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Clinical Ophthalmology
Made Easy
Clinical Ophthalmology
Made Easy
Anina Abraham MS
Fellow in Vitreo-retinal Surgery
LV Prasad Eye Institute
Hyderabad
Sirisha Senthil MS FRCS

Consultant in Glaucoma
LV Prasad Eye Institute
Hyderabad
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Clinical Ophthalmology Made Easy
© 2009, Anina Abraham, Sirisha Senthil
All rights reserved. No part of this publication and photo CD ROM should be reproduced, stored in a
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This book has been published in good faith that the material provided by authors is original. Every
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under Delhi jurisdiction only.
First Edition: 2009
ISBN 978-81-8448-499-1
Typeset at JPBMP typesetting unit
Printed at Rajkamal
Preface
This book 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. This book is primarily meant for postgraduate
students for whom it will be a quick reference in preparing
for the exams and for the practising 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 flowcharts have been added where necessary to add clarity.
Although it provides information on most topics, we wish to
caution readers that this 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 this book will be a useful addition to your library.
Anina Abraham
Sirisha Senthil
Acknowledgements
First and foremost, we would like to thank our patients, our

greatest teachers. We are especially grateful to Dr Kasu Prasad
Reddy, Dr P Muralidhar Rao, Dr Rqjeetha Jaiswal and all
our colleagues for their valuable support and constant
encouragement. We are indebted to all our teachers in Sarojini
Devi Eye Hospital, Hyderabad and Aravind Eye Hospital,
Madurai, for their valuable lessons in ophthalmology, without
which we would not have been able to compile this book.
Many thanks to Mrs Leela Chandy, for extending her
helping hand, to Tamar Chatterjee who has been a great help
in designing the cover page of this book; and to our families,
for always being there for us. And above all, we thank God,
the Maker of the Eye.
Contents
1. Cornea .......................................................... 1
2. Conjunctiva ................................................. 43
3. Sclera .......................................................... 67
4. Glaucoma .................................................... 73
5. Retina ........................................................ 115
6. Neuro-ophthalmology ................................. 189
7. Lens ........................................................... 225
8. Uvea .......................................................... 243
9. Trauma ....................................................... 269
10. Oculoplasty ................................................ 285
11. Pediatrics and Squint ................................. 337
12. Case Taking ............................................... 365
Index .................................................................... 381

CHAPTER 1
Cornea
2 CLINICAL OPHTHALMOLOGY MADE EASY
CORNEAL COLOR CODING

Scars Black
Degenerations Black
Contact lens Black dotted circle
Sutures Black straight lines
Cornea! outline Black
IOL Black
Guttata Black shade
Deep blood vessels Dark red, straight lines ending at limbus
Superficial blood vessels Bright red, wavy branching lines
crossing limbus
Ghost vessels Red dotted straight lines
Hyphema Red
Rose Bengal stain Red
Pterygium Red
Epithelial edema Blue circles
Descemet’s folds Blue wavy lines
Stromal edema Blue shadows
Lens Green
Vitreous Green
Corneal filaments Green
Fluorescein stain Green
Epithelial defect Green
Infiltrates Yellow
Hypopyon Yellow
Iris Brown
Pigment Brown
Keratic precipitates Brown
CORNEA 3
(For color version see plate 1)

BACTERIAL KERATITIS
PREDISPOSING FACTORS
– Contact lens wear may cause epithelial defects; predispose
to Pseudomonas aeruginosa infection
– Pre-existing corneal disease - trauma, 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
– Circum-corneal 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
– P. 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; A–AC reaction;
L – location.
CORNEA 5
Stains & culture media for microbial keratitis
SUSPECTED STAIN MEDIA
ORGANISM
Aerobic bacteria 1. Gram 1. Blood agar
2. Acridine orange 2. Chocolate agar
3. Thioglycollate broth
Anaerobic bacteria 1. Gram stain 1. Anaerobic blood agar
2. Acridine orange 2. Phenylethyl alcohol
agar in anaerobic
chamber
Mycobacteria 1. Gram 1. Blood agar
2. Acid fast 2. Lowenstein-Jensen
3. Lectin medium
Fungi 1. Gram 1. Blood agar (25°)
2. Acridine orange 2. Sabouraud agar
3. Calcofluor white 3. Brain-heart infusion
(25°)
Acanthamoeba 1. Acridine orange 1. Non-nutrient agar
2. Calcofluor white with E. coli overlay
2. Blood agar
3. Buffered charcoal-
yeast extract agar
GRAM’S STAINING
[Gram +ve stains purple; gram –ve stains pink]
1. Heat fix the slide → 2. flood with crystal violet [1 min]
5 3
4. Stain with Gram’s Iodine [1 min] WASH
7
6. Decolorize with Acetone: Alcohol sol. [in 1:1 ratio]
8. Flood with dilute carbol fuschin [1 min] → WASH
THEN AIR DRY
GIEMSA STAINING
Fix slide with absolute methanol [5-10 min]
↓
Stain with Giemsa stain [30 min]
↓
AIR DRY
ACID FAST STAINING

[stains typical and atypical mycobacteria]
Heat fix the slide → flood with carbol fuschin
↓
WASH
↓
Decolorize with 1% H2SO4
↓
Stain with methylene blue
[counter-stain]
KOH MOUNT
A drop of 10% KOH is placed on the slide with the corneal
scraping; a cover slip is placed over it; Fungal elements are
looked for under the microscope.
TREATMENT
– In the form of broad spectrum topical antibiotics
– Oral ciprofloxacin 750 mg BD in juxta-limbal keratitis
– Atropine 3% ointment BD - to prevent posterior synechiae
and decrease pain from ciliary spasm.
CORNEA 7
Antibiotics used in bacterial keratitis
ORGANISM ANTIBIOTIC TOPICAL DOSE
GP cocci Cefazolin 50 mg/ml
Vancomycin 50 mg/ml
GN rods Tobramycin 9-14 mg/ml
Gentamicin 15 mg/ml
Ceftazidime 50 mg/ml
Fluoroquinolones 3 mg/ml
No/multiple Cefazolin + 50 mg/ml
organisms Gentamicin (or) 15 mg/ml
Fluoroquinolones 3 mg/ml
GN cocci Ceftriaxone 50 mg/ml
Ceftazidime 50 mg/ml
Mycobacteria Amikacin 20 mg/ml
* GP = gram positive
* GN = gram negative
Preparation of fortified topical medication

DRUG VIAL STRENGTH HOW TO PREPARE
Cefazolin 1 vial = 500 mg Add 10 ml of AT to vial
[50 rag/ml]
Ceftazidime 1 vial = 500 mg Add 10 ml of AT to vial
[50 rag/ml]
Vancomycin 1 vial = 500 mg Add 10 ml of AT to vial
[50 rag/ml]
Gentamicin 1 vial = 2 ml Add 2 ml from vial to
[15 mg/ml] [40 mg/ml] 5 ml of 0.3%
gentamicin eye drops
* AT = preservative free artificial tears
KERATOMYCOSIS
CAUSED BY
– Filamentary fungi - Fusarium sp., Aspergillus sp
– Yeasts - Candida species (immunocompromised individuals;
pre-existing corneal disease).
PATHOGENECITY
– Hyphae grow along stromal collagen fibers
– Ineffective phagocytosis by host immune system because
hyphae are large - instead digestion of host cells occurs
– Immunosuppression increases fungal growth
– Fungi enter anterior chamber by penetrating intact
Descemet’s 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.
Candida keratitis
– Yellow-white ulcer with dense suppuration
Rx:
• Topical Imidazole 1%
• Topical Flucytosine 1%
• Oral fluconazole 200 - 400 mg/day if severe
CORNEA 9
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
– Hypopyon - thick and immobile - due to direct invasion
of hyphae enmeshed in thick exudates
Rx:
• Topical natamycin 5%,
• Topical amphotericin B 0.15%
• Oral ketoconazole 200 - 600 mg/day if severe
INVESTIGATIONS
– KOH mount – KOH dissolves epithelial cell walls; hyphae
become visible
– Culture media – Sabouraud’s 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]
– Surgery –
• superficial keratectomy - for good drug penetration
• glues - if micro-perforation occurs
• therapeutic keratoplasty - for non-healing ulcers, corneal
perforation.
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 abscess - may be central/
paracentral
– Radial keratoneuritis - perineural infiltrates
– Sub-epithelial keratopathy
– Endothelial plaque, hypopyon
– Frank corneal necrosis
– Pseudo-dendritic keratitis
– Small white satellite lesions
– Slowly progressive stromal opacification; descemetocele
– Scleritis
INVESTIGATIONS
– 10% KOH mount - amebic cysts are seen
– Calcofluor white - a chemofluorescent dye with special
affinity for acanthamoeba cysts
– Gram’s stain, Giemsa stain, Periodic Acid Schiff
– Culture on non-nutrient agar with E. coli overlay; buffered
charcoal yeast extract.
CORNEA 11
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
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 1-2 weeks]
– Pain, photophobia, lacrimation, blepharospasm
– Circum-corneal congestion, cloudy cornea
– Superficial peripheral vascularization
– Anterior uveitis, choroiditis
– Limbitis - raised inflamed sector of limbus from which
deep blood vessels invade
2. FLORID STAGE [from 2-4 months]
– increased inflammation, DM folds
– deep vascularization
– ground glass cornea - diffuse stromal cellular infiltration
– Salmon patch - corneal clouding obscures the outline
of the vessels — looks dull, pinkish red
3. REGRESSIVE STAGE [from 1-2 years]
– clearing starts
– blood vessels become non-perfused → GHOST
VESSELS - may refill later following inflammation -
bleeding occurs
– stromal thinning, scarring, flattening
4. INACTIVE STAGE
– central deep stromal scar; ghost vessels seen
CORNEA 13
COMPLICATIONS
– corneal decompensation, corneal guttata
– band keratopathy, lipid keratopathy
– Salzmann nodular degeneration, astigmatism
– glaucoma
TREATMENT
– Topical steroids - to reduce corneal inflammation and iritis
– Penicillin G given in →
• Primary and secondary syphilis → 1.2 million units i.m
• Tertiary syphilis → 2.4 million units i.m weekly × 3
wks
– Penetrating keratoplasty - for corneal scarring
HERPES SIMPLEX KERATITIS
EPITHELIAL KERATITIS
– present with watering, discomfort, decreased vision, pain
– opaque epithelial cells break down 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
Rx:
1. debridement of dendritic (not geographic) ulcer
2. acyclovir ointment 3% (5 times per day); check for
response in a week; if no response, change the antiviral
agent to -
• trifluorothymidine 1% (6 X/day) or
• ganciclovir gel 0.15% (5 X/day) [5 times per day]
* 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
– infection of keratocytes and endothelium
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 precipitates - WESSELY RING → marks
the junction between viral antigen and host antibody
– mild anterior uveitis; raised IOP
– decreased corneal sensation
CORNEA 15
Treatment
– Topical prednisolone acetate 1% + antiviral cover initially
[if steroids used > 4 times/day]
– If topical prednisolone acetate 0.25% used - no need for
antiviral cover
– Gradually taper steroids over several weeks
STROMAL NECROTIC KERATITIS

– active viral invasion and tissue necrosis
– can have an intact epithelium or epithelial disease
– cheesy/necrotic stroma
– profound interstitial opacification
– anterior uveitis, KPs
– scarring, vascularization, lipid keratopathy, perforation
– Rx:
• epithelial disease is treated with topical antivirals
• severe stromal keratitis associated with anterior uveitis
is treated with steroids (cautiously) + topical antivirals
+ topical antibiotics
Eye disease caused by Herpes simplex virus

and Varicella zoster virus
HERPES VARICELLA-
SIMPLEX ZOSTER
Dermatomal Incomplete Complete
distribution
Pain Less More
Dendrites Large with central Small, medusa-like
ulceration and dendrites without central
terminal bulbs ulceration or terminal bulbs
Dendritic Don’t occur Occur late
mucous plaques
Skin scarring Rare Frequent
Postherpetic Rare Common
neuralgia
Iris atrophy Patchy Sectoral
Bilateral involvement Rare Never
Recurrent lyric Common Never
epithelial keratitis
Corneal Sectoral/diffuse Frequent
hypoesthesia
CORNEA 17
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. Endocrinological - because 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 ring - a line running along the base of the cone
due to iron deposition superficial to the Bowman’s
membrane (complete/incomplete; pigmented/yellow/brown)
– Prominent corneal nerves
– Stromal thinning increases gradually from base of the cone
to the apex
– Vogt’s striae - thin vertical stress lines in the deeper stroma
which disappear on digital pressure
– Endothelial reflex because of increased concavity
– Acute Hydrops - in the center of the cone due to rupture
of the descemet’s membrane and influx of fluid into the
stroma
– Scarring following rupture
– Munson sign - on looking down, the angular curve is

assumed by the lower lid margin
– Axenfeld sign - loss of sensitivity at the apex of the cone
– Benedict sign - conical reflection on the nasal cornea
when torch light thrown from temporal side
INVESTIGATIONS
– Keratometry - non-alignment of the mires
– breaking/doubling of the right lower circle.
– Placido’s disc - irregularities in reflection of illuminated rings
near the corneal center; distortion of the horizontal axis
– Direct ophthalmoscopy - oil drop sign
– Retinoscopy - scissors reflex; 2 shadows move in opposite
direction
– Orbscan detects early keratoconus; bow-tie pattern; called
Forme Frustae keratoconus
OCULAR ASSOCIATIONS
– Vernal keratoconjunctivitis, atopic keratoconjunctivitis [due
to constant rubbing of eye]
– Retinitis pigmentosa; Leber’s congenital amaurosis
– Retrolental fibroplasia
– Macular coloboma
– Ectopia lentis, blue sclera
– Cataract, retinal detachment, optic atrophy
– Xeroderma pigmentosa
– Addison’s disease
– Syndromes - Down’s, Ehlers-Danlos, Marian’s, Crouzon’s,
Apert’s.
CORNEA 19
DIFFERENTIAL DIAGNOSIS
KERATOCONUS KERATOGLOBUS PELLUCID MARGINAL
DEGN
Most common Rare Less common
Bilateral [usually] Bilateral Bilateral
Onset at puberty Onset at birth 20 - 40 years
Inferior paracentral Thinning greatest 1-2 mm band of
thinning in periphery thinning inferiorly
Protrusion at apex Generalized Protrusion superior to
protrusion band of thinning
Fleischer ring present Absent Sometimes present
Scarring common Mild scarring Only after hydrops
Striae are common Sometimes Sometimes
* DEGN - degeneration
TREATMENT
1. Spectacles
2. Contact lenses - RGP [rigid gas permeable]
• Gas-permeable with large diameter - for oval/globus
cones
• Aspherical - for nipple cones
• Small, steep lenses - for severe nipple cones
• Semi-rigid/hard - for 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)
• Thermokeratoplasty - heat is applied to the tip of the

cornea for 1 min which causes shrinkage of collagen
and flattening of the cornea
• Intacts [intra-stromal rings]
– Rx 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 21
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 he very slow or rapid Progression usually slow
Corneal dystrophies
Epithelial Bowman Stromal Endothelial

membrane
1. Map-dot- 1. Lattice (AD)

fingerfrint (AD) (type III AR)
2. Meesmann (AD) 2. Granular (AD)
3. Avellind (AD)
4. Macular (AR)
5. Gelatinous (AR)
1. Reis buckler (AD) 1. Ched (AD)

2. Theil behnke (AD) 2. Posterior
3. Crystalline (AD) polymorphous
dystrophy (AD)
3. Fuch’s
endothelial
dystrophy (AD)
– Cogan microcystic/epithelial basement membrane/map-dot-

fingerprint dystrophy
• dot-like opacities; epithelial microcysts
• map-like patterns; whorled fingerprint-like lines
• not familial/progressive
• cause recurrent bilateral corneal erosions
– Meesmann dystrophy - tiny intraepithelial cysts in the
interpalpebral area; do not reach limbus
– Reis-Buckler dystrophy - gray-white, round and
polygonal opacities in the center of the cornea; decreased
corneal sensation; visual disturbance due to scarring
– Thiel Behnke dystrophy - similar to Reis-Buckler type;
opacities for a honey-comb pattern
– Crystalline dystrophy - scintillating subepithelial
crystalline opacities in the center of a generally hazy cornea
– Lattice type 1 - fine, spidery, branching lattice lines
spreading outward, sparing the periphery
– Lattice type 2 - short, fine, sparse lattice lines; associated
with progressive bilateral cranial and peripheral neuropathies
– Lattice type 3 - thick ropy lines from limbus to limbus
with minimal intervening haze
– Granular - small, white, crumb-like deposits in the central
anterior stroma; not reaching limbus
– Avellino - fine ring /disc-like opacities [dense centrally]
with deep linear opacities
– Macular - grey-white, dense, focal, poorly delineated spots
with diffuse stromal clouding; eventually full thickness
stroma is involved with stromal thinning
– Gelatinous - in familial sub-epithelial amyloidosis; grey
sub-epithelial nodules giving a mulberry - like appearance;
presents with photophobia, watering, decreased vision
CORNEA 23
– Fuch’s 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 I - cornea has a beaten metal appearance
Stage II - endothelial decompensation leads to stromal
edema
Stage III - epithelial edema leading to bullous Keratopathy
Rx - Topical NaCl; bandage contact lens; PKP
– 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 comeal edema
• Blue grey/ground glass appearance/total opacification
– D/D - birth trauma, buphthalmos, sclerocornea.
TREATMENT
– Observation till asymptomatic or manageable vision
– PKP when vision deteriorates
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
• Thygeson’s 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 conjunctivitis - perilimbal injection, fine papillary
conjunctival reaction
• Giant papillary conjunctivitis - increased mucus, Trantas
dots, limbitis
CORNEA 25
2. Corneal-
• Epithelial edema - due to corneal hypoxia (excessive
usage: e.g. Overnight wear)
• Corneal vascularization at the superior limbus
• Sterile corneal infiltrates - epithelial, sub-epithelial,
stromal
• Corneal warping - severe astigmatism
• Microbial keratitis - Pseudomonas 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
1. AGE RELATED:
a. Arcus senilis -
– occurs hi 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
b. Vogt white limbal girdle -
– narrow bilateral crescentic lines
– chalk-like flecks in the interpalpebral fissure along the
nasal and temporal limbus
c. Cornea farinata -
– bilateral minute flour-like deposits in the deep stroma
d. Crocodile shagreen -
– grayish white, polygonal stromal opacities separated
by relatively clear spaces
– in the anterior 1/3 or posterior 2/3
e. Corneal guttata -
– focal accumulation of collagen on the posterior surface
of the descemet’s membrane
– warts or excrescences in the center of the cornea
– called Hassal-Henle bodies if in the periphery
2. LIPID KERATOPATHY:
– Primary - occurs spontaneously in an avascular cornea
– Secondary - occurs following previous ocular disease/
injury which results in vascularization
CORNEA 27
– Yellowish stromal deposits of cholesterol, fats,

Phospholipids occurs
– If associated with corneal vascularization, it is progressive
Rx-
• control underlying disease [inflammation or
vascularization]
• argon laser photocoagulation to arterial feeder vessels
• needle point cautery to feeder vessels
• PKP if severe
3. 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
Rx-
• 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
4. 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
Rx-
• corneal epithelial debridement
• superficial keratectomy
5. 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
Rx-
• superficial keratectomy or debridement
CORNEA 29
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 extensive - called 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 3-4 mm from limbus
– Argon laser photocoagulation
– Sodium chromoglycate 4% drops
– Superficial keratectomy or PKP
PANNUS
– Inflammatory or degenerative in growth of fibrovascular
tissue from the limbus
– Growth of tissue between epithelium and Bowman’s layer
– An inflammatory pannus disrupts the Bowman’s layer; a
degenerative pannus leaves it intact
STAGES OF PANNUS
1. Infiltration - superficial corneal layers are infiltrated by
polymorphonuclear leucocytes (PMNs) and lymphocytes
2. Progressive - new vessels emerge from the limbal plexus
to form a grey vascular mass beneath the epithelium
3. Stationary - resolution of exudates followed by shrinkage
of blood vessels
4. Sclerotic - cicatricial tissue or obliterated remnants of blood
vessels
TYPES OF PANNUS
– Progressive - a leash of vessels in front of which there is
a zone of infiltration and haziness
– Regressive - vessels 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 31
MOOREN’S ULCER
– Chronic painful peripheral corneal ulceration (serpigenous
ulcer) progressing circumferentially and centrally
– Infection or collagen vascular disease is absent
POSSIBLE ETIOLOGY
– autoimmune 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
TYPES
Type 1 Type 2
Prevalence Common form Atypical form
Pathogenic factors Trauma Trauma, helminthiasis
Age > 40 years 20-30 years
Sex Female > male Male > female
Pain Moderate - severe Variable
Course Slowly progressive Rapid
Response to Moderate Poor
treatment
Perforation Rare In 1/3 of cases
Laterality 75% unilateral 75% bilateral
Mooren’s ulcer Terrian’s degeneration

1. Old or young affected 1. Older people affected
2. Pain, watering, photophobia 2. Usually asymptomatic
3. M>F 3. M>F
4. Irregular astigmatism 4. Against the rule astigmatism
5. Interpalpebral region involved 5. Superior cornea involved
6. Stains with fluorescein 6. Does not stain with
fluorescein [no epithelial
defect]
7. Undermining edges 7. Flat edges
8. Type HI autoimmune reaction 8. Unknown etiology
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
– Peritomy - resection of 4 mm perilimbal conjunctiva adjacent
to the ulcer
– Lamellar corneal transplant and conjunctival flaps
– Systemic immunosuppressives
– Glue if corneal perforation
– PKP - if extreme peripheral corneal thinning
CORNEA 33
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)
– Fuch’s 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 surgery - to protect
endothelium from instrument touch
– Wash out all viscoelastic at the end of surgery to prevent
post-operative rise of IOP
– Try to avoid the use of AC lOLs if there already is endothelial
compromise
– Look for cornea guttata and Fuch’s endothelial dystrophy
in pre-operative evaluation → in which case use BSS
(balanced salt solution) or sodium hyaluronate
TREATMENT OF BULLOUS KERATOPATHY

– Hypertonic saline 5% eye drops or 6% eye ointment [draw
out water from the cornea by osmosis]
– A thin, high water content bandage contact lens - for 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
Bowman’s layer; place bandage contact lens for 1-2 weeks
to allow the epithelium to adhere to cornea
– Excimer laser phototherapeutic keratectomy
– Penetrating keratoplasty
CORNEA 35
CORNEAL TRANSPLANT
TYPES
– Optical - for visual rehabilitation
– Tectonic - for re-enforcing altered corneal structure
(descemetocele)
– Therapeutic - tissue substitution for refractory corneal
disease (corneal ulcer)
COMMON INDICATIONS
– Keratoconus with apical scarring; rapid progression
– Aphakic/pseudophakic bullous keratopathy
– Corneal scarring
– Fuch’s endothelial dystrophy
– Failed graft → primary graft failure; graft rejection/infection
– Herpes simplex keratitis causing stromal necrosis
– Ocular trauma - normal posterior segment
– Congenital corneal opacities — Peter’s anomaly,
sclerocornea
– Stevens-Johnson syndrome
– Corneal dystrophies
– Chemical burns
CONTRAINDICATIONS: (Donor Cornea)
ABSOLUTE RELATIVE
– Death of unknown cause – Multiple sclerosis
– AIDS, rabies – Parkinsonism
– Hepatitis, septicemia – Syphilis
– CMV encephalitis – Chronic lymphocytic leukemia
– Congenital rubella – Chronic immunosuppression
– Reye’s syndrome
– Leukemia
– Hodgkin’s disease
– Intrinsic eye disease
– Creutzfeldt-Jakob disease
DONOR TISSUE EVALUATION

– Epithelium - edema, abrasions, foreign body
– Stroma - edema, DM folds
– Breaks in DM
– Endothelium - specular microscopy
DONOR CORNEA PRESERVATION

a. Short term storage - Moist chamber technique
– Whole globe preservation at 4 o C with saline
humidification for up to 48 hrs
– Disadvantages: endothelium undergoes autolysis;
difficult to screen for HIV and HBsAg; HLA typing
can’t be done in aqueous environment
b. lntermediate term storage media (2 wks)
MKM CSEM CSM DM OM K-SOL
TC199 + + - - + +
HEPES + - + + + +
Dextran + - - + + -
Chondroitin sulphate - + + + + +
Gentamicin sulphate - - + + + +
NEAA - - + + + -
MEM - - + + + -
Mercaptoethanol - - + + - -
Sodium bicarbonate - - - - + -
Sodium pyruvate - - - - + -
– Storage up to 2 weeks
– MKM = Mc-Carey Kaufman Medium
– In modified MK medium, 0.025 M of HEPES is used instead
of bicarbonate buffer
– CSEM = chondroitin sulphate enriched medium
– CSM = corneal storage medium
CORNEA 37
– DM = dexsol medium
– OM = optisol medium
– K-SOL = K sol medium
– NEAA = non-essential amino acids
– MEM = minimum essential medium
– TC 99 = Technichium 99
c. Long Term Storage
1. Organ Culture Method
Eagle’s MEM + Earle’s Salts + L-Glutamine +
Decomplemented Calf Serum is used
– Stored at 34°C for 35 days, endothelial side up
– If no growth after 10 days in any microbiological
medium - cornea is fit for transplant
2. Cryopreservation
– Can preserve indefinitely
– Corneo-scleral button passed through a series of solutions
containing increasing concentration of DSMO (Dimethyl
sulphoxide) up to 7.5%
– Placed in each solution for 10 min.
– Frozen up to -80°C; stored at -160°C
– Disadvantages are - Intracellular microcrystal formation;
number of endothelial cells decreases
– Used for lamellar transplant
COMPLICATIONS OF PENETRATING KERATOPLASTY

EARLY COMPLICATIONS
1. PRIMARY GRAFT FAILURE
– Irreversible graft edema in immediate post-op 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 AC; instrument touch
2. GLAUCOMA
– Acute rise in IOP, with/without optic nerve damage or
field loss
Causes:
• retention of visco-elastic
• angle closure
• distortion of Trabecular Meshwork
• inflammation
• steroid induced
3. EPITHELIAL DEFECTS
– Increased chance of rejection, infection, ulceration,
perforation
Causes:
• Storage
• Injury during surgery
• Post-operative lid movement
• Trichiasis
INTERMEDIATE COMPLICATIONS
1. 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: KAYE’S DOTS
• Randomly distributed in Bowman’s membrane
• Usually occurs 10 months following surgery
CORNEA 39
– Stromal rejection:
• sudden onset of peripheral full thickness haze with
circum-corneal 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 I.V. methyl prednisolone followed
by oral prednisolone
2. GRAFT INFECTION:
– bacterial, viral, fungal, acanthamoebic infection
– due to steroid usage
– Infectious crystalline keratopathy - caused by Streptococcus
viridans
3. WOUND DEHISCENCE:
– following high IOP, early suture removal or trauma
LATE COMPLICATIONS
– recurrence of disease - especially herpetic keratitis and corneal
dystrophies
– late graft failure → decompensation due to decreased
endothelial cells
– astigmatism if donor button is slightly larger
LAMELLAR KERATOPLASTY
– Partial thickness graft of cornea
– Anterior lamellar and deep lamellar keratoplasty
INDICATIONS
– Corneal opacity involving superficial 1/3 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 descemet’s
membrane level
– Endothelium is not transplanted – so less chances of
rejection
Indications:
– Disease involving anterior 95% of corneal thickness with
endothelium being normal and no breaks/scars in descemet’s
membrane
– Chronic inflammatory disease like atopic keratoconjunctivitis
Advantages:
– Less astigmatism
– Structurally stronger globe
– No risk of endothelial rejection
– Increased availability of graft material
Complications:
– Corneal perforation during dissection
CORNEA 41
REFRACTIVE SURGERY
CORNEA LENS
MYOPIA - PRK - Clear lens
- LASIK extraction
- Radial - Phakic IOL:
keratotomy iris clipped lenses and
- Intrastromal implantable contact
plastic rings lenses
HYPEROPIA - PRK - Clear lens
- LASIK extraction
- Laser thermo- - Phakic IOL
keratoplasty
ASTIGMATISM - Arcuate keratotomy - Toric IOL implantation
PRESBYOPIA - Conductive keratoplasty - Multifocal IOL
CHAPTER 2
Conjunctiva
PSEUDOMEMBRANOUS &
MEMBRANOUS CONJUNCTIVITIS
CAUSED BY
– C. diphtheriae, beta hemolytic streptococci
– S. pneumoniae, N. gonorrheas, S. aureus, E. coli.
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
& cornea
– membrane peels less readily with bleeding from underlying
surface
– patchy or total membrane over palpebral conjunctiva
– pre-auricular lymphadenopathy
– cornea may ulcerate
– After 6-10 days, slough separates; profuse discharge occurs;
conjunctiva - red & succulent
– symblepharon forms
TREATMENT
1. Topical penicillin (10,000 U/rnl drops)
2. Systemic penicillin
3. Antidiphtheritic serum 4000-10,000 U repeated 12 hourly
– Every case is treated as diphtheria unless proved
otherwise; If culture is negative, treat as purulent
bacterial conjunctivitis
– Removal of membranes - precipitates symblepharon
formation
CONJUNCTIVA 45
PTERYGIUM
– Degenerative condition of subconjunctival tissues which
proliferate as vascularized granulation tissue to invade the
cornea
– Destroy the superficial layers of the cornea (stroma &
basement membrane)
– Covered by conjunctival epithelium
– Appears as triangular encroachment of conjunctiva upon
the cornea
– Has a head, neck, & body
– Usually on nasal side of cornea
– Early stage: thick & vascular
– Late stage: thin & pale (does not grow)
– Formation of dense fibrous tissue - results in corneal
astigmatism (with the rule)
– Decreased vision if it progresses into the pupillary area
– Dry sunny climates, UV light - are aggravating factors
– Stocker’s line — pigmented line of iron deposits in
basement membrane in front of the head of the pterygium
TREATMENT
– Observe until: progression; increased astigmatism
– Lubricating drops for dry eye
– Protect from UV rays
– Topical steroids for inflamed pterygium
– Surgery:
• Avulsion with amputation
• Simple excision [bare sclera technique]
• Excision with primary closure
• Excision with primary conjunctival graft
• Excision with lamellar keratoplasty
• Excision with buccal mucous membrane graft
• Excision with amniotic membrane graft
TRACHOMA
– Caused by Chlamydia trachomatis types A, B, Ba, C
CLINICAL FEATURES
– Diffuse conjunctival inflammation with congestion,
papillary hypertrophy, follicles
– Upper tarsal conjunctiva → red & 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 pannus - lymphoid infiltration with
corneal vascularization
– Herbert’s pits [follicles near the limbus leave depressed pits
on resolution]
– Chronic corneal ulcers - at advancing edge of pannus
– Arlt line - white conjunctival scar at junction of lower
1/3 & upper 2/3 of superior tarsus
Trachomatous ptosis - due to dense infiltration of upper
tarsus
– Ectropion, trichiasis - due to cicatrization
– Tylosis - thickening of tarsal plate
WHO CLASSIFICATION (FISTO)

• Follicles - indicate active disease
• Intense inflammation - needs urgent treatment
• Scarring of conjunctiva - indicates old inactive infection
CONJUNCTIVA 47
• Trichiasis - needs electrolysis/surgery

• Opacities of cornea - cause decreased vision
Stages of trachoma
I Immature follicles on superior tarsus; superficial punctuate
keratopathy; pannus
IIa Florid follicular reaction with mature follicles
IIb Marked papillary hyperplasia, pannus, limbal follicles,
superficial corneal sub-epithelial infiltrates
III Scarring & follicles
IV Marked scarring of upper tarsus; no follicles
Prevention & Treatment

– Oral tetracycline, erythromycin, rifampicin or sulfonamides
(for 3-6 months)
– Topical erythromycin or tetracycline ointment (5 days a
month for 1 yr)
– Single dose of 1 gm oral azithromycin
– Strict personal hygiene
FOLLICULAR CONJUNCTIVITIS
ACUTE FORMS
1. Chlamydial inclusion conjunctivitis
– Swimming pool conjunctivitis
Rx-
• Oral tetracycline 250 mg qid/doxycycline 100 mg bd/
erythromycin 250 mg qid X 14 days
• Single oral dose 1 gm azithromycin
• Ofloxacin 300 mg bd for 7 days
2. Epidemic keratoconjunctivitis
– Caused by adenovirus types 8 & 19
– Scanty exudates; marked inflammatory symptoms;
membranes
– Pre-auricular lymphadenopathy
– Punctuate epithelial infiltrates & sub-epithelial opacities
in cornea after 7-10 days
Rx-
• for symptomatic relief
• topical steroids if very severe
3. Pharyngo-conjunctival fever
– Caused by adenovirus types 3,4,7
– Pharyngitis, fever, pre-auricular lymphadenopathy
– Fine, superficial punctuate keratitis
4. New Castle conjunctivitis
– From dead fowls
– Similar to pharyngoconjunctival fever
5. Hemorrhagic conjunctivitis
– Coxsackie virus; Enterovirus 70
– Also called Apollo conjunctivitis
– Violent inflammatory conjunctivitis with subconjunctival
hemorrhage
– Cornea is unaffected
CONJUNCTIVA 49
6. Acute herpetic conjunctivitis

– Associated with facial lesions in children
– Large follicles
– Corneal vesicles coalesce to form dendritic keratitis
– Decreased corneal sensation
7. Herpes simplex conjunctivitis
– Occurs in adults
– Follicular conjunctivitis with or without microdendrites,
similar to EKC
– Decreased corneal sensation
CHRONIC FORMS
Caused by
– Drugs e.g. Pilocarpine
– Molluscum contagiosum in lids
– Trachoma
ALLERGIC TYPES OF CONJUNCTIVITIS

1. Acute/subacute allergic catarrhal conjunctivitis
– Severe itching; watering (tears contain eosinophils)
– No purulent discharge; less hyperemia
– Recurs on contact with allergen
– E.g. Hay fever, chemicals (cosmetics/dyes), drugs
(atropine, brimonidine)
Rx-
• remove allergen; desensitization
• antihistamines; topical steroids
• mast cell stabilizers (sodium chromoglycate,
olopatadine)
2. Vernal keratoconjunctivitis (spring catarrh)
– Young males; hot weather
– Type I hypersensitivity reaction — mediated by IgE
– Itching, photophobia, watering, ropy discharge
– Foreign body sensation
(a) 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
(b) LIMBAL FORM:
- Horner Trantas dots → white dots consisting of
eosinophils & epithelial debris
- Wall of gelatinous thickening at the limbus
- Opacification of limbus with nodule formation
Cornea-
– Fine, diffuse SPKs
– Severe dry eyes → filamentary keratopathy
– Shield ulcer in upper cornea due to rubbing of the
hypertrophied papillae → heal with scarring;
treated with topical steroids
CONJUNCTIVA 51
Rx-
• 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
3. Giant papillary conjunctivitis
– Type I & IV hypersensitivity reaction
– Large polygonal papillae on superior tarsal conjunctiva;
conjunctival congestion
– Macropapillae : 0.3-1.0 mm
– Giant papillae : 1-2 mm
Causes:
(a) soft hydrophilic contact lens
(b) protruding suture ends
(c) ocular prosthesis
Rx-
• Discontinue contact lenses
• Remove protruding sutures/prosthesis
• Topical steroids
4. Phlyctenular conjunctivitis
– Small round, yellow-grey nodules on bulbar conjunctiva,
at or near limbus
– Congestion of vessels limited to area around phlyctens
– Epithelium over the surface becomes necrotic &
small ulcers form
– Complicated by muco-purulent conjunctivitis
– Probably caused by endogenous tuberculous
proteins or non-specific delayed hypersensitivity
reaction to staphylococcal antigens
– Corneal phlycten - may scar
Rx — steroids, antibiotics, cycloplegics
– Conjunctival phlycten heals rapidly - no scar
Rx — steroids
SUPERIOR LIMBIC KERATOCONJUNCTIVITIS

CLINICAL FEATURES
– Discomfort, foreign body sensation, photophobia,
tearing
– Pseudoptosis, blepharospasm
– Sectoral inflammation & injection of superior bulbar
conjunctiva & limbal cornea
– On upper lid eversion - uniform papillary hypertrophy are
seen
– Cornea - punctate epithelial erosions
– Filaments in precorneal tear film
– Bilateral; probably autoimmune etiology
(e.g. associated thyroid dysfunction)
TREATMENT
• Topical 0.5-1.0% silver nitrate solution (a chemical cautery)
used to promote re-growth of healthy new epithelium
• 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
CONJUNCTIVA 53
AMNIOTIC MEMBRANE GRAFT

– Amniotic membrane consists of a thick basement
membrane, single layer of epithelial cells & 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 & 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
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 & expanded on
amniotic membrane
– Superficial keratectomy done - to 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 & put on long
term immunosuppressive treatment
In Partial Stem Cell Deficiency
– Remove abnormal epithelium & 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
CONJUNCTIVA 55
OPHTHALMIA NEONATORUM
– Mucoid, muco-purulent or purulent discharge from
one or both eyes in the 1st month of life
– Caused by - Neisseria gonorrhoeae, Chlamydia trachomatis,
Streptococcus pneumoniae, Chlamydia oculogenitalis,
herpes simplex virus, chemicals
1. N. gonorrhoeae infection
– In the 1st 48 hours of birth
– Thick, yellow purulent discharge
– Swollen, tense lids; marked chemosis
– Conjunctiva is intensely inflamed, bright red & 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
Rx-
• Gentamycin 0.3% e/d after every feed X 3 days
• Ceftriaxone i.m 125 mg stat (or)
• Cefotaxime i.v 50 mg/kg in 3 divided doses
• Bacitracin eye ointment 2-4 hourly
• Topical & systemic penicillin
2. Chemical induced
– Develops after prophylaxis with silver nitrate solution
– Disappears spontaneously after 24-48 hours
Rx-
• eye wash; erythromycin ointment
3.C. 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
Rx:
• Oral erythromycin 50 mg/kg/d in 4 divided doses (or)
Oral azithromycin 10 mg/kg for 3 days
• Erythromycin/chlortetracycline 1% ointment qid
4. Herpes simplex virus conjunctivitis

– 5-7 days after birth
Rx:
• Acyclovir 3% ointment 5 times/day for a week
CONJUNCTIVA 57
DRY EYE
– Ocular discomfort, foreign body sensation, burning
sensation, blurred vision
– Tear film breaks up into dry spots between blinks - exposing
the corneal & conjunctival epithelium to evaporation
Causes of dry eye

a. AQUEOUS TEAR DEFICIENCY:
1. Congenital – absence of lacrimal gland / lacrimal
nucleus
– Adie’s syndrome
– MEN syndrome
2. Acquired – trauma / surgical removal of lacrimal
gland
– radiation induced damage
3. Inflammation – mumps; trachoma
– Sjögren’s syndrome
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
b. MUCIN DEFICIENCY:
– Goblet cell dysfunction
• primary - Vitamin A deficiency (nutritional)
• secondary - diarrhea, liver disease, pregnancy,
trachoma, burns, SJS, cicatricial pemphigoid
– Drug induced - proctalol, ecothiophate iodine
c. LIPID ABNORMALITIES:
– Congenital absence of meibomian glands
– Altered composition of meibomian gland secretion
e.g. Blepharitis - increases free fatty acids
d. LID ABNORMALITIES:
– Ectropion, coloboma lid - exposure
– Vlln palsy - decreased blink rate, lagophthalmos
– Keratinized lid margin
e. EPITHELIOPATHIES:
– Ulcers, erosions, scars
CONJUNCTIVA 59
TESTS FOR DRY EYE

1. Rose Bengal test
– Rose Bengal has affinity for devitalized cells,
mucus, corneal filaments & plaques
2. Tear film break up time (TBUT)
– 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 &
appearance of the 1st dry spot
– Normal TBUT > 10 seconds
3. Schirmer’s 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 & inserted
into the lower fornix between the middle & outer
1/3 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 min.
– > 15 mm wetting → normal
– 10-15 mm wetting → borderline
Schirmer II – Measure BASIC tear secretion
– ANESTHETIC USED
– Measure wetting after 5 min.
– < 6 mm wetting → failure of secretion
4. 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)
5. Tear osmolality
– In keratoconjunctivitis sicca > 312 mosm/kg
6. Conjunctival impression cytology
– Goblet cells >5 cells/HPF is normal
TREATMENT
1. Tear conservation
– Decrease room temperature, increase humidity
– Moist chamber goggles, tarsorrhaphy
2. Tear substitution
– Eye drops - polyvinyl 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. Immunomodulators
– Cyclosporine
7. Treat associated disease like
– Blepharitis, spring catarrh
8. Hydrophilic contact lens
9. Trans-retinoic acid ointment - reverses squamous
metaplasia of ocular surface
CONJUNCTIVA 61
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 & debris in tear
film which moves en masse with each blink
– Marginal tear strip → only 0.3 mm high (normally
1 mm high); concave; contains mucus & debris
– Lid margin → thickening & telangiectasia
– Tear: lysozyme ratio = 1 : 10
– Associated with desiccation in mucous membranes of
bronchi, vagina, mouth
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 & glands
• E.g. trachoma, burns, pemphigoid, diphtheria
– Prolonged corneal exposure
• E.g. ectropion, proptosis, lagophthalmos
• Epithelium stops secreting mucus → becomes
epidermoid with granular & horny layers
• Meibomian gland activity increases → ocular surface
gets covered with fatty secretion
– Systemic disorder — Vitamin A deficiency
• Bitot spots → triangular white patches on inner & 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
CONJUNCTIVA 63
TEARING
Causes for Hyperlacrimation
1. Supranuclear – Emotional
– Psychological
– Voluntary (CNS)
2. Reflex arc – Corneal/conjunctival disease
– Foreign body
– Iritis, glaucoma
– Pseudoepiphora in yawning, nasal irritation
3. Infranuclear – CPA tumors
– Aberrant regeneration of Vlln (crocodile tears)
4. Direct lacrimal – Inflammation
gland – Neoplasm
stimulation – Parasympathomimetic drugs
– Cholinesterase inhibitors
Causes for Epiphora

1. Lacrimal pump failure • Vlln palsy
• Stiff lid (burns, scars)
2. Decreased tear film • Lid contour deformity
movement • Chalazion
3. Punctum disorder • Punctal occlusion / Malposition
4. Canalicular obstruction • Cicatrizing conjunctiva
• Trauma, laceration
• Post - irradiation
• Drags - phospholine iodine
• Stevens-Johnson syndrome
• Canaliculitis
• Tumors
• Repeated probing
5. Lacrimal sac • Trauma
obstruction • Tumors
• Allergy
6. NLD obstruction • Trauma
• Infiltrative disorders
7. Intranasal pathology • Allergic rhinitis
• Turbinate scarring [post-surgery]
• Tumors, polyps
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 Patent → fluid goes into the nose/mouth
– When →
a. regurgitation from same punctum → canalicular
block
b. 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:
JONES’ TEST: in suspected partial obstruction
Primary test:
– Differentiates partial obstruction from primary
hyperlacrimation
CONJUNCTIVA 65
– 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 & negative if bud
is not stained
(a) Test is positive - no block

(b) Test is negative - NLD block
(c) Test is negative - canalicular block
Secondary test:
– Wash out the residual fluorescein
– Irrigate with saline (syringing)
a. Test is positive if cotton bud gets stained
(indicates partial obstruction of NLD)
b. Test is negative if bud is not stained
(indicates partial obstruction of upper lacrimal
passages or pump failure)
(a) (b)
CHAPTER 3
Sclera
SCLERITIS
– Severe chronic, destructive inflammation of the sclera
CLASSIFICATION
1. Anterior
a. Diffuse
b. Nodular - single/multiple nodules
c. Necrotizing
i. With inflammation
ii. Without inflammation
2. Posterior
Another classification:
a. Infectious:
i. Endogenous
ii. Exogenous
b. Non-infectious
PATHOGENESIS
– Immune mediated vasculitis
CLINICAL FEATURES
– Pain - dull, aching, boring; with facial radiation; nocturnal
worsening
– Decreased vision - in 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
• Early - capillary closure
• Late - area of intense vasodilatation with a central less
injected area
• Advanced - thinning of sclera; bluish sclera
SCLERA 69
ASSOCIATED SYSTEMIC DISEASE

– Rheumatoid arthritis
– Wegener’s granulomatosis
– Relapsing polychondritis
– SLE [systemic lupus erythematosis]
– PAN [polyarteritis nodosa]
– Ankylosing spondylitis
– Reiter’s syndrome
– Giant cell arteritis
– Behcet’s syndrome
NECROTISING SCLERITIS WITH INFLAMMATION

– Severe ocular & periocular pain
– Scleral edema, intense vasodilatation
– Tenderness, thinning, blue sclera [parchment-like]
– Massive infection & loss of scleral tissue
– Raised IOP leads to staphyloma formation
– Corneal ulceration & inflammation
SCLEROMALACIA PERFORANS
[Necrotising scleritis without inflammation]
– Bilateral; females more than males
– Associated with rheumatoid arthritis
– Asymptomatic
– Thinning & 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
POSTERIOR SCLERITIS
– Inflammation of sclera posterior to ora serrata
SYMPTOMS
– Pain, redness, proptosis, decreased vision
– Diplopia, pain on ocular movement
SIGNS
– Exudative retinal detachment
– Retinal/choroidal folds
– Annular choroidal detachment
– Circumscribed mass lesion
– Disc edema, maculopathy
– Uveitis, retinal vasculitis
– Raised IOP
INVESTIGATIONS
– B- scan → scleral thickening, T sign
– CT scan, fundus fluorescein angiography
COMPLICATIONS
– Cornea - stromal keratitis, sclerosing keratitis peripheral
corneal melt, perforation
– Sclera - thinning, necrosis, staphyloma, perforation
– Uvea - uveitis, choroidal granuloma
– Glaucoma, cataract
– Exudative RD, macular edema, optic atrophy
TREATMENT
– NSAIDs - for mild scleritis
– Steroids — oral or I.V. — in severe scleritis
– Cyclophosphamide, cyclosporine, azathioprine,
methotrexate - if disease not controlled by steroids
SCLERA 71
STAPHYLOMA
– Ectasia of the coats of the eyeball along with uveal tissue
TYPES
1. Anterior
a. Congenital
– corneal opacity becomes protruberant
– associated with extremely disorganized anterior segment
– lens may adhere to the posterior cornea
– associated with intra-uterine inflammation or mal-
development
– raised IOP can cause prominent buphthalmic
enlargement
b. Acquired
– following sloughing of corneal ulcer
– iris becomes exposed & inflamed
– layer of exudates covers the iris → organizes into a thin
fibrous layer called pseudocornea - thin & cannot
withstand IOP → bulges
– ‘Bunch of grapes’ appearance
2. Intercalary
– At limbus; immediately in front of ciliary body
3. Ciliary
– Bulging of ciliary body
– Due to thinning of sclera due to scleritis or injury
– Up to 8 mm from limbus
– Bluish, irregular staphyloma
4. Equatorial
– At the regions of sclera perforated by vortex Veins
– Always remains local
– Noticed during surgery
5. Posterior
– In high myopes
– Bulging of sclera at posterior pole
COMPLICATIONS
– Glaucoma due to decreased aqueous outflow
– Retinal detachment - equatorial type
– Lens subluxation, globe rupture
TREATMENT
– Scleral resection
– Staphyloma excised or buckled inwards
– Scleroplasty - staphyloma excised & replaced by sclera
– Evisceration or enucleation with artificial eye implant
CHAPTER 4
Glaucoma
PRIMARY OPEN ANGLE GLAUCOMA

– Glaucoma is a chronic progressive optic neuropathy leading
to optic nerve damage & loss of visual field, intra-ocular
pressure (IOP) being the most common risk factor
– POAG occurs due to increased resistance to aqueous outflow
at the trabecular meshwork
PATHOGENESIS
1. MECHANICAL CHANGES
– Raised IOP causes mechanical pressure on the lamina
cribrosa
– Backward displacement & compaction of the laminar
plates
– Openings through which axons pass become narrow
causing damage to the optic nerve
2. 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 & ganglion cell death → apoptosis
DISC CHANGES
1. Disc size - 50% cupping in a small disc is more significant
than 50% cupping in a large disc
GLAUCOMA 75
2. Asymmetrical cupping > 20% in discs of the same size
3. Cup : disc ratio > 0.5 : 1.0 (esp. in the vertical axis)
4. Neuro-retinal rim -
Pallor
Localized notching
Thinning
ISNT rule - Thickness of Inferior rim>
Superior rim> Nasal rim> Temporal rim
5. Superficial disc hemorrhages at disc margin (splinter

hemorrhage in NTG)
6. Peripapillary atrophy
7. Bayoneting sign; nasal pushing of vessels
8. NFL defect - slit-like/wedge-shaped/diffuse NFL loss (seen
best with a red-free filter) - corresponds to field loss
FIELD DEFECTS IN GLAUCOMA

1. Generalized reduction of sensitivity
2. Relative paracentral scotoma
3. Nasal step
4. Siedel scotoma
5. Arcuate scotoma
6. Double arcuate (ring) scotoma
7. Near-total field defect
ANDERSON’S CRITERIA
– Diagnostic criteria for glaucomatous visual field loss in the
absence of retinal/neurological disease affecting visual field
1. 3 or more non-edge points in a cluster with p = <5%,
one of which has p = <1%
2. CPSD or PSD with p = < 5%
3. GHT outside normal limits
* CSPD - corrected pattern standard deviation
* PSD - pattern standard deviation
* GHT - glaucoma hemifield test
Any defect must be confirmed by repeated testing
GLAUCOMA 77
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 & IOP checked
after 1-2 hours
4. Map stone test [Phenylephrine-pilocarpine test]
– 2% pilocarpine + 10% phenylephrine instilled every half
hour into eye for 2½ hours
NORMO -TENSIVE GLAUCOMA

(low tension glaucoma)
– Mean IOP ≤ 21 mm Hg on diurnal testing
– Glaucomatous optic disc damage; splinter hemorrhages
may be present at disc margin
– Visual field loss - typically closer to fixation; deeper, steeper
& more localized
– Open angles
– Absence of secondary causes
POSSIBLE CAUSES
– nocturnal systemic hypotension
– over treated hypertension
– decreased blood flow velocity in the ophthalmic artery
– peripheral vascular spasm on cooling
– migraine
TREATMENT
• Prostaglandin analogues, beta-blockers, trabeculectomy
• Avoid anti-hypertensives at bed time if patient is on
antihypertensive medication
– POAG - IOP > 21 mm Hg on diurnal variation testing
– AION - Post AION disc pallor can resemble disc changes
in NTG
– Congenital optic disc anomalies
GLAUCOMA 79
OCULAR HYPERTENSION
– IOP > 21 mm Hg on two consecutive occasions in the
absence of detectable glaucomatous damage
– Open angles on gonioscopy
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
– Patients who will be lost for follow up
Central corneal thickness:
– Average normal CCT = 520 μm
– 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 70 μm deviation
in CCT, from 520 μm
TONOMETRY
– Assessment of intraocular pressure
– Used to diagnose glaucoma & monitor anti-glaucoma
medications
1. Digital tonometry
– Like testing fluctuation
– Patient looks down; 2 fingers placed above superior
tarsal plate a small distance apart & pushed backward
alternately
2. 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 & volume of indentation - depend on tension
& distensibility of ocular walls
– Weights used are 5.5, 7.5, 10.0, 15.0 grams
– Calibrated so that equivalent reading in mm Hg are
read off a chart
– False recording in - thick/steep/irregular corneas, high
myopia, high hypermetropia, after ocular surgery, with
miotics/vaso-dilators/vasoconstrictors
3. Applanation tonometry-
– Golmann, Perkin’s, tonopen, non-contact tonometer
– Based on Imbert-Fick principle
– Assesses amount of force needed to flatten or applanate
a known area of cornea
– On applanation
– IOP is directly proportional to pressure applied & inversely
proportional to the area flattened 0.05 ml of aqueous
displaced
Goldmann
• Flat, circular, plexiglass plate
• Applanates 3.06 mm diameter area of corneal surface
• A force of 0.1 gm exerted by a spring & lever system
corresponds to IOP of 1 mm Hg
GLAUCOMA 81
HOW TO TEST CALIBRATION OF

A GOLDMANN TONOMETER
– Set the tonometer in position; tension on circular dial set
at 5 mm Hg. The head should lean slightly forwards
– Twirl the circular dial counter-clockwise until the head rocks
back towards you; the tension should read 0-2 mm Hg
below 0
– Twirl the dial clockwise until the head rocks forward again;
the tension should read 0-2 mm Hg
– Remove the calibration rod from its box.

– Firmly screw into position the holding bracket that slides
along the rod so that the closest mark in front of the center
one is aligned as exactly as you can.
– Slip the rod & 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 20-23 mm Hg
– Twirl the dial counter-clockwise until the head rocks
backwards; the tension on the dial should read 17-20
mmHg
– Remove the rod & holding bracket from the tonometer &
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 60-64 mm Hg
– Twirl the dial counter-clockwise until the head rocks
backward; the tension should read 56-60 mm Hg
GLAUCOMA 83
TONOGRAPHY
– To determine aqueous outflow facility
– Recording IOP during several minutes while the eye is
subjected to the weight of a Schiotz electronic tonometer;
determine how rapidly pressure drops under this load
– Done after surgery or intraocular inflammation when IOP
may be low; gives a warning of future rise in IOP
– Done for POAG
– Used to analyze mode of action of drugs on hydrodynamics
of eye
PROCEDURE
– Patient recumbent - tonometer rests on anesthetized cornea
for 4 min.
– When tonometer applied - 1st IOP increases - then rate
of aqueous outflow increases & IOP falls [no influence on
aqueous formation]
– When aqueous outflow > inflow, IOP begins to fall
PRIMARY ANGLE CLOSURE GLAUCOMA

– Obstruction of aqueous outflow by partial/complete closure
of the angle by peripheral iris
Primary Angle Closure Suspect (PACS)
– Occludable angles
Primary Angle Closure (PAC)
– Occludable angles with raised IOP/glaucomflecken/
peripheral anterior synechiae
Primary Angle Closure Glaucoma (PACG)
– PAC with optic disc damage & visual field loss
ANATOMICALLY PREDISPOSING FACTORS

– Anterior location of the lens - iris diaphragm
– Shallow anterior chamber
– Small lens size - microspherophakia
– Smaller corneal diameter (by 0.25 mm)
– Smaller axial length (hypermetropes, nanophthalmos)
VAN HERICK’S GRADING

Grade 0 Iridocorneal contact
Grade 1 Peripheral AC depth between iris & corneal endothelium
< 1/4 corneal thickness [occludable]
Grade 2 > 1/4 but < ½ of corneal thickness
Grade 3 > ½ of corneal thickness [non-occludable]
GLAUCOMA 85
STAGES
1. Latent-
– Occludable angles; no symptoms
– Rx - prophylactic YAG peripheral iridotomy (PI)
2. Sub-acute-
– Intermittent pupillary block causing sudden rise in IOP
– Spontaneously relieved on physiological miosis
– Presents with transient blurring ; haloes around light
bulbs; headache
– Precipitated on mydriasis (e.g. in a dark room), prone
position , bending to read a book (shallowing of anterior
chamber)
– Rx: YAG PI
3. Acute congestive glaucoma-
– Sudden total angle closure with acute rise in IOP
– Painful decrease of vision
– Circum-ciliary injection, corneal edema, stromal
thickening
– Shallow anterior chamber; peripheral irido-corneal touch
– Anterior chamber reaction with cells & flare
– Dilated iris blood vessels
– Vertically oval, mid-dilated, fixed pupil
– Closed angles on gonioscopy
– Optic disc hyperemia/edema
– Secondary angle closure
– Neovascular glaucoma
– Phacomorphic glaucoma
– Migraine
Always do gonioscopy for the fellow eye !!
TREATMENT
– 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% (1-2 gm/kg body wt) over 45 min. (contra-
indicated in cardiac failure & 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 gm/kg body wt); contraindicated in
diabetics
– Prophylactic YAG PI in the fellow eye
* Topical dorzolamide may be avoided as they exacerbate
or potentiate corneal edema
4. Post - congestive glaucoma
– After an attack of acute congestive glaucoma
– Descemet’s 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
– IOP - normal/increased/decreased
– Narrow angles with trabecular hyperpigmentation with
or without synechiae
– Optic disc hyperemia/pallor
GLAUCOMA 87
5. Chronic angle closure glaucoma

– Mostly asymptomatic
– Course is like POAG but on gonioscopy has variable
degrees of angle closure
– Type 1 - creeping angle closure; gradual progressive
synechial angle closure; Rx: YAG PI
– Type 2 - synechial angle closure due to intermittent
attacks of pupillary block; Rx: YAG PI + medical
treatment
– Type 3 - POAG with narrow angles (combined
mechanism glaucoma); Rx: Patient already on medical
treatment; add YAG PI
6. Absolute glaucoma
– No light perception
– Raised IOP
– NVI may or may not be present
– Rx:
• Antiglaucoma medications
• If very painful -
– trans-scleral cyclophotocoagulation
– trabeculectomy with mitomycin C
– artificial drainage shunts
– evisceration with artificial eye implant
SECONDARY GLAUCOMA
1. Inflammatory glaucoma:
a. Hypertensive uveitis
b. Following inflammation - posterior synechiae formation
c. Glaucomatocyclitic crisis
d. Fuch’s heterochromic iridocyclitis
2. Neovascular glaucoma
3. Corneal perforation - adhesions between iris & cornea
4. Lens induced glaucoma -
a. Phacomorphic glaucoma
b. Phacolytic glaucoma
c. Phacoanaphylactic glaucoma
5. Aphakic glaucoma
6. Pseudophakic glaucoma - AC IOL / PC IOL
7. Steroid induced glaucoma
8. Intra-ocular tumors - infiltration of the angle by neoplastic
tissue
9. Raised episcleral venous pressure -
a. Orbital inflammation
b. Sturge-Weber syndrome
c. Orbital varices
d. Carotico-cavernous fistula
e. 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 89
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
a. Acute anterior uveitis - due to
– Steroid induced raise in IOP
– Trabecular obstruction by inflammatory cells
– Acute trabeculitis
– Inflammation subsides while ciliary body function
returns
b. Chronic anterior uveitis - due to
– Trabecular scarring/sclerosis
4. Fuch’s 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 analogues & 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 40 to 80 mm Hg
– Few cells
– 1 or more fine white KPs
– Open angle - no peripheral anterior synechiae
TREATMENT
– Topical steroids, oral NSAIDs
– Aqueous suppressants to reduce IOP
HYPERTENSIVE UVEITIS
– Uveitis with raised IOP
– Occurs due to swelling & dysfunction of endothelial cells
(or) infiltration & obstruction of trabecular meshwork by
inflammatory material [WBCs, macrophages, fibrin]
– Decreased outflow of aqueous leads to rise in IOP
GLAUCOMA 91
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 CRVO - 100 day glaucoma
– Proliferative diabetic retinopathy
– Ocular ischemic syndrome
– CRAO
– Chronic intra-ocular inflammation
– Long-standing retinal detachment
– Coat’s disease
– Intra-ocular tumors
– Acute congestive glaucoma (look for narrow angles in the
fellow eye)
– Post-vitrectomy inflammation
CLASSIFICATION
NVI Secondary open Secondary angle
angle glaucoma closure glaucoma
New vessels grow Fibrovascular Contraction of
radially over the membrane in the fibrovascular
iris surface angle blocks membrane pulls
trabecular outflow peripheral iris over
trabeculum
Rx: Rx: Rx:
- PRPC - hypotensive agents- - hypotensive agents
topical atropine - topical atropine
- topical steroids - topical steroids
- PRPC - retinal ablation
- trab + mitomycin C
- artificial filtering
shunts
- cyclodestruction
- retrobulbar alcohol
injection
- enucleation [if all else
fails]
CLINICAL FEATURES
– Severe ocular pain; decreased visual acuity
– Circumciliary congestion, corneal edema
– Very high TOP, synechial angle closure
– Mild AC reaction
– Ectropion uveae
MANAGEMENT
– Treat the cause
– PRPC for posterior segment ischemia [wait for 4-6 weeks
for a response]
GLAUCOMA 93
– If
TOP not controlled:
• Trabeculectomy + Mitomycin C
• Aqueous shunt procedure
• Trans-scleral cyclophotocoagulation or endocyclo-
photocoagulation
• Intravitreal bevacizumab [off-label drug] has been found
to reduce rubeosis; it can be also given into the anterior
chamber
PHACOLYTIC GLAUCOMA
– Also called lens protein glaucoma
– Secondary open angle glaucoma
– Lens proteins leak through the intact capsule of a
hypermature cataract & block the trabecular meshwork
– Lens protein laden macrophages also block the trabecular
meshwork
– Phacoanaphylactic uveitis -autoimmune 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
– ECCE with IOL implantation with peripheral iridotomy;
flush out all the proteinaceous material from AC
– Hypotensive agents, topical steroids
PHACOMORPHIC GLAUCOMA
– Secondary angle closure glaucoma caused by an
intumescent cataractous lens
– Equatorial & antero-posterior increase in curvature of the
lens - increases iridolenticular contact; causing a pupillary
block & iris bombe’
– Blurring of vision, severe ocular pain, high IOP
– Circumciliary congestion, corneal edema, shallow anterior
chamber, intumescent lens
– Rx: cataract extraction with IOL implantation
GLAUCOMA 95
MALIGNANT GLAUCOMA
– Also called ciliary block glaucoma or aqueous misdirection
syndrome
IMPORTANT SIGNS
– shallowing or flattening of central or peripheral anterior
chamber in the presence of a patent peripheral iridotomy
– raised IOP
– aggravated with miotics
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 & iris-vitreous diaphragm
a. Cilio-lenticular block → ciliary processes rotate forward
& press against the lens-equator or anterior hyaloid
b. 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
– Choroidal detachment → hypotony; straw colored fluid
can be drained from supra-choroidal space
– Supra-choroidal hemorrhage → high IOP, flat anterior
chamber, severe pain
TREATMENT
• Cycloplegics [atropine]- ciliary paralysis tightens the zonules
& pulls the lens back
• Hyperosmotics [mannitol] - decrease the pressure exerted
by the vitreous
• Carbonic anhydrase inhibitors & beta blockers - decrease
aqueous accumulation
• Argon laser photocoagulation of ciliary processes - decreases
aqueous production
• Nd: YAG laser to disrupt the anterior hyaloid face
SURGERY
– Posterior sclerotomy [Chandler’s procedure]
– Anterior pars plana vitrectomy
– Lens extraction
GLAUCOMA 97
APHAKIC GLAUCOMA
Mechanism of glaucoma in aphakic eyes:
– Primary open angle glaucoma
– Secondary glaucoma due to:
• Immediate post-operative reaction
• “Enzyme glaucoma” - due 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 agents - topical & systemic
– Topical steroids for post-operative inflammation & hyphema
– Relieve pupillary block with atropine/pilocarpine
– Surgical management if not controlled medically
PSEUDOEXFOLIATION SYNDROME
– Secondary trabecular block glaucoma
– Called glaucoma capsulare or pseudoexfoliation glaucoma
PATHOGENESIS
– Grey-white, fibrillogranular, extra-cellular matrix material
deposited on:
Anterior lens capsule, zonules, ciliary body, iris, trabecular
meshwork, conjunctiva, anterior vitreous face
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
- Schwalbe’s line - angle may be narrow
- dandruff-like pseudoexfoliative material in trabecular
meshwork
Iris - pseudoexfoliative material on pupillary margin
- sphincter atrophy; ‘moth-eaten’ appearance
- transillumination defects at pupillary margin
- pigment dispersion
- posterior synechiae
- intra-stromal hemorrhages on mydriasis
Pupil - does not dilate well
- pseudoexfoliative material present
- sphincter atrophy
Lens - nuclear cataract
- zonular instability causes- phacodonesis, lens subluxation,
zonular dialysis, vitreous loss may occur during cataract
surgery
- pseudoexfoliative material on anterior lens capsule → central
disc & a peripheral band with a clear zone in the middle;
sometimes central disc is absent
GLAUCOMA 99
PSEUDOEXFOLIATION GLAUCOMA
– Glaucoma occurs due to:
• clogging up of trabecular meshwork by pseudoexfolia-
tive material/pigment released from iris
• trabecular endothelial dysfunction
– Occurs in the 7th decade; mostly unilateral; more common
in females
– Chronic open angle glaucoma
– Degree of hyperpigmentation in the angle co-relates with
the severity of glaucoma
– Rx:
• antiglaucoma medication
• argon laser trabeculoplasty
• trabeculectomy
BUPHTHALMOS
PATHOGENESIS
– Isolated trabeculo-dysgenesis → absence of angle recess;
iris inserted directly into surface of trabeculum.
– Rat or concave iris insertion
CLASSIFICATION
– True congenital glaucoma → raised IOP during intrauterine
life
– Infantile → Birth - 3 years
– Juvenile → 3-6 years
CLINICAL FEATURES
1. Corneal haze - due toepithelial/stromal edema
– present with lacrimation, photophobia, blepharospasm
2. Buphthalmos (birth to 3 years) -
– Enlarged eye due to stretching when IOP high
– Stretched sclera - thin & translucent → appears blue
– Deep anterior chamber
– Zonular fibers stretch & lens may subluxate
– Axial myopia can cause amblyopia
3. Haab striae -
– Horizontal curvilinear lines
– Healed breaks in DM
– Breaks in DM occur due to stretching of eye ball; this
causes sudden influx of aqueous into stroma
4. Optic disc cupping may regress if treated early
– C:D ratio > 0.3 : 1.0
– Scleral canal enlarges
– Lamina cribrosa may bow posteriorly
GLAUCOMA 101
– Cloudy cornea
• Mucopolysaccharidosis
• Birth trauma
• Congenital Hereditary Endothelial Dystrophy
• Sclerocornea
• Keratitis - rubella
– Megalo cornea
• In myopia; anatomically big cornea
– Lacrimation
• NLD obstruction (delayed canalization)
– Secondary infantile glaucoma
• Retinoblastoma, juvenile xanthogranuloma
• PHPV, ROP
• Trauma, inflammation
• Ectopia lentis
EVALUATION
Under general anesthesia with I.V ketamine
– Evaluate the optic disc
– Measure IOP with Perkin’s tonometer/tonopen
– Measure corneal diameter [>13 mm at any age or > 11
mm up to 1 year - is significant)
– Gonioscopy - with a koeppe lens [direct gonioscope]
SURGICAL TREATMENT
– Medical treatment with beta blockers, ACE inhibitors &
PG analogues can be used before surgery
– Avoid alfa 2 agonists as they can cause sleep apnea &
respiratory failure
– Goniotomy, trabeculotomy
– Trabeculectomy + trabeculotomy
– Aqueous drainage implants
– Trans-scleral cyclophotocoagulation
Vision loss due to — optic damage, corneal scarring, amblyopia,
cataract, lens subluxation
IRIDOCORNEAL ENDOTHELIAL SYNDROME

– Unilateral; 4th decade; females > males
PATHOGENESIS
– Abnormal corneal endothelial cell layer which proliferates
& migrates across the angle onto the iris surface
– Synechial angle closure due to contraction of this abnormal
tissue
1. Progressive Iris Atrophy
– Severe iris changes with stromal atrophy
– Corectopia (malposition of pupil)
– Pseudo polycoria (super-numerary false pupils - hole
formation)
2. Iris Nevus (Cogan-Reese) Syndrome
– Diffuse nevus covers anterior iris (or)
– Pigmented, pedunculated iris nodules
– Smudged, matted iris surface (D/D- iris melanoma)
3. Chandler Syndrome
– Corneal endothelial changes - ‘hammered silver’
appearance
– Corneal edema - blurred vision, haloes
TREATMENT
– Trabeculectomy with mitomycin C
– Filtering shunts
GLAUCOMA 103
SCOTOMA
– An area of decreased visual sensitivity surrounded by an
area of normal sensitivity
TYPES
– Positive - can be perceived
– Negative - cannot be perceived e.g. blind spot
– Absolute - no change in area of scotoma with change in
size or color of stimulus
– Relative - area of scotoma changes with change in the
variables
– Sloping - gradual decrease in visual sensitivity from an area
of normal sensitivity e.g. tumors
– Steep - distinct margin between areas of normal &
decreased sensitivity
– Physiological - e.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 papillo-macular 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 & below blind spot - due to
shadows of large blood vessels
VISUAL FIELD
– An area in space encompassed by visual perception while
the eye fixates in a steady direction.
– Island of vision surrounded by a sea of blindness.
FIELD CHARTING
1. Kinetic:
– Confrontation method
– Bjerrum’s tangent screen
– Goldmann perimetry
2. Static:
– Standard automated perimetry [white on white perimetry]
– Short wave automated perimetry
– Frequency doubling perimetry
– Humphrey’s visual field perimetry
BLIND SPOT
– Corresponds to the region of the optic nerve head
– 15° temporal to fixation extending 2° above & 5° below
– Has an area of
• Absolute scotoma - corresponds to actual optic nerve
head
• Relative scotoma - corresponds to peripapillary retina.
FIELD DEFECTS
1. Binasal hemianopia - seen in
– atheroma of carotids or posterior communicating artery
– dilatation of 3 ventricle [optic nerves get pressed
downwards & outwards against the internal carotids]
GLAUCOMA 105
2. Bitemporal hemianopia - seen in

– Chiasmal lesions, dermatochalasis
– Nasal retinitis pigmentosa, nasal retinoschisis
– Optic nerve hypoplasia, tilted discs [high myopia]
3. 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
4. Right homonymous hemianopia -

– Lesion in left optic tract
– Right temporal & left nasal field loss
5. Right homonymous upper quadrantanopia

– Left optic radiation [temporal lobe lesion]
– ‘Pie in the sky’
6. Right homonymous lower quadrantanopia -

– Left optic radiation - parietal lobe lesion
– ‘Pie on the floor’
7. Homonymous hemianopia with macular sparing

– Anterior visual cortex lesion
– Occlusion of posterior cerebral artery
8. Macular involvement -
– Occlusion of middle cerebral artery
– Lesion at the tip of the calcarine process
9. Centro-cecal scotoma -
– Toxic amblyopia
– Ethambutol toxicity
– Papilloedema
10. Central scotoma -
– Optic neuritis
– AMD, heridomacular degenerations
11. Tubular vision -
– Retinitis pigmentosa
– Advanced glaucoma
12. Ring scotoma -
– Early retinitis pigmentosa
13. Enlargement of blind spot -
– Papilloedema
– High myopia with peripapillary atrophy
14. Altitudinal defect -
– AION
– optic disc drusen
GLAUCOMA 107
UGH SYNDROME
– Uveitis-Glaucoma-Hyphema syndrome
– Complication of cataract extraction with IOL implantation
CAUSES
– ACIOL abrading the iris
– PCIOL in ciliary sulcus
– Spontaneous hyphemas in - iris neoplasms, NVI, blood
dyscrasias
CLINICAL FEATURES
– Rapid decrease in vision over minutes followed by more
gradual resolution over hours to days
– Erythropsia - red vision
– Eye ache due to increased IOP
– Microscopic hyphaema, anterior uveitis, increased IOP
– Hyphema cleared from the anterior chamber within hours
– Gonioscopy - blood in trabecular meshwork between attacks
TREATMENT
– IOL - rotation/exchange/removal
– Steroids - in uveitis
– IOP lowering drugs
TRABECULECTOMY
– Lowers IOP by creating a fistula which allows aqueous
outflow from anterior chamber to sub-Tenon’s space
– Fistula is guarded by superficial scleral flap
POST-OPERATIVE COMPLICATIONS
1. 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 → Lens-corneal touch
Causes:
a. Shallow AC with increased IOP
– Pupillary block [see if peripheral iridotomy is patent]
– Malignant glaucoma
– Suprachoroidal hemorrhage
b. Shallow AC with decreased IOP
– Overfiltration → well formed bleb; Siedel’s test is
negative
– Bleb leak → flat bleb; Siedel’s test is positive
Seidel test — 2% fluorescein instilled into conjunctival
sac or over bleb; If bleb leak is present, fluorescein gets
diluted by escaping aqueous.
TREATMENT
– Topical atropine → prevents pupillary block, pushes lens-
iris diaphragm backwards
– Pinpoint bleb leak → cyanoacrylate or fibrin glue used
– Button holes/ leaky incisions → surgical repair
– Aqueous suppression → decreases aqueous flow through
fistula → allows spontaneous healing
GLAUCOMA 109
– Topical antibiotics [gentamycin] → irritates conjunctival

tissue & induces scarring
– Tamponade → bandage contact lens, pressure patch
2. Filtration failure - due to -
– Subconjunctival & episcleral fibrosis
– Bleb encapsulation
– Over tight suturing of scleral flap
– Scarring in scleral bed
– Blockage of sclerostomy by - vitreous, blood, uvea
– Blockage by thin membranes
Treatment
– Ocular compression
• digital (through lower lid, with eyes closed & patient
looking straight)
• focal (with a cotton bud - at edge of the scleral flap)
– Suture manipulation
• releasable sutures are removed
• argon laser suture lysis done
– Needling of an encysted bleb
– Sub-conjunctival injection of 5-FU
– Nd: YAG laser → gonioscopic re-opening of a blocked
internal ostium
– Re-surgery
3. Blebitis-
– White milky bleb - containing infective material
– Anterior uveitis may or may not be present
– Normal red fundal glow
4. Bleb associated endophihalmitis -
– Rapid worsening of vision
– White milky bleb
– Severe anterior uveitis & hypopyon
– Vitritis; no red glow of the fundus
5. 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
- peripheral anterior synechiae
Treatment:
- Sweating blebs → tissue glue, sutures
- Full thickness holes → conjunctival advancement to
hood existing bleb, conjunctival autograft & removal
of bleb
GLAUCOMA 111
NON-PENETRATING FILTRATION SURGERY

– Fashioning 2 lamellar scleral flaps & excising the deep flap,
leaving behind a thin membrane consisting of trabecular
meshwork or Descemet’s membrane through which aqueous
diffuses from anterior chamber to sub-conjunctival space
– Anterior chamber is not entered
DEEP SCLERECTOMY
– Superficial scleral flap
– 2nd deeper partial thickness scleral flap 4 mm wide, is
dissected forward to the Schlemm’s canal & excised
– Collagen implant drainage device is placed under the
superficial scleral flap which is loosely approximated &
conjunctiva closed
VISCO CANALOSTOMY
– Fornix-based conjunctival flap
– Superficial 1/3 thick scleral flap
– 2nd deeper scleral flap is dissected to provide access to
Schlemm’s canal
– Viscoelastic is injected into Schlemm’s canal with a special
cannula
– Descemet’s window is created by gently dissecting the deep
flap anterior to Schlemm’s canal & excising it
– Viscoelastic is injected into the area of the sclerostomy
– Superficial scleral flap is tightly sutured
– Conjunctiva closed
ARTIFICIAL DRAINAGE SHUNTS

– Artificial shunts which create a communication between
anterior chamber & 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
– Severe conjunctival scarring due to previous surgeries
– Congenital glaucoma where conventional procedures have
failed
– Post-vitrectomy glaucomas
IMPLANT TYPES: Molteno, Krupin, Ahmed
– An open tube with one end in anterior chamber — shunts
aqueous into an encapsulated area around the explant
located 10-12 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
– Ahmed valve is pressure-sensitive; it opens when IOP rises
& closes when IOP falls
COMPLICATIONS
– Increased drainage or leakage → leads to shallow AC
– Corneal decompensation—if tube touches the endothelium
– Cataract—if tube touches lens
– Tube retraction from AC—if tube is short
– Tube erosion through conjunctiva—avoided by placing a
donor scleral flap between tube & Tenon capsule
– Drainage failure if tube gets blocked by iris, vitreous or
blood
– Diplopia—if foot plate passes under muscle
– Bleb encapsulation over the foot plate
– Endophthalmitis
GLAUCOMA 113
Nd: YAG LASER IRIDOTOMY
INDICATIONS
– PACG - acute, intermittent, chronic
– Fellow eye in acute congestive glaucoma
– Narrow occludable angles (opening up to the posterior
trabecular meshwork in 180o or less)
– Secondary angle closure with pupillary block
– POAG with narrow angles - combined mechanism glaucoma
PROCEDURE
– Done in a miosed pupil; apraclonidine 1% drops &
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)
– 4- 8 mJ energy (3-6 mJ X 3 bursts)
Rx following 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 burns - if contact lens is not used
– Glare & diplopia - if large PI inferiorly; not covered by
upper lid
ARGON LASER TRABECULOPLASTY

– Argon laser used
– Laser beam aimed between anterior non-pigmented &
posterior pigmented trabecular meshwork
Indications
– POAG, NTG
– Pigmentary glaucoma
– Pseudoexfoliation glaucoma
Contraindications
– Aphakic glaucoma
– Uveitic glaucoma
– Extensive peripheral anterior synechiae [PAS]
Complications
– PAS - if burns are too posterior or if high energy is used
– Small hemorrhages - if blood vessels on iris are hit
– Increased IOP
– Anterior uveitis - mild
– 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 macrophages to engulf debris in trabecular
meshwork [scavenges trabecular meshwork & cleans it]
CHAPTER 5
Retina
THE LAYERS OF THE RETINA
Layer Sign
- Nerve fiber layer - Flame shaped hemorrhages
- Cotton wool spots
- Large retinal arteries & veins
- Inner nuclear layer - Retinal capillaries
- Microaneurysms
- Outer plexiform layer - Retinal edema
- Deep hemorrhages
- Hardexudates
RETINA 117
CYSTOID MACULAR EDEMA

– Abnormal accumulation of fluid in the neurosensory retina
in the macular area; in the outer plexiform & inner nuclear
layers
– Fluid filled cyst-like changes are seen
PATHOPHYSIOLOGY
Breakdown of inner blood retinal barrier
↓
Diffusion of water & plasma proteins
↓
Expansion of extra-cellular space
↓
Cystoid macular edema
↓
Lamellar hole
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

Causes Treatment
INFLAMMATORY Cataract surgery Anterior vitrectomy
[PC rupture, vitreous if vitreous loss
loss, vitreous occurred &
incarceration in vitreous in wound
wound], (or)
PKP, filtering YAG anterior
surgery, scleral hyaloidotomy
buckling, pars plana
vitrectomy Posterior sub-tenon’s
injection of
triamcinolone
Intermediate uveitis Systemic steroids
Behcet’s disease,
CMV retinitis, ARN
METABOLIC Diabetes mellitus Focal/ grid
photocoagulation;
intravitreal
triamcinolone
ISCHEMIC CRVO, BRVO; Oral acetazolamide;
topical NSAIDs
Choroidal ischemia
HEREDITARY Retinitis pigmentosa, Oral acetazolamide
Dominantly
inherited CME
MECHANICAL Macular pucker, Membrane peeling
Vitreomacular Vitrectomy
traction syndrome
HYDROSTATIC Hypertension Control BP
TOXIC Nicotinic acid, Stop drugs
Topical epinephrine,
Latanoprost
RETINA 119
CENTRAL SEROUS RETINOPATHY

– Localized detachment of the sensory retina at the macula
with or without pigment epithelial detachment [FED]
– Due to hyperpermeability of the retinal pigment epithelium
[RPE]
– M:F= 10:1; 20-45 year age group, type A personality
– Aggravating factors - stress, steroids, hypertension, SLE
CLINICAL FEATURES
– 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 fluid - clear/turbid
– Small precipitates on the posterior surface of the detachment
– May be associated with pigment epithelial detachment
FFA: The two patterns are -
1. In early phase - small hyper fluorescent spot seen; dye
passes into the sub-retinal space & 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 four months, no treatment required
(topical NSAIDs can be tried)
– Focal laser is done if -
• recurrent CSR
• CSR persists > 4 months
• decreased vision in fellow eye
– Photocoagulation done to the site of leakage - unless the
leak is near or within the FAZ
– Optic disc pit
– Circumscribed choroidal hemangioma
– CNVM
– Harada disease [exudative RD]
– Unilateral acute idiopathic maculopathy
RETINA 121
EALES DISEASE
– Primary perivasculitis of the retina associated with recurrent
vitreous hemorrhage in young adults
– Males > females; 20 - 30 year age group; Bilateral in 70-
85%
CAUSES
– Tuberculosis; allergy to tuberculoprotein
– Focal sepsis
– Thrombotic arteriolar occlusion
– Vitamin C deficiency
– Endocrine factors
– Multiple sclerosis
PATHOLOGY
Inflammation
↓ (PMNs infiltrate
around veins)
Obliteration
↓ (endothelial proliferation
into lumen; hypoxia results)
Proliferation
(new blood vessels form
leading to recurrent
vitreous hemorrhage)
STAGES
I. Vasculitis
II. Vaso-occlusion
III. Neovascularization
IV. Fibrovascular proliferation → Tractional RD, vitreous
hemorrhage
CLINICAL FEATURES
– Floaters; decreased vision
– Peri-venous sheathing with white exudates
– Retinal hemorrhages, vitreous hemorrhage
– Multiple quadrants involved with spread from the periphery
– Proliferative retinopathy with recurrent vitreous hemorrhage
– Tractional retinal detachment
– Complicated cataract, glaucoma
FFA
– Areas of non-perfusion seen (capillary drop-out)
– NVE (leaks) at the junction of normal & non-perfused areas
– Retinitis due to HIV, HSV, CMV
– Pars planitis
– Causes of vasculitis like tuberculosis, syphilis, toxocara,
Toxoplasma, leukemia, Behcet’s disease, SLE
TREATMENT
a. Medical - in stage of inflammation
– Steroids - periocular/systemic
– Anti-tubercular treatment if required
b. Laser - in stage of obliteration & neovascularization
c. Surgery - vitrectomy in
– non-resolving vitreous hemorrhage, traction bands,
tractional RD
RETINA 123
LEUCOCORIA
– Amaurotic cat’s eye reflex
– Whitish reflex in the pupillary area
1. Retinoblastoma (discussed later)
2. PHPV (persistent hyperplastic primary vitreous)
– Nystagmus, strabismus, decreased vision
– Unilateral & mostly sporadic
– Associated with microphthalmos
Clinical Features
– Retrolenticular mass into which elongated ciliary
processes are inserted
– The mass contracts & pulls the ciliary processes centrally
– In Anterior PHPV, a small, plaque-like opacity is seen
behind the lens capsule - Mittendorf’s dot
– In posterior PHPV, Bergmiester’s papilla is seen
Associations
– Shallow anterior chamber with angle closure glaucoma
– Optic nerve hypoplasia
– Macular hypoplasia
– Iris & lens coloboma
– Posterior polar cataract
– Lens subluxation
– Persistent pupillary membrane
– Vitreous hemorrhage
Vitrectomy
– Indicated if vitreous hemorrhage occurs
3. Coat’s disease
– severe form of retinal telangiectasia
– unilateral; young boys
Clinical Features
– Decreased vision, squint
– Retinal telangiectasia & aneurysms in inferior &
temporal quadrants
– Intra-retinal or sub-retinal yellowish exudation (especially
in the macular area)
– Exudative retinal detachment
– Neovascular glaucoma
– Uveitis, phthisis bulbi
FFA
– tortuosity, aneurysms [hyperfluorescent], areas of
capillary non-perfusion
– blockage of background choroidal fluorescence due to
exudation
Rx
– photocoagulation of areas of telangiectasia
– cryotherapy - in shallow RD
– vitreo-retinal surgery - in extensive RD
4. Toxocariasis
– chronic endophthalmitis — cyclitic membrane gives a
white pupillary reflex
– Posterior pole granuloma can resemble endophytic
retinoblastoma
5. Retinal astrocytoma
– in tuberous sclerosis
– solid white nodule with multiple areas of calcification
– fossilized mulberry-like appearance
RETINA 125
6. Retinopathy of prematurity
– In premature infants [< 32 wks 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
Zonel Posterior pole: twice the disc-fovea distance, centered
around the disc
Zone 2 From zone 1 to the nasal periphery, temporally equidistant
from the disc
Zone 3 The remaining temporal periphery
Extent - number of clock hours involved
Severity
Stage 1 Flat demarcation line separating No treatment
the vascular posterior retina from
the avascular peripheral retina
Stage 2 Ridged demarcation line No treatment
Stage 3 Ridged demarcation line with Laser
extraretinal fibrovascular photocoagulation
proliferation or cryotherapy if →
threshold disease
Stage 4a Extrafoveal retinal detachment Surgery
4b Subtotal retinal detachment
involving macula
Stage 5 Total retinal detachment Surgery
Threshold disease → atleast 5 contiguous or 8 accumulated

clock hours of stage 3+ disease
Plus disease → engorged veins & tortuous arteries in the
posterior pole
Rush disease → high risk for rapid progression [e.g. Zone
1 with plus disease]
Differential diagnosis:
– Familial exudative vitreoretinopathy
– Incontinentia pigmenti in girls
7. Intermediate uveitis
– causes an inflammatory cyclitic membrane
– can mimic infiltrative type of retinoblastoma
8. Retinal dysplasia
– retina never attains maturity
– associated with microphthalmos, shallow anterior
chamber, elongated ciliary processes
– pink or white retrolental membrane
9. Incontinentia pigmenti
– fibro-vascular proliferation causing cicatricial retinal
detachment
– vesiculo-bullous dermatitis
10. Retinocytoma
– a benign calcified mass with RPE alteration & chorio-
retinal atrophy
RETINA 127
CENTRAL RETINAL VEIN OCCLUSION
PATHOGENESIS
– Thrombotic/atherosclerotic phenomenon
– Vein inflammation; vessel wall abnormalities
– Turbulent blood flow causes thrombosis at lamina cribrosa;
laminar constriction site is a nidus for occlusion
– Increased IOP - POAG or PACG
– Papilloedema
– Orbital tumor/abscess
– Cavernous sinus thrombosis
– Retrobulbar intra nerve sheath injection
– Hypercoagulable states - increased viscosity
– Increased homocysteine levels in the blood
SIGNS
– Disc edema; dilated tortuous veins; deep & superficial
hemorrhages in all 4 quadrants
– Macular edema
– Collaterals over the disc—in old cases
– NVI with neovascular glaucoma - in ischemic type of CRVO
[100 day glaucoma]
Decreased vision due to -
– Macular edema
– RPE atrophy at macula
– Retinal/vitreous hemorrhage
– Tractional retinal detachment, NVG
NON-ISCHEMIC CRVO ISCHEMIC CRVO

Vision > 6/60 Vision < 6/60
Pupil NSRL Pupil -RAPD
Dot & blot hemorrhages Flame shaped hemorrhages
Few cotton wool spots (CWS) Numerous CWS
Relatively normal retina Orange, turbid, edematous
retina
< 10DD of retinal non-perfusion > 10 DD of non-perfusion
Low risk for neovascularization High risk for neovascularization
70% of CRVO cases 30% of CRVO cases
Good prognosis Bad prognosis
ASSOCIATED SYSTEMIC DISEASE

– HTN, DM, cardiovascular disease
– Hyperviscosity syndromes - hypergamaglobulinemia,
hyperfibrinogenemia
– Hyperviscosity states - malignancy, chronic lung disease,
nephrotic syndrome, polycythemia, oral contraceptive use
– AIDS, syphilis - infectious vasculitis
– Behcet’s disease
– Collagen vascular disease - SLE, PAN
– Mitral valve prolapse, migraine, hyperlipidemia
– Head injury, carotid artery disease
– Sickle cell disease
MANAGEMENT
– Refer to physician to rule out & treat systemic vascular
disease & hyperviscosiry syndromes
– Regular follow up to look for NVG
– PRPC if NVD, NVE, NVG develops
RETINA 129
BRANCH RETINAL VEIN OCCLUSION

– Supero-temporal BRVO is more common
– Occlusion occurs at A-V crossings
– Leakage occurs from capillaries - never from the veins/
venules
– Strong association with hypertension
CLINICAL FEATURES
– Present with decreased vision/field loss/are asymptomatic
– Vision loss due to - macular edema, vitreous hemorrhage,
TRD
NON-ISCHEMIC BRVO ISCHEMIC BRVO
80% of BRVOs 20% of BRVOs
Cotton wool spots rare Cotton wool spots common
Collaterals develop NVD, NVE, TRD, vitreous hemorrhage
may occur
Mild macular edema Severe macular edema
< 5 DD of non-perfusion > 5 DD of capillary 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
– PRPC done to the quadrant with capillary non-perfusion,
if neovascularization develops
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 (CRAO may become bilateral in hours)
CLINICAL FEATURES
– Sudden painless unilateral visual loss - vision being CFCF,
HM or even NLP [counting fingers close to face, hand
movements or no light perception]
– Retinal edema - fundus appears white
– Cherry red spot at the fovea
– Optic atrophy eventually occurs
In cilioretinal artery occlusion, central visual acuity
deceases but peripheral field is preserved.
INVESTIGATIONS
– ESR - if raised, urgent referral to rule out Giant cell arteritis
– BP, RBS, VDRL, FTA-ABS, ANA
– TC/ DC, lipid profile, PT/PTT
– Carotid Doppler, ECG
UNDERLYING CAUSES
– HTN, DM, cardiovascular disease
– Infectious endocarditis, valvular heart disease
– Retrobulbar steroid injections
– Migraine, malignancy, trauma, SLE, PAN
– Optic disc drusen - prelaminar compression of central retinal
artery
RETINA 131
TREATMENT
– Paracentesis - to reduce IOP → less compression on central
retinal artery will allow the embolus to pass
– Digital massage → will decrease IOP & cause rebound
arterial dilatation
– Carbogen inhalation for 5-10 min. every hour for 24 hours
→ increases CO2 which causes a rebound vasodilatation
– Breathing into a paper bag increases CO2
– Antifibrinolytic agents like streptokinase can be tried within
6 hours
In Giant cell arteritis & granulomatous vasculitis (Polyarteritis
Nodosa) - treat with systemic steroids
CHERRY RED SPOT

– Superficial retina in the posterior pole becomes opacified
& looks yellow-white except in the region of the foveola,
where the cherry red spot is present
– Ischemic necrosis in the inner half of the retina corresponds
to the whitening
– No ganglion cells in foveola → retina is very thin; underlying
RPE & choroid are visible as the cherry red spot
In inherited metabolic diseases,
– Progressive storage of glycolipids /phospholipids
– Lipids accumulate in ganglion cell layer → appears white
– Foveola retains transparency; it is surrounded by opaque
retina
– Later, ganglion cells die & cherry red spot becomes less
evident
– Atrophy of nerve fiber layer & optic atrophy occurs
eventually
Cherry red spot seen in:
– Central retinal artery occlusion
– Tay-Sachs disease
– Niemann-Pick disease
– Sandhoff’s disease
– Generalized gangliosidosis
– Sialidosis (cherry red spot myoclonus syndrome)
RETINA 133
EYE IN DIABETES MELLITUS

LIDS chalazion, hordeolum internum, hordeolum
externum, blepharitis, ptosis [IIIn 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 IIIn [pupillary sparing], IVn, VIn palsies
ORBIT mucormycosis, orbital cellulitis
DIABETIC RETINOPATHY
KANSKI’S CLASSIFICATION
1. Simple background diabetic retinopathy
– microaneurysms
– hemorrhages - dot, blot, flame-shaped
– hard exudates - arranged in a circulate pattern
– retinal edema [in the outer plexiform layer]
2. Pre-proliferative diabetic retinopathy
– venous beading & looping
– dark blot hemorrhages - hemorrhagic retinal infarcts
– multiple cotton wool spots
– IRMA [intra-retinal microvascular anomalies] - adjacent
to areas of capillary non-perfusion
3. Proliferative diabetic retinopathy
– NVE, NVD [if capillary non-perfusion occurs in
>l/4 of the retina]
– Vitreous hemorrhage, subhyaloid hemorrhage
4. Diabetic maculopathy
– Exudative maculopathy - focal leakage causing hard
exudates formation
– Edematous maculopathy - diffuse macular edema
– Ischemic maculopathy - extensive macular capillary
non-perfusion
MODERN ETDRS CLASSIFICATION

– Mild NPDR — atleast 1 microaneurysm
– Moderate NPDR - microaneurysms, dot & blot
hemorrhages, soft exudates, venous beading
– Severe NPDR - atleast one of: [4-2-1 rule]
• microaneurysms/hemorrhages in 4 quadrants
• venous beading in 2 quadrants
• IRMA in 1 quadrant
RETINA 135
– Very severe NPDR - 2 or more of above

– PDR - new vessels seen
High risk PDR:
• NVD involving 1/3 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
– Retinal edema within 500 um of foveal center
– Hard exudates with adjoining thickening within 500 um
of fovea
– 1 disc diameter of edema encroaching within 1 disc diameter
(1500 um) of foveal center
– Rx: focal or grid photocoagulation
TREATMENT OF DIABETIC RETINOPATHY

Medical:
– Strict blood sugar control
– Vitamin E supplements
– Lipid reduction
Laser:
– PRPC for high risk PDR
– Grid or focal PC for CSME
Surgical Treatment:
– Pars plana vitrectomy for non-resolving vitreous hemorrhage
– Delamination & segmentation for TRD; with or without
silicon oil injection
ETDRS protocol for full scatter laser treatment:
Pan retinal photocoagulation [PRPC]
Spot size - 500 um
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
– Enough energy to small tufts of vessels to produce
intravascular coagulation & occlusion
Indications for photocoagulation in diabetic retinopathy
– High risk PDR
– Extensive capillary non-perfusion, retinal hemorrhage,
venous beading, cotton wool spots
– PDR & CSME - 1st focal/grid PC followed by PRPC 4
to 6 wks later
– Neovascularization of angle/iris
– Endolaser done during vitrectomy
RETINA 137
FUNDUS FLUORESCEIN ANGIOGRAPHY

– Fluorescein is a water soluble dye—remains mainly
intravascular - 80% bound; 20% free
– Outer blood retinal barrier → RPE tight junctions
– Inner blood retinal barrier [BRB] → retinal capillary
endothelial cells
– Disruption of inner BRB leads to leakage of bound & free
fluorescein into extra vascular space
– Fluorescence - property 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 I.V rapidly (in opaque media-
3 ml of 25% sol.)
– Photos taken every 2 seconds, for 5 – 25 sec. after injection;
then after 10 min. & 20 min.
Side Effects
– Skin/urine discoloration, nausea & vomiting
– Itching, hives, laryngeal edema
– Anaphylactic shock
Phases
1. Choroidal/pre-arterial phase -
– Starts 8 to 12 sec. after injection
– Patchy choroidal filling
– Cilioretinal artery if present, gets filled
2. Arterial phase -
– Starts 11 to 18 sec. after injection
– Arterial filling occurs
– Choroidal filling continues
3. Arterio-venous/capillary phase -
– Complete filling of arteries & capillaries
– Choroidal filling continues
After 20-25 seconds of injection, maximum fluorescence occurs
in juxtafoveal/perifoveal capillaries
4. Venous phase -
– early → laminar venous flow
– mid → near complete venous filling
– late → decreased concentration of dye in arteries
5. Late/elimination phase -
– dye absent from angiogram in 5 to 10 min; late staining
of the disc
Dark Fovea due to

– Avascular FAZ [supplied only by choriocapillaries]
– 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. - CSR, PED
– Leakage due to -
• Abnormal choroidal vasculature e.g. CNVM
• Abnormal retinal/disc vasculature e.g. PDR
– Staining - prolonged retention of dye e.g. Drusen
Hypofluorescence
– Blockage of retinal fluorescence
• Vitreous opacities
• Pre-retinal lesions - blood
• Intra-retinal hemorrhages, hard exudates
RETINA 139
– Blockage of background choroidal fluorescence

• Subretinal/sub-RPE lesions - blood
• Increased density of RPE - congenital 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 & emitted
– Reconstitute 40 mg in 2 ml & give I.V
– Rapid serial photos taken; then at 3, 10 & 30 min.
– Used mainly to diagnose & treat occult CNVM
Contraindicated in - pregnancy, iodine allergy
Side effects - stool staining, nausea & vomiting, itching,
sneezing, local skin necrosis, syncope
Phases
1. Early (2-60 sec.)
– Prominent filling of choroidal arteries, early filling of
choroidal veins; retinal arteries are seen
2. Early mid phase (1-3 min.)
– Filling of watershed zone
– More prominent choroidal veins
– Retinal arteries & veins are seen
3. Late mid phase (3-15 min.)
– Diffuse hyperfluorescence due to diffusion from
choriocapillaries
– Fading of choroidal filling
4. Late phase (15-30 min.)
– Hypofluorescence of choroidal vessels against a
background of hyperfluorescence
– Retinal arteries & veins are not seen
RETINA 141
HYPERTENSIVE CHOROIDOPATHY
– Seen in acute hypertension, pregnancy induced hyper-
tension, renal disease, pheochromocytoma, accelerated
hypertension in young adults
CLINICAL FEATURES
– Early phase : Elschnig’s spots → pale white or reddish
patches of outer retina - due to hypoperfusion of underlying
capillaries; necrosis of choriocapillaries
– Focal serous detachment; exudative RD (in pregnancy
induced hypertension)
– Macular star
– Siegrist’s streaks → chains of pigmented spots arranged
like a string of beads along choroidal vessels (fibrinoid
necrosis)
– Chronic Elschnig’s spots → pigmented center with
depigmented halo around it
In the acute phase -
– Ischemic phase → choroidal arterioles severely constrict →
cause Elschnig’s spots
In the chronic phase -
– Occlusive phase - vessels undergo hyperplastic changes with
fibrinoid necrosis → choriocapillaries occluded by thrombi
– Reparative phase - recanalization of blood vessels with focal
necrosis of overlying RPE
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-CLAYGIBNER CLASSIFICATION
Based on:
Generalized narrowing
i. Reduction of artery caliber to 1/2 veins
ii. Reduction of artery caliber to 1/3 veins
iii. Reduction of artery caliber to 1/4 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
Garde 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
RETINA 143
ENDOPHTHALMITIS
– Intra-ocular inflammation which predominantly affects inner
spaces of the eye & their contents → vitreous and/or anterior
chamber
CAUSES
1. Acute post-operative endophthalmitis
a. Infectious-
– Exogenous
• Bacterial flora of lids & conjunctiva
• Staph. aureus — 1st-3rd post-op days
• Staph. epidermidis — 4-10 post-op 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
b. Non-infectious →
– sterile endophthalmitis - usually due to solutions
used during intraocular surgery
2. 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 & posterior capsule
– Increased incidence following YAG capsulotomy
– Organism grows on thioglycolate broth
Rx:
• remove IOL & residual cortex
• vitrectomy + intravitreal antibiotics [cephazolin/
clindamycin/vancomycin]
• topical & periocular steroids
• topical antibiotics
3. Bleb-associated endophthalmitis—usually caused by
Streptococci, H. influenzae
4. Post-traumatic endophthalmitis—caused by Staph.
epidermidis, Bacillus sp.
CLINICAL FEATURES
– Fever, headache, vomiting
– If pain & vision loss is marked, becoming worse
over 6-8 hours, consider infection
– In the exogenous form, edges of wound are yellow / necrotic;
hypopyon occurs
– Ring infiltration, corneal melting
– Proptosis & painful limitation of movement, when
inflammation extends to Tenon’s capsule → called
Panophthalmitis
– Spread of infection - causes orbital cellulitis, cavernous
sinus thrombosis
– Wide spread formation of cyclitic membranes → destruction
of ciliary processes → phthisis bulbi
B-SCAN: shows vitreous exudates; hazy media
RETINA 145
COMPLICATIONS
– Panophthalmitis
– Cataract (due to inflammation/treatment given)
– Rhegmatogenous or fractional RD
– Macular infarction (due to intravitreal aminoglycosides)
– Optic atrophy
– Hypotony
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 taken
– Vitreous tap taken
• 3 mm from the limbus in aphakic & pseudophakic eye
(a more posterior tap may cause retinal dialysis)
• 3.5 mm from limbus in phakic eyes (to avoid trauma
to lens)
– Microscopy - Gram’s stain, Giemsa stain, KOH mount
– Culture sensitivity — blood agar, chocolate agar,
Sabouraud’s dextrose agar (SDA), thioglyocolate broth
1. Intravitreal antibiotics : [can be repeated after 48-72 hours
if no response]
• Gentamycin (GN) + cephazolin (GP) or
• Amikacin (GN) + Vancomycin (GP) or
• Ceftazidime (GN) + Vancomycin (GP)
[GN=gram negative organisms; GP = gram positive
organisms]
Dosage
• Gentamicin 0.2 mg in 0.1 ml
• Amikacin 0.4 mg in 0.1 ml
• Vancomycin 1 mg in 0.1 ml
• Ceftazidime 2 mg in 0.1 ml
2. Anterior sub-tenon’s injection daily for 5-7 days
• Vancomycin 25 mg + ceftazidime 100 mg (or)
• Gentamicin 20 mg + cefuroxime 125 mg
3. Topical antibiotics
• Fortified gentamicin (15 mg/ml) + fortified vancomycin
(50 mg/ml) hourly
4. Systemic antibiotics
• i.v ceftazidime 2 gm every 12 hours
• Oral ciprofloxacin 750 mg bd
5. Steroids
• Periocular — betamethasone 4 mg or dexamethasone
4 mg × 5-7 days
• Topical - dexamethasone 0.1%
• Oral prednisolone 1 mg/kg wt × 10-14 days
• Intravitreal dexamethasone 0.4 mg in 0.1 ml
6. Cycloplegics - prevent posterior synechiae formation
7. Oral acetazolamide/topical beta blockers - to lower IOP
8. Vitrectomy - indications are:
• Vision PL+ (light perception) or worse
• Failure of medical treatment in 48 hours
• Fungal endophthalmitis
• Vitreous abscess
• IOFB removal
• Bleb-associated endophthalmitis
• Post-traumatic endophthalmitis
RETINA 147
FUNGAL ENDOPHTHALMITIS
– delayed onset; minimal discomfort
– snowball exudation in vitreous; vitreous abscess
– increased fibrinoid reaction in AC
– commonest cause - Fusarium sp.
Rx:
• Intravitreal amphotericin B [5 ug in 0.1 ml]
• Oral ketoconazole 400 mg/day
• I.V Amphotericin B 0.25- 0.1 mg, over 6 hours
• Vitrectomy
• NO STEROIDS
PREPARATION OF INTRAVITREAL DRUGS

DRUG VIAL HOW TO PREPARE
STRENGTH INTRAVITREAL DOSE
Vancomycin 1 vial = 500 mg Add 10 ml of SS to vial
[1 mg in 0.1 ml] ↓
Add 0.8 ml SS to 0.2 ml of
reconstituted drag
Ceftazidime 1 vial = 500 mg Add 2 ml of SS to vial
[2.25 mg in ↓
0.1 ml] Add 0.9 ml SS to 0.1 ml of
reconstituted drug
Amikacin 2 ml vial Add 2.3 ml of SS to 0.2 ml
[0.4 mg in = 100 mg of drug
0.1 ml] [0.2 ml = 10 mg]
Gentamycin 2 ml vial Add 1.9 ml of SS to
[0.2 mg in = 80 mg 0.1 ml of drug
0.1 ml] [4 mg in 0.1 ml]
Amphotericin B 1 vial = 50 mg Add 10 ml of 5%
[5 μg in 0.1 ml] dextrose to vial
↓
Add 9.9 ml of 5%
dextrose to 0.1 ml of
reconstituted drug
Ganciclovir 1 vial = 500 mg Add 10 ml of SS to vial.
[400 μg in Take 0.8 ml of reconstituted
0.1 ml] drug & add 0.2 ml of SS
to it [now 1 ml = 40 mg]
↓
Take 0.1 ml of the above
mixture & add 0.9 ml of
SS to it to get a solution in
which 0.1 ml = 400 μg
*[SS = distilled water]

RETINA 149
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)
Fate of Blood
– Fibrinolysis – disperses RBCs in vitreous
– Hemolysis – spontaneously occurs
– Phagocytosis by PMNs; Hemoglobin liberates Heme +
globin + bilirubin, which get absorbed
– Blood clears faster in posterior vitreous
CAUSES OF VITREOUS HEMORRHAGE

– PDR, BRVO, CRVO
– Retinal tear, trauma
– Posterior vitreous detachment [PVD] - sudden collapse of
vitreous
– Sickle cell retinopathy
– Eales’ disease
– Macroaneurysms, telangiectasia
– Anemia
– Valsalva retinopathy
– Choroidal melanoma
– Sub-arachnoid hemorrhage with vitreous hemorrhage -
Terson’s syndrome
– Hemorrhagic disciform macular degeneration
– Familial exudative vitreoretinopathy [FEVR]
– Retrolental fibroplasias
CLINICAL FEATURES
– Visual haze, floaters, photophobia
– Shadows & cob webs
– Sudden decrease in vision
– May give a history of trauma, ocular/systemic disease
– Subhyaloid hemorrhage - unclotted blood, boat shaped
bleed
– Intravitreal hemorrhage -
clotted - gray /yellow globular - adheres to gel unclotted-
shifts with gravity
B SCAN will show
– Extent & density of hemorrhage
– Location & source
– Membranous change (higher amplitude)
TREATMENT
Recent hemorrhage
– Bed rest, patching, head elevation
– Photocoagulation of bleeding vessel
– Posterior hyaloidotomy - Nd:YAG laser disrupts internal
limiting membrane & releases blood into vitreous cavity
– Cryotherapy increases fibrinolysis
– Diathermy
Non-resolving vitreous hemorrhage
– Pars plana vitrectomy
COMPLICATIONS OF VITREOUS HEMORRHAGE

– Hemosiderosis bulbi - due to iron liberated from hemoglobin
– Retinal damage - iron causes degeneration of photoreceptors
→ field loss, nyctalopia, decreased macular function
– Proliferative retinopathy - direct stimulation of fibroblastic
elements by iron
– Ghost cell glaucoma, hemolytic glaucoma
RETINA 151
PERIPHERAL RETINAL DEGENERATION
1. LATTICE DEGENERATION:
– In young myopes, Ehlers-Danlos syndrome, Marian’s
syndrome, Stickler syndrome
TYPES
Typical
– Sharply demarcated, spindle shaped areas of retinal thinning
– Between equator & 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
2. 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
3. DEGENERATIVE RETINOSCHISIS:
– Splitting of sensory retina at the level of outer plexiform
layer into outer choroid & inner vitreous layer
– In hypermetropes
– Microcystoid degeneration with a smooth elevation
of retina (infero-temporal)
– Progresses circumferentially
– Inner layer - immobile & transparent; snowflakes;
sheathing/silver wiring of blood vessels; schisis cavity
bridged by torn gray-white tissue; small round breaks
– Outer layer - beaten metal appearance; white with
pressure; breaks have large rolled edges
– If breaks occur in both layers - RD occurs
RETINA 153
EYE IN LEUKEMIA
– Conjunctiva - spontaneous subconjunctival hemorrhage
– Iris - thickening, iritis
– Anterior chamber - pseudohypopyon, hyphema
– Retina -
• Rame shaped hemorrhages, cotton wool spots
• Roth spots
• Peripheral retinal neovascularization (in CML)
• Leopard spot fundus - secondary to choroidal infiltration
(leukemic pigment epitheliopathy)
– Optic nerve - optic neuropathy
– Orbit involvement - proptosis [due to leukemic infiltration;
retrobulbar hematomal
Changes can be due to

– Leukemic infiltration or
– Anemia/hyperviscosity
OPTIC DISC DRUSEN

– 1st to 8th decade; unilateral or bilateral
– Patients usually have normal visual acuity
PATHOGENESIS
Abnormal axonal transport
↓
intracellular mitochondrial calcification
↓
extrude extracellularly
↓
form calcified microbodies [drusen]
SIGNS
– Afferent pupillary defect
– Defective color vision
– Due to compressive effect - can cause CNVM, CRVO, AION
– Field defects -
• Lower nasal defect
• Sector defect
• Enlargement of blind spot
• Concentric constriction
ASSOCIATIONS
– Angioid streaks
– Glaucoma
– Corneal dystrophies
– Juvenile diabetes mellitus
RETINA 155
FUNDUS
– Round irregular excrescences, mostly nasal to the disc (may
fill the entire optic disc)
– Superficial drusen - whitish yellow, globular; in the form
of dots/granules
– Deep drusen - lack sharp margins
– No disc hyperemia; no dilated capillaries on surface; no
vessel obscuration
– Optic disc elevated; elevation confined to disc
– Commonly in smaller optic discs
– Usually central area of optic disc contains buried drusen
– Premature branching of vessels over the disc
INVESTIGATIONS
– Red-free photography: auto-fluorescence
– FFA: No leakage
PROGNOSIS
– True progressive optic neuropathy - drusen continue to
develop & enlarge - causing progressive nerve fiber layer
atrophy.
– May lose central visual acuity or develop field defects
PNEUMATIC RETINOPEXY
– A gas bubble injected into vitreous cavity
– Patient positioned so that the bubble closes the retinal break,
allowing resorption of SRF, for 5-7 days
– Photocoagulation or cryotherapy around break – to
permanently seal it
– Alternative to scleral buckling
– Out patient procedure
– Usually - 0.3 ml C3 F8 or 0.5 ml SF6 is injected
GAS LASTS FOR ATTAINS LARGEST SIZE EXPANSION
AIR 3 days Immediately Nil
SF6 12 days In 36 hrs Doubles
C3F8 38 days In 3 days Quadruples
CHARACTERISTICS OF GASES
1. Surface tension — allows gas bubble to occlude break &
not pass into the sub-retinal space
2. Buoyancy - force which pushes the uppermost retina back
against the wall of the eye [10 times more than silicon
oil]
INDICATIONS
– Uncomplicated RD with small breaks in 1 or 2 clock hours
in upper 2/3 of peripheral retina
– Superior small breaks with RD
– Single break or break in one quadrant in upper 8 clock
hours
– Macular hole with RD
– Retinoschisis with very posterior outer layer breaks & RD
– Retinal re-detachment following scleral buckling - with
superior breaks
RETINA 157
– Functioning filtering bleb

– Optic pit with serous macular detachment
– Extensively scarred conjunctiva
– Very thin sclera
CONTRAINDICATIONS
– Detached tears 6 clock hours apart
– Inferior breaks
– Severe PVR
– Cloudy media - vitreous hemorrhage
– Inability to maintain positioning - in 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
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 & choroids
• Super fractional crescent
FUNDUS
1. Myopic conus -
– Oval disc
– Temporal crescent (absence of RPE & choroid makes
sclera visible)
[Myopic conus on nasal side → inverse myopia]
2. Posterior staphyloma -
– Localized ectasia involving sclera, choroid & RPE at
the posterior pole
– If macula involved → decreased vision
3. Tigroid & tessellated fundus - due to thinning of retina &
choroid; prominent choroidal vessels
4. Lacquer cracks -
– Rupture of Bruch’s membrane
– Linear/stellate, fine, yellowish white cracks
– Horizontally oriented branching & 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]
RETINA 159
5. Foerster Fuch’s spot

– Dark spot in macula - due 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 & choriocapillaries 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
• Retinopathy of prematurity
• Stickler syndrome, Marfan’s syndrome, Ehlers-Danlos
syndrome
TREATMENT
– Barrage laser for breaks & lattices
– Argon laser photocoagulation or intravitreal ranibizumab
or bevacizumab for active CNVM
PROLIFERATIVE VITREORETINOPATHY
– Growth of cellular membranes within vitreous cavity &
around retina
– Proliferation & 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 RD WITH PVR

GRADE NAME CLINICAL SIGNS
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
C-l - one quadrant
C-2 - two quadrants
C-3 - three quadrants
D Massive - Fixed retinal folds in 4 quadrants
D-l - wide funnel shape
D-2 - narrow funnel shape
D-3 - closed funnel [ONH 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
RETINA 161
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
CP1-12 - Focal/diffuse/circumferential full thickness retinal folds*,
posterior to equator
- Sub-retinal strands*
CA1-12 - 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
Migration of RPE cells onto retinal surface
↓
Proliferate (fibroblastic proliferation)
↓
Membrane formation
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 peering; delamination
– Segmentation of strongly adherent membranes
– Scleral buckling with encircling band & silicon oil
injection
RETINA 163
SUDDEN UNILATERAL PAINLESS LOSS OF VISION
Eye with normal reacting pupils

– Non-ischemic CRVO/BRVO
– Macular lesions
Eye with RAPD

– With central scotoma
• optic neuritis
– Altitudinal field defect
• AION
• Optic neuritis
• Vascular occlusion [branch]
– Central & peripheral field loss
• CRAO
• Ischemic CRVO
• Retinal detachment
VITREOUS OPACITIES
ASYMPTOMATIC
1. Vitreous syneresis
– Vitreous liquefaction
– Condensation of fibrils within the liquefied vitreous -
visible as floaters
– Muscae volitantes - float into optical axis; seen in various
shapes against a black background
2. Asteroid hyalosis
– Mostly unilateral
– Spherical/disc-shaped white bodies in vitreous cavity
– Calcium containing lipid complexes attached to collagen
fibrils, suspended throughout vitreous
– Common in diabetics
– If vision affected - vitrectomy may be done
3. Synchisis scintillans
– Yellow crystalline opacities in vitreous cavity
– In damaged eyes which were subjected to trauma or
inflammation
– Cholesterol crystals - multicolored; they glitter
– Settle in lower part of vitreous cavity due to gravity;
can be thrown up by eye movements as a shower of
iridescence
– Vitreous is liquefied
SYMPTOMATIC: [Patient sees floaters]

1. RBCs seen in-
– proliferative retinopathies like PDR, CRVO, Eales’
disease, sickle cell retinopathy, ROP, sarcoidosis
– PVD, retinal tears
– Wet type of AMD
RETINA 165
2. Pigmented cells in -
– retinal detachment
– malignant melanoma
3. WBCs in-
– Following surgery or trauma—infectious
endophthalmitis, lens induced uveitis, sympathetic
ophthalmitis
– Snow ball opacities in - pars planitis, sarcoidosis, lyme
disease
– Vasculitis - sarcoidosis, Behcet’s disease, ARN, TB,
syphilis, toxoplasmosis, idiopathic
– White dot syndromes - AMPPE, bird shot
chorioretinopathy
– Retinal detachment
• Serous RD - VKH, posterior scleritis, uveal effusion
syndrome, toxoplasmosis
• Tractional/rhegmatogenous RD - ARN, CMV, pars
planitis
HEREDITARY FUNDUS DYSTROPHIES
ROD-CONE DYSTROPHIES
– Atypical pigmentary dystrophy
– Leber’s congenital amaurosis
– Retinitis pigmentosa associated syndromes
CONGENITAL STATIONARY NIGHT BLINDNESS

– Fundus albipunctatus
– Oguchi disease
MACULAR DYSTROPHIES
– Best’s disease
– Stargardt dystrophy
– Familial dominant drusen
– Cone dystrophy
– Congenital retinoschisis
– North Carolina macular dystrophy
– Sorsby pseudo-inflammatory macular dystrophy
CHOROIDAL DYSTROPHIES
– Regional
– Generalized: gyrate atrophy, choroideremia
VITREO-TAPETO RETINAL DYSTROPHIES

– Goldmann-Favre dystrophy
– Wagner’s vitreo-retinal dystrophy
– Stickler’s syndrome
– Snowflake dystrophy
– Familial exudative vitreoretinopathy
RETINA 167
EVALUATION OF MACULAR FUNCTION

1. Visual acuity - for near & distance
2. Slit lamp biomicroscopy - with a strong convex lens
or contact lens
3. Amsler grid -
– Evaluates 10° of visual field surrounding fixation
– Used for screening & monitoring macular disease &
early optic nerve lesions
– Patient is asked to wear reading correction; cover at
a time & 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 reaction - normal in macular disease;
RAPD in optic neuropathies
6. Maddox rod - a large scotoma [loss of the red line viewed
by the patient], indicates macular disease
7. Blue light entoptoscopy - patient views an intense
homogenous blue-light background; WBCs produce shadows
- seen by patient
8. Purkinje’s entoptic phenomenon - a rapidly oscillating
point source of light shone through patient’s 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
OPTICAL COHERENCE TOMOGRAM

– Tornographic imaging of optic nerve head & 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-scan - uses light instead of sound waves
to create images with much higher resolution axially &
laterally
– Fiber optic based interferometer - for anterior & posterior
segment imaging
– Cross-sectional information - derived from time of flight
of reflected or back scattered light
– Delivered using slit-lamp biomicroscope via fiber-optic
– Takes 100 to 200 axial scans in 2.5 sec.
– Axial depth of scan = 3 mm.
Uses in Retinal Disease
– Cystoid macular edema
– Macular hole
– Vitreomacular traction
Uses in Glaucoma
– Analyses NFL loss
– Optic nerve head imaging
RETINA 169
MACULAR HOLE
CLASSIFICATION
1. Partial thickness
a. Outer lamellar
b. Inner lamellar
2. Full thickness
3. Pseudomacular hole - [in overlying epiretinal membranes]
CAUSES
– Idiopathic, trauma, PVD, solar retinitis, CME, CRAO,
CRVO, chorioretinitis, optic pits
CLINICAL FEATURES
– Blurred vision, metamorphopsia
– Watzke-Allen test: when a thin slit is thrown into a
patient’s eye, he will not be able to see it in the region
of the full thickness macular hole
GASS’ STAGING OF MACULAR HOLE:

STAGE 1a- [impending macular hole]
– Yellow spot at the foveola
– Represents an intrafoveal cyst
STAGE 1b - [occult macular hole]

– centrifugal displacement of foveolar retina & xanthophyll
– yellow ring with a bridging interface of vitreous cortex
– 50% resolve with vitreofoveolar separation
STAGE 2 - [early full thickness macular hole]

– eccentric, oval, crescentic, horse-shoe shaped retinal defect
– < 400 um diameter
– ± pseudo-operculum [overlying prefoveal opacity] formed
by contracted prefoveolar cortical vitreous
STAGE 3 - [established full thickness macular hole]

– round retinal defect > 400 um diameter
– attached posterior vitreous face
– ± pseudo-operculum
RETINA 171
STAGE 4 - [full thickness macular hole]

– Enlargement of round defect - surrounded by a cuff
of sub-retinal fluid
– Tiny yellowish deposits at the base of the crater
– Complete PVD — Weiss ring seen
SURGERY
– For full thickness macular holes up to stage 3, visual acuity
worse than 6/18, < 1 year duration
1. Conventional vitrectomy - removal of cortical vitreous &
internal limiting membrane with gas-fluid exchange followed
by strict face down post-operative positioning.
2. Chemical vitrectomy - enzyme [plasmin] injected into
vitreous to chemically detach vitreous from retina; vitreous
lavaged with infusion pipe & vitreous cutter.
AGE-RELATED MACULAR DEGENERATION

– Affects people > 50 years
– Dry AMD - non-exudative/atrophic → drusen, geographical
atrophy of RPE
– Wet AMD - exudative/neovascular → CNVM, sub-retinal
scarring
DRUSEN
– Discrete deposits of abnormal material between RPE &
Bruch’s membrane
– Hard drusen - small, round, discrete, yellow-white spots
associated with focal dysfunction of RPE
– Soft drusen - large, indistinct margins; slowly enlarge &
coalesce; associated with solid drusenoid detachment of
RPE; precursor of atrophic & exudative AMD
– Secondary dystrophic calcification → glistening appearance
of drusen
FFA
– Hyperfluorescence - due to window defects; overlying RPE
atrophy
– Hypofluorescence - a large area of hypofluorescence may
predispose to RPE detachment
Differential diagnosis
Familial dominant drusen, hard exudates, membrano-
proliferative glomerulonephritis fundus flavimaculatus, Stargardt
disease, Alport’s syndrome, benign flecked retina.
RX:
1. Antioxidants & Zinc
2. Home Amsler grid to detect early changes like
metamorphopsia or scotoma
RETINA 173
PIGMENT EPITHELIAL DETACHMENT (PED)

– Thickened Bruch’s 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 [or turbid]
FFA
– Venous phase - increased hyperfluorescence due to pooling
of dye; no increase in size of hyperfluorescence.
ICG
– Oval area of hypofluorescence with a surrounding faint
ring of hyperfluorescence.
COURSE
– Spontaneous resolution
– Geographic atrophy
– Detachment of sensory retina
– Occult CNV
– RPE tear
RPE TEAR
– Occurs spontaneously or following photocoagulation
– At junction of attached & detachment RPE
– Sudden worsening of central vision
– Crescent shaped RPE dehiscence at edge of a prior serous
detachment, with a retracted & folded flap
FFA
• Hypofluorescence over the flap with adjacent hyper-
fluorescence
ATROPHIC AMD
– Slowly progressive atrophy of photo receptors, RPE &
choriocapillaries
– Gradual, progressive decrease in vision
– Hyperfluorescence on FFA
Focal hyperpigmentation/RPE atrophy [drusen present]
↓
Sharply circumscribed circular areas of RPE
atrophy with loss of choriocapillaries
↓
Geographical atrophy with visible large choroidal vessels
[drusen disappear]
EXUDATIVE AMD
– Choroidal neovascular membrane originating from
choriocapillaries, grows through defects in Bruch membrane
– May precede or follow PED
– Metamorphopsia
– Blurring of vision due to leakage of fluid from CNVM
Type 1 - sub-RPE type – gray-green or pinkish yellow; slightly
elevated lesion
Type 2 - subretinal type – subretinal halo or pigmented plaque
Signs: serous retinal elevation, hemorrhages, subretinal hard
exudates
FFA
a. Classic CNV
– Extrafoveal - > 200 urn from FAZ
– Subfoveal - under foveal center
– Juxtafoveal - < 200 um from center of FAZ
– Well-defined membrane fills with dye in a lacy pattern;
it fluoresces brightly - leakage into subretinal space &
around the CNV
RETINA 175
b. Occult CNV - poorly defined membrane; late leakage

c. Fiber vascular FED → CNV + FED
ICG – detects CNV associated with overlying hemorrhage,
pigment or exudates
Course
• Hemorrhagic FED - rupture of blood vessels within CNV
• Vitreous hemorrhage
• Sub-retinal disciform scarring: gradual organization of blood
→ further ingrowth of new vessels from choroids → fibrous
scar
• Massive intraretinal/subretinal exudation - due to chronic
leakage from CNV
Treatment
1. Argon laser photocoagulation
– Extrafoveal/Juxtafoveal CNV with well defined margins
[contraindicated if poor visual acuity or subfoveal CNV]
– Perimeter of lesion treated with overlapping burns - then
enter area covered
2. Photodynamic therapy
– Verteporfin (photosensitizer) - 6 mg/kg wt given i.v for
10 min.
– Activated focally by illumination from a diode laser
source (wavelength corresponds to absorption peak of
compound)
– Has ability to selectively damage tissue
– Given for subfoveal/juxtafoveal classic CNV, < 5400
um; when visual acuity is ≥ 6/60
– Juxtapapillary CNV with subfoveal extension
– Contraindicated in pure occult CNV
– Also used to treat malignant melanoma & retino-
blastoma
3. Surgical treatment
– Submacular surgery- removal of blood & CNV
– Macular translocation - moving fovea away from CNV
– Pneumatic displacement of submacular hemorrhages
(gas in vitreous displaces blood)
4. Transpupillary thermotherapy
– Diode laser used
– Done for occult CNV
5. Intravitreal ranicizumab/bevacizumab/pegabtanib
sodium [macugen]
– Anti-VEGF factors are now being given intravitreally
for active CNVs
RETINA 177
RETINAL DETACHMENT
RHEGMATOGENOUS RD
Symptoms
– Photopsia - in 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
– Floaters - moving vitreous opacities perceived when they
cast a shadow on retina
– Weiss ring - represents the detached annular attachment
to margins of optic disc
– Cobwebs - condensation of collagen fibrils within collapsed
vitreous
– Sudden shower of minute dark spots - in vitreous hemorrhage
– Visual field defect - seen as a dark curtain
– Central vision affected - if subretinal fluid involves fovea
or if bullous RD occurs
Signs
– RAPD - in extensive RD
– Decreased IOP by afleast 5 mm Hg.
– Mild anterior uveitis
– Tobacco dusting - in anterior vitreous
– Retinal breaks - red discontinuities in retina
– PVR changes
FRESH RD
– Convex detached retina - appears opaque & corrugated
– Undulates freely with eye movements
– Retinal blood vessels appear darker than in flat retina
– SRF extends up to ora serrata
– Pseudo-hole if posterior pole is detached
OLD RD
– Retinal thinning secondary to atrophy
– Intra retinal cysts
– Sub-retinal fibrosis
– Sub retinal demarcation lines (high-water marks - due to
proliferation of RPE at junction of flat & detachment retina)
LICOFF’S RULE
a. Superior RD extending a. Break between 11 &
downwards equally on 1 o’clock
both sides of macula
b. Inferior RD extending b. Break between 5 &
upwards equally on 7 o’clock
both sides of macula
c. Asymmetric distribution c. Break within 1-2 clock
of SRF hours of the edge of the
more vertically extensive RD
d. Bullous RD d. Superior break
(See color figures in Plate 02)
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
RETINA 179
– Sub clinical RD - break 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
– Marfan’s, Stickler, Ehlers-Danlos syndrome
– RD in fellow eye
Barrage laser not indicated for:
– Microcystoid degeneration - tiny vesicles on a grayish-white
background
– Snow flakes - minute glistening yellow-white dots diffusely
in peripheral fundus
– Paving stone degeneration - yellow white patches of
chorioretinal atrophy
– Honey comb/reticular degeneration - fine network of
perivascular pigmentation
– Oral pigmentary degeneration → pigmented band running
adjacent to ora serrata
Complications of barrage laser:
– CME, macular pucker
– Choroidal detachment
– Secondary angle-closure glaucoma
– Exudative RD
– Rhegmatogenous RD - secondary tear
– Retinal hemorrhages
RETINAL DETACHMENT SURGERY

1. Scleral buckling -
– 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
RADIAL EXPLANTS CIRCUMFERENTIAL EXPLANTS
At right angles to limbus Parallel to limbus
Dimensions twice Dimensions depends on length
that of tear & breadth of tear
For large ‘U’ shaped tears; For multiple breaks in 1 or 2
posterior breaks quadrants; anterior breaks; dialysis
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 RD - when break can’t be detected
2. SRF drainage -
– If break can’t be localized
– Immobile retina (e.g. in PVR)
– Long standing RD (because SRF is viscid)
– Inferior RD associated with equatorial tears
Complications:
– Hemorrhage — perforation of a large choroidal vessel
– Dry tap [no SRF is drained]
– latrogenic breaks
– Retinal incarceration — does not re-attach
– Fish mouthing - tendency for ‘U’ shaped tears to open
widely following scleral buckle & SRF drainage
3. Intravitreal air injection
4. Pneumatic retinopexy
5. Pars plana vitrectomy
6. Tamponading agents -
– Air
– Expanding gases - SF6, C3F8
– Heavy liquid - perfluorocarbons PFCL
• To unfold giant retinal tears
• To remove posterior dislocated lens fragments/IOL
• To stabilize posterior retina - epiretinal membrane
[ERM] dissection in PVR
– Silicone oils - provide prolonged tamponade
RETINA 181
TRACTIONAL RD
– Vitreoretinal traction develops insidiously
– No photopsia/floaters/acute PVD/breaks
– Detached retina - concave configuration
– Shallow RD - SRF does not extend to ora
– Highest elevation of retina at sites of traction
– Decreased retinal mobility
– No shifting fluid under the detachment
– Combined RD - if TRD develops a break
Surgery
• Delamination - horizontal cutting of individual vascular pegs
connecting membrane to retinal surface
• Segmentation - vertical 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
EXUDATIVE RD
– Detached retina - convex, smooth
– Mobile detached retina - Shifting fluid phenomenon-
SRF detaches the retina under which it accumulates
– No retinal breaks
– May have floaters - if there is vitreitis
– Visual field defect may develop suddenly & progress rapidly
– Scattered areas of subretinal clumping after detachment
resolves → Leopard spot retina
Causes
• Choroidal tumor
• Harada disease
• Malignant hypertension
• Posterior scleritis
• Choroiditis
• Sympathetic ophthalmitis
• CSR
• Uveal effusion syndrome
Treatment
• Treat the cause
RETINA 183
LASERS
– Light amplification by stimulated emission of radiation.
TYPES
Solid → Ruby, Diode, Nd: YAG
Gas → Argon, Krypton, CO2, Neon
Liquid → Dye
Absorption by:
1. Melanin in RPE & choroid - by all lasers
2. Xanthophyll in OPL & IPL - by blue laser
3. Hemoglobin - by blue, green, yellow lasers
COMPLICATIONS
– Accidental foveal burn
– Bleeding (when high power used or blood vessel hit)
– Traction (when fibrous strand treated)
– Bruch’s rupture (when high energy burns given)
– CNVM may form; it may bleed
– Holes (if barrage given within lattice)
– Enlargement of tears [hence lattice should be given atleast
½ DD from margin of lattice]
– Night blindness, glare
– Decreased peripheral field
– Choroidal detachment
– Acute congestive glaucoma, ciliochoroidal effusion
– Increased macular edema
LASER EFFECTS
1. Photochemical - low energy laser radiation converts
absorbing molecule into free radicals [toxic to cell]
2. Photocoagulation - at 30°C
– Proteins get coagulated
– Argon, Xenon, Krypton, Diode laser
– Used for proliferative retinopathy, trabeculoplasty,
tumors, CNVM
3. Photovaporization - at 100°C
– Water content in cell gets evaporated
– CO2 laser
– Used for tissue incision, blepharoplasry, debulking of
conjunctival tumors
4. Photodisruption - at 10,000-20,000°C
– Has an ionizing effect
– Nd: YAG laser
– Used for capsulotomy, iridotomy, vitreolysis
5. Photodynamic therapy -
– dye laser
– Used for melanomas, retinoblastomas, CNV
6. Photoablation -
– Excimer laser (leaves no scar)
– Used for corneal scar removal, refractive surgery
RETINA 185
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 MESHWORK – argon laser trabeculoplasty,
selective laser trabeculoplasty
PUPIL – sphincterotomy, pupilloplasty,
membranolysis
LENS – capsulotomy
VITREOUS – vitreolysis
POSTERIOR SEGMENT USES

• Retinitis proliferans, high risk PDR
• Vessel ablation
• CNV
• CSR
• Holes, lattices - barrage laser
• Neoplasms <4 DD - retinoblastoma, malignant melanoma,
VHL syndrome, choroidal hemangioma
• Coloboma choroid
• Small peripheral retinal detachments
• CSME
• Retinoschisis progressing towards posterior pole
• NVE/NVD/NVG following CRVO or BRVO
• Retinopathy of prematurity
• Familial exudative vitreoretinopathy
• Sickle cell disease
• Bales disease
• During RD surgery, vitrectomy
CYCLOCRYOTHERAPY
– A procedure that employs temperatures of - 80°C to destroy/
ablate a part of the ciliary body
INDICATIONS
– NVG
– Refractory glaucoma [not responding to standard therapy]
– IOP > 40 mm Hg [which may injure a new corneal graft]
– Pain relief in absolute glaucoma
• IOP first increases for 24 hrs - then falls for many months
(may increase later)
• Decreases aqueous production & out flow
PROCEDURE
– N2O, CO2, liquid N2 used
– For effective treatment → -10°C at ciliary processes
– Retrobulbar anesthesia
– Probe placed over ciliary body 3-4 mm from limbus →
create a transconjunctival freeze for 60 seconds
– Single application every clock hour for 6-12 clock hours
– If insufficient IOP lowering in 1 week - repeat procedure
COMPLICATIONS
– Hyphaema, ciliary body hemorrhage
– Iris atrophy, uveitis
– Phthisis bulbi
– Anterior segment ischemia
RETINA 187
RETINAL COLOR CODING

Red - Attached retina
- Attached macula [plus sign]
- Microaneurysms
- Retinal/pre-retinal hemorrhages
- Break [red with blue outline]
Blue - Detached retina
- Macular edema
- Lattice degeneration
Green - Vitreous opacities
- Cotton wool spots
- Fibrous proliferations [pale green]
- White blood in vitreous [dark green]
Purple - New vessels on surface of retina or optic disc
Orange - Elevated new vessels
Yellow - Hard exudates
- Drusen
- Medullated nerve fibers
Black - Retinal pigment
Pink - Red hemorrhage in the vitreous
(For color version see plate 2)

CHAPTER 6
Neuro-
ophthalmology
THE PUPIL
– Normal size : 2-4 mm
– In dark adaptation : 4.5-7 mm
– In light adaptation : 2.5-6 mm
– Miosis : ≤ 3 mm
– Mydriasis : ≥ 6 mm
– Toxic pupil - in neuromuscular blockade

– Adie’s tonic pupil - due to ciliary ganglion block
– Paralytic pupil - in IIIn palsy
– Argyll Robertson pupil - pretectal nucleus lesion
– Marcus Gunn pupil - optic nerve involvement
NEURO-OPHTHALMOLOGY 191
TOXIC PUPIL
– Sudden unilateral dilatation of pupil
– Dilated & fixed pupil
– Due to finger-eye contact of anticholinergic agents
– Neuromuscular blockade occurs
– IIIn [3rd cranial nerve] uninvolved
– 1% pilocarpine will not constrict the pupil
– Acute botulism causes bilateral toxic pupils
ADIE’S 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 supersensitivity - pupil
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)
Adie’s Syndrome
Adie’s pupil + loss of deep tendon reflexes secondary to
degeneration of dorsal root ganglion cells
Causes
– Ciliary ganglionitis - HSV, measles, chickenpox
– Guillain-Barré 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 muscle - causing slow
tonic contraction
– Insufficient catabolism of acetylcholine causes slow
redilatation
ARGYLL ROBERTSON PUPIL

– Accommodation reflex present (ARP)
– Bilateral miotic pupils with irregular margins
– Pupils are asymmetric - in size & response to light
– Precedes other manifestations of neuro-syphilis
– Lesion at pretectal nucleus
Causes
– Tabes dorsalis, diabetes mellitus, Wernicke’s
encephalopathy, encephalitis, hereditary neuropathies,
midbrain tumors
PARALYTIC PUPIL
– In IIIn palsy
– Preganglionic parasympathetic denervation
– Pupil spared in - Diabetes mellitus - because pupillary fibers
are superficially placed & get perineural blood supply
Causes
– Posterior communicating artery aneurysm; cerebral
compression, contusion, inflammation, infiltration
Hippus
– Non-pathological, intermittent, synchronous, rhythmic
contraction & 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 1-3 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
parasympathetic 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 & 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 & greater redilatation
II. Initial stall & greater redilatation
III. Immediate pupillary dilatation
IV. Immediate pupillary dilatation following prolonged
illumination of the good eye for 6 seconds
V. Immediate pupillary dilatation with no secondary
constriction
HORNER’S SYNDROME
– Lesions involving the sympathetic pupillomotor pathway
from the hypothalamus till its termination cause this
syndrome
Clinical Features
1. Miosis-
– Anisocoria of 0.8-1.0 mm; prominent in dim light
– Normal reaction to bright light & accommodation
2. Partial ptosis of the upper lid & inverse ptosis of lower
lid because of paralysis of Muller’s muscle
3. Anhidrosis -
– affecting half body & face - in central lesions
(hypothalamus)
– affecting the face - in lesions proximal to carotid
bifurcation
– absent - in post-ganglionic lesions (distal to superior
cervical ganglion)
4. Enophthalmos - narrowing of palpebral fissure
5. Loss of cilio-spinal reflex — in pre-ganglionic &
post-ganglionic lesions
In congenital Homer’s syndrome — heterochromia iridis
occurs
Causes
– Central — hypothalamus & brain stem lesions
– Pre-ganglionic — Pancoast’s tumor, Klumpke’s paralysis,
breast cancer, lymphoma
– Post- ganglionic — neck trauma, carotid vascular disease,
naso-pharyngeal tumors
Tests
1. COCAINE TEST -
– cocaine prevents reuptake of nor-adrenaline
– normal pupil - dilates after 30-40 min.
– Horner’s pupil - no change in pupillary size
2. HYDROXY AMPHETAMINE (1%) TEST -
– It stimulates nor-adrenaline release at myo-neural
junction
– In central & pre-ganglionic lesions (1st & IInd order
neurons) - pupil dilates
– In post-ganglionic lesions (IIIrd order) - poor dilatation
of pupil
FIELD DEFECTS
IN OPTIC NERVE LESIONS

1. CONGENITAL/HEREDITARY
a. Myelinated nerve fibers -
– enlargement of blind spot
– central/paracentral scotoma
b. Optic nerve coloboma -
– nerve fiber bundle defects
– superior altitudinal defect
– superior nasal depression
c. Optic nerve hypoplasia -
– total blindness
– paracentral scotoma
– bitemporal/binasal hemianopia
– bilateral inferior extension of blind spot
d. Optic nerve head drusen -
– blind spot enlargement
– irregular peripheral contraction
– scotomas
– nasal defects
– slowly progressive defects
e. Optic nerve pit
– gross enlargement of blind spot
f. Tilted disc -
– upper temporal field defect
g. Leber’s Hereditary Optic Neuropathy
– central scotoma
2. PRESSURE ON THE OPTIC NERVE
a. Papilloedema
– gross enlargement of blind spot
– peripheral constriction in post-papilloedemic optic
atrophy
b. Optic nerve glioma

– central scotoma
3. INFLAMMATORY
a. Papillitis
– central scotoma with moderate enlargement of blind
spot
– scotoma for red objects
– centrocecal scotoma
4. VASCULAR
a. AION
– sector type atrophy
– inferior altirudinal defect
5. TRAUMATIC
– central scotoma
– inferior visual field defects
– blindness
6. TOXIC
– central/centrocecal scotoma
– bilateral peripheral field constriction with:
• quinine, chloroquine, salicylates, arsenic
• hyperbaric oxygen, carbon monoxide
• epinephrine
IN CHIASMAL LESIONS
1. INFRACHlASMAL
– Non- scotomatous: lesions in peripheral isopters
– Scotomatous:
• Anterior chiasma - junctional scotoma (one eye
temporal hemianopia; fellow eye peripheral field
defect)
• Posterior chiasma — e.g. pituitary adenoma
– Upper temporal field loss progresses to

hemianopia
– Recovery occurs in opposite direction to field
loss (UN - LN - LT - UT) [UN - upper nasal;
LN - lower nasal; LT - lower temporal; UT -
upper temporal]
2. SUPRACHIASMAL
– Antero- superior
– Postero-superior
• Craniopharyngioma — LT 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 supero-temporal
quadrant
3. PERICHIASMAL
– Inflammatory - arachnoiditis, 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)
4. 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].
MENINGIOMAS
– Olfactory groove meningioma - central hemianopic
scotoma; unilateral blindness
– Tuberculum sellae meningioma - junctional scotoma;
unilateral blindness or central scotoma with contralateral
peripheral field defect
– Frontal lobe meningioma - bitemporal hemianopia
– Sphenoidal ridge meningioma - bitemporal hemianopia with
sloping edges
• Medial - compresses optic nerve early
• Lateral - compresses optic nerve late
• CT scan shows - fullness in temporal fossa due to
hyperostosis
IN POST-CHIASMAL LESIONS
1. 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
2. LATERAL GENICULATE BODY
Crossed fibers end in 1, 4, 6 layers
Uncrossed fibers end in 2, 3, 5 layers
– In occlusion of anterior choroidal artery - upper & lower
quadrants are lost but the central visual field is spared
– In occlusion of lateral choroidal artery - central field
is lost but upper & lower quadrants are spared
3. 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] response - decreased amplitude
& frequency
– Extinction phenomenon - patient 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
4. VISUAL CORTEX
Dorsal part - receives fibers from upper half of retina
Lower part - from lower half of retina
Tip of posterior pole - receives macular fibers
– Congruous homonymous hemianopia with macular
sparing because of bilateral representation &
overlapping blood supply of posterior & middle cerebral
artery
– Visual hallucinations - scintillating 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 & 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 atrophy - primary lesion in the retina, optic
nerve or choroid, e.g. Retinitis pigmentosa, CRAO,
glaucoma, trauma
2. Descending optic atrophy - primary lesion in brain or optic
nerve; proceeds towards eye, e.g. Retrobulbar neuritis,
papilloedema
3. Inherited - congenital, juvenile, Leber’s hereditary optic
neuropathy, Behr’s optic atrophy & Friedreich’s ataxia
OPHTHALMOSCOPIC CLASSIFICATION
1. Primary -
– chalky white optic disc with well defined margins
– retinal blood vessels, periphery & surrounding retina
are normal
– lamina cribrosa well seen
– e.g. retrobulbar neuritis, pituitary tumor, optic nerve
trauma
2. Secondary -
– grey optic disc with poorly defined margins
– physiological cup obliterated
– peripapillary sheathing of blood vessels
– narrow arteries; tortuous veins
– e.g. papillitis, papilloedema
3. Consecutive -
– waxy pallor of optic disc with normal margins
– marked attenuation of arteries; normal cup
– associated retinal pathology
– e.g. retinitis pigmentosa, myopia, choroiditis, CRAO
4. Glaucomatous -
– vertical cup enlargement
– notching & pallor of neuroretinal rim
– laminar dot sign
– bayoneting & nasalization of blood vessels
– peripapillary atrophy
– splinter hemorrhages at disc margin
– Nerve fiber layer defects
5. Segmental or partial -
– temporal pallor e.g. toxic amblyopia
– altitudinal pallor e.g. AION
– wedge shaped pallor e.g. BRAO
ETIOLOGICAL CLASSIFICATION
1. Consecutive -
– post-inflammatory e.g. chorioretinitis
– degenerative e.g. retinitis pigmentosa, myopia
– extensive PRPC
– longstanding retinal detachment
2. Circulatory -
– CRAO, post-hemorrhagic, giant cell arteritis
– arteriosclerosis, carotid artery disease
3. Pressure & traction -
– glaucoma, papilloedema, tumors
– aneurysm of internal carotid artery, basal arachnoiditis
4. Inflammation-
– optic neuritis, intraocular infection, TB, septicemia
5. Toxic-
– tobacco, alcohol, lead, arsenic
– ethambutol, isoniazid, sulfonamide, chloroquine
6. Metabolic-
– diabetes mellitus, thyroid disorder
– cystic fibrosis, nutritional
7. Traumatic optic neuropathy
8. Hereditary -
– Leber’s Hereditary Optic Neuropathy
– Behr’s optic neuropathy
• Band/Bowtie atrophy: pallor only on nasal & temporal
part of optic disc — seen 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 [AION]

– Partial or total infarction of the optic nerve head caused
by occlusion of short posterior ciliary arteries
– Post-laminar 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 syndrome - post AION pallor in
one eye with AION in the fellow eye
– AION never recurs in the same eye
– Optic neuritis
– Compressive or infiltrative optic neuropathy
– Diabetic papillopathy
– Optic disc vasculitis
– Normo-tensive glaucoma
– Papillophlebitis
– PION (posterior ischemic optic neuropathy)
• occlusion of the small pial vessels which supply the
intra-orbital part of the optic nerve
• causes are - acute systemic hypotension, anemia,
vasculitis
• present with acute, severe visual loss
• RAPD; initially normal appearing fundus
ARTERITIC NON-ARTERITIC
F>M F=M
> 60 years 40-60 years
Severe visual loss Moderate visual loss
Vision <6/60 Vision >6/60
Pain may be present Painless
Prior amaurosis episodes Rare
Fellow eye affected in Fellow eye affected in
95%, in days < 30%, in months - years
Optic disc pallor > hyperemia Optic disc hyperemia > pallor
ESR > 40 mm/h ESR 20-40 mm/h
Temporal artery biopsy- giant
cell granulomatous vasculitis —
FFA- optic disc & choroidal FFA- optic disc filling delay
filling delay (choroidal
hypoperfusion)
Associated with Associated with
- Headache - diabetes mellitus
- Scalp tenderness - hypertension
- Palpable, tender, - hemorrhagic shock
non-pulsatile - nocturnal hypotension
temporal artery
- Proximal muscle &
joint aches
- Jaw claudication
- Cranial nerve palsies
Treatment - 1 gm/d i.v methyl Control hypertension
prednisolone X 3 days with & diabetes
oral prednisolone 1 mg/kg/day
× 1 week, tapering to
5 mg/ day; Maintenance dose
5-15 mg/day × 6- 12 months
PAPILLOEDEMA
– 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
& cause an inflammatory response & edema
– Inflammation causes vasomotor instability which 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 & 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 & vomiting
– Transient attacks of blurred vision
– Enlarged blind spot; progressive contraction of visual fields
– Results in optic atrophy ensues
CLASSIFICATION
1. Early papilloedema
– Optic disc hyperemia; splinter hemorrhages
– Blurring of nasal margin followed by superior, inferior
& temporal margins of disc
– Dilated & tortuous vessels
– Absence of spontaneous venous pulsation (if ICT
> 200 mm water)
2. Established papilloedema
– Disc hyperemia; blurring of disc margins
– Dilated tortuous vessels; optic cup obscured
– Microaneurysms & cotton wool spots
– Circumferential retinal folds - Paton’s lines
– Macular star - hard exudates in macula
– Capillary dilatation on optic disc surface
– Intraretinal/subhyaloid/vitreous hemorrhage
3. Chronic papilloedema
– Long standing or vintage papilloedema
– Optic disc elevated - champagne cork appearance
– No cotton wool spots or hemorrhages
– Optociliary shunts because of chronic obstruction of
venous drainage through central retinal vein
– Corpora amylacea - Drusen-like crystalline deposits on
optic disc surface
4. End stage papilloedema
– 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 & cerebellum
→ increased secretion of CSF
– Benign intracranial hypertension - in pseudotumor cerebri,
obese females, 30-40 yr age group; on oral contraceptives/
oral tetracyclines
– Malignant hypertension
– Meningitis, encephalitis → diffuse cerebral edema &
aqueductal stenosis
– Cerebral abscess, subarachnoid hemorrhage, aneurysm,
hydrocephalus
– Pseudoneuritis
• in hypermetropes - reflexes 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
• bilateral, inherited
• no leakage on FFA
– AION
– Compressive thyroid optic neuropathy
– CRVO
– Carotico-cavernous fistula
FFA
– Dilatation of surface capillaries
– Leakage of dye
– Vertical oval pool surrounding the optic disc
TREATMENT
– Relieve the cause of raised ICT
– Timely decompression - removal of tumor
– Watch the visual fields
– Immediate medical treatment - steroids, diuretics, oral
acetazolamide, i.v mannitol (decreases cerebral edema but
increases the chance of uncal herniation) - hence careful
monitoring required
– In benign intracranial hypertension - lateral orbitotomy &
optic nerve sheath decompression
Papilloedema takes 4-6 weeks to appear & 4-6 weeks
to resolve when treated.
UNILATERAL OPTIC DISC SWELLING

Occurs in -
– Papillitis
– AION
– Optic nerve head drusen
– Ocular hypotony
– CRVO
– Thyroid related optic neuropathy
– Pseudotumor
– Posterior scleritis
– Orbital cellulitis
– Retrobulbar hemorrhage
OPTIC NEURITIS
– Inflammation of optic nerve due to demyelinating disease
or spread of infection from orbit or paranasal sinuses
PATHOLOGY
– Perineuritis - due to spread of inflammation from brain/
orbit/sinuses; affects extra-macular fibers
– Axial neuritis - affects macular fibers - occurs in multiple
sclerosis, toxic/nutritional neuropathy
– Transverse neuritis - affects all fibers
CLINICAL FEATURES
– Common in females, 20-40 years of age, mostly idiopathic
– Decreased vision; usually unilateral (can be bilateral in kids
& pregnancy)
– Pain -
• precedes & accompanies visual loss;
• on superior & medial movements, due to traction of
superior & medial recti origins on the optic nerve sheath
at orbital apex
– Blurred vision after exertion - Uhtoff’s phenomenon
– RAPD; red-green color deficiency
– Central/centro-cecal scotoma
– Vision recovery in 2-12 weeks
– Retrobulbar neuritis - optic disc & nerve fiber layer
appear normal
– Papillitis - optic disc swelling, hyperemia, venous
engorgement
– Neuroretinitis - optic disc swelling, macular star.
INVESTIGATIONS
– Decreased contrast sensitivity
– VEP - increased latency, decreased amplitude
– Pupillary light reflex latency - prolonged
– Foveal critical flicker frequency - impaired
ETIOLOGY INVESTIGATION PRESENT WITH

Multiple sclerosis MRI Weakness, ataxia
Viral —mumps, measles WBC Recent illness
TB Chest X-ray, Fever, weight loss,
Mantoux night sweats
Sarcoidosis ACE levels Cough, breathlessness
Toxoplasma TORCH titers H/O contact with cats
Connective tissue ANA Fever, rash, joint pains
disorder
HIV ELISA, PCR Blood transfusion, H/O
exposure
Sinusitis X-ray PNS Headache, cold
CMV ELISA, PCR Organ transplant, HIV
Orbital infection CT scan Periorbital edema,
redness
Behcet’s syndrome HLA typing Oro-genital ulcers
– Papilloedema - bilateral; due to raised ICT; no fall of vision;
normal pupils
– AION - pale disc edema; altitudinal field defect
– Toxic/nutritional amblyopia - bilateral; temporal
– Malingering — pupils normal
– Hypermetropia - bilateral; pupils normal
– LHON-bilateral
– Acute congestive glaucoma - high IOP
TREATMENT
– Treat the cause; treat any infection
– If vision > 6/12 - observe
– I.V methyl prednisolone 1 gm daily X 3 days with 1 mg/
kg/day oral prednisolone; oral steroids should be
continued for 11 days & then rapidly tapered over the next
3 days.
PSEUDOTUMOR CEREBRI
– usually in young obese females, 20-45 years of age
– headache, nausea & vomiting
– no altered consciousness or higher cognitive function
– tinnitus, ocular pain
– transient visual obscurations
– intermittent horizontal diplopia - worsens 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
– Paton’s lines - circumferential retinal folds
– Eventually - optic atrophy occurs
VISUAL FIELDS
– enlarged blind spot, inferior nasal defect, arcuate defect
– generalized constriction, centrocecal scotoma
FOUR CRITERIA
1. Raised ICT - confirmed on lumbar puncture
2. Normal cerebral anatomy
3. Normal CSF analysis
4. Signs & symptoms of raised ICT e.g. papilloedema
THIRD NERVE PALSY

CAUSES
1. VASCULAR
– small blood vessels - DM, HTN, collagen vascular disease
– medium blood vessels - giant cell arteritis, polyarteritis
nodosa, vasospasm
– Large blood vessels - atherosclerosis, aneurysm, AV
malformations
2. INFLAMMATORY
– Post viral infections, sarcoidosis
– Demyelinating diseases, autoimmune disorders
3. NEOPLASTIC
– Meningioma, nasopharyngeal carcinoma
– Pituitary adenoma, craniopharyngioma
– Metastasis
4. CONGENITAL
– Hereditary; developmental anomaly
5. TRAUMATIC
6. UNKNOWN (40%)
CLINICAL FEATURES
– Eyes are divergent & 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)
– Parinaud’s syndrome - vertical gaze palsy
INVESTIGATIONS
(similar for III, IV, & VI n palsies)
– FBS, PLBS - diabetes mellitus
– BP – hypertension
– Angiography - posterior communicating artery aneurysm
– CSF analysis - multiple sclerosis
– CT scan, MRI brain - multiple sclerosis, tumor, trauma
– ESR - GCA (giant cell arteritis)
– Tensilon test - myasthenia gravis
– Thyroid function tests - thyroid 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 & 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 subnucleus - bilateral ptosis occurs
– SR subnucleus - only contralateral superior rectus is affected
– IR, MR, IO subnuclei — only ipsilateral inferior rectus,
inferior oblique & medial rectus affected
– Paired MR subnuclei → wall-eyed bilateral internuclear
ophthalmoplegia [WEBINO] → exotropia, defective
convergence & adduction
• LPS – levator palpebrae superioris
• SR, IR, MR – superior rectus, inferior rectus, medial
rectus
• IO – inferior oblique
Fasciculus - as fibers pass through

– Red nucleus - BENEDIKT’S SYNDROME → ipsilateral
IIIn + contralateral extrapyramidal signs
– Cerebral peduncle - WEBER’S SYNDROME →
ipsilateral IIIn + contralateral hemiparesis
– Superior cerebellar peduncle - NOTHNAGEL
SYNDROME → ipsilateral IIIn + cerebellar ataxia
– CLAUDE SYNDROME → Benedict + Nothnagel
syndrome
Basilar part - [isolated IIIn palsies common]
– Acute painful III n palsy with pupillary involvement - in
aneurysm of posterior communicating artery
– Head trauma → irritative miosis followed by mydriasis &
total IIIn palsy [Hutchinson’s pupil]
Intracavernous part - [associated with IVn, 1st & 2nd
branches of VnJ]
– Causes: diabetes, pituitary apoplexy, caroticocavernous
fistula, Tolosa Hunt syndrome, aneurysm/meningioma in
cavernous sinus
Intraorbital part -
– Superior division - SR & LPS affected
– Inferior division - IR, IO, MR & pupil involved
MANAGEMENT
– Treat the cause
– Commonest cause is vascular [mainly diabetes]
• Observation; strict control of diabetes
• Diplopia is managed with unilateral occlusion
– Trauma - wait 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 positive - greater vertical
deviation with head tilted toward the side of the paretic muscle
– In bilateral superior oblique palsies — positive Bielschowsky
with head tilt in both directions; torsion of images
– Vertical diplopia - difficulty in walking downstairs
– Hypertropia (near > distance), esotropia, face turn to
opposite side, chin depression
– Uncrossed diplopia - maximum 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 in - head trauma, diabetes, herpes zoster
ophthalmicus
MANAGEMENT
– Treat the cause
– Surgery:
a. If vertical deviation is more → Inferior oblique recession
b. If torsional component is more → Harada Ito
procedure [anterior half of superior oblique tendon
is advanced & re-inserted 8 mm behind & 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 Localizing causes
- Raised ICT - Pontine syndromes
- Head trauma - CPA lesions - acoustic neuroma
- Hypertension, DM - Clivus lesions-
- Para-infectious (viral) nasopharyngeal carcinoma
- Basal meningitis - Middle cranial fossa lesions
- Idiopathic - Cavernous sinus thrombosis
- Multiple sclerosis - Superior oblique fissure
- Lumbar puncture syndrome
- Carotico-cavernous fistula
– Raised ICT may damage VI n → false localizing sign

– Septic thrombosis of inferior petrosal sinus → VI n & VII
n palsy
– Base of skull fracture - unilateral /bilateral VI n palsy.
CLINICAL FEATURES
– Esotropia (distance > near); abduction restriction
– Compensatory face turn to affected side
– Muscle sequel - contracture of ipsilateral medial rectus
– Uncrossed diplopia - increased separation towards
affected side
– TRO (thyroid related orbitopathy) - fibrotic medial rectus
– Orbital trauma - medial rectus entrapment
– Congenital defects - Duane’s & Mobius syndrome
– Convergence spasm
– Infantile esotropia
LOCALIZE THE LESION

Nucleus
– Ipsilateral VIn palsy
– Ipsilateral LMN type of Vlln palsy
– Failure of horizontal gaze towards the side of the lesion
Fasciculus - as the fibers pass through
– PPRF – FOVILLE SYNDROME → Ipsilateral V, VI, VII,
VIII n palsy + central Horner syndrome
– Pyramidal tract – MILLARD GUBLER SYNDROME
→ ipsilateral VI n + contralateral hemiplegia
Basilar part
– Acoustic neuroma → VI n palsy + hearing loss + decreased
corneal sensation
– Nasopharyngeal tumors
– Raised ICT - may cause bilateral VI n palsies
– Basal skull fracture
– Gradenigo syndrome → VI, VII, Vin 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 part - supplies the lateral rectus
TREATMENT
– If all tests are normal - observe for 6 months - then correct
surgically
– If pain persists - trial of steroids: 60 mg oral prednisone
× 5 days (If dramatic improvement - could be Tolosa-Hunt
syndrome)
– Surgery
a. With full muscle sequelae → ipsilateral LR resection
+ ipsilateral MR recession
b. 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 ophthalmoplegia - partial/total - involving III, IV,
V (partial), VI n
– Steady boring pain in & around the eye
– Dramatic response to steroids; spontaneous remissions
– Sensory defects in the distribution of ophthalmic branch
of V n
– Pupil may be - normal; dilated & fixed; small; partially
dilated & sluggish
INVESTIGATIONS
CT scan, MRI, arteriography - look for involvement of structures
outside the cavernous sinus.
TREATMENT
Oral prednisolone 1 mg/kg wt daily - gradually taper off
depending on improvement.
OCULAR MYASTHENIA
– Chronic neuromuscular disorder characterized by weakness
& 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
– CPEO
– Pharmacologic myasthenic syndrome
– Orbital apex syndrome, superior orbital fissure syndrome
– IIIn palsy, internal carotid artery aneurysm
CLINICAL FEATURES
1. Ptosis
– unilateral or bilateral
– worsens with fatigue at the end of the day & in sunlight
– Lid fatigue test - worsens on prolonged up gaze
– See saw ptosis - if one upper lid is manually elevated,
the other becomes more ptotic
– Lid hopping - fluttering of a ptotic lid
– Cogan lid twitch - if the eyes are rapidly returned from
down gaze to primary gaze, the upper lid elevates
excessively - then droops/twitches many tunes before
returning to fixed position
– Contralateral upper lid retraction
2. Ophthalmoparesis - causes diplopia
– Can mimic any of the isolated nerve palsies, gaze palsy,
chonic progressive external ophthalmoplegia [CPEO]
3. Saccadic eye movements -
– Small dart-like movements
4. Dissociated nystagmus
5. Epiphora - due to inadequate blink
6. Peek sign - due to orbicularis fatigue
– During gentle eyelid closure eyes gradually open
spontaneously
7. Ectropion - due to fatigue
8. Bell’s phenomenon - decreased or absent (upward &
outward rolling of eyes on forced eyelid closure against
resistance)
9. Pupil fatigue - sluggish responses, anisocoria
INVESTIGATIONS
a. Tensilon test -
– Edrophonium inhibits acetyl cholinesterase - increases
availability of acetylcholine [Ach]
– Dose: 0.15 mg/kg; up to 10 mg

– After administering atropine, 1-2 mg of edrophonium
is injected i.v; look for a positive response
– If no adverse reaction occurs after one minute, slowly
inject 8-9 mg & watch for improvement of ptosis &
extraocular muscle movement within 1 min.
– If improvement is seen, record as positive
b. 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 i.m into the deltoid
– Dose: 0.04 mg/kg in kids
– Peak effect in 30 min.
– Contraindicated in bronchial asthma, cardiac
arrhythmias
c. Sleep test -
– Close eyes & rest for 30 min - ptosis improves
d. Ice pack test - improves ptosis
e. Curare test -
– < 1/10 of d-curarine dose causes paralysis
f. Electrophysiological tests -
– Repetitive supramaximal motor nerve stimulation
– Single-fiber EMG
g. Ach receptor antibody assay
h. Muscle biopsy - quantification of Ach receptors; deposition
of immune complexes at motor end plate
i. CT scan/MRI - to rule out thymoma
MANAGEMENT
1. SYMPTOMATIC TREATMENT
– Acetyl cholinesterase inhibitors: pyridoxine 60 mg BD,
neostigmine 15 mg BD
– Crutch glasses
2. IMMUNOTHERAPIES
– Steroids - 60 mg prednisolone (1 mg/kg wt); then taper
– Cytotoxic therapy - azathioprine 3-5 mg/kg wt
– Plasmapheresis - repeated exchanges over a short period
of time
– i.v immunoglobulin - human gamma globulin 0.4 gm/
kg for 3 days
3. SURGERY
– Thymectomy
• pre-operative plasma exchange
• post-operative anticholinesterase drugs & immuno-
suppressives
HORIZONTAL GAZE PALSIES

INTERNUCLEAR OPHTHALMOPLEGIA (INO)
– Lesion in MLF (medial longitudinal fasciculus)
– Causes: demyelination, trauma, encephalitis, brain stem
tumors, vascular disease, drug-induced
In left INO
– On right gaze there is defective left adduction & ataxic
nystagmus of right eye
– Left gaze is normal
– Convergence is intact
– Vertical nystagmus on attempted up gaze
Investigations:
– FBS, CBP, FTA-ABS, VDRL, Lyme titer, toxicology screen,
MRI
Differential diagnosis:
In multiple sclerosis, bilateral INO can develop
ONE AND A HALF SYNDROME

– Combined lesion of MLF & PPRF on the same side
– Ipsilateral gaze palsy
– Only movement which remains is abduction of the
contralateral eye, with ataxic nystagmus
CHAPTER 7
Lens
SENILE CATARACT
– Cataract: opacification of the crystalline lens
Morphological classification
1. SUBCAPSULAR CATARACT:
– Posterior subcapsular cataract is graded from 10 - 100%
depending on the amount of opacification
– Anterior subcapsular – in
• Atopic dermatitis
• Glaucomflecken following an acute congestive
attack in PACG
2. NUCLEAR CATARACT: grading
I. definite yellowing; vision 20/25 to 20/30
II. yellow ++; vision 20/40
III. yellow/orange; vision 20/60
IV. brown/brunescent; vision <20/80
3. CHRISTMAS TREE CATARACT:
• Needle like deposits
4. CORTICAL CATARACT: grading
I. Cortical cataract with spokes involving one quadrant
of the lens
II. Involving two quadrants

LENS 227
III. Involving three quadrants
IV. Involving four quadrants
Classification according to maturity:

– Immature senile cataract - partially opaque lens
– Mature senile cataract
– Hyper mature senile cataract - Shrunken, wrinkled
anterior capsule due to leakage of water
– Morgagnian senile cataract - total 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
– Poly chromatic luster at posterior pole of lens
– Progresses rapidly if posterior synechiae present
2. Acute congestive glaucoma
– Glaucomflecken - small grey-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
– Leber’s congenital amaurosis
– Gyrate atrophy.
– Stickler syndrome
5. Fuch’s heterochromic iridocyclitis
– Cortical white cataract
LENS 229
AFTER CATARACT (PCO)

– Posterior capsular opacification
– Occurs after extra-capsular cataract extraction
– Decreased visual acuity & contrast sensitivity
– Glare; monocular diplopia
– Can decrease incidence of PCO with acrylic IOL & square
edge design of IOL.
CLINICAL FEATURES
– Elschnig pearls (Bladder/Wedl cells)
• Proliferation & migration of residual equatorial epithelial
cells along the posterior capsule at the site of apposition
between remnants of anterior & 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
4-6 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 endophthalmitis – release of sequestered organism
into vitreous [Propionibacterium acnes]
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 & cortex
– Radial extensions or riders are seen
3. Sutural
– ‘Y’ shaped
– Anterior/posterior
4. Polar cataract
– Anterior polar - pyramidal; associated with anterior
lenticonus, persistent pupillary membrane, Peter’s
anomaly, aniridia
– Posterior polar - associated with PHPV, posterior
lenticonus
LENS 231
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 lentis - bilateral, superio-temporal
dislocation
• Ectopia lentis et pupillae - bilateral; displacement of
pupil & lens in opposite directions
• Aniridia
• Marian’s - bilateral, supero-temporal dislocation; zonules
intact, accommodation retained
• Weil-Marchesani - bilateral inferior dislocation
• Homocystinuria - infero-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 eye - in high myopia, buphthalmos
• Anterior uveal tumors
• Hypermature cataract
CLINICAL FEATURES
– Extreme myopic/hyperopic shift, astigmatism, acquired
aphakia
– Vision may fluctuate dramatically - between phakic &
aphakic vision
– Monocular diplopia
– Lens blocks pupil → secondary angle closure
– Phacodonesis, iridodonesis
TREATMENT
– Glasses (aphakic correction)
– Surgery - when there is cataract, glaucoma, lens can touch
endothelium, uveitis
WEIL-MARCHESANI SYNDROME
– Short stature, brachydactyly, stiff joints, mental retardation
– Ectopia lentis - bilateral, inferior
– Microspherophakia - secondary angle closure glaucoma with
pupillary block
– Nanophthalmos, asymmetrical axial lengths
– Pre-senile vitreous liquefaction
MARFAN SYNDROME
Ophthalmic features:
– Ectopia lentis - bilateral, accommodation retained [unlike
in homocystinuria]
– Microspherophakia - lens may dislocate into anterior
chamber or vitreous; subluxated lens may cause glaucoma
– Angle can show dense iris processes, thickened trabecular
sheets; may cause glaucoma
– RD - associated with lattice degeneration, high myopia
– Flat cornea, blue sclera, squint, hypoplasia of dilator
papillae, peripheral iris transillumination
LENS 233
Systemic features:
– Tall, thin stature, scoliosis, sternum deformity
– Arm span > height
– Arachnodactyly [long, spider-like fingers], mild joint
hypermobility
– Narrow, high arched palate
– Muscular underdevelopment - predisposition to hernias
– Dilatation of ascending aorta → aortic incompetence &
heart failure
– Mitral valve disease, aortic dissection
– Striae, fragility & easy braising of the skin
POST-OP DECREASED VISION
CAUSES
– Corneal edema due to rise in IOP, descemet’s tear
– Striate keratopathy - due to instrument touch during surgery;
more in Fuch’s endothelial dystrophy
– Posterior capsular opacification
– Malposition of IOL
– Iris prolapse - increased astigmatism, chronic uveitis
– Anterior capsular fibrosis (contraction of capsulorhexis-
called capsular phimosis)
– RD – if lattice degeneration, myopia, PC rent, vitreous loss,
vitreous incarceration in wound
– Endophthalmitis
LENS 235
IOL MALPOSITION
– Depends on haptic position & asymmetric bag-sulcus
placement of IOL during surgery
– Fluctuating vision, monocular diplopia, glare, halos,
photosensitivity, optical aberrations
– May cause - aphakia
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
EAST-WEST SYNDROME
[HORIZONTAL DECENTERATION]
CAUSES OF IOL MALPOSITION

– Intra-operative
– Post-operative -
• External force - trauma, rubbing
• Internal force - scarring, 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 IOL - replace with a secondary AC IOL
– Iris/trans-scleral sutures — required to secure IOL in position
– Scleral fixation of lens - iris fixated or clipped IOL
AC IOL decentration can lead to:
– Iris tuck - uveal inflammation, red & tender eye
– Peaked/oval pupil
– If IOL is small - lens is mobile & can cause endothelial
cell loss, CME, glaucoma
Capsular contraction syndrome may be due to:
– Very small capsulorhexis
– Silicon plate IOL design
ANTI-CATARACT DRUGS [tried are]

– Aldose reductase inhibitors
– Pantethine
– Aspirin-like drugs - ibuprofen
– Estrogen replacement therapy
– Naproxen, sulindac - most potent drugs
LENS 237
INTRAOCULAR LENSES
– Made up of optic (central refracting element) + haptics
(sit in contact with ocular structures -capsular bag/ sulcus/
angle of anterior chamber)
– Ideal location - in the bag
DESIGNS
5 generations
• Original Ridley PC lens
• Early AC lens
• Iris support lenses
• Modern AC lens
• Modern PC lens
TYPES OF IOLs
– Rigid lOLs - made entirely from PMMA
– FoldablelOLs:
• Silicone - lower rate of PCO; not preferred for diabetics
• Acrylic
a. hydrophobic - water content < 1%
b. hydrophilic - water content 18 to 35%
• Hydrogel - similar to hydrophilic
• Collamer - mixture of collagen & hydrogel
– Multifocal lOLs
– Accommodative lOLs
CATARACT SURGERY
INDICATIONS
– Visual improvement
– Fundus examination
– Phacolytic/phacomorphic glaucoma
– Cosmetic
PRE-OP EVALUATION
– Vision, cover test
– Pupils - rule out RAPD
– Adnexa - dacryocystitis, blepharitis, conjunctivitis,
lagophthalmos, ectropion, entropion, tear film abnormalities
– Cornea - Fuch’s endothelial dystrophy
– AC - shallow; cells, PAS
– Pseudoexfoliation
– Type of cataract; subluxation; zonular dialysis
– IOP, syringing
– Fundus - indirect ophthalmoscopy, B scan
– A scan, K readings
SURGERIES
– ICCE, ECCE with IOL, SICS with IOL, Phacoemulsification
with IOL placement; under topical/local/general anesthesia.
SURGICAL COMPLICATIONS
Intra-operative Post-operative
1. PC rupture 1. Posterior capsular
opacification
2. Vitreous loss 2. Capsular phimosis
3. Nucleus drop posteriorly 3. Corneal edema
4. IOL drop 4. Bullous keratopathy
5. Expulsive hemorrhage 5. Corneal decompensation
6. Suprachoroidal hemorrhage 6. Secondary glaucoma
7. Iris prolapse 7. IOL malpositioning
8. Descemet’s tear 8. Retinal detachment
9. Zonular dialysis 9. Cystoid macular edema
10. Endophthalmitis
LENS 239
NEEDLES
– Good needle - strong; sharp cutting edge; atraumatic; long

enough to be passed through the wound & retrieved.
1. Round bodied needle
– Sharp point & round shaft
– To suture conjunctiva where watertight wound is required
– Needle track - same diameter as suture
– Decreased tendency for micro-leaks from suture track
e.g. in glaucoma surgeries
2. Conventional cutting needle
– Sharp point & sharp edge along the inside of the shaft
– Minimal damage to deep structures while cutting full
thickness scleral & corneal tissue
3. Reverse cutting needle
– Sharp point with sharp edge on outside of the shaft
– Resist cutting out e.g. skin sutures
4. Spatulated needle
– Sharp cutting point with a flat shaft with side cutting
– For suturing within a structure like cornea, sclera, tarsus
– Strabismus & RD surgery
SUTURES
– Good suture - strong, easy handling; minimum tissue

reaction; can be buried
ABSORBABLE NON-ABSORBABLE
1. Catgut 1. Twisted virgin silk
2. Chromic gut 2. Braided silk [for skin
3. Vicryl [subcutaneous & traction sutures]
& deep closure] 3. Nylon [for corneal wound]
4. Vicryl rapide 4. Nurolon [braided nylon]
5. PDS H [synthetic 5. Prolene [IOL fixation, iris repair]
monofilament] 6. Polyester [retinal surgery]
LENS 241
IOL 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
– Post-op 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 X Refractive
error)
Based on measurements:
1. THEORETICAL FORMULA
n
____________
n × K
__________________
P = –
L – ACD n – K × ACD
n = refractive index far aqueous & vitreous
L = axial length (mm)
ACD = estimated post-op AC depth(mm)
K = corneal curvature (diopters)
2. REGRESSION FORMULA
– SRK formula - Sanders, 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= post-op refraction needed
RF= refraction factor
* In high hypermetropes with axial length < 22 mm,
Brinkhorst or HofferQ formulae are used
* In high myopes with axial length > 26 mm, SRK-T
formula is used
CHAPTER 8
Uvea
UVEITIS
GRANULOMATOUS NON-GRANULOMATOUS
1. Large, greasy, mutton fat KPs 1. Fine KPs
2. Iris nodules 2. Absent
3. Associated with systemic disease 3. Idiopathic
4. Type IV hypersensitivity 4. Allergic/exudative rxn
5. Insiduous onset, chronic 5. Acute onset
6. Dense nodular tissue infiltration 6. Diffuse exudative
phenomenon
ETIOLOGICAL CLASSIFICATION
Inflammatory
– Exogenous – corneal ulcer, penetrating wound
– Endogenous – TB, syphilis, virus, Toxoplasma
– Infection from ocular tissues
– Immune mediated -
• SLE, rheumatoid arthritis, ankylosing spondylitis,
juvenile rheumatoid arthritis, Behcet’s disease
Neoplastic
– Retinoblastoma
– Iris melanoma
– Leukemia
– Reticulum cell sarcoma
– Histiocytic cell sarcoma
Traumatic
– Blunt trauma
– Penetrating trauma
– Surgery
UVEA 245
INVESTIGATIONS FOR UVEITIS

LAB TESTS
SKIN TESTS
1. Mantoux TB
2. Kveim Sarcoidosis
3. Lepromin Leprosy
4. Casoni’s test Hydatid cyst
5. Pathergy test Behcet’s disease
SEROLOGICAL TESTS
l. ANA SLE, dermatomyositis, JRA,
scleroderma, lymphoma, Sjogren’s
syndrome, chronic hepatitis
2. Serum ACE levels Active systemic Sarcoidosis, leprosy,
TB, histoplasmosis
3. HLA antigens B27 - ankylosing spondylitis, Reiter’s
B5- Behcet’s
DR4 - VKH syndrome
A29 - Birdshot chorioretinopathy
4. Rheumatoid factor Rheumatoid arthritis
5. ELISA Toxoplasmosis, toxocariasis, HSV,
CMV, HIV
6. TORCH liters Toxoplasmosis, rubella, CMV
7. ANCA Wegener’s granulomatosis
8. FTA ABS/VDRL Syphilis
9. Hb%, CT/BT, Non-specific
RBS, Serum calcium
HISTO-PATHOLOGY
1. Anterior chamber - microscopy - look for organisms
paracentesis - ACE levels
- LDH levels in retinoblastoma
- immunological tests
- PCR
2. Vitreous tap/biopsy Endophthalmitis
3. Chorio-retinal biopsy B/L acute retinal necrosis
NON-LABORATORY TESTS
X-ray chest TB, Sarcoidosis
X-ray sacro-iliac joint Ankylosing spondylitis
Iris angiography Fuch’suveitis
FFA VKH syndrome, APMPPE, birdshot
chorioretinopathy
B scan, UBM VKH syndrome, toxocariasis
Gallium scan Active sarcoidosis
Lumbar puncture Syphilis, reticulum cell sarcoma
AQUEOUS FLARE
Tyndall Effect
Due to scattering of light by proteins that have leaked into
aqueous humor from damaged iris blood vessels
+1 : Faint; just detectable
+2 : Moderate; iris details clear
+3 : Marked; iris details hazy
+4 : Intense; fibrous exudates
KERATIC PRECIPITATES
– Cellular deposits on endothelium - usually occur in mid
& inferior zones due to convection currents in the anterior
chamber
– Small KPs throughout endothelium - in Fuch’s uveitis
– Endothelial dusting - in acute uveitis
– Medium sized - in acute & chronic uveitis
– Large, mutton-fat, greasy, waxy KPs in - granulomatous
uveitis
– Old KPs - pigmented/ground glass (hyalinized)
UVEA 247
HYPOPYON
– Caused by corneal infection - Bacteria, virus, fungi
– Caused by intraocular inflammation - Behcet’s disease,
HSV, HZV, endophthalmitis, toxoplasmosis, toxocariasis
PSEUDOHYPOPYON
– Tumors—retinoblastoma, malignant melanoma, leukemia,
reticulum cell sarcoma
– Synchisis scintillans in aphakic eyes
– Ghost cell glaucoma
– IOFB
– Phacolytic glaucoma
OCULAR TOXOPLASMOSIS
– Toxoplasma gondii is a protozoan parasite with affinity
towards nerve tissue; it multiplies in ganglion cells & nerve
fibers
– Affects macula - since it has the thickest NFL
CLINICAL FEATURES
– Decreased vision; floaters; metamorphopsia
1. Large destructive retinal lesions
– area of active retinitis > 1 DD
– dense yellowish-white area surrounded by a ring of
retinal edema
– adjacent to old intact pigmented lesion
– severe vitreitis
– Headlight in fog appearance
2. Punctate inner retinal lesions
– Single or multifocal grey areas of active retinitis in
periphery or macula
– Mild retinal edema
3. Punctate outer retinal lesions
– Multifocal grey-white punctate lesions at the level of
the RPE
– Tends to recur in a satellite fashion
– No vitreous reaction
4. Massive granuloma
– 5-6 DD with severe vitreitis
5. Papillitis [Jensen’s choroiditis]
– inflammation at or adjacent to optic disc
– severe vitreitis
– mild anterior chamber reaction
COMPLICATIONS
– chronic iridocyclitis, scleritis
– cataract, glaucoma
– band keratopathy
UVEA 249
– CNVM, CME, RD
– Optic atrophy, BRVO
TREATMENT
ANTIBIOTIC DOSAGE DURATION
Clindamycin 300 mg QID 3 wks
Cotrimoxazole 960 mg BD 4-6 wks
Atovaquone 750 mg TID
Azithromycin 500 mg OD 3 days
Sulphadiazine 2 gm [loading dose]; 3-4 wks
then Igm QID
Pyrimethamine 50 mg [loading dose]; 4 wks
then 25 mg OD
* Systemic steroids are given if severe vitreitis occurs or in

vision threatening lesions
* Sulphonamides are given with clindamycin to prevent
pseudomembranous colitis
TESTS FOR TOXOPLASMOSIS

Sabin Feldman dye test; Indirect hemagglutination test; ELISA;
Toxoplasma skin test; Aqueous humor antibodies; compliment
fixation test.
CONGENITAL TOXOPLASMOSIS
– Transplacental spread in the 3rd trimester
– Triad of: convulsions + cerebral calcification +
chorioretinitis
– Seizures, mental retardation, microcephaly, jaundice,
hydrocephalus
– Chorioretinal atrophy & scarring with pigmented borders
[punched out lesions in macula]
– Unilateral or bilateral
– D/D: macular coloboma, retinoblastoma foci, congenital
HSV, CMV 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 Lubricants
lacriinal gland]
Lepromatous pannus
Interstitial keratitis Steroids
Miliary lepromas [white punctate
sub-epithelial opacities near limbus]
LACREMAL SYSTEM
Acute dacryocystitis Antibiotics
Chronic dacryocystitis DCR/DCT
SCLERA
Episleritis Topical NSAIDs, steroids
Scleritis Steroids, NSAIDs
Scleral necrosis, staphyloma, ectasia
IRIS
Granulomatous uveitis Steroids, Cycloplegics
Iris pearls
Iris holes due to atrophy
Pin point pupil
Ciliary body atrophy
UVEA 251
– 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 & irritation
of the sphincter pupillae
– Iris pearls – chalky-white particles in superficial stroma of
iris, at the pupillary margin; noninflammatory
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 1-2 days]
Late reaction [read in 3-4 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 1-4 mg/kg/day for 6 months
EYE IN TUBERCULOSIS
CLINICAL FEATURES
LIDS - Ulceration of lid margin
- Lupus vulgaris
- Ectropion
CONJUNCTIVA - Parinaud oculoglandular syndrome
- Purulent conjunctivitis
- Pseudomembranous conjunctivitis
- Tuberculomas
CORNEA - Phlyctenular keratoconjunctivitis
- Fascicular keratitis
- Interstitial keratitis
- Suppurative keratitis
UVEA - Granulomatous anterior uveitis
- Conglomerate iris tubercles
- Choroidal granulomas
RETINA - Eales’ disease
- Retinal vasculitis - NVE. BRVO
SCLERA - Deep nodular scleritis
- Tongue-shaped recurrent sclerokeratitis
OPTIC NERVE - Optic neuritis
- Papilloedema
CRANIAL NERVES - Palsies
ORBIT - Orbital cellulitis/abscess
- Periostitis
- Osteomyelitis
- Chronic dacryocystitis
Parinaud oculoglandular syndrome — unilateral follicular

conjunctivitis with ipsilateral lymph node enlargement
TREATMENT
– Systemic disease is treated with antituberculous treatment
– Eye involvement is treated according to the tissues involved
with anti-inflammatory drugs
UVEA 253
EYE IN SYPHILIS
LIDS - Chalazion-like induration

- Madarosis
- Symblepharon
CORNEA - B/L interstitial keratitis
- Keratitis pustuliform profunda
- Keratitis punctata profunda
- Keratitis linearis nigrans
IRIS - Acute plastic iritis
- Gummatous iritis
CHORIORETINA - Diffuse chorioretinitis
- Jensen’s juxta-papillary choroiditis
- Foerster’s multifocal choroiditis
- Neuroretinitis
- Big blind spot syndrome
OPTIC NERVE - Optic neuritis
- Papilloedema
- Ascending/descending/gumma-induced
optic atrophy
PUPIL - Argyll Robertson pupil - light reflex lost;
accommodation reflex present
- Absolute fixed pupil - light & near reflex
lost
- Internal ophthalmoplegia - all reflexes lost
- Accommodation palsy alone
CRANIAL NERVES - IIIn, VIn palsies
- IV n also may be affected
ORBIT - Periostitis
- Proptosis [gumma in orbit]
Acute plastic iritis :

• Jarisch-Hexheimer reaction
• Multiple papules in pupillary region
• Roseolae - dilated iris capillaries
• Posterior synechiae; gumma at root of iris
• Secondary glaucoma, deep keratitis, scleritis
• Localized atrophy of iris stroma - heals
• Dust-like opacities in vitreous
Gummatous iritis:
• Gumma invades - sclera, angle, vitreous
– Foerster’s multifocal choroiditis: bilateral
• Ring scotomas
• Focal areas of chorioretinal atrophy with hyperpig-
mentation
• 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 puncture - to rule out neuro-syphilis
– 12 to 24 MU of aqueous Penicillin i.v daily for 10 days
followed by i.m 2.4 MU for 3 wks
– Oral tetracycline 500 mg qid or
Oral erythromycin 500 mg qid for 3 wks
UVEA 255
EYE IN AIDS
CLINICAL FEATURES
LID - Kaposi’s sarcoma
- Molluscum contagiosum
CONJUNCTIVA - Kaposi’s sarcoma, HSV, HZV, CMV,
squamous cell carcinoma
CORNEA - HSV keratitis - dendrites in peripheral cornea
- HZO, Candida albicans keratitis
- Microsporidial keratitis [bilateral chronic
diffuse punctate epithelial
keratoconjunctivitis]
UVEA - Bilateral anterior uveitis
- Choroiditis - Candida, Toxoplasma,
pneumocystis carinii
VITREOUS - Endophthalmitis
RETINA - Microangiopathy, vascular lesions, CMV
retinitis, ARN, PORN
OPTIC NERVE - Neuritis, optic atrophy
- Papilloedema
ORBIT - Burkitt’s lymphoma
- Kaposi’s sarcoma
- Pseudotumor
CRANIAL NERVES - Palsies
Treatment for Microsporidial Keratitis

– Topical fumagillin, oral albendazole, HAART therapy
SARCOIDOSIS
– Idiopathic multisystem disorder
– Characterized by the presence of non- caseating granulomas
Lungs
Stage I → bilateral hilar lymphadenopathy
Stage II → bilateral hilar lymphadenopathy +
reticulonodular parenchymal infiltrates
Stage III → only parenchymal infiltrates
Stage IV → fibrosis, bronchiectasis
Skin
– Erythema nodosum - tender; on shin
– Cutaneous granulomata - face, buttocks
– Purple lupus
Cranial Nerves
– VII nerve palsy
Eye
– Granulomas on conjunctiva, sclera
– Keratoconjunctivitis sicca - dry eye – due to lacrimal gland
infiltration
– Anterior uveitis - acute & chronic - mutton fat KPs, Busacca
& Koeppe nodules → complicated by glaucoma, cataract,
band keratopathy, peripheral anterior synechiae
– Diffuse vitreitis ; snow balls in inferior anterior vitreous
– Retinal periphlebitis - candle wax drippings → peri-venous
exudates
– BRVO; vascular sheathing; CME
– Retinal granulomas - white/yellow
UVEA 257
– Preretinal granulomata occur interiorly, anterior to equator

→ Lander’s sign
– Choroidal granuloma
– Optic disc - NVD , disc edema, granuloma [does not affect
vision], papilloedema
– Peripheral retinal neovascularization
– Acute sarcoid retinopathy = vitreitis + periphlebitis +
preretinal granulomata + retinal hemorrhages
INVESTIGATIONS
– Chest X-ray
– Biopsy of - lungs, conjunctiva, lacrimal glands
– Serum ACE levels [greater than 8.5 IU]
– Bronchioalveolar lavage - increased activated T-helper
lymphocytes
– Calcium assay - hypercalciuria
– Gallium - 67 scan - increased uptake
– Pulmonary function tests - reduced total lung capacity
– Skin biopsy
– Kviem test - intradermal test - localized granuloma develops.
TREATMENT
– Anterior segment inflammation: topical steroids, cycloplegics
– Posterior segment involvement: systemic steroids
IRIS NODULES
1. Granulomatous Iridocyclitis:
– Koeppe nodules - pupillary border
– Busacca nodules - periphery of iris
2. Juvenile xanthogranuloma:
– Yellow/gray poorly demarcated lesion in 1st year
3. Leiomyoma:
– Localized, diffuse/flat, pigmented
4. Malignant melanoma:
– Nodular/flat
– Inferiorly - sentinel 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 Hansen’s disease
8. Brushfeld spots:
– White to yellow spots — in iris periphery
– In Down’s syndrome
– Normal stroma surrounded by a ring of mild iris
hypoplasia
9. Metastasis:
– Gelatinous white nodules
10. Retinoblastoma:
– White foci on anterior iris surface
UVEA 259
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
PARS PLANITIS
– Ocular inflammation involving intermediate uvea, i.e. pars
plana ciliaris & peripheral retina
– 80% are bilateral
– Children & young adults are mainly affected
CAUSES
– Idiopathic, multiple sclerosis, sarcoidosis
– Lyme disease, inflammatory bowel disease
ETIO-PATHOGENESIS
– Primary peripheral retinal perivasculitis
– Primary vitreal inflammation
– Inflammatory stimulus → tissue reaction → fibroglial
proliferation
CLINICAL FEATURES
– Blurred vision, floaters
– Marked injection (check IOP)
– Decreased central vision due to cataract, CME, organized
vitreous hemorrhage, optic disc edema
– Decreased peripheral vision - glaucoma, RD
– Sarcoidosis, toxocariasis
– Idiopathic iridocyclitis, endophthalmitis
– Sympathetic ophthalmia
– Behcet’s disease, cat scratch disease, lyme disease
UVEA 261
SIGNS
CORNEA - KPs - fine, white
- Band keratopathy
ANTERIOR CHAMBER - Cells, flare - minimal
IRIS - Posterior synechiae , rubeosis
GLAUCOMA - Secondary angle closure [peripheral
anterior synechiae, iris bombe’]
- Steroid induced
- Inflammatory glaucoma
LENS - Anterior epithelial opacities
- Posteror subcapsular cataract
- Intumescent cataract
VITREOUS - Cells in anterior vitreous face
- Snow banking
- Opacities, hemorrhage
- PVD, cyclitic membrane
- Pre-retinal membranes
RETINA - CME; Peripheral vasculitis
- Telangiectasias
- Neovascularization
- Hemorrhage
- Retinal dialysis
- Tractional retinal detachment
- Bone spicule pigmentation
- Heteropia of macula
OPTIC NERVE - Disc edema; optic atrophy
- Neovascularization
TREATMENT
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]
– Cryotherapy - double freeze thaw to the area of snow bank
→ decreases peripheral exudation by eliminating peripheral
neovascularization
– Vitrectomy done if:
• persistent severe vitreal inflammation
• retinal detachment
• epiretinal membranes
• non-clearing vitreous hemorrhage
– Systemic antimetabolites - cyclophosphamide, chlorambucil
UVEA 263
VKH SYNDROME
– Vogt Koyanagi syndrome - poliosis, vitiligo, alopecia, chronic
anterior uveitis
– Harada disease - bilateral posterior uveitis with exudative
RD & CNS abnormalities (pleocytosis in CSF)
– Idiopathic multisystem disorder
CLINICAL FEATURES
1. Prodromal phase:
– Meningitis, headache, neck stiffness
– Tinnitus, vertigo, deafness
– Encephalopathy - convulsion, paresis, cranial nerve
palsies
2. Acute uveitic phase:
– Bilateral pan uveitis
– Bilateral granulomatous anterior uveitis
– Multifocal posterior uveitis/choroiditis
– Exudative RD
3. Convalescent phase:
– Localized alopecia, poliosis, vitiligo
– Sunset glow fundus (old exudative RD)
– Sugiura sign (depigmented limbal lesions)
– Perilimbal vitiligo
4. Chronic recurrent phase:
– Anterior uveitis
DIAGNOSTIC CRITERIA - at least 3 of:
– Skin lesions
– CNS lesions
– Bilateral anterior uveitis
– Sunset glow fundus
TREATMENT
STEROIDS DOSAGE
Oral prednisone 100-200 mg initially, followed by
gradual taper over 3-6 months
Pulse dose of i.v methyl 1 g/day for 3 days, followed by
prednisolone gradual tapering of oral prednisone
over 3-6 months
i.v methyl prednisolone 100-200 mg/day for 3 days
followed by gradual tapering of oral
prednisone over 3-6 months
IMMUNOSUPPRESSIVES
Cyclosporin 5 mg/kg/day
FK506 0.1-0.15 mg/kg/day
CYTOTOXIC AGENTS
Azathioprine l-2.5 mg/kg/day
Mycophenolate mofetil 1-3 g/day
Cyclophosphamide 1-2 mg/kg/day
Chlorambucil 0.1 mg/kg/day [dose adjusted every 3
weeks to a maximum of 18 mg/day
UVEA 265
BEHCET’S DISEASE
– Idiopathic; occurs in young men, 30-40 year age group,
HLA B 51
– Recurrent oral & genital ulcers
CLINICAL FEATURES
– Acute, recurrent, bilateral anterior uveitis - transient, mobile
hypopyon
– Retinitis - scattered white superficial infiltrates
– Retinal vasculitis → occlusions → retinal ischemia → NVE
– Generalized vascular leakage → leads to diffuse retinal
edema, CME, disc edema
– Massive retinal exudation
– Vitreitis - severe, persistent
– End stage - optic atrophy, sheathing of vessels, chorioretinal
scarring
Systemic features
Skin - erythema nodosum, folliculitis, acneiform lesions
CVS - aortitis, arterial/venous thrombosis, aneurysms
Joints - bilateral arthritis [esp. knee joint]
CNS - dural sinus thrombosis
GIT - ulceration
TREATMENT
– Steroids, immunosuppressives (azathioprine)
– Infliximab - safe & effective
DIAGNOSTIC CRITERIA
Recurrent aphthous ulcers [for 1-2 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
– Izdiopathic acute multifocal retinitis
ACUTE RETINAL NECROSIS

– Necrotizing retinitis
Caused by HSV 2 in patients less than 15 years; HSV
1 & VZV in patients more than 15 years
CLINICAL FEATURES
– Painful severe visual impairment
– Insidious onset; complain of floaters
– Anterior granulomatous uveitis, vitritis
– Peripheral retinal periarteritis
– Multifocal, deep, yellow-white retinal infiltrates which
become confluent → full thickness retinal necrosis
– Posterior pole spared till late
– Optic disc edema, choroidal thickening, retinal hemorrhages
INVESTIGATIONS
– Polymerase chain reaction to diagnose HSV/HZV
COMPLICATIONS
– Retinal detachment, AION, retinal vascular occlusion
COURSE
– Resolves in 6-12 weeks leaving behind necrotic retina with
hyper pigmented borders
– Residual visual acuity 6/12 in 50%
TREATMENT
– Acyclovir - i.v (10 mg/kg/day in 3 divided doses for 14 days)
& oral acyclovir 800 mg 5 times daily for 3 months
– Oral famciclovir - 500 mg tid x 3 months
– Systemic steroids - after antivirals are started
– Aspirin - to prevent vascular complications
– Prophylactic argon laser photocoagulation for retinal breaks
– Vitreore retinal surgery — for retinal detachment
UVEA 267
FUCH’S HETEROCHROMIC UVEITIS

– Fuch’s uveitis syndrome
– Chronic, non-granulomatous, anterior uveitis
– Unilateral; young males are mainly affected
CLINICAL FEATURES
– Complain of blurred vision, floaters
– KPs-
• small, round/stellate; grey-white
• scattered throughout endothelium
• never become confluent/pigmented
• filamentary fibrin filaments between KPs
– Anterior chamber - faint flare; cells < +2
– Angle of AC - may have
• fine, radial, twig-like vessels
• membrane
• small irregular peripheral anterior synechiae
– Amsler sign — filiform hemorrhages on paracentesis
– Iris-
• diffuse stromal iris atrophy
• no posterior synechiae
• washed out appearance
• nodules, crystals
• rubeosis iridis
• atrophy of sphincter → mydriasis
• hypochromic iris [90%]
• hyperchromic [10%]
– Cortical/white cataract
– Increased IOP, glaucoma
– Cells in anterior vitreous face
TREATMENT
– Posterior sub-tenon’s injection of triamcinolone [for floaters]
– Cataract surgery with IOL implant
– Vitrectomy - for severe vitreous opacification
MASQUERADE SYNDROMES
– Group of disorders that occur with intraocular inflammation
& are misdiagnosed as chronic idiopathic uveitis
Disorders masquerading as anterior segment
inflammation:
1. Retinoblastoma
2. Leukemia
3. IOFB
4. Malignant melanoma
5. Juvenile xanthogranuloma
6. Drug reactions - sulfonamides, rifabutin
7. Amyloidosis
Disorders masquerading as posterior segment
inflammation:
1. Retinitis pigmentosa
2. Reticulum cell sarcoma
3. Lymphoma
4. Multiple sclerosis
5. Metastatic carcinomas
6. Chronic retinal detachment
7. Sarcoma
8. Malignant melanoma
CHAPTER 9
Trauma
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 & perforation - rare
ALKALI BURNS
– Ammonia, lye (NaOH), lime Ca(OH)2
– Increases pH & produces saponification of fatty components
of cell membrane → cell disruption & death
CLINICAL FEATURES
– Epithelial defect
– Cloudy cornea
– Limbal ischemia
– Anterior chamber reaction - cells, flare
– Raised IOP [due to trabeculitis or shortening of scleral
collagen]
– Cataract
HUGHES CLASSIFICATION
GRADE CORNEA LIMBAL IRIS PROGNOSIS
ISCHEMIA DETAILS
I Epithelial damage Nil Clear Good
II Hazy <1/3 Seen Good
III Total loss of 1/3—1/2 Blurred Guarded
epithelium with
stromal haze
IV Opaque >1/2 Not seen Poor
– Early reparative phase [ERP] → 7-21 days

– Late reparative phase [LRP] → 21 days to months (sterile
stromal ulceration likely)
TRAUMA 271
Complications - Corneal scarring, conjunctivalization of

cornea, dry eye, cataract, symblepharon.
TREATMENT
IMMEDIATE ACUTE [0-7] ERP [7-21] LRP [21-90]
- copius - steroid e/d - steroid e/d* - steroid e/d
irrigation for - timolol e/d - timolol e/d - timolol e/d
½ hour - antibiotic e/d - antibiotic e/d - antibiotic e/d
- remove - cycloplegics - cycloplegics - limbal
particulate - bandage - bandage autograft
matter contact lens contact lens - corneal
- steroid e/d - tarsorrhaphy transplant
- antibiotic e/d [if exposure]
- ascorbic acid
* Discontinue steroids if corneal re-epithelialization does not occur in 10

days
Drugs also started in acute phase are:

– Topical sodium ascorbate 10% 2 hrly
– Tab Vitamin C 2 gm qid
– Topical sodium citrate 10% 2 hrly × 10 days (Decreases
intensity of inflammatory response)
– Tetracyclines - topical & systemic
– Collagenase inhibitors - acetyl cysteine 10-20% used 2
hourly [refrigerated & used for up to 1 week]
SURGERY
EARLY SURGERY LATE SURGERY
• Conjunctival flap • Division of conjunctival bands
[if stromal ulceration occurs] & symblepharon
• Limbal stem cell transplant • Conjunctival & mucous
membrane grafts
• Amniotic membrane graft • PKP → delay by 6 months
• Patch graft or glue [if corneal • Keratoprosthesis - in severely
perforation occurs] 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. IOFB
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
5. → NoPL 5. → No PL
ZONE I. external bulbar I. cornea
conjunctiva,
cornea, sclera
II. anterior segment II. up to 5 mm
up to pars plicata from lirnbus
III. posterior segment III. posterior to zone II
• 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 & an exit wound
For example: A thorn passing through the cornea, getting lodged
in the anterior chamber → perforates the cornea but penetrates
the eye.
TRAUMA 273
BLUNT TRAUMA
ANTERIOR SEGMENT POSTERIOR SEGMENT

1. Cornea - abrasion, edema 1. Vitreous hemorrhage
2. Iris - iritis; iridodialysis2. Berlin’s edema - commotio
retinae
3. Angle - recession 3. Macula - hole, edema,
hemorrhage
4. Anterior chamber-hyphaema 4. Choroidal tears
5. Lens - vossius ring; 5. Retinal detachment;
anterior capsule rupture; retinal dialysis
subluxation; cataract;
zonular dialysis
6. Globe rupture 6. Optic nerve - optic neuropathy;
avulsion; atrophy
TRAUMATIC HYPHEMA
– Microhyphema - circulating RBC in anterior chamber
without gross collection of blood
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
↓
Clot dissolves ← Break down of fibrin
GRADING OF HYPHEMA
Microscopic Circulating RBCs only
I <l/3
II 1/3-1/2
III 1/2 -near total
IV Total or “8 ball”
Rule out:
Bleeding disorders, sickle cell anemia, kidney/liver disease,
anticoagulant therapy
Investigations:
Bleeding time, clotting time, liver function tests, prothrombin
time, platelet count
TRAUMA 275
TREATMENT
SUPPORTIVE MEDICAL SURGICAL
1. Bed rest 1. Steroids 1. Paracentesis with
2. Patching 2. Cycloplegics AC wash
3. Head elevation 3. Mydriatics 2. Peripheral
4. Metal shield to 4. Antifibrinolytics - iridotomy +
prevent further EACA- 50 mg/kg/d trabeculectomy
damage to globe × 5 days 3. Urokinase with
Tranexamic acid - vitrectomy
25 mg/kg tid 4. Automated
5. IOP lowering hyphaemectomy
drugs
INDICATIONS FOR SURGICAL REMOVAL OF

HYPHEMA
– IOP > 50 mmHg × 2 days
> 35 mmHg × 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 2-5 days due to clot lysis
– Glaucoma: due to
• Early - obstruction of trabecular meshwork by RBCs
& platelets; steroid usage
• Late - posterior synechiae, iris bombe’, peripheral
anterior synechiae, angle recession, ghost cell glaucoma
BLOW OUT FRACTURE OF ORBIT
TYPES
– Direct - involves orbital rim & adjacent bone
– Indirect - involves 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 & medial wall]
– Compressive force to orbital rim causes buckling of orbital
floor
CLINICAL FEATURES
– Lid - edema, ecchymosis, hematoma
– Orbital rim - tender, loss of continuity
– Infra-orbital hypo-aesthesia - due to infra-orbital nerve
damage
– Motility disturbance → extra-ocular muscle entrapment or
direct injury → diplopia; FDT positive
– Proptosis with intra-orbital hemorrhage
– Traumatic mydriasis
– Surgical emphysema - if fracture communicates with nasal
sinus
– Epistaxis
– Enophthalmos & pseudo-ptosis
• Immediate -
– due to fat/bone tissue prolapse [herniation into
[antrum]
– edema/hemorrhage causes increased intraorbital
volume, pushing contents into antrum
• Late - due to necrosis & fat atrophy
TRAUMA 277
– Corneal laceration
– Hyphema with raised IOP
– Cataract, RD, choroidal tears
INVESTIGATIONS
CT scan brain & 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 & brain]; observation; treat
infection
– Surgery indicated for orbital floor fracture if:
• > 50% of the floor is fractured
• > 2 mm enophthalmos
• Inferior rectus entrapment causing diplopia [should be
operated within 2 weeks to prevent fibrosis & muscle
sequelae]
Medial wall fracture:
– Periorbital subcutaneous emphysema when one blows nose
– Defective adduction & abduction
Roof fracture:
– Upper lid hematoma, periocular ecchymosis
– Inferior & axial displacement of globe
– Pulsation of globe without bruit (Meningitis may occur!)
Lateral watt fracture:
– Rare; associated with extensive facial damage
INTRAOCULAR FOREIGN BODY [IOFB]
lOFBs Cause
– Mechanical damage, infection, toxic reaction
– Cataract - due to damage to lens capsule
– Vitreous liquefaction, endophthalmitis
– Retinal hemorrhages, retinal breaks
CLASSIFICATION
METALLIC
a. Magnetic - iron, steel, nickel
b. Non-magnetic -
• Inert: gold, silver, platinum
• Irritants:
– copper [worst], bronze, brass
– aluminium [tissue necrosis on contact]
– zinc [retinal atrophy]
– mercury [corneal necrosis; vitreous abscess]
– lead [gets rapidly covered with a layer of carbonate
which prevents further diffusion]
NON-METALLIC
a. Organic - cotton, caterpillar hair, wood, cilia [granulation
tissue formation]
b. Inorganic - stone, sand, concrete, coal, glass, gun powder
[local irritative response → can induce fibrous or suppurative
reaction]
TRAUMA 279
SIDEROSIS BULBI
– Due to retained iron foreign body [FB]
– Iron undergoes electrolyte dissociation & 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
Heber Weiss reaction → oxidation & dissemination of Fe+3
throughout eye causes enzyme inactivation & cell membrane
damage
TYPES
– Direct - iron deposited in immediate neighborhood of FB
– Indirect - iron diffuses throughout tissues of eye
CLINICAL FEATURES
– Cornea - rusty staining; “Coat’s ring” forms
– Secondary open angle glaucoma - due to iron in trabecular
meshwork
– Iris - heterochromia, posterior synechiae
– Pupil - mydriasis due to atrophy of sphincter
– Lens - brownish/greenish dots → large, diffuse, peppery;
beneath & over anterior capsule
– Vitreous - degeneration
– Retina
• pigmentary retinopathy
• arteriosclerotic changes
• optic atrophy & discoloration
• retinal detachment
TREATMENT
1. Remove FB; galvanic de-activation
2. i.v EDTA
3. Desferrioxamine
4. Sub-cutaneous adenosine triphosphate
CHALCOSIS
– Due to retained copper foreign body
PATHOLOGY
– Chronic non-granulomatous inflammation
– Suppurative reaction with abscess formation
– Electrolyte dissociation → chalcosis
CLINICAL FEATURES
– Cornea - greenish blue ring in Descemet’s membrane →
Kayser-Fleischer ring
– Aqueous has multiple metallic particles → brightly refringent
– Iris - greenish discoloration
– Lens - sunflower cataract; thick, powdery deposit under
anterior capsule
– Zonules - impregnation of fibers
– Vitreous - brownish red opacities
– Retina - brilliant deposits [like gold leaf] on surface of retina
& blood vessels
TREATMENT
– Remove FB
– Sodium thiosulphate
– Sodium hyposulphite
– BAL [British anti-lewisite]
TRAUMA 281
LOCALIZATION OF IOFB
1. Direct visualization - by slit-lamp biomicroscopy, indirect
ophthalmoscopy, transillumination
2. Indirect visualization - in hazy media
a. Depending of magnetic property
Magnet brought near globe; when FB is drawn towards
magnet → pain is experienced
b. Depending on electrical conductivity
alternate current
Primary coil Secondary coil
– Alternate current converts primary to secondary coil
– If FB is present - current flows in the secondary
coil
c. Depending on chemical analysis
Intraocular fluids are drawn & analyzed
d. Radiological methods:
i. Direct method
a. Limbal ring method
• metallic ring sutured to limbus
• PA & lateral view X-rays taken
• construct a circle & 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 & X-ray tubes are fixed & patient is asked
to move eyeball → FB moves with globe
iii. Depending on geometric construction -

Eyes are fixed; metal indicators point on center &
temporal side of cornea & X-rays are taken
iv. Stereoscopic method -
2 stereoscopic pictures taken at fixed angles &
displacement of FB’s shadow with reference to
radiopaque marker is noted
v. Delineation of globe using contrast media -Contour
of globe outlined by injecting radiopaque material
into Tenon’s space - to locate the FB
vi. Bone free methods -
If FB in anterior segment & density of FB is equal
to bone density; Dental film placed over inner
canthus & X-rays are directed towards anterior
segment
vii. CT scan - for :
Small FB with low radiographic density, metallic
FB; can’t locate FB if it is in sclera/retina
viii.MRI - for:
Small non-ferromagnetic FB (Plastic); high
resolution images, thinner slices
ix. Ultrasound
FB in opaque media, non radiopaque FB; FBs that
are not anterior.
A mode - steeply rising echospike
B mode - acoustically opaque
3. ERG: Early siderosis - increased ‘a’ amplitude
Late siderosis - decreased ‘b’ amplitude which is
finally extinguished
TRAUMA 283
MANAGEMENT
– Tetanus prophylaxis
– Systemic antibiotics
– Cyclopegics
– Magnetic IOFB: removed with magnets
• hand held magnet (< 1 mm FB)
• giant magnet
• intra ocular magnet
– Anterior segment FB - make limbal incision & 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
• Intra retinal 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
– Cataract
– Endophthalmitis [Bacillus cereus is commonest organism]–
treated with intravitreal antibiotics [400 μg Amikacin +
1 mg Vancomycin + 450 mg clindamycin] + removal of
IOFB
– Fibrotic membranes in vitreous
CHAPTER 10
Oculoplasty
ORBITAL PSEUDOTUMOR
– Non-specific, benign, idiopathic inflammation characterized
by polymorphous lymphocytic infiltrate with varying degrees
of fibrosis
– Usually unilateral; bilateral in kids & in lymphoproliferative
disease
PATHOLOGY
– perivascular lymphocyte cuffing & capillary proliferation
– diffuse retro-orbital soft tissue infiltration
– lymphoid hyperplasia with fibro-fatty tissue
TYPES
– primary - idiopathic
– secondary - in Wegener’s granulomatosis, PAN, systemic
sclerosis, Tolosa-Hunt syndrome, sarcoidosis, ectopic
lacrimal gland
CLINICAL FEATURES
– abrupt onset of painful proptosis
– soft tissue swelling → lid edema, chemosis
– impaired ocular motility → diplopia
– 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
OCULOPLASTY 287
INVESTIGATIONS
– Blood - ESR, ANA, eosinophilia
– CSF - pleocytosis
– Histopathological examination after biopsy
– B scan - ‘T’ sign of the choroid
– CT scan orbit - uniform enlargement of muscle & tendon;
scleral thinning
– Contrast CT scan: contrast enhancement of sclera due to
tenonitis - RING SIGN
SUBTYPES
Dacryoadenitis
– Downward, inward proptosis
– Injection over lacrimal gland; tenderness
– Dry eye; ‘S’ shaped ptosis
Myositis
– Pain on ocular movement which increases in the field of
action of muscle
– Lid edema, ptosis, chemosis
– Diplopia, injection over muscle
– Mild proptosis
– Orbital cellulitis
– Ruptured dermoid cyst
– Malignant orbital tumors
– Wegener’s granulomatosis, PAN
– Sarcoidosis
TREATMENT
Painful proptosis with limitation of movement
↓
Oral prednisolone 60-80 mg +
1% topical prednisolone QID
↓ [if good response - taper]
No response for 2 weeks
Oral pednisolone + i/v dexamethasone
↓ No response for 2 weeks
Oral prednisolone + frozen section biopsy +
injection triamcinolone
↓
Oral prednisolone + irradiation
↓
Repeat steroids + radiotherapy + repeat biopsy +
cyclophosphamide 200 mg/day [cytotoxic therapy]
OCULOPLASTY 289
THYROID RELATED ORBITOPATHY

– Ocular & 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 5-8 times;
becomes firm & rubbery
– Tendons are not involved
PATHOGENESIS
– Organ specific autoimmune disorder
– Congestive stage – there is infiltration by lymphocytes,
plasma cells, macrophages, mast cells
– Proliferation – of fat, lacrimal gland, connective tissue;
causing fluid retention
– Hypertrophy of extraocular muscles (EOMs) - due to increase
in glycosaminoglycans
– Fibrosis – degeneration of muscle fibers
CLINICAL FEATURES
– Active stage: eyes are red & painful
– Quiescent stage: eye are white, painless; motility defects
occur
WERNER’S CLASSIFICATION [NO SPECS]

Class 0 No signs or symptoms
Class 1 Only eye lid signs
Dalyrymple’s sign Upper lid retraction
Von Graef’s sign Upper lid lag on down gaze
Kocher’s sign Starring, frightening look
Griffith’s sign Lower lid lag on up gaze
Boston’s sign Uneven jerky upper lid movement on inferior
movement
Jellinek’s sign Abnormal pigmentation of upper lid
Rosenbach’s sign Tremor of gently closed lid
Stellwag’s sign Incomplete, infrequent blink
Pochin’s sign Decreased amplitude of blink
Class 2 Soft tissue involvement with signs & symptoms

0 - absent
a - minimal
b - moderate
c - marked
Enroth’s sign Lid edema
Goldzether’s sign Deep injection of conjunctiva temporally
Gifford’s sign Difficult eversion of upper lid
Reisman’s sign Bruit over eye lid
Snellen-Donder’s 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
OCULOPLASTY 291
Class 3 Proptosis
0 : absent
a : 3-4 mm over upper limit [upper limit = 21 mm]
b : 5-7 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
Klilder’s sign Jerky horizontal movements
Mohin’s sign Weakness of convergence
Suker’s sign Inability to hold fixation in extreme lateral gaze
Ballet’s sign Paralysis 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
Kneis’s sign Uneven pupillary dilatation in dimness
Loewe’s sign Dilatation of pupil with 1 : 1000 adrenalin
Cowen’s sign Pupillary jerky constriction to consensual reflex
CLINICAL FEATURES
1. Soft tissue involvement :
– Periorbital /lid edema → leads to retro-orbital fat
prolapse into lids; Rx: head elevation, diuretics
– Conjunctival hyperemia - reflects disease activity
– Chemosis; Rx: tear substitutes, taping of lids
– Superior limbic keratoconjunctivitis
Rx: acetyl cysteine 5%
– Keratoconjunctivitis sicca → due to infiltration of
lacrimal gland; Rx: Lubricants
2. Lid retraction - unilateral 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
Rx — recession of lower lid retractors, blepharoplasty,
lateral tarsorrhaphy
3. Proptosis : axial, permanent in 70%
Rx:
– Systemic Steroids - if rapidly progressive &
– Painful proptosis [oral prednisolone 80-100 mg/d × 3
months]
– Radiotherapy
– Surgical decompression:
• 2 Wall [antro-ethmoidal] → 3-6 mm
• 3 Wall [+ lateral wall] → 6-10 mm
• 4 Wall [+ sphenoid] → 10-16 mm retroplacement
OCULOPLASTY 293
4. Restrictive myopathy
– Can cause diplopia in the infiltrative phase or fibrotic
phase
– Inferior rectus & medial rectus are frequently affected;
all recti could be involved
Rx:
• IR/MR recession
• Botulinum toxin injection into the muscle
5. Optic Neuropathy due to -
– Direct compression or
– Compression of blood vessels at apex
Signs:
• Decreased visual acuity, defective red-green
perception
• Central/paracentral scotomas
• Optic atrophy
Rx: steroids, immunosuppression, plasmapheresis,
radiotherapy, surgical decompression
ORBITAL DECOMPRESSION
INDICATIONS
– Graves ophthalmopathy with corneal exposure, visual
changes, optic neuropathy, diplopia, disfigurement
– If fat or fat & muscle expansion occurs & Hotel’s
exophthalmometry reading > 25 mm → orbital fat
decompression may be done [alternative to bony
decompression]
BONY DECOMPRESSION
2 wall (antro-ethmoidal/inferior & medial wall) = 3-6 mm
3 wall (antro-ethmoidal+ lateral wall) = 6-10 mm
4 wall (antro-ethmoidal+ lateral wall + sphenoid) = 10-16
mm of retroplacement
Rule of Thumb
Reduction of exophthalmos is directly proportional to the
number of decompressed walls [2-3 mm per decompressed
wall]
COMPLICATIONS
– Sinusitis
– Lower lid entropion
– CSF leaks
– Numb lips
– Frontal lobe hematoma
OCULOPLASTY 295
BASAL CELL CARCINOMA

– Carcinoma involving basal cell layer of epidermis; invades
the dermis
– Rodent/Jacob ulcer
CARCINOGENESIS
– Chemical carcinogenesis - due to a chemical agents which
act as initiators & promotors
– UV rays
– Xeroderma pigmentosum → deficient DNA repair enzymes
EPIDEMIOLOGY
– Males; > 40 year age group, fair skinned individuals, sun-
exposed individuals
RISK FACTORS
– Congenital → Xeroderma pigmentosum, albinism, Gorlin’s
syndrome
– Acquired → UV rays, ionizing radiation, thermal burns,
scar tissue, arsenic exposure
CLINICAL FEATURES
– Usually occurs above Reed’s line → imaginary line from
tragus to angle of mouth [tear flow area]
1. Localized form → nodular, ulcerative or cystic
• 75%
• Small Papules, pearly appearance, thin epidermis
• Increases in size with central umbilication, erosion or
ulceration
2. Diffuse form → morpheaform or sclerosing type
• 15%
• Flat indurated plaque → whitish pink to yellow in color
• Overlying epidermis intact
3. Superficial form → erythromatous

• On trunk; multifocal
• Slow growing scaly red patches
• Peripheral, translucent rolled out border & central
epidermal atrophy
4. Fibro-epitheliomatous type
• On trunk; sessile with dome-shaped surface
• Nodular plaque
• Polypoid lesion
• Erythromatous/skin colored
5. Pigmented type
• Cells get pigmented on staining with Dopa
PATHOLOGY
– At junction of pilosebaceous duct & epidermis
– 1st sign - nidus of cells in upper dermis
– Club-shaped rete cells & geographic cell patterns in dermis
– Interaction with dermis produces marginal palisade–
surrounded by well organized stroma
* No lymph node involvement - large sized tumor cells do

not pass through the lymphatic channels
* Intially locally invasive tumor; in the late stages–
hematogenous spread
– Squamous cell carcinoma
– Benign hair follicle tumors
• Tricho epithelioma
• Tricho lemmoma
• Pilo matrixoma
• Tricho folliculoma
OCULOPLASTY 297
MANAGEMENT
1. Surgery -
a. Mohr’s micrographic technique →
Excised material processed within 24 hrs; & if margins
show evidence of tumor, the patient is re-operated in
3-4 days & an additional 2 mm is excised from edge
of the margins
b. Small tumor - wide excision
c. Large tumor with skin defect -
• Excision with medium & lateral advancement flap
• Rotational skin flaps
• Skin graft from - supra clavicular area, inner arm,
inner thigh
• Pre-auricular skin graft
• Retro-auricular skin graft
2. Laser treatment - CO2 laser vaporizes the tissue
3. Radiotherapy - inhibits mitosis
4. Cryosurgery - rapid freezing & thawing
5. Curettage - when tissue is soft & friable
6. Chemo Surgery — cauterizing chemical used to evoke
peeling & destruction of superficial lesions; chemicals used
are mono/di /trichloroacetic acid
7. Cytotoxic agents -
• In small superficial BCC—for focal treatment
• Methotrexate, colchicine, podophyllin, cisplantin
8. Photo dynamic therapy -
• I.V Hp D (hematoporphyrin derivative) given 48 hrs
prior to 630 nm of Argon pumped dye laser
• Pigment absorbs dye & facilitates destruction
9. Interferon α
10. Retinoids → etretinate & isoretinoin
XERODERMA PIGMENTOSUM
– Autosomal recessive, congenital
– Inherent defect in DNA repair
– Predisposes to basal cell carcinoma
Stages
1. → Sun sensitivity
2. → Pigmentation
3. → Carcinomas [squamous & basal cell carcinoma of lids
& exposed parts]
UV light → causes changes in DNA segments

Normally: Damaged DNA segments are removed & replaced
by enzymes
In XP: Defective enzymes systems → leads to abnormal DNA
production
Prophylaxis
– Prevent exposure to UV light
OCULOPLASTY 299
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 & arsenic
– Pterygium
– Ocular surface injury
– Vitamin A deficiency
– HSV type I
PREMALIGNANT LESIONS
1. Actinic keratosis
• Flat, scaly keratotic lesions on a telangiectatic base
• Associated with UV light exposure
2. Bowen’s 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 2/3 of upper lid, outer
1/3 of lower lid → Pre-auricular lymph nodes
• From inner canthus, inner 1/3 of upper lid, inner 2/3
of lower lid → Sub-mandibular lymph nodes
– Direct spread - in chronic cases

– Perineural spread - to orbit & intracranial cavity along VIIn
& Vn [7th & 5th cranial nerves]
– Local extension - to orbit, lacrimal passages, eyeball, nose,
face, cranial cavity.
CLINICAL FEATURES
CONJUNCTIVA LIDS
- Lesion at corneo-scleral - Painless small hard nodule or
junction in inter palebral area rough warty keratotic plaque
- From a solar keratosis, - Erosions & fissures
dysplasia or ca-in-situ with crusts
- Roughened, irregular,
exophytic mass
– Pain due to - involvement of supraorbital or infraorbital

nerves
– Late stages → hemorrhage, meningitis, cachexia
OCULOPLASTY 301
TYPES
CONJUNCTIVA LIDS
1. Gelatinous - tufted 1. Ulcerative - base is indurated
superficial blood vessels & hyperemic; edges are
2. Nodular - rapidly hard & undermined
growing; increased 2. Papillomatous
tendency to metastasis 3. Cystic growth
3. Diffuse - least common 4. Cutaneous horn
HISTOPATHOLOGY
– Dysplasia
• mild - involving < 1/3 thickness of epidermis
• moderate - involving <3/4 thickness
• severe—involving 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 type - most common
– Epidermoid cell/pavement/prickle cell type - least common;
large polyhedral cells with large nuclei
– Clear cell → small cells with hyperchromatic nuclei
– Muco-epidermoid/goblet cell - cuboid cells arranged in nests
& 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 -
• Mohr’s microsurgical technique
• Wide excision
• Orbital exenteration - if tumor extends into orbital fat;
or perineural involvement
• Lymph node biopsy
• Enucleation
2. Radiotherapy - Strontium 90, γ irradiation
3. Cryotherapy - N2O cryoprobe
• Repeated rapid freeze & slow thaw
• Probe should never be placed for > 3 sec
4. Immunotherapy/Chemotherapy -
• DNCB [Dinitrochlorobenzene]
• Urea
• Thiotepa
• Cisplatin alone or with doxorubicin, bleomycin,
isotretinoin
Lids:
– Inverted follicular keratosis
– Seborrheic keratosis
– Keratoacanthoma
Conjunctiva:
– Pterygium, pingecula
– Papilloma, nevus
– Pyogenic granuloma
– Dermoid
– Keratoacanthoma
– Mooren’s ulcer
OCULOPLASTY 303
BOWENS’ DISEASE
– Dysplastic changes seen throughout the entire epithelium
but basement membrane not breached
– Also called dysplasia/carcinoma - in situ/ocular surface
squamous metaplasia
– 50 - 60 year 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 grey/reddish grey
– In the interpalpebral fissure area, common at limbus
TYPES
– Gelatinous, velvety, papilliform, leukoplakic, nodular, diffuse
form [masquerades chronic conjunctivitis]
– Malignant melanoma → regular smooth surface
– Papilloma → sessile/pedunculated with a punctate vascular
pattern
– Benign nevi - less pigmented
– Pseudo-epitheliomatous hyperplasia
RELATED CONDITIONS
Xeroderma pigmentosum, HTV, pterygium
INVESTIGATIONS
Exfoliation cytology, impression cytology, Histopathology after
biopsy.
TREATMENT
1. Surgery- Mohr’s micrographic technique
2. Radiotherapy - with Strontium 90 (β irradiation) &
radium (γ 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 micro-circulation → causing infarction of
normal & tumor tissue
4. Immunotherapy - with DNCB & urea
5. Chemotherapy -
• topical mitomycin 0.02% qid for 10-22 days
• Tretinoin → for early dysplasia.
OCULOPLASTY 305
MEIBOMIAN GLAND CARCINOMA

– Common in lids because meibomian glands more; also
occurs in caruncle, eyebrows
– Females more affected; 60-70 years
– Upper lid involvement more common than lower lid
– Spread to → lacrimal gland, naso-lacrimal duct, orbit, pre-
auricular/sub-mandibular/deep cervical lymph nodes
SITES OF ORIGIN
– Meibomian glands, Zeis’ glands, sebaceous gland of
caruncle/eyebrows
PATHOLOGY
– Infiltrating nodules :
• Un-encapsulated masses with infiltrating margins
• Mimics chalazion
• Finely vacuolated frothy cytoplasm
– Conjunctival intra-epithelial spread
– Tumor cells spread down the duct of Zeis or superficially
within epidermis or tarsal conjunctiva
– Cells directly infiltrate epithelium → radially
STRASMA’S CRITERIA
1. Tumor should arise from tarsal plate
2. Should be continuous with tarsus
3. Should have histopathological evidence of meibomian gland
carcinoma
MANAGEMENT
1. Surgery:
– Wide local excision with frozen section
Excision following conjunctival map biopsy → all
quadrants of globe, fornices, tarsal plate – sampled
& mapped
– Exenteration for - bulky caruncular lesions, orbital
invasion, large lid tumors
– Radical surgery → lacrimal gland removed, nasolacrimal
duct sealed
2. Radiotherapy: In very old, ill patients
3. Chemotherapy: for sclerosing/pagetoid type
– Diffuse squamous cell carcinoma
– Kaposi’s sarcoma
– Recurrent chalazion
– Chronic conjunctivitis/blepharitis
– Chronic fungal infection
OCULOPLASTY 307
UPPER LID RECONSTRUCTION

LOWER LID RECONSTRUCTION

OCULOPLASTY 309
ENUCLEATION
– Removal of entire globe, including cornea & 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 & opaque media, with the
slightest suspicion of malignancy
COMPLICATIONS
– 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 & 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
DISADVANTAGES
– no tissue for histopathological examination
– sympathetic ophthalmitis can still occur
EXENTERATION
– Removal of all soft tissues of orbit till the periosteum,
including the globe
– Indications:
• orbital mucormycosis
• malignant epithelial tumors of lacrimal gland
• sarcomas
OCULOPLASTY 311
LATERAL ORBITOTOMY
– An opening made in the lateral wall of the orbit to gain
access to mid & deeper orbital lesions within & 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
a. Primary
• schwannomas
• optic nerve glioma
• optic nerve meningioma
• lacrimal gland tumors
b. 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
OCULOPLASTY 313
SOCKET RECONSTRUCTION
INDICATIONS
– Contracted Socket → When the fornices &/or fundus of
the socket are inadequate to allow retention & motility of
a prosthesis
PROCEDURE
– Incision/excision of scarred tissues
– Full thickness buccal mucosal graft placed in the defect;
fix a silicone stent to the superior & inferior orbital rims
– 6 months later a mold is placed in socket immediately
after removing stent
– A prosthesis is made & fit
INDICATIONS
Congenital:
• Anophthalmos
• Congenital contracted socket
Acquired:
• Enucleation, evisceration
• Phthisis bulbi
• Atrophic eye
ORBITAL IMPLANTS
1. Autogenous:
e.g. - skin/fascia
- mucous membrane
- bone/cartilage
- dermis fat graft
2. Alloplastic:
e.g - glass, titanium
- acrylic, MEDPOR
- hydroxyapatite
3. Conformers
4. Artificial Prosthesis
PTOSIS
– Abnormally low position of upper eye lid (drooping)
CLASSIFICATION
NEUROGENIC MYOGENIC MECHANICAL APONEUROTIC
1. IIIn palsy 1. Myaesthenia 1. Tumors 1. Involutional
2. Homer’s gravis 2. Lid edema 2. Following lid
syndrome 2. Myotonic 3. Dermato- surgery,
3. IIIn dystrophy chalasis trauma,
misdirection 3. Ocular 4. Scars blepharo-
myopathy 5. Anterior chalasis
4. Marcus 4. Simple orbital lesions
Gunn congenital
jaw winking ptosis
5. Blepharo-
phimosis
syndrome
EVALUATION
HISTORY MEASURE- ASSOCIATED PSEUDO-
MENT SIGNS PTOSIS
- Age of onset - MRD1&2 - Contralateral - Lack of globe
- Duration - VFH lid retraction support e.g.
- Diplopia - MCD - Fatigability enophthalmos,
- Systemic - MLD - Cogan twitch micro-
disease - LPS function sign phthalmos
- Diurnal - Pretarsal - Bell’s - Dermato-
variation show phenomenon chalasis
- Fatigue - Herring’s - Hypotropia
reflex - Brow ptosis
- Jaw winking - Contralateral
phenomenon lid retraction
- Ocular motility
defects
* MRD - margin reflex distance
* VFH - vertical fissure height
* MCD - margin crease distance
* MLD - margin limbal distance
OCULOPLASTY 315
SIMPLE CONGENITAL PTOSIS

– Due to failure of neuronal migration/development - with
muscle sequelae
– Absent upper lid crease
– Poor levator function
– 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 elevation – in bilateral ptosis
– Refractive errors – may lead to amblyopia
– Rx - levator resection [in pre-school children]
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
– Rx - 1st correct epicanthus & 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 are intact
– In severe cases, upper lid crease absent
– May get worse at end of day because of fatigue of Muller
muscle
– Rx – levator resection & re-insertion
– anterior levator aponeurosis repair
SURGERIES
FASANELLA - LEVATOR FRONTALIS APONEUROSIS
SERVAT RESECTION SUSPENSION REPAIR
PROCEDURE
Mild ptosis Any ptosis Severe ptosis Aponeurotic
ptosis
LPS ≥ 10 mm LPS ≥ 5 mm LPS < 4 mm LPS ≥ 15 mm
Upper border Shortening of Suspension of Advancement
of tarsus + levator complex tarsus from & suturing of
lower border via anterior frontalis muscle healthy
of Muller → [skin] or with a sling aponeurosis to
excised with posterior made from tarsal plate
overlying [conjunctiva] autologous
conjunctiva approach fascia lata or
non-absorbable
synthetics like
proline/silicone
Done in Done in
Homer’s blepharophimosis
syndrome syn, total IIIn
palsy, Marcus
Gunn Jaw
winking ptosis
* LPS - levator palpebrae superioris function

OCULOPLASTY 317
ENTROPION
• Intuming of the lid margin
TYPES:
1. Involutional/Senile entropion —
– Occurs in lower lid only because upper lid has a broader
tarsus & 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 & fibrous tissues
within the eyelid
– Stretching of canthal tendons & 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 sutures - prevents overriding of
pre-septal orbicularis
• Weis procedure - full thickness horizontal lid splitting;
insertion of everting sutures
• Jones procedure - tightens the lower lid retractors
& creates a barrier between pre-septal & pre-tarsal
orbicularis
– When horizontal lid laxity is present →

• Quickert procedure - transverse lid splitting; insert
everting sutures + horizontal lid shortening
2. 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 cases - replace deficient or keratinized
conjunctiva; replace scarred & contracted tarsus with
composite grafts
3. Congenital entropion -
– Upper lid - secondary to microphthalmos
– Lower lid -
• due to improper development of inferior
• retractor aponeurosis
• absence of lower lid crease
• in turning of lower lid & lashes
– Rx: Hotz procedure - excision of a strip of skin &
muscle; & fixation of skin crease to tarsal plate
OCULOPLASTY 319
ECTROPION
INVOLUTIONAL ECTROPION
Clinical features - Horizontal lid laxity ≥ 8 mm
- Medial canthal tendon laxity
- Lateral canthal tendon laxity
Treatment:
TYPE SURGICAL PROCEDURE
Medial ectropion Lazy T procedure
Generalized ectropion Horizontal lid shortening
Marked generalized Kuhnt-Szymanowski procedure
ectropion with excess skin
CICATRICIAL ECTROPION
Causes: Trauma, burns, icthyosis, dermatitis; [scarring
& contracture of tissue pulls lid away from
globe]
Treatment:
TYPE SURGICAL PROCEDURE
Mild, localized Excision of scar + Z plasty
Severe, generalized Free skin grafts, transposition flaps
PARALYTIC ECTROPION
Causes : VIIn palsy
Clinical features : Brow ptosis, lid retraction, exposure
keratopathy, epiphora
Treatment: Taping of lids, lubricants,
tarsorrhaphy, lateral canthal sling
If medial canthal laxity present Medial wedge resection
If medial canthal tendon intact Medial 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 origin - in 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 2-5 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
– Cafe-au-lait spots
– Sub-ungual hamartomas
– 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) & cardiac (rhabdomyomas)
Triad: epilepsy, mental retardation, adenoma sebaceum
In Eye
• Retinal astrocytomas
• Hypopigmented spots on iris & retina
• Papilloedema
• VI n palsy [due to raised ICT]
OCULOPLASTY 321
von HIPPEL-LINDAU DISEASE

– Angiomatosis retinae
– AD inheritance
– 2nd decade
– Life threatening
In Eye
– Capillary hemangiomas - involving retina &/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
& drained by a dilated & tortuous artery & vein respectively
– Secondary exudative changes → macular star formation
– Tumor grows towards vitreous; may invade choroid
– Cataract, iridocyclitis, phthisis bulbi
– Tumor on optic disc - mimics optic neuritis, papilloedema
(no dilated arteries/veins when on the disc)
FFA
Early phase – delineates the feeding & draining vessels
Late phase – diffuse leakage of dye from tumor (due to
transudative nature)
Systemic Features
– Cerebellar hemangioblastoma - headache, nausea &
vomiting, cerebellar disturbances
– Spinal cord - usually asymptomatic
– Cysts in pancreas, kidney [rife threatening], adrenals, liver,
spleen, ovaries, urinary bladder
– Hypernephroma [life threatening], pheochromocytoma.
TREATMENT
– Diathermy
– Xenon arc photocoagulation (for medium & large sized
lesions)
– Argon laser photocoagulation (for < 0.8 DD angiomas)
– Cryotherapy – triple freeze thaw
• For peripheral angiomas; thick angiomas with
surrounding RD
• Repeated every 6 wks till tumor regresses
Investigations
– CT scan, MRI, ultrasonography, renal angiography
– Family members should be screened
NEUROFIBROMATOSIS
– von Recklinghausen’s disease
– It progresses to invade spinal canal or cranium; can infiltrate
or compress vital organs
– Transformation to sarcoma is rare - called neuro-
fibrosarcoma
Clinical Features
– Cafe 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 & bone growth
– Hemi-hypertrophy of face
– Plexiform neurofibroma
• Contiguous involvement of multiple superficial nerves
• In upper lid, adjacent temple, side of face
OCULOPLASTY 323
– In brain, meninges, spinal cord, cranial nerves

– Any viscera, gut
– Associated with endocrine abnormalities -
• hyperparathyroidism, myxedema, Addison’s disease,
diabetes mellitus, tetany
EYE
CONJUNCTIVA - small localized elevated tumors which 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 - choidal nevi
RETINA - medullary nerve fibers
- hamartomas
OPTIC NERVE - gliomas
LIDS - fibroma molluscum
- schwannoma
- cafe-au-lait spots
- plexiform neurofibroma
- elephantiasis of lids
ORBIT - greater wing of sphenoid absent
- spheno-orbital encephalocele
- pulsatile exophthalmos
GLAUCOMA - angle infiltration by neurofibromatous tissue
- congenital angle anomaly
- angle closure [forward displacement of lens-iris
diaphragm]
- fibrovascular membrane in angle contracts -
Synechial 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 1/3 of face
• Flat; doesn’t 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
Ineye:
– Ipsilateral telangiectasia of conjunctival & episcleral vessels
– Ipsilateral hyperchromic iris
– Spontaneous lens dislocation
– Tortuosity of retinal vessels
– Contralateral homonymous hemianopia
– Glaucoma due to
• congenital malformation of anterior chamber angle
• peripheral anterior synechiae
• raised episcleral venous pressure
– Choroidal hemangioma
• diffuse → Tomato ketchup’ fundus - diffuse thickening
of choroid
• circumscribed → salmon orange color, elevated, sub-
RPE masses with indistinct margins
– Serous retinal detachment
– Cystoid retinal degeneration
OCULOPLASTY 325
PROPTOSIS
CAUSES
1. Congenital -
– pseudoproptosis (myopia)
– meningo-encephalocele
– craniostenosis
– neurofibromatosis
– microphthalmia with cyst
2. Inflammatory -
– Graves’ disease
– pseudotumor
3. Infective -
– orbital cellulitis
– cysticercosis
– hydatid cyst
4. Neoplastic -
– Neural - optic nerve glioma, meningioma, schwannoma,
neurofibroma
– Rhabdomyosarcoma
– Lacrimal gland tumors - benign, malignant
– Cysts - dermoid, epidermoid, teratoma
– Vascular - cavernous hemangioma, capillary
hemangioma, lymphangioma, hemangiopericytoma
– Metastatic - Ewing’s sarcoma, leukemia, neuroblastoma
– Fibro-osseus - fibrous dysplasia, osteoma
– Juvenile xanthogranuloma
– Histiocytic tumors
– Lympho-proliferative tumors
5. Vascular -
– AV fistulas/malformations
– Orbital varices & hemorrhages
ORBITAL CELLULITIS
– Orbital soft tissue infection posterior to orbital septum
CAUSES
– Spread of infection from periorbital structures - brain,
sinuses, lacrimal sac, lids & teeth
– Endogenous →
• Bacteremia
• Endophthalmitis/panophthalmitis
– Exogenous → surgery, trauma
Common pathogens are Staph. aureus, Strept. pyogenes,
Strept. pneumoniae, H. influenzae
CLINICAL FEATURES
– Fever, malaise
– Rapid onset
– Lids are edematous, red & tender
– Conjunctival chemosis
– Proptosis - lateral, downwards
– Optic nerve dysfunction - RAPD, decreased vision, defective
color vision
– Painful ophthalmoplegia
COMPLICATIONS
– Exposure keratopathy
– Glaucoma
– CRAO, CRVO
– Optic neuritis
– Orbital or sub-periosteal
– Brain abscess, meningitis
– Cavernous sinus thrombosis
OCULOPLASTY 327
TREATMENT
KIDS
– Ampicillin 200 mg/kg/d i.v + clavulanic acid i.v 100 mg
/kg/d
ADULTS
– Amoxycillin + clavulanic acid
– Clindamycin
– Vancomycin
– 4th generation cephalosporin + metronidazole
• Assess optic nerve every 4 hours
• Investigations - WBC count, CT scan, lumbar puncture
• Surgery done - if
– decrease in vision
– orbital abscess
– biopsy required
– unresponsive to treatment
CAROTICO - CAVERNOUS FISTULA
HIGH-FLOW CCF
CAUSES
– Congenital
– Atherosclerotic (spontaneous) rupture of intracavernous
aneurysm
– 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 & outward
– Papilloedema → optic atrophy
– Retinal hemorrhages, venous engorgement & tortuosity →
CRVO
– Opacity of media → lens, cornea
– Cornea - exposure 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 & engorgement
of the muscles
HYPOXIC EYEBALL SYNDROME
• Corneal epithelial edema
• AC reaction, iris atrophy, NVI
• Glaucoma, cataract
• Retinal venous dilatation & hemorrhage
OCULOPLASTY 329
PATHOLOGY
– Blood in vein becomes arterialized
– Venous pressure increases
– Decreased arterial pressure & perfusion
LOW-FLOW CCF [Indirect/dural shunt]

– Small, meningeal arterial branches supply dural walls of
cavernous sinus → rupture of these branches causes a low-
flow CCF
Causes: congenital malformations, spontaneous rupture (in
hypertension)
Clinical Features
– Dilated episcleral vessels, raised IOP
– Mild proptosis, ophthalmoplegia
– Bruit, diplopia, transient VI n palsy
– Unilateral headache; chronic, unilateral red eye
Treatment
– Interventional radiology - intravascular balloon introduced
into internal carotid artery via a catheter
CAVERNOUS SINUS THROMBOSIS

– Fever, headache
– Frontal/retro-orbital pain, diplopia
– Ptosis, proptosis, chemosis, ophthalmoplegia
– Hyperesthesia of ophthalmic & maxillary divisions of Vn
– Decreased corneal reflex
– Dilated tortuous retinal veins
– Papilloedema
– Septic cavernous sinus thrombosis is treated with i.v
antibiotics
– Aseptic cavernous sinus thrombosis is treated with urokinase
therapy [thrombolytic agent]; recombinant tissue
plasminogen activator (rtPA) + i.v heparin
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 & pituitary gland
– Decreased visual acuity precedes onset of proptosis
– Unilateral painless, gradual, progressive axial proptosis
– Optic disc - swollen & pale with optociliary shunts
– CT scan - shows concentric enlargement of optic foramen;
J-shaped sella
– MRI – shows intracranial extension
Treatment
– Progressive enlargement with blind eye → Radical surgery;
excise optic nerve & preserve globe
– Chiasmal extension → palliative treatment
OPTIC NERVE MENINGIOMA

– Near sella → early visual field defects, papilloedema, 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 & calcification of optic nerve
• normal optic nerve running through tumor → “Doughnut
sign” on coronal CT scan
OCULOPLASTY 331
RETINOBLASTOMA
– Malignant transformation of primitive retinal cells before
final differentiation
– Usually presents before 3 years of age
HERITABLE NON-HERITABLE
1. 40% of cases 1. 60% of cases
2. Primitive retinal cells 2. Arises at a somatic level in a
predisposed to single retinal cell
malignant transformation
by mutation
3. Autosomal dominant 3. Non-heritable
4. Presents at 18 months 4. At 2 years
5. Bilateral, multiple 5. Single
6. 50% risk of 6. No transmission
transmission to offspring
TYPES
1. Infra-retinal- flat, round, white
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 invasion - multifocal iris invasion, painful
red eye, pseudohypopyon
– Metastasis → lymph nodes, brain
INTERNATIONAL CLASSIFICATION
GROUP RISK TUMOR FEATURES
A Very low Small discrete - ≤ 3 mm, confined to
intraretimal tumors retina
away from foveola - located > 3 mm
& disc from foveola & 1.5 mm
from the disc
B Low All remaining - tumors confined to the
discrete retinal retina not in group A
tumors without - any tumor size &
seeding location
C Moderate Discrete local - discrete tumors
disease with - SRF without gross
minimal subretinal seeding, involving upto
or vitreous seeding 1 quadrant of retina
- local subretinal seeding,
< 5 mm from tumor
- focal fine vitreous seeding
close to tumor
D High Diffuse disease with - massive or diffuse tumors
significant vitreous - SRF upto total RD
or subretinal seeding - diffuse subretinal seeding
- diffuse vitreous disease
with greasy seeds or
avascular tumor masses
E Very high Presence of any - tumor touching lens
one of the poor - NVG
prognostic features - opaque media from
hemorrhage
- tumor anterior to anterior
vitreous face involving
ciliary body or anterior
segment
- diffuse infiltrating
retinoblastoma
- tumor necrosis with
aseptic orbital cellulitis
- phthisis bulbi
OCULOPLASTY 333
REES ELLSWORTH CLASSIFICATION
NO. OF TUMORS POSITION SIZE

I A One Behind equator <4 DD
B Many Behind equator <4 DD
II A One Behind equator 4-10 DD
B Many Behind equator 4-10 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 > ½ retina
B Vitreous seeding
TREATMENT (depends on size & location]

SMALL MEDIUM LARGE
– laser – brachytherapy – chemoreduction
photocoagulation – external beam – enucleation
– transpupillary radiation
thermotherapy – chemotherapy
– cryotherapy with carboplatin +
vincristine + etoposide
– If extraocular extension has occurred → external beam

radiotherapy
– If metastasis has occurred → high dose chemotherapy
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,
2-3 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 involvement - rare
– 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
OCULOPLASTY 335
FFA
– Dual circulation
– Mottled fluorescence in AV phase
Color-coded Doppler
– to differentiate pigmented tumor from hemorrhage
CT scan
– to look for any extraocular extension
TREATMENT
– Brachytherapy → plaque radiotherapy
– Charged particle irradiation with protons & Helium
– Trans-pupillary 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 [when vision is NLP]
– Exenteration → if extraocular extension
– Palliative therapy → if metastasis
CHAPTER 11
Pediatrics
& Squint
AMBLYOPIA
– Defective visual acuity persisting after correction of refractive
error & after removed of, or 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 7-8 years
CLASSIFICATION
1. Stimulus deprivation amblyopia
– May be:
• Complete - in ptosis, mature cataract
• Partial - in lamellar cataract, corneal opacity
2. 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
3. Ametropic amblyopia
– In high bilateral refractive errors
– When refractive error is greater than + 6.00D
or – 10.00D
4. Anisometropic amblyopia
– Meridional [in high astigmatism]
– Anisohypermetropia [due to unequal hypermetropia in
both eyes]
– Anisomyopia [due to unequal myopia in both eyes]
PEDIATRICS & SQUINT 339
NEUTRAL DENSITY FILTER

When placed in front of:
– Normal eye → visual acuity decreases by 2 lines [Snellen’s
chart]
– Eye with organic cause for decreased vision → visual acuity
decreases by 2 lines
– Amblyopic eye → visual acuity remains the same
DIAGNOSIS
– Visual acuity
– Refraction - after full cycloplegia
– Slit lamp & fundus examination
– Compare behavior of one eye with other
• Cover test - eye’s reaction to covering
• Fixation - steady, unsteady, eccentric
• Speed of eye movement [during a cover-uncover test]
• Ability to pick up small grains of sweets with fixing eye
covered
– Assess visual acuity in infants
• Optokinetic nystagmus
• Forced choice preferential looking
• Visual Evoked Response
TREATMENT
– Force the amblyopic eye into use
– Ametropic amblyopia → give full correction of refractive
error
– Anisometropic amblyopia - correct refractive error; allow
2 months before starting occlusion therapy (spontaneous
improvement may occur);
– Reversible up to 11 to 12 years of age; repeat refraction
every 6 months for children below 8 years; children below
18 years should be treated actively
1. OCCLUSION
• Total occlusion - with opaque material on placed on
spectacle lens [plaster]
• Partial occlusion - translucent adhesive tape, atropine
can be used
Precautions
– Prevent occlusion amblyopia by allowing the normal eye
to be used intermittently
– To avoid diplopia, investigate for binocular single vision
before onset of therapy (if fusion is possible → no risk for
diplopia)
PATCHING
Months of age Patching scheme
0-1 no patching
1-2 1-2 hours/day
2-4 2-3 hours/day
4-6 50% of waking hours
6-12 80% of waking hours
12 Full day
24 2:1 [patch 2 of 3 days]
36 3:1 [patch 3 of 4 days]
48 [4 years] 4: 1 [patch 4 of 5 days]
60 [5 years] 5:1 [patch 5 of 6 days]
72 [6 years] onwards 6: 1 [patch 6 of 7 days]
2. PENALIZATION
– Penalize the normal eye so that the amblyopic eye is
made to see.
Penalization may be done by using:
1. 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 & is forced
to be used for near work
2. Glasses -
– Normal eye is under-corrected
– Full refractive correction is given to the amblyopic eye,
which is forced to be used to distance work
3. CAM VISUAL STIMULATOR
– Stimulates the amblyopic eye
4. PLEOPTICS
– Parafoveal area is dazzled with bright light while
protecting the fovea, to stimulate foveal fixation
Methods
1. Bangerster’s 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 & fixation
becomes central
2. Cupper’s 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
NEONATAL CLOUDY CORNEA

S – sclerocornea
T – trauma, tear in descemet’s membrane [infantile
glaucoma]
U – ulcer due to HSV, bacteria, neurotrophic keratopathy
M – mucopolysaccharidosis, metabolic casues, ryrosinosis
P – Peter’s anomaly, posterior keratoconus, posterior corneal
defect, staphyloma
E – endothelial dystrophy (CHED, PPD)
D – dermoid (central)
VISUAL ACUITY TESTING IN PREVERBAL

& VERBAL CHILDREN
PREVERBAL CHILDREN
– Objective way of estimating visual acuity is by assessing
fixation
– Fixation should be central, steady & maintained [CSM]
– Ability to fixate & follow light
– Forced choice preferential looking
– Optokinetic response [OKN]
– Visual evoked response [VER]
– Ability to locate & pick up objects & sweets
– Catford drum
VERBAL CHILDREN
– Sheriden Gardner vision test
– “E” chart
– Landolt’s broken ring test
– Cardiff cards
– Snellen’s charts
CONGENITAL CATARACT
CAUSES
– Unknown - 45%
– Hereditary, genetic
– Intra-uterine infection - rubella, CMV infection, chicken
pox, toxoplasmosis
– Metabolic - galactosemia, diabetes mellitus, hypo-
parathyroidism
– Secondary to coloboma, PHPV
– Associated with microphthalmos, aniridia
– Mesodermal/ectodermal dysgenesis → persistent pupillary
membrane, posterior lenticonus
TYPES
– Zonular - nuclear/lamellar/sutural/capsular
– Polar - anterior/posterior
– Blue dot cataract
– Coronary cataract
– Membranous cataract
– Total/mature cataract
INVESTIGATIONS
– TORCH liters
– Chromosomal analysis [Down’s & Patau’s syndrome]
– Urine analysis [galactosemia]
– Serum calcium & phosphorus
– Fasting & 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
– Cataract with nystagmus
– Bilateral cataract with one eye operated → the other should
be operated within 1-2 weeks to prevent amblyopia
– Bilateral mature cataracts [operate both eyes within 6-8
weeks of birth, with a gap of 1-2 weeks]
Technique
– Lensectomy & anterior vitrectomy [LAV] - via limbal/ pars
plana approach
– Phacoaspiration with primary posterior capsulotomy with/
without anterior vitrectomy, & capsular bag implantation/
optic capture of IOL
IOL Power Calculation
– Aim for residual hypermetropia
• Make emmetropic if > 8 yrs of age
• 90% of emmetropia if 2-8 yrs of age
• 80% of emmetropia if < 2 yrs of age
Post-operative Complications
– Immediate → shallow AC, increased fibrinous reaction
– Late → thick PCO, lens precipitates, pseudophakic
membranes, glaucoma, RD
Visual Rehabilitation
– With glass, contact lens, secondary IOL, occlusion therapy
for amblyopia
CLASSIFICATION OF EXOTROPIA
PRIMARY
a. Intermittent
• Divergence excess: true/pseudo squint
• Convergence insufficiency
b. Constant
• Early onset
• Decompensated divergence excess
SECONDARY
• to ocular pathology
CONSECUTIVE
• Spontaneous
• Post-surgical [following surgical correction for esotropia]
CLASSIFICATION OF ESOTROPIA
PRIMARY
1. Concomitant
a. Accommodative -
• Refractive
• Non-refractive
• Partially accommodative
b. Non-accommodative -
• Infantile
• Acquired:
– Basic
– Acute esotropia
– Cyclic esotropia
– Myopic esotropia
– Convergence excess
– Divergence insufficiency
c. Microtropia
d. Nystagmus blockade syndrome
2. Non-comitant
a. Paralytic - VI n palsy
b. Non-paralytic -
• “A-V” patterns
• restrictive syndromes
• mechanical restrictions
SECONDARY
• to ocular pathology [sensory esotropia]
CONSECUTIVE
• Spontaneous
• Following surgery for exotropia
INFANTILE ESOTROPIA
– Appears 3 to 6 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
1. Dissociated vertical deviation- in 40 to 50%
– slow upward deviation of one/alternate eyes
– no corresponding hypotropia of opposite eye
– may be latent or manifest
– poor BSV & fusion
2. Inferior oblique over action
– V pattern esotropia
– increased elevation in adduction
– onset at 2 to 3 years of age
3. Latent nystagmus -
– nystagmus only when one eye occluded
4. Abnormal OKN -
– normal adducting & weak abducting saccade
TREATMENT
– Spectacle correction if refractive error > +3.00D
– Treat amblyopia → increased chance for fusion
– Surgery :
• Bilateral medial rectus recession [before 3 years of age]
• Bilateral lateral rectus resection
– Follow up
– Pseudo-esotropia → flat broad nasal bridge, prominent
epicanthal folds, narrow interpupillary distance
– Duane’s 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 & accommodate
– < 40 PD esotropia
– Amblyopia in 30-50%
Types
• Fully accommodative - full spectacle correction eliminates
the deviation
• Partially accommodative - residual esotropia despite full
correction of refractive error
CAUSES
– Over-convergence associated with accommodation
– Failure of fusional divergence to correct over-convergence
TYPES
1. Refractive:
– Normal AC/A ratio
– High hyperopia (≥+4.00 D)
– Accommodative effort to overcome hyperopia creates
excessive accommodative convergence
– Rx: Full refractive correction
2. Non - Refractive:
– High AC/A ratio
– Normal refractive error (+2.00 D)
– Increased convergence; normal accommodation
– DN > DD: Deviation greater for near than distance
[atleast 10 PD difference]
– Rx:
• Full distance correction
• Bifocals → to 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 ΔN - ΔD
_____ = IPD (cm) + ____________
A D
Δ N → deviation for near (33 cm)
Δ D → deviation for distance (6 meters)
D → distance of fixation for accommodation
Gradient Method
AC (Δ + L) – (Δ – L)
_____ = ________________________
A D
Δ + L → deviation with concave lens
Δ – L → deviation without lens
D → strength of lens used
NON-SURGICAL MANAGEMENT OF SQUINT

1. Glasses - for accommodative esotropia
a. Accommodative esotropia with hypermetropia:
• Regular plus glasses to relax accommodation &
increase convergence
• Bifocals → if more hyperopia for near
b. Non refractive - voluntary convergence with emmetropia
2. Prisms -
– Only when BSV present
– In acquired paretic squint, vertical palsies, small
deviations
– ESOTROPIA - base in prism used
– EXOTROPIA - base out prism used
– Visual acuity should be almost normal in both eyes
– Prisms - divided equally for both eyes
– Fused with spectacle lenses
3. Orthoptic exercises -
– Increasing fusional amplitude by stimulating
physiological diplopia
– Called anti-suppression exercises
– Increases accommodation amplitude & improves
convergence & fusion
4. Pharmacological -
– Atropine - for penalization of normal eye in
accommodative esotropia
– Miotics - phospholine iodine, pilocarpine
– Botulinum toxin A - chemical denervation
EVALUATION OF SQUINT
COVER TEST
– To detect heterotropia
– Done for near & distance
– Cover the apparently fixing eye & watch movement of
suspected deviating eye
COVER-UNCOVER TEST
– To detect heterophoria
– Uncover the eye & 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)
– Phoria - patient will have straight eyes before & after test
– Tropia - patient will have a manifest deviation
– Quickly cover each eye alternately & watch behavior of
each eye when cover is removed & 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 esotropia - use a base out prism

– For exotropia - use 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
HIRSCHBERG’S 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 ½ way between center of pupil & limbus
→ deviation is 20°
– Reflex ½ way between pupillary margin & 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 (if - manifest 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
Orthophoria or ARC [if squint]
Diplopia
No simultaneous perception [Suppression]
Central suppression scotoma
MADDOX ROD: [when placed in front of right eye]
No horizontal phoria
Esophoria
Exophoria
EVALUATION OF PARALYTIC SQUINT

– Determine cause — history, ocular examination orbital
ultrasonography, neurological examination, CT scan, MRI
– Secondary deviation > Primary deviation
DIPLOPIA CHARTING
Data Obtained
– Areas of single vision & 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 & then left - deviation [&
diplopia] increases in the direction of action of paralyzed
muscle
3. Tilt the head toward each shoulder & look for increase
in deviation [in superior oblique palsy, deviation increases
on tilting the head to the same side as the palsy]
BIELCHOWSKY HEAD TILT TEST

E.g.: In right superior oblique palsy, right hypertropia increases
when head is tilted toward the right shoulder; & disappears
or decreases when head is tilted toward the left shoulder.
MICROTROPIA
– Monofixation syndrome
CAUSES
– Primary
– 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 Δ 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
– 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
– Cyclophoria - torsional deviation
– Over stimulation of convergence with accommodation in
hyperopia → esophoria
– Under stimulation in myopia → exophoria
SYMPTOMS
– Eye strain if deviation ≥ 5-10°
– 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 & 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 - Limited adduction
adduction abduction
- Orthophoria/slight - Orthophoria/slight - Orthophoria/slight
esotropia exotropia 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 TREATMENT IF
– No orthophoria 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, pan-
sinusitis, 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 FDT on elevating globe in adduction
– Ipsilateral head tilt & chin elevation
– Inferior oblique palsy
– Monocular elevation deficit
MOBIUS SYNDROME
CLINICAL FEATURES
Eye
– Horizontal gaze palsy; vertical gaze intact
– Bilateral VI nerve palsy
– Esotropia or orthophoria in primary gaze
– Pseudo-esotropia – in children who learn to cross-fixate
Systemic
– Bilateral facial palsy - asymmetrical, incomplete
• Mask-like facies
• Incomplete lid closure
– IX n and XII n palsy
– Mental retardation, limb anomalies
SUDDEN ONSET DIPLOPIA
CAUSES
– Trauma → blow out fracture; fracture floor of orbit
– Inflammation - superior orbital fissure syndrome, Tolosa
Hunt syndrome, orbital apex syndrome, myositis,
pseudotumor, cellulitis
– Endocrine - thyroid disorders
– Neuromuscular - myasthenia gravis
– Vascular - aneurysm, AV fistula, hypertension, diabetes
– Tumors
• benign – neurofibroma, hemangioma, lymphoma
• malignant – lymphoblastic leukemia
– Parasitic infestations - cysticercosis
– Iatrogenic – following cataract/RD surgery
– Idiopathic → decompensating phorias
– Demyelination → in multiple sclerosis
INVESTIGATIONS
– RBS, Blood pressure
– X-ray skull
– CT scan
– Total count, differential count, ESR
– T3, T4, TSH levels
– Tensilon test
– Carotid angiography
– Eosinophil count
– MRI, CSF analysis
BOTULINUM TOXIN
INDICATIONS
1. Therapeutic -
– Horizontal squint correction
– Upper lid retraction
– Lower lid senile entropion
– Lacrimal gland hypersecretion
– Aberrant VII n regeneration → crocodile tears, Frey’s
syndrome
– Facial dystonias - benign essential blepharospasm,
hemfacial spasm, Meige syndrome
– Chemotarsorrhaphy - done for corneal exposure in
temporary VII n palsy, indolent corneal ulcer or epithelial
defects
– Dry eye syndromes
– Acquired nystagmus
– Oscillopsia
2. Cosmetic -
– Brow lift
– Dynamic facial wrinkles - crow’s feet
3. Other uses -
– Torticollis
– Laryngeal dystonia
– Tics, stuttering, bruxism
– Spastic bladder
ACTION
– At neuromuscular junction, autonomic ganglia, post
ganglionic parasympathetic & sympathetic nerve endings
that release acetylcholine [ACh]
– Decrease release of ACh from pre-synaptic 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 12
Case Taking
EVALUATION OF PROPTOSIS
HISTORY
– Onset, duration & progression of proptosis
– Associated pain; nature of the pain
– Decreased vision
– Diplopia → in which gaze?
– Field defects
– Remissions/exacerbations
– Diurnal variation [painful proptosis worse in the morning
→ Graves’ disease/pseudotumor]
– Trauma
– Fever, upper respiratory tract infection [sinusitis, leukemia]
– Any other cutaneous swellings [neurofibromatosis]
– Epistaxis [nasal communication]
– Dental infection
– Skin lesions [cafe 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 problems - dry skin, excessive sweating
– Neck swelling
– Hand tremors
– Menorrhagia/amenorrhea
– Sleep disturbances
CASE TAKING 367
Past history
– Diabetes [DM] or hypertension [HTN]
– Cardiovascular disease/CNS disorder/respiratory disorder
– Previous ocular disease or surgery
Personal history
– Diet/appetite/bowels/micturition
– Smoking/alcohol intake
Menstrual history
– Amenorrhea
– Menorrhagia
Family history
– Similar complaints in the family
Treatment history
– Remission with steroids or other medication
GENERAL EXAMINATION
– Conscious, coherent, moderately built
– Pallor, icterus, cyanosis, clubbing, lymphadenopathy, pedal
edema [PICCLE]
– Dental & nasal examination
– Thyroid [neck] & breast examination
– Finger/hand tremors
– Skin - dry/scaly; cafe au lait spots
Vital data
– Temperature/BP/respiratory rate/heart rate
Systemic examination
– Heart - sounds; murmurs
– Lung - breath sounds
– Abdomen - hepatosplenomegaly; any masses
OCULAR EXAMINATION
– Best corrected visual acuity for distance & near
– Refraction [high myopes → pseudoproptosis]
– Visual fields, color vision
– Ocular alignment - cover, uncover, alternate cover tests
– Diplopia charting [if present]
– Extraocular movements
– Forced duction [if any movement is restricted]
– IOP; differential IOP; gonioscopy
– Applanation tonometry - check for pulsatile proptosis
– Anterior segment evaluation; especially pupillary reaction
– Fundus — Any signs of optic nerve compression; CRVO;
optic atrophy
PROPTOSIS EVALUATION
– Facial symmetry
– Compensatory head posture
– Lid retraction, bogginess or lid lag
– If ptosis is present - evaluate levator function
INSPECTION
– Naffziger’s sign → on looking tangentially over the patient’s
forehead, palpebrae of the proptosed eye is seen first
– Fullness or mass lesion in the orbit
– Visible pulsations or engorged veins
– Lagophthalmos
– Bell’s phenomenon
– Conjunctival congestion over recti muscles [TRO] diffuse
congestion [vascular anomaly]
– Corneal exposure
– Change in size with Valsalva
CASE TAKING 369
PALPATION
– orbital rim - any irregularity; mass lesion; can you insinuate
your finger between the globe & orbital bones?
– size, shape, surface, margins, skin over swelling, consistency,
signs of inflammation, tenderness, reducibility, motility
– variation with valsalva or bending down of the head
– resistance to retropulsion
– pulsations, thrill
– corneal anesthesia, infraorbital/supraorbital anesthesia
AUSCULTATION
– bruit over lesion/eye ball/ipsilateral forehead
EXOPHTHALMOMETRY
– Reading > 21 mm or a difference of > 2 mm between
the two eyes suggests proptosis
– Reading of 10 - 12 mm suggests enophthalmos
– Hertel’s exophthalmometer reading e.g. Base reading
110 mm; OD 24 mm, OS 20 mm
110 mm
24 mm 20 mm
[OD] [OS]
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] & 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 surgery - under local anesthesia?
– similar complaints in the past
Family history
– others in the family affected
– consanguineous marriage
CASE TAKING 371
OCULAR EXAMINATION
1. Visual acuity for near & distance; without & with correction
is checked, e.g.
D OD 6/12
sc
OS 6/12
[sc = sine correction; without correction]

Visual acuity for distance without correction is 6/12 for
both eyes
N OD N6
cc
OS N6
[cc = cum correction; with correction]
Visual acuity for near with reading addition is N6 for both
eyes
2. Refraction
3. Facial symmetry
4. Compensatory head posture
5. Brow elevation
6. Cover/uncover test, Hirschberg’s corneal reflex, Prism bar
cover test - to test for ocular alignment
7. Extra-ocular movements - full/restricted
8. Lids:
• MRD 1 - margin reflex distance 1 → distance between
upper lid margin & corneal reflection of a pen torch
[patient looking directly at it ] Normal = 4-4.5 mm
• MRD 2 - margin reflex distance 2 → distance between
lower lid margin & corneal reflection of a pen torch
• VFH - vertical fissure height → MRD 1 + MRD 2
Normal: 8-12 mm; Measure in upgaze/ downgaze/
primary gaze
• MCD – margin crease distance - distance between upper

lid margin & lid crease in downgaze; Normal in female
= 10 mm; male = 8 mm
• MLD - margin limbal distance - distance between upper
lid margin & lower limbus in upgaze
• LPS function — place a thumb firmly against patient’s
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 =12-14 mm
– Fair function = 5-11 mm
– Poor function = < 5 mm
• Bell’s phenomenon - present if upward & outward
rotation of the globe occurs on forceful closure of the
lids; if absent - patient may develop post-operative
exposure keratopathy
• Herring reflex → in unilateral ptosis, manually elevate
the ptotic lid & 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 phenomenon - when patient
makes chewing movements with his jaw, the lid
intermittently droops & elevates
• Tests for ocular myasthenia [mentioned under neuro-
ophthalmology]
9. Anterior segment examination
10. Gonioscopy, TOP
11. Fundus examination
CASE TAKING 373
EVALUATION OF CORNEAL ULCER

HISTORY
– onset, duration
– symptoms - pain, watering, discharge
– trauma, fall of foreign body, chemical injury
– viral infection, conjunctivitis
– dry eyes, contact lens wear
– swimming in duly 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 & 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:
• Lids - blepharitis, hordeolum, trichiasis, entropion,
lagophthalmos
• Upper palpebral conjunctiva - giant papillae
• Corneal sensation
• Corneal ulcer - location [central/marginal]; surrounding
edema/infiltrate ; stromal haze; shape & size; margins/
edge/base/floor; satellite lesions; Wessely ring; fluorescein
staining
• Pre-auricular lymphadenopathy
• Anterior chamber reaction; hypopyon
• Pupillary reaction
– Fundus examination
EVALUATION OF GLAUCOMA
HISTORY
– pain, redness, watering
– one/two sided headache or brow ache
– haloes around bulbs; blurred vision
– nausea, vomiting
– use of topical steroids
– trauma
– frequent change of glasses
Family History
– DM/glaucoma/ocular disease
Past History
– similar complaints
– DM/HTN
– ocular surgery; laser
– uveitis
Treatment History
– any medication for glaucoma
– any ocular surgery
OCULAR EXAMINATION
– visual acuity for distance & near; also check with a pin
hole
– refraction
– IOP; gonioscopy
– Visual fields
– Anterior segment examination
Cornea
• epithelial/stromal edema
• pigment on endothelium
• Kruckenberg’s spindle
• pseudoexfoliation [PXF]
CASE TAKING 375
Anterior Chamber
• depth; regularity
• reaction
Iris
• color/pattern
• posterior synechiae
• peripheral anterior synechiae
• NVI
• peripheral iridotomy
Pupil
• size, shape, RAPD
• transillumination defects
• 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
– Central corneal thickness: the thicker the cornea,
applanation tonometry shows a falsely high recording of
IOP
– Visual fields
– GDx, OCT, HRT
EVALUATION OF INCOMITANT 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 &
vomiting [raised ICT]
– nasal symptoms
– defective vision
– tingling & 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 & ENT examination.
CASE TAKING 377
OCULAR EXAMINATION
– Best corrected visual acuity for distance & near;
refraction
– Color vision, visual fields
– Compensatory head posture, facial symmetry
– Lagophthalmos → any facial palsy
– Ocular alignment - Hirschberg corneal reflex, cover/uncover/
alternate cover test, Prism bar cover test, Krimsky test
– Ocular motility - full/restricted
– Diplopia charting
– Forced duction test
– IOP, gonioscopy
– Anterior segment: if ptosis present - evaluate fully
– Posterior segment → any papilloedema?
EVALUATION OF UVEITIS
HISTORY
– onset, duration
– pain, photophobia, redness, watering
– blurred vision, floaters
– trauma
– viral infection e.g. HZO
– 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]
– oro-genital ulcers [Behcet’s 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
– DM/HTN/TB/leprosy
– ocular surgery, previous recurrent attacks
– rheumatoid arthritis, SLE, ankylosing spondylitis
CASE TAKING 379
OCULAR EXAMINATION
– Best corrected visual acuity for distance & near
– Refraction
– IOP, gonioscopy
– Anterior segment examination :
• Conjunctiva - circumciliary congestion
• Sclera - scleritis
• Cornea - keratic precipitates [small/ fine/ white/ stellate/
medium-sized/mutton fat/greasy/inferiorly or throughout
endothelium]; disciform keratitis
• Anterior chamber - cells, flare, hypopyon, hyphema,
peripheral anterior synechiae
• Iris - muddy, loss of crypts, heterochromia iridis, iris
nodules, sector atrophy, new blood vessels
• Pupil - small, reaction to light, posterior synechiae,
occlusion pupillae, seclusio pupillae, NVI, sphincter
atrophy
• Lens - cataract, subluxation
– Posterior segment examination:
• Vitreous cells
• Snow banking, cystoid macular edema
• Choroiditis, vasculitis, papillitis
Index
A Artificial drainage shunts 112

complications 112
Acanthamoeba keratitis 10 implant types 112
clinical features 10 indications 112
investigations 10
treatment 11
Accommodative esotropia 349
B
causes 349 Bacterial keratitis 4
types 349 clinical features 4
Acute retinal necrosis 266 treatment 6
clinical features 266 Basal cell carcinoma 295
complications 266 carcinogenesis 295
investigations 266 clinical features 295
treatment 266 differential diagnosis 296
After cataract (PCO) 229
epidemiology 295
clinical features 229
management 297
complications 229
pathology 296
treatment 229
Allergic types of conjunctivitis 50 risk factors 295
Amblyopia 338 Behcet’s disease 265
classification 338 clinical features 265
diagnosis 339 diagnostic criteria 265
Amniotic membrane graft 53 treatment 265
indications 53 Behcet’s syndrome 69
Anterior ischemic optic neuropathy Blow out fractures of orbit 276
204 clinical features 276
clinical features 204 investigations 277
differential diagnosis 204 management 277
Aphakic glaucoma 97 theories 276
treatment 97 types 276
Argon laser trabeculoplasty 114 Blunt trauma 273
complications 114 Botulinum toxin 362
contraindications 114 action 362
indications 114 complications 363
contraindications 363 Cavernous sinus thrombosis 329
general examination 376 Central retinal artery occlusion 130
history 376 clinical features 130
indications 362 investigations 130
ocular examination 377 pathophysiology 130
Bowen’s disease 303 treatment 131
clinical features 303 Central retinal vein occlusion 127
differential diagnosis 303 management 128
etiology 303 pathogenesis 127
investigations 303 signs 127
treatment 304 Central serous retinopathy 119
types 303 clinical features 119
Branch retinal vein occlusion 129 differential diagnosis 120
clinical features 129 treatment 120
treatment 129 Chalcosis 280
Brown syndrome 359 clinical features 280
causes 359 pathology 280
differential diagnosis 359 Chemical injuries 270
Bullous keratopathy 33 clinical features 270
causes 33 complications 271
symptoms 33 treatment 271
treatment 34 Cherry red spot 132
Buphthalmos 100 Choroidal melanoma 334
clinical features 100 differential diagnosis 334
differential diagnosis 101 pathological classification 334
evaluation 101 treatment 335
pathogenesis 100 Coat’s disease 124
surgical treatment 101 Congenital cataract 343
causes 343
investigations 343
C
types 343
Carotico-cavernous fistula 328 Corneal color coding 2
causes 328 Corneal degenerations 26
clinical features 328 age related 26
pathology 329 band keratopathy 27
Cataract surgery 238 lipid keratopathy 26
indications 238 Salzmann nodular degeneration
pre-op evaluation 238 28
surgeries 238 spheroidal degeneration 28
surgical complications 238 Corneal dystrophies 21
INDEX 383
Corneal transplant 35 pathology 121

contraindications 35 stages 121
indications 35 treatment 122
types 35 Ectopia lentis 231
Corneal vascularization 29 causes 231
etiopathogenesis 29 treatment 232
treatment 29 Ectropion 319
Cyclocryotherapy 186 cicatricial ectropion 319
complications 186 involutional ectropion 319
indications 186 mechanical ectropion 319
procedure 186 paralytic ectropion 319
Cystoid macular edema 117 Ehlers-Danlos syndrome 231
causes 118 Endophthalmitis 143
clinical features 117 causes 143
management 118 clinical features 144
pathophysiology 117 complications 145
management 145
precautionary measures 145
D
Entropion 317
Diabetic retinopathy 134 pathogenesis 317
Kanski’s classification 134 treatment 317
modern ETDRS classification Enucleation 309
134 complications 309
treatment 135 indications 309
Dry eye 57 Epiphora 63
causes 57 Evaluation of glaucoma 374
aqueous tear deficiency 57 Evaluation of incomitant squint
epitheliopathies 58 376
lid abnormalities 58 Evaluation of macular function
lipid abnormalities 58 167
mucin deficiency 57 Evaluation of paralytic squint 355
tests for dry eye 59 Bielchowsky head tilt test 355
treatment 60 diplopia charting 355
Duane syndrome 358 park 3 step test 355
Evaluation of proptosis 366
Evaluation of ptosis 370
E Evaluation of squint 352
Eales disease 121 alternate cover test 352
causes 121 cover test 352
clinical features 122 cover-uncover test 352
differential diagnosis 122 Hirschberg’s test 353
Krimsky test 352 phases 137
prism bar cover test 352 side effects 137
Worth four dot test 353 technique 137
Evaluation of uveitis 378
history 378
G
ocular examination 379
Evisceration 310 Giemsa staining 6
indications 310 Glaucomatocyclitic crisis 90
advantages 310 clinical features 90
disadvantages 310 hypertensive uveitis 90.
Exudative RD 182 treatment 90
Eye in aids 255 Gram’s staining 5
treatment 255
Eye in diabetes mellitus 133 H
Eye in leprosy 250
Hereditary fundus dystrophies 166
Herpes simplex keratitis 14
investigations 251
epithelial keratitis 14
management 250
disciform keratitis 14
treatment 251
stromal necrotic keratitis 15
Eye in leukemia 153
Heterophoria 357
Eye in syphilis 253
symptoms 357
management 254
treatment 357
Eye in tuberculosis 252
Horizontal gaze palsies 224
Horner’s syndrome 193
treatment 252
Hyperlacrimation 63
Hypertensive choroidopathy 141
F clinical features 141
Fleischer ring 17 Hypertensive retinopathy 142
Follicular conjunctivitis 48 Keith-Wagener-Barker classifi-
acute forms 48 cation 142
chronic forms 49 Wagener-Claygibner classifi-
Fourth nerve palsy 216 cation 142
clinical features 216 Scheie classification 142
differential diagnosis 216 Indocyanine green angiography
management 216 140
Fuch’s endothelial dystrophy 23 Infantile esotropia 347
Fuch’s heterochromic uveitis 267 associated findings 347
Fundus fluorescein angiography Inflammatory glaucoma 89
137 treatment 89
INDEX 385
Interstitial keratitis 12 L
causes 12
clinical features 12 Lamellar keratoplasty 40
complications 13 Lasers 183
complications 183
treatment 13
laser effects 183
Intraocular foreign body 278
types 183
classification 278
Lateral orbitotomy 311
Intraocular lenses 237
complications 312
designs 237 indications 311
types 237 Layers of the retina 116
IOL malposition 235 Leucocoria 123
causes 236 differential diagnosis 123
management 236 Licoff’s rule 178
IOL power calculation 241 Limbal stem cell transplant 54
Iridocorneal endothelial syndrome indications 54
102 method 54
pathogenesis 102 Localization of IOFB 281
treatment 102 complications 283
Iris nodules 258 management 283
J M
Jones’ test 64 Macular hole 169
causes 169
K classification 169
Keratoconus 17 Malignant glaucoma 95
differential diagnosis 19 differential diagnosis 96
investigations 18 etiology 95
signs 17
important signs 95
symptoms 17
theories 95
theories 17
treatment 96
treatment 19
Marfan syndrome 232
Keratomycosis 8
causes 8 Masquerade syndromes 268
clinical features 8 Meesmann dystrophy 22
epidemiology 8 Meibomian gland carcinoma 305
investigations 9 differential diagnosis 306
pathogenecity 8 management 306
treatment 9 pathology 305
Microtropia 356 Ocular myasthenia 220
causes 356 clinical features 221
signs 356 differential diagnosis 220
tests 356 epidemiology 220
treatment 356 investigations 221
Mobius syndrome 360 management 222
clinical features 360 pathology 220
Mooren’s ulcer 31 Ocular toxoplasmosis 248
clinical features 31 clinical features 248
etiology 31 complications 248
investigations 32 treatment 249
treatment 32 Ophthalmia neonatorum 55
types 31 Optic atrophy 201
differential diagnosis 203
N etiological classification 202
ophthalmoscopic classification
Nd: YAG laser iridotomy 113 201
indications 113 pathological classification 201
procedure 113 Optic disc drusen 154
complications 113 investigations 155
Needles 239 pathogenesis 154
conventional cutting needle 239 prognosis 155
reverse cutting needle 239 signs 154
round bodied needle 239 Optic nerve glioma 330
Neonatal cloudy cornea 342 Optic nerve meningioma 330
Neovascular glaucoma 91 Optic neuritis 210
causes 91 clinical features 210
classification 92 differential diagnosis 211
clinical features 92 investigations 210
differential diagnosis 91 pathology 210
management 92 treatment 211
pathogenesis 91 Optical coherence tomogram 168
Non-surgical management of Orbital cellulitis 326
squint 351 causes 326
Normo-tensive glaucoma 78 clinical features 326
differential diagnosis 78 treatment 327
treatment 78
Orbital decompression 294
complications 294
O indications 294
Ocular hypertension 79 Orbital pseudotumor 286
treatment 79 clinical features 286
INDEX 387
differential diagnosis 287 Posterior scleritis 70

investigations 287 complications 70
pathology 286 investigations 70
treatment 288 signs 70
types 286 symptoms 70
treatment 70
P Primary angle closure glaucoma 84
Pannus 30 stages 85
differential diagnosis 30 treatment 86
types 30 Primary open angle glaucoma 74
Papilloedema 206 Anderson’s criteria 76
classification 207 disc changes 74
clinical features 207 field defects in glaucoma 75
differential diagnosis 208 pathogenesis 74
etiology 208 provocative tests 77
pathogenesis 206 Proliferative vitreoretinopathy 160
pathology 206 classification 161
treatment 209 pathogenesis 161
Pars planitis 260 risk factors 160
causes 260 treatment 161
clinical features 260 Proptosis 325
differential diagnosis 260 causes 325
Etiopathogenesis 260 Pseudoexfoliation glaucoma 99
signs 261 Pseudoexfoliation syndrome 98
treatment 262 clinical features 98
Pathological myopia 158 pathogenesis 98
pathogenesis 158 Pseudomembranous and mem-
treatment 159 branous conjunctivitis 44
Peripheral retinal degeneration 151 causes 44
degenerative retinoschisis 152 clinical features 44
lattice degeneration 151 treatment 44
snail track degeneration 151 Pseudotumor cerebri 212
Phacolytic glaucoma 94 Pterygium 45
differential diagnosis 94 Ptosis 314
treatment 94 aponeurotic ptosis 315
Phakomatoses 320 blepharophimosis syndrome
Pneumatic retinopexy 156 315
complications 157 classification 314
contraindications 157 evaluation 314
indications 156 simple congenital ptosis 315
Pupil 190 classification according to
Adie’s tonic pupil 191 maturity 227
Argyll Robertson pupil 192 hypermature senile cataract
Marcus Gunn pupil 192 227
paralytic pupil 192 immature senile cataract
toxic pupil 191 227
mature senile cataract 227
morgagnian senile cataract
R 227
Reis-Buckler dystrophy 22 morphological classification
Reiter’s syndrome 69 226
Retinal color coding 187 christmas tree cataract 226
Retinal detachment 177 cortical cataract 226
old RD 178 nuclear cataract 226
rhegmatogenous RD 177 subcapsular cataract 226
signs 177 Siderosis bulbi 279
symptoms 177 clinical features 279
fresh RD 177 treatment 279
Retinoblastoma 331 types 279
clinical features 331 Sixth nerve palsy 217
types 331 causes 217
S
treatment 218
Sarcoidosis 256 Socket reconstruction 313
investigations 257 Spatulated needle 239
treatment 257 Squamous cell carcinoma 299
Schirmer’s test 59 causes 299
Scleritis 68 clinical features 300
classification 68 differential diagnosis 302
clinical features 68 histopathology 301
pathogenesis 68 premalignant lesions 299
Scotoma 103 treatment 302
types 103 types 301
Secondary glaucoma 88 Staphyloma 71
Secondary/complicated cataract complications 72
228 treatment 72
causes 228 types 71
Senile cataract 226 Sturge-Weber syndrome 324
INDEX 389
Sudden onset diplopia 361 Traumatic hyphema 274

investigations 361 grading 274
Superior limbic keratoconjunctivitis treatment 275
52
clinical features 52 U
treatment 52
UGH syndrome 107
causes 107
T
Therapeutic contact lens 24 treatment 107
complications 24 Uveitis 244
uses 24 etiological classification 244
Third nerve palsy 213 investigations 245
causes 213
lab tests 245
non-laboratory tests 246
investigations 214
management 215 V
Thyroid related orbitopathy 289
clinical features 289 Van Herick’s grading 84
pathogenesis 289 Visual acuity testing in 342
pathology 289 preverbal children 342
Tolosa Hunt syndrome 219 verbal children 342
investigations 219 Visual field 104
treatment 219 blind spot 104
Tonography 83 field charting 104
Tonometry 80 kinetic 104
applanation tonometry 80 static 104
digital tonometry 80 field defects 104
indentation tonometry 80 Vitreous hemorrhage 149
Trabeculectomy 108 causes 149
postoperative complications classification 149
108
treatment 108
complications 150
Trachoma 46
clinical features 46 pathogenesis 149
prevention 47 treatment 150
stages 47 Vitreous opacities 164
treatment 47 asymptomatic 164
Tractional RD 181 symptomatic 164
VKH syndrome 263 X
diagnosis criteria 263 Xeroderma pigmentosum 298
differential diagnosis 264 prophylaxis 298
treatment 264 stages 298
Vogt’s striae 17 Xerophthalmia 62
von Hippel-Lindau disease 321 causes 62
treatment 62
W
Z
Wegener’s granulomatosis 69
Weil-Marchesani syndrome 232 Zonular cataract 230
Werner’s classification 290 types 230

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Clinical Ophthalmology

Sirisha Senthil MS FRCS

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

This book is a condensation of information on a wide range

First and foremost, we would like to thank our patients, our

Index .................................................................... 381

CORNEAL COLOR CODING

(For color version see plate 1)

ACID FAST STAINING

Preparation of fortified topical medication

HERPES SIMPLEX KERATITIS

STROMAL NECROTIC KERATITIS

Eye disease caused by Herpes simplex virus

– Munson sign - on looking down, the angular curve is

• Thermokeratoplasty - heat is applied to the tip of the

Epithelial Bowman Stromal Endothelial

1. Map-dot- 1. Lattice (AD)

1. Reis buckler (AD) 1. Ched (AD)

– Cogan microcystic/epithelial basement membrane/map-dot-

– Fuch’s endothelial dystrophy–

THERAPEUTIC CONTACT LENS

COMPLICATIONS OF CONTACT LENS USE

– Yellowish stromal deposits of cholesterol, fats,

Mooren’s ulcer Terrian’s degeneration

TREATMENT OF BULLOUS KERATOPATHY

CONTRAINDICATIONS: (Donor Cornea)

DONOR TISSUE EVALUATION

DONOR CORNEA PRESERVATION

COMPLICATIONS OF PENETRATING KERATOPLASTY

DEEP LAMELLAR KERATOPLASTY

WHO CLASSIFICATION (FISTO)

• Trichiasis - needs electrolysis/surgery

Prevention & Treatment

6. Acute herpetic conjunctivitis

ALLERGIC TYPES OF CONJUNCTIVITIS

SUPERIOR LIMBIC KERATOCONJUNCTIVITIS

AMNIOTIC MEMBRANE GRAFT

LIMBAL STEM CELL TRANSPLANT

3.C. trachomatis inclusion conjunctivitis

4. Herpes simplex virus conjunctivitis

Causes of dry eye

TESTS FOR DRY EYE

– Measure the zone of lysis

Causes for Epiphora

– Hard stop → NLD block

– A drop of fluorescein is instilled into conjunctival

(a) Test is positive - no block

ASSOCIATED SYSTEMIC DISEASE

NECROTISING SCLERITIS WITH INFLAMMATION

PRIMARY OPEN ANGLE GLAUCOMA

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

5. Superficial disc hemorrhages at disc margin (splinter

FIELD DEFECTS IN GLAUCOMA

NORMO -TENSIVE GLAUCOMA

Ocular Hypertension Treatment Study

HOW TO TEST CALIBRATION OF

– Remove the calibration rod from its box.

– Replace the rod in its bracket in the tonometer receptacle;

PRIMARY ANGLE CLOSURE GLAUCOMA

ANATOMICALLY PREDISPOSING FACTORS

VAN HERICK’S GRADING

5. Chronic angle closure glaucoma

IRIDOCORNEAL ENDOTHELIAL SYNDROME