Best Aid To Ophthalmology

BEST AID
to
OPHTHALMOLOGY
BEST AID
to
OPHTHALMOLOGY
Pramod TK MBBS
Research Scholar
Center for Arrhythmia Research
Division of Cardiology
Department of Internal Medicine
University of Michigan, Ann Arbor
Michigan, USA
®
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Best Aid to Ophthalmology
First Edition: 2013

ISBN 978-93-5025-760-9
Printed at
Dedicated to
My mother Nagarathnamma R,
My father Kariyanna R,
My sisters Bharathi TK and Rajashree TK,
My nephews Sushruth, Pranav and Shaan,
and
The god I trust Lord Sri Lakshmiranganatha.
Preface
The time available to master the subject Ophthalmology is very
short. It is a broad subject in itself and is ever expanding like
any other specialty of medicine. The purpose of Best Aid to
Ophthalmology is to make the complex subject simple and
studying a joyful, easy and a loveable task, yet master it in the
limited time available. I hope, I have successfully met the long-
felt need of the student-friendly, yet a complete examination-
oriented book through Best Aid to Ophthalmology. I have invested
my heart and soul to the same.
The notes of mine made referring all the textbooks have been
brought out as a book with lots of needed corrections, additions,
deletions and substitutions. Hence, I myself am the first student
to take the examinations by reading this book, followed by a
couple of my juniors! The book is small and simple but is very
smart. The book is organized in question-and-answer format. A
lot of information has been arranged as tables and flow charts.
Also, the mnemonics makes memorizing an easy task. Diagrams
are in a fashion that they can be easily reproduced in
examinations. This is not a textbook, but a preparatory manual
for examinations. It is also helpful for postgraduates in fast
revision of the subject.
There is no shortcut to success. All are equally blessed by god.
Persistence is the only thing that will help in long run of the MBBS
marathon. Believe in yourself. Keep cool. Impossible is nothing.
viii Best Aid to Ophthalmology
Make the most of "now". It's just a few months from now for you
guys to graduate as doctors. I wish you all a very best for the same
and the journey beyond. Happy studying.
All the comments, corrections, appreciations and criticism
are welcome. I would also like to know if any topic in the book
is not adequately written or if any have been given undue
importance from examination point of view. Kindly let me know,
if I by chance have left out any high yield topic. I will be happy
to receive the mails and will try to reply them at the earliest.
Kindly mail them to drtkpram@gmail.com.
I also welcome you to Best Aid global family, do like our
Facebook page Best Aid to MBBS.
Pramod TK
Acknowledgments
I am grateful to my parents, their visions and sacrifices, which
have made me whatever little I am today in life. My sisters have
nurtured me since I was a kid, I have no words to describe them.
My nephews help me remain cheerful and childish enough even
now!
I wholeheartedly thank Dr Kiran Kumar L, Assistant
Professor, Department of Ophthalmology, Kempegowda Institute
of Medical Sciences, Bengaluru, Karnataka, India, who edited
the book despite his busy schedule.
I am grateful to Dr Prasad Srinivasa, Dr Chethan Murthy and
Dr Tahera Syed, for their time and thorough editing.
I gratefully remember the cooperation rendered by M/s Jaypee
Brothers Medical Publishers (P) Ltd, New Delhi, India, in bringing
out the book in a wonderful fashion. I thank Shri Jitendar P Vij
(Group Chairman), Mr Ankit Vij (Managing Director),
Mr Tarun Duneja (Director-Publishing) and their staff, for their
cooperation and who were there to answer every query of mine.
I am grateful to all the teachers who have taught me till date.
How to Contribute to
“Best Aid to Ophthalmology”
Dear friends,
I request you to share with me high-yield relevant materials you
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from a book or a website, kindly provide full information of the
same. Kindly send in:
• Mnemonics
• Tables
• Flow charts
• Notes
• Diagrams
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send your contributions to drtkpram@gmail.com.
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Contents
1. Applied Anatomy ................................................... 1
2. Physiology of Eye and Vision ............................... 24
3. Optics and Refraction ............................................ 29
4. Diseases of the Conjunctiva .................................. 58
5. Diseases of the Cornea .......................................... 87
6. Diseases of the Sclera .......................................... 123
7. Diseases of the Uveal Tract ................................. 132
8. Diseases of Lens .................................................. 159
9. Glaucoma............................................................. 201
10. Diseases of the Vitreous ...................................... 235
11. Diseases of Retina ............................................... 240
12. Neuro-ophthalmology ......................................... 275
13. Strabismus ........................................................... 297
14. Diseases of Eyelids .............................................. 322
15. Diseases of Lacrimal Apparatus .......................... 350
xiv Best Aid to Ophthalmology
16. Diseases of the Orbit ........................................... 370

17. Ocular Injuries ..................................................... 382
18. Ocular Therapeutics, Laser and
Cryotherapy in Ophthalmology ........................... 399
19. Systemic Ophthalmology .................................... 404
20. Community Ophthalmology ................................ 416
21. Differential Diagnosis, Important
Diagnostic and Darkroom Procedures ................. 424
22. Ophthalmic Instruments ...................................... 454
Bibliography ............................................................... 475
Index ........................................................................... 477

1.
Applied Anatomy
Q. Discuss in brief the structure of the eye ball.

Q. Discuss the structure of the limbus.
The structure of the eye ball (Figs 1.1 and 1.2)
A. Outer fibrous coat
 Sclera: It is a fibrous coat which covers the posterior
5/6th of the eye
 Cornea: It forms the anterior 1/6th of the outer layer
 Limbus:
– It is the transition zone between the cornea and the sclera
– Its internal boundaries are the scleral spur posteriorly
and the Schwalbe’s line anteriorly
Fig. 1.1: Structure of the eye

2 Best Aid to Ophthalmology
Fig. 1.2: Section of the eye and its accessory structures
– Its external boundaries are sclerocorneal junction

anteriorly and sclerolimbal junction posteriorly
– Sclerolimbal junction is one of the most consistent land
marks of the limbus used in surgery
– Limbus contains trabecular meshwork internally,
through which the aqueous humor leaves the anterior
chamber.
B. The middle vascular layer has three layers
 Anterior: Iris, a free circular diaphragm with a central
opening, called pupil
 Intermediate: Ciliary body
 Posteriorly: Choroid.
C. The inner nervous tissue layer—that is the retina.
Applied Anatomy 3
Q. Discuss the structure, blood supply, nerve supply and

functions of cornea.
Q. Discuss the microscopy of cornea.
Q. Discuss the source of nutrition to cornea.
 Cornea is a clear transparent elliptical avascular structure with
smooth shining surface which makes the anterior 1/6 of the
eye ball
 Thickness: 0.5 mm at center and 1 mm at periphery
 Diameter: Vertically 11 mm and horizontally 12 mm
 Refractive index: 1.37
 Dioptric power: +43 D to +45 D
 Corneal transparency is due to:
– Regular arrangement of corneal lamellae
– Avascularity
– Relative state of dehydration
 Histology: It consists of five layers, from outer to inner layer
they are as follows (Mnemonic: ABCDE) (Fig. 1.3)
– A. Anterior epithelium:
• It is of stratified squamous type
• Three cell types are noted: Basal columnar cells, 2 to 3
layers of wing cells and surface cells
– B. Bowman’s membrane:
• It is a layer of condensed collagen fibrils
• It shows significant resistance to infection but once
damaged cannot be replaced, hence causing permanent
corneal opacities
Fig. 1.3: Structure of cornea
– C. Corneal stroma:
• Accounts for 90% of the corneal thickness
• It consists of collagen fibrils arranged in matrix of
proteoglycans and glycoproteins
• Collagen fibrils are not only parallel to each other but
also to the corneal surface
• Among the collagen fibrils are present keratocytes,
wandering macrophages, histiocytes and few
macrophages
– D. Descemet’s membrane:
• It is a strong homogenous membrane
• It is very resistant to trauma and chemicals
• It can regenerate
– E. Endothelium:
• It is a single layer of polygonal cells continuous with
endothelium of the anterior surface of iris
• Cell density: 3000 cells/mm cube
Applied Anatomy 5
 Blood supply: It’s an avascular structure. Hence, it derives

nutrition from:
– Prelimbal blood vessels
– Aqueous humor
– Atmospheric oxygen.
 Nerve supply: The corneal nerve supply is purely sensory.
Corneal nerves are derived from the long and short ciliary
nerves, branches of the ophthalmic division of trigeminal
nerve
 Functions:
– It’s a major refractive medium
– It protects the intraocular contents.
Q. Discuss the structure, blood supply, nerve supply and
functions of sclera.
 Sclera is a fibrous coat which covers the posterior 5/6th of
the eye
 It is thickest posteriorly surrounding the optic nerve (1 mm)
and is thinnest at the site of attachment of intraocular muscles
 It has two large openings: Corneal window anteriorly and
posteriorly an opening for the optic nerve
 Structures piercing sclera are:
– Four vortex veins
– Long and short ciliary nerves and vessels
– Perivascular lymphatics
 Structure of the sclera:
– Episclera: Is loose fibrous tissue with fine capillaries
– Sclera proper: Is dense network of irregular collagen fibers
– Lamina fusca: Is the inner layer adjacent to choroids
 Blood supply: From episclearal and choroidal vessels

 Nerve supply: Short ciliary nerves posteriorly and long ciliary
nerves anteriorly
 Functions:
– Resists stress and strain
– To maintain the shape of the eyeball
– Provides insertion to the extraocular muscles.
Q. Discuss the structure of the Uvea. List the functions of the
same.
 Uvea constitutes the middle vascular layer of the eyeball
 It can be divided into three parts, namely iris, ciliary body and
choroid (Each of which is discussed in detail as follows) (Fig. 1.4)
 Blood supply
 Arterial supply:
• Short posterior ciliary arteries (10–20)
• Long posterior ciliary arteries (2)
• Anterior ciliary arteries (7)
Fig. 1.4: Structure of iris and ciliary body

Applied Anatomy 7
Venous drainage: All three parts are drained by a series of veins

 they drain into four or more vortex veins  superior and
inferior ophthalmic veins  cavernous sinus.
Functions:
Iris Ciliary body Choroid

Iris with its central Formation of aqueous Provides nutrition to
opening, pupil, controls humor outer layer of retina
the amount of light Accommodation
entering the eye Opens canal of Schlemm
Q. What are the structures seen at the angle of anterior chamber?

The structures seen at the angle of anterior chamber are: (Fig. 1.5)
(Mnemonic: I can see Till schwalbe’s line)
 I—Iris root
 Can—Ciliary root
 See—Scleral spur
 Till—Trabecular meshwork
 Schwalbe’s line.
Fig. 1.5: Structures forming angle of the anterior chamber

Q. Discuss the structure and function of the Iris.

 Iris is a colored, free, circular diaphragm
 It has a central aperture, the pupil, measuring about 4 mm
 Its roots are attached to the anterior end of the ciliary body
 Parts: Anterior surface of the iris can be divided into two
zones by a circular ridge called “Collarette” (Fig. 1.6)
– Ciliary zone: Many crypts and ridges are noted here
– Pupillary zone: Is the region between Collarette and
pupillary frill. It is smooth and flat
 Structure of the iris:
– Anterior endothelium: Which is continuous with the
corneal epithelium
– Stroma: It consists of loose connective tissue, blood
vessels, nerves and smooth muscles namely
• Sphincter pupillae: It is circular band surrounding the
pupil. It causes constriction of pupil
• Dilator pupillae: These are radial fibers extending from
ciliary body to the pupillary margin. It causes dilatation
of pupil
– Posterior epithelium: It is two layered and is pigmented
Fig. 1.6: Macroscopic appearance of anterior surface of the iris

Applied Anatomy 9
 Nerve supply:
– Sensory: Nasociliary nerve, branch of 1st division of 5th
cranial nerve
– Sphincter pupillae: Oculomotor nerve
– Dilator pupillae: Cervical sympathetic chain
 Blood supply and function refer above.
Q. Discuss the structure and function of the ciliary body.

 Ciliary body is a ring of tissue that extends from the scleral
spur to the ora serrata of the retina
 Parts:
– Pars plicata: It is the anterior 1/3rd of the ciliary body,
with about 70 visible plications responsible for production
of aqueous
– Pars plana: It is the posterior 2/3rd of the ciliary body and
is relatively avascular. Hence surgical incisions are put
here
 Structure: It resembles an isosceles triangle with its base
forwards. It is about 6 mm thick. Iris is attached to the middle
of the base. The ciliary body consists of four layers
– Supraciliary lamina: Which is condensed stroma and is
continuous with suprachoroidal lamina posteriorly
– Stroma of ciliary body: Consists of collagen and
fibroblasts, embedded in it are ciliary muscles, vessels and
nerves
– Layer of pigment epithelium: It is forward continuation
of the retinal pigment epithelium. Anteriorly it continues
with anterior pigment epithelium of the iris
– Layer of non-pigment epithelium: It consists of cuboidal

epithelium and is forward continuation of the sensory
retina. It continues anteriorly as posterior pigmentary
epithelium of the iris
– Internal limiting membrane: It is forward continuation of
the internal limiting membrane of the retina.
Ciliary processes: They are 70 to 80 fingers like projections of
the pars plicata. They are lined by double layered epithelium,
the core of which contain blood vessels and loose connective
tissue. These are the site of aqueous humor production.
Q. Discuss the structure and function of the Choroid.

 Choroid is a highly vascular area situated between sclera and
retina
 It extends from the ora serrata up to the optic nerve aperture
 Structure (Fig. 1.7):
– Suprachoroidal lamina:
• It is a thin layer of collagen fibers, melanocytes and
fibroblasts
• It is continuous anteriorly with supraciliary lamina
• The space between this membrane and sclera contains
long and short posterior ciliary arteries and nerves
– Vascular layer or stoma: This layer contains loose collagen
tissue, pigment cells, macrophages, mast cells and plasma
cell. Its main bulk is formed by three layers of blood vessels
and they are
Applied Anatomy 11
Fig. 1.7: Structure of choroid
• Layer of large vessels (Haller’s layer)

• Layer of small vessels (Sattler’s layer)
• Layer of choriocapillaries: These nourish the outer
retina
– Bruch’s membrane: It lines the choriocapillaries. It lies in
approximation with the pigment epithelium of the retina
Q. Discuss the anatomy of the angle of anterior chamber.
 Anterior chamber is bounded cornea in the front and behind
by the anterior surface of the iris and the lens which is exposed
at the pupil (Fig. 1.8)
Fig. 1.8: Mechanism of aqueous formation, flow and

outflow pathways in the normal eye
 The peripheral recess of the anterior chamber is known as

angle of glaucoma
 It is bounded anteriorly by corneo-sclera and posteriorly by
the ciliary body and the iris
 At the angle, the inner layer of the sclera contains circular
venous sinus called canal of Schlemm, which is lined by
endothelial cells and its function is to drain aqueous humor
 At the periphery of the angle between the canal of Schlemm
and the recess of the anterior chamber, there lies a loose mesh
of tissue, known as trabacular meshwork
– It is made up of circumferentially disposed flattened bands
which are perforated by numerous oval openings
– Through this tortuous opening, communication exists
between canal of Schlemm and anterior chamber.
Applied Anatomy 13
Q. Discuss the factors which maintain the intraocular pressure

normally.
Q. Discuss the aqueous formation and outflow system.
Aqueous humor is clear fluid filling the anterior chamber (0.25 ml)
and posterior chamber (0.06 ml) of the eyeball.
Its function is to maintain intraocular pressure and provide
nutrition to cornea and lens.
The factors which maintain the intraocular pressure normally
are as follows:
 Formation of aqueous humor by the ciliary epithelium occurs
by:
– Previously, Leber’s theory of simple diffusion from blood
was accepted
– Now it is understood that aqueous humor production takes
place by:
• Secretion, which is an active metabolic process
• Ultrafiltration, which is influenced by blood pressure
in the ciliary capillaries, plasma osmotic pressure and
the level of the intraocular pressure
 Outflow system: It happens through two routes
– Angle of anterior chamber—80 percent (Conventional
route): Secretion of aqueous humor by the ciliary
epithelium  trabacular mesh work  canal of Schlemm
 aqueous vein  venous circulation
– Uveoscleral outflow—20 percent (Unconventional route):
Secretion of aqueous humor by the ciliary epithelium 
suprachoroid space  venous circulation of the ciliary
body, choroid and sclera
 The pressure of the episcleral veins: The pressure difference

(5 mm Hg) between the anterior chamber and the episcleral
veins is responsible for continuous flow of aqueous.
Q. Discuss the structure of crystalline lens.
 The lens is a transparent, biconvex structure of crystalline
appearance placed between the iris and the vitreous
 It is suspended by the suspensory ligament of the lens or
zonules of zinn
 Refractive index 1.39
 Dioptric power: 15–18D
 Diameter: 9–10 mm
 Thickness: 4 mm
 Radius of curvature: Anterior surface 10 mm (less convex),
posterior surface 6 mm (more convex)
Structure:
 Lens capsule:
– It is a thin, transparent, acellular, homogenous membrane
surrounding the lens which is thicker anteriorly than
posteriorly
– It is the anterior basement membrane of the anterior lens
epithelium and is the thickest basement membrane in the
body
 Anterior epithelium:
– It is a single layer of cuboidal cells which lie deep to the
anterior lens capsule
– In the equatorial region these cells become columnar and
elongated and are actively dividing forming new lens fibers
Applied Anatomy 15
 Lens fibers:
– The epithelial cells elongate to form lens fibers
– Mature lens fibers are cells that have lost nucleus
– As the cells are formed throughout life they are arranged
in a compact fashion as nucleus and cortex of lens
– Nucleus of lens: It is the central part which contains the
oldest fibers
It consists of different zones laid down successively as
the development proceeds
In a beam of slit-lamp these are seen as zones of dis-
continuity
Depending on the period of the development the different
zones that involved are (Fig. 1.9):
Nucleus Corresponds to Position/origin

Embryonic Corresponds to lens in It consists of primary lens fibers
nucleus first 3 months of gestation which are formed by elongation of
cells of posterior wall of lens
Fetal From 3 months of It surrounds the embryonic
nucleus gestation till birth nucleus
It’s fibers met at around
sutures which are anteriorly
Y shaped and posteriorly inverted
Y shaped
Infantile Birth to puberty Surrounds the fetal nucleus
nucleus
Adult Puberty to rest of life Surrounds the infantile nucleus
nucleus
Fig. 1.9: Major components of adult lens
– Cortex of lens: It is the peripheral part which consists of

the youngest and the recent fibers
 Suspensory ligament of the lens or zonules of zinn:
– They arise from the sides of the ciliary processes and the
valleys in between them
– They hold the lens in position and enable the ciliary
muscles to act on it
– The zonular fibers are inserted into the anterior and
posterior lens capsule near the equator.
Applied Anatomy 17
Q. Discuss the microscopy of retina.

Retina consists of the three cell types and their synapses arranged
(from without inwards) in the following ten layers (Figs 1.10
and 1.11):
Layers (from Features of the layer
without inwards)
Retina pigment Outermost layer
epithelium It consists of single layer of cells containing pigment
(Melanin)
The cells are taller at the fovea and contain more
pigments
Around the optic disc they heaped up as a ‘choroidal
ring’
The cells are firmly adherent to basal lamina
Layer of rods and The rods (contains Rhodopsin; responsible for scotopsic
cones vision—peripheral vision and vision of low illumination)
and the cones (photopsic vision—highly discriminatory
central vision and color vision) are the end organs of
the vision. They are arranged in a palisade manner
External limiting It is a fenestrated layer formed by supporting fibers
membrane of mullers, through which passes the rods and cones
Outer nuclear layer Contains nuclei of rods and cones
Outer plexiform Consists of connections of rod spherules and cone
layer pedicles with the dendrites of bipolar cells and horizontal
cells
Inner nuclear layer Mainly consists of the cell bodies of the bipolar cells (also
amacrine cells and horizontal cells)
The bipolar cells constitute the first order neurons of
visual pathway
Capillaries from retinal vessels reach up to this layer
Contd...
Contd...
Inner plexiform Consists of connections between the axons of bipolar
layer cells, dendrites of ganglion cells and processes of
amacrine cells
Ganglion cell layer Contains the cell bodies of ganglion cells
The ganglion cells constitute the second order neurons
of visual pathway
Nerve fiber layer Consists of bundles of ganglion cell axons, running
parallel to the retinal surface
It passes through the lamina cribrosa to form the optic
nerve
Internal limiting Innermost layer
membrane It is a basement membrane formed by union of terminal
expansions of Muller’s fibers
Separates the retina from the vitreous
Fig. 1.10: Structure of retina

Applied Anatomy 19
Figs 1.11A and B: (A) Applied anatomy of retina; (B) Normal fundus
Q. Discuss the microscopy of fovea centralis.

 Fovea centralis is a depressed area, located in the central
region of the retina, about 3 mm temporal to the optic disc
Fig. 1.12: Section of the retina

and 0.8 mm below the horizontal meridian. It measures about
1.5 mm
 Its central depression is called as fovea (Fig. 1.12)
 The photoreceptors in the fovea are exclusively cones. All
the other layers are displaced peripherally so that light falls
directly on the cone’s outer segment
 The fovea is nourished solely by the chorio-capillaries and
does not contain any blood vessels and hence called foveolar
avascular zone (FAZ).
Q. Explain in brief the development of the eye.

Q. List the ocular derivatives of Neural Ectoderm/Surface
Ectoderm/Mesoderm.
The PAX6 is the master gene for eye development.
Applied Anatomy 21
Neural Ectoderm* Surface Ectoderm$ Mesoderm

Sensory retina Conjunctiva Corneal stroma
Retinal pigment Corneal epithelium Corneal endothelium
epithelium Eyelash and Descemet’s membrane
Ciliary body Crystalline lens Sclera
epithelium Epithelium of Choroid
Pigmented • Meibomian glands Iris stroma
epithelium of • Glands of Moll Extraocular muscles
the iris • Glands of Zeis Ciliary muscles
Sphincter pupillae • Lacrimal glands Bony orbit
Dialator pupillae • Accessory lacrimal Vitreous
Neural part of the glands
optic nerve
Melanocytes
Eyelids: Both from surface ectoderm and mesoderm
Zonules: Surface ectoderm and mesoderm
Bruch’s membrane: Neural ectoderm and mesoderm
(*Mnemonic: nueroectoder derivatives-MORE—Muscles of Pupil, Optic Nerve, Retina (with
RPE), Epithelium of Iris, Epithelium of Cilliary Body)
($Mnemonic: surface ectoderm with SLE Skin of Eyelids and its derivatives viz. cilia, tarsal
glands, conjunctival gland, Lens, Lacrimal Gland, Epithelium of Conjunctiva, Epithelium of
Cornea, Epithelium of lacrimal passage)
The key points in the development of eye are listed below:

 On either side of the cephalic end of the forebrain, a lateral
depression appears; known as optic pit (3 weeks). Optic pit
is thickened to form the optic plate
 Optic plate changes into primary optic vesicle. Lens plates
appears simultaneously (4 weeks)
 Optic vesicle invaginates to form optic cup. Pigment appears
in the outer layer of the optic cup
 Lens plate changes into lens pit and then into lens vesicle
(end of 4th week)
 Foveal fissure closes. Lens separates from the surface and
primary lens fibers form. Tunica vasculosa lentis (To give
nourishment) begins to develop (6 weeks)
 Sclera, cornea and extraocular muscles differentiate (9 weeks)
 Optic tracts are completed. Pars ciliaris and pars iridica retinae
grow forwards. Lid folds develop (3 months)
 Tunica vasculosa lentis begins to retrogress. Sphincter and
dialator muscles and ciliary muscles develop (4 months)
 Hyaloid artery disappears. Myelination of the optic nerve
reaches lamina cribrosa (9 months)
 Macula leutea finally differentiates 4 to 6 months after birth.
Age Visual development

At birth Eye appears to move randomly and there is no central
fixation
Fovea is not fully developed, visual acuity is roughly 6/60
The retina is almost fully developed at birth, apart from
macula which further develops after birth till 6 months of
age
Myelination of the optic nerve reaches lamina cribrosa
(started at 7 months of intrauterine life)
Hypermetropia of +2 to +3D
Orbit is more divergent (50°) when compared to adults (45°)
AP diameter of the eyeball is 16.5 mm (70% of the adult size
which is attained by 7–8 years)
Corneal diameter is 10 mm (adult size 11.7 mm reached at
2 years of age)
Contd...
Applied Anatomy 23
Contd...
The anterior chamber is shallow, the angle is deep and the
lens is more spherical as compared to the adult eye
1½ months Fixation reflex first becomes apparent and the eye can follow
bright light for a short distance
2–4 months Critical period for development of fixation reflex
4–6 months Fixation reflex develops firmly
Macula differentiates
6–8 months Depth perception starts developing
6 years Fovea develops completely
Full visual acuity attained 6/6
2.
Physiology of Eye and Vision
Q. Discuss the physiology of vision.

Rods and cones serve as sensory nerve endings for visual
sensation.
Physiology of vision is a complex phenomenon involving
the following mechanisms:
 Initiation of vision (Phototransduction), a function of
photoreceptors (rods and cones)
 Processing and transmission of visual sensation, a function
of the image processing cells of the retina and visual pathway
 Visual perception, a function of visual cortex and its related
areas
Each have been discussed below in detail.
Q. Define and discuss in detail Phototransduction.
Q. Discuss the photochemical and electrical charges associated
with vision.
Definition: Phototransduction is the whole phenomenon of
conversion of light energy into nerve impulse.
Physiology of Eye and Vision 25
Light falling upon the retina causes photochemical changes

which in turn trigger a cascade of biochemical reactions that
result in the generation of electrical impulse.
Photochemical changes include:
 Rhodopsin bleaching
 Rhodopsin regeneration
 Visual cycle.
Q. Discuss the theories of color vision.

There are various theories of color vision, the following two are
important:
1. Thomas Young’s trichromatic theory:
 According to this theory retina has three types of cones, each
possesses its own photosensitive substance
 Each type of the cone gives rise to one of the primary colors—
red, blue and green
 The different color sensations are produced by stimulation of
various combination of three types of cones
 For the sensation of white light, all three types of cones are
stimulated equally.
2. Hering’s theory of opposite colors:
 According to this theory retina has three photochemical
substances
 Each substance produces the sensation of particular color by
its breakdown or synthesis.
Substance Also called Breakdown causes Resynthesis causes

sensation of sensation of
First substance White-black White Black
substance
Second substance Yellow-blue Yellow Blue
substance
Third substance Red-green Red Green
substance
This theory can explain the successive contrast and the after
images but not the simultaneous sensation of antagonist color.
Q. What is binocular single vision (BSV)? Discuss the pre-
requisites, components and advantages of the same.
Q. What is fusion reflex?
Q. What is Stereopsis?
 The BSV is the coordinated use of two eyes, in order to
produce a single unified image in three dimensions
 The BSV is a conditional reflex that is not present since birth,
but is acquired during first 6 months and is completed during
first few years (Psycho-optical reflex)
(Mnemonic: 3’s of BSV—3 dimension vision, 3 prerequisites,
3 components)
Prerequisites for BSV: Three factors are required for its
development (Mnemonic CCF)
 C—reasonably Clear vision in both the eyes
 C—precise Coordination between the eyes for all directions
of gaze
Physiology of Eye and Vision 27
 F—ability of the visual areas of brain to promote Fusion of

the two slightly dissimilar objects
Three components (grades) of BSV are:
 Grade 1—Simultaneous macular perception (SMP): This
means the ability to see two dissimilar (but not mutually
antagonist) images simultaneously and to superimpose them.
 Grade 2—Fusion:
– This is the ability to see the slightly dissimilar images
formed in each eye and blend them into one
– Retinal areas which coordinate visually in the occipital
cortex so that such an object is seen with both the eyes as
single objects known as corresponding points. The most
important pair of which is fovea
– Nasal half of one retina corresponds to temporal half of
the other retina in the occipital cortex
– Points on the 2 retina which are not corresponding points
in this sense of term are called disparate points and if
objects forms its retinal points on these, it will be seen
double (binocular diplopia). If disparity is slight, there is
tendency to move the eyes so that the images may be fused
by the means of fusion reflex.
 Grade 3—Stereopsis (depth perception):
– This is the appreciation of the third dimension, allowing
the perception of depth
– For Stereopsis to occur, disparate points should be
stimulated
– Each eye views the world in slight different horizontal

position, so images of both the eyes is different from the
other
– Objects at different distances from the eyes project images
in the two eyes that differ in their horizontal position, giving
the depth perception of horizontal disparity (also known
as retinal disparity/binocular disparity or binasal disparity).
Q. What is fixation reflex?
Since the most accurate vision is attained by fovea, it is necessary
that the eyes be rapidly oriented so that image of an object of
interest falls upon them or that of a moving object retained on
them. This ascendency of fovea is maintained by fixation reflex.
3.
Optics and Refraction
Q. List the uses of following: Prism, convex lens, concave lens,

cylindrical lens.
Uses
Prism Objective measurement of angle of deviation (prism bar
cover test)
Measurement of fusional reserve and diagnosis of microtropia
Used in ophthalmic equipments like gonioscopes,
keratometer and applanation tonometer
Patients of phorias and diplopia
Convex lens Correction of: hypermetropia, Aphakia and Presbyopia
(positive lens) In oblique illumination examination
In indirect ophthalmoscope
As magnifying lens
Concave lens Correction of myopia
(negative lens) Hruby lens for fundus examination with slit lamp
Cylindrical lens To correct astigmatism
As a cross cylinder to check the refraction subjectively
Q. Define Emmetropia and Ametropia.

Emmetropia (optically normal eye): A state of refraction where in
parallel rays coming from infinity are focused at the sensitive layer
of retina with accommodation being at rest (Figs 3.1 and 3.2).
Fig. 3.1: The normal schematic eye
Fig. 3.2: Normal, hypermetropia and myopia

Optics and Refraction 31
Ametropia (a condition of refractive error): A state of

refraction where parallel rays coming from infinity (with
accommodation at rest) are focused either in front or behind the
sensitive layer of retina in one or both the meridians.
This includes myopia, hypermetropia and astigmatism.
Q. Define Hypermetropia/Hyperopia/long-sightedness. Discuss
the etiology, clinical features, complications and management
of the same.
Q. List the complications of hypermetropia.
Definition: Hypermetropia or long-sightedness is the refractive
state of the eye where in parallel rays of light coming from infinity
are focused behind retina with accommodation at rest.
Thus the posterior focal point is behind retina hence blurred
vision (Fig. 3.3).
Fig. 3.3: Hypermetropic eye and correction with convex lens
Etiology:
Mnemonic (ICAAP)
 Index hypermetropia: Hypermetropia results from  RI due
to age or DM
 Curvature hypermetropia: Here curvature of corner or lens

or both is flatter than normal (1 mm  in curvature results in
6 diopters hypermetropia)
 Axial (commonest): Total refractive power is normal but there
is axial shortening of eyeball (1 mm  results in 3 diopters
hypermetropia)
 Absence of crystalline lens
 Positional hypermetropia: Posteriorly placed crystalline lens.
Clinical features:
Symptoms: Vary depending upon the age of patients and degree
of RE.
 Asymptomatic due to accommodation effort
 Asthenopic symptoms: At time the hypermetropia is fully
corrected but due to sustained accommodative efforts, patient
develops asthenopic symptoms like tiredness of eyes, frontal/
frontotemporal headache, watering and mild photophobia
 Defective vision with asthenopic symptoms: When hyper-
metropia is not corrected by voluntary accommodative efforts,
defective vision is developed for near work
 Defective vision only: When amount of HM is very high,
patient do not accommodate specially the adults.
Signs:
 Size of eyeball: small as a whole
 Cornea: smaller than normal
 Anterior chamber: shallow
 Fundus examination:
– Small optic disk which may look more vascular and

simulates papillitis (pseudopapillitis) (Fig. 3.4)
– Retina shines due to greater brilliances of light (short-silk
appearance).
 A-scan USG: short AP length of eyeball.
Complications:
 Recurrent styles, blepharitis or chalazion
 Accommodative convergent squint
 Amblyopia: gradually loss of vision out any pathology
 Predisposition to development of 1° narrow angle glaucoma.
Treatment:
A. Optical treatment: Correction of hypermetropia using convex
lens. Modes of prescription spectacles or contact lens.
Fig. 3.4: Pseudopapillitis

B. Surgical treatment: Is not effective and reliable but following

procedures are done
 Holmium laser thermal kerotoplasty
 Hyperopic LASIK
 Hyperopic PRK (photorefractive keratectomy)
 Conductive kerotoplasty
 Phakic IOL’s.
Q. Discuss the clinical types of Hypermetropia.

The clinical types of hypermetropia are as follows:
Type Means As in
Simple/ Due to normal biological
Developmental variations in development
(commonest) of eyeball. It includes axial
and curvature hypermetropia
Pathological Congenital or acquired Index hypermetropia as in
hypermetropia condition which are acquired cortical sclerosis
outside the normal Positional due to poste-
biological variations of rior subluxation
the development Aphakia
Consecutive hypermetropia
(due to Myopia) surgically
over corrected
Functional Hypermetropia due Third cranial nerve
hypermetropia paralysis of accommodation palsy
Internal ophthalmoplegia
Q. Discuss various components of hypermetropia.

Q. What is Total hypermetropia?
Q. What is Latent hypermetropia?
Q. What is Manifest hypermetropia?
 Total hypermetropia is the total amount of refractive error,
which is estimated after complete cycloplegia with atropine.
Total hypermetropia = latent hypermetropia + manifest
hypermetropia.
 Latent hypermetropia is the amount of hypermetropia (about
1D) which is normally corrected by the inherent tone of ciliary
muscle
– Inherent tone of ciliary muscle is more in children than in
old
– It is disclosed after tone of the muscle is abolished by
atropine.
 Manifest hypermetropia = facultative hypermetropia +
absolute hypermetropia.
 Manifest hypermetropia is the remaining portion of total
hypermetropia, which is not corrected by ciliary tone.
 Facultative hypermetropia is that part of manifest hypermetro-
pia that can be corrected by the patient’s accommodative effort.
 Absolute hypermetropia is the residual part of hypermetropia
that cannot be corrected by the patient’s accommodation
effort.
Q. Define Aphakia. Discuss the etiology, clinical features and

management of the same.
Definition: Aphakia literally means absence of crystalline lens
from eye (Fig. 3.5).
However, from optical point of view it may be considered as
a condition in which the lens is absent from pupillary area.
Aphakia procedure high degree of HM.
Etiology:
Mnemonic: PACTS of Aphakia
 Posterior dislocation
 Aphakia due to absorption of lens matter from due to trauma
 Congenital absence of lens
 Traumatic extrusion of lens due to trauma
 Surgical aphakia.
Aphakia results in:

  HM
  lens power of eye from 60 D to 44 D
 Total loss of accommodation.
Symptoms:
 Defective vision: both far and near due to hypermetropia and
loss of accommodation
Fig. 3.5: Aphakic eye and correction with convex lens

 Erythropsia and Cyonopsia  seeing red and blue images. This

is due to excessive entry of UV and infrared rays because of
aphakia.
Signs:
 Limbal scar is seen in surgical aphakia
 Pupil is jet black
 Anterior chamber is deep
 Iridodonesis: tremulousness of iris
 Purkinje images: only two seen
 Fundus appears like a small disc
 Retinoscopy: reveals high hypermetropia.
Treatment:
Principle: To correct the error by convex lenses of appropriate
power so that images are formed on the retina.
Modalities of correction
 Spectacles
 Contact lens
 IOL
 Refractive corneal surgery:
– Keratophakia: lenticular preparation from donor cornea
placed between lamellae of patient’s cornea
– Epikeratophakia: the lenticule preparation from donor
cornea is stitched over patient’s cornea
– Hyperopic LASIK.
Q. Define pseudophakia/Artephakia. Discuss the clinical
features of the same.
Definition: The condition of aphakia when corrected by an IOL
is referred to as pseudophakia.
Signs: for posterior chamber IOL:

 Scar at limbus
 Anterior chamber: slightly deep
 Mild Iridodonesis
 Purkinje image test: all four images are seen
 Pupil: blackish but when light is thrown shining reflexes are
observed
 On dialatation of pupil, IOL is seen
 Visual status and refraction: varies depending on the power
of IOL. It can be Emmetropia (Most ideal), Consecutive
myopia or Consecutive hypermetropia.
Q. Define myopia/short-sightedness. Discuss the etiology and
clinical types of the same.
Q. What is index myopia?
Definition: Myopia/short-sightedness is a type of refractive error
in which parallel rays coming from infinity are focused in front
of retina when accommodation at rest.
Etiology:
 Axial:  in AP length of eyeball
 Due to  in curvature
 Positional myopia: due to anterior placement of lens
 Index myopia
– This is due to  in RI of lens
– Seen in nuclear sclerosis and diabetes
 Myopia due to excessive accommodation seen in patients with

spasm of accommodation.
Clinically variety:
 Congenital
 Simple/developmental
 Pathological/degenerative
 Acquired: post-traumatic, post-keratitic, drug-induced, space
myopia and night myopia.
Treatment: See next question (Fig. 3.6).
Q. What is pathological myopia/degenerative/progressive
myopia? Discuss the etiopathogenesis, clinical features,
complications and management of the same pathological
myopia/degenerative/progressive myopia.
Q. List the complications of pathological myopia.
Definition: It’s a progressive error starts at 5 to 10 years of age
and rapidly progresses and results in high myopia during early
adult life which is associated with degenerative change.
Fig. 3.6: Myopic eye, correction with concave lens

Etiology:
It results from a rapid axial growth of the eyeball which is outside
the normal biological variations of development (Fig. 3.7).
Two theories have been proposed to explain the same:
A. Role of heredity:
 It is familial
 Race: Chinese, Japanese, Arabs, Jews are commonly affected
 Uncommon in Sudanese and Blacks
 Sclera has distensibility  follows retinal growth  but
choroids undergo degeneration due to stretching  causes
degeneration of retina due to lack of blood supply 
degeneration of vitreous.
Fig. 3.7: Increase in axial length

B. Role of general growth process:

 Lengthening of posterior segment of the globe commences
only during the period of active growth and ends with the
termination of active growth
 Hence factors like nutrition deficiency, endocrinal disorders
which influencing general growth process also causes
development of pothological myopia.
Symptoms:
 Defective vision
 Muscae volitantes: floating black bodies in front of eye due
to degeneration of vitreous
 Nightblindness.
Signs:
 Prominent eyeball, in unilateral cases simulate exophthalmos
 Cornea is large
 Pupils are large, pupillary reaction is sluggish
 Fundus examination (Fig. 3.8)
– Optic disc: (Mnemonic: PSM)
• Peripapillary crescent encircling the disc
• Super tractional crescents on nasal side due to retina
pulled over disc margin (Fig. 3.9)
• Myopic crescent in temporal end
– Degeneration of retina and choroids:
• Foster Fuch’s spots: Which are dark red circular patch
due to subretinal neovascularization and choroidal
hemorrhage
• White atrophy patches in macula
• Cystoid degeneration
Fig. 3.8: Fundus changes in pathological myopia
Fig. 3.9: Temporal and supertractional nasal crescent

– Posterior staphyloma (Fig. 3.10)

– Degenerative changes in vitreous: Liquefaction and
opacities
– Visual fields shows contraction
– ERG is subnormal
Complications:
 Retinal detachment
 Complicated cataract
 Vitreous hemorrhage
 Choroidal hemorrhage
 Strabismus fixus convergence
Fig. 3.10: Posterior staphyloma

Treatment of myopia:
 Basic principle:
– The minimum acceptance providing maximum vision to
be used
– Concave lens are used
 General measures which prevent development of progression
of myopia:
– Good vitamin and protein supplementation
– Early diagnosis and treatment of chronic debilitating
disease
 Low vision aids are given to patient with progressive myopia
with advanced degenerative process
 Prophylaxis: Genetic counseling, as pathological myopia has
strong genetic basis
 Surgery: Basic principles of the surgical methods are that they
induce flattening of the cornea.
Surgical method Used for Complications

what the
range of
myopia
Radial keratotomy: Making deep 1–6 D Cornea is weakened
radial incisions (90% of the corneal so chances of perforation
thickness) in the peripheral part and late rupture after
of the cornea leaving the central trivial trauma
4 mm  these incisions after Astigmatism
healing flatten the cornea  Glare in night
decreasing in refractive error (Fig. 3.11)
Contd...
Contd...
Photorefractive keratectomy by 1–6 D Slow visual recovery with

Excimer laser: Central optical pain for several weeks
zone of the anterior corneal Corneal haze
stroma is ablated after removal Glare and loss of contrast
of epithelium (Fig. 3.13) sensitivity
Automated laser keratectomy 6–32 D Difficult procedure
(ALK): Anterior corneal flap (hence replaced by
(130–160 μ) is raised then corneal lasix)
stroma of desired thickness is
removed by automated microtome
Excimer Laser Assisted In situ 2–12D Flap related complications
Keratomileusis (LASIK): It is similar (up to like:
to ALK only difference is corneal 30 D) Intraoperative flap
stroma ablated by excimer laser amputation
and flap is elevated by micro- Wrinkling of flap on
keratome (Fig. 3.12) repositioning
Epithelization of flap bed
Irregular astigmatism
Postoperative flap
discoloration
Intracorneal ring implantation 1–6 D Unpredictable results
Clear lens extraction: Is a method > 15 D Retinal detachment
that reduces overall refractory Endophthalmitis
power of eye
Fig. 3.11: Radial keratotomy
Fig. 3.12: Excimer laser PRK – Flattening to correct astigmatism, myopia,

hypermetropia
Fig. 3.13: Photorefractive keratectomy (PRK)

Q. List the prerequisites and contraindications of LASIK.

Q. List the advantages and disadvantages of LASIK.
LASIK (Fig. 3.14):
Prerequisites Contraindications Advantages Disadvantages
Age > 20 years Corneal pathology No postoperative Expensive
Stable refraction Corneal ectasia pain Skilled surgeon
for 1 year Corneal thickness Early recovery of needed
Motivated < 450 mm thick vision (vs PRK) Corneal flap
patient (Mnemonic: No risk of corneal related complica-
Absence of C-PET) perforation (Vs RK) tions:
corneal No residual haze • Intraoperative
pathology (Vs PRK) flap amputations
Correction till • Wrinkling of the
–30 D of myopia flap on
repositioning
• Posterior flap
dislocation/
subluxation
• Epithelialization
of flap-bed
interface
• Irregular
astigmatism
Fig. 3.14: Laser-assisted in situ keratomileusis (LASIK)

Q. What is astigmatism? Classify the same.

 Astigmatism is a type of refractive error in which refraction
varies in different meridian
 Consequently the rays of light entering the eye cannot
converge to a focal point but forms focal lines
 Types of astigmatism: Regular and Irregular.
Q. Define regular astigmatism. Discuss the etiology, types,

clinical features and management of the same.
Q. Discuss the types of regular astigmatism and their
treatment.
Definition: Astigmatism is regular when the refractive power
changes uniformly from one meridian to another (i.e. there are 2
principal meridians).
Etiology:
 Cornea astigmatism: Due to abnormal curvature of cornea.
 Lenticular astigmatism (lens): Curvatural, positional, index:
due to variable RI.
 Retinal astigmatism: Due obliquely placed maculae.
Types of regular astigmatism:

Type Refractive error Management
With the rule Two principal meridians are Concave cylinders at
astigmatism placed at right angles to 180° ± 20° or
(Fig. 3.15) one another
But vertical meridian is more Convex cylinders at
curved than horizontal 90° ± 20°
Contd...
Contd...
Named so because similar
astigmatic condition normally
exists, i.e. vertical meridian is
normally rendered 0.25 D more
convex than horizontal by the
pressure of eyelid
Against the rule Horizontal meridian more Convex cylinders at
astigmatism curved than vertical 180° ± 20° or
Concave cylinders
at 90° ± 20°
Oblique Two principal meridians are not If symmetrical:
astigmatism vertical and horizontal but cylindrical lens at 30°
are at Right angles to each eye in both the eyes
other (Ex: 45° and 135°) If asymmetrical:
cylindrical lens at 30°
eye and 150° in other
Bio-oblique Two principal meridians are not Correction
astigmatism vertical and not horizontal and according to the
they are also not at right angles meridians
to each other
Fig. 3.15: ‘With the rule’ astigmatism

Refractive types of regular astigmatism: Depending upon the

position of two focal lines in relation to retina, there are three
types of astigmatism.
Type Comment
Simple astigmatism In one meridian rays are focused on retina
In the other meridian rays are focused:
• either in front of retina ( simple myopic
astigmatism)
• at back of retina (simple hypermetropic
astigmatism)
Compound Compound myopic astigmatism: both meridians
astigmatism focused in front of the retina
Compound hypermetropic: both meridians
focused behind the retina
Mixed astigmatism In one meridian myopic and in the other
hypermetropic
Symptoms:
 Blurring of object
 Object appear elongated
 Asthenopic symptoms: Dull headaches, eyeache, tiredness
of eyes, nausea, drowsiness.
Signs:
 Different power of two meridians revealed by Retinoscopy
 Oval or tilted optic disc
 Heat tilt: Torticollis in an attempt to bring their axes to nearer
to vertical or horizontal meridian
 Half closure of lid: Like myopes to achieve great clarity of

stenopic vision.
Investigations:
 Retinoscopy shows different power in two axis
 Keratometry: Reveals different corneal curvature in two
different meridian in corneal astigmatism
 Asynclintic fan test and Jackon’s cross cylinder test: Are useful
in conforming power and uses of cylindrical lens.
Treatment:
 Optical treatment: Appropriate cylindrical lenses, spectacles
or contact lenses
 Surgical options:
– Astigmatism keratotomy: making transverse cuts in the
mid periphery of corneal margin
– PARK: Photo-astigmatic refractive keratotomy
– LASIK
– Limbal relaxing incision.
Q. Define irregular astigmatism. Discuss the etiology, clinical
features and management of the same.
Definition: Irregular astigmatism is characterized by an irregular
change of refractive power in different meridian. There are
multiple meridians which admit no geometrical analysis.
Etiological types:
 Curvatural irregular astigmatism as in extensive corneal scars
or keratoconus
 Index irregular astigmatism due to variable RI in different

parts of the crystalline lens
 Retinal irregular astigmatism.
Symptoms:
 Distortion of objects
 Polyopia.
Investigations:
 Placido disc reveals distorted circles
 Photokeratoscopy and computerized corneal topography:
reveal irregular corneal curvature.
Treatment:
 Optical treatment by using contact lenses (which replaces the
anterior surface of cornea for refraction)
 PTK—Phototherapeutic keratectomy useful in patients with
superficial cornea scar
 Surgery (Penetrating keratoplasty) is indicated in excessive
corneal scarring.
Q. What is anisometropia? How do you manage the same?
 An optical state in which there is equal refraction in two eyes
is called isometropia
 Condition in which total refraction of the two eyes are unequal
is called as anisometropia
 A difference of power of 1D produces an image of 2 percent
difference size on retina
 Anisometropia is tolerable up to 2.5 D = 5%
 Causes:
– Congenital and developmental
– Acquired anisometropia: Due to Uniocular Aphakia, IOL
 Clinical types:
Type One eye Other eye
Simple anisometropia Normal Either myopic or
hypermetropic
Compound Either myopic Either myopic or
anisometropia or hypermetropic hypermetropic
But one having higher refractive error than the
other
Mixed anisometropia Myopic Hypermetropic
(also called antimetropia)
Simple astigmatic Normal Either myopic astigmatism or
anisometropia hypermetropic astigmatism
Compound Astigmatic Astigmatic
astigmatic
anisometropia But of variable degree
 Treatment:
– Spectacle correction up to a difference of 4 D
– Lens for higher degree of anisometropia
– Anisometropia glasses are of limited value
– IOL for uniocular aphakia
– Refractive corneal surgeries for unilateral high myopia,
astigmatism and hypermetropia
– Removal of crystalline lens for uniocular very high myopia.
Q. What is Presbyopia? Discuss the pathophysiology, clinical

 Presbyopia is an abnormality of accommodation. It is not an
error of refraction but a conclusion of physiological
insufficiency of accommodation leading to a progressive fall
in vision (Fig. 3.16)
 It is sight of old age
Pathophysiology:
 In an emmetropic eye, far point is at infinity and near point
varies with age
 As age increases, the near point of accommodation receeds
behind
 This condition of failing near vision due to age related  in
the amplitude of accommodation or  in punctum proximum
is called Presbyopia
Fig. 3.16: Presbyopia

 Causes of  accommodation power of lens:

– Age related changes in lens like:  elasticity,  size and 
hardness
– Age related  in the power of ciliary muscles.
Symptoms:
 Difficulty of near vision: Specially reading small prints and
in dim light
 Asthenoscopic symptoms due to fatigue of ciliary muscle
while doing near work
 Patient comes with complaint of:
– Inability to thread the needle
– Hands are not long enough for the same.
Treatment:
 Prescribing appropriate convex glass for near work. A rough
guideline is as follows:
Patients age in years Correction

40–45 + 1DS
45–50 +1.5 DS
50–55 +2 DS
55–60 +2.5 DS
 Basic principles of presbyopic correction:

– Always find out refractive error for distance vision and
correct the same
– Find out the presbyopic correction needed in each eye
separately and add it to the distant vision
– Near point fixed based on profession

– Weakest contact lens with which an individual can clearly
see the nearest point should be prescribed
– Presbyopic spectacles may be: unifocal, bifocal, varifocal
 Surgical options available:
– Monovision LASIK
– Monovision conductive keratoplasty
– Scleral expansion
– Bifocal or multifocal IOL
– Monovision with IOL
– Anterior ciliary sclerotomy.
Q. List the material from which lens is made.
Q. List the different types of lenses.
Q. List the advantages of contact lens over spectacles.
Q. List the indications and contraindications for the use of
contact lens.
Different types Different types of contact lenses
of glasses
Crown glass Soft lens: Made of HEMA (Hydroxyethyl methacrylate)
Resin lenses Hard lens: Made of PMMA (Polymethyl methacrylate)
Plastic lenses Rigid gas permeable lens is permeable to oxygen
Triplex lenses
Advantages of contact lens over spectacles Contraindications for lens

Irregular corneal astigmatism can only be Poor motivation
corrected by lens Chronic dacryocystitis
Contd...
Contd...
Not affected by rain or fog Chronic conjunctivitis
Cosmetically better accepted Dry eye syndrome
Provides normal field of vision Corneal dystrophies
Aberrations associated with spectacles Recurrent Episcleritis/
are absent Scleritis/iridocycilitis
Able to retain binocular vision in high
anisometropia
Indication for use of contact lens:

Mnemonic: {Therapy for PCOD}
Indication Examples/as in
Therapeutic indication Corneal diseases: nonhealing ulcers, bullous
keratopathy, recurrent corneal erosion syndrome
Iris: aniridia, Coloboma, albinism to avoid glare
Glaucoma for drug delivery
In amblyopia opaque contact lenses are used
Bandage soft contact lens after kerotoplasty
Preventive indication Symblepharon
Exposure keratitis
Trichiasis
Cosmetic indication To cover corneal scars, cosmetic scleral lenses in
phthisis bulbi, ptosis (haptic contact lens)
Optical indications Anisometropia, unilateral Aphakia, high myopia,
Keratoconus, irregular astigmatism
Operative indication During Goniotomy for congenital glaucoma
Vitrectomy and extraocular photocoagulation
Occupational indication Sportsmen, pilots and actors
Diagnostic indication During Gonioscopy, ERG, examination of fundus in
presence of irregular corneal astigmatism, fundus
photography, Goldman’s 3 mirror examination
4.
Diseases of the Conjunctiva
Fig. 4.1: Structure of conjunctiva

Diseases of the Conjunctiva 59
Fig. 4.2: Parts of conjunctiva
Q. Define conjunctivitis and classify the same.

Definition: Inflammation of conjunctiva is called as
conjunctivitis (Figs 4.1 and 4.2 show the normal structure of
conjunctiva).
Classification:
Etiological classification Clinical classification
Infective conjunctivitis Acute catarrhal or mucopurulent conjunctivitis
Allergic conjunctivitis Acute purulent conjunctivitis
Irritative conjunctivitis Serous conjunctivitis
Keratoconjunctivitis Chronic simple conjunctivitis
associated with diseases Angular conjunctivitis
of skin or mucous Membranous conjunctivitis
membrane Pseudomembrane conjunctivitis
Traumatic conjunctivitis Papillary conjunctivitis
Keratoconjunctivitis of Follicular conjunctivitis
unknown etiology Ophthalmia neonatorum
Granulomatous conjunctivitis
Ulcerative conjunctivitis
Cicatrising conjunctivitis
Q. Discuss the etiology, clinical features, complications and

management of acute mucopurulent conjunctivitis.
Acute mucopurulent conjunctivitis is the most common type of
acute bacterial conjunctivitis.
Etiology:
Causative organisms:
 Staphylococcus aureus
 Koch-Weeks bacillus
 Pneumococcus
 Streptococcus
It is commonly associated with measles and scarlet fever.
Clinical features:
Symptoms Signs
Discomfort and foreign body Conjunctival congestion
sensation in eyes (fiery red eye)
Mild photophobia Chemosis (swelling of eyelids)
Mucopurulent discharge from eyes Petechial hemorrhage
Sticking together of eyelids (in Pneumococcal infection)
Slight blurring sensation of vision Flakes of mucopus in fornices,
due to mucus flakes canthi and lid margin
Colored halos Matted cilia
Complications:
 Marginal corneal ulcer
 Superficial keratitis
 Blepharitis
 Dacryocystitis.
Treatment:
 Cleanliness: Frequent washing of the eyes with warm water
and soap
 Topical antibiotics: This is the main stay of treatment
– Treatment may be started with chloramphenicol (1%),
gentamicin (0.3%) or framycetin
– If the patient does not respond, then alternatively
ciprofloxacin (0.3%), ofloxacin (0.3%) or gatifloxacin
(0.3%) can be used
 Anti-inflammatory and analgesics: Ibuprofen and paracetamol

are commonly used
 Irrigation of conjunctival sac with warm saline
 Dark goggles to avoid photophobia
 No bandage should be applied in patients with mucopurulent
conjunctivitis (Bandage  Rise in temperature  promotes
bacterial growth)
 No steroids: As it will flare up the infection.
Q. What is Pseudomembrane conjunctivitis? Discuss the

etiology, clinical features and management of the same.
Pseudomembrane conjunctivitis is a type of acute conjunctivitis
characterized by formation of psuedomembrane on the conjunctiva.
Pseudomembrane (false membrane) is a membrane that can
be easily peeled off leaving behind intact conjunctive.
Etiology:
Bacterial Viral Chemical
Cornyebacterium diphtheriae Herpes simplex Copper sulfate
Staphylococci Adenovirus Lime
Streptococci Acids
H. Influenzae Ammonia
N. Gonorrhoea Silver nitrate
(Mnemonic: claas
instead of class)
Pathology: Infection  inflammatory fibrinous exudate 

coagulation of the exudation formation of psuedomembrane
Clinical picture:
 Same as features of acute mucopurulent conjunctivitis
 Pseudomembrane formation which is thin yellowish white
membrane seen in the fornices and on the palpable conjunctiva
 Membrane can be peeled off without bleeding.
Treatment: Is similar to acute mucopurulent conjunctivitis.

Q. What is angular conjunctivitis? Discuss the etiology, clinical
Angular conjunctivitis is a type of chronic conjunctivitis
characterized by mild grade inflammation confined to the
conjunctiva and the lid margin near the angles (hence the name)
associated with maceration of the surrounding skin (Fig. 4.3).
Etiology:
 Predisposing factors are:
– Chronic exposure to dust, smoke
– Alcoholism, metabolic diseases
Fig. 4.3: Angular conjunctivitis

– Local irritation: Trichiosis, foreign body

– Eye strain due to refractive errors, convergence
insufficiency.
 Causative organism: Moraxella-Axenfeld (a diplobacilli, hence
the diseases is also called as diplobacillary conjunctivitis)
 Source of infection: Nasal cavity
 Mode of infection: Infection is transmitted from nasal cavity
to eyes by contaminated fingers or handkerchief.
Pathology: Moraxella-Axenfeld  produces proteolytic enzyme
 this collects at the angles due to the action of tears 
maceration of the epithelium of the conjunctiva, lid margin and
the skin  mild grade inflammation.
Clinical features:
Symptoms:
 Irritation, smarting sensation and feeling of discomfort in the
eyes
 History of collection of dirty white foamy discharge at the
angles
 Redness at the angles.
Signs:
 Hyperemia of the bulbar conjunctiva at the canthi
 Hyperemia of the lid margins near the angles
 Excoriation of the skin around the angles

 Presence of foamy mucopurulent discharge at the angles.
Complications: Blepharitis and shallow marginal catarrhal
corneal ulceration.
Treatment:
 Treatment of nasal infection and good personal hygiene
 Oxytetracycline (1%) eye ointment 2 to 3 times a day for 9 to
14 days
 Zinc lotion instilled in day time and Zinc oxide ointment at
bed time inhibits proteolytic action of the enzymes.
Q. Define trachoma. Discuss the etiology, clinical features,
complications and management of the same.
Q. Discuss the WHO classification of trachoma/FISTO
classification of trachoma.
Q. List the squealae of trachoma.
Q. Discuss in detail the clinical features, investigation and
management of trachoma.
Q. What is intermittent treatment for trachoma?
Definition: Trachoma is a chronic granulomatous Kerato-
conjunctivitis, primarily affecting the superficial epithelium of
the conjunctiva and the cornea simultaneously. It is characterized
by mixed follicular and papillary response of the conjunctival
tissue (Trachoma means rough).
Etiology:
Causative agent Predisposing factors Source of Mode of
infection infection
Chlamydia trachomatis Any age Conjunctival Air borne or
Serotypes A, B, Ba, C: Sex: Females > males discharge water born
hyperendemic of the affec- Vector: Eye
trachoma ted person seeking
insects
Serotypes D-K: No race is spared, Material
paratrochoma however less transfer:
(Oculogenital common in Jews iatrogenic,
Chlamydial disease) and blacks contaminated
Dusty and dry tonometers
weather Surma rod,
Lower socio- towel
economic status
Eye seeking flies
Use of kajal or
Surma from same
container by many
Clinical profile:
 Incubation period: 5 to 21 days
 Clinical course: Of the disease is determined by the presence
or absence of secondary infection. Pure trachoma is mild and
asymptomatic
 Natural history of the disease: Incubation period  insidious
in onset  acute disease in first decade  slow progression
 sequelae appear after 20 years after the onset of the disease
 so peak incidence of blinding is in fourth or fifth decade
Symptoms:
In absence of secondary infection: In presence of secondary infection
Minimal symptoms
Mild foreign body sensation Symptoms of mucopurulent
Slight stickiness of the lids conjunctivitis
Scanty mucus discharge
Signs:
A. Conjunctival signs (Fig. 4.5):
 Bulbar congestion
 Follicles: Look like boiled sagograins, commonly found in
upper tarsal conjunctiva and fornix (Fig. 4.4)
 Papillary hyperplasia: Reddish flat topped raised areas
 Conjunctival scarring: Which may be irregular, star shaped
or linear
 Concretions may be formed due to accumulation of dead
epithelial cells and inspissated mucus in depressions called
glands of Henle.
Fig. 4.4: Follicular conjunctivitis

B. Corneal signs:
 Superficial keratitis
 Herbert follicles: are follicles in the Limbal area
 Pannus: Pannus is infiltration of the cornea associated with

vascularization seen in the upper part of the cornea (Fig. 4.6)
– Progressive pannus: Infiltration of cornea is ahead of vas-
cularization
– Regressive pannus: Vessels extend a short distance ahead
of infiltration
Fig. 4.5: Signs of active trachoma (diagramatic)
Fig. 4.6: Pannus

 Corneal ulceration
 Herbert pits: Oval or circular pitted scar left after healing of
Herbert’s follicles
 Corneal scarring.
WHO classification (FISTO) (Figs 4.7A to D):

Category Implies Criteria
Follicles Active disease which needs Trchomatous inflammation,
treatment, if treated will follicles: 5 or more follicles of
recover without scarring at least 5 mm in diameter on
the upper tarsal plate
The deep tarsal plate should
be visible through the follicles
and the papillae
Intense Severe disease which Pronounced inflammatory
needs urgent treatment thickening of upper tarsal
conjunctiva obscures more
than half of the normal deep
tarsal vessels
Scarring Old, now inactive disease Scar in the tarsal conjunctiva
Scars appear as white, bands
or as sheet
Trichiasis Needs corrective surgery Presence of atleast one
trichiatic eyelash
Opacities Previous trachoma, Presence of corneal opacity
may be the cause of covering part of the papillary
visual loss region
Figs 4.7A to D: (A) Subclinical stage; (B) Typical trachomatous lesions;

(C) Stage of scarring; (D) Stage of sequelae and complications
Sequelae of trachoma:
Eyelids Conjunctiva Cornea Lacrimal sac
Ptosis Loss of fornices Herbert’s pits Chronic
Boat shaped lid Xerosis Healed pannus Dacryocystitis
Entropion Symblepharon resulting in hazy
Trichiasis Pigmentation cornea
Tylosis (Round Pseudo- Opacities
lid border) pterygium Loss of sensation
Madarosis Trachomatous
Chalazion nodular keratopathy
Treatment:
A. Treatment of Acute trachoma:
 Tropical antibiotics: 1% tetracycline or 1% erythromycin
eye drops 4 times a day for 6 weeks
 Systemic therapy: Tetracycline or erythromycin 250 mg

4 times a day for 3–4 weeks (alternatively doxycycline
100 mg)
 Combined tropical and systemic treatment in severe cases.
B. Treatment of sequelae:
 Concretions: Removed by hypodermic needle
 Trichiasis: Epilation, electrolysis
 Entropion: Surgical correction
 Xerosis: Artificial tears.
C. Prophylaxis:
 Hygienic measures
 Early treatment of any conjunctivitis
 Blanket treatment/intermittent antibiotic therapy:
– Was advised by WHO as a strategy to treat trachoma in
endemic areas
– It is useful to reduce the severity and intensity of the
disease
– Regimen: 1% tetracycline eye ointment twice daily for
45 days in a month for 6 months.
D. Prevention: SAFE strategy (discussed in community
ophthalmology)
(Mnemonic: Trachoma presents with “HALF SP City”)
H- Herberts pits, A- Arlts line, L- Leber cells, F-Folicles, S-Safe
stratergy, P- Papillary hyperplasia, Pannus, City- Corneal ulcers)
Q. What is Epidemic Keratoconjunctivitis? Discuss the etiology,
clinical stages and management of the same.
Epidemic Keratoconjunctivitis is a type of acute follicular
conjunctivitis mostly associated with superficial punctate keratitis
and usually occurs in epidemics and hence the name.
Etiology: Adenovirus 8 and 19

It spreads mostly through contact with contaminated fingers,
solutions and tonometers.
Clinical picture: It usually affects young individuals
Clinical stages:
Clinical Name Features
stages
1 Acute serous conjunctivitis Conjunctival hyperemia
Mild chemosis
Lacrimation
2 Typical acute follicular Follicles are formed more
conjunctivitis in lower lid
3 Acute psuedomembranous Psuedomembrane is formed on
conjunctivitis the conjunctiva
 Corneal involvement in the form of ‘superficial punctate

keratitis’ after one week after the onset of the disease is a
distinctive feature of Epidemic Keratoconjunctivitis
 Preauricular lymphadenopathy is present in almost all the
cases.
Treatment: Is mainly supportive
 Antiviral drugs are ineffective
 Adenine arabinoside is effective
 Antibiotic eyedrops to prevent secondary infection
 Mild cycloplegics.

management of the Ophthalmia neonatorum.
Ophthalmia neonatorum is the name given to bilateral
inflammation of the conjunctiva occurring in an infant less than
30 days of age.
Etiology:
Causative agents:
 Chemical conjunctivitis: Silver nitrate or other antibiotics used
for prophylaxis
 Gonococcal infection (accounts for 50% of the cases)
 Other bacteria: Staphylococcus, Streptococcus haemolyticus,
Streptococcus pneumoniae
 Neonatal inclusion conjunctivitis: Chlamydia trachomatis
(Serotypes D to K)
 Herpes simplex ophthalmia neonatorum
Source and mode of infection:

 Before birth through infected liquor amnii in mothers with
rupture membranes
 During birth from the infected birth canal (commonest mode)
 After birth: Infection may occur during first bath or from
soiled clothes.
Clinical features:
 Any discharge or even watering from the eyes in the first
week of life should arouse suspicion
 Pain and tenderness of eye ball

 Mucoid or mucopurulent discharge
 Swollen lids
 Conjunctiva: Hyperemia, chemosis
 Cornea: Punctate keratitis in herpes simplex ophthalmia.
Complications: Corneal opacification and staphyloma formation.
Prophylaxis:
 Antenatal: Treatment of genital tract infections in the mother
 Natal: Delivery under aseptic precautions, newborns eyelid
should cleansed
 Postnatal: 1% tetracycline ointment or 1% silver nitrate
solution into the eyes of the baby.
Treatment:
 Chemical ophthalmia is self limiting and requires no treatment
 Gonococcal ophthalmia neonatorum:
A. Topical therapy:
– Hourly saline lavage to eliminate the discharge
– Bacitracin/Nebracin eye ointment four times a day
– Atropine sulfate if there is corneal involvement.
B. Systemic therapy: Ceftriaxone, cefotaxime, ciprofloxacin
(one of these for 7 days).
 Other bacterial Ophthalmia neonatorum: Broad-spectrum
antibiotics
 Neonatal inclusion conjunctivitis: Topical 1% tetracycline or
erythromycin 0.5% eye ointment. Treat the respiratory loci
in parents
 Herpes simplex conjunctivitis: Self limiting, topical antiviral drugs
control the infection more effectively and prevents the recurrence.
Q. Define Vernal Keratoconjunctivitis (VKC) or spring catarrh.

Discuss the etiology, clinical features, complications and
Q. Define warm weather conjunctivitis. Discuss the etiology,
clinical features, complications and management of the same.
Q. What are the three clinical types of Vernal Kerato-
conjunctivitis (VKC)? Discuss their features.
Q. List the various types of vernal keratitis and discuss the
treatment of the same.
Definition: Vernal Keratoconjunctivitis (VKC) is a recurrent,
bilateral, interstitial, self-limiting allergic inflammation of the
conjunctiva having a periodic seasonal incidence.
Etiology:
 It is a hypersensitivity to an exogenous allergen such as grass
pollen
 It is an atopic disorder (IgE mediated and the same is elevated)
 Family history of atopy may be present.
Predisposing factors:
 Age: 4 to 20 years
 Sex: Males are more commonly affected than females
 Season: More in summer, hence the name is a misnomer and
recently it is being called as ‘Warm weather conjunctivitis’
 Climate: Tropics > temperate region, non-existent in cold region.
Clinical features:
Symptoms:
 Marked burning and aching sensation
 Fibrinous/ropy discharge
 Heaviness of lids
 Photophobia
 Lacrimation
 Foreign body sensation
 It is self limiting and regresses in 5 to 10 years.
Signs of Vernal Keratoconjunctivitis can be described in the

following three clinical forms (Fig. 4.8):
Clinical type Features
Polpebral form Upper tarsal conjunctiva is affected
Cobble stone appearance (hard, flat topped papillae)
In severe case papillae may hypertrophy to form giant
papillae
Bulbar form Dusky red triangular congestion of the bulbar conjunctiva
Tranta’s spot: discrete whitish raised dots along the limbus
Mixed Has a picture of above 2 types
Vernal keratopathy: Five types of the lesions are seen and they
are:
 Punctate epithelial keratitis
 Ulcerative vernal keratitis (shield ulceration)
 Venal corneal plaques
 Subepithelial scarring
 Pseudogerontoxon characterized by ‘cupid bow’ outline of
cornea.
Fig. 4.8: Palpebral and bulbar form of spring catarrh

Treatment:
A. Local therapy:
 Topical steroids: Fluromethalone, medrysone, betametha-
sone and dexamethasone are commonly used drugs
 Mast cell inhibitors: Sodium cromoglycate 2% eye drops
 Topical antihistaminics
 Acetylcysteine: Used as a local mucolytic and is useful
for early plaques
 Topical cyclosporine in severe unresponsive cases.
B. Systemic therapy:
 Oral antihistaminics for relief from itching
 Oral steroids in very severe cases.
C. Treatment of large papillae:
 Supratarsal injection of long acting steroid
 Cryo surgery
 Surgical excision of large papillae.
D. General measures:
 Dark goggles to prevent photophobia
 Cold compression and ice packs
 Change of place from hot to cold area.
E. Desensitization (Immunotherapy)
Treatment of vernal keratopathy:
 Punctate epithelial keratitis: Topical steroids
 Venal corneal plaques: Surgical excision and superficial
keratectomy
 Severe shield ulcer:
– Debridment
– Superficial keratectomy or excimer laser keratectomy
– Amniotic membrane transplantation.
Mnemonic:
Cobble stone Cobble stone appearance
Can Cupid’s bow outline
Provide Pseudogerontoxon
Pavement stone appearance
Maximum Maxwell lyon sign (stringy or ropy discharge)
Shield Shield ulcers of the cornea
(In) Hot Horner- Trantas dots
Summer Summer problem rather than in spring
Q. Define Phlyctenular keratoconjunctivitis. Discuss the

Q. Define tubercular keratoconjunctivitis. Discuss the etiology,
Q. What is fascicular ulcer? How do you manage the same?
Definition: Phlyctenular keratoconjunctivitis is an allergic
reaction of the conjunctiva/cornea caused by endogenous
bacterial toxins and characterized by formation of bleb or nodule
formation near the limbus ‘Phlycten’ means a bleb (Fig. 4.9).
Etiology:
It is thought to be because of type IV hypersensitivity reaction
Causative endogenous allergens Predisposing factors
Tubercular proteins Age: 3–15 years
Staphylococcus proteins Sex: Female > male
Moraxella-Axenfeld Overcrowding
Intestinal worms High incidence in spring and summer
Fig. 4.9: Phlyctenular conjunctivitis
Clinical course: True vesicle  necrosis of epithelium  ulcera-

tion  granulation tissue formation  healing without scarring
Clinical features:
Symptoms:
 Mild discomfort of eyes
 Irritation of eyes
 Lacrimation
 Photophobia.
Signs:
 One or more small raised nodule at or near the limbus (gray
or pinkish white in color)
 Bulbar congesion near the limbus
 Secondary infection may result in congesion of whole
conjunctiva and mucopurulent discharge.
Phlyctenular keratitis: Two forms have been noted
A. Ulcerative phlyctenular keratitis: Following three forms have
been noted
 Sacrofulous ulcer: Is a shallow marginal ulcer formed due
to breakdown of Limbal Phlycten
 Fascicular ulcer: Has a prominent parallel leash of blood

vessels. It is superficial but leaves a band shaped opacity
 Miliary ulcers: Small scattered ulcers all over the cornea.
B. Diffuse infiltrative Phlyctenular keratitis: Diffuse infiltration
with characteristic rich vascularization at the periphery.
Investigations: Indicated when phlycten are multiple or recurrent
 To detect TB: Sputum for AFB, ESR, TC, chest X-ray
 ENT consultation top rule out tonsillitis and adenoids
(Staphylococcal/streptococcal source)
 Stool examination for cyst or ova.
Treatment:
General measures: Protein rich diet and Vitamin A, C and D
supplementation
A. Local therapy:
 Topical steroids: Dexamethasone or betamethasone
eyedrops
 Antibiotic eyedrops to avoid secondary infection
 Atropine eyedrops
B. Specific therapy:
 Antitubercular treatment if TB is diagnosed
 Antibiotics for Staphylococcal/streptococcal tonsillitis
 Eradicate parasitic infections.
Q. Differentiate between conjunctival congestion and ciliary

congestion.
Features Conjunctival congestion Ciliary congestion
Site More marked in the fornices More marked around
limbus
Color Bright red Purple or dull red
Arrangement of Superficial and branching Dull and radiating from

vessels the limbus
On moving Congested vessels also move Congested vessels do not

conjunctiva move
On mechanical Vessels fill slowly from Vessels fill rapidly from
squeezing out the fornix towards limbus limbus towards fornices
blood vessels
Blanching, i.e. on Vessels blanch Do not blanch
putting one drop immediately
of 1 in 10000
adrenaline
Common causes Acute conjunctivitis Acute iridocyclitis
Corneal ulcer
Q. Define Pterygium. Discuss the etiology, pathology, types,

Q. List the complication of Pterygium.
Q. How do you treat recurrent pterygium?
Definition: Pterygium is a degenerative wing-shaped fold of
the conjunctiva encroaching upon the cornea from either side of
the interpalpable fissure (Pterygium means wing).
Etiology: Not defined but the following have been attributed:
 More common in people living in hot climate
 Following environmental factors have been attributed: Exposure
to sun (ultraviolet-B radiations), dry heat, high wind and dust.
Pathology:
 It is both degenerative and hyperplastic condition
 The subconjunctival tissue undergoes elastotic degeneration
and proliferates as vascularized granulation tissue which
ultimately encroaches the cornea
 The layer of the cornea that are destroyed are: Corneal
epithelium, Bowman’s membrane and superficial stroma
 Stocker’s line: Deposition of iron may occur anterior to head
of Pterygium. This is called as the stocker’s line.
Parts of the Pterygium (Fig. 4.10):
 Head: Apical part present on the cornea
 Neck: Limbal part
 Body is the scleral part extending between limbus and the canthus.
Fig. 4.10: Pterygium
Fig. 4.11: Pterygium–types
Types (Fig. 4.11):

 Progressive pterygium: It is thick, fleshy and vascular, with
infiltrates in cornea in front of the head (called as the cap of
Pterygium)
 Regressive pterygium: Is thin, atrophic attenuated membrane.
It is having no cap.
Clinical features:
Symptoms:
 Appearance of mass in the interpalpable area more so in nasal
side (because it receive both direct and reflected UV light
from the nose)
 Visual disturbance occurs when it encroaches the pupillary

area or due to corneal astigmatism
 Diplopia due to limited ocular movement.
Signs:
 Decreased visual acuity
 Triangular fold of conjunctival mass encroaching on cornea
 Limitation of movements in a few cases.
Complications:
 Cystic degeneration
 Infection
 Malignant change: Epithelioma, fibrosarcoma, malignant
melanoma.
Treatment: Surgical excision.
Indications for surgical excision:
 Cosmetic reasons
 Progressive type encroaching on pupillary area
 Diplopia.
Management of recurrent pterygium/measures to prevent

recurrence:
 Transplantation of pterygium into the lower fornix
 Postoperative beta irradiation
 Surgical excision with bare sclera
 Surgical excision with free conjunctival graft taken from the

same eye or the other eye (Preferred technique)
 Mitomycin-C solution locally during operation or as drops
postoperatively
 Lamellar kerotoplasty of the affected cornea, along with the
excision of the pterygium.
Fig. 4.12: Simple excision
Fig. 4.13: Strocker line, simple excision, transposition to lower fornix

Q. Differentiate between pterygium and pseudopterygium.

Pterygium Pseudopterygium
Etiology Degenerative process Inflammatory process
Unilateral/ Usually bilateral Unilateral
bilateral
Age of presentation Elders Any age
Site Always situated in the Can occur at any site
palpabral aperture
Stages May be progressive Stationary
or regressive
Probe test A probe cannot be A probe can be passed
passed underneath underneath
Treatment Excision Excision
Recurrence May recur Does not recur
5.
Diseases of the Cornea
Q. Define keratitis and corneal ulcer. Discuss the etiological

classification of the keratitis.
Definitions:
Inflammation of cornea is called keratitis. It is associated with
corneal edema, cellular infiltration and ciliary congestion.
Corneal ulcer is discontinuation in the normal epithelial
surface of the cornea associated with necrosis of the surrounding
corneal tissue.
Etiological classification of the keratitis:
Infective keratitis Bacterial, viral, fungal, chlamydial,
protozoal, spirochetal
Allergic keratitis Phlyctenular keratitis, vernal keratitis,
atopic keratitis
Trophic keratitis Exposure keratitis, neuroparalytic kera-
titis, keratomalacia, atheromatous ulcer
Keratitis associated with diseases Rosacea
of skin and mucous membrane
Keratitis associated with RA, SLE, PAN.
collagen vascular diseases
Contd...
Contd...
Traumatic keratitis Mechanical, thermal, chemical, radiation
Idiopathic keratitis Mooren’s corneal ulcer
Superior limbic keratoconjunctivitis
Superficial punctate keratitis of thygeson
Q. Discuss the etiology, pathogenesis, clinical features,

complications and management of bacterial corneal ulcer.
Q. List the risk factors for corneal ulceration.
Q. List the organisms which can invade intact corneal
epithelium.
Q. Discuss in detail the stages of pathogenesis in bacterial
corneal ulcer.
Q. List the common causes for non healing corneal ulcer. How
do you manage the same?
Q. List the sequelae of bacterial corneal ulcer.
Etiology:
Risk factors Source of infection Common organisms
Corneal abrasion Exogenous infection: Staphylococcus aureus
Epithelial drying From conjunctival sac, Pseudomonas pyocyanea
Necrosis of epithelium dacrocystitis, infected Streptococcus pneumoniae
as in keratomalacia foreign body, water E. Coli
Desquamation of borne or air borne Proteus
epithelial cells as a infections
result of corneal From the ocular tissue Klebsiella
edema as in bullous N. gonorrhoea*
keratopathy N. meningitidis*
epithelial damage C. diphtheriae*
*These three organisms can invade intact corneal epithelium and cause ulceration
Diseases of the Cornea 89
Pathogenesis:
Pathogenesis of corneal ulcer (Fig. 5.1):
1. Stage of progressive infiltration: Characterized by infiltration
of neutrophils and lymphocytes into the epithelium from
peripheral circulation  Subsequent necrosis of involved tissue.
2. Stage of active ulcerations:
 Ulceration is because of necrosis and sloughing of involved
epithelium Bowman’s membrane and stroma
Fig. 5.1: Stages of corneal ulcer

 Walls of active ulcer project owing to swelling of lamellae

by imbibitions of the fluid, circumcorneal congestion occurs
 Iritis due to absorption of toxins
 Hypopyon is formed
 Fate of ulcer: May spread superficially, perforation or
descemetocele may be formed.
3. Stage of regression:
 The necrotic tissue is shedded and edema subsides
 The floor and the edges of the ulcer are smooth and transparent
 The epithelium starts to regrow.
4. Stage of cicatrization (healing)

 Progressive epithelial growth
 Beneath epithelium fibrous tissue is laid down
 The stroma gets thickened and fills in under the epithelium

thus pushing the epithelium anteriorly
 The degree of scarring varies: They are
– In superficial type there is no scarring

– In ulcer which involves Bowman’s membrane and a few
superficial stromal lamellae, the resultant scar is nebula
– Involvement of  1/3rd of stromal lamellae results in
macula and > 1/2 of stroma leukoma
Pathology of perforated corneal ulcer: Perforation occurs when

ulcer is deep up to Descemet’s membrane  Descemet’s
membrane being tough bulges out as descemetocele  exertion
like cough, sneeze, straining for stools will perforate the
descemetocele  aqueous escapes  decrease in intraocular
pressure  iris and lens move forward  this may result in
adherent leukoma.
Pathology of sloughing corneal ulcer and anterior staphyloma
When the infective agent is virulent/host immunity is com-
promised  whole of cornea is destroyed except at the rim 
total prolapse of iris  iris is inflamed, exudates blocks pupil
and covers iris surface forming false cornea  these exudates
get organized and a then fibrous layer is formed over which
grows the conjunctiva/corneal epithelium forming: pseudocornea
 pseudocornea being thin and cant with stand IOP hence bulges
forward with iris tissue to form anterior staphyloma.
Clinical features:
Symptoms:
 Pain and foreign body sensation
 Watering
 Redness of eyes
 Blurring of vision
 Photophobia.
Signs:
 Swollen lids
 Blepharospasm
 Conjunctiva: Chemosis, hyperemia and ciliary congestion

 Corneal ulcer
– Initially is small but later increases in size
– Appears yellowish white in color
– Is irregular or oval in shape
– Margins are swollen and are hanging out
– Floor is covered by necrotic material
– Pupils are small
– IOP is raised due to inflammatory glaucoma
– Anterior chamber: Pus may or may not be present.
Investigations:
 Routine laboratory investigations like: Hb%, TC, DC, ESR,
blood sugar, complete urine and stool examination
 Microbiological investigations: Material for investigation is
obtained from base and margin of corneal ulcer with the help
of a kimura spatula.
The material obtained is used for the following investigations:
 Gram stain and giemsa stain
 10% KOH mount to identify fungal hyphae
 Calcofluor white stain preparation and is viewed under
fluorescent microscope for fungal elements
 Culture in blood agar for anaerobic organisms and in
Sabouraud’s dextrose agar for fungi.
Complications: Sequeal of bacterial corneal ulcer (Figs 5.2 to 5.4)

Complications Sequeal of bacterial corneal ulcer
Toxic iridocylitis Prolapse of iris
Secondary glaucoma Subluxation/dislocation of lens
Descemetocele Anterior capsular cataract
Perforation Corneal fistula
Scarring Purulent uveitis, endophthalmitis, panopthalmitis
Anterior Intraocular hemorrhage
Staphyloma
Fig. 5.2: Descemetocele
Figs 5.3A and B: (A) Adherent leukoma; (B) Anterior staphyloma

Fig. 5.4: Perforated corneal ulcer with prolapse of iris
Treatment:
Treatment of uncomplicated corneal ulcer:
A. Specific treatment:
 Topical antibiotics:
– Initial therapy (till culture sensitivity is obtained) should
be with combination of antibiotics to cover both gram-
positive and gram-negative organisms
– Fortified gentamicin or fortified tobramycin eyedrops
along with fortified cephazoline is used as initial therapy
– After adequate response is obtained, the fortified drops
can be substituted by dilute preparations of ofloxacin,
ciprofloxacin, gatifloxacin, moxifloxacin
 Systemic antibiotics are not indicated.
B. Nonspecific treatment:
 Cycloplegics:
– 1% Atropine and 2% homatropine are commonly used
– Mechanism of action:
• Reduces pain due to ciliary spasm
• Prevents formation posterior synechiae due to
secondary iridocylitis
•  tear content so drugs are more in contact with cornea
• Increases blood flow to anterior uvea, hence brings
more antibiotics in the aqueous humor
• Reduces exudation by decreasing hyperemia and
vascular permeability
 Systemic analgesics and anti-inflammatory (paracetamol and
ibuprofen)
 Vitamin supplementation (A, B-complex and C)
C. Physical and general measures:
 Hot fomentation
 Dark goggles
 Rest, good diet
Treatment of non healing corneal ulcer

Common causes of non healing ulcer are:
Local causes Systemic causes
Raised IOP Diabetes mellitus
Concretions Severe anemia
Misdirected cilia Malnutrition
Impacted foreign body Immunosuppressed condition ( HIV, on steroids)
Dacrocystitis
Inadequate therapy
Wrong diagnosis
Lagophthalmos
Excessive vascularization
of the ulcer
Treatment of non healing corneal ulcer:

 Removal of any of the above causes for non-healing
 Mechanical debridement of ulcer to remove necrosed material
 Cauterization in nonresponding cases
 Bandage soft contact lens
 Peritomy (severing the perilimbal conjunctival vessels may
be performed when excessive corneal vascularization is
hindering the healing)
Treatment of perforated corneal ulcer:
Following are the options available:
 Tissue adhesive glues
 Covering with conjunctival flap
 Use of bandage soft contact lens
 Therapeutic keratoplasty (Best option).
Q. Define hypopyon corneal ulcer/Ulcus Serpens. Discuss the

etiology, clinical features and treatment of the same.
Q. List the organisms causing hypopyon corneal ulcer/Ulcus
Serpens.
Definition: Hypopyon corneal ulcer is a corneal ulcer associated
with hypopyon that is sterile pus in the anterior chamber as a
result of iridocylitis (Fig. 5.5).
Hypopyon is sterile as the leukocytosis is due to the toxins
and not by actual invasion of the bacteria.
The characteristic hypopyon corneal ulcer caused by
Pneumococcus is called Ulcus Serpens.
Fig. 5.5: Hypopyon corneal ulcer
Etiology:
Causative organisms Predisposing factors
Pneumococcus Chronic Dacrocystitis
Pseudomonas pyocyanea Minor injuries like scratch
Staphylococcus Retained foreign body
Streptococcus Old, debilitated and alcoholic patients
Gonococcus Measles, scarlet fever
Moroxella
Pathogenesis:
Corneal ulcer  Toxins diffusion  causes iritis  out-
pouring of inflammatory cells  under the influence of gravity
they settle to form hypopyon (sterile, as there is no invasion of
bacteria).
Clinical features:
Symptoms: Same as bacterial corneal ulcer, but there is less
pain.
Signs: Are similar to bacterial corneal ulcer.
Characteristics of Ulcus Serpens are as follows:

 Ulcus Serpens is grayish white or yellowish white
 It is disc shaped
 The ulcer has tendency to creep over cornea hence it is called
‘serpens’
 The edge along which ulcer spreads shows infiltration, other
edge shows cicatrization
 It is associated with violent iridocylitis
 Hypopyon increases in size rapidly
 It may cause secondary glaucoma
 It has a great tendency for perforation.
Treatment:
Is same as bacterial corneal ulcer. Paracentesis may be done if
the hypopyon is massive.
Q. Discuss the etiology, clinical features and management of
keratomycosis/mycotic/fungal corneal ulcer.
Etiology:
Causative organisms Predisposing factors
Filamentous fungi Yeast like fungi Vegetative injury from crop leaf
Aspergillus Candida Animal tail injury
Fusarium Cryptococcus Local/systemic immunosuppression
Pencillium Dry eyes
Cephalosporium Herpes
Bullous keratopathy
Post-keratoplasty
Clinical features:
Symptoms: Are similar to bacterial corneal ulcer but slow
progression.
Signs (Fig. 5.6):

 Ulcer is dry, grayish white with rolled out margin
 Sterile immune ring (yellow line of demarcation, which is
the junction of fungi and inflammatory cell)
 Feathery finger extensions into surrounding stroma below
intact epithelium
 Multiple, small satellite lesions
 Big nonsterile hypopyon
 Rarely perforation may happen
 Corneal vascularization is rare.
Investigations:
 Gram stain and giemsa stain
 10% KOH mount to identify fungal hyphae
 Calcofluor white stain preparation and is viewed under
fluorescent microscope for fungal elements
 Sabouraud’s dextrose agar for fungi.
Fig. 5.6: Fungal corneal ulcer

Treatment:
A. Specific treatment:
 Local antifungal’s for 6 to 8 week: Natamycin 5%, nystatin
3.5%, fluconazole 0.2%
 Systemic antifungals 2 to 3 week: Ketoconazole.
B. Nonspecific treatment:
 Cycloplegics like homatropine
 Analgesics and anti-inflammatory
 Vitamin supplementation (Vitamin A, B complex, C).
C. General measures:
 Dark goggles
 Hot fomentation
 Good diet.
Mnemonic: Fungal corneal ulcer
We Wesseley’s sterile immune ring (yellow line)

Saw Symptoms milder than signs
Vegetative Vegetative material trauma is the cause
D Dry looking ulcer
P Pseudohypopyon
S Satellite ring
Film Feather finger like extensions into surrounding stroma
Q. Define keratoplasty/corneal grafting. Discuss its types,

indications, contraindications and complications.
Q. List the reasons for graft failure.
Q. Discuss the various ways to preserve the cornea.
Definition: Keratoplasty is an operation in which the patient’s
diseased cornea is replaced by donor’s healthy cornea.
Types of keratoplasty:
 Allograft:
– Full thickness/penetrating
– Partial thickness/lamellar
– Small patch graft/penetrating lamellar
 Rotational autograft:
– This is for small scars on visual axis with surrounding
clear cornea
– Patient’s cornea is used
– There is no risk of graft rejection.
Preservation of donor cornea:
Cornea is to be recovered within six hours after death of the patient.
 Short-term (up to 46–72 hrs): Whole globe in 4°C moist
chamber
 Intermediate duration:
– Up to 10 days
McCarey Kaufman (MK) medium
Optisol medium (contains condritin sulfate)
– Up to 30 days: Organ culture.
Figure 5.7 demonstrates types of keratoplasty and Figure 5.8
demonstrates technique of penetrating keratoplasty.
Long-term: cryopreservation
Figs 5.7A and B: (A) Penetrating and; (B) partial thickness lamellar keratoplasty
Fig. 5.8: Technique of penetrating keratoplasty
Contraindication for collection of eye:

Ophthalmic Medical CNS diseases Malignancy Others
Previous surgeries HIV SSPE Leukemia Unknown
Malignant Hepatitis B Creutzfeldt- Disseminated cause of
melanoma Syphilis Jacob lymphoma death
Retinoblastoma Septicemia disease
Iritis
Corneal pathology
Endophthalmitis
Indications of penetrating keratoplasty: (Mnemonic: OTCT)

O: Optic T:Tectonic: that is C: Cosmetic T: Therapeutic
to preserve the
integrity of cornea
Bullous keratopathy Descemetocele To replace
Keratoconus Stromal thinning infected
Opacity cornea
Dystrophy
Degeneration
Complications of corneal grafting:

Early Late
Primary graft failure Late graft failure
Iris prolapse Recurrence of disease
Flat anterior chamber Astigmatism
Infection Cataract
Secondary glaucoma
Epithelial defect
Causes of graft failure:

Early: Endothelial dysfunction (due to trauma or defective donor)
Late: Immunological.
Q. Discuss the etiology, pathogenesis, clinical features and
management of Herpes Zoster ophthalmicus.
Etiology: Varicella Zoster virus is the causative agent.
Pathogenesis:
Infection in childhood  chicken pox  child develops immunity
 virus dormant gasserian ganglion of V cranial nerve 
depressed cellular immunity  virus replicates  travels down
ophthalmic division of V nerve  Herpes Zoster ophthalmicus.
Ocular lesions: Occur after skin lesions subside

 Conjunctiva:
– Mucopurulent conjunctivitis with petechial hemorrhage
– Acute follicular conjunctivitis with regional lymphadenopathy
 Episcleritis and scleritis
 Iridocylitis with hypopyon or hyphema
 Zonular keratitis: Occurs the following chronological order
(Fig. 5.9)
– Fine or course punctate epithelial keratitis
– Microdendritic epithelial ulcers: Small, fine, multiple,
dendritic or stellate lesions. They are pathognomonic of
Herpes Zoster ophthalmicus
– Numular keratitis: These are multiple granular lesions,
surrounded by a halo of stromal haze
– Disciform keratitis: It involves stroma to cause disc shaped
opacities
– Neuroparalytic ulceration due to sequelae of acute
infections of gasserian ganglion
– Exposure keratitis due to facial palsy
– Mucous plaque keratitis
Fig. 5.9: Superficial punctate, coarse subepithelial, nummular, disciform keratitis

Fig. 5.10: Herpes zoster
 Acute retinal necrosis

 Anterior segment necrosis causing phthisis bulbi
 Secondary glaucoma (may be because of trabeculitis or
synechial angle closure)
 Motor nerve palsy of III, IV, VI, VII cranial nerves
 Optic neuritis.
Hutchison’s rule: Ophthalmic involvement is common if the
side or tip of the nose presents vesicle (cutaneous involvement
of Nasociliary nerve) (Fig. 5.10).
Treatment:
A. Systemic treatment for Herpes zoster:
 Oral antiviral drugs; (Mnemonic: VIT-A: Vidarabine,
Idoxuridine, Trifluorothymidine, Acyclovir)
– Acyclovir 800 mg 5 times for 10 days

– Valacyclovir 500 mg tid
 Analgesic: Following combinations can be used mephenamic
acid + paracetamol or pentazocin or pethedine
 Systemic steroids:
– Prevents postherpetic neuralgia
– Also used in III cranial nerve palsy and optic neuritis
 Cimetidine: Histamine blocker, decreases pain and pruritis
 Amitriptyline for depression.
B. Local Treatment for skin lesions:
 Antibiotic: Steroid skin cream/lotion
 Avoid calamine lotion: It increases crust formation.
C. For local eye lesions:
 For herpetic keratitis, iridocylitis, scleritis
– Topical steroids qid
– Cycloplegics: Atropine 1 %
– Topical Acyclovir ointment 5 times/day
 Antibiotics to prevent secondary infection
 For secondary glaucoma
– 0.5% Timolol / Betaxolol
– Acetazolamide 250 mg qid
 Neuroparalytic corneal ulcer: Lateral tarsorrhaphy
 For persistent epithelial defect
– Lubricating eye drops
– Bandage soft contact lens.
D. Keratoplasty for visual rehabilitation.

Acanthamoeba keratitis.
Acanthamoeba keratitis has gained importance recently because
of its increasing incidence, difficulty in diagnosis and
unsatisfactory treatment.
Etiology:
 Acanthamoeba a free lying amoeba in soil, fresh water, salt
water and sewage
 Two forms of the organism are trophozoites and cysts
 Predisposing factors are: Usually mild trauma is the predis-
posing factor
– Contact lens users: Due to homemade saline (H2O and
saline tablets)
– Salt water diving
– Wind blow
– Organic matter
– Hot tub use
– Muddy water
– Opportunistic infection following: Herpetic keratitis,
bacterial keratitis, bullous keratopathy.
Clinical features:
Symptoms:
 Intense pain (out of proportion of inflammation)
 Watering
 Photophobia
 Blepharospasm
 Blurred vision.
Signs: Signs vary hence the condition is difficult to diagnose.

 Initial lesions: The following signs might be seen
– Limbitis
– Fine/coarse opaque streaks at the limbus
– Epithelial/subepithelial opacities
– Radial keratoneuritis (infiltration along corneal nerves)
 Advanced cases: The following signs might be seen
– Central or paracentral ring shaped opacities
– Ring abscess due to overlying epithelial defect
– Hypopyon.
Investigations: The following investigations are done on the
corneal scrapings
 KOH mount to identify the cysts
 Calcofluor white stain: To identify cysts which appear bright
apple green
 Lactophenol cotton blue mount to identify cyst
 Non nutrient agar enriched with E.coli may show trophozoites
within 48 hours.
Treatment:
A. Nonspecific treatment same as bacterial corneal ulcer.
B. Specific medical treatment (Mnemonic: CNS BP)
 Chlorhexidine
 Neomycin drops
 Steroids (topical)
 Brolene drops 0.1%
 Polyhexamethelene biguanide
 Others: Imidazole (fluconazole, miconazole).
C. Penetrating keratoplasty in nonresponding cases.

Mooren’s ulcer or Chronic Serpiginous ulcer or Rodent ulcer.
It is a chronic progressive peripheral ulcer with unknown
etiology.
Etiology: The exact etiology is not known, the following have
been attributed
 Idiopathic degenerative condition
 Ischemic necrosis resulting from vasculitis of limbal vessels
 Effect of collagenase and proteoglyconase produced from
conjunctiva
 Autoimmunity has also been attributed.
Clinical picture: Two varieties are seen

Benign form Virulent form
Unilateral Bilateral
Affects: Elderly people Affects: Young individuals
Slow progression Rapid progression
Low incidence of scleral involvement High incidence of scleral involvement
Clinical features: Common in elderly males

Symptoms
 Severe pain
 Photophobia
 Lacrimation
 Defective vision.
Signs:
 Ulcer usually starts at the interpalpable area as a patchy gray
infiltrates at the margin
 It spreads slowly undermining the epithelium and superficial

stroma
 Advancing edge of the ulcer has an overhanging edge
 Later it may involve the entire circumference of the cornea
 It also spreads towards the center of the cornea and may
involve the sclera
 Healing takes place from the periphery and the healed area
becomes vascularized, thinned and opaque.
Complications: Perforations and thin nebular opacities in whole
of cornea.
Treatment: Is unsatisfactory
 Topical corticosteroids (hourly)
 Cycloplegics like atropine
 Conjunctival excision: A 3 mm collar of conjunctiva is excised
from the limbus and parallel to the ulcer
 Immunosuppressive therapy specially for the bilateral cases:
Systemic corticosteroids, cyclophosphamide, azothioprin or
methotrexate
 Bandage soft contact lens
 Lamellar sclera-corneal patch graft, if there is threat of
perforation.
Q. Define deep keratitis. Classify the same.
Definition: Inflammation of the corneal stroma with or without
the involvement of the posterior corneal layers is called deep
keratitis.
Classification:
Suppurative type Non-suppurative type
Central corneal abscess Interstitial keratitis
Posterior corneal abscess Disciform keratitis
Sclerotic keratitis
Q. Define interstitial keratitis. List the causes of the same.

Definition: Interstitial keratitis denotes profound inflammation
of the corneal stroma without primary involvement of epithelium
or endothelium.
Causes:
 Congenital and acquired syphilis
 TB
 Cogan’s syndrome
 Trypanosomiasis
 Malaria
 Leprosy
 Sarcoidosis.
Q. Discuss etiology, clinical features and management of

syphilitic interstitial keratitis.
Etiology: The causative organism is Treponema pallidum.
This condition is unilateral in acquired syphilis and bilateral in
congenital syphilis.
Pathogenesis:
 Syphilitic interstitial keratitis has been attributed to immu-
nological reaction (antigen-antibody reaction)
 Treponema pallidum invades cornea and sensitizes it during

the period of generalized diffusion in the fetal stage  small-
scale fresh invasion by the organism or toxins exites
inflammation of the sensitized cornea
 Inflammation is usually triggered by operation or injury.
Clinical features:
Hutchison’s triad: Interstitial keratitis, Hutchison’s teeth,
vestibular deafness
Clinical features are divided into three different stages:
A. Progressive stage (lasts for 2 weeks):
 Begins as endothelial and deep stromal edema
 This is secondary to anterior uveitis
 Symptoms: Pain, lacrimation and photophobia
 Signs:
– Blepharospasm
– Circumcorneal congestion
– Diffuse corneal haze followed by ground glass
appearance of cornea
– Keratic precipitates may be present.
B. Florid stage (lasts for 2 months):
 Eyes are acutely inflamed. Superficial and deep vascula-
rization are noted
 Superficial vascularization: The superficial vessels and the
conjunctiva heap at the limbus like epulit
 Deep vascularization: Radial bundle of brush like vessels
cover the hazy cornea hence get a salmon patch appearance
(Dull reddish pink).
C. Stage of regression (lasts for 2 years): Resolution of acute

inflammation  appearance of vascular invasion  clearing
of cornea is slow and from peripheral to central  lesion
leave behind opacities and ghost blood vessels.
Investigations: VDRL and Treponema pallidum immobilization
test.
Treatment:
A. Local Treatment:
 Topical steroid dexamethasone 0.1%
 Atropine 1% ointment
 Dark goggles.
B. Keratoplasty for dense opacity.
C. Systemic treatment:
 Penicillin high dose to prevent development of further
syphilitic lesions
 Systemic steroids.
Q. What is Cogan’s syndrome? How do you manage the same?

Cogan’s syndrome is interstitial keratitis of unknown origin.
Clinical features:
 The condition is bilateral and is usually seen in middle age
 Interstitial keratitis
 Tinnitus
 Vertigo
 Deafness.
Treatment: Topical and systemic steroids.

Q. Define keratoconus/conical cornea. Discuss the etiology,

Definition: It is a noninflammatory bilateral ectatic condition
of the cornea in axial (central) part.
It usually starts at puberty and has a slow progression.
Etiopathogenesis:
Exact etiology is not clear, following theories have been attributed
 Developmental
 Degeneration
 Endocrinal
 Hereditary dystrophy.
Essential pathological changes are: Thinning and ectasia

(rupture) of cornea.
Basic defect: Defective synthesis of mucopolysaccharide and
collagen.
Association:
Ocular conditions Systemic conditions
Ectopic lentis Marfans syndrome
Congenital cataract Down’s syndrome
Aniridia Ehler-Danlos syndrome
Retinitis Pigmentosa Osteogenesis imperfecta
Vernal Keratoconjunctivitis
Morphological classification: Depending upon size and shape,

keratoconus is classified into:
Name Size Shape

Nipple cone < 5 mm Steep curvature
Oval cone 5–6 mm Ellipsoid
Globus cone > 6 mm Globe
Clinical features:
Symptoms:
 Progressive myopia
 Irregular astigmatism which is not corrected despite full
correction with glasses.
Signs:
 Window reflex is distorted
 Placido disc examination: Shows irregularities of circles
irregular (Fig. 5.11)
 Keratometry: Extreme misalignment of mires.
Fig. 5.11: Placido’s disc (Keratoscope)

 Photokeratoscopy reveals distortion of circles

 Slit lamp examination: Shows
– Thinning and ectasia of central cornea
– Opacity at the apex
– Fleischer’s ring at the base of cone
– Folds in descemet’s and bowman’s membrane
– Vogt line, i.e. very fine vertical, deep stromal striae which
disappear with external pressure on globe
 On retinoscopy: Yawning/scissors reflex and high oblique/
irregular astigmatism
 On distant direct opthalmoscopy:
– Dark shadow (due to total internal reflexion of light)
– This separates central and peripheral part of cornea (oil
drop reflex)
 Munson’s sign: Localized bulging of lower lid when patient
looks down is positive in later stages (Fig. 5.12)
Complications: Acute hydrops due to rupture of Descemet’s
membrane.
Fig. 5.12: Munson’s sign

Treatment:
 Glasses or Contact lens (rigid gas permeable) in early stages
 Penetrating keratoplasty in later stages
 Intacs (intracorneal ring segments) are useful in early stages.
Mnemonic: “I Had a FAMOUS plan”

I Irregular circles on Placido disc examination
Irregular scissors or yawning reflex on Retinoscopy
Irregular astigmatism
Had Hydrops
F Fleischers ring
A Astigmatism
M Myopia
Munson sign
Malaligned mires on Keratometry
O Oil droplet reflex on direct Ophthalmoscopy
U Vogt lines on slit lamp biomicroscopy
S Stromal thinning in central and peripheral areas
Plan Protrusion (anterior) of cornea
Q. Define corneal opacities. Discuss the causes, types and

Q. List the secondary changes seen in corneal opacities.
Definition: Corneal opacity is loss of corneal transparency due
to any reason.
Causes:
 Congenital
 Healed corneal wound
 Healed corneal ulcer.
Clinical features:
 Loss of vision because of opacity in pupillary area
 Blurred vision because of astigmatic effect (Fig. 5.13).
Type Area involved Opacity  decided

by area affected
Nebula Superficial stroma and Faint opacity
Bowman’s membrane
Macula 1/3–1/2 of corneal stroma Semi dense opacity
Leucomatous > 1/2 of corneal stroma Dense white opacity
(leucoma simplex)
Adherent leucoma Due to healed perforation Incarceration of iris
with incarceration of iris
Corneal facets Depressed scar due to -
defective less fibrous tissue
Keratectasia Corneal curvature is -
increased at scar/opacity
Due to weak scar
Figs 5.13A and B: (A) Optical effect of nebula: Irregular astigmatism, (B) Optical
effect of leukoma: Stops all light which falls upon it; loss of brightness but not
definition
Anterior staphyloma: An ectasia of pseudocornea (the scar

formed from organized exudates and fibrous tissue with
epithelium) which results after total sloughing of cornea with
iris plastered behind it.
Secondary changes seen in the opacities are:
 Hyaline degeneration
 Calcareous degeneration
 Pigmentation
 Atheromatous ulceration.
Treatment:
 Optical iridectomy for central macula/leukoma provides
vision improvement with pupillary dialatation
 Keratoplasty for uncomplicated cases with opacities
 PTK—phototherapeutic keratectomy—nebula with laser
 Cosmetic colored contact lens
 Tattooing of Scar: Inks used gold and platinum.
Q. Define dendritic ulcer. Discuss the etiology, clinical features

and management of the same.
Etiology: Recurrent ocular herpes.
Predisposition factors:
 Fever like malaria, flu, exposure to UV radiation
 General ill health
 Emotional/physical exhaustion.
Symptoms:
 Redness
 Lacrimation
 Acute pain
 Photophobia
 Blurring.
Signs:
 Circumciliary congestion
 Superficial punctate keratitis  later they desquamate to
form erosions  erosions coalese with each other and spread
in all directions and send lateral branches with knobbed ends
 resulting in dendritic ulcers
 Staining: Base of the ulcer stains with flourescein and margin
with rose Bengal
 Corneal sensation may be diminished or absent.
Treatment:
 Antiviral Drugs:
– Acyclovir 3% ointment 5 times a day
– Ganciclovir gel
– Treflurothiamine 1% drop
– Vidarabine
 Mechanical debridement of wound
 Atropine 1% eyedrops
 Improvement of general health

 Cryosurgery or cautery for resistant cases.
Q. Define Paracentesis. List the indications for the same.
Definition: Opening the anterior chamber for the purpose of aspiration
of its contents partially/fully is called Paracentesis (Fig. 5.14).
Indications:
Diagnostic: Aqueous humor study for Therapeutic
Intraocular tumor: Cytology and Massive hyphema to control

LDH enzyme assay secondary glaucoma
Intraocular parasite infestation Corneal ulcer with massive
hypopyon
Impending corneal perforation
Central retinal artery occlusion
To control secondary glaucoma
following; Iridocycilitis, traumatic
cataract with soft lens matter in
anterior chamber
Fig. 5.14: Paracentesis

Q. Differentiate between superficial and deep corneal

vascularization.
Superficial corneal vascularization Deep corneal vascularization
Corneal vessels can be traced over Corneal vessel end abruptly at the
the limbus into the conjunctiva limbus
Vessels are bright red and well Vessels are ill-defined and cause only a
defined diffuse reddish blush
Superficial vessels branch in an Deep vessels run parallel to each other
arborescent fashion in a radial fashion
Superficial vessels raise the epithe- Deep vessels do not disturb corneal
lium and make the corneal surface surface
irregular
Q. List the causes of corneal vascularization.

The causes of corneal vascularization are:
Superficial vascularization Deep vascularization
(mnemonic: Graft DISC)
Contact lens users Graft rejection
Superficial corneal ulcer Disciform keratitis
Trachoma Deep corneal ulcers
Rosacea keratitis Interstitial keratitis
Phlyctenular Keratoconjunctivitis Sclerosing keratitis
Chemical burns
6.
Diseases of the Sclera
Q. Define Episcleritis. Discuss the etiology, clinical features,

Q. What is Episcleritis periodica/Episcleritis peri fuxa?
Definition: Episcleritis is recurrent inflammation of episclera,
involving tenon’s capsule but not the underlying sclera (Fig. 6.1).
Etiology:
 Seen in adults
 Females are affected more than male
 Exact etiology is not known
 It is associated with gout, psoriasis, rosacea
 It is considered as a hypersensitive reaction to streptococcal
and tubercular antigens.
Pathology: The following are noted
 Localized lymphocytic infiltration of sclera
 Edema and congestion of tenon’s capsule.
Fig. 6.1: Episcleritis

Clinical features:
Symptoms:
 Redness
 Discomfort: Gritty, burning and foreign body sensation
 Photophobia
 Lacrimation.
Signs: On examination two clinical types are noted

Diffuse Episcleritis Nodular Episcleritis
Although the whole of eye is It is pink/purple flat and surrounded by
involved, 1–2 quadrants are injection
affected more Usually situated 2–3 mm from limbus. It is
firm, tender and the overlying mucosa moves
freely
Clinical course:
 Episcleritis runs a limited course of 10 to 20 days and resolves
spontaneously
 Recurrence is common and tends to occur in bouts. Rarely a
fleeting type of disease Episcleritis periodica/Episcleritis peri
fuxa, may occur.
Differential diagnosis Complications
Inflamed pingecula Recurrence
Due to foreign body Chronic episcleritis
Scleritis Scleritis
Sclerokeratitis
Conjunctival adherence to sclera after
repeated attacks
Diseases of the Sclera 125
Treatment:
 Topical steroids fourth hourly
 Cold compression relieves symptoms
 NSAIDs: Indomethacin, flurbiprofen, oxyphenbutazone.
Q. Define Scleritis. Discuss the etiology, clinical features,

Q. What is Scleromalacia perforans?
Definition: Scleritis is chronic inflammation of sclera proper.
It is a more serious disease than episcleritis.
However, it has a lesser incidence than episcleritis.
Etiology:
 Age affected: 40 to 70 years
 Sex: Affects female than males.
Following are its associations:

 Autoimmune diseases like rheumatoid arthritis and SLE
 Staphylococcal, Herpes Zoster and streptococcal infections
 Metabolic: Thyrotoxicosis
 Granulomatous diseases: TB, syphilis, leprosy, sarcoidosis
 Miscellaneous: Irradiation, chemicals, Vogt-Koyanagi-Harada
syndrome, Behcet’s disease and rosacea
 Surgically induced
 Idiopathic.
Pathology: Deposition of immune complex in the sclera leading

to inflammation  marked infiltration of lymphocytes in the
scleral lamellae with edema breakdown of swollen lamellae
with necrosis scleral thinning simultaneous inflammation
of the uveal tract, causing uveitis.
Classification of scleritis:
A. Anterior scleritis
 Non-necrotizing scleritis
– Diffuse
– Nodular
 Necrotizing scleritis
– With inflammation
– Without inflammation (scleromalacia perforans).
B. Posterior scleritis.
Clinical features:
Symptoms:
 Severe boring pain, making patient to wake up in early
morning and radiates to jaw and temple
 Localized or diffuse redness
 Photophobia
 Lacrimation
 Diminution of vision.
Signs:
Non-necrotizing diffuse scleritis (commonest):
 Involves 1 or more quadrants
 Involved area appears pinkish/purple.
Non-necrotizing nodular scleritis:

 Charecterized by 1 or 2 hard purplish elevated scleral nodules,
near the limbus
 Sometimes the nodules may be arranged in a ring around the
limbus (annular scleritis).
Fig. 6.2: Necrotizing scleritis
Anterior necrotizing scleritis with inflammation (Fig. 6.2):

 Is acute severe form of scleritis associated with severe
inflammation
 Vasculitis causes local infarction and thinning of sclera which
becomes thin and transparent
 Associated with uveitis.
Anterior necrotizing scleritis without inflammation:

(Scleromalacia perforans):
 Typically occurs in elderly females suffering from rheumatoid
arthritis
 Charecterized by development of yellowish patch of melting
sclera (due to obliteration of arterial supply)
 The patch along with overlying conjunctiva and episclera
often separates from the surrounding normal sclera
 This sequestrum of sclera becomes dead white in color and is
absorbed leaving behind a large punched out lesion.
Posterior scleritis:
 It is inflammation of the sclera behind the equator
 The condition is frequently misdiagnosed
 It is associated with: Retinal detachment, macular edema,
proptosis and limited ocular movements.
Fig. 6.3: Sclerosing keratitis

Complications:
 Sclerosing keratitis (Fig. 6.3)
 Keratolysis
 Secondary cataract.
Investigations:
 Complete hemogram
 Urine routine
 Serum for Complement (C3) levels, immune complexes, auto-
immune antibodies, Rh factor
 Montoux, VDRL
 Serum uric acid for gout
 X-ray chest, sacroiliac joints and paranasal sinuses
 B scan to detect posterior uveitis.
Treatment:
A. Non-necrotizing scleritis:
 Topical steroids
 Indomethacin 100 mg/day.
B. Necrotizing scleritis:
 Topical/oral steroids
 Subconjunctival injection of steroids
 Methotrexate and cyclosporine for non-responsive cases.
Q. Compare and contrast Episcleritis and Scleritis.

Episcleritis Scleritis
Definition Episcleritis is recurrent Scleritis is chronic inflammation
inflammation of episclera, of sclera proper
involving tenon’s capsule
but not the underlying sclera
Symptoms Redness is main presentation Severe boring pain is the main
presentation
Signs Less tender More tender nodule
Color: Bright red Purplish in color
No features of uveitis Associated with uveitis
Drug test Quick blanching of blood No such blanching of blood
with 10% vessels vessels
phenylep-
hrine
Prognosis Favorable, complications Poor, complications are
are rare common
Q. What is blue sclera? List the differential diagnosis for the

same.
Blue sclera is a asymptomatic condition charecterized by marked,
generalized blue discoloration of sclera due to thinning.
It is typically associated with the following:
 Osteogenesis imperfecta
 Marfan’s syndrome
 Ehler-Danlos syndrome
 Pseudoxanthoma elasticum
 Buphthalmos
 High myopia
 Healed scleritis.
Q. Define staphyloma. Discuss its types, etiology and
management.
Q. What is anterior staphyloma?
Definition: Staphyloma refers to a localized bulging of a weak
and thin outer layer of eyeball (cornea or sclera); lined by uveal
tissue which shines due to thinned out fibrous coat (Fig. 6.4).
Type of Etiology Affected part of the
staphyloma outer layer of eyeball
Anterior Ectasia of the pseudocornea (Scar Cornea
formed from organized exudates
with fibrous tissue covered by
epithelium which results after
total sloughing of cornea with
iris plastered behind)
Intercalary Peripheral corneal ulcers Limbal area with
Healing perforations backing of root of iris
Ciliary Perforation Sclera lined by ciliary
Scleritis body 2–3 mm from
Absolute glaucoma limbus
Equatorial Scleritis Sclera in the region of
Degeneration of sclera in equator lined by
pathological myopia choroid specially where
vortex veins enter
Posterior Pathological myopia Sclera lined by choroid
Posterior scleritis behind the equator
Perforation injuries
Fig. 6.4: Different types of staphylomas
Treatment:
 Inflammatory conditions of the sclera like scleritis, corneal
ulcer, keratomalacia, rheumatoid arthritis are to be taken care
of
 Local excision and repair with a scleral patch graft can be
performed
 For large unsightly eye:
– Staphylectomy and keratoplasty to be done
– Enucleation with implant placement can be done.
7.
Diseases of the Uveal Tract
Q. Define uveitis. Discuss the classification, etiology, pathology,

clinical features, complications and management of uveitis.
Q. Define and discuss the classification of uveitis.
Q. Discuss the classification, etiology, pathology, clinical
features, complications and management of iridocyclitis or
anterior uveitis.
Q. What are Keratic Precipitates (KP)? Mention its types.
Q. Discuss the anterior chamber signs of iridocyclitis.
Q. What is aqueous flare? Discuss its importance.
Q. What are irish nodules?
Q. What is seclusio pupillae?
Q. What is iris bombe?
Q. What is occlusio pupillae?
Q. List the complications of iridocyclitis.
Q. Discuss the management of iridocyclitis.
Q. What is mydricaine?
Inflammation of uveal tract is called uveitis.
Figure 7.1 shows classification of uveitis depending on the
location.
Diseases of the Uveal Tract 133
Fig. 7.1: Classification of uveitis

Pathology of uveitis:
Inflammation is same as elsewhere in the body but because of the
more vascularity and looseness of the uveal tissue inflammation
is exaggerated and gives special results.
Pathologically uveitis can be classified as follows:
 Suppurative
 Non-suppurative (wood’s classification)
– Granulomatous and non-granulomatous.
Pathology of suppurative uveitis:
 This is due to exogenous infection by pyogenic organisms
 It is usually a part of endophthalmitis or panophthalmitis
 All the cavities (anterior, posterior, vitreous) get filled with pus
 Uveal tissue becomes thick and necrotic.
Pathology of granulomatous uveitis:

 Granulomatous uveitis is a chronic inflammation proliferative
in nature
 Etiology:
– Foreign body in eye
– Hemorrhage or necrotic tissue in eye
– Non-pyogenic and non-virulent organisms: TB, leprosy,

syphilis, brucellosis
– Also seen in Vogt-Koyanagi-Harada disease, sarcoidosis
and sympathetic ophthalmitis
 Pathological features:
– Infiltration and local multiplication of neutrophils and
lymphocytes
– Formation of epithelioid and gaint cells.
Pathology of non-granulomatous uveitis:
 It can be acute or chronic
 Usually involves iris and ciliary body
 It is usually induced by physical insult, toxins and hyper-
sensitivity
 Pathogenesis: Inflammation leads to marked dialatation and
increased permeability of blood vessels leading to fibrinous
exudates and infiltration of WBC’s
Iridocyclitis or anterior uveitis may be:
Acute: Both symptoms and signs are present
Chronic: Symptoms are absent but signs are present.
Symptoms:
 Pain: Dull aching throbbing pain worst at night, radiates to
scalp and forehead
 Redness: Due to circumcorneal congestion
 Photophobia and blepharospasm
 Lacrimation
 Defective vision to total loss of vision.
Signs: Slit lamp biomicroscope examination reveals the following

1. Signs of anterior uveitis (Fig. 7.2)
2. Lid: Mild edema
3. Circumcorneal congestion: Mild in chronic cases and severe
in acute cases. To be differentiated from superficial corneal
congestion occurring in acute conjunctivitis
4. Corneal signs:
a. Corneal edema due to toxic endothelitis and increased IOP
b. Keratic precipitates (KP).
Definition: They are proteinaceous cellular substance at the back
of the cornea arranged in triangular fashion (Due to current of
aqueous humor) (Fig. 7.3).
The composition and morphology of KP varies with:
 Severity
 Size: Small, medium and large
Fig. 7.2: Signs of anterior uveitis

Fig. 7.3: Slit-lamp examination in acute iridocyclitis
 Type
 Age: Fresh and old KP.
Following are the different types of KP:
Type of KP Etiology Composition Number of cells Appearance
Mutton fat Granulomatous Epithelioid cells, 10–15 Thick, fluffy,
KP iridocyclitis macrophages lardaceous, greasy
Medium and Non- Lymphocytes 100s hence Small, discrete,
small KP or granulomatous called as dirty white,
granular KP uveitis endothelial irregularly
dusting arranged
Red KP Hemorrhagic Neutrophils, High in They appear red
uveitis lymphocytes number
and RBC‘s
Old KP Healed uveitis Any of the Any of the Mutton fat KP
above three above have ‘ground glass’
after healing appearance after
healing
Contd...
4. Anterior chamber signs:

a. Aqueous cells: It is an early feature of iridocyclitis
Grading of aqueous cells:
Cell number Grade Tyndall effect on slit lamp
0 – Clear aqueous humor
1–5 –/+ Aqueous humor near clearly
6–10 +1 Cells identifiable
11–20 +2 Cells definitely identifiable
21–50 +3 Hazy iris details
> 50 +4 Aqueous humor appears white, hypopyon may appear
b. Aqueous flare:
 It is because of the protein particles from the damaged
blood vessels, causing a tyndall effect
 It is usually seen in non-granulomatous uveitis and
minimal granulomatous uveitis
 Grading of Aqueous flare:
Flare Grade Tyndall effect

No flare 0 Nil
Faint +1 Just detectable
Moderate +2 Iris details clear
Marked +3 Iris details hazy
Intense +4 Severe fibrinous exudate
c. Hypopyon:
 Heavy, thick, sterile exudate settles down in the lower
part
 Classically seen in Behcet’s syndrome
d. Hyphema:
 Is blood in anterior chamber
 Seen in hemorrhagic uveitis and trauma
e. Change in depth and shape of anterior chamber:
 Deep and irregular in posterior synechiae
 Funnel shaped in iris bombe
f. Changes in angle of anterior chamber:
 This is noted in gonioscopy examination
 In active stage there is cellular deposition and in chronic
stage there is peripheral anterior synechiae.
5. Iris:
a. Loss of normal pattern of iris due to edema in acute phase
and atropic changes in chronic stages
b. Change in iris color: Muddy in acute stage and hypopigmented
in healed areas
c. Irish nodules: Typically seen in granulomatous uveitis
Koeppe’s nodules (Fig. 7.4) Busacca’s nodules
Incidence Most common Relatively rare
Size Smaller Large
Site of appearance Situated in pupillary border Situated on the surface
of iris
Fig. 7.4: Koeppe’s nodules seen in tuberculosis
d. Neovascularization: Is a feature of chronic iridocyclitis

e. Posterior synechiae:
 Definition: It is adhesion between the anterior lens
surface and the posterior surface of iris
 Cause: It is caused due to organization of fibrin rich
exudates
 Morphologically posterior synechiae can be segmental,
annular or total (Figs 7.6A to D)
– Segmental posterior synechiae: Adhesion of iris to
the lens is at some point
– Annular posterior synechiae (Ring synechiae):
• Ring synechiae are 360° adhesions of pupillary
margin to the anterior capsule of lens
• Those prevents the circulation of aqueous humor
from posterior to anterior chamber (Seclusio
Pupillae)
• The aqueous humor collects behind the iris and

pushes it forward leading to Iris bombe formation,
followed by rise in IOP
– Total posterior synechiae (Fig. 7.5):
This is due to total plastering of the posterior surface
of iris to the anterior lens surface. This results in
deepening of anterior chamber.
Fig. 7.5: Posterior synechia
6. Pupillary signs:
 Narrow pupil: Due to irritation and edema of sphincter
pupillae and engorgement of radial veins
 Irregular pupillary size: Due to segmental posterior
synechia
 Ectropion pupillae: Due to contraction of fibrinous exudate
 Pupillary reflex is sluggish or absent
 Occlusio pupillae: Pupil is completely occluded due to
organization of exudates across entire pupillary area.
7. Lens:
 Pigment dispersal is noted on anterior chamber
 Exudates may be deposited on lens
 Complicated cataract.
8. Vitreous: Shows exudates and inflammatory cells
Figs 7.6A to D: (A) Annular or ring synechiae; (B) Total posterior synechiae;
(C) Occlusio-pupillae; (D) Cyclitic membrane
Complications:
 Secondary glaucoma (Early or late)
 Cyclitic membrane: Formed due to fibrosis of exudates behind
lens
 Choroiditis
 Retinal complications: Detachment, degeneration and cystoid
macular edema
 Papillitis
 Band shaped keratopathy
 Phthisis bulbi.
Investigations:
 Hematological:
– TC and DC to have a general information about inflam-
matory response of the body
– ESR to ascertain existence of any chronic inflammation
in the body
– Blood sugars to rule out diabetes
– Blood uric acid levels to rule out gout
– Serological tests to rule out syphilis and toxoplasmosis
– Tests for Rh factor and antinuclear antibodies
 Urine routine to rule out urinary tract infection
 Stools for cyst or ova
 X-ray of following regions to rule out infective foci: Chest,
paranasal sinuses, spine and sacroiliac joints
 Skin test: To rule out TB and Toxoplasmosis.
Treatment of iridocyclitis:
Nonspecific treatment:
1. Local treatment:
A. Mydriatic- cyclopegic drugs:
 Commonly used drugs:
• 1% atropine sulfate
• In case of atropine allergy 2% homatropine or 1%
cyclopentolate is used
• Mydricaine, a mixture of atropine, adrenaline and procaine
 Route of administration:
• 1% atropine sulfate, 2% homatropine and 1%
cyclopentolate: Eye drops or ointments
• Mydricaine is given as subconjunctival injection
 Mechanism of action:
• Relives spasm of iris hence gives comfort and rest
• Prevents formation of synechiae and breaks it if already
formed
• Decreases exudation by decreasing hyperemia and
vascular permeability
• Increase blood supply to anterior uvea by releaving
pressure on the anterior ciliary artery.
B. Corticosteroids:
 Commonly used drugs: Betamethasone, Dexamethasone,
Prednisolone, Hydrocortisone
 Route of administration:
• Eye drops 4 to 6 times daily
• Eye ointment at bed time
• Subtenon injection in severe cases
 Mechanism of action: Anti-inflammatory, anti-allergic and

anti-fibrotic (Mnemonic: 3A’s).
C. Broad-spectrum antibiotics: Used as umbrella cover for
topical steroids
2. Systemic treatment:
A. Corticosteroids:
 Most useful in non-granulomatous uveitis where uveitis
is due to antigen-antibody reaction
 Also indicated in intractable anterior uveitis resistant to
topical therapy
 Mechanism of action: Anti-inflammatory, anti-allergic and
anti-fibrotic (Mnemonic: 3A’s)
 Drug of choice and duration of usage: Prednisolone, 60 to
100 mg as daily or alternate day therapy, tapered
completely in about 6 to 8 weeks.
B. NSAID’s:
 Like aspirin is used
 Phenylbutazone and oxyphenbutazone are useful in uveitis
associated with rheumatoid disease.
C. Immunosuppressive drugs:
Indication Common drugs used Mechanism of action
Severe cases where there Cyclophosphamide Antiproliferative more on B
is risk of blindness cells than on T cells
Specially indicated in Cyclosporine Antiproliferative selective on
the following: T lymphocytes
Vogt-Koyanagi-Harada disease Azathioprine Purine antimetabolite
Sympathetic ophthalmitis Antiproliferative
Behcet’s syndrome Methotrexate Folate antagonist
Pars planitis Chlorambucil Weak immunosuppressant
3. Physical measures:
 Hot fomentation: Is very soothing, diminishes pain,
increases circulation and decreases venous stasis
 Dark Goggles: Give a feeling of comfort by reducing
photophobia, blepharospasm and lacrimation, specially in
sunlight.
Specific treatment of the cause:
 Local treatment decreases uveitis but does not cure the disease
resulting in relapse
 Hence it is important to find out and treat the cause
Ex: Antitubercular drugs in tuberculosis
 Broad-spectrum antibiotics are useful in non-granulomatous
uveitis.
Treatment of complications:
Complications Treatment
Inflammatory glaucoma 0.5% Timolol maleate BID or
Acetazolamide 250 mg TID
Post-Inflammatory glaucoma Laser iridectomy
Due to ring synechiae or Surgical iridectomy
Complicated cataract Lens extraction
Retinal detachment Vitrectomy
Phthisis bulbi Enucleation
Q. Compare and contrast granulomatous and non-granulo-

matous uveitis.
Features Granulomatous uveitis Non-granulomatous uveitis
Onset Insidious Acute
Pain Minimal Marked
Photophobia Slight Marked
Ciliary congestion Minimal Marked
Keratic precipitates Mutton fat KP Small
Aqueous flare Mild Marked
Iris nodules Usually present Absent
Posterior synechiae Thick and broad based Thin and tenuous
Fundus Nodular lesions Diffuse involvement
Q. Compare and contrast acute conjunctivitis and acute

iridocyclitis.
Q. Compare and contrast acute conjunctivitis and acute
congestive glaucoma.
Q. Compare and contrast acute iridocyclitis and acute
congestive glaucoma.
Features Acute Acute Acute congestive

conjunctivitis iridocyclitis glaucoma
Onset Gradual Usually gradual Sudden
Pain Mild Moderate in Severe in eyes
discomfort eye and along the and the entire
first division of trigeminal area
trigeminal nerve
Discharge Mucopurulent Watery Watery
Colored May be present Absent Present
halos
Vision Good Slight impaired Markedly impaired
Congestion Superficial Deep ciliary Deep ciliary
conjunctiva
Tenderness Absent Marked Marked
Pupil Normal Small and irregular Large and vertically
oval
Media Clear Hazy due to KPs, Hazy due to
aqueous flare and edematous cornea
pupillary exudates
Anterior Normal May be deep Very shallow
chamber
Iris Normal Muddy Edematous
Intraocular Normal Usually normal Raised
pressure
Constitutional Absent Little Prostration and
symptoms vomiting
Q. Define posterior uveitis. Discuss the etiology, clinical types,

Q. Define choroiditis. Discuss the etiology, clinical types, clinical
features, complications and management of the same.
Definition: Posterior uveitis or choroiditis refers to inflammation
of the choroid.
Due to the close proximity of the outer layer of retina with the
choroid and also as retina is dependent on choroid for nutrition,
choroiditis almost always involve retina causing chorioretinitis.
Etiology: It is same as uveitis.
Clinical types:
A. Suppurative choroiditis: It is almost always a part of endophthalmitis
B. Non-suppurative choroiditis:
 May be granulomatous or non-granulomatous
 This is usually bilateral
 Depending upon the number of cells and localization of
the lesion, morphologically it can be classified into the
following: Diffuse, disseminated and circumscribed
Type Description/lesion location Etiology
1. Diffuse Diffuse spreading lesion Tuberculosis
Choroiditis Involves most of choroid Syphilis
2. Disseminated Multiple small areas of
Choroiditis inflammation
Spreads all over the choroid
3. Circumscribed Choroiditis (localized or focal) (Fig. 7.7)
Which is once again described by the names depending on the location
Contd...
Contd...
a. Central Macular area Tuberculosis
Choroiditis Syphilis
Toxoplasmosis
Histoplasma
Visceral larva migrans
b. Juxtacaecal Area adjoining optic disc Jensen’s choroiditis
Choroiditis
c. Anterior Peripheral parts of choroid Syphilis
peripheral (Anterior to equator)
Choroiditis
d. Equatorial Only in equator
Choroiditis
Figs 7.7A and B: (A) Types of circumscribed choroiditis;

(B) Features of disseminated choroiditis
Clinical features:
Symptoms:
 Photopsia: Is subjective sensation of flashes of light resulting
due to irritation of rods and cones
 Black spots floating in front of the eye due to large exudative
clumps in vitreous
 Metamorphopsia: Is distorted images of the objects due to
distortion of retinal contour (Fig. 7.8)
 Micropsia: Objects appear small due to separation of rods
and cones
 Macropsia: Objects appear big due to crowding of rods and
cones
 Positive scotoma: That is perception of a fixed large spot in
the field of vision, corresponding to the site of the lesion.
Signs:
 Anterior segment appears to be normal, KPs may be
present
Fig. 7.8: Clinical features of choroiditis

 Vitreous:
– Following are the opacities seen
• Fine opacities: Composed of inflammatory cells
• Coarse opacities: Are result of severe tissue destruction
• Stringy opacities: Are caused by alteration of vitreous
gel
• Snow-ball opacities: Are large opacities found in pars
planitis, sarcoidosis and candidiasis
– Posterior vitreous detachment.
 Fundus: Shows the following features
– Choroiditis:
Features of acute stage Features of healed/atropic stage
Irregular patches Well defined from normal area
Yellow white in color Grayish in color
The lesion is typically deeper The involved area shows white sclera
to the retinal vessels. The over- below the atropic choroid and black
lying retina is often cloudy and pigment clumps at the periphery of the
edematous lesion
– Vasculitis and periphlebitis: Severe periphlebitis in

sarcoidosis results in perivascular granuloma called
“Candle wax dripping”
– Neovascularization
– Exudative retinal detachment
– Optic nerve findings: Optic neuritis or optic atrophy.
Complications:
 Iridocyclitis
 Vitreous degeneration
 Macular edema
 Secondary Periphlebitis retinae
 Retinal detachment
Investigations: Same as iridocyclitis

Treatment:
A. Nonspecific treatment:
 Topical and systemic (septicemic) steroids
 Posterior Subtenon injection of depot corticosteroids
 Rarely immunosuppressant drugs may be required
B. Specific treatment: Directed towards causative agent like ATT,
treatment of toxoplasmosis, treatment of toxocariasis.
Q. Define endophthalmitis. Discuss the etiology, clinical types,
Q. Discuss the clinical picture and management of acute
bacterial endophthalmitis.
Definition: Endophthalmitis is inflammation of the inner
structure of the eye ball (i.e. uvea and retina) associated with
pouring of exudates into anterior chamber, posterior chamber
and vitreous cavity.
Etiology:
A. Infective endophthalmitis:
Causative organisms:
 Bacterial: Mostly gram-positive cocci like Staphylococcus
Epidermidis and Staphylococcus aureus
Other bacterias: Streptococci, Pseudomonas, Pnemococci,
Corynebacterium acne and Actinomyces
 Fungal: Aspergillus, Candida and Fusarium
Modes of infection:
 Exogenous infections: Traumatic perforation, perforation
of corneal ulcer, postoperative infection
 Endogenous infections: Dental infection, Puerperal sepsis,
Septicemia
 Secondary infection from surrounding structures.
B. Non-infective (Sterile) endophthalmitis: This is caused due
to toxin/toxic material
 Postoperative sterile endophthalmitis: Due to chemical
adherent to IOL or instruments
 Post-traumatic sterile endophthalmitis: Due to retained
foreign body like pure copper
 Intraocular tumor necrosis
 Phacoanaphylactic endophthalmitis seen in morgangian
cataract.
Clinical picture of acute bacterial endophthalmitis:
Incidence: 0.1% of all intraocular surgeries.
Source of infection: Periorbital flora, environment source,
contamination from solution and instruments.
Symptoms:
 Acute bacterial endophthalmitis usually occurs seven days
after intraocular surgery
 Severe pain
 Redness
 Lacrimation
 Photophobia
 Loss of vision.
Signs:
 Lids: Red and swollen
 Conjunctiva: Chemosis and circumcorneal congestion
 Cornea: Edematous, cloudy and ring infiltration is noted
 Edges of the wound: Yellow and necrotic
 Anterior chamber: Hypopyon
 Iris: Visible, edematous and muddy
 Pupils: “Yellow reflex”, that is when anterior chamber is filled
with pus, iris and pupil details are not made out
 Vitreous: Is filled with pus. Soon a yellowish white mass is
seen through fixed pupil—“Amaurotic cat’s eye reflex”
 IOP: Initially increases and later decreases as the eyeball shrinks.
Management:
Aqueous or vitreal tap for staining and culture sensitivity to be
taken.
A. Antibiotics: Can be administered in the following ways
1. Intravitreal antibiotics and diagnostic tap:
 This is performed transconjunctively under topical
anesthesia from the area of pars plana
 Two antibiotics are used, one effective against coagulase
negative staphylococci and the other against gram-negative
bacilli
 The following combination can be used
– First choice: Vancomycin 1mg in 0.1 ml plus ceftazi-
dimide 2.25 mg in 0.1 ml
– Second choice: Vancomycin 1 mg in 0.1 ml plus amikacin
0.4 mg in 0.1 ml
– Third choice: Vancomycin 1 mg in 0.1 ml plus gentamycin
0.2 mg in 0.1 ml (Note that gentamicin is retinotoxic)
 If there is no improvement after 48 hours the drug is to be

changed as per culture sensitivity.
2. Subconjunctival injection: For 5 to 7 days to maintain intraocular
concentration
 First choice: Vancomycin 25 mg in 0.5 ml plus ceftazidimide
100mg in 0.5 ml
 Second choice: Vancomycin 25 mg in 0.5 ml plus cefuroxime
125 mg in 0.5 ml.
3. Topical concentrate antibiotic: Used once in every 30 min. A
combination of two drugs one effective against gram-positive
and other against gram-negative organisms
 Vancomycin or cefazoline plus
 Amikacin or tobramycin.
4. Systemic antibiotics: Following are being used, but they have
limited role
 Ciprofloxacin
 Vancomycin and ceftazidime
 Cefazoline and amikacin.
B. Steroidal therapy:
 Use of steroids limits the tissue damage
 Time of usage: 24 to 48 hours after control of infection
 Route of administration: Intravitreal, subconjunctival
injection, topical steroids, systemically
 Drug commonly used: Dexamethasone.
C. Supportive therapy:
 Cycloplegics: 1% atropine/2% homatropine
 Antiglaucoma drugs:
– 0.5% Timolol BID
– Acetazolamide 250 mg TID.
D. Vitrectomy: Is done if conditions would not improve even on

intensive care.
Vitrectomy improves the conditions by removing infective
organisms, toxins and enzymes.
Q. Define panophthalmitis. Discuss the etiology, clinical types,
Definition: Intense purulent inflammation of the whole eyeball
including tenon’s capsule is called panophthalmitis.
Etiology: Same as endophthalmitis
Pathogenesis: Purulent anterior/posterior uveitis  followed
by a short stage of endophthalmitis full fledged picture of
panophthalmitis.
Clinical features:
Symptoms:
 Severe ocular pain
 Headache
 Complete loss of vision
 Profuse watering of eyes
 Purulent discharge
 Marked redness and swelling of eyeball
 Malaise and fever.
Signs:
 Lids: Edema and hyperemia
 Eyeball: Proptosed, ocular movements are limited and painful
 Conjunctiva: Chemosis, circumcorneal and ciliary congestion
present
 Cornea: Cloudy and edematous

 Anterior chamber: Is filled with pus
 Vision: Complete loss of vision, perception of light is absent
 IOP: Raised
 Globe perforation occurs at limbus and the pus comes out.
Complications:
 Orbital cellulitis
 Cavernous sinus thrombosis
 Meningitis and encephalitis.
Treatment:
 Anti-inflammatory and analgesics are to be started to relive
pain
 Broad-spectrum antibiotics to be started
 Evisceration is done to prevent the risk of intracranial infection
(Fig. 7.9).
Fig. 7.9: Evisceration steps in brief

8.
Diseases of Lens
(To make the examination oriented study easy, this chapter has
been discussed under short topics as two long questions may cover
the whole chapter. Also such a thing would be difficult to study.
The questions in examination may be asked in any permutation
and combination)
Q. Define cataract. Classify the same.
Definition: Any opacity of the lens or its capsule whether
congenital or acquired causing visual impairment, is called
cataract (‘Cataract’ means waterfalls).
Classification:
A. Etiological classification:
 Congenital or developmental cataract
 Acquired cataract:
– Senile cataract
– Traumatic cataract
– Complicated cataract
– Metabolic cataract
– Electric cataract
– Radiational cataract
– Toxic cataract, e.g. Steroid induced, miotic induced, copper
(chalosis) and iron induced (siderosis)
– Cataract associated with skin diseases
– Cataract associated with osseous diseases
– Cataract associated with miscellaneous syndrome,
e.g. Down’s syndrome, Lowe’s syndrome.
B. Morphological classification (Fig. 8.1):
Type Subtype if any Part of the lens affected
Capsular Anterior capsular cataract It involves the capsule
cataract Posterior capsular cataract
Subcapsular Anterior subcapsular cataract It involves the superficial
cataract Posterior subcapsular cataract part of the cortex just below
the capsule
Cortical - It involves the major part of
cataract the cortex
Supranuclear - It involves the deeper part of
cataract the cortex, just outside the
nucleus
Nuclear - Involves the nucleus
Cataract
Polar Anterior polar cataract Capsule and superficial part
Cataract Posterior polar cataract of the cortex in the polar
region only
Diseases of Lens 161
Fig. 8.1: Morphological shapes of cataract
Q. What is congenital and developmental cataract? Discuss

the etiology, clinical types and management of the same.
Time at which there is Fibers affected*
disturbance in normal
development of lens fibers
Congenital cataract Before birth Embryonic and/or fetal
fibers are affected
Developmental Infancy to adolescence Infantile and/or adult
cataract fibers
*The fibers laid previously/subsequently will be normal
Etiology: Exact etiology is not known, the following factors have

been attributed:
 Hereditary:
– About 1/3rd of congenital cataracts are hereditary
(Autosomal dominant)
– Common familial cataracts are: Cataract pulverulenta,
zonular cataract, coronary cataract and total soft cataract
 Maternal factors:
– Malnutrition is associated with non-familial zonular
cataract
– Infections: Like rubella, toxoplasmosis and cytomegalo
inclusion disease
– Drug ingestion, e.g. thalidomide, corticosteroids
– Radiation exposure during pregnancy
 Fetal or infantile factors: (Mnemonic: ABCDF)
– A—Anoxia, deficient oxygenation owing to placental
hemorrhage
– B—Birth trauma
– C—Cataract associated with congenital abnormalities,
e.g. as seen in Lowe’s syndrome, myotonia dystrophica
– D—Disorders of metabolism, e.g. Galactosemia
– F—Food factor, malnutrition in early infancy
 Idiopathic (Majority).
Clinical types (Fig. 8.2):

 Congenital capsular cataract (anterior capsular cataract or
posterior capsular cataract)
 Polar cataract (anterior polar cataract or posterior polar cataract)
 Nuclear cataract
 Lamellar cataract
 Sutural and axial cataracts:
– Floriform cataract
– Coralliform cataract
– Spear-shaped cataract
– Anterior axial embryonic cataract
Figs 8.2A to C: (A) Coronary cataract; (B) Anterior capsular cataract;

(C) Posterior capsular cataract
 Generalized cataract:
– Coronary cataract
– Blue dot cataract
– Total congenital cataract
– Congenital membranous cataract.
Clinical features:
Symptoms: It depends on the size and the position of the opacities
 If the opacity is large and central in position, there is marked
visual impairment
 White reflex in the pupillary area
 Abnormal movement of the eye due to squint or nystagmus
might be present.
Signs:
 White reflex is present in the pupillary area
 Plane mirror examination: Black opacity is noted against a
red back round
 Ophthalmoscopic examination: Black opacity is noted against
a red back round
 Detailed examination to note for any associated congenital
abnormalities that may be associated with developmental
cataract: Patent ductus arteriosus, microophthalmos, micro-
cephaly, mental retardation, deafness, dental abnormalities.
Investigations:
 Ocular examination:
– Density and morphology of the cataract is noted based on
child’s vision and ability of the fundus on ophthalmology
– Refraction by retinoscopy under atropine is done in partial

cataract
– Note for any associate ocular pathology like micro-
ophthalmos, glaucoma, rubella retinopathy
– Intraocular pressure is noted
– B-scan USG: To assess posterior segment of the eye in
total cataract to rule out associated retinal detachment or
retinoblastoma
– A-scan USG: To record and compare the axial length of
the two eyes
 Laboratory investigations in non-hereditary cataract to detect
the cause and systemic associations:
– TORCH test: Patient and the maternal serum are tested
for antibody titers
– Test for Galactosemia (reducing substance in urine, RBC
transferase levels and galactokinase levels)
– Lowe’s syndrome: Urine chromatography for amino acids
– Blood sugars for hyperglycemia
– Hypocalcemia by serum calcium, phosphates and X-ray
skull.
Treatment:
 No treatment is required if the vision is good
 Partial cataract and small central cataract which are visually
insignificant can be ignored and observed or may need non-
surgical treatment with pupillary dialatation
 Surgery:
Indications for pediatric Timing of surgery Surgical procedures
cataract surgery employed
All dense cataract Unilateral dense Optical iridectomy
(unilateral or bilateral) cataract: day after Anterior capsulotomy and
the birth, Bilateral irrigation aspiration of lens
dense cataract: matter
within 6 weeks Lensectomy
after birth
 Correction of pediatric aphakia:

– Children above the age of 2 years: Implantation of
PCIOL
– Children below the age of 2 years:
• Extended wear contact lens
• Spectacles may be prescribed in bilateral cases
 Correction of amblyopia (refer the chapter on strabismus).
Q. Define lamellar/zonular cataract. Discuss the etiology,

characters and management of lamellar cataract.
Definition: Lamellar or zonular cataract refers to Developmental
cataract in which the opacities occupy a Discrete zone in the
lens (Fig. 8.3).
Etiology:
 D—Dominant, Autosomal dominant pattern of inheritance
 D—Vitamin D deficiency has been attributed
 D—Disease—Maternal rubella infection
(Mnemonic: 5D’s of lamellar cataract: Developmental cataract,
Discrete pattern in lens, Autosomal Dominant, Vitamin D
deficiency, Disease-maternal rubella)
Fig. 8.3: Zonular cataract
Characteristics: (Mnemonic: LMNOP)

 Laterality: Bilateral and frequently causes severe visual defects
 Main mass (except for the opacities) of the lens internal and
external to the zone of cataract is clear
 Nucleus affected: Fetal nucleus surrounding the embryological
nucleus
 Opacities: Linear opacities, like spokes of a wheel that extend
outwards towards the equator (pathognomonic)
 Photophobia: Child may present with photophobia due to light
scattering.
Treatment: Same as other developmental cataract.
senile cataract.
Q. Discuss the stages of maturation of senile cataract and
Q. Discuss in detail the signs of senile cataract and
Note: You can find the answer for the above questions in smaller
questions below. However, the questions can appear in any
permutation and combination.
Q. Discuss the etiology of senile cataract.

Senile cataract is an age related process. The following have
been attributed for the onset and maturation of senile cataract.
 DNA—Hereditary; plays an important role in onset and
maturation of the cataract
 UltraViolet radiations: Exposure to UV radiations has been
attributed in both onset and maturation of cataract
 Dietary factors: Dietary deficiency of proteins, essential
minerals and vitamins (riboflavin, vitamin E and C) has been
attributed
 Dehydration crisis: Episode of severe dehydration crisis
(diarrhea and cholera)
 Smoking:
– Cyanates in smoke causes carbamylation and protein
denaturation
– 3 hydroxykynurenine and chromophores lead to yellowing.
(Mnemonic: Watching more DVDD’S causes senile cataract -
Dietary factor, ultraViolet radiations, Dehydration crisis, DNA-
Hereditary, Smoking)
Q. Classify senile cataract.
Morphologically senile cataract occurs in two forms:
A. Senile cortical cataract (Soft cataract)
 Cuneiform cataract (70% of all senile cataract cases)
 Cupuliform cataract (5% of all senile cataract cases)
B. Senile nuclear cataract (Hard cataract) (25% of all senile
cataract cases).
Q. Discuss the pathogenesis of senile cataract.

Q. Discuss the mechanism of loss of transparency of lens in
senile cataract.
Mechanism of loss of transparency is different in cortical and
nuclear senile cataract.
Mechanism of loss of transparency in cortical senile cataract:
 With increasing age decrease in the functioning of active
transports pump mechanism of the lens  reversal of the
sodium/potassium pump hydration of fibers
 With increasing age reduced oxidative reaction decrease
levels of amino acids decrease synthesis of proteins in the
lens fibers
 The above lead to denaturation of proteins opacification
of cortical lens fibers.
Mechanism of loss of transparency in nuclear senile cataract:
 Intensification of the age related nuclear sclerosis associated
with dehydration and compaction of the nucleus
 Significant increase in water insoluble proteins, but the total
protein content and the distribution of cations remain normal
 There may or may not be deposition of urochrome and/or melanin.
Q. Discuss in detail the stages of maturation of senile cataract/

nuclear senile cataract/cortical senile cataract.
Stages of maturation of senile cataract:
Stages of maturation of cortical senile cataract:
1. Stage of lamellar separation (Fig. 8.4):
 The earliest senile change is demarcation of cortical fibers
owing to separation by fibers
 This can be demonstrated by slit lamp

 It is reversible change.
2. Stage of incipient cataract: In this stage early detectable
opacities with clear areas in between them are seen. Two types
can be noted in this stage (Fig. 8.5)
 Cuneiform cataract:
– These are wedge shaped spokes of opacities at the
periphery and gradually encroach towards the center
(Opacities are present on both anterior and posterior cortex)
– First seen in lower nasal quadrant
Fig. 8.4: Stage of lamellar separation
Figs 8.5A and B: Diagrammatic depiction of immature senile cataract (cuneiform

type): (A) as seen by oblique ilumination; (B) in optical section with the beam of
the slit-lamp
Fig. 8.6: Incipient cataract
– Visual disturbance are noted at a comparatively later

stage as this form of cataract starts in the periphery and
moves towards the center
 Cupuliform cataract:
– Starts as a saucer shaped opacity in the posterior cortex
just beneath the capsule (Fig. 8.6)
– Cupuliform cataract lies in the pathway of the axial rays
and hence causes an early loss of visual acuity.
3. Immature senile cataract:
 Lens appears grayish white
 Irish shadow is present
 In some patients at this stage (may persist in next stage).
Lens becomes swollen due to continued hydration. This
condition is called as ‘intumescent cataract’ (Fig. 8.7).
Fig. 8.7: Intumescent cataract
4. Mature senile cataract:

 Opacification becomes complete and the whole of the
cortex is involved (Fig. 8.8)
 Lens becomes pearly white in color. Such a cataract is
called ‘ripe cataract’.
5. Hypermature senile cataract:
 Hypermature cataract sets in when mature cataract is left
in situ (Fig. 8.8)
Fig. 8.8: Mature, immature, hypermature cataract

 The hypermature cataract may occur in any of the two forms:

– Morgagnian type: In some patients, cortex liquefies
the lens is converted into a bag of milky fluid small
brownish fluid settles at the bottom (changes the
position with change in position of head) calcium
deposition may happen
– Sclerotic type: In some patients, cortex disintegrates
 water leaks  hence lens shrinks  anterior
chamber becomes deep and iridodonesis is noted.
Stages of maturation of nuclear senile cataract (Fig. 8.9):
 Sclerosis lens becomes inelastic and hard inability to
accommodate obstructs light
 These changes starts centrally and move to the periphery
 Pigmentation may result in different color of the cataract:
– Amber color (most common)
– Brown (cataract brunescence)
– Black (cataract nigra)
– Reddish (cataract rubra).
Fig. 8.9: Senile nuclear cataract

Q. Discuss the clinical features of senile cataract.

Q. What is second sight?
Clinical features of senile cataract:
Symptoms:
 Glare to bright light
 Uniocular polyopia: Doubling or trebling of objects due to
variable refractive error of the lens
 Colored holos: Due to breaking of white light into colored
spectrum due to presence of water droplets in lens
 Black spots in front of the eye
 Image blur, distortion of images and misty vision
 Loss of vision:
– Is painless, gradual and progressive in nature
– Patients with central opacities (e.g. Cupuliform cataract)
have early loss of vision. These people see better when
pupil is dilated in dim light
– In patients with nuclear sclerosis, distant vision deteriorates
due to progressive index myopia. Such patients may be
able to read without Presbyopic glasses (Fig. 8.10). This
improvement in near vision is referred to as ‘second sight’.
But as opacification progresses, vision steadily diminishes,
until only perception of light and accurate projection of
rays remain in stage of mature cataract.
Fig. 8.10: Nuclear cataract—Progressive myopia
Signs of senile cataract:

Examination Different types/stages of senile cataract
Nuclear Immature Mature Hypermature Hypermature
Morgagnian Sclerotic
Visual acuity* 6/9 to PL + 6/9 to FC+ HM+ to PL+ PL+ PL+
Color of lens Gray, Grayish Pearly white Milky white Dirty white
amber white with shrinking with hyper
brownish white spots
nucleus
Irish shadow Seen Seen Not seen Not seen Not seen
Distant direct Central Multiple No red glow No red glow No red glow
opthalmoscopy dark area dark areas but white but white
with dilated against against pupil due pupil
pupil red fundal red fundal to complete
glow glow cataract
Slit-lamp Nuclear Areas of Complete Milky white Shrunken
examination opacity normal cortex is shrunken cataractous
clear with cata- cataractous brownish lens with
cortex ractous nucleus thickened
cortex anterior
capsule
* FC-Finger counting, HM- Hand movement, PL-perception of light
Q. Grade the nucleus hardness on slit-lamp biomicroscopy.

Grading of nucleus hardness on slit-lamp biomicroscopy:
Grades of hardness Description of hardness Color of nucleus
I Soft Greenish yellow
II Soft-medium Yellowish
III Medium-hard Amber
IV Hard Brownish
V Rock hard Blackish
Q. List the complications of senile cataract.

Complications of senile cataract are as follows:
 Phacoanaphylactic uveitis: Due to leakage of lens protein into
anterior chamber from hypermature cataract
 Lens induced glaucoma: Due to swollen lens or leakage of
lens protein
 Subluxation or dislocation of lens.
Q. How do you investigate a case of senile cataract?

Q. Discuss in detail the preoperative investigations of senile
cataract.
Q. Discuss macular function tests in detail.
Investigations prior to surgery are as follows:
A. History:
 Any trauma or inflammation of the eye
 Of drug intake/Drug allergy
 Any posterior segment disease like macular lesions, venous
thrombosis, vitreal hemorrhage in the past
Nature of glasses using in the past

DM, HTN, cardiac problems, bronchial asthma, dental,
ENT problems and urinary problems.
B. Local investigations:
 Ocular examination:
Test Comment/importance of the test

Vision and refraction For documentation
of the eye to be
operated
Perception of light (PL) If the eye has ‘no PL’ a favorable prognosis is unlikely
Projection of rays (PR) It indicates gross function of the peripheral retina. It tells
or light projection nothing about the condition of the macula
‘Accurate’ PR: rules out possibility large retinal detachment
or an absolute field defect
‘Inaccurate’ PR: seen in retinal detachment, chorioretinal
atropy or advanced glaucoma
‘Inaccurate’ PR: does not indicate inoperable situation
Pupil for light reaction To estimate the ability of the pupil to dilate before surgery
Slit lamp examination To evaluate type and extent of cataract
To evaluate health of cornea
To find out evidence of old iridocyclitis
To find out any pathology of anterior segment of the eye
Intraocular pressure To rule out glaucoma
Patency of lacrimal To identify any lacrimal pathology and to treat the
apparatus same before surgery
Fundoscopy To rule out diabetic retinopathy and age related macular
degeneration
 Conjunctival swab for culture and sensitivity (Not routinely

done)
 Calculation of IOL power (see next question)
 Macular function test: It helps to predict the visual potentials

of the eyes with opaque media.
Test Comment/importance of the test
Two point In a dark room patient looks at an opaque disc with 2 holes
discrimination behind which is a light source
If the patient is able to appreciate presence of two light macular
function is good
Maddox rod test The patient is asked to look at a distant light through the Maddox
(Fig. 8.11) rod
If the red line of light is continuous and unbroken macular
function is probably good
Color vision test If the patient is able to identify red, green or blue light in presence
of opaque medium his macular function is probably good
Pupillary light reflex This should be brisk even in the presence of mature cataract 
this indicates good optic nerve function
Purkinje’s Entoptic Patient can see his whole retinal vessels, after pressing his lower
view of retina lid with an illuminated bulb. An intelligent patient can even
detect a patch of Choroiditis or macular degeneration
Blue-field entoplo- It allows the visualization of one’s own leukocytes (‘flying
scopy corpuscles’) flowing in macular retinal capillaries
Illuminated Amsler’s Useful in assessing macular function in eyes with visual acuity
grid test of 6/60 or less
Photo-stress test With the help of an indirect ophthalmoscope, eye is exposed to
a bright light for 15s and the recovery time is note. Recovery is
prolonged in Maculopathy
Laser interferometry Postoperative visual acuity is assessed in both the methods
and potential acuity They are helpful in immature cataract
meter
Foveal-ERG It comments on integrity of macula and optic nerve
USG B-scan Gives valuable anatomical information concerning the vitreous
and entire retina
Figs 8.11A and B: (A) Two point discrimination test; (B) Maddox rod test
 Specula microscopy:
– To count and to study the morphology of corneal cells
(normal count in elderly 2000–2500 cells/sq mm)
– The count is decreased in endothelial dystrophy and special
precautions to be taken in such cases before an IOL
implantation.
C. Systemic investigations:
 BP monitoring
 Blood sugars monitoring
 Complete hemogram
 Urine for albumin, sugars, pus cells
 Serology: HIV, HBsAg and VDRL
 Dental and ENT check up to rule out septic foci
 ECG, chest X-ray.
Q. Discuss in detail the treatment of senile cataract.

Q. Discuss in detail the management (investigation+
treatment) of senile cataract.
Q. Compare and contrast the surgical procedures of cataract.
Q. List the indications for surgical management of cataract.
Q. Compare and contrast ECCE/ICCE/Phacoemulsification.
Q. List the merits and demerits of ECCE/ICCE/Phacoemulsi-
fication.
Treatment of cataract essentially consists of its surgical removal
A. Non-surgical treatment:
(Mnemonic: CID act—Crime investigation department
act—Act (measures) C—against Cause, I—to Improve
vision, D— to Delay Progression)
 Treat the Cause of cataract:
– Adequate control of DM
– Removal of cataractogenic drugs (corticosteroids,
phenothiazides and strong miotics)
– Removal of source of radiation
– Early treatment of ocular diseases like uveitis
 Measures to Delay progression: Supplementation of
– Iodine salts of calcium and potassium
– Vitamin E
– Aspirin delays progression of the disease
 Measures to Improve vision in presence of incipient and
immature cataract: (Mnemonic: RAMU)
– Refractive correction of vision (frequent correction
needed)
– Arrangement of illumination:
• Bright illumination for peripheral opacities
• Dull illumination for central opacities
– Mydriatics in patients with small axial cataract
– Use of dark goggles for patient having central opacities.
B. Surgical management:
The most commonly used techniques are:
 Intracapsular cataract extraction (ICCE): In this technique,
the whole of the crystalline lens including the capsule is
removed leaving behind a clear pupillary area
 Extracapsular cataract extraction: In this technique the
central part of the anterior capsule is excised (anterior
Capsulotomy) followed by the expression of the nucleus
and cortical clearing
– Conventional extracapsular cataract extraction (ECCE):
The posterior capsule, equatorial region and peripheral part
of the anterior capsule are left behind
– Small incision extracapsular cataract extraction (SICS):
ECCE done through a small hole
– Phacoemulsifications:
• It is basically ECCE with the help of a highly
sophisticated instrument called phacoemulsifier. Here
the lens nucleus and cortical matter are emulsified by
ultrasonic vibration and then removed by simultaneous
controlled irrigation and aspiration
• The whole of the posterior capsule and part of the
anterior capsule are left intact as a ‘capsular bag’
Phacoemulsification is the safest of all the methods and is the

method that is preferred these days with IOL placed inside the
bag for allmost all types of cataract.
Technique ICCE SICS Phacoemulsification
General principle See above See above See above
Indications Subluxated or 40 years of age Same as ECCE
dislocated lens High myopia with It is over all the
is absolute degenerated fluid method of choice
indication vitreous
Also indicated in: Procedure of choice
camp surgery, over ICCE
when microsur-
gical instruments
are not available,
untrained surgeon
Dilatation of Required Required Required
the pupil
Magnification Binocular loupe Microscope Microscope
or microscope
Incision Large, 180 degree, Smaller, 120 degree, Smallest, 30 degree,
10–12 mm 7–8 mm 3.2–3.5 mm
Lens removal
Capsulotomy Nil Can opener Rhexis
Nucleus delivery Intact lens delivered Manual sliding Phacoemulsification
Contd...
Contd...
Cortex removal Nil Irrigation and Irrigation aspiration,
aspiration, manual automated
or automated
IOL Anterior chamber Posterior chamber Posterior chamber

or none in the bag in the bag
Sutures Required Not required Not required
(continuous or
interrupted, 5–7)
Merits and demerits of the above procedures:

Merits Demerits
ICCE Relatively simple, quick and cheap Cannot be performed safely on
No chance of after cataract patients below 35 years of age
No chance of developing uveitis Posterior chamber IOL is not possible
and secondary glaucoma due to Incidence of vitreous related anterior
lens particles chamber problem is high (pupillary
Cosmetically looks better block, delayed wound healing,
endothelial decompression,
glaucoma)
Incidence of postoperative cystoid
macular degeneration is high
Incidence of postoperative retinal
detachment is high
Corneal astigmatism is more as the
Limbal incision is large
Contd...
Contd...
ECCE Chances of vitreous loss is very Costly equipments
minimal Takes time to master the technique
Incidence of vitreous related Iridocyclitis and glaucoma due to lens
anterior chamber problem is proteins are common
negligible After cataract occurs in a significantly
Less incidence of postoperative high number of cases
cystoid macular degeneration ECCE cannot be done in dislocated
Less chance of retinal detachment lens and is difficult to do the same in
A posterior chamber IOL is usually subluxated lens
implanted along with ECCE, which
is an ideal IOL
An intact posterior capsule guards
against infection (Endophthalmitis)
for a prolonged period
Phacoemul- Sutureless cataract surgery Expensive equipments
sification More rapid wound healing Most difficult technique to master
Shorter convalescence High incidence of complications in
Early stabilization of refraction beginners (iris damage, corneal
with minimal or no astigmatism decompensation, posterior capsular
Plus all the above merits of ECCE rent or nucleus drop into the vitreous)
It is difficult to perform in white
mature cataract and grade 4+ nuclear
cataract
Plus other demerits of ECCE
Q. List the complications of cataract surgery.

Q. List the complications of local anesthesia in cataract surgery.
The Complications of cataract surgery:
Preoperative Anxiety
complications Nausea, vomiting
Irritation or allergic conjunctivitis to antibiotic drops
Corneal abrasion due to tonometry
Contd...
Contd...
Complications of A-Anaphylaxis
local anesthetics D-Dislocation of lens spontaneous into vitreous cavity
(Mnemonic; R-Retrobulbar hemorrhage
A DROPSS) O-Oculocardiac reflex: bradycardia and cardiac arrhythmia
P-Perforation of Globe
S-Subconjunctival hemorrhage
S-Shock [Lignocaine, shock]
Operative Superior rectus laceration
complications Excessive bleeding
Incision related complications:
• Conventional ECCE—irregular incision
• SICS and phacoemulsification—buttonholing of anterior
wall, premature entry into anterior chamber, scleral
dessection
Descemets detachment
Iridodialysis
Capsularhexsis
Posterior capsular rupture
Early Hyphema
postoperative Iris prolapse
complications Striate keratopathy
Shallow anterior chamber
Anterior uveitis
Endophthalmitis
Late After cataract
postoperative Bullous keratopathy (Pseudophakic)
complications Cystoid macular degeneration
(Mnemonic: Delayed chronic Endophthalmitis
ABCDDEFGI) Detachment Retinal
Epithelial ingrowth
Fibrous down growth
Glaucoma in Aphakia or pseudophakia
IOL related complications
Q. List the postoperative complications associated with IOL.

The postoperative complications associated with IOL are as
follows:
 Cystoid macular edema*
 Corneal endothelial damage*
 Uveitis*
 Secondary glaucoma*
 UGH syndrome *(Uveitis, secondary glaucoma and hyphema)
*common with rigid anterior IOL
 Malposition of IOL:
– Sunset syndrome: Inferior subluxation of IOL
– Sunrise syndrome: Superior subluxation of IOL
– Lost lens syndrome: Complete dislocation of IOL into
vitreous cavity
– Windshield wiper syndrome: It results when a small IOL
is placed in the sulcus. In it the superior sulcus moves to
left and right with the movement of head and damages the
endothelium of cornea.
 Pupillary capture of lens: This follows postoperative
iridocyclitis or proliferation of the remaining lens particles
 Toxic lens syndrome: Is uveal inflammation exited by ethylene
gas used for sterilization or by the lens material itself.
Q. What is vitreous loss/vitreous prolapse? List the signs,
complications, consequences and management of the same.
Vitreous loss/Vitreous prolapse is accidental vitreous loss during
surgery on the lens, cornea and iris.
The vitreous herniates into the anterior chamber or escapes
outside the eye.
Signs:
 Corneal edema due to epithelial damage
 Upward pupil is usually seen due to attachment of vitreous
bands to the pupillary margin and corneoscleral junction
 Macular edema may be associated with massive vitreal loss
 There may be presence of fibrous bands in the vitreous later on
 Aphakic glaucoma may occur at a later stage due to pupillary
block or due to presence of vitreous in the anterior chamber
causing angle closure
 On table findings: Bulging of iris, deep anterior chamber and
gaping of incision.
Complications Consequences
Direct contact of vitreous with cornea A–Astigmatism
Incarceration of vitreous into B–Bullous keratopathy
operative wound C–Cystoid macular degeneration
Fibroplasias of residual vitreous C–Chronic irritation
Inflammation E–Endophthalmitis
F–Fibrous and epithelial ingrowth
G–Glaucoma (secondary)
I–Infection of wound
V–Vitreous opacities
Prophylaxis; all the measures taken preoperatively

(Mnemonic: DAD—DDDADDD)
 D—Decrease vitreal volume by using hyperosmotic agents
(glycerin, mannitol)
 D—Decrease aqueous volume (acetazolamide)
 D—Decrease orbital volume by ocular massage and
compression
 A—Better ocular Akinesia and Anesthesia.

 D—Decrease external pressure on eyeball by not using eye
speculum
 D—Do use flieringa ring to prevent prolapse of sclera
 D—Despite all the measure if IOP is high then postpone the
operation
Treatment: Anterior vitrectomy.
Q. What is snow flake cataract/snow storm cataract/
galactosemia cataract/sunflower cataract/hypocalcemia
cataract/cataract in Lowe’s syndrome/glass blower’s cataract/
electric cataract/syndermatotic cataract?
Cataract type Etiology Important features of cataract/
comment
Snow flake Also called true diabetic cataract Appear as large number of fluid
cataract/snow Seen in diabetic young adults vacuoles  followed by
storm cataract due to osmotic over hydration appearance of bilateral
of the lens snowflake-like white opacities in
the capsule
Galactosemia Classical Galactosemia due to Bilateral cataract (oil droplet
cataract deficiency of: galactose-1 central lens opacities)
phosphate uridyl-transferase Lens changes can be reversed in
(GPUT) early stages if milk and milk
A related disorder due to products are eliminated from the
deficiency of galactokinase diet
Hypocalcemia Parathyroid tetany (may be a Multicolor crystals or small
cataract complication of thyroidectomy) discrete white flecks of opacities
are formed in the cortex
They rarely mature
Contd...
Contd...
Sunflower Wilson’s disease (hepatolen- Green ‘sunflower cataract’ is
cataract ticular degeneration) observed in such patients
Kayser-Fleischer ring (KF ring) is
noted in cornea
Cataract in Lowe’s syndrome (oculocerebro- Congenital cataract
Lowe’s syndrome renal syndrome) is a rare inborn Glaucoma
error of amino acid metabolism
Glass blower’s/ Prolonged exposure to infrared Discoid posterior subcapsular
workers cataract rays opacities and true exfoliation
Most commonly seen in people
working in glass industries
Irradiational Exposure to X-rays,  rays and There is a latent period of 6
cataract neutrons months to few years before
Commonly seen in inadequately cataract develops
protected X-ray technicians,
patients on radiotherapy and
people working in atomic plants
Electric cataract Usually follows electric shock Punctate Subcapsular opacities
Source of which can be a electric which mature rapidly
wire or a flash of lightening
Syndermatotic Associated with skin diseases They are bilateral and occur at
cataract like atopic dermatitis (atopic young age
cataract, most common),
poikiloderma vasculare
atrophicans, scleroderma and
keratosis follicularis
Q. Define complicated cataract. Discuss the etiopathogenesis,

Definition: Complicated cataract refers to opacification of the
lens secondary to some other intraocular disease.
Etiopathogenesis:
Lens nutrition depends on intraocular fluid  therefore any
conditions in which intraocular circulations disturbed or in which
toxins are secreted to the same disturbs nutrition of crystalline
lens complicated cataract (Fig. 8.12).
The following are the etiological agents:
(Mnemonic: Remember GIRD instead of GERD, the etiology
of complicated cataract to your brain, GIRD means to bind)
 G—Glaucoma (primary or secondary): It probably decreases
the intraocular circulation secondary to raised IOP
 I—Inflammatory conditions: Hypopyon corneal ulcer,
iridocycilitis, parsplanitis, choroiditis
 I—Intraocular tumors like retinoblastoma or melanoma
 R—Retinal detachment
 D—Degenerative conditions like retinitis pigmentosa, myopic
chorioretinal degenerations.
Figs 8.12A and B: (A) Complicated cataract; (B) Opacity in the posterior cortex
Management: Investigations and treatment is same as senile

cataract.
Q.Define after cataract/secondary cataract/posterior capsule
opacification (PCO). Discuss the mechanisms, clinical types and
Q. List the different types of after cataract.
Q. List the measures that can prevent PCO/after cataract.
Definition: After cataract/secondary cataract/posterior capsule
opacification refers to opacities which persist or develop after
extracapsular lens extraction.
Mechanism:
 After cataract results from residual lens matter left behind
after surgery may get organized along with fibrin and blood
 After cataract may also results from proliferation of anterior
epithelial cells that may sweep across whole of posterior
capsule.
Clinical types: Three types have been noted (Fig. 8.13):
 Thin membranous type
 Dense membranous type
 Soemmering’s ring: This is a thick ring of after cataract formed
behind the iris enclosed between two layers of capsule
 Elschnig’s pearl: These are vacuolated subcapsular epithelial
cells clustered like soap bubbles and they fill the pupillary
aperture.
Fig. 8.13: Clinical types of after cataracts

Prevention:
 A—Acrylic hydrophobic IOL has least incidence of PCO
 A—Anterior (remaining part) and posterior capsule should
be polished well
 B—‘Biconvex’ PC IOL or plano-convex IOL with convexity
towards the posterior capsule
 B—(Bagging, as I call it)—‘in-the-Bag’ insertion of PC-IOL
 C—Circular anterior capsulotomy
 C—Cortical Cleaning should be good including peripheral
and equatorial parts
 C–CCC–Continuous curvilinear capsulorhexis
 D—Dimension point (as I call it)—In case of capsulorhexis,
the margins of the capsular opening must overlap 0.5 to 1
mm with the margin of the optic of IOL
 E—Square Edge optic designed IOL.
Treatment:
 YAG laser capsulotomy for after cataract that develops after
PC IOL
 Capsulectomy, membranectomy for after cataract that is dense
and adherent to the iris
 Dissection and needling for thin membranes.
Q. List the major classes of IOL.

Q. What is biometer?
Q. Give the formula used to calculate power of IOL.
 IOL is presently the method of choice to correct Aphakia
 Advantages and disadvantages of IOL (refer refraction
chapter)
 IOL is made up of: Polymethylmethacrylate (PMMA)
 Major classes of IOL based on the method of fixation in the eye:
Class Comment
1. Anterior chamber IOL Lies entirely anterior in front of the iris and
supported by the angle of anterior chamber
Not very popular because of higher incidence
of bullous keratopathy
2. Iris supported lenses These are fixed to the iris with the help of
sutures, loops or claws
Not popular because of high incidence of
complications
3. Posterior chamber Rest entirely behind iris
lenses They may be supported by ciliary sulcus or
capsular bag
Recent trend is towards ‘in-the-bag-fixation’
C-loop model of PCIOL is commonly used
Below are the 3 type of PCIOL based on
material they are (Figs 8.14A and B):
• Rigid IOL  made up of PMMA
• Foldable IOL  silicone, acrylic, hydrogel
and collamer. Used in Phacoemulsification
• Rollable IOL  hydrogel. Used in microincision
surgeries (1 mm)
Figs 8.14A and B: (A) One piece PMMA lens; (B) Silicone lens
Calculation of IOL power (biometry):

Calculation is done using SRK formula (Sanders, Retzlaff and
Kraff formula)
The formula is P = A- 2.5 L- 0.9 K, where (Mnemonic: PALAK
green leafy vegetable)
P—is the power of IOL
A—is a constant which is specific for each lens type
L—is axial length of eyeball in mm, determined by A scan
K—is the average curvature, which is determined by Keratometry
The ultrasound machine equipped with A-scan and IOL power
calculation software is called ‘Biometry’.
Q. List the causes of ectopic lentis.

The causes of ectopic lentis are:
Congenital displacements Traumatic Spontaneous
Simple EL Usually associated This is due to any IO disease
EL et pupillae(EL+ slit shaped pupil) with concussion that results in mechanical
EL associated with systemic injuries stretching, disintegration or
abnormalities: Couching is an degeneration of zonules like:
• Marfans syndrome iatrogenic posterior Hypermature cataract
• Homocystinuria dislocation of lens Buphthalmos
• Ehler-Danlos syndrome performed as High myopia
• Hyperlysinemia treatment in Staphyloma
• Weil-marchesani syndrome olden days IO tumors
• Stickler syndrome Uveitis
• Sulphite oxidase deficiency
Q. What is Phakonit?
 Phakonit refers to the technique of phacoemulsification
(PHACO) performed with a needle (N) opening via an
incision (I) using the tip (T) of phacoprobe
 In this technique the size of incision is only 0.9 mm and after
the completion of the operation an ultrathin rollable IOL is
inserted into the capsular bag
 Advantage: It is a nil astigmatism cataract surgery.
Q. What is Laser Phacoemulsification?

 Laser phacoemulsification is a technique under trail which
may soon replace conventional phacoemulsification
 In this technique laser is used to emulsify the lens material
 Advantage: Laser energy that is used in emulsifying lens is
not exposed to any other ocular structures.
Q. What is Subluxation of lens? Discuss the etiology, clinical

Subluxation of lens is partial displacement in which lens is moved
to sideways (up, down, medially or laterally) but remains behind
the pupil (Fig. 8.15).
It results from partial rupture or unequal stretching of zonules.
Etiology:
 Congenital ectopic lentis (causes listed above)
 Acquired conditions:
– Spontaneous:
• Excessive stretching of zonules, as in Buphthalmos,
high myopia or perforation of corneal ulcer
• Degeneration of zonules, as in hypermature cataract
and latent syphilis
– Traumatic: Due to tear of zonules.
Clinical features:
Symptoms:
 Defective vision due to myopic stigmatism
 Uniocular diplopia
Fig. 8.15: Subluxation of lens

Signs:
 Unequal depths of anterior chamber
 Tremulousness of iris (Iridodonesis) and lens (phacodonesis)
 Diagnosis should be confirmed after full dialatation of the
pupil. The edge of the lens is visible as a dark cresentric line
in oblique illumination
 Indirect opthalmoscopy may show, two images of the disc
due to phakic and aphakic zones in the pupil.
Complications:
 Complete dislocation
 Cataractous change
 Uveitis
 Secondary glaucoma.
Treatment:
 If the lens remains clear and there is no irritative symptoms—
Glasses are prescribed against phakic part to correct lenticular
myopic astigmatism
 Alternatively, if the aphakic zone in the pupil is more—
Aphakic correction may be considered
 In the presence of cataract or irritative symptoms:
– For small zonular tear—ECCE with PCIOL may be
considered
– If the zonular tear is more—ICCE with vectis is the
treatment of choice. This is followed by anterior vitrectomy
with or without AC IOL
– Scleral fixation IOL may be tried if the other eye is normal
or pseudophakic.
Q. What is Dislocation/Luxation of lens? Discuss the etiology,

Dislocation or Luxation of the lens is a condition in which the
crystalline lens is completely unsupported by the zonular fibers,
so that the lens is completely displaced from the pupillary area
(Fig. 8.16).
Etiology: Same as subluxation of lens, couching (deliberate
dislocation of lens into vitreous previously used as a treatment
option of cataract)
Fate of dislocated lens:
 Incarceration to the pupil
 Dislocation into anterior chamber
 Dislocation into the vitreous
 To subretinal space
 To subscleral space
 Extruded out of globe (partially or complete).
Symptoms:
 Marked dimness of vision for distance and near, due to high
hypermetropia and loss of accommodation
 Slight improvement of vision in hypermature cataract.
Figs 8.16A and B: (A) Dislocation into the anterior chamber;

(B) Dislocation into the vitreous
Signs:
Signs of Aphakia Signs of anterior Signs of posterior
dislocation dislocation
Deep anterior chamber Ophthalmoscopic Ophthalmoscopic
examination reveals examination reveals
lens in anterior lens in posterior
chamber chamber
Jet black pupil Clear lens looks like
an oil drop in aqueous
Iridodonesis
Absence of 3rd and
4th Purkinje images
but without any
iridectomy or limbal
scar mark
Complications:
 Secondary glaucoma
 Severe iridocycilitis
 Vitreoretinal degeneration.
Treatment:
 In anterior dislocation: ICCE and vitrectomy with or without
AC IOL
 In posterior dislocation:
– No inflammatory sigs: Dislocated lens is kept as such and
only Aphakic glasses are prescribed
– If signs of inflammation are present then lens is extracted
(Lensectomy) along with vitrectomy. A scleral fixation (SF)
IOL can be implanted by an expert.
Q. What is Purkinje-Sanson image test?

 Purkinje-Sanson was the person who introduced the test which
carries his name to diagnose mature cataract and Aphakia.
 The test does not has much significance and thus not
frequently employed in clinical practice
 Normally when a strong beam of light is thrown on the eye,
four images are formed
Image Derived from Characters of the image
1st image Anterior corneal Brightest, erect image and moves in same
surface direction of movement of light source
2nd image Posterior corneal Faint, erect image and lies adjacent to 1st
surface image
3rd image Anterior lens Largest, dim, erect image
surface
4th image Posterior lens Dim, small and inverted (posterior surface
surface of lens is concave) and it moves in opposite
direction of movement of light source
 These images will be better appreciated in a darkroom or with

dilated pupil.
Q. List the drugs which cause cataract.
The drugs which cause cataract are: (Mnemonic: ABCD)
 Amiodarone
 Busulfan
 Chlorpromazine
 Dexamethasone.
9.
Glaucoma
Q. Discuss the clinical features, pathogenesis and management

of congenital glaucoma/buphthalmos/infantile glaucoma/
Juvenile glaucoma/hydrophthalmos.
Definition:
Congenital glaucoma are a type of diverse disorders in which
abnormal high IOP results due to developmental abnormalities
of the angle of the anterior chamber obstructing the drainage of
the aqueous humor.
 If the disease manifests before three years of age, the eyeball
enlarges hence called buphthalmos (Bulls eye)
 Because there is retention of aqueous humor (aqueous = water)
the name hydrophthalmos has also been suggested
Types:
A. Primary developmental/congenital glaucoma: Abnormal high
IOP is due to developmental anomaly of the angle of the anterior
chamber, not associated with any ocular or systemic anomaly
Subtype IOP is raised since
True congenital glaucoma Intrauterine life and child is born with enlarged eye
Infantile glaucoma Manifests before 3 years of age
Juvenile glaucoma Manifests between 3–16 years of age
B. Developmental glaucoma’s with associated ocular

abnormality
Pathogenesis:
 Maldevelopment of the trabeculum including the
iridotrabecular junction
 Flat iris insertion
 Concave iris insertion.
Clinical features:
Symptoms: Photophobia, blepharospasm, lacrimation and eye
rubbing often occur together.
Signs:
 Corneal signs: Corneal edema, corneal enlargement and tears
and breaks in Descemets membrane (Habb’s striae)
 Sclera: Thin and appears blue
 Iris: Iridodonesis and atrophy
 Lens: Becomes flat due to stretching of zonules and may even
subluxated
 IOP is raised (neither marked nor acute)
 Axial myopia (due to increased axial length) may give rise to
anisometropic amblyopia.
Investigations:
 Measurement of IOP by Schiotz tonometry
 Measurement of corneal diameter by using calipers
 Ophthalmoscopy to evaluate the optic disc
 Gonioscopic examination of the angle of anterior chamber.
Glaucoma 203
Treatment:
 Medical treatment: Is of no value. Miotics and beta blockers
are given only for a temporary period prior to surgery
 Surgery: Following are the surgical options available:
– Goniotomy: An arcuate incision is made with a special
knife halfway between the iris and the Schwalbe’s line
(Fig. 9.1)
– Goniopuncture: Is a puncture that is made in the whole
thickness of the trabecular region into the subconjunctival
space
– Trabeculotomy: A fine metal probe is passed into the
Schlemm’s canal, and is then swept into the anterior
chamber, thus exposing the Schlemm’s canal directly to
aqueous humor (Fig. 9.2)
– Combined Trabeculotomy and Trabeculectomy (Preferred
and best option)
– Glaucoma value implants for cases resistant to other
treatment
(Mnemonic: Buphthalmos-5B’s- boys (are affected more than
girls), Bilateral, Blepharospasm, Blue, Bull’s eye, Backward
subluxation of lens)
Fig. 9.1: Goniotomy knife

Fig. 9.2: Harm’s trabeculotome
Q. What is Primary open angle glaucoma? Discuss the risk factors,

pathogenesis, clinical features and management of the same.
Q. What is triad of Primary open angle glaucoma?
Q. Discuss the signs of Primary open angle glaucoma.
Q. Discuss the pathophysiology of optic disc changes and
changes of the disc in Primary open angle glaucoma.
Q. Discuss the Anatomic basis of field defects in glaucoma.
Q. Discuss the progression of field defects in Primary open
angle glaucoma.
Q. Discuss the provocative test for glaucoma.
Q. Grade the severity of glaucoma damage.
Q. Discuss in detail the treatment of Primary open angle glaucoma.
Q. Discuss in detail the medical treatment of Primary open
angle glaucoma.
 Primary open angle glaucoma is a chronic, slowly progressive
condition with insidious onset in which there is no obvious
signs of systemic or ocular cause of rise in intraocular pressure
Glaucoma 205
 Occurs in eye with open angle of anterior chamber

 It is also known as chronic simple glaucoma of adult onset,
where there is slow progressive raised IOP (> 21 mm Hg recor-
ded at least on few occasions) associated with characteristics
optic disc cupping and specific visual field defect.
Etiology:
Risk factors:
 A—Age: elderly between 50 to 70 years
 B—Black > white
 C—Cigarette smoking
 D—Diabetes
 E—MyopEs predisposed
 H—Hereditary—polygenic inheritance
 H—Hypertensives
 T—Thyrotoxicosis.
Pathogenesis of raised intraocular pressure:

  in intraocular pressure is due to  in aqueous outflow facility
due to  resistance to aqueous outflow (Fig. 9.3)
  resistance is because of:
– Thickening and sclerosis of trabecular meshwork
– Absence of giant vacuoles in cell lining the canal of
Schlemm
Fig. 9.3: Mechanism of rise in intraocular pressure in open angle glaucoma
Clinical features:
Symptoms:
 Asymptomatic and insidious in onset till there is significant
painless progressive loss of vision
 Mild headache and eyeache
 Defects in visual field
 Difficulty in doing reading and near work due to accom-
modation failure owing to continuous pressure on ciliary
muscles and its nerve supply
Glaucoma 207
 Hence frequent change in presbyopic glasses

 Delayed dark adaptation.
Signs:
 Anterior segment signs
 Intraocular pressure changes
 Optic disc changes
– Early glaucomatous
– Advanced glaucomatous
– Glaucomatous optic atrophy
 Visual field changes.
Anterior segment signs:

– It is usually normal
– In advanced cases: Cornea: slight haze, Pupil: reflex
becomes sluggish.
Intraocular pressure changes:
 Initially intraocular pressure is not permanently raised
 A variation of 5 mm Hg is suspicious and 8 mm Hg is
diagnostic of glaucoma
 In later stages intraocular pressure is persistently high above
21 mm Hg and ranges between 30 to 45 mm Hg
 In most of patient intraocular pressure falls by evening
opposite to that of closed angle glaucoma.
Optic disc changes:
A. Early glaucomatous change: One or more of the following
may be noted
 Virtual oval cup: Due to selective loss of neural rim tissue
in inferior or superior poles
 Asymmetry of cups: Difference of > 0.2 mm in two eyes

 Large cup > 0.6 mm
 Splinter hemorrhage
 Pallor areas of disc
 Atropy of retinal nerve fiber layer seen on red free light.
B. Advanced glaucomatous changes
 Marked cupping: Excavation may even reach the disc
margin, with steep side (Fig. 9.4)
 Thinning of neurosensory retina: Seen as cresentric shadow
adjacent to disc margin
 Nasal shifting of retinal vessels
 Pulsating of retinal arterioles
 Laminar dot sign: Opening of the (pores) lamina cribrosa
seen in the disc
 Bayoneting sign: It is the double angulations of the blood
vessel, as they turn sharply backwards then run along steep
wall of the excavation again angled at floor of cup (Hence
their path in the steep wall is not seen) (Fig. 9.5).
C. Glaucomatous optic atrophy:
 Disc is total pale and bean shaped cupping is noted
 All the neural tissues of the disc is destroyed
 Optic nerve head is white and deeply excavated.
Figs 9.4A and B: (A) Normal physiological cup; (B) Glaucomatous cup
Glaucoma 209
Figs 9.5A and B: (A) Laminar dot sign; (B) Bayoneting sign
Pathophysiology of disc change: Mechanical factors and
vascular factors play a role in pathophysiology of disc change
A. Mechanical factors:  IOP  forces lamina cribrosa to move
back
Death of neurons is by direct compression.
B. Vascular factors: Ischemia plays a role in obstruction of
axoplasmic flow in response to IOP causes atropy of
axons without corresponding or of supporting glial tissue
large lacunae are formed.
Anatomic basis of field defects:
 Fibers from nasal side of retina come directly to optic disc as
superior and inferior radiation fibers
 Those from macular area comes horizontally as
papulomacular bundles
 Fibers from temporal retina arch above and below the macula
and papulomacular bundle as superior and inferior arcuate
fiber with horizontal raphe in between.
Arrangement of nerve fiber within optic head:

 Those from periphery lie deep in retina and superficial
(or peripheral) in optic disc (Figs 9.6A and B)
 Nerve fibers originating closer to nerve head lie superficial
in retina  and occupy deeper portion of the disc
 The arcuate nerve fiber occupy the superior and inferior
temporal portion, of the optic nerve head
 Arcuate nerve are most sensitive for glaucoma
 Macular fibers are resistant for glaucoma hence vision retained
in this area till end (central vision).
Progression of field defects:
Visual field defects in glaucoma are initially observed in
Bjerrum’s area (10°–20° from fixation).
The natural history of the progressive glaucomatous field loss,
more or less takes the following sequence (Figs 9.7A to G).
Figs 9.6A and B: (A) Arrangement of retinal nerve fibers;

(B) Extent of normal visual field—Right eye
Glaucoma 211
Figs 9.7A to G: (A) Baring of the blind spot; (B) Small scotomatous areas;
(C) Seidel’s sign; (D) Bjerrum’s arcuate scotoma; (E) Double arcuate scotoma or
annular scotoma; (F) Temporal-central island; (G) Peripheral visual field defects
Progressive visual Description

field defects
1. Isopter contraction There is mild generalized contraction of central as well
as peripheral field
Diagnostic value: limited as it occurs in many other
conditions
Contd...
Contd...
2. Baring of blind One of the earliest field defect
spot It means exclusion of the blind spot from the central
field due to inward curve of the outer boundary of
30° central field Diagnostic value: limited
3. Small wing shaped It may appear below or above the blind spot in
paracentral Bjerrum’s area
scotoma Clinically significant
4. Seidels scotoma Sickle shaped, with concavity towards the fixed
point with the passage of time the paracentral
scotoma joins the blind spot to form sickle shaped
scotoma
5. Arcuate/Bjerrum’s This is due to extension of seidels scotoma in an area
scotoma either above or below the fixation point, hence reaches
horizontal line
6. Double arcuate or Develops when the 2 arcuate scotoma join together
ring scotoma
7. Ronne’s central It is created when 2 arcuate scotoma run in different
nasal step areas and meet to form a sharp 90° defect at horizontal
meridian
This is because the arcuate defect in upper and lower
portion of eye do not proceed at same rate
8. Peripheral field May be early or late in onset
defects
9. Advanced and The visual field loss gradually spreads centrally and
glaucomatous peripherally, eventually only a small island of central
field vision might be left (tubular vision)
These islands of vision disappear and Later only
tiny central island of vision is left
Temporal island of vision is most resistant and is
lost at last
Glaucoma 213
Investigation:
 Tonometry: Applanation preferred over schiotz
 Diurnal variation test: To diagnose early cases
 Gonioscopy:
– Reveals wider open angle of anterior chamber
– Its importance in POAG is to rule out other forms of
glaucoma
 Documentation of optic disc changes
 Slit lamp examination to rule out secondary open angle glaucoma
 Perimetry to detect field defects
 Nerve fiber layer analyzer: Helps to detect glaucomatous
damage to retinal nerve fiber before disc changes
 Provocative test:
– Required to diagnose borderline cases
– Commonly performed in water drinking test.
Principle: Glaucomatous eye have great response to water
drinking.
Procedure:
 After 8 hours past-patient is asked to drink 1 liter of water,
baseline IOP is noted, every 15 minutes for 1 hour
 Maximum rise of IOP is noted between 15 to 30 minutes and
returns to baseline at 60 minutes
 A rise of > 8 mm is diagnostic of POAG
 Diagnosis:
IOP Disc
1. POAG > 21 mm Hg Definite disc cupping and
visual field defects
2. Ocular HTN/ > 21 mm Hg Nil
glaucoma suspect
3. Normotensive glaucoma/ < 21 mm Hg Cupping present field
low tension glaucoma defects absent
Severity of Glaucoma damage:

Degree Description
Mild Characterized by optic nerve abnormality with glaucoma
Normal visual field
Moderate Visual field abnormal in one hemisphere and not within 5° of fixation
Severe Severe: Visual field abnormal in both hemispheres
within 5° of fixation
Treatment:
Therapeutic choices:
 Medical therapy: Is the treatment of choice in the early stages
 Filteration surgery: It is considered as a last resort
 Argon or diode laser trabeculoplasty: It is the most advanced
technique.
A. Medical therapy
Basic guidelines for medical therapy:
 Is the treatment of choice in the early stages
 Use the lowest concentration of the drug
 Use minimum concentration of drug per day
 Choose the drug with least side effects
 Combined drug therapy is more effective and convenient to
avoid adverse effects.
Glaucoma 215
Drug Mechanism of action Side effects Note

A. Topical  Reduces aqueous Bronchospasm, Drug of first choice
blockers: secretion bradycardia,
Timolol maleate, arrhythmia, low
Levobunolol, BP, corneal
Betaxolol anesthesia
(except for
Betaxolol)
B. Miotics: Ciliary muscle Myopia Preferred as drug of
Pilocarpine contraction Hyperemia second choice as young
Miosis Retinal patients suffer from
Open spaces in detachment spasm of accommodation
trabecular meshwork Cataract and miosis
C. Prostaglandin Enhances Uveoscleral Hyperemia, iris Drug of first choice if
analogs: Latanoprost, outflow pigmentation, patient is affordable
travoprost, headache
bimetaprost
D. Sympathomimetics: Increases aqueous Of epinephrine: Because of its side effects
Epinephrine, outflow Irritation, it’s not being used as drug
dipivefrine Reduces aqueous conjunctival of first or second choice
hydrochloride and formation by vaso- congestion,
brimonidine constrictor action cystoids
macular edema
E. Carbonic anhydrase Reduces aqueous Paraesthesia, Not suitable for long-term
inhibitors: formation malaise, gastritis, use
acetazolamide, renal stone
methazolamide formation,
Stevens-Johnson
syndrome
F. Hyperosmotic They increase the These are rarely used
agents: Glycerol, plasma tonicity to draw
isosorbide, water out of the eyes
mannitol, urea
B. Surgery:
Indication:
 Uncontrolled glaucoma inspite of max medical therapy and
argon laser trabeculoplasty
 Non-compliance for medical treatment with non-availability

of ALT
 Failure of medical treatment and unsolvable for ALT either
due to lack of cooperation or inability to visualize trabeculum
 Eyes with advanced disease.
Types of surgery:
 Fistulising (filtration) surgery: Which provides new channel
for outflow and hence reduces IOP
 Trabeculectomy: Commonly practiced now. In this procedure
part of trabecular meshwork is removed to create an alternative
drainage route.
C. Argon or diode laser trabeculoplasty (ALT): It causes
trabecular shrinkage on inner aspect of the trabecular meshwork.
Indications: Open angle glaucoma Contraindications Complications
with any of the patients
Not responding to tropical treatment Invisibility of Transient raise in
Poor compliance to medical treatment trabeculum IOP
In elderly patients to temporarily post- Pediatric glaucoma Inflammation
pone the surgery Secondary glaucoma Hemorrhage
Previously failed ALT Uveitis
Peripheral anterior
synechiae
Decreased
accommodation
Q. What is Primary angle closure glaucoma (PACG)? Discuss

the etiology and mechanism for the same.
Q. List the different stages of Primary angle closure glaucoma.
Primary angle closure glaucomaa(PACG) is a type of Primary
glaucoma (where there is no obvious systemic or ocular causes)
Glaucoma 217
in which rise in IOP occurs due to blockage of the aqueous

outflow by closure of a narrow angle of anterior chamber.
Etiology:
Predisposing anatomical General factors Precipitating factors
factors
Hypermetropic eye Age: Common in 5th and Dull illumination
Eyes in which iris–lens 6th decade of life Emotional stress
diaphragm is placed Females are commonly Mydriatic treatment
anteriorly affected
Eye with narrow anterior Caucasian race
chamber Personality: nervous
Plateau iris configuration people with vasomotor
instability
Rainy season
Positive family history
Mechanism of rise in IOP: Predisposing factors  mild

dialatation of pupil increased amount of apposition between
iris and anteriorly placed lens with a considerable pressure
resulting in relative pupillary block aqueous collects in posterior
chamber and pushes the peripheral flaccid iris anteriorly (iris
bombe) results in appositional closure IOP begins to rise
slowly appositional angle closure is converted into synechial angle
closure (due to peripheral anterior synechia) raised IOP.
Clinical presentation: The progression may need not be in an
orderly sequence.
 Latent PACG (suspect)
 Subacute/intermittent
 Acute PACG
 Postcongestive PACG
 Chronic PACG
 Absolute PACG.
Q. What is Latent PACG? Discuss the clinical feature and

Q. Give the Van Herick slit lamp grading of latent PACG.
Q. Discuss provocative test for PACG.
 ‘Latent’ is the term now used for eyes predisposed to ACG
 ‘Suspect’ PACG is now used for the eye with shallow anterior
chamber with occludable angle
 The suspect of latent ACG is done if
– On routine slit lamp examination in a patient coming for
some other complaint
– In fellow eye of the patients presenting with an attack of
acute ACG.
Clinical features:
Symptoms: Absent.
Signs:
 Eclipse sign:
– It indicates decrease depth of anterior chamber
– Can be seen by shining a pen torch from temporal side
and noting a shadow on nasal side
 Slit lamp signs:
– Decrease in axial anterior chamber depth
– Convex shaped iris lens diaphragm
– Close proximity of iris to cornea in periphery
Glaucoma 219
 Gonioscopic examination: Shows very narrow angle (shaffer

grade 1)
 Van Herick slit lamp grading of the angle (Fig. 9.8):
– Slit lamp grading is done when Gonioscopy is not available
– Here peripheral anterior chamber depths in compared with
adjacent corneal thickness.
Grade Name PACD to CT ratio
+ Wide open angle ¾ to 1
3 Mild narrow angle ¼ to ½
2 Moderately narrow PACD = ¼ CT
1 Extremly narrow PACD < ¼ CT
0 Closed angle Nil
Clinical course: Without treatment may follow following course.

 IOP may remain normal
 Sub acute or acute angle closure glaucoma
 Chronic angle closure glaucoma without passing through
stage (ii).
Fig. 9.8: van Herrick method of slit-lamp grading of angle of anterior chamber
Investigations:
Provocative test: For PACG have been designed to precipitate
closure of angle in the hospital where it can be treated promptly.
Following are the two procedures available:
 Prone darkroom test:
– It is a best physiological provocations test for PACG
– Baseline IOP is measured patient is made to lie prone
in a darkroom for one hour he must be awake to keep
pupils dilated after 1 hour IOP is measured again
rise in IOP > 8 mm of Hg is diagnostic of PACG.
 Mydriatic provocative test:
– This test is not preferred because it is not physiological
– In this test either a weak mydriatic (tropicamide) or a
combination of weak mydriatic + miotic (Phenylepherine
+ Pilocarpine) is used to middialated pupil
– An increase in IOP > 8 mm of Hg is diagnostic of PACG.
Inference:
 Positive test indicates the angle is capable of spontaneous
closure
 Negative test in the presence of a narrow angle of anterior
chamber does not rule out a possibility of spontaneous closure.
So patient should be warned of possible attack of PACG.
DD of colored halos in PACG
 Acute purulent conjunctivitis
 Early cataractous change.
Treatment:
Prophylactic laser iridotomy for both eyes.
Glaucoma 221
Q. What is acute primary ACG/Acute primary angle closure

glaucoma/congestive glaucoma? Discuss the clinical feature
An attack of acute primary angle closure glaucoma occurs due to
sudden total angle closure leading to severe rise in IOP (Fig. 9.9).
It usually does not terminate on its own and thus if not treated
becomes a sight threatening emergency.
Clinical features:
Symptoms:
 Eye pain sudden, severe and it radiates along fifth cranial
nerve
Fig. 9.9: Mechanism of the rise in intraocular pressure in angle-closure

glaucoma
 Headache, nausea, vomiting, prostration

 Rapidly progressive impairment of vision
 Redness, photophobia, lacrimation
 Past history of typical attack of subacute angle closure
glaucoma.
Signs:
 Lids: Edematous
 Conjunctiva: Chemosed ciliary and circumcorneal congestion
 Cornea: Edematous and insensitive
 Anterior chamber: Is shallow, aqueous flare/aqueous cells may
be seen
 Angle of anterior chamber: Completely closed (shaffers grade
O)
 Iris: Discolored
 Pupil: Semidialated, vertically oval, fixed, nonreactive for
both light reflex and accommodation (Fig. 9.10)
 IOP: Usually > 40–70 mm Hg
 Optic disc: Edematous and hyperemic
 Signs of fellow eye: Shallow anterior chamber and narrow
angle.
Fig. 9.10: Vertically oval pupil

Glaucoma 223
Clinical course: It may progress to postcongestive glaucoma.

Differential Diagnosis:
 Causes of acute red eye
 Secondary acute congestive glaucoma such as phacomorphic
glaucoma, acute neovascular glaucoma and glaucomatocyc-
litic glaucoma.
Treatment:
A. Medical therapy:
Systemic therapy:
 Sedation, analgesic and antiemetic
 Systemic hyperosmatic agent: To reduce IOP (mannitol)
 Acetazolamide: Carbonic anhydrase inhibitor, to reduce
aqueous formation
 Pressure with moist cotton swab on the central part of the
cornea if the pupil remains blocked. This helps to
mechanically push the iris away from the cornea or indentation
with goniolens is the best method to massage eye ball.
Local treatment:
 Pilocarpine eye drops:
– Started 1 hour after systemic hyperosmotic treatment
– This is because at high IOP iris sphincter is ischemic and
not respond to pilocarpine
 -blocker eye drops (0.5% Timolol, 0.5% Betaxolol): Reduces
aqueous secretion
 Corticosteroid eye drops (Dexamethasone or betamethasone

drops).
B. Surgical Management:
Procedure Indications Mechanism responsible
for reduction in IOP
Peripheral iridectomy Cases where anterior It re-establishes
(Fig. 9.11) synechial is formed communication between
Prophylactic surgery posterior and anterior
chamber, so bypasses
pupillary block
Filteration surgery Failures of medical Provides an alternate to the
(Fig. 9.12) treatment angle of drainage of
Peripheral anterior aqueous from anterior
synechiae formed chamber into sub-
conjunctival space
Trabeculectomy PACG with peripheral A new channel around
anterior synechiae margin of scleral flap
> 1/2 of angle through which
POAG not responding aqueous flow from
to drugs anterior chamber into
Secondary glaucoma subconjunctival space.
not responding to  Uveoscleral feet flow
drugs Tissue dissection
Congnital posterior to scleral spur
glaucoma where  cyclodialysis 
trabeculotomy and Uveoscleral outflow.
goniotomy fails
C. Prophylactic treatment in fellow eye: Prophylactic laser

iridotomy is preferred.
Glaucoma 225
Figs 9.11A to C: (A) Peripheral iridectomy; (B) Iridotomy (after YAG laser
treatment); (C) Laser iridotomy or peripheral iridectomy
Fig. 9.12: Conjunctival filtering bleb following trabeculectomy

Q. What is Absolute PACG? Discuss the clinical feature and

Absolute PACG is the chronic phase of PACG if untreated with
or without the occurrence of intermittent subacute attacks,
gradually posses to this stage.
Clinical features:
 Painful blind eye
 Perilimbal reddish blue zone: i.e. a slight flush around the
cornea due to the dilated anterior ciliary veins
 Cornea:
– Clear but not sensitive. It becomes hazy later
– Epithelial bullae (bullous keratopathy)
– Filaments seen
 Anterior chamber: Shallow
 Iris: Atrophic
 Pupils: Fixed and dilated with greenish hue
 Optic disc: Shows glaucomatous optic disc
 IOP is raised
 Eyeball: Stony hard to feel.
Complications: Atrophia bulbi, phthisis bulbi, staphyloma and

corneal ulcer.
Glaucoma 227
Treatment:
Procedure Mechanism of action/justification
Retrobulbar alcohol injection This results in destruction of ciliary
ganglion and hence relieves pain
Destruction of secondary ciliary Decreases IOP by reduction in
epithelium by: (3C’s) formation of aqueous humor
Cyclocryotherapy or
Cyclophotocoagulation or
Cyclodiathermy
Enucleation for painful blind eye Justification: To relieve chronic
pain
Q. Classify secondary glaucoma’s.

Secondary glaucoma’s classification:
Based on mechanism Based on etiology
Secondary open angle glaucoma Phacogenic glaucoma
Secondary angle closure glaucoma Inflammatory glaucoma
Pigmentary glaucoma
Neovascular glaucoma
Glaucoma associated with irido-
corneal endothelial syndromes
Pseudoexfoliative glaucoma
Glaucoma associated with
intraocular hemorrhages
Steroid induced glaucoma
Traumatic glaucoma
Glaucoma-in-Aphakia
Glaucoma associated with
intraocular tumors
Mnemonic: NIPPLES N–Neovascular,

I–Inflammatory, intraocular hemorrhage, intraocular tumor
P–Phacogenic, pigmentory, pseudoexfoliative
L–Lens absent (aphakia)
E–Iridocorneal endothelial syndrome
S–Steriod induced.
Q. Discuss the pathogenesis, clinical features and treatment
of phacolytic glaucoma (lens protein glaucoma) or glaucoma
induced by hypermature cataract.
Pathogenesis:
 Phacolytic glaucoma is a type of 2° open angle glaucoma
 Leakage of lens material happens through an intact capsule
here trabecular meshwork is clogged by lens protein and
macrophages which have phagocytosed lens protein.
Clinical features:
 Features of acute congestive glaucoma are noted
 Aqueous may contain fine white protein particles.
Treatment:
 Medical line of management for raised IOP
 Extraction of hypermature lens and PCIOL placement.
Q. List the causes of Neovascular glaucoma (NVG). Discuss the

Neovascular glaucoma occurs due to formation of neovascular
membrane involving the angle of anterior chamber (Fig. 9.13).
Causes of Neovascular glaucoma are as follows:
 Diabetic retinopathy
 Central retinal vein occlusion (CRVO)
Glaucoma 229
Fig. 9.13: Neovascular glaucoma
 Central retinal artery occlusion (CRAO)

 Sickle cell retinopathy
 Eale’s disease
 Chronic inflammation, retinal detachment, intraocular tumors.
Treatment:
 Panretinal photocoagulation to prevent further neo-
vascularization
 Medical therapy for raised IOP
 Filtration surgery for raised IOP.
Q. Discuss the etiology and management of Glaucoma’s due

to uveitis.
The rise in IOP is secondary to inflammation of anterior uveal tract.
Types: Two main groups are noted
A. Hypertensive uveitis: Refers to acute inflammation of
anterior uveal tissue associated with increased IOP.
Subtypes Etiology/pathogenesis Treatment

Nonspecific All causes of anterior Treat the cause of
hypertensive uveitis uveitis. Mechanism: anterior uveitis
Trabecular clogging by Beta blocker eye drops
inflammatory cells, Hyperosmotic agents
exudates, turbid aqueous
Trabecular edema Acetazolamide
Prostaglandin induced
rise in IOP
Specific hypertensive Fuch’s uveitis syndrome Corticosteroids
uveitis glaucomatocyclitic crisis
B. Postinflammatory glaucoma
Postinflammatory Pupillary block due to Prophylaxis: Treat the
glaucoma: Raise in anterior synechiae cause of anterior
IOP is because of after Secondary angle closure uveitis
effects of iridocylitis pupil block following Add steroids and
iris bombe atropine to prevent
Secondary angle closure synechiae formation
without pupil block due Treatment: Medical
to organization of inflam- treatment to lower IOP
matory debris in the angle Iridotomy (surgical/
Secondary open angle laser)
glaucoma: due to trabe- Filtration surgery
cular scarring and obstruc-
tion of meshwork
Q. Discuss the etiology, pathogenesis and management of

ciliary block or malignant glaucoma.
Ciliary block or malignant glaucoma is a condition that occurs
as a complication of intraocular surgery.
Glaucoma 231
Etiology: It typically happens in a patient with

 Primary narrow angle glaucoma operated for peripheral
iridectomy or trabeculectomy
 Aphakic eye following vitreous phase disturbance.
Pathogenesis:
 Rarely following intraocular surgeries, the tips of the ciliary
processes rotate forward and press against the lens in phakic
eyes (ciliolenticular block) or against the intraocular lens
(cilio-IOL block) or against the anterior hyaloid phase of the
vitreous in aphakic eyes (ciliovitreal block)
 This blocks the normal flow of the aqueous, which is
diverted posteriorly and collects as aqueous pockets in the
vitreous (Fig. 9.14A)
 Thus the anterior chamber becomes flat and IOP is markedly
raised.
Clinical features:
Symptoms Signs
Severe pain Persistent flat anterior chamber following
Blurring of vision following an an intraocular surgery
intraocular surgery IOP is markedly raised
Note that the other eye is also susceptible for the same fate.
Treatment:
 Medical therapy:
– Atropine drops or ointment to dilate the ciliary ring and
hence break the ciliolenticular block or cilio-IOL block
– Acetazolamide
– Timolol maleate
– IV mannitol
Figs 9.14A and B: (A) Pockets of aqueous in the vitreous; (B) Aspiration of
fluid and air injection in the anterior chamber
 Surgical therapy: Pars plana vitrectomy followed by injection

of air into anterior chamber (Fig. 9.14B).
Q. What is tonometer? List the different types of tonometer.
Q. What is the principle of Schiotz tonometry? List the advan-
tages and disadvantages of the same.
Q. What is Applantation tonometer?
Q. What is Imbert-Fick’s law?
The IOP is measured with the help of an instrument called tono-
meter and the procedure is called as tonometry.
Types:
 Indentation tonometer: Schiotz (manual) tonometer, electronic
tonometer
 Applantation tonometer: Goldman’s Applantation tonometer,
airpuff tonometer.
Glaucoma 233
Schiotz indentation tonometer:

 Principle: This is based on the principle that a plunger will
indent a soft eye more than a hard eye
 It is constructed in such a way that, when placed on the eye,
the plunger together with a presenting weight, indents the
cornea (Fig. 9.15B)
 The amount of indentation is measured on a scale and corres-
ponding IOP can be calculated from an accompanying table
Advantages Disadvantages
Simple It gives false reading when used in eyes
Reliable with abnormal scleral rigidity
Cheap False low levels of IOP are obtained in
Relative accuracy is good eyes with low scleral rigidity (high
Does not require a slit-lamp Myopes and after ocular surgeries)
for measurement of IOP
Figs 9.15A and B: (A) Goldmann applanation tonometer; (B) Schiotz tonometer
Applanation tonometry:
 Principle: It is based on Imbert-Fick’s law which states that
for an ideal thin walled sphere, the pressure inside the sphere
(P) equals to the force necessary to flatten its surface (F)
divided by area of flattening (A)
 P = F/A
 An applanation tonometer measures the IOP by flattening the
cornea over a specific area (3.06 mm)
 Advantage: Its readings are more accurate since the pressure
values recorded are not influenced by scleral rigidity
 Goldmann applanation tonometer is mounted on a slit lamp
and a special plastic prism rests on the cornea, the pressure
being adjusted until it achieves a standard disc of contact as
outlined by a pre-instilled drop of flourescein (Fig. 9.15A).
10.
Diseases of the Vitreous

management of vitreous hemorrhage.
Q. Discuss the fate of vitreous hemorrhage.
Vitreous hemorrhage usually occurs from the retinal vessels.
It may present as:
 Pre-retinal hemorrhage (subhyaloid) (Fig. 10.1A)
 Intragel hemorrhage, which may be anterior, middle, posterior
or whole of vitreous body (intravitreal) (Fig. 10.1B).
Figs 10.1A and B: (A) Subhyaloid hemorrhage; (B) Large intravitreal hemorrhage
Fig. 10.2: Structures of vitreous

Etiology:
Mnemonic: VITREOUS
V: Vascular lesions: CRVO, hypertensive retinopathy
I: Inflammatory: Acute chorioretinitis, periphlebitis retinae
I: Idiopathic
T: Trauma: Blunt or perforating injury
R: Retinopathy due anemia, diabetes and sickle cell disease
E: HEmophilia, scurvy, purpura (Bleeding diseases)
O: Ocular tumors: Retinoblastoma
U: LeUkemia, Polycythemia (Blood dyscrasias)
S: Spontaneous as in peripheral vascular disease.
Clinical features
Symptoms:
 Sudden development of floaters if hemorrhage is small
 Sudden painless loss of vision if hemorrhage is large.
Signs:
 On distant direct ophthalmoscope:
– Small hemorrhage: Black shadow against red glow
– Large hemorrhage: Red glow of fundus is absent
Diseases of the Vitreous 237
 Direct and indirect ophthalmoscope shows presence of blood

in vitreous cavity.
Fate of vitreous hemorrhage:
 Complete absorption
 Organization: Formation of yellowish white debris in
persistent or recurrent hemorrhage
 Complication:
– Vitreous liquefaction
– Vitreous degeneration
– Khaki cell glaucoma (In Aphakia)
– Retinitis proliferans and tractional retinal detachment.
Investigations:
 Blood pressure
 Routine hemogram
 Estimation of blood sugars
 Test for TB
 B scan: Helps to establish the diagnosis and to rule out retinal
detachment
 Macular function tests before surgery.
Treatment:
 Treat the causative agent
 Conservative treatment:
• Bed rest with head end elevation
• Bilateral eye patches helps blood to settle down
 Pars plana vitrectomy with photocoagulation if hemorrhage
is not resolved by 3 months
 Prevention: Early detection of neovascularization in DM, CRVO
and sickle cell disease followed by laser photocoagulation.
Q. Define vitrectomy. Discuss the indications and types of the

same.
Q. What are vitreous substitute? Name them.
Removal and replacement of vitreous is known as vitrectomy.
Indications:
 Persistent vitreous opacities: Hemorrhage, preretinal/vitreous
membranes
 Complications of cataract extraction
 Endophthalmitis with vitreous abscess
 Trauma: Removal of foreign body, removal of subluxated or
dislocated lens
 Complicated retinal detachment: Giant retinal tear, retinal
dialysis, massive vitreous traction
 Congenital cataract and ectopic lentis
 Persistent hyperplastic primary vitreous.
Types:
 Open-sky vitrectomy
 Pars plana vitrectomy.
Open-sky vitrectomy:
This is performed through a large corneal or limbal section. It is
necessary to remove the lens first.
Pars plana (closed) vitrectomy:
 It is employed to restore the optical pathway of eye
 Vitrectomy is done through a small 3 mm incision in the pars
plana
Diseases of the Vitreous 239
 As the vitreous is removed from the eyeball by cutting and

suction physiological solution is infused into the eye to balance
the suction
 An operative microscope with co-axial illumination is
required for the procedure.
Vitreous substitutes:
The vitreous replacement is necessary for:
 Restoration of intraocular pressure
 Repositioning the retina in different vitreoretinal surgeries.
The vitreous substitutes are:

 Air: As in internal tamponade
 Physiological solutions: Normal saline, ringers lactate,
balanced salt solution
 Gases: Are better than air and give longer period of internal
tamponade, e.g. Sulfur hexafluoride (SF6) and octafluoro-
cyclobutane (C3F8)
 Silicone oil
 Donor vitreous: As it is completely inert and acceptable by
the recipient eye
 Perfluorocarbon liquid: Is heavy and mainly used to assist
removal of dislocated lens nucleus or IOL from vitreous
cavity.
11.
Diseases of Retina
Q. What is central retinal artery occlusion (CRAO)? Discuss the

etiology, clinical features, management and complications of
the same.
Central retinal artery occlusion occurs due to obstruction at the
level of lamina cribrosa.
Incidence: More in males than in females, usually unilateral.
Etiology:
 Atherosclerosis
 Embolism
 Retinal arteritis with obliteration
 Angiospasm
 Increased intraocular tension associated with retinal artery
occlusion as in tight encirclage in retinal detachment operation
 Thrombophilic disorders.
Clinical features:
Symptoms:
 Sudden painless loss of vision
 Amaurosis fugax: Transient loss of vision for few minutes
due to occlusion by embolism.
Diseases of Retina 241
Signs (Fig. 11.1):

 Pupillary light reflex absent
 Ophthalmoscopic examination shows:
– Markedly narrowed retinal arteries
– Retina appears to be milk white due to edema
 Central part of the macular area shows “cherry red spots”
due to vascular choroid shining through the thin retina of this
region
 “Cattle trucking”, that is blood column is segmented in retinal
blood vessels
 In obstruction of branched retinal artery, the occlusion is at
bifurcation and usually embolism is the cause.
Management: Unsatisfactory as the retinal tissue cannot survive
ischemia for few hours.
Fig. 11.1: Central retinal artery occlusion

Emergency treatment includes:

 Immediate lowering of intraocular pressure by
– Mannitol
– Intermittent ocular massage
– Paresthesia
 IV acetazolamide
 Vasodilators and inhalation of 95% oxygen and 5% carbon-
dioxide to relieve Angiospasm
 Anticoagulants like heparin
 Intravascular steroids for arteritis.
Complications: Neovascular glaucoma.

Q. Discuss the etiology, clinical features, management and
complications of central retinal vein occlusion.
It is more common than central retinal artery occlusion (CRAO).
Etiology:
Mnemonic: HYPPER
HY: Hyperviscosity of the blood as in
 Polycythemia
 Hyperlipidemia
 Macroglobinemia
P: Pressure
 Pressure on retinal veins by retinal arteries because both
share the same adventitia
 Pressure due to systemic hypertension
P: Periphlebitis retinae- Central or peripheral

E: Erysipelas, Cellulitis, cavernous sinus thrombosis (Note all
are local causes)
R: Raised intraocular pressure as in primary open angle
glaucoma.
Classifications:
 Central retinal vein occlusion (Fig. 11.2B)
– Nonischemic or Venous stasis retinopathy
 Branched retinal vein occlusion
Clinical features:
Nonischemic/venous stasis Ischemic type/Hemorrhagic
retinopathy retinopathy
Incidence: 75% 25%
Clinical features: Clinical features:
Visual acuity is slightly reduced Visual acuity is markedly reduced
Relative afferent pupillary defect is Marked
usually mild
Ophthalmoscopic examination: Ophthalmoscopic examination:
Mild Tortuosity and dialatation of veins Marked
‘Dot’ and ‘Blot’ and ‘flame’ shaped Massive superficial and deep
Hemorrhages are seen throughout Hemorrhages throughout the
all four quadrants of the retina fundus
Cotton wool exudates are usually Cotton wool exudates are common
absent
Mild to moderate swelling of optic disc Optic disc swollen and hyperemic
Macular edema may or may not be Macular edema and hemorrhage
present seen (splashed tomato appearance)
Contd...
Contd...
Fluorescein angiography: shows Fluorescein angiography: retinal
venous stasis but with good retinal capillary non-perfusion noted in later
capillary perfusion stage
Complication: Visual loss due to Complication: Neovascular
chronic macular edema glaucoma, rubeosis iridis
Treatment: Treatment:
Self resolving in 50% Panretinal photocoagulation
Visual loss occurs in rest due to (Fig. 11.2C) or cryoapplication to
cystoid macular degeneration, prevent
Steroids for 4–12 weeks are helpful Neovascular glaucoma
in them
Figs 11.2A to C: (A) Central retinal vein occlusion;

(B) Superior temporal vein occlusion; (C) Pan photocoagulation
Q. Define hypertensive retinopathy. Discuss the etiopatho-

genesis, classification, clinical features and management of the
same.
Q. Discuss in detail Keith-Wegner-Barkar classification.
Q. Discuss the Choroidal changes seen in hypertensive retino-
pathy.
Definition: Hypertensive retinopathy refers to fundus changes
occurring in the patient suffering from systemic hypertension.
Etiopathogenesis:
Hypertensive retinopathy in turn is determined by severity and
duration of hypertension.
 Vasoconstriction: Is the primary response of retinal arterioles
to HTN. It is directly proportional to severity of HTN
 Arteriosclerotic changes: Reflects duration of HTN
 Increased vascular permeability: Systemic chronic HTN
narrowing of retinal arterioles retinal ischemia hypoxia
 increased capillary permeability focal retinal edema,
retinal hemorrhage and hard exudates.
Keith-Wegner-Barkar classification (Figs 11.3 and 11.4):
Grade Features
1 Mild generalized arteriolar attenuation especially small branches
Broadening of arteriolar light reflex
Vein concealment
2 Marked generalized narrowing
Salu’s sign: Focal attenuation of the arterioles with deflection of
veins at AV crossing (‘S’ shaped or ‘Z’ shaped)
Obvious broadening of arteriolar light reflex
3 All features of grade 2 plus the following
Mnemonic: BCG vaccine
Bonnet’s sign: banking of veins distal to AV crossing
Copper wiring of arterioles
Cotton wool spots and hard exudates
Gunn’s sign: tapering of vein on either side of AV crossing
Flame shaped hemmorhage
4 All features of grade 3 plus the following
Silver wiring of arterioles
Papilledema
Increase in amount of soft exudates, flame shaped hemorrhages
and cotton wool spots
Figs 11.3A to C: (A) Normal A-V corssing, (B and C) Hypertensive retinopathy
Fig. 11.4: Hypertensive retinopathy
Choroidal changes seen in hypertensive retinopathy are as

follows:
 Usually seen in young individuals
 Elschnig’s spots:
– These are irregularly scattered bright yellow spots with
black center
– They are focal choroidal infracts
 Seigrist’s line: They are pigment deposition along the
choroidal vessels
 Exudative bullous retinal detachment.
Treatment: It is necessarily control of hypertension.

Q. List the differential diagnosis for cherry red spots.

Q. What are Microaneurysms? List the differential diagnosis
for Microaneurysms in retina.
Q. Define diabetic retinopathy. Discuss the etiopathogenesis,
classification, clinical features and management of the same.
Q. Classify diabetic retinopathy and discuss each class in detail.
Q. Discuss the features of Proliferative diabetic retinopathy.
Q. Discuss the features of diabetic Maculopathy.
Q. List the criteria for clinically significant macular edema.
Diabetic retinopathy is more common in type 1 diabetes than in
type 2.
Risk factors of diabetic retinopathy:
 Duration of diabetes
 Poor metabolic control
 Pregnancy
 Associated hypertension
 Nephropathy
 Smoking, obesity and hyperlipidemia
Pathogenesis:
 Diabetic retinopathy is essentially microangiopathy, primarily
affecting pre-capillary arterioles, arterioles and venules
 Microangiopathy causes microvascular occlusion and leakage
 Microvascular occlusion  retinal ischemia  retinal
hypoxia leading to neovascularization and AV shunt formation
 Microvascular leakage increases vascular permeability
hemorrhage and retinal edema
 Chronic retinal edema leads to deposition of hard exudates at

the junction of healthy and edematous retina.
Classification:
1. Non-proliferative diabetic retinopathy (NPDR) mild,
moderate, severe, very severe
2. Proliferative diabetic retinopathy (PDR)
3. Diabetic maculopathy
4. Advanced diabetic eye disease (ADED).
1. Non-Proliferative diabetic retinopathy (NPDR): Ophthal-
moscopic features are as follows (Fig. 11.5A)
 Microaneurysms in the macular area (Earliest detectable lesion)
 Retinal hemorrhage
– Deep hemorrhage: Dot and Blot hemorrhage
– Superficial hemorrhage: Flame shaped hemorrhage
 Hard exudates: are yellowish white waxy looking patches
are arranged in clumps or in circinate pattern around macula
 Retinal edema characteristic of retinal thickening
 Cotton-wool spots
 Venous abnormalities: Like beading, looping, dilatation
 Dot-blot hemorrhages representing hemorrhagic retinal infarct.
2. Proliferative diabetic retinopathy (PDR) (Fig. 11.5B):

 Develops in more than 50% of the cases after about 25 years
after the onset of the disease
 Therefore it is more common in Type 1 diabetics
Ophthalmoscopic features are as follows:
 Neovascularization:
– Develops only when more than one-fourth of retina is
ischemic
Figs 11.5A and B: (A) Background retinopathy; (B) Proliferative retinopathy

– It may be on the optic nerve head (NVD- new vessel at
disc) or along course of major blood vessel (NVE- new
vessel elsewhere)
– NVD is more dangerous than NVE, as they have greater
propensity to bleed
– Fluorescein angiography: Seen as hyperfluorescent areas
with leakage from new blood vessels.
 Posterior vitreous detachment
 Hemorrhage: May be intraretinal, preretinal or vitreous
hemorrhage
– A preretinal (Subhyaloid) hemorrhage has a boat shaped
configuration which demarcates the level of posterior
vitreous detachment
Types of PDR: Based on high risk characteristics (HRC) PDR
is classified into the following
– PDR without HRC or early PDR
– PDR with HRC or advanced PDR are as follows
• NVD 1/4 to 1/3 of disc are with or without vitreous
hemorrhage (VH) or preretinal hemorrhage (PRH)
• NVD < 1/4 of disc are with VH or PRH
• NVE > 1/2 disc are with VH or PRH
3. Diabetic maculopathy
 Changes in macular lesion requires special mention due to its
effect on vision
 These changes may be associated with NPDR or PDR
 Diabetic macular edema occurs due to increased permeability
of the retinal capillaries
 It is termed as clinically significant macular edema (CSME)
if one of the three criteria is present on the slit lamp
examination with 90D lens:
– Thickening of the retina at the fovea or within 500 microns
of the center of fovea
– Hard exudates at the fovea or within 500 microns of the
center of fovea associated with adjacent retinal thickening
– Development of a zone of retinal thickening one disc
diameter or larger in size, at least a part of which is within
one disc diameter of the Foveal center
 Clinicoangiographically diabetic maculopathy can be
classified into four types
a. Focal exudative maculopathy
 Microaneurysms, hemorrhage and macular edema are
arranged in circinate pattern
 Hard exudates in circinate pattern
 Fluorescein angiography: Focal leak with adequate
macular perfusion
b. Diffuse exudative maculopathy
 Diffuse retinal edema with thickening throughout the
posterior pole
 Few hard exudates
 Fluorescein angiography: Diffuse leakage at posterior pole
c. Ischemic maculopathy:
 Occurs due to microvascular leak
 Clinically characterized by: Marked visual loss with
Microaneurysms, hemorrhages, mild or no macular
edema and a few hard exudates
 Fluorescein angiography: Shows areas of non-perfusion
in early cases seen as enlargement of Foveal avascular
zone (FAZ)
d. Mixed variety.
4. Advanced diabetic eye disease:
Is an end result of uncontrolled PDR
It is marked by complications like:
 Persistent vitreous hemorrhage
 Tractional retinal detachment
 Neovascular glaucoma.
Management:
Investigations:
 Urine examination
 Blood sugar examination
 Fundus Fluorescein angiography.
Treatment:
1. Screening and follow-up for diabetic retinopathy: As follows
No diabetic retinopathy or early NPDR Every year
Moderate NPDR Every 6 months
Severe NPDR Every 3 months
PDR with no risk characteristics Every 2 months
2. Medical treatment: Can be discussed under following

headings:
A. Control of systemic risk factors:
 Strict control of sugars in diabetics
 Lipid reduction
 Control of associated anemia and hypoproteinemia.
B. Role of pharmacological modulation: Drugs are being used
for inhibition of certain biochemical pathways involved
in the pathogenesis of retinal changes in diabetes. These
are
 Protein kinase C inhibitors
 Vascular endothelial growth factors inhibitors
 Aldose reductase and ACE inhibitors
 Antioxidants like vitamin E.
C. Intravitreal steroids reduce diabetic macular edema
Mode of administration:
 Flucinolone acetonide intravitreal implant
 Intravitreal injection of triamcinolone.
3. Photocoagulation:
Remains mainstay of treatment in diabetic retinopathy and
maculopathy.
Either argon or diode laser can be used.
The protocol for laser application is different for macula and
the rest of retina as follows
A. Macular photocoagulation:
 Indications: Clinically significant macular edema
 Contraindication: Ischemic maculopathy
 The procedure should be done before PRP as this will

increase macular edema
 Techniques of macular photocoagulation:
– Focal treatment: With argon-laser photocoagulation
around the Microaneurysms or leaking vessels
– Grid treatment: Photocoagulation is required but
avoiding the fovea (the burns should not be closer
than 500 microns from the foveola).
B. Panretinal Photocoagulation (PRP):
Laser burns are applied 2–3 disc areas from the center of
the macula extending peripherally to equator.
Aim of PRP: To convert the hypoxic area into anoxic area
and thereby to induce involution of new vessels and to prevent
recurrent vitreous hemorrhage.
Indication:
 PDR with HRC’s
 Neovascularization of iris
 Severe NPDR associated with:
– Poor compliance for follow up
– Before cataract surgery/YAG capsulotomy
– Renal failure
– One eyed patient and
– Pregnancy
4. Surgical treatment:
 Is required for advanced cases of PDR
 Pars plana vitrectomy is done for dense vitreous hemorrhage,
tractional retinal detachment and epiretinal membranes.
Q. Define retinitis pigmentosa (RP). Discuss its etiology,

pathogenesis, clinical features, systhemic and ocular
associations and management.
Q. What is classical triad of retinitis pigmentosa (RP)?
Q. List the systemic associations of RP and describe the same.
Definition: Retinitis pigmentosa is defined as a group of
hereditary disorders characterized by night blindness and
constricted visual field.
Typical retinitis pigmentosa or primary pigmentary retinal
dystrophy is a hereditary disorder predominantly affecting rods
more than cones.
Etiology:
Exact etiology is not known but following are the associations
 Inheritance: Autosomal recessive > Autosomal dominant
> X-linked inheritance
 It is mostly bilateral
 Sex: Males are affected more than females
 Age: Appears in childhood and progresses slowly
 Affects all races.
Pathogenesis:
 Degeneration of rods and cones
 Migration of pigments into retina (Fig. 11.6A)
 Degenerated ganglion cells and their axons are replaced by
neuroglial tissue
 Attenuation of blood vessels
 Atrophy of optic disc.
Clinical features:
Symptoms:
 Night blindness
 Progressive visual field defect
 Dark adaptation: Light threshold of peripheral retina is increased
 Tubular vision in advanced cases (Fig. 11.6B).
Fundus changes: The classical triad of RP

1. Retinal pigmentary changes: Resembles bony spicule
 They are perivascular
 Initially equatorial and later spread anteriorly and posteriorly
2. Arteriolar attenuation
3. Waxy-pallor of optic disc, ultimately optic atrophy occurs.
Other fundus changes:
 Colloidal bodies
 Choroidal sclerosis
 Cystoid macular edema
 Atropic maculopathy.
Figs 11.6A and B: (A) Visual retinitis pigmentosa; (B) Visual field changes
Visual field changes:

 Annular or ring scotoma is a characteristic feature which
corresponds to degenerated equatorial zone of retina
 As disease progresses the scotoma increases anteriorly and
posteriorly leaving behind tubular vision.
Electrophysiological changes:
 ERG: Marked subnormal amplitude
 EOG: Shows absence of light peak.
Associations:
Ocular associations of RP are:
 Myopia
 Primary open angle glaucoma
 Microphthalmos
 Conical cornea
 Posterior subcapsular cataract.
Systemic associations of RP:

Systhemic associations Its features
Laurence-Moon-Biedl syndrome RP
Obesity
Hypogenitalism
Polydactyl
Mental retardation
Cockayne’s syndrome RP
Progressive infantile deafness
Dwarfism
Mental retardation
Nystagmus
Ataxia
Contd...
Contd...
Refsum’s syndrome RP
Peripheral neuropathy
Cerebellar ataxia
Usher’s syndromes RP
Labyrinthine deafness
Hallgren’s syndrome RP
Vestibulo-cerebellar ataxia
Congenital deafness
Mental retardation
Bassen-Kornzweig syndrome RP
(Abeta-lipoproteinemia) Ataxia
Acanthocytosis
Fat malabsorption
Kearns-Sayre syndrome Classical triad of
RP
Ocular myopathy
Heart block
Friedreich’s ataxia RP
Posterior column disease
Ataxia
Nystagmus
Subaortic stenosis
Treatment: No effective treatment is available following are being

tried without any breakthrough:
 To prevent progression of the disease the following drugs are
being tried:
– Vasodilators
– Placental extracts
– Transplantation of rectus muscle into subchoroidal space
– Light exclusion therapy
– Vitamin A and E
 Low vision aids in the form of magnifying glasses and night

vision devices
 Socioeconomic rehabilitation
 Prophylaxis:
– Genetic counseling for consanguineous marriage
– Affected patients should avoid concerning.
Q. Define and classify retinal detachment.
Definition: Retinal detachment is separation of neurosensory
retina proper from pigment epithelium.
These two layers are loosely attached two each other with
potential space in between.
Hence actually speaking retinal detachment is a misnomer and
it should be retinal separation.
Classification:
A. Rhegmatogenous (primary)
B. Non-rhegmatogenous (secondary)
 Tractional retinal detachment
 Exudative or solid retinal detachment
Q. Discuss the etiology, clinical features, management and

complications of primary retinal detachment/Rhegmatogenous
retinal detachment.
Rhegmatogenous (primary) retinal detachment is usually
associated with a retinal break (tear or hole) through which the
subretinal fluid (SRF) seeps and separates nuerosensory retina
from pigment epithelium.
Etiology: Not known, following are the predisposing factors

 Age: Most common in 40 to 60 years of age
 Sex: More common in males
 Many cases are myopic
 Myopia
 Aphakia
 Retinal degeneration
 Trauma
 Senile posterior vitreous detachment.
Pathogenesis (Fig. 11.7):

Senile posterior vitreous detachment Retinal degeneration Aphakia Trauma
   
Retinal break

The degenerated fluid seeps through the retinal break and collects as subretinal
fluid (SRF) between neurosensory retina from pigment epithelium

Retinal detachment
Fig. 11.7: Primary retinal detachment

Clinical features:
Prodromal symptoms: Floaters and photopsia.
Symptoms of detached retina:
 Localized relative loss in the field of vision
 Sudden painless loss of vision.
Signs:
 External examination: Eye is normal
 Intraocular pressure: Low
 Marcus Gunn pupil is present in cases with extensive RD
 Plane mirror examination reveals an altered red reflex in
Pupillary area
 Indirect ophthalmoscopy for posterior chamber: shows
following features.
(C/F Mnemonic; 4’F’s – Floaters, Flashes, Falling acuity, Field
loss)
Fresh RD Long-standing RD
Retina is slightly opaque, convex and Retinal thinning
corrugated in appearance Subretinal demarcation
Detached retina freely oscillates with the lines
movement of eye Secondary intraretinal cysts
There is no shifting of fluid Multiple opaque strands of
Breaks appear as red areas (holes or tears) of subretinal fibrosis
discontinuity mainly in peripheral retina
Vitreous shows ‘Tobacco dust’ in the anterior
vitreous with posterior vitreous detachment
 Visual field charting: Reveals scotoma corresponding to area

of RD
 ERG: Subnormal or absent

 USG: Confirms the diagnosis and are useful when media is
hazy.
Complications:
 Proliferative vitreoretinopathy
 Chronic uveitis
 Hypotony
 Phthisis bulbi.
Treatment:
The patient should take rest in recumbent position as far as possible.
Name of the Aim Steps in brief
procedure
1. Sealing of Breaks are found Retinal breaks are detected
retinal breaks and sealed accurately localized and sealed
off using
Cryocoagulation
2. SRF drainage To drain the subretinal Drainage is achieved through a
fluid, hence allows for fine needle inserted through the
immediate apposition sclera and choroid through into
of sensory retina and subretinal space
RPE
3. Scleral To maintain chorioretinal It is a procedure to create an
buckling apposition inward indentation of the sclera
and the choroid
This is achieved by inserting a
solid silicon band or a silicone
sponge and firmly suturing it
into the sclera
Contd...
Contd...
4. Pneumatic To maintain chorioretinal After sealing the breaks with the
retinopaxy apposition cryopexy, an expanding gas
bubbles (SF6 or C3F8) is injected
into the vitreous and patient is
positioned so that the break is
uppermost and the gas bubble
remains in contact with the tear
for 5–7 days
5. Pars plana To maintain Indications:
vitrectomy, chorioretinal All complicated primary RDs
endolaser pho- apposition All tractional RD
tocoagulation Presently even for
and internal uncomplicated primary RD
tamponade
Q. Discuss in brief etiology, clinical features, management and

complications of secondary retinal detachment/Non
Rhegmatogenous retinal detachment.
complications of tractional retinal detachment.
complications of exudative or solid retinal detachment.
Exudative or solid Retinal detachment Tractional Retinal detachment
Mechanism: RD occurs due to the retina Mechanism: RD occurs due to retina
being pushed away by a neoplasm or being mechanically pulled away
accumulation of the fluid beneath the from its bed by the contraction of
retina following inflammation or the fibrous tissue in the vitreous
vascular lesion (Vitreoretinal bands)
Contd...
Contd...
Etiology: Etiology: Mnemonic: 6P’s
A. Systemic diseases: Toxemia of Post-traumatic scar
pregnancy, renal hypertension, Proliferative diabetic retinopathy
blood Dyscarasis and PAN Post-hemorrhagic retinitis
B. Ocular diseases: proliferans
Inflammatory lesions like Orbital Prematurity retinopathy
cellulitis, Scleritis, sympathetic (Retinopathy of prematurity)
ophthalmia Plastic cyclitis
Vascular diseases like central serous Proliferative retinopathy in Eales
retinopathy, exudative retinopathy disease
of coats Pathy- sickle cell retinopathy
Tumors: Retinoblastoma, malignant
melanoma of choroid
Sudden hypotony due to perforation
of globe and intraocular operation
Symptoms: Symptoms:
Floaters are present occasionally Floaters are absent
Photopsia is absent Photopsia is absent
Sudden and rapid loss of vision Slow and progressive loss of visual
field
Signs: Signs:
Retinal breaks are absent Retinal breaks are absent
RD configuration is convex RD configuration is concave
Shifting of fluid is hallmark sign Shifting of fluid is absent
Pattern of retinal vessels disturbed Retinal mobility is reduced
due to neovascularization on the Vitreoretinal bands are seen
tumor summit
Treatment: Treatment: Is difficult
Exudative RD due to transudation, It requires pars plana vitrectomy to
exudation or hemorrhage undergo cut the vitreoretinal retraction
spontaneous regression, thus no bands and internal tamponade
treatment is required
Enucleation in case of
intraocular tumors
Q. Discuss the incidence, genetics, pathology, clinical features,

differential diagnosis and management of retinoblastoma.
Q. Discuss the types and treatment of retinoblastoma.
Q. Discuss the pathology of retinoblastoma.
Q. Discuss in detail management of retinoblastoma.
Q. What are Flexner-Wintersteiner rosettes?
Q. What are Homer-Wright rosettes?
Retinoblastoma is the commonest tumor arising from neuro-
sensory retina.
Incidence:
 It’s a childhood tumor affecting one in 20,000 births
 Age: Usually seen between 1 to 2 years of age
 Sex: Affects both sex
 Race: Common in whites than in blacks
 Bilateral in 30% of the cases.
Genetics and hereditary:

 Deletion of RB gene by two mutations (Knudson’s 2 hit
hypothesis) results in occurrence of retinoblastoma
 RB gene is a cancer suppressor gene, identified as 14 band
on long arm of chromosome 13
 Retinoblastoma is found in two forms: Hereditary and non-
hereditary.
Hereditary Retinoblastoma Non-hereditary Retinoblastoma

Knudson’s 2 hit hypothesis holds good Both the hits occur after fertilizations
Accounts for 40% of all cases Accounts for 60% of all cases
Accounts for 100% of bilateral cases Accounts for 0% of bilateral cases
Accounts for 15% of unilateral cases Accounts for 85% of unilateral cases
It is familial It is not familial
Associated with non-ocular cancers Not associated with non-
ocular cancers
Pathology:
Origin: The tumor arises from immature retinal neural cells called
retinoblasts which have lost tumor suppressor gene.
Gross: A chalky white friable tumor with dense foci of
calcification.
Histology:
 Growth chiefly consists of small round cells with large nuclei
 They resemble cells of nuclear cells of retina
 The cells may be well differentiated or undifferentiated
 Necrosis and calcification may be seen.
Microscopic features (Figs 11.8A to D):

 Flexner-Wintersteiner rosettes: Cells arranged in a single layer
around a central lumen. This is a true rosette and highly
specific of retinoblastoma
 Homer-Wright rosette: Is a radial arrangement of cells around
a central triangle of neural fibers (rather than clear lumen).
Mainly found in neuroblastoma and Medulloblastoma
 Pseudorosette: In necrotic retinoblastoma, several layers of
cells may be seen around blood vessel, within the areas of
extensive necrosis with the formation of pseudorosettes
Figs 11.8A to D: (A) Flexner-Wintersteiner rosettes; (B) Homer-Wright

rosettes; (C) Pseudorosettes; (D) Fleurettes
 Flurette: Is composed of a group of tumor cells and contains

pear shaped eosinophilic processes which project through a
fenestrated membrane
 Histology of metastatic lesion outside retina shows a change
in character of the cell and they resemble sarcomatous cells.
Clinical features: May be divided into four stages
A. Quiescent stage: Lasts for 6 months to 1 year
During this stage the child may develop any of the following features
 Leukocoria or yellowish white pupillary reflex
 Squint
 Nystagmus
 Ophthalmoscopic features: On full mydriasis, fundus
examination may show two patterns (Figs 11.9A and B).
Endophytic Retinoblastoma Exophytic Retinoblastoma
Grows inward from retina into vitreous Growth of the tumor is in
It is well circumscribed polypoidal white mass outward direction
Cottage cheese pattern of calcification noted Separates the retina from
Multiple growths project in to vitreous choroid
Figs 11.9A and B: (A) Exophytic retinoblastoma; (B) Endophytic retinoblastoma
B. Glaucomatous stage:
Symptoms Signs
Severe pain Eyeball is enlarged and proptosed
Redness Conjunctiva is congested
Watering of eyes Cornea is hazy
IOP is raised
Occasionally picture simulating severe, acute uveitis usually
associated with pseudohypopyon and/or hyphema may be
the presenting mode
C. Stage of extraocular extension:

 Growing tumor bursts open through any of these sites: Sclera,
limbus or near optic disc
 Followed by fungation and involvement of extraocular tissue.
D. Stage of distant metastasis:

 Direct spread to optic nerve and brain
 Lymphatic spread to periarticular lymph nodes
 Metastasis to cranial bones and liver.
Differential diagnosis:
 Other causes of Leukocoria (refer Leukocoria)
 Of Endophytic Retinoblastoma: Differentiate from
– Retinal tumors in tuberous sclerosis, neurofibromatosis
– Astrocytoma
– A patch of exudative retinopathy of coats
 Of Exophytic Retinoblastoma: Differentiate from causes of
exudative retinal detachment.
Investigations:
 Indirect ophthalmoscopy
 Plain X-ray of orbit: For presence of calcification and erosion
of optic foramen
 USG: B-scan shows presence of tumor with calcification
 CT scan of the orbit and brain to note the calcification and
spread of the tumor
 Aqueous humor paresthesia: Shows elevated level of LDH
 Carcinoembryonic antigen (CEA) is elevated
 ELISA to differentiate it from Toxocara endophthalmitis
 Lumbar puncture and bone marrow aspiration for evidence
of metastasis
 FNAC when other tests are inconclusive.
Treatment:
A. Tumor destructive therapy:
Indications:
 Diagnosis made in stage 1
 Tumor involving less than half of the retina
 Optic nerve is not involved.
Present recommendation is for sequential aggressive local

therapy (SALT) comprising of multimodality therapy as
follows:
Chemoreduction followed by local therapy (Cryotherapy,
thermochemotherapy, brachytherapy)
 Cryotherapy for small tumors
 Radiotherapy plus chemotherapy for medium sized tumors
 Laser photocoagulation for tumors located posterior to the
equator < 3 mm from fovea
 Thermotherapy for small tumors located posterior to
equator away from macula.
B. Enucleation: Carries good prognosis
Indication:
 Tumor involving > than half of the retina
 Optic nerve involvement
 Glaucoma is present
 Involvement of anterior chamber
Maximum length of optic nerve should be excised.
If optic nerve shows invasion postoperative treatment should
consist of
 Radiotherapy to the apex of orbit
 Chemotherapy (Vincristine, carboplatin, etoposide,
cyclosporine).
C. Palliative therapy is given when prognosis for life is dismal
in spite of aggressive treatment:
Indication: Retinoblastoma with extraocular extension,
intracranial extension, distal metastasis.
Palliative treatment includes:

 Chemotherapy
 Surgical debulking of the orbit or orbital extension
 Radiotherapy.
Poor prognostic factors:
 Optic nerve involvement
 Undifferentiated tumor cells
 Massive choroidal invasion.
Q. What are Pseudogliomas? List the causes for the same.

Pseudogliomas are non-neoplastic conditions that mimic the
clinical picture of retinoblastoma.
Etiology: (Mnemonic: TRP—target rating point)
 T- Toxocara choroiditis and tuberculoma of the choroid
 R- Retinal detachment and retrolental fibroplasia
 P- Plastic iridocyclitis with vitreous abscess and persistent
hyperplastic primary vitreous.
Clinical features:
 Reduced IOP
 Absence of intraocular calcification, enlargement of optic
foramen and calcified mass in cranium in X-rays of orbit,
optic foramen and skull respectively.
Treatment: Treat the cause.
Q. Define Enucleation. Discuss the indications, contra-
indications and steps in brief.
Definition: Enucleation is surgical removal of eyeball.
Indications:
Absolute indications Relative indications
Retinoblastoma Painful blind eye: absolute glaucoma,
Malignant melanoma chronic iridocyclitis, intraocular
Severely traumatized eye hemmorhage
Blind and disfigured eye: Anterior
Collection of donor staphyloma, ciliary staphyloma
eye to eye bank is the Phthisis bulbi
commonest indication Endophthalmitis
Sympathetic ophthalmitis
Contraindications: Panophthalmitis because of the risk of

meningitis through sheath of optic nerve.
Steps in brief (Fig. 11.10):
 The procedure is done under local anesthesia in adults and
under general anesthesia in children
 Universal eye speculum is applied
 Conjunctiva is dissected all around the limbus and the Tenon’s
capsule is separated from the sclera upto the insertion of the
extraocular muscles
 Each rectus is hooked with a squint hook and cut with the
scissors in the order of Superior, Lateral, Inferior and Medial
(Mnemonic: SLIM)
 Speculum is depressed and the eyeball is made to be luxated
out
 Enucleation scissors are introduced with closed-tip along the
lateral side of the globe. Scissors are opened and optic nerve
is severed
Fig. 11.10: Steps of enucleation
 Oblique muscles are severed lastly with same scissors

 Bleeding is stopped by applying pressure within the socket
 Tenon’s capsule and the conjunctiva are suture separately
 Pressure bandage is applied for 48 hours
 Fitting of artificial prosthetic eye may be done after 6 weeks
when healing of the enucleated socket is complete.
Q. What are Phakomatoses.

Q. What are Neurocutaneous markers.
Q. List the features of Sturge-Weber syndrome.
Phakomatoses refer to a group of familial condition (autosomal
dominant transmission) which are characterized by development
of neoplasms in the eye, skin and CNS phakomatoses include:
Phakomatoses Features
Von Hippel Lindau’s syndrome Males are affected more than females
(Angiomatosis retinae) Seen in third and fourth decade of life
Angiomatosis of retina, brain, spinal
cord, kidneys and adrenals
Clinical course of angiomatosis retinae:
Comprises vascular dialation, tortuosity
and formation of aneurysms which vary
in size from small to balloon like
aneurysms followed by hemorrhage
and exudates, retinal detachment and
secondary glaucoma
Tuberous sclerosis Diagnostic triad: Epilepsy, mental
(Bourneville’s disease) retardation and adenoma sebaceum
Associated with hamartomas of brain,
retina and viscera
Ocular lesions: Multiple nodular tumors
seen springing from the optic disc, like
white mulberries (Astrocytoma)
Neurofibromatosis Characterized by multiple tumors in
(von Recklinghausen’s disease) skin, retina and cerebellum
Cutaneous manifestations: Cafe-au-lait
spots to neurofibromatosis
Ocular lesions: neurofibroma of lids and
orbit, glioma of optic nerve and
congenital glaucoma
Contd...
Contd...
Encephalofacial Angiomatosis Angiomatosis in form of port- wine stain
(Sturge-Weber syndrome) involving 1 side of the face
Associated with choroidal
hemangioma, leptomeningeal
angioma and congenital glaucoma
12.
Neuro-ophthalmology
Fundus oculi examination is demonstrated in Figure 12.1.
Fig. 12.1: Fundus oculi examination

Q. Draw the optic tract and the lesions at the various levels.
Mention the cause for the same (Figs 12.2A and B).
Lesion Site of lesion Results in Commonest cause
number
1 Optic nerve Anopsia of right side Optic neuritis (multiple sclerosis)

2 Lateral aspect Right nasal Aneurysm of internal carotid artery
of optic chiasm hemianopsia
Contd...
Contd...
3 Optic chiasm Bitemporal heterony- Craniopharyngioma, pituitary
mous hemianopsia adenoma
4 Optic tract Left homonymous Vascular lesion
hemianopsia
5 Optic radiations Vascular due to occlusion of
posterior cerebral artery
6 Meyer’s loop/ Right homonymous Occlusion of a branch of middle
temporal loop superior quadrantanopia cerebral artery
7 Optic radiations Right homonymous Occlusion of a branch of posterior
to cuneus inferior quadrantanopia cerebral artery
8 Cerebral cortex Right homonymous Occlusion of posterior cerebral
hemianopsia with artery
macular sparing*
*lesion at 8 has macular sparing because this region also receives collateral from middle cerebral artery
Neuro-ophthalmology 277
Figs 12.2A and B: (A) Visual system 1; (B) Visual system 2
Q. Describe the pathway of light reflex.

Q. Describe in detail pupillary reflex.
Pupillary reflex consists of: light reflex, near reflex and
psycosensory reflex (Fig. 12.3).
A. Light reflex:
1. Direct light reflex: When light is thrown on an eye, the
pupil of the same eye constricts. This is direct light reflex.
Fig. 12.3: Pathway of the pupillary light reflex
 Afferent pathway: The optic nerve optic chiasm

optic tract pretectal nucleus Internuncial fibers
 Center: Edinger-Westphal nucleus in brainstem (third
nerve nucleus)
 Efferent pathway: Inferior division of oculomotor nerve
 ciliary ganglion short ciliary nerves sphincter
pupillae.
2. Indirect light reflex: When light is thrown on an eye, the
pupil of the other eye constricts. This is called as indirect
light reflex. This is because fibers from the pretectal
nucleus project into Edinger-Westphal nucleus of both the
sides.
B. Near reflex: Occurs on looking a near object. It has two
components (Fig. 12.4)
Fig. 12.4: Pathway of the near reflex
1. Convergence reflex: Contraction of pupil on convergence

 Afferent: Fibers from the medial rectus  oculomotor
nerve  mesencephalic nucleus of 5th nerve 
convergence center in the tectal and pretectal nucleus
 Center: Edinger-Westphal nucleus in brain stem (third

nerve nucleus)
 Efferent: Oculomotor nerve  accessory ganglion 
sphincter pupillae.
2. Accommodation reflex:
 Afferent: Optic nerve relays bilaterally
 Center: Edinger-Westphal nucleus in brainstem (third
nerve nucleus)
 Efferent: Oculomotor nerve (via accessory and ciliary
ganglion).
3. Miosis
C. Psycosensory reflex: Dialatation of pupil in response to
sensory or psychic stimuli.
Q. What is Marcus-Gunn pupil/Relative afferent pupillary
defect (RAPD)?
 Marcus-Gunn pupil occurs in defect of visual pathway anterior
to chiasma
 It consists of :
– A diminished amplitude of pupillary reaction
– A lengthened latent period and
– Pupillary dilatation with continuous stimulation
 Detection: Swinging flash light test
– Normally, if an illuminated pen light is alternately directed
to each eye, the pupils constrict and do not vary as the
light alternates between the eyes
– In afferent pupillary defect, both the pupils dilate when the
light is moved from the unaffected eye to the affected eye.
But they constrict when light is directed to the normal eye
 Afferent pupillary defect is most conspicuous in unilateral

optic neuritis. It distinguishes the reduction of visual acuity
caused by optic neuritis, from that caused by cytoid macular
edema or central serous retinopathy.
Q. What is Argyll-Robertson pupil?
 Argyll-Robertson pupil is a bilateral abnormality characterized
by failure of the pupils to constrict with light but retention of
constriction present with accommodation.
 Seen in:
– Tabes dorsalis/Neurosyphilis (most common)
– Nonsyphilitic causes diabetes, multiple sclerosis,
hemorrhage, tumors
 Site of lesion: Internuncial fibers between pretectal nucleus
and Edinger-Westphal nucleus at the level of pretectum
 The entire syndrome includes:
– Absence of light reaction
– Presence of accommodation reflex
– Pupils are miotic, irregular, eccentric and unequal
– Pupils fail to dilate with mydriatic
– Presence of good vision in both the eyes
– Pupil does not dilate fully after administration of mydriatic
(atropine).
Q. What is Adie’s pupil/Holme Adie’s pupil/syndrome?
 Adie’s pupil is a disorder of pupil of unknown etiology
associated with degeneration of ciliary ganglion
 It usually occurs in young women and is associated with
absent knee jerk
 Adie’s pupil features;

– Pupil is slightly dilated
– Although reaction to the light appears to absent at first,
careful examination reveals it to be present, as a vermiform
slight constriction
– The reaction to light in affected eye both direct and
consensual are delayed/slight or absent
– The reaction of pupil on convergence is sluggish with long
latent period and is unduly sustained
– The tonic pupil dilates well with atropine. Topical 2.5%
methacoline causes constriction of Adie’s pupil but not of
normal pupil.
Q. What is Hutchison’s pupil?
 Hutchison’s pupil is an abnormal dilated pupil
 Lesion: raised intracranial tension herniation of temporal
lobe into tentorial hiatus or posterior cerebellar or superior
cerebellar artery impingement or compression of the III
cranial nerve Hutchison’s pupil
 Etiology; Cerebral injury/hemorrhage, cerebral abscess/
edema/tumor
 Features: Hutchison’s pupil has three stages of progression
– Initial stage of miosis due to irritation of ipsilateral III nerve
– Dilatation of ipsilateral pupil which still reacts to light and
convergence though the patient is drowsy
– True Hutchison’s pupil, where pupil is dilated with loss of
all reflexes. Increased drowsiness and patient may go into
coma and paresis of extraocular muscles supplied by
cranial nerve III
– In terminal stage contralateral pupil becomes dilated and

fixed. It is a grave prognostic sign and is an indication of
cerebral decompression.
Q. What is Horner’s syndrome?
 Horner’s syndrome consist of miosis, partial ptosis, enophthalmos
and anhydrosis of same side of the face (Fig. 12.5)
 In congenital form it is also associated with the heterochromia
of the iris
 Lesion: Damage to sympathetic innervation of the eye
 Etiology:
– In cervical region: apical bronchial carcinoma, neck gland
tumors
– Centrally: Multiple sclerosis, pontine tumors, syringomyelia
 Treatment: If cosmetically unacceptable, ptosis can be
corrected surgically (Mullerectomy).
(Mnemonic: Horner’s syndrome presents with NOPALM-
eNOphthalmos, Ptosis, Anhidrosis, Loss of ciliospinal reflex,
Miosis. Less common feature associated—4H’s—Hyperactive
accommodation, Hypochromic heterochromia, Hypotony,
Hyperemia)
Fig. 12.5: Horner’s syndrome

Q. Define Optic Neuritis. Discuss the etiology, types, clinical

Q. Define papillitis/Nueroretinitis/retrobulbar neuritis. Discuss
the etiology, clinical features and management of the same.
Q. List the complications of optic neuritis.
Definition: Optic neuritis is inflammation and demyelinating
disease of the optic nerve.
Etiology:
 Idiopathic
 Infective: Acute ethamoiditis, cat scratch fever, syphilis,
cryptococcal meningitis in AIDS
 Hereditary Leber’s disease
 Demyelinating diseases: Multiple sclerosis (commonest)
 Parainfectitious
 Toxic: Toxic amblyopias due to- tobacco, alcohol and methyl
alcohol, drug induced (ethambutol, quinine).
Mnemonic: IDIOPA  Idiopathic, demyelinating diseases,
infection, others–hereditary, parainfectious, alcohols, tobacco
and other toxics.
Anatomical types:
Type Inflammation of (definition)
Papillitis Optic disc (associated with demyelinating disease)
Neuroretinitis Optic disc and surrounding retina in macular area
Retrobulbar neuritis Optic nerve behind the eyeball
Clinical features:
Symptoms:
 Sudden, progressive, profound visual loss
 Markedly lowered dark adaptation
 Visual obscuration in bright light
 Impaired color vision
 Movement and sound phosphenes (phosphenes refers to
glowing sensation produced by nonphotic or inadequate
stimuli)
 Depth perception of moving objects is lost
 Episodic transient obscuration of vision
 Mild pain in eye.
Signs:
 Decrease in visual acuity
 Impaired color vision (Color vision tests)
 Pupil: Marcus Gunn pupil
 Ophthalmoscopic features (Figs 12.6A and B):
– Hyperemic disc
– Blurred margins
– Disc: Edematous and physiological cup is obliterated
– Retinal veins: Tortuous and congested
– Sphincter hemorrhages
– Fine exudates in the disc
– Slit lamp examination:
• Papillitis: Inflammatory cells may be seen in vitreous
• Nueroretinitis: Retinitis signs, macular star formation
• Retrobulbar neuritis: Fundus appears normal (Neither
the patient nor the doctor sees anything)
Figs 12.6A to C: (A) Early changes; (B) Late changes Papillitis; (C) Visual field changes
Fig. 12.7: Retrobulbar neuritis and its field changes
• Visual field changes: Central and centro-cecal scotoma

(Figs 12.6C and 12.7)
• Contrast sensitivity: Impaired
• VER: Decreased amplitude and delay in transmission time.
Differential diagnosis:
Papillitis Acute retrobulbar neuritis
Papilledema Malingering
Pseudopapilledema Hysterical blindness
Cortical blindness
Indirect optic neuropathy
Complications:
 Altered color vision
 Primary optic atrophy
 Postneuritic optic atrophy
 Recurrent papillitis
 Complete blindness.
Investigations: X-ray, CT and MRI may be used to establish

demyelination.
Treatment:
 Treat the cause
 There is no treatment option available for hereditary and
idiopathic demyelinating disease
 Corticosteroids accelerates the rate of recovery
 IV ACTH is an alternative
 Periocular injection of depot steroids
 Inj Vitamin B1, B6, B12 in full dose
 Interferon  is useful in multiple sclerosis.
Q. Define Papilledema. Discuss the etiology, pathogenesis,

types, clinical features and management of the same.
Definition: Papilledema is the bilateral, noninflammatory passive
swelling of the optic disc produced by raised intracranial pressure.
Disc edema (see below) and Papilledema look alike.
Etiology: (Mnemonic: OPTICS)
O: Obstruction of CSF absorption or over secretion of CSF
P: Pseudotumor cerebri
T: Tumors of the spinal cord
I: Intracranial infection: meningitis, encephalitis

I: Intracranial hemorrhage—Cerebral or subarachnoid
I: Intracranial space occupying lesion like abscess, tuberculoma,
gumma
C: Congenital
C: Craniosynostosis
S: Systemic causes- malignant HTN, nephritis, Pre-eclampsia,
blood dyscariasis.
Pathogenesis: Hayreh’s theory: raised CSF pressure 
axoplasmic stasis in optic nerve head  swelling of optic disc
and secondary changes at the disc surface.
Clinical features:
General features Ocular features
Headache Amaurosis fugax
Nausea Visual acuity and pupillary reaction
Vomiting will be normal till late stages
Diplopia
Focal neurological deficit
Papilledema is described in four stages:

Stage Symptoms and Pupillary Visual Ophthalmoscopic
visual acuity reaction field features
Early Absent Normal Fairly Obscuration of disc
(Fig. 12.8A) VA: normal normal margin first in the
nasal margin
Blurring of peripheral
nerve fiber layer
Absence of spontaneous
venous pulsation at the disc
Mild hyperemia of the disc
Contd...
Contd...
Established Amaurosis Fairly Enlargement Optic disc edema is seen
fugax normal of blind spot Fig. 12.9 as forward elevation
for few sec above the plane of retina
VA: usually Physiological cup obliteration
normal Disc: margins blurred,
hyperemic
Soft and hard exudates
Veins: tortuous and engorged
Circumferential grayish white
fold due to separation of optic
nerve fibers by edema
Chronic/ Appear Usually Blind spot Acute hemorrhage
long VA: variable normal enlarged Exudates resolve
standing decrease
Visual field Optic disc appears like dome
begins to of Champagne cork
constrict Central cup obliteration
Corpora amylacea: crystalline
deposition on disc surface
Mnemonic: 7C’S of Chronic
stage, Constricted visual field,
Champagne cork optic disc,
Central Cup obliteration,
Corpora amylacea-Crystalline
deposition on disc surface
Atropic Progress Light Concentric Mnemonic: ABCD
(Fig. 12.8B) VA: severely reflex contraction A– Arterioles narrowed
impaired impaired of peripheral B– Blood vessels, sheathing
field around them
C– Congested veins
D–Disc prominence
decreases
D– Disc appears grayish
white due to atrophy
and gliosis
Figs 12.8A and B: (A) Early changes; (B) Late changes
Fig. 12.9: Papilledema and edematous retina
Treatment:
 It is an emergency
 Identify and treat the cause
 Surgical decompression of the optic nerve.
Q. What is disc edema? List the causes for the same.

Disc edema or disc swelling includes all cases of acute and
passive swelling of disc.
Disc edema and Papilledema look alike.
Etiology: (Mnemonic: DISCO)
D: Disc edema causes are as follows
I: Inflammatory: Papillitis, Nueroretinitis
I: Increased intracranial pressure due to any cause
S: Systemic causes—anemia, uremia, anterior ischemic optic

atrophy
C: Congenital anomalous elevation (Pseudopapilledema)
O: Ocular causes—uveitis, hypotony, CRVO, tumors, Graves’
disease, orbital cellulitis.
Q. Define Optic atrophy. Discuss the classification, clinical
Definition: Optic atrophy is degeneration of the optic nerve,
which occurs as a result of any pathological process that damages
axons of the anterior visual system (retinal ganglion cells to lateral
geniculate body).
Classification:
A. Primary versus secondary optic atrophy
Primary optic atrophy Secondary optic atrophy
Occurs without any local disturbance but Follows the disease of retina,
is associated with the diseases of CNS like causing excessive degeneration
Tabes dorsalis of ganglion cells
Multiple sclerosis (commonest cause) Retinitis pigmentosa
Glaucomatous optic atrophy CRAO
Compression by tumor Retinochoroiditis
B. Ascending versus descending optic atrophy

Ascending optic atrophy Descending optic atrophy
Ascends from retina to lateral Starts at optic nerve fibers anterior
geniculate body to the lateral geniculate body and
terminates at the optic disc
C. Ophthalmoscopic classification
Type Pathology Etiology Ophthalmoscopic features
Primary Lesions proximal Multiple sclerosis Color of disc: chalky white
optic to optic disc Retrobulbar neuritis Edge: sharp outline
atrophy without Leber’s disease Slight recession of complete
antecedent Pituitary tumors optic disc occurs in total
papilledema Traumatic avulsion atrophy
of optic nerve Lamina cribrosa is clearly
Toxic amblyopia seen at the bottom of the
Tabes dorsalis physiological cup (stipling
may be seen)
Retinal vessels: normal
Consecutive Follows Posterior uveitis Color of disc: yellow waxy
optic atrophy destruction of Endophthalmitis Edge: not sharply defined
ganglion cells Retinitis pigmentosa Retinal vessels: attenuated
secondary to Pathological myopia
inflammation CRAO
or degenerative
conditions of
retina or choroid
Postneuritic Squeal of See the causes for Color of disc: dirty white
optic atrophy papilledema the same Edge: blurred
or papillitis Lamina cribrosa not seen
Physiological cup obliterated
Retinal vessels: obliterated,
sheathing present
Glauco- Long standing See the causes for Disc: deep and wide cupping
matous raised IOP the same Nasal shift of blood vessels
optic
atrophy
Vascular/ Disc ischemia Anemia Disc: pale
ischemic Giant cell arteritis Retinal vessels: attenuated
optic Severe hemorrhage
atrophy
Clinical features:
 Loss of vision: sudden or gradual, total or partial
 Pupil:
– Semidilated
– Direct light reflex: sluggish or absent
– Marcus Gunn pupil.
 Visual field loss:
– Generalized in systemic causes
– Central in focal neuritis
– Eccentric in nerve/tract compression.
 Ophthalmoscopic appearance: discussed in detail above
(Fig. 12.10).
Treatment: Treat the underlying cause
Figs 12.10A to C: (A) Primary optic atrophy; (B) Consecutive optic atrophy;
(C) Postneuritic optic atrophy
Q. List the common causes of Hamartopia, Nyctalopia,

Amaurosis fugax
Hamartopia/day Nyctalopia/night Amaurosis fugax (Sudden
blindness blindness painless loss of vision)
Central corneal opacities Vitamin A deficiency TIA
Central lenticular Familial CRAO
degeneration (polar Retinitis pigmentosa Embolism
cataract) Congenital high Hypertensive
Congenital deficiency myopia retinopathy
of cones Oguchi disease Nonischemic CRVO
(Mnemonic: 3 C’s) Paracentral lenticular Giant cell arteritis
opacities/Corneal Papilledema
opacities
POAG
Q. What is toxic amblyopia? Discuss the common etiological

agents and management of the same.
Toxic amblyopia refers to a number of conditions in which optic
nerve fibers are damaged by a number of external agents.
Two types of toxic effect have been noted:
 Central or centrocecal scotoma (Between blind spot and
fixation point)
 Generalized depression of the vision with contraction of the
visual field
Toxic agents Treatment
Tobacco-alcohol amblyopia 1000 units of hydroxyl-cobalamine for 3 months
Methyl alcohol amblyopia Rapid correction of acidosis
Correct dehydration
Contd...
Contd...
Administration of ethyl aclohol which
competes with methyl alcohol for metabolism.
Injection Vitamin B1, B6, B12
Ethambutol amblyopia Discontinue the drug injection
hydroxyl-cobalamine
Quinine amblyopia Discontinue the drug Vasodilators
Other toxic agents that cause amblyopia are: Cannabis

indica, lead, arsenic, carbon disulfide, streptomycin, INH, digoxin.
Q. What is malingering?
 Malingering is a willful, deliberate, and fraudulent feigning
or exaggeration of symptoms of illness or injury (here
blindness) for a desired perceived benefit.
 Such patients may complain loss of vision (complete/partial)
which is usually sudden in onset.
 These perceived benefits may include avoiding work,
obtaining drugs, getting lighter criminal sentences, avoiding
school, or simply attracting attention or sympathy.
Q. Differentiate between Papilledema and Pseudopapillitis.
Q. Differentiate between papillitis and Pseudopapillitis.
Q. Differentiate between Papilledema and papillitis.
Features Papilledema Papillitis Pseudopapillitis
1. Laterality Usually bilateral Usually unilateral May be unilateral
2. Symptoms:
Visual acuity Transient attacks Marked loss of Defective vision
of blurred vision vision of sudden depending upon
Contd...
Contd...
Later vision onset of the degree of
decreases due refractive error hypermetropia
to optic atrophy
Pain and Absent May be present Absent
tenderness with ocular
movements
3. Fundus
examination
Media Clear Posterior vitreous Clear
haze
Disc color Red juicy Marked Reddish
appearance hyperemia
Disc margins Blurred Blurred Not well defined
Disc swelling 2–6 diopters  3 diopters Depending upon
the degree of
hypermetropia
Peripapillary Present Present Absent
edema
Venous More marked Less marked Not Present
engorgement
Retinal Marked Not Present Not Present
hemorrhage
Retinal More marked Less marked Absent
exudates
Macula Macular star Macular fan Absent
might be present might be present
i. Fields Enlarged blind Central scotoma No defect
spot more for colors
ii. Flourescein Vertical oval Minimal leakage No leakage of dye
angiography pool of dye of dye
due to leakage
13.
Strabismus
Q. Discuss the anatomy of extraocular muscles in detail.

Q. Discuss the origin, insertion, nerve supply and action of
extraocular muscles (Figs 13.1 to 13.4).
Extraocular Origin Insertion Nerve supply$ Action*
muscle
Medial rectus Medial part of All the 4 recti are Cranial nerve 3 Adduction
the common inserted into the
tendinous ring sclera by flat
tendons at diffe-
rent distances
from the limbus
Superior rectus Superior part of Cranial nerve 3 Abduction

the common ten-
dinous ring and
adjoining Dura
covering the
optic nerve
Inferior rectus Inferior part of Cranial nerve 3 Elevation, intorsion,

the common adduction
tendinous ring
Lateral rectus Lateral part of Cranial nerve 6 Depression, extorsion,

the common ten- adduction
dinous ring by
2 heads
Contd...
Contd...
Superior Bone above Upper and outer Cranial nerve 4 Intorsion, Depression,
oblique and medial to part of the sclera Abduction
the optic foramen behind the equator
after it turns
around a pulley
Inferior Orbital plate of Lower and outer Cranial nerve 3 Extorsion, Elevation,
oblique the maxilla just part of the sclera Abduction
lateral to the behind the equator
orifice of the
nasolacrimal
duct
# Tendinous ring is also called as the annulus of Zinn and is attached at the apex of the orbit and medial part of the
superior orbital fissure
$ SO4 LR6 Rest supplied by 3
*In the order of primary, secondary and tertiary action
Fig. 13.1: The extraocular muscles of the eye

Strabismus 299
Fig. 13.2: Posterior aspect of right eye
Fig. 13.3: Insertion of recti muscle tendons in sclera

Fig. 13.4: Conjugate movements of the eyeball
Q. Define Amblyopia. Discuss the etiopathogenesis, types,

clinical characters and management of the same.
Q. What is occlusion therapy?
Definition: Amblyopia refers to partial loss of vision in one or
both the eyes in absence of any organic disease of the ocular
media, retina and visual pathway.
Etiopathogenesis:
 Amblyopia is produced by some amblyopic factors operating
during critical period of development of the eye (birth to
6 years of age)
Strabismus 301
 First six months of the age is the most sensitive period to

develop amblyopia and it rarely develops after 6 years of age
 Amblyopic factors include:
– Visual deprivation as it occurs in anisometropia
– Light deprivation, e.g. congenital cataract
– Abnormal binocular interaction, e.g. in strabismus.
Types: Depending upon the cause amblyopia is of the following
types
Type Results from Etiology
Stimulus The non-use of one eye Cataract, leukoma (Opacities
deprivation in infancy and early in the media)
Amblyopia childhood Complete ptosis
Strabismic Develops in a squinting Unilateral constant squint.
amblyopia eye Such patients fixate with one
eye
Anisometropic Occurs in the more Anisohypermetropia>
amblyopia Anisometropic eye, as Aniso-astigmatism>
a result of constantly Anisomyopia
blurred image of an
object falling on its
fovea
Ametropic High refractive errors Commonly bilateral high
amblyopia of both the eyes hypermetropia
Meridional Selective amblyopia for Uncorrected astigmatic
amblyopia a specific visual meridian refractive error
Treatment:
Treatment should be started as early as possible (younger the
child better is the prognosis).
(Mnemonic: FOR amblyopia—indicates first letters of the

treatment principle F—Full correction of refractive errors,
O— Occlusion therapy, R—Removal of the opacities of the
media. R and F should however precede O)
 R—Removal of the opacities of the media*
 F—Full correction of refractive errors*
*these measures are instituted before occlusion therapy is
started
 Occlusion therapy
– The aim is to occlude the sound eye and force to use the
amblyopic eye
– Simplified schedule for occlusion therapy depends on age
(up to 2 years occlusion should be done 2:1, i.e. 2 days in
sound eye and 1 day in amblyopic eye, at 3 years 3:1 , at 4
years 4:1, at 5 years 5:1, after age of 6 years 6:1)
– Duration of occlusion therapy:
• Till visual acuity develops fully or
• There is no further improvement of vision for three
months.
Other treatment options: (Mnemonic: CAP)
 C—CAM stimulator therapy: Consists of viewing rotational
high Contrast stripes of different sizes with amblyopic eye
 A—Atropine penalization: Atropine is used to blur the sound
eye
 P—Pleoptics are methods of foveal fixation and may be
helpful in older children.
Strabismus 303
Q. Define Squint (Strabismus). Classify the same.

Definition: A misalignment of the visual axes of the two eyes is
called Squint.
Classification: (Mnemonic: MLA—Apparent squint, Latent
squint, Manifest squint)
Q. What is apparent squint (pseudostrabismus)? List the causes
for the same.
Apparent squint is a condition in which the visual axes are in
fact parallel, but the eyes seem to have squint.
Types and causes:
Pseudoesotropia (apparent Pseudoexotropia
convergent squint) (Apparent divergent squint)
Prominent epicanthal folds Hypertelorism
Myopia Hypermetropia
Q. What is Heterophoria (latent squint)? Discuss the types,

In heterophoria (latent squint), there is a tendency for deviation
of the eyes is present when fusion is broken. However, the eyes
regain their normal alignment or position with fusion.
Types:
 Esophoria—There is a tendency for deviation of the eyeball
inwards
 Exophoria—There is a tendency for deviation of the eyeball
outwards
 Hyperphoria—There is a tendency for deviation of the eyeball
upwards
 Cyclophoria—There is a tortional deviation of the eyeball

 Anisophoria—The deviation of the eyeball varies with the
direction of the gaze
 Orthophoria—There is no deviation of the eyes even when
the fusion is broken.
Etiology:
 Increase requirement for accommodation and convergence
as in hypermetropia results in Esophoria
 Decrease requirement for accommodation and convergence
as in myopia results in Exophoria
 Occupational requirement too much close work such as
goldsmith and watchmakers
 General poor health, fatigue and advancing age.
Symptoms:
 Eyestrain and headache
 Blurring of prints and overlapping of words or lines while reading
 The patient complains of seeing double objects after close
work for prolonged period (Intermittent squint).
Diagnosis:
Test Principle/comment
Cover test Fusion of the two eyes is abolished by covering one eye
Maddox Rod test This test is done to find out heterophoria for distance. It
alters the appearance of the retinal image in one eye.
There is no stimulation given for fusion
Maddox Wing test The Maddox wing is an instrument that dissociates the
two eyes for near fixation (one-third of a meter) and
measures the amount of heterophoria
Contd...
Strabismus 305
Contd...
Prism vergence test The actual measurement of the deviation and strength
of the muscles involved are tested. The muscles are
forced to act with maximum effort against the prism
Synaptophore To know the range of fusion
evaluation
Treatment (Mnemonic: SHEEPS)

 Smaller degrees of heterophoria which give rise to no
symptom requires no treatment
 General improvement of Health and nutrition is necessary.
Proper position, distance and illumination while doing near
work is maintained with suitable breaks in between
 Errors of refraction should be corrected
 Exercises to increase the fusional reverse and convergence
are advised :
– Pencil exercise: A pencil is held in the hand and is brought
slowly towards the nose until the tip appears double. The
two images are then fused into a single image by an effort.
This is repeated 3 to 4 times a day for several weeks
– Exercise the weak muscles against the prisms
– Exercise the weak muscles by the use of the Synaptophore
 Prisms can be prescribed in the spectacles to correct the defect
optically. The base of the prism is kept towards the muscle to
be helped
 Surgery: It is rarely indicated, especially in a large deviation
and then the heterophoria is to be treated as heterotropia.
Q. Define Concomitant squint. Discuss the types, etiology,

Q. Discuss in detail the management of concomitant squint.
Q. What is Uniocular concomitant squint? Discuss the types,
Q. What is Alternating concomitant squint? Discuss the types,
Q. What is Concomitant convergent squint? Discuss the types,
Q. What is Concomitant divergent squint? Discuss the types,
Definition: Concomitant squint is the dissociation of the eyes,
wherein the angle of deviation remains the same in all directions
of the gaze, irrespective of the eye of fixation.
Etiology:
 In concomitant squint the eyes are not in alignment but they
retain their abnormal relation to each other in all the
movements of the eye.
 The efferent pathway (nerve and muscles) are normal.
However, the afferent pathway is defective due to poor visual
acuity as a result of:
– Defects in the eyes
– Breaking down of fixation and fusional reflex.
Types:
1. Uniocular concomitant squint: convergent/divergent
2. Alternating concomitant squint: convergent/divergent
Strabismus 307
1. Uniocular concomitant squint: When one eye deviates

always and the normal eye takes up and maintains fixation, it
is known as Uniocular concomitant squint
– Concomitant convergent squint:
– In this condition one eye always deviates inwards while
the other eye fixes the object
– This develops typically in early life before the binocular
reflexes are firmly established (before 6 years of age)
– It usually follows debilitating illness.
Etiology: (Mnemonic: DCH MA)
– D—Decompensetion of esophoria
– C—Congenital myopia: due to excessive use of
convergence for near vision
– H—Hypermetropia wherein excessive convergence and
accommodation is needed
– M—Media factor, i.e. opacities in the media (Cornea, lens,
vitreous opacities)
– A—Anatomical factors, e.g. orbital asymmetry, enophthalmos.
 Concomitant divergent squint:
– In this condition one eye always deviates outwards while
the other eye fixes the object.
Etiology:
– In inherent neuromuscular coordination
– Complete loss of vision: The blind eye deviates particularly
in adults
– In myopia commencing at a later age: When the vision in
one eye is greatly reduced, it takes up the position of rest
that is divergence.
2. Alternating concomitant squint:

– In this type of squint one eye fixes, the other eye deviates
either inwards or outwards and either of the eyes can take
up fixation alternately
– In an alternate squint, the visual acuity remains normal in
each eye
– There is no diplopia as the image formed in the deviating
eye is completely suppressed by the brain.
Etiology:
– Weakness of either of medial or lateral rectus of each eye
– Refractive errors.
Symptoms:
 Usually there is no symptom. The squinting of the eye is
noticed by the parents or relatives. There is no diplopia, as
the suppression develops easily in the young age
 In case of Uniocular squint, visual acuity is usually poor
(Strabismic amblyopia). This is maximum with convergent
squint
 There is no limitation of the eye movements.
Signs:
Primary angle of deviation is equal to the secondary angle of
deviation (the primary angle of deviation means, the angle of
deviation of the squinting eye when other eye fixes an object.
Secondary deviation means the angle of deviation of the normal
eye under cover, when the squinting eye is made to fix an object
by covering the normal eye (Fig. 13.5)).
Strabismus 309
Fig. 13.5: Primary and secondary deviation
Evaluation of concomitant squint:

History: enquire for the following
 Age of onset:
– Accommodative squint usually manifest around 3 to 6
years of age
– The squint due to paresis of muscles appear at a very early
age
– The prognosis is better if the age of onset is late
 Any history of acute illness, head injury, mental shock at the
time of onset
 Family history of squint or refractive error may be positive
 Is the squint intermittent or constant
 Is the squint unilateral or alternating
 Diplopia or head posture: To differentiate it from a paralytic
squint.
Examination:
 Visual acuity is tested
 Refraction under atropine to find out any refractive error
 Ocular motility; to find out any limitations
 Cover test
 Anterior segment and the fundus to rule out any organic lesion
which may be the cause of squint
 Measurement of the angle of squint by corneal reflection test
(Hirschberg test): This is a quick and useful method to measure
the angle of squint by position of the corneal reflex when the
light is thrown into the eye from a distance of about 50 cm
 Worth’s ‘four dot’ test: To diagnose the presence of
suppression and abnormal retinal correspondence in a
manifest squint
 State of binocular vision:
– All three grades of binocular vision (simultaneous macular
perception, fusion and Stereopsis) are determined by
Synaptophore
– The alternating squint does not possess any grade of
binocular vision
– In intermittent squint, binocular vision is being maintained
for the part of the time.
Treatment:
Aim: To make the eyes straight and to ensure binocular single
vision.
The treatment should be started as early as possible so that
restoration of binocular single vision is possible (Prognosis is
poor after 6 years of age).
Strabismus 311
Treatment (Mnemonic: 4’O’):

 Optical correction of refractive errors by suitable spectacles.
Some squint (particularly fully accommodative convergent
squint) are completely controlled by spectacle correction
 Occlusion therapy to treat amblyopia
 Orthostatic exercises given to achieve binocular vision and
to increase the range of stereoscopic fusion preoperatively
and postoperatively
 Operative methods:
– Indications for the surgery: When the squint is more than
10º even after wearing suitable glasses and orthoptic
training for a reasonable period
– Two main types of operation are:
1. Weakening procedures that decreases the pull of a
muscle:
Weakening procedure What is done
Recession Muscle insertion site is move posteriorly
Marginal myotomy Partial resection of the muscle
Myotomy Full portion of a muscle is cut
Disinsertion The muscle is disinserted
Faden procedure Suturing the muscle belly to the globe
2. Strengthening procedures that enhance the pull of the muscle:

Strengthening procedures What is done
Resection Effective pull of the muscle is increased by making
it short
Contd...
Contd...
Advancement The muscle is first disinserted and is reinserted
nearer to the limbus
Tucking This effectively shortens the muscle
General principles of squint surgery:

 The degree of resection/recession cannot be calculated. However
1 mm resection/recession of medial rectus corrects about 3º of
deviation and for lateral rectus it is about 2º
 Medial rectus should not be resected more than 5.5 mm (as it
may cause convergence insufficiency). The same is 7 mm for
lateral rectus
 It is wise to err in under correction specially in children (As a
residual 5 to 10 degree will disappear once stereotypic vision
is established)
 It is preferable to operate on elevators than on depressors
(which are important in reading and walking). A 3 mm muscle
resection corrects about 10 degree of vertical squint.
Choice of surgery:
In convergent squint Medial rectus recession and lateral rectus resection
of the squinting eye
Medial rectus recession of both the eyes (Bi-medial
recession)
In divergent squint Lateral rectus recession and Medial rectus resection
of the squinting eye
Lateral rectus recession of both the eyes (Bi-lateral
recession)
In alternating squint Treatment is for cosmetic purpose. Both the eyes are
tuckled to correct the deviation
Strabismus 313
Q. Define paralytic squint. Discuss the etiology, clinical features

Definition: Paralytic squint is the misalignment of the visual
axes as a result of paresis or paralysis of one or more extraocular
muscles.
Etiology:
Lesions affecting the cranial nerves Lesions in the muscle
Nuclear lesions Lesions of the nerve Congenital maldevelopment
Cerebrovascular Head injury of a muscle
accidents Meningitis Direct injury to the muscle
Infections Cavernous sinus Diseases of the muscle:
Neoplasms thrombosis ocular myopathy, thyroid
Aneurysms Fracture of the base myopathy
Toxins (diphtheria) of the skull
Pressure from a
neoplasm or aneurysm
Clinical feature:
 Diplopia in an adult with previous single binocular vision. It
is most marked in the direction of action of paralyzed muscle
 False orientation of the object: Object is projected too far in
the direction of paralyzed muscle, due to increase in secondary
deviation
 Vertigo and nausea secondary to diplopia and false orientation
 Secondary angle of deviation is greater than primary angle
of deviation
 Compensatory head posture: The patient’s head and the face are
turned towards the direction of the action of the paralyzed muscle
 Visual acuity is normal in both the eyes.
Different types of Ocular paralysis:

Type Clinical signs
Total ophthalmoplegia: involves Ptosis
both intrinsic and extrinsic muscles The eyeball is proptosed and
of the eyeball divergent (due to anatomical
In unilateral cases the lesion is in position at the rest)
cavernous sinus or in the superior No movement of eyeball in any
orbital fissure direction
In bilateral cases it is the vascular Fixed dilated pupil (no reaction to
or inflammatory cause of the brainstem light, accommodation and
convergence)
Total loss of accommodation
External ophthalmoplegia: paralysis Same as above except that
of the 6 extraocular muscles and the pupillary reaction and
levator. It is due to nuclear lesion accommodation are normal
without affecting the Edinger-Westphal
nucleus which supplies intrinsic muscles
Internal ophthalmoplegia: intrinsic Fixed dilated pupil (no reaction to
ocular muscles are paralyzed light, accommodation and
convergence)
Total loss of accommodation
Cranial Nerve palsy Features

Third Cranial Nerve palsy Ptosis (levator weakness)
(CN III all extraocular Eyeball rotates downwards and outwards due
muscles except superior to unopposed action of muscles supplied by CN
oblique and lateral rectus) IV and VI
(Fig. 13.6) Intorsion of eyeball on attempted down gaze,
due to the action of superior oblique
Ocular movements are restricted in all directions
except in outward direction
Contd...
Strabismus 315
Contd...
Pupil is dilated and does not constrict to light or
convergence
IV Cranial Nerve palsy Abnormal head posture: chin depression, head
(supplies superior oblique) tilt and slight face turned to the opposite side
(Fig. 13.7) (normal side)
Diplopia in down gaze
Eyeball deviated upwards and inwards
Extorsion of the globe
Restriction of downwards and inwards
movement
VI Cranial Nerve palsy The eyeball is rotated inwards
(Supplies lateral rectus) Defective abduction of eye
(Fig. 13.8) Face turns towards the field of action of
paralyzed muscle (Ex: towards right in
right VI CN palsy)
Fig. 13.6: Third nerve palsy – Right eye

Fig. 13.7: Fourth nerve palsy – Right eye
Fig. 13.8: Sixth nerve palsy – Right eye
Investigations:
 Diplopia charting:
– A spectacle containing a red lens for the right eye
(Mnemonic: RR-red, right) and a green lens for the left
eye is worn by the patient. This dissociates the retinal image
perceived by the eyes (Fig. 13.9)
Strabismus 317
Fig. 13.9: Diplopia chart for right lateral rectus palsy
– In a dark room, a streak light is moved in different areas

of binocular vision with the head being held stationary
– Position of the two images are recorded on a chart with
nine squares (Representing 9 diagnostic positions of the
gaze) marked on it
– Note for the following:
• The area of single vision and diplopia
• The distance between the two images
• The position of the image, weather erect or tilted
• The diplopia is crossed or uncrossed
 Worth’s 4 dot test:
– Procedure: Patient’s eyes are dissociated. A spectacle
containing a red lens for the right eye (Mnemonic: RR-
red, right) and a green lens for the left eye is worn by the
patient. He then views at a box with 4 lights (dots)—
1 red, 2 green, 1 white (Fig. 13.10)
Fig. 13.10: Worth’s four dot test
– The interpretations of the 4 dot test are as follows:

If the patient sees Presence of
All 4 lights Normal fusion
All 3 lights, even in presence Abnormal retinal correspondence
of concomitant squint (ARC)
2 red and 3 green lights Diplopia (paralytic squint)
2 red lights Suppression of the left eye
3 green lights Suppression of the right eye
2 red or 3 green lights alternately Alternate Suppression
 Hess screen (Chart):

– Principle: Dissociation of the two eyes is achieved by red-
green goggles. This test provides the following information:
• A record of primary and secondary deviation
Strabismus 319
• In paralytic squint, it provides information about the

progress of the case if taken at suitable intervals.
– Method:
• The patient wears a red-green filter goggles and holds
a green light projector
• The surgeon holds a red light projection pointer which
is used as a point of fixation
• The surgeon projects the light onto the Hess screen
• The patient is asked to superimpose his green light onto
the red light.
– Interpretation:
• In normal conditions, the two pointers should be nearly
superimposed in all nine positions of the gaze
• In paralytic squint, the greater restriction occurs in the
direction of the paretic muscle, with corresponding over
action of the contralateral synergistic muscle
 Forced duction test (FDT):
– This is a test used to differentiate defective ocular move-
ments due to physical restriction, from a muscle paralysis
– Procedure: After topical anesthesia, the insertion of the
affected muscle is grasped with fixation forceps and gently
attempted to rotate the eyeball in the field of action of
weak muscle (Fig. 13.11)
– Interpretation:
• FDI ‘positive’ means: It is difficult to move the globe
with forceps, (e.g. contracture of muscle as in thyroid
myopathy, trapped muscle in the orbital floor fracture)
Fig. 13.11: Hess chart in right lateral rectus palsy
• FDT “negative” in case of muscle paralysis (Globe can

be easily moved)
 Investigations to find out the cause: Like complete
neurological examination, X-ray skull/CT/MRI of brain and
orbit, thyroid function tests, Tensilon test (for myasthenia
gravis).
Treatment:
 Treat the cause
 Conservative measures: Wait and watch for any self impro-
vement for a period of six months. Give vitamin B complex
supplementation and systemic steroids for nonspecific
inflammation
 Treatment of annoying diplopia:
– Occlusion of affected eye temporarily
– Suitable prism correction for minor diplopia
 Botulinus toxin injection may be tried in some cases—to
prevent contracture of antagonist muscle
 Surgery: Recession of the contralateral synergist or muscle
transposition operation.
Strabismus 321
Q. Differentiate between paralytic squint and nonparalytic

squint.
Features Paralytic squint Nonparalytic squint
Developmental/acquired Mostly acquired Mostly developmental
Age group affected Mostly adults Mostly in infants and
children
Onset Usually sudden Usually slow
Diplopia Usually present Usually Absent
Ocular movements Limited in the direction Full
of the action of the
muscle
False projections It is positive It is negative
Head posture A particular head Normal
posture depending
upon the muscle
paralyzed may be
present
Nausea and vomiting Present Absent
Secondary deviation More than the Equal to primary
primary deviation deviation
In old cases pathological Present Absent
squeal in the muscle
Amblyopia No amblyopia Present
Surgery Results are usually Not satisfactory
good
14.
Diseases of Eyelids
Q. Discuss the structure of eyelid.

Structure of eyelid is as follows (Figs 14.1 to 14.3):
 Skin thinnest in whole body, it is delicate and hairless
 Subcutaneous tissue made up of loose areolar tissue devoid
of fat
 Layer of striated muscle: Consists of
a. Orbicularis (closes lid, supplied by zygomatic branch of
facial nerve)
b. Lipopolysaccharide (LPS) (opens lid, supplied by
oculomotor nerve)
 Submuscular areolar tissue
 Fibrous layer
– Tarsal plate in the lower part
– Orbital septum in the upper part
 Layer of nonstriated muscle: Formed
– Mullers muscle formed by LPS in upper lid
– Extension of ‘Inferior’ rectus in lower lid
 Conjunctiva.
Diseases of Eyelids 323
Fig. 14.1: Structure of eyelid
Fig. 14.2: Structure of lid margin

Fig. 14.3: Glands of eyelids
Q. Discuss the Nerve supply of the eyelid.

Q. Mention the elevator of upper eyelid and its nerve supply.
Nerve supply of the eyelid
Motor supply Orbicularis oculi facial nerve

Levator palpebrae superioris Oculomotor nerve (both are
striated muscles)
Mullers muscle (nonstriated muscle) Sympathetic fibers
Sensory supply By branches of trigeminal nerve
Orbicularis oculi (palpable part) is the elevator of upper eyelid

 Origin: From the sphenoid bone
 Insertion: Into the eyelid, tarsal plate and walls of the eye socket.
Q. What is blepharitis? Discuss the etiology, clinical features

Definition: Blepharitis is the subacute or chronic inflammation
of the eyelids.
Etiology:
 Starts in childhood and continues throughout the life
 Usually bilateral
 Irritation by dusts, smoke and cosmetics
 Uncorrected refractive errors
 Seborrhea of scalp
 Chronic conjunctivitis
 Parasitic infestation: Due to demodex folliculorum and
phthirus pubis.
Types of blepharitis (Figs 14.4A and B):
Ulcerative blepharitis Squamous blepharitis
It is chronic staphylococcal It is not an infective condition. It is
infection of the lid margin usually characterized by hyperemia limited
caused by coagulase positive strains to lid margin
Contd...
Contd...
Symptoms: Symptoms:
Irritation itching Redness of eye margin
Lacrimation Burning and discomfort of eye
Gluing of cilia Epiphora
Photophobia
Symptoms worsen in morning
Signs: Signs:
Yellow crusts at the root of eyelashes White dandruff like scales on the lid
with matting margin
Small ulcers seen on removal of crust On removal of scales hyperemic area
lid margins shows dilated blood is seen
vessels (Rossettes) Madarosis
Thickening of lid margin (tylosis)
Associated seborrheic dermatitis of
scalp
Treatment: Treatment:
Lid scrub: using soda-bicarbonate Treat seborrhea of scalp
solution. Alternatively baby shampoo Lid hygiene: scales on eyelid margins
or 0.1% selenium sulfide solution is removed by moistened cotton- tip
can be used applicator twice a day
Epilate loose and diseased eyelashes Antibiotic drops and ointment
Antibiotic drops and ointment
Figs 14.4A and B: (A) Squamous blepharitis; (B) Ulcerative blepharitis

Oral antibiotics are rarely required

General treatment:
 Ocular hygiene and handwashing
 Avoid hair oil, kajal or other ocular cosmetics
 Correction of refractive errors
 Treatment of louse infestation.
Complications/sequelae:
 Madarosis
 Trichiasis
 Poliosis (Graying of lashes)
 Tylosis
 Ectropion
 Eczema of skin
 Recurrent styles.
Q. What is external Hordeolum/Stye? Discuss the etiology,

External hordeolum (Stye) is an acute suppurative inflammation
of gland of the Zeis or Moll (Fig. 14.5).
Fig. 14.5: Stye

Etiology:
 Causative agent is Staphylococcus aureus
 Following are the associations and the predisposing factors:
– Commonly affects young children and adults
– Common in immunosuppressed patients like diabetics
– Uncorrected refractive error
– Habitual rubbing of eyes
– Fingering of eyes and nose
– Excessive intake of carbohydrates or alcohol.
Clinical features:
Symptoms Signs
Acute pain Localized swelling of the lid
Swelling of the lids Redness and edema
Photophobia Local rise of temperature
Mild lacrimation Swelling is tender
Sense of heaviness Matting of eyelashes
Enlargement of preauricular and/or
submandibular lymph node
Complications:
 Ulcerative blepharitis
 Cellulitis
 Lid abscess
 Cavernous sinus thrombosis.
Treatment:
 Evacuation of pus by epilation of a eyelash/a tiny horizontal
incision
 Systemic analgesics (ibuprofen)

 Local antibiotic eye drops—chloramphenicol/ciprofloxacin
 In recurrent styes, treat the underlying cause.
Q. What is Chalazion/tarsal or meibomian cyst? Discuss the

Definition: Chalazion is a chronic nonsuppurative inflammation
of the meibomian gland.
Etiolopathogenesis:
 Predispositions are similar to external hordeolum
 Pathogenesis: Chronic low grade inflammation of the meibo-
mian gland by low virulent organisms blockage of the duct
of the meibomian gland accumulation of lipid secretions
break down of lipids into components of oleic acid mucosal
irritation cellular infiltration with formation of giant cells
proliferation of fibroblasts ‘granuloma’ formation.
Clinical features:
Symptoms:
 Painless nodular swelling of the eyelid
 Drooping of eyelid in case of multiple or large chalazion.
Signs:
 The swelling is usually of pea size
 Its firm tense and non-tender
 It is usually away from the lid margin
 It usually points towards conjunctiva and rarely towards skin.
Complications:
 Ptosis
 Internal hordeolum
Figs 14.6A to C: (A) Chalazion; (B) and (C) Incision and curettage of chalazion
 Ectropion
 Epiphora
 Calcification
 Secondary infection
 Malignant change.
Treatment:
 Conservative management:
– Hot fomentation
– Topical antibiotic eye drops
– Systemic analgesics
 Intralesional injection of long acting steroid (triamcinolone)
 Incision and curettage (Figs 14.6A to C)
 Diathermy.
Q. What is internal Hordeolum? Discuss the etiology, clinical

Internal hordeolum is acute suppurative inflammation of the
meibomian gland associated with blockages of the duct.
Etiology:
 Primary staphylococcal infection of the meibomian gland
 Secondary infection in a chalazion.
Clinical features:
 Symptoms are similar to external hordeolum except that pain
is more intense
 On examination:
– It can be differentiated from external hordeolum from the
fact that, the point of maximum tenderness and swelling
is always away from the lid margin
– Pus points at the tarsal conjunctiva and not at the root of
the cilia.
Treatment: Is similar to external hordeolum except that when
the pus is formed it is drained by a vertical incision from the
tarsal conjunctiva.
Q. Define Trichiasis. Discuss the etiology, clinical features and
Definition: Trichiasis is inward misdirection of cilia (which rub
against eyeball) with normal position of the lid margin (Fig. 14.7).
Fig. 14.7: Section of the upper eyelid showing normal and abnormal position
of tarsus and eyelashes
Etiology:
 Cicatrizing trachoma
 Ulcerative blepharitis
 Healed membranous conjunctivitis
 Hordeolum irternum
 Mechanical injuries
 Burns
 Postoperative scar.
Symptoms: Foreign body sensation, photophobia, irritation, pain,

lacrimation.
Signs:
 One/more misdirected cilia touching cornea can be noted
 Reflex blepharospasm
 Photophobia if cornea is abraded
 Conjunctival congestion
 Signs of trachoma, blepharitis, or previous surgery may be
seen.
Complications:
 Recurrent corneal ulceration
 Superficial corneal opacities
 Corneal vascularization
 Nonhealing corneal ulcer.
Treatment: A misdirected cilia is treated by

 Epilation: Mechanical removal of misdirected cilia using
forceps. It is a temporary method
 Electrolysis: It is a method of destroying the lashes by electric
current
 Cryoepilation: Cryoprobe (–20°C) applied for 20 to 25s to

lid margin to destroy the misdirected cilia
 Surgical correction is required if many cilia are misdirected.
Q. Define Entropion. Discuss the etiology/types, clinical

Definition: Entropion: It is in turning of the lid margin (Fig. 14.7).
Types: Mnemonic: M(SC)2 (i.e. master of science)
Type Causes
M Mechanical This is due to lack of support by globe to lids as in
Entropion Phthisis bulbi
Enophthalmos
Enucleation
Evisceration
S Spastic Occurs due to spasm of orbicularis muscle in patient with
chronic irritation corneal condition or after light bandage
Most common in lower lid and elderly individuals
S Senile Most common in lower lid and elderly individuals
C Congenital Usually associated with microophthalmos
C Cicatricial Usually affects upper lid. The causes are as follows:
Trachoma
Membranous conjunctivitis
Chemical burns
Pemphigus
Steven Johnson syndrome
Symptoms are same as Trichiasis

Signs: Depending of degree of intruding Entropion is graded as
follows and the same are the signs.
Grade I Only posterior lid border inrolled

Grade II Entropion + intruding up to inter marginal strip
Grade III Whole of lid margin including anterior border
Complications: Same as trichiasis.

Treatment:
Surgery is the choice of treatment. The following are the options
available:
 Resection of skin and muscle: In this operation an elliptical
strip of skin and orbicularis muscle is resected 3 mm away
from lid margin (Fig. 14.8)
 Resection of skin, muscle and tarsus
 Modified Burrow’s operation:
– The procedure is performed from the conjunctival side
– A horizontal incision is made involving conjunction and
tarsal plate in the region of sulcus subtarsalis. Skin is not
cut (Fig. 14.9)
– Temporal side of the strip is incised by a full thickness
vertical incision
– Pad and bandage is applied so that the lid is kept everted
Fig. 14.8: Skin and muscle resection

Fig. 14.9: Burow’s operation
 Jaeschke-Arlt’s operation:
– The lid is split along gray line up to a depth of 3 to 4 mm
from outer canthus just lateral to the puncture
– A 4 mm cresentric strip of skin is removed from 3 mm
above the lid margin. After suturing the skin incision, the
lash line will be transplanted high.
 Modified Ketssey’s operation:
– A horizontal incision is made along the whole length of
sulcus subtarsalis involving conjunctiva and tarsal plate
– Lower piece of tarsal plate is undermined up to lid margin
– Mattress suture are then passed from upper cut ends of the
tarsal plate to emerge on the skin 1 mm above lid margin
– When sutures are tied the Entropion is corrected by
transpositioning conjunctival wedge.
Q. Define Ectropion. Discuss the etiology, clinical features,
Definition: Outrolling or outward turning of the lid margin is
called Ectropion (Fig. 14.7).
Etiology/Types: (Mnemonic MSC – P)

Types Seen in Lid affected
Mechanical Tumors, proptosis, chemosis Any
Spastic Seen in children and young adults following
spasm of Orbicularis Any
Senile Most common in old age (due to loss Lower lid
Ectropion of tone of orbicularis and laxity of tissue
lids)
Cicatricial This is due to scaring Any
Ectropion Causes: burns, lacerating injuries and
skin ulcers
Paralytic Paralysis of facial nerve due to bells Lower lid
palsy, CSOM or head injury
Symptoms:
 Epiphora, if lower lid is affected
 Irritation, discomfort, mild photophobia.
Signs: Lid margin out rolled. The same is graded as follows

Grade I Punctum everted
Grade II Margin everted, palpable conjunctiva visible
Grade III Fornix visible
Signs of scars/facial nerve paralysis may be seen.
Complications:
 Dryness of eye
 Conjunctival thickening
 Exposure keratitis
 Eczema and dermatitis (due to epiphora).
Treatment:
Type Surgical procedure
Mechanical Ectropion Treat the underlying cause
Spastic Ectropion Treat the cause of blepharospasm
Senile Ectropion Medical conjunctivoplasty
Horizontal lid shortening (Fig. 14.10)
Byron smiths modified operation
Cicatricial Ectropion Mild case: V-Y operation – V incision for skin,
followed by suturing of skin in Y shape (Fig. 14.11)
Moderate: Z plasty
Severe variety: Excision of scar and full thickness
skin graft
Paralytic Ectropion Lateral tarsorrhaphy
Fig. 14.10: Full-thickness shortening of the lid
Fig. 14.11: V-Y operation

 In Medical conjunctivoplasty: a spindle cresentric strip of

conjunctival and subconjunctival tissues is removed just
below punctum
 Byron Smiths modified operation:
– For severe degree of ectropion which is more marked on
lateral aspect
– Pentagonal full thickness excision from lateral third of the
eyelid is combined with triangular excision of the skin
from the area just lateral to lateral canthus.
Q. Define Symblepharon. Discuss the etiology, clinical features,
Definition: Symblepharon is a condition in which lids become
adherent with the eyeball as a result of adhesion between palpable
and bulbar conjunctiva.
Etiology:
 Burns
 Membranous conjunctivitis
 Injuries
 Conjunctival ulcerations
 Ocular pemphigus
 Steven Johnson’s syndrome.
Pathology: Results from healing of the opposing raw surfaces

upon the palpable and bulbar conjunctiva.
Clinical features:
 Difficulty in lid movement
 Diplopia: due to  lid movement
 Lagophthalmos
 Cosmetic disfiguration.
Types: Anterior, Posterior – fornix, Whole – total (Fig. 14.12)
Complications:
 Keratinization of conjunctions
 Exposure keratitis.
Treatment:
Prophylaxis
 Sweeping a glass rod with lubricant around the fornix several
times a day
 For a large raw surface, therapeutic contact lenses can be
used.
Curative Treatment:
 Mild cases: Raw area covered by mobilizing the surrounding
conjunctiva
 Severe case: Cover the raw area by graft obtained from
conjunctiva or buccal mucosa.
Fig. 14.12: Types of symblepharon

Q. Define Lagophthalmos. Discuss the etiology, clinical

Q. What is Tarsorrhaphy? Discuss its types and indications.
Q. List the indications for Tarsorrhaphy.
Define: Lagophthalmos is a condition characterized by inability
to voluntarily close the eyelids (Fig. 14.13).
Etiology:
 Paralysis of Orbicularis oculi
 Cicatricial contraction of the lid
 Symblepharon
 Severe ectropion
 Proptosis
 Over resection of levator muscle for ptosis
 Coma
 Physiological: Nocturnal lagophthalmos people sleeping with
open eyes.
Clinical features:
 Incomplete closure of palpable aperture
 Features of associated disease may be seen.
Fig. 14.13: Incomplete closure of palpebral fissure on closing the eyes

Complication:
 Xerosis of cornea and conjunctiva
 Exposure keratitis.
Treatment:
 Artificial tears to prevent exposure keratitis
 Antibiotics to be filled in palpable fissure in cases of nocturnal
lagophthalmos and coma
 Soft bandage contact lens for exposure keratitis
 Tarsorrhaphy.
Tarsorrhaphy:
Tarsorrhaphy is an operation designed to create adhesions are
between a part of the lid margins with the aim to narrow down
or almost close palpable operative (Figs 14A and B).
Figs 14.14A and B: (A) Paramedian tarsorrhaphy; (B) Lateral tarsorrhaphy

Types: Temporary tarsorrhaphy and permanent tarsorrhaphy.

Indications:
Temporary tarsorrhaphy Permanent tarsorrhaphy
To protect cornea when VII nerve Established case of VII nerve palsy with-
palsy is expected to recover out chance of recovery
To assist healing of indolent corneal Established of neuroparalytic keratitis
ulcer with sure loss of corneal sensation
To assist in healing of skin graft of Tarsorrhaphy can be median or
the lids in correct position paramedian
Procedure:
 Incision
– For paramedian tarsorrhaphy, about 5 mm long incision
site is marked on the corresponding parts of upper and
lower lid margins, 3 mm on either side of the midline
– An incision 2 mm deep is made in the gray line on the
marked site and the marginal epithelium is then excised
– Care is to be taken not to damage the ciliary line anteriorly,
sharp lid border posteriorly
 Suturing: raw surface thus created on the opposing parts of
lid margins are then sutured with double armed 6-0 silk sutures
passed through a rubber bolsters.
Permanent tarsorrhaphy technique:
 This is performed at lateral canthus to create permanent
adhesions
 Eyelids are overlapped after excision of triangular flap of
skin and orbicularis from lower lid and corresponding
triangular tarsoconjunctival flap from upper lid are excised.
Q. Define Ptosis. Discuss the etiology, clinical features,

Q. List the causes of ptosis/congenital/acquired ptosis.
Q. What is Marcus Gunn jaw-winking ptosis?
Definition: Abnormal drooping of the upper eyelid is called
ptosis.
Normally, upper lid covers up to 1/6 of cornea or 2 mm. Ptosis
covers more than 2 mm of cornea.
Types and Etiology
A. Congenital ptosis: This is due to congenital weakness/
maldevelopment of levator palpebrae superioris.
 Simple congenital ptosis: not associated with any other
anomaly
 Congenital ptosis: associated with weakness of superior rectus
muscle
 Blepharophimosis syndrome: It comprises of
– Congenital ptosis
– Blepharophimosis (narrow palpable fissure)
– Telecanthus ( distance between the two medial canthus)
– Epicanthus invertus (vertical fold of skin either side of
nose covering the medial canthus)
 Marcus-Gunn jaw-winking syndrome: In this condition there
is retraction of the ptosis lid with jaw movements (that is
with the stimulation of ipsilateral pterygoid muscle).
B. Acquired ptosis: (subtypes can be remembered by Mnemonic
MAN: Mechanical Myogenic, Aponeurotic and Neurogenic)
Type and the reason As in

M Mechanical—Excessive weight Tumors
of the lid Multiple chalazion
Lid edema
Cicatricial ptosis (as in scarring
ocular pemphigoid trachoma)
M Myogenic—Due to acquired Myasthenia gravis
disorder of LPS or myoneural Dystrophia myotonica
junction Ocular myopathy
Oculopharyngeal muscular dystrophy
A Aponeurotic—due to defects Senile ptosis
of levator aponeurosis in the Postoperative ptosis
presence of normal function Trauma
of muscle Disinsertion of aponeurosis
N Neurogenic III cranial nerve palsy
Horner’s syndrome
Ophthalmic migraine
Multiple sclerosis
Diagnosis:
History: Onset, family history, history of trauma, history of eye
surgery, variations in degree of ptosis.
Examination: Examine for the following points
 If ptosis is unilateral or bilateral
 Function of Orbicularis oculi (Fig. 14.15)
 Presence or absence of eyelid crease and Jaw-winking
phenomenon (Figs 14.16 and 14.17)
 Associated weakness of extraocular muscles
 Presence or absence of eye bells phenomenon up- and out-
rolling of the eyeball during forceful closure.
Fig. 14.15: Measurement of levator muscle function
Fig. 14.16: Narrow palpebral aperture (Ptosis)
Fig. 14.17: Ptosis

Measurement of degree of ptosis: Measure amount of cornea

covered by eyelid and subtract by 2 mm (Fig. 14.18).
Mild ptosis = 2 mm, moderate ptosis = 3 mm and severe ptosis
= 4 mm.
Assessment of levator functions:
The brow is immobilized by pressure with the thumb (to remove
the action of frontalis muscle). Patient is asked to look down
and then up and the amount of upper lid excursion is measured
with a ruler held in the hands of examiner.
Levator function is graded as: Normal 15 mm, Good > 8 mm,
Fair 5 to 7 mm and Poor 4 mm or less.
Special investigation
 Ocular motility test
 Tensilon test if myasthenia is suspected
 Phenylephrine test if Horner’s syndrome is suspected
 Neurological investigations for neurogenic ptosis.
Photographic record as a preoperative record.
Fig. 14.18: Measurement of vertical palpebral fissure

Treatment:
Following are the surgical options available:
 Fasanella-Servat operation: Upper lid is everted, upper tarsal
border along with attachment of mullers muscle and
conjunctiva are resected (Fig. 14.19).
 Frontalis sling operation/brown suspension: Lid is attached
to frontalis muscle via a sling. Fascia lata or a non absorbable
suture material is used as the sling (silk) (Fig. 14.20).
Fig. 14.19: Fasanella-Servat operation
Figs 14.20A and B: (A) Fascia lata sling operation; (B) Hess’s operation
 Levator resection: This can be done by two approach, i.e.

Skin approach: suitable for large resection [Everbusch
operation (Fig. 14.21)] Conjunctional approach: suitable for
small resection [Blaskovics operation (Fig. 14.22)].
 Aponeurotic strengthening: done by tuckling the aponeurosis
surgery is almost always required congenital causes, in
acquired cases to find out the cause and treat the same. In
neurogenic cause treatment is conservative and surgery
deferred till 6 m.
Figs 14.21A and B: Everbusch operation (skin side)
Fig. 14.22: Blaskovics operation (conjunctival side)

Procedure Required Amount of Common

levator ptosis treat Indications
function
Fasanella-Servat Good 2 mm Horner’s syndrome
operation
Frontalis sling Moderate Any Large congenital
operation ptosis, Acquired
ptosis
Levator resection- Moderate Any Moderate congenital
Skin approach ptosis, Acquired
ptosis
Levator resection- Moderate Any Acquired ptosis
Conjunctional
approach
Levator resection Poor > 2 mm Marcus Gunn jaw
with aponeurotic winking ptosis
reinsertion
Q. List the causes of bilateral ptosis.

The causes of bilateral ptosis are:
 Senile
 Myasthenia gravis
 Dystrophia myotonica
 Ocular myopathy
 Oculopharyngeal muscular dystrophy
 GB syndrome
 Fascio-muscular dystrophy.
15.
Diseases of Lacrimal
Apparatus
Fig. 15.1: The lacrimal apparatus
Fig. 15.2: Surgical anatomy of lacrimal sac

Diseases of Lacrimal Apparatus 351
Q. Discuss in detail the layers of the tear film.

Q. Give the different layers of the tear film with their functions.
The tear film can be divided into three layers from anterior to
posterior (Fig. 15.3).
(Mnemonic: LAMa, the first word of each layer)
Layer Source Other features Function
Lipid Glands of zeis It is the outermost layer Prevents overflow of the tears
layer Glands of Moll formed at the air-tear Retards evaporation of tears
Meibomian gland interface Acts as a lubricant
Aqueous Main and It is the intermediate layer It is antibacterial due to
layer accessory Forms the bulk of the tear presence of lysozyme,
lacrimal gland Its constituents are: betalysin and lactoferrin
water, sodium chloride,
urea and proteins
It is salty to taste
Mucus Goblet cells of It is the inner most layer Converts hydrophobic
layer conjunctiva It is the thinnest of all corneal layer into
Glands of manz the layers hydrophilic
Fig. 15.3: The tear film

Q. List the functions of the tear film.

The functions of the tear film are as follows:
 Keeps conjunctiva and cornea moist
 Provides oxygen to corneal epithelium
 Washes away debris and toxic irritants
 Prevents infection due to presence of antibacterial substance
 Facilitates movement of eyelid over the globe.
Composition of tear: Mnemonic: water PLUSS  protein,
lysozyme, urea, salts and sugars.
Q. Define dry eye.\ Discuss the etiology, clinical features and
Definition: Dry eye is not a diseases but a symptom complex
that results from deficiency or abnormality of the tear film.
Etiology:
(Mnemonic: A- MILE)
A Aqueous tear Keratoconjunctivitis sicca
deficiency Congenital alacrima
Paralytic hyposecretion
Sjogren’s syndrome
Idiopathic
M Mucin deficiency Hypovitaminosis A
Conjunctival scarring diseases like:
• Steven- Johnson syndrome
• Trachoma
• Burns
• Radiation
I Impaired eyelid Bell’s palsy
function Exposure keratitis
Symblepharon
Contd...
Contd...
Pterygium
Nocturnal lagopthalmos
Ectropion
L Lipid deficiency and Congenital anhydrotic ectodermal dysplasia
abnormalities Chronic blepharitis
Chronic meibomianitis
E Epitheliopathies Corneal ulcer due to any reason results in
of cornea dry eye due to close approximation between
corneal epithelium and tear film
Clinical features:
Symptoms:
 Irritation
 Foreign body sensation/sandy sensation in eye
 Feeling of dryness
 Itching
 Nonspecific ocular discomfort
 Chronically sore eye not responding to a variety of eye drops.
Signs:
 Presence of stingy mucous
 Particulate matter in tear film
 Lusterless ocular surface
 Conjunctival xerosis
 Absence of marginal tear strip
 Cornea: Punctate epithelial erosion.
Investigation:
The patient is diagnosed to have dry eye when any of the
following two tests are positive.
(Mnemonic: STaR: Schirmer- 1 test, T- tear film break up test,

R-Rose Bengal test)
1. Tear film break up time:
 It is a test for “mucus component” of the tear
 Tear film break up time is the time interval between a complete
blink and appearance of first randomly distributed dry spot
on cornea
 It is noted in slit lamp after instillation of fluorescein dye
 Normal Tear film break up time is 15 to 35 seconds
 It is considered abnormal if it < 10 seconds.
2. Schirmer-1 test:
 It checks the total tear secretion
 A 5 × 35 mm strip of Whatman-41 filter paper is kept in the
lower fornix at the junction of the lateral1/3rd and medial
2/3rd. Patient should look up and should not blink (Fig. 15.4)
 After 5 minutes a wetting of
 15 mm Is normal
5–10 mm Mild Keratoconjunctivitis sicca
< 5 mm Severe Keratoconjunctivitis sicca
Fig. 15.4: Schirmer test

3. Rose Bengal test (staining):

 It is useful to detect mild Keratoconjunctivitis sicca
 Three staining patterns are seen.
A Confluent staining Severe Keratoconjunctivitis sicca

B Extensive staining Moderate Keratoconjunctivitis sicca
C Punctate staining Mild Keratoconjunctivitis sicca
Treatment: There is no cure available yet

 Mucolytics: Five percent acetyl cysteine is a mucolytic and
hence reduces the viscosity of the tears.
Mnemonic: MTP  M-Mucolytics, T–Topical cyclosporine,
Topical retinoids tears, P–Preservation of existing tear drop.
 Supplementation with tear substitutes:
– Available as drops, ointments, slow release inserts
– Cellulose derivatives and polyvinyl alcohol are commonly
used
 Topical cyclosporine: Effective in reducing cell mediated
inflammation of lacrimal gland
 Topical retinoids: decreases squamous metaplasia
 Preservation of existing tear drop by:

– Decreasing evaporation by using moist chambers and
protective glasses
– Punctal occlusion by laser, collagen implants or
Electrocautery decreases drainage.
Q. What is watering eye? Discuss the etiology and management

of the same.
Q. Discuss the diagnostic role of lacrimal syringing.
Q. Discuss and interpret Jone’s test.
Characteristic overflowing of tears from the conjunctival sac is
called the watering of eyes. It may be due to:
A. Hyperlacrimation, which is overflow of tears due to excessive
secretion of the same.
B. Epiphora, which is an overflow of tears, usually caused by
insufficient drainage of the tear film from the eye.
Etiology:
A. Hyperlacrimation:
 Primary hyperlacrimation: It is due to direct stimulation of
the lacrimal gland as seen in:
– Tumors of the gland
– Cysts of the gland
– Increased parasympathetic stimulation
 Reflex hyperlacrimation: This is due to stimulation of the
trigeminal nerve due to any of the following causes:
– Lid: Meibominitis, Trichiasis, Entropion
– Conjunctiva: Conjunctivitis due to any etiology
– Sclera: Scleritis, Episcleritis
– Uvea: Iridocyclitis
– Acute glaucoma
– Endophthalmitis or panophthalmitis
– Orbital cellulitis
 Central lacrimation: It is seen in

– Emotional state
– Voluntary lacrimation
– Hysterical lacrimation.
B. Epiphora:
This may be physiological or mechanical (anatomical)
 Physiological: It is due to lacrimal pump failure as in
– Lower lid laxity
– Weakness of Orbicularis oculi
 Mechanical obstruction:
Punctal eversion Old age

Chronic conjunctivitis
Chronic blepharitis
Ectropion
Punctal obstruction Closure following burns, injuries
Small foreign body
Stenosis following use of Pilocarpine or idoxuridine
Obstruction in Congenital obstruction
canaliculi Acquired due to foreign body, trauma, canaliculitis
caused by actinomycetes
Obstruction in Congenital obstruction due to mucous membrane fold
lacrimal sac Dacryocystitis
TB, syphilis
Dacryolithiasis
Tumors
Atonia
Obstruction in Congenital: non-canalization, partial canalization,
Nasolacrimal duct imperforated membrane valves
Acquired causes: Traumatic/inflammatory strictures,
tumors, diseases of the surrounding bone
Clinical evaluation:
A. Ocular examination with diffuse illumination using magnifi-
cation: helps to identify
 Punctal causes
 Any swelling in the sac area
 To detect any cause of reflex hypersecretion.
B. Regurgitation test:
 A steady pressure with index finger is applied over lacrimal
sac above the medial palpable ligament
 Reflux of mucopurulent pus shows obstruction at lower
end of sac or nasolacrimal duct.
C. Fluorescein dye disappearance test:
 Two drops of Fluorescein dye is instilled in both the
conjunctival sac and observation is made after two minutes
 Normally no dye is seen in conjunctival sac after two minutes
 Prolonged retention of the dye shows decreased drainage
due to atonia or obstruction.
D. Lacrimal syringing test:
 Free passage of saline rules out obstruction
 Saline passing under considerable pressure indicates partial
obstruction
 In presence of obstruction no fluid goes to the nose (Figs
15.5 and 15.6)
– If the fluid comes through the same punctum  it
indicates obstruction in the same or common canaliculi
– If it comes out through the opposite punctum  it
indicates obstruction in lacrimal sac or nasolacrimal duct.
Fig. 15.5: Syringing through lower punctum
Figs 15.6A and B: Patency (syringing) test: (A) Fast regurgitation;

(B) Slow regurgitation
E. Jone’s dye test:

 Indication: When partial obstruction is suspected
 Drawback: the test is of no use when there is total
obstruction.
Jone’s dye test 1:
 Objective: To differentiate between partial obstruction and
primary hypersecretion
 Procedure:
– Two drops of two percent fluorescein dye are instilled
in the conjunctiva sac and a cotton bud dipped in
1 percent xylocaine is placed in the inferior meatus at
the opening of the nasolacrimal duct
– After 5 minutes the cotton bud is removed and
inspected.
 Interpretation:
– A dye stained cotton (positive staining)  shows
adequate drainage but hyperlacrimation
– An unstained cotton bud (negative staining)  indicates
partial obstruction or lacrimal pump failure. These two
can be differentiated by Jone’s dye test 2.
Jone’s dye test 2:
 Objective: To differentiate between partial obstruction or
lacrimal pump failure
 Procedure: The cotton bud is again placed in inferior
meatus and syringing is done
 Interpretation:
– Positive test, means the bud is stained with dye 
indicates that the dye was present in the sac but could
not reach the nose due to partial obstruction
– Negative test, means that the bud is not stained,
indicating lacrimal pump failure.
F. Dacryocystography: Is useful to detect the lacrimal pump
failure. It detects site, nature and extent of obstruction.
G. Radionucleotide Dacryocystography: Is a noninvasive method
to study the lacrimal glands functional efficacy (Fig. 15.7).
Treatment: Lies in treating the causative agent.
Q. Classify Dacryocystitis.
Dacryocystitis is classified as follows:
A. Congenital dacryocystitis
B. Acquired dacryocystitis:
 Acute dacryocystitis
 Chronic dacryocystitis.
Q. What is Congenital Dacryocystitis? Discuss the etiology,

Fig. 15.7: Gamma camera images

Q. What is Dacryocystitis Neonatorum/Dacryocystitis of new

born? Discuss the etiology, clinical features and management
of the same.
Q. List the complications of congenital dacryocystitis.
Congenital dacryocystitis is the inflammation of the lacrimal sac
occurring in the newborn infants. Hence it is also called as
dacryocystitis neonatorum.
Etiopathogenesis:
Predisposing factors Common bacteria causing
chronic Dacryocystitis
Congenital blockage of Nasolacrimal duct Staphylococci
Presence of epithelial debris Streptococci
Membranous occlusion at the upper end Pneumococci
near lacrimal sac
Complete non-canalization
Bony occlusion
Pathogenesis: Obstruction due to any cause  collection of

secretion  stasis of secretions  mucocele infection.
Clinical features:
 This condition presents as a mild grade chronic inflammation
 Epiphora: After seven days of life with mucopurulent discharge
 Regurgitation test is positive
 Swelling of lacrimal sac develops eventually.
Complications:
 Acute dacryocystitis
 Chronic dacryocystitis
 Lacrimal abscess
 Fistula formation.
Treatment:
 Massage of the lacrimal sac area and topical antibiotics
constitute the treatment up to 6 to 8 weeks of age
 Lacrimal syringing with normal saline and antibiotics, if the
above is not satisfactory
 Probing of nasolacrimal duct under general anesthesia using
bowman’s probe if there is no cure till 3 to 4 months of age
 Intubation with silicone tube around 6 months of age, is done
if probing fails
 Dacryocystorhinostomy: If all the above treatment fails, this
procedure is done around 4 years of age.
Q. What is chronic dacryocystitis? Discuss the etiology, clinical
Q. What is lacrimal pyocele? How do you manage the same?
Q. List the complications of Chronic Dacryocystitis.
Chronic dacryocystitis is a common chronic suppurative
inflammation of the lacrimal sac that usually results from
obstruction of the nasolacrimal duct.
Etiology:
Predisposing factors Source of infection Causative organisms
Common between 20 to 40 Conjunctiva Staphylococci
years of age nasal cavity Streptococci
Common in females than in males Paranasal sinuses Pneumococci
Whites are affected Pseudomonas
more than blacks Rarely: Pyocyanea
Hereditary (specific facial TB, syphilis,
configuration) rhinosporidiosis
Lower socioeconomic status
Poor personal hygiene
Factors responsible for stagnation of tears:

 Anatomical factors
 Foreign body
 Excessive lacrimation
 Mild grade inflammation of the lacrimal sac due to recurrent
conjunctivitis
 Obstruction of the lower end of the nasolacrimal duct by: polyp,
hypertrophied inferior turbinate, deviated nasal septum, tumors.
Clinical features: Comprises of four stages
Stage Pathology Clinical features
Symptoms Signs
Stage of Mild grade inflammation Watering of On syringing: clear
chronic of the lacrimal sac eyes fluid/few mucoid flakes
catarrhal associated with blockage seen Dacryocystography
Dacryocystitis of nasolacrimal duct reveals block in
nasolacrimal duct
Stage of Chronic infection  blocks Watering of Milky or gelatinous fluid
lacrimal both canaliculi  soft eyes exudates on pressing
mucocele cystic swelling at the inner Distended Negative regurgitation
or hydrops canthus with encysted lacrimal sac test
mucocele
Stage of Pyogenic infection  hence Epiphora Regurgitation test is
chronic mucocele becomes pyocele Recurrent positive with purulent
suppurative If the opening of the conjunctivitis discharge
Dacryocystitis canaliculi are blocked at Swelling on
this stage, it results in the inner
encysted pyocele canthus with
erythema on
overlying skin
Stage of Chronic low grade Epiphora Dacryocystography
chronic inflammation results in Mild Pyogenic reveals small sac with
fibrotic sac thickening of the mucosa discharge irregular folds
 followed by fibrosis
Complications:
 Acute on chronic conjunctivitis
 Ectropion of lower lid with maceration, eczema of skin due
to epiphora
 Even simple corneal abrasion becomes infected and forms
hypopyon
 Endophthalmitis if surgery is done on eye.
Treatment:
 Conservative treatment: Syringing (normal saline and
antibiotics) and probing
 Dacryocystorhinostomy: Is the operation of choice. It is performed
after the control of infection by antibiotics and syringing
 Dacryocystectomy is done if dacryocystorhinostomy is
contraindicated
 Conjunctivodacryocystorhinostomy (CDCR): Is done if both
the canaliculi are blocked.
Q. What is acute dacryocystitis? Discuss the etiology, clinical
Q. List the complications of acute dacryocystitis.
Q. What is lacrimal fistula? How do you manage the same?
Acute dacryocystitis is acute suppurative inflammation of the
lacrimal sac, characterized by presence of painful swelling in
the region of the sac.
Etiology: It may occur in two ways
1. Acute exacerbation of chronic dacryocystitis
2. Acute peridacryocystitis due to direct involvement from the

neighboring area like infected paranasal sinuses, bone or teeth.
Causative organism: Staphylococci, Streptococci, Pneumococci.
Clinical features:
Stage Pathology Clinical features Treatment
Stage of Acute infection and Painful swelling in Systemic and local
cellulitis infiltration of the gland the region of the sac antibiotics
by inflammatory cells Epiphora Systemic analgesics
Malaise
Redness and edema
of cheeks
Stage of Inflammation  occlusion Fever Incision and drainage
lacrimal of canaliculi  pus filled Malaise of abscess
abscess sac  Rupture of anterior Swelling of lacrimal Followed by
wall of sac  pericystic sac: A fluctuant mass Dacryocystorhinostomy
swelling  lacrimal pointing below and or
abscess outside of the sac Dacryocystectomy
(owing to presence
of medial palpable
ligament and gravity)
Stage of Untreated lacrimal abscess Wound with Control of infection using
fistula  bursts open fistula discharging pus antibiotics
External fistula when Followed by fistulectomy
opening is below medial with
palpable ligament Dacryocystorhinostomy
Internal fistula when it or
opens up into the nasal Dacryocystectomy
cavity
Complications:
 Acute conjunctivitis
 Corneal abrasion which gets converted to corneal ulcer
 Lid abscess
 Osteomyelitis of lacrimal bone
 Facial cellulitis
 Sinusitis
 Cavernous sinus thrombosis
 Generalized septicemia
 Death.
Q. What is dacryocystorhinostomy? Discuss the indications and
contraindications of the same.
Q. Discuss the advantages and disadvantages of the
conventional metod over endoscopic dacryocystorhinostomy.
Dacryocystorhinostomy is an operation providing an anastomosis
between the lacrimal sac and the nasal mucosa through an
opening in the lacrimal bone.
Indications Contraindications
Congenital dacryocystitis after the Atropic rhinitis (absolute)
failure of other modes of treatment Active infection of lacrimal sac
Acute dacryocystitis (temporary)
Chronic dacryocystitis
Advantages of the conventional Disadvantages of the conventional

method over endoscopic method over endoscopic
procedure procedure
High success rate Cutaneous scar
Easy to perform/learn More bleeding
Cheaper Potential damage to structures at
Does not require special equipments medial canthus
Lengthy procedure
Significant postoperative morbidity
Procedure of conventional method in brief:

 General anesthesia is preferred in children and local anesthesia
in adults (Fig. 15.8)
 Skin incision 2 cm long, medial to medial canthus. 1/3rd of
which is above medial palpable ligament
 Exposure of medial palpable ligament and anterior lacrimal
crest
 Dessection of lacrimal sac
 Exposure of nasal mucosa
 Preparation of the flaps of sac: A probe is introduced into the
sac through the lower canaliculus and the sac is incised
vertically. To prepare the anterior and posterior flaps a ‘H’
shape incision is made
 First posterior and then anterior flap is sutured
 Skin is sutured
 Nasal packing is done which is removed after 72 hours.
Q. What is dacryocystectomy? Discuss the indications and

contraindications of the same.
Fig. 15.8: Dacryocystorhinostomy

Dacryocystectomy is surgical removal of the lacrimal sac.

Indications Contraindications
Too young (< 4 years) or too old patient Active infection of lacrimal sac
(> 60 years) (temporary)
Marked shrunken or fibrotic sac
TB, syphilis, leprosy
Tumors of the sac
Atropic rhinitis
Unskilled surgeon
Procedure:
 Till the dissection of the sac the steps are same as discussed
above
 Removal of lacrimal sac from the floor of the fundus
 After the sac is well dissected it is grasped with a straight
artery forceps up to its lower end and twisted until it is torn
off from the Nasolacrimal duct
 Curettage of bony Nasolacrimal duct
 Skin is closed.
16.
Diseases of the Orbit
Fig. 16.1: Superior orbital fissure and optic foramen
Q. Define Proptosis and classify the same.

Q. List the causes for Unilateral proptosis/Bilateral proptosis/
Acute proptosis/Intermittent proptosis/Pulsating proptosis.
Definition: Forward displacement of eyeballs beyond orbital
margin is called Proptosis.
Diseases of the Orbit 371
Proptosis is classified into following clinical groups:

Type Causes
Unilateral Congenital: dermoid, teratoma

Proptosis Circulatory causes: angioneurotic edema, aneurysm
(mnemonic: Cysts of orbit: hematic cyst, Implantation cyst, parasite cyst
CoMIT) Mucoceles of paranasal sinuses: frontal, ethmoidal, maxillary
Inflammatory: cellulites, thrombophlebitis, abscess, panophthalmitis
Traumatic: orbital hemorrhage, foreign body, traumatic aneurysm
Tumors
Bilateral Inflammatory: Mikulicz syndrome, last stage of cavernous

Proptosis sinus thrombosis
(mnemonic: Developmental anomalies of skull craniofacial disostosis
IDEOTS) Endocrinal: Thyrotoxic
Osteopathies: Ostitis deformans, Rickets, Acromegaly
Tumors: lymphomas, secondaries from neuroblastoma,
nephroblostoma, Ewing’s sarcoma
Systemic disorders: histocytosis, amyloidosis, Wegner’s
granulomatosis
Acute Orbital emphysema

Proptosis Fracture of middle orbital wall
(rapidly Orbital hemorrhage
growing) Rupture of ethmoidal mucoceles
Intermittent Intermittent proptosis

Proptosis Orbital varix
Periodic orbital edema
Recurrent orbital hemorrhage
Highly vascular tumors
Pulsating Corticocavernous fistula

Proptosis Saccular aneurysm of ophthalmic artery
Meningocele/meningomyelocele
Neurofibromatosis
Traumatic
Q. Discuss the management of proptosis.

Diagnosis:
History:
 Benign lesions have longer history than malignant tumors
 Acute onset of pain indicates inflammatory lesions
 In the past history enquire about thyroid diseases,
malignancies, orbital trauma and sinus diseases.
Clinical examination:
 Measure the degree of protrusion: By standing behind the
patient and viewing from above
 Measurement of proptosis by using a simple ruler or Hertel’s
exophthalmometer (anything less < 20 is normal)
 Detailed ocular examination
 Dynamic properties of proptosis:
– Try to precipitate proptosis by valsalva maneuver.
Proptosis due to orbital varices and hemangioma get
precipitated by the same
– Look for pulsation (better appreciated by slit lamp)
– A bruit on auscultation may indicate cortico cavernous
fistula or highly vascular tumor
 Transillumination to evaluation of anterior orbital lesions
 Systemic examination of thyroid, paranasal sinuses and the
site of primary tumor
Investigations:
 Blood investigations: TLC and DC are specially helpful in
diagnosis of infective or malignant conditions
 Urine analysis for bence-jones proteins in multiple myeloma
 Thyroid function test
 Casoni’s test for hydatid cyst

 Plain X-ray of orbit
 Orbital venography is useful in orbital varices
 CT and MRI
 USG B-scan
 USG guided FNAC
 Incisional and excisional biopsy.
Principles of treatment in proptosis:

A. Medical: For orbital cellulitis, pseudotumors, thyroid
ophthalmology, leukemia
B. Radiotherapy for secondaries and rapidly growing malignant
tumor
C. Surgical:
 Tarsorrhaphy to protect exposed cornea
 Orbitectomy for benign lesions
 Exenteration operation for malignant lesions and secondaries.
Q. Define Enophthalmos. List the causes for the same.

Definition: Enophthalmos is inward displacement of eyeball.
Causes:
 Congenital: Microophthalmos, maxillary hypoplasia
 Traumatic: Blow out fracture of floor of the orbit
 Postinflammatory: Cicatrization of extraocular muscle
following pseudotumor syndrome
 Paralytic: Horner’s syndrome due to paralysis of cervical
sympathetic plexus
 Atropy of orbital contents: Senile atropy, atropy due to space
occupying lesions.
Q. Define orbital cellulitis. Discuss the etiology, clinical

Definition: Orbital cellulitis refers to an acute infection of the
soft tissue of the orbit behind the orbital septum.
Etiology:
 Orbits may be infected by
– Exogenous infection: result from penetrating injury like
foreign body, evisceration, enucleation, dacryocystectomy
– Extension of infection from neighboring structures like
PNS, teeth, face, lids, intracranial structures
– Endogenous: Breast abscess, peripheral sepsis, throm-
bophlebitis, septicemia.
Causative organisms: Staphylococcus aureus, Streptococcus
pyogenes, S. pneumoniae and Haemophilus influenzae
Clinical features:
Symptoms
 Swelling
 Severe pain. Pain increases on eye movement of eyeballs
 Fever, nausea, vomiting, prostration
 Loss of vision.
Signs:
 Lids: swelling, woody hardness, redness
 Conjunctiva: Chemosis, congestion and neurosis
 Eyeball: Proptosed
 Severe restriction of ocular movement
 Fundus examination: Congestion of retinal veins, features of
papillitis and papilledema.
Complications:
 Ocular complications: Blinding, exposure keratopathy, optic
neuritis, central retinal artery occlusion (CRAO)
 Orbital: Subperiostial abscess and orbital abscess
 Temporal/parotid abscess
 Intracranial complications: cavernous sinus thrombosis,
meningitis, brainstem abscess
 Septicemia/pyemia.
Mnemonic: OPTICS O  Ocular complications. P–Pyemia,
P–Parotid abscess T–Temporal abscess, I–Infractranial lesions,
C–nothing, S–Septicemia
Investigations:
 Culture sensitivity of conjunctional, nasal and blood swabs
 Complete hemogram may show elevated TLC and neutrophils
in DC
 X-ray for PNS: To rule out sinusitis
 Orbital ultrasound: To rule out intraorbital abscess
 CT and MRI are useful.
Rx
 Antibiotic:
– For staphylococcal infection: Oxacillin + ampicillin
combination is used
– For H. influenzae in child: chloramphenicol or clavulanic
acid
– Alternatively—ceftriaxone, ciprofloxacin, vancomycin
 Hot fomentation, analgesics and anti-inflammatory
 Surgical intervention:
Indications Procedures
No response to antibiotics Free incision if the abscess points under skin or
Decreased vision conjunctiva
Subperiostial abscess Subperiostial abscess drained from upper
medical aspect
Drain orbit and PNS

Cavernous sinus thrombosis.
Cavernous sinus thrombosis is an acute thrombophlebitis of the
cavernous sinus resulting from spread of sepsis traveling across
its tributaries.
Etiology: The source of infection includes face, PNS, orbit,
meningitis, cerebral abscess, mastoiditis and labyrinthine infections.
Clinical picture:
 Acute in onset can be unilateral or bilateral
 General feature: Severely ill, high grade fever, rigor, vomiting,
headache
 Pain in eye and forehead
 Conjunctiva: Swollen, congested
 Proptosis: Rapidly developed
 Palsy of III, IV, V cranial nerves
 Edema of mastoid is pathognomonic
 Fundus may reveal congestion of retinal veins, papilledema.
Treatment: (Mnemonic 3 A’s)

 Antibiotics: massive and new generation drugs are used
 Analgesics and anti-inflammatory
 Anticoagulants.
Q. Discuss the anatomy of Cavernous sinus in brief.

3 Afferent veins: Sphenoparietal sinus (Vault veins), Superior
middle cerebral vein (Brain), ophthalmic vein (orbit) (Figs 16.2,
16.3 and 16.4)
3 Efferent veins: Superior petrosal sinus, Inferior petrosal sinus,
Communicating vein to pterygoid plexus
3 Contents; Cranial nerves (III, IV, V1,V2 and VI)
3 Areas Drain into it: Vault bones, brain (cerebral hemisphere),
orbit
3 Nerves are related to it: Motor (III, IV, VI), sensory (V1,
V2), sympathetic
Fig. 16.2: Communications of cavernous sinus—lateral view

Fig. 16.3: Communications of cavernous sinus—looking from above
Fig. 16.4: Sagittal section of cavernous sinus and adjacent structures

Q. Discuss the etiology, pathogenesis and management of

Graves’s ophthalmopathy/thyroid eye disease.
Q. Give Warner’s classification of ophthalmic changes in
thyroid eye disease.
Grave’s ophthalmopathy/thyroid eye disease.
Etiology:
 Grave’s ophthalmopathy/thyroid eye disease may be associated
with in hyperthyroid, hypothyroid or euthyroid state
 It is an autoimmune disease
 Common in the age group 20 to 45 years and in females.
Pathogenesis: Circulating thymoglobulin (Tg) and anti

thymoglobulin immune complex may bind the eye tissue and
orbital tissue to produce thyroid ophthalmology.
Pathology:
 Hydroscopic mucopolysaccharide deposition, and inflam-
matory cells infiltration around the orbital tissue including
muscles
 Proliferation of retrobulbar fat and connective tissue.
Clinical features:
 Lid signs:
– Upper lid retraction, lid lag: When globe is moved down
neared the eyelid lags behind
– Difficulty in eversion of upper lid
– Infrequent blinking
 Conjunctiva: Deep injections and chemosis
 Pupil: Inequality of dilatation of the pupil
 Ocular motility defects
 Exophthalmos
 Optic neuropathy
 Exposure caused
– Exposure keratitis
– Sandy gritty sensation
– Lacrimation
– Photophobia.
Warner’s classification of ophthalmic changes:
(Mnemonic: NO SPECS)
CLASS Ocular changes
0 N No signs and symptoms
1 O Only signs
2 S Soft tissue changes
Symptoms: Photophobia, lacrimation, FB sensation
Signs: Conjunctival signs, palpable lacrimal gland
3 P Proptosis
4 E Extraocular muscles involvement (most common: inferior
rectus)
5 C Corneal involvement (Exposure keratopathy or dry eye)
6 S Slight loss of vision due to optic neuropathy or corneal
involvement
Investigations:
 Thyroid function test
 Positional tonometry: To diagnose mild cases
 USG: Both A and B scan
 CT scan
Management
A. Medical, surgical and/or radiological treatment of thyroid
disease
B. Ocular treatment:
 Topical artificial tear drops: for xerosis + lens
 Guanethidine eyedrops  lid retraction caused by over
action of mullers muscle
 Systemic steroids  chemosis, proptosis, optic neuropathy
 Radiotherapy  orbital edema in patient where steroids
are contraindicated
 Lateral tarsorrhaphy for exposure keratitis in cases not
responding for tear drops
 Extraocular muscle surgery: Should be done for left out
diplopic in primary gaze after congestive phase of disease
is over and the angle of duration is constant for 6 months
 Cosmetic surgery: For persistent lid retraction,
implantation of scleral grafts has become popular technique
 Blepharoplasty: Removal of excess fat and redundant skin
from around eyelid.
Q. What are the ocular manifestation of pituitary tumors?
The Ocular manifestation of pituitary tumors.
Mnemonic: DIPLOPS
Di  Diplopia
P  Ptosis
L  Loss of vision
Op  Ocular pain
S  Squint.
17.
Ocular Injuries
Q. What is black eye? List the causes for the same.

Black eye is bruising around the eye commonly due to an injury
to the face rather than an eye injury.
Causes:
 Basilar fracture of skull
 Blow to nose
 Surgery of face, e.g. face lift
 Surgery of nose
 Jaw surgery
 Angioneurotic edema/allergy (rarely).
Q. What is red eye? List the causes for the same.

A red eye is a cardinal sign of ocular inflammation, which can
be caused by several conditions.
Causes:
 Conjunctivitis
 Keratitis
 Iridocyclitis
 Acute glaucoma
 Subconjunctional hemorrhage
Ocular Injuries 383
 Endophthalmitis
 Panophthalmitis.
Q. Discuss the clinical features, complications and management
of extraocular foreign body.
Q. Discuss the management of foreign body in the cornea.
Common site:
 Conjunctiva: Sulcus subtarsalis, fornices, bulbar conjunctiva
 Cornea: Epithelium and stroma.
Common foreign bodies:

 Industrial workers: Iron, emery and coal
 Agriculturist: Husks of paddy, wings of insect
 Lay man: Sand, dust, glass, steel, wood.
Clinical features:
Symptoms:
 Discomfort, profuse watering of eyes, redness
 Pain
 Photophobia
 Defective vision if the cornea is lodged in the cornea.
Signs:
 Blepharospasm
 Ciliary congestion
 Oblique illumination: To localize the foreign body
 If the foreign body is suspected on the cornea then fluorescent
staining followed by slit lamp examination
 Double eversion if the foreign body is located in superior
fornix.
Complications:
 Acute bacterial conjunctivitis
 Corneal ulcer
 Pigmentation and opacities of cornea.
Treatment: Removal of the foreign body as early as possible is
the main stay of the treatment
A. Management of conjunctival foreign body:
 A foreign body in fornix, sulcus subtarsalis, canthi can be
removed with a swab/stick clean handkerchief with or
without topical anesthesia (Fig. 17.1)
 If the foreign body is lodged in the bulbar conjunctiva it
can be removed using hypodermic needle under topical
anesthesia.
B. Management of corneal foreign body:
 Firstly, an attempt is made to remove the foreign body by
saline irrigation
 If it fails, a sterile cotton-tipped swab is used
 If the above fails foreign body can be removed using
hypodermic needle under topical anesthesia
Fig. 17.1: Removal of superficial foreign body with needle

Ocular Injuries 385
 If the foreign body is a magnetic substance than a hand

held magnet can be used to remove the same
 If the foreign body is impacted in the deep stroma then the
foreign body is to removed using operative microscope
with sharp needle
 After removal, topical antibiotics and cycloplegics are
prescribed.
Q. Discuss the mechanisms, modes of damage and clinical
manifestations of blunt trauma to eye.
Mechanisms of blunt trauma to eye:
 Direct impact on the globe
 Compression wave force: That is transmitted through the fluid
content in all directions and strikes the angle of the anterior
chamber, pushes the iris lens diaphragm posteriorly and also
strikes the retina and the choroid
 Reflected compression wave
 Rebound compression wave
 Indirect force from surrounding bony tissue.
Modes of damage:
 Mechanical tearing of tissues
 Damage to tissues sufficient to cause the mechanical
disruption
 Vascular damage
 Tropic changes
 Delayed complications: Secondary glaucoma, hemophthal-
mitis, late rosette formation and retinal detachment.
Clinical manifestations:
Structure of eye Clinical manifestations
Lid Laceration
Black eye
Emphysema of the lid due to involvement of the
Paranasal sinuses
Conjunctiva Chemosis
Laceration
Subconjunctival hemorrhage
Cornea Simple abrasion
Erosion
Partial corneal tears
Blood stained cornea
Corneal opacities
Sclera Partial thickness scleral wound
Anterior chamber Hyphema
Exudates
Pupil Traumatic miosis/mydriasis
‘D’ shaped pupil
Irregular pupil
Iris Radiating tears of iris stroma
Iridodialysis
Antiflexion: is a condition in which the posterior surface
of iris faces anteriorly
Retroflexion: Whole of the iris is double backed into the
ciliary region and becomes invisible
Traumatic aniridia
Traumatic iridocyclitis
Ciliary body Angle recession due to tear between longitudinal and
circular muscle fibers of the ciliary body. This causes
deepening of the anterior chamber
Contd...
Ocular Injuries 387
Contd...
Lens Vossius ring
Traumatic absorption of lens
Dislocation of lens
Subluxation of lens
Concussion cataract
Vitreous Hemorrhage
Liquefaction
Herniation
Choroid Rupture
Hemorrhage
Detachment
Choroiditis
Retina Berlins edema
Retinal hemorrhage
Retinal tears
Retinitis proliferans
Retinal detachment
Concussion changes in macula
Optic nerve Avulsion of optic nerve
Optic nerve sheath hemorrhage
IOP May be elevate or may decrease
Refraction Myopia due to ciliary spasm
Hypermetropia due to loss of accommodation
Lacrimal Traumatic subluxation of the gland
apparatus Injury to the canaliculi
Orbit Proptosis and displacement of the globe
Orbital hemorrhage
Orbital emphysema
Fracture of orbital bones (blowout fracture)
Q. What is Berlin’s edema/commotio retinae?

 Berlin’s edema is the milky cloudiness at the macular area
due to post-traumatic edema
 Central vision may be permanently impaired due to
pigmentary deposing in the macula
 Mechanism: External force is transmitted through the vitreous
to the chorioretinal area to induce outer retinal ischemia
 It may get spontaneously resolved or may get pigmented.
Q. What is vossius ring?

 Vossius ring is brown pigmentation on the anterior capsule
 It occurs due to striking of the contracted pupillary margin
against the crystalline lens
 It is smaller than the size of the pupil.
Q. What is iridodialysis? How do you manage the same?

Iridodialysis is partial tearing away of the iris from the ciliary
body due to blunt trauma (Fig. 17.2).
Clinical features:
 Few are asymptomatic
 Monocular diplopia
 Glaucoma
 Hyphema
 Hypotony.
Fig. 17.2: Anterior dialysis

Ocular Injuries 389
Management:
 Bed rest
 Acetazolamide to reduce IOP
 Surgical repair.
Q. Define hyphema. Discuss the etiology, clinical features and

Definition: Hyphema is blood in anterior chamber.
Etiology:
 Traumatic
 Intraoperative postoperative
 Herpetic iridocyclitis
 Rubeosis iridis
 Blood dyscrasia
 Intraocular malignancies
 Idiopathic
 Juvenile xanthogranuloma.
Source of bleeding:
 Smaller branches of major arterial circle
 Capillaries of minor arterial circle
 Radial vessels at the root of iris, associated with iridodialysis.
Clinical features:
 Blood usually does not clot and settles in the most dependent
part of the anterior chamber and a fluid meniscus is formed
 Frequently minor bleeding is followed by a more severe
bleeding within 48 hours
 Sometimes blood may be clotted, especially in the presence
of sphinctric tear or iridodialysis.
When blood clots, the hyphema appears as small black ball (like
number ‘8’ ball in the billiards game) this is called ‘8’ ball (or
black-ball) hyphema.
Complications:
 Secondary glaucoma
 Secondary optic atropy
 Blood staining of the cornea.
Treatment:
 Complete bed rest
 Sedation
 Patching of the eyes
 Local steroids to minimize risk of uveitis
 Prophylaxis against secondary glaucoma
 Indications for paracentesis:
– If blood is not absorbed after 5 to 7 days
– Persistent high IOP after 3 days
– Early signs of blood staining of cornea.
Q. What is siderosis bulbi? Discuss the clinical features and
Q. What is chalosis bulbi? Discuss the clinical features and
Figs 17.3A to C: (A) Siderosis bulbi; (B) Kayser-Fleischer ring;

(C) Sunflower cataract
Ocular Injuries 391
Siderosis bulbi refers to irreversible degenerative changes

produced by an iron foreign body. It usually affects epithelial
cells (Fig. 17.3A).
Pathogenesis:
Iron particles undergo electrolytic dissociation iron particles
combine with intracellular proteins and produce degenerative
changes.
Clinical signs:
 Iris: Initially appears greenish but later turns brown
 Lens:
– Anterior epithelium and capsule are affected
– Deposition is in the form of a ring and later causes cataract
 Secondary glaucoma due to degeneration of trabacular mesh-
work
 Retina: Pigment degeneration is noted
 Cornea appears rusty
 Electroretinography (ERG) Response is reduced
 Loss of vision
 Iron particles can be stained using prussian blue.
Chalosis bulbi:
This is a reversible condition in which specific changes are
produced by alloys of copper.
Pathogenesis:
Copper undergo electrolytic dissociation and gets deposited
under membranous structure like iron there is no chemical
reaction with the tissue hence the changes are reversible.
Clinical signs:
 Kayser-Fleischer rings (Fig. 17.3B):
– It is a golden brown ring
– It is formed due to deposition of copper under peripheral
parts of Descemet’s membrane of the cornea.
 Sunflower cataract (Fig. 17.3C):
– Copper deposition behind posterior capsule gives brilliant
golden green color
– The arrangement of the copper particles is in the shape of
the petals of a sunflower.
 Retina:
– Deposition of golden plaques are noted
– Light reflects as a golden sheen.
Investigations:
 Slit lamp examination
 Gonidoscopy
 Plain X-ray
 Limbal ring X-ray
 USG B scan
 CT scan
 Use of metal detector.
Treatment:
 Foreign body in anterior chamber:
– For magnetic foreign body handheld magnet is used
– If nonmagnetic pointed forceps is used for its removal
 Foreign body in Iris: Sector iridectomy of the part containing
the foreign body
Ocular Injuries 393
 Foreign body in lens: Removal of the foreign body along

with the lens with replacement of intraocular lens
 Foreign body in vitreous or retina:
– For magnetic foreign body: The particle is removed directly
through posterior route by hand held magnet (Fig. 17.4
and 17.5)
– For nonmagnetic foreign body: Pars plana vitrectomy
(Fig. 17.6).
Fig. 17.4: Removal of magnetic foreign body in the anterior chamber
Fig. 17.5: Removal of magnetic foreign body in the posterior chamber

Fig. 17.6: Removal of nonmagnetic foreign body in the posterior chamber
Q. Define sympathetic ophthalmitis. Discuss the etiology,

pathology, clinical features and management of the same.
Q. Why is ciliary zone called danger zone of the eye?
Definition: Sympathetic ophthalmitis is a serious bilateral
granulomatous panuveitis which follows penetrating trauma.
 It may also occur postsurgical
 The injured eye is called exiting eye and the fellow eye which
develops uveitis is called sympathizing eye.
Etiology:
Predisposing factors:
 Penetrating wounds
 Wounds in ciliary area
 Wounds of incarceration of iris, ciliary body and lens
 More common in children than in adults
 Whites are predisposed than blacks.
Ocular Injuries 395
Ciliary zone is called as the danger zone of the eye because it

is the wound in this region which commonly evokes sympathetic
ophthalmitis.
Pathogenesis: Allergic theory has been attributed. Uveal pigment
acts as an allergen and excites plastic uveitis in sound eye.
Clinical features:
A. Exiting (injured) eye: Features of low grade plastic uveitis
are seen
 Ciliary congestion
 Lacrimation
 Tenderness of globe
 Keratin precipitates
B. Sympathizing (sound) eye:
The sound eye is affected 4 to 8 weeks after the injury
The clinical picture resembles acute plastic iridocyclitis and
is divided into two stages:
1. Prodormal stage:
Symptoms: Photophobia, difficulty in seeing near objects
Signs:
 Retrolental flares/cells
 Keratin precipitates
 Mild ciliary congestion
 Tenderness of globe
 Fine vitreous gaze.
2. Fully developed stage:
 The above symptoms get exaggerated
 Mutton fat KPs
 Cells and flare in anterior chamber
 White choroidal infiltrates

 Vitreous cells.
Prophylaxis:
 Early excision of the injured eye if there is no chance of saving
useful vision
 When there is chance for vision:
– Meticulous repair of the wound with surgery without
incarceration in the wound
– Systemic steroids
– Topical antibiotics, cycloplegics and steroids
– If uveitis is not resolved after two weeks, then eye is to be
excised.
Treatment: If sympathetic ophthalmitis has already set in
 If the patient is brought in prodromal stage and there is no
hope for vision then the eye is excised
 Conservative treatment for sympathetic ophthalmitis:
– Systemic and topical steroids
– Immunosuppressive agents
– Local atropine.
Q. Discuss the types and management of chemical injuries to
eye.
Q. Discuss the management of acid injuries to eye.
Q. Discuss the mechanism, stages and management of alkali
injuries to eye.
Q. List the complications of chemical injury to eye.
Chemical injury may be because of acid or alkali.
Ocular Injuries 397
Modes of chemical injury:

 Domestic
 Agriculture
 Industrial
 Deliberate attack
 Warfare
 Self inflicted.
Alkali burns:
Alkalies are more severe chemicals than acids.
Common alkali: lime, caustic soda, liquid ammonia.
Mechanical of injury:
 Destruction of cell membrane by dissociation and soponi-
fication
 Being hydroscopic it draws water out of the cell and hence
causes necrosis of the cell
 It combines with the lipids causing softening and
gelatinization.
Clinical stages:
 Stage of acute ischemic necrosis: The clinical picture of the
stage is as follows
– Conjunctiva: Edema, congestion, necrosis, purulent
discharge
– Cornea: Sloughing of epithelium, edema, opacities
– Iris: Violent inflammation.
 Stage of repair:
– Epithelial regrowth is seen in cornea and conjunctiva
– Corneal vascularization is noted
– Inflammation of iris subsides.
 Stage of complications: Following complications may develop

– Symblepharon
– Recurrent corneal ulcer
– Complicated cataract
– Secondary glaucoma.
Acid burns:
 Most common acid that cause injury are sulfuric acid, nitric
acid, hydrochloric acid
 The amount of injury is less severe than the alkali attack
 Mechanism of injury: Coagulation of proteins
 Ocular lesions:
– Conjunctiva: Necrosis, Symblepharon
– Corneal: necrosis, staphyloma.
Management of chemical burns:
 Immediate and thorough wash
 Neutralization of chemicals:
– Neutralization of acids by weak alkalies like sodium
bicarbonate
– Neutralization of alkalies by weak acids like Boric acid
and Ethylene diamine tetracetic acid (EDTA)
 Mechanical removal: Particularly in case of lime by using a swab
 Remove necrotic and contaminated tissue by cotton swab stick
 Tropical antibiotics, steroids and atropine
 Prevention of Symblepharon by passing a glass stick with lubricant
 Treatment of complications:
– Secondary glaucoma: 0.5 percent timolol or 250 mg
acetazolamide
– Kerotoplasty for corneal opacity.
18.
Ocular Therapeutics,
Laser and Cryotherapy in
Ophthalmology
Q. Discuss in detail different modes of drug administration.

Ocular pharmacotherapeutical can be delivered in the following
methods
A. Topical instillation into the conjunctival sac
Method Advantage Disadvantage
Eyedrops Simple, suitable for daytime Quickly diluted by
(Fig. 18.1) use immediate action tears
Eye More bioavailability as there is Blurring of vision, suit-
ointment increased tissue contact time able for bedtime use
Gels More bioavailability as there is Costly
increased tissue contact time
No blurring of vision
Ocusets Drug delivery through membrane Costly
Relatively constant rate of release
Commonly used in glaucoma
Soft contact Delivers higher concentration Costly
lens of the drugs in emergency treatment
Fig. 18.1: Instillation of eye drops
B. Periocular injections:
Type Comment
Subconjunctival injection Useful to achieve higher concentration of the drug
Drugs which cannot pass through the cornea due
to high molecular weight can pass through the
sclera
Subtenon injection Anterior Subtenon injection for anterior uveitis
Posterior Subtenon injection for posterior uveitis
Retrobulbar injection To deliver drugs in optic neuritis, papillitis and
posterior uveitis
Retrobulbar block anesthesia
Peribulbar injection Injecting anesthetic agents
C. Intraocular injections: Used in desperate situations to deliver

the drug in maximum concentration (Endophthalmitis). These
include
 Intracameral injection into the anterior chamber
 Intravitreal injection into the vitreous cavity.
Ocular Therapeutics, Laser and Cryotherapy 401
D. Systemic administration:
 Includes intramuscular, intravenous and oral intake of
drugs
 Only drugs which have high lipid solubility and with low
molecular weight can cross the blood aqueous barrier.
Q. List the viscoelastic substances used in ophthalmology. List
their uses.
Viscoelastic substances used in ophthalmology are:
Methylcellulose, sodium hyaluronate, hypromellose and
chondroitin sulfate.
Uses:
 Cataract surgery with or without IOL implantation
 Glaucoma surgery
 Kerotoplasty
 Retinal detachment surgery
 Repair of globe in perforation injuries.
Q. What is LASER? List its properties (rarely tested) and uses

of the same.
Q. List the uses of laser in ophthalmology.
 LASER is an acronym for ‘light amplification by stimulated
emission of radiation’
 Laser light is characterized by monochromaticity, coherence
and collimation. These properties make it the brightest existing
light
 Different types of laser are: Argon, Krypton, Diode, Nd:YAG
and Excimer laser.
Effect produced by laser and Used in treatment of

Mechanism of action
Photocoagulation: Absorption of Eyelid lesions like hemangioma
laser light by tissue pigments  light is Corneal neovascularization
converted into heat temperature of Glaucoma (Iridotomy and trabeculoplasty)
tissues raises  coagulation and denatu- Photomydriasis, sphinctrectomy and laser
ration of tissues/proteins shrinkage of iris cyst
Panretinal photocoagulation in diabetic
retinopathy
Peripheral retinal vascular abnormalities
Intraocular tumors (retinoblastoma)
Macular disease: Central serous retinopathy
and age related macular degeneration
Photodisruption: Laser ionizes the Capsulotomy for thickened posterior capsule
electron of the target tissue producing Membranecetomy for pupillary membranes
a state called plasma  this plasma Phacolysis of phacoemulsification
expands with a momentary pressure as
high as 10 kilobars  exerting a
cutting/incision effect on the tissues
Photoablation: Laser UV light of Photorefractive keratectomy (PRK)
very short wavelength  breaks chemical LASIK
bonds of biological material converting Phototherapeutic keratectomy (PTK)
them into smaller molecules that diffuse
away
Q. List the uses of Cryotherapy.

Q. Discuss the mechanism of action (rarely tested) and uses of
Cryotherapy.
 Cryopexy means to produce tissue injury by application of
intense cold (– 40º to –100ºC)
 This is achieved by a cryoprobe from a cryo unit
 Commonly used cooling agents in the probe: Freon, nitrous
oxide, carbon dioxide gas
Ocular Therapeutics, Laser and Cryotherapy 403
 Modes of action: The required therapeutic effect is brought

about as follows:
– Tissue necrosis as in cyclocryopexy and cryopexy of
tumors
– Adhesion between tissues, e.g. adhesion between retina
and choroid in retinal detachment
– Vascular occlusion as in coats disease
– Adherence of the cryoprobe to the iceball in the tissues
(as in cataract extraction)
 Uses:
Part of the eye Cryotherapy is used for
Lids Cryolysis for trichiasis
Warts and molluscum contagiosum
Basal cell carcinoma and haemangioma
Conjunctiva Hypertrophied papillae of the vernal catarrh
Cornea Herpes simplex keratitis
Lens Cryoextraction of lens
Ciliary body Cyclocryopexy for absolute glaucoma and neovascular
glaucoma
Retina For sealing holes in retinal detachment
Prophylactically to prevent retinal detachment
Anterior retinal cryopexy in retinal ischemic disease
For retinoblastoma and hemangioma
19.
Systemic Ophthalmology
Q. What is Xerophthalmia? Discuss the etiology, WHO

classification/clinical features and management of the same.
Q. What is Bitot’s spots? How do you manage the same?
The term xerophthalmia is now reserved to cover all manifestations
of Vitamin A deficiency, including not only structural changes
affecting the conjunctiva, cornea and occasionally retina but also
biophysical disorders of retinal rods and cones.
Etiology: Decreased intake or decreased absorption of Vitamin
A or both.
WHO classification of Xerophthalmia
XN Night blindness
X1A Conjunctival xerosis
X1B Bitot’s spots
X2 Corneal xerosis
X3A Corneal ulceration/keratomalacia affecting less than one-third of
the corneal surface
X3B Corneal ulceration/keratomalacia affecting more than one-third of
the corneal surface
XS Corneal scar due to xerophthalmia
XF Xerophthalmic fundus
Systemic Ophthalmology 405
Clinical features:
 Night blindness: This is the first clinical feature to appear.
This stage responds to treatment swiftly
 Conjunctival xerosis:
– One or more patches of dry, lusterless, nonwettable cornea
appears
– It appears like “Emerging sand banks at receding tides”
– Most commonly temporal interpalpable conjunctiva is
affected. Rarely whole of bulbar conjunctiva may be
affected.
 Bitot’s spots:
– These are usually bilateral and they appear as raised silvery
white foamy triangular patch of keratinized epithelium
– Most commonly affects bulbar conjunctiva in temporal
side (Fig. 19.1).
 Corneal Xerosis:
– Punctate keratopathy in the lower nasal quadrant is the
first change note in cornea
– Later haziness and granular pebbly dryness appears.
 Corneal ulceration/keratomalacia:
– Ulceration may be in a part or whole of corneal stroma
resulting in permanent structural alteration
Fig. 19.1: Bitot’s spot

– The ulcers are classically round “punched out defects”

– Perforation if occurs gets plugged by iris
– An emergency treatment may prevent blindness.
 Corneal scar: They are results of healed stromal defects
 Xerophthalmic fundus:
– Small white seed like lesions are noted
– These are uniformly distributed at the level of optic disc.
Treatment of Vitamin A deficiency:
A. Local ocular treatment
 In stage of conjunctival xerosis: Artificial eye tear drops
like 0.7% methylcellulose or 0.3% hypromellose
 In stage of keratomalacia: Treat it similar to bacterial
corneal ulcer.
B. Vitamin A therapy: To all stages of xerophthalmia
 Age > 1 year: 2,00,000 IU orally or 1,00,000 IU as IM
injection on 0, 1, 28 days (in case of vomiting, diarrhea)
 Age < 1 year or body weight < 8 kg: Half of above dose
 Women of reproductive age both pregnant or not
– XN, XIA, XIB  10,000 IU for 2 weeks
– X2 onwards 2,00,000 IU orally or 1,00,000 IU as
IM injection on 0, 1, 28 days
 Oral administration is preferred as it is safe, cheap and
highly cost effective.
C. Treat the underlying cause of diarrhea, PEM, measles and
electrolyte imbalance.
Q. Discuss vitamin A prophylaxis.

Q. Discuss vitamin A prophylaxis program.
Q. List the food items rich in vitamin A.
Vitamin A prophylaxis
 Short-term approach
– Children at 9 month of age 1,00,000 IU
– Children between 1 to 6 years of age  2,00,000 IU once
every 6 months
– Infants < 6 months who are not breastfed: 50,000 IU orally
once
– Lactating mothers: 20,000 IU at delivery
 Medium term approach: Food fortification of ghee,
vanaspathi, bread
 Long term: Good quality diet. Following are the food items
rich in Vitamin A (Fig. 19.2)
– Yellow fruits: mango, papaya
– Green leafy vegetables
– Drumsticks
– Carrot
– Milk
– Egg
– Liver.
Fig. 19.2: Foods rich in vitamin A

Q. List the ocular manifestations of HIV
The ocular manifestations of HIV are as follows:
Usual ocular infections Herpes simplex
Herpes zoster ophthalmicus
Toxoplasmosis
TB, syphilis, fungal corneal ulcer
Opportunistic infection Candida endophthalmitis
Cryptococcus
Pneumocystis carinii
Tumors Burkitt’s lymphoma
Kaposis sarcoma
Neuro-ophthalmological lesions Optic nerve involvement, paralysis
of eyelid, extraocular muscles
involvement, loss of vision
Retinal and vascular features Cotton wool spots
of HIV Superficial and deep hemorrhages
Aneurysms
Telangiectasia
Q. List the ophthalmic manifestation of rheumatoid arthritis.

Note similarly any of the following disease can be asked
Disease Ocular manifestation
Rheumatoid arthritis* Keratoconjunctivitis sicca
Scleritis
Ulcerative keratitis
Systemic lupus erythematosus Madarosis
Keratoconjunctivitis sicca
Scleritis
Periulcerative keratitis
Retinal vasculitis
Optic neuropathy
Wegener’s granulomatosis Necrotizing scleritis
Nasolacrimal duct obstruction
Dacrocystitis
Polyarteritis nodosa Necrotizing scleritis
Orbital inflammatory disease
Occlusive retinal periarteritis
Sjogren’s syndrome Keratoconjunctivitis sicca
Aide’s pupil
Systemic sclerosis* Eyelid tightening and telangiectasia
Episcleritis, scleritis, scleral pits
Retinal cotton wool spots
Patches of choroidal non perfusion
Giant cell arteritis Ischemic optic neuropathy
TIA
Contd...
Contd...
Cotton wool spots
CRAO
Ocular ischemic syndrome
Diplopia
Ehlers-Danlos syndrome * Ocular frigidity
Increased vulnerability to mild trauma
Myopia
Retinal detachment
Keratoconus
Blue sclera
Ectopic lentis
Angiod streaks
Marfan’s syndrome* Ectopic lentis
Hypoplasia of dialator pupillae
Angle anomaly
Myopia
Retinal detachment
Microspherophakia
Keratoconus
Megalocornea
Blue sclera
Patau syndrome (trisomy 13)* Anophthalmos/Microophthalmos
Anterior segment dysgenesis
Cycloplegia
Corneal opacities
Cataract/congenital glaucoma
Coloboma
Hypertelorism
Primary hyperplastic primary vitreous
Retinal dysplasia
Contd...
Contd...
Alport’s syndrome* Cataract
(Mnemonic: CRAP) Corneal dystrophy
Retinal flecks
Anterior lenticonus (anterior conical
projection of the anterior surface of
lens)
Posterior polymorphous corneal
dystrophy
Behcet’s syndrome Occlusive periphlebitis
(Mnemonic: ORAL) Retinitis
Anterior uveitis
Leakage from retinal vessels
Ankylosing spondylitis Anterior uveitis
Scleritis
Reiter’s syndrome Anterior uveitis
Scleritis
Episcleritis
Papillitis
Retinal vasculitis
Psoriatic arthritis Anterior uveitis
Conjunctivitis
Marginal corneal infiltration
Secondary Sjogren syndrome
Ulcerative colitis Conjunctivitis
Peripheral corneal infiltration
Scleritis
Episcleritis
Anterior uveitis
Papillitis
Retinal vasculitis
Contd...
Contd...
Chron’s diseases Conjunctivitis
Episcleritis
Peripheral corneal infiltration
Anterior uveitis
Retinal periphlebitis
Sarcoidosis Conjunctival nodules
Uveitis
Behcet’s syndrome* Panuveitis
vasculitis retinae
periphlebitis and the pipe stem
sheathing along with the recurrent
vitreous hemorrhages
Scleritis
Episcleritis
Vogt-Koyanagi-Harada disease* Uveitis
Bilateral exudative retinal detachment
TB* Lupus vulgaris and cold abscess of eyelid
TB conjunctivitis
Keratitis
Scleritis
Anterior uveitis
Choroiditis
Papillary abnormality
Optic neuropathy
Ocular motor palsies
Acquired syphilis* Uveitis
Interstitial keratitis
Madarosis
Contd...
Contd...
Optic neuritis
Argyll Robertson’s pupil
Congenital syphilis* Anterior uveitis
Interstitial keratitis
Pigmentary retinopathy
Leprosy* Neuroretinitis
Oculoglandular syndrome
Focal choroiditis
Panuveitis
Retinal vein occlusion
Maculopathy
Toxoplasmosis* Microophthalmos
Calcification
Chorioretinitis
Nystagmus
Ocular deviations
Onchocerciasis/river blindness* Sclerosing keratitis
Retinitis
Anterior uveitis
Iridocyclitis
Chorioretinitis
Cysticercosis Affects vitreous and retina
Cryptococcosis Choroiditis
Congenital rubella* Cataract
Microophthalmos
Glaucoma
Retinopathy
Keratitis
Contd...
Contd...
Anterior uveitis
Iris atropy
Severe retinitis
Nystagmus
Strabismus
Homocystinuria* Ectopic lentis
Myopia
Retinal detachment
Paget’s disease Optic atrophy
Proptosis
Angiod streaks
Cushing’s disease Steroid induced cataract
Bitemporal hemianopia
Glaucoma
Acromegaly Angiod streaks
(Mnemonic BS in ARChiology) Chiasmal syndrome
Retinopathy
Optic atrophy
Bitemporal hemianopia
See-saw nystagmus
Myasthenia Gravis* Diplopia
Asymptomatic ptosis
Paralytic squint
Gaze evoked nystagmus
Cogan’s lid twitch
Multiple sclerosis* Retrobulbar neuritis
Nystagmus
Contd...
Contd...
Hemianopia
Uveitis
Neurofibromatosis type 1* Glioma, nuerilemmoma
Plexiform neurofibromatosis
Sphenoorbital encephalocele
Eyelid nuerofibroma
Lish nodules in iris
Congenital ectropion uvea
Glaucoma
Thickened corneal nerves
Neurofibromatosis type 2* Cataract
Hamartoma retina
Unilateral Lisch nodules in iris
Meningioma of optic nerve sheath
Orbital nerve glioma
Leukemia Primary or secondary infiltration
Cranial nerve palsies
Orbital hemorrhage
Infarcts
Vascular occlusion
Optic nerve involvement
Parinaud’s dorsal midbrain Convergence retraction nystagmus
syndrome (Mnemonic: CLUES”) Light near dissociation
Upgaze paralysis
Eyelid retraction
Skew deviation
*Indicates most commonly tested topics
20.
Community Ophthalmology
Q. Define: WHO definition of blindness, economic blindness,

social blindness, legal blindness, total blindness and avoidable
blindness.
Term Definition
WHO definition of Visual acuity less than 3/60 (Snellen) or Inability
blindness to count fingers at a distance of 3 m in daylight
Economic blindness Vision in better eye < 6/60 to 3/60
Social blindness Vision in better eye: < 3/60 to 1/60
Legal blindness Vision in better eye < 1/60 to perception of light
Total blindness No perception of light
Avoidable blindness This includes preventable blindness and curable
blindness
Q. What are the causes of avoidable blindness?

This includes preventable blindness and curable blindness
Examples
Preventable blindness: includes the Corneal blindness due to
blindness that can be easily prevented vitamin A deficiency and
by attacking the causative factor trachoma
Curable blindness: includes blindness Cataract in which blindness can be
that can be cured by timely intervention corrected by surgery
Community Ophthalmology 417
Q. List the most common causes of blindness in India. List the

factors responsible for the same.
Common causes of blindness Factors responsible
in India (Fig. 20.1)
Cataract Inadequacy of the ophthalmic personnel
Refractive errors Lack of availability of services near home
Glaucoma Under-utilization of available manpower
Posterior segment pathology Lack of knowledge and concerns, malnutrition,
lack of eye care, superstition and ignorance
Corneal blindness Prevalence of infection
Childhood blindness Quack practice and home remedies
including xerophthalmia
Fig. 20.1: Common causes of blindness
Q. What is Vision 2020: Right to Sight?

Vision 2020 is the global initiative for the elimination of
avoidable blindness, a joint program of the World Health
Organization (WHO) and the International Agency for the
Prevention of Blindness (IAPB) with an international

membership of NGOs, professional associations, eye care
institutions and corporations.
Aim: To eliminate avoidable courses of blindness by 2020
Strategy: Diseases targeted
Disease prevention and control Cataract
Training of eye care personnel Childhood blindness
Strengthening health care Trachoma
delivery system
Resource collection Refractive errors
Use of appropriate technology Onchocerciasis
Glaucoma
Diabetic retinopathy
Age related macular degeneration
Q. List the common causes of blindness in children.

The common causes of blindness in children
 Vitamin A deficiency
 Measles
 Conjunctivitis
 Congenital cataract
 Ophthalmia neonatorum
 Retinopathy of prematurity.
Q. What is SAFE strategy for Trachoma control?

The SAFE strategy for Trachoma control are effective
interventions developed to prevent blindness from trachoma.
S  Surgery to correct lid deformity and prevent blindness
A  Antibiotics for acute infections and community control
F  Facial hygiene
E  Environment change including improved access to water

and sanitation and health education.
Note some of the important abbreviations:
 GET 2020: Global elimination of trachoma 2020
 NPCB: National program for control of blindness
 DA NPCB: Danish assistance for NPCB
 DBDS: District blindness control society
 VFTF: Vision for the future.
Q. What are the objectives of NPBC? What are the basic

components of the same?
Aims and objectives:
 To provide comprehensive eye care facility for primary,
secondary and tertiary levels of health care
 Decrease the prevalence of blindness from 1.38% to 0.31%
by 2000 AD.
Basic components
 Establishment of permanent infrastructure: This is being done
in a three tier system (Figs 20.2A and B)
Level Associated hospitals Caters for
Primary level Primary health centers Ocular prophylaxis at birth
subcenters Vitamin A prophylaxis
Measles vaccination
Avoid hypoxia at birth
Examination of neonatal eye
Nutritional supplementation
Vision screening
Contd...
Contd...
Secondary Taluk hospitals Treatment of vitamin A
level Community health deficiency
centers Surgical problems
Treatment of trachoma
Tertiary level Medical college hospital Treatment of vitamin A
District hospitals deficiency
Regional centers for Surgical problems
ophthalmic excellence Emergency management
Treatment of trachoma
Corneal transplantation
Management of retinal
detachment
Apex institute Dr Rajendra prasad institute
of ophthalmology in AIIMS
Figs 20.2A and B: Primary, secondary, tertiary level of ocular health care
Q. List the corneal causes of blindness.

Corneal causes of blindness:
 Ulcers
 Trachoma and other infections
 Ocular injuries
 Keratomalacia
 Traditional medicine or home remedies, which often harm

the eye rather than relieve pain or improve eyesight
 Corneal opacities.
Q. List the incurable causes of blindness.
The incurable causes of blindness are:
 Optic atrophy
 Congenital deficiency of photoreceptors
 Retinal degeneration
 Cortical lesions
 Phthisis bulbi
 Posterior circulation occlusion.
Q. Discuss the objectives of an eye bank.

Q. List the contraindication for eye collection.
Q. How do you preserve donor eye after collection? How do
you evaluate the eye collected?
The objectives of an eye bank are as follows:
 Collection of donor eye
 Process and storage of donor cornea
 Distribution and utilization of the highest quality of the donor
tissue for transplantation
 Provide for soliciting eye donation from potential donors
 Provide and process eye tissue for teaching or research
purpose
 To promote public health relation system
 To promote hospital corneal retrieval program
The contraindications for eye collection:

Medical Ophthalmic
HIV Previous surgeries
Hepatitis B/C RB
Rabies Malignant melanoma
Prions disease Endophthalmitis
Leukemia Corneal pathology
Septicemia
Prevention of Donor Eye:
A. Up to 4 days (short-term)
 Moist chamber method: Whole globe at 4° in refrigerator
for 24 hours
 M-K medium: MacCarey Kufwanns medium: Compo-
sition: Dextrose, Gentamicin, buffer
B. Intermediate-term preservation (up to 2 week): the following
can be used
 Dexol, Optisol (condritin sulphate) or K SOL medium
C. Long-term months – years
 Viable eye: Organ culture, cryopreservation
 Non viable eye: Glycerin preservation.
Evaluation of donor eye
 Serology: HIV, Hepatitis, Syphilis
– Examination in torch light
– Slit lamp
– Specular microscopy
– Tryptan blue staining
 Microbial culture
 HLA typing
 Ocular examination.
21.
Differential Diagnosis,
Important Diagnostic and
Darkroom Procedures
(*uses and principle of all darkroom procedures and diagnostic

tests mentioned in the chapter are high yield)
Q. List the common causes of sudden painless loss of vision.
(Note: in a similar fashion any of the following symptom/sign
may be tested)
Ocular symptom/sign Causes
Sudden painless loss of vision* Central retinal artery occlusion
(Mnemonic: C the MRI) Massive vitreous hemorrhage
Retinal detachment involving macular area
Ischemic CRVO
Sudden painless onset of Methyl alcohol amblyopia
defective vision* Optic neuritis
(Mnemonic: MONC) Nonischemic CRVO
Central serous retinopathy
Contd...
Differential Diagnosis, Important Diagnostic 425
Contd...
Sudden painful loss of vision* Chemical injuries to the eye ball
(Mnemonic: CAAM) Acute congestive glaucoma
Acute iridocyclitis
Mechanical injuries to the eye ball
Gradual painless defective Progressive pterygium involving macular area
vision* Corneal degeneration
Corneal dystrophies
Developmental cataract
Senile cataract
Optic atrophy
Chorioretinal degeneration
Age-related macular degeneration
Refractive errors
Gradual painful defective Chronic iridocyclitis
vision (3Cs)* Corneal ulceration
Chronic simple glaucoma
Transient loss of vision Carotid artery disease
(Amaurosis fugax)* Papilledema
Giant cell arteritis
Migraine
Raynaud’s syndrome
Severe hypertension
Prodromal symptom of CRAO
Night blindness (Nyctopia)* C—Congenital night blindness
(Mnemonic: CRVO) R—Retinitis pigmentosa
V—Vitamin A deficiency
O—pathological myOpia
and peripheral cortical cataract
Contd...
Contd...
Day blindness (hamarlopia) C—Central nuclear/polar cataract
(Mnemonic: 4 C’s) C—Central corneal opacities
C—Central vitreous opacities
Congenital deficiency of cones
Diminution of vision for Presbyopia
near only Cycloplegia
Internal or total ophthalmoplegia
Insufficiency of accommodation
Black spots/floaters V—Vitreous hemorrhage
(Mnemonic: 3V’s) V—Vitreous degeneration
V—Vitreal exudates
Lenticular opacities
Photopsia/flashes of light Retinal detachment
in front of the eye Retinal tear
(Mnemonic: 3 retinal causes Retinitis
and 2 vitreal causes) Posterior vitreous detachment
Vitreous fractional band
Colored holos C—acute Congestive glaucoma
(Mnemonic: 5 C’s) C—Cataract (early stage)
C—Conjunctivitis-mucopurulent
C—Corneal scarring
C—Contact lens over use (causing abrasion)
Uniocular diplopia* S—Subluxated lens
(Mnemonic: SICKLED) I—Incipient cataract, C
K—Keratoconus, L
E—Eccentric IOL
D—Double pupil
Binocular diplopia* Paralytic squint
Myasthenia gravis
Contd...
Contd...
Diabetes mellitus
Blow out fracture of the floor of the orbit
Anisometropic glasses
After squint correction in presence of
abnormal retinal correspondence
Decreased blinking Trigeminal anesthesia
7th cranial nerve palsy
Muscular diseases
Lagophthalmos Facial nerve palsy
(inability to close eyes)* Extreme degree of proptosis
Symblepharon (adhesions between palpable
and bulbar conjunctiva)
Madarosis (absence of cilia) Chronic blepharitis
(Mnemonic: CML) Myxedema
Leprosy
Poliosis (graying of cilia) Old age
VKH syndrome (Vogt-Koyanagi-Harada)
Vitiligo
Albinism
Small sized eye ball Congenital microophthalmos
(Mnemonic: CAP) Atropic bulbi
Phthisis bulbi ( 5S’s—Small, soft, shrunken,
sightless and shapeless eye ball)
Papillae in conjunctiva* Trachoma
(reddish raised areas with Spring catarrh
flat tops and velvety Allergic conjunctivitis
appearance) Giant papillary conjunctivitis
Contd...
Contd...
Concretions in conjunctiva* Trachoma
(yellowish white hard Conjunctival degenerations
looking raised areas, pin point Idiopathic
to pin head size)
Conjunctival follicles Trachoma
Acute follicular conjunctivitis
Chronic follicular conjunctivitis
Benign foliculosis
Conjunctival cyst Retention cyst
Implantation cyst
Lymphatic cyst
Cysticercosis
Microcornea Congenital
(cornea < 10 mm in diameter) Microophthalmos
Phthisis bulbi
Megalocornea Congenital
(corneal diameter > 13 mm) Buphthalmos
Congenital corneal opacities S—Sclera cornea
(Mnemonic: STUMPED) T—Trauma
U—Ulcer
M—Mucopolysaccharidosis
P—Peter anomaly
ED—Endothelial dystrophy (congenital)
Decreased sensation of cornea Herpetic keratitis
Neuroparalytic keratitis
Leprosy
Diabetis mellitus
Trigeminal block for postherapeutic neuralgia
Absolute glaucoma
Acoustic nueroma
Contd...
Contd...
Shallow anterior chamber* Primary narrow angle glaucoma
(normal depth 2.5 mm) Hypermetropia
Postoperative shallow anterior chamber
(wound leakage)
Malignant glaucoma
Corneal perforations
Anterior subluxation of lens
Intumescent (swollen) lens
Deep anterior chamber* Aphakia
Total posterior synechiae
Myopia
Keratoglobus
Buphthalmos
Keratoconus
Anterior dislocation of lens into anterior
chamber
Posterior perforation of globe
Irregular anterior chamber Adherent leukoma
Iris bombe formation due to annular
synechiae
Tilting of lens in subluxation
Nodules on iris surface Granulomatous uveitis
Melanoma
Tuberculoma
Gumma
Miosis* Local miotic drugs
Effect of systemic morphine
Iridocyclitis
Hornor’s syndrome
Pontine hemorrhage
Contd...
Contd...
Senile rigid miotic pupil
Due to effect of strong light
During sleep (pin point)
Mydriatics* Sympathomimetics drugs
Parasympatholytics
Acute congestive glaucoma
Absolute glaucoma
Optic atropy
Retinal detachment
Internal ophthalmoplegia
3rd nerve palsy
Belladonna poisoning
Leukocoria Congenital cataract
(white reflex in pupil)** Retinoblastoma
Retinopathy of prematurity
Persistent hyperplastic primary vitreous
Toxocara Endophthalmitis
Cheery red spot in macula* Niemann-Pick disease
(Mnemonic: Pick T BAGS) Tay-Sachs disease
Berlin’s edema
CRAO
Gaucher disease
Gangliosidosis
Sialidosis type 1 and 2
Macular edema Trauma
Intraocular operations
Diabetic maculopathy
Uveitis
Hard exudates in fundus* Diabetic maculopathy
(small, discrete yellowish, Circinate retinopathy
Contd...
Contd...
waxy areas with crenated Coat’s disease
margins) Capillary hemangioma of retina
Hypertensive retinopathy
(Mnemonic: DCH)
Microaneurysms of retinal artery
Soft exudates/cotton wool* Diabetic retinopathy
spots in fundus (whitish fluffy Collagen disorders—LE, PAN and scleroderma
spots with irregular margins) Hypertensive retinopathy
Anemic retinopathy
Leukemic retinopathy
Toxemic retinopathy of pregnancy
Retinopathy of AIDS
(Mnemonic: ALTeR DCH)
Microaneurysms CRVO
Eales disease
Hypertensive retinopathy
Sickle cell disease
Neovascularization of retina CRVO
(hypoxic states- CDE’S) Diabetic retinopathy
Eales disease
Sickle cell disease
Proliferative retinopathy* Proliferative diabetic retinopathy
Sickle cell retinopathy
Eales disease
Ocular trauma
Salt and pepper appearance Prenatal influenza
of fundus Prenatal rubella
(Mnemonic: Prenatal CMV) Congenital syphilis
Congenital Leber amaurosis
Contd...
Contd...
Mumps
Varicella
Angiod streaks (dark brown Pseudoxanthoma elasticum
or pigmented streaks which Pagets disease of bone
anastomose with each other, Ehlers-Danlos syndrome
usually confused for blood Sickle cell disease
vessels. They are due to Degenerative conditions of arteries in fundus
changes in the elastic particularly choroidal neovascular
tissue of Bruch’s membrane) membrane at the macula
Arterial pulsations of the disc Aortic regurgitation
(always pathological) Aneurysms
Exophthalmic goiter
Glaucoma
Orbital tumors
Redness of eye* Conjunctivitis
(Mnemonic: GO SUCK: Keratitis
Glaucoma Iridocyclitis
Orbital disease Acute Glaucomas
Scleritis Subconjunctival hemorrhage
Uveitis Endophthalmitis
Conjunctivitis Panophthalmitis
Keratitis) Ocular injuries
Pain in eye Inflammatory lesions of lids, conjunctiva,
cornea, uvea, sclera
Acute glaucoma
Refractive errors
Ocular injuries
Asthenopia
Contd...
Contd...
Foreign body sensation Conjunctival or corneal foreign body
in the eye Trichiasis
Corneal abrasion
Superficial corneal Phlyctenular Keratoconjunctivitis
vascularization Rosacea keratitis
Superficial corneal ulcer
Trachoma
Abnormal corneal surface Corneal abrasion
Corneal ulcer
Keratoconus
Rubeosis iridis* D—Diabetic retinopathy
(neovascularization of iris) E—Eale’s disease
(Mnemonic: DEVS) V—CRVO
S—Sickle cell retinopathy
Chronic iridocyclitis
Retinoblastoma
Iridodonesis Dislocation of lens
Aphakia
Hypermature shrunken cataract
Buphthalmos
Hyphema* Ocular injuries
Postoperative
Herpes zoster iritis
Gonococcal iritis
Intraocular tumors
From Rubeosis iridis spontaneously
Hypopyon* Corneal ulcer
Iridocyclitis
Endophthalmitis
Contd...
Contd...
Panophthalmitis
Retinoblastoma (pseudohypopyon)
Marcus Gunn pupil* Optic neuritis
(in swinging flashlight test, Optic atropy
the pupil on the diseased Retinal detachment
side dilates on transferring CRVO
light to it) CRAO
Enlargement of blind spot Primary open-angle glaucoma
Papilledema
Medullated nerve fibers
Drusen of the optic nerve
Juxtapapillary Choroiditis
Tubular vision Terminal stages of advanced glaucomatous
field defect
Advanced stages of retinitis pigmentosa
Ring scotoma Glaucoma
Retinitis pigmentosa
Central scotoma Optic neuritis
Tobacco amblyopia
Macular hole/cyst/degeneration
Bitemporal hemianopia Pituitary tumors
(Lesion in central chiasma) Suprasellar aneurysms
Craniopharyngioma
Glioma of third ventricle
Meningiomas at tuberculum sellae
Homonymous hemianopia Optic tract lesions
Lateral geniculate body lesions
Contd...
Contd...
Lesions involving total fibers of optic
radiations
Visual cortex lesion (usually with macular
sparing)
Binasal hemianopia Distension of third ventricle
(lateral chiasmal lesions) Atheroma of posterior communicating artery
Drug induced Maculopathy C—Chloroquin, Canthaxanthin (Carotenoids)
(Mnemonic: CPMT- Combined P—Phenothiazides
premedical test) M—Methoxyflurane
T—Tamoxifen
Congenital Leukocoria C—Cicatrical retinopathy of prematurity
(Mnemonic; COP IN Family) C—Coats disease
O—Ocular Toxocariasis
P—Persistent hyperplastic primary vitreous
I—In congenital pigment retinopathy
N—Norrie’s disease
Family—Familial exudative vitreoretinopathy
Interstitial keratitis • Tuberculosis
(Mnemonic: “ TIC TAC’ S “) • Inherited syphilis (Congenital syphilis)
• Trypanosomiasis
• Acquired syphilis
• Cogan’s syndrome
• Sarcoidosis
*Most commonly tested one
Q. What is electroretinogram (ERG)? List the clinical uses of

the same.
Q. Draw a normal Electroretinogram. Discuss the origin of
different waves, advantages, disadvantages and clinical
significance of ERG.
 Electroretinogram means a gross record of electrical potential
changes in the retina after stimulation with light
 Technique: A recorded by placing an active electrode on the
cornea (via a contact lens) and the other on the forehead. The
small voltage is amplified and usually photographed from
the face of the oscilloscope
 Normal ERG wave forms (Fig. 21.1):
– a-wave: It is a negative wave arising from the rods and cones
– b-wave: It is a large positive wave generated by Muller
cells, but represents activity of bipolar cells
– c-wave: It is also a positive wave representing metabolic
activity of the pigment epithelium.
Advantage: ERG is very useful in detecting functional abnormalities
of the retina (bipolar cell layers) much before the ophthalmoscopic
signs appear.
Fig. 21.1: Electroretinogram

Disadvantage: ERG is normal in diseases involving ganglion

cells and the higher visual pathway such as optic atrophy.
Clinical significance:
 ERG is useful guide in diagnosis and prognosis of certain retinal
disorders particularly retinitis pigmentosa, Chorioretinitis, rod-
cone dystrophy
 In siderosis bulbi
 Cortical blindness or hysterical blindness
 Assessing retinal function in presence of opacification of the
media (cataract, corneal opacity)
 Assessing retinal function in babies with impaired vision.
Q. What is electrooculography (EOG)? Mention its clinical

significance*.
 EOG is based on the measurement of resting potential of eye
which exists between the cornea (corneal potential is positive)
and back of the eye (which is negative). It supplements and
complements ERG
 When EOG is used, the increase in the potentials with light
adaptation is measured, to evaluate the condition of retinal
pigment epithelium
 Technique: Electrodes are placed at each canthus and the
changes in potential between these two electrodes are recorded
as the eyes move
 Interpretation of results:
– The results of EOG is interpreted using Arden ratio
Maximum height of light peak
Arden ratio =  100
Minimum height of dark trough
Where, (Light peak = maximum amplitude obtained in light

and dark trough = minimum amplitude obtained in the dark)
– Normal Arden ratio is 300%.
 Uses:
– A value less than 200 indicates defect in photoreceptors
or retinal pigment epithelium
– EOG is affected in retinitis pigmentosa, vitamin A
deficiency, retinal detachment and toxic retinopathies.
Q. What is visual evoked response/potential (VER/VEP)? List
the clinical significance of the same*.
 Definition: Visual evoked response (VER) is EEG recorded
in the occipital lobe (Stimulation of the retina with light,
changes the electrical activity of the cerebral cortex).
 Importance: It is the only clinically objective technique
available to assess the functional state of the visual system
beyond the retinal ganglion cells.
 Since VER is very small, and indistinguishable from the
background other electrical activities, an averaging technique
is necessary to identify its waveforms.
 VER is of two types based on the technique used:
1. Flash VER:
– It is recorded by intense flash stimulation
– It merely indicates that the light has been perceived by the
visual cortex. It is not affected by opacities in lens or cornea
– Clinical significance:
• It can assess the integrity of the macula and visual
pathway in infants, mentally retarded and aphasic
patient
• It can distinguish between organic and psychological

blindness (e.g. malingering and hysterical blindness)
• It can detect visual potentials in eyes with opaque
media
2. Pattern VER:
– It is recorded using some patterned stimulus
– Clinical significance: The pattern reversal VER depends
on form sense and thus may give rough estimate of
visual acuity (useful in children).
Q. List the uses of ocular ultrasound.
Q. List the uses of A scan/B scan*.
Ultrasonic frequencies in the range of 10 MHz are used in
ophthalmic USG.
There are two types of ocular USG: A scan and B scan
A scan:
 A transducer is positioned so that the ultrasonic beam passes
through a chosen ocular meridian. The tracing records a series
of spikes at sites of change in ocular impedance (Fig. 21.2)
 The height of each spike depends on the acoustic density of
the tissue, which varies with cellular composition
 The distance between the spikes, gives a measurement of the
distance from the transducer, as well as distance between the
intraocular structures
 A scan is one dimensional, and hence, amplitude modulated
display provides the information.
 Uses of A scan:
– Axial length measurement for IOL power calculation
– Measurement of depth of anterior chamber, lens thickness
or depth of a lesion
– To detect pathological lesions preoperatively in presence
of opacities in the ocular media
– To differentiate a preretinal membrane from a retinal
detachment
– To differentiate benign and malignant intraocular lesions
– To measure corneal thickness before radial keratotomy
operation or PRK or LASIK.
B scan:
 The testing transducer is moved in a linear fashion across the
eye, to build up a two-dimensional picture of intraocular
structures and the orbit (Fig. 21.2)
 Echoes are plotted as dots instead of spike and the brightness
of the dot indicates the size of the received echoes
 B scan picture is comparable to a histological cross section
of the eye and the orbit
 B scan can be taken in sagittal, horizontal or oblique planes
of the eye
 Uses of B scan:
– To differentiate the space-occupying lesions within the eye
and the orbit
Fig. 21.2: A-scan and B-scan
– To determine the vitreoretinal pathology (retinal

detachment or vitreous hemorrhage) in the presence of
the opacities of the ocular media
– To localize the intraocular foreign body
– To study the muscle thickness, e.g. in thyroid
ophthalmopathy or orbital pseudotumor
– To study the vitreous hemorrhage and its complications,
(e.g. vitreal bands prior to surgery)
– To differentiate types of retinal detachment (tractional,
exudative type).
*Uses/clinical significance is most commonly tested
Q. What is the principle behind Gonioscopy? Discuss types of

Gonioscopy.
Q. List the applications of Gonioscopy.
Q. List the angle structures normally seen in Gonioscopy.
 Purpose of Gonioscopy: To identify abnormal angle structures
and to estimate the width of the chamber angle (it is a dark
room procedure)
 Principle behind Gonioscopy/optics: Normally, the angle
cannot be visualized directly through an intact cornea because
light rays emitted from angle structures undergo total internal
reflection. A gonioscopes eliminates total internal reflection
by replacing the ‘cornea-air interface’ by a new ‘lens-air
interface’ that has a greater refractive index than that of the
cornea and the tears (Fig. 21.3).
Fig. 21.3: Gonioscopic examination of the angle of anterior chamber

 Types of Gonioscopy:
Direct Gonioscopy Indirect Gonioscopy
Goniolenses are used for the same Gonioprism is used for the same
They provide direct view of the angle They provide mirror image of the
opposite angle
Can be used for both diagnostic and Can only be used under a slit lamp,
operative purposes so diagnostic only
e.g. Koppe’s goniolense is most e.g. Goldmann single mirror or three-
commonly used mirror gonioscopes
 Normal angle structures (from anterior to posterior):

– Schwalbe’s line
– Trabecular meshwork and schlemm’s canal
– Scleral spur
– Anteromedial surface of the ciliary body (ciliary band)
– Root of iris
 Application of gonioscopy:
– Classification of glaucoma into open angle and closed
angle based on configuration of the angle
– Localization of the foreign body, abnormal blood vessels
or tumors in the angle
– Demonstration of extent of peripheral anterior synechiae
and hence planning of glaucoma surgery
– Direct goniolense is used during goniotomy.
Q. What is oblique illumination?
 Oblique illumination (also known as focal illumination) is a
(darkroom procedure) method for examination of the
structures of the anterior segment of the eye ball
 In oblique illumination a zone of light is made to fall upon
the structure to be examined so that it is brilliantly illuminated
and stands out with special clarity as compared to the

surrounding which remain in shadow
 There are two main methods of focal illumination:
– Loupe hand lens examination
– Slit lamp examination.
Q. What is the optical principle behind Loupe hand lens
examination?
Q. What are the different types of loupe used for Loupe hand
lens examination?
Loup hand lens examination is a darkroom procedure (Fig. 21.4)
 Optical principle: Loup hand lens examination is based on
the principle that when an object is placed between a convex
lens and its focal point, its image formed is virtual, erect,
magnified and on the same side of the object.
 Different types of loupe: Uniocular loupe and binocular loupe.
Uniocular loupe Binocular loupe: fixed before

surgeon’s eyes by an elastic
band at forehead
Advantages 10 times magnified image Both hands will be free during
examination
Small and handy instrument Depth of the lesion is better
adjusted
Convenient as the surgeon is
away from the patient
Disadvantage Both hands engaged in Low magnification
examination
Inconvenient due to Inter-pupillary distance may
closeness to the patient be difficult to adjust
No depth perception
Fig. 21.4: Binocular loupe
Q. List the uses of Slit lamp.

 Slit lamp is an instrument with bright illumination and various
grades of magnification. It is binocular so depth perception
is accurate (Fig. 21.5)
 It basically has three parts: Illumination system, viewing
system and mechanical devices to adjust the slit lamp.
Fig. 21.5: Slit lamp

 Uses:
– Detailed microscopic examination of the anterior segment
of the eye layer by layer
– For fundus examination by Hruby lens
– For examination of the angle of the anterior chamber by
gonioscopes
– To measure IOP by applantation tonometer
– For fluorescein staining with blue filter
– For anterior segment photography
– As a delivery system to argon and YAG laser.
Q. List the structures that can be examined with a slit lamp
without any additional aid.
The structures that can be examined with a slit lamp without any
additional aid are (Fig. 21.6):
 Lid margin
 Conjunctiva
 Cornea
 Sclera
 Anterior chamber
 Iris and pupil
 Lens
 Anterior part of vitreous.
Q. What is transillumination? Mention its clinical importance.

 Transillumination is a darkroom procedure in which an intense
beam of light is thrown through the conjunctiva and sclera or
pupil and illumination is observed in the pupillary area.
Fig. 21.6: Fundus oculi examination

 Types:
– Transscleral transillumination: When an intense beam of
light is thrown through the sclera, the pupil appears red in
color. But in the presence of solid mass in the path of light,
the pupil remains black, e.g. as in intraocular tumors
– Transpupillary: When an intense beam of light is allowed to
pass obliquely through the dilated pupil. Normally the pupil
is well illuminated but in detached retina, a grayish reflex is seen.
 Clinical significance: Intraocular tumors, retinal detachment
and vitreous hemorrhage are few ocular conditions which can
be diagnosed with the help of transillumination.
Q. What is retinoscopy? What is the optical principle behind

the same?
 Definition: Retinoscopy is an objective method of finding
out the error of refraction by the method of neutralization
 It is the most practical way of estimating the condition of
refraction objectively, with accommodation at rest
 Optics: When light is reflected from a mirror into the observer’s
eye, the direction in which the light will travel across the pupil
will depend upon the refractive state of the eye
 In emmetropic eye parallel rays of light come to a point focus
on the retina, so they are emerging in the same parallel pathway
 If the eye is hypermetropic—parallel rays of light converge
behind the retina and hence the emerging rays are divergent.
Q. What is refractometry (objective optometry)?
 Refractometry is an objective method to find out the errors
of refraction by use of an equipment called as refractometer
 Refractometry utilizes the principle of indirect opthalmoscopy
 At present, the computerized autorefractometers are most
widely used. They quickly give information about the
refractive error of the patient in terms of sphere, cylinder with
axis and interpupillary distance.
 Advantages:
– Good alternative to Retinoscopy in busy practice
– Very useful in mass screening, research programs and
epidemiological study.
Q. What is keratometry (ophthalmometry)? Discuss the

principle and uses of the same.
 Keratometry is an objective method of estimating corneal
astigmatism by measuring the curvature of the cornea
 Principle: Anterior surface of the cornea acts as a convex
mirror, so that the size of the image it produces depends upon
the curvature. Therefore by the size of the image formed on
the anterior surface of the cornea the curvature of the cornea
can be calculated
 Uses: Keratometry is useful in measuring the curvature of
the cornea:
– In contact lens practice
– For diagnosis of certain corneal conditions, e.g. Keratoconus
– Before cataract operation for measuring IOL power
(biometry) and for planning of incision in cataract surgery
to reduce astigmatism
 Disadvantage: They are not of much value in prescribing for
routine refraction as lenticular astigmatism may coexist.
Q. What is ophthalmoscopy? Mention different techniques of
the same.
Q. List the clinical significance of opthalmoscopy?
Q. Differentiate between direct ophthalmoscopy and indirect
ophthalmoscopy.
 Ophthalmoscopy is a clinical examination of the interior of
the eye by means of an ophthalmoscope
 It is primarily done to assess the state of the fundus and detect
the opacities of ocular media.
 There are three different techniques of the same:

1. Distant direct ophthalmoscopy:
– The light is thrown into the patient’s eye sitting in a
semi-darkroom, from a distance of 20 to 25 cm and the
features of red glow in the pupillary area are noted
– Applications of distant direct ophthalmoscopy:
• To diagnose opacities in the ocular media
• To differentiate between mole and a hole in the iris
• To detect retinal detachment or a tumor
• To discover the edge of subluxated or dislocated lens.
2. Direct ophthalmoscopy: Optics principle is as follows
– A convergent beam of light is reflected into the patient’s
pupil
– The emergent rays from any point on the patient’s
fundus reach the observer’s retina through the viewing
hole in the ophthalmoscope
– The emergent rays from the patient’s eye are parallel
and brought to focus on the retina of the emmetropic
observer when accommodation is relaxed
– However, if the patient and/or the observer is/are ametropic,
a correcting lens (equivalent to the sum of the patient’s and
observer’s refractive error) must be interposed.
3. Indirect ophthalmoscopy: Optics principle is to make
the eye highly myopic by placing a strong convex lens in
front of the patient’s eye so that emergent rays from an
area of the fundus are brought to focus as a real, inverted
image between the lens and the observer’s eye.
Features Direct ophthalmoscopy Indirect ophthalmoscopy

(Fig. 21.7) (Fig. 21.8)
Condensing lens Not required Required
Examination distance As close to the patient’s At an arm’s length
eye as possible
Image* Virtual, erect Inverted, real
Magnification About 15 times 4–5 times
Illumination Not so bright, so not Bright, so useful in hazy
useful in hazy media media
Area of field in focus About 2 disc diopters About 8 disc diopter
Stereopsis Absent Present
Accessible fundus view Slightly beyond equator Up to ora serrata
Examination through Not possible Possible
hazy media
Advantages It is a handy procedure It allows a stereoscopic
Easy to perform view of the fundus
High magnification, It allows examination
hence the lesion can be of the hazy media
examined in detail Periphery of the retina till
Orientation and under- the ora serrata can be
standing of the lesion examined
is easy as the image
formed is erect
*Mnemonic: DEVII.R—“DEV”—direct = erect + virtual; “IIR”- Indirect= Inverted+ Real
Fig. 21.7: Direct ophthalmoscopy

Fig. 21.8: Indirect ophthalmoscopy
Clinical applications:
 Direct ophthalmoscopy is used to diagnose optic disc lesions
like papillitis, papilledema, optic atrophy and glaucomatous
cupping
 Direct/indirect ophthalmoscopy is used to diagnose diabetic
retinopathy, hypertensive retinopathy, retinal detachment and
retinitis pigmentosa.
Q. List the macular function tests.
Macular function tests:
 Indirect slit lamp biomicroscopy
 Photo Stress test
 Card board test (2 point discrimination test)
 Amsler grid test
 Maddox rod test
 Entropic view test
In eyes with opaque media:

 Inferometry (Laser)
 Flying corpuscles test
 Potential visual acuity meter.
(Mnemonic: IPS CAME In Flying Potential)
22.
Ophthalmic Instruments
List of Knives
Knives Features Uses
Von Graefe’s Long narrow thin blade To make ab-interno
knife with a sharp tip corneoscleral incision
Cutting edge only on one during cataract
side surgery
Making incision in
iridectomy and four dot
iridotomy
Zeigler’s Knife Fine hook shape blade Incising the after cataract
Sharp pointed tip For doing capsulotomy
during discussion and
extracapsular lens
extraction
Cystitome or Its a small needle knife capsulotomy during
capsulotome Its tip is bent discussion and
extracapsular lens
extraction
Contd...
Ophthalmic Instruments 455
Contd...
Keratome It has a thin diamond • To make valvular (self
shaped blade sealing) corneal
It has 2 cutting edges incisions for entry into
Types: Straight and curved the anterior chamber
in SICS and
phacoemulsification
• To make ab-interno
corneoscleral
incision during
cataract surgery
Paracentesis Lancet shaped needle Paracentesis of hypema
needle with sharp cutting edges and hypopyon associated
It has a guard to prevent with raised IOP
injuries to the deeper
tissues
It resembles Keratome
but is smaller
Foreign body It has a blunt tip and the Removing superficial

spur edges are also blunt on foreign bodies of cornea
the either side
15° side It has a pointed tip and To make small valvular

port entry the cutting edge is only clear corneal incisions
blade on one side (side port incision) in
phacoemulsification SICS
and pars plana
vitrectomy
Contd...
Contd...
MVR or V lance Fine straight triangular Same as 15 degree side
blade knife with cutting edges port entry blade
on both sides
Crescent knife Blunt tipped bevel up knife To make tunnel shaped

having cut-splitting action incision in the sclera and
at the tip and both the the cornea for
sides. Its blade is curved phacoemulsification,
and is mounted on a manual SICS and
metallic handle sutureless
trabeculectomy
Tooke’s knife Short flat blade with To separate conjunctiva

semicircular blunt edge at limbus during
on one side trabeculectomy
Iris repository It consists of a delicate • To replace iris in the

bent blade (45°) with blunt anterior chamber
edges and the tip attached after iridectomy
to a handle. The angle is • To free the iris form the
helpful in intraocular lips of the section
maneuver • To break the posterior
synechiae at the
papillary margin
List of Straight Forceps

Straight forceps Features Uses
Plain forceps It has no teeth To hold skin or conjunctiva
in blunt dissection
During typing of
conrneoscleral sutures
Corneal or one It has 1 × 2 tiny fine teeth To hold cornea during
toothed forceps at the narrow pointed tip corneoscleral suturing
Fixation forceps It may have narrow or wide To fix the eyeball by

jaws holding conjunctiva and
There may be 2 × 3, 4 × 5 episcleral tissue to 6 O’
teeth at the tip clock position while
making corneoscleral
incision during cataract
surgery
Single Curve Forceps

Single curve Features Uses
forceps
Intracapsular Has a cup on the inner side For Intracapsular lens
forceps of the tip of each limb, the extraction (obsolete these
(Arruga’s) margins of which are days)
smooth. It holds the
anterior lens capsule
during lens delivery
Contd...
Contd...
Extracapsular It has 3 × 4 teeth on inner Was used for extracapsular
forceps aspect of the tip of each lens extraction
limb
Mcpherson iris Small delicate forceps with To hold iris during

forceps 1 × 2 teeth iridectomy (for glaucoma,
cataract surgery)
Intraocular lens A small delicate forceps To hold IOL and also capsule
implant forceps with fine limbs and curved
blunt ends
Lens holding These may be direct action To evenly hold acrylic and
forceps for or cross action forceps silicone lenses
floatable
intraocular
lenses
Double Curve Forceps

Double Features Uses
curve forceps
Superior rectus A strong forceps with To hold superior rectus
forceps S-shaped tip having 1 × 2 muscle while passing a stay
teeth suture to fix the eyeball in
downwards gaze in
intraocular operations, e.g.
(cataract, glaucoma
surgery, keratoplasty)
Iris forceps Small delicate forceps with To hold iris for iridectomy
fine limbs, has 1 × 2 teeth for glaucoma, cataract
surgery
Utrata Has very delicate grasping To hold lens capsule after

capsulorhexis tips. Shanks are extremely raising the flap
forceps thin, long and straight
Scissors
Scissors Features Uses
Plain straight Fine pointed To cut conjunctiva, skin
scissors Straight cutting sharp blades and sutures
Contd...
Contd...
Plain curved Fine pointed To cut conjunctiva to make
scissors Curved sharp cutting blades a conjunctival flap in
cataract and glaucoma
surgery
Corneal scissors Is very fine and delicate To enlarge corneal section

or section The curved blades are kept or corneoscleral section in
enlarging apart by spring action cataract surgery
scissors
Vannas scissors Fine delicate scissors To cut vitreous during

Has sharp edges vitreous prolapse
Iridectomy Strong scissors To perform peripheral

scissors or de- Has small V shaped blades button hole iridectomy
wecker’s scissors directed at right angles to
the arm
Contd...
Artery forceps Blunt forceps. • To hold the skin suture

Similar to plain straight • To catch bleeding
scissors in appearance. arteries during
It has multiple straight lacrimal sac
grooves near the tip. surgeries
Enucleation Stout strong scissors. To cut optic nerve during

scissors Has curved sharp blades enucleation surgery
with blunt tips.
Holders
Holders Features Uses
Needle holders It may have straight or For passing sutures in the
curved tips. lids, superior rectus muscle,
It may or may not have conjunctiva, cornea, sclera
catch or muscles
Contd...
Contd...
Blade holding Designed to hold the razor • To make ab-interno
forceps blade firmly corneaoscleral
incision during
cataract surgery
• In trabeculectomy
Cataract Surgery Instruments

Instrument Features Uses/used
Vectis Its a wire shaped loop • To remove dislocated
attached to a metallic or subluxated lens
handle • In ICCE
Irrigating vectis Its a modified vectis Facilitates easy delivery by

Has a hollow interior and providing additional
multiple ports to allow the hydrostatic pressure to
flow from the leading edge push the nucleus out of the
or posterior surface of the anterior chamber through
vectis. This is attached to an the surgical incision
infusion line to assist in
hydraulic separation
Lens expresser Has a flat metal handle with In ICCE to break the zonules
rounded curved ends and express the lens
Contd...
Contd...
Irrigation cannula Its attached to a syringe Irrigation cannula: in ECCE
and air cannula with air or saline for irrigating the lens
Air cannula is thinner than matter present in the
the irrigation cannula anterior chamber
Air cannula: to inject air
into the anterior chamber
after cataract surgery
Suction irrigation Consists of two cannulas For suction and irrigation of
cannula and a long rubber tube lens matter in ECCE
IOL dialer or Fine but stout instrument. • To dial PMMA non-

Sinskey hook The tip engages the dialing foldable IOL in
holes of the IOL proper position in the
capsular bag
• To manipulate
nucleus in
phacoemulsification
and manual SICS
Chopper Its a fine instrument that • To split the nucleus
resembles IOL dialer into small pieces
• To manipulate
nucleus in
phacoemulsification
and manual SICS
Contd...
Contd...
Hydrodissection It is a single bore (25, 27 or To perform hydrodissection
cannula 30 gauge) cannula with a 45 (separation of capsule from
degree angulation at about the cortex) and
10–12 mm from the free end hydrodeliniation
(separation of the cortex
from nucleus) in
phacoemulsification or SICS
Lid Surgery Instruments

Chalazion clamp Is a forceps with screw in To fix chalazion during
the center for tight fixation incision
One arm has a flat disc
which is applied over the
skin surface
The other arm has a small
circular ring which is
applied on the conjunctival
surface of the chalazion
Chalazion scoop Has a small cup with sharp To scoop out contents of
margins attached to a chalazion
narrow handle
Contd...
Contd...
Lid clamp Has a D-shaped plate • Hemostat in lid
opposed by a rim on the surgeries
other side. The plate is • It protects the
towards the conjunctival underlying eye
side so it protects the eye structures
during the lid surgery on the
skin side. The screw faces the
outer side and the handle is
always situated on the
temporal side
Lid spatula Plane simple metal plate To support lid and protect
having mild convex surface the cornea in entropion,
on either side ectropion and ptosis
surgery
Lid retractor A saddle shaped instrument To examine eyeball in cases

folded on itself in one end of marked blepharospasm
Lacrimal Sac Surgery Instruments

Punctum dilator Has a pointed tip and • To dilate the punctum
(Nettleship’s) cylindrical handle during surgery
• Probing
Contd...
Contd...
Lacrimal probe Set of straight metal wires To probe nasolacrimal duct
with blunt rounded ends
Muller’s Self retaining. • As a hemostat in

skin-muscle Made up of 2 limbs with a lacrimal sac surgery
retractor screw fixed to the limbs • Provides a good
Each limb has 3 pins for operative field
engaging the edges of the
skin or muscle
Chisel and Chisel has a sharp edge To cut bone in

hammer dacryocystorhinostomy
Bone punch Has a spring handle and 2 To cut bone in

blades dacryocystorhinostomy
Upper blade has cutting
edges
Lower blade has a
depression
Squint Surgery Instruments

Muscle hook or Is similar to lens expressor To engage the muscle
strabismus hook but without the round knob during the squint surgery,
Enucleation and retinal
detachment surgery
Caliper and rule Caliper resembles a divider To make measurement
with a graduated scale during squint, ptosis and
attached to one arm retinal detachment surgery
The other arm can be moved To localize the foreign body
by a screw over the scale on X-ray films
Miscellaneous
Wire speculum Has two limbs attached at • To separate eye lids
one end during operative
procedures
• To protect the
underlying eye
structures
Contd...
Contd...
Trephine Has a corrugated metal Cutting the corneal disc
handle which can be fixed from donor’s and
into different size circular recipient’s cornea in
blades having sharp cutting corneal grafting
edges
Evisceration Oval scoop attached to a To scoop out contents of

scoop thick metallic handle eyeball in evisceration
Dark Room Procedures

Convex spherical Is a biconvex spherical lens • Hypermetropia
lens with a metal frame • Presbyopia
Images seen through it move • Aphakia
in opposite direction in all • Various ophthalmic
meridians on moving the instruments, e.g.
lens retinoscope, placido’s
disc, slit lamp
Contd...
Contd...
Concave Is a biconvex spherical lens • Myopia
spherical lens with a metal frame • Hurby’s lens
Images seen through it move
in opposite direction in all
meridians on moving the
lens
Convex Images seen through it move Hypermetropic

cylindrical lens in opposite direction on astigmatism whether
moving the lens but at the simple, compound
axis of the cylinder there is or mixed
no movement
Concave Images seen through it move Myopic astigmatism

cylindrical lens in same direction on moving whether simple, compound
the lens but at the axis of the or mixed
cylinder there is no
movement
Contd...
Contd...
Red green glasses Red glasses are kept in front • Diplopia charting
of right eye and green • To test binocular
glasses in front of left eye vision in worth’s four
dot test for
malingering test
Occluder Black opaque disc To occlude one eye while

testing and correcting the
visual acuity of the other
Pin hole Black opaque disc with a To differentiate between

small central hole impaired vision due to
refractive error or any other
ocular pathology. Vision
improves in case of RE as
the central rays passing
through the hole are
straight. The vision
deteriorates or remains
same in presence of ocular
pathology
Contd...
Contd...
Stenopic slit Black opaque disc with a Used for differentiating
vertical or horizontal causes of colored halos
straight slit in the center When stenopic slit is moved
in front of the eye:
• Halos are intact in acute
congestive glaucoma
• Halos are broken in
immature cataract
Maddox rod Consists of 4–5 cylinders of • To detect

red glass prisms fused side heterophoria by
by side in a supporting disc dissociating the two
retinal images
• To test macular
function
Retinoscope Has a plane mirror on one • To determine errors

side and concave mirror on of refraction
the other • To determine the
There is a small hole in the opacities of the media
center of each mirror having
+ 2D lens to exclude
accommodation error
Contd...
Contd...
Trial frame Has 3 compartments: To test and correct
• Inner compartment: refractive errors
for keeping occluder,
pin hole, stenopic slit
• Middle compartment:
for plaicng spherical
lens
• Outer compartment:
for placing cylindrical
lens
Placido’s disc Has alternative dark and To diagnose irregular

light rings corneal surfaces (ulcers,
There is spherical convex keratoconus)
lens in the center of the
disc (+2D)
Contd...
Contd...
Maddox wing Is an instrument that to diagnose and measure
dissociates the retinal latent squint
images of 2 eyes for near
fixation
Bibliography
1. Albert DM, Miller JW, Azar DT, Blodi BA. Albert & Jakobiec's
Principles & Practice of Ophthalmology: 4-Volume Set (Expert
Consult-Online and Print), 3rd edition, Saunders; 2008.
2. Bradford CA. Basic Ophthalmology by American Academy of
Ophthalmology, 8th edition; 2004.
3. Chern KC, Saidel M. Ophthalmology Review Manual, 2nd edition,
Lipincott Williams and Wilkins; 2011.
4. Gerstenblith AT, Rabinowitz MP. The Wills Eye Manual: Office and
Emergency Room Diagnosis and Treatment of Eye Disease, 6th
edition, Lipincott Williams and Wilkins; 2012.
5. Jogi R. Basic Ophthalmology, 4th edition, Jaypee Highlights Medical
Publishers; 2009.
6. Kanski JJ, Bowling B. Clinical Ophthalmology: A Systematic
Approach, 7th edition, Saunders; 2011.
7. Khurana AK. Comprehensive Ophthalmology, 4th edition, New Age
International (P) Ltd; 2007.
8. Nema HV, Nema N. Textbook of Ophthalmology, 6th edition, Jaypee
Highlights Medical Publishers; 2012.
9. Tandon R, Sihota R. Parsons' Diseases of the Eye, 21th edition,
Elsevier; 2011.
Index
Page numbers followed by f refer to figure
A Anatomy of
Acanthamoeba keratitis 107 angle of anterior chamber 11
Accommodation reflex 280 cavernous sinus 377
Acid extraocular muscles 297
burns 398 Angle
injuries 396 closure glaucoma 221f
Acquired of anterior chamber 7, 13
Angular conjunctivitis 63, 63f
dacryocystitis 361
Anisometropia 52
syphilis 412
Anisophoria 304
Acute
Ankylosing spondylitis 411
bacterial
Annular scotoma 211f
endophthalmitis 153, 154
Anterior
congestive glaucoma 147 capsular cataract 163f
conjunctivitis 147 chamber signs of iridocyclitis 132
dacryocystitis 361, 362, 365 ciliary arteries 6
iridocyclitis 136f, 147 dialysis 388f
mucopurulent conjunctivitis 60 endothelium 8
Adherent leukoma 93f epithelium 14
Adie's pupil 281, 409 segment signs 207
Advanced diabetic eye disease 251 staphyloma 93f, 119, 130
Alkali burns 397 uveitis 132
Allergic Apparent squint 303
conjunctivitis 60 Applanation tonometry 234
keratitis 87 Aqueous
Alport's syndrome 411 flare 132
Alternating concomitant squint 308 formation and outflow system 13
Amaurosis fugax 294 humor 5
Ametropia 29 Argyll-Robertson pupil 281
Amiodarone 200 Arrangement of retinal nerve
Amsler grid test 452 fibers 210f
Artery forceps 461 Causes of

Ascending optic atrophy 291 bilateral ptosis 349
Assessment of levator functions 346 blindness 421, 422
Atmospheric oxygen 5 in children 418
ectopic lentis 195
B
graft failure 103
Background retinopathy 249f hamartopia 294
Bacterial corneal ulcer 88 neovascular glaucoma 228
Baring of blind spot 211f ptosis 343
Bassen-Kornzweig syndrome 257 sudden painless loss of vision 424
Bayoneting sign 209f Cavernous sinus thrombosis 376
Behcet's syndrome 145, 411, 412 Central retinal
Berlin's edema 388
artery occlusion 229, 240, 241f
Binocular
vein occlusion 228, 242, 244f
loupe 445f
Chalazion 330f
single vision 26
clamp 464
Bitot's spots 404, 405, 405f
scoop 464
Bjerrum's arcuate scotoma 211f
Chalosis bulbi 390
Black eye 382
Chemical burns 398
Blaskovics operation 348f
Cherry red spots 247
Blepharitis 61, 325
Blue sclera 129 Chlamydia trachomatis 66, 73
Bone punch 466 Chlorpromazine 200
Bowman's membrane 3 Choice of surgery 312
Bruch's membrane 11 Choroidal hemorrhage 43
Burow's operation 335, 335f Choroiditis 150f, 151f
Busulfan 200 Chron's diseases 412
Chronic
C conjunctivitis 325
Calculation of IOL power 194 dacryocystitis 361-363
Canal of Schlemm 12 inflammation 229
Card board test 452 serpiginous ulcer 109
Cataract 180 Cicatrizing
surgery instruments 462 conjunctivitis 60
Causative endogenous allergens 78 trachoma 332
Index 479
Ciliary glaucoma 201

body 2, 6f, 7 rubella 413
congestion 81 syphilis 413
root 7 Conical cornea 114
zone 8 Conjugate movements of eyeball 300f
Classification of Conjunctiva 322
keratitis 87 Conjunctival
scleritis 126 congestion 81, 332
uveitis 132, 133f xerosis 404
Cockayne's syndrome 256 Consecutive optic atrophy 293f
Cogan's syndrome 113 Contact lens 56
Color vision tests 285 Contraindication for collection of
Common causes of blindness 417f eye 102
Commotio retinae 388 Convergence reflex 279
Communications of cavernous Cornea 1, 3
sinus 377f, 378f Corneal
Complication of epithelium 88
cataract surgery 184 grafting 101
congenital dacryocystitis 362 opacities 117
hypermetropia 31 scar 404
iridocyclitis 132 stroma 4
local anesthesia in cataract ulcer 87
surgery 184 ulceration 69, 88, 404, 405
optic neuritis 284 vascularization 122, 332
pathological myopia 39 xerosis 404, 405
pterygium 82 Cornyebacterium diphtheriae 62
senile cataract 176 Coronary cataract 163f
cataract surgery 184 Cortical senile cataract 169
corneal grafting 103 Cover test 304
Concomitant Cranial nerve palsy 314
convergent squint 307 Crescent knife 456
squint 306 Cushing's disease 414
Conductive kerotoplasty 34 Cyclitic membrane 142f
Congenital Cyclophoria 304
dacryocystitis 361 Cysticercosis 413
D retina 240
Dacryocystitis 61 sclera 123
Dacryocystectomy 368 vitreous 235
Dacryocystitis neonatorum 362 Distant direct ophthalmoscopy 450
Dacryocystography 361 Double
Dacryocystorhinostomy 367, 368f arcuate scotoma 211f
Deep curve forceps 459
corneal vascularization 122 Dry eye 352
keratitis 110 E
vascularization 122
Eales disease 229
Dendritic ulcer 119
Ectropion 335
Descemet's membrane 4 Ehlers-Danlos syndrome 410
Descending optic atrophy 291 Electric cataract 188
Development of eye 20 Electroretinogram 436, 436f
Dexamethasone 200 Emmetropia 29
Diabetic Endophthalmitis 153
maculopathy 247, 250 Endophytic retinoblastoma 266, 267f
retinopathy 247 Endoscopic
Diagnostic role of lacrimal dacryocystorhinostomy 367
syringing 356 Endothelium 4
Different types of Enophthalmos 373
ocular paralysis 314 Entropion 333
staphylomas 131f Enucleation 270
Diffuse episcleritis 124 Epidemic keratoconjunctivitis 71
Dilator pupillae 9 Episclera 5
Diode laser trabeculoplasty 216 Episcleritis 123, 123f, 129
Dioptric power 14 periodica 123
Diplopia chart for right lateral rectus Esophoria 303
palsy 317f Evaluation of concomitant squint 309
Direct ophthalmoscopy 449, 450, 451f Everbusch operation 348f
Disc edema 290 Excimer laser PRK 46f
Diseases of Exophoria 303
conjunctiva 58 Exophytic retinoblastoma 266, 267f
cornea 87 Exposure keratitis 339
Index 481
Extraocular G
foreign body 383 Galactosemia cataract 188
muscles 297 Gamma camera images 361f
of eye 298f Ganglion cell layer 18
Eye General principles of squint
bank 422 surgery 312
collection 422 Giant cell arteritis 409
Gland of
F eyelids 324f
Fasanella-Servat operation 347f Zeis or Moll 327
Fascia lata sling operation 347f Glass Blower's cataract 188
Fascicular ulcer 78 Glaucoma 204
Fate of vitreous hemorrhage 237 Glaucomatous optic atrophy 208
Fibrous layer 322 Goldmann applanation tonometer 233f
Fisto classification of trachoma 65 Gonioscopic examination of angle of
Fistula formation 362 anterior chamber 442f
Fixation Gonioscopy 442
forceps 457 Goniotomy knife 203f
reflex 28 Granulomatous conjunctivitis 60
Flexner-Wintersteiner Graves's ophthalmopathy 379
rosettes 264, 266f H
Flying corpuscles test 453
Haller's layer 11
Follicular conjunctivitis 67f
Hallgren's syndrome 257
Four vortex veins 5
Harm's trabeculotome 204f
Fourth nerve palsy 316f Healed membranous conjunctivitis 332
Fovea centralis 19 Herbert pits 69
Friedreich's ataxia 257 Hereditary retinoblastoma 265
Function of Hering's theory of opposite colors 25
choroid 10 Herpes zoster 105f
ciliary body 9 ophthalmicus 103
iris 8 Hess
Fundus oculi examination 275f chart in right lateral rectus
Fungal corneal ulcer 99f, 100 palsy 320f
Fusion reflex 26 operation 347f
Heterophoria 303 Inner

Homer-Wright rosettes 264, 266 nuclear layer 17
Homocystinuria 414 plexiform 18
Hordeolum irternum 332 Insertion of recti muscle tendons in
Horner's syndrome 283, 283f sclera 299f
Hutchison's Instillation of eye drops 400f
pupil 282 Internal hordeolum 330
rule 105 Interstitial keratitis 111
Hyaloid artery disappears 22 Intraocular
Hypermature cataract 228 injections 400
Hypermetropia 31, 35, 46f pressure 205
Hyperopic photorefractive Intumescent cataract 172f
keratectomy 34 Iridocyclitis 132, 134
Hyperphoria 303 Iridodialysis 388
Hypertensive Iris 7
retinopathy 244, 246f bombe 132
uveitis 229 nodules 132
Hyphema 389 root 7
Hypocalcemia cataract 188 Irregular astigmatism 51
Hypopyon corneal ulcer 96, 97f Irritative conjunctivitis 60
I J
Idiopathic keratitis 88 Jaeschke-Arlt's operation 335
Imbert-Fick's law 232 Jone's
Immature senile cataract 170f dye test 360
Incipient cataract 171f test 356
Indentation tonometer 232
Index myopia 38 K
Indications of penetrating Kayser-Fleischer ring 390f
keratoplasty 103 Kearns-Sayre syndrome 257
Indirect Keith-Wegner-Barkar
ophthalmoscopy 449, 450, 452f classification 244, 245
slit lamp biomicroscopy 452 Keratinization of conjunctions 339
Infective Keratitis 87
conjunctivitis 60 Keratoconjunctivitis 60
keratitis 87 sicca 409
Index 483
Keratomalacia 405 Lens

Keratometry 449 capsule 14
Keratomycosis 98 fibers 15
Keratoplasty 101 protein glaucoma 228
for visual rehabilitation 107 Leprosy 413
Koch-weeks bacillus 60 Lid
Koeppe's nodules 138, 139f clamp 465
retractor 465
L spatula 465
Lacrimal surgery instruments 464
abscess 362 Limbus 1
apparatus 350f Lipopolysaccharide 322
fistula 365 Long posterior ciliary arteries 6
probe 466 Lowe's syndrome 188
sac surgery instruments 465 Luxation of lens 198
Lagophthalmos 340
Lamellar cataract 166 M
Laminar dot sign 209f Macroscopic appearance of anterior
Large intravitreal hemorrhage 235f surface of iris 8f
Laser Macular function test 178, 452
assisted in situ keratomileusis 47f Maddox
iridotomy 225f rod test 179, 304, 452
phacoemulsification 195 wing test 304
Latent hypermetropia 35 Major components of adult lens 16f
Lateral tarsorrhaphy 341f Malignant glaucoma 230
Laurence-Moon-Biedl syndrome 256 Marcus-Gunn
Layer of jaw-winking ptosis 343
choriocapillaries 11 pupil 280
large vessels 11 Marfan's syndrome 410
nonstriated muscle 322 Marginal corneal ulcer 61
small vessels 11 Measurement of
striated muscle 322 degree of ptosis 346
tear film 351 levator muscle function 345f
Leber's theory of simple diffusion 13 vertical palpebral fissure 346f
Meibomian cyst 329 O

Miosis 280 Occlusio pupillae 132, 142f
Modes of chemical injury 397 Occlusion therapy 300, 311
Modified Ketssey's operation 335 Ocular manifestation of
Mooren's HIV 408
corneal ulcer 88 pituitary tumors 381
ulcer 109 Onchocerciasis 413
Morphological shapes of cataract 161f One piece PMMA lens 194f
Multiple sclerosis 414 Open
Munson's sign 116f angle glaucoma 206f, 216
Myasthenia gravis 414 sky vitrectomy 238
Mydriatic provocative test 220 Ophthalmia neonatorum 73
Mydricaine 132 Ophthalmic manifestation of
Myopia 46f rheumatoid arthritis 409
Myopic eye 39f Ophthalmometry 449
Ophthalmoscopy 449
N
Optic
Narrow palpebral aperture 345f atrophy 291
Necrotizing scleritis 127f foramen 370f
Neovascular glaucoma 229f neuritis 284
Nerve fiber layer 18 Orbital cellulitis 374
Night blindness 41, 404 Orthophoria 304
Nodular episcleritis 124 Outer
Nonhealing corneal ulcer 332 nuclear layer 17
Non-hereditary retinoblastoma 265 plexiform 17
Nonparalytic squint 321
Non-proliferative diabetic P
retinopathy 248 Paget's disease 414
Non-rhegmatogenous retinal Pan photocoagulation 244f
detachment 262 Panophthalmitis 157
Normal schematic eye 30f Papilledema 287
Nuclear and edematous retina 290f
cataract 175f and papillitis 295
senile cataract 169 and pseudopapillitis 295
Nyctalopia 294 Papillitis and pseudopapillitis 295
Index 485
Paracentesis 121 Photorefractive keratectomy 46f

Paralytic squint 313, 321 Physiology of
Paramedian tarsorrhaphy 341f eye and vision 24
Parinaud's dorsal midbrain 415 vision 24
Pars plana vitrectomy 238 Placido disc 472
Part of Plain forceps 457
conjunctiva 59f Pneumococcus 60
eye 403 Pockets of aqueous in vitreous 232f
Partial thickness lamellar Polyarteritis nodosa 409
keratoplasty 102f Posterior
Patau syndrome 410 aspect of right eye 299f
Pathogenesis of senile cataract 169 capsular cataract 163f
Pathology of epithelium 8
granulomatous uveitis 133 synechia 140f
non-granulomatous uveitis 134 uveitis 149
perforated corneal ulcer 91 Postinflammatory glaucoma 230
retinoblastoma 264 Postneuritic optic atrophy 293f
sloughing corneal ulcer 91 Potential visual acuity meter 453
suppurative uveitis 133 Prelimbal blood vessels 5
uveitis 133 Presbyopia 54, 54f
Pathway of Preservation of donor cornea 101
light reflex 277 Primary
near reflex 279f angle closure glaucoma 216
pupillary light reflex 278f open angle glaucoma 204
Periocular injections 400 optic atrophy 291, 293f
Peripheral iridectomy 225f retinal detachment 258, 259f
Periphlebitis retinae 243 Principles of
Perivascular lymphatics 5 Schiotz tonometry 232
Phacolytic glaucoma 228 treatment in proptosis 373
Phakomatoses 273 Prism vergence test 305
Phakonit 195 Progressive
Phlyctenular myopia 39, 175f
conjunctivitis 79f diabetic retinopathy 247, 248
keratoconjunctivitis 78 proliferative retinopathy 249f
Photo stress test 452 Prone darkroom test 220
Prophylaxis 71 nonmagnetic foreign body in

Proptosis 372 posterior chamber 394f
Provocative test 220 Resists stress and strain 6
Pseudogliomas 270 Retina 17
Pseudomembrane conjunctivitis 62 Retinal
Pseudomonas pyocyanea 97 detachment 43, 229, 258
Pseudopapillitis 33f pigment 21
Pseudopterygium 86 Retinitis pigmentosa 254
Pseudostrabismus 303 Retinoblastoma 264
Psoriatic arthritis 411 Retinoscope 471
Psycosensory reflex 280 Retrobulbar neuritis 286f
Pterygium 82, 83f, 86 Rhegmatogenous retinal
Ptosis 343, 345f detachment 258
Punctum dilator 465 Rhodopsin
Pupillary reflex 277 bleaching 25
Purkinje-Sanson image test 200 regeneration 25
Ring synechiae 142f
R River blindness 413
Radial keratotomy 46f Rodent ulcer 109
Radionucleotide Rose bengal test 355
dacryocystography 361
Raised intraocular pressure 243 S
Recurrent Sattler's layer 11
corneal ulceration 332 Schiotz
pterygium 84 indentation tonometer 233
Refractive index 14 tonometer 232, 233f
Refsum's syndrome 257 Schirmer test 354, 354f
Regular Schwalbe's line 7
arrangement of corneal lamellae 3 Scleral spur 7
astigmatism 48 Scleritis 125, 129
Reiter's syndrome 411 Scleromalacia perforans 125
Relative state of dehydration 3 Sclerosing keratitis 128f
Removal of Seborrhea of scalp 325
magnetic foreign body in Seclusio pupillae 132
anterior chamber 393f Secondary optic atrophy 291
posterior chamber 393f Section of retina 20f
Index 487
Seidel's sign 211f scarring 70f

Senile sequelae 70f
cataract 167, 168, 169, 174, Staphylococcus
176, 180 aureus 60, 328
nuclear cataract 173f proteins 78
Sensory retina 21 Staphyloma 130
Sequelae of bacterial corneal Stereopsis 26
ulcer 88, 93 Strabismus 303
Short posterior ciliary arteries 6 Straight forceps 457
Sickle cell retinopathy 229 Streptococcus haemolyticus 73
Siderosis bulbi 390, 390f Structure of
Signs of anterior uveitis 135f choroid 11f
Silicone lens 194f conjunctiva 58f
Single curve forceps 457 cornea 4f
crystalline lens 14
Sixth nerve palsy 316f
eye 1f
Sjogren's syndrome 409
ball 1
Slit lamp 445f
eyelid 322, 323f
biomicroscopy 176
iris 6f
Solid retinal detachment 262 lid margin 323f
Source of bleeding 389 limbus 1
Sphincter pupillae 9 retina 18f
Squamous blepharitis 325, 326f sclera 5
Squealae of trachoma 65 uvea 6
Squint 303 vitreous 236f
surgery instruments 467 Sturge-Weber syndrome 273
Stage of Subhyaloid hemorrhage 235f
active ulcerations 89 Subluxation of lens 196, 196f
acute ischemic necrosis 397 Submuscular areolar tissue 322
cicatrization 90 Sunflower cataract 188, 390f
corneal ulcer 89f Superficial
lamellar separation 170f and deep corneal
primary angle closure vascularization 122
glaucoma 216 corneal
regression 90, 113 opacities 332
repair 397 vascularization 122
keratitis 61 Trabecular meshwork 7

vascularization 122 Trachoma 65
Superior Tractional retinal detachment 262
orbital fissure 370f Tranta's spot 76
temporal vein occlusion 244f Traumatic
Suprachoroidal lamina 10 conjunctivitis 60
Surgical anatomy of lacrimal sac 350f keratitis 88
Symblepharon 338 Treatment of
Sympathetic ophthalmitis 394 acute trachoma 70
Syndermatotic cataract 188 complications 146
Syphilitic iridocyclitis 143
interstitial keratitis 111 large papillae 77
lupus erythematosus 409 non-healing corneal ulcer 95
sclerosis 409 perforated corneal ulcer 96
primary open angle glaucoma 204
therapy 77
retinoblastoma 264
treatment for herpes zoster 105
senile cataract 180
T sequelae 71
vernal keratopathy 77
Tarsorrhaphy 340
Trichiasis 331
Technique of penetrating
Trophic keratitis 87
keratoplasty 102f Tubercular
Temporal and supertractional nasal keratoconjunctivitis 78
crescent 42f proteins 78
Theories of color vision 25 Two point discrimination test 179f
Third nerve palsy 315f Types of
Thomas young's trichromatic theory 25 blepharitis 325
Thyroid eye disease 379 circumscribed choroiditis 150f
Till Schwalbe's line 7 gonioscopy 442
Tonometer 232 hypermetropia 34
Tooke's knife 456 keratoplasty 101
Total lenses 56
hypermetropia 35 regular astigmatism 48
posterior synechiae 142f symblepharon 339f
Toxic amblyopia 294 vernal keratoconjunctivitis 75
Toxoplasmosis 413 Typical trachomatous lesions 70f
Index 489
U prophylaxis 407
Ulcerative program 407
blepharitis 325, 326f, 332 Vitrectomy 238
colitis 411 Vitreous hemorrhage 43, 235
conjunctivitis 60 Vogt-Koyanagi-Harada
Uniocular concomitant squint 306, 307 disease 145, 412
Uses of V-Y operation 337f
cryotherapy 402
W
laser in ophthalmology 401
ocular ultrasound 439 Warm weather conjunctivitis 75
slit lamp 445 Warner's classification 379, 380
Usher's syndromes 257 Wegener's granulomatosis 409
Uveitis 132 Wesseley's sterile immune ring 100
WHO
V classification of xerophthalmia 404
van Herrick method 219f definition of blindness 416
Vannas scissors 460 Worth's four dot test 318f
Venous drainage 7
Vernal X
keratoconjunctivitis 75 Xerophthalmia 404
keratopathy 76 Xerophthalmic fundus 404
Vertically oval pupil 222f
Vision 2020 417 Z
Visual Zeigler's knife 454
cycle 25 Zinc
retinitis pigmentosa 255f lotion 65
Vitamin oxide ointment 65
A therapy 406 Zonular cataract 166, 167f

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BEST AID

Jaypee Brothers Medical Publishers (P) Ltd

Jaypee Brothers Medical Publishers (P) Ltd

© 2013, Jaypee Brothers Medical Publishers

Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com

Best Aid to Ophthalmology

First Edition: 2013

16. Diseases of the Orbit ........................................... 370

Bibliography ............................................................... 475

Index ........................................................................... 477

Q. Discuss in brief the structure of the eye ball.

Fig. 1.1: Structure of the eye

Fig. 1.2: Section of the eye and its accessory structures

– Its external boundaries are sclerocorneal junction

Q. Discuss the structure, blood supply, nerve supply and

Fig. 1.3: Structure of cornea

 Blood supply: It’s an avascular structure. Hence, it derives

 Blood supply: From episclearal and choroidal vessels

Fig. 1.4: Structure of iris and ciliary body

Venous drainage: All three parts are drained by a series of veins

Iris Ciliary body Choroid

Q. What are the structures seen at the angle of anterior chamber?

Fig. 1.5: Structures forming angle of the anterior chamber

Q. Discuss the structure and function of the Iris.

Fig. 1.6: Macroscopic appearance of anterior surface of the iris

Q. Discuss the structure and function of the ciliary body.

– Layer of non-pigment epithelium: It consists of cuboidal

Q. Discuss the structure and function of the Choroid.

Fig. 1.7: Structure of choroid

• Layer of large vessels (Haller’s layer)

Fig. 1.8: Mechanism of aqueous formation, flow and

 The peripheral recess of the anterior chamber is known as

Q. Discuss the factors which maintain the intraocular pressure

 The pressure of the episcleral veins: The pressure difference

Nucleus Corresponds to Position/origin

Fig. 1.9: Major components of adult lens

– Cortex of lens: It is the peripheral part which consists of

Q. Discuss the microscopy of retina.

Fig. 1.10: Structure of retina

Q. Discuss the microscopy of fovea centralis.

Fig. 1.12: Section of the retina

Q. Explain in brief the development of the eye.

Neural Ectoderm* Surface Ectoderm$ Mesoderm

The key points in the development of eye are listed below:

Age Visual development

Q. Discuss the physiology of vision.

Light falling upon the retina causes photochemical changes

Q. Discuss the theories of color vision.

Substance Also called Breakdown causes Resynthesis causes

 F—ability of the visual areas of brain to promote Fusion of

– Each eye views the world in slight different horizontal

Q. List the uses of following: Prism, convex lens, concave lens,

Q. Define Emmetropia and Ametropia.

Fig. 3.1: The normal schematic eye

Fig. 3.2: Normal, hypermetropia and myopia

Ametropia (a condition of refractive error): A state of

Fig. 3.3: Hypermetropic eye and correction with convex lens

 Curvature hypermetropia: Here curvature of corner or lens

– Small optic disk which may look more vascular and

Fig. 3.4: Pseudopapillitis

B. Surgical treatment: Is not effective and reliable but following

Q. Discuss the clinical types of Hypermetropia.

Q. Discuss various components of hypermetropia.