 | Placido disc.

Plate 9.4 | Placido disc.

4. Corneal scar
5. Keratoplasty
6. Pellucid corneal degeneration
7. Soft eye
8. Corneal ulcer
9. Terrien’s degeneration
10. Limbal dermoid
11. Mooren’s ulcer
12. Any growth at the limbus
Klein keratoscope This is a small self-illuminated keratoscope that can be attached

to the ophthalmoscope handle or operated by a separate source of energy. It utilises the
same principle as that of the Placido disc. It is very handy but far more expensive. It is
used from the same distance as any ophthalmoscope. There are some ophthalmoscopes
that have a built in grill or rings that can be projected onto the cornea to see the curvature.
Photokeratoscopes Keratometers measure the central 3 mm of the cornea and are
used mostly for routine contact lens fitting. They giving very little information regard-
ing peripheral corneal curvature that is required for difficult contact lens fitting. With
ever-increasing frequency of kerato-refractive surgery, knowledge of corneal curvature
has become more necessary than in the past. Photokeratometers examine 55%,
whereas the keratometers examines only 8% of the corneal surface. Hence, the need
for a photokeratoscope that can give a visual display-photograph or a video display.
Photokeratoscope is used to follow progressive keratoconus, radial keratotomy result,
postsurgical astigmatism, e.g. in IOL and keratoplasty.
Automated computerised corneal topography analyser: This gives a colour-coded
map of corneal topography. This is mostly used in photorefractive corneal surgery.
Other Procedures Followed in the Corneal Examination

1. Examination of corneal scraping: Corneal scraping is examined to pinpoint the causative micro-
bial organisms producing a corneal ulcer
2. Examination of the tear film: see disorders of the tear film

3. Examination of ocular adnexa: Examination of the ocular adnexa has significance in finding out
contributory factors for many pathological conditions of the cornea, which may hamper recov-
ery especially of a corneal ulcer; for example chronic dacryocystitis may act as a reservoir for
pneumococci. Coloboma of the lid, lagophthalmos, trichiasis and entropion may not only cause
keratopathy but also delay recovery
(a) Lid margin is examined for coloboma, trichiasis, entropion, ectropion and chronic
blepharitis
(b) Conjunctiva is examined for xerophthalmia, concretions, angular conjunctivitis, phlycten,
spring catarrh and foreign body in the tarsal conjunctiva
(c) Lacrimal sac is examined for chronic dacryocystitis. In the absence of a positive regurgita-
tion test, syringing of the lacrimal passage may have to be done to confirm the patency of
the nasolacrimal duct
4. Examination of intraocular pressure: It should be done only when there is no contraindication
like bacterial corneal ulcer, fungal corneal ulcer. A pneumotonometer that does not touch the
cornea is the best instrument available for this
(a) Skin examination is done for allergy, atrophia and infections like leprosy, herpes zoster and
rosacea
(b) Systemic infection: Gonorrhoea, syphilis, tuberculosis, leprosy, worm infestation, herpes
zoster, simplex and HIV should be taken into consideration
INTERPRETATION OF CORNEAL EXAMINATION
Shape of the Cornea

On a casual look the normal cornea looks circular, though it is a horizontal ellipse.
Vertical diameter is 11.5 mm and horizontal diameter is 12.5 mm. Shape of the cornea
changes only when the eyeball is soft. In hypotony of some duration the vertical diam-
eter becomes less and the cornea looks more elliptical (Fig. 9.4). In phthisis, the
cornea looks quadrilateral in shape (Fig. 9.6) and in extreme degrees of microphthal-
mos, the cornea becomes very small and irregular.
Size of the Cornea

If the horizontal diameter is more than 13 mm, it is called large or megalocornea. Even
to a trained eye it is not possible to say if there is a borderline enlargement of the
cornea or not. The best method to determine the corneal diameter is by corneal cal-
lipers under local anaesthesia in adults and general anaesthesia in children. Diameter
should be measured both vertically and horizontally in both the eyes.
Causes of increased corneal size are:
1. Buphthalmos
2. Megalocornea
3. Macrophthalmos (keratoglobus)
Causes of decreased corneal size are:

1. Microphthalmos
2. Microcornea
3. Phthisis bulbi
4. Atrophic bulbi
5. Nanophthalmos
Curvature of the Cornea (Fig. 9.6A)

Cornea is more curved than sclera hence it bulges beyond the limbus. The average corneal
curvature is 8 mm. Curvature is slightly more in the central 3 mm, which is called the
optical zone. Curvature of the central zone is best measured by the keratometer, while the
peripheral cornea is measured by the photokeratoscope and topography. Cornea is more
curved vertically due to pressure of the lids. Increased curvature results in physiological
myopic astigmatism of 0.5 D in horizontal axis. This is called astigmatism with the rule.
Corneal curvature is increased in:
1. Keratoconus
2. Buphthalmos
3. Keratoglobus
4. Pellucid degeneration
Corneal curvature is decreased in:
1. Microcornea
2. Microphthalmos
3. Cornea plana
4. Phthisis bulbi
5. Hypotony
6. Perforation of globe
7. Postsurgical tight suture
Corneal curvature is irregular in:
1. Pterygium
2. Keratoconus
3. Keratectasia
4. Corneal staphyloma
5. Pellucid degeneration of cornea
6. Ciliary staphyloma
7. Limbal growth
8. Postsurgical
(a) Keratoplasty
(b) Glaucoma surgery
(c) Retinal detachment surgery
Corneal Thickness
Normal cornea does not have uniform thickness. It is thicker (0.9 mm) on the periph-
ery and thinnest in the centre (0.6 mm). This is due to difference in corneal curvature
of the two surfaces. Posterior surface is more curved than the anterior surface. Corneal
thickness is measured by pachometer. Corneal thickness is increased due to oedema of

either stroma or epithelium or both.
Causes of thickened cornea are:
1. Disciform keratitis
2. Endothelial decompensation
3. Epithelial oedema
4. Corneal leucoma
5. Hydrops of cornea
Causes of thin cornea are:
1. Keratoconus
2. Keratectasia
3. Buphthalmos
4. Pellucid degeneration
5. Mooren’s ulcer
6. Terrien’s degeneration
Corneal Transparency
To maintain its optical property cornea has to be transparent, and most of the diseases of
cornea cause a loss of this transparency. Transient or permanent loss of transparency is
called corneal opacity. Corneal opacity can be stationary or progressive. They may vary
in shape, size, number and depth. They may be unilateral or bilateral. Most of the opac-
ities are painless but some of them may be associated with pain due to non-corneal causes.
Corneal opacities are white in colour. However, corneal transparency may be lost
due to encroachment of pterygium, limbal dermoid or deposits like tattoo, band
keratopathy or epithelial down growth.
Corneal opacities are examined under the following headings:
Position, numbers, size, grade, staining, vascularisation, iris incarceration and deposit.
Position: Position of a corneal opacity is noted in relation to the limbus, pupil and
meridian (face of clock) (Fig. 9.16).
Number: Number of corneal opacities may vary from single to multiple.
Shape: corneal opacities may assume various shapes according to position, depth
and pathology. Dendritic pattern is seen in herpes simplex and herpes zoster, phlycten
produces a dome-shaped opacity with base at the limbus, sclerosing keratitis and epithe-
lial down growth produce a tongue-shaped opacity. Arcus senilis may start as an arc on
the periphery. Rupture in the Descemet’s membrane produces whirl like opacities—
Haab’s striation. Trachomatous pannus is continuous with the limbus (Fig. 9.17).
Grades of Opacity
All corneal opacities are white in colour. Their shades vary according to depth.
Opacities of epithelium and superficial stroma are the faintest; those involving full
thickness are the densest. According to density they have been graded as:
1. Nebula
2. Macula
12
1
O
2
O is an opacity, it is situated 1.5 mm from
L 9 4.25 P P 4.25 3 L the limbus between 1 o’clock and
2 o’clock. Its inner margin is 1.5 mm
from pupillary border. It is irregular in
2.5 shape. Leucomatous, not vascularised.
LL is diameter of cornea, PP is diameter
of pupil.
6
11.00
Fig. 9.16 | Recording the position of a corneal opacity.
Epithelial down
growth Trachomatous pannus
Arcus
RK Dendritic pattern
Sclerosing keratitis
Keratoplasty Haab’s striation
Healed phlycten
Fig. 9.17 | Positions of various kinds of corneal opacities.
3. Leucoma
4. Leucoma adherent
(a) Nebula is the faintest and hardly visible if light is thrown at right angle to the opacity; they
are best visualised on oblique illumination
(b) Macula: They are denser and better visualised than nebulae
(c) Leucomas: They are the densest opacity
(d) Leucoma adherent is an opacity to which iris is either incarcerated or there is evidence of
iris incarceration in the past. It need not be leucomatous always. It is identified as a white
opacity with brown pigment in it
➤ The same eye may have opacities of different grades at the same time
Aetiology of Corneal Opacity

1. Congenital
● Rare
2. Trauma
● Physical
● Chemical
● Mechanical
3. Infection
● Very common
● Keratitis
● Corneal ulcer
● Trachoma
● Leprosy
4. Inflammation
● Interstitial keratitis and disciform keratitis
5. Deficiency
● Keratomalacia
6. Allergy
● Phlycten
● Spring catarrh
7. Degeneration
● Arcus senilis
● Band keratopathy
8. Dystrophy
● Relatively rare
9. Vascularisation
● Superficial/Deep
10. Encroachment
● Pterygium
● Limbal dermoid
● Sclerocornea and sclerosing keratitis
11. Deposits
● Krukenberg spindle
● Hudson Stahli line
● Fleischer’s ring
● Kayser Fleischer ring
● Band keratopathy
● Tattoo
● Corneal plaque
● Haemoglobin
● Foreign bodies
Causes of bilateral corneal opacity (age-wise):

1. Congenital
2. Ophthalmia neonatorum
3. Keratomalacia
4. Small pox (in those who suffered from small pox before it was eradicated)
5. Injury
(a) Fire cracker
(b) Chemical (Plate 9.5)
(c) Iatrogenic (Folk medicine)
6. Spring catarrh
7. Infective corneal ulcer (Plates 9.6, 9.7 and 9.8)
Plate 9.5 | Old corneal opacity due to

chemical burn.
Plate 9.6 | Infective corneal ulcer. (Courtesy Dr. Nidhi Pande.)
(Courtesy Dr. S.K. Das.)
Plate 9.7 | Hypopyon corneal ulcer. (Courtesy Dr. Nidhi Pande.) Plate 9.8 | Bilateral corneal opacity due to
infective keratitis in childhood, right
eye esotropic.
9. Trachoma
10. Leprosy
11. Dystrophy
12. Degeneration
(a) Band keratopathy
(b) Pterygium
(c) Arcus—Juveniles (rare)
(d) Arcus—Senilis (very common) (Plate 8.4)
Plate 9.9 | Testing corneal sensation. Loss of sensation in the right cornea, none of the eyes closed on touching the
right cornea, left eye has normal sensation.Touching the left cornea results in closure of both the eyes.
Staining of opacity: A white discolouration of cornea, which stains, is generally not

called opacity but keratitis, which denotes active inflammation while term opacity is
used to denote lesions that do not stain.
Vascularisation of opacity: Presence of vessels in opacity denotes active lesion.
Iris incarceration in opacity: Iris incarceration in an opacity means full thickness
perforation that has been sealed by the iris and is now healed, entrapping the iris in
the process.
Deposits in opacity: The commonest deposits in opacities are foreign bodies.
Others are mucus plaque, tattoo, iris pigment and several other chemical compounds.
Corneal Sensation
The cornea is richly supplied by pain fibres from the trigeminal nerve. In fact all
sensations—touch, temperature, pressure are translated as one sensation, i.e. pain.
➤ Presence of touch sensation is natural; absence of touch sensation has great

diagnostic value
Testing of corneal sensation (Plate 9.9): Testing of corneal sensation is very simple
but is generally ignored as a clinical test. The patient is asked to look straight ahead.
The tip of a sterile wisp of cotton is brought from the temporal side to touch the
cornea. Precaution is taken not to touch the lashes; separate swabs are taken for each
eye to avoid transfer of infection. If the cornea is sensitive, there is immediate closure
of the lids and rolling up of the eyeball as soon as the cornea is touched. The lids of the
other eye also close due to this reflex. In absence of sensation, there is neither closure
of the lids nor rolling of the eyeball. The patient, on questioning, may not be able to
state whether the cornea had been touched. Difficulty arises when there is lagophthalmos
on the side of the cornea being examined. The patient is not able to close the lids.
However, the eyeball will roll up if Bell’s phenomenon is intact. The other eye will close
and will roll up. Corneal sensation should be tested before any anaesthetic agent is
instilled and before Schirmer’s test is performed. If an anaesthetic agent has been used,
the examination of corneal sensation may be postponed by 24 h.
Causes of diminished corneal sensation:
1. Use of local anaesthetic agent within last 12 h for any indication
2. Viral infection of cornea—herpes simplex and herpes zoster
3. Leprosy
4. Corneal scar
5. Corneal degeneration (band keratopathy)
6. Some of dystrophies
7. Prolonged use of contact lens
(a) Postoperative hypesthesia, e.g. following lens extraction, penetrating keratoplasty and encircling
operation
(b) Involvement of the fifth nerve, Gradenigo syndrome, cerebropontine angle tumour, trigeminal
neuralgia, destruction of trigeminal ganglion by injection of alcohol or surgical section of trigem-
inal root, retrobulbar alcohol, leprosy, superior orbital fissure syndrome and young diabetic
Bilateral loss of corneal sensation is rare except in leprosy, herpes simplex and corneal
opacity. Quantitative estimation of corneal sensation is done by various available
anaesthesiometers.
Corneal Vascularisation
Normal cornea is avascular except for the peripheral 1 mm (Table 9.1). Vascularisation
of cornea always means corneal pathology. Physiologically cornea tries to maintain
avascularity; when this mechanism breaks down corneal vascularisation results. Four
types of corneal vascularisation take place (Fig. 9.18):
1. Superficial
2. Deep
3. Intercorneal
4. Retrocorneal
Causes of superficial corneal vascularisation are:
1. Trachoma
2. Leprosy
3. Phlycten
Table 9.1 Difference between superficial and deep vascularisation (Fig. 9.19)
Features Superficial Deep
Colour Bright red Purple

Level of vascularisation Sub-epithelial or Bowman’s membrane Stroma
Continuity of vessels Conjunctival vessels freely grow in the Ciliary vessels grow in stroma where the vessels
cornea. No break at limbus is seen. are not visible. There is a clear zone at limbus
Branching Free and irregular, may anastomose Parallel, straight, branch at acute angle, do not
anastomose
Causes Conjunctival and corneal Uveal and corneal
1 1. Superficial—in the epithelium in front of

Bowman’s membrane⎯conjunctival vessels
3 2. Deep⎯in the stroma—anterior ciliary vessels
2 3. Intercorneal⎯generally in the stroma—
conjunctival vessels
4. Retrocorneal
(a) Retinal neovascularisation
(b) Conjunctival in case of epithelial down growth
4
Fig. 9.18 | Various types of corneal vascularisation.

4. Spring catarrh
5. Riboflavin deficiency
6. Mooren’s ulcer
7. Chemical burn
8. Indolent corneal ulcer
9. Vascularisation of leucoma
Causes of deep corneal vascularisation are:
2. Disciform keratitis
3. Alkali burn
Causes of intercorneal vascularisation other than deep vascularisation are:
1. Superficial vessels encroaching under lamellar keratoplasty
2. Valve-shaped corneal wound near limbus
Causes of retrocorneal vascularisation are:
1. Epithelial down growth
2. Neo-vascularisation of iris
3. Intraocular tumour
Types of superficial vascularisation (Fig. 9.20):
1. Pannus
(a) Progressive
(b) Regressive
2. Fascicular: A localised area of vascularisation by a tuft of superficial vessels as seen in fascicular ulcer
3. Epaulette: Combination of superficial and deep vascularisation. Superficial tuft stands out promi-
nently on the surface like a wreath, commonly seen in syphilitic interstitial keratitis
Corneal Deposits
Band keratopathy, tattoo, mucus plaque, keratic precipitates, Krukenberg spindle,
Hudson Stahli line, Fleischer ring and Kayser Fleischer ring.
Encroachment from conjunctiva over cornea:
1. Pterygium
2. Dermoid
4. Large glaucoma bleb (Plate 8.14)
A. Superficial vascularisation B. Deep vascularisation
Fig. 9.19 | Differences between superficial and deep vascularisation.
Regressive
Progressive
FU
Vascularisation in
phlyctenular kerato-
Vascularisation in conjunctivitis
fascicular ulcer (FU)
Fig. 9.20 | Types of superficial vascularisation.
Corneal Fistula
Whenever there is a corneal perforation, the sequence of events is as follows—aqueous
flows out, AC collapses, pupil constricts, eyeball becomes soft and iris floats into the
wound, plugging it, corneal wound heals and iris is incarcerated. As soon as the wound
heals it becomes watertight and AC reforms the IOP returns to normal, but the pupil
is distorted and AC remains irregular. If the perforation is central and iris fails to plug
it, the wound remains open and aqueous keeps on leaking, leading to flattening of
cornea, absence of AC and soft eye resulting in a corneal fistula. Corneal fistula is lined
by corneal epithelium as a down growth. Factors predisposing corneal fistula are corneal
perforation in presence of widely dilated pupil, which does not constrict, e.g. use of
atropine for a long time, continuation of atropine following central perforation, large
iridectomy, aniridia, coloboma of iris and iris plastered against the lens in the phakic
eye or vitreous in AC.
Corneal fistula is always central. The actual fistula looks like a light-coloured small
depression, through which the aqueous is seen leaking. The fistula is surrounded by
a zone of infiltrates which appears white. The cornea is flat, AC is absent, the eyeball
is soft, painful, and congested, and the vision is greatly reduced. Delayed effects of
corneal fistulae are peripheral anterior synechia complicated cataract and infection.
EXAMINATION OF THE SCLERA
Normal sclera is white and opaque. It is almost avascular. It is less sensitive to pain
than the cornea. Its functions are: protective, keeping the interior of the globe dark,
to act as attachment of extra-ocular muscles and to allow passage of nerves and blood
vessels. It is less curved than the cornea.
Sclera is examined under the headings: size, shape, colour, nodule and ectasia.
Scleral size is reduced in:
1. Microphthalmos
2. Microcornea
3. Phthisis
4. Hypotony
5. Perforation
Shape of the normal sclera is spherical. In phthisis and perforation it looses its spherical
shape to an irregular wrinkled shape.
Colour
Normal colour of adult’s sclera is marble white. At birth and during the first few months,
sclera has a blue tinge; due to its thinness; the underlying uvea shines through. Other
causes of blue sclera are Marfan’s syndrome, osteogenesis imperfecta, blue sclera and brit-
tle bone syndrome. Sclera becomes yellow in jaundice. In sub-conjunctival haemorrhage
sclera seems to be red, though it is not stained with blood, which is localised in the sub-
conjunctival tissue. Localised redness occurs in episcleritis and scleritis. Localised black
spots are seen in congenital melanosis. The sclera assumes a black colour in scleral ectasia.
Nodules
Scleral nodules are seen in episcleritis, scleritis, interscleral nerve loop, small staphy-
loma and sub-conjunctival prolapse of uvea. Nodules of episcleritis should be differ-
entiated from phlycten and other nodular conditions of the conjunctiva.
Sub-conjunctival injection of depot steroid forms a raised sub-conjunctival plaque
over the sclera. Encircling bands, scleral implants and explants, and glaucoma valves
may be visible through the conjunctiva as large nodules. They may extrude through
the conjunctiva or may erode the sclera.
Ectasia of Globe (Fig. 9.21 and Table 9.2)

Ectasias of globe are called staphylomas. They are defined as ectatic cicatrisation of outer
coat of eyeball with uveal incarceration. Thus, staphyloma can be corneal and scleral.
Equatorial
Intercalary staphyloma
staphyloma
Original shape
of eye
Partial anterior
(corneal) staphyloma
Posterior
staphyloma
Ciliary staphyloma
Fig. 9.21 | Various types of staphyloma.
Table 9.2 Comparison of various types of staphylomas
Name of Uvea
staphyloma Outer coat involved incarcerated Anatomical weakness
Partial anterior Part of cornea Iris Centre of the cornea which

is the thinnest
Total anterior Whole of cornea Iris Centre of the cornea
Intercalary Limbus Root of iris Entry of anterior ciliary vessels
Ciliary Sclera between limbus Ciliary body Non-specific
and equator
Equatorial Equator of the globe Choroid Thinnest part of the sclera
Posterior Sclera on posterior pole Choroid Developmentally thin sclera
Corneal staphylomas can be complete or partial depending upon the part of cornea
involved. They are also called anterior staphylomas—cornea is opaque, its surface is
irregular so is its thickness, iris is incarcerated in the opacity, curvature is increased, AC
is irregular, generally there is secondary glaucoma and the eye is blind. There may be var-
ious degrees of squint and nystagmus. Corneal (anterior) staphyloma can be unilateral or
bilateral. It can be caused by small pox, keratomalacia, sloughing corneal ulcer and trauma.
Scleral staphylomas can be intercalary, ciliary, equatorial or posterior according to
their location.
Equatorial staphylomas lie under extra-ocular muscles or are placed very posteriorly
and posterior staphylomas are not visible. They are seen on indirect ophthalmoscopy
or ultrasonography.
The cause of intercalary staphyloma is generally a penetrating wound at the limbus;
the root of iris is incarcerated in the ectatic cornea and sclera (Fig. 9.21). Causes of
ciliary staphyloma are buphthalmos, long-standing absolute glaucoma, scleritis, scle-
romalacia, rhinosporidiosis (Plates 9.10 and 9.11), idiopathic (Plate 9.12) and trau-
matic. Ciliary staphyloma may be single and localised or multiple and diffuse. They
may involve a sector of the sclera or encircle the whole of cornea in the form of annu-
lar staphyloma.
Commonest cause of equatorial staphyloma is congenital, about 6–7% of eyes have
asymptomatic equatorial staphylomas that become visible during surgery for squint or
Plate 9.10 | Scleral staphyloma under conjunctival rhinosporiodiosis. Plate 9.11 | Scleral staphyloma with conjunctival rhi-
nosporidiosis.
Plate 9.12 | Idiopathic scleral staphyloma.

retinal detachment. Other causes are scleritis and trauma. Posterior staphyloma is seen
in pathological myopia where myopia is high; retinoscopy gives different readings at dif-
ferent places in the same meridian. It is best visualised by indirect ophthalmoscopy as
a depression in the posterior pole of the globe into which the passing vessels dip.
Presence of posterior staphyloma is confirmed by ultrasonography, CT and MRI.
■■■ CHAPTER 10
E VALUATION OF AN E YE WITH
D ISORDER OF T EAR F ILM
Tear film is an essential component of the eye and it’s functions are:
1. To keep the cornea and conjunctiva moist
2. Optical
3. Mechanical cleaning of the conjunctiva and cornea
4. To provide nutrition of the cornea
5. To provide lysozymes to the conjunctiva
The tear film consists of the following layers (Fig. 10.1):
1. Lipid layer produced by the meibomian glands and glands of Zeis and Moll
2. Aqueous layer—lacrimal gland and accessory lacrimal glands
3. Mucus layer—conjunctival glands
Functions of the various layers are:
● Lipid—prevents excess evaporation of the aqueous layer and stabilises the surface of the tear
film.
● Aqueous—main layer that has all the properties of the tear film.
● Mucus—binds the aqueous layer to the conjunctiva and cornea.
MALFUNCTIONING OF TEAR FILM
Malfunctioning of the tear film can be brought about by faults in:

1. Tear production
2. Tear spreading
3. Tear quality
4. Tear drainage
Abnormal Tear Production

Abnormal tear production can be either excessive production or diminished production.
Abnormal Spread of Tear

Tears are spread over the outer eye (ocular surface) by:
1. Gravity
2. Capillary action
Atmosphere
Corneal epithelium
Lipid
Aqueous Mucin
Fig. 10.1 | Various layers of the tear film.
3. Smoothness of the conjunctiva and cornea

4. Blinking
5. Intact lid margin
6. Lacrimal pump system
Any fault in the mechanism will hamper the spreading tears leading to dry spots on
the ocular surface.
Abnormal Tear Drainage

Tears are drained by:
1. Intact lid margin
2. A pair of puncta, canaliculi and lacrimal sac
3. Nasolacrimal duct and its ostium
An abnormality of the lid margin or obstruction to any of the remaining parts will
lead to the overflow of tears, called epiphora.
Abnormality of Tears
Abnormality of tears can be:
1. Flooding by tears (epiphora)
2. Reflex tearing (lacrimation)
3. Deficiency of tears (dry eye syndrome)
Tearing is divided into two types:
1. Epiphora
2. Lacrimation (reflex tearing)
Epiphora
There is a normal production of tears in volume and quality; there is an abnormality in
the drainage, leading to passive overflow of tears and constant dribbling that requires
frequent mopping.
EVALUATION OF AN EYE WITH DISORDER OF TEAR FILM 129
Causes of epiphora are:

1. Loss of contact between the lid margin and the globe especially of lower lid—ectropion of lid,
coloboma of lower lid, growth of lid margin and lagophthalmos
2. Obstruction or the absence of puncta or canaliculi, mostly lower, and can be congenital, trau-
matic, post-inflammatory or infective
3. Absence or fibrosis of the sac—dacryocystectomy, fibrosed sac, failed DCR, failed intubation of
sac and NLD
4. Obstruction of the nasolacrimal duct
5. Nasal growth obstructing the opening of NLD
6. Growth of the sac: rhinosporidiosis
Neoplasms of the sac are very rare.
Examination of a case of epiphora

1. History of:
(a) Constant watering without pain or foreign body sensation in the eye
(b) Mucoid discharge on pressure over the sac
(c) Mucoid conjunctival discharge
2. Exclude reflex tearing
3. Examine:
(a) Lid for ectropion, coloboma, growth on margin, lagophthalmos and trichiasis
(b) Puncta
● Puncta Presence
● Pinpoint, everted, occluded
(c) Sac: visible swelling, positive regurgitation test, scar (history of surgery) and chronic
granuloma
(d) Nasolacrimal duct—patency
Reflex Tearing
This is generally referred to as lacrimation. The drainage system is intact and function-
ally competent; there is an over production of tears in the lacrimal gland that the
drainage system fails to cope with. A combination of epiphora and lacrimation worsen
each other.
Disorders of Tears
Disorders of tears can be brought about by:
1. Normal production with impaired outflow (epiphora)
2. Excess production:
● With normal outflow (reflex tearing): keratitis, iridocyclitis, acute glaucoma, trauma
● With impaired outflow (reflex tearing in epiphora): lagophthalmos, ectropion, keratitis in an
epiphoric eye, etc.

3. Reduced production: trachoma, cicatrisation of conjunctiva
4. Alacrima: congenital absence of tear
5. Change in the quality and quantity: dry eye
● Lipid deficiency
Aqueous deficiency
●
Mucus deficiency
●
6. Paradoxical tear: crocodile tears
Examination of an eye with dryness

1. History
2. Redness, irritation with or without diminished watering
3. Fluctuation of vision
4. Dryness of the mouth, and nose
5. Symptoms are generally bilateral
6. Seropositive rheumatoid arthritis
7. Exclude other causes of redness of the eye. Examination of the:
● Conjunctiva
● Cornea
● Tear film
Common causes of dry eye syndrome Common causes of dry eye syndrome are kera-
toconjunctivitis sicca, Sjogren syndrome, trachoma, vitamin A deficiency, ocular pem-
phigus, leprosy, pterygium and seropositive rheumatoid arthritis.
Drugs—antihistaminics, parasympatholytics, betablockers, oral contraceptives and
hormone replacement therapy.
Examination of the conjunctiva in dry eye The conjunctiva may show:

1. Chronic conjunctivitis
2. Folds in the conjunctiva on lateral gaze
3. Bitot’s spot
4. Patch of xerosis
5. Positive stain with rose bengal
6. Keratonisation (keratinisation)
Examination of the cornea in dry eye

1. Punctate opacities, stain with rose bengal
2. Dry lustreless spots
3. Superficial vascularisation
4. Filaments: stain with fluorescein and rose bengal
5. Normal sensation except in neuroparalytic keratitis
EXAMINATION OF THE TEAR FILM
1. Height of the tear meniscus

2. Schirmer test: 1 and 2
3. Basic secretion test
4. Tear break up time
5. Rose bengal stain
6. Impression cytology
Height of the Tear Meniscus

Height of the tear meniscus less than 0.3 mm with positive rose bengal stain and
Schirmer test is highly suggestive. Height of the tear meniscus is measured with the
slit lamp under a cobalt blue filter following instillation of fluorescein.
Schirmer’s Test 1
This evaluates the total tear secretion, i.e. reflex and basic. This is the most reliable test
in the diagnosis of dry eye syndrome. It measures the available resting tear at a given
time. The patient is made to sit in a diffusely illuminated room, no bright light is thrown
on the cornea and all causes of reflex tearing are excluded. This test is avoided if:
1. The patient has common cold
2. Lid has been manipulated within the previous 1 h
3. Corneal sensation has been tested
4. Anaesthetic agent has been used during the previous 6 h
Staining of rose bengal should be done after the Schirmer test.

A specially designed Schirmer’s strip (Plate 10.1) is used. It is a Whatman 41 strip fil-
ter paper, 35-mm long, 5-mm wide, with a notch 5 mm from one end. The strip is bent
at right angles to its long axis at the level of the notch. The smaller end is put in the
lower fornix behind the lower lid at the junction of lateral one-third with medial two-
third. Both eyes are tested simultaneously. The patient is asked to keep the eyes open, look
straight and slightly up, blinking is permissible.
Precaution is taken not to touch the lid margin, lash or cornea while inserting the strip.
The paper is kept in place for 5 min. Tears wet the strip and the tears spread towards
the other end by capillary action. This distance is measured on the millimetre scale
from the notch, 10–20 mm is taken as normal, 5–10 mm is doubtful. Less than 5 mm
is diagnostic of poor lacrimal secretion (Plate 10.2).
Plate 10.1 | Schirmer’s strip. Plate 10.2 | Schirmer’s test 1.

Schirmer’s Test 2
This measures reflex secretion. It is similar to Schirmer test 1 except that the conjunc-
tiva and cornea are anaesthetised and the ipsilateral nasal mucosa is irritated with a
small cotton swab; reading is noted after 2 min. Reading less than 15 mm denotes fail-
ure of reflex secretion.
Basic Secretion Test

Schirmer’s test 1 measures the total reflex and basic secretion. Basic secretion is the
measurement of wetting with and without anaesthesia. If Schirmer’s test 1 shows
hypo-secretion, Schirmer’s test 2 is done with a fresh strip. If the reading is less than
10 mm, failure of basic secretion is diagnosed.
Tear Breakup Time

A drop of 2% fluorescein sodium is instilled in the conjunctival sac. After 1 min the
patient is asked to be seated on a slit lamp for the usual slit lamp examination, a cobalt
blue filter is inserted and the beam is widened to maximum. The patient is asked to blink
a few times and then stop blinking. The cornea is looked through a cobalt blue filter and
after a few seconds black spot or spots develop in the pool of fluorescein on the cornea.
They denote spaces where there is no tear film. Time taken between the last blink and
appearance of a black spot in the tear film is the break up time in seconds. This is clocked
with a stop watch. Normal tear break up time is 10 s. At least three readings should be
taken. Break up time is shortened in mucin deficiency and lipid deficiency. Other causes are
Dellen of the cornea, limbal dermoid, pterygium, corneal scar and leprosy. If a slit lamp
with cobalt blue filter is not available, an ultraviolet lamp used for contact lens fitting is
a good alternative.
Rose Bengal Staining

Rose bengal is a vital stain, like fluorescein, both are available as brownish, water-
soluble crystals (Table 10.1). They are used either as 1–2% aqueous solution or in the
form of pre-sterilised filter paper strips (Whatman 41) impregnated with the dye.
Rose bengal is highly irritating to the cornea and conjunctiva, hence it is used in the
lowest concentration in the form of smallest possible drop. It stains both corneal and
conjunctival devitalised tissues.
To use rose bengal: The conjunctival sac is irrigated to remove the discharge. Excess
fluid is removed; after a minute a single drop is instilled in the lower fornix and the
patient is asked to close his eye for a while. Excess stain is washed off and the eye is
examined under magnification, under white light and the following points are noted.
1. In conjunctiva: In case of keratoconjunctivitis sicca, two triangular, stain-positive
areas develop in the interpalpebral fissure with the apex away from the cornea; free mucus
and epithelial debris will also stain.
2. Cornea: It stains the devitalised epithelium, mucus strands and epithelial debris.
Filaments stain poorly with rose bengal and better with fluorescein. To differentiate
Table 10.1 Comparison between rose bengal and fluorescein
Rose bengal Fluorescein
Vital stain Vital stain

Brownish crystal Brownish crystal
Water soluble Water soluble
Non-fluorescent Fluorescent
Highly irritable Non-irritable
Used as 0.5–1% drop Used as 1–2% drop
Available in strips Available in strips
Stains bright red Stains bright green
Examined under white light Examined under cobalt blue filter or ultraviolet light
Contamination less possible Contamination with pseudomonas is distinctly possible
Stain desiccated tissue, mucin and Stains dead, degenerated and recently traumatized
debris of conjunctiva and cornea corneal tissue, erosions
Table 10.2 Causes of various types of tear deficiency
Type of deficiency Causes
Aqueous (lacrimal secretion) Keratoconjunctivitis sicca—primary or secondary, Sjogren’s

syndrome, sarcoidosis of lacrimal gland, pseudo-tumours,
conjunctival scar and trachoma
Mucin Vitamin A deficiency, acid alkali burn, symblepharon,
radiation and Stevens Johnson syndrome
Lipid Acid alkali burn, loss of lid, accidental or surgical
and trachoma
between the corneal stain and other materials, the patient is asked to blink a few times.
Corneal stains do not move with the blink but other material like, filaments, debris and
mucus move with the blink. The cornea stains bright red (magenta). Excess mucus
is seen in allergic keratoconjunctivitis like spring catarrh. The presence of damaged
epithelial corneal cells indirectly confirm dry eye. In dry eye the staining is seen in the
lower half of cornea. Other conditions that result in a positive rose bengal stain are
chronic conjunctivitis, acute chemical conjunctivitis, exposure keratitis and herpes sim-
plex. To reduce the stinging of rose bengal the following steps are taken: use of a weak
solution, i.e. 0.5% of the smallest possible drop is used, patient is forewarned about the
stinging; conjunctiva can be anaesthetised by proparacaine but not by any other anaes-
thetic agents as they produce false staining.
Paradoxical Tears (Table 10.2)

This is a rare condition due to aberrant regeneration of the facial nerve following facial
palsy. It is generally unilateral. There is tearing during mastication. There is no treat-
ment for it. They are called crocodile tears.
Causes of bloody tears are trauma to the lacrimal passage and conjunctiva, rhino-
sporidiosis of the sac, conjunctival haemangioma and malignancy of the sac.
E XAMINATION OF
A NTERIOR C HAMBER
The eyeball is divided into two unequal parts by a barrier formed by the lens, suspen-
sory ligament and the ciliary body. A larger posterior part is called vitreous chamber
and a smaller anterior part is called aqueous chamber. This is again divided into two
parts by the iris, a bigger anterior chamber and a smaller posterior chamber. They com-
municate with each other via the pupil. If there is a pupillary block this communica-
tion is snapped, which can be re-established by either breaking the block medically
with mydriatics or surgical by iridectomy or iridotomy (Fig. 11.1).
ANTERIOR CHAMBER
Anterior chamber is a space bounded anteriorly by the posterior surface of the cornea and
posteriorly by a small chunk of ciliary body, iris and anterior lens capsule. In aphakia,
vitreous or after cataract replace the lens. In pseudophakia the posterior chamber IOL
forms the posterior boundary of AC. The shape of a normal anterior chamber is plano-
convex. The iris and lens form the flat base, while the cornea forms the vortex. Due to
this peculiar shape AC is deepest in the centre and tapers to zero at the periphery.
The normal content of anterior chamber is aqueous, which is a crystal clear fluid that
moves freely from the posterior chamber to anterior chamber and leaves the anterior
Ciliary body
PC
AC
LENS
Vitreous
Pupil
chamber
Iris
PC
Fig. 11.1 | Chambers of the eye.

EXAMINATION OF ANTERIOR CHAMBER 135
chamber via the angle of anterior chamber. In anterior chamber, the aqueous circu-
lates by convection currents.
Main function of aqueous are:
1. It maintains the intraocular pressure, which is essential to retain the shape of the eyeball
2. It acts as an optical medium
3. It supplies nutrition to the lens and the cornea
4. It removes metabolic waste products
AQUEOUS HUMOUR
This is a vital fluid that fills the aqueous chamber. It is produced in the ciliary epithelium
at a constant rate of 10–12 μl/min in a normal eye. Its clarity changes rapidly in disease.
Normal volume of aqueous is 125 μl. Its osmotic pressure is slightly more than that of the
plasma. As compared to plasma its protein content is very low, i.e. 0.22% against 7% of
plasma. However, the ratio of albumin and globulin is the same as in plasma. Protein con-
tent rises in the inflammations of uvea and following trauma. The aqueous with raised
proteins is called a plasmoid aqueous. Normal aqueous is crystal clear; Plasmoid aqueous
is turbid. It may be tinted pink if there is a minute haemorrhage in AC, bright red if there
is frank blood and white due to accumulation of pus. The aqueous is tinged green due to
fluorescein either through a corneal leaking wound or during angiography of the anterior
segment. Aqueous may have inflammatory and malignant cells, microorganisms, parasites.
Anterior chamber is examined under the following heads: depth, contents and analysis
of aspirated fluid.
DEPTH OF AC
To determine the depth of the anterior chamber either it is inspected from the side
with a beam of light falling at right angles to the cornea or viewing from the front with
the beam of light falling at an angle. Then, the following points are noted:
1. Is it of normal depth?
2. Deep or shallow?
3. Is this depth uneven?
Normal AC depth is 3 mm over the pupil, 2–2.5 mm over the mid iris. At the extreme
periphery, cornea and iris come in contact with each other obliterating the AC.
Depth of AC is increased due to the following causes:
1. Corneal: keratoconus, buphthalmos, keratoglobus and megalocornea
2. Lenticular: aphakia, dislocated lens, subluxated lens, pseudophakia or anterior dislocation of the lens
3. Iris: aniridia, coloboma and posterior synechiae
4. Anterior chamber in myopia is deeper than in emmetropia and hypermetropia
Depth of AC is reduced due to the following causes:
1. Corneal: micro-cornea, microphthalmos
2. Lenticular: swollen lens
3. Glaucoma: narrow angle glaucoma, lens-induced glaucoma and malignant glaucoma. AC becomes
shallow if the aqueous drains out constantly in a perforated wound or an over-filtering bleb
4. Iris: iris bombe, anterior synechiae and corneal staphyloma
5. Others: perforating injury, leaking wound, hypotony and phthisis bulbi
Causes of irregular depth of AC Iris bombe, retroflexion of iris, anteflexion of iris,
adherent leucoma, tilted lens, tilted IOL, iris tumours, cysts and iris prolapse.
ABNORMAL CONTENTS OF AC
1. Plasmoid aqueous (turbid)

2. Pus (hypopyon)
3. Lens—the whole lens, cortical matter, nucleus, intraocular lens, Elschnig’s pearls and
Soemmerring ring
4. Vitreous
5. Parasites
6. Foreign body
7. Malignant cells (pseudo-hypopyon)
8. Tumours and cysts
9. Gas in the anterior chamber
10. Silicone oil in AC
Plasmoid Aqueous
Aqueous humour is called plasmoid when the protein content increases to 7% or more.
Protein particles are suspended as refractile bodies and become visible when light strikes
them. This phenomenon is called aqueous flare, which is best seen on the slit lamp. To
see an aqueous flare the beam of the slit lamp is reduced to a circular shaft of 2 mm
diameter, with maximum intensity and high magnification. As the number of particles
increase, finer details of iris are obscured. A combination of density of particles and
obscuration of iris is graded between 1 and 4⫹.
Causes of plasmoid aqueous are:
1. Anterior uveitis
2. Pan uveitis
3. Trauma
4. Paracentesis
➤ Aqueous flare is not a true sign of active anterior uveitis for which it should
be associated with cells in the aqueous
Aqueous Cells
In inflammations of the anterior uvea, inflammatory cells pour into the aqueous. They
are also refractile like protein particles, but larger in size. They are graded from 0 to
⫹4 according to the number seen on oblique, circular, intense beam of 2 mm size with
maximum illumination. About 5–10 cells per beam is ⫹1, more than 50 is ⫹4.
Hypopyon
Pus in the AC is called hypopyon. It always means a severe uveal reaction. The pus remains
sterile unless it is contaminated from outside. As it is denser than the aqueous it set-
tles down at the most dependent part of the anterior chamber, i.e. if the patient is
upright it will settle in the lowest part of the AC. In a recumbent patient the pus may
spread as a thin film over the iris and becomes almost invisible. The best way to see a
hypopyon is to ask the patient to sit up for few minutes and then direct the beam of
light at the lower part of the AC while at the same time patient is asked to look down.
Hypopyon is examined under the following heads:
1. Its height; does it move with the position of the head; colour and consistency
2. Amount of hypopyon is measured in millimetres from the bottom of AC
3. Recent pus is fluid and changes its position with the movements of the head
4. It becomes organised with time. Pus of fungal infection is fluffy and less mobile
5. Generally pus is white in colour. It may get tinted red in the presence of blood, yellowish in
fungal infection and greenish in pseudomonas infection
6. So long the Descemet’s membrane is intact, the organisms cannot reach the AC to produce pus
Pseudo-hypopyon is a collection of white deposit in the AC other than pus. They can
be malignant cells, accidental injection of depot steroid in AC, cortical material, ghost
cells in glaucoma and silicone oil.
Inverse hypopyon (Plate 11.1): Generally when the head is upright, the pus gravitates
to the lower part of the AC with a horizontal upper border because pus is heavier than
aqueous. In case of silicone oil which is lighter than aqueous, the oil floats up with a
horizontal lower border. The silicone oil moves freely in the AC. This is called inverse
hypopyon, which is a pseudo-hypopyon.
Hypopyon can be simple or associated with a corneal ulcer. Common causes of
hypopyon corneal ulcer are pneumococci, pseudomonas, gonococci, streptococci, Morax
Axenfeld, proteus, E. coli and fungi.
Causes of hypopyon without a corneal ulcer are moderate-to-severe iridocyclitis
endophthalmitis and panophthalmitis.
➤ Presence of white material in the ac should be presumed to be hypopyon and

treated as an emergency unless proved otherwise
Hyphaema
Blood in the anterior chamber is called hyphaema. The amount of blood may be small
enough just to tinge the aqueous pink or may be large enough to fill the whole of the
anterior chamber.
The sources of blood in the AC are iris, ciliary body, limbal blood vessels and vit-
reous haemorrhage in aphakia. Normal iris does not bleed even when it is surgically
Plate 11.1 | Inverse hypopyon.
Plate 11.2 | Hyphaema in post-operative

endophthalmitis.
cut. Iris bleeds when new blood vessels have developed in or over it or is inflamed. In
contrast to the iris, ciliary body bleeds on the slightest trauma and is the commonest
source of hyphaema in blunt injury. The other common source of bleeding is from the
newly formed conjunctival blood vessels across the section in aphakia due to trauma;
the commonest time of such bleeding is the fifth post-operative day. Limbal vessels
can bleed following penetrating injury at the limbus.
Blood being heavier than aqueous settles down at the most dependent part of the ante-
rior chamber. As long as it is fluid it can change its position like a hypopyon. It has a hori-
zontal upper border. The colour of blood changes with time, fresh hyphaema is bright red
in colour while old blood may clot and look blackish (black ball or eight ball hyphaema).
The amount of blood may be just sufficient to give a fine haze to the aqueous best
seen on the slit lamp. It may be in the form of a streak over the iris or lens. It may fill
the whole AC. Hyphaema is measured in mm from the bottom of the AC or may be
described as between the lower border of the pupil and limbus, up to mid pupil, above
the pupil or full. When blood fills the anterior chamber fully it is called total hyphaema.
Causes of hyphaema are:
1. Trauma: blunt or penetrating resulting in
● Iridodialysis
● Rupture of iris stroma
● Tear in the ciliary body
● Cyclodialysis
2. Inflammation (Plate 11.2)

● Gonococcal iridocyclitis
● Herpes simplex
● Rheumatoid arthritis
3. Neovascularisation of iris and ciliary body

4. Blood dyscrasia
● Haemophilia
● Leukaemia
● Purpura
5. Metabolic disorders: diabetes
6. Vascular tumours of the iris and ciliary body
7. Intraocular malignancy: retinoblastoma
8. Miscellaneous
● Juvenile xanthogranuloma
● Retrolental fibroplasia
● Persistent hyperplastic primary vitreous
● Haemophthalmos
Abnormal Structures in the AC (Lens and

Related Structures)
1. Clear or cataractous lens can come into the AC generally following blunt trauma or spon-
taneously in Marfan’s syndrome, homocystinuria, buphthalmos and long-standing uveitis. If the
intact lens comes in the anterior chamber it pushes the iris back causing a deep AC
2. Cortical matter—commonest cause is extra-capsular lens extraction and another cause is
traumatic cataract
● Classical extracapsular cataract extraction
● Needling
● Incomplete removal of cortex in IOL and phacoemulsification
● Traumatic cataract: it may be just a few flakes or may completely fill the AC
3. After cataract: Elschnig pearl or Soemmerring’s ring may be dislocated in the anterior chamber
4. Intraocular lens: anterior chamber and iris clip lenses are put in the AC and posterior chamber
lenses can get dislocated into the AC
Vitreous in Anterior Chamber

The lens and the suspensory ligament form a barrier between the vitreous and AC
though there is no formed capsule of vitreous. It is solid enough, so it does not flow into
the anterior chamber in the absence of the lens or suspensory ligament. For vitreous to
come into the AC, the vitreous should be liquid and there should be a rupture of the
anterior vitreous face. The vitreous may bulge into the AC, may fill the AC or a strand
of vitreous may be incarcerated in the surgical or accidental wound.
Tumours and Cysts in the Anterior Chamber

1. Tumours: primary or secondary tumours of iris and ciliary body may protrude in the AC
2. Cysts
● Implantation cysts from epithelial down growth
● Primary cysts in the iris
● Parasitic cyst as cysticercus or hydatid cyst may be seen in the AC
Parasites in the Anterior Chamber

Common parasites in the AC are thelazia (Plate 11.3), cysticercus, dirofilariasis and
onchocerciasis.
Plate 11.3 | Live parasite thelazia in anterior chamber.

Foreign Bodies in the Anterior Chamber
Single or multiple foreign bodies, organic or inorganic, can get into the anterior cham-
ber following penetrating injury. Deliberate foreign bodies that are left in the AC are
ACIOL and glaucoma implants. Foreign bodies may be in the AC or embedded in
other structures like the cornea, iris, ciliary body or lens. They may be metallic or non-
metallic. Metallic bodies may be inert or may produce a severe reaction, e.g. copper.
Transparent foreign bodies are difficult to visualise.
Gas in the Anterior Chamber

Anterior chamber is reformed with sterile air following lens extraction, glaucoma sur-
gery, paracentesis, repair of anterior segment and penetrating keratoplasty. Artificially
introduced gas in the AC moves freely. However, it may slip into the PC if the pupil
is large or vitreous is incarcerated in the wound.
Pathological gas formation is seen in infection with gas-forming organisms.
EXAMINATION OF THE AQUEOUS AFTER ASPIRATION
Aqueous may be aspirated and subjected to an examination for organisms and bio-
chemical tests. In endophthalmitis, smear, culture and sensitivity of the organism to
antibiotic is a routine examination. Estimation of LDH enzyme is done in retinoblas-
toma. Oncological examination of the stained smear is done for retinoblastoma (see
page 154).
Therapeutic values of paracentesis are as follows:
1. It reduces the intraocular tension
2. Causes miosis
3. Large hyphaema and hypopyon can be removed
4. Antibiotic can be injected in the AC. The injection of drugs in the AC is called an intracameral
injection.
E XAMINATION OF I RIS ,
C ILIARY B ODY AND C HOROID
Iris, ciliary body and choroid constitute the uvea. Due to the anatomical position, cil-
iary body and choroid are not available for direct inspection by oblique illumination.
They are examined by special instruments, e.g. direct and indirect ophthalmoscope
and three-mirror gonioscope.
Iris is situated in the anterior region and is the major part of the uvea. It differs
from the other two in the sense that while the choroid and ciliary body are arranged
parallel to the sclera, iris is at right angles to the sclera. It hangs as a curtain with a hole
in the centre, the pupil. Normally it does not bleed. It is the thinnest part of the uvea.
It divides the aqueous chamber into anterior and posterior chambers. In a normal eye
the lens forms its posterior support on which it glides smoothly. In the absence of lens
it falls back deepening the anterior chamber and developing an anterior posterior
movement—tremulousness or iridodonesis, which is not possible in a phakic eye. Iris in
a phakic eye has only radial movement, which changes the size of pupil unless the
movement is restricted due to drugs or neurological causes e.g. mydriasis or miosis.
Movements are also limited due to adhesions between the iris and lens (posterior
synechiae). Iris pigment gives it its colour. The black of the eye (colour of the iris)
depends upon the amount of pigment present.
FUNCTIONS OF THE IRIS
1. To regulate the amount of light entering the interior of the eye

2. To regulate the flow of aqueous from posterior to anterior chamber
3. To keep the interior of the eye dark
Iris is vascular but does not bleed even on cutting. The mechanism is not well
understood. The commonest hypothesis put forward is that the iris vessels are highly
retractile and they retract following trauma.
Tumours of iris are far less common than those of the choroid and ciliary body.
Congenital anomalies of iris are more common than that of ciliary body and choroid.
Normal iris does not develop adhesion either with the lens posteriorly, or peripheral
cornea anteriorly, unless it is swollen and sticky. Iris does not block a normal angle
even with maximum mydriasis. It also does not block the pupil with extreme miosis.
However, in anatomically predisposed eyes, there may be rise of intraocular pressure
either by miosis or by mydriasis.
EXAMINATION OF IRIS
Iris can be best examined under focal illumination with magnification by a bright flash
light and uniocular corneal loupe. Binocular loupe does not give sufficient magnifica-
tion to examine the iris. It is best examined by a slit lamp.
Examination of iris should be done under following headings:
2. Colour of iris
3. Pattern of iris
4. Coloboma of iris
5. Mobility of pupil
6. Nodule of iris
7. Vascularisation
8. Aqueous flare and KP
9. Cells in AC
10. Hypopyon
11. Hyphaema
12. Intra-ocular pressure
13. Gonioscopy
14. Examination of fluid from AC
15. Examination of sac
RECORDING OF VISION
This should be done, not only on the first visit, but on every subsequent visit espe-
cially in cases of trauma, iridocyclitis and secondary glaucoma, with and without
correction.
COLOUR OF IRIS
Colour of iris varies from light blue to dark brown. The colour is due to a pigment
present in the iris. Absence of the pigment is seen in albinism where the iris looks grey
with a pink pupil. Colour of iris is of no clinical significance; so long, it is equal in both
eyes and uniform in each eye. Darker iris dilates poorly with mydriasis. Difference in the
colour of iris is called heterochromia of iris. The colour difference of iris in same eye is
called heterochromia iridium. Generally it is seen in both eyes and some part of the iris
has a different colour than other parts, then it is called heterochromia iridis.
Causes of heterochromia iridis are:
1. Simple or idiopathic
2. Trauma
EXAMINATION OF IRIS, CILIARY BODY AND CHOROID 143
4. Fuchs’ heterochromic iritis (cyclitis)
5. Posner Schlossman’s syndrome
6. Waardenburg syndrome
7. Uveitis and acute congestive glaucoma may produce necrosis of iris leading to localised white
atrophic patches
PATTERN OF IRIS
The anterior surface of iris is rough, whereas the posterior surface is smooth. Anterior
surface shows radial furrows and scattered pits. There is a circular raised ridge 3 mm
from the pupillary margin. This is called collarette of iris. The pupillary margin is bor-
dered by a ring of dark pigment. The furrows, pits and collarette give the iris a rugged
appearance. This is called normal iris pattern; loss of roughness of iris surface is called
loss of iris pattern.
Causes of loss of iris pattern are:
1. Oedema of iris as seen in inflammations of the iris. The iris stroma gets fluid laden thus distending
the iris. This is similar to an inflated balloon that looses its wrinkles on distension
2. Atrophy of iris: Essential iris atrophy, trauma, herpes zoster, post-acute congestive glaucoma and
trauma
COLOBOMA OF IRIS
Loss of margin or substance is called coloboma.

Causes of coloboma of iris Congenital coloboma of the iris may be localised to the
iris or may extend backwards into the ciliary body and choroid. It may be associated
with coloboma of the lens. Presence of iris coloboma in microphthalmic eyes is very
common.
The various types of congenital coloboma of iris are notch coloboma, typical
coloboma, pseudo-polycoria and iridostasis (Fig. 12.1). A coloboma at the lower part
of iris is called typical coloboma.
A B C D
Notch coloboma Typical coloboma Pseudo-polycoria Iridostasis
Fig. 12.1 | Types of congenital coloboma.

A B C D
Broad based Peripheral basal Peripheral button hole Sphincterotomy
E F G
Optical iridectomy Iridodialysis Four dot iridotomy
Fig. 12.2 | Types of acquired coloboma of iris.
Acquired coloboma of iris is mostly traumatic that can be surgical, post-laser or acci-
dental. Surgical coloboma is either iridectomy, where a piece of iris has been removed
or iridotomy where a hole has been made without removing tissue—laser produces
iridotomy. Various types of iridectomy or iridotomies are (Fig. 12.2) as follows:
1. Broad-based iridectomy
2. Peripheral basal
3. Peripheral button hole
4. Sphincterotomy (the coloboma does not extend up to the root of iris)
5. Optical iridectomy (coloboma reaches up to root of iris)
6. Four dot iridotomy
7. Laser iridotomy
Accidental iridotomies are due to penetrating injury or passage of intraocular foreign

body through the iris substance.
Miscellaneous causes of holes in the iris are essential iris atrophy, dysgenesis of ante-
rior chamber, post-glaucoma and herpes zoster.
Small iridectomies and iridotomies are visible on slit lamp examination, retro-
illumination either with a plane mirror or slit lamp and scleral trans-illumination.
Iridodialysis (Fig. 12.2F): The commonest cause of iridodialysis is blunt injury;
other causes are accidental catching of iris by intracapsular forceps, cryo probe, on
engaging iris by cystotome needle or even with Von Graefe knife, keratome, etc. In iri-
dodialysis, iris is separated from the root, as iris is thinnest at that point. The opening
is a slit-like plano-convex aperture with convex surface towards the limbus. It may be
very small or very extensive. Whole of the iris may be avulsed. The pupil gives a clue
to the presence of a dialysis. The pupil becomes plano-convex, plane border towards
the dialysis and convexity away from the dialysis.
A B C
One pillar Two pillar Basal
Fig. 12.3 | Types of iridencleisis.
Iridencleisis (Fig. 12.3): This was a popular filtering operation for glaucoma where
a part of the iris was incarcerated in the corneo-scleral wound under the conjunctiva.
There are three types of iridencleisis.
1. One pillar
2. Two pillars
3. Basal iridencleisis
PUPIL
Pupil is the natural opening in the centre of the iris. It acts as a communication between
the anterior and posterior chambers. This is the only aperture that allows light to reach
the retina. It constricts in bright light and dilates in the dark. A normal iris is highly
mobile, constricting and dilating with the change of illumination, convergence and
accommodation. Pupil can be examined under following headings:
1. Position of the pupil
2. Number of pupils
3. Size of the pupil
4. Shape of the pupil
5. Pupillary reaction to light
6. Pupillary reaction to accommodation and convergence
7. Colour of the pupil
Position of the Pupil

Though the pupil seems to be in the centre of the iris, in fact, it is situated slightly
nasally and medially. It can be shifted from its normal position as a congenital anom-
aly, as in corectopia or due to trauma, as iris prolapse following corneal, corneo-scleral
or scleral perforation (Fig. 12.4C–E).
Corectopia is a pupil complete with independent constrictor and dilator muscles
and pigmented pupillary margin, but not in its usual position (Fig. 12.4B).
Iris prolapse: Iris can prolapse through the limbus, sclera, or cornea (Fig. 12.4). The
pupil shifts towards the site of prolapse. AC is either absent or very shallow at the site
of prolapse (Plates 12.1 and 12.2).
A B C D E
Normal pupil Corectopia Iris prolapse Iris prolapse Iris prolapse
through cornea through limbus through sclera
Fig. 12.4 | Abnormal positions of the pupil.
Plate 12.1 | Traumatic iris prolapse. Plate 12.2 | Uveal prolapse through sclera away
from the limbus.
Number of Pupils
Most of the eyes have only one central, circular pupil. There may be more than one pupil
either as a congenital defect, trauma or infection. Congenital multiple pupil are called
polycoria. Each pupil reacts independent of the other when a very thin pencil of light is
shone on it. If there is no independent reaction, the condition is called pseudo-polycoria.
Examples are essential iris atrophy, traumatic iridotomy, post-inflammatory (herpes
zoster) and surgical iridectomy.
Size of the Pupil

The normal size varies between 2.5 and 3 mm, dilation of pupil is called mydriasis while
constriction is called miosis. A difference in the size of two pupils is called anisocoria.
Moderate anisocoria is very common. In pathological anisocoria, it is important to
find out which pupil is abnormal, the larger or the smaller one. The pupil that reacts
to light and accommodation is likely to be the normal pupil.
Causes of anisocoria
1. Drug induced
2. Iridocyclitis
3. Trauma
4. Unilateral internal ophthalmoplegia
6. Argyll Robertson pupil
7. Adie’s pupil
Causes of small pupil (miosis)
A. Physiological
(i) Age: pupil of newborns and elderly is small
(ii) Error of refraction: hypermetropic pupil is smaller
(iii) Bright light: pupil constricts in bright light and remains constricted till the stimulus is main-
tained
(iv) Sleep
B. Pharmacological
(i) Use of local miotic (parasympathomimetic), pilocarpine, methacholine, carbachol, physostig-
mine and DFP
(ii) Sympatholytic
(iii) Systemic use of miotics—Morphine, opium and organophosphorous poisoning
➤ In all cases of small pupil, patients should be questioned about the instillation
of local miotic or having ingested systemic miotics, e.g. opium etc
C. Pathological
(i) Iritis
(ii) Iridocyclitis
(iii) Traumatic miosis
D. Neurological
(i) Horner’s syndrome
(ii) Argyll Robertson pupil
(iii) Irritable lesions of third nerve
(iv) Pontine haemorrhage
Causes of large pupil
A. Physiological
(i) Dim light
(ii) Fright, fear and surprise
(iii) Myopia
B. Pharmacological causes
(i) Installation of local mydriatic
● Parasympatholytics—atropine, homatropine, cyclopentolate and tropicamide
● Sympathomimetic—adrenaline, phenylephrine, cocaine and ephedrine
C. Pathological
(i) Chronic simple glaucoma
(ii) Chronic congestive glaucoma
(iii) Absolute glaucoma
(iv) In acute congestive glaucoma the pupil is dilated but vertically oval
(v) Traumatic mydriasis
(vi) Optic atrophy (total)
D. Neurological
(i) Internal ophthalmoplegia
(ii) Oculomotor palsy
(iii) Irritable lesions of cervical sympathetic
(iv) Adie’s pupil
E. Miscellaneous
(i) General anaesthesia stage I, II and IV
(ii) Hutchinson pupil
(iii) Photocoagulation
Causes of fixed dilated pupil Instillation of mydriatic or cycloplegic, therapeutic or

accidental, Hutchinson pupil, amaurotic eye, total optic atrophy, absolute glaucoma,
long-standing total retinal detachment and death.
Shape of the Pupil

Normal pupil is circular. A pupil that is not circular is called irregular. Pupil can be
irregular with normal size or with miosis or mydriasis. Persistent pupillary membrane
(Fig. 12.5) is the only condition where pupil looks irregular with a normal size.
Causes of small irregular pupil
1. Iridocyclitis
2. Iritis
3. Traumatic miosis
Causes of large irregular pupil

1. Congenital coloboma
2. Iris atrophy
3. Broad-based iridectomy
4. Iridencleisis
Central
circular pupil
Root of iris Collarette
Persistent pupillary
Collarette membrane arising
from the anterior
surface of iris
A. Normal pupil with B1 B2

normal collarette
Fig. 12.5 | Persistent pupillary membrane.

5. Iridodialysis
6. Festooned pupil—due to instillation of mydriatic in iritis (Fig. 12.6C)
Pupil in Inflammation of the Iris

In iritis, the iris swells up due to the accumulation of fibrinous transudate (Figs 12.6 and
12.7). If the weight of the iris increases, there is over activity of the parasympathetic
nerve supply. As fluid increases, the iris becomes more oedematous, increases in vol-
ume and spreads towards the centre thus reducing its aperture (pupil). Fibrinous fluid
is sticky in nature. Due to the reduced mobility, the iris gets stuck to the anterior sur-
face of the lens or posterior surface of the cornea. This adhesion is called synechia. It
can be posterior or anterior (Fig. 12.8).
Posterior synechia (Fig. 12.8) is an adhesion between the posterior surface of iris to any
of the following: anterior lens capsule, PCIOL, after cataract, posterior capsule or vitre-
ous as the case may be. The synechia may be very small, visible on slit lamp and break-
ing with mydriatic and cycloplegic. It may be broad and strong, resisting breakage by
drugs, and may have to be cut or broken by photo-iridoplasty. Their number may vary
A B C
Normal pupil Small irregular pupil Large irregular pupil
atropinised in iridocyclitis
Fig. 12.6 | Pupil in iridocyclitis.
PAS
Normal iris
No KP
Normal pattern
Pupil⎯central, circular N
lris pigment on lens
BK
CCC
Large KP
Hypopyon Chronic iridocyclitis (pupil dilated with cycloplegic)

Acute iridocyclitis Circumciliary congestion
Prominent circumciliary congestion Large KP
Fine KPs Fine KP Festooned pupil
Aqueous flare lris nodule (N)
Loss of iris pattern lris pigment on lens
Constricted irregular pupil Peripheral anterior synechiae (PAS)
Hypopyon ± Band keratopathy (BK)
Fig. 12.7 | Comparison of signs in acute and chronic iridocyclitis (Plate 12.3).
IOL
After V
cataract
Small adhesion between the lens Adhesion between

PC IOL and iris Adhesion between iris Adhesion between
capsule and posterior surface of iris
and after cataract vitreous and iris
Fig. 12.8 | Types of posterior synechiae.
A. Peripheral B. Central
Fig. 12.9 | Various types of anterior synechiae.

from single to multiple. A synechia may extend all around and is called annular or ring
synechia. Such synechia prevent the aqueous flow and is called seclusio pupillae.
Persistent pupillary membrane (Fig. 12.5): This is a very common congenital anom-
aly of the iris and anterior chamber. Fine strands of iris tissue are attached to the ante-
rior surface of the iris generally at the collarette. The other end of the strand may pass
across the pupil, may get attached to the lens or float freely in aqueous. These strands
neither interfere with the movement of iris nor with the vision. They are often mis-
taken as posterior synechiae.
Anterior synechiae can be peripheral or central. Peripheral anterior synechiae develop
on the extreme periphery of iris.
Causes of peripheral anterior synechiae are (Fig. 12.9A) as follows:
1. Acute and chronic iridocyclitis
3. Persistent hypotony
4. Corneal fistula
Causes of central anterior synechiae are (Fig. 12.9B) as follows:
1. Perforation of corneal ulcer
2. Penetrating injury of cornea
3. Persistent absence of anterior chamber
A B
Hammock pupil Tear drop pupil
Fig. 12.10 | Hammock pupil and tear drop pupil.
Effect of Mydriatics on Posterior Synechiae

Small and recent posterior synechiae break with the usual dose of local mydriatic. As
the synechiae break, the pupil becomes dilated leaving marks of iris pigment on the
anterior lens capsule. Old and broad synechiae do not break easily. They remain
attached to the anterior lens capsule but the pupil in between the synechiae dilates
giving an exaggerated irregular pupil called Festooned pupil (Fig. 12.6).
Total posterior synechia is a firm adhesion of large posterior surface of iris to the
anterior lens capsule due to prolonged iridocyclitis, swollen lens with iridocyclitis and
prolonged hypotony with iridocyclitis.
Hammock pupil: This is a hammock or boat-shaped pupil which is shifted upwards.
The upper margin of the pupil is not visible. It does not react to light or accommodation.
The commonest cause is vitreous prolapse during intracapsular lens extraction
(Fig. 12.10A).
Tear drop pupil or pear-shaped pupil with the narrow end towards the limbus. On slit
lamp examination a narrow tag of vitreous is found to be incarcerated in the limbal
wound of lens extraction (Fig. 12.10B). Commonest cause is intracapsular lens extraction.
Mobility of Pupil (Pupillary Reaction)

Normal pupil should constrict in bright light and remain constricted in the presence
of light stimulus. It should dilate in dark and remain so in darkness. As intensity of
light is not constant, size of the pupil keeps on fluctuating alternately constricting and
dilating. This is under the control of the autonomic nervous system and integrity of the
visual pathway. There are two types of pupillary reactions: light reflex and near reflex.
Light reflex is further divided into two types (i) direct and (ii) consensual or indirect.
Direct pupillary reaction is the constriction of the ipsilateral pupil in the presence of
light stimulus.
Indirect pupillary reaction is the constriction of the contralateral pupil when light is
shone on the ipsilateral pupil. Normal light reflex is brisk, abnormal can be sluggish
or absent.
Near reflex consists of convergence, accommodation and miosis. For details see neuro-
logical examination of the pupil (Chapter 19).
NODULES OF IRIS
Nodules are often seen on the iris in granulomatous uveitis (Fig. 12.11). They can either
be on the pupillary margin or in the substance of iris. Former is called Koeppe’s nodule
and the latter is called Busacca’s nodule. Nodules are raised areas, 1–2 mm in size, may
be single or multiple.
Other causes of nodules on iris are leprosy, tuberculosis, foreign body granuloma, new
growth of iris, sarcoidosis of uvea, acquired or congenital cysts and secondaries in the iris.
Characteristics of Some Typical Iris Nodules

1. Koeppe’s nodule: Ectodermal in origin, seen on the pupillary border of iris, may project in the
pupil and disappears within a few days. They are equivalent of mutton fat KP
2. Busacca nodule:They are seen in the mid periphery of iris and they last longer
3. Tubercular nodule: These may be single or multiple and seen near the iris root; vessels travel
over them
4. Syphilitic nodule: Seen anywhere on the iris, yellowish red in colour, slight vascular and disap-
pear with systemic treatment of syphilis
5. Leprotic nodule: The two types of nodules seen are pearl and leproma. Leprosy pearl can be
small, shinning white dot on the pupillary margin arranged in an arc.They contain histocytes and
lepra bacilli
NEOVASCULARISATION OF IRIS
In a normal iris, blood vessels are embedded in the substance of iris and are not visi-
ble. They do not bleed on trauma. New vessels are those vessels that develop in or
on the iris, are visible and bleed on trauma. They can either be on the surface of iris
or the substance. They give a red hue to the iris and such an iris is called Rubeosis iridis.
They are visible with uniocular corneal loupe, slit lamp and gonioscope. Surprisingly,
the cause of neovascularisation is not always in the iris. The most common cause is
hypoxia of the retina. Hypoxic retina sends a chemical signal that starts angiogenesis
leading to neovascularisation. Sometimes such signals may be started from the uvea.
Syphilitic nodule Koeppe's nodule
Lepromatous nodule
Busacca's nodule
Tubercular nodule
Fig. 12.11 | Various types of nodules in iridocyclitis.

The other peculiarity of neovascularisation is that it starts from the pupillary margin
and travels towards the root of iris.
Causes of neovascularisation
1. Diabetic retinopathy
2. Central retinal vein obstruction
3. Long-standing glaucoma
4. Uveitis
5. Sickle cell retinopathy
6. Long-standing retinal detachment
7. Coats disease
8. Eales disease
9. Retrolental fibroplasia
10. Intraocular malignancy
11. Carotid artery occlusive disease
12. Aortic arch syndrome
13. Vitrectomy and lensectomy in an already hypoxic eye
Aqueous flare—see plasmoid aqueous.
KERATIC PRECIPITATES (PLATE 12.3)
These are deposits of cells and uveal pigment on the endothelium of cornea and denote
inflammation of the uvea. In uveitis there is an outpouring of cells in the aqueous, the
aqueous becomes plasmoid, the endothelium is oedematous; these two predispose to
the deposition of cells on endothelium. Keratic precipitates (KPs) vary in shape, size,
number, colour and distribution. Small KPs are called dusty KPs; the large ones are
Plate 12.3 | Keratic precipitates in endophthalmitis. (Courtesy Dr. M.L. Garg.)

known as mutton fat KPs; fresh KPs are multiple, circular and white. They are due to
lymphocytes and are seen in anterior uveitis. Old KPs get pigmented with the passage
of time. They have crenated borders; central part of old KPs is pale; they denote extin-
guished activity and are mostly plasmoid cells (see page 135).
Mutton Fat KPs

They are large, generally few and scattered all over the endothelium. They may be large
enough to be seen with the naked eye or binocular loupe and are waxy, yellow and greasy.
When old, they become hyalinised. They are seen in granulomatous uveitis.
Cells in aqueous (see aqueous humour), hypopyon (see examination of AC), and
hyphaema (see examination of AC) (see page 136).
INTRAOCULAR PRESSURE IN INFLAMMATION OF THE UVEA
Intraocular pressure variation in uveitis is unpredictable. It may remain normal, may be

raised or lowered enough to produce hypotony. Hence it is mandatory that in all case
of uveitis, especially anterior uveitis, tension should be examined at regular intervals.
Causes of raised IOP in uveitis
1. Blockage of trabeculum by debris
2. Peripheral anterior synechiae
3. Pupillary block
4. Closure of an anatomically narrow angle due to mydriasis
5. Steroid-induced glaucoma following the prolonged use of local or systemic steroids in a genet-
ically predisposed patient
6. Neovascularisation of the angle
7. Swelling of trabecular meshwork, formation of hyaline membrane or sclerosis of meshwork
GONIOSCOPY
This is an examination of the angle of the anterior chamber by a special device called
gonioscope. Gonioscopy will reveal the formation of goniosynechiae, inflammatory
deposits, membrane formation, pigment deposits, neovascularisation, foreign bodies
and tumour cells besides width of the angle.
EXAMINATION OF FLUID FROM AC (SEE PAGE 140)
Aqueous is collected in a cooled autoclaved syringe by a 30 gauge needle under suit-

able local anaesthesia in adults and general anaesthesia in children with utmost antisep-
sis and asepsis in the same fashion as paracentesis, avoiding blood vessels on the cornea.
0.1–0.2 ml of aqueous is aspirated. It is better avoided in neovascularisation of the

iris. The aqueous is used to:
1. Find out the causative organism and culture them
2. Identify the cell type in inflammation
3. Identify antibody in the aqueous
4. Examination of enzymes
5. Papanicolau stain for malignancy
6. Dark field examination for treponema
7. Demonstration of parasites
One drop of aqueous is put over a dry autoclaved glass slide, stained with Gram or
Giemsa stain and examined for bacteria and cytology. A separate drop can be inocu-
lated on a suitable culture medium for the growth of microorganisms. In cytology, the
cells may be neutrophils in Behcet’s disease, lens-induced uveitis and bacterial uveitis;
macrophages in lens-induced uveitis; eosinophils in parasitic inflammation.
Examination of the sac: In all cases of iritis, especially with hypopyon, the sac should
be examined for the presence of chronic dacryocystitis.
Systemic examination: diabetes, autoimmune diseases, arthritis, gonococcal infection,
syphilis, tuberculosis, leprosy, sarcoidosis, HIV and AIDS should be excluded.
EXAMINATION OF THE CILIARY BODY AND CHOROID
These two parts of the uvea are not visible by simple oblique illumination as they are
hidden behind the iris. However, a part of the choroid is visible by direct ophthalmo-
scope; no part of the ciliary body is visible by direct ophthalmoscope; only a small part
of the ciliary body is visible with the gonioscope. Isolated congenital anomaly of the
ciliary body is extremely rare. Inflammation of the ciliary body alone is also rare except
for pars planitis. The ciliary body, due to its proximity to iris and intimate relation
with the aqueous and anterior vitreous, produces signs that indirectly give a clue to
its involvement in inflammation. Inflammation of the choroid may also involve the
retina, e.g. chorioretinitis. Inflammation of the choroid without involving the ciliary
body does not produce an anterior chamber reaction while they frequently produce
vitreous changes.
Anterior chamber reactions in the disorders of ciliary body are KPs, aqueous flare,
cells in AC, hypopyon, growth protruding in AC, peripheral anterior synechiae.
Changes in the Vitreous in Disorders of the

Ciliary Body
Opacities in the peripheral vitreous, mostly snowball opacities are produced in pars
planitis. Cyclitis mostly produces cells and opacities in the vitreous. Examination of the
ciliary body reveals changes similar to the examination of iris. KPs, aqueous flare, cells in
AC, hypopyon, hyphaema, posterior sub-capsular lenticular opacity and cells in anterior
vitreous are hallmarks of cyclitis. Posterior vitreous cells denote choroiditis.
Methods of examination for posterior uveal involvement consist of:

1. Slit lamp examination with
● Hruby lens
● El Bayadi lens
● ⫹9 0 D
2. Direct ophthalmoscopy
3. Indirect ophthalmoscopy
4. Three-mirror gonioscope
5. Trans-illumination
● Trans-pupillary
● Trans-scleral
6. Ultrasonography
Symptoms of posterior uveitis (choroiditis) depend on the part of the choroid involved.
Diminished vision means involvement of the:
1. Macula
2. Maculopapillar bundle
Floaters: generally seen in peripheral choroiditis.

Pain, redness of eye and AC reaction are absent.
Signs
1. Vitreous signs
2. Fundus changes
Vitreous signs may include:

1. Cells
2. Floaters (opacities)
3. Posterior vitreous detachment
Opacities are noted under the following heads:

1. Shape
2. Size
3. Number
4. Position in relation to its distance from the retina and a fixed landmark like the optic nerve
head, macula or retinal blood vessels
They can be fine, coarse or nodular (snowball).

Causes of snowball opacities The commonest cause is pars planitis. Other causes are
fungal infection of candida, sarcoidosis.
Fundus changes in choroiditis are patches of:
1. Choroiditis
● Single, well defined
● Multiple
● Single, large with irregular shape (geographic)
2. Chorioretinitis
3. Optic neuropathy—papillitis and consecutive optic atrophy

4. Macular oedema
● Exudative
● Tractional
6. Retinal vascularisation
Signs of Active Choroiditis

1. Vitreous opacities, cells and flare
2. Yellowish raised area with diffuse borders. Blood vessels are passing over the lesion
Signs of Healed Choroiditis

Whitish patch of atrophy, clumps of pigment on the periphery of the atrophic patch
and vessels crossing the patch of choroiditis. Not all the signs that have been men-
tioned earlier need be present in all the cases of posterior uveitis.
Signs and symptoms depend upon the:
1. Duration
2. Nature
3. Severity
4. Involvement of:
● Macula
● Optic nerve
Symptoms of Choroiditis
Two prominent symptoms of choroiditis are visual symptoms and floaters. Visual
symptoms can be diminished distant vision and metamorphopsia. Floaters are gener-
ally seen in peripheral lesions. Choroiditis is devoid of pain and redness of eye.
E XAMINATION OF L ENS AND
E VALUATION OF AN E YE FOR
L ENS E XTRACTION
Disorders of lens are the most common ocular diseases next only to errors of refraction.
The lens itself may cause an error of refraction. Not many disease processes affect the
lens. Out of all the disorders of lens, opacity is commonest and may even be known
to layman as cataract or by its local name.
PECULIARITIES OF LENS AS AN ORGAN
1. It starts developing at a very early stage of intrauterine life, i.e. 4.5 mm and keeps on developing
2. Postnatal lens is completely avascular
3. It has no nerve supply-motor, sensory or autonomous
4. It is not capable of developing infection, inflammation or new growth
5. Lens is not affected by allergy because it is avascular
6. Lens can cause allergy. The lens is encapsulated, hence the body does not recognise it as a
foreign protein as long as the capsule is intact
7. Once there is a break in the capsule, the lens protein starts circulating in the body and causes
antigen–antibody reaction
8. In utero, its nutrition is from tunica vasculosa lentis
Cornea
Object
Lens
1
2
3
4
1. First image: brightest, virtual, erect, moves with

2. Second image: virtual, erect, moves with, faint, very near the first
3. Third image: virtual, erect, largest, moves with
4. Fourth image: real, inverted, moves against
Fig. 13.1 | Purkinje images.

EXAMINATION OF LENS 159
9. It has only one function, i.e. to focus light rays on the retina both from distance as well as near
10. With age, its power to converge the light diminishes, more for rays arising from the near point
11. Though the lens acts as a convex spherical medium, its capsule acts as a mirror—
anterior capsule as convex mirror, posterior capsule as concave mirror (Fig. 13.1)
12. It is wider in vertical and horizontal diameters than anterio-posterior thickness
13. Posterior surface is more than curved than the anterior surface
EXAMINATION OF LENS
Examination of the lens is done under following headings:

1. Examination of function
2. Examination of lens morphology
3. Examination of the other parts of eye
4. Special investigation
1. Examination of function
(a) Distant vision
(b) Near vision
(c) Impaired colour vision
2. Examination of lens morphology:
(a) (i) Presence Transparent

(Phakia)
Complete—Mature
cataract
Opaque (cataract)
Partial—Immature cataract
(Plate 13.1)
(ii) Absence Complete
(Aphakia)
Partial—Ectopia, after
(b) Position of lens
cataract
Normal
Dislocation
Subluxation
Absence
(c) Curvature Increased
Spherophakia
Microphakia
Lenticonus
Lentiglobus
Intumescent
Decreased
Buphthalmos
Dehydration
Hypoglycaemia
(d) Transparency
Plate 13.1 | Immature cataract. (Courtesy Dr. Nidhi Pande.)
➤ While examining the lens of one eye the other eye must always be seen, not only for
lenticular changes but also for refraction and fundus changes
3. Examination of the other parts of eye:

(a) Depth of AC
(b) Pupillary reaction
(c) Intraocular pressure
(d) Fundus examination: direct and indirect ophthalmoscopy
(e) Error of refraction
4. Special investigation
5. Systemic Examination
Method to detect the presence of lens in the pupillary area: The first and primary thing
is to ascertain the presence of lens in the pupillary area. An opaque lens does not pose
any difficulty. Its presence is obvious by a grey reflex in the pupillary area.
A transparent lens allows almost all the rays through it; hence it looks as a black hole
in the pupil. Only some rays are reflected by the anterior and posterior surface of the
lens. These surfaces produce two distinct images in pupillary area called the third and
fourth Purkinje images. Presence of the third image confirms the presence of lens unless
the anterior lens capsule is obstructed or absent. Presence of the fourth denotes a trans-
parent lens. It is not possible to have fourth image in the absence of third (Fig. 13.1).
Anterior lens capsule is obscured in following conditions (Table 13.1):
1. Large central corneal opacity
2. Abnormal contents of AC
Table 13.1 Difference between third and fourth Purkinje images
Third Purkinje image Fourth Purkinje image
Large and erect, virtual Smaller and inverted, real

Moves with movement of light Moves against movement of light
Absent only when the anterior capsule Absent in obscured anterior capsule, mature
is opaque/obscured and in aphakia cataract and aphakia
Anterior capsule acts as convex mirror Posterior capsule acts as concave mirror
It is largest in size It is smallest in size
➤ The fourth image is smaller than the third because the posterior surface is more
curved (6 mm) than the anterior surface (10 mm). Position of posterior pole is about
4 mm behind the anterior pole
3. Pinpoint pupil
4. Exudate in pupillary area
Opaque Lens (Cataract)

Any opacity in the lens, acquired or congenital, is called cataract. If the opacity spreads
from capsule to capsule it is called mature cataract, otherwise it is known as immature
cataract.
Mature cataract—Colour of the lens is dense white. Third Purkinje image is present,
fourth is absent. There is no iris shadow.
Immature cataract—Third Purkinje image is present. If the cataract is not very large
and pupil is dilated fourth may be seen. Lens looks light grey. Iris shadow is present;
may be nuclear, cortical or combined.
Some points to be noted in relation to iris shadow.
Causes of absent iris shadow:
1. Mature cataract
2. Aphakia
3. Clear lens
Iris shadow is present in:
2. Dense after cataract
Absence of lens from the pupillary area is called aphakia. It can be totally or par-
tially absent from the pupillary area.
Causes of total absence:
1. Surgical removal (commonest)
2. Dislocation (fairly common), extrusion and absorption (fairly common)
3. Non-formation (congenital)
Examination of an Immature Cataract

Logically any opacity in the lens—capsular, cortical or nuclear is called cataract; as
long as it does not involve whole of the cortex, it is known as immature cataract.
Opacities can be:
1. Single or multiple
2. Unilateral or bilateral
3. Simultaneous and bilateral
4. The other lens may be involved later
5. Only lens may be involved or the other parts of the eye may have a causative or non-causative
pathology
6. May be congenital, traumatic or age related
Location of opacities can be capsular, subcapsular, cortical, nuclear, sutural and
combinations (Fig. 13.2A and B).
Coronary
Posterior cortical
Nuclear View of lens from side
Anterior sub-capsular Posterior polar
Zonular lamellar Cortex

Anterior capsule Coronary 1 2 3 4 5
View of lens from front
Equator of lens Posterior capsule
(A) (B)
Fig. 13.2 | (A) Diagrammatic representation of various lenticular opacities; (B)1—total cataract, mature; 2–5—immature cataract.
Presence of opacity can be demonstrated by following methods; if necessary pupil
should be dilated:
1. Flash light
2. Retinoscope
4. Slit lamp
6. Trans-illuminator
7. Ultrasonography
Examination of Lens with Retinoscope

Plane mirror retinoscope is used for convenience. Pupil is dilated and the patient is
examined as in a case of error of refraction. In clear lens, the reflected light from retina
gives a uniform pink glow that fills the entire pupillary area. If there are opacities in
the media that obstruct the rays, they stand out as black spots against the pink back-
ground. They can be in the lens, behind the lens or in front of the lens. The opacities
in the lens do not move with the movement of the retinoscope or the eye.
Examination of Lens with Direct Ophthalmoscope

1. Examination from 20 cm
2. Examination from the usual distance with ⫹10 interposed in peephole
Examination of Lens with Slit Lamp

1. Diffuse illumination with low magnification will be sufficient for cortical and nuclear opacity, and
iris pigment on lens
2. Optical section with high magnification is useful to see early subcapsular opacity, vacuole
formation, posterior subcapsular opacity and changes in posterior capsular curvature like
posterior lenticonus, remnants of Cloquet’s canal, exfoliation and pseudo-exfoliation of capsule
➤ A nuclear cataract may give an appearance of “lens within lens” when the
cortex gives the usual pink glow and nucleus gives a dull pink glow
Ultrasonography
As such ultrasonography is superfluous in the examination of lens so long as it is not
obscured by either iris or exudates. In such a condition, ultrasonography will not only
demonstrate the presence of lens but also the extent of the opacity, condition of the
posterior capsule and presence of any mass lesion in the vitreous, choroid or retina,
axial length of eye ball, position of displaced lens, intraocular foreign body etc.
Examination of an Aphakic Eye

1. Distant vision—In an uncomplicated aphakia distant vision is 1/60 or less. A better vision is
suggestive of high axial myopia
2. Near vision is lost
3. Scar—In post-operative aphakia—large scar from 3 to 9 O’clock at the upper limbus means
conventional intracapsular or extracapsular lens extraction
A small scar denotes modern extracapsular cataract extraction. A small scar away from the
limbus means phaco-emulsification or pars plana lensectomy
A very small scar inside limbus means needling or aspiration
4. Deep anterior chamber—Aphakic depth—Theoretically AC of an aphakic eye should be
about 6 mm. deep, i.e. 2.5 ⫹ 3.5 mm, but in practice it is about 4.5 mm deep. In pseudophakia
AC is almost normal in depth
5. Tremulousness of iris—In the absence of lens, the iris loses its posterior support and devel-
ops fine anterio-posterior movement (iridodonesis)
6. Iridectomy—In classical lens extraction various types of iridectomies are visible. In microsur-
gical cataract extraction either iridectomy is absent or too small or too peripheral to be seen
7. Purkinje image—Third and fourth Purkinje images are absent in classical aphakia. A history of
lens extraction, slightly deep AC, non-tremulous iris and presence of third and fourth Purkinje
image denote pseudophakia, e.g. PCIOL. The Purkinje image is very bright in PCIOL
8. Jet black pupil—Denotes removal of lens in toto e.g. intracapsular lens extraction
9. After cataract—With all findings of aphakia plus a white membrane in pupillary area means
after cataract following extracapsular lens extraction or trauma
Faint opacity on the posterior capsule is called posterior capsular opacification (PCO)
10. Refraction—Acquired compound hypermetropic astigmatism, which is index in nature and
absolute in type is seen in classical lens extraction in an emmetropic eye
11. Accommodation—Total loss of accommodation
12. Fundus—Small hypermetropic disc, over-all fundus size is reduced
Signs of Atypical Aphakia

1. Scar (a) Absent in spontaneous dislocation of lens or blunt trauma (Table 13.2).
Corneal—Penetrating wound
(b) Small
Limbal—Needling aspiration
(c) Away from limbus

Phaco emulsification
Pars plana lensectomy
Penetrating injury
2. Depth of AC
(a) Normal or slightly deep AC posterior chamber IOL
(b) Shallow
Aphakia with iris prolapse
Vitreous loss
Iris bombe
Leaking wound
Ciliochoroidal detachment
Malignant glaucoma
3. Contents of AC
ACIOL, dislocated PCIOL, cortical matter
4. Absent iridodonesis
(a) Pseudo phakia
(b) Iris prolapse
(c) Vitreous loss (hammock pupil) (Fig. 12.10A)
(d) Leaking wound
5. White reflex in pupillary area in aphakia—After cataract, Elschnig’s pearls, Soemmerring ring,
posterior capsular opacification, retrolenticular mass, endophthalmitis, large retinal detachment
and intraocular tumour.
6. Absent iridectomy—Spontaneous dislocation of lens, blunt trauma, micro-surgical extracapsu-
lar lens extraction and round pupil lens extraction.
7. Refraction—Less than ⫹10 Dioptre hypermetropia is seen in axial myopia and IOL.
8. Fundus—Not visible due to thick after cataract, vitreous haemorrhage and endophthalmitis.
Large disc and high axial myopia.
9. Absent foveal reflex—Cystoid macular edema and ARMD.
Optics of Aphakia
1. Optics of normal eye (phakic) can be broadly divided into two components:
● Corneal
● Lenticular
Table 13.2 Differences between classical post-operative aphakia and pseudophakia
Aphakia Pseudophakia
Scar large at limbus Small scar at limbus or away from limbus

AC depth more than 4 mm Normal or slightly deep
Iridodonesis—Present Absent
Iridectomy—Generally present Generally absent or not visible
Purkinje image—Third and fourth absent Third and fourth present
After cataract
In ICCE absent Thin PCO in 30% adult, 100% in children
In ECCE present
Refraction—Compound hypermetropic Nil or variable according to the power of IOL
astigmatism against the rule
Astigmatism: 1–2 Dcyl 180° May be more, depending upon the number
and type of suture
Fundus—Appears small in size Normal size
2. In aphakia with the removal of lens the eye virtually comes closer to the concept of reduced
eye of Donder
3. It is less convergent than phakic eye. Its diopteric power is reduced to ⫹43 D
4. Parallel rays are brought to a focus 31 mm behind the cornea
5. There is one refractive component, i.e. cornea
6. The two nodal points are very near to each other, i.e. 8 mm from anterior corneal surface
7. The nodal points shift away from the anterior corneal surface
8. The anterior focal point is 23 mm in front of cornea
9. There is no accommodation
Causes of magnification in spectacle correction of aphakia:

It depends on the power and position of the lens used to correct aphakia.
1. A plus lens placed away from the nodal point acts as a stronger converging lens than when
pushed nearer to it
2. This is used to advantage in aphakia. If a distant correction is pushed away from the eye over
the nose, the patient can use it as a near correction as well
3. The hypermetropic eye has a hypothetical minus lens that is neutralised by putting lenses in
front of the eye; in contrast a myopic eye has a hypothetical plus lens that is neutralised by
minus lens
4. Aphakia is an extreme degree of hypermetropia, which is corrected by a ⫹10 D lens placed at
the anterior focal plane
5. ⫹10 D at anterior focal plane is as effective as ⫹17 D at nodal point
6. In aphakia, a hypothetical high minus lens and a ⫹10 D in front of it, creates a condition simi-
lar to Galilean telescope that causes magnification. The diopteric system of the aphakic eye acts
as an ocular, while the spectacle lens acts as an objective lens producing an erect, virtual and
magnified image
Causes of astigmatism in post-operative aphakic can be:

1. Pre-operative
2. Operative
3. Post-operative
1. Pre-existing astigmatism of high degree is bound to influence the post-operative cylindrical

error. It may be reduced or may be enhanced
Table 13.3 Comparison between the optics of phakic and aphakic eye
Comparative features Phakic Aphakic
Refractive media Cornea, lens, aqueous and vitreous Cornea, aqueous, vitreous
Diopteric value ⫹60 D ⫹43 D
Anterior focal point 17 mm in front of anterior 23 mm in front of anterior
surface of cornea surface of cornea
Posterior focal point 24 mm 31 mm
Nodal point 7.8 mm behind anterior 8 mm behind anterior corneal
corneal surface surface
Accommodation According to age of patient Absent
Magnification Nil 33% with spectacle correction
10–15% with contact lens
2. Operative causes of astigmatism are:

(a) Section:
● A corneal section produces more astigmatism than corneo-scleral
● A scleral incision with conjunctival flap produced less astigmatism
● A ragged section produces more astigmatism
(b) Suture—number, pattern and tightness of sutures influence astigmatism. Astigmatism is least
if no suture is used. Tighter sutures produce more astigmatism
(c) Scar—thicker the scar more is the astigmatism
Causes of thick scars are:

1. Iris prolapse
2. Vitreous in the wound
3. Post-operative factors
(a) Cortical matter incarceration
(b) Re-suturing
(c) Lens extraction following filtering surgery
(d) In the first post-operative period astigmatism may be as high as 6–7 Dcyl. It gradually
tapers to one to two by the sixth week and then remains stationary
Examination of Displaced Lens (Ectopia Lentis)

1. Clinically aphakia represents total or partial absence of lens from pupillary area.
2. When lens is partially present in the pupillary area it is called Ectopia Lentis.
3. An ectopic lens can be (Figs 13.3 and 13.4):
(a) Subluxated, i.e. when some of the zonules are attached the between the lens and ciliary body.
(b) Dislocated—when all the suspensory ligaments are broken. According to its position it can
be dislocated:
● In vitreous
● In AC
● Entrapped in the pupil
● Extruded outside the globe
Common causes of ectopia lentis are:

1. Injury
(a) Blunt (commonest)
(b) Penetrating
3
1
4
2
Fig. 13.3 | Lens in position, normal AC. Fig. 13.4 | 1.Ectopia lentis:
Subluxated down—upper part of pupil is aphakic
2. Dislocated in vitreous—whole of the pupil is
aphakic
3. Lens entrapped in pupil
4. Lens dislocated in AC—deep AC, aphakic pupil
5. Lens extruded outside the globe—deep AC,
aphakic pupil, soft eye.
2. Congenital
(a) with skeletal changes
(b) with ocular changes—buphthalmos
3. Chronic uveitis
4. Spontaneous
Congenital ectopia lentis with skeletal anomaly:

1. Marfan syndrome
2. Marchesani
3. Homocystinuria syndrome
4. Ehlers–Danlos syndrome
5. Hyperlysinemia
6. Sulphite oxidase deficiency
7. Mandibulo-facial dysostosis
8. Treacher Collins syndrome
Congenital ectopia lentis with ocular changes (without skeletal anomaly):

1. Congenital primary glaucoma
2. Dysgenesis of AC
3. Aniridia
4. Coloboma of ciliary body
5. Megalocornea
6. High myopia
7. Spherophakia
8. Primary (idiopathic) ectopia lentis
➤ The word ‘ectopia lentis’ is generally used in cases of congenitally displaced lens
Clinical features of ectopia lentis are:

Vision—Patient may have normal vision, diminished distant vision, diminished
near vision and uniocular diplopia.
Anterior chamber—Irregularly deep, deep over the aphakic area, normal or shallow.
Tremulousness of iris—Over aphakic area.
Oblique illumination:
1. If the subluxated lens is opaque, a clear-cut white phakic and jet-black aphakic area is visible
2. In case of clear lens—Purkinje image from the clear lens is visible, aphakic area looks jet-black
without the third and fourth Purkinje images. Edge of the dislocated lens shows a bright cres-
cent shaped reflex
Slit-lamp examination—Strands of suspensory ligaments may be visible. Formed

vitreous may bulge in the aphakic area. Fluid vitreous may be seen in the AC.
Retinoscopy—Aphakic area is hypermetropic, phakic area generally shows index
myopia. The edge of the lens looks dark.
Fundus—With a clear lens two discs are seen. One large through the phakic area
and one small through the aphakic area.
EVALUATION OF AN EYE FOR LENS EXTRACTION
Indications of lens extraction are:

1. Removal of opacity that interferes with vision (cataract)
2. Lens-induced glaucoma
3. To reduce the diopteric power of eye (clear lens extraction in myopia)
4. Subluxated or dislocated lens
5. Cosmetic—mature cataract in a blind eye
6. Prophylactic—removal of mature cataract in a blind eye to prevent lens-induced uveitis and
glaucoma
By far the commonest indication of lens extraction is cataract.
Before embarking on lens extraction for cataract, the following points merit
consideration:
1. Is the diminished vision due to cataract?
2. Is the diminished vision due to causes other than cataract?
3. Is it due to cataract only or is it compounded by other causes like corneal opacity, chronic
uveitis, glaucoma, high errors of refraction, amblyopia, retinal changes, optic nerve changes and
macular pathology?
➤ These causes, when present, will not permit improvement of vision to the expected
levels
It is essential to evaluate an eye before surgery to prevent operative and post-

operative complications and to be warned about the possibility of non-improvement
of vision.
An eye that has to undergo lens extraction is scrutinised under following headings:
1. Examination of lens
2. Examination of structures other than lens
3. Examination of adnexa
Examination of Ocular Structures

1. Vision—minimum vision should be perception of light and projection of light from all quad-
rants. However, there may be a gross macular lesion in the presence of perception of light
and accurate projection that will prevent improvement of vision following lens extraction
2. Cornea—peripheral corneal opacities do not interfere with post-operative vision, central
corneal opacity will greatly reduce vision and even a faint central opacity may hamper vision
after the best possible surgery
3. Anterior chamber—normal anterior chamber gives best results. Deep AC may mean high
myopia, keratoconus, subluxated lens, hypermature cataract
Shallow AC may be due to intumescent lens, narrow angle glaucoma or nanophthalmos.
Abnormal depth of AC may result in poor post-operative vision
4. Pupil—central, circular, brisk reactions both direct and consensual is desirable. It should dilate
well with a short acting mydriatic. A sluggish pupil should warn about the presence of glau-
coma, optic neuropathy, neurological iridoplegia and extensive retinal lesion
5. Iris—should have normal colour and pattern without any patches of atrophy, neovascularisa-
tion, holes and synechia
6. Intraocular tension—should be less than 20 mmHg without medication. If tension is raised, it
should be brought to 20 mm or below and maintained
➤ A bright cornea, normal AC, brisk pupil reacting to direct and indirect light, without
any anti-glaucoma treatment denotes normal IOP
7. Fundus examination: Fundus should be examined by both indirect and direct ophthalmoscope
whenever possible. Indirect ophthalmoscope gives far more information than direct in the
presence of central opacity. The other eye should be examined as routine because it may
give a clue to the presence of macular lesion or peripheral degeneration, which are generally
bilateral
8. Slit-lamp examination is done to exclude aqueous flare, cells in AC, early neovascularisation
and exfoliation
9. Keratometry—this is important to calculate the power of IOL and to rule out borderline
keratoconus
10. Ultrasonography is undertaken to:
(a) Measure the axial length of globe to calculate IOL power
(b) To find out axial emmetropia, position of retina, lens, intraocular growth and vitreous
haemorrhage
11. Biometry—to find out the exact power of IOL
12. Macular function test: This is one of the most important tests on which the ultimate visual
improvement depends
There are various macular function tests available; some are very simple and can be
done in the usual ophthalmic setup without any specialised equipment.
Simple macular function tests are:
1. Two-point discrimination test
2. Maddox rod test
3. Coloured light test
4. Modified photo stress test
5. Entoptic visualisation
Other tests are:

1. Blue field entoptoscopy
2. Laser interferometry
3. Potential acuity meter
Two-Point Discrimination Test

This test is done in a dark room. Two equally bright point sources of light are held in
front of the eye under examination at a distance of 60 cm. The other eye is occluded.
To begin the test the lights are kept very near to each other, i.e. 3 cm from each other.
In such close proximity, the patient cannot differentiate them as two separate points.
Now the lights are gradually shifted from each other and the patient is asked to tell as
soon as he can discriminate two light points. In good macular function, a patient
should be able to clearly see two light points when they are 12 cm apart.
Maddox Rod Test

This test is done in a dark room. The other eye is occluded. A white point source of
light is kept in front of the eye at a distance of 33 cm. A Maddox rod is put in front
of the eye under examination. If the macula is normal, the patient will see a red streak
without break. A break or distortion in the streak means poor macular function.
Coloured Light Test

This test may be done by shinning a white light in the eye after putting a red or green
filter over it or the patient is asked to see a white point of light through the usual red
and green glasses provided in standard trial set. A good macula should be able to
appreciate both colours properly.
Modified Photo-Stress Test

The bright light of an indirect ophthalmoscope is shone in the pupil for loser, after
recording distant vision. Then the light is removed and the time taken to reach the
pre-test level is noted. A recovery time more than 1 min means poor macular function.
This is not a very accurate test as it may be influenced by the density of ocular media.
Entoptic Visualisation
The patient sits in a dark room with both the eyes lightly closed. A point of light is
pressed against the lower lid and moved from side to side. The patient should be able
to see the branching pattern of retinal vessels if macula is functioning. Difficulty with
this test is that the patient needs to be explained actually what he is supposed to see.
Examination of Ocular Adnexa

1. Examination of sac: examination of the sac is the single most important examination as far as
post-operative infection is concerned. Sacs with positive regurgitation test should be subjected
to appropriate surgical management. All cases of epiphora with negative regurgitation should
undergo lacrimal syringing. An eye with nasolacrimal duct obstruction should also be subjected
to surgical management prior to lens extraction
2. Examination of lid: lids are examined for trichiasis, entropion, ectropion, lagophthalmos,
coloboma, growth on lid margin. If any of these is present it should be managed before lens
extraction. Lid margin should be examined carefully for evidence of blepharitis
3. Examination of conjunctiva: chronic conjunctivitis is very common and not an absolute contra-
indication. However, it is better to get a conjunctival smear, culture and sensitivity done. Acute
conjunctivitis is an absolute contra-indication for planned lens extraction
Systemic Examination
1. Examination to exclude diabetes—if the patient is diabetic, his anti-diabetic treatment should
continue in the post-operative period
2. Hypertension—if the patient is a known hypertensive, his treatment should continue as usual. If a
patient is found to be hypertensive for the first time, his cardiovascular work up should be ordered
3. Allergy—history of allergy to drugs should be noted and allergen should be avoided
IOL Power Calculation

Aim of an IOL is to give 6/6 vision without glasses. To achieve this, it is important to
calculate the correct power of the lens that will be implanted.
The most ideal method is estimation of IOL power by SRK formula or its modifi-
cation. For this the following information is needed:
1. Axial length of the globe (Plate 13.2)
2. Keratometric reading (Plate 13.3)
3. A constant of the lens to be used
IOL power is calculated by SRK formula which as follows:
P ⫽ A ⫺ 2.5L ⫺ 0.9K
where P is the power of implant; A, the constant; L, the axial length of the eye in mm
and K is the average keratometry in dioptres.
Generally, modified SRK formula is used.
When facilities for the measurement of axial length and corneal curvature are not
available, following methods may be tried:
1. Eighty percent of the patients are emmetropic, only 20% have an ametropia of more than
2.00 D and out of which 1% have ametropia of more than 5.00 D, in which axial myopia is more
Plate 13.2 | IOL power calculation in a case of traumatic cataract in a child.

Plate 13.3 | Recording of keratometry reading to calculate IOL power.

common than hypermetropia. If the patient gives a reliable history of emmetropia then it is safe
to implant a standard ⫹19 D PCIOL
2. If a patient is able to give the exact power of distant correction, then the following
calculations are done: multiply the existing distant power by 1.25 and add this to ⫹20 power
of standard PCIOL
Example: Instead of ⫹20 Dsph PCIOL a person who has been using 4.00 D for axial myopia
will require ⫹20 – (4 ⫻ 1.25) ⫽ ⫹15.00
For 4.00 D axial hypermetropia the expected power will be:
⫹20 ⫹ (⫹4 ⫻ 1.25) ⫽ ⫹25.00
3. Intraoperative power calculation—When the lens has been removed by usual microsurgical
method, the eye is refracted by a streak retinoscope on the table and the above formula is
used to calculate the power
M EASUREMENT OF
I NTRAOCULAR T ENSION
Intraocular tension is the pressure exerted by the intraocular contents on sclera, cornea
and optic nerve.
Intraocular components that can change intraocular pressure are:
1. Aqueous
2. Lens
3. Uvea
Normal intraocular tension varies between 15 and 20 mmHg with ⫾2.5 D. This is very
high as compared to CSF and far less than the normal blood pressure. Persistent tension
above 22 mm or below 7 mm will produce structural and functional changes in the eye.
Persistent high tension will produce changes in:
1. Optic nerve: cupping, atrophy and field changes
2. Nerve fibre layer of retina: field changes
3. Sclera: thinning and ectasia
4. Cornea: thinning, rupture of Descemet’s membrane, band keratopathy, bullous keratopathy,
myopia and astigmatism
Persistent low tension (hypotony) will produce changes in:
1. Cornea: reduced curvature, folds and opacities
2. AC: shallow
3. Iris: peripheral synechiae
4. Angle: gonio synechiae and delayed secondary glaucoma
5. Macula: cystoid macular oedema
6. Axial length: reduced
7. Refraction: shift towards hypermetropia
METHODS OF MEASURING IOP
Intraocular pressure can be measured by a group of instruments called tonometers.

Digital palpation of eye to find out the pressure is good only in soft eyes. It is better
avoided in normal and glaucomatous eyes. The two types of tonometers are indenta-
tion tonometer and applanation tonometer.
Indentation tonometer is a mechanical tonometer. The commonest model used is
Schiotz tonometer. It is based on the principle that if a fluid-filled sphere (globe) is indented
by a plunger, the plunger will sink in the globe till the pressure of the plunger is equal to
the pressure inside the globe. Thus, depth of indentation is proportional to the pressure
inside. The plunger of the tonometer displaces a large amount of fluid, around 30 ␮l. The
radius of curvature of the footplate of the tonometer is flatter than cornea, i.e. 15 mm
as compared to 8 mm of cornea. The plunger also has a curvature of 15 mm. About
0.005 mm change in the position of the plunger, gives a deflection of one unit (Fig. 14.1).
Applanation tonometer is based on the principle that flattening of a small area of
a fluid-filled sphere can be done by counter pressure exactly equal to the hydraulic
pressure inside the globe (Table 14.1).
There are various types of applanation tonometers, out of which Goldmann tono-
meter is the most popular. It flattens a small area of 3.06 mm of cornea by varying the
weight that displaces 0.56 ␮l fluid. It is not too much influenced by scleral rigidity.
Barrel
Plunger Applanating
head
Foot plate
Cornea
Working of indentation tonometer Working of applanation tonometer
Fig. 14.1 | Diagrammatic representation of working of tonometers.

Table 14.1 Comparison between indentation and applanation tonometer
Indentation Applanation
Schiotz tonometer Goldmann tonometer

Displaces large volume of fluid—30 ␮l Displaces small volume of fluid—0.56 ␮l
Indentation is greatly influenced by scleral Applanation is not too much influenced by
rigidity scleral rigidity
Fully mechanical instrument Partially mechanical and partially optical
Does not require any other instrument to work Requires a slit lamp or its modification
Relatively cheap—can be used only in Costly—can be used only in sitting patient
supine patient Hand held instrument could be used in
supine patient
Can be used in patients under general Cannot be used in patients under general
anaesthesia anaesthesia unless a hand held
instrument is available
It is very small, light and portable Slit lamp make it bulky and it is not portable
Does not require fluorescein and cobalt blue filter Requires fluorescein and cobalt blue filter
Can be effectively sterilised Sterilisation is poor
Can transmit infection from one eye to other Can transmit infection from one eye to other
MEASUREMENT OF INTRAOCULAR TENSION 175
HOW TO USE A SCHIOTZ TONOMETER—DO’S AND DONT’S
1. Explain the patient that it is a painless but essential procedure

2. IOP should be measured in both eyes unless contraindicated
3. Anaesthetise both corneas by 4% Xylocaine. Instill only one drop at a time in the lower fornix
and not over the cornea
4. Patient will close the eyes instantaneously as local anaesthetic agent causes intense burning.
Burning will persist until the cornea is anaesthetised. Some patients may require a second drop.
Right eye takes longer time to get anaesthetised. Proparacaine HCl does not cause burning
5. As soon as the cornea is anaesthetised, the patient will be able to open the lids
6. While the eye is being anaesthetised, clean and sterilise the instrument. See that the plunger
moves freely in the barrel, and the pointer moves smoothly on the scale
7. Ask the patient to keep the other eye open when one eye is being tested
8. Instruct the patient not to blink
9. Do not exert pressure over the globe
10. Separate the lids by thumb and forefinger of one hand and hold tonometer with the other
hand
11. It is a convention to measure tension in left eye first. This is based on the presumption that
people are less sensitive about left eye
12. Ask the patient to look at a spot on the ceiling of the room
13. Put the footplate on the cornea so that the plunger is in front of the pupil and at right angles
to the iris surface (Plate 14.1)
14. Allow the plunger to fall freely on the cornea without exerting pressure
15. Note the deflection on the scale
16. Convert the reading into mmHg from the chart supplied with the instrument
17. Repeat the same in the other eye
18. Lesser the deflection on the scale, more is the tension
19. If the deflection is less than 3 on the scale, use 7.5 and 10 g weights one after the other and
take average of the three readings as mean IOP
20. Do not press the globe with the tonometer or keep it on the cornea for a long time. This
will displace more fluid and show less pressure
Plate 14.1 | Recording of IOP by Schiotzs tonometer.

Methods of Cleaning and Sterilisation of

Schiotz Tonometer
As Schiotz tonometer is made up of stainless steel, it can be sterilised very well. Its
plunger should be dismantled at least once in a week and rubbed clean after dipping
in some sterilising fluid. Inner wall of the barrel should also be cleaned with the brush
(supplied with the instrument) dipped in alcohol. Before using the tonometer the
footplate should be wiped with surgical spirit and dried. The foot plate and the base
of plunger should be wiped clean after every use.
Methods that are used to sterilise a tonometer are:
1. Mechanical cleaning with sterile swab
2. Dry heat and ultraviolet rays
3. Gas sterilisation
Chemicals used are surgical spirit, ether, absolute alcohol, 70% isopropyl alcohol,
1:1000 merthiolate (thimerosal), benzalkonium chloride and hydrogen peroxide.
They destroy common bacteria but not viruses specially adenovirus 7 and 8. They also
fail to destroy HIV and hepatitis B virus. Sodium hypochlorite 500 ppm destroys both
adenovirus and HIV in less than 10 min. The lower end of the tonometer can be kept
dipped in a solution of merthiolate 1:1000 in between uses.
HOW TO USE GOLDMANN APPLANATION TONOMETER
There are many models of applanation tonometers; commonly used are as follows:
1. Goldmann tonometer
2. Perkins handheld tonometer
3. Draeger applanation tonometer
4. Various types of pneumo tonometers
Out of these, Goldmann tonometer is the most widely used.
Eyes are anaesthetised with a suitable local anaesthetic agent. A small drop of fluo-
rescein is instilled in the lower fornix or a fluorescein strip is kept in the lower fornix
for 10 s. This stains the tear film.
The patient sits comfortably in front of the slit lamp with his chin on the chin rest
and forehead against the head band, and fixes a distant object. The beam of slit lamp
is put at maximum. The slit microscope is put at 60⬚ to the slit beam. Magnification
is set at the lowest. Cobalt blue filter is interposed in the illumination system; cobalt
blue beam is focussed on the tip of the prism of the tonometer.
The applanation knob is adjusted at 1.0 scale. The tip of the tonometer is pushed
slowly towards the apex of the cornea.
As soon as the prism touches the cornea, the fluorescein breaks into two semicircles
one above and one below the horizontal corneal line with concavity towards each. If the
applanation pressure is less the semicircles will be away from each other and pressure needs
to be increased by moving the knob of the pressure drum till the two overlap (Fig. 14.2).
I. Tonometer touching the tear film. II. Too much fluorescein III. Too less fluorescein
Fluorescein breaks into two semi-
circles, one above and the other
below the horizontal line
IV. Applanation head in V. End point VI. Proper position of

contact with cornea circles for pressure
measurements
Fig. 14.2 | Position of fluorescein rings in applanation tonometer.
Plate 14.2 | Recording of IOP by Perkins handheld applanation tonometer.

Now, exert more pressure till the inner edge of each semicircle cross one another
and move towards the opposite side. Reduce the pressure till they are aligned to give
the end point.
Multiply the reading on the knob by 10. This gives the intraocular tension in mmHg.
Once pressure in one eye has been recorded the other eye is examined in a similar way.
Perkins Handheld Tonometer

This small, portable instrument uses the principle of a Goldmann tonometer, without
the use of slit lamp. This operates on dry cells and can be used in a recumbent posi-
tion. The method of use is same as with Goldmann tonometer (Plate 14.2).
Method of Cleaning and Sterilisation of

Applanation Tonometer
Mechanically wipe with a disposable mop, re-clean with mop soaked with either 70%
isopropyl alcohol, 3% hydrogen peroxide or 1:10 sodium hypochlorite or soak the tip of
the prism in 70% isopropyl alcohol, 1:1000 hydrogen peroxide or 1:10 sodium hypochlo-
rite. Tonopens and MacKay-Marg’s tonometers are provided with sterile tonofilm covers.
After tension has been recorded one drop of a methyl cellulose containing eye drop
is instilled in each eye to prevent drying of the anaesthetised cornea, especially in dry
hot climate. If methyl cellulose is not available, any antibiotic ophthalmic drop will
suffice.
Tension in the two eyes is generally equal at a given time, in normal conditions,
within a range of 15 mm to 20 mmHg with SD ⫾ 2 with Schiotz tonometer and
slightly less in applanation tonometer.
If there is a difference of more than 5 mm between the two eyes, the eyes should be
evaluated.
1. Patient should be asked if he is using any anti-glaucoma drug locally or orally
2. The eye with higher tension should be examined for evidence of glaucoma by diurnal variation,
provocative test, field and fundus examination
3. Any eye with tension lower than normal should be examined for trauma, uveitis and retinal
detachment
4. Eyes with normal or below normal range of tension may have low-tension glaucoma
5. Eyes may have persistent high tension without glaucomatous change in ocular hypertension
Diurnal Variation in IOP

Intraocular pressure is not uniform throughout the day. There is no known clinical
method to record intraocular pressure during sleep. Changes in IOP during the waking
hours is called diurnal variation.
1. Morning rise: Maximum tension is noted between 6 and 8 AM
2. Forenoon rise: Maximum tension is recorded between 8 AM and 12 noon
3. Biphasic: Tension is high in the morning and late evening and lowest in mid-noon
Phasing This term is used to denote the recording of intraocular pressure

throughout the day at an interval of 4 h. The patient is ambulatory. This gives a base-
line intraocular tension.
Diurnal variation and phasing are used for timing of instillation of local drops. The
drug is so scheduled that its peak effect coincides with the maximum rise of tension.
COMPLICATIONS OF TONOMETRY
Tonometry is a simple and safe procedure. It should not produce any complication.
On rare occasions, following complications may be encountered:
1. Corneal abrasion: This is produced by the edge of the footplate or end of the plunger
2. Desquamation of epithelium: In dry and hot climate, the corneal epithelium may dry up and
desquamate if the lids are kept open for a long time after topical anaesthesia
3. Chemical injury: If the footplate is cleaned with excessive spirit it may find its way inside the
barrel of the tonometer and creep down on the cornea during tonometry producing a circular
corneal ulcer
4. Transfer of infection from one eye to another. If the tonometer is not sterilised this can hap-
pen, especially during an epidemic of conjunctivitis
Infections commonly transmitted via contaminated tonometers are bacterial conjunc-
tivitis and keratitis, HIV, herpes simplex, hepatitis B and lymphadenopathy virus.
NON-CONTACT APPLANATION TONOMETRY
Principles of this are same as an applanation tonometer where a puff of air is used to
flatten the cornea. Light is reflected to a photo sensor in the instrument from the flat-
tened cornea. Time taken to flatten the cornea is directly related to the IOP, which is
digitally displayed and a print out can be taken. This method does not require either
anaesthesia or fluorescein. No slit lamp is needed. It cannot be use in a scarred cornea.
E XAMINATION OF E YES
WITH A BNORMAL
I NTRAOCULAR T ENSION
ABNORMALITY OF IOP
Abnormality of IOP can produce:

1. Glaucoma
2. Ocular hypertension
3. Low and normal tension glaucoma
4. Hypotony
Out of these, glaucomas are the commonest IOP disturbances. Glaucoma is not a single
disease. It is a syndrome complex resulting into
1. Rise of IOP
2. Disc changes
3. Retinal changes
SOME CLINICAL FEATURES OF GLAUCOMA
1. Glaucoma is a major cause of treatable blindness

2. About 2% of the population above 40 years of age suffers from some type and degree of
glaucoma
3. Incidence of glaucoma rises after 40 years of age
4. Vision lost in chronic glaucoma is not fully recoverable even with the best treatment
5. Vision may be restored to almost normal in acute glaucoma if treated within a reasonable
time
6. There are about 40 types of secondary glaucomas
7. Glaucomas, especially primary, are multifactorial, polygenic in nature and have a strong genetic
predisposition
8. Children may be born with congenital glaucoma
9. Two most common causes of secondary glaucoma are trauma and uveitis
10. Cause of raised IOP is mostly obstruction in the circulation of aqueous
11. Though hypersecretion of aqueous has not been proved as a cause of raised IOP, reduced
production of aqueous always lowers IOP both in normal eyes and in glaucoma
EXAMINATION OF EYES WITH ABNORMAL IOT 181
Aqueous Humour Dynamics

Aqueous humour dynamics is worth knowing to understand glaucomas.
Formation
Aqueous humour is formed in the ciliary epithelium at a rate of 2–3 μl/min. Total vol-
ume of aqueous is 125 μl. It shows a diurnal variation. Its formation is reduced by:
1. Drugs—carbonic anhydrase inhibitors and some locally acting anti-glaucoma drugs like beta
blockers, adrenaline and brimonidine
2. Inflammation
3. Trauma
Blood Aqueous Barrier

Tight junctions between the adjacent cells of non-pigmented epithelium and capillary
endothelium constitute the blood aqueous barrier. This allows only selective chemicals
to reach the aqueous. All antibiotics, administered systematically or locally, do not
cross the blood aqueous barrier. Only a few antibiotics can pass the blood aqueous
barrier and only these can be used for intraocular inflammation.
Blood aqueous barrier is broken down by:
1. Trauma—mechanical, chemical, radiation and laser
2. Histamine
3. Prostaglandins
4. Inflammatory endotoxin
Probable modes of formation of aqueous are:
1. Secretion by non-pigmented ciliary epithelium 80%
2. Ultra-filtration
3. Diffusion
Circulation of Aqueous Humour (Fig. 15.1)

1. Aqueous humour is constantly produced in the ciliary process and poured in the posterior
chamber
2. From posterior chamber, it passes through the pupil into anterior chamber
3. In the anterior chamber, it moves by convectional currents
4. 90% leaves the anterior chamber by angle of anterior chamber, 10% by uveo-scleral outflow
5. In the angle, the aqueous finds its way successively through trabecular meshwork—canal of
Schlemm’s collecting channels—episcleral vessels-systemic circulation at the rate of 2 .75 μl/min
6. Obstruction in the flow of aqueous at any or multiple sites will hamper outflow and cause rise
of intraocular tension
Probable sites of obstruction of aqueous outflow could be as follows:
1. Before the angle
2. In the angle
3. Beyond the angle
Ciliary
,
body Schlemm s
PC AC canal
AC
Lens
Vitreous
Pupil
chamber C L C
Iris
PC
PC PC
Sclera
Circulation of aqueous
Chambers of the eye
Aqueous vein
nea
Cor
Conjunctiva
AC
Episcleral vein
Trabecular meshwork
Iris
Lens
a
ler
Suspensory ligament
Sc
Ciliary body
Enlarged view of aqueous flow
Fig. 15.1 | Circulation of aqueous humour.
1. Pre-angular block is due to pupillary block caused by increased contact between pos-
terior surface of iris, and lens, IOL or vitreous. The causes can be:
(a) Extreme miosis due to strong miotics
(b) Physiological iris bombe
(c) Annular synechia
(d) Phacomorphic
● Lens entrapped in pupil
● Micro-spherophakia
● Intumescent cataract
● Subluxated lens
● Cortical matter
(e) Vitreous incarcerated in pupil

(f) Malignant glaucoma
(g) Expanding gas in vitreous
2. Angular block can be:

(a) Pre-trabecular
(b) Trabecular
(c) Retro-trabecular
(i) Pre-trabecular obstruction can be caused by
● Peripheral anterior synechia
● Mydriasis in narrow angle
● Neovascular membrane
● Congenital membrane
(ii) Trabecular block can be produced due to:

● Sclerosis of trabecular meshwork
● Obstruction by large particles, pigment etc.
(iii) Post-trabecular block is brought about by increased episcleral pressure due to dysthyroid
oculopathy, retrobulbar mass, orbital varices, Sturge Weber syndrome and superior vena
cava obstruction
GLAUCOMA
There is no universally accepted definition that can cover all types of glaucoma. The
most accepted definition is “Glaucoma is a state of raised intraocular tension sufficient
to produce derangement of vision.”
It comprises of raised intraocular pressure, changes in optic nerve, field changes.
➤ Chronic rise of intraocular pressure produces more optic atrophy and less
keratopathy while acute rise of intraocular pressure produces more keratopathy
and less neuropathy
Glaucoma can be bilateral or unilateral; one eye may be involved more than the other.
Primary glaucomas are more often bilateral; unilateral rise of tension should always be
suspected to be secondary and investigated as such.
Classification of Glaucoma
There is no single classification that can satisfy all the queries. Traditionally glaucoma
has been put into two broad groups: primary and secondary
Primary glaucomas comprise of those conditions of raised intraocular pressure for
which no ocular cause can be found except obstruction of outflow facility.
Secondary glaucoma comprises of a larger group of conditions of raised intraocular
pressure that can be attributed to some ocular pathology. There are about 40 causes of
secondary rise of intraocular tension.
It was realised that in both the groups the width of angle of anterior chamber was a
crucial factor in diagnosis, management and prognosis.
According to age, glaucoma can be congenital, infantile, juvenile, pre-senile and senile.
This classification fails to meet all the requirements for diagnosis and treatment espe-
cially in the congenital group. It is better to treat congenital glaucomas as an altogether
separate entity comprising of multiple syndromes.
Glaucoma
Primary Secondary
Open angle Closed angle Congenital
Open angle Closed angle
(A) Pretrabecular Trabecular Post-trabecular Posterior force Anterior force
Primary
Open angle
Secondary
Glaucoma
Primary
Closed angle
(B) Secondary
Flowchart 15.1 | Classification of glaucoma.

Symptoms of Raised Intraocular Tension
Symptoms are so variable that it is difficult to enumerate them in a logical way.
Symptoms depend upon:
1. Onset of disease—acute and chronic
2. Age of patient
3. Rise of IOP
● How fast
● How much
● Duration of raised tension
4. Associated ocular diseases: cataract, uveitis, trauma, retinopathy and vascularisation

Acute onset is always associated with high rise of tension and is accompanied with:
1. Fast deterioration of vision
2. Pain
3. Redness
4. Lacrimation
5. Coloured haloes
6. Headache
Gradual rise in IOP as in chronic simple glaucoma or secondary open-angle glaucoma
may go unnoticed to the extent of blindness.
Common Symptoms of Glaucomas

1. No symptoms: early primary open-angle glaucoma
2. Visual
(a) Diminished distant vision

● Sudden—acute glaucoma, both primary or secondary
● Gradual—all chronic glaucomas with moderate rise of tension
(b) Diminished near vision

Early onset of presbyopia and frequent change of presbyopic glasses is seen in chronic simple
glaucoma
(c) Loss of field—Unless there is extensive loss of field, it may go unnoticed; however patient
with good central vision and constricted peripheral field may complain of tubular vision
(d) Coloured haloes are seen in sudden, moderate to high, rise of IOP. Common causes
are prodromal stage of primary angle closure glaucoma, acute secondary glaucoma and
epidemic dropsy glaucoma
(e) Photophobia is seen in congenital glaucoma due to rupture of Descemet’s membrane
3. Lacrimation is prominent feature of congenital glaucoma and acute glaucomas
4. Pain is seen in acute rise of tension, both primary and secondary. In acute congestive glaucoma,
it is a very prominent feature
Unexplained pain in uveitis and corneal ulcer may raise the suspicion of glaucoma. Absolute
glaucomas may have intractable and sometimes unbearable pain that is not relieved by the
usual anti-glaucoma treatment
5. Redness of eye
(a) Circumciliary congestion is seen in acute congestive glaucoma, chronic congestive glau-
coma and some secondary glaucomas
(b) Episcleral congestion is seen in absolute glaucoma and raised episcleral pressure
Examination of a Case of Glaucoma

Symptoms and signs of glaucoma vary from one type to another. In primary glaucomas,
chronic simple glaucoma differs from acute congestive glaucoma not only in onset but
also in physical findings, course and management. In secondary glaucoma it is overshad-
owed by the primary disease.
To evaluate a patient with glaucoma the eyes should be scrutinised under following heads:
1. History
2. Visual acuity
3. Examination of anterior segment—conjunctiva, cornea, anterior chamber, iris, pupil, angle of
anterior chamber, lens and intraocular tension
4. Examination of optic disc
5. Field examination
1. History of
(a) Present disease
(b) Family history of glaucoma
(c) Previous attack of acute glaucoma
(d) Treatment taken for any glaucoma
(e) Trauma, surgery, uveitis, retinopathy
(f) Diabetes, hypertension, dysthyroid condition, epidemic dropsy
(g) Local or systematic use of steroid
(h) Coloured haloes
2. Visual acuity—vision
(a) Without glasses—will give the extent of visual loss
(b) With pinhole—will indicate the limit to which vision can be salvaged with treatment
(c) With spectacle—will show the type of error of refraction, the patient is suffering from. Myopes
are more often associated with POAG while PNAG is commonly seen in hypermetropia.
Many a times, patient may not be aware of diminished vision especially if it is uniocular
➤ In some patients, vision deteriorates with treatment of glaucoma:

Miotics will
(a) Reduce vision in cases associated with central nuclear cataract, central corneal
opacity and macular lesion
(b) Cause diminished night vision
(c) Reduce field of vision
(d) Produce difficulty in near vision
(i) Carbonic anhydrase inhibitors may produce transient myopia
(ii) Anti-glaucoma surgery may produce:
● Troublesome astigmatism
● Persistent hypotony
3. Examination of anterior segment

(a) Conjunctiva
(i) Circumciliary congestion is seen in acute congestive glaucoma, chronic congestive
glaucoma and absolute glaucoma
(ii) Episcleral congestion is seen in raised episcleral pressure
(b) Cornea
(i) Rupture in Descemet’s membrane and Haab’s striations are seen in congenital glaucoma
(ii) Corneal oedema is seen in acute rise of tension
(iii) Krukenberg spindle is sometimes seen in POAG
(iv) KP may be present following acute rise of tension, or uveitis
(v) Band keratopathy is seen in long-standing glaucoma
(vi) Diminished corneal sensation is seen with acute rise of tension
(vii) Bullous keratopathy is seen in absolute glaucoma
(viii) Vascularisation may be present in the absolute stage
(c) Sclera
(i) Thinning and stretching of sclera is very common in congenital glaucoma
(ii) Scleral ectasia is seen in congenital glaucoma and sometimes in absolute glaucoma
(d) Anterior chamber depth
(i) Normal—in chronic simple glaucoma and some secondary glaucomas
(ii) Shallow—in NAG, lens-induced glaucoma and malignant glaucoma
(iii) Deep—buphthalmos, aphakic glaucoma, trauma and pseudo-phakic glaucoma
Measurement of anterior chamber depth
(a) By oblique illumination:With slight practice, it is possible to differentiate normal AC depth from
abnormal depth. Uniocular abnormality is easier to find out by comparing with the other side
(b) Comparing corneal thickness to anterior chamber depth (Van Herick’s sign)—If the average
depth of anterior chamber is less than three times the corneal thickness it denotes narrow
angle. Peripheral depth less than half the thickness of cornea also means narrow angle.This is
examined on the slit lamp biomicroscope. All cases of shallow AC should undergo gonioscopy
(c) Shadow of temporal iris: A beam of light is directed from the temporal side of limbus, direc-
tion of light should be at right angles to limbus. In an eye with normal depth or increased depth
temporal iris will not cast a shadow on the nasal side. However, if nasal iris comes under the
shadow of temporal iris, the AC is shallow and angle is likely to be closed by mydriasis (Fig. 15.2)
T T
Normal AC, no shadow Shallow AC, shadow on nasal side
Fig. 15.2 | Rough estimation of AC depth by oblique illumination.

(d) Pachymetry
● Optical
● Ultrasonic
It gives not only the corneal thickness but also depth of AC.
Iris
(i) Loss of pattern is due to oedema of iris; it is commonly seen in acute congestive attack
of glaucoma, both primary and secondary
(ii) Atrophic patches are seen following iritis glaucomatosa, chronic congestive glaucoma
and absolute glaucoma
(iii) Posterior synechiae—sudden high rise of intraocular tension, anterior uveitis, iritis and
glaucomatosa result in posterior synechiae
(iv) Peripheral anterior synechiae are seen following unrelieved tension in acute congestive
glaucoma, chronic uveitis and neo-vascular glaucoma
(v) Neovascularisation—thrombotic glaucoma
(vi) Coloboma—surgical, laser and trauma
(vii) Holes—(positive trans-illumination) are seen in essential iris atrophy, mesodermal dys-
genesis of anterior chamber, glaucomatocyclitic uveitis, heterochromic uveitis, pigment
dispersion syndrome and herpes zoster
(viii) Flakes are seen in pseudo-exfoliation syndrome
Pupil—examination of the pupil is one of the most important clinical methods in

glaucoma
(i) A large, sluggish pupil with fairly good vision, without a history of use of mydriatic, in
a person past 40 years should raise the possibility of increased intraocular tension unless
proved otherwise
(ii) An afferent pupillary defect in glaucoma denotes unilateral advanced glaucomatous change
in the optic disc
(iii) A semi-dilated, sluggish, vertical pupil in a congested eye means acute narrow-angle
glaucoma
(iv) A constricted pupil should invite enquiry about the instillation of a miotic; its strength
and frequency. All small pupils should be examined to exclude iritis
(v) Widely dilated, very sluggish pupil is seen in absolute glaucoma and after the use of mydriatic
(vi) Distorted pupil is seen in trauma, uveitis, chronic congestive glaucoma and absolute glaucoma
Angle of anterior chamber—examination of angle of anterior chamber is done to

note its (Fig. 15.3):
(i) Width
(ii) Possibility of its closure by—mydriasis and indentation
Cornea Cornea
20°45° 20°
Lens Lens
Grade 3−4 Grade 2
Wide open angle Moderately wide angle,
incapable of closure closure of angle possible
Cornea Cornea
10° 0°
Lens Lens
Grade 1 Grade 0
Very narrow angle Angle closed
high risk of closure
Fig. 15.3 | Grading of angle width.

(iii) Peripheral anterior synechiae
(iv) Pigment deposition
(v) Exfoliated matter
(vi) Neo-vascularisation
(vii) Patency of iridectomy, goniotomy and filtering surgery
(viii) Insertion of iris
(ix) Recession of angle
(x) Foreign body, tumours
➤ Anterior chamber angle in a shallow AC is more likely to close by mydriasis; all eyes
with shallow AC do not develop narrow angle glaucoma, only some eyes with
shallow AC may develop acute closure
Gonioscopy
Gonioscope is an instrument by which the angle can be visualised (Fig. 15.4). Basically,
gonioscope is a contact lens that replaces the cornea as a refracting medium by elimi-
nating the cornea air interface allowing rays arising from the angle to come out of the
angle. These rays are picked up by either a plane mirror or a suitable prism to be visible
by the slit lamp or microscope.
There are two types of gonioscopes (Table 15.1):
1. Indirect gonioscope—where a reflected image of the angle is seen by slit lamp
2. Direct gonioscope—where the image of angle is visible, without reflection, by a microscope
Various Types of Indirect Gonioscopes

1. Goldmann single-mirror gonioscope
2. Goldmann three-mirror gonioscope
A B Slit lamp C Microscope
m = 1.5
m
m = 1.37
Eye without gonioscope. Rays Indirect gonioscope. Light arising Direct gonioscope. Rays arising from
arising from angles undergo from angle is refracted by cornea angle are refracted by tear meniscus
total internal reflection and do and fluid meniscus to reach the plane and gonioscope to reach the micro-
not leave the eye. mirror (m) to be reflected and picked scope without being reflected.
up by slit lamp.
Fig. 15.4 | Optics of gonioscope.
Table 15.1 Comparison between indirect and direct gonioscope
Features Indirect Direct
Position of the patient Sitting Supine

Viewing system Slit-lamp microscope Operating or handheld microscope
Source of light Slit lamp Fibre optic Barken light
Image Inverted image of angle; both Panoramic, erect; both eyes
eyes cannot be examined can be examined at a time
Indentation gonioscopy Possible Not possible
Use in surgery Not possible Possible
3. Zeiss four-mirror gonioscope

4. Posner four-mirror gonioscope
Various Types of Direct Gonioscopes

1. Barkan
2. Swan Jacob
3. Layden
4. Richardson Shaffer
5. Thorpe direct gonioscope
6. Koeppe gonio lens
(a) Lens—lens in glaucoma is examined for its shape, size, position, transparency, exfoliation,
pigments and opacity
(b) Intraocular tension—examination of intraocular tension is the most important clinical pro-
cedure in glaucoma. It gives a clue to the extent of damage when fields and fundus cannot
be examined
➤ Tension in both eyes must be taken every time even when the tension is normal in
one eye
Glaucoma is said to be present if IOP is more than 21 mmHg at any given time in a
given eye.
In an eye suspected to have glaucoma, if any of the following is present then the
eye should be subjected to fundus, field and gonioscopy examination.
1. If there is difference in IOP more than 7 mm between the two eyes
2. Diurnal variation—positive
3. Provocative test—positive
Interpretation/Tension
(a) More than 21 mm
● Established glaucoma
● Ocular hypertension
(b) Less than 21 mm

● Normal
● Glaucoma suspect
(c) Glaucoma under treatment

● Medial
● Post-surgical
● Post-laser
(d) Low-tension glaucoma
Glaucoma Suspect
A patient is suspected to have glaucoma or may develop glaucoma if the following are
present singly or in combination.
1. Family history of glaucoma
(a) In parents
(b) In siblings
2. Myopia
3. Diabetes
4. Person on prolonged steroid
(a) Topical
(b) Systemic
5. Uveitis
6. Blunt trauma
7. Epidemic dropsy
8. Dysthyroid oculopathy
10. Difference in IOP in the two eyes
11. Changes in disc
(a) Large cup
(b) Notching of cup
(c) Vertical enlargement of cup
(d) Asymmetry of cup
12. Krukenberg spindle on cornea
13. Pseudo exfoliation of lens capsule
14. Retinitis pigmentosa
15. Central retinal vein thrombosis
Diurnal Variation
Intraocular tension is not the same through out day and night. It shows a physiolog-
ical variation of 3–4 mm between the lowest and peak tensions. If it exceeds more than
7 mmHg, it is called a positive diurnal variation.
Procedure
Intraocular tension is recorded in an ambulatory patient at intervals of 4 h during waking
hours. All local and systemic drugs that can influence intraocular tension are discontinued
2 days prior to the commencement of the test. There are three types of pressure changes:
1. Morning rise
2. Evening rise
3. Biphasic
Test is positive if:
1. Tension variation is more than 7 mm between the lowest and highest pressure
2. Tension variation more than 7 mm at any time between the two eyes
Importance of Diurnal Variation

1. Diagnosis of glaucoma
2. Planning the frequency of instillation of topical drugs so that therapeutic peak of the drug coin-
cides with peak rise of tension
Provocative Tests for Glaucoma

These are a group of procedures that cause rise of intraocular pressure by hampering
flow of aqueous from the eye, by changing aqueous dynamics or causing obstruction
in outflow mechanisms.
They are divided into two groups:
1. Those, which are suitable for wide-angle glaucoma
2. Those, which are suitable for narrow-angle glaucoma
Provocative test suitable for wide-angles are:
1. Water drinking test
2. Steroid provocative test
Water Drinking Test

Patient is hospitalised. Fluid and food are withheld after 10 PM. Patient is allowed to
go to the toilet in the morning without ingesting any fluid. On return from the toilet,
patient is asked to rest in bed for some time and the first intraocular tension is recorded.
Then the patient is given 1 l of water to drink quickly. IOP is noted every 15 min for
six times and the readings are compared.
A test is considered positive if there is a rise of tension by 7 mm from the lowest.
Corticosteroid Provocative Test
In a genetically predisposed person, there is a rise of intraocular tension following local
instillation of steroid for more than a fortnight. All steroids do not produce an equal
rise of tension. Dexamethasone and betamethasone are the two steroids that produce
maximum elevation of tension. The test consists of administration of topical 0.1%
drop of either of the drugs three times a day for 3 weeks and noting the level of tension
after 3 weeks. Average tension is noted before starting the test. There are three types
of steroid responses in relation to the rise of tension.
1. Low responders—rise does not exceed 5 mm
2. Intermediate responders—rise is between 6 and 15 mm
3. High responders
Intermediate and high responders are at a risk of developing glaucoma and should be
watched for other signs, e.g. field and fundus changes.
As the test consists of prolonged use of strong steroid, any contra-indication for its
use should be excluded before the test is started.
Provocative Tests Suitable for Narrow-Angle Glaucoma

These tests depend upon the ability of the iris to produce obstruction of the angle by
blocking it directly or indirectly. Tests that block the angle without pupillary block are:
1. Dark room test
2. Mydriatic test
Tests that block the angle with pupillary block are:

1. Prone position test
2. Mydriatic cum miotic test
Dark room test: This test is based on the physiological property of a normal pupil
to dilate in darkness and remain dilated till darkness is maintained. Intraocular ten-
sion is recorded as usual. The patient is made to sit in a dark room for 60 min. The
patient is warned not to go to sleep (as sleep induces miosis). Tension is recorded after
60 min. A rise of 7–8 mm is diagnostic of narrow angle, capable of going into acute attack.
After the test, to prevent an acute attack, the pupil is constricted by 2% pilocarpine,
when gonioscopy is not available. Otherwise gonioscopy and preferably indentation
gonioscopy is recommended to see if the angle is likely to be closed.
Mydriatic test: A mydriatic phenylephrine 10% or a short-acting mydriatic as
well as cycloplegic is used to produce mechanical obstruction of the angle and note
the rise of tension. More than 8 mm rise is indicative of a narrow angle. Longer act-
ing cycloplegic like homatropine and cyclopentolate are best avoided. Atropine should
never be used as its effect lasts for more than 10 days.
Prone position test: Intraocular tension is noted and patient is put in a prone
position for 60 min, thereafter IOP is again noted, a rise of 8 mm is diagnostic. Patient
should not go to sleep during the test.
Combined mydriatic and miotic test: Phenylephrine 10% and pilocarpine 2% are
instilled in the eye, for three times at an interval of 1 min. This produces a mild dilation
of pupil. Rise of 8 mm of IOP after the test is diagnostic.
➤ Ideally all provocative tests should be preceded and followed by gonioscopic

examination and indentation gonioscopy
➤ In an eye that can go into an attack following mydriasis, steps should be taken to
avoid acute attack
In case of dark room test, prone position test and mydriatic cum miotic test:
1. Constrict the pupil and treat like prodromal glaucoma
2. If pupil has been dilated by drugs:
(a) Phenylephrine—Pilocarpine will not constrict the pupil in therapeutic dose but cause
cyclotonia that will not avoid the rise of tension but will cause headache
(b) Parasympatholytic—Pilocarpine will neither counteract mydriasis nor cycloplegia
Better alternatives are oral systemic carbonic anhydrase inhibitors, beta blockers or alpha
agonist locally or in combination with oral CAI.
Examination of Optic Disc for Glaucomatous Change

Fundus examination is one of three basic examinations in glaucoma, the other two being
recording of intraocular pressure and plotting of field of vision.
Examination of the optic disc not only confirms presence of glaucoma but it arouses the
suspicion of glaucoma and helps in documentation of the progress of disease (Fig. 15.5).
Fundus should be examined in all the patients above 40 years of age who present
to the ophthalmologist for any complaint even with an undilated pupil.
Methods of Examination of the Optic Disc

(a) With white light—colour of the disc, cup and splinter haemorrhages
1. Normal disc 2. Notch at lower pole 3. Vertically oval enlargement not

extending up to rim
4. Large pale cup reaching 5. Glaucomatous cup with atrophy. Hardly any rim visible.
almost to the temporal rim Cup almost as large as nerve head, which is pale, vessels
on the rim of the cup cannot be traced to the floor of the cup.
Fig. 15.5 | Progressive chronic glaucomatous change in optic disc.

(b) Green light—retinal nerve fibres

(c) Graticule—extent of the cup
(d) Measure the depth of cup in dioptres
3. Directly by slit lamp
(a) Hruby lens
(b) Goldmann contact lens
4. Indirectly by slit lamp
(a) ⫹90 D
(b) El Bayadi ⫹68 D
5. Computerised analysis of optic nerve head
(a) Confocal scanning laser tomography (Heidelberg retinal tomography, HRT)
(b) Scanning laser polarimeter
(c) Optical coherence tomography (OCT)
The changes can be documented by:
1. Writing down the findings in words.
2. Labelled drawing
3. Photography
(a) Flat—black and white or coloured
(b) Stereoscopic
Direct Ophthalmoscopy in Glaucoma

For a detailed examination of the optic nerve, pupil should be widely dilated by a short-
acting mydriatic and cycloplegic unless contra-indicated. It is better to use a narrow
circular beam with bright illumination. Green filter is used for retinal nerve fibre layer.
In children, fundus should be examined under a short-acting general anaesthetic along
with the measurement of IOP and corneal diameter.
Indirect Ophthalmoscope
Glaucoma is a condition where direct ophthalmoscopy scores over indirect ophthal-
moscopy because of its higher magnification and ability to measure the depth of
the cup in diopters. However, indirect ophthalmoscope has a better view in the pres-
ence of central nuclear sclerosis without distortion, which is common with direct
ophthalmoscope.
Glaucomatous Changes in the Optic Disc

While examining the disc in glaucoma, the following points are noted:
1. Size of disc
2. Size of cup
3. Width of neuroretinal rim
4. Cup disc ratio
5. Notching
6. Depth of cup—by adding minus lenses
7. Pallor of cup
8. Position of blood vessels

9. Splinter haemorrhage
10. Peri-papillary halo
11. Retinal nerve fibre layer with ⫹60 D on slit lamp, HRT and OCT
12. Vascular pulsation
The size of disc, cup and width of rim are measured by the graticule provided with
direct ophthalmoscope. When interposed in the beam of the ophthalmoscope, it casts
a large square over the disc. This is divided into smaller squares like in a graph paper;
by counting the smaller squares, the size of the various lesions can be measured. Depth
of cup can be measured by
2. Stereo-photograph
Measurement of Depth of Cup by

Direct Ophthalmoscope
Focus the retina a little away from the disc. In an emmetropic eye, this is generally
achieved by zero in the peephole. Now shift the beam to the bottom of the cup; the view
becomes indistinct. Add minus lenses to the viewing hole till the lamina comes to a focus;
power of the lens required to focus the lamina gives depth in diopters. Three dioptres
are equal to 1 mm in depth. In the presence of error of refraction, appropriate lenses
must first be used to focus the retina and then the minus lenses are added to this.
Characteristics of a Suspicious Cup

1. Difference in the cup size between two eyes
2. Vertically enlarged cup
3. Cup disc ratio ⬎0.3
4. Notching of the cup in any pole
5. Narrow neuroretinal rim
6. Nasal shift of central retinal blood vessels
Changes in the optic disc have been divided into two groups:
1. Definite, also called hard signs
2. Subtle, called soft signs
Hard signs are:
1. Notch in the neural rim
2. Dots in the peripheral rim
3. Enlargement of optic cup
4. Excavation of cup
5. Glaucomatous atrophy
6. Arterial pulsation
Soft signs are:
1. Asymmetry of cup
2. Cup disc ratio more than 0.3
3. Vertically oval disc
4. Laminar dot sign

5. Nasal shift of blood vessels
6. Disc haemorrhage
Differential diagnosis of glaucomatous cup:
1. Physiological cup
2. Coloboma of disc
3. Pits in the optic nerve head
4. Myopia
5. Anterior ischaemic optic neuropathy
6. Primary optic atrophy
Characteristic Features of a Physiological Cup

1. Symmetry of both cups
2. Cup disc ratio is 0.3 or less
3. No notching
4. Concentric enlargement of cup
5. Neural rim is normal, i.e. 1.35 mm2
6. No filling defect in fluorescein angiography
Field Examination in Glaucoma

Field changes in glaucoma represent:
1. Changes in optic nerve head
2. Changes in nerve fibre layer
Recently, it has been well established that changes in the nerve fibre layer may precede
rise of intraocular tension.
Glaucomatous field changes are examined to:
(i) Establish the presence of glaucomatous change
(ii) To record its progress
(a) Arrested
(b) Progressive
Detection of field changes is called “qualitative field defect”, while changes in shape,
size and depth is called “quantitative field defect”.
Various Methods of Examination of

Glaucomatous Field
1. Confrontation—fail to show early changes
2. Tangent screen
3. Perimeter
(i) Arc perimeter: Lister and Aimark
(ii) Bowl perimeter (Plate 15.1)
4. Automated perimeter
5. Multiple pattern field analyser (Fig. 15.6)
Amsler grid has no role in the examination of a glaucomatous field.
Plate 15.1 | Projection perimeter.
Fig. 15.6 | Multiple pattern field analyser.

Perimetry in Glaucoma
1. It is a subjective test
2. It is influenced by
● Vision of the patient
● Ability of the patient to understand instructions of the observer
● Co-operation of the patient

● Reliability of the patient

● Size and colour of the object
● Luminance
A field recording device is said to be kinetic when the object is moved from a non-seeing
to a seeing area in the field of vision at a steady speed. The object has a known size, colour
and luminance. Distance between the patient and the target is fixed.
Static perimeter is a bowl perimeter; here the target (stimulus) is an illuminated spot,
luminance of which can be varied at given place. It is more difficult to master, both in
operation and in interpretation and it is far more costly than any kinetic perimeter. It
gives qualitative estimation of the depth of scotoma, is more effective to detect early
glaucomatous changes than kinetic perimeter. It can be automated and non-auto-
mated. However, there are models in which both static and kinetic perimetry can be
performed with one instrument.
Terms Used in Perimetry

Scotoma is a localised defect in the field of vision.
Field of vision is an island of vision in a sea of blindness (Fig. 15.7).
Positive scotoma: a defect in the field of vision that the person is aware of. They are
generally acute in onset like retinal detachment, macular lesions and optic nerve
lesions. They can be converted into negative scotomas.
Negative scotoma: these are scotomas that the patient is not aware of, blind spot is
an example of a naturally occurring negative scotoma. Glaucomatous field changes are
generally negative scotomas.
Absolute scotoma: absolute scotoma is that scotoma that does not change with the
intensity of the stimulus. Its size is the same even with the maximum stimulus.
Blind spot: it is a negative but absolute scotoma that represents the optic nerve head.
Relative scotoma: these are field defects that change with the intensity. They are pres-
ent with low intensity but shrink in size or may disappear with the maximum stimulus.
The patient complains of seeing through a cloudy medium.
Central field: visual field extending up to 30⬚ all around the point of fixation; it is
circular in shape.
Fixation: this represents the macula of the eye under examination.
Peripheral field: it is the field of vision beyond 30⬚. It is not circular. It is maximum,
95⬚ on temporal side, 60⬚ superiorly, 75⬚ inferiorly and 60⬚ nasally.
M
ON
T
N
Fig. 15.7 | Linear diagram of Traquiair hill of vision (M, macula; ON, optic nerve; T, temporal end of field;
N, nasal end).
Isopter: it is an area outlined by target of same stimulus, i.e. it is a line that joins the
position of successive targets of same size, colour at a given distance under the same
illumination.
Depression: it represents reduced sensitivity.
Arcuate scotoma: these are curved scotomas extending from the blind spot towards
the other side, above or below the horizontal raphe, in a fan-shaped pattern. They do
not cross the horizontal raphe and represent nerve fibre effects.
Luminance: this is a unit of light stimulus measured in ‘Apostilb’ (abc). It is measured
in candles per square meter.
Field Changes in Glaucoma

Field changes are more marked with chronic glaucoma, may it be primary or secondary.
Field changes in glaucoma reflect changes in the optic nerve head; hence they follow
the pattern of retinal fibres (Fig. 15.8).
Field changes and changes in the optic nerve head do not correspond with the level of
intraocular pressure. They are influenced by duration of raised IOP, range of intraocular
pressure, age of the patient, error of refraction, size of the pupil, lenticular opacity, size of
the target used, luminance, associated diseases of the retina and choroid and optic nerve.
➤ Glaucomatous field changes respect the horizontal raphe, chiasmal lesions respect
the vertical raphe
1. Scattered scotomas in 2. Seidel scotoma with 3. Single arcuate (Bjerrum

Bjerrum area scattered scotomas scotoma)
4. Double arcuate scotoma 5. Almost total loss of field with a central

with Roenne’s step and temporal island of vision
Fig. 15.8 | Field changes in chronic glaucoma.

Previously too much importance was given to baring of the blind spot and enlarge-
ment of the blind spot. It has been proved that these changes are due to stimulus
sensitivity threshold.
Glaucomatous field changes can be divided into early field changes and late field
changes.
Early Glaucomatous Changes

They are mostly seen in the central 30⬚.
1. Scattered scotomas in the Bjerrum area (Fig. 15.5)
Bjerrum area is an area, like an arc above or below the point of fixation, beginning at the pole
of the blind spot. The scotomas are scattered between 10⬚ and 20⬚.They may be single or mul-
tiple. They may be adjacent to the blind spot without touching the blind spot
2. Gradually these scotomas enlarge in size, both in width and length and unite to form an arcu-
ate scotoma either above or below the horizontal line. Shape of the scotoma is that of a comet,
the narrow end touches the pole of the blind spot. The other end fans out to reach the hori-
zontal line on the opposite side
3. In case of a double arcuate scotoma (Bjerrum scotoma) the scotomas meet each other on the
horizontal raphe without overlapping each other; the lower scotoma shifts laterally forming
a step-like deformity called Roenne’s nasal step
4. Changes in the blind spot are not as consistent as the nerve fibre changes.They consist of
(a) Vertical enlargement
(b) Horizontal enlargement
(c) Bean-shaped deformity of the vertically enlarged blind spot with concavity towards the
point of fixation
Horizontal enlargement is less marked than vertical enlargement. The bean-shaped

enlargement of the blind spot is called ‘Seidel’s scotoma.
Late Field Changes in Glaucoma (Fig. 15.8)

Late glaucomatous field changes are a continuation of same process and extend both
towards the periphery and centre, till the scotoma spreads over the whole of the field,
leaving an island of vision round the macula and another island of vision in the lower
temporal field, in mid-periphery. The spread of field defects is no more confined to the
central 30⬚. They spread all over the periphery to cover the outer limits of peripheral
field. They are best demonstrated on arc or bowl perimeters. If disease process is not
arrested, the two islands of vision left will also disappear, resulting in the loss of percep-
tion of light and development of glaucomatous optic atrophy. Loss of the peripheral
island of vision occurs earlier than the central island resulting in a tubular field defect.
The most probable explanation of retaining central island are:
(a) Vertical spread of glaucomatous cup is more than the horizontal spread.
(b) Papillo-macular bundle is the last to be affected in glaucoma.
Causes of nerve fibre defects are:
1. Chronic glaucoma
2. Ischaemic optic neuropathy
3. Drusen of optic nerve head
4. Myopia with peripheral degeneration

5. Juxta-papillary choroiditis
6. Localised pressure on the optic nerve
7. Post-laser status
8. Atypical retinitis pigmentosa
Causes of tubular field defects are:
1. Advanced glaucoma
2. Advanced retinitis pigmentosa and allied conditions
3. Central retinal artery occlusion
4. Quinine amblyopia
Causes of enlarged blind spot are:
1. Papilloedema
2. Coloboma of optic disc
3. Myopic crescent
4. Opaque nerve fibres
5. Drusen of the optic nerve head
6. Neuroretinitis
Characteristics of Chronic Simple Glaucoma

(Primary Open-Angle Glaucoma)
1. Incidence:
(a) 2% of the population above 40 years suffer from some type of glaucoma
(b) More than half are primary cases
(c) 80% primary glaucomas are POAG worldwide. In India ANAG is almost as frequent as
POAG
(d) Incidence increases with age
2. Inheritance:
(a) No race is immune; however, it is more amongst coloured races
(b) It is polygenic and multifactorial
3. Epidemiology:
(a) Equal in both sexes
(b) It is a bilateral disease. One eye may be involved earlier than the other; unilateral advanced
glaucoma is seldom POAG
(c) Family history—positive family history is seen mostly in parents, 4% in siblings, 2% in other
close relatives and may be sporadic.
4. More common in myopia and diabetes
Mechanism
Obstruction in the trabecular meshwork.
Symptoms
1. May be symptomless
2. Patient may not be aware of the diminished vision because it is very slow and painless, without
redness, pain or watering
3. Occasionally, the patient may be aware of faulty fields
4. There may be a frequent change in the presbyopic correction
5. Sudden rise of intraocular tension with diminished vision and coloured haloes denote second-
ary open-angle glaucoma like uveitis, glaucomatous cyclitic crisis, pigmentary glaucoma, epi-
demic dropsy and central vein thrombosis.
On investigation, there may be raised intraocular tension with field and fundus changes,
and open angles not capable of closure. In the presence of normal IOP, positive diurnal
variation and positive provocative tests are diagnostic.
Causes of sudden diminished vision in well-controlled POAG:
1. Central retinal vein obstruction
2. Branch retinal vein obstruction
3. Rhegmatogenous retinal detachment
5. Haemorrhage in front of the macula
Differential Diagnosis of Early Chronic

Simple Glaucoma (Table 15.2)
1. All cases of large and sluggish pupils
2. All cases of scattered scotomas in Bjerrum area
3. All cases of arcuate scotoma
4. Myopia
6. Low tension glaucoma
7. Secondary open-angle glaucoma.
9. Coloboma of optic disc
Table 15.2 Comparison between advanced chronic simple glaucoma and immature cataract
Features Chronic simple glaucoma Immature cataract
Common age of onset 50 years and above. 80% of population above

2% of population 50 years have some degree
of cataract
Relation with age Incidence increases with age Incidence increases with age
Type of eye Any. Myopic eyes have higher incidence Any
AC Normal Normal
Iris Patches of atrophy may be Normal
present (late)
Pupil Large, sluggish (late) Central, circular, brisk
Angle Normal open Normal
Lens Variable opacity not related to glaucoma Opacity
Iris shadow Depends upon the extent of lenticular Present
opacity without any relation to
glaucoma
Tension Raised Normal
Diurnal variation More than 7–8 mmHg 3–4 mm
Water drinking Positive Negative
Fundus Glaucomatous changes in optic disc Normal
Field Glaucomatous field changes Normal
10. Congenital pit of optic nerve

Characteristics of Acute Narrow-Angle Glaucoma

Incidence—less common than POAG. Incidence increases with age.
Inheritance—strong hereditary tendency, polygenic and multifactorial.
Epidemiology—more common amongst females, is bilateral, seen in all races, more
common in a high-strung personality. It is a symptomatic disease. Patient is bound to
seek medical help for pain, diminished vision and redness of eye.
Type of eye—hypermetropic eyes are more prone to develop ANAG. These eyes have
a shallow AC, lens iris diaphragm is placed anteriorly, cornea is small in diameter and
thicker than in emmetropes. Microphthalmic and nanophthalmic eyes are more at risk.
Angle of anterior chamber is narrow and liable to be closed by iris but trabecular mesh-
work is normal.
Mechanism:
1. Obstruction of angle mainly by iris
2. Obstruction of angle secondary to pupillary block
Stages of ANAG:
1. Prodromal
2. Stage of constant instability (intermittent)
3. Acute attack
4. Chronic congestive stage
5. Absolute stage
Symptoms—depend on the stage of glaucoma.
Differential Diagnosis of Primary

Narrow-Angle Glaucoma (Table 15.3)
1. Prodromal stage—it requires a high degree of suspicion. Every hypermetropic eye or eyes with
shallow AC should undergo Van Herick test, gonioscopy and provocative tests.
2. Intermittent stage—all cases of coloured haloes should be investigated. Causes of coloured
haloes are:
(a) Incipient stage of cataract
(b) Acute mucopurulent conjunctivitis
(c) Epidemic conjunctivitis
(d) Secondary open-angle glaucoma
(e) Other causes of corneal oedema
3. Acute congestive stage—causes of congested eye are:
(a) Acute mucopurulent conjunctivitis
(b) Epidemic conjunctivitis
(c) Acute iridocyclitis
(d) Secondary-angle closure glaucoma.
(e) Lens-induced glaucoma
(f) Neovascular glaucoma
Table 15.3 Differential diagnosis of primary narrow-angle glaucoma
Stage Symptom Sign Investigation
Prodromal Without symptoms— Shallow AC; normal IOP, Gonioscopy will show narrow
discovered accidentally brisk pupil angle, capable of closure
With symptoms of coloured Raised tension, sluggish pupil, Positive dark room, prone
haloes corneal oedema position and mydriatic test.
Partially closed angle
Stage of constant Blurred vision, coloured No congestion. Mild corneal Narrow, partially closed angle
instability halo, dull pain. Symptoms oedema, pupil sluggish,
subside within hours only raised IOP
to reappear after a few days
Acute attack Rapid fall of vision, severe Lid oedema, CC congestion, Angle closed almost all around
pain, redness, headache corneal oedema, aqueous
and vomiting flare, cells, KP, pupil semi-
dilated vertically oval not
reacting to light. Tension
raised, optic nerve may show
oedema
Chronic Dull pain, redness, CC congestion, corneal Angle partly closed.
congestive stage diminished vision but oedema, AC shallow, iris Peripheral anterior synechia
better than acute stage atrophy, sluggish pupil, KP,
flare, cells and raised tension
4. Chronic-angle closure glaucoma should be differentiated from primary open-angle glaucoma

by gonioscopy.
Course of Acute Attack

An acute attack may have the following courses:
1. Spontaneous relief: It may be due to:
(a) Relief of pupillary block
(b) Relief of angle closure
(c) Reflex ciliary hyposecretion
2. Relief due to medical treatment
3. Failure of medical treatment. It may be due to:
(a) Discontinuation of treatment
(b) Subtherapeutic dose
4. Spontaneous relief followed by another attack
5. Discontinuation of treatment leading to another attack
6. Failure of medical treatment going into chronic congestive stage
Evidence of a Previous Attack of

Angle Closure Glaucoma
1. Old KP
2. Iris atrophy
3. Posterior synechia
4. Peripheral anterior synechia
5. Glaucomflecken
Table 15.4 Comparison between primary open-angle and narrow-angle glaucoma
Features POAG PNAG
Incidence More frequent Less common

Age After 40 After 40
Sex Equal in both sexes More in females
Type of eye Any, more common in myopia Any, more common in hypermetropia
Family history May be positive May be positive
Laterality Bilateral Bilateral
Diseases associated Diabetes, myopia and thyroid Hypermetropia, microphthalmos and
nanophthalmos
Symptoms Almost symptom-less to begin with Symptoms, very prominent from the beginning
Loss of vision Gradual and sustained Acute and recovers
Redness Absent CC congestion
Cornea Bright, may show Krukenberg’s spindle Epithelial oedema
AC Normal Shallow
Pupil Large, sluggish Vertical oval, sluggish
Pupillary block Absent May be present
Trabecular meshwork Obstruction, sclerosis Normal
Provocative test Water drinking, steroid provocative Mydriatic, dark room, prone position
Tension Gradual rise Acute rise
Disc Glaucomatous changes May show hyperaemia even oedema
Visual fields Glaucomatous field changes Enlargement of blind spot may be present otherwise
difficult to chart field during an acute attack
6. Capsular or subcapsular lens opacities

7. Sectorial angle closure
8. Raised IOP
9. Disc changes
10. Field changes
11. Shallow AC
12. Diminished outflow
13. Diminished vision
➤ Sudden lowering of IOP with lowering of vision and sudden field loss should be
investigated for the possibility of rhegmatogenous retinal detachment in glaucoma
Evaluation of a Case of Congenital Glaucoma

Peculiarities of Congenital Glaucoma
1. It is a rare disease
2. It is a major cause of blindness in infancy and childhood
3. It is one of the three commonest congenital causes of blindness in childhood. Other two are—
congenital cataract and retinoblastoma
4. The exact mode of disorder is not clear. It is due to an obstruction at the angle of AC. It is due
to a dysgenesis of trabeculum, iris or cornea or a combination thereof
5. The commonest age of presentation is 1 year
6. In 75% of cases, it is bilateral
7. It may be present in siblings
8. It is more common in males
Classification
Classification of congenital glaucoma is difficult, as the exact mode of causation is not
known. The following classification meets most of the requirements.
1. Simple congenital glaucoma (buphthalmos)
2. Associated congenital glaucoma
3. Secondary infantile glaucoma
Congenital glaucoma can be primary or secondary with angle closure or open angle.
➤ Simple congenital glaucoma is called primary because there are no anomalies

except in the angle. The rest of the eye is normal as far as its development is
concerned. However, almost all intraocular structures are affected as a sequelae
of raised intraocular tension
Buphthalmic Eye (Plate 15.2)

Globe—It is a large eye, the whole globe is enlarged, and maximum enlargement is
in the anterior segment. Eye is expanded in an anterior-posterior direction. There is
pseudo-proptosis.
Cornea is enlarged and stretched. Stretching of the cornea stops after 3 years of age.
Due to stretching the cornea becomes thin, may develop ruptures in the Descemet’s
membrane; there is an over all increase in the corneal curvature with relative flatten-
ing at the centre. There may be epithelial oedema but hydrops never develops.
Corneo-scleral sulcus—it is obliterated.
Sclera is stretched more in the anterior segment, there may be relative thickening
in the posterior part. Colour of the sclera is bluish due to uvea shinning through. In the
late stages there may be ciliary or equatorial staphylomas.
Plate 15.2 | Bilateral buphthalmos.

Causes of deep AC in buphthalmos are:

1. Increased corneal curvature
2. Stretching of zonules
3. Flattening of lens
4. Posterior displacement of lens
5. Subluxation of lens
Iris is lightly pigmented but not heterochromic. It may be atrophic. If lens is sub-
luxated there may be iridodonesis.
Pupil is large due to stretching of the iris at its root. It is sluggish due to stretching,
raised tension and glaucomatous optic atrophy.
Lens is smaller than normal but not micro-spherophakic. It is rather flat due to the
stretch of the zonules. There may be rupture of zonules leading to subluxation.
Angle of anterior chamber holds the key to diagnosis and classification. The angle is
open as in a normal eye. Iris is inserted in or above the scleral spur. The angle is covered
by Barkan’s membrane.
Tension is raised above 40 mmHg.
Disc—in buphthalmos cupping occurs earlier than in adults. It is capable of regres-
sion if the tension is brought down and kept within normal limits. The cup is enlarged
due to stretching of the posterior sclera and loss of neural rim; there may be notching
of the disc.
Examination of a Case of Buphthalmos

Symptoms:
1. In mild cases there may not be any symptom and glaucoma is diagnosed only when the child
grows
2. Commonest symptom is watering
3. Most troublesome symptom is photophobia, the child avoids light. In unilateral cases the child
closes the affected eye as soon as the eye is exposed to bright light. A child with bilateral buph-
thalmos likes to stay in the dark and buries the head under the pillow
4. Large eyes—parents may notice a child with large and watering eyes
(a) Pseudo-proptosis
(b) Increased anterior posterior diameter is more obvious in unilateral cases. It is confirmed
by ultrasonography
(c) Corneal diameter is more than 12 mm, may be as much as 18 mm; any cornea larger than
3 mm should be investigated. Cornea should be measured under general anaesthesia with
a corneal calliper
(d) Corneal curvature is increased, may show irregular rings on keratoscopy
5. Ruptures in the Descemet’s membrane—they may be in the central part or periphery in the
form of a line or whirl called Haab’s line. They are permanent in nature and cause lacrimation and
photophobia
6. Epithelial oedema—there may be generalised corneal haze but true hydrops does not develop
7. Anterior chamber is uniformly deep without any mesodermal tissue. Presence of mesodermal
tissue excludes primary buphthalmos
8. Angle of AC is wide open but the trabecular meshwork is not visible on the affected side. The
iris is attached to the scleral spur or above it, either in straight line or in a crescentic fashion.
No neovascularisation, pigment or gonio-synechia is seen
Plate 15.3 | Simultaneous examination of the two eyes in a buphthalmic child. Tension and gonioscopy should be
done without Desmarres retractor or speculum. Gonioscopy should be done simultaneously in two eyes.
Gonioscopy is best done with 16 mm Koeppe’s direct gonioscope, with Barkan’s light and
handheld microscope or operating microscope. Advantage of direct gonioscopy is that both
the eyes can be examined simultaneously with two separate gonioscopes and compared
(Plate 15.3)
9. Tension should be recorded under general anaesthesia by such an anaesthetic agent that does
not alter IOP. Perkins hand held applanation tonometer is best and in its absence, Schiotz
tonometer can be used
10. Fundus should be examined as in POAG noting the size, shape, notching of cup and vertical
spread of cup. In the presence of corneal opacity indirect ophthalmoscopy is preferred
11. Ultrasonography gives the information regarding ocular dimensions, position of lens
Differential Diagnosis of Buphthalmos (Table 15.5)

Following signs and symptoms may be mistaken for buphthalmos and vice versa:
1. Lacrimation
2. Proptosis
3. Large cornea
4. Hazy cornea
5. Photophobia
Congenital Anomalies that can Produce Associated Buphthalmos

1. Iridocorneal dysgenesis (most common)
(a) Axenfeld anomaly
(b) Rieger’s anomaly
(c) Peters anomaly
2. Phacomatosis
(a) Neurofibromatosis
(b) Sturge Weber Syndrome (Plate 15.4)
Table 15.5 Differential diagnosis of buphthalmos
Signs and symptoms Cause Test
Lacrimation Neonatal conjunctivitis Positive culture for micro-organism

Neonatal lacrimal obstruction Develops after 4 weeks, RT positive
Birth trauma Positive stain
Accidental abrasion of cornea Positive stain
Proptosis Retrobulbar growth Ultrasonography with normal
diameter of globe
Pseudo-proptosis Congenital myopia Ultrasonography shows increased
axial length, myopic refraction.
No growth
Large cornea Keratoglobus Normal tension and no symptoms
Cloudy cornea Interstitial keratitis Positive serology, other stigma of
congenital syphilis
Intrauterine rubella Torch test—positive
Mucopolysaccharidosis Other signs of systemic
involvement
Plate 15.4 | Secondary glaucoma in Sturge Weber syndrome.

3. Ectopia lentis
4. Nanophthalmos
5. Lowe’s syndromes
6. Aniridia
7. Retinoblastoma
Examination of a Case of Absolute Glaucoma

1. History
(a) History of glaucoma
(b) Patient had glaucoma which has:
● Not been treated/partially treated
● Mistaken as cataract (common)
2. Vision
(a) Is grossly reduced
Table 15.6 Comparison between buphthalmos and associated congenital glaucoma (Plate15.5)
Features Primary buphthalmos Associated buphthalmos
Age of first presentation Generally discovered before Generally in the third year unless
the second year looked for at birth
Sex More in males Differ in different types
Laterality 75% bilateral Variable
Inheritance Autosomal recessive Variable
Tissue involved Trabecular, resulting in Cornea and iris, angle involved
trabecular dysgenesis secondary to iridocorneal dysgenesis
Anterior chamber Uniform and normal depth Generally shallow or irregular due
no mesodermal tissue to mesodermal tissue
Pupil Single, large, central Irregular, polycoria, ectopic pupil
pupillary area clear Many show a white reflex, due to
retinoblastoma, persistent primary
hyperplastic vitreous and retinopathy
of pre-maturity
Superficial
Staphyloma vascularisation
Episcleral congestion
KP
+ -
Iris
atrophy Circumciliary Bullae Stain Band
congestion keratopathy
Fig. 15.9 | Absolute glaucoma.

(b) There my be faulty projection
(c) There may be no perception of light
3. Circumcorneal flush, prominent episcleral vessels
4. In children and young adults there may be a divergent squint
5. Cornea has multiple changes (Fig. 15.9)
(a) Bullous keratopathy
(b) Positive stain
(c) Diminished sensation
(d) Superficial vascularisation
(e) Band keratopathy
(f) Perforation
6. Globe may have various types of scleral staphylomas, e.g. ciliary and equatorial. There may be
intercalary staphyloma in aphakic glaucoma; corneal and posterior staphylomas are not seen in
glaucoma
7. AC—depends upon the type of glaucoma
8. Pupil—generally fixed, dilated, amaurotic pupil but may be immobile, semi-dilated, irregular
pupil, with ectropion of iris pigment. Irregularity of pupil in absolute glaucoma is due to iritis
glaucomatous, associated iridocyclitis, atrophic patches on the iris, trauma and surgery
9. Iris—may show patches of atrophy, even holes and there may be neovascularisation
10. Lens—may be clear or may have a variable degree of opacity
11. Tension—generally more than 60 mmHg. May go up to 100 mmHg
12. Fundus—glaucomatous optic atrophy
13. Field—when possible to record it shows either a temporal island of vision and central island
of vision or tubular vision
Ocular Hypertension and Low Tension Glaucoma

These are two diagonally opposite clinical conditions.
Ocular hypertension is a condition where intraocular tension is constantly raised above
the normal range; is generally a bilateral condition. There may be a positive history of
primary especially wide-angle glaucoma in the family. However, there are no field or
fundus changes. Eye with the initial tension above 30 mmHg may develop:
1. Glaucomatous disc and fundus changes at a rate of 1% per year
2. There is another group of eyes that will withstand raised intraocular tension
However, patients in both groups should be under observation for fundus and field
changes specially if there is positive family history of glaucoma.
In contrast, low tension glaucoma (normotensive glaucoma) is a condition where
the intraocular tension is never more than the mean upper limit of normal IOP, i.e.
20 mmHg, but have typical fundus and field changes. These are bilateral with wide
angle, may have a positive provocative test and diurnal variation. It is more common
after 60 years of age and incidence increases with age like POAG. It is more common
in hypertension and diabetics.
Ocular Hypotony
There is no exact definition to describe ocular hypotony. It is said that the ocular functions
can be retained with IOP as low as 6.5 mmHg. Hence a tension that is persistently lower
than 6.5 mm is considered as hypotony. This is one condition that can be diagnosed by
palpation. Tension with Schiotz tonometer is generally non-recordable.
Causes of ocular hypotony are:
1. Leaking wound
Accidental
Surgical
2. Ciliochoroidal detachment
3. Rhegmatogenous retinal detachment
4. Severe iridocyclitis
5. Therapeutic
(a) Large dose of carbonic anhydrase inhibitor
(b) Fast IV mannitol or urea
(c) Combination of local and systemic ocular hypotensive drugs
6. Systemic—dehydration, diabetic coma and shock
7. Vascular—carotid artery occlusion
8. Phthisis bulbi
9. Over-filtering glaucoma bleb (Plate 15.5)
Plate 15.5 | Over-filtering bleb.

Diagnosis of ocular hypotony
1. Vision
(a) Generally there is diminished distant vision due to reduction of the axial length of the
globe, flattening of cornea, shifting of lens, lenticular opacity, folds in the cornea, choroidal
folds and macular oedema and
(b) may be normal
2. Narrow interpalpebral fissure
3. Loss of contour of upper lid
4. Flattening of cornea, folds in cornea or corneal opacity
5. Shallow AC
6. Sluggish pupil
7. Fundus, when visible, will show choroidal folds, oedema of the disc, macular oedema and cilio-
choroidal detachment
8. Unrecordable IOP
E XAMINATION OF THE E YES
R EQUIRING O PTICAL C ORRECTION
Examination of an eye having:

A. Error of refraction
B. Presbyopia
C. Low vision
EXAMINATION OF AN EYE WITH ERROR OF REFRACTION
Errors of refraction are the commonest group of ocular disorders and are the easiest to
treat. A child may be born with an error of refraction or may develop it in later life
due to abnormalities of:
● Axial length of the eye ball
● Curvature of cornea and lens
● Changes in the refractive index, lens and cornea
The normal eye has an average length of 24 mm. A change of 1 mm in length will pro-
duce an error of refraction equal to 3 D; thus a 25 mm long eye will have 3 D of myopia
while a 23 mm long eye will be hypermetropic by 3 D. A large eye can be emmetropic
if optical components are weak. If optical components of a smaller eye are strong it may
become emmetropic or even myopic.
A developed cornea has a curvature of approximately 8 mm. A change of 1 mm of
curvature will produce 6 D of error of refraction. Thus, an eye with keratoconus is
myopic, a flat cornea is hypermetropic. Similarly, increased lenticular curvature will
produce myopia, e.g. lenticonus or lentiglobus, while a lens with less curvature will be
relatively hypermetropic.
An increased refractive index is a very common cause of index myopia in central
nuclear sclerosis. Another common cause of index myopia is uncontrolled diabetes. In
contrast to this hypoglycaemia produces hypermetropia.
➤ Myopia due to corneal oedema is frequent, but not very marked and overlooked due
to associated corneal opacity
A patient with an error of refraction may present with:

1. Diminished distant vision
2. Difficulty in near vision
3. Both
4. May have muscle imbalance
5. Asthenopia
6. Amblyopia
If a patient with diminished distant vision presents for treatment, the first thing to
do is to find out the extent of visual loss. Second thing is to find out if the loss of
vision is due to an error of refraction or some organic lesion or a combination. Once
it has been established that the loss of vision is due to error of refraction, the next step
consists of evaluation of the type and extent of error of refraction.
1. Visual loss is determined by recording visual acuity
2. Presence of error of refraction is found out by the pinhole test (Scheiner test) (Fig. 16.1)
Large circle Small circle of blur

of blur
Eye with error of refraction Effect of pinhole in the same eye
Fig. 16.1 | Principle of pinhole.

Diminished vision
Pinhole
Improvement of vision No improvement of vision
Error of refraction Examine media

See fundus
Exclude amblyopia
Objective
Subjective
examination
examination
Retinoscopy,
keratometry,
Improvement
autorefraction
Confirmed by Post-mydriatic
objective test test
Flowchart 16.1 | Examination of an eye with diminished vision.

EYES REQUIRING OPTICAL CORRECTION 215
3. Extent and type of error of refraction can be determined, either by subjective test or by objec-
tive test
Subjective Test
This consists of putting lenses in the trial frame and finding out the lens that improves
the vision. Glasses thus prescribed may not be correct, especially in astigmatism. It should
not be used in children under 10 years of age as it fails to unmask pseudo-myopia,
i.e. myopia produced due to excess accommodation in emmetropic or hypermetropic
children.
Fogging method—This is the best non-cycloplegic method to abolish accommoda-
tion. It is commonly used to find out the best hypermetropic correction. It is also used
along with an astigmatic fan for cylindrical correction. The eye is made myopic by put-
ting a strong plus lens (⫹4 D). This reduces the distant vision by five or six lines on
the Snellen’s chart. Then plus power is gradually reduced by 0.50 D till the vision
comes to 6/6. One eye is tested at a time.
Objective Test (Retinoscopy)

Retinoscopy is an objective method of finding out the type and extent of error of
refraction by an instrument called the retinoscope. A retinoscope measures the far point
of a given eye indirectly. The purpose of retinoscopy is to illuminate the retina through
the pupil and bring the emerging rays to focus on the pupil of the observer. This is
achieved by using either a plane mirror or concave mirror. A retinoscope is either a
plane or concave mirror that sends reflected rays from a source of light in the pupil.
This light is reflected back by the retina, giving a red reflex in the pupil. The emerg-
ing rays are refracted by the ocular media and brought to focus at far point of the
patient’s eye, e.g. in emmetropia at infinity.
The far point in myopia is a finite point in front of the eye. In hypermetropia it is a
hypothetical point behind the patient’s eyes.
While using a retinoscope, the pupil of the patient and the observer should be in
the same line and level, the light reflected by the retinoscope should travel in this line.
By placing appropriate plus or minus lenses in front of the patient’s eye, the far point
of the patient’s eye can be changed, until it is brought to the observer’s pupil. Once
the far point of the patient’s eye is brought to the pupil of the observer, the end point is
reached. If the distance between the patient’s pupil and pupil of the observer is known
and power required to reach the end point is known, the ametropia can be calculated.
Types of Retinoscopes
There are two types of retinoscopes:
1. One reflects parallel rays (plane mirror effect)
2. One reflects divergent rays (concave mirror effect)
These effects can be produced either by a plane or concave mirror, or a self-illuminat-
ing system of convex lenses.
Plane Mirror Retinoscope

This consists of a plane mirror mounted on a handle. In fact the mirror has a mild
curvature. The mirror is circular in shape. There is either deficiency of silvering in the
centre of the mirror or a hole is bored in the centre. This acts as an aperture through
which the observer can see the pupillary red glow and its movement when the mirror
is moved from side to side. Light reflected by plane mirror is parallel.
Uses of a plane mirror retinoscope are:
1. To find out the error of refraction
2. To locate opacities in ocular media
3. Direct ophthalmoscope (a suitable prism can replace the plane mirror)
Concave Mirror Retinoscope

Instead of a plane mirror a concave mirror with a focal length of 25 cm is used. An
optional ⫹2 D lens is incorporated in the peephole to relax the accommodation of the
observer.
Uses of concave mirror retinoscope are:
1. To find out the error of refraction
2. To locate opacities in ocular media
3. Indirect ophthalmoscopy (incorporated in binocular indirect ophthalmoscope)
Retinoscopy by concave mirror is used less commonly than plane mirror retinoscopy.
It is mostly used when there is high ametropia or media is hazy.
Self-Illuminated Retroscopes
To use a mirror for retinoscopy an external source of light is required. The patient
should be in a sitting position. Later on, self-illuminated and battery-operated retino-
scopes were developed. They are either spot retinoscope or streak retinoscope. These
electric retinoscopes are small and handy. They have a built-in source of light and a
mirror or prism. In between the source of light and mirror is a condensing lens that
can be moved towards or away from the light to give out either parallel rays (plane mir-
ror effect), or diverging rays (concave mirror effect) (Fig. 16.2). In streak retinoscope,
the emerging rays form a narrow streak that instead of illuminating whole of pupil,
Mirror or prism Mirror or prism
Convex lens
Convex lens that can be moved
that can be moved up and down
up and down
Bulb Bulb
Lens near the bulb gives out parallel rays Lens away from the bulb gives out convergent rays
(Plane mirror effect) (Concave mirror effect)
Fig. 16.2 | Electric retinoscope.

illuminates only one meridian. This streak can be rotated at various meridians to get
the axis of astigmatism. Rest of the procedure is similar to mirror retroscopy.
Note:
1. Reflecting surface used in a direct ophthalmoscope head is either a plane mirror or a prism that
reflects parallel rays from a source of light
2. Concave mirror is used in an indirect ophthalmoscope
3. Retinoscope is used to find out the position of opacities in the optical axis of the eye.They can-
not be used to localise foreign bodies in the eye
Types of Retinoscopy
There are two types of retinoscopy: (I) static and (II) dynamic.
Static retinoscopy is performed under full cycloplegia. This measures the diopteric
power of the eye for distance. Aphakic and pseudo-aphakic refractions are always static
in nature.
Dynamic retinoscopy is where no cycloplegic is used. It can measure the diopteric power
of the eye both for distance as well as for near. It requires more practice. Refraction done
under a mydriatic only is a dynamic retinoscopy.
How to Use a Mirror Retinoscope (Retinoscopy)

(Plate 16.1)
The patient sits in front of the observer at a distance of roughly 1 m. Pupils are dilated
with cycloplegic. It can be done with or without cycloplegic by an experienced person.
Plate 16.1 | Retinoscopy at arms length. (Courtesy Shri. K.G. Birla.)

The room is darkened. A light of about 40 W is placed behind and little away from the
head of the patient slightly on the temporal side, in such a way that the face of the
patient is in dark. The observer puts the retinoscope near his eyes and reflects the light
into the pupil of the patient. Pupil of the patient and observer should be in same line.
The peephole of the retinoscope is kept in front of the observer’s pupil so that the red
glow of the patient’s pupil can be seen by the observer. If the media are clear the pupil
looks uniformly pink. Any opacity in the media stands out as a black spot against red
glow. The aim of retinoscopy is to find out the lens which when placed in front of the
eye under examination will focus the emerging rays on the pupil of the observer.
The Following Steps are Executed

1. Move the retinoscope from side to side, and from above downward and note the movement
of the pink glow. Observe if the glow moves
(i) With the movement of the retinoscope?
(ii) Moves against the movement?
(iii) Is stationary?
(iv) Is the movement equal in all directions?
(a) If it moves with the movements of the retinoscope then interpose a ⫹1.50 D in front of the
patient’s eye and observe the movement of the glow
1. If the glow stops moving, the patient has no error of refraction, i.e. emmetropia
2. If the reflex still moves with the movement of the retinoscope, keep on adding plus lenses
till the movement is abolished. This means that the patient has hypermetropia
3. If the image starts moving against with ⫹1.5 D in front of the eye then the eye has myopia
less than 1 D. Gradually reduce plus lenses till the movement stops. This will give the myopic
refraction of the eye
(b) If the reflex moves against without putting any lens in front of the eye, it means myopia more
than 1D. Keep adding minus lenses till the movement stops.This will give the myopic refraction
(c) If there is no movement without any lens in front then the eye has myopia of 1 D
(d) If the movements are different in two meridians, the eye is astigmatic.
Summary If images move with the movement of retinoscope without keeping any
lens in front, then the eye is emmetropic, hypermetropic or has myopia less than 1 D.
If the image is stationary then the eye is myopic by ⫺1 D.
If the image moves against then the eye has myopia more than ⫺1 D.
➤ These movements are reserved when concave mirror is used for retinoscopy.
In myopia of 1 D, no movement is seen with either of the mirrors
Post-Mydriatic Test (PMT)

The findings of retinoscopy though the objective method are not precise. The glasses
accepted by the patient may be different from retinoscopic findings. Generally,
glasses accepted by a myopic will be more than the retinoscopic findings by 1.5 D.
In case of hypermetropia, it will be less than the retinoscopic findings by 1.5 D.
Post-mydriatic test is in fact post-cycloplegic test. It is undertaken when the effect of
cycloplegia has passed off. In case of homatropine, cyclopentolate and tropicamide,
it is done after 24 h. In case of atropine it should be done after 15 days. To find out
the post-cycloplegic power 1.5 D is subtracted from the retinoscopy findings; one
dioptre for the distance at which retinoscopy was performed and half dioptre for the
cycloplegic used. If atropine is used to produce cycloplegia, 1 D is subtracted instead
of half dioptre. More is the distance between the patient and the examiner, more pre-
cise will be the findings and less dioptres will have to be subtracted from the retinoscopy
findings.
Table 16.1 gives the amount to be subtracted at a given distance.
For all practical purposes, retinoscopy is done at an arms length for the convenience of
the examiner.
Examples
Retinoscopy under homatropine
Note: Subtracting ⫹1.5 D from a given number is equivalent to adding ⫺1.5 D to
the same amount (Table 16.2).
Table 16.1 Amount to be subtracted at

various distances
Distance (cm) Subtraction (D)
133 0.75
100 1.00
67 1.50
50 2.00
Table 16.2 Relation between retinoscopy and final power
Retinoscopy Subtraction (D) Power

⫹1.5
⫹1.5 1.5 0
⫹2.5
1.5 ⫹1.0 Dsph
⫹2.5
⫺1
1.5 ⫺2.5 Dsph
⫺1
⫹0.5
1.5 ⫺1.00 D Dcyl 180
⫹1.5 ←
⫹1.5
1.5 ⫺1.00 Dcyl 90
⫹0.5
From the above two tables it seems that if ⫹1.5 is subtracted from the retinoscopy,
the resultant should be accepted by the patient. In practice, it is not true because for
comfort of the patient at least 1/3 of accommodation should be left in reserve. During
the post-mydriatic test the pupil comes to the normal size, and cuts off the peripheral
rays, which increases the depth of focus. It also cuts off peripheral lenticular opacities
in cortical cataract. A constricted pupil may be obstructed by existing corneal or cen-
tral lenticular opacity.
➤ While prescribing glasses the most comfortable number, even with slightly less
vision should be prescribed
Use of various cycloplegics and mydriatics:
➤ All cycloplegics are mydriatics. Mydriatics are not cycloplegics
Phenylephrine in a dose of 5–10% is used as a mydriatic. It has no cycloplegic

effect hence it is not useful in retinoscopy when accommodation is active, e.g. under
40 years of age. However, when this is added to other cycloplegics, onset and duration
of mydriasis is enhanced some common combinations are 0.5% tropicamide with
10% phenylephrine and 0.8% tropicamide with 5% phenylephrine. Similarly homa-
tropine and cyclopentolate can be used in various combinations with phenylephrine.
Sometimes a combination of two cycloplegics is also used, e.g. 0.5% of tropicamide
with 1% cyclopentolate or homatropine.
Atropine sulphate is used in children under 10 years of age, preferably as ointment,
at a frequency of two times a day for 3 days for retinoscopy. If pupil is not dilated at
the time of retinoscopy, 5–10% phenylephrine may be used, one drop every 10 min
for three instillations. Homatropine, cyclopentolate and tropicamide are used between
10 and 40 years of age. Phenylephrine 10% can be used in persons after 40 years of age.
Aphakics do not have any accommodation so there is no logic in using a cycloplegic.
However, some aphakic eyes do not dilate well with mydriatic only, so a combination
of mydriatic cum cycloplegic may be required (Table 16.3).
Automated Refractometers
These are sophisticated refractometers that use an infrared light source instead of
white visible light and a sensor, which measure various meridians of the eye under
Table 16.3 Time of PMT in relation to cycloplegic
Cycloplegic Onset of action Duration PMT
Atropine sulphate (1/2–1%) 1h 10–15 days After 15 days

Homatropine hydrobromide (2%) 1h 12 h 24 h
Cyclopentolate hydrochloride (1%) 30 min 12 h 24 h
Tropicamide (1%) 15 min 4h 12 h
Plate 16.2 | Autorefractometer in use.
examination, which is then converted into optical terms in the form of a print out
(Plate 16.2). For accurate reading the instrument should be in line with the patients
visual axis, accommodation should be relaxed, pupil need not be dilated but should
be of moderate size. The automated instrument is objective, but some of the instru-
ments have a built-in adjustment for subjective testing also. Otherwise, findings of
the automated instrument should be tested subjectively. They are good for mass screen-
ing of errors of refraction in a short time, non-cooperative children and illiterate
patients.
Examination of an Eye with Astigmatism

Peculiarities of Vision in Astigmatism
1. Even small amounts of astigmatism can produce asthenopic symptoms
2. When astigmatic patients are asked to read the Snellen’s chart, they may confuse the letters
with slanting sides like ANMW
3. On E chart they may be able to correctly recognise the direction of arms of E when E is
vertical but may not be able to point the direction when placed horizontally and vice versa
4. Vision with a pinhole does not improve to the extent to which it would in case of a
purely spherical error. For example, a patient with ⫺1 D spherical refraction will improve to
6/6 from 6/36 with pinhole, but an astigmatic of same amount will not improve beyond
6/12 with PH
5. On subjective test, value of cylinder is always more than the value of corresponding sphere. Say
a patient with 6/9 vision will improve to 6/6 or 6/5 by 0.5 Dsph, but to attain the same correc-
tion an astigmatic may require as much as ⫺1.00 to 1.25 or more cylinder. In other words high
astigmatism produces less visual loss in contrast to spherical errors
6. Uncorrected astigmatic develops reading difficulty even in pre-presbyopic age that is overcome
by astigmatic correction without near correction
Retinoscopy in Astigmatism
Retinoscopy in suspected astigmatism should be done under cycloplegia. Steps of
retinoscopy are the same as in spherical error of refraction. Only difference is that
the retinoscopy findings are not uniform in all the meridians. Difference between the
two meridians is the power of the cylinder.
Steps to find out the power of glasses in astigmatism:
1. Refract the eye under cycloplegia
2. Find out difference between two principle meridians.This will give value of cylindrical correction
3. The lower value is the power of sphere
4. To this, add cylindrical value in appropriate axis
5. If the vertical meridian has more power than the horizontal meridian, the horizontal reading
will be the value of sphere and the axis will be 180°
6. In case the horizontal meridian is of higher value, the cylinder will be at 90° axis
7. There may be other axes also
➤ Value of cylinder will not change by adding or subtracting for PMT or

presbyopic correction. The axis will change by 90° with the addition of
sphere of opposite sign
Checking the Astigmatic Correction

Many a times the patient may not be able to state correctly as to which position of the
cylinder is the best. To find out the correct axis and power of the cylindrical correction
the following methods are used.
1. PMT on E chart: Axis and power that give the clearest vision in all Es of the same line is the
power and axis to be prescribed
2. Astigmatic fan or dial: This consist of lines radiating from a common point above a horizontal
line like protractor, or a point all round. All the lines are at uniform intervals of 15°. They are
of the same width, length and brightness (Fig. 16.3).The test is done at 6 m distance. One eye
is tested at a time
The patient is asked to state:
● Are all lines equally clear? Is the distance between all lines equal all over the fan? If answer is yes,
the axis of the cylinder is correct. If a particular line is blurred, this means that the axis is not
fully correct and the axis of the cylinder should be shifted accordingly
Astigmatic dial Astigmatic fan Astigmatism at 180⬚—patient's

view of astigmatic fan
Fig. 16.3 | Astigmatic fan and dial.

● The test is subjective. It requires maximum co-operation, attentiveness and intelligence of the
patient. It require a lot of explanation to the patient.Though this is most accurate of all subjec-
tive tests, it is least utilised. Use of an autorefractometer eliminates these problems
● Cross-cylinder (Jackson’s Cross-Cylinder)
This is a lens mounted in a frame with a handle. The lens consists of a sphere and
a cylinder. The power of sphere is half than that of cylinder but the signs are oppo-
site, e.g. ⫹0.5 Dsph with ⫺1.00 Dcyl. This has the effect of two cylinders of equal
strength but opposite signs at right angles to each other. The spherical equivalent of
a cross-cylinder is always zero. The above power can be expressed in various ways as
follows:
1. ⫹0.5 Dsph ⫺1.00 Dcyl 180°

2. ⫺0.5 Dsph ⫹1.00 Dcyl 90°
3. ⫹0.5 Dcyl 90° ⫺0.5 Dcyl 180°
4. ⫹0.5 Dcyl 180° ⫺0.5 Dcyl 90°
In a cross-cylinder the axes are at 45° and 135° instead of 90° and 180°. The handle
is in such a position that its long axis is in between axes of two cylinders in 90°. The
cross-cylinders can be of various combinations most common is a combination of
⫹0.25 Dsph with ⫺0.5 Dcyl (Fig. 16.4). Cross-cylinder is used to find out exact axis
of astigmatism and correct power of the cylinder.
1. While examining one eye the other is occluded
2. Patient looks at Snellen’s chart at 20 ft
3. Sphere and cylinder are put in the trial frame at an axis determined by retinoscopy
4. First axis of cylinder is corrected
5. Then the power of cylinder is refined
Procedure The cross-cylinder is placed in such a way that the axis of the cross-
cylinder is 45° away from the cylinder in the trial frame on each side. This is called
straddling of the cross-cylinder, for example the axis of cylinder in trial frame is at 90°
the cross-cylinder will have its two axes at 45° and 135°.
Now the cross-cylinder is rotated by 180°, e.g. flipped, so the axis that was at 45°
becomes 135° and vice versa. If the vision is blurred equally in either position, the axis
Fig. 16.4 | Jackson’s cross-cylinder.

of the cylinder in trial frame is correct. If the vision is better in one position then the
axis of cylinder in trial frame is not correct.
To correct the axis of cylinder in trial frame, the cross-cylinder is removed and the
cylinder in trial frame is moved. If the cylinder in trial frame is plus, it is shifted
towards plus side of the cross-cylinder.
Next step is to straddle the cross-cylinder again and repeat the procedure. This is
repeated till vision is equally blurred in both the positions of cross-cylinder. To correct
the power plus cylinder of cross-cylinder is superimposed on the cylinder of trial
frame. Then the minus cylinder is superimposed in the same way and power of cylin-
der in trial frame is increased or decreased till vision is same in both positions.
Duochrome Test
This test is based on the principle of chromatic aberration of optical system. Green rays
are refracted more than red because they have a shorter wavelength. In a myopic eye all
rays come to focus in front of the retina. As green part of the white light comes to focus
more in front of the retina than red components, the green rays are more myopic than
the white and the red rays. Thus in a myopic eye red letters against black background
will look better than green letters against black background. In a hypermetropic eye all
the rays are focused behind the retina. In hypermetropic eye green letters against black
background are seen clearer than red. In emmetropia or properly corrected ametropia
both green and red are equally clear. Actually the eye prefers to focus yellow.
The instrument for the Duochrome test (Fig. 16.5) consists of two panels of equal
size; one has red letters, the other has green letters. Letters corresponding to Snellen’s
6/18 to 6/6 of black colour are inscribed on these panels. The panels are electrically
illuminated; illumination should be equal on both panels. One eye is examined at a
time. The patient is asked to state which panel has clearer vision. If the red side looks
clearer then the eye is still myopic and needs addition of more minus lenses. In hyper-
metropia reverse is the rule.
Sometimes there is confusion in adding lenses, which is avoided by following dictum:
“If green is better it means ‘go ahead’ as in traffic signal to go ahead mean adding;
if patient has better vision with green panel then add if not then subtract”.
➤ Duochrome test is not influenced by colour vision of the patient, it cannot be used
to test colour vision
O L E C C L A E F RI END
H A T N O H L O
Fig. 16.5 | Panels of Duochrome and Friend test.

EXAMINATION OF A PATIENT WITH NEAR-VISION

DISORDER (PRESBYOPIA)
Generally an emmetrope develops near-vision difficulty at about 40 years of age. This

is a gradual process. The person may not realise that he is developing near-vision
difficulty because, it can be compensated by moving the object away from the eye,
increasing illumination or both. However, those who have to work at close quarters
will report earlier than others.
Whenever a person complains about near-vision difficulty, the following things should
be asked—age of the patient, usual distance at which he is required to do near work, dis-
tant vision, any corrective glasses that the person is using, is the patient instilling any drug
in the eyes, is the person on any drug that can cause cycloplegia, diabetic status etc.
Age—A patient develops presbyopia, at about 40 years of age, which is physiolog-
ical but if a patient below 40 years of age develops diminished near vision other causes
of diminished near vision should be found out. They are: uncorrected hypermetropia
and astigmatism, over-corrected myopia, instillation of cycloplegic, neurological cyclo-
plegia, internal ophthalmoplegia, post-diphtheria cycloplegia, short near-work dis-
tance, e.g. goldsmith, engravers, tailors, miniature painters, stamp and coin collectors
and jewellers.
Many drugs with para-sympatholytic effect, e.g. antispasmodic and psychosomatic
drugs, may produce near-vision defect.
Commonest cause of early prescription of near-vision correction is uncorrected
hypermetropia where most of the accommodation is used in distant vision. These
patients will be relieved by the proper distant correction and may not require near
correction till they reach presbyopic age.
To examine a presbyopic the following steps are followed:
1. Distant vision—patient may resent examination of distant vision saying that distant vision is alright
2. Even if distant vision is 6/6 BE exclude facultative hypermetropia by adding plus lenses till the
patient remains 6/6
3. If there is diminished distant vision, it should be corrected
4. Find out the patients near working distance and compare it with his physiological distance for
that particular age
5. Find out the near point of accommodation (NPA) and near point of convergence (NPC)
6. Examine the eyes for opacity in media, macular lesion, phoria, amblyopia and anisometropia
7. Exclude diabetes
Near Point of Accommodation

NPA is the shortest distance at which maximum accommodation is exerted and object
is seen clearly. In children it is very near the eye; at 10 years of age it is 7 cm. It recedes
with age; at 40 years it is 25 cm, at 60 years it is 100 cm.
To measure NPA a target that requires accommodation (e.g. small letters or num-
bers) is gradually moved at eye level and the patient is asked to indicate the distance
at which it is no longer clear. NPA should be measured separately in each eye and then
Table 16.4 Relation between accommodation power to near point
Accommodation
Age in years power Near point (cm)
10 14.0 7
20 10.0 10
30 7.0 14
40 4.0 25
50 2.5 40
60 1.0 100
70 0.5 200
in both eyes together. The patient should wear distant vision correction if needed. The
distance is measured in centimetres, and then changed to dioptres by a formula.
Near Point of Convergence

NPC is the closest distance at which maximum convergence is available and an object
is seen singly. Like NPA it is very close to the eyes in children and recedes with age.
To measure NPC, a small target, usually a letter or number is moved slowly at the level
of eye towards it. As the target moves towards the eyes, convergence is increased. As
maximum convergence is reached, patient can no longer maintain convergence or
fusion resulting in diplopia. This distance is measured in centimetres (Table 16.4).
How to Measure Near Point

1. The patient is given any reading material and asked to read. Distance at which the patient keeps
the reading material is roughly the reading distance of the patient. It need not be the physio-
logical near point corresponding to age
2. The patient is given a standard near-vision chart and asked to read it at the usual reading dis-
tance for patient’s age. At 40 years, a person should be able to read the smallest point at 30 cm.
There are two methods to find out near point by near-vision chart
● Note the distance at which patient can read the smallest point, e.g. N5 or J1
● Note the line that patient can read at 30 cm, e.g. N18 or N24
The other method, which is more accurate, is the use of either RAF gauge or Livingston’s
binocular gauge (Plate 16.3).
In these instruments, point of near vision is given in centimetres and amplitude of
accommodation in dioptres.
While prescribing presbyopic correction, the following should be taken into consideration:
1. Plus lenses are added to the distance correction to reinforce accommodation
2. At least one-third of accommodation should be left uncorrected for the comfort of the patient
and to give a range of working distance
3. A patient with good distant vision will prefer a greater working range while a patient with dimin-
ished distant vision prefers a shorter working distance as it gives a larger retinal image
Example—An emmetrope has diminished near vision. On examination, it is found
that his near point has receded to 33 cm while his actual working distance is 25 cm
Plate 16.3 | RAF gauge in use.

and amplitude of accommodation is 3 D. The patient requires 4 D of accommodation
for a working distance of 25 cm. Out of 3 D of amplitude of accommodation, one-
third is left in reserve. So the available accommodation is ⫹2 D. For a working dis-
tance of 25 cm, an addition of ⫹2 D to his distant correction will give him comfort-
able near vision. Distant correction of an emmetrope is 0 so his near correction will
be ⫹2 DSph. Suppose his distant correction was ⫹1.0 Dsph then his near correction
will be ⫹1.0 D ⫹ 2.0 D ⫽ ⫹3.0 D. In myopia of ⫺1.00 near correction will be
⫺1.0 D ⫹ 2.0 D ⫽ ⫹1.0 D for the same age.
➤ Prescription of near correction is not a simple sum of powers. It is highly individual,

depending on age, profession, illumination, general health of patient and
interpupillary distance for near vision
Interpupillary distance has an important role to play in spectacle fitting. The dis-
tance between the optical centres of the spectacle must correspond with the inter-
pupillary distance. Interpupillary distance for near vision is shorter by about 3 mm as
compared to distant vision.
There are various instruments to measure interpupillary distance (Plate 16.4).
Simplest method is to use a transparent scale. The distance between the nasal edge of
one pupil and temporal edge of the other pupil is measured, provided the pupils are
of equal size. Most accurate measurement is given by a synoptophore.
EXAMINATION OF A PATIENT WITH LOW VISION
Examination of an eye with low vision is one of the most difficult clinical tasks in oph-
thalmology. The most frustrating part is recording of vision before and after treatment.
The greatest difficulty faced by an ophthalmologist is to draw the line between legal
blindness, low vision, and a partially seeing patient. The following definitions are helpful.
Plate 16.4 | Interpupillary distance measuring device. To measure IPD the circle in the centre of right glass is
centred in front of the right pupil. The other glass is moved over the horizontal bar till it is in front of
the left pupil. The distance between the two pupils is read from the scale inscribed on the horizontal
metal bar above.
Legal Blindness
If the vision in the better eye with the best correction is less than 6/60 or periph-
eral field is less than 20° at its maximum diameter, the person is designated as legally
blind.
Low vision is that central vision or field loss, which even with the best optical cor-
rection interferes with the routine functions
Functionally blind are those patients whose best corrected vision interferes with their
ability to read, write, identify familiar objects by sight and travel safely in unfamiliar places.
Partially seeing child is one who has distant vision between 6/24 and 6/60 with the
best optical correction that does not improve reading and writing.
Travel vision is defined as a vision of 1/60 or less with visual fields extending up to
50° at its maximum diameter.
Legal blindness may be treatable, reversible and preventable. Preventable blindness
are vitamin A deficiency, trachoma, infective keratitis etc. Common examples of
reversible blindness are cataract and corneal opacity.
History plays a dominant role in the management of low vision. Inquire about the
age of the patient, age of onset and education of the patient. Visual requirement for
(a) distant, (b) near, (c) both and (d) field of vision. Is the vision better in bright light
or dim light? Finally the motivation of the patient as to why he wants a low vision aid.
All patients do not improve with low vision aids; some of the patients may not
co-operate and may be resigned to the present state of vision. Educated patients pre-
fer better near vision than distant vision. History of systemic diseases should be taken
specially arthritis, tremors, diabetes, hypertension and hemiplegia.
➤ The principle of low vision aid is to exploit the residual vision and use it to improve
the vision to the best possible level
Recording of Vision
Recording of vision in low vision is one of the most important steps because it gives
the following information:
1. Extent of residual vision.
2. To what extent can it be improved?

3. Which type of low vision will be most advantageous to the patient?
Recording of vision in a patient with low vision differs from that in a sighted person.
Ordinary vision charts are not useful for recording vision in these patients. Usual dis-
tance at which vision is recorded ranges between 1.5 and 3 m. The charts used are
Modified Snellen’s, Bausch and Lomb, Solan, Straub for distant vision and Keeler’s charts
for near vision (Plates 16.5 and 16.6).
Keeler’s near-vision chart for low vision not only denotes vision but also indicates
the magnification required for near vision. Keeler’s charts are read at 25 cm. They con-
sist of 20 lines that are marked as A1 to A20. A1 corresponds to the usual newsprint,
A2 is equal to 80% of A1, while A3 is 80% of A2 and only 64% of A1. Thus A20
equals 1.4% of A1.
Solan’s charts are read at 40 cm. They contain series of M. They are numbered between
m1 and m20. It directly gives the magnification required, e.g. a person reading m7
will require seven times magnification for usual book prints.
Examination of Eye
All forms of ocular examination should be carried out to determine the type of the
lesion and its location. It will also give some idea about the choice of near vision aid
Plate 16.5 | Charts for low vision.

(Courtesy Dr. Subhash Mishra.)
Plate 16.6 | Charts for low vision.
(Courtesy Dr. Subhash Mishra.)
to be prescribed. It is better to postpone low vision aid to a patient with an active lesion.
The lesions are grouped according to the location, aetiology and combination of both.
➤ All patients do not improve with low vision aids
The conditions that are favourable are cataract, macular degeneration, chorio-retinal
scar, high myopia, irregular cornea and albinism. Unfavourable conditions are glaucoma,
retinitis pigmentosa, diabetic and hypertensive retinopathy and secondary optic atrophy.
➤ It should be noted that those who have lost sight for many years do not improve so
well as compared to blindness of shorter duration
Old persons require more illumination than children. Old patients require more time
to get adjusted to low vision aids.
Children use their own accommodation; hence require less magnification for near.
Retinoscopy in Low Vision

Retinoscopy in low vision is sometimes impossible due to opacities in the media,
squint and nystagmus. More reliance is given to subjective correction than objective.
Whenever retinoscopy is required it should be done at the shortest possible distance, this
gives a brighter illumination.
Types of Low Vision Aids

Low vision aids (Plate 16.7) are mostly optical for visual improvement. Mobility may
be enhanced by walking canes, guide dogs etc.
Plate 16.7 | Some of the low vision aids. (Courtesy Dr. Subhash Mishra.)
Fig. 16.6 | Braille alphabets.
Optical devices can be:

1. Spectacle and modified spectacle devices
2. Non-spectacle devices
Spectacle devices are high-power spectacles, spectacle mounted telescopes and
microscopes.
Non-spectacle devices are various types of magnifiers, both hand held or stand
magnifiers. Braille is a special type of script, which can be read with touch (Fig. 16.6).
Totally blind persons can develop sufficient proficiency to become teacher, lawyers,
etc. Old persons learn Braille with difficulty. Computer and television screens are very
helpful to partially sighted persons as here the letters (objects) can be enlarged as
required.
E XAMINATION OF A
C ASE OF S QUINT
Patients with misaligned eyes may present with complains of deviation of one eye, alter-
nate eye or rarely both eyes. Sometimes patients with asthenopia are found to have latent
squint or phoria. The word squint is generally used to denote manifest squint, i.e. tropia.
EXAMINATION OF SQUINT
Examination of manifest squint differs from that of latent squint in many ways.
If a patient presents with manifest squint, the first thing is to find out whether it is:
1. Pseudo-squint or
2. Real squint
BROAD CLASSIFICATION OF OCULAR DEVIATION
1. Pseudo-squint (they look like tropias)

2. Latent squint (heterophoria)
3. Manifest squint (heterotropia)
(a) Concomitant squint
(b) Non-concomitant squint
● Paralytic squint
● Restrictive squint
4. Miscellaneous
PSEUDO-SQUINT
Pseudo-squint is a state of ocular position that gives a false impression of manifest

squint. It can be pseudo-convergent or pseudo-divergent. Vertical pseudo-squints are rare.
Causes of pseudo-squint are:
1. Epicanthic folds
2. Large-angle kappa
3. Broad nasal bridge
4. Telecanthus
EXAMINATION OF A CASE OF SQUINT 233
Causes of pseudo-convergent squint are broad nasal bridges, epicanthal folds, negative-
angle kappa.
Causes of divergent pseudo-squint are telecanthus, positive-angle kappa and reduced
length of interpalpebral fissure on temporal side.
Characteristics of pseudo-squint are:
1. Generally seen in children, may disappear with age
2. Does not show any deviation undercover
3. Disappears if epicanthal fold is obliterated
4. Measurement of large-angle kappa is demonstrable
➤ Psuedo-squint may co-exist with true squint. It may worsen or neutralise the
appearance of true squint. An epicanthus with convergent squint will worsen it,
but may neutralize divergence
Once it has been established that a patient has manifest squint (tropia) it should be
evaluated if it is
(a) Paralytic: non-concomitant
(b) Non-paralytic: concomitant (Table 17.1)
Primary deviation is the deviation of the squinting eye when the other eye fixes. It is
equal undercover or without cover. Secondary deviation is the deviation of the sound
eye when paralytic eye fixes or is forced to fix. The sound eye deviates more than the
deviation of the paralytic eye due to Hering’s law of equal innervation.
Angle Kappa
In normal eyes, the visual axis, i.e. the imaginary line joining the point of fixation with
the fovea and the pupillary line, i.e. an imaginary line passing through centre of the
Table 17.1 Comparison between paralytic and non-paralytic squint
Features Paralytic Non-paralytic
Symptoms Cosmetic deviation Cosmetic deviation

Diplopia No diplopia
Abnormal head posture No abnormal head posture
May have giddiness No giddiness
Heredity Absent May be hereditary
Vision Variable. Unrelated to squint Variable. Diminished vision may be
the cause
Error of refraction Does not cause paralytic squint May be the cause of deviation
Onset Sudden Gradual
Movement Restricted Normal
Secondary changes in Common Very rare
muscles
Primary deviation Secondary deviation is more Equal to secondary deviation
than primary
Spontaneous recovery May be possible Nil
Change to concomitant Can become concomitant Nil
P Pupillary axis
V K P V Visual axis
K Angle kappa
Positive Negative
Angle kappa Positive and negative angle kappa
Fig. 17.1 | Angle kappa.

pupil perpendicular to the cornea should coincide, but like many other physiological
conditions, this is an exception rather than the rule. These two lines meet each other
to form an angle. This angle is called angle kappa. Angle kappa is called positive if
light reflex is formed on the nasal side of cornea giving an impression of exodeviation.
In negative angle kappa the impression is that of esodeviation. A positive angle kappa
of 5⬚ is normal in emmetropia (Fig. 17.1).
How to Measure Angle Kappa

Angle kappa can be measured in two ways: (1) objectively and (2) subjectively.
1. Objective measurement is done on Lister’s perimeter in degrees (arc). The patient fixes the
central point of perimeter at 33 cm. A small point of light is moved over the arc of the perimeter
until it is centred on the cornea. Difference between point of fixation and this light gives angle
kappa in degrees
2. Subjective test is done on the synoptophore with special slides that have a central point on the
horizontal line; line on each side of the central point is calibrated. The calibrations are marked
either by numbers or alphabets. The light in the tube of the synoptophore is switched on; the
patient is asked to fix the central spot of the slide. Position of the corneal reflex is noted. If it is
decentred, the patient is asked to move the gaze on the horizontal line of the slide from number
to number unless the light is centred on the cornea
➤ Angle kappa is negative in myopia and positive in hypermetropia
Causes of decentred corneal reflex are:

1. Large-angle kappa
2. Tropia
3. Ectopic macula
4. Eccentric fixation
5. Corectopia and coloboma iris
TYPES OF TROPIA
Causes Wise
A manifest squint (heterotropia) is said to be:
1. Concomitant, when deviation is not due to paralysis of extra-ocular muscles
2. Paralytic (non-concomitant), when at least one extra-ocular muscle is paralysed
3. Restrictive, when restriction of the muscle is not neurological but is mostly myogenic as follow-
ing fracture of orbit, dysthyroid myopathy, myasthenia and congenital fibrosis
Direction Wise
If the eye is deviated medially, it is called esotropia and when deviated laterally it is
called exotropia. Upwards deviation is called hypertropia. If 12 O’ Clock of cornea rotates
medially, it is incyclotropia; if it rotates laterally, it is called excyclotropia. Term hypotropia
is no more in clinical use.
Laterality Wise
Uniocular—When one eye always takes up fixation and the other eye deviates. When
the fixing eye is covered the deviating eye takes up fixation and fixing eye undercover
deviates. On removal of the cover the eye that was undercover takes up fixation and
the originally squinting eye goes back to the deviated position.
Alternate squint—Both eyes deviate from time to time. When one eye squints the
other eye fixes.
Characteristics of alternate squint:
1. Generally, angle of deviation is large
2. Convergent squint is more likely to alternate
3. Vision in both eyes is near normal; when sub-normal, it is almost equal in both eyes
4. Error of refraction when present is low
5. If the fixing eye is covered it deviates undercover and the deviating eye takes up fixation. On
removing the cover the eye that was undercover remains deviated
6. There is central fixation in both eyes
7. Amblyopia is rare
8. There is no fusion
9. Abnormal retinal correspondence is present
Bilateral squint—This is relatively rare. Both eyes may squint simultaneously as in
bilateral sixth nerve palsy, Moebius syndrome and dysthyroid myopathy.
COVER TESTS
This is a very simple test of great diagnostic value. This helps in determining if a devia-
tion is latent, manifest, pseudo, concomitant, paralytic, uniocular or alternate. The test
does not require any gadget. To perform the test the patient is asked to fix an object with
both eyes. If one eye deviates in relation to other, the patient has a manifest squint (tropia)
that could be concomitant or paralytic. If concomitant, it could be uniocular or alternate.

Straight eyes do not exclude deviation; a straight eye can have latent squint (phoria).
Cover test consists of:
1. Alternate cover test
2. Cover–uncover test (for manifest/Latin deviation)
Alternate Cover Test (Fig. 17.2)

The patient fixes a small target. One of the patient’s eye is covered for a while, then the
cover is moved over the other eye for a while, then the cover is moved back over the
Right esotropia
Right eye covered, no

movement in any eye
Left eye covered, right

eye takes up fixation
Right eye covered

again, squinting left
eye, takes up fixation
straight
Fig. 17.2 | Alternate cover test.

Normal or phoria
Right eye covered,

esophoric
Both eyes uncovered

and straight
Normal or phoria
Left eye covered,

esophoric
Both eyes uncovered

and straight
Fig. 17.3 | Cover–uncover test for phoria.

first eye. The process of covering alternate eyes is continued and the eye is watched for
any movement as the cover is moved. Alternate cover test does not distinguish between
phoria and tropia.
Cover–uncover test for phoria (Fig. 17.3): Once the patient fixes an object and
both eyes look to be straight, any of the eyes is covered for about 2 s and then the cover
is removed. When the cover is removed the observer notes:
1. Has the eye undercover made any movement? Does it take up fixation after the cover is
removed? If yes, it means phoria
2. There is no movement of either eye when it is covered and then uncovered. This means that
there is no phoria, a microtropia syndrome may be present that requires investigation or
pseudo-tropia is present, which can be unmasked by suitable tests
➤ The cover–uncover test distinguishes unilateral squint from alternate squint
Cover–Uncover Test for Tropia (Figs 17.4 and 17.5)

The patient fixes an object:
1. The fixing eye is covered and movement of the squinting eye is observed—it will move to take
up fixation. If it moves out to take fixation this means that it was originally deviated in (esotropic).
Similarly an exotropic eye will move inward to take up fixation
2. The non-fixing eye when covered
(a) Will not show any movement if the squint is unilateral (Fig. 17.5)
A
1
B
3
4
5
5
6
Fig. 17.4 | (A) 1. Both eyes uncovered, right eye squints. 2. Right eye covered, no movement in either eye. 3. Both
eyes uncovered. (B) 3. Left eye covered, right eye takes up fixation, left eye squints under cover. 4. Both
eyes uncovered, right eye remains squinting. 5. Both eyes uncovered, right eye goes into its original squint
(uniocular squint). 6. Both eyes uncovered, right eye does not move, left eye squints (alternate squint).
Fig. 17.5 | Detection of heterotropia.
(b) The fixing eye deviates undercover.The squinting eye takes up fixation; the eye undercover
remains deviated when the cover is removed and this denotes that this is a case of alter-
nate squint (Fig. 17.4)
Cover and Prism Test

The test is quantitative; it measures the actual deviation when both eyes are uncovered.
It is mostly used in small-angle esotropia. This test has two parts, e.g. alternate cover
test and prism cover test (Plates 17.1 and 17.2).
The fixing eye is covered; the deviating eye moves to take up fixation. A prism is
put in front of the uncovered eye that was originally squinting; base-out for esotropia
and base-in for exotropia. The cover is removed from the other eye. The normal eye
will take up fixation and eye behind prism will deviate. The power of prism is gradu-
ally increased till movement of the eye behind the prism stops. On inspection both
the eyes will look straight. Power of the prism that stops the movement is the angle of
deviation in prism dioptres. This test is not suitable in small children and in restrictive
squint.
Plate 17.1 | Vertical prism bar. (Courtesy Dr. Anil Gupta.) Plate 17.2 | Horizontal prism bar. (Courtesy Dr. Anil Gupta.)
MEASUREMENT OF DEVIATION IN TROPIA
Corneal Light Reflex or Hirschberg’s Test (Fig. 17.6)

It measures the relative the position of light reflex on cornea. The patient is asked to
look straight ahead. A small fixation light is held in front of the eyes at the level of
pupil at 33 cm distance. The position of the corneal reflex is noted in relation to pupil
or limbus. 1 mm of decentering of the reflex denotes 7⬚ or 14 prism dioptre (PD) of
deviation. If the reflexes are symmetrical in both eyes, there is no manifest squint. If
the reflex is formed on nasal side of cornea the eye is deviated out (exotropic) and vice
versa. The test is effective when the patient is attentive. With useful vision and central
fixation, it may be influenced by angle kappa. It is not suitable for small deviations,
e.g. microtropia.
Krimsky Test with Prism

This test is based on the principle that light deviates towards the apex of the prism.
Hence by placing a prism in front of cornea; the corneal light reflex can be shifted
depending on the power of the prism and relative position of its base.
The test comprises of two steps:
1. Hirschberg test to locate the corneal reflex
2. Placing of prism with appropriate base and gradually increasing the power in front of the fixing
eye unless the corneal reflex is central—base out for esotropia, base in for exotropia and base
down for hypertropia
Fig. 17.6 | Hirschberg test.

Perimeter Test
The patient sits on a Lister’s perimeter and fixes the 0 mark with fixing eye. The other
eye deviates. Observer moves a small light on the arc of the perimeter in front of the
deviating eye from periphery to centre till the image coincides with centre of the
pupil. Distance of the light from zero mark gives the deviation in degrees.
Amblyoscope (Synoptophore)
This instrument consists of a base on which two tubes are fixed in such a way that they
can be moved in various directions. The tubes can be moved away from each eye to meas-
ure various interpupillary distances. The tubes can be moved separately or simultane-
ously. Each tube is shaped like the alphabet L with a small arm and a long arm; terminal
of small arm is the eyepiece. The end of the long arm has an arrangement to place trans-
parent slides, which are internally illuminated. The slides can be illuminated simulta-
neously, separately or alternately. There is a plane mirror fixed at the junction of the
long and short arms at 45⬚ to the axis of both the tubes. This reflects the picture from
the slide into the eyepiece, which has a plus 6.5 D lens. The reflected image is formed at
infinity (Fig. 17.7). An emmetropic eye need not accommodate to see this object. The
pictures in the slide are projected separately in each eye. If the light of one of the slide is
switched off, this acts as an occluder for that eye. The eyepiece is provided with slots, sim-
ilar to a trial frame. Corrective glasses can be put into them if required. By putting minus
lenses in these slots desired amount of accommodation and convergence can be induced.
To examine a patient on the synoptophore, the patient sits in front of the eyepieces.
Height of the instrument and position of eyes of the patient can be adjusted according
to need. The patient puts his chin on the chin rest and forehead on the forehead rest.
Interpupillary distance is adjusted. The tubes are put on zero mark on each side.
The lights in the tubes are put on. In an orthophoric patient the light coming from
the tubes should be centred in the pupil. If the lights are decentred a manifest squint
Image of
targets at
infinity
Transparent slide
Transparent slide
Light Plane mirror Light
Lens 6.5D
Fig. 17.7 | Optics of synoptophore.

is present, which can be measured by moving the arm in front of the deviating eye till
the light reflex is placed in the centre of pupil.
Effect of occlusion can be introduced by putting the light off in one of the tubes.
By switching the light on and off in alternate tubes, alternate cover test can be done.
The instrument is used in the sensory evaluation of squint; it is used to measure
angle kappa, interpupillary distance, objective and subjective angle of squint, angle of
anomaly, grades of vision, suppression and abnormal retinal correspondence.
Besides the diagnostic use it has a therapeutic role in orthoptic treatment. It can be
used to detect uniocular malingering also.
Objective methods of measuring ocular deviation are:
1. Hirschberg’s test
2. Krimsky test
3. Prism and cover test (P⫹C)
4. Simultaneous prism and cover test (SP⫹C)
Subjective methods of measurement of ocular deviation are:
1. Maddox rod
2. Maddox wing
3. Maddox tangent
4. Double Maddox rod (red and white)
5. Maddox double prism
6. Hess’ Screen
7. Red green glass test
8. Diplopia field
Measurement of Objective Angle of Squint by Synoptophore

The patient sits on the synoptophore. After adjusting IPD and measuring the angle of
kappa, the tubes of synoptophore are put at zero on each side. Two dissimilar slides of
Simultaneous macular perception
Fusion
C
Stereopsis
Fig. 17.8 | Slides for synoptophore.
simultaneous macular perception test are put in each tube, e.g. lion in front of right eye
and cage in front of left eye. The patient is asked to fix the lion. Now the left tube is moved
until the corneal reflex comes to an identical position. This gives objective angle of squint.
Measurement of Subjective Angle of Squint by Synoptophore

After objective angle of squint has been measured, the usual slides of lion and cage are
put in the synoptophore. Lion is in front of the right eye and cage in front of the left
eye (Fig. 17.8A). The patient is asked to put the lion in the cage. The angle between
two tubes is noted. This gives subjective angle of squint.
Angle of anomaly denotes the difference between subjective and objective angle of
squint. If subjective and objective angles are same, the patient has simultaneous per-
ception and normal correspondence.
ASSESSMENT OF BINOCULAR FUNCTION
There are three grades of binocular vision:

1. Simultaneous perception
2. Fusion
3. Stereopsis
Testing Grades of Vision—Simultaneous Perception

Simultaneous perception is the most primitive binocular function. It has the ability to
fuse even those points that are projected outside the corresponding retinal areas. The
person interprets two separate impulses from the two maculae as one. It is tested on
the synoptophore by placing two dissimilar slides that need not be fused, but do not
antagonize each other. Say a lion and a cage; a sentry and a sentry box.
Measure the objective angle of the squint. Ask the patient to put the lion in the
cage. If he can put the lion in the cage, he has simultaneous perception. If the patient
has no angle of anomaly, he has simultaneous perception and retinal correspondence.
Absence of simultaneous perception may be due to uniocular or alternate suppression.
Simultaneous perception is first step towards the next grade of binocular vision, i.e.
fusion. There are various types of slides to measure simultaneous perception like
foveal, macular or paramacular perception.
Fusion
Fusion is the ability to fuse images projected on corresponding retinal points. This is
a central function. This is second faculty to be acquired in the development of binocular
vision. In this two pictures with very slight differences are combined into one picture.
For example, one bunny with tail, and the same bunny with a bunch of flowers in hand
without tail; a cat with a butterfly but no tail, the other side has a cat with tail but no
butterfly (Fig. 17.8B).
To test fusion, the first prerequisite is simultaneous perception. The tubes are so set
that the pictures are seen separately by the two eyes. The patient is asked to move the
tubes to complete the picture. Amplitude of fusion can also be measured. Absence of
fusion in a squint has poorer prognosis.
Stereopsis
It is the most developed faculty in binocular vision. This is the ability to appreciate
the third dimension. This is tested on synoptophore (Fig. 17.8C) and various types of
stereoscopes.
1. Variable prism stereoscope (Fig. 17.9)
2. Non-variable prism stereoscope (Fig. 17.10)
3. Kinetic stereoscope
The principle of stereopsis test is to present a field to each eye at a given time; each
field contains elements imaged on corresponding retinal areas. Stereopsis should
ideally be tested for near as well as distance.
Other methods to test stereopsis are:
1. Two pencil stereopsis test (Langs)
2. Titmus fly test
3. TNO test
4. Random dot stereo test
5. Frisby stereo test
6. Langs stereo test
Images of
targets at
infinity
Left eye target Right eye target

Left eye target Right eye target
Mirrors
Lenses
Fig. 17.9 | Principles of prism stereoscope. Fig. 17.10 | Principles of reflecting (mirror)
stereoscope.
7. Holmes stereoscope
8. Keystone stereoscope
9. Asher law stereoscope
The two pencil test does not require any special instruments. Two pencils are about 6 in.
long each or any thin cylindrical stick will suffice. The examiner holds a pencil at about an
arm’s length in front of the patient who has similar pencil in his hand. The patient is asked
to touch the tip of the pencil with the bottom end of his pencil. The patient should be
able to touch the tip with his pencil when both eyes are open but not with one eye closed.
Commonly used stereoscope is Titmus Fly test.
To test stereopsis with a synoptophore special slides are used; they look similar but
have minor differences. The slide on right tube sees more towards right and slide on
the left tube sees more towards left.
Advantages of binocular single vision are as follows:
1. Binocular vision is better than uniocular vision
2. Binocular field is larger
3. Binocular vision gives stereopsis
4. Binocular single vision compensates for blind spot and other binocular defects
MADDOX ROD TEST
This instrument presents dissimilar images to the two eyes at a time, one red streak
and one white light. This dissociates the eyes resulting into diplopia.
Maddox rod consists of six or seven hemicylinders arranged side by side (Fig. 17.11).
They are fitted in a metal frame like any other trial lens. One surface is corrugated,
whereas the other surface is plane. Generally, the colour of Maddox rod is red but can
Fig. 17.11 | Maddox rod.
No horizontal phoria No vertical phoria
Right hyperphoria
Exophoria; corrected corrected with prism
with prism base in base down before OS
Right hyperphoria
Esophoria; corrected corrected with prism
with prism base out base up before OS
Fig. 17.12 | Maddox rod test.

be white also. The cylinders have power only at right angles to their long axis, thus when
light passes through a Maddox rod parallel rays are converted in to a streak instead of
a point. This converts a white light in to a red streak.
Maddox rod can be rotated through 360⬚ if required. While using, the flat surface
is put towards the eye of the patient. The test can be done at 6 m and 33 cm.
The instrument is used to measure ocular deviation both in phoria and tropia. Phoria
and tropia cannot be differentiated by this method. Traditionally this test is used to
measure phorias only.
To perform the test the room is darkened (Fig. 17.12). Patient puts on the trial
frame. Maddox rod is put in front of right eye with its axis at 180⬚. This gives a verti-
cal streak. The other eye is kept open and the patient looks at a white light. When he
sees through the Maddox rod, it looks like a red streak. To the other eye the fixation
light looks like any ordinary bulb. If there is no phoria, the streak passes through the
white light in all meridians through which the Maddox rod is rotated. If the streak
passes on the left of the light this means exophoria and crossed diplopia; if it passes on
right side of the light it means esophoria. Similarly in hyperphoria the streak will pass
below the white light. Angle of deviation is equal to distance of the streak from the light
which can be measured by a suitable prism—for exo-deviation the prism is put base in
and in eso-deviation the prism is put base out, in hyper-deviation, the prism is put base
down. In a very dark room, deviation can be measured roughly on Maddox tangent.
To perform the test, the patient should have good enough vision to see both the red
streak and white light. If the patient has error of refraction, the distant correction should
be incorporated in the trial frame. The child should be mature enough to correlate the
position of the streak to the light. There should be normal retinal correspondence.
RED GLASS TEST AND MADDOX TANGENT
This also dissociates the two images thus producing diplopia. Here instead of a Maddox
rod, a red glass which is generally used to test diplopia is utilised. The red glass is put
in front of the eye with better vision; the other eye is kept open. The patient is asked
to look at a tangent scale. The tangent scale (Fig. 17.13) consists of two black wooden
or metallic sheets, one longer which is horizontal and one shorter which is vertical, at
right angles to each eye. A small white point of light is placed at the intersection of the
two arms. This is the point of fixation. The horizontal and vertical arms are marked in
degrees from 1° to 10° horizontally and 1⬚–5⬚ vertically. One is nearer to the point of
fixation. There are two types of marking, the large ones for examination from 5 m and
small ones for examination from 1 m. When the eye looks through red glass, the light
looks like a red spot. The patient is asked to fix the white light; if there is no phoria,
the red spot will overlap the white light; otherwise it can be either on the left or right
of the white light. Position of red spot is measured directly on the scale.
The examination is performed in a dark room; the red glass should be dark enough
so that the patient sees the central white light as a red spot and not the white letters
•
3
•
2
•
1
5 • 4 • 3 • 2 • 1 • 0 • 1 • 2 • 3 • 4 • 5
20 18 16 14 12 10 8 7 6 5 4 3 2 1 0 1 2 3 4 5 6 7 8 10 12 14 16 18 20
1
•
2
•
3
•
Fig. 17.13 | Maddox tangent scale.

on the scale. If the glass is lighter, the patient will see two images of the outline of the
scale that produces confusion. Like Maddox rod test this also fails to differentiate between
phoria and tropia. The patient should be cooperative for the test.
Measurement of phoria for near is done by the Maddox Wing and Cover test while
the patient fixes a near object.
MADDOX WING TEST
The principle of this test is presenting two dissimilar images to the two eyes simultane-
ously, causing diplopia for near (Fig. 17.14). The instrument consists of a black square
panel on which the numbers are inscribed in a horizontal and a vertical line at right
angles to each other. These lines do not bisect each other. The horizontal line is slightly
above the midline of the panel. Under the horizontal numbers is a white arrow, the tip
of which corresponds with zero of the horizontal numbers. The zero is not in the mid-
dle of the horizontal line. It is shifted slightly towards right. The letters on the right of
the arrow are marked as 1, 3, 5, 7, etc. up to 15. Letters on the left are 2, 4, 6, etc. up
to 22. Letters on the right of the arrow denote esophoria and the left letters denote
exophoria. Similarly the vertical rows of letters denote vertical deviation and are mea-
sured by a red arrow, which is parallel to the horizontal line and on the right side of
the panel. The vertical row of numbers cut the horizontal row at the level of number 8.
The zero of the vertical row is below the horizontal line at the level of 8. Upper vertical
Left Hyperphoria
22
20
18
16
14
12
10
22-20-18-16-14-12-10-8-6-4-2-0-1-3-5-7-9-11-15
8
Exophoria 6 Esophoria
4
incy
2
0
1
excy
3
5
7
9
11
13
Right Hyperphoria
Notations in Maddox wing
Fig. 17.14 | Maddox wing.

letters denotes vertical deviation of the left eye, i.e. left hyperphoria. The lower vertical
letters measure right hyperphoria. The panel is fixed at one end of two rigid metallic
walls that converge towards the other end; the converging end terminates into two see-
ing apertures similar to a trial frame. The distance between the trial frame and the panel
is 30 cm. There is a vertical slanting partition that divides the panel in such a way the
right eye can see only the white arrow and horizontal numbers.
The left eye can see only the red arrow and vertical numbers. The whole of the
instrument has a rigid frame to which a handle is fixed. To use the instrument the
patient holds the instrument in one hand and brings it near the eye so that the bridge
of the trial frame sits on the nose bridge of the patient. The patient looks at the panel
through the trial frames, both eyes are kept open. To test phoria the patient is asked
to see through the viewing hole and tell against which letters the white and red arrows
are positioned. The white arrow measures horizontal phoria the red arrow measures
vertical phoria. Corrected glasses can be incorporated in the viewing slot.
MEASUREMENT OF CYCLODEVIATION
Cyclodeviations are far less common than horizontal or pure vertical deviations
but are most troublesome as far as symptoms and correct diagnosis are concerned.
Cyclodeviation can be latent or manifest. Manifest cyclodeviation is detected by the
cover test and measured by prism with appropriate base. Cyclophorias are measured
by Maddox double prism and double Maddox rod tests.
Maddox Double Prism

The instrument consists of two clear prisms of 4 prism dioptre each mounted in a trial
lens held base to base (Figs 17.15–17.17). When the patient looks at a horizontal line
through the double prism (the other eye is occluded), he sees two lines; the lines look
parallel to each other but shifted vertically away from each other. When the patient
opens the other eye, the line viewed by the eye that does not have double prism in
front will be seen in between two lines and parallel to them, if no cyclophoria is pres-
ent. In presence of cyclophoria the intermediate line will be oblique.
The test is done in a normal room light. It is only a qualitative test and cannot differ-
entiate between phoria and tropia. Quantitative test is done by Maddox double-rod test.
A B
Fig. 17.15 | Maddox double prism.

Double Maddox Rod Test

Double Maddox rod test is a quantitative test for measurement of both cyclodevia-
tions, e.g. cyclophoria and cyclotropia (Fig. 17.18). The appliances required are a good
trial frame, a red Maddox rod, a white Maddox rod, a 6 D prism, a white fixation light
Fig. 17.16 | Principles of Maddox double prism.
No cyclophoria Right incyclophoria Right excyclophoria
Fig. 17.17 | Interpretation of Maddox double prism.
Red Maddox rod in

front of right eye
A White Maddox rod in
front of left eye
Left Right
Left Right
Fig. 17.18 | Maddox double-rod test for cyclodeviations.

in a dark room. Red Maddox rod is put in front of the eye suspected to have cyclode-
viation; white Maddox rod is put in front of the other eye. Both are positioned in such
a way that their axes are at 90⬚ angle of the trial frame. The prism is put behind the white
Maddox rod to separate the two images. If there is already a vertical deviation, the prism
need not be used. In case of orthophoria, two streaks, one white and other red will be par-
allel to each other. In case of cyclodeviation the red streak will be inclined to the white line.
The red rod is now rotated until both the lines are parallel. This will give the magnitude
and direction of cyclodeviation. It does not differentiate between phoria and tropia.
SUPPRESSION AND ECCENTRIC FIXATION
Suppression is an acquired cerebral function that is used by the patient to avoid con-
fusion and diplopia. A patient may not be aware of suppression. It may be present
even in a straight eye, associated with amblyopia and abnormal retinal correspon-
dence. A patient may have alternate or uniocular suppression. Suppression scotoma is
present only in tropias, both eso and exo. The suppression scotomas prevent diplopia.
Suppression takes place only when both eyes are open and only in the eye that is
deviating at the time of examination. Vision in such an eye is always poorer, depth of
suppression varies in various gazes and with intensity of illumination.
Suppression is tested by:
1. Worth four dot test
2. Prism 4 PD base out test
3. Red glass test
4. Synoptophore
Worth Four Dot Test

The equipment consists of a self-illuminated panel of two green, one red and one white
light arranged in diamond pattern (Fig. 17.19A). The spots are of the same size and
intensity of illumination is equal in all spots. The test is generally done at 6 m but can
be done at 1 m with dots mounted on a flash light. The patient should have fairly good
vision and should put on best corrected glasses. Patient wears a red-green glass; red in
front of the right eye. When the patient looks through the red glass, he can see only the
red spot, the white spot looks pink. While looking through the green glass the patient
can seen only green spots, the white spot looks light green. When a normal patient
looks with both eyes open, he sees two green, one red and one mixture of red and green.
A B C D
Fig. 17.19 | Worth four dot test.

In case of left suppression, the patient will see two red lights (Fig. 17.19B). When
there is right suppression patient will see three green lights (Fig. 17.19C).
If the patient sees five lights in presence of ocular deviation, the patient has diplopia
and normal retinal correspondence (Fig. 17.19D).
If a patient sees four spots in presence of ocular deviation the patient has anom-
alous retinal correspondence.
Worth four dot test is only a gross test. It cannot be used in deep amblyopia.
Base Out Prism Test

This is used to detect suppression in small-angle esotropia and surgically corrected large
angle squint.
The patient fixes a small source of light with both eyes open; a four dioptre prism
with base out is quickly slipped in front of the right eye and the observer looks for any
movement of the left eye. The test is repeated by fixing the light with the right eye and
placing the base out prism in front of the left eye.
Red Glass Test

A patient with deviation and normal vision in each eye should experience diplopia
unless he is either ignoring it or suppressing it. If the patient fixes a white light and a
red glass is put in front of the deviated eye, the patient will become aware of the sec-
ond image as a red light. If there is deep suppression only white light will be visible.
Synoptophore
Special slides are used to detect suppression on a synoptophore. Depth of suppression
can be measured by altering the illumination of the slides.
ABNORMAL RETINAL CORRESPONDENCE (ARC)
A person is said to have normal retinal correspondence (NRC) when anatomically

corresponding areas of the two eyes correspond with each other. Abnormal retinal cor-
respondence is a crude method of retaining binocular vision in squint. In abnormal
retinal correspondence an extra-foveal area of the squinting eye and fovea of the fix-
ing eye have a common visual direction. Magnitude of ARC depends upon age of the
patient and duration of squint. ARC develops early in children and in squint of long
duration. It develops more in microtropia than large-angle squint.
It is diagnosed by:
1. Bagolini striated glasses
2. Worth four dot test
3. Synoptophore
4. After image test
Suppression, one eye Straight eye, central Foveal suppression, NRC in deviated eye
fixation NRC straight eye—NRC,
squint-ARC
Fig. 17.20 | Bagolini striated glass test.
NRC Central fixation Right esotropia ARC— Right exotropia ARC—

uncrossed (homonymous) crossed (heteronymous)
diplopia diplopia
Fig. 17.21 | Hering–Bielschowsky after image test.

Bagolini lenses are plane glasses; on one surface multiple parallel lines are etched.
When a spot of light is seen through a Bagolini glass, the spot is converted into a streak.
The glasses are mounted on a usual trial frame. Test is done at 33 cm and 6 m. Both
eyes are kept open, corrective glasses should be added if needed. The lenses are put one
in front of each eye. The lens in front of the right eye is positioned in such a way that
the lines are at 45⬚ axis and the left eye at 135⬚ axis (Fig. 17.20).
If the patient sees only one slanting line, the other eye is suppressed. If the lines
cross each other in a perfect cross, the eyes are straight and have central fixation, patient
has normal retinal correspondence.
If there is a deviation and a perfect X, the patient has abnormal retinal correspondence.
After Image Test (Hering–Bielschowsky Test)

(Fig. 17.21)
A shining vertical light is thrown on the fovea of the right eye and a similar horizontal
light is thrown on fovea of the left light. Intensity and size of the light beams and dura-
tion should be the same. After the foveae have been exposed to light for 20 s, the
patient looks at a fixation point. Patient with central fixation and normal retinal cor-
respondence will see a perfect cross of two after images with a central gap. A patient with
ARC and right exotropia with central fixation will see the vertical after image shifted
to right. In case of esotropia the vertical line is shifted to the left.
ECCENTRIC FIXATION
A normal eye when looking at an object gets an inverted image of the object on the
macula; this is central fixation. In a squinting eye which is amblyopic, light reflexes
are decentred when the other eye is occluded. The image is formed at places other than
the fovea. This is called eccentric fixation. This is a uniocular phenomenon. When images
are being formed on each fovea, it is called central fixation otherwise eccentric. A posi-
tion in between central and eccentric fixation is called eccentric viewing. According to
the position of the image, the eccentric fixation has been classified as: Para-foveal, para-
macular, peripheral and paradoxical.
Eccentric fixation depend upon multiple factors like angle of deviation, age of onset
of squint, type of squint and age of onset of amblyopia.
Eccentric fixation can be diagnosed by (1) corneal reflex test and (2) visuscope
(visuoscope).
Corneal Reflex Test for Eccentric Fixation

Here the corneal reflex is decentred but does not move on covering the dominant eye.
It may be influenced by angle kappa.
Visuscope (Visuoscope)
This is a specially designed ophthalmoscope that has a star incorporated in the beam
of light. First the patient is examined for the presence of squint and/or amblyopia. The
patient is asked to close the dominant eye, light from the visuscope is thrown through
the dilated pupil on the macula and the patient is asked to fix the star projected on
the macula. In central fixation the star will be superimposed on the macula and will
remain on the macula, so long the fixation is maintained; otherwise the star will drift
away from the macula. As per the position of the star in relation to the fovea, it is clas-
sified as paracentral, parafoveal etc.
AMBLYOPIA
Amblyopia is a very common disorder seen in squint. It has been defined in various
ways. It denotes a decrease in vision in an otherwise normal eye that cannot be improved
by correcting glasses. Fundus examination and other tests like colour vision, pupillary
reactions are normal. It develops more commonly in children. It is important that
amblyopia is detected early and treated before it becomes irreversible.
➤ In all cases of squint, amblyopia should be suspected unless proved otherwise
Diagnosis
Vision in an amblyopic eye is less than that in the normal eye by two to three lines.
Crowding phenomenon—The patient may not be able to read a complete line but
when letters from same line are presented separately, patient has no difficulty in
recognising the letters.
Missing parts of the letters—An amblyopic eye may miss a part of the letters in
Snellen’s chart, e.g. E looks like F, T or I, and C, G and Q look like O.
Error of refraction—Refraction must be done under complete cycloplegia.
Hypermetropia and hypermetropic astigmatism are more common than myopia.
Anisometropia is common in amblyopia.
Fundus—Fundus changes do not contribute to amblyopia.
Strabismus—Amblyopia can develop in any squint but is more common in
esodeviation.
Neutral density filter—A neutral density filter reduces vision in a normal eye by
two or three lines. In case of organic amblyopia, vision is reduced by five or six
lines. In case of functional amblyopia (reversible) it may remain unchanged or may
even improve.
Eccentric fixation test by visuscope is positive.
EXAMINATION OF HETEROPHORIA (LATENT SQUINT)
As the name suggests, patient and onlookers are not aware of a deviation. Small degree
latent squints (phorias) may be symptomless. Adults can tolerate up to 10⬚ of heteropho-
ria without any symptoms, children are asymptomatic for even larger deviations.
Types of Horizontal Phorias

Esophoria:
(a) Convergence excess—esophoria more for near
(b) Divergence weakness—esophoria more for distance
(c) Non-specific—equal for near and distance
Exophoria:
(a) Convergence weakness—exophoria more for near
(b) Divergence excess—exophoria more for distance
(c) Non-specific—equal for near and distance
Symptoms of Heterophoria
Asthenopia—Asthenopia is the commonest symptom.
Blurred vision—Vision is generally good in phorias, subnormal vision in phorias gen-
erally correctable. However, patient may experience blurred vision in the direction of
maximum phoria. The patient may have difficulty in distant vision if deviation is
greater for distance; patient may have reading difficulty in convergence insufficiency.
Vertical phorias and cyclophorias are more troublesome than horizontal phorias.
Measurement of phoria—Maddox tangent scale, Maddox rod and Maddox wing are
used.
Refraction—All types of errors of refraction are possible. Hypermetropia is more

likely to produce esophoria while myopia produces exophoria. An uncorrected
presbyopia may cause exophoria.
Amblyopia—Amblyopia is absent in phorias.
Dissociating factors that can break down phoria into tropia are:
1. Short-term occlusion: cover–uncover test
2. Prolonged occlusion: pad and bandage
3. Shape difference: Maddox rod test
4. Colour difference: Worth four dot test
5. Asthenopia
Main causes of asthenopia are:
1. Uncorrected error of refraction
2. Presbyopia
3. Muscle imbalance
4. Convergence insufficiency
Symptoms of asthenopia are eyestrain, blurred vision, intermittent diplopia, headache,
pain in and around the eyes, watering, unexplained redness especially after near work.
To differentiate between a refractive and a muscular cause, patch one eye during near
vision for 1 week. If asthenopia persists, it is due to an error of refraction.
EXAMINATION OF A CASE OF HETEROTROPIA
For examination of any ocular deviation a fixed protocol is followed that may vary
from clinician to clinician. A rough outline consists of the following:
History
1. Age of onset: congenital, infantile, childhood or adult
2. Sudden or gradual: Sudden heterotropias are generally paralytic or a phoria may suddenly
break into tropia
3. Diplopia is generally seen in paralytic squint
4. Family History: Concomitant squint has a strong hereditary background that lacks in paralytic
squint
Inspection
The observer stands at a distance of 1–2 m and observes the child, without touching,
in a diffuse light. This makes the child cooperative and the following points are noted.
(a) Is either eye misaligned (squint)?
(b) Does the same eye squint constantly?
(c) Does squint shift to the other eye (alternation)?
(d) Direction of deviation
(e) Width of interpalpebral aperture
(f) Abnormal head posture

● Face turn: right/left
● Position of chin: elevated/depressed
● Tilt of head: towards right shoulder or left shoulder
● A combination of the above
Abnormal head posture is rarely seen in a purely concomitant squint. Presence of an abnor-
mal head posture in a concomitant squint denotes spread of comitance in paralytic squint. It
may be present in a congenital anomaly, e.g. Brown’s syndrome. Abnormal head posture is a
characteristic of recent paralytic squint
(g) Facial asymmetry: Asymmetry of face is common with superior oblique mal-development and
cranio-facial abnormality
(h) Is it a real squint? Epicanthus produces pseudo-esotropia, which is neutralised by obliterating
the epicanthus. Negative angle kappa produces esotropia while positive angle kappa presents
as pseudo-exotropia
(i) Once it has been decided that it is a real squint, it should be ascertained whether it is a con-
comitant or paralytic squint
Measure squint in primary position by:
● Hirschberg test
● Prism and cover test
● Synoptophore
(j) Measure squint in

● Up gaze—A/V phenomena
● Down gaze—A/V phenomena
A esotropia—convergent squint decreases in down gaze and increases in up gaze

A exotropia—divergence increases in down gaze
V esotropia—convergence is more in down gaze
V exotropia—divergence is more in up gaze
Note: Deviation is measured by prism and cover test (Fig. 17.22)
While examining A/V phenomena the eye is moved 25⬚ up and 35⬚ down
(k) Vision is examined in both eyes separately and together; with and without glasses. The power
and type of glasses is noted
(l) Refraction—All cases of squint need not have errors of refraction. Hypermetropia is more
likely to produce esotropia; myopia is generally present with exotropia. However, the reverse
is also possible
(m) In children below 10 years of age refraction should be done under atropine
Exotropia Esotropia
more in up gaze more in up gaze
MR MR
LR LR LR LR
MR MR
Esotropia Esotropia
more in down gaze more in down gaze
over action of IO over action of SO
Fig. 17.22 | A and V pattern in horizontal strabismus.

(n) Measurement of AC/A or accommodative convergence—convergence ratio. It is a ratio that

denotes how many prism dioptres of convergence is produced for each dioptre of accom-
modation. The normal ratio is 4 D of convergence for each dioptres of accommodation.
Following are the methods to measure AC/A
● Heterophoria method: Patient’s interpupillary distance is measured in centimetres (PD).
Distant deviation (D) is measured in prism dioptre, near deviation (N) is measured simi-
larly at 1/3 m. AC/A is calculated by the formula:
AC/A ⫽ (PD) ⫹ (N ⫺D)/near fixation distance in dioptre
Note:
1. As the name suggests this test is suitable for phoria only
2. Measurement of deviation is done by prism and cover test
3. By convention, esodeviation is given (⫹) sign and exodeviation (⫺) sign for calculation
● Lens gradient method: In this method deviation is measured by prism and alternate cover.
The patient should wear full refractive correction. After the deviation has been noted, addi-
tional convex or concave lenses of three dioptre are put in front of each eye. Convex lens
reduces accommodation as well as convergence for a given distance. Concave lenses
increase both for a given distance. Deviation is measured in the usual way, either with ⫹3 D
or ⫺3 D. AC/A is calculated by following formula:
AC/A ⫽ (⌬2 ⫺ ⌬1)/D
where ⌬1 is original deviation in prism dioptre, ⌬2 is deviation in prism dioptre after put-
ting the lenses and D is the power of new lens in dioptres
● Synoptophore method: Patient’s interpupillary distance and angle of deviation is measured
using slides for foveal fixation. ⫺3 D lenses are inserted in the lens holder in front of each
eye and measurements are repeated. AC/A is calculated by the same formula.
AC/A ratio is normal, when measurements for distance and near are equal. It is low when
measurement for distance is more than the measurement for near and high when meas-
urement for near is more than for distance
(o) Grades of vision
(p) Abnormal retinal correspondence
(q) Eccentric fixation
(r) Tests for amblyopia
Causes of restrictive squint:
● Ocular Graves’ disease (dysthyroid myopathy/orbitopathy)
● Fracture orbit
● Moebius syndrome
● Brown’s syndrome
Table 17.2 Comparison between paralytic and restrictive squint
Features Paralytic Restrictive
Onset Sudden Gradual

Laterality Generally unilateral May be bilateral
Movement Restricted in the direction of Restricted in the
action of involved muscle opposite direction
Ductions and versions Duction more than version Equal
Forced duction test Negative Generally positive
● Strabismus fixus
● Congenital fibrosis of muscles
● Pseudo-tumour of orbit
● Excessive resection of muscle
● Encircling operation for retinal detachment
● Duane’s retraction syndrome (sometimes)
● Long-standing chronic external ophthalmoplegia
● High axial myopia
Miscellaneous causes of ocular deviation:

1. Duane’s retraction syndrome
2. Myasthenia gravis
5. Double depressor palsy
Paralytic squint may result in the following combination of cranial nerve palsy (Table 17.3):
1. Single nerve supplying single extra-ocular muscle
(a) Isolated sixth nerve
(b) Isolated fourth nerve
2. Single nerve supplying multiple extra-ocular muscles
(a) Total third nerve palsy—SR, MR, IR, IO, LPS, iris and ciliary body
(b) Partial third nerve palsy
● Upper division: LPS and SR
● Lower division: MR, IR and IO
● Internal ophthalmoplegia
3. Multiple cranial nerves palsy

(a) Third, fourth, sixth—Total ophthalmoplegia (very common)
(b) Third and Fourth: Ipsilateral third with contralateral fourth due to single one-sided lesion
at the junction of mid brain and pons (rare)
Table 17.3 Clinical features of various neurological syndrome
Syndrome Neurological involvement
Gradenigo’s Facial pain in distribution of first division of trigeminal with facial weakness, ipsilateral
sixth nerve palsy, conductive deafness and otitis media
Godtfredsen’s Ophthalmoplegia with hypoglossal palsy due to nasopharyngeal carcinoma
Foville’s Ipsilateral sixth, seventh nerve weakness, Horner’s syndrome, facial analgesia and
deafness (all lesions on the same side)
Millard-Gubler’s Abducent and facial palsy with contralateral hemiplegia
Weber’s Ipsilateral third nerve palsy with contralateral hemiplegia
Claude’s Ipsilateral third nerve palsy with contralateral tremors
Benedict’s Ipsilateral third nerve palsy, contralateral hemiplegia with contralateral tremors
Nothnagel’s Cerebellar ataxia with third nerve palsy on the same side
Raymond’s Ipsilateral sixth nerve palsy, contralateral hemiplegia
Kernohan notch Pupillary dilatation, contralateral paresis
Fischer’s syndrome (modified Bilateral oculomotor palsy, ataxia and areflexia
Gullian–Barre syndrome)
Jacod’s Total third, fourth and sixth nerve palsy, trigeminal neuralgia, amaurosis
(c) Fifth, sixth and seventh—Gradenigo’s syndrome

(d) Third, fourth, and sixth—Godtfredsen’s syndrome with hypoglossal palsy
(e) Sixth, seventh, dorsal pons and sympathetic—Foville’s syndrome
4. Cranial nerve with tract lesion
(a) Single cranial nerve
(b) Multiple cranial nerve
(c) Single cranial nerve with tract involvement
(i) Third nerve with cortico spinal tract involvement—Weber’s syndrome
(ii) Third nerve with red nucleus—Claude’s syndrome
(iii) Third nerve with red nucleus and cortico spinal tract—Benedict’s syndrome
(iv) Third nerve at superior cerebellar peduncle—Nothnagel’s syndrome
(v) Sixth nerve and cortio spinal tract at the level of pons—Raymond’s syndrome
(d) Multiple cranial nerve with tract lesion—sixth and seventh with corticospinal tract
lesion—Millard Gubler syndrome
EXAMINATION OF PARALYTIC SQUINT (Table 17.4)
1. Paralytic squint can be acquired or congenital

2. Only one muscle may be involved, e.g. lesion of fourth or sixth cranial nerve
3. Multiple muscles supplied by one cranial nerve may be involved
4. All extra-ocular muscles may be involved due to a lesion of third, fourth and sixth nerve
5. Generally unilateral but may be bilateral
6. There may be complete paralysis of one or a group of muscles or there may be paresis of
muscles or combination of paralysis and paresis may be present
7. Diagnosis of recent single muscle palsy is not difficult, multiple muscle involvement pose prob-
lem in diagnosis
8. Horizontal muscle palsy is easy to diagnose, while cyclovertical muscle palsy pose clinical
difficulty
9. Secondary changes in muscle may present an altogether different clinical pattern in the long
run
10. All paralytic squints of recent origin present as tropias, depending on the muscle or muscles
involved
Table 17.4 Comparison between congenital and acquired paralytic squint
Features Congenital Acquired (recent)
Onset At birth or intrauterine Sudden

Diplopia Only in paretic gaze position Present
Abnormal head posture Present, patient may not be aware. Old Position may be absent, old
photographs will show abnormal head posture photographs do not show abnormality
Past pointing Absent Common
Image tilt Absent Diagnostic
Forced duction test May be positive Absent
Comitance Spread of comitance Incomitant
Secondary muscle change May or may not be present Always present
Amblyopia Frequent Absent (may develop in children)
Hess Chart Field of same size Smaller field in affected eye
To Diagnose Paralytic Element in a Case of

Heterotropia
A. First and foremost step is to differentiate between concomitant and paralytic squint.Then, the
following steps are taken
B. History—diplopia, change in position of eye, restricted movement of eye
C. Examination
1. Vision—Vision in both eyes is noted separately and together. As children are prone to
develop amblyopia early, their vision must be monitored on every visit and steps taken to
prevent amblyopia
2. Inspection
(a) Head posture
(b) Position of globe
(c) Palpebral fissure
(d) Movement of globe
● Uniocular—duction (Fig. 17.23)
● Binocular—version and vergence (Fig. 17.24)
(e) Measurement of deviation (Fig. 17.22)

3. Refraction—especially in children, in case of esotropia
4. Fundus examination
5. Examination of III, IV, V, VI, VII and VIII CN
6. Diplopia charting
7. Forced duction test
8. Pharmacological test
9. CT, MRI and X-ray
10. Neurological examination
The conjugate movements are in red and names of the muscles are in blue
(Fig. 17.25).
Fig. 17.23 | Uniocular movement of eye.

Dextroversion Levoversion
Supraversion Infraversion
Dextrocycloversion Levocycloversion
1. Conjugate movement, movement in
the same direction
Convergence Divergence
1. Disconjugate, horizontal movements in
the opposite direction
SR IO SR (IO) SR (IO) IO SR
Dextroelevation Sursum version Levoelevation
LR MR MR LR
Dextroversion Primary position Levoversion
IR SO IR(SO) IR(SO) SO IR
Dextrodepression Deosrum version Levodepression
Fig. 17.24 | Binocular movements.
Table 17.5 Nine cardinal positions of conjugate movements and muscles involved
Dextroelevation Elevation Levo (Laevo) elevation

Rt. S.R. and Lt IO Rt SR, Rt IO Rt IO and Lt SR
LE SR, Lt IO
(Both superior recti and inferior oblique)
Dextroversion Primary Levoversion
Rt. L.R. and Lt MR Position Rt MR and Lt LR
Dextrodepression Rt IR Rt SO Levodepression
RIR and LSO LE IR Lt SO LIR and RSO
Both inferior recti and both superior oblique
Depression
A. Normal looking right B. Normal looking left
C. Mild overaction of LMR E. Mild underaction of LLR
D. Severe overaction of LMR F. Severe underaction of LLR
Fig. 17.25 | Examples of overaction and underaction of horizontal muscles.
LSR LMR LIR Crossed Uncrossed

MR LR
Adductors SR IO Abductors
IR SO
LLR LSO LIO
Fig. 17.26 | Typical diplopia chart in isolated extra-ocular muscle palsy.

Diplopia
Tests (Fig. 17.26) are done to find out:
1. Whether it is crossed diplopia or uncrossed?
2. Direction of gaze in which diplopia is maximum
3. To which eye the paralytic muscle or muscles belong?
4. Which muscle is involved?
5. Which muscle is underacting and which muscle is over acting?
6. Effect of treatment on diplopia
Points 3–5 are more relevant for cyclovertical muscles than horizontal muscles.
To pinpoint the paralysed muscle other clinical signs like abnormal head posture,
forced duction test must also be taken in to consideration.
Evaluation of Diplopia
Find out if the symptom is really diplopia or blurring of image, running of image or
jumping of letters.
Once the above points are settled, find out if the symptom is diplopia or polyopia.
In cases of polyopia bright linear or crescent-shaped lights appear as multiple images.
It is most commonly seen in early immature cataract.
Once it has been established that the patient has double vision, find out if it is
uniocular diplopia or binocular diplopia. Uniocular diplopia will disappear on closing
the affected eye only. Closure of other eye does not abolish diplopia. In contrast,
binocular diplopia will disappear on closing either eye. Commonest cause of binocu-
lar diplopia is paralytic squint and requires evaluation.
➤ In case of paralytic squint, diploma will be absent if there is very poor or absent
vision, deep amblyopia, pupillary area is covered by lid, or image is being formed
in the far periphery of any eye
False and True Images

False image is the image formed in the deviated eye at a point other than the macula.
It is blurred as compared to the true image. It may be separated from the true image
and may be tilted. Distance between the true and false images may vary at different
positions of gaze and head.
Crossed and Uncrossed Diplopia

Crossed diplopia is that diplopia in which the false image is projected across the mid-
line. The false image is formed in the direction opposite to that of the displacement, i.e.
if the globe is deviated out the false image will be formed on the inner side and vice versa.
Analysis of Diplopia (Table 17.6)

1. Separation of two images is maximum in the field of action of weak muscle
2. Find out the direction of gaze in which the separation is maximum
3. In case of vertical diplopia, only vertical separation is taken into consideration
4. In vertical diplopia find out which muscles, elevators or depressors, are at fault
5. In case of vertical diplopia if the eye is (a) abducted—rectus is at fault; (b) adducted—oblique
is at fault
6. With red glass in front of the right eye, the red image belongs to the right eye and the green
image to left eye
7. More peripheral image belongs to paretic eye.This is found out by the cover–uncover test on one
eye. Find out which of the two images disappears. The disappeared image belongs to the eye
undercover
8. Crossed diplopia is caused by paralysis of adductors of the eye, i.e. medial rectus, superior and
inferior recti. Uncrossed diplopia is caused by paralysis of abductors of the eye, i.e. lateral rectus,
superior and inferior obliques
Table 17.6 Direction of diplopia
Types of diplopia Muscle involved
Horizontal Lateral and medial recti

Cyclovertical Superior and inferior recti and obliques
Crossed Adductors—Medial rectus
Superior and inferior recti
Uncrossed Abductors—Lateral rectus
Superior and inferior obliques
➤ Superiors are intorters—SR and SO

➤ Inferiors are extorters—IR and IO
Mnemonic SINRAD (cyclovertical muscles only)

S represents superior, i.e. SR and SO, IN stand for intortion
R for recti SR, IR and AD for adduction
Thus it is summarised that: superiors will intort, inferiors will extort, Recti adduct
and obliques abduct when cyclovertical muscles are concerned. This rule does not apply
to horizontal muscles.
Sequelae of Extra-Ocular Muscle Palsy
1. Contracture of antagonist of the same side
2. Overaction of contralateral synergist
3. Secondary inhibition of contralateral antagonist
4. Spread of comitance: comitance spreads away from the weak muscle
Example (Fig. 17.25)
(a) Rt LR palsy
● Overaction of LMR
● Contracture of RMR
● Inhibition of LLR
(b) Rt SR palsy
● Overaction of LIO
● Contracture of RIO
● Inhibition of LSR
Abnormal Head Posture

Abnormal head posture consists of the following:
1. Head turn
2. Chin up or down
3. Head tilt
4. Combination
Head turn towards right:
1. Rt lateral rectus palsy
2. Rt medial rectus contracture
3. Duane syndrome type I and III
4. Lt medial rectus palsy
Head turn toward left:
1. Rt medial rectus palsy
2. Left lateral rectus palsy
3. Left medial rectus contracture
4. Duane’s II and III
Causes of head turn in restricted medial movement:
1. Third nerve palsy
2. Duane syndrome II and III
3. Lateral rectus contracture

4. Medial rectus palsy
Causes of head turn in restricted lateral movement:
1. Sixth nerve palsy
2. Medial rectus contracture
3. Duane syndrome I and III
Other causes of head turn are infantile esotropia with nystagmus and sometimes DVD.
Causes of elevation of chin following ocular motility defect:
1. Superior rectus palsy
2. Inferior oblique palsy
4. A—Esotropia
5. V—Exotropia
6. Brown syndrome
7. Thyroid myopathy
8. Fracture floor of orbit
Causes of depression of chin:
1. Inferior rectus palsy
2. Superior oblique palsy
3. V—esotropia
4. A—exotropia
5. Thyroid myopathy
Causes of ptosis with tropia Congenital ptosis is very often associated with mal-
functioning of superior rectus. It could be unilateral or bilateral.
Bilateral causes are:
1. Congenital ptosis
2. Bilateral third nerve palsy
3. Myasthenia (elevation of eye may be normal)
4. Chronic progressive external ophthalmoplegia
Unilateral causes are:
1. Congenital ptosis
2. Unilateral third nerve palsy
3. Double elevator palsy with ptosis
Causes of sudden esotropia:
1. Sixth nerve palsy
2. Infantile esotropia
3. Decompensated esophoria
4. Uncorrected hypermetropia
Causes of limitation of adduction—Adductors of the eye are medial, superior and infe-
rior recti. Paralysis or paresis of these muscles will cause limited adduction. They are:
1. Isolated palsy of these muscles or complete third nerve palsy
2. Myasthenia
3. Thyroid myopathy
4. Disinsertion of medial rectus
5. Internuclear ophthalmoplegia
6. Excessive resection or fibrosis of lateral rectus
Causes of limited abduction—Abductors of the eyeball are lateral rectus and the obliques.
Paralysis or paresis of these will prevent the eye from moving externally. They are:
1. Lateral rectus palsy (Plate 17.3)
2. Medial rectus entrapped in fracture of medial wall of orbit
3. Laceration, disinsertion or slipped lateral rectus
4. Essential infantile esotropia
6. Moebius syndrome
7. Thyroid myopathy
Restriction of elevation—Superior rectus and inferior oblique are the elevators of
eyeball. Paralysis or paresis of these muscles will restrict upward movement of the eye-
ball (Plate 17.4). The causes can be neurological or restrictive. They are:
1. Superior rectus palsy—Isolated or with LPS
3. Inferior oblique palsy
4. Brown syndrome
5. Myasthenia
6. Thyroid myopathy
7. Blow out fracture of orbital floor
8. Fibrosis of inferior rectus
9. Myositis
10. Pseudo-tumour of orbit
Restriction of depression of eyeball—Inferior rectus and superior oblique are the depres-
sors of the eyeball. Paralysis or paresis of these muscles will prevent downward move-
ment of the eyeball. The causes can be neurological or restrictive. They are:
1. Paralysis of inferior rectus
2. Paralysis of superior oblique
Plate 17.3 | Limited abduction left eye. Plate 17.4 | Bilateral limited elevation.
3. Myasthenia
4. Trauma to superior oblique or inferior rectus
Forced Duction Test

This test is of great value in differentiating between neurological and mechanical causes
of restriction of ocular movement. Some mechanical causes are given below.
Contracture of muscle, fibrosis of muscle, excessive shortening of muscle following
surgery, thyroid myopathy, fracture floor or medial wall of orbit, congenital fibrosis of
interior rectus.
In adults, the test is done under local anaesthesia and in children, under general
anaesthesia.
The conjunctiva is fully anaesthetised with three or four installations of 4% Xylocaine.
A cotton applicator dipped in local anaesthesia may be handy if the patient complains
of discomfort; in that case the cotton applicator is pressed on the conjunctiva just ante-
rior to the insertion of muscle that is being tested. The patient is asked to look at his
own outstretched hand; the outstretched hand is used to move the eyeball. The eye is
grasped with a toothed forceps near the limbus. The grip should include the conjunc-
tiva and episclera. Otherwise, the conjunctiva may be lacerated.
The eye is moved in the direction opposite to the one in which mechanical restric-
tion is suspected, i.e. the eye is moved medially to test mechanical restriction of lateral
rectus. While doing the test the globe should not be pushed in the orbit because this
gives a false sense of normal ocular motility in presence of mechanical restriction.
Forced duction test should be performed before and after every squint surgery.
Pharmacological Test in Paralytic Squint

Tensilon Test
This is a diagnostic test for myasthenia gravis. It is not very specific because some non-
myasthenic patients may also give a false positive test. Test should be done when the
symptoms are obvious. It consists of intravenous injection of fast-acting anticholine
esterase drug edrophonium hydrochloride (tensilon). The drug is available in 1 ml vial
containing 10 mg of drug.
Procedure—Inject 0.4 mg of atropine sulphate IM 15 min before starting the actual
test; this prevents undesirable side effects of Tensilon, e.g. colic, bronchospasm, bradycar-
dia and angina. Take 1 ml of Tensilon in a tuberculin syringe, inject 2 mg in vein and flush
it with normal saline. Wait for 2 min for any change. If improvement occurs, the result is
considered significant. If no response or very little response is visible, the remaining 8 mg
is injected quickly and flushed with normal saline. In a positive result ptosis will vanish,
diplopia will disappear, movements will improve. There are three types of responses:
1. Improvement in ptosis and tropia—Ptosis is either abolished or becomes milder. Large mani-
fest squint becomes smaller or may disappear
2. Worsening—ptosis and tropia increase
3. Reversal—A left hypertropia becomes right hypertropia. Response 2 and 3 may be seen in
non-myasthenic patients also
If tensilon is not available other anticholine esterase drugs can be given either intra-
muscular or intravenously. In intramuscular injection response is delayed. Commonest
used drug is prostigmine.
Causes of generalized limitation of ocular movement (they can be uniocular or binocu-
lar, equal or asymmetrical):
1. Thyroid myopathy
2. Myasthenia
4. Chronic progressive external ophthalmoplegia
6. High myopia—axial length more than 30 mm
7. Progressive supranuclear gaze palsy
Causes of painful ophthalmoplegia: Generally all muscles are involved but sometimes
only third nerve palsy may present with pain. It could be unilateral or bilateral.
1. Superior orbital fissure syndrome (Tolosa Hunt syndrome)
2. Gradenigo syndrome
3. Diabetic oculomotor palsy
4. Oculomotor palsy due to aneurysm of posterior communicating artery
5. Myositis (Pseudo-tumour)
6. Acquired Brown syndrome
7. Orbital tumours
8. Parasellar tumours
9. Fungal granuloma of orbit
Characteristics of medial rectus palsy:
1. Exotropia
2. Diminished adduction
3. Head turn towards contralateral side
4. Overaction of lateral recti
5. Crossed horizontal diplopia
6. Rarely, may be associated with ptosis
Characteristics of lateral rectus palsy: can be congenital or acquired. Isolated lateral
rectus palsy has no localising value.
1. Esotropia
2. Diminished abduction (Plates 17.5 and 17.6)
3. Overaction of medial rectus of both eyes
4. Head turn towards the side of paralysis, e.g. in right lateral rectus palsy head will be turned
towards right side
5. Uncrossed horizontal diplopia
6. Differential diagnosis consists of Moebius syndrome, Duane’s retraction syndrome, essential
infantile esotropia and entrapment of medial rectus
Characteristics of superior rectus palsy:
1. Hypotropia of ipsilateral eye
2. Hypotropia increases in field of involved SR
3. Excyclotropia
Plate 17.5 | Limited abduction left eye. Primary position and

left gaze.
Plate 17.6 | Limited abduction left eye. Primary position
and left gaze.
4. Overaction of ipsilateral inferior rectus and contralateral inferior oblique

5. Ipsilateral ptosis
6. Pseudo-ptosis due to hypotrophic position of the eye when L.P.S. has good function
7. Elevation of chin
8. Bielschowsky test with head tilt may be positive
9. Diplopia—vertical crossed diplopia
Differential Diagnosis
Double elevator palsy, inferior rectus fibrosis, entrapment of inferior rectus, myasthenia,
thyroid myopathy, contralateral superior oblique palsy may produce pseudo-paralysis
of SR.
Characteristics of Inferior Rectus Palsy

1. Ipsilateral hypertropia
2. Hypertropia increases in the field of involved inferior rectus
3. Incyclotropia
4. Overaction of ipsilateral superior rectus and contralateral superior oblique
5. Depression of chin
6. Pseudo-ptosis of the sound eye
7. Bielschowsky head tilt test may be positive
8. Diplopia—vertical crossed and image tilted
Superior Oblique Palsy

This can be congenital or acquired, unilateral or bilateral. Bilateral superior oblique palsy
is generally acquired and neurological. It is sometimes not obvious and its presence has
to be unmasked. Congenital SO palsy is generally due to anatomical misalignment of
the tendon and is unilateral. The features are:
1. Hypertropia of involved eye
2. Maximum hypertropia on adduction
3. Ipsilateral excyclotropia
4. Head tilt and turn towards uninvolved side
5. Overaction of ipsilateral inferior rectus and contralateral superior rectus
6. Bielschowsky head tilt test is diagnostic
7. There may be depression of chin
8. Vertical uncrossed tilted diplopia
9. Diplopia is more for near work
10. There may be asymmetry of face in congenital palsy
11. Old photographs may show abnormal head posture in congenital palsy
Inferior Oblique Palsy

Isolated inferior oblique palsy is very rare. When present it is mostly congenital. Less
common cause is trauma to the muscle itself. The features are:
1. Hypotropia of involved eye
2. Hypotropia increases in adduction
3. Incyclotropia
4. Chin is elevated
5. Head tilt towards paralysed side
6. Bielschowsky test is diagnostic
7. Overaction of ipsilateral superior oblique and contralateral superior rectus
8. Vertical uncrossed tilted diplopia
Diagnosis of Cyclovertical Squint

Cyclovertical squint may be caused by under action of any of the eight cyclovertical
muscles. To pinpoint the single offending muscle out of the eight muscles, i.e. supe-
rior and inferior recti and obliques of both eyes, requires three steps. The patient fixes
a distant point, prism and cover test is performed.
Step one—Cover test: Find out whether patient has right or left hypertropia in pri-
mary position. Say the patient has right hypertropia, causes of which can be attributed
to only four muscles. Two underacting, depressors belonging to right eye, i.e. RSO
and RIR; two underacting elevators belonging to left eye i.e. LSR and LIO.
Step two—Ask the patient to move the eye toward right and then left and observe
if the hypertropia increases on right gaze or left gaze.
If hypertropia increases on right gaze, number of offending muscles is reduced to
two but not in same eye. They may be RIR or LIO.
Step three—In the final step the head is tilted to right and then left to observe which
tilt produces greater hypertropia. If hypertropia increases on left head tilt, final diag-
nosis is RIR palsy.
Causes of right hypertropia:
1. Left inferior oblique palsy
2. Right inferior rectus palsy
3. Right superior oblique palsy
4. Left superior rectus palsy
Causes of left hypertropia:
1. Right superior rectus palsy
2. Left superior oblique palsy
3. Left inferior rectus palsy

4. Right inferior oblique palsy
EXAMINATION OF CRANIAL NERVES THAT

SUPPLY THE EYE AND ADNEXA
1. Cranial nerves that serve the eye and its adnexa are optic, oculomotor, trochlear, trigeminal,
abducent and facial nerves
2. Out of these oculomotor, trochlear and abducent are involved in ocular movements.The ocu-
lomotor also supplies intrinsic muscles of the eye
3. These muscles may be involved individually or in combination
4. Their involvement is generally uniocular, but may be bilateral
5. They may be involved in congenital lesions or may suffer from acquired anomalies
6. They may be associated with other neurological defects
7. The lesions can be supranuclear, nuclear, fascicular, basilar, in the cavernous sinus
and in the orbit
8. In about one-fourth cases of involvement of these nerves, no cause can be pin pointed
9. In the remaining 75% aetiology varies from congenital anomaly to neoplasm. The causes are as
follows:
(a) Vascular: Diabetes, hypertension, atherosclerosis, aneurysm, intraneural haemorrhage and
intraneural infarct. Diabetes and hypertension are the primary causes of third and sixth
nerve palsy while they are second most common cause of fourth nerve involvement.
Aneurysm is a very common cause of isolated third nerve palsy with involvement of pupil,
the commonest site being posterior communicating artery. Aneurysm as a cause of fourth
and sixth nerve lesions is less common; however, isolated sixth nerve palsy may be caused
due to aneurysm of internal carotid artery inside cavernous sinus.This is painless in contrast
to isolated third nerve palsy due to posterior communicating artery aneurysm, which is painful
(b) Trauma is the commonest cause of fourth nerve palsy but may affect the third and sixth
nerves also. It can be bilateral
(c) Inflammation—They can cause various combinations of third, fourth and sixth nerves lesions.
Common infections are tuberculosis, syphilis, otitis media and cavernous sinus thrombosis.
Acute lesions are produced by basal meningitis and herpes zoster
● Anterior cavernous sinus inflammation or inflammation in the superior orbital fissure
produces painful ophthalmoplegia—Tolosa Hunt syndrome

● Vasculitis due to polyarthritis and temporal arteritis also causes ophthalmoplegia
(d) New growth—Generally they involve the sixth nerve due to their expansion but no nerve
is immune
Oculomotor (III Nerve) Palsy

Localising Features of Third Nerve Involvement
Nuclear: can be total, unpaired or paired.
1. Nuclear involvement will have following features:
(a) Unilateral palsy of LPS, SR, IR, IO, and MR
(b) Contralateral LPS and SR
2. Midline lesion will produce bilateral LPS underaction
3. Unilateral partial third nerve palsy with contralateral underaction of SR
4. Isolated ipsilateral MR, IR IO palsy
Following Conditions Cannot be Nuclear Third Nerve Palsy

1. Unilateral ptosis
2. Unilateral third nerve palsy without involvement of contralateral SR. May or may not involve
the pupil
3. Unilateral internal ophthalmoplegia
Fascicular lesions: During its course in the midbrain, fibres of third nerve come in close
relation with various structures that produce other neurological signs. They can be:
Weber’s Syndrome
● Ipsilateral third nerve palsy
● Contralateral hemiplegia due to involvement of cortico spinal tract
Claude’s syndrome
● Ipsilateral III nerve palsy
● Contralateral ataxia and tremor due to involvement of red nucleus in the region of tegmentum
of midbrain
Benedict’s syndrome
● Contralateral hemiplegia and tremor due to lesion in dorsal mesencephalon
Nothnagel’s syndrome
● Ipsilateral cerebellar ataxia, due to lesion in superior cerebellar peduncle
Basilar lesion: Once the third nerve leaves the midbrain and travels forward to reach
the cavernous sinus, it does not come in relation with any cranial nerve. Hence basi-
lar lesions produce isolated third nerve palsy as it passes first between posterior cere-
bral and superior cerebellar arteries and courses parallel to posterior communicating
artery. Commonest cause of isolated third nerve palsy is an aneurysm of posterior
communicating artery at this site.
Features of Diabetic Third Nerve Palsy

Acute, painful, isolated or associated with other cranial nerve palsy. Third nerve palsy
may be total or partial, pupillary fibres are always spared, self-limiting, may reoccur and
may involve the other side.
Features of Posterior Communicating Artery Aneurysm

Acute, painful, isolated third nerve palsy with pupillary involvement without sponta-
neous recovery; may have signs of subarachnoid haemorrhage.
➤ An acute isolated painful oculomotor palsy with pupillary involvement in a

diabetic should arouse suspicion of an aneurysm and should be investigated
The cause of pupillary sparing in diabetic third nerve palsy lies in the position of pupillo-
motor fibres in the third nerve trunk. The pupillomotor fibres lie superficially in the supe-
rio median part of nerve trunk and get blood supply from pial vessels. Rest of the nerve
derives its blood supply from vasa nervorum, which are affected by micro-vasculopathy
in diabetes. A mass lesion like aneurysm will compress pial vessels as well as other vessels,
hence pupil is always involved in aneurysm and spared in diabetes.
Cavernous Sinus Lesion

In the cavernous sinus third nerve is involved along with fourth, fifth, sixth nerves and
ocular sympathetic resulting in ipsilateral painful multiple cranial nerve palsy. Logically
pupil should also be involved (dilated) but due to the superimposed oculo sympathetic
palsy that produces miosis the pupil comes to its usual normal size.
Orbital Lesions of Third Nerve

Involvement depends upon the size and extent of orbital lesions. If it involves both the
trunks of the third nerve then all the muscles supplied by the third nerve including
pupil will be involved. There may be involvement of fourth and sixth nerves as well.
Isolated upper division lesions will produce involvement of LPS and SR only while
similar lesions of lower division will produce underaction of MR, IR and IO along
with involvement of pupil.
Aberrant Regeneration
Aberrant regeneration of the third nerve is seen following trauma and aneurysm but
not diabetes. It produces paradoxical movement of muscles supplied by the third
nerve. It can rarely be bilateral.
Ophthalmoplegic Migraine
This is seen in children and young adults either with a past history or family history
of migraine. It consists of ocular pain, peri-orbital pain, nausea, vomiting, and oph-
thalmoplegia. Pain generally subsides with the onset of palsy. Ocular palsy generally
improves to near normal. There may be recurrent episodes.
Trochlear Nerve (IV Nerve) Palsy

Localising Features of Trochlear Nerve
1. Trochlear nerve is a unique cranial nerve
2. It has the longest intracranial course
3. It is thinnest cranial nerve
4. It is the only cranial nerve that decussates completely
5. It has the smallest fascicular course
6. It is the only cranial nerve that decussates dorsally
7. It is the only cranial nerve that emerges from the brain posteriorly
8. It is generally not affected by moderate amounts of retro-bulbar anaesthesia
9. It innervates contralateral single extra-ocular muscle, i.e. superior oblique
10. It enters the orbit through superior orbital fissure outside the annulus of Zinn
Nuclear and Fascicular Lesions of Trochlear Nerve

Fascicular part of the fourth nerve is very small and there is no other structure along its
fascicular course. Therefore, it is extremely difficult to differentiate nuclear lesions from
fascicular lesions. In the anterior medullary velum a single small lesion can involve both
the nerves. Commonest cause of bilateral fourth nerve palsy is closed head injury.
➤ If a patient with head injury complains of diplopia in the post-traumatic period,

bilateral fourth nerve involvement should be suspected unless proved otherwise
Basilar Lesions of Trochlear Nerve

The fourth nerve after emerging from the brain stem turns anteriorly around the brain
stem, under the free edge of tentorium and passes between the posterior cerebral and
superior cerebellar artery lateral to the third nerve. Basilar part is yet another position
that is subjected to blunt injury. The offending cause lies in the edge of the tentorium.
In fact, the same trauma may travel and involve the nerve in anterior medullary velum.
Cavernous Sinus Lesion

In the cavernous sinus the fourth nerve lies lateral and inferior to the third nerve; iso-
lated lesion at this level is very unlikely. It is involved generally with third, fifth and
sixth nerves.
Orbital Lesion
Fourth nerve enters the orbit via superior orbital fissure outside the annulus of Zinn
and supplies the superior oblique. Isolated fourth nerve involvement in orbit is rare;
it is generally associated with third and sixth nerves.
Superior Oblique Palsy

Superior oblique palsy can be congenital or acquired. It can be unilateral or bilateral.
Isolated superior oblique palsy is best diagnosed by the three-step test.
Clinical features of isolated superior oblique palsy are:
1. Hyperdeviation on the same side
2. Excyclodeviation on the same side
3. Limited depression on adduction
4. Depressed chin
5. Head turn to other side
6. Head tilted to other shoulder
Examination of superior oblique in the presence of third nerve palsy—Superior oblique is
a depressor, intorter and abductor. Its primary function is intortion, which is best in
abduction. In third nerve palsy the eye is already in abduction, so if the patient just
looks down, the eye will intort.
Abducent (VI Nerve) Palsy (Plate 17.3)

Localising features of abducent nerve: Abducent nerve has more similarity with the
trochlear nerve than with the other cranial nerves, i.e. it has a long intracranial course
and supplies only one extra-ocular muscle.
Isolated sixth nerve involvement has no localising importance. It can be involved as a

congenital anomaly; head injury can cause bilateral involvement.
Nuclear Lesions
Nuclear lesion of sixth nerve is always associated with ipsilateral gaze palsy due to
involvement of PPRF and facial palsy due to involvement of facial nerve fascicles, as
they encircle the sixth nerve nucleus. Hence, it is not possible to have isolated sixth
nerve palsy in nuclear lesions.
Fascicular Lesions
Three lesions are possible due to its proximity to the seventh nerve fascicle, PPRF, sen-
sory part of fifth nerve, sympathetic chain, eighth nerve and pyramidal tract. The lesions
can be dorsal, ventral and combined.
Dorsal Fascicular Lesion:
● Foville’s syndrome: It produces ipsilateral lesions comprising of ipsilateral sixth nerve palsy, horizon-
tal gaze palsy, facial paresis, facial analgesia, Horner’s syndrome and deafness
Ventral Fascicular Lesion:
● Millard–Gubler’s syndrome: It produces ipsilateral sixth and seventh nerve palsy with contralateral
hemiplegia due to involvement of pyramidal tract. If the lesion is big many of the dorsal signs
may be present. Generally there is a facial palsy rather than paresis
Combined Lesion:
● Raymond’s syndrome: This comprises features of both dorsal and ventral lesions. Commonest
cause is involvement of anterior inferior cerebellar artery causing haemorrhage or infarction.
Other causes are tumour, demyelination or chronic inflammation. It produces ipsilateral abdu-
cent palsy and contralateral hemiplegia
Basilar Lesions
Basilar lesions are more numerous and varied due to the involvement of various struc-
tures, e.g. cerebropontine angle structures, nasopharyngeal growth, clivus and apex of
petrous bone. Raised intracranial tension and trauma may produce both unilateral as
well as bilateral lesions.
● Cerebropontine angle tumour (acoustic neuroma): It produces sixth nerve palsy with loss of
corneal sensation and hearing impairment
➤ First symptom of cerebropontine angle tumour is hearing loss and first sign is
impaired corneal sensation
● Battle’s sign: It comprises of leak of blood and CSF from ears and ecchymosis over mastoid. It is
due to fracture base of skull, as in closed head injury, that may cause bilateral sixth and seventh
nerve palsy
● Raised intracranial tension: Raised intracranial tension produces bilateral sixth nerve palsy due to
downward shift of brain stem, which stretches the sixth nerve over the tip of petrous bone. It
has no localising sign. Other intracranial causes of bilateral sixth nerve palsy are tumours of the
posterior fossa and benign intracranial hypertension
Plate 17.7 | Duane’s retraction syndrome. Primary position. Plate 17.8 | Looking right, narrowing of left IPA.
Plate 17.9 | Looking left, widening of left IPA.

● Gradenigo’s syndrome: It comprises of severe pain in the distribution of fifth nerve, sixth and sev-
enth nerve palsy and deafness. It is secondary to chronic otitis media, generally seen in children
Cavernous sinus: Lesions of the cavernous sinus may produce unilateral, sometimes
bilateral, isolated sixth nerve palsy or may be involved with third, fourth, fifth and
sympathetic nerves.
Orbital: Orbital lesions produce multiple extra-ocular nerve palsy.
Causes of bilateral sixth nerve underaction:
1. Moebius syndrome
2. Raised intracranial tension
3. Benign intracranial hypertension

4. Post-lumbar puncture
5. Cavernous sinus thrombosis
6. Strabismus fixus
Congenital lesions of innervation of extra-ocular muscles:
2. Brown tendon sheath syndrome
4. Moebius syndrome
5. Marcus Gunn phenomena
6. Vertical retraction syndrome
Duane’s retraction syndrome: The eyeball retracts during horizontal movement, which
depends upon the duction of the eyeball. According to this it has been divided into
three types (Plates 17.7–17.9).
Type I: Decreased abduction, normal adduction
Type II: Decreased adduction, normal abduction
Type III: Decreased abduction and adduction
Type I is the commonest type where there is a narrowing of the interpalpebral aper-
ture on medial gaze and retraction of the eyeball. On lateral gaze there is a widening
of interpalpebral aperture. In the primary position the eye is straight. The adducted
eye moves into a position of elevation. It is more commonly seen in the left eye but
can be bilateral and hereditary. The condition is generally confused with paralysis of
the sixth nerve and esotropia in children.
N EUROLOGICAL E XAMINATION
OF THE P UPIL
Normal pupillary reaction is a kinetic indicator of normal iris, optic pathway, third
nerve and oculo sympathetic path.
Examination of the pupil is required in the evaluation of :
1. Local disorders of pupil
● Congenital
● Traumatic
● Anterior uveitis
● Glaucoma
2. Neuro-ophthalmic conditions
● Diseases of visual pathway
● Disorders of third nerve
● Disorders of autonomic nervous system
Some terms used in pupillary examination:
1. Miosis: Pupil smaller than normal

2. Mydriasis: Pupil larger than normal
3. Fixed dilated pupil: Pupil not reacting to light or near reflex
4. Anisocoria: One pupil is smaller or larger than the other, by birth or may be acquired. About 20%
of persons have anisocoria. Simple anisocoria does not produce any symptom and does not
require any treatment. Important point is to find out if anisocoria is physiological or pathological. In
pathological anisocoria, it is essential to decide if the pupil under observation is normal and other
is dilated or constricted and vice versa
5. Hippus: A physiological condition where the pupil keeps on changing size under same
illumination
6. Mydriatics: Drugs that dilate the pupil
● Centrally acting
● Locally acting
● Pure mydriatics as adrenaline, phenylephrine
● Mydriatic cum cycloplegic as atropine, cyclopentolate, homatropine and tropicamide
7. Cycloplegic: Drugs that paralyse accommodation. All cycloplegics are mydriatic also, pure mydri-
atics are not cycloplegic
8. Cyclotonic: Drugs that constrict the ciliary muscle. All locally acting parasympathomimetics are
cyclotonics
NEUROLOGICAL EXAMINATION OF THE PUPIL 279
EXAMINATION OF PUPILLARY REACTION
1. Examination of pupillary reaction does not require elaborate instruments. A simple bright flash-
light that can give both a diffuse as well as pinpoint focus is all that is required
2. A slit lamp gives information regarding subtle pupillary change in Argyll–Robertson pupil and is
helpful in eliciting hemianopic pupillary reaction and vermiform movement in tonic pupil
3. There should be an arrangement to darken the area of examination while the test is per-
formed. There is no need of a dark room
4. Following drugs should be available to evaluate autonomic disorder of pupil
(a) Weak solution of 0.125% pilocarpine
(b) 2.5% Mecholyl
(c) 4–10% Cocaine
(d) 1% Paredrine (hydroxyamphetamine)
5. Initial observation of pupil should be done in diffuse illumination. The patient looks at a distant
object and following points are noted in the eyes:
(a) Colour of iris and pupil
(b) Size of pupil
(c) Equality of pupil
6. There are two types of pupillary reactions:
(a) Light reflex
(I) Direct light reflex
(II) Indirect light reflex
(b) Near reflex
To Elicit Direct Light Reaction

Patient fixes a distant object; this eliminates accommodation-induced miosis. Light is
thrown in one eye and its reaction is observed in the same eye. It is better to keep the
other eye covered. If direct reaction is present, the pupil will immediately constrict and
remain constricted so long the light stimulus is maintained, and spring back to the orig-
inal size on removal of stimulus. If direct reaction is absent, the pupil will not constrict
and will dilate so that the size becomes larger than resting size; near reflex remains normal.
Causes of absent light reflex are:
1. Use of mydriatic and cycloplegic
3. Optic nerve lesion: severe optic neuritis, total optic atrophy, central retinal artery occlusion,
ischaemic optic neuropathy, severe trauma to optic nerve, trans-section of nerve and avulsion
of optic nerve
To elicit indirect reaction, eyes are kept open. Pupil does not constrict when light is
thrown in ipsilateral pupil but constricts when light is thrown in contralateral pupil.
Swinging Flash Light Test

Normal
Step I: Shine bright light in the eye (right). Allow it to constrict to minimum possible
size. Keep the light in position. Allow the pupil to dilate to intermediate size.
Step II: Quickly shift the light to the other eye (left), which is in state of intermedi-
ate size. This will constrict to minimum and escape to intermediate size.
Step III: As soon as the left pupil starts re-dilating, the light is swung to right eye.
Right pupil constricts as in step II. Amount of constriction, time taken to
constrict and time to re-dilate in the right eye is equal to left eye.
Abnormal indirect reaction: abnormal reaction is called Marcus Gunn pupil (relative
afferent pupillary defect, RAPD), which is said to exist if the right pupil promptly dilates
in step three and constricts to normal when light is swung back to left.
Causes of Marcus Gunn pupil are:
1. Unilateral optic neuropathy
2. Bilateral optic neuropathy when vision in one eye is grossly reduced
3. Extensive retinal damage
4. Amaurotic eye
Conditions of diminished vision that do not produce Marcus Gunn pupil are:
➤ Any degree of opacity in the media, maculopathy and amblyopia
➤ There is no bilateral Marcus Gunn pupil
Amaurotic Pupil
1. Both the pupils are of same size
2. Direct reaction in blind eye is absent
3. Consensual reaction in normal eye is absent
4. When normal eye is stimulated both pupils constrict
5. Near reflex is normal in both eyes
Near Reflex
1. This is not a single reflex
2. It is triad of:
(a) Accommodation
(b) Convergence
(c) Miosis
3. All of those components can act independently or collectively
4. Accommodation can be neutralised by convex lens and induced by minus lens. It can be abol-
ished by cycloplegia: therapeutic or neurological. Miosis can be abolished by mydriatic or cyclo-
plegic. Convergence can be modified by appropriate prisms
5. Vision is not required for near reflex
6. Absence of near reflex in presence of light reflex is not possible
7. Accommodation reflex can be present in absence of light reflex
8. There is no need to test near reflex if light reflex is present
Hemianopic Pupil
Examination of hemianopic pupil requires examination by a narrow beam of light
preferably on a slit lamp. The test is elicited by directing a beam of light on affected
side of the retina, i.e. temporal of right and nasal side of left eye.
Hemianopic pupil is seen in lesions of optic radiation and chiasma. In mid-line lesions
of the chiasma light thrown on the temporal field produces less constriction of pupil than
when nasal side is stimulated. Anterior chiasmal lesion with involvement of posterior part
of optic nerve produces Marcus Gunn pupil on the side of the involved optic nerve and
contralateral hemianopic pupil.
Reflexes that Produce Changes in Pupil

A. Bilateral miosis
B. Unilateral miosis
C. Bilateral mydriasis
Cochlear stimulus by sound produces mydriasis followed by miosis; stimulation of
cornea by touch first produces constriction followed by dilation.
Tonic Pupil (Adie’s Pupil) (Table 18.1)

This is mostly seen in females in third decade. In 80% of the cases, it is unilateral and
deep tendon reflexes are absent. The cases are diagnosed on routine examination and
may be confused with uniocular glaucoma or iridoplegia. Generally aetiology is not
known; condition does not require any treatment. It can be idiopathic or due to her-
pes zoster, varicella, temporal arteritis and syphilis. The lesion is either in the ciliary
ganglion or in the short ciliary nerve.
The affected pupil is large. Both light and accommodation reflexes are diminished.
There is relative mydriasis in bright illumination. Light reflex is either absent or minimal.
Table 18.1 Relation between size of the pupil and stimulus
Condition of the pupil Reflex Stimulus
A. Bilateral miosis Light reflex Illumination

Near reflex Accommodation, convergence
Vagotonic Expiration
B. Unilateral miosis Orbicularis Forceful closure of lid
C. Bilateral mydriasis Vestibular Caloric
Psycho sensory Psychic
Table 18.2 Comparison between Argyll–Robertson pupil and Adie’s pupil
Features ARP Adie’s
Vision Good Good

Pupil Constricted Dilated
Laterality Bilateral; may be unilateral Unilateral; may become bilateral
Effect of illumination Nil Larger in bright light
Light reflex Absent Absent/poor
Near reflex Brisk Tonic
Atropine No mydriasis Mydriasis
Miotic Constrict Constrict with very weak solution
Lesion Pretectal Ciliary ganglion
Re-dilatation of pupil is slow. Accommodation is slow. The pupil is tonic. On slit-

lamp examination, there is vermiform movement of iris. The pupil is hypersensitive to
cholinergic drugs. A normal pupil will not constrict with 0.125% of pilocarpine, but
a tonic pupil will constrict with 0.125% of pilocarpine and 2.5% mecholyl. The pupil
responds to mydriatics.
Argyll–Robertson Pupil (Table 18.2)

Characteristics of Argyll–Robertson pupil are:
1. Absent light reflex; accommodation reflex present
2. Seen mostly in fourth decade
3. Mostly bilateral
4. Almost normal vision
5. Intact near vision with correction
6. Miosis
7. Irregular pupil
8. Poor dilatation with mydriatic
9. Asymmetry of pupil
10. Patches of iris atrophy
11. Hypersensitive to miotics
12. Size of pupil does not change with intensity of light
13. Commonest cause is neuro-syphilis
14. Unilateral cases later become bilateral
Other causes that may produce Argyll–Robertson like pupillary change are as follows:
1. Juvenile diabetes
2. Multiple sclerosis
3. Trauma
4. Herpes zoster
5. Tumours
6. Mid-brain haemorrhage
7. Tuberculosis
Other causes of near-light dissociation are given below:
1. Tonic pupil
2. Rostral mid-brain lesion
3. Aberrant regeneration of third nerve
4. Advanced glaucoma
5. Extensive retinal lesion
Inverse Argyll–Robertson pupil is a rare bilateral condition. The lesion is in the mid-brain
between Edinger–Westphal and Perlia’s nucleus. Light reflex is present, near reflex is sub-
normal. Causes are diphtheria and growth near the corpora quadrigemina.
Horner’s Syndrome—Oculosympathetic Syndrome

This consists of:
1. Ptosis
2. Upside down ptosis
Table 18.3 Effect of sympathomimetic drugs in pupil at various levels of Horner’s syndrome
Drug Central Pre-ganglion Post-ganglion
4% Cocaine Poor Poor Nil

Adrenaline 1:1000 Nil Moderate Good
10% Phenylephrine Slight Moderate Good
Hydroxyamphetamine Slight Moderate Nil
3. Narrow interpalpebral aperture

4. Enophthalmos
5. Miosis
6. Heterochromia of iris
7. Warm skin
8. Brittle and dry hair
9. Action of LPS and SR normal
10. Pupil does not dilate in dark
The lesion is in the cervical sympathetic. It can be central, pre-ganglionic or post
ganglionic.
Inferences
1. Cocaine will dilate a normal pupil but not in Horner’s syndrome
2. Hydroxyamphetamine will dilate the pupil in pre-ganglion lesion but not in post-ganglion lesion
Pupil in Coma and Head Injury (Hutchinson’s Pupil)

1. In early stages of coma, pupil on the side of expanding lesion is small due to irritation of the third
nerve
2. Pupil on the side of injury dilates due to inhibition of the third nerve nucleus
3. Contralateral pupil constricts due to irritation of the third nerve
4. Both pupils dilate
Neurological Causes of Fixed Dilated Pupil

Pupil does not react to light, near reflex or accommodation
2. Mid-brain lesion
3. Oculomotor nerve trunk palsy
It may be difficult to differentiate between trunk lesion and nuclear lesion
4. Lesion at ciliary ganglion
5. Lesion of short ciliary nerve
IMPORTANT POINTS TO REMEMBER IN

PUPILLARY DISORDERS
1. Commonest cause of sluggish pupillary reaction is poor illumination of torch

2. Other causes of sluggish pupillary reaction are—residual effect of mydriatic, e.g. local or sys-
temic ingestion of parasympatholytic drugs, psychosomatic drugs and central stimulants
3. Common causes of small pupil are:

● Patient fixing at a near object
● Brightly lit place of examination
● Light falling directly on eye
4. To elicit Argyll–Robertson pupil first requisite is good distant vision

5. Adie’s pupil will constrict by weak cholinergic drug
6. Horner’s syndrome is best examined in dull light
7. Measurement of pupil is best done by infra-red pupillometry
8. For pharmacological testing of pupil, the drugs should be put in eyes
9. Ganglion for sympathetic is superior cervical ganglion
10. Ganglion for parasympathetic is ciliary ganglion
E XAMINATION OF THE
O RBIT AND R ADIOLOGY OF
O PHTHALMIC I NTEREST
Orbits are not organs, they are natural anatomical spaces. One on each side of the
nose, they house tissues of various origin and function (Figs 19.1 and 19.2). Disorders
of these tissues constitute orbital diseases. Proximity of orbit to paranasal sinuses and
brain greatly influence orbital disorders.
Greater wing of sphenoid
Frontal nerve
Lacrimal nerve Trochlear nerve
Superior-ophthalmic vein
Circle of Zinn
Superior orbital fissure
Optic foramen
Recurrent meningeal artery
Optic nerve
Upper division of III nerve
Ophthalmic artery
Nasociliary nerve
Sympathetic nerve
VI nerve
Lower division of Ill nerve Inferior ophthalmic vein
Lesser wing of sphenoid
Fig. 19.1 | Structures passing through optic foramen and superior orbital fissure.
SO = superior oblique
Lacrimal nerve SO SR = superior rectus
Frontal nerve LPS = levator palpebrae superior
LPS
SR
MR = medial rectus
Trochlear nerve supplying SO Optic nerve
Upper division of III nerve IR = inferior rectus
supplying SR and LPS LR IO = inferior oblique
MR CG = ciliary ganglion
Abducent supplying LR
Inferior division of III nerve
Nerve to IO and CG supplying MR, IR, IO, and CG
IQ IR
Not to scale
Red lines represent extraocular muscles
Blue lines represent motor nerves
Red dot represents ophthalmic artery
Fig. 19.2 | Diagram representing muscles and nerves at the orbital apex.
COMMONEST FEATURE OF ORBITAL DISORDERS IS

DISPLACEMENT OF THE GLOBE
1. Pushed forward
(a) Proptosis
(b) Exophthalmos
2. Pulled backward
(a) Enophthalmos
3. Absence of the contents
(a) Congenital anophthalmos
(b) Acquired
● Enucleation
● Evisceration
● Exenteration
Orbital disorders are due to the involvement of the following:

(a) Orbital walls
(b) Contents of orbit
(c) Paraorbital structures
● Paranasal sinuses
● Teeth and gum
● Nasopharynx
● Cranial cavity
● Cavernous sinus
(d) Globe
(e) Systemic disorders
● Thyroid dysfunction
● Leukaemia
● Sarcoidosis
● Chronic infection
● Parasites
● Secondaries
● Storage diseases
Causes of orbital disorder can be:

1. Congenital
2. Infection
(a) Orbital cellulitis—acute and chronic
(b) Cavernous sinus thrombosis
3. Inflammation—pseudo-tumours, fungal granuloma, tubercular granuloma and Wegener’s gran-
uloma
4. Tumours
(a) Primary: benign and malignant
(b) Secondary
5. Extension from paraorbital structures
6. Trauma
7. Vascular
8. Storage diseases
EXAMINATION OF THE ORBIT 287
9. Blood disorders like leukaemia

10. Parasites
Symptoms of Orbital Disorders

1. Cosmetic
(a) Prominence of the eye ball
(b) Displacement of the eye ball
(c) Squint
(d) Inability to close the lids
2. Ocular
(a) Redness, watering and pain in eye
(b) Restricted movement; diplopia
(c) Diminished vision
3. Headache and fever
Signs of Orbital Disorders

1. Proptosis or exophthalmos
2. Enophthalmos
3. Lid retraction
4. Lid lag
5. Ptosis—true/pseudo
6. Lagophthalmos
7. Puffiness of lids
8. Squint
9. Exposure of cornea
10. Chronic conjunctivitis
12. Afferent pupillary defect
13. Papilloedema and optic atrophy
14. Raised intraocular pressure
EXAMINATION OF PROPTOSIS
Earlier proptosis and exophthalmos where used to denote forward displacement of the
globe due to retro-ocular mass and thyrotoxicosis, respectively. Presently, exophthalmos
is used exclusively for cases of dysthyroid myopathy. In a suspected case of proptosis,
before embarking on extensive examination and investigation, following questions
should be answered:
1. Is the eyeball in normal position?
2. If so, is the contralateral eye ball sunken (enophthalmic)?
3. Is the eye ball proptosed?
Signs of normal position of the globe:
1. The upper lids should cover 1/5 of the upper part of normal cornea or 2 mm from the
upper limbus
Plate 19.1 | Examination of a suspected case of proptosis.

2. Lower lids should just touch the cornea at lower limbus
3. No strip of sclera should be visible either above or below the cornea
4. If a straight measuring scale is put in front of the eyeball in such a position that the upper part
rests over mid-point of eyebrow and lower part rests on the maxilla, then the outer margin of
upper lid should just touch inner edge of the scale. If it pushes the scale away, the eyeball is pushed
forward. If there is a gap between the inner edge of scale and lid the eyeball is pulled in
5. Patient is seated comfortably in a chair. The observer stands behind and the patient’s head is
tilted back slightly. The observer looks at the most prominent part of the upper lid (Plate 19.1).
Normally the centre of upper lid should be just visible at the level of upper rim of the orbit. If
it protrudes beyond the upper rim, the eye ball is proptosed. If it is hidden under the superior
orbital rim, the eye ball is sunken.
6. Exophthalmometry reading should not exceed 18 mm or be less than 15 mm
Pseudo-Proptosis
Sometimes, the eyeballs seem to be proptosed without really being so. This is called
pseudo-proptosis.
Causes of pseudo-proptosis:
1. Causes in the globe
(a) Enlargement
● High myopia
● Buphthalmos
● Anterior and large ciliary staphylomas
Generally the above factors give a false impression of proptosis on the affected side when
they are unilateral.
(b) Diminished size
● Microphthalmos
● Microcornea
● Phthisis
Generally the above factors in one eye give an impression of contralateral proptosis.
2. Causes in lid
(a) Lagophthalmos
(b) Lid retraction
(c) Contralateral ptosis
3. Causes of extraocular muscles
(a) Unilateral extraocular muscle palsy
(b) Retraction of globe (contralateral)
4. Causes of globe retraction
(a) Fracture of the orbit
(b) Post-squint surgery
(c) Retractive tumours of orbit e.g. metastatic breast carcinoma
(d) Post-radiation status
Once it has been decided that there is proptosis, the examiner proceeds to explore the
following points.
1. Is proptosis uniocular or binocular?
2. Is the onset acute or gradual?
3. Measurement of proptosis
4. Direction of proptosis
5. Compressibility of proptosis
6. Intermittence of proptosis
7. Factors aggravating proptosis
8. Pulsation of proptosis
9. Bruit over proptosis
10. Palpation of any mass in the orbit
11. Other examination related to proptosis, i.e. systemic conditions
12. Special investigations for proptosis: X-ray, CT, MRI and ultrasonography
Unilateral Proptosis
Unilateral proptosis can be seen at any age. In children it could be life threatening, e.g.
neuro blastoma, retinoblastoma, rhabdomyosarcoma and leukaemia. Unilateral cases
can be acute or chronic. It could be due to local, ocular, orbital or systemic causes.
Occasionally unilateral proptosis may become bilateral, e.g. ophthalmic Graves’ disease,
leukaemia and cavernous sinus thrombosis.
Plate 19.2 | Proptosis due to glioma of optic nerve,

lateral view.
Plate 19.3 | Proptosis due to glioma of optic nerve,
front view.
Causes of unilateral proptosis are:

1. Inflammation or infection
(a) Orbital cellulitis
(b) Cavernous sinus thrombosis
(c) Orbital abscess
(d) Pseudo-tumour
(e) Parasites
2. Traumatic
(a) Air causing surgical emphysema due to fracture of paranasal sinuses
3. Vascular
(a) Haemorrhage
(b) Aneurysm of ophthalmic artery
(c) Carotico-cavernous fistula
(d) Orbital varix
(e) Haemangioma
4. Tumours
(a) Dermoid
(b) Glioma of optic nerve (Plates 19.2 and 19.3)
(c) Meningioma of optic nerve sheath
(d) Retinoblastoma (Plates 19.4 and 19.5)
(e) Neuroblastoma
(f) Rhabdomyosarcoma (Plate 19.6)
(g) Secondaries
(h) Leukaemia (Plate 19.7)
(i) Lacrimal gland tumours
5. Systemic disorders
(a) Ocular Graves’ disease (dysthyroid orbitopathy)
(b) Blood disorders
(c) Sarcoid
(d) Storage disorders
6. Cysts and parasites: mostly on left side
(a) Cysticercosis
(b) Hydatid cyst
7. Rarely congenital anomaly
Plate 19.4 | Proptosis due to retinoblastoma. Plate 19.5 | Proptosis due to retinoblastoma.
Plate 19.6 | Proptosis and displacement of globe upward

due to rhabdomyosarcoma.
Plate 19.7 | Bilateral proptosis due to leukaemia.
Bilateral Proptosis
1. Could be congenital or acquired.
2. Congenital proptosis is more likely to be bilateral.
3. Onset may be sudden and rapid or gradual and slow.
4. One eye may be proptosed more than the other or both eyes may be involved simultaneously
and equally.
5. Progress in both eyes need not be equal.
Causes of bilateral proptosis (Plate 19.8):
1. Congenital
● Oxycephaly
2. Inflammatory
● Cavernous sinus thrombosis
● Pseudo-tumours
● Wegener’s granuloma, tuberculosis and fungal granuloma

Plate 19.8 | Bilateral, slow, congenital proptosis.

3. Metabolic
● Ocular Graves’ disease and sarcoid
4. Tumours
● Retinoblastoma
● Lymphoma
● Lymphosarcoma
● Leukaemia
Proptosis in Children (Table 19.1)

1. Orbital cellulitis
2. Leukaemia
3. Neuroblastoma
4. Retinoblastoma
5. Rhabdomyosarcoma
6. Optic nerve glioma
7. Pseudo-tumour
8. Crouzon’s syndrome
9. Dermoid
10. Orbital foreign body
11. Panophthalmitis
12. Parasitic cyst
Three common causes of infective acute proptosis are (Table 19.2):
● Orbital cellulitis
● Cavernous sinus thrombosis
● Panophthalmitis
All the signs given below need not be present in all cases. Some of them are so sub-
tle that they have to be looked for carefully.
The important and frequent signs are:
1. Upper lid retraction
2. Diminished blinking
Table 19.1 Some probable causes of proptosis in children
Features Probable causes
Pale child, moderately ill, bleeding from gums; Leukaemia

unilateral or bilateral proptosis
Palpable abdominal mass, enlarged liver, Neuroblastoma
ecchymosis of lids and proptosis
Unilateral fast growing proptosis, fever, Orbital cellulitis
toxic child and pain
Fast growing unilateral proptosis with Rhabdomyosarcoma
palpable mass in orbit
Proptosis with white reflex in the pupil Retinoblastoma
Unilateral axial proptosis with early visual loss Optic nerve glioma
Bilateral proptosis, fever and toxaemia Cavernous sinus thrombosis
Bilateral slow, progressive proptosis Congenital anomaly of
with deformity of face skull or face
Unilateral proptosis, pain, fever, hazy cornea Panophthalmitis
and loss of vision
Table 19.2 Comparison between various infective proptosis
Features Orbital Cavernous sinus Panophthalmitis

cellulitis thrombosis
History Generally no contributory Boil in the surgical Surgery (intraocular),

factor. Rarely may be due danger zone, stye, penetrating injury
to penetrating injury or infected chalazion, lid of globe
retained orbital foreign abscess and retained
body foreign body
Age More frequent in children Any Any
Laterality Unilateral Unilateral, may become Unilateral
bilateral
Proptosis Marked Moderate Mild to moderate
Movement Restricted due to myositis Restricted due to Absent due to myositis
of globe ophthalmoplegia
Tenderness Globe Mastoid Globe
Discharge Nil Nil Profuse
AC reaction Absent Absent Severe, may have a
large hypopyon
3. Fullness of upper lid

4. Weakness of convergence
5. Limitation of ocular movement
Grades of Thyroid Orbitopathy: Warner’s Van Dyke

Modified Classification
Thyroid orbitopathy is divided into six classes from 0 to 6, each class is further divided
into mild, moderate or severe.
➤ The first letter of each class form the acronym = no specs

Table 19.3 Eponyms used for various ocular signs in dysthyroid oculopathy
Eponyms Sign
Ballet sign Extraocular muscle palsy

Dalrymple sign Retraction of upper lid
Boston sign Jerky movement of upper lid on looking down
Graefe’s sign Upper lid lag
Enroth’s sign Fullness of both lids
Gifford’s sign Difficulty in everting the upper lid
Jellinek’s sign Increased pigmentation of upper lid
Stellwag’s sign Infrequent blinking
Rosenbach’s sign Tremors of closed lid
Moebius sign Weakness of convergence
Kocher’s sign Globe lag on looking up
Griffith’s sign Lower lid lag on looking up
Cowen’s sign Jerky pupillary reaction
Lowy’s sign Hypersensitivity to sympathomimetics (adrenaline)
Table 19.4 Ocular signs of thyroid ophthalmopathy
Class Symptoms First letter of sign
0 No sign or symptom N
1 Only sign no symptom O
2 Soft tissue involvement S
3 Proptosis P
4 Extraocular muscle involvement E
5 Corneal involvement C
6 Sight loss S
An earlier classification divided exophthalmos into two group, e.g. thyrotropic and
thyrotoxic (Table 19.5).
Causes of proptosis in adults:
1. Ocular Graves’ disease
2. Pseudo-tumour of the orbit
3. Lacrimal gland tumour
4. Secondary extension from paranasal sinuses
5. Orbital cellulitis: bacterial or fungal
6. Parasitic cyst
7. Meningioma
8. Lymphomas
9. Orbital varices
11. Carotico-cavernous fistula
12. Aneurysm of ophthalmic artery
13. Posterior scleritis
14. Orbital foreign body
Table 19.5 Comparison between thyrotropic and thyrotoxic exophthalmos
Features Thyrotropic Thyrotoxic
Probable cause Seen in normal thyroid (euthyroid) Hyperthyroid status

hyper or hypothyroid
Lid retraction Mild, may disappear Prominent feature
Conjunctival chemosis Moderate to severe Absent
Exophthalmos Severe, progressive Moderate, slow progress
Reducibility Irreducible Mostly reducible
Ophthalmoplegia External ophthalmoplegia Partial ophthalmoplegia
Cornea Exposure common Less common exposure
Vision May be lost Generally retained
Fundus Papilloedema Normal
Causes of acute proptosis (all ages):

1. Retrobulbar haemorrhage
2. Surgical emphysema of orbit
3. Acute orbital cellulitis
5. Panophthalmitis
6. Acute dacryoadenitis (mumps)
7. Rhabdomyosarcoma (fast developing)
Causes of gradual proptosis:

1. Cranio-facial dysostosis (bilateral)
3. Dysthyroid orbitopathy
4. Orbital tumours
5. Orbital parasites
6. Leukaemia
7. Peri-orbital tumours
9. Optic nerve meningioma
11. Orbital varices
Intermittent Proptosis
Intermittent proptosis is caused by varices of the orbital vein in elderly people. They
are unilateral; dilated vessels may be visible over the conjunctiva. Degree of proptosis
changes with the position of head. They increase if the patient bends forward and
reduce if the head is tilted back. Proptosis is increased with Valsalva manoeuvre. They
are generally associated with phlebolith in the orbital vein which is visible as calcified
spots in X-ray and CT. Other less common causes are recurrent emphysema, recurrent
retrobulbar haemorrhage that absorbs and re-bleeds.
Pulsating Proptosis
Pulsating proptosis is seen in the following cases:
2. Aneurysm of internal carotid
3. Carotid cavernous fistula
4. Encephalocele
5. Meningocele
6. Rarely dermoid or neurofibromatosis
There is a visible and palpable pulsation. Patient complains of hearing rhythmic
sounds, corresponding with the heart beat. There is an auscultable sound over the prop-
tosis. It is invariably unilateral.
MEASUREMENT OF PROPTOSIS
Well-established proptosis, as in retinoblastoma, rhabdomyosarcoma and optic nerve

glioma, hardly require measurement. Measurement is important is initial stages and to
record improvement.
Proptosis is measured by a group of instruments called the exophthalmometer or
proptometer. There are various types of exophthalmometers: optical or mechanical. All
the instruments are meant to measure the distance between apex of the cornea and the
lateral rim of the orbit.
1. Optical can be of two types:
(a) Transparent scale—Luedde’s transparent scale
(b) Hertels mirror exophthalmometer
2. Mechanical
(a) Gormaz exophthalmometer (Plate 19.10)
All instruments are meant to measure the distance between apex of cornea and lateral
wall of the orbit.
Luedde’s Transparent Scale (Plate 19.9)

Luedde’s transparent scale consists of a transparent rectangular scale with a tapering end.
The tapering end has a notch for the lateral orbital rim. The notch is at right angles to the
sharp end. The scale is calibrated in millimetres, 0–30, with 0 at the lower end and higher
number at the upper end. To measure proptosis, the patient either sits or lies down. No
anaesthesia is required. The scale is put at right angles to the lateral wall. The patient is then
asked to fix a distant object. The apex of the cornea is viewed through the transparent scale
and reading is taken in millimetres. Normal reading varies between 15 and 20 mm.
Both the eyes should be measured; a difference of 2 mm is significant. This method is
not very accurate. This should be correlated with other clinical signs (Plate 19.9).
Hertels Exophthalmometer
This is the most commonly used exophthalmometer. This can measure the trans-
orbital distance as well as proptosis of both eyes simultaneously. In this, the apex of
Plate 19.9 | Twin Luedde’s transparent exophthalmometer.
Plate 19.10 | Gormaz exophthalmometer.

cornea is seen in two mirrors. The distance is given in millimetres. No anaesthesia is
required. The instrument can be used either in erect position or in recumbent position.
Gormaz Exophthalmometer (Plate 19.10)

This has a horizontal calibrated metal bar. At right angles to this horizontal bar are two
vertical arms with notch for lateral orbital margins. One of the vertical arms is fixed. The
other is movable. To measure the distance between the two lateral orbital rims, the fixed
vertical arm is kept on the lateral orbital rim of right orbit, and the other arm is moved
till the notch is over the lateral orbital margin of the other orbit. Distance between the
two arms is read in millimetres. This part of examination does not require anaesthesia.
There is another vertical arm that can be moved along the horizontal scale as well as it can
be lowered in a vertical direction. This gives the distance between the lateral orbital rim
and apex of cornea. To measure proptosis, the patient lies down on the examination table,
and both cornea are anaesthetised. The instrument is positioned to measure intraorbital
distance and the patient is asked to look straight at the roof of the room. The vertical scale
is brought over the right cornea and gently lowered on the cornea. The distance is read on
the vertical scale etched on the vertical arm. The test is repeated on the left cornea. Care
should be taken not to injure the cornea with the metallic foot plate of the instrument.
DIRECTION OF PROPTOSIS
There are various directions in which the globe can be pushed.

1. Anterio-posterior
2. Down and in
3. Vertically up
4. Up and out
5. Down and out
6. Lateral
7. Vertically down
8. Medially
9. Combination
Axial Proptosis
This is due to a mass in the muscle cone. Commonest cause is glioma of optic nerve
in children and optic nerve meningioma in adults. Other causes are a pocket of pus in
muscle cone, retrobulbar haemorrhage and foreign body inside the muscle cone.
● Down and out proptosis is caused by growth from frontal, sphenoidal and ethmoidal sinuses
(Plate 19.11).
● Down and medial proptosis is caused by growth in lacrimal gland
● Upward shift is due to growth from maxillary sinus or floor of orbit (Plate 19.12)
● Vertically down is due to growth from the roof of orbit
Compressibility of Proptosis
The globe is pushed back in the orbit by pressure of fingers or palm of the observer
through closed lids. If the globe can be pushed back and it springs back to its original
position after release of pressure, the proptosis is said to be compressible.
OTHER EXAMINATIONS RELATED TO PROPTOSIS
1. Examination of lids
(a) Lid retraction:This is due to sympathetic over activity and brought about by the contrac-
tion of Muller’s muscle. It is seen mostly in dysthyroid orbitopathy. Presence of lid retraction
is almost a sure sign of absence of tumour
Plate 19.11 | Growth from ethmoid causing Plate 19.12 | Proptosis with upward displacement of globe due to down-
wards extraocular spread of retinoblastoma.
bilateral proptosis and lateral
displacement of globes.
(b) Lid lag:The patient is asked to look down; normally the upper lid should follow the globe.
If it fails to follow the globe in down gaze, it is called a lid lag. This is seen in dysthyroid
orbitopathy or scar of upper lid
(c) Lagophthalmos: This is a late feature of malignancy of lacrimal gland
2. Extraocular muscles
Restrictive squint is common in dysthyroid orbitopathy and pseudo-tumours of the orbit.
Ophthalmoplegia is common in cavernous sinus thrombosis
3. Forced duction test is positive in cases of ocular Graves’ disease
4. Corneal exposure is common in high degree of proptosis and malignant exophthalmos. It may
range from scattered keratitis to vascularisation or sloughing of cornea
5. Pupillary reaction—Marcus Gunn pupillary reaction suggests optic nerve compression
6. Differential intraocular tension recording—Rise of tension on movement is suggestive of dysthy-
roid orbitopathy
7. Refractive error—Shift towards hypermetropia is suggestive of a retro-ocular growth
8. Fundus examination
(a) Optic nerve
● Primary optic atrophy
● Papilloedema
● Post-papilloedematous optic atrophy
(b) Choroidal folds are seen in a mass pushing the posterior pole
SPECIAL INVESTIGATIONS IN PROPTOSIS
1. Haematological for blood dyscrasia

2. Otorhinological
(a) Nasopharynx
(b) Examination of paranasal sinuses
3. Thyroid function tests
4. X-ray: orbit and skull

5. Ultrasonography of:
(a) Eye ball: axial length and intraocular growth
(b) Soft tissues of orbit: growth, fibrosis and deposit in muscles
6. CT scan
7. MRI
8. Orbital venography
9. Fine needle biopsy
10. Excision biopsy
X-Ray Orbit
Following X-rays are helpful in localising orbital pathology:
1. Caldwell view: In this view, the petrous pyramids (apexes) do not obstruct orbital details. This
shows greater and lesser wing of sphenoid. Superior orbital fissure, most of the paranasal sinuses
2. Water’ view:This gives details of orbital rim, orbital roof and floor and maxillary sinuses
3. Lateral view:This shows sphenoid, sphenoid air sinuses, anterior clinoid and sella turcica
4. Axial (basal view)
5. Optic foramen view: X-ray of both the foramen should be taken for comparison especially in
optic nerve glioma
What to Look for in X-Ray Orbit

1. Size of orbit
2. Symmetry of orbit
3. Bone changes
4. Intraorbital calcification
5. Changes in paranasal sinuses
6. Retained intraorbital foreign body
7. Changes in optic foramen and optic canal
8. Superior orbital fissure width
Size of the orbit: Both orbits are almost of the same size. Bilateral symmetrical mild
enlargement of orbit may not lead to any definite conclusion. Unilateral enlargement
is diagnostic. In children enlargement takes place within 2 to 3 months, in adults it
takes a minimum of 1 year to produce enlargement. Enlargement may be symmetrical
or asymmetrical.
Symmetrical enlargement is seen in intraconal masses, e.g. optic nerve glioma, hae-
mangioma, neurofibroma, retinoblastoma and pseudo-tumours of orbit.
Asymmetrical enlargement is seen in extraconal lesions, e.g. rhabdomyosarcoma and
dermoid.
Diminished orbital size is seen in:
● Congenital anomaly: anophthalmos and microphthalmos
● Enucleation of eye in childhood
● Phthisis in children
● Trauma
Asymmetry of orbit is seen in trauma, radiation, extension of growth from paraor-
bital spaces, dermoid and encapsulated lacrimal gland tumour.
Bone changes in orbit: Orbital lesions may produce either enhanced or decreased
bone density.
Causes of increased bone density are sphenoidal ridge meningioma, chronic periostitis,
osteoblastic metastasis, Paget’s disease and fibrous dysplasia.
Causes of decreased bone density are dermoid, mixed cell tumour of lacrimal gland,
malignant tumours of lacrimal gland and extension of tumour from paranasal sinuses.
Intraorbital calcification It can be:
A. Intraocular
B. Extraocular
Intraocular calcification is seen in:
1. Long-standing mature cataract
2. Chronic uveitis
3. Retinoblastoma
4. Osteoma of choroid
5. Intraocular foreign body
6. Drusen
Extraocular calcification is seen in:
1. Retinoblastoma
2. Phlebolith in orbital varices
3. Meningioma of optic nerve
4. Glioma of optic nerve
5. Lacrimal gland carcinoma
6. Parasitic cyst
7. Aneurysm
8. Dermoid
Changes in superior orbital fissure Widening of SOF is seen in intracavernous
aneurysm of internal carotid, intracranial extension from orbit and intraorbital exten-
sion from brain.
Changes in optic canal and foramen Optic canals form an angle of about 40°
with midline; hence they cannot be projected simultaneously in a single X-ray. The
size of two optic foramina is almost constant, around 7 mm. Any difference greater
than 1 mm between the two denotes optic nerve glioma in children and optic nerve
sheath meningioma in adults, or intracranial extension of retinoblastoma or neurofi-
bromatosis.
Optic nerve glioma produces symmetrical, smooth enlargement while others pro-
duce irregular enlargement. Changes in optic canal are best seen in computerised
tomography in different sections.
Computerised Tomography of Orbit

Following types of tomography are done in orbital diseases:
1. Axial tomography:This is the most commonly used mode to locate intraorbital lesions
2. Coronal tomography demonstrates bone erosion in malignant tumours, mostly of lacrimal gland
3. Lateral tomography is used to see blow out fracture of orbit. Computerised tomography can be
done without or with contrast. Contrast tomography is helpful in vascular lesions
Uses of Computerised Tomography

To see:
1. Intraocular lesions
2. Intraorbital lesions
3. Paraorbital lesions
4. Intracranial lesions
It is generally indicated in exophthalmos, fracture of orbit, expanding lesions of orbit,
foreign bodies in orbit and to see size of optic nerve, optic canal and extraocular muscles.
Causes of enlargement of optic nerve—Diffuse in cases of raised intracranial pressure
and localised in glioma and meningioma.
Thickening of extraocular muscles is seen in Graves’ disease, pseudo-tumour and
secondary infiltration.
MRI of Orbit
This is a non-invasive method of imaging. It differs from X-ray or CT scan as it does not
use either X-ray radiation or ionisation radiation. It works on rearrangement of hydro-
gen nuclei when tissue has been exposed to an electromagnetic pulse. It produces a
tomographic picture, similar to CT. It is useful in intracanalicular lesions, chiasmal
and post-chiasmal lesions.
Orbital Venography
This is a minor, invasive, radio-diagnostic procedure. Radio-opaque dye is introduced
in the ophthalmic veins to make them opaque. Most of the veins all over the body are
very inconsistent in their course. Hence they are generally not taken as surgical land-
marks. Ophthalmic veins have a fairly constant anatomical location. Hence their loca-
tion and shape have diagnostic importance. The superior ophthalmic veins forms a
parallelogram in axial view. Changes in the shape of the parallelogram differentiates
intraconal lesions from extraconal lesions. Venography may show any of the following
changes or a combination of changes:
1. Displacement of the arms of the parallelogram
(a) Opening of parallelogram
(b) Closing of parallelogram
2. Obstruction in the venous system
(a) Pre-conal
(b) Inter-conal
(c) Post-conal
3. Abnormal circulation
Procedure of orbital venography—This is an outdoor procedure in adults. The
patient lies on the examination table with the head end lowered; a headband is put on
the forehead. These two procedures will make the angular, facial and frontal veins
prominent. The most prominent vein is punctured by needle of 21 ga. That is

attached to a 10 cc glass syringe containing Conray 280.
A control picture is taken and thereafter 5 ml of dye is injected rapidly in 2–3 s. A film
is taken, the remaining solution is injected and another film is exposed. While injecting
the dye, other veins on face are compressed to prevent filling of extraorbital veins.
A. Intraconal lesions:
1. Will open up the parallelogram, making the angles more obtuse
2. Elevation of second and third part of the superior ophthalmic vein
B. Extraconal lesions:
1. The parallelogram will collapse and the angles will become more acute.
2. Pathological venous circulation is seen in cases of orbital varices, malignant growths, cavernous
haemangioma, neurofibroma and pseudo-tumour of orbit.
Ophthalmic Ultrasonography
This is a non-invasive investigation that utilises ultrasound in place of light or X-ray
to produce a visible image that can be printed on suitable paper or film. Sound used
in ultrasonography is inaudible to human ears. Ophthalmic ultrasonography uses high
frequency sound vibration at 500 mega cycles/s, 8–10 MHz. There are two modes of
ultrasonography. They are A Scan and B Scan.
A scan is time amplitude scan that gives a linear unidimensional picture. B scan is
intensity modulated and gives a two-dimensional cross-sectional view in the form of
dots (Figs 19.3 and 19.4). Each of them has a specific use in ophthalmology. Inter-
pretation of A scan requires more skill than B scan. A scan is most useful in finding out
the ocular dimensions like depth of AC, thickness of lens, axial length of eye ball and
thickness of cornea (Fig. 19.5). It has a limited value in diseases of globe or orbit.
B scan on the other hand not only gives information regarding geometrical dimensions
but also the geography of the intraocular and orbital structures (Fig. 19.6).
Fig. 19.3 | A scan time amplitude gives linear spikes. Fig. 19.4 | Scan intensity modulated display,
echoes are displayed as dots.
Transducer
AC = Anterior chamber
L = Lens
V = Vitreous
RD = Retinal detachment
Pulser SRF = Sub-retinal fluid
RBF = Retrobulbar fat
AC NR = Normal retina
L SRF
V RBF
Cornea Ant. RD NR Post

capsule wall
Receiver
Signal
Display Printout
processor
Various frequencies used in ultrasonography

Higher the frequency lower is the penetration
Part Frequency
Cornea 12–15 MHz
AC 12–15 MHz
Eyeball 10–12 MHz
Orbit 7 MHz
Body 5 MHz
1 MHz = 1 million cycles per second
Fig. 19.5 | A scan.

Ciliary body
Foreign body
A Posterior lens capsule
Cornea
C
Vitreous
Iris
Detached retina
Sub-retinal fluid
Fig. 19.6 | B scan.

Orbits contain less acoustic landmarks than the eye ball. Acoustic landmarks of globe
are anterior and posterior surface of cornea (aqueous is acoustically homogenous, so does
not produce any change), posterior capsule of lens, iris and ciliary body. Normally placed
retina, choroid and sclera give a common deflection. Normal vitreous is acoustically
homogenous. However, clotted blood, vitreous bands, opacities, foreign bodies, cysts, etc
produce detectable changes in both the modes of ultrasonography. Detached retina and
choroid are also visible. Tumours arising from retina or choroid show a definite pattern.
Normally, transparent lens does not give any acoustic response except the posterior
capsule. Rupture of posterior capsule, posterior lenticonus, subluxation and dislocation
of lens are visible.
The posterior surface of the globe gives a uniform smooth concave contour with
concavity towards cornea. Retrobulbar fat gives a uniform pattern in the form of let-
ter W; the notch of W is represented by optic nerve.
By changing the direction of the probe (transducer), extraocular muscles can be
outlined.
High-resolution B scan ultrasonography gives non-invasive, radiation-free, auto-
matic mode of evaluation of orbital disorders. It is better than X-ray or A scan for
orbital examination. Findings of B scan depend upon (a) plane of acoustic section and
(b) gaze of the patient.
Common lesions where B scan ultrasonography is used are meningioma, mucocele,
dermoid, parasitic cysts, ocular Graves’ disease, tumours of optic nerve (both glioma
and meningioma), neurofibroma and lymphomas. All the above lesions have typical
ultrasonic appearance that differentiates one from the other.
RADIOGRAPHY OF OPHTHALMIC INTEREST
Radiology of orbit is an important investigation in the diagnosis of orbital disorders.

However, X-ray of orbit may give additional information in the disorders of globe and
skull as well. In unilateral lesions of the orbit, the other orbit acts as a control and is of
great value in early changes in orbital size, density of bones and size of optic foramen.
Common X-Rays Ordered in Ophthalmology

● X-ray orbit
● X-ray globe
● X-ray paranasal sinuses
● X-ray skull
● X-ray chest, hands, bones and joints
Radiological and non-radiological imaging procedures in ophthalmology are (1) non-
invasive and (2) invasive.
Non-invasive procedures are as follows:
● X-rays
● Tomography
● Computerised tomography
● Ultrasonography
● MRI
● Use of radioactive tracer with Gamma camera
● OCT
Invasive procedures are as follows:

● Dacryocystography—simple and macro-DCG
● Orbital venography
● Arteriography
Disadvantages of Eye as Subject of Radiology

1. The globe does not have any bone or opaque landmark
2. The orbits are irregular prismoids, walls are not parallel and size of all the walls is not similar
(Fig. 19.7)
3. Orbits are surrounded by air containing paranasal sinuses on three sides
4. The occipital bone and apex of petrous bone encroach on true AP or PA view of orbit
5. In lateral view findings of opposite side overlap findings of side of interest
Common positions used in ophthalmic radiology:
1. Caldwell projection
2. Water’s view
3. Towne’s view
4. Lateral view
5. Submento-vortex view
6. Optic foramen—Rhese’s view and Ruggiero’s view
7. Limbal ring for intraocular foreign body
8. Sweets localisation
Radiological Examination of an Eye with

Suspected Intraocular Foreign Body
It should be remembered that a single PA or lateral view is not sufficient to find out
if there is a radio-opaque substance in the orbit being evaluated.
Fig. 19.7 | Relation of lateral wall and medial wall to globe.

A lateral view may show a radio-opaque shadow that may be in the other orbit,
between the two orbits, even extraorbital or extracranial. A posterio-anterior view may
not be sufficient to say if the opacity is intraorbital or intracranial.
First pre-requisite is to find out if the foreign body is in the orbit or not; is it sin-
gle or multiple. Next step is to find if it is intraocular or extraocular.
A posterior-anterior and lateral views will confirm the presence of foreign body in
the orbit. For this the following views are taken:
1. Looking straight
2. Looking up
3. Looking down
If the foreign body is intraocular, it will move with the movement of eye except
sometimes when it may be on the posterior pole where movement is negligible.
However, foreign bodies embedded on the outer surface of sclera and extraocular mus-
cles will also show movement.
Once it has been established that the foreign body is intraocular, its position in rela-
tion to limbus, sclera and meridian must be localised by limbal ring or Sweets localisers.
Limbal Ring Localisation of Intraocular

Foreign Body
Take pilot X-ray of lateral and PA view to find out if the foreign body is intraorbital.
If the answer is positive, find out if the foreign body is intraocular and, if so, proceed
with limbal ring.
Procedure
Anaesthetise the cornea and the conjunctiva with 4% Xylocaine. Stitch a limbal ring
of 12 mm diameter at four places—12, 3, 6 and 9 O’clock firmly on the limbus. Take
a PA view. Take two true lateral views, one looking straight ahead and the other look-
ing up. A true lateral view should project the limbal ring as a straight line and not an
oval. After the film has been dried, find out the geometric centre of the globe by the
usual method and draw a circle with 12 mm radius on both PA and lateral view and
measure the distance of foreign body from limbus, and the meridian.
X-Ray of Globe
Separate X-ray of globe is limited to bone-free X-ray of globe for intraocular foreign
body. This has very limited value. Various X-rays of orbit are sufficient to give away
the position of intraocular radio-opaque shadow. The purpose is better served by USG
or CT. MRI is contraindicated in metallic foreign bodies.
Common causes of intraocular radio-opaque shadows are:
1. Exogenous
● Intraocular foreign body
2. Endogenous (Plate 19.13)

(a) Mature cataract of long standing
(b) Retinoblastoma
Plate 19.13 | Intraocular calcification. 1. Calcified complicated cataract 2. Bone formation in choroids.
(c) Bone formation in choroid
(d) Osteoma of choroid
(e) Intraocular calcified parasites
➤ All metallic foreign bodies are radio-opaque; iron, steel, copper, brass, bronze, lead
give dense opacities. Glass, unless it contains lead, is transparent; plastic, rubber,
wood are non-opaque. They are better seen in ultrasonography or CT scan
X-ray skull of ophthalmic interest:

1. For raised intracranial tension, silver beaten appearance (in case of papilloedema). However,
papilloedema may occur in the absence of silver beaten appearance.
2. Intracranial calcification is seen in congenital toxoplasmosis, adenoma, meningioma, healed
tubercular meningitis and cranio-pharyngioma.
3. Changes in pituitary fossa.
Pituitary tumours, being a common cause of field defects, optic nerve changes and
blindness, are very often subjected to X-ray investigation; commonest view is lateral
view. The pituitary fossa is examined for:
1. Its size—enlargement is seen in pituitary tumours
2. Suprasellar calcification
3. Double floor of the sella
4. J-shaped pituitary fossa
5. Empty sella syndrome
6. Destruction of posterior clinoid
E XAMINATION OF
R ETINA AND M ACULA
Retina has only one function—visual. It may be form vision, colour vision, field of
vision, scotopic vision (night vision) and photopic vision (day vision).
SYMPTOMS OF RETINAL DISORDERS
1. Check if it is primary retinal involvement or

2. It is associated with involvement of:
● Choroid
● Optic nerve
● Vitreous
● Blood vessels
● Visual pathway
● Combination
3. Part of retina involved:

● Central
● Peripheral
● Both
Symptoms of Central Retinal (Macular) Involvement

1. Loss of central vision
2. Altered colour vision
3. Diminished fine vision
4. Distorted vision (metamorphopsia)
Symptoms of Peripheral Retinal Involvement

1. Diminished peripheral field
2. Poor night vision
3. Poor dark adaptation
4. Flashes of light
OVERALL SYMPTOMS OF RETINAL DISORDERS

2. Diminished detailed vision (fine vision)
3. Altered colour sense

4. Positive scotoma
5. Micropsia, macropsia and metamorphopsia
6. Diminished night vision
7. Flashes of light (photopsia)
8. Loss of peripheral field
9. Black spots in front of the eye
10. White reflex in the pupillary area
DISORDERS OF RETINA
Retinal involvement may be unilateral or bilateral. One eye may be involved earlier than
the other; they may be symmetrical or otherwise. A retina involved earlier need not be
more damaged than the one involved later.
Retina may be involved in following conditions:
1. Congenital
2. Infection
3. Inflammation
4. Vascular disorder
● Arterial
● Venous
● Capillary
● Combination
● Primary
● Secondary
6. Dystrophies
● Peripheral
● Central
● Combined
7. Degeneration
8. Trauma
● Direct
● Indirect
9. Neoplasm
● Benign
● Associate
● Malignant
● Secondaries
EXAMINATION OF RETINA
Retina is examined under the following headings:

1. Visual acuity
2. Vision with pinhole
EXAMINATION OF RETINA AND MACULA 311
3. Vision with distant correction

4. Near vision with correction
5. Refraction
6. Colour vision
7. Direct ophthalmoscopy
8. Indirect ophthalmoscopy
9. Slit-lamp examination of posterior pole
10. Three-mirror gonioscopic examination of posterior pole and periphery
11. Pupillary reaction—Marcus Gunn
12. Recording of IOP
13. Field examination
● Central 10°: Amsler grid
● Central 30°: Bjerrum screen
● Peripheral: Kinetic and static

15. Electroretinography
16. Visually evoked response
17. Ultrasonography
18. MRI
19. OCT
20. Dark adaptometry
21. Trans-illumination
All cases of retinal disorder do not require all the above listed examination.
Some diagnoses are straight forward; others require elaborate examination for diag-
nosis, differential diagnosis and treatment. Out of the large list, following are more
useful than others—recording of vision, examination of fundus, examination of
posterior segment by slit lamp, field examination, fluorescein angiography and ultra-
sonography.
Fundus Examination
Fundus is the visible part of retina. It not only allows observation of retina, but also
optic nerve, retinal blood vessels, vitreous and, to a limited extent, choroid. Retinal
blood vessels reflect the condition of vessels of same size elsewhere like brain, heart,
coronary and kidney, hence have a great prognostic value.
Fundus can be visualised by following methods:

1. Ophthalmoscopy:
● Direct ophthalmoscopy
● Indirect ophthalmoscopy
2. Slit-lamp examination
3. Hruby lens—minus lens 55 D
4. El Bayadi—Plus lens 68 D
5. Volk—Plus 90 D
6. Goldmann three mirror
Direct Ophthalmoscope
This is a versatile, compact, handy optical instrument with multiple functions, the
most important being examination of the fundus. Other uses are (Plate 20.3):
1. Focal illumination for examination of the anterior segment
2. To see opacities in the media
3. Rough estimation of spherical error of refraction
There are various types of direct ophthalmoscopes. They generally work on dry battery
or mains with a suitable step down transformer that can be housed either in the han-
dle of the ophthalmoscope or available as a separate unit. The direct ophthalmoscope
may have accessories for various purposes:
1. Uniocular indirect ophthalmoscope
2. Cobalt blue filter (fluoroscopy)
3. Red-free filter (nerve fibre layer)
4. Trans-illuminator (Plate 20.1)
5. Graticule (graph) to measure the size of lesion
6. Star for eccentric fixation
7. Slit for macular lesions
Plate 20.1 | Keeler trans-illuminator with step down transformer. (Courtesy Dr. Santosh Patel.)
Parts of Direct Ophthalmoscope

Following are the parts of a direct ophthalmoscope:
1. Body—To hold dry battery or step down transformer. The body has a switch with a rheostat
that can control illumination
2. Head of the ophthalmoscope—This is attached to one end of the body. It has (a) source of
illumination, (b) a reflecting mirror or a prism that throws an almost parallel beam of light and
(c) a viewing aperture just above the edge of the reflector and (d) series of movable spherical
lenses. These lenses focus the retina in ametropia, to correct ametropia of the observer, to mea-
sure elevation of the lesion, to measure the depth of cup and posterior staphyloma
The body acts as a handle of the ophthalmoscope. The viewing aperture can be made small,
intermediate or large. Small aperture is used to see the fundus through an undilated pupil.
Optics of Direct Ophthalmoscope

Direct ophthalmoscope uses optics of the eye under examination (Fig. 20.1). Illuminated
retina acts as the object and diopteric system of the eye as a magnifying lens of 60
D in an emmetropic eye. The retina comes within the focal length of the diopteric sys-
tem. The system thus acts as a simple magnifier producing an erect, magnified, virtual
image on the same side as the object. Magnification is roughly 15. Size of the image
follows a simple rule of magnification, M D/4, where M stands for magnification,
D is the dioptre of the eye under observation. Thus, a hypermetropic eye which is less
converging than an emmetropic eye produces a smaller image than emmetropia.
Conversely, myopia produces a larger image (Table 20.1).
Observed
Observer image
Mirror
Source of light
Fig. 20.1 | Principle of direct ophthalmoscopy.

Table 20.1 Relation between error of refraction and magnification
Error of refraction Dioptre Magnification
Emmetropia 60 60/4 15
Hypermetropia 10 60 10 50 50/4 12.5
Aphakia 43 43/4 10.8
Myopia 10 70 70/4 17.4
Area seen by a direct ophthalmoscope is 10° at a time, thus to see a large area, the
spot of light has to be shifted from place to place to scan the fundus. Still the periphery
is not visible as it is obscured by the over-hanging anterior border of the sclera. There
is no stereopsis. The greatest advantage is an erect image that need not be oriented.
Small central lesions like macular lesions or lesions on the disc can be seen with greater
magnification. It is very easy to master the art of direct ophthalmoscopy. Ophthalmoscopy
can be done either with dilated or normal-sized pupil. It is better to dilate the pupil for
ophthalmoscopy to bypass central lenticular and corneal opacities.
Indirect Ophthalmoscope
Indirect ophthalmoscope is yet another optical device without which examination of
the retina is not complete. Undergraduate students must understand its optical principle,
method of use and its comparative merits and demerits vis-à-vis direct ophthalmo-
scope (Table 20.2). All postgraduates, teachers and consultants must master use of this
instrument as it opens up a flood gate of information regarding posterior segment
which otherwise would have to be noted down as “fundus not visible”.
There are two types of indirect ophthalmoscopes:
1. Binocular indirect ophthalmoscope
2. Uniocular (rarely used)
The instrument consists of three parts:
1. Illumination system
2. Viewing system
3. Image forming system
Illumination system This is attached to a headband and worn on the forehead by

the examiner. It can also be fitted to a sturdy spectacle frame. Energy for the illumina-
tion is provided by a step down transformer attached to mains or may be worked on dry
battery. Besides the bulb as a source of illumination it consists of a reflecting mirror that
gives an almost parallel beam of rays. The mirror can be tilted on a pivot when required.
Brightness of the illumination system can be regulated by a rheostat on the transformer.
Table 20.2 Comparison between direct and indirect ophthalmoscope
Features Direct Indirect
Image
Nature Virtual, erect, magnified 15 Real, inverted magnified 1 to 4
Position Towards the retina of the patient Between the condensing lens and
observer
Brightness Less bright Very bright
Stereopsis Nil Good
Resolution Poor Better
Field Small 10° Large 37°
Peripheral view Not possible Well seen
Working distance Very short Long
Scleral indentation Not possible Possible
Viewing system This consists of four plane mirror or prisms (Fig. 20.2). There are
two on each side to reduce the inter-pupillary distance of the observer from 60 to
15 mm. There is an eyepiece in front of each eye that has 2 Dsph to relax accommo-
dation of the observer. The observer should wear his own distant correction. Cobalt
blue and red-free filter can be interposed in front of the viewing system.
Image forming system This consists of a condensing lens (Fig. 20.3). Power of con-
densing lens may be 15 D, 20 D or 30 D; each has its own utility. Commonly used
lens is 20 D. The lenses have a large diameter for easy grip and larger field. They are
coated with anti-reflecting coating. Condensing lenses are either made of glass or plas-
tic, are aspheric, can be biconvex or planoconvex. While using a planoconvex lens the
convex surface should face the observer.
15 mm
Second mirror
First mirror
First mirror
Eye piece of the

ophthalmoscope
60 mm
Fig. 20.2 | Viewing system of indirect binocular ophthalmoscope (Inter-pupillary distance is reduced from usual 60 to 15 mm by a
pair of reflecting plane mirrors that are parallel to each other with reflecting surfaces facing each other).
Fig. 20.3 | Principle of indirect ophthalmoscopy.

Function of the condensing lens is to condense the rays at the anterior focal point
of the eye just behind the iris and form an image of the retina in space between the
condensing lens and the observer. It also magnifies the image. Size of the image is
inversely proportional to the distance between the image and the condensing lens. In
myopia, image is nearest to the condensing lens and is the largest.
The image formed by the condensing lens is real, inverted, magnified and laterally
reversed. Sharpness of the picture depends upon the focal length of the lens. Shorter
the focal length nearer should the condensing lens be held from the eye; 15 D is kept
at 3, 20 D at 2 and 30 D at 1.5. Higher the power of the condensing lens, larger
is the field, brighter the illumination but lesser is the magnification. Macula and optic
disc are better seen with 15 D while periphery is best seen with 30 D. For a begin-
ner 20 D planoconvex lens with large diameter is the best.
Optics of Indirect Ophthalmoscope

Optics of the indirect ophthalmoscope are similar to the optics of an astronomical tel-
escope where retina is the object, image of retina is formed in space after it passes
through the condensing lens and is picked up by the dioptre system of the observer.
Indirect Ophthalmoscopy
This is generally done with patient lying on an examination table but can be done with
a patient sitting erect (Plate 20.2). The latter is done usually by a monocular indirect
ophthalmoscope for rough estimation of fundal pathology followed by a detailed
examination with a binocular indirect ophthalmoscope. Similarly indirect ophthalmo-
scope is done with maximum mydriasis but can be done through undilated or smaller
pupil by special adjustment of small pupil indirect ophthalmoscopy. Generally, pupil is
Plate 20.2 | Indirect ophthalmoscopy. (Courtesy Dr. Santosh Patel.)

dilated with a combination of mydriatic and cycloplegic. Cycloplegic helps to overcome

glare and has a synergistic effect on mydriasis. A widely dilated pupil enables exami-
nation of larger area, and it circumvents opacities in media. Both the pupils should be
dilated and both the eyes examined for comparison as a rule unless contraindicated.
To examine the fundus the patient lies down on an examination table about 2 ft high
with sufficient space for the observer to move about on the head side of the patient and
examine from either side of the patient. The height of the table allows the observer to work
at an arm’s length. The room is darkened with sufficient illumination to draw the diagram
of the fundus on a chart, which is kept on the chest of the patient with 12 O’clock point-
ing towards the feet of the patient (Fig. 20.4 and Plate 20.3). The patient is explained the
procedure with emphasis that it is a painless procedure and his co-operation is required
for the examination to go smoothly. He is further explained to keep both eyes open and
fix at the roof of the room. If one eye is closed, the other eye has a tendency to roll up
due to Bell’s phenomenon. To begin with illumination of the ophthalmoscope should
Fig. 20.4 | Retinal drawing chart. 12 O’ clock point towards the feet of the patient. O—Optic nerve,
M—Macula.
Plate 20.3 | Direct ophthalmoscopy. (Courtesy Dr. Anil Gupta.)

be dim enough to see the pink glow only and is gradually increased in intensity. While
the condensing lens is held between the thumb and index finger of the left hand, the
right hand is free to draw the diagram as seen, and to hold the scleral depressor when
required. A strict protocol should be followed while doing indirect ophthalmoscopy.
The media that seems to be too hazy to perform direct ophthalmoscopy, looks light
enough to see the fundus through it, because the illumination of indirect ophthalmoscope
is very bright and fundus can be visualised by the side of opacities in the media, like
corneal, lenticular and vitreous opacity, vitreous haemorrhage and endophthalmitis. While
drawing the fundus picture international code of colour and symbols must be adhered to.
The normal structure seen with indirect ophthalmoscope (Fig. 20.5; Table 20.3).
As the image of indirect ophthalmoscope is inverted and laterally reversed, the observer
should be able to orient his own position vis-à-vis retinal image. To see a lesion, the
observer should post himself away from the site of suspected lesion. Ask the patient to
look towards the lesion, i.e. to see a lesion in the lower fundus, the observer should
stand at the head end of the patient and ask the patient to look towards his own feet.
Examination of Retina by Slit Lamp

Direct ophthalmoscope gives an erect and 15 magnified image of the retina but has the
drawback that there is no stereopsis and field is small. Indirect ophthalmoscope has advan-
tage of stereopsis and large field but magnification is very low, and the image inverted and
laterally reversed. Slit lamp is better of the two, i.e. it magnifies and there is stereopsis.
Outermost circle represents pars plana

SC Irregular circle with serrated border is ora
SC
V V The imaginary circle passing through

LC M LC vertex ampullae is position of equator
V V
LC is long ciliary nerve
SC is short ciliary nerve
SC O is optic nerve
SC
M is macula
V is vortex vein
Fig. 20.5 | Indirect ophthalmoscopy. (Courtesy Dr. Anil Gupta.)
Table 20.3 Colour codes
Attached retina Red

Detached retina Blue
Retinal break Red with blue outline
Flap of tear Blue
Lattice degeneration Blue outline with blue hatching
Thinning of retina Blue outline, red hatching
Retinal exudate Yellow
Retinal pigment Black
Vitreous opacity Green
Retinal veins Blue
Retina can be viewed with slit-lamp biomicroscope by direct or indirect method. It

can be done by
A. A minus lens kept:
1. In contact with cornea (Goldmann) (Fig. 20.6)
2. Away from the cornea (Hruby lens)
Viewing of retina by minus lenses is called the direct method.
B. Placing a plus lens away from cornea (El Bayadi)
The retina cannot be visualised with slit lamp unless the optics of the eye are modified to form
an image that is in focus of the biomicroscope.This can be achieved either by:
1. A Goldmann contact lens that replaces corneal surface by a focal flat surface. This produces
an erect image in the mid-vitreous that can be focussed by slit lamp (Fig. 20.7)
Table 20.4 Comparison between various dioptres of condensing lenses
Features ⴙ15 D ⴙ20 D ⴙ30 D
Distance from eye 3 in. 2 in. 1.5 in.

Magnification 5 3 2
Field 30° 50° 60°
Stereopsis Normal ¾ normal ½ normal
Illumination Low Medium Bright
Fig. 20.6 | Relative position of various parts of Goldmann three-mirror lens.
Fig. 20.7 | Image formed by lens kept in contact with the cornea.
H I E
I
Position of image by Hruby lens. Virtual Position of image by EI Bayadi lens. Real inverted
image 18 mm in front of retina image 17 mm in front of (towards the observer) lens
Fig. 20.8 | Image formed by Hruby and El Bayadi lens.

2. A Hruby lens comprises of a –60 D lens that neutralises the total diopteric power (60 D)
of the eye and forms a virtual image 18 mm in front of the patient’s retina which is smaller
than normal in size, due to reduction of pupillary size. The Hruby lens should be placed
10–12 mm in front of the patient’s cornea (Fig. 20.8)
3. With 60 D or more lens—The El Bayadi lens forms an inverted real image without magni-
fication between the lens and the observer 17 mm in front of the lens (Fig. 20.8)
4. Panfundoscopic lens—This is a heavy lens that is either illuminated by an external fibre optic
system or by slit lamp. It forms an inverted, laterally reversed image as in indirect ophthal-
moscopy that is seventy percent less than the normal retinal size
Retinal periphery is examined to see following features:
1. Retinal degenerations
2. Retinal breaks—holes, tears and dialysis
3. Traction bands
4. Neovascularisation
5. Vitreous condensation
6. Chorio-retinal scars
8. Retinal dystrophies
9. Retinoschisis
10. Scars of cryo, diathermy
Indirect ophthalmoscope is not only used as a diagnostic tool but also as an essential
accessory for retinal surgery.
➤ All retinal surgeries must be done under direct vision of an indirect ophthalmoscope
only
To examine the fundus, a strict protocol should be followed.

To examine with the direct ophthalmoscope patient can be either seated or may be
recumbent. To examine the right eye the observer stands on the right side of the
patient with the ophthalmoscope in the right hand and uses his right eye. To see the
left eye, the observer stands on the left side, uses his left hand and left eye. The patient is
asked to fix a distant point with both eyes open. If the patient fixes the light on the oph-
thalmoscope only macula will be visible. In a squinting eye, if the other eye is covered,
the squinting eye will generally take up fixation and can be examined with ease. While
doing ophthalmoscopy the patient is asked to move the eye as per instruction to visu-
alise as far as possible.
Fundus Should Be Examined Under the

Following Topics
(1) Media, (2) disc, (3) general appearance of the retina, (4) blood vessels (5) exudates,
(6) haemorrhage, (7) scar, (8) macula, (9) periphery for degeneration, dystrophies,
holes and neovascularisation and (10) detachment.
➤ Both the fundi should be examined on the first visit unless there is a valid reason
not to do so
Media
Transparent media gives a better visualisation for finer points. The position of
opacities can be made out by examining at a distance of 20 cm or by interposing plus
lenses and gradually reducing the distance while examining with the direct ophthal-
moscope.
Disc
Optic disc is examined for shape, size, colour, margin, cup, elevation, crescent, super-
traction, haemorrhage on the surface, abnormal tissues on the surface, neovascularisa-
tion on the disc and pulsation of vessels.
Shape—Normal disc is almost circular. It looks oval in astigmatism. Vertically oval
disc is more common than horizontally oval. In case of subluxated clear lens two disc
images may be visible, a large one through the phakic area and a small one through
the aphakic area.
Size—Normal disc is 1.5 mm in diameter. In aplasia and hypoplasia, it is smaller.
In aphakia it looks smaller. Size of disc varies with refractive error of the eye. In
coloboma of the disc, the disc is large. Myopic discs look larger than the emmetropic
disc and hypermetropic smaller.
Colour—Optic disc being part of a nerve has white colour. It looks pink due to small
capillaries on the disc, which are normally between 10 and 15 in number. Capillaries
more than these give a hyperaemic appearance and less than this gives a pallor.
Causes of pale disc are—severe systemic anaemia, central retinal artery obstruction,
ischaemic optic neuropathy, optic atrophy (primary optic atrophy gives a chalk white
colour, while secondary optic atrophy gives a waxy pale colour), glaucoma, coloboma
of disc and myopia.
Causes of hyperaemic disc are—optic neuritis, papilloedema, venous obstruction,
neovascularisation of disc and trace of blood on the disc surface. Sometimes splinter
haemorrhages are visible on the disc surface.
Pigmentation—There may be deposit of pigment on the optic nerve in benign nevus.
Margin—Normal margin of disc is sharp. Causes of blurred disc margin are pseudo-
neuritis, optic neuritis, papilloedema, post-papilloedema optic atrophy, drusen of optic
disc, opaque nerve fibre and venous obstruction.
Physiological cup of the optic nerve—A normal depression in the optic nerve head is
due to backward bowing of lamina cribrosa. It occupies almost one-third of the lateral
side of the disc bed. Its lateral floor has a gradual slope towards centre. In a normal eye,
it is paler than rest of the disc. It shows small bluish dots on its floor, which represent holes
in the lamina. The holes remain visible in primary and glaucomatous optic atrophy. They
are prominent in congenital pits of optic nerve. They become obscured in hypoplasia of
disc, pseudo-neuritis, papillitis, papilloedema, secondary optic atrophy, drusen of optic
nerve and venous congestion of the disc. The cup is examined for its size and depth.
Size is noted in relation to diameter of the disc head. It increases in glaucoma. In an
advanced case of glaucoma, the cup may be very large and extend up to margin of the
disc. Vertical spread and presence of notch are suggestive of chronic simple glaucoma.
Neuro-retinal rim—This is a part of the disc that surrounds the cup. It is pale in
neurological disorders and narrow in advanced glaucoma.
Depth of the cup is measured by direct ophthalmoscope. First retina adjacent to disc is
focussed then the beam of the light is shifted to the cup and minus lenses are added till the
bottom of the cup is clearly visible. Three dioptre of change in depth represent 1 mm of
excavation. Depth of cup is increased in chronic glaucoma, myopia, and coloboma of disc.
Elevation of disc is measured by adding plus lenses to make the apex of elevation
visible, 3 dioptre is equal to 1 mm of elevation. Disc surface is raised in pseudo-neuritis,
optic neuritis, papilloedema, drusen of disc, and venous congestion.
Crescent of optic disc—Normally choroid and retina reach up to the margin of the
disc but when they fail to do so a crescent shape gap is seen adjacent to the disc with
concavity towards the disc. Commonest crescent is seen on the temporal side. In high
myopia, it may encircle whole of the disc.
Haemorrhage on the disc—Splinter haemorrhages are seen in chronic simple glau-
coma. There may be superficial haemorrhages in papilloedema, papillitis, central vein
obstruction, central Eales’ and neovascularisation of disc.
Abnormal tissue on the disc surface—Remains of hyaloid artery may be present at
optic nerve head as Bergmeister’s papilla. Sometimes a thin translucent membrane
may also be seen as a congenital anomaly.
Neovascularisation of the disc—It is seen as a part of new vessel formation in prolif-
erate diabetic retinopathy, central Eale’s, venous obstruction and sickle cell retinopathy.
General Appearance of Fundus (Retina and Choroid)

Retina is a transparent membrane and though it has its own blood vessels, they hardly
impart any colour to the retina. The pink colour of the fundus is due to choroid shin-
ning through the retina. When retina is separated, inflamed or oedematous, it
becomes white and obscures the choroid. Retina looks pale in anaemia, obstruction of
central retinal artery, attenuation of retinal artery due to toxin, retinal oedema, retini-
tis and retinal detachment.
Retina becomes hyperaemic due to venous congestion of any cause which may be
obstructive or inflammatory.
Tigroid or tessellated fundus is a normal phenomenon where pattern of choroidal

blood vessels become visible due to loss of pigment from pigment epithelium of retina.
It is more prominent in dark individuals, old age and myopia. It is not to be confused
with sclerosis of choroidal vessels.
General retinal background may be superimposed by exudates, haemorrhages, pig-
ments, scars, and new vessels formation. They may be present singly or in combina-
tion; a combination of exudate and haemorrhage is very common.
Blood Vessels
Central retinal artery after or just before piercing lamina divides into two main branches,
temporal and nasal. They again divide into superior and inferior branches. Each branch
sweeps away from the disc in an arcuate fashion with concavity inwards on their course
towards periphery. They divide and re-divide two to three times to be reduced to cap-
illaries. Each arteries has its corresponding venous component. The blood column is
almost four times the thickness of the wall at the entry of artery in the substance of the
disc. After the artery passes through the lamina, the wall is reduced to half of its thickness.
This is due to a lack of muscle coat and elastic lamina after the first bifurcation. The reti-
nal arteries are true arteries up to the second bifurcation; after that they are arterioles.
Arteries and veins are identified by their distinct characteristics. Arteries are thin,
rounded and paler than veins. Veins are broad, flatter and dark. Normal ratio of calibre
of artery to vein is 2 : 3. The artery may cross the vein either above or below. At the arterio-
venous crossing they have a common sheath. There are classical changes at the arterio-
venous crossing in arteriosclerosis, and hypertension. Artery being harder, is more prone
to sclerosis, and having a higher blood pressure, produce pressure changes in veins and not
the vice versa. In normal retina neither the arteries nor veins anastomose with each other.
They do not anastomose either among themselves or with choroidal vessels. Development
of anastomosis in retinal blood vessels is always abnormal—congenital or acquired.
Blood vessels are examined under following topics:
(1) calibre, (2) tortuosity, (3) irregularity, (4) changes in vessel wall, (5) aneurysm, (6)
anastomosis, (7) neovascularisation, (8) exudates, (9) haemorrhage and (10) chorio-
retinal scar.
Calibre—Normal ratio between artery and vein is 2:3. Veins get dilated more often
than arteries. Arteries get thinned more often than veins.
Causes of venous dilation are venous obstruction, papilloedema, angiomatosis and
haemangioma.
Causes of arterial dilatation are leukaemia, polycythaemia.
Causes of arterial thinning are central retinal artery or branch obstruction, retinitis
pigmentosa, arteriosclerosis, atheroma, drug induced spasm.
Tortuosity—Generally the course of retinal vessels is smooth. They can be tortuous
as in a congenital anomaly or in arteriosclerosis, hypertension, diabetes.
Irregularity of arteries is seen in arteriosclerosis, atheroma, hypertension. Venous
irregularity is seen in periphlebitis, neovascularisation, congenital malformation.
Changes in vessel wall are produced by increased light reflex from the anterior wall due to
sclerosis of the wall. There are silver wire appearance, copper wire appearance, sheathing
of the outer wall of the vessel or change in contents of vessels, e.g. lipaemia.
Aneurysms—Micro aneurysms are most commonly seen in diabetic retinopathy. Other

causes are CRVT, Eales disease, Coats disease. They look like small circular dots. Macro-
aneurysms are very rare; there may be aneurysmal dilatation in angiomatosis retinae.
Anastomosis—Generally retinal blood vessels do not anastomose with each other.
However there may be anastomosis between retinal artery and cilioretinal artery. In
angiomatosis retinae there is a prominent feeding artery that ends in a dilated mass
with a draining vein. There may be anastomosis formation between an artery and a
vein following trauma, toxoplasmosis.
Neovascularisation—New vessel formation always means hypoxia of retina. It can
develop anywhere. It can be on the optic disc and is called neovascularisation of disc
(NVD) Neovascularisation elsewhere (NVE) can be peripheral or central. They look
like tufts of blood vessels and are present either on the surface of retina, sub-retinal,
or may project in the vitreous.
Exudates
Retinal exudations are due to leak of serum, protein and fibrin from a diseased wall.
They may be due to trauma, infection, inflammation, degeneration of the vessel wall, dia-
betes, hypertension, arteriosclerosis, toxaemia of pregnancy. According to the level at
which they develop, they are called superficial and deep. Sometimes both types may be
present in the same eye.
Superficial or soft exudates (cotton wool exudate)—They are present in the nerve
fibre layers. They are due to anoxia and ischaemia following occlusion of small
capillaries; this is followed by oedema and proliferation of neural element. They rep-
resent axoplasmic residue. Soft exudates are seen in hypertension, toxaemia of preg-
nancy, central and branch vein thrombosis, retinitis, chorio-retinitis, Eale’s disease and
Coat’s disease.
Deep exudates or hard exudates—They are small with clear-cut border, waxy yel-
low in colour, circular in shape, situated in retinal layers deeper than the nerve fibre
layer. They are mostly seen in diabetic retinopathy. They should not be confused with
drusen of retina.
Haemorrhage
Retinal haemorrhages are caused due to escape of whole blood from the retinal blood
vessels. Haemorrhages in the fundus can be:
1. Intra-retinal
2. Sub-retinal
3. Pre-retinal (sub-hyaloid)
4. Combined
Intra-retinal haemorrhage Intra-retinal haemorrhages are by far capillary in nature

but can be arterial or venous.
They are of two types: superficial and deep; however, both can co-exist.
Superficial haemorrhages due to their shape and colour are also called flame-shaped
and splinter haemorrhages. They are seen in the nerve fibre layer of retina. They may
vary in shape, size, number and location and may be associated with exudates.
The common causes of superficial haemorrhages.

Hypertension, arteriosclerosis, central and branch vein obstruction, Eales disease,
Coats disease, papilloedema, papillitis, retinitis, anaemia, purpura, leukaemia, trauma
and sickle cell disease.
Deep haemorrhages Deep haemorrhages are like small pinpoint dots. They
may be single or in clusters. They are generally seen at the posterior pole. They are
in the deeper layers of retina and are generally seen with deep exudates. Superficial
haemorrhages and exudates may coexist with them. They are mostly seen in dia-
betic retinopathy. They are to be differentiated from microaneurysms, which have
a similar appearance and location. Both are seen in diabetic retinopathy. Fluorescein
is blocked by haemorrhages while micro-aneurysms become visible on fluorescein
angiography.
Pre-retinal haemorrhage Pre-retinal haemorrhages are also called sub-hyaloid
haemorrhages. They occur between the anterior limiting membrane of the retina and
vitreous. They are essentially large retinal haemorrhages mostly arising from unsup-
ported new vessels. To begin with, they are circular in shape and uniformly bright red
in colour; with gravity blood settles down at the lower part, in the shape of keel of a
boat with a horizontal level. They vary in size. Their location is generally at the pos-
terior pole. They may be small or may be large enough to obscure visibility of the fun-
dus behind. When they are large, they may invade the vitreous. They may absorb leav-
ing no trace. Recurrent haemorrhages cause development of vitreous bands.
Common causes of sub-hyaloid haemorrhages are Eales disease, proliferative dia-
betic retinopathy, central vein thrombosis and trauma.
Roth’s spots are a special type of superficial exudate in the centre of a patch of a
superficial haemorrhage. There may be more than one spot visible in fundus. They are
seen in anaemia, purpura, leukaemia and sub-acute bacterial endocarditis.
Sub-retinal haemorrhage They are generally localised and give a dark raised cir-
cular appearance. They occur between the choroid and pigment epithelium of retina.
The retinal vessels travel over them. They are caused due to trauma and neovascular-
isation of choroid. They block fluorescence. They must be differentiated from
melanoma of choroid. They are also known as neovascularisation of choroid. They
may be localised around the macula or away.
The common causes of sub-retinal vascularisation:
1. Age-related macular degeneration
2. Choroidal rupture
3. Histoplasmosis
4. Angioid streak
Chorio-Retinal Scar
Initially, they are raised diffuse, waxy pale areas that obscure retinal vessels and choroidal
pattern. Vitreous opacity in front of an acute chorio-retinal scar is common. On healing
they become white in colour and irregular edges and pigments. Causes are trauma,
rupture of choroid, retinitis, toxoplasmosis, diathermy, cryo and laser.
Retinal Detachment
When fluid accumulates between the sensory retina and the pigment epithelium, the
former is pushed away from the latter and a retinal detachment takes place. Retinal
detachments are invariably caused by a retinal tear or hole. A detached retina is raised
from its surroundings. It is white in colour and there are corrugations on the surface
of detached retina. Blood vessels travel over the detached retina, and colour of blood
vessels over the detachment is darker than normal.
Retinal detachment can occur anywhere in the retina depending upon the position
of the causative hole or holes. It may be localised, may spread to involve a large area
which may be the whole of retina.
Pigments in the Fundus

Pigments can be congenital, which are relatively rare, are circular in shape and seen in
clumps. More important are the spider-shaped pigments of retinal dystrophy that develop
in the mid-periphery. Pigments of chorio-retinal scar are of an irregular shape and size.
Causes of sub-retinal neovascularisation:
1. Age-related maculopathy
2. Myopic degeneration
3. Angioid streak
4. Optic nerve drusen
5. Toxoplasmosis
6. Rubella
7. Choroidal rupture
8. Coloboma choroid
9. Post photo-coagulation
10. Central choroidopathy
Retinal Breaks (Fig. 20.9)

These are full thickness defects in the neuroretina establishing a communication between
the vitreous cavity and pigment epithelium (Figs 20.10 and 20.11). Vitreous can percolate
through the breaks and separate the neuroretina from the pigment epithelium resulting
into retinal detachment. It should be noted that all holes do not produce retinal detach-
ment all the time. A retinal detachment due to a break is called Rhegmatogenous while those
due to pull by tractional band is called a traction detachment, that may be worsened by the
6b. Horse-shoe tear with detachment

6a. Horse-shoe tear
1. Circular small holes in aphakia
Lattice degeneration
2a. Hole without operculum
5. Retinal tear with traction band and flap
2b. Hole with operculum
Vitreous opacity
Retinal exudate 3. Dialysis with shallow detachment
4. Hole with pigment on the periphery
Fig. 20.9 | Various types of retinal lesions.

presence of a break or tear. When all the layers of retina are lifted from the choroid, it
is called secondary detachment.
According to their shape, size and position they are called holes, tear or dialysis. Holes
are generally circular. They may be with or without an operculum. Tears are generally
irregular, triangular or arrow head shaped. They too may have an operculum. Dialysis or
disinsertion is separation of retina from periphery. They are large, the border is concave.
The edge may be rolled up.
Primary retinal detachment must be differentiated from secondary retinal detachment,
choroidal detachment and retinoschisis (Figs 20.12 and 20.13). It is better to call a
rhegmatogenous detachment a retinal separation while separation of all the layers of
retina from choroid should be called retinal detachment. For convenience sake, the
first is called primary retinal detachment and latter is called secondary (serous or solid).
Tractional detachment holds a place in between the two. Sometimes simple oph-
thalmoscopy, direct and indirect, may not be sufficient to clinch the diagnosis. Following
points may be noted to differentiate them (Table 20.5).
Vitreous
Sensory retina
Pigment
epithelium Choroid
Sclera
Note: Gap between the sensory retina and pigment
epithelium is the potential space where retinal
separation occurs
Fig. 20.10 | Normal relation of retina to other structures.
Fig. 20.11 | Primary rhegmatogenous retinal detachment. Sub-retinal fluid between sensory retina and pigment
epithelium.
Sensory retina
Pigment epithelium Choroid
Fluid or moss
Sclera
Fig. 20.12 | Retina and choroid lifted off from the sclera.
Retinoschisis
This is a less common condition. In contrast to retinal detachment where there is a sep-
aration between the sensory retina and pigment epithelium, in retinoschisis there is a split
in-between the layers of sensory retina. There are two forms, juvenile and adult (senile).
Juvenile form is rarer than senile. Retinoschisis may be unilateral or bilateral; it is gener-
ally seen in inferotemporal part. It is more common in hypermetropia and produces an
absolute scotoma. It is thought to be an exaggerated form of cystoid retinal degeneration.
It has two layers. The inner layer is thin and bulges towards vitreous, with a beaten
metal shine; there may be many round holes in the inner layer. Inner layer is transpar-
ent with small snowflake deposits. The deeper layer has larger holes, it is hazy, and
details of choroid are not seen through it. Retinoschisis is mistaken for retinal detach-
ment, which may otherwise be its complication if there are holes in both the layers.
Retinoschisis
Hole
Pigment
epithelium Choroid
Sclera
Fig. 20.13 | Retinoschisis is a separation between the layers of sensory retina.
Table 20.5 Comparison between rhegmatogenous, traction and exudative detachment
Features Rhegmatogenous Traction Exudative or solid
Incidence Common Common Less common

Break Always present and are the Are not present initially. May Nil
cause of detachment. May develop later and worsen
not be visible in aphakia the condition
Shape Convex surface with convex Concave surface Convex
border with concave border
Size May be small but expands Generally smaller, does not Small, never involves whole
soon, may involve whole reach ora retina
retina
Sub-retinal fluid Does not shift Does not shift Shifts
Elevation May be shallow or ballooned, Variable; generally low Depends upon the size of
more marked in upper holes sub-retinal lesion
Fluorescein Non-contributory May show changes in blood Leaking and pooling of the dye
angiography vessels; may have window in sub-retinal fluid
defect
Ultrasonography Shows detachment but not the Non-contributory May show the cause
cause
Trans-Illumination Non-contributory Non-contributory Growth may obstruct light
Surface Corrugated due to inter-retinal Smooth Smooth
oedema
Colour of new vessels Absent May be present Seen at the apex of tumour
IOP Normal or low Normal May be raised
Symptoms and signs of retinal detachment:

1. No symptoms—Many times a shallow retinal detachment, away from macula in the lower
part, may not produce any symptom
2. Floaters—Patients may complain of floaters, which may suddenly increase in number and size
3. Photopsia—Flashes of light generally in the periphery
4. Diminished vision—So long the macula and para-macular area are not detached, patient may
not complain of diminished vision. Once macula is involved, there is a rapid fall in vision
Causes of diminished central vision in retinal detachment are:
● Involvement of macula
● Spread of detachment to macula
● Overhanging upper detachment
● Large vitreous floater
● Bleeding from torn vessels at the site of tear
5. Loss of field—Lower and temporal field losses are detected earlier than upper and nasal field loss
6. Pupillary reaction—Early and small detachment do not produce any pupillary change. In
advanced retinal detachment, there is afferent pupillary defect
7. Intraocular tension—Eye with retinal detachment have lower tension by 4.5 mmHg
8. Retinoscopy—A detached retina due to its pale colour gives a grey fundal glow especially if
the posterior pole is involved. Due to forward shift of retina there may be relative hypermetropia,
i.e. reduction in myopia and increase in hypermetropia
9. Direct ophthalmoscopy—may reveal retinal detachment but may fail to demonstrate retinal
break. Due to lack of stereopsis shallow detachments may not be appreciated
10. Indirect ophthalmoscopy is the best instrument to diagnose retinal detachment. If needed,
scleral depressor may be used. The only difficulty is that the image is inverted and laterally
reversed. This requires proper orientation
11. Ultrasonography shows retinal detachment clearly and helps in differentiating between the
various types of detachment
Pre-disposing factors in rhegmatogenous retinal detachment:
1. Heredity
2. Myopia
3. Aphakia
4. Pseudophakia
5. Blunt trauma
6. Penetrating injury
7. Lattice degeneration
8. Posterior vitreous detachment
9. Use of strong miotics
10. Retinoschisis
11. Congenital coloboma of choroid
Pre-disposing factors in tractional detachment:
1. Vascular
(a) Diabetic retinopathy
(b) Sickle cell anaemia
(c) Central vein thrombosis
(d) Eale’s disease
(e) Retrolental fibroplasia
(f) Persistent hyperplastic primary vitreous
2. Inflammation
(a) Pars planitis
(b) Healed endophthalmitis
(c) Toxoplasmosis
(d) Toxocariasis
3. Trauma
(a) Surgical
● Lens extraction with vitreous disturbance
● Repeated needling in congenital cataract
● Laser capsulotomy in myopic eyes
(b) Perforating injury

(c) Retained intraocular foreign body
Characteristics of tractional detachment:
1. Vitreo retinal band
2. Spreads slowly
3. Sub-retinal fluid is uveal in nature rather than vitreous.Vitreous may find its way through a break
4. Detachment has maximum elevation at the site of attachment of the traction band
5. Fluorescein angiography may show window defect
Conditions that mimic rhegmatogenous retinal detachment (Table 20.6):
1. Tractional detachment
2. Exudative detachment
3. Solid detachment
4. Ciliochoroidal detachment
Table 20.6 Comparison between rhegmatogenous retinal detachment (RRD) and

ciliochoroidal detachment (CCD)
Features RRD CCD
Holes Essential pre-requisite Nil

Location Between sensory retina and Between uvea and sclera
pigment epithelium
Nature of sub-retinal fluid Mostly fluid vitreous, rarely blood Transudate from choroid
Predisposing factor Myopia, aphakia, trauma, peripheral Intraocular surgery,
degeneration, posterior trauma, hypotony, uveitis,
vitreous detachment nanophthalmos
Position Any part of the retina Limited between scleral
spur and vortex ampulla
Shape Convex. Funnel shape in total RRD Convex. In total CCD four
quadrilateral elevations
separated by a cleavage
Surface Corrugated Smooth
White Greyish black
Blood vessels—dark Normal colour
AC Normal Shallow
Ciliary body Normal Moves forward
Iris lens diaphragm Normal Pushed forward
IOP Normal or low Very low
Recovery Spontaneous recovery not possible May resolve spontaneously
Surgery Essential May be required
5. Retinoschisis
6. Retinal tumour
7. Retinal cyst
8. Endophthalmitis
9. Unabsorbed vitreous haemorrhage
10. Lens dislocated in vitreous
Causes of exudative retinal detachment:
1. Inflammatory
(a) Posterior uveitis
(b) Chorioretinitis
(c) Posterior scleritis
(d) Vogt Koyanagi Harada syndrome
(e) Sympathetic ophthalmia
2. Retinal pigment epithelial disease
(a) Central
(b) Retinal pigment epithelium detachment
3. Sub-retinal neovascularisation
(a) Presumed ocular histoplasmosis
(b) Age-related macular degeneration
4. Systemic disorder
(a) Toxaemia of pregnancy
(b) Malignant hypertension
(c) Renal failure
5. Neoplasm
(a) Choroidal melanoma
(b) Malignant melanoma
(c) Retinoblastoma
6. Miscellaneous
(a) Choroidal effusion syndrome
(b) Extensive photo-coagulation
(c) Excessive cryo
(d) Post operative ciliochoroidal detachment
● Intra capsular lens extraction
● Filtering surgery
● Leaking wound
7. Congenital
(a) Nanophthalmos
(b) Morning glory syndrome
Common Peripheral Retinal Degenerations

Peripheral retinal degeneration are very common. They are generally bilateral. They may
begin in childhood. Some of them may predispose to retinal detachment. Appearance
of peripheral degeneration does not present their true nature as far as retinal detach-
ment is concerned.
Common peripheral retinal degenerations are:
1. Lattice degeneration
2. Paving stone degeneration
3. Cystoid degeneration
4. Retinoschisis
5. Snow flake degeneration
COMPARISON BETWEEN APHAKIC AND PSEUDO-PHAKIC

RETINAL DETACHMENT (Table 20.7)
Before intraocular lens implant became a routine procedure it was thought that reti-
nal detachment was far less common in pseudophakia than in aphakia. With ever
increasing number of patients under going PCIOL surgery it has been found that
pseudo-phakic retinal detachment is not so uncommon as was thought to be.
Common vascular disorders of retina:
1. Retinopathy of prematurity
2. Retinal vasculitis (Eale’s disease)
3. Arterial occlusion
(a) Central retinal artery
(b) Branch
4. Venous occlusion
(a) Central vein occlusion
(b) Branch vein occlusion
5. Coats disease
6. Vascular retinopathies
(a) Diabetic retinopathy
● Pre-proliferative
● Proliferative
(b) Hypertensive retinopathy

(c) Toxaemia of pregnancy
(d) Sickle cell retinopathy
7. Retinal telangiectasis
Table 20.7 Comparison between aphakic retinal detachment and pseudo-phakic retinal
detachment
Features Aphakic retinal detachment Pseudo-phakic retinal detachment
Incidence 1% of all cases Slightly higher, more common

following YAG capsulotomy
Time lapse Less common in first Most common in first
post-operative year post-operative year
Holes Multiple round small holes Generally single and
on the periphery; may not well visualised, large
be visible with ophthalmoscope
Symptoms Develop late Symptoms appear early as
vision is better following pseudophakia
Extension of Has tendency to develop total Depends upon the location of holes but
detachment detachment less likely to develop total detachment
Relation to Needling or capsulotomy by YAG capsulotomy produces
management of after knife produced tractional rhegmatogenous detachment
cataract detachment
FUNDUS EXAMINATION IN RETINOPATHY OF PREMATURITY

(RETROLENTAL FIBROPLASIA)
This is a bilateral proliferative retinopathy commonly seen in children who have

weight less than 1300 g and have also been exposed to high ambient O2 concentra-
tion. Generally these infants are premature. The condition is potentially blinding.
The fundi of these children should be examined by indirect ophthalmoscope with
maximum pupillary dilatation after 4–6 weeks of chronological age or 31–33 weeks
post-conceptual age (Fig. 20.14).
Post conceptual age Gestational age Chronological age
To draw ROP chart:
1. Use usual retinal chart with macula as centre
2. To draw zone 1
(a) Take centre of optic disc as centre
(b) Draw a circle with radius 2 times the distance between the centre of disc and macula
3. To draw zone 2 draw a circle with O as centre and diameter up to nasal periphery
4. The remaining temporal crescent is zone 3
Stages of Retinopathy of Prematurity

Stage 1: Stage of line of demarcation, separating the avascular immature retina from
vascularised mature retina
Stage 2: Stage of ridge of demarcation
Stage 3: Stage of extra retinal fibro vascular growth, which may be mild, moderate or severe.
Stage 4: Stage of retinal detachment
Stage 4a: Subtotal detachment with spared macula
Stage 4b: Macular involvement in retinal detachment
Stage 5: Total retinal detachment
Plus disease: Tortuous dilated vessels in zone 1
Threshold disease: Plus disease associated with stage 3 in zone 1 and zone 2 spread over
5 contagious or 8 non-contagious clock hours
Post conceptual age ⫽ Gestational age ⫹ Chronological age

12
Zone 3
Zone 2
Nasal ora
Zone 1
Temporal ora
Optic nerve
6
Macula
Fig. 20.14 | Chart to draw fundus picture of ROP.

Classification of Diabetic Retinopathy

There are many classifications of diabetic retinopathy, most commonly used classifi-
cations are:
1. Early treatment diabetic retinopathy study (ETDRS) classification (Flowchart 20.1)
2. Diabetic retinopathy study (DRS) classification
DRS classification:
1. Early non-proliferative retinopathy
(a) Without maculopathy
(b) With maculopathy
2. Advanced non-proliferative retinopathy
(a) Without maculopathy
(b) With maculopathy
3. Proliferative retinopathy
(a) Without high risk
(b) With high risk
High risk factors:
1. Neovascularisation of disc (NVD) 1/3 – 1/2 DD with pre retinal haemorrhage
2. NVD 1/2 DD with or without pre retinal haemorrhage
3. Neovascularisation elsewhere (NVE) 1/2 DD with pre retinal haemorrhage
Maculopathy consist of focal or diffuse macular oedema, cystoid macular oedema
and ischaemic changes (see examination of macula).
ETDRS classification
Non-proliferative diabetic retinopathy (NPDR) Proliferative diabetic retinopathy (PDR)
Mild–minimum micro aneurysms NVD/NVE
or
Moderate – Venous haemorrhage
Cotton wool exudate Pre-retinal/Vitreous haemorrhage
Intra retinal micro-
vascular changes or
Severe – Fibrous tissue proliferation

All quadrants show retinal (Presence of any of above is diagnostic of PDR)
haemorrhages and micro
aneurysm
At least two quadrants have

venous haemorrhage
One quadrant shows intra-

retinal micro vascular changes
Flowchart 20.1 | ETDRS classification.

Table 20.8 Stages of hypertensive retinopathy
Group Characteristics
I Often missed, seen in mild hypertension, transient narrowing of arterioles or

spasm of arterioles, no exudate or haemorrhage, have good life expectancy
II Obvious fundus changes, well-established hypertension, narrowing
of arteriole, AV ratio may be 1 : 3 (normal 2 : 3). Expected mortality
within five years 40–45%
III Marked fundus changes. Severe narrowing of arterioles,
straightening of arterioles with acute branching, arteriovenous
crossing defects, flame-shaped haemorrhages, soft exudates,
retinal haemorrhage without change in disc. Mortality rate high
IV Severe form of group III with papilloedema, very poor prognosis
Classification of Hypertensive Retinopathy

As per old classification, retinopathy is divided into following groups (Table 20.8).
Arteriosclerotic and Arteriovenous Crossing Changes

Sclerotic changes in arterioles denote:
1. They reflect similar changes in brain, heart and kidney (which are not available for visual examination)
2. Roughly indicate duration
3. Reflect prognosis
Arteriosclerotic changes consists of:
1. Changes in transparency of vessel wall (arteriole)
2. Changes in light reflex
(a) Copper wire
(b) Silver wire
3. Arteriovenous crossing changes
(a) Compression of the vein by artery
(b) Banking of the vein
(c) Widening of venous column distant to disc
(d) Deflection of veins at AV crossing
Modern Classification of Hypertensive Retinopathy

Keith–Wagner–Baker Classification (Table 20.9)
Table 20.9 Keith–Wagner–Baker classification
Stage Characteristics
Stage I Minimal arteriolar thinning

Stage II Localised irregularity in arterial blood column, focal constriction
of lumen, generalised narrowing, AV crossing changes
Stage III All above changes in greater degree
with superficial exudates and haemorrhages.
A few hard exudates may be present
Stage IV Stage III changes with papilloedema
Table 20.10 Comparison between non-ischaemic and ischaemic central retinal vein obstruction
Features Non-ischaemic Ischaemic
Incidence More common: 75–80% Less frequent: only 20–25%

Visual loss Painless, slight or moderate, Painless, marked, unilateral but
generally unilateral generally patient becomes
aware of loss of vision
Pupil May be normal; In the long run, may Marcus–Gunn pupil develops early,
develop Marcus–Gunn pupil may be present at first visit
Fundus changes
Venous dilatation Mild to moderate Well marked
Retinal haemorrhage Flame-shaped at the periphery Severe superficial haemorrhages
involving mostly posterior pole
Cotton wool spots Absent Frequent
Macular changes May or may not be present, late Early and marked
to develop
Disc swelling Mild Moderate to severe
FFA Good capillary perfusion, venous Extensive capillary non-
stagnation perfusion
Complication Some vision may be regained. Visual loss due to neovascular
50% may have almost normal vision glaucoma and proliferative
retinopathy
EXAMINATION OF MACULA
Macula is that part of the retina which is responsible for central vision, colour vision
and stereopsis. In each eye it is situated temporal to the optic nerve. Its inner border is
two-disc diameter away from the temporal border of the optic nerve. (Fig. 20.15) It is
circular in shape. A point 0.33 mm in diameter at the centre of this circle is called
foveola, which is surrounded by an avascular zone of 0.5 mm. The foveola and the
avascular zone are surrounded by the less sensitive fovea, diameter of which is 1.5 mm.
The temporal retinal arteries arch over the macula, they may reach the outer periph-
ery of the fovea. The fovea gets its blood supply from the chorio-capillaries under-
neath. Macula is the thinnest part of retina.
Macular disorders may be congenital and present at birth, e.g. coloboma of mac-
ula, hypoplasia of macula and scar of toxoplasmosis. They have profound visual effects.
Vision loss due to macular disorders may be associated with squint and nystagmus.
It may be congenital/hereditary but manifest in childhood or later. The heredo-macular
degeneration and dystrophies are generally bilateral.
The acquired lesions can be traumatic, inflammatory, vascular, dystrophies and
degenerations.
They are:
1. Commotio retinae (Berlin’s oedema)
2. Central serous chorio-retinopathy
3. Central choroiditis
4. Macular dystrophies
Macula lutea
1.5 mm
Fovea 1.5 mm
1.5 mm 5 mm Foveola 0.33 mm
Fig. 20.15 | Relative position of macula and size of its different parts.
5. Macular oedema
(a) Traumatic
(b) Secondary to vascular retinopathy
6. Macular cyst
7. Macular hole
8. Chorio-retinal scar involving macula
9. Storage diseases (Cherry red spot)
10. Haemorrhage over the macula
12. Solar retinitis
13. Laser burn (accidental)
14. Radiation retinopathy
15. Drug-induced maculopathy
16. Macular pucker
17. Sub-retinal neovascularisation
Causes of macular oedema can be unilateral or bilateral and need not be equal or
simultaneous.
Characteristics of clinically significant macular oedema:
1. A zone of retinal thickening of one disc diameter or more located within one disc diameter
from the centre of macula
2. Hard exudate with thickening of surrounding retina within 500 micron from the centre of macula
3. Thickening of retina all around located 500 micron from the centre of macula
The causes are:
1. Trauma
● Commotio retinae
● Electric shock
● Radiation retinopathy
● Excess photo-coagulation
2. Inflammation
● Anterior uveitis
● Posterior uveitis
● Parsplanitis
● Intra retinal nematode
3. Retinopathy
●Central vein thrombosis

●Coats disease
4. Central serous retinopathy
5. Congenital pit of optic nerve
6. Vascular malformation
7. Haemangioma choroid
8. Macular dystrophy
Causes of sub-retinal neovascularisation:
1. High myopia
2. Angioid streak
3. Rupture of choroid
4. Chorio-retinitis
5. Rubella retinopathy
6. Presumed ocular histoplasmosis
7. Choroidal naevus
8. Melanoma choroid
9. Haemangioma choroid
10. Serpiginous choroiditis
11. Best’s disease
12. Excessive photo-coagulation
Age-Related Macular Degeneration (ARMD)

Age-related macular degeneration (ARMD), formely known as senile macular degene-
ration, is one of the common causes of legal blindness in non-diabetic, aged persons.
The incidence increases with age. It is a bilateral, slowly progressive disease without a
satisfactory management. The two clinical types of ARMD are (1) Dry and (2) Wet
(Table 20.11).
Symptoms of Macular Disorders

Visual Symptoms
2. Diminished near vision in both presbyopic and pre-presbyopic age which is independent of
accommodation. Pre-presbyopes complain of diminished near vision. Presbyopes have difficulty
with usual near correction
3. Diminished fine vision
4. Micropsia, macropsia and metamorphopsia
5. Diminished colour sense (late)
6. Positive central scotoma
7. Poor photopic vision
8. Poor stereopsis
Methods of Examination of Macula

1. History—any or many of the above symptoms may be present. Acute symptoms are generally
unilateral
Table 20.11 Comparison between dry and wet ARMD
Features Dry Wet
Age Past 50 Past 50

Visual loss Gradual Rapid and progressive
Vision Loss of central vision, Fast deteriorating central vision, spreads to
peripheral vision maintained periphery. Not correctable
Metamorphopsia Present Present
Near vision Not correctable, diminished Late onset but not correctable
Fundus Dull or absent foveal reflex, RPE detachment, dome-shaped
atrophy of RPE, capillary elevation, sub-retinal neovascular membrane,
drop out, Mottling of pigment leaking SRNVM may lead to vitreous
haemorrhage and formation of disciform scar
Management Low vision aids Laser photo-coagulation of neovascularisation
followed by low vision aid
(a) Naked eye vision. Range between 6/9 and 6/60
➤ Isolated largest macular lesion will not produce loss of perception of light
(b) Vision with pinhole—No improvement or little improvement. May become worse
(c) Vision with distant correction—less than what it used to be before the onset of macular
disorder
3. Amsler grid—central scotoma
4. Brightness—not changed
5. Photo-stress test—positive: This is a crude method to evaluate photoreceptors to re-synthesise
visual pigment following exposure to bright light.To perform the photo-stress test, distant vision is
noted. If necessary full distant correction is given.Vision with distant correction is noted. Effected
eye is exposed to light of indirect ophthalmoscope held at 3 cm distance for 10 s. After 10 s, the
patient is asked to read the best corrected line on Snellen’s chart. Soon after exposure to bright
light, vision on Snellen’s chart is diminished.The vision returns to original line in 20–30 s in normal
patients. In macular lesion, this time becomes 50 s or more. In unilateral lesion the normal eye acts
as a control.
6. Examination of macula by slit-lamp microscope
(a) With strong minus lenses
(b) With strong plus lenses
8. Ultrasonography
9. Optical coherence tomograph (OCT)
(This can also be used to analyse tension of optic nerve head and retina)
Fluorescein Angiography
Invention of fundus fluorescein angiography (FFA) in diagnosis and photo-coagulation
in management are two most important advances in the management of vascular disor-
ders of retina, macula and choroid.
Properties of fluorescein—Fluorescein is available as a water soluble crystal. Both solid
and aqueous solutions have fluorescent property, which is maximum in blue light. Its pH
Table 20.12 Comparison between macular and optic nerve lesions
Features Macular Optic nerve
Distant vision Diminished Diminished

Scotoma Positive Holes in field
Central Centrocaecal
Metamorphopsia Positive Negative
Colour vision Slightly disturbed Grossly disturbed
Pupillary reaction Brisk May be Marcus Gunn (RAPD)
Brightness No change Dull
Amsler grid Positive Holes in grid sometimes
Photo-stress test Positive Negative
is 7.4. It is commercially available as 5, 10 and 25% sterile aqueous solution for intra-
venous injection. On intravenous injection 75% dye gets bound to serum albumin and
rest circulates as free fluorescein. Injected or orally ingested fluorescein is excreted in
urine in two to four hours. It stains the urine yellowish green and gives the skin a jaun-
diced look. When injected in antecubital vein, it takes 8–10 s for the dye to reach reti-
nal circulation and 3–4 s for it to clear out of retinal circulation. Hence it is to be given
in a bolus form and pictures are taken in quick succession at an interval of 1 s for 5 s.
Fluorescein when injected intravenously, is not visible with both direct and indirect
ophthalmoscope, or slit lamp in white light. To see the fluorescein and to photograph
its passage through circulation a blue light is a prerequisite. Observation of fluorescein
by ophthalmoscope is called fluoroscopy. It has a very limited value but is helpful where
FFA is not available.
For fluorescein angiography a specially designed fundus camera is required. Some
molecules when subjected to stimulation by light in short wavelength emit longer
wavelength. This property is called fluorescence.
The camera, besides having its having its usual arrangement for quick photography
by automatic clicking, has two more important components that differentiate it from
other cameras
(a) A blue exciting filter 490 nm
(b) A yellow green barrier filter 530 nm
A camera can take either still or movie photographs. Some of the cameras have time
markers that get photographed on the film.
For FFA pupils should be widely dilated; presence of opacities in the media inter-
fere with clarity of pictures. The patient sits on a fluorescein unit. Patient is explained
the outline of the test.
A tray containing emergency medicine with a disposable 2 cc syringe, and fitting
needle is kept handy. It is better to keep a separate fluid line running at bare minimum
flow for emergency. Injection of dye in this fluid line dilutes the dye. Hence, fluores-
cein is injected in bolus form by a separate 10 cc syringe directly. Concentration of
dye does not influence adverse reaction. Common untoward effects are nausea, dizzi-
ness, red after image, fainting; serious complications are syncope, laryngeal oedema,
bronchospasm and anaphylactic shock.
Fluorescein injected is either 10 cc of 5%, 5 cc of 10% or 2.5 cc of 20% solution,

in the antecubital vein. A picture is taken before dye reaches the eye. There after pho-
tographs are taken at an interval of one second between 5 and 20 s. Later pictures can
be taken at 5, 10 and 20 min. Arrival of dye in eye is enhanced in anaemia and delayed
in obstruction of carotid.
The dye passes freely through the smallest capillary lumen but not through normal
capillary endothelium. Thus any leak in vessel wall is pathological. Dye also does not pass
through retinal pigment epithelium and large choroidal vessels. Dye however passes
through very fine chorio-capillaries.
Dye reaches the fundus in two distinct phases:
1. Choroidal phase—Choroidal phase represents filling of choroidal vasculature via long posterior
ciliary artery
2. Retinal phase—Retinal phase follows the former. It is due to filling of retinal vessels. It has follow-
ing components:
● Arterial
● Capillary
● Venous
1. Arterial phase begins with the appearance of dye in central retinal artery and completes with fill-
ing of whole of the arterial tree
2. Capillary phase denotes beginning of emptying of arteries and start of laminar flow in veins; in
between these two phases there is complete filling of capillaries
3. Venous phase is sub-divided into early, intermediate and late venous phase. Early venous flow is
seen as two streaks of dye in the vein. In venous phase whole of the vasculature stands out promi-
nently against dull choroidal background except the foveal area that looks black due to:
● Foveal avascular zone
● Increased xanthophyll
● Excess of melanin in retinal pigment epithelium.
Fluorescein is blocked due to obstruction of view by:

1. Pigment—xanthophyll, melanin and lipofuscin
2. Blood—haemorrhage
3. Exudates—soft and hard
4. Oedema
5. Obstruction in flow
● Closure of capillary, non-perfusion
● Absence of vessels—myopia and choroideraemia
The above phenomenon is called hypofluorescence.

Causes of hypofluorescence are:
1. Retinal haemorrhage
2. Pre-retinal haemorrhage
3. Hard and soft exudates
4. Healed choroiditis
5. Retinal vascular obstruction
6. Choroidal naevus
7. RPE hyperplasia
8. Choroidal haemorrhage
Hyperfluorescence is visibility of dye in excess of normal. It is caused by:

1. Defect in RPE, window defect
2. Accumulation of dye under detached RPE
3. Break down of blood retinal barrier
4. Bleeding from retinal or chorio-capillaries
5. Retention of dye due to any cause
6. Albinism
7. Drusen
8. Coloboma of choroid
9. Angioid streak
10. RPE atrophy
11. RPE detachment
12. Central serous retino choroidopathy
13. Retinal vasculitis (Eale’s)
14. Chorio-retinal scar
15. Diabetic retinopathy
16. Coat’s disease
17. Sickle cell retinopathy
19. Angiomatosis retinae
20. Malignant melanoma
Purpose of fluorescein angiography:

1. To see the characteristics of blood flow in vessels—Narrowing, obstruction, non-perfusion, leak,
new vessels formation, anastomosis
2. Outline details of area that are otherwise not visible with ophthalmoscope e.g. micro
aneurysms, sub-retinal neovascularisation, hypoxic areas
3. To document:
(a) Progress of a lesion
(b) Regression of a lesion
(c) New lesion
Indocyanine green (ICG) angiography

Indocyanine green shows fluorescence in infra red range (835 nm). It does not leak
from choroidal vessels including chorio-capillaries. It enhances outline of choroidal ves-
sels and choroidal neovascularisation which is not well delineated by fluorescein.
Indocyanine green is used as intravenous fluid, 98% of it is bound to plasma protein.
It is mostly used in choroidal vascular disorders but can be used in retinal disorders of
some patients allergic to fluorescein.
E XAMINATION OF V ITREOUS
Till a few decades ago the vitreous was supposed to be an unwanted evil without any
function except to fill the gap between the lens and the retina. With popularisation of
indirect ophthalmoscopy, biomicroscopy of the posterior pole, advent of fluorescein angio-
graphy and ultrasonography its role in various disorders of eye has been understood better
and vitreous is no more an inert jelly.
PECULIARITIES OF VITREOUS
1. Vitreous is a gel with 99% water and 1% other constituents, mostly hyaluronic acid that
imparts its viscosity
2. It is avascular, but retinal vessels can grow into it
3. It is not affected by primary infection or inflammations
4. When micro-organisms find their way into the vitreous they multiply and thrive, since the vit-
reous acts as a good naturally occurring medium
5. Infection and inflammation both reach it via retina and choroid
6. Exogenous entry of micro-organisms invariably leads to severe inflammation
7. Vitreous is not known to cause an allergic reaction
8. There are no known growths of vitreous, however retinal and uveal growths can protrude
into the vitreous
9. It does not have a formed capsule
10. Vitreous is said to have three stages of development; primary, secondary (adult vitreous) and
tertiary vitreous (zonules of lens)
11. The primary vitreous starts developing from a very early stage and continues up to the 13 mm
stage. It is this central core of vitreous over which secondary vitreous is laid down. The pri-
mary vitreous gradually regresses after the 13 mm stage and disappears well before birth. Its
incomplete disappearance results in (a) Bergmeister papilla (on the disc), (b) Mittendorf ’s dot
(behind the lens) and (c) persistent hyperplastic primary vitreous.
The former two do not require treatment. The last one is a major ophthalmic problem in a child
12. It gets liquefied when degenerated
PERSISTENT HYPERPLASTIC PRIMARY VITREOUS
This condition is seen in those eyes in which the primary vitreous, that form a part of the
hyaloid system of vessels does not regress and there is hyperplasia of posterior vitreous.
These eyes are generally small and may be microphthalmic. It is invariably unilateral
and is a cause of white reflex in the pupillary area.
The affected eye is invariably blind and strabismic. The ciliary processes get elongated
and are visible through the clear lens. Due to rupture of the posterior lens capsule a com-
plicated cataract develops that may cause secondary glaucoma as the anterior chamber
is shallow, otherwise glaucoma may be independent of lens change.
EXAMINATION OF VITREOUS CONSISTS OF THE

FOLLOWING PROCEDURES
1. Distant vision with and without correction

2. Vision with PH
3. Examination of anterior vitreous
(a) Focal illumination
(b) Retinoscopy for retinal glow to locate opacities
(c) Slit-lamp biomicroscopy
(d) Ophthalmoscopy
4. Examination of posterior vitreous
(a) Indirect ophthalmoscopy with indentation
(b) Bio-microscopy with
● Hruby lens
● El Bayadi lens
● Volk lens
● Goldmann three-mirror contact lens to see the posterior pole and periphery
5. Fluorescein angiography for new vessel formation

6. Ultrasonography—B Scan
7. Vitreous aspiration for smear, culture and sensitivity of organism in endophthalmitis
8. Overall examination of the eye
ATTACHMENTS OF VITREOUS
Vitreous fills the space between the retina and the lens. It is a semi-solid gel. Normal vit-
reous does not move with movement of the eye because it is firmly attached to various
parts of the retina. These parts are (i) ora serrata, (ii) macula, (iii) rim of the optic nerve
and (iv) a loose attachment of vitreous to the internal limiting membrane of retina (Fig.
21.1). Hence if there is any traction, which is always pathological, there is every chance
of retina being pulled along with it and can cause a retinal break and traction detachment.
SYMPTOMS OF VITREOUS DISORDERS
Symptoms consist of :
1. Floaters
2. Diminished vision
3. Flashes of light
EXAMINATION OF VITREOUS 345
Fig. 21.1 | Attachments of vitreous.

Floaters
Any particle that is suspended in the vitreous is seen as a floater. The patients complain of
seeing either small pinpoint spots singly or in strings. The floaters may be large enough to
obscure the visual axis for a while. The causes of floaters are exogenous and endogenous.
Exogenous floaters consist of light foreign bodies suspended in the vitreous and
parasites. Endogenous causes of vitreous floaters are as follows:
A. Muscae volitantes
B. Blood products—RBC, leucocyte and pigment
C. Cholesterol crystals—Synchisis scintillans
D. Calcium salts. Asteroid hyalopathy
E. Parasites
Muscae volitantes: They represent very fine residue of the unabsorbed hyaloid vascular
system. They are seen as single or multiple pinpoint bodies in a string formation that
move freely in the vitreous. The shadow of these particles is projected in space and is
seen in normal light against a white background or sky. They do not need any treat-
ment nor do they cause any complication. They are not visible with the retinoscope or
the ophthalmoscope.
Synchisis scintillans: They may present as vitreous floaters and are generally seen in
traumatised eyes or in eyes that have previous history of inflammation. Rarely, they may
be idiopathic. These are cholesterol particles in liquid vitreous. The patient may not
be aware of them. They are visible as a golden shower on movement of eye on oblique
illumination when the lens is clear. Following intra-capsular cataract extraction they
may be seen in the anterior chamber.
Asteroid Hyalitis: These are non-symptomatic, mostly uniocular shinning bodies sus-
pended in solid vitreous. They are a mixture of calcium and lipid. They may obscure
part of the retina.
Diminished Vision
Causes of diminished vision in disorders of vitreous are:
1. Vitreous haemorrhage
2. Vitreous bands (retinitis proliferans)
3. Retinal detachment: tractional/rhegmatogenous

4. Retrolental fibroplasia
5. Persistent hyperplastic primary vitreous
6. Endophthalmitis
7. Haemophthalmos
8. Complicated cataract
9. Secondary glaucoma
VITREOUS HAEMORRHAGE
Vitreous is not capable of bleeding as it is avascular. The so-called vitreous haemorrhage

is, in fact, haemorrhage from the retinal blood vessels. The vessels may be retinal surface
vessels or newly formed vessels that invade the vitreous.
Causes of vitreous haemorrhages are:
A. Leak from inflamed vessels—Eale’s disease
B. Rupture of newly formed vessels
(i) Diabetic retinopathy
(ii) Sickle cell retinopathy
(iii) Retinal vein obstruction
(iv) Retinopathy of prematurity
C. Trauma—Blunt injury, penetrating injury, retinal tear, cryopexy, photo-coagulation and vitrectomy.
D. Terson’s syndrome. Spread of blood by the side of optic nerve in the sub-hyaloid space in sub-
arachnoid haemorrhage
Vitreous haemorrhage can be sub–hyaloid, intra–vitreal or both.
Symptoms
Symptoms of vitreous haemorrhage depend upon the position and amount of the
haemorrhage. A small pre-macular blood clot causes more visual loss than a large clot
in the periphery.
Loss of Vision
1. Vitreous haemorrhage is one of the most common causes of painless, sudden loss of vision
2. Loss of vision may be as low as perception of light
3. There may be no visual loss
Vitreous Signs
Only fresh blood in anterior vitreous is visible on oblique illumination, a greyish white
reflex may be visible in old haemorrhage.
Retinoscopy: A large haemorrhage result in the absence of fundal pink glow.
Fundus examination: Direct ophthalmoscopy—small opacities, smaller than 10° in
diameter may be visible with direct ophthalmoscopy, while a large haemorrhage obscures
fundal details.
EXAMINATION OF VITREOUS 347
Indirect ophthalmoscopy: Best method to examine vitreous is by indirect ophthal-

moscopy. It delineates the limits of haemorrhage and its depth. The causative factors like
retinopathy, periphlebitis, vitreous bands and peripheral breaks, etc can be made out.
Slit-lamp biomicroscopy has a limited part to play in the diagnosis of vitreous
haemorrhage.
Ultrasonography
This is useful in total vitreous haemorrhage (haemophthalmos), vitreous bands, tractional
detachment, foreign bodies and organised inflammation.
➤ In cases of vitreous haemorrhage, examination of the other eye is mandatory. It may

reveal the cause of haemorrhage when details of fundus are not visible in the
affected eye. The other eye may be involved more but may be asymptomatic
VITREOUS DETACHMENT (FIGS 21.2–21.5)
The vitreous can get detached from its usual attachments. There are two types of vitreous
detachments.
Fig. 21.2 | Small peripheral detachment of vitreous. Fig. 21.3 | Infundibular detachment of vitreous.
Fig. 21.4 | Posterior detachment of vitreous. Fig. 21.5 | Anterior detachment of vitreous.
1. Anterior detachment:The vitreous gets separated from the posterior lens capsule, zonule or ora
2. Posterior detachment
(a) Simple
(b) Detachment with collapse
Common causes of vitreous detachment are:
1. Idiopathic
2. Myopia
3. Senile
4. Blunt injury
5. Chronic uveitis
6. Retinal detachment with break
7. Post-operative
Symptoms
Anterior detachment can be symptomless, whereas posterior detachment is associated
with floaters and photopsia.
Moore’s flashes: Flashes of light seen in the darkness on the temporal side and they
are generally intermittent.
Examination
Direct ophthalmoscopy may not reveal vitreous detachment, occasionally it may show
a ring-shaped opacity with a central hole. Indirect ophthalmoscopy, biomicroscopy
examination with plus lenses are very useful. A detachment with collapse may be seen in
ultrasonography.
Abnormal contents of vitreous:
1. Blood: Partial/total (haemophthalmos)
2. Pus: endophthalmitis
3. Foreign body
4. Intra-vitreal parasite
5. Air
6. Intact transparent lens
7. Cataract
8. Cortical material
9. IOL
10. Silicone oil
11. Sulphur hexafluoride
12. Donor vitreous
Note: 10–12 are generally used in vitreous and retinal surgery.
E XAMINATION OF THE
O PTIC N ERVE AND THE
V ISUAL PATHWAY
Before embarking on the examination of the optic nerve it is worth noting some pecu-
liarities of the optic nerve.
SOME PECULIARITIES OF THE OPTIC NERVE
1. Optic nerve is not a true nerve. It is better considered as a tract

2. It is surrounded by dura, arachnoid and pia. Dura forms the outermost covering; pia is inner-
most and is firmly adherent to the optic nerve. In between the two lies the arachnoid. The space
between the pia and the arachnoid is called sub-arachnoid space, while the space between the
dura and the arachnoid is called sub-dural space. These two spaces are direct extension of
the same spaces surrounding the brain (Fig. 22.1)
3. It has only sensory function (visual)
4. Its fibres start in the retinal ganglions
5. The fibres are not uniform in size, length and thickness
6. The fibres are mainly of two types:
(a) Maculo papillar
(b) Peripheral
7. The fibres above the horizontal raphe of the retina do not meet those below and vice versa
8. This respect for the horizontal raphe and the peculiar arrangement of the central and the
peripheral fibres are the cause of various shapes and sizes of scotomas. Maculo papillar lesions
Arachnoid
Dura
Sub-dural space
Optic nerve Pia
Sub-arachnoid
space
Fig. 22.1 | Diagram showing coverings of optic nerve (not to scale).

produce central, centrocaecal, small circular defects while peripheral fibre lesions produce arcu-
ate and altitudinal field defects
9. The pink colour of the disc is due to fine capillaries on the surface
10. Optic nerve has a dual blood supply:
(a) Retinal
(b) Posterior ciliary
11. Size of the average optic nerve is 1.5 mm. The retrobulbar part is thicker, about 3.0 mm
12. There is no decussation of fibres in the optic nerve. The fibres decussate in the chiasma
13. The optic nerve carries fibres of both light and pupillary reflexes
BLOOD SUPPLY OF OPTIC NERVE HEAD
In spite of being a very small part of the visual pathway, 1.5 ⫻ 0.7 mm, the optic nerve
head (papilla) has an elaborate blood supply that comes from the ophthalmic artery
and has two distinct components.
1. Central artery of retina
2. Posterior ciliary artery
Blood supply of the optic nerve head is further sub-divided into pre-laminar, laminar
and retro-laminar. The pre-laminar part is supplied by peri-papillary choroidal vessels.
The laminar blood supply is from posterior choroidal vessels. The retrolaminar part
gets its blood supply from centrifugal branches of the central retinal artery and cen-
tripetal branches of pial vessels.
Causes of hyperaemia of optic nerve:
1. Optic neuritis
2. Papilloedema
3. Pseudo-neuritis
4. Neovascularisation of the disc, that may be due to
● Central retinal vein occlusion
● Central Eale’s disease
● Sickle cell retinopathy
● Neuroretinitis
Causes of optociliary shunt vessels:

2. Late papilloedema
3. Meningioma
5. Glaucoma
SYMPTOMS OF DISORDERS OF OPTIC NERVE
Symptoms and signs depend upon:

1. Part of the nerve involved
● Optic nerve head
EXAMINATION OF THE OPTIC NERVE AND THE VISUAL PATHWAY 351
1. Central 2. Centrocaecal 3. Paracentral
4. Enlargement of the blind spot 5. Arcuate scotoma 6. Altitudinal 7. Sectorial
Fig. 22.2 | Field changes in disorders of optic nerve.
●Retrobulbar part
●Intercanalicular part
● Junction with chiasma
2. Involvement of other structures

● Primary involvement of optic nerve only
● Secondary involvement of retina, choroid or both
3. Involvement of orbit, brain and meninges

As the main function of the optic nerve is visual, the symptoms of its disorders are visual
only (Fig. 22.2). The optic nerve does not have any pain sensation of its own. However,
the coverings of the optic nerve and the vessels are involved in the pain sensation.
Symptoms can be unilateral or bilateral but are rarely equal on both sides and simulta-
neous. They are:
1. Diminished central vision
2. Diminished colour sense
3. Central or paracentral scotoma
4. Pain on movement of the eyeball
5. Tenderness at the insertion of superior rectus
6. Proptosis
Disorders of the optic nerve can be congenital or acquired. Congenital anomalies

are few and cause permanent diminished vision. Common among them are:
1. Hypoplasia of the optic nerve
2. Tilting of optic nerve
3. Coloboma of the optic nerve
4. Drusen of optic nerve
5. Bergmeister papilla
Acquired anomalies include:

1. Inflammation
2. Infection
3. Demyelination
Plate 22.1 | Optic nerve glioma.

Manifestations of the above three separately or in combination are designated as
neuritis.
4. Vascular obstruction
● Arterial—trunk or branch
● Venous—trunk or branch
5. Glaucoma
6. New vessel formation
7. Toxins and drugs
8. Nutritional deficiency
9. Degeneration
10. Neoplasms—optic nerve glioma (Plate 22.1), optic sheath meningioma
11. Trauma
12. Metabolic disorders
13. Disorders of PNS, orbit, meninges, brain
EXAMINATION OF OPTIC NERVE
Examination of the optic nerve is basically examination of the visual function and fun-
dus examination. It consists of:
1. Examination of distance and near vision with and without correction
2. Colour vision
3. Field of vision:
● Central
● Peripheral
4. Pupillary reactions
5. Intraocular pressure
6. Ophthalmoscopy
7. Slit-lamp biomicroscopy
9. X-ray skull, PNS, optic foramen, canal and orbit
10. Ultrasonography
11. CT Scan
12. MRI
13. OCT
14. Visually evoked response
EXAMINATION OF A CASE OF PAPILLOEDEMA
The term papilloedema should be used for bilateral swollen disc either due to raised
intracranial tension or systemic condition. Rest should be labelled as disc swelling.
Common space occupying lesions that produce papilloedema are:
Neoplasm
● Primary or secondary
● Extension from neighbouring structures
Intracranial granuloma
● Tuberculoma
● Intracranial cysts
● Brain abscess
● Encephalitis
● Meningitis
Expanding haematoma
● Trauma
● Cerebrovascular accident
● Pseudo-tumour cerebri
● Hydrocephalus
● Congenital anomalies of the skull
Common systemic causes of raised intracranial tension are:
● Malignant hypertension
● Pulmonary emphysema
● Toxaemia of pregnancy
● Blood dyscrasias
● Anaemia (Hb ⬍10 g)
Toxins and drugs are:
● Methyl alcohol
● Lead
● Carbon dioxide
● Large doses of vitamin A
● Oral contraceptives
➤ Sub-tentorial space occupying lesions produce early and more papilloedema than
supra tentorial lesions of same size and duration
Symptoms of Papilloedema
As papilloedema is caused by raised intracranial tension, ocular symptom may be over-
shadowed by systemic complaints. Those are headache, vomiting, giddiness, fever,
convulsion, weakness of limbs and fits.
Ocular symptoms of papilloedema are:
1. Nil—It may be discovered on routine examination
2. Transient blurring of vision for 10–20 s
3. Persistent diminished vision
4. Diplopia
5. Ocular deviation
Diagnosis of Papilloedema
Diagnosis is made on symptoms, ocular examination, fundus examination and backed
by investigations that include central and peripheral field, fluorescein angiography, fun-
dus photography, X-ray, CT, MRI and USG.
Fundus Findings in Papilloedema

1. Early—blurring of disc margin and hyperaemia of disc. Obliteration of physiological cup is gener-
ally a late feature
2. Established papilloedema—changes are bilateral and almost equal. To the above findings the fol-
lowing are added:
Peri-papillary retinal oedema into which dilated and tortuous veins are embedded. There are
superficial linear or flame-shaped haemorrhages. Some exudates may be seen, venous pulsation
is absent. If venous pulsation is present at the disc margin papilloedema is ruled out
3. Chronic papilloedema—The disc oedema is more than ⫹4.0 D. The vessels disappear in the
swollen and mushroomed-hyperaemic disc. There are retinal striations and formation of mac-
ular star
4. Late papilloedema—There is sheathing of blood vessels, pallor and waxy discoloration of
the disc. Post-papilloedematous optic atrophy replaces the disc hyperaemia. Macular star may
persist
Once optic atrophy sets in the vision starts falling and the peripheral field starts
constricting. Pupil gradually becomes sluggish and once there is complete loss of per-
ception of light pupils become immobile and dilated.
Field Changes in Papilloedema

1. Early stages—enlargement of the blind spot
2. Late stages—peripheral constriction
Fundus Fluorescein Angiography (FFA)

in Papilloedema
There is a diffuse fluorescence of the optic nerve head. This is due to the retention of
the dye in the retinal veins and oedematous fluid over the disc. The veins are dilated.
In the venous phase there is a lack of fluorescence over the disc.
Other causes of enlargement of the blind spot are:
1. Drusen of the optic nerve head
2. Chronic simple glaucoma
3. High myopia
4. Coloboma of the optic nerve
5. Peri-papillary oedema of the retina
6. Opaque nerve fibre
Uniocular causes of disc swelling are:

It is better not to use the term papilloedema for uniocular swelling of the disc
because the causes of uniocular swelling are local, either ocular or orbital.
However in some instances one optic nerve may show papilloedema earlier to be
followed by same in the other.
The ocular causes are ocular hypotony, post-inflammatory, post-traumatic, acute
congestive glaucoma, impending central retinal vein thrombosis, optic nerve glioma,
papillophlebitis, optic neuritis, anterior ischaemic optic neuropathy, Leber’s optic neu-
ropathy, drusen of optic nerve head, Bergmeister papilla, unilateral hypermetropia,
contralateral myopia and pseudo-neuritis.
The orbital causes are thyrotoxicosis, pseudo-tumours of the orbit, lymphomas,
retrobulbar growth, leukaemic infiltration and orbital tumours (primary or
secondary).
➤ Whatever may be the cause of disc swelling, the mechanism of production and
pathogenesis is similar in true bilateral papilloedema and uniocular disc swelling
Differential Diagnosis of Papilloedema

(Tables 22.1 and 22.2)
● The diagnosis of papilloedema in early stages is difficult
● The difficulty is compounded if the swelling is bilateral
● The mild unilateral disc swelling with diminished vision is invariably not papilloedema
● The two conditions that merit mentions in this group are pseudo-neuritis and drusen of the
optic nerve head
Differential Diagnosis of Unilateral

Disc Swelling
1. Papillitis
Table 22.1 Comparison between papilloedema, pseudo-neuritis and drusen
Features Papilloedema Pseudo-neuritis Drusen
Age Any age after the Congenital Congenital, manifests

sutures have closed few years after birth
Laterality Bilateral Bilateral Mostly bilateral
Ocular symptoms Nil Nil Nil
Refraction Emmetropic or Mostly hypermetropic Any, rare in myopia
hypermetropic. Myopic may be emmetropic
eyes do not generally
develop papilloedema
Disc colour Hyperaemia ⫹ ⫹ ⫹ ⫹ Hyperaemia ⫹ Pink or yellow
Margin Blurred Blurred Blurred
Lamina Lost late Not visible Not visible
Haemorrhage On disc or peri-papillary Nil Peri-papillary
(less common)
Retinal oedema Present Absent Absent
Visual field Enlargement of blind spot Normal Enlargement of blind spot
Vision Good initially Good Good
Venous Absent Present Present
pulsation
Sequel Secondary Nil May remain stationary
Optic atrophy or increase in size
Table 22.2 Comparison between papilloedema and optic neuritis
Features Papilloedema Optic neuritis
Visual loss Minimal, gradual and late Acute, marked

Visual recovery Diminished vision continues unless Acute loss is followed by
primary cause is relieved, otherwise recovery to the normal level,
loss of vision is inevitable loss of vision may recur
Scotoma Enlarged blind spot Central, centrocaecal more for colours
Visual field Peripheral constriction of field Transient central field effect,
is a late feature suggesting peripheral field remains normal
onset of secondary optic atrophy
Laterality Generally bilateral Often unilateral
Pain Nil May be present over the
insertion of superior rectus
Systemic symptoms Headache, vomiting, giddiness, Generally absent
diplopia may be present
Fundus findings:
Disc swelling More than 3 D Less than 2 D
Venous dilatation Marked Usually mild
Haemorrhage More marked Few, linear
Retinal oedema Less marked Marked around the disc
Macular star Frequent and large Absent or small
Vitreous haze Absent Present
3. Leber’s optic neuropathy

4. Papillophlebitis
6. Juxta papillary choroiditis
7. Pseudo-neuritis
Papilloedema in Relation to Management

1. Urgent management—In head injury, sub-arachnoid haemorrhage, meningitis, encephalitis and
brain abscess
2. Semi urgent—In hypertension and renal retinopathy
3. Planned—In intracranial space occupying lesion
EXAMINATION OF THE EYE WITH OPTIC NEURITIS
Optic neuritis denotes inflammation of the optic nerve but there may be causes other
than inflammation, e.g. demyelination, compression, infiltration, etc. However inflam-
matory reaction is a major histopathological feature in all cases.
On the basis of ophthalmoscopic features and symptoms, optic neuritis is divided into:
1. Optic neuritis
(a) Early
(b) Fully established
(c) Late
2. Retrobulbar neuritis—acute/chronic
3. Neuroretinitis
Characteristics of Papillitis
1. Affection of the visible part of the optic nerve
2. No age is immune—common between 15 and 50 years
3. Optic neuritis in children differs from adults in many ways
4. Slightly more common in females
5. Generally unilateral
6. Main symptoms are visual
(a) Sudden fall in visual acuity which may be lowered to perception of light only in two to
three days
(b) Stationary diminished vision for 2 to 3 weeks
(c) Recovery to original levels in 2 to 3 weeks
(d) Relapse is common
(e) Other eye may be involved when the originally effected eye has recovered (demyelination)
(f) If vision does not improve in eight weeks, investigations for pressure or infiltration should
be done
7. Scotoma – Patient may complain of positive scotoma, relative or absolute
8. Colour vision is generally diminished
9. Depth perception is faulty
10. Pain on movement of eye
11. Pupillary reactions
(a) Pupillary size is normal in spite of gross loss of vision
(b) Afferent pupillary defect is prominent, may be present in spite of moderate or good vision
(c) Consensual and near reflexes are normal
12. Fundus changes

(a) Early—There may be no change in an early case or there may be slight hyperaemia of
disc. Foggy vision with afferent pupillary defect goes in favour of optic neuritis. At this
stage macular lesion should be differentiated
(b) Fully developed papillitis—There is elevation of disc but not more than ⫹3 D. Physiological
cup is lost. Disc is hyperaemic, there may be linear or superficial haemorrhages on and near
the disc. Surrounding retina may be oedematous. In severe neuritis there may be a macu-
lar star. On slit-lamp examination there is vitreous haze in front of the disc
(c) Late—It takes 8–12 weeks and repeated attacks to develop these changes.The disc loses
its colour from hyperaemia to pallor, waxy yellow discoloration is common, margins remain
blurred and vessels become narrow and sheathed. A fully developed post-neuritic optic
atrophy takes place, which is difficult to differentiate from post-papilloedematous atrophy
13. Differential diagnosis.
(a) Differentiate between disc lesion and macular lesion
(b) Differentiate between various causes of unilateral disc swelling
● With diminished vision—acute ischaemic optic neuropathy
● Without diminished vision
(c) Differentiate between early papilloedema and neuritis
Optic Neuritis in Children

Optic neuritis in children differs from adult optic neuritis in many ways. In adults
demyelination is a major cause while in children infection is a prominent cause of
optic neuritis.
● It is generally viral and post-viral
● It is more commonly bilateral
● Loss of vision is more severe
● Complaint of scotoma is common
● Recovery is good
● Recurrence is less common
Eyes that do not develop swelling of the disc can be due to:
1. Already atrophied disc
2. Raised intraocular tension, more than 30 mmHg
3. Moderate and high myopia
4. Coloboma of the disc
Diagnosis of Acute Retrobulbar Optic Neuritis

1. It has all the features of optic neuritis without any fundus changes
➤ The patient does not see anything, the observer does not see any
change in the fundus
2. There may be an afferent pupillary defect
Differential Diagnosis of Retrobulbar Neuritis

Posterior ischaemic optic neuropathy, drug-induced neuropathy, functional, recently
detected uniocular error of refraction, anisometropia, and amblyopia.
EXAMINATION OF AN EYE WITH OPTIC ATROPHY
➤ Optic atrophy is not a disease, it is end result of disorders of axons of optic nerve or
ganglions of retina
To diagnose optic atrophy there should be:

1. Pallor of disc
2. Decreased vision
3. Pupillary changes
4. Field changes when detectable
5. Defective colour vision
Causes of pale disc:

1. Optic atrophy
2. Infants
3. Myopia
4. Coloboma of the disc
5. Central retinal artery occlusion
6. Severe anaemia
Classification of optic atrophy Optic atrophy can be classified according to the:

1. Ophthalmoscopic appearance
2. Pathological process
3. Aetiology
4. Part involved
(a) Ascending
(b) Descending
5. Onset
(a) Acute
● Avulsion of optic nerve
● Trans-section of optic nerve
● Central retinal artery occlusion
(b) Chronic
● Neuritis
● Papilloedema
Ophthalmoscopic Appearance of Optic Atrophy

This is the most commonly used clinical classification followed by the clinicians. It
depends upon:
1. Degree of pallor (number of vessels on the disc)
2. General colour of the retina
3. Margins of the disc
4. Vascular changes on the disc
5. Retinal and choroidal changes
6. Visibility of lamina
7. Depth of cup
Table 22.3 Correlation between ophthalmoscopic changes and probable causes of optic atrophy
Name Ophthalmoscopic changes Probable causes
Primary Disc margins sharp, chalky white colour, prominent Tabes dorsalis, pituitary tumour, retrobulbar
physiological cup, C/D ratio normal, lamina visible, neuritis, posterior ischaemic optic neuro-
absent vascular, retinal or choroidal changes pathy, trauma to optic nerve, idiopathic
Secondary Blurred disc margins, dirty yellow colour, lamina not Optic neuritis, optic disc swelling,
visible, absent cup, vascular sheathing, no retinal or papilloedema
choroidal changes. Paton’s line may be present
Consecutive Margins normal, pale yellow colour, lamina not visible, Retinitis pigmentosa and other tapeto-retinal
cup shallow or normal, evidence of chorio-retinal or dystrophies, chorioretinitis, macular lesions,
vascular changes excess cryo or photo-coagulation
Glaucoma Margins normal, peri-papillary halo, large pale glauco- Advanced glaucoma of any type
matous cup. Cup disc ratio changed, lamina well
preserved, nasal shift of blood vessels, retinal vessels
normal, retina normal
Vascular Findings between primary and glaucomatous optic Central retinal artery obstruction
atrophy with extreme thinning of blood vessels
Types of optic atrophy (Table 22.3):

1. Primary
2. Secondary
● Post-neuritic
● Post-papilloedematous
3. Consecutive
4. Glaucomatous
5. Vascular
6. Heredofamilial
Some Special Types of Optic Atrophy

Temporal pallor—Architecture of the disc is within normal limits except that there is
localised pallor of the disc on the temporal side, mostly involving the maculo-papillar
bundle. Generally seen in congenital anomalies of the disc and macula, cerebromacu-
lar degeneration, macular lesions, retrobulbar neuritis, rupture of the choroid and
localised photo-coagulation.
Segmental pallor—Only one segment adjacent to juxtapapillary choroiditis shows
pallor. Other causes are localised photo-coagulation, rupture of the choroid, central
artery branch occlusion and solitary large patch of choroiditis.
Altitudinal pallor—This is seen as a horizontal pallor generally of the lower part in
ischaemic optic neuropathy.
Bow tie pallor—This is seen as a horizontal band of pallor of the disc in chiasmal,
retrochiasmal and pre-geniculate lesions. It is associated with bitemporal hemianopic
field loss. The pallor is horizontally wider towards periphery than centre. Disc above
and below the pallor looks normal. In retrochiasmal and pre-geniculate lesions, it is
on the contralateral side of the lesion. Occasionally nerve fibre defects may also pro-
duce such an appearance.
Foster Kennedy Syndrome

This comprises of primary optic atrophy on the side of the intracranial tumour and
papilloedema or post-papilloedematous optic atrophy on the other side. In early stages,
the other side may present with a normal disc. The combination is seen in tumours of
the sphenoidal ridge, olfactory groove, sella and rarely frontal lobe. Optic nerve on the
side of the lesion is compressed first to produce primary optic atrophy without the rise
of intracranial pressure. By the time the tumour is large enough to produce rise of
intracranial pressure, the disc on one side has already undergone atrophy that prevents
it from developing papilloedema but the other side disc develops swelling.
Pseudo-Foster Kennedy Syndrome

This is seen in ischaemic optic neuropathy but the swelling is not due to raised intracra-
nial pressure. Loss of vision is profound and differentiates it from true papilloedema.
Cause of contra-lateral primary optic atrophy is not well understood.
Characteristics of Ischaemic Optic Neuropathy

1. This disorder is far more common than it was thought to be
2. There is a devastating, painless and permanent loss of vision in one eye
3. Other eye may follow with similar results
4. It occurs in patients more than 50 years of age. Incidence increases with age
5. Topographically, it is divided into two types:
(a) Acute ischaemic anterior neuropathy
(b) Acute ischaemic posterior neuropathy
The latter is less common and more often missed
6. Aetiology of ischaemic optic neuropathy is divided into two groups:
(a) Arteritic
(b) Non-arteritic
7. Pre-disposing factors in ischaemic optic neuropathy are:
(a) Age more than 50 years
(b) Systemic conditions as temporal arteritis, peri-arteritic nodosa, hypertension, diabetes, hyper-
lipidaemia, hyperviscosity syndrome, acute loss of blood, hypotension, migraine and syphilis
(c) Ocular conditions as a small or hypoplastic disc, drusen of the optic nerve, raised intraoc-
ular tension, reduced cup disc ratio, narrow retinal arteries, uncomplicated lens extraction
and history of amaurosis fugax
Amaurosis fugax It is defined as a recurrent, transient, painless loss of vision in
one eye lasting more than few seconds but not exceeding 30 min; may be bilateral.
Causes of amaurosis fugax:
1. Narrowing of the internal carotid artery
2. Stenosis of the ophthalmic artery
3. Arrhythmias, mitral valve prolapse, myocardial infarction, hypertension and hypotension
4. Anaemia, sickle cell syndrome
5. Arteritis
6. Diabetes
7. Retinal migraine
8. CRA spasm
Symptoms of Arteritic Ischaemic Optic

Neuropathy (IONP)
1. Ocular—sudden painless loss of central vision over a few hours without recovery in a patient
in the sixth or seventh decade, more often in females. Loss of vision may start as an altitudinal
field defect. There may be diplopia
2. Non-ocular symptoms—temporal headache, tenderness over a thickened temporal artery, low
grade fever, night chills, weight loss, anorexia, fatigue, neck stiffness and most strikingly a claudi-
cation of the muscles of mastication
Early signs:
1. Profound, non-correctable diminished vision
2. Afferent pupillary defect
3. Pale but swollen disc
4. Peri-papillary superficial haemorrhages
5. Altitudinal field defect
Late signs:
1. No improvement in vision
2. Cupping of disc with atrophy similar to that in chronic simple glaucoma
3. Pseudo-Foster Kennedy syndrome
➤ Raised ESR in an elderly patient with sudden painless, monocular loss of

vision is a diagnostic feature of arteritic ischaemic optic neuropathy. This
may be confirmed by a temporal artery biopsy
Table 22.4 Comparison between idiopathic and arteritic IONP
Features Idiopathic Arteritic
Age Fifth and sixth decade Sixth decade and above

Sex Equal in both More in females
Systemic disease Hypertension Hypertension may be present.
Temporal arteritis is the
commonest cause
Loss of vision Moderate Profound
Involvement of other eye 30–40% 75–80%
Fundus changes Minimal Disc pallor with swelling,
peri-papillary haemorrhages
ESR Normal More than 40 mm
Systemic steroid No effect Other eye may be salvaged
Table 22.5 Some characteristic features of chiasmal, pre-chiasmal and retrochiasmal lesions
Characteristic features Pre-chiasmal Chiasmal Retrochiasmal
Laterality Unilateral Bilateral Bilateral

Vision Reduced Central vision may be present,
poor on temporal side.
Light reflex May be sluggish Variable Normal
Type of field change Central scotoma Bitemporal hemianopia Homonymous
(heteronymous) hemianopia
Causes of optic atrophy in children:

1. Heredofamilial optic neuropathy
(a) Dominant
(b) Recessive
(c) Intermediate
2. Consecutive to retinal and macular dystrophy
Table 22.6 Sites and types of field defects at various levels of the visual pathway
I II III IV V
Site Laterality Ipsilateral changes Contralateral Type of scotoma

changes
Retina Unilateral Varied Nil Depending on the location
of the retinal lesion
Disc Unilateral Central, centrocaecal, arcuate Nil Depending upon the type
of the maculo-papillar lesion
Optic nerve Unilateral Central, Centrocaecal, arcuate, Nil Central
may be total loss of vision
Anterior angle Bilateral Total Contralateral Variable
of chiasma hemianopia
Mid chiasma Bilateral Temporal loss Temporal loss Bitemporal hemianopia
Tract Bilateral Nasal half Temporal Homonymous hemianopia
Radiation Bilateral Nasal Temporal Homonymous hemianopia
Cortex Bilateral Nasal half; macular sparing Temporal Central homonymous hemianopia
Fig. 22.3 | Example of visual field defect.

Table 22.7 Aetiology of various field defects
Types of field defects Common causes
Monocular total Optic nerve lesions—optic atrophy

Bitemporal hemianopia Mid chiasmal lesion, pituitary tumour
Monocular nasal hemianopia Pressure on the outer side of the chiasma.
Aneurysm of internal carotid
Pie in the sky Lesions of anterior–inferior optic radiation
Pie on the floor Lesions of superior optic radiation
Pseudo-bitemporal hemianopia Tilted disc, sectorial retinitis pigmentosa, large central
or centrocaecal scotoma
T T N N
Bitemporal hemianopia Binasal hemianopia

T T
Pseudo-bitemporal hemianopia defect

does not respect vertical meridian
Fig. 22.4 | Heteronymous field defects.
Fig. 22.5 | Right homonymous hemianopia.

3. Associated with systemic disease
4. Space occupying lesion
It will be observed that:
1. Pre-chiasmal field changes are ipsilateral (Fig. 22.3)
2. Chiasmal field changes are bilateral heteronymous (Fig. 22.4)
3. Retrochiasmal field changes are bilateral homonymous (Fig. 22.5)
E XAMINATION OF E YES IN
PAEDIATRIC AGE
It is difficult to classify ocular disorders in this age group due to overlapping with the
disorders of adults. They are classified in various groups depending upon the age of
onset, tissue involved, chronology of disorder and clinical presentation.
According to age onset, they could be: (1) intrauterine, (2) neonatal, (3) between
1 and 5 years, (4) between 5 and 10 years and (5) between 10 and 15 years.
INTRAUTERINE CAUSES
Generally produce mild-to-severe deformity and visual loss. Intrauterine causes can be
genetic, infective or traumatic in nature.
Intrauterine Factors Producing Ocular Malformation

1. Genetic: They may be due to
(a) Inherited genetic defect
(b) Genetic mutation
(c) Effect of exogenous factors, e.g. drugs and radiation
(d) Chromosomal aberration
2. Trans-placental
(a) Infection: In early pregnancy rubella, toxoplasmosis, syphilis and cytomegalovirus diseases
are common causes
(b) Drugs taken by mother in first trimester
(c) Deficiency: Dietary
3. Mechanical factors: Pressure over the eyes and face during development due to intrauterine
bands, fibroid, umbilical cord etc
4. Intrauterine trauma
NEONATAL CAUSES
1. Infective: Either contracted during delivery or soon after, or their sequelae, e.g. gonorrhoea, inclu-
sion conjunctivitis, trachoma and herpes simplex
2. Maldevelopment of various structures of the eye, single or in various combinations and their
residual effect. They could be anophthalmos, microphthalmos, micro-cornea, limbal dermoid,
blue sclera, dysgenesis of the anterior chamber, uveal coloboma, polycoria, aniridia, cataract
(total or partial), ectopia lentis, congenital myopia, glaucoma (primary, associated or secondary).
Retina may show congenital folds, detachment and coloboma. Macula may have hypoplasia, scar.
Others may be strabismus (paralytic or concomitant) white reflex in the pupillary area, persist-
ent hyperplastic primary vitreous and meningoencephalocele
3. Effect of prematurity: Retinopathy of prematurity and myopia of prematurity
Causes between 1 and 5 years
1. Sequel and complication of:
(a) Intrauterine infection
(b) Developmental anomalies
(c) Neonatal infection
(d) Trauma
(e) Dietary deficiency
2. Inborn errors of metabolism
4. Strabismus
5. Glaucoma
6. Intraocular tumours
7. Orbital tumours
8. Allergy
(a) Endogenous
(b) Exogenous
9. Autoimmune diseases
10. Infections
(a) Local
(b) Systemic
11. Degenerations and dystrophies
Causes between 5 and 10 years

Residual effect of above, infection, allergy or trauma can be super added to any of
the causes mentioned earlier. Trauma becomes more common. Errors of refraction and
squint are more frequent in this age group. Amblyopia if it has not been detected and
managed in early childhood may manifest as a permanent disability in this age group.
Boys should be tested for colour-vision deficiency at this age to plan their future
occupational training.
EYES AT BIRTH
In a normal full-term child, eyes are well formed. Structurally they are smaller in size
and subnormal in function. As a sensory system, it is better developed than expected in
comparison to its size.
The pupils are smaller than adult, but react well to direct and indirect light. Near
reflex and convergence cannot be tested.
Vision is very poor, about 2/60.
The eyeballs are small but compared to other organs, they are proportionately larger.
The eyeball of a neonate is about 16.5–17.5 mm in diameter. Volume of the eyeball is
EXAMINATION OF EYES IN PAEDIATRIC AGE 367
2.88 cc as compared to 7.0 cc of an adult. The smaller diameter makes the eye hyperme-
tropic by three to four diopters but by 5 years the eye assumes adult size and becomes
emmetropic.
The orbits are small, shallower and round. This give a false impression of prominent
eyeballs.
Interpalpebral aperture is about 18 mm as compared to 30 mm of an adult eye. There
is a broad nasal bridge giving a false impression of convergent squint.
The cornea is 10 mm in diameter but as IPA is short there is an impression of cornea
being larger. Cornea has a mild haze that clears in a few days.
The anterior chamber is well formed and contents are clear. AC depth is less than that
of an adult. The angles are wide open and pupil can dilate fully without any danger
of glaucoma.
The pupil is slightly shifted down and nasally. It is miotic, reacts to direct and indirect
light. Near reflex and convergence cannot be tested. There is less pigment in iris hence it
looks lighter, a few vessels may be visible which disappear with development of normal
pigment.
The lens is more spherical than adult and transparent. Diameter of lens is 6 mm as
compared to 9 mm of an adult lens.
The ciliary body is small.
The fundus is visible but paler than in adults, as is the disc. Macula is not well
developed and foveal reflex is absent. The retinal periphery is also pale.
The nasolacrimal duct is patent. Lacrimal secretion is absent or very scanty, con-
junctival secretion is present. The paediatric conjunctiva is normally sterile.
Congenital anomalies seen at birth can be unilateral or bilateral. There may be a dif-
ference in severity between the two eyes in bilateral cases. In unilateral cases the other
eye may be fully developed structurally and functionally and continues to be so for the
rest of the life, while the defective eye may be mildly to severely affected. Skeletal defects
are very commonly associated with many ocular anomalies. In fact they share the same
etiological predisposition.
The congenital anomalies can involve eyes or adnexa and are as follows:
1. Cranio-facial
2. Mandibulo-facial
3. Associated with other skeletal anomalies—ear, digit, skin, bones, heart, brain and errors of
metabolism
COMMON DISORDERS AT INFANCY THAT

REQUIRE URGENT MANAGEMENT
1. Ophthalmia neonatorum—Gonococcal/non-gonococcal
2. Complete cataract—premature child
3. Coloboma of the upper lid
4. Proptosis
5. Orbital cellulitis
6. Premature child
Table 23.1 Vision at various ages
Age Vision
Birth to 2 months 2/60

6 months 6/60
1 year 6/36
2 years 6/18
3 years 6/9
5 years 6/6
➤ Under one year of age accurate vision is difficult to test. It can be tested only by
optokinetic nystagmography, which may be available only in very advanced centers
➤ Vision should be considered to be normal in a child under one year of age if the
media are clear, there is no error of refraction, pupils are central, circular, react
briskly to direct and indirect light, there is no squint or nystagmus, fundus is
normal, with usual milestones of general development
Various methods of testing vision in children and infants are:

A. Subjective methods
● Snellen’s chart
● STYCAR (Snellen’s test for young children and retarded)
● Landolt’s broken C
● Pictorial charts—Allen
● Pictorial cubes
● Sheridan Gardener cards
● Dots
● Lippman’s HOTV test
● Cardiff acuity cards
● Catford drum test
● Teller acuity card test
B. Objective
● Visual evoked potential (VEP)
● Preferential looking technique
A child under 3 years may not be able to read letters on Snellen’s chart but is able to
tell the direction of opening in the E and C charts. This requires explaining the pro-
cedure to the child before starting the test. It is better to have a smaller version of
the E chart and show it to the child from a close quarter. STYCAR charts are better
alternatives. Pictorial and dots are not very good charts.
While examining a child’s vision the following steps are helpful:
1. Let the attendant (most of the time one of the parents) be present at the time of examination
but ask them not to prompt
2. Let the child read with both eyes open first—this gives confidence to the child
3. Then examine the better eye first
4. Examine the poorer eye thereafter. If the child has very poor vision in one eye, the child under
3 years resists closer of better eye. Children under 1 year may even cry on closing the better eye
(Fig. 23.1)
Fig. 23.1 | Athechild resents covering of the seeing eye, if

other eye is amblyopic.
Fig. 23.2 | Cross-fixation in a child—the left eye fixes the
object on the right side and the right eye fixes
the object on the left side.
5. While examining one eye, the other eye should be fully occluded. Otherwise, the child may
look over or by the side of the occluder
6. Instead of asking the child to read the chart from top to bottom, point towards a letter and ask
the child to identify it. Except in suspected amblyopia, children are known to memorise the let-
ters in a Snellen’s chart
7. Single letter presentation is not suitable in amblyopia because an amblyopic child may recog-
nise letters when presented singly but fail to read complete line
8. A child with convergent squint may cross fixate (Fig. 23.2)
SOME COMMON CRANIO-FACIAL ANOMALIES WITH

OCULAR MANIFESTATIONS
Oxycephaly—There is premature closure of sutures, and the skull grows vertically. It is

more common among males. At birth the child may look normal. The ocular signs are
bilateral proptosis, strabismus, ptosis, corneal exposure, conjunctival chemosis, errors
of refraction, papilloedema, optic atrophy and cataract.
Crouzon’s disorder—There is a frog-like face, exophthalmos, exophoria V pattern,
nystagmus, cataract, there may be mental retardation, other skeletal deformity and
neurological defects.
Apert’s syndrome—This is similar to Crouzon’s syndrome, the prominent features
being syndactyly of hands and feet and mental retardation. There may be involvement
of the heart. Maxilla is hypoplastic. Ocular features consist of hypertelorism, proptosis,
prolapse of globe that can be reposited and downwards slanted palpebral fissure.
Mandibulo-facial dysostosis—Out of the many mandibulo-facial dysostosis, the
commonest is Franceschetti syndrome. It consists of hyperplasia of maxilla and
mandible, macrostomia, deformity of external ear, mental retardation, downward dis-
placement of canthi, coloboma of lower lid, trichiasis, corneal irritation and corneal
opacities. The condition is due to maldevelopment of the first and second branchial
arches.
Plate 23.1 | Cut section of the globe showing retinoblastoma extending to the optic nerve.
(Courtesy Dr. Alka Das.)
Plate 23.2 | White reflex in the pupillary area, case of intraocular retinoblastoma.
(Courtesy Dr. Alka Das.)
Causes of white reflex in pupillary area (Leucocoria) in childhood:

1. Cataract
(a) Congenital
(b) Traumatic
(c) Complicated
2. Retinoblastoma (Plates 23.1 and 23.2)
3. Persistent hyperplastic primary vitreous
4. Posterior uveitis
(a) Metastatic
(b) Parasitic:Toxocara
5. Retinopathy of prematurity (retrolental fibroplasia)
7. Retinal dysplasia
8. Large coloboma of choroid
SOME COMMON SKELETAL DEFORMITIES

SEEN WITH OCULAR DISORDERS
Kyphosis, scoliosis, high-arched palate, deformity of ear, barrel chest, long arm, arach-
nodactyly, syndactyly, meningocele and meningoencephalocele.
The three common skeletal disorders associated with ocular defects are:
1. Marfan’s syndrome
2. Homocystinuria
3. Weill Marchesani syndrome
All three have multiple systemic disorders. Ectopia lentis is the commonest factor in
all the three conditions.
Causes of ectopia lentis
Frequent causes are:
1. Marfan’s syndrome
2. Familial
3. Blunt trauma
4. Homocystinuria
5. Weill Marchesani syndrome
6. Buphthalmos
Less common syndromes are:

1. Aniridia
2. Crouzon’s syndrome
3. Treacher Collins syndrome
4. Rieger’s syndrome
5. Alport’s syndrome
6. Ehler’s Danlos syndrome
7. Klinefelter syndrome
8. Pfandlers syndrome
Common inborn errors of metabolism seen in ocular disorders:
1. Galactosaemia
2. Aminoaciduria
3. Mucopolysaccharidosis
4. Albinism
5. Homocystinuria
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I NDEX
A Fluorescein 42, 47, 78, 79, 96, 107, 108, Atropine 4, 13, 73, 123, 192, 219, 220,
A esotropia 256, 265 109, 130, 131, 132, 133, 135, 156, 256, 267, 278, 281
A exotropia 40, 256 174, 176, 177, 179, 196, 311, 325, Atropine sulphate 220, 267
A scan 303, 304, 305 328, 330, 339, 340, 341, 342, 343, Automated perimeters 32
A typical retinitis pigmentosa 201 344, 353, 354, 355 Axenfeld anomaly 208
A/V phenomena 256 Indocyanine 342 Axial proptosis 293, 298
Aberrant regeneration of the third nerve Angle kappa 232, 233, 234, 239, 241,
273 253, 256 B
Abnormal head posture 38, 233, 256, Angle of anterior chamber 135, 181, 183, B scan 303, 304, 305
259, 262, 264, 270 187, 203, 207 Bagolini striated glasses 251, 252
Absolute scotoma 198, 328 Angular conjunctivitis 9, 87 Bailey-Lovie Logmar 16
Acute congestive glaucoma 3, 6, 8, 37, Anisocoria 146, 147, 278 Ballet sign 294
107, 121, 143, 148, 185, 186, 187, Ankyloblepharon 40, 59, 60, 64 Band keratopathy 109, 118, 119, 121,
355 Anomalies of accommodation 2 122, 149, 173, 186, 209
Acute iridocyclitis 3, 7, 8, 149, 203 Anomalous trichromats 30 Barkan 189
Acute ischaemic optic neuropathy 3, 5, Anophthalmos 40, 67, 100, 286, 300, Basal cell carcinoma 59, 60, 99
38, 203, 358 365 Basic secretion test 130, 132
Acute proptosis 292, 295 Anti-monogoloid obliquity 40 Battle’s sign 275
Adie’s pupil 147, 148, 281, 284 Aortic arch syndrome 153 Bausch and Lomb chart 229
Adrenaline 181, 278, 283, 294 Apert’s syndrome 369 Bell’s phenomenon 54, 60, 68, 72, 317
Afferent pupillary defect 359, 358 Aphakia 4, 7, 22, 27, 38, 39, 134, 135, Benedict’s syndrome 259, 272
After cataract 7, 134, 139, 149, 150, 161, 137, 138, 159, 160, 161, 163–165, Benzalkonium chloride 176
163, 164 166, 313, 321, 326, 328, 329, 330, 332 Beta blockers 130, 181, 193
After image test 251, 252 Applanation tonometer 173, 174, 176, Bilateral proptosis 291, 293, 299, 369
Albinism 7, 10, 11, 29, 142, 230, 342, 371 177, 178, 179, 208 Bilateral squint 235
Allen pictures 15 Aqueous 3, 79, 106, 123, 127, 128, 130, Binocular corneal Loupes 44
Alport’s syndrome 371 132–138, 141, 142, 149, 150, 153, Binocular vision 14, 242–244, 251
Alternate cover test 236, 237, 241 154, 155, 165, 169, 173, 180–182, Binomag 43
Alternate squint 235, 237 191, 204, 304, 339, 340 Biometry 169
Altitudinal pallor 360 Aqueous flare 106, 136, 142, 149, 155, 169 Bitot’s spot 8, 85, 96, 130
Amaurosis fugax 361 Arachnoid 349 Bjerrum scotoma 200
Amaurotic pupil 209, 280 Arcuate scotoma 35, 199, 200, 202, 351 Black eye 10, 50
Amblyopia 2, 3, 11, 13, 65, 68, 168, 201, Arcus-Juveniles 119 Blepharitis 10, 52, 54, 55, 56, 114, 170
214, 225, 235, 250, 251, 253, 254, Arcus-Senilis 119 Blepharophimosis 40, 41, 64, 65
257, 259, 260, 263, 280, 358, 366, Argyll–Robertson pupil 147, 279, 281, Blind spot 32, 33, 34, 35, 198, 199,
369 282, 284 200, 201, 205, 244, 351, 354, 355,
Anisometropic 3 ARMD 164, 338, 339 356
Strabismic 3, 344 Arteriography 306 Blood dyscrasia 9, 138, 299
Amblyoscope (Synoptophore) 240 Arteritic ischaemic optic neuropathy Haemophilia 138
Ametropia 39, 171, 215, 216, 224, 313 (IONP) 362 Juvenile xanthogranuloma 139
Aminoaciduria 371 Atrophy in children 363 Leukaemia 91, 139, 286, 287
Amsler grid 32, 33, 196, 311, 340 Asher law stereoscope 244 Purpura 91, 139, 325
Anastomosis 323, 324, 342 Aspherial lenses 29 Retrolental fibroplasias 139, 153, 329,
Aneurysm of ophthalmic artery 290, 294, Lens aspherical 29 333, 346, 376
295, 296 Asthenopia 11, 214, 232, 255 Persistent hyperplastic primary vitreous
Aneurysms 324, 325, 334, 342 Astigmatic fan or dial 222 139, 329, 343, 346
Angiography 108, 135, 156, 196, 311, Astigmatism 3, 6, 11, 27, 57, 65, 112, Haemophthalmos 139, 346, 347, 348
325, 328, 330, 339, 340, 342, 343, 113, 115, 163, 164, 165, 166 Blood staining 10
344, 353, 354, 355 Atrophic bulbi 101, 115 Blood staining of cornea 10
380 INDEX
Blow out fracture of the orbit 6 Chamber 10, 47, 48, 86, 134–139, 140, Colour blindness 4, 30, 32
Blue field entoptoscopy 169 154, 141, 144, 150, 155, 164, 168, Coloured haloes 2, 6, 184, 185, 202, 203
Boston sign 294 181, 183, 185, 186, 187, 203, 207, Compound sphero-cylinder 24, 26
Bow tie pallor 360 304, 344, 345, 366, 367 Compressibility of proptosis 289, 298
Bowens disease 99 Aqueous 3, 79, 106, 123, 127, 128, Computerised tomography 301, 302, 305
Braille alphabets 231 130, 132, 133, 134, 135, Computerised tomography of orbit 301
Branch artery occulusion 2 136–138, 154, 141, 142, 149, Concave mirror 159, 160, 215, 216, 217,
Branch vein occlusion 2, 332 150, 153, 136, 154, 155, 165, 218
Brightness 30, 45, 222, 314, 340 169, 173, 180, 181, 182, 191, Concave mirror retinoscope 216
Brimonidine 181 204, 304, 339, 340 Concomitant squint 232, 255, 256
Brown’s syndrome 256, 257, 265 Anterior 10, 41, 43, 44, 45, 47, 48, Concretion 84, 97
Bullous keratopathy 173, 186, 209 52, 83, 84, 86, 87, 88, 96, 104, Condensing lens 42, 43, 216, 314, 315,
Buphthalmic eye 206 105, 106, 109, 110, 111, 112, 316, 318
Buphthalmos 41, 62, 88, 101, 104, 114, 115, 124, 125, 134–140, 141, Confocal microscope 106
115, 116, 125, 135, 139, 159, 143, 144, 145, 148, 149, 150, Confrontation method 32
206–209, 289, 371 151, 154, 155, 159, 160, 161, Congenital cataract 10, 205, 330
162, 163, 165, 167, 168, 181, Congenital fibrosis of muscles 258
C 183, 184, 185, 186, 187, 196, Congenital glaucoma 110, 180, 185, 186,
Carbonic anhydrase inhibitors 186, 193 203, 204, 206, 207, 267, 271, 205, 206, 209
Cardiff acuity cards 368 274, 275, 278, 281, 289, 300, Congenital ptosis 65, 70, 72, 265
Carotico-cavernous fistula 290, 294 304, 307, 312, 314, 316, 323, Congruous 5
Carotid artery occlusive disease 153 325, 337, 344, 345, 346, 347, Conjunctivitis acute allergic 8, 9, 10, 90
Caruncle 81, 83 348, 355, 361, 363, 366, 367 Consecutive optic atrophy 2, 157
Cataract 3, 4, 5, 6, 7, 10, 12, 13, 30, 66, Posterior 4, 5, 6, 11, 24, 43, 44, 47, Convex mirror 111, 112, 159, 160
124, 134, 139, 149, 150, 158, 160, 80, 88, 96, 101, 105, 106 Corectopia 145, 146, 234
161–164, 168, 171, 182, 184, 186, Characteristics of ischaemic optic Cornea 1, 3, 6, 7, 8, 10, 29, 40, 41, 44,
202, 203, 205, 209, 220, 228, 230, neuropathy 361 47, 48, 52, 54, 63, 64, 69, 70, 71, 72,
262, 301, 307, 308, 330, 332, 344, Chemosis of conjunctiva 89 81, 82, 86, 87, 88, 92, 93, 99, 100,
345, 346, 348, 366, 369 Chorioretinitis 155, 156, 331, 360 101, 102–106
Catford drum test 368 Choroidal dystrophy 5 Corneal Fistula 123, 150
Causes of pale disc 321, 359 Chromatopsia 2, 6 Corneal loupe 42, 43, 44, 103, 110, 142,
Cavernous sinus 37, 57, 86, 271, 271, Chromosomal aberration 365 152
272–277, 286, 289, 290, 291, 292, Chronic congestive glaucoma 8, 10, 11, Corneal plaque 118
293, 294, 295, 299 86, 88, 147, 150, 185, 187 Corneal topography 103, 112, 113
Central 3, 5, 6, 7, 12, 20, 21, 29, 32, 33, Chronic dacryocystitis 9, 75, 76, 86, 87, Corneal ulcer 3, 8, 9, 10, 37, 54, 55, 62,
34, 35, 36, 38, 47, 70, 90, 111, 112, 90, 114, 155 83, 113, 114, 118, 119, 122, 125, 137
113, 115, 123, 135, 146, 148, 149, Chronic glaucomas 2, 185 Cornu cutaneum 58
150, 153, 160, 168, 169, 185, 186, Chronic optic neuropathy 2, 3 Cortical blindness 3
190, 194, 195, 198, 199, 200, 201, Chronic simple glaucoma 7, 21, 88, 147, Cover and prism test 238
202, 207, 211, 213, 220, 228, 234, 184, 185, 186, 201, 202, 322, 355, Cover uncover test 236, 237
235, 239, 243, 246, 252, 253, 279, 362 Cowen’s sign 294
283, 309, 310, 311, 314, 321, 322, Cicatricial or spastic 52 Cranio-facial Anomalies 369
323, 324, 325, 326, 329, 331, 332, Ciliary epithelium 135, 181 Crouzan’s disorder 369
336, 338, 339, 340, 341, 342, 343, Ciliary staphyloma 41, 115, 125 Crowding phenomenon 254
348, 349, 350, 351, 352, 354, 355, Circle of least diffusion 18 Cup disc ratio is 0.3 or less 196
356, 359, 360, 362, 363, 364, 368 Classification of optic atrophy 359 Cyanopsia 6
Central artery occlusion 3 Claude’s syndrome 258, 259, 272 Cyanosis 85
Central field 5, 32, 34, 36, 198, 356 Cloquet’s canal 162 Cyclodialysis 138
Central nuclear cataract 5, 7, 186 Coats disease 153, 324, 325, 332, 338 Cyclopentolate 147, 192, 218, 220, 278
Central nuclear sclerosis 12, 194 Cobalt blue filter 42, 47, 103, 107, 131, Cycloplegic 7, 220, 278, 279
Central serous retinopathy 3, 6, 338 132, 174, 176, 312 Cyclotonic 278
Centrocecal field defects 33 Cocaine 279 Cyclovertical squint 270
Field defect central 5, 34 Cocaine 147, 279, 283 Cysticercus 139
Field defect peripheral 32, 35, 36, 198, Coloboma congenital of iris 143, 148 Cysticercosis 98, 230
309, 310, 354 Acquired 5, 30, 40, 52, 59, 65, 68, 70, Cystoid macular oedema 2, 173, 334
Field defect altitudinal 35, 362 109, 144, 152, 161, 243, 250, Cytomegalovirus 365
Centrocecal scotomas 33, 35 259, 268, 269, 271, 274, 278,
Cerebropontine angle tumour 121, 275 286, 291, 323, 336, 351 D
Chalazion 10, 12, 51, 52, 55, 56, 57, 58, Typical 18, 143, 152, 211, 262, 305 Dacryoadenitis 10, 37, 75, 295
97, 293 Coloboma of optic disc 201, 202 Dacryocystectomy 129
INDEX 381
Dacryocystitis 9, 10, 75, 76, 79, 86, 87, Dry eye syndrome 96, 128, 130, 131 Essential iris atrophy 143, 144, 146, 187
90, 114, 155 Duane’s retraction syndrome 258, 266, Eviscerated socket 40, 67
Dacryocystography 77, 79 268, 276, 277 Exenteration Evisceration 100
Macrodacryocystography 79, 80 Duochrome test 224 Exophoria 245, 247, 254, 255, 369
Lacrimal scintillography 77, 80 Dura 349 Exophthalmos 10, 37, 41, 96, 102, 286,
Dalrymple sign 294 Dye recovery test 77, 78 287, 294, 295, 299, 302, 369
Dark room test 192, 193 Dynamic retinoscopy 217 Exotropia 40, 235, 238, 239, 252, 256, 268
DCR 77, 78, 79, 129 Dyslexia 7 Eyes at birth 366
Demodex 59 Dysthyroid oculopathy 6, 38, 64, 86,
Deosrum version 261 190, 294 F
Depression 38, 39, 123, 126, 199, 261, Dysthyroid orbitopathy 41, 86, 290, 295, Face turn 256
265, 266, 269, 270, 274, 322 298, 299 Facultative hypermetropia 22, 225
Desmarre’s retractor 83, 84 Dysthyroid state 13 Farnsworth-Munsell:D-15 test 31
Dextro depression 261 Farnsworth-Munsell:100 hue test 31
Dextrocycloversion 261 E Fascicular ulcer 62, 96, 122, 123
Dextroelevation 261 Eales disease 153, 324, 325 Fibrosed sac 129
Dextroversion 261 Eccentric fixation 234, 250, 253, 254, Field changes in papilloedema 354
Diabetes 11, 57, 91, 139, 155, 185, 190, 257, 312 Field of vision 1, 5, 6, 14, 32, 39, 45,
201, 205, 213, 225, 228, 271, 273, Ecchymosis 66, 92, 275, 293 186, 193, 198, 228, 352
282, 323, 324, 361 Eccentric viewing 253 Filtering bleb 93, 94, 95, 136, 212
Diabetic maculopathy 2 Ectasia of globe 124 First Purkinje image 111, 112
Diabetic retinopathy 2, 13, 153, 322, Ectopia lentis 166, 167, 209, 366, 371 Fischer’s syndrome (modified
324, 325, 329, 332, 334, 337, 342, Ectropion 9, 52, 53, 54, 60, 96, 110, Gullian–Barre syndrome) 258
346, 350 114, 129, 170, 209 Fixation 32, 33, 34, 35, 36, 70, 198, 200,
Diabetic third nerve palsy 272 Edridge green lantern 31 233, 234, 235, 236, 237, 238, 239,
Diagnosis of papilloedema 354, 355 Edrophonium hydrochloride 73, 267 245, 246, 249, 250, 252, 253, 254,
Diminished vision in bright light 2, 5 Ehler’s Danlos syndrome 371 257, 312, 321, 369
Dioptre 26, 27, 111, 164, 219, 239, 248, Elschnig pearl or Soemmerring’s ring 139 Fixed dilated pupil 148, 278, 283
251, 257, 313, 316, 322 Elschnig’s pearls 136, 164 Fleischer’s ring 109, 118, 122
Diplopia 2, 5, 6, 28, 65, 68, 69, 73, 167, Emphysema 51, 92, 290, 295, 353 Fluorescein angiography 108, 156, 196,
226, 233, 241, 244, 245, 246, 247, Endo-illuminator 42 311, 330, 339, 340, 342, 343, 344,
250, 251, 252, 255, 259, 260 Endophthalmitis 3, 8, 10, 11, 51, 87, 88, 353, 354, 355
Binocular 6, 14, 43, 44, 45, 48, 61, 137, 138, 154, 153, 164, 318, 330, Fluorescein 42, 47, 78, 79, 96, 107, 131
103, 142, 136, 216, 226, 331, 344, 346, 348 Follicle 82, 84, 85, 89, 90
242–244, 251, 261, 263, 268, Enophthalmos 40, 53, 68, 100, 102, 283, Forced duction test 257, 259, 260, 262,
289, 314, 315, 316 286, 287 267, 299
Uniocular 6, 14, 22, 43, 44, 45, 61, Enroth’s sign 294 Formix
101, 103, 110, 142, 152, 167, 186, Entoptic visualisation 169, 170 Upper formix 83
235, 236, 237, 241, 243, 244, 250, Entropion 9, 52, 53, 55, 101, 107, 110, Lower formix 81
253, 260, 263, 268, 271, 281, 289, 114, 170 Lateral formix 81
312, 314, 345, 355, 358 Enucleated socket 40, 53 Medial formix 81
Diptheria 13 Enucleation 100, 286, 300 Foster kennedy syndrome 361, 362
Direct 42, 44, 189, 194, 310 Epaulette 122 Foville’s syndrome 258, 259, 275
Direct papillary reaction 151 Ephedrine 147 Fracture of orbit 10, 102, 235, 302
Indirect papillary reaction 151 Epicanthic folds 232 Fresnel prisms 27
Dirofilariasis 139 Epicanthus 41, 64, 65, 233, 256 Frisby stereo test 243
Dichromatopsia 30 Epidemic dropsy 185, 190 Fuch’s heterochromic iritis 143
Disciform keratitis 110, 116, 118, 122 Epidermoid carcinoma 67, 93, 95, 99 Functionally blind 228
Distichiasis 52, 54, 64 Epiphora 9, 53, 54, 60, 64, 77, 78, 128, Fundus findings in papilloedema 354
Diurnal variation in IOP 178 129, 170 Fundus fluorescein angiography in
Dorsal fascicular lesion 275 Episcleral congestion 82, 86, 185, 186 papilloedema 295
Double depressor palsy 39, 258 Episcleritis 8, 10, 13, 85, 86, 87, 88, 95, Fungal granuloma 268, 286, 291
Double elevator palsy 39, 258, 265, 266, 96, 124 Fusion 64, 226, 235, 242, 243
269, 277 Errors of refraction 2, 56, 287, 366
Double Maddox rod 241, 248, 249 Erysipelas 75 G
Draeger applanation tonometer 176 Erythropsia 6 Galactosaemia 371
Drusen 200, 201, 301, 322, 324, 326, Esophoria 245, 246, 247, 254, 255, 265 Genetic mutation 365
338, 342, 351, 355, 356, 357, 361 Esotropia 40, 235, 236, 238, 239, 251, Gifford’s sign 295
Drusen of optic nerve head 200, 338, 252, 256, 260, 265, 266, 268, 277 Glands 55, 57, 64, 74, 75, 84, 86, 127
355, 357 Essential blepharospasm 61, 62 Glands lacrimal 133, 290, 300
382 INDEX
Glands conjunctival 87 Homonymous 362, 364 Accidental 98, 211

Glands Meibomian 74 Hordeolum internum 56 Broad-based 144, 148
Glands Zeis 55 Horner’s syndrome 40, 63, 69, 72, 102, Four dot 144, 250, 251, 255
Glands moll 55 143, 147, 258, 275, 282–284, 371 Iridectomy 123, 134, 144, 146, 148,
Glare 2, 6, 7, 29, 317 Hudson Stahli line 118, 122 163, 187
Glaucoma suspect 190 Hue 30, 31, 152 Laser 144, 169, 181, 187, 190, 194,
Glaucomatous changes 194, 198, 200, Hutchinson pupil 148, 283 201, 325, 330, 337, 339
202, 205 Hydatid cyst 98, 139, 290 Optical 17, 45, 106, 111, 127, 174, 187
Glaucomflecken 204 Hydrogen peroxide 176, 178 Peripheral 5, 18, 20, 21, 29, 32, 35,
Godtfredsen’s syndrome 258, 259 Hydrops of cornea 116 36, 47, 48, 86, 110, 113, 115,
Goldmann three mirror contact lens 47 Hyperaemia of optic nerve 350 121, 124, 140, 141, 144, 149,
Goldmann three-mirror 187, 319, 344 Hyperglycaemia 7 150, 155, 156, 157, 163, 169,
Goldmann tonometer 174, 176, 177 Hyperlysinemia 167 173, 183, 185, 186
Gonioscope 28, 42, 47, 141, 152, 140, Hypertensive retinopathy 2, 13, 230, Peripheralbutton hole 144
155, 156, 187, 189, 208 332, 335 Iridencleisis 145, 148
Gonorrhoea 13, 114, 365 Hypertropia 68, 73, 235, 239, 267, Iridocyclitis 3, 7, 8, 10, 11, 13, 86, 129,
Gormaz exophthalmometer 296, 297 269, 270 137, 138, 142, 147, 148, 149, 150,
Gradenigo’s syndrome 121, 258, 259, 276 Hyphaema 12, 137, 138, 140, 142, 151, 152, 203, 209
Gradual proptosis 295 136, 155 Iridodialysis 6, 138, 144, 149
Graefe’s sign 294 Hypofluorescence 341 Iridostasis 143
Granulomatous uveiis 152, 154 Hypoglycaemia 7, 159, 213 Iridotomy 134, 144, 146
Griffith’s sign 294 Hypopyon 119, 136, 137, 138, 140, 142, Iris bombe 136, 164, 182
149, 136, 155, 293 Adherent leucoma 136
H Hypothyroidism 10, 39 Anteflexion of iris 136
Haab’s line 207 Hypotony 7, 13, 40, 68, 101, 114, 115, Retroflexion of iris 136
Haemangioma of conjunctiva 9 124, 136, 140, 150, 151, 173, 180, Iritis 10, 11, 143, 147, 148, 149, 155, 187
Haemophthalmos 139, 346, 347, 348 186, 211, 212, 330 Irridodonesis 141, 163, 164, 207
Haemorrhage 3, 8, 84, 85, 87, 88, 91, 92, Hypotropia 235, 268, 270 Ischaemic optic neuropathy 3, 5, 38, 196,
124, 135, 137, 147, 164, 169, 195, 200, 202, 203, 279, 321, 355, 358,
196, 202, 271, 272, 275, 282, 290, I 360, 361
295, 298, 318, 321, 322, 323, 324, Incongruous 5 Ishihara plates 30
325, 331, 334, 335, 336, 337, 339, Incyclotropia 235, 269, 270 Isolated superior oblique palsy 274
341, 345, 346, 347, 356, 357 Indentation tonometer 173, 174 Isopropyl alcohol 176, 178
Hamartomas 39 Indirect 42, 310, 314, 316, 340, 367 Isopter 199
Hammock pupil 151, 164 Indirect ophthalmoscope 28, 43, 48, 141,
Hand-held slit lamp 103 162, 169, 170, 194, 216, 217, 312, J
Hardy Rand Rittler plates 31 314, 316, 318, 320, 333, 339 Jackson’s cross-cylinder 223
Head posture 6, 37, 38, 68, 233, 256, Inferior oblique palsy 265, 266, 270, 271 Jacod’s syndrome 258
259, 260, 262, 264, 270 Inferior rectus palsy 265, 269, 270, 271 Jaeger’s near vision chart 22
Headache 11, 184, 193 Inflammatory endotoxin 181 Jaw winking 65, 66, 72
Hemianopic pupil 280, 281 Influenza 75 Jet black pupil 163, 167
Heredofamilial optic neuropathy 2, 363 Infrared lights 29 Jones I test 78
Hering-Bielschowsky test 252 Intensity 18, 30, 32, 136, 151, 198, 250, Jones II test 78
Herpes zoster 8, 54, 121, 187, 271, 282 252, 282, 303, 318 Juxta-papillary choroiditis 201
Herpes zoster ophthalmicus 3 Intermittent proptosis 295
Hertels mirror exophthalmometer 296 Internal ophthalmoplegia 4, 147, 148, K
Hess’ screen 241 225, 258, 272, 279, 283 Kayser Fleischer ring 118, 122
Heterochromia iridis 142 Interpupillary distance 227, 228, 240, Keeler’s near-vision chart 229
Heterochromia iridium 142 241, 257 Keith-Wagner-Baker classification
Heteronymous 5, 32, 252, 362, 364 Interscleral nerve loop 124 Keratoplasty 109, 110, 111, 113, 121, 122
Heterophoria (latent squint) 254 Interstitial keratitis 3, 7, 62, 107, 110, Keratectasia 115, 116
Hidradenitis 57 118, 119, 122, 209 Keratic precipitates 122, 153
Hippus 278 Intra epithelial epithelioma of Bowen 93 Keratitis 3, 7, 8, 9, 55, 56, 61, 62, 86, 87,
Hirschber’s test 239–247, 256 Intraocular tension 140, 173, 175, 177, 107, 109, 110, 116, 117, 118, 119,
Histamine 181 178, 179, 180, 181, 183, 184, 185, 120, 122, 129, 130, 133, 179, 209,
Holmes stereoscope 244 187, 189, 191, 192, 196, 202, 206, 228, 299
Homatropine 147, 192, 218, 219, 220, 211, 299, 358 Keratoconjunctivitis sicca 107, 132
278 Intraorbital calcification 300, 301 Keratoconus 7, 104, 107, 109, 110, 111,
Homocystinuria 139, 167, 371 Inverse Argyll-Robertson pupil 282, 288 112, 113, 115, 116, 135, 168, 169,
Homocystinuria syndrome 167 Inverse hypopyon 137, 138 213
INDEX 383
Keratomalacia 83, 118, 125 223, 240, 241, 244, 248, 252, 257, M
Keratometer 48, 111, 112, 115 280, 303, 304, 305, 311, 313, 314, MacKay-Marg’s tonometer 178
Keratometry 103, 110, 171, 172, 214 315, 316, 318, 319, 320, 321, 330, Macrophthalmos 114
Keratonisation 130 331, 332, 343, 344, 345, 348, 361, Macropsia 310, 338
Keratoscopy 103, 112, 207 367 Macula 3, 18, 20, 30, 68, 109, 116, 117,
Kernohan notch syndrome Hruby 47, 156, 194, 311, 319, 320, 156, 157, 170, 173, 198, 200, 202,
Keystone stereoscope 244 344 234, 253, 263, 309, 311, 313, 315,
Kinetic perimetry 198 Goldmann 47, 174, 176, 177, 187, 316, 317, 318, 319
Kinetic stereoscope 243 194, 311, 319, 344 Macular Degenerations and dystrophies 2
Klein keratoscope 113 El Bayadi 47, 156, 194, 319, 320, 344 Macular oedema 2, 6, 7, 157, 173, 212,
Klinefelter syndrome 371 Panfundoscopic 320 334, 337
Kocher’s sign 294 Lensometer 26 Madarosis 52, 55, 56, 61, 83
Koeppe 152, 189 Lenticular 20, 29, 135, 155, 160, 162, Maddox double prism 28, 241, 248, 249
Koeppe’s nodule 164, 199, 202, 212, 213, 220, 314, Maddox rod 17, 169, 170, 241, 244, 245,
Krimsky test with prism 239 318 247–250, 254, 255
Krukenberg spindle 118, 122, 186, 190 Leprosy 10, 13, 39, 40, 49, 53, 54, 55, Maddox tangent 241, 246
61, 110, 114, 118, 119, 121, 130, Maddox wing 241, 247, 254
L 132, 152, 155 Malingering 3, 38, 241
Lacrimal sac 9, 74, 76, 77, 78, 103, 114, Leprotic nodule 152 Mandibulo-facial dysostosis 64, 167, 369
128 Leucoma 109, 116, 117, 122, 136 Manifest squint 232, 233, 235, 239, 240
Lacrimal scintillography 77, 80 Leucoma adherent 109, 117 Marcus Gunn pupil 280, 281
Lacrimation 9, 53, 54, 55, 61, 128, 129, Leukaemia 91, 139, 286, 287, 289, 290, Marfan syndrome 167
184, 185, 207, 208, 209 291, 292 Mature cataract 161, 168, 301, 307
Lagophthalmos 9, 10, 60, 61, 68, 96, Levocycloversion 261 Immature cataract 3, 5, 6, 7, 30, 160,
107, 110, 114, 120, 129 Levodepression 261 161, 202, 262
Landolt’s broken C Levoelevation 261 Measurement of depth 195
Landolt’s C and E charts Levoversion 261 Mecholyl 279, 282
Langs stereo test 243 Lid abscess 10, 51, 57, 83 Medial rectus palsy 264, 265, 268
Laser interferometry 169 Lid hook 83 Megalocornea 101, 114, 135, 167
Latent squint 41, 232, 236, 254 Lid lag 64, 102, 287, 294, 299 Meibomian cell carcinoma 59
Lateral rectus palsy 264, 266, 268 Lid retraction 10, 40, 63, 102, 287, 289, Melkersson Rosenthal syndrome 61
Layden 189 292, 295, 298 Membranous 9, 53, 83, 87, 89, 91
LDH enzyme 154 Lid retraction 10, 40, 63, 102, 287, 289, Meningitis 13, 271, 308, 353, 357
Left hypertropia 267, 270 292, 295, 298 Meniscus 29, 130, 131, 189
Legal blindness 228, 338 Lid retractor 83 Lens meniscus 29, 130, 131, 189
Lens El Bayadi 47 Light reflex 70, 71, 151, 234, 239, 241, Merthiolate 176
Lens contact 47, 90, 108, 110, 111, 113, 279, 280, 281, 282, 323 Metamorphopsia 2, 6, 33, 34, 157, 309,
121, 132, 165, 188, 194, 344 Limbal dermoid 93, 94, 113, 116, 118, 310, 338
Lens plano 24, 28, 44, 47, 134, 144 132, 365 Micro-cornea 110, 135, 365
Lens convex 27, 28, 44, 47, 103, 111, Limbal ring localization 307 Microphthalmos 40, 67, 100, 101, 114,
215, 216, 257, 280, 315 Limbus 40, 70, 81, 86, 87, 90, 93, 94, 115, 124
Lens concave 27, 28, 47, 257 95, 96, 99, 102, 106, 110, 113, 115, Micropsia 310, 338
Lens biconvex 24, 315 116, 117, 121, 122, 125, 138, 144, Microscope 26, 28, 43, 45, 46, 47, 48, 105,
Lens plano concave 24, 47 145, 146, 151, 163, 164, 186, 239, 106, 111, 176, 187, 189, 208, 339
Lens plano convex 24, 44, 144 267, 287, 288, 307 Mikulicz syndrome 75
Lens concave convex Limitation of adduction 365 Millard-Gubler’s syndrome 258, 259, 275
Lens convexo concave 24 Limited abduction 266, 269 Miosis 140, 141, 146, 147, 148, 151,
Lens intraocular 136, 139, 332 Lippman’s HOTV test 368 182, 192, 273, 278, 279, 280, 281,
Lens Hruby 47 Lister’s lamp 103, 104 282, 283
Lens Volk 47, 311, 344 Lister’s perimeter 234, 240 Mixed sphero-cylinders 24
Lens 3, 6, 13, 22, 23, 24, 25, 26, 27, 28, Localising features of trochlear Modified photo stress test 169, 170
29, 37, 42, 43, 44, 47, 48, 90, 103, nerve 273 Moebius sign 294
106, 108, 110, 111, 112, 113, 121, Low tension glaucoma 202, 211 Moebius syndrome 235, 257, 266, 268,
123, 132, 134, 135, 136, 138, 139, Low vision 22, 27, 213, 227, 228, 229, 276, 277
154, 141, 143, 149, 150, 151, 155, 230, 339 Molluscum 51, 58
156, 158, 159, 160, 161, 162, 163, Lowe’s syndromes 209 Mongoloid obliquity 40
164, 165, 166, 167, 168, 169, 170, Luedde’s transparent scale 227, 296 Mooren’s ulcer 113, 116, 122
171, 172, 173, 182, 185, 186, 187, Luminance 198, 199 MRI of orbit 302
189, 190, 194, 195, 202, 203, 205, Lymphoma 292 Mucocele of sac 76, 78
207, 208, 212, 213, 215, 216, 218, Lymphosarcoma 292 Mucopolysaccharidosis 209, 371
384 INDEX
Mumps 75, 295 Operating loupes and telescope 43 Partially seeing 227, 228
Muscae volitantes 345 Operating microscope 43, 208 Peculiarities of congenital glaucoma 205
Muscles–orbicularis 49 Operating telescopes 45 Peculiarities of vitreous 343
Levator palpebral superioris 49 Ophthalmia neonatorum 9, 83, 118 Pediculus 59
Muller’s muscles 49 Ophthalmic ultrasonography 303 Pellucid corneal degeneration 104, 113
Mutton fat KPs 152, 154 Ophthalmoplegic migraine 273 Perception of light 20, 21, 168, 339,
Myasthenia 6, 40, 66, 68, 69, 73, 235, Ophthalmoscope 27, 28, 42, 43, 48, 113, 346, 357
258, 265–269 141, 155, 162, 169, 170, 193, 194, Perimeters 32
Myasthenia gravis 6, 258, 267 195, 216, 217, 253, 312–318, Perimeter arc 32, 35, 196, 234
Mydriasis 29, 140–142, 146, 148, 183, 320–322, 332, 333, 339, 340, 342, Perimeter bowl 32, 35, 198, 200
186, 187, 193, 220, 278, 281, 316, 317 345 Perimeter automated 32, 196
Mydriasis or miosis 141 Direct 28, 42, 43, 44, 47, 48, 61, 91, Perimeter Goldmann 35, 47
Mydriatic cum miotic test 192, 193 92, 104, 105, 137, 141, 151, 155, Perimeter Tubinger 35
Myodisc 29 156, 160, 162, 169, 187, 189, Perimeter kinetic 198
Lens myodisc 29 193, 194, 195, 208, 216, 217, Perimeter static 198
Myositis 10, 266, 268, 293 279, 280, 310, 311, 312, 313, Perimeter Lister’s 35, 234, 240
Myotonic dystrophy 66, 268 314, 317, 318, 319, 320, 321, Peripheral field 32, 35, 185, 198, 309,
Myxoedema 51 322, 327, 329, 340, 346, 348, 310, 354, 356
349, 366, 367, 368 Perkins handheld tonometer 176, 177
N Indirect 28, 42, 43, 48, 91, 104, 106, Persistent hyperplastic primary vitreous
Naevus 50, 58, 59, 338, 341 125, 126, 141, 151, 156, 160, 162, 139, 329, 343, 346, 370
Nagel’s anomaloscope 31 169, 170, 187, 189, 194, 208, 216, Persistent pupillary membrane 148, 150
Nanophthalmos 101, 115, 168, 205, 209, 217, 279, 280, 310, 311, 312, 314, Peters anomaly 208
330, 331 315, 316, 318, 319, 320, 327, 329, Pfandlers syndrome 371
Near point of accommodation 225 333, 339, 340, 343, 344, 347, 348, Phacomatosis 208
Near point of convergence 225, 226 366, 367, 368 Aphakia 4, 7, 22, 27, 38, 39, 134, 135,
Near reflex 151, 279–283, 367 Optic nerve glioma 292, 293, 295, 300, 137, 138, 159, 160, 161, 163–166,
Nebula 109, 116, 117 301, 350, 352, 355 313, 321, 326, 328, 329, 330, 332
Negative scotoma 5, 198 Optic neuritis 5, 10, 279, 322, 350, Lenticonus 159, 162, 213, 305
Neuro fibroma 59 355–360 Lentiglobus 159, 213
Neurofibromatosis 66, 208, 296 Optic neuritis in children 357, 358 Microphakia 159
Neuro-fibromatosis 39 Optic sheath meningioma 352 Phakia 159, 164
Neutral density filter 254 Optical pachometer 111 Spheropha
Nevus 10, 99, 321 Optociliary shunt vessels 350 Phenylephrine 63, 147, 192, 220, 278, 283
Night vision 1, 4, 14, 186, 309, 310 Orbital abscess 290 Phlycten 8,10, 86, 87, 92–94, 118, 121,
Nodule of iris 142 Orbital cellulitis 10, 37, 286, 290–295, 367 122, 123
Non-concomitant squint 232 Orbital varix 290 Phlyctenular keratoconjunctivitis 7,
Non-variable prism stereoscope 243 Orbital venography 300, 302, 306 62, 122
Nothnagel’s syndrome 259, 272 Oxycephaly 291 Photogrey 30
Nystagmus 30, 37, 41, 125, 230, 265, Photo-iridoplasty 149
336, 368, 369 P Photokeratoscopes 113
Pachymetry 48, 103, 111, 187 Photophobia 2, 6, 7, 61, 185, 207, 208
O Painful ophthalmoplegia 268 Photopsia 2, 6, 310, 348
Objective angle of squint 241, 242 Pannus 90, 110, 116, 117, 122 Photo-stress test 170, 339, 340
Objective test 214, 215 Pannus progressive 122 Photosun 30
Oblique illumination 42, 117, 141, Pannus regressive 122 Phthiriasis 59
155, 167, 186, 187, 346 Pannus fascicular 122 Phthisis 40, 68, 101, 102, 114, 115, 124,
Occluder 17, 21, 240, 369 Papanicolau 155 136, 211, 289, 300
Occluder hand-held 17 Papillae 82, 84, 85, 89, 90 Phthisis bulbi 101, 102, 115, 136, 211
Ocular grave’s disease 12, 158, 184 Papillitis-characteristic of 357 Pia 349
Ocular hypertension 178, 180, 190, Papilloedema 201, 287, 295, 299, 308, Pictorial charts 368
202, 211 321–323, 325, 335, 350, 353–361, Pin hole 17
Ocular hypotony 211, 212, 355 369 Pinguecula 85–87, 91, 92, 94
Ocular pemphigus 53, 96, 130 Papilloma 9, 91, 93, 94, 99 Pits in the optic nerve head 196
Ocular symptoms of papilloedema Papilloma of the conjunctiva 9 Pituitary tumours 5, 308
Oculomotor (III Nerve) palsy Paracentral scotomas 35 Plane mirror retinoscope 162, 216
Oculomotor palsy 11, 40, 148, 258, 268, Paralytic squint 6, 11, 41, 232, 233, 255, Plasmoid aqueous 135, 136, 153
272 256, 258–260, 263, 267 Plica semilunaris 81
Oculosporidiosis 9 Paredrine 279 Poliosis 40
Onchocerciasis 139 Parsplanitis 337 Polycoria 143, 146, 209, 366
INDEX 385
Polyopia 2, 6, 262 Puncta occluded 129 Rieger’s anomaly 208

Position of chin 256 Puncta pin point 56, 271 Right hypertropia 73, 267, 270
Posner four-mirror 189 Pupillary block 134, 140, 182, 192, 203, Rose Bengal 96, 107–109, 130–133
Posner Schlossman’s syndrome 143 204, 205 Rosenbach’s sign 294
Post-operative entrapment of muscles 6 Purkinje images 112, 158, 160, 161, 163, Crossed diplopia 245, 262, 263, 269
Posterior uveitis 11, 88, 156, 157, 331, 164, 167 Rubella 13, 209, 326, 338, 365
337, 370 Pyocele of sac 76 Rubeosis iridis 152
Posterior vitreous detachment 6, 156, 329
Post-mydriatic test 218, 220 R S
Potential acuity meter 169 Random dot stereo test 243 Sarcoidosis 75, 133, 152, 155, 156, 286
Preferential looking technique 368 RAPD 280, 340 Saturation 30
Presbyopia 1, 4, 11, 12, 22, 27, 185, 213, Raymond’s syndrome 259 Scheiner test 214
225, 255 Red glass test 250, 251 Schiotz tonometer 173, 174, 176, 178, 211
Primary glaucomas 183, 185, 201 Reduced eye of Donder Schirmer’s test 1 130, 132
Primary herpes simplex 51 Regurgitation test 75–78, 129, 170 Schirmer’s test 2 72, 130, 132
Primary narrow-angle glaucoma 204 Reiters disease 167 Schlemm’s collecting channels 181, 182
Primary postion 72 Relative scotoma 5, 34, 198 Sclera 40, 41, 63, 64, 81, 82, 84, 85, 89,
Prism 4 PD base out test 250 Restriction of depression of eyeball 266 100, 101, 103–105, 107, 109, 111,
Prism dioptre 27, 239, 248, 257 Restriction of elevation 266 113, 115
Prisms 17, 27, 28, 46, 248, 280, 315 Restrictive squint 232, 257, 299 Scleral ectasia 124, 186
Progressive external ophthalmoplegia 66, Restrictive strabismus 6, 102 Scleral staphyloma 101, 126
258, 265, 268 Retinal breaks 326 Scleritis 8, 10, 13, 85–88, 95, 124–126,
Projection of light 20, 21, 168 Retinal detachment 3, 5, 6, 12, 13, 20, 294, 331
Projection perimeter 197 21, 38, 66, 115, 126, 148, 153, 157, Scotoma 5, 33, 34, 198–200, 202, 250,
Prone position 192, 193, 205 164, 198, 202, 205, 211, 258, 304, 310, 328, 338–340, 351, 356–358,
Proparacaine 107, 133, 175 310, 320, 322, 326–333, 346, 348, 362–364
Proptosis 9, 10, 11, 37, 41, 63, 75, 82, 370 Congruous 5
92, 96, 102, 110, 206–209, 286–299, Retinal dysplasia 370 Incongruous 5
351, 367, 369 Retinal dystrophy 4, 5, 21, 326 Homonymous 5, 32, 252, 362–364
Proptosis in children 292, 293 Retinal vein obstruction 153, 202, Heteronymous 5, 32, 252, 362, 364
Prostaglandins 181 336, 346 Scotoma absolute 33, 198, 228
Provocative test for corticosteroid 112 Retinal vein thrombosis 3, 190, 350, Scotoma arcuate 35, 198–200
Provocative test for glaucoma 191 355, 356 Scotoma central 5, 33
Provocative test for water drinking 191 Retinitis 1, 4, 5, 11, 190, 201, 230, Scotoma centrocecal 35
Provocative test suitable for narrow angle 322–325, 337, 338, 345, 360, 364 Scotoma peripheral 5
glaucoma 192 Retinitis pigmentosa 1, 4, 5, 190, 201, Scotoma paracentral 34, 35
Pseudo-foster kennedy syndrome 361, 230, 360, 364 Scotoma relative 5, 198
362 Retinitis proliferans 345 Screen Bjerrum 33–35
Pseudo-hypopyon 136, 137 Retinoblastoma 10, 139, 154, 205, 209, Screen tangent 32, 34, 196
Pseudo-membrane 9, 89 289–293, 296, 299, 300, 301, 307, Seclusio pupillae 150
Conjunctivitis membranous 9 331, 370 Secondary glaucoma 125, 142, 173, 180,
Conjunctivitis pseudo-membranous 9 Retinopathy of prematurity 332, 333, 183, 185, 209, 344, 346
Pseudo-neuritis 322, 350, 355–357 346, 366, 370 Secondary optic atrophy 2, 230, 321,
Pseudophakia 4, 27, 134, 135, 163, 164, Retinoschisis 320, 327, 328, 329, 331, 332 322, 356
329, 332 Retinoscope 42 Segmental pallor 360
Pseudo-polycoria 143, 146 Retinoscopy 126, 214–220, 222, 223, Seidel’s scotoma 199, 200
Pseudo-proptosis 206, 207, 209, 288 230, 344, 346 Senile cataract 10
Pseudo-pterygium 88, 93 Retrobulbar growth 6, 7, 209, 355, Sheridan Gardener cards 368
Pseudoptosis 10, 38, 39, 40, 101, 102 Retrobulbar neuritis 5, 10, 13, 358, 360 Sickle cell retinopathy 153, 322, 332,
Pseudo-squint 64, 232, 233 Retrobulbar optic neuritis 358 342, 346, 350
Pseudo-tumour of orbit 258, 266, 268, Retrolental fibroplasias 139, 153, 329, Simple blepharospasm 61
295, 303 333, 346, 370 Simultaneous perception 242, 243
Pterygium 8, 10, 11, 85–88, 91–93, 112, Retro-ocular mass 287 single-mirror 187
115, 116, 118, 119, 122, 130, 132 Rhabdomyosarcoma 289, 290–293, 295, SINRAD 264
Ptosis 10, 38, 39, 40, 41, 63–73, 265, 296, 300 Sinusitis 10
267–269, 272, 282, 289, 369 Rheumatoid arthritis 130, 138 Sjogren syndrome 96, 130
Ptosis - tru/pseudo 287 Rhinosporidiosis 76, 79, 91, 97, 125, Slit lamp 27, 42, 43, 45–48, 103, 111,
Pulsating proptosis 296 126, 129, 133 131, 132, 136, 138, 142, 144, 149,
Puncta 9, 74–79, 128, 129 Richardson Shaffer 189 152, 156, 162, 174, 176, 177, 179,
Puncta everted 29 Riddley’s rotating prism 28 186, 187
386 INDEX
Small pox 118, 125 Suppression 250–252 Thyrotoxic 294, 295

Snellen’s chart 14–19, 21, 215, 254 Supraversion 261 Thyrotoxicosis 89, 287, 355
Snowball opacities 155, 156 Infraversion 261 Thyrotropic 294, 295
Sodium hypochlorite 176, 178 Sursum version 261 Titmus fly test 243, 244
Soemmerring ring 136, 164 Suspicious cup 195 TNO test 243
Spasm of accommodation 4 Swan Jacob 189 Tomography 194, 301, 302, 305
Spectacles 11, 13, 22, 27, 45, 231 Symblepharon 84, 96, 133 Tonic pupil (Adie’s pupil) 281
Specular microscopy 106, 110 Anterior symblepharon 96 Tonometers 173, 174, 176, 178, 179
Spot retinoscope 216 Posterior symblepharon 96 Tonopens 178
Spring catarrh 8, 9, 10, 49, 87, 90, 93, Sympathetic Ophthalmia 10, 40, 331 Toric lenses 28
94, 110, 114, 118, 122, 133 Symptoms of retinal disorders 309 Total ophthalmoplegia 4
Squamous blepharitis 55 Synaptophore 27, 28 Toxic amblyopia 13
Squamous cell carcinoma 59 Synchisis scintillans 345 Toxocara 370
Squint 3, 6, 10, 11, 13, 37, 41, 64, 66, Synechia 42, 124, 149–151, 169, 182, Toxoplasmosis 308, 324–326, 330, 336,
82, 125, 230, 232, 233, 235–243, 183, 204, 207 365
245, 247, 249, 251–260, 263, 265, Anterior 47, 106, 125, 134, 135, 138, Trachoma 9, 10, 13, 53–55, 83, 87, 89, 90,
267, 269–271, 273, 275, 277, 287, 143, 144, 148, 149, 150, 155, 110, 118, 119, 121, 129, 130, 133,
289, 299, 336, 366–369 165, 267 228, 365
SRK formula 171 Central 314, 321–326, 329, 331, 332, Trans-illuminator 42, 48, 162, 312
Staphyloma anterior 41, 104, 125 336, 338–343, 348–352, Traquiair hill of vision 198
Staphyloma ciliary 41, 115, 125 354–356, 359, 360, 362, 363 Traumatic cataract 139, 171
Staphyloma equatorial 125 Posterior 106, 125, 141, 181, 182, Travel vision 228
Staphyloma intercalary 125, 210 272, 298, 305, 325, 341 Treacher Collins syndrome 167, 371
Staphyloma posterior 125, 126, 210 Peripheral 5, 18, 20, 21, 29, 32, 35, Tremulousness of iris 163, 167
Staphyloma scleral 125, 126, 210 36, 47, 48, 86, 110, 113, 115, Trial frame 17, 215, 223, 224, 240, 246,
Staphyloma 10, 41, 85, 101, 104, 115, 121, 124, 140, 141, 144, 149, 248–250, 252
124–126, 136, 209, 313 150, 155–157, 163, 169, 173, Trichiasis 9, 52, 54–56, 64, 101, 107,
Staphyloma corneal 115, 125, 136 183, 185–187, 195, 198, 200, 110, 114, 129, 170, 369
Static perimeter 36, 198 201, 204, 220, 228, 253, 263, Trigeminal neuralgia 37, 258
Static retinoscopy 217 309, 310, 311 Tritanopia
Stellwag’s sign 294 Ring 18, 39, 109, 118, 122, 136, 139, Tropicamide 147, 218, 220, 278
Stenopeic slit 17 143, 150, 164, 306, 307, 348 True images 263
Stereopsis 44, 45, 242–244, 314, 318, Synoptophore 227, 234, 240, 241–244, True membrane 89
319, 329, 336, 338 250, 251, 256, 257 True ptosis 69
Stereopsis test 243 Syphilis 13, 75, 114, 152, 155, 209, 271, Tuberculosis 13, 75, 99, 114, 152, 155,
Steroid hyalopathy 345 281, 282, 361, 365 271, 282, 291
Steroid-induced cataract 13 Syphilitic nodule 152 Tunica vasculosa lentis 158
Stevens Johnson syndrome 53, 133 Syringing 75–79, 114, 170 Two pencil stereopsis 243
Still’s disease 13 Two-point discrimination test 169
Stilling plates 31 T Tylosis 52, 55
Strabismus fixus 258, 277 Tangent scale 246, 254
Straub’s chart 229 Tangent screen 32, 34, 196 U
Streak retinoscope 172, 216 Tarsal cyst 58, 67 Ulcerative blepharitis 54–56
Sturge Weber syndrome 39, 66, 183, 208, Tarsal plate 50, 81, 88 Ultrasonic pachometer 111
209 Taste test 78, 289 Ultraviolet 7, 29, 36, 62, 107, 132, 133,
STYCAR (Snellen’s test for young Tattoo 116, 118, 120, 122 176
children & retarded) 14, 16, 368 Tear breakup time 132 Light ultraviolet 7, 36, 107, 133
Stye 10, 12, 51, 52, 55–57, 83, 293 Tear meniscus 130, 131, 189 Unilateral disc swelling 355, 358
Sub-Conjunctival Haemorrhage 8, 84, Telecanthus 64, 232, 233 Unilateral proptosis 289, 290, 293
85, 87, 88, 91, 92, 124 Teller acuity card test 368 Uniocular Corneal Loupe 43, 44, 103,
Subjective angle of squint 241, 242 Temporal pallor 360 110, 142, 152
Subjective test 197, 215, 221, 234 Tensilon (Edrophonium hydrochloride) 73 Uniocular vision 14, 244
Subluxated lens 6, 135, 167, 168, 182 Tensilon test 68, 69, 73, 267 Upside down ptosis 282
Sub-retinal neovascularisation 2, 326, Terrien’s degeneration 113, 116 Acquired 5, 30, 40, 52, 59, 65, 68, 70,
331, 337, 338, 342 Terson’s syndrome 346 109, 144, 152, 161, 243, 250,
Sulphite oxidase deficiency 167 Thelazia 139 259, 268, 269, 271, 274, 278,
Superior oblique palsy 265, 269, 270, 274 Thorpe 189 286, 291, 323, 336, 351
Superior orbital fissure syndrome 10, 121, Thrombosis 3, 10, 37, 38, 57, 86, 190, Congenital 10, 30, 38–40, 49, 52, 55,
268 202, 271, 277, 286, 289–295, 299, 59, 64–66, 68, 70, 72, 77, 98, 101,
Superior rectus palsy 265, 268, 270 324, 325, 329, 338, 350, 355, 356 109, 110, 117, 118, 124, 125, 129,
INDEX 387
141, 143, 145, 146, 148, 150, 152, Variable prism stereoscope 243 Vitreous detachment 6, 156, 329, 330,
155, 161, 167, 180, 183, 184–186, Vascularisation 53, 54, 55, 102, 109, 110, 347, 348
203, 205, 206, 208, 209, 235, 255, 116, 118, 120–123, 130, 142, 157, Vitreous haemorrhage 3, 164, 318, 331,
256, 258, 259, 265, 267–271, 274, 184, 186, 210 334, 345, 346, 347
275, 277, 278, 286, 290, 291–293 Ventral fascicular lesion 275 Vogt koyanagi syndrome 11
Neurogenic 66, 69 Vertigo 11
Myogenic 66, 69, 235 Vision charts 22, 229 W
Pseudo 9, 30, 63, 64, 66, 68, 69, 75, Visual evoked potential (VEP) 368 Waardenburg syndrome 143
88, 89, 93, 133, 136, 137, 143, Visual hallucinations 7 Weber’s syndrome 66
146, 162, 164, 186, 187, 190, Visual agnosia 7 Wegener’s granuloma 286, 291
206, 207, 209, 215, 217, 232, Visuscope 253, 254 Weill Marchesani syndrome 371
233, 235, 237, 256, 258, 266, Vitamin A deficiency 4, 96, 130, 133, 228 Window reflex 112
268, 269, 287, 288, 290, 291 Vitiligo 10, 40, 49 Worth four dot test 250, 251, 255
Upside 65, 282 Vitreous bands 305, 325, 345, 347
Uvea 101, 121, 124, 125, 135, 136, 137, Vitreous chamber 134 X
140, 141, 146, 152, 153, 154, 156, Aqueous chamber 134, 135, 141 Xanthelasma 49, 58
155, 173, 206, 330, 343 Anterior chamber 10, 47, 48, 86, Xanthopsia 6
Uveo-scleral outflow 181 134–139, 140, 141, 144, 150, Xeroderma pigmentosa 59, 60, 95
154, 155, 163, 167, 168, 181, Xanthosis 85
V 183, 185–188, 203, 207, 210, Xylocaine 78, 79, 107, 175, 267, 307
V esotropia 40 304, 344–366, 367
V exotropia 256, 265 Posterior chamber 134, 139, 164, Z
Van Herick’s sign 186 181 Zeiss four-mirror 50, 189

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Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann and

All rights are reserved. No part of this publication may be reproduced,

Medical knowledge is constantly changing. As new information becomes

Published by Elsevier, a division of Reed Elsevier India Private Limited,

Printed and bound in India at

SYMPTOMS IN OPHTHALMIC DISORDERS

Symptoms in ophthalmic disorders are as follows:

Visual Symptoms of Ocular Disorders

● Diminished vision in bright light

● Consecutive optic atrophy

● Secondary optic atrophy

(d) Chronic maculopathy

● Cystoid macular oedema

● Chronic macular oedema, secondary to vascular lesion, inflammation, trauma or drug

● Branch artery occlusion

● Branch vein occlusion

● Ex anopsia (form vision deprivation)

(a) Errors of refraction are myopia, hypermetropia and astigmatism

by opacities of cornea, which may be post-traumatic and post-infective, vascularisation of

Diminished colour vision This is commonly known as colour blindness.

image or may be separated by a gap. It may be displaced horizontally or vertically, may

Polyopia (seeing multiple) The patient complains of seeing multiple images of

Glare is seen in:

Non-Visual Symptoms of Ocular Disorders

➤ Unilateral redness of eye is seldom conjunctivitis

➤ Acute watering is generally lacrimation

➤ Trachoma, pterygium and phlycten do not cause itching per se

➤ White eyes are generally not painful

Whitening of eyebrows and lashes The causes are physiological, sympathetic

Mixed Symptoms of Ocular Disorders

HISTORY TAKING IN OCULAR DISORDERS

History of Present Illness

catarrh by steroids may develop diminished vision due to steroid-induced cataract,

Past History of Systemic Disease

Allergy and Drug Reaction

From Chapter 1 it is obvious that ocular symptoms outnumber non-ocular symptoms.

Fig. 2.1 | Snellen’s chart. Fig. 2.2 | E test types.

Fig. 2.3 | C chart. Fig. 2.4 | Allen pictures.

The charts are of two types:

If there is shortage of space, then instead of 6 m, 3 m distance is used with changed

Method of Recording of Vision

Fig. 2.7 | Notation in a trial frame.

CONSTRUCTION OF LETTERS IN SNELLEN’S CHART

➤ One degree ⴝ 1/360th of a circle. 1/60 degree ⴝ 1 min

Fig. 2.8 | Construction of Snellen’s letter and Landolt’s ring.

Fig. 2.9 | H, C and E subtend an angle of 5 min at 36, 24 and 12 m, respectively.

HOW TO RECORD LEVEL OF DISTANT VISION

Vision is recorded as a fraction in which the denominator denotes the distance at

How to Test Perception of Light

➤ Perception of light is the ability to perceive light anywhere on the retina.

Causes of loss of perception of light

➤ Projection of light denotes gross retinal function at the periphery

How to Examine Projection of Light

Points to Remember in Recording Distant Vision

Method of Documenting Distant Vision

Recording of Near Vision

Examination of Spectacles of the Patient

Biconvex Plano-convex Concavo-convex Biconcave Plano-concave Convexo-concave

Fig. 2.11 | Types of lenses.

Fig. 2.12 | Movement of image in a plus sphere.

2. Movement is equal in all directions

Characteristics of minus sphere