Ophthalmology Concept Book

Concept Based Learning
Video Companion on Each Chapter
Next Generation
Comprehensive Review Series
“OPHTHALMOLOGY”
Active Recall Based
Integrated Edition
Published by Delhi Academy of Medical Sciences (P) Ltd.
HEAD OFFICE
Delhi Academy of Medical Sciences (P.) Ltd.
4-B, Grovers Chamber, Pusa Road,
Near Karol Bagh Metro Station,
New Delhi-110 005
Phone : 011-4009 4009
http://www.damsdelhi.com
Email: info@damsdelhi.com
ISBN : 978-93-89309-25-6
First Published 1999, Delhi Academy of Medical Sciences
© 2021 DAMS Publication

All rights reserved. No part of this book may be reproduced or transmitted in any form or by any
means, electronic, mechanical, including photocopying, recording, or any information storage and
retrieval system without permission, in writing, from the author and the publishers.
This book contains information obtained from authentic and highly regarded sources. Reprinted
material is quoted with permission. Reasonable efforts have been made to publish reliable data and
information, but the authors and the publishers cannot assume responsibility for the validity of all
materials. Neither the authors nor the publishers, nor anyone else associated with this publication,
shall be liable for any loss, damage or liability directly or indirectly caused or alleged to be caused
by this book.
Neither this book nor any part may be reproduced or transmitted in any form or by any means,
electronic or mechanical, including photocopying, microfilming and recording, or by any
information storage or retrieval system, without permission in writing from Delhi Academy of
Medical Sciences. The consent of Delhi Academy of Medical Sciences does not extend to copying
for general distribution, for promotion, for creating new works, or for resale. Specific permission
must be obtained in writing from Delhi Academy of Medical Sciences for such copying.
Trademark notice: Product or corporate names may be trademarks or registered trademarks, and are
used only for identification and explanation, without intent to infringe.
Typeset by Delhi Academy of Medical Sciences Pvt. Ltd., New Delhi (India).
Contents
Chapter 1 Anatomy and Embryology 1 – 11
Chapter 2 Lens 12 – 36
Chapter 3 Cornea and Sclera 37 – 63
Chapter 4 Conjunctiva 64 – 82
Chapter 5 Retina 83 – 116
Chapter 6 Neurophthalmology 117 – 140
Chapter 7 Glaucoma 141 – 168
Chapter 8 Orbit 169 – 191
Chapter 9 Eyelids and Lacrimal drainage system 192 – 214
Chapter 10 Uvea 215 – 234
Chapter 11 Squint 235 – 256
Chapter 12 Optics 257 – 284
1 Anatomy and Embryology
CONCEPTS
Â Concept 1.1 Basic anatomy
Â Concept 1.2 Vascular and lymphatic supply
Â Concept 1.3 Embryology

2 | Ophthalmology
Concept 1.1: Basic anatomy
Learning objectives
To know about layers of eye and its components
To learn about chambers and segments of eye
Time Required
st
1 reading 20 mins
2nd look 5 mins
Basic Anatomy
The eye is placed in a bony socket called the orbit
Three parts – outer fibrous, middle vascular, inner neural
Fig.1.1:
Outer Fibrous:
Anterior 1/6th — transparent cornea, posterior 5/6th opaque sclera. Junction is called
limbus
Middle Vascular (Uveal Tissue):

From anterior to posterior, it consists of iris, ciliary body and choroid
Anatomy and Embryology | 3
Iris: Controls amount of light entering the eye
Ciliary body: aqueous humour production, accommodation
Choroid: supplies oxygen and nutrition to outer layers of retina
Inner Neural (Retina):

It extends from the optic disc posteriorly to the ora serrata anteriorly
Anterior and Posterior Chambers (Anterior Segment)

There are two fluid filled areas in the eye – known as the anterior and posterior chambers.
The anterior chamber is located between the cornea and the iris, and the posterior
chamber between the iris and ciliary processes.
The vitreous cavity (Posterior segment) lies between the lens and the back of the
eye. A jellylike substance called vitreous humor fills the cavity, nourishing the inside of
the eye and helping the eye hold its shape.
4 | Ophthalmology
Concept 1.2: Vascular and lymphatic supply
Learning Objectives
To know major vessels supplying eye structures
Time Required
1st reading 20 mins
nd
2 look 10 mins
The eyeball receives arterial blood primarily via the ophthalmic artery. (branch of the
internal carotid artery)
The ophthalmic artery gives rise to many branches, which supply different components
of the eye.
• The central artery of the retina is the most important branch – supplying the internal
surface of the retina.
Fig.1.2:
• The ciliary arteries are divisible into three groups, the long posterior, short posterior,
and the anterior.
A. Short posterior ciliary arteries -
2 trunks from ophthalmic artery
↓
Each trunk divides into 10-20 branches
↓
Pierce sclera around optic nerve
Supplies the choroid
B. Long Posterior ciliary Arteries –
2 in number
Nasal and Temporal
↓
Run in suprachoroidal space to reach the ciliary muscle
↓
Anastamose with each other and anterior ciliary arteries
↓
Major Arterial Circle – [Circulus Arteriosus Major] (At root of iris)
C. Anterior ciliary Arteries – (7)
Derived from muscular branches of ophthalmic artery
↓
Pass anteriorly in episclera
↓
Give branches to sclera – limbus and conjunctiva
↓
Pierce sclera near limbus to enter ciliary muscle
↓
form Major Arterial Circle
↓
Some branches B
ranches run supply ciliary radially through
iris processes towards pupillary margin to
form ‘Circulus arteriosus minor’.
Venous drainage of the eyeball is carried out by vortex veins, central retinal vein into
the superior and inferior ophthalmic veins. These drain into the cavernous sinus, a dural
venous sinus behind the eye.
LYMPHATIC DRAINAGE
Fig.1.3:
From lateral half – into preauricular nodes

From medial half – submandibular nodes
6 | Ophthalmology
Concept 1.3: Embryology
Learning objectives
To learn about derivatives of eye and its implications
Time Required
1st reading 30 mins
2nd look 10 mins
Surface Ectoderm Neural Ectoderm Mesoderm Neural Crest
• Conjunctival • Iris and • Extraocular • Corneal stroma keratocytes and endothelium

and corneal ciliary body muscles • Sclera
epithelium epithelium • Temporal Sclera • Iris stroma
• Lacrimal • Retina • Vascular
glands • Ciliary muscles
• Smooth muscle endothelium of
• Eyelid of Iris eye and orbit • Choroidal stroma
skin and • Optic nerve • Part of vitreous • Trabecular meshwork
appendages • Orbital bones
• Part of the
• Lens vitreous • Orbital connective tissue
• Connective tissue sheath and muscular layer of
ocular and orbital blood vessels
• Uveal and conjunctival melanocytes
• Meningeal sheaths of optic nerve
• Schwann cells of ciliary nerves
• Ciliary ganglion
Formation of OPTIC VESICLE and STALK

Neural plate
A
Thickening
Optic sulcus
C
Optic veside
D
Prosencephalon
E F
H
Optic vesicle
Optic stalk
Optic vesicle
G H
Fig.1.4:
During the folding of the neural tube, a ridge of cells comprising the neural crest develops
from the tips of the converging edges and migrates to the dorsolateral aspect of the
tube. Neural crest cells from this region subsequently migrate and give rise to various
structures within the eye and the orbit.
FORMATION OF LENS VESICLE AND CUP
Fig.1.5:
DEVELOPMENT OF LENS FIBRES
Fig.1.6:
Hyaloid vasculature
Hyaloid vessel extends from the optic disc through the vitreous humor to the lens.
It starts regressing at 4 months and disappear by 8th month.
• Persistence after birth is called Persistent Hyperplastic primary vitreous.
• Anterior remnant of hyaloid artery is known as Mittendorf spots and posterior remnant
of hyaloid artery is known as Bergmeister’s papilla.
8 | Ophthalmology
Fig.1.7: Persistent Hyperplastic primary vitreous

Fig.1.8: Mittendorf dot Fig.1.9: Bergmister papilla
Coloboma
Colobomas due to defective closure of the embryonic cleft. Typical coloboma occur in
the lower part of the eye.
Fig.1.10:

Fig.1.11: Iris coloboma Fig.1.12: Eyelid coloboma

Fig.1.13: Lens coloboma Fig.1.14: Choroid coloboma
10 | Ophthalmology
Worksheet
• DO THIS CHAPTER FROM DQB
• EXTRA POINTS FROM DQB

• Name the structures of eye in the pic
e
a
b
c
d
• Name derivatives of Surface ectoderm
• Identify _________________
• Identify _________________
2 Lens
CONCEPTS
Â Concept 2.1 Anatomy, Physiology and
Investigations
Â Concept 2.2 Etiology of cataracts
Â Concept 2.3 Senile Cataract
Â Concept 2.4 Management of Cataract
Â Concept 2.5 Complications of Cataract Surgery
Â Concept 2.6 Congenital Anomalies and

Ectopia lentis
Lens | 13
Concept 2.1: Structure and physiology of lens
Learning objectives
To know basic lens anatomy and physiology
Time Required
st
1 reading 20 mins
2nd look 10 mins
• 80% glucose is metabolized anaerobically.
• Lens derives its nutrition from aqueous humour.
• Antioxidant system of the lens constitutes: Vitamin C, vitamin E, and glutathione.
• Weigerts Ligament - It is adhesion between lens and anterior vitreous (hyaloid)
• Zonules of lens are suspensory ligaments which support the lens.
Anatomy:
Biconvex.
Diameter: 9-10 mm.
Refractive index: 1.39
Total power : 16-17 D.
Two surfaces:
Anterior and Posterior.
Anterior surface has a radius of curvature of 10 mm while posterior surface has 6mm
(more convex and stepper than anterior surface).
Lens capsule Thickest - pre - equator Thinnest - At
poles- thinnest at posterior pole.
Anterior epithelium Single layer of epithelial cells.
Cuboidal cells at centre.
Anterior capsule
Become columnar at periphery.
Lens fibres Nucleus (old lens fibers) Anterior epithelium
Embryonic (1-3 months of gestation)

Foetal ( 3months of gestation till birth)
Cortex
Infantile (birth to puberty)
Adult (puberty to rest of life). Adult
Cortex (youngest lens fibers).
Nucleus
Infantile
Foetal
Parts of nucleus: Embryonic
1. Embryonic nucleus
2. Fetal nucleus
3. Infantile nucleus
4. Adult nucleus
Fig.2.1:
14 | Ophthalmology
Concept 2.2: Etiology of cataracts
Learning objectives
To know and identify different types of congenital and acquired cataracts
To learn morphologies of various cataracts
Time Required
st
1 reading 40 mins
nd
2 look 15 mins
Congenital and Developmental Cataract:

Etiology:
Idiopathic Heredity: Maternal Factors: Malnutrition. Foetal or Infantile Factors:
Usually dominant. TORCH infections. Metabolic :
Drugs: Thalidomide, corticosteroids • Galactosemia.
radiation.
Congenital anomaly:
• Lowe’s syndrome.
• Myotonia dystrophica.
Birth Trauma.
Malnutrition.
Types of Congenital and Developmental Cataract: cryg gene

1. Punctate Cataract:
a. Blue dot cataract: Most common
Fig.2.2:
Lens | 15
b. Sutural cataract/Anterior axial embryonic cataract: When these blue dots are
crowded in the Y sutures.
c. Cataracta centralis pulverulenta: Central sphenoidal or biconvex opacity consisting
of powdery fine white dots within the embryonic or fetal nucleus.
2. Zonular Cataract (Lamellar Cataract):
Most common type of congenital cataract causing diminution of vision
• In foetal nucleus.
• Small linear opacities towards equator – Rider and spokes
Fig.2.3:
Acquired Cataracts:
Diabetic Cataract
• Snow-flake or snow-storm cataract
• Sorbitol accumulation in lens due to aldose reductase pathway leads to overhydration
of lens
Fig.2.4:
16 | Ophthalmology
Traumatic Cataract (Blunt Trauma): Rosette shaped cataract
Fig.2.5:
Vossius ring – iris pigments on lens capsule after blunt trauma
Fig.2.6:
Radiational Cataract: Glass Blower’s or Glass- worker’s cataract
Wilson’s disease:
• Hepatolenticular degeneration
• Sunflower cataract
Fig.2.7:
Lens | 17
• Kayser – Fleischer Ring: In Descement’s membrane of cornea
Fig.2.8:
Myotonic dystrophy: Christmas tree cataract
Fig.2.9:
Atopic dermatitis: Shield cataract
Fig.2.10:
18 | Ophthalmology
Galactosaemic cataract:
• Deficiency of GPUT [Galactose Uridyl Transferase]: Oil-droplet cataract
Fig.2.11:
• Deficiency of Galactokinase:Lamellar cataract
Lowe’s syndrome (Oculo- cerebro-renal syndrome):

• Congenital cataract. Glaucoma, Microphakia
• Posterior lenticonus
Complicated Cataract: develops as a result of some other primary ocular

disease like
• Uveitis
Fig.2.12:
• Degenerative – Myopia, Retinitis pigeentosa

• Tumours
Lens | 19
Drugs causing Cataract:
Steroids
Miotics
Chlorpromazine (Phenothiazines)
Gold
Busulphan
Amiodarone
Morphologies of cataracts
Fig.2.13:
Anterior capsular/polar cataract: due to corneal perforation (penetrating injury)

Posterior polar cataract- due to persistence of posterior part of the vascular sheath
of lens
Anterior subcapsular cataract – Amiodarone, shield, Chlorpromazine
Posterior subcapsular cataract – Steroids, radiation, busalphan
20 | Ophthalmology
Concept 2.3: Senile Cataract
Learning objectives
To know and identify different types and stages of senile cataract
Time Required
st
1 reading 20 mins
2nd look 10 mins
Senile Cataract:
Stages of maturation of cortical cataract
NUCLEAR CORTICAL
Increased age related Decreased level of total

nuclear sclerosis proteins, amino acids
and potassium
+
Increased insoluble Increased concentration
proteins of Sodium
Deposition of Melanin Hydration and

and Urochrome conagulation of
Pigments proteins
Cuneiform-
Radial Spokes and
Cupulliform-Posterior
subcapsular
Fig.2.14:
Nuclear sclerosis
• Second sight phenomeon (due to myopic shift)
• Vision improves with pin hole
Nuclear sclerosis Type of Cataract

Brown Cataracta brunescens
Black Cataracta nigra
Red Cataracta – rubra
Nuclear cataract
• Hemeralopia (day blindness)
• Vision does not improve with pin hole
Lens | 21

Fig.2.15: Nuclear Sclerosis Fig.2.16: Cuneiform cataract
Fig.2.17: Posterior Subcapsular Cataract
Fig.2.18:
Incipient/Intumuscent stage – frequent change of glasses, coloured haloes

(Fincham’s Test differentiates haloes between cataract and angle closure glaucoma)
22 | Ophthalmology
Concept 2.4: Management of Cataract
Learning objectives
To know about different surgeries to manage cataract
To learn steps of phacoemulsification
To know different IOLs used in cataract surgery
Time Required
st
1 reading 45 mins
nd
2 look 15 mins
There is no role of medical therapy in cataract
Surgeries:
Congenital Acquired
• Mydriatics/ Optical iridectomy for stationary • Intracapsular cataract extraction (ICCE)
central cataracts • Extracapsular cataract extraction (ECCE)
• Lens aspiration with primary posterior • Small incision cataract surgery (SICS)
capsulotomy with anterior vitrectomy • Phacoemulsification.
Anaesthesia In Cataract Surgery:

It can be of following types:
Topical Commonly paracaine eye drops are
used
Peribulbar In peribulbar space around the eyeball
Retrobulbar space behind the equator of the eye Greater risk of retrobulbar haemorrhage,
globe perforation and optic nerve
damage.
The last muscle to be rendered akinetic is superior oblique, as it is supplied by the fourth
nerve which is outside the muscle cone
Steps of Phacoemulsification
1. Preparation
Retrobulbar, peribulbar or topical anesthesia
2. Clear corneal tunnel/Limbal incisiom
Stab incision with 2.75-3.2 mm keratome for main wound
3. Fill anterior chamber with viscoelastic
4. Continuous circular capsulorrhexis- trypan blue dye can be used
5. Hydrodissection (cleavage between cortex and capsule) and hydrodelineation
(cleavage between nucleus and epinucleus)
Lens | 23
Fig.2.19:
6. Phacoemulsification of nucleus
Fig.2.20:
Fig.2.21:
24 | Ophthalmology
7. Soft lens aspiration
Aspirate soft lens with automated infusion- aspiration cannula
8. IOL implantation
Insert foldable IOL into capsular bag
9. Wound closure if necessary
FEMTOSECOND LASER ASSISTED CATARACT SURGERY (FLACS)-

The femtosecond laser (1053 nm wavelength) can be used to create cleavage planes via
photodisruption in tissues. Used for craeting
• Wounds
• Anterior capsulotomies
• Nuclear fragmentation
Also used in keratoplasty and arcuate keratotomies
Other cataract surgeries
Fig.2.22: Extracapsular Catract Extraction (ECCE)
Fig.2.23: SICS
Lens | 25
Fig.2.24: ICCE
Intra Ocular Lens (IOLs):

Ideal site of IOL implantation is Posterior Chamber.
Non-foldable lenses-PMMA.
Foldable lenses are: Hydrogel, Silicon, Acrylic.
Fig.2.25:
PCIOL
AC-IOL. – examples are Kelman multiflex., Iris-supported-worst’s or Singh’s iris claw
lens
26 | Ophthalmology
Fig.2.26: ACIOL
Fig.2.27: Scleral fixated IOL (placed behind iris, done when there is no posterior capsule support)
Biometry:
• It is the process of calculating the power of IOL
SRK Formula:
• P= A-2.5L-0.9 K
A= constant
L=Axial length
K= Curvature of cornea
Lens | 27
Fig.2.28: ULTRASOUND A and B scan
Fig.2.29: Keratometry
28 | Ophthalmology
Concept 2.5: Complications of Cataract Surgery
Learning objectives
To learn about various complications during and after cataract surgery
Time Required
1st reading 30 mins
nd
2 look 10 mins
Complications of Cataract Surgery:

Operative Early Post- Late Post-Operative IOL-Related
Operative
Irregular incision. Hyphema. After cataract UGH syndrome
Injury to cornea, Iris prolapse. Cystoid macular edema Malpositions of IOL.
Descment detachment.
Iris injury and
iridodialysis.
Accidental rupture of Bullous keratopathy Bullous keratopathy Toxic anterior
lens capsule. Vitreous segment syndrome
loss. (TASS)
Expulsive suprachoroidal Endophthalmitis Retinal detachment
haemorrhage.
Malignant glaucoma Endophthalmitis
Pupil block glaucoma Epithelial in-growth.
Fibrous down growth
• Endophthalmitis. Most common organism is Staphylococcus epidermidis.
• Most common late complication is –After cataract / Posterior capsular opacification/
Elschnig’s Pearls and Soemmerings Ring- treatment by laser capsulotomy (Nd- YAG
laser)

Fig.2.30: Elschnig pearls Fig.2.31: Posterior capsular opacification
Lens | 29
Fig.2.32: Pupil block GLAUCOMA
Cornea
Ciliary Body
Aqueous
Lens
Vitreous
Aqueous
Fig.2.33: A
QUEOUS MISDIRECTION SYNDROME/ MALIGNANT GLAUCO
30 | Ophthalmology
Concept 2.6: Congenital Anomalies and Ectopia lentis
Learning objectives
To know some terms of congenital anamoly of lens
To learn about causes of subluxation
Time Required
st
1 reading 20 mins
2nd look 10 mins
Congenital Anomalies of Lens:

Coloboma Failure to close embryonic fissure
Lenticonus Anterior - Alports Syndrome.
Posterior - Lowes Syndrome.
Microphakia Lowe’s syndrome - lens small and disc like
Micro spherophakia Small and spherical lens:
Weil Marchesani Syndrome.
Fig.2.34: Lens coloboma
Fig.2.35: Anterior and posterior lenticonus

Lens | 31
Ectopia lentis
Subluxation is displacement of the Lens in patellar fossa
Simple Ectopia Lentis Symmetrical and upwards.
Ecoptia lentis et pupillae Pupil displaced in direction opposite to the lens.
Marfans syndrome Upwards and temporal
Homocystinuria Down and nasally
Sulphite oxidase deficiency
Hyperlysinaemia
Aniridia
Well-Marchesani syndrome Inferior subluxation

Microspherophakia. anterior dislocation
Fig.2.36: Subluxation of lens in Marfans
Fig.2.37: Anterior dislocation of lens

32 | Ophthalmology
Worksheet

Lens | 33
• Oldest lens fibres are _____________
• Antioxidant system of the lens constitutes _________________________________
• Rider and spokes are seen in ____________________________
• Identify - ____________________________
Write the name of cataract morphologies in boxesSteps of phacoemulsification

34 | Ophthalmology
1
2
3
4
5
6
7
8
• SRK Formula = __________________________
• Ideal site of IOL implantation is _______________________
• Treatment of this complication of cataract surgery is _______________________
• Identify - _______________
Lens | 35
• Identify the IOL - _______________
List some causes of subluxation of lens

1
5
36 | Ophthalmology
EXTRA POINTS:
3 Cornea and Sclera
CONCEPTS
Â Concept 3.1 A
natomy, Physiology and
Investigations
Â Concept 3.2 Infective keratitis
Â Concept 3.3 C
orneal Degenerations and
depositions
Â Concept 3.4 Corneal ectasias
Â Concept 3.5 Corneal Dystrophy
Â Concept 3.6 Keratoplasty
Â Concept 3.7 Sclera

38 | Ophthalmology
Concept 3.1: Anatomy, Physiology and Investigations:

Learning objectives
To know basic cornea anatomy and physiology
To know about some special investigations of cornea
Time Required
st
1 reading 30 mins
nd
2 look 10 mins
It is a transparent, avascular structure, forming 1/6th of the outer fibrous coat of eyeball
Horizontal diameters -11.7 mm.
Vertical diameter of anterior surface is 10.6 mm while that of posterior is 11.7 mm.
Refractive power: 43-45D
Refractive index: 1.376.
Structure:
It consists of six distinct layers (from anterior to posterior):
Fig.3.1:
Cornea and Sclera | 39
• Epithelium.
• Bowman’s membrane, Not a true membrane but a condensed superficial part of
stroma.
• Stroma: 90 % thickness
• Dua’s layer
• Descemet’s membrane: Ends at the anterior limit of trabecular meshwork as
Schwalbe’s ring.
• Endothelium.
Physiology:
Cornea is avascular, dehydrated, transparent structure with aerobic metabolism.
Factors Responsible for Maintaining the Transparency of Cornea:
1. Epithelium :. Made up of stratified squamous non-keratinized epithelial cells. Have
microvilli.
2. Stroma: regular arrangement of collagen fibrils in a lattice form separated from
each other by less than the wavelength of light [4000-7000A]. Stroma pressure has
also role in maintain transparency.
3. Endothelium: barrier function and pump function. It has Na+/K+ ATPase pump.
Made up of a single layer flat polygonal cells. Cell density in young adults is 3000
cells/mm2. The most metabolically active layer of cornea is endothelium.
4. Avascular cornea
Nervous supply
Fig.3.2:
40 | Ophthalmology
Special investigations related to cornea:
Pachymetry Measures cornea thickness
Specular microscopy Evaluates corneal endothelium
Keratometry Measures corneal curvature
Keratoscopy/Placido disc/ Topography Detects abnormalities of corneal shape
Vital stainings Flourescein stain stains corneal defects
Rose-Bengal stain: It stains dead cells and mucous
Placido disc
Normal Aspheric cornea Keratoconus
Fig.3.3:
Fig.3.4: SPECULAR MICROSCOPY and normal endothelial cells
Fig.3.5: AESTHESIOMETER
Concept 3.2: Infective keratitis/Corneal ulcer:
Learning objectives
To know and identify various forms of infective keratitis
To learn about different corneal opacities
Time Required
st
1 reading 60 mins
2nd look 20 mins
General symptoms
Watering, photophobia (1st), redness, pain, mild discharge, diminuition of vision

Fig.3.6: FUNGAL CORNEAL ULCER Fig.3.7: FUNGAL CORNEAL ULCER with hypopyon

Fig.3.8: ACANTHAMOEBA KERATITIS Fig.3.9: BACTERIAL CORNEAL ULCER

Fig.3.10: H
ERPES SIMPLEX Fig.3.11:
Dendritic ulcer
42 | Ophthalmology
Fungal Acanthamoeba Viral Bacterial

Organism Most common Protozoa Herpes Most common in India is:
in India is: simplex>Herpes Staphylococcus epidermidis
Aspergillus zoster
fumigatus
Pseudomonas (MC cause of
keratitis in contact lens users).
Important Trauma by a Soft contact lens
Pedisposing vegetative matter wearers who use tap
factor water for cleaning
the lenses
Special clinical Signs are more Symptoms are more Decreased corneal Pathogens which can penetrate
features than symptoms than signs sensations intact corneal (epithelium) are:
• Neisseria gonorrheae/
Ulcer – dry and Blurred vision Epithelium meningitis
rough. and pain are involement- • Corynebacterium
Stromal infiltrates characteristically Dendritic ulcer: The diphtheriae.
with feathery severe and bed of ulcer stains • Listeria.
hyphate edges disproportionate with
• Haemophilus
Satellite lesions
to the extent of fluorescein and
ocular involvement. virus laden cells at
in periphery.
This occurs due to the margin of ulcer Pneumococcal keratitis is
Associated perineural invasion called ‘Hypopyon Corneal
take up Rose Bengal
hypopyon: Ulcer’and the ulcer is called
stain.
Unsterile. “Ulcus serpens”.
Multifocal patchy
anterior stromal Stromal involement-
infiltrates which Due to direct
gradually enlarge viral invasion and
and coalesce to form destruction. Stroma
are complete, central has cheesy, necrotic
or paracentral non- appearance with
suppurative ring associated uveitis.
Pseudo dendrites. Interstitial keratitis

– hypersensitivity
reaction to virus,
Salmon patch seen
Endothelium
Involvement –
Disciform ulcer,
Trophic ulcer - also

called Metaherpetic
keratitis- due to
denervation and
drug toxicity.
Corneal Smear Smear Examination: PCR Gram stain

scraping sample examination: Calcoflour white, Blood/Choclate agar
KOH wet Acridine orange
preparation. Culture medium:
Gomori’s Non-Nutrient Agar
methamine silver with E coli.
stain.
Culture:
Saboraud’s
glucose agar.
Treatment Topical 5% Combination of Epithelium – topical Fortified topical antibiotics:
Natamycin propamidine and Acyclovir a. Tobramycin : 13 mg/ml.
polyhexamethylene
b. Cefazoline : 50 mg/ml.
biguanide eye drops.
Others Interstitial and
Other drugs: disciform – topical
a. Topical :
Fluconazole a. chlorhexidine steroids
(0.2%) 0.02%,
b. Oral: b. neomycin 0.175% Trophic – stop
Fluconazole, c. clotrimazole 1% causative drug,
iatraconazole. d. Miconazole 1%. lubricants
Steroids are
contraindicated in
epithelial keratitis
Topical cycloplegics are adjuvant treatment for keratitis
HERPES ZOSTER KERATITIS

Hutchisons rule / sign: When the tip of the nose is involved then eye will be involved.
This is because the involvement of nasocilliary nerve is generally associated with ocular
complications
Ocular Lesions
External Lesions:
• Conjunctivitis.
• Episcleritis.
• Scleritis – less common.
Corneal Lesions:
• Punctate epithelial keratitis
• May be associated with filamentary keratitis.
• Micro dendritic ulcers (Pseudodendrites).
• Nummular Keratitis – involves superficial stroma.
• Disciform keratitis. Anterior uveitis.
Neurological Complications:
• Cranial nerve palsies – all 3rd, 4th and 6th can be involved.
• Optic neuritis.
• Encephalitis.
• Contralateral hemiplegia.
44 | Ophthalmology

Fig.3.12:
Interstitial Keratitis:
It is an inflammation of the corneal stroma with no primary involvement of the epithelium
or endothelium.
Fig.3.13:
Salmon patch –Interstitial keratitis

Causes:
1. Congenital syphilis: Deep vessels [Ghost vessels]– “Salmon – patch”.
2. Tuberculosis.
3. Cogan’s syndrome: Interstitial keratitis associated with deafness.
4. Sarcoidosis.
5. Leprosy.
6. Filiariasis
Moorens Ulcer:
It’s a peripheral ulcerative keratitis caused by ischemic necrosis caused by vasculitis of
limbal vessels. Vasculitis occurs due to the enzyme collagenase and proteoglyconase
produced from adjacent conjunctiva. It is of two types:
• Limited form: Usually unilateral and affects the elderly.
• Progressive form: Usually bilateral and affects the young individuals.
Corneal Opacities:
1. Nebula: superficial scars involving bowman’s layer and superficial stroma (less than
1/3rd). Treatment is keratectomy by excimer laser or by lamellar keratoplasty.
2. Macular opacity: Semi dense opacity resulting from scarring of about 1/3rd to 2/3rd
cornea stroma. Treatment is optical iridectomy or by keratoplasty.
3. Leucoma: Dense opacity resulting from scarring of more than 2/3rd of stroma.
Treatment is same as Macular one.
4. Adherent leucoma: Healing occurs after perforation of cornea with incarcination of
iris.
Fig.3.14:
Neurotrophic Keratopathy: Loss of neural influence causes edema and exfoliation of

epithelial cell
• HSV.
• HZO.
• DM.
• Leprosy.
• Section of Vth nerve.
Photophthalmia:
Keratoconjunctivitis due to exposure of UV rays especially from 311 to 290 nm
46 | Ophthalmology
Concept 3.3: Corneal Degenerations and depositions:
Learning objectives
To know and identify various degenerations of cornea
To learn the layers in which depositions are seen in various conditions
Time Required
st
1 reading 30 mins
nd
2 look 10 mins
Arcus Senilis:
Bilateral lipid deposition starting in superior and inferior perilimbal cornea and progress
circumferentially to form 1 mm wide band.
Age related or it may be associated with hyper lipoproteinaenmia
Fig.3.15:
Band –Shaped Keratopathy:

It is the deposition of calcium on the cornea in the shape of a band.
Etiology:
1. Pthisis bulbi.
2. Chronic uveitis in children.
3. Hypercalcemia.
4. Idiopathic.
Treatment: Chelation which is done with EDTA
Fig.3.16: Band shaped keratopathy

Corneal Pigmentations and depositions:
Iron (Epithelial Deposition):
Fleischer’s ring Keratoconus.
Hudson-Stahli line Idiopathic.
Stocker’s line Pterygium.
Ferry’s line Filtering bleb.

Siderosis Iron foreign body
Silver In Agyrosis in descement’s membrane.

Gold In Chrysiasis in the epithelium and stroma
Copper In Wilson’s disease [Kayser- Fleischers ring] In descement’s membrane.
Melanin In pigment dispersion syndrome [Krukenberg spindle] in the endothelium.
Drugs Vortex keratopathy in the epithelium
(Amiodarone/Chloroquine/NSAIDs)
whorled pattern
Protein Spheroidal degeneration In anterior stroma
Hyaline Salzman nodular generation Superficial stromal opacities
Fig.3.17: KAYSER –FLEISHER RING Fig.3.18: VORTEX KERATOPATHY
Fig.3.19: SPHEROIDAL DEGENERATION Fig.3.20: S

ALZMAN NODULAR
DEGENERATION
48 | Ophthalmology
Concept 3.4: Corneal ectasias:
Learning objectives
To know various corneal thinning disorders of cornea
To learn about signs keratoconus and its management
Time Required
st
1 reading 30 mins
nd
2 look 15 mins
Ectatic Degenerations:
a. Keratoconus.
b. Keratoglobus.
c. Pellucid marginal degeneration
d. Terriens marginal degeneration
Keratoconus:
Non-inflammatory, usually bilateral ectasia of the cornea giving it a conical shape with
resultant myopia with irregular astigmatism.
Keratoconus – Clinical features
Symptom Impaired vision due to progressing myopia and irregular
astigmatism
Uniocular diplopia
Slit–lamp examination Vogt’s Striae
Prominent corneal nerves
Hurricane keratopathy - Whorl pattern of sub-
epithelialkeratopathy due to effect of contact lens.
Retinoscopy Scissors reflex/Yawning refle
Keratometry Irregular astigmatism
Keratoscopy Irregularity
Munsons Sign V-shaped deformity of lower lid in down gaze
Fleischers ring Iron deposition in epithelium
Acute hydrops Sudden hydration of corneal stroma due to rupture of
Descements membrane.
Investigations: Corneal topographic is diagnostic (Pentacam/Orbscan)
Treatment:
Astigmatic spectacles → Rigid gas permeable contact lens [RGPs] → collagens crosslinking
(C3 R) → Penetrating Keratoplasty.

Fig.3.21: Keratoconus Fig.3.22: FLEISHER RING under
Cobalt blue light

Fig.3.23: Fig.3.24: OIL DROPLET REFLEX

Fig.3.25: VOGT’s striae Fig.3.26: PROMINENT CORNEAL NERVES
50 | Ophthalmology
Concept 3.5: Corneal Dystrophy:
Learning objectives
To know various corneal dystrophies and their salient features
Time Required
st
1 reading 40 mins
2nd look 10 mins
Corneal Dystrophy:
Group of spontaneous appearing, usually inherited, bilateral, stationary or slowly
progressive corneal alterations that develop in absence of inflammation.
Corneal Dystrophies
Layer Dystrophy Causative Inheritance Deposit
gene characteristics
Epithelial - Microcystic (Cogans) TGFb1 Limited familial cases Dot-like or finger-

subepithelial (epithelial basement print
membrane) KRT3 Autosomal dominant
Meesmann’s Tiny epithelial
cysts.
Epithelial - Reis – Buckler’s TGFb1 Autosomal dominant Lack of
stromal Lattice TGFb1 Autosomal dominant hemidesmosomes
Granular TGFb1 Autosomal dominant amyloid
hyaline
Stromal Macular CHST6 Autosomal recessive Mucopoly
saccharodosis
Endothelial Fuch’s endothelial COL8A2 Autosomal dominant corneal guttatae
Posterior COL8A2 Autosomal dominant Vesicular
polymorphous or band-like
opacities

Fig.3.27: Cogan microcystic Fig.3.28: Meesman
Fig.3.29: Reis – Buckler
Fig.3.30: LATTICE TYPE

52 | Ophthalmology

Fig.3.31: GRANULAR TYPE

Fig.3.32: MACULAR TYPE
Fig.3.33: ENDOTHELIAL CORNEAL DYSTROPHY : FUCH’S DYSTROPHY

Concept 3.6: Keratoplasty:
Learning objectives
• To know various types of keratoplasty and their indications
Time Required
st
1 reading 25 mins
2nd look 10 mins
Keratoplasty:
Replacement of diseased cornea by a graft of homologous tissue. It is of two types
i.e. penetrating and lamellar. Donor cornea should be obtained from cadaveric eyes
preferably within 6 hours, but can be permitted till 12 hrs.
Keratoplasty
Type Purpose Indications
Optical To improve vision keratoconus, scarring, corneal dystrophies
Tectonic to preserve corneal integrity descemetocele
Therapeutic facilitates removal of infected corneal Corneal ulcer
tissue
Cosmetic to improve the appearance of the eye Rarely done
Penetrating Keratoplasty:
Replacement of whole (full-thickness) cornea.
Lamellar Keratoplasty:
Replacement of partial thickness of cornea.
Types:
a. Inlay lamellar keratoplasty – can be anterior (Anterior lamellear keratoplasty) or
posterior (Descement Stripping Endothelial keratoplasty)
b. Onlay lamellar keratoplasty – Epikeratoplasty/Epikeratophakia.
Fig.3.34: PENETRATING KERATOPLASTY

54 | Ophthalmology
Fig.3.35: LAMELLAR KERATOPLASTY (in lays)
Fig.3.36: ANTERIOR LAMELLAR KERATOPLASTY

Fig.3.37: POSTERIOR LAMELLAR KERATOPLASTY
Keratoprostheses
They are artificial corneal implants used in patients unsuitable for keratoplasty.
Indicated in bilateral blindness from severe but inactive anterior segment disease with
no realistic chance of success from conventional keratoplasty, e.g. Stevens–Johnson
syndrome, ocular cicatricial pemphigoid, chemical burns and trachoma.

Fig.3.38: Boston keratoprosthesis Fig.3.39: Osteo-odonto keratoprosthesis
56 | Ophthalmology
Concept 3.7: Sclera:
Learning objectives
To learn salient features of scleritis and episcleritis
To know about types of staphylomas
Time Required
st
1 reading 25 mins
nd
2 look 10 mins
Episeleritis Scleritis
Pathophysiology Idiopathic inflammation Autoimmune dysregulation
Symptoms Acute onset Mild pain Redness, Subacute onset Severe pain Pain with eye
irritation movement Blurred vision/vision loss Photophobia
Physical Exam Mobile vessels Adherent vessels
Blanch with phenylephrine drops Does NOT blanch with phenylephrine drops
Reddish hue Bluish hue
Slit lamp may reveal nodules, scleral thinning, and
corneal changes
Systemic inflammation (joint pain, rashes, etc)
Treatment Self-limited Ophthalmology consult
Consider topical steroids in Systemic steroids/NSAIDs +/- Topical antibiotics
refractory cases

Fig.3.40: Episcleritis Fig.3.41: Scleritis
Scleromalacia Perforans:
It is anterior necrotizing scleritis without inflammation.
Common in women with long-standing seropositive rheumatoid arthritis. Spontaneous
perforation is rare, unless intraocular pressure is elevated.
Staphyloma:
It is an ectatic condition of the eyeball with herniation of uveal tissue
Type Uveal tissue lining Cause
Anterior staphyloma Iris plastered behind Pseudocornea (the scar formed from organized
sloughed cornea exudates and fibrous tissue covered by epithelium)
Intercalary staphyloma Occurs at limbus, lined Causes are secondary angle closure glaucoma,
internally by root of iris and cataract surgery, scleromalacia perforans, anterior
anterior portion of ciliary scleritis, marginal corneal ulcer and injuries to
body. limbus.
Ciliary staphyloma Ciliary body is incarcerated in Causes are scleritis, trauma, developmental
the region of sclera ectasia. glaucoma, end stage primary/secondary glaucoma.
Equatorial staphyloma Occurs at equatorial region Causes are uncontrolled glaucoma, scleritis,
of the eye with incarceration degenerative myopia.
of the choroid.
Posterior staphyloma Occurs at posterior pole and is Degenerative high axial myopia is a major cause
lined by choroid from inside.
Fig.3.42:

Fig.3.43: Anterior Fig.3.44: Intercalary
58 | Ophthalmology

Fig.3.45: Ciliary Fig.3.46: Posterior
Worksheet

60 | Ophthalmology
• Most vital layer of cornea is _____________
• Investigation to measure corneal thickness is ______________________________
• Satellite lesions are characteristic of which corneal ulcer _______________________
What is checked with this device? ____________________________
What is the treatment of this? ____________________________
Name the conditions in which these lines are seen

Fleischer’s ring
Hudson-Stahli line
Stocker’s line
Ferry’s line
Siderosis
Write some important signs of keratoconus

Identify the deposit and layer of cornea involved- _______________
Identify _______________
Identify the procedure _______________

62 | Ophthalmology
Fill the boxes for type of staphylomas

Fill in the remaining points
Corneal Dystrophies
Layer Dystrophy Deposit characteristics

Epithelial - subepithelial Microcystic (Cogans)(epithelial basement
membrane)
Tiny epithelial cysts.
Epithelial - stromal
Stromal Macular
Endothelial Fuch’s endothelial
Posterior polymorphous Vesicular
or band-like opacities
EXTRA POINTS:
4 Conjunctiva
CONCEPTS
Â Concept 4.1 Basic Anatomy and histology
Â Concept 4.2 Allergic Conjunctivitis
Â Concept 4.3 Trachoma
Â Concept 4.4 Viral conjunctivitis
Â Concept 4.5 Bacterial Conjunctivitis
Â Concept 4.6 Cicatricial Conjunctivitis
Â Concept 4.7 Conjunctival degenerations

Conjunctiva | 65
Concept 4.1: Basic Anatomy and histology
Learning objectives
• To know basic conjunctival anatomy and histology
Time Required
st
1 reading 10 mins
nd
2 look 3 mins
Parts Special point
Palpebral conjunctiva Begins from the anterior margin of the edge of the lids. 3 parts: Marginal,
Tarsal and Orbital parts
Conjunctival fornix Continuous cul- de-sac uniting the palpebral and bulbar conjunctiva
Bulbar conjunctiva Covers the anterior part of the eye ball over sclera and limbus
Fig.4.1:
66 | Ophthalmology
Layer Special point

Epithelium Stratified squamous non-keratinized epithelium
Adenoid layer fine connective tissue reticulum
Fibrous layer contains all the blood vessels and nerves
Goblet cells: Occurs throughout the conjunctiva. More dense on the nasal side
Melanocytes: Present in limbus, fornix, caruncle and at the site of anterior ciliary
vessels
Langerhans cells: All over conjunctiva
Epithelium
Adenoid
Layer
Substantia
Propria
Fibrous
Layer
Fig.4.2:
Conjunctiva | 67
Concept 4.2: Allergic Conjunctivitis
Learning objectives
• To know important features of Vernal and Phlyctenular conjunctivitis
Time Required
1st reading 20 mins
nd
2 look 5 mins
Vernal Keratoconjunctivitis:
• Also called spring catarrh
• Bilateral condition, Type I hypersensitivity to exogenous antigen, like pollen or dust.
• It is a conjunctivitis with no follicular reaction, only papillary reaction.
• Common in ages of 4-20 years.
• More common in male children
• VKC patients have increased incidence of keratoconus.
Clinical Features: Intense ocular itching, lacrimation, photophobia, foreign body
sensation, burning, thick mucus ropy like discharge
Palpebral VKC Limbal VKC
Papillary hypertrophy most marked on superior tarsus. Limbal papillae with smooth, round surface
Papillae – become large – Cobble-stone appearance. “Horner-Trantas spots” composed predominantly
of eosinophils.
Fig.4.3: Conjunctival papillae Fig.4.4: Shield ulcer
Fig.4.5: Pseudo gerontoxon – Cupids bow

68 | Ophthalmology
Treatment:
• Topical steroids and topical mast-cell stabilizers i.e. sodium cromoglycate.
• New drugs: Epinastine and Olopatadine: These are both mast cell stabilizers and
antihistaminics.
Phlyctenular Keratoconjunctivitis:
• Unilateral mostly.
• Type 4 hypersenstivity- non-specific delayed hypersensitivity reaction to
Staphylococcus (most common) or tubercular antigens
• Predominantly affects children
• Small pinkish – white nodule near the limbus, surrounded by hyperaemia called
corneal Phlycten
• Corneal involvement: Fascicular ulcer or Sacrofulous ulcer
Fig.4.6:
Treatment:
• Topical steroids.
• Any associated staphylococcal blepharitis must be treated.
Conjunctiva | 69
Concept 4.3: Trachoma
Learning objectives
• To learn and identify clinical signs of trachoma and to know its management
Time Required
1st reading 20 mins
nd
2 look 5 mins
• Chronic Keratoconjunctivitis.
• By Chlamydia trachomatis – Serotypes A, B, Ba, C.
• Conjunctival reaction in trachoma is both follicular and papillary
• Chlamydia trachomatis is epitheliotropic and produces intra – cytoplasmic inclusion
bodies called H.P bodies (Halber Staedter – Prowazeke bodies)
• Major vector of infection is flies
• Incubation period is 5-12 days
• Clinical features: 1-9 year child presents with lot of itching and watering. There are
follicles (boiled Sago grain appearance) in the upper palpebral conjunctiva and upper
limbus.
• SAFE strategy : It is a WHO strategy to control trachoma in a community.It stands for
Surgery, Antibiotics, Facial Cleanliness, Environment.
• Treatment: The choice of treatment is Azithromycin.
• Other drugs: Tetracycline ointment 1%, Topical erythromycin eye ointment and
topical sulphonamides eye drops and ointmen
WHO classification of trachoma: Mnemonic- FISTO:

Trachomatous inflammation follicular (TF)- Presence of five or more
follicles with 0.5 mm in diameter in the upper tarsal conjunctiva.
Follicles
Trachomatous inflammation (TI)- Inflammatory thickening of the
tarsal conjunctiva that obscures more than half of the normal deep
tarsal vessels
Trachomatous scarring (TS)- The presence of scarring in the tarsal
conjunctiva. Arlt’s line: Linear scar in sulcus subtarsalis
Arlt’s line
Trachomatous trichiasis (TT)- At least one eyelash rubs on the eyeball
Corneal Opacity (CO)-
Trichiasis and corneal opacity

70 | Ophthalmology
Fig.4.7: H
erbert’s pits: Cicatrized follicles at the Fig.4.8: P
annus: Infiltration of cornea associated with
superior limbus. vascularization
Conjunctiva | 71
Concept 4.4: Viral Conjunctivitis:
Learning objectives
• To learn features of adenoviral conjunctivitis
Time Required
1st reading 10 mins
nd
2 look 5 mins
Typical viral lesion is a keratoconjunctivitis.

Causes- Adenovirus, HSV, Herpes zoster virus, Poxvirus, Myxovirus, Paramyxovirus.
Adenoviral Keratoconjunctivitis:
Usually affects children with Upper respiratory tract infection
Fig.4.9: Chemosis of conjunctiva
Clinical features Types

Watering, discomfort, photophobia Pharyngo conjunctival fever
Follicular response Epidemic kerato conjunctivitis
Preauricular adenopathy
Severe causes
• Subconjunctival haemorrhage
• Chemosis
• Pseudo membranes
• Focal white subepithelial/anterior stromal infiltrates-probably as
an immune response to the virus
Treatment – Conservative, cold compresses, topical antibiotics (to prevent secondary
infection)
72 | Ophthalmology
Concept 4.5: Bacterial Conjunctivitis:
Learning objectives
• To learn few examples and salient features of bacterial conjunctivitis
Time Required
1st reading 25 mins
nd
2 look 10 mins
The most common isolates are Streptococcus pneumoniae, Staphylococcus aureus

(most common), Haemophilus influenzae and Moraxella catarrhalis
• Acute onset of redness, grittiness, burning and discharge
• The discharge can initially be watery, mimicking viral conjunctivitis, but rapidly
becomes mucopurulent (can lead to Coloured halos sometimes)
• Hyperacute purulent discharge may signify gonococcal or meningococcal conjunctivitis,
which may have lymphadenopathy as well
Fig.4.10: Mucopurulent discharge
Treatment
Topical antibiotics
Systemic antibiotics for Haemophilus influenza, gonococcal or meningococcal
conjunctivitis
Conjunctiva | 73
Conjunctivitis Organisms Treatment

Acute Membranous • Corynebacterium diptheriae Topical penicillin and topical
Conjunctivitis • Virulent type of Streptococous antidiphtheric serum
haemolyticus
Pseudomembranous Severe Adenoviral infection Topical antibiotics and anti-
Conjunctivitis Ligneous conjunctivitis. inflammatory.
(it does not bleed on Gonococcal conjunctivitis.
peeling)
Autoimmune conjunctivitis.
Streptococcus haemolyticus.
Low virulent diphtheria infection.
Chemical causes: Lime, Acids, Ammonia,
Copper sulfate.
Angular Conjunctivitis Morax-Axenfeld diplobacilli (diplobacillary Oxytetracycline- inhibits the growth of
conjunctivitis) organisms
Zine lotion- It inhibits proteolytic
enzymes.
Acute Haemorrhagic Bacterial -Pneumococcus and Haemophilus. Self–limiting – resolves in 7 days
Conjunctivitis Virus - Picorna viruses: Enterovirus 70 (most
common) and coxsackie A24. Adenovirus type
11, Echovirus 34
Ophthalmia Chlamydial: manifest after 5-14 days. Prophylaxis: 0.5% eryhthromycin and 1%
Neonatorum tetracycline ointment
(conjunctival Gonococcal: manifest after 1-4 days.
inflammation that Specific treatment:
Chemical: due to 1% silver nitrate given to
occurs during the first
prevent gonococcal conjunctivitis- within Gonococcus: Systemic ceftriaxone,
month of life)
hours. ciprofloxacin, penicillin G etc.
Staphylococcus aureus –end of 1st week HSV: Acyclovir eye ointment or systemic
Herpes simplex: It occurs due to HSV-2- Acyclovir.
manifest 1to 2 weeks Chlamydia trachomatis: eryhthromycin
eye ointment, oral erythromycin.
Fig.4.11: M
embranous conjunctivitis Fig.4.12: G
ONOCOCCAL CONUNCTIVITIS
Fig.4.13: Hemorragic conjunctivitis

74 | Ophthalmology
Concept 4.6: Cicatricial Conjunctivitis:
Learning objectives
• To learn features of Keratoconjunctivitis Sicca and Xerophthalmia
• To lean few investigations for dry eyes
Time Required
st
1 reading 40 mins
2nd look 15 mins
Pre-corneal tear film has three layers:

Tear film layer Glangs producing
Lipid layer Meibomian and Zeiss
Aqueous layer Main lacrimal glands (95%) and accessory lacrimal glands of Krause and Wolfring
Mucin layer Goblets cells, Glands of Henle and Manz
Fig.4.14:
Keratoconjunctivitis Sicca (KCS):

It refers to any eye with some degree of dryness. It primarily resulting from aqueous
layer deficiency.
Sjogren syndrome is an autoimmune inflammatory disease of which dry eyes is a
feature
Conjunctiva | 75
Dry eyes classified as:
Aqueous-deficient Evaporative
Sjögren
syndrome dry Non-Sjögren
Intrinsic Extrinsic
eye (primary or syndrome
secondary
Non-Sjogren syndrome dry eye.

• Lacrimal deficiency: primary (e.g. age-related dry eye, familial dysautonomia) or
secondary (e.g. inflammatory and neoplastic lacrimal gland infiltration)
• Lacrimal gland duct obstruction, e.g. trachoma, cicatricial pemphigoid, chemical
injury, Stevens–Johnson syndrome
Intrinsic
• Meibomian gland deficiency, e.g. posterior blepharitis, rosacea.
• Disorders of lid aperture, e.g.lid retraction, proptosis
• Low blink rate, e.g. Parkinson disease, prolonged computer monitor use, reading,
watching television.
Extrinsic
• Vitamin A deficiency.
• Contact lens wear.
• Allergic conjunctivitis.
Investigations:
Tear film break- up time Normal – 34 seconds.
< 10 seconds → abnormal.
Rose Bengal Staining
Fluoroscein staining
Lissamine staining
Schirmers test Normal > 15 mm.
Borderline → Between 5 mm and 10 mm.
Abnormal - <5 mm.
Phenol red thread test
Lactoferrin level in tears It decreases in dry eye.
Tear osmolality measurements It is raised in patients of dry eye.

76 | Ophthalmology
Fig.4.15: CICATRICIAL CONJUNCTIVITIS Fig.4.16: PHENOL RED THREAD test
Fig.4.17: SCHIRMER test Fig.4.18: ROSE BENGAL STAINING
Treatment:
1. Tear substitutes:
a. Cellulose derivatives.
b. Polyvinyl alcohol.
2. Mucolytic Agents – 5% acetylcysteine drops.
3. Reduction of tear drainage – Punctal Occlusion.
Xerophthalmia describes a dry eye associated with vitamin A deficiency
The WHO classification of vitamin A deficiency is as follows:

XN Night blindness
X1A Conjunctival xerosis
X1B Bitot's spot
X2 Corneal xerosis
X3A Corneal ulceration/keratomalada involving one-third or less of the cornea
X3B Corneal ulceration/keratomalada involving one-half or more of the cornea
XS Corneal star
XF Xerophthalmic fundus
Conjunctiva | 77
Prevalance for XEROPHTHALMIA
Criteria Prevalence in population at risk
Night blindness >1%
Bitot's spots >0.5%
Corneal xerosis/corneal uiceration/keratomaJacia >0.01%
Corneal ulcer >0.05%
Serum Retinol(<10 mcg/dl) >5%
Fig.4.19: BITOT SPOT Fig.4.20: KERATOMALACIA
Treatment:
A. Local Ocular Therapy:
a. Topical artificial tears.
b. If Keratomalacia – full-fledged treatment of corneal ulcer.
B. Vitamin A Therapy:
Age Oral dose at 0,1 and 14 days
< 6 months 50000 IU
6 m – 1 year 1 lakh IU
>1 year 2 lakh IU
C. Treatment of underlying conditions–

a. Treatment of PEM – Protein Energy Malnutrition.
b. Other nutritional disorders, diarr- hoea, dehydration and electrolyte imbalance.
Prophylaxis of Xerophthalmia:
• 6-12 months – 1 lakh IU orally every 3-6 months.
• 1-6 years – 2 lakhs IU orally every 6 months.
• < 6 months – 50,000 IU orally.
• Lactating mothers – 20,000 IU orally once at delivery or during next 2 months.
78 | Ophthalmology
Concept 4.7: Conjunctival degenerations:
Learning objectives
• To learn about pterygium and pingencula
Time Required
1st reading 20 mins
nd
2 look 5 mins
Pterygium
• Degenerative and hyperplastic condition of conjunctiva.
• The subconjunctival tissue undergoes elastotic degeneration and proliferates as
vascularized tissue.
• Corneal epithelium, bowman’s layer and stroma is destroyed.
• Etiology: UV rays, dry heat, dusty environment.
• It appears to be a triangular fold encroaching over the cornea in the area of palpebral
aperture, usually on nasal side.
• It is an asymptomatic condition in early stages except for cosmetic intolerance.
Visual disturbance due to encroachment of pterygium on papillary area or corneal
astigmatism.
• Diplopia can very occasionally occur due to ocular movement limitation.
Treatment:
Asymptomatic is best left alone.
Otherwise surgery is the only effective treatment.
Simple excision or Bare sclera technique is associated with high recurrence (80%), so
conjunctival autografting is the most popular approach

Fig.4.21: Stocker line (iron deposition in epithelium of cornea)
Pingencula
Asymptomatic elastotic degeneration of the conjunctival
stroma. A yellow–white fatty like mound is seen on the
bulbar conjunctiva. Calcification is occasionally present.
Treatment is usually unnecessary
Fig.4.22
Conjunctiva | 79
Worksheet

80 | Ophthalmology
• Phlyctenular Keratoconjunctivitis is which hypersensitivity reaction _____________
• Chlamydia trachomatis is caused by which serotypes ________________________
__________
Most common cause of vision deterioration in this is - ____________________________
Name some causative agents

Acute Haemorrhagic Conjunctivitis Bacterial -.
Virus -
Angular Conjunctivitis Organism? Treatment?
• Give two differentials of this
Fill in the values

Schirmers test Normal > .
Borderline →
Abnormal - <5
Tear film layer Glangs producing
Lipid layer
Aqueous layer
Mucin layer
Treatment for 2 year old child with this is _______________________
Conjunctiva | 81
Identify the line marked by arrow - _______________
Identify the IOL - _______________
List WHO classification of xerophthalmia

82 | Ophthalmology
EXTRA POINTS:
5 Retina
CONCEPTS
Â Concept 5.1 Basic Structure
Â Concept 5.2 Layers of retina
Â Concept 5.3 V
ascular supply of retina and related
investigations
Â Concept 5.4 Retinal detachment
Â Concept 5.5 Diabetic Retinopathy
Â Concept 5.6 Hypertensive Retinopathy
Â Concept 5.7 Retinal vein occlusions
Â Concept 5.8 Retinal artery occlusions
Â Concept 5.9 Retinal degenerations
Â Concept 5.10 Retinal dystrophy
Â Concept 5.11 Retinopathy of Prematurity

84 | Ophthalmology
Concept 5.1: Basic Structure
Learning objectives
• To know basic retinal structure and parts
Time Required
1st reading 15 mins
nd
2 look 5 mins
• Retina extends from optic disc (thickest) to ora serrata (thinnest)

• Ora serrata corresponds to the insertion of the rectus muscles. Its thickness is 0.10
mm
• The surface area of the retina is 266 mm2
Fig.5.1:
Diameter Visual field

Optic disc 1.5 mm Blind spot Vertically oval,
1.76 mm horizontally and 1.88 mm vertically.
Macula 5.5 mm 15° Contains xanthophyll
carotenoid pigments lutein and zeaxanthin in
higher concentration
than the peripheral retina
Fovea- Centralis 1.85 mm 5° depression at the centre of macula
Foveola 0.35 mm 1° 2 disc dioptre away from temporal margin of optic
disc
• Umbo- tiny depression at centre of foveola. Seen as foveal reflex.
• FAZ- (Foveal Avascular Zone): It doesn’t contain any capillaries, hence the name.
Inside the fovea but outside foveolar. determined with accuracy only by fluorescein
angiography (0.8 mm diameter)
Retina | 85
Concept 5.2: Layers of retina
Learning objectives
• To know and identify retinal layers
Time Required
1st reading 20 mins
nd
2 look 5 mins
RETINA HISTOLOGY
Fig.5.2:
9 Nerve fiber layer 10 Inner limited membrane

Axons at surface of retina
passing via optic nerve,
8 Ganglion cell layer chiasm and tract to lateral
geniculate body
7 Inner plexiform layer Ganglion cell
Muller cell
6 Inner nuclear layer (supporting glial cell)
Bipolar cell
Amarcine cell
5 Outer plexiform layer
Horizontal cell
Rod
Cone
4 Outer nuclear layer
3 Outer limiting
membrane Pigment cells
2 Photoreceptor layer
1. Pigment epithelium
Choroid
Fig.5.3:
86 | Ophthalmology
Layer
Internal limiting membrane
Nerve fibre layer Axons of ganglion
cells running centrally into the optic nerve
Ganglion cell layer
Inner plexiform layer consisting of synapses
Inner nuclear layer the nuclei of the bipolar, Muller, amacrine, horizontal cells
Outer plexiform layer consisting of synapses
Outer nuclear layer the nuclei
of the rods and cones
External limiting membrane
Photoreceptors This layer transform light energy to the visual impulse. There are
120 million rod cells and 6 million cone cells
Retinal Pigment Epithelium Hexagonal cells, firmaly adherent to bruch’s membrane and
loosely to rods and cones of the sensory retina. This layer provide
metabolic support to neuro- sensory layer. Other important
fuctions are photoreceptor renewal, integrity of subretinal space,
phagocytic of photoreceptor, regenerative and reparative
Most radiosensitive layer of the retina: Rods and cones.
Most radioresistant layer of the retina: Ganglion cell layer.
Fig.5.4: NORMAL Optical Coherence Tomography

Retina | 87
Concept 5.3: Vascular supply of retina and related investigations
Learning objectives
• To learn blood supply of retina
• To learn about angiography
Time Required
st
1 reading 20 mins
2nd look 10 mins
Retinal vascular system Inner six layers derive its nutrition from central retinal artery. The retinal
vessels are end arteries and do not anastomose with each other.
Choroidal vascular system Outer four layers of retina get its nutrition from choriocapillaries i.e.
choroidal vascular system (short posterior ciliary artery)
There is anastomosis of central retinal artery and short posterior artery with the arterial
circle of Zinn or Haller.
Blood supply of optic nerve head/optic disc.

• Surface nerve fibre layer: Derived from retinal arterioles
• Prelaminar region: Vessels of ciliary region.
• Lamina cribrosa: Short post ciliary artery and circle of Zinn.
• Retrolaminar region: Both ciliary and retinal circulation.
Blood-Retinal Barrier:
• Inner: Tight junctions of retinal capillary endothelial cells.
• Outer: Retinal pigment epithelial cells.
Arteriole Venule
Inner limiting membrance
Superficial
capillary Retinal nerve fibre layer
network
Ganflion cell layer
Ineer plexiform layer
Deep
capillary Ineer nuclear layer
network
Outer plexiform layer
Outer nuclear layer

Outer limiting
membrance
Rod and cone layer
Pigment epithelium
Fig.5.5:
88 | Ophthalmology
Fluorescein Angiography (FA):
FA is used in studying the normal physiology of the retinal and choroidal circulation and
to detect any abnormalities.
Procedure:
5 ml of 10% Fc is injected in antecubital vein and photograph taken at 1sec interval
between 5 and 25 s after injection.
Findings:
It may be normal, hypoflourescence or hyperflourescence.
Hypoflourescence: It may be due to blocked fluorescence as a result of haemorrhage
or exudates OR due Capillary Non-Perfusion.
Hyperflourescence: It occurs either due to leakage or RPE defects. A leakage will
increase in size but size of RPE defects will remain normal.
Indocyanine Angiography:
ICG angiography is helpful for diagnosing choroidal lesions as it is 98% bound to the
plasma proteins.
Fig.5.6: NORMAL ANGIOGRAPHY

Retina | 89
Concept 5.4: Retinal Detachment
Learning objectives
• To learn about different types of detachment
• To learn about Central Serous Retinopathy
Time Required
st
1 reading 35 mins
2nd look 15 mins
Separation of sensory retina from retinal pigment epithelium (RPE) by subretinal fluid.
Type of Pathology and Features Configuration Treatment
detachment cause
Rhegmatogenous Due to break • Floaters: opacities Convex Vitreo-retinal
formation in the vitreous surgery
either due to cavity (Pars plana
traction, trauma • Photopsia: flash of vitectomy)
or predisposing light seen by the or
degenerations. patient. It occurs Scleral buckling
due to irritation of
rods and cones.
• Decreased visual
acuity if macula is
involved.
• Visual field defect
Mobility: Detached
retina undulates
freely.
Tractional Vascular • Decreased visual Concave Vitreo-retinal
pathology of acuity if macula surgery
retina like DM, is involved. (Pars plana
CRVO, Eales • Visual field defect vitectomy)
disease • Mobility:
Reduced
Exudative Due to choroidal • Floaters: They Convex Treatment of the
lesions like are seen due to primary choroidal
tumour associated vitritis. lesions
[Melanoma, • Vision
Hemangioma or diminuition
metastasis] or is sudden and
Central Serous progresses rapidly
Retinopathy • Smooth retina
• Shifting fluid:
Present
90 | Ophthalmology
Grey reflex: in old detached retina on distant direct ophthalmoscopy
Vitreous substitutes that can be used are Air, SF6, perflourocarbons like C3F8 and
silicone oil.
Scleral buckling - Aim of treatment in rhegmatogenous RD is closure of break.
a. Drainage of SRF [subretinal fluid].
b. Injection into vitreous: To repose the detached retina:
c. Cryotherapy: To seal retinal break
d. Explant: Buckling is done to internally indent the sealed break. It is done with buckle
explant or encirclage band
RETINAL DETACHMENT
Fig.5.7: PARS PLANA VITRECTOMY(PPV)
Fig.5.8: SCLERAL BUCKILING

Retina | 91
Fig.5.9: SILICONE OIL IN ANTERIOR CHAMBER
Central Serous Retinopathy (CSR):

Idiopathic, self-limited disease of young or middle –aged adult males (20-40 years).
Pathogenesis:
Dysfunction of RPE
↓
Accumulation of fluid in subretinal space
↓
Local detachment of sensory retina at macula
Clinical features
Sudden onset of blurred vision (painless)
Micropsia
Metamorphopsia
VA is 6/9 → 6/12 – mild vision loss
Elevation of sensory retina at posterior pole, borders of which are outlined by glistening reflex [Ring Reflex
Fig.5.10: C
ENTRAL SEROUS RETINOPATHY Fig.5.11: INK BLOT/SMOKE STACK IN CSR
Treatment:
• Spontaneous resolution is common (by 6-12 months).
• Laser photocoagulation – hasten symptomatic relief by speeder resolution of serous
detachment.
92 | Ophthalmology
Concept 5.5: Diabetic Retinopathy
Learning objectives
• To learn about different types of detachment
• To learn about Central Serous Retinopathy
• To learn about Cystoid macular edema
Time Required
st
1 reading 60 mins
nd
2 look 20 mins
Prevalence of DR is higher in IDDs (> 5 years) than in NIDDs (can present with DR at
time of diagnosis).
Risk Factors for DR:

• Duration of diabetes: Most important factor.
• Good metabolic control: Delays the development of DR by few years.
• Miscellaneous Factors: Pregnancy, anaemia, hypertension, renal disease.
It’s a microangiopathy affecting the retinal precapillary arterioles, capillaries and venules.
Pathogenesis:
• Aldose reductase reduces glucose to sorbitol resulting in its accumulation which further
results in activation of protein kinase C,oxidative stress and increased production of
growth factors (VEGF-A, IGF, EGF, PDGF, TGF-B).
• The above said factors lead to the endothelial and metabolic dysfunction which lead
to microangiopathy and features of diabetic retinopathy.
Features of DR
Non-Proliferative DR Proliferative DR
Microaneurysm: First clinically detectable lesion of Neovascularisation – NVD, NVE, Rubeosis iridis:
DR (Inner nuclear layer) NVG
Intra-retinal Haemorrhage: Dot and blot (deep); RD: Tractional RD can later lead to Rhegmatogenous
flame-shaped (superficial). RD
Hard exudates: Lipid deposits within the retina Haemorrhage: intravitreal, pre-retinal
Soft exudates/ cotton wool spots: Due to disturbance
of axoplasmic flow which causes accumulation of
waste product in nerve fibre layer
Venous looping, beading and sausage-like
segmentation.
IRMA (intra-retinal microvascular abnormalities).
A-V shunts due to capillary closure.
Retina | 93
Classification of DR
Grade Features
No DR No abnormality
Mild NPDR Microaneurysm a only
Moderate NPDR More than just microaneurysms and less than severe NPDR
Severe No signs of PDR
NPDR Presence of any one of the following
4 quadrants of intra retinal hemorrhages
(> 20/quadi ant)
Venous beading in >2 quadrants
IRMA in >1 quadrant
PDR Presence of neovascularization
Presence of preretinal or vitreous hemorrhage
Follow up for mild/moderate NPDR

Treatment of severe NPDR: Strict follow-up to watch for changes of PDR. Consider
PRP in high risk cases
Treatment of PDR: PRP- Pan-retinal photocoagulation.
Pars plana vitrectomy: when RD or persistent vitreous haemorrhage
Few Studies Done in DR:
• DRS: Diabetic retinopathy study.
• ETDRS: Early treatment diabetic retinopathy study.
• DRVS: Diabetic retinopathy vitrectomy study
Fig.5.12: M
ICRO-ANEURYSMS Fig.5.13: NON-PROLIFERATIVE RETINOPATHY
94 | Ophthalmology
Fig.5.14: Fig.5.15:
Fig.5.16: PROLIFERATIVE DR Fig.5.17: PAN-RETINAL PHOTOCOAGULATION
Cystoid Macular Edema (CME):

Accumulation of fluid in the outer plexiform (Henle’s) and inner nuclear layers of the
retina, centred about the foveola
Etiology of CME Treatment
Ischemia CRVO, Diabetic retinopathy Anti VEGF intravitreally /Laser photocoagulation
Inflammation uveitis, post operative CME) Steroids
Drugs Epinephrine in aphakia, latanoprost Stop drugs

and betaxolol
Mechanical vitreous traction on macula Vitrectomy
Heredity retinitis pigmentosa, inherited Systemic carbonic anhydrase inhibitors

CME
CSMO (Clinically significant macular oedema) IN DIABETIC RETINOPATHY

It is detected on clinical examination as defined in the ETDRS
Retina | 95
Retinal thickening within 500 µm of the centre of the macula

Exudates within 500 µm of the centre of the macula, if associated with retinal thickening
Retinal thickening one disc area (1500 µm) or larger, any part of which is within one disc diameter of the
centre of the macula
Treatment: FA → Laser photocoagulation/anti VEGF injections intravitreally
Fig.5.18: CME on OCT
Fig.5.19: Flower petal appearance on Angiography

96 | Ophthalmology
Concept 5.6: Hypertensive Retinopathy
Learning objectives
• To learn grading and signs of Hypertensive retinopathy
Time Required
1st reading 15 mins
nd
2 look 5 mins
Keith –Wagner Grading:

Grade I Mild-to-Moderate generalised arteriolar attenuation
Grade II • Moderate-to-Marked narrowing of arterioles.
• Generalised and focal narrowing of arterioles.
• Salus sign (deflection at AV crossing)
Grade III • Bonnet sign (banking of veins), Gunn’s sign (tapering of veins on either side of the
crossing).
• Haemorrhages(superficial or flame shaped).
• Cotton wool patches.
• Retinal edema
Grade IV Grade III changes + silver wiring of arterioles + disc swelling
(Papilledema) – Macular star appearance
Other Ocular Manifestations of Hypertension:
• Subconjunctival haemorrhage.
• Retinal vein occlusion
• Elschnig’s spots- ischemic choroidal infarcts.
• Macroaneurysms.
• Ischemic optic neuropathy [Non-Arteritic AION].
• Ocular motor nerve palsies
Fig.5.20: Macular star appearance in Grade 4

Retina | 97
Concept 5.7: Retinal vein occlusions
Learning objectives
• To learn and identify features of Retinal Vein Occlusions
Time Required
1st reading 20 mins
nd
2 look 5 mins
Predisposing factors:
• Increasing age – 6th/7th decade.
• Unilateral.
• Systemic hypertension, Diabetic mellitus, Arteriosclerosis.
• Blood dyscrasias – Hyperviscosity
• Raised IOP.
• Hypermetropia
• Periphlebitis – Sarcoidosis, Behcet’s disease.
• Use of OCPs
Clinical features:
• Decreased visual acuity.
• Loss of part of the visual field.
• Dilated and tortuous veins, flame- shaped and deep haemorrhages. Retinal edema,
cotton-wool spots.
Complications:
• CME
• Neovascularisation leads to vitreous haemorrhage and TRD
Fig.5.21: Central Retinal Vein Occlusion Fig.5.22: Branch Vein Occlusion

98 | Ophthalmology
Non-ischemic CRVO Ischemic CRVO

Frequency 75-80% 20-25%
Visual acuity Better than 6/60 Worse than 6/60
RAPD Slight or nil Marked
Visual field defect Rare Common
Fundus Less hemorrhages and cotton wool spots Extensive hemorrhages and cotton wool spots
FFA Good perfusion Non-perfusion > 10DD
ERG Normal Reduced b-wave amplitude
Prognosis 50%, 6/60 or better 60% Rubeosis or MVG
Splashed sauce appearance: Multiple flame-shaped haemorrhages around disc in
ischemic CRVO
100-day glaucoma: Neovascular glaucoma in ischemic CRVO is seen to occur after
100 days of occlusion hence the name.
Treatment: CRVO – PRP, BRVO - Scatter laser photocoagulation
Retina | 99
Concept 5.8: Retinal artery occlusions
Learning objectives
• To learn and identify features of Retinal artery Occlusions
Time Required
1st reading 20 mins
nd
2 look 5 mins
Central Retinal Artery Occlusion: Due to emboli from atherosclerosis from heart or
carotid artery
Fig.5.23:
Clinical features:
• Acute and profound, PAINLESS loss of vision.
• White cloudy/milky white retina due to intracellular edema- Cherry-red spot
• Marcus - Gunn pupil
• Segmentation of blood column in venules and arterioles: Cattle –Track Appearance
of blood flow.
Treatment: Ocular emergency:

• Lower IOP - Firm ocular massage/Intravenous acetazolamide –500 mg.
• Inhalation of carbogen i.e. a mixture of 5% CO2 and 95% of O2.
• Anterior chamber paracentesis.
• Alteplase or tPA can be given.
Different Diagnosis oF CHERRY-RED
SPOT:
1. CRAO
2. Tay sachs disease (GM1 Gangliosidosis –
type I)
3. Niemann-pick disease.
4. GM1 Gangliosidosis – type I
5. Sialidosis
6. Berlins edema.
Fig.5.24: C
RAO with cilio-retinal artery
7. Gaucher disease
sparing (Central retina is spared)
100 | Ophthalmology
Concept 5.9: Retinal Degenerations
Learning objectives
• To learn names and features of various retinal degenerations
• To learn about features of Age-Related Macular Degeneration
Time Required
st
1 reading 25 mins
2nd look 10 mins
Predisposing Vitreo-Retinal Degenerations to Retinal Detachment

Latttice Degenerations Common in high myopes
Circumferentially oriented, spindle- shaped areas of
retinal thinning
May be associated with holes or retinal tears
Snail-track Denegerations
Acquired retinoschisis
White with pressure
White without pressure
Myopic Maculopathy degeneration

Annular crescent / temporal crescent surrounding optic disc
Lacquer cracks- can lead to choroidal neovascularisation. These are cracks in the bruch’s membrane –can
have holes/break
Rhegmatogenous RD
Fuchs spots/Fuch’s flecks: Haemorrhage and pigment accumulation in the macula.
Chorioretinal atrophy at posterior pole
Macular holes
Posterior staphyloma.
Age-Related Macular Degeneration (ARMD)

It is a degenerative disorder affecting the macula in old age
Retina | 101
Types of ARMD
Non-exudative (Dry) Exudative (Wet)
Most common – 90% of cases 10% of the cases
Gradual, mild to moderate impairment of vision over Visual impairment is within days and may lead to
months or years loss of all central vision
Drusens Choroidal neovascularisation

RPE atrophy Leakage of fluid
RPE detachment. RPE detachment
No effective treatment. As below

• Low visual aids
• Antioxidants
• Vitamin E (400 IU)
• Vitamin C (500 mg)
• Lutein (10 mg).
• Zeaxanthin (2 mg).
• Zinc (25–80 mg)
• Copper (2 mg)
Fig.5.25: Drusens in Dry ARMD Fig.5.26:
Treatment of Wet ARMD

Extrafoveal more than 200 µm from centre of FAZ (foveal Laser photocoagulation
avascular zone)
Juxtafoveal Not involving centre but closer than 200 µm. Laser photocoagulation/ PDT
(Photodynamic therapy)
Subfoveal Involving centre of FAZ PDT
Anti-VEGF agents: All CNV subtypes respond to anti-VEGF therapy, but benefit is only
likely in the presence of active disease They inhibit the growth of new blood vessels.
They are:
Aflibercept (Eylea), Ranibizumab (Lucentis), Bevacizumab (Avastin), Pegaptanib
(Macugen)
102 | Ophthalmology
PDT – It relies on photochemical injury to the vessel wall and selective damage to the
target tissue while sparing the adjacent normal tissue.
PDT requires two components:
• Photo sensitizer –Commonly used is Benzoporphyrin derivative – Verteporfin.
• A specific laser light corresponding to the absorption peak of the dye (690nm)
Choroidal Neovascularisation:
Proliferation of fibrovascular tissue from choriocapillaris through defects in Bruch’s
membrane into sub- RPE space and later into the sub –retinal space.
Cuses of Choroidal Neovascularisation
Wet ARMD
POHS – Presumed Ocular Hstoplasmosis syndrome.
Severe myopia.
Angioid streaks
Choroidal rupture
Inappropriate laser photocoagulation.
Optic disc drusen.
Retina | 103
Concept 5.10: Retinal Dystrophy
Learning objectives
• To learn names and corresponding layers of various retinal dystrophies
• To learn about features of Retinitis pigmentosa
• To learn about Electroretinogram and Elecrooculogram
Time Required
1st reading 40 mins
nd
2 look 15 mins
Retinitis Pigmentosa:
It’s a photoreceptor dystrophy with damage to rod system is predominant
Sporadic Most common

AD Most common mode of inheritance
Best prognosis
X-linked recessive Worst prognosis and least common
Clinical features:
• Nyctalopia/night blindness-due to impaired rod function.
• Impaired dark adaptation.
• Tunnel vision in later stages
Classical Triad of signs:

• Arteriolar attenuation.
• Retinal bone-spicule pigmentation: These changes are perivascular
• Pale, waxy disc (consecutive optic atrophy)
Fig.5.27:
Investigations:
Subnormal amplitude of ERG mainly scotopic. EOG is also subnormal in later stages
Perimetry: In initial stage of the disease there is ring scotoma due to involvement of the
midperipheral retina whereas in the late stage patient has tubular vision.
104 | Ophthalmology
Treatment: No effective treatment
Vitamin A and Docosahexonoic acid can be given
Atypical Retinitis Pigmentosa:

• Retinitis punctata albescens: White dots instead of bony spicules.
• Sector RP: One sector of the retina is involved
• Pericentric RP: Disease starts from the centre
• Retinitis pigmentosa sine pigmento: Salt and pepper picture instead of bony spicule
Ocular associations of RP
CME: Cystoid macular edema
Open angle glaucoma
PSC: Posterior subcapsular cataract
Keratoconus
Myopia
Disc drusen
Systemic associations of RP
Ushers syndrome –RP with deafness. It is the most common
Refsum’s syndrome
Bassen-kornzweig syndrome
Kearns- sayre syndrome – associated with ocular myopathy and heart defects
Bardet-Biedl syndrome − mental handicap, polydactyly.
Laurence − Moon syndrome − features of Bardet- Biedl syndrome with spastic paraplegia
Cockaynes syndrome.
Friedreich’s ataxia
Best vitelliform and Stargardt dystrophy

Best vitelliform disease Stargardt disease
AD AR
Signs > Symptoms Symptoms > Signs
accumulation of lipofuscin within the RPE- egg accumulation of lipofuscin within the RPE-
yolk appearance beaten-bronze aapearence
Later stages – scrambled egg appearance
FA shows corresponding hypofluorescence due to FA: ‘dark choroid’ due to masking
masking. of background choroidal fluorescence
Autofluoroscence - hyperautofluorescent lesion in Autofluoroscence - hyperautofluorescent flecks
center of retina
EOG is severely subnormal during all stages EOG is commonly subnormal
Retina | 105
Treatment: No effective treatment
Fig.5.28: BEST DISEASE –egg yolk stage Fig.5.29: BEST DISEASE –scrambled egg stage
Fig.5.30: AUTOFLUOROSCENCE in Stargardts showing hyperfluoroscence
Angioid Streaks
These are crack-like dehiscences in the collagenous and elastic portions of the bruch’s
membrane with secondary changes in RPE and choriocapillaris.
Fig.5.31:
106 | Ophthalmology
It can be idiopathic or is associated with:
Pseudoxanthoma elasticum.
Paget’s disease.
Ehler-Danlos syndrome
Sickle cell anemia
Incontinenta pigmenti
Congenital stationary night blindness (CSNB)

• With normal appearing fundus
• CSNB with abnormal looking fundus
Fundus albipunctatus
Oguchi’s disease - Patients demonstrate Mizuo’s phenomenon (retina exhibits
yellow sheen with light exposure, which disappears with dark adaptation)
Differential Diagnosis of Night Blindness:

1. Retinitis Pigmentosa
2. Xerophthalmia.
3. Congenital stationary night blindness
5. High myopia.
6. Advanced case of Primary open angle glaucoma
Bull’s Eye Maculopathy:

Central foveolar hyperpigmentation surrounded by depigmented zone and encircled by
a hyperpigmented ring. There is moderate reduction in VA- 6/18 to 6/24.
Causes:
• Chloroquine toxicity
• Cone dystrophy
• Battens disease/Batten-Mayo syndrome: It is a cerbromacular degeneration
Electrophysiological Tests:
Electroretinogram[ERG] It is the record of the action potential produced by the retina when it
is stimulated by the light of adequate intensity. It is elicited both in
photopic and scotopic state
A wave- due to rods/cones
B wave- due to bipolar/muller cells
c- due to RPE
Electrooculogram[EOG It measures the standing action potential between the cornea
and the back of the eye. It reflects the activity of the RPE and the
photoreceptors [eg BEST”S Ds].
Visual Evoked Potential When light falls on the retina, the series of nerve impulses generated
and passed into the visual cortex is measured by VEP. It indicates
activity from ganglion cell layer to the visual cortex.
Retina | 107
Concept 5.11: Retinopathy of Prematurity
Learning objectives
• To learn risk factors, staging and treatment of ROP
Time Required
1st reading 30 mins
nd
2 look 15 mins
It is a proliferative retinopathy which affects pre-term infants exposed to high ambient

oxygen concentrations. Incompletely vascularized temporal retina is particularly
susceptible to oxygen damage.
Risk factors:
• Prematurity: Gestational age <32 weeks (most important)
• Birth weight <1.5kg.
• Oxygen therapy: Excessive oxygen use
Pathogenesis:
Excessive free radicals
↓
Inhibit spindle cell migration
↓
Produces angiogenic factors
↓
ROP
Stage I Demarcation line
Stage III Ridge formation
Stage III Ridge with extra retinal fibrovascular proliferation
Stage IV Sub-total Tractional Retinal Detachment
Stage V Total retinal detachment.
108 | Ophthalmology
Vascularized retina Isolated neovascular tufts
Demarcation line Ridge
Severe
extraretinal Detached retina
fibrovascular
proliferation
Fig.5.32:
Fig.5.33: Zones of ROP

Retina | 109
Screening of ROP:
The most useful time is between 32 weeks and 36 weeks post conception. After 36
weeks, ROP rarely develops.
Before 28 weeks – screening after 2-3 weeks of birth
After 28 weeks – screening after 4 weeks of birth
Early Treatment of Retinopathy of Prematurity (ETROP)
Classification:
Type 1 ROP should be treated:
Zone I any stage of ROP with plus disease Zone I Stage 3 ROP with or without plus
disease Zone II Stage 2 or 3 ROP with plus disease
Type 2 should be observed, and only undergo treatment if it progresses

to type I or threshold disease:
Zone II Stage 1 or 2 ROP without plus disease
Zone II Stage 3 ROP without plus disease
ROP is treated immediately if disease is threshold disease which is:

Stage –III disease
involving Zone 1 and 2 Location
-5 contiguous clock hours or 8 noncontiguous clock hours with plus Disease.
(Plus Disease involves arteriolar and venous dilatation)
Treatment of ROP:
• Ablation of avascular immature retina by either cryotherapy or laser photocoagulation.
• Vitamin – E therapy – Its antioxidant role helps in prevention of the ROP.
• If Retinal detachment present → Vitreoretinal surgery
110 | Ophthalmology
Worksheet

Retina | 111
• Identify the cell marked _____________
• This is seen after which surgery? _______________________

112 | Ophthalmology
• Identify the sign and stage of diabetic retinopathy? ____________________
• Fill in for severe NPDR

Grade Features
No DR No abnormality
Mild NPDR Microaneurysm a only
Moderate NPDR More than just microaneurysms and less than severe NPDR
Severe
NPDR
PDR Presence of neovascularization

Presence of preretinal or vitreous hemorrhage
• What is the treatment of this if its due to diabetic retinopathy? _________________

Retina | 113
• Fill in the blank spaces
Non-ischemic CRVO Ischemic CRVO
Frequency 75-80% 20-25%
Visual acuity Better than 6/60 Worse than 6/60
RAPD
Visual field defect Rare Common
Fundus
FFA Good perfusion Non-perfusion > 10DD
ERG Normal Reduced b-wave amplitude
Prognosis 50%, 6/60 or better 60% Rubeosis or MVG
• Write some D/D of cherry red spot
Identify the deposit and diagnosis- _______________

114 | Ophthalmology
Classical Triad of signs of this are:
- _______________ , ______________ , ______________
Identify the layer having this pathology - _______________
Fill in the remaining stages

Stage I
Stage III
Stage III Ridge with extra retinal fibrovascular proliferation
Stage IV Sub-total Tractional Retinal Detachment
Stage V
Retina | 115
Fill in the remaining points
Early Treatment of Retinopathy of Prematurity (ETROP)
Classification:
Type 1 ROP should be treated:
Type 2 should be observed, and only undergo treatment if it progresses

to type I or threshold disease:
Zone II Stage 1 or 2 ROP without plus disease
Zone II Stage 3 ROP without plus disease
116 | Ophthalmology
EXTRA POINTS:
6 Neurophthalmology
CONCEPTS
Â Concept 6.1 Visual pathway and its lesions
Â Concept 6.2 Pupillary reflex
Â Concept 6.3 Optic neuritis
Â Concept 6.4 Papilledema
Â Concept 6.5 Optic atrophy
Â Concept 6.6 S
upranuclear Disorder of Eye
Movement
Â Concept 6.7 Nystagmus

118 | Ophthalmology
Concept 6.1: Visual pathway and its lesions
Learning objectives
• To learn about visual pathway and identify various visual field defects in lesion of
structures involved in it
Time Required
st
1 reading 40 mins
nd
2 look 15 mins
Fields of vision
Nasal
hemiretinas
Total blindness
Temporal of pslateral eye
hemiretinas
Bitemporal
Optic heteronymous
tract hemianopsia
Loop of Ipsilateral nasal

Archambault hemianopsia
(Meyer) Contralateral
homonymous
hemianopsia
Contralateral
lower quadrantie
anopsia
Contralateral
Optic
upper quadrantie
radiation anopsia
Contralateral
homonymous
Cuneus Lingual hemianopia
Callcarine with macular sparing
gyrus
sulcus
Fig.6.1:
Neurophthalmology | 119
Lesion Visual field defects

Optic Nerve Ipsilateral blindness
Chiasma Bitemporal hemianopia. It is a heteronymous hemianopia
Anterior junction syndrome (Junctional will lead to ipsilateral central scotoma and contralateral
scotoma of Traquair: Lesion at the junction of superotemporal quandrantopia.
the chiasma and the optic nerve)
Optic Tract Incongruous homonymous hemianopia
Wernicke’s hemianopic pupil
Optic atrophy
Lateral geniculate body (Pupillary reflex Homonymous key hole defects
normal)
Optic Radiations (Pupillary reflex normal) Congruous homonymous defects
• Lesions of Temporal Radiations C/L homonymous Superior quadrantopia (Pie in sky)
• Lesions of Parietal Radiations C/L homonymous Inferior quadrantopia (Pie on the floor)
Occipital Cortex (Pupillary reflex normal)
• Occlusion of posterior cerebral artery Macula sparing congruous homonymous hemianopia
• Occlusion of middle cerebral artery Congruous homonymous macular defects
Chiasma lesions
Fig.6.2:
120 | Ophthalmology
Concept 6.2: Pupillary reflex
Learning objectives
• To learn about pupillary pathway and abnormal pupils
• To learn about sympathetic pathway and Horner syndrome
Time Required
1st reading 40 mins
nd
2 look 15 mins
Fig.6.3: LIGHT REFLEX/Pupillary/Parasympathetic pathway – afferent 2nd nerve, efferent 3rd nerve
Abnormal pupil reactions

Marcus Gunn Pupil Relative Afferent Pupillary Defect [RAPD]:In Retrobulbar neuritis.
TAPD Total Afferent Pupillary Defect: In Optic atrophy.
Argyl Robertson Pupil Light reflex absent but near reflex present.
Holmes-Adie Pupil Tonic pupil with slow response to light and near. Due to denervation of post –
ganglionic supply.
Horner’s Syndrome Due to disruption of sympathetic pathway. Characterised by ptosis, miosis (same
in dark conditions), enophthalmos. Pupillary reaction to both light and near are
normal. Heterochromia iridis in congenital cases.
Fig.6.4: RELATIVE AFFERENT PUPILLARY DEFECT (RAPD)

122 | Ophthalmology
Fig.6.5: ARGYLL –ROBERSTON PUPIL
Fig.6.6: HOLMES –ADIE PUPIL

Fig.6.7: S
ympathetic pathway – Central (from hypothalamus to C8-T2), Pre ganglionic – till superior cervical
ganglion, Post-ganglionic – to iris dilator muscle
Fig.6.8: HORNER’S SYNDROME

124 | Ophthalmology
Concept 6.3: Optic neuritis
Learning objectives
• To learn about parts of optic nerve
• To learn about various causes of optic neuritis
Time Required
st
1 reading 50 mins
2nd look 20 mins
Optic nerve
It is 3.5 cm to 5.5 cm long from optic disc to chiasma. It is divided into
intraocular (1 mm)
intraorbital (25-30mm)
intracanalicular (6-9 mm)
intracranial (10 mm)
Clinical Features of Optic Nerve Disease:

• Diminished visual acuity
• Visual field defects - Impaired central vision (most common field defect is central or
centrocecal scotoma) and defective contrast sensitivity.
• Diminished pupillary light reactions i.e. APD [Afferent Pupillary defect].
• Impairment of color vision
• Diminished light brightness sensitivity
• Near reflex is intact in unilateral optic nerve involvement
Bipolar cells 1st order neuron
Optic nerve 2nd order neuron (made up of Axons of ganglion cells, 1.2 million axons are there)
Lateral geniculate Body 3rd order neuron
OPTIC NEURITIS
Optic neuritis is an acute inflammatory optic nerve disease.
Fig.6.9:
It can be divided into:
Retrobulbar neuritis The fundus examination is normal as the affected part of the optic nerve is behind
the eye ball
Papillitis inflammation of optic nerve head
Neuroretinitis inflammation of optic nerve and nerve fibre layer of retina.
Etiology of optic neuritis:

Idiopathic
Ischemic Arteritic and non-arteritic AION
Viral infections Whooping cough, measles, mumps, varicella zoster.
Demyelinating disorders Multiple sclerosis, Devic’s disease
Metabolic/Nutritional deficiency Vitamin B1 deficiency, Vitamin B12 deficiency, Vitamin B2 deficiency,
Folic acid deficiency, Diabetes Mellitus
Hereditary Leber’s hereditary optic neuropathy
Infections Lyme’s disease, syphilis, cat scratch, cryptococcal meningitis in
AIDS, TB
Toxic amblyopia See later
Most common cause of optic neuritis is Multiple sclerosis
• Painful eye movements seen in upward and medial direction due to attachment of a
few fibres of superior rectus and medial rectus to the durameter of optic nerve.
• Uhthoff sign (worsening of symptoms with exercise or increase in body temperature)
and Pulfrich phenomenon (altered perception of moving objects).
• Visual evoked response shows reduced amplitude and delayed transmission time.
• Treatment - IV steroids 3 days IV methylprednisolone (1g/day) plus 11 days of oral
prednisolone (1mg/kg/day)
Lebers heredity optic neuritis

Maternal Mitochondrial DNA mutations
Clinical features:
Typically in males - third decade.
Initially unilateral visual loss, fellow eye involved within 2 months.
Bilateral optic atrophy
Pupillary reactions to light often remain fairly brisk
Signs:
Dise hyperemia and dilated capillaries (telangiectatic microangiopathy).
Vascular tortuosity.
Swelling of peripapillary nerve fibre layer
126 | Ophthalmology
Fig.6.10:
Treatment:
Prognosis is relatively poor with generally severe, bilateral and permanent visual loss.
• High–dose systemic steroids are used in some cases.
• Stop smoking and excessive drinking.
Anterior ischemic optic neuritis

It occurs due to infarction of the short posterior ciliary arteries. It is of two types-
arteritic and non-arteritic.
Arteritic AION Non-Arteritic AION
In patients of giant cell arteritis Unknown but the major risk factor is hypertension
Sudden loss of vision with associated headaches, Sudden painless loss of vision, mostly in morning
Amaurosis fugax
Visual acuity markedly reduced Slightly decreased visual acuity

Swollen optic disc. Sectoral or diffuse edema of the disc. Optic nerve
• Flame-shaped haemorrhages around the disc head is either pale or hyperaemic. Flame –shaped
haemorrhages around the disc.
Associated symptoms- Frontal or occipital
headache with scalp tenderness, jaw claudication
and polymyalgia rheumat- ica.
I/V steroids [Hydrocortisone] for 3-4 days alongwith Treatment:
oral prednisolone which is tapered gradually • To check for viscosity affecting factors like
fibrinogen and PCV which could be responsible
for the ischemia.
• Manage the BP.
• Manage the underlying disease.
• To stop smoking.
Fig.6.11: Arteritic ischemic optic neuritis Fig.6.12: Non - Arteritic ischemic optic neuritis
Pseudo - Foster- Kennedy Syndrome: in NAION

Foster- Kennedy Syndrome:
Ipsilateral optic atrophy with contralateral papilloedema. It occurs due to tumor in orbital
surface of frontal lobe, olfactory groove or pituitary body.
128 | Ophthalmology
Concept 6.4: Papilledema
Learning objectives
• To learn about stages of papilledema
• To learn about pseudotumour cerebri
Time Required
st
1 reading 20 mins
2nd look mins
Papilloedema
Papilledema is bilateral optic nerve head swelling secondary to raised intracranial
pressure
Increased CSF pressure
↓
Due to disturbance of pressure gradient across the lamina cribosa.
↓
Stasis of axoplasm in prelaminar area
↓
Axonal swelling
↓
Venous congestion
↓
Extra-cellular edema
Fig.6.13:
Stage Early Established Chronic Atrophic
Visual acuity (VA) VA normal • Transient visual VA impaired VA severely

Disturbances Constricted VF impaired
• VA normal or
impaired
• Enlarged blind
spot
Optic disc vascular • Hyperemia of • Venous tortuosity

changes margins and dilation
• Loss of • Peripapillary
spontaneous flame-shaped
venous hemorrhage
pulsation • Cotton wool spots
(absent in 20% • Hard exudates
of normal
individuals)
Optic disc Blurring of • Elevated disc “Champagne Secondary optic

mechanical changes margins (superior • Obliteration of cork” appearance atrophy
and inferior cup Optociliary
margin first) • Retinal/choroidal shunts
folds
Treatment: According to the cause
Pseudotumour Cerebri:
Also known as Benign Intracranial Hypertension
Risk factors Clinical features Investigations Treatment
Obesity. • Headache. • CT scan – No • Diet and lifestyle:

OCPs. • B/L disc edema neurological lesion. Weight loss.
Hypervitaminosis A. • U/L or B/L sixth • Increased CSF • Carbonic anhydrase
Tetracycline nerve palsy leads to pressure. inhibitors i.e.
diplopia. • Normal CSF Acetazolamide
Nalidixic acid.
• Transient visual composition.
Steroids
obscuration.
• Visual field defects:
Enlargement of
blind spot and later
constriction of visual
field.
130 | Ophthalmology
Concept 6.5: Optic atrophy
Learning objectives
• To learn about types of optic atrophy
• To learn about toxic amblyopia
Time Required
st
1 reading 20 mins
2nd look 5 mins
Optic Atrophy:
It is the end result of any pathological process that damages the axons coursing between
retinal ganglion cells and LGB
Primary optic atrophy Secondary optic Glaucomatous optic Consecutive optic
atrophy atrophy atrophy
Chalky white in color, Disc is dirty white in Pathologically - Pale waxy disc.
disc margins are clear colour, with blurred Cavernous optic atrophy
margins
Ex –Trauma Ex - papillitis or Ex -Retinitis pigmentosa

Toxins papilloedema
Tumours
Nutritional
Fig.6.14: PRIMARY OPTIC ATROPHY Fig.6.15: SECONDARY OPTIC ATROPHY

Fig.6.16: GLAUCOMA OPTIC ATROPHY Fig.6.17: CONSECUTIVE OPTIC ATROPHY
Toxic Amblyopia (Toxic Optic Neuropathy)

Refers to conditions in which optic nerve fibres are damaged by exogenous poisons.
Its mostly bilateral and clinically leads to retrobulbar neuritis
Causes:
• Tobacco- Cyanide acts as a toxic agent which causes degeneration of the ganglionic
cells of the macular area
• Ethambutol.
• Deficiency of Vitamins- Thiamine, B12
• Ethyl alcohol.
• Methyl alcohol- Methyl alcohol poisoning is more dangerous than ethyl alcohol because
it leads to direct damage of ganglion cells.
• Quinine.
• Chloroquine.
• Isoniazid.
• Digoxin.
• NSAIDs.
132 | Ophthalmology
Concept 6.6: Supranuclear Disorder of Eye Movement
Learning objectives
• To learn about features of Supranuclear eye Disorder
• To learn about Internuclear ophthalmoplegia and one and half syndrome
Time Required
st
1 reading 20 mins
2nd look 5 mins
Features are:
• Gaze palsies.
• Normal vestibulo-ocular reflexes.
• Absence of diplopia.
Horizontal Gaze Centre: It is located in pons, known as PPRF i.e. Pontine Parareticular
Formation. PPRF controls the lateral rectus of the same side whereas the medial rectus
of the opposite side is controlled by MLF [Medial Longitudinal Fasciculus].Lesion of MLF
leads to Internuclear Ophthalmoplegia
Internuclear Ophthalmoplegia (INO):

• Due to lesion of MLF i.e. Medial Longitudinal Fasciculus.
• Defective adduction of ipsilateral eye.
• Ataxic nystagmus of the contralateral abducting eye.
Right Medial Longitudinal

BASELINE
fasciculus lesion (MLF)
Right Internuclear
Ophthalmoplegia (INO)
Left abduction
nystagmus magnus
R L
Fig.6.18:
One And A Half Syndrome:
It occurs due to lesion of PPRF and MLF of the same side.
An alternative anatomical cause is a lesion of the abducens nucleus (VI) on one side
(resulting in a failure of abduction of the ipsilateral eye and adduction of the contralateral
eye = conjugate gaze palsy towards affected side), with interruption of the ipsilateral
medial longitudinal fasciculus after it has crossed the midline from its site of origin in the
contralateral abducens (VI) nucleus (resulting in a failure of adduction of the ipsilateral
eye).
Right one BASELINE

and half
syndrome
Left abduction nystagmus
Fig.6.19:
134 | Ophthalmology
Concept 6.7: Nystagmus
Learning objectives
• To learn about basic types of nystagmus
Time Required
1st reading 20 mins
nd
2 look 5 mins
It is the repetitive, involuntary to and fro oscillation of the eyes.
Clinical Types:
a. Pendular:
Velocity is equal in each direction.
b. Jerk:
Has slow drift and a fast phase.
c. Mixed:
Pendular in primary position and jerk in lateral gaze.
Causes:
a. Physiological:
Optokinetic nystagmus [OKN]. It consists of saccadic and pursuit movements.
Defect in OKN indicates parietal lobe lesion
End gaze
Vestibular – COWS (cold water induces nystagmus to opposite side)
b. Motor Imbalance:
Congenital nystagmus.
Spasmus nutans: It is associated with head nodding.
Latent nystagmus: In Infantile Esotropias
Ataxic nystagmus In Internuclear ophthalmoplegia
See-saw nystagmus: seen in patients with bitemporal hemianopia.
c. Ocular Nystagmus: Due to sensory deprivation.
Worksheet

136 | Ophthalmology
• Fill in the visual field defects _____________
Optic Radiations
• Lesions of Temporal Radiations--------
• Lesions of Parietal Radiations-----------
Occipital Cortex
• Occlusion of posterior cerebral artery-
• Occlusion of middle cerebral artery-
LIGHT REFLEX pathway – afferent ___ nerve, efferent ___ nerve

• Identify? _______________________
• A miotic pupil remains miotic in dark. Likely pathology? ____________________
• Sympathetic pathway –
Central _______________,
Pre ganglionic –_____________,
Post-ganglionic – ____________
• Write some features of the diagnosis
• Most common cause of optic neuritis is _________________
• Which are these 3 optic neuritis?

138 | Ophthalmology
Fill in the blank spaces
Primary optic atrophy Secondary optic Glaucomatous optic Consecutive optic
atrophy atrophy atrophy
Write some drugs causing toxic neuropathy

Where is the lesion?
BASELINE
Left abduction
nystagmus magnus
R L
140 | Ophthalmology
EXTRA POINTS:
7 Glaucoma
CONCEPTS
Â Concept 7.1 Definitions and Basic physiology
Â Concept 7.2 Investigations in glaucoma
Â Concept 7.3 Open angle glaucomas
Â Concept 7.4 Closed angle glaucomas
Â Concept 7.5 Treatment modalities in glaucoma
Â Concept 7.6 Developmental glaucomas
Â Concept 7.7 Secondary glaucomas

142 | Ophthalmology
Concept 7.1: Definitions and Basic physiology
Learning objectives
• To know about different terms in glaucoma
• To learn basic acqueous physiology
Time Required
1st reading 35 mins
nd
2 look 10 mins
Definition:
Glaucoma is a multifactorial optic neuropathy in which there is characteristic optic nerve
damage
Formation and Drainage of Aqueous Humour:

Rate of Formation: 2.3 µl/minute. Formation occurs through non-pigmented epithelial
cells by Pars plicata of ciliary body.
• By secretion.
• By ultrafiltration.
• By diffusion.
Glaucoma | 143
Aqueous humour consists of: Proteins, Na+, K+, Mg++, Urea and Glucose (Less than
blood plasma). Cl, lactate, pyruvate, Bicarbonate, Ascorbate (More than blood plasma).
Classification:
Primary Glaucoma
Glaucomas
Secondary Glaucoma
Developmental
Glaucoma
Primary Glaucoma
• Open angle Primary open angle Glaucoma IOP high, VF and OD changes+
Normal tension Glaucoma IOP Normal, VF and OD changes+
Ocular Hypertension IOP high, VF and OD Normal
• Closed angle Primary angle closure suspect IOP , VF and OD Normal

Primary angle closure IOP high, VF and OD Normal
Primary angle closure glaucoma IOP high, VF and OD changes+
Secondary glaucoma
Developmental glaucoma Primary congenital Glaucoma
Glaucoma associated with congenital

anomalies/ syndrome
IOP= Intraocular pressure, VF = Visual field, OD = optic disc
closed angle
ar tra
b e cut k b
me ecuta
tra hwor shw r
s ork
me
Fig.7.1:
144 | Ophthalmology
Concept 7.2: Investigations in glaucoma
Learning objectives
• To know about investigations done in glaucoma patient
Time Required
1st reading 60 mins
nd
2 look 25 mins
Gonioscopy:
Bimicroscopic examination of anterior chamber angle
Indirect Angle is examined by reflected light
Ex- Goldman, Zeiss, Posner, Susman
Direct Keoppe, Barkan, Thorpe and Swan Jacob goniolenses
Identification of Angle Structures on Gonioscopy (From Anterior Posterior):

• Schwalbe’s line
• Trabecular meshwork
• Scleral spur
• Ciliary body
• Root of Iris
Grading of anterior chamber angle (Based on Von-Herick i.e iris to corneal

angle separation):
Grade 4 Wide open angle (Iris to cornea angular separation of 35-45 degree)
Grade 3 Moderately open angle (Iris to cornea angular separation of 20-35 degree)
Grade 2 Moderated narrow angle (Iris to cornea angular separation of 20 degree)
Grade 1 Extremely narrow angle( Iris to cornea angular separation of 10 degree).
Grade 0 Closed angle (Iris to cornea angular separation of 0 degree).
(Image of Iridocorneal Angle)
Gonioscope
Gonioscope Mirror
Ocular
Lubricant Cornea
Iridocorneal
Angle
Lens Iris
Fig.7.2: Fig.7.3:
Glaucoma | 145
Normal Anterior chamber depth is 2-3 mm.
Deep anterior chamber: Myopics, Males.
Shallow anterior chamber: Hypermetropes, Old people, Females
Measurement of IOP:
• Goldmann
• Perkin
• Schiotz
• Malkalov
• Non contact
• Drager
Applanation Indentation
Applanation
• Tonopen and Dynamic
• Mak-Kay-Marg Indentation Contour
• PASCAL
Another type - Rebound tonometer is home based

Goldmann is gold standard tonometer
Tonography: It is used to measure the ‘facility of aqueous outflow’

Fig.7.4: GOLDMANN’S TONOMETER
Fig.7.5: PERKIN’S TONOMETER

146 | Ophthalmology
Fig.7.6: NON-CONTACT TONOMETER Fig.7.7: MALKALOV tonomete
Fig.7.9: TONOPEN
Fig.7.10: REBOUND TONOMETER
Fig.7.8: INDENTATION TONOMETER - Schiotz
Fig.7.11: PASCAL’S DYNAMIC CONTOUR

TONOMETER
Glaucoma | 147
Evaluation of Optic Nerve Head (ONH)
Visual Field Testing: [Perimetry]
Kinetic
• Lister
• Tangent Screen / Bjerrum Screen
Static
• Automated Perimetry
Octopus
Humphey field analyser
Combined kinetic and static: Goldmann Perimeter
Campimetry: Central visual field evaluation (Central 30°)

Fig.7.12: C
onfrontation visual Fig.7.13: Goldmann kinetic Perimeter Fig.7.14: H
umphrey automated
fiel exam perimetry static
148 | Ophthalmology
Provocative Tests:
For PACG For POAG
• Mydriatic test: Rise in IOP of >8mmHg after instillation of Water drinking test
tropicamide
• Dark Room/ prone provocative test: Patient in dark room for 60-90
min. If >8 mmHg in IOP; test is +ve
• Phenylephrine: Pilocarpine test: 10% phenylephrine and 2% pilo-

carpine – causes middilated pupil
Glaucoma | 149
Concept 7.3: Open angle glaucoma
Learning objectives
• To learn about different entities in open angle glaucoma
• To learn signs and management in open angle glaucomas
Time Required
st
1 reading 50 mins
2nd look 20 mins
Open Angle Glaucoma

Risk factors
• Heredity.
• Age - common elderly.
• Myopes
• Diabetics
• Hypertension
• Cigarette smoking.
• Thyrotoxicosis.
Rise in IOP is due to decreased outflow of aqueous humour from the trabecular meshwork
– This is due to thickening and sclerosis of trabeculae and absence of giant vacuoles in
the cells lining schlemn canal.
Clinical Features:
• Mild headache/Eye ache
• Difficulty in reading and close work
• Frequent change of presbyopic glasses
• Delayed dark adaptation
Signs:
IOP Changes:
Increase in IOP (The normal range of IOP is between 10- 21mmHg
Exaggeration of normal diurnal variation of IOP of >8 mmHg (Normal variation is around
5mmHg)
Optic Disc Changes in glaucoma:

• Assymmetry of cup.
• Flam shaped haemorrhages at disc – splinter hemorrages (in NTG)
• Retinal nerve fibre layer damage/atrophy
• Increase Cup: disc ratio of 0.7 to 0.9
• Thinning/Notching of neuroretinal rim
• Bayonetting sign : double bending of vessels
• Pulsation of retinal arterioles at disc margins
• Lamellar dot sign ie pores in lamina cribrosa
150 | Ophthalmology
OPTIC NERVE HEAD CHANGES IN GLAUCOMA
Fig.7.15: Normal optic nerve head Fig.7.16: Glaucomatous cupping
Fig.7.17: NASAL BENDING OF BLOOD VESSELS Fig.7.18: LAMINAR DOT SIGN

AND BAYONETTING SIGN
Visual Field Defects:
Fig.7.19: SPLINTER HEMORRAGE Fig.7.20: Normal retinal fibres

Glaucoma | 151
Fig.7.21: VISUAL FIELD DEFECTS in Glaucoma
• Isopter contraction: Earliest but non specific visual field defect. Mild constriction of
central and peripheral field.
• Paracentral scotoma: Small ring shaped sotoma which happens to be either above
or below the blind spot in bjerrum’s area. Earliest clinically significant field defect.
152 | Ophthalmology
• Siedel’s scotoma: It is a sickle shaped scotoma formed by paracentral joining of
the blind spot.
• Bjerrum’s or Arcuate scotoma: Extension of scotoma in the area either above or
below the fixation point.
• Double arcuate or ring scotoma: When two arcuate scotomas join together, it is
called double arcuate scotoma.
• Roenne’s central nasal step: Two arcuate scotomas run in different arcs and meet
to form a sharp right angled defect
Temporal visual field is last to be affected in glaucoma
Normal Tension Glaucoma - Normal IOP. Disc Changes. Field defects

Ocular Hypertension -IOP > 21mmHg, No disc change, No field defects
Treatment of POAG and NTG – Medical management→ Laser trabeculoplasty→

Surgery
Glaucoma | 153
Concept 7.4: Closed angle glaucoma
Learning objectives
• To learn about different entities in closed angle glaucoma
• To learn signs and management in closed angle glaucomas
Time Required
st
1 reading 30 mins
2nd look 10 mins
Angle Closure Glaucoma

• Sex - Females are more prone. Female: Male- 4:1.
• Family history - Positive.
Predisposing anatomical Risk Factors:

• Hypermetropic eyes with shallow anterior chamber.
• Iris - Lens diaphragm placed anteriorly.
• Plateau iris configuration
• Large lens
• Small corneal diameter.
PACS and PAC

The patient is asymptomatic but sometimes can complain of halos around the lights and
transient haziness of the vision. This happens when some part of the angle closes when
the pupil is mid dilated and then reopens. Only during the closure, the patient complains
of such symptoms. Otherwise the eye is white and quiet.
PACG
Characterized by all the features of open angle glaucoma i.e. IOP changes, fundus
changes and field defects, but the angle is closed.
Treatment of angle closure – Laser peripheral iridotomy→ Medical management →
Surgery
Acute congestive/acute angle closure glaucoma:
Dim light or pupil mid dilating precipitate the pupil block and lead to high rise in IOP.
Features
• Whole 360 degree angle is closed.
• Patient suffers from severe pain associated with nausea and vomiting.
• The IOP is in the range of 60 mmHg (40-70 mm Hg).
• Coloured halos due to corneal edema
• Severely congested eye associated with lid oedema.
• Shallow AC.
• Closed angle
• Vertically oval semidilated pupil - non reactive to light
154 | Ophthalmology
• Field defects are not prominent in this stage
• Vogt’s Triad:
• Pigment dispersion on the corneal endothelium
• Sector iris atrophy
• Glaucomaflecken
Definitive treatment of choice is surgery. Laser peripheral iridotomy (Nd-Yag)
angle open to
trabecular meshwork
tra
b
me ecuta
shw r
ork
Fig.7.22:
Before going on for surgical procedures, it is important to control the raised IOP. IV
mannitol or IV acetazolamide is used for this purpose. Once the IOP is down, laser/
surgical procedure is performed
Absolute glaucoma: It’s a painful blind eye. The eye is stony hard. Cyclophotocoagulation
is done to decrease IOP.
Glaucoma | 155
Concept 7.5: Treatment modalities in glaucoma
Learning objectives
• To learn about different treatment options in glaucoma
• To know major side effects of glaucoma medications
Time Required
st
1 reading 60 mins
2nd look 25 mins
Medical therapy
Drugs Mechanism of action Side effects
beta blockers Decrease aqueous production Precipitation of bronchial asthma
Selective: Betaxolol. Arrhythmias
Non- selective: Timolol Dry eyes
Nasolacrimal duct blockage
Miotics: Pilocarpine Increase trabecular outflow Uveitis
Ciliary spasm
Myopia
Cataract
Iris cyst
Retinal detachment
Sympathomimetics: Decrease aqueous Allergic conjunctivitis
Non selective- Adrenaline, production Angle closure glaucoma
dipivefrine Increase uveoscleral outflow Adrenachrome deposition
Selective –Brimonidine, Aphakic cystoid macular edema
Apraclonidine Drowsiness
Lid retraction
Carbonic anhydrase inhibitors Decrease aqueous C/I in sulfa drug allergics.
Dorzolamide and Brinzolamide production Acetazolamide: Hypokalemia,
(Topical). Acetazolamide metabolic acidosis, kidney stones,
(Systemic). chronic renal failure.
Dorzolamide and Brinzolamide:
corneal decompensation.
PG analogues: Increase uveoscleral Uveitis
Latanoprost, Travoprost, outflow Iris hyperchromia
Bimatoprost Blephroconjunctivitis
Trichomegaly
Hyperosmotics: Dehydrates vitreous Decompensation in congestive heart
Mannitol, glycerol failure, pulmonary edema
156 | Ophthalmology
Fig.7.23: HYPERPIGMENTED IRIS BY PROSTAGLANDIN ANALOGUES
Fig.7.24: HYPERTRICHOSIS BY Fig.7.25: Lid retraction by alpha agonists

PROSTAGLANDIN ANALOGUES
Fig.7.26: BLACK CONJUCTIVAL DEPOSIT BY EPINEPHRINE
Newer Glaucoma Agents:

Rhopressa (netarsudil 0.02% ophthalmic solution) – it inhibits rho-associated protein
kinase (ROCK)(increases drainage) and norepinephrine transporter (NET) (reduced
aqueous production)
Vyzulta (latanoprostene bunod 0.024% ophthalmic solution) - increasing aqueous humor
outflow through both the trabecular meshwork via nitric oxide, and the uveoscleral route
via latanoprost
Glaucoma | 157
Laser Therapy:
Argon Laser Trabeculoplasty: Laser burn to trabeculum at the junction of the
pigmented and non-pigmented parts – increases drainage of acqueous, more useful in
open angles with pigmented trabecular meshwork like pigmentary or pseudoexfoliation
glaucoma
Nd: YAG Laser iridotomy
Fig.7.27: LASER IRIDOTOMY
Surgical Treatment:
Trabeculectomy- Creation of new channel for aqueous outflow between the anterior
chamber and subtenon’s space
Bleb Diagram showing

flow of aqueous
through a normal
Ostium trabeculectomy
Flow of aqueous
Fig.7.28: TRABECULECTOMY
Antimetabolites in Trabeculectomy: It is used in cases in which there is high risk of

failure of the surgical procedure.
a. 5- FU.
b. Mitomycin C.
Artificial filtering Shunts/Setons

It is used in cases where conventional filtering procedure has failed or likely to fail.
These are plastic devices which create a communication between the anterior chamber
and subtenon’s space.
158 | Ophthalmology
• Express
• Molteno Implant.
• Schoket Implant.
• Ahmed Glaucoma Valve (AGV)
• Xen
• iStent
DRAINAGE IMPLANTS
Fig.7.29: AHMED VALVE Fig.7.30: AHMED VALVE
Fig.7.31: ISTENT
Fig.7.32: XEN implant (SUBCONJUNCTIVAL bypass)

Glaucoma | 159
Concept 7.6: Developmental glaucoma
Learning objectives
• To learn about features of congenital glaucoma
Time Required
1st reading 20 mins
nd
2 look 10 mins
Primary Congenital Glaucoma: Inheritance is- AR [Autosomal Recessive]

True Congenital.
Infantile Before 3 years of age.
Juvenile 3 - adolesence.
Developmental anomaly of angle of anterior chamber – Trabeculodysgenesis

Clinical features
Photophobia, blepharospasm, lacrimation
Buphthalmous
Corneal enlargement - (>13 mm) Haab’s Striae - break in DM, Corneal edema
Blue and thin sclera
Deep AC
Flat lens; which may sub-luxate.
IOP - Raised but neither marked nor acute.
Enlarged C:D ratio may be either due to neuronal loss or enlargement of scleral canal - reversible
Fig.7.33:
160 | Ophthalmology
Treatment:
• Goniotomy - It is the choice of surgery done for congenital glaucoma. In this procedure
cuts are given through the angle.
• Trabeculotomy - It is the procedure to cut open the schlemn canal. It is done if
corneal haze is there and angle not visualised
• Combined trabeculotomy and trabeculectomy
Secondary Congenital Glaucomas:

• With irido-corneal dysgenesis: Axenfeld’s anomaly, Riegers anomaly, Peter’s anomaly
• With Aniridia.
• Associated with ectopia-lentis syndromes
• Nanophthalmos.
• Naevus of ota
• Lowe’s syndrome.
• Phacomatosis: Sturge - Weber syndrome, Von-Recklinghausen’s Disease.
Glaucoma | 161
Concept 7.7: Secondary glaucomas
Learning objectives
• To learn about features of congenital glaucoma
Time Required
1st reading 30 mins
nd
2 look 15 mins
Lens - Induced Glaucoma:

Phacomorphic Glaucoma Intumescent lens –swollen lens block meshwork
Phacotopic glaucoma Subluxation or dislocation of lens.
Phacolytic Glaucoma Morgagnian cataractous lens → Leakage of lens protein through
intact capsule → Clogging of trabecular meshwork by lens
proteins and macrophages.
Lens Particle Glaucoma/Phacotoxic Rupture of lens capsule → Lens particle in aqueous humour →
Glaucoma Clogging of trabecular meshwork.
Inflammatory Glaucoma:
Due to Uveitis:
Secondary ACG with pupil Secondary ACG without pupil Secondary OAG
block block
Due to posterior synechiae. Due to anterior synechiae. Inflammatory cells blocking
meshwork
Pigmentary Glaucoma:
• In pigment dispersion syndrome.
• Pigments block the trabecular meshwork, iris transillumination, Krukenburg spindles
• Treatment- On lines of POAG.
Pseudo-Exfoliative Glaucoma - (Glaucoma Capsulare):

• Due to deposition of grey dandruff- like material in the trabecular meshwork.
• Treatment - On lines of POAG.
NVG- Neovascular Glaucoma:

Associated with neovascularisation of iris (Rubeosis iridis).
Causes:
• DR.
• CRVO.
• Eales disease.
• Sickle - Cell retinopathy.
162 | Ophthalmology
Treatment - Panretinal photocoagulation with Artifical shunt operation.
Steroid - Induced Glaucoma:

It occurs due to accumulation of mucopolysaccharides in the trabecular meshwork.
Traumatic Glaucoma:
Blunt injury-
• Angle Recession Glaucoma
• Inflammatory Glaucoma
• Due to intra-ocular haemorrhage:
Red cell Glaucoma Due to RBCs.
Haemolytic Glaucoma Due to macrophages laden with RBCs
Ghost cell Glaucoma In vitreous haemorrhage.
Hemosiderotic Glaucoma Due to iron from phagocytosed haemoglobin
Ciliary Block Glaucoma (Malignant Glaucoma)

Increased IOP with shallow or absent anterior chamber. It occurs due to sequestration of
aqueous humour into the vitreous cavity. It can be seen after trabeculectomy or cataract
surgery
Glaucoma associated with iridocorneal endothelial syndromes: It’s a

proliferative endotheliopathy
The disease has three forms:
Progressive Iris Atrophy There is stromal atrophy and hole formation in the iris.
Cogan-Rhese syndrome It is characterized by diffuse naevus and pedunculated
nodules in the iris.
Chandler’s syndrome Corneal changes are more prominent leading to corneal
edema.
Fig.7.34: HYPHEMA Fig.7.35: PSEUDOEXFOLIATION GLAUCOMA

Glaucoma | 163
Fig.7.36: PIGMENTARY GLAUCOMA (IRIS ILLUMINATION)
Cornea
Ciliary Body
Aqueous
Lens
Vitreous
Aqueous
Fig.7.37: AQUEOUS MISDIRECTION SYNDROME/ MALIGNANT GLAUCOMA
Fig.7.38: NEOVASCULARISATION INDUCED

164 | Ophthalmology
Worksheet

Glaucoma | 165
Primary Glaucoma
• Open angle ____________________ IOP high, VF and OD changes+
Normal tension Glaucoma _____________________
Ocular Hypertension IOP high, VF and OD Normal
• Closed angle ____________________ IOP , VF and OD Normal

_____________________ IOP high, VF and OD Normal
Primary angle closure glaucoma IOP high, VF and OD changes+
Fill in the Tonometers and principles
Applanation Indentation
Applanation
and
Indentation
• PASCAL
• __________ tonometer is home based
• Which laser is used to do this? _______________________

166 | Ophthalmology
• Which drug can cause this? _______________________
• Earliest clinically significant field defect in glaucoma? ____________________

• This sign is seen in which glaucoma?
• Which implant is this?

Glaucoma | 167
• Identify the striae
Write some features of congenital glaucoma
What is this sign?
Fill in
Red cell Glaucoma
Haemolytic Glaucoma
Ghost cell Glaucoma
Hemosiderotic Glaucoma
168 | Ophthalmology
EXTRA POINTS:
8 Orbit
CONCEPTS
Â Concept 8.1 Orbit Anatomy
Â Concept 8.2 Orbital Fissures
Â Concept 8.3 Blow out Fracture of Orbit
Â Concept 8.4 Proptosis
Â Concept 8.5 Dysthyroid Ophthalmopathy
Â Concept 8.6 Developmental Glaucomas
Â Concept 8.7 Orbital Cellulitis
Â Concept 8.8 Retinoblastoma

170 | Ophthalmology
Concept 8.1: Orbit anatomy
Learning objectives
• To know about different bones making orbital walls
Time Required
1st reading 20 mins
nd
2 look 5 mins
Bony orbits are quadrangular, truncated pyramids with volume of 30cc
Fig.8.1:
(a) Simplifed geometry of the orbits (b) The orbits from above
Medial
wall
Lateral
Lateral wall wall
Medial
wall
Floor
Fig.8.2:
Orbital walls and bones

Medial wall Thinnest medial wall is formed by:
• frontal process of maxilla,
• lacrimal bone,
• orbital cribiform plate of ethmoid body of sphenoid
Floor • Orbital surface of maxillary bone
• orbital surface of zygomatic bone
• palatine bone
It is commonly involved in blow-out fracture
Lateral wall • Zygomatic bone
• greater wing of sphenoid
Superior wall (roof) • Orbital plate of frontal bone
• lesser wing of sphenoid
Orbit | 171
Concept 8.2: Orbital fissures
Learning objectives
• To know about different fissures in orbit and relates syndromes
Time Required
1st reading 30 mins
nd
2 look 10 mins
Inferior orbital fissure: Between floor and lateral wall

Superior orbital fissure: It is at orbital apex, lateral to optic foramen. Between 2
wings of sphenoid
Optic canal/Optic foramen: Formed by lesser wing of sphenoid at orbital apex
Fig.8.3: Structures passing through superior orbital fissure and inferior orbital fissure
172 | Ophthalmology
Superior orbital fissure Syndrome
It is also known as Rochen-Duvigneaud syndrome: is a collection of symptoms caused
by compression of structures just anterior to the orbital apex. Cranial nerves passing
through superior fissure: IIIrd, IVth, V-1, VIth.
Clinical features:
• Onset is slow
• Proptosis (ptosis masked by proptosis)
• Dereased corneal sensation (due to V-1/ ophthalmic branch of trigeminal nerve).
• Ophthalmoplegia due to III,IV and VI nerves
Orbital Apex Syndrome: Orbital apex = superior orbital fissure syndrome+ involvement
of optic nerve
Orbit | 173
Concept 8.3: Blow out fracture of orbit
Learning objectives
• To know different Xray views and blow out fracture
Time Required
1st reading 20 mins
nd
2 look 5 mins
Blow-Out Fracture:
It is the fracture of orbital floor which typically occurs by a sudden increase in the orbital
pressure by a striking object > 5 cm in diameter such as a fist or tennis ball.
Two types:
• Pure blow-out fracture -Does not involve the orbital rim.
• Impure blow-out fracture - Involves the rim
Fig.8.4: Tear-drop sign
Clinical Features:
• Ecchymosis
• Subcutaneous emphysema: It occurs only if medial wall is also fractured.
• Enophthalmos.
• Infraorbital nerve anesthesia: It leads to decreased sensation on the affected cheek.
• Diplopia.
• Tear drop sign
Treatment:
• Conservatively by antibiotics and anti-inflammatory.
• Surgery: If no improvement in enophthalmos or diplopia then surgical intervention
is needed.
174 | Ophthalmology
X-Ray Views of Orbit:
NAME VIEWS STRUCTURES SEEN
Caldwell-luc view PA View Superior orbital fissure.
Occipitofrontal Greater and lesser wing of sphenoid. Ethmoid
and frontal sinus.
Floor of sella.
Town’s view AP view. Frontooccipital Dorsum sellae of sphenoid bone.
Inferior orbital fissure.
Water’s View Occipito-meatal. Maxillary sinus and floor of orbit. (in blow-out
fractures)
Rhese view For optic foramen.
Orbit | 175
Concept 8.4: Proptosis
Learning objectives
• To know about different tests and examples of proptosis
Time Required
1st reading 40 mins
nd
2 look 15 mins
Proptosis
Forward protrusion of normal- sized eyeball > 21 mm beyond the lateral orbital margin
or > 2mm protrusion compared to the other eye.
Measurement of proptosis:
Nafzigger test Inspection of the eyeballs from behind the patient looking over his
forehead.
Hertel’s Exophthalmometre To measure the distance between the apex of cornea and lateral orbital
margin.
Leude’s Exophthalmometre It is useful in children.
Topometre Useful for non-axial proptosis.
Simple plastic rule
Fig.8.5: Hertel’s EXOPHTHALMOMETRY Fig.8.6: Nafzigger test
Bilateral proptosis
Painful Cavernous sinus- thrombosis
Painless Grave’s disease
Pseudotumor
Lymphoma
Carotico-cavernous fistula
Leukemia
Metastasis
Developmental anomalies
176 | Ophthalmology
Unilateral proptosis
Painful Painless
Axial • Orbital haemorrhage. • Hemangioma
(central • Orbital cellulitis. • Meningioma
protusion) • Orbital mucocoele • Glioma
• Cavernous sinus thrombosis • Schwanoma
• Pseudotumor
Non-axial • Adenoid cystic carcinoma of lacrimal • Down and medial- Dermoid, lacrimal
(non-central gland gland tumors
protusion) • Nasopharyngeal carcinoma • Down and temporal - Frontoethmoid
• Metastasis mucocoele, lacrimal sac tumours
• Superior - Maxillary sinus tumor and
mucocele.
Pseudoproptosis:
The eye ball appears to be proptosed by actually there is no forward displacement.
• High axial myopia
• Shallow orbit due to craniofacial synostosis
• Retraction of the upper eyelids
• Enophthalmos of the other eye
Orbit | 177
Concept 8.5: Dysthyroid Ophthalmopathy
Learning objectives
• To know about signs of Thyroid eye disease
Time Required
1st reading 40 mins
nd
2 look 15 mins
May or may not be associated with hyperthyroidism. The patient may be euthyroid,
hyperthyroid or hypothyroid
Fig.8.7: Axial proptosis Fig.8.8: Superior limbic keratoconjunctivitis
Fig.8.9: Von Graefe’s Sign (Right Eye)
Normal Grave's ophthalmopaty
Retroorbital
fat
Retroorbital
muscles
Fig.8.10
178 | Ophthalmology
Eye Lid Signs Soft tissue Proptosis Restrictive thyroid optic

involvement myopathy neuropathy
The earliest and • Conjunctival It can be axial or Enlargement of Due to

most common injection. non- axial/ Extraocular muscle compression
symptom is upper • Chemosis. painful or painless/ without enlargement of optic nerve
eyelid retraction • Edema and unilateral or of tendon is the at orbital apex
(Dalrymple’s sign) fullness of bilateral hallmark by increased
Fibrosis of the eyelids. It is due to the intraorbital
inferior rectus deposition of pressure
• Superior limbic Kocher’s sign-
leads to rebound keratoconjunc- mucopolysachharides
Staring appearance
overaction of SR- tivitis of eyes. Sequence of
LPS complex involvement of
Stellwag’s muscle is: IR→ MR
sign- Decreased → SR→ LR.
frequency of
blinking. Patient presents with
diplopia and squint.
Treatment: Treatment: Treatment: Restrictive myopathy RAPD+
Surgical. • Tear substitutes If progressive and is diagnosed by Treatment
Medical: • For superior painful: Forced-Duction Test. -Intravenous
Topical limbic kerato- Systemic Steroids. steroids
guanethidine conjunctivitis Radiotherapy:
- depletes • Acetylcysteine For its anti-
sympathetic storage [It dissolves the inflammatory
sites. mucus]. effect.
Chemodeneravation Surgery:
of LPS by Decompression
botulinum toxin surgery
Orbit | 179
Concept 8.6: Orbital tumours
Learning objectives
• To know features of few important intraorbital tumours
Time Required
1st reading 40 mins
nd
2 look 15 mins
Lacrimal Gland Tumors:

Benign:
Most common tumor of lacrimal gland is Pleomorphic adenoma (mixed -cell tumor). Lacrimal
gland tumor cause non-axial proptosis i.e. down and medial displacement of eyeball.
Malignant:
• Adenoid cystic carcinoma : It is the most common malignant tumour, painful as there
is perineural invasion.
• Pleomorphic adenocarcinoma
• Mucoepidermoid carcinom
Fig.8.11: LACRIMAL GLAND TUMOUR
Optic nerve tumours

Optic Nerve Glioma Optic nerve sheath meningioma
Common in children, Female > males 3rd-5th decade of life, Female > males
Majority are of astrocytic origin Arises from meningothelial cells
25-50% patients have associated neurofibromatosis -2
neurofibromatosis -I
Nearly 75% of optic nerve gliomas arise from optic
chiasma and adjacent optic nerve while 25% arise
from orbital part of optic nerve.
Presentation is generally with visual loss, RAPD. Unilateral loss of vision (gradual in onset).
Slow growing tumor; proptosis is a late feature Optociliary shunt
Optic atrophy
Imaging - Fusiform enlargement of nerve along with Imaging - Tubular appearance of nerve along with
enlargement of optic canal. calcification
180 | Ophthalmology
For both-Treatment:
1. Observation.
2. Surgery.
3. Radiotherapy.
Fig.8.12: OPTIC NERVE GLIOMA Fig.8.13: OPTIC NERVE SHEATH

MENINGIOMA
Most common benign intraorbital tumor in children is – Dermoid

Most common primary malignant orbital tumor in children is – Rhabdomyosarcoma.
Most common cause of benign intraorbital tumour in adults- Cavernous hemangioma.
Most common primary malignant orbital tumor in adult is – Lymphoma
Fig.8.14: DERMOID CYST Fig.8.15: CAPILLARY HEMANGIOMA
Fig.8.16: RHABDOMYOSARCOMA Fig.8.17: CAVERNOUS HEMANGIOMA

Orbit | 181
Concept 8.7: Orbital cellulitis
Learning objectives
• To know features and classification of orbital cellulitis
Time Required
1st reading 30 mins
nd
2 look 10 mins
Orbital Cellulitis
It is the inflammation in the orbit behind the orbital septum.
Fig.8.18:
Etiology Clinical features Treatment

• Sinusitis- Most commonly • U/L painful proptosis- Abrupt • Admit the patient as it is an
after ethmoid sinusitis. onset. ocular emergency.
• From adjacent areas like • Restriction of extraocular • Parenteral antibiotics , both
Dacryocystitis movements aerobic and anaerobic with full
• Mid-facial infections and • Diplopia. coverage for gram positive and
dental infections. gram negative organisms.
• Post-traumatic- Any injury that
penetrates the orbital septum.
It occurs after 48-72hrs after
injury
• Post-surgical
182 | Ophthalmology
Chandler classification for orbital cellulitis
1 Inflammatory Eyelid edema and erythema
edema NormaJ extraocular movement
Normal visual acuity
II Orbital cellulitis Diffuse edema of orbital contents without discrete abscess
formation
III Subperiosteal Collection of purulent exudate3 beneath periosteum of lamina
abscess papyracea
Displacement of globe downward/laterally
IV Orbital abscess Purulent collection within orbit3
Proptosis
Chemosis
Ophthalmoplegia
Decreased vision
V Cavernous sinus Bilateral eye findings
thrombosis Prostration
Meningismus
Cavernous Sinus Thrombosis

Clinical features:
• Mastoid tenderness
• Cerebral symptoms with vomiting and rigor – meningismus
• Involvement of opposite eye –first being paralysis of sixth nerve, hence limited
abduction of the other eye.
• Decreased corneal and cheek sensation due to the involvement of the fifth nerve.
• Complete limitation of eye ball movement due to involvement of 3rd, 4th and 6th
nerves.
• Pupil dilated and fixed due to involvement of the third nerve.
• Disc edema
• Engorgement of retinal veins.
• Rapidly developing proptosis.
Orbit | 183
Ant. cerebral a.
Int. carotid a.
Ant. clinoid process

Subarachnoid
space
Optic
chiasma
Oculomotor (III) n.
Trochlear (IV) n.
Hypophysis
Oculomotor (V1) n.
Maxillary (V2) n.
Sphenold
sinus Pia
Arachnold
Dura
Abducens (VI) n.
Fig.8.19: CAVERNOUS SINUS
INVESTIGATION: Magnetic resonance angiograohy is the investigation of choice which

will show absence of flow in thrombosed sinuses.
Treatment: I/V Antibiotics. Prognosis is poor.
184 | Ophthalmology
Concept 8.8: Retinoblastoma
Learning objectives
• To learn in detail about retinoblastoma
• To learn orbital surgeries
Time Required
st
1 reading 45 mins
2nd look 15 mins
Most common cause of malignant intraocular tumour in children is –Retinoblastoma.

Most common cause of malignant intraocular tumour in adults – Choroidal malignant
melanoma.
Retinoblastoma arises from primitive multi-potential neuroectodermal cells of retina.
Most common age of diagnosis is 18 months.
Genetics:
• Inheritance – AD, but only 6% cases are familial.
• Unilateral in 70-75% while bilateral is 25%-30%
• Familial cases have early onset, bilateral involvement and are predisposed to develop
non- ocular malignancy including pinealoblastoma and osteogenic sarcoma.
• B/L retinoblastoma with pinealoblastoma is termed as trilateral retinoblastoma.
• The specific area corresponding to retinoblastoma gene was identified on
• 14 band, on long arm of chromosome 13 – i.e. 13 q 14.
• 13q syndrome - Retinoblastoma when associated with other dysmorphic features
(microcephaly, broad nasal bridge, hyperteleorism and mental handicap).
• Knudson’s two hit hypothesis: In hereditary retinoblastoma, first genetic change/hit
in RB gene is inherited from an affected parent while second mutation (second hit)
occurs in post natal life and both alleles are lost.
• In non-hereditary retinoblastoma, both mutations (first and second hits) occur in post
natal life.
Clinical features:
Mode of presentations are:
• Leukocoria (60%): It is the most common mode of presentation.
• Strabismus (20%): It is the second most common mode of presentation.
• Secondary glaucoma.
• Pseudouveitis.
• Orbital inflammation - mimicking orbital cellulitis.
• Proptosis.
• Heterochromia iridis, rubeosis iridis.
Growth patterns
• Exophytic: towards choroid
• Endophytic: towards vitreos
• Diffuse infitrating
Orbit | 185
Pathology:
Gross:
• Chalky white friable mass with dense foci of calcification and necrosis.
• Seeding into vitreous cavity.
• Extension to uvea, epibulbar structures, optic nerve and orbit.
Microscopic:
Basophillic mass with light eosinophillic areas due to necrosis.
A. Well - differentiated:
Flexner-Wintersteiner rosette (specific for retinoblastoma).
Homer- Wright roset.
Fleurette formation.
Poorly differentiated: Poor prognosis.
Investigations:
X-ray- Rheese view will show enlargement of optic foramen
USG: B scan. It helps to visualize calcification in tumour.
CT-Scan - (for intracranial extension).
MRI- Investigation to choice to assess spread of tumour (via optic nerve).
Enzymes found to be raised in acquous are:

• LDH- Lactic acid dehydrogenase.
• PGI- Phosphoglucoisomerase.
• NSE- Neuron- Specific- Enolase
Staging and treatment of retinoblastoma

1 Intraocular Group Findings A-Laser photocoagulation/
Cryotherapy
A Tumor thickness <3 mm
B Tumor thickness >3 mm; located within the temporal
arcade B, C, D- Neoadjuvant
chemotherapy to decrease
C Localized vitreous body or subretinal metastasis
the size of the tumour
D Diffuse vitreous body or subretinal metastasis Drugs used are Vincristine,
E Massive tumor with no chance of preserving the eye Etopside and Carboplatin
Followed by laser/cryo
E- enucleation
2 Optic nerve Most common mode of spread is via optic nerve Enucleation with
invasion radiotherapy/Chemotherapy
3 Orbital Exenteration
extension
4 Distant- Palliative
Metastasis
186 | Ophthalmology
Enucleation: Removal of the eyeball with long piece of optic nerve
Laser Photocoagulation: for posterior tumours
Cryotherapy: Tripple freezing - thaw technique, for anterior tumours
Differential Diagnosis of Leukocoria: It is collectively known as Pseudogliomas (These
are the conditions which simulate retinoblastoma due to the presence of leukocoria)
Differentiating features of pseudoglioma from retinoblastoma:
• IOP is raise in Retinoblastoma while decreased/normal in pseudoglioma
• There is intraocular calcification in retinoblastoma which is not seen in pseudoglioma.
• Congenital cataract.
• PHPV [Persistent hyperplastic primary vitreous].
• ROP [Retinopathy of prematurity].
• Toxocariasis.
• Coats disease.
• Coloboma of optic nerve.
• Retinal astrocytoma: It is the benign counterpart of retinoblastoma.
• Fungal endophthalmitis.
• Retinal dysplasias.
Enucleation: Evisceration: Exenteration:
Removal of eyeball with stump Removal of entire intraocular Complete removal of eyeball, the
of optic nerve leaving behind the contents of the eye, leaving the retrobulbar orbital soft tissues,
extra ocular muscles scleral shell and extraocular and most or all of the eyelids, uptil
muscle attachements intact. periosteum
Blind painful eye. Expulsive choroidal hemorrage Orbital extension of Malignancies.
Intraocular tumor. Pan-ophthalmitis Mucormycosis.
Pthisis bulbi. Bleeding anterior staphyloma Chronic orbital pain.
Microphthalmia. Severe trauma with risk of Orbital deformities.
sympathetic ophthalmitis.
Fig.8.20: Leukocoria Fig.8.21: Calcification in retinoblastoma

Orbit | 187
Worksheet

188 | Ophthalmology
Inferior orbital fissure: Between ______________
Superior orbital fissure: Between ______________
Optic canal/Optic foramen: Formed by ____________
• Name some nerves passing from upper part of superior orbital fissure and
inferior orbital fissure
• Identify the sign? _______________________
• Fill in the blank spaces

NAME VIEWS STRUCTURES SEEN
Caldwell-luc view PA View
Occipitofrontal
Town’s view AP view. Frontooccipital
Occipito-meatal. Maxillary sinus and floor of orbit. (in blow-

out fractures)
Rhese view
• Which test is being done? _______________________

Orbit | 189
Name some examples of Bilateral proptosis

Painful
Painless
• Which sign is this in thyroid eye disease? _____________________
• Earliest muscle involved in thyroid eye disease? ____________________
• Which sign is this in thyroid eye disease?

190 | Ophthalmology
• Which syndrome its associated with?
• Write some features of cavernous sinus thrombosis
Mode of presentations of retinoblastoma:

• __________: It is the most common mode of presentation.
• ___________: It is the second most common mode of presentation
What is this sign?
Fill in
Most common benign intraorbital tumor in children is –
Most common primary malignant orbital tumor in children is –
Most common cause of benign intraorbital tumour in adults-
Most common primary malignant orbital tumor in adult is –
Orbit | 191
EXTRA POINTS:
9 Lacrimal
Eyelids
drainage system
and
CONCEPTS
Â Concept 9.1 Eyelid anatomy and muscles
Â Concept 9.2 Ptosis
Â Concept 9.3 Entropion and Ectropion
Â Concept 9.4 M
iscellaneous eyelid and eylash
disorders
Â Concept 9.5 Lacrimal drainage system

Eyelids and Lacrimal drainage system | 193
Concept 9.1: Eyelid anatomy and muscles
Learning objectives
• To know about layers of eyelid
• To learn important muscles in eyelid
Time Required
st
1 reading 20 mins
2nd look 5 mins
Fig.9.1:
Eyelid Anatomy
The eyelid is divided into the upper lid and lower lid. It has 7 layers
Skin- Thinnest skin in body
Subcutaneous tissue
Striated muscles
▫ Orbicularis oculi: Three portions: Orbit, Palpebral (Preseptal and Pretarsal) and
Lacrimal – supplied by 7th nerve
▫ Levator palpebral superioris – supplied by 3rd nerve
Submuscular areolar tissue- contains veseels and nerves
Orbital septum and Tarsal plate (Fibrous skeleton of lids containing Meibomian
glands)
Smooth muscle – Muller
Palpebral conjunctiva
Fig.9.2: Levator palpebral superioris – elevation of Fig.9.3: Origin: Lesser wing of sphenoid
upper eyelid
194 | Ophthalmology
Insertion:
• Skin crease
• Medial and lateral palpebral ligaments (including Whitnall’s ligament)
• Anterior surface of tarsal plate
Fig.9.4: ORBICULARIS OCULI –closing of eyelids

Concept 9.2: Ptosis
Learning objectives
• To know about different types of ptosis
• To learn about management of congenital ptosis
Time Required
st
1 reading 50 mins
2nd look 20 mins
It is drooping of upper eyelid in relation to the globe

Congenital ptosis Acquired Ptosis
Simple congenital ptosis- Neurogenic
• Due to developmental dystrophy of levator muscle. • Third nerve palsy
• Lid lag sign+ • Horner’s syndrome
• Absence of eyelid crease
• Head tilt with chin elevation
Complicated ptosis Mechanical
Marcus gunn jaw-winking syndrome: Increased weight due to tumor, oedema,
• It is due to aberrant connection between the LPS and dermatochalasis
the lateral Pterygoid muscle. It is because of trigemino-
occulomotor synkinesis
Blepharophimosis Syndrome (BPES) Myogenic
• AD • Myasthenia gravis
• Telecanthus (Increased distance between the two medial • Myotonic dystrophy
canthus, but the IPD is normal)
• Ptosis
• Epicanthus inversus (Extra fold of skin on the medial
canthus arising from the lower lid)
• Lower lid ectropion
• Flat nasal bridge with hypoplasia of superior orbital rim
Aponeurotic
Localized dehiscence of aponeurosis
disinsertion-
• Involutional or senile ptosis
• Post operative ptosis
196 | Ophthalmology
Fig.9.5: CONGENITAL PTOSIS Fig.9.6: Epicanthus
Fig.9.7: Marcus Gunn Jaw Winking Phenomeon Fig.9.8: Blepherophimosis–Ptosis–Epicanthus

inversus
Fig.9.9: NEUROLOGICAL PTOSIS Fig.9.10: MYOGENIC PTOSIS
Fig.9.11: MYASTHENIA GRAVIS
Fig.9.12: MECHANICAL PTOSIS Fig.9.13: INVOLUTIONAL/APONEUROTIC

Clinical Evaluation:
• MRD: Marginal reflex distance between upper lid margin and light reflex in primary
gaze
• Amount of ptosis: Mild: 2 mm / Moderate: 3-4 mm / Severe: >4 mm
Fig.9.14:
• LPS muscle action (Upper lid excursion): N→ 15 mm or more. If it is 4mm or less, it

is poor action
Fig.9.15:
198 | Ophthalmology
• Bell’s Phenomenon: If Bell’s phenomenon is absent, then it is a contraindication for
surgery
• Tensilon Test: It is done for myasthenia gravis
• Phenylepherine Test: On instilling 10% phenylephrine, if within 10-15 minutes the
ptosis improves, it is due to muller muscle underaction as in Horner’s syndrome
• Upper lid crease: M- 10 mm; F - 8 mm.
• Vertical fissure height: M: 7-10 mm, F: 8-12 mm
Treatment of acquired ptosis – treatment of underlying cause
For mild ptosis-Fasanella: Servat procedure

Fig.9.16:
For moderate ptosis - Levator Resection
Fig.9.17:
Blasckovics operation: Conjunctival route.

Everbusch’s operation: Cutaneous route.
For severe ptosis -Frontalis Brow Suspension or Sling operation
The material of choice is fascia lata
Fig.9.18:
200 | Ophthalmology
Concept 9.3: Entropion and Ectropion
Learning objectives
• To know about different causes and treatment of entropion and ectropion
Time Required
1st reading 40 mins
nd
2 look 15 mins
Entropion- It is the inward turning of the lid margin

Involutional Age related No excess horizontal laxity-Weis procedure
(transverse lid split and everting sutures)
Excess horizontal laxity-Quickert’s
procedure (Weis procedure plus horizontal
lid shortening)
Jones procedure
(plication of lower lid retractors)
Modified wheelers operation
Cicatrical Cicatrical pemphigoid, Stevens Treat the cause like trichiasis etc
- Johnson syndrome, Trachoma, Tarsal fracture
chemical burns. Mucus membrane grafts
Congenital lower eyelid retractors not well- Hotz procedure

developed
Spastic entropion Treat the cause of the spasm.
Injection of botulinum toxin
ENTROPION
Fig.9.19: INVOLUTIONAL/SENILE ENTROPION Fig.9.20: CICATRICIAL

Fig.9.21: SPASTIC Fig.9.22: CONGENITAL
Ectropion: Outward turning of eyelid margin

Involutional Age related No horizontal lid laxity — medial
conjunctivoplasty (excision of a diamond of
tarso-conjunctiva)
Mild horizontal lid laxity — Lazy-T
procedure (medial conjunctivoplasty plus full
thickness lid excision)
Severe horizontal lid laxity —
Bick procedure.
Modified kuhnt szymanowski procedure.
Cicatrical Due to trauma, burns Excision of scar with Z- plasty,
transposition flaps or free skin grafts.
Congenital lower eyelid retractors not Skin grafts
well- developed
Paralytic Due to facial nerve palsy Temporary: Artificial tears,ointment
If very poor bells phenomenon- tarsorrhaphy.
Permanent:
• Medial canthoplasty.
• Prosthetic devices - silicone rings
Mechanical Due to eyelid tumours Treat the cause

202 | Ophthalmology
ECTROPION
Fig.9.23: INVOLUTIONAL/SENILE Fig.9.24: CICATRICIAL

Fig.9.25: PARALYTIC Fig.9.26: MECHANICAL
Fig.9.27: CONGENITAL
Concept 9.4: Miscellaneous eyelid and eyelash disorders
Learning objectives
• To learn and identify various terminology in eyelids and eyelash disorders
Time Required
1st reading 30 mins
nd
2 look 15 mins
Chalazion (Meibomian Cyst):

It is a chronic lipogranulomatous inflammation of the meibomian glands. It is caused
by blockage of meibomian gland orifices and stagnation of sebaceous secretions. It
presents as a painless swelling on the lid. It is treated by incision and drainage or by
intralesional injection of triamicilone acetate.
Fig.9.28: CHALAZION
External Hordeolum (Stye):

Stye is a small abscess (suppurative inflammation) caused by an acute staphylococcal
infection of a lash follicle and its associated gland of Zeis or hair follicles. It presents
as a painful swelling at the lid margin. It is treated with hot fomentation, oral anti-
inflammatory and if needed epilation of the hair follicle.
Fig.9.29: STYE
204 | Ophthalmology
Internum Hordeolum: It is small abscess caused by an acute staphylococcal infection
of meibomian gland. It presents as a painful swelling in the lid. It is treated with hot
formentation, oral antibiotics and anti-inflammatory. Incision and drainage if required,
can be done.
Trichiasis: Misdirection of the eyelashes. It presents as irritation, pain, lacrimation,
blepharospasm. It can lead to punctuate epithelial erosions, corneal ulcer and pannus.
Distichiasis:It is a congenital anomaly characterized by extra row of lashes
Symblepharon: It is the adhesion of lid with the globe. It can occur due to burn,
chemical injuries, ulcers or after surgeries.
Ankyloblepharon: Adhesion of the margins of both the lids and both palpebral
conjunctiva. Causes are same as symblepharon.
Lagophthalmos: Inability to close the eyes.
It can lead to exposure keratopathy. Causes are: Cicatrization of the lids, Paralysis of
orbicularis oculi and proptosis
Madarosis: Loss of eyelashes or loss of eyebrows, both are termed as madarosis.
Causes:

Local:

Blepharitis Trachoma, S. J. syndrome.

Infilterating tumors.

Burns.
Radiotherapy or cryoth of lid tumors.

Skin:
▫ Psoriasis.
▫ Generalized alopecia.
Systemic:
▫ Myxoedema.
▫ Leprosy.
▫ Syphilis.
▫ SLE.
Following Removal:
▫ Iatrogenic trichiasis.
▫ Trichotillomania.
Poliosis: Whitening of eye lashes is known as poliosis.
Causes:
Local:
▫ Chronic blepharitis.
▫ Sympathetic uveitis.
Systemic:
▫ VKH syndrome.
▫ Waardenberg syndrome.
Fig.9.30: Poliosis Fig.9.31: Distichiasis
Fig.9.32: Symblepharon Fig.9.33: Ankyloblepharon
Fig.9.34: Madarosis Fig.9.35: Lagophthalmous
Malignant Eyelid Tumors:

a. Basal cell carcinoma: It is the most common tumour of the eyelid. Most common site
is lower lid and then medial canthus. It is a slow growing tumour, locally invasive.
b. Squamous cell carcinoma: It is the second most common tumour of the eyelid. It is a
fast growing tumour which metastasizes to the regional lymph node.
c. Sebaceous cell carcinoma: It arises from the meibomian glands. It may present as
Recurrent chalazion.
d. Malignant melanoma.
e. Kaposis sarcoma.
206 | Ophthalmology
Concept 9.5: Lacrimal drainage system
Learning objectives
• To learn about lacrimal drainage system
• To learn tests for watering eyes
• To learn about dacryocystitis
Time Required
st
1 reading 40 mins
nd
2 look 20 mins
Fig.9.36:
LACRIMAL APPARATUS OF EYE
Fig.9.37:
Watering of Eyes
Lacrimation: It is the over-production of the tear.
Epiphora- It is overflowing of the tear due to blockage of the drainage system
Causes of Blockage:
Anatomical:
Strictures.
Obstruction.
Foreign body
Tumor
Physiological:
Lacrimal pump failure.
Tests of Lacrimal Drainage System:

Regurgitation test.
Syringing
Jones dye test.
Dacryocystography
Dacryoscintillography
Syringing/irrigation with saline

Soft stop
Diagnosis: Complete canaliculi block
Reflex from upper canaliculi — common canaliculi block
Reflex from lower canaliculi — lower canaliculi block
Hard stop
If no saline enters nose/mucoid reflux into puncta: Diagnosis: Complete NLD block
If saline enters nose: Possibilities: Hypersecretion, partial obstruction or lacrimal pump
Fig.9.38: JONES DYE TEST 1 Fig.9.39: JONES DYE TEST 2

208 | Ophthalmology
Jones primary dye test 1
• Positive (dye in nose): Diagnosis: Hypersecretion (1)
• Negative: Possibilities: Partial obstruction or lacrimal pump failure
Proceed with Jones secondary dye test 2

• Positive (dye in nose after flushing): Diagnosis: Partial obstruction NLD
• Negative: Diagnosis: lacrimal pump failure
Fig.9.40: DACRYOCYSTOGRAPHY Fig.9.41: Arrow pointing towards block
Dacrocystitis:
It is the inflammation of the lacrimal sac at the medial canthus region. It may be:
Congenital (chronic) or acquired (either acute or chronic).
Congenital dacrocystitis:
It is due to congenital blockade of the lacrimal duct.
Usually presents as mild grade chronic inflammation.
Characterised by:
Epiphora
Regurgitation of mucopurulent discharge on applying pressure over lacrimal sac
region, (positive regurgitation test).
Swelling over the sac area.
Fig.9.42: DACRYOCYSTITIS
Treatment:
• Upto 9 months -Massage over the lacrimal sac region with topical antibiotics
• 9 months to 4 years -Probing of Nasolacrimal duct:Bowman’s probe is used for this
purpose.
• After 4 years -Dacrocystorhinostomy
Fig.9.43: BOWMAN’S PROBING
Acquired Dacrocystitis:
It may be acute or chronic.
a. Acute dacrocystitis: It is acute suppurative inflammation having marked swelling,
tenderness, redness over lacrimal region with the presence of epiphora.
Treatment:
Cellulitis stage: Systemic and topical antibiotics are given. Systemic anti inflammatory
and analgesics are added along with hot fomentation to relieve pain and swelling.
Lacrimal abscess stage: In addition to above treatment, when the pus starts
pointing out on the skin,it should be drained with a small incision. Later on, either DCR
(Dacrocystorhinostomy)
External lacrimal fistula: After controlling the acute infection with systemic antibiotics,
fistulectomy along with DCR.
Chronic dacrocystitis: It is more common than acute form. It occurs as a result of
obstruction of NLD due to various causes like chronic inflammation of nasal mucosa or
by polyp pressure etc. Treated by DCR.
Dacryocystectomy – reoval of lacrimal sac - Indications

• lacrimal sac tumor
• Chronic dacryocystitis following failed dacryocystorhinostomy (DCR)
• Dacryocystitis in setting of granulomatosis with polyangiitis (Wegeners granulomatosis)
that is refractory to conventional management
210 | Ophthalmology
Worksheet

Levator palpebral superioris –
Action ______________
Origin: __________
Insertion: ___________
Write some features of

Simple congenital ptosis-
•
Whats the diagnosis?
Name some nerves passing from upper part of superior orbital fissure and inferior orbital
fissure
• Which is being tested? _______________________
• Phenylepherine Test in ptosis is done for ________________

• What is the treatment of this? _____________________
212 | Ophthalmology
• What is the diagnosis and treatment?
• Name the diagnosis?

• Write some indications for Dacryocystectomy
Which test is this?
Treatment of congenital nasolacrimal duct obstruction:

• Upto 9 months -_________________________
• 9 months to 4 years -____________________
• After 4 years -__________________
214 | Ophthalmology
EXTRA POINTS:
10 Uvea
CONCEPTS
Â Concept 10.1 Uveal anatomy
Â Concept 10.2 Uveitis
Â Concept 10.3 S
ystemic Associations of Uveitis:
Arthritis
Â Concept 10.4 S
ystemic Associations of Uveitis:
Infections
Â Concept 10.5 O
ther Systemic Associations of
Uveitis
216 | Ophthalmology
Concept 10.1: Uveal anatomy
Learning objectives
• To know about basic anatomy of uveal layer
Time Required
1st reading 25 mins
nd
2 look 10 mins
Iris
Circular disc, 12 mm in diameter with an aperture of 3-4 mm called pupil. Its is thinnest
at its root. The anterior surface is divided into ciliary zone and pupillary zone by a zig-
zag line called Collarette (represents attachment of pupillary membrane).
Microscopic:
Anterior limiting layer (anterior most condensed part of stroma). Has melanocytes and fibroblast
Stroma (contains vessels, nerves, sphincter pupillae, dilator muscle)
Anterior epithelial layer
Posterior pigmented epithelial layer.
• Disinsertion of iris from its root is called iridodialysis. The pupil in iridodialysis becomes
D-shaped.
• Aniridia - The iris may be apparently absent, however, a narrow rim exists at the
ciliary border. Wilms tumour is associated with sporadic cases.
• Polycoria –multiple pupil, corectopia – displaced pupil
Fig.10.1: ANIRIDIA Fig.10.2: POLYCORIA/CORECTOPIA
Fig.10.3: IRIDO-DIALYSIS
Uvea| 217
Ciliary Body
It’s a forward continuation of choroid at ora-serrata.
It is divided into two parts:
• Pars plicata.
• Pars plana.
Microscopic:
Supraciliary lamina (outermost condensed stroma), consists of pigmented collagen fibres Stroma (consists
of longitudinal, circular and radial fibres and vascular stroma)
Layer of pigmented epithelium
Layer of non-pigmented epithelium
Internal limiting membrane.
Accomodation is mainly done by circular and radial muscles. The resting tone of ciliary
muscles is +1D.
Choroid
Extremely vascular membrane. From retina to sclera, it has
• Thin elastic membrane, membrane of Bruch.
• Capillary plexus of fenestrated vessels, the choriocapillaris.
• the layer of medium-sized vessels, while most externally are the large vessels, the
whole being held together by a stroma consisting of branched pigmented connective
tissue cells.
• It is not firmly adherent to sclera - potential space between the two structures - the
suprachoroidal space.
218 | Ophthalmology
Concept 10.2: Uveitis
Learning objectives
• To know about classification of uveitis
• To learn features of different types of uveitis
Time Required
st
1 reading 50 mins
2nd look 20 mins
Uveitis: Inflammation of the uveal tract.
Classification:
Anatomical Clinical Pathological
Anterior uveitis Acute uveitis: Granulomatous
Intermediate uveitis Sudden onset and persists less than 6 weeks Nongranulomatous
Posterior uveitis Chronic uveitis:
Panuveitis Insidous onset and persists months or years
Fig.10.4:
Anterior Uveitis:
Inflammation of iris (iritis) and anterior part of ciliary body i.e. pars plicata, (iridocyclitis).
Most common form of uveitis accounting for 70% cases (approx).
Uvea| 219
Causes of Anterior Uveitis:
Autoimmune Psoriasis, ankylosing Spondylitis, Inflammatory bowel disease, Sarcoidosis, Behcet’s disease.
Infections Herpes zoster, Herpes simplex, TB, Syphilis, Leprosy, leptospirosis.
Malignancy Leukemia, retinoblastoma, malignant melanoma, lymphoma
Others Idiopathic, trauma, Fuch’s heterochromatic iridocyclitis.
Most common cause of anterior uveitis is IDIOPATHIC.
Clinical features:
• Photophobia, pain, redness, decreased vision, lacrimation.
• Circumcorneal (ciliary) congestion
• Keratic precipitates (KP): Proteinaceous cellular deposits at the back of the cornea.
It is a pathognomic sign.
Mutton fat KPs Large and are composed of epitheloid cells and macrophages. Seen in
granulomatous inflammation.
Small Granular KPs Also known as They are composed of lymphocytes, and are characteristic of
non-granulomatous uveitis.
Red KPs Composed of RBCs and inflammatory cells. Seen in haemorrhagic uveitis.
Old KPs In healed uveitis with crenated margins.
Fig.10.5: Mutton fat KPs Fig.10.6: Fine KPs
• Iris Nodules: features of granulo-matous inflammation).

Koeppe nodule: At the pupillary border.
Busacca nodule: At the base of the iris.
Fig.10.7: Busaca Fig.10.8: Koeppe

220 | Ophthalmology
• Aqueous cells: Sign of active inflammation. They may settle in anterior chamber as
hypopyon (sterile)
Fig.10.9 (a): cells in anterior chamber Fig.10.9 (b): Hypopyon
• Aqueous flare: Due to leakage of proteins from the inflamed capillaries of the iris
and pars plicata. It is based on Tyndal phenomenon/Brownian movements.
• Posterior Synechiae
Fig.10.10: Seclusio pupillae
Posterior synechiae extending 360° causing papillary block.

↓
Iris bombe
↓
PAS (Peripheral anterior synechiae leading to raised intraocular pressure due to angle
closure.)
Occlusio papillae: Obstruction of aqueous flow due to organization of exudates across
the entire pupil which block the pupil, also known as blocked pupil.
• Anterior vitreous cells.
• Pupil constricted. If posterior synechiae, irregular and constricted pupil, called
Festoon-shaped Pupil. Sluggish pupillary reaction.
Treatment:
Steroids: Topical
Mydriatics with strong cycloplegic action (Atropine).
Uvea| 221
Intermediate Uveitis or Pars Planitis
Primary
Idiopathic, insidious, chronic, intra-ocular inflammation typically affecting children or
young adults.
Secondary:
• Sarcoidosis
• Retinitis pigmentosa
• Multiple sclerosis
• TB, syphilis, Lyme’s disease, toxocara
Clinical features:
• Floaters
• Diminished vision- if associated with Cystoid macular edema
• Vitritis: Cells, Snow balls or cotton balls. Mild peripheral periphlebitis. Sheathing of
terminal venules (Snow – Banking): Hallmark of pars planitis.
Fig.10.11:
Complications:
• CME.
• Secondary cataract.
• Tractional RD.
• Cyclitic membranes.
Treatment:
It is four step approach.
• Periocular steroid injections.
• Systemic steroid and cytotoxic drugs.
• Cryotherapy of vitreous base.
• Vitrectomy
222 | Ophthalmology
Posterior Uveitis:
It is the inflammation of the choroid along with associated structures i.e. vitreous, optic
disc, macula, peripheral retina and retinal veins. It is usually insidious in nature.
Clinical features:
• Choroiditis: It is seen as round yellowish patches.
• Cystoid macular edema: CME.
• Vitritis
• Papillitis
• Retinal edema
• Periphlebitis
There is no pain, photophobia, lacrimation or circumcorneal congestion.
Most common cause of posterior uveitis is Toxoplasmosis
Treatment:
• Local steroids: Sub-tenon injections of triamicilone acetate.
• Systemic steroids.
Complications of Uveitis:
In the Cornea Iris Lens In the Globe Posterior Segment
• Sclerosing • Atrophy • Complicated • Secondary • CME
keratouveitis • Rubeosis cataract Glaucoma • RD
• Corneal edema • Pthisis bulbi. • Cyclitic membrane
• Bullous keratopathy formation →
• Disciform keratitis Cilio- Choroidal
• Band-shaped detachment →
keratopathy Hypotony.
• Choroidal
neovascular
membrane
Uvea| 223
Concept 10.3: Systemic Associations of Uveitis: Arthritis
Learning objectives
• To know about some arthritis related uveitis
Time Required
st
1 reading 15 mins
2nd look 5 mins
Uveitis Associated with Arthritis:

Disease Features
Ankylosing Spondylitis HLA -B27 associated.
Acute, recurrent non-granulomatous iritis.
Negative RA factor.
Reiters Syndrome Urethritis.
Conjunctivitis.
Sero-negative arthritis
HLA- B27 associated.
Psoriatic Arthritis Sero-negative arthritis.
HLA- B27 associated
Conjunctivitis.
Acute iritis.
Keratitis.
Secondary sjogren’s syndrome
Juvenile Chronic Arthritis Children below age of 16 years Sero-negative arthritis.
Divided into 3 types:
Systemic onset
Polyarticular (> 5 joints involved)
Pauciarticular (< 5 joints involved)
Uveitis is commonest in Pauciarticular JCA.
Chronic non-granulomatous, bilateral anterior uveitis.
Also called “White Uveitis"
224 | Ophthalmology
Concept 10.4: Systemic Associations of Uveitis: Infections
Learning objectives
• To know about some infections associated with uveitis
Time Required
st
1 reading 20 mins
2nd look 5 mins
Systemic Associations of Uveitis: Infections

Disease Main Uveitis Features Treatment
Toxoplasmosis: Iridocyclitis: Granulomatous or non- Systemic steroids
(Most commonly is in foetal granulomatous.
life and later it reoccurs in old Sulphonamide
healed chorio-retinal scar due Posterior Uveitis:
to rupture of cyst) “Headlight in Fog Appearance”. Pyrimethamine
Deep retinitis (involving outer retinal Co-trimoxazole

layer) Clindamycin
Syphilis Acute granulomatous or non- 12-24 MU of aqueous penicillin
granulomatous panuveitis I/V for
Iris Roseola 10 days followed by 2.4 MU
Unifocal choroiditis I/M for 3 weeks.
Other important feature –
“Salt and pepper fundus”
Argyll- Robertson pupil
Tuberculosis Chronic granulomatous panuveitis ATT Drugs.
Chronic iridocyclitis:
Most frequent feature
Choroditis: Focal or multifocal.
Retinal vasculitis.
Moderate vitritis.
Severe ischemic periphlebitis.
Peripheral capillary closure →
neovascularisation.
Uvea| 225
AIDS CMV Retinitis: It is the most I/V Gancyclovir.

(Retinal Microangiopathy common opportunist ocular infection I/V Foscarnet.
is the most common of AIDS - Sauce and Cheese Intravitreal Gancyclovir
ocular manifestation of Retinopathy” implants
HIV infection -Cotton-
wool spots, haemorrhages, Varicella- Zoster Retinitis: It causes
microaneurysms) Acute Retinal Necrosis
Cryptococcal and Histoplasmal

Choroiditis
Leprosy Acute iritis: It occurs due to
(Ocular involvement is more deposition of immune complexes in
in lepromatous leprosy than in the anterior uvea.
tuberculoid leprosy) Chronic uveitis: It occurs due
to direct invasion of the bacilli.
The pathognomic feature is IRIS
PEARLS. These are histiocytes
containing bacilli arranged along
the pupillary border. It resembles a
necklace.
River Blindness Chorio-retinitis: Chronic, non- Ivermectin:
(Onchocerciasis) granulomatous Given only to those at high risk
of blindness because treatment
can lead to severe, acute,
systemic, inflammation (called
MAZZOTI’S REACTION) that
can cause death.
Fig.10.12: Toxoplasmosis Fig.10.13: Cytomegalo retinitis

226 | Ophthalmology
Concept 10.5: Other Systemic Associations of Uveitis
Learning objectives
• To know about some infections associated with uveitis
Time Required
st
1 reading 50 mins
2nd look 20 mins
Sarcoidosis:
It is an idiopathic, multisystem disorder characterised by presence of non-caseating
granulomata in lungs and other organs.
Ocular features:
Adnexa Granuloma conjunctiva, episclera, sclera.
KCS- due to involvement of lacrimal gland
Anterior uveitis Chronic granulomatous iridocyclitis
Iris nodules
Fundus Changes Periphlebitis- Advanced stage of vascular sheathing leads to Candle- wax
drippings.
Pre-retinal nodules- Lander’s sign
Snow ball opacities in vitreous
Disc granuloma
Optic atrophy
Fig.10.14: Periphlebitis in sarcoidosis Fig.10.15: Sarcoidosis
Behcet’s Disease:
Idiopathic multisystem disorder, affecting young men leading to obliterative vasculitis
due to circulating immune complexes.
Uvea| 227
Clinical Features:
• Oral ulceration.
• Recurrent genital ulceration.
• Skin lesions: Erythema nodosum
• Positive pathergy test.
• HLA- B5 associated.
• Eye involvement- Severe bilateral nongranulomatous panuveitis (Acute recurrent
iridiocyclitis with transient hypopyon, retinitis, vitritis, vasculitis)
Vogt- Koyanagi- Harada Syndrome [VKH]:

Idiopathic multisystem disorder which typically affects pigmented individuals.
HLA-DR4 associated.
Skin and Hair Neurological Features: Auditory Ocular Features
Changes: symptoms
Alopecia Meningeal Irritation Tinnitus Bilateral granulomatous panuveitis
Poliosis Encephalopathy Vertigo Dalen-Fuchs nodules (inflammatory cells
Vitiligo CSF- Lymphocytosis Deafness. in RPE and Bruch’s membrane)
(Suguiras sign) Pigment epithelial atrophy (sunset glow
fundus)
Multifocal choroiditis and exudative RD
Fig.10.16: Vogt–Koyanagi–Harada syndrome

228 | Ophthalmology
Sympathetic Ophthalmitis:
• Bilateral, granulomatous panuveitis.
• Occurs after accidental penetrating trauma.
• Traumatized eye is the exciting eye and the fellow eye is sympathizing eye.
• 65% of cases occur between 2 weeks and 3 months after injury.
• 90% of cases occur within first year.
Blurring of vision due to loss of accommodation- 1st symptom
Retrolental flare: 1st sign
Ocular Signs – similar to VKH syndrome but with sparing of choriocapillaries and absence
of systemic features
Treatment:
• Vigorous steroid therapy by all possible routes of administration.
• Immunosuppressive therapy: with chlorambucil, cyclophosphamide or cyclosporin, in
severe steroid – resistant cases.
• Enucleation- within 2 weeks of injury will prevent sympathetic uveitis
Fig.10.17: SYMPATHETIC OPHTHALMITIS
Ophthalmia Nodosum
Severe, granulomatous iridocyclitis with nodule formation, due to caterpillar hair inside
the eye
Eales Disease (Periphlebitis Retinae):

Mainly affects young males. B/L, idiopathic
Etiology:
• Idiopathic.
• Hypersensitivity to tuberculo protein leads to peripheral retinal vasculitis.
Uvea| 229
Presentation:
• Sudden blurring of vision with floaters as a result of vitreous haemorrhage.
• Sheathing of small peripheral retinal veins.
• Massive proliferative retinopathy → Vitreous or retinal haemorrhage → TRD.
Treatment:
1. PRP
2. Pars plana vitrectomy
Specific uveitis syndromes

Posner Schlossman Syndrome: Fuch’s Uveitis Syndrome or
Glaucomatocyclitic crisis Fuch’s Heterochromic Cyclitis
Young patient Middle age patient
Non-granulomatous, anterior uveitis Non-granulomatous, anterior uveitis
possibly cytomegalovirus
(CMV) or H. pylori may play a role
Acute blurring of vision and halos Asymptomatic, sometimes with blurring of vision
Few depigmented KPs Heterochromia iridis
No posterior synechiae Iris atrophy
IOP-: 40-60mmHg No posterior synechiae
Gonioscopy shows open angles. Keratic precipitates- small, stellate and grey- coloured;
Optic nerve – No cupping Rubeosis (fine): Amsler’s sign - acute
Visual field is normal. hyphema following ocular decompression such as paracentesis
Complications:
Cataract.
Glaucoma – usually of open- angle type
Treatment for both:

Topical steroids with anti-glaucoma drugs to decrease the IOP.
Fig.10.18: FUCH’S HETEROCHROMIC Fig.10.19: Amsler sign

IRIDOCYCLITIS
230 | Ophthalmology
Endophthalmitis:
It is an inflammation of the inner eye fluids and tissues ie uveal tissue, retina, vitreous
humor and aqueous humor.
Outer coat ie sclera is spared.
Most common cause of endophthalmitis is intraocular surgery.
It may also occur after a penetrating trauma, entry of the microbes endogenously or by
metastatic spread.
Organisms:
Exogenous endophthalmitis:
• Post-operative: Acute post-operative ie within 7 days after surgery: Staphylococcus
epidermidis, Staphylococcus aureus, Streptococcus. Delayed onset i.e. from a week
to months after surgery: Fungi, P. acne (most common).
• Post traumatic: Bacillus, Staphylococcus epidermidis, Fungi, Streptococcus.
Endogenous endophthalmitis: Bacillus cereus (drug abusers), Staphylococcus aureus,
Streptococcus, Haemophilus influenzae, meningococci etc.
Clinical features:
• Severe ocular pain.
• Redness.
• Lacrimation.
• Photophobia and marked loss of vision.
• Swollen lids.
• Chemosis of conjunctiva.
• Conjunctival and circumcorneal congestion.
• Hypopyon.
• Corneal edema.
• Amourotic cat’s eye reflex.
Treatment:
Intravitreal antibiotics
Topical and systemic steroids
Pars plana vitrectomy
Panophthalmitis:
Inflammation of all the structures of the eye
Complications include:
• Orbital cellulitis.
• Cavernous sinus thrombosis.
• Meningitis.
• Encephalitis.
Treatment:
Eviseration
Systemic antibiotics
Uvea| 231
Worksheet

232 | Ophthalmology
• Identify
• Name the KPs whose description is given

Large and are composed of epitheloid cells and macrophages. Seen in
granulomatous inflammation.
Also known as They are composed of lymphocytes, and are characteristic of
non-granulomatous uveitis.
Composed of RBCs and inflammatory cells. Seen in haemorrhagic uveitis.
In healed uveitis with crenated margins.
• Write features of
Reiters Syndrome ______________
Ocular Features of VKH syndrome
• Name the iris nodules? _______________________

Uvea| 233
• The most common ocular manifestation of HIV infection -______________
• Acute hyphema following ocular decompression such as paracentesis in Fuch’s uveitis
is _________________
• Endophthalmitis is inflammation of ___________________________-
Write some features of Bechets disease
• Sympathetic Ophthalmitis:
Critical period of development is _______________
1st symptom in sympathising eye - ___________
1st sign in sympathising eye - ___________
• Identify the organism causing it

234 | Ophthalmology
EXTRA POINTS:
11 Squint
CONCEPTS
Â Concept 11.1 Extraocular muscles and actions
Â Concept 11.2 Squint: Definition and tests
Â Concept 11.3 C
oncomitant vs Inconcomitant
squint
Â Concept 11.4 Tests for binocular vision

236 | Ophthalmology
Concept 11.1: Extraocular muscles and actions
Learning objectives
• To know about extrocular muscles, their origin, insertion and actions
• To learn about laws governing extraocular muscles
Time Required
st
1 reading 40 mins
2nd look 20 mins
EXTRAOCULAR MUSCLES
Fig.11.1: Actions, Origin and insertion of extraocular muscles

Squint| 237
Muscle Primary Secondary Tertiary Origin Insertion

Medial rectus Adduction - - Annulus of Zinnn Anterior sclera (5.5 mm)
Lateral rectus Adduction - - Annulus of Zinnn Anterior sclera (7 mm)
Inferior rectus Depression Extorsion Adduction Annulus of Zinnn Anterior sclera (6.5 mm)
Superior rectus Elevation Intorsion Adduction Annulus of Zinnn Anterior sclera (7.5 mm)
Inferior oblique Extorsion Elevation Adduction Body of maxilla Posterior sclera
Superior oblique Intorsion Depression Adduction Body of sphenoid Posterior sclera
The number in bracket is distance of muscle insertion from limbus
Superiors are intorters
Recti are adductors
• The vertical recti run in line with the orbital axis and are inserted in front of the
equator. They therefore form an angle of 23° with the visual axis
• The obliques are inserted behind the equator and form an angle of 51° with the visual
axis
GAZE POSITIONS
Fig.11.2:
Hering’s law: It states that during any conjugate eye movement, equal and simultaneous
innervation flows to the yolk muscles.
Sherrington’s Law of reciprocal innervations: It states that increased innervation
and contraction of a muscle is automatically associated with a reciprocal decrease in
innervations and relaxation of its antagonists.
Primary position of gaze: Position of eyes in binocular vision when, with the head
erect, the object of regard is at infinity and lies at intersection of saggital plane of the
head and horizontal plane passing through the centre of rotation of the two eye balls.
Secondary position: Supreversion, Infraversion, Levoversion, Dextroversion.
Tertiary position: Vertical + Horizontal position i.e. dextroelevation, Levoelevation,
dextrodepression, Levodepression.
238 | Ophthalmology
Concept 11.2: Squint: Definition and tests
Learning objectives
• To know about types of squint
• To learn various tests to determine squint
Time Required
st
1 reading 50 mins
2nd look 25 mins
The misalignment of the visual axis of the two eyes is known as squint or strabismus.
Strabismus is classified as:
Latent squint [Phorias]: It is further classified as exophoria, esophoria, hypophoria or
hyperphoria.
Manifest squint [Tropias]: It can be classified as: Esotropia, Exotropia, Hypeotropia or
Hypertropia
Fig.11.3:
Tests for Squint:

Hirschberg Test: Deviation of the corneal light reflex from the centre of the pupil.
Reflex at the inner border of the pupil indicates squint of 15°.
Reflex at the centre of the inner and outer border of the pupil indicates a squint of 30
degrees.
Reflex at the limbus indicates squint of 45°.
Squint| 239
In general, for every 1 mm that the light is decentered, the eye is turned about 15 prism
diopters (7 degrees from center).
Fig.11.4:
Cover-uncover test:
• Cover component:
Detects heterotropias
Cover straight eye
Look at uncovered deviated eye (movement indicates tropia)
• Uncover component:
Detects heterophorias
Uncover straight eye
Look at uncovered eye for deviation and refixation (movement indicates phoria in this
eye)
Alternate –Cover Test: In this test we alternate cover both the eyes with the cover
and see the movement of the uncovered eye.
240 | Ophthalmology
COVER TEST FOR TROPIAS
Fig.11.5:
Squint| 241
COVER-UNCOVER TEST FOR PHORI
AS/LATENT SQUINT
Fig.11.6:
Krimky’s test/Prism bar test: Prisms of increasing power are placed in front of
deviated eye till the eye appears straight or light reflex is aligned straight. It measures
heterotropias. [Light rays are deviated towards the base of the prism, and the objects
appear displaced towards the apex].
Fig.11.7: PRISM BARS

242 | Ophthalmology
Fig.11.8: PRISM BAR COVER TEST
Alternate prism cover test: Measures total deviation (heterotropias and phorias).
Prism over deviated eye and alternate cover each eye until no movement is seen.
Maddox rod and Maddox wing are used to assess the latent squint.
In Maddox wing -Dissociates two eyes for near fixation
In Maddox rod - Dissociates two eyes for distance fixation. It consists of series of fused
high power cylinder red rods.
Fig.11.9:
Squint| 243
Concept 11.3: Concomitant vs Inconcomitant squint
Learning objectives
• To know about types of squint
• To learn various tests to determine squint
Time Required
st
1 reading 60 mins
2nd look 25 mins
Concomitant vs Inconcomitant [Paralytic squint]

• Non-Paralytic/Concomitant- Primary deviation is equal to secondary deviation.
Primary deviation is the deviation of the squinted eye, whereas secondary deviation
is the deviation of the normal eye.
• Paralytic/Incomitant- Secondary deviation is more than the primary deviation.
This is due to Herring’s Law.
Features of Paralytic squint:

Diplopia.
Confusion.
Nausea and vertigo.
Ocular deviation.
Diplopia (Double Vision):

Horizontal – Images are side by side.
Vertical – Images are up and down.
Torsional - oblique
Horizontal Diplopia may be:

Uncrossed: When the false image is on the same side as the deviating eye.
Crossed – When false image is on opposite side of deviating eye.
Convergent Squint: Uncrossed diplopia

Divergent Squint: Crossed diplopia
Uniocular Diplopia: Causes:
Subluxated lens.
Double pupil.
Incipient cataract.
Keratoconus.
Binocular Diplopia: Causes:

Paralytic squint.
Restrictive squint.
Anisometropic glasses- (uniocular aphakic glass).
After squint correction
244 | Ophthalmology
Third Nerve Palsy:
Ptosis.
Eye is - Down and Out.
Defective – adduction, elevation and depression.
Dilated pupil with defective accommodation.
Webino: [Wall-Eyed Bilateral Internu- clear Ophthalmoplegia]. Due to lesions involving
paired medial rectus subnuclei. Defective convergence and adduction.
Benedickt’s Syndrome : Ipsilateral third nerve palsy and contralateral hemitremor.
Weber’s Syndrome: Ipsilateral third nerve palsy and a contralateral hemiparesis.
Fig.11.10: Left 3rd nerve palsy
Fourth Nerve Palsy:

• Hyperdeviation.
• Excyclotorsion: Compensated by head tilt to opposite shoulder.
• Limited depression in adduction.
• Diplopia: Vertical. Worse on looking down
Bielchowsky’s sign: Increase of the hyperdeviation on tilting the head to the ipsilateral
shoulder. This is a feature of fourth nerve palsy.
Fig.11.11: Left 4th nerve palsy
Sixth Nerve Palsy:

• Defective abduction.
• Convergent strabismus.
• Horizontal diplopia.
• Face turn into field of action of paralysed muscle
Squint| 245
Millard Gubler Syndrome : Ipsilateral sixth nerve palsy with contralateral hemiplegia.
Fig.11.12: Left 6th nerve palsy
Concomitant squint
Concomitant esotropia:
• Infantile esotropia- Presents at 6 months of birth Large angle (> 30 prism
D).Alternating fixation in primary position but cross
• Accomodative esotropia- Refractive- corrected by spectacles. Non refractive- high
AC/A ratio (accommodative convergence/accommodation_- corrected by bifocals.
Mixed- components of both
• Sensory esotropia (disruption of binocular single vision in children e.g. congenital
cataract)
• Consecutive esotropia (after correction for exotropia)
Concomitant exotropia:
• Infantile exotropia- Present at birth, large and constant angle
• Intermittent exotropia- Convergence insufficiency (worse for near, needs MR resection
or recess-resect). Divergence excess (worse for distance, needs LR recession):
• Sensory exotropia (disruption of binocular single vision in children e.g. congenital
cataract)
• Consecutive exotropia (after correction for esotropia)
Treatment :
Incomitant/Paralytic Squint:
Wait for 5-6 months, if no improvement do surgery.[For an underacting muscle we do
resection and for a overacting muscle we do recession].
Concomitant Squint / No-Paralytic squint:

Sequence of management is as follows:
Refraction » Occlusion » Orthoptic Excercises » Surgery
Fig.11.13: ORTHOPTICS: EXCERCISES

246 | Ophthalmology
Concept 11.4: Tests for binocular vision
Learning objectives
• To know about different tests to evaluate binocularity and stereopsis
Time Required
1st reading 40 mins
nd
2 look 15 mins
The synoptophore
Test of Binocular single vision
It dissociates two eyes for both near and distance fixation
Fig.11.14: SYNAPTOPHORE
Binocular Vision:
Defined as that state of simultaneous vision with two seeing eyes that occurs when
an individual fixes his visual attention on an object of regard. It is assessed by a
synaptophore.
Grades:
I – Grade- Simultaneous perception
II- Grade – Fusion.
III- Grade – Stereopsis
Horopter:
It is the sum total of points in physical space; that stimulate corresponding retinal
elements of the two eyes.
Panum’s Area:
The field in front of and behind the horopter in which the expected diplopia does not
occur is known as “Panums fusional space”.
Squint| 247
Visual reflex (fixation) in infants starts developing at 6 weeks of age and develops fully
till 4 month of age.
Binocular function fully develops by 6 years and orthoptic exercises are most useful till
8-9 years of age.
Visual acuity is a measure of form sense.
Fig.11.15: SIMULTANEOUS PERCEPTION
Fig.11.16: FUSION
248 | Ophthalmology
Fig.11.17: STEREOPSIS
OTHER TESTS FOR STEREOPSIS

TITMUS STEREO TEST:
FLY TEST, ANIMAL TEST & CIRCLES TEST
Fig.11.18:
Squint| 249

Fig.11.19: Randot E Fig.11.20: TNO

Fig.11.21: Lang Fig.11.22: Frishy
Fig.11.23: WORTH FOUR DOT TEST

250 | Ophthalmology
Tests binocular vision and suppression
a. Shown to patient
b. If 4 lights are seen, indicates normal fusion
c. If 2 lights are seen, indicates left suppression
d. If 3 lights are seen, indicates right suppression
e. If 5 lights are seen, indicates diplopia
Fig.11.24: Bagolini striated glasses
Tests binocular vision and suppression

Squint| 251
Worksheet

252 | Ophthalmology
Muscle Origin Insertion Primary action

Superior rectus
Inferior rectus
Superior oblique
Medial rectus
• The obliques are inserted behind the equator and form an angle of ____ with the
visual axis
• Write the diagnosis for each

Squint| 253
• What test is being done?
• If the patient is normal, he will _________ from right eye and _______ from left eye
• Uniocular Diplopia: Causes:

254 | Ophthalmology
• The test is used for? ___________
• Convergent Squint: ____________diplopia

• Divergent Squint: ____________diplopia
• Name the nerve involved here _______________________
• Write the features of the diagnosis

Squint| 255
• Identify the device
• What does c and d indicate here?

256 | Ophthalmology
EXTRA POINTS:
12 Optics
CONCEPTS
Â Concept 12.1 Basics
Â Concept 12.2 Visual acuity charts
Â Concept 12.3 Slit lamp and Ophthalmoscopes
Â Concept 12.4 Errors of Refraction
Â Concept 12.5 Pin hole and macular function tests
Â Concept 12.6 Amblyopia
Â Concept 12.7 Retinoscopy
Â Concept 12.8 Refractive procedures

258 | Ophthalmology
Concept 12.1: Basics

Learning objectives
• To know basic points regarding slit refractive power and index of eye
• To know about visual angles
• To learn about Purkinje images
Time Required
1st reading 20 mins
nd
2 look 5 mins
• Total diopteric power of eye is 58 D to 60 D.

• Reduced eye: Simplified optics of eye is referred as reduced eye.
• Refractive power of the cornea is 44D
• Refractive power of the lens is:16D-17D
• Refractive index of the cornea is 1.376.
• Refractive index of lens is 1.386-1.406.
• Refractive index of aqueous and vitreous humor is 1.33
Visual angles:
a. Angle Alpha (α):
Angle between optical axis and visual axis at the nodal point.
b. Angle Gamma (γ):
Angle between optical axis and fixation axis at the centre of rotation of the eyeball.
c. Angle Kappa (κ):
Angle between visual axis and pupillary line at cornea
Fig.12.1:
Optics| 259
Positive angle kappa – Pseudo exotropia. It is a feature of hypermetropia.
Negative angle kappa- Pseudo esotropia. It is a feature of myopia.
Purkinje image:
Formed when strong beam of light is projected on eye.
• Ist and IInd image- by anterior and posterior surface of cornea.
• IIIrd and IVth image- by anterior and posterior surface of lens.
• IVth image- is inverted.
In aphakia, 2 images are absent (3rd and 4th).
In pseudophakia, 4 images
Fig.12.2:
260 | Ophthalmology
Concept 12.2: Visual acuity charts

Learning objectives
• To know about different vision testing charts
Time Required
st
1 reading 30 mins
nd
2 look 10 mins
Visual acuity measurement by Snellen chart

Letters are made of different sizes and designated by distance at which letter subtends
5 min of ARC, e.g. letters on 6/6 line subtend 5 min of ARC when viewed at 6m, each
part (stroke) of the letter subtends 1 min of arc. It measures minimum resolvable visual
acuity. In Normals, the minimum resolvable angle is 30 s to 1 min of arc.
Fig.12.3: Snellen chart
Snellen chart
Near visual acuity is assessed commonly at 40 cm, using charts with different size print
samples. Jaeger, Snellen are examples.
Optics| 261
Fig.12.4: Near vision chart
Fig.12.5: Landolt C chart
Landolt C chart chart is a way to check vision for illiterate or mute patients.
262 | Ophthalmology
ETDRS chart (Early Treatment of Diabetic Retinopathy Study Chart)
Fig.12.6:
Same number of letters per row (five letters per row). When using a LogMAR chart, visual
acuity is scored with reference to the logarithm of the minimum angle of resolution. It
is done at 4 m.
Vision testing in infant: The pattern visual evoked potential (VEP) and preferential
looking behaviour by Teller chart. An objective measure of the visual acuity may also be
made by utilizing the phenomenon of opticokineticnystagmus.
Fig.12.7: Opticokineticnystagmus drum

Optics| 263
Other charts used in children:
Cardiff acuity cards for children 2–4 years of age.
Lea figure testing in a young child. The child matches the presented figure. The child
points to one of four choices to match the figure or letter he or she sees on the computer
monitor or chart in the distance.
HOTV acuity testing. The child is asked to match the indicated letter on the chart with
a hand-held card displaying the HOTV letters.
STYCAR (sight testing for young children and retards)

264 | Ophthalmology
Concept 12.3: Slit lamp and Ophthalmoscopes

Learning objectives
• To know basic points regarding slit lamp and ophthalmoscopes with lenses used
Time Required
st
1 reading 20 mins
nd
2 look 5 mins
Fig.12.8: SLIT LAMP
SLIT LAMP
The slit-lamp is essential for a thorough examination of the eye. The magnification can
be varied by changing the power of the eye pieces and the objective lens. It can view
upto anterior 1/3rd of vitreous. Coupled with additional lens, fundus and optic disc can
also be seen (slit lamp biomicroscopy)
For an emmetropic, magnification of Direct ophthalmoscope is 15 times, image formed
is virtual and erect and is used to see central retina.
Magnification of Indirect ophthalmoscope with 20D lens is 3 times, image formed is real
and inverted and is used to see the periphery of the retina.
Optics| 265

Fig.12.9: DIRECT OPHTHALMOSCOPE Fig.12.10: INDIRECT OPHTHALMOSCOPE
Fig.12.11: 20D – FOR INDIRECT OPHTHALMOSCOPY

90D/78D – FOR SLIT LAMP
BIOMICROSCOPY
266 | Ophthalmology
Concept 12.4: Errors of Refraction

Learning objectives
• To know about various errors of refraction
• To learn about presbyopia
Time Required
st
1 reading 40 mins
nd
2 look 15 mins
Errors of Refraction:
Myopia:
It is a refractive error where the light rays are focused in front of the retina. It is
corrected by using concave lens. Any myopia of more than 6D is called high myopia.
Myopia with fundus changes is called pathological myopia.
Far Point and Near Point Come Nearer in Myopia.
Hypermetropia:
It is a refractive error where the light rays are focused behind the retina. It is corrected
by convex lenses.
The fundus changes are:
• Pseudopapillitis.
• Silk shot appearance.
• Degenerative retinoschisis.
Near Point Becomes Distant in Hypermeropia.
Refractive Error
Fig.12.12:
Optics| 267
Astigmatism:
When the refractive power in the two principal axis of the eye is different, it is called
astigmatism. It is corrected by cylindrical lenses.
It can be due to corneal curvature abnormality, lenticular curvature abnormality/oblique
position of lens and oblique displacement of macula.
Fig.12.13:
Types of astigmatism (can be classified in different ways)

Simple myopic Regular With the rule astigmatism – vertical axis (90 Corneal
(refractive degree) is steeper
Simple power change Lenticular
hypermetropic regularly Against the rule astigmatism – horizontal axis
from one (0/180 degree) is steeper
meridian to Retinal
Compound other)
myopic Oblique – When the 2 mridians are not
horizontal or vertical, but at 90 degress
Compound
hypermetropic Irregular Bioblique - When the 2 mridians are not at 90
(like in degree to each other
keratoconus,
Mixed corneal
opacity)
268 | Ophthalmology
Fig.12.14:
Anisometropia:
When the total refraction of the two eyes is unequal by > 2.5 D.
Aniseikonia:
When the images projected to the visual cortex from the two retina are abnormally
unequal in size and/or shape.
Pseudomyopia:
• Due to excessive ciliary muscle tone which causes increase in accommodation leading
to increase in the power of the lens.
• Distant vision is decreased while near vision is good.
• Present in children who try to compensate their refractive error
• Can also be drug induced eg. Cholinergic drugs since it causes ciliary spasm and will
increase the tone of the ciliary muscle.
Aphakia:
Absence of the Lens:
• Eye becomes highly hypermetropic.
• Total power of eye is reduced to + 44 D from + 60 D [less by 16D-17D].
• Total loss of accommodation.
• Best available treatment for aphakia is posterior chamber intraocular lens.
Other methods of correcting aphakia:

• Spectacles.
• Contact lens.
• Refractive surgery:
Optics| 269
Keratophakia.
Epikeratophakia.
Hyperopic Lasik.
Disadvantages of spectacle correction in aphakia

• Problem of spherical and chromatic aberration
• Prismatic effect of thick lenses
• Roving ring scotoma (Jack in the box phenomenon)
• Field of vision is limited
• Not useful in unilateral aphakia as it causes diplopia
Fig.12.15: Pincushion Distortion
Fig.12.16: Jack in box phenomeon

270 | Ophthalmology
Presbyopia
Presbyopia is when eyes gradually lose the ability to see near things clearly due to
decrease in accommodation with age. It is a normal part of aging. Presbyopia usually
becomes noticeable in your early to mid-40s.
Common symptoms of presbyopia are:

• having eyestrain or headaches after reading or doing close work
• having difficulty reading small print
• having fatigue from doing close work
Treatment
Near glasses (plus)
Bifocals (if patient has refractive error for far as well)
Fig.12.17: BIFOCALS
Fig.12.18: BIFOCALS (executive) – preferably in pediatric patients

Optics| 271
Concept 12.5: Pin hole and macular function tests

Learning objectives
Time Required
st
1 reading 20 mins
nd
2 look 5 mins
PIN-HOLE
Pinhole aperture compensates for the effect of refractive errors, and consists of an
opaque occlude perforated by one or more holes of about 1 mm diameter. If the vision
is subnormal, the visual acuity is again determined by asking the patient to read the
letters through a pinhole. If it improves, it indicates an underlying refractive error.
However, visual acuity in patients with macular disease and posterior lens opacities may
be worse with pin hole.
Fig.12.19:
Macula function tests

272 | Ophthalmology
Fig.12.20: Normal Amsler grid Fig.12.21: Amsler grid with metamorphosia and
positive scotoma
Optics| 273
Concept 12.6: Amblyopia

Learning objectives
Time Required
st
1 reading 20 mins
nd
2 look 5 mins
Amblyopia:
It is defined as deficiency of form sense resulting in reduction in visual acuity of greater
than two lines between the eyes or an absolute reduction in acuity below 6/9.
Squint is the most common cause of amblyopia.
Pathophysiology: Cell shrinkage in parvocellular layers of lateral geniculate body.
Signs and symptoms:

• Decreased visual acuity.
• Decreased accommodation ability.
• Afferent pupillary defect- in severely affected eye.
• Eccentric viewing.
• Enhanced crowding phenomenon.
• Neutral density filters decrease vision in normal eye and not in amblyopic eye.
Types:
• Strabismic Amblyopia – due to squint
• Form deprivation Amblyopia: congenital cataract, rubella keratitis.
• Refractive Amblyopia:
Anisometropic Amblyopia.
Ametropic Amblyopia.
Meridional Amblyopia.
Treatment:
• Refractive correction.
• Occlusion.
• Penalisation (with atropine).
• CAM stimulator (high contrast square wave gratings of different frequency).
• Pleoptics – Stimulation of fovea by means of after–images in case of eccentric fixation.
• Drug therapy: Levodopa/Carbidopa:
• Occlusion therapy is the mainstay of the treatment in which NORMAL eye is occluded
274 | Ophthalmology
Concept 12.7: Retinoscopy
Learning objectives
• To know steps of retinoscopy
• To know about refractive error prescription
• To learn basics of contact lenses
Time Required
st
1 reading 40 mins
nd
2 look 15 mins
Retinoscopy
Also called Skiascopy or shadow test, is an objective method of finding out the error of
refraction by the method of neutralisation.
Fig.12.22: Retinoscopes Fig.12.23: Priestley Smith Retinoscope
Observation:
Depending upon the movement of red reflex, when a plane mirror retinoscope is used,
reflex direction is seen like these 3:
"Against"
Fig.12.24:
Optics| 275
Plus lens are added if reflex moves in same direction with movement of retinoscope
Minus lens are added if reflex moves in opposite direction with movement of retinoscope
Deduction for distance:

If retinoscopy is performed at a distance of 1m, 1D is deducted. If retinoscopy is
performed at a distance of 67cm, 1.5D is deducted.
Deduction of cycloplegic:
Atropine- 1D: <7 yrs of age: Atropine should be used for cycloplegic.
Atropine ointment is the choice of cycloplegic in children. 1% ointment is given 3 times
a day for 3 days.
Homatropine- 0.5D
This is done in two axis. The final prescription is given as- example
Add is given for near vision if required

If retinoscopy is done from 1 m with no cycloplegia, then the results are interpreted as
below:
• No movement of red reflex indicates myopia of 1 D.
• When red reflex moves along with the movement of the retinoscope, it indicates
either emmetropia or hypermetropia or myopia of less than 1 dioptre
• Against the movement indicates myopia of more than 1D.
Contact Lens:
Contact lens is a small polymer material designed to rest on the cornea or sclera
Purpose:
• Optical- used to correct refractive errors.
• Therapeutic – Bandage contact lens
• Cosmetic – coloured contact lenses
Types:
Material:
• Hard- Gas-impermeable –PMMA (Poly methyl methacrylate)
• RGP-Rigid gas-permeable –
CAB- Cellulose Acetate Butyrate.
Styrene.
Siloxane- methacrylate.
Fluoro based or fluorinated silicon.
276 | Ophthalmology
• Soft:
Hydrogel- HEMA.
Elastomer- Silicon rubber.
• Patients using soft contact lens (if use tap water for cleaning the lens) are at increased
risk of Acanthamoeba Keratitis.
• DK- Symbolises oxygen permeability of contact lens; where D is diffusion co- efficient
and K is solubility co-efficient.
• DK/t: Denotes oxygen transmissibility, where t is the thickness of the contact lens.
• Fluorescein: Is not used in soft- lens fitting evaluation as it stains the lens. Except for
large molecules fluorescein like Flourexon.
• Benzalkonium chloride should never be used for disinfecting soft contact lens.
• Toric lenses- For correcting astigmatism, contact lenses with cylindrical power are
called toric lenses.
• X- chrom lenses- These lenses transmit light in red part of the spectrum and are
useful to patients with red-green defective vision.
Optics| 277
Concept 12.8: Refractive procedures

Learning objectives
• To know some refractive procedures and range of refractive error they can correct
• To know basic of LASIK
Time Required
st
1 reading 40 mins
nd
2 look 15 mins
REFRACTORY PROCEDURES
Procedure Detail Range
Radial keratotomy Linear radial incisions (80% depth) are made in Upto - 6 D
peripheral cornea sparing a central optic zone
thereby flattening it
Intracorneal rings or inserted in a paracentral corneal stromal pocket Upto - 6 D
segments lead to central flattening
Photorefractive keratotomy Excimer laser ablation of the superficial layer of Upto -4D
(PRK) the cornea, after removing the epithelium. Astigmatism up to
around 3 D and low–
moderate hypermetropia
Laser assisted epithelial Resembles excimer laser PRK with an epithelial
keratomileusis (LASEK) flap.
Laser-assisted in situ Excimer laser beam reshapes the cornea by +4 to -12D
keratomileusis (LASIK) ablating the superficial stroma to a predetermined astigmatism up to 5 D
extent after lifting a flap of the cornea with a
sharp
Microkeratome or femtosecond laser
Refractive lenticule Refractive lenticule extraction (ReLEx) uses a +4 to -12D
extraction (SMILE) femtosecond laser to cut a lens-shaped piece of astigmatism up to 5 D
corneal tissue (a lenticule) within the intact
cornea. This is then removed a minimally
invasive 4 mm incision (small incision lenticule
extraction – SMILE).
Clear lens extraction -15D

Phakic intraocular lens Concave intraocular lenses of appropriate power +10 to -20D
are fitted in the anterior chamber or posterior
chamber anterior to the natural
crystalline lens.
Holmium:YAG laser or conductive thermokeratoplasty is suitable for lower hyperopia of
11 D to 12.5 D
278 | Ophthalmology

Fig.12.25: Refractive lenticule extraction (SMILE)
Fig.12.26:
Optics| 279
PHOTOREFRACTIVE KERATECTOMY
Laser epithelial keratomileusis
Fig.12.27: PHAKIC IOLs

280 | Ophthalmology
Worksheet

Optics| 281
• Write the diagnosis of each
Refractive Error
• What is the refractive error
• This vision chart is tested from _____m?

282 | Ophthalmology
• Identify the device
• Aniseikonia is __________________________
• Identify the spectacles
• _____ lens are added if reflex moves in same direction with movement of retinoscope
• This chart is used for ___________________
Optics| 283
Laser-assisted in situ keratomileusis (LASIK) Range? _______________
• Which laser is used in this step of LASIK?

284 | Ophthalmology
EXTRA POINTS:

Ophthalmology Concept Book

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Ophthalmology Concept Book

Uploaded by

Copyright:

Available Formats

Concept Based Learning

Video Companion on Each Chapter

Comprehensive Review Series

First Published 1999, Delhi Academy of Medical Sciences

© 2021 DAMS Publication

Â Concept 1.2 Vascular and lymphatic supply

Â Concept 1.3 Embryology

Middle Vascular (Uveal Tissue):

Inner Neural (Retina):

Anterior and Posterior Chambers (Anterior Segment)

From lateral half – into preauricular nodes

Surface Ectoderm Neural Ectoderm Mesoderm Neural Crest

• Conjunctival • Iris and • Extraocular • Corneal stroma keratocytes and endothelium

Formation of OPTIC VESICLE and STALK

FORMATION OF LENS VESICLE AND CUP

DEVELOPMENT OF LENS FIBRES

Fig.1.7: Persistent Hyperplastic primary vitreous

• EXTRA POINTS FROM DQB

• Name derivatives of Surface ectoderm

Â Concept 2.2 Etiology of cataracts

Â Concept 2.3 Senile Cataract

Â Concept 2.4 Management of Cataract

Â Concept 2.5 Complications of Cataract Surgery

Â Concept 2.6 Congenital Anomalies and

Embryonic (1-3 months of gestation)

Congenital and Developmental Cataract:

Types of Congenital and Developmental Cataract: cryg gene

Vossius ring – iris pigments on lens capsule after blunt trauma

Radiational Cataract: Glass Blower’s or Glass- worker’s cataract

Myotonic dystrophy: Christmas tree cataract

Atopic dermatitis: Shield cataract

• Deficiency of Galactokinase:Lamellar cataract

Lowe’s syndrome (Oculo- cerebro-renal syndrome):

Complicated Cataract: develops as a result of some other primary ocular

• Degenerative – Myopia, Retinitis pigeentosa

Anterior capsular/polar cataract: due to corneal perforation (penetrating injury)

Increased age related Decreased level of total

Deposition of Melanin Hydration and

Nuclear sclerosis Type of Cataract

Fig.2.17: Posterior Subcapsular Cataract

Incipient/Intumuscent stage – frequent change of glasses, coloured haloes

There is no role of medical therapy in cataract

Anaesthesia In Cataract Surgery:

FEMTOSECOND LASER ASSISTED CATARACT SURGERY (FLACS)-

Other cataract surgeries

Fig.2.22: Extracapsular Catract Extraction (ECCE)

Intra Ocular Lens (IOLs):

Fig.2.28: ULTRASOUND A and B scan

Complications of Cataract Surgery:

Fig.2.32: Pupil block GLAUCOMA

Congenital Anomalies of Lens:

Fig.2.34: Lens coloboma

Fig.2.35: Anterior and posterior lenticonus

Marfans syndrome Upwards and temporal

Homocystinuria Down and nasally

Sulphite oxidase deficiency

Well-Marchesani syndrome Inferior subluxation

Fig.2.36: Subluxation of lens in Marfans

Fig.2.37: Anterior dislocation of lens

• EXTRA POINTS FROM DQB

Write the name of cataract morphologies in boxesSteps of phacoemulsification

List some causes of subluxation of lens

Â Concept 3.2 Infective keratitis

Â Concept 3.4 Corneal ectasias

Â Concept 2.6 Congenital Anomalies and