Clinical Ophthalmology

CLINICAL
OPHTHALMOLOGY
Made Easy
CLINICAL
OPHTHALMOLOGY
Made Easy
SECOND EDITION
Editor-in-Chief
Anina Abraham MS
Fellow (Vitreoretinal Surgery)
LV Prasad Eye Institute
Hyderabad, Andhra Pradesh, India
Vitreoretinal Consultant
Swarup Eye Center
Editor
Sirisha Senthil MS FRCS
Consultant in Glaucoma
Foreword
Kasu Prasad Reddy
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Clinical Ophthalmology Made Easy

First Edition: 2009
Second Edition: 2013
ISBN: 978-93-5090-518-0
Printed at
Dedicated to
THE CREATOR
of every cell of the eye,
which is so fearfully and
wonderfully made
Contributors
Anina Abraham MS Nitesh Narayen MS DNB

Fellow (Vitreoretinal Surgery) Former Fellow
LV Prasad Eye Institute LV Prasad Eye Institute
Hyderabad, Andhra Pradesh, India Hyderabad, Andhra Pradesh, India
Vitreoretinal Consultant Cataract, Cornea and
Swarup Eye Center Refractive Surgeon
Hyderabad, Andhra Pradesh, India Maxivision Eye Hospitals
Mayur R Moreker MS DOMS FCPS DNB Ritesh Narula MS
FRCS Former Fellow
(Glasgow, Scotland, UK) LV Prasad Eye Institute
Former Fellow Hyderabad, Andhra Pradesh, India
LV Prasad Eye Institute Consultant, Ophthalmologist and
Hyderabad, Andhra Pradesh, India Vitreoretinal Specialist
Consultant and Eye Surgeon Center for Sight, New Delhi, India
Bombay Hospital and
Medical Research Center Sirisha Senthil MS FRCS
Mumbai, Maharashtra, India Consultant in Glaucoma
Mohammad Javed Ali MD
FRCS FRCGP Sunayana Bhat MS
Consultant Former Fellow
Department of Ophthalmic Plastics and LV Prasad Eye Institute
Facial Asthetic Surgery Hyderabad, Andhra Pradesh, India
Consultant Consultant in Pediatric Ophthalmology
Department of Orbits and Strabismus
Ocular Oncology and Neuro-ophthalmology
LV Prasad Eye Institute Vasan Eye Care
Hyderabad, Andhra Pradesh, India Mangalore, Karnataka, India
Foreword
A wise man once said nothing succeeds like success

and in my view, the definition of success is hard work,
combined with the blessings of your elders and the will of
God. All these three components are there with Dr Anina
Abraham and Dr Sirisha Senthil, with whom I had the
pleasure of working together at Maxivision Eye Hospitals,
Hyderabad, Andhra Pradesh, India. The first edition of
Clinical Ophthalmology Made Easy by them was such a
success that they are going for the next edition. At my
age of 63, I feel academic activities by some among us are a gift and they both
are gifted to that extent.
The book I found to be extremely useful as an excellent and concise pocket
book for quick reference in a clinical situation. Having done thousands of
procedures and having got involved in many technical advances in eye care, I
still keep the book with me in all my travels for a quick reference. When I was
a resident, then after all the degrees, I still continue to be a resident meaning,
the learning process never ends. Lastly, my observations are that the young
ophthalmologists are far more informed and talented than us, the old ones and
I am sure that these young oculists will contribute further to better the book.
Kasu Prasad Reddy MBBS MS DO MRC (Ophth)

Chairman
Maxivision Eye Hospitals
Preface to the Second Edition
Clinical Ophthalmology Made Easy is a condensation of information on a wide

range of topics in clinical ophthalmology. It is compiled from major textbooks
and the latest peer-reviewed journals. It aims to simplify reading of vast complex
topics, making quick reference in the clinics possible. It gives the reader a practical
and concise summary of various ophthalmic diseases and management for
better understanding.
We hope to constantly update information in future editions, for which we
need your support, encouragement and constructive criticism. We sincerely wish
that the book will be a useful addition to your library.
Anina Abraham
Sirisha Senthil
Preface to the First Edition
Clinical Ophthalmology Made Easy is a condensation of information on a wide

range of topics from major textbooks in the respective fields of ophthalmology.
It aims to simplify the difficult topics and give the reader a practical and concise
summary for better understanding. The book is primarily meant for postgraduate
students for whom it will be a quick reference in preparing for the examinations
and for the practicing ophthalmologists in dealing with common problems in
day-to-day practice.
Each chapter has been divided into etiology, pathology, clinical features,
management and follow-up. Diagrams, tables, and flow charts have been added
where necessary to add clarity. Although it provides information on most topics,
we wish to caution readers that the book should not be a substitute for detailed
reading from standard textbooks.
We hope to constantly update information in the future editions for which
we need your constant support, encouragement and constructive criticisms. We
sincerely wish that the book will be a useful addition to your library.
Anina Abraham
Sirisha Senthil
Acknowledgments
First and foremost, we would like to thank our patients, our great teachers. We
are especially grateful to Dr Kasu Prasad Reddy (Chairman) and all our colleagues
at Maxivision Eye Hospitals, Hyderabad, Andhra Pradesh, India, for their valuable
support and constant encouragement. We are indebted to all our teachers
Dr G Chandrashekar, Dr Subhadra Jalali, Dr Ajit Babu, Dr Nazimul Husain, Dr Rajeev
Reddy, and Dr Annie Mathai, LV Prasad Eye Institute, Hyderabad, Andhra Pradesh,
India, for their valuable lessons in vitreoretina and glaucoma. Many thanks to
our Professors at Sarojini Devi Eye Hospital, Hyderabad, Andhra Pradesh, India,
and Aravind Eye Hospital, Madurai, Tamil Nadu, India, for teaching us the basics
in ophthalmology without which the book would not have been possible.
We are thankful to Tamar Chatterjee, who has been a great help in designing
the cover page of the book, and to our families, for always being there for us and
above all, we thank God, the creator of the eye.
Contents
1. Patient Evaluation 1
Evaluation of Glaucoma 1
Evaluation of Squint 3
Evaluation of Uveitis 7
Evaluation of Proptosis 8
Evaluation of Ptosis 11
Evaluation of Corneal Ulcer 13
2. Glaucoma 14
Visual Field 14
Scotoma 17
Tonometry 18
Calibration of a Goldmann Tonometer 19
Gonioscopy 21
Primary Open Angle Glaucoma 23
Normotensive Glaucoma 26
Ocular Hypertension 27
Primary Angle Closure Glaucoma 28
Secondary Glaucoma 30
Inflammatory Glaucoma 31
Glaucomatocyclitic Crisis 32
Neovascular Glaucoma 33
Phacolytic Glaucoma 34
Phacomorphic Glaucoma 35
Malignant Glaucoma 36
Aphakic Glaucoma 38
Pseudoexfoliation Syndrome 39
Iridocorneal Endothelial Syndrome 40
Uveitis-Glaucoma-Hyphema Syndrome 41
Buphthalmos 42
Nd: YAG Laser Iridotomy 44
Argon Laser Trabeculoplasty 45
Trabeculectomy 46
Non-Penetrating Filtration Surgery 49
Artificial Drainage Shunts 50
In the Clinic 51
3. Retina 52
Layers of the Retina 52
Retinal Color Coding 53
Fundus Fluorescein Angiography 54
Indocyanine Green Angiography 56
Optical Coherence Tomogram 57
xviii Clinical Ophthalmology
Clinical Electrophysiology 58
Evaluation of Macular Function 62
Cystoid Macular Edema 63
Central Serous Chorioretinopathy 65
Pigment Epithelial Detachment 67
Retinal Pigment Epithelium Tear 68
Macular Hole 69
Age-related Macular Degeneration 72
Anti-VEGF Therapy 75
Idiopathic Macular Telangiectasia 76
Polypoidal Choroidal Vasculopathy 78
Central Retinal Vein Occlusion 80
Branch Retinal Vein Occlusion 82
Central Retinal Artery Occlusion 83
Cotton Wool Spots 85
Ocular Ischemic Syndrome 86
Diabetic Retinopathy 89
Hypertensive Retinopathy 91
Hypertensive Choroidopathy 92
Eales Disease 93
Vitreous Hemorrhage 95
Retinopathy of Prematurity 97
Lasers 98
Hereditary Fundus Dystrophies 101
Peripheral Retinal Degeneration 102
Pathological Myopia 103
Retinal Detachment 105
Tractional Retinal Detachment 108
Exudative Retinal Detachment 109
Proliferative Vitreoretinopathy 111
Leukocoria 113
Endophthalmitis 115
Preparation of Intravitreal Drugs 118
In the Clinic 119
4. Uvea 120
Uveitis120
Investigations for Uveitis 122
Iris Nodules 124
Intermediate Uveitis 125
Ocular Toxoplasmosis 126
Fuchs Heterochromic Uveitis 129
Vogt-Koyanagi-Harada Disease 130
White Dot Syndromes 132
Acute Posterior Multifocal Placoid 133
Pigment Epitheliopathy 133
Birdshot Retinochoroidopathy 135
Multifocal Choroiditis and Panuveitis 137
Multiple Evanescent White Dot Syndrome 138
Punctate Inner Choroidopathy 139
Serpiginous Choroiditis 140
Immunosuppressive Drugs 141
Contents xix
5. Cornea 142
Corneal Color Coding 142
Bacterial Keratitis 144
Keratomycosis 146
Acanthamoeba Keratitis 148
Interstitial Keratitis 149
Herpes Simplex Keratitis 150
Keratoconus 152
Corneal Dystrophies 155
Therapeutic Contact Lens 157
Corneal Degenerations 158
Corneal Vascularization 161
Pannus 162
Moorens Ulcer 163
Bullous Keratopathy 165
Corneal Transplant 166
Lamellar Keratoplasty 169
6. Conjunctiva 170
Pseudomembranous and Membranous Conjunctivitis 170
Pterygium 172
Trachoma 173
Follicular Conjunctivitis 175
Allergic Types of Conjunctivitis 177
Superior Limbic Keratoconjunctivitis 179
Amniotic Membrane Graft 180
Limbal Stem Cell Transplant 181
Ophthalmia Neonatorum 182
Dry Eye 184
Tests for Dry Eye 186
Keratoconjunctivitis Sicca 188
Xerophthalmia 189
Tearing 190
7. Sclera 193
Scleritis193
Posterior Scleritis 195
Staphyloma 196
8. Pediatrics and Squint 197

Amblyopia197
Visual Acuity Testing in Preverbal and Verbal Children 200
Neonatal Cloudy Cornea 201
Congenital Cataract 202
Classification of Exotropia 204
Classification of Esotropia 205
Infantile Esotropia 206
Accommodative Esotropia 207
Microtropia 209
Heterophoria 210
Duane Syndrome 211
xx Clinical Ophthalmology
Brown Syndrome 212

Moebius Syndrome 213
Nonsurgical Management of Squint 214
Sudden Onset Diplopia 215
Botulinum Toxin 216
9. Neuro-ophthalmology 218
The Pupil 218
Field Defects 221
Optic Atrophy 226
Anterior Ischemic Optic Neuropathy 228
Papilledema 230
Optic Neuritis 233
Third Nerve Palsy 235
Fourth Nerve Palsy 238
Sixth Nerve Palsy 239
Tolosa-Hunt Syndrome 241
Ocular Myasthenia 242
Horizontal Gaze Palsies 245
Horners Syndrome 247
Pseudotumor Cerebri 248
10. Oculoplasty 249
Non-Specific Orbital Inflammatory Disease 249
Thyroid-related Orbitopathy 251
Orbital Decompression 254
Basal Cell Carcinoma 255
Xeroderma Pigmentosum 257
Squamous Cell Carcinoma 258
Bowen's Disease 261
Meibomian Gland Carcinoma 262
Lateral Orbitotomy 265
Socket Reconstruction 266
Blepharoptosis 267
Entropion 269
Ectropion 271
Phakomatoses 272
Proptosis 276
Orbital Cellulitis 277
Carotico-Cavernous Fistula 279
Optic Nerve Glioma 281
Optic Nerve Meningioma 282
Retinoblastoma 283
Choroidal Melanoma 285
11. Lens 287

Senile Cataract 287
Secondary/Complicated Cataract 288
After Cataract 289
Zonular Cataract 290
Ectopia Lentis 291
Cataract Surgery 293
Contents xxi
Intraocular Lenses 294

Intraocular Lens Power Calculation 295
Intraocular Lens Malposition 296
Postoperative Decrease in Vision 298
12. Trauma 299

Chemical Injuries 299
Traumatic Hyphema 302
Blowout Fracture of Orbit 304
Intraocular Foreign Body 306
Localization of Intraocular Foreign Body 307
Siderosis Bulbi 309
Chalcosis 310
13. Systemic Diseases 311

Eye in Aids 311
Cytomegalovirus Retinitis 313
Acute Retinal Necrosis 314
Eye in Tuberculosis 316
Eye in Sarcoidosis 318
Eye in Syphilis 319
Behets Disease 320
Eye in Leprosy 321
Index 323
chapter
Patient Evaluation 1
EVALUATION OF GLAUCOMA
History
Pain, redness, watering
One/two-sided headache or brow ache
Haloes around bulbs; blurred vision
Nausea, vomiting
Use of topical/systemic steroids
Trauma
Frequent change of glasses
Family History
Diabetes mellitus/glaucoma/ocular disease
Past History
Similar complaints in the past
Diabetes, hypertension
Ocular surgery, laser
Uveitis, asthma
Treatment History
Glaucoma medication, use of homeopathy medications, inhalational
steroids, antihypertensive (beta-blockers), antimigraine drugs (Topiramate)
Ocular Examination
Visual acuity for distance and near; vision improvement with pin hole
Refraction
Intraocular pressure with applanation tonometry
Gonioscopyopen angle, closed angle, occludable angle, goniosynechiae,
blotchy pigments, angle recession, foreign body, new vessels, silicone oil,
patency of the internal osteum
Pachymetry for central corneal thickness
Visual fields
Anterior segment examination
Cornea
Epithelial/stromal edema/scars
Pigment on endothelium
Krukenbergs spindle
Pseudoexfoliation (PXF)
2 Clinical Ophthalmology
Anterior Chamber
Depth (central and peripheral); regularity
Reaction
Iris
Color/pattern
Posterior synechiae
Peripheral anterior synechiae
Rubeosis iridis
Peripheral iridotomy/iridectomy
Pupil
Size, shape, reaction to light
Transillumination defects, sphincter atrophy
Pseudoexfoliation
Lens
Opacification, subluxation
Dislocation, glaucomflecken
Pseudoexfoliative material
Fundus Examination
Size/shape of optic disc
Neuroretinal rim (pallor/notching/thinning/ISNT rule)
Splinter hemorrhages
Peripapillary atrophy
NFL loss
PRPC (laser) marks
Vein occlusions
Choroidal detachment
Investigations
Central corneal thickness
Visual fields
GDx, OCT, HRT
EVALUATION OF SQUINT
History
Onset, duration, intermittent/constant
Progression/regression
Ocular pain, headache (with aura)
Diplopia (variability), lid droop (variability)
Trauma to head/face/eye
Fever (viral meningitis)
Tremors, hemiparesis, weakness
Hearing loss, tinnitus, vertigo
Long standing early morning headache with nausea and vomiting (raised
ICT)
Nasal symptoms
Defective vision
Tingling and numbness (multiple sclerosis)
Past History
DM/HTN/cardiovascular disease
Stroke, multiple sclerosis
Drug allergies
Ocular surgery
Previous episodes with remissions/exacerbations
Malignancy
General Examination
Including CNS examination and ENT examination
Ocular Examination
Best corrected visual acuity for distance and near; refraction
Color vision, visual fields
Compensatory head posture, facial symmetry
Lagophthalmos any facial palsy
Ocular alignmentHirschberg corneal reflex, cover/uncover/alternate cover
test, Prism bar cover test, Krimsky test
Ocular motilityfull/restricted
Diplopia charting
Forced duction test
IOP, gonioscopy
Anterior segment: if ptosis presentevaluate fully
Posterior segment any papilloedema?
Cover Test
To detect heterotropia
Done for near and distance
Cover the apparently fixing eye and watch movement of suspected deviating
eye
Cover-uncover Test
To detect heterophoria
Uncover the eye and watch its movement
If eye deviated under cover on uncover, it will manifest a re-fixation
movement on being uncovered
Alternate Cover Test
Interrupts binocular fusion
Reveals total deviation (phoria + tropia)
Phoriapatient will have straight eyes before and after test
Tropiapatient will have a manifest deviation
Quickly cover each eye alternately and watch behavior of each eye when
cover is removed and transferred to the other eye
Krimsky Test
Prism in front of seeing eye which fixates a target
Increase strength of prism till corneal reflex is centered in blind eye
Prism Bar Cover Test
Precisely measures angle of deviation
Alternate cover test performed
Prisms of increasing strengths are placed in front of one eye with base
opposite the direction of deviation
For esotropiause a base out prism
For exotropiause a base in prism
Amplitude of ocular re-fixation movements gradually decreases
End point is when ocular movements are negated
Then, angle of deviation = strength of prism
Hirschbergs Test
Light thrown into the eyes from 60 cm distance with an ophthalmoscope
or focused light beam
Patient is asked to look at the light
1 mm of deviation of corneal reflex = 7 deviation

If reflex is at the pupillary margin deviation is 15
If reflex is seen way between center of pupil and limbus deviation
is 20
Reflex way between pupillary margin and limbus deviation is 30
If reflex seen at limbus deviation is 45
Worth Four Dot Test

If all 4 lights seen normal fusion or abnormal retinal correspondence
(ifmanifest squint)
2 red lights seen LE suppression
3 green lights RE suppression
2 red + 3 green seen diplopia
Red and green alternately seen alternate suppression
Bagolini Striated Glasses
Glasses placed in front of both eyes
Patient is asked to look at a point source of light
Maddox Rod (When Placed in Front of Right Eye)

Evaluation of Paralytic Squint
Determine causehistory, ocular examination orbital ultrasonography,
neurological examination, CT-scan, MRI
Secondary deviation > Primary deviation
Diplopia Charting
Data obtained:
Areas of single vision and diplopia
Distance between 2 images in diplopia
Image tilt/erect
Image on same level or not
Crossed/homonymous diplopia
Park 3 Step Test
1. Identify hypertropic eye
2. Patient looks horizontally right and then leftdeviation (and diplopia)
increases in the direction of action of paralyzed muscle
3. Tilt the head toward each shoulder and look for increase in deviation (in
superior oblique palsy, deviation increases on tilting the head to the same
side as the palsy)
Bielschowsky Head Tilt Test
For example: In right superior oblique palsy, right hypertropia increases when
head is tilted toward the right shoulder; and disappears or decreases when head
is tilted toward the left shoulder
EVALUATION OF UVEITIS
History
Onset, duration
Pain, photophobia, redness, watering
Blurred vision, floaters
Trauma
Viral infection, e.g. herpes zoster ophthalmicus
Fever, weight loss, night sweats, cough, shortness of breath (TB, sarcoidosis)
Diarrhea, constipation (inflammatory bowel disease)
Low back pain (ankylosing spondylitis)
Small joint pains (rheumatoid arthritis)
Orogenital ulcers (Behets disease)
Exposure (HIV, venereal disease)
Skin lesions like erythema nodosum, dermographia
Treatment History
Any long-term treatment for TB, leprosy
Any topical medication like steroids for similar episodes in the past
Past History
Diabetes/hypertension/tuberculosis/leprosy
Ocular surgery, previous recurrent attacks
Rheumatoid arthritis, SLE, ankylosing spondylitis
Ocular Examination
Best corrected visual acuity for distance and near
Refraction
IOP, gonioscopy
Anterior segment examination:
Conjunctivacircumciliary congestion
Sclerascleritis
Corneakeratic precipitates (small/fine/white/stellate/medium-
sized/mutton fat/greasy/inferiorly or throughout endothelium);
disciform keratitis
Anterior chambercells, flare, hypopyon, hyphema, peripheral
anterior synechiae
Irismuddy, loss of crypts, heterochromia iridis, iris nodules, sector
atrophy, new blood vessels, iris bombe
Pupilsmall, reaction to light, posterior synechiae, occlusion pupillae,
seclusio pupillae, NVI, sphincter atrophy
Lenscataract, subluxation
Posterior segment examination:
Vitreous cells
Snow banking, cystoid macular edema
Choroiditis, vasculitis, papillitis
EVALUATION OF PROPTOSIS
History
Onset, duration and progression of proptosis
Associated pain; nature of the pain
Decreased vision
Diplopia in which gaze?
Field defects
Remissions/exacerbations
Diurnal variation; trauma
Systemic History
Fever, upper respiratory tract infection (sinusitis, lymphangioma, leukemia)
Any other cutaneous swellings (neurofibromatosis)
Epistaxis (nasal communication)
Dental infection
Skin lesions (caf au lait spots in NF-1)
Allergies, nasal discharge, nasal polyps
Breast lumps, chronic cough, shortness of breath, hemoptysis (metastasis)
History Specific to Thyroid Orbitopathy
Increased/decreased appetite
Weight loss/gain
Palpitations, chest pain, shortness of breath
Hyperactivity/lethargy
Skin problemsdry skin, excessive sweating
Neck swelling
Hand tremors
Menorrhagia/amenorrhea
Sleep disturbances
Past History
Diabetes mellitus (DM) or hypertension (HTN)
Cardiovascular disease/CNS disorder/respiratory disorder
Previous ocular disease or surgery
Personal History
Diet/appetite/bowels/micturition
Smoking/alcohol intake
Family History
Similar complaints in the family
Treatment History
Use of steroids or other medication
General Examination
Conscious, coherent, moderately built
Pallor, icterus, cyanosis, clubbing, lymphadenopathy, pedal edema (PICCLE)
Dental and nasal examination
Thyroid (neck) and breast examination
Finger/hand tremors
Skindry/scaly; caf au lait spots
Vital data
Temperature/BP/respiratory rate/heart rate
Systemic Examination
Heartsounds; murmurs
Lungbreath sounds
Abdomenhepatosplenomegaly; any masses
Ocular Examination
Best corrected visual acuity for distance and near
Refraction (high myopes pseudoproptosis)
Visual fields, color vision
Ocular alignmentcover, uncover, alternate cover tests
Diplopia charting (if present); extraocular movements
Forced duction test (if any movement is restricted)
IOP; differential IOP; gonioscopy; applanation tonometrycheck for
pulsatile proptosis
Anterior segment evaluation; especially pupillary reaction
Fundusany signs of optic nerve compression; CRVO; optic atrophy
Proptosis Evaluation
Facial symmetry; compensatory head posture
Lid retraction or lid lag, periocular fullness
If ptosis is presentevaluate levator function
Inspection
Naffzigers sign on looking tangentially over the patients forehead,
palpebrae of the proptosed eye is seen first.
Birds view or Worms view can help in picking up subtle proptosis and
differences between the two eyes.
Fullness or mass lesion in the orbit; visible pulsations or engorged veins
Lagophthalmos, Bells phenomenon; corneal exposure
Conjunctival congestion over recti muscles (thyroid eye disease) diffuse
congestion (vascular anomaly)
Change in size with Valsalva
Palpation
Orbital rimany irregularity; mass lesion; can you insinuate your finger
between the globe and orbital bones?
Size, shape, surface, margins, skin over-swelling, consistency, signs of

inflammation, tenderness, reducibility and mobility
Variation with valsalva or bending down of the head
Resistance to retropulsion; pulsations, thrill
Corneal anesthesia, infraorbital/supraorbital anesthesia
Auscultation
Bruit over lesion/eyeball/ipsilateral forehead (Best heard with the bell of the
stethoscope)
Exophthalmometry
Reading > 21 mm or a difference of > 2 mm between the two eyes suggests
proptosis
Reading of 1012 mm suggests enophthalmos
Hertels exophthalmometer reading, e.g. base reading 110 mm, OD 24 mm,
OS 20 mm
Measure horizontal displacement: Mark a point (P) on the center of the

bridge of the nose; place a scale over the bridge; measure the distance between
(P) and the nasal limbus of both eyes
Measure vertical displacement: Place a scale perpendicular to the lateral
canthus; measure the vertical displacement with a scale held perpendicular to
the first scale
EVALUATION OF PTOSIS
History
Sudden/gradual in onset
Duration present since birth?
Trauma
Diurnal variation worse in the evening?
Worse in sunlight
Diplopia
General fatigue
Past History
Diabetes mellitus, hypertension
Previous ocular surgeryunder local anesthesia?
Similar complaints in the past
Family History
Others in the family affected?
Consanguineous marriage
Ocular Examination
1. Visual acuity for near and distance, without and with correction is checked;
refraction
2. Facial symmetry
3. Compensatory head posture
4. Brow elevation
5. Cover/uncover test, Hirschbergs corneal reflex, Prism bar cover test (test
ocular alignment)
6. Extra-ocular movementsfull/restricted
7. Lids:
MRD 1margin reflex distance 1 distance between upper lid margin
and corneal reflection of a pen torch (patient looking directly at it)
Normal = 44.5 mm
MRD 2margin reflex distance 2 distance between lower lid margin
and corneal reflection of a pen torch
VFHvertical fissure height MRD 1 + MRD 2; Normal: 812 mm;
Measure in upgaze/ downgaze/primary gaze
MCDmargin crease distancedistance between upper lid margin
and lid crease in downgaze; Normal in female = 10 mm; male = 8mm
MLDmargin limbal distancedistance between upper lid margin
and lower limbus in upgaze
LPS functionplace a thumb firmly against patients brow to negate the
action of the frontalis; then patient looks up as far as possible; measure
the excursion of the lid
Normal function = 15 mm
Good function = 1214 mm
Fair function = 511 mm

Poor function = < 5 mm
Bells phenomenonpresent if upward and outward rotation of the
globe occurs on forceful closure of the lids; if absentpatient may
develop post-operative exposure keratopathy
Herring reflex in unilateral ptosis, manually elevate the ptotic lid and
look for drooping of the fellow upper lid (it may show a subtle bilateral
ptosis in which case surgery may induce ptosis in the fellow eye)
Marcus Gunn jaw winking phenomenonwhen patient makes chewing
movements with his jaw, the lid intermittently droops and elevates
Tests for ocular myasthenia (mentioned under neuro-ophthalmology)
8. Anterior segment examination, gonioscopy, IOP
9. Fundus examination
EVALUATION OF CORNEAL ULCER

History
Onset, duration
Symptomspain, watering, discharge
Trauma, fall of foreign body, chemical injury
Viral infection, conjunctivitis
Dry eyes, contact lens wear
Swimming in dirty pools
Topical steroid use or other medication (keratitis medicamentosa)
Itching (shield ulcer)
Facial weakness
Past History
Recurrence; similar episodes in the past
DM, HTN, ocular surgery
TB, leprosy (neurotrophic ulcer)
Ocular Examination
Visual acuity for distance and near; any improvement with pin hole; refraction
Digital tonometry (applanation tonometry should not be done when keratitis
exists)
Syringing; reflux of material with pressure over lacrimal sac; any discharge
Anterior segment examination:
Lidsblepharitis, hordeolum, trichiasis, entropion, lagophthalmos
Upper palpebral conjunctivagiant papillae
Corneal sensation
Corneal ulcerlocation (central/marginal); surrounding edema/
infiltrate; stromal haze; shape and size; margins/edge/base/floor;
satellite lesions; Wessely ring; fluorescein staining
- Pre-auricular lymphadenopathy
- Anterior chamber reaction; hypopyon
- Pupillary reaction
Fundus examination
chapter
Glaucoma 2
VISUAL FIELD
An area in space visible to a steadily fixating eyes darkness
Island of vision surrounded by a sea of darkness
Field Charting
Kinetic
Confrontation method
Bjerrums tangent screen
Goldmann perimetry
Static
Standard automated perimetry (white on white perimetry) SITA (Swedish
Interactive Thresholding Algorithm)
Short wave automated perimetry
Frequency doubling perimetry
Blind Spot
Corresponds to the region of the optic nerve head
15 temporal to fixation extending 2 above and 5 below
Has an area of:
Absolute scotomacorresponds to actual optic nerve head
Relative scotomacorresponds to peripapillary retina
Field Defects
Binasal Hemianopia
Atheroma of carotids or posterior communicating artery
Dilatation of 3 ventricle (optic nerves get pressed downwards and outwards
against the internal carotids)
Glaucoma 15
Bitemporal Hemianopia
Chiasmal lesions, dermatochalasis
Nasal retinitis pigmentosa, nasal retinoschisis
Optic nerve hypoplasia, tilted discs (high myopia)
Junctional Scotoma
Tuberculum sellae meningioma
Damage to anterior knee of Willibrand at optic chiasma (lower nasal fibers)
Unilateral central scotoma (or unilateral blindness) + Contralateral upper
temporal field loss
Right Homonymous Hemianopia

Lesion in left optic tract
Right temporal and left nasal field loss
Right Homonymous Upper Quadrantanopia

Left optic radiation (temporal lobe lesion)
Pie in the sky
Right Homonymous Lower Quadrantanopia

Left optic radiationparietal lobe lesion
Pie on the floor
Homonymous Hemianopia with Macular Sparing

Anterior visual cortex lesion
Occlusion of posterior cerebral artery
Macular Involvement
Occlusion of middle cerebral artery
Lesion at the tip of the calcarine process
Centrocecal Scotoma
Toxic amblyopia; ethambutol toxicity; papilloedema
Central Scotoma
Optic neuritis; AMD; heredomacular degenerations
Tubular Vision
Retinitis pigmentosa; advanced glaucoma
Ring Scotoma
Early retinitis pigmentosa
Enlargement of Blind Spot
Papilloedema
High myopia with peripapillary atrophy
Altitudinal Defect
AION; optic disc drusen
Chorioretinal coloboma
Glaucoma 17
SCOTOMA
An area of decreased visual sensitivity surrounded by an area of normal
sensitivity
Types
Positivecan be perceived
Negativecannot be perceived, e.g. blind spot
Absoluteno change in area of scotoma with change in size or color of
stimulus
Relativearea of scotoma changes with change in the variables
Slopinggradual decrease in visual sensitivity from an area of normal
sensitivity, e.g. tumors
Steepdistinct margin between areas of normal and decreased sensitivity
Physiologicale.g. blind spot
Pathological scotomas are:
Central involving the point of fixation, e.g. optic neuritis, ethambutol
toxicity
Paracentral involving area near the point of fixation but sparing
fixation
Centrocecal involving papillomacular bundle
Arcuate involving the radial arcuate fibers, e.g. glaucoma, optic disc
coloboma
Altitudinal hemifield defect; respects the horizontal meridian; e.g.
AION
Junctional ipsilateral centrocecal scotoma + contralateral upper
temporal quadrantanopia
Angioscotomas above and below blind spot due to shadows of
large blood vessels
TONOMETRY
Assessment of intraocular pressure
Used to diagnose glaucoma and monitor IOP. IOP is the only modifiable
risk factor in glaucoma and is useful in the diagnosis and management of
glaucoma anti-glaucoma medications
Digital Tonometry
Like testing fluctuation
Patient looks down; 2 fingers placed above superior tarsal plate a small
distance apart and pushed backward alternately
Indentation Tonometry (Schiotz)

Measures depth of indentation of anesthetized cornea, produced by a
weighted stylet
Measured by a lever which travels over a scale
Depth and volume of indentationdepend on tension and distensibility
of ocular walls
Weights used are 5.5, 7.5, 10.0, 15.0 g
Calibrated so that equivalent reading in mm Hg are read off a chart
False recording inthick/steep/irregular corneas, high myopia,
high hypermetropia, after ocular surgery, with miotics/vasodilators/
vasoconstrictors
Applanation Tonometry
Goldmann applanation tonometry (GAT)gold standard
Based on Imbert-Fick principle: assesses amount of force needed to flatten
or applanate a known area of cornea; IOP is directly proportional to pressure
applied and inversely proportional to the area flattened 0.05 mL of aqueous
displaced
A force of 0.1 g exerted by a spring and lever system corresponds to IOP of
1 mm Hg
Goldmann assumed a uniform central corneal thickness (CCT) of 520 microns
IOP recorded is affected by CCT and GAT overestimates IOP in thicker corneas
and underestimates IOP in thinner corneas
Correction factor: 5 mm Hg for each 70 difference in CCT; deviating from
520 microns, for example, if recorded IOP is 24 mm Hg and CCT is 590 , the
corrected IOP is 19 mm Hg
In thinner corneas, the IOP is underestimated and in thicker corneas the IOP
is overestimated
Perkins tonometer principle is applanation
Tonopen principle is applanation (surface applanated is very small)
Non-contact tonometer uses air puff; principle ocular response analyzer
(bidirectional applanation)
Dynamic contour tonometer (DCT) principle is contour matching
Rebound tonometer measures IOP by rebound method, portable
Glaucoma 19
CALIBRATION OF A GOLDMANN TONOMETER

Should be calibrated at 0, 2 and 6; The acceptable error is 2 mm Hg at 0 level of
testing, 3 mm Hg at 2 (corresponds to 20 mm Hg), 4 mm Hg at 6 (corresponds
to 60 mm Hg)
Checking the Calibration at 0

Set the tonometer in position; tension on circular dial set at 0.05; the
head should lean slightly forwards; twirl the circular dial counter-clockwise
until the head rocks back towards you; the tension should read 02 mm Hg
below 0
Twirl the dial clockwise until the head rocks forward again; the tension
should read 02 mm Hg

Remove the calibration rod from its box; firmly screw into position the
holding bracket that slides along the rod so that the closet mark in front of
the center one is aligned as exactly as you can
Slip the rod and its holder into the receptacle on the right side of the
tonometer; the head will rock backwards towards you
Twirl the dial clockwise until the head rocks forwards; the tension reading on
the dial should be 2023 mm Hg
Twirl the dial counter-clockwise until the head rocks backwards; the tension
on the dial should read 1720mm Hg

Remove the rod and holding bracket from the tonometer and reposition
the bracket so that it is aligned exactly with the most forward mark on the
rod
Replace the rod in its bracket in the tonometer receptacle; the tonometer
head should rock backwards, towards you.
Twirl the dial clockwise until the head rocks forwards; the tension should
read 6064 mm Hg
Twirl the dial counter-clockwise until the head rocks backward; the tension
should read 5660 mm Hg
Glaucoma 21
GONIOSCOPY
Angle of the anterior chamber is examined:
1. To decide if the angle is open or occludableif more than 1800 of the
posterior trabeculum is visible on gonioscopy (without indentation), the
angle is considered open (dark room; minimum slit lamp illumination with
reduced height and width so that light does not fall on the pupil as miosis
may cause artificial opening of angle)
2. To look for abnormalities in the angle like trabecular hyperpigmentation,
angle recession, peripheral anterior synechiae, new vessels, pigment clumps
(examine with bright light pupil constricts and angle structures can be
examined)
Types
1. Directthe anterior curve of the contact lens (goniolens) is such that the
critical angle is not reached and the light rays are refracted at the contact
lens/air interface, e.g. Koeppe goniolens
2. Indirectlight rays are reflected by a mirror in the contact lens (gonioprism)
and leave the lens at nearly a right angle to the contact lens-air interface; can
be with or without indentation; e.g. Goldmann three mirror lens, Sussman,
Zeiss, Posner four mirror lens
Grading of the Angle

Grade Van Herrick Shaffer Modified Shaffer
4 > : 1 45 35 Ciliary body band visible
3 -:1 35 20 Scleral spur visible
2 : 1 20 Anterior trabeculum visible
1 <:1 10 or less Schwalbes line visible
0 Closed angle Closed angle Schwalbes line not visible
Van Herricks Grading

Grade 4: Peripheral anterior chamber depth between iris and corneal
endothelium is more than the corneal thickness
Grade 3: Peripheral chamber depth is between and corneal thickness
Grade 2: Peripheral chamber depth is corneal thickness
Grade 1: Peripheral chamber depth is between less than corneal thickness
Grade 0: Iridocorneal contact
Indentation gonioscopy helps to identify plateau iris configuration
Sine-wave sign double hump pattern of the iris on indentation;
Peripheral hump produced by the anteriorly inserted iris root and ciliary
processes
Central hump produced by the peripheral lens contour
Dilated pupil is not a contraindication for gonioscopy
Contraindications
Hyphema
Compromised cornea
Lacerated/perforated globe
Glaucoma 23
PRIMARY OPEN ANGLE GLAUCOMA

Glaucoma is a chronic progressive optic neuropathy leading to optic nerve
damage and loss of visual field, intraocular pressure (IOP) being the most
common risk factor
POAG occurs due to increased resistance to aqueous outflow at the
trabecular meshwork
Pathogenesis
Mechanical Changes
Raised IOP causes mechanical pressure on the lamina cribrosa
Backward displacement and compaction of the laminar plates
Openings through which axons pass become narrow causing damage to
the optic nerve
Vascular Perfusion
Decreased capillary blood flow due to mechanical compression at the lamina
cribrosa
Lack of auto-regulatory mechanism
Occurs in acute hypotension, acute blood loss, vasospasm
Decreased optic nerve head perfusion causes decreased axoplasmic flow
and ganglion cell death apoptosis
Disc Changes
1. Disc size50% cupping in a small disc is more significant than 50% cupping
in a large disc; CDR (cup-disc ratio) varies with disc size
2. Asymmetrical cupping > 20% in discs of the same size

3. Cup:disc ratio > 0.5 : 1.0 (especially in the vertical axis)
4. Neuroretinal rim
Pallor
Localized notching
Thinning
ISNT ruleThickness of Inferior rim>
Superior rim> Nasal rim> Temporal rim (followed in 80% eyes);
Inferior rim : temporal rim = 2 : 1
Superior rim : temporal rim = 1.5 : 1
5. Superficial disc hemorrhages at disc margin (splinter hemorrhage in NTG)

6. Peripapillary atrophy
7. Bayoneting sign; nasal pushing of vessels
8. Nerve fiber layer (NFL) defectslit-like/wedge-shaped/diffuse NFL loss
(seen best with a red-free filter) - corresponds to field loss; touches the disc
and fans out; appears dark compared to surrounding retina
Lenses Used for Disc Evaluation
1. 60 D : 1 (magnification factor)
2. 78 D : 1.15
3. 90 D : 1.45
4. Goldmann 3 mirror: 1.13 (central lens)
Field Defects in Glaucoma
1. Generalized reduction of sensitivity
2. Relative paracentral scotoma
3. Nasal step
4. Siedel scotoma
Glaucoma 25
5. Arcuate scotoma
6. Double arcuate (ring) scotoma
7. Near-total field defect
Points to Note in Glaucoma Evaluation
1. Look at the reliability criteria
2. Does the defect/scotoma appear like a glaucomatous defect (arcuate area)?
3. Does it correlate with the optic disc changes?
Andersons Criteria
Diagnostic criteria for glaucomatous visual field loss in the absence of retinal/
neurological disease affecting visual field
3 or more non-edge points in a cluster with p = <5%, one of which has
p = <1%
CPSD or PSD with p = < 5%
GHT outside normal limits
- CSPDcorrected pattern standard deviation
- PSDpattern standard deviation
- GHTglaucoma hemi-field test
Any defect must be confirmed by repeated testing
Provocative Tests
1. Water drinking test(done for POAG)
Patient drinks 1 liter of water; IOP measured after 1 hour
Test is positive if IOP rise > 8 mm Hg
Tests to determine whether a narrow angle is actually occludable:
2. Prone provocative test
Patient lies face down for 1 hour without sleeping
This is due to anterior movement of the lens (not mydriasis)
3. Mydriatic test
Weak cycloplegic agent instilled into eye and IOP checked after 12
hours
4. Map stone test (Phenylephrine-pilocarpine test)
2% pilocarpine + 10% phenylephrine instilled every half hour into eye
for 2 hours
NORMOTENSIVE GLAUCOMA
Low Pressure Glaucoma
Mean IOP 21 mm Hg on diurnal testing
Glaucomatous optic disc damage; splinter hemorrhages may be present at
disc margin
Visual field losstypically closer to fixation; deeper, steeper and more
localized
Open angles
Absence of secondary causes
Possible Causes
Nocturnal systemic hypotension
Over treated hypertension
Carotid artery occlusion
Systemic vascular insufficiency
Hypercholesterolemia
Decreased blood flow velocity in the ophthalmic artery
Peripheral vascular spasm when exposed to cold (Raynauds phenomenon)
Migraine
Treatment
Prostaglandin analogues, 2 agonists, trabeculectomy
Avoid antihypertensives at bed time if patient is on antihypertensive
medication
Differential diagnosis:
POAGIOP > 21 mm Hg on diurnal variation testing
AIONPost-AION disc pallor can resemble disc changes in NTG
Congenital optic disc anomalies
Glaucoma 27
OCULAR HYPERTENSION
IOP > 21 mm Hg on two consecutive occasions in the absence of detectable
glaucomatous damage
Open angles on gonioscopy
Average corneal thickness
No other ocular pathology
Ocular Hypertension Treatment Study

Identified baseline factors that predicted POAG development
Older age
Larger vertical or horizontal C/D ratio
Higher IOP (>30 mm Hg)
Low central corneal thickness
Treatment is Considered for
One-eyed
Patients unable to do a visual field
Persistent elevated IOP
Thinner corneas
Patients who will be lost for follow-up
Central Corneal Thickness
Average normal CCT = 520 m (for the purpose of Goldman applanation
tonometry)
Thicker corneas record a falsely high IOP; thinner corneas record a falsely
low IOP with Goldmann tonometer
Apply a correction of 5 mm Hg for every 70100 m deviation in CCT, from
520 m; [subtract if corneas are thicker than 520 ; add if corneas are thinner
than 520]
14 thickness deviation = 1 mm Hg; (correction factor)
PRIMARY ANGLE CLOSURE GLAUCOMA

Obstruction of aqueous outflow by partial/complete closure of the angle
by peripheral iris
Mechanism
1. Pupillary block
2. Anterior insertion of iris and ciliary body
3. Trabecular obstruction
Primary Angle Closure Suspect (PACS)
Occludable angles
Primary Angle Closure (PAC)
Occludable angles with raised IOP/glaucomflecken/peripheral anterior
synechiae/pupillary sphincter atrophy
Primary Angle Closure Glaucoma (PACG)
PAC with optic disc damage and visual field loss
Anatomically Predisposing Factors
Anterior location of the lens iris diaphragm
Shallow anterior chamber
Women more prone than men
Anatomical Abnormalities Causing Secondary Angle Closure
Small lens sizemicrospherophakia
Smaller corneal diameter (by 0.25 mm)
Smaller axial length (hypermetropes, nanophthalmos)
Management
1. PACS:
Observation; periodic gonioscopy
Yag PI (if patient needs repeated dilated retinal examination)
Fellow eye has PAC/PACG
Post-dilated raised IOP
2. PAC:
Yag PI medical treatment
3. PACG:
Yag PI medical treatment surgical treatment
Acute Congestive Glaucoma (ACG)
Sudden total angle closure with acute rise in IOP
Painful decrease of vision
Circumciliary injection, corneal edema, stromal thickening
Shallow anterior chamber; peripheral irido-corneal touch
Glaucoma 29
Anterior chamber reaction with cells and flare

Dilated iris blood vessels
Vertically oval, mid-dilated, fixed pupil
Closed angles on gonioscopy
Optic disc hyperemia/edema
Differential Diagnosis
Secondary angle closure
Neovascular glaucoma
Phacomorphic glaucoma
Migraine
Always do gonioscopy for the fellow eye !!
Treatment of ACG
Indentation gonioscopy or pressure on the center of the cornea with a cotton
bud can break the attack by pushing the aqueous into the angle
IV acetazolamide 500 mg; oral acetazolamide 500 mg QID
IV mannitol 20% (12 g/kg body wt) over 45 min (contraindicated in cardiac
failure and renal compromise)
Topical steroids
Topical beta blockers
Topical pilocarpine 2% (every 15 min for 1 hour followed by every hour for
4 hours); will not work when iris ischemia is present when IOP is very high
Oral glycerol 50% (1 g/kg body wt); contraindicated in diabetics
Prophylactic YAG PI in the fellow eye
Post Congestive Glaucoma
After an attack of acute congestive glaucoma
Descemets folds (if IOP is decreased suddenly)
AC (anterior chamber) reaction; pigment on endothelium
Stromal iris atrophy
Fixed, mid-dilated pupil due to paralysis of the sphincter
Glaucomflecken due to focal necrosis of the lens epithelium; small gray
anterior capsular or subcapsular opacities
IOPnormal/increased/decreased
Narrow angles with trabecular hyperpigmentation with or without synechiae
Optic disc hyperemia/pallor
Absolute Glaucoma
No light perception
Total glaucomatous optic atrophy
Raised IOP
NVI may or may not be present
Rx:
Antiglaucoma medications
If very painfultrans-scleral cyclophotocoagulation/evisceration +
prosthesis
SECONDARY GLAUCOMA
1. Inflammatory glaucoma:
Anterior uveitis
Pars planitis
Glaucomatocyclitic crisis; Posner-Schlossman syndrome
Fuchs heterochromic iridocyclitis
2. Neovascular glaucoma
3. Corneal perforationadhesions between iris and cornea
4. Lens induced glaucoma:
Phacomorphic glaucoma
Phacolytic glaucoma
Phacoanaphylactic glaucoma
5. Aphakic glaucoma
6. Pseudophakic glaucomaAC IOL/PC IOL
7. Steroid induced glaucoma
8. Intraocular tumorsinfiltration of the angle by neoplastic tissue
9. Raised episcleral venous pressure:
Orbital inflammation
Sturge-Weber syndrome
Orbital varices
Carotico-cavernous fistula
Primary pulmonary hypertension
10. Pigmentary glaucoma
11. Malignant glaucoma
12. Pseudo-exfoliation syndrome
13. Angle recession glaucoma
14. Ghost cell glaucoma
15. Hemolytic glaucoma
Glaucoma 31
INFLAMMATORY GLAUCOMA
1. Angle closure with pupillary block
Pupillary block may be relieved with a YAG PI
2. Angle closure without pupillary block
Synechial angle closure
3. Open angle glaucoma in
Acute anterior uveitis - due to
Steroid induced raise in IOP
Trabecular obstruction by inflammatory cells
Acute trabeculitis
Inflammation subsides while ciliary body function returns
Chronic anterior uveitis - due to
Trabecular scarring/sclerosis
4. Fuchs heterochromic iridocyclitis
Secondary open angle glaucoma due to trabecular sclerosis
5. Posner-Schlossman syndrome
Acute trabeculitis
Treatment
Topical steroids/NSAIDs
Treat the cause of inflammation
IOP lowering drugs
Drugs contraindicated are PG analogs and pilocarpine
GLAUCOMATOCYCLITIC CRISIS
Posner-Schlossman syndrome
Recurrent attacks of unilateral, acute, secondary open angle glaucoma
associated with mild anterior uveitis
Probably due to acute trabeculitis; associated mild uveitis
Males, young people, association with HLA - Bw 54
Clinical Features
Blurring of vision, haloes
Mild discomfort
White eye
Corneal epithelial edema
IOP 4080 mm Hg
Few cells
1 or more fine white KPs
Open angleno peripheral anterior synechiae
Treatment
Topical steroids, oral NSAIDs
Aqueous suppressants to reduce IOP
Glaucoma 33
NEOVASCULAR GLAUCOMA
Pathogenesis
Severe, diffuse, chronic retinal ischemia
Hypoxic retina produces vaso-proliferative growth factors which diffuse into
the anterior segment
Neovascularization of the angle (NVA) blocks aqueous outflow in the
presence of an open angle
Later the neovascular membrane contracts causing a secondary angle
closure
Causes
Ischemic CRVO100-day glaucoma
Proliferative diabetic retinopathy
Ocular ischemic syndrome, CRAO
Chronic intra-ocular inflammation
Long-standing retinal detachment
Coats disease, intraocular tumors
Classification Pathology Management

Rubeosis iridis New vessels grow radially Panretinal photocoagulation;
over iris surface Intravitreal bevacizumab
Secondary open angle Fibrovascular membrane in Hypotensive agents;
glaucoma the angle blocks trabecular Topical atropine;
outflow Topical steroids;
Panretinal photocoagulation;
Anterior retinal cryopexy;
Intravitreal bevacizumab
Secondary angle Contraction of fibrovascular Hypotensive agents;
closure glaucoma membrane pulls the Topical atropine;
peripheral iris over Topical steroids;
trabeculum Panretinal photocoagulation;
Trabeculectomy + mitomycin C;
Aqueous drainage implants;
Trans-scleral cyclophoto-coagulation
Retrobulbar alcohol injection
Enucleation (painful blind eye)
Clinical Features
Severe ocular pain; decreased visual acuity
Circumciliary congestion, corneal edema
Very high IOP, synechial angle closure, NVI, NVA
Mild AC reaction
Ectropion uveae, cataract
Acute angle closure glaucoma
Absolute glaucoma
PHACOLYTIC GLAUCOMA
Also called lens protein glaucoma
Secondary open angle glaucoma
Lens proteins leak through the intact capsule of a hypermature cataract and
block the trabecular meshwork
Lens protein laden macrophages also block the trabecular meshwork
Phacoanaphylactic uveitisautoimmune reaction to lens proteins following
anterior capsule rupture
Clinical Features
Corneal edema; deep anterior chamber, open angles on gonioscopy
Floating white particles in aqueous pseudohypopyon
Treatment
Cataract extraction with IOL implantation with peripheral iridotomy; flush
out all the proteinaceous material from AC
Hypotensive agents, topical steroids
Glaucoma 35
PHACOMORPHIC GLAUCOMA
Secondary angle closure glaucoma caused by an intumescent cataractous
lens
Equatorial and anteroposterior increase in curvature of the lensincreases
iridolenticular contact; causing a pupillary block and iris bombe
Blurring of vision, severe ocular pain, high IOP
Circumciliary congestion, corneal edema, shallow anterior chamber,
intumescent lens
Treatment: Cataract extraction with IOL implantation
Lens induced glaucomas with rise in IOP of duration more than 23 weeks,
combined cataract surgery with glaucoma filtering surgery is required
MALIGNANT GLAUCOMA
Also called ciliary block glaucoma or aqueous misdirection syndrome
Important Signs
Shallowing or flattening of peripheral anterior chamber in the presence of
a patent peripheral iridotomy
Raised IOP
Etiology
Following surgery for PACG (incisional iridectomy)
Following YAG PI for PACG
Following retinal detachment surgery
Trauma, inflammation, infection
Spontaneous
Aphakia, pseudophakia
CRVO, ROP
Theories
1. Posterior pooling of aqueous causes forward displacement of iris-lens and
iris-vitreous diaphragm
Cilio-lenticular block ciliary processes rotate forward and press
against the lens-equator or anterior hyaloid
Anterior hyaloid obstruction breaks in the hyaloid near the vitreous
base allows posterior diversion of aqueous
2. Slackness of zonules leads to forward movement of lens-iris diaphragm; due
to severe prolonged angle closure or ciliary muscle spasm
Pupillary block glaucoma iris bombe; centrally deep anterior chamber
with 3600 posterior synechiae
Choroidal detachment central and peripheral shallowing of anterior
chamber; low IOP
Supra-choroidal hemorrhage high IOP, flat anterior chamber, severe pain
Treatment
Cycloplegics (atropine)ciliary paralysis tightens the zonules and pulls the
lens back
Hyperosmotics (mannitol)decrease the pressure exerted by the vitreous
Carbonic anhydrase inhibitors and beta-blockersdecrease aqueous
accumulation
Argon laser photocoagulation of ciliary processesdecreases aqueous
production
Glaucoma 37
Nd: YAG laserdisrupts the anterior hyaloid face; opens-up the

communication from anterior vitreous to the anterior chamber
Surgery
Posterior sclerotomy (Chandlers procedure)
Pars plana vitrectomy with anterior hyaloidotomy and peripheral iridectomy
Lens extraction with anterior vitrectomy and peripheral iridectomy
APHAKIC GLAUCOMA
Mechanism of Glaucoma in Aphakic Eyes
Primary open angle glaucoma; collapse of trabecular meshwork channels
Secondary glaucoma due to:
Immediate postoperative reaction
Enzyme glaucomadue to use of alfa-chymotrypsin
Pupillary block glaucoma
Hyphema
Peripheral anterior synechiae - causing a shallow anterior chamber
Malignant glaucoma
Vitreous in anterior chamber blocking the angle
Prolonged post-operative inflammation
Ghost cell glaucoma - vitreous hemorrhage
Implantation cysts in anterior chamber
Epithelialization of anterior chamber
Retained lens matter blocking the angle
Chronic uveitis due to retained lens matter
Steroid induced glaucoma
Treatment
IOP lowering agentstopical and systemic
Topical steroids for postoperative inflammation and hyphema
Relieve pupillary block with atropine/pilocarpine
Surgical management if not controlled medically
Glaucoma 39
PSEUDOEXFOLIATION SYNDROME
Pathogenesis
Gray-white, fibrillogranular, extra-cellular matrix material deposited on:
Anterior lens capsule, zonules, ciliary body, iris, trabecular meshwork,
conjunctiva, anterior vitreous face, cornea, pupil, iris
Clinical Features
Cornea Pseudoexfoliative material on endothelium [mimics KPs]

Pigment deposition on endothelium [diffuse/Krukenberg spindle]
Decreased number of endothelial cells [propensity to corneal decompensation]
Anterior Mild flare (pseudo-uveitis)
chamber
Angle Trabecular hyperpigmentation
Sampaolesi line (band of pigment anterior to Schwalbes line)
Dandruff-like pseudoexfoliative material in trabecular meshwork
Usually open; may be narrow
Iris Moth eaten appearance
Transillumination defects at pupillary margin
Pigment dispersion
Intrastromal hemorrhages on mydriasis
Pupil Does not dilate well
Pseudoexfoliative material at pupillary margin
Sphincter atrophy
Lens Nuclear cataract
Zonular instabilityphacodonesis, lens subluxation, zonular dialysis
Pseudoexfoliative material on anterior lens capsule
Pseudoexfoliation Glaucoma
Glaucoma occurs due to:
Clogging-up of trabecular meshwork by pseudoexfoliative material/
pigment released from iris
Trabecular endothelial dysfunction
Occurs in the 6th - 7th decade; more common in females
Bilateral with assymetric presentation or unilateral
Chronic open angle glaucoma
Degree of hyperpigmentation in the angle may correlate with the severity
of glaucoma
Treatment:
Anti-glaucoma medication
Argon laser trabeculoplasty
Trabeculectomy
IRIDOCORNEAL ENDOTHELIAL SYNDROME

Unilateral; 4th decade; females > males
Pathogenesis
Abnormal corneal endothelial cell layer which proliferates and migrates
across the angle onto the iris surface
Synechial angle closure due to contraction of this abnormal tissue
Progressive Iris Atrophy
Severe iris changes with stromal atrophy
Corectopia (malposition of pupil)
Pseudo polycoria (super-numerary false pupils hole formation)
Iris Nevus (Cogan-Reese) Syndrome
Diffuse nevus covers anterior iris (or)
Pigmented, pedunculated iris nodules
Smudged, matted iris surface (D/D- iris melanoma)
Chandler Syndrome
Corneal endothelial changeshammered silver appearance
Corneal edemablurred vision, haloes
Treatment
Trabeculectomy with mitomycin C
Aqueous drainage devices
Glaucoma 41
UVEITIS-GLAUCOMA-HYPHEMA SYNDROME
Uveitis-Glaucoma-Hyphema syndrome
Complication of cataract extraction with IOL implantation
Causes
ACIOL abrading the iris
PCIOL in ciliary sulcus
Spontaneous hyphemas iniris neoplasms, NVI, blood dyscrasias
Clinical Features
Rapid decrease in vision over minutes followed by more gradual resolution
over hours to days
Erythropsiared vision
Eye ache due to increased IOP
Microscopic hyphaema, anterior uveitis, increased IOP
Hyphema cleared from the anterior chamber within hours
Gonioscopyblood in trabecular meshwork between attacks
Treatment
IOLrotation/exchange/removal
Steroidsin uveitis
IOP lowering drugs
BUPHTHALMOS
Classification
True congenital glaucoma raised IOP during intrauterine life
Infantile from birth 3 years
Juvenile 36 years
Pathogenesis
Isolated trabeculo-dysgenesis absence of angle recess; iris inserted
directly into surface of trabeculum
Flat or concave iris insertion
Clinical Features
1. Corneal hazedue to epithelial/stromal edema
present with lacrimation, photophobia, blepharospasm
2. Buphthalmos (birth to 3 years):
Enlarged eye due to stretching when IOP increases
Stretched sclera - thin and translucent appears blue
Deep anterior chamber
Zonular fibers stretch and lens may subluxate
Axial myopia can cause amblyopia if untreated
3. Haab striae:
Horizontal or circular curvilinear lines
Healed breaks in DM
Breaks in DM occur due to stretching of eyeball; this causes sudden
influx of aqueous into stroma leading to stromal edema
4. Optic disc cupping may regress if treated early
C:D ratio > 0.3 : 1.0
Scleral canal enlarges
Lamina cribrosa may bow posteriorly
Cupping may regress if treated early and appropriately
Vision loss due tooptic damage, corneal scarring, amblyopia, cataract,
lens subluxation
Cloudy cornea
Mucopolysaccharidosis, birth trauma
Congenital hereditary endothelial dystrophy
Sclerocornea, keratitis (rubella)
Megalo cornea
In myopia; anatomically big cornea
Lacrimation
Nasolacrimal duct obstruction (delayed canalization)
Glaucoma 43
Secondary infantile glaucoma

Retinoblastoma, juvenile xanthogranuloma
PHPV, ROP, Trauma, inflammation
Ectopia lentis
Evaluation
Under general anesthesia
Measure IOP with Perkins tonometer/tonopen
Measure corneal diameter (>13 mm at any age or >11 mm up to 1 year
is significant)
Gonioscopywith a koeppe lens (direct gonioscope)
Retinoscopy
Optic disc evaluation
Surgical Treatment
Medical treatment with beta blockers and ACE inhibitors - before surgery
Avoid 2 agonists as they can cause sleep apnea and respiratory failure in
children
Goniotomy, trabeculotomy
Trabeculectomy + trabeculotomy
Aqueous drainage implants
Trans-scleral cyclophotocoagulation
Follow-up
Life long
Appropriate refractive and amblyopia therapy
Treat media opacities like corneal scars and cataract
Nd: YAG LASER IRIDOTOMY

Indications
PACG, PAC and acute angle closure
Fellow eye in acute angle closure, PAC, PACG
Secondary angle closure with pupillary block
POAG with narrow anglescombined mechanism glaucoma
Procedure
Done in a miosed pupil; apraclonidine 1% drop and anesthetic drop instilled
into eye
Abraham iridotomy lens is inserted
Site in superior iris chosen because it is covered by eyelid no diplopia
PI done as peripheral as possible to decrease damage to lens
Non-perpendicular beam aimed towards peripheral retina (to avoid macular
burn)
48 mJ energy (36 mJ 3 bursts)
Following the Procedure
One drop of 1% apraclonidine
Topical steroids for 1 week
IOP lowering agents depending on IOP
Complications
Bleeding
Increased IOP
Iritis posterior synechiae
Corneal burnsif contact lens is not used or laser beam not focused well
Glare and diplopiaif large PI inferiorly; not covered by upper lid
Glaucoma 45
ARGON LASER TRABECULOPLASTY

Argon laser beam aimed between anterior non-pigmented and posterior
pigmented trabecular meshwork
Indications
POAG, NTG
Pigmentary glaucoma
Pseudoexfoliation glaucoma
Contraindications
Aphakic glaucoma
Uveitic glaucoma
Extensive peripheral anterior synechiae (PAS)
Complications
Peripheral anterior synechiaeif burns are too posterior or if high energy
is used
Small hemorrhagesif blood vessels on iris are hit
Increased IOP
Anterior uveitismild
Increased incidence of encapsulated blebs following filtration surgery
Selective Laser Trabeculoplasty

Frequency doubled YAG
Only done for POAG, pigmentary glaucoma, pseudoexfoliation glaucoma
Can be repeated since no scarring is induced
Creates an inflammatory response inflammatory mediators attract macro
phages to engulf debris in trabecular meshwork (scavenges trabecular
meshwork and cleans it)
Following laser, patients should not be given topical/systemic NSAIDs or
steroids
TRABECULECTOMY
Lowers IOP by creating a fistula which allows aqueous outflow from anterior
chamber to sub-Tenons space
Fistula is guarded by superficial scleral flap
Postoperative Complications
Shallow Anterior Chamber
Results in peripheral anterior synechiae, endothelial damage, cataract
formation
Grading of Severity
1. Peripheral iris apposition to cornea
2. Pupillary border apposition to cornea
3. Corneolenticular touch
Causes
Shallow AC with increased IOP
Pupillary block [see if peripheral iridotomy is patent]
Malignant glaucoma
Suprachoroidal hemorrhage
Shallow AC with decreased IOP
Overfiltering blebs well-formed bleb; Seidels test is negative
Bleb leak flat bleb; Seidels test is positive
Seidels test 2% fluorescein instilled into conjunctival sac or over bleb; if
bleb leak is present, fluorescein gets diluted by escaping aqueous
Management of Bleb Leak

Topical atropine (cycloplegics) prevents pupillary block, pushes lens-iris
diaphragm backwards
Pinpoint bleb leak bandage contact lens, pressure patch; cyanoacrylate
or fibrin glue
Button holes/leaky incisions surgical repair
Aqueous suppression decreases aqueous flow through fistula allows
spontaneous healing
Topical antibiotics irritates conjunctival tissue and induces scarring
Management of Over-filtering Bleb

Aqueous suppressants
Decrease the dose of topical steroids
Simmonds shell
Patching the eye
Compression sutures
Additional suture to the scleral flap
Glaucoma 47
Filtration Failure - Due to

Subconjunctival and episcleral fibrosis
Bleb encapsulation
Over tight suturing of scleral flap
Scarring in scleral bed
Blockage of sclerostomy by vitreous, blood, uvea
Blockage by thin inflammatory membranes
Management
Ocular compression
Digital (through lower lid, with eyes closed and patient looking straight)
Focal (with a cotton budat edge of the scleral flap, adjacent to area
of bleb)
Suture manipulation
Releasable sutures are removed
Argon laser suture lysis
Needling of an encysted bleb
Subconjunctival injection of 5-FU
Nd: YAG laser gonioscopic re-opening of a blocked internal ostium
Re-surgery
Blebitis
White milky bleb - containing infective material
Anterior uveitis may or may not be present
Normal red fundal glow
Bleb-associated Endophthalmitis
Rapid worsening of vision
White milky bleb
Severe anterior uveitis and hypopyon
Vitritis; no red glow of the fundus
Late Bleb Leak
Due to dissolution of conjunctiva over sclerostomy (mitomycin C causes
necrosis of epithelium)
Complications
Thin overfiltering blebs
Scleral necrosis
Chorioretinal folds, hypotonous maculopathy
Infection
Corneal decompensation
Treatment
Sweating blebs tissue glue, sutures
Full thickness holes
Conjunctival advancement to hood existing bleb
Excision of bleb with conjunctival autograft
Rotational autograft
Scleral patch graft
Amniotic membrane grafting
Glaucoma 49
NON-PENETRATING FILTRATION SURGERY

Fashioning 2 lamellar scleral flaps (superficial and deep) and excising
the deep flap, leaving behind a thin membrane consisting of trabecular
meshwork or Descemets membrane through which aqueous diffuses from
anterior chamber to sub-conjunctival space
Anterior chamber is not entered
Indications
Ocular hypertension
POAG requiring moderate IOP control (5 mm Hg)
Deep Sclerectomy
Superficial scleral flap is made
2nd deeper partial thickness scleral flap 4 mm wide, is dissected forward to
the Schlemms canal and excised
Collagen implant drainage device is placed under the superficial scleral flap
which is loosely approximated and conjunctiva closed
Visco Canalostomy
Fornix-based conjunctival flap
Superficial 1/3rd thick scleral flap
2nd deeper scleral flap is dissected to provide access to Schlemms canal
Viscoelastic is injected into Schlemms canal with a special cannula
Descemets window is created by gently dissecting the deep flap anterior
to Schlemms canal and excising it
Viscoelastic is injected into the area of the sclerostomy
Superficial scleral flap is tightly sutured
Conjunctiva closed
Canaloplasty
Similar to viscocanalostomy
A fiber optic probe is passed around the Schlemms canal and prolene suture
is inserted
Sutures ends are tied tight enough to keep the canal open without tearing
it
ARTIFICIAL DRAINAGE SHUNTS

Artificial shunts which create a communication between anterior chamber
and sub-Tenon space
Tube is attached to a posterior episcleral explant
Have pressure sensitive valves for regulation of aqueous flow
Indications
Refractory glaucoma despite previous trabeculectomy with antimetabolites
Secondary glaucomas, neovascular glaucoma, aniridia, angle recession
glaucoma X
Severe conjunctival scarring due to previous surgeries
Congenital glaucoma where conventional procedures have failed
Post-vitrectomy glaucomas
Implant Types
1. Valved devices (Ahmed, Krupin, Joseph, OptiMed, White shunt pump) offer
a certain resistance and allow unidirectional flow of aqueous; Ahmed valve
is pressure-sensitive
2. Non-valved devices (Baerveldt, Molteno) are passive and do not offer any
resistance to either anterograde or retrograde flow
Mechanism
An open tube with one end in anterior chamber shunts aqueous into
an encapsulated area around the explant located 1012 mm posterior to
limbus
IOP reduction due to passive pressure dependent flow of aqueous across
the capsular wall
Thicker the capsule higher the IOP
Larger the surface area of encapsulation lower the IOP
Complications
Hypotony; suprachoroidal hemorrhage
Increased drainage or leakage leads to shallow AC
Corneal decompensationif tube touches the endothelium
Cataractif tube touches lens
Tube retraction from ACif tube is short; in children (due to growth of
eyeball)
Tube erosion through conjunctivaavoided by placing a donor scleral flap
between tube and Tenon capsule
Drainage failure if tube gets blocked by iris, vitreous or blood
Diplopiaif extraocular muscle damaged; large blebs
Bleb encapsulation over the implant; Extrusion of implant
Endophthalmitis; compressive optic neuropathy
Glaucoma 51
IN THE CLINIC
Patient can have 20/20 vision and still have glaucoma!!
Rise in IOP following pupillary dilatationlook for closed angles on
gonioscopy; if angles are openrule out pseudoexfoliation or pigment
dispersion syndrome
Dilated pupil is not a contraindication for gonioscopy; if the angle is open
even after dilatation, it is open; an occludable/closed angle requires repeat
gonioscopy without dilatation
In unilateral angle closure rule out a secondary cause (subtle lens
subluxation, ciliary body pathology)
High hyperopia with angle closure glaucoma in the young rule out
nanophthalmos
High myopia with angle closure glaucoma in the young rule out
microspherophakia
In young patients with raised IOP and open angles with/without posterior
subcapsular cataract rule out steroid induced glaucoma
Following peripheral iridotomy, if the angle is still occludable rule out
plateau iris syndrome
Gonioscopy must be repeated yearly as an open angle can eventually close
(with increasing age and anteroposterior diameter of the lens)
Glaucoma must not be treated based on Schiotz or non-contact tonometry
recordings (only Goldmann applanation tonometry)
Dilated disc evaluation is mandatory whenever a field test is done correlate
the disc and visual fields
Borderline IOP with a healthy disc check central corneal thickness before
starting glaucoma medication
Patient on brimonidine presenting with itching/blepharitis/dermatitis stop
the drug and substitute with a non- alpha agonist
IOP and disc evaluation must be routinely done following penetrating
keratoplasty and vitreoretinal surgery
Enlarged corneal diameter, photophobia and lacrimation in a child with
normal IOP rule out glaucoma
chapter
Retina 3
LAYERS OF THE RETINA
Layer Sign
Nerve fiber layer Flame-shaped hemorrhages
Cotton wool spots
Large retinal arteries and veins
Inner nuclear layer Retinal capillaries
Microaneurysms
Outer plexiform layer Retinal edema
Deep hemorrhages
Hard exudates
Retina 53
RETINAL COLOR CODING

Red Attached retina; attached macula (+ sign); microaneurysms; retinal/pre-retinal/
fresh vitreous hemorrhages; break (red with blue outline)
Blue Detached retina; macular edema; lattice degeneration; retinal veins
Green Vitreous opacities; cotton wool spots; fibrous proliferation
Purple Flat NVE/NVD
Orange Raised NVE/NVD
Yellow Hard exudates; drusen; medullated nerve fibers
Black Pigmentary changes; disc outline; scars; laser/cryotherapy marks; buckle effect
Brown Pigment epithelial detachment; choroidal melanoma
FUNDUS FLUORESCEIN ANGIOGRAPHY

Fluorescein is a water-soluble dyeremains mainly intravascular80%
bound; 20% free
Outer blood retinal barrier [BRB] RPE tight junctions
Inner blood retinal barrier [BRB] retinal capillary endothelial cells
Disruption of inner BRB leads to leakage of bound and free fluorescein into
extra vascular space
Fluorescenceproperty of molecules to emit light energy of longer
wavelength when stimulated by light energy of shorter wavelength
Technique
Red-free photograph is taken first
Inject 5 mL of 10% solution or 3 mL of 25% solution intravenously
Photos taken every 2 sec, for 525 sec after injection; then after 10 min and
20 min
Side Effects
Skin/urine discoloration, nausea and vomiting
Itching, hives, laryngeal edema
Anaphylactic shock
Phases
Choroidal/Prearterial Phase
Starts 812 sec after injection
Patchy choroidal filling
Cilioretinal artery if present, gets filled
Arterial Phase
Starts 1118 sec after injection
Arterial filling occurs
Choroidal filling continues
Arteriovenous/Capillary Phase
Complete filling of arteries and capillaries
Choroidal filling continues
After 2025 sec of injection, maximum fluorescence occurs in juxtafoveal/
perifoveal capillaries (best time to assess integrity of foveal avascular zone)
Venous Phase
Early laminar venous flow
Mid near complete venous filling
Late decreased concentration of dye in arteries
Late/Elimination Phase
Dye absent from angiogram in 510 min; late staining of the disc
Retina 55
Dark Fovea Due to

Avascular FAZ (supplied only by choriocapillaris)
Increased density of xanthophyll
Increased RPE cells at fovea (contain more melanin)
Hyperfluorescence Seen in
Window defects (RPE atrophy)
Pooling of dye (breakdown of outer BRB); e.g. CSCR, PED
Leakage due to:
Abnormal choroidal vasculature, e.g. CNVM
Abnormal retinal/disc vasculature, e.g. PDR; perivascular leakage from
inflamed vessel, e.g. Eales disease
Stainingprolonged retention of dye, e.g. Drusen, ERM
Hypofluorescence
Blockage of Retinal Fluorescence
Vitreous opacities
Pre-retinal lesionsblood
Intraretinal hemorrhages, hard exudates
Blockage of Background Choroidal Fluorescence
Subretinal/sub-RPE lesionsblood
Increased density of RPEcongenital hypertrophy of the RPE
Choroidal nevi
Filling Defects
Vascular occlusion (capillary drop-out)
Loss of vascular bed (myopic degeneration, choroideremia)
INDOCYANINE GREEN ANGIOGRAPHY

To study choroidal circulation
Infrared light readily penetrates xanthophyll, melanin, blood, exudates; is
absorbed by the dye and emitted
Reconstitute 40 mg in 2 mL and give intravenously
Rapid serial photos taken; then at 3, 10 and 30 min
Used mainly to diagnose and treat occult CNVM
Contraindicated inpregnancy, iodine allergy
Side-effectsstool staining, nausea and vomiting, itching, sneezing, local
skin necrosis, syncope
Phases
Early (260 sec)
Prominent filling of choroidal arteries, early filling of choroidal veins; retinal
arteries are seen
Early Mid-Phase (13 min)
Filling of watershed zone
More prominent choroidal veins
Retinal arteries and veins are seen
Late Mid-Phase (315 min)
Diffuse hyperfluorescence due to diffusion from choriocapillaris
Fading of choroidal filling
Late Phase (1530 min)
Hypofluorescence of choroidal vessels against a background of hyper
fluorescence
Retinal arteries and veins are not seen
Retina 57
OPTICAL COHERENCE TOMOGRAM

Tomographic imaging of optic nerve head and nerve fiber layer
Performs high resolution, cross-sectional imaging using low coherence light
Non-contact, non-invasive method
Correlates with histological measurement of the tissue
Not limited by pupil aperture or ocular optical aberrations
Analogous to B-scanuses light instead of sound waves to create images
with much higher resolution axially and laterally
Fiber optic based interferometerfor anterior and posterior segment
imaging
Cross-sectional informationderived from time of flight of reflected or back
scattered light
Normal Retina
Nerve fiber layerhigh reflective (red)
Plexiform layersmoderate back scattering (yellow)
Nuclear layersminimum back scattering (green)
Photoreceptorsdark layer
RPE and choriocapillarishigh reflective (red)
Choroid and scleralow reflectivity
Interpretation
Retinal thickness: Increased edema, traction
Reflectivity
Hyper-reflectivity: Inflammatory infiltrate, hard exudates, blood
Hypo-reflectivity: Retinal edema, media haze, shadowing from hyper-
reflective tissues
Distinction Between
Serous fluid, blood, cloudy exudate
Detachments of neurosensory retina and RPE
Operculum, posterior hyaloid, ERM
Uses in Retinal Disease
CSCR, CNVM
Vitreomacular traction
Polypoidal choroidal vasculopathy
Foveal schisis
Staging of macular holes
Evaluating vitreo-retinal interface
Quantifying retinal thickness (macular edema)
Uses in Glaucoma
Analyses NFL loss
Optic nerve head imaging
CLINICAL ELECTROPHYSIOLOGY
Components and Origin
Retinal pigment epitheliumEOG
Photoreceptors (a-wave), Muller and bipolar cells (b-wave), RPE (c-wave),
oscillatory potential (amacrine cells)Flash ERG
Macular photoreceptors (P50), Ganglion cells (N95)PERG (pattern ERG)
Optic Nerve to Visual CortexVEP
Basic ISCEV Flash ERG Response

Scotopic
Isolated rod response: Almost no a wave; slow rising, broad-peaked, b-wave
(rod function)
Maximal combined response: A sharp a wave and a much larger, rapidly

rising peaked b wave which comes to baseline very slowly (rod and cone
function)
Retina 59
Oscillatory potentials: High frequency oscillations that occur on the

ascending limb of the b-wave of the maximal combined response; Normal
response is characterized by 3 major peaks followed by a smaller peak
(middle/inner retina function)
Photopic
Single flash cone response: Small, rounded a wave and a very sharply rising
b wave that rapidly returns to the baseline (cone function)
30 Hz flicker response: Normal responses are such that the peak of a given
response falls just before the stimulus onset for the next response; if the
response peaks fall on the vertical stimulus line or immediately after the
stimulus line, it depicts a delay in the responses (cone function)
Negative ERG
a wave is larger than the b wave in scotopic maximal combined response
Seen in:
Congenital stationary blindness
X-linked retinoschisis
Retina 61
Central retinal artery obstruction

Quinine toxicity
Melanoma associated retinopathy
Batten disease
Cone Rod dystrophy
ERG Findings in
Cone dystrophy marked abnormal cone flicker response with normal rod
response
Lebers congenital amaurosis extinguished ERG
Inverse/central retinitis pigmentosa scotopic and photopic responses
show reduction in amplitude and increased latency
Advanced retinitis pigmentosa nearly extinguished ERG
Congenital stationery night blindness normal a wave and a very small b
wave
PDR reduction in amplitude of oscillatory potential
Ocular ischemic syndrome nearly extinguished oscillatory potentials;
delayed latency with reduced amplitudes of the flicker ERG responses
CRVO reduced b wave amplitude and increased 30 Hz flicker latency
indicate ischemia
CRAO negative ERG (absent b wave, normal a wave)
Ophthalmic artery occlusion non-recordable ERG
Siderosis bulbi marked reduction of a and b wave amplitude
EVALUATION OF MACULAR FUNCTION

1. Visual acuityfor near and distance
2. Slit lamp biomicroscopywith a strong convex lens or contact lens
3. Amsler grid:
Evaluates 10 of visual field surrounding fixation
Used for screening and monitoring macular disease and early optic
nerve lesions
Patient is asked to wear reading correction; cover at a time and look at
the central dot on the grid; he must report any distortion, blurred areas
or missing lines on the grid
4. Photo stress testing:
Patient asked to fixate light of a pen torch held 3 cm from eye for 10
seconds
Photo stress recovery time (PSRT)time taken to read any 3 letters of
the pre-test visual acuity line
Normal: 27 11 seconds (<50 sec)
PSRT is prolonged in maculopathy but not in optic neuropathy
5. Pupillary light reactionnormal in macular disease; RAPD in optic
neuropathies
6. Maddox roda large scotoma (loss of the red line viewed by the patient),
indicates macular disease
7. Blue light entoptoscopypatient views an intense homogenous blue-light
background; WBCs produce shadows seen by patient
8. Purkinjes entoptic phenomenona rapidly oscillating point source of
light shone through patients closed eyelids; he can detect shadow images
of his retinal vasculature
9. Potential acuity meter
10. Flying corpuscle test
11. Electroretinography
12. Visual evoked response
Retina 63
CYSTOID MACULAR EDEMA

Abnormal accumulation of fluid in the neurosensory retina in the macular
area
In the outer plexiform and inner nuclear layers
Fluid filled cyst-like changes seen
Pathophysiology
Clinical Features
Decreased vision [especially for near], metamorphopsia, positive central
scotoma
Cysts are seen on retro-illumination with a 78D lens
FFA
Early phase Fluorescein leaks from perifoveal capillaries; hyperfluorescence
Late phase Dye collects in cystic spaces arranged radially around the center
of the fovea; flower petal appearance
Causes and Management

Inflammatory
1. Following surgery:
Cataract surgery (PC rupture, vitreous loss, vitreous incarceration in
wound)
Penetrating keratoplasty
Glaucoma filtering surgery
Scleral buckling
Pars plana vitrectomy
Management
Anterior vitrectomy if vitreous loss occurs following PC rupture
Yag anterior hyaloidotomy if vitreous in wound
Topical NSAIDs nepafenac, bromfenac, ketorolac
Triamcinolone posterior sub-Tenons (40 mg in 1 mL) or intravitreal
(4 mg in 0.1 mL)
Intravitreal anti-VEGF avastin (bevacizumab 1.25 mg in 0.05 mL),
lucentis (ranibizumab 0.5 mg in 0.05 mL)
2. Intermediate uveitis treat with systemic steroids

3. Behcets disease intravitreal triamcinolone
4. CMV retinitis intravitreal ganciclovir
5. Acute retinal necrosis antiviral therapy
Metabolic
Diabetes mellitus:
Photocoagulation focal/grid
Intravitreal anti-VEGF/triamcinolone or combination
Ischemic
CRVO and BRVO
Intravitreal anti-VEGF/triamcinolone or combination
Macular grid photocoagulation
Hereditary
Retinitis pigmentosa oral acetazolamide/topical dorzolamide may be tried
Dominantly inherited CME
Mechanical
Macular pucker vitrectomy with ERM peeling
Vitreomacular traction syndrome vitrectomy
Hydrostatic
Hypertension control blood pressure
Toxic
Nicotinic acid
Topical epinephrine (used during cataract surgery)
Latanoproststop drug
Retina 65
CENTRAL SEROUS CHORIORETINOPATHY

Idiopathic chorioretinal disorder characterized by serous neural retinal
detachment in the macular region
Due to hyperpermeability of the retinal pigment epithelium (RPE)
M:F = 9:1; 2045 years age group, type A personality
Aggravating factorsstress, steroids, hypertension, SLE
Steroidsincreased capillary fragility and hyperpermeability; decom
pensation of choroidal circulation and leakage of fluid into the subretinal
space
Types
Typical/Classic/Acute
Younger people
Acute localized detachment of the retina
Mild to moderate VA loss
One/few focal leaks on FFA
Chronic
Diffuse retinal pigment epitheliopathy
Decompensated RPE
Chronic presence of shallow subretinal fluid
Widespread RPE pigment alteration
Increased risk of CNVM
usually bilateral
Bullous Retinal Detachment
Located inferiorly
Shifting sub-retinal fluid
After organ transplants, steroid use
Pathogenesis
Breakdown of blood retinal barrier at RPE level
Widespread choroidal hyperpermeability (detected on ICG angiography)
Abnormal choroidal circulation
Clinical Features (Acute CSCR)

Sudden onset of unilateral blurred vision
Micropsia, metamorphopsia, defective color vision
Positive relative scotoma
Acquired hyperopia
Round/oval sensory detachment at the macula causing a ring reflex
Sub-retinal fluidclear/turbid
Small precipitates on the posterior surface of the detachment
May be associated with pigment epithelial detachment
FFA
1. In early phase: Small hyper fluorescent spot seen; dye passes into the sub-
retinal space and ascends vertically
Smoke stack appearance
In late phase: Dye spreads laterally giving a mushroom or umbrella
configuration; whole detachment gets filled with dye
2. In early phase: Small hyperfluorescent spot seen; (RPE defect); gradually
enlarges centrifugally ink blot pattern
In late phase: Entire detachment gets filled with dye
Treatment
For the 1st two months, no treatment required (topical NSAIDs can be tried)
Focal laser is done if:
Recurrent CSCR
CSCR persists > 2 months
Decreased vision in fellow eye
Focal photocoagulation to the site of leakageunless the leak is near or
within the FAZ
Alternative treatment options
Photodynamic Therapy (full-fluence or more commonly half-fluence)
Intravitreal anti-VEGF
In acute CSCR, RPE increases its function to absorb subretinal fluid (disease
is self-limiting)
In chronic CSCR, RPE decompensates (leakage persists gradual progressive
loss of central vision)
Optic disc pit
Circumscribed choroidal hemangioma
CNVM
VKH syndrome (exudative RD)
Unilateral acute idiopathic maculopathy
Retina 67
PIGMENT EPITHELIAL DETACHMENT

Thickened Bruchs membrane - impedes movement of fluid from RPE to
choroid
Presents with unilateral metamorphopsia; impaired central vision
Sharply circumscribed, dome-shaped elevation at posterior pole
Subretinal fluid clear
FFA
Uniform bright hyperfluorescence in early phase
Smooth contour to RPE in middle phase
Little if any leakage at the borders in late phase (remain brightly
hyperfluorescent)
ICG
Oval area of hypofluorescence with a surrounding faint ring of
hyperfluorescence
Course
Spontaneous resolution; geographic atrophy
Occult CNV; RPE tear
Types of PED
1. Fibrovascular PED stippled hyperfluorescence along surface of RPE; later
pooling of dye in the overlying subsensory retinal space; Occult CNV
2. Serous PED
3. Hemorrhagic PED blocks choroidal fluorescence
4. Drusenoid PED fluoresce faintly during the transit; do not progress to bright
hyperfluorescence; reticulated pigment clumping overlying the large, soft,
confluent drusen
RETINAL PIGMENT EPITHELIUM TEAR

Occurs spontaneously; following photocoagulation/PDT; following
intravitreal injection
At junction of attached and detachment RPE
Sudden worsening of central vision
Crescent-shaped RPE dehiscence at edge of a prior serous detachment, with
a retracted and folded flap
FFA
Denuded RPE marked early hyperfluorescence (fluorescein does not leak
from here)
Late staining of choroid and sclera
Retracted (folded) RPE mound blocks fluorescence (if it leaks later due
to underlying CNV)
Retina 69
MACULAR HOLE
Classification
1. Partial thickness (inner and outer lamellar)
2. Full thickness
3. Pseudomacular hole (in overlying epiretinal membranes)
Causes
Idiopathic, trauma, solar retinitis, CME, CRAO, CRVO, inflammation, myopia
Clinical Features
Blurred vision, metamorphopsia, central scotoma
Watzke-Allen test: When a thin slit is thrown into a patients eye, he will not
be able to see it in the region of the full thickness macular hole
Hole Formation
1. Hole initiation: Focal adhesion of the vitreous to the macula leads to
mechanical deformation of the fovea (pseudocyst) formation dehiscence
full thickness hole
2. Hole expansion: Forces acting tangentially on the surface of the retina like
epiretinal membranes, tend to expand the hole
3. Hole closure: 3050% of stage 1a and 1b lesions will arrest or resolve
spontaneously glial proliferation
OCT Staging of Macular Hole

1a Partial thickness pseudocyst with peri-foveal PVD
1b Full thickness pseudocyst with roof
2a Partial opening of roof; focal vitreous attachment to flap
2b Operculated; traction to retina released
3 400 diameter; operculated hole
4 Complete PVD; vitreous face not seen on OCT
Biomicroscopic Staging of Macular Hole (Gass)

1a Foveolar detachment; yellow spot at fovea; posterior hyaloid attached to ILM
1b Foveal detachment; yellow ring
2a Centric: full thickness tear begins at foveal center; expands symmetrically
Pericentric: begins eccentrically; extends in a can-opener fashion; crescentic hole
3 400 diameter; operculated hole; white deposits at base of hole
4 Complete PVD
Lamellar hole Pseudohole

Results from an abortive process of macular Due to centripetal contraction of an ERM
hole formation or a complication of chronic CME
Avulsion of part of the macular tissue Entire macular tissue becomes bunched up
Split foveal edges Steepened foveal pit; small pit diameter
Thin, irregular foveal floor Normal or increased central foveal thickness
Near-normal perifoveal retinal thickness Increased perifoveal thickness
Retina 71
Surgery
Full thickness macular holes up to stage 3; < 1 year duration better prognosis
1. Vitrectomy with ILM peeling; fluid gas exchange; face down postoperative
positioning for 14 days
Dyes used for ILM Staining:
Triamcinolone acetonide, Indocyanine green, Infracyanine green
Brilliant Blue, Trypan Blue
2. Chemical vitrectomy enzyme (plasmin) injected into vitreous to chemically
detach vitreous from retina; vitreous lavage with infusion pipe and vitreous
cutter
Epiretinal Membrane
Proliferation of fibrocellular membranes on the retinal surface
Classification
Grade 0 Cellophane maculopathy
(translucent membrane with cellophane light reflex)
Grade 1 Surface wrinkling retinopathy
(membrane causes folds in the inner retina)
Grade 2 Macular pucker
(distinct greyish membrane partly obscuring the underlying retinal
vessels)
Pathogenesis
ILM defects astrocytes reach retinal surface collagen deposition ERM
Causes
Idiopathic age > 50 years
Retinal vascular disease diabetic retinopathy, retinal vein occlusion
Inflammation uveitis, toxoplasmosis
Trauma
Intraocular tumors
Following retinal laser/cryotherapy/retinal surgery
Symptoms and Signs
Asymptomatic, blurred vision, metamorphopsia, diplopia
Straightening or tortuosity of vessels, foveal ectopia, punctate hemorrhages,
cotton wool spots
Pseudohole, RPE changes
Associated CME
Investigations
FFA and OCT (detects early ERM)
Management
Observation in the early stage
Surgery (vitrectomy with membrane peeling) if vision or metamorphopsia
worsens
ILM peeling during surgery reduces the recurrence rate
AGE-RELATED MACULAR DEGENERATION
Early AMD
Few (< 20) medium-sized drusen (63124) (few small hard drusen not
AMD)
Pigment abnormalities (hyperpigmentation/hypopigmentation)
Intermediate AMD
At least one large drusen ( 125) width of retinal vein crossing optic
nerve
Numerous (> 20) medium-sized soft drusen
Geographic atrophy not involving center of macula
Advanced AMD
Geographic atrophy extending under center of macula
CNVM
Dry AMDnon-exudative/atrophic drusen, geographical atrophy of RPE
Wet AMDexudative/neovascular CNVM, sub-retinal scarring
Drusen
Discrete deposits of abnormal material between RPE and Bruchs membrane
Hard drusensmall, round, discrete, yellow-white spots; focal dysfunction
of RPE
Soft drusenlarge, indistinct margins; slowly enlarge and coalesce;
associated with solid drusenoid detachment of RPE (drusenoid PED);
precursor of atrophic and exudative AMD
FFA
Hyperfluorescencedue to window defects; overlying RPE atrophy
Hypofluorescencea large area of hypofluorescence may predispose to
RPE detachment
Familial dominant drusen, hard exudates, membrano-proliferative glomerulo-
nephritis fundus flavimaculatus, Stargardt disease, Alports syndrome, benign
flecked retina
Atrophic AMD
Slowly progressive atrophy of photoreceptors, RPE and choriocapillaris
Gradual, progressive decrease in vision; central negative scotoma
Hyperfluorescence on FFA
Retina 73
Exudative AMD
Choroidal neovascular membrane (CNVM) pathological growth of new
blood vessels from pre-existing choroidal vessels into the sub-retinal space
New vessels lie between choroid and RPE
Subretinal neovascular membrane (SRVNM) lies between RPE and
neurosensory retina (seen in idiopathic parafoveal telangiectasias)
Signs
Serous retinal elevation, hemorrhages, sub-retinal hard exudates
FFA
1. Classic CNV
Extrafoveal > 200 m from FAZ
Subfovealunder foveal center
Juxtafoveal< 200 m from center of FAZ
Well-defined membrane fills with dye in a lacy pattern; it fluoresces
brightly leakage into subretinal space and around the CNV
2. Occult CNVpoorly-defined membrane; late leakage
3. Fiber vascular PED CNV + PED
ICG detects CNV associated with overlying hemorrhage, pigment or exudates
Course:
Hemorrhagic PED rupture of blood vessels within CNV
Vitreous hemorrhage
Sub-retinal disciform scarring with retinal angiomatous proliferans
(RAP)retinal anastomoses into fibrovascular tissue
Massive intraretinal/subretinal exudationdue to chronic leakage from
CNV
Treatment
1. Argon laser photocoagulation:
Extrafoveal CNV with well-defined margins
Perimeter of lesion is treated with overlapping burns then enter area
covered
2. Photodynamic therapy:
Verteporfincomplexed with LDL and injected intravenously 6 mg/
kg wt for 10 min
Verteporfin taken up selectively by rapidly proliferating endothelial cells

that have increased number of LDL receptors their plasma membranes
Has ability to selectively damage neovascular net without affecting
overlying retinal tissue
Activated focally by illumination from a diode laser source (wavelength
corresponds to absorption peak of compound)
Greatest linear dimension (GLD) is determined from FFA; laser spot size
used to activate verteporfin = 1 mm + GLD (when ICG is done, 1 mm
not added)
Laser is set at a standard fluence rate of 50 J/cm2; which indicates
83 sec at 600 mW/cm2
Given for:
Subfoveal/juxtafoveal classic CNV < 5400
Juxtapapillary CNV with subfoveal extension
Malignant melanoma, retino-blastoma, choroidal hemangioma
Chronic CSCR
3. Intravitreal ranibizumab/bevacizumab/pegabtanib sodium (anti-VEGF):
Ranibizumab given monthly (3 injections), bevacizumab and pegabtanib
given every 6 weeks (3 injections) followed by injections as and when
required based on OCT findings
Intravitreal injection given 3.5 mm from limbus in phakic eyes and
3 mm from limbus in aphakic and pseudophakic eyes
4. Surgical treatment:
Submacular surgeryremoval of blood and CNV
Macular translocationmoving fovea away from CNV
Pneumatic displacement of submacular hemorrhages (gas in vitreous
displaces blood)
5. Transpupillary thermotherapy (being used less frequently):
Diode laser used
Done for occult CNV
Retina 75
ANTI-VEGF THERAPY
Wet AMD occurs due to the formation of new fragile vessels under the retina
(angiogenesis)
Vascular endothelial growth factor (VEGF) is the major chemical mediator
responsible for this and is secreted in high concentration by the retinal RPE
cells in WET AMD
Anti-VEGF drugs block VEGF from stimulating the growth of these new
vessels which can damage the overlying retinal photoreceptors
Anti-VEGF Drugs
1. Macugen (pegatanib sodium)first anti-VEGF therapy used to treat AMD;
Selective VEGF 125 inhibitor; dose 0.3 mg in 90 L
2. Lucentis (ranibizumab)Pan VEGF inhibitor; dose 0.5 mg in 0.05 mL
3. Avastin (bevacizumab)not FDA approved but commonly used as an off
label drug; Pan VEGF inhibitor; dose 1.25 mg in 0.05 mL.
Other Indications of Anti-VEGF Therapy
Macular edema in vein occlusion (due to the antipermeability property of
anti-VEGF)
Diabetic macular edema (may be used in combination with triamcinolone)
Non-resolving vitreous hemorrhage
Prior to vitrectomy in PDR to decrease intraoperative bleeding
Non-resolving postoperative CME
CSCR acute and chronic (not proved to benefit)
IDIOPATHIC MACULAR TELANGIECTASIA
Type 1
Aneurysmal telangiectasia
Unilateral; mostly in men
Variable-sized aneurysms capillary/venular/arteriolar
Larger aneurysms in the superficial circulation
Patchy ischemia, lipid deposition, CME
No crystalline deposits/pigment migration
No SRNVM (subretinal neovascular membrane)
Subgroup 1A: Clinical detection of aneurysmal and telangiectatic exudative
vessels in the juxtafoveal area
Subgroup 1B: Focal exudative telangiectasia limited to 2 clock hours or less
in the juxtafoveal area
Type 2
Perifoveal telangiectasia
Mostly bilateral, asymmetric
Associated with diabetes, hypertension
Loss of transparency in temporal juxtafoveal area which progressively
surrounds the fovea (grayish oval zone around fovea)
Vitreoretinal interface crystalline deposits
Inner lamellar cyst at fovea
Subretinal plaques of pigmentation
Dilated right-angle retinal vessels (venules/arterioles)
Retinalretinal anastomoses within the retina or extending to communicate
with new vessels beneath the retina (SRNVM)
SRNVM originates from deep retinal circulation; presents with neurosensory
detachment, subretinal hemorrhage, fibrosis, visual decline; PED is rare
Subgroup 2A
Stage 1 occult vascular abnormalities evident only by mild staining with
fluorescein
Stage 2 mild loss of transparency without clinically evident telangiectatic
vessels
Stage 3 prominent dilated right-angle retinal venules
Stage 4 retinal pigment hyperplasia extending into the retina
Stage 5 SRNVM originating from proliferation of intraretinal capillaries
beneath the neurosensory retina
Subgroup 2B
Familial disorder; perifoveal telangiectasia in the young
Yannuzzis Classification
Non-proliferative stage exudative telangiectasia and foveal atrophy
Proliferative stage subretinal neovascularization
Retina 77
OCT Findings
Retinal thickening 1st detectable change
Inner lamellar cyst at the fovea bordered by ILM
Progressive loss of outer retina foveal atrophy
SRNVM detect neurosensory detachment
Type 3
Occlusive telangiectasia
Perifoveal capillary non-perfusion
Ocular manifestation of systemic/cerebral familial disease
POLYPOIDAL CHOROIDAL VASCULOPATHY

Hemorrhagic disorder of the macula characterized by recurrent subretinal
and sub-RPE bleeding
Posterior uveal bleeding syndrome
Pathology
Primary abnormality of the choroidal vasculature
Inner choroidal vascular network of vessels end in an aneurysmal bulge or
outward projection
Dilated thin-walled vessels of choriocapillaris
Sub-RPE, intra-Bruchs vascular lesion
Within Bruchs membrane cavernous vascular channels
Clinical Features
Mostly bilateral; 5065 years of age; women; pigmented races
Multiple recurrent serosanguineous detachments of the RPE and
neurosensory retina secondary to leakage and bleeding
Dilated choroidal vascular channels ending in orange, polyp-like dilatations
in the peripapillary and macular area
Recurrent subretinal and vitreous hemorrhage; hemorrhagic PED
Lack of drusen
Relatively minimal fibrous scarring
Absence of retinal vascular disease/pathological myopia/intraocular
inflammation
Exudative neurosensory detachment
Polypoidal lesions
Appear larger when outer choroidal vessels involved; smaller when middle
choroidal vasculature is involved
Peripapillary area, central macula, midperiphery
In juxtapapillary lesions vascular channels may follow a radial arching
pattern; may be interconnected with smaller spanning branches (numerous
at the edge of the lesion)
ICG
Early filling of the larger vessels of the PCV network prior to retinal vessels
(area within the lesion and immediately surrounding the lesion remains
hypofluorescent)
Small hyperfluorescent polyps seen within the choroid
Late phase reversal of the pattern of fluorescence area surrounding the
lesion is hyperfluorescent and center of the lesion is hypofluorescent
Very late stage dye disappears from the non-leaking lesions (washout)
Leaking lesions remain hyperfluorescent
Retina 79
OCT
Dome-like elevation of the RPE; nodular appearance beneath the RPE
Characteristic hyper-reflectivity in the choroidal layers
Management
Thermal laser to the peripapillary polypoidal lesions - if vision is threatened
PDT to macular lesions
Asymptomatic PCV in the periphery can be observed
Role of anti-VEGF agents is controversial
CENTRAL RETINAL VEIN OCCLUSION
Pathogenesis
Thrombotic/atherosclerotic phenomenon
Vein inflammation; vessel wall abnormalities
Turbulent blood flow causes thrombosis at lamina cribrosa
Increased IOP POAG or PACG
Papilloedema
Orbital tumor/abscess
Clinical Features
Sudden painless loss of vision
Disc edema; dilated tortuous veins
Retinal hemorrhages in all 4 quadrants blood and thunder appearance
Macular edema, soft exudates
Collaterals over the disc, disc pallor in old cases
NVI with neovascular glaucoma in ischemic type of CRVO (100-day
glaucoma)
Decreased vision due to:
Macular edema/ischemia
Retinal/vitreous hemorrhage
Consecutive optic atrophy; RPE atrophy
Tractional RD, combined RD
Non-ischemic CRVO Ischemic CRVO
Vision better than 20/200 Vision worse than 20/200
Pupil RRL or RAPD <0.7 log units RAPD > 0.7 log units
Dot and blot hemorrhages Flame shaped hemorrhages
Relatively normal appearing retina Orange, turbid, edematous retina
<10 DD of retinal non-perfusion >10 DD of retinal non-perfusion
Few cotton wool spots Numerous cotton wool spots
Low risk for neovascularization High risk for neovascularization
70% of CRVO cases 30% of CRVO cases
Good prognosis Bad prognosis
ERG shows 60% Reduction of b Wave Amplitude in Ischemic CRVO
Associated Systemic Disease

HTN, DM, cardiovascular disease, hyperlipidemia
Hyperviscosity syndromeshypergamaglobulinemia, hyperfibrinogenemia
Hyperviscosity statesmalignancy, chronic lung disease, nephrotic
syndrome, polycythemia, oral contraceptive use
Retina 81
AIDS, syphilisinfectious vasculitis

Behets disease
Collagen vascular diseaseSLE, PAN
Mitral valve prolapse, migraine, hyperlipidemia
Head injury, carotid artery disease
Sickle cell disease
Management
Investigations
FFA: To rule-out macular ischemia and to differentiate ischemic and non-
ischemic CRVO
OCT: To estimate the degree of macular edema
ERG: To differentiate ischemic and non-ischemic CRVO
Gonioscopy at regular intervals to r/o NVA; regular IOP check-up
Rule-out systemic vascular disease, hypertension and hyperviscosity
syndromes
Check blood pressure, blood sugar, lipid profile, ESR, CBC, platelet count
In young patients:
Elevated plasma homocysteine
Antithrombin III deficiency
Decreased activated Protein C resistance
Protein C deficiency
Protein S deficiency
Antiphospholipid antibodies
Treatment
1. Intravitreal injectionsto reduce macular edema and neovascularization
Triamcinolone 1 mg in 0.1 mL
Anti-VEGF drugs:
Avastin (bevacizumab) 1.25 mg in 0.05 mL
Lucentis (ranibizumab) 0.5 mg in 0.05 mL
Macugen (pegabtanib sodium) 0.3 mg in 0.9 mL
Combination of intravitreal triamcinolone and anti-VEGF
2. Panretinal photocoagulationif NVD, NVE, NVG develops
BRANCH RETINAL VEIN OCCLUSION

Supero-temporal BRVO is more common
Occlusion occurs at A-V crossings; rarely following ocular inflammation
(vasculitis)
Risk factors: Hypertension, diabetes, hyperlipidemia, glaucoma, smoking
Clinical Features
Decreased vision/field loss/asymptomatic
Vision loss due to macular edema, vitreous hemorrhage, TRD, combined RD
Non-ischemic BRVO Ischemic BRVO

80% of BRVO cases 20% of BRVO cases
Usually mild macular edema Usually severe macular edema
Cotton wool spots are rare Cotton wool spots common
Collaterals develop Risk of neovascularization NVE, NVD, TRD
<5 DD of retinal non-perfusion >5 DD of retinal non-perfusion
50% Rule
If BRVO in one-quadrant ~ 50% chance of developing 5 DD of capillary non-
perfusion
If 5 DD of non-perfusion ~ 50% chance of developing NVD, NVE
If NVD/NVE develop ~50% chance of a vitreous hemorrhage
Treatment
Sectoral laser photocoagulation done to the quadrant with capillary non-
perfusion, if neovascularization develops
Intravitreal anti-VEGF +/- triamcinolone helps to reduce/resolve macular
edema (macular edema may resolve spontaneously)
Macular grid photocoagulation to reduce macular edema
Vitrectomy for recurrent/non-resolving vitreous hemorrhage and retinal
detachment
Retina 83
CENTRAL RETINAL ARTERY OCCLUSION

Pathophysiology
Emboli from carotid artery or heart lodge in the central retinal artery at the
laminar constriction site, intra-luminal thrombosis
Vasospasm, circulatory collapse
Dissecting aneurysm, hemorrhage under atherosclerotic plaque
Giant cell arteritis
Clinical Features
Preceding history of amaurosis fugax indicates embolic cause
Sudden painless unilateral visual lossvision being CFCF, HM or even LP
(counting fingers close to face, hand movements or light perception)
Superficial retina in posterior pole-opacified (cloudy swelling); yellow-white
appearance due to ischemic necrosis of inner half of retina
Cherry red spot at the fovea (underlying RPE and choroid are visible)
Segmentation/ boxcarring of blood column in arteries and veins
Simultaneous bilateral CRAO giant cell arteritis. Cardiac valvular disease,
vascular inflammation
Rubeosis iridis at the time of obstruction concomitant carotid artery
obstruction
APD even if fundus is normal (early phase)
In 46 weeks: Retinal opacification resolves; pale disc, narrowed retinal vessels
In cilioretinal artery occlusion central visual acuity deseases but peripheral
field is preserved
In ophthalmic artery occlusion vision is reduced to no light perception
Underlying Causes
HTN, DM, cardiovascular disease
Infectious endocarditis, valvular heart disease
Retrobulbar steroid injections
In the young migraine, cardiac disorders, trauma, sickling hemo
globinopathies, optic disc drusen, SLE, PAN, Protein C/S deficiency,
antithrombin deficiency
Investigations
ESRif raised, urgent referral to rule-out giant cell arteritis
Blood pressure, blood sugar, lipid profile, ECG, carotid doppler,
echocardiogram
VDRL, ACE, ANA, ANCA, RA factor, chest X-ray
FFA
Delay in retinal arterial filling
Presence of an arterial dye front
Delay in retinal arteriovenous transit time (normally 11 sec)
Choroidal vascular bed fills normally (marked delay in choroidal filling in

ophthalmic artery obstruction)
FFA can revert to normal as retinal circulation has a marked propensity to
re-establish circulation
ERG
Decreased b wave amplitude (Muller and bipolar cell function)
Normal a wave (photoreceptor function)
decreased in ophthalmic artery obstruction
May be normal in the presence of decreased vision if retinal blood flow is
re-established
Visual Field
Residual temporal island of vision (nasal retina supplied by choroidal vessels)
Treatment
Within 24 hours of onset of vision loss
Ocular massage with Goldmann contact lens or digitally to dislodge
embolus
(apply pressure for 1015 sec followed by sudden release)
Inspiration of 95% oxygen (diffuses from choroid to surface of retina) + 5%
carbon dioxide (vasodilator)
Anterior chamber paracentesis to reduce IOP less compression on central
retinal artery will allow the embolus to pass
Systemic Acetazolamide to reduce IOP
Antifibrinolytic agents like streptokinase can be tried within 6 hours
(increases risk of systemic bleeding)
In giant cell arteritis and granulomatous vasculitis (polyarteritis nodosa)
treat with systemic steroids
Retina 85
COTTON WOOL SPOTS

Seen in
Diabetic retinopathy
Hypertensive retinopathy
Collagen vascular disease
Cardiac valvular disease
AIDS
Retinal vein occlusion
Leukemia
Trauma
Radiation retinopathy
High altitude retinopathy
Severe anemia
Acute blood loss
Papilloedema
Papillitis
Septicemia
Intravenous drug abuse
Acute pancreatitis
Aortic arch syndrome (pulseless disease)
OCULAR ISCHEMIC SYNDROME

In severe carotid artery obstructive disease; common carotid or internal
carotid artery
Earlier called venous stasis retinopathy
Mostly men, around 65 years of age
Mostly unilateral; 20% bilateral
>90% stenosis of the ipsilateral carotid arterial system (50% reduction of
ipsilateral central retinal artery perfusion pressure)
Associated systemic arterial hypertension, diabetes mellitus, peripheral
vascular disease, stroke
5-year mortality rate 40%
Causes
Atherosclerosis within the carotid artery
Dissecting aneurysm of the carotid artery
Giant cell arteritits (bilateral loss of vision)
Symptoms
Visual loss over a period of weeks (majority of cases)
Abrupt loss of vision (12%) cherry red spot may be seen
Prolonged recovery following exposure to bright light (due to macular
ischemia)
Scintillating scotomata resembling migraine aura in dissection of internal
carotid artery
Amaurosis fugax (10%) fleeting loss of vision for seconds to minutes due
to emboli or vasospasm
Ocular angina pain (40%) in the affected eye or orbital region dull ache
Pain secondary to NVG can occur
Signs
Visual acuity ranges from 20/20 to finger counting vision
Absence of light perception in NVG
Rubeosis iridis (in 2/3rds patients) only half of them may develop an
increase in IOP
Hypotony due to impaired ciliary body perfusion decreased aqueous
production
Aqueous flare (if rubeosis), cells in anterior chamber
Lens becomes cataractous
Prominent collaterals on the forehead
Retinal arteries narrowed
Retinal veins dilated but not tortuous; beading
Some cases retinal arteries and veins are narrowed
Retinal hemorrhages in the mid-periphery, can extend into posterior pole
Retina 87
Mostly dot and blot hemorrhages less numerous than CRVO, never
confluent
Microaneurysms mostly outside the posterior pole
Retinal telangiectasia may be seen
NVD (25%), NVE (8%), vitreous hemorrhage (4%)
Cherry red spot (12%) central retinal artery obstruction by emboli or IOP
exceeding the perfusion pressure within the central retinal artery
Cotton wool spots (4%)
Spontaneous retinal arterial pulsations (4%) more pronounced; may extend
a DD out from the disc into the surrounding retina
Light digital pressure on the upper lid of the affected eye during
ophthalmoscopy retinal arterial pulsations can be readily induced
Cholesterol emboli within the retinal arteries (2%)
AION may occur
Acquired arteriovenous communications of the retina rare
FFA
Delayed arm-to-choroid and arm-to-retina circulation times
Well-demarcated leading edge of fluorescein dye within a retinal artery
(secondary to hypoperfusion)
Patchy or delayed choroidal filling (>5 sec) high specificity
Prolongation of retinal arteriovenous transit time high sensitivity, low
specificity
Major retinal veins may not fill throughout the FFA in severe cases (normally
fill in 1011 sec after the 1st appearance of dye within the corresponding
retinal arteries)
Retinal vascular staining (all vessels due to chronic hypoxic damage to
endothelial cells)
Macular edema (due to endothelial damage within the smaller retinal vessels
and leakage from microaneurysms)
Hyperfluorescence of the optic disc not swollen
Retinal capillary non-perfusion
Bilateral simultaneous intravenous fluorescein angiography to diagnose
unilateral ocular ischemic syndrome
ERG
a and b waves diminution of amplitude or absent
In central retinal artery obstruction only b wave amplitude is decreased
(inner retinal function)
Oscillatory potential of b wave reduction in amplitude retinal ischemia
secondary to carotid artery stenosis
Management
Carotid angiography 90% or more obstruction of the ipsilateral internal/
common carotid artery
Duplex ultrasonography, oculoplethysmography non-invasive test for

carotid artery obstruction
Visual evoked potential attenuation after light exposure
Ophthalmodynamometry to detect decreased ocular perfusion
In 100% obstruction of carotid artery extracranial to intracranial bypass
surgery
<100% obstruction carotid endarterectomy severe increase in IOP may
occur following the procedure
Panretinal photocoagulation in rubeosis iridis and retinal neovascularization
If anterior chamber angle is completely closed by fibrovascular tissue
and there is no posterior segment neovascularization retinal laser is not
indicated unless glaucoma filtering procedure is being considered
Intravitreal triamcinolone/anti-VEGF agents to treat macular edema
Anti-VEGF agents to reduce rubeosis iridis and posterior segment
neovascularization
Retina 89
DIABETIC RETINOPATHY
Kanskis Classification
Simple background diabetic retinopathy:
Microaneurysms
Hemorrhages dot, blot, flame-shaped
Hard exudates arranged in a circinate pattern
Retinal edema (in the outer plexiform layer)
Preproliferative diabetic retinopathy:
Venous beading and looping
Dark blot hemorrhages
Multiple cotton wool spots
IRMA (intra-retinal microvascular anomalies) adjacent to areas of capillary
non-perfusion.
Proliferative diabetic retinopathy:
Neovascularization on disc and elsewhere
Vitreous hemorrhage, subhyaloid hemorrhage
Tractional and combined retinal detachment
Diabetic maculopathy:
Exudative maculopathyfocal leakage causing hard exudates formation
Edematous maculopathydiffuse macular edema
Ischemic maculopathyextensive macular capillary non-perfusion
Modern ETDRS Classification

Mild NPDR at least 1 microaneurysm
Moderate NPDR microaneurysms, dot and blot hemorrhages, soft exudates,
venous beading
Severe NPDR at least one of [4-2-1 rule]
Microaneurysms/hemorrhages in 4 quadrants
Venous beading in 2 quadrants
IRMA in 1 quadrant
Very severe NPDR 2 or more of above
PDR new vessels seen
High-risk PDR:
NVD involving 1/3rd to 1/2 disc area
NVD with vitreous/pre-retinal hemorrhage
NVE of 1/2 disc area with pre-retinal or vitreous hemorrhage
Clinically Significant Macular Edema (CSME)

Retinal edema within 500 of foveal center
Hard exudates with adjoining retinal thickening within 500 of fovea
1 disc diameter of retinal edema encroaching within 1 disc diameter
(1500 ) of foveal center
Treatment of Diabetic Retinopathy

Medical
Strict blood sugar control
Vitamin E supplements
Lipid lowering drugs (in cases of hyperlipidemia)
Laser
Panretinal photocoagulation for high-risk PDR
Focal laser or grid photocoagulation for CSME
PASCAL laser:
PRP can be completed in a single sitting
Uniform burns of very small duration are applied
Patient has minimal pain
Cannot be done if media is hazy
Intravitreal Injections
Avastin\Lucentis
To reduce macular edema as monotherapy (repeated injections at
monthly intervals for first 3 months then as needed based on OCT)
About 4 weeks before macular grid photocoagulation (to ensure better
laser uptake)
12 weeks before vitrectomy in PDR (to decrease intraoperative
bleeding)
Triamcinolone acetonide
Alone or in combination with anti-VEGF to reduce macular edema
Surgical Treatment
Pars plana vitrectomy with delamination and segmentation of membranes
for:
TRD involving posterior pole and threatening macula
Combined RD
ETDRS Protocol for Full Scatter Laser Treatment
Pan retinal photocoagulation (PRP)
Spot size 500
Duration 0.1 s
No. of burns 1200 to 1600
Laser used argon laser
Burns of moderate intensity placed one-half to one burn apart, divided
between 2/more episodes
Small tufts of vessels intravascular coagulation and occlusion
Retina 91
HYPERTENSIVE RETINOPATHY
Keith-Wagener-Barker Classification
Grade I Mild-moderate narrowing/sclerosis of smaller arterioles
Grade II Moderate-severe narrowing of arterioles; exaggeration of light
reflex; changes at AV crossings
Grade III Focal constriction; AV crossing changes; retinal edema, cotton wool
spots, flame-shaped hemorrhages
Grade IV All of the above with papilloedema
Wagener-Clay-Gibner Classification
Based on
Generalized narrowing:
i. Reduction of artery caliber to 1/2 veins
ii. Reduction of artery caliber to 1/3rd veins
iii. Reduction of artery caliber to 1/4th veins
iv. Thread-like arteries
Sclerosis:
i. Brightening of arterial wall with depression of veins at crossings
ii. Copper wiring with depression of veins
iii. Silver wiring with widening of AV crossings
iv. Fibrous cord without blood
Scheie Classification
Hypertension
Grade 0 no changes
Grade 1 barely detectable arteriolar narrowing
Grade 2 obvious arteriolar narrowing with focal irregularities
Grade 3 grade 2 + retinal hemorrhages and/or exudates
Grade 4 grade 3 + papilloedema
Arteriolar Sclerosis
Grade 0 normal
Grade 1 barely detectable light reflex changes
Grade 2 obvious increased light reflex
Grade 3 copper-wire arterioles
Grade 4 silver-wire arterioles
HYPERTENSIVE CHOROIDOPATHY
Seen in acute hypertension, pregnancy induced hypertension, renal disease,
pheochromocytoma, accelerated hypertension in young adults
Clinical Features
Early phase: Elschnigs spots pale white or reddish patches in outer retina
due to hypoperfusion of underlying capillaries; necrosis of choriocapillaris
Focal serous detachment; exudative RD (in pregnancy-induced hypertension)
Macular star
Siegrists streaks chains of pigmented spots arranged like a string of beads
along choroidal vessels (fibrinoid necrosis)
Chronic Elschnigs spots pigmented center with depigmented halo around
it
Pathogenesis
In the Acute Phase
Ischemic phase choroidal arterioles severely constrict cause Elschnigs
spots
In the Chronic Phase
Occlusive phase vessels undergo hyperplastic changes with fibrinoid
necrosis choriocapillaris occluded by thrombi
Reparative phase recanalization of blood vessels with focal necrosis of
overlying RPE
Retina 93
EALES DISEASE
In healthy young adults; 2030 years of age; male predominance
Bilateral involvement in 7080%
Characterized by
Retinal perivasculitis
Peripheral nonperfusion
Retinal neovascularization
Causes
Tuberculosis; allergy to tuberculoprotein
Focal sepsis
Thrombotic arteriolar occlusion
Stages
Inflammatory
Peripheral retinal perivasculitis (with or without BRVO), in one or more
quadrants
Arterioles may also be affected
Exudates around retinal veins
Superficial retinal hemorrhages
Ischemic
Sclerosed cords of venules appear as fine white solid lines
Pigmentation along the venules
Junction between antero-peripheral nonperfusion and posterior perfused
retina is usually sharply demarcated
Vascular anastomosis, microaneurysms, hard exudates and cotton wool
spots
Proliferative
NVE 3684%
NVD 9%
TRD 38.9%
Combined RD 11%
Radial retinal fold 17%
Vitreous hemorrhage recurrent
Stage 1 Mild periphlebitis of small peripheral retinal capillaries
Stage 2 Perivasculitis of large veins and venous capillary system
Stage 3 Neovascularization, retinal and vitreous hemorrhage
Stage 4 TRD and retinitis proliferans
Symptoms
Mostly asymptomatic
Floaters
Sudden painless decrease in vision
FFA
Active stage staining with extravasation of dye
Ischemic stage capillary non-perfusion
staining without extravasation
shunts
Proliferative stage leakage from new vessels
Lab Investigations
CBC, ESR, blood sugar, VDRL, ANA
Mantoux test, chest X-ray
Pars planitis
Behets disease, sarcoidosis, SLE
Syphilis, viral retinitis
IRVAN (idiopathic retinal vasculitis, aneurysms and neuroretinitis)
Treatment
a. Observation in regressed/inactive vasculitis
b. Medical in stage of inflammation
Steroids periocular/systemic
Anti-tubercular treatment if required
c. Photocoagulation in proliferative stage
d. Surgery vitrectomy in non-resolving/recurrent vitreous hemorrhage,
tractional RD involving posterior pole, combined RD
Retina 95
VITREOUS HEMORRHAGE
Classification
Pre-retinal/Sub-hyaloid hemorrhage
Intravitreal hemorrhage
Combined hemorrhage
Pathogenesis
Rupture of normal/abnormal blood vessels
Extension of sub-retinal hemorrhage into vitreous (AMD, choroidal
melanoma)
Causes
PDR, BRVOcommon
Retinal tear, posterior vitreous detachment (PVD)
Sickle cell retinopathy
Eales disease, CRVO
Macroaneurysms, telangiectasia
Anemia, Valsalva retinopathy
Choroidal melanoma
Hemorrhagic disciform macular degeneration (breakthrough bleeding from
CNV)
Familial exudative vitreoretinopathy (FEVR)
Retrolental fibroplasias
Sub-arachnoid hemorrhage with vitreous hemorrhage Tersons syndrome
Clinical Features
Floaters, shadows and cob webs seen
Sudden decrease in vision
May give a history of trauma, ocular/systemic disease
Subhyaloid hemorrhageunclotted blood, boat-shaped bleed
Intravitreal hemorrhageclotted blood; yellowish - adheres to gel
Treatment
Recent Hemorrhage
Bed rest, patching, head elevation
Examine fellow eye for PDR/BRVO/CRVOmay give a hint to the diagnosis
In case of retinal tearbarrage laser/cryotherapy depending on location
of break and media haze (vitrectomy may be required if neither can be done)
For localized premacular hemorrhageposterior hyaloidotomyNd:YAG
laser disrupts internal limiting membrane and releases blood into vitreous
cavity
Intravitreal anti-VEGF injection in case of PDR when laser cannot be done

due to poor visibility and pre-operatively to reduce risk of intraoperative
bleeding
Non-Resolving Vitreous Hemorrhage
Pars plana vitrectomy
Complications of Vitreous Hemorrhage

Hemosiderosis bulbidue to iron liberated from hemoglobin
Retinal damageiron causes degeneration of photoreceptors field loss,
nyctalopia, decreased macular function
Proliferative retinopathydirect stimulation of fibroblastic elements by iron
Ghost cell glaucoma, hemolytic glaucoma
Retina 97
RETINOPATHY OF PREMATURITY
In premature infants (< 32 weeks gestation)
Low-birth weight (<1.5 kg)
On supplemental oxygen due to hypoxemia or hypercarbia
Clinical Features
Decreased vision, myopia, squint
Retinal dragging, retinal detachment, lattice degenerations
Avascular peripheral retina
Classification
Location
Zone 1 Posterior pole (twice the disc-fovea distance, centered around disc)
Zone 2 From zone 1 to nasal periphery; temporally equidistant from disc
Zone 3 Remaining temporal periphery
Extent number of clock hours involved
Severity
Stage 1 Flat demarcation line separating the vascular No treatment required

and avascular retina
Stage 2 Ridged demarcation line No treatment required
Stage 3 Ridged demarcation line with extra-retinal Laser photocoagulation or
fibrovascular proliferation cryotherapy
Stage 4 Extrafoveal RD or subtotal RD involving Surgery
macula
Stage 5 Total RD Surgery
Threshold disease at least 5 contiguous or 8 accumulated clock hours of

stage 3 + disease
Plus disease engorged veins and tortuous arteries in the posterior pole;
non-dilating pupil; vitreous haze
Aggressive Posterior ROP (Rush disease) high-risk for rapid progression
(e.g. Zone 1 with plus disease)
Familial exudative vitreoretinopathy
Incontinentia pigmenti
LASERS
Light amplification by stimulated emission of radiation
Types
Solid Ruby, Diode, Nd: YAG
Gas Argon, Krypton, CO2, Neon
Liquid Dye
Absorption by
Melanin in RPE and choroidall lasers
Xanthophyll in outer and inner plexiform layersblue laser
Hemoglobin blue, green, yellow lasers
Complications
Accidental foveal burn
Bleeding (when high power used or blood vessel hit)
Traction (when fibrous strand treated)
Bruchs rupture (when high energy burns given)
CNVM may form; it may bleed
Holes (if barrage given within lattice)
Night blindness, glare (extensive PRP)
Decreased peripheral field
Choroidal detachment
Exudative retinal detachment
Acute congestive glaucoma, ciliochoroidal effusion
Increased macular edema, ERM
Secondary angle-closure glaucoma
Rhegmatogenous RD secondary tear
Laser Effects
1. Photochemical: Low-energy laser radiation converts absorbing molecule
into free radicals (toxic to cell)
2. Photocoagulation: At 30C
Proteins get coagulated
Argon, Xenon, Krypton, Diode laser
Used for proliferative retinopathy, trabeculoplasty, tumors, CNVM
3. Photovaporization: At 100C
Water content in cell gets evaporated
CO2 laser
Used for tissue incision, blepharoplasty, debulking of conjunctival
tumors
4. Photodisruption: At 10,00020,000C
Has an ionizing effect
Nd: YAG laser
Used for capsulotomy, iridotomy, vitreolysis
Retina 99
5. Photodynamic therapy:
Dye laser
Used for melanomas, retinoblastomas, CNV
6. Photoablation:
Excimer laser (leaves no scar)
Used for corneal scar removal, refractive surgery
Anterior Segment Uses

Lid Trichiasis, blepharoplasty,
capillary hemangioma
Conjunctiva Suturolysis of trabeculectomy
sutures
Cornea Scars, dystrophies, band
keratopathy, vascularizations,
refractive surgery
Iris Iridotomy, iridoplasty
Ciliary body Trans-scleral
cyclophotocoagulation
Trabecular Argon laser trabeculoplasty
Meshwork selective laser trabeculoplasty
Pupil Sphincterotomy, pupilloplasty,
membranolysis
Lens Capsulotomy
Vitreous Vitreolysis
Posterior Segment Uses

PDR, BRVO, CRVO
CNV, CSCR, CSME
Retinal breaks and lattices
Neoplasms <4 DDretinoblastoma, malignant melanoma, VHL syndrome,
choroidal hemangioma
Coloboma choroid
Small peripheral retinal detachments
Retinoschisis progressing towards posterior pole
Retinopathy of prematurity
Sickle cell retinopathy
During RD surgery, vitrectomy
Indications for Prophylactic Barrage Laser

Tear > hole (tear is more dangerous than a hole)
Large breaks > small breaks
Symptomatic breaks (flashes/floaters)
Superior breaks > inferior breaks
Equatorial breaks > oral breaks
Subclinical RDbreak surrounded by SRF

Pigmentation around break (low-risk of RD)
Breaks in aphakia (when vitreous loss has occurred)
Breaks in pseudophakia (after YAG capsulotomy)
High myopia with lattice degeneration
One eyed with breaks
Family history of retinal detachment
Marfans, Stickler, Ehlers-Danlos syndrome
Horse shoe tear with or without localized RD
Lattice degeneration with horse shoe tears
Symptomatic lattice degeneration with or without holes
Lattice degenerationin high myopia, one-eyed, history of RD in fellow eye
Asymptomatic lattice degeneration before planning cataract/refractive
surgery
Barrage Laser Not Indicated for

Microcystoid degenerationtiny vesicles on a grayish-white background
Snowflakesminute glistening yellow-white dots diffusely in peripheral
fundus
Paving stone degenerationyellow-white patches of chorioretinal atrophy
Honey comb/reticular degenerationfine network of perivascular
pigmentation
Oral pigmentary degeneration pigmented band running adjacent to ora
serrata
Retina 101
HEREDITARY FUNDUS DYSTROPHIES

Rod Cone Dystrophies
Retinitis pigmentosa
Atypical pigmentary dystrophy
Lebers congenital amaurosis
Retinitis pigmentosa associated syndromes
Congenital Stationary Night Blindness

Fundus albipunctatus
Oguchi disease
Macular Dystrophies
Bests disease
Stargardt dystrophy
Familial dominant drusen
Cone dystrophy
Congenital retinoschisis
North Carolina macular dystrophy
Sorsby pseudoinflammatory macular dystrophy
Choroidal Dystrophies
Regional
Generalized: Gyrate atrophy, choroideremia
Vitreotapeto Retinal Dystrophies

Goldmann-Favre dystrophy
Wagners vitreoretinal dystrophy
Sticklers syndrome
Snowflake dystrophy
PERIPHERAL RETINAL DEGENERATION

Lattice Degeneration
In young myopes, Ehlers-Danlos syndrome, Marians syndrome, Stickler
syndrome
Types
Typical:
Sharply demarcated, spindle-shaped areas of retinal thinning
Between equator and posterior border of vitreous base
Discontinuity of internal limiting membrane
Atrophy of underlying sensory retina
Commonly SUPERO - TEMPORAL
Arborizing network of tiny white lines
Overlying vitreous is synchytic
Atypical:
Radially oriented
Continuous with peripheral blood vessels
Seen in Stickler syndrome
Complications
Acute PVD (photopsia, floaters) can cause fractional tears along posterior
edge of an island of lattice
Atrophic holes within lattices may cause retinal detachment
Snail Track Degeneration

Sharply demarcated bands of tightly packed snow flakes
White frost-like appearance of periphery
Overlying vitreous liquefaction
Hole formation can cause retinal detachment
Degenerative Retinoschisis
Splitting of sensory retina at the level of outer plexiform layer into outer
choroid and inner vitreous layer
In hypermetropes
Microcystoid degeneration with a smooth elevation of retina (infero-
temporal)
Progresses circumferentially
Inner layerimmobile and transparent; snowflakes; sheathing/silver wiring
of blood vessels; schisis cavity bridged by torn gray-white tissue; small round
breaks
Outer layerbeaten metal appearance; white with pressure; breaks have
large rolled edges
If breaks occur in both layersRD occurs
Retina 103
PATHOLOGICAL MYOPIA
Myopia of more than -6 D; axial length > 26 mm; with progressive choroidal
degeneration at the posterior pole
Pathogenesis
Due to increased axial elongation
Progressive distention of posterior pole stretches the outer coats which
causes:
Straightening of outer retinal vessels
Thinning of retina and choroids
Super fractional crescent
Fundus
1. Myopic conus:
Oval disc
Temporal crescent (absence of RPE and choroid makes sclera visible)
(Myopic conus on nasal side inverse myopia)
2. Posterior staphyloma:
Localized ectasia involving sclera, choroid and RPE at the posterior pole
If macula involved decreased vision
3. Tigroid and tessellated fundusdue to thinning of retina and choroid;
prominent choroidal vessels
4. Lacquer cracks:
Rupture of Bruchs membrane
Linear/stellate, fine, yellowish white cracks
Horizontally oriented branching and criss-crossing occurring at the
deepest layer of retina
Pigmentary mottling at border of cracks
May be associated with:
CNVM
Focal degenerative lesions
Sudden macular hemorrhage (coin hemorrhages)
5. Foerster Fuchs spot:
Dark spot in maculadue to proliferation of RPE
Develops after a macular hemorrhage has absorbed
6. Sub-retinal neovascular membrane:
Usually subfoveal
Causes decreased vision
Usually no scarring occurs
7. Paving stone degeneration:
Peripheral chorioretinal atrophy
8. Geographical atrophy of RPE and choriocapillaris at the macula
9. Exudative maculopathy secondary to CNVM
10. Macular hole
11. Areas of focal atrophy
Can be Associated with

POAG (early onset), pigmentary glaucoma, steroid responsiveness
Posterior subcapsular cataract; early onset of nuclear sclerosis
Retinal detachment
Stickler syndrome, Marfans syndrome, Ehlers-Danlos syndrome
Retina 105
RETINAL DETACHMENT
Rhegmatogenous RD
Symptoms
Inferior RD (not extending under macula) may be asymptomatic
Field defectlike a curtain dropping
Sudden painless loss of vision (partial/complete)
Photopsiain acute PVD due to traction on retina at sites of vitreo-retinal
adhesion; stops on complete tearing away of a piece of retina at site of
adhesion
Sudden shower of minute dark spotsin vitreous hemorrhage associated
with acute retinal tears; floatersmoving vitreous opacities perceived when
they cast a shadow on retina
Signs
RAPDin extensive RD
Decreased IOP
Mild anterior uveitis
Tobacco dustingin anterior vitreous
Retinal breaks
PVR changes
Fresh RD
Convex detached retinaappears opaque and corrugated
Undulates freely with eye movements
Retinal blood vessels appear darker than in flat retina
Old RD
Retinal thinning secondary to atrophy
Intraretinal cysts
Subretinal fibrosis, PVR changes
Subretinal demarcation lines (high-water marksdue to proliferation of
RPE at junction of flat and detachment retina)
Lincoffs Rule
Extent of RD Location of break
Superior RD extending downwards equally on Between 11 and 1 oclock
both sides of macula
Inferior RD extending upwards equally on both Between 5 and 7 oclock
sides of macula
Asymmetric distribution of SRF Within 12 clock hours of the edge of more
vertically extensive side of RD
Bullous RD Superior break
Retinal Detachment Surgery

Scleral Buckling and SRF Drainage
Creating inward indentation of sclera (buckle)
Closes retinal breaks by apposing RPE to sensory retina
To reduce dynamic vitreoretinal traction at sites of vitreoretinal adhesion
Local explants:
Circumferential explants
Radial explants
Encircling explants:
Placed around entire globe circumference
Used for:
Breaks involving 3 or 4 quadrants
Lattice degeneration/snail track degeneration in 3 or 4 quadrants
Extensive RDwhen break cannot be detected
SRF drainage:
If break cannot be localized
Immobile retina (e.g. in PVR)
Inferior RD associated with equatorial tears
Complications:
Hemorrhage perforation of a large choroidal vessel
Dry tap (no SRF is drained)
latrogenic breaks
Retinal incarcerationdoes not re-attach
Fish mouthingtendency for U shaped tears to open widely following
scleral buckle and SRF drainage
Pneumatic Retinopexy
Photocoagulation or cryotherapy around breakto permanently seal it
A gas bubble injected into vitreous cavity
Patient positioned so that the bubble closes the retinal break, allowing
resorption of SRF, for 57 days
Usually0.3 mL C3 F8 or 0.5 mL SF6 is injected
Retina 107
Gas Lasts For Largest Size Expansion

Air 3 days Immediately Nil
SF6 12 days 36 hours Doubles
C3F8 38 days 72 hours Quadruples
Indications:
Uncomplicated RD with small breaks in 1 or 2 clock hours in upper 2/3rds
of peripheral retina
Superior small breaks with RD
Single break or break in one-quadrant in upper 8 clock hours
Impending macular hole (recent study)
Retinoschisis with very posterior outer layer breaks and RD
Retinal re-detachment following scleral bucklingwith superior breaks
Functioning filtering bleb
Optic pit with serous macular detachment
Extensively scarred conjunctiva; very thin sclera
Contraindications:
Detached tears 6 oclock hours apart
Inferior breaks
Severe PVR
Cloudy mediavitreous hemorrhage
Inability to maintain positioningin old patients, kids, people with back/
neck problem
Extensive lattice degeneration
Aphakia/pseudophakia
Complications:
CRAO
Cataract (if patient sleeps face up)
Ciliary block glaucoma in aphakic eye
Pars Plana Vitrectomy
20 g, 23 g and 25 guage
Tamponading Agents
Air
Expanding gases - SF6, C3F8
Heavy liquidperfluorocarbons (PFCL)
To unfold giant retinal tears
To remove posterior dislocated lens fragments/IOL
To stabilize posterior retinaepiretinal membrane (ERM) dissection in PVR
Silicone oilsprovide prolonged tamponade
TRACTIONAL RETINAL DETACHMENT

Vitreoretinal traction develops insidiously
No photopsia/floaters/acute PVD/breaks
Detached retinaconcave configuration
Shallow RD - SRF does not extend to ora
Highest elevation of retina at sites of traction
Decreased retina mobility
No shifting fluid under the detachment
Combined RDif TRD develops a break
Causes
Proliferative diabetic retinopathy
BRVO, CRVO
Eales disease
Surgery
Virtectomy with membrane peeling and tamponade with gas/silicon oil
Membrane peeling done by:
Delaminationhorizontal cutting of individual vascular pegs
connecting membrane to retinal surface
Segmentationvertical cutting of ERM into smaller segments; band
causing traction focally is cut
Surgical Complications
1. Increased IOP due to:
Over-expansion of gas
Silicone oil in AC
Blockage of trabecular meshwork
Ghost cell glaucoma
Steroid-induced glaucoma
2. Cataract
3. Retinal re-detachment after removal of oil, or when gas bubble is absorbed
Retina 109
EXUDATIVE RETINAL DETACHMENT

Detached retinaconvex, smooth
Mobile detached retinaShifting fluid phenomenon SRF detaches the
retina under which it accumulates
No retinal breaks
May have floatersif there is vitritis
Visual field defect may develop suddenly and progress rapidly
Scattered areas of subretinal clumping after detachment resolves Leopard
spot retina
Causes
Idiopathic
Idiopathic CSCR
Coats disease
Congenital
Optic nerve pit
FEVR
Morning glory syndrome
Post-surgical
PRP
Hemorrhagic choroidal detachment
Repair of retinal detachment
Inflammatory
Scleritis
Orbital cellulitis
Orbital pseudotumor
Neoplastic
Malignant melanoma
Choroidal nevus
Choroidal hemangioma
Metastasis
Lymphoma
Combined hamartoma
Retinoblastoma
Secondary to Uveitis
Posterior uveitis
Cysticercosis
Vogt-Koyanagi-Harada syndrome
Sympathetic ophthalmia
Vascular (Hemodynamic)
Toxemia of pregnancy
Hypertensive retinopathy
Diabetic retinopathy
Chronic renal failure
Hematologic
Thrombotic thrombocytopenic purpura
Sickle cell disease
Leukemia
Retina 111
PROLIFERATIVE VITREORETINOPATHY (PVR)

Growth of cellular membranes within vitreous cavity and around retina
Proliferation and contraction of membranes on:
Inner retinal surface (epiretinal membrane)
Posterior surface of detached hyaloid
Outer retinal surface (subretinal membrane)
Failure of RD surgery
Classification of Retinal Detachment with PVR
Grade Name Classification

A Minimal Diffuse vitreous haze
Tobacco dusting
Pigmented cells on inferior retina
B Moderate Retinal breaks with rolled edges
Wrinkling of inner retinal surface
Tortuous blood vessels
Retinal stiffness
Decreased mobility of vitreous gel
C Marked Full thickness retinal folds
C1 one quadrant
C2 two quadrants
C3 three quadrants
D Massive Fixed retinal folds in 4 quadrants
D1 - wide funnel shape RD
D2 - narrow funnel shape RD
D3 - closed funnel RD (disc not visible)
Risk Factors
Horse shoe tears, giant retinal tear
Posterior vitreous detachment
Vitreous hemorrhage, vitreous liquefaction
Myopic/aphakic RD, re-surgery
Excessive cryotherapy/photocoagulation/diathermy
Classification of PVR
Grade Features
A Diffuse vitreous haze
Vitreous pigment clumps
Pigmented clusters on inferior retina
B Retinal breaks with rolled edges
Wrinkling of inner retinal surface
Tortuous wood vessels
Retinal stiffness
Decreased mobility of vitreous gel
CP 112 Focal/diffuse/circumferential full thickness retinal folds,* posterior
to equator
Sub-retinal strands
CA 112 Focal/diffuse/circumferential full thickness retinal folds,* anterior
to equator
Sub-retinal strands
Anterior displacement
Condensed vitreous with strands
*Expressed in number of clock hours involved
Pathogenesis
Medical Treatment
In Active Stage of Inflammation
Systemic colchicine 2 mg/day 6 months; followed by 1 mg/d 2 months
Intravitreal dexamethasone, triamcinolone, 5-fluorouracil, colchicine,
penicillamine have been tried
Surgery
Sector iridectomy to prevent pupillary block glaucoma
Core vitrectomy with removal of membranes
Membrane peeling: delamination and segmentation of strongly adherent
membranes
Scleral buckling with encircling band and silicon oil injection
Retina 113
LEUKOCORIA
Amaurotic cats eye reflex
Whitish reflex in the pupillary area
Retinoblastoma
Discussed under oculoplasty
PHPV (Persistent Hyperplastic Primary Vitreous)
Nystagmus, strabismus, decreased vision
Unilateral and mostly sporadic
Associated with microphthalmos
Clinical features:
Retrolenticular mass into which elongated ciliary processes are inserted
The mass contracts and pulls the ciliary processes centrally
In anterior PHPV, a small, plaque-like opacity is seen behind the lens capsule
Mittendorfs dot
In posterior PHPV, Bergmiesters papilla is seen
Associations:
Shallow anterior chamber with angle closure glaucoma
Optic nerve hypoplasia
Macular hypoplasia
Iris and lens coloboma
Posterior polar cataract
Lens subluxation
Persistent pupillary membrane
Vitreous hemorrhage.
Vitrectomy if vitreous hemorrhage occurs
Coats Disease
Severe form of retinal telangiectasia
Unilateral; young boys
Clinical features:
Decreased vision, squint
Retinal telangiectasia and aneurysms in inferior and temporal quadrants
Intra-retinal or sub-retinal yellowish exudation (especially in the macular
area)
Uveitis, phthisis bulbi
FFA:
Tortuosity, aneurysms (hyperfluorescent), areas of capillary non-perfusion
Blockage of background choroidal fluorescence due to exudation
Treatment:
Photocoagulation of areas of telangiectasia
Cryotherapyin shallow RD
Vitreoretinal surgeryin extensive RD
Toxocariasis
Chronic endophthalmitis cyclitic membrane gives a white pupillary reflex
Posterior pole granuloma can resemble endophytic retinoblastoma
Retinal Astrocytoma
In tuberous sclerosis
Solid white nodule with multiple areas of calcification
Fossilized mulberry-like appearance
Intermediate Uveitis
Causes an inflammatory cyclitic membrane
Can mimic infiltrative type of retinoblastoma
Retinal Dysplasia
Retina never attains maturity
Associated with microphthalmos, shallow anterior chamber, elongated
ciliary processes
Pink or white retrolental membraness
Incontinentia Pigmenti
Fibrovascular proliferation causing cicatricial retinal detachment
Vesiculobullous dermatitis
Retinocytoma
A benign calcified mass with RPE alteration and chorioretinal atrophy
Retina 115
ENDOPHTHALMITIS
Intra-ocular inflammation which predominantly affects inner spaces of the eye
and their contents (vitreous and/or anterior chamber)
Causes
Acute Postoperative Endophthalmitis
Infectious:
Exogenous
Bacterial flora of lids and conjunctiva
Staphylococcus aureus 13 postoperative days
Staphylococcus epidermidis 410 postoperative days
Clinical features:
Severe ocular pain, decreased vision, lid edema, chemosis
Conjunctival injection, increased AC reaction, hypopyon
No red glow; B-scan shows multiple low-medium reflective echoes in
vitreous cavity
Rapid progression of signs
Differential diagnosis:
Retained lens material, severe uveitis, toxic reaction to irrigating fluids
Endogenous
Bacteremia, fungemia
Non-infectious:
Sterile endophthalmitisusually due to solutions used during intraocular
surgery
Delayed Onset Pseudophakic Endophthalmitis
Presents > 1 month after surgery
Sudden decrease in vision, increased AC reaction, no red glow
Propionibacterium acnes (gram +ve rod)causes recurrent granulomatous
inflammation
White plaque between IOL and posterior capsule
Increased incidence following YAG capsulotomy
Organism grows on thioglycolate broth
Treatment:
Remove IOL and residual cortex
Vitrectomy + intravitreal antibiotics (cephazolin/vancomycin)
Topical and periocular steroids
Topical antibiotics
Bleb-associated Endophthalmitis
Usually caused by Streptococci, H. influenzae
Post-Traumatic Endophthalmitis
Caused by Staphylococcus epidermidis, Bacillus species
Complications
Panophthalmitisproptosis and painful limitation of movement, when
inflammation extends to Tenons capsule
Orbital cellulitis, cavernous sinus thrombosis
Cataract (due to inflammation/treatment given)
Rhegmatogenous or tractional RD
Macular infarction (due to intravitreal aminoglycosides); optic atrophy
Wide spread formation of cyclitic membranes destruction of ciliary
processes phthisis bulbi
Precautionary Measures
Treat risk factors like chronic blepharitis, dacryocystitis
Povidone-iodine should be instilled into conjunctival sac before surgery
Strict asepsis
Prophylactic topical antibiotics may be given
Management
Anterior chamber paracentesis 0.1 mL of aqueous tapped
Vitreous tap taken
3 mm from the limbus in aphakic and pseudophakic eye (a more
posterior tap may cause retinal dialysis)
3.5 mm from limbus in phakic eyes (to avoid trauma to lens)
MicroscopyGrams stain, Giemsa stain, KOH mount
Culture sensitivityblood agar, chocolate agar, Sabourauds dextrose agar
(SDA), thioglyocolate broth
1. Intravitreal antibiotics (can be repeated after 4872 hours if no response):
Amikacin + Vancomycin
Ceftazidime + Vancomycin
Dosage:
Amikacin 0.4 mg in 0.1 mL
Vancomycin 1 mg in 0.1 mL
Ceftazidime 2.25 mg in 0.1 mL
2. Anterior sub-Tenons injection daily for 57 days:
Vancomycin 25 mg + ceftazidime 100 mg
3. Topical antibiotics:
Fortified gentamicin (15 mg/mL) + fortified vancomycin (50 mg/mL)
hourly
4. Systemic antibioticsif panophthalmitis develops:
Intravenous ceftazidime 2 g every 12 hours
Oral ciprofloxacin 750 mg BD
Retina 117
5. Steroids:
Periocularbetamethasone 4 mg or dexamethasone 4 mg 57 days
Topical dexamethasone or prednisolone
Oral prednisolone 1 mg/kg wt 1014 days
Intravitreal dexamethasone 0.4 mg in 0.1 mL (if fungal infection is ruled-
out)
6. Cycloplegics prevent posterior synechiae formation
7. Vitrectomy indications are:
Vision PL+ (light perception) or worse
Failure of medical treatment in 48 hours
Fungal endophthalmitis
Vitreous abscess
Removal of intraocular foreign body
Bleb-associated endophthalmitis
Post-traumatic endophthalmitis
Fungal Endophthalmitis
Delayed onset; minimal discomfort
Snowball exudation in vitreous; vitreous abscess
Increased fibrinoid reaction in anterior chamber
Commonest cause Fusarium species
Treatment
Core vitrectomy + intravitreal antifungal drugs
Intravitreal amphotericin B (5 in 0.1 mL) or
Intravitreal voriconazole 50 in 0.1 mL
Oral ketoconazole 400 mg/day
Steroids are contraindicated
PREPARATION OF INTRAVITREAL DRUGS
Drug 1 vial contains Intravitreal dose preparation

Vancomycin 500 mg Add 10 mL of DW to vial; take 0.2 mL of this and
(1 mg in 0.1 mL) add 0.8 mL of DW
Ceftazidime 500 mg Add 2 mL of DW to vial; take 0.1 mL of this and add
(2.25 mg in 0.1 mL) 0.9 mL of DW
Amikacin 2 mL = 100 mg Add 2.3 mL of DW to 0.2 mL of drug
(0.4 mg in 0.1 mL)
Amphotericin B 50 mg Add 10 mL of 5% D to vial; take 0.1 mL of this and
(5 g in 0.1 mL) add 9.9 mL of 5% D
Ganciclovir 500 mg Add 10 mL of DW to vial; take 0.04 mL for injection
(2000 g in 0.1 mL)
DW = distilled water; 5% D = 5% dextrose

Retina 119
IN THE CLINIC
If clinical findings and vision do not correlate 1st re-check vision
Following uneventful cataract surgery, if vision does not improve to 20/20
look for CME (provided no other pre-operative cause for vision loss)
RPE alterations in the macula of one eye of a young/ middle-aged man, with
mild-to-moderate vision loss rule-out resolved CSCR
Full thickness macular hole cannot present with 20/20 vision; look for ERM
could be a pseudo-hole
CNV not responding to intravitreal injections rule-out polypoidal choroidal
vasculopathy
CRVO with profound vision loss and retinal opacification in the macula
rule-out combined CRVO and CRAO
Young man with one cotton wool spot and no hypertension or diabetes
rule-out HIV microangiopathy
Subhyaloid/vitreous hemorrhage in a long standing diabetic rule-out PDR
even if new vessels on the disc/retina are not glaring at you!
In bilateral venous stasis retinopathy rule-out poly-cythemia
One/few isolated retinal hemorrhages and no other sign check blood
pressure
Yellowish blob on the macula may be an old preretinal hemorrhage
If there is a rhegmatogenous RD in one eye look for retinal breaks/lattices
in the fellow eye
If PVD has recently occurred, or an ERM has spontaneously peeled, look for
a retinal tear
Scan the disc on slit lamp biomicroscopy for glaucoma/ mild blurring of disc
margin/collaterals/NVD/pallor
In a patient who had undergone cataract surgery presenting with aphakia
look for dropped IOL
Patient referred for dropped IOL look for a dropped nucleus as well!
If the disc and macula are normal, and vision is poor look at the cornea
Unilateral macular star and disc edema of long duration may be a brain
tumor!
All cases of blunt trauma look for retinal dialysis
In localized corneal scar with cataract look for an intraocular foreign body
chapter
Uvea 4
UVEITIS
Granulomatous Non-granulomatous
Large, greasy, mutton fat KPs Fine KPs
Iris nodules Absent
Mostly associated with systemic disease May be idiopathic
Type IV hypersensitivity Allergic/exudative reaction
Insiduous onset, chronic Acute onset
Etiological Classification
Inflammatory
Exogenouscorneal ulcer, penetrating wound
EndogenousTB, Syphilis, Viral, Toxoplasma
Infection from ocular tissues
Immune-mediated
SLE, rheumatoid arthritis, ankylosing spondylitis, juvenile rheumatoid
arthritis, Behets disease
Neoplastic
Retinoblastoma
Iris melanoma
Leukemia
Reticulum cell sarcoma
Histiocytic cell sarcoma
Traumatic
Blunt trauma
Penetrating trauma
Surgery
Aqueous Flare
Grading:
1+ : Mild; just detectable
2+ : Moderate; iris details clear
3+ : Marked; iris and lens hazily seen
4+ : Intense; fibrous exudates
Uvea 121
Aqueous Cells
Grading:
0 : 0 cells
Trace : 15 cells
1+ : 615 cells
2+ : 1625 cells
3+ : 2650 cells
4+ : >50 cells
Vitreous Cells
Grading:
0 : 0 cells
Trace : 220 cells
1+ : 2150 cells
2+ : 51100 cells
3+ : 101250 cells
4+ : >250 cells
Vitreous Haze
Grading:
0/trace : Clear view of fundus
1+ : 2nd order vessels seen
2+ : Optic nerve head and 1st order vessels seen
3+ : Faint view of optic nerve head
4+ : Optic nerve head obscured
Keratic Precipitates
Cellular deposits on endotheliumusually occur in mid and inferior zones due
to convection currents in the anterior chamber (Arlts triangle)
Stellate keratic precipitates (KPs) throughout endotheliumin Fuchs hetero-
chromic uveitis
Endothelial dustingin acute uveitis
Medium-sizedin acute and chronic uveitis
Large, mutton-fat, greasy, waxy KPs ingranulomatous uveitis
Old KPspigmented/ground glass (hyalinized)
INVESTIGATIONS FOR UVEITIS

Laboratory Tests
Skin Tests
Mantoux Tuberculosis
Kveim test Sarcoidosis
Lepromin test Leprosy
Casonis test Hydatid cyst
Pathergy test Behets disease
Serological Tests
Antinuclear antibodies SLE, Juvenile rheumatoid

arthritis, scleroderma,
dermatomyositis
ACE levels Active systemic sarcoidosis,
leprosy, tuberculolsis,
histoplasmosis
HLA antigens B27 (Ankylosing spondylosis,
Reiters syndrome, inflammatory
bowel disease, psoriatic arthritis)
B5 (Behets disease)
DR4 (VKH syndrome)
A29 (Birdshot chorioretinopathy)
Rheumatoid factor Rheumatoid arthritis
ELISA HIV, CMV, HSV, toxoplasmosis, toxocariasis
TORCH titers Toxoplasmosis, rubella, CMV
ANCA Wegeners granulomatosis, polyarteritis nodosa
FTA-ABS / VDRL Syphilis
RBS, Hb%, BT/CT, Serum calcuim Non-specific
Histopathology
Anterior chamber paracentesis Microscopy, ACE levels, LDL levels
(Retinoblastoma), immunological tests, PCR (HSV,
tuberculosis)
Vitreous tap/biopsy Endophthalmitis
Chorioretinal biopsy Bilateral acute retinal necrosis
Uvea 123
Non-laboratory Tests
X-ray chest Tuberculosis, sarcoidosis
X-ray sacroiliac joint Ankylosing spondylitis
Iris angiography Fuchs heterochromic uveitis
FFA VKH syndrome, APMPPE,
Birdshot chorioretinopathy
B-scan, UBM VKH syndrome, toxocariasis
Gallium scan Active sarcoidosis
Lumbar puncture Syphilis, reticulum cell sarcoma
IRIS NODULES
1. Granulomatous iridocyclitis:
Koeppe nodulespupillary border
Busacca nodulesperiphery of iris
2. Juvenile xanthogranuloma:
Yellow/gray poorly demarcated lesion in 1st year
3. Leiomyoma:
Localized, diffuse/flat, pigmented
4. Malignant melanoma:
Nodular/flat
Inferiorlysentinel vessels may be seen
May be amelanotic
5. Tapioca melanoma:
Nodules over a part/all of iris
Translucent to lightly pigmented
6. Lisch nodules:
Neurofibromas; multiple
Tan to dark brown; pinhead size; flat/raised
7. Iris pearls:
Granulomas in Hansens disease
8. Brushfeld spots:
White to yellow spotsin iris periphery
In Downs syndrome
Normal stroma surrounded by a ring of mild iris hypoplasia
9. Metastasis:
Gelatinous white nodules
10. Retinoblastoma:
White foci on anterior iris surface
11. Leukemia:
Nodular/diffuse milky lesions with intense hyperemia
12. Iris nevus:
Discrete mass/nodule
Has varied pigmentation
13. Iris nevus syndrome:
Diffuse nevus with ipsilateral glaucoma
14. Fungal endophthalmitis:
Irregular, yellow-white mass on iris
15. Retained foreign body:
Becomes secondarily pigmented
Uvea 125
INTERMEDIATE UVEITIS
Intraocular inflammation involving anterior vitreous, peripheral retina and
pars plana
80% are bilateral
Children and young adults are mainly affected
Chronic; periods of exacerbation and remission
Causes
Idiopathic, multiple sclerosis, sarcoidosis
Lyme disease, inflammatory bowel disease, thyroid disease
Etiopathogenesis
Primary peripheral retinal perivasculitis
Primary vitreal inflammation
Inflammatory stimulus tissue reaction fibroglial proliferation
Symptoms
Blurred vision, floaters
Signs
Cornea Fine white KPs in inferior portion of cornea; band keratopathy
Anterior chamber Mild to moderate inflammation; minimum cells and flare
Iris Posterior synechiae; rubeosis iridis
Lens Anterior opacities; posterior subcapsular cataract; intumescent cataract
Vitreous Cells in anterior vitreous face (vitritis); snow balls; PVD; hemorrhage
Retina CME, peripheral vasculitis, NVE, hemorrhages, TRD, pigmentation
Optic nerve Papillitis, NVD, optic atrophy
Glaucoma Secondary angle closure (iris bombe); steroid induced; inflammatory
IOP High or low (hypotony due to contraction of cyclitic membranes)
Management
Treat if vision is 6/12 or worse; or if patient has severe floaters with vision better
than 6/12
Steroids:
Periocular (if unilateral)
Systemic (if bilateral)
Cryotherapydouble freeze thaw to the area of snow bank decreases
peripheral exudation by eliminating peripheral neovascularization
Vitrectomy done if:
Persistent severe vitritis
Retinal detachment
Epiretinal membranes
Immunosuppressivescyclosporine A, methotrexate, azathioprine
OCULAR TOXOPLASMOSIS
Toxoplasma gondii is a protozoan parasite with affinity towards nerve
tissue; it multiplies in ganglion cells and nerve fibers; causes toxoplasmic
retinochoroiditis
Affects maculasince it has the thickest NFL
Symptoms
Young childrenreduced visual acuity, strabismus, nystagmus, leucocoria
Teenagers and adultsdecreased vision, floaters, photophobia, pain,
hyperemia (anterior uveitis)
Signs
Lesions are solitary/multiple/satellite (adjacent to a scar)
Typical congenital lesionmacular cicatricial lesion with radial deposition
of pigment around a central necrotic zone
Infects primarily the retina with secondary involvement of the choroid and
vitreous
Initial lesionlocalizing necrotizing granulomatous retinochoroiditis at the
edge of a pigmented retinal scar
Gray-white focus of retinal necrosis exudation with undefined margins
Headlight in fog appearancewhen the retinal inflammation can just be
seen through the dense vitritis
Cicatrization occurs from the periphery towards the center with variable
pigmentary hyperplasia and choroidal atrophy
Diffuse/segmental vasculitis adjacent or distant from active lesion
Nodular arteritis Kyrieleis arterilitis
Disc edema, vascular occlusions, CNVM
Retinochoroiditis adjacent to the discJensens choroiditis
Vitreousinflammation, opacifications, hemorrhage, pigmentation, PVD
Vitreous haze may take more than a year to resolve
Granulomatous anterior uveitismutton fat KPs, fibrin/cells/flare in anterior
chamber, Koeppe and Busacca nodules, posterior synechiae
Glaucoma, cataract
Atypical Presentations
Punctate outer retinitismultifocal small gray-white lesions at the level of
outer retina and RPE; mild vitritis; severe involvement of optic nerve head
Neuroretinitisactive lesions adjacent to an edematous/hyperemic disc;
venous dilatation, hemorrhage, severe vitritis
PapillitisAPD; sudden decrease in vision
Pseudo-multiple retinochoroiditis multiple retinal lesions (apparently
active); after regression only one scar (from the real focus of infection)
Intraocular inflammation without retinochoroiditis
Unilateral pigmentary retinopathy simulating retinitispigmentosa
Fuchs like anterior uveitis
Uvea 127
Scleritis associated with severe retinitis

Multifocal or diffuse retinochoroiditis mimicking ARN
Complications
Chronic iridocyclitis, scleritis
Cataract, glaucoma
Band keratopathy
CNVM, CME, RD
Optic atrophy, BRVO
Laboratory Tests
Sabin Feldman dye testin research centers
ELISAto detect IgG, IgM, IgA, IgE; recent infection presence of IgM/IgA/
IgE
IgG avidity testhigh avidity indicates that infection is more than 35
months old
Aqueous humor studyantibodies, parasite detection, PCR
FFA
Early hyperfluorescence in the margins of the active lesion spreads to the
whole lesionfuzzy hyperfluorescence
Scars are hypofluorescent with hyperfluorescent margins
ICG
Active lesionshyperfluorescent throughout angiogram
Scarshypofluorescent throughout
Management
Combination Regimens
1. Pyrimethamine, sulfadiazine, folinic acid, prednisone
2. Pyrimethamine, clindamycin, folinic acid, prednisone
3. Trimethoprime-sulphamethoxazole, prednisone
4. Tetracycline/minocycline and prednisone
Drug Formulation Adult dose
Pyrimethamine 25 mg tab 100 mg (1st day), 75 mg (2nd day), 50
mg (3rd day); then 25 mg OD for 46 wks
Folinic acid 10 mg tab 7.515 mg on alternate days
Sulfadiazine 500 mg tab 4 g daily in 4 divided doses
Clindamycin 75/150/300 mg 150400 mg every 68 hours
Bactrim/septran 80 mg + 400 mg BD for 46 wks
(trimethoprim+sulfamethoxazole)
Spiramycin 250/500 mg tab 1 g BD
Azithromycin 250/500 mg tab 1 g (1st day), then 500 mg OD3 wks
Tetracycline 250/500 mg tab 500 mg QID (1st day),
then 250 mg QID for 46 wks
Oral Corticosteroids
Must be initiated at least 24 hours after antiparasitic drugs
1 mg/kg/day followed by tapering depending on response
Must be stopped at least 10 days before the antiparasitic drugs
Topical steroids and mydriatics are given:
Immunocompromised Patients
Treat for 6 or more weeks
After complete resolution, start secondary prophyllaxis with sulfadiazine,
pyrimethamine and folinic acid, can be discontinued when CD4 count >200
cells/l for 6 months
During Pregnancy
1st trimesterspiramycin, sulfadiazine
2nd trimesterspiramycin, sulfadiazine, pyrimethamine, folinic acid
3rd trimesterspiramycin, pyrimethamine, folinic acid
Uvea 129
FUCHS HETEROCHROMIC UVEITIS

Chronic anterior segment inflammatory syndrome
Chronic, non-granulomatous, anterior uveitis
Unilateral; 3rd and 4th decades of life
Herpes simplex, ocular toxoplasmosis, rubella may be responsible
Clinical Features
Usually asymptomatic; may complain of blurred vision and floaters
Absence of acute symptomsredness, pain, photophobia
Keratic precipitates:
Small, round/stellate; gray-white
Scattered throughout endothelium
Never become confluent/pigmented
Filamentary fibrin filaments between KPs
Anterior chamberfaint flare; < +2 cells
Angle of anterior chambermay have
Fine, radial, twig-like blood vessels
Usually open; no peripheral anterior synechiae (rarely small irregular
PAS)
Iris:
Diffuse stromal iris atrophy
Posterior synechiae do not develop
Washed out appearance
Koeppe nodules (pupillary margin), Busacca nodules (on iris surface)
Rubeosis iridis
Atrophy of sphincter irregular pupil with poor light reflex
Hypochromic iris (90%)
Hyperchromic (10%)
Posterior subcapsular/cortical cataract
Increased intraocular pressure
Vitreous cells in the anterior face
Amslers signIris and trabecular meshwork show abnormal vesselslead
to hyphema after paracentesis, surgery, trauma, gonioscopy, tonometry,
spontaneously
Treatment
Low-grade anterior chamber reactionno treatment
Occasional, short time use of topical steroidsif acute exacerbation occurs
Glaucoma not responding to medical treatmenttrabeculectomy with
mitomycin C
Cataract surgerywhen inflammatory process is controlled for 3 months
Vitrectomyfor severe vitreous opacification
VOGT-KOYANAGI-HARADA DISEASE
Multisystem autoimmune disorder primarily affecting pigmented tissues in
the ocular, auditory, integumentary and central nervous system
Directed against antigens in choroid, meninges, inner ear, skin
No history of surgical/accidental ocular trauma
Bilateral chronic, diffuse granulomatous uveitis
Diagnostic Criteria
Complete VKH Disease
1. No history of penetrating ocular trauma
2. No evidence of other ocular/systemic disease
3. Bilateral ocular disease
a. Early manifestations:
i. Diffuse choroiditis with focal areas of subretinal fluid or bullous se-
rous retinal detachments
ii. FFA shows focal delayed choroidal perfusion, pinpoint leakage,
pooling of fluorescein within the subretinal fluid, optic nerve stain-
ing
iii. B-scan shows diffuse choroidal thickening (due to inflammatory
cell infiltration) without evidence of posterior scleritis
b. Late manifestations:
i. Ocular depigmentation sunset glow fundus, Sugiuras sign
ii. Nummular chorioretinal depigmented scars
iii. RPE clumping with or without migration
iv. Recurrent or chronic anterior uveitis
4. Neurological/auditory findings:
a. Meningismus
b. Tinnitus
c. CSF pleocytosis
5. Integumentary findings (not preceding CNS/ocular disease)
a. Alopecia
b. Poliosis
c. Vitiligo
Incomplete VKH Disease
Criteria 13; and 4 or 5 from above
Probable VKH Disease
Isolated ocular disease (only criteria 13 from above)
Clinical Features
Prodromal Phase
Meningitis, headache, neck stiffness
Tinnitus, vertigo, deafness
Encephalopathyconvulsion, paresis, cranial nerve palsies
Uvea 131
Acute Uveitic Phase

Bilateral panuveitis
Bilateral granulomatous anterior uveitis
Multifocal choroiditis, vitritis, papillitis
May have shallow anterior chamber due to ciliary body edema or
ciliochoroidal detachment
Convalescent Phase
Localized alopecia, poliosis, vitiligo
Sunset glow fundus (old exudative RD)
Sugiuras sign (perilimbal vitiligo)within a month of onset of disease
Perilimbal vitiligo
Chronic Recurrent Phase
Bilateral anterior uveitis
Management
Prompt and aggressive use of systemic corticosteroids
1g intravenous methyl prednisolone daily for 3 days followed by high dose
oral corticosteroidsgradually tapered over 6 months depending on
response
If nonresponsive to steroidsgive oral cyclosporine
If no response to cyclosporinegive cyclophosphamide/chlorambucil/
azathioprine
Differential Diagnosis of Bilateral Panuveitis

History of Ocular Trauma
a. Sympathetic ophthalmia
b. Uveal effusion syndrome
No History of Trauma
a. Malignancyprimary intraocular B-cell lymphoma
b. Inflammatory VKH, sarcoidosis, posterior scleritis, MEWDS, APMPPE
c. Infectioustuberculosis, syphilis
d. Othersuveal infusion syndrome
WHITE DOT SYNDROMES

Acquired diseases that cause inflammation and multifocal lesions at the
level of the outer retina, RPE and inner choroid
Healthy individuals
They are:
APMPPE (acute posterior multifocal placoid pigment epitheliopathy)
Birdshot retinochoroidopathy
Multifocal choroiditis and panuveitis syndrome
MEWDS (multiple evanescent white dot syndrome)
Punctate inner choroidopathy
Serpiginous choroiditis (geographical helicoid peripapillary
choroidopathy)
Acute retinal pigment epithelialitis
Presumed ocular histoplasmosis syndrome
Subretinal fibrosis and uveitis syndrome
Uvea 133
ACUTE POSTERIOR MULTIFOCAL PLACOID

PIGMENT EPITHELIOPATHY
Acuterecover within 3 weeks
Posteriorposterior pole involvement
Multifocalmultiple foci of yellow-white lesions
Placoidround, discrete lesions
Pigment epitheliopathyat the RPE level; choriocapillaris may be the primary
site of inflammation
Young patients
Flu-like prodrome
Bilateral rapid painless decrease in vision
Central/paracentral scotomas
Rapid recovery in visual acuity
Pathogenesis
Choroidal microvasculitischoroidal lobule closure and secondary RPE
changes
Lesions are focal infarcts of the RPE
Signs
Posterior polemultifocal, large, yellow-white placoid lesions at the level
of the RPE and inner choroid; may form one large central lesion
Mid-peripheryoval/Linear lesions with the long axis oriented radially
The disease is remarkable for the rate at which pigment changes develop
(in 12 weeks)
Associated findings:
Papillitis, serous RD
Retinal vasculitis, macular edema, vitritis
Superficial retinal hemorrhages
Corneal infiltrates, episcleritis
CNVvery rare
Resolution of the lesions within 3 weekswell-defined scarsareas of
depigmentation and pigment epithelial clumping
Systemic associations:
Erythema nodosum; cerebral vasculitis
Adeno virus type-5 infection
Neurosensory hearing loss
FFA
Acute lesions:
Early hypofluorescence secondary to RPE cell edema, leukocyte
infiltration, and capillary non-perfusion
Late hyperfluorescence, as leakage occurs from the choriocapillaris
through damaged RPE cells, and persists for up to 30 minutes
Inactive lesions:
Window defects due to atrophy and depigmentation of RPE
ICG
Active stageareas of choroidal hypofluorescence resulting from capillary
non-perfusion
Later stages of the diseasehypofluorescence persists, becoming smaller
and less pronounced as the lesions heal
EOGmarkedly abnormal
ERGnormal
1. Serpiginous choroiditis:
Older patients
No viral prodrome
Severe choroidal scarring
Shape of the lesions
Normal optic nerve
Resolves more slowly
Recurrences happen over years
2. VKH disease:
Multifocal, gray-white patches at the level of the retinal pigment
epithelium
Less well-defined
Accumulation of dye in the subretinal space on FFA
Management
No proven treatment
Systemic steroids severe; macular involvement
Systemic and neurological evaluation:
Exclude cerebral vasculitis, sarcoidosis, nephropathy, thyroiditis, and
tuberculosis
If headachelook for cerebral vasculitisTreatment: high-dose steroids,
cyclosporin A
Uvea 135
BIRDSHOT RETINOCHOROIDOPATHY
Focal depigmentation of choroidal melanocytes vitiliginous choroiditis
BirdshotMultiple, small, white spots that have the pattern seen with
birdshot in the scatter from a shotgun
RetinoDysfunction of all retinal layers
ChoroidopathyLesions in the outer choroid, associated with large
choroidal vessels
Features
Older females
Painless gradual bilateral blurring of vision, floaters
Loss of color vision; difficulty in night vision
White eye; minimal AC reaction, few KPs
Posterior vitritis, CME
Disc edema, peripapillary atrophy
Retinal vasculitischange in vessel caliber, perivascular exudates and
sheathing
Intraretinal hemorrhages in the posterior pole
Spots of depigmentation:
cream-colored; < DD; densest surrounding the optic nerve and nasally
Bead-like arrangement, paralleling the course of the choroidal veins,
radiating towards the periphery, sparing macula
No associated hyperpigmentation/clumping of melanin
No apparent changes in the sensory retina or RPE
Indistinctbecause of their deep location and lack of secondary RPE
reaction
Patient may present with vitritis and vasculitis, with no fundus lesions
initially
Retinal and subretinal neovasularization
FFA
Lesions are more apparent by ophthalmoscopy than by FFA
Early hypofluorescence of lesions
Late slight diffuse hyperfluorescencedeep-seated inflammatory focus
gradually accumulates fluorescein
Vasculitisleakage from vessels or late vessel wall staining
Disk leakage and cystoid macular edema
ICG
Hypofluorescent dark spots between large choroidal vessels
ERG
Negative ERG: Preserved a-wave with diminished amplitude and increased latency
of b-wave, suggesting impairment of the inner retina with relative sparing of
the photoreceptor-RPE-choroids complex
Supernormal ERG: Representing increased retinal irritability
In advanced disease,
a-wave and b-wave amplitudes are decreased, suggesting dysfunction of
all retinal layers, including the photoreceptors
EOG abnormalrepresenting RPE dysfunction
Dark adaptation abnormalitiesthe rod system is more affected than cones
Systemic Associations
Systemic hypertension, coronary artery disease, cerebro-vascular accident
Vitiligo, auto-immune sensorineural hearing loss
Myelodysplasia syndrome, Psoriasis
Complications
Chronic CME, epiretinal membrane formation
CNV, NVD, NVE, optic atrophy, cataract, glaucoma
Rhegmatogenous RD
Management
Periocular/systemic steroidsvitritis, vasculitis, CME
Low-dose cyclosporine (2.55 mg/day) or a combination of azathioprine
and cyclosporine
Intravenous immunoglobulin
Ketoconazole: adjunct therapy to cyclosporinedelays metabolism of
cyclosporine
Course
Exacerbations and remissions
Progressive disease with threat to central vision
May stabilize in 34 years
Poor long-term prognosis
Uvea 137
MULTIFOCAL CHOROIDITIS AND PANUVEITIS

Multifocalmultiple foci (several hundred)
Choroiditisyellow lesions at the level of RPE and choriocapillaris
Panuveitiscells in anterior chamber, non-granulomatous KPs, posterior
synechiae, vitritis, choroiditis
Features
Young women; bilateral
Chronic, recurrent nature
Floaters; decreased central vision (CME, CNV)
Paracentral scotomata, photopsias, photophobia
VA: 20/20 light perception
Anterior uveitis, vitritis
Lesions:
Round/oval; peripapillary/mid-periphery; arranged singly/clusters/linear
Small amounts of subretinal fluid
Leaves a deep, round, atrophic, pigmented scar (increases with time)
Disc edema
Peripapillary scarring white, napkin-ring
Disc pallor, narrowing of retinal vessels
Periphlebitis, NVE, NVD
FFA
Early hypofluorescence
Late leakage; Scarswindow defects
ICG
Demonstrates many more lesions
Hypofluorescent round spotsstay hypofluorescent throughout the
angiogram
Represent inflammatory products in the inner choroid
Choroidal ischemia
Fields
Enlargement of the blind spot
Large temporal field defects; scotomata
MULTIPLE EVANESCENT WHITE DOT SYNDROME

Multiplemany dots made of aggregates of small white dots
Evanescenttemporary/momentary (vanish in 6 weeks)
White Dotflat, gray-white lesions
Features
Young females
Acute, painless, unilateral loss of vision
Photopsias, temporal scotoma
Near total recovery of vision in 39 weeks
Visual acuity 20/20 20/300; RAPD present
Cells in posterior vitreous
Disc-blurred margins
Macula granular orange/yellow dots (foveal granularity)
Paramacular area and beyond the arcadesmultiple white dots
Flat, multifocal, gray-white lesions at the RPE level; 100300
White dots vanish may leave scattered chorioretinal scarring/pigment
mottling
Progressive geographic circumpapillary discolorationgiant white spot
may lead to peripapillary scarring
FFA
Early punctate hyperfluorescence in areas corresponding to the white dots;
wreath-like pattern
Late staining of the lesions
Diffuse, patchy late staining at level of RPE and retina
Disc capillary leakage
Window defects in maculaafter lesions resolve
ICG
Multiple hypofluorescent spots in the posterior pole and hypofluorescence
around the optic nerve head
Fields
Blind spot enlargementpersists after resolution of the white dots
Electrophysiology
Reduced ERG a-wave = photoreceptor dysfunction
Abnormal focal ERG = inner retinal dysfunction
Prolonged Early receptor potential = RPE and outer retina dysfunction
Abnormal EOG = reduced light-to-dark ratio, impaired RPE function
Abnormal VER = decreased P100 component and prolonged latency
suggestive of optic nerve dysfunction
Management
No treatment
Spontaneous recovery is the rule
Uvea 139
PUNCTATE INNER CHOROIDOPATHY

Punctate tiny, discrete, yellow lesions
Inner choroidopathy at the level of the inner choroid
Features
Young healthy women
Bilateral; blurred central vision
Flashing lights; scotomas
Small grey/yellow opaque spotsscattered randomly from posterior pole
to mid-periphery
Sub-RPE/inner choroidal lesions
Serous detachments overlying the choroidal lesions
No signs of inflammation (aqueous or vitreous cells, vasculitis, disc edema)
an inflammation without an inflammation
Evolve into chorioretinal atrophic pigmented cylindrical punched-out scars
CNVsarise from parafoveal scars through breaks in the Bruchs membrane
Optic discnormal
FFA
Arterial phasehyperfluorescence
AV phasestaining
ICG
There is early hypofluorescence
Larger vessels may be seen to cross these lesions and exhibit localized points
of hyperfluorescence
Fields
Paracentral defects, enlarged blind spot
ERG, EOGnormal
Management
Oral steroids in CNV can stabilize vision and reduce leakage from new vessels
Lesions may respond to oral and regional corticosteroids
SERPIGINOUS CHOROIDITIS
Serpiginous: Lesions emanate from the disc with finger-like polypoid extensions
spreading outward in a serpentine fashion
Choroiditis: Grayish-yellow fuzzy lesions at RPE level or inner choroid. Also called
Geographic helicoid peripapillary choroidopathy (GHPC)
Geographic: Geographic shape with a light boundary
Helicoid: Lesions spread in a helicoid/spiral fashion out to the equator
Peripapillary: Lesions emanate from the optic nerve head
Choroidopathy: At the RPE/inner choroid
Features
Bilateral chronic, recurring inflammatory disease
Decreased visionin case of foveal involvement
Normal optic nerve
Grayish-yellow, fuzzy lesions
A light border demarcates the leading edge of the lesion from normal tissue
Circumvent the fovea (macular GHPC involves the fovea)
Older lesionsfibrous scar tissue, loss of choroidal tissue, marked RPE
hyperplasia adjacent to areas of atrophy
Anterior uveitis, CME, retinal vasculitis, BRVO
Retinal detachment, CNV
FFA
Early hypofluorescence
Late soft, fuzzy hyperfluorescencestarts from the edge of the lesion and
spreads inwards
Late staining of scar tissue
ICG
Hypofluorescence throughout all phases
Choroidal nonperfusion + blockage by exudation or edema at the level of
the outer retina, RPE, choriocapillaris
Management
Anti-inflammatory agentssteroids
Immunosuppressivescyclosporin, azathioprine, cyclophosphamide,
chlorambucil
Uvea 141
IMMUNOSUPPRESSIVE DRUGS
Guidelines for the Use of Prednisolone in Uveitis

Parameter Suggested guideline
Initial dose 1 mg/kg/day
Maximum oral dose 6080 mg/day
Tapering schedule Over 40 mg/day, decrease by 10 mg/day every 12 wks
4020 mg/day, decrease by 5 mg/day every 12 wks
2010 mg/day, decrease by 2.5mg/day every 12 wks
100 mg/day, decrease by 12/5 mg/day every 14 wks
Monitor Blood pressure, weight, glucose Q 3 months
Cholesterol, triglycerides Q yearly
Bone density within 1st 3 months and yearly thereafter
Supplemental treatment Calcium 1500 mg daily
Vitamin D 800 IU daily
Proton pump inhibitors like Pantoprazole 40 mg daily
Immunosuppressive Drugs for Ocular Inflammation
Oral Initial dose Maximum Laboratory Comments

formulation dose test
Azazthio- 50 mg tab 1 mg/kg/d 2.54.0 CBC Q 4-6 wks; OD or BD
prine (50 mg OD) mg/kg/d LFT Q 12 dosage
Methotrexate 2.5 mg tab 7.512.5 25 mg/wk CBS, LFT Folic acid
mg/wk Q 68 wks 1mg daily
Cyclosporine 25/50 /100 mg 2.55.0 mg/ 10 mg/kg/d Creatinine BD dosage;
kg/d (50 mg Q 4 wks; CBC, Check blood
OD) LFT, Mg+2Q pressure
12 wks
Cyclophos- 25/50 mg tab 2 mg/kg/d 3 mg/kg/d CBC, urine May cause
phamide analysis hemorrhagic
Q 14 wks cystitis
Chlorambucil 2 mg tab 0.1 mg/kg/d 0.2 mg/kg/d CBC Q
14 wks
Side Effects
Bone marrow suppression, GI upset, hepatotoxicity azathioprine,
methotrexate
Pneumonitis, abortionsmethotrexate
Renal dysfunction, hirsuitism, gum hyperplasia, tremor cyclosporine
Bone marrow suppression, risk of malignancy, sterility, infection
cyclophosphamide, chlorambucil
Hemorrhagic cystitis, alopeciacyclophosphamide
chapter
Cornea 5
CORNEAL COLOR CODING
Red Deep blood vessels (dark red; straight lines ending at limbus), superficial blood vessels
(bright red; wavy branching lines crossing the limbus), ghost vessels (dotted straight
lines), hyphema, pterygium
Blue Epithelial edema (circles), Descemets folds (wavy lines), stromal edema (blue shade)
Green Lens, vitreous, corneal filaments, fluorescein stain, epithelial defect
Yellow Infiltrates, hypopyon, fresh keratic precipitates
Black Scars, degenerations, corneal outline, IOL, guttata (black shade), sutures (straight
line), loose suture (straight line with a circle around it), contact lens (dotted circle)
Brown Iris, pigment, old keratic precipitates
Cornea 143
BACTERIAL KERATITIS
Predisposing Factors
Contact lens wear may cause epithelial defects; predispose to Pseudomonas
aeruginosa infection
Pre-existing corneal diseasetrauma, bullous keratopathy, exposure
keratopathy, decreased corneal sensation
Chronic blepharitis; chronic dacryocystitis
Tear film deficiency; topical steroid usage; Vitamin A deficiency
Clinical Features
Pain, photophobia, redness, foreign body sensation, lid edema, discharge
Circumcorneal congestion
Sharp epithelial demarcation with underlying dense suppurative stromal
inflammation, surrounded by stromal edema
Epithelial defect surrounded by infiltrate
Endothelial inflammatory plaque
Anterior uveitis with hypopyon
Pseudomonas aeruginosa produces stromal necrosis with a shaggy surface
and adherent mucopurulent exudate
Corneal perforation is a complication
The Pneumonic PEDAL is Used for Infectious Keratitis
P pain; E epithelial defects; D discharge; AAC reaction; L location
Treatment
Broad spectrum topical antibiotics
Oral ciprofloxacin 750 mg BD in juxtalimbal keratitis
Atropine 3% ointment BDto prevent posterior synechiae and decrease
pain from ciliary spasm
Antibiotics Used in Bacterial Keratitis

Organism Antibiotic Topical dose
Gram-positive cocci Fortified cefazolin 50 mg/mL
Fortified vancomycin 50 mg/mL
Gram-negative rods Tobramycin 914 mg/mL
Fortified gentamicin 15 mg/mL
Fortified ceftazidime 50 mg/mL
Fluoroquinolones 3 mg/mL
No organisms/ Fortified cefazolin + Fortified
multiple organisms gentamicin (OR) fluoroquinolones
Gram-negative cocci Fortified ceftriaxone 50 mg/mL
Fortified ceftazidime 50 mg/mL
Mycobacteria Fortified amikacin 2550 mg/mL
Cornea 145
Preparation of Fortified Topical Medication

Drug 1 Vial contains Preparation
Cefazolin (50 mg/mL) 500 mg Add 10 mL of TS to vial
Ceftazidime (50 mg/mL) 500 mg Add 10 mL of TS to vial
Vancomycin (50 mg/mL) 500 mg Add 10 mL of TS to vial
Gentamicin (15 mg/mL) 2 mL (40 mg/mL) Add 2 mL from vial to 5mL of 3%
gentamicin eyedrops
TS = tear substitute
KERATOMYCOSIS
Caused by
Filamentary fungiFusarium sp., Aspergillus sp.
YeastsCandida species (immunocompromised individuals; pre-existing
corneal disease)
Pathogenicity
Hyphae grow along stromal collagen fibers
Ineffective phagocytosis by host immune system because hyphae are
largeinstead digestion of host cells occurs
Immunosuppression increases fungal growth
Fungi enter anterior chamber by penetrating intact Descemets membrane
Epidemiology
Trivial injury with organic matter
Windy and dry season; rural areas; agriculturists are more prone
Clinical Features
Signs >>> symptoms
Gradual onset, foreign body sensation, photophobia, blurred vision,
discharge
Slow progression, less painful
Investigations
KOH mountKOH dissolves epithelial cell walls; hyphae become visible
Culture mediaSabourauds dextrose agar, potato dextrose agar
Treatment
Topical antifungals up to 6 weeks
Cycloplegics
Hypotensive agents
Systemic antifungals (oral fluconazole 150 mg BD; if severe or if
endophthalmitis occurs)for large ulcers > 3 mm
Surgery:
Superficial keratectomyfor good drug penetration
Gluesif micro-perforation occurs
Therapeutic keratoplastyfor nonhealing ulcers, corneal perforation
Candida Keratitis
Yellow-white ulcer with dense suppuration
Cornea 147
Treatment
Topical imidazole 1%
Topical flucytosine 1%
Oral fluconazole 200400 mg/day if severe
Filamentous Keratitis
Gray stromal infiltrate with a dry texture and indistinct margins
Surrounding satellite lesions
Feathery finger-like lesions
Immune ring infiltrates (Wessely ring)
Endothelial plaque
Hypopyonthick and immobiledue to direct invasion of hyphae
enmeshed in thick exudates
Treatment
Topical natamycin 5%,
Topical amphotericin B 0.15%
Oral ketoconazole 200600 mg/day if severe
ACANTHAMOEBA KERATITIS
Caused by a ubiquitous free-living protozoan
Cysts become trophozoites which produce enzymes
tissue penetration and destruction
Contact lens wearers at particular risk
Clinical Features
Severe pain, blurred vision
Symptoms >> signs
Photophobia, foreign body sensation
Conjunctival injection, chemosis
Stromal ring infiltrate ring abscessmay be central/ paracentral
Radial keratoneuritisperineural infiltratescauses severe pain
Sub-epithelial keratopathy
Endothelial plaque, hypopyon
Frank corneal necrosis
Pseudodendritic keratitis
Small white satellite lesions
Slowly progressive stromal opacification; descemetocele
Scleritis
Investigations
10% KOH mountamebic cysts are seen
Calcofluor whitea chemofluorescent dye with special affinity for
acanthamoeba cysts
Grams stain, Giemsa stain, Periodic Acid Schiff
Culture on non-nutrient agar with E. coli overlay; buffered charcoal yeast
extract
Treatment
Topical:
1. PHMB (polyhexamethylene biguanide) 0.02% + propamidine isothionate
(brolene) 0.1%
2. Chlorhexidine (monotherapy)
3. Neomycin + brolene
Also used are:
4. Miconazole 1%
5. Clotrimazole 1%
6. Dipropamidine isothionate 0.15%.
Oral: Ketoconazole (optional)
Surgery: Therapeutic penetrating keratoplasty
Cornea 149
INTERSTITIAL KERATITIS
Non-ulcerative, non-suppurative inflammation of corneal stroma, often with
subsequent vascularization
Causes
Congenital/acquired syphilis (90%)
TB, leprosy, lyme disease
HSV, HZV, mumps, influenza, rubella
Chromium deficiency, gold toxicity
Onchocercariasis, cysticercosis, infectious mononucleosis
Malaria, leishmaniasis, trypanosomiasis
Clinical Features
1. Progressive stage (from 12 weeks)
Pain, photophobia, lacrimation, blepharospasm
Circumcorneal congestion, cloudy cornea
Superficial peripheral vascularization
Anterior uveitis, choroiditis
Limbitisraised inflamed sector of limbus from which deep blood
vessels invade
2. Florid stage (from 24 months)
Increased inflammation, DM folds
Deep vascularization
Ground glass corneadiffuse stromal cellular infiltration
Salmon patchcorneal clouding obscures the outline of the vessels
looks dull, pinkish red
3. Regressive stage (from 12 years)
Clearing starts
Blood vessels become non-perfused GHOST VESSELSmay refill later
following inflammationbleeding occurs
Stromal thinning, scarring, flattening
4. Inactive stage
Central deep stromal scar; ghost vessels seen
Complications
Corneal decompensation, corneal guttata
Band keratopathy, lipid keratopathy
Salzmann nodular degeneration, astigmatism
Glaucoma
Treatment
Topical steroidsto reduce corneal inflammation and iritis
Penicillin G given in
Primary and secondary syphilis 1.2 million units IM
Tertiary syphilis 2.4 million units IM weekly 3wks
Penetrating keratoplastyfor corneal scarring
HERPES SIMPLEX KERATITIS

Epithelial Keratitis
Present with watering, discomfort, decreased vision, pain
Vesicles are seen in the initial stages which coalesce to form linear, branching,
dendritic ulcer with terminal bulbs (ulcer bed stains with fluorescein; margin
stains with Rose Bengal)
Centrifugal enlargement geographical/ameboid ulcer
Decreased corneal sensation
Treatment
1. Debridement of dendritic (not geographic) ulcer
2. Acyclovir ointment 3% (5 times a day); if ulceration persists after 2 weeks,
rule out:
a. HSV dendritic epitheliopathy
b. Neurotrophic ulcer
Low-dose oral acyclovir (400 mg BD for 1 yr) reduces the rate of recurrent herpetic
eye disease; this is indicated in patients prone to frequent recurrences
Disciform Keratitis
Possible Etiologies
Exaggerated hypersensitivity reaction to viral antigens
Clinical Features
Gradual onset of blurred vision and haloes; no pain
Central, disc-like zone of epithelial edema overlying an area of stromal
thickening, with KPs and DM folds
Ring of stromal precipitatesWESSELY RING marks the junction between
viral antigen and host antibody
Mild anterior uveitis; raised IOP
Treatment
Topical prednisolone acetate 1% + antiviral cover
Gradually taper steroids over several weeks
Stromal Necrotic Keratitis

Active viral invasion and tissue necrosis
Cheesy/necrotic stroma
Profound interstitial necrosis
Anterior uveitis, KPs
Scarring, vascularization, lipid keratopathy, perforation
Treatment
Severe stromal keratitis associated with anterior uveitis is treated with
steroids (cautiously) + topical antivirals + topical antibiotics
Advanced stages require tissue adhesive with bandage contact lenses to
prevent perforation and in cases of descemetocele
Cornea 151
Eye Disease Caused by Herpes Simplex Virus and Varicella Zoster Virus
Herpes simplex virus Varicella zoster virus

Dermatomal distribution Incomplete Complete
Pain Less More
Dendrites Large with central Small, medusa-like dendrites
ulceration and terminal without central ulceration or
bulbs terminal bulbs
Dendritic mucus plaques Do not occur Occur late
Skin scarring Rare Frequent
Post-herpetic neuralgia Rare Common
Iris atrophy Patchy Sectoral
Bilateral involvement Rare Never
Recurrent lytic epithelial keratitis Common Never
Corneal hypoesthesia Sectoral/diffuse Frequent
KERATOCONUS
Non-inflammatory ectasia of cornea resulting in visual impairment, owing
to a high degree of irregular myopic astigmatism
Adolescence; bilateral/unilateral
Theories
1. Developmental delay in separation of lens fibers from cornea
2. Degeneration of elastic fibers
3. Secondary to disease process or malnutrition
4. Endocrinologicalbecause of association with hypothyroidism and
pregnancy
Symptoms
Decreased visual acuity; ghost images; glare
Can present with irritation and frequent rubbing of the eye
Signs
Central/eccentric cone
Fleischer ringa line running along the base of the cone due to iron
deposition superficial to the Bowmans membrane (complete/incomplete;
pigmented/yellow/brown)
Prominent corneal nerves
Stromal thinning increases gradually from base of the cone to the apex
Vogts striaethin vertical stress lines in the deeper stroma which disappear
on digital pressure
Endothelial reflex because of increased concavity
Acute hydropsin the center of the cone due to rupture of the Descemets
membrane and influx of fluid into the stroma
Scarring following rupture
Munson signon looking down, the angular curve is assumed by the lower
lid margin
Axenfeld signloss of sensitivity at the apex of the cone
Benedict signconical reflection on the nasal cornea when torch light
thrown from temporal side
Investigations
Keratometrynon-alignment of the mires
Breaking/doubling of the right lower circle
Placidos discirregularities in reflection of illuminated rings near the
corneal center; distortion of the horizontal axis
Direct ophthalmoscopyoil drop sign
Retinoscopyscissors reflex; 2 shadows move in opposite direction
Orbscan detects early keratoconus; bow-tie pattern; called Forme Frustae
keratoconus
Cornea 153
Ocular Associations
Vernal keratoconjunctivitis, atopic keratoconjunctivitis (due to constant
rubbing of eye)
Retinitis pigmentosa; Lebers congenital amaurosis
Retrolental fibroplasia
Macular coloboma
Ectopia lentis, blue sclera
Cataract, retinal detachment, optic atrophy
Xeroderma pigmentosa
Addisons disease
SyndromesDowns, Ehlers-Danlos, Marians, Crouzons, Aperts
Keratoconus Keratoglobus Pellucid marginal degeneration

Most common Rare Less common
Bilateral (usually) Bilateral Bilateral
Onset at puberty Onset at birth 2040 years
Inferior paracentral thinning Thinning maximum at 12 mm band of thinning inferiorly
periphery
Protrusion at apex Generalized protrusion Protrusion superior to band of
thinning
Fleischer ring present Absent Sometimes present
Scarring common Mild scarring Only after hydrops
Striae are common Rare Rare
Treatment
1. Spectacles
2. Contact lensesRGP (rigid gas permeable)
Gas-permeable with large diameterfor oval/globus cones
Asphericalfor nipple cones
Small, steep lensesfor severe nipple cones
Semi-rigid/hardfor steep oval cones
Piggy bag lenses
Scleral contact lenses (Boston lenses)
3. Surgery:
Anterior lamellar keratoplasty
Epikeratoplasty
Deep lamellar keratoplasty
Penetrating keratoplasty (use same-sized donor button)
Thermokeratoplastyheat is applied to the tip of the cornea for 1 min
which causes shrinkage of collagen and flattening of the cornea
Intacts/Kera-rings (intra-stromal rings) to reduce irregular astigmatism
so that the patient is comfortable with contact lenses or glasses
4. Corneal collagen cross-linking (C3R)with riboflavin one time application

of riboflavin solution to the eye and is activated by the illumination of ultra
violet A rays; delays/halts the progression of keratoconus
Treatment of acute hydrops:
Hypertonic saline drops
C3F8 (14%) injection into the anterior chamber
Posterior Keratoconus
Increased curvature of the posterior corneal surface with normal curvature
of the anterior corneal surface
May be focal/generalized; central/eccentric
Unilateral; present from birth
Associated with posterior corneal opacity, anterior lenticonus, aniridia, iris
atrophy, ectropion uveae
Amblyopia and strabismus may be present
Associated features: Hypertelorism, webbed neck, short stature, mental
retardation, abnormal development of bridge of the nose
Cornea 155
CORNEAL DYSTROPHIES
A dystrophy is a bilateral, symmetric, inherited condition that appears to have
little or no relationship to environmental or systemic factors
Degeneration Dystrophy
Opacity often peripheral Central opacity
May be asymmetric Bilateral and symmetric
Presents later in life Presents early in life
Associated with aging Hereditary
Progression can be very slow or rapid Progression usually slow
Classification
1. EpithelialMap-dot-fingerprint (AD), Meesmann (AD)
2. Bowman membraneReis-Buckler (AD), Thiel Behnke (AD), Crystalline (AD)
3. StromalLattice (mostly AD), Granular (AD), Avellino (AD), Macular (AR),
Gelatinous (AR)
4. EndothelialCHED (AD), posterior polymorphous dystrophy (AD), Fuchs
endothelial dystrophy(AD)
AD autosomal dominant; AR autosomal recessive
Map-dot-fingerprint/Cogan microcystic/epithelial basement membrane
dystrophy
Dot-like opacities; epithelial microcysts
Map-like patterns; whorled fingerprint-like lines
Not familial/progressive
Cause recurrent bilateral corneal erosions
Meesmann dystrophytiny intraepithelial cysts in the interpalpebral area;
do not reach limbus
Reis-Buckler dystrophygray-white, round and polygonal opacities in the
center of the cornea; decreased corneal sensation; visual disturbance due
to scarring
Thiel Behnke dystrophysimilar to Reis-Buckler type; opacities for a honey-
comb pattern
Crystalline dystrophyscintillating subepithelial crystalline opacities in
the center of a generally hazy cornea
Lattice type 1fine, spidery, branching lattice lines spreading outward,
sparing the periphery
Lattice type 2short, fine, sparse lattice lines; associated with progressive
bilateral cranial and peripheral neuropathies
Lattice type 3thick ropy lines from limbus to limbus with minimal
intervening haze
Granularsmall, white, crumb-like deposits in the central anterior stroma;
not reaching limbus
Avellinofine ring/disc-like opacities (dense centrally) with deep linear
opacities
Maculargray-white, dense, focal, poorly-delineated spots with diffuse

stromal clouding; eventually full thickness stroma is involved with stromal
thinning
Gelatinousin familial sub-epithelial amyloidosis; grey sub-epithelial
nodules giving a mulberry-like appearance; presents with photophobia,
watering, decreased vision
Fuchs Endothelial Dystrophy
Middle-aged women
Increased incidence of POAG
Central corneal guttata which spread to the periphery
Blurred vision especially in the morning which clears during the day
Stage Icornea has a beaten metal appearance
Stage IIendothelial decompensation leads to stromal edema
Stage IIIepithelial edema leading to bullous Keratopathy
Stage IVgrowth of avascular sub-epithelial connective tissue
causing reduced vision from scarring
Treatment
Topical NaCl; bandage contact lens for symptomatic relief
Penetrating keratoplasty (PK)
Deep lamellar endothelial keratoplasty (DLEK)
Descemet stripping endothelial keratoplasty (DSEK)
Descemet membrane endothelial keratoplasty (DMEK)
Soft shell technique for cataract surgerysodium hyaluronate 1% (healon)
used for cataract procedure under the shell of chondroitin sulfate 4%; sodium
hyaluronate 3% (viscoat) which is used to coat the endothelium.
Posterior Polymorphous Dystrophy
Endothelium displays features of epithelium
Vesicular/band-like/geographical endothelial patterns
Associated with peripheral anterior synechiae, glaucoma, ectropion uveae
Congenital Hereditary Endothelial Dystrophy
Focal/generalized absence of endothelium
Diffuse bilateral corneal edema
Blue grey/ground glass appearance/total opacification
Differential diagnosis: Birth trauma, buphthalmos, sclerocornea
Treatment: Observation till asymptomatic or manageable vision; PKP when
vision deteriorates
Cornea 157
THERAPEUTIC CONTACT LENS

Uses
1. Optical
Irregular astigmatism, e.g. Keratoconus
Superficial corneal irregularities
Anisometropia for binocular single vision
2. Promote epithelial healing
Persistent epithelial defects
Recurrent corneal erosions
3. Pain relief
Bullous keratopathy
Wet filamentary keratitis
Trichiasis
Thygesons SPK
4. Preservation of corneal integrity
Descemetocele
Corneal wound apposition
5. Miscellaneous
Ptosis props to support the upper lid in patients with ocular myopathies
Prevent symblepharon in eyes with cicatrizing conjunctivitis
Drug delivery (hydrogel lenses soaked in topical medication)
Complications of Contact Lens Use
1. Conjunctival
Allergic conjunctivitisperilimbal injection, fine papillary conjunctival
reaction
Giant papillary conjunctivitisincreased mucus, Trantas dots, limbitis
2. Corneal
Epithelial edemadue to corneal hypoxia (excessive usage, e.g.
overnight wear)
Corneal vascularization at the superior limbus
Sterile corneal infiltratesepithelial, sub-epithelial, stromal
Corneal warpingsevere astigmatism
Microbial keratitisPseudomonas aeruginosa, Acanthamoeba
CORNEAL DEGENERATIONS
Degeneration of a tissue is a physiological decomposition of tissue elements and
deterioration of tissue functions; it is distinguished from dystrophies in being
non-hereditary and usually unilateral
Age Related
Arcus Senilis
Occurs in elderly individuals
A ring of lipid deposition in the peripheral cornea (1 mm band)
Separated from the limbus by a clear zone
Also seen in Type II hyperlipoproteinemia (presents early)
Usually bilateral; unilateral in ocular hypotony and carotid artery disease
Vogt White Limbal Girdle
Narrow bilateral crescentic lines
Chalk-like flecks in the interpalpebral fissure along the nasal and temporal
limbus
Cornea Farinata
Bilateral minute flour-like deposits in the deep stroma
Crocodile Shagreen
Grayish white, polygonal stromal opacities separated by relatively clear
spaces
In the anterior 1/3rd or posterior 2/3rds
Corneal Guttata
Focal accumulation of collagen on the posterior surface of the Descemets
membrane
Warts or excrescences in the center of the cornea
Called Hassal-Henle bodies if in the periphery
Lipid Keratopathy
Primaryoccurs spontaneously in an avascular cornea
Secondaryoccurs following previous ocular disease/injury which results
in vascularization
Yellowish stromal deposits of cholesterol, fats, phospholipids occurs
If associated with corneal vascularization, it is progressive
Treatment
Control underlying disease (inflammation or vascularization)
Argon laser photocoagulation to arterial feeder vessels
Needle point cautery to feeder vessels
PKP if severe
Cornea 159
Band Keratopathy
Deposition of calcium salts in the sub-epithelial space and anterior portion
of the Bowman membrane
Causes
a. Ocular
Chronic anterior uveitis
Interstitial keratitis, severe superficial keratitis
Phthisis bulbi
Silicon oil instillation in an aphakic eye
b. Age-related band keratopathy
c. Metabolic
Hypercalcemia caused by hyperparathyroidism, vitamin D toxicity,
milk-alkali syndrome, sarcoidosis
Hyperphosphatemia with normal serum calcium (in some renal failure
patients)
d. Hereditary transmission primary hereditary band keratopathy
Clinical Features
Peripheral interpalpebral calcification separated from the limbus by a clear
zone
Gradual central spread band-like chalky plaque
Nodular elevated lesions in advanced stages
Discomfort due to epithelial breakdown
Treatment
Chelation with a neutral solution of EDTA (sodium edetate) 150 mg/mL
after large chips of calcium are removed with forceps and the epithelium
is scraped off (mix a 20 mL vial with 100 mL of sterile ophthalmic irrigation
solution and warm it)
Excimer laser keratectomy
Deep anterior lamellar keratoplasty (DALK) in cases of deeper involvement
Spheroidal Degeneration
Also called corneal elastosis; Labrador keratopathy; climatic droplet
keratopathy (due to increased exposure to UV light)
Amber-colored spheroidal granules in the superficial stroma, in the
interpalpebral strip
Treatment
Corneal epithelial debridement
Superficial keratectomy
Deep anterior lamellar keratoplasty (DALK) in cases of deeper involvement
Salzmann Nodular Degeneration

Secondary to chronic keratitis as in trachoma, phlyctenulosis
Discrete, elevated, gray superficial lesions
Stromal opacities form nodules which elevate the epithelium
Located over scarred cornea or at the edge of a scar in a clear cornea
Treatment
Superficial keratectomy or debridement with amniotic membrane graft
Cornea 161
CORNEAL VASCULARIZATION
Etiopathogenesis
Traumatic/inflammatory/toxic/nutritional insult causes blood vessels to
gain access into a swollen and edematous tissue
The normally present vasoinhibitory factors are abolished in pathological
state
Classification
1. Superficial vascularization:
Originates from the superficial limbal plexus
From branches of anterior ciliary arteries
Confined to a segment or extend around the limbus
Preceded by edema, exudation or epithelial disturbance
When extensivecalled pannus
2. Interstitial vascularization:
Straight non-anastomozing blood vessels from anterior ciliary arteries
Seem to disappear from view
Invade the cornea at the level of the pathological process
3. Deep vascularization:
Retrocorneal pannus
Proliferation of deep blood vessels by budding from anterior ciliary
arteries
Treatment
Radiation given at the onset of superficial vascularization; obliterative
end arteries develop due to trauma to the endothelium
Peritomy is done 34 mm from limbus
Argon laser photocoagulation
Sodium chromoglycate 4% drops
Superficial keratectomy or PKP
Intracameral injection of bevacizumab (2.5 mg/0.1 mL)partial regression
of corneal neovascularization
PANNUS
Inflammatory or degenerative in growth of fibrovascular tissue from the
limbus
Growth of tissue between epithelium and Bowmans layer
An inflammatory pannus disrupts the Bowmans layer; a degenerative
pannus leaves it intact
Stages
1. Infiltrationsuperficial corneal layers are infiltrated by polymorphonuclear
leucocytes (PMNs) and lymphocytes
2. Progressivenew vessels emerge from the limbal plexus to form a grey
vascular mass beneath the epithelium
3. Stationaryresolution of exudates followed by shrinkage of blood vessels
4. Scleroticcicatricial tissue or obliterated remnants of blood vessels
Types
Progressivea leash of vessels in front of which there is a zone of infiltration
and haziness
Regressivevessels extend beyond the area of infiltrated cornea
Superior limbic keratoconjunctivitis; phlyctenulosis
Vernal keratoconjunctivitis; atopic conjunctivitis
Herpes simplex keratitis; trachoma
Contact lens wear; toxic/chemical keratitis
Cornea 163
MOORENS ULCER
Chronic painful peripheral corneal ulceration (serpigenous ulcer) progressing
circumferentially and centrally
Infection or collagen vascular disease is absent
Possible Etiology
Auto-immune reaction, helminthiasis
Chronic hepatitis C
Corneal injury; surgery; burns
HSV/HZV
Clinical Features
Pain, photophobia, lacrimation
Decreased vision, blepharospasm
Starts as a peripheral infiltration in the interpalpebral fissure area near the
limbus
Marginal furrow ulcer with overhanging edge and sloping peripheral border
The infiltration breaks into a circumferential ulcer
Type 1 Type 2
Prevalence Common form Atypical form
Pathogenic factors Trauma Trauma, helminthiasis
Age > 40 years 2030 years
Sex Female > male Male > female
Pain Moderatesevere Variable
Course Slowly progressive Rapid
Response to treatment Moderate Poor
Perforation Rare In 1/3rd of cases
Laterality 75% unilateral 75% bilateral
Investigations
To rule-out systemic association:
Total count/differential count; platelet count; ESR; Hemoglobin%
Rheumatoid factor; ANA; pANCA; cANCA
Treatment
Topical steroids; oral steroids
Topical cycloplegics
Bandage contact lens
Peritomyresection of 4 mm perilimbal conjunctiva adjacent to the ulcer
Lamellar corneal transplant and conjunctival flaps
Systemic immunosuppressives
Glue if corneal perforation
PKPif extreme peripheral corneal thinning
Moorens ulcer Terriens degeneration

Old or young affected Older people affected
Pain, watering, photophobia Usually asymptomatic
Females > males Males > females
Irregular astigmatism Against the rule astigmatism
Interpalpebral region involved Superior cornea involved
Stains with fluorescein Does not stain
Undermining edges Flat edges
Autoimmune reaction Unknown etiology
Cornea 165
BULLOUS KERATOPATHY
Symptoms
Poor vision, haloes around light bulbs, pain, photophobia, foreign body sensation
Causes
Endothelial damage during cataract surgery
Pseudophakic bullous keratopathy due to AC IOL touching endothelium or
raised IOP following surgery
Aphakic bullous keratopathy due to vitreous in anterior chamber, which
touches the endothelium
Congenital hereditary endothelial dystrophy (CHED)
Fuchs endothelial dystrophy
Posterior polymorphous dystrophy
Chandler syndrome (ICE syndrome)
Acute angle closure glaucoma
Herpetic disciform keratitis
Corneal transplant rejection
Prevention of Corneal Edema Following

Cataract Surgery
Choose the type of cataract surgery depending on the type of cataract
(phacoemulsification for a hard cataract will cause more endothelial
damage)
Use viscoelastics liberally during surgeryto protect endothelium from
instrument touch
Wash out all viscoelastic at the end of surgery to prevent postoperative rise
of IOP
Try to avoid the use of AC lOLs if there already is endothelial compromise
Look for cornea guttata and Fuchs endothelial dystrophy in preoperative
evaluation in which case use BSS (balanced salt solution) or sodium
hyaluronate
Treatment
Hypertonic saline 5% eyedrops or 6% eye ointment (draws out water from
the cornea by osmosis)
A thin, high water content bandage contact lensfor pain relief
Control IOP if it is high
Remove AC lOLs and iris-clipped if they are the cause for bullous keratopathy
Anterior stromal puncture with a 25 g needle, multiple small superficial
punctures are made in the cornea, at/below Bowmans layer; place bandage
contact lens for 12 weeks to allow the epithelium to adhere to cornea
Excimer laser phototherapeutic keratectomy
Penetrating keratoplasty, deep lamellar endothelial keratoplasty (DLEK),
Descemet stripping endothelial keratoplasty (DSEK), Descemet membrane
endothelial keratoplasty (DMEK)
CORNEAL TRANSPLANT
Types
Opticalfor visual rehabilitation
Tectonicfor re-enforcing altered corneal structure (descemetocele)
Therapeutictissue substitution for refractory corneal disease (corneal
ulcer)
Indications
Keratoconus with apical scarring; rapid progression
Aphakic/pseudophakic bullous keratopathy
Corneal scarring
Fuchs endothelial dystrophy
Failed graft primary graft failure; graft rejection/infection
Herpes simplex keratitis causing stromal necrosis
Ocular traumanormal posterior segment
Congenital corneal opacities Peters anomaly, sclerocornea
Stevens-Johnson syndrome
Corneal dystrophies
Chemical burns
Contraindications (Donor Cornea)

Absolute
Death of unknown cause
AIDS, rabies
Hepatitis, septicemia
CMV encephalitis
Congenital rubella
Reyes syndrome
Leukemia
Hodgkins disease
Intrinsic eye disease
Creutzfeldt-Jakob disease
Relative
Multiple sclerosis
Parkinsonism
Syphilis
Chronic lymphocytic leukemia
Chronic immunosuppression
Donor Tissue Evaluation
Epitheliumedema, abrasions, foreign body
Stromaedema, folds in Descemets membrane
Breaks in Descemets membrane
Endotheliumspecular microscopy
Cornea 167
Donor Cornea Preservation

a. Short-term storage: Moist chamber technique
Whole globe preservation at 4C with saline humidification for up to 48 hrs
Disadvantages: Endothelium undergoes autolysis; difficult to screen for
HIV and HBsAg; HLA typing cannot be done in aqueous environment
b. lntermediate-term storage media (2 wks):
TC199, HEPES, Dextran, Chondroitin sulphate, non-essential amino
acids, minimum essential medium
c. Long-term storage:
1. Organ culture method: Eagles MEM + Earles salts + L-Glutamine +
Decomplemented calf serum is used
Stored at 34C for 35 days, endothelial side up
If no growth after 10 days in any microbiological mediumcornea
is fit for transplant
2. Cryopreservation
Can preserve indefinitely
Corneo-scler
al button passed through a series of solutions contain-
ing increasing concentration of DSMO (dimethyl sulphoxide) up to
7.5%
Placed in each solution for 10 min
Frozen up to -80C; stored at -160C
Disadvantages areintracellular microcrystal formation; number
of endothelial cells decreases
Used for lamellar transplant
Complications (Early)
Primary Graft Failure
Irreversible graft edema in immediate postoperative period
No period of graft clarity
Due to endothelial damage
Causes:
Donor tissue with endothelial cell count < 1500/mm3
Improper preservation
Trauma during surgery, stretching of cornea; shallowing of anterior chamber;
instrument touch
Glaucoma
Acute rise in IOP, with/without optic nerve damage or field loss
Causes:
Retention of viscoelastic
Angle closure
Distortion of trabecular meshwork
Inflammation
Steroid induced
Epithelial Defects
Increased chance of rejection, infection, ulceration, perforation
Causes:
Storage
Injury during surgery
Postoperative lid movement
Trichiasis
Intermediate Complications
Graft Rejection
Epithelial rejection:
Elevated rejection line which stains with fluorescein/Rose Bengal
Represents zone of destruction of donor epithelial cells
Occurs usually 3 months following surgery
Subepithelial infiltrates: Kayes dots
Randomly distributed in Bowmans membrane
Usually occurs 10 months following surgery
Stromal rejection:
Sudden onset of peripheral full thickness haze with circumcorneal
congestion
Associated with endothelial rejection
Endothelial rejection:
Khoudadoust line
Diffuse KPs
Linear arrangement of endothelial precipitates
Edematous cornea
Risk factors for rejection:
Vascularization
Previous graft failure
Large, eccentric, bilateral grafts
Younger patients
Treatment of graft rejection:
Topical hourly steroids
Systemic steroids
In severe rejection, pulsed IV methyl prednisolone followed by oral
prednisolone
Graft Infection
Bacterial, viral, fungal, acanthamoebic infection
Due to steroid usage
Infectious crystalline keratopathycaused by Streptococcus viridans
Wound Dehiscence
Following high IOP, early suture removal or trauma
Late Complications
Recurrence of diseaseespecially herpetic keratitis and corneal dystrophies
Late graft failure decompensation due to decreased endothelial cells
Astigmatism if donor button is slightly larger
Cornea 169
LAMELLAR KERATOPLASTY
Partial thickness graft of cornea
Anterior lamellar and deep lamellar keratoplasty
Indications
Corneal opacity involving superficial 1/3rd of stroma, not caused by recurrent
disease
Marginal corneal thinning, e.g. pterygium, Terrien marginal degeneration,
limbal dermoids
Localized thinning or descemetocele
Keratoconus
Deep Lamellar Keratoplasty

All opaque corneal tissue is removed to the Descemets membrane level
Endothelium is not transplantedso less chances of rejection
Indications
Disease involving anterior 95% of corneal thickness with endothelium being
normal and no breaks/scars in Descemets membrane
Chronic inflammatory disease like atopic kerato-conjunctivitis
Advantages
Structurally stronger globe
No risk of endothelial rejection
Increased availability of graft material
Complications
Corneal perforation during dissection
Refractive Surgery
Cornea Lens
Myopia PRK Clear lens extraction
LASIK Phakic IOL (iris clipped lens,
implantable contact lens)
Radial keratotomy
Intrastromal PMMA rings
Hyperopia PRK Clear lens extraction
LASIK Phakic IOL
Laser thermokeratoplasty
Astigmatism LASIK Toric IOL implantation
Arcuate keratotomy
Presbyopia Conductive keratoplasty Multifocal IOL
chapter
Conjunctiva 6
PSEUDOMEMBRANOUS AND MEMBRANOUS

CONJUNCTIVITIS
Caused by
Adenovirus, Corynebacterium diphtheriae, beta hemolytic streptococci
Streptococcus pneumoniae, N. gonorrheae, S. aureus, E. coli
Ligneous conjunctivitischronic; unknown cause
Clinical Features
Mild
Lid swelling, mucopurulent discharge
Palpebral conjunctiva covered with a white membrane which peels off easily
without bleeding called pseudomembrane
Severe
Lids are brawny
Conjunctiva permeated with semisolid exudates which prevent formation
of free discharge; necrosis of conjunctiva and cornea
Membrane peels less readily with bleeding from underlying surface
Patchy or total membrane over palpebral conjunctiva
Preauricular lymphadenopathy
Cornea may ulcerate
After 610 days, slough separates; profuse discharge occurs; conjunctiva -
red and succulent
Symblepharon forms
Treatment
Preventive
Immunization
Isolation of patients
Curative
Complete bed rest (in case of myocarditis and heart failure)
Antidiphtheritic serum 4000060,000 units TM
Systemic penicillin injection
Conjunctiva 171
Local antibiotic eyedrops

Local antidiphtheritic serum
Local antibiotic ointment to prevent symblepharon
Every case is treated as diphtheria unless proved otherwise; if culture is
negative, treat as purulent bacterial conjunctivitis
Removal of membranesprecipitates symblepharon formation
PTERYGIUM
Elastotic degenerative condition of subconjunctival tissues which proliferate
as vascularized granulation tissue to invade the cornea
Destroy the superficial layers of the cornea (stroma and basement
membrane)
Covered by conjunctival epithelium
Appears as triangular encroachment of conjunctiva upon the cornea
Has a head, neck and body
Usually on nasal side of cornea
Early stage: Thick and vascular
Late stage: Thin and pale (does not grow)
Formation of dense fibrous tissueresults in corneal astigmatism (with the
rule)
Decreased vision if it progresses into the pupillary area
Dry sunny climates, UV lightare aggravating factors
Stockers linepigmented line of iron deposits in basement membrane in
front of the head of the pterygium
Treatment
Observe initially
Surgical indications: Progression into visual axis, increased astigmatism,
cosmesis
Lubricating drops for dry eye
Protect from UV rays
Topical steroids for inflamed pterygium
Surgery:
Avulsion with amputation
Simple excision (bare sclera techniquehas a high recurrence rate)
Excision with primary closure
Excision with primary conjunctival graft
Excision with lamellar keratoplasty
Excision with buccal mucous membrane graft
Excision with amniotic membrane graft
Conjunctiva 173
TRACHOMA
Caused by Chlamydia trachomatis types A, B, Ba, C
Clinical Features
Diffuse conjunctival inflammation with congestion, papillary hypertrophy,
follicles
Upper tarsal conjunctiva red and velvety with jelly-like thickening
Trachomatous follicle (0.5 mm diameter)
Typically 5 or more in number
Start in lower fornix
More in upper fornix
Form a row along upper margin of tarsus
Cicatrization of follicles appear as minute stellate scars
Superficial keratitis in upper cornea
Trachomatous pannuslymphoid infiltration with corneal vascularization
Herberts pits (follicles near the limbus leave depressed pits on resolution)
Chronic corneal ulcersat advancing edge of pannus
Arlt linewhite conjunctival scar at junction of lower 1/3rd and upper 2/3rds
of superior tarsus. Trachomatous ptosisdue to dense infiltration of upper
tarsus
Ectropion, trichiasisdue to cicatrization
Tylosisthickening of tarsal plate
Stages of Trachoma (McCallan Classification)
Stage Sign
1 Early stage of follicles
IIa Large, gelatinous follicles
IIb Papillary enlargement and follicles
IIc Trachoma complicated by gonococcal conjunctivitis
III Cicatrization has commenced
IV Cicatrization is complete
WHO Classification (FISTO)

Folliclesindicate active disease
Intense inflammationneeds urgent treatment
Scarring of conjunctivaindicates old inactive infection
Trichiasisneeds electrolysis/surgery
Opacities of corneacause decreased vision
Inflammatory stagesFollicular inflammation ( TF), trachomatous
inflammation (TI), Scarring stages trachomatous scarring (TS), trachomatous
trichiasis (TT), corneal opacity (CO)
Prevention and Treatment

Oral tetracycline, erythromycin, rifampicin or sulfonamides (for 36 months)
Topical erythromycin or tetracycline ointment (5 days a month for 1 year)
Single dose of 1 g oral azithromycin
Strict personal hygiene
SAFE protocol adopted by WHO to eradicate trachoma by 2020:
S Surgery for trichiasis
A Antibiotic treatment of clinically active chlamydial infection
F Facial cleanliness and improvement of
E Environmental conditions; safe water, adequate disposal of feces
Conjunctiva 175
FOLLICULAR CONJUNCTIVITIS
Acute Forms
Chlamydial Inclusion Conjunctivitis Swimming Pool Conjunctivitis
Treatment:
Oral tetracycline 250 mg QID/doxycycline 100 mg BD/erythromycin 250 mg
QID X 14 days
Single oral dose 1 g azithromycin
Ofloxacin 300 mg BD for 7 days
Epidemic Keratoconjunctivitis
Caused by adenovirus types 8 and 19
Scanty exudates; marked inflammatory symptoms; membranes
Punctuate epithelial infiltrates and subepithelial opacities in cornea after
710 days
Treatment:
For symptomatic relief
Topical steroids if very severe
Pharyngoconjunctival Fever
Caused by adenovirus types 3, 4, 7
Pharyngitis, fever, preauricular lymphadenopathy
Fine, superficial punctuate keratitis
New Castle Conjunctivitis
From dead fowls
Similar to pharyngoconjunctival fever
Hemorrhagic Conjunctivitis
Coxsackie virus; Enterovirus 70
Also called Apollo conjunctivitis
Violent inflammatory conjunctivitis with subconjunctival hemorrhage
Cornea is unaffected
Acute Herpetic Conjunctivitis
Associated with facial lesions in children
Large follicles
Corneal vesicles coalesce to form dendritic keratitis
Herpes Simplex Conjunctivitis

Occurs in adults
Follicular conjunctivitis with or without microdendrites, similar to EKC
Chronic Forms
Caused by
Drugs, e.g. Pilocarpine
Molluscum contagiosum in lids
Trachoma
Conjunctiva 177
ALLERGIC TYPES OF CONJUNCTIVITIS

Acute/Subacute Allergic Catarrhal Conjunctivitis
Severe itching; watering (tears contain eosinophils)
No purulent discharge; less hyperemia
Recurs on contact with allergen
For example Hay fever, chemicals (cosmetics/dyes), drugs (atropine,
brimonidine)
Treatment
Remove allergen; desensitization
Antihistamines; topical steroids
Mast cell stabilizers (sodium chromoglycate, olopatadine)
Vernal Keratoconjunctivitis (Spring Catarrh)

Young males; hot weather
Type I hypersensitivity reaction mediated by IgE
Itching, photophobia, watering, ropy discharge
Foreign body sensation
Palpebral Form
Palpebral conjunctiva is hypertrophied
Polygonal raised areas; flat-topped hard nodules cobblestone appearance;
contain eosinophils
Epithelium over them thickened giving a milky hue
Limbal Form
Horner Trantas dotswhite dots consisting of eosinophils and epithelial
debris
Wall of gelatinous thickening at the limbus
Opacification of limbus with nodule formation
Cornea
Fine, diffuse SPKs
Severe dry eyesfilamentary keratopathy
Shield ulcer in upper cornea due to rubbing of the hypertrophied papillae
heal with scarring; treated with topical steroids
Treatment
Topical steroids, mast cell stabilizers
Sub-tarsal triamcinolone injection
Topical olopatadine BD/iodoxamide QID
Acetyl cysteine eye drops 10% or 20%to control excess mucus secretion
In severe cases, debridement of ulcer and amniotic membrane graft
Giant Papillary Conjunctivitis

Type I and IV hypersensitivity reaction
Large polygonal papillae on superior tarsal conjunctiva; conjunctival
congestion
Macropapillae: 0.31.0 mm
Giant papillae: 12 mm
Causes
Soft hydrophilic contact lens
Protruding suture ends
Ocular prosthesis
Treatment
Discontinue contact lenses
Remove protruding sutures/prosthesis
Topical steroids
Phlyctenular Conjunctivitis
Small round, yellow-gray nodules on bulbar conjunctiva, at or near limbus
Congestion of vessels limited to area around phlyctens
Epithelium over the surface becomes necrotic and small ulcers form
Complicated by mucopurulent conjunctivitis
Probably caused by endogenous tuberculous proteins or non-specific
delayed hypersensitivity reaction to staphylococcal antigens
Corneal phlyctenmay scar
Treatment
Steroids, antibiotics, cycloplegics
Conjunctival phlycten heals rapidlyno scar
Conjunctiva 179
SUPERIOR LIMBIC KERATOCONJUNCTIVITIS

Clinical Features
Discomfort, foreign body sensation, photophobia, tearing
Pseudoptosis, blepharospasm
Sectoral inflammation and injection of superior bulbar conjunctiva and
limbal cornea
On upper lid eversionuniform papillary hypertrophy are seen
Corneapunctate epithelial erosions
Filaments in precorneal tear film in the upper quadrant
Bilateral; probably autoimmune etiology (e.g. associated thyroid dysfunction)
Treatment
Topical 0.51.0% silver nitrate solution (a chemical cautery) used to promote
re-growth of healthy new epithelium; acts by retracting the conjunctiva and
inducing its adherence to the underlying sclera
Bandage contact lens; pressure patching
Tear substitutes
4% cromolyn sodium
Lacrimal punctal occlusion (especially upper puncta)
Acetyl cysteine 5%
Surgical resection of superior bulbar conjunctiva peritomy from 102
oclock and resection of a 5 mm large arcuate segment of conjunctiva and
Tenons capsulebest results
AMNIOTIC MEMBRANE GRAFT

Amniotic membrane consists of a thick basement membrane, single layer
of epithelial cells and an avascular stromal matrix
Human amniotic membrane is non-immunogenic; does not express any
HLA antigen; hence use to treat various ocular surface disorders
Indications
1. In acute chemical and thermal burns (within 2 weeks after injury)
Promotes re-epithelialization
Decreases inflammation
Prevents scarring
2. Primary pterygium
Prevents recurrence
As good as conjunctival autograft with mitomycin C
3. Severe neurotrophic corneal ulcers
Herpes zoster ophthalmicus, Herpes simplex keratitis
Radiation, acoustic neuroma
4. Severely damaged corneas in
Pemphigoid
5. Non-healing infected corneal ulcers after treatment with sufficient
antibacterials/antifungals/antivirals (amniotic membrane soaked in anti-
infective agents before transplantation)
6. Conjunctival surface reconstruction
Restores large conjunctival defect created during surgical removal of
conjunctivochalasis
7. Non-traumatic corneal perforations, descemetocele
8. After surgical removal of band keratopathy
9. Used as therapeutic contact lens to treat epithelial defects without stromal
ulceration
Conjunctiva 181
LIMBAL STEM CELL TRANSPLANT

Limbal stem cells are necessary to maintain a healthy ocular surface
Limbal stem cell deficiency causes conjunctivalization of cornea, corneal
vascularization, chronic inflammation, recurrent epithelial defects
Transplantation of epithelial cells from limbus of fellow eye Auto-
transplant
Transplantation from live related donor or amniotic membrane cultured
limbal stem cell transplant Allo transplant
Indications
1. Severely damaged corneas as in:
Ocular pemphigoid
Chemical/thermal burns
2. Conditions destroying limbal area of peripheral cornea when PKP is not
enough
Method
Specimens of limbal epithelial cells from healthy fellow eyes are used directly
or are cultured and expanded on amniotic membrane
Superficial keratectomy doneto remove fibrovascular ingrowth
Amniotic membrane with a sheet of limbal epithelial cells is transplanted
to denuded corneal surface of damaged eye
Patients are followed up meticulously and put on long-term immuno
suppressive treatment
In Partial Stem Cell Deficiency
Remove abnormal epithelium and allow denuded cornea to resurface with
cells derived from intact epithelium
In Total Stem Cell Deficiency
Autologous graft: Taken from normal fellow eye
Homologous graft: Taken from living/cadaveric donors
OPHTHALMIA NEONATORUM
Mucoid, mucopurulent or purulent discharge from one or both eyes in the
1st month of life
Caused by: Neisseria gonorrheae, Chlamydia trachomatis, Streptococcus
pneumoniae, Chlamydia oculogenitalis, herpes simplex virus, chemicals
Neisseria Gonorrheae Infection

In the 1st 48 hours of birth
Thick, yellow purulent discharge
Swollen, tense lids; marked chemosis
Conjunctiva is intensely inflamed, bright red and swollen with
pseudomembranes
Organism invades intact corneal epithelium
Perforated corneal ulcer just below the center of the cornea
Sudden perforation causes iris prolapse, lens extrusion
Complications are anterior synechiae, adherent leucoma, anterior
staphyloma, cataract, panophthalmitis
Treatment
Gentamycin 0.3% e/d after every feed 3 days
Ceftriaxone IM 125 mg stat (or)
Cefotaxime IV 50 mg/kg in 3 divided doses
Bacitracin eye ointment 24 hourly
Topical and systemic penicillin
With resistance emerging against penicillin, tetracycline and
fluoroquinolones, a single dose of intramuscular/intravenous
ceftriaxone 2550 mg/kg is the preferred treatment
Hospitalization and hourly saline irrigation of the conjunctival fornices
Chemical Induced
Develops after prophylaxis with silver nitrate solution
Disappears spontaneously after 2448 hours
Treatment:
Eye wash; erythromycin ointment
Chlamydia trachomatis Inclusion Conjunctivitis
After 1st week of birth
Venereal infection from cervix or urethra of mother
Conjunctival chemosis; no follicles unless infection has become chronic (>3
months)
Superficial keratitis is a rule
Differs from that of an adultno follicular response in neonate; greater
mucopurulent discharge and tendency to form membranes on the palpebral
conjunctiva
Conjunctiva 183
Treatment:
Oral erythromycin 50 mg/kg/day in 4 divided doses (or) Oral azithromycin 10
mg/kg for 2 weeks to treat the pneumonitis and otitis media accompanying
the conjunctivitis
Erythromycin/chlortetracycline 1% ointment QID
Mother and her sexual partners oral erythromycin/ tetracycline for a week
Herpes Simplex Virus Conjunctivitis
57 days after birth
Treatment:
Acyclovir 3% ointment 5 times/day for a week
DRY EYE
Ocular discomfort, foreign body sensation, burning sensation, blurred vision
Tear film breaks up into dry spots between blinksexposing the corneal
and conjunctival epithelium to evaporation
Causes of Dry Eye

Aqueous Tear Deficiency
Sjgrens syndrome:
1. Primary
2. SecondaryRheumatoid arthritis, SLE, PAN, systemic sclerosis
Non-Sjgrens syndrome dry eye:
1. Congenital Absence of lacrimal gland/lacrimal
nucleus
Adies syndrome
MEN syndrome
2. Acquired Trauma/surgical removal of
lacrimal gland
Radiation induced damage
3. Infection/inflammation Mumps, trachoma
4. Infiltration Sarcoidosis; amyloidosis
Leukemia, lymphoma
5. Drug-induced Antihistamines, decongestants
Antidepressants
Propranolol, clonidine
Thiabendazole
6. Neuroparalytic hyposecretion:
Brain stem lesions
CPA tumors
Lesions at the sphenopalatine
ganglion
Mucin Deficiency
Goblet cell dysfunction
Primaryvitamin A deficiency (nutritional)
Secondarydiarrhea, liver disease, pregnancy, trachoma, burns, SJS,
cicatricial pemphigoid
Drug-inducedproctalol, ecothiophate iodine
Lipid Abnormalities
Congenital absence of meibomian glands
Altered composition of meibomian gland secretion, e.g. Blepharitis
increases free fatty acids
Conjunctiva 185
Lid Abnormalities
Ectropion, coloboma lidexposure
Vlln palsydecreased blink rate, lagophthalmos
Keratinized lid margin
Epitheliopathies
Ulcers, erosions, scars
TESTS FOR DRY EYE

Rose Bengal Test
Rose Bengal has affinity for devitalized cells, mucus, corneal filaments and
plaques
Interpalpebral bulbar conjunctival and corneal staining is characteristic of
keratoconjunctivitis sicca
Tear Film Break-up Time (TFBUT)

To assess stability of precorneal tear film
Instill fluorescein into lower fornix without touching cornea
Blink for even spreading of the fluorescein-stained tear film
TBUT is the time interval between the last blink and appearance of the 1st
dry spot
Normal TBUT > 10 seconds (mean of 3 tests is taken)
Schirmers Test (Done for Aqueous Deficiency)

Measure the amount of wetting of a special filter paper
35 5 mm
Paper is folded 5 mm from one end and inserted into the lower fornix
between the middle and outer 1/3rd of lower lid - without touching the
cornea
Patient is asked to blink normally
Schirmer I Measures total tear secretion
No anesthetic used
Measure wetting after 5 minutes
>15 mm wettingnormal
10-15 mm wettingborderline
Schirmer II Measure BASIC tear secretion
Anesthetic used
Measure wetting after 5 minutes
< 6 mm wettingfailure of secretion
Lysozyme assay:
Place a wetted filter paper into an agar plate containing specific bacteria
Incubate for 24 hours
Measure the zone of lysis
In keratoconjunctivitis sicca, decreased lysozyme concentrations (< 1 mg/
mL)
Tear osmolality:
In keratoconjunctivitis sicca > 312 mOsm/kg
Conjunctival impression cytology:
Goblet cells >5 cells/HPF is normal
Conjunctiva 187
Treatment
1. Tear conservation
Decrease room temperature, increase humidity
Moist chamber goggles, tarsorrhaphy
2. Tear substitution
Eye dropspolyvinyl alcohol, hydroxypropyl methyl cellulose,
carboxymethyl cellulose, mucomimetics
Ointments, gels
Sodium hyaluronate
3. Mucolytics
Acetyl cysteine drops 5% QID
4. Reduce tear drainage
Temporary punctal occlusion with dissolvable collagen plugs
Permanent punctal occlusion with silicon plugs or thermal cautery
5. Systemic therapy
Steroids, bromohexidine
6. Immunomodulatorscyclosporine
7. Treat associated disease like blepharitis, spring catarrh
8. Hydrophilic contact lens
9. Transretinoic acid ointmentreverses squamous metaplasia of ocular
surface
KERATOCONJUNCTIVITIS SICCA
Deficiency of aqueous component of tears
Autoimmune pathology
More in females; after menopause
Associated with rheumatoid arthritis
Clinical Features
Chronic irritative symptoms
Punctate epithelial erosions in inferior cornea; dellen
Filamentary keratopathy
Earliest sign increased mucus and debris in tear
film which moves en masse with each blink
Marginal tear striponly 0.3 mm high (normally 1mm high); concave;
contains mucus and debris
Lid marginthickening and telangiectasia
Tear: lysozyme ratio = 1:10
Associated with desiccation in mucous membranes of bronchi, vagina,
mouth
Conjunctiva 189
XEROPHTHALMIA
Dry, lusterless condition of conjunctiva due to mucin deficiency
Occurs only when secretory activity of conjunctiva is impaired (not when
lacrimal gland is extirpated)
Causes
Cicatricial degeneration of conjunctival epithelium and glands
For example trachoma, burns, pemphigoid, diphtheria
Prolonged corneal exposure
For example ectropion, proptosis, lagophthalmos
Epithelium stops secreting mucusbecomes epidermoid with granular
and horny layers
Meibomian gland activity increasesocular surface gets covered with
fatty secretion
Systemic disorder Vitamin A deficiency
Bitot spotstriangular white patches on inner and outer sides of cornea
covered by foam-like material; not wetted by tears (Foam-like material
is due to gas production by Corynebacterium xerosis)
Treatment
Tear substitutes
Mucomimetic agents
Vitamin A supplements
TEARING
Causes
Hyperlacrimation causes
Supranuclear Emotional, psychological, voluntary (CNS)
Reflex arc Corneal/conjunctival disease, foreign body, iritis, glaucoma, yawning
(pseudoepiphora)
Infranuclear Cerebellopontine angle tumors, aberrant regeneration of facial nerve
(crocodile tears)
Direct lacrimal gland Inflammation, neoplasm, parasympathomimetic drugs, cholinesterase
stimulation inhibitors
Epiphora causes
Lacrimal pump failure Facial nerve palsy, stiff lid (burns/scars)
Decreased tear Lid contour deformity, chalazion
film movement
Punctum disorder Punctual occlusion or malposition
Canalicular Cicatrizing conjunctiva, trauma, laceration, Steven-Johnson
obstruction syndrome, canaliculitis, tumors, repeated probing
Lacrimal sac obstruction Trauma, tumors, allergy
Nasolacrimal duct Trauma, infiltrative disorders
obstruction
Intranasal pathology Allergic rhinitis, turbinate scarring (postsurgery), tumors, polyp
Jones Test: In Suspected Partial Obstruction

Primary Test
Differentiates partial obstruction from primary hyperlacrimation
A drop of fluorescein is instilled into conjunctival sac
After 5 minutes, a cotton bud is placed under the inferior turbinate
Test is positive if bud gets stained and negative if bud is not stained
Conjunctiva 191
Test is positiveno block

Test is negativeNLD block
Test is negativecanalicular block
Secondary Test
Wash out the residual fluorescein
Irrigate with saline (syringing)
Test is positive if cotton bud gets stained (indicates partial obstruction
of NLD)
Test is negative if bud is not stained (indicates partial obstruction of
upper lacrimal passages or pump failure)
Diagnosis
1. External examination:
Lids-movement, ectropion, puncta
Marginal tear strip
2. Pressure over sac regurgitation
Palpate sac for tumors/stones
3. Probing
Soft stop canalicular block
Hard stop NLD block

4. Syringing
NLD (nasolacrimal duct) patent fluid goes into the nose/mouth
When
regurgitation from same punctum canalicular block
regurgitation from upper punctum common canalicular/NLD
block
5. Dye test
Estimate if the dye has entered the mouth/nose
6. Nasal examination
7. X-ray of lacrimal sac
8. Dye disappearance test
chapter
Sclera 7
SCLERITIS
Severe painful inflammatory process centered in the sclera
May involve cornea, adjacent episclera, underlying uvea
50% have underlying systemic disease
Classification
1. Anterior scleritis
Diffuse
Nodularsingle/multiple nodules
Necrotizing
With inflammation
Without inflammation
Scleromalacia perforans
2. Posterior scleritisinflammation of sclera posterior to insertion of rectus
muscles
Diffuse
Nodular
Necrotizing
Pathogenesis
Immune-mediated vasculitis
Episcleritis Scleritis
Inflammation confined to superficial episcleral Inflammation of the sclera
tissue (not the deep episcleral tissue overlying
the sclera)
Conjunctival and superficial episcleral vascular Deep episcleral plexus is displaced outward by
plexuses are displaced outward from the sclera edematous sclera
Mild, non-vision threatening inflammation Severe; may threaten vision (posterior scleritis)
Usually idiopathic Mostly associated with systemic disease
Usually other ocular structures not involved Cornea, episclera, uvea may be involved
Symptomsredness, grittiness Symptomspain, globe tenderness, redness
Distinct red hue Bluish violet hue
Can be blanched with 2.510% phenylephrine Cannot be blanched
or 1:1000 epinephrine
Nodular/diffuse Diffuse/nodular/necrotizing
Clinical Features
Paindull, aching, boring; with facial radiation; nocturnal worsening
Decreased visionin corneal/posterior segment involvement
Redness, watering, photophobia
Scleral edema (differentiates it from episcleritis)
Intense injection due to dilatation of deep episcleral vascular plexus
Tenderness of globe
Signs of scleral necrosis:
Earlycapillary closure
Latearea of intense vasodilatation with a central less injected area
Advancedthinning of sclera; bluish sclera
Associated Systemic Disease

Rheumatoid arthritis
Wegeners granulomatosis
Relapsing polychondritis
Systemic lupus erythematosis (SLE)
Polyarteritis nodosa (PAN)
Ankylosing spondylitis
Reiters syndrome
Giant cell arteritis
Behets syndrome
Necrotizing Scleritis with Inflammation

Severe ocular and periocular pain
Scleral edema, intense vasodilatation
Tenderness, thinning, blue sclera (parchment-like)
Massive infection and loss of scleral tissue
Raised IOP leads to staphyloma formation
Corneal ulceration and inflammation
Scleromalacia Perforans
(Necrotizing scleritis without inflammation)
Bilateral; females more than males
Associated with rheumatoid arthritis
Asymptomatic
Thinning and atrophy of episcleral tissue
Loss of normal episcleral vasculature
Localized areas of yellow-white infarcted tissue
No tenderness or vascular dilatation
Exposed choroid comes into contact with conjunctiva
Astigmatism may result
Sclera 195
POSTERIOR SCLERITIS
Inflammation of sclera posterior to ora serrate
Symptoms
Pain, redness, proptosis, decreased vision
Diplopia, pain on ocular movement
Signs
Retinal/choroidal folds
Annular choroidal detachment
Circumscribed mass lesion
Chorioretinal granulomas
Disc edema, maculopathy, cotton wool spots
Uveitis, retinal vasculitis
Ciliary body rotation secondary to uveal effusionsecondary angle closure
glaucoma
Investigations
B-scan scleral thickening (>2 mm), T sign
CT-scan, fundus fluorescein angiography
Complications
Corneastromal keratitis, sclerosing keratitis peripheral corneal melt,
perforation
Sclerathinning, necrosis, staphyloma, perforation
Uveauveitis, choroidal granuloma
Glaucoma, cataract
Exudative RD, macular edema, optic atrophy
Treatment
NSAIDsfor mild scleritis
Steroids oral or IV in severe scleritis
Cyclophosphamide, cyclosporine, azathioprine, methotrexateif disease
not controlled by steroids
STAPHYLOMA
Ectasia of the coats of the eyeball along with uveal tissue
Types
Anterior
Congenital
Corneal opacity becomes protruberant
Associated with extremely disorganized anterior segment
Lens may adhere to the posterior cornea
Associated with intrauterine inflammation or maldevelopment
Raised IOP can cause prominent buphthalmic enlargement
Acquired
Following sloughing of corneal ulcer
Iris becomes exposed and inflamed
Layer of exudates covers the iris organizes into a thin fibrous layer
called pseudocorneathin and cannot withstand IOP bulges
Bunch of grapes appearance
Intercalary
At limbus; immediately in front of ciliary body
Ciliary
Bulging of ciliary body
Due to thinning of sclera due to scleritis or injury
Up to 8 mm from limbus
Bluish, irregular staphyloma
Equatorial
At the regions of sclera perforated by vortex veins
Always remains local
Noticed during surgery
Posterior
In high myopes
Bulging of sclera at posterior pole
Complications
Glaucoma due to decreased aqueous outflow
Retinal detachmentequatorial type
Lens subluxation, globe rupture
Treatment
Scleral resection
Staphyloma excised or buckled inwards
Scleroplastystaphyloma excised and replaced by sclera
Evisceration or enucleation with artificial eye implant
chapter
Pediatrics and Squint 8
AMBLYOPIA
Unilateral or bilateral reduction in best corrected visual acuity of equal to
or more than 2 lines, in the absence of any ocular pathology
A condition of diminished vision, form, sense which is not associated with
any structural abnormality or disease of media/fundi/visual pathways; not
overcome by correction of refractive error; which in appropriate cases is
reversible by therapeutic measures
Onset: Birth to 78 years
Classification
Stimulus Deprivation Amblyopia
Unilateral or bilateral
May be:
Completein ptosis, mature cataract
Partialin lamellar cataract, corneal opacity
Strabismic Amblyopia
In constant unilateral strabismus
Both fovea not focused on same object brain receives 2 dissimilar images
produces blurred or double vision
Reversible until 9 years of age
Ametropic Amblyopia
In high bilateral refractive errors
When refractive error is greater than +6.00D or 10.00D
Anisometropic Amblyopia
Meridional (in high astigmatism)
Anisohypermetropia (due to unequal hypermetropia in both eyes)
Anisomyopia (due to unequal myopia in both eyes)
Neutral Density Filter

When placed in front of:
Normal eye visual acuity decreases by 2 lines (Snellens chart)
Eye with organic cause for decreased vision visual acuity decreases by
2 lines
Amblyopic eye visual acuity remains the same
Assessment
Visual acuity
Refractionafter full cycloplegia
Slit lamp and fundus examination
Compare behavior of one eye with other
Cover testeyes reaction to covering
Fixationsteady, unsteady, eccentric
Speed of eye movement (during a cover-uncover test)
Ability to pick-up small grains of sweets with fixing eye covered
Visual acuity in infants
Optokinetic nystagmus
Forced choice preferential looking
Visual evoked response
Management
Begins with correction of underlying cause:
Appropriate refractive correction
Removal of the underlying cause of stimulus deprivation (cataract, ptosis)
Strabismus surgery
Methods
Occlusion/Patching
Based on type of occlusion:
Total occlusionwith opaque material placed on the seeing eye
Partial occlusiontranslucent adhesive tape (no longer advocated)
Based on duration of occlusion:
Full-time
Part-time: Patching is done for a few hours in a day, depending on the severity
of amblyopia
Severity Snellen visual acuity Hours of patching
Mild < 6/12 24 hours
Moderate 6/126/24 24 hours
Severe 6/306/120 46 hours/day or 50% of waking
hours in infants
A part time total occlusion is recommended for all newly diagnosed cases
of amblyopia
Other measures may be useful in unresponsive non-compliant cases
Sensory amblyopia: >6 hrs to full-time regimen
Precautions:
To avoid diplopia, investigate for binocular single vision before onset of therapy
(if fusion is possible no risk for diplopia)
Penalization
Penalize the normal eye so that the amblyopic eye is made to see
Penalization may be done by using:
Atropine:
1% atropine drops are instilled in the normal eye
Vision becomes defective for near but vision for distance is reasonably
maintained
Refractive correction is given to normal eye and is forced to be used for near
work
Glasses:
Normal eye is under-corrected
Full refractive correction is given to the amblyopic eye, which is forced to
be used to distance work
Cam Visual Stimulator
Stimulates the amblyopic eye
Pleoptics
Parafoveal area is dazzled with bright light while protecting the fovea, to
stimulate foveal fixation
Methods
Bangersters Method
Dazzle eccentric fixing retinal area with a disc projected onto fundus
Followed by intermittent stimulation of macula by flashes of light
Continued till central scotoma diminishes and fixation becomes central
Cuppers Method
Application of after images elicited by a modified ophthalmoscope that
contains black discs which stimulate other areas while protecting fovea
Used for older children with established eccentric fixation
VISUAL ACUITY TESTING IN PREVERBAL AND

VERBAL CHILDREN
Preverbal Children
Objective way of estimating visual acuity is by assessing fixation
Fixation should be central, steady and maintained (CSM)
Ability to fixate and follow light
Forced choice preferential looking (Teller acuity cards)
Optokinetic response (OKN)
Visual evoked response (VER)
Ability to locate and pick-up objects and sweets
Catford drum
Verbal Children
Sheriden Gardner vision test
E chart
Landolts broken ring test
Cardiff cards
Snellens charts
NEONATAL CLOUDY CORNEA

Causes
S Sclerocornea
T Trauma, tear in Descemets membrane (Infantile glaucoma)
U Ulcer due to HSV, bacteria, neurotrophic keratopathy
M Mucopolysaccharidosis, metabolic causes, tyrosinosis
P Peters anomaly, posterior keratoconus, posterior corneal defect,
staphyloma
E Endothelial dystrophy (CHED, PPD)
D Dermoid (central)
CONGENITAL CATARACT
Causes
Unknown45%; hereditary; genetic
Intrauterine infectionrubella, CMV infection, chickenpox, toxoplasmosis
Metabolicgalactosemia, diabetes mellitus, hypoparathyroidism
Secondary to coloboma, persistent hyperplastic primary vitreous (PHPV)
Associated with microphthalmos, aniridia
Mesodermal/ectodermal dysgenesispersistent pupillary membrane,
posterior lenticonus
Types
Zonularnuclear/lamellar/sutural/capsular
Polaranterior/posterior
Blue dot cataract
Coronary cataract
Membranous cataract
Total/mature cataract
Investigations
TORCH liters
Chromosomal analysis (Downs and Pataus syndrome)
Urine analysis (galactosemia)
Serum calcium and phosphorus
Fasting and post-prandial blood sugar
Surgery
Indications
Visually significant cataract (occupying >3 mm of the pupillary area)
Unilateral partial/complete cataract (operate within 4 weeks of birth if
visually significant)
Cataract with strabismus/nystagmus
Bilateral cataract with one eye operatedthe other should be operated
within 12 weeks to prevent amblyopia
Bilateral mature cataracts (operate both eyes within 68 weeks of birth, with
a gap of 12 weeks)
Technique
Up to 6 months Lens aspiration with primary posterior capsulorrhexis and anterior vitrectomy;
Postoperative rehabilitation is done with aphakic glasses and secondary IOL
placement at the age of 4 years
6 months to Lens aspiration with primary posterior capsulorrhexis and anterior vitrectomy
78 years with IOL implantation
>8 years Lens aspiration with IOL implantation
IOL Power Calculation

Aim for residual hypermetropia
Make emmetropic if > 8 yrs of age
90% of emmetropia if 28 yrs of age
80% of emmetropia if < 2 yrs of age
Postoperative Complications
Immediateshallow AC, increased fibrinous reaction
Latethick PCO, lens precipitates, pseudophakic membranes, glaucoma,
RD
Visual Rehabilitation
With glass, contact lens, secondary IOL, occlusion therapy for amblyopia
CLASSIFICATION OF EXOTROPIA
Primary
Intermittent
Divergence excess
Convergence insufficiency
Constant
Early onset
Decompensated divergence excess
Secondary
To ocular pathology
Consecutive
Postsurgical (following surgical correction for esotropia)
CLASSIFICATION OF ESOTROPIA
Primary
Concomitant
Accommodative:
Refractive
Non-refractive
Partially accommodative
Non-accommodative:
Infantile
Acquired:
Basic
Acute esotropia
Cyclic esotropia
Myopic esotropia
Convergence excess
Divergence insufficiency
Microtropia
Nystagmus blockade syndrome
Non-concomitant
ParalyticVI nerve palsy
Non-paralytic:
A-V patterns
Restrictive syndromes
Mechanical restrictions
Secondary
To ocular pathology (sensory esotropia)
Consecutive
Following surgery for exotropia
INFANTILE ESOTROPIA
Appears 36 months after birth
Size of deviation > 40 PD (prism diopters)
Constant deviation (does not change with change in accommodative effort)
Comitant deviation (may change in up gaze or down gaze due to A or V
pattern)
Refraction normal for age (low plus)
Correcting the refractive error will not correct the deviation
Associated Findings
Dissociated Vertical Deviation: in 4050%
Slow upward deviation of one/alternate eyes
No corresponding hypotropia of opposite eye
May be latent or manifest
Poor BSV and fusion
Inferior Oblique Over-action
V-pattern esotropia
Increased elevation in adduction
Onset at 23 years of age
Latent Nystagmus
Nystagmus only when one eye occluded
Abnormal OKN
Normal adducting and weak abducting saccade
Treatment
Spectacle correction if refractive error > +3.00D
Treat amblyopiaincreased chance for fusion
Surgery:
Bilateral medial rectus recession (can be treated as early as 6 months of
age to improve postoperative fusional result)
Bilateral lateral rectus resection
Follow-up
Pseudoesotropia flat broad nasal bridge, prominent epicanthal folds,
narrow interpupillary distance
Duanes retraction syndrome
Early accommodative esotropia
VI nerve palsy
Mobius syndrome VI + VII nerve palsy
Nystagmus blockade syndrome increased convergence to dampen
nystagmus
ACCOMMODATIVE ESOTROPIA
Present at 18 months 3 years
When child begins to look at detail and accommodate
<40 PD esotropia
Amblyopia in 3050%
Fully accommodativefull spectacle correction eliminates the deviation.
Partially accommodativeresidual esotropia despite full correction of
refractive error.
Causes
Over-convergence associated with accommodation
Failure of fusional divergence to correct over-convergence
Types
Refractive
Normal accommodative convergence to accommodation ratio (AC/A ratio)
Moderate hyperopia ( +4.00 D and less than +8.00 D)
Accommodative effort to overcome hyperopia creates excessive accom-
modative convergence
Treatment: Full refractive correction
Non-refractive
High AC/A ratio
Normal refractive error (+2.00 D)
Increased convergence; normal accommodation
DN > DD: Deviation greater for near than distance (at least 10 PD difference)
Treatment:
Full distance correction
Bifocalsto relieve additional deviation at near
Accommodative Convergence/Accommodation
AC/A ratio
Normally 5 (in children), 6 (in adults)
High AC/A excess convergence makes DN > DD
Low AC/A insufficient convergence makes DD > DN
Measuring AC/A Ratio

Heterophoria Method
AC N D
= IPD (cm) +
A D
N deviation for near (33 cm)
D deviation for distance (6 meters)
D distance of fixation for accommodation
Gradient Method
+ L deviation with concave lens
L deviation without lens
AC ( + L) ( + L)
=
A D
D strength of lens used
MICROTROPIA
Monofixation syndrome
Causes
Primary or following surgery for a large deviation
Signs
Very small esotropia 5 deviation ( 8 PD)
Anisometropia with hypermetropia or hypermetropic astigmatism
Minor or moderate amblyopia (1 or two lines difference in visual acuity
between the two eyes)
Harmonious ARC (anomalous retinal correspondence)
No confusion because of central suppression scotoma in the deviating eye
Normal peripheral fusional amplitudes; reduced stereopsis
Tests
Bagolini striated glasses: Cross is seen with a gap in the oblique line perceived
by the microtropic eye
4 base-out test:
When this prism is placed in front of:
Normal eye refixation movement occurs (due to sudden displacement
of image from fovea to a parafoveal point)
Microtropic eye no movement occurs (because image is shifted within
the central suppression scotoma)
Treatment
Spectacle correction of anisometropia
Occlusion for amblyopia (never successful in restoring bifoveal fixation)
HETEROPHORIA
Latent strabismus
Operative tendency to misalignment of visual axes which is corrected by
the fusional capacity of the eyes
Strabismus is equally shared between the two eyes
Esophoria, exophoria, hyperphoria
Cyclophoriatorsional deviation
Overstimulation of convergence with accommodation in hyperopia
esophoria
Understimulation in myopia exophoria
Symptoms
Eye strain if deviation 510
Hyperphoria, cyclophoria increased discomfort
Deviation may become manifest in fatigue
In convergence insufficiency exophoria appears when near objects are
regarded
Treatment
Correct refractive error
Exercise weak muscles against prisms (base of prism in direction of deviation)
Prism in spectacles to correct the deviation (total prismatic error should be
divided equally between the two eyes)
Surgery
Convergence insufficiency orthoptic exercises can be done distance at
which diplopia occurs is gradually shortened (e.g. a pencil is brought toward
the nose)
DUANE SYNDROME
Retraction of globe on attempted adduction caused by co-contraction of
medial and lateral rectus
May be associated with perceptive deafness, speech disorder
Huber Classification
Type I Type II Type III

Limited abduction Limited adduction Limited abduction
Normal/decreased Normal/decreased abduction Limited adduction
Orthophoria/slight esotropia Orthophoria/slight exotropia Orthophoria/slight esotropia
On attempted adduction globe retraction + narrowing of palpebral fissure

On attempted abduction globe comes back to its normal position +
widening of palpebral fissure
Upshoot/downshoot in adduction Leash or Bridle phenomenon (because
a tight lateral rectus slips over/under the globe respectively)
Surgical Indications
No orthotropia in primary gaze
Patient assumes an abnormal head posture to achieve fusion
Cosmetic correction required
BROWN SYNDROME
Superior oblique tendon sheath syndrome
Causes
Congenital
Idiopathic
Impaired movement of superior oblique tendon through trochlea
Surgery if hypotropia in primary gaze or abnormal head posture
Acquired
latrogenic damage to trochlea or superior oblique tendon
Inflammation of tendon in rheumatoid arthritis, pansinusitis, scleritis
Treat with steroids (oral steroids or steroid injection near trochlea)
Clinical Features (In Right-Sided Brown Syndrome)

Orthophoria/hypotropia
Limited right elevation in adduction
Down shoot on adduction
Normal right elevation in abduction
No superior oblique overaction
Positive forced duction test on elevating globe in adduction
Ipsilateral head tilt and chin elevation
Inferior oblique palsy
Monocular elevation deficit
MOEBIUS SYNDROME
Clinical Features
Eye
Horizontal gaze palsy; vertical gaze intact
Bilateral VI nerve palsy
Esotropia or orthophoria in primary gaze
Pseudoesotropiain children who learn to cross-fixate
Systemic
Bilateral facial palsyasymmetrical, incomplete
Mask-like facies
Incomplete lid closure
IX nerve and XII nerve palsy
Mental retardation, limb anomalies
NONSURGICAL MANAGEMENT OF SQUINT

Glasses: For accommodative esotropia
Accommodative esotropia with hypermetropia:
Regular plus glasses to relax accommodation and increase convergence
Bifocals if more hyperopia for near
Non-refractivevoluntary convergence with emmetropia
Prisms:
Only when BSV present
In acquired paretic squint, vertical palsies, small deviations
Esotropiabasein prism used
Exotropiabaseout prism used
Visual acuity should be almost normal in both eyes
Prismsdivided equally for both eyes
Fused with spectacle lenses
Orthoptic exercises:
Increasing fusional amplitude by stimulating physiological diplopia
Called anti-suppression exercises
Increases accommodation amplitude and improves convergence and fusion
Pharmacological:
Atropinefor penalization of normal eye in accommodative esotropia
Mioticsphospholine iodine, pilocarpine
Botulinum toxin Achemical denervation
SUDDEN ONSET DIPLOPIA

Causes
Trauma blow out fracture; fracture floor of orbit
Inflammationsuperior orbital fissure syndrome, Tolosa Hunt syndrome,
orbital apex syndrome, myositis, pseudotumor, cellulitis
Endocrinethyroid disorders
Neuromuscularmyasthenia gravis
Vascularaneurysm, AV fistula, hypertension, diabetes
Tumors
benignneurofibroma, hemangioma, lymphoma
malignantlymphoblastic leukemia
Parasitic infestationscysticercosis
Iatrogenicfollowing cataract/RD surgery
Idiopathicdecompensating phorias
Demyelinationin multiple sclerosis
Investigations
Blood sugar, blood pressure
X-ray skull, CT-scan, MRI, CSF analysis
Total count, differential count, eosinophil count, ESR
T3, T4, TSH levels
Tensilon test
Carotid angiography
BOTULINUM TOXIN
Indications
Therapeutic
Horizontal squint correction
Upper lid retraction
Lower lid senile entropion
Lacrimal gland hypersecretion
Aberrant VII nerve regeneration crocodile tears, Freys syndrome
Facial dystoniasbenign essential blepharospasm, hemfacial spasm, Meige
syndrome
Chemotarsorrhaphydone for corneal exposure in temporary VII nerve
palsy, indolent corneal ulcer or epithelial defects
Dry eye syndromes
Acquired nystagmus
Oscillopsia
Cosmetic
Brow lift
Dynamic facial wrinklescrows feet
Other Uses
Torticollis
Laryngeal dystonia
Tics, stuttering, bruxism
Spastic bladder
Action
At neuromuscular junction, autonomic ganglia, post-ganglionic
parasympathetic and sympathetic nerve endings that release acetylcholine
(ACh)
Decrease release of ACh from presynaptic motor neurons
Contraindications
Amyotropic lateral sclerosis
Motor neuropathy
Myaesthesia gravis
Eaton-Lambert syndrome
Pregnancy
Areas of active infection
Complications
Upper lid ptosis
Ectropion, entropion
Lagophthalmos
Diplopia
Eyelid hematoma
Functional epiphora due to lacrimal pump failure
Dry eye
chapter
Neuro-ophthalmology 9
THE PUPIL
Normal size: 24 mm
In dark adaptation: 4.57 mm
In light adaptation: 2.56 mm
Miosis: 3 mm
Mydriasis: 6 mm
AR pupilArgyll Robertson pupil; PTNPretectal nucleus

EWNEdinger Westphal nucleus; APDAfferent pupillary defect
II nOptic nerve; III nOculomotor nerve
Toxic pupiloccurs in neuromuscular blockade

Adies tonic pupildue to ciliary ganglion block
Paralytic pupilin III n palsy
Argyll Robertson pupilpretectal nucleus lesion
Marcus Gunn pupiloptic nerve involvement
Toxic Pupil
Sudden unilateral dilatation of pupil
Dilated and fixed pupil
Due to finger-eye contact of anticholinergic agents
Neuromuscular blockade occurs
III n (3rd cranial nerve) uninvolved
1% pilocarpine will not constrict the pupil
Acute botulism causes bilateral toxic pupils
Adies Tonic Pupil

Unilateral dilated pupil; common in females
Slow tonic contraction of iris in near response; slow redilatation
Dilates well with mydriatics
Blurring of vision while reading
Parasympathetic denervation supersensitivitypupil constricts after 1/8%
pilocarpine
Vermilliform movements of the pupillary margin seen on slit lamp (due to
selective activation of small segments of the sphincter margins)
Adies Syndrome
Adies pupil + loss of deep tendon reflexes secondary to degeneration of dorsal
root ganglion cells
Causes
Ciliary ganglionitisHSV, measles, chickenpox
Guillain-Barr syndrome, diabetes mellitus, Ross syndrome
Shy-Drager syndrome, alcohol, surgery, trauma, ischemic episodes
Mechanism
Loss of neurons in the ipsilateral ciliary ganglion
Acetylcholine from collaterals is not released directly into synaptic troughs
of the sphincter musclecausing slow tonic contraction
Insufficient catabolism of acetylcholine causes slow re-dilatation
Argyll Robertson Pupil

Accommodation reflex present (ARP)
Bilateral miotic pupils with irregular margins
Pupils are asymmetricin size and response to light
Precedes other manifestations of neuro-syphilis

Lesion at pretectal nucleus
Causes
Tabes dorsalis, diabetes mellitus, Wernickes encephalopathy, encephalitis,
hereditary neuropathies, midbrain tumors
Paralytic Pupil
In III n palsy
Preganglionic parasympathetic denervation
Pupil spared inDiabetes mellitusbecause pupillary fibers are superficially
placed and get perineural blood supply
Causes
Posterior communicating artery aneurysm; cerebral compression, contusion,
inflammation, infiltration
Hippus
Nonpathological, intermittent, synchronous, rhythmic contraction and
dilatation of pupils
Marcus Gunn Pupil

De-afferented pupil causing a relative afferent pupillary defect (RAPD)
The swinging flashlight test is used to determine RAPD
Patient should fix his gaze at a distant object in a dark room
Light is swung from eye to the other every 13 seconds
RAPD is paradoxical dilatation of pupil when light is thrown in the eye
Mechanism
Impaired nerve transmission Edinger-Westphal nucleus gets fewer light
elicited impulses exerts less para-sympathetic tone so pupil dilates
instead of constricting
RAPD can be checked even in IIIn palsy, corneal opacity, atropinized pupil
by checking reflexes in the other eye
Not useful in bilaterally symmetrical optic nerve lesions
Quantified by using neutral density filters before the normal eye and
repeating the test with increasing density filters in the fellow eye until
pupillary responses are equal
Grading of RAPD
I. Weak initial constriction of pupil and greater re-dilatation
II.
Initial stall and greater re-dilatation
III.
Initial immediate pupillary dilatationcalled pupillary escape
IV. Immediate pupillary dilatation following prolonged illumination of the good
eye for 6 seconds
V. Immediate pupillary dilatation with no secondary constriction
FIELD DEFECTS
In Optic Nerve Lesions
Congenital/Hereditary
Myelinated nerve fibers:
Enlargement of blind spot
Central/paracentral scotoma
Optic nerve coloboma:
Nerve fiber bundle defects
Superior altitudinal defect
Superior nasal depression
Optic nerve hypoplasia:
Total blindness
Paracentral scotoma
Bitemporal/binasal hemianopia
Bilateral inferior extension of blind spot
Optic nerve head drusen:
Blind spot enlargement
Irregular peripheral contraction
Scotomas
Nasal defects
Slowly progressive defects
Optic nerve pit:
Gross enlargement of blind spot
Paracentral scotoma
Tilted disc:
Upper temporal field defect
Lebers hereditary optic neuropathy:
Central scotoma
Pressure on the Optic Nerve

Papilledema
Gross enlargement of blind spot
Peripheral constriction in postpapilledemic optic atrophy
Optic nerve glioma
Central scotoma
Inflammatory
Papillitis
Central scotoma with moderate enlargement of blind spot
Scotoma for red objects
Centrocecal scotoma
Paracentral scotoma
Vascular
AION
Sector type atrophy
Inferior altitudinal defect
Traumatic
Central scotoma
Inferior visual field defects
Blindness
Toxic
Central/centrocecal scotoma
Bilateral peripheral field constriction with:
Quinine, chloroquine, salicylates, arsenic
Hyperbaric oxygen, carbon monoxide, epinephrine
In Chiasmal Lesions
Infrachiasmal
Non-scotomatous: Lesions in peripheral isopters
Scotomatous:
Anterior chiasmajunctional scotoma (one eye temporal hemianopia;
fellow eye peripheral field defect)
Posterior chiasmae.g. pituitary adenoma
Upper temporal field loss progresses to hemianopia

Recovery occurs in opposite direction to field loss (UNLNLTUT)
(UNupper nasal; LNlower nasal; LTlower temporal; UTupper
temporal)
Suprachiasmal
Anterosuperior
Posterosuperior
CraniopharyngiomaLT defect progresses to hemianopia (LT UT
UN LN)
Dilatation of the IIIrd ventricle

Small bilateral inferior quadrant scotoma close to fixation, progresses
to involve the superotemporal quadrant
Perichiasmal
Inflammatoryarachnoiditis, basal meningitis
Bitemporal hemianopia
Binasal hemianopia
Homonymous hemianopia
Concentric contraction of field
Aneurysms of internal carotid artery
Subclinoid (within cavernous sinus)
Supraclinoid (above cavernous sinus)
Intrachiasmal
Glioma/tumors
Field defects depend on direction of tumor growth
Bizarre form of bitemporal hemianopia
Injuries
Permanent bitemporal hemianopia with macular split (direct injury to
nerve fibers or ischemic necrosis)
In Meningiomas
Olfactory groove meningiomacentral hemianopic scotoma; unilateral
blindness
Tuberculum sellae meningiomajunctional scotoma; unilateral blindness
or central scotoma with contralateral peripheral field defect
Frontal lobe meningiomabitemporal hemianopia
Sphenoidal ridge meningiomabitemporal hemianopia with sloping edges
Medialcompresses optic nerve early
Lateralcompresses optic nerve late
CT-scan showsfullness in temporal fossa due to hyperostosis
In Post Chiasmal Lesions

Optic Tract
Extreme incongruity of fields
Negative optokinetic response (OKN)
Optic tract syndrome:
Type I: Involves anterior optic tract
Ipsilateral decreased visual acuity with afferent pupillary defect (APD)

Contralateral homonymous hemianopia
Caused by mass lesions
Type II: Involves posterior optic tract
Normal visual acuity
Contralateral APD
Caused by demyelination, infarction, mass lesions
Lateral Geniculate Body
Crossed fibers end in 1, 4, 6 layers
Uncrossed fibers end in 2, 3, 5 layers
In occlusion of anterior choroidal arteryupper and lower quadrants are
lost but the central visual field is spared
In occlusion of lateral choroidal arterycentral field is lost but upper and
lower quadrants are spared
Optic Radiation
Longest, most vulnerable pathway
Within the internal capsule:
Contralateral hemianesthesia/hemiplegia
Complete homonymous hemianopia
Temporal lobe:
Homonymous wedge-shaped defect in upper visual field
Pie in the sky defect
Due to tumors, abscesses
Parietal lobe:
Homonymous hemianopia densest in the lower quadrant
Pie in the floor defect
Positive optokinetic (OKN) responsedecreased amplitude and frequency
Extinction phenomenonpatient may not pay attention to one-half of the
field when both sides are simultaneously stimulated (not a true field defect)
Occipital lobe:
Dorsal horizontal part gets fibers from medial segment of lateral geniculate
body (LGB)
Ventral horizontal part gets fibers from lateral segment of LGB
Vertical communicating part from intermediate segment of LGB
Visual Cortex
Dorsal partreceives fibers from upper half of retina
Lower partfrom lower half of retina
Tip of posterior polereceives macular fibers
Congruous homonymous hemianopia with macular sparing because of
bilateral representation and overlapping blood supply of posterior and
middle cerebral artery
Visual hallucinationsscintillating scotomas
Total cortical blindness
Hemianopic dyschromatopsia
Checkboard quadrantanopia
OPTIC ATROPHY
Abnormal pallor of optic disc
Loss of conducting function of optic nerve, with increase in pallor of optic
disc as a result of gliosis and loss of capillaries of the disc
Normally the optic disc is pink because light is reflected back from the disc
capillaries
Pathological Classification
1. Ascending optic atrophyprimary lesion in the retina, optic nerve or
choroid, e.g. retinitis pigmentosa, CRAO, glaucoma, trauma
2. Descending optic atrophyprimary lesion in brain or optic nerve; proceeds
towards eye, e.g. retrobulbar neuritis, papilledema
3. Inheritedcongenital, juvenile, Lebers hereditary optic neuropathy, Behrs
optic atrophy and Friedreichs ataxia
Ophthalmoscopic Classification
Primary
Chalky white optic disc with well-defined margins
Retinal blood vessels, periphery and surrounding retina are normal
Lamina cribrosa well seen
Example: Retrobulbar neuritis, pituitary tumor, optic nerve trauma
Secondary
Gray optic disc with poorly-defined margins
Physiological cup obliterated
Peripapillary sheathing of blood vessels
Narrow arteries; tortuous veins
Example: Papillitis, papilledema
Consecutive
Waxy pallor of optic disc with normal margins
Marked attenuation of arteries; normal cup
Associated retinal pathology
Example: Retinitis pigmentosa, myopia, choroiditis, CRAO
Glaucomatous
Vertical cup enlargement
Notching and pallor of neuroretinal rim
Laminar dot sign
Bayoneting and nasalization of blood vessels
Peripapillary atrophy
Splinter hemorrhages at disc margin
Nerve fiber layer defects
Segmental or Partial
Temporal pallor, e.g. toxic amblyopia
Altitudinal pallor, e.g. AION

Wedge-shaped pallor, e.g. BRAO
Etiological Classification
Consecutive
Post-inflammatory, e.g. chorioretinitis
Degenerative, e.g. retinitis pigmentosa, myopia
Extensive PRPC
Longstanding retinal detachment
Circulatory
CRAO, post-hemorrhagic, giant cell arteritis
Arteriosclerosis, carotid artery disease
Pressure and Traction
Glaucoma, papilledema, tumors
Aneurysm of internal carotid artery, basal arachnoiditis
Inflammation
Optic neuritis, intraocular infection, TB, septicemia
Toxic
Tobacco, alcohol, lead, arsenic
Ethambutol, isoniazid, sulfonamide, chloroquine
Metabolic
Diabetes mellitus, thyroid disorder
Cystic fibrosis, nutritional
Traumatic Optic Neuropathy
Hereditary
Lebers hereditary optic neuropathy
Behrs optic neuropathy
Band/Bowtie atrophy: Pallor only on nasal and temporal part of optic
discseen in chiasmal syndrome with bitemporal hemianopia
Temporal pallor: Degeneration of axial fibers of retrobulbar optic nerve
causing atrophy of papillomacular bundle, producing a centrocecal
scotoma
Optic disc coloboma
Optic disc drusen
Morning glory syndrome
Optic disc pit
Medullated nerve fibers
Optic nerve hypoplasia
ANTERIOR ISCHEMIC OPTIC NEUROPATHY

Partial or total infarction of the optic nerve head caused by occlusion of
short posterior ciliary arteries; postlaminar infarct
Clinical Features
Sudden painless unilateral loss of vision
Defective color vision; RAPD
Altitudinal/central field defect
Pale disc edema with flame-shaped hemorrhages; may be sectoral
May be associated with CRAO, cilioretinal artery occlusion, diplopia (because
of ischemia of extraocular muscles)
Pseudo Foster Kennedy Syndromepost AION pallor in one eye with AION
in the fellow eye
Anterior ischemic optic neuropathy (AION) never recurs in the same eye
Optic neuritis
Compressive or infiltrative optic neuropathy
Diabetic papillopathy
Optic disc vasculitis
Normotensive glaucoma
Papillophlebitis
PION (posterior ischemic optic neuropathy)
Occlusion of the small pial vessels which supply the intraorbital part of
the optic nerve
Causes areacute systemic hypotension, anemia, vasculitis
Present with acute, severe visual loss
RAPD; initially normal appearing fundus
Arteritic Non-arteritic
Females > Males Females = Males
More than 60 years of age 4060 years of age
Severe visual loss Mild to moderate visual loss
Vision worse than 6/60 Vision better than 6/60
Pain may be present Painless
Previous episodes of amaurosis Rare
Fellow eye affected in 95% within days Fellow eye affected in <30%
Optic disc pallor > hyperemia Optic disc hyperemia > pallor
ESR >40 mm/hour ESR <40 mm/hour
Temporal artery biopsy giant cell granulomatous No biopsy required
vasculitis
FFA optic disc and choroidal filling delay FFA optic disc filling delay
Treatment intravenous corticosteroids Treatment control blood pressure/sugar
Arteritic AION
Associated Features
Headache, scalp tenderness
Palpable, tender, non-pulsatile temporal artery
Proximal muscle and joint aches
Jaw claudication; cranial nerve palsies
Treatment
1 g/day intravenous methyl prednisolone for 3 days with oral prednisolone
1 mg/kg/day for 1 week, tapering to 5 mg/day; Maintenance dose515
mg/day 612 months
PAPILLEDEMA
Bilateral, passive, hydrostatic, non-inflammatory edema of the optic disc
Secondary to raised intracranial tension (ICT)
Pathogenesis
Toxic elements from CSF pass through optic nerve sheath and cause an
inflammatory response and edema
Inflammation causes vasomotor instability that leads to optic disc edema
Pressure on cavernous sinus causes congestion of ophthalmic veins
Retrograde axonal flow: From LGB to ganglion cells
In hypertension
Hypertensive encephalopathy raised ICT
Vascular occlusion leads to ischemia axoplasmic stasis
Swelling of optic disc due to accumulation of fluid between nerve fibers
If there is sudden increase in ICT subhyaloid hemorrhage
Pathology
Signs of passive edema
No sign of inflammation
Swelling of nerve fibers in optic nerve head due to axoplasmic stasis
Physiological cup is filled
Internal limiting membrane (ILM) raised
Nerve fibers are swollen and varicose degenerate
Cystoid bodies present in front of lamina cribrosa
Macular fan due to edema in nerve fiber layer (NFL) raising ILM in folds
Clinical Features
Headache due to stretching of meninges
Nausea and vomiting
Transient attacks of blurred vision
Enlarged blind spot; progressive contraction of visual fields
Results in optic atrophy ensues
Classification
Early Papilledema
Optic disc hyperemia; splinter hemorrhages
Blurring of nasal margin followed by superior, inferior and temporal margins
of disc
Dilated and tortuous vessels
Absence of spontaneous venous pulsation (if ICT > 200 mm water)
Established Papilledema
Disc hyperemia; blurring of disc margins
Dilated tortuous vessels; optic cup obscured
Microaneurysms and cotton wool spots
Circumferential retinal foldsPatons lines
Macular starhard exudates in macula

Capillary dilatation on optic disc surface
Intraretinal/subhyaloid/vitreous hemorrhage
Chronic Papilledema
Long standing or vintage papilledema
Optic disc elevatedchampagne cork appearance
No cotton wool spots or hemorrhages
Optociliary shunts because of chronic obstruction of venous drainage
through central retinal vein
Corpora amylaceaDrusen-like crystalline deposits on optic disc surface
End Stage Papilledema
Decreased vision, optic atrophy
Glial cell proliferation, perivascular cuffing
Etiology
Congenital aqueductal stenosis
Space occupying lesions obstruction of CSF flow
Venous stasis decreased absorption of CSF
Tumors of midbrain, parieto-occipital region and cerebellum increased
secretion of CSF
Benign intracranial hypertensionin pseudotumor cerebri, obese females,
3040 years age group; on oral contraceptives/oral tetracyclines
Malignant hypertension
Meningitis, encephalitis diffuse cerebral edema and aqueductal stenosis
Cerebral abscess, subarachnoid hemorrhage, aneurysm, hydrocephalus
Pseudoneuritis
In hypermetropesreflexes cause disc margins to appear blurred
Swelling of disc < 2 DD
No venous engorgement, edema or exudates
No leakage on FFA
Optic neuritis
RAPD, decreased visual acuity
Optic disc drusen
Bilateral, inherited
No leakage on FFA
AION, CRVO
Compressive thyroid optic neuropathy
FFA
Dilatation of surface capillaries
Leakage of dye
Vertical oval pool surrounding the optic disc
Treatment
Relieve the cause of raised ICT
Timely decompressionremoval of tumor
Watch the visual fields
Immediate medical treatmentsteroids, diuretics, oral acetazolamide,
IV mannitol (decreases cerebral edema but increases the chance of uncal
herniation)hence careful monitoring required
In benign intracranial hypertensionlateral orbitotomy and optic nerve
sheath decompression
Papilledema takes 46 weeks to appear and 46 weeks to resolve when treated
OPTIC NEURITIS
Inflammation of optic nerve due to demyelinating disease or spread of
infection from orbit or paranasal sinuses
Pathology
Perineuritisdue to spread of inflammation from brain/orbit/sinuses; affects
extramacular fibers
Axial neuritisaffects macular fibersoccurs in multiple sclerosis, toxic/
nutritional neuropathy
Transverse neuritisaffects all fibers
Clinical Features
Common in females, 2040 years of age, mostly idiopathic
Decreased vision; usually unilateral (can be bilateral in kids and pregnancy)
Pain:
Precedes and accompanies visual loss
On superior and medial movements, due to traction of superior and
medial recti origins on the optic nerve sheath at orbital apex
Blurred vision after exertionUhtoffs phenomenon
RAPD; red-green color deficiency; central/centro-cecal scotoma
Vision recovery in 212 weeks
Retrobulbar neuritisoptic disc and nerve fiber layer appear normal
Papillitisoptic disc swelling, hyperemia, venous engorgement
Neuroretinitisoptic disc swelling, macular star
Investigations
Decreased contrast sensitivity
VEPincreased latency, decreased amplitude
Pupillary light reflex latencyprolonged
Foveal critical flicker frequencyimpaired
Etiology Features Investigations

Multiple sclerosis Weakness, ataxia MRI
Viral (mumps, measles) Recent illness WBC count
Tuberculosis Fever, weight loss, night sweats Mantoux, chest X-ray, ELISA
Sarcoidosis Cough, breathlessness Serum ACE levels
Toxoplasmosis History of contact with cats TORCH titers
Connective tissue Fever, rash, joint pains ANA, anti-ds DNA
disorders
HIV History of blood transfusion ELISA, PCR
CMV Organ transplant, ELISA, PCR
immunosuppressed
Orbital infection Periorbital edema CT scan
Behets disease Orogenital ulcers HLA typing
Papilledemabilateral; due to raised ICT; no fall of vision; normal pupils
AIONpale disc edema; altitudinal field defect
Toxic/nutritional amblyopiabilateral; temporal
Malingeringpupils normal
Hypermetropiabilateral; pupils normal
LHONbilateral
Acute congestive glaucomahigh IOP
Optic disc drusen
Treatment
Treat the cause
Intravenous methyl prednisolone 1 g daily 3 days with 1 mg/kg/day oral
prednisolone; oral steroids should be continued for 11 days and then rapidly
tapered over the next 3 days
THIRD NERVE PALSY

Causes
Vascular
Small blood vesselsDM, HTN, collagen vascular disease
Medium blood vesselsgiant cell arteritis, polyarteritis nodosa, vasospasm
Large blood vesselsatherosclerosis, aneurysm, AV malformations
Inflammatory
Post-viral infections, sarcoidosis
Demyelinating diseases, autoimmune disorders
Neoplastic
Meningioma, nasopharyngeal carcinoma
Pituitary adenoma, craniopharyngioma
Metastasis
Congenital
Hereditary; developmental anomaly
Traumatic
Unknown (40%)
Clinical Features
Eyes are divergent and depressed
Ptosis; crossed diplopia (unless there is total ptosis)
Dilated pupil (unless it is a pupil-sparing palsy)
Multiple cranial nerve palsies
Chronic progressive external ophthalmoplegia
Ocular myasthenia
Congenital fibrosis
Thyroid related orbitopathy
Generalized orbital inflammation
Double elevator palsy
Orbital floor fracture (inferior oblique/inferior rectus trapped in antrum)
Parinauds syndromevertical gaze palsy
Investigations
(Similar for III, IV and VI n Palsies)
Blood sugar, blood pressure
Angiographyposterior communicating artery aneurysm
CSF analysismultiple sclerosis
CT scan, MRI brainmultiple sclerosis, tumor, trauma
ESRgiant cell arteritis

Tensilon testmyasthenia gravis
Thyroid function teststhyroid related orbitopathy
Antinuclear antibodies (ANA)collagen vascular disease
Forced duction test to rule-out restrictive pathology in nerve palsies of short
duration
Hess chart to determine the prognosis and recovery
Diplopia chart to determine the extraocular muscles involved, crossed/
uncrossed diplopia, extent of diplopia
Localizing the Lesion
Nuclear Complex (in Midbrain @ Superior Colliculus)

LPS subnucleusbilateral ptosis occurs
SR subnucleusonly contralateral superior rectus is affected
IR, MR, IO subnucleionly ipsilateral inferior rectus, inferior oblique and
medial rectus affected
Paired MR subnuclei wall-eyed bilateral internuclear ophthalmoplegia
(WEBINO) exotropia, defective convergence and adduction
LPSlevator palpebrae superioris
SR, IR, MRsuperior rectus, inferior rectus, medial rectus
IOinferior oblique
Fasciculusas fibers pass through:
Red nucleusBenedicts syndrome ipsilateral III n + contralateral
extrapyramidal signs
Cerebral peduncleWebers syndrome ipsilateral III n + contralateral
hemiparesis
Superior cerebellar peduncleNothnagel syndrome ipsilateral III n
+ cerebellar ataxia
Claude Syndrome Benedict + Nothnagel syndrome
Basilar Part (Isolated III n Palsies Common)
Acute painful III n palsy with pupillary involvement in aneurysm of
posterior communicating artery
Head trauma irritative miosis followed by mydriasis and total III n palsy
(Hutchinsons pupil)
Intracavernous Part (Associated with IV n, 1st and 2nd Branches of V n)
Causes: Diabetes, pituitary apoplexy, caroticocavernous fistula, Tolosa Hunt
syndrome, aneurysm/meningioma in cavernous sinus
Intraorbital Part
Superior divisionSR and LPS affected
Inferior divisionIR, IO, MR and pupil involved
Management
Treat the cause
The most common cause is vascular (mainly diabetes)
Observation; strict control of diabetes
Diplopia is managed with unilateral occlusion
Traumawait for at least 6 months before surgical correction
Surgery: Ipsilateral lateral rectus recession + superior oblique tenotomy
medial rectus resection
First correct the extraocular muscles; then the ptosis
FOURTH NERVE PALSY

Clinical Features
Compensatory contralateral head tilt
Head tilt is toward the side opposite the defective eye
Bielschowsky forced head tilt test positivegreater vertical deviation with
head tilted toward the side of the paretic muscle
In bilateral superior oblique palsiespositive Bielschowsky with head tilt
in both directions; torsion of images
Vertical diplopiadifficulty in walking downstairs
Hypertropia (near > distance), esotropia, face turn to opposite side, chin
depression
Uncrossed diplopiamaximum separation of images on levodepression in
right superior oblique palsy
Causes (Apart from those Mentioned Above)
Decompensated congenital ptosis
Posterior fossa tumor
Cavernous sinus/superior oblique fissure syndromes
Neurosurgical procedures
Isolated IV n palsy inhead trauma, diabetes, herpes zoster ophthalmicus
Management
Treat the cause
Surgery:
If vertical deviation is more Inferior oblique recession
If torsional component is more Harada I to procedure (anterior) half
of superior oblique tendon is advanced and re-inserted 8 mm behind
and just above the superior border of lateral rectus
Myasthenia gravis
TRO (thyroid-related orbitopathy)fibrotic inferior oblique/superior rectus
Idiopathic orbital inflammatory syndrome
Injury to trochlea
SIXTH NERVE PALSY

Causes
Non-Localizing Causes
Raised intracranial tension, head trauma
Hypertension, diabetes mellitus
Idiopathic
Para-infectious (viral)
Multiple sclerosis
Lumbar puncture
Localizing Causes
Pontine syndromes
Cerebello-pontine angle lesions (acoustic neuroma)
Clivus lesions (nasopharyngeal carcinoma)
Middle cranial fossa lesions
Cavernous sinus thrombosis
Superior oblique fissure syndrome
Raised ICT may damage VI n false localizing sign
Septic thrombosis of inferior petrosal sinus VI n and VII n palsy
Base of skull fractureunilateral/bilateral VI n palsy
Clinical Features
Esotropia (distance > near); abduction restriction
Compensatory face turn to affected side
Muscle sequelcontracture of ipsilateral medial rectus
Uncrossed diplopiaincreased separation towards affected side
Myasthenia gravis
TRO (thyroid-related orbitopathy)fibrotic medial rectus
Idiopathic orbital inflammatory syndrome
Orbital traumamedial rectus entrapment
Congenital defectsDuanes and Mobius syndrome
Convergence spasm
Infantile esotropia
Localize the Lesion

Nucleus
Ipsilateral VI n palsy
Ipsilateral LMN type of Vll n palsy
Failure of horizontal gaze towards the side of the lesion
Fasciculusas the Fibers Pass through

PPRF - Foville syndrome Ipsilateral V, VI, VII, VIII n palsy + central Horner
syndrome
Pyramidal tractMillard Gubler syndrome ipsilateral VI n + contralateral
hemiplegia
Basilar Part
Acoustic neuroma VI n palsy + hearing loss + decreased corneal sensation
Nasopharyngeal tumors
Raised ICTmay cause bilateral VI n palsies
Basal skull fracture
Gradenigo syndrome VI, VII, VIII n affected
Intracavernous Part
III, IV, VI are also affected
VI n more prone to damage as it runs in the middle of the sinus, in close
relation with the internal carotid artery
Intraorbital PartSupplies the Lateral Rectus
Treatment
If all tests are normalobserve for 6 monthsthen correct surgically
If pain persiststrial of steroids: 60 mg oral prednisone 5 days (If dramatic
improvementcould be Tolosa-Hunt syndrome)
Surgery:
With full muscle sequelae ipsilateral LR resection + ipsilateral MR
recession
Incomplete muscle sequelae ipsilateral LR resection + contralateral
MR recession
TOLOSA-HUNT SYNDROME
Non-specific granulomatous inflammation, acute or subacute in onset,
involving the superior orbital fissure or anterior cavernous sinus
Painful ophthalmoplegiapartial/totalinvolving III, IV, V (partial), VI n
Steady boring pain in and around the eye
Dramatic response to steroids; spontaneous remissions
Sensory defects in the distribution of ophthalmic branch of V n
Pupil may benormal; dilated and fixed; small; partially dilated and sluggish
Investigations
CT-scan, MRI, arteriographylook for involvement of structures outside the
cavernous sinus
Treatment
Oral prednisolone 1 mg/kg wt dailygradually taper off depending on
improvement
OCULAR MYASTHENIA
Chronic neuromuscular disorder characterized by weakness and fatigability
of voluntary muscles
Pathology
Acquired autoimmunity to motor end plate leads to decreased number of
ACh receptors
Involves only extraocular muscles, orbicularis oculi
Epidemiology
Females affected more than males in < 40-year age group
Males are more affected in > 50-year age group
Chronic progressive external ophthalmoplegia
Pharmacologic myasthenic syndrome
Orbital apex syndrome, superior orbital fissure syndrome
III n palsy, internal carotid artery aneurysm
Clinical Features
1. Ptosis
Worsens with fatigue at the end of the day and in sunlight
Lid fatigue testworsens on prolonged up gaze
See saw ptosisif one upper lid is manually elevated, the other becomes
more ptotic
Lid hoppingfluttering of a ptotic lid
Cogan lid twitchif the eyes are rapidly returned from down gaze to
primary gaze, the upper lid elevates excessivelythen droops/twitches
many tunes before returning to fixed position
Contralateral upper lid retraction
2. Ophthalmoparesiscauses diplopia
Can mimic any of the isolated nerve palsies, gaze palsy, chronic
progressive external ophthalmoplegia (CPEO)
3. Saccadic eye movements
Small dart-like movements
4. Dissociated nystagmus
5. Epiphoradue to inadequate blink
6. Peek signdue to orbicularis fatigue
During gentle eyelid closure eyes gradually open spontaneously
7. Ectropiondue to fatigue
8. Bells phenomenondecreased or absent (upward and outward rolling of
eyes on forced eyelid closure against resistance)
9. Pupil fatiguesluggish responses, anisocoria
Investigations
1. Tensilon test:
Edrophonium inhibits acetyl cholinesteraseincreases availability of
acetylcholine (ACh)
Dose: 0.15 mg/kg; up to 10 mg
After administering atropine, 12 mg of edrophonium is injected IV;
look for a positive response
If no adverse reaction occurs after one minute, slowly inject 89 mg and
watch for improvement of ptosis and extraocular muscle movement
within 1 min
If improvement is seen, record as positive
2. Neostigmine test:
In children; when minimum there are ocular manifestations
0.6 mg atropine 20 min before the procedure, is administered
1.5 mg neostigmine IM into the deltoid
Dose: 0.04 mg/kg in kids
Peak effect in 30 min
Contraindicated in bronchial asthma, cardiac arrhythmias
3. Sleep test:
Close eyes and rest for 30 minptosis improves
4. Ice pack test improves ptosis
5. Curare test:
< 1/10 of d-curarine dose causes paralysis
6. Electrophysiological tests:
Repetitive supramaximal motor nerve stimulation
Single-fiber EMG
7. ACh receptor antibody assay
8. Muscle biopsyquantification of ACh receptors; deposition of immune

complexes at motor end plate
9. CT-scan/MRIto rule out thymoma
Management
Symptomatic Treatment
Acetyl cholinesterase inhibitors: pyridoxine 60 mg BD, neostigmine 15 mg
BD
Crutch glasses
Immunotherapies
Steroids60 mg prednisolone (1 mg/kg wt); then taper
Cytotoxic therapyazathioprine 35 mg/kg wt
Plasmapheresisrepeated exchanges over a short period of time
Intravenous immunoglobulinhuman gamma globulin 0.4 gm/kg for
3 days
Surgery
Thymectomy
Preoperative plasma exchange
Postoperative anticholinesterase drugs and immunosuppressives
HORIZONTAL GAZE PALSIES

Internuclear Ophthalmoplegia (INO)
Disorder of conjugate lateral gaze
Affected eye show impairment of adduction
Lesion in MLF (medial longitudinal fasciculus)
Causes
Demyelination, trauma, encephalitis, brain stem tumors
Vascular disease, drug-induced
Multiple sclerosis
Bilateral INO can develop
In Right INO
On left gaze there is defective right adduction and ataxic nystagmus of
left eye
Right gaze is normal
Convergence is intact
Vertical nystagmus on attempted up gaze
Investigations
Blood sugar, complete blood count
FTA-ABS, VRDL
Lyme titer, toxicology screen, MRI
Myasthenia gravis
One and a Half Syndrome

Combined lesion of MLF and PPRF (paramedian pontine reticular formation)
on the same side
Conjugate horizontal gaze palsy in one direction and an internuclear
ophthalmoplegia in the other
Ipsilateral gaze palsy; only movement which remains is abduction of the
contralateral eye, with ataxic nystagmus
HORNERS SYNDROME
Lesions involving the sympathetic pupillomotor pathway from the
hypothalamus till its termination cause this syndrome
Clinical Features
1. Miosis:
Anisocoria of 0.81.0 mm; prominent in dim light
Normal reaction to bright light and accommodation
2. Partial ptosis of the upper lid and inverse ptosis of lower lid because of
paralysis of Mullers muscle
3. Anhidrosis:
Affecting half body and facein central lesions (hypothalamus)
Affecting the facein lesions proximal to carotid bifurcation
Absentin postganglionic lesions (distal to superior cervical ganglion)
4. Enophthalmosnarrowing of palpebral fissure
5. Loss of cilio-spinal reflexin preganglionic and post-ganglionic lesions
In congenital Homers syndrome heterochromia iridis occurs
Causes
Centralhypothalamus and brain stem lesions
PreganglionicPancoasts tumor, Klumpkes paralysis, breast cancer,
lymphoma
Postganglionicneck trauma, carotid vascular disease, nasopharyngeal
tumors
Tests
Cocaine Test
Cocaine prevents reuptake of noradrenaline
Normal pupildilates after 3040 min
Horners pupilno change in pupillary size
Hydroxy Amphetamine (1%) Test
It stimulates noradrenaline release at myoneural junction
In central and preganglionic lesions (1st and IInd order neurons)pupil
dilates
In postganglionic lesions (IIIrd order)poor dilatation of pupil
PSEUDOTUMOR CEREBRI
Usually in young obese females, 2045 years of age
Headache, nausea and vomiting
No altered consciousness or higher cognitive function
Tinnitus, ocular pain
Transient visual obscurations
Intermittent horizontal diplopiaworsens with valsalva maneuver
No RAPD
Fundus
Bilateral, hyperemic edematous optic discs
Striations within the nerve fiber layer
Engorged tortuous veins
Peripapillary hemorrhages, cotton wool spots
Patons linescircumferential retinal folds
Eventuallyoptic atrophy occurs
Visual Fields
Enlarged blind spot, inferior nasal defect, arcuate defect
Generalized constriction, centrocecal scotoma
Four Criteria
1. Raised ICTconfirmed on lumbar puncture
2. Normal cerebral anatomy
3. Normal CSF analysis
4. Signs and symptoms of raised ICT, e.g. papilledema
chapter
Oculoplasty 10
NON-SPECIFIC ORBITAL INFLAMMATORY

DISEASE (NSOID)
Non-specific, benign, idiopathic inflammation characterized by poly
morphous lymphocytic infiltrate with varying degrees of fibrosis
Usually unilateral; bilateral in kids and in lymphoproliferative disorders
Pathology
Perivascular lymphocyte cuffing and capillary proliferation
Diffuse retro-orbital soft tissue infiltration
Lymphoid hyperplasia with fibro-fatty tissue
Types
Primaryidiopathic
Secondaryin Wegeners granulomatosis, PAN, systemic sclerosis, Tolosa-
Hunt syndrome, and sarcoidosis
Clinical Features
Soft tissue swelling lid edema, chemosis
Impaired ocular motility diplopia
Abrupt onset of painful proptosis
Ptosis, defective vision
Associated papilloedema or iritis in kids
Ill-defined orbital mass
Course
Spontaneous remission in a few weeks
Prolonged intermittent episodes with eventual remission
Severe prolonged inflammation with progressive fibrosis of orbital tissues
Frozen orbit
Investigations
BloodESR, ANA, Rh factor, C-ANCA, anti dsDNA, SS-A, SS-B, ACE, serum
calcium
Histopathological examination after biopsy
B-scanT sign of the choroid
CT-scan orbituniform enlargement of muscle and tendon; scleral thinning
Contrast CT-scan: Contrast enhancement of sclera due to tenonitisRing

sign
CSFpleocytosis
Subtypes
1. Dacryoadenitis
Downward and inward proptosis
Injection over lacrimal gland; tenderness
Dry eye; S shaped ptosis
2. Myositis
Pain on ocular movement that increases in the field of action of muscle
Lid edema, ptosis, chemosis
Diplopia, injection over muscle
Mild proptosis
3. Anterior NSOID
4. Apical NSOID
5. Diffuse NSOID
Orbital cellulitis
Ruptured dermoid cyst
Malignant orbital tumors
Wegeners granulomatosis, PAN
Sarcoidosis
Treatment
Oculoplasty 251
THYROID-RELATED ORBITOPATHY
Ocular and orbital pathology due to secondary response to immunological
disorders mediated against the thyroid gland
Patients may be in hyperthyroid state (70%), euthyroid state (20%),
hypothyroid state (10%)
Pathology
The bulk of extra-ocular muscles increases 58 times; becomes firm and
rubbery
Tendons are not involved
Pathogenesis
Organ specific autoimmune disorder
Congestive stage there is infiltration by lymphocytes, plasma cells,
macrophages, mast cells
Proliferationof fat, lacrimal gland, connective tissue; causing fluid retention
Hypertrophy of extraocular muscles (EOMs)due to increase in glycos
aminoglycans
Fibrosis degeneration of muscle fibers
Clinical Features
Active stage: Eyes are red and painful
Quiescent stage: Eye are white, painless; motility defects occur
Werners Classification (No Specs)
Class 0 No signs or symptoms
Class 1 Only eye lid signs
Dalrymples sign - Upper lid retraction
Von Graefes sign - Upper lid lag on down gaze
Kochers sign - Starring, frightening look
Griffiths sign - Lower lid lag on up gaze
Bostons sign - Uneven jerky upper lid movement on inferior movement
Jellineks sign - Abnormal pigmentation of upper lid
Rosenbachs sign - Tremor of gently closed lid
Stellwags sign - Incomplete, infrequent blink
Pochins sign - Decreased amplitude of blink
Class 2 Soft tissue involvement with signs and symptoms
0absent
aminimal
bmoderate
cmarked
Enroths signLid edema
Goldzihers signDeep injection of conjunctiva temporally
Giffords sign - Difficult eversion of upper lid
Reismans sign - Bruit over eyelid

Snellen-Donders sign - Bruit over globe
R - resistance to retropulsion
E - edema of conjunctiva
L - lacrimal gland enlargement
I - injection of conjunctiva
E - edema of lid
F - fullness of lids
Class 3 Proptosis
0 : Absent
a : 34 mm over upper limit (upper limit = 21 mm)
b : 57 mm over upper limit
c : 8 mm or more over upper limit
Class 4 Extraocular muscle involvement
0 : Absent
a : Limitation of movement in extreme gaze
b : Evident restriction of movement
c : Fixation of globe
Kildares signJerky horizontal movements
Mohins signWeakness of convergence
Sukers signInability to hold fixation in extreme lateral gaze
Ballets signParalysis of one or more extraocular muscles
Class 5 Corneal involvement
0 : Absent
a : Exposure keratopathy
b : Ulceration
c : Perforation
Class 6 Sight loss (due to optic nerve involvement)
0 : Absent
a : Disc pallor/papilloedema; vision 6/6 6/18
b : Disc pallor/papilloedema; vision 6/24 6/60
c : Optic atrophy; vision < 6/60
Kneiss signUneven pupillary dilatation in dimness
Loewes signDilatation of pupil with 1 : 1000 adrenalin
Cowens signPupillary jerky constriction to consensual reflex
Clinical Features
Soft Tissue Involvement
Periorbital/lid edema leads to retro-orbital fat prolapse into lids;
Treatment: head elevation, diuretics
Conjunctival hyperemia - reflects disease activity
Chemosis; Treatment: tear substitutes, taping of lids
Superior limbic keratoconjunctivitis
Treatment: acetyl cysteine 5%
Keratoconjunctivitis sicca due to infiltration of lacrimal gland; Treatment:
lubricants
Oculoplasty 253
Lid RetractionUnilateral or Bilateral

Levator muscle:
Undergoes contraction, fibrosis, adhesions
Over action due to tethering of inferior rectus
Muller muscle:
Sympathetic over-stimulation due to raised T4
Treatment: Recession of lower lid retractors, blepharoplasty (recession
of LPS; fillers in upper and lower lids), lateral tarsorrhaphy
Proptosis: Axial, Permanent in 70%
Treatment:
Systemic steroidsif rapidly progressive and
Painful proptosis
Intravenous methyl prednisolone
Radiotherapy
Surgical decompression:
2 wall (antro-ethmoidal) 36 mm
3 wall (+ lateral wall) 610 mm
4 wall (+sphenoid) 1016 mm retroplacement
Restrictive Myopathy
Can cause diplopia in the infiltrative phase or fibrotic phase
Inferior rectus and medial rectus are frequently affected; all recti could be
involved
Treatment:
IR/MR recession
Botulinum toxin injection into the muscle
Optic Neuropathy Due to
Direct compression or
Compression of blood vessels at apex
Signs
Decreased visual acuity, defective red-green perception
Optic atrophy
Treatment
Steroids, immunosuppression, plasmapheresis, radiotherapy, surgical
decompression
ORBITAL DECOMPRESSION
Indications
Graves ophthalmopathy with corneal exposure, visual changes, optic
neuropathy, diplopia, disfigurement
If fat or fat and muscle expansion occurs and Hertels exophthalmometry
reading >25 mm orbital fat decompression may be done (alternative to
bony decompression) in a quiescent stage
Bony Decompression
2 wall (antro-ethmoidal/inferior and medial wall) = 36 mm
3 wall (antro-ethmoidal + lateral wall) = 610 mm
4 wall (antro-ethmoidal + lateral wall + sphenoid) = 1016 mm of
retroplacement
Rule of Thumb
Reduction of exophthalmos is directly proportional to the number of
decompressed walls (23 mm per decompressed wall)
Complications
Sinusitis
Lower lid entropion
CSF leaks
Numb lips
Frontal lobe hematoma
Oculoplasty 255
BASAL CELL CARCINOMA

Carcinoma involving basal cell layer of epidermis; invades the dermis
Rodent/Jacob ulcer
Carcinogenesis
1. Xeroderma pigmentosum deficient DNA repair enzymes
2. UV rays
3. Chemical carcinogenesisdue to a chemical agents which act as initiators
and promoters
Epidemiology
Males; > 40 years age group, fair-skinned individuals, sun-exposed
individuals
Risk Factors
Congenital Xeroderma pigmentosum, albinism, Gorlin-Goltz syndrome
Acquired UV rays, ionizing radiation, thermal burns, scar tissue, arsenic
exposure
Clinical Features
Usually occurs above Reeds line imaginary line from tragus to angle of
mouth (tear flow area)
Localized form nodular, ulcerative or cystic
- 75%
- Small papules, pearly appearance, thin epidermis
- Increases in size with central umbilication, erosion or ulceration
Diffuse form morphea form or sclerosing type
- 15%
- Flat indurated plaque whitish pink to yellow in color
- Overlying epidermis intact
Superficial form erythromatous
- On trunk; multifocal
- Slow growing scaly red patches
- Peripheral, translucent rolled-out border and central epidermal
atrophy
Fibro-epitheliomatous type
- On trunk; sessile with dome-shaped surface
- Nodular plaque
- Polypoid lesion
- Erythromatous/skin colored
Pigmented type
- Cells get pigmented on staining with Dopa
Pathology
At junction of pilo-sebaceous duct and epidermis
1st signnidus of cells in upper dermis
Club-shaped rete cells and geographic cell patterns in dermis

Interaction with dermis produces marginal palisade-surrounded by well-
organized stroma
Retraction space
No lymph node involvementlarge-sized tumor cells do not pass through
the lymphatic channels
Initially locally invasive tumor; in the late stageshematogenous spread
Squamous cell carcinoma
Pigmented sebaceous gland carcinoma
Placoid dermal melanomas
Management
1. Surgery:
a. Mohs micrographic technique
b. Small tumorwide excision
c. Large tumor with skin defect:
Excision with medium and lateral advancement flap
Rotational skin flaps
Skin graft fromretroauricular area, supra clavicular area, inner
arm, inner thigh
2. Cryosurgery: Rapid freezing and thawing
3. Laser treatment: CO2 laser vaporizes the tissue
4. Radiotherapy: Inhibits mitosis
5. Chemosurgerycauterizing chemical used to evoke peeling and destruction
of superficial lesions; chemicals used are mono/di/trichloroacetic acid
6. Cytotoxic agents:
In small superficial BCC topical imiquimod 5% cream twice daily x 16
weeks
Methotrexate, colchicine, podophyllin, cisplantin
7. Photdynamic therapy:
IV Hp D (hematoporphyrin derivative) given 48 hrs prior to 630 nm of
Argon pumped dye laser
Pigment absorbs dye and facilitates destruction
8. Interferon-
9. Retinoids etretinate and isoretinoin
Oculoplasty 257
XERODERMA PIGMENTOSUM
Autosomal recessive, congenital
Inherent defect in DNA repair
Predisposes to basal cell carcinoma and squamous cell carcinoma
Stages
1. Sun sensitivity
2.
Pigmentation
3.
Carcinomas (squamous and basal cell carcinoma of lids and exposed parts)
UV light causes changes in DNA segments
Normally: Damaged DNA segments are removed and repaired by enzymes
In XP: Defective enzymes systems leads to abnormal DNA repair defective
DNA
Prophylaxis
Prevent exposure to UV light
SQUAMOUS CELL CARCINOMA

Predominant cell type is squamous or prickle cell of epidermis
Causes
UV light DNA damage
HPV type 16 Conjunctival neoplasia
Conjunctivalization of cornea
Exposure to dust/wind/chemicals like trifluridine and arsenic
Pterygium
Ocular surface injury
Vitamin A deficiency
Premalignant Lesions
1. Actinic keratosis:
Flat, scaly keratotic lesions on a telangiectatic base
Associated with UV light exposure
2. Bowens disease:
Isolated erythematous, scaly, crusty, pigmented, keratotic plaque at
limbus
3. Radiation dermatosis:
Early erythema, edema, pigmentation
Late Skin atrophy with necrosis
4. Xeroderma pigmentosum
Spread
Lymphatic spread:
From outer canthus, outer 2/3rds of upper lid, outer 1/3rd of lower lid
Preauricular lymph nodes
From inner canthus, inner 1/3rd of upper lid, inner 2/3rds of lower lid
Submandibular lymph nodes
Direct spreadin chronic cases

Perineural spreadto orbit and intracranial cavity along VII n and V n (7th
and 5th cranial nerves)
Local extensionto orbit, lacrimal passages, eyeball, nose, face, cranial
cavity
Oculoplasty 259
Conjunctiva Lids
Clinical Lesion at corneoscleral junction in Painless small hard nodule or rough
features interpalpebral area warty keratotic plaque
Rough, irregular, exophytic mass Erosions and fissures with crusts
Types 1. Gelatinous tufted superficial blood vessels 1. Ulcerative base is indurated
and hyperemic; edges hard and
undermined
2. Nodular rapidly growing; increased 2. Papillomatous
tendency to metastasis
3. Diffuse 3. Cystic growth
4. Cutaneous horn
Pain due toinvolvement of supraorbital or infraorbital nerves

Late stages hemorrhage, meningitis, cachexia
Histopathology
Dysplasia
Mildinvolving < 1/3rd thickness of epidermis
Moderateinvolving <3/4th thickness
Severeinvolving full thickness; atypical cells
Carcinoma-in situ dysplasia + loss of normal surface layer
Invasive squamous cell carcinoma invasion of substantia propria after
basal epithelial layer breached
Spindle cell typemost common
Epidermoid cell/pavement/prickle cell typeleast common; large
polyhedral cells with large nuclei
Clear cell small cells with hyperchromatic nuclei
Mucoepidermoid/goblet cellcuboid cells arranged in nests and cords
with secreted pools of mucin in extracellular spaces
Dyskeratosis
Presence of epithelial pearls
Compressed laminated masses with peripheral cylindrical cells, central
squamous cells undergoing cornification which are surrounded by large
prickle cells
Treatment
1. Surgery:
Mohs microsurgical technique
Wide excision
Orbital exenterationif tumor extends into orbit, or perineural
involvement
Lymph node dissection
Enucleation if intraocular extension
2. RadiotherapyStrontium 90, -irradiation

3. CryotherapyN2O cryoprobe
Repeated rapid freeze and slow thaw
Double freeze thaw
4. Immunotherapy/Chemotherapy:
DNCB (Dinitrochlorobenzene)
Urea
Thiotepa
Cisplatin alone or with doxorubicin, bleomycin, isotretinoin
For superficial lesions topical imiquimod 5% BD x 16 weeks along with
aloe vera cream
Lids
Inverted follicular keratosis
Seborrheic keratosis
Keratoacanthoma
Conjunctiva
Pterygium, pingecula
Papilloma, nevus
Pyogenic granuloma
Dermoid
Keratoacanthoma
Moorens ulcer
Oculoplasty 261
BOWENS DISEASE
Dysplastic changes seen throughout the entire epithelium but basement
membrane not breached
Also called dysplasia/carcinoma-in situ/ocular surface squamous metaplasia
5060 years age group; males affected more than females
Etiology
Same as for squamous cell carcinoma
Clinical Features
Slightly elevated, sharply demarcated nodule
Accompanied by feeding vessels
Pearly gray/reddish gray
In the interpalpebral fissure area, common at limbus
Types
Gelatinous, velvety, papilliform, leukoplakic, nodular, diffuse form
Malignant melanoma regular smooth surface
Papilloma sessile/pedunculated with a punctate vascular pattern
Benign neviless pigmented
Pseudoepitheliomatous hyperplasia
Related Conditions
Xeroderma pigmentosum, HTV, pterygium
Investigations
Exfoliation cytology, impression cytology, histopathology after biopsy
Treatment
1. SurgeryMohs micrographic technique
2. Radiotherapywith Strontium 90 (-irradiation) and radium (-irradiation)
Complications dry eye, cataract, telangiectasias, symblepharon, corneal
perforation
3. Excision of tumor + 2 mm of healthy conjunctiva followed by cryotherapy
(double freeze thaw)
Destroys cells by thermal effect
Obliterates microcirculation causing infarction of normal and tumor
tissue
4. Immunotherapywith DNCB, urea, topical imiquimod
5. Chemotherapy:
Topical mitomycin 0.02% QID for 1022 days
Tretinoin for early dysplasia
MEIBOMIAN GLAND CARCINOMA

Most common malignant lid tumor in India
Common in lids because meibomian glands more; also occurs in caruncle,
eyebrows
Females more affected; 6070 years
Upper lid involvement more common than lower lid
Spread to lacrimal gland, nasolacrimal duct, orbit, preauricular/
submandibular/deep cervical lymph nodes
Sites of Origin
Meibomian glands, Zeis glands, sebaceous gland of caruncle/eyebrows
Pathology
Infiltrating nodules:
Unencapsulated masses with infiltrating margins
Mimics chalazion
Finely vacuolated frothy cytoplasm
Conjunctival intraepithelial spread
Tumor cells spread down the duct of Zeis or superficially within epidermis
or tarsal conjunctiva
Cells directly infiltrate epithelium radially
Types
1. Nodular
2. Noduloulcerative
3. Pagetoid (diffuse)
Strasmas Criteria
1. Tumor should arise from tarsal plate
2. Should be continuous with tarsus
3. Should have histopathological evidence of meibomian gland carcinoma
Management
Surgery
Wide local excision with frozen section
Excision following conjunctival map biopsy all quadrants of globe,
fornices, tarsal plate sampled and mapped (17 points to be sampled)
Exenteration fororbital invasion, pagetoid variants
Radical surgery lacrimal gland removed, nasolacrimal duct sealed
Radiotherapy
In very old, ill patients
Oculoplasty 263
Chemotherapy
For sclerosing/pagetoid type
Upper Lid Reconstruction
Lower Lid Reconstruction
Diffuse squamous cell carcinoma
Kaposis sarcoma
Recurrent chalazion
Chronic conjunctivitis/blepharitis
Chronic fungal infection
Enucleation
Removal of entire globe, including cornea and sclera
Indications
Severely traumatized eye which have an increased risk of sympathetic
ophthalmia enucleate within 14 days
Intraocular malignancy
To prevent extraocular extension or distant metastasis
Care must be taken not to open the globe
Gentle handling of tissue required to minimize risk of dissemination
Painful blind eye without potential for useful vision, e.g. absolute glaucoma,
inextricable foreign body
Deformed phthisical eye
Eye with no light perception and opaque media
Hemorrhage, infection
Globe perforation
Perforation of bony orbit
Failure to get an adequate length of optic nerve
Evisceration
Removal of contents of globe leaving sclera and optic nerve intact
Indications
Acute suppurative endophthalmitis or panophthalmitis not responding to
treatment
Painful blind eye, e.g. absolute glaucoma
Blind deformed eye: Cosmetic correction evisceration with artificial eye
implant
Advantages
Less chances of fat atrophy due to less disruption of orbital anatomy
Good motility of prosthesis because extraocular muscles remain attached
to scleral coat
Decreased chance of contamination of orbit or intracranial extension
Disadvantage
Sympathetic ophthalmitis can still occur
Infected scleral rims left behind may cause recurrent infections
Exenteration
Removal of all soft tissues of orbit along with the periosteum, including the
globe
Indications:
Orbital mucormycosis
- Eyelid tumors with orbital extension
- Extensive orbital malignancies without intracranial extension
Oculoplasty 265
LATERAL ORBITOTOMY
An opening made in the lateral wall of the orbit to gain access to mid and
deeper orbital lesions within and outside the muscle cone
Indications
1. Choristomas
Dermoid cyst
Epidermoid cyst
Teratoma
Ectopic lacrimal gland
2. Hamartomas
Hemangioma
Lymphangioma
Neurofibroma
AV malformations
3. Inflammation
Orbital abscess
Graves disease
Fronto-orbital mucocele
4. Implantation cyst in the orbit
5. Neoplasms
Primary
Schwannomas
Optic nerve glioma
Optic nerve meningioma
Lacrimal gland tumors
Secondary
Astrocytoma
Sphenoidal ridge meningioma
Complications
Hemorrhage
Conjunctival prolapse/dessication
Diplopia due to extensive traction on lateral rectus
Fibrous adhesions
Ptosis
Dry eye due to removal of lacrimal gland
Damage to pupillary fibers
Damage to cranial nerves
Loss of corneal sensation
Retinal detachment
Intraocular hemorrhage
Vision loss due to:
Direct manipulation of optic nerve
Damage to posterior ciliary artery
Blind dissection of tumors attached to optic nerve
CRAO
AION
SOCKET RECONSTRUCTION
Contracted socket When the fornices and/or volume of the socket are
inadequate to allow retention and motility of a prosthesis
Procedure
Incision/excision of scarred tissues
For surface contractionFull thickness buccal mucosal graft placed in the
defect; fix a silicone stent to the superior and inferior orbital rims with a
fornix formation suture
Six months later a mold is placed in socket immediately after removing stent
A prosthesis is made and fit
For volume loss secondary implants or dermis fat graft
Indications
Congenital
Anophthalmos
Congenital contracted socket
Acquired
Enucleation
Evisceration without implants
Phthisis bulbi
Atrophic eye
Trauma
Orbital Implants
1. Autogenous:
ExampleSkin/fascia
Mucous membrane
Bone/cartilage
Dermis fat graft
2. Alloplastic:
ExampleGlass, titanium
Acrylic, MEDPOR
Hydroxyapatite
3. Conformers
4. Artificial prosthesis
Oculoplasty 267
BLEPHAROPTOSIS
Abnormally low position of upper eyelid (drooping)
Classification
Neurogenic Myogenic Mechanical Aponeurotic
III n palsy Myasthenia Tumors Involutional
gravis
Horners syndrome Myotonic dystrophy Lid edema Post-trauma
III n misdirection Ocular myopathy Dermatochalasis Post-lid surgery
Marcus Gunn jaw Simple congenital Scars Following
winking ptosis dermatochalasis
Blepharophimosis Anterior orbital
syndrome lesions
Evaluation
History Measurement Associated signs
Age of onset Margin reflex distance 1 and 2 Contralateral lid retraction
Duration Vertical fissure height Fatigability
Diplopia Margin crease distance Cogan twitch sign
Systemic disease Margin limbal distance Bells phenomenon
Diurnal variation LPS function Herings reflex
Fatigue Pretarsal show Jaw winking phenomenon
Trauma Ocular motility defects
Surgery
Neck swelling
Pseudoptosis
Lack of globe support, e.g. enophthalmos, microphthalmos
Dermatochalasis
Hypotropia
Brow ptosis
Contralateral lid retraction
Simple Congenital Ptosis

Due to failure of neuronal migration/developmentwith muscle sequelae
Absent upper lid crease (not always)
Poor levator function (not always)
In down gaze, the ptotic lid is higher than normal due to poor relaxation of
the levator
May be associated with superior rectus weakness
Compensatory chin elevationin bilateral ptosis

Refractive errorsmay lead to amblyopia
Treatment: Temporary sling with ethibond; to decide later on LPSR based
on LPS action
Blepharophimosis Syndrome
Symmetrical ptosis with poor levator function
Short horizontal palpebral aperture
Telecanthus, epicanthus inversus
Lateral ectropion of lower lids
Poorly developed nasal bridge
Hypoplasia of superior orbital rims
Treatment: 1st correct epicanthus and telecanthus; then after some months,
ptosis is corrected by bilateral frontalis suspension
Aponeurotic Ptosis
Dehiscence, disinsertion or stretching of levator aponeurosis
Restricts transmission of force from a normal levator muscle to the upper
lid
Variable bilateral ptosis with good levator function
High upper lid crease ( 12 mm) because posterior attachments of
aponeurosis to tarsus have detached but anterior attachments to skin are
intact
In severe cases, upper lid crease absent
May get worse at end of day because of fatigue of Muller muscle
Treatment:
Levator re-insertion and resection
Anterior levator aponeurosis repair
Oculoplasty 269
ENTROPION
Inturning of the lid margin
Types
Involutional/Senile Entropion
Occurs in lower lid only because upper lid has a broader tarsus and is stable
Pseudo-trichiasis rubbing of lashes against cornea results in punctate
epithelial erosions, ulcer, pannus in the cornea
Pathogenesis:
Age-related degeneration of elastic and fibrous tissues within the eyelid
Stretching of canthal tendons and tarsal plate horizontal lid laxity
Attenuation, dehiscence, disinsertion of lower lid retractors vertical lid
instability
Weakness of lower lid retractors decreased excursion of lower lid in down
gaze
Over-riding of pre-tarsal orbicularis by pre-septal orbicularis during lid
closure upper border of tarsus moved towards globe
Treatment:
Lubricants, taping
Botulinum toxin injection into orbicularis muscle
Bandage contact lens when cornea is involved
Surgery:
When horizontal lid laxity is absent
Transverse everting suturesprevents over-riding of preseptal orbicularis
Weis procedurefull thickness horizontal lid splitting; insertion of
everting sutures
Jones proceduretightens the lower lid retractors and creates a barrier
between pre-septal and pretarsal orbicularis
When horizontal lid laxity is present
Quickert proceduretransverse lid splitting; insert everting sutures +
horizontal lid shortening
Cicatricial Entropion
Severe scarring of palpebral conjunctiva pulls lid margin towards globe
Causes:
Trachoma, cicatrizing conjunctivitis, cicatricial pemphigoid, chemical injury,
trauma
Treatment:
Bandage contact lens
Mild cases transverse tarsotomy (tarsal fracture) with anterior rotation of
lid margin
Severe casesreplace deficient or keratinized conjunctiva; replace scarred

and contracted tarsus with composite grafts
Congenital Entropion
Upper lidsecondary to microphthalmos
Lower lid:
Due to improper development of inferior
Retractor aponeurosis
Absence of lower lid crease
In turning of lower lid and lashes
Treatment:
Hotz procedureexcision of a strip of skin and muscle; and fixation of skin
crease to tarsal plate
Oculoplasty 271
ECTROPION
Involutional Ectropion
Clinical Features
Horizontal lid laxity 8 mm
Medial canthal tendon laxity > 2 mm
Lateral canthal tendon laxity > 2 mm
Treatment
Medial ectropionLazy T procedure
Generalized ectropion Horizontal lid shortening
Marked generalized ectropion with excess skinKuhnt-Szymanowski
procedure
Cicatricial Ectropion
Causes
Trauma, burns, icthyosis, dermatitis
Scarring and contracture of tissue pulls lid away from globe
Treatment
Mild, localizedExcision of scar + Z plasty
Severe, generalizedFree skin grafts, transposition flaps
Paralytic Ectropion
Causes
VII n palsy
Clinical Features
Brow ptosis, lid retraction, exposure keratopathy, epiphora
Treatment
Taping of lids, lubricants, tarsorrhaphy, lateral canthal sling
If medial canthal laxity presentMedial wedge resection
If medial canthal tendon intactMedial canthoplasty
Mechanical Ectropion
Causes
Tumors at/near lid margin
Treatment
Remove the cause
PHAKOMATOSES
Group of developmental anomalies
Tumor-like malformations (hamartomas) in tissues of ectodermal originin
skin, eyes, CNS
Hamartoma congenital tumor made of an abnormal mixture of tissue
elements or an abnormal proportion of a single element, usually found in
the organ
Tuberous Sclerosis (Bourneville Disease)

Clinical Features
Adenoma sebaceum:
Presents at 25 years of age; in 90% of patients with tuberous sclerosis
Multiple reddish-brown nodules over nose
Cheeks in a butterfly pattern
Enlarge until puberty
Telangiectasias on nose
Shagreen patches:
Leathery, thickened skin plaques on the lower back
Caf-au-lait spots
Subungual hematomas
Skin tags: Molluscum fibrosum pediculum
Fibrous plaques on forehead
Ash leaf spots: Hypopigmented patches on trunk, limbs, scalp (Detected by
woods lamp in infants)
Scattered astrocytic cerebral hamartomas (in all patients)
Renal (angiomyolipomas) and cardiac (rhabdomyomas)
Triad: epilepsy, mental retardation, adenoma sebaceum
In Eye
Retinal astrocytomas
Hypopigmented spots on iris and retina
Papilledema
VI n palsy (due to raised ICT)
Von Hippel-Lindau Disease

Angiomatosis retinae
AD inheritance
2nd decade
Life-threatening
In Eye
Capillary hemangiomasinvolving retina and/or optic nerve head
Blurring of vision due to macular exudates/retinal detachment
Ocular pain due to secondary glaucoma
Localized reddish-yellow mass in retinal mid-periphery; fed and drained by
a dilated and tortuous artery and vein respectively
Oculoplasty 273
Secondary exudative changes macular star formation

Tumor grows towards vitreous; may invade choroid
Cataract, iridocyclitis, phthisis bulbi
Tumor on optic discmimics optic neuritis, papilloedema (no dilated
arteries/veins when on the disc)
FFA
Early phase delineates the feeding and draining vessels
Late phase diffuse leakage of dye from tumor (due to transudative nature)
Systemic Features
Cerebellar hemangioblastomaheadache, nausea and vomiting, cerebellar
disturbances
Spinal cordusually asymptomatic
Cysts in pancreas, kidney (life-threatening), adrenals, liver, spleen, ovaries,
urinary bladder
Renal cell carcinoma, pheochromocytoma
Treatment
1. Xenon arc photocoagulation (for medium and large-sized lesions)
2. Argon laser photocoagulation (for < 0.8 DD angiomas)
3. Cryotherapy triple freeze thaw
For peripheral angiomas; thick angiomas with surround-ing RD
Repeated every 6 wks till tumor regresses
4. Plaque brachytherapy with I131 or Ru106
Investigations
CT-scan, MRI, ultrasonography, renal angiography
Family members should be screened
Neurofibromatosis
von Recklinghausens disease
It progresses to invade spinal canal or cranium; can infiltrate or compress
vital organs
Transformation to sarcoma is rarecalled neurofibrosarcoma
Clinical Features
Caf-au-lait spots: 6 in number
Tan colored, macular (flat) configuration with smooth edges
Hyperpigmentation of basal cell layer of epidermis
Fibroma molluscum: Soft pedunculated nodules over body
Abnormal sexual maturation and bone growth
Hemi-hypertrophy of face
Plexiform neurofibroma
Contiguous involvement of multiple superficial nerves
In upper lid, adjacent temple, side of face
In brain, meninges, spinal cord, cranial nerves

Any viscera, gut
Associated with endocrine abnormalities:
Hyperparathyroidism, myxedema, Addisons disease, diabetes mellitus,
tetany
Conjunctiva Small localized elevated tumors that are firm, non-tender, fixed, covered by
normal epithelium
Cornea Lignes grises large hyperplastic prominent intrastromal corneal nerves
Iris Lisch nodules, congenital ectropion uveae, mamillations
Choroid Choroidal nevi
Retina Medullary nerve fibers, hamartomas
Optic nerve Gliomas
Lids Fibroma molluscum, S shaped eyelid, schwannoma, caf-au-lait spots, plexiform
neurofibroma (bag of worms on palpation), elephantiasis of lids
Orbit Greater wing of sphenoid absent, spheno-orbital encephalocele, pulsatile
exophthalmos (transmitted pulsations)
Glaucoma Angle infiltration by neurofibromatous tissue, congenital angle anomaly, angle
closure (forward displacement of lens-iris diaphragm), fibrovascular membrane
in angle contractssynechial angle closure
Sturge-Weber Syndrome
Encephalofacial angiomatosis
No genetic transmission
Clinical Features
Port wine stain/Nevus flammeus:
Facial angiomatosis
1 or more red patches, unilateral
Over upper 1/3rd of face
Flat; does not change with age
Ipsilateral hemi-hypertrophy of face
Ipsilateral lepto-meningeal angioma
In the occipito-parietal area
Calcification of small blood vessels Train track sign
Epilepsy, mental retardation, hemiplegia
Jacksonian
Angiomas in kidney, spleen, ovaries, adrenals, thyroid, lungs
In Eye
Ipsilateral telangiectasia of conjunctival and episcleral vessels
Ipsilateral hyperchromic iris
Spontaneous lens dislocation
Tortuosity of retinal vessels
Contralateral homonymous hemianopia
Oculoplasty 275
Glaucoma due to:

Congenital malformation of anterior chamber angle
Raised episcleral venous pressure
Choroidal hemangioma
Diffuse Tomato ketchup fundusdiffuse thickening of choroid
Circumscribed salmon orange color, elevated, sub-RPE masses with
indistinct margins
Serous retinal detachment
Cystoid retinal degeneration
Treatment
1. Manage glaucoma
2. Choroidal hemangioma:
plaque brachytherapy with I131 or Ru106
Photodynamic therapy
PROPTOSIS
Causes
Congenital
Pseudoproptosis (myopia)
Meningo-encephalocele
Craniosynostosis
Neurofibromatosis
Microphthalmia with cyst
Inflammatory
Graves disease
Pseudotumor
Infective
Orbital cellulitis
Cysticercosis
Hydatid cyst
Neoplastic
Neuraloptic nerve glioma, meningioma, schwannoma, neurofibroma
Rhabdomyosarcoma
Lacrimal gland tumorsbenign, malignant
Cystsdermoid, epidermoid, teratoma
Vascularcavernous hemangioma, capillary hemangioma, lymphangioma,
hemangiopericytoma
MetastaticEwings sarcoma, leukemia, neuroblastoma
Fibro-osseusfibrous dysplasia, osteoma
Juvenile xanthogranuloma
Histiocytic tumors
Lympho-proliferative tumors
Vascular
AV fistulas/malformations
Orbital varices and hemorrhages
Oculoplasty 277
ORBITAL CELLULITIS
Orbital soft tissue infection posterior to orbital septum
Causes
Spread of infection from periorbital structuresbrain, sinuses, lacrimal sac,
lids and teeth
Endogenous
Septicemia
Endophthalmitis/panophthalmitis
Exogenous surgery, trauma
Common pathogens are Staphylococcus aureus, Streptococcus pyogenes,
Streptococcus pneumoniae, H. influenzae
Clinical Features
Fever, malaise
Rapid onset
Lids are edematous, red and tender
Conjunctival chemosis
Proptosislateral, downwards
Optic nerve dysfunctionRAPD, decreased vision, defective color vision
Painful ophthalmoplegia
Complications
Exposure keratopathy
Glaucoma
CRAO, CRVO
Optic neuritis
Orbital or subperiosteal
Brain abscess, meningitis
Cavernous sinus thrombosis
Treatment
In Children
If discharge occurs do culture/sensitivity
If subperiosteal/orbital abscess drain culture/sensitivity
Emperical treatment: Intravenous cephalosporins and aminoglycosides; C/S
guidance
In Adults
Amoxycillin + clavulanic acid
4th generation cephalosporin + metronidazole
Assess optic nerve every 4 hours
InvestigationsWBC count, CT-scan, lumbar puncture
Surgery doneif
- Decrease in vision
- Orbital abscess
- Biopsy required
- Unresponsive to treatment
Oculoplasty 279
CAROTICO-CAVERNOUS FISTULA (CCF)

High-flow CCF
Causes
Congenital
Atherosclerotic (spontaneous) rupture of intracavernous aneurysm,
hypertension
Traumatic frontal head injury, basal skull fracture
Clinical Features
Pulsating proptosis, ptosis
Painless, abrupt onset becomes painful
Noise heard in head, synchronous with the pulse
Thrill, bruit widely transmitted; abolished by ipsilateral carotid artery
compression in neck
Conjunctival edema, congestion
Globe displaced downward and outward
Papilloedema optic atrophy
Retinal hemorrhages, venous engorgement and tortuosity CRVO
Opacity of media lens, cornea
Corneaexposure keratopathy, dehydration
Nasal mucosa congestion epitasis
Increased IOP due to raised episcleral venous pressure
Decreased visual acuity
Ophthalmoplegia due to damage/stretching of cranial nerves supplying
the extraocular muscles and engorgement of the muscles
Hypoxic Eyeball Syndrome

Corneal epithelial edema
AC reaction, iris atrophy, NVI
Glaucoma, cataract
Retinal venous dilatation and hemorrhage
Pathology
Blood in vein becomes arterialized
Venous pressure increases
Decreased arterial pressure and perfusion
Low-flow CCF (Indirect/Dural Shunt)

Small, meningeal arterial branches supply dural walls of cavernous sinus
rupture of these branchesb causes a low-flow CCF
Causes
Congenital malformations, spontaneous rupture (in hypertension)
Clinical Features
Dilated episcleral vesselsmedusa head appearance; raised IOP
Mild proptosis, ophthalmoplegia
Bruit, diplopia, transient VIn palsy
Unilateral headache; chronic, unilateral red eye
Treatment
Interventional radiologyintravascular balloon introduced into internal
carotid artery via a catheter and embolized
Cavernous Sinus Thrombosis

Fever, headache
Frontal/retro-orbital pain, diplopia
Ptosis, proptosis, chemosis, ophthalmoplegia
Hyperesthesia of ophthalmic and maxillary divisions of V n
Decreased corneal reflex
Dilated tortuous retinal veins
Papilloedema
Septic cavernous sinus thrombosis is treated with IV antibiotics along with
anticoagulants
Aseptic cavernous sinus thrombosis is treated with urokinase therapy
(thrombolytic agent); recombinant
tissue plasminogen activator (rtPA) + IV heparin
Oculoplasty 281
OPTIC NERVE GLIOMA

Females affected more than males; present in 1st decade
Associated with neurofibromatosis
Intracranial extension chiasma involved (in 50%), ICT, function of
hypothalamus and pituitary gland
Decreased visual acuity precedes onset of proptosis
Unilateral painless, gradual, progressive axial proptosis
Optic discswollen and pale with optociliary shunts
CT-scanshows concentric enlargement of optic foramen; J-shaped sella
MRI shows intracranial extension
Treatment
Progressive enlargement with blind eye radical surgery; excise optic nerve
and preserve globe
Chiasmal extension sterotactic radiotherapy
OPTIC NERVE MENINGIOMA

Near sella early visual field defects, papilledema, optic atrophy
Tumors outside dural sheath burst through dura become exophytic
Proptosis followed by vision loss
Triad: optociliary shunts, vision loss, optic atrophy
Arises from optic nerve sheath
CT-scan:
Tram Track Sign
Lucent center (in optic nerve glioma denser in center)
Tubular thickening and calcification of optic nerve
Normal optic nerve running through tumor Doughnut sign on
coronal CT-scan
Oculoplasty 283
RETINOBLASTOMA
Malignant transformation of primitive retinal cells before final differentiation
Usually presents before 3 years of age
Heritable Non-heritable
40% of cases 60% of cases
Primitive retinal cells predisposed to malignant Arises at a somatic level in a retinal cell
transformation by mutation
Autosomal dominant Non-heritable
Presents around 18 months of age Presents around 2 years of age
50% risk of transmission to offspring No transmission to offspring
Types
1. Infiltrative: Flat, round, white intraretinal infiltration (usually seen in older
children)
2. Endophytic:
Arises from retinal surface
Friable white mass with blood vessels on surface secondary calcification
resembles cottage cheese
Vitreous seeding
3. Exophytic:
Multiglobulated white mass
May have an overlying retinal detachment
Vitreous hemorrhage
Clinical Features
Leucocoria, strabismus, proptosis
Secondary glaucoma, orbital inflammation
Masquerade syndrome
Anterior segment invasionmultifocal iris invasion, painful red eye,
pseudohypopyon
Metastasis brain, bone marrow and regional lymph nodes
International Classification of Intraocular Retinoblastoma
Group Risk Tumor Features

A Very low Small discrete intraretinal <3 mm confined to the retina; located
tumors away from foveola > 3 mm from foveola and >1.5 mm the disc
and disc
B Low All remaining discrete retinal Tumors confined to the retina not in group
tumors without seeding A; any tumor size and location
C Moderate Discrete local disease with Subretinal fluid without gross seeding,
minimal subretinal/vitreous involving up to one-quadrant of retina; local
seeding subretinal seeding <5 mm from tumor; focal
fine vitreous seeding close to tumor
Contd...
Contd...
Group Risk Tumor Features

D High Diffuse disease with Massive/diffuse tumors, almost total retinal
significant vitreous/ detachment; diffuse subretinal seeding; diffuse
subretinal seeding vitreous disease with greasy seeds or avascular
tumor masses
E Very high Presence of any Tumor touching lens, neovascular glaucoma, opaque
one of the poor media from hemorrhage, tumor anterior to anterior
prognostic features vitreous face involving ciliary body or anterior
segment, diffuse infiltrating retinoblastoma, tumor
necrosis with aseptic orbital cellulitis, phthisis bulbi
Rees Ellsworth Classification
Number of tumors Position Size

I A One Behind equator <4 DD
B Many Behind equator <4 DD
II A One Behind equator 410 DD
B Many Behind equator 410 DD
III A One Anterior to equator Any size
B One Behind equator >10 DD
IV A Many >10 DD
B One Anterior to ora Any size
V A More than one Involving more than retina
B Vitreous seeding
Treatment (Depends on Size and Location)

Small Tumors
Laser photocoagulation
Transpupillary thermotherapy
Cryotherapy
Medium Tumors
Brachytherapy
External beam radiation
Chemotherapy (carboplatin + vincristine + etoposide)
Large Tumors
Chemoreduction
Enucleation
If extraocular extension has occurred high-dose chemotherapy
(36 cycles) enucleation/evisceration EBRT continued high-dose
chemotherapy for 12 cycles
If metastasis has occurred metastasis protocols with stem cell rescue
Oculoplasty 285
CHOROIDAL MELANOMA
Pathological Classification
Spindle cell melanomas
Pure epitheloid cell melanomas
Mixed cell melanomas
Necrotic melanomas
Clinical Features
Decreased vision; field defects
Photopsia balls of light passing across visual field, 23 times/day
Elevated, oval, sub-retinal mass
Brown (mottled with pigment) or amelanotic
Orange pigment lipofuscin on tumor surface
Mushroom-shaped if it breaks through bruch membrane
Secondary exudative retinal detachment
Choroidal folds
Masquerade syndrome
Glaucoma, cataract
Optic nerve head involvementrare
Nevus, choroidal hemangioma, choroidal metastasis
Retinal detachment, choroidal detachment
Choroidal granulomas
Posterior scleritis, age-related macular degeneration
B-Scan
Acoustic hollowness
Orbital shadowing
Choroidal excavation
FFA
Dual circulation
Mottled fluorescence in AV phase
Color-coded Doppler
Give to differentiate pigmented tumor from hemorrhage
CT-scan
To look for any extraocular extension
Treatment
Brachytherapy plaque radiotherapy for medium-sized tumors
Charged particle irradiation with protons and helium
Transpupillary thermotherapy with diode laser for small tumors near

optic disc/fovea
Laser photocoagulation for small recurrences
Trans-scleral local resection for rumors < 16 mm
Enucleation for large tumors
Exenteration if extraocular extension
Palliative therapy if metastasis dicarbazine base protocols
chapter
Lens 11
SENILE CATARACT
Cataract: Opacification of the crystalline lens
Morphological Classification
Subcapsular Cataract
Posterior subcapsular cataract is graded from 10100% depending on the
amount of opacification; may be steroid induced
Anterior subcapsular in
Atopic dermatitis
Glaucomflecken following an acute congestive attack in PACG
Nuclear Cataract Grading
I. Definite yellowing; vision 20/2520/30
II. Yellow ++; vision 20/40
III. Yellow/orange; vision 20/60
IV. Brown/brunescent; vision <20/80
Christmas Tree Cataract
Needle-like deposits
Cortical Cataract Grading
I. Cortical cataract with spokes involving one quadrant of the lens
II. Involving two quadrants
III. Involving three quadrants
IV. Involving four quadrants
Classification According to Maturity

Immature senile cataractpartially opaque lens
Mature senile cataract
Hyper mature senile cataractshrunken, wrinkled anterior capsule due to
leakage of water
Morgagnian senile cataracttotal liquefaction of the cortex has allowed
nucleus to sink inferiorly
SECONDARY/COMPLICATED CATARACT
Cataract occurring secondary to other primary ocular disease
Causes
1. Chronic anterior uveitis
Polychromatic luster at posterior pole of lens
Progresses rapidly if posterior synechiae present
2. Acute congestive glaucoma
Glaucomfleckensmall gray-white anterior subcapsular opacities
within pupillary area
Focal infarct of lens epithelium
3. Pathological myopia
Early onset nuclear sclerosis
Posterior subcapsular cataract
4. Hereditary fundus dystrophy
Retinitis pigmentosa
Lebers congenital amaurosis
Gyrate atrophy
Stickler syndrome
5. Fuchs heterochromic iridocyclitis
Cortical white cataract
Lens 289
AFTER CATARACT
Posterior capsular opacification (PCO)
Occurs after extra-capsular cataract extraction
Decreased visual acuity and contrast sensitivity
Glare; monocular diplopia
Decreased incidence of PCO with acrylic hydrophobic IOL and square edge
design IOL
Clinical Features
Elschnig pearls (Bladder cells)
Proliferation and migration of residual equatorial epithelial cells along the
posterior capsule at the site of apposition between remnants of anterior
and posterior capsule
Vacuolated appearance
Common in children (if primary posterior capsulotomy is not done)
Capsular fibrosis
Due to fibrous metaplasia of epithelial cells
Treatment
Nd: YAG laser capsulotomy (preferably not done before 46 months
following cataract surgery); opening of 3 mm is adequate
Complications
Pitting (damage) of IOL
Cystoid macular edema
Rhegmatogenous RD in high myopes
Transient rise in IOP
Posterior subluxation/dislocation of IOL
Chronic endophthalmitisrelease of sequestered organism into vitreous
(Propionibacterium acnes)
Anterior Capsular Phimosis

Fibrosis of the anterior capsule with capsulorrhexis shrinkage
Degree of phimosis is related topseudoexfoliation syndrome, diabetic
retinopathy, retinitis pigmentosa, myotonic dystrophy
Treatment:
Limited form (without invasion of the optical zone)YAG laser
capsulotomy
Severe form (dense fibrous plaques)surgery
ZONULAR CATARACT
Opacity occupies a discrete zone in the lens
Types
1. Nuclear
Opacification confined to embryonic or fetal nucleus
Fine, pulverulent cataract or dense, central cataract
2. Lamellar
Cataract sandwiched between clear nucleus and cortex
Radial extensions or riders are seen
3. Sutural
Y shaped
Anterior/posterior
4. Polar cataract
Anterior polarpyramidal; associated with anterior lenticonus,
persistent pupillary membrane, Peters anomaly, aniridia
Posterior polarassociated with PHPV, posterior lenticonus
Lens 291
ECTOPIA LENTIS
Displacement of lens from its normal position
Luxated lens completely dislocated
Subluxated part of the lens still in pupillary area
Causes
Hereditary
Familial ectopia lentisbilateral, supero-temporal dislocation
Ectopia lentis et pupillaebilateral; displacement of pupil and lens in
opposite directions
Aniridia
Marfans syndromebilateral, supero-temporal dislocation; zonules intact,
accommodation retained
Weil-Marchesani syndromebilateral inferior dislocation
Homocystinuriainfero-nasal dislocation; zonules disintegrate (due to
high-cysteine levels)accommodation is lost
Hyperlysinemia
Sulphite oxidase deficiency
Stickler syndrome
Ehlers-Danlos syndrome
Acquired
Spontaneous dislocation
Trauma
Large eyein high myopia, buphthalmos
Anterior uveal tumors
Hypermature cataract
Clinical Features
Extreme myopic/hyperopic shift, astigmatism, acquired aphakia
Vision may fluctuate dramaticallybetween phakic and aphakic vision
Monocular diplopia
Lens blocks pupil secondary angle closure
Phacodonesis, iridodonesis
Treatment
Glasses (aphakic correction)
Lensectomyindications are:
Lens in the anterior chamber
Lens induced uveitis/glaucoma
Lenticular opacity with poor visual function
Anisometropia or refractive error not amenable to optical correction
(prevent amblyopia in children)
Impending lens dislocation
Surgical procedures:
<1 quadrant subluxationcapsular tension ring
<2 quadrant subluxationCionni ring
>2 quadrant subluxationLensectomy + scleral fixated/anterior
chamber IOL
Weil-Marchesani Syndrome
Short stature, brachydactyly, stiff joints, mental retardation
Ectopia lentisbilateral, inferior
Microspherophakiasecondary angle closure glaucoma with pupillary
block
Nanophthalmos, asymmetrical axial lengths
Pre-senile vitreous liquefaction
Marfan Syndrome
Ophthalmic Features
Ectopia lentisbilateral, accommodation retained (unlike in homocystinuria)
Microspherophakialens may dislocate into anterior chamber or vitreous;
subluxated lens may cause glaucoma
Angle can show dense iris processes, thickened trabecular sheets; may cause
glaucoma
RDassociated with lattice degeneration, high myopia
Flat cornea, blue sclera, squint, hypoplasia of dilator papillae, peripheral iris
transillumination
Systemic Features
Tall, thin stature, scoliosis, sternum deformity
Arm span > height
Arachnodactyly (long, spider-like fingers), mild joint hypermobility
Narrow, high arched palate
Muscular underdevelopmentpredisposition to hernias
Dilatation of ascending aorta aortic incompetence and heart failure
Mitral valve disease, aortic dissection
Striae, fragility and easy braising of the skin
Lens 293
CATARACT SURGERY
Indications
Visual improvement
Fundus examination
Phacolytic/phacomorphic glaucoma
Cosmetic
Preoperative Evaluation
Vision, cover test
Pupilsrule out RAPD
Adnexadacryocystitis, blepharitis, conjunctivitis, lagophthalmos,
ectropion, entropion, tear film abnormalities
CorneaFuchs endothelial dystrophy
ACshallow; cells, PAS
Pseudoexfoliation
Type of cataract; subluxation; zonular dialysis
IOP, syringing
Fundusindirect ophthalmoscopy, B-scan
A-scan, K readings
Surgical Complications
Intraoperative complications Postoperative complications

Posterior capsular rupture Posterior capsular opacification
Vitreous loss Cystoid macular edema
Nucleus drop posteriorly Corneal edema
IOL drop Bullous keratopathy
Expulsive hemorrhage Corneal decompensation
Suprachoroidal hemorrhage Secondary glaucoma
Iris prolapse IOL malpositioning
Descemets tear Retinal detachment
Zonular dialysis Anterior capsular phimosis
Endophthalmitis
INTRAOCULAR LENSES
Made up of optic (central refracting element) + haptics (sit in contact with
ocular structurescapsular bag/sulcus/angle of anterior chamber)
Ideal locationin the bag
Designs
Five generations:
Original Ridley PC lens
Early AC lens
Iris support lenses
Modern AC lens
Modern PC lens
Types of IOLs
Rigid lOLsmade entirely from PMMA
Foldable lOLs:
Siliconelower rate of PCO; not preferred for diabetics
Acrylic
- Hydrophobicwater content < 1%
- Hydrophilicwater content 18 to 35%
Hydrogelsimilar to hydrophilic
Collamermixture of collagen and hydrogel
Multifocal lOLs
Diffractive:
- Designed to use both diffractive and refractive optics to provide
distance, intermediate and near vision
- Use 40% of available light for distance, 40% for a second focal
point, 20% lost to destructive interference
- Available lenses areAcrysof Restor (Alcon), Tecnis Multifocal
(advanced medical optics), Acri LISA (Zeiss)
Refractive:
- Designed with several optical zones on the IOL which provide
various focal points allowing for an improvement in distance,
intermediate and near vision
- Available lensReZoom
Accomodative IOLsdesigned to accommodate or adjust, like a natural eye,
to see at multiple distances, e.g. Crystalens IOLs, 1CU lenses, Synchrony
lenses
Lens 295
INTRAOCULAR LENS POWER CALCULATION

Based on basic refraction:
IOL insertion in capsular bag + 20D lens
IOL in pupillary plane +19D lens
IOL on anterior capsule 17D lens
Postoperative refraction will be same as pre-existing refraction; which is the
Idem lens power
If there was a pre-existing refractive error: IOL power for emmetropia = Idem
lens power + (1.25 refractive error)
Based on Measurements
Theoretical Formula
n nK
P=
L ACD n K ACD
L ACD n K ACD
n = refractive index far aqueous and vitreous
L = axial length (mm)
ACD = estimated postoperative AC depth (mm)
K = corneal curvature (diopters)
Regression Formula
SRK formulaSanders, Retzlaff, Kraff
SRK-I
P = A 2.5 L 0.9 K
L = axial length
K = average keratometric reading
A = specific constant for each type of lens (used only when L = 22 to 24.5
mm)
SRK-II
IOL power = P(RT RF)
P = power got from SRK-I
RT = refraction needed
RF = refraction factor
In high hypermetropes with axial length <22 mm, Brinkhorst or Hoffer Q
formulae are used
In high myopes with axial length >26 mm, SRK-T formula is used
INTRAOCULAR LENS MALPOSITION

Depends on haptic position and asymmetric bagsulcus placement of IOL
during surgery
Fluctuating vision, monocular diplopia, glare, halos, photosensitivity, optical
aberrations
May causeaphakia
Sunrise Syndrome (IOL Subluxates Superiorly)

Due to
Misplacement of superior haptic in ciliary sulcus while inferior haptic placed
in the bag
Superior zonular dialysis or PC rent
Small IOL size; placement in sulcus
Sunset Syndrome (IOL Subluxates Inferiorly)

Due to
PC rupture extending inferiorly allowing inferior haptic to escape through
defect
Inferior Zonular dialysis
Small-sized IOL placed in sulcus
Lens 297
East-West Syndrome (Horizontal Decentration)
Causes of IOL Malposition

Intraoperative
Postoperative:
External forcetrauma, rubbing
Internal forcescarring, peripheral anterior synechiae, capsular
contraction
Management
Reposition IOL
Move lens from bag to sulcus or sulcus to bag
Place optical portion in front of iris
Create a pupillary capture
Remove IOLreplace with a secondary AC IOL
Iris/trans-scleral suturesrequired to secure IOL in position
Scleral fixation of lensiris fixated or clipped IOL
AC IOL Decentration can Lead to
Iris tuck uveal inflammation, red and tender eye
Peaked/oval pupil
If IOL is smalllens is mobile and can cause endothelial cell loss, CME,
glaucoma
Capsular Contraction Syndrome May be Due to
Very small capsulorrhexis
Silicon plate IOL design
POSTOPERATIVE DECREASE IN VISION

Causes
Corneal edema due to rise in IOP, Descemets tear
Striate keratopathydue to instrument touch during surgery; more in Fuchs
endothelial dystrophy
Posterior capsular opacification
Malposition of IOL
Iris prolapseincreased astigmatism, chronic uveitis
Anterior capsular fibrosis (contraction of capsulorrhexiscalled capsular
phimosis)
RDif lattice degeneration, myopia, PC rent, vitreous loss, vitreous
incarceration in wound
Endophthalmitis
chapter
Trauma 12
CHEMICAL INJURIES
Acid Burns
Caused by H2SO4, HCl, acetic acid
Coagulates proteins in corneal epithelium; this prevents further penetration
of acid into eye; hence acid burns are not as dangerous as alkali burns
Sterile ulceration and perforation rare
Alkali Burns
Ammonia, lye (NaOH), lime Ca(OH)2
Increases pH and produces saponification of fatty components of cell
membrane cell disruption and death
Clinical Features
Epithelial defect
Cloudy cornea
Limbal ischemia
Anterior chamber reactioncells, flare
Raised IOP (due to trabeculitis or shortening of scleral collagen)
Cataract
Modified Classification of Ocular Chemical Injuries
Grade Cornea Limbal Ischemia Conjunctival Prognosis

involvement
I Clear; epithelial damage only None None Good
II Clear; epithelial damage only < 1/3 < 1/3 Good
III Hazy cornea > 1/3(OR) > 1/3 Guarded
Acute phase 0 7 days

Early reparative phase (ERP) 721 days
Late reparative phase (LRP) 21 days to months (sterile stromal ulceration
likely)
Complications: Corneal scarring, conjunctivalization of cornea, dry eye,
cataract, symblepharon
Treatment
Immediate Acute ERP LRP
Copious irrigation Topical steroids Topical steroids Topical steroids
for hour
Remove particulate Topical antibiotics Topical antibiotics Topical antibiotics
matter
Steroid eyedrops Timolol eyedrops Timolol eyedrops Timolol eyedrops
Antibiotic eyedrops Cycloplegic eyedrops Cycloplegic eyedrops Limbal autograft
Tab ascorbic acid Bandage contact lens Bandage contact lens Corneal transplant
Tarsorraphy (if exposure)
Discontinue steroids if corneal re-epithelialization does not occur in 10 days
Drugs also started in acute phase are:

Topical sodium ascorbate 10% 2 hourly
Tab Vitamin C 2 g QID
Topical sodium citrate 10% 2 hourly 10 days (decreases intensity of
inflammatory response)
Tetracyclinestopical and systemic
Collagenase inhibitorsacetyl cysteine 1020% used 2 hourly (refrigerated
and used for up to 1 week)
Surgery
Early surgery Late surgery
Conjunctival flap (if stromal ulceration occurs) Division of conjunctival bands and
symblepharon
Limbal stem cell transplant Conjunctival and mucous membrane grafts
Amniotic membrane graft Penetrating keratoplasty (after 6 months)
Patch graft or glue (if corneal perforation occurs) Keratoprosthesis (in severely damaged eyes)
Classification of Globe Injuries

Closed globe Open globe
Type A. Contusion A. Rupture
B. Superficial foreign body B. Penetrating injury
C. Lamellar laceration C. Intraocular foreign body
D. Mixed D. Perforating
E. Mixed
Grade 1 6/12 vision 1 6/12 vision
2 6/18 6/36 2 6/18 6/36
3 6/36 3/60 3 6/36 3/60
4 2/60 PL 4 2/60 PL
Zone 5 NoPL 5 NoPL
I - external bulbar conjunctiva, cornea, sclera I cornea
II anterior segment up to pars plicata II - Up to 5 mm from limbus
III posterior segment III posterior to zone II
Trauma 301
A penetrating wound passes into a structure; it has only a wound of entry

A perforating wound passes through a structure; it has an entry and an exit
wound
For example:
A thorn passing through the cornea, getting lodged in the anterior chamber
perforates the cornea but penetrates the eye
Blunt Trauma
Anterior segment Posterior segment
Corneaabrasion, edema Vitreous hemorrhage
Irisiritis, iridodialysis Berlins edema, commotion retinae
Anglerecession Macular hole, macular edema, macular
hemorrhage
Anterior chamberhyphema Choroidal rupture
LensVossius ring, subluxation, cataract, Retinal detachment, retinal dialysis
zonular dialysis
Globe rupture Optic neuropathy, optic nerve avulsion, optic
atrophy
TRAUMATIC HYPHEMA
Blunt Trauma Causes
Stretching of limbal tissue
Equatorial scleral expansion
Posterior displacement of lens/iris diaphragm
Raised IOP
Bleeding Occurs from
Major arterial circle, recurrent choroidal arteries, ciliary body veins, iris vessels
Fate of the Blood
Plasminogen in AC Plasmin Breakdown of fibrin Clot dissolves
Grading of Hyphema
Microscopic Circulating RBCs only
I < 1/3
II 1/31/2
III 1/2near total
IV Total or 8 ball
Rule Out
Bleeding disorders, sickle cell anemia, kidney/liver disease, anti-coagulant
therapy
Investigations
Bleeding time, clotting time, liver function tests, prothrombin time, platelet count
Treatment
Supportive
Bed rest, patching, head elevation, metal shield (to prevent further damage
to globe)
Medical
Topical steroids/cycloplegics/mydriatics
Antifibrinolytics EACA 50 mg/kg/day for 5 days; Tranexamic acid 25 mg/
kg TID
IOP lowering drugs
Surgical
Paracentesis with AC wash
Peripheral iridotomy + trabeculectomy
Urokinase with vitrectomy
Automated hyphemectomy
Trauma 303
Indications for Surgical Removal of Hyphema

IOP > 50 mm Hg 2 days or > 35 mm Hg 7 days (to prevent optic atrophy)
Blood staining of cornea
Compromised endothelial function
Pre-existing glaucomatous damage
Sickle cell disease (IOP > 26 mm Hg 2 days)
Prolonged resistant clot in AC > 10 days
Total hyphema > 5 days
Complications of Hyphema
Re-bleed after 25 days due to clot lysis
Glaucoma due to:
Earlyobstruction of trabecular meshwork by RBCs and platelets;
steroid usage
Lateposterior synechiae, iris bombe, peripheral anterior synechiae,
angle recession, ghost cell glaucoma
BLOWOUT FRACTURE OF ORBIT

Types
Directinvolves orbital rim and adjacent bone
Indirectinvolves bones in orbital cavity, not orbital rim; pure blow out
fracture
Theories
When striking object is > 5 cm in diameter (fist/tennis ball), a compressive
force is directed posteriorly causing a sudden rise in intraorbital pressure
fracture of weak portions of orbit (floor and medial wall)
Compressive force to orbital rim causes buckling of orbital floor
Clinical Features
Lidedema, ecchymosis, hematoma
Orbital rimtender, loss of continuity
Infraorbital hypoesthesiadue to infraorbital nerve damage
Motility disturbance extraocular muscle entrapment or direct injury
diplopia; FDT positive
Proptosis with intraorbital hemorrhage
Traumatic mydriasis
Surgical emphysemaif fracture communicates with nasal sinus
Epistaxis
Enophthalmos and pseudoptosis
Immediate:
- Due to fat/bone tissue prolapse (herniation into antrum)
- Edema/hemorrhage causes increased intraorbital volume, push-
ing contents into antrum
- Latedue to necrosis and fat atrophy
Corneal laceration
Hyphema with raised IOP
Cataract, RD, choroidal tears
Investigations
CT-scan brain and orbits, diplopia charting, forced duction test, exophthalmometry,
cheek sensation testing, X-ray PNS/skull
Management
Conservative
Blowing nose should be avoided (because infected sinus contents can pass
into orbit and brain); observation; treat infection
Surgery indicated for orbital floor fracture if:
>50% of the floor is fractured
>2 mm enophthalmos
Trauma 305
Inferior rectus entrapment causing diplopia (should be operated within

2 weeks to prevent fibrosis and muscle sequelae)
Medial Wall Fracture
Periorbital subcutaneous emphysema when one blows nose
Defective adduction and abduction
Roof Fracture
Upper lid hematoma, periocular ecchymosis
Inferior and axial displacement of globe
Pulsation of globe without bruit (meningitis may occur!)
Lateral Wall Fracture
Rare; associated with extensive facial damage
INTRAOCULAR FOREIGN BODY

Intraocular foreign bodies cause:
Mechanical damage, infection, toxic reaction
Cataractdue to damage to lens capsule
Vitreous liquefaction, endophthalmitis
Retinal hemorrhages, retinal breaks
Classification
Metallic

Magneticiron, steel, nickel
Non-magnetic:

Inert: Gold, silver, platinum
Irritants:
- Copper (worst), bronze, brass
- Aluminum (tissue necrosis on contact)
- Zinc (retinal atrophy)
- Mercury (corneal necrosis; vitreous abscess)
- Lead (gets rapidly covered with a layer of carbonate which pre-
vents further diffusion)
Non-metallic
Organiccotton, caterpillar hair, wood, cilia (granulation tissue formation)
Inorganicstone, sand, concrete, coal, glass, gun powder (local irritative
response can induce fibrous or suppurative reaction)
Trauma 307
LOCALIZATION OF INTRAOCULAR FOREIGN BODY

1. Direct visualizationby slit-lamp biomicroscopy, indirect ophthalmoscopy,
transillumination
2. Indirect visualizationin hazy media
Depending of magnetic property:
Magnet brought near globe; when FB is drawn towards magnet pain
is experienced
Depending on electrical conductivity:
Alternate current
Primary coil Secondary coil
Alternate current converts primary to secondary coil
If FB is presentcurrent flows in the secondary coil
Depending on chemical analysis:
Intraocular fluids are drawn and analyzed
Radiological methods:
i. Direct method:
a. Limbal ring method
Metallic ring sutured to limbus
PA and lateral view X-rays taken
Construct a circle and find relationship of IOFB to it
b. Contact lens method
Zeiss contact lens has lead markers in 4 quadrants
Worst Lonac contact lens has a central hole with metal
tube marker
With contact lens on, X-ray is taken to locate position of
the FB
ii. Depending on rotation of globe: Lead and X-ray tubes are fixed and
patient is asked to move eyeball FB moves with globe
iii. Depending on geometric construction: Eyes are fixed; metal indicators
point on center and temporal side of cornea and X-rays are taken
iv. Stereoscopic method: Two stereoscopic pictures taken at fixed an-
gles and displacement of FBs shadow with reference to radiopaque
marker is noted
v. Delineation of globe using contrast media: Contour of globe outlined
by injecting radiopaque material into Tenons spaceto locate the
FB
vi. Bone free methods: If FB in anterior segment and density of FB is
equal to bone density; Dental film placed over inner canthus and
X-rays are directed towards anterior segment
vii. CT-scan for: Small FB with low radiographic density, metallic FB; can-
not locate FB if it is in sclera/retina
viii. MRI for: Small non-ferromagnetic FB (plastic); high resolution im-
ages, thinner slices
ix. Ultrasound: FB in opaque media, non-radiopaque FB; FBs that are
not anterior
A modesteeply rising echo spike

B modeacoustically opaque, cast an acoustic shadow
3. ERGEarly siderosisincreased a amplitude
Late siderosisdecreased b amplitude which is finally extinguished
Management
Tetanus prophylaxis
Systemic antibiotics
Cycloplegics
Magnetic IOFB: Removed with magnets
Hand-held magnet (<1 mm FB)
Giant magnet
Intraocular magnet
Anterior segment FBmake limbal incision and remove with a simple
forceps/hand held magnet
Posterior segment FB:
In vitreous cavity vitrectomy + sclerostomy + removal of FB
In posterior part TPPV (total pars plana vitrectomy) + pars plana
sclerostomy
Intraretinal FB can be removed:
Trans-sclerally trap door scleral flap
Trans-vitreally TPPV + removal of IOFB with forceps
Subretinal FB retinotomy + barrage laser; then forceps removal of
FB
Complications
Vitreous hemorrhage
Retinal detachment
Cataract
Endophthalmitis (Bacillus cereus is the most common organism)treated
with intravitreal antibiotics (400 mg amikacin + 1 mg vancomycin + 450 mg
clindamycin) + removal of IOFB
Sympathetic ophthalmia
Fibrotic membranes in vitreous
Trauma 309
SIDEROSIS BULBI
Due to retained iron foreign body (FB)
Iron undergoes electrolyte dissociation and gets widely deposited in eye;
deposition in the lens carries the best prognosis but in the ciliary body/
retina has the worst prognosis
Chronic degenerative process
Haber Weiss reaction oxidation and dissemination of Fe+3 throughout
eye causes enzyme inactivation and cell membrane damage
Types
Directiron deposited in immediate neighborhood of FB
Indirectiron diffuses throughout tissues of eye
Clinical Features
Cornearusty staining; Coats ring forms
Secondary open angle glaucomadue to iron in trabecular meshwork
Irisheterochromia, posterior synechiae
Pupil mydriasis due to atrophy of sphincter
Lensbrownish/greenish dots large, diffuse, peppery; beneath and over
anterior capsule
Vitreousdegeneration
Retina
Pigmentary retinopathy
Arteriosclerotic changes
Optic atrophy and discoloration
Retinal detachment
Treatment
Remove foreign body; galvanic deactivation
Intravenous EDTA
Desferrioxamine
Subcutaneous adenosine triphosphate
CHALCOSIS
Due to retained copper foreign body
Pathology
Chronic non-granulomatous inflammation
Suppurative reaction with abscess formation
Electrolyte dissociation chalcosis
Clinical Features
Corneagreenish blue ring in Descemets membrane Kayser-Fleischer
ring
Aqueous has multiple metallic particles brightly refringent
Irisgreenish discoloration
Lenssunflower cataract; thick, powdery deposit under anterior capsule
Zonulesimpregnation of fibers
Vitreousbrownish red opacities
Retinabrilliant deposits (like gold leaf ) on surface of retina and blood
vessels
Treatment
Remove foreign body
Sodium thiosulphate
Sodium hyposulphite
BAL (British anti-lewisite)
chapter
Systemic Diseases 13
EYE IN AIDS
Anterior Segment Manifestations
1. Lids Kaposis sarcoma; Molluscum contagiosum
2. Conjunctiva Kaposis sarcoma; squamous cell carcinoma, viral conjunctivitis
3. Cornea:
HSV keratitis (dendrites in peripheral cornea)
Herpes zoster ophthalmicussevere
Candida albicans keratitis
Microsporidial keratitisbilateral chronic diffuse punctate epithelial
keratoconjunctivitis treated with topical fumagillin, oral albendazole,
HAART therapy
4. OrbitBurkitts lymphoma, Kaposis sarcoma, pseudotumor
Posterior Segment Manifestations

Microvasculopathy
Cotton wool spots in posterior pole may be large and simulate CMV retinitis
(no associated uveitis/intralesional hemorrhages; do not enlarge)
Microaneurysms (occasionally on FFA)
Asymptomatic (large cotton wool spots may cause scotomas)
Ischemic maculopathy, macular edema, serous maculopathy rare
Marker for patients with severely immuno-compromised status (low CD4+
counts)
Large Vessel Disease
BRAO, CRVO, BRVO very rare
Frosted branch vasculitis
Malignancies
Non-Hodgkins lymphoma causes cortical visual loss
Intraocular NHL necrotizing retinitis, choroidal infiltrates, vitritis
Optic Neuropathies
Perineuritis, papilledema normal vision and pupillary reaction
Papillitis visual loss and APD
Retrobulbar neuritis mostly infectious
Optic atrophy
Opportunistic Infections
Retinitis
Necrotizing herpetic retinopathy progressive outer retinal necrosis
(PORN), rarely acute retinal necrosis (ARN)
Toxoplasmic retinochoroiditis bilateral, multifocal, not associated with
chorioretinal scars; associated vitritis, iritis, choroiditis, papillitis
HIV retinitis peripheral multifocal retinitis associated with low grade
vitritis and vasculitis
CMV retinitis discussed later
Choroiditis
Pneumocystis carinii conjunctivitis, orbital mass, optic neuropathy,
bilateral multifocal choroiditis (yellowish well-demarcated lesions in
posterior pole; no associated vitritis/vasculitis)
Cryptococcus papilloedema, retrobulbar neuritis, CNS involvement,
VIth nerve palsy, headache
- Tuberculosis
- Candida albicans
- Toxoplasma gondii
CYTOMEGALOVIRUS RETINITIS
In patients with CD4 counts < 50 cells/L
Clinical Findings
Fulminant form confluent retinal necrosis with hemorrhage mostly in the
posterior retina; associated papillitis may occur
Indolent form granular lesion in peripheral retina with little/no associated
hemorrhage
Frosted branch angiitis
Management
Depends on location of the active retinitis and immune status of the patient
HAART alonehelps resolve small peripheral lesions (may take months)
Vision threatening posterior pole involvement HAART + anti-CMV agents
Newly diagnosed or recurrent CMVR oral valganciclovir 900 mg BD for
3 weeks (or intravenous ganciclovir 5 mg/kg) followed by maintenance
dose of 900 mg OD
Intravitreal ganciclovir 2 mg in 0.1 mL bi-weekly for 3 weeks followed by
weekly injections
Progressive Outer Retinal Necrosis
ARN PORN
Healthy individuals; AIDS patients with mild Severely immunocompromised individuals
immune dysfunction
Peripheral retinitis progresses to posterior Mostly posterior retinitis (multifocal areas of
pole deep outer retinal)whitening throughout
the macula which coalesce rapidly to confluent
sheets
Vitritis, retinal vasculitis, KPs No signs of inflammation
Inner retina involved Clinical sparing of inner retina
Retinal vasculitis with no clearing Perivascular clearing of retinal necrosis-cracked
mud appearance
Treatment of PORN
Intravenous and intravitreal injections of ganciclovir and foscarnet
Intravenous foscarnet: Induction dose 90 mg/kg every 12 hours for 23
weeks; maintenance dose 90 mg/kg once daily (given over 2 hours)
Intravitreal foscarnet: 2400 g twice a week for 3 weeks followed by weekly
injections
ACUTE RETINAL NECROSIS

Mostly occurs in immunocompetent patients
Caused by HSV 1 and 2, VZV, CMV and EBV
Bilateral involvement in 2/3rds cases; Retinal detachment in 75%
Clinical Features
Severe and diffuse uveitis + retinal vasculitis (occlusive vasculopathy) +
retinal necrosis
Anterior uveitis ocular/periocular pain, redness, photophobia, blurred
vision, floaters
KPs, posterior synechiae, scleritis, raised IOP
Retinitis starts as multifocal, deep, yellow-white lesions in the peripheral
retina progress to thick, well delimited necrotic plaques (full thickness
necrosis)
Rapid circumferential progression in 510 days; posterior pole spared till
late
Retinal vasculitis arteriolar, occlusive, associated choroidal vasculitis
Moderate or severe vitritis progresses with the retinal necrosis
Optic nerve edema, dyschromatopsia, RAPD, visual field defect
Optic neuritis may precede ARN
Rhegmatogenous retinal detachment
Diagnostic Criteria (American Uveitis Society)

1. Designation of ARN should be based only on clinical appearance and course of
infection; clinical characteristics:
One/more foci of retinal necrosis with discrete borders in peripheral
retina (rarely macula)
Rapid progression of disease in absence of treatment (advancement of
lesion borders or development of new foci of necrosis)
Circumferential spread
Occlusive vasculopathy with arteriolar involvement
Prominent inflammatory reaction in the vitreous and anterior chamber
2. Characteristics that support diagnosis (not required for diagnosis)
Optic neuropathy
Scleritis
Pain
3. The definition does not depend on:
Extent of necrosis
Immunological status of the host
Isolation of any virus/pathogen from ocular tissue/fluid
Treatment
Intrwavenous acyclovir (10 mg/kg every 8 hours for 14 days) followed by:
Oral acyclovir 800 mg 5 times daily for 14 weeks (to prevent fellow eye
involvement) or
Oral famciclovir500 mg TID x 14 weeks
Occlusive vasculopathy and optic neuropathy:
Oral prednisolone 60 mg/day (started one day after antiviral medication,
used for a week and tapered)
Tab aspirin 325 mg/day in acute stage
Early diagnosed cases:
Intravitreal foscarnet +
Oral acyclovir/valacyclovir (1 g every 8 hours)
Prophylactic argon laser photocoagulationretinal breaks; posterior to
healed ARN in 34 rows (ARN progresses through laser marks if active)
Vitrectomy with endolaser and silicon oil injection for retinal detachment
Clinical stability 4872 hours after initiation of therapy
Early pigmentation of lesions in 14 days
Complete resolution of inflammation in 612 weeks
EYE IN TUBERCULOSIS
Clinical Features
Lids Ulceration of lid margin, lupus vulgaris, ectropion

Conjunctiva Parinaud oculoglandular syndrome (unilateral follicular conjunctivitis with
ipsilateral lymph node enlargement), purulent conjunctivitis, pseudo
membranous conjunctivitis, tuberculomas
Cornea Phlyctenular keratoconjunctivitis, fascicular keratitis, interstitial keratitis,
suppurative keratitis
Uvea Bilateral granulomatous anterior uveitis, conglomerate iris tubercles, choroidal
granulomas, pars planitis, multifocal choroiditis
Retina Eales disease, retinal vasculitisNVE. BRVO
Sclera Deep nodular scleritis, tongue-shaped recurrent sclerokeratitis
Optic nerve Optic neuritis, papilledema
Cranial nerves Palsies
Orbit Orbital cellulitis/abscess, periostitis, osteomyelitis, chronic dacryocystitis
Tuberculosis (TB) should be considered strongly in:

Alcoholics who are homeless, living alone, low economic status
HIV-positive patients, residents of prison
Health care professionals
People who have been exposed in the past to active TB
Negative chest X-ray, markedly positive Mantoux test, some type of
extrapulmonary TB
Drug abuse, homosexual activity
Investigations
1. Skin testing (Mantoux) record diameter of erythema and induration;
vesiculation
Positive indicates that the patient at some time in the past has been
infected with TB or BCG vaccination was given
Conversion from negative to positive indication for ATT for 1 year
Positive (<10 mm of induration and erythema and no other evidence)
no treatment
Positive (1020 mm of induration) treat or monitor carefully
Positive (>25 mm of induration) treat for 1 year
2. Radiography chest X-ray may show classic evidence of TB; may be normal
in extrapulmonary TB
3. Microbiology Mycobacterium culture positive in sputum or urine treat
4. Histopathology acid fast organisms in biopsied tissue treat
5. PCR of ocular fluids/tissues
6. ELISA Serum IgG, IgM , IgA assay

7. Therapeutic trial response to ATT in 46 weeks
Treatment
Systemic disease is treated with antituberculous treatment
Eye involvement is treated according to the tissues involved with anti-
inflammatory drugs
EYE IN SARCOIDOSIS
Idiopathic multisystem disorder
Characterized by the presence of non-caseating granulomas
Clinical Features
Granulomas on conjunctiva, sclera
Keratoconjunctivitis siccadry eye due to lacrimal gland infiltration
Anterior uveitisacute and chronicmutton fat KPs, Busacca and Koeppe
nodules complicated by glaucoma, cataract, band keratopathy, peripheral
anterior synechiae
Diffuse vitritis; snow balls in inferior anterior vitreous
Retinal periphlebitiscandle wax drippings perivenous exudates
BRVO; vascular sheathing; CME
Retinal granulomaswhite/yellow
Preretinal granulomata occur interiorly, anterior to equator Landers sign
Choroidal granuloma
Optic discNVD, disc edema, granuloma (does not affect vision),
papilledema
Peripheral retinal neovascularization
Acute sarcoid retinopathy = vitritis + periphlebitis + preretinal granulomata
+ retinal hemorrhages
Investigations
Chest X-ray
Biopsy oflungs, conjunctiva, lacrimal glands
Serum ACE levels
Bronchioalveolar lavageincreased activated T-helper lymphocytes
Calcium assayhypercalciuria
Gallium67 scanincreased uptake
Pulmonary function testsreduced total lung capacity
Skin biopsy
Kviem testintradermal testlocalized granuloma develops
Treatment
Anterior segment inflammation: Topical steroids, cycloplegics
Posterior segment involvement: Systemic steroids
EYE IN SYPHILIS
Lids Chalazion-like induration, madarosis, symblepharon

Cornea Bilateral interstitial keratitis, keratitis pustuliform profunda, keratitis punctata
profunda, keratitis linearis nigrans
Iris Acute plastic iritis, gummatous iritis
Pupil Argyll Robertson pupil (light reflex lost; accommodation reflex present)
Absolute fixed pupillight and near reflex lost
Internal ophthalmoplegiaall reflexes lost
Accommodation palsy alone
Choroid, retina Diffuse chorioretinitis, Jensens juxta-papillary choroiditis, Foersters multifocal
choroiditis, neuroretinitis, big blind spot syndrome
Optic nerve Optic neuritis, papilledema, ascending/descending/gumma-induced optic
atrophy
Cranial nerves III n, VI n palsies, IV n also may be affected
Orbit Periostitis, proptosis (gumma in orbit)
Acute Plastic Iritis

Jarisch-Herxheimer reaction
Multiple papules in pupillary region
Roseolaedilated iris capillaries
Posterior synechiae; gumma at root of iris
Secondary glaucoma, deep keratitis, scleritis
Localized atrophy of iris stromaheals
Dust-like opacities in vitreous
Gummatous Iritis
Gumma invadessclera, angle, vitreous
Foersters multifocal choroiditis: bilateral
- Ring scotomas
- Focal areas of chorioretinal atrophy with hyperpigmentation
- Extensive pigmentary changes with perivascular bony spicules
night blindness
Neuro-retinitis:
- Disc edema, engorged veins, macular star
- Cotton wool spots, flame-shaped hemorrhages
- Blood vessels reduced to white threads; optic atrophy
Management
Lumbar punctureto rule out neuro-syphilis
12 to 24 MU of aqueous Penicillin IV daily for 10 days followed by IM 2.4 MU
for 3 wks
Oral tetracycline 500 mg QID or Oral erythromycin 500 mg QID for 3 wks
BEHETS DISEASE
Idiopathic; occurs in young men, 3040 year age group, HLA B51
Recurrent oral and genital ulcers
Clinical Features
Acute, recurrent, bilateral anterior uveitistransient, mobile hypopyon
Retinitisscattered white superficial infiltrates
Retinal vasculitis occlusions retinal ischemia NVE
Generalized vascular leakage leads to diffuse retinal edema, CME, disc
edema
Massive retinal exudation
Vitritissevere, persistent
End stageoptic atrophy, sheathing of vessels, chorioretinal scarring
Systemic Features
Skinerythema nodosum, folliculitis, acneiform lesions
CVSaortitis, arterial/venous thrombosis, aneurysms
Jointsbilateral arthritis (especially knee joint)
CNSdural sinus thrombosis
GITulceration
Treatment
Steroids, immunosuppressives (azathioprine)
Infliximabsafe and effective
Diagnostic Criteria
Recurrent aphthous ulcers (for 12 wks) + any two of:
1. Recurrent genital ulcers
2. Eye lesions
3. Skin lesions
4. Pathergy test: Skin inflammatory reactivity to scratches
Spondyloarthopathies
Acute retinal necrosis
Idiopathic acute multifocal retinitis
EYE IN LEPROSY
Clinical features Management

Lids Superciliary madarosis, madarosis
Lagophthalmos Tarsorrhaphy
Lower lid ectropion Tarsal strip procedure
Upper lid entropion Blepharoplasty
Trichiasis Electrolysis
Cornea Exposure keratitis Tarsorrhaphy
Neurotrophic keratitis Tarsorrhaphy, lubricants
Dry eyes (denervation of lacrimal gland) Lubricants
Lepromatous pannus
Interstitial keratitis Topical steroids
Military lepromas (white punctate
subepithelial opacities near limbus)
Lacrimal Acute dacryocystitis Topical and oral antibiotics
system
Chronic dacryocystitis DCR or DCT
Sclera Episcleritis Topical NSAIDs
Scleritis Topical steroids, oral NSAIDs
Scleral necrosis
Staphyloma
Uvea Granulomatous uveitis Topical steroids, cycloplegics
Iris pearls
Iris hole (due to atrophy)
Ciliary body atrophy
Pupil Pin-point pupil
Fulminant granulomatous uveitis is due to deposition of immune complexes

Chronic low-grade uveitis is due to direct invasion of organisms
Pin-point pupil due to atrophy of dilator pupillae and irritation of the
sphincter pupillae
Iris pearls chalky-white particles in superficial stroma of iris, at the pupillary
margin; non-inflammatory microlepromas
Ciliary body atrophy causes early presbyopia, hypotony
IOP may increase or decrease due to early autonomic neuropathy
Investigations
Lepromin test: Early reaction (read in 12 days)
Late reaction (read in 34 wks)
Decreased Vision Due to

1. Hypotensive maculopathy (in ciliary body atrophy)
2. Cystoid macular edema
3. Dapsone toxicity
Treatment
Paucibacillary Therapy
Dapsone 50 mg/day for 6 months + rifampicin 600 mg OD every month for
6 months
Multibacillary Therapy
Dapsone 50 mg/day + rifampicin 600 mg OD every month for 6 months +
clofazimine 14 mg/kg/day for 6 months
Eye in Diabetes Mellitus
Lids Chalazion, hordeolum internum/externum, blepharitis, ptosis (III n palsy),

xanthelasma
Conjunctiva Microcirculatory abnormalities, vasoconstriction of conjunctival vessels
Cornea Decreased sensation, neurotrophic ulcers, increased thickness, persistent
epithelial defects, infective keratitis, decreased endothelial cell count
Sclera Episcleritis
Glaucoma POAG, NTG, PACG, NVG, pseudoexfoliation glaucoma, steroid induced
glaucoma, ghost cell glaucoma (following vitreous hemorrhage)
Refraction Myopia, hypermetropia, early presbyopia
Lens Snow flake cataract, intumescent cataract
Vitreous Asteroid hyalosis
Retina Diabetic retinopathy, lipoma retinalis, CRAO, CRVO, ocular ischemic syndrome
Optic nerve Papillitis, AION, diabetic papillopathy
Cranial nerves III n (pupil sparing), IV n, VI n palsies
Orbit Mucormycosis, orbital cellulitis
Index
A Anemia 95
Acanthamoeba keratitis 148 Aneurysms of internal carotid artery 223
Accommodative esotropia 207 Angle
Acid burns 299 closure
Acoustic hollowness 285 glaucoma 113
Actinic keratosis 258 with pupillary block 31
Active without pupillary block 31
sarcoidosis 123 recession glaucoma 30
systemic sarcoidosis 122 Anisometropic amblyopia 197
Acute Ankylosing spondylitis 123, 194
angle closure glaucoma 33, 165 Anterior
anterior uveitis 31 capsular phimosis 293
blood loss 85 chamber 2, 39, 125
congestive glaucoma 28, 288 paracentesis 122
dacryocystitis 321 reaction 299
esotropia 205 hyaloidotomy 37
herpetic conjunctivitis 175 ischemic optic neuropathy 228
hydrops 152 scleritis 193
plastic iritis 319 segment
postoperative endophthalmitis 115 inflammation 318
retinal necrosis 64, 314, 320 manifestations 311
trabeculitis 31 sub-Tenons injection 116
Adenovirus 170 uveitis 30
Adies vitrectomy 63
syndrome 219 Anti-glaucoma medication 39
tonic pupil 219 Anti-VEGF
Advanced retinitis pigmentosa 61 drugs 75
Age-related macular degeneration 72 therapy 75
Alkali burns 299 Antiviral therapy 64
Allergic types of conjunctivitis 177 Aphakic glaucoma 30, 38
Alternate cover test 4 Aponeurotic ptosis 268
Amblyopia 197 Applanation tonometry 18
American Uveitis Society 314 Aqueous
Ametropic amblyopia 197 cells 121
Amikacin 118 flare 120
Amniotic membrane graft 180 tear deficiency 184
Amphotericin B 118 Arcuate scotoma 25
Amsler Arcus senilis 158
grid 62 Argon laser
sign 129 photocoagulation 73
Amyotropic lateral sclerosis 216 trabeculoplasty 39, 45
Andersons criteria 25 Argyll Robertson pupil 219
Arteriolar sclerosis 91 Blockage of

Artificial background choroidal fluorescence
drainage shunts 50 55
prosthesis 266 retinal fluorescence 55
Astigmatism 169 Blowout fracture of orbit 304
Atopic keratoconjunctivitis 153 Blue
Atrophic light entoptoscopy 62
AMD 72 sclera 153
eye 266 Blunt trauma 120, 301, 302
Atypical pigmentary dystrophy 101 Blurring of vision 32
Autoimmune disorders 235 Bone free methods 307
Axenfeld sign 152 Bony decompression 254
Azazthioprine 141 Bostons sign 251
Azithromycin 127 Botulinum toxin 216
Bourneville disease 272
B Bowens disease 258, 261
Bowman membrane 155
Bacterial keratitis 144
Brain abscess 277
Bagolini striated glasses 5, 209
Branch retinal vein occlusion 82
Band keratopathy 127, 159
Bruchs membrane 67
Bangersters method 199
Brushfeld spots 124
Basal cell carcinoma 255
Bullous keratopathy 165, 293
Batten disease 61
Buphthalmos 42
Behets
Burkitts lymphoma 311
disease 64, 81, 94, 122, 233, 320
syndrome 194
Behrs optic neuropathy 227 C
Benedicts Calibration of Goldmann tonometer 19
sign 152 Canaloplasty 49
syndrome 236 Candida
Bests disease 101 albicans 312
Bielschowsky head tilt test 6 keratitis 311
Bilateral keratitis 146
acute retinal necrosis 122 Capsular contraction syndrome 297
chronic diffuse punctate epithelial Cardiac valvular disease 85
keratoconjunctivitis 311 Caroticocavernous fistula 30, 231, 279
panuveitis 131 Carotid artery disease 81
Binasal hemianopia 14, 223 Casonis test 122
Biomicroscopic staging of macular hole Cataract 127, 289, 299
69 surgery 63, 293
Birdshot Causes of
chorioretinopathy 123 dry eye 184
retinochoroidopathy 135 IOL malposition 297
Bitemporal hemianopia 15, 223 Cavernous sinus thrombosis 277, 280
Bjerrums tangent screen 14 Cefazolin 145
Bleb-associated endophthalmitis 47, 115 Ceftazidime 118, 145
Blepharophimosis syndrome 268 Central
Blepharoplasty 321 corneal thickness 18, 27
Blepharoptosis 267 hump 22
Blind spot 14 retinal artery
enlargement 221 obstruction 61
Index 325
occlusion 83 Cicatricial
retinal vein occlusion 80 ectropion 271
retinitis pigmentosa 61 entropion 269
scotoma 16, 221, 222 Ciliary body 99
serous chorioretinopathy 65 atrophy 321, 322
Centrocecal scotoma 16, 221 Circumferential retinal folds 230
Chalcosis 310 Classification of
Chandler esotropia 205
procedure 37 exotropia 204
syndrome 40, 165 globe injuries 300
Chemical injuries 299 PVR 112
Chemosis 280 retinal detachment 111
Chemotherapy 263 Clindamycin 127
Chiasmal lesions 222 Clinically significant macular edema 89
Chlamydia Cloudy cornea 42, 299
oculogenitalis 182 Coats disease 33, 109, 113
trachomatis 182 Cocaine test 247
inclusion conjunctivitis 182 Cogan-Reese syndrome 40
Chlamydial inclusion conjunctivitis 175 Collagen vascular disease 81, 85, 235
Chorioretinal Coloboma choroid 99
biopsy 122 Complete
coloboma 16 homonymous hemianopia 224
Choroid 274, 319 VKH disease 130
Choroidal Complications of
detachment 36 hyphema 303
dystrophies 101 vitreous hemorrhage 96
excavation 285 Compressive thyroid optic neuropathy
hemangioma 99, 109 231
melanoma 95, 285 Cone
microvasculitis 133 dystrophy 61, 101
nevus 109 rod dystrophy 61
thickening 130 Confrontation method 14
Choroiditis 7, 140 Congenital
Choroidopathy 135 cataract 202
Christmas tree cataract 287 entropion 270
Chronic fibrosis 235
anterior hereditary endothelial dystrophy 156,
segment inflammatory syndrome 165
129 malformation of anterior chamber
uveitis 31, 288 angle 275
conjunctivitis/blepharitis 263 retinoschisis 101
dacryocystitis 321 rubella 166
fungal infection 263 stationary
intra-ocular inflammation 33 blindness 60
iridocyclitis 127 night blindness 61, 101
lymphocytic leukemia 166 Conjunctiva 7, 99, 170, 260, 274, 311,
papilledema 231 316, 322
progressive external ophthalmoplegia Conjunctival
235, 243 chemosis 280
renal failure 110 impression cytology 186
Conjunctivitis 170, 175 Deep

Connective tissue disorders 233 blood vessels 142
Constant rubbing of eye 153 hemorrhage 52
Contralateral keratitis 319
hemianesthesia/hemiplegia 224 lamellar
homonymous hemianopia 274 endothelial keratoplasty 165
Cornea 1, 7, 39, 99, 125, 142, 274, 311, keratoplasty 169
316, 319, 321, 322 sclerectomy 49
Corneal vascularization 161
color coding 142 Degenerative retinoschisis 102
decompensation 293 Delayed onset pseudophakic
degenerations 158 endophthalmitis 115
dystrophies 155 Demyelinating diseases 235
edema 293 Dendrites in peripheral cornea 311
epithelial edema 32, 279 Dendritic mucus plaques 151
filaments 142 Denervation of lacrimal gland 321
haze 42 Dermatomyositis 122
hypoesthesia 151 Dermoid cyst 265
opacity 173 Descemet
perforation 30 folds 142
transplant 166 membrane 201
rejection 165 endothelial keratoplasty 165
vascularization 161 stripping endothelial keratoplasty
Cortical cataract grading 287 165
Corynebacterium diphtheriae 170 tear 293
Cotton wool spots 52, 85, 311 Diabetes mellitus 64, 227, 239
Cover Diabetic
test 3 maculopathy 89
uncover test 4 papillopathy 228
Cowens sign 252 retinopathy 85, 89, 110
Cranial nerves 316, 319, 322 Diffuse
Craniopharyngioma 235 retinal pigment epitheliopathy 65
Craniosynostosis 276 squamous cell carcinoma 263
Creutzfeldt-Jakob disease 166 Digital tonometry 18
Crystalline dystrophy 155 Dilated tortuous retinal veins 280
Cuppers method 199 Diplopia 217
Curare test 243 charting 6
Cyclic esotropia 205 Direct visualization 307
Cyclosporine 141 Disciform keratitis 150
Cystic fibrosis 227 Dissociated vertical deviation 206
Cysticercosis 109 Donor cornea 166
Cystoid Double
macular edema 7, 63, 293, 322 arcuate scotoma 25
retinal degeneration 275 elevator palsy 235
Cytomegalovirus retinitis 313 Doughnut sign 282
Downs
D and Pataus syndrome 202
Dalrymples sign 251 syndrome 124
Dark fovea 55 Drusen 72
Index 327
Dry eye 184, 217, 321 proptosis 8

syndromes 216 ptosis 11
Duanes and Mobius syndrome squint 3
Dynamic contour tonometer 18 uveitis 7
Dyskeratosis 259 Exposure
keratitis 321
E keratopathy 277
Expulsive hemorrhage 293
Eales disease 93, 95
Exudative
Early
AMD 73
papilledema 230
retinal detachment 109
retinitis pigmentosa 16
Eye in
East-West syndrome 297
AIDS 311
Eaton-Lambert syndrome 216
diabetes mellitus 322
Ectopia lentis 153, 291
leprosy 321
Ectopic lacrimal gland 265
sarcoidosis 318
Ectropion 271
syphilis 319
Edema of
tuberculosis 316
conjunctiva 252
Eyelid hematoma 217
lid 252
Electrophysiological tests 243
Encephalofacial angiomatosis 274 F
Encircling explants 106 Familial
End stage papilledema 231 dominant drusen 101
Endophthalmitis 115, 122, 293, 308 exudative vitreoretinopathy 97, 101
Endothelial rejection 168 Fate of blood 302
Enlargement of blind spot 16, 221 Fever 280
Enroths sign 251 Fibroma molluscum 273
Entropion 269 Filamentous keratitis 147
Enucleation 264, 266 Flame shaped hemorrhages 52
Enzyme glaucoma 38 Fleischer ring 152
Epidemic keratoconjunctivitis 175 Fluorescein stain 142
Epidermoid cyst 265 Foerster
Epiretinal membrane 71, 125 Fuchs spot 103
Episcleritis 321 multifocal choroiditis 319
Epithelial Folinic acid 127
basement membrane dystrophy 155 Follicular inflammation 173
defect 299 Freys syndrome 216
edema 142 Frontal lobe meningioma 223
keratitis 150 Fronto-orbital mucocele 265
rejection 168 Fuchs
Epithelialization of anterior chamber 38 endothelial dystrophy 156, 165
Equatorial scleral expansion 302 heterochromic
Ethambutol toxicity 16 iridocyclitis 30, 31, 288
Evaluation of uveitis 123, 129
corneal ulcer 13 Fundus
glaucoma 1 albipunctatus 101
macular function 62 fluorescein angiography 54
paralytic squint 5 Fungal endophthalmitis 117, 124
G Herpes
Galactosemia 202 simplex
Gallium scan 123 conjunctivitis 176
Gelatinous white nodules 124 keratitis 150
Gentamicin 145 virus 151, 182, 183
Ghost zoster ophthalmicus 311
cell glaucoma 30, 38, 95 Herpetic disciform keratitis 165
vessels 142 Heterophoria 210
Giant High altitude retinopathy 85
cell arteritis 194, 235, 236 Hirschbergs test 4
papillary conjunctivitis 178 Histiocytic cell sarcoma 120
Giffords sign 251 Histoplasmosis 122
Glaucoma 14, 125, 127, 274, 277, 322 HIV retinitis 312
filtering surgery 63 Hodgkins disease 166
Glaucomatocyclitic crisis 30, 32 Hole
Goldmann closure 69
applanation tonometry 18 expansion 69
Favre dystrophy 101 Homonymous hemianopia 223
perimetry 14 Horizontal
Goldzihers sign 251 gaze palsies 245
Gonioscopy 1, 21 squint correction 216
Grading of Horners syndrome 247, 267
angle 21 Hotz procedure 270
hyphema 302 HSV keratitis 311
severity 46 Huber classification 211
Graft infection 168 Hydatid cyst 122, 276
Granulomatous Hydroxy amphetamine test 247
iridocyclitis 124 Hyperfluorescence 55
uveitis 321 Hyperlipidemia 81
Graves disease 265, 276 Hyperopia 169
Griffiths sign 251 Hypertension 64, 91, 239
Gummatous iritis 319 Hypertensive
choroidopathy 92
retinopathy 85, 91, 110
H
Hypertrophy of extraocular muscles 251
Haab striae 42 Hyphema 22, 38, 142
Haber Weiss reaction 309 Hypotensive maculopathy 322
Hard exudates 52, 89 Hypotropia 267
Head injury 81 Hypoxic eyeball syndrome 279
Headache 280
Hemangioma 265
Hemolytic glaucoma 30, 96 I
Hemorrhage 89, 106, 265 Ice syndrome 165
Hemorrhagic Idiopathic
choroidal detachment 109 acute multifocal retinitis 320
conjunctivitis 175 chorioretinal disorder 65
Hemosiderosis bulbi 96 macular telangiectasia 76
Hepatitis 166 orbital inflammatory syndrome 239
Hereditary fundus dystrophies 101, 288 retinal vasculitis 94
Heredomacular degenerations 16 Incomplete VKH disease 130
Index 329
Indentation tonometry 18 K
Indocyanine green angiography 56 Kanskis classification 89
Infantile Kaposis sarcoma 263, 311
esotropia 206 Keith-Wagener-Barker classification 91
glaucoma 201 Keratoacanthoma 260
Infiltrative optic neuropathy 228 Keratoconjunctivitis sicca 188
Inflammatory glaucoma 30, 31 Keratoconus 152
Inner nuclear layer 52 Keratomycosis 146
Intermediate uveitis 64, 114, 125 Kneiss sign 252
Internuclear ophthalmoplegia 245 Kochers sign 251
Interstitial keratitis 149, 321 Koeppe nodules 124
Intraocular Krimsky test 4
lens 294 Krukenbergs spindle 1
malposition 296 Kveim test 122
power calculation 295
pressure 23 L
tumors 30, 33
Intravitreal Lacquer cracks 103
antibiotics 116 Lacrimal
injections 81 gland
triamcinolone 64 enlargement 252
Intrinsic eye disease 166 hypersecretion 216
Inverted follicular keratosis 260 tumors 265
Ipsilateral system 321
hyperchromic iris 274 Lacrimation 42
telangiectasia of conjunctival and Lamellar keratoplasty 169
episcleral vessels 274 Landers sign 318
Iridocorneal endothelial syndrome 40 Large
Iris 2, 7, 39, 99, 125, 274, 319 blood vessels 235
angiography 123 retinal arteries and veins 52
atrophy 151 vessel disease 311
diaphragm 302 Laryngeal dystonia 216
hole 321 Laser photocoagulation 284
melanoma 120 Late bleb leak 47
nevus 40, 124 Latent nystagmus 206
syndrome 124 Lateral
nodules 124 geniculate body 224
pearls 124, 321 orbitotomy 265
prolapse 293 wall fracture 305
Irregular peripheral contraction 221 Lattice degeneration 102
Isolated trabeculodysgenesis 42 Layers of retina 52
Lebers
congenital amaurosis 61, 101, 153
J hereditary optic neuropathy 221, 227
Jarisch-herxheimer reaction 319 Leiomyoma 124
Jellineks sign 251 Lens 2, 7, 125, 141, 287, 322
Jones test 190 extraction with anterior vitrectomy
Junctional scotoma 15 and peripheral iridectomy 37
Juvenile induced glaucoma 30
rheumatoid arthritis 122 subluxation 113
xanthogranuloma 124 Lepromatous pannus 321
Lepromin test 122, 321 Meesmann dystrophy 155

Leprosy 122 Megalo cornea 42
Leukemia 85, 110, 120, 124, 166 Melanoma associated retinopathy 61
Leukocoria 113 Meningioma 223, 235
Lids 260, 274, 311, 319, 321 Meningitis 277
Ligneous conjunctivitis 170 Meningoencephalocele 276
Limbal Methotrexate 141
ischemia 299 Microsporidial keratitis 311
stem cell transplant 181 Microtropia 205, 209
Lincoffs rule 105 Migraine 29, 81
Lipid keratopathy 158 Military lepromas 321
Lisch nodules 124 Mitral valve prolapse 81
Loewes sign 252 Mixed cell melanomas 285
Low Moderate enlargement of blind spot 221
flow CCF 279 Modern ETDRS classification 89
pressure glaucoma 26 Modified classification of ocular chemical
Lower lid injuries 299
ectropion 321 Moebius syndrome 213
entropion 254 Mohs micrographic technique 256
reconstruction 263 Molluscum contagiosum 311
senile entropion 216 Moorens ulcer 163, 260
Lumbar puncture 123 Morning glory syndrome 109, 227
Lymph node dissection 259 Motor neuropathy 216
Mucin deficiency 184
Lymphangioma 265
Mucopolysaccharidosis 201
Lymphatic spread 258
Multibacillary therapy 322
Lymphoma 109
Multifocal choroiditis 137
Multiple
M cranial nerve palsies 235
Macular evanescent white dot syndrome 138
coloboma 153 sclerosis 166, 233, 239
dystrophies 101 Munson sign 152
grid photocoagulation 64 Myasthenia gravis 236, 238, 239
hole 69 Mycobacteria 144
hypoplasia 113 Mydriatic test 25
Madarosis 321 Myesthesia gravis 216
Maddox rod 5, 62 Myopia 169, 276
Malaise 280 Myopic
Malignant conus 103
glaucoma 30, 36, 38 esotropia 205
melanoma 99, 109, 124, 261
orbital tumors 250 N
Management of Nasopharyngeal carcinoma 235
bleb leak 46 Nd: YAG laser iridotomy 44
over-filtering bleb 46 Near-total field defect 25
Map stone test 25 Necrotic melanomas 285
Marcus Gunn pupil 219, 220 Necrotizing
Marfan syndrome 292 herpetic retinopathy 312
Medial wall fracture 305 scleritis
Medium blood vessels 235 with inflammation 194
Medullated nerve fibers 227 without inflammation 194
Index 331
Neisseria gonorrhoeae 182 Ophthalmoparesis 243

infection 182 Ophthalmoplegia 280
Neonatal cloudy cornea 201 Ophthalmoscopic classification 226
Neostigmine test 243 Opportunistic infections 312
Neovascular glaucoma 29, 30, 33 Optic
Neovascularization of angle 33 atrophy 226
Nerve fiber disc
bundle defects 221 coloboma 227
layer 52 drusen 227
Neurofibroma 265 pit 66, 227
Neuroretinitis 319 vasculitis 228
Neurotrophic nerve 125, 274, 316, 319, 322
keratitis 321 dysfunction 277
keratopathy 201 glioma 221, 265, 281
Neutral density filter 197 head drusen 221
New castle conjunctivitis 175 hypoplasia 113, 227
Nicotinic acid 64 lesions 221
Non-contact tonometer 18 meningioma 265, 282
Non-Hodgkins lymphoma 311 pit 109, 221
Non-penetrating filtration surgery 49 neuritis 16, 228, 233, 277
Non-resolving vitreous hemorrhage 96, neuropathies 311, 314, 315
125 radiation 224
Non-Sjgrens syndrome dry eye 184 tract syndrome 223
Non-specific orbital inflammatory disease Optical coherence tomogram 57
249 Oral corticosteroids 128
Non-surgical management of squint 214 Orbit 274, 316, 319, 322
Normal optic nerve 134 Orbital
Normotensive glaucoma 26, 228 abscess 265
North Carolina macular dystrophy 101 cellulitis 109, 250, 276, 277
Nuclear cataract grading 287 decompression 254
Nystagmus 113 floor fracture 235
blockade syndrome 205 inflammation 30
pseudotumor 109
O shadowing 285
Outer plexiform layer 52
Occlusion of middle cerebral artery 16
Occlusive vasculopathy 315
OCT 79 P
staging of macular hole 69 Pain relief 157
Ocular Painful ophthalmoplegia 277
hypertension 27 Panretinal photocoagulation 81
ischemic syndrome 33, 61, 86 Papilledema 221, 230
myasthenia 235, 242 Papillophlebitis 228
toxoplasmosis 126 Paracentral scotoma 221
Oculoplasty 249 Paralytic
Oguchi disease 101 ectropion 271
Olfactory groove meningioma 223 pupil 219, 220
Opacification of crystalline lens 287 Parinauds syndrome 235
Open angle glaucoma 31 Pars
Ophthalmia neonatorum 182 plana vitrectomy 37, 63, 96, 107
Ophthalmic artery occlusion 61 planitis 30, 94
Partial stem cell deficiency 181 displacement of lens 302

Pathergy test 320 ischemic optic neuropathy 228
Patons lines 230 keratoconus 154
Paucibacillary therapy 322 polar cataract 113
Paving stone degeneration 103 polymorphous dystrophy 156, 165
Penetrating keratoplasty 63, 165 scleritis 193, 195
Penetrating trauma 120 sclerotomy 37
Peripapillary atrophy 16 staphyloma 103
Peripheral synechiae 319
anterior synechiae 275 uveitis 109
hump 22 vitreous detachment 95
iridectomy 37 Post-herpetic neuralgia 151
retinal degeneration 102 Post-traumatic endophthalmitis 116
Periphery of iris 124 Post-viral infections 235
Perkins tonometer 18, 43 Preproliferative diabetic retinopathy 89
Persistent Presbyopia 169
hyperplastic primary vitreous 113 Primary
pupillary membrane 113 angle closure glaucoma 28
severe vitritis 125 open angle glaucoma 23, 38
Peters anomaly 201 pulmonary hypertension 30
Phacoanaphylactic glaucoma 30 Prism bar cover test 4
Phacolytic glaucoma 30 Progressive
Phacomorphic glaucoma 30, 35 iris atrophy 40
Pharyngoconjunctival fever 175 outer retinal necrosis 313
Phenylephrine-pilocarpine test 25 Proliferative
Phlyctenular conjunctivitis 178 diabetic retinopathy 33, 89
Photo stress testing 62 vitreoretinopathy 111
Photodynamic therapy 73, 99 Prone provocative test 25
Phthisis bulbi 266 Proptosis 9, 276, 280
Pigment Provocative tests 25
epithelial detachment 67 Pseudoexfoliation 1
epitheliopathy 133 glaucoma 39
Pigmentary syndrome 30, 39
glaucoma 30 Pseudoneuritis 231
retinopathy 309 Pseudophakic glaucoma 30
Pin-point pupil 321 Pseudoproptosis 276
Pituitary adenoma 235 Pseudoptosis 267
Pneumatic retinopexy 106 Pseudotumor 276, 311
Pneumocystis carinii 312 cerebri 248
Pochins sign 251 Pterygium 142, 172, 260
Polar cataract 290 Ptosis 280
Polyarteritis nodosa 122, 194, 235 Punctate
Polypoidal choroidal vasculopathy 78, 95 inner choroidopathy 139
Port wine stain 274 outer retinitis 126
Posner-Schlossman syndrome 30-32 Pupil 2, 7, 39, 218, 319, 321
Posterior Pupillary
capsular block glaucoma 36, 38
opacification 293 light reaction 62
rupture 293 Pure epitheloid cell melanomas 285
Index 333
Purkinjes entoptic phenomenon 62 Retrolental fibroplasia 153

Pyogenic granuloma 260 Reyes syndrome 166
Pyrimethamine 127 Rheumatoid arthritis 122, 194
Right homonymous
Q hemianopia 15
lower quadrantanopia 15
Quinine toxicity 61
upper quadrantanopia 15
Ring
R abscess 148
Radiation scotoma 16, 319
dermatosis 258 Rod cone dystrophies 101
retinopathy 85 Roof fracture 305
Raised Rose bengal test 186
episcleral venous pressure 30 Rosenbachs sign 251
intracranial tension 239 Rubeosis iridis 33
Recent hemorrhage 95 Rule of thumb 254
Recurrent Ruptured dermoid cyst 250
chalazion 263 Rush disease 97
genital ulcers 320
lytic epithelial keratitis 151
S
Rees Ellsworth classification 284
Refraction 322 Saccadic eye movements 243
Refractive surgery 169 Salzmann nodular degeneration 160
Regression formula 295 Sarcoidosis 94, 122, 123, 233, 250
Reis-Buckler dystrophy 155 Scarring of conjunctiva 173
Reismans sign 252 Scheie classification 91
Reiters syndrome 194 Schirmers test 186
Repair of retinal detachment 109 Sclera 7, 193, 316, 321, 322
Restrictive myopathy 253 Scleral
Retained buckling 63
foreign body 124 necrosis 321
lens matter blocking angle 38 Scleritis 109, 127, 193, 314, 319, 321
Reticulum cell sarcoma 120, 123 Sclerocornea 201
Retina 52, 125, 274, 316, 322 Scleroderma 122
Retinal Scleromalacia perforans 194
astrocytoma 114 Scotoma 17, 221
capillaries 52 Seborrheic keratosis 260
color coding 53 Secondary
detachment 105, 106, 125, 293, 309 angle closure 29
dysplasia 114 glaucoma 33
edema 52, 89 glaucoma 30, 293
pigment epithelium tear 68 infantile glaucoma 43
tear 95 open angle glaucoma 33
vascular disease 71 Seidels test 46
vein occlusion 85 Selective laser trabeculoplasty 45
Retinitis pigmentosa 16, 64, 101, 153 Senile cataract 287
Retinoblastoma 99, 109, 113, 120, 124, Septicemia 166
283 Serological tests 122
Retinocytoma 114 Serous retinal detachment 275
Retinopathy of prematurity 97 Serpiginous choroiditis 134, 140
Severe Sticklers syndrome 101

anemia 85 Stimulus deprivation amblyopia 197
choroidal scarring 134 Stockers line 172
Shallow anterior chamber 46, 113 Strabismic amblyopia 197
Short wave automated perimetry 14 Streptococcus
Shortening of scleral collagen 299 pneumoniae 170, 182, 277
Sickle cell pyogenes 277
disease 81, 110 viridans 168
retinopathy 95 Stromal
Siderosis bulbi 61, 309 edema 142
Simple congenital ptosis 267 necrotic keratitis 150
Sine-wave sign 21 rejection 168
Sinusitis 254 Sturge-Weber syndrome 30, 274
Sixth nerve palsy 239 Subacute allergic catarrhal conjunctivitis
Sjgrens syndrome 184 177
Skin Subcapsular cataract 287
scarring 151 Sub-retinal neovascular membrane 103
tests 122 Sudden onset diplopia 215
Sleep test 243 Sulfadiazine 127
Slit-lamp biomicroscopy 62 Sunrise syndrome 296
Small Sunset syndrome 296
blood vessels 235 Superciliary madarosis 321
peripheral retinal detachments 99 Superficial
Smoke stack appearance 66 blood vessels 142
Snail track degeneration 102 vascularization 161
Snellens charts 200 Superior
Snellen-Donders sign 252 altitudinal defect 221
Snow banking 7 limbic keratoconjunctivitis 179
Snowflake dystrophy 101 nasal depression 221
Socket reconstruction 266 Suprachoroidal hemorrhage 36, 293
Sorsby pseudoinflammatory macular Swedish interactive thresholding
dystrophy 101 algorithm 14
Spastic bladder 216 Swimming pool conjunctivitis 175
Sphenoidal ridge meningioma 223 Sympathetic ophthalmia 109
Spheroidal degeneration 159 Syphilis 94, 166
Spindle cell melanomas 285 Systemic lupus erythematosis 194
Spiramycin 127
Spondyloarthopathies 320 T
Spontaneous lens dislocation 274 Tapioca melanoma 124
Spring catarrh 177 Tarsal strip procedure 321
Squamous cell carcinoma 258, 261, 311 Tarsorrhaphy 321
Standard automated perimetry 14 Tear osmolality 186
Staphylococcus Temporal pallor 227
aureus 115, 227 Tensilon test 236, 243
epidermidis 115 Tetracycline 127
Staphyloma 196, 321 Therapeutic contact lens 157
Stargardt dystrophy 101 Thiel Behnke dystrophy 155
Stellwags sign 251 Third nerve palsy 235
Stereoscopic method 307 Thrombotic thrombocytopenic purpura
Steroid induced glaucoma 30, 38 110
Index 335
Thyroid ptosis 217

disorder 227 reconstruction 263
function tests 236 retraction 216
related orbitopathy 236, 239, 251 Uvea 120, 316, 321
Tolosa-Hunt syndrome 241 Uveitis 120
Tonometry 18 glaucoma-hyphema syndrome 41
Topical
antibiotics 116
V
atropine 46
steroids 321 Valsalva retinopathy 95
Total Van Herricks grading 21
blindness 221 Vancomycin 118, 145
stem cell deficiency 181 Varicella zoster virus 151
Toxemia of pregnancy 110 Vascular perfusion 23
Toxic Vernal keratoconjunctivitis 153, 177
amblyopia 16 Vertical gaze palsy 235
pupil 219 Viral
Toxocariasis 114, 123 conjunctivitis 311
Toxoplasma gondii 126, 312 retinitis 94
Toxoplasmic retinochoroiditis 312 Visual
Toxoplasmosis 233 acuity 62
Trabeculectomy 39, 46 cortex 225
Trabeculitis 299 Vitrectomy 113, 117
Trachomatous Vitreomacular traction syndrome 64
inflammation 173 Vitreous
scarring 173 cells 7, 121
trichiasis 173 haze 121
Tractional retinal detachment 108 hemorrhage 38, 95, 113
Train track sign 274, 282 loss 293
Transpupillary thermotherapy 74, 284 tap/biopsy 122
Traumatic Vogt Koyanagi-Harada
hyphema 302 disease 130, 134
optic neuropathy 227 syndrome 109, 123
Treatment of Vogt
diabetic retinopathy 90 striae 152
graft rejection 168 white limbal girdle 158
PORN 313 Von Graefes sign 251
True congenital glaucoma 42 Von Hippel-Lindau disease 272
Tuberculosis 122, 123, 233, 312, 316
Tuberculum sellae meningioma 15, 223 W
Tuberous sclerosis 272
Wagener-Clay-Gibner classification 91
Tubular vision 16
Wagners vitreoretinal dystrophy 101
Water drinking test 25
U Watzke-Allen test 69
Unilateral Webers syndrome 236
acute idiopathic maculopathy 66 Wegeners granulomatosis 122, 194, 250
blindness 15 Weil-Marchesani syndrome 292
central scotoma 15 Werners classification 251
Upper lid White
entropion 321 dot syndromes 132
punctate subepithelial opacities near Y

limbus 321 YAG anterior hyaloidotomy 63
WHO classification 173 Yannuzzis classification 76
Worth four dot test 5
Wound dehiscence 168
Z
X Zeiss contact lens 307
Zonular
Xeroderma pigmentosum 257, 258 cataract 290
Xerophthalmia 189 dialysis 293
X-ray
chest 123
sacroiliac joint 123

Clinical Ophthalmology

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CLINICAL

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Jaypee Brothers Medical Publishers (P) Ltd.

Jaypee Medical Inc. Jaypee Brothers Medical Publishers (P) Ltd.

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2013, Jaypee Brothers Medical Publishers

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Clinical Ophthalmology Made Easy

Anina Abraham MS Nitesh Narayen MS DNB

A wise man once said nothing succeeds like success

Kasu Prasad Reddy MBBS MS DO MRC (Ophth)

Clinical Ophthalmology Made Easy is a condensation of information on a wide

Clinical Ophthalmology Made Easy is a condensation of information on a wide

8. Pediatrics and Squint 197

Brown Syndrome 212

11. Lens 287

Intraocular Lenses 294

12. Trauma 299

13. Systemic Diseases 311

1 mm of deviation of corneal reflex = 7 deviation

Worth Four Dot Test

Maddox Rod (When Placed in Front of Right Eye)

Size, shape, surface, margins, skin over-swelling, consistency, signs of

Measure horizontal displacement: Mark a point (P) on the center of the

Fair function = 511 mm

EVALUATION OF CORNEAL ULCER

Right Homonymous Hemianopia

Right Homonymous Upper Quadrantanopia

Right Homonymous Lower Quadrantanopia

Homonymous Hemianopia with Macular Sparing

Indentation Tonometry (Schiotz)

CALIBRATION OF A GOLDMANN TONOMETER

Checking the Calibration at 0

Checking the Calibration at 2

Checking the Calibration at 6

Grading of the Angle

Van Herricks Grading

PRIMARY OPEN ANGLE GLAUCOMA

2. Asymmetrical cupping > 20% in discs of the same size

3. Cup:disc ratio > 0.5 : 1.0 (especially in the vertical axis)

5. Superficial disc hemorrhages at disc margin (splinter hemorrhage in NTG)

Ocular Hypertension Treatment Study

PRIMARY ANGLE CLOSURE GLAUCOMA

Anterior chamber reaction with cells and flare

Classification Pathology Management

Nd: YAG laserdisrupts the anterior hyaloid face; opens-up the

Cornea Pseudoexfoliative material on endothelium [mimics KPs]

IRIDOCORNEAL ENDOTHELIAL SYNDROME

Secondary infantile glaucoma

Nd: YAG LASER IRIDOTOMY

ARGON LASER TRABECULOPLASTY

Selective Laser Trabeculoplasty

Management of Bleb Leak

Management of Over-filtering Bleb

Filtration Failure - Due to

NON-PENETRATING FILTRATION SURGERY

ARTIFICIAL DRAINAGE SHUNTS

LAYERS OF THE RETINA

RETINAL COLOR CODING

FUNDUS FLUORESCEIN ANGIOGRAPHY

Dark Fovea Due to

INDOCYANINE GREEN ANGIOGRAPHY

OPTICAL COHERENCE TOMOGRAM

Basic ISCEV Flash ERG Response